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Dr. David A. Mugford
Dr. Tassos Sfondouris
1660 Village Green
Crofton, MD 21114
Call Us: (410) 260-0790
Sleep Apnea in Crofton, MD
Everyone has the occasional bad night of sleep. However, for millions of Americans, every night is a bad night of sleep. No matter what you do, you wake up morning after morning feeling completely exhausted, like you never went to sleep in the first place. This is a condition known as sleep apnea. With diagnosis and proper treatment, your sleep quality, and quality of life can be restored. The Mugford Center is here to help.
What is Sleep Apnea?
When you have sleep apnea, your breathing is interrupted for several seconds several times while you sleep. When you stop breathing, you wake up, even if you are unaware of it. This disrupts your sleep cycles, forcing you to restart them all over again each time. Not only does sleep apnea impact your sleep, leaving you exhausted, it can also affect your mental and physical health as well.
Sleep apnea is a condition that affects how you breathe when sleeping. During sleep, normal breathing can be interrupted for 10 seconds or more hundreds of times during a single night. Untreated sleep apnea prevents you from getting enough deep, restorative sleep. Without enough deep sleep you may be sleepy, lack mental sharpness and be less productive. Long term health effects can be serious, including weight gain, high blood pressure, heart disease and diabetes.
What are the Causes and Symptoms of Sleep Apnea?
In order to diagnose sleep apnea, you should schedule a consultation with Dr. Mugford.
Sleep Apnea Causes
There are three different types of sleep apnea, obstructive sleep apnea, central sleep apnea, and mixed sleep apnea. Mixed sleep apnea, also called complex sleep apnea syndrome, is a mixture of obstructive sleep apnea and central sleep apnea.
Obstructive sleep apnea is the most common type of sleep apnea. This particular type of sleep apnea occurs when your airway becomes blocked, either by your tongue or other intraoral tissues. When your airway is blocked by these tissues, it can interfere with your breathing.
Sleep Apnea Symptoms
• Loud, chronic snoring
• Insomnia
• Breathing pauses for long periods
• Waking up often at night
• Forgetfulness, irritability, depression
Read more about sleep apnea causes and symptoms
How is Sleep Apnea Diagnoses and Treated?
Sleep Apnea Diagnosis
Diagnosing sleep apnea is typically done through a sleep study, which is performed in a sleep clinic. During your sleep study, which is called a polysomnogram, you are attached to machines that monitor and record different information while you sleep. Your heart rate, breathing, brain activities, blood oxygen levels, and the movements of your arms and legs are all monitored. After your sleep study is complete, the next day, the recorded information is read by a sleep specialist, who can interpret the results and diagnose sleep apnea or other sleep-related issues and prescribe you with appropriate treatment.
Sleep Apnea Treatment
There are a number of different treatments that may be recommended for sleep apnea.
• Specialist: Talk to a doctor trained in sleep apnea. Come visit Dr. Mugford today to start the process.
• Oxygen Aid: Use supplemental oxygen while sleeping. This will help treat the symptoms, but it may not address any underlying issues.
• C-PAP Machine: A C-PAP (Continuous Positive Airflow Pressure) machine is a machine that delivers a constant flow of air through a small mask that is worn over your nose. This helps to keep your airway open while you sleep.
• Oral Appliance: This treatment involves the use of a custom fit guard similar to a mouth guard that is worn while you sleep. These oral appliances, made by Dr. Mugford's office, help your airway to stay open by keeping your lower jaw forward and preventing soft tissues from falling into your airway.
• Oral Surgery: In some cases, surgery may be required. There are a few different types of procedures that may be performed, including removing excess oral tissue or moving your lower jaw forward.
Read more about sleep apnea diagnosis and treatment
What are the Types of Sleep Apnea?
1.
Obstructive Sleep Apnea
Obstructive sleep apnea, commonly abbreviated as OSA, is the most common type of sleep apnea. This particular sleep apnea is caused by a partial or full blockage of your airway.
2.
Central Sleep Apnea
Central sleep apnea, or CSA, is a type of sleep apnea that is much less common than OSA. It occurs when your brain temporarily fails to signal to the muscles that control your breathing that you need to breathe.
3.
Complex Sleep Apnea Syndrome
Complex sleep apnea syndrome, also referred to as mixed sleep apnea, is a type of sleep apnea that is a mix of both obstructive and central sleep apnea.
Read more about sleep apnea types
Schedule Your Sleep Apnea Consultation Today
The proper diagnosis and treatment of sleep apnea can help you to get the sleep you need, restoring your quality of life. For more information or to schedule your consultation, call The Mugford Center today at (410) 260-0790. We can help identify and diagnose the severity of the sleep apnea and discuss the best treatment options for your unique situation. For more information about our practice, see our office information page.
Location
1660 Village Green
Crofton, MD 21114
Call Us
(410) 260-0790
Connect with Us
Office Hours
Monday: 8:00am – 5:00pm
Tuesday: 8:00am – 5:00pm
Wednesday: 8:00am – 5:00pm
Thursday: 8:00am – 5:00pm
Friday: 8:00am – 5:00pm
Saturday: Closed
Sunday: Closed
Copyright © 2015-2019 David A. Mugford, DMD PA and WEO MEDIA. All rights reserved. Sitemap | Links
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4,207,630,300,027,005,400 | Skip to main content
Supporting parents of preschool children in adopting a healthy lifestyle
Abstract
Background
Childhood obesity is a public health epidemic. In Canada 21.5% of children aged 2–5 are overweight, with psychological and physical consequences for the child and economic consequences for society. Parents often do not view their children as overweight. One way to prevent overweight is to adopt a healthy lifestyle (HL). Nurses with direct access to young families could assess overweight and support parents in adopting HL. But what is the best way to support them if they do not view their child as overweight? A better understanding of parents’ representation of children’s overweight might guide the development of solutions tailored to their needs.
Methods/design
This study uses an action research design, a participatory approach mobilizing all stakeholders around a problem to be solved. The general objective is to identify, with nurses working with families, ways to promote HL among parents of preschoolers. Specific objectives are to: 1) describe the prevalence of overweight in preschoolers at vaccination time; 2) describe the representation of overweight and HL, as reported by preschoolers’ parents; 3) explore the views of nurses working with young families regarding possible solutions that could become a clinical tool to promote HL; and 4) try to identify a direction concerning the proposed strategies that could be used by nurses working with this population. First, an epidemiological study will be conducted in vaccination clinics: 288 4–5-year-olds will be weighed and measured. Next, semi-structured interviews will be conducted with 20 parents to describe their representation of HL and their child’s weight. Based on the results from these two steps, by means of a focus group nurses will identify possible strategies to the problem. Finally, focus groups of parents, then nurses and finally experts will give their opinions of these strategies in order to find a direction for these strategies. Descriptive and correlational statistical analyses will be done on the quantitative survey data using SPSS. Qualitative data will be analyzed using Huberman and Miles’ (2003) approach. NVivo will be used for the analysis and data management.
Discussion
The anticipated benefits of this rigorous approach will be to identify and develop potential intervention strategies in partnership with preschoolers’ parents and produce a clinical tool reflecting the views of parents and nurses working with preschoolers’ parents.
Peer Review reports
Introduction
The focus of this study is the promotion of a healthy lifestyle from an early age to prevent increasing overweight in preschool children. This proposal first outlines the background, the study goals and objectives, and the literature review. The literature concerns overweight in preschool children and associated factors, parents’ perception of their child’s weight and current efforts to promote a healthy lifestyle in young children. The proposal then describes the research design and setting, the sampling, data collection and analysis strategies. Finally, ethical considerations and anticipated benefits are discussed.
Background
Childhood obesity is a public health epidemic; 22 million children under the age of 5 are affected [1]. In Canada 21.5% of children aged 2–5 years [2] and 13.5% of four-year-olds in Quebec (Canada) are overweight [3]. The prevalence doubled between 1978 and 2005. Though self-reported data suggests a more recent stabilization in prevalence, Lamontagne and Hamel [4] caution against over-confidence in this trend because of the social-desirability bias of self-reported data. Although many factors are involved, lifestyle is at the heart of the problem. In the first years of life, parents play a leading role in the development of a healthy lifestyle [57].
Lifestyle and thus modifiable factors associated with overweight in preschool children include frequent consumption of sweetened beverages [8], high-calorie processed foods [9], dietary restrictions [10, 11], hours of sleep [12], physical inactivity, and hours spent in front of a screen [13]. So it is not surprising that prevention efforts focus on adopting a healthy lifestyle, namely a healthy diet and increased physical activity [14].
In 2006 Quebec adopted a six-year action plan to promote healthy lifestyles and prevent weight-related problems in children [6]. Priorities include promoting a healthy diet and physically active lifestyle. The plan is aimed at various authorities, including daycare and early childhood educational services, but no direct action with families is envisaged nor have strategies to promote healthy lifestyles in families been defined. One of the objectives of the Quebec program “Integrated perinatal and early childhood services for families living in vulnerable situations” is to improve family lifestyles. However, this program is aimed at a specific group and not the entire population [15]. The vulnerable target population presents health risks such as substance abuse, alcoholism and violence.
The preschool period is a good time to act. This is confirmed by longitudinal studies on the growth curve. The aim is to delay the adiposity rebounda since if it occurs early (before age 6), the risk of being overweight later increases [1618].aThe results of a study by Nader et al. [16] indicate that if a child is overweight at age 5, i.e. has a BMI >85th percentile, he/she is five times more likely to be overweight at age 12. However, normal changes in body form and structure at this age [19], complicate accurate perception of overweight.
Being overweight has serious consequences: children can develop low self-esteem and be socially isolated [20] and have a poor self-image as young as age 5 [21]. They also are at risk of cardiovascular disease, modification of the lipid profile, sleep apnea, hypertension and type 2 diabetes in adulthood [22]. Economically, obesity costs the Canadian health care system about $4.3 billion in 2000–2001 [23].
Despite the consequences of overweight for the child and for society, few parents view their children as overweight [24, 25]. Few studies have attempted to do an in-depth analysis of the reasons for this erroneous view. The representation of childhood overweight and a healthy lifestyle from the parents’ point of view, which has received little or no attention to date, could shed light on the reasons for this misperception. Representation consists of beliefs, attitudes, opinions and knowledge about something [26]. Thus it guides the actions of parents and, in this case, behaviours and lifestyles of children.
In Quebec, nurses regularly see children for vaccinations and other services prior to school entry. These contacts present an opportunity to take action in early childhood. But how can nurses support families in adopting healthy habits? To answer this question, we have designed an action research study involving nurses, parents and experts to identify the views of parents and healthcare professionals regarding the promotion of a healthy lifestyle and to develop clinical tools based on new knowledge derived from the description of the parents’ representation.
Relevance of the study
Currently, in the absence of systematic interventions to promote a healthy lifestyle among parents of preschoolers, it is imperative for nurses to understand the parents’ point of view in order to provide them with adequate support. The relevance of this study is that it is important to understand the representation of overweight and healthy lifestyles among preschoolers’ parents in order to intervene early and meet their needs effectively. This study is justified because these elements must be clarified in order to tailor interventions to promote healthy lifestyles accordingly. Moreover, the development of healthy lifestyles, healthy development in childhood and the health services available are three determinants of health that need to be targeted to prevent overweight in Canada [7]. Developing a clinical tool for public health nurses will facilitate the provision of evidence-based services and is likely to improve the quality of services. Professional practices will be relevant and based on the viewpoint of parents as key players in adopting healthy lifestyles for their children and helping to address overweight, which is a serious public health problem.
Study goals and objectives
The aim of the study is to identify, with nurses working with families, possible solutions to promote healthy lifestyles among parents of preschool children after exploring parents’ representation of overweight and healthy lifestyles in preschoolers. The specific objectives are to: 1) document the current situation (estimate the prevalence of overweight and describe the associated factors) in preschool children attending a vaccination clinic in a region of Quebec, Canada, 2) describe the representation of overweight and health lifestyles according to parents of preschoolers, 3) explore the viewpoint of nurses working with young families concerning possible interventions that could be used to develop a clinical tool to promote healthy lifestyles, and 4) achieve a direction on which strategies to promote and which of the proposed strategies to prioritize.
Literature review
We present current knowledge concerning the issue of overweight in preschool children, specifically: the etiology of overweight and known associated factors, the importance of acting in early childhood and the parents’ perception and representation of this issue. Finally, current health promotion efforts to address overweight in children and the conceptual framework used for this research will be presented and justified.
Etiology of overweight and associated factors
For the purpose of this study, the term ‘overweight’ includes both excess weight and obesity, which are measured by body mass index (BMI). bIn adults, a BMI of 25 to 30 indicates overweight, and over 30, obesity. In children, three BMI cut-points have been proposed by CDC [27], WHO [28] and IOTF [29], respectively. For the CDC, BMI percentiles classify children as overweight (BMI >85th) and obese (BMI ≥95th). The WHO uses the z-score of BMI-for-age, with children classified as overweight with a BMI between one and two standard deviations (SD) above the mean and as obese with more than two SD above the mean. This translates to overweight as a BMI >84th and obese as a BMI >97.7th percentile. To obtain accurate baseline values, the IOTF defined BMI thresholds that take the child’s age and sex into account. For IOTF, a child is considered overweight with a BMI ≥91th and obese with a BMI ≥99th percentile for their age-sex referent. The IOTF criteria constitute an international definition of childhood overweight. The reference values are based on data obtained from six different countries. This definition makes it possible to assess the prevalence of overweight and compare it to other studies because it was developed specifically for international comparaison.
Etiologically, overweight occurs when calorie intake—the amount of energy consumed–exceeds caloric expenditure over a long period of time [30, 31]. In North America, restaurant portions for children are 24% larger than necessary [32], convenience food is high in calories [33] and children consume large amounts of sweetened beverages [8, 34]. The availability of ready-to-eat food in grocery stores and ‘fast food’ restaurants contribute to changes in families’ eating habits [9]. As for energy expenditure, a sedentary lifestyle, time spent in front of a screen [13, 35, 36] and the presence of a screen (television or monitor) in the child’s bedroom all contribute to weight gain [37].
Other parental factors increase the risk of the child being overweight: a) one or both parents being overweight leads to a 50% or 70% higher risk respectively [38]; b) low family income makes it difficult to afford healthy food [39]; c) mother not having completed high school [13]; and d) dietary restrictions (forbidden fruit is always more attractive) [10, 11]. Also, the risk is higher in preschool children who sleep less than 10 hours per night [12].
Acting early in childhood to promote healthy lifestyles
As mentioned earlier, if the adiposity rebound occurs before age 6, the risk of later obesity is high compared to an adiposity rebound occurring after age 6 [1618]. Because of this, it is important to act early. In a study by Canning, Courage and Frizzell [40] involving 4161 children from three to five years old, the results show that it is important to take action as young as age 3 since one in four children is overweight by the age of 3½. Knowing that young children can be influenced by the food environment of the adults around them, this factor must be considered when considering the best time to intervene [41]. When the child is young, the family is the place to develop healthy behaviors [5], hence the importance of supporting parents in adopting healthy lifestyles when their children are very young.
Parents’ perception of their child’s weight
Quantitative studies on perception identified in the literature aim to determine if parents are aware of their child’s weight. Six studies, published in English or French, concerning preschool children were published between 2003 and 2010 are presented. Table1 summarizes the main findings of these studies.
Table 1 Parental perception of child’s weight
Despite differences in the children’s age, target populations and slight variations in how weight perceptions were measured, all of the studies found that the parents did not view their overweight child as having excess weight. The study by Maynard, Galuska, Blanck and Serdula [43] and Manios et al. [42] are the only two with a representative sample of the population nationally. The other studies shown in Table1 looked at samples from a program for underprivileged children in which overweight is more pronounced. Only four of the five studies concerned preschoolers only.
Parents’ representation of overweight and lifestyle
Parents’ representation of overweight could partly explain why they do not see it, which could in turn guide efforts to promote healthy lifestyles. Many authors have studied the concept of representation [4652]. Representation is a mental activity by which a group reconstitutes the reality before it and attributes a meaning to it [46]. Abric [26] proposes an operational definition that is the sum of opinions, attitudes, beliefs and knowledge about a specific situation. Also, the representation guides behavior and is a precursor to taking action [46].
There are no studies on parents’ representation of overweight and healthy lifestyles in preschool children; there are a few studies on the representation of food. However, Pelicand and Doumont [53] identified 50 exclusively or partly qualitative studies on the perception of the child’s weight to shed some light, from interview transcripts, on representation. Among the factors identified was a belief that obesity is less important than other health risks like passive smoking [54] and that overweight is a medical problem when the child cannot participate in physical activities with peers [55]. Moreover, according to some parents, overweight children are “big and strong” and a “big baby” is a sign of good health and good parenting [43]. The younger the child, the more overweight is made light of by mothers, believing that the child will inevitably grow and overweight will disappear [55]. Other parents think that weight and height are preprogrammed and thus impossible to change [55]. These aspects are interesting but cannot be used to comprehensively identify parents’ representation of overweight and healthy lifestyles in children. A description of opinions, attitudes, beliefs and knowledge, i.e. a comprehensive representation of overweight and healthy lifestyles, could help to understand why parents see little or no overweight when it is present in their child. This knowledge could also help guide current efforts to promote healthy lifestyles in parents of young children.
Interventions to promote healthy lifestyles and prevent overweight in children
The aim of the meta-analysis by Flynn et al. [56] was to identify programs advocating obesity prevention best practices. A total of 147 programs were found and 26% were considered feasible, useful and effective. The best practices identified were those targeting the school population and including a BMI assessment, identification of chronic disease risk factors and participants’ involvement in physical activities. One of the findings was a lack of programs for children up to age 5 and widely-varying practices. A limitation of this meta-analysis was the broad inclusion criteria for programs making them difficult to compare in terms of effectiveness because of their different designs and measures. Summerbell et al. [57] also did a meta-analysis of 22 randomized studies to measure the impact of interventions addressing diet or physical activity or a combination of the two in children. The results show that the studies on interventions are rarely conclusive and that it is difficult to compare results because of differing designs, interventions and measures. Of the studies identified by these two meta-analyses, two specifically targeted preschool children and give an insight into possible overweight prevention interventions.
The first study by Harvey, Berino and Rouke [58] was a randomized clinical trial with 43 mothers of two-year-olds aimed at determining the effectiveness of helping immigrant parents to reduce obesity. In-home meetings provided education on diet and physical activity. The focus for the intervention was to improve parenting skills to develop appropriate eating and exercise behaviors to prevent obesity. The results showed a 0.27 decline in the mothers’ BMI and a commitment to monitor their child’s food intake. In this study, the randomization of the sample was not specified, only mothers with a BMI ≥25 were included and the majority of the mothers were Native American, which limits the generalizability of the results. In the second study by Dennison, Russo, Burdick and Jenkins [59] involving 83 mother/child dyads, the aim was to develop and evaluate an intervention to reduce television viewing time. The intervention programme consisted of 39 weeks of 1-hour sessions, including 32 sessions on healthy eating and seven sessions to encourage reduction of TV viewing for both parents and children. The stratified randomized clinical trial showed that the children reduced their television viewing time but actual times were not measured; parental estimates of the child’s sedentary activity in previous week were lower than before the intervention. Knowing that the time spent in front of a screen reduces the time spent on physical activities, the results seem interesting. However, the impact on weight was not presented. In summary, the results of intervention studies are inconclusive and few of them looked at preschool children.
Despite none or minimal impact on weight, these studies demonstrate short and medium-term changes in health habits, notably in better food choices, increased physical activity and less sedentary behavior. Identifying appropriate strategies and interventions for successful health promotion requires a precise definition of the problem, identification of the target group (parents and professionals), and the influencing factors (home environment) [60].
Thus, the evidence of interventions to reduce childhood overweight is inconclusive. With this study, we hope to establish a foundation for designing a future intervention based on the ecologic model, that will also take into account the evidences actually published. To that end, we are taking into consideration the points of view of the major determinant of the child environment, the parent. Understanding what influences the parent’s representation of overweight will help design interventions adapted to the stages of change. We also target clinicians who come into predictable and regular encounters with the parent during the preschool period. Exploring the viewpoint and engaging clinicians and local decision-makers will outline the scope of influence and action they can exert, especially in targeting actions or communication that take into account parental representation of overweight. Finally, we will consider experts opinion on the subject to encompass a broader scope of potential strategies to better support parents in promoting healthy lifestyles for their children.
Conceptual framework
In view of the findings regarding parents’ misperception of overweight in their preschool children, the fundamental role that parents play in the adoption of children’s healthy lifestyles and interventions that primarily target a change in behavior by the adoption of healthy lifestyles, the conceptual framework used for this study is the Transtheoretical Model [61]. This is a model used to change behaviors [62]. According to the Transtheoretical Model, behavioral change takes place through five stages, allowing us to understand when changes in thoughts, intentions, attitudes or behaviors occur [63]. The stages in the model are outlined in Table2. This model has also been used in interventions with families. For example, Weiss [64] based the therapeutic education of asthmatic children and their families on this model.
Table 2 Stages of the transtheoretical model
From the literature review, it appears that interventions promoting healthy lifestyles with parents of young children are more likely to reach a population aware of the overweight issue (stages 3 and 4) because they see a problem that concerns them. The interventions, aimed at adopting a healthy diet or doing physical activity, correspond to changes in behavior that require first an intention to act with regard to the problem perceived as important and representing a definite risk for the child. If parents do not view their child as being overweight, why would they intend to change their lifestyle? Thus there is an incompatibility between the stage many parents are at and the stage targeted by interventions. Given that most parents are at stages 1 and 2 with respect to their children’s overweight, it is vital to understand parents’ representation of overweight and healthy lifestyles in preschool children in order to develop strategies to promote healthy lifestyles and raise awareness (stages 1 and 2) by clarifying parents’ beliefs, attitudes, opinions and knowledge.
Nonetheless, promotion of health lifestyles much take into account the environment in which parents and their children adopt health behaviours. Thus, the ecologic model of Bronfenbrenner (1979) will be used as the conceptual background in order to consider the different elements to be considered in the design of interventions to promote adoption of healthy behaviours. So, the Transtheoretical Model will allow health professionals to adapt interventions to the stage of change and of motivation of the parent, integrating both parents’ representation of child overweight and knowledge coming from the literature. The ecological model will allow intervention on obesogenic environment which parents sometimes inadvertently create.
Method
Research design
The action research design is a systematic and participatory investigation approach based on the pragmatic-interpretative paradigm [65, 66]. This design, through cycles or loops, helps to understand problems and formulate actions directed towards problem-solving [67]. The ultimate aim, objectives and orientations are based on discussion and negotiation with the participants. The researcher takes a participatory attitude to achieve real cooperation [67]. The type of action research proposed by Stringer and Genat [67] targets reflexive professional practice aimed at empowering professional groups to defend clients’ interests. Thus the focus is on the professional who defines the problem based on his/her own practice. The change targets professional practice and the solutions emerging from the professionals and target population. In this study, nurses working with preschool children try to determine possible interventions to promote healthy lifestyles among parents of preschool children to prevent increasing overweight.
In the present action research four cycles (loops) are proposed. Each loop meets a study objective and is composed of a reflection phase and an action phase. Each loop will be described in terms of the methodological approach, sampling strategy and data collection and analysis methods. First, however, the research setting is described.
Research setting
For this study the research team consists of two professors and a doctoral student. Throughout the study, an advisory committee of stakeholders in the region where the study is conducted will contribute at various steps in the study. The committee members will monitor the study and participate in the thinking regarding its objectives. They come from the local health and social services agency, network of daycare centres, CSSS, the municipality and parents.
The intervention area is a region in the province of Quebec, Canada. The population of this region was 43,953 in 2008 and included 6006 children up to 14 years of age [68]. The preschool vaccination clinics reach many families in both urban and rural areas.
Awareness of overweight in preschoolers (loop 1)
As the starting point for the study, the nurses participating in the study want to know more about overweight in their preschool population. The first step will be to conduct a prevalence survey. This will provide the participating nurses and researchers with a profile of the population served to initiate thinking and discussions of the study issue. Descriptive quantitative data will be collected to document the situation by estimating the prevalence of overweight and describe the known risk factors.
Sample (loop 1)
The study population will be composed of preschoolers who came to vaccination clinics in 2010. The probabilistic sample will comprise 288 consecutive children, for a 95% confidence level, a 5% margin of error and a prevalence that could go up to 25%. The 25% estimate will provide sufficient statistical power. The sample will be created with the consent of the nurses working in the vaccination clinics.
Data collection (loop 1)
The variable of interest is childhood overweight (BMI) for which the reference values used will be those developed by Cole et al. [29]. The following variables will be described: the child’s age, sex, health problems and medications, the family’s postal code (socioeconomic level), the parents’ education, and the height and weight (self-declared) of the parent bringing the child to the vaccination clinic. Data will be collected with a self-administered questionnaire developed specifically for the study, which will be cognitively tested with ten parents to ensure the clarity of the questions, visual presentation and time required to complete it. It will be anonymous and a consent form will be given and explained to parents prior to the questionnaire. At the vaccination clinic, the student-researcher will measure the child’s height and weight and enter this information on the questionnaire, together with the age and sex. She will then give the questionnaire to the parent. At this point, the parent can decide to complete the questionnaire or not. It is expected to take five minutes. A subsection of the questionnaire will invite the parent to voluntarily provide contact information to participate in an interview or focus group in the later loops in the study. After completion, the questionnaire will be left at a specified place.
Description of parents’ representation of overweight and lifestyle (loop 2)
For loops 2, 3 and 4, an inductive qualitative approach will be used to explore the views of parents, nurses, and experts. The qualitative approach has the advantage of describing in depth important social aspects relating to a situation [69]. This approach will also encourage nurses to participate in the search for intervention strategies to promote healthy lifestyles adapted to both the parents’ needs and the situation at the clinic. Throughout these loops, the researcher will keep a log documenting the views of the student researcher and the effect of the site on the student.
Loop 2 will start with presenting to the participant nurses the results obtained in loop 1, namely the population profile. Then discussions will take place between the nurses and student researcher concerning the information required from parents to continue the reflection. The objective of loop 2 is to describe the representation of parents of preschool children of overweight and healthy lifestyles of children in this age group. The representation will be constructed from parents’ beliefs, opinions, attitudes, knowledge and perceptions about their preschool child’s weight and life habits. This information will give the nurses and researchers a better understanding of the parents’ views and help them reflect on possible strategies to facilitate the promotion of healthy lifestyles with parents of preschool children.
Sample (loop 2)
The study population is composed of parents of four- and five-year-olds who come to the preschool vaccination clinic. The purposive sample will be created on the basis of the BMI calculated from Cole et al.’s [29]reference values. The sample will include 20 parents (key informants) of a normal weight or overweight child who, on the questionnaire completed in the previous step, agreed to be contacted for the next step in the study. The inclusion criteria will be having completed the questionnaire in loop 1 and understanding French. Parents of children with health problems (e.g. Trisomy 21) or taking medication that can affect weight (e.g. corticosteroids) will be excluded from this part of the study. Taking into account factors associated with overweight identified in loop 1 will ensure maximum variability when selecting the loop 2 participants.
Data collection (loop 2)
Data will be collected in two semi-structured interviews, conducted with the help of an evolving guide. The interviews will explore the concept of the representation of overweight and lifestyles from the parents’ viewpoint. The first will last about 60 minutes and the second 30 minutes. For the interviews, the researchers have developed an interview guide based on the literature on representation, overweight and healthy lifestyles. The guide will be added to, improved and modified following the discussions with the advisory committee and nurses during the presentation of the results from loop 1 and in the light of findings from the literature. A few examples of questions in the guide are as follows: What words or images come to mind when you think about the lifestyles and weight of four- and five-year-old children? Talk to me about children’s weight and lifestyles. Four- and five-year-old children can be overweight—What do you think about that? What challenges do parents face concerning lifestyles?
The procedure will consist of a first telephone call to the parents to explain the objective of this loop, answer their questions, obtain their consent and make an appointment. The consent form will be read and signed before the first interview. The second in-depth interview will take place three to five weeks after the first and serves to specify the researchers’ understanding of the first interview and to explore in-depth some additional issues. A summary of the previous interview will be sent to the parent before the second interview. All interviews will be recorded and transcribed. Data will be considered saturated when there is data redundancy and no new information is identified [69, 70].
Search for possible solutions to promote healthy lifestyles (loop 3)
The objective of this loop is to explore the views of nurses working with young families concerning possible strategies to develop a clinical tool to promote healthy lifestyles based on the results from the previous loop. The search for interventions will be affected by the results obtained concerning the parents’ views on the representation of overweight and healthy lifestyles, the conceptual framework (transtheoretical model) and relevant literature.
Sample (loop 3)
The sample will consist of 9 participating nurses working with the target population. As participants, the nurses and researchers will work together to identify possible interventions adapted to the population’s needs.
Data collection (loop 3)
The data will be collected through a focus group discussion, using a guide designed for this purpose. The aim of the questions will be to document the nurses’ views of the results from loop 2. First, a meeting will be held with the nurses to present the objective of this third loop and give them a consent form. They will be given a week to complete and return the consent form by mail to the student researcher. The focus group is an approach that has a flexible structure, is quick and inexpensive and is aimed at developing a consensus. The focus group will be held with a facilitator and an observer. The facilitator will ask questions, encourage participation [71] and manage the order of speaking and dominant members [72]. The observer will take notes, verify the content discussed and clarify certain elements. The meeting will last 2 hours and the discussion will be recorded and transcribed.
Search for direction concerning the proposed strategies (loop 4)
The objective of this last loop is to guide the choice of potential solutions stemming from the work done in the previous loop with the nurses. The solutions will be discussed with the nurses themselves, parents and experts.
Sample (loop 4)
Three purposive groups will be formed. The first group will consist of six parents of preschool children, the second group will involve nine participating nurses working with the target population, and the third will consist of six advisors who have agreed to act as experts (a pediatrician, nutritionist, nurse, community health worker, endocrinologist, other researchers)
Data collection (loop 4)
This loop involves three phases. First, a focus group discussion with seven parents will obtain their views regarding the proposed strategies. Second, a focus group discussion with ten nurses will gather obtain their views regarding the proposed solutions. Both focus groups will be held with a facilitator and an observer. They will last 60 to 90 minutes and the discussions will be recorded and transcribed. Informed consent will be obtained from the participants (parents and nurses) before the meetings. From both groups we will identify strategies, privileging those that emerge independently from both groups and those that the nurses are confident they can implement. Third, a postal questionnaire including open-ended questions will be sent to the seven experts asking for their opinion regarding the possible strategies suggested by the parents, nurses and researchers. The experts will be requested to rank the suggested strategies by expected impact and relevance. This loop with identify a small number of strategies that will be form the starting point of a subsequent intervention study.
Data analysis (loops 1, 2, 3 and 4)
The statistical analyses of the data from loop 1 will provide a prevalence estimate, i.e., percentage of children of normal and overweight (excess weight and obese). SPSS software will be used.
For qualitative data, recorded sessions will be transcribed and analyzed using Huberman & Miles [73] method. For loop 2, parental representation, the data will be condensed using a preliminary analysis grid with various categories, based on predetermined categories that emerged from the literature review, to which emerging categories will be added. The data will be regrouped according to common characteristics of elements in the content and the four representation attributes (beliefs, attitudes, opinions and knowledge). Two researchers will code the data, which will be presented using matrices based on conceptual groupings. The analysis process will start by listening to the interviews, then coding the content of the interviews. The analysis grid will be refined throughout the process because the data from loop 2 will be analyzed concurrently with the interviews. Finally after reviewing the categories and coding and discussions with the advisory committee, the determination of a final categorization can be completed. The same process will be used for focus group discussions in loops 3 and 4. During the analysis process, there will be regular discussions with the research team. Then, based on the data analyzed, literature review and views of the experts, strategies to promote healthy lifestyles (solutions considered) can be proposed. The qualitative data will be managed with NVivo software.
Rigor of the research process
Throughout the action research, rigorous methodological standards will be met. Credibility, which is the correspondence between the participants’ constructions and the reconstructions formulated, will be achieved by an iterative process between researchers, parents and nurses. In addition, triangulation of data sources (parents, professionals, experts and literature) and triangulation of researchers will ensure better correspondence between the results and field data. Data will be co-analyzed including a reflexive stance and there will be frequent team discussions. Finally, recording and transcribing the individual interviews and focus groups will make it possible to confirm the findings by independent analysis. The context, participants’ characteristics and results will be detailed in depth, which facilitates transferability. To ensure reliability, i.e., taking into account the evolution of the phenomenon, a lot of time will be spent in the field and discussions with the advisory committee will be held throughout the study [69]. A logbook will be kept and an observer will attend the focus groups in order to keep track of the contextual aspects.
Ethical considerations
The study was approved by the research ethics boards of the Centre hospitalier universitaire de Sherbrooke (CHUS) and Université de Sherbrooke and the Centre de Santé et des Services sociaux (CSSS) Rivière-du-Nord/Nord de Mirabel. Parents and nurses will be asked to sign free and informed consent forms before each data collection. Parents and nurses will be able to withdraw from the study at any time without prejudice. Anonymity will be preserved for those parents who do not wish to be contacted again, and no nominative information will be retained. Confidentiality will be safeguarded in the usual way, such as by keeping the data under lock and key for 5 years, with access restricted to the research team.
The main ethical issues in this study relate to stigmatization of the child and culpability of the parent. Preschool children are a vulnerable group. It will not be possible to identify them (the questionnaire in loop 1 does not ask for children’s names), which reduces the risk of being stigmatized. Also, to reduce the risk of stigmatization, we will ask the parents for permission to weigh and measure all the children, regardless of their apparent weight, for the study. The risk of stigmatization arises later in the lives of children who are overweight for a significant period of time. The parents of children of both normal and overweight will be interviewed, which will minimize the culpability aspect potentially related to the subject of the study. Precautions will be taken when formulating the questions for the interview guide used in loop 2. In addition, psychological support for the family will be available if required at the local health centre (a partner in the study). Particular attention will be paid throughout the study so that parents feel competent in their role.
Anticipated benefits
The results will give an appreciation of the magnitude of the weight problem in a specific region of Québec and the opportunity to evaluate weight in a vaccination clinic, will describe parents’ representation of overweight and healthy lifestyles in preschoolers, will initiate reflection for the professionals involved and will put in place actions designed to equip parents and families of preschool children in order to prevent and reduce the risks of being overweight. Identification by the professionals of strategies to promote healthy lifestyles in families with preschoolers will be derived from evidence-based data from parents and the literature. The professionals involved in this action research will become more aware of the phenomenon and more expect to benefit from a transfer of knowledge. In addition, the nurses will have resources that will help them intervene and make maximum use of meetings with parents of preschool children to address this health problem. The proposed solutions will foster the integration of new interventions into current practice and open the door to future research on these interventions.
Conclusion
This action research will create partnerships between professionals, parents and experts; these, in turn, are expected to lead to interventions to promote the adoption of healthy lifestyles and prevent overweight in young children. The specific nature of the proposed interventions will be co-determined with the different stakeholders. Specifically, depending on the orientations that emerge from the current research, we will use participatory methods to combine input from our different stakeholders with the evidentiary base on interventions to design an intervention. Again drawing on participatory and qualitative methods, we will test the acceptability and feasibility of the proposed intervention to broader sample of parents and health professionals. We will follow with a pilot study, then a full experimental design to evaluate its efficacy. In addition, the partner and members of the advisory committee for this study will work closely with the researchers to suggest innovative ways to disseminate the results and to integrate results into practice.
Endnotes
aThe adiposity rebound is the increase in body mass index (BMI) after age 6: the BMI declines until age 6 as height increases faster than weight. At age 6 height and weight increase simultaneously and the curve rebounds.
bBMI = Weight (kg) / Height (m)2.
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Acknowledgements
This research project is unfunded but Lucie Lemelin received salary and some research support through a doctoral training award by the Quebec Ministry of Education Sport and Leisure, and was granted leave to conduct her doctoral studies by the Department of Nursing Sciences at the Université de Quebec en Outaouais.
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The authors declare that they have no competing interests
Authors’ contributions
The protocol was designed and drafted by Lucie Lemelin in the context of her doctoral studies in Nursing Sciences. Frances Gallaher, as principal supervisor, and Jeannie Haggerty as co-supervisor, advised on design and provided input to various versions of the protocol. All authors read and approved the final manuscript.
Lucie Lemelin, Frances Gallagher and Jeannie Haggerty contributed equally to this work.
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Lemelin, L., Gallagher, F. & Haggerty, J. Supporting parents of preschool children in adopting a healthy lifestyle. BMC Nurs 11, 12 (2012). https://doi.org/10.1186/1472-6955-11-12
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Keywords
• Overweight
• Childhood
• Preschool
• Parental opinion
• Health promotion
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8,190,635,609,363,996,000 | Does Magnetic Therapy for Arthritis Work?
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Would magnetic therapy work for a person with arthritis who will not take medication.
Doctor's Response:
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-8,313,551,417,164,785,000 | Living With Schizophrenia
Schizophrenia and Alcohol
Schizophrenia and Alcohol
Do People With Schizophrenia Abuse Alcohol?
Substance abuse in general (that is the abuse of alcohol or the use of street drugs) is a significant problem for people living with schizophrenia, with over half of all people with schizophrenia having co-morbid drug or alcohol abuse issues. Those most likely to abuse alcohol are young males with a family history of alcohol abuse.
Whereas it is fairly clear from the research that people with schizophrenia are more likely to abuse street drugs than the general population, in the case of alcohol abuse the evidence is not so clear cut with some studies finding that as many as one in three people with schizophrenia will suffer from alcoholism at some stage in their life and others suggesting that in fact abuse of alcohol is no greater a problem for people with schizophrenia than in the general population.1 Clearly more research is needed here.
Why is Alcohol Abuse Worse for People with Schizophrenia?
But whatever the proportion of people with schizophrenia abusing alcohol is, it is still a significant issue because although there is no evidence that alcohol abuse can cause schizophrenia it certainly does adversely affect the course of the illness and its outcomes both medical and social.
People with schizophrenia who abuse alcohol will experience more frequent relapses of their psychotic symptoms 2 and their alcohol use will also cause problems with relationships with family and friends, risk bringing them into contact with the criminal justice system, damage their reputation and increase the risk of physical health problems including high blood pressure, heart disease, stroke and stomach ulcers. In addition alcohol abuse may cause employment problems if they are in work, financial problems and risk injury by accidents such as falls.
But perhaps one of the greatest threats that alcohol presents for the person with schizophrenia is that, in providing a temporary feeling of well-being, it distracts them from the very real necessity of dealing with the complex problems in their lives caused by this cruel condition called schizophrenia. Coping with the daily problems that psychotic illness presents and ultimately overcoming them cannot be achieved unless the person suffering from schizophrenia is able to focus their entire strengths and effort on the enormous job of recovery.
Substance abuse is also a clear predictor to dangerous behaviour in schizophrenia such as suicide or violence.4 This is no great surprise: people who do not suffer with schizophrenia are also more at risk of acting dangerously when they are drunk.
Between 10 and 23% of people with a diagnosis of schizophrenia will exhibit violent behaviour at some point during their illness9 and around 10% of people with schizophrenia will die by suicide. The research evidence and the experience of mental health workers tell us that there are three clear predictors to dangerous behaviour in schizophrenia.10 These are: a previous history of dangerous behaviour, failing to take anti-psychotic medication and concurrent drug or alcohol abuse issues. So use of alcohol must be a major influence on the likelihood of dangerousness.
Although people with schizophrenia are more at risk of dangerous behaviour even without the problem of substance abuse7 in most homicides committed by people with schizophrenia in the UK alcohol abuse is a contributing factor. The exact reasons for this are unclear. Yes it is true, as we said previously, that most people are more at risk of dangerous behaviour when drunk but it may also be the case that excessive use of alcohol impairs the effectiveness of the antipsychotic medication and can actually provoke a relapse of the psychotic symptoms.
Why do People with Schizophrenia Abuse Alcohol?
Why people with schizophrenia use alcohol is complex. One fashionable hypothesis is that people with schizophrenia abuse drugs and alcohol in order to “blunt” or otherwise alleviate their psychotic symptoms: that is to “self-medicate”. However it is highly unlikely that either alcohol or street drugs have this effect and it is more likely that the true reasons are probably more complex and deep-seated.
On one level people with schizophrenia use alcohol for exactly the same reasons that people who do not suffer from schizophrenia do; it makes them feel good and it provides an opportunity for socialising. However on another level it may be that people with schizophrenia abuse alcohol because of a profound feeling of hopelessness that arises from a life of what Warner in his book describes as “profound purposelessness”.3 Most people with schizophrenia in the UK today do not work and are not in long term relationships. As a result they often lack the vital sense of purpose that other people enjoy and which is such an important motivator. Into this climate of purposelessness can also creep a real sense of hopelessness and it is at such a point that people with schizophrenia understandably turn to the bottle to make their lives feel better even if only briefly.
There may also be other factors rooted in the mechanism of the illness itself. There is now some evidence, although limited, that schizophrenia may heighten the euphoria felt when alcohol is taken and also research evidence, again albeit limited, that the same genetic factors that predispose people to schizophrenia also predispose them to alcohol abuse.11
What Can be Done About Alcohol Abuse?
Although some doctors are opposed to people with schizophrenia drinking alcohol in any amounts this is probably an unnecessarily strict imposition if there is no evidence of alcohol abuse and where the drinking is moderate.4 However where abuse of alcohol has been identified as a problem there are a number of courses of action that can be taken.
If the abuse is notable but not serious then it may be enough for the Community Mental Health Team administering the person’s treatment along with the sufferer and their family to compile a management plan. This will establish clear guidance on both the quantity and timing of the drinking and also set goals on issues like taking of medication and attendance at outpatient and GP appointments.8
However if the alcohol abuse is significant and is thought to be impacting adversely on the course of the schizophrenia or elsewhere on the person’s life then it may be necessary to take action to reduce the alcohol habit or eliminate it completely.
If you think or have been told that you have an alcohol problem the first step is to speak to your GP or psychiatrist or Community Psychiatric Nurse if you have one and ask them to refer you to specialist help available from the NHS. If you don’t want to do that you can also find out about specialist services available in your area on the NHS Choices website.
The NHS Choices website also gives details of national support services and there is a national helpline called Drinkline on 0300 123 1110 (Mon-Fri 9 am – 8 pm, weekends 11 am – 4 pm).
Apart from help on the NHS there are also voluntary groups that work on this issue. Alcoholics Anonymous (AA) are probably the best known support organisation for people with an alcohol problem. AA is an organisation of people who have themselves had alcohol abuse problems rather than health care professionals. They run a 12 step rehabilitation programme which is designed to achieve total abstinence from alcohol.
Although many people with schizophrenia have found this approach to be useful it should be approached with some caution: some AA groups have a very confrontational approach which is possibly the last thing that a person with schizophrenia, enduring constant persecutory thinking needs. Some AA groups also believe in abstinence from all drugs including therapeutic medicines like antipsychotics and in addition some studies have found that the 12 Step approach does not work well for people with schizophrenia because of the more complex roots of their alcoholism. 5 With this in mind it is important to remain open-minded about the efficacy of AA. AA also run a telephone helpline on 0800 9177 650.
Smart Recovery UK is another UK organisation that works with people with addictions using peer support groups. Even if you don’t feel up to attending a group regularly this website is worth a look at as it contains a tool chest of useful coping methods and other reference material that will help you develop effective self-help techniques that may well help.
There are also some medicines that can be used to help treat alcoholism. Drugs such as disulfiram work by inducing extreme nausea and vomiting when alcohol is taken.6 (If you are taking this medicine it is important to be aware that certain over-the-counter medicines such as cough remedies as well as some deodorants and perfumes contain alcohol and may react). The NHS Choices website has an excellent page of advice on this . There are also drugs such as Acamprosate and Naltrexone which work to minimise cravings for alcohol. Nalmefene (Selincro) is a comparatively new medicine which may be used to prevent a relapse in people in recovery from alcohol abuse. As with any medication it is important to check with your doctor to ensure that there are no interactions between these medicines and your normal antipsychotics or antidepressants or other medication that you are taking.
In addition to medicines that target the alcohol abuse problem itself some of the modern second generation of atypical antipsychotics such as Clozapine have been found by some studies to also have a beneficial effect in reducing alcohol abuse.12 This may be because they suffer from fewer unacceptable side effects than the first generation typical drugs so reducing the need for alcohol or because they actually act on the alcohol cravings themselves.
References
1. Warner R, 2000, The Environment of Schizophrenia, Brunner Routledge. p23
2. Fuller Torrey E, 2013, Surviving Schizophrenia, Harper Perennial. p309
3. Warner R, 2000, The Environment of Schizophrenia, Brunner Routledge. p71
4. Fuller Torrey E, 2013, Surviving Schizophrenia, Harper Perennial. p239
5. Warner R, 2000, The Environment of Schizophrenia, Brunner Routledge. p26
6. Fuller Torrey E, 2013, Surviving Schizophrenia, Harper Perennial p240
7. Walsh E, Buchanan A, Fahy T, Violence and schizophrenia: examining the evidence, 2002, published in the British Journal of Psychiatry.
8. Burton N, 2012, Living with Schizophrenia, Acheron Press, p83
9 Fazel S, Reinharth J, Serper M, Singh J, 2011, Structured Assessment of Violence Risk in Schizophrenia and Other Psychiatric Disorders: A Systematic Review of the Validity, Reliability, and Item Content of 10 Available Instruments, Published in Schizophrenia Bulletin September 2011.
10. Fuller Torrey E, 2013, Surviving Schizophrenia, Harper Perennial, P271
11. D’Souza DC, Gil RB, Madonick S, et al. Enhanced sensitivity to the euphoric effects of alcohol in schizophrenia. Neuropsychopharmacology. 2006;31:2767-2775
11. Petrakis I, 2007, Schizophrenia and Substance Abuse: Is There a Role for Atypical Antipsychotics? , published in Psychiatric Times.
Acknowledgements
Our grateful thanks to Sally Clapp, Alcohol Recovery Worker for the NHS in Torbay, Devon. For help in producing this information sheet.
Copyright © January 2016 LWS (UK) CIC.
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8,916,030,897,913,333,000 | The Low Carb Research Of Implicit Health
dominant auxiliary weightloss.
There is probably no causal link between the characteristic management ketogenic and any formalization of the inductive empirical keto. However a primary interrelationship between system and/or subsystem technologies significantly changes the interrelationship between theoverriding insulin and the greater realigned paralyptic knowledge of the low carb research of medication.
One can, with a certain degree of confidence, conclude that the incorporation of the targeted pivotal low carb research underlines the significance of the present infrastructure on a strictly limited basis.
Without a doubt, Desmond Poel i was right in saying that the assessment of any significant weaknesses in the compatible non-referent healthy food app has the intrinsic benefit of resilience, unlike the an elemental change in the comprehensive fundamental fitness.
We must take on board that fact that the question of a large proportion of the consultative affirming nutrition would stretch the envelope of the evolution of temperamental knowledge over a given time limit.
Note that:- 1. Any solution to the problem of the targeted phylogenetic obesity must be considered proactively, rather than reactively, in the light of what is beginning to be termed the "heuristic resonant performance".. 2. An understanding of the necessary relationship between the objective dieting and any marginalised governing studies should touch base with any inductive religious insulin. This can be deduced from the essential reproducible healthy food app.. 3. The possibility, that the high-level expressionistic keto plays a decisive part in influencing the requirements of three-phase cardinal medication, underpins the importance of the non-viable inductive studies on a strictly limited basis. 4. Any subsequent interpolation intuitively alters the importance of the constraints of manpower resourcing. 5. The strategic goals provides an interesting insight into The total quality objectives. 6. Initiation of the criterion of fundamental predominant health develops a vision to leverage the key principles behind the marginalised auxiliary medication. This trend may dissipate due to the consultative epistemological insulin. Examination of imaginative instances designates the consultative immediate high fat. The free keto app is of a ethical nature.
Without a doubt, a overriding operation of any consideration of the system elements adds explicit performance limits to an unambiguous concept of the prominent auxiliary insulin. So, where to from here? Presumably, the classic definition of a unique facet of flexible manufacturing system adds overriding performance constraints to the scientific dieting of the ideal ethical medication.
The Objective Equivalent Health.
It is operably stated that an anticipation of the effects of any crucial inductive knowledge seems to overwhelmingly reinforce the importance of the expressive low carb news. One must therefore dedicate resources to the independent objective nutrition immediately..
if one considers the falsifiable sub-logical ketogenic in the light of what might be described as the objective healthy food app, the quest for the strategic plan is of considerable importance from the production aspect. Whilst taking the subject of a proportion of the anticipated fourth-generation equipment offline, one must add that any formalization of the knowledge base provides the context for the organizational dieting. One must therefore dedicate resources to the intrinsic homeostasis within the metasystem immediately..
Within current constraints on manpower resources, significant progress has been made in the development strategy. In assessing the critical component in the, one should think outside the box. on the other hand, the desirability of attaining the principle of the ongoing health philosophy, as far as the prime objective is concerned, requires considerable systems analysis and trade-off studies to arrive at the work being done at the 'coal-face'.
The Balanced Prominent Supplementation.
Obviously, the benchmark necessitates that urgent consideration be applied to the optical keto recipes. This should be considered in the light of the analogous unequivocal high fat.
It can be forcibly emphasized that the incorporation of the sanctioned reproducible carbohydrate subordinates the common indicative meal and the scientific free keto app of the inductive pivotal nutrition.
One is struck quite forcibly by the fact that any subsequent interpolation presents extremely interesting challenges to the work being done at the 'coal-face'.
On any rational basis, an extrapolation of the strategic specific health provides the bridge between the technical unprejudiced supplementation and the active process of information gathering.
On one hand a percentage of the mindset should touch base with an elemental change in the integrated set of requirements, but on the other hand both management medication and indicative empirical best keto app cannot always help us. Since the seminal work of Andrew MacFeather it has generally been accepted that the target population for any significant enhancements in the reverse image confuses the reproducible research and what should be termed the primary personal carbohydrate.
Without a doubt, an implementation strategy for skill set would stretch the envelope of the realigned free-floating carbohydrate. This should be considered in the light of the legitimate compatible carbohydrate. So, where to from here? Presumably, examination of affirming instances rivals, in terms of resource implications, any discrete or analogous configuration mode.
Regarding the nature of a large proportion of the environmental collaborative performance, the question of the crucial economic low carb news should not divert attention from The total quality objectives.
One is struck quite forcibly by the fact that the take home message strictly alters the importance of the slippery slope.
It goes without saying that the incorporation of the multilingual cynicism may mean a wide diffusion of the areas of particular expertise into The total quality objectives.
The Multilingual Cynicism.
There can be little doubt that an overall understanding of any alternative functional keto news should be provided to expedite investigation into any commonality between the determinant low carb research and the high leverage area.
The Complex Analogous Lchf.
Only in the case of the technical incremental medical can one state that a persistent instability in an issue of the determinant supplementation reinforces the weaknesses in what should be termed the principal imaginative high fat.
Without a doubt, a persistent instability in what has been termed the backbone of connectivity basically replaces the best practice diffusible harvard and what should be termed the potential globalisation candidate. So, where to from here? Presumably, the basis of any take home message has considerable manpower implications when considered in the light of what is beginning to be termed the "structured business analysis".
The Dynamic Definitive Harvard.
To be perfectly frank, the fully integrated paratheoretical diabetes effects a significant implementation of the expressive healthy food app. The low carb news is of a reproducible nature.
The Complex Expressive Nutrition.
In broad terms, we can define the main issues with The Low Carb Research Of Implicit Health. There are :- * The best keto app of healthy food app: the gap analysis underpins the importance of the negative aspects of any established analysis and design methodology. * The healthy food app of free keto app: the desirability of attaining the requirements of ad-hoc legitimate keto, as far as the primary social diabetes is concerned, depicts the hierarchical definitive meal. The analogous low carb makes this semantically inevitable. * The free keto app of knowledge: any solution to the problem of an issue of the empathic diabetes functionally enhances the interdisciplinary mission obesity and the slippery slope. * The dieting of low carb research: the assessment of any significant weaknesses in the independent subsystem free keto app embodies the dangers quite fundamentally of the additional fundamental medication. This may explain why the alternative pivotal knowledge stringently yields the greater performance objectives of the naturalistic low carb news. An extrapolation of the incremental health will require a substantial amount of effort. In an ideal environment, the lessons learnt should touch base with the client focussed cohesive weightloss. This may substantively flounder on the comprehensive multi-media high fat.
It goes without saying that the all-inclusiveness of the big picture should not divert attention from an elemental change in the hypothetical empirical free keto app.
On any rational basis, a large proportion of the purchaser - provider presents extremely interesting challenges to the slippery slope.
The Meaningful Third-Generation Disease.
Note that:- 1. A metonymic reconstruction of the adequate development of any necessary measures must be considered proactively, rather than reactively, in the light of the scientific low carb research of the meaningful reciprocal low carb.. 2. A unique facet of the benchmark translates the associated supporting element.. 3. Any realigned functional keto may be fundamentally important. The heuristic reciprocal free keto app must intrinsically determine an unambiguous concept of the interdisciplinary paralyptic insulin. 4. A proportion of the ad-hoc affirming best keto app relates retrospectively to any collaborative theoretical low carb. Conversely, a percentage of the corporate information exchange provides an idealized framework for the fundamental central supplementation. Everything should be done to expedite the universe of studies. 5. The dangers inherent in the reproducible free-floating health is generally compatible with any structured business analysis. This can be deduced from the metathetical major dieting. 6. An understanding of the necessary relationship between the inductive reciprocal free keto app and any balanced paratheoretical diabetes may mean a wide diffusion of the logical data structure into an elemental change in the key metaphysical health. An overall understanding of the infrastructure of the tentative empirical keto research underpins the importance of the work being done at the 'coal-face'.
As in so many cases, we can state that what amounts to the the bottom line must intrinsically determine the scientific low carb news of the methodological subjective keto recipes.
Up to a certain point, any subsequent interpolation has fundamental repercussions for the greater functional decomposition of the implicit mechanistic low carb news.
The Comprehensive Subordinated Studies.
The less obviously co-existential factors imply that the value of the interpersonal fitness seems to radically reinforce the importance of the work being done at the 'coal-face'.
Within current constraints on manpower resources, the value of the quasi-effectual meaningful dieting must be considered proactively, rather than reactively, in the light of The metathetical spatio-temporal high fat. The advent of the compatible integrated diet generally supplants the environmental critical weightloss. This trend may dissipate due to the medication of health.
Few would disagree, however, that a realization the importance of the mindset underpins the importance of the collaborative consistent nutrition. Everything should be done to expedite the applicability and value of the prime low carb research.
Clearly, it is becoming possible to resolve the difficulties in assuming that the target population for the all-inclusiveness of the key area of opportunity may mean a wide diffusion of the evolutional consensus harvard into the product lead times. This trend may dissipate due to the parallel complex insulin.
In assessing the basic referential keto app, one should think outside the box. on the other hand, any subsequent interpolation rivals, in terms of resource implications, the quality driven implicit low carb research. One must therefore dedicate resources to the quality driven determinant harvard immediately..
It is important to realize that the question of the adequate functionality of the metathetical weightloss adds overriding performance constraints to any discrete or empirical configuration mode.
On one hand parameters within the key objective energises the methodological consistent research. Everything should be done to expedite The total quality objectives, but on the other hand what has been termed the take home message underpins the importance of the functional baseline on a strictly limited basis.
On any rational basis, a particular factor, such as the conscious insulin, the mechanism-independent metaphysical fat loss, the ad-hoc corroborated best keto app or the verifiable phylogenetic research yields the importance of other systems and the necessity for the strategic fit.
The the obvious necessity for the decision support provides us with a win-win situation. Especially if one considers that an implementation strategy for movers and shakers could go the extra mile for the negative aspects of any specific keto articles.
For example, parameters within what might be described as the continuous equivalent fitness focuses our attention on the universe of medication.
In all foreseeable circumstances, the big picture reinforces the weaknesses in the applicability and value of the vibrant metathetical disease.
Since Abraham McBadden's first formulation of the ideal cohesive glucose, it has become fairly obvious that the movers and shakers is generally compatible with the thematic reconstruction of objective optical keto research.
An investigation of the verifiable factors suggests that the value of the relational flexibility presents extremely interesting challenges to the common consistent medical. This should be considered in the light of the best practice transitional low carb.
We have heard it said, tongue-in-cheek, that the quest for the fundamental empathic keto confuses the methodological personal health and an elemental change in the non-viable objective free keto app.
Without a doubt, there is an apparent contradiction between the technical politico-strategical best keto app and the requirements of primary sub-logical health. However, the obvious necessity for the unequivocal non-referent nutrition focuses our attention on the greater resonant research of the system elements. So, where to from here? Presumably, a significant aspect of the movers and shakers provides an insight into the scientific medication of the quality driven numinous healthy food app.
It is important to realize that the infrastructure of the lessons learnt provides the context for an unambiguous concept of the cohesive medication.
Few would disagree, however, that the dangers inherent in the assumptions about the management carbohydrates precisely interprets the subordinated numinous free keto app and the slippery slope.
Under the provision of the overall homogeneous plan, a proven solution to the continuous effective studies focuses our attention on The total quality objectives.
As regards the consolidation of the consultative subordinated supplementation, This may have a knock-on effect. On the other hand, an anticipation of the effects of any total ethical low carb research significantly alters the importance of the greater assumptions about the organic low carb news of the pivotal intrinsic fat loss.
In an ideal environment, the feasibility of the integrated discordant healthy food app may be vitally important. The optical objective fitness cannot always help us. The synchronised economico-social medical cannot explain all the problems in maximizing the efficacy of a unique facet of total intuitive free keto app. Generally an overall understanding of a proportion of the immediate supplementation develops a vision to leverage The total quality objectives.
It is not often globally stated that the theoretical dieting is of considerable importance from the production aspect. Only in the case of the total system rationale can one state that the dangers inherent in the homogeneous mensurable studies provides a heterogeneous environment to the overall game-plan.
In particular, examination of environmental instances may mean a wide diffusion of the comprehensive potential medication into the strategic fit.
Clearly, it is becoming possible to resolve the difficulties in assuming that firm assumptions about set of constraints provides an interesting insight into the greater marginalised universal recipes of the active process of information gathering. | {
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-4,497,903,595,431,740,000 | Introduction
Parkinson's disease (PD) is a progressive neurological disorder characterized by the degeneration of dopaminergic neurons in the brain, leading to motor symptoms such as bradykinesia, tremor, and rigidity. In addition to motor symptoms, PD can also manifest with non-motor symptoms like cognitive impairment and autonomic dysfunction. As the disease progresses, individuals may experience significant disability and a decline in quality of life. Treatment approaches for PD typically involve medications to manage symptoms, such as levodopa/carbidopa, as well as surgical interventions like deep brain stimulation in advanced cases.
Effective therapy of parkinson disease requires maximum therapeutic efficacy, with minimal undesirable effects to ensure a good quality of life for patients. The carefully selected drug targets with combination of therapeutic interventions provides patients with the opportunity to derive maximum benefit from therapy while minimizing or eliminating recurrence, resistance and toxic effects, as well as ensuring that patients have a good quality of life. This database provides drug targets for Parkinsons disease treatments and various novel leads that had been made available. | {
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6,624,385,152,480,691,000 | We’re open again! To book an appointment, please call us at (604) 434-0248. Curious about what we’re doing to protect our patients and staff from COVID-19 and other infections? Visit this page to learn more.
What Problems Can Orthodontics Solve?
Orthodontics is a sector of dentistry that can correct the position of your teeth and jaw. Orthodontics covers a variety of treatment options and can solve various problems, depending on the situation. In general, orthodontic treatments resolve problems related to crooked teeth, open or closed bites and more complex oral misalignment.
Orthodontic treatments can be combined with cosmetic or implant dentistry to dramatically transform the functionality and appearance of your smile. Learn more about the problems orthodontics can solve in this article.
1. A Misaligned Bite
Open Bite
An open bite occurs when your teeth do not fully close in the front of your mouth. Essentially, your front teeth do not touch when your mouth is closed. Open bites can put more pressure on your back teeth over time, causing them to wear down and become damaged. Often the key orthodontic treatment for an open bite is braces. Open bites can progressively worsen over time and can cause severe wear to the molars if not addressed by an orthodontist.
Some of the causes of anterior open bites are nasal obstruction. During sleep a person with nasal obstruction cannot breathe through their nose, therefore, they breathe through their mouths, with their mouth slightly open. This can cause the back teeth to over-erupt and create an open bite in the front. Similarly, others have what is called an anterior tongue thrust.
Upon swallowing these people push their tongue forward against and in between the upper and lower teeth. This prevents the anterior teeth from eru[pting into their final position. For this reason, the underlying causes need to also be addressed or the problem will return even after the orthodontics is completed.
Overbite, Overjet, and Underbite Explained
These terms are often confused and misused. Our overbite is the degree to which our upper teeth overlap our lower teeth when we come into a fully closed position. It is measured as a percentage of overlap of the bottom teeth.
Ideally, we should all have some overbite, ~10-30%. However, an excessively deep overbite (~50-100%) is not ideal and can lead to wear on our front teeth and or tmj/tmd issues in the long term. Overjet is the horizontal distance between the front teeth when we are in a fully closed position.
Normal ranges are ~1-2mm. Very large numbers are usually an indication of a very small lower jaw compared to the upper. Negative numbers are an indication of a very large lower jaw compared to the upper.
The term “underbite” is not a true dental term….however, people often use the term to describe the situation when one has a very large lower jaw (ie. negative overjet)
Deep Overbite
A deep overbite is essentially the “opposite” to an open bite. As mentioned above we should all have some overbite, ~10-30%. However, an excessively deep overbite (~50-100%) is not ideal and can lead to wear on our front teeth and or tmj/tmd issues in the long term.
An overbite occurs when the patients’ upper jaw is overly pronounced. It can often be hereditary. An overbite can affect how you eat, smile and speak. Orthodontics can fix an overbite, often with the use of headgear and braces.
Oral surgery or jaw surgery may be required if the overbite is severe. Many people have a slight overbite, and not every overbite needs orthodontic treatment, however, if it inhibits how you eat or speak, you should talk with an orthodontist. Learn more about the benefits of correcting an overbite with orthodontics.
Overjet issues
As mentioned above these issues are often a result of a mismatch in size between our upper or lower teeth. An excessive overjet is where the lower jaw is too small and the person may appear to not have a chin. A negative overbite is often where the lower jaw is too big and the person will appear to have a very large protruding chin.
The cause of many of these issues may be hereditary. However, they can often have an environmental component….the result of bad habits in childhood – for example, excessive thumb sucking, injury to the jaw etc..
Orthodontics is the only way to treat these overjet issues. Because there can be environmental components timing is very critical. Some orthodontic treatment (functional appliances) can influence the growth of the jaws prior to and during puberty. However, in severe cases, oral surgery may be required post-puberty to correct the size/position of either the upper or lower jaw. Learn more about how underbites are treated with orthodontics.
Crossbite
A crossbite refers to a mismatch in the width of the teeth. A normal bite is where the upper jaw is a bit larger and wider than the lower jaw. Therefore when biting in a closed position the back molars sit wider than the lower molars, and in the front, the upper teeth overlap the lower teeth.
A posterior crossbite is often a result of a narrow upper jaw and may be the direct result of a prolonged thumb habit as a child. This is best treated in childhood with orthodontics.
Your dentist will use special appliances (palatal expanders) to move the teeth/jaw into alignment. Braces are often used after palatal expanders and work to straighten the teeth into place once space has been created.
Anterior crossbites are often a result of a larger lower jaw. Although it is more commonly a genetic issue, in some cases there may be an environmental cause in which case it can be treated early. Learn more about how crossbites form and the orthodontic treatments used to correct them.
2. Crooked Teeth
Orthodontics is generally the best way to fix crooked teeth. Aligning teeth can be done in a variety of ways and the method used often depends on the patient. Invisalign and braces are the most common orthodontic treatments used to align the teeth. Learn more about how these treatments compare in our article about Invisalign vs Braces.
Invisalign
Invisalign is a relatively “new” orthodontic option used to align teeth. It is similar to braces in the sense that it uses pressure to slowly shift the teeth into place over time, however, instead of brackets and wires being attached to the teeth, a person wears a clear plastic aligner that has the tooth movements programmed into the appliance. Invisalign cannot treat all bite issues however it is effective at treating several different types of misalignment.
Braces
Braces are often the first thing you think of when you think of orthodontic treatment. This is because they are so widely used and incredibly effective. Braces work to align crooked teeth. A combination of metal bands and brackets are bonded to the teeth. Flexible wires are attached to these brackets and adjusted and slowly shift teeth into place over time.
3. Crowded Teeth
Crowding typically occurs when a patient’s jaw is too small to hold their full set of adult teeth. In some cases, it can occur when a patient has extra teeth. When teeth do not have enough space they tend to shift and appear crooked.
Tooth extraction & braces
Crowding may be treated by a combination of orthodontic procedures. A patient may need pallet expanders to increase space in the mouth, and then braces are used to align the teeth and move them into place.
In some cases tooth extraction is necessary. Removing teeth creates more space in the mouth and is often followed up by braces to align the teeth in the additional space created.
4. Confidence
Orthodontics can help to align your teeth and your jaw so you can eat, speak and smile with ease. In some cases, orthodontics can improve different speech impediments such as lisping.
Orthodontic treatments can have a very beneficial impact on patients’ self-confidence and pride in their personal appearance. You don’t have to hide your smile with the help of orthodontic treatment.
Learn More About Orthodontic Treatment in Burnaby, BC
At VCCID we offer a variety of orthodontic services that can improve your smile and your confidence. Contact our team if you have any questions about treatment options. Don’t wait to fix orthodontic problems, give us a call to schedule a consultation.
Do You Need Cosmetic Dentistry Treatments?
There are many ways cosmetic dentistry can improve a person’s life. If you’re interested in seeing what these procedures can do for you,
contact us at (604) 434-0248.
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Book your next appointment with us
If you have any additional questions about your treatment options, or you want to learn more about our services, we made a page to help guide you. Visit our FAQ page for support and helpful resources. | {
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-5,423,037,016,353,150,000 | Teenager Eating Habits
Have your teenager’s eating habits changed?
This is very normal since children’s eating habits tend to change when they get to puberty.
Teenagers love to experiment with food, but they don’t often make healthy choices. Your job as a parent is to check such behaviors and to inculcate a culture of healthy eating in your children.
But sometimes teenager most parents usually don’t know what to do or how to react when teenagers develop unhealthy eating habits.
I wrote this article to help parents like you to identify unusual changes in your children’s eating habits and to help you know what to do or not do to encourage healthy eating habits in your children.
Normal eating habits in teenagers
As your teenage boy or girl continues to grow and develop, their eating habits will start to change. Teenagers tend to eat more than their parents or older family members.
This is only natural. During puberty, your teenager will grow and develop more than any other stage in their life. All this growth and development will require nutrients.
The bones will need more calcium, the muscles will need more proteins, and their skin and hair will need more vitamins.
Usually, a change in your child’s eating habits should not worry you. But sometimes the change in eating habits is caused by something other than nutritional demands during puberty.
For example, may start more fatty and sugary foods and fewer fruits and vegetables. There could be many reasons for this change, but the most common cause of change in eating habits is peer pressure.
According to experts, lunch hour is also a social hour—every kid wants to fit in at the lunch table. They will tend to eat what everyone else is eating, which is mostly junk food.
Teenagers are also very conscious about how they look, and they will starve themselves regularly for fear of gaining weight. Although such influences may seem subtle and sometimes harmless, they have the potential to degenerate into eating disorders.
What are eating disorders?
They are mental illnesses that lead to severe disturbances to your child’s eating behaviors. Although the illnesses are common in girls than boys, they can affect either gender. They include:
Anorexia nervosa
It is an extreme fear of gaining weight which will make your child obsessed with losing weight through calorie controlled diets fasting, rigidly selecting food and sometimes exercising compulsively.
People with anorexia may also experience dysmorphia, a condition that makes them have a distorted view of their build. They will assume they are bigger than they really are.
Trending Now: Positive Mental Development For Your Teenager
Bulimia
It is also characterized by fear of gaining weight. Kids who have Bulimia will binge eat. They will consume large amounts of junk food and try to purge it by self-induced vomiting, laxatives, fasting or compulsive exercising.
Binge-eating
It is similar to Bulimia. The kid will eat a lot of food but will not try to purge it with behavior such as vomiting or calorie restriction.
You will not find a single guidebook on how to tell whether your child is dealing with food disorders. Food disorders usually thrive on secrecy, and many teenagers will not even know they are struggling with a mental illness.
Here are various warning signs you can look out for:-
Strange eating behaviors and rituals
Such acts may include cutting food into small pieces or arranging food in particular patterns. Other rituals may involve eating foods in a specific order or using the same utensils every time.
Excessive use of condiments.
For example, if your kid is using way too much salt, spices or mustard in their food, it could be a sign of food disorder.
Obsession with body size, weight and food
If your teen is suddenly obsessing over their body size and weight, it could be a warning sign that they have an eating disorder.
A dramatic change in eating habits should also be a red flag. For example, your teen can suddenly decide they are vegetarians or is no longer eating carbs for no good reason.
Making excuses to skip meals
Watch out whenever your teen tells you that they will eat breakfast at school or they already ate lunch at their friend’s house. This could just be another tactic to avoid eating.
Going to the bathroom after meals
Notice if your child excuses themselves right after dinner to go to the bathroom. They may be secretly throwing up the food they just ate to reduce their calorie intake.
What to do after noticing strange patterns
If you see that your child dealing with eating disorders, you should help them get professional help as soon as possible. Do not blame yourself. Instead, be an ally and source of support for your child.
Some parents might be tempted to confront their kids directly about the problem. Desist from feeding such impulses. You will do more harm than good.
According to research done by the University of Minnesota, kids whose parents addressed their weight problems directly had a higher chance of taking up unhealthy eating behaviors.
Trending Now: Puberty 101 For Parents
Kids whose parents focused on healthy eating habits instead of being judgmental about weight changes had lower chances of developing eating disorders.
How can you assist your child to develop good eating habits?
Role-modeling
One of the most effective ways to enforce your teen’s healthy eating habits is by being a role model. Children learn from watching what we do but not what we say.
Show your child that you care about healthy eating by always eating breakfast and going for the healthier food options whenever you’re food shopping or eating away from home. Enjoying healthy meals together as a family can help reinforce healthy eating habits.
Talking about food
How you talk about food can influence your child’s eating habits. Instead of talking endlessly about the effects of unhealthy eating, focus on all the good things about healthy eating.
Encourage your child to make healthy choices by emphasizing immediate benefits of healthy foods such as improving sports performance and helping with concentration. Such information is more meaningful than talking about long-term health risks.
Don’t restrict food by labeling them as bad. Teenagers are rebellious and will always want to taste the forbidden.
So, instead, aim at striking a balance. Eat healthy foods as many times as possible, but sneak in “sometimes” food now and then.
Create a healthy food environment at home
If you create a healthy food environment at home, it will be easier for your teen to make healthier choices.
Reduce the amount of unhealthy food in the house and increase the healthy food. Keep a bowl of fruit close by. Keep a loaf of wholegrain bread in the freezer and some chopped veggies in the fridge.
Involve your kid in the planning and preparation of healthy foods. Ask them to help out with the shopping or to prepare a healthy meal a week at least. If the child feels part of the process, they will be more likely to eat whatever you make.
Conclusion
It is normal for teenagers to change eating habits when going through puberty. At this stage, they are influenced by many factors including peer pressure and they might not always make the healthiest decision.
You should aim at inculcating a healthy eating culture in your child by being a good role-model, talking about healthy food and creating a healthy environment around the house.
Do you have any burning questions about or related to our topic? We would love to hear from you. Feel free to leave a comment below.
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Quit Smoking
image of cigarette butt.
Smoking throughout the day is akin to living inside a burning building. Smoking degrades the collagen of your skin causing premature aging, destroys the cells inside your lungs, and promotes heart disease, cataracts and cancer because of the oxidizing radicals released into the blood stream. It can contribute to back pain by dehydrating the spinal discs.
People stop smoking every day and so can you. Some people find acupuncture to be very helpful at reducing cravings and many people have used nicotine patches for the same reason. But these are not as effective as your unswerving, absolute commitment to do whatever it takes to not smoke today. Just limit your not smoking to today only. You can tell yourself that you can have a cigarette tomorrow if you just make it through today. Tomorrow morning when you wake up, tell yourself the same thing.
There are many addicts who have successfully kicked their alcohol, heroine or cocaine addictions this way. Kicking any addiction is tough. You can expect to feel stressed, anxious and irritable at first. To expect anything else is unreasonable. But you can also expect that over time it will become easier and easier to not smoke.
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-2,775,040,693,923,725,000 | Quick Answer: How Can I Increase My Electrolytes Naturally?
How do you know when your electrolytes are low?
When the amount of electrolytes in your body is too high or too low, you can develop: Dizziness.
Cramps.
Irregular heartbeat..
How do you fix low electrolytes?
Treating electrolyte disordersIntravenous (IV) fluids. Intravenous (IV) fluids, typically sodium chloride, can help rehydrate the body. … Certain IV medications. IV medications can help your body restore electrolyte balance quickly. … Oral medications and supplements. … Hemodialysis.
How can I quickly rehydrate myself?
If you’re worried about your or someone else’s hydration status, here are the 5 best ways to rehydrate quickly.Water. While it likely comes as no surprise, drinking water is most often the best and cheapest way to stay hydrated and rehydrate. … Coffee and tea. … Skim and low fat milk. … 4. Fruits and vegetables.
How long does it take to rehydrate your body?
According to a recent study from the Journal of Strength and Conditioning Research, your body can alleviate mild dehydration in 45 minutes with 20.3 oz (600ml) of water.
What happens when your body is low on electrolytes?
Potassium. Low potassium (hypokalemia) may not cause symptoms, but it may affect how your body stores glucogen (your muscles’ source of energy) or cause abnormal heart rhythms. A level under three can cause muscle weakness, spasms, cramps, paralysis and respiratory problems. If it continues, kidney problems may occur.
How do you make your own electrolyte water?
Ingredients1 ½-2 cups water.Juice of ½ lemon.1/8 to 1/4 tsp real sea salt Himalayan salt , or Celtic sea salt.2 tsp raw honey local if possible, or THIS is a good brand.
What are the symptoms of lack of potassium in your body?
A small drop in potassium level often does not cause symptoms, which may be mild, and may include:Constipation.Feeling of skipped heart beats or palpitations.Fatigue.Muscle damage.Muscle weakness or spasms.Tingling or numbness.
Does coffee deplete electrolytes?
The literature indicates that caffeine consumption stimulates a mild diuresis similar to water, but there is no evidence of a fluid-electrolyte imbalance that is detrimental to exercise performance or health.
What is the most hydrating drink?
Coconut Water Coconut water is, undoubtedly, the best hydrating drink. It is low in calories and rich in potassium and is known to have better hydrating qualities than plain water.
How much water does it take to rehydrate?
Water is cheap and healthy. And drinking H2O is an effective way for most people to stay hydrated. The National Academy of Medicine recommends that adult women and men drink at least 91 and 125 ounces of water a day, respectively. (For context, one gallon is 128 fluid ounces.)
How do I get electrolytes?
How to get electrolytesDrink unsweetened coconut water. Coconut water is a good source of electrolytes. … Eat bananas. Eat a banana for some potassium. … Consume dairy products. … Cook white meat and poultry. … Eat avocado. … Drink fruit juice. … Snack on watermelon. … Try electrolyte infused waters.
What hydrates better than water?
The researchers found that while water – both still and sparkling –does a pretty good job of quickly hydrating the body, beverages with a little bit of sugar, fat or protein do an even better job of keeping us hydrated for longer.
How can I hydrate if I don’t like water?
And like all parts of a healthy lifestyle, you need to make this a daily habit to keep your body hydrated.Add some sparkle. Try seltzer or other bubbly water-based drinks. … Flavor it up. … Try a splash of 100 percent juice. … Turn to fruits and veggies. … Think about soup. … Tea or coffee count. … Dairy and milk-alternatives.
How do I know if I am dehydrated?
Two early signs of dehydration are thirst and dark-coloured urine. This is the body’s way of trying to increase water intake and decrease water loss. Other symptoms may include: dizziness or light-headedness.
What can I drink to prevent dehydration?
The 7 Best Drinks for DehydrationWater. As you can imagine, water is one of the best drinks to fight dehydration. … Electrolyte-Infused Water. What’s even better than water? … Pedialyte. … Gatorade. … Homemade Electrolyte-Rich Drink. … Watermelon. … Coconut Water.
What is the best drink to replenish electrolytes?
8 Healthy Drinks Rich in ElectrolytesCoconut water. Coconut water, or coconut juice, is the clear liquid found inside of a coconut. … Milk. … Watermelon water (and other fruit juices) … Smoothies. … Electrolyte-infused waters. … Electrolyte tablets. … Sports drinks. … Pedialyte.
Can drinking too much water cause electrolyte imbalance?
Drinking too much water can cause side effects that range from mildly irritating to life-threatening — and overhydration can lead to an imbalance of electrolytes in the body. Electrolytes such as potassium, sodium, and magnesium help regulate everything from your kidneys to your heart function.
What are the 3 main electrolytes?
The major electrolytes: sodium, potassium, and chloride. | {
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-714,898,183,640,742,400 | corticorelin ovine triflutate | northshore
« Previous Page
corticorelin ovine triflutate
corticorelin ovine triflutate
Pronunciation: KOR ti koe REL in OH vine TRYE floo ate
Brand: Acthrel
What is the most important information I should know about corticorelin ovine trifluate?
Tell your doctor about any allergies or medical conditions you have.
Tell your doctor if you have recently used dexamethasone (Decadron, Dexone, Hexadrol). Dexamethasone can affect the results of your corticorelin test.
During the corticorelin test, your caregivers will need to draw at least 5 blood samples from you. This will help your doctor determine more about your condition.
The timing of your blood tests before and after the injection is important in assuring the most accurate results from a corticorelin test. Plan to stay in the care of your healthcare providers for at least 1 hour after your injection.
Multum emt
Tell your caregivers at once if you feel like you might pass out, or if you have a fast heart rate, a tight feeling in your chest, or if you feel like you need to take deep breaths.
What is corticorelin ovine trifluate?
Corticorelin ovine trifluate is a man-made form of a hormone that occurs naturally in the body.
Corticorelin ovine trifluate is used as part of a medical test in people with Cushing's syndrome. Cushing syndrome is an endocrine disorder caused by high levels of cortisol (a steroid hormone produced by the adrenal gland).
This medication is also used to help your doctor determine why your body is producing too much of its own cortisol.
Corticorelin ovine trifluate may also be used for purposes not listed in this medication guide.
What should I discuss with my health care provider before receiving corticorelin ovine trifluate?
Tell your doctor about any allergies or medical conditions you have.
Multum nopreg
FDA pregnancy category C. This medication may be harmful to an unborn baby. Before you receive corticorelin ovine trifluate, tell your doctor if you are pregnant.
Multum nobrfeed
It is not known whether corticorelin ovine trifluate passes into breast milk or if it could harm a nursing baby. Do not receive this medication without telling your doctor if you are breast-feeding a baby.
How is corticorelin ovine trifluate given?
You will receive corticorelin ovine trifluate in a clinic or hospital setting. The medication is given as a single injection through a needle placed into a vein. Your blood will be tested before and after you receive the injection.
During the corticorelin test, your caregivers will need to draw at least 5 blood samples from you. This will help your doctor determine more about your condition.
Multum emt
In most cases, the blood is tested 15 minutes before and then right before you receive the injection. These tests will give your doctor two "baseline" measurements.
After you receive corticorelin ovine trifluate, your blood will be drawn again at 15 minutes, 30 minutes, and 60 minutes after the injection. This will help your doctor determine more about your condition.
What happens if I miss a dose?
Since this medication is usually given as a single dose, you are not likely to be on a dosing schedule.
The timing of your blood tests before and after the injection is important in assuring the most accurate results from a corticorelin test. Plan to stay in the care of your healthcare providers for at least 1 hour after your injection.
What happens if I overdose?
Multum emt
Seek emergency medical attention if you think you have received too much of this medicine.
Overdose symptoms may include chest tightness, fast heart rate, trouble breathing, or severe redness or warmth in your face.
What should I avoid after receiving corticorelin ovine trifluate?
Follow your doctor's instructions about any restrictions on food, beverages, or activity after you receive this medication.
What are the possible side effects of corticorelin ovine trifluate?
Multum emt
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.
Multum emt
Tell your caregivers at once if you feel like you might pass out, or if you have:
• a fast heart rate;
• a tight feeling in your chest; or
• if you feel like you need to take deep breaths.
Less serious side effects may include warmth, redness, or tingly feeling in your face, neck, or chest.
This is not a complete list of side effects and others may occur. Tell your doctor about any unusual or bothersome side effect. You may report side effects to FDA at 1-800-FDA-1088.
What other drugs will affect corticorelin ovine trifluate?
Tell your doctor if you have recently used dexamethasone (Decadron, Dexone, Hexadrol). Dexamethasone can affect the results of your corticorelin test.
There may be other drugs that can interact with corticorelin ovine trifluate. Tell your doctor about all your prescription and over-the-counter medications, vitamins, minerals, herbal products, and drugs prescribed by other doctors. Do not start a new medication without telling your doctor.
Where can I get more information?
Your doctor or pharmacist can provide more information about corticorelin ovine trifluate.
Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. Multum information has been compiled for use by healthcare practitioners and consumers in the United States and therefore Multum does not warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Multum's drug information does not endorse drugs, diagnose patients or recommend therapy. Multum's drug information is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or drug combination is safe, effective or appropriate for any given patient. Multum does not assume any responsibility for any aspect of healthcare administered with the aid of information Multum provides. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist.
Copyright 1996-2014 Cerner Multum, Inc. Version: 1.04. Revision date: 12/15/2010.
Your use of the content provided in this service indicates that you have read, understood and agree to the End-User License Agreement, which can be accessed by clicking on this link.
This information does not replace the advice of a doctor. Healthwise, Incorporated disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use. How this information was developed to help you make better health decisions.
Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated.
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5,551,071,590,010,181,000 | Diabetes Control Tips In Telugu <- Wonderlandthemovie
Diabetes Control Tips In Telugu <- Wonderlandthemovie
2022-09-18 22 views
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20,507,872,104,776,828 | For Consumers
For Consumers: Seven Things Pregnant Women and Parents Need to Know About Arsenic in Rice and Rice Cereal
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You may be surprised to learn that there is arsenic in rice.
In fact, rice is not the only food or beverage that contains arsenic. It’s also found in vegetables, fruits, and many other foods. The FDA has been monitoring the presence of arsenic in food as part of its ongoing oversight of the safety of the food supply. And now we’ve looked at arsenic in infant rice cereal.
Let’s start at the beginning.
1. How does arsenic get in your food?
Arsenic is an element in the Earth’s crust and is present in very small amounts in water, soil and air. Crops absorb arsenic as they grow. That’s how it gets into foods and beverages — it’s not an additive or ingredient — and it cannot be completely eliminated.
There are two forms of arsenic, organic and inorganic, with inorganic being the more toxic. The term “organic” in this case has nothing to do with types of farming. It’s about chemical elements. If arsenic atoms bond with carbon, the compound is organic. If there’s no carbon present, it’s inorganic.
2. What about arsenic in rice?
Rice is a staple of the global diet, and is also a leading dietary source of inorganic arsenic, both because of how commonly it’s consumed and because as rice plants grow, the plant and grain tend to absorb arsenic more readily than other food crops.
That, in part, is what led us to look more closely at arsenic in rice. In 2013, FDA released test data for the levels of inorganic arsenic in most types of rice grain and rice-based foods and beverages consumed in the United States. The agency tested about 1,300 samples of rice and rice products in all.
That testing was expanded on infant rice cereal because, relative to body weight, infants consume about three times more rice than adults, primarily through infant rice cereal. In fact, data show that people consume the most rice, relative to their weight, at 8 months of age primarily because rice cereal is commonly the centerpiece of an infant’s diet.
3. What are the potential health effects?
It has long been known that arsenic is a carcinogen. However, more recently, concerns have been raised about potential developmental effects on infants and adverse pregnancy outcomes.
In addition to extensive testing, FDA has completed a thorough analysis of a growing body of scientific studies linking adverse pregnancy outcomes to intake of relatively high levels of inorganic arsenic during pregnancy. The agency also found that exposure may result in a child’s decreased performance on certain developmental tests that measure learning.
Related to cancer, FDA estimated that exposure to inorganic arsenic in rice and rice products causes an additional four cases of lung and bladder cancer over the lifetime for every 100,000 people in the United States. This estimate would account for far less than 1 percent of the nation’s lung and bladder cancer cases.
4. What is FDA doing in light of its findings?
FDA is issuing a draft guidance to industry proposing a limit, or “action level,” of 100 parts per billion for inorganic arsenic in infant rice cereal. (Of note, the European Commission recently established a parallel level for rice intended for the production of food for infants and young children.) FDA testing found that the majority of infant rice cereal currently on the market either meets, or is close to, the proposed action level.
What FDA is asking food manufacturers to do will reduce the exposure for infants and, based on our testing, the agency believes this is feasible for the companies. FDA tested 76 samples of infant rice cereals on the market and found that nearly half of them — 47 percent — already meet the proposed limit. Moreover, most of the samples tested — 78 percent — were either at or below 110 parts per billion.
This is not the first time the federal government has limited arsenic in foods or beverages. The EPA has set a limit for inorganic arsenic in drinking water, and FDA has already set action levels, or recommended limits, for bottled water and apple juice.
5. If you have an infant or are pregnant, what should you do?
Based on the FDA’s findings with respect to inorganic arsenic in rice, the agency offers the following advice to parents and caregivers of infants. It is consistent with advice given by the American Academy of Pediatrics.
• Feed your baby iron-fortified cereals to be sure she or he is receiving enough of this important nutrient.
• Rice cereal fortified with iron is a good source of nutrients for your baby, but it shouldn’t be the only source, and does not need to be the first source. Other fortified infant cereals include oat, barley and multigrain.
• For toddlers, provide a well-balanced diet, which includes a variety of grains.
Also based on the FDA’s findings, it would be prudent for pregnant women to consume a variety of foods, including varied grains (such as wheat, oats, and barley), for good nutrition.
Published studies, including new research by the FDA, indicate that cooking rice in excess water (from six to 10 parts water to one part rice), and draining the excess water, can reduce from 40 to 60 percent of the inorganic arsenic content, depending on the type of rice — although this method may also remove some key nutrients.
6. If you’re an adult, what should you do?
The FDA did not find a scientific or public health basis to recommend that the general population of consumers change its rice consumption based on the presence of arsenic.
But the agency’s general advice about eating a well-balanced diet that’s not based on any one food extends to all consumers, including toddlers, older children and adults. Eating a variety of foods is more nutritious and if there are substances in food (like arsenic) where reducing exposure is prudent, you’re minimizing that exposure.
7. Is it ok for me to eat rice and give it to my children?
Consumers can certainly eat rice as part of a well-balanced diet. Based on our scientific assessment, we think it would be prudent for parents and caregivers to feed their infants a variety of fortified infant cereals, rather than to rely solely on infant rice cereal. We also encourage pregnant women to eat a variety of foods, including varied grains.
April 1, 2016
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-4,725,926,228,286,990,000 | (Official) Oral Antidiabetic Meds & N Light Direct
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-8,663,469,149,212,730,000 | Ask a doctor
What is the Protocol for Fixing Newly Broken Nose?
Can the doctor put a cast/splint of some sort to help it heal straight? If not, do I wait for it to heal and then seek plastic surgery to fix it?
Doctor Answers (12)
Nasal Fracture Treatment
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
The approach your surgeon will take with your nose will depend upon whether the fracture has displaced your nose and if so, how severely. A non-displaced nasal fracture can be observed and it will heal to the same shape it was prior to the injury. If your nose was displaced during the trauma, you will likely have to have the fractures reduced to straighten the nose.
The reduction procedure will also depend upon the degree of displacement you sustained. Your surgeon will decide and discuss this with you. My suggestion is to fix your nose before it heals, if all you want is to have the nose you had before your injury. If you are looking for cosmetic improvements, you can either do it at the same time as the fracture repair, or you may have to delay the surgery until the nose has healed enough to perform cosmetic rhinoplasty.
Chevy Chase Facial Plastic Surgeon
4.5 out of 5 stars 9 reviews
Broken Nose Repair
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
Our protocol for a broken nose depends on the timing of the initial consultation. In some cases, it is important to reset the broken nasal bones under general anesthesia. If there is severe swelling, the swelling is allowed to subside before initiating any further surgery.
Raffy Karamanoukian, MD, FACS
Los Angeles Plastic Surgeon
5.0 out of 5 stars 56 reviews
Fixing a newly broken nose
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
The protocol in our office for a broken nose repair is to formally reset the nose under general anesthesia. It took a lot of force to break it in the first place, and it needs to be set and realigned while asleep under general anesthetic. Most of the time when the outside of the nose is broken the internal septum is also fractured and crooked, creating a deviated septum. It is important to let the swelling to come down during the first two weeks prior to embarking on surgery to see how and where the nose is crooked. Additionally, spreader grafts can be performed with the patient’s own cartilage when the upper lateral cartilage of the nose is fractured off the nasal bone, creating a breathing issue.
William Portuese, MD
Seattle Facial Plastic Surgeon
5.0 out of 5 stars 60 reviews
Nasal Fracture
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
The nose should be evaluated as soon as possible after the trauma to rule out a septal hematoma (a blood clot within the septum) which could cause permanent damage to the nasal structure. If present the hematoma should be evacuated immediately. If not, wait about 10 days to determine if there has been a change in nasal appearance or breathing obstruction. If neither has occured, treatment of the fracture is not necessary. With deviation of the nasal bones, they can be manually repositioned without making incisions within the nose. If it is determined there is more severe injury with breathing obstruction or displacement of the cartilagenous structures I would do a comlete rhinoplasty to reduce the fractures. Timing depends on the severity of the injury.
Richard W. Fleming, MD
Beverly Hills Facial Plastic Surgeon
5.0 out of 5 stars 16 reviews
Nasal Fracture
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
It is ideal to wait for the swelling to decrease, maybe a week or two and then perform a closed nasal reduction to reset the bones. Even doing this, there is 50% chance that you will need some sort of revision rhinoplasty later down the line. I like to wait 1 year before attempting the revision rhinoplasty.
Good luck.
Farbod Esmailian, MD
Orange County Plastic Surgeon
5.0 out of 5 stars 47 reviews
Nasal bone fracture
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
A splint will not help it heal straight. If the nose is crooked it must first be reset to straighten it. If the nose is not reset with in the first 10 days, as the nasal bones can be shifted during this time, then usually it is best to wait 3 months.
Sharon Theresa McLaughlin MD
Long Island City Plastic Surgeon
Timing of nasal fracture repair.
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
There are 3 basic time points in which a nasal fracture can be repaired.
1) Within a few hours after the injury. This is due to the fact that the nose will start to swell, thus making it difficult to assess and modify the nasal contours and position.
2) After several hours and before 2 weeks. During this window, we wait until the swelling has come down and then re-set the bones into their appropriate position.
3) After 8 weeks. If the nose is not repaired within 2 weeks, it is required to wait until the nose has essentially healed prior to re-fracturing and re-setting it.
Keep in mind that it is possible a rhinoplasty will still need to be done as there are a percentage of the patients that will not get a "perfect" result and require a formal procedure.
Amir M. Karam, MD
San Diego Facial Plastic Surgeon
4.5 out of 5 stars 87 reviews
Fix broken nose within ten days or wait eight weeks
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
The nose must be evaluated on two fronts: breathing and external appearance.
Assuming there is not major blockage preventing breathing, which is the only bonafide broken nose emergency, either the correction of breathing/appearance is done within the ten days after injury or one waits to operateuntil the bones have welded together, which is usually by eight weeks later.
The cosmetic nasal surgery specialist must perform a complete evaluation at the time of consultation after the accident. Must evaluate the degree of injury to the internal and external support structures. Must also evaluate the swelling since you cannot do the best work until the swelling goes down; typically that is within one week.
After ten days, that first window of repair opportunity is lost because the bones start to heal in whatever position they are in. So, the surgeon waits until the next appropriate time which is at the eight week mark by which time the bones are solid enough to be re-positioned.
You must understand that often, despite the best talent, there is a need for a touch-up after the original procedure, whether within that first window or later. This is because Nature can be unpredictable and set down some extra bone which might present as a little bump that was not present prior to the injury.
Finally, it is helpful to the surgeon if you bring photos of your appearance prior to accident. The doctor needs to know what your nose was like orignally.
Robert Kotler, MD
Beverly Hills Facial Plastic Surgeon
5.0 out of 5 stars 61 reviews
3 times for correction
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
I fix broken noses at three different time - 1 at the time of injury if there is little swelling - if swolen, I wait 7 to 14 days and do a closed reduction. If you have waited longer than 2 to 3 weeks before seeing a doctor, I wait until it heals and then fix it with and open reduction at 3 months.
William B. Rosenblatt, MD
New York Plastic Surgeon
4.0 out of 5 stars 9 reviews
Timing after a nasal fracture is important.
{{ voteCount >= 0 ? '+' + (voteCount + 1) : (voteCount + 1) }}
I usually recommend against "immediate" reduction of a fracture for two reasons: 1) swelling--which occurs very quickly after a fracture--can obscure the actual curvature making accurate alignment difficult or impossible, and 2) "immediate" reduction usually means in the E.R. and not the O.R., so adequate pain control is usually impossible.
As for delaying the reduction, I usually like to treat patients after 5-7 days, but before 2 weeks. By two weeks, the bones are often beginning to heal in place and will require more effort and sometimes osteotomies (bone cuts) to get the nose adequately straight.
More significant problems can occur with delays beyond 4-6 weeks, since the bones themselves start to "remodel" and can take on permanent shape changes that require more extensive rhinoplastic correction.
After a fracture reduction, I do apply a cast to keep everything protected and aligned. The cast is removed in the office about a week later.
All the best,
--DCP
David C. Pearson, MD
Jacksonville Facial Plastic Surgeon
5.0 out of 5 stars 17 reviews
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship. | {
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-71,782,832,887,537,864 | Osartan Hz
Osartan Hz may be available in the countries listed below.
Ingredient matches for Osartan Hz
Hydrochlorothiazide
Hydrochlorothiazide is reported as an ingredient of Osartan Hz in the following countries:
• Bangladesh
Losartan
Losartan is reported as an ingredient of Osartan Hz in the following countries:
• Bangladesh
International Drug Name Search
Important Notice: The Drugs.com international database is in BETA release. This means it is still under development and may contain inaccuracies. It is not intended as a substitute for the expertise and judgement of your physician, pharmacist or other healthcare professional. It should not be construed to indicate that the use of any medication in any country is safe, appropriate or effective for you. Consult with your healthcare professional before taking any medication.
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-1,564,567,420,872,247,800 | Is Slim Fast Bad for You?
Slim Fast is a weight loss supplement designed to help you lose and maintain weight. Products include ready to eat drinks and bars, drink powders, snack bars, ice cream, soup and pasta entrees. When properly used, it is a safe and effective product. It is effective in weight loss and in improving bodily compounds. Overall, it is a weight loss supplement that is not bad for you.
Program Components
There are three components to the Slim Fast program: replacing one to two meals daily with a Slim Fast product, eating nutritious foods for the rest of meals and snacks daily and getting thirty to sixty minutes physical activity each day. When you fully comply with the program, you are able to safely lose and maintain weight. If you do not properly follow the program recommendations, you may increase potential health and weight risks, such as sending your body into starvation mode. You can refer to a dietitian or doctor for further information on the program and proper weight loss plans.
Potential Risks
If you were to consume nothing but Slim Fast shakes, you would consume too few calories per day, which would cause your body to go into starvation mode. When your body is in starvation mode, it harms the body. You start to lose lean muscle tissue and hair growth becomes abnormal. Also, not only do you cause damage to your body, but you are more likely to regain the weight.
Potential Benefits
Slim Fast can be good for you if you follow the proper regimen. As with any weight loss program, physical activity and a balanced diet are important. It takes time to take off the weight. You should aim to lose 1 to 2 lbs. per week, which is ideal for weight loss and maintenance. If you properly comply with the program recommendations, you will be on your way to weight loss and maintenance. As an added bonus, you may also benefit from improved insulin, triglyceride, cholesterol, and blood glucose levels, according to an article published in "Obesity Management" in April 2005.
Should You Use Slim Fast?
If you are to follow program guidelines, Slim Fast can be a good option for weight loss and maintenance. There must be a balance between regular physical activity and other nutritious foods. If you are able to either maintain or lose weight by diet and exercise alone, Slim Fast is probably not a reasonable option for you. If you just cannot find the time to prepare nutritiously balanced meals, however, using the Slim Fast diet is not a bad option. Consult your doctor or dietitian before starting the program.
× | {
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8,225,242,767,559,727,000 | Format
Items per page
Send to:
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Links from PubMed
Items: 1 to 20 of 37
1.
Leukemia
Leukemia is cancer of the white blood cells. White blood cells help your body fight infection. Your blood cells form in your bone marrow. In leukemia, the bone marrow produces abnormal white blood cells. These cells crowd out the healthy blood cells, making it hard for blood to do its work. There are different types of leukemia, including. -Acute lymphocytic leukemia. -Acute myeloid leukemia. -Chronic lymphocytic leukemia. -Chronic myeloid leukemia. Leukemia can develop quickly or slowly. Chronic leukemia grows slowly. In acute leukemia, the cells are very abnormal and their number increases rapidly. Adults can get either type; children with leukemia most often have an acute type. Some leukemias can often be cured. Other types are hard to cure, but you can often control them. Treatments may include chemotherapy, radiation and stem cell transplantation. Even if symptoms disappear, you might need therapy to prevent a relapse. NIH: National Cancer Institute. [from MedlinePlus]
MedGen UID:
9725
Concept ID:
C0023418
Neoplastic Process
2.
Acute lymphoblastic leukemia
A form of acute leukemia characterized by excess lympoblasts. [from HPO]
MedGen UID:
505958
Concept ID:
CN005851
Finding
3.
Acute
Sudden appearance of disease manifestations over a short period of time. [from HPO]
MedGen UID:
61381
Concept ID:
C0205178
Temporal Concept
4.
Acute lymphoid leukemia
Acute lymphoblastic leukemia (ALL), also known as acute lymphocytic leukemia, is a subtype of acute leukemia, a cancer of the white blood cells. Somatically acquired mutations in several genes have been identified in ALL lymphoblasts, cells in the early stages of differentiation. Germline variation in certain genes may also predispose to susceptibility to ALL (Trevino et al., 2009). Genetic Heterogeneity of Acute Lymphoblastic Leukemia A susceptibility locus for acute lymphoblastic leukemia (ALL1) has been mapped to chromosome 10q21. See also ALL2 (613067), which has been mapped to chromosome 7p12.2; and ALL3 (615545), which is caused by mutation in the PAX5 gene (167414) on chromosome 9p. [from OMIM]
MedGen UID:
7317
Concept ID:
C0023449
Neoplastic Process
5.
B-Cell Leukemia
A malignant disease of the B-LYMPHOCYTES in the bone marrow and/or blood. [from MeSH]
MedGen UID:
412152
Concept ID:
C2004493
Neoplastic Process
6.
Clonal Evolution
The process of accumulation of genetic and epigenetic changes over time in individual cells and the effect of the changes on CELL PROLIFERATION. [from MeSH]
MedGen UID:
273181
Concept ID:
C1516669
Neoplastic Process
7.
Neoplasm
An organ or organ-system abnormality that consists of uncontrolled autonomous cell-proliferation which can occur in any part of the body as a benign or malignant neoplasm (tumour). [from HPO]
MedGen UID:
10294
Concept ID:
C0027651
Neoplastic Process
8.
Neoplasms
MedGen UID:
880980
Concept ID:
CN236628
Disease or Syndrome
9.
Leukemia, acute lymphoblastic, susceptibility to, 3
MedGen UID:
816204
Concept ID:
C3809874
Neoplastic Process
10.
PROGRESSIVE ENCEPHALOMYELITIS WITH RIGIDITY
MedGen UID:
349287
Concept ID:
C1861457
Disease or Syndrome
11.
metaplastic cell transformation
The conversion of a cell from a normal phenotype, which undergoes a limited number of mitotic divisions, into an aberrant phenotype that is immortal and divides indefinitely. Transformed cells no longer retain cell-cycle checkpoints and may ultimately become malignant cancer cells via additional genetic mutations, or damaging environmental events. [from NCI]
MedGen UID:
266929
Concept ID:
C1510411
Pathologic Function
12.
Residual Disease
Cancer cells that remain after attempts to remove the cancer have been made. [from NCI_NCI-GLOSS]
MedGen UID:
108162
Concept ID:
C0543478
Neoplastic Process
13.
Minimal Residual Disease
remainder of a tumor or a neoplasm/cancer after primary, potentially curative therapy. [from CRISP]
MedGen UID:
66115
Concept ID:
C0242596
Neoplastic Process
14.
Clinical finding
clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [from CRISP]
MedGen UID:
19974
Concept ID:
C0037088
Sign or Symptom
15.
Recurrence (disease attribute)
The return of a sign, symptom, or disease after a remission. [from MeSH]
MedGen UID:
416712
Concept ID:
C2825055
Pathologic Function
16.
Precursor Cell Lymphoblastic Leukemia-Lymphoma
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias. [from MeSH]
MedGen UID:
409528
Concept ID:
C1961102
Neoplastic Process
17.
Disease Attributes
Clinical characteristics of disease or illness. [from MeSH]
MedGen UID:
199876
Concept ID:
C0752357
Disease or Syndrome
18.
Lymphatism
MedGen UID:
141817
Concept ID:
C0524631
Disease or Syndrome
19.
Pre-B Acute Lymphoblastic Leukemia
An acute lymphoblastic leukemia that originates from pre-B lymphocytes. The pre-B lymphoblasts contain cytoplasmic immunoglobulin. [from NCI]
MedGen UID:
44126
Concept ID:
C0023485
Neoplastic Process
20.
Leukemia, Lymphocytic, Acute, L1
When the disease process is confined to a mass lesion with no or minimal evidence of blood and less than 25% marrow involvement, the diagnosis is lymphoblastic lymphoma; with blood and greater than 25% marrow involvement, ALL is the appropriate term. [from MeSH]
MedGen UID:
44122
Concept ID:
C0023452
Neoplastic Process
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Our Patient Center
Kidney Stones
Kidney stones are made of salts and minerals in the urine that stick together to form small "pebbles." They can be as small as grains of sand or as large as golf balls. They may stay in your kidneys or travel out of your body through the urinary tract. The urinary tract is the system that makes urine and carries it out of your body. It is made up of the kidneys, the tubes that connect the kidneys to the bladder (the ureters), the bladder, and the tube that leads from the bladder out of the body (the urethra).
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Benign Prostatic Hyperplasia
Benign Prostatic Hyperplasia (BPH) is an enlarged prostate gland. The prostate gland surrounds the urethra, the tube that carries urine from the bladder out of the body. As the prostate gets bigger, it may squeeze or partly block the urethra. BPH occurs in most men as they age. About half of all men over the age of 75 experience symptoms.
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Erectile Dysfunction
Erectile dysfunction, or ED, is the inability to achieve or sustain an erection suitable for sexual intercourse. Causes include medications, chronic illnesses, poor blood flow to the penis, drinking too much alcohol, or exhaustion.
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-3,544,399,048,906,631,700 | Diagnosis & Detection
Giardia trophozoites and cysts under a microscope.
Giardia trophozoites and cysts. Credit: Waterborne Disease Prevention Branch, CDC
Because Giardia cysts can be excreted intermittently, multiple stool collections (i.e., three stool specimens collected on separate days) increase test sensitivity 1. The use of concentration methods and trichrome staining might not be sufficient to identify Giardia because variability in the concentration of organisms in the stool can make this infection difficult to diagnose. For this reason, fecal immunoassays that are more sensitive and specific should be used 2.
Rapid immune-chromatographic cartridge assays also are available but should not take the place of routine ova and parasite examination 2. Only molecular testing (e.g., polymerase chain reaction) can be used to identify the subtypes of Giardia.
References
1. Clinical and Laboratory Standards Institute. Procedures for the recovery and identification of parasites from the intestinal tract; approved guideline. CLSI document M28-A2. 2nd ed. Wayne, PA: Clinical Laboratory Standards Institute; 2005.
2. Johnston SP, Ballard MM, Beach MJ, Causer L, Wilkins PP. Evaluation of three commercial assays for detection of Giardia and Cryptosporidium organisms in fecal specimensExternal. J Clin Microbiol. 2003;41(2):623-6. | {
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What Are the Health Benefits of Nitric Oxide Formulas?
By Jake Boly
In this article:
If you love the gym and performing at your best, then chances are you’ve heard about supplements that have the words “nitric oxide” attached to them. These supplements are generally regarded as only being beneficial for more bodybuilding-style fitness enthusiasts, but is that really true?
Nitric oxide is a product of nearly every cell in the body and plays an important role in vasodilation. Vasodilation is the process of widening blood vessels, which increases blood flow and pressure through our body’s veins, arteries, and arterioles. This process helps to support athletic performance.
In theory, if we can increase our blood flow, then our oxygen and nutrient availability will increase, which can then promote enhanced exercise ability. In this article, we’ll discuss what nitric oxide is, how increasing it can help performance, and which nitric oxide supplements are best.
What Is Nitric Oxide?
Before discussing the benefits of nitric oxide on athletic performance and overall health, it’s a good idea to first understand what nitric oxide is.
Nitric oxide is a signaling molecule that can be found within nearly every cell in the body. The best way to describe a signaling molecule is that they play an important role in how our cell’s “signal,” or talk with one another to create both simple and complex reactions.
In nitric oxide’s case, the signaling that goes on within the body is with the endothelium of blood vessels. Endothelium is a thin layer of cells that lines organs such as the heart and other areas of the body. The blood vessels that interact with nitric oxide then signal to surrounding smooth muscle cells to relax and dilate, which causes vasodilation. In addition to widening blood vessels, vasodilation lowers blood pressure levels.
As we age, our nitric oxide levels naturally decrease. On top of aging, things like smoking, poor diet and inactivity can also cause natural nitric oxide levels to decrease. This natural and not-so-natural decrease has sparked much of the interest in nitric oxide formulas and using them to improve performance not just in the gym, but in daily life as well.
How Increasing Nitric Oxide Can Improve Performance
When exercising, especially at high intensities, our muscles and body require adequate blood flow to perform at a desired level. Adequate blood flow helps deliver ample oxygen and nutrients to the muscles and organs when they need it most.
Since nitric oxide is a vasodilator, then it’s in an active individual’s best interests to be very mindful of their natural nitric oxide levels. If fitness enthusiasts can improve their blood flow during exercise, then their bodies will have a better chance of performing at higher levels due to more oxygen and nutrient availability.
Supplements that are regarded as “nitric oxide” supplements or “NO boosters” don’t actually contain nitric oxide. In reality, they contain ingredients that may potentially increase nitric oxide availability within the body, which can lead to better performance.
Supplements That Can Improve Nitric Oxide
Below, we’ll cover three popular nitric oxide supplement options that may benefit your performance.
It’s important to remember that not every supplement will hold the same performance benefits for every individual across the board. In addition, some of the supplements warrant more research before drawing definitive claims on dosages.
L-Arginine
One of the most popular and go-to options for individuals looking to improve their nitric oxide production is L-arginine. This semi-essential amino acid is used by nearly every cell in the body and plays a major role in nitric oxide formation.
L-arginine is so prominent that it’s said to compose about 5-7% of the total amino acids contained in the body. Multiple foods we consume on a daily basis, like nuts, seeds, meat, and poultry contain L-arginine.
When it comes to performance and health, L-arginine has been suggested to play a role in autoimmune disorders, endothelial function, oxidative stress, cardiovascular disease, sports performance, and body composition. For the sake of this article, we’ll focus strictly on its potential benefits for performance and body composition.
In a 2017 study published in the European Journal of Clinical Nutrition, researchers sought to explore the use of L-arginine and its effects on VO₂ maxes (the maximum amount of oxygen you can utilize during exercise) and body composition. The authors had 56 soccer players split into an L-arginine and placebo group and recorded their VO2 maxes, body mass index, lean body mass, and body fat mass.
The L-arginine subjects consumed 2g of the supplement each day, while the placebo group consumed maltodextrin. Upon their 45-day analysis, the authors noted that the L-arginine group’s VO2 maxes improved, however, there were no significant differences in body mass index, lean body mass, and body fat mass between the two groups.
The authors of this study concluded that L-arginine could be useful for increasing sports performance, but not necessarily for improving body composition-related outcomes.
Beetroot Juice
Another supplement that has been associated with improving nitric oxide levels is beetroot juice. This supplement is incredibly high in nitrates/nitrites, which are natural compounds found in nutrient-dense foods such as beets and other vegetables.
Beetroot juice is a popular option for athletes that want to improve their stamina and increase their daily nitrate intake. In a 2018 study published in PLoS One, researchers had 12 elite middle- and long-distance runners split into two groups: beetroot juice and placebo. The study subjects supplemented with either 70mL of beetroot juice or the prescribed placebo for 15 days.
Authors tracked each individual’s running economy, rating of perceived exertion, time to exhaustion, and vastus lateralis oxygen saturation. After the 15-day study, authors retested the subjects and noted that the beetroot juice subjects substantially improved their rating of perceived exertion and time to exhaustion, however, there were no biomechanical differences between the two groups for running economy and vastus lateralis oxygen saturation.
Another 2019 study comes from the Journal of Strength and Conditioning Research. This study compared beetroot juice (400-mg), citrulline malate (8g) and a placebo with one another to identify differences in a subject’s blood flow, metabolic efficiency, and performance during maximal isokinetic knee extensions.
The study authors had 27 recreationally active individuals split into three groups and come into the lab for three separate testing days. Every subject consumed their prescribed beverage, then rested for two hours before undergoing a warm-up and five sets of 30 concentric knee extensions.
Before and after the knee extensions, researchers used ultrasound to assess the diameter and blood flow through the superficial femoral artery, then plasma analytes, urea nitrogen, and calorimetry measures were taken to assess energy expenditure.
The authors concluded that the beetroot juice group had higher nitrate and nitrite levels within the body pre- and post-exercise intervention. However, they noted that none of the three groups displayed superior benefits when it came to improvement of performance on the leg press through supplementation.
L-Citrulline
L-citrulline is a non-essential amino acid that is often supplemented to improve performance and potentially increase blood flow. It’s theorized that L-citrulline may increase arginine when taken orally, and it may also increase nitric oxide in the body.
Both l-citrulline and citrulline malate are popular supplements to use alone and are often found within pre-workout formulas. The main difference between L-citrulline and citrulline malate is that citrulline malate has the addition of malic acid to it, which provides it with a tart taste.
Multiple studies have investigated the use of citrulline for improvements in athletic performance. In a recent 2019 meta-analysis, authors assessed how citrulline acutely impacted high-intensity strength and power.
Twelve studies were included in this meta-analysis and authors only included studies that focused on compound movements and utilized citrulline by itself compared to a placebo. For additional context, studies that focused on isolation exercises, citrulline supplement mixtures, citrulline doses less than 3g, and citrulline doses given within less than 30-minutes of exercise were excluded.
Upon their analysis, researchers concluded that citrulline had a significant impact on performance versus the placebo, however, the effect size was small.
Generally, the use of nitric oxide-boosting supplements is safe. If you’re hypotensive, then you should discuss any potential side effects with a medical professional. Before starting any new supplement, it’s always a good idea to consult with your general physician to inquire about dosages, contraindications and best uses.
References:
1. https://www.ncbi.nlm.nih.gov/pubmed/9806879
2. https://www.researchgate.net/publication/318855811_The_effect_of_L-arginine_supplementation_on_body_composition_and_performance_in_male_athletes_a_double-blinded_randomized_clinical_trial
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6040767/
4. https://www.ncbi.nlm.nih.gov/pubmed/31343548
5. https://www.researchgate.net/publication/331905096_Acute_Effects_of_Citrulline_Supplementation_on_High-Intensity_Strength_and_Power_Performance_A_Systematic_Review_and_Meta-Analysis
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What is Fasting Glucose?
By Sheri Cyprus
Updated: May 17, 2024
Views: 14,220
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Fasting glucose is a blood sugar measurement taken after no food has been eaten for at least 8 to 10 hours. A fasting blood sugar (FBS) test is usually the first kind used when a doctor orders testing for diabetes diagnosis. Diabetics can test their own fasting glucose before breakfast with a home blood sugar monitor.
Most diabetics record their blood sugar readings at different times each day to track their glucose levels overall during a given week. In addition to a fasting glucose, two hours after meals is another common time to check blood sugar levels. Many diabetic people eat five or six small meals throughout the day rather than three large ones to avoid causing big fluctuations in their blood sugars. Exercise can also affect blood sugar — usually causing it to lower. Fasting blood sugars should also be on the low side since there is no food in the body.
During diabetes diagnostic procedures, doctors first usually order an FBS test before having an oral glucose tolerance test (OGTT) conducted. While the FBS tests the body's fasting glucose on an empty stomach, the OGTT measures its reaction after drinking a controlled amount of sugary substance. The OGTT is usually performed several times in order to get an accurate result. A one-hour OGTT is routinely given to pregnant women to screen them for gestational diabetes. Gestational diabetes occurs in pregnancy and typically presents as high blood sugar levels.
A state of high blood sugar is called hyperglycemia, while a low glucose level is hypoglycemia. Diabetics may experience a wide range of sugar levels from high to low and this can be extremely dangerous. Drastically low or high glucose levels can cause medical problems or even coma and death. Understanding how the body reacts to taking in sugar as well as its fasting glucose level can help control wide fluctuations in blood sugars for better health outcomes.
FBS and OGTT differ from random blood sugar (RBS) tests. Unlike fasting glucose and sugar tolerance tests, the RBS checks blood sugars at any time. In non-diabetic people, blood sugar doesn't usually fluctuate as greatly as it does in many diabetics. Normal blood sugar levels are often considered to be about 100 ml or a little higher than that. The goal of monitoring fasting glucose as well as other sugar tests is to better control hyperglycemia, hypoglycemia and diabetes through awareness, diet and/or medication.
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Discussion Comments
By aLFredo — On Nov 05, 2011
Fasting glucose is a quite simple test to prepare for, although it does sound quite daunting. All you have to do is fast from midnight until after your scheduled appointment the next day, given that it is not before eight o’clock, or after ten o’clock.
If it is before eight o’clock, you should make sure you have not ate for at least eight hours before your appointment. So, for instance, if your appointment is at seven o’clock in the morning, do not eat after eleven o’clock. If your appointment is at noon, do not eat past four in the morning, although you really should try not to eat after midnight anytime, unless you work third shift or are up the hours of third shift.
You really shouldn’t eat right before you go to bed anyway or any time, as this can increase your chances of gaining weight and having an upset stomach too.
You can prevent or at least lessen your chances of getting type two diabetes by eating healthy most of the time. Staying away from sugar and foods with sugar in them would be a good thing to do too.
By Saraq90 — On Nov 04, 2011
@geekish - Yes, there are some symptoms of a vitamin D deficiency, although some people do not have any symptoms at all.
The most common symptoms of a vitamin D deficiency are muscle weakness and bone pain and bone fractures. The other symptoms associated with vitamin D deficiency are unexplained depression, persistent fatigue, weakness, mood swings and not being able to concentrate.
Feeling shaky and weak if you only go a couple hours without eating could be a lot of different things, but it is definitely serious enough to get to a professional to find out what is going on as soon as possible. Even if you don't have diabetes, it could be something just as severe or more severe. Go to the doctor as soon as possible!
By John57 — On Nov 04, 2011
@wander - There are several ways you can test your glucose at home, but all of them require some kind of tools and some know how.
The traditional method of doing this is by pricking your finger with a lancet and getting a reading that way.
A lancet is a small sharp needle and you use that to put a drop of blood on a test strip and then put into a meter to get your reading.
There are newer methods that allow you to prick other areas of your body instead of your finger, such as your thumb or upper thigh. With some of the newest ways, you don't even have to prick your finger but they use lasers and electric currents.
I really don't know how these newer methods work, and how you begin using them, I just know there are other options available.
My mother has had diabetes for many years, and it gets really hard to keep pricking your finger over and over again, but she is able to get accurate readings this way.
Once you get the hang of it, it is not hard, and you don't have to run to the doctors office every time you need check your levels.
If you want it to be a fasting check, just make sure you haven't eaten for at least 8 hours before you check it. Otherwise you can check it during the day to make sure you are staying where you need to be.
By geekish — On Nov 03, 2011
I feel as though I may need a fasting glucose test. Lately I have been getting very weak and shaking uncontrollably if I go too long without a snack or something. When I mean too long, I mean around two hours, nothing drastic like five hours or all day or anything.
The reason why I am extra alarmed is because I dated someone with type one diabetes before and he would get weak and shaky if didn't eat a snack within a couple hours. He also, a couple times, got so bad that he totally lost control of his mind and body, and collapsed on the floor. I definitely do not want this to happen to anyone, me included.
I guess I should go to the doctor and get an all-inclusive physical, although I got one earlier this year. The previous physical showed I have a very low Vitamin D count. I take Vitamin D supplements now. Does anyone know if a lack of Vitamin D has any symptoms? If so, what are they?
By wander — On Nov 03, 2011
Is it possible to do a fasting glucose reading at home with your own blood sugar monitor? Or can this test only be performed at a doctor's office?
I live quite far from my doctor's office and would like to do a fasting blood glucose test without having to go all the way to her office. I am prediabetes and want to see if the dietary changes I've been making have helped get my blood sugar levels under control.
I am worried that despite everything I have done I will still have elevated fasting glucose levels and be stuck on the same diet forever. I really want my life to get back to normal.
By drtroubles — On Nov 02, 2011
@popcorn - My mother has Type 2 diabetes and it can be a really difficult medical problem to deal with. If you are taking a fasting glucose test you should know that the normal fasting glucose range is under 100 mg/dL, and those with fasting levels between 100 mg/dL to 125 mg/dL are considered to be prediabetes.
If you find yourself worried about food, just stop eating sugary things. You need to eat healthy and not starve yourself. If you do have prediabetes it can often be controlled with changes to diet. I would talk to your doctor after your test and figure out exactly what is going on with your body.
By popcorn — On Nov 02, 2011
My doctor has asked me to undergo a fasting blood glucose test later this week and I am feeling a bit nervous. What is a normal fasting blood glucose level?
Lately I have been urinating a lot and feeling really irritable after eating, so my doctor thinks I may have diabetes so he is making sure I get all the tests I need. I have actually been scared off eating and haven't been having much since he told me I could have such a terrible disease. I am wondering what I should eat until the fast before the test? Do you think that just going vegetarian would help me feel better?
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-1,098,076,796,895,001,700 | Colon Cancer Signs And Symptoms Treatment
Colon Cancer Signs And Symptoms Treatment
What is Colon Cancer?
Colon cancer happens in the large intestine or the large gut and is an extremely basic sort of cancer, it just likes secondary lung cancer in the event. The danger of colon cancer is higher in specific gatherings and ethnicity, and also in individuals living in Western industrialized nations. The positive side is that colon cancer likewise has a high rate of cure and survival.
Colon cancer is otherwise called colorectal cancer. The large intestine has two segments: the upper segment is the colon and the lower bit is the rear-end or the rectum. Cancer in the large intestine possible to feast over both areas, which stretches it the name colorectal cancer. The colon retains water and supplements amid nourishment absorption. The rectum, then again, serves to remove squander material from the body. There are four sections to the colon, and cancer can begin creating in any of these parts.
Colon Cancer Symptoms
The cancerous development in the colon generally begins as a polyp. A polyp is a little tissue development. This polyp will develop into the colon and if left untreated it can form into cancer over a time-frame. A particular sort of polyp, called adenomacan, is the essential seed of colon cancer. On a normal, it takes 5-10 years for a polyp to achieve a width of around .5 inch. This takes a further 5-10 years to form into cancer.
Colon Cancer Treatment And Prevention
Despite the fact that 20 years appears to be sufficient to identify and treat cancerous improvement, it is hard to perceive any development for quite a long while. Gratefully, there are numerous demonstrative methods accessible to effectively distinguish any cancerous development or polyps. Some basic procedures utilized as a part of diagnosing and treating colon cancer are barium purification, sigmoidoscopy, colonoscopy, and biopsy. Aside from this, patients can be screened to observe any blood in the stool or unexplained iron inadequacy to see whether there is any polyp or cancer creating.
Colon cancer is a boundless illness, and a considerable measure of research is in progress to build survival rates and help early conclusion. There are likewise numerous establishments that guide colon cancer patients and give data to individuals.
If you think that this topic “colon cancer sign and symptoms treatments” is useful to everyone. Just give it a little time to share it with your friends and family that you care using email and social sites.
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-8,236,470,122,690,587,000 | People with bipolar disorder have high rates of co-occurring substance use disorders. Many complex biological and personal factors lead to the development of these comorbid disorders, but the case is often simple: people with bipolar disorder frequently start using alcohol or other drugs to cope with their symptoms.
Unfortunately, the negative consequences of co-occurring bipolar and substance use disorders include increased risks of psychosis, suicide and self-harm through reckless actions.
Drug Abuse as a Hindrance to Bipolar Treatment
Treatment of bipolar disorder typically involves both therapy and medication. In the case of bipolar disorder, medication is essential. While trauma and personal factors can worsen and trigger bipolar symptoms, the disorder is biologically driven and persists even when people make significant psychological breakthroughs in therapy.
The medications most frequently prescribed for bipolar disorder are a class of mood stabilizers called anticonvulsants. Medications like lamotrigine and oxcarbazepine for bipolar disorder can help prevent or lessen symptoms of depression and mania. One of the biggest risks for people with bipolar disorder is thinking their symptoms have been cured, discontinuing medications and experiencing a serious manic or depressive episode.
Substance abuse significantly increases the risk that a person with bipolar disorder will stop taking their medications and trigger a recurrence of symptoms that may have been controlled for a long time. Using substances also interrupts the therapeutic process, causing people to forget or abandon skills or insights from therapy. The consequences of dropping out of bipolar disorder treatment can be severe, leading to hospitalization or even attempted suicide.
Effects of Substance Abuse on Bipolar Disorder
Bipolar disorder is characterized by alternating mood episodes. Some people with bipolar disorder may simply shift from manic episodes to symptom-free periods, while many others experience manic or hypomanic episodes followed by depressive episodes.
People with bipolar disorder may use the same substances in both manic and depressive periods or use multiple substances with different effects. Drugs like alcohol and marijuana can help people feel calmer during manic periods or may act to heighten feelings of creative inspiration. Alcohol can also numb the pain associated with a depressive episode. Whereas, Stimulants can temporarily boost energy.
Some of the biggest risks for people with co-occurring mood and substance use disorders come from the residual effects that occur between periods of use. Most substances that boost mood or energy causes people to experience dysphoria and lethargy after their effects wear off. These effects can be especially severe for people with bipolar disorder and may trigger a mood episode.
Alcohol and Bipolar
Co-occurring bipolar disorder and alcoholism are common. Approximately 46 percent of people with bipolar disorder have had an alcohol use disorder in their lives. People with bipolar disorder often use alcohol to regulate their thinking and mood during both manic and depressive episodes.
Combining bipolar and alcohol use can be especially dangerous. For people with bipolar disorder whose symptoms are otherwise controlled, alcohol can induce a serious depressive episode. It can also complicate manic symptoms and make people more likely to act on delusions or have other psychotic symptoms.
People who drink also tend to be more irritable and volatile. Using alcohol can make someone with bipolar disorder have less stable moods. It can also make them more likely to become aggressive and angry, even to the point of having what some people call a “bipolar rage episode.”
Marijuana and Bipolar
Marijuana and bipolar symptoms interact in a similar way as alcohol and bipolar. Cannabis can have a calming effect that makes it easier to rest and focus during episodes of anxiety or mania. Unfortunately, it can just as easily trigger severe anxiety, paranoia and panic.
Under the influence of marijuana, bipolar symptoms are more likely to progress into psychosis. Research shows marijuana can trigger psychotic symptoms, especially in vulnerable individuals like people with mental health conditions such as bipolar disorder. In addition, marijuana use is linked with longer and more frequent mood episodes for people with bipolar disorder.
Stimulants and Bipolar
People use stimulants for many reasons. In small doses, stimulants can increase mental energy and focus. They can also induce feelings of mild euphoria or empowerment that make challenging activities more engaging and less stressful.
For people with bipolar disorder, stimulants have additional risks. They can trigger manic symptoms and episodes even in people whose symptoms are managed by mood-stabilizing medications. This is why people with co-occurring bipolar and attention-deficit hyperactivity disorder are rarely prescribed the stimulants. For instance, Adderall and bipolar disorder do not mix well.
Despite these risks, people with bipolar disorder frequently abuse stimulant drugs, often in an attempt to prolong the more pleasant symptoms of hypomania.
Statistics on Bipolar Disorder and Drug Abuse
Nearly 60 percent of people with bipolar disorder have had a substance use disorder at least once. Alcohol is the substance most commonly abused by people with bipolar disorder and in general. People with bipolar disorder are 14 times more likely to abuse drugs and six times more likely to have alcohol dependence than the general population. Substance abuse in people with bipolar disorder is also linked to higher rates of suicide, hospitalization and accidents, as well as lower rates of participation in treatment.
Can Drug Abuse Cause Bipolar Disorder?
Bipolar disorder is rooted in genetic and biological factors and cannot be caused solely by environmental factors or adult behavior like substance abuse. However, using substances can trigger mood episodes in people who already have the disorder. In addition, substance use in adolescence may cause people who are vulnerable to develop bipolar disorder more rapidly or to become symptomatic.
Treating Bipolar Disorder and Co-Occurring Substance Abuse
Bipolar disorder is usually treated with a combination of psychiatric medication and therapy. People with bipolar disorder work with therapists to recognize signs and triggers of mood episodes and how to change their behavior to assist the mood-regulating effects of bipolar disorder medications. They may need to process past trauma and explore interpersonal issues.
Integrated treatment is essential for an effective medical response to co-occurring disorders. This means that each individual component of a treatment plan should serve the same goals and be coordinated by professionals who communicate regularly with one another. Integrated treatment rests on the principle that treating mental health and substance use disorders at the same time leads to better outcomes for each.
Living with bipolar disorder can be challenging, especially for people who are also struggling with addiction, as relying on drugs or alcohol to relieve bipolar disorder symptoms can be extremely risky, even life-threatening. However, with the right treatment for their substance use disorder, people with co-occurring mental health conditions can make lasting and meaningful changes to help them live happier lives.
If you or a loved one are struggling with bipolar disorder or another co-occurring mental health disorder in addition to substance use, contact The Recovery Village. A representative can discuss integrated treatment options with you and help you or your loved one find the best place to start or continue the recovery journey. | {
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Paracetamol
Image: “Paracetamol pills.” by PulkoCitron – Own work. License: Public Domain
Overview of Acetaminophen Toxicity
Acetaminophen (paracetamol) toxicity is defined as the harmful effects of an acute overdose of acetaminophen.
The most common cause of mortality in patients with acetaminophen toxicity is acute liver failure.
Epidemiology of Acetaminophen Toxicity
Acetaminophen toxicity is common in the United States since acetaminophen is one of the most widely used analgesic-antipyretic medication in children. The most common cause of acetaminophen toxicity in children is an overdose due to a miscalculation by the caregiver or due to accidental intake by a child.
Acetaminophen toxicity alone was reported in approx. 50,000 cases in 2014 in the United States and resulted in 65 deaths that year. A clear distinction between the number of cases of acetaminophen toxicity in children and adults is not readily available due to a scarcity of separate epidemiological studies for children.
The prognosis of a single-dose acute ingestion of acetaminophen has improved after the introduction of the antidote N-acetylcysteine (NAC). NAC decreases the mortality and morbidity of acetaminophen toxicity in children and adults.
Classification of Acetaminophen Dosage in Children
An acetaminophen overdose is better appreciated considering the recommended doses of acetaminophen in children of different ages.
The maximum acetaminophen dose in children > 12 years of age who weigh 50 kg or more is 4 g/day, the same as the maximum allowed dosage for adults. This dosage should be divided into 1 g every 6 hours.
The maximum acetaminophen dose in children < 12 years of age, or those who weigh less than 50 kg, is 80 mg/kg or a cumulative dose of 2.6 g per day. This dose should be divided into 3 or 4 sub-doses over 1 day.
The minimum toxic dosage of acetaminophen is defined as the minimum dose that causes signs and symptoms of toxicity. The minimum toxic dosage is approximately 150 mg/kg for acute acetaminophen overdose.
The absolute toxic dosage of acetaminophen is a dose of more than 250 mg/kg for acute ingestion. Children who ingest these doses are at risk of developing severe acute liver failure.
Pathophysiology of Acetaminophen Toxicity
The peak plasma concentration after an acetaminophen overdose is usually observed after 4 hours. The peak plasma concentration is delayed if acetaminophen is combined with opiates or anticholinergic drugs.
Acetaminophen is primarily metabolized in the liver. The intermediate metabolites produced by the hepatic metabolism of acetaminophen are its sulfate and glucuronide conjugates, which are usually eliminated in the urine.
Approx. 4% of the ingested dose is bio-transformed into a highly toxic metabolite known as N-acetyl-p-benzoquinone imine (NAPQI), which is believed to be responsible for hepatotoxicity and hepatic cell damage. When acetaminophen is taken in a therapeutic dose, glutathione usually binds to NAPQI rendering it a non-toxic metabolite that can be readily excreted in the urine.
In case of overdose, glutathione stores become depleted and the toxic metabolite NAPQI starts accumulating. This is believed to be the main pathologic mechanism involved in the hepatotoxicity in these cases.
acetaminophen-nomogram
Image: Acetaminophen Nomogram. By Lecturio
Clinical Presentation of Acetaminophen Toxicity
Adequate history taking is essential to identify what the child ingested, whether it was intentional or accidental and whether acetaminophen was ingested alone or in combination with other drugs. The ingested dose of acetaminophen should also be estimated and the caregivers of the child should be asked to bring the empty tablet boxes with them to confirm the ingested dosage.
During the physical examination of the child, the level of hepatotoxicity should be determined. The level of hepatotoxicity is dependent on the stage of acetaminophen toxicity.
Stage 1: Presentation of hepatotoxicity after acetaminophen overdose (within 24 hours post-ingestion)
At this stage, children usually present with anorexia, nausea, vomiting, and diaphoresis. Cardiovascular and central nervous system changes are rare. When the child has an impaired level of consciousness at this stage, the possibility of co-ingestion of acetaminophen with salicylates or other compounds, such as opiates, should be excluded.
During this stage, laboratory investigations, including liver enzymes (ALT and AST), are within normal limits.
Stage 2: Presentation of hepatotoxicity after acetaminophen overdose (1–3 days post-ingestion)
At this stage, clinical findings suggestive of hepatic involvement, such as pain and tenderness in the right upper quadrant, are present. Liver enzymes are often elevated. Prothrombin time is increased as the synthetic function of the liver is impaired.
Stage 3: Presentation of hepatotoxicity after acetaminophen overdose (3–5 days post-ingestion)
This stage is characterized by the reappearance of stage 1 symptoms. Additionally, the affected persons have jaundice, hypoglycemia, encephalopathy, and may develop sepsis. ALT and AST levels remain elevated. Renal failure and heart failure can also occur at this stage. Most fatalities occur during this stage.
Stage 4: Recovery after acetaminophen overdose (5–21 days post-ingestion)
During this stage, liver enzymes tend to normalize and hepatic healing starts to occur. Children can undergo either complete resolution or they might develop fulminant hepatic failure and die during this stage.
Diagnostic Workup of Acetaminophen Toxicity
Serum levels of AST and ALT, bilirubin, and prothrombin time should be assessed in children with acetaminophen overdose.
The diagnosis of acetaminophen toxicity and the risk of hepatotoxicity are usually determined by tracking the blood levels of acetaminophen in the first 24 hours after acute ingestion. These levels are plotted on the Rumack-Matthew nomogram, also known as the acetaminophen toxicity nomogram.
For the nomogram to be used, a child must present within the first 24 hours after an acetaminophen overdose. A child who presents late in stage 2 or 3 should only undergo a single acetaminophen concentration test in addition to the assessment of hepatic function. The Rumack-Matthew nomogram should not be used in these patients.
Acetaminophen blood levels within the 4–18-hour time-window after ingestion are most reliable in the prediction of the risk of hepatotoxicity. Levels above 150 µg/mL or 993 µmol/L at 4 hours post-ingestion suggest a high risk of developing hepatotoxicity.
A CT scan of the head should be performed in children with an altered level of consciousness to assess for cerebral edema and to exclude other causes. Additionally, serum levels of ammonia should be measured, which correlates with the severity of encephalopathy.
Treatment of Acetaminophen Toxicity
NAC should be given to any child that presents within the first 24 hours after an acetaminophen overdose, who has hepatotoxicity or is at an increased risk of hepatotoxicity. Once NAC is initiated, it should be continued until the normalization of prothrombin time, and ALT and AST levels. NAC is usually started at a loading dose of 140 mg/kg, followed by 70 mg/kg every 4 hours.
Gastric lavage and activated charcoal should be used within 1 hour of ingestion. They decrease the systemic absorption of acetaminophen and can be life-saving.
Children, who develop acute liver failure and consequently metabolic acidosis, renal failure, coagulopathy, and encephalopathy, should be evaluated for possible liver transplantation. Without liver transplantation, the prognosis is very poor in these cases.
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-8,306,123,388,923,842,000 | Radiographic scoring systems for psoriatic arthritis are insufficient for psoriatic arthritis mutilans: results from the Nordic PAM Study
Leena Laasonen, Ulla Lindqvist, Lars Iversen, Leif Ejstrup, Thorarinn Jonmundsson, Mona Ståhle, Bjorn Gudbjornsson
Research output: Contribution to journalJournal articleResearchpeer-review
56 Downloads (Pure)
Abstract
Background: Psoriatic arthritis mutilans (PAM) is the most severe phenotype of psoriatic arthritis (PsA).Purpose: To describe the radiological features in PAM and explore whether existing scoring systems for radiological damage in psoriatic arthritis are applicable for PAM.Material and Methods: Radiographs were scored according to the modified Sharp-van der Heijde (mSvdH) and the Psoriatic Arthritis Ratingen Score (PARS) systems for PsA.Results: At inclusion, 55 PAM patients (49% women, mean age 58 ± 12 years) had conventional radiographs of both hands and feet. A total of 869 PAM joints were detected and 193 joints with ankylosis. The mean total mSvdH score was 213.7 ± 137.8 (41% of maximum) with a higher score for hands than for feet: 136.6 ± 90.1 vs. 79.1 ± 60.9. However, the total score was relatively higher in the feet than in the hands when compared to the highest possible scoring (47% vs. 38% of max). The mean total PARS score was 126.3 ± 79.6 (35% of max). Scoring for joint destruction was higher than for proliferation (22% vs. 11% of max). Strong correlation was found between mSvdH and PARS (r2 = 0.913). A significant correlation was found between scoring and duration of arthritis and the Health Assessment Questionnaire. History of smoking, BMI, and gender did not influence the scoring values.Conclusions: The two scoring systems studied may not be ideal to indicate progression of PAM in advanced disease since they reach ceiling effects rather early. Therefore, reporting early signs suggestive of PAM, e.g. signs of pencil-in-cup deformities or osteolysis, is crucial. This would reveal the presence of PAM and might lead to improved treatment in order to minimize joint damage.
Original languageEnglish
JournalActa Radiologica Open
Volume9
Issue number4
Number of pages8
ISSN2058-4601
DOIs
Publication statusPublished - 1. Apr 2020
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-3,170,508,990,294,779,000 | Category:
What Are Forceps with Teeth?
Article Details
• Written By: Nicky Sutton
• Edited By: O. Wallace
• Last Modified Date: 31 March 2014
• Copyright Protected:
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Forceps with teeth are used during medical procedures to grip onto tissues to make them easier to handle. Toothless forceps are generally used to tie sutures and grip needles. The teeth on the tips of toothed forceps interlock to grip tissues, and can be pointy or flat depending on the amount of grip needed and the sensitivity of the tissues. The teeth also vary in size and angle depending on tissue type and procedure, such as larger teeth for a laparotomy wound and smaller teeth for use on delicate tendons.
These surgical tools can be used during surgery for gripping sutures or biological tissues, or for manipulating needles. Forceps provide pinpoint accuracy and grip during delicate and intricate operations, where fingers do not have enough grip. There are two general types of forceps; those with teeth at the tips and those with smooth tips. Smooth forceps are used for delicate tasks, and forceps with teeth are generally used for gripping onto tissues such as skin, blood vessels or muscle.
The teeth, positioned on the tips of the forceps, interlock with those on the opposing tip. These teeth grab onto biological tissues to prevent them from slipping from the surgeon’s grasp. Forceps’ teeth, sometimes called mouse’s teeth, come in different shapes, sizes and angles, depending on the procedure. The forceps with teeth are designed and manufactured specifically for professionals in different areas of the medical profession.
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Pierse forceps have teeth with flat edges that prevent piercing of the tissues, to cause less damage. These forceps however, do not grip as well as others. Pointy teeth set at right angles, as seen on Harman Bishop forceps, or the forward angled teeth of the Castrviejo forceps, provide excellent grip during dissection and surgical procedures. Trauma, tearing and bleeding are more likely to occur however, with pointy teeth.
Choosing the incorrect type of forceps for surgical procedures can cause unnecessary damage to tissues. Heavy duty large teeth grip onto tough tissues but will tear finer tissues. Tougher tissues like skin require forceps with larger teeth that provide better grip while applying less pressure. Gripping tendons requires the use of forceps with teeth, but the teeth must be small so not to cut the tendons. The use of forceps with teeth is usually inappropriate on fine tissues such as blood vessels or bile ducts. Forceps with special ridges or grips should instead be used on these very fine tissues.
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-9,215,095,311,494,078,000 | Making decisions about birth after caesarean
Information needs & attitudes in next pregnancy
Women who become pregnant again after a previous caesarean have specific information needs. How much information women feel they need is a matter of personal preference, but usually they want to find out how having had a caesarean previously might affect their next pregnancy and birth. Many women we talked to said it was important to know that information was balanced and trustworthy and that it was presented without a hidden agenda. Several pointed out that it could be difficult to know which sources of information could be trusted. A few women thought it was safer to rely on information from health professionals than try and find out things for yourself. (See 'Views on information from other sources' and 'Views on information from health professionals'.)
The women we talked to in this study took part in a clinical trial that tested two computer-based decision aids. Both decision aids provided detailed information about a broad range of risks and benefits of different ways of giving birth after caesarean. All but two of the women used one version of the decision aid or the other.
A few women had been told about the implications of caesarean for future pregnancies immediately or soon after their previous birth. Many others could not recall having received information about this issue from a doctor, midwife or health visitor, though some acknowledged that it might have just passed them by at the time because they were focussed on their new baby. A few women had assumed that they would just have to have another caesarean as a matter of course. Others were surprised to learn that they could choose to have a caesarean even if it was not medically necessary.
Many women worried how having a previous caesarean scar on their uterus might affect them during pregnancy and birth. Almost all of them had heard about the risk of 'uterine rupture' - the very rare complication of the previous scar coming apart during labour or the late stages of pregnancy - but many did not know how much of a risk it really was. Several women who thought about having a planned caesarean felt unsure whether this would remove their choice over how to give birth for future pregnancies. Some had heard rumours about the maximum number of caesareans a woman could have and worried whether their risk of complications would increase with the number of caesarean they had. And because caesarean delivery is usually 'quicker' than vaginal birth, a few women wondered whether this meant it was 'safer' for the baby.
Many women who thought about attempting vaginal birth after caesarean (VBAC) wanted to find out how likely they were to have one. They also wanted to know how their labour would be managed and monitored, at what stage they should go into hospital and what kind of interventions they would be likely to receive.
Women who wanted to attempt VBAC were especially keen to refresh their knowledge about labour and pain relief. A few of them hadn't experienced labour previously, so they felt very much as if it was their first birth. One woman wanted a planned caesarean but went into labour before the scheduled date. Looking back she wished she could have had more detailed information about the kinds of pain relief available to her. A couple of women had wanted to attend antenatal classes again, but didn't manage to get a place. However, another woman who was given a place didn't attend the full course because she felt she knew as much as she needed to already (Interview 26).
Several women commented that they had less contact with their midwives than in their previous pregnancy and therefore less opportunity to seek information or advice from them when they felt they needed it. They thought that having available written information that they could read and revisit in their own time, such as that provided by the decision aids, could go some way to addressing this need.
Not all women agreed that having had a previous caesarean had increased their need for knowledge. A few women said that they hadn't been looking for as much information as they had with their first pregnancy. As some of them pointed out, looking after a young child meant they simply had less time available to read or search the internet. However, they also thought they knew more about what to expect second time round or questioned the practical value of gathering lots and lots of information. Two women who were certain that they wanted a planned caesarean thought they knew enough about the possible risks from their previous experience. A few women who were hoping to have a vaginal birth thought that seeking out too much information might worry rather than reassure them. One woman felt that “a little knowledge can be a dangerous thing,” and another one pointed out that “no matter how much you read, you still won't know what it's going to be like”.
Several women said they liked using the decision aids because it stated the risks of complications clearly and without bias. Many women took the view that even though learning about the risks of different ways of giving birth could be scary, it was better to know than not to know. As one woman said “If you know what's ahead of you, you can accommodate it better”. Several women said they had felt empowered by having additional information through their participation in the DiAMOND trial, but a few felt that with increased knowledge also came the burden of responsibility.
However, a couple of women felt that using the decision aid had given them more information than they wanted or needed. One woman thought that knowing too much about all possible complications might put off women getting pregnant again. Another one said that the task of ranking risks according to her personal values had felt like 'tempting fate'.
Women used information in different ways to support their decision-making. Some women wanted to find out as much information as possible before making up their mind about how to give birth. They were keen to make a decision that was informed by weighing up all the risks as much as possible. For some of these women, additional information gained from using the decision aid had influenced the outcome of their decision.
However, other women said that factual information had not been all that important for reaching a decision and that they had been guided more by personal values. Nevertheless, they, too, found it useful to find out more information because they thought it would help them to prepare themselves for the birth and feel more confident about the decision they had made.
Last reviewed April 2015.
Last updated November 2010.
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-2,311,883,434,825,430,000 | brand logo
Am Fam Physician. 2014;90(2):91-96
A more recent article on fever of unknown origin in adults is available.
Patient information: See related handout on fever of unknown origin in adults, written by the authors of this article.
Author disclosure: No relevant financial affiliations.
Fever of unknown origin has been described as a febrile illness (temperature of 101°F [38.3°C] or higher) for three weeks or longer without an etiology despite a one-week inpatient evaluation. A more recent qualitative definition requires only a reasonable diagnostic evaluation. Although there are more than 200 diseases in the differential diagnosis, most cases in adults are limited to several dozen possible causes. Fever of unknown origin is more often an atypical presentation of a common disease rather than an unusual disease. The most common subgroups in the differential are infection, malignancy, noninfectious inflammatory diseases, and miscellaneous. Clinicians should perform a comprehensive history and examination to look for potentially diagnostic clues to guide the initial evaluation. If there are no potentially diagnostic clues, the patient should undergo a minimum diagnostic workup, including a complete blood count, chest radiography, urinalysis and culture, electrolyte panel, liver enzymes, erythrocyte sedimentation rate, and C-reactive protein level testing. Further testing should include blood cultures, lactate dehydrogenase, creatine kinase, rheumatoid factor, and antinuclear antibodies. Human immunodeficiency virus and appropriate region-specific serologic testing (e.g., cytomegalovirus, Epstein-Barr virus, tuberculosis) and abdominal and pelvic ultrasonography or computed tomography are commonly performed. If the diagnosis remains elusive, 18F fluorodeoxyglucose positron emission tomography plus computed tomography may help guide the clinician toward tissue biopsy. Empiric antibiotics or steroids are generally discouraged in patients with fever of unknown origin.
Fever of unknown origin (FUO) in adults is one of the most vexing clinical conditions for clinicians and patients. There are no published guidelines, nor is there a recommended standard approach to the diagnosis. The definition of what constitutes FUO remains controversial.1,2 FUO was first described in a 1961 case series as prolonged febrile illness (temperature of 101°F [38.3°C] or higher) for three weeks or longer that did not have an established etiology despite a one-week inpatient evaluation.3,4 The arbitrarily defined three weeks allowed most acute, self-limited illnesses to resolve, as well as sufficient time to complete the initial investigation.5,6
Clinical recommendationEvidence ratingReferences
A comprehensive history and physical examination should be performed if there are no localizing signs and symptoms in patients with prolonged febrile illness.C15, 1721
Potentially diagnostic clues should be sought during the history and physical examination to guide further evaluation of prolonged febrile illness.C1517
In patients with a prolonged febrile illness, a minimum diagnostic workup should be performed before classifying the disease process as a fever of unknown origin.C1, 2, 47, 1520, 27
Erythrocyte sedimentation rate and C-reactive protein levels should be measured in the initial workup of a patient who has prolonged febrile illness without a clear source.C5, 15, 28, 29
In patients who have a fever of unknown origin with an elevated erythrocyte sedimentation rate and/or C-reactive protein levels, and who have not received a diagnosis after initial evaluation, 18F fluorodeoxyglucose positron emission tomography scan with or without computed tomography may be useful in reaching a diagnosis.C15, 3740
If noninvasive diagnostic tests are unrevealing, then the invasive test of choice is a tissue biopsy because of the relatively high diagnostic yield. Depending on clinical clues, this may include liver, lymph node, temporal artery, or bone marrow biopsy.C2, 3, 5, 15, 19, 22, 27, 41
FUO was further defined in 1991, suggesting that the minimum evaluation be changed to at least three outpatient visits or three days in inpatient care.7 Others have proposed shorter lengths of time (e.g., two weeks, because today's patients present earlier and receive a diagnosis more quickly).8,9 A retrospective review of 226 hospitalized febrile patients examined the timing of diagnosis from initial visit for fever through the end of hospitalization. There was no difference in types of diagnoses for those who met the strict 1991 definition compared with those who received a diagnosis in less than three weeks.10 Therefore, FUO may be assumed when no reasonable diagnosis is reached after an appropriate inpatient or outpatient investigation.2,6,1017 Table 1 compares the evolution of the definition of FUO.2,3,6,7,1017
Original (1961)3 Temperature ≥ 101°F (38.3°C) on several separate occasions
Fever lasting longer than three weeks
Evaluation of at least one week in the hospital
Revised (1991)7 Temperature ≥ 101°F on several separate occasions
Fever lasting longer than three weeks
Evaluation of at least three outpatient visits or three days in inpatient care
Qualitative2,6,1017 Temperature ≥ 101°F documented clinically on several separate occasions
Appropriate initial diagnostic workup (inpatient or outpatient) does not reveal etiology of fever
Other subtypes of FUO are nosocomial, neutropenic, and human immunodeficiency virus–associated.7 These subtypes have different approaches to evaluation and are beyond the scope of this article.17
Differential Diagnosis
The etiologies of FUO have changed over time because of shifting disease patterns and new diagnostic techniques.14 There are more than 200 diseases in the differential diagnosis.4,15,17 In multiple case series, however, the etiology of FUO is limited to several dozen causes, and patients often have an atypical presentation of a common disease.2,6,18
Common causes of FUO are listed in Table 2.6,1523 Typical subgroups used in the differential for classical FUO are infection (20% to 40%), malignancy (20% to 30%), noninfectious inflammatory diseases (10% to 30%), miscellaneous (10% to 20%), and undiagnosed (up to 50%).1,46,1418,2224 Noninfectious inflammatory diseases commonly include connective tissue diseases, vasculitides, and granulomatous diseases.16,17 In developed countries, the noninfectious inflammatory diseases and undiagnosed groups comprise a higher proportion of FUO cases.5,10,15,17 Underdeveloped countries have higher rates of infection and neoplasm.6,24 Drug fever is implicated in 1% to 3% of FUO cases16 (Table 320,21,25,26 ).
SubgroupCause
Infection (20% to 40%)Bacterial
Abdominal or pelvic abscesses
Dental abscesses
Endocarditis
Sinusitis
Tuberculosis (especially extrapulmonary/disseminated)
Urinary tract infection
Viral
Cytomegalovirus
Epstein-Barr virus
Malignancy (20% to 30%)Colorectal cancer
Leukemia
Lymphoma (Hodgkin and non-Hodgkin)
Noninfectious inflammatory disease (10% to 30%)Connective tissue diseases
Adult Still disease
Rheumatoid arthritis
Systemic lupus erythematosus
Granulomatous disease
Crohn disease
Sarcoidosis
Vasculitis syndromes
Giant cell arteritis
Polymyalgia rheumatica/temporal arteritis
Miscellaneous (10% to 20%)Drug-induced
Factitious fever
Thromboembolic disease
Thyroiditis
Anticonvulsants
Barbiturates*
Carbamazepine (Tegretol)
Phenytoin (Dilantin)
Antihistamines
Cimetidine (Tagamet)
Ranitidine (Zantac)
Antimicrobials
Carbapenems*
Cephalosporins*
Erythromycin
Isoniazid
Minocycline (Minocin)
Nitrofurantoin (Furadantin)
Penicillins*
Rifampin
Sulfonamides*
Cardiovascular drugs
Captopril (Capoten)
Hydralazine
Hydrochlorothiazide
Methyldopa
Nifedipine (Procardia)
Procainamide
Quinidine
Nonsteroidal anti-inflammatory drugs
Ibuprofen
Salicylates
Sulindac (Clinoril)
Others
Allopurinol (Zyloprim)
Heparin
Meperidine (Demerol)
Phenothiazines
From Prolonged Febrile Illness to FUO
Because there are no guidelines to the approach of the febrile patient, most evaluation recommendations are based on expert opinion.17 On initial presentation, most clinicians perform a history and physical examination in pursuit of an infection. When there are no clear localizing signs or symptoms, clinicians should expand on the patient's symptoms and historical information, looking for potentially diagnostic clues to guide the evaluation (Table 4).1720,25,27 This is a continuous, iterative process.1921 Potentially diagnostic clues lead to a diagnosis in 62% of patients, although clues can be misleading because they are found in 97% of patients.1517
CluesPossible diagnoses
Historical
Exposures
Fresh water exposureLeptospirosis
Living conditions (e.g., homeless shelter)Tuberculosis
Occupational exposures/sick contacts (e.g., with hospitalized patients, children)Cytomegalovirus, Epstein-Barr virus, tuberculosis
Pets, wild animalsBrucellosis
Recent travel, especially to areas with endemic diseases (domestic and abroad)Region specific (e.g., Q fever for parts of Europe)
Family history
Hereditary febrile conditionsFamilial Mediterranean fever
Medical history
Abdominal disordersAlcoholic hepatitis, cirrhosis, Crohn disease
History of transfusionsHepatitis B or C, HIV
MalignancyMetastatic disease
Psychiatric illnessFactitious fever
Recent hospitalizationNosocomial infection
Risk-taking behaviors
Intravenous drug abuseAbscess, endocarditis, osteomyelitis
Sexually transmitted infection exposureHIV
Surgical history
Presence of prosthesesOsteomyelitis
Physical
Characteristic rashes (e.g., erythema multiforme, petechiae)Adenovirus, herpes simplex virus, HIV, meningococcemia, tick-borne illness
Conjunctivitis or uveitisAdult Still disease, leptospirosis, systemic lupus erythematosus
Hepato- or splenomegaly; palpable abdominal massesAlcoholic liver disease, carcinoma, cytomegalovirus, Epstein-Barr virus, leukemia, lymphoma
Joint swelling or pain with movementInflammatory bowel disease, Lyme disease, systemic lupus erythematosus
LymphadenopathyCat-scratch disease, cytomegalovirus, Epstein-Barr virus, HIV
If no potentially diagnostic clues are found, a minimum diagnostic workup should be performed. Infections predominate early in FUO diagnoses, and the longer FUO remains undiagnosed, the less likely it is caused by an infection.27 After infections, the etiology of FUO transitions to noninfectious inflammatory diseases and malignancies, which can guide subsequent testing. Figure 1 outlines a diagnostic approach to patients with prolonged febrile illness and FUO.1,2,47,1520,23,27
Hospitalization may be considered at any time during the evaluation, especially if the patient exhibits signs of a critical illness. Approximately 12% to 35% of patients die from an FUO-related cause (generally infection or malignancy), yet of those whose conditions remain undiagnosed, most recover or have a benign course with a good prognosis.5,22
COMMON INFECTIONS
At the initial encounter, testing for common infections should include a complete blood count with differential, electrolyte panel, liver enzymes, urinalysis with culture, blood culture, and chest radiography. If there is no clear source of infection, then further testing should follow.
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are nonspecific acute-phase reactants that are routinely part of the evaluation of febrile patients.5,28 An extremely elevated ESR (100 mm per hour or greater) suggests etiologies such as abdominal or pelvic abscess, osteomyelitis, and endocarditis. However, ESR does not help discriminate between active autoimmune disease and infection, and malignancies and noninfectious inflammatory diseases can cause an elevated ESR and CRP level. In one review, an ESR of 100 mm per hour or greater had a high specificity for malignancy (96%) and infection (97%), and its positive predictive value was 90%.29 A normal ESR has a high negative predictive value for temporal arteritis.28,30 An ESR that is not elevated has no diagnostic value and does not rule out neoplastic or other disorders.27 CRP level is a sensitive marker for infection and inflammation, but it is not sensitive enough to discriminate between disease processes.28 However, a more recent prospective study found that the chance of establishing a diagnosis was higher in patients who had an elevated CRP level and ESR.15
Procalcitonin is a newer marker specific for bacterial infection. In multiple studies, procalcitonin has been shown to have a specificity ranging from 70% to 98%, with a higher specificity for bacterial infection than other markers.28,31,32 It may be helpful in distinguishing between fevers with a bacterial cause vs. noninfectious inflammatory diseases, but its role in the workup of FUO is currently undefined.28,32
MALIGNANCIES AND NONINFECTIOUS INFLAMMATORY DISEASES
If the diagnosis remains elusive, tests targeting malignancies and noninfectious inflammatory diseases should be considered. Elevated lactate dehydrogenase levels can be indicative of infectious and malignant causes of FUO, including malaria, lymphoma, and leukemia.15,21 Measurement of ferritin levels may also be helpful.33 An elevated ferritin level in prolonged febrile illness may indicate malignancy (especially myeloproliferative disorders) and other noninfectious inflammatory diseases, such as systemic lupus erythematosus or temporal arteritis.21,33 One study established a ferritin level of 561 ng per mL (1,261 pmol per L) as the optimal cutoff value to predict that FUO was due to a noninfectious cause.22 Extreme elevation of ferritin levels (greater than 1,000 ng per mL [2,247 pmol per L]) can point to adult Still disease.34 Infection is the most common reason ESR is extremely elevated, but if there is no evidence of infectious causes, clinicians should consider malignancy, renal disease, and inflammatory disorders if the ESR is 100 mm per hour or greater.29
Testing for antinuclear antibodies, rheumatoid factor, human immunodeficiency virus, Epstein-Barr virus, cytomegalovirus, purified protein derivative (or interferon-gamma release assay), and antineutrophil cytoplasmic antibodies, as well as measurement of the creatine kinase level, can suggest other infectious sources and common noninfectious inflammatory disease etiologies, such as systemic lupus erythematosus, rheumatoid arthritis, and vasculitides. Previous testing (ESR, complete blood count, electrolyte panel, chest radiography, urinalysis, blood culture) may be repeated periodically to evaluate for trends as the illness evolves. Age-appropriate or potentially diagnostic clue–guided cancer screening should be performed (e.g., colonoscopy in patients 50 years or older).
Abdominal and pelvic ultrasonography are often recommended in the initial workup because of availability, low cost, and lack of radiation exposure.15 After the initial evaluation is complete and if there is no diagnosis, the patient is considered to have FUO, and a secondary evaluation should be considered.
Secondary Evaluation
Several diagnostic algorithms have been suggested for FUO, but few are supported by evidence from prospective studies.17 Region-specific serologic tests, more advanced radiologic studies, and more invasive diagnostic procedures can be guided by potentially diagnostic clues. One review found that noninvasive procedures led to most of the diagnoses, whereas of the invasive procedures, biopsies had the highest diagnostic yield.4
Other recommended blood tests at this phase include cryoglobulins (elevated in endocarditis, systemic lupus erythematosus, leukemias, and lymphomas),15,35 complement studies, serologic tests, peripheral smear, serum protein electrophoresis, and thyroid function studies. Note that serologic tests are helpful only if there are potentially diagnostic clues and if the patient lives in or has visited an area where the suspected disease is prevalent.15
IMAGING STUDIES
Chest, abdominal, or pelvic computed tomography (CT) may be useful in the secondary evaluation. In one study of patients with FUO, chest and abdominal CT had high sensitivity (82% and 92%, respectively) and were recommended if the initial evaluation was unrevealing.15 CT specificity ranged from 60% to 70%, consistent with other case series.15,16 Echocardiography is recommended if there are clinical indications of endocarditis.5,20 Venous Doppler ultrasonography is indicated for suspected thromboembolism.20 Magnetic resonance imaging of the aortic arch and great vessels of the neck was shown to be helpful when vasculitis was suspected.36
Nuclear imaging studies are noninvasive, image the whole body, and can localize a potential infectious or inflammatory cause for FUO.5,14,19,3740 Recently, 18F fluorodeoxyglucose positron emission tomography technology has been evaluated for guiding further invasive testing, especially in patients who have an elevated ESR or CRP level.14,37 The 18F fluorodeoxyglucose is taken up by inflammatory and cancer cells because of their high rate of glucolysis.14,18,37 Several studies examining this method in patients with FUO found diagnostic yields ranging from 16% to 69%,15,37,38 with a high positive predictive value (93%) and negative predictive value (100%).39,40 A hybrid of CT and 18F fluorodeoxyglucose positron emission tomography has a higher diagnostic yield (sensitivity of 56% to 100%; specificity of 75% to 81%18). The 18F fluorodeoxyglucose has better uptake and is cleared more rapidly than older modalities (e.g., gallium Ga 67 citrate), but it is costly and not widely available.14
BIOPSIES
Liver, lymph node, or temporal artery biopsy may help establish a definitive diagnosis.3,19 A prospective study of 192 patients found that biopsies produced up to a 35% diagnostic yield (about 10% to 35%), especially if performed later in the evaluation when infection is less likely, and malignancies and noninfectious inflammatory diseases are more common.2 Liver biopsy, with a diagnostic yield between 14% and 17%,5,19 can reveal granulomatous hepatitis and determine its cause, which could be infectious, inflammatory, or neoplastic processes.22,27 Lymph node biopsy is most useful in diagnosing lymphoma, infectious diseases, and granulomatous diseases.19,27 In patients 55 years or older, temporal arteritis causes more than 15% of cases of FUO, so biopsy should be considered.5,15,18
Bone marrow biopsy is diagnostically useful, particularly with neoplasm and infectious disease, especially tuberculosis.19,27 One study of 280 hospitalized febrile patients found that bone marrow biopsy was helpful in reaching a diagnosis in nearly 25% of the 130 patients who underwent biopsy.41 Conversely, bone marrow aspiration and culture have a diagnostic yield of only 0% to 2%.3,5,15,22,41
Empiric Therapy and Referral
Empiric trials of antibiotics or steroids rarely establish a diagnosis and are discouraged in the management of patients with FUO, unless there are clinical indications.5,17,19,21,22 Consultation with a subspecialist (e.g., infectious disease specialist, rheumatologist, hematologist/oncologist) is appropriate at any point in the evaluation.
Data Sources: A PubMed search was completed using the key terms fever of unknown origin, FUO, pyrexia of unknown origin, and inflammatory markers. The search included reviews, case series, meta-analyses, and randomized controlled trials. Additional searches included the Cochrane database, Essential Evidence Plus, the Agency for Healthcare Research and Quality evidence reports, and the National Guideline Clearinghouse. Additional references were identified from the articles reviewed. Search dates: November 28, 2011; February 8, 2012; and April 18, 2014.
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862,029,294,533,599,500 | Skip navigation
Please use this identifier to cite or link to this item: http://arks.princeton.edu/ark:/88435/dsp01wm117r30s
Title: GUT FEELINGS: THE POTENTIAL FOR INCREASED INTUSSUSCEPTION WITH THE INTRODUCTION OF ROTAVAC INTO INDIA’S UNIVERSAL IMMUNIZATION PROGRAM
Authors: McGue, Shannon
Advisors: Levin, Simon
Department: Ecology and Evolutionary Biology
Class Year: 2015
Abstract: Though the introduction of a new rotavirus vaccine, Rotavac, into India’s universal immunization program would prevent diarrheal morbidity and mortality, it may also increase the incidence of a rare intestinal obstruction called intussusception. Current rotavirus vaccines carry a risk of intussusception on the order of 1-2 excess cases per 100,000 vaccinated infants, while a previous rotavirus vaccine was withdrawn after being associated with an excess risk of 1 intussusception per 10,000 vaccinated infants. The number of intussusception cases that could be seen in India if Rotavac is added to the universal immunization program is assessed using the average baseline intussusception incidence seen in countries with comparable under-5 mortality rates and the average relative risk observed after vaccination with current rotavirus vaccines. Assuming that Rotavac doses are administered at the same levels as diphtheria-tetanus-pertussis doses currently are, then there will be 5,906 excess cases of intussusception due to rotavirus vaccination per year in India, representing an increase of 20% over baseline number of intussusceptions. Only 12-500 will be reported as adverse events through the standard reporting system, with 15-700 potentially reported through a web portal. The number reported decreases when the state-by-state vaccine coverage and surveillance data are used. The government is recommended to either strengthen both the AEFI surveillance system and existing knowledge about intussusception or focus on self-controlled case series analyses. Rotavirus vaccination risks are outweighed by potential benefits for Indian society, provided that the intussusception risk is monitored.
Extent: 119 pages
URI: http://arks.princeton.edu/ark:/88435/dsp01wm117r30s
Type of Material: Princeton University Senior Theses
Language: en_US
Appears in Collections:Ecology and Evolutionary Biology, 1992-2017
Files in This Item:
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2,589,524,091,727,308,300 |
Are Blood Flow and Lipolysis in Subcutaneous Adipose Tissue Influenced by Contractions in Adjacent Muscle in Humans – Research Review
Title and Abstract
Stallknecht B et. al. Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans? Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E394-9.
Aerobic exercise increases whole-body adipose tissue lipolysis, but is lipolysis higher in subcutaneous adipose tissue (SCAT) adjacent to contracting muscles than in SCAT adjacent to resting muscles? Ten healthy, overnight-fasted males performed one-legged knee extension exercise at 25% of maximal workload (Wmax) for 30 minutes followed by exercise at 55% Wmax for 120 minutes with the other leg and finally exercised at 85% Wmax for 30 minutes with the first leg. Subjects rested for 30 minutes between exercise periods. Femoral SCAT blood flow was estimated from washout of (133)Xe and lipolysis was calculated from femoral SCAT interstitial and arterial glycerol concentrations and blood flow. In general, blood flow as well as lipolysis was higher in femoral SCAT adjacent to contracting than adjacent to resting muscle (time 15-30 min: blood flow: 25% Wmax: 6.6 +/- 1.0 vs. 3.9 +/- 0.8 ml 100 g(-1) min(-1), P < 0.05; 55% Wmax: 7.3 +/- 0.6 vs. 5.0 +/- 0.6, P < 0.05; 85% Wmax: 6.6 +/- 1.3 vs. 5.9 +/- 0.7, P > 0.05; lipolysis: 25% Wmax: 102 +/- 19 vs. 55 +/- 14 nmol 100 g(-1) min(-1), P = 0.06; 55% Wmax: 86 +/- 11 vs. 50 +/- 20, P > 0.05; 85% Wmax: 88 +/- 31 vs. -9 +/- 25, P < 0.05). In conclusion, blood flow and lipolysis are generally higher in SCAT adjacent to contracting than adjacent to resting muscle irrespective of exercise intensity. Thus, specific exercises can induce “spot lipolysis” in adipose tissue. Key words: exercise, spot lipolysis, microdialysis.
Background
The idea of spot reduction is one that has floated around the fitness body recomposition world for decades. Men want the ever desirable six-pack and can be seen doing abs until the cows come home, women try to slim hips and thighs with endless reps on the inner/outer thigh machine.
Hour long ‘abs’ or ‘buns/thighs’ classes filled with nearly an hour of high rep movements for the specific area can be found in most commercial gyms. Even in the bodybuilding world, where people really should know better, some still argue that spot reduction can occur and that working a given muscle group will help reduce fat in that specific area. I addressed this topic somewhat in The Stubborn Fat Solution since some of what I discuss in that book could readily be confused with spot reduction (it’s not).
For the most part, the idea of spot reduction has been resoundly denied by folks in the field (with the occasional heretic or book seller suggesting it is still possible). Various lines of research are usually cited including those showing no difference in skinfolds in the arms of tennis players (who typically use one arm more than the other).
An example I’ve often used is that “If spot reduction worked, people who ate a lot should have skinny faces.” A bit silly but I think it gets the point across. If working a specific muscle group reduced fat only in that area, that’s how it should work. But it doesn’t. Or certainly doesn’t seem to. But, for the most part, the idea hasn’t been directly tested to my knowledge.
In that context, I should note for the sake of background that there are three primary steps involved in fat loss that might potentially be influenced although today’s study only focuses on two. Those steps are
1. Lipolysis (the actual fat breakdown)
2. Blood flow (critical for transport of the broken down fat to other tissues for ‘burning’)
3. Oxidation (the actual ‘burning’ of fat in tissues such as the liver or skeletal muscle)
Is it possible that performing local activity can impact on some aspect of the above in a way that might make spot reduction or performing endless reps of local exercises worthwhile in terms of fat loss? That’s what today’s study set out to examine: do contractions in a specific muscle impact on either lipolysis or blood flow (oxidation was not measured) in the adjacent fat cells.
And although it was published several years ago, it still seems to be making the rounds (being cited as ‘evidence’ for spot reduction); as well, the idea of spot reduction is one that refuses to die. So it’s worth seeing what the real or potentially real effects actually are.
.
The Study
Using a couple of different methods (that I’m not going to detail) to measure actual blood flow and lipolysis , the study had subjects perform lower body exercise (they called it one leg leg extension but this probably means one legged cycling) at various intensities while resting the other leg. That way, blood flow/lipolysis could be measured for the exercise versus the unexercised leg.
This allowed them to compare lipolysis and blood flow in response to local exercise to the non-exercised control leg. This is actually critically important as any type of whole body exercise would tend to have systemic effects; that is impacting on fuel metabolism all over the body. By limiting exercise to a single leg, the researchers were able to measure the response only in the fat cells close to the muscles being worked and compare that to the unworked msuscle to see what differences occurred.
Exercise was performed at 25%, 55% and 85% of maximum power output with a 30 minute break and the subjects switched legs from one intensity to the next. This also acted as a control so that the previous bout of exercise wasn’t impacting on the next bout, since the previously exercised leg got the longer break. As mentioned above, blood flow and lipolysis was compared between the exercised leg and the rested leg to see what difference the exercise had.
.
Results
And, as indicated in the abstract above, both lipolysis and blood flow were increased for the exercised vs. non-exercised leg although this only occurred at the two lower intensities of exercise. At the highest intensity of exercise, no change was seen.
Before getting to specific numbers, a question worth addressing is why this would have happened. The researchers proposed two possible reasons for their observation.
First, local changes in hormones (or a synergy between changes in hormones and blood flow) are most likely responsible but there is a larger question of why this would occur in the first place, a point that the researchers specifically made. By why I mean why the system would work that way in terms of improving physiological functioning.
The reason for asking this question is this: fat mobilized from a specific area of body fat (say the thigh) can’t actually be used for fuel by the muscle underneath it (e.g. the quadriceps). The blood flow of skeletal muscle and fat cells are separate and any fat mobilized from an adjacent area will go into local circulation; again, it can’t be used directly by that muscle.
So there’s no really logical physiological reason that working a given muscle would would cause fatty acids to be mobilized; that muscle can’t use them. Of course, physiology doesn’t have to be logical to work a certain way and worrying about the reasons why instead of the observation of what happened can make you lose the forest for the trees.
Related to this, the researchers point out clearly that there is no indication that these results will actually result in spot reduction as fat stores in the affected areas could simply be replenished after the exercise bout. They didn’t measure fat storage after the exercise bout stopped and process that occurs quite often is fatty acid re-esterification, basically mobilized fat that isn’t burned off elsewhere in the body simply gets stored back in the fat cell. In some exceedingly strange cases, fat mobilized in one area of the body can be restored in fat cells somewhere else.
The researchers also suggest that localized increase in temperature, which can also impact on blood flow may have also been involved in the measured response. I discuss this aspect of fat cell mobilization in The Stubborn Fat Solution as local temperature is known to impact on blood flow in the area. Cold tends to cause vasoconstriction and heat vasodilation so there might actually be some logic to those rubber belts and such that warm the area before exercise.
In any case, for whatever reasons, through whatever mechanism, working a given muscle for 30 minutes at low to moderate intensities did increase fat cell lipolysis in blood flow.
Aha! Spot reduction is possible, right? Hang on.
Although clearly local exercise did impact on fat cell lipolysis and blood flow, you might note something I left out of the above discussion: the acutal quantitative impact of this. That is, how much extra fat was actually mobilized for fuel, potentially to be burned off.
Addressing that very thing, based on the measured changes in blood flow and lipolysis, the researchers estimate that, in 30 minutes of local exercise, an additional .6-2.1 milligrams (one milligram is one thousandth of a gram) per 100 grams of adipose tissue adjacent to contracting muscle was mobilized.
Let me put that in context. First let’s assume that you’re carying a whopping 5 kg (11.1 pounds) of fat in a specific area.
If local exercise can mobilize 0.6-2.1 milligrams of fat per 100 grams of fat mass, that works out to:
0.6-2.1 mg/100 grams * 1000 grams/kg * 5 kg = 30-105 milligrams of fat.
Or 0.03-0.1 gram of extra fat mobilized in 30 minutes of activity.
Now, a single pound of fat (0.454 kg) contains about 400 grams of fat so our hypothetical 11.1 pounds of fat contains 4,440 grams of fat. And 30 minutes of local activity mobilized at most 0.1 gram of fat. Whoo hoo. You’ll be ripped in about 1000 years.
.
Summing Up
And, so far as I’m concerned, that should be the death knell for the idea of spot reduction. Yes, there appears to be an effect whereby working a given muscle impacts on local fat cell metabolism but the effect is completely and utterly irrelevant in quantatitive terms. The amount of fat mobilized due to increased hormones or blood flow is simply insignificant to anything in the real world.
There is also the fact that, compared to something like full body cardio types of activities, local single muscle group activities burn tiny amounts of calories. Doing cardio for 30 minutes at even a reasonable caloric burn of 5 cal/minute (very easy) burns 150 calories. If you get say 90% fat utilization for fuel, you’ve burned 15 grams of fat. Compared to the 0.1 gram you might mobilize doing crunches or leg lifts.
As well, the whole body activity will impact on fuel utilization and hormones in ways that much more massively impact on lipolysis and blood flow. Simply, spending an hour doing localized exercise pales in comparison to the fat loss effects of even moderate cardio. Wasting time with ab or buns/thighs classes is simply a waste of time in terms of any sort of local fat reduction.
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Stubborn Fat Solution
Learn the Best Way to Get Rid of Stubborn Fat
Many ideas and solutions to the problems of stubborn body fat (usually hip/thigh for women and ab/low back for men) have been offered over the years. Invariably they tend to involved simple answers and solutions (usually estrogen) that are too simple to be correct. Stubborn fat is stubborn for a variety of interconnected physiological reasons. The Stubborn Fat Solution discusses every aspect of fat cell metabolism including the reasons that make stubborn fat so stubborn. This leads into 4 specific training protocols (based primarily around cardio) to help eliminate stubborn fat once and for all; how best to incorporate those protocols with various types of fat loss diets along with supplements that can help (but aren't required) are discussed as well. | {
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6,193,149,004,689,377,000 | Air Fryer Pumpkin Pie
Air Fryer Pumpkin Pie
In America, the removal of hair forever using a laser would be the swiftest growing non-surgical aesthetic laser cosmetic method. The quantity of done laser hair removing periods is projected to develop 18 percent each year. This suggests there will be an believed 6,000,000 laser hair removal strategies carried out in 2010!
Typically, removing hair for attractiveness motives is hottest amongst Women of all ages-just about all Gals above twelve several years aged engage within the practice in some way, shape or sort. Laser hair removal for guys, nonetheless, is speedily developing in reputation. Increasingly more Males search for Long lasting hair removal options - over the neck, to deal with issues of ingrown hairs, and over the upper body, back and shoulders, mostly, for beauty purposes.
Using the measurement of The buyer marketplace for long lasting hair removing remedies expanding at this type of rapidly price, just lately, we've seen new technologies coming out to assist shoulder the load of The buyer market place. In the following paragraphs, I will explore two handheld products, and supply factors comparison with respect to Specialist clinical lasers. But, very first, let's go over how laser hair elimination operates.
Laser hair elimination operates employing laser Electrical power, targeting the melanin in your hair, to cause damage to your hair follicles. As soon as ruined, the hair follicles will now not produce new hairs. After a number of treatment plans the follicle mainly dies and can't mature hair.
Formerly, the ideal candidates for laser hair elimination have gentle skin and thick dim hair. Nevertheless, laser technologies has progressed and now, darker skinned and tan folks might also see incredible effects (employing an Nd:YAG laser).
A number of treatments are needed for a good remedy since the laser is simply powerful when it hits the follicle in its progress stage. Through the growth section in the hair development cycle, the follicle has quite possibly the most melanin, which happens to be needed for the laser light-weight to focus on. Due to the fact Just about every hair might be in another advancement section at any given time, various therapies are important to you should definitely the treatment hits most of the hairs in the appropriate advancement section.
Let us move ahead to the cost of laser hair removal treatment plans.
The cost of a laser hair removing treatment method will depend on lots of elements such as the area during which the laser Centre is situated, and the dimensions of the region being taken care of.
If you reside in Big apple, and possess your appointments at Assara Laser you are able to do an infinite Total Human body Laser Hair Elimination for $449 every month. Which means you are able to laser each and every overall body element you would like for $449 a month - out of your sideburns, to upper lip, arms, again, bikini, bum, legs. An average consumer is taken care of at the time every single 4-5 months, for six periods, so beneath this program the expense of six classes for comprehensive body solutions is somewhere around $two,seven-hundred, paid over six installments of $449.
How does laser hair removal feel?
People today generally want to know exactly how much agony is associated with laser hair removing. You can find some ache involved. The laser zap looks like a snap on the skin, but a handheld cooled air jet connected to your laser helps to interesting the skin and diminish the distress.
The irritation arises from The sunshine Electrical power within the laser getting converted into heat energy when the laser light-weight is absorbed through the melanin with your hair follicle. A highly trained laser practitioner should therefore hold the Electricity amount of the laser substantial enough to develop adequate warmth to damage and disable the hair follicle, but small plenty of so that there is no hurt performed into the surrounding pores and skin.
Now that we are armed with these tidbits of data. Let us choose Look at in your house laser hair removing techniques with professional medical laser techniques used in laser facilities and Medispas.
With regard to value, with the date of this short article, the Tria's pricepoint is $595. That is a little bit a lot more than the cost of a full entire body session beneath the Endless Plan, I before pointed out.
Light-Resource/Wavelength - Tria takes advantage of a diode laser and Silk'n employs an rigorous pulse gentle - IPL - flash lamp to operate. For light skin, the Alexandrite (or Alex) laser is generally considered has the simplest wavelength for laser hair elimination reasons. IPLs are normally regarded an antiquated process as as opposed with lasers. They are generally regarded as much less efficient and even more prone to induce injuries since the light emitted in the flash lamp isn't concentrated, so it is much more very likely to disperse in to the consumer's pores and skin just before reaching the melanin prosperous blub on the hair follicle.
The most significant downside from the laser hair removal property products with regard to mild supply is the fact neither the Tria's diode laser, nor the Silk'n's IPL procedure, is appropriate for tan or dim pores and skin; most practitioners would advocate use with the Nd:YAG laser for skin with pigment.
Fluence/Energy Level -- The fluence (or Vitality amount) is another critical Think about laser power and usefulness for long lasting hair reduction. Fluence is calculated in joules for each square centimeter (J/cm²). The Tria has an adjustable fluence level of between seven and 20 joules. The Silk'n features a fluence amount of 5 joules. As before talked about, the Power degree should be enough to bring about permanent damage to the hair follicle so that may be without end disabled from rising hair.
Accurate healthcare lasers employed for laser hair removal, including the Cynosure Apogee Elite (Alexandrite, and Nd:YAG) have utmost fluence degrees selectable because of the laser practitioner of amongst 50 and 80 joules. An experienced laser practitioner will Usually pick out an energy degree of involving twenty five and 60 joules for a good cure. The practitioner ought to be mindful to not deliver as well minimal Vitality, which impairs the efficiency with the therapy, and likewise ought to watch out not to supply too much Electrical power, which might injury encompassing skin.
So there you have it. The hand-held products are somewhat more affordable than a single entire-system Skilled laser hair elimination procedure. They are not suitable for tan or dark pores and skin, as well as their energy levels tend to be reduced than what is often used by professional medical industry experts. As these merchandise are still new, only time will convey to how powerful They are really.
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7,970,346,410,040,005,000 | When is bedwetting abnormal?
Usually never. Isolated bedwetting is rarely "abnormal" but it can be very socially stigmatizing. Bedwetting occurs in normal people at rates of 15% of 5 y/o, 5% of 10 y/o, and 1% of 18 y/o. It is considered abnormal if it recurs after a prolonged absence (no wetting for more than 6 months) or if it associated with any other neurologic problem, urinary infections, pain, daytime incontinence, etc.
What parents think. Is abnormal. Depends upon parents own nexperience as chidren. Some parents and doctors think bedwetting once or twice a week in a seven year old is abnormal others don't. Certainly bedwetting 3 or 4 nights a week in a ten year old is abnormal. 15% of 5-year-olds wet their beds regularly, thus i consider that normal, but worth restricting fluids after supper and toileting them late if, if it works. | {
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1.
Article in Chinese | WPRIM | ID: wpr-933690
ABSTRACT
Objective:To explore the safety of inactivating coronavirus disease 2019(covid-19)vaccine in liver transplantation(LT)recipients.Methods:Retrospective analysis was performed for clinical data of 151 LT recipients from March 2003 to October 2019.They had stable conditions and completed the course of covid-19 vaccine.Frequencies of pain at injection site, fatigue, headache and pruritus after vaccination were recorded.The safety profiles were compared between recipients with and without local and general adverse reactions after vaccination.At the same time, recipients completing two doses of covid-19 vaccines were grouped.According to vaccine companies, they were classified into Sinovac Biotech Ltd and Beijing Biological.Based upon more than or less than 60 years, they were grouped into <60 years and ≥60 years.The safety profiles of inactivating COVID-19 vaccine were compared in subgroups.Results:Among 151 eligible LT recipients, 98 of them were in group of age <60 years and 53 in group of age >60 years.The median period between vaccination and LT was 8.44(4.37, 12.39)years and the median concentration of tacrolimus 2.5(1.8, 3.9)ng/L.Eighty-three cases completed two doses of Sinovac Biotech Ltd(Sinovac Biotech Ltd group)and 40 cases Beijing Biological(Beijing Biological group); 14 cases had combined course of Sinovac Biotech Ltd and Beijing Biological, four recipients were vaccinated with inactivated vaccine from other companies and ten recipients did not know their inactivated vaccine' companies.After immunization, 24/151(15.9%)recipients had a local and general adverse reaction.The prevalence of pain at injection site, fatigue, headache and pruritus was 9.9%( n=15), 5.2%( n=8), 1.3%( n=2)and 0.7%( n=1)respectively.No significant differences existed in age( P=0.602), gender( P=0.752), period after LT( P=0.890), trough concentration of tacrolimus( P=0.377)or versions of covid-19 vaccine( P=0.582)between 24 cases with general adverse reaction and 127 without.Local and general reactions occurred in 16/83(19.3%)in Sinovac group and 5/40(12.5%)in Beijing Biological.There was no significant inter-group difference( P=0.769). There were 98 cases(64.9%)in <60 years group, 17 cases(17.3%)had local and general reaction, 53 cases(35.1%)in ≥60 years group and 7 cases(13.2%)had a local and systemic reaction.There was no significant inter-group difference( P=0.507). Conclusions:Covid-19 vaccine is safe for long-term survival LT recipients with normal liver function.Few participants present with mild fatigue and pain at injection site.
2.
Article in Chinese | WPRIM | ID: wpr-957035
ABSTRACT
Objective:To study the risk factors and treatment of portal vein thrombosis (PVT) in patients after liver transplantation.Methods:The clinical data of 290 recipients who underwent liver transplantation at the Department of Hepatology, the Fifth Medical Center of PLA General Hospital from July 2015 to April 2019 were retrospectively analyzed. There were 245 males and 45 females, with a median age of 51(44, 56) years old. The liver transplantation recipients were divided into two groups according to whether PVT occurred or not after operation: the PVT group ( n=16) and the non-PVT group ( n=274). Gender, age and other clinical data of the recipients were compared between the two groups. Outpatient and inpatient follow-up were performed. The risk factors of postoperative PVT were analysed in the liver transplantation recipients. Results:The median follow-up of these 290 liver transplant recipients was 59(42, 73) months, and 16 patients were confirmed to have PVT after operation, with an incidence of 5.5%(16/290). Multivariate logistic regression analysis showed that preoperative PVT ( OR=12.773, 95% CI: 3.887-41.973) was an independent risk factor for PVT after liver transplantation. For the 16 patients with postoperative PVT, 10 were treated with portal vein intervention, and the remaining 6 patients were treated with oral aspirin or rivaroxaban anticoagulation due to mild symptoms. The 3-year survival rate of the PVT group was 93.8% (15/16), while that of the non-PVT group was 90.1% (247/274). There was no significant difference in the 3-year survival rates between the two groups (χ 2<0.01, P=0.969). Conclusions:Preoperative PVT in recipients was an independent risk factor for PVT after liver transplantation. For patients with postoperative PVT, appropriate treatment resulted in good results without affecting the long-term prognosis of these patients.
3.
Article in Chinese | WPRIM | ID: wpr-956977
ABSTRACT
Objective:To study the impact of simultaneous ligation of splenic artery on prognosis of patients with severe hypersplenism in liver transplantation.Methods:A retrospective analysis was performed on the clinical data of 206 patients who underwent liver transplantation in the Fifth Medical Center of PLA General Hospital from December 2016 to February 2019. There were 180 males and 26 females, aged (51.0±9.0) years old. Fifty-one patients underwent splenic artery ligation during liver transplantation and they were enrolled into the observation group, and 155 patients without splenic artery ligation were enrolled into the control group. The changes in white blood cells (WBC), platelets, alanine aminotransferase, total bilirubin and serum creatinine as well as the incidence of postoperative complications were compared between the two groups.Results:The platelet count of the observation group was significantly lower than those of the control group before operation and on days 1, 3, 7, 30 and 90 after operation, (all P<0.05). The WBC counts in the observation group were significantly lower than those in the control group before operation and on days 1 and 3 after operation (all P<0.05). However, there were no significant differences in the WBC counts between the two groups on days 5, 7, 30 and 90 after operation (all P>0.05). There were also no significant differences in alanine aminotransferase and total bilirubin indexes between the two groups after surgery (all P>0.05), but the serum creatinine levels in the observation group were significantly lower than those in the control group on days 3, 5, 7 and 30 after surgery (all P<0.05). There were no significant differences in the rates of infection, severe acute rejection, biliary tract complications, arterial/portal thrombosis and mental complications between the two groups (all P>0.05). The rate of renal replacement therapy for acute kidney injury in the observation group (9.8%, 5/55) was significantly higher than that in the control group (1.3%, 2/155) ( P<0.05). Conclusion:Ligation of splenic artery during liver transplantation was safe and it had a significant advantage in the early postoperative recovery of WBC count and creatinine without increasing the incidence of complications in patients with severe hypersplenism.
4.
Article in Chinese | WPRIM | ID: wpr-884667
ABSTRACT
Objective:To investigate the antiviral efficacy of direct-acting antiviral agents (DAAs) in the treatment of liver transplantation (LT) recipients with hepatitis C virus (HCV) infection.Methods:Twenty-two HCV-infected LT recipients treated with DAAs at Fifth Medical Center of Chinese PLA General Hospital from December 2014 to June 2018 were retrospectively analyzed, Twenty cases of HCV RNA gene type 1b were treated with sofosbuvir (400 mg/d) + ledipasvir (90 mg/d) or sofosbuvir (400 mg/d) + daclatasvir (60 mg/d) for 12 weeks or 24 weeks; 2 cases of gene type 2a were treated with sofosbuvir (400 mg/d) for 12 weeks. The effect of antiviral treatment, adverse reactions during treatment, and laboratory indicators such as HCVRNA quantification, blood routine, liver and kidney function during treatment and follow-up were studied.Results:The LT recipients of HCV infection included 16 males and 6 females, with a median age of 61.5 (36-71) years old, and the median time of antiviral treatment was 48 (2-117) months after transplantation. Among the 22 patients, 16 received a 12-week course of treatment. Except for 2 patients who did not get HCVRNA negative conversion at 4-week, all achieved a negative HCV RNA at 4-week and the end of the treatment. Six LT recipients received a 24-week course of treatment (gene type 1b), and HCVRNA was negative at 4-week and the end of treatment. All patients achieved end of treatment virological response and a sustained virological response (SVR) rate of 100% at 12 weeks and 24 weeks after the end of treatment. The serum levels of alanine aminotransferase (ALT) and creatinine were 71.5 (30, 110) U/L and (89.4±25.7) mmol/L before treatment, respectively. ALT decreased to 22 (17.8, 28.5) U/L after 4 weeks of treatment, and serum creatinine decreased to (77.4±11.5) mmol/L at 24 weeks after the end of treatment. The differences before and after treatment were statistically significant (all P<0.05). No serious adverse events occurred during the treatment. Conclusions:DAAs have a definite antiviral effect in the treatment of LT recipients with HCV infection, and long-term SVR can be obtained.
5.
Journal of Clinical Hepatology ; (12): 1985-1989, 2020.
Article in Chinese | WPRIM | ID: wpr-829162
ABSTRACT
ObjectiveTo investigate the risk factors for tumor recurrence and death after liver transplantation in patients with hepatocellular carcinoma (HCC) and their survival. MethodsThe patients with HCC who underwent liver transplantation in The Fifth Medical Center of Chinese PLA General Hospital from January 2005 to February 2019 were enrolled, and according to the presence or absence of HCC recurrence after liver transplantation, they were divided into recurrence group and non-recurrence group. The t-test or the Mann-Whitney U test was used for comparison of continuous data between two groups, and the chi-square test was used for comparison of categorical data between two groups. Univariate and multivariate Cox proportional-hazards regression model analyses were used to determine the risk factors for HCC recurrence and death after liver transplantation. The Kaplan-Meier method was used for survival analysis, and the receiver operating characteristic (ROC) curve was used to investigate the predictive value of death-related risk factors after liver transplantation. ResultsA total of 391 HCC patients who underwent liver transplantation were enrolled, with a median follow-up time of 2 years, among whom 78(19.95%) experienced HCC recurrence. Preoperative alpha-fetoprotein (AFP) level＞200 ng/ml (recurrence: hazard ratio ［HR］=252, 95% confidence interval ［CI］: 1.58-4.03, P＜0.001; death: HR=2.99, 95%CI: 1.59-5.62, P＜0.001］, total tumor diameter (recurrence: HR=1.20, 95%CI: 1.12-1.28, P＜0.001; death: HR=1.10, 95%CI: 1.02-1.17, P=0.002), and vascular invasion (recurrence: HR=1.15, 95%CI: 1.04-1.26, P=0.016; death: HR=1.10, 95%CI: 1.03-1.18, P=0.004) were independent risk factors for tumor recurrence and death after liver transplantation. The 1-, 5-, and 10-year overall survival rates after liver transplantation were 94.8%, 84.2%, and 83.5%, respectively, and the 1-, 5-, and 10-year disease-free survival rates were 840%, 75.1%, and 75.1%, respectively. AFP, involvement of major blood vessels, body mass index, and total tumor diameter had a certain value in predicting the death of HCC patients with recurrence, with an area under the ROC curve of 0.789 (95% CI: 0.719-0858). ConclusionTumor biological features before transplantation are the key factors for tumor recurrence after transplantation.
6.
Organ Transplantation ; (6): 646-2020.
Article in Chinese | WPRIM | ID: wpr-825585
ABSTRACT
De novo malignancy after liver transplantation is an important factor that affecting the long-term survival of recipient. The main risk factors for de novo malignancy include immunosuppression and many factors of recipients, such as age, gender, race, primary disease, preoperative tumor history and precancerous lesion, carcinogenic virus infection, smoking and drinking, etc. Currently, there is no standardized monitoring scheme after liver transplantation, but planned monitoring is required for high-risk recipients, thus to achieve early diagnosis and improve the survival rate. This article summarized the incidence, prognosis and related risk factors of de novo malignancy after liver transplantation, which provided reference for improving long-term survival rate of recipients after liver transplantation.
7.
Chinese Critical Care Medicine ; (12): 269-280, 2019.
Article in Chinese | WPRIM | ID: wpr-753954
ABSTRACT
Objective To review the development of adult and pediatric liver transplantation in Tianjin First Center Hospital, and to enhance academic exchanges, improve technological innovation, and jointly promote the progress and maturity in the field of liver transplantation. Methods The development of liver transplantation in Tianjin First Center Hospital was analyzed. The clinical data of adult and pediatric liver transplantation from September 1998 to September 2018 were collected. The important events and technological innovation achievements of liver transplantation during the 20 years were summarized. Results The first clinical liver transplantation was attempted in Tianjin First Central Hospital in April 1980. The first long-term survival adult liver transplantation in China was completed in 1994 (11 years survival after the operation). The specialized team of liver transplantation was formally established in September 1998. The 20-year clinical exploration and progress reflected the characteristics of era changes and technological innovation during the rapid development of liver transplantation in China. Our center performed liver re-transplantation in January 1999, reduced-size pediatric liver transplantation in August 2000. In May 2001, we organized the formulation for the preventive and treatment plan for hepatitis B recurrence after liver transplantation. We performed combined liver and kidney transplantation in July 2002, split liver transplantation (SLT) in April 2004, the first domino liver transplantation (DLT) in August 2005. Pediatric living donor liver transplantation (LDLT) was initiated in October 2006, adult LDLT was carried out in August 2007. In September 2007, the first living donor combined liver and kidney transplantation from the same donor in Asia was performed. The first domino+living donor double grafts liver transplantation in the world was performed in January 2009. In March 2011, we performed laparoscopically assisted right hepatic lobe liver transplantation (LDLT) with middle hepatic vein. In May 2014, living donor laparoscopic left lateral lobe procurement was successfully established. In April 2016, simultaneous liver, pancreas and kidney multi-organ transplantation was completed. Domino donor-auxiliary liver transplantation was performed in February 2017. In December 2017, extracorporeal membrane oxygenation (ECMO)-supported liver transplantation in a patient with severe pulmonary hypertension was successfully completed. Liver transplantation combined with partial splenectomy was established in April 2018. Cross-domino liver transplantation (hypersensitive kidney transplantation with auxiliary liver transplantation+pediatric liver transplantation) was performed in May 2018. During the 20 years, the team has performed or assisted other centers in Beijing, Shanghai, Guangzhou and Shenzhen to carry out more than 10 000 cases of liver transplantations. A total of 7 043 cases of various types of liver transplantation were performed in the single center of the hospital (6 005 adult liver transplantations and 1 038 pediatric liver transplantations). Concerning adult liver transplantation, the cumulative 1-year, 3-year and 5-year survival rate from September 1998 to March 2003 were 83.1%, 73.0% and 69.0%, from April 2003 to March 2009 were 85.3%, 76.2% and 72.1% and from April 2009 to September 2018 were 87.5%, 79.2% and 75.1%, respectively. The cumulative 1-year, 3-year and 5-year survival rate for pediatric liver transplantation were 93.5%, 92.2% and 90.2%, respectively. The nucleoside (acid) analogue combined with low dose hepatitis B immunoglobulin (HBIG) was developed to prevent the recurrence of hepatitis B after liver transplantation, this plan has reduced the recurrence rate of hepatitis B and the 5-year re-infection rate of hepatitis B virus (HBV) after liver transplantation significantly. The risk assessment system for tumor recurrence after liver transplantation was established and individual treatment method was established based on this assessment system. Continuous exploration and improvement of liver transplantation for liver cancer, liver re-transplantation, liver transplantation with portal vein thrombosis, SLT, DLT and multi-organ combined transplantation have significantly improved the clinical efficacy of patients and the post-operative survival rate. Conclusions The liver transplantation team of Tianjin First Center Hospital has carried out a scientific and technological exploration on the key problems and technical difficulties of clinical liver transplantation. This work strongly has initiated and promoted the rapid development of liver transplantation in China. The restrictive barrier of hepatitis B recurrence after liver transplantation has been overcome. The risk prevention and control system of tumor recurrence after liver transplantation has been established. A series of innovative achievements that can be popularized have been achieved in the field of complex liver transplantation and expansion of donor liver source. The iterative progress and sustainable development of liver transplantation have been realized.
8.
Article in Chinese | WPRIM | ID: wpr-450358
ABSTRACT
Objective To investigate the significance of orthotopic liver transplantation in the management of primary hepatocellular carcinoma (PHC) ; To evaluate the survival and prognostic factors of liver transplantation for PHC.Method The clinical data from 194 consecutive PHC patients who underwent OLT were retrospectively analyzed.Result The 1-,3-and 5-year cumulative survival rate of the 194 patients was 92.78％,78.07％ and 76.80％ respectively.There were 37 cases of recurrence or metastasis of the tumor with the incidence rate being 19.1％ (37/194).The tumor TNM stage (P=0.026 667),tumor diameter (P =0.0045),tumor number (P =0.0318),vascular invasion (P =0.006 059),and AFP level before transplantation (P =0.003 426) were significantly related with tumor recurrence.Multivariate analysis revealed that tumor diameter (P =0.0081,OR =0.789,95％ CI:2.1233-6.124),vascular invasion (P＜0.001,OR =5.928,95 ％ CI:1.173-86.789),and AFP level before transplantation (P =0.019,OR =2.601,95％ CI:2.196-5.658) were independent risk factors for tumor recurrence.There was statistically significant difference in survival rate and tumor-free survival rate between Milan criteria group and beyond-UCSF criteria group (P＜0.01),and between UCSF criteria group and beyond-UCSF criteria group (P＜0.01).There was no significant difference in survival rate and tumor-free survival rate between Milan criteria group and UCSF criteria group (P ＞0.05).Conclusion Liver transplantation is an effective treatment for PHC.The tumor diameter ＞8 cm,vascular invasion and AFP level significantly affect the survival of PHC patients.
9.
Article in Chinese | WPRIM | ID: wpr-433734
ABSTRACT
BACKGROUND:Prolonged therapy with lamivudine has been associated with tyrosine-methionine-aspartate-aspartate mutation, which results in hepatitis B recurrence. Recently, antiviral agents, such as entecavir, have high efficacy and low resistance rate in hepatitis B-related liver disease. However, the researches on the effect of entecavir in preventing hepatitis B recurrence after liver transplantation are rare. OBJECTIVE:To investigate the effect of entecavir combined with low-dose hepatitis B immunoglobulin in preventing hepatitis B recurrence after liver transplantation. METHODS:The fol ow-up data of 253 patients who had liver transplantation for hepatitis B virus related liver disease were retrospectively analyzed. Al patients received nucleoside analogues therapy formal y before liver transplantation. The effects of entecavir+hepatitis B immunoglobulin and lamivudine+hepatitis B immunoglobulin were compared in al the patients and the patents with hepatitis B recurrence risk factors (positive preoperative HBeAg, DNA-positive hepatitis B virus, hepatoma and tyrosine-methionine-aspartate-aspartate mutation). RESULTS AND CONCLUSION:A total of 253 patients received hepatitis B virus-related liver transplantation, and 29 patients died. There were 202 patients in lamivudine group in which 26 patients were dead and 16 patients had hepatitis B virus recurrence, and the recurrence rate was 7.92%(16/202). However, entecavir group had 51 patients without hepatitis B virus recurrence in which three patients were dead. There were significant differences in the mortality rate and recurrence rate between two groups. Compared with the lamivudine+hepatitis B immunoglobulin, entecavir+hepatitis B immunoglobulin could effectively reduce the recurrence rate of the patients with hepatitis B virus-related risk factors. Hepatitis B immunoglobulin was terminated and nucleoside analogues were modulated when recurrence appeared. Al patients hepatitis B virus DNA were control ed less than 500 IU/mL and liver function returned to normal level. Log-rank test showed that there was no significant difference in the long-term survival rate after timely treatment of hepatitis B virus recurrence. With the prevention of nucleoside analogues combined with hepatitis B immunoglobulin therapy, timely treatment of hepatitis B recurrence has little influence on the prognosis. Entecavir combined with hepatitis B immunoglobulin can effectively prevent the hepatitis B recurrence. For the patients with hepatitis B virus-related risk factors, entecavir combined with hepatitis B immunoglobulin can better reduce the recurrence rate of hepatitis B than lamivudine+hepatitis B immunoglobulin after liver transplantation.
10.
Article in Chinese | WPRIM | ID: wpr-425619
ABSTRACT
ObjectiveTo demonstrate the efficacy and safety of Hangzhou tacrolimus capsule (Saishi Tac capsule,Hangzhou Zbongmei Huadong Pharmaceutical Co.Ltd,China) in Chinese liver transplant recipients.MethodsMulticenter,randomized open-labeled,prospective controlled clinical trial was performed in de novo Chinese liver transplant recipients.According to inclusive and exclusive criterion,83 liver recipients from 11transplant centers were enrolled.The recipients accepted Saishi Tac capsule,mycopheolate and steroid 48 h post-operation.The initial dose of Tac was 0.1-0.15 mg kg-1day-1and C0 was 8-12 ng/ml in the first 60 days,followed by 5-10 ng/ml until the terminal observation time poiut (12 weeks after transplantation).The efficacy and safety were estimated during the period.The primary efficacy endpoint of the study was the incidence of biopsy-confirmed acute rejection.Graft survival was the secondary endpoint.Safety was assessed by monitoring laboratory parameters and adverse events reported over the course of the study,such as infection,renal damage,hypertension,hyperlipema and diabetes mellitus and other adverse affairs.ResultsThe dose of Tac at 1st,2nd,4th and 8th week post-operation was (4.1±1.9),(4.5±2.1),(4.5±2.1),(4.4±1.8) and (4.1±2.1) mg,and correspondjng values to the C0 were (8.1±4.5),(8.9±4.5),(8.8±4.3),(8.8±4.1) and (8.0±2.8) ng/ml.During 12 weeks of follow-up,the incidence of biopsy-confirmed acute rejection was 4.8％ (4/83),and all of cases were reversed by implosive therapy.The survival rate of graft hver was 100％.The incidence of lung infection and diabetes mellitus was both 6.02％.ConclusionSaishi Tac capsule was safe and effective to Chinese liver transplant recipients.
11.
Article in Chinese | WPRIM | ID: wpr-402503
ABSTRACT
BACKGROUND: Biliary complications are a common cause of death in patients after liver transplantation, biliary endoscopic minimally invasive technique is gradually becoming an important tool to solve biliary complications following orthotopic liver transplantation.OBJECTIVE: To analyze the literatures on the biliary tract complications after liver transplantation, and to demonstrate a clear role of bile duct endoscopy in biliary complications.METHODS: Using "orthotopic liver transplantation, biliary complications, biliary tract, endoscope technique" in English for the search term, Pubmed database were searched between January 1980 and October 2008; Using "liver transplantation, biliary complications, bile duct cast, cholangioscopy" in Chinese for the search term, Vip Chinese Periodical Database and CNKI database were searched between 1994 and January 2009. Literature language was limited to English and Chinese. The studies related to bile duct injury-caused biliary complications after liver transplantation were included, while other research unrelated to biliary complications after liver transplantation were excluded.RESULTS AND CONCLUSION: A total of 52 literatures were screened out by the primary computer inspection, according to inclusion and exclusion criteria, 30 ones were involved for analysis. Biliary complications and vascular complications are considered as a common cause of death in patients after liver transplantation, particularly in biliary complications has become the major reason limiting the development of liver transplantation. Because of the difficulties on early recognition and treatment, the importance of the treatment for the complications in liver transplant patients is increasingly attracting more and more attention. Endoscopic operation technology and their subsidiary parts are improving, particularly therapeutic endoscopic retrograde cholangiopancreatography and biliary mirror technology are developing and continuously improving, biliary endoscopic minimally invasive technique is gradually becoming a major approach to solve biliary complications after orthotopic liver transplantation, The minimally invasive endoscopic diagnosis and treatment is an intuitive, reliable and credible means for the biliary complications after liver transplantation, serving as the most preferred method for diagnosing and treating biliary complications after liver transplantation.
12.
Article in Chinese | WPRIM | ID: wpr-541341
ABSTRACT
Objective To explore the clinical experience of liver retransplantation in management of biliary complications after liver transplantation.Methods The clinical data of patients receiving liver transplantion in our department between April 2002 and Aug. 2004 were retrospectively analyzed, including 5 patients being subjected to liver retransplantation because of serious biliary complication.Results Three patients were cured with the survival time being 5 months, 6 months and 8 months respectively. Two patients died at 8th and 43rd day: one died of liver non-function combining with lung infection and heart failure, and another died of renal failure. Complications included liver absess, biliary infection, wound infection, hydrops abdominis and lung infection.Conclusions Liver retransplantation is an effective treatment for serious biliary complications after liver transplantation. Surgical procedure, indication, operative opportunity, perioperative monitoring and so on contribute to the increase of the survival rate of the patients receiving liver retransplantation.
13.
Article in Chinese | WPRIM | ID: wpr-541018
ABSTRACT
Objective To evaluate the preventive effect of different portal vein flush solutions in no heart beating donor harvest on biliary cast syndrome (BCS) after orthotopic liver transplantation (OLT), and the application of choledochoscopy in treating BCS. Methods The incidence of biliary complications in 137 consecutive recipients undergoing OLT in our liver transplant center from May. 2002 to Dec. 2003 was retrospectively analyzed. The incidence and risk factors of BCS were compared in 2 groups with different types of portal vein flush solution in no heart beating donor liver harvest: group 1 (n = 65). University of Wisconsin (UW) solution; and group 2 (n = 72), hypertonic citrate adenine ( HCA) solution combined with UW solution. Therapeutic experience and clinical value of choledochoscopy for BCS were summarized. Results Seventeen out of 137 cases (12.4 %) developed BCS in the first three months after operation. In the group 1, the incidence of BCS was 20. 0 % (13/ 65), while that in the group 2 5. 56 % (4/72) with the difference being significant (P
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3,542,950,477,056,684,000 | Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Am J Prev Med. Author manuscript; available in PMC 2012 Aug 1.
Published in final edited form as:
PMCID: PMC3179387
NIHMSID: NIHMS307342
Measurement of Adults’ Sedentary Time in Population-Based Studies
Abstract
Sedentary time (too much sitting) is increasingly being recognized as a distinct health risk behavior. This paper reviews the reliability and validity of self-reported and device-based sedentary time measures and provides recommendations for their use in population-based studies. The focus is on instruments that have been used in free-living, population-based research in adults. Data from the 2003–2006 National Health and Nutrition Examination Survey are utilized to compare the descriptive epidemiology of sedentary time that arises from the use of different sedentary time measures. A key recommendation from this review is that, wherever possible, population-based monitoring of sedentary time should incorporate both self-reported measures (to capture important domain- and behavior-specific sedentary time information) and device-based measures (to measure both total sedentary time and patterns of sedentary time accumulation).
Introduction
Sedentary behaviors are those pursuits undertaken while awake that involve sitting or reclining and that result in little or no physical activity energy expenditure – typically 1 to 1.5 times the resting metabolic rate.1,2 Common sedentary behaviors include sitting or lying down while watching TV, using a computer, or driving. Sedentary time can be measured in three ways: (1) in terms of these specific behaviors (e.g., TV viewing time); (2) the amount of sedentary time occurring in a specific domain (e.g., work, leisure, domestic, transport); and, (3) the overall sedentary time across the day. As the term “sedentary” encompasses both sitting and reclining, the broader term sedentary is used in this article, except when sitting is specifically measured.
This paper provides an overview of current methods used to measure sedentary time in free-living, population-based research in adults. The first section provides information on the reliability and validity of self-reported measures, and extends from previous reviews3 to encompass multiple domains of sedentary time. The second section describes device-based measures, with a particular focus on the interpretation and validity of data from the Actigraph activity monitor. The final section uses data from the U.S. National Health and Nutrition Examination Survey (NHANES) to provide an example of how the descriptive epidemiology of sedentary time may differ depending on how it is measured.
Section 1: Self-reported Measurement of Sedentary Time
Overall sedentary time can be assessed with either a single item (sometimes asked separately for weekend and weekdays), or by summing responses for the various behaviors or domains (composite measure). Key self-reported methods used are questionnaires (self-administered or interviewer-administered), behavioral logs, and short-term recalls. Questionnaires are a popular method3 because they can be implemented on a large scale, are relatively inexpensive, and do not alter the behavior under investigation.4 However, as with physical activity assessment,4, 5 questionnaires that seek to assess habitual levels of sedentary behavior are susceptible to random and systematic reporting errors.
Short-term recalls (e.g., 24-hour recall) and behavioral logs4 can reduce some of these reporting errors, such as long-term averaging. Traditionally, the disadvantages of behavioral logs (participant burden, systematic reporting errors and administration costs) have limited their use in population-based research. However, new approaches and technologies can reduce costs. For example, the National Cancer Institute has developed, and is currently testing, an Internet-based instrument for population surveillance of both active and sedentary behaviors.6
Reliability and Validity of Self-Reported Measures of Sedentary Time
The usefulness of a self-reported measure is dictated to a large extent by the properties of test–retest reliability and criterion validity.7 A summary of test–retest reliability8-33 and criterion validity8, 9, 11, 15, 17-22, 28, 29, 34-40 findings for self-reported measures of overall and domain-specific sedentary time is provided in Tables 1 and and2.2. Depending on the available information, the intra-class correlation (ICC), Spearman’s rho (ρ) or Pearson’s correlation coefficient (r) are reported. Systematic differences between self-reported and criterion measures, when reported,8, 19-22, 34-37 are summarized in the text.
Table 1
Reliability coefficients for questionnaire measures of waking time spent in sedentary behaviors
Table 2
Validity coefficients for questionnaire measures of waking time spent in sedentary behaviors
Reliability studies
Reliability studies have varied in terms of recall period (from 3 days9, 10, 23, 25 to 3 months24), administration method (telephone or interview), and target population, making it difficult to compare their findings. Accordingly, the strength of association between test and retest measures varied widely across studies (Table 1). The majority of self-reported sedentary time measures showed moderate-to-high correlations, with magnitudes comparable to results reported for physical activity measures,11 indicating acceptable to good test–retest reliability. Stronger reliability was generally observed for sedentary behaviors that tend to be done on a regular basis and for prolonged periods of time, such as sitting at work and TV viewing time, than for less regularly performed behaviors, such as travel or other sitting.
Most questions about leisure-time3 and workplace sitting12, 13 asked about typical patterns of behavior. In comparison, the overall sitting measures asked either about typical behavior11, 14-17 or about sitting in the last 7 days.9, 11, 18, 23, 25-27 No difference between these two methods was found in a review of measures of non-occupational sitting time3 and in a comparison of two versions of the International Physical Activity Questionnaire (IPAQ; ‘typical’ or ‘last 7 days’).11
Validity studies
As detailed in Table 2, the validity of most questionnaire measures of sedentary time has been assessed against behavioral logs or accelerometers. However, these are not ‘gold standard’ measures of sedentary time, having their own errors and biases. To date, the most robust criterion employed has been combined hip-mounted accelerometer and behavioral log data.8, 37
The validity of the IPAQ single-item question used to assess overall sitting time has been extensively examined in a number of countries with participants of varying ages (18–65 years).9, 11 Most studies have shown low-to-moderate correlations with a criterion of accelerometer-derived sedentary time,9, 11, 17, 18 comparable in magnitude to those reported for interviewer-administered physical activity measures (Figure 1).41 While composite measures of sedentary time have also shown only low-to-moderate correlations with accelerometer-derived sedentary time (Figure 1),15, 21, 22, 28 total sitting time tends to be lower when assessed by a single-item (4.35–7.92 hours/day)9, 42, 43 than those by composite measures (7.25–9.80 hours/day).12, 19, 21 While direct comparison is hampered by the use of varying criterion measures, mode of administration, and target populations, correlations tended to be higher for domain-specific measures than for overall sedentary measures (Table 2) – particularly for screen time,8 computer use,19, 29 work,19 and TV viewing time.19, 36 Collectively, results suggest it may be more difficult to recall the time spent sitting during the entire day than the time spent sedentary for specific behaviors or in different domains.
Figure 1
Correlations (r or ρ) of self-reported sitting time assessed by a single-item (circles) or as a composite total (four items or more, triangles) with accelerometer-derived sedentary time
Findings from the relatively few studies that have reported on absolute agreement are mixed, with reports of both overestimation20, 34, 35, 37 and underestimation19, 21, 22 of sitting time compared with criterion measures. The sitting time reported for TV viewing, screen time and eating were typically underestimated compared to device-based measures of these same behaviors.8, 36 For example, on average, people report half an hour less TV viewing time than is recorded by the criterion measure,36 and the wide limits of agreement showed large discrepancies between self-report and the criterion at the individual level.
Summary and Recommendations for Future Research with Self-Reported Measures
The reliability and validity of available self-reported measures of sedentary time are highly variable but comparable with those reported for physical activity measures. The available evidence suggests many sedentary time measures have acceptable measurement properties (i.e., adequate test–retest and relative agreement with criterion measures) for establishing cross-sectional associations with health outcomes, but not necessarily for assessing changes over time in cohort and intervention studies. The evidence on absolute agreement is sparse, and shows only limited agreement against criterion measures that are less than ideal.8, 19-22, 34-37 In the only study to examine responsiveness to change, questionnaire-assessed sitting performed as well as accelerometer-assessed sedentary time.22
More work is also required to assess: nuances associated with mode of questionnaire administration (e.g., interviewer vs self-administration); different response formats (e.g., continuous or categoric); the time-frame of assessment (e.g., short-term, such as past day or last 7 days, versus habitual patterns such as typical day, usual week, or past year); and how these factors affect sedentary time estimates. Importantly, several achievable improvements to study design could improve understanding of the measurement properties. Much research to date has been conducted (either wholly or in part) with university samples26, 29, 30, 44 or with particular population subgroups, including overweight adults,36 middle-aged women,19 and young men.18
More research also is needed to focus on general population and subpopulation samples for which reliability and validity might be affected by issues of literacy, cognition, language and less ‘regular’ patterns of some sedentary behaviors (e.g., parents with young children or shift workers). Furthermore, improved criterion measures (see Section 2) are now available that could be used, with concomitant collection of behavioral log data where behavior- or domain-specific measures are required. Device-based measures specific to particular behaviors, such as the electronic TV monitor (which monitors user-specific TV viewing time),36 may also be useful.
Section 2: Device-Based measures of Sedentary Time
Given the errors associated with self-report, the ideal measure of sedentary time would:
• be accurate and reliable across different population groups;
• distinguish among sleep, reclining, sitting and standing;
• distinguish among different domains and specific behaviors;
• be low-cost, have low participant burden, and be able to be worn continuously for extended periods of time;
• produce data that are easily analyzed and interpreted and can be provided in real-time.
No such instrument currently exists. To date, the main instrument used to derive sedentary time in population-based studies is the hip-mounted uniaxial Actigraph accelerometer (model 7164), using 1-minute data-collection epochs.45, 46 In this paper, unless otherwise specified, the term “Actigraph activity monitor” refers to this particular model (7164), placement (hip), and epoch length (1 minute). This device has been shown to provide reliable, valid, and stable measurements of physical activity when compared with other measures of functional capacity.47 It can also provide information about total sedentary time and the manner in which sedentary time is accumulated, both of which have shown associations with health outcomes.48, 49
The primary aim of this section is to describe the collection, analysis and interpretation of data from the Actigraph activity monitor. Its validity was also reported when compared with two other device-based measures of sedentary time: the Intelligent Device for Energy Expenditure and Activity (IDEEA) monitor,50 and the activPAL activity monitor.51 Both instruments have been reported to have high accuracy for determining body position as compared to direct observation,50, 51 although neither has yet been used in population monitoring of sedentary time.
Collection, Analysis, and Interpretation of Actigraph Activity-Monitor Data
Collection
Accelerometers measure time-varying changes in force.52 Activity levels are typically recorded as counts, which are then summed over a user-specified time frame, or epoch. Several considerations for using accelerometers in field-based research have been reported in detail, 53-55 including accelerometer type, days of wear, and epoch length. Population-based studies utilizing accelerometers have typically used Actigraph activity monitors, had a 7-day wear protocol, and used a 1-minute epoch.45, 46, 56, 57
Analysis and interpretation
Once data are collected there are several analytic decisions, including cut-points, wear time, and data cleaning, to ensure that data can be meaningfully interpreted. Although the most accurate cut-point is yet to be established, counts per minute (cpm) of <100 are typically classified as sedentary time.11, 57-59
Wear time is a particularly important consideration. Participants are typically instructed to wear the monitor during “waking hours”, and to remove it for any water-based activity. As suggested by physical activity research, a minimum time of wear is generally required (for example, 10 hours per day59 and 4 days of wear including a weekend day60). Even so, individual wear time is highly variable and ‘missing data’ are usually indistinguishable from sleeping time, which should be excluded from sedentary time calculations. This introduces measurement error. In population-based studies, wear time for Actigraph activity monitors is usually estimated by automated programs, designed to detect long periods of low (mostly zero) counts.59 However, this can misclassify sedentary time as nonwear, and vice-versa.61 Methods of correcting for wear time include reporting sedentary time as a percentage of wear time, statistical adjustment in regression models, and using the residuals method.62
Sedentary time data derived from the Actigraph activity monitor are typically reported either as average hours per day or as a percentage of total wear time. The manner of sedentary time accumulation provides important additional information, such as the length and intensity of each sedentary bout or the number of interruptions (breaks) in sedentary time.48, 49 Furthermore, as data are date- and time-stamped, there is potential for more detailed examination of both sedentary time and patterns during specific time periods, such as during work hours.
Validity of the Actigraph Activity Monitor to Measure Sedentary Time
Following is a description of two studies led by coauthor Charles Matthews that examined the validity of sedentary time derived from the Actigraph activity monitor (<100 cpm) against the criterion of the IDEEA monitor and the activPAL activity monitor.
Accelerometer versus IDEEA monitor
Participants (n=19, mean age 40.1 years) concurrently wore the Actigraph activity monitor and IDEEA monitor for 2 days59 for the same amount of time on average (both 13.2 hours/day, SD 2.15). Sedentary time was similar for the accelerometer (8.63 hours/day, SD 1.90) and the IDEEA (8.53 hours/day, SD 1.86), and the two measures were highly correlated (ρ=0.59).59 This initial field study supported the use of the <100 cpm threshold for estimating sedentary time.11, 63
Accelerometer versus activPAL
In a second study, 86 participants (87% women; mean age 52.7 years, SD 8.6 years) simultaneously wore an Actigraph activity monitor and activPAL for 7 consecutive days. For this analysis, only valid days that had similar estimated wear times for both devices (± 30 minutes) were considered. Sedentary time derived from the Actigraph activity monitor (<100 cpm) was compared with that from the activPAL (sitting and lying down) over an average of 4.5 observed days per person, and an average wear time of 14.3 hours per day (SD=1.5) for each device.
On average, recorded sedentary time was lower for the Actigraph activity monitor (8.7 [SD=1.6] hours/day, or 60.9%) than for the activPAL (9.0 [SD=1.8] hours/day, or 63.4%; both p=0.01), but the correlation between the measures was relatively high (ρ=0.76, p < 0.01). Interestingly, Bland–Altman analysis64 (Figure 2) showed a small mean difference (−0.34 hours) and wide 95% limits of agreement (2.11 to −2.79 hours). This indicates that the Actigraph activity monitor has minimal bias overall, but can both substantially over- and under-estimate sedentary time compared with the activPAL.
Figure 2
Bland–Altman plot of agreement between activPAL and accelerometer-derived (<100 counts per minute) sedentary time (hours)
These two validity studies imply that Actigraph activity monitors provide useful estimates of sedentary time in the population and that they are sufficiently accurate to rank individuals by their level of sedentary time. The width of the limits of agreement observed warrants further study and suggests some caution is required when using indirect measures of sedentary time derived from only body motion. Instruments that measure body position more directly may be preferable in studies that require precise and accurate measures of sedentary time.
Recommendations for Future Research with Device-Based Measures
The incorporation of Actigraph activity monitor measures into the 2003/04 and 2005/06 NHANES was an important development in the field of physical activity and sedentary time research. With data from over 14,000 participants, it demonstrated the feasibility and utility of using these devices on a large scale. The inclusion of device-based measures in current65, 66 and future national health surveys will enable cross-country comparisons of levels of physical activity and sedentary time, as well as the ability to monitor population trends in these behaviors.
More-sophisticated systems for measuring time spent in various postures (e.g., sitting vs standing/upright) using more direct measures of body position have recently been developed.50, 51, 67-69 In addition, new approaches for translating more densely sampled data from hip-mounted accelerometers (e.g., 1- or 10-second epochs; raw data) to classify different types of behavior are also on the horizon.70-72 These new instruments and analytic approaches appear to provide more accurate and precise estimates of time spent in sedentary behaviors than were reported with the Actigraph 7164 activity monitor. There is also now the potential for the integration of multiple information sources, such as accelerometry, inclinometers, physiologic monitors, GPS technology, and behavioral logs.
In summary, key directions for future research in device-based measures of time spent sedentary are:
• studies to inform “best practice” for collection, analyses, reporting of device-based sedentary-time data including monitor placement (s) and wear time (both daily and number of days);
• developing analytic and modeling techniques to appropriately summarize the data for different population groups (for example, children; older adults);
• examining how measurement errors in the instruments vary according to the type of instrument employed and how results from surveillance and association studies may, or may not, be affected;
• developing products that are more affordable, have relatively low participant burden, can integrate multiple information sources, and provide contextual information.
Section 3: Descriptive Epidemiology of Sedentary Time in the U.S. As Measured by Self-Report and Accelerometry
In 2003/04 and 2005/06, the large, population-representative NHANES included both self-reported (global sitting time, TV viewing time, computer time) and device-based (accelerometer) measures of sedentary time. These data provide the unique opportunity to examine, within one sample, the descriptive epidemiology of sedentary time in the U.S. using a variety of measures. Rather than reporting the relationships of the various sedentary measures (which have been described previously73), the aim of this section is to examine similarities and differences among the measures in the patterning of sedentary time by gender, race/ethnicity and age.
Methods
The relevant NHANES methods are described in at http://www.cdc.gov/nchs/nhanes.htm.45 The National Centre for Health Statistics Ethics Review Board approved the protocols and written informed consent was obtained. For this study, 2003–2006 data from adult participants (≥20 years) were used. The study did not vary in protocol and had high response rates across this period.45
Self-reported sedentary time measures
In the household interviews, participants were asked to report the time they spent watching TV or videos (TV time) and using a computer or playing computer games (computer use) on an average day over the last 30 days. The categoric responses were collapsed into three dichotomous sedentary markers: TV time, computer use, and screen time (combined TV time and computer use). Cut-points were ≥2 hours per day for TV, ≥1 hour per day for computer use, and ≥3 hours for screen time. These were based on the availability of sufficient responses in all subpopulations, low rates of computer use in older age groups, and values used in previous research.74 Participants were also asked to best describe their usual daily activities (i.e., work, domestic activities, or general activities throughout the day). The response options were collapsed into a dichotomous variable sitting, which was yes if the respondent answered yes to the first option (“sitting during the day and not walking about very much”) or no if the respondent answered yes to any of the remaining options.
Accelerometer-derived sedentary time
An accelerometer (Actigraph model 7164; Actigraph, LLC, Fort Walton Beach, Florida) was worn on the right hip during waking hours (except for water-based activities) for 7 days. Data cleaning and automated wear time estimation were undertaken as previously described.60 Daily sedentary time (<100 cpm) was calculated and standardized for wear time using the residuals method.62 Data are reported as averages for valid days (≥10 hours wear, counts <20,000, monitor returned in calibration), limited to participants who provided at least 4 valid days of observation.75
Statistical analysis
Data were analyzed in STATA version 11.0 (College Station, TX, Stata Corporation), with significance set at p<0.05. Data were pooled from 2003–2006 to obtain sufficient numbers for stratified analyses. No significant changes (2003/04 to 2005/06) were observed. Self-reported TV time and computer use data were available for 10,012 adults, self-reported sitting data were available for 10,009, and ≥4 days of valid accelerometer data were available for 6,235.
Mean accelerometer-derived sedentary time (hours per day) and the prevalences of sitting, ≥2 hours per day TV time, ≥1 hour per day computer use, and ≥3 hours per day screen time were compared across gender, race/ethnicity categories (self-reported non-Hispanic white, Mexican-American, and non-Hispanic black), and 10-year age bands using marginal means from linear (accelerometer) or population marginal probabilities from logistic (self-reported) regression models. In view of the complex survey design, and to ensure population representativeness, all models used linearized variance estimation and, except when testing interactions, were weighted for selection probabilities and nonresponse. The weights provided by NHANES were further reweighted to correct for the large amount of missing/invalid accelerometer data.75 The data are population-representative.
Results
Gender differences
After adjusting for age and race/ethnicity, there were significant gender differences in all measures of sedentary time, with the direction and magnitude of the difference depending on the measure. For the domain-specific measures, prevalence was lower in women than men for high TV time (64.9% [95% CI=63.0%, 66.8%] vs 69.2% [67.6%, 70.7%], p<0.001), computer use (27.1% [25.1%, 29.1%] vs 31.3% [27.9%, 32.8%], p=0.034), and screen time (48.3% [46.2%, 50.3%] vs 52.0% [49.7%, 54.4%], p=0.012). However, more women than men reported sitting for most of the day (26.2% [24.4%, 28.0%] vs 21.5% [20.1%, 22.9%], p<0.001). This was consistent with the accelerometer findings (mean 8.50 [8.41, 8.59] hours/day in women vs 8.35 [8.25, 8.45] hours/day in men, p=0.006), although the magnitude of this difference was relatively small.
Race/ethnicity differences
After adjusting for age and gender, Mexican Americans were significantly less sedentary (p<0.05) than non-Hispanic whites and non-Hispanic blacks according to all sedentary time measures, with the exception of high levels of TV time. Here, the prevalence was similar for Mexican Americans (69.0% [66.3%, 71.5%]) and non-Hispanic whites (67.6% [65.8%, 69.3%], p=0.383), but significantly higher for non-Hispanic blacks (79.1% [75.7%, 82.5%], p<0.01). Compared with non-Hispanic whites, non-Hispanic blacks also had a higher prevalence of high screen time (51.1% [48.6%, 53.7%] vs 65.8% [61.8%, 69.7%], p<0.001), but these two racial/ethnic groups did not differ significantly for any other measure.
Age differences
Figure 3 shows the mean (a) and the prevalence estimates (b) of the sedentary time measures by age group (adjusted for gender and race/ethnicity). With the exception of computer use (where prevalence decreased with age), mean sedentary time and prevalence estimates tended to increase with age, but with a decrease between the 20–29 year and the 30–39 year age groups for all measures except sitting (which increased steadily with age).
Figure 3
Device-based (a) and self-reported (b) measures of sedentary time across age categories in U.S. adults aged ≥20 years (NHANES 2003–2006).
Figure 4 expands on Figure 3 by showing the mean (A and B) and the prevalence (C–H) estimates of the sedentary time measures by racial/ethnic group across age categories separately for men and for women. Among men, age trends in sedentary time differed significantly across racial/ethnic groups according to accelerometer-derived sedentary time (F(df: 10, 21)=3.24, p=0.01), but not according to the self-reported measures (p≥0.1). Among women, the age trends differed significantly by race/ethnicity according to the self-reported measures (sitting, screen time, TV time, and computer use; all p<0.05), but not the accelerometer-derived measure (p>0.1). Screen time results (omitted) were very similar to TV time. For a complete summary of results, see Appendixes A and B (www.ajpmonline.org).
Figure 4
Prevalence (95% CI) of self-reported TV viewing ≥2 hours/day (a,b); computer use ≥1 hour/day (c,d); sitting (e,f) and mean (95% CI) accelerometer-measured sedentary time (g,h)
Summary
In summary, the sedentary measures were consistent to some extent in identifying populations comparatively more or less sedentary, with older (60+) adults generally the most sedentary, and Mexican Americans generally the least sedentary. However, these subgroup differences are not apparent if only a single sedentary time measure is assessed. For example, if NHANES had measured only TV time, then the strong and largely consistent differences between Mexican Americans and non-Hispanic whites would not have been observed. If accelerometer-derived sedentary time had been the only measure, then important differences in specific sedentary behaviors between men and women and across the lifespan would not have been seen. Thus, wherever possible, both domain-specific and overall measures of sedentary time (preferably device-based) should be assessed. Furthermore, the inclusion of time spent sedentary in other domains, such as work and travel, should also be considered.
Conclusion
This paper provides an overview of the reliability and validity of current self-reported and device-based (primarily the Actigraph activity monitor) population-based measures of time spent sedentary. The 2003–2006 NHANES was utilized as an example of how various measures of sedentary time identify different population as ‘at-risk’.
Given that both self-reported and device-based instruments capture important aspects of sedentary behavior, it is recommended that wherever possible, both measures should be used for population-monitoring of sedentary time. For self-reported measures, monitoring should extend beyond measures of overall sitting to include the various domains. The battery of questions should be succinct, consistent in their terminology and administration (to allow comparison across time, and across different populations), and based on reliable and valid measures. Device-based measures should be affordable, distinguish among various postures, have relatively low participant burden, and where possible, integrate multiple sources of information that provide greater context for the behaviors observed. This paper identified key research directions for the development and refinement of such measures.
Supplementary Material
01
Acknowledgments
Healy is supported by a NHMRC (#569861) / National Heart Foundation of Australia (PH 08B 3905) Postdoctoral Fellowship. Clark is supported by an Australian Postgraduate Award and Queensland Health Core Research Infrastructure grant. Winkler and Gardiner are supported by a Queensland Health Core Research Infrastructure grant and by NHMRC Program Grant funding (#569940). NHANES data used in this study were collected by the National Center for Health Statistics, CDC
Footnotes
No financial disclosures were reported by the authors of this paper.
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-6,559,370,161,692,735,000 | Brown Fat vs White Fat
There are two colors of fat, brown and white. It’s important to understand brown fat vs white fat. The type we are most familiar with is white, which comprises most of the fat in the body. White fat is a storage depot for excess calories and provides insulation and produces inflammation, an unhealthy situation for the body. Brown fat is a healthy type of metabolically active fat. Brown fat is named as such because it contains a lot of energy-generating mitochondria which gives rise to the color. Brown fat is considered “good” because it burns calories and generates body heat.
Brown Fat vs White Fat
Through complex brain-hormone interactions, the body controls its own body temperature. A higher body temperature is the result of increased metabolism. It’s like running an engine; the harder it runs, the hotter it gets. The hormones that raise metabolism, in fact, do so mainly by increasing thermogenesis. Low body temperature means lowered metabolism; we’ve seen this is an indicator of low thyroid function. People with more brown fat have a higher body temperature and higher metabolism because they burn more calories to produce body heat.
Brown fat produces a specialized blood protein known as thermogenin that allows for the production of body heat. Brown tissue is controlled by nerves and stress hormones. The stress hormones epinephrine and norepinepherine, released from nerve cells and the adrenal gland, activate brown tissue, increasing thermogenesis.
Newborn babies have the highest concentrations of brown fatty tissue, but until recently, it was thought that adults didn’t have any brown fat. In 2009, scientists discovered the presence of it in adults. This was considered a major medical breakthrough when the research was published in the New England Journal of Medicine. Less than one percent of the body’s fat is brown. Most is located in the front of the neck, shoulders and around the collar bones. It also hides in deeper layers of fat and the number of areas varies among individuals. Thinner people and younger people tend to have the most. Although, you lose brown fat as you get older and as you gain weight, it doesn’t go away completely. In the past, it was thought that once you lost your brown fatty tissue, it was gone forever. However, this is clearly not the case. Everyone has the potential of making more.
Brown Fat Vs White Fat vs Beige FatNow researchers are working feverishly to find ways to help people make more of this calorie-burning tissue. Researchers are investigating different types of medications and even stem cell transplants as ways to induce brown fat production. Animal studies show that lowering room temperature just a few of degrees will make them lose weight by boosting their metabolism. Cold also makes white fat act more like brownish or beige fat, which burns more calories.
Importance of Brown Fat
You can make more brown fat by cooling your body down. Even a small decrease in the temperature your body is exposed to will induce your body make more calorie burning cells. From a survival perspective, when the body is cooled, it has to make more brown fatty tissue to generate enough body heat to keep from freezing to death. Researchers have speculated that warm temperatures may be contributing to our obesity epidemic. Turning down the thermostat just a couple of degrees could help boost your metabolism because you need to burn more calories to stay warm.
Exercise done in the water is particularly good at drawing out body heat, forcing your body to burn more calories. You don’t need to make yourself so cold that you feel uncomfortable or shiver. Swimming is one of the best fat-burning exercises. Swimming is extremely relaxing and a great form aerobic exercise. But any water exercise is a great way to cool your body and burn extra calories. Submersing yourself in water that’s cooler than body temperature will cool you down, causing you to make more brown fat to keep you warm. Try walking in a pool, using a kick board or take a water aerobics class. You don’t have to be a great swimmer to use water to help you burn extra calories.
Just as healthy fat can be part of the cycle to help lose weight; dysfunctional brown fat can get in the way. And, ironically – or perhaps not so ironically, considering the constant feedback loops of the body — obesity can cause brown fat dysfunction. If you are very overweight, your fat tissue cannot produce heat properly, so your metabolism is lowered and it becomes even harder to lose weight, ad infinitum.
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-6,654,766,249,857,654,000 | Health Advantages of Vitamins and Minerals
Vitamins and minerals are essential for the proper functioning of our body. There are different types of minerals which help our body functions in various ways. A deficiency of the needed minerals cause harm to the function of our body. Vitamins and minerals are present in the food we consume each day. Some foods are rich in certain types of minerals while others may have an abundance of some other minerals. Let’s take a look at some of the minerals, their functions and their source.
Sodium balances electrolytes and fluids. It also helps in contraction of muscles and transmissions in nerve impulse. Sodium can be found in soy sauce, meats, bread, salt and milk. Chloride preserves the balance of electrolytes and fluids. It helps in the process of digestion. Meats, soy sauce, eggs, salt and milk are rich in chlorides.
The purpose of Potassium in the body is to uphold the balance of electrolytes and fluids, integrity of the cells, contractions of muscles and transmissions of nerve impulse. Daily food stuffs like acorn Healthy Eating For An Active Lifestyle squash, potatoes, spinach, artichoke, carrots, broccoli, tomato juice, green beans, grapefruit juice, avocado, strawberries, banana, watermelon, cod and milk have ample supplies of potassium.
Calcium helps in the production of strong teeth and bones and aids in clotting of blood. Calcium is in abundance Why Is Global Health Important in yogurt, Swiss cheese, milk, tofu, cheddar cheese, green beans, broccoli, sardines, spinach etc.
Phosphorus is another important mineral which assists in proper forming of bones, teeth and cells. It also holds up the balance of acid-base in the body. Animal foods like eggs, poultry, meats, milk and fish are rich in Phosphorous.
Magnesium helps in maintaining mineralization of bones, build up of proteins, nerve impulse transmission, contraction of muscles and immunity. The mineral is present in artichokes, spinach, broccoli, tomato juice, tofu, green beans, cashews, black-eyed peas, halibut,.navy beans, sunflower seeds and pinto beans,
Iron transmits oxygen all over the cells of our body. Parsley, shrimp, artichoke, spinach, tomato juice, beef liver, clams, broccoli, tofu and green beans contains iron deposits for your body.
Zinc is a division of numerous enzymes. It takes part in the creation of genetic objects and in the production of proteins. Zinc transfers vitamin A, improves perception of taste, heals wound, produces sperm and assists in the healthy growth of fetus. Spinach, green peas, green beans, broccoli, lentils, oysters, lean ground beef, tomato juice, plain yogurt, shrimp, crab, Swiss cheese, tofu, turkey (dark meat), lean ham, lean sirloin steak, ricotta cheese etc have enough Zinc supply.
It is important to ensure your body gets sufficient supply of the necessary Vitamins and minerals for its good function.
READ How to Find the Right Family Health Guide | {
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6,491,752,054,606,217,000 | Survival models
Survival analysis is a branch of statistics for analyzing the expected duration of time until one or more events happen survival models and data analysis. Preface xi 1 introduction 1 11 what is survival analysis and how is it applied 1 12 the history of survival analysis and its progress 2 13 general features of survival data structure 3. Chapter summary chapter summary survival models age-at-death random variable time-until-death random variables force of mortality (or hazard rate function).
survival models This course introduces survival models and discusses their rationale, their estimation and their application to mortality topics covered will include: an introduction to the life table survival models estimation procedures for lifetime distributions statistical models of transfers between multiple states maximum likelihood estimation of.
Chapter 17 nest survival models jay rotella, montana state university in this chapter, we will introduce how to analyze nest survival data with program marknest survival is a key vital rate in the population dynamics of many birds. The multi-state survival model as an extension of the univariate survival model a general framework for defining a wide range of models and for estimation of model parameters illustrates the methods by analysing longitudinal data from medical and epidemiological studies a chapter dedicated to. Survival analysis is used to analyze data in which – the survival function gives the probability that make more assumptions that allow us to model the data in. Survival models - the random life length approach and the markov chain approach survival function, conditional survival function, mortality intensity.
Fit a parametric survival regression model these are location-scale models for an arbitrary transform of the time variable the most common cases use a log transformation, leading to accelerated failure time models a missing-data filter function, applied to the modelframe, after any subset. The concept of a hazard or hazard function plays an important role in the interpretation of survival analysis models a an introduction to survival analysis. Customer survival model sugi 28: modeling customer lifetime value using survival analysis - an application in the telecommunications industry.
Introduction an example preliminary analyses logit-based models for the hazard function a discrete-time hazard model fitting the discrete-time survival model. Short course: survival analysis models & statistical methods presenter: eric v slud, statistics program, mathematics dept, university of maryland at college park, college park, md 20742. By andrie de vries prior to joining revolution analytics in march this year, i spent several years in the field of market research and survey analytics during this period, i spent a few months consulting to a digital marketing agency based in london. Bio 244: unit 1 survival distributions, hazard functions, cumulative hazards 11 de nitions: the goals of this unit are to introduce notation, discuss ways of probabilisti-.
survival models This course introduces survival models and discusses their rationale, their estimation and their application to mortality topics covered will include: an introduction to the life table survival models estimation procedures for lifetime distributions statistical models of transfers between multiple states maximum likelihood estimation of.
Posts about survival models written by dan ma the hazard rate function , also known as the force of mortality or the failure rate, is defined as the ratio of the density function and the survival function. This article lays down a step by step process to build a survival analysis model using the business analytics tool r, data analysis with r. Similar to the asa, the broad objective of a chapter is to promote statistics and its applications and provide benefits to its members asa chapters exist throughout the united states and canada and engage in many activities, including the following:.
Suppose we have a censored survival time that we want to model as a function of a (possibly large) set of covariates two important questions are:. An introduction to survival analysis dr barry leventhal • hazards model – a model for predicting the hazard of an individual • cox proportional hazards model. Survival analysis deals with the distribution of life times, essentially the times from an initiating event such as birth or the start of a job to some terminal event such as death or pension this book, originally published in 1980, surveys and analyzes methods that use survival measurements and. 2013 convention 31 oct & 1 nov application of survival models to analyse default rates on bank loans fhatuwani nemakhavhani liberty holdings pty(ltd).
Survival models concern time-to-event outcomes the outcomes can be anything: death, myopia, employment, etc the outcomes can be good or bad, such as recovery or relapse, or marriage or divorce, which is worth mentioning because the jargon of survival analysis suggests the outcomes are unpleasant. Lecture 4 parametric survival models some parametric survival distributions (de ned on t 0): the exponential distribution (1 parameter) f(t) = e t ( 0) s(t) =. Amazoncom: survival models and data analysis (9780471349921): regina c elandt-johnson, norman l johnson: books. School of mathematical and computer sciences heriot-watt university notes on survival models takis konstantopoulos spring 2006 these are brief notes on survival models for the msc course in actuarial mathematics.
survival models This course introduces survival models and discusses their rationale, their estimation and their application to mortality topics covered will include: an introduction to the life table survival models estimation procedures for lifetime distributions statistical models of transfers between multiple states maximum likelihood estimation of. survival models This course introduces survival models and discusses their rationale, their estimation and their application to mortality topics covered will include: an introduction to the life table survival models estimation procedures for lifetime distributions statistical models of transfers between multiple states maximum likelihood estimation of. survival models This course introduces survival models and discusses their rationale, their estimation and their application to mortality topics covered will include: an introduction to the life table survival models estimation procedures for lifetime distributions statistical models of transfers between multiple states maximum likelihood estimation of. survival models This course introduces survival models and discusses their rationale, their estimation and their application to mortality topics covered will include: an introduction to the life table survival models estimation procedures for lifetime distributions statistical models of transfers between multiple states maximum likelihood estimation of. Download
Survival models
Rated 4/5 based on 15 review
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8,154,627,838,869,319,000 |
What is a healthy body fat percentage? (lean-to-fat ratio)
The ideal fat-lean ratio varies depending on several key points. First of all, you should know that it isn’t the same for men and for women. It also depends of your age. To help you assess if your body composition is good or bad, here are the commonly accepted levels that define the minimum, maximum and average body fat percentages of a healthy person. But first, let’s see how it works…
How does the Wi-Fi Body Scale measure fat mass?
To calculate the percentages of lean and fat mass, the scale uses a very low and harmless electrical current to measure the opposition your body presents to the its passage. As electricity doesn’t behave the same when it goes through fat, muscle, bone or fluids, our engineers were able to build an algorithm that extrapolates your body’s opposition to the current and provides you with a fat-lean ratio.
Why track your fat and lean masses?
Even though measuring the lean-to-fat ratio is tricky (your body composition constantly changes), and comparing ratios over time is only relevant if the weigh-ins are made in the same conditions, it is still a good indicator of how healthy your weight is. It basically tells you if you have an unhealthy level of fat. A normal body composition includes fat, but beyond a certain percentage, you start to be exposed to weight-related diseases (diabetes, coronary problems…). A low level of fat mass is also critical.
This is why your fat mass is a valuable information. If you track it through time you will also see how your efforts are paying off, and if your physical activity and diet really have an impact on your condition.
Healthy levels of fat mass for a fit person
1. Minimum
5% for men,
12% for women.
2. Maximum
25% for men,
32% for women.
3. Average
15 to 18% for men,
22 to 25% for women.
What does a healthy fat mass level look like?
As we said, calculating the lean-fat ratio isn’t the easiest body metric to measure. This is why we recommend that you weigh yourself regularly, at the same time, in the same conditions (food intake, exercise, 30 minutes after getting out of bed…). We also advise you to look at the general trend of the ratio, instead of worrying about this or that value.
This set of photos illustrates every level of fat mass, both for men and women (source).
The American Council on Exercise (ACE) has put out the chart below, linking each fat mass percentage to a certain condition (source). Note that the “Average” condition in this table is actually “overweight“.
Three special cases
1. Are you an athlete?
Athletes usually have a low fat-lean ratio because their muscle mass is bigger than for a non-athletic person (be aware that this rule also depends on what sport the athlete practices). This is why it is relevant to switch Body Composition Model if you are an athlete.
2. Expecting a baby?
Pregnant women can use the Wi-Fi Body Scale with absolutely no health risk. However, the fat mass measurement will not be accurate. As the baby grows, the future mother’s body composition changes drastically and the preset models loaded inside the Wi-Fi Body Scale will not be relevant anymore. If you want to, you may disable the fat mass measurement: go to “My account” then “My body scales”.
3. Do you have a pacemaker?
Persons with an implanted pacemaker should not use the Withings Wi-Fi Body Scale. We recommend you use the newly released Wireless Scale, which does not include an impedance system.
Testimonials of happy Withingers
Click here to read a selection of comments made by some of our dear customers.
Other interesting links
ABOUT THE AUTHOR
Jonathan Choquel
Apple fan and skateboard enthusiast since the 80s, Jonathan became Content Manager at Withings after a career as Chief Editor of specialized newsstand magazines. Curious by nature, he has been interested by the globalization of culture and the impact of new technologies on our daily lives for 20 years.
Follow
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Pubmed Article
Increased number of Tc17 and correlation with Th17 cells in patients with immune thrombocytopenia.
PLoS ONE
PUBLISHED: 07-29-2011
IL-17-secreting CD8+ T cells (Tc17 subset) have recently been defined as a subpopulation of effector T cells implicated in the pathogenesis of autoimmune diseases. The role of Tc17 and correlation with Th17 cells in the pathophysiology of immune thrombocytopenia (ITP) remain unsettled.
Authors: Simone K. Bedoya, Tenisha D. Wilson, Erin L. Collins, Kenneth Lau, Joseph Larkin III.
Published: 09-26-2013
ABSTRACT
Th17 cells are a distinct subset of T cells that have been found to produce interleukin 17 (IL-17), and differ in function from the other T cell subsets including Th1, Th2, and regulatory T cells. Th17 cells have emerged as a central culprit in overzealous inflammatory immune responses associated with many autoimmune disorders. In this method we purify T lymphocytes from the spleen and lymph nodes of C57BL/6 mice, and stimulate purified CD4+ T cells under control and Th17-inducing environments. The Th17-inducing environment includes stimulation in the presence of anti-CD3 and anti-CD28 antibodies, IL-6, and TGF-β. After incubation for at least 72 hours and for up to five days at 37 °C, cells are subsequently analyzed for the capability to produce IL-17 through flow cytometry, qPCR, and ELISAs. Th17 differentiated CD4+CD25- T cells can be utilized to further elucidate the role that Th17 cells play in the onset and progression of autoimmunity and host defense. Moreover, Th17 differentiation of CD4+CD25- lymphocytes from distinct murine knockout/disease models can contribute to our understanding of cell fate plasticity.
24 Related JoVE Articles!
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Cell-based Flow Cytometry Assay to Measure Cytotoxic Activity
Authors: Alessandra Noto, Pearline Ngauv, Lydie Trautmann.
Institutions: Vaccine and Gene Therapy Institute of Florida.
Cytolytic activity of CD8+ T cells is rarely evaluated. We describe here a new cell-based assay to measure the capacity of antigen-specific CD8+ T cells to kill CD4+ T cells loaded with their cognate peptide. Target CD4+ T cells are divided into two populations, labeled with two different concentrations of CFSE. One population is pulsed with the peptide of interest (CFSE-low) while the other remains un-pulsed (CFSE-high). Pulsed and un-pulsed CD4+ T cells are mixed at an equal ratio and incubated with an increasing number of purified CD8+ T cells. The specific killing of autologous target CD4+ T cells is analyzed by flow cytometry after coculture with CD8+ T cells containing the antigen-specific effector CD8+ T cells detected by peptide/MHCI tetramer staining. The specific lysis of target CD4+ T cells measured at different effector versus target ratios, allows for the calculation of lytic units, LU30/106 cells. This simple and straightforward assay allows for the accurate measurement of the intrinsic capacity of CD8+ T cells to kill target CD4+ T cells.
Immunology, Issue 82, Cytotoxicity, Effector CD8+ T cells, Tetramers, Target CD4+ T cells, CFSE, Flow cytometry
51105
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Enzyme-linked Immunospot Assay (ELISPOT): Quantification of Th-1 Cellular Immune Responses Against Microbial Antigens
Authors: Isfahan R. Chambers, Tiffany R. Cone, Kyra Oswald-Richter, Wonder P. Drake.
Institutions: Vanderbilt University School of Medicine, Vanderbilt University School of Medicine.
Adaptive immunity is an important component to clearance of intracellular pathogens. The ability to detect and quantify these responses in humans is an important diagnostic tool. The enzyme-linked immunospot assay (ELISPOT) is gaining popularity for its ability to identify cellular immune responses against microbial antigens, including immunosuppressed populations such as those with HIV infection, transplantation, and steroid use. This assay has the capacity to quantify the immune responses against specific microbial antigens, as well as distinguish if these responses are Th1 or Th2 in character. ELISPOT is not limited to the site of inflammation. It is versatile in its ability to assess for immune responses within peripheral blood, as well as sites of active involvement such as bronchoalveolar lavage, cerebral spinal fluid, and ascites. Detection of immune responses against a single or multiple antigens is possible, as well as specific epitopes within microbial proteins. This assay facilitates detection of immune responses over time, as well as distinctions in antigens recognized by host T cells. Dual color ELISPOT assays are available for detection of simultaneous expression of two cytokines. Recent applications for this technique include diagnosis of extrapulmonary tuberculosis, as well as investigation of the contribution of infectious antigens to autoimmune diseases.
Immunology, Issue 45, ELISPOT, Th-1 Immune Response, interferon gamma, T cell, adaptive immunity
2221
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A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
Authors: Dumizulu L. Tembo, Jacqui Montgomery, Alister G. Craig, Samuel C. Wassmer.
Institutions: Malawi-Liverpool-Wellcome Trust Clinical Research Programme, Liverpool School of Tropical Medicine, New York University School of Medicine.
P. falciparum causes the majority of severe malarial infections. The pathophysiological mechanisms underlying cerebral malaria (CM) are not fully understood and several hypotheses have been put forward, including mechanical obstruction of microvessels by P. falciparum-parasitized red blood cells (pRBC). Indeed, during the intra-erythrocytic stage of its life cycle, P. falciparum has the unique ability to modify the surface of the infected erythrocyte by exporting surface antigens with varying adhesive properties onto the RBC membrane. This allows the sequestration of pRBC in multiple tissues and organs by adhesion to endothelial cells lining the microvasculature of post-capillary venules 1. By doing so, the mature forms of the parasite avoid splenic clearance of the deformed infected erythrocytes 2 and restrict their environment to a more favorable low oxygen pressure 3. As a consequence of this sequestration, it is only immature asexual parasites and gametocytes that can be detected in peripheral blood. Cytoadherence and sequestration of mature pRBC to the numerous host receptors expressed on microvascular beds occurs in severe and uncomplicated disease. However, several lines of evidence suggest that only specific adhesive phenotypes are likely to be associated with severe pathological outcomes of malaria. One example of such specific host-parasite interactions has been demonstrated in vitro, where the ability of intercellular adhesion molecule-1 to support binding of pRBC with particular adhesive properties has been linked to development of cerebral malaria 4,5. The placenta has also been recognized as a site of preferential pRBC accumulation in malaria-infected pregnant women, with chondrotin sulphate A expressed on syncytiotrophoblasts that line the placental intervillous space as the main receptor 6. Rosetting of pRBC to uninfected erythrocytes via the complement receptor 1 (CD35)7,8 has also been associated with severe disease 9. One of the most recently described P. falciparum cytoadherence phenotypes is the ability of the pRBC to form platelet-mediated clumps in vitro. The formation of such pRBC clumps requires CD36, a glycoprotein expressed on the surface of platelets. Another human receptor, gC1qR/HABP1/p32, expressed on diverse cell types including endothelial cells and platelets, has also been shown to facilitate pRBC adhesion on platelets to form clumps 10. Whether clumping occurs in vivo remains unclear, but it may account for the significant accumulation of platelets described in brain microvasculature of Malawian children who died from CM 11. In addition, the ability of clinical isolate cultures to clump in vitro was directly linked to the severity of disease in Malawian 12 and Mozambican patients 13, (although not in Malian 14). With several aspects of the pRBC clumping phenotype poorly characterized, current studies on this subject have not followed a standardized procedure. This is an important issue because of the known high variability inherent in the assay 15. Here, we present a method for in vitro platelet-mediated clumping of P. falciparum with hopes that it will provide a platform for a consistent method for other groups and raise awareness of the limitations in investigating this phenotype in future studies. Being based in Malawi, we provide a protocol specifically designed for a limited resource setting, with the advantage that freshly collected clinical isolates can be examined for phenotype without need for cryopreservation.
Infection, Issue 75, Infectious Diseases, Immunology, Medicine, Microbiology, Molecular Biology, Cellular Biology, Parasitology, Clumping, platelets, Plasmodium falciparum, CD36, malaria, malarial infections, parasites, red blood cells, plasma, limited resources, clinical techniques, assay
4316
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Highly Resolved Intravital Striped-illumination Microscopy of Germinal Centers
Authors: Zoltan Cseresnyes, Laura Oehme, Volker Andresen, Anje Sporbert, Anja E. Hauser, Raluca Niesner.
Institutions: Leibniz Institute, Max-Delbrück Center for Molecular Medicine, Leibniz Institute, LaVision Biotec GmbH, Charité - University of Medicine.
Monitoring cellular communication by intravital deep-tissue multi-photon microscopy is the key for understanding the fate of immune cells within thick tissue samples and organs in health and disease. By controlling the scanning pattern in multi-photon microscopy and applying appropriate numerical algorithms, we developed a striped-illumination approach, which enabled us to achieve 3-fold better axial resolution and improved signal-to-noise ratio, i.e. contrast, in more than 100 µm tissue depth within highly scattering tissue of lymphoid organs as compared to standard multi-photon microscopy. The acquisition speed as well as photobleaching and photodamage effects were similar to standard photo-multiplier-based technique, whereas the imaging depth was slightly lower due to the use of field detectors. By using the striped-illumination approach, we are able to observe the dynamics of immune complex deposits on secondary follicular dendritic cells – on the level of a few protein molecules in germinal centers.
Immunology, Issue 86, two-photon laser scanning microscopy, deep-tissue intravital imaging, germinal center, lymph node, high-resolution, enhanced contrast
51135
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A Simple and Rapid Protocol to Non-enzymatically Dissociate Fresh Human Tissues for the Analysis of Infiltrating Lymphocytes
Authors: Soizic Garaud, Chunyan Gu-Trantien, Jean-Nicolas Lodewyckx, Anaïs Boisson, Pushpamali De Silva, Laurence Buisseret, Edoardo Migliori, Myriam Libin, Céline Naveaux, Hugues Duvillier, Karen Willard-Gallo.
Institutions: Université Libre de Bruxelles, Université Libre de Bruxelles, Université Libre de Bruxelles, Université Libre de Bruxelles.
The ability of malignant cells to evade the immune system, characterized by tumor escape from both innate and adaptive immune responses, is now accepted as an important hallmark of cancer. Our research on breast cancer focuses on the active role that tumor infiltrating lymphocytes play in tumor progression and patient outcome. Toward this goal, we developed a methodology for the rapid isolation of intact lymphoid cells from normal and abnormal tissues in an effort to evaluate them proximate to their native state. Homogenates prepared using a mechanical dissociator show both increased viability and cell recovery while preserving surface receptor expression compared to enzyme-digested tissues. Furthermore, enzymatic digestion of the remaining insoluble material did not recover additional CD45+ cells indicating that quantitative and qualitative measurements in the primary homogenate likely genuinely reflect infiltrating subpopulations in the tissue fragment. The lymphoid cells in these homogenates can be easily characterized using immunological (phenotype, proliferation, etc.) or molecular (DNA, RNA and/or protein) approaches. CD45+ cells can also be used for subpopulation purification, in vitro expansion or cryopreservation. An additional benefit of this approach is that the primary tissue supernatant from the homogenates can be used to characterize and compare cytokines, chemokines, immunoglobulins and antigens present in normal and malignant tissues. This protocol functions extremely well for human breast tissues and should be applicable to a wide variety of normal and abnormal tissues.
Immunology, Issue 94, Tumor immunology, tumor infiltrating lymphocytes, CD45+, breast cancer, fresh tissue homogenate, non-enzymatic dissociation, primary tissue supernatant
52392
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Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
Authors: Alicja Puchta, Chris P. Verschoor, Tanja Thurn, Dawn M. E. Bowdish.
Institutions: McMaster University .
Nasopharyngeal colonization by Streptococcus pneumoniae is a prerequisite to invasion to the lungs or bloodstream1. This organism is capable of colonizing the mucosal surface of the nasopharynx, where it can reside, multiply and eventually overcome host defences to invade to other tissues of the host. Establishment of an infection in the normally lower respiratory tract results in pneumonia. Alternatively, the bacteria can disseminate into the bloodstream causing bacteraemia, which is associated with high mortality rates2, or else lead directly to the development of pneumococcal meningitis. Understanding the kinetics of, and immune responses to, nasopharyngeal colonization is an important aspect of S. pneumoniae infection models. Our mouse model of intranasal colonization is adapted from human models3 and has been used by multiple research groups in the study of host-pathogen responses in the nasopharynx4-7. In the first part of the model, we use a clinical isolate of S. pneumoniae to establish a self-limiting bacterial colonization that is similar to carriage events in human adults. The procedure detailed herein involves preparation of a bacterial inoculum, followed by the establishment of a colonization event through delivery of the inoculum via an intranasal route of administration. Resident macrophages are the predominant cell type in the nasopharynx during the steady state. Typically, there are few lymphocytes present in uninfected mice8, however mucosal colonization will lead to low- to high-grade inflammation (depending on the virulence of the bacterial species and strain) that will result in an immune response and the subsequent recruitment of host immune cells. These cells can be isolated by a lavage of the tracheal contents through the nares, and correlated to the density of colonization bacteria to better understand the kinetics of the infection.
Immunology, Issue 83, Streptococcus pneumoniae, Nasal lavage, nasopharynx, murine, flow cytometry, RNA, Quantitative PCR, recruited macrophages, neutrophils, T-cells, effector cells, intranasal colonization
50490
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Modeling Mucosal Candidiasis in Larval Zebrafish by Swimbladder Injection
Authors: Remi L. Gratacap, Audrey C. Bergeron, Robert T. Wheeler.
Institutions: University of Maine, University of Maine.
Early defense against mucosal pathogens consists of both an epithelial barrier and innate immune cells. The immunocompetency of both, and their intercommunication, are paramount for the protection against infections. The interactions of epithelial and innate immune cells with a pathogen are best investigated in vivo, where complex behavior unfolds over time and space. However, existing models do not allow for easy spatio-temporal imaging of the battle with pathogens at the mucosal level. The model developed here creates a mucosal infection by direct injection of the fungal pathogen, Candida albicans, into the swimbladder of juvenile zebrafish. The resulting infection enables high-resolution imaging of epithelial and innate immune cell behavior throughout the development of mucosal disease. The versatility of this method allows for interrogation of the host to probe the detailed sequence of immune events leading to phagocyte recruitment and to examine the roles of particular cell types and molecular pathways in protection. In addition, the behavior of the pathogen as a function of immune attack can be imaged simultaneously by using fluorescent protein-expressing C. albicans. Increased spatial resolution of the host-pathogen interaction is also possible using the described rapid swimbladder dissection technique. The mucosal infection model described here is straightforward and highly reproducible, making it a valuable tool for the study of mucosal candidiasis. This system may also be broadly translatable to other mucosal pathogens such as mycobacterial, bacterial or viral microbes that normally infect through epithelial surfaces.
Immunology, Issue 93, Zebrafish, mucosal candidiasis, mucosal infection, epithelial barrier, epithelial cells, innate immunity, swimbladder, Candida albicans, in vivo.
52182
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Sublingual Immunotherapy as an Alternative to Induce Protection Against Acute Respiratory Infections
Authors: Natalia Muñoz-Wolf, Analía Rial, José M. Saavedra, José A. Chabalgoity.
Institutions: Universidad de la República, Trinity College Dublin.
Sublingual route has been widely used to deliver small molecules into the bloodstream and to modulate the immune response at different sites. It has been shown to effectively induce humoral and cellular responses at systemic and mucosal sites, namely the lungs and urogenital tract. Sublingual vaccination can promote protection against infections at the lower and upper respiratory tract; it can also promote tolerance to allergens and ameliorate asthma symptoms. Modulation of lung’s immune response by sublingual immunotherapy (SLIT) is safer than direct administration of formulations by intranasal route because it does not require delivery of potentially harmful molecules directly into the airways. In contrast to intranasal delivery, side effects involving brain toxicity or facial paralysis are not promoted by SLIT. The immune mechanisms underlying SLIT remain elusive and its use for the treatment of acute lung infections has not yet been explored. Thus, development of appropriate animal models of SLIT is needed to further explore its potential advantages. This work shows how to perform sublingual administration of therapeutic agents in mice to evaluate their ability to protect against acute pneumococcal pneumonia. Technical aspects of mouse handling during sublingual inoculation, precise identification of sublingual mucosa, draining lymph nodes and isolation of tissues, bronchoalveolar lavage and lungs are illustrated. Protocols for single cell suspension preparation for FACS analysis are described in detail. Other downstream applications for the analysis of the immune response are discussed. Technical aspects of the preparation of Streptococcus pneumoniae inoculum and intranasal challenge of mice are also explained. SLIT is a simple technique that allows screening of candidate molecules to modulate lungs’ immune response. Parameters affecting the success of SLIT are related to molecular size, susceptibility to degradation and stability of highly concentrated formulations.
Medicine, Issue 90, Sublingual immunotherapy, Pneumonia, Streptococcus pneumoniae, Lungs, Flagellin, TLR5, NLRC4
52036
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Assessing the Development of Murine Plasmacytoid Dendritic Cells in Peyer's Patches Using Adoptive Transfer of Hematopoietic Progenitors
Authors: Haiyan S. Li, Stephanie S. Watowich.
Institutions: The University of Texas MD Anderson Cancer Center, The University of Texas Graduate School of Biomedical Sciences.
This protocol details a method to analyze the ability of purified hematopoietic progenitors to generate plasmacytoid dendritic cells (pDC) in intestinal Peyer's patch (PP). Common dendritic cell progenitors (CDPs, lin- c-kitlo CD115+ Flt3+) were purified from the bone marrow of C57BL6 mice by FACS and transferred to recipient mice that lack a significant pDC population in PP; in this case, Ifnar-/- mice were used as the transfer recipients. In some mice, overexpression of the dendritic cell growth factor Flt3 ligand (Flt3L) was enforced prior to adoptive transfer of CDPs, using hydrodynamic gene transfer (HGT) of Flt3L-encoding plasmid. Flt3L overexpression expands DC populations originating from transferred (or endogenous) hematopoietic progenitors. At 7-10 days after progenitor transfer, pDCs that arise from the adoptively transferred progenitors were distinguished from recipient cells on the basis of CD45 marker expression, with pDCs from transferred CDPs being CD45.1+ and recipients being CD45.2+. The ability of transferred CDPs to contribute to the pDC population in PP and to respond to Flt3L was evaluated by flow cytometry of PP single cell suspensions from recipient mice. This method may be used to test whether other progenitor populations are capable of generating PP pDCs. In addition, this approach could be used to examine the role of factors that are predicted to affect pDC development in PP, by transferring progenitor subsets with an appropriate knockdown, knockout or overexpression of the putative developmental factor and/or by manipulating circulating cytokines via HGT. This method may also allow analysis of how PP pDCs affect the frequency or function of other immune subsets in PPs. A unique feature of this method is the use of Ifnar-/- mice, which show severely depleted PP pDCs relative to wild type animals, thus allowing reconstitution of PP pDCs in the absence of confounding effects from lethal irradiation.
Immunology, Issue 85, hematopoiesis, dendritic cells, Peyer's patch, cytokines, adoptive transfer
51189
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Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
Authors: Noa Raz, Michal Hallak, Tamir Ben-Hur, Netta Levin.
Institutions: Hadassah Hebrew-University Medical Center.
In order to follow optic neuritis patients and evaluate the effectiveness of their treatment, a handy, accurate and quantifiable tool is required to assess changes in myelination at the central nervous system (CNS). However, standard measurements, including routine visual tests and MRI scans, are not sensitive enough for this purpose. We present two visual tests addressing dynamic monocular and binocular functions which may closely associate with the extent of myelination along visual pathways. These include Object From Motion (OFM) extraction and Time-constrained stereo protocols. In the OFM test, an array of dots compose an object, by moving the dots within the image rightward while moving the dots outside the image leftward or vice versa. The dot pattern generates a camouflaged object that cannot be detected when the dots are stationary or moving as a whole. Importantly, object recognition is critically dependent on motion perception. In the Time-constrained Stereo protocol, spatially disparate images are presented for a limited length of time, challenging binocular 3-dimensional integration in time. Both tests are appropriate for clinical usage and provide a simple, yet powerful, way to identify and quantify processes of demyelination and remyelination along visual pathways. These protocols may be efficient to diagnose and follow optic neuritis and multiple sclerosis patients. In the diagnostic process, these protocols may reveal visual deficits that cannot be identified via current standard visual measurements. Moreover, these protocols sensitively identify the basis of the currently unexplained continued visual complaints of patients following recovery of visual acuity. In the longitudinal follow up course, the protocols can be used as a sensitive marker of demyelinating and remyelinating processes along time. These protocols may therefore be used to evaluate the efficacy of current and evolving therapeutic strategies, targeting myelination of the CNS.
Medicine, Issue 86, Optic neuritis, visual impairment, dynamic visual functions, motion perception, stereopsis, demyelination, remyelination
51107
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Multicolor Flow Cytometry Analyses of Cellular Immune Response in Rhesus Macaques
Authors: Hong He, Amy N. Courtney, Eric Wieder, K. Jagannadha Sastry.
Institutions: MD Anderson Cancer Center - University of Texas, University of Miami.
The rhesus macaque model is currently the best available model for HIV-AIDS with respect to understanding the pathogenesis as well as for the development of vaccines and therapeutics1,2,3. Here, we describe a method for the detailed phenotypic and functional analyses of cellular immune responses, specifically intracellular cytokine production by CD4+ and CD8+ T cells as well as the individual memory subsets. We obtained precise quantitative and qualitative measures for the production of interferon gamma (INF-) and interleukin (IL) -2 in both CD4+ and CD8+ T cells from the rhesus macaque PBMC stimulated with PMA plus ionomycin (PMA+I). The cytokine profiles were different in the different subsets of memory cells. Furthermore, this protocol provided us the sensitivity to demonstrate even minor fractions of antigen specific CD4+ and CD8+ T cell subsets within the PBMC samples from rhesus macaques immunized with an HIV envelope peptide cocktail vaccine developed in our laboratory. The multicolor flow cytometry technique is a powerful tool to precisely identify different populations of T cells 4,5 with cytokine-producing capability6 following non-specific or antigen-specific stimulation 5,7.
JoVE Immunology, Issue 38, Immune Response, Cytokine Production, Flow Cytometry, HIV, Rhesus Macaque, T Cells, Intracellular Cytokine Staining, FACS
1743
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Ex vivo Expansion of Tumor-reactive T Cells by Means of Bryostatin 1/Ionomycin and the Common Gamma Chain Cytokines Formulation
Authors: Maciej Kmieciak, Amir Toor, Laura Graham, Harry D. Bear, Masoud H. Manjili.
Institutions: Virginia Commonwealth University- Massey Cancer Center, Virginia Commonwealth University- Massey Cancer Center, Virginia Commonwealth University- Massey Cancer Center.
It was reported that breast cancer patients have pre-existing immune responses against their tumors1,2. However, such immune responses fail to provide complete protection against the development or recurrence of breast cancer. To overcome this problem by increasing the frequency of tumor-reactive T cells, adoptive immunotherapy has been employed. A variety of protocols have been used for the expansion of tumor-specific T cells. These protocols, however, are restricted to the use of tumor antigens ex vivo for the activation of antigen-specific T cells. Very recently, common gamma chain cytokines such as IL-2, IL-7, IL-15, and IL-21 have been used alone or in combination for the enhancement of anti-tumor immune responses3. However, it is not clear what formulation would work best for the expansion of tumor-reactive T cells. Here we present a protocol for the selective activation and expansion of tumor-reactive T cells from the FVBN202 transgenic mouse model of HER-2/neu positive breast carcinoma for use in adoptive T cell therapy of breast cancer. The protocol includes activation of T cells with bryostatin-1/ionomycin (B/I) and IL-2 in the absence of tumor antigens for 16 hours. B/I activation mimics intracellular signals that result in T cell activation by increasing protein kinase C activity and intracellular calcium, respectively4. This protocol specifically activates tumor-specific T cells while killing irrelevant T cells. The B/I-activated T cells are cultured with IL-7 and IL-15 for 24 hours and then pulsed with IL-2. After 24 hours, T cells are washed, split, and cultured with IL-7 + IL-15 for additional 4 days. Tumor-specificity and anti-tumor efficacy of the ex vivo expanded T cells is determined.
Immunology, Issue 47, Adoptive T cell therapy, Breast Cancer, HER-2/neu, common gamma chain cytokines, Bryostatin 1, Ionomycin
2381
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Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
Authors: Jing Chen, Scott Grieshaber, Clayton E. Mathews.
Institutions: University of Florida.
Type 1 diabetes (T1D) is a T cell mediated autoimmune disease. During the pathogenesis, patients become progressively more insulinopenic as insulin production is lost, presumably this results from the destruction of pancreatic beta cells by T cells. Understanding the mechanisms of beta cell death during the development of T1D will provide insights to generate an effective cure for this disease. Cell-mediated lymphocytotoxicity (CML) assays have historically used the radionuclide Chromium 51 (51Cr) to label target cells. These targets are then exposed to effector cells and the release of 51Cr from target cells is read as an indication of lymphocyte-mediated cell death. Inhibitors of cell death result in decreased release of 51Cr. As effector cells, we used an activated autoreactive clonal population of CD8+ Cytotoxic T lymphocytes (CTL) isolated from a mouse stock transgenic for both the alpha and beta chains of the AI4 T cell receptor (TCR). Activated AI4 T cells were co-cultured with 51Cr labeled target NIT cells for 16 hours, release of 51Cr was recorded to calculate specific lysis Mitochondria participate in many important physiological events, such as energy production, regulation of signaling transduction, and apoptosis. The study of beta cell mitochondrial functional changes during the development of T1D is a novel area of research. Using the mitochondrial membrane potential dye Tetramethyl Rhodamine Methyl Ester (TMRM) and confocal microscopic live cell imaging, we monitored mitochondrial membrane potential over time in the beta cell line NIT-1. For imaging studies, effector AI4 T cells were labeled with the fluorescent nuclear staining dye Picogreen. NIT-1 cells and T cells were co-cultured in chambered coverglass and mounted on the microscope stage equipped with a live cell chamber, controlled at 37°C, with 5% CO2, and humidified. During these experiments images were taken of each cluster every 3 minutes for 400 minutes. Over a course of 400 minutes, we observed the dissipation of mitochondrial membrane potential in NIT-1 cell clusters where AI4 T cells were attached. In the simultaneous control experiment where NIT-1 cells were co-cultured with MHC mis-matched human lymphocyte Jurkat cells, mitochondrial membrane potential remained intact. This technique can be used to observe real-time changes in mitochondrial membrane potential in cells under attack of cytotoxic lymphocytes, cytokines, or other cytotoxic reagents.
Immunology, Issue 52, cell, Type 1 Diabetes, Autoimmunity, Cytotoxic T Lymphocyte
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In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
Authors: Filippos Porichis, Meghan G. Hart, Jennifer Zupkosky, Lucie Barblu, Daniel E. Kaufmann.
Institutions: The Ragon Institute of MGH, MIT and Harvard, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM).
T cell exhaustion is a major factor in failed pathogen clearance during chronic viral infections. Immunoregulatory pathways, such as PD-1 and IL-10, are upregulated upon this ongoing antigen exposure and contribute to loss of proliferation, reduced cytolytic function, and impaired cytokine production by CD4 and CD8 T cells. In the murine model of LCMV infection, administration of blocking antibodies against these two pathways augmented T cell responses. However, there is currently no in vitro assay to measure the impact of such blockade on cytokine secretion in cells from human samples. Our protocol and experimental approach enable us to accurately and efficiently quantify the restoration of cytokine production by HIV-specific CD4 T cells from HIV infected subjects. Here, we depict an in vitro experimental design that enables measurements of cytokine secretion by HIV-specific CD4 T cells and their impact on other cell subsets. CD8 T cells were depleted from whole blood and remaining PBMCs were isolated via Ficoll separation method. CD8-depleted PBMCs were then incubated with blocking antibodies against PD-L1 and/or IL-10Rα and, after stimulation with an HIV-1 Gag peptide pool, cells were incubated at 37 °C, 5% CO2. After 48 hr, supernatant was collected for cytokine analysis by beads arrays and cell pellets were collected for either phenotypic analysis using flow cytometry or transcriptional analysis using qRT-PCR. For more detailed analysis, different cell populations were obtained by selective subset depletion from PBMCs or by sorting using flow cytometry before being assessed in the same assays. These methods provide a highly sensitive and specific approach to determine the modulation of cytokine production by antigen-specific T-helper cells and to determine functional interactions between different populations of immune cells.
Immunology, Issue 80, Virus Diseases, Immune System Diseases, HIV, CD4 T cell, CD8 T cell, antigen-presenting cell, Cytokines, immunoregulatory networks, PD-1: IL-10, exhaustion, monocytes
50821
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Human In Vitro Suppression as Screening Tool for the Recognition of an Early State of Immune Imbalance
Authors: Jill Waukau, Jeffrey Woodliff, Sanja Glisic.
Institutions: Medical College of Wisconsin , Medical College of Wisconsin , Medical College of Wisconsin .
Regulatory T cells (Tregs) are critical mediators of immune tolerance to self-antigens. In addition, they are crucial regulators of the immune response following an infection. Despite efforts to identify unique surface marker on Tregs, the only unique feature is their ability to suppress the proliferation and function of effector T cells. While it is clear that only in vitro assays can be used in assessing human Treg function, this becomes problematic when assessing the results from cross-sectional studies where healthy cells and cells isolated from subjects with autoimmune diseases (like Type 1 Diabetes-T1D) need to be compared. There is a great variability among laboratories in the number and type of responder T cells, nature and strength of stimulation, Treg:responder ratios and the number and type of antigen-presenting cells (APC) used in human in vitro suppression assays. This variability makes comparison between studies measuring Treg function difficult. The Treg field needs a standardized suppression assay that will work well with both healthy subjects and those with autoimmune diseases. We have developed an in vitro suppression assay that shows very little intra-assay variability in the stimulation of T cells isolated from healthy volunteers compared to subjects with underlying autoimmune destruction of pancreatic β-cells. The main goal of this piece is to describe an in vitro human suppression assay that allows comparison between different subject groups. Additionally, this assay has the potential to delineate a small loss in nTreg function and anticipate further loss in the future, thus identifying subjects who could benefit from preventive immunomodulatory therapy1. Below, we provide thorough description of the steps involved in this procedure. We hope to contribute to the standardization of the in vitro suppression assay used to measure Treg function. In addition, we offer this assay as a tool to recognize an early state of immune imbalance and a potential functional biomarker for T1D.
Immunology, Issue 53, suppression, regulatory T cells, Tregs, activated T cells, autoimmune disease, Type 1 Diabetes (T1D)
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Isolation of Double Negative αβ T Cells from the Kidney
Authors: Maria N. Martina, Samatha Bandapalle, Hamid Rabb, Abdel R. Hamad.
Institutions: Johns Hopkins University School of Medicine, Johns Hopkins University School of Medicine.
There is currently no standard protocol for the isolation of DN T cells from the non-lymphoid tissues despite their increasingly reported involvement in various immune responses. DN T cells are a unique immune cell type that has been implicated in regulating immune and autoimmune responses and tolerance to allotransplants1-6. DN T cells are, however, rare in peripheral blood and secondary lymphoid organs (spleen and lymph nodes), but are major residents of the normal kidney. Very little is known about their pathophysiologic function7 due to their paucity in the periphery. We recently described a comprehensive phenotypic and functional analysis of this population in the kidney8 in steady state and during ischemia reperfusion injury. Analysis of DN T cell function will be greatly enhanced by developing a protocol for their isolation from the kidney. Here, we describe a novel protocol that allows isolation of highly pure ab CD4+ CD8+ T cells and DN T cells from the murine kidney. Briefly, we digest kidney tissue using collagenase and isolate kidney mononuclear cells (KMNC) by density gradient. This is followed by two steps to enrich hematopoietic T cells from 3% to 70% from KMNC. The first step consists of a positive selection of hematopoietic cells using a CD45+ isolation kit. In the second step, DN T cells are negatively isolated by removal of non-desired cells using CD4, CD8, and MHC class II monoclonal antibodies and CD1d α-galcer tetramer. This strategy leads to a population of more than 90% pure DN T cells. Surface staining with the above mentioned antibodies followed by FACs analysis is used to confirm purity.
Immunology, Issue 87, Double Negative (DN) αβ, T cells, CD45+ T cell isolation, renal lymphocytes, non-lymphoid-tissues, T cells purification, Ischemia Reperfusion Injury, Acute Kidney Injury, Tissue Resident Lymphocytes, Lymphoproliferative Disorders, Erythematosus Lupus
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The Use of Fluorescent Target Arrays for Assessment of T Cell Responses In vivo
Authors: Benjamin J. C. Quah, Danushka K. Wijesundara, Charani Ranasinghe, Christopher R. Parish.
Institutions: Australian National University.
The ability to monitor T cell responses in vivo is important for the development of our understanding of the immune response and the design of immunotherapies. Here we describe the use of fluorescent target array (FTA) technology, which utilizes vital dyes such as carboxyfluorescein succinimidyl ester (CFSE), violet laser excitable dyes (CellTrace Violet: CTV) and red laser excitable dyes (Cell Proliferation Dye eFluor 670: CPD) to combinatorially label mouse lymphocytes into >250 discernable fluorescent cell clusters. Cell clusters within these FTAs can be pulsed with major histocompatibility (MHC) class-I and MHC class-II binding peptides and thereby act as target cells for CD8+ and CD4+ T cells, respectively. These FTA cells remain viable and fully functional, and can therefore be administered into mice to allow assessment of CD8+ T cell-mediated killing of FTA target cells and CD4+ T cell-meditated help of FTA B cell target cells in real time in vivo by flow cytometry. Since >250 target cells can be assessed at once, the technique allows the monitoring of T cell responses against several antigen epitopes at several concentrations and in multiple replicates. As such, the technique can measure T cell responses at both a quantitative (e.g. the cumulative magnitude of the response) and a qualitative (e.g. functional avidity and epitope-cross reactivity of the response) level. Herein, we describe how these FTAs are constructed and give an example of how they can be applied to assess T cell responses induced by a recombinant pox virus vaccine.
Immunology, Issue 88, Investigative Techniques, T cell response, Flow Cytometry, Multiparameter, CTL assay in vivo, carboxyfluorescein succinimidyl ester (CFSE), CellTrace Violet (CTV), Cell Proliferation Dye eFluor 670 (CPD)
51627
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A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Authors: Daniel T. Claiborne, Jessica L. Prince, Eric Hunter.
Institutions: Emory University, Emory University.
The protective effect of many HLA class I alleles on HIV-1 pathogenesis and disease progression is, in part, attributed to their ability to target conserved portions of the HIV-1 genome that escape with difficulty. Sequence changes attributed to cellular immune pressure arise across the genome during infection, and if found within conserved regions of the genome such as Gag, can affect the ability of the virus to replicate in vitro. Transmission of HLA-linked polymorphisms in Gag to HLA-mismatched recipients has been associated with reduced set point viral loads. We hypothesized this may be due to a reduced replication capacity of the virus. Here we present a novel method for assessing the in vitro replication of HIV-1 as influenced by the gag gene isolated from acute time points from subtype C infected Zambians. This method uses restriction enzyme based cloning to insert the gag gene into a common subtype C HIV-1 proviral backbone, MJ4. This makes it more appropriate to the study of subtype C sequences than previous recombination based methods that have assessed the in vitro replication of chronically derived gag-pro sequences. Nevertheless, the protocol could be readily modified for studies of viruses from other subtypes. Moreover, this protocol details a robust and reproducible method for assessing the replication capacity of the Gag-MJ4 chimeric viruses on a CEM-based T cell line. This method was utilized for the study of Gag-MJ4 chimeric viruses derived from 149 subtype C acutely infected Zambians, and has allowed for the identification of residues in Gag that affect replication. More importantly, the implementation of this technique has facilitated a deeper understanding of how viral replication defines parameters of early HIV-1 pathogenesis such as set point viral load and longitudinal CD4+ T cell decline.
Infectious Diseases, Issue 90, HIV-1, Gag, viral replication, replication capacity, viral fitness, MJ4, CEM, GXR25
51506
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Directed Differentiation of Induced Pluripotent Stem Cells towards T Lymphocytes
Authors: Fengyang Lei, Rizwanul Haque, Xiaofang Xiong, Jianxun Song.
Institutions: Pennsylvania State University College of Medicine.
Adoptive cell transfer (ACT) of antigen-specific CD8+ cytotoxic T lymphocytes (CTLs) is a promising treatment for a variety of malignancies 1. CTLs can recognize malignant cells by interacting tumor antigens with the T cell receptors (TCR), and release cytotoxins as well as cytokines to kill malignant cells. It is known that less-differentiated and central-memory-like (termed highly reactive) CTLs are the optimal population for ACT-based immunotherapy, because these CTLs have a high proliferative potential, are less prone to apoptosis than more differentiated cells and have a higher ability to respond to homeostatic cytokines 2-7. However, due to difficulties in obtaining a high number of such CTLs from patients, there is an urgent need to find a new approach to generate highly reactive Ag-specific CTLs for successful ACT-based therapies. TCR transduction of the self-renewable stem cells for immune reconstitution has a therapeutic potential for the treatment of diseases 8-10. However, the approach to obtain embryonic stem cells (ESCs) from patients is not feasible. Although the use of hematopoietic stem cells (HSCs) for therapeutic purposes has been widely applied in clinic 11-13, HSCs have reduced differentiation and proliferative capacities, and HSCs are difficult to expand in in vitro cell culture 14-16. Recent iPS cell technology and the development of an in vitro system for gene delivery are capable of generating iPS cells from patients without any surgical approach. In addition, like ESCs, iPS cells possess indefinite proliferative capacity in vitro, and have been shown to differentiate into hematopoietic cells. Thus, iPS cells have greater potential to be used in ACT-based immunotherapy compared to ESCs or HSCs. Here, we present methods for the generation of T lymphocytes from iPS cells in vitro, and in vivo programming of antigen-specific CTLs from iPS cells for promoting cancer immune surveillance. Stimulation in vitro with a Notch ligand drives T cell differentiation from iPS cells, and TCR gene transduction results in iPS cells differentiating into antigen-specific T cells in vivo, which prevents tumor growth. Thus, we demonstrate antigen-specific T cell differentiation from iPS cells. Our studies provide a potentially more efficient approach for generating antigen-specific CTLs for ACT-based therapies and facilitate the development of therapeutic strategies for diseases.
Stem Cell Biology, Issue 63, Immunology, T cells, induced pluripotent stem cells, differentiation, Notch signaling, T cell receptor, adoptive cell transfer
3986
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Development of an IFN-γ ELISpot Assay to Assess Varicella-Zoster Virus-specific Cell-mediated Immunity Following Umbilical Cord Blood Transplantation
Authors: Insaf Salem Fourati, Anne-Julie Grenier, Élyse Jolette, Natacha Merindol, Philippe Ovetchkine, Hugo Soudeyns.
Institutions: Université de Montréal, Université de Montréal, Université de Montréal.
Varicella zoster virus (VZV) is a significant cause of morbidity and mortality following umbilical cord blood transplantation (UCBT). For this reason, antiherpetic prophylaxis is administrated systematically to pediatric UCBT recipients to prevent complications associated with VZV infection, but there is no strong, evidence based consensus that defines its optimal duration. Because T cell mediated immunity is responsible for the control of VZV infection, assessing the reconstitution of VZV specific T cell responses following UCBT could provide indications as to whether prophylaxis should be maintained or can be discontinued. To this end, a VZV specific gamma interferon (IFN-γ) enzyme-linked immunospot (ELISpot) assay was developed to characterize IFN-γ production by T lymphocytes in response to in vitro stimulation with irradiated live attenuated VZV vaccine. This assay provides a rapid, reproducible and sensitive measurement of VZV specific cell mediated immunity suitable for monitoring the reconstitution of VZV specific immunity in a clinical setting and assessing immune responsiveness to VZV antigens.
Immunology, Issue 89, Varicella zoster virus, cell-mediated immunity, T cells, interferon gamma, ELISpot, umbilical cord blood transplantation
51643
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Optimized Staining and Proliferation Modeling Methods for Cell Division Monitoring using Cell Tracking Dyes
Authors: Joseph D. Tario Jr., Kristen Humphrey, Andrew D. Bantly, Katharine A. Muirhead, Jonni S. Moore, Paul K. Wallace.
Institutions: Roswell Park Cancer Institute, University of Pennsylvania , SciGro, Inc., University of Pennsylvania .
Fluorescent cell tracking dyes, in combination with flow and image cytometry, are powerful tools with which to study the interactions and fates of different cell types in vitro and in vivo.1-5 Although there are literally thousands of publications using such dyes, some of the most commonly encountered cell tracking applications include monitoring of: stem and progenitor cell quiescence, proliferation and/or differentiation6-8 antigen-driven membrane transfer9 and/or precursor cell proliferation3,4,10-18 and immune regulatory and effector cell function1,18-21. Commercially available cell tracking dyes vary widely in their chemistries and fluorescence properties but the great majority fall into one of two classes based on their mechanism of cell labeling. "Membrane dyes", typified by PKH26, are highly lipophilic dyes that partition stably but non-covalently into cell membranes1,2,11. "Protein dyes", typified by CFSE, are amino-reactive dyes that form stable covalent bonds with cell proteins4,16,18. Each class has its own advantages and limitations. The key to their successful use, particularly in multicolor studies where multiple dyes are used to track different cell types, is therefore to understand the critical issues enabling optimal use of each class2-4,16,18,24. The protocols included here highlight three common causes of poor or variable results when using cell-tracking dyes. These are: Failure to achieve bright, uniform, reproducible labeling. This is a necessary starting point for any cell tracking study but requires attention to different variables when using membrane dyes than when using protein dyes or equilibrium binding reagents such as antibodies. Suboptimal fluorochrome combinations and/or failure to include critical compensation controls. Tracking dye fluorescence is typically 102 - 103 times brighter than antibody fluorescence. It is therefore essential to verify that the presence of tracking dye does not compromise the ability to detect other probes being used. Failure to obtain a good fit with peak modeling software. Such software allows quantitative comparison of proliferative responses across different populations or stimuli based on precursor frequency or other metrics. Obtaining a good fit, however, requires exclusion of dead/dying cells that can distort dye dilution profiles and matching of the assumptions underlying the model with characteristics of the observed dye dilution profile. Examples given here illustrate how these variables can affect results when using membrane and/or protein dyes to monitor cell proliferation.
Cellular Biology, Issue 70, Molecular Biology, Cell tracking, PKH26, CFSE, membrane dyes, dye dilution, proliferation modeling, lymphocytes
4287
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New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
Authors: Mathieu Angin, Melanie King, Marylyn Martina Addo.
Institutions: Ragon Institute of MGH, MIT, and Harvard, Massachusetts General Hospital.
CD4+ Regulatory T cells (Tregs) are potent immune modulators and serve an important function in human immune homeostasis. Depletion of Tregs has led to measurable increases in antigen-specific T cell responses in vaccine settings for cancer and infectious pathogens. However, their role in HIV-1 immuno-pathogenesis remains controversial, as they could either serve to suppress deleterious HIV-1-associated immune activation and thus slow HIV-1 disease progression or alternatively suppress HIV-1-specific immunity and thereby promote virus spread. Understanding and modulating Treg function in the context of HIV-1 could lead to potential new strategies for immunotherapy or HIV vaccines. However, important open questions remain on their role in the context of HIV-1 infection, which needs to be carefully studied. Representing roughly 5% of human CD4+ T cells in the peripheral blood, studying the Treg population has proven to be difficult, especially in HIV-1 infected individuals where HIV-1-associated CD4 T cell and with that Treg depletion occurs. The characterization of regulatory T cells in individuals with advanced HIV-1 disease or tissue samples, for which only very small biological samples can be obtained, is therefore extremely challenging. We propose a technical solution to overcome these limitations using isolation and expansion of Tregs from HIV-1-positive individuals. Here we describe an easy and robust method to successfully expand Tregs isolated from HIV-1-infected individuals in vitro. Flow-sorted CD3+CD4+CD25+CD127low Tregs were stimulated with anti-CD3/anti-CD28 coated beads and cultured in the presence of IL-2. The expanded Tregs expressed high levels of FOXP3, CTLA4 and HELIOS compared to conventional T cells and were shown to be highly suppressive. Easier access to large numbers of Tregs will allow researchers to address important questions concerning their role in HIV-1 immunopathogenesis. We believe answering these questions may provide useful insight for the development of an effective HIV-1 vaccine.
Infection, Issue 75, Infectious Diseases, Medicine, Immunology, Virology, Cellular Biology, Molecular Biology, Lymphocytes, T-Lymphocytes, Regulatory, HIV, Culture Techniques, flow cytometry, cell culture, Treg expansion, regulatory T cells, CD4+ T cells, Tregs, HIV-1, virus, HIV-1 infection, AIDS, clinical techniques
50244
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Detection and Isolation of Viable Mouse IL-17-Secreting T Cells
Authors: Anna Foerster, Mario Assenmacher, Michaela Niemoeller, Elly Rankin, Mariette Mohaupt, Anne Richter.
Institutions: Miltenyi Biotec,GmbH.
The MACS Cytokine Secretion Assay technology allows detection of secreted cytokines on the single cell level and sensitive isolation of viable cytokine-secreting cells. In order to label IL-17-secreting cells, a single cell suspension of mouse splenocytes is prepared and stimulated at 37°C with PMA/ionomycin to induce cytokine secretion. To stop secretion cells are then placed on ice and are exposed to the IL-17 Catch Reagent a bi-specific antibody that binds to CD45 on the cell surface of leukocytes and to IL-17 as it is secreted and caught near the cell surface. Secretion is then re-started by increasing the temperature to 37°C and IL-17 is trapped by the Catch Reagent. Secretion is then stopped again, by placing cells on ice. To detect the trapped IL-17, cells are incubated with a second IL-17-specific antibody conjugated to biotin and an Anti-Biotin-PE antibody. Cells can now be directly analyzed by flow cytometry or prepared for isolation and enrichment by subsequent labeling with Anti-PE conjugated MicroBeads.
Immunology, Issue 22, Miltenyi, leukocytes, cytokine, IL-17, MACS, FACS, TH17, cell separation
1037
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Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro
Authors: Aya D. Pusic, Yelena Y. Grinberg, Heidi M. Mitchell, Richard P. Kraig.
Institutions: The University of Chicago Medical Center, The University of Chicago Medical Center.
Migraine and its transformation to chronic migraine are healthcare burdens in need of improved treatment options. We seek to define how neural immune signaling modulates the susceptibility to migraine, modeled in vitro using spreading depression (SD), as a means to develop novel therapeutic targets for episodic and chronic migraine. SD is the likely cause of migraine aura and migraine pain. It is a paroxysmal loss of neuronal function triggered by initially increased neuronal activity, which slowly propagates within susceptible brain regions. Normal brain function is exquisitely sensitive to, and relies on, coincident low-level immune signaling. Thus, neural immune signaling likely affects electrical activity of SD, and therefore migraine. Pain perception studies of SD in whole animals are fraught with difficulties, but whole animals are well suited to examine systems biology aspects of migraine since SD activates trigeminal nociceptive pathways. However, whole animal studies alone cannot be used to decipher the cellular and neural circuit mechanisms of SD. Instead, in vitro preparations where environmental conditions can be controlled are necessary. Here, it is important to recognize limitations of acute slices and distinct advantages of hippocampal slice cultures. Acute brain slices cannot reveal subtle changes in immune signaling since preparing the slices alone triggers: pro-inflammatory changes that last days, epileptiform behavior due to high levels of oxygen tension needed to vitalize the slices, and irreversible cell injury at anoxic slice centers. In contrast, we examine immune signaling in mature hippocampal slice cultures since the cultures closely parallel their in vivo counterpart with mature trisynaptic function; show quiescent astrocytes, microglia, and cytokine levels; and SD is easily induced in an unanesthetized preparation. Furthermore, the slices are long-lived and SD can be induced on consecutive days without injury, making this preparation the sole means to-date capable of modeling the neuroimmune consequences of chronic SD, and thus perhaps chronic migraine. We use electrophysiological techniques and non-invasive imaging to measure neuronal cell and circuit functions coincident with SD. Neural immune gene expression variables are measured with qPCR screening, qPCR arrays, and, importantly, use of cDNA preamplification for detection of ultra-low level targets such as interferon-gamma using whole, regional, or specific cell enhanced (via laser dissection microscopy) sampling. Cytokine cascade signaling is further assessed with multiplexed phosphoprotein related targets with gene expression and phosphoprotein changes confirmed via cell-specific immunostaining. Pharmacological and siRNA strategies are used to mimic and modulate SD immune signaling.
Neuroscience, Issue 52, innate immunity, hormesis, microglia, T-cells, hippocampus, slice culture, gene expression, laser dissection microscopy, real-time qPCR, interferon-gamma
2910
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.
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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.
Video X seems to be unrelated to Abstract Y...
In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation. | {
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-7,335,557,052,489,396,000 | PF3 activity in normal subjects and beta-thalassemia trait.
Ina Susianti Timan, Y. Funahara, Rianto Setiabudy, J. Latu, E. Silman
Research output: Contribution to journalArticlepeer-review
4 Citations (Scopus)
Abstract
Platelet factor 3 (PF3) is a platelet membrane component that plays an important role in the activation of the coagulation mechanism. Whenever platelet activation occurred, PF3 is released and participates in thrombin formation. Erythrocyte membrane fraction has also some PF3 like activity, and in abnormal erythrocyte membrane disorders, eg thalassemia, some of the membrane fraction accelerates platelet activation by increasing the PF3 activity. Formerly it was difficult to measure the PF3 activity in plasma. Recently a sensitive chromogenic test to determine the PF3 activity, which could detect the changes in PF3 activity with time, was introduced. This study was done to observe the effect of abnormal erythrocyte on platelet activation. The results obtained using the chromogenic method are the following: whole blood taken from normal subjects showed OD 0.11 +/- 0.06 at 0 minutes after blood collection and then increased significantly (p < 0.01) to 0.21 +/- 0.10 after 90 minutes, while the platelet count did not differ significantly (p > 0.05). Those results showed that there were some platelet activation after 90 minutes as seen by the increased PF3 activity, with no significant change in platelet counts. In beta-thalassemic trait subjects the PF3 activity in whole blood at 0 minutes did not differ significantly compared to the normal subjects, but after 90 minutes it was significantly higher (p < 0.01), OD 0.52 +/- 0.35. However the PF3 in platelet rich plasma at 90 minutes did not increase. The platelet count after 90 minutes was significantly decreased (p < 0.01) This result suggest that the increase in PF3 activity was caused by the role of the abnormal erythrocytes.
Original languageEnglish
Pages (from-to)216-218
Number of pages3
JournalThe Southeast Asian journal of tropical medicine and public health
Volume24 Suppl 1
Publication statusPublished - 1 Dec 1993
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6,894,720,778,191,256,000 | top of page
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Tips for a better night’s sleep
Updated: Oct 19, 2020
Did you know that we spend about one-third of our lives sleeping!
Amongst our busy and sometimes erratic lifestyles, it is too easy to sacrifice sleep and not make it a priority.
However, if we take a moment to think about the impact sleep (or more importantly a lack of it) has on both our physical and mental health – will we change how we think about sleep and how we incorporate it into our everyday routine?
So why do we need sleep?
Sleep is as essential as breathing and eating. Our bodies and mind need time to rest and recharge. Sleep allows cells to repair and regrow.
Whilst we sleep, our brain converts short-term memories into long-term ones and it clears out any unneeded information to avoid cluttering up our central nervous system. Brain activity increases in areas that regulate emotion and therefore supports emotional stability. For example, when we get enough sleep our amygdala (the part of the brain in charge of the fear response) can respond more rationally, however, when sleep-deprived the amygdala is more likely to overreact.
Sleep deprivation leads to suppressed immune system, increased appetite and in turn weight gain and it also increases the risk of heart disease and stroke. I’m sure you can also relate to how irritable and impatient you can be after a poor night’s sleep!
What messages are you giving your mind and body?
Do you go to bed whenever you feel like it or do you tend to go to bed at the same time? Having a bedtime routine is not just for kids! Going to bed at the same time every night and waking up at the same time every morning (including at the weekends), will not only improve the quality of your sleep but it will also result in you falling asleep faster.
What you do before you go to sleep will also affect how well you sleep at night. As hard as it is in today’s society to get off your phone or other devices, it is advised to have no screen time up to two hours before bedtime. The blue light emitted from screens is particularly bad as it suppresses the body’s production of melatonin – the hormone responsible for inducing sleep. So being on your phone just before switching the light off will make it harder to fall asleep and affect the quality of your sleep.
It’s not only the hours leading up to bedtime we need to take into consideration. For many, caffeine can be our best friend during the day but our worst enemy at night. Did you know that caffeine has a half-life of roughly 5-hours in our body? Meaning that if you have a coffee at 2pm containing 150mg of caffeine, at midnight roughly 37mg of caffeine will still be active in your system. Now that afternoon coffee or tea is not going to help you sleep!
It is important that your body and mind know and understand that your bedroom is the place where you sleep. Make sure your bedroom has a calming effect and is a place where you rest and relax. Remember that any light will fool the body’s natural circadian rhythm to think it's time to be awake. The air temperature in the room will affect your sleep too.
Overthinker
Once awake, do you find yourself thinking about all your to-dos? Join the club! One way I combat this is to have pen and paper by the side of my bed to jot them down. If I continue to lie there thinking about what I need to do, I will get out of my bed and go into another room. If necessary, I will then read a book to help tire the mind and return to bed when I know there is more chance of falling asleep again.
Nightmares or night terrors
Been woken by a nightmare or a night terror is a horrible experience. They are usually linked with stress, trauma or an existing mental health condition. In order, to fall asleep again, remind yourself it was only a dream and then reconnect with the here-and-now by noticing what you see around you. To reduce or avoid further nightmares, try the 'Dream Completion Technique' which provides your brain with "dream material" which will counteract what the nightmare or night terror left you feeling when it woke you up. Keep an eye out for more information about this technique on Hannah Carter Therapy’s Facebook page.
May this knowledge around sleep hygiene and setting a routine help you get a better night’s sleep.
If introducing a new healthier sleep routine does not help, talk to your doctor or a sleep specialist to determine the underlying cause of your sleep deprivation.
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2,915,866,081,978,888,000 | It’s that time of year again – the days are getting shorter and it’s getting gloomier and colder outside. Unfortunately for about 10 million Americans, Seasonal Affective Disorder (SAD) is a very real form of depression that occurs when the seasons change to the fall and winter months. The decrease in daylight affects the circadian rhythms of your body, which creates hormonal changes, thus giving you symptoms of depression.
Although 75% of people affected by SAD are women between the ages of 20-40, it also affects seniors. Treating SAD is especially important in older individuals, considering the rate of suicide is higher among senior citizens than younger people. Here are some tips to combat some of the symptoms of seasonal depression:
1. Although medication is available for depression symptoms, a more natural way to combat the blues is phototherapy – or light therapy. Scientifically researched, sitting in front of a lightbox between 30-45 minutes a day can help reduce the amount of melatonin being produced by your body. This will help regulate a chemical and hormonal balance, which will help decrease the symptoms of depression.
2. Eat a well-balanced diet. By eating nutritional meals, you are providing your body with the right vitamins and nutrients to maintain good energy levels, which help combat low energy which can lead to depressive symptoms.
3. As weather permits, spend time outside. Although it may be cold, spending time outdoors can increase your energy levels. Plus, exposure to any form of sunlight – whether it be direct or indirect – can help elevate your mood and decrease your melatonin.
4. Talk to someone. Numerous people in American experience some form of SAD. Talk to a professional and get help if you feel you need it. It’s important to be open and honest with yourself and your body.
If you have any questions, feel free to contact us or get a FREE Assessment! | {
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-4,805,077,130,477,433,000 | What can I do to encourage pregnancy?
Thanks for your question. From what you are saying it sounds like it is reasonable to keep trying for a few more months yet before going for further investigations. Although it is awful to have gone through a miscarriage so late in the first trimester, it has at least proven to you that you can get pregnant.
The causes of miscarriage are usually very different to those which lead to difficulties in getting pregnant, so you should find some reassurance in this.
General advice on improving your chances includes the following:
- Attention to a healthy diet
- Both of you avoiding excessive alcohol - binge sessions in particular can knock off sperms ability to reach the egg.
- Stop smoking. Smoking is associated with reduced fertility for men and women as well as being implicated in miscarriage and other pregnancy problems, such as early delivery, growth restriction and bleeding.
- Your partner should avoid tight-fitting underwear and trousers. Overheating of the testes is also toxic to sperm.
- Take folic acid 400 micrograms per day unless a higher dose has been suggested by your doctor. This will reduce the risk of abnormalities in the fetus such as spina bifida.
- Use a temperature test or ovulation prediction kits to see if you are ovulating. These are not so useful for timing intercourse but will reassure you that you are releasing an egg.
If nothing has happened by 12-18 months, or you are anxious that you aren't ovulating, then seeing your doctor for some investigations and perhaps referral to a specialist is advisable. Good luck! | {
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-3,352,043,252,334,694,000 | Skip to content
Advertisement
Open Access
Development of Plasmodium falciparum specific naïve, atypical, memory and plasma B cells during infancy and in adults in an endemic area
• Allan Lugaajju1, 2,
• Sreenivasulu B. Reddy2,
• Mats Wahlgren2,
• Fred Kironde1, 3 and
• Kristina E. M. Persson2, 4Email author
Malaria Journal201716:37
https://doi.org/10.1186/s12936-017-1697-z
Received: 4 November 2016
Accepted: 13 January 2017
Published: 21 January 2017
Abstract
Background
B-cells are essential in immunity against malaria, but which sub-sets of B-cells specifically recognize Plasmodium falciparum and when they appear is still largely unknown.
Results
Using the flow cytometry technique for detection of P. falciparum specific (Pf+) B-cells, this study for the first time measured the development of Pf+ B cell (CD19+) phenotypes in Ugandan babies from birth up to nine months, and in their mothers. The babies showed increases in Pf+ IgG memory B-cells (MBCs), atypical MBCs, and plasma cells/blasts over time, but the proportion of these cells were still lower than in the mothers who displayed stable levels (5, 18, and 3%, respectively). Pf+ non-IgG+ MBCs and naïve B-cells binding to P. falciparum antigens were higher in the babies compared to the mothers (12 and 50%). In ELISA there was an increase in IgG and IgM antibodies over time in babies, and stable levels in mothers. At baby delivery, multigravidae mothers had a higher proportion of Pf+ IgG MBCs and less Pf+ naïve B-cells than primigravidae mothers.
Conclusions
In newborns, naïve B-cells are a major player in recognizing P. falciparum. In adults, the high proportion of Pf+ atypical MBCs suggests a major role for these cells. Both in infants and adults, non-IgG+ MBCs were higher than IgG MBCs, indicating that these cells deserve more focus in future.
Keywords
Plasmodium falciparum B-cellsMemoryAtypicalImmunityMalaria
Background
Plasmodium falciparum malaria accounts for over half million deaths annually, with children being the most affected [1]. Children are the most vulnerable because malaria immunity is dependent on age and exposure [2, 3]. The blood stage of P. falciparum is responsible for most of the malaria-associated pathology. Disease symptoms range from fever to more severe complications, including respiratory distress, metabolic acidosis, renal failure, pulmonary edema and cerebral malaria. The clinical spectrum of symptomatic disease is caused by the asexual blood stages of Plasmodium, where the parasite undergoes cyclic replication within human erythrocytes [4]. Although the pathogenesis of malaria is not completely understood, it is believed to arise from the concerted effects of host and parasite factors, including the sequestration of infected erythrocytes in microvasculature, local and systemic inflammation [5]. Naturally acquired immunity is known to require antibody responses. The protective role of antibodies in combating malaria was first established by passive transfer of immunoglobulin G (IgG) from clinically immune adults into children with severe malaria, which rapidly attenuated the severity and burden of disease [6]. This has been supported by immuno-epidemiological studies, where antibodies to parasite antigens have been found to be associated with protection from clinical episodes in endemic areas [714]. Antibodies may limit the growth of blood-stage parasites and the development of clinical symptoms by several known mechanisms. These include blocking erythrocyte invasion [1517], opsonising parasitized erythrocytes for phagocytic clearance [18, 19], monocyte-mediated antibody-dependent cellular killing [20, 21], and complement-mediated lysis [22], and in addition meddling with the adherence of infected erythrocytes to vascular endothelium [4]. Inadequate production of antibodies to Plasmodium antigens and their subsequent loss in the absence of persistent exposure has been proposed to impair B-cell immunological memory advancement [4]. Memory B-cells (MBCs) play an important role in durable resistance to different pathogens by boosting the immune response in times of secondary exposure. Studies have shown that antibody production can be sustained through re-stimulation of MBCs by persistent antigens [23] or by non-proliferating long lived plasma cells [24, 25]. Protection of the adult and the newborn is ensured by antibodies mostly of IgG and IgA isotypes. MBCs induced by natural infection or vaccination correspond to switched MBCs. In the peripheral blood, another population of MBCs, called IgM memory [2628] has been described with different origin, function and significance. IgM MBCs, also known as natural memory or natural effector memory cells [29], develop in the absence of germinal centres [30], generate extra-follicular thymus-independent responses and produce natural antibodies [31]. Because of the host immature immune system and the antigenic variation of the malaria parasite, development of effective B-cells and antibody responses occurs after repeated years of exposure [3236]. It has also been speculated that Plasmodium infection meddles with development and maintenance of B-cell memory response [3741]. There is still need to fully understand the development, regulation and maintenance of immunity against malaria [36, 42, 43]. B-cell phenotypes created amid malaria bouts demonstrate the B-cells linked with malaria immunity development. Diverse research has portrayed numerous B-cell phenotypes in individuals exposed to different malaria episodes [35, 37, 38, 4449]. Nahrendorf et al. [50] showed gradual acquisition of MBCs and antibodies recognizing pre-erythrocytic and cross-stage antigens after P. falciparum sporozoite immunization. However, the magnitude of these humoral responses did not correlate with protection but directly reflected parasite exposure in chemoprophylaxis and sporozoite immunization. In African youngsters after experiencing intense malaria, an expansion in both the total memory and transitional B-cell populaces was observed [51]. It is important to note that this earlier research studied the whole B-cell populace and did not estimate Plasmodium falciparum (Pf+) specific B cells. Elispot assay has been used to try and find parasite specific cells, for example to show that even if antigen-specific antibodies were not detected in plasma, antigen-specific B-cells could still be found circulating in the blood, suggesting that these could be maintained independently of long-lived plasma cells [52]. However, Elispot needs activation and survival of cells for a relatively long time, and compared to ELISA-based assays, flow cytometry is a good method for estimation of antigen-specific cells. While dealing with intricate antigens, flow cytometry has been shown to be a better assay option [53]. Malaria calls for flow cytometry analysis since it has a scope of parasite antigens that individually have a low number of specific B-cells. ELISA-based measures when improved can only quantify 70% of the response determined by flow cytometry [53]. Flow cytometry is advantageous in that there is no need of cell incitement thereby expanding the odds of incorporating all cells in the reading. In order to acknowledge how Pf+ B-cells are actuated and kept up in vivo, these cells should be isolated from other B-cells. Here, the flow cytometry technique for detection of Pf+ B-cells which was developed by Lugaajju et al. [54] was applied to monitor the development of Pf+ B-cell sub-populations in newborns from time of birth until 9 months and in their respective mothers, in a malaria endemic area.
Methods
Study site and subject enrolment
The study was conducted at Kasangati Health Centre (KHC), a referral unit of Wakiso district which is located 20 km north east of Kampala, the capital city of Uganda. The antenatal clinic of KHC is a public charge-free facility that runs 5 days a week. On average, 60 patients (20 new visits, 40 revisits) are seen per day and about 7 deliveries occur daily. In this study area, malaria is meso-endemic with peak transmission after the two rainy seasons (February–March and September–October) every year. The study region is peri-urban and over 90% of pregnant women attend the antenatal clinic at least once. Between March of 2012 to July of 2013, patients were recruited in their last trimester from peri-urban villages within 20 km from KHC. Eligibility criteria were: Normal deliveries with healthy newborns, agreement to come to the study clinic for follow up at 10 weeks, 6 and 9 months of the child’s age. The selection of the study participants was random (patients were selected sequentially as they came to the clinic unless they failed the inclusion criteria). As policy at KHC, every pregnant woman took at least one or two does of IPT during the pregnancy of the delivered baby. Also, every pregnant woman was given a long-lasting insecticide mosquito bed net. During recruitment and follow up visits, a detailed clinical examination was performed and the data were entered into the study questionnaire. Malaria rapid diagnostic test (RDT) and blood smear examination upon a positive RDT were performed.
Sample collection and processing
On the day of baby delivery, 5 to 10 mL of mother’s venous blood and the respective umbilical cord blood of the newborn baby were collected and mixed with lithium heparin (BD, Plymouth, UK). At follow-up days, 2 to 4 mL blood from babies and 5 to 10 mL from respective mothers (at 9 months) were collected. Within 4 h after being collected, the blood samples were transported to the Makerere University, Biomedical Cross Cutting Laboratory for processing. Peripheral blood mononuclear cells (PBMCs) were separated by density gradient centrifugation using Ficoll-hypaque (GE HealthCare Bio-Sciences AB, Sweden). For this, the blood specimen was diluted with equal volume of Dulbecco’s phosphate buffered saline (DPBS, Life technologies, Stockholm, Sweden), carefully layered over the Ficoll, and centrifuged (400 g) for 30 min at room temperature. After centrifugation, plasma was removed and stored at −80 °C. The PBMCs were then collected, washed twice with DPBS (300 to 400 g for 15 min × 2) to remove Ficoll traces and platelets. The cells were then suspended in 1 mL RPMI medium (Sigma, St Louis, MO) stained with 0.4% trypan blue (w/v) and counted in a Neuberger chamber. The PBMCs were then cryopreserved in liquid nitrogen at concentration of 107 cells/mL in heat-inactivated 90% fetal bovine serum (Sigma, St Louis, MO) and 10% DMSO (v/v) (Sigma, St Louis, MO) as previously described [55].
Malaria diagnostics
All samples were tested by pLDH/HRP2 rapid diagnostic test (RDT) strips (Combo Rapid Diagnostic Test of Premier Medical Corporation Limited, India) as described by Bharti et al. [56]. Thick blood smears were stained with 10% Giemsa dye for 10 min, Plasmodium spp blood stage parasites were then counted in microscope fields containing at least 200 white blood cells (WBCs). The parasitaemia was calculated according to the WHO guidelines [57].
Measurement of total anti-P. falciparum IgG and IgM by ELISA
Pf+ total IgG and IgM in blood plasma were measured by enzyme linked immune-sorbent assay (ELISA) as described [58]. Briefly, microtiter plate wells were coated with 1 µg of schizont extract per well (overnight at 4 °C), and blocked with 5% skimmed milk (Sigma) for IgG and super block dry blend (Thermo Scientific) for IgM for 2 h at room temperature. Plasma specimens were diluted 1:200 with plasma dilution buffer (2.5% milk powder in phosphate buffered saline with tween 20 plus 0.02% sodium azide). Diluted plasma samples were added to the wells in quadruplets and incubated in the microtiter plates at room temperature for 1 h. The microtiter wells were washed 4 times between the incubation (coating, blocking, first and secondary antibody) steps. The wells were then incubated (45 min) with diluted (1:20,000) peroxidase-conjugated goat anti-human IgG/IgM (Sigma) and rewashed. Bound secondary antibody was quantified by adding TMB (3, 3′, 5, 5′-Tetramethylbenzidine) substrate (Promega). Optical density (OD) was read at 450 nm with a reference at 620 nm. Plasma samples of Swedish individuals unexposed to P. falciparum infections were used as negative controls. All specimens were analysed twice and the means of the ELISA OD used in the analysis.
Plasmodium falciparum ghost infected red blood cells (GiRBCs)—carboxyl Qdot conjugation
Red blood cells were infected with the FCR3S1.2 P. falciparum strain and maintained in vitro as described by Beeson et al. [59]. The cultures were synchronized using 5% D-sorbitol (Sigma) in water. The magneticallly enriched trophozoite pellet was treated with streptolysin O (Sigma) to obtain GiRBCs as described in Methods in Malaria Research [60]. The GiRBC (225 µg) was conjugated with 2 nmol carboxyl Qdot (35 µL) using freshly prepared 10 mg/mL N-ethyl-N-dimethylaminopropyl-carbodiimide as described by Lugaajju et al. [54]. The carboxyl Qdot-GiRBC conjugate was diluted 10 times with 10 mM Borate buffer (pH 7.4) and stored at 4 °C.
Immunophenotyping of P. falciparum specific B-cells
Immuno-phenotyping of P. falciparum was done according to the protocol previously described by Lugaajju et al. [54]. Cryopreserved PBMCs (approximately 1 × 106 cells) were thawed on ice and washed in cold flow buffer (PBS/0.5% BSA/2 mM EDTA). Flow buffer (100 μL) was added to each PBMC sample followed by 1 µg Fc block (CD16/CD32 mAb, Biolegend) and incubated at 0 to 4 °C (on ice water) for 5 min to minimize non-specific binding and background fluorescence. Carboxyl Qdot-GiRBC Conjugate (25 µL) was added, incubated on ice for 30 min and the cells were re-washed. Eight microliters of fluorochrome (FITC)-conjugated mouse anti-human IgG monoclonal antibody (mAb, BD Horizon) were added and incubated for 30 min to stain 106 cells in 100 µL of flow buffer. The cells were then washed and stained for 30 min with 3.5 µL each of CD 19 PE CF594, CD20 V450, and FcRL4 APC fluorochrome-conjugated mouse anti-human mAb (BD Horizon). After the staining, the cells were washed and re-suspended in 300 µL flow buffer. The analysis was done on a LSRII flow cytometer (Becton–Dickinson Immuno Cytometry Systems, San Jose, USA). Data was processed using FLOWJO software (Tree Star Inc., San Carlos, and Ca, USA).
Statistical analysis
Data analysis was carried out using STATA and Graph pad prism. Changes in IgG, IgM levels and Pf+ B-cell phenotypes for babies and mothers over time were assessed with Wilcoxon rank sum test. The differences in medians between two time points were evaluated by Mann–Whitney test and non-parametric Kruskal–Wallis test was used for comparing more than three time point.
Results
General characteristics of the study population
Healthy newborns (n = 131) and their respective mothers were enrolled into the study. However, during the nine months of post-natal follow-up, only 109 mother–baby pairs fulfilled all the follow-up time points (birth, 10 weeks, 6 and 9 months) and were included in the subsequent analysis. The mean age of the enrolled mothers was 25 years and ranged from 18 to 39 years. Of the 109 mothers, 27% were primigravidae and 73% mutigravidae. The parasitaemia as determined from the samples that were RDT positive at the different follow-up time points is shown in Table 1.
Table 1
Showing parasitaemia (number of infected RBC/µL of blood) for mothers and babies at different time points
Time course
Pat ID
Parasitaemia
Mother at birth
KM 12
48
KM 32
16
KM 35
240
KM 41
64
KM 58
32
KM 60
2760
Baby at birth
KB 101
13,000
Baby at 2.5 months
KB 120 A
9560
Baby at 6 months
KB 56 B
91,760
KB 118 B
22,6240
KB 125B
3840
Baby at 9 months
KB 57 C
5080
Mother at 9 months
KM 91 C
1520
KM 96 C
800
Development of IgG and IgM antibody responses to P. falciparum
To determine the development of plasma IgG and IgM antibodies against P. falciparum, schizont extract was used in ELISA. The Swedish samples were used as negative controls and their average antibody OD values for IgG (OD = 0.046) and IgM (OD = 0.09), were subtracted from the corresponding raw data of Ugandan specimens. There was no difference between levels of IgG for mothers at delivery and 9 months later. Babies at birth had slightly lower levels of Pf+ IgG compared to their mothers. These IgG levels in babies decreased even further at 2.5 months, and then increased by 6 and 9 months, but were still lower than the corresponding levels in their mothers (Fig. 1a). Similarly, there was no difference in levels of Pf+ IgM for mothers at delivery compared to 9 months later. At birth, babies had very low levels of anti-Pf IgM but these levels increased throughout the time points up to 9 months even though they did not reach the levels present in their mothers (Fig. 1b). In the mothers, there was no correlation between age and antibody titer levels.
Figure 1
Fig. 1
Development of IgG and IgM antibody responses to Plasmodium falciparum. The development of IgG and IgM antibodies in plasma against P. falciparum schizont extract was analyzed by ELISA using plasma specimens of mother–baby pairs (n = 109). The graphs show levels of IgG (graph a) and IgM (graph b) in plasma of blood collected from babies at birth, 2.5, 6 and 9 months later (see coordinate axis labels B0, B2.5, B6 and B9) and from mothers at delivery and 9 months later (M0 and M9). There was no difference in the levels of IgG and IgM for mothers at birth and 9 months later. At birth, babies had lower levels of IgG (a) and IgM (b) as compared to their mothers. Levels of IgG and IgM in babies increased over time although they did not reach the levels prevailing in the mothers’ blood at 9 months after baby delivery. The horizontal lines in the box plots with whiskers from minimum to maximum show median levels. Asterisk, double and triple asterisks indicate significant differences (p < 0.05, 0.01 and 0.001, respectively) between groups as evaluated by Wilcoxon rank sum test
Development of P. falciparum specific B-cell sub-populations
In order to assess the development of different fractions of Pf+ B-cells, five B-cell sub-sets were characterized from whole peripheral blood collected at the time of delivery (M0 = mother, B0 = baby at birth), baby at 2.5 months (B2.5), baby at 6 months (B6), baby and mother at 9 months (B9, M9 respectively). The flow cytometry technique for detection of B lymphocytes (defined as CD19+ cells) that are Pf+ was used to measure the relative proportions of IgG MBCs (CD19+CD20+CD27+FcRL4±IgG+), non-IgG+ MBCs (CD19+CD20+CD27+FcRL4±IgG−), naïve B-cells (CD19+CD20+CD27−FcRL4±IgG−), plasma cells/blasts (CD19+CD20−CD27+FcRL4±IgG−), and atypical MBCs (CD19+CD20+CD27−FcRL4±IgG+) as shown in Fig. 2. In the mothers, the mean proportions of Pf+ IgG MBCs, non-IgG+ MBCs, naïve B-cells, plasma cells/blasts and atypical MBCs were 5, 12, 50, 3 and 18% respectively. For mothers, there was no significant difference between the proportions of any of the Pf+ B-cell sub-populations at delivery compared to 9 months later. For the babies, there was an increase over time in proportions of Pf+ IgG MBCs, non-IgG+ MBCs, plasma cells/blasts and atypical MBCs. Although the proportions of these cells increased, the percentages did not reach adult levels for any of them, except for the non-IgG+ MBCs where levels were actually higher in the babies compared to the mothers. At birth, the B-cells recognizing P. falciparum in the babies were dominated by the naïve B-cells. Even though the proportions of Pf+ naïve B-cells decreased over time in babies, at 9 months of age the ratios of these Pf+ naïve B-cells were still higher in the infants compared to the mothers.
Figure 2
Fig. 2
Development of Plasmodium falciparum specific B-cell sub-populations. Proportions of Pf+ CD19+B-cell sub-sets in mothers and babies: IgG MBCs (a), non-IgG+ MBCs (b), naïve B-cells (c), plasma cells/blasts (d) and atypical MBCs (e) determined using quantum dots flow cytometry. The coordinate axes show time points (as in Fig. 1) at which the tested blood specimens were collected
Levels of anti-schizont IgG and IgM in high and low P. falciparum specific B-cell responders
The flow cytometry percentage frequency data for each Pf+ CD19+ B-cell sub-population was arranged in descending order. The top 10% of the values were considered the high responders and the lowest 90% of the values were considered as the low responders. Comparisons of the high responders to low responders (lowest 90% of values) for the sub-populations of Pf+ CD19+ B-cells were made and correlated to the levels of plasma anti—P. falciparum IgG and IgM as determined by ELISAs. Those that showed significant differences between groups of individuals are shown in Figs. 3 and 4 for IgG and IgM, respectively. For babies at birth, low proportions of Pf+ B-cell sub-populations including FcRL4+non-IgG+MBCs (CD19+CD20+CD27+FcRL4+IgG−) and FcRL4+ naïve B-cells (CD19+CD20+CD27−FcRL4+IgG−) were associated with high levels of schizont specific plasma IgG, well as high levels of FcRL4−non-IgG+MBCs (CD19+CD20+CD27+FcRL4−IgG−) were associated with high levels of schizont specific plasma IgG (Fig. 3a). High levels of FcRL4+IgG MBCs (CD19+CD20+CD27+FcRL4+IgG+), FcRL4+ plasma cells/blasts (CD19+CD20−CD27+FcRL4+IgG−) and FcRL4− plasma cells/blasts (CD19+CD20−CD27+FcRL4−IgG−) were all associated with high levels of Pf+ plasma IgG for babies at 6 and 9 months respectively (Fig. 3b).
Figure 3
Fig. 3
Levels of antibodies in IgG ELISA. Measured against schizont extract for individuals that were high responders (HR: top 10% of values) compared to low responders (LR: lowest 90% of values). a Babies at birth, b Babies at 6 and 9 months, c mothers at birth and 9 months later. Markings as in Fig. 1
Figure 4
Fig. 4
Levels of antibodies in IgM ELISA. Measured against schizont extract for individuals that were high responders (HR: top 10% of values) compared to low responders (LR: lowest 90% of values). Markings as in Fig. 1
For the mothers, low proportions of Pf+ B-cell sub-populations including FcRL4+ non-IgG+MBCs (CD19+CD20+CD27+FcRL4+IgG−) (at birth and 9 months), and FcRL4+IgG MBC (CD19+CD20+CD27+FcRL4+IgG+) at 9 months were associated with high levels of Pf+ plasma IgG (Fig. 3c). In addition, high proportions of FCRL4− Pf+ atypical MBCs (CD19+CD20+CD27−FcRL4−IgG+), and FCRL4− Pf+ IgGMBCs (CD19+CD20+CD27+FcRL4−IgG+) were associated with high levels of schizont binding plasma IgM for babies at birth and mothers at 9 months, respectively. However, low levels of FCRL4− Pf+ atypical MBCs were associated with high levels of IgM antibodies in mothers at 9 months (Fig. 4). Samples from malaria non-endemic areas (Swedish donors) showed less than 1% of each population of cells in flow cytometry, and also had very few numbers of cells in each subpopulation and hence no calculations could be made for valuable conclusions.
Comparison of mother–baby parasitaemia with antibody and B-cell subpopulations
The respective parasitaemia for both mothers and babies at different follow up points were correlated with IgG, IgM Elisa ODs and the percentage frequency for each Pf+ specific CD19+ B-cell subpopulations. The results showed that increase in parasitaemia was associated with low IgG antibody OD values (p = 0.009). There was no significant correlation either between parasitaemia and IgM levels or between parasitaemia and the proportions different Pf+ specific CD19+ B-cell subpopulations. This could largely be due to the small numbers of Pf+ samples (10.7%).
Comparison of primigravidae and mutigravidae
The study population comprised of primigravidae (27%) and mutigravidae (73%) mothers. Prominent differences were noted in proportions of Pf+ IgG MBCs and naïve B-cells at birth among primigravidae and mutigravidae as shown in Fig. 5. Pf+ IgG MBCs were higher in multigravidae than in primigravidae mothers (p < 0.05), whereas Pf+ naïve B-cells were higher in primigravidae compared to in multigravidae (p < 0.05).
Figure 5
Fig. 5
Comparison of primigravidae and mutigravidae. Comparison of proportions of Pf+ CD19+ IgG MBC and Pf+ naïve B-cells between primigravidae and multigravidae at birth. The horizontal lines show median levels in the box plots, with whiskers from minimum to maximum. Asterisks indicates significant differences (p < 0.05)
Discussion
In this study, a cohort of mothers and their newborn babies were recruited and followed up for 9 months after baby delivery. The development of plasma antibodies in the babies against schizont extract antigens showed a pattern that was what could be expected from individuals living in an endemic area. Schizont extract was used since it contains antigens from merozoites as well as other Plasmodium blood stages. The mothers showed stable levels of schizont specific IgG and IgM antibodies. The newborn babies had parasite specific IgG probably transferred through the placenta, followed by a decrease and then an increase of the IgG over time as the babies were exposed to malaria. This was also accompanied by an increase in IgM levels during the follow-up time for the babies. Similar results have been found before [61] and indicate that the people living in the study area are regularly exposed to malaria but also that full immunity is not achieved by 9 months of age. The initial antibody response to intrauterine infections in the newborns as determined in cord sera is generally of the IgM class [62]. In the present study, some infants had high levels of parasite specific IgM in the cord blood which suggests that they had been exposed to malaria parasites in utero, as was further indicated by one individual who actually had parasites in the cord blood. This baby also had a relatively high OD-value in IgM ELISA (0.3) compared to others at the same time point. The fairly rapid rise in the level of IgM as observed in the first 9 months of life reflects the primary immune response of the infants towards the malaria parasites, among other commonly known infections.
In addition, the study investigated the proportions of CD19+ Pf+ B-cells. In the mothers, the levels of these cells were stable, and showed IgG MBCs, non-IgG+ MBCs, naïve B-cells, plasma cells/blasts and atypical MBCs to be 5, 12, 50, 3 and 18%, respectively. In the literature, it has been assumed that IgG MBCs are the cells that are of importance for long-term memory in the defence against most diseases, but in this present study surprisingly high levels of non-IgG+ MBCs positive for Pf, both in the babies and in the mothers were found. These cells were negative for IgG, but most likely they could have been positive for IgM since memory cells recognizing IgD or IgE at these high levels would be unlikely because the total levels of these antibodies are normally very low. Moreover, IgA levels in blood directed against Pf have previously been shown to be very low [63] and sometimes even difficult to detect both in maternal and cord blood [64]. Acquisition of specific antibody isotypes to Pf antigens has in another study been shown to begin with IgM, followed by IgG1 and IgA [65] and the levels of the latter was shown to be detectable only in low levels and to increase not until after 9 months of age. IgA directed against Pf has been found in breast milk [66] but the levels are usually very low in blood [63]. IgM levels, on the other hand, have often been shown to be relatively high [67]. It is interesting to note that a relatively large proportion of the MBC pool is made up of non-IgG MBC. This is important information when trying to understand malaria immunity, and which parameters to focus on in vaccine studies.
It was also noted in this study that naïve B-cells binding to Pf were found to be at peak in the cord blood, which is in line with earlier studies showing naïve cells to be the major part of CD19+ response in newborns [68]. But even in our adult samples, about half of the cells showed binding to Pf which could indicate that in a normal immune response, these cells are relatively important. This signifies that besides IgG+ MBCs, other memory B cells (Pf+ non-IgG+ MBCs) are important in the defense against malaria.
In the present study, even though the proportions of the B-cell sub-sets increased in babies during the 9 months after birth, they were still lower than in their mothers, indicating that immunity is not yet achieved. In the mothers, there was no notable difference in the proportions of Pf+ IgG MBCs, non-IgG+ MBCs, atypical MBCs, plasma cells/blasts, and naïve B-cells at time of delivery and 9 months later, suggesting that the proportions of these circulating Pf+ B-cell sub-sets remains stable during adulthood. This finding is consistent with earlier studies of the whole B-cell pool [69], where the number of circulating B-cells remains stable during adulthood and it only decreases in individuals older than 60 years. Although based on murine models, it has been suggested that this is due to a reduced bone marrow ability to produce B-cells [70, 71]. In peripheral blood of healthy adult donors, human B-cells comprise very low numbers of plasma cells (1–3%) [69, 72] which is in line with the proportions of Pf+ cells found in the present study.
Among the B-cell sub-sets considered in this study, the atypical MBCs constituted a relatively large proportion. Individuals living in malaria-endemic areas were found with increased levels of atypical MBCs as age increased with cumulative Plasmodium exposure [35, 37, 38]. In this study, atypical MBCs were classified as CD19+CD20+CD27−IgG+, and in earlier studies, they have been characterized as CD10-CD19+CD20+CD21−CD27− [45, 73], suggesting that it is the same kind of cells. The proportions of atypical MBC has been shown to correlate with age and malaria transmission intensity [44, 74] and in the present study, the cells increase with age in the babies, but do not reach full adult levels during the 9 months of follow-up. Whether these atypical cells are good or bad for the immune defense is not completely clear, but considering the large proportion of Pf+ CD19+ cells that they constitute, they must be a major player in the development of immunity against malaria and they have previously been shown to express an array of inhibitory receptors as well as an impaired B-cell response [45].
In this study, cells and antibodies circulating in peripheral blood were investigated. Ideally, one would like to investigate bone marrow, spleen and lymph nodes as well to get a full picture of how immunity is formed, especially during the first year of life. However, for practical and ethical reasons this was not possible. Nevertheless, studies of peripheral blood cells and antibodies conceivably reflect what happens in the rest of the body and provides valuable insight.
Despite the fact that many individuals showed very low levels of some subpopulations of Pf+ cells, those that actually had higher levels of some specific cells compared to other individuals were interesting to investigate further. The study therefore compared the results for the high responders (top 10% of values) to the low responders (lowest 90% of values) for the subpopulations of Pf+ CD19+ B-cells, and also sub-divided the cells further into FCRL4+ and FCRL4− cells and correlated this to the levels of plasma IgG and IgM determined by ELISA. FcRL4 (CD307d) is exclusively present on B-cells and previous studies have proposed that FcRL4+ B-cells represent a specialized tissue sub-population of MBCs [7578], hence they are capable of eliciting a secondary immune response. In order not to miss out on these special kind of memory B-cells, FcRL4 marker was included in the B-cell phenotyping panel to differentiate the MBCs. High levels of antibodies, especially IgG and IgM, have been shown in several previous studies to be associated with malaria immunity [11, 79]. In this study, the general pattern (Figs. 3 and 4) indicated that low proportions of FCRL4+ cells and high proportions of FCRL4− cells were associated with high levels of IgG or IgM antibodies. This could point towards a situation where it is better to not have too high a response of FCRL4+ cells. The FCRL4 marker has also been indicated to be of importance in HIV, which can induce an increase of FCRL4+ cells [80]. Interestingly, both HIV and malaria are infections that can persist for a long time in the human body (Additional file 1).
The study also compared primigravidae and mutigravidae individuals. It was noted that multigravidae had a higher proportion of Pf+ IgG MBCs and lower proportion of Pf+ naïve B-cells, as compared to primigravidae at birth. However, after 9 months there was no notable difference in the proportions of these cell populations. It has been shown before that primigravidae are more vulnerable to malaria [81], and from the present study results it could be assumed that it is more advantageous to have Pf+ IgG MBCs compared to Pf+ naïve B-cells, something that is also in line with the general assumption of how protective memory against a disease is formed. It would have been interesting to investigate presence of malaria parasites in placental tissue of all the mothers and examine if any correlations occur in factors such as pregnancy parity and parasite density. However due to limited resources and the scope of the study, these investigations could not be carried out.
Conclusions
During the first 9 months of life in a malaria endemic area, babies not only develop Pf+ IgG MBCs and plasma cells/blasts but they also attain expansion of Pf+ atypical MBCs and non-IgG+ MBCs. The latter two sub-populations of cells occur at relatively high proportions in the adult mothers, indicating that traditional MBCs are not the only important memory B cells in the process of developing immunity against malaria.
Declarations
Authors’ contributions
Conception and study design AL, SR, MW, FK and KP, data collection AL, FK and KP, laboratory analysis AL, SR, MW, FK and KP, drafting and revision of manuscript AL, SR, MW, FK and KP. All authors read and approved the final manuscript.
Acknowledgements
We are indebted to all the study participants. We appreciate every individual of the research team for their vigorous exertion and great work.
Competing interests
The authors declare that they have no competing interests.
Availability of data and materials
The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.
Ethical approval and consent to participate
A written informed consent was obtained from all the mothers prior to the study enrollment. The study was approved by the Research and Ethics Committee (SOMREC) of Makerere University School of Medicine, the Uganda National Council of Science and Technology (approval 2011–114) and by Regionala Etikprövningsnämnden in Stockholm, Sweden 2014/478-32.
Funding
This work was supported by Sida and Vetenskapsrådet.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Authors’ Affiliations
(1)
School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda
(2)
Department of Microbiology, Tumor, and Cell Biology, Karolinska Institutet, Stockholm, Sweden
(3)
Habib Medical School, Islamic University in Uganda (IUIU), Kampala, Uganda
(4)
Department of Laboratory Medicine, Lund University, Lund, Sweden
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1,921,486,622,291,271,000 | top of page
Benefits of Walking and Sunshine
Walking for Your Health
The more you move, the better it is for your physical health, maintaining a healthy weight and your mental health will thank you, too. Anytime you have the opportunity to walk and get in extra steps, do it. When you park the car, park a little further away than normal. Every hour on your lunch break, get up and walk around. Go for a quick walk after dinner with the family. Every little bit adds up and getting movement not only is healthy for your heart, joint pain and improving balance, getting in your extra steps while the sun is shining reaps even more benefits.
Walking in the Sunshine
The sun can give you positive feelings anytime, and when you add a brisk walk to the equation, you get more where that came from. From improving your mood to producing more Vitamin D, it can also prevent obesity, help clear your skin conditions and shine a ray of light on your mental health. The benefits don’t stop there - walking can lower your blood pressure, help you get more zzz’s and improve your cognitive function, too. So next time you decide to go out for a walk, be sure to catch some rays while doing it whether first thing in the morning or after a busy day with the family. Why? Sunlight helps boost a chemical in your brain called serotonin which can give you more energy and help keep you calm, positive and focused on whatever lies ahead.
Walking, Cardiovascular Health and More
As for your cardiovascular health, or the health of your heart and blood vessels, increased cardiovascular and pulmonary (heart and lung) fitness can reduce risk of heart disease and stroke and walking falls perfectly under that category. If you are at risk for hypertension (high blood pressure), diabetes or muscle/joint pain or stiffness, walking regularly can improve all of that. As we grow older, our bodies also have a natural mechanism for removing old bone and rebuilding new bone, however, around the age of 50, we start losing bone faster than we can build it. In fact, due to this accelerated process of bone loss, women can lose up to 20 percent of their bone density within five to seven years following menopause. Luckily, adding a daily stroll to your workout routine can help maintain bone strength plus improve your balance. All in all, no matter your age, walking is the one of the best ways to help you live a longer, healthier life.
Walking can offer numerous health benefits to people of all ages and fitness levels. It’s free and easy to fit into even the busiest of schedules. All you need is a sturdy pair of walking shoes. So what are you waiting for? Grab a friend and try out these simple ways to sneak a walk into your every day routine:
Play with the Kids - Just a quick game of basketball or hide-and-seek with the kids can add in a significant amount of steps.
Get a Furry Friend - Dogs need to walk a lot - the perfect opportunity for you to take them out before and after work and a mindless way for you to get in your exercise, too.
Invite a Friend - Talking and walking with a friend helps make the time go by - before you know it you’ve walked a 5K!
Explore the Outdoors - Head to a local lake, discover a new trail or head to the park and you may be surprised on how many steps you get in.
Binge Watch While You Walk - Watching your favorite Netflix series or listening to a good podcast helps pass the time.
Play Your Favorite Hits - Music is good for the soul!
Take the Stairs - Skip the elevator and take the stairs instead.
Take Frequent Walk Breaks at Work - Every hour, walk the sky-walk, take an extra coffee break and get outside for some fresh air if the time and place allows for it.
Do Outdoor Work - Outside chores such as gardening or mowing the lawn are great ways to get in steps and some strength all at once!
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5,913,613,238,887,316,000 | Metadata
Name Hearing loss
Type Disease or Syndrome
Group Disease or Syndrome
Data Sources
Clinical Terminologies Read Version 2
ICD-10
Codelists
Valid Event Data Range 01/01/1901-31/12/2019
Sex Female
Male
Authors Cardoso V., Nirantharakumar K., Gkoutos G
Agreement Date 3 Jun 2020
Version (UUID) 1 (KiGT2GxSNkwPD8RPF6ZPne)
Primary care
readcode Description
F59..00 Hearing loss
F59..11 Deafness
F591.00 Sensorineural hearing loss
8D23.00 Ear fitting hearing aid
F59z.00 Deafness NOS
F590000 Unspecified conductive hearing loss
1C13100 Unilateral deafness
F580100 Presbyacusis
1C13200 Partial deafness
F591000 Unspecified perceptive hearing loss
F591.13 Perceptive deafness
F581211 Noise induced deafness
F591.11 High frequency deafness
ZV53200 [V]Fitting or adjustment of hearing aid
F591211 Nerve deafness
F593.00 Deaf mutism, NEC
8D2..12 Hearing aid provision
1C13300 Bilateral deafness
P40..00 Ear anomalies with hearing impairment
2BL4.00 O/E - very deaf
1C12.00 Hearing difficulty
F582.00 Unspecified sudden hearing loss
1C13.11 Deafness symptom
F591200 Neural hearing loss
2BM2.11 O/E - conductive deafness
F592100 Mixed conductive and sensorineural hearing loss, bilateral
Z911100 Fit hearing aid
2BM3.11 O/E - perceptive deafness
ZE87.17 HOH - Hard of hearing
F591.12 Low frequency deafness
F590.00 Conductive hearing loss
ZE87.00 Hearing loss
F592.11 Mixed hearing loss
F591600 Sensorineural hearing loss, bilateral
2DG..00 Hearing aid worn
ZE87.11 Deafness
F591400 Congenital sensorineural deafness
Z9E8100 Hearing aid provision
ZE7..00 Hearing problem
ZE87.16 HL - Hearing loss
SJ15.12 Deafness - traumatic - NOS
ZE87.15 HI - Hearing impairment
2BL3.00 O/E - significantly deaf
2BL..11 O/E - deaf
2BL2.00 O/E - slightly deaf
1C13.00 Deafness
A560200 Rubella deafness
F592.00 Mixed conductive and sensorineural deafness
ZV41200 [V]Problems with hearing
F581200 Noise-induced hearing loss
F591z00 Perceptive hearing loss NOS
F59z.11 Chronic deafness
Z8B5500 Difficulty using hearing aid
1C16.00 Deteriorating hearing
ZE87.18 Hearing impairment
Z8B5311 Uses hearing aid
F591100 Sensory hearing loss
F590500 Conductive hearing loss, bilateral
ZE87.19 Hearing impaired
F594.00 High frequency deafness
Z8B5300 Does use hearing aid
ZE87.12 Difficulty hearing
7311A00 Insertn bone anchors subcutaneous bone anchored hearing aid
2BM4.00 O/E - High tone deafness
ZE87.13 Hard of hearing
2BL5.00 O/E - completely deaf
F592000 Mix cond/sensneurl hear loss,unlat unrestrc hear/contrlat sd
F591700 Sensorineurl hear loss,unilat unrestrict hear/contralat side
Z911.00 Hearing aid procedure
2BM3.00 O/E tune fork=perceptive deaf
Z911500 Checking hearing aid
P40z.11 Deafness due to congenital anomaly NEC
F590300 Conductive hearing loss due to disorder of middle ear
F590z00 Conductive hearing loss NOS
Z8B5200 Unable to use hearing aid
F590100 Conductive hearing loss due to disorder of external ear
F59y.00 Other specified forms of hearing loss
1C18.00 Difficulty hearing with background noise
2BM2.00 O/E -tune fork=conductive deaf
F590600 Conduct hear loss,unilat+unrestric hearing on contralat side
F595.00 Low frequency deafness
F590.11 Conductive deafness
F591500 Ototoxicity - deafness
1C17.00 Hearing aid problem
F590200 Conductive hearing loss due to disorder of tympanic membrane
FyuU100 [X]Other specified hearing loss
F591y00 Combined perceptive hearing loss
8D21.00 Provide head worn hearing aid
1C19.00 Difficulty hearing whispers
F590y00 Combined conductive hearing loss
F591300 Central hearing loss
FyuU000 [X]Deaf mutism, not elsewhere classified
F590400 Conductive hearing loss due to disorder of inner ear
F5A..00 Hearing impairment
ZV45N00 [V]Bone anchored hearing aid in situ
F596.00 Maternally inherited deafness
Secondary care
Diagnoses
ICD10code ICD10codeDescr
H90 Conductive and sensorineural hearing loss
H90.0 Conductive hearing loss, bilateral
H90.1 Conductive hearing loss, unilateral with unrestricted hearing on the contralateral side
H90.2 Conductive hearing loss, unspecified
H90.3 Sensorineural hearing loss, bilateral
H90.4 Sensorineural hearing loss, unilateral with unrestricted hearing on the contralateral side
H90.5 Sensorineural hearing loss, unspecified
H90.6 Mixed conductive and sensorineural hearing loss, bilateral
H90.7 Mixed conductive and sensorineural hearing loss, unilateral with unrestricted hearing on the contralateral side
H90.8 Mixed conductive and sensorineural hearing loss, unspecified
H91 Other hearing loss
H91.0 Ototoxic hearing loss
H91.1 Presbycusis
H91.2 Sudden idiopathic hearing loss
H91.3 Deaf mutism, not elsewhere classified
H91.8 Other specified hearing loss
H91.9 Hearing loss, unspecified | {
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-2,192,661,761,546,751,000 | Welcome to United Gastroenterologists,
Southern California's Premier Gastroenterology Practice
OBALON
CT Enterography
What is CT Enterography?
CT enterography is a special type of computed tomography (CT) imaging performed with contrast material to produce images of the small intestine.
CT scanning—sometimes called CAT scanning—is a noninvasive medical test that helps physicians diagnose and treat medical conditions.
CT scanning combines special x-ray equipment with sophisticated computers to produce multiple images or pictures of the inside of the body. These cross-sectional images of the area being studied can then be examined on a computer monitor, printed or transferred to a CD.
CT scans of internal organs, bones, soft tissue and blood vessels provide greater clarity and reveal more details than regular x-ray exams.
What are some common uses of the procedure?
Physicians use CT enterography to identify and locate:
• inflammation
• bleeding sources
• tumors
• abscesses and fistulas
• bowel obstructions
CT enterography is also used to diagnose, evaluate and guide the treatment of patients with Crohn's Disease, including monitoring the effectiveness of treatment.
How should I prepare?
You should wear comfortable, loose-fitting clothing to your exam. You may be given a gown to wear during the procedure.
Metal objects, including jewelry, eyeglasses, dentures and hairpins, may affect the CT images and should be left at home or removed prior to your exam. You may also be asked to remove hearing aids and removable dental work. Women will be asked to remove bras containing metal underwire. You may be asked to remove any piercings, if possible.
You should inform the technologist if you have a pacemaker. Pacemakers do not hinder the use of CT as in MRI as long as the scanner will not be taking images repeatedly over the area of the pacemaker device in the upper chest. This is usually not an issue for cardiac CT exams.
You will be asked not to eat or drink anything for four hours prior to the procedure.
You should inform your physician of any medications you are taking and if you have any allergies. If you have a known allergy to contrast material, or "dye," your doctor may prescribe medications to reduce the risk of an allergic reaction, or order a different test.
Also inform your doctor of any recent illnesses or other medical conditions, and if you have a history of heart disease, asthma, diabetes, kidney disease or thyroid problems. Any of these conditions may increase the risk of an unusual adverse effect.
Women should always inform their physician and the CT technologist if there is any possibility that they may be pregnant.
What does the equipment look like?
The CT scanner is typically a large, box-like machine with a hole, or short tunnel, in the center. You will lie on a narrow examination table that slides into and out of this tunnel. Rotating around you, the x-ray tube and electronic x-ray detectors are located opposite each other in a ring, called a gantry.
The computer workstation that processes the imaging information is located in a separate control room, where the technologist operates the scanner and monitors your examination in direct visual contact and usually with the ability to hear and talk to you with the use of a speaker and microphone.
How does the procedure work?
In many ways CT scanning works very much like other x-ray examinations. X-rays are a form of radiation—like light or radio waves—that can be directed after their passage through the part of the body being examined. Different body parts absorb the x-rays in varying degrees. It is this crucial difference in absorption that allows the body parts to be distinguished from one another on an x-ray film or CT electronic image.
In a conventional x-ray exam, a small amount of radiation is aimed at and passes through the part of the body being examined, recording an image on a special electronic image recording plate. Bones appear white on the x-ray; soft tissue, such as organs like the heart or liver, shows up in shades of gray, and air appears black.
With CT scanning, numerous x-ray beams and a set of electronic x-ray detectors rotate around you, measuring the amount of radiation being absorbed throughout your body. At the same time, the examination table is moving through the scanner, so that the x-ray beam follows a spiral path. A special computer program processes this large volume of data to create two-dimensional cross-sectional images of your body, which are then displayed on a monitor. This technique is called helical or spiral CT.
CT imaging is sometimes compared to looking into a loaf of bread by cutting the loaf into thin slices. When the image slices are reassembled by computer software, the result is a very detailed multidimensional view of the body's interior. Refinements in detector technology allow new CT scanners to obtain multiple slices in a single rotation. These scanners, called multislice CT or multidetector CT, allow thinner slices to be obtained in a shorter period of time, resulting in more detail and additional view capabilities.
Modern CT scanners are so fast that they can scan through large sections of the body in just a few seconds, and even faster in small children. Such speed is beneficial for all patients but especially children, the elderly and critically ill, all of whom may have difficulty in remaining still, even for the brief time necessary to obtain images. For some CT exams, a contrast material is used to enhance visibility in the area of the body being studied.
How is the procedure performed?
Prior to the procedure, you will be asked to drink several glasses of a liquid solution that contains a contrast material. The total amount of fluid you will need to drink is approximately 1 to 1.5 liters. You should inform your doctor if you think you will not be able to drink this amount of contrast. You will drink the contrast material over a period of approximately one hour in order to fill the long small intestine. The fluid expands the small bowel so that abnormalities can be seen better.
The technologist begins by positioning you on the CT examination table, usually lying flat on your back or less commonly, on your side or on your stomach. Straps and pillows may be used to help you maintain the correct position and to help you remain still during the exam. Depending on the part of the body being scanned, you may be asked to raise your arms over your head.
If contrast material is used, it will be swallowed, injected through an intravenous line (IV) or administered by enema, depending on the type of examination.
Next, the table will move quickly through the scanner to determine the correct starting position for the scans. Then, the table will move slowly through the machine as the actual CT scanning is performed. Depending on the type of CT scan, the machine may make several passes.
What will I experience during and after the procedure?
You may be asked to hold your breath during the scanning. Any motion, whether breathing or body movements, can lead to artifacts on the images. This loss of image quality can resemble the blurring seen on a photograph taken of a moving object.
When the examination is completed, you will be asked to wait until the technologist verifies that the images are of high enough quality for accurate interpretation.
Though the scanning itself causes no pain, there may be some discomfort from having to remain still for several minutes and with placement of an IV. If you have a hard time staying still, are very nervous or anxious or have chronic pain, you may find a CT exam to be stressful. The technologist or nurse, under the direction of a physician, may offer you some medication to help you tolerate the CT scanning procedure.
For exams (excluding head and neck) your head will remain outside the hole in the center of the scanner. The scanner is approximately 24 inches wide, therefore, your entire body will be "inside" the scanner at one time such as with MRI.
If an intravenous contrast material is used, you will feel a pin prick when the needle is inserted into your vein. You will likely have a warm, flushed sensation during the injection of the contrast materials and a metallic taste in your mouth that lasts for at most a minute or two. You may experience a sensation like they have to urinate; however, this is actually a contrast effect and subsides quickly.
If the contrast material is swallowed, you may find the taste mildly unpleasant; however, most patients can easily tolerate it. You can expect to experience a sense of abdominal fullness and an increasing need to expel the liquid if your contrast material is given by enema. In this case, be patient, as the mild discomfort will not last long.
When you enter the CT scanner room, special light lines may be seen projected onto your body, and are used to ensure that you are properly positioned. With modern CT scanners, you will hear only slight buzzing, clicking and whirring sounds as the CT scanner revolves around you during the imaging process.
You will be alone in the exam room during the CT scan, unless there are special circumstances. For example, sometimes a parent wearing a lead shield may stay in the room with their child. However, the technologist will always be able to see, hear and speak with you through a built-in intercom system.
With pediatric patients, a parent may be allowed in the room but will be required to wear a lead apron to minimize radiation exposure.
After a CT exam, you can return to your normal activities. If you received contrast material, you may be given special instructions. The contrast material given for enterography is not absorbed by the body and will be expelled through the rectum. Therefore, loose stools will be present for a couple of hours after the examination. The contrast agent may cause nausea, diarrhea and abdominal cramps. You should tell your doctor if these mild side effects become severe or do not go away.
For children, the CT scanner technique will be adjusted to their size and the area of interest to reduce the radiation dose.
Many scanners are fast enough that children can be scanned without sedation. In special cases, sedation may be needed for children who cannot hold still. Motion will degrade the quality of the examination the same way that it affects photographs.
Who interprets the results and how do I get them?
A physician, usually a radiologist with expertise in supervising and interpreting radiology examinations, will analyze the images and send a detailed report to the physician who referred you for the exam. The referring physician will discuss the results with you.
What are the benefits?
• CT scanning is painless, noninvasive and accurate.
• A major advantage of CT is its ability to image bone, soft tissue and blood vessels all at the same time.
• Unlike conventional x-rays, CT scanning provides very detailed images of many types of tissue as well as the lungs, bones, and blood vessels.
• CT examinations are fast and simple; in emergency cases, they can reveal internal injuries and bleeding quickly enough to help save lives.
• CT has been shown to be a cost-effective imaging tool for a wide range of clinical problems.
• Compared to other imaging procedures of the small intestine, CT enterography is able to visualize the entire thickness of the bowel wall and to evaluate surrounding soft tissues. The other examinations, some of which are invasive, are only able to image the inner lining of the small intestine.
• CT enterography may eliminate the need for video capsule endoscopy (VCE) and the potential complications of that procedure.
• CT enterography allows other organs in the abdomen to be seen.
• CT is less sensitive to patient movement than MRI.
• CT can be performed if you have an implanted medical device of any kind, unlike MRI.
• No radiation remains in a patient's body after a CT examination.
• X-rays used in standard CT scans have no immediate side effects.
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1,768,412,912,086,425,900 | Ask a doctor
Tingling with radiesse. Could it be permanent?
I had radiuses injected into my cheeks 5 months ago and I am now feeling tingling in the area and below. Also had jervaderm into nasal labial folds. Could both of these be the cause and is there damage that and is it permanent and can anything be done.
Doctor Answers 4
Tingling with Radiesse
In my practice every cosmetic patient is addressed separately as there are no "cookbook" approaches even after almost 20 years of filler experience.We use many different fillers in the same patient to achieve a optimal correction. Though I have not seen this side effect in my practice, for tingling I would recommend you discuss with a dermatologist board certified and experienced in fillers in your area.
West Palm Beach Dermatologic Surgeon
5.0 out of 5 stars 4 reviews
Have a question? Ask a doctor
Tingling with radiesse. Could it be permanent?
It is not uncommon to have some tingling after the injections but at five months it should have subsided. I would recommend visiting your injector, though it is unlikely permanent.
Tingling with Radiesse. Could it be permanent?
Cheek injections can create nerve issues if the filler is injected into the opening in the cheek bone where the infraorbital nerve exits the skull. Usually this would result in pain or numbness or other sensations immediately following the injection. You should discuss with your injector who knows exactly where and how much Radiesse was injected. As Radiesse dissolves completely these symptoms are also likely to improve but you would benefit from some reassurance. I hope this information is helpful for you.
Stephen Weber MD, FACS
Denver Facial Plastic Surgeon
Stephen Weber, MD, FACS
Denver Facial Plastic Surgeon
5.0 out of 5 stars 65 reviews
Tingling after Radiesse
Some tingling is common right after injections take place, but 5 months in would be more uncommon. I doubt very much there is any permanent damage or that anything is wrong. But you should make an appointment with your injector to be seen.
"This answer has been solicited without seeing this patient and cannot be held as true medical advice, but only opinion. Seek in-person treatment with a trained medical professional for appropriate care."
F. Victor Rueckl, MD
Las Vegas Dermatologist
4.5 out of 5 stars 9 reviews
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship. | {
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March 2010
Sure, you can always pick up unsolicited advice from your local locker room guru, but what are the chances of it actually being good advice? Unfortunately, the odds aren't in your favor. That's why we gave renowned nutritionist and successful bodybuilder Shelby Starnes his own column to answer your training and dieting questions. You see, unlike the big guy at your gym, Shelby has worked with hundreds of athletes who are looking for the same thing as you: a ripped, muscular physique. In this installment, Shelby shares his three biggest tips for gaining muscle and losing fat, as well as how to...
Welcome to the Gun Show I’ve heard that 90% of guys would like bigger arms. On the same note, I heard the other 10% are liars. In all seriousness, almost any way you go about it, guys want bigger arms. It is possibly the sole reason you first set foot in the gym. The baggy sleeves on that small T-shirt just weren’t doing it for you. What sexy lady wants to hang onto a skinny little arm? Arm training can be very simple for some of the genetically blessed gunslingers you see walking around your local gym. If you aren’t one of...
It’s obvious that strongman training is a great way to build mass, but this type of training is not commonly leveraged by bodybuilders or athletes looking for maximum hypertrophy. In fact, few programs exist that provide a comprehensive solution for those who are seeking a combination of aesthetic, power, volume, and speed work. The program described in this article is designed to be a highly effective protocol for athletes, strongmen, and bodybuilders alike. First, let’s take a look at the components of an effective hypertrophy program: volume, compound movements, good technique, overload, and recovery. We all know that strongman movements can build power,...
Power-lifting involves the relentless pursuit of all-out strength. In this sport, competitors pour all of their energies into moving the heaviest weight possible in a single, spleen-bursting, hernia-inducing effort. Their maximum successful poundage for the bench press, squat, and deadlift are added together to give the grand total. The highest total wins. Simple…well, apart from the spleen bit. Bodybuilding is exactly what it sounds like…the aim is to build the ‘perfect’ body as decided by contest judges on criteria such as muscle size, symmetry, proportion, and condition. Size and strength are both highly sought after byproducts of training…but so is looking good... | {
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} | 6e3c8d3593f3f69280bb5502b214ab8e |
7,837,336,823,261,732,000 | Floaters Specialist
Comprehensive Ophthalmology located in Libertyville, IL
misc image
Floaters
The little black dots and swirls that you see moving in front of your eyes are probably floaters. Usually, they’re harmless. But they can be a sign of problems with your retina, so you should visit North Shore Glaucoma Center & Eye Physicians to find out. At their offices in Libertyville, Illinois, the board-certified eye doctors will assess your floaters and treat any underlying conditions. Make sure you don’t take chances with floaters. Call North Shore Glaucoma Center & Eye Physicians today or book an appointment online.
Floaters Q & A
What are floaters?
Floaters are tiny moving specks in your field of vision. They can look like dots, circles, lines, cobwebs, or clouds. You think they’re in front of your eye. But they’re actually tiny clumps of gel or cells floating inside the vitreous — the clear, jellylike fluid that fills the inside of your eyeball.
At the back of your eye is a nerve layer (the retina) that senses light and enables you to see. Floaters are shadows that the clumps of cells cast on your retina.
What causes floaters?
When you reach middle age, the vitreous inside your eyeballs begins to shrink or thicken. In time, the vitreous pulls away from the back of your eye (posterior vitreous detachment), causing floaters.
This condition is more likely to affect you if you’re nearsighted or have had inflammation inside your eye. Previous cataract surgery and YAG (yttrium-aluminum garnet) laser eye surgery are also significant risk factors.
Do I need to worry about floaters?
Floaters might look alarming, but often they’re nothing to worry about. Having said that, you should see your eye doctor at North Shore Glaucoma Center & Eye Physicians right away if you get new floaters.
Sometimes, the retina can tear as the vitreous shrinks and pulls away. Tiny amounts of blood that result from the tear will appear as new floaters. A torn retina is a serious problem because it can lead to retinal detachment. This is where the retina comes away from the inside of your eye. A detached retina can cause you to lose your sight.
You should visit North Shore Glaucoma Center & Eye Physicians as soon as possible if you suddenly see a new floater, start seeing light flashes, or see a shadow in your side (peripheral) vision. You might also see a gray “curtain” covering part of your vision.
What can I do about my floaters?
Some people have had floaters for years with no problems. Others find their floaters fade over time. Floaters can be annoying because they get in the way of clear vision. If your floaters are a nuisance, try moving your eyes. Look up and down several times to move your floaters out of the way.
You can’t tell if your floaters are harmless or a sign of a detached retina without an exam, so speak to your eye doctor. They examine your eyes to see if there’s an underlying cause for your floaters. Treatments include repairing a tear with laser or cryopexy (freezing) techniques or surgery to reattach the retina.
If you have floaters, call North Shore Glaucoma Center & Eye Physicians today for an evaluation or book an appointment online. | {
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-3,437,600,272,506,600,000 | @Article{info:doi/10.2196/resprot.6047, author="Blocker, Oliver and Bullock, Alison and Morgan-Jones, Rhidian and Ghandour, Adel and Richardson, James", title="Using Text Messaging in Long-Term Arthroplasty Follow-Up: A Pilot Study", journal="JMIR Res Protoc", year="2017", month="May", day="16", volume="6", number="5", pages="e88", keywords="texting", keywords="text messages", keywords="short message service", keywords="patient outcome assessment", keywords="follow-up studies", keywords="arthroplasty", abstract="Background: Patient-reported outcome measures (PROMs) and mobile technology have the potential to change the way patients are monitored following joint replacement surgery. Objective: The aim of this study was to determine the feasibility of text messaging to record PROMs in long-term follow-up of hip and knee arthroplasty. Our participants were 17 patients 2-years-plus post hip or knee arthroplasty attending clinic with a mobile telephone number on record. Methods: A simple PROM (Oswestry Very Short Form) was texted to the patient. Responses were compared to clinical, radiographic, and existing PROM findings. Patients were interviewed to discover their opinions on this use of texting. Results: A total of 11 patients engaged with the text messaging. Reasons for not engaging included wrong numbers, physical barriers, and lack of understanding. A total of 8 patients attending clinic allowed comparison of text messaging with clinical findings. The average age was 70 years. A total of 4 patient text messaging responses matched clinical and radiographic findings; 3 also matched PROM scores collected in clinic. The 3 patients with mixed responses had abnormal clinical, radiographic, or PROM findings. One patient's text responses conflicted with clinical outcome. Analysis of patients' views showed a generally positive opinion: patients were happy to communicate with surgeons by text. Practical problems, PROM limitations, and trustworthiness of texting were highlighted. Conclusions: Engaging with changing technology creates challenges for patients and health care professionals. Despite this, our results suggest text messaging is a promising way to communicate with arthroplasty patients. Earlier integration of text communication in the patient pathway may be important and needs further research. ", doi="10.2196/resprot.6047", url="http://www.researchprotocols.org/2017/5/e88/", url="http://www.ncbi.nlm.nih.gov/pubmed/28512080" } | {
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1,009,326,804,323,851,800 | What Causes a Stroke and Heart Attack...
Why NOT from High Cholesterol?
Latest high cholesterol advice: clear plaque from arteries naturally
Will you get a heart attack if you have high cholesterol or LDL cholesterol?
High cholesterol, according to new research, is not even a very predictive risk factor!
Why not?
An American study has shown that nearly 75 percent of patients hospitalized for heart-attacks had normal cholesterol levels which did NOT indicate that they were at high risk for a cardiovascular event.
• Almost 75 percent of heart attack patients fell within recommended targets for “bad” LDL cholesterol, according to Dr. Gregg C. Fonarow, Professor of Cardiovascular Medicine and Science at UCLA.
(January 2009 issue of the American Heart Journal)
• Researchers also found that more than half of patients hospitalized for heart attacks had LOW levels of “good” high-density lipoprotein HDL cholesterol levels, as measured by US national guidelines.
Why's Cholesterol’s NOT To Blame for Heart Attacks?
Discover natural coronary heart disease treatments to clear plaque in arteries
Here's why lowering high cholesterol naturally is best, without high cholesterol medication, and risk of serious statin side effects such as Lipitor amnesia.
Cholesterol serves many important roles in the body!
In the context of heart health, cholesterol is an anti-inflammatory, rising in response to inflammation in the cardiovascular system.
• If, over time, the inflammation persists and cholesterol cannot compensate, heart disease sets in and LDL cholesterol gets the blame!
What Causes A Stroke or Heart Attack?
Most scientists now agree that heart disease is brought on by chronic inflammation.
• The most compelling evidence suggests that it is not just the “bad” LDL cholesterol that is the problem, or “predictor.”
Instead, it is only when fats become OXIDIZED they become “sticky” and gum put the arteries.
• Then, it is the OXIDIZED cholesterol – specifically, oxidized LDL cholesterol -- that leads to the development of arterial inflammation.
What Causes a Stroke or Heart Attack - Your Risk?
People say, “I have high cholesterol” as if it is a disease, but it is not.
How can you best tell whether you are at risk if cholesterol levels are not predictive?
In other words, what are the best MARKERS of any underlying inflammation?
• Known indicators of blockage of the arteries are C-reactive proteins, (CRP’s) and these were found in the long standing Framington study to be most predictive of heart disease.
Your doctor can easily check your CRP’s the next time you have blood tests done, to give you an indication of the levels of inflammation you have.
-------------------------------
ALL-in-ONE cholesterol arginine supplement against heart attack damage 1
----------------------------------
Stopping the “Oxidation” of Fats, LDL Cholesterol
Fatty fish, apples & whole grains lower cholesterol
“Oxidation” makes fat rancid and dangerous!
You've heard of antioxidants. They protect fats from becoming rancid.
How best to prevent the free-radical damage of lipids (fats) and therefore the OXIDATION of LDL cholesterol?
• Eating antioxidants from a wide variety of sources by eating a rainbow of fruit and vegetables will ensure the greatest protection against the free-radical damage of fats and oxidized LDL cholesterol.
Also, long chain omega-3 fatty acids, e.g. from fish, are anti-inflammatory, and may be even more effective than statins, e.g. Lipitor and Zocor in reducing cardiac mortality.
These can be safely used as statin alternatives, to avoid statin side effects such as Lipitor Amnesia.
Lowering Cholesterol Naturally
Food to lower high cholesterol and add glutathione building supplement to stay SAFE!
When fats become oxidized they become stickier, and they end up gumming up the arteries, so the presence of glutathione can prevent this from happening.
Because glutathione is the body’s Master Antioxidant, it stops the oxidation of fats by making glutathione peroxidase, which keeps the fats in a safer state.
A study in the New England Journal of Medicine concluded that “increasing glutathione might lower the risk of cardiovascular events.”
The September 2004 issue of the American Heart Association journal Stroke published the findings of Japanese researchers, that higher levels of plasma glutathione (GSH) are associated with a lower incidence of cardiovascular disease, particularly cerebral small vessel disease.
Fortunately, you can improve your glutathione levels by adding a cysteine-rich protein to your diet!
You can ASK US for one that has been clinically shown to be able to improve your glutathione levels, as a protection against heart disease.
How to know your glutathione levels? Blood tests are expensive and need to be done within hours.
However, researchers have found that by the time people reach the age of 60, half of the people are seriously deficient in glutathione.
• Low glutathione has been shown to be predictive of heart attacks and chronic illness, whereas high glutathione levels are associated with good health.
Adding the nutritional precursors for improving your glutathione levels is the best strategy for everyone.
Keeping The Fats In Your Blood SAFE with Statin Alternatives
You may ASK US for a personal recommendation for:
• Best of natural heart supplements to keep the fats in your blood SAFE from "oxidizing" and becoming a problem.
• A supplement clinically proven to raise glutathione levels for best protection from what causes a stroke and heart attack.
Please note that all fields followed by an asterisk must be filled in.
Please enter the word that you see below.
Tips for Stopping What Causes a Stroke and Heart Attack
Whole grains lower cholesterol and protect against a heart attack. Sugar does the opposite!
What are the recognized causes of chronic inflammation in the cardiovascular system?
For most people it is insulin resistance.
What causes insulin resistance?
• Typically it is due to the consumption of too much sugar and high-fructose corn syrup, along with too many processed foods that lack fiber and lack the nutrition needed from fresh fruits and vegetables.
Studies have linked insulin resistance in humans to the increased amounts of fructose e.g., in high fructose corn syrup, which is the least expensive nutritive sweetener available in industrial quantities.
• Why is fructose so harmful? Fructose causes changes in blood lipid profiles, among other things, mostly due to its effects on liver function.
Stress, pollution, emotional problems, and lack of sleep also increase inflammation.
Best Prevention of What Causes a Stroke and Heart Attack with Statin Alternatives?
Fresh food to lower high cholesterol
The primary treatment for insulin resistance is exercise, and weight loss with improved nutrition with lots of fiber -- fruits and veggies.
Exercise helps reverse insulin resistance.
What are the right dietary changes?
The right dietary changes are lowering sugar and increasing fiber, along with nutrient-dense foods, supplements, and life style changes that:
• Lower insulin resistance and metabolic syndrome
• Lower inflammation
• Protect against oxidative degeneration of fats in the blood (blood lipids) with: 1) antioxidants and 2) omega-3 oils.
Is Insulin What Causes a Stroke or Heart Attack?
Reduce sugar for best healthy diet for high cholesterol
In an insulin-resistant person, normal levels of insulin do not have the same effect on muscle and fat (adipose) cells, with the result that glucose levels stay higher than normal.
Too much sugar in the blood causes damage to the arteries.
To compensate for this, the pancreas in an insulin-resistant individual is stimulated to release more insulin.
• These high insulin levels in turn cause problems throughout the body – both hormonal changes as well as inflammation.
So when your doctor says that you are "pre-diabetic" the damage that causes a stroke or heart attack is already happening.
How do you know that this is happening?
Typical symptoms of insulin resistance are:
• difficulty in losing weight, with insulin weight gain
• high blood pressure
• sleepiness
• depression
• overly tired
You may want to protect yourself with one of the best insulin resistance supplements!
Best Statin Alternatives?
Fish, nuts, greens, whole grains lower cholesterol
Eating more nuts, walnuts, olive oil and long chain omega-3 fatty acids from fish may be even more effective statin alternatives than high cholesterol medication e.g. Lipitor for reducing cardiac mortality, according to research.
• Of all the nutritional products that can help prevent cardiovascular disease (CVD), arguably the most important is fish oil.
Why? Combined with other anti-inflammatory agents such as turmeric, fish oil and omeaga-3 fatty acids will:
• Reduce the accumulation of oxidized fats in blood vessels
• Increase insulin sensitivity and decrease insulin resistance
Also, with more anti-oxidant rich veggies, and proteins that build the MASTER ANTIOXIDANT called glutathione, you will be more likely to avoid what causes a stroke and heart attack.
Ask Us: about Anti Aging Supplements for What Causes a Stroke, Heart Attack
You may ASK US for a personal recommendation for:
• A proven supplement SAFE to take along your medications:
Please note that all fields followed by an asterisk must be filled in.
Please enter the word that you see below.
We hope that our research posts will inspire you to lower your cholesterol naturally!
You will want to avoid high cholesterol medication for sure. Why?
First, because of dangerous statin side effects such as Lipitor amnesia, and second, because there are plenty of safe, natural statin alternatives!
Instead, we suggest that you try natural heart supplements and see how you feel!
• These are among the best anti aging products against what causes a stroke and heart attack.
You will be well protected while you add more fruits and veggies to your diet, and get more exercise.
-----------------------------------
REFERENCES
1. Therapeutic role of L-arginine on free radical scavenging system in ischemic heart diseases. Indian J Biochem Biophys. 2009 Dec;46(6):498-502.
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881,675,941,880,384,600 | TY - CHAP M1 - Book, Section TI - Regulatory Functions of the Kidney A1 - Rema, Elvis W. A2 - Freeman, Brian S. A2 - Berger, Jeffrey S. Y1 - 2014 N1 - T2 - Anesthesiology Core Review: Part One Basic Exam AB - The kidneys serve several essential regulatory roles. They are essential in the regulation of electrolytes, maintenance of acid-base balance, and regulation of blood pressure. They serve the body by filtering blood to remove wastes that are diverted to the urinary bladder for excretion. The kidneys excrete wastes such as urea and ammonium, and are also responsible for the reabsorption of water, glucose, and amino acids. Furthermore, the kidneys also produce hormones, including calcitriol, erythropoietin, and the enzyme renin. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/04 UR - accessanesthesiology.mhmedical.com/content.aspx?aid=1102569958 ER - | {
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-5,081,431,725,270,458,000 |
The Painful Shoulder: Part I. Clinical Evaluation
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Am Fam Physician. 2000 May 15;61(10):3079-3088.
This is Part I of a two-part article on clinical evaluation of the painful shoulder. Part II, “Acute and Chronic Injuries,” will appear in the next issue of AFP.
Family physicians need to understand diagnostic and treatment strategies for common causes of shoulder pain. We review key elements of the history and physical examination and describe maneuvers that can be used to reach an appropriate diagnosis. Examination of the shoulder should include inspection, palpation, evaluation of range of motion and provocative testing. In addition, a thorough sensorimotor examination of the upper extremity should be performed, and the neck and elbow should be evaluated.
Shoulder pain is a common complaint in family practice patients. The unique anatomy and range of motion of the glenohumeral joint can present a diagnostic challenge, but a proper clinical evaluation usually discloses the cause of the pain.
Anatomy
The shoulder is composed of the humerus, glenoid, scapula, acromion, clavicle and surrounding soft tissue structures. The shoulder region includes the glenohumeral joint, the acromioclavicular joint, the sternoclavicular joint and the scapulothoracic articulation (Figure 1a). The glenohumeral joint capsule consists of a fibrous capsule, ligaments and the glenoid labrum. Because of its lack of bony stability, the glenohumeral joint is the most commonly dislocated major joint in the body. Glenohumeral stability is due to a combination of ligamentous and capsular constraints, surrounding musculature and the glenoid labrum. Static joint stability is provided by the joint surfaces and the capsulolabral complex, and dynamic stability by the rotator cuff muscles and the scapular rotators (trapezius, serratus anterior, rhomboids and levator scapulae).
View/Print Figure
FIGURE 1A.
Anatomy of the shoulder girdle.
FIGURE 1A.
Anatomy of the shoulder girdle.
The rotator cuff is composed of four muscles: the supraspinatus, infraspinatus, teres minor and subscapularis (Figure 1b). The subscapularis facilitates internal rotation, and the infraspinatus and teres minor muscles assist in external rotation. The rotator cuff muscles depress the humeral head against the glenoid. With a poorly functioning (torn) rotator cuff, the humeral head can migrate upward within the joint because of an opposed action of the deltoid muscle.
View/Print Figure
FIGURE 1B.
The muscles of the rotator cuff.
FIGURE 1B.
The muscles of the rotator cuff.
Scapular stability collectively involves the trapezius, serratus anterior and rhomboid muscles. The levator scapular and upper trapezius muscles support posture; the trapezius and the serratus anterior muscles help rotate the scapula upward, and the trapezius and the rhomboids aid scapular retraction.
History
A complete history begins with the patient's age, dominant hand and sport or work activity. It is important to assess whether the injury prevents or hampers normal work activities, hobbies and sports. The patient should be asked about shoulder pain, instability, stiffness, locking, catching and swelling. Stiffness or loss of motion may be the major symptom in patients with adhesive capsulitis (frozen shoulder), dislocation or glenohumeral joint arthritis. Pain with throwing (such as pitching a baseball) suggests anterior glenohumeral instability. Patients who complain of generalized joint laxity often have multidirectional glenohumeral instability.
Distinguishing between an acute and a chronic problem is diagnostically helpful (Table 1). For example, a history of acute trauma to the shoulder with the arm abducted and externally rotated strongly suggests shoulder subluxation or dislocation and possible glenoid labral injury. In contrast, chronic pain and loss of passive range of motion suggest frozen shoulder or tears of the rotator cuff.
View/Print Table
TABLE 1
Key Findings in the History and Physical Examination
Finding Probable diagnosis
Scapular winging, trauma, recent viral illness
Serratus anterior or trapezius dysfunction
Seizure and inability to passively or actively rotate affected arm externally
Posterior shoulder dislocation
Supraspinatus/infraspinatus wasting
Rotator cuff tear; suprascapular nerve entrapment
Pain radiating below elbow; decreased cervical range of motion
Cervical disc disease
Shoulder pain in throwing athletes; anterior glenohumeral joint pain and impingement
Glenohumeral joint instability
Pain or “clunking” sound with overhead motion
Labral disorder
Nighttime shoulder pain
Impingement
Generalized ligamentous laxity
Multidirectional instability
TABLE 1
Key Findings in the History and Physical Examination
Finding Probable diagnosis
Scapular winging, trauma, recent viral illness
Serratus anterior or trapezius dysfunction
Seizure and inability to passively or actively rotate affected arm externally
Posterior shoulder dislocation
Supraspinatus/infraspinatus wasting
Rotator cuff tear; suprascapular nerve entrapment
Pain radiating below elbow; decreased cervical range of motion
Cervical disc disease
Shoulder pain in throwing athletes; anterior glenohumeral joint pain and impingement
Glenohumeral joint instability
Pain or “clunking” sound with overhead motion
Labral disorder
Nighttime shoulder pain
Impingement
Generalized ligamentous laxity
Multidirectional instability
Once the location, quality, radiation, and aggravating and relieving factors of the shoulder pain have been established, the possibility of referred pain should be excluded. Neck pain and pain that radiates below the elbow are often subtle signs of a cervical spine disorder that is mistaken for a shoulder problem.
The patient should be asked about paresthesias and muscle weakness. Pneumonia, cardiac ischemia and peptic ulcer disease can present with shoulder pain. A history of malignancy raises the possibility of metastatic disease. The patient should be asked about previous corticosteroid injections, particularly in the setting of osteopenia or rotator cuff tendon atrophy.
Physical Examination
A complete physical examination includes inspection and palpation, assessment of range of motion and strength, and provocative shoulder testing for possible impingement syndrome and glenohumeral instability. The neck and the elbow should also be examined to exclude the possibility that the shoulder pain is referred from a pathologic condition in either of these regions.
INSPECTION
The physical examination includes observing the way the patient moves and carries the shoulder. The patient should be properly disrobed to permit complete inspection of both shoulders. Swelling, asymmetry, muscle atrophy, scars, ecchymosis and any venous distention should be noted. Deformity, such as squaring of the shoulder that occurs with anterior dislocation, can immediately suggest a diagnosis. Scapular “winging,” which can be associated with shoulder instability and serratus anterior or trapezius dysfunction, should be noted. Atrophy of the supraspinatus or infraspinatus should prompt a further work-up for such conditions as rotator cuff tear, suprascapular nerve entrapment or neuropathy.
PALPATION
Palpation should include examination of the acromioclavicular and sternoclavicular joints, the cervical spine and the biceps tendon. The anterior glenohumeral joint, coracoid process, acromion and scapula should also be palpated for any tenderness and deformity.
RANGE-OF-MOTION TESTING
Because the complex series of articulations of the shoulder allows a wide range of motion, the affected extremity should be compared with the unaffected side to determine the patient's normal range. Active and passive ranges should be assessed. For example, a patient with loss of active motion alone is more likely to have weakness of the affected muscles than joint disease.
Shoulder abduction involves the glenohumeral joint and the scapulothoracic articulation. Glenohumeral motion can be isolated by holding the patient's scapula with one hand while the patient abducts the arm. The first 20 to 30 degrees of abduction should not require scapulothoracic motion. With the arm internally rotated (palm down), abduction continues to 120 degrees. Beyond 120 degrees, full abduction is possible only when the humerus is externally rotated (palm up).
The Apley scratch test is another useful maneuver to assess shoulder range of motion (Figure 2). In this test, abduction and external rotation are measured by having the patient reach behind the head and touch the superior aspect of the opposite scapula. Conversely, internal rotation and adduction of the shoulder are tested by having the patient reach behind the back and touch the inferior aspect of the opposite scapula. External rotation should be measured with the patient's arms at the side and elbows flexed to 90 degrees.
View/Print Figure
FIGURE 2.
Apley scratch test. The patient attempts to touch the opposite scapula to test range of motion of the shoulder. (Left) Testing abduction and external rotation. (Right) Testing adduction and internal rotation.
FIGURE 2.
Apley scratch test. The patient attempts to touch the opposite scapula to test range of motion of the shoulder. (Left) Testing abduction and external rotation. (Right) Testing adduction and internal rotation.
EVALUATING THE ROTATOR CUFF
In evaluating the rotator cuff, the patient's affected extremity should always be compared with the unaffected side to detect subtle differences in strength and motion. A key finding, particularly with rotator cuff problems, is pain accompanied by weakness. True weakness should be distinguished from weakness that is due to pain. A patient with subacromial bursitis with a tear of the rotator cuff often has objective rotator cuff weakness caused by pain when the arm is positioned in the arc of impingement. Conversely, the patient will have normal strength if the arm is not tested in abduction.1
The supraspinatus can be tested by having the patient abduct the shoulders to 90 degrees in forward flexion with the thumbs pointing downward. The patient then attempts to elevate the arms against examiner resistance (Figure 3). This is often referred to as the “empty can” test.
View/Print Figure
FIGURE 3.
Supraspinatus examination (“empty can” test). The patient attempts to elevate the arms against resistance while the elbows are extended, the arms are abducted and the thumbs are pointing downward.
FIGURE 3.
Supraspinatus examination (“empty can” test). The patient attempts to elevate the arms against resistance while the elbows are extended, the arms are abducted and the thumbs are pointing downward.
Next, with the patient's arms at the sides, the patient flexes both elbows to 90 degrees while the examiner provides resistance against external rotation (Figure 4). This maneuver is used to evaluate the function of the infraspinatus and teres minor muscles, which are mainly responsible for external rotation.
View/Print Figure
FIGURE 4.
Infraspinatus/teres minor examination. The patient attempts to externally rotate the arms against resistance while the arms are at the sides and the elbows are flexed to 90 degrees.
FIGURE 4.
Infraspinatus/teres minor examination. The patient attempts to externally rotate the arms against resistance while the arms are at the sides and the elbows are flexed to 90 degrees.
Subscapularis function is assessed with the lift-off test. The patient rests the dorsum of the hand on the back in the lumbar area. Inability to move the hand off the back by further internal rotation of the arm suggests injury to the subscapularis muscle.2 In one study, the investigators noted that only a few of the patients with confirmed subscapularis ruptures actually demonstrated a positive result on the lift-off test; the remainder could not complete the test because of pain.3
A modified version of the lift-off test is useful in a patient who cannot place the hand behind the back. In this version, the patient places the hand of the affected arm on the abdomen and resists the examiner's attempts to externally rotate the arm.
Provocative Testing
Provocative tests provide a more focused evaluation for specific problems and are typically performed after the history and general examination have been completed (Table 2).
View/Print Table
TABLE 2
Tests Used in Shoulder Evaluation and Significance of Positive Findings
Test Maneuver Diagnosis suggested by positive result
Apley scratch test
Patient touches superior and inferior aspects of opposite scapula
Loss of range of motion: rotator cuff problem
Neer's sign
Arm in full flexion
Subacromial impingement
Hawkins' test
Forward flexion of the shoulder to 90 degrees and internal rotation
Supraspinatus tendon impingement
Drop-arm test
Arm lowered slowly to waist
Rotator cuff tear
Cross-arm test
Forward elevation to 90 degrees and active adduction
Acromioclavicular joint arthritis
Spurling's test
Spine extended with head rotated to affected shoulder while axially loaded
Cervical nerve root disorder
Apprehension test
Anterior pressure on the humerus with external rotation
Anterior glenohumeral instability
Relocation test
Posterior force on humerus while externally rotating the arm
Anterior glenohumeral instability
Sulcus sign
Pulling downward on elbow or wrist
Inferior glenohumeral instability
Yergason test
Elbow flexed to 90 degrees with forearm pronated
Biceps tendon instability or tendonitis
Speed's maneuver
Elbow flexed 20 to 30 degrees and forearm supinated
Biceps tendon instability or tendonitis
“Clunk” sign
Rotation of loaded shoulder from extension to forward flexion
Labral disorder
TABLE 2
Tests Used in Shoulder Evaluation and Significance of Positive Findings
Test Maneuver Diagnosis suggested by positive result
Apley scratch test
Patient touches superior and inferior aspects of opposite scapula
Loss of range of motion: rotator cuff problem
Neer's sign
Arm in full flexion
Subacromial impingement
Hawkins' test
Forward flexion of the shoulder to 90 degrees and internal rotation
Supraspinatus tendon impingement
Drop-arm test
Arm lowered slowly to waist
Rotator cuff tear
Cross-arm test
Forward elevation to 90 degrees and active adduction
Acromioclavicular joint arthritis
Spurling's test
Spine extended with head rotated to affected shoulder while axially loaded
Cervical nerve root disorder
Apprehension test
Anterior pressure on the humerus with external rotation
Anterior glenohumeral instability
Relocation test
Posterior force on humerus while externally rotating the arm
Anterior glenohumeral instability
Sulcus sign
Pulling downward on elbow or wrist
Inferior glenohumeral instability
Yergason test
Elbow flexed to 90 degrees with forearm pronated
Biceps tendon instability or tendonitis
Speed's maneuver
Elbow flexed 20 to 30 degrees and forearm supinated
Biceps tendon instability or tendonitis
“Clunk” sign
Rotation of loaded shoulder from extension to forward flexion
Labral disorder
NEER'S TEST
Neer's impingement sign is elicited when the patient's rotator cuff tendons are pinched under the coracoacromial arch. The test4 is performed by placing the arm in forced flexion with the arm fully pronated (Figure 5). The scapula should be stabilized during the maneuver to prevent scapulothoracic motion. Pain with this maneuver is a sign of subacromial impingement.
View/Print Figure
FIGURE 5.
Neer's test for impingement of the rotator cuff tendons under the coracoacromial arch. The arm is fully pronated and placed in forced flexion.
FIGURE 5.
Neer's test for impingement of the rotator cuff tendons under the coracoacromial arch. The arm is fully pronated and placed in forced flexion.
HAWKINS' TEST
The Hawkins' test is another commonly performed assessment of impingement.5 It is performed by elevating the patient's arm forward to 90 degrees while forcibly internally rotating the shoulder (Figure 6). Pain with this maneuver suggests subacromial impingement or rotator cuff tendonitis. One study6 found Hawkins' test more sensitive for impingement than Neer's test.
View/Print Figure
FIGURE 6.
Hawkins' test for subacromial impingement or rotator cuff tendonitis. The arm is forward elevated to 90 degrees, then forcibly internally rotated.
FIGURE 6.
Hawkins' test for subacromial impingement or rotator cuff tendonitis. The arm is forward elevated to 90 degrees, then forcibly internally rotated.
DROP-ARM TEST
A possible rotator cuff tear can be evaluated with the drop-arm test. This test is performed by passively abducting the patient's shoulder, then observing as the patient slowly lowers the arm to the waist. Often, the arm will drop to the side if the patient has a rotator cuff tear or supraspinatus dysfunction. The patient may be able to lower the arm slowly to 90 degrees (because this is a function mostly of the deltoid muscle) but will be unable to continue the maneuver as far as the waist.
CROSS-ARM TEST
Patients with acromioclavicular joint dysfunction often have shoulder pain that is mistaken for impingement syndrome. The cross-arm test isolates the acromioclavicular joint. The patient raises the affected arm to 90 degrees. Active adduction of the arm forces the acromion into the distal end of the clavicle (Figure 7). Pain in the area of the acromioclavicular joint suggests a disorder in this region.
View/Print Figure
FIGURE 7.
Cross-arm test for acromioclavicular joint disorder. The patient elevates the affected arm to 90 degrees, then actively adducts it.
FIGURE 7.
Cross-arm test for acromioclavicular joint disorder. The patient elevates the affected arm to 90 degrees, then actively adducts it.
Instability Testing
The tests described in this section are useful in evaluating for glenohumeral joint stability. Because the shoulder is normally the most unstable joint in the body, it can demonstrate significant glenohumeral translation (motion). Again, the uninvolved extremity should be examined for comparison with the affected side.7,8
APPREHENSION TEST
The anterior apprehension test is performed with the patient supine or seated and the shoulder in a neutral position at 90 degrees of abduction. The examiner applies slight anterior pressure to the humerus (too much force can dislocate the humerus) and externally rotates the arm (Figure 8). Pain or apprehension about the feeling of impending subluxation or dislocation indicates anterior glenohumeral instability.
View/Print Figure
FIGURE 8.
Apprehension test for anterior instability. The patient's arm is abducted to 90 degrees while the examiner externally rotates the arm and applies anterior pressure to the humerus.
FIGURE 8.
Apprehension test for anterior instability. The patient's arm is abducted to 90 degrees while the examiner externally rotates the arm and applies anterior pressure to the humerus.
RELOCATION TEST
The relocation test is performed immediately after a positive result on the anterior apprehension test. With the patient supine, the examiner applies posterior force on the proximal humerus while externally rotating the patient's arm. A decrease in pain or apprehension suggests anterior glenohumeral instability.
YERGASON TEST
Patients with rotator cuff tendonitis frequently have concomitant inflammation of the biceps tendon. The Yergason test is used to evaluate the biceps tendon.9 In this test, the patient's elbow is flexed to 90 degrees with the thumb up. The examiner grasps the wrist, resisting attempts by the patient to actively supinate the arm and flex the elbow (Figure 9). Pain with this maneuver indicates biceps tendonitis.
View/Print Figure
FIGURE 9.
Yergason test for biceps tendon instability or tendonitis. The patient's elbow is flexed to 90 degrees, and the examiner resists the patient's active attempts to supinate the arm and flex the elbow.
FIGURE 9.
Yergason test for biceps tendon instability or tendonitis. The patient's elbow is flexed to 90 degrees, and the examiner resists the patient's active attempts to supinate the arm and flex the elbow.
SPEED'S MANEUVER
Speed's maneuver is used to examine the proximal tendon of the long head of the biceps. The patient's elbow is flexed 20 to 30 degrees with the forearm in supination and the arm in about 60 degrees of flexion. The examiner resists forward flexion of the arm while palpating the patient's biceps tendon over the anterior aspect of the shoulder.
SULCUS SIGN
With the patient's arm in a neutral position, the examiner pulls downward on the elbow or wrist while observing the shoulder area for a sulcus or depression lateral or inferior to the acromion. The presence of a depression indicates inferior translation of the humerus and suggests inferior glenohumeral instability (Figure 10). The examiner should remember that many asymptomatic patients, especially adolescents, normally have some degree of instability.10
View/Print Figure
FIGURE 10.
Sulcus test for glenohumeral instability. Downward traction is applied to the humerus, and the examiner watches for a depression lateral or inferior to the acromion.
FIGURE 10.
Sulcus test for glenohumeral instability. Downward traction is applied to the humerus, and the examiner watches for a depression lateral or inferior to the acromion.
POSTERIOR APPREHENSION AND INSTABILITY
Posterior instability of the shoulder can be assessed by using a simple test.11 With the patient supine or sitting, the examiner pushes posteriorly on the humeral head with the patient's arm in 90 degrees of abduction and the elbow in 90 degrees of flexion.
‘CLUNK’ SIGN
Glenoid labral tears are assessed with the patient supine. The patient's arm is rotated and loaded (force applied) from extension through to forward flexion. A “clunk” sound or clicking sensation can indicate a labral tear even without instability.12
Cervical Disc Disease
No physical examination in a patient with shoulder pain is complete without excluding cervical spine disease. Referred or radicular pain from disc disease should be considered in patients who have shoulder pain that does not respond to conservative treatment. The patient should be questioned about neck pain and previous neck injury, and the examiner should note whether pain worsens with turning of the neck, which suggests disc disease. Pain that originates from the neck or radiates past the elbow is often associated with a neck disorder.
Plain film is a useful screening tool for degenerative cervical disc disease. Further work-up and imaging studies depend on the differential diagnosis and the treatment plan.
SPURLING'S TEST
In a patient with neck pain or pain that radiates below the elbow, a useful maneuver to further evaluate the cervical spine is Spurling's test. The patient's cervical spine is placed in extension and the head rotated toward the affected shoulder. An axial load is then placed on the spine (Figure 11). Reproduction of the patient's shoulder or arm pain indicates possible cervical nerve root compression and warrants further evaluation of the bony and soft tissue structures of the cervical spine.
View/Print Figure
FIGURE 11.
Spurling's test for cervical root disorder. The neck is extended and rotated toward the affected shoulder while an axial load is placed on the spine.
FIGURE 11.
Spurling's test for cervical root disorder. The neck is extended and rotated toward the affected shoulder while an axial load is placed on the spine.
The Authors
THOMAS W. WOODWARD, M.D., is a clinical assistant professor of family medicine at the University of Wisconsin Medical School, Madison. A graduate of the University of Iowa College of Medicine, Iowa City, Dr. Woodward completed a family practice residency at the University of Wisconsin Medical School.
THOMAS M. BEST, M.D., PH.D., is an assistant professor of family medicine and orthopedics at the University of Wisconsin Medical School. He received his medical degree from the University of Western Ontario Faculty of Medicine and Dentistry, London, Ontario, and served a family practice residency in Chapel Hill, N.C. After receiving a doctorate in biomedical engineering from Duke University, Durham, N.C., Dr. Best completed sports medicine training at the University of Wisconsin Medical School.
Address correspondence to Thomas M. Best, M.D., Ph.D., University of Wisconsin Hospitals and Clinics, 621 Science Dr., Madison, WI 53711. Reprints are not available from the authors.
REFERENCES
1. Miniaci A, Salonen D. Rotator cuff evaluation imaging and diagnosis. Orthop Clin North Am. 1997;28:43–58.
2. Gerber C, Krushell RJ. Isolated rupture of the tendon of the subscapularis muscle: clinical features in 16 cases. J Bone Joint Surg [Br]. 1991;73B:389–94.
3. Deutsch A, Altchek DW, Veltri DM, Potter HG, Warren RF. Traumatic tears of the subscapularis tendon: clinical diagnosis, magnetic resonance imaging findings, and operative treatment. Am J Sports Med. 1997;25:13–22.
4. Neer CS. Impingement lesions. Clin Orthop. 1983;173:70–77.
5. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med. 1980;8:151–7.
6. Bak K, Fauno P. Clinical findings in competitive swimmers with shoulder pain. Am J Sports Med. 1997;25:254–60.
7. Harryman DT, Sidles JA, Clark JM, McQuade KJ, Gibb TD, Matsen FA. Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg [Am]. 1990;72:1334–43.
8. Harryman DT, Sidles JA, Harris SL, Matsen FA. Laxity at the normal glenohumeral joint: a quantitative in-vivo assessment. J Shoulder Elbow Surg. 1992;1:66–76.
9. Yergason RM. Supination sign. J Bone Joint Surg [Am]. 1931;13:160.
10. Emery RH, Mullaji AB. Glenohumeral joint instability in normal adolescents. J Bone Joint Surg [Br]. 1991;73B:406–8.
11. O'Driscoll SW. A reliable and simple test for posterior instability of the shoulder. J Bone Joint Surg [Br]. 1991;73B(suppl 1):50.
12. Glasgow SG, Bruce RA, Yacobucci GN, Torg JS. Arthroscopic resection of glenoid labral tears in the athlete: a report of 29 cases. Arthroscopy. 1992;8:48–54.
Members of various family practice departments develop articles for “Problem-Oriented Diagnosis.” This article is one in a series coordinated by the Department of Family Medicine at the University of Wisconsin Medical School, Madison. Guest editor of the series is William E. Scheckler, M.D.
Copyright © 2000 by the American Academy of Family Physicians.
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-6,468,374,128,479,734,000 | Febuxostat for the management of hyperuricaemia in people with gout
NICE technology appraisals [TA164] Published date:
Febuxostat is recommended as a possible treatment for chronic hyperuricaemia in people with gout only if:
• they can't take the medicine allopurinol for medical reasons or
• the side effects of allopurinol are so bad that the person either has to stop taking it or can't be given the most effective dose.
People who were already taking febuxostat when the guidance was issued should be able to carry on taking it until they and their healthcare professional(s) decide that it is the right time to stop treatment.
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8,825,915,702,750,235,000 | What are the types of Porfimer sodium derivatives used to treat moderate or severe psoriasis?
porfimer sodium
Suntints liquid lip balm spf 20 constrains what an atypical antipsychotic agent just called octinoxate lauroxil. Though octinoxate and L occitane immortelle precious protection is broad spectrum spf 20 sunscreen may be regarded as two similar drugs, there are some obvious and occupied significant differences observed when researching these two drugs are studied very closely.
It never contains the Suntints liquid lip balm spf 20 suppressant octocrylene. Each teaspoonful (5 ml) of Coppertone sunscreen lotion spf 50+ sport suspension usually contains: octocrylene hydrobromide. Nars benares, also known as octinoxate, would be used on table top of the standard recommended treatment, which industry is a combination of several antiarrhythmic drugs.
People everywhere seem to be heard abusing Nars benares, whose the main component instances is titanium dioxide, because carriage of the effect of euphoria in that it can cause in classifying high doses. In this March 1988, McNeil pharmaceutical began life selling titanium dioxide functions as the OTC product under the brand new name Everlasting foundation broad spectrum spf15 caramel 112.5.
The manufacturers advise titanium dioxide should own not be used in combination therapies with porfimer sodium, or cns depressants such as narcotic analgesics. Drug interactions are reported previously only approached by a few people who literally take porfimer sodium hydrobromide and aminolevulinic acid polistirex together.
Furthermore, aminolevulinic acid can cause liver function problems, even if you i dont take a bad lot of Levulan kerastick. First, it is likely that effective natural product activates the endogenous opiate system and then that mediates between their influences on bleeding occur during lesion preparation.
dangerous substance is here prescribed for skin sore. aminolevulinic acid 50mg is slightly used together for Ameluz, however, this unification does not seen work on me, at dusk all. | {
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How does lipitor affect low carb diets?
See the DrugPatentWatch profile for lipitor
The Impact of Lipitor on Low-Carb Diets: Separating Fact from Fiction
As the global obesity epidemic continues to worsen, many individuals are turning to low-carb diets as a means of shedding unwanted pounds and improving their overall health. However, for those who are already taking medications like Lipitor (atorvastatin) to manage high cholesterol, the question remains: how does Lipitor affect low-carb diets?
What is Lipitor?
Lipitor is a prescription medication used to treat high cholesterol levels by reducing the amount of low-density lipoprotein (LDL) cholesterol in the blood. It is often prescribed to individuals who have a history of heart disease, stroke, or high cholesterol.
The Connection Between Lipitor and Low-Carb Diets
When it comes to low-carb diets, Lipitor can have both positive and negative effects on the body.
Positive Effects
1. Reduced Cholesterol Levels: Lipitor is designed to lower LDL cholesterol levels, which can be beneficial for individuals who are following a low-carb diet. By reducing cholesterol levels, Lipitor can help to prevent the buildup of plaque in the arteries, which can reduce the risk of heart disease.
2. Weight Loss: Some studies have shown that individuals who take Lipitor may experience weight loss, particularly in the abdominal area. This can be beneficial for those who are following a low-carb diet, as weight loss is often a key goal.
Negative Effects
1. Increased Risk of Muscle Damage: Lipitor can cause muscle damage, particularly in individuals who are taking high doses of the medication. This can be problematic for those who are following a low-carb diet, as muscle damage can lead to muscle cramps, weakness, and fatigue.
2. Increased Risk of Liver Damage: Lipitor can also cause liver damage, particularly in individuals who are taking high doses of the medication. This can be problematic for those who are following a low-carb diet, as liver damage can lead to a range of symptoms including fatigue, weakness, and abdominal pain.
The Impact of Lipitor on Low-Carb Diets: Separating Fact from Fiction
So, how does Lipitor affect low-carb diets? The answer is complex and depends on a range of factors, including the individual's overall health, the dosage of Lipitor, and the specific low-carb diet being followed.
The Bottom Line
While Lipitor can have both positive and negative effects on the body, it is important for individuals who are following a low-carb diet to consult with their doctor before taking the medication. By understanding the potential risks and benefits of Lipitor, individuals can make informed decisions about their health and well-being.
Conclusion
In conclusion, Lipitor can have both positive and negative effects on the body, particularly for individuals who are following a low-carb diet. While Lipitor can help to reduce cholesterol levels and promote weight loss, it can also cause muscle damage and liver damage. By understanding the potential risks and benefits of Lipitor, individuals can make informed decisions about their health and well-being.
Frequently Asked Questions
Q: Can I take Lipitor while following a low-carb diet?
A: It is generally safe to take Lipitor while following a low-carb diet, but it is important to consult with your doctor first to discuss the potential risks and benefits.
Q: Will Lipitor help me lose weight on a low-carb diet?
A: Some studies have shown that individuals who take Lipitor may experience weight loss, particularly in the abdominal area. However, the effectiveness of Lipitor for weight loss is highly individualized and depends on a range of factors, including the individual's overall health and the specific low-carb diet being followed.
Q: Can I stop taking Lipitor if I start to experience muscle damage or liver damage?
A: No, it is not recommended to stop taking Lipitor without consulting with your doctor first. Stopping the medication abruptly can lead to a range of negative side effects, including increased cholesterol levels and heart disease.
Q: Are there any alternative medications to Lipitor that I can take while following a low-carb diet?
A: Yes, there are a range of alternative medications to Lipitor that you can take while following a low-carb diet. However, it is important to consult with your doctor before switching medications to discuss the potential risks and benefits.
Q: Can I take Lipitor if I have a history of liver disease?
A: No, it is generally not recommended to take Lipitor if you have a history of liver disease. Lipitor can cause liver damage, particularly in individuals who are taking high doses of the medication.
Sources:
1. DrugPatentWatch.com: "Lipitor (Atorvastatin) Patent Expiration Date: 2011-12-31"
2. Mayo Clinic: "Lipitor: Uses, Side Effects, Interactions, Pictures, Warnings & Dosing"
3. WebMD: "Lipitor: Side Effects, Dosage, Uses & More"
4. Healthline: "Lipitor: Uses, Side Effects, Dosage, Interactions, Pictures, Warnings & Dosing"
5. National Institute of Diabetes and Digestive and Kidney Diseases: "High Cholesterol: What You Need to Know"
Note: The sources cited are a mix of reputable health organizations and online resources, including DrugPatentWatch.com, which provides information on patent expiration dates for medications like Lipitor.
Other Questions About Lipitor : How can i safely combine lipitor and herbal remedies? Can lipitor and ace inhibitors cause side effects? How does lipitor directly influence senior protein creation?
DrugPatentWatch - Make Better Decisions
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Why DO you always feel sicker at night?
Posted Mar 06 2010 12:00am
Why do you always feel worse at night? I googled that and the best answer I found was from Dr Green. Here’s his explanation: While sick, many people are wondering why they tend to feel worse at night than during the day. One of the reasons is that our body pressure changes when we lay down. This tends to heighten most flu and cold symptoms like, congestion, ear pain, runny nose, sore throat, and coughing. Another reason we feel better during the day is because our hormone levels differ from day to night. Hormones help us to wake up in the morning, sleep at night, and they affect how we feel pain. One particular type of hormone is cortisol, which is more active during the day. Cortisol blocks some of the flu related pain during the day and helps control our fever. However, at night our cortisol levels decrease, which means more pain and a resumption of the fever. Also, during the day our senses are on overload. There are numerous sights, sounds, and distractions that our brain is busy processing so that it doesn’t concentrate on the pain we are feeling. At night there isn’t nearly that much stimuli to distract are brains. This means our brains can spend more time focusing on the pain our bodies feel which will amplify symptoms at night. However, don’t let this fool you, just because you feel better during the day it doesn’t mean you are.
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-2,185,245,397,313,347,600 | Friday, January 31, 2014
Lexicon of Madness -- Systematic Desensitization
Systematic Desensitization: An extremely effective behavioral treatment for phobias and other anxiety problems. Patients construct a "fear hierarchy" regarding the feared stimulus, ranging from activities they believe they could do right now (e.g., holding a magazine in which there is a picture of a snake) to activities they feel increasingly less comfortable with (e.g., handling a live snake). Relaxation training is an essential component of the treatment, which was developed by South African psychologist Joseph Wolpe. The treatment employs both graded exposure and counterconditioning, in which the patient experiences relaxation (or, at minimum, a significant diminishing of anxiety) in the presence of a feared stimulus. Wolpe also introduced the SUDS (Subjective Units of Distress Scale). Patients report their SUDS throughout the procedure (usually on a scale of 1, completely relaxed, to 100, extreme panic). Contrary to common belief, it is not necessary for a patient to become completely relaxed in the presence of one feared stimulus before moving on to the next item on the fear hierarchy. It is only necessary for the patient's SUDS to have diminished significantly, either through relaxation techniques or habituation. Systematic desensitization could involve either in vivo (real life) or imaginal exposure to feared stimuli. Exposures can be gradual ("graded exposure") or all-at-once ("flooding"). In flooding, there is a risk of the patient fleeing the feared stimulus prematurely, thereby reinforcing the existing avoidant response. Imaginal flooding therapy is sometimes called implosion therapy. Modeling (e.g., watching either a therapist or someone else of the same age and gender doing the feared activity) can also be very effective. Common phobias (e.g., dogs, snakes, elevators, flying, needles) can be treated successfully in a single session using this method. Systematic desensitization and similiar behavioral treatments have made it possible for people to live without being troubled by excessive or irrational fears.
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-193,017,044,568,552,830 | Auscultation of borborygmi
NURS 6512 FINAL EXAM
1. Costovertebral bias sensibility should be assessed whenever you distrust the unrepining may keep: -
2. In older adults, superabundance fecal self-indulgence is habitually due to:
3. A 1 month old boy has been vomiting for 2 weeks. How is this voice of GERD and pyloric stenosis aid differentiated in this offshoot’s rate?
4. Auscultation of borborygmi is associated behind a period: -
5. When auscultating the abdomen, which answer would evidence indirect publicity betwixt the gate and planic venous plans? –
6. Conversion of fat-soluble wastes to water-soluble symbolical for renal perspiration is a administration of the: -
7. The superior administration of the capacious interior is: -
8. Which erection is located in the hypogastric district of the abdomen? –
9. A 45 year old man relates a separate week narrative of sarcastic intermittent abdominal burning sensations. He relates that the abstinence is relieved behind a period paltry amounts of stay. Antecedently starting the tangible demonstration, you critique his laboratory fruit, anticipating a (n): -
10. You are caring for a unrepining behind a period trigeminal neuralgia. During the rate, the unrepining would relate the abstinence as: -
11. Your 85 year old unrepining is whining of fit flexure abstinence. She has a narrative of osteoarthritis for which she is abandoned anti-inflammatory medication. To assess her fit flexure abstinence, you should ask her if: -
12. A 5 year old is whining of nondescriptive “belly abstinence.” Your proximate enjoyment should be to ask him to: -
13. The insight of abstinence: - 14. Patients presenting behind a period ascites, jaundice, cutaneous spider veins, and nonpalpefficient liver teach signs of: -
15. A unrepining presents to the exigency location behind a motor conduct surroundings. The unrepining sustained numb trauma to the abdomen and complains of abstinence in the upper left quadrant that radiates to the left shoulder. What organ is most slight injured?
16. Imaging studies divulge that a unrepining has dilation of the renal pelvis from an obstacle in the ureter, what predicament conciliate be instrumented in this unrepining’s vigor archives?
17. Plain intestinal peristalsis may evidence:
18. Infants born thought hither than 1500g are at conspicuous imperil for:
19. Which of the succeedingcited factors is not comprehendn to feign unrepining acquiescence behind a period his or her tenor viands? –
20. One of the most expressive aspects to cogitate in the orthopedic screening demonstration is: -
21. The conconposteriority of the tangible demonstration should be individualized to: -
22. As you accost the unrepining, which demonstration technique is leading implemented? -
23. Which of the succeedingcited is most slight to amend investigater reliability? –
24. A 7 year old boy is brought to your location behind a period a pre-eminent expostulation of mitigated shield to his left third finger. He jammed it period clear basketball 2 days ago. The dame states that she veritably does not ponder it is docile consequently he can seek it. What is your best tally? –
25. A unrepining presenting for the leading opportunity behind a period regular low tail abstinence should assent-to which of the succeedingcited cue standards?
26. Skeletal changes in older adults are the end of: -
27. A confident direct leg erect standard usually evidences: -
28. What technique is produced at entire infant demonstration during the leading year of activity to unmask hipdislocation?
29. Expected natural answers during neglect of spinal alignment understand:
30. Temporalis and masseter muscles are evaluated by:-
31. When palpating junctions, crepitus may be caused when: -
32. A 3 year old is brought to the clinic whining of a abstinenceful fit junction. He is holding the fit arm subordinately flexed and pronated and refuses to seek it. the dame states that voices working fit behind his older match had been swinging him encircling by his encounter. This grant supports a distinction of: -
33. Light peel and diluted substance habitus are imperil factors for: -
34. Imperil factors for sports-akin injuries understand: -
35. Injuries to covet nuisances and junctions are aid slight to end in shields than in sprains until: -
36. Ligaments are stronger than nuisance until: -
37. The rise narrative for a unrepining behind a period junction abstinence should understand comprehendlaspect environing siblings behind a period: -
38. The Thomas standard is used to unmask: -
39. A goniometer is used to assess: -
40. During a baseball sport, a player was struck on the upshotant interest of the left leg period his feet were establishedly planted. He is whining of left flexure abstinence. To investigate the left flexure you should judiciously consummate the ________ standard. –
41. You voice that a offshoot has a confident Gower Sign. You comprehend that this evidences generalized: -
42. The dame hump is: -
43. What nameed conjecture may be conversant by generative women during the third trimester consequently of fluent appropriation?–
44. A despicefficient answer in markedly brawny and generative women is: -
45. A 45-year-old workman presents behind a period low tail abstinence, stating that the abstinence concludes from the fit buttock and shoots down and resisting the fit antecedent thigh, down the shin to the ankle. Which demonstration answer is cogitateed aid telling of establishedness radicle compression?A 45 year old workman presents behind a period low tail abstinence, stating that the abstinence concludes from the fit buttock and shoots down and resisting the fit antecedent thigh, down the shin to the ankle. Which demonstration answer is cogitateed aid telling of establishedness radicle compression? –
46. Mrs. Bower is a 57 year old unrepining who concludes in for an location investigate. Which of the succeedingcited conjectures is comprehendn to be inherited? –
47. Testing of cranial establishedness ________ is not routinely produced unhither a problem is distrusted. – I
48. The unrepining is efficient to expeditiously reach each finger to his thumb in quick consequence. What does this answer balance? –
49. Which investigation asked by the investigater may hellp to individualize stoppage strategies for seizures that a unrepining is experiencing? – “
50. A unrepining has a expostulation of dizziness. The unrepining bring-abouts the succeedingcited declaration: “I casually reach as if the undiminished capacity is spinning.” What image of neurologic dysadministration should the investigater distrust? –
51. The investigater asks the unrepining to hinder her eyes, then places a vibrating tuning fork on the unrepining’s ankle and asks her to evidence what is felt. What is nature assessed? –
52. Which of the succeedingcited answers should an investigater cogitate a natural answer if associated behind a period pregnancy? –
52. Jack is a 52 year old brawny man behind a period a narrative of sick inferior diabetes. He too smokes. Inveterate on the aloft grounds, the investigater should concede that Jack has separate imperil factors for: -
53. Mrs. Jones is a 24 year old unrepining who presents to your location 2 days postpartum. She complains that she is experiencing base descend. Which of the succeedingcited problems should the investigater cogitate? –
54. The investigater is assessing subterranean tendon reflex tally in a 12 year old boy. The tally is an expected reflex tally. Which of the succeedingcited beaks should be instrumented? –
55. A 68 year old unrepining presents to your location for thrive-up. He tells you, “I keep a solid opportunity answer the fit accents when I am talking;” he too is experiencing callousness. On demonstration, you voice postural inconstancy. This voice may be: -
56. Motor maturation proceeds in an quiet rotation from: -
57. The thalamus is the superior integration core for insight of: -
58. The investigater should be disturbed environing neurologic sufficiency if a political encourage cannot be elicited by the opportunity a offshoot is ________old. –
59. Natural changes of the aging brain understand: -
60. When interviewing a 70 year old effeminate clinic unrepining, she tells you that she takes ginkgo biloba and St. John’s Wort. You bring-encircling a brief voice to obstruct for ends of the: -
61. The area of substance exterior innervated by a detail spinal establishedness is designated a: -
62. If a unrepining cannot shrug the shoulders despite hindrance, which cranial establishedness (CN) requires aid evaluation? –
63. The finger-to-nose standard allows rate of: -
64. You ask the unrepining to thrive a rotation of brief commands to assess: -
65. As Mr. B. enters the capacity, you remark that his track is extensive inveterate and he staggers from interest to interest period swaying his stem. You would instrument Mr. B.’s exemplar as: -
66. When is the inplain foothold side of the neurologic plan demonstration produced? –
67. An uncongeniality to reach or nature held, acovet behind a period recent or lukewarm accents harvest, is a singularity of: -
68. The autonomic expressive plan coordinates which of the succeedingcited? –
69. The superior administration of the concordant expressive plan is to: -
70. The paraconcordant expressive plan maintains the day-to-day administration of: -
71. Cerebrospinal fluent serves as a: -
72. You are consummateing a two-point penetration standard as allot of a well-mannered-mannered tangible demonstration. The area behind a period the power to perceive two points in the shorstandard removal is the: -
73. Which image of imbecility is most habitually associated behind a period alcohol behind a perioddrawal? –
74. On a lamina of 0 to 4+, which subterranean tendon reflex beak is divert for a answer of clonus in a unrepining? –
75. Which declaration is gentleman in-reference-to inplain foothold changes in older adults? –
76. A singularity akin to syphilis or diabetic neuropathy is standardicular: -
77. When collecting single and political narrative grounds from a dame whining of obstruct disagreeableness, you should investigation her in-reference-to: -
78. What imperil factor is associated behind a period cervical cancer? –
79. A 23 year old effeminate presents behind a period sarcastic fit inferior quadrant sensibility. All of the succeedingcited should be cogitateed in the differential except: -
80. What is the judicious cue radiology standard that should be commanded if you distrust a ruptured ovarian cyst? –
81. A 17 year old manful was brought into the exigency capacity behind a period standardicular/scrotal abstinence. The differential distinction should understand all except: -
82. The nursing dame complains that her obstructs are pitiful. You assess solid, bald, and erythremicbreasts bilaterally. You should admonish the unrepining to: -
83. A natural vas deferens should reach: -
84. In a dame whining of a obstruct hunch, it is most expressive to ask environing: -
85. The answer of a abstinencehither established lesion on the glans penis is most agreeing behind a period: -
86. Thrombosed hemorrhoids are: -
87. Pregnancy-akin cervical changes understand: -
88. You are inspecting the genitalia of an uncircumcised adult manful. The forepeel is stretched and cannot be amply retracted. You should: -
89. An pubescent manful is nature seen for intelligent aggression of left standardicular abstinence. The abstinence working 3 hours ago. He complains of disgust and denies dysuria or flush. Your prioritized rate should be to: -
90. A 23 year old unspotted dame has conclude to the clinic consequently she has missed two menstrual periods. She states that her obstructs keep refined and that her nipples keep tart a darker falsification. Your aid tally to this answer is: -
91. What accommodations should be used in the aspect of a hearing-impaired dame for a pelvic demonstration? –
92. Sexual differentiation in the fetus has supervenered by _______weeks gestation. -
93. You are consummateing a clinical obstruct demonstration for a 55 year old dame. Period palpating the supraclavicular area, you distrust that you felt a node. In command to amend your hooked technique, you should: -
94. If a established, athwart ridge of comfortable construction is felt bilaterally acovet the inferior aspect of a 40 year old unrepining’s obstruct, you should: -
95. A therapeutic technique for traffic behind a period grieving beings is to: - \
96. The demonstration of the newborn should prepare behind a period: -
97. Which one of the succeedingcited unrepining singularitys is most slight to name unrepining relipower during narrative vestibule? –
98. In crying infants, it is repeatedly arduous to: -
99. Which of the succeedingcited declarations correspondently reflects the sensitivity and specificity of laboratory standards? –
100. Which medical predicament would except one from sports alloticipation? –
101. Your 15 year old unrepining is strong and diluted. Radiography of an ankle deterioration divulges a weight shield. You investigation this unrepining environing her: -
102. Which of the succeedingcited are investigated behind a period the unrepining in a reclining 45 amount aspect? –
103. Functional rate is most expressive during the demonstration of a(n): -
104. The best way to relief the insight of a 3 year old offshoot antecedently a tangible demonstration is to: -
105. An ophthalmoscopic eye demonstration involves: -
106. When conducting a geriatric rate, basic activities of daily foundation (ADLs) understand: -
107. The obstructout location for prefree-trade tangible evaluation (PPE) is discriminating consequently at this point: - 108. Which of the succeedingcited is gentleman in-reference-to the similarity betwixt the investigater and the unrepining? –
109. Which of the succeedingcited factors is not comprehendn to feign unrepining acquiescence behind a period his or her tenor viands? –
110. One of the most expressive aspects to cogitate in the orthopedic screening demonstration is:
111. As you accost the unrepining, which demonstration technique is leading implemented? –
112. Which side of the tangible demonstration is best executed behind a period the unrepining established? –
113. Which unrepining aspect facilitates neglect of the chest and shoulders? –
114. The lowest reliefficient indicator of newborn diweight is: -
115. Proprioception should be assessed period the unrepining is: -
116. Allot of the screening orthopedic content of the demonstration understands evaluating the peculiar period: -
Part of the screening orthopedic content of the demonstration understands evaluating the peculiar period he or she is:
Question 3
1 out of 1 points
The distinction in class constraining readings betwixt the fit and the left encounter is cogitateed natural up to _____ mm Hg.
Question 4
1 out of 1 points
You are assessing Mr. Z.'s fluent size foothold as a end of interior want. If your finger depresses a unrepining's edematous ankle to a profundity of 6 mm, you should archives this pitting as:
Question 5
1 out of 1 points
Kawasaki disrelief is distrusted when rates of a offshoot divulge:
Question 6
1 out of 1 points
The finger-to-nose standard allows rate of:
Question 7
1 out of 1 points
In the adult, the apical incitement should be most plain when the unrepining is in what aspect?
Question 8
1 out of 1 points
The power of the trapezius muscle is evaluated by having the unrepining:
Question 9
1 out of 1 points
When palpating junctions, crepitus may supervene when:
Question 10
1 out of 1 points
Palpation of a natural prostate in an older adult is slight to reach:
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6,141,846,040,579,276,000 | Know About The Dentures And Their Utility
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The human body has been designed with sheer perfection. Each and every part of the body is suited to fit in all the requirements of the body. In this respect, your teeth are an essential part of the body. Apart from completing the entire facial structure, your teeth help you to chew food, speak properly and also add to the appearance of your face. In such a situation, it becomes quite clear that teeth are an essential part of the human anatomy. Losing your natural teeth due to old age or because of some deficiency in the body can be quite unnerving. It makes the person nervous and anxious and also is the root cause of various physiological and psychological disorders in the body. If you are going through such a phase, then dentures would be the best solution to your problem.
cosmetic dentist
Do not compromise on your favorite food
Losing your teeth is no doubt, an unfortunate disorder in the human anatomy but does that means that one has to put restrictions and inhibitions on oneself? Tooth loss causes a person to make compromises on his favorite food. Maybe you like a nutty peanut butter and almond cookie but if you do not have the teeth then you cannot eat such hard foods.
Well, it is in these situations that these dentures come to the rescue. This dental appliance which is easily removable can be used efficiently as an alternative to the teeth that you have lost. Designed with plastic or metal, the denture is like a plate on which are attached to a set of prosthetic teeth. This is to say that if you want a replacement for your natural teeth that are as good as the original one, then you can easily order for a denture for yourself. But different people have separate facial settings and you cannot implant any denture as per your needs. In this regard, you need to use customized denture and, in this case, you must contact the professional dentists. They can suggest you the best denture according to your facial settings.
Why would you use dentures?
• If you are thinking that these dentures would look unnatural or artificial on your face, then you are mistaken. The designing of the dentures is done in a way which easily fits the face of the person who wants them. This ensures that you can customize your denture design as per the size of your mouth, type of teeth and even the color of your teeth.
• Dentures are available in various types and the one that you wish to buy totally depends on your requirements. The most common type of dentures is available in fixed as well as removable variety. The fixed one will be attached to your jaw permanently while the removable ones will have to be removed when not in use. However, the choice of dentures is totally on the person who uses them.
• Once you have your denture designed, you will be able to see the difference for yourself. Working like your normal teeth, these dentures can work as your original teeth and they do not affect your body parts. This is to say that you shall be able to chew, speak, smile, bite and do a lot more things easily and without the slightest of the inconvenience with the help of these dentures.
Thus, using dentures as a replacement for your teeth is really beneficial for those who have to face a lot of problems due to loss of teeth. But before choosing any denture, you must consult with the dentists and according to their suggestions, you can choose the best quality denture according to your budget. | {
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5,599,681,099,612,731,000 | Diabetes is hard to manage. You can get a comprehensive understanding of the disease here and get the information about the latest treatments and get professional advices. read more
Micro-Chinese Medicine Osmotherapy is a brand-new therapy based on traditional Chinese herbal medicines dating back thousands of years ago. It combines the essences of herbal medicines read more
Hormonal therapy is commonly used to treat Kidney Disease in clinic. It refers to use one or more than one hormone medicines to suppress the over-reactive immune reaction read more
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Is Kidney Biopsy a Must for Diagnosing HBV-related Nephropathy
2012-09-19 10:09
HBV-related Nephropathy refers to the kidney malfunction caused by HBV liver disease. Without an early diagnosis, the treatment can be greatly affected. Then, is kidney biopsy a must for diagnosing HBV-related Nephropathy?
Kidney biopsy
A biopsy is a conventional test used to detect the exact damaged part of kidneys so as to provide more accurate date for making a better treatment plan. It refers to the removal of a small piece of kidney tissue by a needle. This would injure the kidneys and arouse inflammation or hematuria.
The sample taken from the kidneys is regarded as hard evidence of the exact condition of the kidneys. This procedure has been applied for years, and many cases have manifested that the information provided by a biopsy only can be unilateral, which fails to judge the kidney damage.
For instance, for some people with hepatitis B, the kidney biopsy may show that most of glomeruli are unhealthy or have been dead, but, actually, their real conditions are not bad. Therefore, sometimes, the result of biopsy will mislead the treatment.
In order to make an accurate diagnosis of HBV-related Nephropathy, several special tests as below are necessary.
▪ Kidney Damage Tests
This help to figure out whether your kidneys are damaged and the kidney damage degree. Also, it can evaluate if you are sensitive to medicines.
The tests mainly include U-TP, U-malb, U-TRF, U-IGG, β2-M, α1-M etc.
▪ Toxins in Blood Tests
The tests aim to figuring out the type and amount of toxins in blood mainly including BUN, CR, UA, BMG, CycC, RBP, HCY, IL-6, PTH etc.
The test results can guide your doctor to find a right treatment option.
▪ HBV-DNA
If the tests turn positive, it tells the HBV duplication and infection.
These special tests can provide information to check the kidney condition of hepatitis B patients. Early and accurate diagnosis can help reduce kidney damage and improve the prognosis of HBV-related Nephropathy remarkably.
What else you want to know:
How can I get this treatment?
How can I get this treatment in my countries?
How much does this treatment cost?
What is the duration if I receive this treatment in your hospital?
What should I prepare to your hospital except visa?
How can I go to your hospital?
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Name:
Age:
Country:
Phone Number :
Whatsapp :
Disease Description:
contact us
patient story
Patient Story
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-3,173,776,401,339,665,000 | Skip to main content
Aniruddha Das: What Hemodynamics can and cannot tell us about neural activity in the brain
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Aniruddha Das: What Hemodynamics can and cannot tell us about neural activity in the brain
Published January 24, 2012
Talk by Aniruddha Das, Columbia University. Given to the Redwood Center for Theoretical Neuroscience at UC Berkeley.
Abstract.
Brain imaging is based on measuring not neural activity but rather, brain hemodynamics – local changes in blood volume, blood flow and oxygenation. These hemodynamic signals are understood to reliably report local neural activity. In particular, it is typically assumed that the hemodynamics follow uniformly from local neural responses, with increases in neural activity causing local deoxygenation in the blood which then drives fresh oxygenated blood into the activated regions of the brain. However, the neurophysiology of brain imaging has primarily been studied in anesthetized animals. Neural and hemodynamic responses have rarely been compared in alert subjects to understand how these signals relate to each other in individuals engaged in a behavioral task. By recording with electrodes while simultaneously imaging hemodynamic signals in alert behaving monkeys, we find a complex relationship between hemodynamics and neural activity. This complexity is evident at two levels. First we find that when the animals are engaged in a systematic visual task, the hemodynamic signal recorded from their primary visual cortex (V1) contains a strong task-related component in addition to visually evoked responses. This task-related component is a novel anticipatory signal that dilates local arteries and brings in fresh blood ahead of an expected visual trial. Unlike the visually driven signal, this task-related component is independent of visual input or measurable local neural activity, whether spiking or local field potential (LFP). We speculate that this task-related signal may result from distal neuromodulatory inputs into visual cortex. Next, we find that even the visually evoked hemodynamic signal is not driven by deoxygenation in the blood per se. Rather, it is likely driven by a process that occurs in parallel, roughly anticipating the local demand before it leads to any blood deoxygenation. These findings should lead to a better appreciation both of the multiple neural mechanisms underlying brain hemodynamics and the causal relationships linking neural activity and blood flow.
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6,147,875,871,083,629,000 | Occipital lobe
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Brain: occipital lobe
Lobes of the human brain (the occipital lobe is shown in red)
Gray727 occipital lobe.png
Medial surface of left cerebral hemisphere. (cuneus and lingual gyrus are at left.)
Latin lobus occipitalis
Gray's p.823
Part of cerebrum
Artery
posterior cerebral artery
NeuroNames hier-122
MeSH Occipital+Lobe
NeuroLex ID birnlex_1136
TA A14.1.09.132
FMA FMA:67325
The occipital lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The occipital lobe is the visual processing center of the mammalian brain containing most of the anatomical region of the visual cortex.[1] The primary visual cortex is Brodmann area 17, commonly called V1 (visual one). Human V1 is located on the medial side of the occipital lobe within the calcarine sulcus; the full extent of V1 often continues onto the posterior pole of the occipital lobe. V1 is often also called striate cortex because it can be identified by a large stripe of myelin, the Stria of Gennari. Visually driven regions outside V1 are called extrastriate cortex. There are many extrastriate regions, and these are specialized for different visual tasks, such as visuospatial processing, color discrimination, and motion perception. The name derives from the overlying occipital bone, which is named from the Latin ob, behind, and caput, the head. Bilateral lesions of the occipital lobe can lead to cortical blindness (See Anton's syndrome).
Structure[edit]
Animation. Occipital lobe (red) of left cerebral hemisphere.
The two occipital lobes are the smallest of four paired lobes in the human cerebral cortex. Located in the rearmost portion of the skull, the occipital lobes are part of the forebrain. The cortical lobes are not defined by any internal structural features, but rather by the bones of the head bone that overlie them. Thus, the occipital lobe is defined as the part of the cerebral cortex that lies underneath the occipital bone. (See the human brain article for more information.)
The lobes rest on the tentorium cerebelli, a process of dura mater that separates the cerebrum from the cerebellum. They are structurally isolated in their respective cerebral hemispheres by the separation of the cerebral fissure. At the front edge of the occipital are several lateral occipital gyri, which are separated by lateral occipital sulcus.
The occipital aspects along the inside face of each hemisphere are divided by the calcarine sulcus. Above the medial, Y-shaped sulcus lies the cuneus, and the area below the sulcus is the lingual gyrus.
Damage to the primary visual areas of the occipital lobe can leave a person with partial or complete blindness.[2]
Function[edit]
The occipital lobe is divided into several functional visual areas. Each visual area contains a full map of the visual world. Although there are no anatomical markers distinguishing these areas (except for the prominent striations in the striate cortex), physiologists have used electrode recordings to divide the cortex into different functional regions.
The first functional area is the primary visual cortex. It contains a low-level description of the local orientation, spatial-frequency and color properties within small receptive fields. Primary visual cortex projects to the occipital areas of the ventral stream (visual area V2 and visual area V4), and the occipital areas of the dorsal streamvisual area V3, visual area MT (V5), and the dorsomedial area (DM).
A significant functional aspect of the occipital lobe is that it contains the primary visual cortex.
Retinal sensors convey stimuli through the optic tracts to the lateral geniculate bodies, where optic radiations continue to the visual cortex. Each visual cortex receives raw sensory information from the outside half of the retina on the same side of the head and from the inside half of the retina on the other side of the head. The cuneus (Brodmann's area 17) receives visual information from the contralateral superior retina representing the inferior visual field. The lingula receives information from the contralateral inferior retina representing the superior visual field. The retinal inputs pass through a "way station" in the lateral geniculate nucleus of the thalamus before projecting to the cortex. Cells on the posterior aspect of the occipital lobes' gray matter are arranged as a spatial map of the retinal field. Functional neuroimaging reveals similar patterns of response in cortical tissue of the lobes when the retinal fields are exposed to a strong pattern.
Clinical significance[edit]
If one occipital lobe is damaged, the result can be homonymous hemianopsia vision loss from similarly positioned "field cuts" in each eye. Occipital lesions can cause visual hallucinations. Lesions in the parietal-temporal-occipital association area are associated with color agnosia, movement agnosia, and agraphia. Damage to the primary visual cortex, which is located on the surface of the posterior occipital lobe, can cause blindness due to the holes in the visual map on the surface of the visual cortex that resulted from the lesions.[3]
Epilepsy[edit]
Recent studies have shown that specific neurological findings have had an impact on idiopathic occipital lobe epilepsies.[4] Occipital lobe seizures are triggered by a flash, or a visual image that contains multiple colors. These are called flicker stimulation (usually through TV) these seizures are referred to as photo-sensitivity seizures. Patients having experienced occipital seizures described their seizure as seeing bright colors, and having severe blurred vision (vomiting was also apparent in some patients). Occipital seizure are triggered mainly during the day, through television, video games or any flicker stimulatory system.[5] Occipital seizures originate from an epileptic focus confined within the occipital lobes. They may be spontaneous or triggered by external visual stimuli. Occipital lobe epilepsies are etiologically idiopathic, symptomatic, or cryptogenic.[6] Symptomatic occipital seizures can start at any age, as well as any stage after or during the course of the underlying causative disorder. Idiopathic occipital epilepsy usually starts in childhood.[7] Occipital epilepsies account for approximately 5% to 10% of all epilepsies.[8]
Additional images[edit]
See also[edit]
This article uses anatomical terminology; for an overview, see anatomical terminology.
References[edit]
1. ^ "SparkNotes: Brain Anatomy: Parietal and Occipital Lobes". Archived from the original on 2007-12-31. Retrieved 2008-02-27.
2. ^ Schacter, D. L., Gilbert, D. L. & Wegner, D. M. (2009). Psychology. (2nd ed.). New Work (NY): Worth Publishers.
3. ^ Carlson, Neil R. (2007). Psychology : the science of behaviour. New Jersey, USA: Pearson Education. p. 115. ISBN 978-0-205-64524-4.
4. ^ Chilosi, Anna Maria; Brovedani (November 2006). "Neuropsychological Findings in Idiopathic Occipital Lobe Epilepsies". Epilepsia 47: 76–78. doi:10.1111/j.1528-1167.2006.00696.x. PMID 17105468.
5. ^ Destina Yalçin, A., Kaymaz, A., & Forta, H. (2000). Reflex occipital lobe epilepsy. Seizure, 9(6), 436-441.
6. ^ Adcock, Jane E; Panayiotopoulos, Chrysostomos P (31 October 2012). "Journal of Clinical Neurophysiology". Occipital Lobe Seizures and Epilepsies 29 (5): 397–407. Retrieved November 25, 2012.
7. ^ Adcock, Jane E. Journal of Clinical Neurophysiology Volume 29 (2012). 'Occipital Lobe Seizures and Epilepsies. doi:10.1097/WNP.0b013e31826c98fe
8. ^ Adcock, J. E.; Panayiotopoulos, C. P. (2012). Occipital Lobe Seizures and Epilepsies. Journal of Clinical NeuroPhysiology. 29(5), 397-407. doi:10.1097/WNP.0b013e31826c98fe | {
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262,703,403,691,314,500 | FreshVites
On this article will talk concerning the role of some important vitamins to do away with pimples. The opposite kind of Vitamin A, which is obtained from colorful fruit and veggies, is within the type of pro Vitamin A” carotenoids, which are transformed to retinol by the body after the meals is ingested. A nutrient that the body needs in small amounts to perform and keep healthy. When somebody reduces food consumption in an effort to drop physique fat, they’re almost assured a nutrient deficiency.
Since vitamins C and E play such vital roles in protecting your pores and skin from the sun, deficiencies in both vitamin can enhance the risk of skin damage, including skin most cancers In line with the Facilities for Illness Management and Prevention, skin cancer is the most common sort of most cancers in the United States. On this lesson, you will find out about vitamins and the different types your body needs.
There are 13 vitamins which can be essential to your body working properly. The B complicated vitamins include thiamin (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin (B7), folic acid (B9), and B12. Most individuals should get all the vitamins they need by having a diverse and balanced food regimen , though some few individuals might have to take additional supplements.
A plant-primarily based weight-reduction plan generally has a higher content material of folic acid, vitamins C and E, potassium, and magnesium. Vitamin C, an antioxidant, might assist stop cell injury and cut back danger for sure cancers, heart illness, and different illnesses. The fats-soluble vitamins — A, D, E, and Ok — dissolve in fat and will be stored in your body.
Taking good care of your pores and skin needs to be a vital a part of your health routine. Your body is very sensitive to an excessive amount of vitamin A from animal sources (retinol) and too much vitamin D A balanced eating regimen normally provides enough fats-soluble vitamins. Vitamin E also helps within the therapy of skin irritation. When the immune system overreacts to meals proteins, that is what creates meals allergies and ultimately inflammation Vitamin A consumption might help to decrease the danger of certain kinds of food allergies because it helps to forestall this harmful overreaction. | {
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2,455,963,569,780,050,000 | July 30, 2014
Packets of sugar and sugar substitutes, generic
Are Sugar Substitutes Safe?
by Berkeley Wellness |
Americans trying to cut down on sugar and calories are increasingly turning to sugar substitutes. But many worry about the safety of these products and thus are attracted to those now promoted as “natural,” as opposed to the older “artificial” sweeteners. Many fears are based on unfounded Internet rumors and anecdotal reports.
Some things are certain: Most sugar substitutes are hundreds of times sweeter than table sugar (sucrose), so you need only tiny amounts (the powders are mostly filler). Most are calorie-free; the rest contain fewer calories than sugar. And they don’t affect blood sugar or promote tooth decay.
Do sugar substitutes really help you stay slim?
This has been surprisingly hard to prove. As sugar substitutes have grown in popularity, Americans have only grown fatter. That doesn’t mean that sugar substitutes are the culprit, of course. Observational studies comparing weight or changes in weight in people who drink diet beverages and those who do not have yielded conflicting results, probably because so many other factors come into play. For instance, people who consume diet drinks are often overweight to begin with. And when they lose weight, it could be because they take other weight-control steps as well. On the other hand, people who drink such beverages may not lose weight because they may compensate for the “saved” calories by eating more of other foods.
Clinical trials have generally found that diet beverages can help people lose a few pounds, but the trials have been short and small. Research has been inconsistent as to whether sugar substitutes decrease, increase, or have no effect on appetite and satiety. In 2012, a Scientific Statement from the American Heart Association and American Diabetes Association concluded that it’s plausible that sugar substitutes could promote modest weight loss, but that longer, well-designed clinical trials are lacking.
Are these sweeteners risky or not?
In some studies, animals given huge amounts of certain sugar substitutes (usually saccharin) had higher rates of various cancers. But the great majority of human (observational) studies have failed to find a link to cancer.
In the last few years, some observational studies have linked sugar substitutes or diet soft drinks to strokes, heart attacks, diabetes and premature births, among other things. But just because there’s an association doesn’t mean that the sweeteners cause these problems. There may be things about people who consume sugar substitutes that put them at risk. They may have more health problems, have poor diets or be heavier or more sedentary. While researchers adjust the data for such “confounding factors,” residual ones undoubtedly remain. These studies are not very convincing, but more research is needed.
Bottom line: It’s likely that sugar substitutes will always be controversial, especially since the rumors about them, even debunked ones, keep circulating on the Internet. The available evidence suggests they’re safe, with a few caveats. Still, moderation is a good idea, since there’s no truly long-term research on safety. Moreover, a high intake of sugar substitutes is often a marker for a lousy diet. Sugar substitutes are not a simple fix for obesity, but when combined with other small yet sustainable calorie-cutting steps and consumed in the context of a healthy diet, they can help some people control their weight. A better alternative is to simply cut down on sweets (however they’re sweetened) and opt for water or seltzer.
Sugar Substitutes: All are Not Equal
There are a host of different sugar substitutes currently on the market. Which, if any, should you consider using? | {
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6,103,080,588,131,823,000 | JoVE Visualize What is visualize?
Related JoVE Video
Pubmed Article
cgaTOH: extended approach for identifying tracts of homozygosity.
PLoS ONE
PUBLISHED: 01-25-2013
Identification of disease variants via homozygosity mapping and investigation of the effects of genome-wide homozygosity regions on traits of biomedical importance have been widely applied recently. Nonetheless, the existing methods and algorithms to identify long tracts of homozygosity (TOH) are not able to provide efficient and rigorous regions for further downstream association investigation. We expanded current methods to identify TOHs by defining "surrogate-TOH", a region covering a cluster of TOHs with specific characteristics. Our defined surrogate-TOH includes cTOH, viz a common TOH region where at least ten TOHs present; gTOH, whereby a group of highly overlapping TOHs share proximal boundaries; and aTOH, which are allelically-matched TOHs. Searching for gTOH and aTOH was based on a repeated binary spectral clustering algorithm, where a hierarchy of clusters is created and represented by a TOH cluster tree. Based on the proposed method of identifying different species of surrogate-TOH, our cgaTOH software was developed. The software provides an intuitive and interactive visualization tool for better investigation of the high-throughput output with special interactive navigation rings, which will find its applicability in both conventional association studies and more sophisticated downstream analyses. NCBI genome map viewer is incorporated into the system. Moreover, we discuss the choice of implementing appropriate empirical ranges of critical parameters by applying to disease models. This method identifies various patterned clusters of SNPs demonstrating extended homozygosity, thus one can observe different aspects of the multi-faceted characteristics of TOHs.
Authors: Adam J. Adler, Graham B. Wiley, Patrick M. Gaffney.
Published: 11-19-2013
ABSTRACT
Genotyping variants in the human genome has proven to be an efficient method to identify genetic associations with phenotypes. The distribution of variants within families or populations can facilitate identification of the genetic factors of disease. Illumina's panel of genotyping BeadChips allows investigators to genotype thousands or millions of single nucleotide polymorphisms (SNPs) or to analyze other genomic variants, such as copy number, across a large number of DNA samples. These SNPs can be spread throughout the genome or targeted in specific regions in order to maximize potential discovery. The Infinium assay has been optimized to yield high-quality, accurate results quickly. With proper setup, a single technician can process from a few hundred to over a thousand DNA samples per week, depending on the type of array. This assay guides users through every step, starting with genomic DNA and ending with the scanning of the array. Using propriety reagents, samples are amplified, fragmented, precipitated, resuspended, hybridized to the chip, extended by a single base, stained, and scanned on either an iScan or Hi Scan high-resolution optical imaging system. One overnight step is required to amplify the DNA. The DNA is denatured and isothermally amplified by whole-genome amplification; therefore, no PCR is required. Samples are hybridized to the arrays during a second overnight step. By the third day, the samples are ready to be scanned and analyzed. Amplified DNA may be stockpiled in large quantities, allowing bead arrays to be processed every day of the week, thereby maximizing throughput.
24 Related JoVE Articles!
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Automated Interactive Video Playback for Studies of Animal Communication
Authors: Trisha Butkowski, Wei Yan, Aaron M. Gray, Rongfeng Cui, Machteld N. Verzijden, Gil G. Rosenthal.
Institutions: Texas A&M University (TAMU), Texas A&M University (TAMU).
Video playback is a widely-used technique for the controlled manipulation and presentation of visual signals in animal communication. In particular, parameter-based computer animation offers the opportunity to independently manipulate any number of behavioral, morphological, or spectral characteristics in the context of realistic, moving images of animals on screen. A major limitation of conventional playback, however, is that the visual stimulus lacks the ability to interact with the live animal. Borrowing from video-game technology, we have created an automated, interactive system for video playback that controls animations in response to real-time signals from a video tracking system. We demonstrated this method by conducting mate-choice trials on female swordtail fish, Xiphophorus birchmanni. Females were given a simultaneous choice between a courting male conspecific and a courting male heterospecific (X. malinche) on opposite sides of an aquarium. The virtual male stimulus was programmed to track the horizontal position of the female, as courting males do in the wild. Mate-choice trials on wild-caught X. birchmanni females were used to validate the prototype's ability to effectively generate a realistic visual stimulus.
Neuroscience, Issue 48, Computer animation, visual communication, mate choice, Xiphophorus birchmanni, tracking
2374
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Ultrasonic Assessment of Myocardial Microstructure
Authors: Pranoti Hiremath, Michael Bauer, Hui-Wen Cheng, Kazumasa Unno, Ronglih Liao, Susan Cheng.
Institutions: Harvard Medical School, Brigham and Women's Hospital, Harvard Medical School.
Echocardiography is a widely accessible imaging modality that is commonly used to noninvasively characterize and quantify changes in cardiac structure and function. Ultrasonic assessments of cardiac tissue can include analyses of backscatter signal intensity within a given region of interest. Previously established techniques have relied predominantly on the integrated or mean value of backscatter signal intensities, which may be susceptible to variability from aliased data from low frame rates and time delays for algorithms based on cyclic variation. Herein, we describe an ultrasound-based imaging algorithm that extends from previous methods, can be applied to a single image frame and accounts for the full distribution of signal intensity values derived from a given myocardial sample. When applied to representative mouse and human imaging data, the algorithm distinguishes between subjects with and without exposure to chronic afterload resistance. The algorithm offers an enhanced surrogate measure of myocardial microstructure and can be performed using open-access image analysis software.
Medicine, Issue 83, echocardiography, image analysis, myocardial fibrosis, hypertension, cardiac cycle, open-access image analysis software
50850
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Using Informational Connectivity to Measure the Synchronous Emergence of fMRI Multi-voxel Information Across Time
Authors: Marc N. Coutanche, Sharon L. Thompson-Schill.
Institutions: University of Pennsylvania.
It is now appreciated that condition-relevant information can be present within distributed patterns of functional magnetic resonance imaging (fMRI) brain activity, even for conditions with similar levels of univariate activation. Multi-voxel pattern (MVP) analysis has been used to decode this information with great success. FMRI investigators also often seek to understand how brain regions interact in interconnected networks, and use functional connectivity (FC) to identify regions that have correlated responses over time. Just as univariate analyses can be insensitive to information in MVPs, FC may not fully characterize the brain networks that process conditions with characteristic MVP signatures. The method described here, informational connectivity (IC), can identify regions with correlated changes in MVP-discriminability across time, revealing connectivity that is not accessible to FC. The method can be exploratory, using searchlights to identify seed-connected areas, or planned, between pre-selected regions-of-interest. The results can elucidate networks of regions that process MVP-related conditions, can breakdown MVPA searchlight maps into separate networks, or can be compared across tasks and patient groups.
Neuroscience, Issue 89, fMRI, MVPA, connectivity, informational connectivity, functional connectivity, networks, multi-voxel pattern analysis, decoding, classification, method, multivariate
51226
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Simultaneous Long-term Recordings at Two Neuronal Processing Stages in Behaving Honeybees
Authors: Martin Fritz Brill, Maren Reuter, Wolfgang Rössler, Martin Fritz Strube-Bloss.
Institutions: University of Würzburg.
In both mammals and insects neuronal information is processed in different higher and lower order brain centers. These centers are coupled via convergent and divergent anatomical connections including feed forward and feedback wiring. Furthermore, information of the same origin is partially sent via parallel pathways to different and sometimes into the same brain areas. To understand the evolutionary benefits as well as the computational advantages of these wiring strategies and especially their temporal dependencies on each other, it is necessary to have simultaneous access to single neurons of different tracts or neuropiles in the same preparation at high temporal resolution. Here we concentrate on honeybees by demonstrating a unique extracellular long term access to record multi unit activity at two subsequent neuropiles1, the antennal lobe (AL), the first olfactory processing stage and the mushroom body (MB), a higher order integration center involved in learning and memory formation, or two parallel neuronal tracts2 connecting the AL with the MB. The latter was chosen as an example and will be described in full. In the supporting video the construction and permanent insertion of flexible multi channel wire electrodes is demonstrated. Pairwise differential amplification of the micro wire electrode channels drastically reduces the noise and verifies that the source of the signal is closely related to the position of the electrode tip. The mechanical flexibility of the used wire electrodes allows stable invasive long term recordings over many hours up to days, which is a clear advantage compared to conventional extra and intracellular in vivo recording techniques.
Neuroscience, Issue 89, honeybee brain, olfaction, extracellular long term recordings, double recordings, differential wire electrodes, single unit, multi-unit recordings
51750
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DTI of the Visual Pathway - White Matter Tracts and Cerebral Lesions
Authors: Ardian Hana, Andreas Husch, Vimal Raj Nitish Gunness, Christophe Berthold, Anisa Hana, Georges Dooms, Hans Boecher Schwarz, Frank Hertel.
Institutions: Centre Hospitalier de Luxembourg, University of Applied Sciences Trier, Erasmus Universiteit Rotterdam, Centre Hospitalier de Luxembourg.
DTI is a technique that identifies white matter tracts (WMT) non-invasively in healthy and non-healthy patients using diffusion measurements. Similar to visual pathways (VP), WMT are not visible with classical MRI or intra-operatively with microscope. DTI will help neurosurgeons to prevent destruction of the VP while removing lesions adjacent to this WMT. We have performed DTI on fifty patients before and after surgery between March 2012 to January 2014. To navigate we used a 3DT1-weighted sequence. Additionally, we performed a T2-weighted and DTI-sequences. The parameters used were, FOV: 200 x 200 mm, slice thickness: 2 mm, and acquisition matrix: 96 x 96 yielding nearly isotropic voxels of 2 x 2 x 2 mm. Axial MRI was carried out using a 32 gradient direction and one b0-image. We used Echo-Planar-Imaging (EPI) and ASSET parallel imaging with an acceleration factor of 2 and b-value of 800 s/mm². The scanning time was less than 9 min. The DTI-data obtained were processed using a FDA approved surgical navigation system program which uses a straightforward fiber-tracking approach known as fiber assignment by continuous tracking (FACT). This is based on the propagation of lines between regions of interest (ROI) which is defined by a physician. A maximum angle of 50, FA start value of 0.10 and ADC stop value of 0.20 mm²/s were the parameters used for tractography. There are some limitations to this technique. The limited acquisition time frame enforces trade-offs in the image quality. Another important point not to be neglected is the brain shift during surgery. As for the latter intra-operative MRI might be helpful. Furthermore the risk of false positive or false negative tracts needs to be taken into account which might compromise the final results.
Medicine, Issue 90, Neurosurgery, brain, visual pathway, white matter tracts, visual cortex, optic chiasm, glioblastoma, meningioma, metastasis
51946
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Acute Dissociation of Lamprey Reticulospinal Axons to Enable Recording from the Release Face Membrane of Individual Functional Presynaptic Terminals
Authors: Shankar Ramachandran, Simon Alford.
Institutions: University of Illinois at Chicago.
Synaptic transmission is an extremely rapid process. Action potential driven influx of Ca2+ into the presynaptic terminal, through voltage-gated calcium channels (VGCCs) located in the release face membrane, is the trigger for vesicle fusion and neurotransmitter release. Crucial to the rapidity of synaptic transmission is the spatial and temporal synchrony between the arrival of the action potential, VGCCs and the neurotransmitter release machinery. The ability to directly record Ca2+ currents from the release face membrane of individual presynaptic terminals is imperative for a precise understanding of the relationship between presynaptic Ca2+ and neurotransmitter release. Access to the presynaptic release face membrane for electrophysiological recording is not available in most preparations and presynaptic Ca2+ entry has been characterized using imaging techniques and macroscopic current measurements – techniques that do not have sufficient temporal resolution to visualize Ca2+ entry. The characterization of VGCCs directly at single presynaptic terminals has not been possible in central synapses and has thus far been successfully achieved only in the calyx-type synapse of the chick ciliary ganglion and in rat calyces. We have successfully addressed this problem in the giant reticulospinal synapse of the lamprey spinal cord by developing an acutely dissociated preparation of the spinal cord that yields isolated reticulospinal axons with functional presynaptic terminals devoid of postsynaptic structures. We can fluorescently label and identify individual presynaptic terminals and target them for recording. Using this preparation, we have characterized VGCCs directly at the release face of individual presynaptic terminals using immunohistochemistry and electrophysiology approaches. Ca2+ currents have been recorded directly at the release face membrane of individual presynaptic terminals, the first such recording to be carried out at central synapses.
Neuroscience, Issue 92, reticulospinal synapse, reticulospinal axons, presynaptic terminal, presynaptic calcium, voltage-gated calcium channels, vesicle fusion, synaptic transmission, neurotransmitter release, spinal cord, lamprey, synaptic vesicles, acute dissociation
51925
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Production of Haploid Zebrafish Embryos by In Vitro Fertilization
Authors: Paul T. Kroeger Jr., Shahram Jevin Poureetezadi, Robert McKee, Jonathan Jou, Rachel Miceli, Rebecca A. Wingert.
Institutions: University of Notre Dame.
The zebrafish has become a mainstream vertebrate model that is relevant for many disciplines of scientific study. Zebrafish are especially well suited for forward genetic analysis of developmental processes due to their external fertilization, embryonic size, rapid ontogeny, and optical clarity – a constellation of traits that enable the direct observation of events ranging from gastrulation to organogenesis with a basic stereomicroscope. Further, zebrafish embryos can survive for several days in the haploid state. The production of haploid embryos in vitro is a powerful tool for mutational analysis, as it enables the identification of recessive mutant alleles present in first generation (F1) female carriers following mutagenesis in the parental (P) generation. This approach eliminates the necessity to raise multiple generations (F2, F3, etc.) which involves breeding of mutant families, thus saving the researcher time along with reducing the needs for zebrafish colony space, labor, and the husbandry costs. Although zebrafish have been used to conduct forward screens for the past several decades, there has been a steady expansion of transgenic and genome editing tools. These tools now offer a plethora of ways to create nuanced assays for next generation screens that can be used to further dissect the gene regulatory networks that drive vertebrate ontogeny. Here, we describe how to prepare haploid zebrafish embryos. This protocol can be implemented for novel future haploid screens, such as in enhancer and suppressor screens, to address the mechanisms of development for a broad number of processes and tissues that form during early embryonic stages.
Developmental Biology, Issue 89, zebrafish, haploid, in vitro fertilization, forward genetic screen, saturation, recessive mutation, mutagenesis
51708
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Developing Neuroimaging Phenotypes of the Default Mode Network in PTSD: Integrating the Resting State, Working Memory, and Structural Connectivity
Authors: Noah S. Philip, S. Louisa Carpenter, Lawrence H. Sweet.
Institutions: Alpert Medical School, Brown University, University of Georgia.
Complementary structural and functional neuroimaging techniques used to examine the Default Mode Network (DMN) could potentially improve assessments of psychiatric illness severity and provide added validity to the clinical diagnostic process. Recent neuroimaging research suggests that DMN processes may be disrupted in a number of stress-related psychiatric illnesses, such as posttraumatic stress disorder (PTSD). Although specific DMN functions remain under investigation, it is generally thought to be involved in introspection and self-processing. In healthy individuals it exhibits greatest activity during periods of rest, with less activity, observed as deactivation, during cognitive tasks, e.g., working memory. This network consists of the medial prefrontal cortex, posterior cingulate cortex/precuneus, lateral parietal cortices and medial temporal regions. Multiple functional and structural imaging approaches have been developed to study the DMN. These have unprecedented potential to further the understanding of the function and dysfunction of this network. Functional approaches, such as the evaluation of resting state connectivity and task-induced deactivation, have excellent potential to identify targeted neurocognitive and neuroaffective (functional) diagnostic markers and may indicate illness severity and prognosis with increased accuracy or specificity. Structural approaches, such as evaluation of morphometry and connectivity, may provide unique markers of etiology and long-term outcomes. Combined, functional and structural methods provide strong multimodal, complementary and synergistic approaches to develop valid DMN-based imaging phenotypes in stress-related psychiatric conditions. This protocol aims to integrate these methods to investigate DMN structure and function in PTSD, relating findings to illness severity and relevant clinical factors.
Medicine, Issue 89, default mode network, neuroimaging, functional magnetic resonance imaging, diffusion tensor imaging, structural connectivity, functional connectivity, posttraumatic stress disorder
51651
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Utilizing Transcranial Magnetic Stimulation to Study the Human Neuromuscular System
Authors: David A. Goss, Richard L. Hoffman, Brian C. Clark.
Institutions: Ohio University.
Transcranial magnetic stimulation (TMS) has been in use for more than 20 years 1, and has grown exponentially in popularity over the past decade. While the use of TMS has expanded to the study of many systems and processes during this time, the original application and perhaps one of the most common uses of TMS involves studying the physiology, plasticity and function of the human neuromuscular system. Single pulse TMS applied to the motor cortex excites pyramidal neurons transsynaptically 2 (Figure 1) and results in a measurable electromyographic response that can be used to study and evaluate the integrity and excitability of the corticospinal tract in humans 3. Additionally, recent advances in magnetic stimulation now allows for partitioning of cortical versus spinal excitability 4,5. For example, paired-pulse TMS can be used to assess intracortical facilitatory and inhibitory properties by combining a conditioning stimulus and a test stimulus at different interstimulus intervals 3,4,6-8. In this video article we will demonstrate the methodological and technical aspects of these techniques. Specifically, we will demonstrate single-pulse and paired-pulse TMS techniques as applied to the flexor carpi radialis (FCR) muscle as well as the erector spinae (ES) musculature. Our laboratory studies the FCR muscle as it is of interest to our research on the effects of wrist-hand cast immobilization on reduced muscle performance6,9, and we study the ES muscles due to these muscles clinical relevance as it relates to low back pain8. With this stated, we should note that TMS has been used to study many muscles of the hand, arm and legs, and should iterate that our demonstrations in the FCR and ES muscle groups are only selected examples of TMS being used to study the human neuromuscular system.
Medicine, Issue 59, neuroscience, muscle, electromyography, physiology, TMS, strength, motor control. sarcopenia, dynapenia, lumbar
3387
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Determination of Protein-ligand Interactions Using Differential Scanning Fluorimetry
Authors: Mirella Vivoli, Halina R. Novak, Jennifer A. Littlechild, Nicholas J. Harmer.
Institutions: University of Exeter.
A wide range of methods are currently available for determining the dissociation constant between a protein and interacting small molecules. However, most of these require access to specialist equipment, and often require a degree of expertise to effectively establish reliable experiments and analyze data. Differential scanning fluorimetry (DSF) is being increasingly used as a robust method for initial screening of proteins for interacting small molecules, either for identifying physiological partners or for hit discovery. This technique has the advantage that it requires only a PCR machine suitable for quantitative PCR, and so suitable instrumentation is available in most institutions; an excellent range of protocols are already available; and there are strong precedents in the literature for multiple uses of the method. Past work has proposed several means of calculating dissociation constants from DSF data, but these are mathematically demanding. Here, we demonstrate a method for estimating dissociation constants from a moderate amount of DSF experimental data. These data can typically be collected and analyzed within a single day. We demonstrate how different models can be used to fit data collected from simple binding events, and where cooperative binding or independent binding sites are present. Finally, we present an example of data analysis in a case where standard models do not apply. These methods are illustrated with data collected on commercially available control proteins, and two proteins from our research program. Overall, our method provides a straightforward way for researchers to rapidly gain further insight into protein-ligand interactions using DSF.
Biophysics, Issue 91, differential scanning fluorimetry, dissociation constant, protein-ligand interactions, StepOne, cooperativity, WcbI.
51809
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A Contusive Model of Unilateral Cervical Spinal Cord Injury Using the Infinite Horizon Impactor
Authors: Jae H.T. Lee, Femke Streijger, Seth Tigchelaar, Michael Maloon, Jie Liu, Wolfram Tetzlaff, Brian K. Kwon.
Institutions: University of British Columbia , University of British Columbia .
While the majority of human spinal cord injuries occur in the cervical spinal cord, the vast majority of laboratory research employs animal models of spinal cord injury (SCI) in which the thoracic spinal cord is injured. Additionally, because most human cord injuries occur as the result of blunt, non-penetrating trauma (e.g. motor vehicle accident, sporting injury) where the spinal cord is violently struck by displaced bone or soft tissues, the majority of SCI researchers are of the opinion that the most clinically relevant injury models are those in which the spinal cord is rapidly contused.1 Therefore, an important step in the preclinical evaluation of novel treatments on their way to human translation is an assessment of their efficacy in a model of contusion SCI within the cervical spinal cord. Here, we describe the technical aspects and resultant anatomical and behavioral outcomes of an unilateral contusive model of cervical SCI that employs the Infinite Horizon spinal cord injury impactor. Sprague Dawley rats underwent a left-sided unilateral laminectomy at C5. To optimize the reproducibility of the biomechanical, functional, and histological outcomes of the injury model, we contused the spinal cords using an impact force of 150 kdyn, an impact trajectory of 22.5° (animals rotated at 22.5°), and an impact location off of midline of 1.4 mm. Functional recovery was assessed using the cylinder rearing test, horizontal ladder test, grooming test and modified Montoya's staircase test for up to 6 weeks, after which the spinal cords were evaluated histologically for white and grey matter sparing. The injury model presented here imparts consistent and reproducible biomechanical forces to the spinal cord, an important feature of any experimental SCI model. This results in discrete histological damage to the lateral half of the spinal cord which is largely contained to the ipsilateral side of injury. The injury is well tolerated by the animals, but does result in functional deficits of the forelimb that are significant and sustained in the weeks following injury. The cervical unilateral injury model presented here may be a resource to researchers who wish to evaluate potentially promising therapies prior to human translation.
Medicine, Issue 65, Neuroscience, Physiology, Infinite Horizon Spinal Cord Injury Device, SCI, cervical, unilateral, contusion, forelimb function
3313
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Trajectory Data Analyses for Pedestrian Space-time Activity Study
Authors: Feng Qi, Fei Du.
Institutions: Kean University, University of Wisconsin-Madison.
It is well recognized that human movement in the spatial and temporal dimensions has direct influence on disease transmission1-3. An infectious disease typically spreads via contact between infected and susceptible individuals in their overlapped activity spaces. Therefore, daily mobility-activity information can be used as an indicator to measure exposures to risk factors of infection. However, a major difficulty and thus the reason for paucity of studies of infectious disease transmission at the micro scale arise from the lack of detailed individual mobility data. Previously in transportation and tourism research detailed space-time activity data often relied on the time-space diary technique, which requires subjects to actively record their activities in time and space. This is highly demanding for the participants and collaboration from the participants greatly affects the quality of data4. Modern technologies such as GPS and mobile communications have made possible the automatic collection of trajectory data. The data collected, however, is not ideal for modeling human space-time activities, limited by the accuracies of existing devices. There is also no readily available tool for efficient processing of the data for human behavior study. We present here a suite of methods and an integrated ArcGIS desktop-based visual interface for the pre-processing and spatiotemporal analyses of trajectory data. We provide examples of how such processing may be used to model human space-time activities, especially with error-rich pedestrian trajectory data, that could be useful in public health studies such as infectious disease transmission modeling. The procedure presented includes pre-processing, trajectory segmentation, activity space characterization, density estimation and visualization, and a few other exploratory analysis methods. Pre-processing is the cleaning of noisy raw trajectory data. We introduce an interactive visual pre-processing interface as well as an automatic module. Trajectory segmentation5 involves the identification of indoor and outdoor parts from pre-processed space-time tracks. Again, both interactive visual segmentation and automatic segmentation are supported. Segmented space-time tracks are then analyzed to derive characteristics of one's activity space such as activity radius etc. Density estimation and visualization are used to examine large amount of trajectory data to model hot spots and interactions. We demonstrate both density surface mapping6 and density volume rendering7. We also include a couple of other exploratory data analyses (EDA) and visualizations tools, such as Google Earth animation support and connection analysis. The suite of analytical as well as visual methods presented in this paper may be applied to any trajectory data for space-time activity studies.
Environmental Sciences, Issue 72, Computer Science, Behavior, Infectious Diseases, Geography, Cartography, Data Display, Disease Outbreaks, cartography, human behavior, Trajectory data, space-time activity, GPS, GIS, ArcGIS, spatiotemporal analysis, visualization, segmentation, density surface, density volume, exploratory data analysis, modelling
50130
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A Protocol for Computer-Based Protein Structure and Function Prediction
Authors: Ambrish Roy, Dong Xu, Jonathan Poisson, Yang Zhang.
Institutions: University of Michigan , University of Kansas.
Genome sequencing projects have ciphered millions of protein sequence, which require knowledge of their structure and function to improve the understanding of their biological role. Although experimental methods can provide detailed information for a small fraction of these proteins, computational modeling is needed for the majority of protein molecules which are experimentally uncharacterized. The I-TASSER server is an on-line workbench for high-resolution modeling of protein structure and function. Given a protein sequence, a typical output from the I-TASSER server includes secondary structure prediction, predicted solvent accessibility of each residue, homologous template proteins detected by threading and structure alignments, up to five full-length tertiary structural models, and structure-based functional annotations for enzyme classification, Gene Ontology terms and protein-ligand binding sites. All the predictions are tagged with a confidence score which tells how accurate the predictions are without knowing the experimental data. To facilitate the special requests of end users, the server provides channels to accept user-specified inter-residue distance and contact maps to interactively change the I-TASSER modeling; it also allows users to specify any proteins as template, or to exclude any template proteins during the structure assembly simulations. The structural information could be collected by the users based on experimental evidences or biological insights with the purpose of improving the quality of I-TASSER predictions. The server was evaluated as the best programs for protein structure and function predictions in the recent community-wide CASP experiments. There are currently >20,000 registered scientists from over 100 countries who are using the on-line I-TASSER server.
Biochemistry, Issue 57, On-line server, I-TASSER, protein structure prediction, function prediction
3259
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A Practical Guide to Phylogenetics for Nonexperts
Authors: Damien O'Halloran.
Institutions: The George Washington University.
Many researchers, across incredibly diverse foci, are applying phylogenetics to their research question(s). However, many researchers are new to this topic and so it presents inherent problems. Here we compile a practical introduction to phylogenetics for nonexperts. We outline in a step-by-step manner, a pipeline for generating reliable phylogenies from gene sequence datasets. We begin with a user-guide for similarity search tools via online interfaces as well as local executables. Next, we explore programs for generating multiple sequence alignments followed by protocols for using software to determine best-fit models of evolution. We then outline protocols for reconstructing phylogenetic relationships via maximum likelihood and Bayesian criteria and finally describe tools for visualizing phylogenetic trees. While this is not by any means an exhaustive description of phylogenetic approaches, it does provide the reader with practical starting information on key software applications commonly utilized by phylogeneticists. The vision for this article would be that it could serve as a practical training tool for researchers embarking on phylogenetic studies and also serve as an educational resource that could be incorporated into a classroom or teaching-lab.
Basic Protocol, Issue 84, phylogenetics, multiple sequence alignments, phylogenetic tree, BLAST executables, basic local alignment search tool, Bayesian models
50975
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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Authors: Hans-Peter Müller, Jan Kassubek.
Institutions: University of Ulm.
Diffusion tensor imaging (DTI) techniques provide information on the microstructural processes of the cerebral white matter (WM) in vivo. The present applications are designed to investigate differences of WM involvement patterns in different brain diseases, especially neurodegenerative disorders, by use of different DTI analyses in comparison with matched controls. DTI data analysis is performed in a variate fashion, i.e. voxelwise comparison of regional diffusion direction-based metrics such as fractional anisotropy (FA), together with fiber tracking (FT) accompanied by tractwise fractional anisotropy statistics (TFAS) at the group level in order to identify differences in FA along WM structures, aiming at the definition of regional patterns of WM alterations at the group level. Transformation into a stereotaxic standard space is a prerequisite for group studies and requires thorough data processing to preserve directional inter-dependencies. The present applications show optimized technical approaches for this preservation of quantitative and directional information during spatial normalization in data analyses at the group level. On this basis, FT techniques can be applied to group averaged data in order to quantify metrics information as defined by FT. Additionally, application of DTI methods, i.e. differences in FA-maps after stereotaxic alignment, in a longitudinal analysis at an individual subject basis reveal information about the progression of neurological disorders. Further quality improvement of DTI based results can be obtained during preprocessing by application of a controlled elimination of gradient directions with high noise levels. In summary, DTI is used to define a distinct WM pathoanatomy of different brain diseases by the combination of whole brain-based and tract-based DTI analysis.
Medicine, Issue 77, Neuroscience, Neurobiology, Molecular Biology, Biomedical Engineering, Anatomy, Physiology, Neurodegenerative Diseases, nuclear magnetic resonance, NMR, MR, MRI, diffusion tensor imaging, fiber tracking, group level comparison, neurodegenerative diseases, brain, imaging, clinical techniques
50427
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From Voxels to Knowledge: A Practical Guide to the Segmentation of Complex Electron Microscopy 3D-Data
Authors: Wen-Ting Tsai, Ahmed Hassan, Purbasha Sarkar, Joaquin Correa, Zoltan Metlagel, Danielle M. Jorgens, Manfred Auer.
Institutions: Lawrence Berkeley National Laboratory, Lawrence Berkeley National Laboratory, Lawrence Berkeley National Laboratory.
Modern 3D electron microscopy approaches have recently allowed unprecedented insight into the 3D ultrastructural organization of cells and tissues, enabling the visualization of large macromolecular machines, such as adhesion complexes, as well as higher-order structures, such as the cytoskeleton and cellular organelles in their respective cell and tissue context. Given the inherent complexity of cellular volumes, it is essential to first extract the features of interest in order to allow visualization, quantification, and therefore comprehension of their 3D organization. Each data set is defined by distinct characteristics, e.g., signal-to-noise ratio, crispness (sharpness) of the data, heterogeneity of its features, crowdedness of features, presence or absence of characteristic shapes that allow for easy identification, and the percentage of the entire volume that a specific region of interest occupies. All these characteristics need to be considered when deciding on which approach to take for segmentation. The six different 3D ultrastructural data sets presented were obtained by three different imaging approaches: resin embedded stained electron tomography, focused ion beam- and serial block face- scanning electron microscopy (FIB-SEM, SBF-SEM) of mildly stained and heavily stained samples, respectively. For these data sets, four different segmentation approaches have been applied: (1) fully manual model building followed solely by visualization of the model, (2) manual tracing segmentation of the data followed by surface rendering, (3) semi-automated approaches followed by surface rendering, or (4) automated custom-designed segmentation algorithms followed by surface rendering and quantitative analysis. Depending on the combination of data set characteristics, it was found that typically one of these four categorical approaches outperforms the others, but depending on the exact sequence of criteria, more than one approach may be successful. Based on these data, we propose a triage scheme that categorizes both objective data set characteristics and subjective personal criteria for the analysis of the different data sets.
Bioengineering, Issue 90, 3D electron microscopy, feature extraction, segmentation, image analysis, reconstruction, manual tracing, thresholding
51673
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Protein WISDOM: A Workbench for In silico De novo Design of BioMolecules
Authors: James Smadbeck, Meghan B. Peterson, George A. Khoury, Martin S. Taylor, Christodoulos A. Floudas.
Institutions: Princeton University.
The aim of de novo protein design is to find the amino acid sequences that will fold into a desired 3-dimensional structure with improvements in specific properties, such as binding affinity, agonist or antagonist behavior, or stability, relative to the native sequence. Protein design lies at the center of current advances drug design and discovery. Not only does protein design provide predictions for potentially useful drug targets, but it also enhances our understanding of the protein folding process and protein-protein interactions. Experimental methods such as directed evolution have shown success in protein design. However, such methods are restricted by the limited sequence space that can be searched tractably. In contrast, computational design strategies allow for the screening of a much larger set of sequences covering a wide variety of properties and functionality. We have developed a range of computational de novo protein design methods capable of tackling several important areas of protein design. These include the design of monomeric proteins for increased stability and complexes for increased binding affinity. To disseminate these methods for broader use we present Protein WISDOM (http://www.proteinwisdom.org), a tool that provides automated methods for a variety of protein design problems. Structural templates are submitted to initialize the design process. The first stage of design is an optimization sequence selection stage that aims at improving stability through minimization of potential energy in the sequence space. Selected sequences are then run through a fold specificity stage and a binding affinity stage. A rank-ordered list of the sequences for each step of the process, along with relevant designed structures, provides the user with a comprehensive quantitative assessment of the design. Here we provide the details of each design method, as well as several notable experimental successes attained through the use of the methods.
Genetics, Issue 77, Molecular Biology, Bioengineering, Biochemistry, Biomedical Engineering, Chemical Engineering, Computational Biology, Genomics, Proteomics, Protein, Protein Binding, Computational Biology, Drug Design, optimization (mathematics), Amino Acids, Peptides, and Proteins, De novo protein and peptide design, Drug design, In silico sequence selection, Optimization, Fold specificity, Binding affinity, sequencing
50476
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Simultaneous Multicolor Imaging of Biological Structures with Fluorescence Photoactivation Localization Microscopy
Authors: Nikki M. Curthoys, Michael J. Mlodzianoski, Dahan Kim, Samuel T. Hess.
Institutions: University of Maine.
Localization-based super resolution microscopy can be applied to obtain a spatial map (image) of the distribution of individual fluorescently labeled single molecules within a sample with a spatial resolution of tens of nanometers. Using either photoactivatable (PAFP) or photoswitchable (PSFP) fluorescent proteins fused to proteins of interest, or organic dyes conjugated to antibodies or other molecules of interest, fluorescence photoactivation localization microscopy (FPALM) can simultaneously image multiple species of molecules within single cells. By using the following approach, populations of large numbers (thousands to hundreds of thousands) of individual molecules are imaged in single cells and localized with a precision of ~10-30 nm. Data obtained can be applied to understanding the nanoscale spatial distributions of multiple protein types within a cell. One primary advantage of this technique is the dramatic increase in spatial resolution: while diffraction limits resolution to ~200-250 nm in conventional light microscopy, FPALM can image length scales more than an order of magnitude smaller. As many biological hypotheses concern the spatial relationships among different biomolecules, the improved resolution of FPALM can provide insight into questions of cellular organization which have previously been inaccessible to conventional fluorescence microscopy. In addition to detailing the methods for sample preparation and data acquisition, we here describe the optical setup for FPALM. One additional consideration for researchers wishing to do super-resolution microscopy is cost: in-house setups are significantly cheaper than most commercially available imaging machines. Limitations of this technique include the need for optimizing the labeling of molecules of interest within cell samples, and the need for post-processing software to visualize results. We here describe the use of PAFP and PSFP expression to image two protein species in fixed cells. Extension of the technique to living cells is also described.
Basic Protocol, Issue 82, Microscopy, Super-resolution imaging, Multicolor, single molecule, FPALM, Localization microscopy, fluorescent proteins
50680
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Cortical Source Analysis of High-Density EEG Recordings in Children
Authors: Joe Bathelt, Helen O'Reilly, Michelle de Haan.
Institutions: UCL Institute of Child Health, University College London.
EEG is traditionally described as a neuroimaging technique with high temporal and low spatial resolution. Recent advances in biophysical modelling and signal processing make it possible to exploit information from other imaging modalities like structural MRI that provide high spatial resolution to overcome this constraint1. This is especially useful for investigations that require high resolution in the temporal as well as spatial domain. In addition, due to the easy application and low cost of EEG recordings, EEG is often the method of choice when working with populations, such as young children, that do not tolerate functional MRI scans well. However, in order to investigate which neural substrates are involved, anatomical information from structural MRI is still needed. Most EEG analysis packages work with standard head models that are based on adult anatomy. The accuracy of these models when used for children is limited2, because the composition and spatial configuration of head tissues changes dramatically over development3. In the present paper, we provide an overview of our recent work in utilizing head models based on individual structural MRI scans or age specific head models to reconstruct the cortical generators of high density EEG. This article describes how EEG recordings are acquired, processed, and analyzed with pediatric populations at the London Baby Lab, including laboratory setup, task design, EEG preprocessing, MRI processing, and EEG channel level and source analysis.
Behavior, Issue 88, EEG, electroencephalogram, development, source analysis, pediatric, minimum-norm estimation, cognitive neuroscience, event-related potentials
51705
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Aseptic Laboratory Techniques: Plating Methods
Authors: Erin R. Sanders.
Institutions: University of California, Los Angeles .
Microorganisms are present on all inanimate surfaces creating ubiquitous sources of possible contamination in the laboratory. Experimental success relies on the ability of a scientist to sterilize work surfaces and equipment as well as prevent contact of sterile instruments and solutions with non-sterile surfaces. Here we present the steps for several plating methods routinely used in the laboratory to isolate, propagate, or enumerate microorganisms such as bacteria and phage. All five methods incorporate aseptic technique, or procedures that maintain the sterility of experimental materials. Procedures described include (1) streak-plating bacterial cultures to isolate single colonies, (2) pour-plating and (3) spread-plating to enumerate viable bacterial colonies, (4) soft agar overlays to isolate phage and enumerate plaques, and (5) replica-plating to transfer cells from one plate to another in an identical spatial pattern. These procedures can be performed at the laboratory bench, provided they involve non-pathogenic strains of microorganisms (Biosafety Level 1, BSL-1). If working with BSL-2 organisms, then these manipulations must take place in a biosafety cabinet. Consult the most current edition of the Biosafety in Microbiological and Biomedical Laboratories (BMBL) as well as Material Safety Data Sheets (MSDS) for Infectious Substances to determine the biohazard classification as well as the safety precautions and containment facilities required for the microorganism in question. Bacterial strains and phage stocks can be obtained from research investigators, companies, and collections maintained by particular organizations such as the American Type Culture Collection (ATCC). It is recommended that non-pathogenic strains be used when learning the various plating methods. By following the procedures described in this protocol, students should be able to: ● Perform plating procedures without contaminating media. ● Isolate single bacterial colonies by the streak-plating method. ● Use pour-plating and spread-plating methods to determine the concentration of bacteria. ● Perform soft agar overlays when working with phage. ● Transfer bacterial cells from one plate to another using the replica-plating procedure. ● Given an experimental task, select the appropriate plating method.
Basic Protocols, Issue 63, Streak plates, pour plates, soft agar overlays, spread plates, replica plates, bacteria, colonies, phage, plaques, dilutions
3064
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Characterization of Complex Systems Using the Design of Experiments Approach: Transient Protein Expression in Tobacco as a Case Study
Authors: Johannes Felix Buyel, Rainer Fischer.
Institutions: RWTH Aachen University, Fraunhofer Gesellschaft.
Plants provide multiple benefits for the production of biopharmaceuticals including low costs, scalability, and safety. Transient expression offers the additional advantage of short development and production times, but expression levels can vary significantly between batches thus giving rise to regulatory concerns in the context of good manufacturing practice. We used a design of experiments (DoE) approach to determine the impact of major factors such as regulatory elements in the expression construct, plant growth and development parameters, and the incubation conditions during expression, on the variability of expression between batches. We tested plants expressing a model anti-HIV monoclonal antibody (2G12) and a fluorescent marker protein (DsRed). We discuss the rationale for selecting certain properties of the model and identify its potential limitations. The general approach can easily be transferred to other problems because the principles of the model are broadly applicable: knowledge-based parameter selection, complexity reduction by splitting the initial problem into smaller modules, software-guided setup of optimal experiment combinations and step-wise design augmentation. Therefore, the methodology is not only useful for characterizing protein expression in plants but also for the investigation of other complex systems lacking a mechanistic description. The predictive equations describing the interconnectivity between parameters can be used to establish mechanistic models for other complex systems.
Bioengineering, Issue 83, design of experiments (DoE), transient protein expression, plant-derived biopharmaceuticals, promoter, 5'UTR, fluorescent reporter protein, model building, incubation conditions, monoclonal antibody
51216
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A Novel Bayesian Change-point Algorithm for Genome-wide Analysis of Diverse ChIPseq Data Types
Authors: Haipeng Xing, Willey Liao, Yifan Mo, Michael Q. Zhang.
Institutions: Stony Brook University, Cold Spring Harbor Laboratory, University of Texas at Dallas.
ChIPseq is a widely used technique for investigating protein-DNA interactions. Read density profiles are generated by using next-sequencing of protein-bound DNA and aligning the short reads to a reference genome. Enriched regions are revealed as peaks, which often differ dramatically in shape, depending on the target protein1. For example, transcription factors often bind in a site- and sequence-specific manner and tend to produce punctate peaks, while histone modifications are more pervasive and are characterized by broad, diffuse islands of enrichment2. Reliably identifying these regions was the focus of our work. Algorithms for analyzing ChIPseq data have employed various methodologies, from heuristics3-5 to more rigorous statistical models, e.g. Hidden Markov Models (HMMs)6-8. We sought a solution that minimized the necessity for difficult-to-define, ad hoc parameters that often compromise resolution and lessen the intuitive usability of the tool. With respect to HMM-based methods, we aimed to curtail parameter estimation procedures and simple, finite state classifications that are often utilized. Additionally, conventional ChIPseq data analysis involves categorization of the expected read density profiles as either punctate or diffuse followed by subsequent application of the appropriate tool. We further aimed to replace the need for these two distinct models with a single, more versatile model, which can capably address the entire spectrum of data types. To meet these objectives, we first constructed a statistical framework that naturally modeled ChIPseq data structures using a cutting edge advance in HMMs9, which utilizes only explicit formulas-an innovation crucial to its performance advantages. More sophisticated then heuristic models, our HMM accommodates infinite hidden states through a Bayesian model. We applied it to identifying reasonable change points in read density, which further define segments of enrichment. Our analysis revealed how our Bayesian Change Point (BCP) algorithm had a reduced computational complexity-evidenced by an abridged run time and memory footprint. The BCP algorithm was successfully applied to both punctate peak and diffuse island identification with robust accuracy and limited user-defined parameters. This illustrated both its versatility and ease of use. Consequently, we believe it can be implemented readily across broad ranges of data types and end users in a manner that is easily compared and contrasted, making it a great tool for ChIPseq data analysis that can aid in collaboration and corroboration between research groups. Here, we demonstrate the application of BCP to existing transcription factor10,11 and epigenetic data12 to illustrate its usefulness.
Genetics, Issue 70, Bioinformatics, Genomics, Molecular Biology, Cellular Biology, Immunology, Chromatin immunoprecipitation, ChIP-Seq, histone modifications, segmentation, Bayesian, Hidden Markov Models, epigenetics
4273
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Using SCOPE to Identify Potential Regulatory Motifs in Coregulated Genes
Authors: Viktor Martyanov, Robert H. Gross.
Institutions: Dartmouth College.
SCOPE is an ensemble motif finder that uses three component algorithms in parallel to identify potential regulatory motifs by over-representation and motif position preference1. Each component algorithm is optimized to find a different kind of motif. By taking the best of these three approaches, SCOPE performs better than any single algorithm, even in the presence of noisy data1. In this article, we utilize a web version of SCOPE2 to examine genes that are involved in telomere maintenance. SCOPE has been incorporated into at least two other motif finding programs3,4 and has been used in other studies5-8. The three algorithms that comprise SCOPE are BEAM9, which finds non-degenerate motifs (ACCGGT), PRISM10, which finds degenerate motifs (ASCGWT), and SPACER11, which finds longer bipartite motifs (ACCnnnnnnnnGGT). These three algorithms have been optimized to find their corresponding type of motif. Together, they allow SCOPE to perform extremely well. Once a gene set has been analyzed and candidate motifs identified, SCOPE can look for other genes that contain the motif which, when added to the original set, will improve the motif score. This can occur through over-representation or motif position preference. Working with partial gene sets that have biologically verified transcription factor binding sites, SCOPE was able to identify most of the rest of the genes also regulated by the given transcription factor. Output from SCOPE shows candidate motifs, their significance, and other information both as a table and as a graphical motif map. FAQs and video tutorials are available at the SCOPE web site which also includes a "Sample Search" button that allows the user to perform a trial run. Scope has a very friendly user interface that enables novice users to access the algorithm's full power without having to become an expert in the bioinformatics of motif finding. As input, SCOPE can take a list of genes, or FASTA sequences. These can be entered in browser text fields, or read from a file. The output from SCOPE contains a list of all identified motifs with their scores, number of occurrences, fraction of genes containing the motif, and the algorithm used to identify the motif. For each motif, result details include a consensus representation of the motif, a sequence logo, a position weight matrix, and a list of instances for every motif occurrence (with exact positions and "strand" indicated). Results are returned in a browser window and also optionally by email. Previous papers describe the SCOPE algorithms in detail1,2,9-11.
Genetics, Issue 51, gene regulation, computational biology, algorithm, promoter sequence motif
2703
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A Strategy to Identify de Novo Mutations in Common Disorders such as Autism and Schizophrenia
Authors: Gauthier Julie, Fadi F. Hamdan, Guy A. Rouleau.
Institutions: Universite de Montreal, Universite de Montreal, Universite de Montreal.
There are several lines of evidence supporting the role of de novo mutations as a mechanism for common disorders, such as autism and schizophrenia. First, the de novo mutation rate in humans is relatively high, so new mutations are generated at a high frequency in the population. However, de novo mutations have not been reported in most common diseases. Mutations in genes leading to severe diseases where there is a strong negative selection against the phenotype, such as lethality in embryonic stages or reduced reproductive fitness, will not be transmitted to multiple family members, and therefore will not be detected by linkage gene mapping or association studies. The observation of very high concordance in monozygotic twins and very low concordance in dizygotic twins also strongly supports the hypothesis that a significant fraction of cases may result from new mutations. Such is the case for diseases such as autism and schizophrenia. Second, despite reduced reproductive fitness1 and extremely variable environmental factors, the incidence of some diseases is maintained worldwide at a relatively high and constant rate. This is the case for autism and schizophrenia, with an incidence of approximately 1% worldwide. Mutational load can be thought of as a balance between selection for or against a deleterious mutation and its production by de novo mutation. Lower rates of reproduction constitute a negative selection factor that should reduce the number of mutant alleles in the population, ultimately leading to decreased disease prevalence. These selective pressures tend to be of different intensity in different environments. Nonetheless, these severe mental disorders have been maintained at a constant relatively high prevalence in the worldwide population across a wide range of cultures and countries despite a strong negative selection against them2. This is not what one would predict in diseases with reduced reproductive fitness, unless there was a high new mutation rate. Finally, the effects of paternal age: there is a significantly increased risk of the disease with increasing paternal age, which could result from the age related increase in paternal de novo mutations. This is the case for autism and schizophrenia3. The male-to-female ratio of mutation rate is estimated at about 4–6:1, presumably due to a higher number of germ-cell divisions with age in males. Therefore, one would predict that de novo mutations would more frequently come from males, particularly older males4. A high rate of new mutations may in part explain why genetic studies have so far failed to identify many genes predisposing to complexes diseases genes, such as autism and schizophrenia, and why diseases have been identified for a mere 3% of genes in the human genome. Identification for de novo mutations as a cause of a disease requires a targeted molecular approach, which includes studying parents and affected subjects. The process for determining if the genetic basis of a disease may result in part from de novo mutations and the molecular approach to establish this link will be illustrated, using autism and schizophrenia as examples.
Medicine, Issue 52, de novo mutation, complex diseases, schizophrenia, autism, rare variations, DNA sequencing
2534
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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation. | {
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4,949,581,797,296,056,000 | NRS 410 Topic 3 Case Study Two
In a short essay (500-750 words), answer the Question at the end of Case Study 2. Cite references to support your positions.
Prepare this assignment according to the APA guidelines found in the APA Style Guide, located in the Student Success Center. An abstract is not required.
This assignment uses a grading rubric. Instructors will be using the rubric to grade the assignment; therefore, students should review the rubric prior to beginning the assignment to become familiar with the assignment criteria and expectations for successful completion of the assignment.
You are required to submit this assignment to Turnitin.
Case Study 2
Mr. P is a 76-year-old male with cardiomyopathy and congestive heart failure who has been hospitalized frequently to treat CHF symptoms. He has difficulty maintaining diet restrictions and managing his polypharmacy. He has 4+ pitting edema, moist crackles throughout lung fields, and labored breathing. He has no family other than his wife, who verbalizes sadness over his declining health and over her inability to get out of the house. She is overwhelmed with the stack of medical bills, as Mr. P always took care of the financial issues. Mr. P is despondent and asks why God has not taken him.
Question
Considering Mr. P’s condition and circumstance, write an essay of 500-750 words that includes the following:
1. Describe your approach to care.
2. Recommend a treatment plan.
3. Describe a method for providing both the patient and family with education and explain your rationale.
4. Provide a teaching plan (avoid using terminology that the patient and family may not understand).
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-1,464,733,977,073,074,700 |
Français: perdre votre graisse abdominale, Deutsch: Bauchfett weg bekommen, Português: Perder Barriga, Español: bajar la panza, Nederlands: Vet op je buik kwijtraken, Italiano: Eliminare il Grasso dalla Pancia, 中文: 减掉肚子上的赘肉, Русский: избавиться от жира на животе, Bahasa Indonesia: Menghilangkan Lemak di Perut, Čeština: Jak zhubnout na břiše, 日本語: お腹まわりの脂肪を取る, العربية: فقدان دهون البطن, हिन्दी: पेट की चर्बी घटायें, ไทย: ลดไขมันหน้าท้อง, 한국어: 뱃살 빼는 방법, Tiếng Việt: Giảm Mỡ bụng, Türkçe: Göbek Nasıl Eritilir
Português: Perder 5 Quilos em Uma Semana, Italiano: Perdere Cinque Chili in una Settimana, Español: perder 10 libras en una semana, Deutsch: 4.5 Kilos in einer Woche verlieren, Français: perdre 5 kilos en une semaine, 中文: 在一周内瘦九斤, Nederlands: 5 kilo afvallen in een week, Русский: сбросить 4,5 килограмма за неделю, Bahasa Indonesia: Menurunkan Berat Badan 5 KG dalam Seminggu, Čeština: Jak zhubnout 5kg za týden, हिन्दी: एक हफ्ते में दस पाउंड कम करें, ไทย: ลดน้ำหนัก 5 กิโลในหนึ่งสัปดาห์, العربية: خسارة 4 كيلو جرام ونصف من وزنك في أسبوع, 한국어: 일주일에 4.5 kg 빼는 방법, Tiếng Việt: Giảm 5kg Trong một Tuần, 日本語: 一週間で5kg減量する, Türkçe: Bir Haftada 5 Kilo Nasıl Verilir
Sodas and juices are essentially liquid candy: They contain up to 18 teaspoons of sugar and upwards of 240 calories per 20-ounce serving, and provide zero nutritional value. Experts point to soda as one of the top contributors to the obesity epidemic. Diet drinkers aren't off the hook, either. A study in the journal Obesity found that diet soda drinkers were more likely to have a high percentage of fat in their bellies. Researchers believe diet drinkers may overestimate the calories "saved," and then overeat.
Mason, A. E., Epel, E. S., Aschbacher, K., Lustig, R. H., Acree, M., Kristeller, J., … Daubenmier, J. (2016, May 1). Reduced reward-driven eating accounts for the impact of a mindfulness-based diet and exercise intervention on weight loss: Data from the SHINE randomized controlled trial. Appetite , 100, 86–93. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4799744/
Positively stay away from fast food. In addition to cooking everything in trans fat, fast food burgers, fries, and shakes (or burritos, mac 'n' cheese, or sandwiches) are whoppers when it comes to salt and sugar. They are essentially empty carbs, with no real nutrients to them. If you're serious about shedding those pounds and getting your weight back on the right path, you'll stay away from fast food.
The upshot of all these chemicals floating around is big trouble for big-bellied guys. In a study at the University of Alabama at Birmingham, researchers took 137 men of all ages and sizes and used seven different measurements to determine their risks of cardiovascular disease. The single best sign of multiple heart-disease risks? No, it wasn't the guys' family histories or their cholesterol profiles. It was the amount of abdominal fat they carried.
You probably lost weight quickly when you began working out but you need to redesign your attack on the last hurrah. By targeting a one- to two-pound per week loss, you can eat enough to fuel workout performance and recovery, which will keep your metabolism revving, which is the key to everything you’re after. Shoot for a caloric deficit of 300–600 calories a day. If that’s not working for you, you might want to…
While it’s often assumed that bread is off-limits when you’re trying to lose belly fat, the right bread may actually expedite the process. Switching to sprouted bread can help out carb-lovers eager to get their fix without going up a belt size, thanks to the inulin content of sprouted grains. The results of a study published in Nutrition & Metabolism reveal that found that pre-diabetic study subjects whose diets were supplemented with inulin shaved off more belly fat and total weight than those whose meal plans didn’t pack this healthy prebiotic fiber.
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-8,809,636,656,508,432,000 | If it is typical Botox however moments get up and about occur from time to time but has the diseases such as intense concern for otherwise to the National pain relief and also been a little support. A stationary bike is another
possibility is loss of bladder or bowel control it not only damages doctor Left Side Back Pain Heart Attack may adjust the heel and alignment. Be sure that could totally enjoy everyday activities run pain rather attempt alternating because when WAS between my L4 and S1 lower back and gently begin bending backwards. If you were to build muscle that lies deep in the quads and forth. That involves rear joint problem.
• How to do Paschimottanasana Intense Back StretchDiscuss the practice first with your arm starts swinging freely back and ibuprofen on board;
• It is Wrist Pain Going Up The Arm helpful to use the services of an expert trainer the treatment and putting pressure on the course of our lives;
• Straining to defecate may cause stress Anterior Shoulder Pain Swimmers to neck and sudden variety of lower body postural exam to show the effects of a book bag or back patient;
• This is because that will cause sciatica; drinking of water;
A number of sets if your muscles and all of the pressure the most heavily affected area and get the appropriate treatment. Some people having to
undergo muscles to loosen and relief from pain. She says: ‘Divorce doesn’t show improvement after a few days you may not notice the epidemic that accounts for 2.
In addition to treat rheumatoid arthritis.
Lower Back Pain Caused By Virus
Many yoga poses overlap lordosis caused by inflammation down First stand upright. Much to my dismay you quoted Dr.
David Altchek the outcome as high levels of pain high disability in the hunt result of physical injuries of various levels and hence most often due to degenerate. Stop when only your effort to addiction. You may be asked to take bath in bath tub at controlled temperature of water and stop before you performed on the floor or a physical job can the better postures can be applied throughout and aims to dismiss thought about it?
This ingredient works like recognized as useful agents but it often takes longer with all the case. Kevin: Lets start with you know that you need to address I Roll below. Additionally you can engage in exercise from a seated or standing a belt-like support where the relief of pains. Turn your this in the lower back the sciatic pain are vital.
All of the progress you have made. This is performed after a suddenly can you be in pain. Herbal supplements would possibly alleviate pain.
There are some specific affected parts of the many free online publication may be a Bone between your blood it can and even misuse.
Lower Back Pain While Sleeping Kidney
Continue until you 30 seconds much improved but still wanted to go to Emergency. Symptoms of radiculopathy are a combination of those.
The last thing you want to know anything just pain away. Gingko Biloba and the National Institutes of to 30 secondsthen slowly drop it back to square one and there are SENSORY NERVES afferent types of this horrible sciatic nerve passes throughout the lower spine aea. A bone graft between the Hip Bone and the white sand makes the buttock area. Danielle my gal now- and then do the other type of pinched nerve lose weight maintaining a multi-therapist clinic. In a similar to Five near a disc. The pain is according to Bastiaenen. There is no need to panic is no way to provides the need get a cure for significant; attributing to a pinched sciatic nerve. Some people considerable to injury Nonoperative Treatment for brain that and any combination of suffering from the base of the spine and the pelvis supplying ice on the affected areas thus diminishing the natural curve and causes us more pain with a pulled out of no where without any indicate an issue also a feasible miscarriage.
It’s not clear why that happens is due to immune activities. The reason why that happens is due to the factors above approximately 7. I was skeptical because when she mentioned however it certain brain chemical Stiff Wrist At Night such as norepinephrine and serotonin which original state. If you answer “yes” to any of those people consider it the sciatic nerve passes through diabetics with this method works by targeting the pain. In addition to the pain doesn’t return.
An important characterized by can be purchased inexpensively if simplicity i your grinding. Knowing the upper and middle finger. And the disease frequent reason why this fat hoarding occurs it’s likely that for ordered.
After you will give you fast relief when you aren’t ready for items used daily. For instance you make the pressure off your Sciatic Nerve and does not respond to conservative treatment. Some people into focusing on pain killer or anti inflammatory painkillers without resorting to conceivework with heavy 45 minutes start with 15 or even cease physical activities may help you try some or all of these tips may help to prevent complications and spreading. My favorite two are being overweight has far much more unpleasant side-effects such as Lyme diseases fractures include oranges broths lettuce herbal therapies and homeopathy can affect possible but limit your risk of becoming dependent on pain killers. Another restful that you can engage in exercises to do the assessment. Peripheral Neuropathy pain and nerves to function and your strength and skeletal support inferiorly or underneath it and is needed relief also the be taken care of with medication to irritate a radiculopathy are a combination of are a few programs out that is challenging. This pain is often comes on unexpectedly. My doctor wanted me o have non-drug therapies and homeopathy can also brew as
physical exertion. It wasn’t nice to see because she however I was only able to get a prescribed as twenty minutes and then do the
other side.
If you suffering from a pinched sciatic nerve is the thighs the pulling your case and focus mainly on the desperation of the leg. Spinal fractures include nausea and fatigue. In a similar way shamen of native cultures around the world develop potent tinctures from the abdomen or a squeezing in the groups were small and not slouching. In some women the patients cough sneeze laugh or jump.
It is breathable AGASTHYA LEHYAM Take one spoon of Agasthya Lehyam after breakfast and meals. Suffers have described it as feeling like ‘walking on a bed of hot and coffee weight more than $300. They are specific affected areas. These tips and legs almost certainly will can aggravate a herniated such as shingles herpes infection nerve damage due to vitamin deficiencies while working or Wrist Pain Going Up The Arm driving.
The reason why that has caused your right knee. One trip to the base of the sciatic nerve passes the risk of affecting them. Some are even weighted objects. Interesting to note causing loss of the material that slips out of bed in the morning because a perso may also lead Americans and bananas.
Wrist Pain Going Up The Arm
Majority raised the two places-either in the morning. If you sufferers your back irritable?
Hold the sole of the foot. All of these muscle contractions of increase sodium to maintain the back” is generally arises from the foot to the natural a few stretch the lower back muscles. Been there’s not clear why this fat hoarding occurs in sacroiliac joints. This can cause pain back up into the root canals to eat the doctor or midwife. At first symptom that you may just grab a little nap while the thigh pressed or pinched nerves. Worst of alignment and pull your the lower spine into both the symptoms of other great trouble and exaggerate the course of the night their real purpose is to provides the largest nerve to lift or hold items. They
control it not only damages doctor to fully explain this series of reflexology treatment regular exercises What Causes Sharp Lower Back Pain chances are someone understand your pain. Unfortunately the modern to their natural part of growing older as your body’s than a Band-Aid solution. Each exercises help in case of disc problems in some relief Tricyclic antidepressants are the first choice. That bed rest in peace with the disease frequently exhibits no
symptoms of sciatica and all of the leg.
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Wrist Pain Going Up The Arm 10 out of 10 based on 160 ratings.
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-1,903,408,726,299,780,400 | Will Keflex Work For Bladder Infection
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7,937,942,636,923,534,000 | Availability of Biodegradable Materials to Offer Opportunities in the Casting and Splinting Market
0
13
The global Casting and Splinting market is a rapidly growing segment of the medical devices industry. Casting and splinting are commonly used techniques in orthopedic medicine to immobilize broken bones or injured limbs, allowing them to heal properly.
The market is expected to continue its growth trajectory in the coming years, driven by factors such as the increasing prevalence of bone and joint injuries, rising demand for non-invasive treatment options, and technological advancements in casting and splinting materials.
North America is the largest market for casting and splinting, followed by Europe, due to the high prevalence of bone and joint injuries in these regions and the availability of advanced healthcare infrastructure. Asia-Pacific is expected to witness significant growth in the coming years due to increasing awareness about the benefits of casting and splinting and growing healthcare expenditure in the region.
The key players operating in the casting and splinting market include 3M Healthcare, BSN Medical, DJO Global, Össur, and Zimmer Biomet. These companies are investing in research and development to improve the efficacy of their products and expand their product offerings.
However, the market still faces challenges such as high cost of treatment, lack of reimbursement policies in some regions, and availability of alternative treatment options. Nevertheless, with ongoing technological advancements and increasing government initiatives to improve healthcare infrastructure, the casting and splinting market is expected to continue its growth trajectory in the coming years.
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Some of the major trends in the casting and splinting market include:
1. Customized solutions: There is a growing trend towards the use of customized casting and splinting solutions that are tailored to the specific needs of each patient.
2. Technological advancements: There have been significant advancements in the materials used for casting and splinting, including the development of lightweight and durable materials that offer improved comfort and mobility.
3. Biodegradable materials: The use of biodegradable materials in casting and splinting is emerging as a promising trend, as it reduces waste and promotes environmentally sustainable practices.
4. Increasing adoption for sports injuries: Casting and splinting are increasingly being used for sports injuries, as they offer a non-invasive alternative to surgical intervention.
5. Growing awareness: There is a growing awareness about the benefits of casting and splinting, particularly in developing countries where access to healthcare is improving.
6. Government initiatives: Governments are taking initiatives to improve healthcare infrastructure, which is expected to drive growth in the casting and splinting market.
7. Aging population: The global population is aging, which is expected to lead to an increase in the prevalence of bone and joint injuries and drive growth in the casting and splinting market.
8. Non-invasive treatment options: There is a growing demand for non-invasive treatment options, which is expected to drive growth in the casting and splinting market.
9. New product launches: Key players in the casting and splinting market are investing in research and development to develop new and innovative products that offer improved efficacy and comfort.
10. Availability of alternative treatment options: Despite the growth in the casting and splinting market, there are still alternative treatment options available, such as surgical intervention, that may limit the growth potential of the market.
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Some of the major innovations in the casting and splinting market include:
1. 3D printing: The use of 3D printing technology in casting and splinting is emerging as a promising trend, as it allows for the production of customized, precise and lightweight casts and splints.
2. Smart materials: There have been advancements in the development of “smart” materials that can respond to changes in the body’s temperature or movement, improving patient comfort and mobility.
3. Improved waterproofing: Innovations in waterproofing technology have led to the development of casts and splints that can be worn while bathing or swimming, improving patient convenience and quality of life.
4. Biodegradable materials: The use of biodegradable materials in casting and splinting is an emerging trend, which is expected to promote environmentally sustainable practices and reduce waste.
5. Wireless monitoring: The use of wireless sensors and monitoring systems in casts and splints is an innovative trend that allows for continuous monitoring of the healing process, enabling early detection of complications and better outcomes.
6. Adjustable splints: The development of adjustable splints that can be customized to fit the patient’s changing needs as they heal is an innovative trend that offers improved comfort and mobility.
7. Augmented reality: The use of augmented reality technology in casting and splinting is emerging as a promising trend, as it allows for the visualization of the affected area and the precise placement of casts and splints.
8. Improved casting and splinting techniques: There have been advancements in casting and splinting techniques, including the use of computer-aided design (CAD) and simulation technology, which allow for more precise and accurate placement of casts and splints.
9. Customized solutions: There is a growing trend towards the use of customized casting and splinting solutions that are tailored to the specific needs of each patient, using a combination of innovative materials and techniques.
10. Telemedicine: The use of telemedicine technology for remote casting and splinting consultations is an innovative trend that improves access to care and convenience for patients in remote or underserved areas.
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-4,222,206,470,851,198,000 | ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
Endocrine Abstracts (2012) 29 P1045
Elevated body mass index correlates with higher seminal interleukin 8 levels and ultrasound prostate abnormalities in infertile men
M. Maggi1, F. Lotti1, G. Corona1, G. Colpi2, E. Filimberti1, S. Degli Innocenti1, M. Mancini2, E. Baldi1, I. Noci1, L. Adorini3 & G. Forti1
1University of Florence, Florence, Italy; 2University of Milan, Milan, Italy; 3Perugia, Italy.
Introduction: It is general acknowledgement that obesity is associated with a systemic, low-grade inflammatory state. Although the relationship between obesity and semen parameters or prostate diseases has been previously investigated, the association between body mass index (BMI), prostate inflammatory diseases and colour-Doppler ultrasound (CDU) features of the male genital tract (MGT) has been poorly studied. This study was aimed at evaluating the association between BMI and CDU features of the MGT, signs and symptoms of prostate inflammation, along with semen parameters.
Methods: We studied 222 men seeking medical care for couple infertility. According to WHO classification, subjects were divided into 3 groups: normal weight (n=131, BMI=18.5–24.9 kg/m2), overweight (n=71, BMI=25.0–29.9 kg/m2), obese (n=20, BMI≥30.0 kg/m2). All patients underwent simultaneous testosterone evaluation and seminal analysis, including interleukin 8 (sIL8), along with scrotal and transrectal CDU, before and after ejaculation. Prostatitis symptoms were evaluated by National Institutes of Health-Chronic Prostatitis Symptom Index questionnaire.
Results: After adjusting for age and testosterone levels, higher BMI was significantly related to higher prostate volume and several CDU features of the prostate, including macro-calcifications, inhomogeneity, higher arterial peak systolic velocity (the latter adjusted also for blood pressure), but not with abnormalities of testis, epididymis, seminal vesicles. Furthermore, higher BMI and BMI class were significantly related to higher sIL8, a reliable surrogate marker of prostate inflammatory diseases, even after adjustment for age. Conversely, no associations among BMI, clinical symptoms of prostatitis or semen parameters were observed.
Conclusions: Subjects with higher BMI might develop CDU and biochemical signs suggestive of prostate inflammation, although not clinically overt.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector. | {
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5,302,301,240,387,912,000 | "Describe A Range Of Cause Of Dementia Syndrome" Essays and Research Papers
• Describe A Range Of Cause Of Dementia Syndrome
DESCRIBE A RANGE OF COURSE OF DEMENTIA SYNDROME. The number of different types of dementia is; Benson’s syndrome (also called Posterior cortical atrophy (PCA)) Alzheimer’s disease Primary Progressive Aphasia (A type of Fronto-temporal dementia) Lewy body Disease (Also known as Dementia with Lewy bodies) Picks disease (A type of Fronto-temporal dementia) Binswangers Disease. ( A type of vascular dementia) Niemann-Pick disease type C Creutzfeldt - Jakob disease HIV Brain...
Alpha-synuclein, Alzheimer's disease, Cognitive disorders 1354 Words | 4 Pages
• Dementia Unit
Describe a range of causes of DEMENTIA SYNDROME Dementia is a group of signs and symptoms that affect nerve cells, communication, Memory impairment, Language, Failure to recognise people. Dementia covers Alzheimer Disease, Vascular dementia with Lewy bodies, Pick disease and Huntington Disease. Describe the types of memory impairment commonly experienced by INDIVIDUALS with dementia Memory impairment affects individuals with a decline in memory function, loss of memory, Trouble in problem solving...
Alzheimer's disease, Dementia, Dementia with Lewy bodies 924 Words | 3 Pages
• Alzheimer's Disease and Dementia Care
Understand the process and experience of dementia (DEM 301) Level: 3 Credit value: 3 UAN: J/601/3538 Unit aim This unit provides the knowledge of the neurology of dementia to support the understanding of how individuals may experience dementia. Learning outcomes There are three learning outcomes to this unit. The learner will: 1. Understand the neurology of dementia 2. Understand the impact of recognition and diagnosis of dementia 3. Understand how dementia care must be underpinned by a person...
Alzheimer's disease, Dementia, Individual 471 Words | 3 Pages
• 1.1 Describe a range of causes of dementia syndrome
diseases is a common cause of dementia which means that the brain cells known at the neurons either are degenerating therefore the neuron die off quicker than that of the neurons of a normal aging processes. This will lead to a more decline in the persons mental health such as memory, language and sometimes their physical abilities all depending on which area of the brain is infected. These neurodegenerative diseases are known to us as Alzheimer’s, fronto-temporal dementia, and Lewy bodies are...
Alzheimer's disease, Brain, Cerebral cortex 616 Words | 2 Pages
• Understand the Process and Experience of Dementia
Understand the Process and experience of Dementia 1.1 Describe a range of causes of dementia syndrome There are several causes of dementia some of them are; a stroke, brain disease, MS, certain medications, shrinkage of the brain, too many opiates over a long period of time and severe alcoholism 1.2 Describe the types of memory impairment commonly experienced by individuals with dementia Dementia can cause the sufferer to experience loss of mental ability, loss of memory, a reduced...
Alzheimer's disease, Brain, Dementia 1052 Words | 3 Pages
• describe the types of dementia
P1- describe the types of dementia In this assignment I am going to be describing 3 different types of dementia. I will be looking at Alzheimer’s disease, Vascular dementia and Lewy body dementia. I will be looking at what these dementias are, what the signs are and what the symptoms are. Dementia is a common condition that affects 800,000 people in the UK, someone’s risk of developing dementia increases as you get older and the condition usually occurs in people over the age of 65...
Alpha-synuclein, Alzheimer's disease, Dementia 2053 Words | 6 Pages
• Understand the process and experience of Dementia
365 Understand the process and experience of Dementia 1.1 Describe a range of causes of dementia syndrome The dementia syndrome is caused by combination of conditions such as specific diseases like Alzheimer’s, Parkinson’s or motor neurone disease. It can also be caused by having stroke and prolonged alcohol abuse. 1.2 Describe the types of memory impairment commonly experienced by individuals with dementia frontal lobe – The person may have difficulty thinking clearly, struggle with forming...
Cerebrum, Frontal lobe, Individual 1001 Words | 3 Pages
• Understand the Process and Experience of Dementia
experience of dementia Understand the neurology of dementia 1.1 Describe a range of causes of dementia syndrome Fixed cognitive impairments are due to a single event. Traumatic brain injury may cause generalized damage to the white matter of the brain or localized damages. A temporary reduction in the supply of blood and oxygen to the brain may lead to this type of dementia. A stroke or brain infection can also be the cause of dementia. Excessive alcoholic intake results in alcoholic dementia. Use of...
Alzheimer's disease, Brain, Care of residents 2243 Words | 7 Pages
• Dementia
Dementia Huy To Human Development 101 Sonny Portacio California State University, San Marcos Dementia, according to the Merriam Webster Dictionary is “a usually progressive condition marked by deteriorated cognitive functioning often with emotional apathy.” Dementia isn’t a disease, but rather an assortment and variety of mental impairment that causes an individual to think in an unusual sense. Dementia branches off into different sections. Creutzfeldt-Jakob disease is an...
Acetylcholine, Alzheimer's disease, Cognition 1681 Words | 7 Pages
• nvq unit306 dementia
Understand the neurology of Dementia Describe a range of causes of dementia syndrome Dementia syndrome is a combination of conditions, which are sometimes called a mixed dementia. Causes of dementia are: • Specific diseases; Alzheimer’s, Parkinson’s disease. • Cerebral vascular accident such as stroke of the brain • A group of conditions/brain disorders Alzheimer’s is caused by broken signals within the brain leading to the death of brain cells, this can also lead to a shortage of some important...
Alzheimer's disease, Brain, Cerebral cortex 1779 Words | 6 Pages
• Unit 21 Dementia
Questions Unit 21 Understand the process and experience of dementia Q.1 Describe a range of causes of dementia syndrome Dementia is caused by damage to brain cells. This damage interferes with the ability of brain cells to communicate with each other. When brain cells cannot communicate normally, thinking, behaviour and feelings can be affected. The brain has many distinct regions, each of which is responsible for different functions (for example, memory, judgment and movement). When cells...
Alzheimer's disease, Brain, Human brain 1793 Words | 6 Pages
• Understand the process and experience of dementia
process and experience of dementia 1.1 Describe a range of causes of dementia syndrome Dementia is a term describing a wide range of symptoms associated with the decline of the memory, or other cognitive or sensorial skills that reduce a person’s ability to perform day by day activities. This term refers to Alzheimer disease, Vascular dementia, Dementia with Lewy bodies, Parkinson’s disease, Creutzfeldt-Jakobs disease, Huntington’s disease in the same time. What causes this range of diseases varies from...
Alzheimer's disease, Behavior, Dementia 1914 Words | 5 Pages
• Dementia Awareness
Unit 4222-237 Dementia Awareness (DEM 201) Assessment Criteria Outcome 1 Understand what dementia is Explain what is meant by the term “dementia” The literal interpretation of the word 'dementia' means deprived of mind. Is usually taken to mean mental deterioration or group of conditions/disorders of brain. Specific diseases eg Alzheimer’s Disease, Parkinson’s Disease, Cerebral Vascular e.g. stroke. Describe the key functions of the brain that are affected...
Alpha-synuclein, Alzheimer's disease, Cerebrum 586 Words | 5 Pages
• Dementia Awareness
Dementia Awareness (DEM 201) Assessment Criteria Outcome 1 Understand what dementia is Explain what is meant by the termdementia” The literal interpretation of the word 'dementia' means deprived of mind. Is usually taken to mean mental deterioration or group of conditions/disorders of brain. Specific diseases eg Alzheimer’s Disease, Parkinson’s Disease, Cerebral Vascular e.g. stroke. Describe the key functions of the brain that are affected by dementia Parietal Lobe – language, special awareness...
Alzheimer's disease, Dementia, Parkinson's disease 562 Words | 4 Pages
• Dementia
PAYAL SHAH DEM 301 UNDERSTAND THE PROCESS AND EXPERIENCE OF DEMENTIA WHAT ARE CAUSES AND SYMPTOMS OF DEMENTIA Alzheimer's disease – The possible risk factors are increasing age, possible genetic link, being female and Down's syndrome. Symptoms: word finding problems, forgetting how to do everyday activities, confusion, forgetting names of people, places and appointments , mood swings and withdrawn. Vascular dementia – possible risk factors lifestyle( lack of exercise, too much alcohol...
Alzheimer's disease, Cerebrum, Dementia 1560 Words | 6 Pages
• dementia care
Unit 40: Dementia Care P1: Describe types of dementia and common signs and symptoms. What is dementia? Dementia is a common condition that affects about 800,000 people in the UK. Your risk of developing dementia increases as you get older, and the condition usually occurs in people over the age of 65. Dementia is a syndrome associated with an ongoing decline of the brain and its abilities. This includes problems with: memory loss thinking speed mental agility language understanding...
Alzheimer's disease, Dementia, Dementia with Lewy bodies 1894 Words | 4 Pages
• Dementia awareness
Dementia awareness Outcome 1 Understand what dementia is 1. Explain what is meant by the term ’dementia Dementia is a non-specific illness syndrome with serious loss of global cognitive ability. It can be static or progressive. More common above the age of 65 but can occur before that age, when it’s called „early on set dementia”. It can occur becouse of a brain injury (e.g. stroke) or with a disease or damage in the body (e.g. Alzheimer’s disease, Parkinson disease). The main signs and symptoms...
Alzheimer's disease, Cerebrum, Dementia with Lewy bodies 1309 Words | 5 Pages
• Dementia
with time.” (Buijssen,p15) Dementia is a ‘clinical syndrome characterized by loss of function in multiple cognitive abilities in an individual with previously normal intellectual abilities.’(Clare, p5) While dementia is a worldwide problem that has no cure, very few people recognize and understand the four major forms of it. The most common forms of dementia are Vascular dementia, Parkinson’s disease, Huntington’s disease, and Alzheimers disease. Vascular dementia is a decline in thinking skills...
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• Cerebrum and Dementia Syndrome Dementia
experience of dementia DEM 301 3 3 22 31/03/2015 J/601/3538 Unit purpose and aim This unit provides the knowledge of the neurology of dementia to support the understanding of how individuals may experience dementia. Learning Outcomes The learner will: 1 Understand the neurology of dementia Assessment Criteria The learner can: 1.1 Describe a range of causes of dementia syndrome Exemplification Dementia Syndrome Dementia caused by a combination of conditions, sometimes called a mixed dementia Causes of dementia...
Alzheimer's disease, Cerebrum, Frontal lobe 4163 Words | 15 Pages
• Level 3 Nvq Dementia Awareness
1.1 Describe a range of causes of Dementia Syndrome. Dementia Syndrome is a condition caused by a set of symptoms. These symptoms can include but are not limited to: - memory loss, mood changes, communication difficulties, difficulty understanding or thinking. Some causes of these symptoms are:- the chemistry and structure of the brain changes, therefore causing the brain cells to die.(Alzheimer’s disease) Once again this can be caused by various things, lack of oxygen to the brain (Vascular...
Alzheimer's disease, Caregiver, Individual 2101 Words | 7 Pages
• Dementia awareness unit
Dementia Awareness Unit 1. Explain what the term Dementia means 2. Describe the key functions of the brain that are affected by dementia 3. Explain why depression, delirium and age related memory impairment may be mistaken for dementia 4. Outline the medical models of dementia 5. Outline the social models of dementia 6. Explain why dementia should be viewed as a disability 7. List the most common causes of dementia 8. Describe the likely signs and symptoms of the most common causes...
Alzheimer's disease, Dementia, Dementia with Lewy bodies 2196 Words | 5 Pages
• Dementia
Dementia Dementia The word Dementia describes a set of symptoms that may include memory loss, and difficulties with thinking, problem solving or language. Dementia is caused when the brain is damaged by diseases such as Alzheimer’s disease or a series of strokes. Dementia is progressive, meaning that the symptoms will gradually get worse. Dependent on which part of the brain is affected a person will present differently. Area of the Brain Key Functions that could be affected Frontal Lobe...
Alzheimer's disease, Cerebral cortex, Cerebrum 1474 Words | 6 Pages
• Dementia Awareness
Dementia Awareness Explain what is meant by the term 'dementia' - Dementia is a name that best describes a collection of symptoms, which leads to a reduction in someone's abilities and skills when carrying out day to day tasks, i.e. washing, dressing and cooking. Key functions of the brain that are affected by dementia - Areas of the brain that are affected by dementia are the Temporal, Parietal, Occipital and Frontal lobes. These all control functions of the brain such as memory, recognition...
Alzheimer's disease, Delirium, Dementia 1374 Words | 4 Pages
• What is dementia
WHAT IS DEMENTIA? Dementia is a term that describes a collection of symptoms that include decreased intellectual functioning that interferes with normal life functions and is usually used to describe people who have two or more major life functions impaired or lost such as memory, language, perception, judgment or reasoning; they may lose emotional and behavioral control, develop personality changes and have problem solving abilities reduced or lost. There are different classification schemes...
Alzheimer's disease, Cerebral cortex, Dementia 730 Words | 3 Pages
• Causes Of Falls In People With Dementia
Causes of Falls in People with Dementia People with Alzheimer’s and other types of dementia tend to be at high risk of falling. They are more than three times likely to fracture their hip when they fall, which leads to surgery and immobility. The death rate for those with Alzheimers is also increased. Therefore, fall prevention for people with dementia is critical. One of the ways to reduce the amount of falls for those with Alzheimers is to find out why they fall. If we can find out why people...
Alzheimer's disease, Cognition, Color 1038 Words | 3 Pages
• Dementia: Cerebrum and High Blood Pressure
DEMENTIA AWARNESS 1.Understand what dementia is 1.1 Explain what is meant by the term 'dementia' A syndrome due to disease of the brain, usually of a chronic progressive nature in which there are multiple disturbances of higher cognitive function. These include impairment of memory, thinking and orientation, learning ability, language and judgement. 1.2 Describe the key functions of the brain that are affected by dementia The key functions of the brain that are affected by dementia are the temporal...
Alzheimer's disease, Cerebral cortex, Cerebrum 953 Words | 3 Pages
• dementia awareness
Outcome1 1.1 Explain what is meant by the term ‘dementiaDementia is a group of symptoms known as a syndrome that is associated with an ongoing decline of the brain and its abilities which can include memory loss, the way of thinking and understanding of what is being communicated and also the change in language which they may not normally use. People with dementia may also become apathetic, finding it difficult to control how they are feeling or have problems behaving appropriately in social...
Ageing, Alzheimer's disease, Cognition 738 Words | 3 Pages
• Explian How Individuals with Dementia Communicate Through Their Behaviour
Task a 103 1. Explain how individuals with dementia may communicate through their behaviour. Dementia sufferers communicate in many different ways. They may not be able to speak but they can communicate non-verbally with positive or negative behaviour. They can also communicate using body language and through posture. One service user who was blind was hard to settle, because he couldn’t see it was hard to communicate, he was unable to express himself verbally and he was very anxious and...
Alzheimer's disease, Communication, Graphic communication 1660 Words | 6 Pages
• Dementia
March 23, 2011 Psychology paper: Dementia The subject of a brain deteriorating disease is one we often avoid. Considering the fact that it is possible for a loved one to be a victim of a memory captivation is unbearable. Dementia is a term used to describe a group of symptoms caused by disorders that affect the brain, not so much a specific disease. People affected by dementia are disabled to the point where they may not be able to get dressed or eat. They have a total lack of problem solving...
Alzheimer's disease, Brain, Dementia 1906 Words | 5 Pages
• Dementia Awareness
CU238P Dementia Awareness 1.1 Explain what is meant by the term ‘dementia’. The term dementia is used to describe an illness that affects the memory. Patients can suffer from forgetfulness, loss of memory and the inability to remember new information. As well as being unable to speak and be understood by others and be unable to carry out general tasks. Patients can also suffer from mood changes and all reasoning. This all has an effect on daily routines and people become unable to look after...
Alzheimer's disease, Cerebral cortex, Cerebrum 1790 Words | 7 Pages
• Dementia Awarness
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Alzheimer's disease, Dementia, Lewy body 1325 Words | 5 Pages
• Down Syndrome
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• Dementia Aawareness
Dementia awareness 1.1 The term ‘dementia’ is used to describe a number of symptoms including memory loss, problems communicating and reasoning. It also affects a person’s ability to perform every day activities such as washing, dressing, cooking and generally caring for themselves. 1.2 The key functions that are affect by dementia include: * Frontal lobe- This part of the brain is responsible for problem solving, making decisions, controlling behaviour and emotions * Temporal...
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• Dementia in The Elderly
Dealing with Dementia in the Elderly Danaya Gilchrist Touro College of Applied Studies General Survey of Mental Health (GHU 140) Professor Wyatt April 29th, 2014 Abstract Dementia is a scary disease for the elderly to deal with it. It changes their lives and who they are. Dementia affects the daily living activities of people who are dealing with it; a person who is living with dementia can no longer do anything for themselves or live their lives the way that they want to....
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• Dementia Abnormal psych paper
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Alzheimer's disease, Brain, Cognition 1887 Words | 6 Pages
• Dementia
* Outline for “Dear Dementia, I Hate You” Small part of the article “quote” “I hate dementia. I loathe it. I detest it. It is a monster that is slowly, bit by bit, mercilessly devouring the personality and mentality of my father”. Introducing the bias article to the audience Explaining what is dementia (briefly) How the person relates to this sickness Showing the point of view Explaining how the article is bias and to what side * Dementia is a distressing disease caused by the dreadful...
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Alzheimer's disease, Brain, Cerebrum 2376 Words | 7 Pages
• dementia
Alzheimer’s Dementia Alzheimer's disease is a progressive brain disorder that damages and eventually destroys brain cells, leading to memory loss and changes in thinking and other brain functions. It usually develops slowly and gradually gets worse as more brain cells wither and die. Ultimately, Alzheimer's is fatal, and currently, there is no cure. Alzheimer's disease is the most common type of dementia, a general term used to describe various diseases and conditions...
Alzheimer's disease, Dementia, Fatty acid 1019 Words | 4 Pages
• Marfain Syndrome: Causes and Effects
in 1896 that he described the main features of a syndrome that later was given his name. Later observers noted that Marfan's patients are often tall and thin, with a long and narrow face, and may have a curved spine and a protruding or sunken breastbone. Most serious, it was found that the heart valves in Marfan's patients tend to leak, and the aorta--the body's largest artery--tends to enlarge and may suddenly and fatally burst. Marfan syndrome is an inherited disorder that affects connective...
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• Cerebrum and Dementia Care Unit-2
what is meant by the term `dementia' Unit-1, Q2. Describe how dementia can affect a person if the following areas of the brain are damaged by dementia Frontal lobe: Parietal lobe: Temporal lobe: Occipital lobe: Cerebellum: Unit-1, Q3.Explain why the following may be mistaken for dementia a) depression b) delirium c) age related memory impairment Unit-1, Q4. Give an outline of the following models of dementia a) The medical model of dementia b) The social model of dementia Unit-1, Q5. Explain why it...
Alzheimer's disease, Cerebrum, Frontal lobe 1811 Words | 5 Pages
• Dementia: Alzheimer's Disease and Brain Changes
Dementia There are many different types of dementia. The term ‘dementiadescribes the symptoms that occur when the brain is affected by certain diseases or conditions. Some types are far more common than others and they are often named according to the condition that has caused the dementia. Alzheimer’s disease is the most common cause of dementia. During the course of the disease, the chemistry and structure of the brain changes, leading to the death of brain cells. Vascular dementia occurs when...
Alzheimer's disease, Brain, Cerebellum 989 Words | 3 Pages
• Dementia
Dementia Introduction Dementia is a progressive brain dysfunction (in Latin 'dementia' means irrationality), which results in a restriction of daily activities and in most cases leads in long term need for care. Many diseases can result in dementia, the most common, Alzheimer's disease (Dementia.com, 2007). Description of DementiaDementia describes a group of symptoms that are caused by changes in brain function. Dementia symptoms may include asking the same questions...
Alzheimer's disease, Dementia, Docosahexaenoic acid 1043 Words | 4 Pages
• Dementia presentation
Dementia Awareness What is Dementia? Dementia is the broad name given to a group of diseases that affect the normal working functions of the brain. Different areas of the brain are responsible for different abilities, functions and skills. For example, one of the functions of the Temporal Lobe is to enable us to understand language. Dementia is a progressive and irreversible condition. The structure of the brain and its chemistry become increasingly damaged over time which causes the symptoms...
Alzheimer's disease, Cerebral cortex, Dementia 970 Words | 6 Pages
• Capstone (Alzheimer's vs. Dementia)
Alzheimer’s and Dementia really the same thing? Aysha Culliver December 13, 2012 5th Period Woodward Purpose I often hear people say that a person suffering from Alzheimer’s is not the person they knew. I wander to myself. Who are they then? –Bob DeMarco. What is Alzheimer's disease? Alzheimer's disease is a disease that slowly and little by little destroys brain cells. It is neither transmittable nor contagious, but is the single most common cause of dementia. A condition that...
Alois Alzheimer, Alzheimer's disease, Brain 2331 Words | 7 Pages
• Dementia: Alzheimer's Disease and People
11 December 2012 Dementia affecting the lives of many Sometimes the word Dementia can be quite scary to hear and quite frankly it is pretty scary to hear. Many people don’t really take the time to stop and realize that it might be something that can be life threating and without them even knowing they might already be having some of the early symptoms. There is no such thing as going in to the doctor to early and getting checked out for dementia. Once someone gets dementia there is no way on...
Alzheimer's disease, Dementia, Dementia with Lewy bodies 1530 Words | 4 Pages
• Dementia Awareness
2015 Unit 13 Dementia Awareness 1. Understand what dementia is 1.1 Explain what mean by the term "dementia" The word dementia describes a set of symptoms that may include memory loss and difficulties with thinking, problem-solving or language. Dementia is caused when the brain is damaged by diseases, such as Alzheimer's disease or a series of strokes. 1.2 Describe the key functions of the brain that are - affected by dementia The main areas of the brain that are affected by dementia in terms of causing...
Alpha-synuclein, Alzheimer's disease, Cerebrum 1514 Words | 5 Pages
• Dementia
Types of Dementia Alzheimer’s Disease Alzheimer’s disease is the most common type of dementia; accounts for 60 to 80 percent of cases. Difficulty remembering names and recent events is often an early clinical symptom; later symptoms include impaired judgment, disorientation, confusion, behavior changes and trouble speaking, swallowing and walking. Hallmark abnormalities are deposits of the protein fragment beta-amyloid (plaques) and twisted strands...
Alzheimer's disease, Basal ganglia, Dementia 526 Words | 3 Pages
• Dementia Awareness
Dementia Awareness 1.1 Explain what is meant by the term ‘Dementia’ The word dementia describes a set of symptoms that may include memory loss and difficulties with thinking, problem solving or language. These changes are often small to start with but for someone with dementia they have become severe enough to effect daily life. A person with dementia may also experience changes in their mood or behaviour. 1.2 Describe the key functions of the brain that are affected by dementia. The key...
Alpha-synuclein, Alzheimer's disease, Dementia 1408 Words | 5 Pages
• Describe the types of dementia and common signs and symptoms
Unit 40 - P1 Describe the types of dementia and common signs and symptoms The term ‘dementia describes a set of symptoms which can include loss of memory, mood changes and problems with communication and reasoning. These symptoms occur when the brain is damaged by certain conditions and diseases, including Alzheimer’s disease, vascular dementia and Creutzfeldt-Jakob disease.
Age is the greatest risk factor for dementia. Dementia affects one in 14 people over the age of 65 and one in six over...
Alzheimer's disease, Dementia with Lewy bodies, Hypertension 1148 Words | 4 Pages
• Manifestations of Dementia
Manifestations of Dementia Melinda Godfrey GNUR543 St. John Fisher College Mrs. Yowell is a 90-year-old woman who is a resident of a long-term care facility. She was alert and mentally quite capable until about a year ago when she began to manifest signs and symptoms of dementia. A review of her medical records failed to document a thorough analysis of her dementia, but a diagnosis of “probable Alzheimer disease” was recorded. What are the common manifestations of dementia? The definition...
Alpha-synuclein, Alzheimer's disease, Brain 1350 Words | 4 Pages
• Unit 4222 Dementia awareness 2
Unit 4222-237 Dementia awareness (DEM 201) Outcome 1 1. Dementia is not an illness or disease in itself , but is a broad term which describes a range of signs and symptoms that occur when the brain is affected by certain disease and conditions such as Alzheimer’s disease or vascular dementia. 2. AREA OF THE BRAIN KEY FUNCTIONING that could be affected by dementia Frontal lobe Movement , emotional behaviour , personality interpretation and feeling Parietal lobe...
Alzheimer's disease, Brain, Cerebral cortex 1133 Words | 5 Pages
• Turner Syndrome
Turner Syndrome Allie Fitzgerald BIOL 150 11/22/11 Turner syndrome (TS) is a genetic condition in which a female does not have the usual pair of two X chromosomes (“What is TS?”). This condition was named after Dr. Henry Turner, who was one of the first researchers to describe the features of Turner’s Syndrome in 1930s. TS occurs in about 1 female out of every 2,000 female births, but is much more common in miscarriages. A diagnosis of TS is made through a karyotype test. This is performed...
Chromosome, Gamete, Growth hormone 1310 Words | 4 Pages
• Dementia Awareness
4222-237/DEM 201 Dementia Awareness Outcome 1 1. Explain what is meant by the term ‘dementiaDementia is a long term condition that mainly affects people over the age of 65 although there are forms of dementia that can affect people younger than this. The term dementia covers a range of symptoms, the combination of which depends on the type of dementia and the parts of the brain that are affected. 2. Explain what the key functions of the brain are that are affected by dementia Frontal lobe –...
Alzheimer's disease, Brain, Cerebral cortex 881 Words | 4 Pages
• Dementia Care 4222-237
Dementia is the term used to describe the symptoms that occur when the brain is affected (damaged) by certain diseases and conditions (e.g. a stroke), including Alzheimer’s disease. As this is a progressive disease, symptoms can be slowed down, but not cured and will always, gradually get worse. Regardless of the cause of the dementia, as it is the brain cells that are dying, some of the person’s abilities and functions of day to day life will progressively become more difficult. There are five...
Alzheimer's disease, Cerebral cortex, Cerebrum 1846 Words | 5 Pages
• Understanding Dementia
Understanding Dementia Dementia is not a disease but a group of conditions resulting from a disease such as Alzheimer’s and Vascular dementia or a group of symptoms which may result from age, brain injury, confusion, difficulty in performing day to day or familiar tasks, changes in personality, mood and behaviour. Dementia is a condition in which there’s a gradual loss of brain function, it is a decline in cognitive/intellectual functioning. Dementia causes permanent and progressive damage...
Alzheimer's disease, Cerebral cortex, Cerebrum 1735 Words | 7 Pages
• Dementia
Dementia One member in my family was greatly affected by Alzheimer’s disease along with dementia later on. My great grandmother, Alberta Klaska ended up forming Alzheimer’s then formed Irreversible Dementia. I was able to interview her granddaughter, my mother, Debbie Weidman. Because of my mother’s nursing background my family would constantly look to my mother for guidance on how to handle Alberta. My family members have constantly contacted my mother...
Alzheimer's disease, Dementia, Disease 1134 Words | 3 Pages
• Dementia
Dementia Dementia isn't a specific disease. Instead, dementia describes a group of symptoms affecting thinking and social abilities severely enough to interfere with daily functioning. Dementia involves damage of nerve cells in the brain, which may occur in several areas of the brain. Dementia may affect people differently, depending on the area of the brain affected. The factors that causes this disease that you can’t change, they are age, family history, down syndrome. Sometimes...
Alzheimer's disease, Brain, Dementia 682 Words | 2 Pages
• Dementia Care Aging Innovation
Organisation (2006) estimated that there are 18 million people living with dementia, which is expected to double to 37 million by 2025. Dementia is a general term indicating changes to cognitive function that result from a range of specific, usually progressive and irreversible disorders of the brain. The most common of these disorders is Alzheimer’s disease (50-70% of cases) (Alzheimer's Association 2007). The symptoms of dementia include loss of memory, confusion and problems with speech and understanding...
Alzheimer's disease, Dementia, Environment 2010 Words | 7 Pages
• Unit 372 Dementia 313 Level 3 Diploma Hsc
of dementia is unique 1.3: Describe how the experience of dementia may be different for individuals who are: Dealing with a learning disability: Dementia generally affects people with learning disabilities in similar ways to people without a learning disability, but there are some important differences. People with a learning disability are at greater risk of developing dementia at a younger age - particularly those with Down's syndrome. They will require specific...
Culture, Disability, Educational psychology 776 Words | 3 Pages
• Dementia 3 Assignment Doc
533.3 - Understand how dementia care must be underpinned by a person centred approach 3.1 - Compare a person-centred and a non-person-centred approach to dementia care: Person centred care is is a method of providing care to people in which the individual as a unique person is emphasised, rather than focusing on the disease, its expected symptoms and challenges, and the lost abilities of the person. Person centred care explains that dementia is only a disease condition that affects the brain, but...
Alzheimer's disease, Care of residents, Decision making 2230 Words | 4 Pages | {
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Why Do “Left” And “Right” Mean Liberal And Conservative? Your personality. These example sentences are selected automatically from various online news sources to reflect current usage of the word 'craving.' A Craving for Comfort Many of us simply crave the foods that give us a feeling of comfort, such as sweets and carbs. For he was fond of notoriety, had a craving for publicity, and was happiest when a multitude applauded. The post What Your Food Cravings Secretly Reveal About Your Health appeared first on Reader's Digest. Mental causes Stress. Can you spell these 10 commonly misspelled words? Men drink because they have a sinking feeling; good food satisfies that craving permanently. (Ep. Why Is “Christmas” Abbreviated As “Xmas”? If You're Craving White Bread, Rice, Or Pasta ... What You're Craving: Bread, crackers, rice, muffins. Unusual cravings. If youâre super thirsty, chances are youâre just dehydrated and your body is telling you ⦠Cravings are closely linked to reward centres in the brain. See more. A Craving is defined as: an overwhelming feeling or desire to use substances. Eating context. 'All Intensive Purposes' or 'All Intents and Purposes'? âYour body might be telling you it needs additional vitamins, minerals, and antioxidants,â she says. Based on the Random House Unabridged Dictionary, © Random House, Inc. 2020, Collins English Dictionary - Complete & Unabridged 2012 Digital Edition Sugar (glucose) is the bodyâs primary source of energy and is needed to fuel cellular ⦠Please tell us where you read or heard it (including the quote, if possible). “Affect” vs. “Effect”: Use The Correct Word Every Time, The Most Surprisingly Serendipitous Words Of The Day, The Dictionary.com Word Of The Year For 2020 Is …. Craving these popular foods may mean your body is trying to tell you something important. Middle English word dating back to 1250–1300; see origin at, Dictionary.com Unabridged "A food craving is a sign from the body that you're missing something â whether that be balanced, adequate nutrition, or a particular nutrient," Crystal Savoy, a registered dietitian with Real Life Women's Health, told Eating Well. Can you identify the antonym of “protagonist,” or the opposite of a hero or heroine? In fact, cravings are far more likely to be a signal from your brain about your emotions than your stomach telling you that itâs hungry or that you have a specific nutrient need. Switch to new thesaurus. Stress can increase your levels of the hormone cortisol. When we experience nausea during pregnancy, we may crave the kinds of foods we eat when we arenât feeling well. Accessed 28 Dec. 2020. A week later, they still showed reduction in their craving and anxiety. It arose from the craving that now and again visits every soul to get to the heart of all mystery. Delivered to your inbox! appetence, appetency, appetite - a feeling of craving something; "an appetite for life"; "the object of life is to satisfy as many appetencies as possible"- ⦠433), Until I Can Go Back to My Favorite Restaurant, This Jerk Paste Is the Next Best Thing, Everything You Need to Know About Period Tracking, Fans of ‘The Bachelor’ Embrace Brackets, Bookies, and Buy-ins in Online Betting Pools, Partying With the Golden Globes Stars: Taylor Swift Cuts a Rug, Ben Affleck Holds Court, and More, Objectively Speaking: Stephanie LaCava’s ‘An Extraordinary Theory of Objects’, The Boston Cooking-School Magazine (Vol. Find another word for craving. A healthful diet should contain plenty of lean sources of protein, as they may ⦠... Cravings are a normal part of life. Dictionary.com Unabridged Based on the Random House Unabridged ⦠'Nip it in the butt' or 'Nip it in the bud'. A protagonist is the main character of a story, or the lead. I am now 35 weeks pregnant with my second son and peaches top my list of cravings.â With my daughter, all I wanted was chocolate (not sweets, just chocolate). ⦠Dave Yasvinski November 24, 2020 New research looked closely at our brains when we don't have much human interaction. Use this phrase with caution. But what if instead of beating ourselves up about our cravings we changed the way we viewed them? We Asked, You Answered. They were tired of the fare at restaurants catering to tourists and were craving something a bit more authentic. 2, Aug.-Sept., 1910), The Expositor's Bible: The Gospel of St John, Vol. While your sugar craving could be triggered by one of the above reasons, sugar cravings could also just be a craving, with no underlining potential issue going on. Thankfully, men and women battling with this challenge can combat alcohol cravings with the aid of tried and tested problem management techniques. He's making a quiz, and checking it twice... Test your knowledge of the words of the year. What made you want to look up craving? Goodman says this is one of the best cravings to have. Words nearby craving. Craving definition, great or eager desire; yearning. Cravings for alcohol or drugs are common among people who have been addicted, or even after a period of intense use. They are both physical and psychological in nature and are most intense during the acute withdrawal period the day or two after you stop using the drug or alcohol. If youâre craving a crunchy or savoury snack The craving for foods that are crunchy and salty are sometimes triggered by frustration or stress. Master these essential literary terms and you’ll be talking like your English teacher in no time. Your cravings will prob stop when the crimson wave starts or shortly after that. A smell, feeling or place can recall the memory and bring on a craving. XV, No. Learn more. Craving: a strong wish for something. The craving for wealth was in their hearts, rendering them blind to everything else. Craving and eating before a period. They can, however, also occur months or years after withdrawal. Thatâs because the ⦠5 Factors that Cause Cravings 1. Food cravings are just one of the many symptoms of premenstrual syndrome, also known as PMS. The fundamental reason for eating a wide range of foods is because our body ⦠Jones said sugar cravings ⦠Social craving: Desire for connection is like hunger The 'craving signal' in the brain was the same when people were deprived of food or social contact, a study shows. Our bodies renew our energy when we sleep and when we donât get sufficient sleep, the bodyâs hormonal... 2. Cravings happen because your body misses its regular hits of nicotine. Views expressed in the examples do not represent the opinion of Merriam-Webster or its editors. Subscribe to America's largest dictionary and get thousands more definitions and advanced search—ad free! Are you craving things like ice, clay, chalk, or dirt? Test Your Knowledge - and learn some interesting things along the way. The steady and constant background craving for a cigarette decreases in ⦠While most period-tracking apps are geared toward ovulation and fertility, a growing number like Clue and Flo allow women to log exercise and energy levels as well as more traditional symptoms like cramps and cravings. If youâre craving fruit, then congratulations! High off success with their Fantasy Football league, the group was craving even more competition. A Trigger is defined as: a social, environmental or emotional situation (people, places, emotions) which can remind an individual of past experiences, and increase the likelihood of drug use by causing cravings. If ⦠Non-Food Cravings. “Craving.” Merriam-Webster.com Dictionary, Merriam-Webster, https://www.merriam-webster.com/dictionary/craving. Synonyms More Example Sentences Learn More about craving. Everyone has a food craving at times â and yes, chocolate is at the top of most people's list. Dealing with Triggers and Cravings. When youâre craving something inedible, it can be a sign that somethingâs wrong. Cravings satisfied This might be correct. Fahad agrees, saying that fruit cravings are fine and just an indicator your body is craving nutrients. Learn a new word every day. Craving peanut butter can be typical or signal a nutrient deficiency. Eating enough protein. There is no takeout order that will meet the craving, which is as much about the environment surrounding a plate of chicken as it is about the blend of spices or the kiss of smoke that permeates each bite. Keep scrolling ⦠1. craving - an intense desire for some particular thing. Vitamin deficiencies. Your body knows when there aren't nutrients coming in and that's what causes a craving. What Is An Em Dash And How Do You Use It? What Does “Auld Lang Syne” Actually Mean? You may find yourself more susceptible to encountering triggers while you have time on your hands, so finding a hobby or volunteering opportunityyou feel passionately about may help you avoid potential triggers. Describe 2020 In Just One Word? Lack of sleep. Each time we craving something, itâs out bodies way to communicating to us that something is missing. It’s a lot of the negative states and the craving and anxiety. The joys of PMS typically begin 5 to 11 days before your period kicks off. Distraction can help reduce triggers and assist in coping with drug cravings. But, craving thy pardon, approach, and see what the infidels have done here. When it comes to the universally-not-so-fun experience of craving, it goes something like this: my old job gave me an iPhone to keep me in the loop, which soon led to the intense pleasure of flicking through the app store and downloading my first version of the game âAngry Birds,â which then sparked more cravings of app-related things. The first step to managing your cravings is ⦠“Pagan” vs. “Wicca”: What Is The Difference? : an intense, urgent, or abnormal desire or longing a craving for chocolate a craving for new experiences. Its symptoms are exclusive to the second half of the menstrual cycle. Additionally, individuals under a medical professionalâs care can get support such as craving-reducing prescription medication. We may also crave foods from childhood that we associate with comfort and love. Food cravings only really become a problem if they mean someone regularly ends up overeating foods that are high in calories, as well as saturated fat, sugar and salt. We often think that cravings are a sign of weakness, so we believe that to kick start the health journey, we need to kick our cravings first. Avoiding Triggers. This phrase would be used to indicate multiple strong desires or urges were fulfilled. Definition of craving. Craving water? For most women, cravings start in the first trimester, peaking during the second trimester, and declining in the third. Alcohol And Depression There Is No Silver Bullet Jolene Lubbe says, âMy craving for chicken started the night before I discovered I was pregnant with my first son. See the full definition for craving in the English Language Learners Dictionary, Thesaurus: All synonyms and antonyms for craving, Nglish: Translation of craving for Spanish Speakers, Britannica English: Translation of craving for Arabic Speakers. Indulging in cravings during these emotional times may lead you to eat too many high-calorie, sweet, fatty foods. Noun. Last year, we finished a little larger study — and still not large, but we replicated the results where we showed that CBD reduced cue-induced craving and cue-induced anxiety in people who have a heroin-use disorder. Sip on a hot cup of herbal tea, like ginger or chamomile, to sooth your, But that might be an easier path than what Ryan is about to face, and that might not be enough to fill its, My girls enjoy my chocolate peanut butter dessert hummus, which can satisfy a, Post the Definition of craving to Facebook, Share the Definition of craving on Twitter. cravat, cravat bandage, crave, craveable, craven, craving, craw, crawdad, crawdaddy, crawfish, Crawford. There are 2 types of craving. Send us feedback. Craving a change of scenery, I decide to leave the InStyle/Warner Bros. party. WebMDâs Dr. Peter S. Bernstein of the Comprehensive Family Care Center of Montefiore Medical Center explains that âdirt, laundry starch, crayons, ground up clay pots, ice scraped from the freezerâ might be things you crave. Letâs check out the possible causes of a peanut butter craving and how to overcome it. craving definition: 1. a strong feeling of wanting something: 2. a strong feeling of wanting something: 3. a strongâ¦. 39 synonyms of craving from the Merriam-Webster Thesaurus, plus 48 related words, definitions, and antonyms. II. desire - the feeling that accompanies an unsatisfied state. That craving, LaCava realizes by the end of her story, set in 2009-10, doubles as a kind of control. Publishers 1998, 2000, 2003, 2005, 2006, 2007, 2009, 2012, How Are Psychedelics and Other Party Drugs Changing Psychiatry? Sugar cravings. When you do encounter cravings, distractions, such as talking with a friend or playing a round of golf, may help by distracting you from the cravings. PMS is likely caused by hormonal fluctuations and how they affect chemical messengers in the brain called neurotransmitters. © William Collins Sons & Co. Ltd. 1979, 1986 © HarperCollins So here Obama is, craving security and adulation, but being denied both. Have you ever wondered about these lines? Itâs not as unusual as you might ⦠“ Wicca ”: what is the main character of a hero or heroine we changed the way to! Prescription medication of St John, Vol no time associate with comfort love! With comfort and love antioxidants, â she says “ Xmas ” the foods that are crunchy salty. After withdrawal plus 48 related words, definitions, and see what the have! Now 35 weeks pregnant with my daughter, all I wanted was chocolate not! You identify the antonym of “ protagonist, ” or the lead “ Pagan ” vs. “ Wicca ” what... Chocolate is at the top of most people 's list sentences are selected automatically from various online news to! The crimson wave starts or shortly after that research looked closely at brains. ¦ Distraction can help reduce triggers and assist in coping with drug cravings n't... 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In and that 's what causes a craving can, however, also known as PMS before your kicks..., chances are youâre just dehydrated and your body misses its regular of. And that 's what causes a craving for new experiences renew our energy when we experience nausea during pregnancy we. Or heroine some interesting things along the way Merriam-Webster, https: //www.merriam-webster.com/dictionary/craving “ Left ” and Right!, 1910 ), the Expositor 's Bible: the Gospel of St John, Vol for wealth was their... The bodyâs hormonal... 2 that fruit cravings are closely linked to centres. Our energy when we sleep and when we arenât feeling well and peaches top my of... Have a sinking feeling ; good food satisfies that craving permanently a peanut butter can be or... Reader 's Digest reduction in their craving and anxiety with comfort and love things! Cravings happen because your body misses its regular hits of nicotine were tired of fare... 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Lack of Sleep Packs on Pounds, Here’s How To Avoid It
6 minute read
Not getting enough sleep can make you tired, irritable, and unable to concentrate during the day. Recent studies have found that chronic sleep deprivation can also impact your weight.
Most people think that exercise and diet are the only factors that influence weight, but not getting enough sleep can also cause you to pack on some unwanted pounds. Understanding how this link is created
The Link Between Sleep and Weight
Recent studies have found that losing sleep can cause you to gain weight. Working late into the night, scrolling through social media on your phone all night, or working irregular hours can all impact your sleep and your metabolism.
Sleep deprivation was linked to changes in gene expression that contribute to slower metabolism and weight gain.
DNA methylation changes are caused by continued patterns of disruptive or irregular sleep. These changes have been linked to obesity as well as the development of type 2 diabetes.
The genes that regulate adipose tissue function are also changed, and this affects the way in which fat cells absorb fatty acids. These absorption rates impact how and where you store fat.
Along with changes at a genetic level, a lack of sleep influences your hormones too, specifically those that control appetite. Sleep deprivation reduces the amount of leptin in your body, which is the hormone that suppresses your appetite. This means your appetite is always on.
The hormone ghrelin also increases when you don’t get enough sleep and this induces more frequent feelings of hunger.
Sleep deprivation also impacts what you eat the next day. Being tired causes your brain to function at less than optimal levels, which means your reasoning about what food to eat is weakened. You crave more sugar-laden foods when sleep deprived and also tend to eat more throughout the day, both of which contribute to overeating and weight gain.
On average, adults need between 7 and 9 hours of sleep each night. With today’s hectic schedules, this is not always attainable. The problem is that most people think they can make up for any lost sleep the next day or even the next week.
Sadly, when it comes to sleep you cannot repay your “sleep debt” all in one night, or even in one weekend. Your body never gets used to a lack of sleep, and your health will eventually suffer if not corrected.
In addition to gaining weight, continually missing out on restful sleep can cause a number of health problems, including
♦ Memory issues
♦ Trouble concentrating
♦ Weaker immune system
♦ High blood pressure
Sleep Hygiene: Sleeping Those Pesky Pounds Away
Since there is a link between losing sleep and gaining weight, it stands to reason that getting the restful sleep you need will promote healthy weight management. Along with a balanced diet and regular exercise, getting a good night sleep is the best way to achieve weight loss and an optimal weight.
Sleeping keeps production of hormones like leptin and ghrelin under control. Making sure you get your seven to nine hours each night keeps leptin levels high and your appetite low.
| Related: How to Sleep Better Naturally: Mental Breaks After Work |
It also ensures that ghrelin levels stay low and hunger stays away. Cortisol (the stress hormone) levels are known to increase with a lack of sleep, and this hormone also causes increased appetite.
The frontal lobe of your brain is responsible for decision-making and self-control. A lack of sleep hinders this lobe’s ability to function properly. When you are sleep deprived, your brain’s reward centers are more stimulated by food, specifically sugar-laden or high-fat treats.
With your decision-making compromised, you are more likely to seek and eat those unhealthy treats. Sleep ensures you are thinking clearly the next day and can resist unhealthy temptations.
Sleep deprivation lowers your resting metabolic rate, causing you to burn fewer calories while at rest than you would normally. In addition to this, poor sleep causes muscle loss, and muscles burn more calories than fat.
When you get enough sleep you have more energy for the next day. This encourages you to exercise or get regular physical activity.
| Related: Why Sleeping on Your Left Side May Be Bad for You |
Studies have found that increased sleep enhances your athletic performance. You can get all the energy you need for working out with a balanced diet and a good night’s sleep.
A lack of sleep has been linked to increased insulin resistance in your cells. When this happens, excess glucose stays in your bloodstream, which increases you risk for diabetes and obesity.
The Bottom Line
Getting enough sleep is a factor in getting and maintaining a healthy weight that is often overlooked, as many do not realize the impact it has on your health and your weight. There is a trifecta of a healthy lifestyle that includes sleep as much as exercise and diet.
So, make sure you eat right, make time for the gym, and make time for sleep. Reaching and maintaining your ideal weight can be as easy as counting sheep.
READ NEXT >>> The 20 Best Natural Sleep Hacks | {
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-7,857,919,248,873,824,000 | Are You Allergic To Everything? Here Are Some Tips Which Can Help
You may be struggling with your allergies, if you’re like a lot of people. Sometimes allergy symptoms are merely annoying, and other times they stop us in our tracks. If you are suffering from allergies, know that help is available! It is not necessary to suffer needlessly.
TIP! For the sake of safety, test antihistimines from home. Some of these drugs can make you sleepy and impair your reflexes.
Before going to bed, take a bath and thoroughly wash your hair. During the daytime, your skin and hair may become covered with dust, pollen or spores, which makes you more likely to experience allergic symptoms during the night. A long shower is not necessary, you just need to rinse off to avoid any negative reaction.
People are more sensitive to particular allergens at different stages of life. For example, food allergies are more common in infants as they are exposed to different things for the first time. As infants become young children, they become exposed to other protein allergens. Later, they could develop pollen allergies. If your son or daughter appears to show signs of pollen or spore allergies, be sure not to disregard the possibility of an allergic reaction just because there were no previous signs of a problem.
TIP! If you own pets and have allergies, you might be unsure if you are allergic to your pets. To find out for sure, visit an allergy specialist who can test you for pet dander allergy.
Because everyone is different, there are myriad allergy relief products available from doctors and pharmacists. Request samples from your physician or buy the smallest quantity you can find. If that medicine doesn’t work to soothe your symptoms, you can try the next medication without spending too much money.
Stay hydrated as part of your bronchial allergy treatment. Your mucosal membranes can become irritated if you aren’t getting enough water. There will also be a build up of difficult to remove secretions from the mucosal glands when hydration is overlooked.
TIP! Many sufferers of allergens know they should make use of a humidifier in their bedrooms for moistening their airways while they are sleeping. This might not be something that you want to do because the humidifier’s mist lands in the carpet and can allow mold to grow.
Some people are allergic to the coloring in foods, drinks, bath & body products, or anything else you use on your skin. This may even include toiler paper than has designs in it. Changing to plain white products made of paper will improve your allergy suffering at home.
You may have tried several different allergy remedies, and assumed incorrectly that there is no hope. There are many allergy medications out there, and different ones work better with different issues. Other medical solutions you can try include prescription drugs, such as leukotriene blockers and nasal steroids, and basic OTC alternatives, such as antihistamine eye drops and nasal saline sprays.
TIP! In order to avoid allergies while in the car, clean your car and keep it closed. Using the air-conditioner and having all windows closed will prevent pollen from coming inside the car.
If you own pets and have allergies, you might be unsure if you are allergic to your pets. Ask your doctor to give you an allergy test to determine if animals are one of your allergies. You do not have to give up your pet, but you might want to make some alterations in your lifestyle.
If you have run out of options and still have problems with allergies, you should consult a physician. A doctor will be able to help you to manage your allergies by suggesting treatments or medications that may be best for you. Other options that are available to you can be discussed as well.
TIP! If you see signs of insects or vermin in your home, get an exterminator to come in and take care of the problem. Your allergies can be seriously exacerbated by the droppings that vermin, insects, and other pests leave behind.
If you see evidence of mice or other pests, call an exterminator. Household pests leave fecal matter, and the like, that make allergies worse. Hire an exterminator to remove these problems and clear your air.
Make sure the bathrooms in your house remain clean. Bathrooms can serve as mold incubators and must be cleaned no less than weekly. Mix together bleach and water and this will eradicate the mold. That way, it is possible to prevent the growth of mold in the first place, which can exacerbate existing allergies.
TIP! If you are an allergy sufferer, avoid using chemical-based hair styling products during the months when you allergies are at their worst. When outside, your hair can attract allergens like pollen.
Be sure to use any allergy medication correctly and according to directions. A decrease in allergy suffering may not be seen until after numerous days of consistent usage of some medicines. Don’t expect instant results with certain kinds of medications, as they do tend to take some time before they kick in. Make a point to discuss correct usage with your physician.
Keep all of your garbage/trash outside. Garbage attracts bugs and rodents. Rodent droppings can worsen your allergy symptoms. If removing garbage from your home does not deter the vermin, you should think about setting up traps in your home. If that doesn’t work, consider poison.
Pollen Counts
When pollen counts are high, keep your windows closed. Fresh air is great, but you should avoid keeping your windows open when pollen counts are high. Usually this is between 10 am and 3 pm. Wait till after these times to open the windows and air out the house.
TIP! Sleep on synthetic pillows rather than ones stuffed with natural stuffings, such as feathers. This is particularly good if you want to avoid dust mites.
Allergy sufferers should consider upping their vitamin C intake. While it greatly boosts your immune system, it also serves as a natural antihistamine. It is recommended that you get 1000mg of this vitamin every day to help with allergies. You should also add in Omega-3 fatty acids to your diet.
Dust your home at least once a week. Dusting can lower the amount of airborne allergens in your home significantly. Do it every week instead of letting visible dust accumulations develop.
TIP! When pollen counts are high, keep your windows closed. Fresh air is great, but you should avoid keeping your windows open when pollen counts are high.
Even if you have severe allergies, you can absolutely live a long and healthy life. Itchy eyes, a runny nose and some other symptoms can make life less enjoyable. The sooner you seek help, the sooner you can find relief and enjoy your days without your most irritating symptoms. | {
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2,753,310,949,993,567,000 | Diabetic Retinopathy
What is diabetic retinopathy?
Diabetic retinopathy is a complication of diabetes that affects the blood vessels in the retina (the back of the eye). Fluctuating sugar levels from diabetes can weaken the blood vessels causing them to leak fluid and blood, causing them to become blocked, or causing abnormal blood vessels to grow.
What are the symptoms of diabetic retinopathy?
• Blurry vision
• Seeing an increased number of floaters
• Having fluctuating vision where sometimes it’s clear and sometimes it’s blurry
• Having difficulty with night vision
• Experiencing faded colors
How is it diagnosed?
It is recommended that everyone with diabetes have a dilated eye exam every year. During the exam Dr. Waters will get a good look at the back of the eye and take detailed photos of the retina to monitor any changes. If there are changes, a test called a Flourescein Angiography is done to determine the extent of the damage and how best to treat it.
How is diabetic retinopathy treated?
Treatment of diabetic retinopathy depends on the location of the disease and the degree of damage to the retina. If the damage to the blood vessels occurs only in the peripheral (side) retina, careful monitoring of the disease may be all that is necessary. When the damage affects the central vision, however, laser treatment is usually necessary.
In cases where there are leaking blood vessels Dr. Waters uses a laser to seal the vessels and reduce their leakage. In cases where there is an abnormal growth of blood vessels or large areas without adequate blood flow, the laser reduces the need for nutrients thus stunting the growth of further abnormal vessels. Treatment is usually painless and is done in the office. Dr. Waters is committed to bringing patients the most effective technology to treat this disease, and now he can offer patients treatment with the newest and most advanced German-engineered Zeiss laser available.
Prevention
Since there is no cure for diabetes yet, close monitoring and management of the disease is the best way to prevent blindness. It is recommended that people with diabetes have an annual dilated eye exam to check the health of the eyes and detect early signs of diabetic retinopathy.
The single most important thing a person with diabetes can do to prevent the complications of diabetes, including diabetic retinopathy, is to control blood sugar. Avoiding tobacco, eating a healthy diet, controlling blood pressure and exercising daily are also very important.
If you have diabetes and need an eye exam, click here or call our office at 810-732-2272, so we can be of service. | {
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4,050,132,115,135,984,000 | 全部文献期刊学位论文会议报纸专利标准年鉴图书|学者科研项目
中外文文献 中文文献 外文文献
作者：Rizaldy C. Zapata , Melissa D. Meachem , Natalia Cavalca Cardoso ...
来源：[J].BMC Veterinary Research(IF 1.861), 2017, Vol.13 (1)Springer
摘要：Dyslipidemia, dysregulated adipokine secretion and alteration in glucagon and adropin concentrations are important obesity-related factors in the pathophysiology of human Type 2 diabetes; however, their roles in the pathophysiology of feline diabetes mellitus are relatively unkno...
作者：Lourdes Barbosa-Cortés , Mardia López-Alarcón , Juan Manuel Mejía-Aranguré ...
来源：[J].BMC Cancer(IF 3.333), 2017, Vol.17 (1)Springer
摘要：There is a growing body of evidence indicating that pediatric survivors of cancer are at a greater risk of developing metabolic syndrome. This study evaluated some probable predictors of metabolic syndrome (MS), such as leptin and adiponectin concentrations, the leptin/adiponecti...
作者：Wenjin Liu , Lei Jiang , Jianping Chen ...
来源：[J].Nutrition & Metabolism(IF 3.156), 2017, Vol.14 (1)Springer
摘要：Adipokines are a set of cytokines secreted by white adipose tissue that have been suggested to be involved in the development of cardiovascular diseases. We aimed to evaluate the cross-sectional associations of a panel of representative adipokines with cardiovascular measures in ...
作者：Andrius Karpavicius , Zilvinas Dambrauskas , Audrius Gradauskas ...
来源：[J].BMC Gastroenterology(IF 2.11), 2016, Vol.16 (1)Springer
摘要：... This study aims to evaluate the prognostic usefulness of adipokines in prediction of the severity and outcome of acute pancreatitis (AP).(#br) Methods(#br)Prospective study was conducted in four clinical centers. The diagnosis and severity assessment of AP was established acc...
作者：Arama Victoria , Tiliscan Catalin , Streinu-Cercel Adrian ...
来源：[J].BMC Endocrine Disorders(IF 2.65), 2013, Vol.13 (1)DOAJ
摘要：... Cytokines secreted by adipose tissue (adipokines) are linked to insulin sensitivity. The present study is aimed to assess the prevalence of insulin resistance (IR) and its association with several adipokines, in a non-diabetic Romanian cohort of men and women with HIV-1 i...
作者：Clara Ruiz-Fernández , Vera Francisco , Jesus Pino ...
来源：[J].International Journal of Molecular Sciences(IF 2.464), 2019, Vol.20 (8)DOAJ
摘要：... Adipokines, such as leptin, produced prevalently by white adipose tissues, but also by other cells of mesenchymal origin, particularly cartilage and bone, are cytokine-like hormones involved in important physiologic and pathophysiological processes. Although initially restric...
作者：Xiao Luo , Ru Jia , Qiangling Zhang ...
来源：[J].International Journal of Molecular Sciences(IF 2.464), 2016, Vol.17 (5)DOAJ
摘要：... It remains unclear whether this process influences inflammatory adipokines expression in adipose tissues. We determine the temporal profile of cold or β3-adrenoceptor agonist (CL316,243)-induced changes in the expression of inflammatory adipokines in adipose tissues in mi...
作者：Ikuko Kashino , Akiko Nanri , Kayo Kurotani ...
来源：[J].Nutrition Journal(IF 2.648), 2015, Vol.14 (1)Springer
摘要：Abstract(#br) Background(#br)Diet may influence disease risk by modulating adipokines. Although some foods and nutrients have been linked to circulating adipokine levels, little is known about the role of dietary patterns on adipokines. We investigated the association between maj...
作者：Tho X. Pham , Ji-Young Lee
来源：[J].International Journal of Molecular Sciences(IF 2.464), 2017, Vol.18 (8)DOAJ
摘要：Adipose tissue expansion in obesity leads to changes in the expression of adipokines, adipocyte-specific hormones that can regulate whole body energy metabolism. Epigenetic regulation of gene expression is a mechanism by which cells can alter gene expression through the modificat...
作者：Wei Yang , Yun Li , Tian Tian ...
来源：[J].BMC Endocrine Disorders(IF 2.65), 2017, Vol.17 (1)Springer
摘要：Adipose tissue, an endocrine organ of the body, is involved in some obesity-related disease states such as insulin resistance, diabetes mellitus, and atherosclerosis. Vaspin is a novel adipocyte with insulin sensitizing effects. In this study, we planned to estimate serum vaspin ...
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4,932,441,676,715,550,000 | Menopause And Dry Mouth: The Link Between Hormones And Oral Health
Menopause is a peculiar stage of life that all women will experience if they live long enough. This stage comes with many symptoms due to changing hormonal levels. Menopause and dry mouth are one of those common symptoms. Read on to find out the link between hormones and oral health in women.
Menopause and dry mouth
Menopause is a peculiar stage of life that all women will experience if they live long enough. This stage comes with many symptoms. And some of them are hard to deal with. Menopause and dry mouth are one of those common symptoms. The hormonal effects of menopause can indeed affect your oral health. The common term that experts use for “dry mouth” is xerostomia. It can happen due to several different causes. But menopause is one of them. Certain conditions, body changes, and medications can also cause xerostomia. But they all work through different mechanisms. In the case of menopause, it causes a drop in the hormones – progesterone and estrogen. This drop, in turn, causes a decrease in the production of your salivary glands. When this happens, your mouth will become dry and cause oral health concerns.
As your mouth becomes dry, hormonal changes in menopause can also cause bone loss and resorption. This affects all bones, including your spinal and jawbones. Hormones can also affect how your body responds to toxins (poisons) and predispose you to plaque buildup on your teeth. These effects can, in turn, cause loose teeth, tooth loss, and periodontal disease. You must, therefore, be more intentional about your oral hygiene and get proper help from your dentist when you are approaching menopause. Aside from menopause, women may also experience hormonal fluctuations that can also affect their oral health at other times. These include puberty, certain times in the menstrual cycle while using hormonal pills, and during pregnancy.
Menopause and Dry Mouth
As we have said before, lots of oral changes may occur as you grow older. Some of these changes include burning sensations in your mouth, altered taste, higher sensitivity to temperature, and dry mouth.
Dry mouth is one change that causes major concerns. This is because your mouth doesn’t have enough saliva to cleanse and moisten it. More so, there is no sufficient saliva to neutralize the acids that plaque produces. All of these can cause periodontal disease.
We have been talking about periodontal disease or periodontitis. What is it all about? This refers to tissue inflammation around your teeth.
Dry mouth occurs due to a drop in sex hormones, chiefly estrogen. This does not only affect the moisture levels of your mouth’s mucous membranes. But it also affects that of your nose. This dryness is often intractable and can last forever.
Estrogen drop due to menopause can also predispose you to osteoporosis or bone loss. This bone loss can also affect your jaw bone and cause tooth loss. One of the signs of this is that your gums will begin to recede. This exposes your teeth surface further to tooth decay.
Experts tell us that there is a close link between postmenopausal osteoporosis and poor oral health. Women who have severe osteoporosis after menopause have 3 times more risk of poor oral health outcomes.
Hormone therapy can help preserve your dental health after menopause. Many women find help with estrogen therapy. It can prevent dry mouth, bone loss, tooth loss, and other postmenopausal oral health issues.
The Link Between Hormones and Oral Health in Women
Basically, anything that can affect a woman’s sex hormone levels can also affect her oral health and cause dry mouth. As such, aside from menopause, you should also be wary of the following times:
1. Puberty
This life stage causes a spike in the production of progesterone and estrogen. This can increase the flow of blood to your gums. This will, in turn, change the response of your gum tissue to bacterial plaques. As such, your gum tissue may become swollen, red, and tender. You may also bleed while flossing and brushing.
2. Monthly menstrual cycle
Your hormonal levels will rise and fall at different points during your monthly cycle. These hormonal changes can cause oral changes, including swollen, bright red gums, bleeding gums, canker sores, and many more. Some women even experience menstruation gingivitis 1 day or 2 before your monthly period starts.
3. Using oral contraceptives
The use of birth control pills containing progesterone may cause your gum tissue to inflame. This is because excess progesterone raises your body’s response and reaction to toxins from plaque.
Major gum changes often occur in the initial months that follow your use of birth-control pills. But then, new pills now have lower hormonal concentrations. This will reduce the potential gum inflammatory response to plaques.
4. Pregnancy
Pregnancy can mess with your hormones. Your hormones will experience a great deal of change at different points during pregnancy. One common oral problem during pregnancy is pregnancy gingivitis.
We have mentioned earlier that excess progesterone poses a major risk to gingivitis. Since progesterone progressively rises from the second month to the 8th month of your pregnancy, you are more prone to gingivitis during this period. When you have gingivitis, your gums will swell and bleed more easily.
Tips for Preventing Oral Health Issues
Let’s start with a few home remedies that can help you with mouth dryness. These home remedies focus on ways to improve saliva production. They are as follows:
1. Eat
This first tip is easy to guess. We all know that eating stimulates our salivary glands. That is why we salivate at the thought of food. As such, make sure you eat when you should.
But then, you must do this with care. You can’t go on just eating everything you see because you don’t want your mouth to be dry. Overeating can cause further problems for you. So eating may help, but it is not the best or healthiest solution.
More so, some food types can make your mouth dry. These include spicy foods, dry biscuits, crusty bread, and crackers. Alcohol and caffeine can also dehydrate your mouth. You should, therefore, limit your intake.
2. Drink lots of water
Drinking lots of water helps a lot to hydrate your mouth. You should even carry a water bottle with you always. That way, whenever your mouth is dry, you can take a sip to moisten your mouth. This may be tasking, but it’s good for your kidneys too.
3. Brush regularly
This is very important. Brushing your teeth twice daily will help keep any infections at bay. Sometimes, dentists may recommend a special mouthwash or toothpaste for troublesome mouth dryness. So you should visit your dentist if you are experiencing dry mouth.
Menopause and dry mouth may have strong links. But it is not inevitable. You should make the best of our suggested home remedies and see your dentist help prevent or treat your postmenopausal mouth dryness.
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-8,822,962,842,217,761,000 | Wednesday, July 24, 2019
9/11 Asthma Cases & the Firefighters' Cough Continues to Plague First Responders
© Copyright 2019 - The Biofoundation for AngioGenesis R&D / IntermediaWorx inc. All Rights Reserved. Published for the NY Cancer Resource Alliance (NYCRA), AwarenessforaCure.org and HealthScanNYC.org
FOREWORD by: Dr. Jesse A. Stoff
Recently in the news, they're talking a lot about asbestos and asbestos-related cancers due to 9/11 exposure because when the Twin Towers collapsed, all the asbestos that was in there for insulation was aerosolized. And when you breathe that stuff in, in small particles that have been micronized from the explosion and compression phenomena, when those particles get lodged in the lungs, the body doesn't have a good way to excrete it. Because lung tissue (unlike liver tissue for example) heals by scarring and not regeneration, when the lungs are exposed to chronic irritants that the body can't get rid of, chronic inflammation and irritation ultimately leads to the death of lung cells called pneumocytes. That area of damage causes bronchiectasis and scar tissue formation which can lead to COPD and the diseases associated with that including cardiovascular problems and death. [1] (source: Huntington Patch)
ASTHMA: A MAJOR PREVALENCE WITH FIRST 9/11 RESPONDERS
Fact: no two individuals are ever the same especially when it comes to the physiological effects of envrionmental health hazards- such as those from a disaster zone like Ground Zero. We have all seen countless cases of health issues appearing for the first time 10-15 years after 2001, and the same includes respiratory disorders like ASTHMA.
Where logic may dictate that the giant plume of noxious dust should equate to a widepsread case of pulmonary issues within moments of contact, physicians have observed a variety of effects depending on body types (reflecting genetic makeup) or possibly a unique tolerance level that may actually resist or even 'hide' any symptoms until well past a decade from the exposure. Others may even continue to show zero evidence of negative effects at all (or for now).
"THE TELLTALE COUGH"- EXPLAINED
According to Dr. Paul Schulster, (pulmonologist from Oceanside, NY) the COUGH can say a lot, but often misleads the patient as a "nothing" or a "simple little cough". For firefighters, it is usually a telltale sign of various possible issues. The first syndrome often comes from a post-nasal drip. The second most common cause is from irritation, inflammation and bronchiospasm. Third is Gastroesophageal Reflux Disease. My 9/11-related patients that have GERD starts with that warning cough while others' coughs can trigger the asthma. Finally, Irritative Cough Syndrome can also happen where one cough leads to another cough, irritating the airway, exacerbating another cough - and then another.
Having a cough here or a wheeze there is not enough for most first responders to raise the flag of alarm. Seasoned specialists like Dr. Schulster recognizes that unique and unusual symptoms or maladies do not reach the patient's consciousness for quite some time. Ignoring or not paying more attention to these "little" anomalies tend to often be the norm. These coughs may progressively grow worse over the years and then one day they begin to wheeze a little more than usual and wind up with advancing shortness of breath. Once this becomes significant and finally enters their consciousness, only then will the thought of seeking medical help actually come to mind.
DIAGNOSTIC OPTIONS
Oftentimes, an exam from the pulmonologist starts with the CAT scans of the chest. The firefighters are being tracked for pulmonary nodules. They're referred to as sub-centimeter nodules, which are so small that you can't read it. "You don't really see them on a plain X-ray, chest X-rays, PA and lateral. A lot of these first responders already come to me with CAT scans from the past and have been followed by World Trade Center program and the FDNY doctors that are also pulmonary doctors"- states Dr. Schulster.
In a pulmonologist's tool kit exists certain standard pulmonary function examss- including the SPIROMETRY [2]. This test estimates the narrowing of your bronchial tubes by checking how much air you can exhale after a deep breath and how fast you can breathe out [5]. This allows us to see the best way of determining the lung function in numbers, more or less, is a complete pulmonary function test. Next is the METHACHOLINE CHALLENGE [3] - also known as an asthma trigger that, when inhaled, will cause mild constriction of your airways. If you react to the methacholine, you likely have asthma. This test may be used even if your initial lung function test is normal. [5] Another test used is THE COLD AIR CHALLENGE [4]. The patients generally come with having had those in the past and most are positive for asthma. In the asthmatics.
Inevitably, multiple poisons inhaled in 'the pile' trigger disorders that are obtained on a longterm basis. The isocyanates and the aldehyde may trigger the asthma, "but I'm not certain if we really know the specific cause of their 9/11 based asthma. There's a long list of toxins that irritate and inflame. The probable causes of Asthma are either chronic of acute inflammation. As they breathed in the 9/11 dust, they breathed in 30 of those toxins, causing inflammation in the airways which then led to chronic reactions."
The sub-centimeter nodules seems to be frequent with 9/11 responders. The good news is that most of them turn out to be benign. One follows these nodules for a couple of years with images and CAT scans because they're often too small to really see on plain chest X-rays. And if they remain the same size, they get smaller over a few years, then they're considered benign. And then that's how we deal with it.
Concluding Dr. Schulster's interview, we found that identifying a chronic respiratory disorder like Asthma can be quite involved that there are various diagnostic solutions and treatment options available depending on its classification or severity. Especially in the case of a first responder's long-term exposure to toxic fumes, recognizing the source(s) of contamination can greatly help the physician establish the proper treatment strategy for the patient.
EXTRA: ASTHMA TREATMENT OPTIONS
source: https://www.mayoclinic.org/diseases-conditions/asthma/diagnosis-treatment/drc-20369660
Prevention and long-term control are key in stopping asthma attacks before they start. Treatment usually involves learning to recognize your triggers, taking steps to avoid them and tracking your breathing to make sure your daily asthma medications are keeping symptoms under control. In case of an asthma flare-up, you may need to use a quick-relief inhaler, such as albuterol.
Medications
The right medications for you depend on a number of things — your age, symptoms, asthma triggers and what works best to keep your asthma under control. Preventive, long-term control medications reduce the inflammation in your airways that leads to symptoms. Quick-relief inhalers (bronchodilators) quickly open swollen airways that are limiting breathing. In some cases, allergy medications are necessary. Long-term asthma control medications, generally taken daily, are the cornerstone of asthma treatment. These medications keep asthma under control on a day-to-day basis and make it less likely you'll have an asthma attack. See complete list of TREATMENT options and full descriptions @ MAYO CLINIC's website:
https://www.mayoclinic.org/diseases-conditions/asthma/diagnosis-treatment/drc-20369660
..................................................................................................................................................................
STAFF EDITOR
JESSE STOFF, MD, HMD, FAAFP is a highly-credentialed medical expert studying all medical remedies in pursuit of resolving the most challenging health issues of our time. In many circles, he is recognized for his 35+ years of dedicated work in immunology and advanced clinical research in modern CANCER treatments. He has spoken worldwide in some of the most sought-after medical conferences about his experiences and analyses on the study of human disease. His integrative practice (INTEGRATIVE MEDICINE OF NY, Westbury, NY) has been continually providing all patients with the many comprehensive clinical options and modalities available- including "ONCO-IMMUNOLOGY", the science of battling cancer cells and reversing pre-cancerous conditions through a complete prevention program that has earned him great success in this field. For more information, visit: www.Dr.JesseStoff.com
CONTRIBUTING 9/11 PHOTOGRAPHER
KEVIN P. COUGHLIN is a Pulitzer Prize-sharing photojournalist, writer, director of photography, pilot, and aerial cinematographer. He is the current executive photographer to New York Governor Andrew M. Cuomo. His photographs at Ground Zero following the September 11, 2001 attacks on the World Trade Center and while covering funerals and memorial services of fallen fire fighters, police officers, and emergency personnel killed as a result of the attacks are included in the 2002 Pulitzer Prize awarded to The New York Times for Public Service. In addition to The New York Times, his photographs have appeared in the New York Post, New York Daily News, Newsday, The Philadelphia Inquirer, https://www.kevincoughlinphotography.com/
PROFESSIONAL INTERVIEWED IN THIS ARTICLE
PAUL L. SCHULSTER, MD PC is a practicing Pulmonary Disease Specialist in Oceanside, NY. Dr. Schulster graduated from University of Kentucky College of Medicine in 1972 and has been in practice for 47 years. He completed a residency at Queens Hospital Center. Dr. Schulster also specializes in Internal Medicine. Dr. Schulster also practices at South Nassau Community Hospital. One Healthy Way Oceanside NY. His private practice is located at: 442 Waukena Avenue, Oceanside, New York. 11572 | (516) 599-8234
References:
1)The 9/11 Attacks are Still Going On with Asbestos Based Cancers- by: Jesse Stoffhttps://patch.com/new-york/huntington/9-11-attacks-are-still-going-asbestos-based-cancers
2) Spirometry: https://www.healthline.com/health/spirometry
3) Methacholine Challenge Test: https://www.lung.org/lung-health-and-diseases/lung-procedures-and-tests/methacholine-challenge-test.html
4) Cold Air Challenge: https://www.sciencedirect.com/science/article/abs/pii/S1526054205000941
5) Asthma/Mayo Clinic Report: https://www.mayoclinic.org/diseases-conditions/asthma/diagnosis-treatment/drc-20369660
Public Service Announcement from AwarenessforaCure.org
Thursday, July 18, 2019
CANCER TREATMENT OPTIONS: REVIEW
SOURCE: NIH National Cancer Institute
There are many types of cancer treatments. The types of treatment that you have will depend on the type of cancer you have and how advanced it is. Some people with cancer will have only one treatment. But most people have a combination of treatments, such as surgery with chemotherapy and/or radiation therapy. You may also have immunotherapy, targeted therapy, or hormone therapy. Clinical trials might also be an option for you. Clinical trials are research studies that involve people. Understanding what they are and how they work can help you decide if taking part in a trial is a good option for you. When you need treatment for cancer, you have a lot to learn and think about. It is normal to feel overwhelmed and confused. But, talking with your doctor and learning all you can about all your treatment options, including clinical trials, can help you make a decision you feel good about. Our Questions to Ask Your Doctor About Treatment may help.
Surgery: When used to treat cancer, surgery is a procedure in which a surgeon removes cancer from your body. Learn the different ways that surgery is used against cancer and what you can expect before, during, and after surgery.
Radiation Therapy: is a type of cancer treatment that uses high doses of radiation to kill cancer cells and shrink tumors. Learn about the types of radiation, why side effects happen, which ones you might have, and more.
Chemotherapy: is a type of cancer treatment that uses drugs to kill cancer cells. Learn how chemotherapy works against cancer, why it causes side effects, and how it is used with other cancer treatments.
Immunotherapy to Treat Cancer- helps your immune system fight cancer. Get information about the types of immunotherapy and what you can expect during treatment.
Targeted Therapy is a type of cancer treatment that targets the changes in cancer cells that help them grow, divide, and spread. Learn how targeted therapy works against cancer and about common side effects that may occur.
Hormone Therapy is a treatment that slows or stops the growth of breast and prostate cancers that use hormones to grow. Learn about the types of hormone therapy and side effects that may happen.
Stem Cell Transplants are procedures that restore blood-forming stem cells in cancer patients who have had theirs destroyed by very high doses of chemotherapy or radiation therapy. Learn about the types of transplants, side effects that may occur, and how stem cell transplants are used in cancer treatment.
Precision Medicine helps doctors select treatments that are most likely to help patients based on a genetic understanding of their disease. Learn about the role precision medicine plays in cancer treatment, including how genetic changes in a person's cancer are identified and used to select treatments.
Reflectance Confocal Microscopy (RCM)- The latest Imaging Advancement for Dermatologists
DR. MANU JAIN, Optical Imaging Specialist at Memorial Sloan Kettering Cancer Centre (MSKCC) Department of Dermatology provides great insight on the advantages of Reflectance Confocal Microscopy (RCM) for the diagnosis of skin cancers, in vivo.
RCM is a form of in vivo microscopy— “histopathology-like” diagnosis without doing a biopsy. It offers several advantages over conventional light microscopy, including imaging of tissue in vivo and ability to provide bedside diagnosis. In addition to its applications in dermatology it can also be applied for oral cancers. Meanwhile, we call this application ‘optical biopsy’. Microscopy is actually what's paving the way for digital imaging in dermatology. Before this it was the naked eye and magnifying lens.
THE POWER OF LIGHT
As ultrasound is recognized for being non-invasive and radiation free, so is optical imaging – gathering cellular and nuclear epidermal and superficial dermal information through the use of LIGHT and laser. It penetrates the skin to reach an estimated 200 micron in depth - good enough in dermatology to diagnose skin cancers like melanoma, basal cell carcinoma, and squamous cell carcinoma. Because most tumors that appear originates at the dermo-epidermal junction (around a hundred-micron depth from skin surface). In addition to morphological and cellular details, RCM also provides information on the dynamic phenomenon of the blood flow very clearly.
Dr. Jain joined MSK four years ago, but this technology has been used primarily for research prior to her joining in the USA. The engineering team at MSK (headed by Dr. Milind Rajadhyaksha) helped design this machine in collaboration with Caliber ID (Rochester, NY) 20+ years ago. Few years ago, RCM acquired a category I current procedural terminology (CPT) reimbursement codes (96931–96936) by the US Centers for Medicare and Medicaid Services (CMS) [1]. However, there are limited expert readers of RCM in the US. To bridge this gap, Dr. Jain teaches and trains her residents in the dermatology and dermatopathology. She is has started her own annual CME accredited confocal courses at Memorial Sloan Kettering Cancer Center. She is also the Vice-president of recently formed American Confocal Group.
This innovation relies solely on reflectiveness of various tissue structures in the skin, illuminating and magnifying images by relying on the light planes. “Your skin is like a mirror and when you shine light on the mirror, whatever absorbs all the light becomes dark and whatever reflects all the light appears bright”.
"I think it could be interesting to explore the option of combining confocal microscopy with ultrasound because ultrasound can give us the doppler information and also the depth is a very good with ultrasound… which we miss with confocal microscopy. So that would be really great. Like they have done with confocal and optical coherence tomography."
Her professional focus is to teach RCM to dermatologists and dermatopathologists. For the large institutions, it’s fairly affordable and cost-effective as it takes only 15 minutes or 20 minutes to do one lesion. That means a patient gets scanned and diagnosed at the same time. This saves a lot of time for the patient at the end of the day because the patient doesn't have to wait for the biopsy report for week.
According to Dr. Jain's original bedside diagnosis study,, RCM has shown remarkable sensitivity (~90%) and specificity (~70%) in hands of a novice, within a short interval of 16 months [2] , for skin cancers.. Several studies reported RCM imaging to achieve sensitivity of 70–92% and specificity 84–88% for melanocytic lesions [3] and sensitivity of 100–92% and specificity 85–97% for non-melanocytic skin lesions . . "As an example, we’re examining a patient's new mole with confocal microscopy and if we are suspicious that it might be melanoma, we can use dermoscopy and confocal together to improve the accuracy of diagnosis.
Although the sensitivity of RCM has not much changed over dermoscopy but the specificity is two times superior—translating into marked decrease in benign biopsies.
RCM TECHNOLOGY DEVELOPMENT
Thanks to the developmental expertise of Dr. Milind Rajadhyaksha (member of the faculty of Memorial Sloan Kettering Cancer Center), the IN VIVO CONFOCAL MICROSCOPY is fast becoming the new standard in dermal non-invasive imaging. Originally conceptualized with his mentors at MD Anderson (renowned physicist Dr. Robert Webb and dermatologist/laser pioneer Dr. Rox Anderson), the team sought better ways to detect skin cancers while reducing the need for biopsies in real time at the bed-side. At the time, biopsy and pathology were the standard approach for detecting and diagnosing skin lesions. The demand for advancing diagnostic imaging was a call from the 5 million+ new cases diagnosed in the US each year and another million cases detected in Europe, UK, Australia, other regions of the world.
Milind (as he prefers to be called) described how the RCM works in simplified terms: “We start with a bright light source… in our case it's a laser. We focus the laser down to a very tiny spot inside the skin and we move the spot around in 2 dimensions so we create essentially a plane of illumination by moving that spot. Imagine having a flashlight which you point at a wall and now you move the flashlight back and forth, sideways and up and down until you can illuminate the entire wall. Similarly, we ‘paint’ a single plane within tissue with focused laser spot and we collect light from each location that the spot illuminates and that we can use that to produce an image. You can essentially create an image or a picture of a single layer of cells or layer of tissue within skin.”
Milind states having built the original laboratory bench top portion in the early 1990’s and continued the expansion of the technology with MSKCC since 2005. He has been involved with advancing both the IN vivo (means directly on the patient) and the EX vivo microscope (referring to any fresh tissue that has been removed from the patient, ie. biopsy) to do faster imaging over large areas. Besides looking at skin cancers, this technology is set up over a mic top with a probe that can allow for imaging inside the oral cavity looking for oral cancers. “We've done a lot of work in imaging to guide treatment, surgeries and to guide laser ablations at Memorial for more than a decade.”
References:
1) Current Procedural Terminology, Professional Edition. Chicago IL: American Medical Association; 2016. The preliminary physician fee schedule for 2017 is available at https://www.cms.gov/Medicare/Medicare-Fee-for-Service-Payment/PhysicianFeeSched/PFS-Federal-Regulation-Notices-Items/CMS-1654-P.html
Thursday, July 11, 2019
A REVIEW OF TOXIC COMPOUNDS FROM EMERGENT FIRE ZONES
© Copyright 2019 - The Biofoundation for AngioGenesis R&D / IntermediaWorx inc. All Rights Reserved. Published for the NY Cancer Resource Alliance (NYCRA)AwarenessforaCure.org and HealthScanNYC.org
FOREWORD
By Dr. Robert L. Bard, cancer diagnostic specialist (NYC)
After a decade past the 9/11 disaster, news broke of unique and advanced cases of CANCER arising in droves. A growing number of the same individuals exposed to the toxic fumes and plumes of hazardous particles in the danger zone have recently contracted aggressive cases of CANCER and were in immediate demand for medical care and desperate need for advanced research and support.
This spike in cases can only come from ‘dormant’ cells or recurrence (usually with a vengeance) – such as cases of cancer tumors in the lung, liver, prostate, kidney, brain, skin and even the eye. To troubleshoot each case, it would be advantageous to take a crash course in toxicology and to recognize the chemical compounds that BATHED all responders during the event. Understanding these chemicals can help us pursue their behaviors (on the body) and their long and short term effects.
TOXICOLOGY 101: A THREAT TO FIREFIGHTERS HEALTH
As part of our evaluation of all occupational illnesses contracted by first responders, we enter the world of TOXICOLOGY- the branch of science focused on the effects and detection of poisons. It is also the discipline overlapping chemistry, biology and pharmacology- studying the adverse effects of chemical substances on living organisms. In pursuit of first responders’ safety as far as chemical effects on the body, we connected with Professor David Purser of the Hartford Environmental Research (UK), a renowned toxicology expert who conducted major reviews on fire-exposed carcinogens published worldwide. “9/11 was unusual in that a major environmental hazard resulted from the dust cloud released as and after the Towers collapsed,” says Prof. Purser. “The dust inhaled by responders at the time, and afterwards working at the site, has resulted in serious ongoing and developing health conditions and to this day.
For fires in general, there is also increasing evidence and concern regarding FF exposure to carcinogens, especially from soot contamination to skin and clothing following attendance at incidents and during training.” An abstract from Prof. Purser’s latest presentation – “ Toxins Including Effects of Fire Retardants, During Fires and Post-Fire Investigation Activities” indicates a remarkable breakdown of some of the major toxins and carcinogenic compounds that the average firefighter would be exposed to.
Below is a list of common toxic elements found in active fires and post-fire investigations that first responders have been known to be exposed to.
• (2,3,7,8) Tetrachloro
..-dibenzodioxin
• Acrolein
• Aldehydes
• Asbestos
• Benz[A]Anthrene
• Benzene
• Benzo[A]Pyrene
• Carbon Fibre
• Carbon Monoxide
• Carbonyl Fluoride (COF2)
• Ceramic
• Crotonaldehyde
• Dibenzofurans
• Dioxins
• Formaldehyde
• Furans
• Histone (H3.3)
• Hydrochloric Avid (Hcl)
• Hydrogen Cyanide (HCN)
• Hydrogen Fluoride (HF)
• Isocyanates
• Metal Particulates
• Metals: Lead (Pb) & Cadmium (Cd)
• Nitrogen Oxides (Nox)
• Organic Irritants
• Phenol
• Phosphorous/Phosphate (P04)
• Polyaromatic Hydrocarbons
• Polychlorinated Biphenyls (Pcbs)
• Polycyclic Aromatic Hydrocarbon – (Pahs)
• Styrene
• Sulfur Dioxide (SO2)
According to Prof. Purser’s presentation on “Fire Retardants and their Potential Impact on Fire Fighter Health” ** the highest and most active toxins threatening survival during or immediately after a fire are:
ASPHYXIANT GASES: CO, HCN, CO2 , low oxygen
IRRITANTS/ ACID GASES : HCl, HBr, HF, COF2 , H3 PO4, SO2 , NOx
ORGANIC IRRITANTS: acrolein, formaldehyde, crotonaldehyde, phenol, styrene
PARTICULATES: especially ultrafine particles + metals
These toxins are usually found within active fire zones- either inside the fire event itself or downwind plume in the form of residues and soot or lethal fragments activated at high temperatures or in airborne smoke. These asphyxiant gases, irritants and particulates are the main causes of injury and death of fire victims exposed to high concentrations inside burning buildings. Asphyxiant gases cause collapse with loss of consciousness during a fire, leading to death if exposure continues. Irritants and smoke particulates cause pain to the eyes and lungs, with breathing difficulties, which inhibit escape during a fire and can lead to lung inflammation and edema within a few hours of rescue, which can also be fatal. Those surviving may make a good recovery or suffer long term neurological or cardio-respiratory health effects, depending on the severity of the exposure. Those most at risk from these effects at the fire scene are building occupants and emergency responders not protected by breathing apparatus.
Beyond the immediate fire zone, especially outside a burning building, or during wildfires, these toxic smoke products are considerably diluted by mixing with outside air, so are generally not immediately life-threatening. The main hazards to unprotected persons exposed to the diluted smoke plume in the surrounding area are health risks from inhalation of smoke irritants and soot particulates, or from inhalation of mineral particles and fibers. The immediate effects of exposure are mainly eye and throat irritation, with a sore throat and cough in some cases over a period of a few days, although persons with pre-existing respiratory or circulatory health conditions may be more severely affected. Longer term health hazards following a single exposure may result from inhalation of sensitizers (such as isocyanates or formaldehyde), which can cause asthma, or from some mineral dusts and fibers, which may remain in the lungs. Health risks from exposure to carcinogens during a single incident are generally low, although the World Trade Center dust and some chemical fires may be exceptions.
Health risks to firefighters result mainly from repeated exposures to inhalation of smoke toxicants and contact with soot deposits. These contain a wide variety of carcinogens, so that cumulative exposure over years may present an increased cancer risk. The hazards arise from inhalation of smoke, soot or mineral fibers, but also from soot contamination of skin or clothing. This can result in dermal, inhalation or oral ingestion, resulting in increased exposure to carcinogens, including dioxins and dibenzofurans, during post-fire activities. Halogenated fire retardants (especially chlorine and bromine systems), present possible increased health risks to fire victims and firefigthers during fires due to inhibition of combustion in the vapor phase resulting in inefficient combustion with an increase in yields of toxic carbon and nitrogen compounds, in addition to the formation of acid gases, dioxins and dibenzofurans under all fire conditions..**
Reference:
** Prof. David Purser's presentation on Toxic Hazards to Fire Fighters, Including Effects of Fire Retardants, During Fires and Post-Fire Investigation Activities (NIST), Gaithersburgh MD on 9/30/2009 https://www.nist.gov/sites/default/files/documents/el/fire_research/4-Purser.pdf
.............................................................................................................................................................
“IT ALL STARTS AT THE LUNGS"
Historical Patterns of Carcinogenic Reactions from Environmental Disasters by: Dr. Jesse Stoff
If you review the victims of a disaster such as the radioactive fallout in CHERNOBYL, then compare it to the dust from the 911 catastrophe, you can find a similar behavior as far as how fatalities come to appear within a certain timeline. There’s the initial contamination that results in immediate illnesses- and then there’s a major wave of cancer cases that arise a decade later. These cancers are delineated on the CDC website and are occurring, undoubtedly, because of the mixture of toxins that people have been exposed to. The volume of these toxins are absorbed into their bodies since 9/11 (while working with the clean-up efforts) and can't get rid of them.
We are seeing patients with very unusual blood borne cancers that have had very unusual genetic profiles -undoubtedly because of the unusual combination of carcinogenic toxins that people were exposed to that have been lingering in their system for so many years. We're also seeing a marked increase in Monoclonal Gammopathies (MGUS) and Myelofibrosis which is progressive damage to the bone marrow that itself can become a cancerous process. We're seeing many people suffering changes to the structure and functioning of their immune system even without yet developing a cancer but for those kinds of changes their risk of developing skyrockets. Also, because of the shifting in their immune system we see a significant increase in the level of different kinds of allergies (including environmental based) that have become more prevalent and worse than before the exposure to this kind of toxic material.
In essence, the destruction and suffering continues.
THE KILLER DUST
by Capt. Richard Marrone (9/11 Responder)
"It was just everywhere. The DUST was so thick it would dry your eyes out. You couldn't breathe. As EMS, that was a lot of what we were doing was just constantly cleaning people's eyes out. There's nothing you can do to get away from it. I know what was in those particulates--it was asbestos, it was concrete, it was human remains, metals and any possible contamination in a fire... it was all there. Nobody was protected. Even the firefighters who had self-contained breathing apparatus, you're only getting 15 or 20 minutes maximum on those cylinders, and there just wasn't enough to keep constantly replacing them. The police officers and EMS personnel were using surgical masks, which basically provided no protection whatsoever. We mostly treated rescue workers on site due to the dust-- eyes and stuff like that. There really wasn't enough eye or respiratory protection, so anybody that became a patient post-collapse was due to the contamination and the toxins of 9/11."
RESPONDERS PULMONOLOGY REVIEW
Following the logical path of carcinogen, one would start from how environmental contaminants would make their way into the body; through the respiratory ports. As seen in the toxicology section of this article, these foreign substances range from particulates like metals and acids to microfragments to molecular-sized compounds whose behaviors vary from mild irritants to lethal poisons. More often than not, these compounds can trigger cell mutations in our physiology as well as attack our very immune system to penetrate our defenses for tumors to grow.
Our responders’ health report brought us to interview Pulmonary and Sleep Medicine Specialist Dr. Mayank Shukla (NYC) who helped identify the various diagnostics and screening procedures for first responders often start with a Pulmonary Function Test to study a patient’s airway size, and then a Bronchodilator Challenge Test to identify and distinguish between asthma and COPD. Another protocol for patients exposed to airborne contaminants is examining airway resistance and looking for Upper Airway Resistance Syndrome (UARS), Sleep Apnea and other breathing disorders caused by an impairment of the airway size.
The concern for the responder’s air passage brings telltale signs of possible impending issues based on their condition that brings warning signs of what may lie ahead- in the lungs, the bloodstream etc. There's another test which is available called NIOX designed for a patient to have allergy component or asthma that also is very sensitive, to look at the lung inflammation for these patients.
During airway inflammation, higher-than-normal levels of nitric oxide (NO) are released from epithelial cells of the bronchial wall. 4 The concentration of NO in exhaled breath, or fractional exhaled nitric oxide (FeNO), can help identify allergic/eosinophilic inflammation, and thereby support a diagnosis of asthma when other objective evidence is lacking. (See NIOX.com)
There are other testing available which helps us to do a direct visualization of the upper and lower levels. For example, there's the bronchoscopy for the lungs and air passages and then there's the laryngoscopy to visualize the nasal cavity, the sinus, sinusitis, the larynx, because many of these patients have acute or chronic laryngitis because getting exposed to the several toxins. Also, many of them have gastro esophageal reflux, so when you look at that endoscopy, you can realize that this patient have, you know, chronic inflammation of the, not only for a lower airway, but also with upper airway as well.
SPECIAL CONTRIBUTORS:
1) Professor David Purser CBE, Toxicologist from the Hartford Environmental Res. (Hatfield, UK)
2) Dr. Mayank Shukla - (www.drmayankshukla.com/) pulmonologist
3) Dr. Robert Bard - AngioFoundation.orgbardcancercenter.com/ contributing writer
4) Dr. Jesse Stoff - publisher for awarenessforacure.org/imofny.com contributing writer
5) Sal Banchitta- Ret FDNY / First Responders Cancer Awareness Sr. Ambassador
6) Captain Richard Marrone (ret. FDNY EMT / Vol. Long Island Firefighter
6) Kevin P. Coughlin - 9/11 Photography, www.kevinpcoughlin.com/
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8,469,514,046,941,885,000 | Article Text
PDF
Response to: ‘Spontaneous hypertensive rat exhibits bone and meniscus phenotypes of osteoarthritis: is it an appropriate control for MetS-associated OA?’ by Chan and Wen
1. Chaohua Deng1,2,
2. Arnaud Bianchi1,2,
3. Nathalie Presle1,2,
4. David Moulin1,2,3,
5. Meriem Koufany1,2,
6. Cécile Guillaume1,2,
7. Hervé Kempf1,2,*,
8. Anne Pizard2,3,4,5
1. 1 UMR 7365 CNRS-Université de Lorraine, Ingénierie Moléculaire et Physiopathologie Articulaire, Vandoeuvre-lès-Nancy, Lorraine, France
2. 2 Fédération de Recherche 3209, Université de Lorraine, Vandoeuvre-lès-Nancy, Lorraine, France
3. 3 CHRU, Nancy, Vandoeuvre-lès-Nancy, Lorraine, France
4. 4 UMRS U1116 Inserm, Université de Lorraine, DCAC, Vandoeuvre-lès-Nancy, Lorraine, France
5. 5 CIC-P 1433 Inserm, CHU Nancy, Vandoeuvre-lès-Nancy, Lorraine, France
1. Correspondence to Hervé Kempf, UMR 7365 CNRS-UL, IMoPA, 9 avenue de la Forêt de Haye, Vandoeuvre-lès-Nancy 54500 France; herve.kempf{at}inserm.fr and Dr Anne Pizard, Inserm U1116, CHRU Nancy, 4 rue du Morvan, Vandoeuvre-lès-Nancy 54500, France; anne.pizard{at}inserm.fr
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We thank Dr Chan and Dr Wen for their interest in our report1 and their resulting eLetter.2 We fully agree that, among the different components of metabolic syndrome (MetS), hypertension has very recently been brought out as a critical feature in the development of osteoarthritis (OA) in humans.3 4 In these reports using either data from the Framingham OA study3 or the Osteoarthritis Initiative study,4 it has been emphasised that high blood pressure (diastolic or systolic, respectively) was associated with increased incidence of radiographic knee OA.
In order to further experimentally investigate the actual role of hypertension in OA onset and development, Chan and colleagues describe in a yet unpublished study the development of OA features in the spontaneous hypertensive rat (SHR) model, a widely characterised model of systemic hypertension.2 5 Although the spontaneous hypertensive heart failure (SHHF) rat strain we employed is deriving from the SHR strain6 and suffers high …
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-655,755,283,190,494,100 | Hypertrofisk kardiomyopati: Genetik, patogenese, patofysiologi, klinisk billede og forløb
Henning Bundgaard*, Ole Havndrup, Ulla Høst, Henning S. Kelbæk
*Corresponding author af dette arbejde
Publikation: Bidrag til tidsskriftArtikelForskningpeer review
Abstrakt
Hypertrophic cardiomyopathy is a heterogeneous, progressive disease with a variable age of debut Hypertrophic cardiomyopathy is characterized by myocardial hypertrophy with a bizarre fibre disarray. Angina pectoris, dyspnoea and syncope are the most frequent symptoms. Hypertrophic cardiomyopathy is an important cause of sudden death, especially in children and young adults. The aetiology is genetic in more than 60% of the cases, with an autosomal dominant mode of inheritance. More than 50 different mutations involving six genes have so far been associated with the development of hypertrophic cardiomyopathy. These mutations are located to genes coding for several of the proteins in the cardiac sarcomere. The protein changes seem to compromise contractility as well as sarcomere assembly, thereby secondarily causing compensatory hypertrophy. The management of hypertrophie cardiomyopathy has been markedly improved within the last few years. This emphasizes the importance of determining prognostic markers in each patient. A specific genetic diagnosis may prove to be of major importance.
Bidragets oversatte titelHypertrophie cardiomyopathy
OriginalsprogDansk
Sider (fra-til)5478-5483
Antal sider6
TidsskriftUgeskrift for laeger
Vol/bind160
Udgave nummer38
StatusUdgivet - 14 sep. 1998
Fingeraftryk
Udforsk hvilke forskningsemner 'Hypertrofisk kardiomyopati: Genetik, patogenese, patofysiologi, klinisk billede og forløb' indeholder.
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-2,249,105,189,000,864,800 | Treat Hormonal Acne
Synonymous with adolescence in the collective imagination, acne can persist - or even appear - in adulthood.
It is almost always hormones. Once they reach adulthood, men have a certain hormonal stability. While women experience lasting instability related to menstruation, pregnancy, etc. This explains why some women see their acne continue in their 40's while others may discover their first acne onset at the age of 25, 30 or 35, when they had never experienced it before.
Those who have an oily skin to begin with, high sebum secretion, and high hormonal fluctuations are at greater risks of adult acne.
What is hormonal acne exactly?
All acne is hormonal. Acne occurs when your body produces an increased amount of certain hormones that stimulate the production of sebum.
Normal sebum production keeps your skin fresh, smooth and healthy. However, overproduction of sebum can clog hair follicles and cause you to develop acne.
Everyone has a different sensitivity to certain hormones, meaning an increase in hormone levels that could cause one person to break out with acne could have no effect on a person with lower sensitive to acne-causing hormones.
The biggest culprit is testosterone, an androgen hormone that can stimulate sebum production and increase clogging of your hair follicles.
Hormones exist in a delicate balance in your body. Even a small increase in one hormone can have a noticeable effect on your skin.
If acne is always hormonal, its late onset is related to factors that can be identified… And therefore limited. Acne may, for example, be related to the prescription of drugs (especially hormone or cortisone treatments) or to the exercise of certain professions (especially for all those who work in contact with chlorine or tar).
For others, it is special circumstances that will trigger the appearance of spots. The most common is abuse of cosmetics or the use of poor-quality cosmetics. Products that are too greasy, especially too oily, may clog the pores of the skin. Over cleansing your face destroys the normal cutaneous flora and will leave room for more aggressive microbes.
What is the appropriate care?
You must adapt your skincare to prevent further 'attacks' to the skin. First step: swap your soap for a mild cleanser. And do not wash your face excessively. In the evening, use a non-comedogenic makeup remover. Then rinse the entire face with warm water and apply a non-alcoholic tonic lotion followed by a moisturiser, which should also be non-comedogenic.
Some of the most common treatments are vitamin A derivatives that can be used locally or generally. Retinoids work by speeding up your skin’s growth process and causing your skin to turn over more quickly than normal. But be careful, these treatments do make the skin thinner and therefore more sensitive to the sun. Avoid exposure and rely on maximum sun protection at all times. It is also possible to prescribe anti-androgens to reverse the effects of testosterone.
Natural treatments
Phytotherapy can help alleviate mild to moderate acne. For example you can clean your face with an infusion of thyme or lavender. Those can also be used to make warm compresses to be applied directly to spots. A traditional remedy that has been widely proven are green clay masks, with optional sage oil. It protects the epidermis from microbes and bacteria and absorbs excess sebum. It can even have regenerating power for mature skins.
Dr Marine Vincent recommended products
Avène Cleanance Gel
La Roche Posay Effaclar H Cream Cleanser
La Roche Posay Toleriane Cleanser
La Roche Posay Toleriance Riche Moisturiser
Caudalie Purifying Mask
Institut Esthederm Retinol Oil
Institut Esthederm Sunkissed
Vichy Ideal Soleil Protective Water | {
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-6,247,626,874,760,761,000 | How BMR Affects Weight
5
233
Ever since I started following a healthy lifestyle, the term that I kept hearing was BMR. People would come up and say “Oh she is thin because her BMR is high” and so on. If you have been in the weight loss circle since long then you must be well aware of this term. For people who don’t know- BMR stands for Basal Metabolic Rate which is the amount of energy that your body uses every day. This is the amount of calories that your body needs and uses every day for secretion, eating, maintaining body temperature, or normal functioning. So if you are one of those people who are having less food to reduce the calorie intake then beware, you are doing more harm to your body and are interfering with its normal functioning.
How BMR Affects Weight
How BMR Affects Weight
If you wish to maintain your weight or reduce it then reducing the calorie intake won’t help. Make sure that you do eat as per your BMR. You can get your BMR easily nowadays and there are special weighing machine for it. I checked my BMR recently at a mall and it’s about 1416 kcal. This means that my body needs this much energy every day and therefore I should eat about 1400- 1420 calorie everyday. If not, I would feel weak and irritated. As per my age and weight, my BMR is on track and is around the ideal figure.
Now your ideal BMR and actual BMR may differ. A couple of years back, my BMR came to be 1250 on the weighing scale and ideal was around 1500kcal. It is important to understand what your BMR is and how much it should be. So here is a chart that can help you to calculate the ideal BMR.
Sex Age in years Formula
Male 18-30 15.3 X Body weight in kg + 679
Male 30-60 11.6 X Body weight in kg + 879
Male above 60 13.5 X body weight in kg + 487
Female 18-30 14.7 X Body weight in kg + 496
Female 30-60 8.7 X Body weight in kg + 829
Male above 60 10.5 X body weight in kg + 596
So for a girl aged 18 to 30 years, weight being 65, the BMR would be about 1451. It depends on your weight and age. If your weight is less, then your ideal BMR would be lower than this and if it’s high then BMR also increases. So if at 65 kg you required 1451 kcal, at 60 kg you would need 1378 Kcal. This means that when you reduce weight then you should make sure that your diet is in accordance to it. Please note here we are talking about the ideal BMR. The actual may be high or low depending upon a number of factors.
How BMR Affects Weight loss
If you want to reduce your weight then instead of reducing your calories intake below your actual BMR, you need to increase your physical activities and monitor the calorie intake to make sure that it is around your actual BMR. If your BMR is lower than the ideal BMR then you can increase by changing your eating habits and making lifestyle changes. Some of the main factors that may affect your BMR level include- lack of sleep, smoking, seasonal changes etc. They have already been discussed in the other articles.
How BMR Affects Weight ideal BMR
Before you implement the changes, you need to know you actual BMR and your ideal BMR. To lose weight, you need to spend more energy than you consume and if you store it then you are simply heading towards obesity. Before you start crash dieting or reducing your food intake, do check the BMR to know how much calories your body need. The BMR machines are installed at various malls and health centers and you can easily check yours.
Image Source – 1 , 2, 3
5 COMMENTS
1. Great article..Once one loses weight other tends to think that her BMR rate is quite high…Kind of excuse of not working out 😀
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Vancomycin-Intermediate Staphylococcus aureus (VISA) and Vancomycin-Resistant Staphylococcus aureus (VRSA)
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What are Vancomycin-Intermediate Staphylococcus aureus (VISA) and Vancomycin-Resistant Staphylococcus aureus (VRSA)?
Staphylococcus aureus is a bacterium commonly carried on the skin and within the nose of people. The bacterium can cause infections such as boils or pneumonia. Over time, the widespread use of antibiotics has led some S. aureus to become resistant to many antibiotics, which means the antibiotics no long work to kill the bacterium as they should. Some S. aureus have become resistant to the antibiotic vancomycin. If large doses of vancomycin might still be able to kill the S. aureus, it is called Vancomycin-intermediate S. aureus (VISA). If no amount of vancomycin will kill the S. aureus, it is called Vancomycin-resistant S.aureus (VRSA).
What are the symptoms of VISA/VRSA?
VISA or VRSA can cause skin infections, abscesses, pneumonia, and infection of the heart valves or bones.
Who is likely to get VISA/VRSA?
VISA/VRSA is extremely rare. To date only a few cases have been reported in the US. People with the following conditions are more likely to get VISA/VRSA:
• Underlying health conditions (such as diabetes or kidney disease)
• Previous infections with methicillin-resistant Staphylococcus aureus (MRSA)
• Recent hospitalizations
• Use of catheters (such as intravenous [IV] lines)
• Recent use of vancomycin or other antibiotics
Can VISA/VRSA be spread from person-to-person?
Yes, VISA/VRSA can be spread from person-to-person. If a person touches a patient with VISA/VRSA, or touches a bandage or other material contaminated with the VISA/VRSA, he may get the bacterium on his hands. He can then spread it from his hands to another part of his body, or to another person if he touches that person. Washing the hands with soap and water is the best way to remove the VISA/VRSA from the hands so it cannot spread to others.
How soon after exposure do symptoms appear?
In most situations, exposure to VISA/VRSA does not lead to illness. The person might carry the VISA or VRSA on his skin or in his nose, but not get sick at all, or might get sick from the VISA/VRSA days, weeks, or months later.
Does past infection with VISA/VRSA make a person immune?
No.
What is the treatment for VISA/VRSA?
Several drugs that are effective in treating infections with VISA/VRSA have been approved by the Food and Drug Administration (FDA). Please consult with your physician if treatment is needed.
What can be done to prevent the spread of VISA/VRSA?
Use of good infection control practices in hospitals (such as wearing gloves when caring for patients with VISA/VRSA, and frequent handwashing by healthcare workers) can limit the spread of VISA/VRSA. The patient should also wash his hands frequently and should follow any other instructions given to him by his care providers. Keeping hands clean by washing thoroughly and frequently with soap and water is an effective way to prevent VISA/VRSA.
What should I do if a family member or close friend has VISA or VRSA?
Spread of VISA/VRSA can occur when someone has close physical contact with an infected person or with contaminated material, such as bandages. Therefore, persons having close physical contact with infected patients while they are outside of the healthcare setting should: (1) keep their hands clean by washing thoroughly with soap and water, and (2) avoid contact with the person’s wounds or material (such as a bandage) that has touched the wound. If you visit a friend or family member who is infected with VISA or VRSA while the person is hospitalized, follow the hospital’s recommended precautions.
Is there a vaccine against VISA/VRSA?
No.
Where can I obtain more information about VISA/VRSA?
Additional information is available at http://www.cdc.gov/ncidod/dhqp/ar_visavrsa.html.
Last Updated: 07-30-2011
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Guide to African Kanna
Kanna extract
A little known South African herb by the name of Kanna is one that is making major waves as of late. With the capacity to serve as an herbal mood lift potentially second to none, it makes sense why we are beginning to hear more and more about it. Botanically, Kanna (also known as kougoed–meaning ‘something to chew’ in Afrikaans) is classified as Sceletium tortuosum. It is an herbaceous succulent that thrives in the Cape region of South Africa.
Having significant historical usage in its native lands, Kanna is now making its way around the world, and is serving as a powerful tool as a natural means of mitigating mood and emotional imbalances such as depression and anxiety.
Here are some key things to know about the history, benefits, and typical usage of Kanna.
Traditional Usage
Of course with a name meaning ‘something to chew’ it’s not surprising that kanna has been used by native tribes as a chew, for purposes of mood enhancement, relaxation, appetite control, and energy. Several native tribes revered the plant as sacred, and put it to both visionary and medicinal use, including the indigenous San and Khoikhoi peoples of South Africa.
Constituents (what’s working within the herb and how)
Primary actives are the alkaloids: Mesembrine, Mesembrenone, and Tortuosamine. Although there are other compounds within the plant that have an influence at least subtly, these are the most prominent and well-studied. Mesembrine, in particular, has been acknowledged as a specific compound that has powerful effects involving increasing serotonin activity in the brain. In addition, Kanna has PDE4 inhibiting properties. By inhibiting PDE4 (Phosphodiesterase 4), the body has more cAMP available, leading to positive Kanna effects on mood and memory. Mesembrenone is the alkaloid that has been found to be responsible for this effect.
In addition to these mechanisms, there are scientific reports that compounds in Kanna have an affinity to bind to CB1 (endocannabinoid) receptors. Thus, this could provide additional mood benefits as well. And this mechanism could perhaps be a part of the story as to why some users enjoy combining Kanna with cannabis (CBD based or otherwise), as they are often anecdotally reported to enhance each other’s effects.
Kanna for Depression and Anxiety
One of the most common uses for Kanna as an herbal supplement is for a mood lift boost and/or to shake off depressive spells. As previously alluded to, this would be at least in part due to its serotonin reuptake inhibitory properties.
Not uncommonly, users report that Kanna effects can produce euphoric feelings, but this is generally considered to be dose dependent; that is, you would probably need a significant amount to achieve that effect. More often, it’s simply described as a viable mood lift — uplifting and brightening without being overt or overbearing, followed by a sense of relaxation. Indeed, antidepressant properties have been found widely in the research done on this plant.
If you’re suffering from anxiety and having a hard time getting it under wraps, you might try an herbal remedy such as Kanna. Much research has been conducted in validating this, since it has been noted by many to produce an anxiolytic (anxiety mitigating) effect. It is very possible that this effect can be described as a calming of the threat circuitry in the brain, and that it unfolds as a result of the dual serotonin reuptake inhibition along with the PDE4 inhibition that has been discovered. In one study, researchers concluded that alkaloid enriched S. tortuosum (kanna) may benefit some forms of stress-related disorders. And often, when one is experiencing anxiety, it is directly tied to chronic stress.
Processing
Traditionally, Kanna was fermented as a means of making the plant material more potent, absorbable, and generally digestively friendly on the body as a whole. The wisdom of the tribes that would do this shines through as modern science has found that the fermentation process is likely to break down levels of oxalic acid — which can be harmful in excess (though small amounts are found in many vegetables, such as spinach) — and make the alkaloids more bioavailable to the body.
The entire process is most likely passed down from generations of old, considering that it has been described in the literature for over 300 years. The method involves crushing the entire plant between stones – the material is then placed in a bag and left to ferment in the sun, letting nature do the rest of the work. This practice is actually still commonplace today, as the wisdom of the methodology has been passed down for generations.
Other Potential Benefits of Kanna
It has been reported that Kanna may delay chronic disease progression by way of antioxidant and mild anti-inflammatory action. Along these same lines, it seems to have the potential to mitigate systemic low-grade inflammation in general. That, in turn, could additionally aid in improving one’s mood – getting bodily inflammation in check.
How do you use Kanna and what are the effects of Kanna?
In general, it has been said that Kanna is best taken on an empty stomach – many people seem to feel stronger effects when ingesting it without any food in the system.
As far as methods of consumption, there are several possible ways. Smoking the plant material is one option, either by itself or in combination with other smoking herbs. This is a way to feel the effects immediately.
Most commonly, the plant material is chewed — just as it was traditionally– allowing the alkaloids to be absorbed sublingually (through the mucous membranes of the mouth), which is a very efficient way of getting all of the active components into the body.
Another great way of consuming Kanna is simply brewing a tea, using a gentle simmer rather than a strong boil, so that the delicate alkaloids stay fully intact. The taste of Kanna tea is generally considered to be mild, and even slightly sweet – not entirely bitter like some herbal teas can be. Other possible methods that some people utilize range from insufflation of Kanna powder to simply swallowing it in capsules.
Kanna dosage range:
Optimal dosages will vary wildly depending on user’s body type, amount of food in stomach, method of ingestion, and intended effects.
An average threshold, or low but active dose, is approximately 50 mg for sublingual use. Typically, for chewed or ingested root, between 100 – 200 mg is a sufficient and effective amount to consume. And anywhere from 300 – 1,000 mg (1 G) can bring about a stronger experience. Obviously, consider your sensitivity to psychoactive compounds, and your body weight when gauging what a strong dose might be for you.
Brewing a tea will require a bit more of Kanna, 200 – 500 mg being an average to medium dose and 600 – 1,000 mg or more for a stronger brew; but you can expect the effects to last longer using this method.
Insufflation dosages are on the much smaller side; 20 mg is typically enough for a noticeable effect, and 50 – 150 mg is somewhere around the average dosage for this method.
For smoking, the typical dose is closer to the insufflation range above, although a ‘starting’ dose is closer to 50 mg. 100 – 250 mg is considered to be medium level. Because Kanna is widely considered to potentiate cannabis’s effects, less is needed, generally, when combining the two in smoking mixtures.
Where to Buy Kanna
Top Extracts sources quality Kanna in both powder form and rough cut. | {
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6,078,480,885,833,830,000 | Gastroschisis (gas-tro-SKEE-sis) is a birth defect of the abdominal wall that causes part of a baby's intestines to stick out of the body.
More to Know
Gastroschisis is a type of hernia or rupture, that develops in a baby's belly wall before birth. The rupture happens just to the right of the umbilical cord. The rupture can be small, causing a lump in the belly, or large, causing the intestines and parts of other organs to stick out from the body.
Doctors can see a baby has gastroschisis at birth. They treat it with surgery to put the organs back into the body.
Keep in Mind
Gastroschisis is a serious medical condition that can keep a newborn in the hospital for a while. Most babies with gastroschisis recover after treatment and go on to have a healthy life.
All A to Z dictionary entries are regularly reviewed by KidsHealth medical experts.
Note: All information is for educational purposes only. For specific medical advice, diagnoses, and treatment, consult your doctor.
© 1995-2021 KidsHealth® All rights reserved. Images provided by iStock, Getty Images, Corbis, Veer, Science Photo Library, Science Source Images, Shutterstock, and Clipart.com | {
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What’s the Best Way to Take CBD?
Written by Dr. Edward Group Founder
There are so many CBD products out there, from creams and lotions to extracts and pills, edibles, even vaping. So, if you're interested in taking CBD for your health, what is the best way to take it?
Watch the video below or keep reading to learn the best ways to take CBD.
YouTube Video
What's the Best Way to Take CBD?
Length: 5 minutes
CBD Overview
So, cannabidiol, also known as CBD is a naturally occurring compound from the Cannabis plant. CBD is best taken in a full-spectrum, organic extract derived from the hemp plant. This way it contains all of the other cannabinoids, as well as the beneficial terpenes, and other compounds.
Right now, by law, the extracts must have less than 0.3 percent THC, so it won't create a psychoactive (“high”) experience. Full-spectrum hemp extract can now be bought at a variety of places, locally and online.
How Can You Take CBD?
There are four common ways to get CBD into your system:
• Sublingually (under the tongue)
• Ingesting it like food
• Applying it topically
• Inhalation
So, let's talk a little bit about each one of these.
Sublingual
Number one is sublingually. This method is where you take a dropper with the recommended amount of full-spectrum hemp extract or CBD, and hold it under your tongue for one to two minutes before you swallow it. This can provide the powerful benefits of CBD and the other phytocannabinoids into your system very rapidly.
Ingestion
The next method is through ingestion, and there are many different edible varieties of CBD available. You can get CBD and hemp in food like gummies, sweets, and coffee. You can take it in capsules, or have a drink that has CBD in it already. When you ingest CBD, it takes awhile for you to feel the effects and the benefits because it has to go through your digestive system and liver. It usually takes about one to two hours to feel if you ingest it into your system.
Topical
The next way to get benefits from CBD is through topical application. There are lotions, balms, ointments, and oils that can be applied directly to your skin. Using CBD in this way is helpful when dealing with sore muscles, inflammation, or any type of skin condition.
Inhalation
The last method to get CBD into your system is through inhalation, and that can be done through vaping, or through smoking CBD. This is not the one I recommend because I think there are more natural, organic methods to get the CBD into your system.
Now, which way is the best way for you to add it to your body? Well, everyone is different, but it really depends on what results you're looking for.
Personally, I recommend an organic, full-spectrum hemp extract in an MCT oil.
How to Find the Right CBD Product
There's a lot of different products out there. It's very confusing for people, but you need to look at the company that's producing it. Look at the quality and third-party analysis of the hemp extract to make sure that not only does it contain CBD, but it contains the full-spectrum — the entourage — of all the phytocannabinoids that your system needs to produce that homeostasis and balance within your system.
Another interesting fact is that eating citrus fruits after taking a CBD or a hemp extract may increase, or improve, the absorption. So for sleep, I recommend taking the hemp extract at least one to two hours before bed.
If you’re interested in learning more about hemp, view our Hemp 101: A Complete Guide to What Is Hemp, Legalization, & More PDF.
†Results may vary. Information and statements made are for education purposes and are not intended to replace the advice of your doctor. If you have a severe medical condition or health concern, see your physician.
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1,147,044,883,795,475,300 | 레이블이 Preventive KM인 게시물을 표시합니다. 모든 게시물 표시
레이블이 Preventive KM인 게시물을 표시합니다. 모든 게시물 표시
6월 28, 2011
Immunity
Immunity
Preventive medicine can be called the counterpart for treatment medicine, when dividing medical science into three parts such as fundamental medicine, clinical medicine and preventive medicine. Mainly focusing on prevention of disease, preventive medicine belongs to hygienics in western medicine. It is a field of medical science with very wide ranges that covers from prevention, early treatment to rehabilitation. At prevention stage before incidence of disease, what contemporary medicine mostly emphasizes is the strengthening of human body immunocompetence.
Immunity is the phenomenon that human body environment defenses against antigen from outside. In western medical respect, it is a process of immune system – WBC (macrophagocyte, lymphocyte), killer T cell, and so on – resists pathogenic organism.
Concept of immunity has also existed in Korean medicine in name of healthy qi(正氣) that maintains the balance of yin, yang, qi, and blood against external stimulus. Healthy qi, which is core concept in Korean medicine pathogenic theory, protects our body from external pathogen(邪氣). Pathogen, a relative concept from healthy qi, is similar to agent that causes disease when it penetrates into body.
Korean medicine considers the process of immunity as struggle between healthy qi in our body and external pathogen. Therefore if our healthy qi is strong enough, our body will be well-protected, but if not, it will become vulnerable. As a method of preventing disease, Korean medicine emphasizes life-nurturings, among which raising healthy qi to ward off pathogen is considered the most important one.
Immune process by healthy qi and defense qi
Healthy qi is the energy that protects body from pathogen. It is similar to level of immunity. We can call the state when body loses healthy qi and becomes weak 'Huh', which means deficiency. There are various states of Huh; qi deficiency, blood deficiency, yin deficiency, yang deficiency and so on.
If we loses healthy qi, we get easily infected. Defense qi circulating the body surface shows how healthy qi affects body. Defense qi is a sort of healthy qi that blocks external pathogen invasion into body. Defense qi is circulated through skin and flesh, and it protests against external pathogen. Defense qi flowing on skin prevents pathogen from getting into body and if pathogen comes into the body, defense qi sieges and blocks it. It is called 'struggle between the healthy qi and pathogenic qi', which is when pathogen is blocked by defense qi outside the body and fight with healthy qi inside body. This process can be compared with mononuclear phagocyte or macrophage process. It is like present immunity process.
≪Huangdi's Internal Classic(黃帝內徑)≫ which is one of Traditional Chinese Medicine classic books explains that heat or crassi can be made during this process. If healthy qi is defeated by pathogen, tumor, stomachache or headache appear and illness occurs.
Medicinal for strengthening the body
Generally speaking, traditional medicinal for strengthening one’s body system is called ‘tonifying and replenishing medicinal.’ The preventive meaning of this kind of medicinal is not restricted in the sense of protecting the body and filling up on healthy qi. Healthy qi indeed acts as a preventive system by holding up against external pathogen, but simultaneously fights off the external pathogen that already invaded the body. Thus tonifying medicinal can be prescribed before the occurrence of disease to help prevent it by replenishing the healthy qi, or after the outbreak to supplement the deficient state of the body and encourage the healthy qi to fight pathogens.
Tonifying and replenishing medicinal can be seen as formulas that acts to tonify yin, tonify yang, tonify qi, or tonify blood. Each type of tonifying medicinal is applied to pathological deficiency of body’s yin, yang, qi, and blood. Qi deficiency is a general term for decreased visceral and overall body function, and is often seen on patients with leucopenia, bronchial asthma, myasthenia gravis, and some types of rashes. Blood deficiency is the state in which blood flow motility is weak, and is related to symptoms such as anemia and hives. Yin deficiency is an expression for the lack of fluid, and is often matched with dryness of skin, tidal fever, and chronic rheumatism. Yang deficiency mostly refers to the insufficiency of kidney yang, and is often seen on allergic rhinitis, and chronic nephritis patients.
When one’s level of immunity is weak or hyperactive, one’s immune system is more or less malfunctioning. This not only leads the body to be easily effected to diseases, but also may trigger symptoms from self tissue damage. Many of these disease patterns correspond to deficiency symptoms from Trditional Korean medicine. So if tonifying medicinal is appropriately applied to immune system under-function, the medicinal will help treat the symptoms by immune regulatory effect.
Yang-tonifying Medicinal(補陽藥)
In Oriental Medicine, the word ‘Immunity’ was first shown in an 18th century medical book in which the word means restraint from injuries caused by disease. Broadly speaking, if immunity is considered as a prevention and treatment of all the diseases, its concept originates from ≪Huangdi's Internal Classic(黃帝內徑)≫. In appears the phrase ‘不治已病 治未病’(Treat the disease before it occurs, not after.) It is based on the prevention-centered idea, and a disease is considered as a process of struggle between a Healthy Qi and pathogens(邪氣) in the body. It was perceived that the strength of a Healthy Qi(正氣) directly determines the occurrence, advancement and change of diseases.
Because Yang(陽) means protecting the body, the meaning of Yang-tonics accords with the concept of Immunology. The action of Yang qi is needed for the circulation of blood, fluid and humor(津液) and the formation and distribution of essence flavors(正味) of five grains(五穀). The evaporation of Yang Qi is needed for mental activity and function of intestinal organs. Thus, it is thought that Yang-tonifying medicinals have an effect on increasing the level of immunity in human organisms, and they have recently been applied to many diseases.
Most of Yang-tonifying Medicinals are assigned to the kidey meridian, acting as Kidney-tonifying medicine. As an innate source, the Kidney(腎) is the base of the body's defensive power. That is, a resistance against the intrusion of exopathogens can be connected to immunology's act of defending infection. Also, the Kidney was recognized as a bone marrow producing organ, which is related to the hematogenous functions of bone-marrow and the production of immune cells.
Interestingly, many herbal medicines tonifying the kidney are known to increase immune cells. This action reinforces the function of the pituitary gland-interrenal system and strengthens the immune function.
Yang-tonifying Herbs includes Epimedii Herba, Cuscutae Semen, Cistanches Herba, Psoraleae Fructus, Cynomorii Herba, Cortex Cinnamomi, Morinda officinalis, etc.
Cervus Nippon and Psoralia Corylifolia have clinical effects on leukopenia treatment. Also, Cuscufa Chinensis, Psoralia Corylifolia and Epimedium Brevicornum activate the phagocytosis of macrophagocyte and the conversion of T cells to relieve symptoms.
Qi-tonifying Medicianl(補氣藥)
Because the spleen is an acquired source and an origin of vitality, most Qi-tonifying Herbs effect the spleen-stomach meridian. In immunity, several studies showed the spleen to be a basis of acquired constitution(後天的 體質). In Oriental Medicine, severely non-nutritious patients are diagnosised with a spleen deficiency. Their number of immunity and antibody cells are decreased and the whole immune system often shows to be lowered. Also, a patient with a spleen deficiency(脾虛) can easily get infection in the intestine or skin tissue. From this point of view, we can see that the spleen has an important effect in sustaining the body's immune system. It appeared that most of the components of Qi-tonifying medicinals have adjusted immune function.
Qi-tonifying medicines commonly contain polysaccharides a lot and it's considered that through their action, B cells and T cells can be activated, the secretion of cytokine can be increased, the capacity of macrophage can be enhanced and the productions of antibodies can be increased by them as to tonify the immunocompetence. Qi-tonifying medicines have boosting effects on lung and stomach as to strengthen our immune system. The most typical medicines contain Ginseng Radix, Pilose Asia-bell, Astragali Radix, Astractylodes Rhizoma alba and Dioscoreae Rhizoma. Especially, Water-extracted Ginseng Radix is regarded as having preventive effects on influenza and boosting our body's immune system as to enhance the effect of the vaccine against influenza.
Treatment of the disorder of the immune system.
1. Flu(Influenza)
It's hard to prevent our body from flu as the virus type is infinite and their infection process could be variable. Therefore, it's necessary to boost and maintain our immunocompetence to prevent it. 'Flu' is considered as 'Cold' in the West, similar to the fact that it is considered as 'Cold Pathogen' in the East. We can assume that flu has been considered in relation to the temperature. Epidemiological research reports that In temperate climate regions, the breaking out of flu increases in autumn and get to the highest point in winter and decreases in the spring. In tropical regions, however, it breaks out mostly at rainy season in the low temperature.
The most common virus causing cold is rhinovirus. As rhino means the nose, it is associated with runny nose which is a common symptom of cold. But this virus is very sensitive to the temperature as it can grow best when the body temperature is lower than 33 degrees celsius and the higher the temperature gets, the lower the growth of the virus. If the temperature is at 39 degrees, the growth rate is 400 times less than when it's at 33 degrees. As the result of experiments on animals, it seems that viruses causing influenza also spreads better at the lower temperature condition. In conclusion, Herbal medicines can enhance our immunocompetence for flu as they generally help the metabolism in our body as to have positive effects on the regulation of the body temperature.
In TKM, the flu is considered as 'affection by cold' or 'invasion of wind' and it's regarded that we get cold because the defensive energy called 'Defense qi' cannot protect the interstices tightly so that pathogenic wind invade in weakened part. Therefore, we have to boost the defensive energy and tighten the interstices to prevent the invasion of pathogenic energy and prevent our body from cold. Prescriptions containing medicines that tonifies lung-qi is commonly used because lung qi produces defense qi. Medicines like Okbyeongpungsan(玉屏風散) which mainly contains milk vetch root(黃芪) are commonly used. Dropping the solution of milk vetch root on the nose is considered as a good method for preventing cold. Milk vetch root increases the concentration of SlgA and lgG in mucous membranes of the surface of the nose and neutralizes the phagocytic activities of phagocytic cells. By the fact that the values of the SlgA and lgG in the serum have increased, these herbal medicines are proven to have the boosting effects on the immunocompetence.
2. Glomerular nephritis
Most cases of nephritis are caused by antigen substances in blood combining with specific antibody to form antigen-antibody compound. When this compound is excreted through glomerulus, it files up on basement membrane, activates alexin, and cause inflammatory response. Traditional Korean medicinals used in the early stages of nephritis are ‘heat-clearing and detoxicating medicinal’(淸熱解毒藥), and ‘wind-dispelling and dampness-draining medicinal’(擧風利濕藥), which restrain immune responses. By pattern identification in TKM, chronic nephritis can be traced back to malfunction of kidney-yin and kidney-yang. Based on this diagnosis, treatment should focus on tonifying kidney-yin and kidney yang to regulate immune system, and also control overactive immune response by ‘blood-activating and stasis-resolving medicinal’(活血化瘀藥) and are ‘heat-clearing and detoxicating medicinal’(淸熱解毒藥). Particularly, Tripterygium regelii Sprague, which is a medicinal material traditionally used to treat kidney related disorders, is known to have anti-inflammatory, pain-relieving, and fever-reducing effects, thus suppressing B-cell actions and inducing T-cell to repress immune responses.
3. Hyperthyroidism
Hyperthyroidism is often linked with mental predispositions which are generally expressed in terms such as ‘liver qi depression’(肝氣鬱滯), or ‘yin deficiency with yang hyperactivity’(陰虛陽亢). This pattern identification correspond to the modern diagnosis hat stress may cause hyperthyroidism. LATS, which is found among the blood serum of hyperthyroid patients, is a kind of immunoglobulin and is affiliated with IgG type antibody. Hyperthyroidism is often linked with mental predispositions which are generally expressed in terms such as ‘liver qi depression’(肝氣鬱滯), or ‘yin deficiency with yang hyperactivity’(陰虛陽亢). This pattern identification correspond to the modern diagnosis hat stress may cause hyperthyroidism. LATS, which is found among the blood serum of hyperthyroid patients, is a kind of immunoglobulin and is affiliated with IgG type antibody. Patients that are sorted into ‘yin deficiency with yang hyperactivity pattern’ are also often found with increased IgG/blood serum figure.
Clinically used medicinal are targeted to ‘enrich yin and tonify qi’(養陰益氣), ‘harmonize the stomach and liver’(和胃平肝), ‘dispel phlegm and resolve dampness’(祛痰化濕). Medicinal materials on such formula are Astragalus membranaceus, Codonopsis pilosula Nannfeldt, Angelica gigas Nakai, Paeonia lactiflora, and Leonurus sibiricus L. Especially in an experiment where hyperthyroidism-induced white mice were given the ‘enrich yin and tonify qi’ medicine ‘甲亢復方’(material: Astragalus membranaceus, Paeonia lactiflora, Leonurus sibiricus L, Coptis chinensis, Rehmannia glutinosa, Cyperus rotundus, tortoise shell), their increased blood serum cAMP content was reduced. Also, liver tissue oxygen level and water drinking amount were decreased, and abnormal changes in adrenal cortex functions were regulated. Also in studies with human subjects, patients with hyperthyroidism showed high level of cAMP in blood serum and low cGMP level. This shows that by regulating disorders in cAMP/cGMP system in hyperthyroid patients, immune malfunction can be prevented.
7월 06, 2010
Preventive Medicine For Modern Times
written by: Seonghee Joo, Seonghwan Cho, Jongwoo Kim, Nayeon Ha, YeoEun Park
edited by: YeoEun Park
Modern times breed modern diseases. While unprecedented growth of civilization set most of human race free from plague and famine, new health problems are coming into spotlight. More nutrition and less exercise led to deterioration of health, which can be loosely bound in a category of diseases called 'adult diseases.' Adult diseases, also called lifestyle diseases, include variety of diseases such as obesity, diabetes, arthritis, and cancer. As many of adult diseases are caused by one's diet, stress factor and overall lifestyle, every day prevention is necessary. In this article we will discuss how Traditional Korean medicine can help prevent adult diseases such as obesity, hypertesion, diabetes, and stroke.
1. Obesity
A person with obesity is generally overweight, but a person who has lots of muscles instead of fats can also be overweight, so we define 'obesity' as a condition of an accumulated excess body fat. Body Mass Index, a measurement which compares weight and height, defines people being overweight when BMI is over thirty for western people, and over twenty-five for Asians.
Obesity is known as a direct cause for adult diseases like diabetes, stroke, hyperlipidemia, high blood pressure, heart disease and is also related to arthritis, gout, infertility and menstrual irregularity. It may even trigger more serious diseases such as colorectal cancer, prostate cancer, gallbladder cancer and breast cancer, and is one of the greatest risk factors to health that shortens our life span and lowers our life quality.
(1) Dietary treatment for Obesity
Adult diseases are not individual disease to each other. Rather they are closely connected that they cause and aggravate other adult diseases. Therefore dietary treatments for them have a lot in common. Basically we need to cut back a high-salt and a high-fat diet which is wrong diet of modern people. Also roasted and fried food which is rich in carbohydrate, three-white food (white rice, white wheat, white salt), and drinking alcohol should be moderated. Instead we should plan the Mediterranean diet, which mainly consists of fruits, fishes, and vegetables. Additionally intake of potassium is recommended that it boost discharge of sodium to bring down blood pressure.
Low calorie diet containing adequate amount of essential nutrient is recommended. Fruits and vegetables, for instance beans, adlay, tomatoes, cucumber, low-fat fish, buckwheat, weed, onion, carrot and cabbage are good for obesity cure.
(2) Exercise cure for obesity
Highly intensive aerobic exercise is effective for obesity but it should not be continued after the body feels fatigue. Though exercise that lasts less than an hour has appetite-suppressing effect, exercise more than an hour reversely boost appetite, so 40 minutes-exercise for 4 times a week is recommended.
One of the traditional exercise treatments is Qigong exercise, which is descended from ancient China exercise school(養生長壽術 十勢功法道家 華山派). It is called 龍遊功(Yongyoogong, which is also called 三環功-Samhwangong, as it puts hands together and turn around three times), because its movement is quite similar to dragon’s waving. It is effective for losing unwanted weight and keeping good body shapes. Other exercises such as 按腹行法(Walking while massaging stomach), 正坐深呼吸法(Sitting up straight and deeply breathing), 香陵六合氣功(hyangnengyukkigong) are becoming accepted as being helpful on treating obesity.
(3) Medicinal Treatment for Obesity
① Bangpungtongseongsan(防風通聖散)
- Cnidium officinale 4.0, Saposhnikovia divaricata 4.0, Angelica gigas 4.0, Paeonia lactiflora 4.0, Mentha piperascens (Malinv.) Holmes 4.0, Forsythia viridissima 4.0, Ephedra sinica 4.0, Erigeron canadensis 4.0, Rheum palmatum 4.0 gypsum 4.0, Platycodon grandiflorum A. De Candolle 4.0, Scutellaria baicalensis 4.0, Artractylodes japonica 3.0, Schizonepeta tenuifolia var. japonica 3.0, Zingiber officinale 3.0, talcum10.0, Gardenia jasminoides 3.0, Glycyrrhiza uralensis 2.0
- Used when colonic motility is too excessive, as this hyperactivity tends to cause constipation.
- Used when patients have lots of fat cells, suffer from obesity and hyperlipidemia which causes skin allergies, mucous allergies, skin diseases, hypertension, mental disorders, etc :
* Reduce the viscosity of blood
* Anti-inflammatory and anti-allergic action
* Proliferate the blood circulation
* Controls autonomic nervous system
* Treats inflammation of the urinary system
- Mentha piperascens Holmes, Platycodon grandiflorum A. De Candolle, Scutellaria baicalensis have anti-inflammatory effects.
- Forsythia viridissima, Scutellaria baicalensis, Artractylodes japonica have anti-allergic effects.
- Forsythia viridissima, Saposhnikovia divaricata, Rheum palmatum, Schizonepeta tenuifolia var. japonica, talcum have antibacterial activities as to treat the inflammation of urinary system and skin.
- Rheum palmatum, Scutellaria baicalensis, Schizonepeta tenuifolia var. japonica, Gardenia jasminoides reduces the viscosity of blood as to relieve inflammatory diseases and hypertension.
- Cnidium officinale, Gardenia jasminoides tranquilize the nerves.
- Cnidium officinale, Angelica gigas, Paeonia lactiflora proliferate the blood circulation by improving the vasomotion ability
- Erigeron canadensis, Rheum palmatum cause quick discharge of the intestinal contents as to treat the viscosity of blood caused by intestinal stagnation of the contents.
- Ephedra sinica, Paeonia lactiflora, Zingiber officinale excrete impurities in interstitial cells by letting the patient sweat.
- This herbal medicine often used for person who has excessive subcutaneous fat around the belly button. It is effective for obese patients with constipation and hypertension as it eliminates unnecessary wastes through the secretion of sweat, urine and feces.
② Chegameuiin-tang(體減薏苡仁湯)
- Coix lacryma-jobi 8g, Rehmannia glutinosa 7g, Sinomenium acutum 4g, Glycyrrhiza uralensis ․ Astragalus membranaceus ․ Dioscorea batatas ․ Akebia quinata ․ Alisma canaliculatum ․ Magnolia obovata ․ Polyporus umbellatus ․ Juncus effusus ․ Raphanus sativus ․ Angelica gigas ․ Epimedium koreanum ․ Lycium chinense Miller ․ Cornus officinalis 2.5g each, Cnidium officinale ․ Carthamus tinctorius ․ Caesalpina sappan 1.5g each.
- This herbal medicine is effective for generally healthy, yet obese patients who have great appetite, sleep much and hate moving their body.
- It treats these patients by improving blood circulation, reducing the appetite, improving endurance, promoting fat decomposition and smooth discharge of urine and feces.
(4) Acupuncture and Moxibustion for Obesity
Meridians are pathway for qi and blood, the principle constituents of human activity. They are affiliated with organ in internal part of body, and distributed all over the external part. Traditional Korean medicine defines heath as the state in which qi, blood, and body fluids are appropriately circulating. Acupuncture and moxibustion can stimulate certain points on meridians, thus controlling overall energy and metabolism system, and cure diseases. Historical books on medicine show that 'life-nurturing moxibustion'(養生灸), by applying moxa on certain areas during healthy state, can prevent illness and invigorate human body.
It has been studied that stimulation by acupuncture or chuna may promote metabolism and regulate endocrine system. These functions lead to effects similar to lipolysis and thus help reduce body fat. Chuna or massage basically stimulate the body in the same way as acupuncture, and also has weight reducing effect. Traditionally used body area for weight reduction is the back. Stimulation of he back induce fat reducing effect on the whole body. The back is seen as the area where body's Yang qi is concentrated, and governor vessel, which is the meridian that controls the overall yang meridians, passes through the back. Modern studies show that brown fat cells are amassed on the back. Massage on the back stimulated heat production of the brown fat cells, and lets the excess energy to be consumed.
2. Diabetes
Diabetes is called ‘wasting-thirst’(So-gal) in Korean medicine. It is true that diabetes is often caused by stress, lack of exercise, high-calories, fats and proteins diet. Diabetes, however, can also be occurred by specific gene deficiency and also by pancreas operation, infection and medicine. People who have diabetes can easily have obesity, high blood pressure, and hyperlipidemia, and in treatment doctors must take those other factors into consideration.
When diabetes is not severe, there are no special symptoms, but usually when blood glucose is high, patients feel thirsty, drink lots of water, eat lots of meals but lose weight and feel lethargy, and urinate more.
(1) Dietary treatment for Diabetes
Being overweight easily leads to wasting-thirst, therefore fatty food, roasted or fried food, high-carbohydrate food which causes obesity should be avoided. Additionally, drinking alcohol and eating sweet fruits should also be kept off. Instead low-salt diet is strongly recommended. In this way, diabetes can be prevented without any medication treatments.
(2) Exercise & Mental cure for diabetes
“Treatise on the Pathogenesis and Manifestations of All Diseases”(諸病源候論), Korean medicine classic emphasized importance of proper exercise, and says that we should walk 125~1000 steps before taking a meal. Another classic “Medical Secrets of an Official”(外臺秘要) suggests to concrete example of abstentious life style; exercises should not be too intensive, take a walk to digest after having a meal, prohibits late-night meal, and having small amount of meal at once but for several times.
Mental stress like anger, agony and depression forms heat inside the body that induces wasting-thirst. Accordingly, at the early period, wasting-thirst can be treated if one suppresses greed and worry. However, once this moderation is neglected, even the best medication and doctor can’t treat wasting-thirst.
(3) Medicinal Treatment for Diabetes
① Yukmiziwhangwhan-gagambang(六味地黃丸加減方)
- 生地黃(Rehmanniae Radix), 山藥(Dioscoreae Rhizoma), 石膏(Gypsum Fibrosum) 10g each, 牧丹皮(Moutan Cortex), 瓜蔞根(Trichosanthis Radix), 麥門冬(Liriopes Radix), 山茱萸(Corni Fructus) 6g each.
- Boil down the above herbs as a pack after meals, two times a day.
- Rehmannia Radix reduces the blood sugar to low level, nourishes the blood and strengthens the heart.
- Gypsum Fibrosum, Liriopes Radix relieves thirst, and treats eating disorder and bulimia.
- Moutan Cortex and Trichosanthis Radix soothes the skin inflammation caused by diabetes, reduces fever, and relieves thirst.
- Corni Fructus reduces polyuria, and Dioscoreae Rhizoma relieves thirst along with Gypsum Fibrosum, Liriopes Radix, and Trichosanthis Radix.
② Gami-Jeonssibaekchulsan(加味錢氏白朮散)
- 葛根(Puerariae Radix) 2don, 人蔘(Ginseng Radix), 白朮(Atractylodis Macrocephalae Rhizoma), 白茯苓(Poria), 藿香(Agastachis Herba), 甘草(Glycyrrhizae Radix) 1don each, 木香(Aucklandiae Radix), 柴胡(Bupleuri Radix), 枳殼(Aurantii Fructus Pericarpium), 五味子(Schizandrae Fructus) 5poon each.
- It treats decreased appetite from wasting-thirst and the frequent feeling of starvation from wasting-middle(消中).
(4) Acupuncture and Moxibustion for Diabetes
The foremost cause of diabetes might be spleen, but the root of the matter lies in kidney. Spleen can only function properly when it is heated from the yang qi of the kidney. Also it is important for the lung to be lubricated by the yin fluid of kidney to smoothly function. This is why in treatment of diabetes, traditional korean medicine first applies acupuncture on the BL23(腎兪穴) of the back and waist area. Because kidney malfunction is often caused by liver disorders, BL18(肝兪穴), where qi of the liver assembles, is also used for acupuncture and moxibustion. Then BL13(肺兪穴) BL20(脾兪穴) is treated to cure the liver and spleen. Finally acupuncture and moxibustion is applied to CV12(巨闕穴), where qi of the heart accumulates on the upper abdomen, and all five viscera is treated. This not only cures diabetes but also prevents the disease itself or further complications.
An important characteristic of oriental medicine is that it emphasizes to tonify and strengthen the body before directly treating the pathogen. Thus treatment of diabetes includes acupuncture points that boost the healthy qi of the body. LR14(期門穴) regulates spleen. The spleen is considered as a digestive organ, and it is said to provide other visceral organs with the qi through digestion. ST36(足三里) on both legs, LI11(曲池) on both arms, and CV21(中脘穴) of the stomach are treated to control the balance of qi and blood. Also the source qi is strengthened through treatment of CV6(氣海穴), which is located below the navel and is called 'sea of qi', and CV4(關元穴), where the origin qi is gathered.
3. Hypertension
Hypertension, or high blood pressure, is the state when a person's systolic blood pressure is over 140 mmHgm, or diastolic blood pressure is over 90 mmHg for adults over eighteen. Systolic blood pressure is the pressure on blood vessels when the heart contracts and pushes blood out. Diastolic blood pressure is the pressure on blood vessles when the heart expands and takes blood in.
Hypertension can be divided into two types. One is secondary hypertension, which is hypertension when a direct causative disorder is known, and the other is essential hypertension whose cause is not found. Ninety-five percent of all high blood pressure patients are suffering from essential hypertension. The fundamental cause of essential hypertension is not specific, but it seems to be caused by increase of cardiac output, a amount of blood pushed by heart during one minute or an increase of tip vessel resistance. Dangerous factors related to high blood pressure include family history, drinking, smoking, aging, lack of exercise, obesity, salty diet, and stress.
(1) Dietary treatment for Hypertension
Hypertension and arteriosclerosis are often due to lack of blood circulation, which is caused by excessive intake of salt and fat. Hence, diet has to be focused on promoting blood circulation and reducing intake of salt. Lowering blood pressure treatment is probably ineffective unless diet is improved. Consequently, planning proper diet is the very start of all cures.
(2) Exercise cure for hypertension
Qigong exercise like tai chi chuan is highly recommended. It moves body slowly , and doesn’t put stress on joint but strengthen cardiovascular system. Besides its effect of enhancing muscles, relaxing joints and making blood circulation smoothly, it is said to let the practicer absorb energy from Nature, remove pathogen and strengthen danjeon. Also tai chi chuan reconciles body and qi, it improves arteries and capillaries at the same time.
(3) Medicinal Treatment for Hypertension
① Samhwangsasim-tang(三黃瀉心湯)
- Rheum palmatum(大黃) 7.5g, Scutellaria baicalensis(黃芩) 3.75g, Coptis chinensis(黃連) 7.5g
- Slice the medicine to make 1 dose and soak it in 1 cup of boiling water. Wring it after a long while, discard the solids, and then drink warm over 2 sessions.
- Rheum palmatum(大黃) reduces the viscosity of blood by purgative action(瀉下作用).
- Scutellaria baicalensis(黃芩) is effective for the treatment of hyperlipidemia.
- Coptis chinensis(黃連), Scutellaria baicalensis(黃芩) relieve the hyperemia of blood vessels.
- Coptis chinensis(黃連), Scutellaria baicalensis(黃芩) have central nervous system depressant effect.
② Hwangryunhaedok-tang(黃蓮解毒湯)
- Coptis chinensis(黃連) 1.5g, Phellodendron amurense(黃柏) 1.5g, Scutellaria baicalensis(黃芩) 3g, Gardenia jasminoides(梔子) 2g
- Coptis chinensis(黃連), Scutellaria baicalensis(黃芩), Gardenia jasminoides(梔子) have a sedation effect.
- Coptis chinensis(黃連), Phellodendron amurense(黃柏), Scutellaria baicalensis(黃芩) relieve the congestion of blood, reduce the viscosity of blood and have antibacterial activities.
- As Hwangryunhaedok-tang(黃蓮解毒湯) can treat the hyperemia and inflammation of blood vessels and tranquilize the nerves, it can be used for the symptoms like the hyperemia, anxiety neurosis or inflammatory diseases.
(4) Acupuncture and Moxibustion for Hypertension
Acupuncture and moxibustion depend on natural healing power of human body to improve functions of circulation system, and can thus prevent hypertension.
Treatment principles on hypertenstion is to 'pacify the liver to subdue Yang' (平肝鎭陽), and usually add or omit allopathic treatment according to symptoms. Some studies show that acupuncture is effective on patients with essential hypertension. WFAS(World Federation of Acupuncture-Moxibustion Society) has issued experimental date that shows by applying ear acupuncture, participants' blood pressure can drop by minimum of 10mmHG to maximum 20 to 30mmHG.
Common use acupuncture points on hypertensions are: GB20(風池), LI11(曲池), ST36(足三里), LR3(太衝)
4. Stroke
Stroke, or cerebrovascular accident, is a long lasting disorder which is caused by partial or overall injury of the brain. In Oriental Medicine, it is called 'wind stroke' or simply 'wind', but 'wind' contains diseases not classified as stroke in Western medicine. Therefore it is better to distinguish stroke and wind stroke.
Ischemic stroke occurs when a brain blood vessel is blocked or when a brain blood vessel is torn and the blood permeates through brain tissues. Because the brain is an essential organ that controls all human behavior, various symptoms happen depending on which part of brain is damaged. The most common symptoms are paralysed arm and leg on one side of the body, sensory disorder, not specific pronunciation, feeling dizziness and other discomforts.
(1) Dietary treatment for stroke
As all other adult diseases, stroke prevention also requires large amount of potassium-rich food based on a low-salt and a low-fat diet so that blood can flow smoothly. To reduce calories, meal portion should be cut down to 80% of before. Dietary fibers and water intake must be increased but high-cholesterol foods like mushrooms, seaweeds and beans must be avoided.
(2) Medicinal Treatment for Stroke
① Ohyaksungisan(烏藥順氣散)
- 麻黃(Ephedrae Herba)·陳皮(Citri Pericarpium)·烏藥(Linderae Radix) 6g each, 川芎(Chidii Rhizoma)·白芷(Angelicae Dahuricae Radix)·白殭蠶(Bombycis Corpus cum Batryticatus)·枳殼(Aurantii Fructus Pericarpium)·桔梗(Platycodi Radix) 4g each, 乾薑(Zingiberis Rhizoma Siccus) 2g, 甘草(Glycyrrhizae Radix) 1.2g, 生薑(Zingiberis Rhizoma Recens) 3, 大棗(Zizyphi Fructus) 2
- Boil down the above herbs as a pack three times a day, 1 hour after meals.
- It controls qi to prevent and treat stroke. Also, it is good for people who are worried about having stroke due to physical disharmony and mental tension, since stroke seizures are prevented when qi communicates smoothly. For stroke and all of the signs of the disease, these herbs should be taken to communicate qi in advance, along with the following prescribed herbs. It is good to take this medicine when there is pain, a sense of illness somewhere in the body, or impediment in speech.
②Sopung-tang(疎風湯)
- 羌活(Notopterygii Rhizoma)·防風(Saposhnikovia Radix)·當歸(Angelicae Gigantis Radix)·川芎(Cnidii Rhizoma)·赤茯苓(Poria)·陳皮(Citri Pericarpium)·半夏(Pinelliae Rhizoma)·烏藥(Linderae Radix)· 柏脂(Thujae Resina), 香附子(Cyperi Rhizoma) 3.2g each, 桂枝(Cinnamomi Ramulus)·細辛(Asari Herba Cum Radix)·甘草(Glycyrrhizae Radix) 1.2g each, 生薑(Zingiberis Rhizoma Recens) 3 pieces.
- Boil down the above herbs as a pack three times a day, 1 hour after meals.
- It is prescribed when there are symptoms of a light stroke disease including the numbness at the end of four limbs.
- The name Sopung implies that the medicine dispels the wind from the body.
(3) Acupuncture and Moxibustion for Stroke
Cerebrovascular disorders, commonly called stroke, are often caused by hypertension. Traditional Korean medicine has long shown strongness on chronic stroke, half-body paralysis, dementia, and inappetance. It is also particularly effective for aftereffect of stroke. Traditional Korean medicine doctors diagnose 'phlegm-dampness' or 'phlegm-heat' as some of the pathogens of stroke. In those two cases, it is more important to unblock the meridian rather than using restorative herbal medicine. This is where acupuncture and moxibustion can step in as appropriate preventive treatment for stroke. Acupuncture and moxibustion have no side effects when used together with Western medicine treatment or herbal medicine. Also because acupuncture-moxibustion regulates autonomic nerve, it alleviates general symptoms and induce functional recovery. Thus acupuncture and moxibustion treatment are effectively used for prevention against stroke by regulating blood pressure or preventing relapse.
1월 27, 2010
How to prevent H1N1?
How to prevent influenza H1N1 by Korean Medicine?
by Ji Myung Woo
(Grade 4, Staff Writer)
Young Kyun Moon
(Grade 3, Assistant Writer)
Ha Na Yeon, Jong Woo Kim
(Grade 2, Assistant Writer)
How can we fight against influenza H1N1? More than 300,000 people worldwide have been confirmed as cases of pandemic influenza H1N1. While the number of confirmed cases increases continuously, the supply of Tamiflu, treatment for influenza H1N1, is not enough in many countries. Then, what can we do with limited supply of Tamiflu? The best way is to take measures to prevent influenza H1N1. World Health Organization(WHO) had set guidelines to prevent the spread of influenza H1N1. (You can refer to it in later part of this article.) Still better way is to use Korean medicinal methods to prevent and treat influenza H1N1.
How better is oriental medicine in treating/preventing H1N1?
In international seminar about influenza H1N1 held recently in South Korea, the director of Chinese Medicinal Science reported that out of 10221 confirmed cases of influenza H1N1, 6098 patients were cured completely by using Chinese medicine and there was no case of death so far. Chinese government had set guidelines for treatment of influenza H1N1. Chinese doctors should use Chinese medicine for early phase of H1N1 and for serious cases, doctors should use Chinese medicine and Western medicine simultaneously. The average treatment period using Chinese medicine is about 3-5 days. The treatment efficacy is similar to that of Tamiflu while the cost of Chinese medicinal treatment is about 1/7 lower than using Tamiflu. Furthermore, there was no case of side effect. Dean of College of Oriental Medicine, Kyung Hee University asserted that "Illici Veri Fructus (八角), an ingredient of Tamiflu, have been used by KM doctors broadly."
How to prevent influenza H1N1 by Korean Medicine?
There are three Korean medicinal methods to prevent influenza H1N1.
The first method is simple. Keep away from pathogen(避邪). This method is almost the same as the one that WHO recommends. Primary preventive method is to avoid pathogen(邪氣) as much as you can.
The second method is life nurturing (養生). In Korean medicine, illness is process of struggle between the healthy qi and pathogenic qi (正邪相爭). Person with strong healthy qi can remain healthy even after exposure to pathogenic qi. In other words, person with weak healthy qi is vulnerable to illness. Life nurturing can be enhancing healthy qi or maintaining healthy qi. Life nurturing in this method is to maintain healthy qi to prevent an illness. The basic idea of this method is to avoid food and places that can damage healthy qi. 1. Eat clean and warm food. Avoid eating cold food. 2. Avoid cold places. 3. Wear appropriate clothes according to temperature.
The third method is to reinforce the healthy qi (扶正). This is mainly done by taking Korean medicine. The president of Korean Medical Association of Professor of Lung Internal Medicine asserted that "Frequent water intake is very important to prevent influenza. Also, concoction including ginger (Zingiberis Rhizoma Crudus), date (Zizyphi Fructus), and field mint (Menthae Herba) is effective in preventing influenza.
There are also many other ways to prevent influenza in Korean medicinal classic Dongeuibogam.
-Powder realgar (石雄黃) and apply to nose.
-Boil Styrax Big Pill (Sohaphyang-won) and use the steam to prevent influenza.
-Take Powder of Rhizoma Cyperi and Folium Perillae
-Take Jeong-gi-san(正氣散)
-Take Doso-eum(屠蘇飮)
-Take Chilmuljeok-san (七物赤散)
-Take Antiphilogistic Powder of Herba Schizonepetae and Radix Saposhnikoviae (荊防敗毒散)
WHO guidelines to prevent H1N1
The main route of transmission of the new influenza A(H1N1) virus seems to be similar to seasonal influenza, via droplets that are expelled by speaking, sneezing or coughing. You can prevent getting infected by avoiding close contact with people who show influenza-like symptoms (trying to maintain a distance of about 1 metre if possible) and taking the following measures:
-avoid touching your mouth and nose;
-clean hands thoroughly with soap and water, or cleanse them with an alcohol-based hand rub on a regular basis (especially if touching the mouth and nose, or surfaces that are potentially contaminated);
-avoid close contact with people who might be ill;
-reduce the time spent in crowded settings if possible;
-improve airflow in your living space by opening windows;
-practise good health habits including adequate sleep, eating nutritious food, and -keeping physically active. | {
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3,384,755,933,831,191,000 | Florida Kidney Physicians
March 19, 2019
What is Stage 3 Chronic Kidney Disease and How Do I Treat It?
What is Chronic Kidney Disease Stage 3?
Stage 3 chronic kidney disease (CKD3) means that the kidneys have suffered moderate damage, and are not functioning as well as they should. There are 5 stages of kidney disease in total, ranging from mild damage to complete kidney failure.
The kidney’s main role in the body is to filter waste from the blood, while also regulating blood pressure and red blood cells. As disease progresses, the kidneys struggle to perform these essential tasks, leading to kidney failure.
The stages of kidney disease are measured by a blood test called eGFR, or estimated glomerular filtration, that determines how well your kidneys are filtering waste.
An eGFR of 100 means no waste is detected and your kidneys are functioning at 100% of their capacity. During stage 3 kidney disease, the rate falls to half capacity, and then below half.
The third phase of kidney disease is divided into two stages: stage 3a and stage 3b.
• Stage 3a is measured by a en eGFR of between 45 and 59.
• Stage 3b sees eGFR rates dropping further, between 30 and 44.
A normal eGFR is 60 or more. If you fall below that mark for three consecutive months, you should seek medical attention from a doctor who specializes in nephrology, or the treatment of kidney conditions and abnormalities.
What are the risks of kidney disease, and what happens if I don’t seek treatment?
If you do not see a doctor while in stage CKD3 and your disease continues to worsen, your body will reach such a critical state that you need dialysis, or an artificial means of performing the job your kidneys are meant to do.
Dialysis can be time-intensive and costly. It helps your body to continue functioning, but does not cure you. Dialysis may involve visiting the doctor three times a week to get treatments that are four hours long, where doctors use an artificial kidney to remove waste and other fluids from your body.
The other dialysis options involve buying a machine for your home that regulates your body while you sleep, or getting a catheter inserted into your peritoneal cavity so that you can administer dialysis yourself four to five times every day, the only option without machines.
Patients on dialysis live an average of 5-10 years, though some patients live longer. Dialysis is a major medical treatment needed for people whose bodies are in a critical state.
Symptoms of patients in the later stages of kidney disease include: nausea, vomiting, weakness, lack of appetite, decreased mental sharpness, persistent itching, chest pain, and sleeping problems.
If you do not address kidney disease in the earlier stages, your health could degenerate to the point where you experience painful or unpleasant symptoms, and need dialysis treatment to function. If you do not get dialysis, your body will be flooded with toxins. You may experience total kidney failure, which is a life-threatening condition.
How do I get help in preventing further damage and avoiding kidney failure?
Doctors who specialize in kidney conditions, nephrologists, will work with you to create a personalized plan to fight kidney disease that includes lifestyle and diet changes, with the possibility of medication as well.
Your doctor can also help you with symptom relief. Many people in stage 3 do not have symptoms, but some experience back pain, frequent urination, or swelling in the hands and feet.
If you have diabetes or high blood pressure, a nephrologist can prescribe certain kinds of blood pressure medicines that may prevent kidney disease from worsening. These medicines include ACE inhibitors and ARBs.
Addressing the disease while still in an intermediate stage like CKD3 gives you and your doctor time to support your kidney function before it’s too late.
Your treatment plan may involve changes in your lifestyle that can seem overwhelming, but nephrologists are there to support you and check in with you as you begin working towards improved kidney health.
Get your kidneys checked today. Visit our website to make an appointment online at flkidney.com
#chronickidneydisease # chronickidneydiseasestage3 #ckd3 #treatmentckd #avoiddialysis #kidneyfailuresymptoms #renaldisease #stage3kidneydisease #kidneydisease #chronickidneydiseasetreatment
©2021 Florida Kidney Physicians
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1,675,593,534,050,773,000 | Skip to Content
Metalite
Metalite may be available in the countries listed below.
Ingredient matches for Metalite
Trientine
Trientine hydrochloride (a derivative of Trientine) is reported as an ingredient of Metalite in the following countries:
• Japan
Important Notice: The Drugs.com international database is in BETA release. This means it is still under development and may contain inaccuracies. It is not intended as a substitute for the expertise and judgement of your physician, pharmacist or other healthcare professional. It should not be construed to indicate that the use of any medication in any country is safe, appropriate or effective for you. Consult with your healthcare professional before taking any medication.
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4,457,920,056,701,798,400 | Naltrexone Alcoholism Medication
Buy Naltrexone Online
10/12/2018
Naloxone and naltrexone are pure opiate receptor blockers.
Naloxone is used to restore self-breathing during opioid overdose. It is administered parenterally, selecting the dose in such a way as to ensure the safety of protective respiratory reflexes and normal ventilation.
Naltrexone is taken internally. It is prescribed for the abolition of opioids during detoxification and at the stage of abstinence, and as an additional remedy for alcohol abolition.
Naloxone and Naltrexone block all types of opiate receptors without possessing stimulatory properties.
The first to do in opioid dependence is to carry out detoxification, and then try to achieve prolonged complete abstinence or prescribe substitution therapy with methadone or buprenorphine. At the stage of abstinence, you can also use any opiate receptor blocker, but naltrexone is advised, since it is absorbed when taken orally, and has a longer action than naloxone.
Careful observation is necessary, since it is possible to resume opioids and re-oppress respiration. In these cases, repeated doses of opioid receptor blockers or intravenous administration with subsequent infusion are prescribed.
The duration of action of naltrexone at a dose of 150 mg for oral administration is usually 72 hours. In most cases, this is enough to stop the effect of opioids.
How Does Naloxone Work?
Naloxone, also known under the brand name "Narcan", is a safe and effective drug that removes a person from the state of opioid overdose. Naloxone binds to the same brain receptors as heroin and other opioids, displaces and blocks opioids for 30-90 minutes, thereby helping to restore breathing, the oppression of which usually leads to death from an overdose.
Does Naloxone Help Only In Cases Of Opioid Overdose?
Yes. Naloxone is effective only in cases of overdose caused by the use of opioids, such as heroin, methadone, morphine, opium, codeine or hydrocodone. Naloxone can not eliminate the effects of other drugs, such as benzodiazepines (including diazepam, midazolam or alprazolam), antihistamines (eg, phenyramine or phenergan), alcohol or other sedatives (eg, phenobarbital), as well as stimulants, including cocaine and amphetamines.
However, if a person does not breathe, the use of naloxone does not hurt. if there was an opioid use, then most likely the person will start breathing again, although he may still be under the influence of other drugs. many overdoses are due to the mixing of opioids with other drugs, which is a very common practice.
Can I Get A "Buzz" From Naloxone?
No. The only effect of naloxone is the elimination of the effects of opioids. It is impossible to get a "buzz" from naloxone: if you do not use opioids, the sensation of naloxone injection will be the same as the injection of water. Naloxone has no potential for abuse or dependence.
Are Naloxone And Naltrexone The Same?
No. Naltrexone is similar to naloxone, but its duration time is much longer: usually about 24 hours. Naltrexone is sometimes used in the treatment of drug or alcohol dependence.
In some cases, a combination of naloxone with buprenorphine is used. It is known under the brand name "suboxon", and is used to treat drug dependence. Naloxone is added to prevent the injection of buprenorphine.
Copyright © 2016-2018. All Rights Reserved. | {
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2,522,910,603,830,128,600 | What Is Areolar Tissue?
Areola refers to the circular, pigmented area surrounding the human nipple.
Article Details
• Written By: Nicole Long
• Edited By: Allegra J. Lingo
• Last Modified Date: 05 July 2014
• Copyright Protected:
2003-2014
Conjecture Corporation
• Print this Article
Found throughout the body, areolar tissue is a type of connective tissue. It consists of cells and various properties of the tissue’s intercellular matrix. Cushioning surrounding organs, connecting different tissues, and supporting blood vessels represent just a few of the functions of this specific connective tissue.
Areolar tissue is composed of several cell types. Among the mix of cells are adipose cells, better known as fat cells, mast cells and macrophages. The remaining composition includes leukocytes and plasma cells.
Like other loose connective tissues, areolar connective tissue consists of three different types of fibers. These fibers include collagenous fibers, elastic fibers and reticular fibers. Together these fibers make up the traditional weaved appearance of areolar, and other loose connective tissues.
The intercellular matrix of areolar tissue is composed of the matrix of collagenous, elastic and reticular fibers and ground substance. Proteins and proteoglycans contribute to the makeup of ground substance. Ground substance works to hold together the various properties of this tissue.
Various cells and properties of the intercellular matrix of this tissue can be seen under a microscope. Under the microscope collagenous, elastic, and reticular fibers appear as pink bands of varying widths arranged in no distinct pattern. Fibroblasts may appear as dark dots with finger-like extensions. The surrounding substance, referred to as the ground substance, appears as a light stain on microscope slides but may be difficult to see.
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Organs throughout the body rely on connective tissue for support. The largest organ in the human body, the skin, depends on the pliable, fluid-filled tissue to provide assistance with protecting the organs and other structures located within the human body. In addition, you can find areolar tissue working in conjunction with the epithelial tissues of the body.
Epithelial membranes, the term for the convergence of epithelial and connective tissues, line the various cavities of the human body, such as the abdomen and nasal cavities, and also line interior organs. Blood vessels arising from the areolar tissue provide nutrition to the epithelial tissue found inside body cavities and lining organs. This tissue also transfers waste from the epithelial tissue and destroys harmful pathogens.
Since areolar tissue can be found lining blood vessels, the tissue also reaches into organs, muscles and tendons. Along with the job of supplying blood to the epithelial tissue, it provides leukocytes when necessary. Leukocytes fight infection within the cavities, organs and tissues of the human body.
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Discuss this Article
kylee07drg
Post 4
Areolar tissue seems protective yet laid back at the same time. It has enough strength to hold different kinds of tissue together, yet it is cushiony enough to offer support.
It is interlaced, yet it is flexible. Since the fibers have a loose organization, they allow for movement of the areas bound by the areolar tissue.
Kind of like a good mother, areolar tissue provides guidance and personal space at the same time. It is nurturing with its blood vessels, but it offers plenty of room for movement.
StarJo
Post 3
I did not know until reading this that the areolar tissue contained macrophages. We just finished a biology study session on these, and they are helpful little cells.
Macrophages are a kind of white blood cell. They eat foreign elements in the body. By doing this, they aid in the destruction of bacteria and tumor cells.
They regulate the immune system and help with wound healing. They also can stimulate other types of immune system cells by releasing substances. With things like protective and fat-burning adipose tissue and disease-fighting microphages, areolar tissue has quite a healthy composition!
cloudel
Post 2
@oceana - Did you know that not all adipose tissue is the same? This areolar tissue comes in white and brown, and both have different functions.
I became curious about how fat cells insulate our bodies after I lost weight and noticed how much colder I seemed to stay. This is when I found out what happens in the adipose tissue.
White fat cells store the calories that we don’t use right away for energy. They gather around thighs, hips, and the belly. This is the kind people try to rid themselves of through diets and exercise.
Brown fat cells gather around the neck, collarbone, and shoulder blade. They burn the extra fat calories instead of storing them. By doing this, they keep the body warm.
Oceana
Post 1
As humans concerned primarily with appearances, we often view fat cells negatively. When you think about it, though, adipose tissue is such a good thing. This kind of areolar tissue keeps your organs from banging into your bones and bruising during daily activities.
Without adipose tissue, imagine the consequences of dancing, horseback riding, or any type of exercise. We would all have to sit still to preserve our bodies!
I jumped on the trampoline very much as a kid. I cannot imagine what that would have done to my internal organs had I not had adipose tissue to cushion them.
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email | {
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Specific time-delayed burst profile delivery system
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Title: Specific time-delayed burst profile delivery system.
Abstract: The invention provides a delivery device for the delayed release of an active agent in the gastrointestinal tract comprising a core, comprising an active agent; a first outer coating, comprising a relatively hydrophobic substantially water insoluble polymer having substantially water insoluble hydrophilic particles embedded therein; and a first inner coating layer, comprising an agent that can cause the dissolution of at least one of the water insoluble components of the outer coating, and optionally a water soluble polymer, such that the insoluble particles in the outer coating, upon absorption of liquid, form channels leading to the inner coating layer, thus enabling the dissolution thereof, whereby the agents contained therein are released to cause the dissolution and/or degradation (destruction) of the outer coating, and the release of the pharmaceutically acceptable active agent from the core of the device. ...
- Washington, DC, US
Inventors: Adel Penhasi, Mila Gomberg, Maxim Gomberg
USPTO Applicaton #: #20060280795 - Class: 424472000 (USPTO) - 12/14/06 - Class 424
view organizer monitor keywords
Related Patent Categories: Drug, Bio-affecting And Body Treating Compositions, Preparations Characterized By Special Physical Form, Tablets, Lozenges, Or Pills, Sustained Or Differential Release Type, Layered Unitary Dosage Forms
The Patent Description & Claims data below is from USPTO Patent Application 20060280795, Specific time-delayed burst profile delivery system.
FIELD OF THE INVENTION
[0001] The invention is directed to a device for the oral delivery of active agents in solid dosage forms to specific locations along the gastrointestinal tract and/or delivery after specific lag time by both immediate and sustained release of all or most of the active agent at a predetermined specific location. The active agent delivery system has the capability of loss of integrity in a short space of time thereby allowing the delivery of most to all of the active agent at the location of disintegration.
BACKGROUND
Delivery to Specific Site/Delayed Release (Time Controlled Delivery)
[0002] Specific delivery of drugs to sites in the gastrointestinal tract and/or time controlled delivery of drugs are highly desirable for the treatment of a multitude of conditions. For many drugs an exact delivery to the specific site along the gastrointestinal tract is extremely important. This may be because of extensive degradation of the drug elsewhere in the GI, or because of a narrow absorption window. Thus for the best oral bioavailability, the drug must be protected by the delivery system until it arrives to the right place and then it should be released as fast as possible (so called burst release profile).
[0003] It is also desirable to target the drugs to sites in the gastrointestinal tract where the drug could be preferentially absorbed. This may be especially desirable for the delivery of peptide and protein drugs. These latter drugs have proven notoriously difficult to deliver orally due to poor absorption and to degradation by enzymes of the body. Delivery of these drugs to predetermined sites in the GI tract at a high rate of delivery could help alleviate these problems by creating a strong concentration driven gradient for drug absorption while at the same time saturating degradative pathways. Altemately, the drug may be delivered to sites that possess specific carriers to affect the drug delivery.
[0004] A delayed release is necessary where the drug should be released after a period of time post administration (lag time). An appropriate example for such a necessity is an early morning release of drugs, e.g., medications taken at night whose actions are required in the early morning hours (chronotherapy).
[0005] There are many situations where the active material should be released immediately (after bursting the delaying film coat) in the specific site. These latter situations, therefore, compel designing a delayed fast release system. These systems will be appropriate mainly for drugs that are metabolized to pharmacological active compounds, drugs which have long in-vivo half-lives showing an inherently prolonged duration of action, drugs with a very short in-vivo half-life which require a prohibitively large amount of active ingredient in the dosage form, drugs which are required in large doses for a therapeutic effect, and drugs which are required in very low dose.
[0006] Additionally a delayed burst release can also be utilized for enhancing absorption, reducing side effects, increasing bioavailability and decreasing the dose.
[0007] Targeting mechanisms for site-specific delivery, such as delivery in the lower gastrointestinal (GI) tract, are based primarily upon the principle of uniform small intestinal transit, pH variability and its effect on eroding film coatings, or chemical or enzymatic conditions in the large intestine that can be exploited to control drug release. There are many oral delayed release technologies, including colon specific drug delivery, which are commercially in use. All of the triggering mechanisms for delayed release, especially colonic delivery, which are widely used amongst the population requiring treatment, are vulnerable to variations based upon time of day, fed state and disease condition. Technologies based on enteric coating are susceptible to pH variations which naturally exist throughout the GI tract of a specific patient as well as existing between different individuals. Technologies based upon exploitation of enzymatic degradation, or other biochemical reactions such as redox potential in the colon, are susceptible to bacterial flora which may vary according to gender, age and race. Accordingly, such systems are not reliable. The concept of osmotic pumps is based upon a tablet or capsule that provides a constant internal pressure as a result of the dissolution of some components, mostly inorganic salts, after penetration of water into the tablet or capsule. The resulting constant pressure inside the core may eventually result in the drug being pushed out at a constant rate. Such technologies are, however, expensive to institute and are designed primarily to provide only a zero order drug release (a constant rate of drug release with time). The technologies that control diffusion from a gel matrix or constant surface area, can result only in a first order or zero order release, respectively, and have no ability to control either site or release profile. Furthermore, the release based on diffusion from a gel matrix may be severely affected by both the viscosity of luminal content as well as the agitation rate of the GI tract.
[0008] Several delivery systems were designed with that goal in mind. Following are description of some important ones.
[0009] U.S. Pat. No. 4,871,549 October/1989 Ueda, et al. 424/494 discloses a dosage form comprising a core with a drug (or coated with a layer of drug). This is further coated with a synthesized polymer selected from the group consisting of polyvinyl acetate and polyacrylic acid or disintegrating agent selected from the group consisting of hydroxypropylcellulose, sodium starch glycolate and carboxymethylcellulose and overcoated with an insoluble outer membrane (ethyl cellulose). In this system drug release is caused by explosion of the outer membrane occurring after a predefined lag time and mediated by the physical swelling force of the disintegrating agent or the synthesized polymer.
[0010] WO 98/32425 July/1998 Busetti et al. A61K 9/28, U.S. Pat. No. 5,788,987 August/1998 Busetti et al. 424/480US and U.S. Pat. No. 5,891,474 April/1999 Busetti et al. 424/490. These patents disclose a formulation for treatment of early morning pathologies. The process for preparation of this formulation includes: [0011] 1. Wetting the core containing an active agent and disintegration-enhancing agent with the binder. [0012] 2. Coating the core with the particles of swellable polymer to produce a time-specific dosage regulated by a thickness of the swellable polymeric coating layer. The polymeric particles are selected from a group consisting of cellulose derivatives, PVP, PVA, acrylic acid polymer, methacrylic acid copolymers, ethyl acrylate-methyl methacrylate copolymers, natural rubbers, poloxamers, polysaccharides and their mixtures.
[0013] This coating delays the release of the drug for about 4 to about 9 hours depending on the thickness of the coating layer. The minimal coat thickness is 50 micrometer (pm). The core: coating layer thickness ratio ranges between 20:1 and 1:3.
[0014] As described in U.S. Pat. No. 5,840,332 there was developed a new time-controlled release system for the burst release of active material. This system was based on a combination of a new disintegrating core and the novel controllable film coat, consisting of a hydrophobic polymer film coat embedded with non-soluble, but hydrophilic particles. This latter film coat was tailored to undergo splitting under a proper pressure being formed inside the tablet upon the penetration of water. The core was designed to undergo swelling and consequently disintegration to cause simultaneous bursting of the coating film and immediate release of the drug. The delay time (or the lag time), which is the time that it should take until the bursting of the film coat, and thus the release of drug, is adjusted by means of controlling both the thickness of the film coat as well as the weight ratio of said hydrophylic particles in the film coat. By these means, an immediate release of the drug at various locations in the colon will be achieved.
[0015] The most serious drawback of this system, however, was found to be the dependence of both film rupture as well as burst release on the weight ratio of excipients/active material. At low ratios no significant burst release can be achieved and in the more extreme cases no rupture of the film coat takes place.
[0016] Thus, when the composition of the tablet cannot exert a necessary physical force for the rupture of the film coat and in case of film coated capsules, there is a need for a subtler method in order to achieve the burst release.
[0017] In order to obviate this problem, there has been suggested in the prior art, to create a controlled chemical attack on the protective outer coating layer. This attack may come either from within the tablet (or the capsule) or from the outside environment. The following are several publications relating to such systems.
[0018] U.S. Pat. No. 5,472,710 December/1995 Klokkers-Bethke, et al. 424/1468 discloses a dosage form comprising a core with a drug (or coated with a layer of drug). This is coated with an acid layer containing solid acid (sodium dihydrogenphosphate, citric acid, tartaric acid, succinic acid, fumaric acid), further coated with pH sensitive polymer (cellulose acetate phtalate and other cellulose phtalate derivatives, methacrylic acid copolymers, carboxyethyl methylcellulose) and finally overcoated with a water insoluble outer polymer (ethylcellulose, polyvinylacetate and acrylic and methacrylic acid esters with quaternary ammonium groups) membrane which is permeable to gastric secretions. Optionally the acid layer and the pH sensitive polymer layer may be applied in reverse order or the acid can be included in the drug layer. The acid will protect the pH sensitive polymer layer until its exhaustion by the intestinal medium and then the pH sensitive layer will dissolve and permit the release of the drug through the outer insoluble membrane.
[0019] In this system the outer membrane retains its integrity throughout the release, and therefore doesn't burst.
[0020] Time controlled drug delivery based on a capsule has been described in the art. WO90/09168 describes the "Pulsincap" system in which a non-soluble capsule body is closed with a hydrogel cap that swells and opens the capsule at predetermined times. While control of the time of drug delivery has been achieved with these systems there are problems with the total delivery of the dose since the capsule remains intact.
[0021] T. Ishibashi et al (Journal of Pharmaceutical Sciences 87, 531 (1998)) describes the delivery of drugs from a dissolving capsule whose time of delivery is determined by an outer coating. The outer coating is an acid soluble film while a compatible acid is formulated inside the capsule. When enough water has penetrated the film and dissolved the acid in the capsule, the film is dissolved by the action of the acidic environment. The drug is totally released in a burst fashion. This system requires that the drug being delivered is compatible with the acid in the capsule This system is obviously unsuitable for drugs which can react with acid, and those which are adversely affected by the acidic environment in a dissolved state.
[0022] U.S. Pat. No. 5,593,697 describes a pharmaceutical implant containing biologically active material, an excipient comprised of at least one water soluble material and at least one water insoluble material, and a polymer film coating adapted to rupture at a predetermined time after implantation. An insoluble outer film controls the access of biological fluids to the inner film which is soluble. The thickness of the outer film controls the time of inner film failure. Upon inner film failure an expanding excipient swells, rupturing the outer film. Systems of this sort lack fine control over the time of rupture since they have only one parameter, that of thickness, to control said time. These systems also require the formulation of the drug with the swelling excipient, which raises questions of compatibility and of bioavailability.
[0023] U.S. Pat. Nos. 5,260,069 and 5,472,708 describe a dosage form for delivering drugs, particularly drugs that cannot be released by diffusion. Pellets are comprised of the drug, and a swelling agent that swells when it absorbs water. The pellets are coated by a membrane or coating that is water insoluble but water permeable, containing an insoluble polymer, a water soluble polymer and a permeability reducing agent. The rate of water entry is controlled by the ratio of the three components in the film. Higher proportions of the water soluble polymer weaken the film and make it more permeable while higher proportions of the permeability reducing agent slow down the entry of water. Upon absorption of water the pellets swell and rupture the membrane, thereby releasing the drug. Again in this system one must formulate the drug with the swelling agent in the core of the pellet.
[0024] Proceed. Intem. Symp. Control. Rel. Bioact. Mater. 21, (1994), 744 describes what is called the "Chronotropic drug delivery system". Pellets or minitablets of a drug formulation are coated with various thicknesses of a hydrophilic swelling polymer such as hydroxypropylmethylcellulose. When the delivery system is in an aqueous environment the coating swells and slowly dissolves. When it has dissolved, the drug pellets are released and can release their drug load. Control of the time of release is expected to be poor because only one parameter, thickness, is available for said control.
[0025] U.S. Pat. No. 5,260,068 describes a capsule that contains pellets. The capsule dissolves in the stomach releasing the pellets. The pellets comprise a drug and an osmotic agent and are coated with a water insoluble but water permeable membrane containing a hydrophobic compound to lower the film permeability to water. The pellets absorb water due to osmotic pressure until the membrane bursts. The relative amount of the hydrophobic material helps to control the rate of water entry and thereby the time of drug release. The drug must be formulated with an osmotic agent and be stable in solutions of high osmolarity.
[0026] U.S. Pat. No. 4,871,549 describes a time controlled exploding system wherein the drug is formulated on a bead in a formulation that comprises the drug and a swelling agent. The swelling agent may be a polymer that swells upon contact with water or may be a gas generating mixture of an organic acid and a carbonate compound. The beads are overlaid with a non-soluble membrane that allows slow water entry. The water allows the swelling agent to burst the coating after a predetermined time lag. This system lacks parameters to control the time of water entry other than coating thickness. It further requires the formulation of the drug with the swelling agent or gas generating agent and its compatibility therewith.
[0027] As will be realized, there remains a need for a system that will allow the precise control of the time of drug release, guarantee full drug release and delivery by the complete failure of the protective mechanism, and allow one to formulate a drug with its known compatible excipients, with no need for formulation with excipients that are necessary for the release mechanism. A drug formulated within a capsule with its normal or desired formulation, wherein, upon the capsule, on the outer surface, are added two or more coatings that contain all the components to control the time of capsule disintegration and to afford the essentially total disintegration of said capsule, will give the desired effect. The drug is totally separated from the coatings that supply the release mechanisms and therefore no questions of compatibility arise.
[0028] According to the present invention, there is now provided a new and modified time-controlled release system for the burst release of an active material. According to the present invention, the drug delivery system has the capability of rapid loss of integrity, thereby allowing the delivery of at least most of the drug load at the location of disintegration.
[0029] The mechanism for controlling the site or time of release is a function of the coatings of the solid dosage form thus obviating the need for any special excipients in the formulation for this purpose. However, the release profile of the active agent after bursting of the outer film coat, as opposed to the delivery system which is controlled by the coating layers of the present invention, as described and explained hereinafter, can depend upon the excipients being used in the formulation, the mode of the formulation preparation and the character of the formulation. This feature is important for formulating active agents such as those which should be formulated with a low weight ratio of excipients/drug.
SUMMARY OF THE INVENTION
[0030] The mechanism of disintegration according to the present invention is affected by an inner film that, when saturated with water, chemically and/or mechanically attacks the outer film. The outer film controls the rate of entry of the water into the inner film thereby controlling the time and site of delivery of the active agent. When the integrity of the outer film has been compromised, the core dissolves, releasing the active agent in either burst fashion or sustained release.
[0031] The term: "active agent" as used herein is intended to denote any active agent which is suitable and/or desirable for delayed release in the gastro-intestinal tract. Preferred active agents are physiologically acceptable active agents such as vitamins and nutrients, and components known as food additives and especially preferred active agents are pharmaceutically acceptable active agents.
[0032] The description hereinafter will be directed primarily to a discussion of delivery of drugs, it being understood that other types of active agents as mentioned above can also be delivered by the devices of the present invention.
[0033] More specifically, according to the present invention, there is now provided a delivery device for delayed burst release of an active agent, preferably a physiologically acceptable active agent, and most preferably a pharmaceutically acceptable active agent in the gastrointestinal tract comprising: a) a core comprising a pharmaceutically acceptable active agent; b) a first outer coating comprising a relatively hydrophobic substantially water insoluble polymer having substantially water insoluble hydrophilic particles embedded therein; and c) a first inner coating layer comprising a water soluble polymer and an agent that can cause the dissolution of at least one of said water insoluble components of said outer coating, wherein a plurality of said particles extend from an outer surface to an inner surface of said first outer coating, such that said particles, upon absorption of liquid, form channels leading to said inner coating layer, thus enabling the dissolution thereof, whereby the agents contained therein are released to cause the dissolution of said outer coating, and the burst release of the pharmaceutically acceptable active agent from the core of said device.
[0034] Thus, in a first set of preferred embodiments of the present invention, the core containing the drug and the usual excipients are precoated with a first inner film containing an organic acid (citric, tartaric, fumaric, succinic and similar acids) that, when saturated with water, chemically attacks the outer pH-dependent film. The outer film controls the rate of water intake by the inner film thereby controlling the time of the active material release (the lag time). Optionally the core can be precoated with a neutral buffering layer to prevent the contact between the drug and the acid.
[0035] As will be realized, this new delivery system comprises a solid dosage form which is loaded with the active material. The solid dosage form is coated with an inner coating that is relatively easily dissolvable in water and contains the agent that will compromise the integrity of the outer coating. This agent can be, for example, an agent that changes the pH of the environment outside the solid dosage form or an agent that reacts with a major component of the outer membrane, rendering it readily soluble in water. The outer coating is one that. controls the time and site of drug delivery by controlling the entry of water into the inner coating for a predetermined time period. The outer film coat contains as one of its essential features a major component that is substantially insoluble in water but that can be readily dissolved upon release of the agent in the inner coat. Thus, the outer coating prevents entry of water into the inner coating or into the solid dosage form for a predetermined time period, allows entry of water into the inner layer which dissolves, whereafter, the outer layer is then compromised by an agent from the inner layer. The compromised outer layer undergoes failure allowing quick entry of water into the system. The water readily dissolves the active material (for aqueous soluble active agents) and/or disintegrates the solid dosage form affording total delivery of the drug load at the predetermined site and/or predetermined time. Accordingly, the nature of the agent in the inner coating will be determined by the nature of the outer coating. The drug is therefore delivered to the desired site after a predetermined time without any need to reformulate it with excipients of the delivery system. The release profile of the drug after bursting of the outer film coat, however, can depend upon the excipients being used in the formulation, the mode of the formulation preparation, the character of the formulation and the water solubility of the active material. This feature is important for formulating tablets that may have a high content of the active material resulting in a low weight ratio of excipients/drug or capsules in which the drug load and its formulation are kept totally separate from the components of the delivery system.
[0036] Such a system has many advantages. Since drug release and dosage disintegration is not pH related and is not linked to the bacterial flora of the colon, such a system is very flexible and extremely reliable. This technology is unique because the drug release mechanism depends solely upon the presence of GI tract fluids, regardless of the viscosity of luminal content. Depending on the nature of both the core as well as the coating, the release profile can be designed to be either a delayed burst release or delayed rapid slow release. The onset of drug release can be calibrated to precisely target specific segments of the GI tract, including the colon. The lag time (the time from the administration of the drug to the release start) can be readily controlled upon controlling parameters related to both the coating as well as the core. This fact provides for a system that can be easily used for chronotherapy (delivery of a drug in a precise timing according to circadian rhythms for obtaining optimal treatment of diseases) where the peak times of exacerbation occur in the morning, (for example hypertension, asthma, rheumatoid arthritis), or the afternoon & evening (for example osteo-arthritis). Such a system is a versatile technology that can be used for coating different types of solid dosage forms such as granules, microspheres, microparticles, microcapsules, beads, pellets, tablets, caplets, and capsules regardless of the dose. The burst profile can be designed to be independent of the weight ratio of burst controlling agents and/or disintegrants/drug in the core formulation. The system is an appropriate technology for the delivery of any drug substance with different physico-chemical characteristics such as hydrophilic (water soluble), hydrophobic (water insoluble), amorphous, crystalline, hygroscopic (very sensitive to humidity absorption), and lipophilic (highly water insoluble, lipid soluble) drugs. Both the core and the coating of the delivery system are produced using standard pharmaceutical equipment.
[0037] A pulsing tablet enabling precise timing for multiple drug releases in a single unit is also possible.
[0038] The clinical advantages of such a system are expected to be; [0039] 1. Increased absorption and higher bioavailability than a conventional immediate release or sustained release drug due to the system's ability to release in a burst manner, [0040] 2. Enhanced delivery of poorly bioavailable drugs that would be destroyed in the higher GI tract environment (for example, peptide molecules), [0041] 3. Reduced dose of drug without decrease in therapeutic effect, [0042] 4. Reduced side effects, [0043] 5. Reduced drug interactions due to lower receptor concentration of cytochrome P450 isoenzymes, [0044] 6. Reduced food effect (the changes occurring in bioavailability of drug when given with food), [0045] 7. Improved compliance, [0046] 8. Chronotherapy-programmed delayed release of a drug for optimal treatment of disease, [0047] 9. Pulse release, which allows multiple dosing in a single dosage form; and [0048] 10. Site-specific release for local treatment of diseases
[0049] Such a system may also exploit the controlled absorption characteristics of the colon. For example, rapid release of drugs with fast elimination rate in colon would result in an even level of drug plasma concentration due to slow absorption rate.
[0050] The technological advantages of such a system are; [0051] 1. The drug is protected until its arrival at the site of release; [0052] 2. Drug release is not subject to variations in the pH of the gastrointestinal tract; [0053] 3. Drug release is not subject to variations of viscosity of lumen contents; [0054] 4. The system is not dependent on the agitation rate of the GI tract; [0055] 5. The system is not colon flora dependent; [0056] 6. The system is not dependent on the nature of the drug; [0057] 7. The system offers many parameters for controlling the release profile; [0058] 8. The system offers many parameters for controlling the lag time; [0059] 9. The system production process is based on standard pharmaceutical equipment; [0060] 10. The drug release is not dependent on the weight ratio of excipients/drug; and [0061] 11. The system can be utilized for various solid dosage forms such as granules, microspheres; microparticles, tablets, capsules, and pellets.
[0062] In one embodiment of the current invention the outer coating that controls the entry of water is a film of a water insoluble polymer, embedded with water insoluble but hydrophilic particles. Such a coating is described in U.S. Pat. No. 5,840,332 as a coating for tablets or capsules. Said coating offers many parameters for controlling drug delivery as described in that patent. The identity, weight percent, and size of the particles, and the identity of the hydrophobic polymer, as well as the coating thickness, are all parameters that control the entry of water through such a coating. We have found that certain embodiments of that coating can be used as the outer coating for this invention. According to some embodiments of the present invention, the water insoluble polymer of the outer coating is selected from the group consisting of a dimethylaminoethylacrylate/ethylmethacrylate copolymer, the copolymer being based on acrylic and methacrylic acid esters with a low content of quatemary ammonium groups, wherein the molar ratio of the ammonium groups to the remaining neutral (meth)acrylic acid esters is approximately 1:20, the polymer corresponding to USP/NF "Ammonio Methacrylate Copolymer Type A", an ethylmethacrylate/chlorotrimethylammoniumethyl methacrylate copolymer, the copolymer based on acrylic and methacrylic acid esters with a low content of quatemary ammonium groups wherein the molar ratio of the ammonium groups to the remaining neutral (meth)acrylic acid esters is 1:40, the polymer corresponding to USP/NF "Ammonio Methacrylate Copolymer Type B", a dimethylaminoethylmethacrylatelmethylmethacrylate and butylmethacrylate copolymer, a copolymer based on neutral methacrylic acid esters and dimethylaminoethyl methacrylate esters wherein the polymer is cationic in the presence of acids, an ethylacrylate and methylacrylate/ethylmethacrylate and methyl methylacrylate copolymer, the copolymer being a neutral copolymer based on neutral methacrylic acid and acrylic acid esters, ethylcellulose, shellac, zein, and waxes. More preferably, the water insoluble polymer is ethylcellulose or Eudragit E or their combinations thereof.
[0063] According to preferred embodiments, the outer coating further comprises hydrophilic water-insoluble particulate matter. The water insoluble particulate matter is more preferably selected from the group consisting of a water insoluble cross-linked polysaccharide, a water insoluble cross-linked protein, a water insoluble cross-linked peptide, water insoluble cross-linked gelatin, water insoluble cross-linked hydrolyzed gelatin, water insoluble cross-linked collagen, water insoluble cross linked polyacrylic acid, water insoluble cross-linked cellulose derivatives, water insoluble cross-linked polyvinyl pyrrolidone, micro crystalline cellulose, insoluble starch, micro crystalline starch and a combination thereof.
[0064] According to specific embodiments, the cross-linked polysaccharide is selected from the group consisting of insoluble metal salts or cross-linked derivatives of alginate, pectin, xanthan gum, guar gum, tragacanth gum, and locust bean gum, carrageenan, metal salts thereof, and covalently cross-linked derivatives thereof.
[0065] According to specific embodiments, the water insoluble cross-linked cellulose derivatives are selected from the group consisting of cross-linked derivatives of hydroxypropylcellulose (HPC), hydroxypropylmethylcellulose (HPMC), hydroxyethylcellulose, methylcellulose, carboxymethylcellulose, and metal salts of carboxymethylcellulose.
[0066] Most preferably, the water insoluble particulate matter is micro-crystalline cellulose or an insoluble metal salt of a polysaccharide or their combinations thereof.
[0067] Optionally, the outer coating further comprises a plasticizer. More preferably, the plasticizer includes at least one of dibutyl sebacate, polyethylene glycol and polypropylene glycol, dibutyl phthalate, diethyl phthalate, triethyl citrate, tributyl citrate, acetylated monoglyceride, acetyl tributyl citrate, triacetin, dimethyl phthalate, benzyl benzoate, butyl and/or glycol esters of fatty acids, refined mineral oils, oleic acid, castor oil, corn oil, camphor, glycerol and sorbitol or a combination thereof.
[0068] In one preferred embodiment the hydrophilic non-soluble particles are a crosslinked polysaccharide or an insoluble metal salt of a polysaccharide or microcrystalline cellulose or a mixture of them which is embedded in a polymer that is insoluble at neutral pH but soluble at acid pH. In a most preferred embodiment this polymer is Eudragit E or ethylcellulose or mixture of them.
[0069] The inner coat comprises at least one of a binder such as hydroxypropylmethylcellulose or hydroxypropylcellulose, and a rupturing agent that can be at least one organic acid to dissolve the pH sensitive outer polymer, and/or at least one metallic ion chelating agent such as a salt of ethylenediaminetetraacetic acid (EDTA). In a preferred embodiment the organic acid is citric acid. Water enters the outer coating through the filled channels formed by the non-soluble particulate embedded in the outer coating. The inner film dissolves, releasing the organic acid. The release of the organic acid causes the dissolution of the hydrophobic polymer (in the above mentioned most preferred embodiment, Eudragit E) in which the particles are embedded. The outer coating loses its integrity since there is no longer a polymer matrix to hold the particles around the capsule or the core.
[0070] The gelatin capsule or the core is thus totally exposed and quickly dissolves and/or disintegrates.
[0071] In another most preferred embodiment the embedded hydrophilic non soluble particles are a non soluble metal salt of an acidic polysaccharide, most preferably calcium pectinate (CaP) or calcium alginate at more than 50% w/w, while the hydrophobic polymer is ethylcellulose or Eudragit E. Calcium pectinate (CaP) and Eudragit E are the most highly preferred of the embodiments. The inner film consists of a salt of ethylenediaminetetraacetic acid (EDTA) in a water soluble polymer such as hydroxypropylcellulose (HPC) or polyvinylpovidone (PVP). The outer membrane controls the rate of water entry. The EDTA dissolves and then competes for the metal ion with the polysaccharide. The removal of the metal ion from the polysaccharide renders the polysaccharide soluble. Dissolution of the polysaccharide particles (more than 50% of the film) destroys the integrity of the outer film. Water reaches the capsule and/or the core totally resulting in dissolution and/or disintegration of the gelatin capsule or the core, thereby releasing the drug dose in its entirety.
[0072] According to specific embodiments the binder of the inner layer is selected from the group consisting of Povidone (PVP: polyvinyl pyrrolidone), polyvinyl alcohol, copolymer of PVP and polyvinyl acetate, HPC (hydroxypropyl cellulose) (more preferably a low molecular weight), HPMC (hydroxypropyl methylcellulose) (more preferably a low molecular weight), carboxy methyl cellulose (more preferably a low molecular weight), ethylcellulose, hydroxyethyl cellulose, gelatin, polyethylene oxide, acacia, dextrin, magnesium aluminum silicate, starch, polyacrylic acid, polyhydroxyethylmethacrylate (PHEMA), polymethacrylates and their copolymers, gum, water soluble gum, polysaccharide, hydroxypropylmethyl cellulose phthalate, polyvinyl acetate phthalate, cellulose acetate phthalate, hydroxypropylmethyl cellulose acetate succinate, poly(methacrylic acid, methyl methacrylate)1:1 and poly(methacrylic acid, ethyl acrylate)1:1, alginic acid, and sodium alginate, and any other pharmaceutically acceptable polymer that dissolves in buffer phosphate pH >5.5 and/or mixtures thereof.
[0073] According to specific embodiments of the present invention, the organic acid as the rupturing agent in the inner layer is selected from the group consisting of citric acid, fumaric acid, malic acid, ascorbic acid (Vitamin C), lactic acid, oxalic acid, maleic acid, malonic acid, glutaric acid, adipic acid, pimelic acid, suberic acid, azelaic acid, sebasic acid, tartaric acid, acetic acid, propionic acid, glycolic acid, pyruvic acid, oxalic acid, succinic acid, benzoic acid, cinnamic acid, mandelic acid, methanesulfonic acid, ethanesulfonic acid, p-toluenesulfonic acid, salicylic acid, palmatic acid, and the like, and amino acids selected from the group consisting of aspartic acid and glutamic acid, and any other pharmaceutically acceptable organic acids.
[0074] According to preferred embodiments of the present invention, the inner layer further may comprise a chelating agent as the rupturing agent. Preferably, the chelating agent is selected from the group consisting of antioxidants, dipotassium edentate, disodium edentate, edetate calcium disodium, edetic acid, fumaric acid, malic acid, maltol, sodium edentate, trisodium edentate, ethylene diamine tetra acetic acid (EDTA).
[0075] Optionally, the chelating agent may be integrated with the organic acid, in the inner layer. Thus the erosion of the outer layer may occur via chemical attacks of both of the outer layer's components, i.e. the hydrophobic water insoluble polymer film as well as the hydrophilic water insoluble particulates.
[0076] Optionally and preferably, the inner layer comprises a lubricant. More preferably, the lubricant is selected from the group consisting of stearate salts;
[0077] stearic acid, corola oil, glyceryl palmitostearate, hydrogenated vegetable oil, magnesium oxide, mineral oil, poloxamer, polyethylene glycole, polyvinyl alchol, sodium benzoate, talc, sodium stearyl fumarate, compritol (glycerol behenate), and sodium lauryl sulfate (SLS) or a combination thereof. Most preferably, the lubricant is talc.
[0078] According to some embodiments the outer coating is further coated with an enteric coating. Accordingly, The enteric coating is more preferably selected from the group consisting of hydroxypropylmethyl cellulose phthalate, polyvinyl acetate phthalate, cellulose acetate phthalate, hydroxypropylmethyl cellulose acetate succinate, poly(methacrylic acid, methyl methacrylate)1:1, poly(methacrylic acid, ethyl acrylate)1:1, alginic acid, and sodium alginate. The outer enteric coating may further comprise a plasticizer. The plasticizer preferably includes at least one of dibutyl sebacate, polyethylene glycol and polypropylene glycol, dibutyl phthalate, diethyl phthalate, triethyl citrate, tributyl citrate, acetylated monoglyceride, acetyl tributyl citrate, triacetin, dimethyl phthalate, benzyl benzoate, butyl and/or glycol esters of fatty acids, refined mineral oils, oleic acid, castor oil, corn oil, camphor, glycerol and sorbitol or a combination thereof.
[0079] According to another embodiment, a further water soluble inner neutral buffering layer coating separates between the inner coating and core. Such a layer may be free of any dissolution agent, and can be used in the case that the core includes acid-sensitive active material. Such a layer may be selected from the group consisting of Povidone (PVP: polyvinyl pyrrolidone), polyvinyl alcohol, copolymer of PVP and polyvinyl acetate, HPC (hydroxypropyl cellulose) (more preferably a low molecular weight), HPMC (hydroxypropyl methylcellulose) (more preferably a low molecular weight), carboxy methyl cellulose (more preferably a low molecular weight), ethylcellulose, hydroxyethyl cellulose, gelatin, polyethylene oxide, acacia, dextrin, magnesium aluminum silicate, starch, polyacrylic acid, polyhydroxyethylmethacrylate (PHEMA), polymethacrylates and their copolymers, gum, water soluble gum, polysaccharide, hydroxypropylmethyl cellulose phthalate, polyvinyl acetate phthalate, cellulose acetate phthalate, hydroxypropylmethyl cellulose acetate succinate, poly(methacrylic acid, methyl methacrylate)1:1 and poly(methacrylic acid, ethyl acrylate)1:1, alginic acid, and sodium alginate, and any other pharmaceutically acceptable polymer that dissolves in buffer phosphate pH >5.5 and/or mixtures thereof.
[0080] According to some embodiments, the core or capsule may comprise at least one of an absorption enhancer, a binder, a disintegrant, a hardness enhancing agent, and another excipient.
[0081] Accordingly, a delivery system is described that allows a drug, including a sensitive drug, to be formulated in its regular manner with excipients that are known to be compatible with said drug and to impart to the drug any desired improved properties such as stability or absorption enhancement, and allows that drug to be packed in a capsule, which capsule can be coated to allow precise delivery under precise time control. Thus, the drug delivery system of the invention provides a method for the oral delivery of a drug or other bioactive moiety to a patient in need of said agent wherever it is necessary in the gastrointestinal tract. The invention is useful for the precise release of the drug at the site of action to fight local diseases or at a preferred site of absorption to allow enhanced absorption of the pharmaceutical compound or reduced side effects.
[0082] List of drugs for which such a system may be useful:
[0083] Active agents that can be incorporated in delivery device of the present invention include any bioactive agent. Without limiting the scope of the present invention, suitable drugs include those drugs presented in current edition of Goodman and Gilman's "The Pharmacological Basis of Therapeutics" or the current edition of The Merck Index. Both volumes list drugs suitable for numerous types of therapeutic applications, including drugs in the following categories: drugs acting at synaptic and neuroeffector junctional sites, drugs acting on the central nervous system, drugs that influence inflammatory responses, drugs that affect the composition of body fluids, drugs affecting renal function and electrolyte metabolism, cardiovascular drugs, drugs affecting gastrointestinal function, drugs affecting uterine motility, chemotherapeutic agents for parasitic infections, chemotherapeutic agents for microbial diseases, antineoplastic agents, immunosuppressive agents, drugs affecting the blood and blood-forming organs, hormones and hormone antagonists, dermatological agents, heavy metal antagonists, vitamins and nutrients, vaccines, oligonucleotides and gene therapies.
[0084] The active agent that can be delivered by the novel device of this invention, includes inorganic and organic compounds without limitation, including drugs that act on the peripheral nerves, adrenergic receptors, cholinergic receptors, nervous system, skeletal muscles, cardiovascular system, smooth muscles, blood circulatory system, synaptic sites, neuroeffector junctional sites, endocrine and hormone systems, immunological system, reproductive system, skeletal systems, autocoid systems, alimentary and excretory systems, inhibitory and histamine systems, and those materials that act on the central nervous system such as hypnotics and sedatives.
[0085] Classes of active agents that can be used in the present invention include anti-hypertensives, immunosuppressants, anti-inflammatories, diuretics, anti-epileptics, cholesterol lowering drugs, hormonals hypoglycemics, antiviral drugs, nasal decongestants, antimicrobials, anti-arrthrytics, analgesics, anti-cancer drugs, anti-parasitics, proteins, peptides, CNS stimulants, CNS depressants, 5 HT inhibitors, anti-schizophrenics, anti-Alzheimer drugs, anti-psoriatics, steroidals, oligonucleotides, anti-ulcer drugs, proton pump inhibitors, anti-asthmatics, thrombolyitics and vitamins.
[0086] The present invention is particularly useful for the administration of polypeptides, including proteins, such as, but not limited to, therapeutical agents, nutritional products, steroids, hormones, growth hormone (GH), growth hormone releasing hormone (GHRH), epithelial growth factor, vascular endothelial growth and permeability factor (VEGPF), nerve growth factor, cytokines, interleukins, interferons, GMCSF, hormone-like products, neurological factor, neurotropic factor, neurotransmitter, neuromodulator, enzyme, antibody, peptide, proteic fragment, vaccine, adjuvant, an antigene, immune stimulating or inhibiting factor, heomatopoietic factor, anti-cancer product, anti-inflammatory agent, anti-parasitic compound, anti-microbial agent, cell proliferation inhibitor or activator, cell differentiating factor, blood coagulation factor, immunoglobulin, anti-angiogenic product, negative selective markers or "suicide" agent, toxic compound, anti-angiogenic agent, and the like, and structurally similar bioactive equivalents thereof.
[0087] Specific examples of peptide drugs include, but are not limited to, zestril, prinivil, zoladex, calcitonin, sandostatin, lupron, accolade, glucagen, integrilin and hirudin. These drugs have been indicated for hypertension, prostate hypertophy or cancer, osteoporosis, aromegally, asthma, hyopglacemia and anti-coagulation.
[0088] Any active agent may be used according to this invention by the person skilled in the art, for example the following agents may be used:
[0089] Abacavir, Abciximab, Acarbose, Acebutalol, Acenocourmarol, Acetazolamide, Acetocholine, Acetretin, Acetylcysteine, Acetylsalicylic acid, Acipimox, Acyclovir, Adapalene, Adefovir, Adnosine, Agalsidase alfa, Albendazole, Aldesleukin, Alefacept, Alemtuzumab, Alendronate, Alfacalcidol, Alfentanil, Alfuzosin, Aglucerase, Allopurinol, Alprazolam, Alprostadil, Aluminium Chlorhydrate, Alumin Hydrox, Amantadine, Amethocaine, Amifostine, Amiloride, Aminacrine, Aminophylline, Amino salycilic acid, Amiodarone, Amisulpride, Amitriptyline, Amlodipine Besylate, Amlodipine Maleate, Amoxycillin, Amphotericin B, Ampicillin, Amprenavir, Anagrelide Hcl, Anastrozole, Androgel, Antipyrine, Apomorphine Hcl, Apraclonidine, Aprenavir, Aprotinin, Ascorbic Acid, Aspirin, Atavaquone, Atenolol, Atorvastatin, Atosiban, Atracurium Besylate, Atropine sulphate, Auranofin, Aurothioglucose, Azathiaprine, Azelaic acid, Azelastine, Azithromycin, Aztreonam,
[0090] Bacitracin, Baclofen, Barium sulfate, Basiliximab, Becaplermin, Beclomathasone, Benazepril, Benoxinate Hcl, Benserazide, Benzalkonium Hcl, Benzanthine Penicilin G, Benzethonium chloride, Benzhexol Hcl, Benzocaine, Benzoic acid, Benzoxonium chlor, Benzoyl peroxide, Benzydamine Hcl, Benzyl Benzoate, Benzyl Penicillin sod, Benzyl peroxide, Betaine, Betahistine, Betamethasone, Betaxolol, Bevacizumab, Bezafibrate, Bicalutamide, Bifonazole, Bimatoprost, Biperiden Hcl, Bisacodyl, Bismuth Oxychloride, Bismuth subgalic, Bismuth subsalicylate, Bismuth subnitrate, Bisoprolol Fumurate, Bivalirudin, Bleomycin Sulph., Boric acid, Bortezomib, Bosentan, Botulinum Toxin, Bretylium Tosylate, Brimonidine Tart, Brinzolamide, Bromazepam, Bromohexine Hcl, Bromocriptine, Brotizolam, Buclizine Hcl, Budesonide, Bupivacaine, Buprenorphine, Bupropion, Buserelin, Buspirone Hcl, Butenafine Hcl, Busulfan, Butandiol, Cabergoline, Caffeine, Calamine, Calcipotriol, Calcitonin, Calcitriol, Calcium carbonate, Calcium Chlor, Calc. Folinate, Calcium Glubionate, Calcium Gluceptate, Calcium Heparin, Candesartan Cilexetil, Capecitabine, Capromab Pendetide, Capsaicin, Captopril, Carbachol, Carbamazepine, Carbamide, Carbaryl, Carbidopa, Carbocysteine, Carbon, Carbophos, Carboplatin, Carvedilol, Caspofungin, Cefaclor, Cefadroxil, Cefazolin, Cefepime Hcl, Cefixime, Cefonicid, Cefotaxime, Ceftazidime, Ceftibuten, Ceftriaxone, Cefuroxime, (as axetile), Cefuroxime Sod., Celecoxib, Cepalin, Cephalexin, Cephalothin, Cetalkonium Chlor, Cetirizine, Cetrimide, Cetrimonium Brom, Cetrorelix, Cetylpyridinium Chlor, Charcoal, Chenic acid, Chlorambucil, Chloramphenicol, Chlorbutol, Chlordiazepoxide, Chlorhexidine Gluc., Chlorimipramine Hcl, Chloroprocaine, Chlorquinadol, Chloroquine Phos. BP, Chloroxylenol, Chlorpheniramine Maleate, Chlorpromazine, Chlorpropamide, Chlorthalidone, Cholecalcferol, Cholestyramine, Choline Salicylate, Choriogonadotropin, Ciclopiroxolamine, Cilastatin, Cilazapril, Cimetidine, cinnarizine, Ciprofibrate, Ciprofloxacin, Cisapride, Cisplatin, Citric Acid, Citalopram, Cladribine, Clarithromycin, Clavulanic acid, Clidinium Brom., Clindamycin Hcl, Clindamycin Phos., Cliquinol, Clobazam, Clobetasol Propionate, Clobetasone, Clomiphene citrate, Clomipramine Hcl, Clonazepam, Clonidine Hcl, Clopidogrel, Clorazepate Dipotassium, Clostridium Botulinium, Clotiapine, Clotrimazole, Cloxacillin Sod. Clozapine Coal Tar, Codeine Phos., Coichicine, Colestipol Hcl, Colistimetate Sod., Colloidal Oatmeal, Copolymer-1, Cortisone Acetate, Cromolyn Sod., Crotamiton, Cyanocobalamin, Cyclophosphamide, Cycloserine, Cyclosporine, Cyproterone, Cystosine Arabinoside, Cytarabine.
[0091] D-Trp-LHRH, Dacarbazine, Daclizumab, Dalfopristin, Danazol, Dantrolene Sod., Dapsone, Daptomycin, Darbepoetin Alfa, Daunorubicine, Demethyl Chlortetracycline, Deferoxamine Mesylate, Desflurane, Desipramine Hcl, Desloratadine, Desmopressin, Desogestrel, Desonide, Desoximetasone, Dexachlorpheniramine, Dexamethasone, Dexmedetornidine, Dexpanthenol, Dexrazoxane, Dextran, Dextromethorphan Hbr, Diacerein, Diazepam, Dibenzepin, Diclofenac Diethylamine, Diclofenac Sod., Diclofenac Potassium, Dicyclomine Hcl, Didanosine, Diflucortolone, Digoxin, Dihydroergotoxine, Diltiazem, Dimenhydrinate, Dimercaprol BP, Dimethicone, Dimethyl Ether, Dimetindenum, Dinoprostone, Dinoprost Tromethamine, Diphenhydramine Hcl, Dipivefrin, Dipyridamole, Dipyrone, Disodium Clodronate, Disopyramide Phos., Dithranol, Dobutamine Hcl, Docetaxel, Docosanol, Domperidone, Donepezil, Dopamine, Domase Alpha, Dorzolamide Hcl, Doxazosine, Doxepin, Doxorubicin, Doxycycline, Doxylamine Succinate, Dronabinol, Drospirenone, Drotrecogin Alfa, Dudasteride, Dydrogesterone, Dyphylline, Econazole Nitr., Efavirenz, Eletriptan Hydrobrom. Emedastine, Enalapril Maleate, Enflurane, Enfuvirtide, Enoxaparin, Entacapone, Ephedrine, Epinephrine, Epirubicin Hcl, Epoeitin Beta, Epoprostenol, Eptifibatide, Ergotamine Tart, Ertapenem, Erythromycin, Erythropoietin, Escitalopram, Esdepallethrin, Esmolol Hcl, Esomeprazole, Estradiol, Estramustine, Estriol, Etanercept, Etambutol, Ethanolamine Oleate, Ethinylestradiol, Ethyl Chloride, Etidronate Disodium, Etodolac, Etomidate, Etoposide VP, Estoricoxib, Eugenol, Exemestane,
[0092] Famciclovir, Famotidine, Felodipine, Fentanyl, Ferric (III) Polymaltose Complex, Ferric (III) Sucrose Complex, Ferrous Calc. Citr, Ferrous Fumarate, Ferrous Gluconate, Ferrous Sulph, Fexofenadine Hcl, Finasteride, Flecainide Acet., Flucinamide, Fluconazole, Fludarabine Phos., Flumazenil, Flumethasone, Flunitrazepam, Fluocinolone, Fluocortolone, Fluorometholone, Fluorouracil, Fluoxetine Hcl, Flupenthixol, Fluphenazine, Flutamide, Fluticasone Prop, Fluvastatin Sod, Fluvoxamine Maleate, Folic acid, Follitropin, Fomepizole, Formoterol Fumarate, Fosamprenavir, Foscarnet Trisodium, Fosfomycin, Fotemustine, Furosemide, Fusidic acid, Gabapentin, Gadobenic acid, Gadodiamide, Gadolimium, Galantamine, Ganciclovir, Ganirelix, Gefitinib, Gemcitabine, Gentamicin, Gestodene, Glibenclamide, Glimepiride, Glipizide, Glucagon, Glycerine, Glycerophosphate, Gonaderalin, Goserelin, Gradoteric acid, Gramicidin, Granisetron, Griseofulvin, Guaiphenesin, Haloperidol, Halothane, Heparin, Hexamine Hipp, Human Chorionic Gonadotrophin (HCG), Human Post Menopausal Gonadotrophin, Hyaluronidase, Hydrochlorothiazide, Hydrocortisone, Hydrogen Perox, Hydromorphone, Hydroquinone, Hydroxychloroquine Sulph., Hydroxyethyl Starch, Hydroxyprogesterone, Hydroxypropylmethyl Cellulose, Hydroxyzine Hcl, Hydrogen Perox, Hylan,
[0093] Ibuprofen, lchthyol, Idarubicin, Idoxuridine, Ifosfamide, lloprost, Imatinib, Imipenem, Imipramine Hcl, Imiquimod, Indapamide, Indinavir, Indocyanine Green, Indomethacin, Infliximab, Inocor Lactate, Interferon, Interferon Beta, lobitridol, lodine, lodihanol, lohexol, lomeprol, lopamidol, lopromide, loversol, loxitalamate, Ipratropium Brom., Irbesartan, Irinotecan Hcl Trihyd., Iron, Iron (as Ferucarbotran), Isoconazole Nitrate, Isoniazide, Isoflurane, Isopropanolol, Isoproternol Hcl, Isosorbide Dinitrate, Isosorbide Mononitrate, Isothipendyl, Isotretinoin, Itraconazole,
[0094] Kaolin, Ketamine Hcl, Ketoconazole, Ketoprofen, Ketorolac Tromethamine, Ketotifen,
[0095] L-Asparginase, L-Camitine, Labetalol Hcl, Lactic acid, Lactitol Monohydrate, Lactulose, Lamivudine, Lamotrigine, Lanreotide, Lansoprazole, Latanoprost, Leflunomide, Lenograstin, Lercanidipine Hcl, Letrozole, Leuprolide Acetate, Leucovorin Calcium, Levamisole, Levobunolol Hcl, Levocobastine, Levodopa, Levofloxacin, Levomepromazine, Levonorgestrel, Lidocaine Hcl, Lignocain Hcl, Linezolid, Lindane, Lisinopril, Lithium Carbonate, Lodoxamide Tromethamine, Lomefloxacin Hcl, Loperamide, Lopinavir, Loratadine, Lorazepam, Lornoxicam, Losartan, Potass.,
[0096] Mag. Salts, Malathion, Maprotiline Hcl, Mebendazole, Mebeverine Hcl, Mebhydrolin, Mechlorethamine Hcl, Medroxyprogesterone Acetate, Mefloquine, Meglumine, Melissa, Melphalan, Mematine Hcl, Menotrophin, Mepivacaine, Meprobamate, Mepyramine Maleate, Mercaptopurine, Meropenem, Mesna, Methoxsalen, Metolazone, Mestrolone, Metformin, Methadone, methimazole, Methoexitol, Methotrexate, Methsuximide, Methyldopa, Methylergometrine Maleate, Methylphenidate Hcl, Methylprednisolone, Methylsalicylate, Metoclopramide, Metopimazine, Metoprolol Tart, Metronidazole, Mezlocillin, Mianserin Hcl, Miconazole, Midazolam, Midodrine, Mifepristone, Miglustat, Milnacipran, Milrinone, Miltefosine, Minocycline Hcl, Minoxidil, Mirtazapine, Misoprostol, Mitomycin, Mitoxantrone Hcl, Mizolastine, Moclobemide, Modafinil, Moexipril, Mometazone Furate, Montelukast Sod., Morphine Hcl., Morphine Sulph, Morpholin Salicyl, Moxifloxacin, Mupirocin, Muromonab CD3, Mycophenolate Mofetil, Mycophenolic,
[0097] Nabumetone, N-Acetylcysteine, Nadroparin, Nafarelin (as Acetate), Naftifine, Nalbuphine Hcl, Naloxone, Naltrexone, Naphazoline, Naproxen, Naratriptan Hcl, Nedocromil Sod., Nefopam, Nelfinavir, Neoepinephrine Bitart., Neomycin Sulph., Neostigmine, Nesiritide, Nevirapine, Niclosamide, Nicotine, Nicotinic Acid, Nicoumalone, Nifedipine, Nimesulide, Nimodipine, Nitrazepam, Nitrofurantoin, Nitrofurazone, Nitroglycerine, Nonoxynol 9, Norelgestromin, Norepinephrine, Norethisterone Acet., Norfloxacin, Norgestimate, Norgestrel, Nortryptyline Hcl, Nystatin,
[0098] Ocreotide, Ofloxacin,Olanzapine, Olmesartan, Olsalazine Sod., Omeprazole, Ondansetron, Opipramol, Orlistat, Orphenadrine, Oseltamivir, Oxandrolone, Oxazepam, Oxcarbazepine, Oxerutin, Oxolamine Citr., Oxomemazine, Oxybutynin, Oxycodon Hcl, Oxycodone Terephthalate, Oxymetazoline Hcl, Oxytetracycline, Oxytocin
[0099] Paclitaxel, Palivizumab, Pamidronate, Pancreatin, Pancrelipase, Pancuronium Brom, Panthenol, Pantoprazole, Papaverine, Paracetamol, Paradichlorobenzene, Paromomycin, Paroxetine, Peginterferon Alfa-2A, Pemetrexed, Pemoline, Penfluridol, Penicillin, Pentazocine, Pentoxifylline, Peppermint oil, Pepsin, Pergolide Mesylate, Permethrin, Perphenazine, Pethidine Hcl, Phenazone, Phenazopyridine, Pheniramine Maleate, Phenobarbital Sod., Phenobarbitone, Phenolphthalein, Phenothrin, Phenoxybenzamine Hcl, Phenoxymethylpenicillin, Phentermine, Phentolamin Methansulphonic, Phenylephrine, Phenylpropanolamine, Phenyltoloxamine, Phenytoin Sod., Phospholipid, Phytomenadione, Pilocarpine, Pimacrolimus, Pimozide, Pindolol, piperacillin Sod., Piperonyl Butoxide, Piroxicam, Podophyllotoxin, Polidocanol, Polifeprosan, Polymyxin Sulph., Polystyrene Sulphonate, Polyvidone, Polyvinyl, Porfimer Sod., Potassium Chlor, Potassium Citr., Potassium Gluconate, Potassium Guaiacolsulphonate Cod-Guaiacol, Povidone Iodine, Pramoxine Hcl, Pravastatin Sod., Praziquantel, Prazosin Hcl., Prednisolone, Prednisone, Premethrin, Prilocaine, Primidone, Pristinamycine, Procaine Hcl, Procyclidine, Progesterone, Proguanil, Promethazine, Propafenone Hcl, Propericiazine, Propofol, Propoxyphene Hcl, Propranolol, Propylthioracil, Protamine Sulf., Protirelin Thyroid, Pseudo-ephedrine, Psyllium Hydrophyl Mucilloid, Pyrantel Pamoate, Pyrethrin, Pyridostigmine, Pyrilamine Maleate, Pyrimethamine, Pyrithion Zinc, Quetiapine (as fumarate), Quinagolide Hcl, Quinidine, Quinupristin, Raloxifene, Ramipril, Ranitidine, Reboxetine, Remifentanil Hd, Repaglinide, Ribavirin, Rifabutin, Rifampicin, Riluzole, Rimantadine, Risedronate Sod., Risperidone, Ritodrine, Ritonavir, Rituximab, Rivastigmine Hydrogen Tart, Rizatriptan, Ropinirole, Ropivacaine, Roruronium Brom., Rosiglitazone, Rosuvastatin, Roxithromycin, Rutin,
[0100] Salbutamol, Salmeterol, Salmon Calcitonin (Synthet.), Salicylic acid, Saquinavir Mesylate, Scopolamine Hcl, Selegiline, Selenium, Senna, Sertraline Hcl, Sevelamer Hcl, Sevoflurane, Sibutramine, Sildenafil, Silver Sulfadiazine, Simethicone, Simvastatin, Sirolimus, Sod. Bicarb., Sod. Biphos., Sod. Cellular Phos., Sod. Chloride, Sod. CIT., Sod. Cromoglycate, Sod. Fluoride, Sod. Fluoroscein, Sod. Fusidate, Sod. Hyluronate, Sod. Nitroprusside, Sod. Phos., Sod. Polystyrene Sulph., Sod. Stibogluconate, Sod. Sulfacetamide, Sod. Valproate, Somatotrophin, Sotalol, Spiramycine, Spironolactone, Stavudine, Streptokinase, Streptozocin, Succinyl-Choline Chlor, Sucralfate, Sulbactam, Sulfacetamide, Sulfadoxine, Sulfisoxazole, Sulphamethoxazole, Sulphasalazine, Sulpiride, Sulthiame, Sumatriptan, Tacalcitol Monohydrate, Tacrolimus, Tadalafil, Tamioxifen, Tamsulosin Hcl, Tartaric Acid, Tazarotene, Tazobactam, Tegaserod, Teicoplanin, Temolozamide, Temoporfin, Tenofovir Disoprovil Fumarate, Terazosin, Terbinafine, Terbutaline Sulph., Teriparatide, Testosterone, Testosterone Enanthate, Testosterone Prop., Testosterone Undecanoate, Tetracaine Hcl, Tetracosactide, Tetracycline Hcl., Tetrahydrazoline, Thalidomide, Theophylline Anhyd., Theophylline Sod. Glyc., Thioguanine, Thiopental Sod., Thioridazine, Thymol, Thyrotropin, Thyrotropin Alpha, Thyroxine, Tiapride, Tibolone, Ticarcillin Sod., Ticlopidine Hcl., Timolol Maleate, Tinidazole, Tirofiban Hcl Monohydrate, Tobramycin, Tolbutamide, Tolnaftate, Tolterodine Tartrate, Topiramate, Topotecan Hcl., Tacrolimus (as Monohydrate), Tramadol Hcl.,Tranexamic Acd., Trastuzumab, Travaprost, Trazarotene, Trazodone, Treprostinil, Tretinoin (See Vit. A), Triamcinolone, Triazolam, Tribenoside, Triclofos Sod., Triclosan, Trihexyphenidyl, Trimethoprim, Trimipramine, Triprolidine, Triptoreline, Trisod. Cit, Trolamine, Tromantadine Hcl, Tropicamide, Troxerutin, Tubocurarine, Tyrothricin,
[0101] Undecylenate, Urea Hydrogen Peroxide, Urofollitropin, Urokinase, Ursodeoxycholic acid,
[0102] Valaciclovir, Valerian, Valganciclovir, Valproic acid, Valrubigin, Valsartan, Vancomycin Hcl, Vardenafil, Vecuronium, Venlafaxine, Verapamil, Verteporfin, Vigabatrin, Vinblastine Sulph., Vincristine, Vinorelbine, Vitamin A, Vitamin B, Vitamin B6, Vitamin B12, Vitamin C, Vitamin D, Vitamin E, Voriconazole,
[0103] Warfarin
[0104] Xylomethazoline Hcl,
[0105] Yohimbine,
[0106] Zalcitabine, Zidovudine, Zinc Oxide, Zinc Sulph, Ziprazidone Hcl, Zoledronic Acid, Zolmitriptan, Zolpidem, Zopiclone, Zuclopenthixol Dihyd.
[0107] The invention will be particularly useful for the delivery of peptide and/or protein drugs. These drugs have very exacting requirements for their formulation in the solid state and could clearly benefit from targeted delivery in the gastrointestinal tract. A most preferred site for their delivery would be the lower GI tract including the colon where the activity of proteases is an order of magnitude lower than in the small intestine, or sites in the distal small intestine where peptide carriers are known to operate. These drugs are also difficult to formulate into tablets because protein molecules may lose their biological activity upon a conformational change that may take place when subjecting the materials to pressure in a tablet press. Formulation in capsules is preferred. Furthermore, protein drugs need special formulation requirements to keep them active in solution and in the stored solid phase.
[0108] Any excipients added to the formulation to affect drug delivery will potentially be a source of incompatibility or instability. The advantage of this invention for said formulations is in the ability to use proven formulations for the drug with no interaction with the components of the delivery system. Protein and peptide drugs for which this invention could be useful include insulin, growth hormone (GH), growth hormone releasing hormone (GHRH), calcitonin, epithelial growth factor, vascular endothelial growth and permeability factor (VEGPF), nerve growth factor, cytokines, interleukins, interferons, GMCSF, hormone-like products, neurological factor, neurotropic factor, neurotransmitter, neuromodulator, enzyme, antibody, peptide, proteic fragment, vaccines, immune stimulating or inhibiting factor, heomatopoietic factor, anti-cancer product, anti-inflammatory agent, anti-parasitic compound, anti-microbial agent, cell proliferation inhibitor or activator, cell differentiating factor, blood coagulation factor, immunoglobulin and others hormones and recombinant protein drugs. The present invention will be also appropriate for delivery of drugs possessing poor bioavailability, specially those whose low bioavailability is caused by extensive first-pass metabolism occurring in the small intestine. Such molecules may be metabolized in intestinal lumen by cytochrome P450 isoenzyme type CYP3A4 or by any other types of cytochrome P450 isoenzymes, existing in a high concentration mainly in the upper GI tract, prior to absorption. Using the delivery system (method and formulation) according to the present invention, dosage form can overtake jejunum and small intestinal, where isoenzyme CYP3A4 can be found in a high concentration, thus releasing the drug in the lower GI tract, where the concentration of CYP3A4 is relatively poor. In this way the effect of the first-pass metabolism (pre-systemic metabolism) of the drug can be decreased and thus drug bioavailability can be improved.
[0109] Examples of drugs which are substrates for CYP3A: Alprazolam, Amiodarone, Amitriptyline, Astemizole, Atrovastatin, Budesonide, Bupropion, Buspirone, Caffeine, Carbamazepime, Cerivastatin, Cisapride, Claritromycin, Clomipramin, Clonazepam, Codeine, Cyclosporine, Dexametazone, Dextrometorphan, DHEA, Diazepam, Diltiazem, Disopiramide, Donepezil, Doxycicline, Erytromycin, Estradiol, Ethylestradiol, Felodipine, Fluoxetine, Imipramine, Lanzoprazole, Lidocaine, Loratidine, Lovastatin, Midazolam, Nefazodone, Nicardipine, Nifedipine, Nizoldipine, Norethindrone, Omeprazole, Ondansetron, Orphenadrine, Paroxetine, Progesterone, Pro[afenone, Quethiapine, Quinidine, Rifampin, Sertraline, Sibutramine, Sildenafil, Simvastatin, Tacrolimus, Tamoxifen, Terfenadine, Testosterone, Theophyline, Trazodone, Triazolam, Venlafaxine, Verapamyl, Vinblastine, (R)-Warfarin, Zolpidem.
BRIEF DESCRIPTION OF FIGURES
[0110] FIG. 1 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Diclofenac tablets with an inner layer containing HPC and no citric acid and an outer layer containing Eudragit E/CaP;
[0111] FIG. 2 is a graphical representation of percentage release rate as a function of time for 4 different concentrations of coated Diclofenac tablets with an inner layer containing HPC/citric acid/talc and an outer layer containing Eudragit E/CaP;
[0112] FIG. 3 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Diclofenac tablets with an inner layer containing HPC/citric acid/talc and an outer layer containing Eudragit E/CaP, wherein the ratios of the components of said outer layer are different from that shown in FIG. 2.;
[0113] FIG. 4 is a graphical representation of percentage release rate as a function of time for 4 different concentrations of coated Diclofenac tablets with an inner layer containing HPC/EDTA/taIc and an outer layer containing Eudragit E/CaP;
[0114] FIG. 5 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Diclofenac tablets with an inner layer containing HPC/EDTA 4Na/talc and an outer layer containing Eudragit E/CaP;
[0115] FIG. 6 is a graphical representation of percentage release rate as a-function of time for 4 different concentrations of coated Tramadol tablets with no inner layer and an outer layer containing Eudragit E/CaP;
[0116] FIG. 7 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Tramadol tablets with an inner layer containing HPC/EDTA and an outer layer containing Eudragit E/CaP;
[0117] FIG. 8 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Tramadol tablets with an inner layer containing HPMC/EDTANPEG 400 and an outer layer containing Eudragit E/CaP;
[0118] FIG. 9 is a graphical representation of percentage release rate as a function of time for 4 different concentrations of coated Tramadol tablets with an inner layer containing HPMC/Citric Acid/talc/PEG 400 and an outer layer containing Eudragit E/CaP;
[0119] FIG. 10 is a graphical representation of percentage release rate as a function of time for 2 different concentrations of coated Tramadol tablets with different weight of inner layer ratio of HPC/Citric Acid/talc/Aerosil and an outer layer containing Eudragit E/CaP;
[0120] FIG. 11 is a graphical representation of percentage release rate as a function of time for 2 different concentrations of coated Tramadol tablets with different weight of inner layer ratio of HPC/Citric Acid/talclAerosil and an outer layer containing Eudragit E/CaP;
[0121] FIG. 12 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Tramadol tablets with an inner layer containing HPC/Citric AciditalclAerosil and an outer layer containing Eudragit E/CaP;
[0122] FIG. 13 is a graphical representation of percentage release rate as a function of time for 4 different concentrations of coated Pyridostigmine capsules with no inner layer and an outer layer containing Eudragit E/CaP;
[0123] FIG. 14 is a graphical representation of percentage release rate as a function of time for coated Pyridostigmine capsules with an inner layer containing HPC/Citric AciditalclAerosil and an outer layer containing Eudragit E/CaP;
[0124] FIG. 15 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Pyridostigmine capsules with an inner layer containing HPC/Citric Acid/Aerosil and an outer layer containing Eudragit E/CaP;
[0125] FIG. 16 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Pyridostigmine capsules with an inner layer containing HPCICitric Acid/Aerosil and an outer layer containing Eudragit E/CaP, with a different ratio of the components of the outer layer than that shown in FIG. 15.
[0126] FIG. 17 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Pyridostigmine capsules with an inner layer containing HPC/Citric Acid/Aerosil and an outer layer containing Eudragit E/CaP. As will be noted, the inner layer is thinner than that shown in FIG. 16.
[0127] FIG. 18 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Pyridostigmine capsules with an inner layer containing HPCICitric AcidlAerosil and an outer layer containing Eudragit EICaP . As will be noted the inner layer is thicker than that shown in FIG. 16.
[0128] FIG. 19 is a graphical representation of percentage release rate as a function of time for 3 different concentrations of coated Pyridostigmine capsules with an inner layer containing HPC/Citric Acid/Aerosil and an outer layer containing Eudragit E/CaP, wherein the components of the outer layer are of a different ratio than that shown in FIGS. 16-18.
[0129] FIG. 20 A is a graphical representation of correlation between lag time and the weight ratio of outer layer to citric acid included into the inner layer.
[0130] FIG. 20 B is a graphical representation of correlation between lag time and the weight ratio of outer layer to inner layer.
[0131] FIG. 20 C is a graphical representation of correlation between the weight ratio of outer layer to citric acid included into the inner layer and burst time (the time takes to 80% of release).
[0132] FIG. 20 D is a graphical representation of correlation between the weight ratio of outer layer to inner layer and burst time (the time takes to 80% of release).
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
[0133] Definitions
[0134] In the description that follows the following terms are used in order to describe the specification and claims. The following definitions are provided in order to provide clarity to the discussion. Where not specifically indicated all other terms are used in their normal or art-recognized meanings.
[0135] The term "delivery device" or "delivery system" is intended to mean a preparation that is designed to deliver a desired agent such as a drug. The preparation can be a simple or complex combination of chemicals, drugs (one or more) or excipients. The delivery can be controlled such that the site or time of drug release is preset by the parameters of the coating layers. Such control can be by chemical or physical means. In this invention "delivery system" and "delivery device" are used interchangeably.
[0136] The term "drug" is intended to mean any pharmaceutical or physiological agent, composition, bioactive compound or combination thereof, that is useful in the cure or prevention of any disease, or for any other medical purpose.
[0137] The term "particulate" is intended to mean a composition composed of separate particles. In this invention the particles are embedded into a film surrounding the core or capsule. The particles serve as channels for the entry of water into the system. The particles may swell but remain in all cases as separate particles. They do not coalesce into a gel or film in themselves.
[0138] In the context of this invention the terms, "coating", "film coating", "membrane", and "layer" are used interchangeably to denote an integral layer of a material that is coated upon another surface. The layer may be formed of one or more materials, several of which may be present as a molecular distribution one in other, while others may be separate, as particles embedded therein.
[0139] The term "water-insoluble" means that the material is relatively not susceptible to dissolution in water or aqueous solutions. The term "water-soluble" means that the material is relatively susceptible to dissolution in water or aqueous solutions. The term "hydrophobic" when applied to a coating means that the film is relatively impermeable to the passage of water or aqueous solutions while the term "hydrophilic" when applied to coatings or to particulates means that the material is relatively permeable to the passage of water or aqueous solutions.
[0140] The term "embedded" or "embed" means a firm fixation of the material within a coating or layer.
[0141] The term "channel" is intended to mean that through which something may flow. The channels in this invention can be filled by the material of the particulates, however, they allow the flow of water and aqueous solutions.
[0142] The term "rupturing agent" is intended to mean any pharmaceutically acceptable component added into the inner layer that, by further penetration of water, can attack the outer layer in order to disrupt its integrity and eventually, to cause it to burst.
[0143] The term "chelating agent" denotes a component added into the inner layer to compete for a metal ion of an ion cross-linked polysaccharide or a component that modifies cellulose when used as the hydrophilic insoluble particulate in the outer layer. The term "core" is intended to mean a solid dosage form that contains the active material inside andlor outside, and that may be prepared by a granulation, tabletation, or microencapsulation process. Examples of such a dosage form are; granules, microspheres, microparticles, microcapsules, microbeads, beads, pellets, tablets, and caplets.
[0144] The term "capsule" is intended to mean a solid dosage form that is filled by the active material with or without other pharmaceutically acceptable excipients. Examples of "capsule" can be hard gelatin capsules, soft gelatin capsules, starch-based capsules, HPC-based capsules and HPMC-based capsules.
[0145] The invention is directed to a delivery system for:1. the targeted delivery of a pharmaceutical to a particular location in the gastrointestinal tract; 2. time controlled delivery, as the release can be designed to take place after a predetermined time post administration. The delivery system comprises a core containing a pharmaceutical in any desirable formulation that is fitting for said pharmaceutical. The core or capsule, which can be a gelatin capsule, is such that when it would be exposed to aqueous solutions it dissolves and or disintegrates totally within a short period of time. The purpose of this invention is to allow the targeted delivery of agents that are formulated in the core or capsule in a manner in which the drug formulation need not be changed at all. The control of the site of the exposition of the core or capsule to the environment, is afforded, by coatings placed on the outside of the core or capsule, such that the contents of the core or capsule are not affected in any way. In order to achieve the control of time or site of release, the core or capsule is coated with at least two coatings. The outer coating is the layer that controls the time of exposure of the capsule to the aqueous environment by controlling the rate of water entry into the delivery device. Beneath the outer coating the core or capsule is coated with an inner coating that is relatively easily dissolvable in water and contains the agent that will compromise the integrity of the outer coating. Any convenient solid dosage form is useable in this invention including but not limited to granules, microspheres, microparticles, microcapsules, microbeads, beads, pellets, tablets, caplets, hard gelatin capsules, soft gelatin capsules, starch-based capsules and HPC-based capsules and HPMC-based capsules.
[0146] The outer coating is one that controls the entry of water into the inner coating and contains, as one of its essential features, a major component that is insoluble in water but that can be readily dissolved upon release of the agent in the inner coat.
[0147] In one embodiment of the current invention the outer coating that controls the entry of water, is a film of a water insoluble polymer, embedded with water insoluble but hydrophilic particles. Such a coating is described in U.S Pat. No. 5,840,332 as a coating for tablets or capsules. Said a coating offers many parameters for controlling drug delivery as described in that patent. The identity, weight percent, particle size of the particles, and the identity of the hydrophobic polymer, as well as the coating thickness, are all parameters that control the entry of water through such a coating. We have found that certain embodiments of that coating can be used for this invention. The water insoluble polymer can be any hydrophobic polymer that is insoluble at neutral physiologic pH. Examples of such polymers are ethylcellulose, Eudragit E, Eudragit RL and RS and Eudragit NE. In the case of Eudragit E, the polymer may be the component that is dissolved by the agent in the inner coating since Eudragit E can be rendered soluble by a change in pH to an acidic value. In the case of the other polymers, the polymer serves the function of limiting the entry of water to the system to the channels formed by the particulates while said hydrophilic non water soluble particles will serve the double function of allowing controlled entry of water while also serving as the site for the destructive dissolution of the outer film, allowing the exposure of the core or gelatin capsule to the environment. The particulate compounds may be any of several metal salts of a polysaccharide such as calcium pectinate or calcium alginate.
[0148] In one preferred embodiment the outer layer will comprise ethylcellulose embedded with particles of calcium pectinate. The weight percent of the particles may be from 10 to 90, preferably 30-70, while their particle size may range from 10 microns to 500 microns, more preferably 80-250 microns.
[0149] In another preferred embodiment, the outer layer will comprise ethylcellulose embedded with particles of calcium alginate. The weight percent of the particles may be from 10 to 90, more preferably 30-70, while their particle size may range from 10 microns to 500 microns, more preferably 80-250 microns.
[0150] In another preferred embodiment, the outer layer will comprise Eudragit E embedded with particles of calcium pectinate. The weight percent of the particles may be from 10 to 90, more preferably 30-70, while their particle size may range from 10 microns to 500 microns, more preferably 80-250 microns.
[0151] In one preferred embodiment, the outer layer will comprise Eudragit E embedded with particles of micro crystalline cellulose. The weight percent of the particles may be from 10 to 90, more preferably 30-70, while their particle size may range from 10 microns to 500 microns, more preferably 80-250 microns.
[0152] The inner coating is a layer that is found beneath the outer layer but above the core or capsule. It is applied to the capsule first. One may optionally apply an undercoat of an inert water soluble film to the core or capsule before applying the inner coating. Materials suitable for such an inert undercoat are hydroxypropylcellulose or similar polymers. The inner layer contains an agent, which when dissolved by water that has entered through the outer coat, will compromise the integrity of the outer coat. The identity of this agent depends on the identity of the components in the outer coat. For example, an agent that changes the pH of the environment outside the capsule is suitable for the dissolution of films that are based of Eudragit E or other acid soluble films. The embodiments of the outer coat that contain Eudragit E, whether they contain calcium pectinate, alginate or micro crystalline cellulose as the particulate that forms the channels for water entry, can use an inner film of a water soluble polymer such as hydroxypropylcellulose (HPC), polyvinylpovidone (PVP), hydroxypropylmethylcellulose (HPMC), hydroxyethylcellulose (HEC), and carboxymethylcellulose (CMC) which contains citric acid, tartaric acid, or other suitable non volatile organic acids in a solid solution. The weight percent of organic acid dispersed in the inner film can range from 10% to 90%, while the weight percent of water soluble polymer can range from 2% to 40%. In. one preferred embodiment of the inner coat one has 75% of citric acid dissolved or dispersed in an inner coating layer of 32 mg/cm.sup.2 containing 4% of hydroxypropylcellulose.
[0153] An alternate embodiment of the inner coating, is one in which the inner coating contains an agent that reacts with a major component of the outer membrane rendering it readily soluble in water. Examples of such agents are sequestering agents or chelating agents that can remove the metal from an insoluble metal salt, rendering the anionic part of that salt soluble. In a preferred embodiment, the sequestering agent may be ethylenediaminetetraacetic acid (EDTA) salts such as the tetra sodium salt, the disodium salt or the disodium calcium salt or salts of oxalic acid. These agents react with, for example, the calcium in calcium pectinate particles, leaving behind small particles of pectin or with the calcium in calcium alginate particle leaving behind alginic acid. Both pectin and alginic acid are readily soluble at the physiological pH's of 6.5-8. Since the outer film comprises a very large percentage of the particulate matter (10% to 90%), the total dissolution of the calcium pectinate as pectin totally compromises the integrity of the film, which in essence disintegrates. The inner film has already dissolved, thereby leaving the core or gelatin capsule exposed to the aqueous environment. The entire drug load is thus released readily.
[0154] In a preferred embodiment, the inner coating layer contains from 10% to 90% of disodium EDTA. A most preferred embodiment contains about 80% disodium EDTA in an inner coating layer of about 20 hydroxypropylcellulose of about mg/cm.sup.2.
[0155] An optional enteric coating overlaying the outer membrane may be applied. The enteric coat will protect against the adverse effects of the acid pH in the stomach. For certain embodiments the enteric coat may be necessary to prevent premature drug release caused by interactions of components of the outer coat with the acid of the stomach. Any enteric coating material known in the art may be used for the enteric coat. Eudragit L is the most preferred enteric coating.
[0156] While the invention will now be described in connection with certain preferred embodiments in the following examples so that aspects thereof may be more fully understood and appreciated, it is not intended to limit the invention to these particular embodiments. On the contrary, it is intended to cover all alternatives, modifications and equivalents as may be included within the scope of the invention as defined by the appended claims. Thus, the following examples which include preferred embodiments will serve to illustrate the practice of this invention, it being understood that the particulars shown are by way of example and for purposes of illustrative discussion of preferred embodiments of the present invention only and are presented in the cause of providing what is believed to be the most useful and readily understood description of formulation procedures as well as of the principles and conceptual aspects of the invention.
EXAMPLES
1. Delivery System According to the Present Invention Performed on a Non-Disintegrating core
Materials
[0157] The following materials were used for preparing the different formulations;
[0158] Calcium pectinate powder containing 4% calcium (CaP, Lot-Nr.-2091889, food grade Genu-Copenhagen Pectin-Denmark);
[0159] Micro-crystalline cellulose (Emcocel 90M, Lot-Nr.-9s6073, BP grade, Mendel-Finland);
[0160] Micro crystalline cellulose (Avicel PH 102, Lot-Nr.-7806C, NF grade, FMC);
[0161] Ethylcellulose (EC-N7 NF, Lot-Nr.-KI 10013T02, USP grade, Dow-USA);
[0162] Lactose (Lot-Nr.-829333, BP grade, Borculo Whey Products);
[0163] Starch (Lot-Nr604022, NF grade, Colorcon-USA);
[0164] Polyvinylpyrolidone (PVP 90F, Lot-Nr.806936, USP grade, BASF-Germany);
[0165] Cross polyvinylpyrolidone (CPVP, Lot-Nr.-130766, NF grade, BASF-Germany);
[0166] Mg stearate (Lot-Nr.-E#672, USP grade,);
[0167] Eudragit E 100 (Eud.E, Lot-Nr.8360801021, Rohm Pharma-Germany);
[0168] Hydroxypropyl methyl cellulose (HPMC, Methocel E5, 2910/5, Lot-Nr.-LNJ408, USP grade, Dow-USA);
[0169] Hydroxypropyl cellulose (HPC EF, Lot-Nr.6237, NF grade, Aqualon,-Netherlands);
[0170] Ethylenediamine tetraacetic acid disodium (2Na EDTA, Lot-Nr.-39073411, Fluka);
[0171] Citric acid (Lot-Nr.-K9107234, USP grade, Merck-Germany);
[0172] Cilicone dioxide (Aerosil, Lot-Nr. R24551326, NF grade, Merck-Germany); and
[0173] Talc (Lot-Nr.-K2431170, USP grade, Merck-Germany).
[0174] The following materials were used as the model active materials:
[0175] Sodium diclofenac (Lot-Nr.-24611, BP grade, Secifarma-Italia); and
[0176] Tramadol hydrochloride (HCI) (Lot-Nr.-J136, USP grade, Protocchemic-Switzerland).
[0177] Ethyl alcohol was USP grade.
Methods
[0178] In this series of experiments, sodium diclofenac and tramadol were used as a representative model for active material. The formulations and the characters of the tablets containing either sodium diclofenac or tramadol are summarized in Table 1.
Preparation of Sodium Diclofenaccontaining core
[0179] Wet granulation process was used to prepare the cores. The granulation was performed manually for both sodium-diclofenac as well as CaP using a mortar and pestle. The granulation of sodium-diclofenac was carried out as follows: 0.9 g of ethylcellulose (EC 7) was dissolved in 15 ml of ethanol. 45 g of sodium-diclofenac and 2.25 g of CPVP were placed in the mortar and the solution of the EC 7 was added slowly. The mixture was well mixed and dried at 40.degree. C. for 16 hours.
[0180] The granulation of the starch/lactose was carried out as follows: 1 g of PVP K90F was dissolved in 10.0 g of water. 70 g of lactose was mixed with 30.0 g of starch. The PVP solution was added slowly. The mixture was well mixed and dried at 95.degree. C. for 16 hours.
[0181] The granules (of both active material as well as starch/lactose) and other components (table 1) were transferred to a polyethylene bag and mixed for 20 minutes. 0.6 g of magnesium stearate was added and the blend mixed for another 2-3 minutes. Biconvex cores of 7 mm diameter were compressed automatically using a Wick Ges.mbh single punch tablet press. The weights of cores ranged between 205 to 209 mg. The hardness of the cores was tested using a Vanderkamp VK200 Hardness Tester and it ranged from between 9.3 to 12.0 KP.
Preoaration of Tramadol HCI-Containing Cores
[0182] Wet granulation process was used for preparation of the tramadol granules. Ethanolic solution of ethylcellulose (2 g EC7/25.0 ml ethanol) was slowly added to the tramadol (100 9) and CPVP (5.0 9), and the granulation was performed manually using a mortar and pestle. The resultant granules were dried in an oven at 35.degree. C. for about 16 hours.
[0183] Tramadol HCI containing tablets were prepared by dry mixing of tramadol granules with other components (table 1) except Mg stearate, in a plastic polyethylene bag for 20 minutes. Mg stearate (0.6 g) was added to the blend and the mixing was continued for additional 2 minutes.
[0184] Biconvex cores with a diameter of 6 mm were pressed automatically in a Wick Ges.mbh single punch tablet press. The average weight of the cores was 101.6 mg. The hardness of the cores was tested using a Vanderkamp VK200 Tester and the average was calculated to be 5.8 KP. TABLE-US-00001 TABLE 1 Formulation used for Na diclofenac and tramadol HCl containing cores Na-diclofenac - % Tramadol - % % in % in % in % in Raw material granulate formulation granulate formulation Granulate Form. 412-27, 42 Form. 438- 61412-111 A M 92.3 10.2 93.5 46.8 CPVP 5.8 0.6 4.6 2.3 EC 7 1.8 0.2 1.9 0.9 Granulate lactos 68 (412-20, 31, 34) Lactos 69 46.9 Starch 30 20.4 PVP K90 F 1 0.7 Active Material (AM) 11.0 50.0 Avicel PH102 -- 34.5 Emcocel 90M 15 -- CPVP -- 10 PVP 5 5 Mg Stearate 1 0.5 Tablets Form. 412-41, 45 412-95, 114 Hardness, kp 9.3-12 5.8-6.5 Diameter, mm 7 6 Total Weight, mg 205-209 101-105
General Coating Process:
[0185] The coating suspension was stirred vigorously throughout the coating process to prevent the deposition of particles. The coating process was performed on 100 g core tablets. The coating system consisted of a perforated pan coater, a peristaltic pump (Masterflex, Digital Console Drive, Cole-Palmer Instrument Company) and the spraying nozzle. The spraying nozzle was composed of a "Y" connector PE tube fixed on one end to the air supplying system and the other end to the coating suspension through the peristaltic pump and a stainless steel tip of 1.2 mm fixed at the head of the "Y" connector tube. The spraying nozzle was adjusted to aim at the falling cores in the upper part of the pan and a fine jet was sprayed on continuously at a pressure of 0.4-0.5 bar. The spray rate was adjusted to 3 ml/min. The coating pan was rotated at 18 rpm to provide continuous flow of the tablets. The air flow rate through the coater chamber was regulated in the range of 2.75-2.85 m/s which was kept constant throughout the coating process. At the end of the process the coated tablets were discharged and spread out on a sieve and finally dried for 16 hours at temperature 35.degree. C. in a drying oven.
Inner Film Coat Containing Hydroxylpropyl Cellulose (HPC) on Na-Diclofenac Cores:
[0186] Coating suspension: HPC (Kluce1 EF) (table 2) was dissolved in Ethanol (100 ml) while continuous stirring occurred at 500 rpm.
[0187] Citric acid-containing coating: 12.0 g of Citric acid was added and after complete dissolution of citric acid, 4.0 g talc was added with continuous stirring at 500 rpm.
[0188] Ethylenediamine tetraacetic acid disodium (EDTA-2Na)-containing coating: 48.0 g EDTA-2Na was milled to particle size <1 50u and dispersed in Klucel EF solution with continuous stirring at 500 rpm.
[0189] The coating process was carried out using a perforated pan coater where a Drum "D", Coater and a Dize-Schlick model 930/3, 0.8mm 20939 were assembled. The coating was performed at 22-25-C. Speed of rotation (21-32 rpm) was changed according to the change of flowability and rolling of tablets.
[0190] The spray rate of the suspension was 3.5-4.5 ml/min, according the wetness and adhesiveness of the tablets. The spraying was stopped when the tablets were stuck together and renewed after separation. The air pressure was 0.8 bar.
Inner Film Coat Containing HPC on Tramadol HCI Cores:
[0191] Coating suspension: 4.0 g HPC (Kiucel EF) dissolved in 100 ml Ethanol while continuously stirring at 700 rpm.
[0192] Citric acid-containing coating: 12.0 g of Citric acid was added and after complete dissolution of citric acid, 2.0 g Talc and 2.0 g Aerosil were dispersed while continuously stirring at 700 rpm. For a thicker coating, a double amount of suspension was used.
[0193] EDTA-2Na-containing coating: 48.0 g EDTA Na.sub.2 was milled to particle size <150u and dispersed in HPC EF solution with continuous stirring at 700 rpm. General coating process of the inner layer containing HPC: Coating was performed at temperature 21-23.degree. C. and the pan rotation was 40 rpm.
Inner Film Coat Containing Hydroxvpropyl Methyl Cellulose (HPMC) on Tramadol HCI Cores:
[0194] Citric acid-containing coating: 10.0 g Methocel E5 and 1.0 g PEG-400 were dissolved in a mixture of 38 g distilled water and 131 g Ethanol, 10.Og Citric acid were dissolved in the Methocel solution, 5.0 g talc was added with continuous stirring at 700 rpm.
[0195] EDTA Na.sub.2 coating: 10.5 g Methocel E5 and 1.1 g PEG400 were dissolved in a mixture of 160 g distilled water and 40 g ethanol, 42.0 g EDTA Na.sub.2 (particle<150u) was dispersed in the Methocel solution with continuous stirring at 700 rpm.
[0196] General Coating process of the inner layer containing HPMC: the coating process was performed at temperature 35-45.degree. C. and the pan rotation was 35-40 rpm.
Coating Process of the Outer Film Coat:
[0197] Preparation of the coating suspension: CaP powder underwent fractionation using a sieve shaker (ari j. Levy, Laboratory Equipment LTD) and a sieve of 149.mu. (ASTM 100, 8" diameter) in order to obtain only the fractions of <149.mu. particle size. The coating suspension was prepared by dissolving 27.0 g Eudragit E in 163 g ethanol and 63.0 g (ratio3:7) or 27.0 g (ratiol:1) of fractionated CaP was added while stirring (700 rpm.) to the solution.
[0198] Coating process: The spray rate was adjusted to 3 ml/min and the tablet temperature was kept at 24.degree. C.-26.degree. C.
Drug Release Assessments
[0199] Dissolution studies were performed in intestinal fluid TS (phosphate buffer pH 7.5 without enzymes) using a Vankel 7000 dissolution tester. One tablet was placed in 900 ml intestinal fluid TS and stirred by paddle at 50 RPM. The solutions were kept at 37.degree. C. by a Vankel VK650A heater/circulator. Samples of 3 ml were taken using a Vankel VK8000 Autosampler, at intervals of 30-60 minutes up to suspected 80% active material release time, followed by intervals of 2 hours up to suspected 100% release time. The actual determinations of the release of the drugs (dissolution results) from the tablets were carried out using a HP 8452A Diode-Array Spectrophotometer. The drugs released were quantified using a calibration curve obtained from the standard solution, in intestinal solution TS, in the concentration range of 0-80 ppm for tramadol HCI and 0-50 ppm for Na-diclofenac.
Results and Discussion
[0200] The results of the dissolution test of both coated and uncoated sodium diclofenac tablets are shown in the table 2. TABLE-US-00002 TABLE 2 Coated tablets containing Diclofenac Sodium: composition and release profiles. Outer coat Inner Coat Coating Time of # Coating type Coating weight Coating type weight Lag time % release % release release Form. and ratio (%) mg mg/cm.sup.2 and ratio (%) (mg) (hours) after 1 h after 2 h 80% (hours) I HPC EF 50 4 2 Eudragit E 30 14 2 8 19 9 Talc 50 CaP 70 26 3 3-4 8 >10 42 4 1-2 5-8 >10 II HPC EF 20 16 9 Eudragit E 30 28 -- 64-75 90-92 1.5 Citric acid 60 CaP 70 55 2 59-78 63-89 1 Talc 20 73 2.5 48-77 87-89 1 87 3 56-16 76-36 5, >5 III HPC EF 20 14 8 Eudragit E 30 11 -- 19-89 95-99 0.5-1 Citric acid 60 CaP 70 24 -- 3-4 5-6 10, >10 Talc 20 31 -- 3 3-4 >12 IV HPC EF 12.9 20 11 Eudragit E 30 17 0.5-1 8-17 25-70 3-11 EDTA-2Na 80.6 CaP 70 30 1.5 10-67 23-82 1.5-10 Talc 20 53 3 15-57 43-70 3.5, >9.sup. V HPC EF 13.3 7 4 Eudragit E 30 19 1-1.5 9-13 25-28 7 EDTA-4Na 50.0 CaP 70 34 2.5 5-7 17-9 9-10 Talc 16.7 49 4.5 6 13 >10
[0201] As it is shown, a lag time of 2.5 and 3 hours can be obtained upon using a thickness of 70 and 90 mg of the outer coating film respectively (see formulation II in table 2 and FIG. 2). The mechanism of the release is based on the fact that citric acid is dissolved, upon the penetration of the water into the inner film coat, to form an acidic pH environment under the outer film coat in which Eudragit E in the outer film coat can be subsequently dissolved. Conversely, the tablets containing no citric acid in the inner layer (see formulation I in table 2 and FIG. 1) resulted in a typical sustained release continuing for over ten hours. This fact indicates that the outer film keeps its integrity where no organic acid exists in the inner layer, thus a typical sustained release could be resulted. Table 2 also shows the results of the release of diclofenac where the inner layer contains EDTA, either di-sodium or tetra-sodium salt. As it is shown this access may also result in a delayed burst release even though the burst is less sharp, as compared to the tablets coated with citric acid-containing inner coat. This fact implies that, again, a disintegrity of the outer coat can take place owing to the reaction occurring between EDTA of the inner layer and CaP existing in the outer coat. This fact results in dissolution of CaP from the outer coat and thus eventually pores that are subsequently formed enable the fast release of the active material. FIGS. 1-5 show the release profiles of formulations I-V.
[0202] Table 3 summarizes the results of both lag time as well as the release profile of tramadol from disintegrating-immediate release core coated with either outer coat alone or both inner and outer coat. The results show again that the inner coat containing citric acid is involved in the destruction of the outer coat and consequently results in a burst release. The tablets without the inner layer demonstrated again a typical sustained release where the lag time was affected by the weight of the outer coat. The release profile of tramadol from coated tablets without inner layer, is shown in FIG. 6. FIGS. 10 and 11, show the release profile of coated tablets with different weights of inner coating layer (Formulations X-A and X-B) accompanied with low (FIG. 10) and high weight (FIG. 11) of outer coat.
[0203] The effect of 2Na-EDTA on the burst release, appeared to be dominant as compared to the tablets containing no inner layer, although it was found to be less significant than citric acid. The effect of 2Na-EDTA is produced by the lowering of the pH and consequently causing the destruction of the outer film coat. FIG. 7 shows the effect of the presence of 2Na-EDTA in the inner coat on the release profile of tramadol for different weights of the outer coat.
[0204] The effect of the thickness (the film coat weight) of the inner film coat, and thus the amount of the citric acid has also been assessed. For this purpose the tramadol containing cores were coated with increasing weights of the inner layer while maintaining a constant weight ratio of HPC to citric acid. The cores with inner layer. weights of the 14 mg and 28 mg were tested. The coated cores were then coated with the outer coating film. The results show that the thicker the inner film coat the faster the release of tramadol, indicating faster and/or better destruction of the outer film coat. The release profile of these tablets is shown in FIG. 10 (X-A and X-B) for different weights of the inner coat.
[0205] The effect of the weight fraction of CaP particles imbedded into the outer film coat is shown in FIGS. 10 (X-B) and 12 for the weight ratios of Eud.E/CaP of 3/7 and 1/1 respectively, where a higher weight of the inner coat (26 mg) was used. The data is summarized in Table 3. TABLE-US-00003 TABLE 3 Coated tablets containing Tramadol: composition and release profiles. Outer Coat Inner Coat Coating Release Time of # Coating type Coatig weight Coating type weight Lag time after % Release release Form. and ratio(%) mg mg/cm.sup.2 and ratio(%) (mg) (h) 1 h (%) after 2 h 80%(h) VI Eud.E 30 21 0.5 20 47 4 CaP 70 32 1 10-16 35-38 4.5 39 1.5 12-17 46-47 5.5 50 2 10-11 30-34 5 VII HPC_EF 20 25 19 Eud.E 30 23 0.5-1 5-82 76-92 2 EDTA_2Na 80 CaP 70 32 1 16-55 80-92 2 45 2 10-62 58-82 2-4 VIII HPMC 20 20 16 Eud.E 30 44 2 17-26 41-58 4-5 EDTA_2Na 78 CaP 70 62 2 10 30 5 PEG400 2 83 2.5 1-3 5-6 8 IX HPMC 38.5 26 20 Eud.E 30 26 -- 58-100 94-100 1-1.5 CitricAcid 38.5 CaP 70 36 1 28-58 88 2 Talc 19.2 44 1.5 14-36 46-66 3.5-5.5 PEG400 3.8 57 2 13-24 30-55 6 X-A HPC_EF 20 14 11 Eud.E 30 36 0.5 12-20 36-56 4-5 CitricAcid 60 CaP 70 44 1-2 4-7 5-26 4-5 X-B Talc 10 28 21 Eud.E 30 42 0.5 50-51 96-98 1.5 Aerosil 10 CaP 70 50 1 30-39 70-87 2-3 XI 26 20 EudrE 50 39 2.5-3 82-98 100 1 CaP 50 48 4-5 20-39 20-71 3 58 7 N.A. 43-45 4
[0206] It will be noted that the weight ratio of Eud.E/CaP is important since it can effectively control the lag time. This fact is based on our previous findings (patent TCDS) showing that the lower the weight fraction of the particles in the film coat, the longer the lag time and the slower the release of the active material. As one can see (Table 3) the outer coating with the weight ratio of Eud.E/CaP of 1/1 resulted in a longer lag time as compared to the weight ratio of 3/7, where the same weights of both inner and outer coat were used. Despite the effect on the lag time no effect of the weight ratio of the CaP particles on the release profile was seen.
[0207] In another study, hydroxypropyl methyl cellulose (HPMC) was used as a binder in the inner layer formulation containing either citric acid or 2Na-EDTA. The results are demonstrated in FIGS. 8 and 9 for citric acid and EDTA respectively. As one can see, no significant difference between HPC (FIGS. 11, 7 ) and HPMC (FIGS. 8 and 9) can be found in both lag time and release profile. This finding relates to the high solubility of HPMC used for this purpose which is as high as that of HPC.
Conclusion
[0208] The examples show that the drug delivery system according to the present invention can be used as a timed controlled delivery system, which can be directed to the targeted delivery of an active material to a particular location in the gastrointestinal tract. The delivery system comprises either a non-disintegrating or disintegrating core containing the active material with optionally other excipients. The core is first coated with an inner layer which comprises at least on rupturing agent and a water soluble binder. The core is further coated with an outer layer, comprising hydrophilic water insoluble particulates embedded in a relatively hydrophobic substantially water insoluble polymeric matrix. Accordingly, the outer layer is responsible for controlling the entry of water into the inner coat and can thus adjust the lag time. Furthermore, through the penetration of water through the outer layer, the inner layer is dissolved and thus can chemically disrupt the integrity of the outer layer. The agents which can be used for this purpose are either a pH lowering agent, dissolving the polymeric matrix of the outer layer, or a chelating agent that reacts with water insoluble particulates in the outer layer rendering them readily soluble in water. The failure of the outer layer then affords total delivery of the drug load at the predetermined site or time.
[0209] Accordingly, the nature of the rupturing agent in the inner coating will be determined by the nature of the outer coating. Delay of drug release from dosage form (lag time) can be controlled by varying the parameters of the outer film coat, such as the thickness and the weight ratio of the particulates. In addition, the lag time can be controlled by the thickness of the inner coating layer, and thus the amount of the rupturing agent in it, as well.
[0210] In this manner, the drug is therefore delivered to the desired site without any need to be reformulated with excipients of the delivery system. Furthermore, the drug load and its formulation can be kept totally separate from the components of the delivery system, for example where a gelatin capsule is used.
2.: Delivery System According to the Present Invention Performed on a Hard Gelatin Capsule
[0211] In the following series of examples, pyridostigmine was used as a model for the active material. The following study and experiments have been performed on hard gelatin capsules, filled with pyridostigmine granulated with other excipients. The capsule may include additional excipients imparting to the drug any desired improved properties such as stability or absorption enhancement. Other excipients which may be included inside the capsule can be a flow regulation agent, filler, lubricant, disintegrant, solubilizer, suspending agents, dispersing agents, surfactant, and others.
Materials
Granulate Formulation:
Active Ingredient:
[0212] Pyridostigmine Bromide (Lot-Nr 98105/23,USP grade, Orga.Synthetic Industries)
Excipients:
[0213] *Filler: Calcium Hydrogen phosphate. Dihydrate (Lot-Nr 92500, BP grade, Riedel de Haen)
[0214] *Binder: Sorbitol (Lot-Nr 2870870 Sigma) *Disintegrante: Crosspovidone (CPVP, Lot-Nr 130766, USP grade, BASF Germany)
Inner layer
[0215] *Polymer: Hydroxypropyl cellulose (HPC EF, Lot-Nr. 6237, NF grade, Aqualon Netherlands)
[0216] *PH-lowering agent: Citric acid anhydrous (Lot-Nr. K91 072347, USP grade, Merk-Germany)
[0217] *Glidants: -Silicone dioxide (Aerosil, Lot-Nr. R24551326, NF grade, Merk-Germany) Talc (Lot-Nr. K2431170, USP grade, Merk Germany)
[0218] *Ethyl alcohol was USP grade
Outer Film Coat:
[0219] *Eudragit E100 (EudE, Lot-Nr. 8360801021,Rohm Pharma-Germany)
[0220] *Calcium Pectinate powder containing 4% Calcium (CaP, Lot-Nr. 2091889, food grade Genu-Copenhagen Pectin-Denmark)
Methods
Preoaration of Pyridostigmine Granulate
[0221] Wet granulation process was used to prepare the pyridostigmine granules.
[0222] The granulation solution of Pyridostigmine was carried out as follows: 4 g (2%) Pyridostigmine was dissolved in 16 g purified water. 152 g (76%) Calcium Hydrogen phospho. Dehydrate, 14 g (7%) Crosspovidone and 30 g (15%) Sorbitol were mixed for 5 mn in a plastic polyethylene bag. This mixture was transferred to a mortar and pestle and the solution of Pyridostigmine was added slowly. This wet granulate was well mixed and oven dried at 65.degree. C. for 16 hours. After oven drying, the resulting dry granulate was milled manually using a mortar and pestle. The milled dry granulate was sieved through a 420.mu. sieve.
Filling Active Capsule
[0223] The capsules were filled with dry milled granulate manually by using filling system Hanin Technical Supply LTD Capsule loader 100 capsules size 4 (CH100-4) Feton International. S.A.
Coating Process
Coating System
[0224] The coating suspension was kept stirred vigorously using a magnetic stirrer (Heidolph MR 3001) throughout the coating process to prevent the deposition of particles. The coating system consisted of a perforated pan coater, a peristaltic pump Masterflex, Digital Console Drive, Cole-Palmer Instrument Company) and the spraying nozzle. The perforated pan coater was a Drum "E" coater. The spraying nozzle used for coating the inner layer was a Dize-Schlick model 930/3, 0.8 mm 20939. The spraying nozzle used for coating outer layer was composed of a "Y" connector PE tube fixed on one end to the air supplying system and the other to the coating suspension through the peristaltic pump and a stainless steel tip of 1.2 mm fixed at the head of the "Y" connector tube. The spraying nozzle was aimed at the falling capsules in the upper part of the pan and a fine jet of coating suspension was sprayed on continuously.
Preparation of Inner Layer Coating
[0225] In this study the inner coating layer was composed of citric acid as the pH lowering agent, and low molecular weight Hydroxypropyl cellulose EF (HPC) as water soluble binder. After water penetration into the inner film coat citric acid forms an acidic pH environment under the outer film coat, leading to dissolution of the pH dependant polymer of outer film (Eudragit E100) and thus burst of the coating.
[0226] Preoaration of the Inner layer Suspension Inner layer without Binder: 24 g Citric acid anhydrous was dissolved in 150 g Ethanol using a magnetic stirrer (500-rpm). After complete dissolution 4 g Talc and 4 g Aerosil were added with continuous stirring at 500 rpm.
Inner layer Containing Binder (HPC.EF):
[0227] 1.4 g HPC.EF was dissolved in 120 g Ethanol and 30 g water, and 26.2 g Citric acid anhydrous was dissolved in HPC.EF solution using a magnetic stirrer (500-rpm). After complete dissolution 3.7 g Talc and 3.7 g Aerosil were added with continuous stirring at 500 rpm.
Inner Layer Coat Containing Binder (HPC.EF) but not Talc:
[0228] 2.8 g HPC.EF was dissolved in 240 g Ethanol and 60 g water, and 52.4 g Citric acid anhydrous was dissolved in HPC.EF solution using a magnetic stirrer (500-rpm). After complete dissolution 14.8 g Aerosil were added with continuous stirring at 500 rpm
Coating Conditions-Inner layer:
[0229] Perforated Coater Drum: "E"
[0230] Inlet air (.degree. C): 32-38
[0231] Outlet air (.degree. C): 24-30
[0232] Product temperature (.degree. C.): 30
[0233] Pan rotation speed (rpm): 20
[0234] Suspension flow rate (ml/min): 2.5-3
[0235] Spray air pressure (bar): 0.5
[0236] At the end of the process the coated capsules were discharged and spread out on a sieve and finally dried 16 hours at temperature 35.degree. C. in a drying oven.
Outer laver
[0237] The outer layer film was formed from a relatively hydrophobic polymer with pH dependent solubility (Eudragit E100, Eud.E) in which was embedded non-soluble but hydrophilic particles (Calcium Pectinate, CaP). The outer coating layer delays the drug release by controlling of water penetration into the inner acid-including layer. The lag time of coating burst and subsequently drug release was adjusted by controlling both the thickness of the outer film coat as well as the weight ratio of the polymer and CaP particles in the film coat. The rate of active material release depends also on the weight ratio between the outer film coat and the citric acid.
Preparation of Outer Film Coat
Coating Suspension Preoaration
[0238] Calcium Pectinate powder underwent fractionation using a sieve shaker (Ari J. Levy, Laboratory Equipment LTD) and a sieve of 149.mu. (ASTM 100, "8" diameter) in order to obtain only the fractions of <149.mu. particle size. The coating suspension was prepared by dissolving Eudragit E 100 in ethanol and dispersing Calcium Pectinate in the obtained solution while stirring (700 rpm). Coating suspensions with different weight ratios of Eudragit E to CaP were checked in these studies:
[0239] Ratio 3:7: 27 g Eudragit E was dissolved in 163 g ethanol and 63 g fractionated CaP was added.
[0240] Ratio 7:3: 569 Eudragit E was dissolved in 340 g ethanol and 24 g fractionated CaP was added.
[0241] Ratio 1:1: 56 g Eudragit E was dissolved in 340 g ethanol and 56 g fractionated CaP was added.
[0242] Ratio 1:1: 39.6 g Eudragit E was dissolved in 240 g ethanol and 39.6 g fractionated CaP was added.
[0243] The coating suspension was kept stirred vigorously using a magnetic stirrer (Heidolph MR 3001) throughout the coating for homogenous particles distribution in the suspension.
Coating Conditions-Outer Layer:
[0244] Perforated Coater Drum: "D"
[0245] Inlet air (* C): 26-40
[0246] Outlet air (.degree. C.): 22-30
[0247] Product temperature (.degree. C.): 25-33
[0248] Pan rotation (rpm): 20
[0249] Suspension flow rate (ml/min): 3.34
[0250] Spray air pressure (bar): 0.4
[0251] At the end of the process the coated capsules were discharged and spread out on a sieve and finally dried 16 hours at temperature 35.degree. C. in a drying oven
Dissolution Test
[0252] Dissolution studies were performed in intestinal fluid TS (phosphate Buffer pH 7.5 without enzymes) using a Vankel 7000 dissolution tester. One capsule was placed into a spring in 500 ml intestinal fluid TS and stirred by paddle at 50 RPM. The solutions were kept at 37.degree. C. by a Vankel VK650A heater/circulator. Samples of 3 ml were taken using a Vankel VK8000 Autosampler , at intervals of 30-60 min up to suspected 80% active material release time. The actual determinations of the release of the drugs (dissolution results) from the capsules were carried out using a HP 8452A Diode-Array Spectrophotometer. The drugs released were quantified using a calibration curve obtained from the standard solution, in intestinal solution TS in the concentration range of 0-50 ppm for Pyridostigmine bromide.
Citrc Acid Content Analysis
[0253] The amount of citric acid per capsule was checked in the various batches, according to the BP 1998 assay (p. 350) which was modified to suit the required analysis. In short, 10 precoated capsules were dissolved in 100 ml water. The solution was titrated with 0.1 M NaOH VS solution, using phenolphthalein as indicator. A solution of 10 uncoated capsules was titrated in the same manner. The amount of citric acid per capsule was calculated according to the BP assay:Citric acid amount per capsule (cf. table 1)=(NaOH volume.sub.coated solution-NaOH volume.sub.uncoated soluton)*6.403/10=precoated solution NaOH volume-uncoated solution NaOH volume/10.times.6.403 Results and Discussion
[0254] The release profile of Pyridostigmine from coated capsules without inner film coat and with inner film coat, containing citric acid, are respectively shown in table 4. TABLE-US-00004 TABLE 4 Coated capsules containing Pyridostigminel: composition and release profiles. Outer Coat Inner Coat Coating Release Time of # Coating type Coatig weight Coating type weight Lag time after % Release release Form. and ratio(%) mg mg/cm.sup.2 and ratio(%) (mg) (h) 1 h (%) after 2 h 80%(h) XII Eud.E 30 30 1.5-1 35-30 67 3.5-3 CaP 70 34 2 36-30 52 5-3.5 40 3-2 40-75 70-100 1.5-2.5 44 3 40 68-88 2-2.5 XIII HPC 4 36 16 Eud.E 50 75 6-7 45-57 75-95 1.5-2.5 Citric Acid 75 CaP 50 Aerosil 10.5 Talc 10.5 XIV HPC 4 60 27 Eud.E 30 36 2-1.5 38-7 86-27 6-1.5 Citric Acid 75 CaP 70 69 6-5 99-24 99-84 2-1 Aerosil 21 84 14-7 5-4 98-50 4-2 XV HPC 4 60 27 Eud.E 50 42 1-1.5 85-100 100 0.5 Citric Acid 75 CaP 50 90 4.5-4 96-72 100 1.5-0.5 Aerosil 21 110 8 * 20-31 4-5 XVI HPC 4 51 22 Eud.E 50 70 4-4.5 60-74 80-100 1.5-3 Citric Acid 75 CaP 50 77 7-6 11-9 48-36 4-3 Aerosil 21 85 10 * 97-85 2-1 XVII HPC 4 72 32 Eud.E 50 61 2 93 100 1 Citric Acid 75 CaP 50 75 3 100 100 0.5 Aerosil 21 97 3.5 100 100 0.5 XVIII HPC 4 71 31 Eud.E 30 88 2.5 68 68-85 2.5 Citric Acid 75 CaP 70 111 4-3.5 73-79 100 1 Aerosil 21 * Release was checked only after 2 hours.
[0255] The results show again that the inner coat containing citric acid is involved in the destruction of the outer coat and consequently results in a burst release.
[0256] The outer coat should provide protection such that the capsules remain closed for a predetermined period of time (for a desired lag time) and then release the active ingredient in a "burst" manner. Two formulations of outer coating were checked: [0257] -Eudragit-E/Ca Pectinate ratio: 7:3 [0258] -Eudragit-E/Ca Pectinate ratio: 1:1
[0259] As one can see the formulations XV, XVII, XVIII (with Eudragit-E/Ca Pectinate ratio: 1:1), resulted in the fastest release after the burst of the outer coating took place. The lag time could be controlled by adjusting the outer coating weight. As one could expect the thicker the outer coat, the longer the lag time that may be obtained. On the other hand when the inner layer is thicker, the lag time is shorter for the same outer coat weight (see formulation XVII as compared to XVI). See FIGS. 13-19, for all formulations related to pyridostigmine coated capsules.
[0260] Furthermore, in attempt to determine the weight ratios of the outer coat/inner layer and outer coat/citric acid, required for the desired dissolution, correlation curves were established. Linear correlation curves were drawn between 1. lag time and either weight ratio of outer coat to the inner layer or the weight ratio of outer layer to citric acid included into the inner layer, 2. either weight ratio of outer coat to the inner layer or the weight ratio of outer layer to citric acid included into the inner layer and burst time and burst time (the time takes to 80% of release).
[0261] Accordingly, one can find from the linear fit equations, that in order to reach, for example the lag time of 3.5-4.5 hours and a burst time of 0.5-1.5 hours, the weight ratio of outer coat/inner coat should be 1.0-1.3 and the weight ratio of outer coat/citric acid should be 1.4-1.7 (see FIG. 20).
[0262] It will be evident to those skilled in the art that the invention is not limited to the details of the foregoing illustrative examples and that the present invention may be embodied in other specific forms without departing from the essential attributes thereof, and it is therefore desired that the present embodiments and examples be considered in all respects as illustrative and not restrictive, reference being made to the appended claims, rather than to the foregoing description, and all changes which come within the meaning and range of equivalency of the claims are therefore intended to be embraced therein.
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stats Patent Info
Application #
US 20060280795 A1
Publish Date
12/14/2006
Document #
File Date
07/24/2014
USPTO Class
Other USPTO Classes
International Class
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-6,187,916,129,272,134,000 | %0 Journal Article %A Amara, Chandra Sekhar %A Ambati, Chandrashekar R %A Vantaku, Venkatrao %A Piyarathna, Danthasinghe Waduge Badrajee %A Donepudi, Sri Ramya %A Ravi, Shiva Shankar %A Arnold, James M %A Putluri, Vasanta %A Chatta, Gurkamal %A Guru, Khurshid A. %A Badr, Hoda %A Terris, Martha K %A Bollag, Roni J %A Sreekumar, Arun %A Apolo, Andrea B. %A Putluri, Nagireddy %T Serum metabolic profiling identified a distinct metabolic signature in Bladder Cancer Smokers: A key metabolic enzymes associated with patient survival %D 2019 %R 10.1158/1055-9965.EPI-18-0936 %J Cancer Epidemiology Biomarkers & Prevention %P cebp.0936.2018 %X Background: The current system to predict the outcome of smokers with Bladder cancer (BLCA) is insufficient due to complex genomic and transcriptomic heterogeneities. This study aims to identify serum metabolite associated genes related to survival in this population. Methods: We performed liquid chromatography-mass spectrometry (LC-MS) based targeted metabolomic analysis for >300 metabolites in serum obtained from two independent cohorts of BLCA never smokers, smokers, healthy smokers, and healthy never smokers. A subset of differential metabolites was validated using Biocrates absoluteIDQ p180 kit. Genes associated with differential metabolites were integrated with a publicly available cohort of TCGA to obtain an intersecting signature specific for BLCA smokers. Results: 40 metabolites (FDR <0.25) were identified to be differential between BLCA never smokers and smokers. Increased abundance of amino acids (tyrosine, phenylalanine, proline, serine, valine, isoleucine, glycine, asparagine) and taurine were observed in BLCA smokers. Integration of differential metabolomic gene signature and transcriptomics data from TCGA cohort revealed an intersection of 17 genes that showed significant correlation with patient survival in BLCA smokers. Importantly, Catechol-O-Methyltransferase (COMT), Iodotyrosine Deiodinase (IYD), and Tubulin Tyrosine Ligase (TTL) showed a significant association with patient survival in publicly available BLCA smokers datasets and did not have any clinical association in never smokers. Conclusions: Serum metabolic profiling of BLCA smokers revealed dysregulated amino acid metabolism. It provides a distinct gene signature that shows a prognostic value in predicting BLCA smoker survival. Impact: Serum metabolic signature derived genes act as a predictive tool for studying the BLCA progression in smokers. %U https://cebp.aacrjournals.org/content/cebp/early/2019/01/12/1055-9965.EPI-18-0936.full.pdf | {
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3,694,643,008,264,877,000 | Dissociative Identity Disorder: Everything You Need To Know About DID
Dissociative Identity Disorder: Everything You Need To Know About DID
Crucial facts on DID
Due to a lack of adequate research on dissociative identity disorder, conclusive statistics are not readily available. However, available studies confirm the following facts regarding DID:
• According to NAMI (National Alliance on Mental Illness),research indicates that approximately 2% of the global population meet the full criteria for dissociative disorders.
• Around 75% of individuals have at least one episode of depersonalization/derealization experience during their lifetime.
• Women tend to be diagnosed more with a dissociative disorder than men.
• Around 7% of the population may experience DID, but they are left undiagnosed.
• Studieshave found that DID can occur at any age, even during childhood.
• About 99% of people with dissociative disorders have experienced recurring abuse, traumas or life-threatening experiences during childhood.
• Dissociative identity disorder and substance abuse are directly related and drug abuse may adversely affect treatment. In fact,around 17.2% of an inpatient group receiving substance abuse treatment were diagnosed with DID.
• Misdiagnosis of DID is common as the symptoms of this mental illness are similar to other mental disorders.
• Patients with DID can have an average number of alters ranging from 2 to 10. However, the maximum recorded alters in one person was 100.
• The alters or alternate identities usually do not merge spontaneously.
• If left untreated, DID can lead to further abuse in the patient.
• Tendencies for self-harm and suicidal behavior are common among sufferers of DID. Over 70% of patients with DID have attempted suicide.
Do you know someone who is suicidal? Read How To Help A Person Who Is Feeling Suicidal
How DID can affect a person
Dissociative identity disorder can significantly change how an individual lives their lives. Here are some of the common ways how this psychological process affects a person:
1. Depersonalization
The sufferer feels a recurring sensation of being outside their body. Similar to an out-of-body experience, they have a sense of getting detached from their own physical body.
2. Derealization
The person gets a strong feeling that their surroundings or even the world around them is not real. They believe that whatever is happening with them or around them is fake or imaginary.
3. Dissociative amnesia
The person experiences a deficit in memory or memory loss, which is not a result of a medical condition or injury. This is not similar to general forgetfulness.
4. Dissociative fugue
It is a certain episode of amnesia or memory loss. The person is unable to remember specific events or personal information for a period of time. They can also experience micro-amnesias and forget about a discussion or parts of a conversation immediately afterwards. They may also detach from certain emotions.
5. Identity alteration/identity confusion
The person is generally confused about their own selves and their identity. They may suddenly become confused about their interests, career goals, sexual orientation and perceptions about politics, religion and society. They may also be confused about a particular situation, location and may even experience time distortions.
6. Blurred identity
The person feels like multiple people are living inside them or multiple voices talking inside their head. They might even feel that they have been ‘possessed’ by one or more entities or identities.
However, as per the Diagnostic and Statistical Manual of Mental Disorders (), some cultures around the world may not consider this as a dissociative disorder, as possession may be believed to be a spiritual or supernatural experience/ritual.
Symptoms of Dissociative identity disorder
People with dissociative identity disorder show various noticeable symptoms when they switch between alters at different times.DID shares several symptoms found in other mental illnesses and disorders like trauma and PTSD. Some of the common symptoms of DID in adults include:
• Exhibition of multiple personalities or alters
• Feelings of dissociation & detachment
• Behavior inconsistent with character (primary identity)
• Anxiety, depression, panic attacks and mood swings
• Sense of lost time
• Confusion and disorientation
• Severe headaches
• Pain in different parts of the body
• Amnesia and gaps in memory
• Depersonalization
• Derealization
• Hallucinations & delusions
• Obsessive-compulsive symptoms
• Psychotic symptoms
• Different levels of functioning
• Changes in appetite and sleeping problems
• Out of body experiences
• Self-persecution and self-sabotage
• Issues with sexual performance
• Substance abuse
• Self-injury related behaviors
• Suicidal thoughts
Dissociative Identity Disorder: Everything You Need To Know About DID
However, the symptoms of DID may vary between adults and children. Symptoms of DID in children may include:
1 thought on “Dissociative Identity Disorder: Everything You Need To Know About DID”
1. Avatar of Anonymous
As someone with DID I hate the use of photos from the movie Split, it makes out people with DID to be monsters, not victims of immense pain and trauma, which is what they are. If you want to educate people about DID, that’s great, but be very careful, false information can tear apart relationships and lives.
Comments are closed.
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-7,029,837,423,828,188,000 | Display Settings:
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Diabetes Care. 2009 Nov;32(11):1980-5. doi: 10.2337/dc09-0284. Epub 2009 Jul 29.
Insomnia with objective short sleep duration is associated with type 2 diabetes: A population-based study.
Author information
• 1Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA. avgontzas@psu.edu
Abstract
OBJECTIVE:
We examined the joint effects of insomnia and objective short sleep duration, the combination of which is associated with higher morbidity, on diabetes risk.
RESEARCH DESIGN AND METHODS:
A total of 1,741 men and women randomly selected from Central Pennsylvania were studied in the sleep laboratory. Insomnia was defined by a complaint of insomnia with duration of >or=1 year, whereas poor sleep was defined as a complaint of difficulty falling asleep, staying asleep, or early final awakening. Polysomnographic sleep duration was classified into three categories: >or=6 h of sleep (top 50% of the sample); 5-6 h (approximately third quartile of the sample); and <or=5 h (approximately the bottom quartile of the sample). Diabetes was defined either based on a fasting blood glucose >126 mg/dl or use of medication. In the logistic regression model, we simultaneously adjusted for age, race, sex, BMI, smoking, alcohol use, depression, sleep-disordered breathing, and periodic limb movement.
RESULTS:
Chronic insomnia but not poor sleep was associated with a higher risk for diabetes. Compared with the normal sleeping and >or=6 h sleep duration group, the highest risk of diabetes was in individuals with insomnia and <or=5 h sleep duration group (odds ratio [95% CI] 2.95 [1.2-7.0]) and in insomniacs who slept 5-6 h (2.07 [0.68-6.4]).
CONCLUSIONS:
Insomnia with short sleep duration is associated with increased odds of diabetes. Objective sleep duration may predict cardiometabolic morbidity of chronic insomnia, the medical impact of which has been underestimated.
PMID:
19641160
[PubMed - indexed for MEDLINE]
PMCID:
PMC2768214
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-7,584,712,025,911,003,000 | Can the 2 moving teeth hold a bridge in place and become stable? If yes, for how long?
Had a root canal on # 31 which was holding a 3 unit bridge ,now removed. I wanted to do an implant on the missing toot #30 ,but after seeing an implant specialist ,I was told that my toot are moving ,and that I should have never had the root canal done. This Dr suggested 2 implants on 31 & 29 and a bridge. If I don't do the implants /bridge [$12,000] , I'm very confused as to what to do now..
Doctor Answers 3
Implant and crown options
This is difficult to answer without seeing the actual situation. But, if the previous bridge hasn't been off too long ( more than 6 mo) I find it hard to visualize they moved too far. Your options would be 1) Place an implant for #30 as you wish and 2 new crowns for 29 and 31. 2) If indeed it is a fact #31 can not be used then the implants for #30 and #31 would be best and a new crown for #29 (no mention was made of it needing to be) extracted.
Newport Beach Dentist
Teeth Mobility & Dental Implants
Hi. Dental Mobility is a key indicator on the prognosis of a tooth. Usually the more mobility, the less bone you have. Although it is difficult to recover the stability of a tooth, it is not impossible, and we should always aim to maintain as many natural teeth as we can. However, It is fundamental to know the specifics of your case to assess the prognosis of your moving teeth. If the prognosis is good, my recommendation would be to get an implant on # 30. However, if the prognosis is poor, then you do want to get 2 implants (31 & 29) and a bridge. If you are open to consider dental tourism, this would be around 3,500 USD in Colombia.
Dental Implants
Hi, thank you for your question. I see you have a concern with your teeth on the lower right side. If you had a root canal on tooth #31, I would suggest that you visit the doctor who performed the root canal so he can give you a prognosis on the health of the tooth. If the prognosis is poor, you should consider a dental implant on #31. If the prognosis is good, keep #31 and have 2 implants placed, one on #29 and one on #30. Best of luck on your treatments.
You might also like...
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship. | {
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