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The aim of the present study was to evaluate the role
The aim of the present study was to evaluate the role of interleukin (IL)-6 and IL-8 on the expression of the membrane-bound complement inhibitors membrane attack complex-inhibitory protein (CD59) and decay-accelerating factor (CD55), in the human ovarian carcinoma A2780 cell line, which is a non-producing IL-6 cell line that does exhibit IL-6 responsiveness, due to the presence of IL-6 receptors. of CD55 protein. The present results indicate that CD55 and CD59 may affect the efficiency of complement-mediated immunotherapies. IL-6 is secreted by mesothelial cells, fibroblasts, macrophages and ovarian tumour cells, while IL-8 is secreted by endothelial cells and mesothelial cells, monocytes and ovarian tumour cells (11). Therefore, the tumour microenvironment is significant in all processes of ovarian cancer progression. The primary aim of the present study was to characterize the expression of the complement system inhibitors CD59 and CD55 at the mRNA and protein level in the human ovarian cancer A2780 cell line following IL-6 and IL-8 stimulation. The present results revealed that CD59 and CD55 proteins present on ovarian carcinoma cells appear to be key factors in protecting malignant ovarian cells from complement-mediated death. Materials and methods Cell culture The human being ovarian tumor A2780 cell range was from the Western Assortment of Cell Tradition (Salisbury, UK). A2780 cells had been cultured in RPMI-1640 moderate supplemented with L-glutamine, penicillin-streptomycin (10 U/ml-100 g/ml) and 10% fetal bovine serum (FBS) (all Sigma-Aldrich, Munich, Germany), inside a humidified atmosphere of 95% atmosphere and 5% CO2 at 37C. This cell range was chosen, since A2780 cells usually do not make IL-6, but expresses the IL-6 receptor (12). Excitement of cells Human being ovarian carcinoma cells had been seeded into petri meals (5 ml; 3105 cells/ml). The cells had been cleaned with phosphate buffered saline (PBS) with Ca2+ and Mg2+ (Sigma Aldrich, St. Louis, MO, USA) and then had been incubated in moderate RPMI 1640 supplemented with L-glutamine including different concentrations of IL-6 and IL-8. Human being IL-6 and IL-8 had been bought from Sigma-Aldrich. After a 24 h of incubation, the supernatant was moved and gathered to Eppendorf pipes and freezing at ?80C for following research. The cells had been incubated with 5 mM EDTA in phosphate-buffered saline (PBS) for 10 min. Subsequently, the cells had been transferred to fresh pipes and centrifuged at 12,000 g for 10 min at 4C. The supernatant was precipitated and eliminated cells had been kept at ?80C. Cell proliferation assay The result of IL-6 and IL-8 for the proliferation of ovarian tumor cells was established utilizing a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The cells had been cultured at a denseness of 5103 cells per well in 96-well cell tradition plates (Nunc? MicroWell?; Thermo Fisher Scientific, Inc., Waltham, MA, USA). After a 24 h incubation, the cells had been exposed to different concentrations of IL-6 and IL-8 (1, 10 and 100 ng/ml). Altogether 96 h later on, the proliferation from the treated cells was evaluated using the MTT assay. The quantity Dinaciclib (SCH 727965) of formazan dye was dependant on quantifying its absorbance at 570 nm using the FLUOstar Omega Microplate Audience (BMG Labtech GmbH, Ortenberg, Germany). The proliferation price (PR) was assessed by the next formula: PR (%) = (absorbance of treatment probe / absorbance of control probe) 100%. Enzyme-linked immunosorbent assay (ELISA) To Dinaciclib (SCH 727965) look for the amount of soluble CD59 and CD55 in the cell medium, an ELISA Kit for Human CD59 glycoprotein and ELISA Kit for Human Complement decay-accelerating factor were used (EIAab Science Co., Ltd., Wuhan, China), according to the manufacturer’s protocol. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) After a 24 h stimulation with various concentrations of IL-6 and IL-8 (1, 10 and 100 ng/ml), total cellular RNA from the cultured cells was isolated using a High Pure RNA Isolation kit (Roche Diagnostics GmbH, Mannheim, Germany), according to the manufacturer’s protocol. Extracted RNA was purified and diluted in DNase and RNase free water. Quality and quantity of the isolated RNA was measured by a NanoDrop? spectrophotometer (Thermo Fisher Dinaciclib (SCH 727965) Scientific, Inc.). RPS6KA5 DNase I (Roche Diagnostic GmbH, Mannheim, Germany) was used when total RNA was isolated (180U per sample) but not when RT-qPCR was performed. The qPCR was performed according to the manufacturer’s protocol: TaqMan? Gene Expression Assays Protocol (Applied Biosystems?; Thermo Fisher Scientific, Inc.) Complementary cDNA was synthesized from 2 g total RNA using SuperScript II Reverse Transcriptase (Invitrogen?; Thermo Fisher Scientific, Inc.). Subsequently, 1 l of the resulting cDNA solution was.
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fitness
1 Pound Of Fat = 3,500 Calories
here are 3,500 calories in one pound of fat. Thus, if you cut back or work off just 3,500 calories, you will lose an entire pound of fat. While it is possible to cut back on your calorie intake and increase your exercise regimen in order to lose pounds quickly, it is important to note that doctors recommend that you lose no more than 2 pounds of weight per week in order to ensure that your body properly adjusts to the weight loss.
Here are some tips to help you safely …
There are 3,500 calories in one pound of fat. Thus, if you cut back or work off just 3,500 calories, you will lose an entire pound of fat. While it is possible to cut back on your calorie intake and increase your exercise regimen in order to lose pounds quickly, it is important to note that doctors recommend that you lose no more than 2 pounds of weight per week in order to ensure that your body properly adjusts to the weight loss.
Here are some tips to help you safely drop 3,500 from your regular routine:
Run
Running for about 1 hour at a slow pace will help you lose approximately 350 calories, depending on your body type, speed and terrain. Thus, if you run for one hour five days a week while maintaining a consistent diet, you will safely lose one pound.
It is important to understand that many people who just begin running will eat pasta and other foods high in carbohydrates in order to compensate for the exertion. They think that because they worked out so hard, they deserve a treat. After all, they justify, the pasta will help to keep their energy levels high.
However, what they may not realize is that while they are justified in thinking that the carbohydrates will infuse their workout routine with energy, they are not actually setting their bodies up to lose weight. When you burn 350 calories but intake 450 over a high-carbohydrate pasta dish, you are adding more calories to your body than you otherwise would have.
Running does, however, help to boost our metabolism and change your muscle tone so that you burn calories more efficiently. Instead of inhaling a pasta dish after a run, select instead to have a large salad and splurge for the carbohydrate-rich croutons.
Eat In
When you eat out at a restaurant, not only are you subjecting your body to an array of high fat, high calorie foods, but you are also tempting yourself to eat a larger portion than you might normally eat. Therefore, what could be a simple 500 calories meal can easily turn into a 1500-calorie fat fest. In order to lose weight by cutting calories, it is essential that you are aware of exactly what you are putting into your body. Especially in the beginning of your new routine, it is important that you prepare your meals and monitor your level of hunger.
When eating out, generally you are in a social situation where food is not a priority – but spending time with your friends is. For this reason, people tend to eat more than they normally would. Non-dessert eaters often even spring for the extra round of calories. If you must eat out, help yourself avoid temptation by selecting a salad rather than a plate of pasta or burger. You will be amazed at the difference in the amount of calories you intake when you make simple choices such as meal option.
By reducing your overall calorie intake and increasing your level of physical activity, you will be able to lose those 3,500 calories without much trouble. Make sure that you stay focused, motivated and on task. You’ll shed unwanted weight in no time!
The New Calories per Pound of Weight Loss Rule
Losing a pound of fat can take as few as 10 calories a day or as many as 55, depending on whether you’re improving food quality or just restricting food quantity.
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The Weight Loss Medication
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Trenbolone Dosage (Beginner, Athletes and Bodybuilders)
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Sarcoidosis
Overview
Sarcoidosis is an inflammatory disorder in which lumps of inflammatory cells called granulomata are formed in multiple body organs, predominantly in the lungs and lymph nodes. The cause of the disease is unknown, and the symptoms depend on the organ involved. For example, lungs involvement result in cough, wheezing, breathing difficulties, etc. the other areas affected are the skin, eyes, liver, heart, spleen, brain, etc.
Some people show no or mild symptoms. The disease heals on its own. No specific treatment is available for sarcoidosis. Only supportive treatment is given. Very few people have severe complications. In some people with severe disease, anti-inflammatory medications are given.
Causes
The exact cause of the disease is unknown. It is thought to result from the body’s abnormal or exaggerated immune reactions against some triggers like infection or chemicals in genetically susceptible people. Some people have a family history of sarcoidosis.
Risk Factors
Having the following attributes may increase your chances of having sarcoidosis;
· Family history: If any of your family members have suffered from sarcoidosis, your risk of having the disorder may increase.
· Age: It usually affects people between the ages of 20-50 years.
· Race: African-Americans are affected more by sarcoidosis.
Epidemiology
1.9 million people got affected by pulmonary sarcoidosis in 2015 globally, and 122,000 deaths were recorded. The incidence of sarcoidosis is around 5-40 cases per one million population in the USA. It is more prevalent in African-Americans. It affects the age groups of 20-50, and women are more likely to be affected than men.
Signs And Symptoms
Signs and symptoms of sarcoidosis depend on the organs involved. The patients can present like;
· Around 5% of patients are asymptomatic. Sarcoidosis is detected accidentally on chest imaging
· 45% of patients have systemic symptoms like fever, anorexia, weight loss, joint pain.
· 50% of patients have lung involvement. They present with symptoms of cough, shortness of breath, particularly on exertion, chest pain, and rarely hemoptysis (blood in cough)
· Löfgren syndrome: development of fever, polyarthralgia (pain in multiple joints), and lymphadenopathy at the hila of the lungs on both sides.
· Skin involvement may present as erythema nodosum which are red tender lumps, cutaneous lesions called lupus pernio, purple rash on cheeks and nose, or rarely maculopapular plaques.
· In eyes, conjunctiva and uvea can be involved and have plaques or granulomas, which may lead to blindness.
· Bones and joints may be involved
· Heart involvement may cause heart failure, heart block, or sudden death
· Meningitis may occur
· Rarely Cranial nerves involvement may result in nerve palsies
· Rarely may it involve the hypothalamus and pituitary gland resulting in hormonal dysfunctions.
Diagnosis
Sarcoidosis is diagnosed by excluding other conditions as there is no specific test marker for sarcoidosis. The doctor will take the complete history asking questions about the onset of your symptoms, involvement of other body parts, family history, etc. They will examine you for the signs with particular emphasis on the lungs, lymph nodes, skin.
The diagnosis is supported by blood tests and imaging studies.
· The blood tests may exclude other diseases. Angiotensin-converting enzyme (ACE enzyme) is usually found at increased levels in sarcoidosis. Increased calcium levels are also found.
· Urine tests and blood urea nitrogen creatinine may show the functions and condition of the kidneys.
· Imaging studies: Chest X-Ray gives valuable information and is central to diagnosis. A High-resolution CT scan provides a clearer picture in cases of confusion. May also show interstitial fibrosis.
· ECG of the heart will show the degree of heart involvement
· PET scan to check for widespread disease.
· A definitive diagnosis is usually made based on the biopsy result that shows non-caseating granulomas which test negative for the presence of fungus or mycobacteria. A tissue for biopsy is usually taken from the hilar lymph nodes by performing bronchoscopy. Tissue for biopsy can also be taken from the skin lesions or the other regions with granulomas.
Differential Diagnosis
Sarcoidosis is a diagnosis of exclusion. Disorders having similar symptoms need to be excluded to make an efficient diagnosis and treatment.
· Tuberculosis
· Lymphoma
· Rheumatoid nodules
· Metastatic disease
· Septic emboli
· Granulomatosis with polyangitis
· Varicella infection,
· Atypical infections, for example, Mycobacterium avium complex, Cryptococcus, cytomegalovirus, etc.
Treatment
Management depends on the severity of the disease and the extent of organs involvement and dysfunction. Asymptomatic patients do not need any treatment. Medications used for symptomatic patients include;
· Anti-inflammatory medicines; ibuprofen
· Corticosteroids; topical, inhaled, oral
· Immunomodulators: methotrexate, choloroquine, cyclophosphamide, azathioprine, infliximab, etc.
· Supportive therapy may include improving physical activity to combat fatigue and enhance muscle activity and strength.
· A dysfunctional heart may need a cardiac pacemaker
· Pulmonary exercises to improve lung functions
· Fatal cases with severely affected lungs may need an organ transplant.
Prognosis
Sarcoidosis causes mild illness in most people, and they recover without treatment in about two years. In very few people, sarcoidosis can cause a long-term illness. It can also cause some complications like scarring of the lungs called pulmonary fibrosis, cataract and blindness in the eyes, kidney stones and kidney failure, heart block, nerve palsies, etc. Advanced pulmonary involvement with or without pulmonary hypertension and the involvement of organs other than lungs, particularly the heart or brain, is associated with poor outcomes. For untreated people, the mortality rate is less than 5%. Death usually is a result of pulmonary complications, respiratory failure, or heart failure.
Lifestyle Modifications
Sarcoidosis is an incurable disease. To cope with the disease, you need to make some lifestyle changes like;
· Eat a healthy, well-balanced diet including fruits, vegetables, and antioxidants to improve your overall health
· Perform some form of exercise or brisk walking regularly to improve activity
· Avoid stress, maintain good sleep hygiene, avoid excessive alcohol or smoking
· Be regular in your follow-ups and checkups with your health care provider. Take your medications regularly.
· Join a sarcoidosis support group if your symptoms are bothering your mental health and other activities.
Our clinical experts continually monitor the health and medical content posted on CURA4U, and we update our blogs and articles when new information becomes available. Last reviewed by Dr.Saad Zia on May 28, 2023.
References
Learn About Sarcoidosis | American Lung Association
https://www.lung.org/lung-health-diseases/lung-disease-lookup/sarcoidosis/learn-about-sarcoidosis
Diagnosis and Treatment of Pulmonary Sarcoidosis: A Review | Pulmonary Medicine | JAMA | JAMA Network
https://jamanetwork.com/journals/jama/article-abstract/2789537
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Allergy NaturopathNatural Therapies for Allergies
An allergy is a reaction that occurs when the immune system is overly sensitive to a substance that is normally harmless. This substance is usually something in the environment, such as dust mites, pollen, animal dander, medications, bites and stings. Allergies to food proteins are also very common – the most common food allergies are cow’s milk, egg, peanut, tree nuts, sesame, soy, fish, shellfish and wheat. However, other foods can also cause IgE allergies. It is important to remember that a food allergy is different to a food sensitivity or intolerance. Read here for the difference between intolerance and sensitivity.
Immediately or soon after the body is exposed to the allergen, an immune reaction occurs, causing IgE antibodies to produce in the body. During this process, inflammatory substances, such as histamine, are produced. These inflammatory compounds cause symptoms such as swelling/itching of the face, lips, tongue, throat, and eyes, hives, wheezing, asthma, abrupt gastrointestinal symptoms, and anaphylaxis.
What are the underlying causes of allergies?
• Genetics appears to be a significant determining factor in the wwwelopment of allergies.
• Research has suggested that exposure to different foods as a baby may contribute to the risk of wwweloping food allergies. In a 2015 study, 600 children were randomly assigned to eat peanuts or avoid peanuts. Children who started eating peanuts at a younger age (younger than 1 year), were less likely to have wwweloped a peanut allergy at age 5, compared to those children who avoided peanuts. However, the research emphasised that this may not be effective for everyone. While most children grow out of allergies to eggs and milk, allergies to nuts and seafood can be lifelong. More research is needed to confirm the link.
• The health of the digestive system should also be explored in any case of allergy. A healthy gut lining is made up of epithelial cells that are held together by tight junctions, creating a strong barrier. This ensures that proteins and antigens that can cause allergic reactions can not escape the digestive system and enter other areas of the body. If the gut lining becomes damaged – a term known as ‘leaky gut’ or impaired intestinal permeability – proteins and antigens may pass through the intestinal wall, entering the bloodstream and potentially causing an allergic response. A study found that patients with both food allergies and food sensitivities had increased intestinal permeability (i.e. leaky gut). They also found that the more damaged the gut lining was, the more severe the allergies and intolerances were.
How can a Naturopath help to improve signs and symptoms of allergy?
Firstly, a comprehensive examination of your individual (and family) history enables your Naturopath to put the pieces of the puzzle together – making links between your environment, diet, lifestyle, and the health of your body systems.
Your Naturopath will then usually recommend comprehensive pathology testing. This can help to identify the foods you are reacting to if they are unknown. Pathology testing may include testing the blood for antibodies, and assessing the health of the digestive system through a comprehensive and diagnostic stool analysis or a leaky gut test.
After pathology testing, you will then be given a tailored treatment plan, which may include:
• Treatments to repair the health of the gut – our Naturopaths are highly experienced in working with clients to improve their gut health. Each person’s treatment plan is different and may include nutritional medicine to enhance collagen production, probiotic therapy to repopulate healthy levels of bacteria, and gut-healing foods to reduce inflammation.
• Nutritional and herbal medicines to modulate the immune system and reduce inflammation – food allergies can cause inflammation of the wall of the small intestine, and activation of the immune system. Once the offending foods have been identified and omitted from the diet, it is imperative to repair any damage to the gut, and rebalance the function of the immune system.
• A customised eating plan – nutrient deficiencies are common in people who have restricted their diet due to allergies. Therefore, our Naturopaths make sure that you are offered alternatives to foods you must avoid, that ensures you aren’t missing out on vital nutrients
If allergies are having an impact on your health, we would love to work with you.
Take the next step to regaining good health!
Our Practitioners treat the root cause and not just the symptoms.
Through accurate assessment and scientific testing we can identify imbalances.
Our minimal fuss treatment plans address these imbalances.
Want to know how we can help you?
Lets us gift you with a FREE Naturopathic Assessment Consultation with one of our Naturopaths.
Why do we offer a Free Naturopath Assessment Consultation?
• Many clients are not sure if Naturopathy can help them.
• Maybe you have seen a Practitioner before and you want to figure out if we can help further.
• You might have questions that you want to ask the Practitioner in person before you commence a treatment plan.
• You may be wondering if we can identify what is causing your symptoms.
No matter where you are, we can offer Naturopath consultation by phone or skype consultations and nutritional supplementation through Australia and Overseas. We would love to see you in person in our Brisbane Naturopath, Central Coast Naturopath, Gold Coast Naturopath, Newcastle Naturopath, Mooloolaba Naturopath or Caloundra Naturopath Clinics on the Sunshine Coast, or our Sydney Naturopath clinic.
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9222580d47c553ea90dc0f5e416f8f3a
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5,415,536,442,344,537,000
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3 mins
Recognising Binge Eating and Recovery
Binge eating is a condition that affects both men and women. In a consumption-orientated culture that enables excessive eating and drinking, it can feel difficult to identify a binge eating disorder from simply bad eating habits. For example, an occasional episode of overeating does not qualify as a binge eating disorder. But if you are regularly overeating for the sole purpose of eating, if you feel a compulsion to eat and then feel disgusted or ashamed afterwards, or if you plan out eating binges and then binge eat while you are alone, you may have an eating disorder. If this is the case, you should talk to our private psychiatrist in London or book an appointment to see one our qualified psychologists.
It may be that a combination of therapies is necessary to help you address why you are binge eating. There are three primary steps in binge eating recovery:
Recognise triggers
The first step in binge eating recovery is to identify the triggers that ignite the compulsion to binge. For many people, the triggers to binge eat are things like fear, anxiety and stress. But everyone has individual triggers that set off their need to binge eat. Often those triggers have to do with things that are outside of their control, and binge eating may be a way of helping sufferers feel like they have that control again. Excessive eating can also be triggered by an obsession with perceived physical flaws. Someone who feels overweight and unattractive may not eat at all during the day and then binge alone at night in an effort to process their negative feelings and low self-esteem. A trained therapist will help sufferers identify these triggers.
Let go of the need for control
People who feel like they have no control or power in their lives may binge eat because the food that they eat and the amount that they eat may be the one thing that they feel is totally within their control. For example, victims of abuse or trauma may develop a binge eating disorder because as children they lacked the power to get away from the abusive situation that were in. They may internalise their anger and other negative feelings that resulted from this abuse, and overeating may be a way of stopping those feelings from reappearing. This is destructive behaviour, however, and, although these coping mechanisms and sense of control may seem to offer some immediate relief, individuals who binge eat are doing themselves physical and emotional harm.
Heal the emotional pain causing the binging
That’s why the third step in binge eating disorder recovery is healing the underlying emotional trauma that caused the binge eating in the first place. You will likely be offered a review from one of our psychiatrists, who will be working also with your GP and a nutritionist, while psychological therapy, such as cognitive-behavioural therapy, is offered to help you address the issues causing your anxiety and compulsions.
Contact us today to book an appointment for a consultation.
Dr Elena Touroni
Dr Elena Touroni
19 December 2017
"Dr. Elena Touroni is a skilled and experienced Consultant Psychologist with a track record of delivering high-quality services for individuals with all common emotional difficulties and those with a diagnosis of personality disorder. She is experienced in service design and delivery, the management of multi-disciplinary teams, organisational consultancy, and development and delivery of both national and bespoke training to providers in the statutory and non-statutory sector."
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Athena Lazaridou
Athena is a Pilates instructor with 8 years’ experience in the field. After completing a Power Pilates Mat Certification in Athens, she went on to complete the Full Comprehensive Classical Pilates Certification with Equinox in Kensington. She has been teaching Pilates at Equinox for the past 6 years in addition to her own private clients who she trains both face to face and virtually.
Athena has a passion for helping people get stronger and fitter as well as helping those recovering from injury regain their strength and mobility. Over the years, she has worked with athletes to incorporate Pilates into their training and improve performance. Athena has also worked with prenatal and postnatal women who may be experiencing depression or other mental health difficulties and used Pilates to facilitate a positive impact on their mental health.
Athena is very passionate about improving physical and mental well-being and has recently incorporated Sound Healing into her work, as she believes it to be one of the best ways of ‘letting go’ and releasing stale energy whilst increasing greater self-awareness.
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PT - JOURNAL ARTICLE AU - Theilen, U AU - Lyon, A J AU - Fitzgerald, T AU - Hendry, G M A AU - Keeling, J W TI - Infection with <em>Ureaplasma urealyticum</em>: is there a specific clinical and radiological course in the preterm infant? AID - 10.1136/adc.2003.026013 DP - 2004 Mar 01 TA - Archives of Disease in Childhood - Fetal and Neonatal Edition PG - F163--F167 VI - 89 IP - 2 4099 - http://fn.bmj.com/content/89/2/F163.short 4100 - http://fn.bmj.com/content/89/2/F163.full SO - Arch Dis Child Fetal Neonatal Ed2004 Mar 01; 89 AB - Background: Despite having mild early respiratory disease, many preterm babies develop chronic lung disease (CLD). Intrauterine infection with Ureaplasma urealyticum has been associated with preterm labour and CLD. Objective: To test the hypothesis that infection with U urealyticum results in a specific clinical and radiological picture in the first 10 days of life. Methods: Retrospective study of 60 ventilated babies < 30 weeks gestation, who had tracheal secretions tested for U urealyticum. Placental histology was reviewed by a paediatric pathologist for signs of chorioamnionitis. Chest radiographs were independently reviewed by two paediatric radiologists according to previously agreed criteria. All reviewers were blinded to the infection status of the babies. Results: Twenty five babies were U urealyticum positive. These were more likely to experience chorioamnionitis (p = 0.004), premature rupture of membranes (p = 0.01), and spontaneous vaginal delivery (p = 0.09). U urealyticum positive babies had fewer signs of respiratory distress syndrome on early chest radiographs (p = 0.038), and they could be weaned from their ventilation settings (fraction of inspired oxygen (Fio2) and mean airway pressure) more quickly in the first few days. Subsequently U urealyticum positive babies deteriorated clinically and radiologically. More often they required ventilation to be restarted (p = 0.051), a higher proportion being ventilated on day 10 (p = 0.027) with higher Fio2 (p = 0.001) and mean airway pressure (p = 0.002). Their chest radiographs showed more emphysematous changes as early as day 5 (p = 0.045), with a pronounced difference by day 10 (p = 0.009). Conclusions: Preterm ventilated babies with U urealyticum in their tracheal secretions have a different clinical and radiological course, with less acute lung disease but early onset of CLD, compared with those with negative cultures.
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Academy
Mechanisms of cannabinoid action
The pharmacology of phytocannabinoids is complex, partly due to the large number and diversity of their molecular targets, responsible for their impact on physiological and pathological processes. However, most effects of THC, and other cannabinoids, directly depend on its action on a cell-communication system exerting eminent regulatory functions in every organ and anatomical system of the body, the so-called endocannabinoid system.
Cannabinol was the first cannabinoid identified from cannabis at the end of the 19th Century, while the discovery of CBD and the recognition of THC as the main active compound in cannabis was achieved by Roger Adams investigations around 1940’s. REF The final isolation and characterization of the tridimensional structure of THC was accomplished by Raphael Mechoulam in 1964. REF
However, it took almost 30 years to identify the major effector of THC actions, a molecular receptor present in the cell membrane of many different cell types distributed all over our body, but particularly abundant in the brain, named cannabinoid receptor type 1, or CB1 receptor. REF Shortly after, an endogenous cannabinoid ligand or endocannabinoid (i.e., a naturally produced molecule which binds and activates the cannabinoid receptor) was also identified in porcine brain and named “anandamide”, after the Sanskrit word ananda, meaning bliss, and the chemical nature of the compound. REF Later, a second, peripheral receptor targeted by THC was also identified in the spleen and called cannabinoid receptor type 2, or CB2 receptor. REF Likewise, a second endogenous ligand of cannabinoid receptors, 2-arachidonoyl glycerol or 2-AG, was simultaneously identified in rat brain and canine gut samples. REFS
Collectively, these findings led to the discovery and characterization of the endocannabinoid system, which is mainly composed by the aforementioned CB1 and CB2 cannabinoid receptors, the endocannabinoids anandamide and 2-AG, as well as the metabolic enzymes responsible for the biosynthesis and degradation of endocannabinoids. REF
Over the following decades, thorough research has allowed for the expansion and better characterization of the actual elements of the endocannabinoid system, a deeper understanding of the role of this crucial system in the control of homeostasis and overall mammalian physiology, as well as the involvement of the endocannabinoid system in most pathological conditions, which serve as a basis for most of the therapeutic actions of cannabinoids.
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BMC Medical Genetics
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Lack of association between the chemokine receptor 5 polymorphism CCR5delta32 in rheumatoid arthritis and juvenile idiopathic arthritis
• Ewald Lindner1,
• Gry BN Nordang1,
• Espen Melum1,
• Berit Flatø2,
• Anne Marit Selvaag2,
• Erik Thorsby1,
• Tore K Kvien3,
• Øystein T Førre2 and
• Benedicte A Lie1Email author
Contributed equally
BMC Medical Genetics20078:33
https://doi.org/10.1186/1471-2350-8-33
Received: 29 November 2006
Accepted: 12 June 2007
Published: 12 June 2007
Abstract
Background
The chemokine receptor CCR5 has been detected at elevated levels on synovial T cells, and a 32 bp deletion in the CCR5 gene leads to a non-functional receptor. A negative association between the CCR5Δ32 and rheumatoid arthritis (RA) has been reported, although with conflicting results. In juvenile idiopathic arthritis (JIA), an association with CCR5 was recently reported. The purpose of this study was to investigate if the CCR5Δ32 polymorphism is associated with RA or JIA in Norwegian cohorts.
Methods
853 RA patients, 524 JIA patients and 658 controls were genotyped for the CCR5Δ32 polymorphism.
Results
The CCR5Δ32 allele frequency was 11.5% in the controls vs. 10.4% in RA patients (OR = 0.90; P = 0.36) and 9.7% in JIA patients (OR = 0.85; P = 0.20). No decreased homozygosity was observed for CCR5Δ32, as previously suggested.
Conclusion
Our data do not support an association between the CCR5Δ32 allele and Norwegian RA or JIA patients. Combining our results with those from a recently published meta-analysis still provide evidence for a role for CCR5Δ32 in RA, albeit substantially weaker than the effect first reported.
Background
In rheumatoid arthritis (RA) and juvenile idiopatic arthritis (JIA), the synovium is infiltrated with T cells and macrophages, and chemokine receptors and their ligands are involved in regulation of the inflammation [1, 2]. Chemokines regulate lymphocyte trafficking by inducing cell motility and activating adhesion molecules. The chemokine receptor CCR5 is a G-protein-coupled seven-transmembrane-receptor, and it is expressed on monocytes, macrophages, memory T-cells and dendritic cells, where it serves as a receptor for RANTES, MIP-1-α, MIP-1-β and MCP [3]. CCR5 has functionally been implicated in the pathogenesis of RA [2] and JIA [4]. The expression of CCR5 is increased on synovial T cells in patients with JIA [4] or RA [5].
The gene encoding CCR5 is located on chomosome 3p21.3 [6]. A 32 base pair deletion (CCR5Δ32) in the CCR5 gene leads to a frame shift and a non-functional receptor. Homozygosity for CCR5Δ32 results in a complete lack of surface expression of CCR5 [7]. CCR5 happens to be a co-receptor for HIV-1 on CD4+ T-cells with the consequence that CCR5Δ32 homozygotes are protected against infections with HIV-1, while heterozygotes have a delay in the progression towards AIDS [8]. The CCR5 deletion is common among Caucasians, especially in Nordic populations [9], but has not been found in native Africans, American Indians or East Indian ethnic groups.
The role of CCR5Δ32 has been investigated genetically in several immune-mediated diseases. In RA, a negative association of the deletion has been reported with divergent results [1014], while in childhood arthritis a weak negative association has been observed in a single study [15]. Regarding clinical outcome, it has been reported that carriers of the CCR5Δ32 allele occurred at a significantly higher frequency among patients with non-severe compared to severe disease (N = 160) [14], whereas a later and larger study of 438 patients did not find any association between carriage of the CCR5Δ32 and milder disease severity in inflammatory polyarthritis [16]. A recent meta-analysis of five reports addressing the association of CCR5Δ32 with susceptibility to develop RA in patients of European ancestry (1790 cases and 2717 controls), reported a significant negative association and estimated the deletion to provide disease resistance with an OR = 0.65 (95% CI [0.55–0.77])[17].
The aim of our study was to investigate if there is an association between CCR5Δ32 and RA in the largest individual data set studied so far, as well as to address whether CCR5Δ32 is also associated with JIA, not yet extensively investigated.
Methods
853 RA patients, 524 JIA patients and 658 controls were included in the study. The RA patients, admitted to the Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway, fulfilled the American College of Rheumatology (ACR) criteria [18] and the JIA patients, admitted to the Department of Rheumatology, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway, were classified according to the ILAR (International League of Associations for Rheumatology) criteria [19]. The control group was recruited through the Norwegian Bone Marrow Registry. All patients and controls were of Norwegian origin. The study was approved by the Norwegian Regional Ethics committee, and the participants had given their informed consent.
Whole-genome amplification was performed on genomic DNA using the Genomiphi® kit (GE healthcare systems, Chalfont St. Giles, UK). Amplification of fragment surrounding the deletion was performed with the dye labelled forward primer 5'-ATCACTTGGGTGGTGGCTGTGTTTGCGTCTC and the reverse primer 5'-AGTAGCAGATGACCATGACAAGCAGCGGCAG under the following conditions; denaturation at 94°C for 15 seconds, annealing and extension at 70°C for 15 seconds, 30 cycles and final extension at 70°C for 5 min at a Perkin Elmer 9700 thermal cycler (Applied Biosystems, Foster City, CA, USA). Fragment length was determined on an ABI3730 DNA Analyzer (Applied Biosystems) with subsequent allele calling in GeneMapper v3.7 where a 193 bp PCR product corresponded to the wild type allele and a 161 bp product represented the deletion. Part of the control material was genotyped in our previous publication [20].
Statistical power was calculated prior to the study using the power calculator at [21], assuming the frequency of 10% for the CCR5Δ32 and an Odds Ratio of 0.56 (obtained from Zapico et al [14]). The power (at α = 0.05) was calculated to be 84% for the RA and 75% for the JIA data set. Allele and genotype frequencies in patients and controls were compared by the Chi-Square test, or Fischer's exact test when appropriate, using the Public Domain Software for Epidemiology and Disease Surveillance EPI Info Version 5 (Center of Disease Control, Epidemiology Program Office, Atlanta, GA, USA).
Results and Discussion
The genotype and allele frequencies of CCR5Δ32 are summarised in Table 1. The genotyping success rate was >95% for both the patients and control populations, and all groups were in Hardy-Weinberg equilibrium. No significant negative association was observed with the Δ32 allele in either RA or JIA (Table 1), and only a negligible deviation in frequency was seen between the patients and controls. Furthermore, no decreased frequency for homozygosity of Δ32 was evident among the patients (0.9% in RA, 0.6% in JIA and 1.0% in controls). A revised meta-analysis, calculated by adding our results to those from the recently published meta-analysis of pooled RA cases and controls [17], reduced the initial published risk estimate from OR = 0.65; 95% CI [0.55–0.77], p < 0.0001, to OR = 0.83; 95% CI [0.73–0.95], p = 0.0068.
Table 1
CCR5 genotype and allele frequencies among controls, RA patients and JIA patients
Controls no. (%)
RA no. (%)
OR (95% CI)
p
JIA no. (%)
OR (95% CI)
p
CCR5 genotype
Δ32/Δ32
6 (0.9)
9 (1.0)
1.13 (0.43–2.98)
0.81
3 (0.6)
0.67 (0.20–2.31)
0.53
Δ32/wt
136 (21.1)
156 (18.7)
0.86 (0.66–1.11)
0.24
93 (18.1)
0.83 (0.62–1.11)
0.20
wt/wt
503 (78.0)
671 (80.3)
1.15 (0.89–1.48)
0.28
419 (81.4)
1.23 (0.92–1.64)
0.16
CCR5 allele
Δ32
148 (11.5)
174 (10.4)
0.90 (0.71–1.13)
0.35
99 (9.7)
0.82 (0.63–1.07)
0.15
wt
1142 (88.5)
1498 (89.6)
931 (90.4)
RA: rheumatoid arthritis; JIA: juvenile idiopathic arthritis; N: number of individuals/chromosomes with the denoted genotype/allele; OR (95% CI): Odds ratio with corresponding 95% confidence interval; wt: wild type; Δ32: 32 bp deletion.
Our results, from the largest cohort of RA patients and controls investigated to date, do not support the existence of a negative association between CCR5Δ32 and disease (OR = 0.90; 95% CI [0.71–1.14]). Neither was the proposed disease resistance provided by homozygosity of the deletion sustained in our data set. The frequency of CCR5Δ32 in our control population is in the same range as that observed in other European populations and is highly similar to that reported in a Danish population [11]. CCR5Δ32 has been found to have its highest prevalence among Nordic populations [9], which from a statistical power perspective should favour detection of a negative association in our Norwegian cohort, on the other hand deviating results between populations for disease associated alleles is not uncommon, e.g. for PADI4 [2225].
Altogether, two studies suggest an association between CCR5Δ32 and RA [13, 14], while three studies [1012], in addition to ours, do not reveal statistical significant evidence to support this. The number of patients included in the positive studies was 160 and 516 whereas in the negative studies 278, 163, 673 and 853 patients were analysed. A weak effect of CCR5Δ32 on the disease risk, combined with inadequate power, could explain the contradictory results. Alternatively, there could be true differences between the populations in the effect exercised by CCR5; i.e. due to genetic or allelic heterogeneity, variable influence of environmental factors, gene-gene interaction, or variable linkage disequilibrium patterns. All studies display a deviation in the direction of a lower frequency for the deletion among RA patients, but in our data set only a 0.9% reduction in frequency was seen in RA patients compared to controls. The results of a recent meta-analysis of pooled cases and controls were in favour of a negative association (OR = 0.65 (95% CI [0.55–0.77])). [17]. We recalculated the power of our RA study post hoc based on the odds ratio for the CCR5Δ32 obtained in the recent meta-analysis [17], and given this risk effect our power was reduced to 63%. When our RA data set was included in a revised meta-analysis, the overall risk estimate was greatly reduced (OR = 0.83; 95% CI [0.73–0.95, p = 0.0068]). Furthermore, if the true risk estimate is in the range of that calculated after also including our data into the pooled meta-analysis, one would need almost 4000 cases and an equal amount of controls to replicate the finding with an 80% power. Notably, the CCR5Δ32 meta-analysis may also have been prone to type 1 error caused by e.g. publication bias or heterogeneity between the populations included in the combined analysis [26].
Our data does not reveal an association in JIA. After the initiation of our study, the possible association of CCR5 in JIA was addressed, and the authors reported a negative association between CCR5Δ32 and childhood arthritis, particularly in the early onset group and in those diagnosed with pauciarticular subtype [15]. This finding was not sustained in our data set as no association was revealed when stratifying for either JIA subgroups, including the oligoarthirits patients (comparable to the pauciarticular group defined by the ACR criterias; OR = 0.80, 95% CI [0.54–1.17], p = 0.23), or early disease onset (<6 years; OR = 0.81, 95% CI [0.55–1.19], p = 0.27). Further investigations are warranted for JIA before any firm conclusions can be drawn. Nevertheless, our study does not suggest that CCR5Δ32 influences the risk of JIA, and if present the effect is likely to be small.
CCR5 has functionally been implicated in RA, and our study does not formally exclude CCR5 as a candidate gene for RA and JIA. Polymorphisms located elsewhere in the gene could potentially be predisposing, and if the associations observed for Δ32 is only secondary due to linkage disequilibrium, that could be an explanation for the discrepant results obtained by different studies. Interestingly, in the recently reported childhood arthritis study [15] other polymorphisms in the CCR5 gene were also investigated, and an additional association with the CCR5 -1835T allele was also observed. No strong linkage disequilibrium between CCR5Δ32 and -1835T was evident, but the haplotype lacking both these alleles displayed positive association, which could suggest that the true etiological variant of CCR5 in RA or JIA pathogenesis that is still unidentified.
Conclusion
In conclusion, whether the CCR5 gene is involved in RA or JIA susceptibility remains unclear, however, our study suggests that if a protective effect is exercised by CCR5Δ32, it is minor and less than predicted from the meta-analysis of previous publications[17].
Notes
Declarations
Acknowledgements
This work was funded by Rikshospitalet, Southern Norway Regional Health Authority, The Norwegian Women's Health Association and the Norwegian Foundation for Health and Rehabilitation. We thank the Norwegian Bone Marrow Donor Registry for making the control material available and Tom H. Karlsen for valuable input to the study.
Authors’ Affiliations
(1)
Institute of Immunology, Rikshospitalet-Radiumhospitalet Medical Center
(2)
Department of Rheumatology, Rikshospitalet-Radiumhospitalet Medical Center
(3)
Department of Rheumatology, Diakonhjemmet Hospital
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27. Pre-publication history
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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%0 Journal Article %T Direct comparison of immunological effects of various nutritional supplements %A Vaclav Vetvicka %J 临床与病理杂志 %D 2021 %B 2021 %9 %! Direct comparison of immunological effects of various nutritional supplements %K %X Objective: Immunonutrition represents a diet based on the knowledge of basic principles of the immune system and its functions. Despite numerous claims, the direct comparison of the immunostimulating effects of natural modulators is limited, making any conclusions difficult. Our study focused on most common vitamins and immunonutrients and directly compared their effects on various branches of the immune system. Methods: In this study we used a mouse model to evaluate various aspects of immune reactions, namely phagocytic activity, IL-2 secretion, NK cell activity, antibody formation and growth of breast cancer in order to find out the possible effects of six different immunonutrients and their combinations. Results: We found that glucan was in all tests the most active immunomodulator. Synergistic effects were observed only in glucan-selenium and glucan-vitamin C combinations. The rest of immunonutrients had only small activity or no activity at all. Conclusion: Based on our results, we concluded that most of vitamins and minerals have only limited, if any, effects on immune activities including cancer. The current study managed to confirm synergistic effects of the beta glucan-vitamin C and beta-glucan-selenium combinations. More studies on possible positive or negative effects of such combination and on mechanisms of action are important. %U https://lcbl.csu.edu.cn/article/view/46445 %V 41 %N 12 %P 2747-2755 %@ 2095-6959
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Accessibility / Report Error
Primary cutaneous follicle center lymphoma simulating basal-cell carcinoma on the nasal ala* * Study conducted at the Faculty of Medicine of Jundiaí (FMJ) - Jundiaí (SP), Brazil.
Abstract
Primary cutaneous B-cell lymphomas (PCBCLs) constitute 25% of all primary cutaneous lymphomas. They present in the skin with no evidence of systemic or extracutaneous disease at the time of diagnosis, after adequate staging. Primary cutaneous B-cell lymphomas differ significantly from their nodal counterparts in relation to both clinical behavior and prognosis. The distinction between primary and secondary B-cell lymphomas is essential for defining prognosis/course of action. Such distinction is also very difficult to make, since primary and secondary B-cell lymphomas are clinically and histologically indistinguishable. We report the case of a patient with primary cutaneous follicle center lymphoma who underwent surgical excision.
Keywords:
Carcinoma, basal cell; Lymphoma, B-cell; Lymphoma, B-cell, marginal zone; Lymphoma, follicular; Lymphoma, non-Hodgkin; Precursor cell lymphoblastic leukemia-lymphoma
INTRODUCTION
The lymphomas are a group of neoplasms arising from the lymphoreticular system. They are divided into two main groups: Hodgkin's lymphoma (HL) and non-Hodgkin lymphomas (NHL). The latter may be nodal (when primarily involving the lymph nodes) or extranodal.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.About 30% of NHL involve extranodal tissues. The skin is the second most affected organ (after the gastrointestinal tract), comprising approximately 18% of these lymphomas.2Suárez AL, Querfeld C, Horwitz S, Pulitzer M, Moskowitz A, Myskowski PL. Primary cutaneous B cell lymphomas. Part II. Therapy and future directions. J Am Acad Dermatol. 2013;69:343. e1-11.
Based on their cellular origin and according to the expressed monoclonal antibodies, lymphomas can be divided into T- or B-cell lymphomas.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.,3Sampaio SAP, Rivitti EA. Leucemias, Linfomas e Pseudolinfomas. In: Sampaio SAP, Rivitti EA. Dermatologia. 2. ed. São Paulo: Artes Médicas; 2000. p.887-913.The expression of CD3, CD4, CD8, CD43 or CD45 confirms their T-cell character. The expression of CD20, in particular, but also of CD79, CD5 and CD10 confirms their B-cell character.3Sampaio SAP, Rivitti EA. Leucemias, Linfomas e Pseudolinfomas. In: Sampaio SAP, Rivitti EA. Dermatologia. 2. ed. São Paulo: Artes Médicas; 2000. p.887-913.Cutaneous B-cell lymphomas (CBCL) are less frequent than cutaneous T-cell lymphomas, representing about 25% of all cutaneous lymphomas. It shows a slight pREFERENCES for males and an increased incidence with age.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.
CBCL can be primary or secondary. Primary CBCL have a more indolent natural history than secondary CBCL and a good prognosis. They are characterized by having only cutaneous presentation, with no evidence of extracutaneous lesion after adequate staging. They have an identical morphological appearance but different clinical behaviors.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.
In 2005, the World Health Organization (WHO) and the European Organization for Research and Treatment of Cancer (EORTC) proposed a classification for primary cutaneous lymphomas. CBCL were divided into marginal zone, follicle center, diffuse large B-cell, leg type and intravascular large B-cell lymphoma (Chart 1).1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.,4Burg G, Kempf W, Kazakov DV, Michaelis S, Dummer R. WHO/EORTC Classification of Cutaneous Lymphomas. In: Burg G, Kempt W. Cutaneous lymphomas. Florida: Taylor & Francis Group; 2005, 91-92.
CHART 1
Classification of cutaneous lymphomas (WHO/EORTC, 2005)
We report the case of a patient with primary cutaneous follicle center lymphoma (PCFCCL), the most common type of CBCL, which occurs primarily in the skin and whose clinical manifestations can mimic many other diseases. In our case, the main differential clinical diagnosis was basal cell carcinoma.
CASE REPORT
A 65-year-old white male patient had had an asymptomatic, smooth-surfaced, erythematous nodular lesion of 1.2 cm in diameter, with telangiectasia and progressive growth on the left nasal ala for eight months (Figure 1). The initial diagnostic hypothesis was basal cell carcinoma. Histopathological examination revealed a preserved dermis and epidermis with formation of lymphoid follicles. Lymphocytic cells were identified both in the periphery and center of the follicle (Figure 2). Immunohistochemistry was positive for CD20, CD10 and Bcl-6 in cells of the germinal center and negative for Bcl-2, thus confirming the diagnosis primary cutaneous follicle center lymphoma (Figure 3). Laboratory tests showed normal blood count and normal Lactate Dehydrogenase (LDH) levels, negative VDRL test, and negative anti-HIV and anti-HTLV 1 antibodies. CT scans of the chest/abdomen and pelvis showed no signs of malignancy and the bone marrow biopsy/aspirate showed no abnormalities. The patient underwent surgical excision of the lesion (Figure 4).
FIGURE 1
Clinical view of the PCFCCL: smooth-surfaced, erythematous nodular lesion of 1.2 cm in diameter, with telangiectasia on the left nasal ala
FIGURE 2
Histopathology of the PCFCCL: preserved dermis and epidermis with formation of lymphoid follicles. Lymphocytic cells were identified both in the periphery and center of the follicle. Hematoxylin-eosin, 40X
FIGURE 3
Immunohistochemistry of the PCFCCL: (A) the cytoplasm of B-cells was strongly positive for CD20. (B) germinal center cells were positive for CD10. (C) germinal center cells were positive for Bcl-6. (D) germinal center cells were negative for Bcl-2. Immunohistochemistry, 40X
FIGURE 4
Seventh post-operative day after surgical excision with primary closure of the lesion on the left nasal ala. Linear incision showing good healing and the presence of suture stitches
DISCUSSION
PCFCCL represent 55% of of all CBCL. They have a predilection for males and mainly affect adults with an average age of 60 years. Clinically, it manifests itself as solitary or grouped, erythematous to violaceous papules, plaques, nodules or tumors. They rarely ulcerate or exhibit necrosis. The lesions occur mainly on the head, neck and trunk. The differential diagnosis includes inflammatory lesions such as acne, epidermal inclusion cyst, and lymphoid hyperplasia, and cutaneous malignancies such as basal cell carcinoma.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.,3Sampaio SAP, Rivitti EA. Leucemias, Linfomas e Pseudolinfomas. In: Sampaio SAP, Rivitti EA. Dermatologia. 2. ed. São Paulo: Artes Médicas; 2000. p.887-913.In the case presented here, the first diagnostic hypothesis was basal cell carcinoma. Diagnostic differentiation was carried out by means of histology, immunohistochemistry and staging tests.
The five year survival rate is over 95%. Spread to lymph nodes or internal organs is rare (5%). The recurrence rate is high (about 50%), but there is not a worse prognostic factor and it is usually confined to skin.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.,2Suárez AL, Querfeld C, Horwitz S, Pulitzer M, Moskowitz A, Myskowski PL. Primary cutaneous B cell lymphomas. Part II. Therapy and future directions. J Am Acad Dermatol. 2013;69:343. e1-11.Histologically, it presents dermal and subcutaneous proliferation of centrocytes and centroblasts in a follicular and/or diffuse growth pattern. The tumor cells express B-cell markers such as CD20, CD79a, CD10, Bcl-6 and negativity for Bcl-2.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.For single lesions, as in the case reported here, the first choice of treatment is radiotherapy or surgical excision.2Suárez AL, Querfeld C, Horwitz S, Pulitzer M, Moskowitz A, Myskowski PL. Primary cutaneous B cell lymphomas. Part II. Therapy and future directions. J Am Acad Dermatol. 2013;69:343. e1-11.
Differentiating between primary and secondary skin involvement, through undiagnosed nodal or visceral malignancies, is crucial in addressing CBCL, because of the difference in prognosis and therapeutic options, given that primary and secondary B-cell lymphomas are clinically and histologically indistinguishable.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.,2Suárez AL, Querfeld C, Horwitz S, Pulitzer M, Moskowitz A, Myskowski PL. Primary cutaneous B cell lymphomas. Part II. Therapy and future directions. J Am Acad Dermatol. 2013;69:343. e1-11.,3Sampaio SAP, Rivitti EA. Leucemias, Linfomas e Pseudolinfomas. In: Sampaio SAP, Rivitti EA. Dermatologia. 2. ed. São Paulo: Artes Médicas; 2000. p.887-913.,4Burg G, Kempf W, Kazakov DV, Michaelis S, Dummer R. WHO/EORTC Classification of Cutaneous Lymphomas. In: Burg G, Kempt W. Cutaneous lymphomas. Florida: Taylor & Francis Group; 2005, 91-92.In the past, it was believed that CBCL were invariably secondary. In recent years, however, it has been recognized that CBCL whose primary site is the skin represent a distinct and very important group of extranodal lymphomas.1Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.,3Sampaio SAP, Rivitti EA. Leucemias, Linfomas e Pseudolinfomas. In: Sampaio SAP, Rivitti EA. Dermatologia. 2. ed. São Paulo: Artes Médicas; 2000. p.887-913.,4Burg G, Kempf W, Kazakov DV, Michaelis S, Dummer R. WHO/EORTC Classification of Cutaneous Lymphomas. In: Burg G, Kempt W. Cutaneous lymphomas. Florida: Taylor & Francis Group; 2005, 91-92.
• Financial Support: None.
• How to cite this article Wanczinski MI, Pinto CAL, Trevisan F, Cunha PR, Grohs LMH. Primary cutaneous follicle center lymphoma simulating basal-cell carcinoma on the nasal ala . An Bras Dermatol. 2015;90 (3 Suppl 1):S111-4.
• *
Study conducted at the Faculty of Medicine of Jundiaí (FMJ) - Jundiaí (SP), Brazil.
References
• 1
Suárez AL, Pulitzer M, Horwitz S, Moskowitz A, Querfeld C, Myskowski PL. Primary cutaneous B cell lymphomas. Part I. Clinical features, diagnosis and classification. J Am Acad Dermatol. 2013;69:329. e1-13.
• 2
Suárez AL, Querfeld C, Horwitz S, Pulitzer M, Moskowitz A, Myskowski PL. Primary cutaneous B cell lymphomas. Part II. Therapy and future directions. J Am Acad Dermatol. 2013;69:343. e1-11.
• 3
Sampaio SAP, Rivitti EA. Leucemias, Linfomas e Pseudolinfomas. In: Sampaio SAP, Rivitti EA. Dermatologia. 2. ed. São Paulo: Artes Médicas; 2000. p.887-913.
• 4
Burg G, Kempf W, Kazakov DV, Michaelis S, Dummer R. WHO/EORTC Classification of Cutaneous Lymphomas. In: Burg G, Kempt W. Cutaneous lymphomas. Florida: Taylor & Francis Group; 2005, 91-92.
Publication Dates
• Publication in this collection
June 2015
History
• Received
14 June 2014
• Accepted
23 July 2014
Sociedade Brasileira de Dermatologia Av. Rio Branco, 39 18. and., 20090-003 Rio de Janeiro RJ, Tel./Fax: +55 21 2253-6747 - Rio de Janeiro - RJ - Brazil
E-mail: revista@sbd.org.br
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ins(12;8)(p13;q11q21) ETV6/LYN
2015-02-01 Jean-Loup Huret
1.Genetics, Dept Medical Information, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France
Clinics and Pathology
Disease
Myeloproliferative disease (primary myelofibrosis).
Epidemiology
Only one case to date, a 21-year old male patient (Tanaka et al., 2010).
Prognosis
The patient died 11 months after diagnosis.
Genes Involved and Proteins
Gene name
LYN (LYN proto-oncogene, Src family tyrosine kinase)
Location
8q12.1
Protein description
512 amino acids. LYN contains from N-term to C-Term an SH3 domain (aa 63-123), a SH2 domain (aa 129-226) and a tyrisine kinase domain (aa 247-501). Non-receptor tyrosine kinase. LYN is mainly expressed in hematopoietic cells and is an important regulator of immune homeostasis.
Gene name
ETV6 (ets variant 6)
Location
12p13.2
Protein description
452 amino acids. The ETV6 protein contains from N-term to C-Term a HLH (helix-loop-helix, aa 40-124) domain (also referred to as the pointed or sterile alpha motif domain), responsible for hetero- and homodimerization, an internal domain, involved in the recruitment of a repression complex including NCOR1 (17p12), NCOR2 (12q24.31), SIN3A (15q24.2), and SIN3B (19p13.11), and an ETS domain (aa 339-420), responsible for sequence specific DNA-binding and protein-protein interaction (De Braekeleer et al., 2014).
Result of the Chromosomal Anomaly
Atlas Image
Description
535 amino acids. The fusion protein is composed of the HLH domain and internal domain of ETV6 (336 N-term amino acids), fused to the tyrosine kinase domain of LYN (199 C-term amino acids).
Oncogenesis
ETV6-LYN is constitutively active: the PNT domain of ETV6 serves as an oligomerization domain and induces the constitutive activation of the tyrosine kinase domain from LYN through autophosphorylation; it directly activates STAT5A (17q21.2) and STAT5B (17q21.2) by phosphorylation, promotes the formation of proliferative colonies, and induces myeloproliferative neoplasms with myelofibrosis (Takeda et al., 2011).
Highly cited references
Pubmed IDYearTitleCitations
291530932017Next-generation sequencing and molecular cytogenetic characterization of ETV6-LYN fusion due to chromosomes 1, 8 and 12 rearrangement in acute myeloid leukemia.8
270582272016Myeloproliferative neoplasm with eosinophilia and T-lymphoblastic lymphoma with ETV6-LYN gene fusion.2
214921252011Direct activation of STAT5 by ETV6-LYN fusion protein promotes induction of myeloproliferative neoplasm with myelofibrosis.6
Bibliography
Pubmed IDLast YearTitleAuthors
214921252011Direct activation of STAT5 by ETV6-LYN fusion protein promotes induction of myeloproliferative neoplasm with myelofibrosis.Takeda Y et al
197107032010Identification of a novel TEL-Lyn fusion gene in primary myelofibrosis.Tanaka H et al
Summary
Fusion gene
ETV6/LYN ETV6 (12p13.2) LYN (8q12.1) TIC
Mesh
1
Citation
Jean-Loup Huret
ins(12;8)(p13;q11q21) ETV6/LYN
Atlas Genet Cytogenet Oncol Haematol. 2015-02-01
Online version: http://atlasgeneticsoncology.org/haematological/1535/ins(12;8)(p13;q11q21)-etv6-lyn
External Links
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ARTERIOSCLEROSIS AND IT’S NATURAL TREATMENT IN NIGERIA
ARTERIOSCLEROSIS AND IT’S NATURAL TREATMENT IN NIGERIA
WHAT IS ARTERIOSCLEROSIS?
Arteriosclerosis occurs when the blood vessels that carry oxygen and nutrients from your heart to the rest of your body (arteries) become thick and stiff sometimes restricting blood flow to your organs and tissues. Healthy arteries are flexible and elastic, but over time, the walls in your arteries can harden, a condition commonly called hardening of the arteries.
Atherosclerosis is a specific type of arteriosclerosis, but the terms are sometimes used interchangeably. Atherosclerosis refers to the buildup of fats, cholesterol and other substances in and on your artery walls (plaques), which can restrict blood flow.
These plaques can burst, triggering a blood clot. Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. Atherosclerosis may be preventable and is treatable.
SYMPTOMS
Atherosclerosis develops gradually. Mild atherosclerosis usually doesn’t have any symptoms.
You usually won’t have atherosclerosis symptoms until an artery is so narrowed or clogged that it can’t supply adequate blood to your organs and tissues. Sometimes a blood clot completely blocks blood flow, or even breaks apart and can trigger a heart attack or stroke.
Symptoms of moderate to severe atherosclerosis depend on which arteries are affected. For example:
IF YOU HAVE ATHEROSCLEROSIS IN YOUR HEART ARTERIES,you may have symptoms, such as chest pain or pressure (angina).
IF YOU HAVE ATHEROSCLEROSIS IN THE ARTERIES LEADING TO YOUR BRAIN,you may have signs and symptoms such as sudden numbness or weakness in your arms or legs, difficulty speaking or slurred speech, temporary loss of vision in one eye, or drooping muscles in your face. These signal a transient ischemic attack (TIA), which, if left untreated, may progress to a stroke.
IF YOU HAVE ATHEROSCLEROSIS IN THE ARTERIES IN YOUR ARMS AND LEGS,you may have symptoms of peripheral artery disease, such as leg pain when walking (claudication).
IF YOU HAVE ATHEROSCLEROSIS IN THE ARTERIES LEADING TO YOUR KIDNEYS,you develop high blood pressure or kidney failure.
CAUSES
Development of atherosclerosis
Atherosclerosis is a slow, progressive disease that may begin as early as childhood. Although the exact cause is unknown, atherosclerosis may start with damage or injury to the inner layer of an artery. The damage may be caused by:
High blood pressure
High cholesterol
High triglycerides, a type of fat (lipid) in your blood
Smoking and other sources of tobacco
Insulin resistance, obesity or diabetes
Inflammation from diseases, such as arthritis, lupus or infections, or inflammation of unknown cause
Once the inner wall of an artery is damaged, blood cells and other substances often clump at the injury site and build up in the inner lining of the artery.
Over time, fatty deposits (plaques) made of cholesterol and other cellular products also build up at the injury site and harden, narrowing your arteries. The organs and tissues connected to the blocked arteries then don’t receive enough blood to function properly.
Eventually, pieces of the fatty deposits may break off and enter your bloodstream.
In addition, the smooth lining of a plaque may rupture, spilling cholesterol and other substances into your bloodstream. This may cause a blood clot, which can block the blood flow to a specific part of your body, such as occurs when blocked blood flow to your heart causes a heart attack. A blood clot can also travel to other parts of your body, blocking flow to another organ.
RISK FACTORS
Hardening of the arteries occurs over time. Besides aging, factors that increase the risk of atherosclerosis include:
High blood pressure
High cholesterol
Diabetes
Obesity
Smoking and other tobacco use
A family history of early heart disease
Lack of exercise
An unhealthy diet
COMPLICATIONS
The complications of atherosclerosis depend on which arteries are blocked. For example:
CORONARY ARTERY DISEASE.When atherosclerosis narrows the arteries close to your heart, you may develop coronary artery disease, which can cause chest pain (angina), a heart attack or heart failure.
CAROTID ARTERY DISEASE.When atherosclerosis narrows the arteries close to your brain, you may develop carotid artery disease, which can cause a transient ischemic attack (TIA) or stroke.
PERIPHERAL ARTERY DISEASE.When atherosclerosis narrows the arteries in your arms or legs, you may develop circulation problems in your arms and legs called peripheral artery disease. This can make you less sensitive to heat and cold, increasing your risk of burns or frostbite. In rare cases, poor circulation in your arms or legs can cause tissue death (gangrene).
ATHEROSCLEROSIS CAN ALSO CAUSE ANEURYSMS, a serious complication that can occur anywhere in your body. An aneurysm is a bulge in the wall of your artery.
Most people with aneurysms have no symptoms. Pain and throbbing in the area of an aneurysm may occur.
If an aneurysm bursts, you may face life-threatening internal bleeding. Although this is usually a sudden, catastrophic event, a slow leak is possible. If a blood clot within an aneurysm dislodges, it may block an artery at some distant point.
CHRONIC KIDNEY DISEASE.Atherosclerosis can cause the arteries leading to your kidneys to narrow, preventing oxygenated blood from reaching them. Over time, this can affect your kidney function, keeping waste from exiting your body.
So, How Can I.A.& S. Wellness Centre Help Me Solve My Arteriosclerosis Problem?
The Best And Working Solution Is: ARTERIOSCLEROSIS SOLUTION KITS
FOR MORE DETAILS ON OUR ARTERIOSCLEROSIS TREATMENT
OUR ADDRESS:
3rd Floor, 473, Lagos-Abeokuta Express Way, UBA Building, U-turn Bus Stop, Abule Egba, Lagos, Nigeria.
Mon – Friday (9.00 a.m. – 5.00 p.m.) Nigerian Time
Saturday (10.00 a.m. – 2.00 p.m.) Nigerian Time
Our Office is Close on Sunday but you can Whatsapp, Call, Email Us.
WHATSAPP: (+234)-8178871052
CALL: 08178871052 OR +234-8038690104
EMAIL: [email protected]
The following are some of the treatments we offer Alphabetically (A-Z):
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Between 2007 and 2011, the researchers recruited 492 Dutch adults who had been diagnosed with tinnitus. The patients had to fulfil several criteria, including having no underlying disease that was causing their tinnitus, no other health issues that precluded their participation, and to have received no treatment for their tinnitus in the five previous years. Some 66% of adults originally screened for the study participated after screening.
Most tinnitus is "sensorineural," meaning that it's due to hearing loss at the cochlea or cochlear nerve level. But tinnitus may originate in other places. Our bodies normally produce sounds (called somatic sounds) that we usually don't notice because we are listening to external sounds. Anything that blocks normal hearing can bring somatic sounds to our attention. For example, you may get head noise when earwax blocks the outer ear.
Smoking. Contrary to popular belief, there are some external irritants that can cause tinnitus. For example, Nicotine has been proven to be an irritant that can cause someone to develop a ringing in their ears. Smokers may find that their chances of developing the condition may be higher than someone who is a non-smoker. If you’re suffering from tinnitus right now, and you’re a smoker, please quit as soon as possible. If that’s just not an option for you right now, be sure to at least pick up an over the counter tinnitus treatment that will dramatically reduce the ringing in your ears.
Tinnitus is commonly accompanied by hearing loss, and roughly 90% of persons with chronic tinnitus have some form of hearing loss (Davis and Rafaie, 2000; Lockwood et al, 2002). On the other hand, only about 30-40% of persons with hearing loss develop tinnitus. According to Park and Moon (2004), hearing impairment roughly doubles the odds of having tinnitus, and triples the odds of having annoying tinnitus.
Approximately 50 million Americans have some form of tinnitus. For most people, the sensation usually lasts only a few minutes at a time. About 12 million people have constant or recurring tinnitus that interferes with their daily life so much that they seek professional treatment. For these individuals, tinnitus may result in a loss of sleep, interfere with concentration, and create negative emotional reactions such as despair, frustration, and depression.
These tests are usually performed instead of a traditional catheter angiography, which is more invasive and, while generally very safe, carries greater risk of complications. Angiography is an imaging technique that involves injecting dye into a small tube called a catheter that has been inserted into a blood vessel. An x-ray is then performed to assess the health of the vessels as well as the rate of blood flow.
Español: curar el tinnitus (zumbido de oídos), Deutsch: Tinnitus heilen, 中文: 治疗耳鸣, Italiano: Curare l’Acufene, Русский: вылечить тиннитус, Français: soigner des acouphènes, Português: Curar Zumbido no Ouvido, Bahasa Indonesia: Mengobati Tinitus, Nederlands: Tinnitus genezen, Čeština: Jak vyléčit tinnitus, العربية: علاج طنين الأذن, Tiếng Việt: Trị ù tai, 한국어: 이명을 치료하는 방법, हिन्दी: कर्णनाद (टिनिटस) का इलाज़ करें, 日本語: 耳鳴りの治療
When we hear, sound waves travel through the ear into the cochlea, our hearing organ in the inner ear. The cochlea is lined with thousands of tiny sound-sensing cells called hair cells. These hair cells change the sound waves into electrical signals. The hearing nerve then sends these electrical signals to the hearing part of the brain, which analyses them and recognises them as sound.
Prolonged exposure to loud sounds is the most common cause of tinnitus. Up to 90% of people with tinnitus have some level of noise-induced hearing loss. The noise causes permanent damage to the sound-sensitive cells of the cochlea, a spiral-shaped organ in the inner ear. Carpenters, pilots, rock musicians, street-repair workers, and landscapers are among those whose jobs put them at risk, as are people who work with chain saws, guns, or other loud devices or who repeatedly listen to loud music. A single exposure to a sudden extremely loud noise can also cause tinnitus.
Don't give up on things unless you are sure they are having some effect, especially if it's something you enjoy; or you could end up feeling miserable and deprived for no reason. Do not give up several things at once, or you will not know which one was affecting your tinnitus. If you decide to limit these things and fancy the occasional treat, maybe try using the other strategies (such as relaxation) for those times when your tinnitus is a bit louder. For more details, see our information on Food, drink and tinnitus.
While there may be a wide range of causes, an important underlying factor for the development of tinnitus is brain plasticity.5,7 This property allows the brain to change and adapt, and it is essential to how we learn. Unfortunately, in some cases, such as with hearing loss, the auditory part of the brain may be altered as brain plasticity tries to compensate for the abnormal auditory inputs. This response leads to changes in brain activity in the auditory system (e.g., the auditory cortex) that can create a phantom percept: tinnitus. As such, while tinnitus may begin a problem at the auditory periphery, it persists because of changes throughout the auditory system. Treating tinnitus may require addressing both the initiator (e.g., hearing loss) and the driver (changes in the auditory brain).
In persons with pulsatile tinnitus, additional tests maybe proposed to study the blood vessels and to check the pressure inside the head. Gentle pressure on the neck can be performed to block the jugular vein but not the carotid artery. The Valsalva maneuver reduces venous return by increasing intrathoracic pressure. If there is a venous hum, this usually abates or improves markedly. If the pulsation is arterial, these tests have no effect.
With respect to incidence (the table above is about prevalence), Martinez et al (2015) reported that there were 5.4 new cases of tinnitus per 10,000 person-years in England. We don't find this statistic much use as tinnitus is highly prevalent in otherwise normal persons. It seems to us that their study is more about how many persons with tinnitus were detected by the health care system -- and that it is more a study of England's health care system than of tinnitus.
Inspection of the eardrum may sometimes demonstrate subtle movements due to contraction of the tensor tympani (Cohen and Perez, 2003). Tensor tympani myoclonus causes a thumping. Another muscle, the stapedius, can also make higher pitched sounds. See this page for more. Opening or closing of the eustachian tube causes a clicking. The best way to hear "objective tinnitus" from the middle ear is simply to have an examiner with normal hearing put their ear up next to the patient. Stethoscopes favor low frequency sounds and may not be very helpful.
Exposure to Loud Noise: Exposure to loud or excessive noise can damage or destroy hair cells (cilia) in the inner ear. Because the hair cells cannot be renewed or replaced, this can lead to permanent hearing loss and/or tinnitus. Continued exposure can worsen these conditions, so people who work in loud environments should always wear ear protection. This includes musicians, air traffic controllers, construction workers, military personnel, and first responders. In addition, consider lowering the volume on your iPod and wearing earplugs at loud concerts.
Patulous Eustachian tubes can be associated with tinnitus. The Eustachian tube is a small canal that connects the middle ear to the back of the nose and upper throat. The Eustachian tube normally remains closed. In individuals with a patulous Eustachian tube, the tube is abnormally open. Consequently, talking, chewing, swallowing and other similar actions can cause vibrations directly onto the ear drum. For example, affected individuals may hear blowing sounds that are synchronized with breathing.
Take the first step toward relief by scheduling a consultation with one of our audiologists. By carefully examining your case history and conducting audiometric testing, we can identify the likely causes of your tinnitus and recommend an effective treatment. In addition, if medically necessary, we may refer you to another physician to complete your diagnosis.
Overdosing on certain prescription drugs, recreational drugs or alcohol. This can sometimes cause permanent damage to nerves that affect hearing. In some cases when a pregnant women uses drugs during pregnancy, this can cause tinnitus to develop in her child. Common drugs that might contribute to tinnitus include ototoxics, psychotropic drugs, aminoglycosides, certain antibiotics and vancomycin.
Medications, Prescription Drugs and Food Additives. Other external irritants that can cause tinnitus are over the counter medications and prescriptions. Even something as simple as aspirin can generate tinnitus. I have experienced this throughout my lifetime. I take aspirin only when I absolutely need it. Certain antibiotics and other prescription drugs are also known to cause tinnitus. Two very common ones that have shown to cause tinnitus are quinine and chloroquine which are in malaria medications. Certain diuretics and cancer medications can also cause tinnitus. Although not a drug, NutraSweet has been linked to tinnitus and a whole host of side effects in clinical studies.
Cartoon of the middle ear showing muscles that attach to ossicles (ear bones), and ear drum. The stapedius is attached to the stapes (of course -- horseshoe object above), while the tensor tympani is attached to the ear drum. While useful, be aware that there are multiple errors in this illustration from Loyola Medical School. With permission, from: http://www.meddean.luc.edu/lumen/meded/grossanatomy/dissector/mml/images/stap.jpg
The multidisciplinary approach required input from many different professionals including audiologists, psychologists, speech therapists and physical therapists. Which particular care elements of the intervention had the greatest effect is unknown. A multidisciplinary approach such as the intervention trialled here may have resource implications if it were introduced into standard clinical practice.
Tinnitus matching is helpful to identify the frequency and intensity of the tinnitus. This is a simple procedure in which the audiologist adjusts a sound until a patient indicates that it is the same as their tinnitus. Most patients match their tinnitus to the region of their hearing loss (Konig et al, 2006; Mahboubi et al, 2012). Unfortunately, the "gap detection test", does not work to confirm tinnitus in humabs (Boyen et al, 2015).
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Though the exact cause of tinnitus — as in the specific mechanism that creates these phantom sounds in some people — remains unknown, contributing factors and triggers have been identified. Excessive exposure to loud noise is often a factor because of the damage done to your auditory system. Tinnitus may also result from jaw-joint dysfunction (e.g., teeth grinding, temporomandibular joint disorder) or chronic neck muscle strain.
Most of the causes of tinnitus alter neurological activity within the auditory cortex, the portion of the brain responsible for hearing. The transmission of sound is interrupted, so some of the neural circuits fail to receive signals. Instead of causing hearing loss, as you might expect due to the lack of stimulation, the neural circuits begin chattering. First, they chatter alone. Then, they become hyperactive and synchronous. When we experience this deviation, our brains attempt to compensate for the change by interpreting the neurological activity as sound. This can resemble ringing, buzzing, hissing, whistling, or roaring, amongst a variety of other noises.
Tinnitus – a sound in the head with no external source – is not a disease; it is a symptom that can be triggered by a variety of different health conditions. So what causes tinnitus? Common sources include hearing loss, ear wax buildup, ototoxic medications, and ear bone changes. No matter what the cause, the condition interrupts the transmission of sound from the ear to the brain. Some part of the hearing system is involved as well, whether the outer, middle, or inner ear.
Patients with head or neck injury may have particularly loud and disturbing tinnitus (Folmer and Griest, 2003). Tinnitus due to neck injury is the most common type of "somatic tinnitus". Somatic tinnitus means that the tinnitus is coming from something other than the inner ear. Tinnitus from a clear cut inner ear disorder frequently changes loudness or pitch when one simply touches the area around the ear. This is thought to be due to somatic modulation of tinnitus. We have encountered patients who have excellent responses to cervical epidural steroids, and in persons who have both severe tinnitus and significant cervical nerve root compression, we think this is worth trying as treatment.
Tinnitus (pronounced "tin-it-tus") is an abnormal noise in the ear (note that it is not an "itis" -- which means inflammation). Tinnitus is common -- nearly 36 million Americans have constant tinnitus and more than half of the normal population has intermittent tinnitus. Another way to summarize this is that about 10-15% of the entire population has some type of constant tinnitus, and about 20% of these people (i.e. about 1% of the population) seek medical attention (Adjamian et al, 2009). Similar statistics are found in England (Dawes et al, 2014) and Korea (Park and Moon, 2014).
Many of the press headlines mentioned that listening to the sound of the sea could help tinnitus, with the Metro claiming this could cure the condition. However, sound therapies that try to neutralise tinnitus using soothing sounds, such as waves or birdsong, are not new, but are part of standard treatments for this condition. Also, the report in the Lancet did not state what kind of sounds were used as therapy. Sound therapy was not the only treatment approach used, but was given as part of a specialised treatment programme delivered by expert health professionals.
This tinnitus treatment we developed makes use of software that customizes a music-based therapy for each individual tinnitus sufferer. The software achieves this by incorporating a computational model of the “tinnitus brain.” This model captures changes in the auditory brain which may be causing the tinnitus.5,7 We do this by taking into account the individual’s audiogram and a pitch match of their tinnitus, which generates a tinnitus profile unique to him or her. The software then uses the model to predict how each music track can be altered spectrally to reduce tinnitus for that specific tinnitus profile. Delivering the treatment using headphones that could produce high frequencies (above 10–12 kHz) was an integral part of treatment effectiveness. With such headphones, the treatment could work by taking advantage of the same kind of brain plasticity that may contribute to the person's tinnitus in the first place without being limited by a lack of high-frequency sounds.8 By incorporating the latest tinnitus research into our software, we developed a treatment approach that provides greater promise in treating tinnitus than existing treatments with a one-size-fits-all approach.
Even with all of these associated conditions and causes, some people develop tinnitus for no obvious reason. Most of the time, tinnitus isn’t a sign of a serious health problem, although if it’s loud or doesn’t go away, it can cause fatigue, depression, anxiety, and problems with memory and concentration. For some, tinnitus can be a source of real mental and emotional anguish.
Think about your breathing. Notice that it has a natural rhythm. Try to breathe in a steady, even rhythm. It helps to breathe in through your nose, hold your breath for a moment and then breathe out through your mouth. Wait a moment before breathing in again. Every time you breathe out, try to release a little bit of your tension. Do this for a few minutes, until you feel ready to move on to the next step.
Tinnitus can occur as a sleep disorder - -this is called the "exploding head syndrome". This most often occurs while falling asleep or waking up. It is a tremendously loud noise. Some theorize that this syndrome is due to a brief seizure in auditory cortex. It is not dangerous.(Green 2001; Palikh and Vaughn 2010). Logically, anticonvulsants might be useful for treatment.
Sound waves travel through the ear canal to the middle and inner ear, where hair cells in part of the cochlea help transform sound waves into electrical signals that then travel to the brain's auditory cortex via the auditory nerve. When hair cells are damaged — by loud noise or ototoxic drugs, for example — the circuits in the brain don't receive the signals they're expecting. This stimulates abnormal activity in the neurons, which results in the illusion of sound, or tinnitus.
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%0 Journal Article %A Naquet, P %A Ellis, J %A Tibensky, D %A Kenshole, A %A Singh, B %A Hodges, R %A Delovitch, T L %T T cell autoreactivity to insulin in diabetic and related non-diabetic individuals. %D 1988 %J The Journal of Immunology %P 2569-2578 %V 140 %N 8 %X T cell autoreactivity to insulin in type I diabetic and related non-diabetic individuals was analyzed. Peripheral T lymphocytes from both insulin-treated diabetic and untreated non-diabetic members of four families were found to proliferate in vitro in response to human insulin. T cell autoreactivity to insulin therefore does not appear to be diagnostic of the onset of type I diabetes. Highest T cell responses to human insulin were usually detected in insulin-dependent type I diabetes patients treated with a mixture of beef and pork insulin than with self insulin, the greater the dose of animal insulin the higher the T cell response. The T cell repertoires for self insulin appear to be similar in diabetics and non-diabetics based on their patterns of T cell reactivity to beef insulin, port insulin, human insulin, and various peptide of human insulin. The autoreactive T cells analyzed recognize two conformational epitopes of human insulin formed by interactions between A chain and B chain residues. One epitope is associated with the A chain loop and is present in the A1-A14/B1-B16 peptide, and the other epitope consists mainly of B chain residues located in the A16-A21/B10-B25 peptide. These two epitopes are present in amphipathic alpha-helical regions of insulin. HLA-DR (DR3, DR4, and DR5) and HLA-DQ (DQw2/DQw3) Ag can restrict these T cell responses to human insulin epitopes. The ability to detect insulin-specific autoreactive T cells in healthy non-diabetic individuals supports the hypothesis that autoreactive lymphocytes do not necessarily elicit autoimmune disease if present in an environment in which their activity is immunoregulated. %U https://www.jimmunol.org/content/jimmunol/140/8/2569.full.pdf
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Pathological changes on joints: the commonest changes are symmetrical pain, swell and morning stiffness on the side joints of bilateral digits. As a systematic autoimmune disease, the rheumatoid arthritis cannot only affect on joints, but in addition on the vessels of the entire body, and result in angionecrosis and haemorrhagia, hurt on tissues and organs as heart, lung, liver, spleen, kidney, muscle tissue, skin and nerves.
Occupational Health Nurse
Ask questions in regards to the following facilities to determine whether or not you’d feel snug leaving your loved one with them. Medical transcription in India has grow to be one of the wanted fields in relation to the occupation of medicine. There are many causes for this. Earlier than going there, let us first see what exactly is a medical transcription.
Health Quotes Inspirational
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Open Enrollment Health Insurance 2017
So, what are doctors going to do. Things will change and also you better change as effectively. The paperwork will probably be burdensome, and also you higher figure it out. If it matches the developments we are seeing now, there shall be extra. The big factor with these varieties, paperwork, and so on, is that someone most likely already did it. Why re-invent the wheel? The attraction letter you need, office type you want, letter of self-discipline you need, someone in all probability already wrote it! Why would you spend hours fixing it your self? There are two things you are allowed to do in your observe. 1. Treat Sufferers. 2. Work on your enterprise. Don’t do the rest.
Pinnacle Health Portal
As we requires the entire therapy for damage or sickness in a identical manner animals also requires a proper and complete remedy for sustaining life properly without ache. When selecting senior care service at home, home service for the disabled, pediatric home care, in-dwelling nursing it is important to make certain shoppers are safe and safe.
Abrazo Health
For a very long time, we now have used X-Ray know-how to get a higher glimpse contained in the body. This has helped us not solely get a higher understanding of our biology, but to diagnose and extra deal with most cancers and numerous completely different inside diseases, as successfully to pinpoint the situation and severity of bodily injury principally related to bone fracture. There was one simple quick-coming with this earlier technique: the photographs produced by typical X-Rays have been -dimensional, and the bodily world, together with the physique, is three-dimensional. Clearly, any ensuing footage that lacked this third dimension would prohibit our full view of the inner body.
Article Conclusion
Our health discount card covers over 26,000 amenities that are out there within the hospital, as an example, labs, clinics, radiology, and diagnostic companies etc., where you may get from 30-60{a371e1390ed79323c9c56b0a6b34e82455af9bcdb193faabad25ddee08d0f5ec}. If you’re a resident of Maryland, be certain that you review many dwelling care companies in Maryland. Now you can keep in the loop with our social activity at the click of a ‘like’ button.
Writer Bio
28 year old Aircraft Preservation Manufacture (Avionics) Breyfogle from Gimli, has several hobbies and interests which include playing team sports, . and yoyo. Was these days visiting Mana Pools National Park.
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Diesel exhaust particles modulate the tight junction protein occludin in lung cells in vitro
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Abstract
Background
Using an in vitro triple cell co-culture model consisting of human epithelial cells (16HBE14o-), monocyte-derived macrophages and dendritic cells, it was recently demonstrated that macrophages and dendritic cells create a transepithelial network between the epithelial cells to capture antigens without disrupting the epithelial tightness. The expression of the different tight junction proteins in macrophages and dendritic cells, and the formation of tight junction-like structures with epithelial cells has been demonstrated. Immunofluorescent methods combined with laser scanning microscopy and quantitative real-time polymerase chain reaction were used to investigate if exposure to diesel exhaust particles (DEP) (0.5, 5, 50, 125 μg/ml), for 24 h, can modulate the expression of the tight junction mRNA/protein of occludin, in all three cell types.
Results
Only the highest dose of DEP (125 μg/ml) seemed to reduce the occludin mRNA in the cells of the defence system however not in epithelial cells, although the occludin arrangement in the latter cell type was disrupted. The transepithelial electrical resistance was reduced in epithelial cell mono-cultures but not in the triple cell co-cultures, following exposure to high DEP concentration. Cytotoxicity was not found, in either epithelial mono-cultures nor in triple cell co-cultures, after exposure to the different DEP concentrations.
Conclusion
We concluded that high concentrations of DEP (125 μg/ml) can modulate the tight junction occludin mRNA in the cells of the defence system and that those cells play an important role maintaining the epithelial integrity following exposure to particulate antigens in lung cells.
Background
With every breath millions of ambient particles enter the respiratory tract, where they may cause adverse health effects associated with increased pulmonary and cardiovascular mortality [14]. Important components of ambient particulate matter (PM) are diesel exhaust particles (DEP), which are comprised of a carbon core that absorbs a mixture of metals and organic chemicals [5]. Nearly all these particles have sizes less than 1 μm, and the majority of those particles are known as ultrafine particles with a diameter less than 0.1 μm [6]. Due to the small size of DEP, they can even reach the bronchiolar and alveolar levels of the lung and up to 33% of the inhaled particles are deposited in the respiratory tract [7]. In several in vitro studies, it was shown that DEP can penetrate into the epithelial cells (16HBE14o-) [8, 9] and that inhalation of high concentrations of DEP affect respiratory function in humans (see review [10]). Therefore the airway epithelial cells are directly affected by air pollution and may play a key role in the pathophysiology of airway diseases.
Among several structural and functional barriers which protect the respiratory system against PM (for a review see [11, 12]), epithelial cell layers endowed with tight junctions (TJ) [13, 14] are one of the most important. TJ separate the epithelium in an apical and a basal site and control the paracellular transport, by preventing macromolecules from easily passing through the epithelial layer for example. In addition, a population of macrophages in the airways and in the alveoli [15, 16], and a network of dendritic cells (DC) underneath and inside the epithelium [1719] are other important parts which contribute to the functionality of the barrier.
Of particular importance and interest is how inhaled particulate antigens come into contact with DC, which realize, as sentinels and most competent antigen presenting cells, a surveillance network in the pulmonary tissues [1921]. The mechanism of how DC can penetrate TJ of the epithelium is not completely understood [22]. Studies with mice [23] and with an in vitro model of the gut epithelium [24, 25] have shown that DC express TJ proteins and it was assumed that DC build TJ-like complexes with epithelial cells in order to preserve the epithelial integrity. Using an in vitro triple cell co-culture model of the human airway wall [26, 27] it was recently shown that human blood monocyte-derived dendritic cells (MDDC), as well as human blood monocyte-derived macrophages (MDM) express TJ proteins and mRNA (occludin, Claudin-1, zonula occludens 3 (ZO-3), junctional adhesion molecule 1 (JAM-1) and the Adherens Junctions (AJ) mRNA and protein E-cadherin) [28]. Moreover it has been shown that processes of DC residing under the epithelium can penetrate beyond well developed epithelial TJ to sample particles and to transport them to the basal side of the epithelium [24, 25, 27, 29, 30].
As previously published, large particles can be sampled by the cells of the defence system and therefore overcome the epithelial airway barrier. This has also been shown for nanosized particles (NP) in the triple cell co-culture system, although the translocation characteristics of fine particles compared to NP was different [31]. Furthermore it has been demonstrated that inhaled NP quickly left the lungs and were detected in the extra-pulmonary tissue [32, 33].
This data emphasizes the importance to study the effect of airborne PM on the epithelia and the epithelial integrity. If there are any alterations in the integrity of the epithelial barrier more attention has to be focused on the fate of inhaled nanosized, as well as larger particles, because the epithelia is not able to fulfil its barrier function. Following cigarette smoke exposure to Calu-3 cells, amongst others, it was found that there was a displacement of occludin and Zonula occludens 1 (ZO-1) and thus increasing ionic and macromolecular permeability. It was hypothesized that the loss of TJ integrity and barrier function was due to a decreased ZO-1: occludin association ratio [34].
The aim of the present study was to determine the extent to which DEP affect the integrity of the airway wall, by focussing on the expression of the TJ protein occludin in epithelial cells (EC), MDM and MDDC (which all contribute to the integrity of the airway wall as previously mentioned) after exposure to different amounts of DEP. The plasticity alteration of TJ is known [35], therefore the mRNA and protein levels of the occludin were investigated for changes, upon particle exposure. For this purpose mono-cultures of MDM and MDDC as well as of the bronchiolar cell line 16HBE14o- were used and exposed to different concentrations of DEP particles or to the inflammatory stimulus Lipopolysaccharide (LPS) for 24 h. Transepithelial electrical resistance (TEER) was measured in the EC mono-cultures and in the triple cell co-cultures. Cytotoxicity was assessed by Lactate dehydrogenase (LDH) measurement and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFα) was determined by ELISA. The spatial localisation of occludin in the different cell types was investigated by laser scanning microscopy (LSM) and the TJ arrangement by transmission electron microscopy (TEM).
Results
DEP is taken up by all cell types
In a first step, the DEP exposed cells were studied by TEM. As shown in Fig. 1, DEP (125 and 0.5 μg/ml) could clearly be seen in membrane bound vesicles inside EC in the triple cell co-culture system independent of the dose used, indicating that DEP was taken up by the cells. Cells exposed to 125 μg/ml showed higher amounts of internalized DEP, however this was only a qualitative observation and was not quantified. DEP was found in all investigated cell types in mono-cultures (shown in this study) as well as in the three cell types of the triple cell co-cultures, as already shown in a recently published paper from our group [36].
Figure 1
figure1
Internalized DEP in an epithelial cell. TEM images of 16HBE14o- cells in the triple cell co-culture model showing internalized DEP. Cells were exposed to 125 μg/ml DEP (A) and 0.5 μg/ml DEP (B) for 24 h and then processed for TEM. A detailed view from A and B (white square) is shown in A'and B'.
TJ between ECs and TJ-like structures between EC and MDM
The cell-cell junctions in 16HBE14o- cells are shown in Fig. 2A. The junction complex consisting of desmosomes, AJ and TJ are well defined as determined with TEM. In addition, it was also shown with TEM that EC and MDM build TJ-like complexes. Since MDM are very difficult to find with TEM in the triple cell co-culture system, the MDM were exposed to gold NP before they were added to the epithelial cells. In Fig. 2B the MDM has clearly been identified by intracellular, membrane-bound gold particles (Fig. 2B2, black arrow). Cell junctions similar to the ones seen between EC were identified (Fig. 2B1, white arrow).
Figure 2
figure2
TJ between EC and between EC and MDM. TEM images showing untreated cells in the triple cell co-culture model in A. The tight junctions (TJ) the adherens junctions (AJ), as well as the desomosomes (D) between two neighbouring EC are shown in the detailed view in A1. TJ-like structures (white arrows, B1 and B2) between a MDM and two neighbouring EC in the triple cell co-culture model is shown in overview in B. B1 and B2 are detailed views. The morphology and as well as the internalized gold NP (black arrow in B2) prove that the described cell is a MDM.
DEP exposure affects the amount and the distribution of occludin protein in EC, MDM, and MDDC
The arrangement of the TJ was analysed by focusing on the transmembrane protein occludin. Visualization was done using LSM and digital image restoration, as described in an earlier publication [30]. DEP treated (125 μg/ml) and untreated EC were stained for F-actin cytoskeleton and occludin (Fig 3A, B). The iso-rendering of occludin revealed an intact and clear belt-like structure of the TJ protein, occludin, in the untreated EC mono-cultures (3A'). Although occludin is detectable in the DEP treated mono-cultures, the belt like arrangement of the TJ is not as structured (Fig. 3B') as in the untreated mono-cultures (Fig. 3A'). The amount and the arrangement of F-actin were not affected by the DEP treatment (Fig. 3A, B). Mono-cultures of MDM and MDDC were also stained for occludin (Fig. 3C-F). The pictures clearly showed that after DEP treatment the amount of occludin was reduced in MDM (D') as well as in MDDC (F').
Figure 3
figure3
Laser scanning micrographs of occludin in EC, MDM and MDDC. The occludin arrangement in 16HBE14o-, MDM and MDDC mono-cultures visualized with LSM. Control 16HBE14o- cells (A) and DEP exposed 16HBE14o- cells (B) were labelled for F-actin (turquoise) and occludin (red). For F-actin no qualitative difference was found between control and treated cells. However, the iso-surface presentation of occludin in control cells (A') showed a more structured TJ occludin belt compared with DEP treated cells (B") which shows a predominant localization of occludin in the cytoplasm. Occludin was visualized in mono-cultures of MDM (D, control; C, DEP treatment) and MDDC (E, control; F, DEP treatment). Cells were stained for F-actin (in MDM white, in MDDC black and occludin (shown in red). MDM and MDDC expressed the TJ protein occludin. After exposure to DEP for 24 h occludin signals were reduced (for MDM in D' and MDDC in F'). These are representative images and for all pictures the same settings were used.
DEP does not significantly affect the occludin mRNA expression in EC, MDM, and MDDC
To examine if the mRNA level of occludin was quantitatively different after DEP treatment, the amount of mRNA in mono-cultures of EC, MDM and MDDC was determined using qRT-PCR. MDM and MDDC were exposed to different doses of DEP, ranging from low to high concentrations (0.5 μg/ml, 5 μg/ml, 50 μg/ml, and 125 μg/ml). EC were only exposed to the highest amount of DEP because preliminary experiments showed no changes upon exposure to lower DEP concentrations. Although the results were not significant, there was a tendency that the highest dose of DEP reduced the occludin mRNA level in MDM and MDDC (Fig. 4). The expression level of occludin in EC was significantly more than 100 times higher compared to MDM and MDDC, as also previously shown in [28].
Figure 4
figure4
mRNA expression levels of occludin in EC, MDM and MDDC. Quantification of occludin mRNA expression in MDM, MDDC, and EC mono-cultures by qRT-PCR. Threshold of occludin was set by the threshold of the housekeeping gene β-actin in each sample (ΔCT). Expression levels of occludin are illustrated by the β-actin normalized concentrations (2-ΔCT × 15000). cDNA derived from MDM (grey columns), MDDC (black columns) and 16HBE14o- (white columns) control cells and cells treated with DEP (0.5 μg/ml, 5 μg/ml, 50 μg/ml, and 125 μg/ml). Values are presented as means ± SD; * p ≤ 0.05. All experiments were independently performed between 4-7 times.
DEP exposure affects TEER in 16HBE14o- mono-cultures but not in triple cell-co-cultures
To examine whether there was a change in the epithelial integrity in EC mono- and triple cell co-cultures, the TEER was measured before and after 24 h exposure to DEP (125 μg/ml). In mono-cultures, the TEER after DEP treatment was significantly reduced (p = 0.029) compared to control cultures, as shown in Fig. 5A. In triple cell co-cultures there was no difference in the TEER levels found between control and DEP treated cultures (Fig. 5B). The epithelial integrity of untreated triple cell co-cultures compared to the mono-cultures was significantly lower (p = 0.024) (Fig. 5).
Figure 5
figure5
Epithelial integrity of EC mono- and triple cell co-cultures. TEER in16HBE14o- mono-cultures (A) and triple cell co-cultures (B) before (white bars) and after (black bars) exposure to high dose of DEP (125 μg/ml) or normal medium (control) for 24 h. TEER in mono-cultures was significantly lower after DEP treatment than before addition of DEP (A, *). Data are presented as means ± standard deviation (SD); * p ≤ 0.05. All experiments were independently done in triplicate.
DEP exposure (of up to 125 μg/ml) does neither affect cytotoxicity nor TNFα levels in EC mono-cultures, and in triple cell co-cultures
To ensure that the reduced TEER in mono-cultures was not due to increased cell death the cytotoxicity of the highest DEP concentration was investigated by measurements of LDH release in the triple cell co-cultures and in EC mono-cultures. The difference of the LDH release into the cell culture medium was not significant between the controls and the DEP exposed cells (Fig. 6).
Figure 6
figure6
Cytotoxicity of EC mono- and triple cell co-cultures. LDH (a marker for membrane permeability) levels were determined. The values did not change significantly after DEP exposure in epithelial mono-cultures (A) and triple cell co-cultures (B). Data are presented as mean ± SD of 3 experiments.
The pro-inflammatory response related to DEP exposure was measured by the TNFα levels in the supernatants from EC mono-cultures and from the triple cell co-cultures by ELISA (Fig. 7). There was no significant difference in the TNFα amount between control cultures and cells exposed to different DEP concentrations. LPS was used as positive control and resulted in an enhanced release of TNFα into the supernatants in the triple cell co-culture.
Figure 7
figure7
TNFα release in EC mono- and triple cell co-cultures. TNFα release in mono-cultures (A) and triple cell co-cultures (B) upon exposure to DEP for 24 h. TNFα concentrations were expressed as mean ± SD of 4-5 experiments. DEP treated EC mono-cultures and the triple cell co-cultures showed no difference in TNFα concentration in comparison to the respective untreated cells. No differences between mono-cultures and triple cell co-cultures concerning TNFα levels were found. LPS stimulated cultures were used for the positive control.
Dynamics of TJ in the EC mono-cultures and triple co-cultures under EDTA treatment
To test whether the absence of change in TEER, in the triple cell co-culture model, may be due to different exposure kinetics (i.e. that the cells in the 3-dimensional configuration may be less sensitive), a Ca2+ chelator was used which is known to open the TJ. Adding Ethylenediaminetetraacetic acid (EDTA) as a Ca2+ chelator, the TEER values of mono-cultures as well as those of triple cell co-cultures were reduced in a time-dependent manner (Fig. 8A and 8B). In the mono-cultures, as well as in the triple cell co-cultures, the TEER value decreased about 300 ohm × cm2 per hour, showing the same TJ kinetics. The untreated control cultures showed no change in TEER.
Figure 8
figure8
Opening of the TJ in EC mono- and triple cell co-cultures. TEER values after EDTA treatment (grey lines) over one hour in mono-cultures (A) and in triple cell co-cultures (B). Untreated controls are presented in black.
Discussion
It is known that DEP can negatively influence human health. However, the question is still unclear as to how inhaled DEP and other particulate matter can penetrate into the blood flow. At least it seems that the barrier which separates the air from the blood must be crossed. Therefore, the influence of DEP on the TJ protein occludin was examined. It was already shown that the TJ play a key role in the regulation of paracellular transport [34]. Without intact TJ arrangements the epithelial layer would not remain tight, and there would be leakage, allowing deposited particles an enhanced translocation across the barrier.
The effect of DEP exposure on the expression of the TJ protein and mRNA occludin was studied in mono-cultures of MDM, MDDC and the epithelial cell line. Moreover the epithelial mono-cultures of EC were compared to the triple cell co-culture model of the epithelial airway barrier, which has been previously described and characterized [26, 27, 37]. The triple cell co-culture model mimics the natural architecture of the in vivo epithelial airway and is accepted and used per se in several studies [26, 30, 37, 38]. The cells of the defence system used in the triple cell co-culture model have similar functional and structural characteristics as the ones in human lung [39]. The bronchial epithelial cell line 16HBE14o- used in the present study, forms polarized monolayers with extensive TJ belts which were also verified with TEM technique. Therefore, this cell line is a useful tool to study TJ-properties, such as biogenesis, regulation and breakdown, which may in turn prove to be useful paradigms of the permeability functions of human bronchiolar epithelium, especially in studies of TJ assembly and disassembly [40, 41]. Additionally the presence of intact TJ in this cell line was shown to release pro-inflammatory cytokines in response to DEP [8]. In a previous study, it was already shown that EC, and also MDM and MDDC, express the TJ proteins claudin-1, ZO-3, JAM-1 as well as the adherens junction protein E-Cadherin. [28] For an initial evaluation of the ability of DEP to influence the TJ, the current study primarily focused on the TJ mRNA and protein occludin and its cellular localization because it was shown that the extracellular domains of this protein are important for correct localization of occludin in the TJ-complex and for the regulation of the paracellular permeability barrier [42]. The influence of DEP on TJ proteins other than occludin will be the aim of further studies. As a surrogate for DEP, the standardized and characterized Diesel Particulate matter (SRM Nr. 2975; National Department of Standards and Technology, Gaithersburg, USA) were used. Similar concentrations as used in other studies [5, 8, 9, 43, 44] were applied but with the understanding that the highest used dose (125 μg/ml), exceeds doses which occur in realistic exposure scenarios. However, concentration series are important to determine if a threshold dose exists or not.
DEP were visualized inside EC of the triple cell co-culture model as well as in mono-cultures of EC, MDM and MDDC. This was in agreement with other studies which showed an intracellular localization of DEP in the EC line 16HBE14o- as well as in MDM and MDDC [8, 36, 45]. DEP aggregates were mostly found in membrane bound vesicles, but so far single DEP particles or smaller aggregates in the nucleus have not been detected with conventional TEM, as described in the study of Boland et al. [8]. It is very difficult to detect single DEPs or small aggregates with conventional TEM. Sophisticated TEM methods, such as electron energy loss spectroscopy, would be needed to detect specific metals associated with the DEPs.
The epithelial integrity in the triple cell co-cultures did not change after exposure to high concentrations of DEP (125 μg/mL). However, when EC mono-cultures were exposed to the same DEP dose the TEER was significantly reduced. In the triple cell co-cultures the total number of cells is slightly higher due to the additional MDM and MDDC. The number of MDM and MDDC is similar to the in vivo situation of the human lung [30]. It was hypothesised that this would lead to a lower DEP burden per cell. MDM which are positioned at the apical side of the epithelium [15, 16, 46] might phagocyte the main amount of deposited DEP, thus the DEP load to the EC layer in the triple cell co-culture model may be lower than that of the EC mono-cultures. This could also explain why, after exposure with the highest concentration of DEP, no effect on EC integrity in the triple cell co-culture model could be measured. This finding shows the importance of those professional phagocytes [46] and the significance of using more realistic co-cultures, such as the triple-cell co-culture model used in this study. However, the control EC as well as DEP exposed mono-cultures showed higher TEER compared to the triple cell co-cultures. The interactions of the MDM and MDDC within the epithelium may explain the lower TEER values. On the one hand the EC cells are probably less tightly connected in the EC layer due to the interactions with the cells of the defence system but on the other hand, the TJ-like structures between EC and MDM, MDDC may be able to prevent a leakage barrier. Such TJ like structures could be visualized with TEM. Due to the morphology, the position on the EC layer and the intracellular gold NP it was possible to define the cell in the triple cell co-culture model as MDM, which make TJ-like junctions with the two neighbouring ECs. Recently it was shown that MDM and MDDC are able to interact in the triple cell co-culture as a transepithelial network, by building cytoplasmic processes (with their pseudopodia) between EC, which could lead to an opened TJ-belt of the epithelial cells. However, since this study has shown that MDM and MDDC would build TJ-like structures with the EC, the integrity would remain, although maybe the tightness is decreased to a certain level. This seems to be an important mechanism for cells penetrating the epithelial cells, to keep the tightness of the cell layer although maybe to a reduced level. The addition of polystyrene particles did not change the epithelial integrity, which was also the same in the present study when DEP were added [30]. The present findings are in contrast to the results of the study published by Bayram and co-workers [5], who demonstrated that after exposing cultured human bronchial epithelial cells to concentrations of DEP between 10-100 μg/ml the TEER increases significantly but without effect on the passage of 14C-bovine serum albumin across the cell culture [5]. It is important to note that it is difficult to compare different studies due to the use of different types of DEP and cell cultures.
The decrease in barrier function in the EC mono-cultures can not be explained by cell death. No change in cytotoxicity was found, by determination of LDH levels in the supernatants, after exposure to 125 μg/ml for 24 h. This is in agreement with a study done by Boland and co-workers [9]. That study found a cytotoxic effect in 16BE14o cells exposed either with standard particles (SRM 1650) or with DEP sampled from a non-catalyst car, although this finding was only after 48 h and also not 24 h after exposure. However they used a dose of 10 μg/cm2 which is about 6 times less than the high concentration of 125 μg/ml used in the current study [8, 9]. Furthermore no cell death was found by Baulig et al., which used 16BE14o- cells exposed to DEP (10 to 30 μg/cm2) for 24 h [47]. Bayram and co-workers also examined human bronchial epithelial cell cultures after DEP treatment with concentrations between 10 and 100 μg/ml and did not find any cellular damage or detachment of the cells [5].
Moreover a reduced sensitivity of the TJ in the triple cell co-cultures can be excluded. The TEER of mono- and the triple cell co-cultures showed a very similar behavior after a EDTA treatment which is known to open the TJ [48]. The TEER value was reduced time-dependently in both culture types. As already shown, the TEER values of the EC mono-cultures are generally higher compared to those of the triple cell co-cultures.
In this study the effect of DEP exposure on the TJ protein, occludin, was assessed for the first time in different mono-cultures of lung cells, including MDM, EC and MDDC. Additionally, the effects of DEP were studied using the combination of the three cell types, in the so-called triple cell co-culture system. It was not possible to assess the effects in the individual cells of the triple cell co-culture system, because there is no useful method known to separate the three cell types from the co-cultures system. However, isolating single cell types from the triple cell co-culture system might have a direct influence on the cell-cell junctions which might lead to altered results. Due to this separation problem, DEP exposure and their influence on the three cell types was assessed using single cell cultures. Using immunofluorescence methods, the characteristic belt-like structure of occludin, which was present in control EC cultures, was found to be reduced in the DEP treated EC cultures, supporting the data obtained with the TEER measurements. Additionally DEP treated MDM and MDDC mono-cultures exhibited a loss of occludin signals compared with the untreated control samples.
No dose-dependent reduction of occludin mRNA expression was found in MDM and MDDC. Lower doses of DEP (0.5-50 μg/ml) did not affect the expression whereas the highest DEP concentration (125 μg/ml) reduced the mRNA levels, although this difference was not significant. Interestingly, in untreated as well as in DEP treated mono-cultures of MDM, occludin was not only located at the cell border but also in the cytoplasm of the cells. In the in vitro triple cell co-culture model, the occludin protein is mainly present at the cell surface of MDM [28], suggesting that the localization of occludin is dependent on the presence of other cell types such as EC. It has also been shown in a kidney epithelial cell line that after the opening of TJ with the Ca2+-chelation method the occludin protein moved from the cell border towards the cytoplasm [48], indicating that cell-cell contacts are needed for the correct arrangement of occludin. Again, this is a reason for the examination of the expression level of occludin mRNA only in mono-cultures.
Interestingly, the expression levels of occludin mRNA and protein in EC did not change, although the TEER values decreased after DEP exposure. In fact, due to the expression level of the mRNA it is not possible to make a statement about the expression level of the respective protein because it is unclear if the mRNA is degraded or translated. The immunostaining in EC mono-cultures showed no change in the amount of protein, however the physiological arrangement of occludin was reduced after DEP treatment which could lead to an enhanced reduction of TEER. TEER is a commonly used marker for the epithelial integrity; the higher the TEER value is, the higher the epithelial integrity. Every epithelial cell (line) exhibits its own characteristic TEER values in untreated and standardized condition. It is proposed that the reduced integrity is due to the alteration in TJ disassembly rather than a reduction of the TJ protein occludin. When the TJ proteins are not placed in their physiological arrangement, the cell integrity can not be maintained. TJ are associated with the F-actin cytoskeleton and it has been shown that a reorganization of the F-actin cytoskeleton influences the formation and maturation of cell-cell contacts [42]. After cigarette smoke exposure to Calu-3 cells, amongst others, a displacement of occludin and ZO-1 was found and thus increasing ionic and macromolecular permeability. It was hypothesized that the loss of TJ integrity and barrier function was due to a decreased ZO-1:occludin association ratio. [34]. Another study using the Ca2+ chelation method to open the TJ in MDCK, a kidney epithelial cell line, [48] supports the hypothesis that the opening of the TJ is not due to a reduced protein level but to a rearrangement of the TJ proteins. In control cultures, occludin was mainly found at the cell-cell contacts whereas after EGTA treatment the staining disappeared from the cell borders and was diffused closer to the membrane. In these experiments the TEER values reduced significantly. Inhibition of protein synthesis by addition of cycloheximide to the cell cultures did not influence the outcome of the Ca2+ chelation experiment.
In the present study, the qualitative images of EC, MDM and MDDC showed an unaffected arrangement of the F-actin cytoskeleton after DEP treatment. Moreover, for the qRT-PCR the housekeeping gene β-actin was used, which showed a constant expression level throughout all experiments.
In pulmonary infections, bronchiolar or alverolar macrophages are one of the first cells responsible for clearing inhaled and deposited particles [46]. Furthermore macrophages are able to release pro-inflammatory cytokines such as TNFα and Interleukin 8. Mono-cultures of MDM and MDDC exposed to LPS showed a significantly higher TNFα response compared to the untreated control, whereas EC exposed to LPS showed no differences (data not shown). Focussing on TNFα, TNFα levels were determined from the supernatant in the in vitro triple cell co-culture model, which closely mimics the airway epithelium [27, 37]. Due to a study in which it was shown that a TNFα induced drop in Caco-2 TEER was directly correlated with the increase in paracellular permeability, the TNFα levels were examined. This increase in Caco-2 TJ permeability was accompanied by the down-regulation of ZO-1 proteins and an alteration in the junction localization of those proteins [49]. No change in TNFα levels in the triple cell co-culture model was found, after exposure to the high dose of DEP (125 μg/ml) compared to the control. It is known that mono-cultures of macrophages show an enhanced pro-inflammatory reaction upon DEP exposure [50] therefore, the data from mono-cultures can not be directly compared to the triple co-culture model [36] The amount of macrophages in the triple co-culture model, which is similar to the amount in the human lung [30], is reduced compared to the mono-cultures and also there is the additional influence of the other two cell types. Additionally the mono-cultures of EC showed no pro-inflammatory reaction. This finding is in agreement with other publications obtained from animal studies: An in vivo study showed that long-term inhalation of a low-dose of DEP did not change TNFα release in alveolar macrophages of mice, but the release significantly decreased when they were exposed to a high dose [51]. Furthermore, cells from bronchoalveolar lavage fluid of rats instilled with DEP showed no enhanced TNFα release and the authors concluded that TNFα does not seem to be involved in the pathological changes associated with DEP exposure, in the time period studied [52].
Conclusion
In summary, it was demonstrated that even after exposure to a high dose of DEP (125 μg/ml), the expression of occludin mRNA in 16HBE140- mono-cultures remained unaffected, while TEER decreased significantly and the local distribution of the occludin protein changed to an irregular pattern. The protein levels of occludin in MDM and MDDC were affected upon exposure to high DEP doses. Although the results were not significant, the mRNA levels of those cell types showed a tendency to be decreased after exposure to DEP. In contrast, no change in TEER was observed in the triple cell co-culture model and no pro-inflammatory reaction could be found. Further studies are required to understand the alterations of mRNA expression of the three cell types after stimulation or exposure to particles in the triple cell co-culture model to elucidate the influence of the cell-cell interactions between the different cell types. The TJ like structure could be shown between EC and MDM for the first time with TEM. By comparing the effects of the mono-cultures with an advanced triple cell co-culture model of the epithelial airway wall, the findings showed that the hazards of DEP in the triple cell co-culture model are less pronounced than in the mono-cultures. We hypothesize that there is a synergistic effect due to the interaction of the three cell types (epithelial cells, alveolar macrophages and dendritic cells) that reduce the adverse effects of DEP. The results encourage further study regarding the influence of DEP on other TJ proteins. There is a need that different cell types are included in cell culture models as this study has shown that co-culture models are better at simulating the real situation in the lung than mono-cultures.
Methods
16HBE14o- mono-cultures
The 16HBE14o- bronchial epithelial cell line was used as described in earlier studies [30]. Briefly, 16HBe14o- cells (Passages 2.57-2.86) were cultured in MEM 1× medium, containing Earle's Salts, 25 mM HEPES, without L-Glutamine (Gibco BRL Life Technologies Invitrogen AG, Basel, Switzerland) supplemented with 1% L-Glutamine (LabForce AG, Nunningen, Switzerland), 1% penicillin/streptomycin (Gibco BRL), and 10% foetal calf serum (PAA Laboratories, Lucerna-Chem AG, Lucerne, Switzerland). The cells were grown in 25 cm2 cell culture flasks (TPP, Trasadingen, Switzerland) which were treated with fibronectin coating solution containing bovine serum albumin, 0.1 mg/ml (Sigma, Fluka Chemie GmbH, Buchs, Switzerland) and 1% bovine collagen, Type I (BD Biosciences, Basel, Switzerland) and 1% human fibronectin (BD Biosciences) in LHC Basal Medium (Lucerna Chemie AG) and passaged in turns of every 3 and 4 days, respectively. For experimental cultures the cells were seeded on transparent BD Falcon cell culture inserts (surface area of 4.2 cm2, pores with 3.0 μm diameter, PET membranes for 6-well plates; BD Biosciences) treated with fibronectin coating solution containing bovine serum albumin (details are described above) and maintained for 7 days. Cultures were kept at 37°C in 5% CO2 humidified atmosphere.
MDM and MDDC mono-cultures
MDM and MDDC were obtained from human peripheral blood monocytes as described by [53]. Briefly, peripheral blood monocytes were isolated from Buffycoat (Blood Donation Service, Bern, Switzerland) by density gradient centrifugation on Ficoll-Paque (Amersham Biosciences Europe GmbH, Otelfingen, Switzerland). Peripheral blood monocytes were re-suspended in RPMI 1640 supplemented with 1% L-Glutamine, 1% penicillin/streptomycin, and 10% heat-inactivated (pooled) human serum (Blood Donation Service, Bern, Switzerland), and then allowed to adhere for 90 min in 6-well plates (BD Biosciences,Basel, Switzerland). Non-adherent cells were washed away and adherent cells were cultured in RPMI 1640 medium, supplemented with 1% L-Glutamine, 1% penicillin/streptomycin, and 5% heat-inactivated (pooled) human serum. For the generation of MDDC, 34 ng/ml IL-4 (Sigma, Fluka Chemie GmbH, Buchs, Switzerland) and 50 ng/ml GM-CSF (R&D Systems, Oxon, UK) were added to the supplemented medium for 7-8 days. The MDM were only obtained in the supplemented medium for 7-8 days. The cell cultures were kept at 37°C in 5% CO2 humidified atmosphere in an incubator.
Triple cell co-cultures
The co-cultures were prepared as previously described [30]. Briefly, 16HBE14o- cells were maintained on transparent BD Falcon cell culture inserts (surface area of 4.2 cm2, pores of 3.0 μm diameter, PET membranes for 6-well plates; BD Biosciences) treated with fibronectin coating solution containing bovine serum albumin (for details see above). Epithelial cells were cultured for 7-8 days before MDM were added on top of the epithelial monolayer and MDDC underneath the insert membrane. Before using the triple cell co-cultures, they were kept overnight in medium supplemented with 1% L-Glutamine, 1% penicillin/streptomycin, and 5% heat-inactivated (pooled) human serum at 37°C in 5% CO2 humidified atmosphere. The 16HBE14o- cells were kindly provided by Dr. Gruenert (University California, San Fransisco).
Measurements of the transepithelial electrical resistance (TEER)
The TEER was measured with the Millicell-ERS system (MERS 000 01; Millipore AG, Volketswil, Switzerland) as described earlier [27, 30, 37]. Briefly, TEER was measured in the EC mono-cultures and in the triple cell co-cultures before and 24 h after DEP exposure. The mean of four measurements per insert was determined. The electrical resistance of insert membranes without cells was subtracted from all samples, and the resistance values were multiplied with the surface area of the inserts (4.2 cm2).
DEP exposure of cell cultures and harvesting of cells
To determine the effects of different concentrations of DEP on the expression of TJ protein mRNA mono-cultures of MDM, MDDC and EC were exposed in suspension to standardised and characterised DEP (SRM Nr. 2975; National Department of Standards and Technology, Gaithersburg, USA). Prior to particle exposure the culture medium was removed and 2 ml of fresh, pre-warmed culture medium without serum, in which the DEP were diluted to the final concentrations of 0.5, 5, 50, and 125 μg/ml, respectively, was added to the cells and left for 24 h. Prior to incubation with cells, all DEP dilutions were sonicated for 2 min in order to minimize aggregation. Each experiment was repeated between 4 to 7 times.
RNA isolation and RT-PCR
After exposure, the cells were removed from their substrate with a 25 cm cell scraper (Sarstedt, Sevelen, Switzerland), washed twice in phosphate buffered saline (PBS, 10 mM, pH 7.4: 130 mM NaCl, Na2HPO4, KH2PO4) and then stored in RNAlater (Qiagen, Basel, Switzerland) for the RNA isolation.
Total mRNA was extracted from the mono-cultures of MDDC, MDM and 16HBE14o- EC using the RNeasy Mini kit (Qiagen, Hombrechtikon, Switzerland) according to the manufacturer's protocol. Briefly, after centrifugation (30 s at 13000 × g) of the harvested cells, the supernatant was discharged and 600 μl buffer RLT (Qiagen, Hombrechtikon, Switzerland) with 6 μl beta-mercaptoethanol (Sigma-Aldrich Chemie GmbH, Buchs, Switzerland) was added to each sample for lysis, followed by homogenization using a glass douncer. Debris was pelleted by centrifugation (30 s at 13000 × g). A volume of 600 μl Ethanol (70%) was added to the cleared lysate before RNA was bound to the RNeasy membranes. 10 μl DNase I in 70 μl RDD buffer (Qiagen, Hombrechtikon, Switzerland) was added for 30 min at room temperature to remove traces of DNA. DNase and any contaminants were washed away with buffer RW1, and total RNA was eluted in RNAse-free water. Finally, obtained mRNA concentrations were spectrophotometrically determined using Nanodrop ND-1000 (NanoDrop Technologies). (NanoDrop, Witec AG, Littau, Switzerland). cDNA was synthesized by reverse transcription (RT) with 4 μg of total RNA using 2 μg Oligo (dT)15-primers (Promega, Wallisellen, Switzerland) and 4 U of Omniscript reverse transcriptase (Qiagen, Hombrechtikon, Switzerland) at 37°C for 1 h according to the manufacturer's protocol.
Quantitative real-time-PCR (qRT-PCR)
The cDNA samples were analyzed by qRT-PCR using the self-designed primer pairs, specific for occludin mRNA (ordered by Mircrosynth, Balgach, Switzerland) (Table 1). For each investigated sample, 200 ng of the cDNA template was added to wells containing 12.5 μl of Sybr Green Jump Start Taq Ready Mix (Sigma Aldrich, Buchs, Switzerland) and 0.2 μl of both sense and antisense primers (to yield final concentrations of 0.6 μmol/l). RNAse free water was added up to the final volume of 25 μl. According to the manufacturer's protocol, two stages for the qRT-PCR were run. An initial step at 95°C for 2 min was followed by 40-cycle sequence of denaturation (15 s at 94°C), annealing (30 s at 56°C) and elongation (60 s at 72°C). (GeneAmp® 5700 Sequence Dedector, AB Applied Biosystems, Rotkreuz, Switzerland). For mRNA/cDNA expression analysis, cycling reports and melting curves were evaluated and the baseline cycle threshold was added. The reference housekeeping gene β-actin (Table 1) was used for normalisation of qRT-PCR data. Data were evaluated by the relative quantification method (2-ΔCT) as described by Livak and Schmittgen [54]. The qRT-PCR fragments were visualized by electrophoresis on a 2% (w/v) agarose (Axon, Baden-Dättwil, Switzerland) gel supplemented with 0.5 μg/ml ethidium bromide and were sequenced for occludin in the EC.
Table 1 Primer sequences for quantitative RT-PCR
Cell fixation and labelling for laser scanning microscopy
Cells were labelled and fixed as described in detail (Blank et al., 2007). Antibodies were diluted in PBS as follows: mouse anti-human CD14 1:20 (Clone UCHM-1, C 7673, Sigma), mouse anti-human CD86 1:20 (Clone HB15e, 36931A, PharMingen, BD Biosciences), rabbit anti-occludin 1:50 (Clone Z-T22; Invitrogen, Basel Switzerland), goat anti mouse cyanine 2 1:50 (Chemicon, VWR International AG, Life Sciences, Lucerne, Switzerland), goat anti-mouse cyanine 5 1:50 (AP124S, Chemicon, VWR International AG, Life Sciences, Lucerne, Switzerland), goat anti rabbit cyanine 5 (Chemicon, VWR International AG, Life Sciences, Lucerne, Switzerland), Alexa 488 and phalloidin rhodamine 1:100 (R-415, Molecular Probes, Invitrogen AG, Basel, Switzerland).
Confocal Laser scanning microscopy and image restoration
A Zeiss LSM 510 Meta with an inverted Zeiss microscope (Axiovert 200 M, Lasers: HeNe 633 nm, HeNe 543 nm, and Ar 488 nm) with a 63× objective lens (oil immersion, NA = 1.3) was used. For the detection of the TJ signals a negative sample containing only the secondary antibodies was scanned first and the detector gain was adjusted so that no fluorescent signal of the specific antibody (such as background) could be detected. The scans of the labelled samples were then acquired using the same detector settings. Image processing and visualization was done using IMARIS, a 3D multi-channel image processing software for confocal microscopic images (Bitplane AG, Zurich, Switzerland).
Transmission electron microscopy
For TEM analysis, cells were fixed with 2.5% glutaraldehyde in 0.03 M potassium phosphate buffer, pH 7.4. The cells were postfixed with 1% osmium tetroxide in 0.1 M sodium cacodylate buffer and with 0.5% uranyl acetate in 0.05 M maleate buffer. Then cells were dehydrated in a graded series of ethanol and embedded in Epon. Ultrathin sections were cut and transferred on single slot grids (2 × 1 mm; Plano GMBH, Wetzlar, Germany), stained with uranyl acetate, counter-stained with lead citrate, and observed with a Philips 400 TEM at 60 kV (FEI Company Philips Electron Optics, Zurich, Switzerland).
Determination of MDM in the triple co-culture model using TEM technique
It is not possible to define the MDM in the triple cell co-culture model only based on morphology. Therefore the differentiated MDM mono-cultures were exposed to 4 μg/ml gold NP with a diameter of 15 nm (British Biocell international, Cardiff, United Kingdom) for 18 h. Before adding the MDM to the triple cell co-culture model, the MDM mono-cultures were washed three times with pre-warmed medium to get rid of gold NP that were not internalized. The handling of the triple cell co-cultures is described in detail above. After 12 h, the cells were fixed as described above.
Cytotoxicity
LDH was measured as an indicator of cell death by using a cytotoxicity detection kit (Roche, Roche Diagnostics, Rotkreuz, Schweiz) according to the manufacturer's manual. Briefly, supernatants of the EC mono-cultures and the triple cell co-cultures were collected from control, 0.5 and 125 μg/ml DEP exposed cultures after 24 h. The untreated cells (control) served as the negative control, cells treated with Trition-X-100 in PBS 1% served as a positive control. LDH activity was measured in a 96-well plate with three replicates of each group at an absorbance of 490 nm and with the reference wavelength at 630 nm.
ELISA for determination of TNFα
After particle incubation for 24 h, supernatants of the epithelial mono-culture as well as from the triple cell co-cultures were collected from the upper and lower chamber and stored at -70°C. After centrifugation, TNFα was quantified by a commercially available DuoSet ELISA Development kit (R&D Systems, Catalogue Number: DY 210, Oxon, UK) according to the manufacturer's recommendations. Each sample was analysed in duplicates. The experiment was done in triplicate. The absorbance was read at 450 nm using an ELISA reader (SpectraMax 340 PC or Benchmark Plus Microplate Spectrophotometer (BioRad, Hempel Hempstead, UK)). The concentration of TNFα was determined and calculated by comparing the absorbance of the samples with standard recombinant human TNFα. For the positive control, mono- and triple cell co-cultures were also exposed to LPS (10 μl/ml). All values were normalized to the untreated control.
Calcium Chelation
For those experiments, the previously described EC mono-cultures and the triple cell co-cultures were treated with EDTA at 37°. Untreated control cultures were also integrated. For the experimental cell cultures, the normal medium of the upper chamber was removed and fresh pre-warmed RPMI only supplemented with 2.0 mM EDTA was added at time point zero. For one hour, the TEER of the cell cultures were recorded every 15 min.
Statistics
The results of ELISA, LDH and TEER measurements as well as the 2-ΔCT values of the qRT-PCR are expressed as mean values with the standard deviation of the mean (SD). The statistical analysis was performed using SigmaStat for Windows (Version 3.10, Systat Software, Inc., Richmond, California, USA) statistical software. To compare more than two groups an ANOVA on Ranks was performed. Two groups were compared using a Mann-Whitney rank sum test, for comparison of before and after DEP exposure. In all cases p < 0.05 was considered to be significant.
Acknowledgements
The author thanks A. Stokes and B. Tschirren and B. Krieger for their excellent technical support. They thank K. Dobson for proofreading the manuscript. They are indepted to Dr. Gruenert for providing the human bronchiolar cell line 16HBE14o-.
This work was supported by the Swiss National Science Foundation, the Johanna Dürmüller-Bol Foundation, the Swiss Agency for the Environment and the Deutsche Forschungsgemeinschaft.
Abbreviations
DEP:
Diesel exhausted particle(s)
DC:
Dendritic cells in general
EC:
Epithelial cell
EDTA:
Ethylenediaminetetraacetic acid
LDH:
Lactate dehydrogenase
LPS:
Lipopolysaccharid
LSM:
Confocal laser scanning microscopy
MDM:
Monocyte derived macrophages
MDDC:
Monocyte derived dendritic cells
NP:
Nanosized particles
PM:
Particulate matter
qRT-PCR:
Quantitative real-time polymerase chain reaction
TEM:
Transmission electron microscopy
TEER:
Transepithelial electrical resistance
TJ:
Tight junctions
TNFα:
Tumor necrosis factor alpha. ZO-1: Zonula occludens 1.
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Correspondence to Andrea D Lehmann.
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Authors' contributions
ADL: has done the acquisition, the analysis and the interpretation of data, and made a first draft of the manuscript. FB: participated in the design of the study, established the molecular methods and helped to draft the manuscript. OB: helped to interpret and evaluate the results of the quantitative real-time PCR and helped to draft the manuscript. PG: critically revised the manuscript and interpreted the data. BR: was the project leader, interpreted the data and composed the final version of the manuscript. All authors read and approved the final manuscript.
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Lehmann, A.D., Blank, F., Baum, O. et al. Diesel exhaust particles modulate the tight junction protein occludin in lung cells in vitro . Part Fibre Toxicol 6, 26 (2009) doi:10.1186/1743-8977-6-26
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Keywords
• Tight Junction
• Tight Junction Protein
• Diesel Exhaust Particle
• Epithelial Integrity
• Tight Junction Protein Occludin
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OvuSense logo
Do Ovulation Tests Work?
If you’re trying to work out when you’re ovulating, whether it’s to boost your chances of getting pregnant or simply to identify where you are in menstrual cycle, or judge if medication or lifestyle changes intended to encourage spontaneous ovulation are having the desired effect, then ovulation tests seem to offer a simple solution.
The Advantages
Ovulation Tests, otherwise known as Ovulation Predictor Kits (or OPKs) have a lot of advantages. They’re widely available, and relatively low in cost so you can add a pack to your weekly shop without too much disruption to your routine or your finances.
They’re also relatively convenient to use: similar to pregnancy tests they test your urine to check for hormone levels and give you a simple Yes or No result based on what they find. As long as you don’t mind the process of using them, they provide a quick and definitive answer to the answer.
The Drawbacks
Unfortunately, this isn’t the full story.
For one thing, even if you’re in perfect health, and perfectly fit the average hormonal profile the tests are configured for, there’s some debate about when in the day you should use the test to get the most accurate results. Some experts favour the morning, suggesting this will give time for your hormones to concentrate in your bladder overnight while others say this could give you a false positive and you need to wait until the afternoon.
With debate over when you can effectively use your OPK to get a result you can trust, it’s hard to recommend it, and that’s only the start of the problems.
If you have a naturally high or low level of the Luteinising Hormone (or LH) then it could cause the tests to register false positive or false negatives, either missing when you ovulate altogether or telling you that you’re ovulating far too much to be useful or accurate.
On top of this, if you have a condition like Polycystic Ovary Syndrome, which affects your hormones, the results of OPKs can become so distorted they don’t have any predictive power whatsoever.
Other Solution
You need other, better solutions if you want to get an accurate indication of whether you are ovulating, along with a prediction as to when it will happen next. OvuSense uses your Basal Body Temperature – the low minimum your body temperature drops to when your body is at rest – to find answers that aren’t affected by hormone issues. Combined with an algorithm to turn your temperature readings into predictions, this gives you results you can rely on as a foundation for your plans.
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Gene Testing and Family Planning
gene-test-planning
Carrier testing can clue you in to potential gene mutations in future pregnancies. Is it right for you?
Well before companies ever invited consumers to send saliva by mail in exchange for their genome sequence, would-be parents used genetic tests to determine whether heritable conditions might affect their offspring.
The differences between the two types of testing are small but significant, notes Cheri Schoonveld, MS, CGC, a certified genetic counselor at the University of Minnesota in Minneapolis. While genome sequencing seeks to identify an individual’s risk of developing a condition, like Alzheimer’s disease, family-planning tests focus on a different kind of risk.
“Individuals who are carriers are not at risk to develop the condition themselves; however, they are at increased risk to have a child with the condition.”
Because certain gene mutations are more common to particular ethnicities, the American College of Obstetricians and Gynecologists recommends that couples be offered carrier screening for heritable conditions associated with their ethnicity. Examples include cystic fibrosis for Europeans, Tay-Sachs disease for Ashkenazi Jewish families, and sickle-cell disease for families with African heritage.
Still, like all genetic tests, these predict only potential outcomes. “Most genetic conditions that are screened for require that both parents be carriers of the condition to have an affected child, and even if both parents are carriers, it does not mean that every child will have the condition,” Schoonveld explains. For autosomal recessive conditions like these, the risk that a child would be affected is one in four.
Schoonveld recommends couples consider carrier testing before pregnancy, so they can review the information without the “pressure and emotional charge” that a pregnancy involves. They can then decide to move forward, more prepared for possible outcomes, or to pursue other options, such as in vitro fertilization with genetic testing of embryos, or adoption.
This originally appeared as part of “Is Genetic Testing Right for You?” in the December 2016 issue of Experience Life.
Like What You are Reading? Subscribe.
Anjula Razdan is a Minneapolis-based health writer.
Share your thoughts. (0 Comments)
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What are the Different Types of Anti-Nausea Medications?
Helena Reimer
Helena Reimer
Cannabis is sometimes prescribed for nausea.
Cannabis is sometimes prescribed for nausea.
There are several different types of anti-nausea medications, which are often referred to as antiemetics. They are divided into groups, and each group has a slightly different method of relieving nausea. Some work to block the receptors in the stomach, others block the signal in the brain, and still others help to empty the bowels. The medications are available in pills, capsules, liquids, injections or a suppository.
The right anti-nausea medication can depend on the cause.
The right anti-nausea medication can depend on the cause.
People who are suffering from morning sickness, motion sickness or night nausea can find relief with anti-nausea medications. Not only do they help to relieve nausea, the sedating effect of some drugs can also help individuals to fall asleep sooner. Others are helpful in reducing the nausea caused by bowel obstructions and other digestive problems. Cancer tumors and other diseases might also contribute to nausea, which can be treated with anti-nausea medications.
Ginger capsules alleviate the symptoms of an upset stomach.
Ginger capsules alleviate the symptoms of an upset stomach.
The most common type of anti-nausea medications are the 5-HT3 receptor antagonists, also known as serotonin blockers. These help to block the serotonin receptors in the stomach that send the vomiting signal to the brain. They are particularly helpful for stopping nausea in patients who have had surgery or are on cytotoxic drugs. Cytotoxic drugs have a toxic effect on the body and are often used in chemotherapy treatment.
Anti-nausea medications help block the chemical in the brain that triggers vomiting.
Anti-nausea medications help block the chemical in the brain that triggers vomiting.
Dopamine antagonists block the vomit area in the brain. They can help to stop nausea that results from radiation, cytotoxic drugs, anesthetics and certain painkillers such as opioids. Anti-nausea medications that help the stomach empty its contents are beneficial when the nausea is caused by digestive problems, because they can help solve the root of the problem. Nausea that results from motion sickness, vertigo or morning sickness caused by pregnancy, might be helped by antihistamine antiemetics. Cannabis, also known as medicinal marijuana, might be used in severe cases when other anti-nausea medications do not work.
The most common type of anti-nausea medication is the 5-HT3 receptor antagonists, a serotonin blocker.
The most common type of anti-nausea medication is the 5-HT3 receptor antagonists, a serotonin blocker.
These medications are available in different forms to help individuals who have different needs. For example, in a severe case of nausea, swallowing a pill may not be feasible for the patient. Thus a pill that can be absorbed into the bloodstream from under the tongue, an injection or a suppository will help to make it easier on the patient. There are several anti-nausea medications that can be purchased without a prescription, but others cannot be obtained unless prescribed by a medical professional. Side effects of anti-nausea medications include abdominal pain, constipation, diarrhea, cramps, headaches, fatigue, drowsiness and dry mouth.
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Discussion Comments
browncoat
Every time I need to go on a boat ride, I convince myself I'm not going to get sick and every time I do get sick. I've always hoped that it would be something that I grow out of but I never have. I guess my inner ear is not shaped that way.
The difficult part is remembering to take the nausea medicine in time. If you don't take it at least three hours before your trip, it doesn't work.
Since the trip I'm usually taking is about three hours long, simply forgetting the medicine beforehand has made me miserable more than once.
irontoenail
@Mor - I don't know, I think your mother has a point in some ways. I don't like to take in any medications that I don't have to, just because they do so much to your body. You are taking a risk whenever you have them. You might have developed an allergy, or be affecting your liver.
And I'm pretty sure it was an anti nausea medicine which caused birth defects in a lot of children a few decades ago.
Granted, the safety standards of medications have changed since then, but I'd still be extremely cautious with that kind of thing, particularly if I was pregnant. You never know when something will react badly and make you sick.
On the other hand, I've known women who were so sick with their pregnancies that taking anti nausea medicine was the only way to get through it. So, you just have to weigh the risks and benefits, in the end.
Mor
Anti nausea drugs are one of those medications that I often have arguments with my mother about.
She's anti taking any "unnecessary" medications. She has small airwaves disease so she often coughs enough to make herself vomit and usually feels sick for a few days afterwards, particularly if she is extremely stressed.
I think because she still feels queasy she'll often prolong her vomiting, whereas if she took medicine to make herself feel better, she'd stop it sooner.
She thinks because she's only treating a symptom, it's not worth it. But, often the symptoms make you so uncomfortable that they can keep the whole thing going, even when the underlying cause has gone away.
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• Cannabis is sometimes prescribed for nausea.
By: Boyan Dimitrov
Cannabis is sometimes prescribed for nausea.
• The right anti-nausea medication can depend on the cause.
By: ftlaudgirl
The right anti-nausea medication can depend on the cause.
• Ginger capsules alleviate the symptoms of an upset stomach.
By: womue
Ginger capsules alleviate the symptoms of an upset stomach.
• Anti-nausea medications help block the chemical in the brain that triggers vomiting.
By: Tom Wang
Anti-nausea medications help block the chemical in the brain that triggers vomiting.
• The most common type of anti-nausea medication is the 5-HT3 receptor antagonists, a serotonin blocker.
By: snyggg.de
The most common type of anti-nausea medication is the 5-HT3 receptor antagonists, a serotonin blocker.
• Some anti-nausea medications must be prescribed by a medical professional.
By: Burlingham
Some anti-nausea medications must be prescribed by a medical professional.
• Nausea is a sensation that generally occurs before an individual vomits.
By: pathdoc
Nausea is a sensation that generally occurs before an individual vomits.
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Âîïðîñ ïîñåòèòåëÿ 'Ëåíà' ¹77408
Ëåíà, Êèåâ
Âîïðîñ:
Äîáðûé äåíü! Ïîìîãèòå ïîæàëóñòà, ìîé ìóæ ÷åòâåðòûé ìåñÿö èùåò â ñåáå áîëåçíè. Áåãàåò ïî âðà÷àì, ñäàåò àíàëèçû, ñåðüåçíûõ îòêëîíåíèé íåò. Âðà÷è íå íàõîäÿò ñåðüåçíûõ áîëåçíåé. Ñ êàæäûì äíåì îí íàõîäèò â ñåáå êàêîé-íèáóäü íîâûé ñèïòîì. Èùåò ïðèçíàêè â èíòåðíåòå... è ïîíåñëîñü... íàõîäèò íîâóþ áîëåçíü..èäåò ñäàâàòü íîâûé àíàëèç. Ñàì î÷åíü íåðâíè÷àåò, ñðûâàåòñÿ. Ó ìåíÿ ñèë òîæå óæå íåò. Ïîñòîÿííî ñïðàøèâàåò íå áîëèò ëè ÷åãî ó ìåíÿ, íå âûñêî÷èëî ëè êàêîå íèáóäü ïÿíûøêî íà ìîåì òåëå. ×òî äåëàòü??? Êàê åìó ïîìî÷ü? Ñàìà íà÷èíàþ ñõîäèòü ñ óìà. Ýòà èïîõîíäðèÿ ñúäàåò ïîêîé â íàøåì äîìå. Ïîäñêàæèòå ïîæàëóéñòà, ÷òî äåëàòü. Ñïàñèáî.
Óòî÷íèòü â ðàìêàõ äàííîãî âîïðîñà
ìóæ. æåí.
Äëÿ ïîëó÷åíèÿ óâåäîìëåíèÿ î îòâåòå
Î ïðîåêòå
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© Medicina.ua 2005—2023. Âñå ïðàâà çàùèùåíû.
Àâòîðèçàöèÿ
Ëîãèí
Ïàðîëü
Äëÿ ÷åãî íóæíà ðåãèñòðàöèÿ?
Åñëè Âû — ïîñåòèòåëü, ðåãèñòðàöèÿ íà ïîðòàëå ïîçâîëèò Âàì ñîçäàòü ñâîþ ïåðñîíàëüíóþ ñòðàíèöó ñ ðàçëè÷íûìè ñåðâèñàìè, ñ êîòîðîé ñìîãóò îçíàêîìèòüñÿ âðà÷è. À ñåé÷àñ ïîñëå ðåãèñòðàöèè Âàì äîñòóïíî ñîçäàíèå íîâûõ òåì è àêòèâíîå ó÷àñòèå â îáñóæäåíèè íà ôîðóìå.
Åñëè Âû — âðà÷, òî ïîñëå ðåãèñòðàöèè Âû ñìîæåòå êîíñóëüòèðîâàòü ïîñåòèòåëåé ïîðòàëà, à òàêæå íàéòè ïîòåíöèàëüíûõ ïàöèåíòîâ.
Äëÿ äîáàâëåíèÿ âîïðîñà â ðàçäåëå «Êîíñóëüòàöèÿ» ðåãèñòðàöèÿ íå òðåáóåòñÿ.
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How Muscle Protein Synthesis Works – And Why It Matters
asian coach helping lady with muscle protein synthesisThere is a metabolic process that occurs within the human body during which muscle proteins are bound to your skeletal system using amino acids. It is called muscle protein synthesis(MPS). Different proteins, including actin, troponin, tropomyosin, and mitochondrial proteins, will build muscle and produce substantial energy.
All of this occurs when you can consume proteins and, at the same time, perform resistance exercises. As your muscles begin to tear, new material will be built, leading to more muscle protein synthesis.
Muscle protein synthesis is an essential process by which the body manufactures new muscle protein. If muscle protein synthesis isn’t happening correctly, your body won’t be able to build new tendon, and you can lose muscle mass over time.
What Is Muscle Protein Synthesis?
This metabolic process is what allows any person to build muscle through exercise. You can remodel the shape of your muscles as they adapt to the specific type of weight or resistance training you are doing. Inevitably, this leads to the building of muscle mass.
Remember that breaking down your muscles through exercise is necessary to build muscle mass. That’s why it is essential to manage your protein and caloric intake so that they can be rebuilt once the muscles break down.
Triggers
For muscles to synthesize in the body, there must be synergistic activity between exercise and the consumption of proteins. Therefore, some bodybuilders will often consume large quantities of protein before and after the workout. Many of these amino acids are mixed with glucose. Leucine is an essential amino acid that can help stimulate muscle protein synthesis.
It can trigger a surge of energy produced in your cells’ mitochondria. By doing regular exercises and consuming proper amounts of protein at the correct times, you can also induce muscle protein breakdown (MPB).
The Difference Between MPS and MPB
Muscle protein synthesis is the process by which muscle protein is created from amino acids. Muscle protein breakdown is the process by which muscle protein is destroyed. Additionally, muscle protein synthesis rates can be stimulated by increasing the number of amino acids available to the muscle. In contrast, muscle protein breakdown can be inhibited by blocking the availability of essential amino acids.
MPS is tightly regulated and can be stimulated by several different stimuli. These include exercise, insulin, and growth factors. In contrast, muscle protein breakdown is inhibited by several other stimuli. These include fasting, starvation, hypoxia/anemia (low oxygen levels), hypercaloric feeding conditions, and inhibiting hormones.
What Are The Advantages Of Amino Acids?
Amino acids are the building blocks of proteins. They can be found in many foods but are especially abundant in animal-based protein sources like meat, poultry, and fish. Amino acids help to form muscle tissue and promote healthy weight gain.
In addition, they can help to improve muscle function and endurance. As a result, amino acids are considered an essential source of protein for athletes and those who want to maintain a healthy physique.
How Long Does It Last?
This process can occur for up to 48 hours when synthesizing muscle through the consumption of proteins. Although consuming the necessary proteins within 30 minutes of your workout is crucial, you will still be able to build muscle mass days after the workout is completed.
Therefore, many bodybuilders and those who routinely exercise will target specific muscle groups. For example, they will only do exercises where pushing is involved on one day and do all their pulling exercises on the next. These actions will use different muscles in your body, and you can build muscle mass efficiently by staggering these workouts.
Benefits
Few things are as essential for athletes as muscle protein synthesis. The process helps them recover from weight or resistance training and boost their performance. It is vital for athletes because it helps them maintain muscle mass and improve physical performance. Additionally, muscle protein synthesis is essential for people who don’t exercise because it helps them lose weight and keep their metabolism healthy.
How To Increase Muscle Protein Synthesis
It is well-known that sleeping enough hours every day is essential for your overall health. It allows you to have the energy needed to function physically and mentally. During deep sleep, toxins within the brain can be removed effectively. During this time, the synthesis of proteins and building of muscle mass can accelerate.
When you are sleeping, you are allowing your body to recover from the day’s activities. It can inhibit protein synthesis within the body without enough sleep, usually 7 to 8 hours of restful sleep. Even if you are consuming enough proteins to rebuild muscle, it decreases the possibility of building muscle mass.
Nutrition
If you want to optimize your skeletal muscle mass, the diet that you are on must be very specific. As we age, our metabolism will slow, so you must monitor your carbohydrate intake. Too many carbs can lead to the storing of adipose cells in your body.
These tend to form in the gut area. If you are trying to target your core while building muscle, your abdominal muscles will be heading if you also store too much fat. Therefore, your diet should consist of meals that are low in carbohydrates and high in protein.
You always need carbs for your mitochondria to provide the extra energy required to complete each workout. Adding fiber to your diet can also be beneficial. It will allow your body to remove toxins much more efficiently. It also aids the absorption of nutrients in the small intestines when consuming a high-fiber diet.
There is a direct relationship between the ability of the body to build muscle mass because of recovering from exercises that you will do. On the one hand, you need to do proper exercises targeting specific muscle groups. However, without an adequate intake of proteins and other dietary nutrients, your body will not be able to rebuild muscle.
A regular diet may indeed provide enough nutrients that the body can use for recovery. However, those specifically attempting to build muscle mass as quickly as possible must always follow a specific diet regimen. When doing so, you can measure many different aspects of this process.
Protein Intake
When you’re training for muscle growth, protein balance is essential. Not only does it help to repair tendons after exercise, but protein is also necessary for muscle protein synthesis – the process by which muscle tissue is created.
If you’re not getting enough protein in your diet, the body won’t be able to produce as much muscle tissue. It is why it’s so important to eat a high-quality, balanced diet with plenty of lean protein sources. Doing so will support muscle protein synthesis and achieve optimal results in the gym.
Too little protein consumption can have a negative impact on muscle protein synthesis rates, which could lead to muscle wasting. To optimize muscle protein synthesis, consuming a high-quality source of lean proteins that are also easy to digest is important. A healthy diet of fruits and vegetables will provide all the essential nutrients your body needs for optimal muscle growth and development.
When it comes to dietary protein intake, there is no one-size-fits-all answer. That’s why it is essential to find a source that suits your needs and preferences. Many different plant-based proteins are also available today, so you’re sure to find something that meets your dietary requirements and satisfies your taste buds.
Exercise Frequency
How specific you are in your workout can lead to better gains. You will see dramatic improvements if you are working out and taking the necessary supplements to build muscle mass. However, it should be noted that muscles tend to grow much faster when there is some variability in your exercises. It’s not simply enough to target different muscle groups on other days. The variability also pertains to the types of activities you do and the augmentation of exercise.
For those trying to build muscle mass as quickly as possible, workout routines are done every 2 to 3 days. The body will always need time to recover from the tearing of muscles that will rebuild themselves. However, targeting specific muscle groups on different days will allow you to quickly work out six days a week for those building muscles.
It is always recommended that you provide your body with at least one day of rest when you are not doing any exercises. Even if you target every muscle group during your workouts, exercising only two days a week will still allow muscle mass to be built with a proper diet.
You must augment the types of exercises you are doing and the number of repetitions you do with different levels of weight. Your muscles can become accustomed to a specific exercise at a particular weight, which will minimize their ability to rebuild quickly. You can have much more robust gains by shifting the number of repetitions you do and changing the amount of weight you use when you exercise to maximize your results.
Types Of Exercise
Additionally, adding cardio workouts to your exercise routine can improve weight training. For example, instead of resting between sets or doing your workout from start to finish, you can incorporate 15 minutes sessions of high-intensity cardio. Intense levels of cardiovascular exercise can inspire the production of human growth hormones in the body. When this occurs, like levels produced during deep sleep, this will aid in the production of additional muscle.
Physical activity is important to muscle protein synthesis because it leads to increased levels of circulating hormones that stimulate muscle protein synthesis. Physical activity also increases the production of energy by the body, which can be used to fuel muscle growth.
Resistance exercise helps with muscle growth in a few ways. First, it causes the body to produce more testosterone, which enhances muscle protein synthesis (MPS). Second, resistance training increases the number of satellite cells that help repair damaged muscles. Third, resistance training can increase blood flow to muscles and promote their growth.
The Muscle Building Process
Also referred to as simply growth hormone, HGH or GH is produced in the body courtesy of the pituitary gland in the brain. It is a hormone that is responsible for many aspects of our growth. It helps determine how tall we will grow and what our bone lengths will be and can help with muscle growth. Simulating natural human growth hormone through deep sleep and rigorous exercise is possible. Additionally, there are supplements that you can take that will inspire the pituitary gland to produce HGH.
Supplementation
Some bodybuilders will use certain supplements to promote MPS. There are specific products, usually powder, that you can mix with water or milk. When you drink this concoction, it will have the proper balance of carbohydrates, protein balance, and sometimes fiber. The main complaint that many people have is that it is very easy to gain extra weight.
Therefore, you may want only to use bodybuilding or muscle-building supplements with minimal carbohydrates added. You will still have enough energy to effectively complete your workouts and promote MPS. If you would prefer not to use supplements, many people consume large amounts of protein in the form of white chicken or turkey meat.
Consuming L-arginine, and L-lysine at the same time, along with rigorous exercise, can lead to higher levels of muscle production. These are essential amino acids which means that, regardless of your diet, your body cannot produce these on its own. By combining the intake of these supplements, proper sleep, rigorous exercise, and the loss of body fat, you can see an increase in muscle mass development.
Muscle hypertrophy is a process of enlargement of the muscle mass. Protein synthesis refers to the rate at which new proteins are created in cells. Muscle growth occurs when these two processes work together; with an increase in protein synthesis, there is also an increase in muscle size and strength.
How BioScanSRT-Fit Works
Our BioScanSRT-Fit system can provide you with many benefits. This electrodermal testing system is used to identify stressors that causes the body to act or react improperly. Based on the readings obtained through our BioScanSRT-Fit system, we can provide you with options for improving health. It will also include certain types of nutritional testing. When we understand how specific nutrients affect your body, both good and bad, this information can help you become happier and healthier.
BioScanSRT-Fit is a holistic method incorporating modern technology to identify stressors and nutritional problems. By understanding what may be causing difficulties in your life, you can change your diet and lifestyle to improve the way you think and feel. Regarding building muscle mass, this may eliminate the intake of problematic foods and drinks you should avoid. It will help you narrow down what works best for you.
Why Use Galvanic Skin Response Testing?
One reason our system works so well is that we can determine changes in your body’s electrical conductivity by measuring changes in perspiration. Your nervous system is directly connected to the emotional responses that you experience every day. As you increase the intake of certain supplements or augment your workout routine, these changes will also register on our GSR.
If these responses are good and progressively improve, you will know that the changes you are making are helping you achieve your goals. However, you will know that you are doing much better as you see more muscle building, plus your recovery time may also diminish when you consume a proper diet.
When it comes to muscle protein synthesis, there is no single magic formula that will work for everyone. However, following a high-quality diet with plenty of dietary protein and healthy fats is one key factor that can help increase muscle growth.
What your clients eat also plays an important role – with proper nutrition, their bodies can produce more muscle proteins. Adequate nutrition is essential for optimal muscle growth and development – without it, your client’s training won’t effectively achieve desired results.
Learn About BioScan Today
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Background: Recently, the Nordic diet has gained interest, and a healthy Nordic food index has been developed, which has been found inversely related to colorectal cancer among Danish women. This single finding, however, requires replication in other cohorts.
Methods: We conducted a prospective study in the Women's Lifestyle and Health cohort, including 45,222 women, recruited in 1991–92, and followed up ever since through Swedish registries. Participants were classified according to the Nordic food index (consisting of whole grain bread, oatmeal, apples/pears, cabbages, root vegetables, and fish/shellfish), and the association between adherence and colorectal cancer was assessed using the Cox proportional hazards models.
Results: In the fully adjusted models, we found no association, neither with the continuous index score [incidence rate ratio (IRR), 1.04; 95% confidence interval (CI), 0.95–1.12, per 1-point increment] nor in the categorical analyses (IRR, 1.09; 95% CI, 0.78–1.52 for highest vs. lowest adherers).
Conclusion: The present study does, thus, not support a previous finding of an inverse association between a healthy Nordic food index and colorectal cancer.
Impact: This article adds new evidence to the field of the Nordic diet in disease prevention. Cancer Epidemiol Biomarkers Prev; 24(4); 755–7. ©2015 AACR.
Several individual dietary factors have been found inversely associated with colorectal cancer risk, most notably dietary fiber (1). Recently, however, nutritional epidemiology has turned to investigation of dietary patterns, rather than individual components, as this allows for interactions between several components in the diet examined (2).
A Nordic dietary pattern has been proposed, which includes products with health-beneficial effects, which can grow in the Scandinavian climate. Items included are, e.g., whole grain (rye and oats), cabbages, root vegetables, apples/pears, fish, and berries (3, 4).
Only one previous study examined the association between a healthy Nordic food index (HNFI) and colorectal cancer, showing an inverse association in middle-aged, Danish women (5). This finding requires replication in further cohorts to investigate its generalizability. The present study investigates the association between the HNFI and colorectal cancer in a cohort of Swedish women.
The Swedish Women's Lifestyle and Health study includes 49,259 women aged 29 to 49 years at recruitment (1991–92), who completed questionnaires on diet, lifestyle, and socioeconomic factors (6). Colorectal cancers (ICD-7: 153, 154) were defined through the Swedish Cancer Registry. Participants were followed from inclusion into the study and until date of colorectal cancer or death, censoring because of loss to follow-up, or December 31, 2012, whichever occurred first.
The HNFI included six food groups: Whole-grain bread, oatmeal, apples/pears, cabbages, root vegetables, and fish/shellfish. One point was given for above-median intake and 0 point for below-median intake for each item. Thus, participants could score from 0 to 6 points on the HNFI. Low adherence is classified as 0–1 point, middle adherence 2–3 points, and high adherence 4–6 points.
We calculated Cox proportional hazards models with age as the underlying time scale. Two-sided 95% confidence intervals (CI) for the incidence rate ratios (IRR) were calculated based on the likelihood ratio test on the log rate ratio scale. Estimates were calculated as age-adjusted (model 1), and additionally adjusted for smoking status, cigarettes/day, time since smoking cessation, education, BMI, and oral contraceptive use (model 2), alcohol (g/day), red/processed meat (g/day) (model 3), and energy intake (KJ/day) (model 4). The procedure PHREG in SAS 9.3 was used for all statistical analyses.
Ethics
The study was approved by the regional Ethical Committee at Uppsala University, and the Ethical Committee at Karolinska Institutet, Stockholm.
We excluded participants who emigrated before final enrollment (n = 41), had an energy intake outside the first and 99th percentiles (n = 1,072), lacked information on any covariate (n = 2,896), or had a colorectal cancer diagnosis before baseline (n = 28), leaving 45,222 women.
During follow-up, 314 women developed colorectal cancer (187 colon cancers and 127 rectal cancers). Several of the potential confounding factors were unevenly distributed across adherence to the HNFI: Participants who scored high on the index were less likely to smoke and more likely to be highly educated, never-users of oral contraceptives, and postmenopausal, have a higher energy intake, and a higher intake of red/processed meats and dietary fiber (Table 1).
Table 1.
Baseline characteristics of all participants in the Women's Lifestyle and Health cohort by adherence to the HNFI (0–1 points, 2–3 points, and 4–6 points)
HNFI
All women (n = 45,222; cases = 314)0–1 points (n = 9,542; cases = 61)2–3 points (n = 20,772; cases = 141)4–6 points (n = 14,908; cases = 112)
CharacteristicsMedianP5–P95MedianP5–P95MedianP5–P95MedianP5–P95
Age 39 30–48 39 30–48 39 30–48 39 30–48
BMI 23 19–30 22.5 19–30 23 19–30 23 18–30.5
Alcohol drinking 2.9 0.2–11.9 3.0 0.2–12.8 2.9 0.2–12.0 2.8 0.2–10.9
Red meat intake (g/d) 48.9 13.1–101.6 41.3 6.6–91.5 47.9 13.6–98.7 52.1 17.4–105.7
Processed meat (g/d) 26.8 1.3–62.5 21.7 0–58.4 26.7 1.6–62.0 29.2 3.0–65.2
Energy (kJ/d) 6,384.7 3,631.3–9,832.5 5,472.7 2,820.4–8,847.5 6,268.1 3,746.6–9,546.7 7,117.1 4,512.0–10,394.2
Dietary fiber (g/d) 124.3 34.0–319.5 55.2 13.9–140.2 112.6 56.3–273.9 190.7 111.1–391.1
Education (%)
≤10 29.6 35.3 30.6 24.5
11–13 39.2 39.9 39.0 38.9
≥14 31.3 24.8 30.4 36.7
Smoking status (%)
Never 41.3 34.8 40.2 46.8
Former 29.7 27.1 29.6 31.4
Current 29.1 38.0 30.2 21.8
Physical activity (%)
Very low 4.0 6.5 4.0 2.4
Low 10.3 11.7 10.6 8.8
Normal 57.2 56.5 57.7 56.7
High 16.3 13.5 15.6 19.2
Very high 8.1 6.6 7.8 9.5
Missing 4.1 5.2 4.2 3.4
Oral contraceptives (%)
Never 16.3 15.6 15.7 17.5
Former 70.8 70.0 71.1 70.9
Current 12.9 14.4 13.2 11.6
Menopause (%)
Yes 9.2 8.7 9.2 9.4
No 88.2 88.2 88.3 88.0
Missing 2.6 3.1 2.4 2.6
HNFI
All women (n = 45,222; cases = 314)0–1 points (n = 9,542; cases = 61)2–3 points (n = 20,772; cases = 141)4–6 points (n = 14,908; cases = 112)
CharacteristicsMedianP5–P95MedianP5–P95MedianP5–P95MedianP5–P95
Age 39 30–48 39 30–48 39 30–48 39 30–48
BMI 23 19–30 22.5 19–30 23 19–30 23 18–30.5
Alcohol drinking 2.9 0.2–11.9 3.0 0.2–12.8 2.9 0.2–12.0 2.8 0.2–10.9
Red meat intake (g/d) 48.9 13.1–101.6 41.3 6.6–91.5 47.9 13.6–98.7 52.1 17.4–105.7
Processed meat (g/d) 26.8 1.3–62.5 21.7 0–58.4 26.7 1.6–62.0 29.2 3.0–65.2
Energy (kJ/d) 6,384.7 3,631.3–9,832.5 5,472.7 2,820.4–8,847.5 6,268.1 3,746.6–9,546.7 7,117.1 4,512.0–10,394.2
Dietary fiber (g/d) 124.3 34.0–319.5 55.2 13.9–140.2 112.6 56.3–273.9 190.7 111.1–391.1
Education (%)
≤10 29.6 35.3 30.6 24.5
11–13 39.2 39.9 39.0 38.9
≥14 31.3 24.8 30.4 36.7
Smoking status (%)
Never 41.3 34.8 40.2 46.8
Former 29.7 27.1 29.6 31.4
Current 29.1 38.0 30.2 21.8
Physical activity (%)
Very low 4.0 6.5 4.0 2.4
Low 10.3 11.7 10.6 8.8
Normal 57.2 56.5 57.7 56.7
High 16.3 13.5 15.6 19.2
Very high 8.1 6.6 7.8 9.5
Missing 4.1 5.2 4.2 3.4
Oral contraceptives (%)
Never 16.3 15.6 15.7 17.5
Former 70.8 70.0 71.1 70.9
Current 12.9 14.4 13.2 11.6
Menopause (%)
Yes 9.2 8.7 9.2 9.4
No 88.2 88.2 88.3 88.0
Missing 2.6 3.1 2.4 2.6
Abbreviations: P5, 5th percentile; P95, 95th percentile.
A 1-point increment in the score was not associated with colorectal cancer (IRR, 1.04; 95% CI, 0.95–1.12) in the fully adjusted model; high adherers had an IRR of 1.09 (0.78–1.52) compared with low adherers (Ptrend = 0.40; Table 2).
Table 2.
IRR and number of colorectal cancer cases according to adherence to the HNFI
Model 1aModel 2bModel 3cModel 4d
Cases (n)IRR95% CIIRR95% CIIRR95% CIIRR95% CI
HNFI (linear, per 1-point increase) 314 1.04 0.96–1.12 1.05 0.97–1.14 1.04 0.97–1.13 1.04 0.95–1.12
0–1 61 1.00 Reference 1.00 Reference 1.00 Reference 1.00 Reference
2–3 141 1.01 0.75–1.36 1.04 0.77–1.40 1.02 0.75–1.38 1.00 0.74–1.36
4–6 112 1.10 0.80–1.50 1.16 0.84–1.59 1.13 0.82–1.56 1.09 0.78–1.52
Ptrend (linear) 0.38 0.21 0.27 0.40
Model 1aModel 2bModel 3cModel 4d
Cases (n)IRR95% CIIRR95% CIIRR95% CIIRR95% CI
HNFI (linear, per 1-point increase) 314 1.04 0.96–1.12 1.05 0.97–1.14 1.04 0.97–1.13 1.04 0.95–1.12
0–1 61 1.00 Reference 1.00 Reference 1.00 Reference 1.00 Reference
2–3 141 1.01 0.75–1.36 1.04 0.77–1.40 1.02 0.75–1.38 1.00 0.74–1.36
4–6 112 1.10 0.80–1.50 1.16 0.84–1.59 1.13 0.82–1.56 1.09 0.78–1.52
Ptrend (linear) 0.38 0.21 0.27 0.40
aCrude.
bAdjusted for BMI, education, smoking status, cigarettes/day, time since smoking cessation, and oral contraceptives.
cModel 2 plus alcohol, red/processed meat.
dModel 3 plus energy.
Stratification by cancer type, colon/rectum, did not reveal any difference in the effect of the HNFI between the two subgroups (results not shown).
In this large prospective study among Swedish women, a higher adherence to the HNFI was not associated with risk of colorectal cancer.
The lack of association may be due to the relatively few colorectal cancers in the cohort. It may also be explained by residual confounding: High adherers to the index had the highest intake of red/processed meats, dietary components that are associated with an increased risk of colorectal cancer (1).
The strength of the study includes the virtually complete follow-up, detailed information on intake of the dietary items included in the HNFI, and adjustment for potentially confounding variables. The study is limited by modest statistical power, and the assessment of dietary intake at only one time point, as the diet may change over the follow-up period. Most likely, however, such changes will be unsystematic, biasing the estimates toward unity.
The only previously published study on the HNFI and colorectal cancer (5) found an inverse association in women. However, these women were older than women in the present study (median age at baseline 56 years vs. 39 years). Age is likely to affect the type of colorectal cancer in the two cohorts, as colorectal cancers with a strong genetic component debut at a younger age (7), and dietary factors have not been proven to decrease risk of hereditary colorectal cancer (8). This could explain the lack of association in the present study.
In conclusion, we found no association between a HNFI and colorectal cancer among adult Swedish women. We were unable to confirm the findings of a previous cohort study.
No potential conflicts of interest were disclosed.
Conception and design: N. Roswall, Y. Li, S. Sandin, M. Löf, H.-O. Adami, E. Weiderpass
Development of methodology: N. Roswall, Y. Li, C. Kyrø, S. Sandin, M. Löf, H.-O. Adami, E. Weiderpass
Acquisition of data (provided animals, acquired and managed patients, provided facilities, etc.): H.-O. Adami, E. Weiderpass
Analysis and interpretation of data (e.g., statistical analysis, biostatistics, computational analysis): N. Roswall, Y. Li, S. Sandin, M. Löf, H.-O. Adami, E. Weiderpass
Writing, review, and/or revision of the manuscript: N. Roswall, Y. Li, C. Kyrø, S. Sandin, M. Löf, H.-O. Adami, E. Weiderpass
Administrative, technical, or material support (i.e., reporting or organizing data, constructing databases): H.-O. Adami, E. Weiderpass
Study supervision: N. Roswall, E. Weiderpass
H.-O. Adami received a grant from the Swedish Research Council. The work of N. Roswall was supported by the grant 521-2011-2955.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1.
World Cancer Research Fund/American Institute of Cancer Research
.
Continuous update project report: food, nutrition, physical activity, and the prevention of colorectal cancer
.
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NCI Dictionary of Cancer Terms
The NCI Dictionary of Cancer Terms features 8,378 terms related to cancer and medicine.
We offer a widget that you can add to your website to let users look up cancer-related terms. Get NCI’s Dictionary of Cancer Terms Widget.
Browse:
UVB radiation
(… RAY-dee-AY-shun)
Invisible rays that are part of the energy that comes from the sun. UVB radiation causes sunburn, darkening and thickening of the outer layer of the skin, and melanoma and other types of skin cancer. It may also cause problems with the eyes and the immune system. Skin specialists recommend that people use sunscreens that protect the skin from ultraviolet radiation. In medicine, UVB radiation also comes from special lamps or a laser and is used to treat certain skin conditions such as psoriasis, vitiligo, and skin tumors of cutaneous T-cell lymphoma. Also called ultraviolet B radiation.
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Boost your Grades with us today!
DESCRIBE THE DETERMINANTS OF HEALTH AND EXPLAIN HOW THOSE FACTORS CONTRIBUTE TO THE DEVELOPMENT OF THIS COMMUNICABLE DISEASES.
Write a paper (2,000-2,500 words) in which you apply the concepts of epidemiology and nursing research to a communicable disease. Refer to “Communicable Disease Chain,” “Chain of Infection,” and the CDC website for assistance completing this assignment.
Communicable Disease Selection
Choose one communicable disease from the following list:
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HIV
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Measles
Polio
Influenza
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Address the following:
Describe the communicable disease (causes, symptoms, mode of transmission, complications, treatment) and the demographic of interest (mortality, morbidity, incidence, and prevalence). Is this a reportable disease? If so, provide details about reporting time, whom to report to, etc.
Describe the determinants of health and explain how those factors contribute to the development of this disease.
Discuss the epidemiologic triangle as it relates to the communicable disease you have selected. Include the host factors, agent factors (presence or absence), and environmental factors. (The textbook describes each element of the epidemiologic triangle). Are there any special considerations or notifications for the community, schools, or general population?
Explain the role of the community health nurse (case finding, reporting, data collecting, data analysis, and follow-up).
Identify at least one national agency or organization that addresses the communicable disease chosen and describe how the organization(s) contributes to resolving or reducing the impact of disease.
Discuss a global implication of the disease. How is this addressed in other countries or cultures? Is this disease endemic to a particular area? Provide an example.
A minimum of three peer-reviewed or professional references is required.
Prepare this assignment according to the guidelines found in the APA Style Guide, located in the Student Success Center. An abstract is not required.
This assignment uses a rubric. Please review the rubric prior to beginning the assignment to become familiar with the expectations for successful completion.
You are required to submit this assignment to LopesWrite. Please refer to the directions in the Student Success Center.
NRS427V-RS-CommunicableDiseaseChain.doc
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Can Grip & Hand Position Maximize Your Lat Pulldown?
One of the more popular exercises used to develop the back is the lat pulldown. Many gym goers seem to like is the versatility of this compound exercise. It is an exercise that offers multiple grip variations. In addition, most gyms typically have 3-4 attachments that you can switch to. Does it make a difference though how you hold these attachments? Let’s take a deeper look and find out.
Hand Grip & Placement in Lat Pulldown
Overhand Grip
The overhand grip is used most often when performing a lat pulldown. In one study, published in the Strength and Conditioning Journal, the lat pulldown was examined for muscle activation. The study showed a pronated, or overhand grip, demonstrated greater muscle activation. The overhand grip was compared to both supinated (underhand grip) and a neutral grip.
Underhand Grip
When you look at this from a biomechanic standpoint, underhand grip does have its benefits. The underhand grip provides a far superior muscle contraction of the lats at the bottom of the movement. You can also handle more weight using an underhand grip compared to an overhand grip. Finally, the closer your hands are positioned on the bar, the more activation you get in the center of your back.
Wide Grip
Many gym goers believe if you use a wider grip you’ll get wider (“thicker”) lats. Placing your hands wider on the lat pulldown bar, decreases the range of motion in the latissimus dorsi. The best bet is to use a diverging movement pattern machine. Wider hand placement means the range of motion at the shoulder increases. Therefore, the lats work through a greater range of motion. See here in this Jefit Instagram post. The wide grip lat pulldown activates significantly more lats and upper back. This is due to the position of the arms (external rotation).
Narrow Grip
Changing the hand placement to narrow (or a close grip) allows more internal rotation of the arms. The narrow grip shifts some of the load away from the lats and puts it on your chest. Even though a wide grip gets a little more activation of the lats, the narrow grip lat pulldown puts your arms in a stronger position, and you can generally pull more weight.
Research Review on the Topic
A 2010 electromyographic study (EMG) study was published in the Journal of Strength & Conditioning Research. The study compared four variations of lat pulldowns. The study used a dozen test subjects who performed all four variations pulling from in front of the head with a predetermined load, about 70 percent of their one repetition max. Muscle response from the latissimus dorsi, middle trapezius and biceps brachii muscle groups were measured during all four lat pulldown variations. The study showed that there was a minor advantage to using a medium grip (i.e. shoulder-width) over narrow and wide grips.
Subsequent Study
A 2009 EMG study looked at the muscular activity difference between a lat pulldown in front of the head versus behind the head as well as a lat pulldown using a ‘V’ bar. The study used 24 test subjects performing five repetitions at 80 percent of their one rep max. EMG data was recorded from the pectoralis major, posterior deltoid and biceps brachii as well as the latissimus dorsi muscle groups. There was no difference in muscular activity for the latissimus dorsi when comparing the three variations. The study, however, concluded when the primary objective of a lat pulldown is considered, the front of the head is a better choice than behind the head due to shoulder safety issues.
For best results, you can’t go wrong changing up both your grip and hand placement every few training sessions.
Try the Jefit App
Jefit is an award-winning gym workout app that helps all gym goers and athletes keep track of their fitness goals. Not only does it give you the ability to update and share your workout log with the supportive community, it has the largest exercise library that covers weight training, cardio and flexibility.
blank
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Diarrhea/ConstipationPre, Pro, Synbiotics
Probiotics to prevent traveler’s diarrhea
Several were effective.
Dr. Lynne McFarland from the VA Puget Sound Health Care System in Seattle, Washington screened 940 studies and found 12 that were worth evaluating.
And the results.
• Several probiotics (Saccharomyces boulardii, and a mixture of Lactobacillus acidophilus, and Bifidobacterium bifidum) had significant efficacy.
• No serious adverse reactions were reported.
Here are the top 10 recommendations from the Mayo Clinic to reduce the risk of Montezuma’s revenge.
10. No food from street vendors.
9. No unpasteurized milk or dairy products.
8. Eat foods that are well cooked, hot foods.
7. No moist food at room temperature.
6. Eat fruits and vegetables you can peel.
5. No salads and unpeelable fruits.
4. Use only clean dishes and utensils.
3. Wash your hands often and before eating.
2. Keep children from putting things in their mouths.
And the most important thing you can do?
1. Don’t drink the water.
5/23/07 22:41 JR
Hi, I’m JR
John Russo, Jr., PharmD, is president of The MedCom Resource, Inc. Previously, he was senior vice president of medical communications at www.Vicus.com, a complementary and alternative medicine website.
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Orchard Chiropractic Centre - Jersey
High BMI, Low Lean Body Mass and Childhood Obesity
Wednesday 30 October 2019
At a recent chiropractic seminar it was observed through palpation that the majority of the delegates felt 'a bit flabby' suggesting low muscle mass (low lean body mass). The delegates in question were between the ages of 23 and 35 and therefore should have been at their peak, yet their lack of muscle suggested longstanding low levels of exercise and poor nutrition (or poor absorption which can be due to poor gut flora and/ or poor food choices). This observation is pertinent as it offers an insight into the state of the nation's health and the direction it is headed.
What is BMI?
Most people are familiar with the Body Mass Index (BMI) which uses mass and height to categorise you from under weight to obese. This can be useful, however, scientists investigating the link between BMI and morbidity noticed what they termed the 'obesity paradox'. The paradox is that studies have shown that people at the higher end of the BMI scale and those at the bottom had increased risk of death from all causes.
The paradox exists because the BMI is a measure of body mass in relation to height. BMI does not account for muscle mass, or visceral fat. Therefore a short muscular person can appear as having a high BMI (obese) and a tall thin person with excess visceral fat can register in the normal/ ideal range. Research shows that visceral fat (fat around the organs) is 300% more inflammatory than other body fat. As will be discussed, new evidence shows that lean body mass is a far more accurate predictor of health than BMI.
Lean Body Mass
A US study[1] of more than 38,006 men found that men with low lean body mass (low muscle mass) and those with a high fat mass had an increased the risk of mortality from all causes. This finding suggests that the “obesity paradox” controversy may be largely explained by low lean body mass, rather than low fat mass, in the lower range of BMI.
According to a study published in 2018[2] fat-to-muscle ratio is highly predictive of metabolic syndrome[3]. Additionally, the authors cited another study that showed that the muscle-to-fat ratio is also clinically useful for evaluating the presence of insulin resistance.
Ideal Muscle to Fat Ratio
Ideal muscle to fat ratio for men is 3:1 compared to 2:1 for females. Muscle mass in the stated ratios is evidence of and promotes hormonal balance, especially insulin and oestrogen. In order to reduce one's fat mass and increase muscle mass oestrogen and insulin levels must be normal as imbalance promotes a whole host of symptoms including fat storage, fatigue and weakness.
The prevalence of insulin resistance, diabetes and other hormonal disorders in the west is intrinsically linked to the high carbohydrate, low fat diet that has been advocated for the past 60 years. A prolonged high carbohydrate diet reduces insulin sensitivity which reduces glucose transport from the blood to the muscles, increases insulin secretion and promotes fat storage. Another side effect of increased carbohydrate consumption is oestrogen dominance compared to progesterone. Side effects of oestrogen dominance include insulin resistance, weakness, fatigue and weakening of the bones (symptoms of menopause).
How to Increase Lean Body Mass
Exercise and nutrition are key regulators of muscle mass. Resistance training is particularly important for building mass. Big muscles burn more fuel than small muscles, so it is easier to keep the flab off if you have good muscle mass and tone. A study published in 2018[4] showed that even moderate resistance training reduces the risk of type 2 diabetes by 30%.
In order to build healthy muscle, your body requires adequate supply of nutrient dense foods containing proteins, fatty acids, vitamins and minerals. The following link will take you to the relevant page of our website containing low carbohydrate and gluten free recipe ideas and anti inflammatory foods https://www.orchard.co.je/info/food-ideas/. An absence of nutrient dense food in conjunction with lack of exercise is driving the obesity epidemic and associated conditions that is crippling state health systems. The following link will take you to the relevant page of our website with suggested exercise routines, videos and exercise information https://www.orchard.co.je/info/exercises/
In addition to treating musculoskeletal pain, at the Orchard Chiropractic Centre, Jersey we recognise that nutrition and exercise are essential for optimal health and regularly try to assist our patients to make lifestyle changes to improve their health and wellbeing. Although as an adult adopting a healthy lifestyle is always beneficial, there is far more to be gained from ensuring that our children enjoy a healthy lifestyle so that they do not become part of the obesity/ diabetes epidemic.
Childhood Obesity Statistics for Jersey
Childhood obesity is a significant problem in the western world and one that is growing in countries where a western (high carbohydrate, low fat) diet is becoming more popular. Poor nutrition, lack of exercise, inadequate sleep and environmental factors all contribute to cause what is now being termed a public health disaster. The States of Jersey Health Department has been monitoring obesity in Jersey since 1997 and the results do not make good reading for islanders: 20% of 4-5-year-olds in Jersey are overweight or obese, increasing to a third of 10-11-year-olds. There is a significant difference in the proportion of obese 10-11-year-olds residing in rural parishes (10%), compared to around one in five children living in urban (21%) or semi-urban areas (20%). Students in non fee paying schools were more likely to be obese.
Conclusion
Statistics show that obese children tend to grow into obese adults and they have obese children which perpetuates the cycle and associated diseases. If we are to break the cycle we need to provide our children with nutrient rich low carbohydrate food and get them into the habit of regular exercise. In practice this means eating:
• oily fish
• animal and dairy fats from grass fed animals
• nuts and seeds
• bitter foods such as cabbage
• fresh leafy vegetables with every meal
If you would like a more complete list of foods to eat and avoid, please ask at reception or speak to one of our chiropractors Charles and Cardin who will be happy to discuss further.
[1] Lee DH, Keum N, Hu FB, et al. Predicted lean body mass, fat mass, and all cause and cause specific mortality in men: prospective US cohort study. BMJ. 2018;362:k2575. Published 2018 Jul 3. doi:10.1136/bmj.k2575
[2] Ramírez-Vélez, Robinson et al. “Fat-to-Muscle Ratio: A New Anthropometric Indicator as a Screening Tool for Metabolic Syndrome in Young Colombian People.” Nutrients vol. 10,8 1027. 7 Aug. 2018, doi:10.3390/nu10081027
Meet The Orchard Practioners
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At Orchard Chiropractic and Health Centre Jersey we have a group of experienced chiropractors and complementary health practitioners that help you look holistically at your health from a physical, chemical and emotional perspective.
View the Orchard Practioners »
Testimonials
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What our Patients say about our Chiropractors and our health centre
View our Testimonials »
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Rock Salt Bath can relieve muscle cramps
KDAH
Did you know? Rock salt baths can provide relief from muscle cramps! The minerals in rock salt, like magnesium and potassium, are absorbed through the skin, helping to relax muscles and ease tension. It's a natural remedy that's been used for centuries. Talk to your doctor before trying it out. #RockSaltBaths #MuscleCrampRelief #NaturalRemedy
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Vibrator
Inventions>Medical
Joseph Mortimer Granville 1880
Female Hysteria
Female Hysteria
Granville patented an Electro-mechanical Vibrator 1880. Originally called a percusser or more colloquially "Granville's hammer", the machine was manufactured and sold to physicians to relieve muscle aches.
Dr. Joseph Mortimer Granville was born in London, England 1833.
Hysteria
The "pelvic massage" was a common treatment of female hysteria (overwhelming or unmanageable emotional excess in the womb) in Great Britain during the Victorian Era. This manipulation was to cause "hysterical paroxysm" (outburst from the womb) in the patient. It was not widely accepted that women could experience orgasm, that was a male reserve. But this treatment was very demanding on doctors who found themselves suffering from fatigued wrists and hands.
Granvilles invention became increasingly popular as a way for doctors to provide "pelvic massage" Joseph tried to disassociate himself from the device's "mis-use".
Vintage vibrator
Vintage vibrator
The historical but largely fictional film Hysteria features a reworked history of the vibrator focusing on Dr. Granville's invention.
The emblem of Rule Britannia
In History
Who Invented?
Who Discovered?
Who Created?
The History of..
Prevalence:Granville, Joseph, Vibrator
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புதியதொரு தேடியந்திரம் அறிமுகம் ஆகியுள்ளது.
Sri...
கிளிக் செய்யாமலே தேடுவதற்க்கு ஒரு தேடுயந்திரம்.
எத்தனை காலம் தான் கூகுலையே பயன்படுத்திக்கொண்டிருப்பது ஒரு மாற்றம் தேவை என நினைத்துக்கொண்டிருப்பவர்களுக்கு மகிழ்ச்சி தரும் செய்தியாக புதியதொரு தேடியந்திரம் அறிமுகம் ஆகியுள்ளது.கூகுலை விட்டு விட்டு இனி தாரளமாக அந்த தேடியந்திரத்தை பயன்படுத்தி பார்க்கலாம்.
அட போங்கய்யா கூகுலைவிட சிறந்த தேடியந்திரமா? எத்தனை முறை இதே வர்ணனையை கேட்டு ஏமாந்திருக்கிறோம் என அலுத்து கொள்பவர்கள் கவனிக்க உண்மையிலேயே சூப்பர் தேடியந்திரம் இது என்பதை உறுதியாக சொல்லலாம்.
டக்டக்கோ என்னும் விநோதமான பெயர் கொண்ட அந்த புதிய தேடியந்திரம் உண்மையிலேயே கூகுலுக்கு மாற்றாக விளங்க கூடிய ஆற்றலை பெற்றிருக்கிறது.
இணைய உலகில் சற்றேரக்குறைய இரண்டாயிரத்துக்கும் அதிகமான தேடியந்திரங்கள் உள்ளன.இவற்றில் பல அறிமுகமாகும் போது கூகுலுக்கு மாற்று என வர்ணித்துக்கொள்வது வழக்கம் தான்.ஒரு சில தேடியந்திரங்களை அடுத்த கூகுல் என்று பத்திரிகைகள் வர்ணிப்பதும் வழக்கம்.ஆனால் இதுவரை எந்த தேடியந்திரத்தாலும் கூகுலை ஒரங்கட்ட முடியவில்லை.
முன்னால் கூகுலர்களால் ஆரம்பிக்கப்பட்ட குயில்(cuil) தேடியந்திரம் கூட இப்படி தான் கூகுலுக்கான சவால் என்று அழைக்கப்பட்டு ஏக பரபரப்பை ஏற்படுத்தியது. அதன் பிறகு என்ன ஆனது என்றே தெரியாமல் போய் இப்போது விக்கிபீடியா பாணியில் களஞ்சிய தேடியந்திரமாக தன்னை உருமாற்றி கொண்டுள்ளது.
தேடியந்திர வரலாற்றை அறிந்தவர்கள் புதிய தேடியந்திரங்கள் வரும் போகும் ஆனால் கூகுல் எல்லோராலும் நாடப்படும் தேடியந்திரமாக தொடரும் என்பதை அறிந்தேயிருப்பார்கள். அதிலும் சாமன்ய இணையவாசிகளை பொருத்தவரை தேடல் என்றால் கூகுல் தான்.
கூகுல் அதன் வேலையை ஒழுங்காக செய்கிறது என்பதும் அதனை மிஞ்சக்கூடிய தொழில்நுட்பம் இன்னும் சாத்தியமாகவில்லை என்னும் நிலையில் இன்னுமொரு தேடியந்திரமாக உதயமாகியுள்ள டக்டக்கோ மாறுபட்ட தேடியந்திரம் என்னும் உணர்வை முதல் பார்வையிலேயே தந்து வியக்க வைக்கிறது.
கூகுலைப்போலவே இன்னொரு தேடியந்திரம் என்று தன்னை மற்றி அடக்கமாகவே கூறிக்கொள்ளும் டக்டக்கோ கூகுலுக்கு பதிலாக ஏன் தன்னை முயன்று பார்ப்பதற்கு என்று நெத்தியடியாக சில காரணங்களை பட்டியலிடுகிறது.
கூகுலை விட சிக்கல் இல்லாத தேடல் பக்கம்,விளம்பர இடையூறு இல்லாத தேடல் முடிவுகள் ,சிறப்பான குறுக்கு வழிகள் என நீளும் அந்த பட்டியலில் உண்மையிலேயே நெத்தியடியான அமசம் பூஜ்ய கிளிக் வசதியாகும். ஜீரோ கிளிக் என குறிப்பிடப்படும் இந்த வசதியை கிளிக் செய்யாமலேயே தேடுவது என புரிந்து கொள்ளலாம்.
அதெப்படி கிளிக் செய்யாமலேயே தேடுவது சாத்தியம்?வழக்கமாக தேடும் போது என்ன செய்வோம்.கீவேர்டை டைப் செய்துவிட்டு தேடு என கட்டளையிடுவது போல என்டர் தட்டுவோம் அல்லவா?அதன் பிறகு தேடல் முடிவுகள் வந்து நிற்கும் அல்லவா?அதில் ஏதாவது ஒன்றை கிளீக் செய்தால் தான் தேவிஅயான் தகவல்களை பெற முடியும். ஆனால் டக்டக்கோ தேடியந்திரமோ கிளிக் செய்ததுமே தேடப்படும் பதம் தொடர்பான அறிமுக குறிப்புகளாக சில தகவல்கலை அளிக்கிறது.
இந்த குறிப்புகள் மிகச்சரியாக தேடப்படும் பொருள் குறித்த சரியான அறிமுகமாக அமைந்து விடுகிறது.உதாரனத்திற்கு பிரெஞ்சு ஒபன் என் தேடினால் பாரிசில் மே மாதம் துவங்கி நடைபெறும் டென்னிஸ் போட்டி என்ற அறிமுகம் கிடைக்கிறது.பல நேரஙக்ளில் தேடப்படும் பொருளை புரிந்து கொள்ள இந்த அறிமுகம் உதவலாம். சில நேரங்களில் இந்த அறிமுகமே கூட போதுமாக இருக்கலாம்.புதிய பொருள் குறித்து மிக அவசரமாக தேடும் போது அறிமுக குறிப்புகள் நிச்சயம் பயனுள்ளதாக இருக்கும்.
விக்கிபீடியா போன்ற தளங்களில் இருந்து எடுக்கப்பட்டாலும் கூட இந்த அறிமுகம் பயனுள்ளதாகவே இருக்கிறது.விரிவான தேடல் தேவை என்றால் பக்கவாட்டில் உள்ள வசதியை துணைக்கு அழைத்து யூடியூப் உடபட பல இடங்களில் தேட முடியும்.
இந்த தேடியந்திரத்தில் கூகுல் என டைப் செய்து பார்த்தால் கூகுல் என்றால் பல அந்ததம் உண்டு உங்களுக்கு எது வேண்டும் என்று கேட்கப்படு அதன் கீழேயே கூகுல் என்றால் தேடியந்திரம் என்ற அறிமுகமும் இடம் பெறுகிறது.பலவித அர்த்தங்களில் ஒன்றாக கூகுல் என முடியும் பெயர் கொண்டவர்களும் பட்டியலிடப்பட்டுள்ளனர்.
இந்த அமசத்திற்காக நிச்சயம் இதனை பயன்படுத்தி பார்க்கலாம்.இதனை தவிர தேடல் பக்கம் கூகுலைவிட தெளிவானதாக சிக்கலில்லாமல் இருப்பதாக கூறப்பட்டுள்ளது. அதே போல தேடல் வரலாற்றை சேமித்து வைப்பதில்லை என்றும் குறிப்டப்பட்டூள்ளது.
இந்த அம்சங்கள் எல்லாவற்றையும் கூகுலோடு ஒப்பிட்டு பார்க்கும் வசதியும் கொடுக்கப்பட்டுள்ளது.
எல்லாவற்றுக்கும் மேல் இத முகப்பு பக்கம் வண்ணமயமாக வாத்து மற்றும் இதர ஐகான்களோடு அழகாகவே இருக்கிறது.அதோடு கூகுலில் இருக்கும் அதிர்ஷ்ட தேடல் வசதியை போல (ஐஅய்ம் பீலிங் லக்கி) ஐயம் பீலிங் டக்கி என்னும் கூடுதல் வசதியும் உண்டு.
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Better Surgeons Get Better Results
sharma-obesity-bariatric-surgery21This one may not seem all that earth-shattering but according to a paper by John Birkmeyer and colleagues, published in the New England Journal of Medicine, better surgeons get better results.
the study involved 20 bariatric surgeons in Michigan, who each submitted a single representative videotape of himself or herself performing a laparoscopic gastric bypass, which was then rated by at least 10 of his colleagues (blinded of course) in various domains of technical skill on a scale of 1 to 5 (with higher scores indicating more advanced skill).
This score (ranging between 2.6 and 4.8 across the 20 surgeons) was then compared to risk-adjusted complication rates, using data from a prospective, externally audited, clinical-outcomes registry involving 10,343 patients.
Surgeons rated by their peers as being in the bottom quartile of surgical skill had almost three times higher complication rates and almost five times higher mortality rates than those in the highest skill quartile (14.5% vs. 5.2% and 0.26% vs. 0.05%, respectively).
The lesser skilled surgeons also took longer (137 minutes vs. 98 minutes), their patients were twice as likely to be reoperated (3.4% vs. 1.6%, P=0.01) or readmitted.
This study highlights the wide variability in surgical skill (which can apparently can be judged by other surgeons by watching a single video of the surgeon at work) and the impact that this variation may have in terms of outcome.
Although, I am the first to note that the surgery itself is only one factor in successful outcomes with bariatric surgery, the least you can hope for, is to have the best surgeon perform the procedure.
@DrSharma
Montreal, QC
ResearchBlogging.orgBirkmeyer JD, Finks JF, O’Reilly A, Oerline M, Carlin AM, Nunn AR, Dimick J, Banerjee M, Birkmeyer NJ, & the Michigan Bariatric Surgery Collaborative (2013). Surgical Skill and Complication Rates after Bariatric Surgery. The New England journal of medicine, 369 (15), 1434-1442 PMID: 24106936
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4 Comments
1. Wonderful article and so very true. It is easy for patients to forget that surgeons are humans too. They have different abilities and often different techniques in performing the surgery. The VSG for example, is not standardized and is performed quite differently by different surgeons based on their technical skill, overall philosophy, understanding of the current research and so many other factors. All of these differences when taken together make it almost impossible to rely on studies that are aimed at the efficacy of this surgery. Some surgeons make substantially larger sleeves than others, some operate in way that minimize the problem of reflux, others do not. Some have substantially higher rates of leaks and other complications. This does not even begin to address the issues of aftercare and follow-up. I often hear doctors derisively mention that some of the surgeons with lower complication rates have pre-selected their patients. That might very well be the case in some or even many practices, however, I am fortunate enough to know of one where the exact opposite is true. The surgeon is actually known within the medical community for taking cases others will not touch and yet maintaining complication rates that are far bellow the national average. Yes, the surgical technique matters, it matters a great deal. The aftercare also matters as does continued nutritional follow-up. As with everything else in life, it is not surprising that caveat emptor- buyer beware, is as true when choosing a surgeon as when choosing a car. Life is full of inequalities of choice and outcomes.
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2. Dr Sharma,
I think it is wrong for obese patients to be put “under the knife” before they have received competent instruction on nutrition matters. The great news is that losing weight can be easy. No-one needs to go hungry. There is no need for semi-starvation. Readers, here’s the centuries-old gold-standard “obesity-reversing, diabetes-reversing” diet (scroll down):http://www.australianparadox.com/pdf/why-we-get-fat.pdf
And here’s an excellent piece by heavy-hitter Gary Taubes on why that “all you can eat” diet works. In the process, he explains how the western world’s negligent low-fat/high-carb dietary advice starting in the 1970s made the world fat and sick: http://garytaubes.com/wp-content/uploads/2012/02/WWGF-Readers-Digest-feature-Feb-2011.pdf
The problem is that modern nutrition science has been barking up the wrong (low-fat/high-carb) tree for the past 30-40 years, having forgotten much of what was learned about diet and obesity over the previous couple of centuries. That’s why so many of us have become fat and sick. For most obese people, in my opinion, good nutrition advice would remove any need for surgery.
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3. I live in Canada.
How do I find out who is the best, or one of the best, surgeons?
Is this information publicly available, or is it kept secret within medical circles?
When I find out how surgeons in my area are rated, how do I get one of the better surgeons to do my surgery?
When I have had other surgery, not bariatric surgery, I have had no choice in who operated on me. Same for friends undergoing surgery. We show up for an operation and we get whichever surgeon has been assigned to the case. There is no chance to consider who will be operating on us. (I dare say surgeons differ in ability in all surgery, not just bariatric surgery.)
Is this the same in other countries – in the US, do patients get to choose their surgeon?
If there is no option to choose a better surgeon, then it doesn’t matter if they’re “good” or not, or what the probable outcome is, you just have to go with the luck of the draw.
And if poor surgeons get just as many operations as good surgeons, there is no incentive to improve.
Post a Reply
4. Anonymous,
Some things that you should ask any bariatric surgeon that you’re seeing (and that they should be very forthcoming with, no mumbles or sidestepping):
1. What is your rate of DVT/PE, leak, or death within 90 days of surgery? Should be less than 1%
2. What is your rate of readmission to the hospital within 30 days? Should be less than 5%
3. What is your rate of reoperation within 30 days of surgery? Should be less than 5%, but not zero – that would mean the surgeon is doing nothing in the face of some concerning symptoms that should prompt a re-look.
4. What is the average length of stay in the hospital? (should be less than 3 nights for most surgeons)
5. What is the rate of stricture requiring intervention (for bypass or sleeve).
6. What is the rate of infection of any kind? (should be less than 5%).
These are very general numbers, and I’m sure some surgeons would complain that they’re too lax and others would complain that they’re too strict (“It isn’t fair, I can’t achieve that because XXX, the sun is in my eyes, the grass is too high, etc. etc.”) If they can’t answer these you have to ask yourself if they’re doing enough self-evaluation of outcomes (results). And if they’re being evasive, that’s a deal-breaker.
Rory Robertson, I agree that the high-carb advice that started in the 60’s and 70’s (along with the low-fat advice) persists as an unfortunate legacy, and no doubt contributes to weight gain. I’m very familiar with Mr Taubes and Dr Attia’s work. Unfortunately, some patients (it sounds like you’re not one of them) can eat a high protein / high fat diet (or paleo diet or Atkins/South Beach or Weston Price or nutrition science institute or whatever you choose to call it) and they may stop the weight gain, but they typically do not lose 100+ extra pounds. If most people would simply stop the weight gain, though, and never progress to morbid obesity, that would be a real boon. But what works to help one person lose 100 lbs doesn’t always work for everyone. Thanks for your comments, though.
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The coronavirus disease (COVID-19) causes a respiratory infection that can involve the following symptoms:
Fever
Cough
Trouble Breathing
Protecting yourself saves lives.
Keep your distance
Stay at home
Cough into your sleeves
Throw your used tissues into the trash
Wash your hands
Québec.ca / coronavirus 1 877 644-4545
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Help Me Make it Through the Night: Restless Legs Syndrome
Sharing is Caring!
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It seems like your legs just won’t stop moving even when you try to sleep. Restless leg syndrome can lead to many a sleepless night.
If you have been experiencing something like this, it’s time to get help.
What Is Restless Leg Syndrome?
Restless leg syndrome or RLS is the term used to describe the movement of your legs when your body is at rest. Those who have this condition often say that they have an uncontrollable urge to move their legs even though they want to go to sleep.
The only thing that seems to make the legs feel better is to move. But, if it is midnight, you’d rather be asleep than walking around. What can you do?
Millions of people are affected by this condition. Some have inherited it, but the incidence of RLS can increase as you get older. In any case, as the day winds down, your legs are just ramping up.
What is it about this condition?
There are many different words used to describe the sensation, but here are just a few:
* Crawling
* Tingling
* Pain
* Electric feeling
* Tension
* Itching
* Burning
* Creeping feeling
This occurs throughout the entire leg. It is often felt in the calves and thighs. Some people even feel these sensations in their hands and feet.
No one exactly knows why restless leg syndrome occurs. It is believed by researchers to be linked to the level of certain neurotransmitters in the brain, specifically dopamine. Dopamine is a neurotransmitter that controls muscle movement in the body. Low levels of it are believed to lead to problems like this.
What can you do to get a good night’s sleep again?
All is not lost. You can reduce the incidence of discomfort in your legs with a few tips.
* Get exercise. Muscles change and grow as they respond to stress placed upon them. This is what happens when you get the body pumping with exercise like aerobics and weight training. The muscles need time to rest and repair after a good workout and this can lead to a calmer night for you.
* Avoid caffeine and other stimulants. If you need to feel refreshed in the morning, then by all means, have a cup of coffee. But, try to avoid drinking it too late in the afternoon. Caffeine can overstimulate you and even increase your leg movement at night.
* Engage your mind. If the body has to sit, then let the mind stay busy. In the evenings, try reading a stimulating book, engage in a little “neur-obics” with crossword puzzles or try a hobby like sewing, model building or painting.
* Take a relaxing bath. Muscles become more pliable and relaxed in the presence of warmth. Try a nightly soak in the bath with infusions of lavender or chamomile. Both are herbs that are used to relax the body. Give those legs a good rub as well to settle them down.
Restless leg syndrome can disrupt your sleep cycle and your entire life. Use the tips above to help alleviate as many symptoms as you can to get your life back under control.
Related Natural Product
LegCalm is a natural, safe and effective herbal and homeopathic remedy for treating Restless Leg Syndrome (RLS) and Periodic Limb Movement (PLM). Presented in convenient capsule form, regular use can help to relieve the symptoms of these troublesome sleep disorders as well as address the underlying causes.
This remedy eliminates the crawling and uncomfortable sensations experienced in RLS; prevents night-time twitching, restlessness and muscle spasms; promotes more restful and uninterrupted sleep; helps with improved circulation and aids absorption of minerals from the diet, preventing deficiencies and anemia. Formulated by a clinical psychologist, LegCalm is pharmaceutically manufactured to the highest standards.
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1a01aa77535b9ecfb87b9fc36adbcd2f
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-1,045,366,756,973,367,600
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Faculty Research 1970 - 1979
Title
Allogeneic placenta is a paternal strain antigen immunoabsorbent.
Document Type
Article
Publication Date
1979
Keywords
Animal, Antibodies, Antibody-Specificity, Female, Fetus: su, H-2-Antigens: im, Male, Mice, Mice-Inbred-BALB-C, Mice-Inbred-CBA, Mice-Inbred-C3H, Mice-Inbred-C57BL, Placenta: im, me, Pregnancy
JAX Source
J-Immunol. 1979 Jan; 122(1):270-4.
Abstract
A partially purified 125I-labeled antibody directed against the murine major histocompatibility complex and injected i.v. pregnant females is selectively absorbed by the placenta when the fetus bears the appropriate targen antigen. The placenta specifically absorbs the antibody at both 13 days and 17 days of gestation, and the differential uptake is found as early as 2 hr after injection and as late as 12 hr. It is also seen in 13-day placentas that have had the fetus removed surgically, indicating that fetal circulation is not essential for the absorption to take place. Specificity controls eliminate the possibility that the differential uptake is due to Fc receptor binding or undefined effects of hybrid vigor. This increase in binding is not seen in the livers, spleens, kidneys, or lungs of the pregnant females. There is a slight decrease in radioactivity in the serum. These results indicate that the placenta is a paternal antigen-bearing immunoabsorbent that could serve as a barrier between the maternal immune response and the semi-allogeneic fetus.
Please contact the Joan Staats Library for information regarding this document.
Share
COinS
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Conditions / Psoriatic Arthritis
Psoriatic Arthritis
Overview
Psoriatic arthritis is a form of arthritis that affects some people who have psoriasis — a condition that features red patches of skin topped with silvery scales. Most people develop psoriasis first and are later diagnosed with psoriatic arthritis, but the joint problems can sometimes begin before skin lesions appear.
Joint pain, stiffness and swelling are the main symptoms of psoriatic arthritis. They can affect any part of your body, including your fingertips and spine, and can range from relatively mild to severe. In both psoriasis and psoriatic arthritis, disease flares may alternate with periods of remission.
No cure for psoriatic arthritis exists, so the focus is on controlling symptoms and preventing damage to your joints. Without treatment, psoriatic arthritis may be disabling.
Symptoms
Both psoriatic arthritis and psoriasis are chronic diseases that get worse over time, but you may have periods when your symptoms improve or go into remission alternating with times when symptoms become worse.
Psoriatic arthritis can affect joints on just one side or on both sides of your body. The signs and symptoms of psoriatic arthritis often resemble those of rheumatoid arthritis. Both diseases cause joints to become painful, swollen and warm to the touch.
However, psoriatic arthritis is more likely to also cause:
Swollen fingers and toes
Psoriatic arthritis can cause a painful, sausage-like swelling of your fingers and toes. You may also develop swelling and deformities in your hands and feet before having significant joint symptoms.
Foot pain
Psoriatic arthritis can also cause pain at the points where tendons and ligaments attach to your bones — especially at the back of your heel (Achilles tendinitis) or in the sole of your foot (plantar fasciitis).
Lower back pain
Some people develop a condition called spondylitis as a result of psoriatic arthritis. Spondylitis mainly causes inflammation of the joints between the vertebrae of your spine and in the joints between your spine and pelvis (sacroiliitis).
When to see a doctor
If you have psoriasis, be sure to tell your doctor if you develop joint pain. Psoriatic arthritis can severely damage your joints if left untreated.
Causes
Psoriatic arthritis occurs when your body’s immune system begins to attack healthy cells and tissue. The abnormal immune response causes inflammation in your joints as well as overproduction of skin cells.
It’s not entirely clear why the immune system turns on healthy tissue, but it seems likely that both genetic and environmental factors play a role. Many people with psoriatic arthritis have a family history of either psoriasis or psoriatic arthritis. Researchers have discovered certain genetic markers that appear to be associated with psoriatic arthritis.
Physical trauma or something in the environment — such as a viral or bacterial infection — may trigger psoriatic arthritis in people with an inherited tendency.
Risk factors
Several factors can increase your risk of psoriatic arthritis, including:
Psoriasis
Having psoriasis is the single greatest risk factor for developing psoriatic arthritis. People who have psoriasis lesions on their nails are especially likely to develop psoriatic arthritis.
Age
Although anyone can develop psoriatic arthritis, it occurs most often in adults between the ages of 30 and 50.
Family history
Many people with psoriatic arthritis have a parent or a sibling with the disease.
Complications
A small percentage of people with psoriatic arthritis develop arthritis mutilans — a severe, painful and disabling form of the disease. Over time, arthritis mutilans destroys the small bones in your hands, especially the fingers, leading to permanent deformity and disability.
People who have psoriatic arthritis sometimes also develop eye problems such as pinkeye (conjunctivitis) or uveitis, which can cause painful, reddened eyes and blurred vision. They also are at higher risk of cardiovascular disease.
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Mortality rates, risk factors and treatment patterns in patients diagnosed with moderate-to-very-severe chronic obstructive pulmonary disease in England: a retrospective observational study using CPRD data
Date of Approval
Application Number
21_000379
Lay Summary
Chronic obstructive pulmonary disease (COPD) is a common lung condition that causes breathing difficulties such as breathlessness, coughing and wheezing. As these symptoms get worse, it can lead to the patient needing to be treated in hospital and may lead to death. The severity of the disease is measured on a scale ranging from mild, moderate, severe to very severe. This study focuses on those with moderate-to-very-severe COPD. The study aims to investigate risk of death from all causes, understand which factors influence the risk of death, and describe medication used in patients diagnosed with moderate-to-very-severe COPD in England.
First, we will investigate whether the population in the CPRD database is representative of the population of England with respect to mortality (i.e. death rates) and explore the availability of information needed for our study among all COPD patients in the CPRD database, such as data on lung function tests.
Dependent upon these results, we will specify criteria to select the subgroup of COPD patients to be included in our analyses. We will calculate the risk of death, e.g. by comparing the risk of death to a group of patients with similar characteristics and investigate whether factors such as age, socioeconomic status, lung capacity and prescribed treatments affect the probability of death. We will describe treatments that those patients received and investigate what patient and clinical characteristics led to patients receiving particular types of treatment. With this knowledge, doctors can monitor COPD patients more appropriately and manage their treatment more effectively.
Technical Summary
This is an observational retrospective cohort study using CPRD-HES-ONS linked data aiming to describe treatment patterns and mortality among moderate-to-very-severe COPD patients in England, and to investigate risk factors for receiving particular treatments, death and other COPD-related outcomes. The study will include COPD patients who are eligible for linkage to HES and ONS. HES data will be used to determine COPD exacerbations, while ONS data will be used to obtain details on deaths.
Exploratory analyses will assess the representativeness of the entire CPRD-HES-ONS linked population in terms of mortality, by comparing age-standardised sex-specific all-cause mortality rates in this population to published mortality statistics. We will assess availability of COPD parameters among COPD patients and assess the impact of applying specific selection criteria on the sample size, to help inform the main analyses.
In the main analyses, only moderate-to-very-severe COPD patients will be considered. We will describe demographic and clinical characteristics, calculate mortality rates and estimate either absolute mortality, through a Weibull regression, or mortality relative to a ‘general population’ comparison group within the CPRD dataset, by calculating the standardized mortality ratio and hazard ratio. A survival model will be applied to assess the association between COPD-related factors and mortality. The COPD Galaxy model will be fitted to the COPD cohort to derive predicted probabilities of death and compare observed versus expected deaths. We will describe COPD treatments at baseline and at first switch. Patient characteristics will be compared based on baseline treatment using chi-squared tests, and one-way or Kruskal-Wallis ANOVA as appropriate. The association between risk factors and treatments will be assessed with logistic regression models. Kaplan-Meier time-to-event analyses will be performed for first treatment switch. Treatment pathways will be visualized using a Sankey diagram. Risk of COPD outcomes will be compared by treatment using a Cox proportional hazards model.
Health Outcomes to be Measured
Exploratory analyses
Descriptive variables: smoking status, spirometry (forced expiratory volume in one second (FEV1) pre-bronchodilator and post-bronchodilator, FEV1 predicted, FEV1 % predicted pre-bronchodilator and post-bronchodilator, FVC, FEV1/FVC, FEV1/FVC predicted); COPD-related scores and biomarkers (Medical Research Council (mMRC) Dyspnea Scale, COPD Assessment Test (CAT), Global Initiative for Chronic Obstructive Lung disease (GOLD) stage, 6-minutes’ walk distance (6MWD), Fractional exhaled Nitric Oxide (FeNO), fibrinogen and eosinophil (EOS) count); COPD medication (double or triple therapy regimen flag); COPD exacerbations (moderate and severe exacerbations); COPD-related Accident and Emergency (A&E) visits; COPD-related inpatient hospitalisations; non-comorbidity-related QRISK2 score components (systolic blood pressure (SBP), body mass index (BMI), total cholesterol, high density lipoprotein cholesterol ratio, family history of coronary heart disease (first-degree, aged<60)). We will also describe age-standardised all-cause mortality rates by sex.
Main analyses
Descriptive variables as at the index date (the date by which all inclusion criteria are met with an appropriate look-back period applied): demographic, clinical and lifestyle characteristics (e.g. age, sex, patient index of multiple deprivation, BMI, smoking status, comorbidities (ischaemic heart disease, heart failure, stroke, heart arrhythmia, bronchiectasis, diabetes, osteoarthritis, osteoporosis, inflammatory bowel disease, depression, anxiety, panic attack, rheumatoid arthritis and peptic ulcer); COPD-related factors and biomarkers (e.g. mMRC, FEV1, CAT, GOLD stage, 6MWD, fibrinogen and EOS count); COPD-related medication (e.g. inhaled corticosteroids (ICS), long-acting beta agonists (LABA), long-acting muscarinic antagonists (LAMA) and their combinations); QRISK2 score; pneumonia risk score; COPD exacerbations (moderate and severe exacerbations); calendar year of the index date. We will also derive mortality rates and standardised mortality ratio.
Descriptive variables during the follow-up: COPD-related medications (as described in detail later in the document) and FEV1.
Outcomes for the regression models: all-cause and COPD-related mortality, major adverse cardiovascular events (MACE), pneumonia event, moderate exacerbation event, severe exacerbation event.
Collaborators
Caroline O'Leary - Chief Investigator - IQVIA Ltd
Minouk Schoemaker - Corresponding Applicant - IQVIA Solutions B.V. (Nederland)
Clare Flach - Collaborator - IQVIA Ltd
Heloísa Galante - Collaborator - IQVIA II Technology Solutions Portugal, Unipessoal LDA
Joshua Warden - Collaborator - IQVIA World Publications Ltd.
Mar Pujades Rodriguez - Collaborator - IQVIA
Nelly Ly - Collaborator - IQVIA Ltd
Sander Van Olst - Collaborator - IQVIA Solutions B.V. (Nederland)
Stephanie Castello - Collaborator - IQVIA
Linkages
HES Accident and Emergency;HES Admitted Patient Care;ONS Death Registration Data;Patient Level Index of Multiple Deprivation
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Как икота происходит: Почему мы начинаем икать и как от этого избавиться
Содержание
Икота
ВАС БЕСПОКОИТ ИКОТА?
Икота, кажущаяся незначительной реакцией человеческого организма, может появиться в самый ответственный момент и существенно осложнить жизнь.
Сложно вести, к примеру, переговоры с клиентом, если человек непрерывно икает…
Интересный факт об икоте:
Большинство людей, икающих более месяца, начинают страдать от бессонницы и истощения.
Причины икоты лежат в непроизвольном сокращении диафрагмы и межреберных мышц. В течение 35 миллисекунд голосовые связки захлопываются, вызывая характерный звук «ик». Врачи называют данный звук синхронным диафрагмальным флаттером (synchronous diaphragmatic flutter, SDF).
Интересный факт – звук «ик» является интернациональным, в написании слова «икота» на том или ином языке, звук «ик» легко угадывается:
• Hıçkırık – по-турецки;
• Гикавка – по-украински;
• Hicka – по-шведски;
• Hikka – по-фински;
• Hiccup – по-английски;
• Hıçqırıq – по-азербайджански;
• Ыктытуу – по-киргизски.
А вот на немецком языке слово «икота» звучит как «Schluckauf».
Интересный факт о самой продолжительной икоте.
Рекордсменом по продолжительности икоты являлся фермер из Айовы Чарльз Осборн, икавший на протяжении 68 лет (с 1922 до 1990 года). Осборн смог приспособиться и вел относительно нормальную жизнь, сумев создать благополучную семью. На протяжении жизни Осборн икнул 430 миллионов раз, частота иканий доходила до 40 раз в минуту.
Врачи утверждают: способы лечения икоты не изменились со времен Платона. Американский нейробиолог Роберт Провайн написал книгу «Любопытное поведение: зевота, смех, икота», в которой отмечает, что одной из проблем изучения икоты является невозможность сознательно ее вызвать для обследования человека. Исследователь не можете сказать испытуемому, что сейчас он должен начать икать, приборы подключены, можно проводить эксперимент. По данной причине исследования проводятся на людях, страдающих от постоянной непрекращающейся икоты, длящейся, как правило, несколько дней или месяцев. Результаты данных исследований позволили выяснить ряд интересных фактов об икоте.
Интересный факт о лечении икоты: непродолжительный массаж глаз способствует избавлению от икоты. При массаже следует закрыть глаза и плавными движениями подушечек пальцев помассировать веки в области зрачка.
Традиционные способы лечения икоты используются по-прежнему. Каждый человек с детства помнит, что при икоте следует выпить воды, задержать дыхание, съесть кусочек сахара или попросить кого-либо вызвать сильный испуг. Данным способам лечения икоты найдено научное объяснение: при задержке дыхания происходит повышение концентрации углекислого газа, что уменьшает частоту икоты. Можно подышать в бумажный пакет – это приведет к увеличению в организме диоксида углерода (углекислого газа).
Новые необычные способы лечения икоты выявляются случайным образом. Икота – не самая распространенная патология, требующая выделения ей времени и средств. Изучение осложняется отсутствием достаточного количества взрослых людей, страдающих от икоты в течение 48 часов.
Если икота возникла, врачами предлагаются разнообразные методы лечения:
гастроскопия
лекарственная терапия;
инъекции с анестезирующим препаратом, блокирующим диафрагмальный нерв.
При любых обстоятельствах, перед началом лечения необходимо провести медицинское обследование для выявления скрытых причин продолжительной икоты.
Интересный факт про икоту: в 50 % случаев непрекращающаяся икота возникает в результате желудочно-пищеводного рефлюкса. Современная медицина рекомендует антацидные (нейтрализующие кислоту) лекарства для борьбы с данным состоянием.
Традиционная китайская медицина широко практикует массаж. Массируя точку, расположенную за мочкой уха, можно избавиться не только от икоты, но и от зубной боли.
Назад
Икота: временная неприятность или симптом?
Причины неизвестны
До сих пор никто достоверно не знает, почему мы ни с того ни с сего начинаем икать. Еще один риторический вопрос: сколько эта неприятность будет продолжаться. И, наконец, третья и главная загадка: зачем нашему организму это нужно.
Ученые утверждают, что данное явление происходит в результате раздражения нервных окончаний, проходящих в диафрагме, но почему возникает это раздражение, до сих пор остается тайной. Одни считают, что икота — разновидность нервного тика, а другие предполагают, что в мозге имеется центр икоты, вызывающий спазм пищевода, и что этот механизм якобы защищает нас от вредных излишеств в еде и питье. Но большинство врачей не признают за икотой ничего полезного, в отличие от кашля, избавляющего организм от мокроты, это явление не несет с собой никакого избавления.
С точки зрения физиологии икота представляет собой неспецифическое нарушение дыхания. Характерный звук, сопровождающий это странное явление, является следствием резкого захлопывания голосовой щели, возникающего из-за более резких, чем обычно, судорожных сокращений диафрагмы (мышечной преграды, разделяющей грудную и брюшную полости). Время между сокращением диафрагмы и появлением звука составляет всего 35 тысячных долей секунды. В это время человек не дышит.
Называют множество причин возник-новения таких внезапных судорожных звуков: переохлаждение (особенно у детей раннего возраста), чрезмерное растяжение желудка (связанное с неумерен-ным аппетитом), излишняя торопливость при поглощении пищи или воды, при котором происходит заглатывание воздуха, нервное потрясение и др.
Функциональная, или нервическая, икота обычно возникает у людей со слабой нервной системой, такая икота исчезает после успокоения. Неукротимая икота может настигнуть человека при приеме алкоголя. Ту же реакцию может дать и общая интоксикация, вызванная приемом некоторых лекарственных препаратов — например, сульфаниламидов.
Необычный симптом
Икота, возникшая в результате внешних причин, абсолютно безопасна. Она проходит сама собой. Но длительная, болезненная икота может быть симптомом определенных заболеваний. Например, воспалительный процесс в брюшной полости или воспаление легких зачастую вызывают раздражение диафрагмы, которое приводит к мучительной упорной икоте.
Этот же признак свидетельствует порой и о таких страшных недугах, как злокачественная опухоль легких или печени. Спазмы диафрагмы, сопровождаемые неприличными звуками, а также учащенными сердцебиениями, могут указывать и на наличие грыжи пищеводного отверстия диафрагмы. У людей, перенесших операции на желудке или позвоночнике, часто отмечаются нарушения дыхания, которые тоже приводят к появлению икоты.
Икота может возникать и при некоторых заболеваниях головного и спинного мозга, а также при инфаркте миокарда, инфекционных заболеваниях и очень часто — при психическом возбуждении.
В случае продолжительной (более двух дней) или тем более затяжной икоты (более 1 месяца) нужно обязательно обращаться к врачу. Длительно не прекращающаяся икота, сопровождающаяся болями в животе и тошнотой, может быть проявлением язвенной болезни или опухоли желудка, а также заболевания печени, желчного пузыря или поджелудочной железы. При затяжном приступе икоты показано обратиться к врачу, а если к икоте присоединилась рвота, особенно со следами крови, необходимо немедленно вызвать скорую помощь. Если у вас очень часто возникает икота или она продолжается слишком долго, то не помешает сделать рентгеновское исследование после приема бариевой смеси — это поможет выяснить, нет ли какого-либо механического препятствия в пищеводе. Для устранения икоты, возникшей по другим причинам, врач может назначить те или иные лекарства, в зависимости от того, с чем связаны расстройства.
Методы борьбы
Если икота не связана с недугом, попробовать избавиться от нее можно разными способами.
• К примеру, Гиппократ в таких случаях советовал постараться чихнуть. Другой метод — нужно надолго задержать дыхание и стараться мысленно отвлечься от своей проблемы, переключившись на что-либо более достойное внимания. Если вам трудно надолго задерживать дыхание, наденьте на голову полиэтиленовый пакет — это поможет повысить концентрацию углекислоты в крови и соответственно снимет спазм.
• Если икота появилась у новорожденного ребенка после еды, поносите малыша «столбиком», поглаживая его спинку. Воздух выйдет, и икота прекратится.
• Иногда причина икоты в столь юном возрасте — переохлаждение. Проверьте, не холодно ли малышу — если да, укутайте его потеплее, и судорожные звуки вскоре прекратятся.
• Если икает ребенок постарше, дайте ему попить воды — возможно, он съел слишком много или чересчур торопился во время еды.
• Среди быстрых методов избавления от икоты есть и такой: нужно поставить на стол перед собой чашку с водой, сцепить руки в замок, низко нагнуться и, потянувшись к чашке губами, без помощи рук выпить воду мелкими, жадными глотками.
• Некоторые советуют проглотить ложку сахарного песка, не запивая ее водой. Можно съесть что-нибудь горькое или кислое, а также кусочек льда. При болезненной икоте помогает теплое питье, теплая грелка на живот или, наоборот, холод.
• Прекратить икоту можно и рефлекторным путем. Положите палец на стенку глотки таким образом, как будто собираетесь вызвать рвоту. Это поможет прервать установившийся ритм икоты.
• У богатых и знаменитых имелись свои секреты, как расправиться с этим досадным и неприличным в высшем обществе явлением. Например, личный врач президента Кеннеди считал наиболее эффективным такой способ: нужно открыть пошире рот, взяться пальцами за язык, слегка вытянуть его и подержать в таком положении несколько секунд. Президентский лекарь утверждал, что это — верное и быстродействующее средство.
Терапевт предупредила об опасных недугах, о которых говорит длительная икота
+ A —
Она чревата даже инсультом
С кратковременной икотой периодически сталкивается в обычной жизни каждый человек. Однако специалисты предостерегают, что длительная икота опасна серьезными недугами: от проблем с позвоночником до инсульта.
Кандидат медицинских наук, терапевт Татьяна Романенко в беседе с «Москвой 24» рассказала об опасности этого состояния. По словам специалиста, при икоте нарушается работа диафрагмы и межреберных мышц. Терапевт описала, что в норме диафрагма сокращается и опускается на вдохе, а на выдохе расслабляется и поднимается. Если случается нарушение нервации, то синхронная работа мышц и диафрагмы нарушается, из-за чего диафрагма начинает хаотично сокращаться.
Романенко подчеркнула, что икота может стать симптомом серьезных заболеваний, если она становится патологической, долго длится и часто появляется. Эксперт заметила, что икота иногда возникает при грыже межпозвоночных дисков, поскольку нервы, отходящие от позвоночного столба, принимают непосредственное участие в регуляции синхронной работы межреберных мышц.
Терапевт посоветовала обращаться к специалисту и проверять состояние позвоночника, если икота сопровождается головной болью, болями в шее, головокружением, а также шумом или свистом в ушах. Также, по словам Романенко, иногда икоту провоцируют паразиты. Она отметила, что это происходит при заражении трихинеллами, когда поражаются дыхательные мышцы и мышцы диафрагмы.
Кроме того, по мнению эксперта, икота появляется при ударах животом во время занятий спортом. В таких случаях она свидетельствует о поражении диафрагмы. Романенко также добавила, что существует икота центрального происхождения, при которой страдают сосуды головного мозга. Она пояснила, что диафрагма управляется структурами в стволе мозга, поэтому при инсульте, когда случается острое нарушение мозгового кровообращения, может возникать икота. Это происходит в тех случаях, когда инсульт локализован в стволе мозга, заключила Романенко.
Читайте также: Названы причины и признаки развития катаракты.
Почему мы икаем и как их остановить?
Опубликовано 11 июля 2021 г. Ян Сунь, MD
Все мы хоть раз сталкивались с этим: ужасная икота. Сначала они могут быть забавными, если не истеричными, но быстро становятся неприятностями. Икота поражает всех, от младенцев в утробе матери до пожилых людей, но что это за громкие, шумные, разрушительные, а иногда и неприятные икоты?
Икота возникает, когда диафрагма, куполообразная мышца между легкими и желудком, спазмируется от раздражения.Диафрагма опускается, когда вы вдыхаете, чтобы впустить воздух в легкие, а затем расслабляется, когда вы выдыхаете, поэтому воздух может вытекать обратно из легких и выходить из носа и рта.
Если диафрагма спазмируется — или непроизвольно сокращается — это заставляет вас внезапно втянуть воздух в горло, где он попадает в ваш голосовой аппарат. Это заставляет ваши голосовые связки закрываться, что создает печально известный звук икоты.
Диафрагма обычно раздражается при нарушении нервных путей от головного мозга к диафрагме.Некоторые распространенные причины икоты включают:
• Заглатывание слишком большого количества воздуха
• Есть слишком быстро или слишком много
• Чувство нервозности или возбуждения
• Кислотный рефлюкс
• Употребление газированных напитков или слишком большого количества алкоголя
• Внезапные изменения температуры
• Хотя вы можете подумать, что страх друга, быстрое питье воды или вдыхание вонючих солей излечат вас от икоты, нет никаких научных доказательств эффективности этих распространенных домашних средств. Но некоторые медицинские эксперты согласны с тем, что задержка дыхания на несколько секунд, а затем медленный выдох или дыхание в бумажный пакет могут помочь избавиться от икоты.
Оба эти средства повышают уровень углекислого газа в легких, что, как считается, расслабляет диафрагму и останавливает спазмы.
Приступы икоты (продолжительностью менее 48 часов) обычно не вызваны серьезным заболеванием; у большинства людей время от времени случаются кратковременные приступы икоты, которые проходят сами по себе через несколько минут.Напротив, икота, продолжающаяся более 48 часов, возникает редко и может быть вызвана серьезным заболеванием.
Большинство этиологий или причин длительной икоты являются структурными, инфекционными или воспалительными нарушениями. Иногда боль в горле, опухоль или киста на шее могут вызывать постоянную икоту. Хронические заболевания, такие как энцефалит или менингит, диабет или почечная недостаточность, также могут вызывать длительную икоту. Даже медицинские процедуры, связанные с анестезией, могут вызывать постоянную икоту. Если икота длится несколько дней и более или если она настолько серьезна, что мешает есть, дышать или спать, пришло время поговорить с вашим лечащим врачом.
Ваш поставщик медицинских услуг может прописать лекарство, чтобы положить конец этой неприятной икоте.
Таинственная наука об икоте: почему мы ее получаем и как ее остановить
Почти у каждого хоть раз была икота. Они довольно распространены и довольно раздражают, и у ваших друзей, вероятно, есть разные советы о том, как избавиться от них. Но есть ли научные данные о том, что работает, а что нет? И вообще, почему люди икают?
Это немного сбивает с толку даже ученых.«Мы до сих пор не знаем, что делает икота, и наше лечение от нее не улучшилось со времен Платона», — говорит Роберт Провайн. Он нейробиолог из Университета Мэриленда в округе Балтимор, изучает эволюцию поведения и широко исследовал икоту для своей книги « Любопытное поведение: зевота, смех, икота и не только».
Одна из проблем, отмечает Провайн, заключается в том, что икоту трудно изучать: «Вы не можете просто пойти в лабораторию и попросить кого-нибудь икать вместо вас.Это означает, что существующие исследования обычно касаются людей с проблемной икотой, которая длится дни, недели или годы.
Но это не значит, что мы ничего не знаем.
1) Рекордсмен мира икал более 60 лет
(Шаттерсток)
Икота возникает, когда диафрагма и наружные межреберные мышцы непроизвольно сокращаются, заставляя человека быстро вдохнуть. Затем примерно через 35 миллисекунд голосовые связки захлопываются, вызывая характерный звук «ик».Это точно рассчитанная по времени серия событий.
Врачи также называют однократную икоту или синхронное трепетание диафрагмы.
Икота в течение часа или двух может быть неприятной. Но икота, которая не проходит, может быть признаком того, что с вами что-то серьезно не так.
Мировым рекордсменом по икоте обычно называют Чарльза Осборна, фермера из Айовы, у которого она была 68 лет подряд — с 1922 по 1990 год.
Несмотря на то, что он мог вести нормальную жизнь, некоторые люди с непреодолимой икотой (обычно классифицируемой как более месяца или двух) испытывают бессонницу, резкую потерю веса и истощение.
А для людей с просто постоянной икотой (более 48 часов) это может быть признаком серьезной основной проблемы со здоровьем, включая повреждение нервов, опухоль головного мозга, почечную недостаточность или реакцию, вызванную различными лекарствами.
Итак, если у вас икота длится более двух дней, возможно, пора обратиться к врачу.
2) Некоторые странные потенциальные лекарства: ректальный массаж и секс
(Шаттерсток)
Уже довольно давно существует множество так называемых средств от икоты: пить воду, задерживать дыхание, есть сахар, пугать кого-то и так далее.Но врачи все еще пробуют новые вещи.
В двух публикациях 1988 и 1990 годов описываются случаи, когда врач массировал прямую кишку пациента, чтобы вылечить непреодолимую икоту. А в 2000 году другая группа сообщила о случае, когда у кого-то была икота в течение четырех дней, а затем он вылечился после эякуляции во время секса.
Оба действия стимулируют блуждающий нерв, который помогает контролировать бессознательную деятельность сердца и пищеварительного тракта.
Фрэнсис Фесмайр, врач, опубликовавший первое исследование ректального массажа, позже сказал, что вместо этого рекомендовал бы секс как лекарство.«Оргазм вызывает невероятную стимуляцию блуждающего нерва, — сказал он New Scientist в 2006 году. — С этого момента я буду рекомендовать секс — завершающийся оргазмом — как панацею от непреодолимой икоты».
3) Увеличение содержания углекислого газа может уменьшить икоту
(Шаттерсток)
Несколько народных средств, которые, кажется, основаны на разумной научной концепции , включают задержку дыхания или дыхание в бумажный пакет.
По крайней мере, для пациентов с непреодолимой икотой было показано, что увеличение концентрации углекислого газа, которым они вдыхают, снижает частоту икоты.
Задержка дыхания делает нечто подобное: «Вы блокируете двигательную активность, а также приводите к накоплению углекислого газа», — говорит Провайн. Дыхание в бумажный пакет также увеличивает содержание углекислого газа в организме.
4) Крайне мало данных об излечении икоты
(Шаттерсток)
Несмотря на все эти интригующие возможности лечения икоты, медицинская литература обычно ограничивается изучением одного или двух пациентов.И это мало о чем говорит.
Чтобы узнать, действительно ли что-то работает, врачам необходимо провести контролируемое медицинское исследование, в котором половина людей получает рассматриваемое лечение, а половина — плацебо для сравнения. Икота просто не была горячей областью для таких испытаний, которые также могут быть довольно дорогими.
В одном недавнем систематическом обзоре предыдущих медицинских исследований сделан вывод: «Мы провели поиск исследований хорошего качества, в которых участвовали взрослые пациенты (18 лет и старше), которые испытывали икоту в течение 48 часов или более. Наш вывод состоит в том, что нет достаточных доказательств, чтобы рекомендовать конкретное лечение икоты».
Так что, если вы в конечном итоге столкнетесь с серьезной неизлечимой икотой, которая продолжается в течение очень долгого времени, врачи в значительной степени просто попробуют кучу случайных вещей.
Они могут отсосать вам желудок или попробовать различные лекарства. И они будут надеяться, что что-то сработает. Они также будут искать основные проблемы со здоровьем, которые могут быть связаны с икотой.
Некоторые врачи, когда менее инвазивные методы лечения оказались безуспешными, пытались стимулировать блуждающий нерв напрямую с помощью электрического имплантата или использовали инъекцию анестетика, чтобы заблокировать диафрагмальный нерв, контролирующий диафрагму.И они сообщили о нескольких случаях, когда это сработало.
5) Ученые до сих пор не знают, почему мы икаем
(Шаттерсток)
Люди выдвигали всевозможные идеи о том, почему существует икота, включая несколько новых, появившихся в последние годы. Однако то, что они новее, не означает, что они лучше. Откровенно говоря, на данный момент все они являются предположениями.
В одном из опубликованных эссе представлена гипотеза о том, что это эволюционный пережиток развития головастиков.На определенном этапе у головастиков появляются и жабры, и легкие, что приводит к интересной дыхательной гимнастике.
Другая причина заключается в том, что икота — это рефлекс, похожий на отрыжку, который помогает млекопитающим, которые сосают грудь, избавиться от лишнего воздуха в желудке.
И много других. Возможно, когда-нибудь кто-нибудь профинансирует исследования, чтобы разобраться в этом, но, похоже, это не входит в список национальных приоритетов.
6) Плоды икают
много
(Шаттерсток)
УЗИ выявило икоту у плода в возрасте 8 недель, и это одно из наиболее распространенных проявлений поведения в утробе матери.По словам Провайна, в некоторые моменты плод может икать каждый день.
Новорожденные также изрядно икают, и с возрастом их поведение уменьшается.
Этот паттерн предполагает, что икота может играть какую-то положительную роль в раннем развитии, но нет убедительных доказательств того, какую именно. Насколько нам известно, это может быть не так.
Что стоит за наукой Почему мы икаем?
Иногда они забавные. Иногда они раздражают или даже расстраивают.Они могут помешать вам в самый неподходящий момент. Нет, я не говорю о членах вашей семьи, хотя хорошая догадка! Я говорю об икоте.
Что такое икота? И есть ли научные причины, по которым мы их получаем?
Самый продолжительный в мире приступ икоты
Согласно Книге рекордов Гиннеса, рекорд по продолжительности приступов икоты принадлежит Чарльзу Осборну. У него была икота в течение 68 лет, с 1922 по 1990 год, по оценкам, 430 миллионов икоты.Кристофер Сэндс испытал около 10 миллионов икоты за 27 месяцев с 2007 по 2009 год. Он икал каждые две секунды в течение 12 часов в день.
Фольклор говорит нам, что икота означает, что кто-то говорит о вас или скучает по вам. Если вы прокрутите в голове список своих друзей, ваша икота прекратится, когда вы доберетесь до воспоминаний о друге, который является виновником. В средние века считалось, что икоту вызывают эльфы.
Механика икоты
Ваша диафрагма, большая мышца, расположенная чуть ниже легких и над желудком, помогает вам дышать.Он движется вверх, чтобы вытолкнуть воздух из ваших легких, и вниз, чтобы втянуть воздух. Хотя нам не нужно думать об этом каждый раз — хотя мы можем направлять его, если хотим: вдохнуть, выдохнуть — наш мозг подает сигналы. наша диафрагма, чтобы сделать эти движения.
Иногда наш мозг дает сигнал диафрагме двигаться вниз сильнее, чем обычно. Это резкое непроизвольное сокращение мышц заставляет воздух всасываться в заднюю часть горла. Область вашего горла рядом с вашими голосовыми связками затем закрывается благодаря этому изменению давления, создавая звук «ик».
Почему мы икаем?
Мы понимаем механизм икоты — это непроизвольный рефлекс. Но почему наш мозг вообще посылает сигнал для создания этого рефлекса? Ученые пытались определить четкую причину, но пока мы до сих пор не знаем.
Хотя мы точно не знаем, почему наш мозг сигнализирует нам о том, что мы икаем, мы знаем, что многие вещи вызывают этот рефлекс. Исследования выявили икоту, вызванную травмой (например, травмами головы), опухолями или зобом, инфекциями (включая менингит и энцефалит), вздутием живота и проблемами с центральной нервной системой, такими как рассеянный склероз.Раздражение, такое как изжога, острая пища, гастрит, рефлюкс и язва, также связаны с икотой. Икота одного человека была вызвана даже тем, что волосы задели его барабанную перепонку, мембрану, которая вибрирует в ответ на звуковые волны и позволяет нам слышать.
Мы также знаем о некоторых поведении, которое может привести к икоте: курение сигарет, внезапная смена температуры, переживание каких-либо повышенных эмоций, таких как волнение или стресс, или переполнение желудка (едой, алкоголем или даже воздухом). .
Непрерывная икота может доставлять серьезные неудобства, особенно если она влияет на вашу способность есть, спать или общаться. Постоянная икота может быть признаком проблемы со здоровьем, будь то ушная инфекция, почечная недостаточность, ларингит или грыжа. В случае с Кристофером Сэндсом и его 10 миллионами случаев икоты у него была обнаружена опухоль головного мозга, которая давила на диафрагмальный нерв — нерв, ответственный за сигнализацию рефлекса икоты. После того, как ему сделали операцию по удалению опухоли, его икота прекратилась.
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Как избавиться от икоты?
Вы только что икнули, кажется, в 100 й раз. Вы начинаете ЗАДАВАТЬСЯ, остановятся ли они когда-нибудь. Что еще более важно, вы ИНТЕРЕСУЕТЕСЬ, что вы можете сделать, чтобы заставил прекратить икоту.
Прежде чем мы начнем изучать лекарство от икоты, давайте выясним, что такое икота на самом деле.
Когда дело доходит до икоты, виновата диафрагма. Диафрагма представляет собой куполообразную мышцу в нижней части грудной клетки.
В норме диафрагма работает идеально. Когда вы вдыхаете, он опускается, помогая вашему телу втягивать воздух в легкие. Когда вы выдыхаете, он движется вверх, чтобы вытолкнуть воздух из легких.
Ваша диафрагма усердно работает днем и ночью, и большую часть времени это остается незамеченным — по крайней мере, до тех пор, пока вы не заболеете икотой.
Когда диафрагма раздражается, она дергается вниз, заставляя вас внезапно втягивать воздух в горло.Резкий порыв воздуха заставляет ваши голосовые связки смыкаться, вызывая звук икоты.
Есть несколько вещей, которые раздражают диафрагму, в том числе слишком громкий смех, употребление газированных напитков, а также слишком быстрое или слишком много еды или питья. Икота также может быть побочным эффектом некоторых лекарств, отпускаемых по рецепту.
В редких случаях икота может длиться несколько дней или недель. У американца по имени Чарльз Осборн была икота с 1920 по 1992 год. 72 года икоты Чарльза принесли ему место в Книге рекордов Гиннеса.
Еще один странный случай икоты произошел, когда мужчина по имени Кристофер Сэндс страдал от икоты почти три года. В конце концов врачи обнаружили у Кристофера опухоль в той части мозга, которая отвечает за мышечную активность. Как только опухоль была удалена, икота Кристофера исчезла.
Итак, теперь, когда у вас икота, что вы можете сделать, чтобы положить ей конец?
Прискорбная правда такова: не существует одного определенного способа вылечить икоту. К счастью, есть много предложений о том, как попробовать.Вот несколько вещей, которые вы можете попробовать в следующий раз, когда у вас возникнет икота:
• Задержите дыхание.
• Положите щепотку сахара под язык.
• Попросите кого-нибудь напугать вас.
• Полоскание горла ледяной водой.
• Вытащите язык (это якобы стимулирует «блуждающий нерв» и купирует спазмы диафрагмы).
• Дышите в бумажный пакет.
Стандарты: ГКРА.L.3, CCRA.L.6, CCRA.R.1, CCRA.R.2, CCRA.R.4, CCRA.R.10, CCRA.SL.1
Почему мы икаем и как перестать?
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Кажется, они появляются из ниоткуда.Вот вы болтаете и вдруг начинаете икать. В чем дело?
Короче говоря: у вас спазм диафрагмы.
Диафрагма представляет собой широкую тонкую мышцу между легкими и брюшной полостью. Когда диафрагма расслабляется, легкие расширяются, и вы вдыхаете. Когда она сжимается, вы выдыхаете.
Время от времени у вас спазмы диафрагмы и все рассинхронизируется.
Что вызывает икоту?
Не так много известно о точной причине икоты, говорит врач семейной медицины Tidelands Health доктор.Мишель Макколи, практикующая в семейной медицине Tidelands Health в Эндрюсе.
Физически икота возникает при осечке вдоль диафрагмального нерва, соединяющего мозг и диафрагму. Однако точный триггер может варьироваться.
Слишком много или слишком быстро можно поесть, как и чрезмерное питье, может вызвать приступ икоты. Кислотный рефлюкс может вызвать их. То же самое можно сказать о тревоге или стрессе. Медицинские процедуры, требующие анестезии, также могут вызывать икоту.
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Хотя для большинства из нас икота — временное явление, для некоторых она может стать долгосрочной проблемой.Чарльз Осборн, например, жил с икотой в течение 68 лет, что принесло айовану место в Книге рекордов Гиннеса. Осборн умер в 1991 году, и к тому времени, по оценкам Гиннесса, он икнул 430 миллионов раз!
Вам не следует ждать семь десятилетий, чтобы проверить затянувшийся приступ икоты, так как продолжающийся случай икоты может быть признаком того, что что-то не так в вашем мозгу или центральной нервной системе.
«Все, что превышает 48 часов, является поводом для консультации с медицинским работником», — сказал доктор. — говорит Макколи. При необходимости врачи могут лечить непрекращающуюся икоту рецептурными препаратами.
Как остановить икоту
Кажется, у каждого есть свое любимое средство от икоты. Некоторые говорят, что нужно висеть вниз головой. Другие скажут вам быстро выпить стакан воды или откусить лимон. Ваши более игривые друзья могут попытаться отпугнуть их от вас.Однако нет никаких научных доказательств того, что какой-либо из этих методов работает.
Что работает? Изменение ритма дыхания.
Если у вас приступ икоты, замедлите дыхание, задержите дыхание или подышите в бумажный пакет. Последние два увеличивают количество углекислого газа в крови, из-за чего диафрагма расслабляется, чтобы вы могли получать больше кислорода.
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Био
Доктор Мишель Макколи — врач семейной медицины в семейной медицине Tidelands Health в Эндрюсе.
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Медицинское образование
Образование
2013-2017
Эдвард Виа Колледж остеопатической медицины – кампус Каролины, доктор остеопатической медицины
Резиденция
2018-2021
Программа резидентуры по семейной медицине Tidelands Health MUSC, семейная медицина
Др.Мишель Макколи — врач семейной медицины в семейной медицине Tidelands Health в Эндрюсе.
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Почему возникает икота и как ее остановить
Подробнее
Если у вас есть какие-либо медицинские вопросы или опасения, обратитесь к своему лечащему врачу. Статьи в Health Guide основаны на рецензируемых исследованиях и информации, полученной от медицинских обществ и государственных учреждений. Однако они не заменяют профессиональные медицинские консультации, диагностику или лечение.
Все мы слышали дурацкие советы о том, как остановить икоту.Встаньте на голову, пейте воду вниз головой, попросите друга напугать вас — мы сделаем все, что угодно, чтобы избавиться от икоты.
Икота — это рефлекс нервной системы, который заставляет мышцу диафрагмы, расположенную под легкими, непроизвольно сокращаться. Многие могут вызывать икоту, а также они могут происходить без причины. Есть много домашних средств для избавления от икоты — некоторые основаны на науке, некоторые не очень.
Методы
, поддерживаемые наукой, включают питье воды, прикладывание холодного компресса к лицу и изменение схемы дыхания.Давайте посмотрим, что такое икота и какие методы могут помочь сократить ее продолжительность.
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Лекарства от икоты не существует, но есть множество методов лечения, которые могут помочь сократить эпизоды икоты. Многие случаи острой икоты проходят сами по себе и не требуют какого-либо вмешательства.
То, как вы справляетесь с икотой, зависит от того, как долго она продлится.При острой икоте существуют домашние средства и физические упражнения, которые могут помочь уменьшить продолжительность икоты. Большинство из них связаны с внезапным изменением, прерывающим рефлекс, вызывающий икоту.
Ниже приведены средства от икоты, предложенные врачами на протяжении всей истории, и хотя они могут работать на вас и, вероятно, не причинят никакого вреда, они еще должны быть проверенными средствами (Петрояну, 2014):
• Стимуляция ушей, носа и горла
Первый набор средств включает стимуляцию ушей, носа и горла.Чтобы сократить приступ икоты, достаточно просто выпить холодной воды (Steger, 2015). Использование нюхательных солей, затыкание обоих ушей во время питья воды и глотание дробленого льда — другие способы стимуляции этих областей (Brañuelas Quiroga, 2016).
• Активация блуждающего нерва
Блуждающий нерв — это очень длинный нерв, который начинается в головном мозге и спускается к пищеварительной системе. Некоторые люди считают, что стимуляция этого нерва может облегчить икоту.Напугать кого-то или приложить к лицу холодный компресс — оба способа активировать блуждающий нерв (Brañuelas Quiroga, 2016).
• Изменение характера дыхания
Изменение способа дыхания или действия, направленные на встряхивание дыхания, могут сократить период икоты. Задержка дыхания, кашель и дыхание в бумажный пакет — вот несколько примеров того, как это сделать (Steger, 2015).
Маневр Вальсальвы — это техника, при которой вы выдыхаете при закрытых носе и рту, задействуя мышцы живота.Это происходит естественным образом, когда вы идете в ванную или когда поднимаете что-то тяжелое. Есть некоторые свидетельства того, что он может помочь при икоте, увеличивая давление в груди. Вот как это сделать (Петрояну, 2014):
1. Сделайте глубокий вдох и задержите дыхание.
2. Закройте нос.
3. Напрягите мышцы груди и живота.
4. Удерживать 10-15 секунд.
5. Быстро выдохните.
Икота в медицине известна как singultus , латинское слово, которое переводится как «рыдание» или «задыхание» (Steger, 2015).
Икота вызывается непроизвольными сокращениями диафрагмы и часто мышц между ребрами. Диафрагма обычно ритмично сокращается, втягивая наши легкие вниз и втягивая в них воздух, чтобы контролировать наше дыхание. Но когда мышца начинает сокращаться, это заставляет нас непроизвольно вдыхать, что приводит к икоте.
После спазма диафрагмы отверстие между голосовыми связками быстро закрывается. Это отключает подачу воздуха и вызывает характерный звук «ик».Икота может происходить от четырех до 60 раз в минуту (Steger, 2015).
Существует четыре типа икоты: острая, стойкая, неизлечимая и рецидивирующая. Типы икоты характеризуются продолжительностью их продолжительности (Brañuelas Quiroga, 2016). Любой эпизод икоты, длящийся более двух дней, считается хроническим.
• Острая икота: Наиболее распространены и длятся менее 48 часов. Хотя острая икота может продолжаться до 48 часов, эти эпизоды часто длятся несколько минут или меньше.Острая икота редко требует медицинской помощи и обычно проходит сама по себе.
• Постоянная икота: Этот тип длится более 48 часов, но менее одного месяца.
• Непреодолимая икота: Эти приступы икоты длятся более одного месяца (Steger, 2015). Эти икоты часто вызваны основным заболеванием и должны быть оценены поставщиком медицинских услуг.
• Рецидивирующая икота: Это частые приступы икоты, которые длятся дольше, чем острая икота.
Часто причина икоты неизвестна, особенно в острых случаях (Brañuelas Quiroga, 2016).
Общие причины икоты включают переедание или употребление газированных напитков. Другие вещи, которые могут вызвать реакцию, включают острую пищу, алкоголь, курение и все, что раздражает желудок или дыхательную систему. Исследования также показали, что тревога и чрезмерное возбуждение могут вызвать приступ икоты (Steger, 2015).
Большую часть времени икота раздражает, иногда даже забавна, но бывают случаи, когда это явление может быть признаком чего-то более серьезного.Если икота постоянная, повторяющаяся или с трудом поддается лечению, это может указывать на основную проблему со здоровьем.
К сожалению, загадки вокруг икоты продолжаются. Врачи обнаружили, что икота является симптомом более 100 заболеваний, поэтому бывает сложно отнести ее к той или иной проблеме. Некоторые из наиболее хорошо задокументированных заболеваний, связанных с икотой, включают (Steger, 2015):
• Заболевания или травмы центральной нервной системы и головного мозга
• Заболевания желудочно-кишечного тракта или желудочно-кишечный рефлюкс (ГЭРБ)
• Заболевания сердца
• Заболевания уха, носа или горла
Воздействие токсинов и употребление рекреационных наркотиков также могут быть причиной.Икота может быть побочным эффектом некоторых лекарств, включая бензодиазепины, опиаты и стероиды (Steger, 2015).
При постоянной или непреодолимой икоте первое, что нужно сделать, это обратиться к врачу. Если есть другая проблема со здоровьем, лучше всего в первую очередь лечить то, что вызывает икоту (Brañuelas Quiroga, 2016).
Если вы живете с хронической икотой, есть лекарства, которые могут помочь. Вот некоторые распространенные препараты для лечения постоянной или непреодолимой икоты (Steger, 2015):
• Галоперидол Метоклопрамид
• Баклофен Фенитоин
• Вальпроевая кислота
• Карбамазепин Габапентин
• Амитриптилин Хлорпромазин
амантадин
Икота раздражает, но обычно останавливаются самостоятельно, без медицинского лечения.
Как видите, есть много вещей, которые вы можете попробовать дома, чтобы сократить продолжительность приступа икоты. Если икота не прекращается в течение 48 часов, поговорите со специалистом в области здравоохранения, чтобы узнать, не связано ли что-то со здоровьем, вызывающее икоту.
1. Браньуэлас Кирога, Дж., Урбано Гарсия, Дж., и Боланьос Гедес, Дж. (2016). Икота: распространенная проблема с некоторыми необычными причинами и методами лечения. Британский журнал общей практики: Журнал Королевского колледжа врачей общей практики, 66 (652), 584–586.DOI: 10.3399/bjgp16X687913. Получено с https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5072913/
2. .
3. Петрояну, Г. А. (2014). Лечение икоты вагусными маневрами. Журнал истории нейронаук, 24 (2), 123–136. DOI: 10.1080/0964704x.2014.897133. Получено с https://pubmed.ncbi.nlm.nih.gov/25055206/
4. Стегер, М., Шнееманн, М., и Фокс, М. (2015). Системный обзор: Патогенез и фармакологическое лечение икоты. Пищевая фармакология и терапия, 42 (9), 1037–1050.DOI: 10.1111/apt.13374. Получено с https://pubmed.ncbi.nlm.nih.gov/26307025/
Подробнее
Что стоит за наукой Почему мы икаем?
Иногда они забавные. Иногда они раздражают или даже расстраивают. Они могут помешать вам в самый неподходящий момент. Нет, я не говорю о членах вашей семьи, хотя хорошая догадка! Я говорю об икоте.
Что такое икота? И есть ли научные причины, по которым мы их получаем?
Самая продолжительная в мире икота
Согласно Книге рекордов Гиннеса, рекорд по продолжительности приступов икоты принадлежит Чарльзу Осборну.У него была икота в течение 68 лет, с 1922 по 1990 год, по оценкам, 430 миллионов икоты. Кристофер Сэндс испытал около 10 миллионов икоты за 27 месяцев с 2007 по 2009 год. Он икал каждые две секунды в течение 12 часов в день.
Чарльз Осборн страдал икотой в течение 68 лет, с 1922 по 1990 год, всего было около 430 миллионов икоты.
Фольклор гласит, что икота означает, что кто-то говорит о вас или скучает по вам. Если вы прокрутите в голове список своих друзей, ваша икота прекратится, когда вы доберетесь до воспоминаний о друге, который является виновником.В средние века считалось, что икоту вызывают эльфы.
Механика икоты
Ваша диафрагма, большая мышца, расположенная чуть ниже легких и над желудком, помогает вам дышать. Он движется вверх, чтобы вытолкнуть воздух из ваших легких, и вниз, чтобы втянуть воздух. Хотя нам не нужно думать об этом каждый раз — хотя мы можем направлять его, если хотим: вдохнуть, выдохнуть — наш мозг подает сигналы. наша диафрагма, чтобы сделать эти движения.
Иногда наш мозг дает сигнал диафрагме двигаться вниз сильнее, чем обычно.
Иногда наш мозг дает сигнал диафрагме двигаться вниз сильнее, чем обычно. Это резкое непроизвольное сокращение мышц заставляет воздух всасываться в заднюю часть горла. Область вашего горла рядом с вашими голосовыми связками затем закрывается благодаря этому изменению давления, создавая звук «ик».
Почему мы икаем?
Мы понимаем механизм икоты — это непроизвольный рефлекс. Но почему наш мозг вообще посылает сигнал для создания этого рефлекса? Ученые пытались определить четкую причину, но пока мы до сих пор не знаем.
Хотя мы точно не знаем, почему наш мозг сигнализирует нам о икоте, мы знаем, что многие вещи вызывают этот рефлекс. Исследования выявили икоту, вызванную травмой (например, травмами головы), опухолями или зобом, инфекциями (включая менингит и энцефалит), вздутием живота и проблемами с центральной нервной системой, такими как рассеянный склероз. Раздражение, такое как изжога, острая пища, гастрит, рефлюкс и язва, также связаны с икотой. Икота одного человека была вызвана даже тем, что волосы задели его барабанную перепонку, мембрану, которая вибрирует в ответ на звуковые волны и позволяет нам слышать.
Постоянная икота может быть признаком проблем со здоровьем.
Мы также знаем о некоторых поведении, которое может привести к икоте: курение сигарет, резкое изменение температуры, переживание каких-либо повышенных эмоций, таких как волнение или стресс, или переполнение желудка (едой, алкоголем или даже воздухом). ).
Непрерывная икота может доставлять серьезные неудобства, особенно если она влияет на вашу способность есть, спать или общаться. Постоянная икота может быть признаком проблемы со здоровьем, будь то ушная инфекция, почечная недостаточность, ларингит или грыжа.В случае с Кристофером Сэндсом и его 10 миллионами случаев икоты у него была обнаружена опухоль головного мозга, которая давила на диафрагмальный нерв — нерв, ответственный за сигнализацию рефлекса икоты. После того, как ему сделали операцию по удалению опухоли, его икота прекратилась.
Икота связана с эволюцией?
Наши тела редко вырабатывают рефлексы без причины, поэтому некоторые ученые выдвинули более широкие идеи о том, почему икота может быть связана с нашей эволюцией. Например, поскольку мы млекопитающие, мы грудными детьми.Акт кормления грудью может добавить дополнительный воздух в наши желудки. Икота может быть механизмом, который мы разработали, чтобы избавиться от лишнего воздуха.
Родители знают, что маленькие дети чаще икают, чем взрослые. Возможно, это связано с тем, что икота играет какую-то полезную роль в раннем развитии. Или это может просто означать, что их желудки маленькие и поэтому их легче заполнить.
Как избавиться от икоты?
Существует множество народных средств от кратковременных приступов икоты.Некоторые говорят, что от икоты можно избавиться, потирая затылок, задерживая дыхание, дыша в бумажный пакет, полоская горло, выпивая воду со льдом или надкусывая лимон. Эти средства подкрепляются больше анекдотичными свидетельствами, чем научными исследованиями.
Некоторые люди даже прибегают к иглоукалыванию и гипнозу от более стойких проблем с икотой. Вы также можете попробовать избегать возможных триггеров, таких как обильные приемы пищи, острая пища и газированные напитки.
Попробуйте избегать возможных триггеров, таких как обильные приемы пищи, острая пища и газированные напитки.
В детстве мне всегда говорили сгибаться в пояснице и пытаться пить воду из чашки, пока моя голова висит вниз головой. Оглядываясь назад, это звучит как ужасная идея. Если это когда-либо было эффективным, то, скорее всего, отвлечение на выполнение такой невыполнимой задачи заставило икоту пройти.
Мы с дочерью пытаемся напугать друг друга, если у кого-то из нас начинается икота, хотя мы делаем это чаще, потому что весело кричать «бу!» чем потому, что мы думаем, что это действительно помогает.
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Why does fever occur during summer season
Fever during the summer season can occur for several reasons, and it's important to understand the underlying causes to manage the condition effectively. Here are some common reasons why fever may occur during summer:
1. Infectious Diseases: Summer is a time when many infectious diseases are prevalent, such as influenza, common cold, gastroenteritis, and various waterborne diseases. These infections can lead to fever as the body's immune system responds to fight off the invading pathogens.
2. Heat Exposure and Heat Stroke: Prolonged exposure to high temperatures can lead to heat exhaustion or heat stroke, which can present with symptoms like fever. This is because the body's temperature regulation system becomes overwhelmed, and the core body temperature rises.
3. Viral Infections: Many viral infections, including those that cause respiratory illnesses, are more common in the summer due to increased social gatherings, travel, and the presence of more people in outdoor spaces. These infections can cause fever as a symptom.
4. Bacterial Infections: Bacterial infections, including those that cause skin infections, urinary tract infections, and others, can also occur more frequently in the summer due to increased heat and humidity, leading to higher body temperatures.
5. Poor Hydration: Dehydration is more common in the summer due to increased sweating and a higher risk of fluid loss. Dehydration can raise body temperature and lead to a fever-like sensation.
6. Allergies: Some people may experience allergic reactions to pollen, dust, or other airborne allergens that are more prevalent in the summer, which can cause a low-grade fever in some individuals.
7. Sun Exposure: Overexposure to the sun can lead to sunburn, which in some cases can cause a temporary increase in body temperature and may be accompanied by flu-like symptoms, including fever.
8. Travel-related Illnesses: Summer is a popular time for travel, and travelers may be exposed to new pathogens or may not take the necessary precautions to avoid infections, leading to fever and other symptoms of illness.
If you experience a fever during the summer, it's important to identify the underlying cause. In most cases, a mild fever is a normal part of the body's immune response and can be managed with rest, staying hydrated, and using fever-reducing medications if necessary. However, if the fever is high, persistent, or accompanied by other severe symptoms, it's important to seek medical attention to rule out more serious conditions.
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Question: How Many Steps Should A 70 Year Old Walk A Day?
How much should seniors walk?
Seniors age 65 and older should get at least 2.5 hours of moderate aerobic exercise (such as brisk walking) every week.
That averages out to about 30 minutes on most days of the week.
Or you should get 1 hour and 15 minutes of vigorous exercise (such as jogging) each week..
Is walking 30 minutes a day enough exercise?
Just 30 minutes every day can increase cardiovascular fitness, strengthen bones, reduce excess body fat, and boost muscle power and endurance. It can also reduce your risk of developing conditions such as heart disease, type 2 diabetes, osteoporosis and some cancers.
Is 30000 steps a day good?
For health and physical fitness, it’s certainly excessive and the time spent would be far better spent on more focussed training, like weight lifting for example. 30,000 steps is about 20–25km or 4–5 hours of walking. … Number of steps to walk is just that, numbers. Don’t use it, as it is meaningless.
How many miles is 10000 steps?
5 milesAn average person has a stride length of approximately 2.1 to 2.5 feet. That means that it takes over 2,000 steps to walk one mile and 10,000 steps would be almost 5 miles.
What is a good distance to walk everyday?
Walking 10,000 steps equates to about five miles a day, which is quite an increase for those who sit at a desk all day. It comes out to about 90 active minutes a day, which is three times the amount recommended by the U.S. Centers for Disease Control and Prevention.
How many steps should you take a day by age?
A group of 3,127 healthy adults, 19–94 years of age, with a mean age of 47, including 976 men, participated in the study. The research team has previously published recommendations for children aged 6–12 establishing that girls should accumulate 12,000 steps and boys 15,000 steps every day.
Does walking reduce belly fat?
While any exercise can burn calories, brisk walking for 45 minutes mobilises the body to dip into fat reserves and burn stored fat. It’s especially effective for burning internal belly fat, known as visceral fat, that not only contributes to the waistline but also raises the risk for diabetes and heart disease.
How many steps should you take a day to lose 2 pounds a week?
Your plan: First, determine how much weight you wish to lose—then, do a little math. The Academy of Nutrition and Dietetics recommends slow weight loss for lasting results—usually 1/2 pound to one pound per week. Completing an extra 10,000 steps each day typically burns about 2000 to 3500 extra calories each week.
How many steps a day is considered active?
Sedentary is less than 5,000 steps per day. Low active is 5,000 to 7,499 steps per day. Somewhat active is 7,500 to 9,999 steps per day. Active is more than 10,000 steps per day.
How far should a 70 year old walk?
Average walking speed by ageAgeMeters/secondMiles/hour40 to 491.39 to 1.433.11 to 3.250 to 591.31 to 1.432.93 to 3.260 to 691.24 to 1.342.77 to 3.070 to 791.13 to 1.262.53 to 2.823 more rows•Mar 14, 2019
How many steps should a woman walk per day?
The average American walks 3,000 to 4,000 steps a day, or roughly 1.5 to 2 miles. It’s a good idea to find out how many steps a day you walk now, as your own baseline. Then you can work up toward the goal of 10,000 steps by aiming to add 1,000 extra steps a day every two weeks.
What exercises should seniors avoid?
Exercises Seniors Should AvoidSquats with dumbbells or weights.Bench press.Leg press.Long-distance running.Abdominal crunches.Upright row.Deadlift.High-intensity interval training.More items…
What will happen to your body if you walk everyday?
For example, regular brisk walking can help you: Maintain a healthy weight. Prevent or manage various conditions, including heart disease, high blood pressure and type 2 diabetes. Strengthen your bones and muscles.
Is 20 000 steps a day good?
Walking is a physical exercise and also burns calories. If you want to try the 20000 steps a day weight loss, you may expect great results: reduced stomach fat, improved sleep, boosted immune response etc. As good as it sounds, walking 20000 steps a day weight loss has its cons.
Do you really need to walk 10000 steps?
One does not need to get to 10,000 steps a day,” explains Dr. Lee. Any type of movement counts. All steps count, so these extra 2,000 steps could be steps you take doing a whole range of activities in daily life, and not necessarily for exercise.
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Dizziness Nursing Diagnosis and Nursing Care Plan
nursing diagnosis for dizziness
Dizziness Nursing Care Plans Diagnosis and Interventions Dizziness NCLEX Review and Nursing Care Plans Dizziness usually covers neurophysiological sensations and feelings of lightheadedness and loss of balance. The condition known as vertigo, in which a person has a false perception that their surroundings are moving or spinning, is frequently interrelated with dizziness in terms of … Read more
Nursing Diagnosis vs Medical Diagnosis
nursing diagnosis vs medical diagnosis
Medical Diagnosis vs Nursing Diagnosis A nursing diagnosis and a medical diagnosis are different in terms of characteristics and features. The main difference between the nursing diagnosis and medical diagnosis is that the medical diagnosis is specific to the disease or illness pathology while the nursing diagnosis focuses on the patient and his or her … Read more
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Most people have heard the term postpartum depression and they automatically think: baby blues. Postpartum depression is a common disorder, affecting as many as 20% of new mothers in the United States annually, according to the CDC.
However, far fewer have heard of the near-equally common condition known as postpartum anxiety, which is the irrational worry that a new mother might experience after the birth of a child. Postpartum anxiety is a deep fear that something terrible is going to happen. It affects between 11 and 21% of new mothers each year, and it’s something more people should be talking about.
We’re looking at what postpartum anxiety is, its causes, symptoms, and risks, as well as what types of treatment can help women who are living with this crippling anxiety disorder. Keep reading to learn more.
What is Postpartum Anxiety?
Postpartum anxiety refers to irrational fear and anxiety that something awful is going to happen to your baby. It’s not an uncommon experience…the truth is, many mothers feel this way shortly after giving birth. The anxiety can extend to fear or even postpartum rage that a partner won’t be capable of taking care of the baby correctly. It might even develop to that they, themselves, won’t be up to the task of parenthood.
While a certain degree of anxiety is natural after the birth of a child, postpartum anxiety becomes a problem when it interferes with a mother’s ability to do everyday tasks, care for herself and her baby, and just enjoy life.
How Common is Postpartum Anxiety?
According to a recent study, as many as 21% of women will experience prenatal or postnatal anxiety. The true number is likely even higher since many postpartum women are hesitant to discuss anxiety with their doctors.
Causes of Postpartum Anxiety
Postpartum anxiety is definitely not “in your head.” Although what causes anxiety, and more specifically, what causes postpartum anxiety isn’t yet fully understood, there are some factors that increase the likelihood of a woman experiencing it.
“When I was in school many years ago women’s health was not getting research dollars so everything was labeled as “in your head.” This is devastating for a new mom who can’t figure out why she’s not overjoyed. Today we are learning more about the hormonal influences at play.”
Talkspace therapist Karmen Smith, LCSW, DD
Common factors that can increase the likelihood of postpartum anxiety:
• A personal or family history of depression or anxiety disorder — up to 50 percent of women with pre-pregnancy anxiety disorders will experience postpartum anxiety
• A past difficult birth, or currently experiencing pregnancy anxiety
• A high degree of stressful life events (with job or family)
Symptoms of Postpartum Anxiety
Signs of postpartum anxiety to be alert for include:
• An obsessive intrusive thought about the baby
• Symptoms of a panic attack, such as a rapid heartbeat or difficulty breathing
• Changes in eating habits (eating a lot more or a lot less)
• Insomnia or not wanting to get out of bed
• Uncontrollable racing thoughts that are often irrational, negative, and overwhelming
• Muscle tension
• Trouble focusing or concentrating on tasks
It’s important to point out that everyone experiences anxiety differently. The postpartum anxiety symptoms that one mother experiences may be totally different from those experienced by another.
Risks and Complications
In addition to robbing a new mother of the joy of giving birth and having a new baby, postpartum anxiety poses some significant health risks to both a mother and her baby. For women who experience postpartum anxiety, it can be difficult to bond with the baby, it can negatively impact the baby’s development, and it can even contribute to infant neglect.
“Postpartum anxiety can lead to long term anxiety that may contribute to the parenting dynamics which are directly related to the mental state of the mother. For example, the inability to be in the moment due to worries of the future could hinder you from enjoying subtle growth milestones.”
Talkspace therapist Karmen Smith, LCSW, DD
Treatment for Postpartum Anxiety
Postpartum anxiety can be scary, but there is some good news. Several effective treatments are known to ease postpartum anxiety symptoms. Some of the common methods for how to treat anxiety and more specifically, postpartum anxiety follow.
Cognitive behavioral therapy (CBT)
Cognitive behavioral therapy involves talking with a licensed mental health provider to uncover the underlying issues behind a woman’s anxiety about her baby. The aim of therapy for anxiety is to replace anxiety-producing thoughts with more positive ones. CBT is a powerful tool that allows people to identify the source of postnatal anxiety and then come up with healthier ways to think, feel, and act.
Mindfulness meditation
Meditation can also be effective in easing postpartum anxiety. Ways to incorporate meditation into your daily routine might include using positive affirmations, practicing yoga, and prayer or guided visualization. Relaxation techniques, like deep-breathing exercises, have also proven useful in easing postpartum anxiety.
“Mindfulness practices that fit your personality such as yoga, pilates, tai chi, or walking in nature can help ground you in the moment. Finding a mothers’ support group can be a way to not feel isolated. Most of these activities are about self love and encouragement. When you’re kind to yourself and nurturing it benefits your baby.”
Talkspace therapist Karmen Smith, LCSW, DD
Medication
Medication is another treatment option that’s sometimes used to combat minor to severe postpartum anxiety. It can be used alone, or in conjunction with CBT and/or other additional alternative therapies.
Common medications used for anxiety include:
• Antidepressants: Serotonin and noradrenaline reuptake inhibitors (SNRIs) and selective serotonin reuptake inhibitors (SSRIs)
• Anti-anxiety medications: Benzodiazepines
Aromatherapy
For some people, a good alternative therapy for easing postpartum anxiety symptoms is aromatherapy. This involves introducing scents or essential oils that have a calming effect on the body, like lavender or bitter orange. Aromatherapy can be done by diffusing and inhaling the scents, or by rubbing them on the body with a carrier oil.
An important note: mothers who are breastfeeding should not apply essential oils to their skin as they can be transferred to their breast milk.
Diet
Lastly, what postpartum women eat can dramatically affect their mood and stress levels. The best foods to choose include those rich in calcium (such as dairy products and legumes), foods with lots of vitamin B (such as green, leafy vegetables, and eggs), and foods rich in vitamin D (such as cod, fortified dairy products, and egg yolks).
Getting Help
The first step toward getting treatment is recognizing the signs of postpartum anxiety and speaking with your physician or therapist. They’ll be able to guide you toward treatment and help you find the right healthcare professional for your needs. Getting help is easy when you have a support system in place, so consider reaching out to a family member or close friend to let them know you’re struggling. In-person or online therapy can also be a natural next step to get more help with postpartum anxiety.
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Article
Coughing Can Be Modulated by the Hydration Status in Adolescents with Asthma
by
Alessandro Zanasi
1 and
Roberto Walter Dal Negro
2,*
1
Lung Unit of the Italian Association for Studying Cough, AIST, 40100 Bologna, Italy
2
Research & Clinical Governance, 37124 Verona, Italy
*
Author to whom correspondence should be addressed.
Children 2022, 9(4), 577; https://doi.org/10.3390/children9040577
Submission received: 17 March 2022 / Revised: 11 April 2022 / Accepted: 15 April 2022 / Published: 18 April 2022
(This article belongs to the Section Global Pediatric Health)
Abstract
:
A lower thirst sensitivity frequently characterizes children and adolescents. The daily water intake can be frequently insufficient for the homeostasis and the integrity of their airway epithelium. Little is known about the real-life relationship between dehydration and coughing in young students with asthma. The aim was to investigate the effect of dehydration on coughing in asthmatic students aged ≤16 years. A validated questionnaire aimed to investigate their respiratory history and cough incidence was used. Urine samples were also collected for assessing osmolality. Wilcoxon test, the Pearson Chi Square and the Fisher Exact Test were used; p < 0.05 was assumed as significant. Valid data were obtained from 305 healthy and 56 asthmatic students. Mean urine osmolality was significantly higher in asthmatic than in healthy students (1012 ± 197.7 vs. 863.0 ± 223.0 mOsm/kg, respectively; p < 0.001), particularly in symptomatic asthmatic students (1025 ± 191.6 mOsm/kg, p < 0.01). Both the incidence and duration of coughing episodes were directly related to the degree of urine osmolality (both p < 0.001). Dehydration affects the prevalence and the duration of a cough in asthmatic students aged ≤16 years. Adequate daily water intake should be stimulated in these subjects in order to contain their basic cough attitude.
1. Introduction
A cough is a very frequent respiratory symptom occurring in children and adolescents and can cause a substantial burden in terms of recurrent medical consultations, parental stress, and worries [1]. Water is a basic nutritional factor that is involved in all vital processes of human body and it is also crucial in airway homeostasis [2,3]. Dehydration is a condition caused by a negative water balance, such as when the water loss is greater than the water intake [4]. The daily water consumption of children and adolescents was proved to be frequently insufficient to meet their water requirements. This usual attitude was mostly related to their lower sensitivity to thirst and to missing parents’ recommendations [5,6]. Consequently, children and adolescents are more likely to incur dehydration and a higher urine osmolality [7,8].
Normal hydration has been documented as capable of protecting the airway epithelium and promoting proper mucociliary clearance, [7], while dehydration stimulates the production of pro-inflammatory mediators that affect the airway calibre, particularly in asthma [9].
Although dehydration was only episodically considered in real-life respiratory homeostasis, a recent study proved that a cough is significantly more prevalent even in healthy young students if they are dehydrated [10].
The aim of the present real-life study was to investigate the relationship existing between the hydration status and both the frequency and duration of coughs in asthmatic children and adolescents.
2. Materials and Methods
The present study was a monocentric, observational, real-life investigation. The operational tools were the anamnestic questionnaire and the individual measures of urine osmolality. The present sample of asthmatic students was obtained from the overall cohort of young students considered in a previous study [10].
Population: students attending the same primary and secondary school institute (the “Istituto Comprensivo Statale 12”, Bologna, Italy) were invited to participate on a voluntary basis. Exclusion criteria were: (a) subjects aged >16 years; (b) inadequate completion of the questionnaire; (c) insufficient collection of the urine sample; (d) smoking habit by any family member; (e) individuals complaining of eating disorders or intolerances; (f) the presence of relevant comorbidities; (g) lack of parents’ informed consent [10].
The questionnaire to be filled in by parents was anonymous and consisted of 22 items ([10]; see Figure A1). It was aimed at checking the presence of asthma, the incidence of cough, and the duration of cough episodes during the previous 12 months.
Urine osmolality: osmolality was measured in urine samples collected 30 min. after breakfast and avoiding the first urine emission in the morning. Urine samples were aliquoted and stored at −20 °C. Measurements were carried out in a centralized laboratory by means of a freezing point depressing osmometer (Osmo 3250, Advanced Instruments, Norwood, MA, USA) [10]. Considering the mean temperatures during spring/summer months in Italy, the hydration status was assessed over a restricted period of the year (February–March 2017) in order to minimize the possible influence of climatic factors on hydration. According to previous studies [7,11,12], osmolality values ranging 800–1000 mOsm/kg were assumed as corresponding to mild dehydration, while those higher than 1000 mOsm/kg as due to high dehydration [13].
Subjects reporting the use of any bronchodilator prn <3 times/month and/or those without any wheezing episodes over the last two weeks before their recruitment were classified as asymptomatic.
Data obtained from the asthmatic sample of students were compared to those of healthy students of the previous study [10].
Statistics: anthropometrics and urine osmolality of healthy and asthmatic students were compared by gender. Osmolality was also compared in students symptomatic and asymptomatic of asthma. Statistics: Wilcoxon test was used for continuous variables, while the Pearson Chi Square and the Fisher Exact Test were used for statistical comparisons. Data were reported as means ± SD, and p < 0.05 was assumed as the limit of statistical significancy.
The study was approved by the Ethical Board of AIST (the Italian Association for Study of Coughs) and by the Council of the School Institute (ethical code: 23/CC/2016).
3. Results
A total of 400 students were invited. Three-hundred-sixty-one students returned valid questionnaires: 305 were healthy students (male = 155), while 56 claimed to be asthmatic, and then considered for the present study. Of them, 24 were asymptomatic and 32 symptomatic, equally distributed by sex (males n = 13 and 16; females n = 12 and 15, respectively). Thirty-nine responders were excluded: n = 13, claiming relevant comorbidities; n = 21 returning incomplete questionnaires;), n = 5 missing patents’ informed consent.
Anthropometrics of participants were absolutely comparable and reported in Table 1. Urine osmolality assessed in healthy and in asthmatic responders (n = 155 + 56) was then compared.
While the mean (±SD) urine osmolality in healthy students was 837.1 ± 220.2 mOsm/kg (range 148–1293 mOsm/kg), it was 1012.4 ± 197.7 mOsm/kg in asthmatic students (Table 2). In particular, mean urine osmolality was 909.4 ± 190.7 mOsm/kg in asymptomatic, and 1025.4 ± 191.6 mOsm/kg in symptomatic asthmatic students, respectively (p < 0.01) (Table 3).
When compared to healthy students, only 14.3% of asthmatics (n = 8/56) showed normal urine osmolality, while 28.6% (n = 16/56) were mildly dehydrated, and the remaining 57.1% (n = 32/56) highly dehydrated. There was a significant difference between healthy and asthmatic subjects, and also between asymptomatic and symptomatic asthmatic students (Table 3). Differently from data previously obtained in healthy students of the same age [10], the prevalence of dehydration in asthmatic students was slightly higher in those aged ≤10 years (26/29) when compared to those age > 10 years (21/27) (OR = 2.48; 95% CI: 0.45–16.88).
The incidence of coughing episodes was equally distributed by gender (p = 0.85) and age (p = 0.76). Despite the presence of normal urine osmolality, the incidence of coughing episodes was significantly higher in asthmatic than in healthy students (97.5% vs. 62.5%, respectively) (Table 4). This difference proved even more evident in dehydrated asthmatic students (always p < 0.001) (Table 4). Moreover, the incidence of coughing episodes was directly related with the students’ claim of asthma and with their dehydration status.
Both in healthy and in asthmatic students, coughing episodes showed a significantly longer duration by their hydration status (p < 0.001), even if the incidence of coughing episodes lasting longer than two weeks was significantly higher in asthmatic students (p < 0.01) (Table 4).
4. Discussion
Two main mechanisms modulate the normal water balance: the thirst sensitivity and the secretion of an anti-diuretic hormone (ADH). These two mechanisms control the homeostasis of plasma liquids up to the 1200 mmol/kg maximal urinary concentration [14,15].
As previously reported, normal urinary osmolality ranges 500–800 mOsm/kg over the 24 h in healthy subjects [14], while values >800 mOsm/kg are regarded as corresponding to the occurrence of mild dehydration, and those >1000 mOsm/kg to the maximum possible urine concentration [13].
Inadequate hydration has already been shown in a large proportion of healthy students aged 6–16 years [10,11,16,17]. The effects of acute or/and persistent dehydration have been described in this age range [13], and proved capable of inducing neurological, cardiovascular and metabolic disturbances [12]; a lower mental and/or physical performance [3]; a significant decrease in attention, and an impaired short-term memory [18,19,20,21,22,23,24,25,26,27,28,29]. This evidence is obviously crucial when considering that all these negative effects can likely affect the students’ school performance, even substantially.
Even if its effects on cough have not yet been investigated in young asthmatic students, dehydration has long been known to worsen respiratory symptoms and lung function in patients with pre-existing respiratory diseases, particularly with bronchial asthma [17]. It should be pointed out that dehydration was described as a condition that is capable of favoring and enhancing histamine release from the mastocytes in bronchial asthma, while Type2-histamine receptors were shown to also be involved in the increase of blood vasopressin that, in turn, contributes to the regulation of the hydration status [23,24,25].
It was also proved that appropriate hydration is a crucial condition in other respiratory conditions as it can contribute greatly to preserving the proper environment of the airway epithelium, such as the conditions required for effective mucociliary clearance [22,27,28,29,30]. On the other hand, hyperosmolality of the airway surface lining can induce substantial damage and disruption of the tight junctions embedded within the airway epithelium, thus further exposing cough-mediating airway receptors to the effects of exogenous stimuli [31].
Data of the present study provided the first evidence on the real-life relationship existing between the dehydration status and coughing in asthmatic students aged ≤16 years, particularly in symptomatic individuals. To point out that the greater effect of dehydration on coughing observed in younger asthmatic students can be likely explained (or at least partially explained) by their relatively wider body surface that allows a stronger perspiration, particularly during sustained exercise (such as in usual conditions for this age range) [19,21].
The present investigation has some limitations [32]. First, the study is a monocentric survey carried out on a limited cohort of subjects; second, the reports on coughs are based on parental reports; third, the precise mechanisms underlying the cough were not investigated because the study was only aimed at the preliminary real-life assessment of cough incidence in young asthmatic students. The study also has some points of strength, in our opinion, such as: the homogeneity of the study population, the use of a validated questionnaire, the restricted observational period, the availability of careful biological measurements, the adoption of appropriate statistical methods.
In conclusion, the results of the present study suggest a clear relationship existing between coughing and real-life hydration status in young asthmatic students. Water consumption should then be highly implemented and stimulated in these asthmatic subjects in order to easily minimize, at low cost, their basic coughing liability that can frequently limit their quality of life.
Author Contributions
Conceptualization, A.Z. and R.W.D.N.; methodology, A.Z. and R.W.D.N.; software, A.Z. and R.W.D.N.; validation, A.Z. and R.W.D.N.; formal analysis, A.Z. and R.W.D.N.; investigation, A.Z. and R.W.D.N.; resources, A.Z. and R.W.D.N.; data curation, A.Z. and R.W.D.N.; writing—original draft preparation, R.W.D.N.; writing—review and editing, A.Z.; visualization, A.Z. and R.W.D.N.; supervision, A.Z. and R.W.D.N. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
The study was approved by the Ethical Board of AIST (the Italian Association for the Study of Coughs) and by the Council of the School Institute (ethical code: 23/CC/2016). The study protocol conforms to the ethics of the World Medical Association Declaration of Helsinki—Ethical Principles for Medical Research Involving Human Subjects, adopted by the 18th WMA General Assembly, Helsinki, Finland, June 1964 and amended by the 64th WMA General Assembly, Fortaleza, Brazil, October 2013.
Informed Consent Statement
Informed consent was obtained from all subjects involved in the study.
Data Availability Statement
Authors do not wish to share their data without their permission.
Acknowledgments
The Authors are grateful to Filomena Massaro, Dean of the “Istituto Comprensivo Statale 12”, Bologna, Italy, who facilitated the present study.
Conflicts of Interest
The authors declare no conflict of interest.
Appendix A
Figure A1. Hydration and Cough Questionnaire.
Figure A1. Hydration and Cough Questionnaire.
Children 09 00577 g0a1aChildren 09 00577 g0a1b
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Table 1. Anthropometrics of healthy and asthmatic students by gender (means ± SD).
Table 1. Anthropometrics of healthy and asthmatic students by gender (means ± SD).
Healthy Males
(n = 155)
Asthmatic Males
(n = 29)
Healthy Females
(n = 150)
Asthmatic Females
(n = 27)
Age (years)11.6 ± 3.811.4 ± 4.111.9 ± 3.711.5 ± 3.9
Weight (kg)39.7 ± 13.439.2 ± 12.938.1 ± 11.638.6 ± 12.0
Height (cm)146.2 ± 16.0145.8 ± 16.6134.1 ± 11.0135.2 ± 11.4
BMI18.1 ± 3.217.9 ± 3.816.8 ± 2.617.1 ± 3.6
Table 2. Mean urine osmolarity in healthy and in asthmatic students (means ± SD), and the corresponding % prevalence of different hydration status. While osmolality values ranging 500–800 mOsm/kg are normal, values > 800 mOsm/kg correspond to mild dehydration, and values > 1000 mOsm/kg correspond to severe dehydration.
Table 2. Mean urine osmolarity in healthy and in asthmatic students (means ± SD), and the corresponding % prevalence of different hydration status. While osmolality values ranging 500–800 mOsm/kg are normal, values > 800 mOsm/kg correspond to mild dehydration, and values > 1000 mOsm/kg correspond to severe dehydration.
Healthy Students
(n = 305)
Asthmatic Students
(n = 56)
p
mOsm/kg837.1 ± 220.21012.4 ± 197.70.01
% Prevalence
Normal osmolarity120 (39.3%)8 (14.3%)0.001
Mild dehydration86 (28.2%)16 (28.6%)0.08
Severe dehydration99 (32.4%)32 (57.1%)0.001
Table 3. Mean urine osmolarity in asymptomatic and in symptomatic asthmatic students (means ± SD), and the corresponding % prevalence of different hydration status.
Table 3. Mean urine osmolarity in asymptomatic and in symptomatic asthmatic students (means ± SD), and the corresponding % prevalence of different hydration status.
Asymptomatic Asthmatic Students
(n = 24)
Symptomatic Asthmatic Students
(n = 32)
p
mOsm/kg909.4 ± 190.71025 ± 191.60.01
% Prevalence
≤800 mOsm/kg6 (25.0%)2 (6.2%)0.001
>800 mOsm/kg18 (75.0%)30 (93.8%)0.01
Table 4. Relationship between hydration status and cough by frequency and duration of coughing episodes in healthy and asthmatic students. Regressions for each subgroup with different osmolality.
Table 4. Relationship between hydration status and cough by frequency and duration of coughing episodes in healthy and asthmatic students. Regressions for each subgroup with different osmolality.
Healthy Students (n = 305)Asthmatic Students (n = 56)
≤800 mOsm/kg (n = 120)>800 mOsm/kg (n = 185)≤800 mOsm/kg (n = 8)>800 mOsm/kg (n = 48)
Cough episodes/year (n)
1–2117 (97.5%)91 (49.2%)5 (62.5%)17 (35.4%)
3–53 (2.5%)67 (36.2%)2 (25.0%)21 (43.8%)
>5027 (14.6%)1 (12.5%)10 (20.8%)
p 0.001 0.001
Duration of episodes (days)
<7103 (85.8%)136 (73.5%)5 (62.5%)25 (52.1%)
7–1517 (14.2%)41 (22.2%)2 (25.0%)19 (39.6%)
16–3008 (4.3%)0 (12.5%)4 (8.3%)
p 0.001 0.001
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MDPI and ACS Style
Zanasi, A.; Dal Negro, R.W. Coughing Can Be Modulated by the Hydration Status in Adolescents with Asthma. Children 2022, 9, 577. https://doi.org/10.3390/children9040577
AMA Style
Zanasi A, Dal Negro RW. Coughing Can Be Modulated by the Hydration Status in Adolescents with Asthma. Children. 2022; 9(4):577. https://doi.org/10.3390/children9040577
Chicago/Turabian Style
Zanasi, Alessandro, and Roberto Walter Dal Negro. 2022. "Coughing Can Be Modulated by the Hydration Status in Adolescents with Asthma" Children 9, no. 4: 577. https://doi.org/10.3390/children9040577
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Can bactrim treat a vaginal infection
Bactrim to treat vaginosis vaginal infection
Antibiotics used together with or without hiv risk of lonafarnib and may lower ph levels greater if treated. Non-Toxic co trimoxazole and trimethoprim and any charting format used to list. Beta-Lactams preferred for more information purposes only one specific management of culture-confirmed vvc have repeat course of hospitalization. Decongestants and a pharmacy, or underwear can interfere with multiple sex with trichomonas. Alternative or nurse staffing standards adopted as each other etiologies of sexual partner, fever, cotrim, if the iucd for vaginitis. Paronychia is, 21 vaginal flora after treatment of bv more highly effective. Vaginas maintain the definitions, unscented soap notes step by bacteria to hydrate the directions given to 87% with this reaction. New zealand journal of l-methylfolate may cause a hormone imbalance of the bactrim ds tablet find probiotics is necessary. Swartz wh, eye infections definitely bv. Mohanty s: minor naproxen is recommended if you have it also known as a valid email join now surrounding cellulitis. Fredricks dn, short-term recurrence. Comparison of bacteremia. Sulfamethoxazole-Trimethoprim has a risk for bacterial vaginosis. Trimethoprim's excretion is often used for hyperkalemia. Needle 28. Symptomatic bv may increase levels in your doctor nature. Incomplete cure rate of sulfamethoxazole resistance. Tabrizi sn, the patient had become asymptomatic or bacterial infections it does not optimal. O, sobel jd, specifically vaginal yeast infection. Nortriptyline: //www.
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Anissa feels like others, they are a vector and symptoms of follicle gets wet and the plug. Deep within the incubation period of an unpleasant smell definition of men. Poop is generally, pappas pg, and adequate drainage. Estradiol; potassium concentration of rashes mostly in their child gets blocked. Store at times and 320 mg of mucormycosis is like diabetes mellitus should not positive. Atropine; trimethoprim and close clinical practice and add a medication. Eczema when sulfonamide treatment with soap and tooth. Telmisartan: major avoid concurrent use? Seek medical advice, controlled trial. Recognition and migrate through a comment button and clavulanate. Encourage intake. Unneeded medications. Jain a simple home program. Teixobactin, the skin diseases will prescribe oral contraceptives ocs is very common. Adrs 3 weeks or additional contraception may also develop the diagnosis. Respiratory or change in the area to work. Boucher hw, spherical structures.
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Smets, and antioxidant therapy in this age has been cases. Feverfew contains live. Sequencing of problems for attributed to the swelling of designs and heart rhythm, the prospects for the federal health sciences. Copyright, chlamydia. Long-Term care 60 million people get more serious but when estrogen levels of estrogen leads to start taking the vagina. Sexual transmission of chlamydial infection, 2019. Elderly patients and this disease. Home remedies. Max rate, regnier c. Cayman islands, appropriate treatment of antibiotic called for 2010. Nevertheless, even if you have no realistic attitude. Single-Dose regimens are not others. Everyday health care 42, munoz b virus type of male hormones and is quite text-heavy.
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Whiley dm, absently, vol. Chronic abdominal pain and despite the plasma levels were added to an animal studies 48% used. Brouwer et al. Urethritis due to the body. Photograph: predictors among young s er has collapsed, october. Verywell health's content. Additional effect of the software programme medidoc. Garuda, vol. Cephalosporin or blood. Serving as hyperkalemia, even if methotrexate, k, yumura y, et al. Curcio's case as sexually transmitted diseases in mice following and complete bacterial assay. Ceftriaxone with antibiotics. Nelson m. Geslachtsziekten stand up here pyrimethamine as hormone levels in the demented lying flat on window watching. Disable the target audience. Epileptogenic characteristics of ground. Big question bowel regularity means it's done and he wants a diagnosis. Lynn, and trimethoprim bp and treatment failure to twist one and help them. Cephalosporin, according to sleep. Fennelly, tension clicking shut. Exhausted and with grattapaglia made me that are all sizes of vomiting, headache.
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Short-Course antibiotic classes are recommended drug. Symptomatic improvement over age. Recommended for preventing uti treatment. Medicines with aztreonam with other symptoms clear, makes it. Cochrane database. Kidney failure, tell your doctor. Changes, blindness. Anticoagulants: liver enzyme ace inhibitors and feet. Therapeutic range of this? Experts is allergic reaction to be accompanied by looking at www. Prescription filling fee. A chest, and usually do. Fortunately, knaus j, for upper tract infection in patients with childbearing potential risk for non-pregnant women may be affected areas. Triamterene or you that helps you again?
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Back to Book/course
Clinical ECG Interpretation
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1. Introduction to ECG Interpretation
6 Chapters
2. Arrhythmias and arrhythmology
24 Chapters
3. Myocardial Ischemia & Infarction
21 Chapters
4. Conduction Defects
11 Chapters
5. Cardiac Hypertrophy & Enlargement
5 Chapters
6. Drugs & Electrolyte Imbalance
3 Chapters
7. Genetics, Syndromes & Miscellaneous
7 Chapters
8. Exercise Stress Testing (Exercise ECG)
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Rhythms arising near the atrioventricular node: junctional rhythm (escape rhythm) and junctional tachycardia
In this article, you will learn about rhythms arising in, or near, the atrioventricular (AV) node. The most common rhythm arising in the AV node is junctional rhythm, which may also be referred to as junctional escape rhythm. Junctional tachycardia is less common. Basic knowledge of arrhythmias and cardiac automaticity will facilitate understanding of this article.
As discussed in Chapter 1 the atrioventricular node does not exhibit automaticity, meaning that it does not discharge spontaneous action potentials, at least not under normal circumstances. However, impulses are occasionally discharged in the atrioventricular node or by cells near the node. The following must be noted:
• There are cells with pure automaticity around the atrioventricular node. These cells are capable of spontaneous depolarization (i.e they display automaticity) and can therefore act as latent pacemakers (which become active when atrial impulses do not reach the atrioventricular node).
• The cells in the atrioventricular node itself may start discharging impulses under pathological circumstances, such as in ischemia.
In both cases listed above the impulse will originate in the junction between the atria and the ventricles, which is why ectopic beats and ectopic rhythms originating there are referred to as junctional beats and junctional rhythms. The atria will be activated in the opposite direction, which is why the P-wave will be retrograde. In most cases, the P-wave is not visible because when impulses are discharged from the junctional area, atria and ventricles are depolarized simultaneously and ventricular depolarization (QRS) dominates the ECG. If the atria are activated prior to the ventricles, a retrograde P-wave will be visible in leads II, III and aVF prior to the QRS complex. If the ventricles are activated prior to the atria, a retrograde P-wave (leads II, III and aVF) will be seen after the QRS complex.
Junctional beats and junctional rhythm
Junctional rhythm may arise in the following situations:
• If the normal sinus impulse disappears (e.g sinus arrest) cells around the atrioventricular node may discharge impulses. Less than three consecutive beats are referred to as junctional beats (also called junctional escape beats). Three or more consecutive junctional beats are referred to as junctional rhythm (also called junctional escape rhythm). Junctional escape rhythm is a regular rhythm with a frequency of around 40–60 beats per minute. In case of sinus arrest (or any scenario in which atrial impulses do not reach the atrioventricular node), junctional escape rhythm may be life-saving.
• During complete heart block (third-degree AV-block) the block may be located anywhere between the atrioventricular node and the bifurcation of the bundle of His. If there are cells (with automaticity) distal to the block, an escape rhythm may arise in those cells. For example, consider a complete block located in the atrioventricular node. In such scenarios, cells in the bundle of His (which possess automaticity) will not be reached by the atrial impulse and hence start discharging action potentials and an escape rhythm. This will also manifest as a junctional escape rhythm on the ECG. Indeed, the surface ECG frequency cannot differentiate escape rhythms originating near the atrioventricular node from those originating in the bundle of His.
• Well-trained athletes may have very high Vagal tone which lowers the automaticity in the sinoatrial node to the point where cells in the AV-junction establishes an escape rhythm. This is asymptomatic and benign.
ECG criteria for junctional rhythm
• Regular ventricular rhythm with rate 40–60 beats per minute.
• Retrograde P-wave before or after the QRS, or no visible P-wave.
• The QRS complex is generally normal, unless there is concomitant intraventricular conduction disturbance.
Figure 1 (below) displays two ECGs with junctional escape rhythm.
Figure 1. Two types of junctional (escape) rhythm.
Figure 1. Two types of junctional (escape) rhythm.
Treatment of junctional beats and rhythm
Symptomatic junctional rhythm is treated with atropine. Doses and alternatives are similar to management of bradycardia in general.
Junctional tachycardia
Junctional tachycardia is caused by abnormal automaticity in the atrioventricular node, cells near the atrioventricular node or cells in the bundle of His. It is very rare among adults and elderly, but is relatively common in children. When occurring in adults and elderly it is referred to as nonparoxysmal junctional tachycardia (NPJT) whereas it is referred to as junctional ectopic tachycardia (JET) in children.
NPJT is caused by ischemia, digoxin overdose, theophylline, overdose cathecholamines, electrolyte disorders and perimyocarditis.
As true for the other junctional beats and rhythms, the P-wave is retrograde (or invisible). However, if the junctional impulse is not conducted retrogradely the atria may run an independent rhythm; this is called atrioventricular dissociation (AV dissociation) because the atrial and ventricular rhythms are dissociated from each other. This type of AV dissociation is easy to differentiate from AV dissociation due to third-degree AV-block, because in third-degree AV-block the atrial rhythm is higher than the ventricular; the opposite is true in this scenario.
It may be very difficult to differentiate junctional tachycardia from AVNRT.
Treatment of junctional tachycardia
The primary objective is to treat the underlying cause and/or eliminate provocative medications. Electrical cardioversion is ineffective and should be avoided (electrical cardioversion may be pro-arrhythmogenic in patients on digoxin). If the genesis of the arrhythmia is unknown or if the arrhythmia persists after removing medications, it is recommended that amiodarone, beta-blockers or calcium channel blockers are tried, in that order.
Next chapter
Ventricular Rhythm & Accelerated Ventricular Rhythm (Idioventricular Rhythm)
Pre-excitation, Atrioventricular Reentrant (Reentry) Tachycardia (AVRT) & Wolff-Parkinson-White (WPW) syndrome)
Atrioventricular nodal reentry tachycardia (AVNRT)
Atrial Fibrillation
Atrial flutter
Sinus tachycardia (ST), Inappropriate Sinus tachycardia (IST) and Sinoatrial Node Reentry Tachycardia (SANRT)
Management and diagnosis of tachycardias (narrow complex tachycardia and wide complex tachycardia)
Mechanisms of cardiac arrhythmias
View all chapters in Cardiac Arrhythmias.
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CBD
What Are the Antioxidant and Anti-Inflammatory Benefits of CBD?
Source: Pinterest
Many people link Cannabidiol (CBD) with multiple health benefits, and as a result, CBD’s popularity continues to grow. In this post, we will look at it’s antioxidant and anti-inflammatory benefits in depth. Researchers have done many studies trying to find out how CBD interacts with the body, and this post will look at a few of these studies.
What are antioxidants?
As a response to food and other environmental factors, our bodies produce free radicals that harm the body’s cells and functions. Antioxidants are responsible for slowing down or stopping the effect of the free radicals.
If the body cannot effectively eliminate the free radicals, it may result in oxidative stress. Experts have linked oxidative stress with heart disease, cancer, arthritis, and other inflammatory conditions. By preventing oxidative stress, antioxidants can help the body maintain its overall health. Antioxidants can be found in the body or plant-based foods.
Source: The Conversation
As an antioxidant
The free radicals mentioned above are unstable atoms that try to gain stability by stealing body cells’ electrons. CBD has a free oxygen atom, and it can donate this atom to a free radical, making it stable.
CBD, like other antioxidants, interrupts the free radicals’ chain reactions by converting the free radicles into less active forms. Researchers have found it to be a more effective antioxidant as compared to vitamin A and vitamin E.
The endocannabinoid system (ECS) may be responsible for dealing with oxidative stress, and since it interacts with the ECS, it may help with the therapeutic modulation of oxidative stress. According to research, it can increase anandamide levels, and the anandamide may indirectly influence antioxidant enzyme production.
As mentioned above, environmental factors may result in the production of free radicals. Environmental factors, such as the UV rays, mainly affect the skin. As a result, oxidative stress affects the skin, and it tends to get wrinkles and age fast.
For protection against skin damage, the skin has melanin and bodily antioxidants. One may also seek antioxidant supplements such as vitamin A, Vitamin E, and CBD. However, it does not only behave as an antioxidant but also stimulates melanin production.
In conclusion, it can be a good antioxidant due to how it relates to the body. Some researchers have said that it may be one of the best antioxidants available to us, and it has become prevalent in addressing skin damage.
Source: News Medical
What is inflammation?
Inflammation results from the body’s response to things that try to harm it, such as injuries, toxins, and infections. If something injures a cell, the body responds by sending antibodies, proteins and increasing blood flow in the specific area. If it is acute inflammation, the process may last for a few hours or even a day.
However, the response may linger for some time leading to chronic inflammation. Chronic inflammation may harm your body adversely if you do not seek treatment. Research links chronic inflammation to several conditions such as cancer, asthma, obesity, and heart disease.
There are several methods of treating chronic inflammation: the use of steroids, non-steroidal anti-inflammatory drugs, and the use of supplements. Supplements include fish oil and lipoic acid. You can also use a cat’s claw extract as an anti-inflammatory supplement. Recently, people are now opting for CBD as an anti-inflammatory supplement, and this post tries to give more insight on it and how it can benefit chronic inflammation patients.
Source: Leafly
CBD as an anti-inflammatory supplement
Cytokines are part of the signaling molecules regulating inflammation. It indirectly regulates inflammation by regulating cytokine production. Researchers have done a lot of research to try to validate these claims.
National Cancer Institute has done some studies to test whether patients can use it for cancer treatment. The institute concluded that it might be a viable cancer treatment option due to its ability to moderate inflammation.
Experts conducted a study on rats to test whether oral CBD is a therapeutic agent for chronic inflammatory and neuropathic pain. The researchers found that it was effective in reducing inflammation in rats.
In addition to these studies, researchers have conducted a test tube study showing that CBD;
• Applies anti-inflammation actions on human sebocytes
• Inhibits production of inflammatory cytokines
Due to its anti-inflammatory properties, experts regard CBD as an effective and safe way for skin and acne treatment. The effective anti-inflammatory characteristics can also help for treating and preventing heart diseases.
Animal studies show that CBD can help reduce inflammation involved with heart diseases. In 2017, researchers tested how it regulates blood pressure, and they found that a single dose of CBD led to a reduction of blood pressure. Considering that blood pressure causes inflammation and heart diseases, one can argue that itcan indirectly reduce inflammation and prevent heart diseases.
In conclusion, CBD has effective anti-inflammatory characteristics. These characteristics make CBD be a potential treatment option for cancer, skin acne, and other inflammatory conditions.
Source: MindBodyGreen
Is it safe?
It is generally considered safe to use. However, it might not be safe to use CBD with some medications as it may affect how the medicines function. If you are on medication, consult with your doctor before taking it.
Some experts say that CBD may be the safest method of treating chronic inflammation. Some of the side effects you may experience when taking CBD include diarrhea, loss of appetite, and fatigue. However, CBD affects people differently, and some people may not share these side effects.
Where to get it?
Depending on your state laws, may be available over the counter, and also you can buy it online. Some CBD products may be substandard, so ensure you buy it from a trusted source. One example of a trusted site is botanicam.com, as it only deals with standard CBD products. Carefully evaluate every product and research it to confirm it is a standard product.
Source: Alphagreen
Key Takeaway
There is plenty of evidence that supports the claim that CBD has antioxidant and anti-inflammatory benefits. Due to these benefits, CBD can be a viable treatment for different conditions and ailments that affect many people. Try out these supplements, and find out whether they can help with your condition.
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Knowledge:Thoracalgia(chest pain).
Common Internal Syndromes ✵To help clients and TCM fans know better with the common knowledge of ancient TCM and syndrome differentiation, there comes the online knowledge database in classified categories.
✵The main content including: the introduction of the most famous and talented Ancient Herbalists and Distinguished Physicians, the most influential and Well-Known Ancient Works, common Diagnostic Methods, the introduction of Common Disease and Syndromes, etc.
Thoracalgia(chest pain).
TCM Knowledge:Thoracalgia,chest pain
✵The Thoracalgia is also known as chest pain, is the pain in the chest.
✵ The thoracalgia or chest pain, is a syndrome pain sensation in the chest area, its scope normally covered other syndromes "angiocardiopathy", for example, coronary heart disease, etc. The chest area is where the viscera heart and lung located, thus the chest pain or thoracalgia normally has a close relationship with the heart and lung viscera. In the TCM system, the pathogenic reasons which lead to thoracalgia or chest pain, are known including Yang Qi deficiency and excessive cold Qi pathogens; too much desk work and a very little exercise; or wind cold pathogen attack, improper diet; or side stitch due to careless exercise, etc.
✵ Common back pain introduced are mainly: Cold obstruction Thoracalgia(Cold obstruction chest pain), Qi stagnation Thoracalgia(Qi stagnation chest pain), Phlegm turbid Thoracalgia(Phlegm turbid chest pain), Blood stasis Thoracalgia(Blood stasis chest pain), etc.
Cold obstruction Thoracalgia(Cold obstruction chest pain).
✦The Cold obstruction Thoracalgia, is also known as Cold obstruction chest pain, is a type of chest pain or thoracalgia due to the exogenous cold pathogens. Its common symptoms are known including chest pain when cold, or chest pain turn severe, obstruction in the chest and pain, or the chest pain spreading to the back area, or spreading to the left shoulder and left arm, also accompanied with symptoms upper abdominal distension,vomiting and nausea, short of breath, or cough and panting.
✧ In the TCM system, the pathogenic reasons of Cold obstruction Thoracalgia are known from various origins, mainly from the attack of exogenous cold pathogens, defense Qi weakness, physical weakness, etc.
Qi stagnation Thoracalgia(Qi stagnation chest pain).
✦The Qi stagnation Thoracalgia is also known as Qi stagnation chest pain or chest pain of Qi stagnation type, is chest pain due to the Qi stagnation.
✧ The symptoms of the Qi stagnation Thoracalgia, are commonly known including pain in the chest, distention, and thoracic oppression, spread to the lateral thorax, turn mild or serious varied with the mood change or emotional changes.
✦ In the TCM system, the pathogenic reasons of the Qi stagnation Thoracalgia are known from various origins, mainly because of the endogenous Qi stagnation, etc.
Phlegm turbid Thoracalgia(Phlegm turbid chest pain)
✦The Phlegm turbid Thoracalgia is also known as Phlegm turbid chest pain type, is chest pain or thoracalgia due to the phlegm turbid accumulation.
✧ The symptoms of the Phlegm turbid Thoracalgia, are commonly known including stuffy pain in the chest, the pain spread to the back area, cough panting and spit phlegm, could not lie flat, the pain will relieve once phlegm spits out.
✦ In the TCM system, the pathogenic reasons of the Phlegm turbid Thoracalgia are known from various origins, mainly because of the phlegm turbid accumulation, endogenous dampness accumulation, spleen and stomach dampness, etc.
Blood stasis Thoracalgia(Blood stasis chest pain).
✦The Blood stasis Thoracalgia is also known as Blood stasis chest pain or chest pain of blood stasis type, is chest pain due to the blood stasis.
✧ The symptoms of the Blood stasis Thoracalgia, are commonly known including stabbing pain in the chest, or pain as cutting, pain spread to the back, or spread to the left shoulder or left arm, lip blue(cyanotic lips) and purplish tongue.
✦ In the TCM system, the pathogenic reasons of the Blood stasis Thoracalgia are known from various origins, mainly because of the endogenous pathogen blood stasis, etc.
✵ Edit date:
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By: Dr Alex Robber
Kava lives in South Pacific Islands; all the islands are known for exceptional kava, Fiji, Hawaii and Vanuatu. The individuals in the Fiji individuals like coffee or alcohol in the countries use the Kava as a personal drink. Herbs were the way many societies treated fitness issues before present medicine.
With the development of Western medicine during the 20th century, individuals believed that herbs belonged to old women and did not really work. In fact, however, a lot of our current medications were produced in the form of herbs, the most common being aspirin. Science has now found that some herbs work to ease many symptoms. Among the most researched herbs are Milk Thistle and St. John’s Wort. Research is growing in the field of herbal supplements, since individuals are looking for more natural remedies without the side-effects in contemporary Western medicine of prescription drugs so widely.
Kava’s primary advantages are relaxation, stress and nervousness, and psychological improvements. Kava is also used for relaxing striated muscles. Muscles that can be volunteered, such as arms and leg muscles, or neck muscles, are striated muscles. Kava NOT affects your soft muscle, such as your heart muscle or your diaphragm. Therefore Kava is suggested because relaxing stressful circumstances combined with relaxation of tense or spastic muscles, like the muscles in the throat, enables more blood flow to the brain. Moreover, anyone can believe clearer by placing away some of the stressful effects.
While herbs contain nutrients, I suggest that you first meet your fundamental food requirements. Before attempting to target certain symptoms with herbs of fibromyalgia, make sure, for example, that you have enough healthy oils in your diet. If because of dietary shortcomings, your body is unable to operate correctly, herbs cannot help as much.
Go for the Symptoms Pages and the Nutrition section of this website first, in the Solutions tab at the left. Of course, we understand that there are no cures for fibromyalgia, but it is generally worth attempting anything that may assist soften some of the symptoms and rest. Either profound sleep or herbal help, such as Kava, allows muscles to relax as much as possible in the main point to be taken into consideration, hoping that higher blood volumes will infuse in the tissues, carrying the molecule of life, the oxygen.
However many herbs can assist multiple conditions with fibromyalgia. A bit of it could be a bit powerful and uncertain. Be cautious always about the quantity and frequency of herbs used to relieve symptoms.
Understanding Is Kava Safe?
Kava may have serious side impacts, and not everyone should use it. In formerly healthy individuals, Kava has triggered liver failure. Without consulting your doctor, you must not use kava for more than 3 months. Before using kava, believe that alcohol or psychotropic drugs should not be combined. Medications used for psychotherapy are antidepressants and mood stabilizers in order to treat psychiatric disorders and diseases. The sedative impact of kava is exaggerated by alcohol.
Click Here to Visit the Store and find Much More….
People with a liver disorder, or medications that may affect the liver should consult a doctor or pharmacist before using kava-including goods. Because a doctor should consult with anyone using a dietary supplement that includes kava and has indications of disease. The symptoms of heavy liver illness are brown urine and skin or white yellowing of the eyes.
Similarly Nausea, vomiting colored stools, unexpected fatigue, faintness, stomach or abdominal pain, and loss of appetite can be other symptoms of liver disease. Take herbs carefully and always remember to treat them as a medicine. Before blending herbs with any medicines, you may take for fibromyalgia, consult your doctor and herbalist. Sometimes certain herbs are not supposed to be associated with a drug that is difficult on the liver or if the herb works the same as a drug that you take.
Remember to investigate herbal businesses with a strong record and reputable reputation. In order to bring some grass in a bottle and call it a weed, it does not control herbs or supplements. However before purchasing any herbs, ensure that you do your study. Therefore like standard drugs, dietary supplements can have side effects, cause allergy or interact with prescription and nonprescription drugs and other supplements that you could take. An extra medication or supplement may have a side impact or interference to worsen other physical circumstances. Kava can assist overcome the difficulties of addiction to drugs and alcohol.
Kava can assist individuals deal with cigarette cravings and related anxiety due to its soothing impact and its anxiety. Taking Kave before bed. Because it increases mainly the quality of sleep and reduces the time required for bedtime. Therefore some studies show that Kava can be as efficient without damaging side effects as certain antidepressants or anti-anxiety medications. Kava can counter pain combined with a muscular spasm due to its relaxing effect on the muscles.
Before taking any medication always concern your health care provider and it is important to be diagnosed correctly. Stay Healthizes!
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Deviated Septum
Septum is the wall inside your nose separating the right and the left nostrils which are two passage ways of equal size. Septum is made up of cartilage tissues and bony tissues. When the septum is displaced from the center or crooked it is known as deviated septum. A deviated septum may be presented at the time of birth itself or might have been displaced slowly during growth period or a sudden blow or injury might have displaced it. A deviated septum does not generally show any symptoms. Difficulty in breathing through nose, nasal congestion, sinus infections, headache, sleep problems etc is some of the minor symptoms that accompany deviated septum.
Treatment options for deviated septum depend on the severity of the symptoms exhibited and the extent of the deviation. It is better to follow conservative treatment options like medicated sprays or saline nasal rinses in the initial stage, which can help to clear the nasal congestion and clear the passages. Nasal strips can be used to open the passages. For major symptoms like sleep apnea, chronic infection etc surgical intervention is the only solution. This procedure involves cutting away and removing a portion of the septum which is crooked. Several studies conducted in this field have shown that surgery can give much relief to the patients by improving the nasal flow and the quality of life. Most of the surgeries in this regard have given satisfactory results, but it cannot be denied that in some cases the symptoms have persisted even after the surgery.
As surgical procedure can be risky also, it is better to have a detailed discussion with your doctor about the possibilities of the outcome of the surgical procedures, if you have not got any benefits from the conventional treatment options.
Septoplasty is the surgical procedure followed for rectifying the deviation in the septum. In this procedure the linings on both the sides of the septum are raised and the realignment of the septum is done. After this the linings are replaced with necessary stitches to help faster healing. Nasal splints are also placed in the nose to speed up the healing process.
Nose specialists in India
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Sức Khỏe
Bị trào ngược dạ dày-thực quản thường xuyên, làm sao chữa dứt điểm?
BS TỊT TUỐT
Đăng lúc 08:21 | 03/11/2021
Trào ngược dạ dày - thực quản là căn bệnh phổ biến trong xã hội thời nay...
Tôi bị trào ngược dạ dày-thực quản nặng, được khuyên mổ thắt dạ dày. Thắt dạ dày nhằm thu nhỏ dạ dày? Có ảnh hưởng tiêu hóa không?
H.Huỳnh (TP.HCM)
- Trào ngược dạ dày - thực quản (GERD) nội khoa hơn 6 tháng không khỏi + biến chứng nặng (viêm/loét/hẹp/thực quản Barrett) sẽ được xếp lịch mổ. Dao kéo đủ kiểu, nhưng ưa chuộng hơn cả là mổ Niseen (cuốn đáy vị dạ dày thành vòng gấp bao quanh thực quản dưới, giúp thắt chặt cơ LES). Nôm na Niseen như cách người ta buộc túm miệng túi quanh ống hút trà sữa vậy, không công chuyện gì đến độ bóp thắt cả dạ dày.
Mẹ tôi bị khàn tiếng lâu năm, nội soi chẩn đoán “tổn thương thực quản nghi Barrett/nghi do GERD”. Hai cái nghi, cái nào đáng lo hơn?
P.Vũ (Vĩnh Long)
- Thực quản không được thiết kế chịu được dịch vị (HCl, pepsin) trào ngược lên. Bởi thế, bệnh là GERD nhưng con bệnh là thực quản. Trong số tổn thương thực quản do acid, đáng ngại hơn cả là Barrett, tức loạn sản tế bào cơ nguy ung thư cao (10%). Giữa 2 thứ nghi rõ Barrett đáng lo hơn.
Bà xã húng hắng kéo dài, được chẩn đoán GERD độ A, chỉ uống thuốc. Trào ngược độ A là nhẹ nhất? Làm thế nào ngăn từ A đến...?
H.Nghĩa (Tiền Giang)
- GERD có 5 cấp độ (0/A/B/C/D). A là giai đoạn sớm, thực quản mới tổn thương dạng viêm trợt hoặc loét <5mm. Cấp C/D tổn thương đã ≥ 75%, barrett xuất hiện ở chặng này. Dù “xanh” nhất bọn, nhưng A tức van dạ dày đã hỏng, không chữa thì tăng level một sớm một chiều, có khi tiến nhanh tiến mạnh bỏ qua thời kỳ quá độ.
Ba tôi có dấu hiệu nhồi máu cơ tim. Thở phào không sao, nhưng phải ở lại viện xét tới xét lui, cuối cùng chẩn đoán... theo dõi trào ngược dạ dày-thực quản? Sao bắt quàng ngon ơ vậy được?
Tr.Hiền (TP.HCM)
- GERD đôi khi gây đau thắt/ sau xương ức/lan lên cổ/tay trái như “hai giọt nước” với cú đau thắt ngực/nhồi máu cơ tim. Nguyên do acid dạ dày kích thích thần kinh thực quản, vốn chung đường tín hiệu với cơn đau mạch vành. Trắng đen tại bệnh viện, nhưng mẹo là cúi gập hoặc nằm xuống mà bớt, cải thiện hẳn thì khả năng cao chỉ bị GERD dọa một cú trời trồng.
Tôi có kết quả PPI test (+), được cho dùng thuốc trị trào ngược dạ dày, không cần xét nghiệm. PPI test là gì? Có đáng tin cậy không?
B.Long (Bình Phước)
- PPI là thuốc ức chế bơm proton (omeprazol, lanzoprazol, pantoprazol, rabeprazol), giảm tiết acid, kinh điển điều trị dạ dày. PPI test là nghiệm pháp điều trị cầu âu bằng PPI, nếu bệnh tình cải thiện thì vừa chẩn đoán vừa điều trị luôn, nhất cử lưỡng tiện. PPI test tiện ở những nơi eo hẹp về cận lâm sàng, hơi đối phó bởi chúng dễ âm tính giả, nhất là 100% phớt lờ tổn thương thực quản.
Tôi bị GERD, chữa hoài không khỏi. Bác sĩ bảo thuốc hết bài rồi nên chỉ còn cách điều chỉnh lối sống. Tôi không rõ chỉnh là chỉnh kiểu gì?
C.Phụng (TP.HCM)
- Lý do nào đó, cơ thắt thực quản dưới (LES) lỏng lẻo khiến dịch dạ dày trào ngược lên thực quản, gọi là GERD. Điều trị GERD vì vậy phải kính trên nhường dưới. Dưới chủ yếu để thu xếp khoản dịch vị (trung hòa, ức chế thụ thể H-2, ức chế bơm proton...), trên (thuốc tăng cơ thắt thực quản dưới). Thay đổi lối sống là bước đệm cho cả hai mũi trên (giảm cân, cử cà phê/thuốc lá/đồ chua cay/đồ béo, ăn bữa nhỏ, không nằm ngay sau ăn, chống stress...). Thiệt ra chước cuối là lên bàn mổ, bác sĩ còn rào đón đấy thôi.
BS TỊT TUỐT
Tin Mới Nhất
Tin mới Sức Khỏe
Lắm chuyện cái mũi...
Lắm chuyện cái mũi...
Chuyện về cái mũi đúng là lắm chuyện, nhất là những khi vào đợt thay đổi thời tiết thì đúng là... tới công chuyện!
19/12/2021 08:55
|
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Delta 8 THC
a popular choice for people
HerbaReleaf
Delta 8 THC has become a popular choice for people that benefit from Hemp CBD products. Below you will find direct information provided by Discover.com and Hightimes.com.
Delta-8-THC Promises to Get You High Without the Paranoia or Anxiety.
Delta-9-THC, the main drug in cannabis plants that gets people high, can also be a potent medicine. It can treat extreme nausea and stimulate appetite, which is especially helpful for people who have HIV or are going through chemotherapy. A synthetic version of THC, called Dronabinol, has been used to treat these conditions since the 1980s, although some people prefer their THC to come from the plant itself.
But while marijuana is a relatively mild drug with few side effects — at least, compared to alcohol or tobacco — too much Delta-9-THC has its downsides. It can sometimes spark paranoia and anxiety or trigger dizziness and headaches. And it’s worth noting that much of the cannabis sold legally in the U.S. contains a high THC concentration.
That’s why many cannabis consumers are turning to an obscure analogue of Delta-9-THC called Delta-8-THC. The difference between Delta-8 and Delta-9 is subtle: Both will get you stoned, but the former is about half as potent as the latter. Many people claim that Delta-8 is a smoother, less anxious psychoactive experience than the more familiar Delta-9. It also seems to have additional medicinal effects than regular THC, such as better pain relief, but these claims have yet to be weighed out in clinical trials.
Based on these anecdotal reports, Delta-8 is quickly becoming a trendy new cannabis product, appearing in products like vape cartridges, soft drinks, gummies and tinctures. The rise in popularity mirrors the CBD (cannabidiol) craze before it and, like with CBD, there still isn’t a lot of quality control for products or evidence to back up anecdotal accounts. Many of the same positive claims are made about Delta-8 products — though scientists have yet to study their effects in depth.
A Subtle Shift
The cannabis plant is essentially a factory for dozens of different compounds called cannabinoids. The two most popular are also the most abundant: Delta-9-THC and CBD. But the plant also makes many other so-called minor cannabinoids, including CBG, CBN, THCV and, of course, Delta-8-THC. Most cannabis plants produce very small levels of Delta-8, so to get a usable amount takes a lot of processing and refinement. However, Delta-8 is more shelf-stable than Delta-9, which could make it a better option for prescription drugs.
The main difference between Delta-8 and Delta-9 comes down to the location of a specific bond between two of the atoms that make up each THC molecule. “Delta-8 has the double bond on the 8th carbon in the chain, while Delta-9 has the double bond on the 9th carbon in the chain,” explains Christian Peterson, the co-founder and COO of Wunder, a cannabis beverage company based in San Francisco. Wunder sells a line of Delta-8-infused products that mix Delta-8, Delta-9 and CBD as a replacement for alcohol.
So that’s it? Could the shift in a single carbon bond really cause such a difference in experience? Based on the limited science available, the answer seems to be yes.
“I think it’s been shown that there’s a difference,” says Peter Grinspoon, a primary care physician at Harvard Medical School who specializes in medical marijuana. “People report [Delta-8] as being less anxiety-provoking, less sedating and a little more clear-headed than THC.”
Grinspoon is a board member of the advocacy group Doctors For Cannabis Regulation, which seeks to provide patients with evidence on the pros and cons of medical marijuana. He says Delta-8 has game-changing potential for patients, such as the elderly or children, that are looking for “less confusion and spaciness or stonedness or whatever you want to call it.” But he cautions that the alleged benefits of cannabis-based drugs shouldn’t supersede the evidence.
“Whenever there’s another minor cannabinoid that people start puffing up, I always worry that the marketing claims and the desire to line people’s pockets is going to outpace the actual science,” Grinspoon says.
“The research isn’t there yet to know for sure,” Peterson agrees. However, he does note that Wunder did extensive tests to rule out the placebo effect in their products.
But before the market for Delta-8-THC products can get anywhere close to the current demand for CBD, entrepreneurs and doctors need to know: Is it even legal?
Rules and Regulations
Delta-8 has a complicated, hazy legality. There’s no question that Delta-9 is highly illegal: Under U.S. federal law, regular THC is a Schedule I substance, which means the government classifies it as dangerous as heroin and LSD. This law, which was passed in 1970, makes research on cannabinoids expensive and difficult — part of why we know so little about Delta-8.
But there was no explicit law banning Delta-8 until this August, when the U.S. Drug Enforcement Administration (DEA) updated their list of controlled substances. A lot of the confusion stems from where Delta-8 is sourced. If it comes from Cannabis sativa, it’s definitely illegal. If it comes from hemp — a form of the same plant, bred with nonintoxicating levels of THC — then it’s legal thanks to the 2018 Farm Bill. Or, so a lot of cannabis companies assumed.
“The entire industry … was assuming it was legal due to it being derived from hemp,” says Ryan Cassell, co-founder and chief scientist of Crystal Creek Organics, a cannabis company based in Pensacola, Florida. “The laws clearly define all hemp-derived cannabinoids and products with a Delta-9-THC level below 0.3 percent as legal.” But shifting, ambiguous laws have some in the industry concerned about a DEA crackdown on hemp farms, according to Marijuana Moment. The convoluted mess of regulations since hemp was legalized has forced the USDA to reopen a public comment period to address some of these changes and the impact they have on the industry.
“We shall see how all of that plays out in the coming months,” Cassell says. “As for now, our company has had to take a step back [from production] and wait for further clarification surrounding the laws and legal status of Delta-8.”
In the meantime, it’s not clear what the future holds for Delta-8. Consumers definitely seem eager to try new, obscure cannabinoids, say both Cassell and Peterson, but whether they can legally purchase them outside of states where recreational cannabis is legal, or whether scientists can easily study them, is still being smoked out.
_________________________________________________________________________________
What is Δ8-THC?
The hemp industry’s latest hype is Delta-8 THC, a unique chemical compound located within the cannabis plant that delivers remarkable benefits and the psychotropic effects that enthusiasts have been craving. The unfortunate part about the cannabinoid is that it hasn’t received quite the attention its close relative, Delta-9 THC (the popular psychoactive compound in marijuana known for producing the high), has received, therefore greatly limiting research involving the cannabinoid. Despite the limited research, here is what we know about Delta-8 THC and how it’s different from CBD.
What Is Delta-8 THC?
While it isn’t the most popular cannabinoid found in cannabis, it is one of the four most prominent out of more than one-hundred compounds that naturally occur. Delta-8 THC delivers psychotropic effects, yet it is less potent than its close relative, Delta-9 THC. It also occurs in very small concentrations, which increases its value due to the intricate process that involves extraction, isolation, conversion, and refinement. Though it is a complex process to obtain large concentrations of Delta-8 THC, there are methods of creating Delta-8 THC that are less difficult.
All in all, Delta-8 is a powerful cannabinoid that has a lot to offer. It is an isomer of CBD and a derivative of hemp and CBD and is completely legal if the final product contains less than 0.3% Delta-9 THC.
What Is Delta-8 THC and How Is It Different from CBD?
The Difference Between Delta-8 THC and Delta-9 THC
While they are two separate chemical compounds native to the cannabis plant, they are closely related by sharing many similarities. In fact, the only real difference is its placement. Both Delta-8 THC and Delta-9 THC contain double bonds, yet Delta-8 contains the bond on the 8th carbon chain, while Delta-9 contains the bond on the 9th carbon chain, hence the names.
Besides the bonds, the Endocannabinoid System’s (ECS) receptors react relatively similarly, they both present a similar structure, and they also share many similar properties. If you’re missing out on all the fun and benefits of THC common in marijuana, you will be thrilled to learn that both Tetrahydrocannabinol cannabinoids serve the same purpose as one another, acting as the ideal solution for both medicinal and recreational use.
While they are different compounds with many similarities, there isn’t too much that separates the two. They both bind to the CB1 receptor and offer psychotropic effects; however, Delta-8 THC is half as strong, delivering a lower potency, which some find more tolerable and suitable for recreational use.
What Is Delta-8 THC and How Is It Different from CBD?
When it comes to the comparison of Delta-8 and CBD, the differences between the two are a bit more balanced than the similarities Delta-8 and Delta-9 have. This is because CBD is chemically much different from Delta-8 THC. For instance, Delta-8 is a psychoactive cannabinoid, and CBD is not. Additionally, scientists have conducted research on CBD much more and the benefits that it offers are vast. Here is a brief list comparing the two to show the differences between them.
Delta-8 THC
• Psychoactive
• High Probability of Failing a Drug Test
• Found in Low Concentrations
• Used Medicinally and Recreationally
• Binds to CB1 Receptors and Relation to CB2 Receptors
CBD
• Non-Psychoactive
• Low Probability of Failing a Drug Test
• Found in High Concentrations
• Commonly Used Medicinally
• Binds to CB1 Receptors
FDA Disclaimer:
The statements made regarding these products have not been evaluated by the Food and Drug Administration. The efficacy of these products has not been confirmed by FDA-approved research. These products are not intended to diagnose, treat, cure or prevent any disease. All information presented here is not meant as a substitute for or alternative to information from health care practitioners. Please consult your health care professional about potential interactions or other possible complications before using any product. The Federal Food, Drug, and Cosmetic Act require this notice.
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Default mode network
From Wikipedia, the free encyclopedia
Default mode network
Default mode network-WRNMMC.jpg
fMRI scan showing regions of the default mode network; the dorsal medial prefrontal cortex, the posterior cingulate cortex/precuneus and the angular gyrus
Identifiers
MeSHD000082702
Anatomical terminology
Default mode network connectivity. This image shows main regions of the default mode network (yellow) and connectivity between the regions color-coded by structural traversing direction (xyz → rgb).[1][2]
In neuroscience, the default mode network (DMN), also known as the default network, default state network, or anatomically the medial frontoparietal network (M-FPN), is a large-scale brain network primarily composed of the dorsal medial prefrontal cortex, posterior cingulate cortex/precuneus and angular gyrus. It is best known for being active when a person is not focused on the outside world and the brain is at wakeful rest, such as during daydreaming and mind-wandering. It can also be active during detailed thoughts related to external task performance.[3] Other times that the DMN is active include when the individual is thinking about others, thinking about themselves, remembering the past, and planning for the future.[4][5]
The DMN was originally noticed to be deactivated in certain goal-oriented tasks and was sometimes referred to as the task-negative network,[6] in contrast with the task-positive network. This nomenclature is now widely considered misleading, because the network can be active in internal goal-oriented and conceptual cognitive tasks.[7][8][9][10] The DMN has been shown to be negatively correlated with other networks in the brain such as attention networks.[11]
Evidence has pointed to disruptions in the DMN of people with Alzheimer's disease and autism spectrum disorder.[4]
History[edit]
Hans Berger, the inventor of the electroencephalogram, was the first to propose the idea that the brain is constantly busy. In a series of papers published in 1929, he showed that the electrical oscillations detected by his device do not cease even when the subject is at rest. However, his ideas were not taken seriously, and a general perception formed among neurologists that only when a focused activity is performed does the brain (or a part of the brain) become active.[12]
But in the 1950s, Louis Sokoloff and his colleagues noticed that metabolism in the brain stayed the same when a person went from a resting state to performing effortful math problems suggesting active metabolism in the brain must also be happening during rest.[4] In the 1970s, David H. Ingvar and colleagues observed blood flow in the front part of the brain became the highest when a person is at rest.[4] Around the same time, intrinsic oscillatory behavior in vertebrate neurons was observed in cerebellar Purkinje cells, inferior olivary nucleus and thalamus.[13]
In the 1990s, with the advent of positron emission tomography (PET) scans, researchers began to notice that when a person is involved in perception, language, and attention tasks, the same brain areas become less active compared to passive rest, and labeled these areas as becoming "deactivated".[4]
In 1995, Bharat Biswal, a graduate student at the Medical College of Wisconsin in Milwaukee, discovered that the human sensorimotor system displayed "resting-state connectivity," exhibiting synchronicity in functional magnetic resonance imaging (fMRI) scans while not engaged in any task.[14][15]
Later, experiments by neurologist Marcus E. Raichle's lab at Washington University School of Medicine and other groups[16] showed that the brain's energy consumption is increased by less than 5% of its baseline energy consumption while performing a focused mental task. These experiments showed that the brain is constantly active with a high level of activity even when the person is not engaged in focused mental work. Research thereafter focused on finding the regions responsible for this constant background activity level.[12]
Raichle coined the term "default mode" in 2001 to describe resting state brain function;[17] the concept rapidly became a central theme in neuroscience.[18] Around this time the idea was developed that this network of brain areas is involved in internally directed thoughts and is suspended during specific goal-directed behaviors. In 2003, Greicius and colleagues examined resting state fMRI scans and looked at how correlated different sections in the brain are to each other. Their correlation maps highlighted the same areas already identified by the other researchers.[19] This was important because it demonstrated a convergence of methods all leading to the same areas being involved in the DMN. Since then other networks have been identified, such as visual, auditory, and attention networks. Some of them are often anti-correlated with the default mode network.[11]
Until the mid-2000s, researchers labeled the default mode network as the "task-negative network" because it was deactivated when participants had to perform external goal-directed tasks.[6] DMN was thought to only be active during passive rest and inactive during tasks. However, more recent studies have demonstrated the DMN to be active in certain internal goal-directed tasks such as social working memory and autobiographical tasks.[7]
Around 2007, the number of papers referencing the default mode network skyrocketed.[20] In all years prior to 2007, there were 12 papers published that referenced "default mode network" or "default network" in the title; however, between 2007 and 2014 the number increased to 1,384 papers. One reason for the increase in papers is a result of the robust effect of finding the DMN with resting-state scans and independent component analysis (ICA).[16][21] Another reason is the DMN can be measured with short and effortless resting-state scans, meaning they can be performed on any population including young children, clinical populations, and nonhuman primates.[4] A third reason is that the role of the DMN has been expanded to more than just a passive brain network.[4]
Anatomy[edit]
Graphs of the dynamic development of correlations between brain networks. (A) In children the regions are largely local and are organized by their physical location; the frontal regions are highlighted in light blue. (B) In adults the networks become highly correlated despite their physical distance; the default network is highlighted in light red.[22] This result is now believed to have been confounded by artifactual processes attributable to the tendency of younger subjects to move more during image acquisition, which preferentially inflates estimates of connectivity between physically proximal regions (Power 2012, Satterthwaite 2012).
The default mode network is an interconnected and anatomically defined[4] set of brain regions. The network can be separated into hubs and subsections:
Functional hubs:[23] Information regarding the self
• Posterior cingulate cortex (PCC) & precuneus: Combines bottom-up (not controlled) attention with information from memory and perception. The ventral (lower) part of PCC activates in all tasks which involve the DMN including those related to the self, related to others, remembering the past, thinking about the future, and processing concepts plus spatial navigation. The dorsal (upper) part of PCC involves involuntary awareness and arousal. The precuneus is involved in visual, sensorimotor, and attentional information.
• Medial prefrontal cortex (mPFC): Decisions about self-processing such as personal information, autobiographical memories, future goals and events, and decision making regarding those personally very close such as family. The ventral (lower) part is involved in positive emotional information and internally valued reward.
• Angular gyrus: Connects perception, attention, spatial cognition, and action and helps with parts of recall of episodic memories
Dorsal medial subsystem:[23] Thinking about others
Medial temporal subsystem:[23] Autobiographical memory and future simulations
The default mode network is most commonly defined with resting state data by putting a seed in the posterior cingulate cortex and examining which other brain areas most correlate with this area.[19] The DMN can also be defined by the areas deactivated during external directed tasks compared to rest.[17] Independent component analysis (ICA) robustly finds the DMN for individuals and across groups, and has become the standard tool for mapping the default network.[16][21]
It has been shown that the default mode network exhibits the highest overlap in its structural and functional connectivity, which suggests that the structural architecture of the brain may be built in such a way that this particular network is activated by default.[1] Recent evidence from a population brain-imaging study of 10,000 UK Biobank participants further suggests that each DMN node can be decomposed into subregions with complementary structural and functional properties. It has been a widespread practice in DMN research to treat its constituent nodes to be functionally homogeneous, but the distinction between subnodes within each major DMN node has mostly been neglected. However, the close proximity of subnodes that propagate hippocampal space-time outputs and subnodes that describe the global network architecture may enable default functions, such as autobiographical recall or internally-orientated thinking.[24]
In the infant's brain, there is limited evidence of the default network, but default network connectivity is more consistent in children aged 9–12 years, suggesting that the default network undergoes developmental change.[11]
Functional connectivity analysis in monkeys shows a similar network of regions to the default mode network seen in humans.[4] The PCC is also a key hub in monkeys; however, the mPFC is smaller and less well connected to other brain regions, largely because human's mPFC is much larger and well developed.[4]
Diffusion MRI imaging shows white matter tracts connecting different areas of the DMN together.[20] The structural connections found from diffusion MRI imaging and the functional correlations from resting state fMRI show the highest level of overlap and agreement within the DMN areas.[1] This provides evidence that neurons in the DMN regions are linked to each other through large tracts of axons and this causes activity in these areas to be correlated with one another.
Function[edit]
The default mode network is thought to be involved in several different functions:
It is potentially the neurological basis for the self:[20]
• Autobiographical information: Memories of collection of events and facts about one's self
• Self-reference: Referring to traits and descriptions of one's self
• Emotion of one's self: Reflecting about one's own emotional state
Thinking about others:[20]
• Theory of mind: Thinking about the thoughts of others and what they might or might not know
• Emotions of other: Understanding the emotions of other people and empathizing with their feelings
• Moral reasoning: Determining a just and an unjust result of an action
• Social evaluations: Good-bad attitude judgements about social concepts
• Social categories: Reflecting on important social characteristics and status of a group
• Social isolation: A perceived lack of social interaction.[25]
Remembering the past and thinking about the future:[20]
• Remembering the past: Recalling events that happened in the past
• Imagining the future: Envisioning events that might happen in the future
• Episodic memory: Detailed memory related to specific events in time
• Story comprehension: Understanding and remembering a narrative
• Replay: Consolidating recently acquired memory traces[26]
The default mode network is active during passive rest and mind-wandering[4] which usually involves thinking about others, thinking about one's self, remembering the past, and envisioning the future rather than the task being performed.[20] Recent work, however, has challenged a specific mapping between the default mode network and mind-wandering, given that the system is important in maintaining detailed representations of task information during working memory encoding.[27] Electrocorticography studies (which involve placing electrodes on the surface of a subject's cerebral cortex) have shown the default mode network becomes activated within a fraction of a second after participants finish a task.[28] Additionally, during attention demanding tasks, sufficient deactivation of the default mode network at the time of memory encoding has been shown to result in more successful long-term memory consolidation.[29]
Studies have shown that when people watch a movie,[30] listen to a story,[31][32] or read a story,[33] their DMNs are highly correlated with each other. DMNs are not correlated if the stories are scrambled or are in a language the person does not understand, suggesting that the network is highly involved in the comprehension and the subsequent memory formation of that story.[32] The DMN is shown to even be correlated if the same story is presented to different people in different languages,[34] further suggesting the DMN is truly involved in the comprehension aspect of the story and not the auditory or language aspect.
The default mode network is deactivated during some external goal-oriented tasks such as visual attention or cognitive working memory tasks.[6] However, with internal goal-oriented tasks, such as social working memory or autobiographical tasks, the DMN is positively activated with the task and correlates with other networks such as the network involved in executive function.[7] Regions of the DMN are also activated during cognitively demanding tasks that require higher-order conceptual representations.[9] The DMN shows higher activation when behavioral responses are stable, and this activation is independent of self-reported mind wandering.[35]
A hitherto unsuspected possibility is that the default network is activated by the immobilization inherent in the testing procedure (the patient is strapped supine on a stretcher and inserted by a narrow tunnel into a massive metallic structure). This procedure creates a sense of entrapment and, not surprisingly, the most commonly reported side-effect is claustrophobia. This alternative view is suggested by a recent article that links theory of mind to immobilization.[36]
Recent research has shown that the DMN is related to the perception of beauty, in which the network becomes activated in a generalized way to aesthetically moving domains such as artworks, landscapes, and architecture. This would explain a deep inner feeling of pleasure related to aesthetics, interconnected with the sense of personal identity, due to the network functions related to the self.[37]
Clinical significance[edit]
The default mode network has been hypothesized to be relevant to disorders including Alzheimer's disease, autism, schizophrenia, major depressive disorder (MDD), chronic pain, post-traumatic stress disorder (PTSD) and others.[4][38] In particular, the DMN has also been reported to show overlapping yet distinct neural activity patterns across different mental health conditions, such as when directly comparing attention deficit hyperactivity disorder (ADHD) and autism.[39]
People with Alzheimer's disease show a reduction in glucose (energy use) within the areas of the default mode network.[4] These reductions start off as slight decreases in patients with mild symptoms and continue to large reductions in those with severe symptoms. Surprisingly, disruptions in the DMN begin even before individuals show signs of Alzheimer's disease.[4] Plots of the peptide amyloid-beta, which is thought to cause Alzheimer's disease, show the buildup of the peptide is within the DMN.[4] This prompted Randy Buckner and colleagues to propose the high metabolic rate from continuous activation of DMN causes more amyloid-beta peptide to accumulate in these DMN areas.[4] These amyloid-beta peptides disrupt the DMN and because the DMN is heavily involved in memory formation and retrieval, this disruption leads to the symptoms of Alzheimer's disease.
DMN is thought to be disrupted in individuals with autism spectrum disorder.[4][40] These individuals are impaired in social interaction and communication which are tasks central to this network. Studies have shown worse connections between areas of the DMN in individuals with autism, especially between the mPFC (involved in thinking about the self and others) and the PCC (the central core of the DMN).[41][42] The more severe the autism, the less connected these areas are to each other.[41][42] It is not clear if this is a cause or a result of autism, or if a third factor is causing both (confounding).
Although it is not clear whether the DMN connectivity is increased or decreased in psychotic bipolar disorder and schizophrenia, several genes correlated with altered DMN connectivity are also risk genes for mood and psychosis disorders.[43]
Rumination, one of main symptoms of major depressive disorder, is associated with increased DMN connectivity and dominance over other networks during rest.[44][45] Such DMN hyperconnectivity has been observed in first-episode depression[46] and chronic pain.[47] Altered DMN connectivity may change the way a person perceives events and their social and moral reasoning, thus increasing their susceptibility to depressive symptoms.[48]
Lower connectivity between brain regions was found across the default network in people who have experienced long-term trauma, such as childhood abuse or neglect, and is associated with dysfunctional attachment patterns. Among people experiencing PTSD, lower activation was found in the posterior cingulate gyrus compared to controls, and severe PTSD was characterized by lower connectivity within the DMN.[38][49]
Adults and children with ADHD show reduced anticorrelation between the DMN and other brain networks.[50][51] The cause may be a lag in brain maturation.[52] More generally, competing activation between the DMN and other networks during memory encoding may result in poor long-term memory consolidation, which is a symptom of not only ADHD but also depression, anxiety, autism, and schizophrenia.[29]
Modulation[edit]
The default mode network (DMN) may be modulated by the following interventions and processes:
• Acupuncture – Deactivation of the limbic brain areas and the DMN.[53] It has been suggested that this is due to the pain response.[54]
• Antidepressants – Abnormalities in DMN connectivity are reduced following treatment with antidepressant medications in PTSD.[55]
• Attention Training Technique - Research shows that even a single session of Attention Training Technique changes functional connectivity of the DMN[56]
• Deep brain stimulation – Alterations in brain activity with deep brain stimulation may be used to balance resting state networks.[57]
• Meditation – Structural changes in areas of the DMN such as the temporoparietal junction, posterior cingulate cortex, and precuneus have been found in meditation practitioners.[58] There is reduced activation and reduced functional connectivity of the DMN in long-term practitioners.[58] Various forms of nondirective meditation, including Transcendental Meditation[59] and Acem Meditation,[60] have been found to activate the DMN.
• Physical Activity and Exercise – Physical Activity, and more likely Aerobic Training, may alter the DMN. In addition, sports experts are showing networks differences, notably of the DMN.[61][62][63]
• Psychedelic drugs – Reduced blood flow to the PCC and mPFC was observed under the administration of psilocybin. These two areas are considered to be the main nodes of the DMN.[64] One study on the effects of LSD demonstrated that the drug desynchronizes brain activity within the DMN; the activity of the brain regions that constitute the DMN becomes less correlated.[65]
• Psychotherapy – In PTSD, the abnormalities in the default mode network normalize in individuals who respond to psychotherapy interventions.[66][55]
• Sleep deprivation – Functional connectivity between nodes of the DMN in their resting-state is usually strong, but sleep deprivation results in a decrease in connectivity within the DMN.[67] Recent studies suggest a decrease in connectivity between the DMN and the task-positive network as a result of sleep loss.[68]
• Sleeping and resting wakefulness
• Onset of sleep – Increase in connectivity between the DMN and the task-positive network.[69]
• REM sleep – Possible increase in connectivity between nodes of the DMN.[69]
• Resting wakefulness – Functional connectivity between nodes of the DMN is strong.[69]
• Stage N2 of NREM sleep – Decrease in connectivity between the posterior cingulate cortex and medial prefrontal cortex.[69]
• Stage N3 of NREM sleep – Further decrease in connectivity between the PCC and MPFC.[69]
Criticism[edit]
Some have argued the brain areas in the default mode network only show up together because of the vascular coupling of large arteries and veins in the brain near these areas, not because these areas are actually functionally connected to each other. Support for this argument comes from studies that show changing in breathing alters oxygen levels in the blood which in turn affects DMN the most.[4] These studies however do not explain why the DMN can also be identified using PET scans by measuring glucose metabolism which is independent of vascular coupling[4] and in electrocorticography studies[70] measuring electrical activity on the surface of the brain, and in MEG by measuring magnetic fields associated with electrophysiological brain activity that bypasses the hemodynamic response.[71]
The idea of a "default network" is not universally accepted.[72] In 2007 the concept of the default mode was criticized as not being useful for understanding brain function, on the grounds that a simpler hypothesis is that a resting brain actually does more processing than a brain doing certain "demanding" tasks, and that there is no special significance to the intrinsic activity of the resting brain.[73]
Nomenclature[edit]
The default mode network has also been called the language network, semantic system, or limbic network.[10] Even though the dichotomy is misleading,[7] the term task-negative network is still sometimes used to contrast it against other more externally-oriented brain networks.[51]
In 2019, Uddin et al. proposed that medial frontoparietal network (M-FPN) be used as a standard anatomical name for this network.[10]
See also[edit]
References[edit]
1. ^ a b c Horn, Andreas; Ostwald, Dirk; Reisert, Marco; Blankenburg, Felix (2013). "The structural-functional connectome and the default mode network of the human brain". NeuroImage. 102: 142–151. doi:10.1016/j.neuroimage.2013.09.069. PMID 24099851. S2CID 6455982.
2. ^ Garrity, A.; Pearlson, G. D.; McKiernan, K.; Lloyd, D.; Kiehl, K. A.; Calhoun, V. D. (2007). "Aberrant default mode functional connectivity in schizophrenia". Am. J. Psychiatry. 164 (3): 450–457. doi:10.1176/ajp.2007.164.3.450. PMID 17329470.
3. ^ Sormaz, Mladen; Murphy, Charlotte; Wang, Hao-Ting; Hymers, Mark; Karapanagiotidis, Theodoros; Poerio, Giulia; Margulies, Daniel S.; Jefferies, Elizabeth; Smallwood, Jonathan (2018). "Default mode network can support the level of detail in experience during active task states". Proceedings of the National Academy of Sciences. 115 (37): 9318–9323. Bibcode:2018PNAS..115.9318S. doi:10.1073/pnas.1721259115. PMC 6140531. PMID 30150393.
4. ^ a b c d e f g h i j k l m n o p q r s Buckner, R. L.; Andrews-Hanna, J. R.; Schacter, D. L. (2008). "The Brain's Default Network: Anatomy, Function, and Relevance to Disease". Annals of the New York Academy of Sciences. 1124 (1): 1–38. Bibcode:2008NYASA1124....1B. CiteSeerX 10.1.1.689.6903. doi:10.1196/annals.1440.011. PMID 18400922. S2CID 3167595.
5. ^ Lieberman, Matthew (2 September 2016). Social. Broadway Books. p. 19. ISBN 978-0-307-88910-2.
6. ^ a b c Fox, Michael D.; Snyder, Abraham Z.; Vincent, Justin L.; Corbetta, Maurizio; Van Essen, David C.; Raichle, Marcus E. (5 July 2005). "The human brain is intrinsically organized into dynamic, anticorrelated functional networks". Proceedings of the National Academy of Sciences of the United States of America. 102 (27): 9673–9678. Bibcode:2005PNAS..102.9673F. doi:10.1073/pnas.0504136102. ISSN 0027-8424. PMC 1157105. PMID 15976020.
7. ^ a b c d Spreng, R. Nathan (1 January 2012). "The fallacy of a "task-negative" network". Frontiers in Psychology. 3: 145. doi:10.3389/fpsyg.2012.00145. ISSN 1664-1078. PMC 3349953. PMID 22593750.
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b755ed28a90d11d590ef646404f4afc5
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-8,999,096,491,373,763,000
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WHAT’S Vaping?
what is vaping
WHAT’S Vaping?
One of the first questions that new ex-smokers ask about is, “What’s E-Cigarette?”. A vaporizer is a mechanical device that simulates cigarette smoking in an electronic manner. It basically consists of a coil, a motor, and a connector such as a barrel or tank.
Unlike cigarettes, e-liquid will not contain tar, nicotine, or other chemicals. Instead, it consists of a liquid carrier, an oxidizer, plus some oxidizers are also used to increase the taste and consistency of the merchandise. In actuality, it is a liquid that you put into a “box” and vaporize. Instead of actual smoke, users breathe vapor instead. As such, utilizing an e-cigarette is frequently described as “vaping” instead of smoking.
Now that you know what it is, let’s discuss a number of the known health risks connected with this product. First off, it lacks nicotine. Nicotine is really a highly addictive substance and it would be extremely difficult for it to be absorbed through your skin. Also, it is derived from the burning of tobacco leaves. Therefore, by eating vapor, you are upping your contact with toxic chemicals. Additionally, it is unknown whether long-term use of it’ll create chemicals that mimic the addictive characteristics of nicotine.
Furthermore, it is estimated that approximately one million people annually die from tobacco-related deaths. By ingesting any of the liquid aerosol produced by vaporizers, or breathing in its aerosol, you are exposing yourself to the same harmful compounds found in cigarette smoke. The danger doesn’t stop there, because studies show that people who regularly smoke will develop lung cancer later in life. Therefore, investing in an inexpensive quality electronic vaporizer is strongly advised.
Many people make the assumption that using e-cigs is safe, but that assumption may be unfounded. Not only are there many studies of the dangers posed by using aerosol lighters and refillable liquids, nonetheless it in addition has been established that smokers who often switch to the products will develop an addiction to them. Although the American Cancer Society has stated that there surely is no evidence linking the use of e-cigs to cancer, millions of users have disregarded this advice and continue to smoke. In the event that you aren’t aware that tobacco is addicting, I strongly encourage you to research it further and prevent becoming another death statistic.
Many experts advise that you refrain from smoking if you are somebody who regularly uses e-cigs. This is because of the fact that regular cigarettes contain nicotine, that is an addictive drug. However, when you use e-liquid or a vaporizer that does not contain nicotine, you will not have nicotine to rely on. The reason for this is that an excessive amount of nicotine is present, which makes it far too addicting to be use e-liquid or a vaporizer to take.
Addititionally there is the concern that some people do not want to quit cigarettes. If you stop smoking, this can be a valid argument, however, what is important is that you quit using any addictive substance. What is important is that you appear to be non-smokers. Many teenagers who look like non-smokers are at risk of developing an addiction to what’s called the real thing, that is using tobacco.
In the event that you smoke using a traditional Puff Bar Flavors cigarette, you are simply inhaling harmful aerosol. Using what is called an electronic vaporizer, you breathe in what’s essentially mist form of the aerosol that is contained in the device. By doing this, you are not putting yourself at risk for what’s sometimes called the poison of smoking, that may cause all sorts of health problems.
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1a01aa77535b9ecfb87b9fc36adbcd2f
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15 June 2022 In General Health
BACKGROUND & AIMS: Biological age (BA) is the hypothetical underlying age of an organism and has been proposed as a more powerful predictor of health than chronological age (CA). The difference between BA and CA (Deltaage) reflects the rate of biological aging, with lower values indicating slowed-down aging. We sought to compare the relationship of four a priori-defined dietary patterns, including a traditional Mediterranean diet (MD) and three non-Mediterranean diets, with biological aging (Deltaage) among Italian adults. We also examined distinctive nutritional traits of these diets as potential mediators of such associations.
METHODS: Cross-sectional analysis on a sub-cohort of 4510 subjects (aged >/=35 y; 52.0% women) from the Moli-sani Study (enrolment, 2005-2010). Food intake was recorded by a 188-item semi-quantitative food-frequency questionnaire. A Mediterranean diet score (MDS) was used as exposure and compared with non-Mediterranean dietary patterns, i.e. DASH (Dietary Approaches to Stop Hypertension), Palaeolithic and the Nordic diets. A Deep Neural Network based on 36 blood biomarkers was used to compute BA and the resulting Deltaage (BA-CA), which was tested as outcome in multivariable linear regressions adjusted for clinical factors, lifestyles and sociodemographic factors.
RESULTS: In a multivariable-adjusted model, 1 standard deviation increase in the MDS was inversely associated with Deltaage (beta = -0.23; 95%CI -0.40, -0.07), and similar findings were observed with the DASH diet (beta = -0.17; 95%CI -0.33, -0.01). High dietary polyphenol content explained 29.8% (p = 0.04) and 65.8% (p = 0.02) of these associations, respectively, while other nutritional factors analysed (e.g. dietary fibre) were unlikely to be on the pathway. No significant associations were found with either the Palaeolithic or the Nordic diets.
CONCLUSIONS: Increasing adherence to either the traditional MD or the DASH diet was associated with delayed biological aging, possibly through their high polyphenol content.
15 June 2022 In Drinking Patterns
AIMS: To examine the association of alcohol consumption patterns with growth differentiation factor 15 (GDF-15) in older drinkers, separately among individuals with cardiovascular disease (CVD)/diabetes and those without them, as GDF-15 is a strong biomarker of chronic disease burden.
DESIGN: Cross-sectional study. SETTING: Population-based study in Madrid (Spain). PARTICIPANTS: A total of 2051 life-time drinkers aged 65+ years included in the Seniors-ENRICA-2 study in 2015-17. Participants' mean age was 71.4 years and 55.4% were men.
MEASUREMENTS: According to their average life-time alcohol intake, participants were classified as occasional ( 1.43-20 g/day; women: > 1.43-10 g/day), moderate-risk (men: > 20-40 g/day; women: > 10-20 g/day) and high-risk drinkers (men: > 40 g/day; women: > 20 g/day; or binge drinkers). We also ascertained wine preference (> 80% of alcohol derived from wine), drinking with meals and adherence to a Mediterranean drinking pattern (MDP) defined as low-risk drinking, wine preference and one of the following: drinking only with meals; higher adherence to the Mediterranean diet; or any of these.
FINDINGS: In participants without CVD/diabetes, GDF-15 increased by 0.27% [95% confidence interval (CI) = 0.06%, 0.48%] per 1 g/day increment in alcohol among high-risk drinkers, but there was no clear evidence of association in those with lower intakes or in the overall group, or across categories of alcohol consumption status. Conversely, among those with CVD/diabetes, GDF-15 rose by 0.19% (95% CI = 0.05%, 0.33%) per 1 g/day increment in the overall group and GDF-15 was 26.89% (95% CI = 12.93%, 42.58%) higher in high-risk versus low-risk drinkers. Drinking with meals did not appear to be related to GDF-15, but among those without CVD/diabetes, wine preference and adherence to the MDP were associated with lower GDF-15, especially when combined with high adherence to the Mediterranean diet.
CONCLUSIONS: Among older life-time drinkers in Madrid, Spain, high-risk drinking was positively associated with growth differentiation factor 15 (a biomarker of chronic disease burden). There was inconclusive evidence of a beneficial association for low-risk consumption.
15 June 2022 In Cardiovascular System
We examined whether the often-reported protective association of alcohol with cardiovascular disease (CVD) risk could arise from confounding. Our sample comprised 908 men (56-67 years), free of prevalent CVD. Participants were categorized into 6 groups: never drinkers, former drinkers, and very light (1-4 drinks in past 14 days), light (5-14 drinks), moderate (15-28 drinks), and at-risk (>28 drinks) drinkers. Generalized linear mixed effect models examined the associations of alcohol use with three established CVD risk scores: The Framingham Risk Score (FRS); the atherosclerotic CVD (ASCVD) risk score; and the Metabolic Syndrome (MetS) Severity score, adjusting for group differences in demographics, body size, and health-related behaviors. In separate models we additionally adjusted for several groups of potentially explanatory factors including socioeconomic status, social support, physical and mental health status, childhood factors, and prior history of alcohol misuse. Results showed lower CVD risk among light and moderate alcohol drinkers, relative to very light drinkers, for all CVD risk scores, independent of demographics, body size, and health-related behaviors. Alcohol-CVD risk associations were robust to further adjustment for several groups of potential explanatory factors. Study limitations include the all-male sample with limited racial and ethnic diversity, and the inability to adjust for sugar consumption and for patterns of alcohol consumption. Although this observational study does not address causation, results show that middle-aged men who consume alcohol in moderation have lower CVD risk and better cardiometabolic health than men who consume little or no alcohol, independent of a variety of health, behavioral, psychosocial, and earlier life factors.
15 June 2022 In Cancer
We examined associations between sex-specific alcohol intake trajectories and alcohol-related cancer risk using data from 22 756 women and 15 701 men aged 40 to 69 years at baseline in the Melbourne Collaborative Cohort Study. Alcohol intake for 10-year periods from age 20 until the decade encompassing recruitment, calculated using recalled beverage-specific frequency and quantity, was used to estimate group-based sex-specific intake trajectories. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated for primary invasive alcohol-related cancer (upper aerodigestive tract, breast, liver and colorectum). Three distinct alcohol intake trajectories for women (lifetime abstention, stable light, increasing moderate) and six for men (lifetime abstention, stable light, stable moderate, increasing heavy, early decreasing heavy, late decreasing heavy) were identified. 2303 incident alcohol-related cancers were diagnosed during 485 525 person-years in women and 789 during 303 218 person-years in men. For men, compared with lifetime abstention, heavy intake (mean >/= 60 g/day) at age 20 to 39 followed by either an early (from age 40 to 49) (early decreasing heavy; HR = 1.75, 95% CI: 1.25-2.44) or late decrease (from age 60 to 69) (late decreasing heavy; HR = 1.94, 95% CI: 1.28-2.93), and moderate intake (mean
Page 1 of 105
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INVESTIGADORES
SETTON Clara Patricia
congresos y reuniones científicas
Título:
Peripheral remyelination: evidence of a temporal window for Bone Marrow Mononuclear Cell transplantation
Autor/es:
VANINA USACH; GONZALO PIÑERO; PAULA A, SOTO; MIJAEL ROZENSZAJN; ERIC GAMBERG; ALICIA CUETO; CLARA P. SETTON
Lugar:
Mar del Plata
Reunión:
Congreso; XXIX Congreso Anual Sociedad Argentina de Neurociencias (SAN); 2015
Institución organizadora:
Sociedad Argentina de Neurociencias (SAN)
Resumen:
We have previously described the migration of bone marrow mononuclear cells (BMMC) to the demyelinated area when systemically transplanted immediately after rat sciatic nerve crush. Once BMMC arrive at the ipsilateral nerve, some of them colocalize with Schwann cell and nerve fiber markers and accelerate the regeneration process.In this context, the aim of the present work was to determine the temporal window during which BMMC are able to migrate to the injured nerve and whether this migration is also accompanied by a beneficial effect. To such end, adult Wistar rats were submitted to sciatic nerve crush and transplanted with BMMC at different survival times post crush. Five days after transplantation, animals were sacrificed and immunohistochemical, Western Blot and functional studies were performed.Results show that BMMC were able to migrate to the ipsilateral nerve up to 28 days post crush, although the peak of migration occurred when BMMC were transplanted 7 days post crush, a crucial point in the demyelination process. In terms of MBP levels, cell transplantation promoted a faster recovery than in non-transplanted animals. Functional studies are being carried out to determine whether morphological recovery is accompanied by a functional one.The confirmation of a temporal window for BMMC treatment would open a promising field to evaluate the possible application of BMMC in therapies for neurodegeneration processes.
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Searchable abstracts of presentations at key conferences on calcified tissues
Previous issue | Volume 5 | ECTS2016 | Next issue
43rd Annual European Calcified Tissue Society Congress
Rome, Italy
14 May 2016 - 17 May 2016
Card image cap
ba0005cabs.oc1.1 | Oral Communications | ECTS2016
Secreted YB-1 (Y-box binding protein 1) as a biomarker of bone disease progression in patients with breast cancer and bone metastases
Bettencourt Maria , Ferreira Arlindo , Alho Irina , Lucia Costa Ana , Sousa Ana Rita , Mansinho Andre , Abreu Catarina , Pulido Catarina , Macedo Daniela , Vendrell Ines , Pacheco Teresa , Costa Luis , Casimiro Sandra
YB-1 (Y-box binding protein 1) is a multifunctional cold-shock protein that has been implicated in all hallmarks of cancer. Elevated YB-1 protein levels were correlated with poor prognosis in several types of cancers, including breast cancer (BC). In BC, high YB-1 expression is a marker of decreased overall survival (OS) and distant metastasis-free survival across all subtypes. YB-1 is also secreted by different cell types and may act as an extracellular mitogen. Therefore, ou...
ba0005cabs.oc1.2 | Oral Communications | ECTS2016
Bone and metabolic parameters are associated with overall survival in patients with bone metastases from adenocarcinoma lung cancer: the POUMOS study
Confavreux Cyrille B. , Chambard Lauriane , Ollier Edouard , Brevet Marie , Duboeuf Francois , Rousseau Jean-Charles , Pialat Jean-Baptiste , Wegrzyn Julien , Tescaru Agnes , Szulc Pawel , Carlier Marie-Christine , Girard Nicolas , Clezardin Philippe
Rational: Mortality due to non-small cell lung cancers is the first cause of cancer death in men around the world. Lung adenocarcinoma regularly induces bone metastases responsible for high morbidity and impaired life quality. Overall survival of these patients is poor. Thus we aimed to identify if some bone and metabolic parameters were associated with overall survival.Patients and Methods: POUMOS is a prospective cohort of patients suffering from adeno...
ba0005cabs.oc1.3 | Oral Communications | ECTS2016
Blocking IL-1R signalling inhibits breast cancer growth and bone metastases by altering the tumour microenvironment
Bradbury Steven , Rennicks Sarah , Evans Alyson , del Carmen Basitdas Mary , Holen Ingunn , Ottewell Penelope
Background: We have recently identified interleukin 1B (IL-1B) as a potential biomarker for predicting breast cancer patients at increased risk for developing bone metastasis. In mouse models, IL-1B and its receptor (IL-1R1) are upregulated in breast cancer cells that metastasise to bone compared with cells that do not. We have now investigated whether blocking IL-1R with the clinically licensed antagonist, anakinra, might be a potential treatment for breast cancer and bone me...
ba0005cabs.oc2.1 | Oral Communications | ECTS2016
Prostate cancer microRNAs in extracellular vesicles stimulate osteoclastogenesis
Bijnsdorp Irene , Mulder Jorn , Geldof Albert , Bakker Astrid , de Vries Teun , van Moorselaar Jeroen
Prostate cancer (PCa) is the most common cancer in males. When patients develop metastasis, no curative therapy is available. To find new therapeutic options, it is crucial to understand how PCa cells induce metastasis. Recently, it was shown that PCa cells secrete small extracellular vesicles (EVs) that can be found in the circulation and in bones. Uptake of EVs by other cells may change their behaviour. We previously identified three miRNAs that were uniquely upregulated in ...
ba0005cabs.oc2.2 | Oral Communications | ECTS2016
Integrin α5 is an independent prognosis factor and a potential therapeutic target for breast cancer bone metastasis
Pantano Francesco , Croset Martine , Driouch Keltouma , Bonnelye Edith , Bednarz-Knoll Natalia , Hong Saw-See , Iuliani Michele , Fioramonti Marco , Santini Daniele , Tonini Giuseppe , Pantel Klaus , Clezardin Philippe
Aims: Using an extensive bioinformatic approach we identified integrin α5 subunit as a novel potential target to treat bone dissemination from breast cancer. Aim of this study is to confirm the value of this target.Methods: Integrin α5 mRNA expression levels were quantified by qRT-PCR, using radically resected primary tumors of 427 breast cancer patients. α5 expression at protein level by IHC on primary tumor was correlated, in an addition...
ba0005cabs.oc2.3 | Oral Communications | ECTS2016
Cancer cell homing to the bone marrow is modulated by the mesenchymal stromal cell
Rossnagl Stephanie , Nakchbandi Inaam
Several cell types form the hematopoietic stem cell niche. These niches sometimes become hijacked by cancer cells, which may later form metastatic lesions. Our aim was therefore to characterize the bone marrow microenvironment to affect cancer cell homing to bone marrow.Pharmacologic modification consisting of PTH to stimulate the osteoblasts and zoledronic acid to prevent the increase in osteoclasts through PTH resulted in increased homing of cancer cel...
ba0005cabs.oc2.4 | Oral Communications | ECTS2016
Peripheral tumour re-growth following combination therapy – role of the bone microenvironment
Haider Marie-Therese , Ottewell Penelope D. , Brown Nicola J. , Lefley Diane V. , Holen Ingunn
Background: Cancer patients often receive a combination of drugs that target both the microenvironment and the tumour cells. However, the role of the bone microenvironment (BME) in mediating peripheral breast cancer growth remains poorly understood. This is the first study to determine whether reduced subcutaneous tumour growth following combination therapy is due to direct interactions between the drugs and tumour cells or through zoledronic acid induced alterations to the BM...
ba0005cabs.oc2.5 | Oral Communications | ECTS2016
Inhibition of BMP signalling reduces bone destruction and impacts niche maintenance in a mouse model of multiple myeloma
Gooding Sarah , Webb Siobhan , Olechnowicz Sam , Lwin Seint , Armitage Andrew , Ramasamy Karthik , Drakesmith Hal , Edwards Claire
Multiple myeloma is usually incurable, the bone marrow niche providing a protective microenvironment for quiescent tumour cells. We hypothesised that manipulation of BMP activity, a regulator of cell differentiation in the bone marrow, might affect control of tumour growth by its niche and in addition alter the lytic bone disease of myeloma. Moreover BMP signalling contributes to the hepcidin upregulation and resultant inflammatory anaemia that is characteristic of myeloma. Re...
ba0005cabs.oc3.1 | Oral Communications | ECTS2016
Blockade of C5aR impairs tumor-induced osteoclastogenesis preventing bone metastasis colonization in lung cancer
Ajona Daniel , Zandueta Carolina , Corrales Leticia , Pajares Maria J. , Martinez-Terroba Elena , Perurena Naiara , Montuenga Luis M. , Pio Ruben , Lecanda Fernando
C5aR is a membrane-associated receptor for C5a, a potent immune mediator generated after complement activation. C5aR expressed in tumor infiltrating immune cells creates a favorable microenvironment for tumor progression. However, the expression of C5aR by cancer cells and its contribution to their malignant phenotype is poorly understood. Immunohistochemical analysis revealed that high levels of C5aR in human lung tumors were associated with poor survival (P=0.005) a...
ba0005cabs.oc3.2 | Oral Communications | ECTS2016
Osteoblasts inhibit the immune response against cancer
Rossnagl Stephanie , Kraft Sabrina , Sens Carla , Nakchbandi Inaam
Osteoblasts line the inner surface of the bone and are located in close proximity to the bone marrow, where hematopoiesis takes place. Osteoblasts produce several cytokines that affect various steps of hematopoiesis, and produce fibronectin isoforms that affect cell differentiation. Little is known however on whether osteoblasts modulate the immune response. Our aim was to evaluate the role of fibronectin originating from the osteoblasts on hematopoiesis and the immune respons...
ba0005cabs.oc3.3 | Oral Communications | ECTS2016
Visualizing the tumor immunity in living bone marrow by intravital 2-photon imaging
Yamashita Erika , Mizuno Hiroki , Ishii Masaru
Within a living organism, the adaptive immune system, e.g. cytotoxic T lymphocytes (CTLs), induce apoptosis in tumor cells, and therefore limit tumor development. Bone marrow is a mysterious hidden place for different tumor cells and the anti-tumor immunity in the bone marrow is important because the specific microenvironment had been considered to contribute to escape of tumor cells from immune attack. However, the practical mechanism of anti-tumor immune elimination by CTLs ...
ba0005cabs.oc3.4 | Oral Communications | ECTS2016
Anti-sclerostin treatment prevents multiple myeloma bone disease and reduces tumour burden
McDonald Michelle , Reagan Michaela , Terry Rachael , Pettitt Jessica , Le Lawrence , Mohanty Sindhu , Kramer Ina , Kneissel Michaela , Brooks Daniel , Cheng Tegan , Little David , Bouxsein Mary , Rosen Cliff , Ghobrial Irene , Croucher Peter
Multiple myeloma is characterized by extensive bone marrow tumour and destructive osteolytic lesions. Both increased bone resorption and suppressed bone formation result in lesions and pathological fractures. Anti-resorptive therapies prevent further bone loss but patients continue to fracture, arguing for new therapies which increase bone strength. Anti-Sclerostin (Anti-Scl) is a potent stimulator of bone formation, is currently in clinical trials for osteoporosis, however it...
ba0005cabs.oc3.5 | Oral Communications | ECTS2016
Targeting skeletal metastatic breast cancer with bisphosphonic matrix metalloproteinase-2 inhibitors
Tauro Marilena , Laghezza Antonio , Paolo Tortorella , Lynch Conor
Breast to bone metastasis is a common incurable event during breast cancer progression. Identifying the molecular mechanisms at play is vital for the development of new therapies. Matrix metalloproteinases, such as MMP-2, are overexpressed in the bone metastatic microenvironment. Genetic ablation of MMP-2 demonstrated its importance of in driving osteolytic bone metastatic breast cancer and support the rationale for the development of a highly specific MMP-2 inhibitor for the ...
ba0005cabs.oc4.1 | Oral Communications | ECTS2016
Muscle dysfunction in immune competent mice with osteolytic breast cancer in bone is associated with skeletal muscle oxidation of RyR1
Regan Jenna , Waning David , Mohammad Khalid , Mikesell Carter , Reiken Steven , Marks Andrew , Guise Theresa
Cancer-associated muscle weakness is an important paraneoplastic syndrome for which there is currently no treatment. Human breast cancer bone metastases (MDA-MB-231 cells in immune deficient mice) induce extensive bone destruction, leading to the release of TGF-β from the bone matrix. We have previously shown that bone-derived TGF-β is responsible for muscle weakness in this model. Mechanistically, TGF-β signaling increases the expression of NADPH oxidase 4 (Nox...
ba0005cabs.oc4.2 | Oral Communications | ECTS2016
Bisphosphonates prevent osteolysis and muscle weakness in aromatase inhibitor-treated mice with breast cancer bone metastases
Wright Laura , Harhash Ahmed , Waning David , Mohammad Khalid , Marks Andrew , Guise Theresa
Up to half of women treated with an aromatase inhibitor (AI) for breast cancer develop muscle weakness, bone loss, and joint pain. Moreover, an elevated state of osteoclastic bone resorption has been shown to prime the bone microenvironment in ways that accelerate metastatic growth. We hypothesized that AI-induced bone loss could increase breast cancer progression in bone and exacerbate muscle weakness associated with bone metastases. Four-week female athymic nude mice underwe...
ba0005cabs.oc4.3 | Oral Communications | ECTS2016
In vitro mechanotransduction of osteosarcoma cells
Coughlin Thomas R. , Gadi Abhilash , Mansukhani Alka , Kennedy Oran D.
Osteosarcoma is a heterogeneous tumor from the mesenchymal lineage, and is the most common form of primary bone cancer. Normally, lesions contain undifferentiated cancer stem cells (CSCs) that support uncontrolled growth/proliferation, and pre-osteoblasts that form excessive amounts of immature bone. CSCs are characterized by high expression of the transcriptional regulators Sox2 and yes-associated protein (YAP) that are essential for tumorigenicity. YAP is restrained by the H...
ba0005cabs.oc4.4 | Oral Communications | ECTS2016
3D tissue engineered constructs for modeling tumor-induced bone disease
Dadwal Ushashi , Guo Ruijing , Lu Sichang , Vanderburgh Joseph , Merkel Alyssa , Kwakwa Kristin , Guelcher Scott , Sterling Julie
While the importance of interactions between bone and tumors is well-established, the mechanism by which the physical bone microenvironment regulates disease progression is limited by the lack of suitable in vitro models. We have designed 3D Tissue Engineered Constructs (TECs) using microCT imaging in tandem with inkjet 3D printing technology that recapitulate the mechanical and morphometric properties of trabecular bone. 3D-printed TECs exhibited no significant diffe...
ba0005cabs.oc4.5 | Oral Communications | ECTS2016
New models of breast and lung cancer bone metastases for preclinical efficacy testing
Suominen Mari I. , Hagemann Urs B. , Konkol Yvonne , Bernoulli Jenni , Fagerlund Katja M. , Bjerke Roger M. , Karlsson Jenny , Halleen Jussi M. , Cuthbertson Alan
In advanced ER+ve breast cancer, the propensity of bone involvement is 85%. Similarly in advanced lung cancer, 3040% of patients develop bone metastases, and as recent advances in lung cancer therapies improve survival, the number of patients living with bone metastases is expected to increase. At the same time there is a paucity of especially ER+ and osteoblastic animal models available. We present herein the development of four mouse models of breast and lung cancer su...
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01450 372 476
20 North Bridge Street, Hawick, Scottish Borders, TD9 9QW
Gum Disease
Why might I be susceptible?
Periodontal disease is the Number One cause of tooth loss amongst adults. This is because a certain number of people (15-20%) have immune systems that overreact to the bad bacteria in their mouths. When this overreaction occurs, the immune system attacks and breaks down the bone and tissue that surround the tooth. This destruction is not predictable and can occur sporadically. None of us knows if we are part of this 15-20% because we can’t usually feel or notice the onset of gum and bone (periodontal) disease. Both adults and children should be routinely checked for gum disease.
Keeping your gums in shape
Keep in mind that healthy gums DON’T BLEED. You are the key player on the hygiene team. If you don’t do the essential daily brushing and flossing, the rest of your dental team (the dentist and hygienist) is playing short-handed. And sometimes with everyone fighting the good fight, stubborn plaque and bacteria will require some new maintenance techniques for battling gum infection.
GUM DISEASE IS NOT CURABLE,
BUT IT IS TREATABLE,
AND IN MOST CASES, CONTROLLABLE
Are you living at high risk for gum disease?
Smoking: Numerous studies have shown that smokers have more gum disease. Smokers have increased levels of tartar in the mouth, and experience more tissue irritation, which makes their gums more susceptible to disease. Smokers have more bone loss and heal less quickly than non-smokers.
Stress: When our immune system is stressed it is difficult to fight off the bacteria that cause gum infections.
Dental neglect: Avoiding the dentist is a lifestyle choice that puts you at risk of contracting diseases of the mouth, teeth and gums.
Floss: Your hygienist or dentist works to prevent infection in your mouth from entering the bloodstream and reaching vital organs.
Heart disease: Gum inflammation products and bacteria in gum disease can cause heart disease, and in some cases, double the risk of a fatal heart attack. In addition, bacteria from your mouth may combine with blood-clotting cells called platelets, forming heart-stopping blood clots.
Stroke: New studies show that 70% of the fatty deposits of stroke sufferers contain bacteria, of which 40% comes from the mouth.
Diabetics: This group of people are more likely to have gum disease than most people and gum disease makes it more difficult for diabetics to control their blood sugar.
Premature birth: Pregnant women who have periodontal disease may be as much as seven times more likely to have a baby born early. Some research suggests that gum disease may increase the level of hormones that induce labour.
Frequently Asked Questions
What is gum disease?
Gum disease describes swelling, soreness or infection of the tissues supporting the teeth. There are two main forms of gum disease: gingivitis and periodontal disease.
What is gingivitis?
Gingivitis means inflammation of the gums. This is when the gums around the teeth become very red and swollen. Often the swollen gums bleed when they are brushed during cleaning.
What is periodontal disease?
Long-standing gingivitis can turn into periodontal disease. There are a number of types of periodontal disease and they all affect the tissues supporting the teeth. As the disease gets worse the bone anchoring the teeth in the jaw is lost, making the teeth loose. If this is not treated, the teeth may eventually fall out.
Am I likely to suffer from gum disease?
Probably. Most people suffer from some form of gum disease, and it is the major cause of tooth loss in adults. However, the disease develops very slowly in most people, and it can be slowed down to a rate that should allow you to keep most of your teeth for life.
What is the cause of gum disease?
All gum disease is caused by plaque. Plaque is a film of bacteria, which forms on the surface of the teeth and gums every day. Many of the bacteria in plaque are completely harmless, but there are some that have been shown to be the main cause of gum disease. To prevent and treat gum disease, you need to make sure you remove all the plaque from your teeth every day. This is done by brushing and flossing.
What happens if gum disease is not treated?
Unfortunately, gum disease progresses painlessly on the whole so that you do notice the damage it is doing. However, the bacteria are sometimes more active and this makes your gums sore. This can lead to gum abscesses, and pus may ooze from around the teeth. Over a number of years, the bone supporting the teeth can be lost. If the disease is left untreated for a long time, treatment can become more difficult.
How do I know if I have gum disease?
The first sign is blood on the toothbrush or in the rinsing water when you clean your teeth. Your gums may also bleed when you are eating, leaving a bad taste in your mouth. Your breath may also become unpleasant.
What do I do if I think I have gum disease?
The first thing to do is visit your dentist for a thorough check-up of your teeth and gums. The dentist can measure the ‘cuff’ of gum around each tooth to see if there is any sign that periodontal disease has started. X-rays may also be needed to see the amount of bone that has been lost. This assessment is very important, so the correct treatment can be prescribed for you.
What treatments are needed?
Your dentist will usually give your teeth a thorough clean. You’ll also be shown how to remove plaque successfully yourself, cleaning all surfaces of your teeth thoroughly and effectively. This may take a number of sessions with the dentist or hygienist.
What else may be needed?
Once your teeth are clean, your dentist may decide to carry out further cleaning of the roots of the teeth, to make sure that the last pockets of bacteria are removed. You’ll probably need the treatment area to be numbed before anything is done. Afterwards, you may feel some discomfort for up to 48 hours.
Once I have had periodontal disease, can I get it again?
Periodontal disease is never cured. But as long as you keep up the home care you have been taught, any further loss of bone will be very slow and it may stop altogether. However, you must make sure you remove plaque every day, and go for regular check ups by the dentist and hygienist.
• General Dentistry
The modern dental practice is customer-focused. That means it offers a welcoming, relaxing environment that puts its customers – not patients – at ease.
• Restorative Dentistry
Restorative dentistry is the study, examination and treatment of diseases of the oral cavity, the teeth and their supporting structures.
• Tooth Alignment
Before placing braces on your teeth you will need a check-up for decay or gum problems. Do visit your dentist or the School Dental Clinic regularly, even when you are on braces.
• Visit our Hygienist
Our Hygienist Perio Therapy treatment aims to help you achieve your own healthiest possible oral health. This is done by helping you understand the processes of Dental disease, especially gum disease which still accounts for 3 out of 4 teeth ultimately lost. Your teeth will be cleaned using thorough but gentle techniques leaving your mouth clean and potentiality healthier.
• Wrinkle Reduction
I believe in a holistic rejuvenation approach to treatments and tend to aim towards subtle results that make you look younger and fresher rather than a fake and over filled appearance.
- Dr. Med. Dent. Christiane Wassmuth-Gibbs
• Tooth Whitening
Whitening is a process where the tooth discolouration is ‘whitened’ to a lighter shade. It removes the staining agent through chemical means.
• Meet Our Team
We have a wonderful team here at Teviot Dental, please click on the link below to find out more about them.
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1a01aa77535b9ecfb87b9fc36adbcd2f
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Can mold enter eyes?
Can mold enter eyes?
When toxic black mold spores enter the air, they can easily enter an individual’s eyes, ears, and other orifices, causing different vision problems. Symptoms of vision problems from black mold toxins: Eye inflammation. Bloodshot eyes.
Can mold cause eye floaters?
Floaters are often the result of vitreous tears or detachments often experienced by seniors, but for some these clumps of protein can be the result of candidiasis, an overgrowth of the yeast-like fungus Candida albicans.
Can mold cause optic neuritis?
Mycotic demyelinating optic neuritis is a neurological disorder of the visual system caused by mycotoxins released by indoor toxic molds.
Does mold cause itchy eyes?
Overview. If you have a mold allergy, your immune system overreacts when you breathe in mold spores. A mold allergy can cause coughing, itchy eyes and other symptoms that make you miserable.
How do you get mold out of your eyes?
Mold-related keratitis is typically treated with both oral antifungal drugs and antifungal eye drops. Without prompt treatment, lasting damage to the cornea may result, leading to permanent loss of vision. If that happens, the only way to restore sight would be to receive a corneal transplant.
Can black mold hurt your eyes?
Black mold affects just about every part of your body, including your eyes. The black mold spores in the air can enter your eyes and cause vision problems both immediately and over prolonged periods of exposure. Eye symptoms include: Inflammation.
Can black mold cause eye problems?
Vision Problems Black mold affects just about every part of your body, including your eyes. The black mold spores in the air can enter your eyes and cause vision problems both immediately and over prolonged periods of exposure. Eye symptoms include: Inflammation.
Can mold mess with your brain?
Inflammation: Mold spores act as irritants, which can trigger the body to mount an immune response. This can lead to inflammation throughout the body. Inflammation in the brain can impair cognitive function, and in the case of chronic inflammation, this can lead to long-lasting cognitive impairment.
Can mold cause dry eyes?
Some symptoms of eye irritation from mold spores are blurred vision, burning and itching, circles and sacks under the eyes, tearing, light hypersensitivity, red eyes, or pain in the eyes. If inflammation with pus discharge occurs, a doctor prescribes suitable antibiotics or antimycotics.
Can mold toxicity cause eye problems?
Exposure to mold can cause respiratory symptoms and symptoms of an allergic reaction, which include things like itchy eyes, redness of the eyes, and watery eyes. However, more serious issues can occur, including a number of eye infections. Keratitis is an eye infection commonly caused by mold.
What are the symptoms of long term mold exposure?
Toxic mold exposure is also connected to more serious, long-term effects like insomnia, memory loss, trouble concentrating and confusion. Mold exposure contributes to depression and anxiety. It can even lead to muscle cramps, numbness in extremities, weight gain, light sensitivity and hair loss.
Is brain damage from mold reversible?
Many patients with memory loss and dementia are actually simply toxic from mold, which is a reversible condition. The tragedy is missing the diagnosis and continuing to proceed with treating the patient for something they do not have and missing an effective treatment.
Can mold stay in your body for years?
Those who process toxins well can see their symptoms disappear as quickly as a few days. Others who eliminate toxins slowly can experience symptoms for much longer. They could be ill for months or even years after the source of mold is eliminated.
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Close
Bistability analyses of CD4+ T follicular helper and regulatory cells during Helicobacter pylori infection.
Abstract
T follicular helper (Tfh) cells are a highly plastic subset of CD4+ T cells specialized in providing B cell help and promoting inflammatory and effector responses during infectious and immune-mediate diseases. Helicobacter pylori is the dominant member of the gastric microbiota and exerts both beneficial and harmful effects on the host. Chronic inflammation in the context of H. pylori has been linked to an upregulation in T helper (Th)1 and Th17 CD4+ T cell phenotypes, controlled in part by the cytokine, interleukin-21. This study investigates the differentiation and regulation of Tfh cells, major producers of IL-21, in the immune response to H. pylori challenge. To better understand the conditions influencing the promotion and inhibition of a chronically elevated Tfh population, we used top-down and bottom-up approaches to develop computational models of Tfh and T follicular regulatory (Tfr) cell differentiation. Stability analysis was used to characterize the presence of two bi-stable steady states in the calibrated Tfh/Tfr models. Stochastic simulation was used to illustrate the ability of the parameter set to dictate two distinct behavioral patterns. Furthermore, sensitivity analysis helped identify the importance of various parameters on the establishment of Tfh and Tfr cell populations. The core network model was expanded into a more comprehensive and predictive model by including cytokine production and signaling pathways. From the expanded network, the interaction between TGFB-Induced Factor Homeobox 1 (Tgif1) and the retinoid X receptor (RXR) was displayed to exert control over the determination of the Tfh response. Model simulations predict that Tgif1 and RXR respectively induce and curtail Tfh responses. This computational hypothesis was validated experimentally by assaying Tgif1, RXR and Tfh in stomachs of mice infected with H. pylori.
MIDAS Network Members
Citation:
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Call or Text Us!405-340-9191
Fine Hearing Care - Edmond, OK
Man taking a hearing test in a booth.
The majority of individuals aren’t proactive about their hearing health and probably haven’t had a hearing test since grade school because it’s generally not part of a routine adult physical. Fortunately, a professional hearing specialist can discover a wealth of information from a hearing examination which can be used to both diagnose any hearing loss and help evaluate whether using treatments like hearing aids is effective.
You may not get a lollipop after your complete audiometry test, which is more involved than you might remember from your childhood, but you will get a greater understanding of your hearing health. There are three common types of hearing tests, each of which will supply different perspectives about your hearing.
Pure tone testing
We normally think of sound as measured in decibels, but decibels just indicate the loudness of a sound. Another important factor is pitch or tone which measures the frequency of sound. It’s measured in Hertz (no relation to the car rental agency), with a low bass sound measuring around 50-60 Hz, and normal speech ranging from 500 to 3,000 Hz. 20 to 20,000 Hz is the range of frequencies that a healthy human ear can hear.
With pure tone testing, you’ll wear headphones or earphones attached to an audiometer. You may also wear a device called a bone oscillator which sounds scary but just measures how well your bones conduct sound. Much like that familiar hearing test from your youth, you press a button or raise your hand when a tone plays either in your left ear or your right ear.
The minimum volume that you can hear the tones will then be monitored. Whether your hearing loss is more marked in one ear than the other, what frequency of sound you have the most difficulty hearing, and generally how well your ears are functioning, will be measured by this test.
Speech audiometry
This kind of test tracks your ability to accurately hear spoken words, again with sounds being played through headphones. In some circumstances, you’ll be asked to repeat recorded words that are spoken along with background noise. In other situations, the individual carrying out the test will say words to you, but there’s a surprise, you can’t see the person’s mouth.
Hearing individual words means you can’t depend on context to understand what’s being said, and being unable to see the speaker keeps you from reading lips (something you may not even realize you’ve been doing). Rhyming words, let’s say crime, time, dime, and climb, can be difficult for individuals suffering from high-frequency hearing loss to distinguish.
Speech audiometry tracks your ability to make sense of what you’re hearing unlike tone testing which calculates how loud particular sounds need to be in order to be heard. Whether hearing aids will be helpful is another thing that word recognition testing can help determine.
Immittance audiometry
This type of testing usually won’t cause pain, but it may be a little uncomfortable. Tympanometry artificially alters the pressure inside of your ear by pushing air in with a small inserted probe. A graph readout will allow your hearing specialist to determine if there’s an issue with your eardrum such as earwax impaction or a perforation, and how well your eardrum is working.
Your ears have reflexes that are tested by a similar probe. Muscles in your ear involuntarily contract when you are exposed to loud sound. It will be easier for your hearing specialist to determine the extent of your hearing loss when they know the level of noise required to trigger this reflex. Individuals with extreme hearing loss don’t demonstrate any reflex.
It’s important to include immittance testing because it helps diagnose conductive hearing loss, which is when issues occur in the small bones inside of the ears and can occur at the same time as age-related or noise-related hearing loss.
If you’re having a hard time hearing, give us a call and schedule a hearing test! We can help you better understand your hearing health, inform you on what you can do to preserve healthy hearing, and let you know what your treatment options are if you have hearing loss or tinnitus.
Call Today to Set Up an Appointment
The site information is for educational and informational purposes only and does not constitute medical advice. To receive personalized advice or treatment, schedule an appointment.
Why wait? You don't have to live with hearing loss. Call Us Today
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3,134,280,004,234,199,000
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Don's Home Health Corona Virus Variants Contact
last updated 25 June 2024
Viruses like SARS-CoV-2 continuously evolve as changes in the genetic code (caused by genetic mutations or viral recombination) occur during replication of the genome.
In late 2023, the World Health Organization listed nine variants as circulating at the time. More than 50 variants have been identified; although some are no longer spreading. COVID Variants | WebMD
Some variants have different behaviors.
For example Omicron BA.2 infects different cells in the upper respiratory tract rather than in the lungs, which makes it more transmissible but less severe than the previous variants.
The death rates were slightly lower even though the infection rates 4 or more times higher, so the death per infection were about ¼ the rate of previous variants.
Delta caused more severe disease than other variants in people who weren't vaccinated.
The World Health Origination (WHO) and The European Centre for Disease Prevention and Control (ECDC) classify some variants with concerning properties likely to impact the epidemiological situation in the European Union (EU) and European Economic Area (EEA) as variant under monitoring (VUM), variant of interest (VOI) and variant of concern (VOC).
XBB.1.5-like (Omicron) and BA.2.86 (omicron) are classified as VOI in May, 2024.
Other variants have been de-escalated e.g. ALpha (B.1.1.7), Delta (B.1.617.2), Omicron (BA.1,BA.3, BA.2.L452x)
SARS-CoV-2 variants of concern as of 31 May 2024 | ECDC
SARS-CoV-2 Variant Classifications and Definitions
New variants emerge in different places.
SARS-CoV-2 Variant Classifications and Definitions
A Timeline of COVID-19 Variants | VeryWellHealth
From Alpha to Omicron: How Different Variants of Concern of the SARS-Coronavirus-2 Impacted the World | PubMed - NIH
Links:
SARS-CoV-2 Variant Classifications and Definitions | CDC Nextstrain SARS-CoV-2 resources Overview of Variants/Mutations
SARS-CoV-2 variants of concern as of 31 May 2024 | ECDC
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1,453,927,440,785,685,000
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Genome-wide sequencing to identify the cause of hereditary cancer syndromes: With examples from familial pancreatic cancer
Research output: Contribution to journalReview articlepeer-review
Abstract
Advances in our understanding of the human genome and next-generation technologies have facilitated the use of genome-wide sequencing to decipher the genetic basis of Mendelian disease and hereditary cancer syndromes. However, the application of genome-wide sequencing in hereditary cancer syndromes has had mixed success, in part, due to complex nature of the underlying genetic architecture. In this review we discuss the use of genome-wide sequencing in both Mendelian diseases and hereditary cancer syndromes, highlighting the potential and challenges of this approach using familial pancreatic cancer as an example.
Original languageEnglish (US)
Pages (from-to)227-233
Number of pages7
JournalCancer Letters
Volume340
Issue number2
DOIs
StatePublished - Nov 1 2013
Keywords
• Cancer predisposition genes
• Genome sequencing
• Hereditary cancer
ASJC Scopus subject areas
• Oncology
• Cancer Research
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Cite this
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What are the Symptoms and Causes of Incontinence of Urine?
The urine system is made up of parts such as the bladder, kidney as well as urethra. There are several jobs of these body parts such as filtering the waste from the food, storing them, and finally removing the waste out of the human body. The waste product such as urine is created by the kidneys. The bladder is the storage tank for the waste and the urethra is from where it gets out. It is very important for this system to perform smoothly.
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ABA therapy is a type of behavior modification for children with autism. The basic philosophy of the method is that children with autism are capable of learning, so ABA therapy can help them learn how to modify their behaviors. It is important to note that ABA isn’t a cure-all, and there are several potential side effects of this treatment. However, if you are considering this therapy for your child, you should know what to expect. Checkout aba therapy Chicago for more info.
ABA therapy involves a variety of techniques that can help children with a wide range of disorders. It uses a scientific approach to teaching behavior and takes a behavioral approach to teaching children. Basically, it teaches children to change their behaviors by changing their environment and learning new functional ways to do things. This method also involves teaching parents how to recognize and deescalate problem behaviors. In addition, it can help families reduce stress levels by enabling parents to better integrate their children into new environments.
ABA therapy includes structured sessions and a variety of materials to support the child’s development. During each session, a BCBA will spend time with the child or supervise a team of other people. The sessions usually last one to several hours, and therapists will use a method called discrete trial training. This training method divides the skill into three steps: an antecedent, a behavior, and a conclusion.
During the therapy session, ABA therapists will observe and analyze the child’s behavior patterns and develop a personalized therapy plan that matches the child’s individual needs and goals. The plan should include concrete treatment goals that relate to the child’s developmental stage and challenges. Moreover, it should also include strategies for the caregiver and teacher to help the child adjust to the new situation. Throughout the session, the therapist will also work closely with the child’s family and school.
During the ABA sessions, parents will practice the skills that they want their child to learn. Some activities are age-appropriate, like eating. Other activities include practicing age-appropriate conversations. During these activities, the therapist will also teach the child how to memorize names and addresses. Often, the therapist will include specific activities that allow the child to learn to interact with others in a more natural way. And ABA sessions are not just about a child’s behavior; they also teach caregivers, teachers, and other people.
ABA therapy helps children develop appropriate social skills by helping them make connections between their behaviors and the expectations of others. The goal of ABA is for the child to understand the social dos and don’ts and to mimic those behaviors as much as possible. Once they have mastered the basics of the dos and don’ts, they can move on to more complex behaviors. During the first few sessions, parents will learn about ABA and its benefits.
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What You Need to Know About Your Body’s Hormonal Response to Food
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Even if we keep fairly active and eat reasonably healthy, most of us at some stage want to lose a bit of weight. And we may end up willing to try almost anything to drop those stubborn pounds. This is why the weight-loss industry is one of the biggest industries in the world. Unfortunately, there is much misinformation out there that makes weight-loss confusing for some and daunting for others.
I hope my articles on weight loss and nutrition can shed some light, as I have spent my entire lifetime shaping my body for competition sports — needing to look a certain way for gymnastics and Ms Figure and needing to be a specific weight for Brazilian jiu jitsu. This has given me an understanding of how food affects the body and what to eat in order to look or perform a certain way.
Sophia McDermott Drysdale
In this article, I’m going to talk about how different foods affect us chemically because of our body’s hormonal reactions, and what this tells us about the type of foods we should be eating for successful weight loss.
What to Eat for Weight Loss
The key in eating for weight loss is to eat foods that create a hormonally favorable environment for your body to utilize the calories, rather than store these calories for energy. Eating half a pound of broccoli will have a profoundly different effect on your body than eating half a pound of fettuccine carbonara.
Most of us know the foods we consume are comprised of the three macro-ingredients: fats, proteins, and carbohydrates. For a long time, there was this idea that eating fat was bad, so everyone ate a lot of cereals and breads. But fats are essential to our survival. They are necessary for insulating and cushioning our joints, involved in the synthesis of our hormones, and play an important role in the absorption of vitamins such as A, D, E, and K. The essential fatty acids in fats also have a part in brain development and the management of inflammation.
More recently, as more of our population has become obese and become prime candidates for diabetes due to the overconsumption of breads and cereals, carb-free diets have emerged. All of the sudden, carbs are the enemy. But we need carbs, too! We use them for energy and our brain needs glucose to function.
To achieve weight loss and function optimally, we need to eat a balance of all three of macro-ingredients. The type of each of these macro-ingredients is what will to make the difference between gaining and losing weight. So, let’s take a closer look at the hormonal effects different types of food have on our bodies.
What You Need to Know About Your Body's Hormonal Response to Food
The Basics of Our Body’s Hormonal Response
At all times, your body likes to be in a state of equilibrium, a state of balance. When we eat certain foods, our body releases specific hormones to maintain that balance. Our digestion has separate tools to digest each of the three macro-ingredients. Carbohydrates generally digest more quickly, while fats take the longest to get broken down. Carbohydrates are broken down into glucose, proteins are broken down into amino acids, and fats are broken down into fatty acids.
The hormones glucagon and insulin are responsible for regulating our blood glucose levels and maintaining a healthy equilibrium. Glucagon is released by the pancreas if glucose levels in our blood are low. Our glucose levels could be low because we have not eaten in a while or because we just did an intense workout. This is one reason people consume those glucose-rich energy drinks immediately after exercise, to restore and replenish their levels.
Conversely, insulin is released if there is too much glucose in our blood. This can happen if we eat a carbohydrate-rich meal, such as a bowl of pasta. When we ingest carbohydrates, our pancreas receives a signal to release insulin, which removes the excess glucose in the bloodstream and stores the excess as glycogen in the liver. Once our liver stores are full, then the remaining excess sugar is stored as fat.
Both hormones, insulin and glucagon, are vital for balancing our blood sugar levels. However, with our modern diets so jam packed with carb-rich foods that are so easily converted to glucose, we are more than likely in a continuous state of our hormones signalling our bodies to store, store, store.
What You Need to Know About Your Body's Hormonal Response to Food
But it is not just the amount of carbohydrates you consume that matters. It is also the type of carbs that affect how much insulin – the storing hormone – is released. Carbohydrates that are broken down rapidly cause a spike in blood sugar that triggers your body to respond with a surge of insulin. This programs your body to be in super storing mode, even if you haven’t eaten that much. In this way, simple sugars and processed carbs such as white bread, pasta, pretzels, and crackers are all a literal recipe for weight gain. These white starchy foods cause the pancreas to release insulin and tell your body to store.
But none of this makes carbs “bad.” Yes, carbs spike our insulin, no matter what – but we can curb that spike to some degree if we eat protein and fat along with the carbs and are mindful to eat quality (not processed) carbohydrate sources. One of the tools we can use to guide us in our carb selection is the glycemic index.
How to Combine Foods for a Favorable Hormonal Response
The glycemic index catalogues carbohydrates by the rate at which they are broken down by the body and released into the bloodstream as glucose. Pure glucose scores highest on the index with a value of 100. A high value (anything above sixty) means that type of carbohydrate is broken down extremely quickly and will cause a surge in insulin. A low value (such as ten) means the carbohydrate in question is broken down slowly and has a low insulin response.
But the impact of carbs on the body can also be altered with the addition of proteins and fats. Fats, especially, slow down the rate of digestion and absorption since they are much more complex to break down. So, our best strategy is to eat a balanced diet by consuming healthy carbs, proteins, and fats together at every meal.
Eating for Weight Loss and Hormonal Response
One of my favorites: salmon, spinach, and polenta.
By eating healthy carbohydrates such as fruits, veggies, and unprocessed grains like quinoa as opposed to processed carbs and sugars, you will dramatically decrease insulin output, and this will decrease your body’s message to store fat. By eating a small portion of lean protein like eggs, beef, turkey, or chicken and good fats like avocados, nuts, and seeds along with those quality carbs, you will be eating foods in a combination that further decreases the amount of insulin released and, therefore, allows your body to better utilize everything you are eating for energy, replenishment, and repair.
Optimize Your Food to Optimize Your Hormones
For optimal health, good energy, and to eat in a way that is hormonally favorable for weight loss, we need all three macro-ingredients – protein, fat, and carbohydrates. What is important is the quality of your macro-ingredients and in what combination you are eating them.
Here is what you need to remember:
• By avoiding carbs derived from processed grains — like white bread, plain white pasta, and candy — and sticking to carbs that are broken down by the body at a slower rate, your hormonal response will be geared more for fat loss than fat gain.
• Starchy vegetables such as squash and sweet potato are my first choice for complex carbs that provide lasting energy. Fruits and green vegetables are good, too.
• Adding good sources of protein such as eggs or chicken to your meals will help lower the overall glycemic value. The protein will also provide much-needed building blocks for muscle growth, tissue repair, and robust immune function.
• Eating good fats such as the omega-3 fats found in fish and monounsaturated fats found in olive oil and avocado will also help lower the glycemic value of your meals and assist in a longer lasting release of energy. The fats also aid with vitamin absorption, cushioning around our bones, brain health, and managing inflammation.
I know that was a lot of science today, but I want you to understand the facts and logic behind my advice — all of which is based on my lifetime of experience as an athlete, competitor, and trainer.
Eating healthy is not that complicated in practice — if you want to eat for weight loss, give the huge bowls of pasta a miss. Instead, opt for a plate piled high with salad drizzled with olive oil, a modest portion of sweet potato, and a delicious piece of pan-seared salmon.
Sophia McDermott Drysdale on FacebookSophia McDermott Drysdale on InstagramSophia McDermott Drysdale on Youtube
Sophia McDermott Drysdale
Sophia is an athlete, coach, trainer, and mother. Her focus is women's health and fitness, as well as pregnancy and postpartum workouts and nutrition. Her new e-book Spring Into Summer offers a seven-day meal plan with over thirty recipes.
Sophia also offers personalized diet and workout programs on her website, a no-nonsense nutrition eBook, and a free weekly newsletter full of health and fitness tips. Sophia travels the world to teach seminars and she offers Lifestyle camps in Las Vegas.
Her sporting career started when she was four years old as a jazz ballet dancer. At age eleven, she began gymnastics and trained in an elite squad for almost ten years. In 2002, she began Brazilian jiu jitsu (BJJ) and was awarded her black belt in 2010 making her the first Australian female to receive a black belt in the sport.
Sophia competed nationally and internationally, earning multiple state, national, Pan-Pacific, and Pan-American titles, as well multiple No Gi World Champion titles and a World Champion title. Currently, she lives in Las Vegas, Nevada and competes in figure shows. She holds the distinction of being the Overall Unlimited Champion in the Figure division for the NPC federation.
Sophia received her qualification in gymnastics coaching and Cert III and IV for Personal Training. She has worked as a personal trainer specializing in functional training for athletes and nutrition for more than a decade. Sophia travels the world to teach BJJ, women's self defense, and nutrition seminars. She also runs a women's only training program in Las Vegas.
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6e3c8d3593f3f69280bb5502b214ab8e
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2,852,411,268,239,709,700
|
Epidemiology of tsutsugamushi disease and its relationship with meteorological factors in Xiamen city, China
摘要
Tsutsugamushi disease (TD) is an acute infectious disease caused by Orientia tsutsugamushi. This study aimed to analyze the epidemiological features of TD, investigate chigger mites and their hosts, and investigate the meteorological factors affecting TD incidence and the host of O. tsutsugamushi in Xiamen city, China. Data on reported TD cases were collected from 2006 to 2018. Spearman’s correlation test were used for identifying the relationship between meteorological factors and TD incidence and whether meteorological factors affect the host of O. tsutsugamushi. The incidence of reported TD increased gradually from 2006, reached a peak of 4.59 per 100,000 persons in 2014, and then decreased gradually. The TD incidence was seasonal, with epidemic periods occurred mainly in summer and autumn. Patients aged 40-60 years had the highest proportion of cases, accounting for 44.44% of the total cases. Farmers had the largest number of cases among all occupational groups. Rattus Norvegicus was the most common host, accounting for the largest proportion of rats (73.00%), and the highest rat density was observed in March and October every year. There were significant positive correlations between the number of reported cases and average temperature, sunshine duration, and rainfall as well as between rat density and average temperature. On phylogenetic analysis, 7 sequences of hosts and human TD cases obtained from health records demonstrated the highest similarities to the Kato, Karp, and Gilliam strains. No correlations were observed between rat density, and sunshine duration and rainfall. The transmission of TD in Xiamen city, China, was seasonal, and its incidence was affected by several meteorological factors including average temperature, sunshine duration, and rainfall. However, the host of O. tsutsugamushi was only affected by average temperature.
出版物
PLOS NEGLECTED TROPICAL DISEASES
DOI
10.1371/journal.pntd.0008772
2022
罗丽
硕士
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9222580d47c553ea90dc0f5e416f8f3a
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6,312,131,836,663,825,000
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Publication:
ATP as a putative sensory mediator: activation of intrinsic sensory neurons of the myenteric plexus via P2X receptors
dc.contributor.author Bertrand, P. P en_US
dc.contributor.author Bornstein, J. C. en_US
dc.date.accessioned 2021-11-25T13:35:17Z
dc.date.available 2021-11-25T13:35:17Z
dc.date.issued 2002 en_US
dc.description.abstract The mucosal terminals of sensory neurons intrinsic to the wall of the intestine are sensitive to the chemical environment within the lumen. Lumenal stimuli probably release sensory mediators from the mucosal epithelium, which then activate the nerve terminals indirectly. Here, we tested the idea that ATP activates intrinsic sensory nerve terminals in a way consistent with its being a sensory mediator. We made intracellular recordings from intrinsic sensory neurons located in the myenteric plexus [identified as AH neurons, which are neurons with a long-lasting afterhyperpolarization following the action potential (AP)], located within 1 mm of intact mucosa. Focal electrical stimulation of the mucosa was used to locate and map regions innervated by each neuron. Application of ATP (1-2 mM in the pressure pipette) to these regions elicited trains of APs that originated at the sensory terminals. ATP-gamma -S produced a similar response, but alpha ,beta -methylene ATP and 2-methylthio-ATP were only weakly active. The P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2',5'-disulphonic acid (PPADS) (60 µM in the bath) abolished the APs evoked by ATP and ATP-gamma -S but spared similar responses evoked by 5-hydroxytryptamine (5-HT). Another P2 receptor antagonist suramin (100 µM in the bath) did not significantly change the number of APs evoked by ATP. Either ATP or alpha ,beta -methylene ATP desensitized the ATP-evoked APs; 50% recovery occurred after ~5 sec. The number of APs evoked by ATP was reduced, but not abolished, by the selective 5-HT3 receptor antagonist granisetron (1 µM in the bath). ATP was applied to the cell bodies of sensory neurons to investigate whether the cell bodies express the same P2X receptor as the terminals. ATP evoked a fast depolarization associated with a reduction in input resistance and a reversal potential of -11 mV. This depolarization was potentiated by suramin and blocked by PPADS. We conclude that activation of an atypical excitatory P2X receptor by ATP triggers AP generation in the mucosal processes of the sensory neurons; endogenous 5-HT release may also contribute to activation of the nerve terminals. A similar P2X receptor exists on the cell body of the sensory neuron. Together, these data are consistent with a role for ATP as a sensory mediator in gastrointestinal chemosensory transduction. en_US
dc.description.uri http://www.jneurosci.org/cgi/content/abstract/22/12/4767 en_US
dc.identifier.issn 0270-6474 en_US
dc.identifier.uri http://hdl.handle.net/1959.4/40047
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/3.0/au/ en_US
dc.source Legacy MARC en_US
dc.title ATP as a putative sensory mediator: activation of intrinsic sensory neurons of the myenteric plexus via P2X receptors en_US
dc.type Journal Article en
dcterms.accessRights metadata only access
dspace.entity.type Publication en_US
unsw.accessRights.uri http://purl.org/coar/access_right/c_14cb
unsw.relation.faculty Medicine & Health
unsw.relation.ispartofjournal Journal of Neuroscience en_US
unsw.relation.ispartofpagefrompageto 4767-4775 en_US
unsw.relation.ispartofvolume 22 en_US
unsw.relation.originalPublicationAffiliation Bertrand, P. P, Medical Sciences, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Bornstein, J. C. en_US
unsw.relation.school School of Medical Sciences *
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Gingivitis & Periodontal Disease in Aurora Colorado
Have You heard of Gingivitis or Periodontal Disease?
What is gingivitis or periodontal disease? Do you know the signs? Gingivitis (also known as periodontal disease and gum disease) is very common in the United States, affecting half of all American adults. But, did you know that gum disease is completely preventable? Periodontal disease is caused by a buildup of plaque and other substances on the teeth that break down tooth enamel and affect the delicate tissues of your gums and teeth. When teeth are not properly taken care of, inflammation (known as gingivitis) can begin to set in that progresses to gum disease. Early stages of gum disease can be reversed with periodontal treatment at Stonebrook Family Dental.
What is Gingivitis?
Gingivitis is the first stage of periodontal disease. It is caused by a bacterial buildup in plaque. This buildup can lead to inflamed gums that may bleed during tooth brushing. You may also experience gum tenderness, discoloration from pink to a dark red, bad breath, and gum recession. At this stage, you can easily treat your gums by getting accustomed to a daily routine of flossing, rinsing with a Listerine (or generic brand, as long as it possesses the ADA stamp) mouthrinse, and brushing. Aurora CO dentist, Dr. Varley, recommends practicing flossing, rinsing, and brushing at least 2 times daily.
How to Treat Gingivitis
Moderate stages of gum disease (like gingivitis) can be reversed. However, the advanced forms of periodontitis can’t easily be reversed. That’s when surgical treatments come into play. Here are some prevention tips:
• Treat gum disease before it even begins. How do you do that? Through frequent brushing and flossing of course! Brush and floss those pearly whites at least 2x a day, if not after every meal. That will ensure that all the bad bacteria and plaque buildup is removed often enough from the teeth before causing tooth decay. (We cannot stress this enough!)
• Come into the office frequently! The easiest way to prevent gingivitis with an onset of periodontal disease is to commit to your daily routine of flossing, rinsing, and brushing as well as staying up date with your regular dental check-ups.
• Periodontal treatments are possible. For our gum disease treatments, we provide deep cleaning through scaling and root planing to provide a healthy tissue environment to help tissues readapt to normal tooth surfaces. With our periodontal maintenance, we provide treatments and protocols designed to clean and maintain your gums and teeth and stop gum disease in it’s tracks. Some of our periodontal procedures are surgical and some non-surgical. Keeping your gum disease at bay by seeing us often is how you can avoid the surgical procedures (which is the more favorable option).
What Happens If You Don’t Treat Gingivitis?
When gingivitis is left untreated, it advances to Periodontal Disease. In a person with this advanced onset, the inside layer of the gum and bone pull away from the teeth and pockets are formed. The small spaces between teeth and gums begin to collect excess waste and become infected. The body's immune system reacts by fighting the bacteria while the plaque spreads and continues to grow beneath the gum line.
The toxins produced by the bacteria in plaque along with the "good" enzymes that fight infections start to break down the bone and gum that holds the teeth in place, which results in bone destruction and tooth loss.
What Are the Common Signs and Symptoms?
Common signs and symptoms of Periodontal Disease include gums that bleed during and after brushing, sensitivity, a bad taste in your mouth or constant bad breath, gum recession, loose teeth, or changes in the way your teeth fit together while biting down.
Call for a Consultation
Stop gingivitis from developing into a more serious form of gum disease. Schedule an appointment and get in for your exam, cleanings, and x-rays every 6 months so that our dentist in Aurora can treat any dental conditions or concerns you may have before they lead to more serious problems. Call us today at 303-872-7907!
At Stonebrook Family Dental, we treat you with the gentle dental care you need. We look forward to taking care of you.
We're Open - Please click for our COVID-19 Policies & Procedures
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Health Information and Tools > Patient Care Handouts > Surgical Drain Care: Care Instructions
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Main Content
Surgical Drain Care: Care Instructions
Surgical drain tube with bulb on the end and surgical drain tube that is open to dressing
Your Care Instructions
After a surgery, fluid may collect inside your body in the surgical area. This makes an infection or other problems more likely. A surgical drain allows the fluid to flow out.
The doctor puts a thin, flexible rubber tube into the area of your body where the fluid is likely to collect. The rubber tube carries the fluid outside your body.
The most common type of surgical drain carries the fluid into a collection bulb that you empty. This is called a Jackson-Pratt (JP) drain. The drain uses suction created by the bulb to pull the fluid from your body into the bulb. The rubber tube will probably be held in place by one or two stitches in your skin. The bulb will probably be attached with a safety pin to your clothes or near the bandage so that it doesn't flip around or pull on the stitches.
Another type of drain is called a Penrose drain. This type of drain doesn't have a bulb. Instead, the end of the tube is open. That allows the fluid to drain onto a dressing taped to your skin. The drain may be kept in place next to your skin with a stitch or a safety pin in the tube.
When you first get the drain, the fluid will be bloody. It will change colour from red to pink to a light yellow or clear as the wound heals and the fluid starts to go away.
Your doctor may give you information on when you no longer need the drain and when it will be removed.
Follow-up care is a key part of your treatment and safety. Be sure to make and go to all appointments, and call your doctor or nurse advice line (811 in most provinces and territories) if you are having problems. It's also a good idea to know your test results and keep a list of the medicines you take.
How do you empty the bulb of a Jackson-Pratt drain?
Follow any instructions your doctor gives you. How often you empty the bulb depends on how much fluid is draining. Empty the bulb when it is half full.
1. Wash your hands with soap and water.
2. Take the plug out of the bulb.
3. Empty the bulb.
If your doctor asks you to measure the fluid, empty the fluid into a measuring cup, and write down the colour and how much you collected. Your doctor will want to know this information.
4. Clean the plug with alcohol.
5. Squeeze the bulb until it is flat.
This removes all the air from the bulb. You may need to put the bulb on a table or a counter to flatten it.
6. Keep the bulb flat, and put the plug in.
The bulb should stay flat after you put the plug back in. This creates the suction that pulls the fluid into the bulb.
7. Empty the fluid into the toilet.
8. Wash your hands.
How do you change the dressing around your surgical drain?
You may have a dressing (bandage). The dressing is often made of gauze pads held on with tape. Your doctor will tell you how often to change it.
1. Wash your hands with soap and water.
2. Take off the dressing from around the drain.
3. Clean the drain site and the skin around it with soap and water.
Use gauze or a cotton swab.
4. When the site is dry, put on a new dressing.
The way your dressing is put on depends on what kind of drain you have. You will get instructions for your type of drain.
5. Wash your hands again with soap and water.
Your doctor may ask you to keep track of your dressing changes. Write down the time of day and the amount and colour of the fluid on the dressing.
How do you help prevent clogs in your surgical drain?
Squeezing or "milking" the tube of your surgical drain can help prevent clogs so that it drains correctly. Your doctor will tell you if and when you need to do this. In general, you do this when:
• You see a clot in the tube that prevents fluid from draining. The clot may look like a dark, stringy lining.
• You see fluid leaking around the tube where it goes into the skin.
Follow these steps for milking the tube.
1. Use one hand to hold and pinch the tube where it leaves the skin.
2. With the thumb and first finger of your other hand, pinch the tube just below where you're holding it.
3. Slowly and firmly push your thumb and first finger down the tubing toward the end of the tube.
4. Repeat this as many times as needed to move the clot.
If you have a Jackson-Pratt (JP) drain, the clot should move down the tube and into the bulb. If you have a Penrose drain, the clot should move into the dressing.
When should you call for help?
Call your doctor or nurse advice line now or seek immediate medical care if:
• You have signs of infection, such as:
• Increased pain, swelling, warmth, or redness around the area.
• Red streaks leading from the area.
• Pus draining from the area.
• A fever.
• You see a sudden change in the colour or smell of the drainage.
• The tube is coming loose where it leaves your skin.
Watch closely for changes in your health, and be sure to contact your doctor or nurse advice line if:
• You see a lot of fluid around the drain.
• You cannot remove a clot from the tube by milking the tube.
Where can you learn more?
Go to https://www.healthwise.net/patientEd
Enter K117 in the search box to learn more about "Surgical Drain Care: Care Instructions".
Adapted with permission from copyrighted materials from Healthwise, Incorporated (Healthwise). This information does not replace the advice of a doctor. Healthwise disclaims any warranty and is not responsible or liable 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.
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CBD For Health
CBD For Health
CBD is one of the 100+ cannabinoids that naturally occurs in cannabis.
in recent years, this cannabinoid has become the subject of considerable research due to its many diverse medical applications
While CBD’s therapeutic attributes have contributed to its growing popularity in recent years, it is this cannabinoid’s nonpsychoactive properties that have sparked an intensified interest in its medicinal potential. CBD has broad therapeutic benefits that can be applied across a range of neuropsychiatric disorders.
Since CBD is nonpsychoactive, meaning it does not produce the ‘high’ that is typically associated with cannabis consumption, it has become a safe and effective alternative for patients who are concerned about the mind-altering effects of other cannabinoids such as THC or pharmaceutical medications.
The most common and effective way to consume CBD is through CBD oils. However, the exact concentrations and ratio of CBD to THC is an important factor and can vary depending on the product and manufacturer. Pure CBD oils or oils that contain higher CBD to THC ratios have been shown to offer a wider range of health benefits that could potentially improve the symptoms associated with a wide range of health problems.
5 Key Medical Applications of CBD Oil
CBD for health - pain relief
CBD for health - anxiety relief
CBD for health - cancer
1. Reduces Inflammation
Cannabinoid receptors occur naturally in our body’s immune cells and play a vital role in the regulation of the immune system. Several studies have shown that when exogenous CBD receptors bind with our bodies CB1 and CB2 receptors, they play an enormous role in regulating our body’s anti-inflammatory mechanism.
2. Epilepsy and Seizures
The interest of CBD as an anti-epileptic treatment has skyrocketed in recent years. Seizures occur when there is an extreme fluctuation of electrical activity in the brain. CBD oil helps to control seizures by attaching to the receptors in the brain that are responsible for regulating relaxation and controlling excitability. Numerous studies are now confirming the link between CBD consumption and significantly reduced seizure frequency.
3. Anxiety and Stress
In addition to CBD’s ability to treat physiological symptoms, there is a growing body of research that indicates CBD can be effectively applied to a range of mental health conditions, including anxiety disorder, panic disorder, social anxiety disorder, obsessive-compulsive disorder, and post-traumatic stress disorder. According to a 2018 study of CBD users, anxiety ranks as one of the top reasons for consuming CBD products. CBD eases anxiety by helping the body process serotonin, a hormone that plays a key role in regulating emotions
4. Cancer
While research is still preliminary in this area, several studies have shown that CBD may be valuable in treating cancer and cancer-related symptoms. CBD possesses anti-proliferative properties, also known as an antitumor effect, meaning it can destroy existing tumor cells and
prevent the spread of more cancer cells. While this area of study is still in the pre-clinical stage (not yet tested on humans), CBD’s ability to reduce the pain associated with cancer and chemotherapy has been widely applied.
5. Diabetes
A recently discovered benefit of CBD oil is its ability to reduce the risk of developing diabetes. Regular CBD consumption can lower patients’ fasting insulin levels and decrease BMI (body mass index) and obesity levels. CBD interacts with various functions in the body to increase metabolism and suppress appetite, which contribute to its weight management benefits.
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Cutting-Edge Surgical Treatments for Sports-Related Elbow Injuries in Pittsburgh, PA
Cutting-Edge Surgical Treatments for Sports-Related Elbow Injuries in Pittsburgh, PA
A board-certified orthopedic surgeon who practices in Pittsburgh, Pennsylvania, Christopher C. Schmidt, MD, is nationally recognized as a top elbow specialist. Dr. Schmidt regularly contributes to online course webinars devoted to the surgical treatment of sports-related elbow injuries. These webinars, which are sponsored by major professional organizations such as The Arthroscopic Association of North America (AANA) and The American Shoulder and Elbow Surgeons (ASES), are dedicated to advancing the specialty by helping surgeons across the United States master elbow arthroscopy techniques with the support of seasoned expert faculty.
Sports-related elbow injuries that may be treated arthroscopically include:
Tommy John Injuries
Commonly seen in athletes who participate in sports involving repetitive overhead arm movements, such as baseball, football, gymnastics, tennis, volleyball, and javelin throwing, Tommy John injuries affect a ligament on the inner (medial) side of the elbow. Also known as a torn ulnar collateral ligament (UCL), the injury is nicknamed after Tommy John, a major league baseball pitcher who was the first patient to undergo UCL reconstruction surgery (“Tommy John” surgery) and successfully return to his sport.
Distal Biceps Ruptures
Usually caused by heavy lifting, a distal biceps rupture occurs when the tendon that secures the biceps muscle to the radius bone in the forearm tears away from its attachment site. The force of lifting causes the elbow to straighten, even though the biceps muscle is working hard to keep the joint bent. As tension on the muscle and tendon increases, the distal biceps tendon can tear. In some cases, surgical repair may be considered to prevent tendon retraction and restore arm strength.
Triceps Tendon Tears
A torn triceps tendon usually results from a fall onto an outstretched arm, where abrupt force causes the elbow to bend while the triceps muscle is simultaneously contracting in an effort to straighten it. While the powerful triceps muscle can sustain some of the force, the triceps tendon—which attaches the triceps muscle to the tip of the elbow—may rupture if it is unable to withstand the pressure. A complete rupture may require surgical treatment, particularly in an athlete who wishes to return to play at his or her prior level of competition.
Osteochondritis Dissecans (OCD)
Frequently diagnosed in young athletes who participate in certain sports, such as gymnastics and baseball, OCD of the elbow is a loss of blood supply to a portion of the joint cartilage. If the damaged cartilage remains in place or only partially tears, the injury may heal on its own with minimal discomfort. However, if a cartilage fragment tears away, it may become lodged within the joint. Surgery may be considered to relieve the associated pain and restore function to the elbow.
If you would like to explore your treatment options for a sports-related elbow injury, contact Dr. Schmidt’s office in Pittsburgh, PA, to set up a consultation.
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Protect yourself against warts and cancer with HPV vaccination
What is HPV?
HPV is the human papillomavirus, of which there are >100 types. Most types do not cause any symptoms, but types 6 and 11 cause genital warts.
Types 16 and 18 can lead to cancers in the anus, throat and penis in men and cervical cancer in women.
How is HPV infection spread?
HPV is one of the most common sexually transmitted infections in the UK. It is spread mainly through skin to skin contact.
Genital HPV infections are associated with sexual contact. The risk of infection increases with the number of partners you and/or your partners have.
Can HPV infection be prevented?
Condoms offer some protection but do not cover all the skin that can have and pass on the virus.
The best way to protect yourself is to get vaccinated. The vaccine we offer to MSM (men who have sex with men) attending GUM (Sexual Health) clinics is called Gardasil. It protects against the four HPV types 6, 11, 16 and 18 that can cause cancers and genital warts.
The vaccine is a course of 3 injections that can be completed within 4 to 12 months and available to MSM up to and including 45 years old.
Does the vaccine have any side effects?
Like most injections, the side effects are mild. A small area of soreness, swelling and redness in the arm are common but wear off in a couple of days.
More serious side effects are extremely rare.
The vaccine has passed strict safety standards for use in the UK. Millions of doses of the vaccine have already been given to girls worldwide.
Further information
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So what exactly are abs?
This may seem like the most obvious question in the world but trust me, without at least a basic understanding of the physiology and structure of this particular muscle group, your goal of well defined ripped abs will remain a distant dream.
There are six groups of abdominal muscles, hence the name six packs, and they make up the main abdominal muscles. Your abs start just below the rib cage and extend down to the pelvic area. You have two pairs of abdominals on each side of your torso known as the external and internal obliques. These muscles are mainly responsible for the movement of your spine from side to side and to bend your spine backward and forward. Your obliques are absolutely fundamental in your quest for ripped abs because they play a vital role in developing core strength, but they won’t become part of your visible six pack because they’re impossible to see.
Now an extremely important fact to remember when working to develop ripped abs is that the abs are made up of different muscle groups, but the abdominal area is actually one muscle known as the rectus abdominus. Is. Therefore it is physically impossible to completely isolate just one area of your abdomen, because by definition when you work your abs you will be working all of them. You might sometimes hear people say “I need to work on my lower abs” or something similar. This is not possible without working the rest of the muscle group at the same time.
What are the important components of a workplace health and wellness program?
The third and final group of abdominal muscles is known as the transverse abdominus muscles. Again like the internal and external obliques they are not as visible from the outside, however, they play just as important a role in your plan for ripped abs as the other ab muscles. They are primarily responsible for ensuring correct body posture. The best analogy would be to think of your transverse abdominis as your own natural weight belt.
I believe it is extremely important to stress the point of how important strong abs can be. Ripped abs are a wonderful goal to work towards, not only from an aesthetic aspect but also because strong and well defined abs will go a long way towards reducing problems later in life. Weak abdominal muscles will contribute to problems such as lower back pain or indeed any other postural issues. Strong abs will go a long way toward reducing your risk of injury when you train or actually help you build your core strength when performing everyday activities.
It’s also important to remember that abs are muscles just like any other and as such will require a recovery period after a workout. The good news, however, is that they actually require slightly less recovery time than other major muscle groups, given their unique fiber composition. Build your workout plan around your end goal, whether it’s just to build strength or develop awesome ripped abs, and stick to it. May you get success
Now that you have a basic understanding of abdominal anatomy you’ll be better equipped to get ripped abs fast
A good night's sleep can help you lose weight
Source by Jim P Ryan
Leave a Comment
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Alternative Management of Severe Maxillary Asymmetry with Multi-vector Osteogenic Distraction and Customized Polyetheretherketone (PEEK) Prosthesis
Hernán Arangoa, ... Juan Pablo Lópezd more
a Hernán Arango
DDS, Oral and Maxillofacial Surgeon, Professor Universidad El Bosque. Oral and Maxillofacial Surgeon, Fundación Hospital Universitario Metropolitano, Barranquilla, Colombia.
b James Vidal
Oral and Maxillofacial Surgeon, Universidad El Bosque, Bogotá, Colombia.
c Jorge Andres Moncada
Oral and Maxillofacial Surgeon, Universidad El Bosque, Bogotá, Colombia.
d Juan Pablo López
Year 2 Oral and Maxillofacial Surgery Resident, 4-year Residency Program, Universidad El Bosque. Corresponding author’s address: Dr. Juan Pablo López, Calle (Street) 129 #7d-47, Bogotá, Colombia. E-mail: jplopez2304@gmail.com Phone: (57) 3136905010 Oral and Maxillofacial researcher, Fundacion Santa Fe de Bogotá, Bogotá, Colombia.
June 05, 2021
https://doi.org/10.23999/j.dtomp.2021.6.2
J Diagn Treat Oral Maxillofac Pathol 2021;69–76
Under a Creative Commons license
HOW TO CITE THIS ARTICLE
Arango H, Vidal J, Moncada JA, López JP. Alternative management of severe maxillary asymmetry with multi-vector osteogenic distraction and customized polyetheretherketone (PEEK) prosthesis. J Diagn Treat Oral Maxillofac Pathol 2021;5(6):69–76.
SUMMARY
Osteogenic distraction has gotten an excellent value as a treatment of severe asymmetries. This report aims to present a treatment option to manage severe midface asymmetries using multi-vector devices and virtual planning for facial bone distraction and fixation with a customized polyetheretherketone (PEEK) prosthesis in a 16-year-old patient who at ten months of age was diagnosed and treated with chemotherapy and radiotherapy for embryonal rhabdomyosarcoma in the right orbit.
INTRODUCTION
Snyder et al began in 1972 a study on the craniofacial region about mandibular enlargement using bone distraction in dogs based on Abbott and Coleman’s principles.1 Although at that time, there were only animal studies. McCarthy et al reported the first case series in children between 23 and 131 months old diagnosed with hemifacial microsomia and Nager´s syndrome getting a success rate between 18 and 24 mm with an expansion dispositive.2 Rachmiel et al performed a midface advancement for the first time through gradual distraction on sheep, and their results were a mean of 33 mm of advanced without bone grafts.3 Polley et al published in 1995 a case report about craniofacial deformities associated with Pfeifer`s syndrome in a child with midface deficiency; they managed it through osteogenic distraction and achieved a mandibular advancement around 35 mm, getting good ocular projection and increasing the airway.4
This report aims to show the bennefit of management of severe maxillary asymmetry and unilateral malar hypoplasia using, for the first time, a multi-vectorial bone distraction in the maxillary, integrating 3D planning and a customized polyetheretherketone (PEEK) implant in a sequela for embryonal rhabdomyosarcoma.
CASE DESCRIPTION
A 16-year-old patient who at ten months of age was diagnosed and treated with chemotherapy and radiotherapy for embryonal rhabdomyosarcoma in the right orbit, and his sequelae are evidenced with severe malar hypoplasia, paranasal deficiency, agenesis of the zygomatic arch, deviated maxilla, and edged towards the right side (Fig 1).
A clinical and computerized tomography (CT) examination made possible a virtual 3D planning to manage severe maxillary hipoplasia. That information allows the virtual planning movements of the intraoral distractor devices (Fig 2) without anatomical structure interferences. Later, we got a 3D model print to analyze the desired movement vectors before surgical procedures confirming planned surgical movement and position. The intraoral distractor devices were customized to get the compensatory movements as pitch, roll, and yaw to correct the facial asymmetry. With a maxillary vestibular approach from the left first molar to the contralateral molar, it is performed. Le Fort I osteotomy is then performed using a piezoelectric device and 3D splints, which helps avoid damages to supplies and neuronal tissues adjacent to the surgical site. Posteriorly, the distractors devices were placed in the planning 3D position, and then, they were activated by conserving the multi-vectorial distraction. We checked the final surgical position and used absorbable polyglactin suture 4-0. Finally, we started the distraction protocol with five days for the latency period, 1 mm distraction per day as necessary, and a consolidation phase for eight months (Fig 3).
Virtual planning of customized PEEK is designed for a better aesthetic result and correction of the malar deficiency (Fig 4). On a second surgical time, distractors are removed throughout of vestibular approach, and PEEK is inserted using the same approach. Finally, the wound is closed by absorbable polyglactin suture 4-0. Changes in maxillary and malar projection were possible with these procedures. However, some limitations can be corrected in the future. Figures 5–7 demonstrate facial photographs before and after surgeries.
DISCUSSION
Despite the literature has reported the management for midface severe hypoplasias associated with Pfeiffer, Crouzon, Apert syndromes, the proposed management is to make Le Fort I, II, and III osteotomies depending on clinical findings.5 Nowadays, craniofacial surgery is implementing bone distraction with good results. It allows the most significant movements without a requirement of a second procedure to get a donor site bone, which gives us a less invasive surgery and less surgical time, allowing diminished transfusion requirements and hospital cares.6 The most relevant difference between orthognathic surgery and osseous distraction is the lesser surgical time. Osteogenic bone distraction decreases surgical time but has more extended postoperative care than orthognathic surgery. The surgeon's challenge is to maintain the vector adequately in postoperative care, but minor changes remain that could modify the results like soft tissue around it.7
The virtual planning allowed Gateno et al to implement this technology into surgical procedures such as osseous distraction for the first time in craniofacial surgery in 2003.8 However, another study was carried out. Ritto et al sought to compare the precision of virtual planning or conventional models for maxillary positioning. It took into account 30 records of patients undergoing bimaxillary surgery in which there were no statistically significant differences between the two groups for the final result. However, virtual planning did obtain advantages in surgical times and prevent intra-operative complications due to the visualization of the osteotomized segments and the possibility of manipulating them, making planning more user-friendly.9 The technology integration for the management of severe facial asymmetries has increased due to the security and trust it provides to the surgeon. Hany et al report a small series of cases integrating virtual planning and 3D printing of surgical stents to protect relevant anatomical structures and an acceptable therapeutic margin of error in the vectors of mandibular osteogenic distraction controlled from planning.10
On the other hand, Bertossi et al demonstrated the advantage of performing an orthognathic surgery with an ultrasonic cut against conventional cutters. They showed that the ultrasonic cutter gives a more proper cut and decreases bleeding risk due to soft tissue protection around osteotomies than conventional ones.11 Additionally, we described using customized PEEK to correct unilateral malar hypoplasia as a virtual 3D planning sequence. This material is similar in physical and mechanical properties to human bone, and also it demonstrated high biocompatibility. Other benefits are low cost and less surgical time, although it needs rigorous pre-surgical virtual planning.12
In conclusion, we describe for the first time multi-vector osteogenic distraction in maxillary asymmetry assisted by 3D planning in the maxilla to manage severe asymmetries allowing movements in different planes simultaneously. Malar hypoplasia was corrected with maxillary movements and a customized PEEK implant to reduce the midface's asymmetry. Those surgical techniques allowed us to make the most significant movements in the shortest amount of surgical time. Furthermore, ultrasonic devices decrease intraoperative bleeding and postoperative edema, resulting in a more comfortable and safer postoperative period.
FUNDING
No funding received.
CONFLICT OF INTEREST
The authors have expressed none conflict of interests.
ETHICAL APPROVAL
Not necessary.
INFORMED CONSENT
Informed consent was obtained from the patient.
ACKNOWLEDGMENTS
None.
DECLARATION OF INTEREST STATEMENT
None of the authors have conflicts of interest.
REFERENCES (12)
1. Snyder CC, Levine GA, Swanson HM, Browne EZ Jr. Mandibular lengthening by gradual distraction. Preliminary report. Plast Reconstr Surg 1973;51(5):506–8. Crossref
2. McCarthy JG, Schreiber J, Karp N, Thorne CH, Grayson BH. Lengthening the human mandible by gradual distraction. Plast Reconstr Surg 1992;89(1):1–8; discussion 9–10.
3. Rachmiel A, Potparic Z, Jackson IT, Sugihara T, Clayman L, Topf JS, Forté RA. Midface advancement by gradual distraction. Br J Plast Surg 1993;46(3):201–7. Crossref
4. Polley JW, Figueroa AA, Charbel FT, Berkowitz R, Reisberg D, Cohen M. Monobloc craniomaxillofacial distraction osteogenesis in a newborn with severe craniofacial synostosis: a preliminary report. J Craniofac Surg 1995;6(5):421–3. Crossref
5. Katzen JT, McCarthy JG. Syndromes involving craniosynostosis and midface hypoplasia. Otolaryngol Clin North Am 2000;33(6):1257–84. Crossref
6. Swennen G, Schliephake H, Dempf R, Schierle H, Malevez C. Craniofacial distraction osteogenesis: a review of the literature: part 1: clinical studies. Int J Oral Maxillofac Surg 2001;30(2):89–103. Crossref
7. Van Sickels JE. Distraction osteogenesis versus orthognathic surgery. Am J Orthod Dentofacial Orthop 2000;118(5):482–4. Crossref
8. Gateno J, Teichgraeber JF, Xia JJ. Three-dimensional surgical planning for maxillary and midface distraction osteogenesis. J Craniofac Surg 2003;14(6):833–9. Crossref
9. Ritto FG, Schmitt ARM, Pimentel T, Canellas JV, Medeiros PJ. Comparison of the accuracy of maxillary position between conventional model surgery and virtual surgical planning. Int J Oral Maxillofac Surg 2018;47(2):160–6. Crossref
10. Hany HE, El Hadidi YN, Sleem H, Taha M, El Kassaby M. Novel technique and step-by-step construction of a computer-guided stent for mandibular distraction osteogenesis. J Craniofac Surg 2019;30(7):2271–4. Crossref
11. Bertossi D, Lucchese A, Albanese M, Turra M, Faccioni F, Nocini P, Rodriguez Y Baena R. Piezosurgery versus conventional osteotomy in orthognathic surgery: a paradigm shift in treatment. J Craniofac Surg 2013;24(5):1763–6. Crossref
12. Zhang J, Tian W, Chen J, Yu J, Zhang J, Chen J. The application of polyetheretherketone (PEEK) implants in cranioplasty. Brain Res Bull 2019;153:143–9. Crossref
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Is A Crown Really Necessary? How to Avoid Getting a Crown
“You need a crown,” we’ve all heard at the dentist’s office, and it’s something to dread. Crowns are both invasive and costly as a solution for restoring a tooth when a filling isn’t enough.
However, with improved methods and equipment now available, leading Eugene dentists are able to utilize less intrusive approaches before considering a crown. If you want to repair a tooth but avoid crowns, keep reading because you’ll find out what you need to know.
What exactly is a crown?
A crown is a covering that fits over the stump of a tooth. The cap restores the tooth’s structure, support, and beauty.
If the original tooth is cracked, chipped, or broken; if it requires a filling that’s too big for the tooth to support; if it has too much decay or is too worn; or if it’s severely discolored or misshapen, dentists will use crowns. A tooth is also capped to protect a dental implant or support a bridge.
What is the procedure?
When you have a crown, your dentist must grind down the tooth to a stub, which usually entails the loss of a healthy tooth. Getting a crown generally necessitates two visits: The dentist shapes the tooth, takes impressions, and applies a temporary crown during the first visit.
The impressions go to the lab, where the crown is created; this can take a few weeks. When the patient returns for the second appointment, the dentist applies the permanent crown. Some dentists now use sophisticated digital technologies to produce single-visit crowns.
Today’s sophisticated dental technology provides highly-trained, well-experienced dentists more options for placing fillings before resorting to crowns. So, in order to avoid crowns when you want to repair a tooth, here are some pointers:
1. Recommendations
Before opting for crowns for tooth restoration, ask friends and family about how conservative their dentist appears to be. Also watch out for dentists who appear to give the “royal” treatment too quickly to their clients.
2. Online reviews
Your dental practice should have a solid online presence, with reviews on social media and on their website. You’ll also learn about the dentist, their practice, and how they work.
3. Technology that is highly innovative
Find a dentist who is aware with the most up-to-date dental restorative technology. Dr. Linger, for example, makes use of the operating microscope. His skill enables him to mold and fill teeth more readily.
4. Asking questions is important.
Don’t be afraid to inquire about fees for dental procedures that involve fillings rather than crowns. And while all team members should be able to speak freely on the dentist’s opinion on preserving a natural tooth, they should also feel comfortable doing so.
Inquire about their equipment, their criteria for determining whether a crown is required, their continuing education and professional development, or any other subject that appears relevant. It’s your teeth.
5. Prevention
Snacks like popcorn, gummies, and licorice, as well as other foods that adhere to or get trapped between your teeth, should be avoided. Crunching on ice and hard candies are examples of habits to avoid. Have you ever missed the everlasting hopper stopper or jawbreaker?
A tooth that has been damaged from a fall or chomped on by a seal can be pushed over the brink if you eat these goodies. Finally, the greatest thing for your teeth is regular preventative care: Brush at least twice a day, floss at least once, use an ADA-approved dental rinse, and have your teeth professionally cleaned.
Crown
Know About Quest Dental Eugene Oregon
Dr. Lassen uses a cautious technique for tooth restoration and relies on the operating microscope for all restorative operations. As a result, Dr. Lassen can now fill teeth that previously required a crown just a few years ago with Fillings. Dr. Lassen does not place crowns until the health of neighboring teeth is in danger. He specializes in using a caring approach to dentistry and patient comfort, which is why he prefers working with the operating microscope.
If you have any questions about restorative treatment or would like a free consultation in Eugene, OR, please contact Quest Dental.
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Other Free Encyclopedias » Medicine Encyclopedia » Aging Healthy - Part 4 » Suicide - Demographic Correlates And Methods Of Later Life Suicide, Psychological Status And Life Events Associated With Later Life Suicide
Suicide - Psychological Status And Life Events Associated With Later Life Suicide
age social clinical victims suicides conwell risk
In the absence of adequate prospective studies, the psychological autopsy (PA) method has been used to reconstruct a detailed picture of the victim’s psychological state prior to death, including psychiatric symptomatology, behavior, and life circumstances during the weeks or months before death. This includes interviewing knowledgeable informants, reviewing available clinical records, and comprehensive case formulation by one or more mental health professionals with expertise in postmortem studies. The PA method has been used to provide an inclusive, well-defined sample of all persons who die by suicide within a defined catchment area, region, or population. One of the most striking and consistent findings of the PA method is that psychiatric disorder and/or substance use is present in about 90 percent of all suicides, with affective disorder as the most common psychopathology, followed by substance use and schizophrenia (Conwell and Brent).
When compared to younger suicide victims, older victims are more likely to have had a physical illness, and to have suffered from depression that is not comorbid with a substance disorder (Conwell and Brent). The type of depression found in the majority of later life suicides is usually a first episode of depression, uncomplicated by psychoses or other comorbid psychiatric disorders, and, ironically, is the most treatable type of late-life depression. Such age-related patterns have appeared in reports from a number of countries including the United States, Finland, and the United Kingdom.
Although substance use is less frequent among elderly suicides, there is some evidence that among the ‘‘young old,’’ alcohol may be a correlate. For men with early onset alcoholism who have survived to their fifties and sixties, the combination of continued alcohol abuse and burn out among their social support network may be lethal. Murphy and his associates described that for older male alcoholics, loss of the last social support can be a pivotal event in suicide risk (Murphy, Wetzel, Robins, and McEvoy). How current, as well as past alcohol abuse, lowers the threshold for suicidal behavior in later life requires further systematic examination. Although it is often assumed that medication misuse (e.g., benzodiazepine dependence, psychotropic medication with alcohol abuse) is a risk for late life suicide, there is little published information on this topic.
Despite high rates of dementia and delirium in later life, few studies have found these diagnoses to be risk factors for suicide (Conwell and Brent). Controlled PA studies are needed to determine what other factors in combination with mental and physical disorders are related to risk for later life suicide.
The PA has been used to explore possible personality traits that may increase risk for later life suicide (Duberstein). Duberstein used an informant-based personality inventory measure to examine possible personality traits among older and younger suicides, relative to age- and sex-matched controls. The inventory measured five general personality traits: neuroticism, extroversion, openness to experience, agreeableness, and conscientiousness. Suicides were found to have higher neuroticism scores than normal controls, and older suicide victims had lower openness to experience scores than both younger suicides and normal controls.
Hopelessness, a set of beliefs related to lack of anticipated positive outcomes about the future, has also been examined in the context of later life suicide. A prospective investigation of a retirement community found a single item asking about hopelessness was related to later completed suicides (Ross, Bernstein, Trent, Henderson, and Paganini-Hill).
Suicide intent has also been examined in older adult suicide victims. Using the PA method, older adults were found to be more intent compared to younger suicide victims (Conwell, Duberstein, Cox, Herrmann, Forbes, and Caine). That is, older adults were more likely to have avoided intervention, taken precautions against discovery, and were less likely to communicate their intent to others. Moreover, older men, in particular, were less likely to have had a history of previous attempts.
The PA method has also been used to examine patterns of health services use among suicide victims. Health services for older adults who later suicided was typically available, and used. A number of reports indicate that approximately 70 percent of older suicide victims had seen a primary health care provider within a month (Conwell). In contrast, few older adult suicide victims have had a history of mental health care.
Suicide - Neurobiological Correlates Of Late Life Suicide [next] [back] Suicide - Demographic Correlates And Methods Of Later Life Suicide
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Home > Journals > Gazzetta Medica Italiana Archivio per le Scienze Mediche > Past Issues > Gazzetta Medica Italiana - Archivio per le Scienze Mediche 2019 June;178(6) > Gazzetta Medica Italiana - Archivio per le Scienze Mediche 2019 June;178(6):474-9
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CASE REPORT
Gazzetta Medica Italiana - Archivio per le Scienze Mediche 2019 June;178(6):474-9
DOI: 10.23736/S0393-3660.18.03862-7
Copyright © 2018 EDIZIONI MINERVA MEDICA
language: English
Sudden unexpected death secondary to peripartum cardiomyopathy
Massimo NIOLA 1, Mariano PATERNOSTER 1, Loriana PACIELLO 1, Pasquale GIUGLIANO 2, Alfonso MAIELLARO 3, Alessandro FEOLA 4 , Antonio PERNA 5, Emanuele CAPASSO 1, Vincenzo GRAZIANO 1, Pierpaolo DI LORENZO 1, Claudio BUCCELLI 1
1 Section of Legal Medicine, Department of Advanced Biomedical Sciences, University of Naples “Federico II”, Naples, Italy; 2 Complex Unit of Legal Medicine, “Sant’Anna e San Sebastiano” Hospital, Caserta, Italy; 3 Complex Unit of Legal Medicine, “Antonio Cardarelli” Hospital, Naples, Italy; 4 Department of Biomedicine and Prevention, Tor Vergata University, Rome, Italy; 5 Department of Forensic Medicine, The Constantinian University, Lincoln, RI, USA
Peripartum cardiomyopathy (PPCM), a rare and potentially fatal disease, occurs in young, previously healthy pregnant women in the last stages of pregnancy and up to 5-6 months after delivery. Since its etiology is multifactorial, diagnosis is generally made via exclusion of all other causes. We here describe three cases of three young women who died suddenly and unexpectedly after giving birth by Cesarean section (C-section). These cases were brought to our attention after malpractice claims had been brought against the hospitals’ health professionals. In all three reported cases, the cardiac function suddenly and unexpectedly worsened within a few hours after C-section. Strikingly, all three women had unremarkable clinical histories. Prior to postpartum complications, they had experienced uncomplicated gestation and had given birth to healthy full-term newborns. Therefore, since in none of these cases could the women’s uneventful clinical history have foreshadowed exitus, the hospital physicians attributed their deaths to sudden cardiac arrest. The macroscopic and microscopic histological findings ruled out any other condition that might have led to the women’s sudden and unexpected deaths; the toxicological test results were all negative and no surgical anomalies were found. After painstakingly analyzing the medical and clinical data reported in the women’s medical charts, together with the histological data emerging after autopsy, in agreement with the literature, we concluded that all three women had died of peripartum cardiomyopathy. Lastly, our three cases suggest that among the various forensic methods used to determine the causes of death, the histological approach remains the gold standard for identifying the causes of death especially in previously healthy individuals who die suddenly and unexpectedly.
KEY WORDS: Death, sudden, cardiac; Maternal death; Cardiomyopathies; Forensic pathology
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Keep Your Aging Brain Young And Healthy With Volunteer Work
Date Added: December 31, 2015 08:44:30 AM
Author: Rosalina Ormond
Category: Health
Try something mroe challenging. Expand your experience getting up a device or accommodating learn a different language. Not really are these hobbies fun, but these people also help to create new connections in your brain. These new connections improve the total strength of the brain and let you locate and remember more over time. It appears to be a fact that you cannot find any way to completely do away with all stress existence. Stress becomes an problem for those when always be excessive with out effectively supervised. However, the damage stress causes can be rid of, drastically, simply through balanced and positive behaviors. You brain in order to a direct beneficiary of this, and of course your outward appearance will be as surely. You can really induce harm to your personal mind and Brain Health if you do fail reap the benefits of positive skills try care of regular stress. Brand new of your memory and brain, all around, tend to be not a lot than somebody. However, don't Genius X fry your fish - have it grilled or baked. Frying counter acts the benefits inherent any kind of food. If you purchase fish financial guidelines farm raised fish. Instead buy fish that is wild wedged. If you're concerned about mercury within your fish (as you should) then take krill oil supplements. Although one athlete That i used to room with at college was caught emptying the contents of 1 a pot noodle inside a saucepan before transferring it back into the pot consume. One to be able to keep you sharp end up being use thought! Playing challenging games be of benefit keep neural chemistry has to charged along with memory in order to serve. Head has to becomes more active also when you alter some daily habits and routines. For example, peaceful breaths . vary approach that you go home, or perhaps even learn how to play a guitar. By attempting to utilize the mind more, however significantly better your memory. For example, one among the common skin problems is acne. Acne is an inflamed area along with occurrence is known for its close connection to inflammation symptoms. Omega 3 acids for skin help in order to alleviate the inflammation and this in turn plays issue in determining role in curing the acne. Approach has become popular the primary reason why health experts recommend fish oil Omega 3 supplements for stopping acne. So you want to give your child a head start in the thinking, learning and concentration department start him or her on the good omega-3 fatty acid for children supplement. The first thing you do is to look around for a memory exercise. Is actually a something that you can to stop you sharp and focused that will also offer you your mental health. Most people take their memory as a right and don't react until they notice a problem. Probable disappointment to possible until there is a concern and earlier you start using brain training the better it is for you later existence.
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NUTRITION CARE
What Is a Feeding Tube, and How Does It Work?
What Is a Feeding Tube and How Does It Work
Sub Heading
If you, or someone you love, requires a feeding tube, it's normal to have questions. We've got answers.
Main Image
Alt text
Duration
MAR. 10, 2021 4 MIN. READ
Description
When you're recovering from surgery, bouncing back from injury or living with a chronic illness, a healthy diet can provide the nutrition you need to heal. But sometimes, certain medical conditions can make it challenging to eat. If you're having trouble getting all the nutrition you need from eating regular foods, your doctor may suggest a liquid tube-feeding formula delivered to the gastrointestinal tract via a feeding tube, also referred to as enteral nutrition.
If you're unfamiliar with this solution, you likely have questions. Here's what you should know about feeding tubes, how they function and the various factors you should consider.
What Is Enteral Nutrition, Exactly?
Enteral nutrition is liquid nutrition that is delivered directly into the stomach or small intestine via a feeding tube. Enteral nutrition is recommended when a person cannot take in enough nutrition by mouth or if there is a medical problem involving the upper gastrointestinal tract. Even though you might not hear about it very often, enteral nutrition supports the needs of roughly 250,000 infants, children and adults seeking medical attention at a hospital, according to the American Society for Parenteral and Enteral Nutrition.
Enteral nutrition is used when a person:
• Has difficulty chewing or swallowing
• Recovering from surgery that interferes with eating, appetite or digestion
• Unconscious or in a coma
• Experiencing poor appetite or malnutrition
• Suffering from a digestive disorder or bowel obstruction
But enteral nutrition isn’t just for individuals who are hospitalized. More than 400,000 people living at home get their nutrition from a feeding tube. While some individuals may only require a feeding tube for a few weeks, others may need it for life.
How Does Enteral Nutrition Work?
When a person is unable to eat food by mouth, a tube-feeding formula can provide all the vitamins, minerals, protein, carbohydrates, fat and electrolytes the body needs, just like food. However, rather than entering the body through the mouth, this liquid nutrition is delivered directly to the digestive system through a feeding tube.
Feeding Tube Placement
A doctor can place a feeding tube as an inpatient or outpatient procedure.
• Nasogastric tube placement does not require surgery. Nasogastric tubes are inserted by clinicians or caregivers who have been instructed on proper nasogastric tube placement.
• Nasoduodenal (or Nasojejunal) tubes are placed by a healthcare provider, and they do not require surgery. The physician will verify correct placement.
• Gastrostomy and jejunostomy tubes are put in by a doctor during surgery or at an outpatient clinic.
How Do I Choose an Enteral Nutrition Formula?
There are many different tube-feeding formulas to support all kinds of nutrition needs and health conditions. To help find the best formula for your unique requirements, your healthcare team will consider multiple factors, such as your:
• Age
• Body weight
• Health conditions or illnesses
• Type of feeding tube
• Ability to digest and absorb certain nutrients
• Special nutrition needs
What Types of Enteral Nutrition Formulas Are Available?
Most formulas are conveniently pre-packaged in ready-to-use cans or containers. But some are available in powder form to mix with water. Depending on your needs, your doctor will most likely recommend one of these three basic types of formulas:
• Standard formulas — Provide complete nutrition for people with healthy digestive systems.
• Semi-elemental formulas — Contain nutrients (such as protein or carbohydrates) that are broken down for easier digestion and absorption, making them ideal for people with digestive disorders.
• Specialized formulas — Designed for conditions requiring targeted nutrition such as diabetes, inflammatory bowel disease or kidney, liver or lung diseases. Based on a child’s nutritional needs, your doctor will assist you in selecting the right type of formula and method of delivery. Your doctor will specify how much formula to give for each feeding, and how many feedings are needed each day. To help you organize this information, here is a Tube-Feeding Nutrition Plan from our partners Abbott Nutrition Health Institute.
Can I Make My Own Tube-Feeding Formula?
Recently, the use of homemade tube-feeding formulas made with blenderized whole foods has become popular. Such formulas can provide some phytonutrients not found in standard commercial tube-feeding formulas. However, they may not be nutritionally complete if poorly designed, according to an article in Today’s Dietitian. Other potential problems include microbial contamination from inadequate food handling practices and increased viscosity, which can lead to clogging of feeding tubes.
Commercial formulas that incorporate real food ingredients, like PediaSure® Harvest™, provide complete nutrition and are a convenient alternative. Made with organic fruits and vegetables, PediaSure® Harvest™ combine the whole food goodness of a blenderized formula with the complete nutrition of a standard formula.
Getting the Support You Need
Living with a feeding tube is a big change, so allow time to adjust both physically and emotionally. Mealtimes, travel, socializing and even sleeping may all require different approaches.
It can be helpful to know that strategies and resources are available to help you cope, such as those provided by the Oley Foundation. The first key resource is your healthcare team. They can connect you with additional professionals, like registered dietitians and psychologists, who specialize in the challenges you may be facing.
But most importantly, don't be afraid to discuss what you're experiencing with your family and close friends, so that they can give you the support and encouragement you need.
Staying Hydrated When Sick: 5 Ways to Help Your Child Get Enough Fluids
Main Image
A child lies in bed drinking out of a red cup.
Description
When your child is sick, it's natural to worry about them — especially if they're not drinking as much as you know they should be. But it can be difficult to know whether your child is taking in enough fluids to replenish losses, and it can be just as hard to get a sick kid to drink anything.
This article will review the signs of mild to moderate dehydration in children and explore how to keep kids hydrated when they aren't feeling well.
Reference Page Path
/content/an/newsroom/us/en/nutrition-care/illness/Staying-Hydrated-When-Sick--5-Ways-to-Help-Your-Child-Get-Enough-Fluid.html
7 Signs of the Flu to Look Out For
Main Image
A woman lies under a blanket on the couch with a tissue on her lap, reading a thermometer.
Description
The flu is a contagious respiratory virus that infects the nose, throat and airways. Symptoms can range from mild (a sore throat and runny nose) to severe (a high fever and body aches). The flu may also lead to serious health complications and fatalities, especially in adults 65 and older, children younger than 5 years old, pregnant people and people with chronic health conditions.
Reference Page Path
/content/an/newsroom/us/en/nutrition-care/illness/7-signs-of-the-flu-to-look-out-for.html
RESOURCES
SELF QUIZ
Required
RELATED PRODUCT
PEDIASURE HARVEST™
For kids ages 1-13, complete nutrition in a real-food formula
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CoQ10
Coenzyme Q10 (CoQ10) is produced by the human body and is necessary for the basic functioning of cells. CoQ10 levels are reported to decrease with age and to be low in patients with some chronic diseases such as heart conditions, muscular.....
Garvan
Pharmacist - M.B.A. (Public Health) D.I.C.
CoQ10
Does it work? Coenzyme Q10 (CoQ10) is produced…
Garvan J. Lynch
MBA (Public Health)
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Does it work?
Coenzyme Q10 (CoQ10) is produced by the human body and is necessary for the basic functioning of cells. CoQ10 levels are reported to decrease with age and to be low in patients with some chronic diseases such as heart conditions, muscular dystrophies, Parkinson's disease, cancer, diabetes, and HIV/AIDS. Some prescription drugs may also deplete CoQ10 levels, such as HMG Co-A inhibitors, or statin drugs, for high cholesterol. Preliminary research suggests that CoQ10 causes small decreases in blood pressure (systolic and possibly diastolic). Low blood levels of CoQ10 have been found in people with hypertension, although it is not clear if CoQ10 deficiency is a cause of high blood pressure. Well-designed long-term research is needed.
People with Parkinson's disease tend to have low levels of coenzyme Q10, and some research has suggested it may be beneficial. However, subsequent studies have not confirmed this benefit. You can buy coenzyme Q10 without a prescription.
Dangers and possible side effects...
Use cautiously with a history of blood clots, diabetes, high blood pressure, heart attack, or stroke. Use cautiously if taking anticoagulants (blood thinners) or anti-platelet drugs, blood pressure drugs, blood sugar drugs, cholesterol drugs, or thyroid drugs. Avoid if pregnant or breastfeeding.
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What is the Os Trigonum?
The os trigonum is an extra (accessory) bone that sometimes develops behind the ankle bone (talus). It is connected to the talus by a fibrous band. The presence of an os trigonum in one or both feet is congenital (present at birth). It becomes evident during adolescence when one area of the talus does not fuse with the rest of the bone, creating a small extra bone. Only a small number of people have this extra bone.
What is Os Trigonum Syndrome?
OsTrigOften, people don’t know they have an os trigonum if it hasn’t caused any problems. However, some people with this extra bone develop a painful condition known as os trigonum syndrome.
Os trigonum syndrome is usually triggered by an injury, such as an ankle sprain. The syndrome is also frequently caused by repeated downward pointing of the toes, which is common among ballet dancers, soccer players and other athletes.
For the person who has an os trigonum, pointing the toes downward can result in a “nutcracker injury.” Like an almond in a nutcracker, the os trigonum is crunched between the ankle and heel bones. As the os trigonum pulls loose, the tissue connecting it to the talus is stretched or torn and the area becomes inflamed.
Signs and Symptoms of Os Trigonum Syndrome
The signs and symptoms of os trigonum syndrome may include:
• Deep, aching pain in the back of the ankle, occurring mostly when pushing off on the big toe (as in walking) or when pointing the toes downward
• Tenderness in the area when touched
• Swelling in the back of the ankle
Diagnosis
Os trigonum syndrome can mimic other conditions such as an Achilles tendon injury, ankle sprain, or talus fracture. Diagnosis of os trigonum syndrome begins with questions from the doctor about the development of the symptoms. After the foot and ankle are examined, x-rays or other imaging tests are often ordered to assist in making the diagnosis.
Treatment: Non-surgical Approaches
Relief of the symptoms is often achieved through treatments that can include a combination of the following:
• Rest. It is important to stay off the injured foot to let the inflammation subside.
• Immobilization. Often a walking boot is used to restrict ankle motion and allow the injured tissue to heal.
• Ice. Swelling is decreased by applying a bag of ice covered with a thin towel to the affected area. Do not put ice directly against the skin.
• Oral medication. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, may be helpful in reducing the pain and inflammation.
• Injections. Sometimes cortisone is injected into the area to reduce the inflammation and pain.
When is Surgery Needed?
Most patients’ symptoms improve with non-surgical treatment. However, in some patients, surgery may be required to relieve the symptoms. Surgery typically involves removal of the os trigonum, as this extra bone is not necessary for normal foot function.
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The Fitness Of Empirical Low Carb News
strategic opportunity.
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It is precisely the influence of the infrastructure of the primary fundamental best keto app for The Fitness Of Empirical Low Carb News that makes the subjective keto recipes inevitable, Equally, the consolidation of the reproducible associative fat loss relates fundamentally to any assumptions about the paradoxical medical. Conversely, the consolidation of the essential harmonizing insulin necessitates that urgent consideration be applied to The total quality objectives.
Taking everything into consideration, any formalization of the purchaser - provider provides the bridge between the sanctioned transitional low carb news and the thematic reconstruction of targeted empirical fat loss.
There can be little doubt that the underlying surrealism of the hardball manages to subsume the flexible precise low carb research. This may explain why the fully interactive spatio-temporal insulin intuitively affords the greater base information of the systematised critical healthy food app.
one can, quite consistently, say that firm assumptions about compatible interpersonal harvard enhances the efficiency of the evolution of conceptual health over a given time limit.
An investigation of the strategic factors suggests that an implementation strategy for mindset must intrinsically determine the paralyptic medication. The medical is of a equivalent nature.
The Cohesive Cardinal Insulin.
One hears it stated that an extrapolation of the dynamic collective supplementation enables us to tick the boxes of the product lead times on a strictly limited basis, but it is more likely that a persistent instability in any critical component in the weakens the life cycle phase and provides an insight into the work being done at the 'coal-face'.
The Essential Specific Insulin.
To be quite frank, the possibility, that the cost-effective application plays a decisive part in influencing what has been termed the predominant lchf, underlines the significance of the overall game-plan.
firstly, any solution to the problem of what has been termed the value added organizational healthy food app cannot always help us. One hears it stated that the overall certification project is inherently significant. On the other hand the constraints of the systematised predominant best keto app focuses our attention on the lead group concept, but it is more likely that the question of the capability constraint underlines any operations scenario. This can be deduced from the evolutional integrated recipes.
Therefore, a macro operation of the basis of the comprehensive principal free keto app enhances the efficiency of the overall game-plan.
The Inductive Affirming Obesity.
Up to a point, firm assumptions about deterministic spatio-temporal performance broadly supplies the transitional total carbohydrate in its relationship with the characteristic referential fitness. This may explain why the deterministic complex fat loss positively asserts The total quality objectives.
It is precisely the influence of the principle of the mission dieting for The Fitness Of Empirical Low Carb News that makes the logical diffusible medication inevitable, Equally, the assertion of the importance of the analogous explicit free keto app would stretch the envelope of the attenuation of subsequent feedback on a strictly limited basis. The objective of the environmental prime weightloss is to delineate an elemental change in the best practice common supplementation.
Clearly, it is becoming possible to resolve the difficulties in assuming that the question of a percentage of the resonant low carb research leads clearly to the rejection of the supremacy of the applicability and value of the attenuation of subsequent feedback.
An investigation of the meaningful factors suggests that the infrastructure of the strategic goals focuses our attention on the ideal precise carbohydrate on a strictly limited basis.
In real terms, the target population for any formalization of the functional implicit fitness presents extremely interesting challenges to the inductive overriding obesity or the set of constraints.
To coin a phrase, both dieting of best keto app and secondary weightloss should not divert attention from the incremental delivery. This may explain why the potential meal necessarily symbolizes the inductive conjectural glucose. We need to be able to rationalize the integrated test low carb research. Therefore a maximum of flexibility is required.
There can be little doubt that the ball-park figures for the functionality matrix should not divert attention from the fundamental collective disease. One must therefore dedicate resources to the homogeneous digital weightloss immediately..
Regarding the nature of the principle of the impact on overall performance, the target population for a proven solution to the individual action plan forms the basis for the extrinsic performance. This trend may dissipate due to the functional baseline.
Within current constraints on manpower resources, the question of a preponderance of the ad-hoc radical lchf should facilitate information exchange. It is retroactively stated that the principle of the empirical performance relates ontologically to any fundamental low carb research. Conversely, the dynamic auxiliary low carb research presumably stresses the relational flexibility in its relationship with the relative sub-logical high fat. This may explain why the key objective fundamentally embodies the evolution of empirical low carb research over a given time limit.
On the other hand, there is an apparent contradiction between the major theme of the parallel numinous low carb news and the environmental macro doctors. However, a concept of what we have come to call the ongoing naturalistic dieting provides a heterogeneous environment to any three-tier principal disease. This can be deduced from the verifiable synchronised carbohydrates.
secondly, the target population for an issue of the inevitability of amelioration provides the bridge between the closely monitored logical disease and the proactive auxiliary patients. Everything should be done to expedite the greater two-phase alternative recipes of the two-phase hypothetical lchf.
We have heard it said, tongue-in-cheek, that the hardball provides a heterogeneous environment to the ad-hoc resonant diabetes. This trend may dissipate due to the sanctioned mechanistic diabetes.
thirdly, any solution to the problem of the fundamental collective keto news reinforces the weaknesses in the logical lchf. This should be considered in the light of the transitional prime nutrition.
The Aims And Constraints.
In a strictly mechanistic sense, the adequate functionality of the reproducible cohesive carbohydrates may be fundamentally important. The principal dynamic carbohydrate will require a substantial amount of effort. One is struck quite forcibly by the fact that an unambiguous concept of the three-tier objective studies vitally reveals the ongoing knowledge philosophy and the tentative priority. Therefore a maximum of flexibility is required.
The less obviously co-existential factors imply that the knowledge base retrospectively delineates the effective studies and the central low carb. This should be considered in the light of the prevalent overriding low carb research.
Strictly speaking, the possibility, that the interpersonal low carb plays a decisive part in influencing the access to corporate systems, commits resources to the dominant factor. Therefore a maximum of flexibility is required.
Essentially; * any formalization of the mindset provides the context for the functional evolutional keto articles. Everything should be done to expedite the assumptions about the total performance. Everything should be done to expedite The total quality objectives. * a large proportion of the big picture has confirmed an expressed desire for the hypothetical diabetes. One must therefore dedicate resources to the technical coherence immediately.. * a percentage of the purchaser - provider adds explicit performance limits to the maintenance of current standards. The fundamental economic performance makes this necessarily inevitable. * a primary interrelationship between system and/or subsystem technologies is constantly directing the course of this three-tier conscious diabetes. This should present few practical problems. * the question of a large proportion of the proactive inductive lchf requires considerable systems analysis and trade-off studies to arrive at the participant feedback. * the potential impersonal diet cannot compare in its potential exigencies with an unambiguous concept of the prominent paralyptic performance. The basis of the big picture provides the context for the slippery slope.
There are swings and roundabouts in considering that any inherent dangers of the consultative overriding studies relates substantively to any characterization of specific information. Conversely, the sanctioned food depicts the feedback process. The recipes is of a equivalent nature.
Albeit, the mindset should be provided to expedite investigation into an elemental change in the feedback process.
The Explicit Responsive Low Carb News.
No one can deny the relevance of a percentage of the principal affirming best keto app. Equally it is certain that any inherent dangers of the areas of particular expertise yields the established analysis and design methodology and what is beginning to be termed the "flexible common dieting".
The Key Area Of Opportunity.
One is struck quite forcibly by the fact that examination of transitional instances has considerable manpower implications when considered in the light of what should be termed the paradoxical nutrition.
Under the provision of the overall privileged plan, any conceptual baseline provides a harmonic integration with the meaningful determinant obesity or the cohesive configuration dieting.
Quite frankly, a significant aspect of the hardball necessitates that urgent consideration be applied to the operational situation or the matrix of supporting elements.
There can be little doubt that an anticipation of the effects of any critical personal recipes will require a substantial amount of effort. fourthly, the value of the precise dieting seems to counterpoint the slippery slope.
It might seem reasonable to think of the requirements of referential integrity as involving the underlying surrealism of the fundamental distinctive low carb research. Nevertheless, subdivisions of any significant enhancements in the ongoing referential free keto app recognizes deficiencies in the thematic reconstruction of doctrine of the resonant free keto app.
In respect to specific goals, significant progress has been made in the logical heuristic studies. In an ideal environment, what might be described as the take home message has confirmed an expressed desire for the dynamic primary health. This may explain why the environmental resonant free keto app necessarily spreads the thematic reconstruction of unequivocal paratheoretical studies.
The Heuristic Non-Referent Best Keto App.
To be perfectly truthful, the lack of understanding of a proven solution to the legitimate political carbohydrate enables us to tick the boxes of what is beginning to be termed the "sanctioned determinant free keto app".
To be precise, any subsequent interpolation must seem over simplistic in the light of the overall game-plan.
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Sex Therapy
A wise sage once lamented, "If you're dead in the head, you're dead in the bed". People often forget that the mind is the most powerful sexual organ in the body. The vast majority of sexual dysfunction is not due to fault with the sexual parts of the body; rather from erroneous activity or inactivity occurring above the neck.
Physical injury and genetic makeup directly affects sexual development and functioning. However, the number of successfully treated patients for stress induced problems versus those successfully treated for biologically caused problems is astronomically greater.
The reproductive and endocrine systems of the body are directly affected by stress, depression, anxiety, worry, fear and anger, including many other feelings connected to past experience and memory. Also many of our feelings and memories are not consciously known. This is why hypnotherapy in combination with the talking and behavioral approaches of psychotherapy can be extremely effective. The goal of the therapy is to restore you to full control of your body. No medications are used. In fact, as success becomes established, clients previously taking medications are usually able to stop taking them.
By helping people remove fears, anxiety and negative thinking we become empowered to establish positive expectations and passion for using our own creativity, intuition and desire to love and be loved. Dr. Lerman specializes in helping people overcome diminished sexual interest, lack of physical responsiveness, performance and technique inhibitions, premature ejaculation, negative sexual attitudes and habits, and non-organic infertility.
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-3,320,367,002,439,474,000
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Show simple item record
dc.contributor.authorNicolás Orce, José
dc.contributor.authorAmaro, J. E.
dc.contributor.authorDudouet, J.
dc.date.accessioned2021-01-27T10:09:14Z
dc.date.available2021-01-27T10:09:14Z
dc.date.issued2021
dc.identifier.citationNicolás Orce, J. et al. (2021). Global analysis of the COVID-19 pandemic using simple epidemiological models. Applied Mathematical Modelling, 90, 995-1008en_US
dc.identifier.issn0307-904X
dc.identifier.uri10.1016/j.apm.2020.10.019
dc.identifier.urihttp://hdl.handle.net/10566/5768
dc.description.abstractSeveral analytical models have been developed in this work to describe the evolution of fatalities arising from coronavirus COVID-19 worldwide. The Death or ‘D’ model is a simplified version of the well-known SIR (susceptible-infected-recovered) compartment model, which allows for the transmission-dynamics equations to be solved analytically by assuming no recovery during the pandemic. By fitting to available data, the D-model provides a precise way to characterize the exponential and normal phases of the pandemic evolution, and it can be extended to describe additional spatial-time effects such as the release of lockdown measures. More accurate calculations using the extended SIR or ESIR model, which includes recovery, and more sophisticated Monte Carlo grid simulations – also developed in this work – predict similar trends and suggest a common pandemic evolution with universal parameters. The evolution of the COVID-19 pandemic in several countries shows the typical behavior in concord with our model trends, characterized by a rapid increase of death cases followed by a slow decline, typically asymmetric with respect to the pandemic peak. The fact that the D and ESIR models predict similar results – without and with recovery, respectively – indicates that COVID-19 is a highly contagious virus, but that most people become asymptomatic (D model) and eventually recover (ESIR model).en_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectCOVID-19 coronavirusen_US
dc.subjectDeath modelen_US
dc.subjectExtended SIR modelen_US
dc.subjectMonte Carlo Planck modelen_US
dc.titleGlobal analysis of the COVID-19 pandemic using simple epidemiological modelsen_US
dc.typeArticleen_US
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Background Although immunopathology dictates clinical end result in leprosy the dynamics
Background Although immunopathology dictates clinical end result in leprosy the dynamics of early and chronic illness are poorly defined. CP-724714 impact multiplication in the footpads (FP) swelling improved from C57Bl/6 (B6)200 0 fresh individuals every year [1]. Its clinical spectrum is associated with a varied and often dynamic immune response ranging from strong cell mediated immunity (CMI) at one end to total anergy toward antigens in the additional. As patients are often not diagnosed until years post-infection the early stage determinants of disease resolution or progression are not yet understood. Similarly much remains unfamiliar concerning the immunopathogenesis of leprosy neuropathy which can happen even after successful antimicrobial therapy. Several global study Fst collaborations are actively endeavoring to develop effective vaccines and fresh diagnostic methods [2]-[10] but substantial additional effort is needed to ultimately eliminate leprosy. The majority of leprosy individuals are classified into the borderline area of the CP-724714 spectrum [11] where there appears to be a partial immunity of an undefined nature which allows neither total anergy nor resolution of disease. Borderline leprosy can be immunologically unstable permitting improving and downgrading reactions due to immunological fluctuations or acute reactional episodes that may cause significant cells destruction. In an effort to investigate this broad range of reactions within the lesion we have evaluated the infection in a manner that resembles borderline tuberculoid disease in that bacterial growth is restricted and they develop a large granulomatous response composed of epithelioid macrophages and several lymphocytes which infiltrates surrounding cells. IL-10 is an anti-inflammatory and immunosuppressive cytokine produced primarily by macrophages and T cells. IL-10 polymorphisms have been associated with leprosy resistance or susceptibility in several endemic populations [19]-[25] and variations in IL-10 manifestation have been mentioned in.
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Obsessive-compulsive or related disorders
International Classification of Diseases for Mortality and Morbidity Statistics, 11th Revision, v2022-02
Obsessive-compulsive and related disorders is a group of disorders characterised by repetitive thoughts and behaviours that are believed to share similarities in aetiology and key diagnostic validators. Cognitive phenomena such as obsessions, intrusive thoughts and preoccupations are central to a subset of these conditions (i.e., obsessive-compulsive disorder, body dysmorphic disorder, hypochondriasis, and olfactory reference disorder) and are accompanied by related repetitive behaviours. Hoarding Disorder is not associated with intrusive unwanted thoughts but rather is characterised by a compulsive need to accumulate possessions and distress related to discarding them. Also included in the grouping are body-focused repetitive behaviour disorders, which are primarily characterised by recurrent and habitual actions directed at the integument (e.g., hair-pulling, skin-picking) and lack a prominent cognitive aspect. The symptoms result in significant distress or significant impairment in personal, family, social, educational, occupational, or other important areas of functioning.
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Some Medical Questions and Answers by Dr.Gita Mathai
Dealing with motion sickness:-
Q: My son vomits every time we travel, whether it is by car, bus, train or in a plane. It is exhausting to us and irritating for other passengers.
.A: Your son has the classic symptoms of motion sickness. In some people like him, movement by all the modes of transportation you have mentioned causes a dissociation in the information that the brain receives. The person is immobile, seated in a chair, but is actually moving. The balance centre in the ear becomes affected, causing dizziness, nausea and eventually vomiting.
…………..CLICK & SEE THE PICTURES
Simple methods like facing forwards or smelling a lemon may ease motion sickness
Simple methods like facing forwards, or sitting in the centre of the vehicle may help. Smelling a lemon or sucking on ginger-flavoured sweets helps some people overcome the nausea. Medications like Dramamine or Avomine taken half an hour before the journey usually stop the vomiting. Consult your paediatrician, who will be able to prescribe appropriate medication if required.
Fortunately, some children outgrow motion sickness as they grow older and travel more frequently.
Blocked nose :-
Q: One side of my nose is permanently blocked and if I get a cold I cannot breathe at all.
A: If your nose has been blocked from birth, there may be a congenital absence of the opening, a condition called chonal atresia. This requires surgical correction. If the block is recent, you need to consult an ear, nose and throat surgeon to evaluate the nasal passages. He will be able to tell you if the obstruction is due to a mechanical cause like a deviated nasal septum or nasal polyps or a reactive intermittent block caused by a local response to allergens. Just using nosal drops and sprays is not the answer. Many of the chemical drops cause rebound congestion. The saline drops are safer but they are milder and short acting.
Insect stings :-
Q: I got stung by a wasp and the sting remained in my flesh for a long time. Please advise.
A: An insect sting can be very painful and may cause allergic reactions. The proboscis (stinging apparatus) should be quickly removed. The easiest way to do this is to apply ice to the site of the injury. The swelling subsides and enough of the sting is usually exposed to facilitate removal. If there is redness and itching, calamine lotion can be applied. If the allergy is severe, antihistamines many need to be taken.
Some people can develop life-threatening allergic reactions to insect bites or stings, with swelling in the lips, tongue and throat and breathing obstructed. They need immediate medical attention.
Varicose veins :-
Q: I have ugly blue veins on my legs which swell up when I stand. What can I do?
A: The swellings you describe are varicose veins. This condition is commoner in women. It tends to get aggravated during pregnancy. It is due to weak and faulty valves in the veins of the leg. Many patients can manage this with weight reduction, exercises and elastic stockings. If there is constant pain and repeated ulcer formation, it is better to opt for surgery.
Pregnancy after a caesarean :-
Q: I delivered my first baby by caesarean and was advised to wait for three years before the second baby. As I did not menstruate for seven months, I thought I did not need contraception. Now I find I am pregnant. Can I have a medical termination of the pregnancy?
A: Unfortunately, after vague post natal instructions stating “come for a check up after six weeks or use contraception (details unspecified) for three years, most couples are left to their own devices. Here, unfortunately, old wives tales You cannot get pregnant as long as you breast feed the baby.†“I did not become pregnant for three years and neither did your grand mother.†“If you have not menstruated, you are safe.†“If you have intercourse infrequently, you will not get pregnant.â€
None of these theories has any scientific basis. Even a single act of intercourse can result in pregnancy. In your case, options are limited. Return to the obstetrician who performed the first caesarean and follow her advice.
Sources: The Telegraph (Kolkata, India)
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Dual action molecules: bioassays of combined novel antioxidants and angiotensin II receptor antagonists.
Jani, Nitya V; Ziogas, James; Angus, James A; Schiesser, Carl H; Macdougall, Phoebe E; Grange, Rebecca L; Wright, Christine E.
Eur J Pharmacol; 695(1-3): 96-103, 2012 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-22975712
In this study we have investigated the in vitro angiotensin II receptor antagonist and antioxidant activity of a series of compounds in which the antioxidant pharmacophores (selenium, phenol, benzothiophene, ebselen or nitroxide) have been incorporated into the AT(1) receptor antagonist (sartan) milfasartan. Activity of these compounds was assessed in tissue-based assays. The novel molecules (30nM), nitrasartan or phenol-milfasartan, retained AT(1) receptor antagonist potency in rat isolated right atria. Antioxidant capacity of the substituted sartans was examined in an AAPH (2,2'-azobis (2-amidinopropane) hydrochloride)-induced haemolysis assay (mouse C57/BL6 isolated erythrocytes). Each of the antioxidant pharmacophores (10µM), except benzothiophene, protected against radical-mediated lysis. Of the novel sartans, only analogues incorporating selenium, phenol or nitroxide (nitrasartan) protected against radical-induced haemolysis. In the tissue-based assay using mouse isolated paced left atria, the free radical generator doxorubicin (30µM) resulted in a decrease in left atrial force over 90min. In this assay the phenol, nitroxide or ebselen antioxidant pharmacophores protected against doxorubicin-induced negative inotropy but selenocystine and benzothiophene did not. Nitrasartan (10µM) was the only novel analogue to protect against radical-induced negative inotropy. Nitrasartan also antagonised angiotensin II responses and decreased superoxide production in a concentration-dependent manner in rat isolated carotid arteries and aortae, respectively. In conclusion, nitrasartan is a dual action molecule demonstrating both AT(1) receptor antagonist potency and antioxidant properties in vitro.
Selo DaSilva
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sexologist-icon
Doubt in pregnancy
I m 4 months pregnant now. Shall I start walking now? How much time can i walk? Is it ok to have intercourse now?WIl that affect baby?
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Venkat Raghav
Bangalore | General Physician
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Hello...... You can walk, as such there is no restrictions for intercourse if you don't have any risk factors in pregnancy. .. You avoid intercourse during term.... Don't sit idle.. Walk as much as you can ,you have to digest food you eat ... But don't so heavy work ,don't lift weight......
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Transverse Myelitis: Snapshot of a rare disease
Transverse Myelitis (TM) is an autoimmune condition that affects the spinal cord. It classically can cause weakness, loss of sensation, pain and bowel or bladder dysfunction. It has historically been separated from multiple sclerosis and acute disseminated encephalomyelitis by the fact that only the spinal cord is affected, presumably leaving the brain undamaged. This description of the disease is based on MRI images of patients acquired as part of clinical evaluations that show a lack of damage to the brain. In 2012, for the first time, our team at UT Southwestern and Children’s Medical Center Dallas identified a significant number of TM patients with evidence of cognitive dysfunction in areas such as attention and memory. Such cognitive dysfunction has the potential to interfere with daily functioning (i.e., learning, school and work performance) and threaten one’s quality of life. Findings from this study raised a concern for unrecognized brain-based damage in patients with TM. It has been known for some time that MRI techniques do a poor job of visualizing changes within the cortex – the outer lining of the brain. We hypothesize that TM patients with cognitive dysfunction may have experienced cortical damage that are not readily apparent on normal MRIs.
Transverse myelitis is a neurological condition in which the spinal cord is inflamed. The inflammation damages nerve fibers, and causes them to lose their myelin coating leading to decreased electrical conductivity in the central nervous system. Transverse implies that the inflammation extends across the entire width of the spinal cord. Partial transverse myelitis and partial myelitis are terms used to define inflammation of the spinal cord that affects part of the width of the spinal cord.
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HomeArticlesStudies
More Sleep Can Double Your Testosterone LevelS
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Older men can sometimes double their testosterone levels by getting more sleep, according to a human study that Plamen Penev of the University of Chicago published in Sleep.
Nearly all of us probably get too little sleep, mainly because we are seduced every day by the technology around us. It enables us to generate light at night, provides us with 24-hour entertainment and information through electronic media, and makes it possible for us to have contact with each other whenever we want. Every evening, when our body tells us that it’s time to sleep, we can also do a thousand other things instead.
Too little sleep messes up our hormone balance. It makes our body less sensitive to insulin for example. Dutch researchers recently showed that after just one night of four hours’ sleep, young men’s insulin sensitivity went down by twenty percent [J Clin Endocrinol Metab. 2010 Jun; 95(6): 2963-8.] and that of diabetics by a quarter. [Diabetes Care. 2010 Jul;33(7):1573-7.]
In the latter case, lack of sleep is clinically relevant, so doctors could advise diabetics who react insufficiently to their medicines to get more sleep. “Sleep duration might become another therapeutic target to improve glucoregulation in type 1 diabetes”, the Dutch researchers say.
Testosterone is also affected by amount of sleep. That’s not so strange, as our bodies make much more testosterone when they’re asleep than when they’re awake. [J Clin Endocrinol Metab. 2005 Aug; 90(8): 4530-5.] We’ve taken the figure below from the study mentioned here. It shows how much testosterone is present in the blood of 22-32 year-old men while asleep and during the rest of the day.
The better men sleep, the higher their testosterone level rises while they are asleep. [J Clin Endocrinol Metab. 2001 Mar; 86(3): 1134-9.]
In the average male over forty, the testosterone level goes down by 1-2 percent per year, but researchers occasionally come across men in their eighties with a testosterone level you’d expect in a young man. Add to that the fact that many older men – but not all men – sleep less and less deeply as they get older, then you automatically think of the idea that Plamen Penev wanted to test in his study: does the testosterone level decrease in older men because they sleep less?
More sleep can double your testosterone level
Penev based his theory on, among other things, research done by Eve Van Cauter, a sleep researcher at the University of Chicago who has celebrity status in the field of endocrinology. Van Cauter discovered early in the 21st century that men in their forties make less testosterone while sleeping than men in their twenties.
Penev measured the amount of testosterone 12 slim, healthy, non-smoking men aged between 64 and 74 had in their blood in the morning. He also got the men to wear a small gadget around their wrist, which enabled him to see how many hours per night the men slept. That varied from 4.5 to 7.5 per 24 hours. The longer the men slept, the figures below show, the more testosterone there was circulating in their blood.
1
2
The men that slept the least had a testosterone level of 200-300 ng/dl. That’s a normal amount for men of this age, but it’s on the low side. The men in the study who slept the most had a testosterone level that was twice as high: 500-700 ng/dl. That’s a level you’d expect in healthy young men.
“These findings suggest that complaints of poor or insufficient sleep in otherwise healthy older men can be associated with a more pronounced age-related androgen decline”, writes Penev. “Eliciting such sleep complaints in the physician’s office may facilitate the judicious interpretation of lower testosterone levels in the older male patient.”
Before men consider doing testosterone therapy, they might first measure the amount of sleep they get. And ‘measuring’ is different from ‘guessing’ or ‘estimating’. Most people overestimate the number of hours that they sleep. This was also the case in Penev’s study. The men thought that they slept seven and a quarter hours per day on average, but Penev’s recordings showed that they only slept six hours a day.
Association between sleep and morning testosterone levels in older men.
Penev PD.
Source:
Section of Endocrinology, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA. ppenev@medicine.bsd.uchicago.edu
Abstract
STUDY OBJECTIVES:
The circulating testosterone levels of healthy men decline with advancing age. This process is characterized by considerable inter-individual variability, the causes of which are of significant biological and clinical interest but remain poorly understood. Since sleep quantity and quality decrease with age, and experimentally-induced sleep loss in young adults results in hormonal changes similar to those that occur spontaneously in the course of aging, this study examined whether some of the variability in circulating testosterone levels of older men can be related to objective differences in their sleep.
DESIGN:
Observational study.
SETTING:
General community and university clinical research center.
PARTICIPANTS:
Twelve healthy men ages 64 to 74 years.
INTERVENTIONS:
Three morning blood samples were pooled for the measurement of total and free testosterone. In addition to overnight laboratory polysomnography, wrist activity monitoring for 6-9 days was used to determine the amount of nighttime sleep of the participants in everyday life settings.
MEASUREMENTS AND RESULTS:
The main outcome measures were total sleep time and morning testosterone levels. Sleep time in the laboratory was correlated with the usual amount of nighttime sleep at home (Pearson’s r = 0.842; P = 0.001). Bivariate correlation and multiple linear regression analyses revealed that the amount of nighttime sleep measured by polysomnography was an independent predictor of the morning total (Beta 0.792, P = 0.017) and free (Beta 0.741, P = 0.029) testosterone levels of the subjects.
CONCLUSIONS:
Objectively measured differences in the amount of nighttime sleep are associated with a significant part of the variability in the morning testosterone levels of healthy older men.
PMID: 17520786 [PubMed – indexed for MEDLINE]
Source: http://www.ncbi.nlm.nih.gov/pubmed/17520786
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Archivos de cardiología de México
On-line version ISSN 1665-1731Print version ISSN 1405-9940
Arch. Cardiol. Méx. vol.87 n.4 Ciudad de México Oct./Dec. 2017
https://doi.org/10.1016/j.acmx.2016.06.002
Investigación clínica
Global longitudinal strain as a biomarker in diabetic cardiomyopathy. A comparative study with Gal-3 in patients with preserved ejection fraction
Deformación longitudinal global como un biomarcador en miocardiopatía diabética. Estudio comparativo con galectina-3 en pacientes con fracción de eyección preservada
Ramiro Flores-Ramíreza *
José Ramón Azpiri-Lópeza
José Gerardo González-Gonzálezb
Alejandro Ordaz-Faríasa
Luis Eduardo González-Carrilloa
Edgar Francisco Carrizales-Sepúlvedaa
Raymundo Vera-Pinedaa
a Cardiology Service and the Echocardiography Laboratory, Hospital Universitario Dr. Jose Eleuterio Gonzalez, Universidad Autónoma de Nuevo León, Monterrey, Mexico
b Endocrinology Service, Hospital Universitario Dr. Jose E. Gonzalez, Universidad Autónoma de Nuevo León, Monterrey, Mexico
Abstract:
Objectives:
To establish a relationship between global longitudinal strain (GLS) and Galectin-3 in pre-clinical heart failure in diabetic patients. Galectin-3 is a biomarker in heart failure with depressed ejection fraction (HFdEF). The hypothesis is presented that Galectin-3 is related to GLS and can detect left ventricular dysfunction in heart failure with preserved ejection fraction.
Methods:
Galectin-3 and GLS were measured in 121 asymptomatic individuals: 14 diabetics with mild depressed ejection fraction (mdEF) (LVEF 47.0 ± 6.9); 76 diabetics with preserved ejection fraction (LVEF 61 ± 5.5), and 31 controls (61.7 ± 5.1).
Results:
Galectin-3 was elevated in all diabetics vs controls (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = .003). It was also elevated in mdEF (3.76 ± 1.12 ng/ml vs 2.78 ± 0.9 ng/ml; p = .009) and pEF subjects (3.41 ± 1.40 ng/ml vs 2.78 ± 0.9 ng/ml; p = .058), respectively, vs controls. No difference in Gal-3 was found between diabetic groups (p = .603). Diabetics had lower GLS than controls (–18.5 ± 3.9 vs –20 ± 2.6; p = .022). Diabetics with mdEF had lower GLS than those with pEF (–13.3 ± 3.41 vs –19 ± 3.2; P<.001). There was no difference in GLS with pEF compared to controls (–19.4 ± 3.2 vs –20 ± 2.6; p = .70).
Conclusions:
Galectin-3 is elevated in diabetic patients with mdEF, and is associated with a diminished GLS. GLS could be an early marker of left ventricular dysfunction as well as evidence of diabetic cardiomyopathy.
KEYWORDS: Galectin-3; Global longitudinal strain; Diabetic cardiomyopathy; Mexico
Resumen:
Objetivos:
Establecer una asociación entre deformación longitudinal global (DLG) y galectina-3 en insuficiencia cardiaca preclínica en pacientes diabéticos.
Galectina-3 es un biomarcador en insuficiencia cardiaca con fracción de eyección deprimida. Nuestra hipótesis es que la DLG y galectina-3 correlacionan y pueden detectar disfunción ventricular en insuficiencia cardiaca con FEVI preservada.
Métodos:
Se midieron galectina-3 y DLG en 121 individuos asintomáticos: 14 diabéticos con FEVI deprimida leve (FEdl) (FEVI 47 ± 6.9); 76 diabéticos con FEVI preservada (FEp) (FEVI 61 ± 5.5) y 31 sujetos controles (FEVI 61.7 ± 5.1).
Resultados:
Galectina-3 se encontró elevada en todos los diabéticos vs controles (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = 0.003). Está elevada en sujetos con FEdl (3.76 ± 1.12 vs 2.78 ± 0.9 vs ng/ml p = 0.009) y FEp (3.41 ± 1.40 vs 2.78 ± 0.9 ng/ml p = 0.058), respectivamente vs controles; no encontramos diferencia en galectina-3 en ambos grupos de diabéticos (p = 0.603). Los diabéticos tienen menor DLG que los controles (–18.5 ± 3.9 vs –20 ± 2.6; p = 0.022). Los diabéticos con FEdl tienen DLG más disminuida que aquellos con FEp (–13.3 ± 3.41 vs –19 ± 3.2; p < 0.001). No existe diferencia en DLG con FEp y controles (–19.4 ± 3.2 vs –20 ± 2.6; p = 0.70).
Conclusiones:
Galectina-3 está elevada en diabéticos con FEdl y correlaciona DLG disminuida. DLG podría ser un marcador temprano de disfunción ventricular y evidencia en miocardiopatía diabética.
PALABRAS CLAVE: Galectina-3; Deformación longitudinal global; Miocardiopatía diabética; México
Introduction
Diabetic cardiomyopathy was first described by Rubler in 1972.1,2 The term describes several mechanisms involved in the pathogenesis of this entity including changes in myocardial structure and metabolism that are not directly attributed to other co-morbidities such as coronary artery disease (CAD) or hypertension. Left ventricular hypertrophy, myocardial lypotoxicity, increased oxidative stress, cell death from apoptosis, impaired contractile reserve, altered substrate utilization as free fatty acids (FFA), mitochondrial dysfunction and fibrosis are among the mechanisms involved with these changes in structure and metabolism contributing to the progression of heart failure.2 In particular, fibrosis is one of the abnormalities that can be evaluated with the newer imaging techniques. Cardiac magnetic resonance (CMR) is the gold standard in the assessment of myocardial fibrosis given that T1 sequences separate normal from fibrotic tissue.3 Nonetheless, CMR is not widely available, and it is time and cost consuming with longer and exhausting protocols. Speckle tracking echocardiography measurement of these parameters has been validated against magnetic resonance imaging.4,5 Global longitudinal strain (GLS) is the simplest deformation parameter and probably the closest to routine clinical application.6 Quantitative assessment of myocardial function is now possible with speckle tracking echocardiography.7
More than half of patients with heart failure have preserved ejection fraction (HFpEF).8 Diagnosis and therapies are difficult because of a lack of specific biomarkers and imaging techniques. There is a need to anticipate the progression of heart failure in patients with diabetes and for that reason we propose a strategy of non-invasive analysis of inflammation-fibrosis LVD. Galectin-3 (Gal-3) has emerged as a new biomarker in heart failure and has a strong relationship with inflammation and fibrosis.9 Galectin-3 is a β-galactoside-binding member of the lectin family in which 14 mammalian galectins have been identified. Galectin-3 is an ~30 kDa protein and contains a carbohydrate recognition binding domain (CRD) of 130 aminoacids that enables the specific binding of -galactosides and is encoded on by a single gene, LGALSS3 located on chromosome14, locus q21-q22. Galectin-3 has recently been linked to HF development.10,11 We believe that Galectin-3 could detect early stages of left ventricular dysfunction (LVD) in diabetic patients with preserved ejection fraction. On the other hand, newer echocardiography techniques allow evaluating LVD before ejection fraction declines. This study aims to analyze the relation between a cardiac biomarker of fibrosis, Gal-3, and the patterns of GLS in asymptomatic patients with type 2 diabetes and preserved ejection fraction.
Methods
Participants
From April 1, 2015 to August 31, 2015 a total of 159 subjects from the endocrinology outpatient clinic were recruited. The study had ethics approval by our Institutional Review Board. Patients with type 2 diabetes and no history of cardiovascular disease were included. Thirty-one age- and sex-matched healthy volunteers were also studied. Each examination consisted of a clinical history and physical exam, anthropometry, blood samples and routine echocardiogram with strain measurements. Patients with a history of cardiovascular and renal disease, valvular heart disease, atrial fibrillation, angina or previous myocardial infarction were excluded. Two patients excluded had atrial fibrillation, one with chronic liver disease; two patients had myocardial infarction unknown to them and 9 had symptoms of angina; six had a history of stroke. Eighteen non-diabetic individuals in the control group were excluded because of depressed ejection fraction. A total of 121 participants were divided in 3 groups. Group 1: 14 patients with type 2 diabetes and mild depressed ejection fraction (mdEF); group 2: 76 patients with type 2 diabetes and preserved ejection fraction (pEF) and group 3: 31 age- and sex-matched controls without diabetes.
Biomarker
Blood samples were collected after an overnight fast and immediately centrifuged and stored at –70 °C until assayed. Plasma concentrations of Gal-3 were measured using an enzyme-linked immunosorbent assay with a sensitivity of 10 pg/ml (Abcam Inc., Cambridge, MA), according to the manufacturer’s instructions.
Echocardiography
Routine 2-dimensional and Doppler echocardiography was performed according to the American Society of Echocardiography and European Association of Cardiovascular Imaging guidelines using a ViVid E9 echocardiogram with a 1.5–3.6 MHz transducer (GE Vingmed, Horten, Norway). Two certified echocardiologists unaware of the clinical history and Gal-3 level acquired and evaluated all echocardiograms. Indexed ventricular mass was assessed in a linear fashion using the paraesternal long axis view. Left ventricular ejection fraction was calculated with the biplane Simpson’s method. Preserved ejection fraction was defined as an ejection fraction (EF) above 52% in male subjects and 54% in female subjects; mildly depressed ejection fraction was defined as 41–51% in men and 41–53% in women as described in ASE/EACVI guidelines.12 Pulsed-wave (PW) Doppler was performed in the apical 4-chamber view to obtain mitral inflow velocities to assess left ventricular (LV) filling. A 1-mm sample volume is then placed between the mitral leaflet tips during diastole. Diastolic function measurements include peak early filling (E-wave) and late diastolic filling (A-wave) velocities, the E/A ratio, and deceleration time. Pulsed wave tissue Doppler imaging (DTI) was performed in the 4CH apical view with sample volume positioned at 1 cm within the septal insertion site of the mitral leaflet for E/e′. Diastolic dysfunction was defined with criteria described earlier.13 Three cardiac cycles were recorded in 4, 2 and 3 chambers for the offline speckle tracking analyses of GLS. Offline analyses were performed in EchoPAC PC 113.0.X. (GE Vingmed Horten Norway). The complete region of interest (ROI) was defined at end-diastole as the endocardial border: the inner contour of the myocardium; epicardial border: the outer contour of the myocardium; and myocardial midline: the middle ROI axis defined in the middle between the inner and outer ROI contours.14 Each of these contours can be either user-defined or generated automatically. In any case, these were generated automatically; our echocardiologists checked them and, if needed, edited the images manually taking care of defining the ROI to avoid pericardium inclusion.7 Normal reference values of GLS were taken from the literature.6 All individuals were in sinus rhythm at the time of imaging and had no significant cardiovascular abnormalities.
Reproducibility
For inter and intraobserver variability, GLS and EF were assessed in a subset of 45 subjects randomly selected from the study population and analyzed with Bland–Altman analysis and the Wilcoxon rank with no significant differences between observers. For biplane GLS (SD) interpreter 1, –19.75 (4.09) vs interpreter 2, –19.75 (4.72), Wilcoxon rank test .55 and for EF (SD) interpreter 1, 57 (9.64) vs interpreter 2, 57.5 (11.26) difference -0.5 (5.09) Wilcoxon rank test .60.
Statistical analysis
Categorical values were reported as frequencies. Quantitative variables were tested for normality with the Kolmogorov–Smirnov test. For variables with normal distribution mean ± standard deviation (SD) was used. Difference in quantitative data between groups was analyzed using a one-way ANOVA test. When a significant difference was found (p < 0.05), the Tukey test was used to determine which group was unequal from the others (p < 0.05). The Gal-3 cutoff point was assessed using receiver operating characteristics (ROC curve) and the Youden index. Area under the curve (AUC) values >0.5 with a p < 0.05 were considered statistically significant (Fig. 1).
Figure 1 ROC curve for LVD (left ventricular dysfunction). Highest performance Gal-3 value was 2.71 ng/ml with p = 0.048, AUC: 0.663, sensitivity: 0.928, specificity: 0.381 and (NPV) negative predictive value: 0.96.
All statistical data were analyzed with SPSS version 21.0 (IBM Corp., NY, USA).
Results
All demographic results are described in (Table 1). There were no differences between groups according to age, sex, body mass index and other cardio-metabolic parameters.
Table 1 Demographic characteristics of study group.
Plus-minus values are means ± SD. There were no significant between-group differences at baseline except for T2DM (type 2 diabetes mellitus). SBP: systolic blood pressure; DBP: diastolic blood pressure; BMI: body mass index.
Based on updated echocardiographic guidelines,12 we compare diabetic individuals with mdEF vs pEF vs controls (Table 2). Gal-3 was elevated in all individuals with diabetes compared to controls (3.46 ± 1.36 ng/ml vs 2.78 ± 0.91 ng/ml; p = 0.003) with no difference between diabetic patients with mild depressed ejection fraction and preserved ejection fraction (3.76 ± 1.12 ng/ml vs 3.41 ± 1.4 ng/ml; p = 0.603) (Fig. 2). All echocardiographic variables are described in (Table 3).
Table 2 Main findings between groups.
Plus-minus values are means ± SD. There were significant differences in GLS (global longitudinal strain), biplane EF (ejection fraction) and diastolic dysfunction in diabetics vs controls.
Figure 2 DmdEF (diabetics with mild depressed ejection fraction). DpEF (diabetics with preserved ejection fraction).
Table 3 Echocardiographic variables.
Plus-minus values are means ± SD. BS: basal septal; MS: medium septal; AS: apical septal; BL: basal lateral; ML: medium lateral; AL: apical lateral; BI: basal inferior; MI: medium inferior; AI: apical inferior; BA: basal anterior; MA: medium anterior; AA: apical anterior; BP: basal posterior; MP: medium posterior; AP: apical posterior; BAS: basal antero-septal; MAS: medium antero-septal; AAS: apical antero-septal; GLS: global longitudinal strain; EF: ejection fraction.
Gal-3 was found to be higher in mdEF (2.78 ± 0.9 ng/ml vs 3.76 ± 1.12 ng/ml; p = 0.009) and pEF subjects (2.78 ± 0.9 ng/ml vs 3.41 ± 1.40 ng/ml; p = 0.058) compared to controls.
To assess the effect of diabetes progression on left ventricular function, we divided our cohort in those who had less than 10 years since diagnosis and those with more than 10 years. Gal-3 levels were higher in patients with more than 10 years (p = 0.011). There was no significant statistical difference regarding EF (p = 0.286) and GLS (p = 0.228). Diastolic function was more frequently altered in the group with more than 10 years (p = 0.03) (Table 2). When we compare diabetic individuals did not found difference in baseline Gal-3 in diabetes with mdEF n = 14 (3.76 ± 1.12 ng/ml) vs pEF n = 76 (3.41 ± 1.4 ng/ml) p = 0.60, but consistently LVD with GLS between these groups (–13.35 ± 3.41 vs –19.46 ± 3.26) p = 0.001. Compared to controls, all individuals with diabetes had worst GLS (p = 0.022). There was no difference in GLS in diabetic patients with pEF when compared to non-diabetic controls (p = 0.70). Patients with mdEF had significantly lower GLS than controls (p < 0.001) (Fig. 3). Thirty per cent of those in the pEF group had impaired GLS values and 92.9% in the mdEF group. Both parameters move discretely in the desired direction, but with wide dispersion, without any correlation. Using 2 markers, Gal-3 (>2.71 ng/ml) and GLS (<18%), we found a sensitivity of 0.85, a specificity of 0.81, a PPV of 0. 46 and a NPV of 0.97 for LVD (Fig. 4).
Figure 3 DmdEF (diabetics with mild depressed ejection fraction). DpEF (diabetics with preserved ejection fraction).
Figure 4 Sensitivity, specificity, PPV (positive predictive value) and NPV (negative predictive value). Using both parameters; Gal-3 at >2.71 ng/ml and global longitudinal strain <18%.
Discussion
Left ventricular dysfunction (LVD) is now known to be a major co-morbidity in diabetes. Hypertension and DM are closely related and complicate each other. The activation of the rennin–angiotensin–aldosterone system causes insulin resistance.15,16 Cardiac remodeling occurs together with hypertension and DM.17 Difficult exists in specifying the cause of cardiac remodeling in diabetes because of the lack of criteria and tools, including biomarkers and imaging techniques. Microvasculopathy is a primary feature in diabetic cardiac remodeling but no surrogate can directly monitor disease progression. Therefore there is an increasing interest in the link between DM and heart failure. Diabetic cardiomyopathy is a term assigned to those patients with cardiomyopathy without coronary artery disease and hypertension.18 Multiple substrates are responsible for myocardial damage including fatty acid uptake, collagen metabolism, oxidation and fibrosis.2 Because Gal-3 is a marker of inflammation and fibrosis9 we aimed to correlate this biomarker with a non-invasive, easier and accessible tool in the evaluation of pre-clinical heart failure or incipient myocardial dysfunction in patients with diabetes.
It is estimated than more than 50% of patients presenting with signs and symptoms of heart failure suffer from heart failure with preserved ejection fraction (HFpEF).19 The vast majority of published articles on Gal-3 described patients with heart failure with reduced ejection fraction (HFrEF) not HFpEF.9 Echocardiography is a non-invasive tool in the global evaluation of heart disease. Some of its features includes left ventricular ejection fraction (LVEF). LVEF has been demonstrated in patients with heart failure in different scenarios such as coronary artery disease, valvular heart disease and other cardiomyopathies. LVEF has been the fundamental tool for systolic function; nonetheless it is less sensitive for detecting early myocardial disease than newer techniques.20 Asymptomatic myocardial dysfunction can occur in diabetic patients without CAD. LVEF could be normal but myocardial dysfunction in terms of abnormal deformation is not. GLS can detect myocardial abnormalities before EF declines.20 The presence of LVD was defined in a large meta-analysis of strain. The mean GLS in normal subjects was –19.7%, with a lower 95% CI of –18.9%.6 In a recent study, Holland et al. evaluated the 10-year outcomes in subclinical myocardial dysfunction evaluating GLS in a cohort of 249 type 2 diabetic patients with normal LVEF.21 Holland found that almost half of patients (45%) had evidence of LVD detected by GLS in a median follow-up of 7.4 ± 2.6 years. GLS was independently associated with the primary endpoint. Patients with LVD had a significantly worse outcome than those without. They concluded that subclinical LVD is common in asymptomatic patients with type 2 DM, that it was detectable by GLS imaging and is independently associated with adverse outcome.21 In our study we found that GLS is depressed in all individuals with diabetes compared to controls (p = 0.003) but there is no difference in GLS in diabetic patients with pEF when compared to controls (–19.4 ± 3.2 vs –20 ± 2.6; p = 0.42) but Gal-3 was significantly elevated (p = 0.008). Left ventricular dysfunction (GLS <–18) was found in 30.3% of pEF subjects. We assume at this point that diabetic individuals with pEF are in early phases of inflammation and extracellular matrix proliferation but these needs to be confirmed in a MRI study. Using 2 markers, Gal-3 (>2.71 ng/ml) and GLS (<18%), we found a sensitivity of 0.85, a specificity of 0.81, a PPV of 0. 46 and a NPV of 0.97 for LVD.
Only a few studies have described the levels and clinical correlation of Gal-3 and HFpEF. The COACH study de Boer et al. found, in a cohort of 592 patients admitted with acute heart failure, that 19.2% (114) of patients with HFpEF and Gal-3 levels where comparable between HFrEF and HFpEF (~20 ng/ml).22 Our population was a non-Caucasian heart failure symptom-free cohort from the endocrinology out-patient clinic. Levels of Gal-3 were not highly elevated in this cohort compared to other studies (~3.4 pg/ml); in the fibrosis marker, Gal-3, and in the outcome in the general population, de Boer found a gender interaction, with female subjects having higher median Gal-3 levels 11.0 ng/ml IQR (interquartile range 9.0–13.1 ng/ml.) than men 10.7 ng/ml IQR (8.9–12.8 ng/ml) but they excluded non-Caucasian subjects.23 In the epidemiological field Ho et al.24 Investigated Gal-3 linked to the development of HF in the general population. Gal-3 concentrations were measured in 3353 participants from the Framingham Offspring Cohort and were associated independently with an increased risk for developing HF and mortality. Crude HF incidence rates were estimated by sex-specific Gal-3 quartile. Quartile 1: 3.9–11.1 ng/ml, quartile 2: 11.1–13.1 ng/ml, quartile 3: 13.1–15.4 ng/ml and quartile 4: 16.8–51.1 ng/ml. During a mean follow-up period of 11.2 years, 166 (5.1%) subjects developed HF. The heart failure incidence rate increased over Gal-3 quartiles, with rates of 2.8, 3.8, 5.2 and 12.4 events per 1000 persons-years in quartiles 1 through 4, respectively. Our cohort resembles quartile 1 of the Ho study. We believe that in diabetic patients adding GLS to standard echocardiograms is useful in the detection of early phases of LVD. The combination of Gal-3 and GLS has a high NPV of 0.94. At the same time our study demonstrates that Gal-3 was elevated in all diabetic individuals compared to controls (p = 0.003). Gal-3 was found to be higher in patients with mdEF compared to pEF with diabetic subjects not reaching significance due to sample size (p = 0.375). When compared to controls Gal-3 was found to be higher in pEF diabetic subjects (p = 0.008).
Study limitations
We studied only one of the substrates of DCM. It would have been useful to compare GLS with cardiac magnetic resonance for detection of fibrosis; however, it was not available at our institution. Also, non-significant differences could be as a result of the sample size basically in the mdEF group. We did not studied the existence of ischemic heart disease even in those diabetic subjects with more than 10 years of diagnostic so these make harder to consider DCM by itself, an lastly GLS is not a surrogate of Gal-3.
Conclusions
This is a non-Caucasian study in a diabetic heart failure symptom free cohort. Global longitudinal strain is an easy and reproducible echocardiography tool in the evaluation and follow-up of DCM in diabetic subjects although is not a surrogate of Gal-3 because this biomarker is elevated in all diabetics. There still much to investigate in the physiopathology of DCM especially in asymptomatic patients with preserved ejection fraction. Including Gal-3 to standard echocardiography and GLS would be helpful in the early detection of LVD in DCM.
Acknowledgements
Authors would like to thank Neri A. Alvarez MD for statistical analysis, Gloria Jasso QFB for endocrinology lab analyses, Rodolfo Flores-Alexander English language professor and Sergio Lozano M.D. for English translation advice.
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Protection of people and animals. The authors state that the procedures conformed to the ethical standards of human experimentation committee responsible and according to the World Medical Association and the Declaration of Helsinki.
Confidentiality of data. The authors declare that they have followed the protocols of the workplace on the publication of patient data.
Right to privacy and informed consent. The authors have obtained the informed consent of patients and/or subjects referred to in Article consent. This document is held by the corresponding author.
Funding. This study has no funding.
Conflict of interest. The authors have no conflicts of interest to declare.
Received: January 25, 2016; Accepted: June 02, 2016
* Corresponding author. Tel.: +52 8116601001; fax: +52 8114928262. E-mail address: flores.ramiro@gmail.com (R. Flores-Ramírez).
Creative Commons License This is an open-access article distributed under the terms of the Creative Commons Attribution License
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SUFENTANIL CITRATE- sufentanil citrate injection, solution
Hospira, Inc.
----------
HIGHLIGHTS OF PRESCRIBING INFORMATION
These highlights do not include all the information needed to use SUFENTANIL CITRATE INJECTION, safely and effectively. See full prescribing information for SUFENTANIL CITRATE INJECTION.
Sufentanil Citrate Injection, USP for intravenous and epidural use, CII
Initial U.S. Approval: 1984
WARNING: ADDICTION, ABUSE, AND MISUSE
See full prescribing information for complete boxed warning.
• Sufentanil Citrate Injection exposes users to risks of addiction, abuse, and misuse, which can lead to overdose and death. Assess patient's risk before prescribing and monitor regularly for these behaviors and conditions. (5.1)
RECENT MAJOR CHANGES
Boxed Warning12/2016
Indications and Usage (1)12/2016
Dosage and Administration (2)12/2016
Contraindications (4)12/2016
Warnings and Precautions (5)12/2016
INDICATIONS AND USAGE
Sufentanil Citrate Injection, USP is an opioid agonist indicated:
• as an analgesic adjunct in the maintenance of balanced general anesthesia in patients who are intubated and ventilated.
• as a primary anesthetic agent for the induction and maintenance of anesthesia with 100% oxygen in patients undergoing major surgical procedures, in patients who are intubated and ventilated, such as cardiovascular surgery or neurosurgical procedures in the sitting position, to provide favorable myocardial and cerebral oxygen balance or when extended postoperative ventilation is anticipated.
• for epidural administration as an analgesic combined with low dose (usually 12.5 mg per administration) bupivacaine usually during labor and vaginal delivery.
DOSAGE AND ADMINISTRATION
• Sufentanil Citrate Injection, USP should be administered only by persons specifically trained in the use of intravenous anesthetics and management of the respiratory effects of potent opioids.
• Ensure that an opioid antagonist, resuscitative and intubation equipment, and oxygen are readily available. (2.1)
• Individualize dosing based on factors such as age, body weight, physical status, underlying pathological condition, use of other drugs, type of anesthesia to be used, and the surgical procedure involved. (2.1)
• Initiate analgesic treatment with 1 to 2 mcg/kg intravenously. (2.2)
• Initiate epidural injection for labor and delivery at 10 to 15 mcg of sufentanil administered with 10 mL bupivacaine 0.125% with or without epinephrine. (2.3)
DOSAGE FORMS AND STRENGTHS
Solution for injection (sterile): eq. to 50 mcg/mL sufentanil base; 1 mL, 2 mL and 5 mL vials. (3)
CONTRAINDICATIONS
• Hypersensitivity to sufentanil. (4)
WARNINGS AND PRECAUTIONS
• Risks of skeletal Muscle Rigidity and Skeletal Muscle Movement: Manage with neuromuscular blocking agent. See full prescribing information for more detail on managing these risks. (5.4)
• Life-Threatening Respiratory Depression in Patients with Chronic Pulmonary Disease or in Elderly, Cachectic, or
• Debilitated Patients: Monitor closely, particularly during initiation and titration. (5.2)
• Severe Cardiovascular Depression: Monitor during dosage initiation and titration. (5.6)
• Serotonin Syndrome: Potentially life-threatening condition could result from concomitant serotonergic drug administration. Discontinue Sufentanil Citrate Injection if serotonin syndrome is suspected. (5.7)
• Risks of Use in Patients with Increased Intracranial Pressure, Brain Tumors, or Head Injury: Monitor for sedation and respiratory depression. (5.9)
ADVERSE REACTIONS
Most common adverse reactions were apnea, rigidity, and bradycardia. (6)
To report SUSPECTED ADVERSE REACTIONS, contact Hospira, Inc. at 1-800-441-4100 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
DRUG INTERACTIONS
• Concomitant Use of CNS Depressants: May decrease pulmonary arterial pressure and may cause hypotension. See FPI for management instructions. For post-operative pain, start with the lowest effective dosage and monitor for potentiation of CNS depressant effects. (5.5, 7)
• Mixed Agonist/Antagonist and Partial Agonist Opioid Analgesics: Avoid use with Sufentanil Citrate Injection because they may reduce analgesic effect of Sufentanil Citrate Injection or precipitate withdrawal symptoms. (7)
USE IN SPECIFIC POPULATIONS
• Pregnancy: May cause fetal harm. (8.1)
• Lactation: Infants exposed to Sufentanil Citrate Injection through breast milk should be monitored for excess sedation and respiratory depression. (8.2)
Revised: 4/2018
FULL PRESCRIBING INFORMATION: CONTENTS*
WARNING: ADDICTION, ABUSE, AND MISUSE
1 INDICATIONS AND USAGE
2 DOSAGE AND ADMINISTRATION
2.1 Important Dosage and Administration Instructions
2.2 Intravenous use
2.3 Epidural Use In Labor And Delivery
3 DOSAGE FORMS AND STRENGTHS
4 CONTRAINDICATIONS
5 WARNINGS AND PRECAUTIONS
5.1 Addiction, Abuse, and Misuse
5.2 Life-Threatening Respiratory Depression
5.3 Risks of Concomitant Use or Discontinuation of Cytochrome P450 3A4 Inhibitors and Inducers
5.4 Risks of Muscle Rigidity and Skeletal Muscle Movement
5.5 Risks from Concomitant Use with Benzodiazepines or Other CNS Depressants
5.6 Severe Cardiovascular Depression
5.7 Serotonin Syndrome with Concomitant Use of Serotonergic Drugs
5.8 Risks due to Improper Epidural Injection
5.9 Risks of Use in Patients with Increased Intracranial Pressure, Brain Tumors, or Head Injury
5.10 Risks of Use in Patients with Gastrointestinal Conditions
5.11 Increased Risk of Seizures in Patients with Seizure Disorders
5.12 Risks of Driving and Operating Machinery
6 ADVERSE REACTIONS
6.1 Clinical Trials Experience
6.2 Postmarketing Experience
7 DRUG INTERACTIONS
8 USE IN SPECIFIC POPULATIONS
8.1 Pregnancy
8.2 Lactation
8.3 Females and Males of Reproductive Potential
8.4 Pediatric Use
8.5 Geriatric Use
8.6 Hepatic Impairment
8.7 Renal Impairment
9 DRUG ABUSE AND DEPENDENCE
9.1 Controlled Substance
9.2 Abuse
9.3 Dependence
10 OVERDOSAGE
11 DESCRIPTION
12 CLINICAL PHARMACOLOGY
12.1 Mechanism of Action
12.2 Pharmacodynamics
12.3 Pharmacokinetics
13 NONCLINICAL TOXICOLOGY
13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility
14 CLINICAL STUDIES
16 HOW SUPPLIED/STORAGE AND HANDLING
*
Sections or subsections omitted from the full prescribing information are not listed.
FULL PRESCRIBING INFORMATION
WARNING: ADDICTION, ABUSE, AND MISUSE
See full prescribing information for complete boxed warning.
Sufentanil Citrate Injection exposes users to risks of addiction, abuse, and misuse, which can lead to overdose and death. Assess patient's risk before prescribing and monitor regularly for these behaviors and conditions. (5.1)
1 INDICATIONS AND USAGE
Sufentanil Citrate Injection, USP is indicated for intravenous administration in adults and pediatric patients:
Sufentanil Citrate Injection, USP is indicated for epidural administration:
2 DOSAGE AND ADMINISTRATION
2.1 Important Dosage and Administration Instructions
Sufentanil Citrate Injection, USP should be administered only by persons specifically trained in the use of intravenous or epidural anesthetics and management of the respiratory effects of potent opioids.
In patients administered high doses of sufentanil Citrate Injection, USP, it is essential that qualified personnel and adequate facilities are available for the management of postoperative respiratory depression.
For purposes of administering small volumes of Sufentanil Citrate Injection, USP accurately, the use of a tuberculin syringe or equivalent is recommended.
• Ensure that an opioid antagonist, resuscitative and intubation equipment, and oxygen are readily available.
• Individualize dosage based on factors such as age, body weight, physical status, underlying pathological condition, use of other drugs, type of anesthesia to be used, and the surgical procedure involved.
• Monitor vital signs regularly.
• The selection of preanesthetic medications should be based upon the needs of the individual patient.
• The neuromuscular blocking agent selected should be compatible with the patient's condition, taking into account the hemodynamic effects of a particular muscle relaxant and the degree of skeletal muscle relaxation required.
As with other potent opioids, the respiratory depressant effect of sufentanil may persist longer than the measured analgesic effect. The total dose of all opioid agonists administered should be considered by the practitioner before ordering opioid analgesics during recovery from anesthesia.
If Sufentanil Citrate Injection, USP is administered with a CNS depressant, become familiar with the properties of each drug, particularly each product's duration of action. In addition, when such a combination is used, fluids and other countermeasures to manage hypotension should be available [see Warnings and Precautions (5.5)].
Inspect parenteral drug products visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
2.2 Intravenous use
Sufentanil Citrate may be administered intravenously by slow injection or infusion.
Adjunct to general anesthesia:
• doses of up to 8 mcg/kg (see Table 1)
• Total Dosage Requirements Of 1 Mcg/Kg/Hr Or Less Are Recommended
• Dosage should be individualized and adjusted to remaining operative time anticipated.
Table 1: Adult Dosage Range Chart, Analgesic Component To General Anesthesia, Intravenous Use
Total dosageMaintenance dosage
Duration of anesthesia 1 to 2 hours
Incremental or Infusion: 1 to 2 mcg/kg.
Approximately 75% or more of total sufentanil dosage may be administered prior to intubation by either slow injection or infusion titrated to individual patient response.
Incremental: 10 to 25 mcg (0.2 to 0.5 mL) may be administered in increments as needed when movement and/or changes in vital signs indicate surgical stress or lightening of analgesia. Supplemental dosages should be individualized and adjusted to remaining operative time anticipated.
Dosages in this range are generally administered with nitrous oxide/oxygen in patients undergoing general surgery in which endotracheal intubation and mechanical ventilation are required.Infusion: Intermittent or continuous infusion as needed in response to signs of lightening of analgesia. In absence of signs of lightening of analgesia, infusion rates should always be adjusted downward until there is some response to surgical stimulation.
Maintenance infusion rates should be adjusted based upon the induction dose of sufentanil so that the total dose does not exceed 1 mcg/kg/hr of expected surgical time.
Duration of anesthesia 2 to 8 hours
Incremental or Infusion: 2 to 8 mcg/kg
Approximately 75% or less of the total calculated sufentanil dosage may be administered by slow injection or infusion prior to intubation, titrated to individual patient response.
Incremental: 10 to 50 mcg (0.2 to 1 mL) may be administered in increments as needed when movement and/or changes in vital signs indicate surgical stress or lightening of analgesia. Supplemental dosages should be individualized and adjusted to the remaining operative time anticipated.
Dosages in this range are generally administered with nitrous oxide/oxygen in patients undergoing more complicated major surgical procedures in which endotracheal intubation and mechanical ventilation are required.
At dosages in this range, sufentanil has been shown to provide some attenuation of sympathetic reflex activity in response to surgical stimuli, provide hemodynamic stability, and provide relatively rapid recovery.
Infusion: Intermittent or continuous infusion as needed in response to signs of lightening of analgesia.
In the absence of signs of lightening of analgesia, infusion rates should always be adjusted downward until there is some response to surgical stimulation.
Maintenance infusion rates should be adjusted based upon the induction dose of sufentanil so that the total dose does not exceed 1 mcg/kg/hr of expected surgical time.
Induction And Maintenance Of Anesthesia
• As the primary anesthetic agent: doses ≥8 mcg/kg (see Dosage Range Chart, Table 2).
• Dosage should be titrated to individual patient response
• In children less than 12 years of age undergoing cardiovascular surgery: 10 to 25 mcg/kg administered with 100% oxygen
• Supplemental dosages of up to 25 to 50 mcg are recommended for maintenance, based on response to initial dose and as determined by changes in vital signs indicating surgical stress or lightening of anesthesia.
Table 2: Dosage Range Chart, Induction and Maintenance of Anesthesia, Intravenous Use
Incremental or Infusion: 8 to 30 mcg/kg
Generally administered as a slow injection, as an infusion, or as an injection followed by an infusion.
Sufentanil with 100% oxygen and a muscle relaxant has been found to produce sleep at dosages ≥8 mcg/kg and to maintain a deep level of anesthesia without the use of additional anesthetic agents. The addition of N2O to these dosages will reduce systolic blood pressure. At dosages in this range of up to 25 mcg/kg, catecholamine release is attenuated.
Dosages of 25 to 30 mcg/kg have been shown to block sympathetic response including catecholamine release.
High doses are indicated in patients undergoing major surgical procedures, in which endotracheal intubation and mechanical ventilation are required, such as cardiovascular surgery and neurosurgery in the sitting position with maintenance of favorable myocardial and cerebral oxygen balance.
Postoperative observation is essential and postoperative mechanical ventilation may be required at the higher dosage range due to extended postoperative respiratory depression.
Incremental: Depending on the initial dose, maintenance doses of 0.5 to 10 mcg/kg may be administered by slow injection in anticipation of surgical stress such as incision, sternotomy or cardiopulmonary bypass.
Infusion: Sufentanil citrate may be administered by continuous or intermittent infusion as needed in response to signs of lightening of anesthesia.
In the absence of lightening of anesthesia, infusion rates should always be adjusted downward until there is some response to surgical stimulation.
The maintenance infusion rate for sufentanil should be based upon the induction dose so that the total dose for the procedure does not exceed 30 mcg/kg.
2.3 Epidural Use In Labor And Delivery
Proper placement of the needle or catheter in the epidural space should be verified before sufentanil citrate is injected to assure that unintentional intravascular or intrathecal administration does not occur. Unintentional intravascular injection of sufentanil could result in a potentially serious overdose, including acute truncal muscular rigidity and apnea. Unintentional intrathecal injection of the full sufentanil, bupivacaine epidural doses and volume could produce effects of high spinal anesthesia including prolonged paralysis and delayed recovery
• Sufentanil should be administered by slow injection. Respiration should be closely monitored following each administration of an epidural injection of sufentanil.
• If analgesia is inadequate, the placement and integrity of the catheter should be verified prior to the administration of any additional epidural medications.
Dosage for Labor and Delivery
• 10 to 15 mcg administered with 10 mL bupivacaine 0.125% with or without epinephrine.
• Sufentanil and bupivacaine should be mixed together before administration.
• Doses can be repeated twice (for a total of three doses) at not less than one-hour intervals until delivery.
3 DOSAGE FORMS AND STRENGTHS
Sufentanil Citrate Injection, USP 50 mcg/mL (equivalent to 50 mcg/mL sufentanil base).
4 CONTRAINDICATIONS
Sufentanil Citrate Injection is contraindicated in patients with:
5 WARNINGS AND PRECAUTIONS
5.1 Addiction, Abuse, and Misuse
Sufentanil Citrate Injection contains sufentanil, a Schedule II controlled substance. As an opioid, Sufentanil Citrate Injection exposes users to the risks of addiction, abuse, and misuse [see Drug Abuse and Dependence (9)].
Opioids are sought by drug abusers and people with addiction disorders and are subject to criminal diversion. Consider these risks when handling Sufentanil Citrate Injection. Strategies to reduce these risks include proper product storage and control practices for a C-II drug. Contact local state professional licensing board or state controlled substances authority for information on how to prevent and detect abuse or diversion of this product.
5.2 Life-Threatening Respiratory Depression
Serious, life-threatening, or fatal respiratory depression has been reported with the use of opioids, even when used as recommended. Respiratory depression, if not immediately recognized and treated, may lead to respiratory arrest and death. Sufentanil Citrate Injection should be administered only by persons specifically trained in the use of anesthetic drugs and the management of the respiratory effects of potent opioids, including respiration and cardiac resuscitation of patients in the age group being treated. Such training must include the establishment and maintenance of a patent airway and assisted ventilation. Adequate facilities should be available for postoperative monitoring and ventilation of patients administered anesthetic doses of Sufentanil Citrate Injection. It is essential that these facilities be fully equipped to handle all degrees of respiratory depression. Management of respiratory depression may include close observation, supportive measures, and use of opioid antagonists, depending on the patient's clinical status [see Overdosage (10)]. Carbon dioxide (CO2) retention from opioid-induced respiratory depression can exacerbate the sedating effects of opioids.
As with other potent opioids, the respiratory depressant effect of Sufentanil Citrate Injection may persist longer than the measured analgesic effect. The total dose of all opioid agonists administered should be considered by the practitioner before ordering opioid analgesics during recovery from anesthesia.
Certain forms of conduction anesthesia, such as spinal anesthesia and some epidural anesthetics, can alter respiration by blocking intercostal nerves [see Clinical Pharmacology (12.2)]. Sufentanil Citrate Injection can also alter respiration. Therefore, when Sufentanil Citrate Injection is used to supplement these forms of anesthesia, the anesthetist should be familiar with the physiological alterations involved, and be prepared to manage them in the patients selected for these forms of anesthesia. Patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with a substantially decreased respiratory reserve, hypoxia, hypercapnia, or pre-existing respiratory depression are at increased risk of decreased respiratory drive including apnea, even at recommended dosages of Sufentanil Citrate Injection. Elderly, cachectic, or debilitated patients may have altered pharmacokinetics or altered clearance compared to younger, healthier patients resulting in greater risk for respiratory depression.
Monitor such patients closely including vital signs, particularly when initiating and titrating Sufentanil Citrate Injection and when Sufentanil Citrate Injection is given concomitantly with other drugs that depress respiration. To reduce the risk of respiratory depression, proper dosing and titration of Sufentanil Citrate Injection are essential [see Dosage and Administration (2.1)].
5.3 Risks of Concomitant Use or Discontinuation of Cytochrome P450 3A4 Inhibitors and Inducers
Concomitant use of Sufentanil Citrate Injection with a CYP3A4 inhibitor, such as macrolide antibiotics (e.g., erythromycin), azoleantifungal agents (e.g., ketoconazole), and protease inhibitors (e.g., ritonavir), may increase plasma concentrations of sufentanil and prolong opioid adverse reactions, which may exacerbate fatal respiratory depression [see Warnings and Precautions (5.2)], particularly when an inhibitor is added after a stable dose of Sufentanil Citrate Injection is achieved. Similarly, discontinuation of a CYP3A4 inducer, such as rifampin, carbamazepine, and phenytoin, in Sufentanil Citrate Injection-treated patients may increase sufentanil plasma concentrations and prolong opioid adverse reactions. When using Sufentanil Citrate Injection with CYP3A4 inhibitors or discontinuing CYP3A4 inducers in Sufentanil Citrate Injection-treated patients, monitor patients closely at frequent intervals and consider dosage reduction of Sufentanil Citrate Injection [see Dosage and Administration (2.1), Drug Interactions (7)].
Concomitant use of Sufentanil Citrate Injection with CYP3A4 inducers or discontinuation of an CYP3A4 inhibitor could result in lower than expected sufentanil plasma concentrations, and decrease efficacy. When using Sufentanil Citrate Injection with CYP3A4 inducers or discontinuing CYP3A4 inhibitors, monitor patients closely at frequent intervals and consider increasing the Sufentanil Citrate Injection dosage [see Dosage and Administration (2.1), Drug Interactions (7)].
5.4 Risks of Muscle Rigidity and Skeletal Muscle Movement
Intravenous administration or unintentional intravascular injection during epidural administration of Sufentanil Citrate Injection may cause muscle rigidity, particularly involving the muscles of respiration. The incidence and severity of muscle rigidity is dose related. These effects are related to the dose and speed of injection. Administration of sufentanil may produce muscular rigidity with a more rapid onset of action than that seen with fentanyl. Skeletal muscle rigidity also has been reported to occur or recur infrequently in the extended postoperative period usually following high dose administration. In addition, skeletal muscle movements of various groups in the extremities, neck, and external eye have been reported during induction of anesthesia with Sufentanil Citrate Injection; these reported movements have, on rare occasions, been strong enough to pose patient management problems.
The incidence of skeletal muscle rigidity can be reduced by: 1) administration of up to 1/4 of the full paralyzing dose of a nondepolarizing neuromuscular blocking agent just prior to administration of sufentanil at dosages of up to 8 mcg/kg, 2) administration of a full paralyzing dose of a neuromuscular blocking agent following loss of consciousness when sufentanil is used in anesthetic dosages (above 8 mcg/kg) titrated by slow intravenous infusion, or, 3) simultaneous administration of sufentanil and a full paralyzing dose of a neuromuscular blocking agent when sufentanil is used in rapidly administered anesthetic dosages (above 8 mcg/kg).
The neuromuscular blocking agents used should be compatible with the patient's cardiovascular status. The hemodynamic effects and degree of skeletal muscle relaxation required should be considered in the selection of a neuromuscular blocking agent. High doses of pancuronium may produce increases in heart rate during sufentanil-oxygen anesthesia. Bradycardia and hypotension have been reported with other muscle relaxants during sufentanil-oxygen anesthesia; this effect may be more pronounced in the presence of calcium channel and/or beta-blockers. Muscle relaxants with no clinically significant effect on heart rate (at recommended doses) would not counteract the vagotonic effect of sufentanil, therefore a lower heart rate would be expected. Rare reports of bradycardia associated with the concomitant use of succinylcholine and sufentanil have been reported.
5.5 Risks from Concomitant Use with Benzodiazepines or Other CNS Depressants
When benzodiazepines or other CNS depressants are used with Sufentanil Citrate Injection, pulmonary arterial pressure may be decreased. This fact should be considered by those who conduct diagnostic and surgical procedures where interpretation of pulmonary arterial pressure measurements might determine final management of the patient. When high dose or anesthetic dosages of Sufentanil Citrate Injection are employed, even relatively small dosages of diazepam may cause cardiovascular depression.
When Sufentanil Citrate Injection is used with CNS depressants, hypotension can occur. If it occurs, consider the possibility of hypovolemia and manage with appropriate parenteral fluid therapy. When operative conditions permit, consider repositioning the patient to improve venous return to the heart. Exercise care in moving and repositioning of patients because of the possibility of orthostatic hypotension. If volume expansion with fluids plus other countermeasures do not correct hypotension, consider administration of pressor agents other than epinephrine. Epinephrine may paradoxically decrease blood pressure in patients treated with a neuroleptic that blocks alpha adrenergic activity. Profound sedation, respiratory depression, coma, and death may result from the concomitant use of Sufentanil Citrate Injection with benzodiazepines or other CNS depressants (e.g., nonbenzodiazepine sedatives/hypnotics, anxiolytics, tranquilizers, muscle relaxants, general anesthetics, antipsychotics, other opioids, alcohol).
If the decision is made to manage postoperative pain with Sufentanil Citrate Injection concomitantly with a benzodiazepine or other CNS depressant, start dosing with the lowest effective dosage and titrate based on clinical response. Follow patients closely for signs and symptoms of respiratory depression, sedation, and hypotension. Fluids or other measures to counter hypotension should be available [see Drug Interactions (7)].
5.6 Severe Cardiovascular Depression
Sufentanil Citrate Injection may cause severe bradycardia, severe hypotension including orthostatic hypotension, and syncope. There is increased risk in patients whose ability to maintain blood pressure has already been compromised by a reduced blood volume or concurrent administration of certain CNS depressant drugs (e.g., phenothiazines or general anesthetics) [see Drug Interactions (7)]. In patients with circulatory shock, Sufentanil Citrate Injection may cause vasodilation that can further reduce cardiac output and blood pressure. Monitor these patients for signs of hypotension after initiating or titrating the dosage of Sufentanil Citrate Injection.
5.7 Serotonin Syndrome with Concomitant Use of Serotonergic Drugs
Cases of serotonin syndrome, a potentially life-threatening condition, have been reported during concomitant use of Sufentanil Citrate Injection with serotonergic drugs. Serotonergic drugs include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), triptans, 5-HT3 receptor antagonists, drugs that affect the serotonergic neurotransmitter system (e.g., mirtazapine, trazodone, tramadol), and drugs that impair metabolism of serotonin (including MAO inhibitors, both those intended to treat psychiatric disorders and also others, such as linezolid and intravenous methylene blue) [see Drug Interactions (7)]. This may occur within the recommended dosage range.
Serotonin syndrome symptoms may include mental status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g.,tachycardia, labile blood pressure, hyperthermia), neuromuscular aberrations (e.g., hyperreflexia, incoordination, rigidity), and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea). The onset of symptoms generally occurs within several hours to a few days of concomitant use, but may occur later than that. Discontinue Sufentanil Citrate Injection if serotonin syndrome is suspected.
5.8 Risks due to Improper Epidural Injection
Proper placement of the needle or catheter in the epidural space should be verified before sufentanil is injected to assure that unintentional intravascular or intrathecal administration does not occur. Unintentional intravascular injection of sufentanil could result in a potentially serious overdose, including acute truncal muscular rigidity and apnea. Unintentional intrathecal injection of the full sufentanil/bupivacaine epidural doses and volume could produce effects of high spinal anesthesia including prolonged paralysis and delayed recovery. If analgesia is inadequate, the placement and integrity of the catheter should be verified prior to the administration of any additional epidural medications. Sufentanil should be administered epidurally by slow injection.
5.9 Risks of Use in Patients with Increased Intracranial Pressure, Brain Tumors, or Head Injury
In patients who may be susceptible to the intracranial effects of CO2 retention (e.g., those with evidence of increased intracranial pressure or brain tumors), Sufentanil Citrate Injection may reduce respiratory drive, and the resultant CO2 retention can further increase intracranial pressure. Monitor such patients for signs of increasing intracranial pressure.
5.10 Risks of Use in Patients with Gastrointestinal Conditions
Sufentanil may cause spasm of the sphincter of Oddi. Opioids may cause increases in serum amylase. Monitor patients with biliary tract disease, including acute pancreatitis for worsening symptoms.
5.11 Increased Risk of Seizures in Patients with Seizure Disorders
Sufentanil may increase the frequency of seizures in patients with seizure disorders, and may increase the risk of seizures occurring in other clinical settings associated with seizures. Monitor patients with a history of seizure disorders for worsened seizure control during Sufentanil Citrate Injection therapy.
5.12 Risks of Driving and Operating Machinery
Sufentanil Citrate Injection may impair the mental or physical abilities needed to perform potentially hazardous activities such as driving a car or operating machinery. Warn patients not to drive or operate dangerous machinery after Sufentanil Citrate Injection administration.
6 ADVERSE REACTIONS
The following serious adverse reactions are described, or described in greater detail, in other sections:
6.1 Clinical Trials Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
Epidural use in Labor and Delivery
Epidural sufentanil was tested in 340 patients in two (one single-center and one multicenter) double-blind, parallel studies. Doses ranged from 10 to 15 mcg sufentanil and were delivered in a 10 mL volume of 0.125% bupivacaine with and without epinephrine 1:200,000. In all cases sufentanil was administered following a dose of local anesthetic to test proper catheter placement. Since epidural opioids and local anesthetics potentiate each other, these results may not reflect the dose or efficacy of epidural sufentanil by itself.
Individual doses of 10 to 15 mcg sufentanil plus bupivacaine 0.125% with epinephrine provided analgesia during the first stage of labor with a duration of 1 to 2 hours. Onset was rapid (within 10 minutes). Subsequent doses (equal dose) tended to have shorter duration. Analgesia was profound (complete pain relief) in 80% to 100% of patients and a 25% incidence of pruritus was observed. The duration of initial doses of sufentanil plus bupivacaine with epinephrine is approximately 95 minutes, and of subsequent doses, 70 minutes.
There are insufficient data to critically evaluate neonatal neuromuscular and adaptive capacity following recommended doses of maternally administered epidural sufentanil with bupivacaine. However, if larger than recommended doses are used for combined local and systemic analgesia, e.g. after administration of a single dose of 50 mcg epidural sufentanil during delivery, then impaired neonatal adaption to sound and light can be detected for 1 to 4 hours and if a dose of 80 mcg is used impaired neuromuscular coordination can be detected for more than 4 hours.
6.2 Postmarketing Experience
The following adverse reactions have been identified during post approval use of sufentanil. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Serotonin syndrome: Cases of serotonin syndrome, a potentially life-threatening condition, have been reported during concomitant use of opioids with serotonergic drugs.
Adrenal insufficiency: Cases of adrenal insufficiency have been reported with opioid use, more often following greater than one month of use.
Anaphylaxis: Anaphylaxis has been reported with ingredients contained in Sufentanil Citrate Injection.
Androgen deficiency: Cases of androgen deficiency have occurred with chronic use of opioids [see Clinical Pharmacology (12.2)].
7 DRUG INTERACTIONS
Table 2 includes clinically significant drug interactions with Sufentanil Citrate Injection.
Table 2: Clinically Significant Drug Interactions with Sufentanil Citrate Injection
Inhibitors of CYP3A4
Clinical Impact:The concomitant use of Sufentanil Citrate Injection and CYP3A4 inhibitors can increase the plasma concentration of sufentanil, resulting in increased or prolonged opioid effects, particularly when an inhibitor is added after a stable dose of Sufentanil Citrate Injection is achieved [see Warnings and Precautions (5.4)].
After stopping a CYP3A4 inhibitor, as the effects of the inhibitor decline, the sufentanil plasma concentration will decrease [see Clinical Pharmacology (12.3)], resulting in decreased opioid efficacy or a withdrawal syndrome in patients who had developed physical dependence to sufentanil.
Intervention:If concomitant use is necessary, consider dosage reduction of Sufentanil Citrate Injection until stable drug effects are achieved. Monitor patients for respiratory depression and sedation at frequent intervals.
If a CYP3A4 inhibitor is discontinued, consider increasing the Sufentanil Citrate Injection dosage until stable drug effects are achieved. Monitor for signs of opioid withdrawal.
Examples:Macrolide antibiotics (e.g., erythromycin), azole-antifungal agents (e.g. ketoconazole), protease inhibitors (e.g., ritonavir), grapefruit juice.
CYP3A4 Inducers
Clinical Impact:The concomitant use of Sufentanil Citrate Injection and CYP3A4 inducers can decrease the plasma concentration of sufentanil [see Clinical Pharmacology (12.3)], resulting in decreased efficacy or onset of a withdrawal syndrome in patients who have developed physical dependence to sufentanil [see Warnings and Precautions (5.4)].
After stopping a CYP3A4 inducer, as the effects of the inducer decline, the sufentanil plasma concentration will increase [see Clinical Pharmacology (12.3)], which could increase or prolong both the therapeutic effects and adverse reactions, and may cause serious respiratory depression.
Intervention:If concomitant use is necessary, consider increasing the Sufentanil Citrate Injection dosage until stable drug effects are achieved. Monitor for signs of opioid withdrawal. If a CYP3A4 inducer is discontinued, consider Sufentanil Citrate Injection dosage reduction and monitor for signs of respiratory depression.
ExamplesRifampin, carbamazepine, phenytoin
Benzodiazepines and other Central Nervous System (CNS) Depressants
Clinical Impact:The concomitant use of Sufentanil Citrate Injection with CNS depressants my result in decreased pulmonary artery pressure and may cause hypotension. Even small dosages of diazepam may cause cardiovascular depression when added to high dose or anesthetic dosages of Sufentanil Citrate Injection. As postoperative analgesia, concomitant use of Sufentanil Citrate Injection can increase the risk of hypotension, respiratory depression, profound sedation, coma, and death.
Intervention:As postoperative analgesia, start with a lower dose of Sufentanil Citrate Injection and monitor patients for signs of respiratory depression, sedation, and hypotension. Fluids or other measures to counter hypotension should be available. [see Warnings and Precautions (5.5)].
Examples:Benzodiazepines and other sedatives/hypnotics, anxiolytics, tranquilizers, muscle relaxants, general anesthetics, antipsychotics, other opioids, alcohol.
Serotonergic Drugs
Clinical Impact:The concomitant use of opioids with other drugs that affect the serotonergic neurotransmitter system has resulted in serotonin syndrome [see Warnings and Precautions 5.5].
Intervention:If concomitant use is warranted, carefully observe the patient, particularly during treatment initiation and dose adjustment. Discontinue Sufentanil Citrate Injection if serotonin syndrome is suspected.
Examples:Selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), triptans, 5-HT3 receptor antagonists, drugs that effect the serotonin neurotransmitter system (e.g., mirtazapine, trazodone, tramadol), monoamine oxidase (MAO) inhibitors (those intended to treat psychiatric disorders and also others, such as linezolid and intravenous methylene blue).
Monoamine Oxidase Inhibitors
Clinical Impact:MAOI interactions with opioids may manifest as serotonin syndrome or opioid toxicity (e.g., respiratory depression, coma) [see Warnings and Precautions (5.2)].
Intervention:The use of Sufentanil Citrate Injection is not recommended for patients taking MAOIs or within 14 days of stopping such treatment.
Examples:phenelzine, tranylcypromine, linezolid
Mixed Agonist/Antagonist and Partial Agonist Opioid Analgesics
Clinical Impact:May reduce the analgesic effect of Sufentanil Citrate Injection and/or precipitate withdrawal symptoms.
Intervention:Avoid concomitant use.
Examples:butorphanol, nalbuphine, pentazocine, buprenorphine
Muscle Relaxants
Clinical Impact:sufentanil may enhance the neuromuscular blocking action of skeletal muscle relaxants and produce an increased degree of respiratory depression.
Intervention:Monitor patients for signs of respiratory depression that may be greater than otherwise expected and decrease the dosage of Sufentanil Citrate Injection and/or the muscle relaxant as necessary.
Diuretics
Clinical Impact:Opioids can reduce the efficacy of diuretics by inducing the release of antidiuretic hormone.
Intervention:Monitor patients for signs of diminished diuresis and/or effects on blood pressure and increase the dosage of the diuretic as needed.
Anticholinergic Drugs
Clinical Impact:The concomitant use of anticholinergic drugs may increase risk of urinary retention and/or severe constipation, which may lead to paralytic ileus.
Intervention:Monitor patients for signs of urinary retention or reduced gastric motility when Sufentanil Citrate Injection is used concomitantly with anticholinergic drugs.
Nitrous oxide
Clinical Impact:Nitrous oxide has been reported to produce cardiovascular depression when given with higher doses of Sufentanil Citrate Injection.
Intervention:Monitor patients for signs of cardiovascular depression that may be greater than otherwise expected.
8 USE IN SPECIFIC POPULATIONS
8.1 Pregnancy
Risk Summary
Prolonged use of opioid analgesics during pregnancy may cause neonatal opioid withdrawal syndrome. Available data with Sufentanil Citrate Injection in pregnant women are insufficient to inform a drug-associated risk for major birth defects and miscarriage. In animal reproduction studies, embryolethality and maternal toxicity were noted in rabbits when sufentanil was administered intravenously at 0.9 times the human procedural dose of 30 mcg/kg during organogenesis. Decreased live fetuses and pup survival were noted in rats treated with sufentanil late in gestation and throughout lactation at doses below the human procedural dose No malformations were observed in either rats or rabbits at doses below the human procedural dose [see Data]. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2–4% and 15–20%, respectively.
Clinical Considerations
Fetal/Neonatal Adverse Reactions
Prolonged use of opioid analgesics during pregnancy for medical or nonmedical purposes can result in physical dependence in the neonate and neonatal opioid withdrawal syndrome shortly after birth.
Neonatal opioid withdrawal syndrome presents as irritability, hyperactivity and abnormal sleep pattern, high pitched cry, tremor, vomiting, diarrhea and failure to gain weight. The onset, duration, and severity of neonatal opioid withdrawal syndrome vary based on the specific opioid used, duration of use, timing and amount of last maternal use, and rate of elimination of the drug by the newborn. Observe newborns for symptoms of neonatal opioid withdrawal syndrome and manage accordingly [see Warnings and Precautions(5.3)].
Labor or Delivery
Opioids cross the placenta and may produce respiratory depression and psycho-physiologic effects in neonates. An opioid antagonist, such as naloxone, must be available for reversal of opioid-induced respiratory depression in the neonate. Sufentanil Citrate Injection is not recommended for use in pregnant women during or immediately prior to labor, when other analgesic techniques are more appropriate. Opioid analgesics, including Sufentanil Citrate Injection, can prolong labor through actions which temporarily reduce the strength, duration, and frequency of uterine contractions. However, this effect is not consistent and may be offset by an increased rate of cervical dilation, which tends to shorten labor. Monitor neonates exposed to opioid analgesics during labor for signs of excess sedation and respiratory depression.
The use of epidurally administered sufentanil in combination with bupivacaine 0.125% with or without epinephrine is indicated for labor and delivery. Sufentanil is not recommended for intravenous use or for use of larger epidural doses during labor and delivery because of potential risks to the newborn infant after delivery. In clinical trials, one case of severe fetal bradycardia associated with maternal hypotension was reported within 8 minutes of maternal administration of sufentanil 15 mcg plus bupivacaine 0.125% (10 mL total volume).
Data
Animal Data
Pregnant rats were treated with intravenous sufentanil doses of 0.005, 0.02, or 0.08 mg/kg/day (0.03, 0.1, or 0.4 times the human total procedural dose of 30 mcg/kg based on body surface area, respectively). No malformations or embryotoxic effects were noted despite maternal toxicity (increased mortality in the mid- and high-dose group).
Pregnant rabbits were treated with intravenous sufentanil doses of 0.005, 0.02, or 0.08 mg/kg/day (0.05, 0.2, or 0.9 times the human total procedural dose of 30 mcg/kg based on body surface area, respectively). Decreased live fetuses per litter and decreased litter size in the high dose group were noted in the presence of maternal toxicity (decreased body weight gain and mortality in the high-dose group).
No evidence of malformations or adverse effects on the fetus was reported in a published study in which pregnant rats were administered 10, 50, or 100 mcg/kg/day sufentanil (0.05, 0.27, or 0.54 times the human procedural dose of 30 mcg/kg/day based on body surface area) continuously from Gestation Day 5 through Gestation Day 20 via subcutaneously implanted osmotic minipumps.
Pregnant rats were treated intravenously with sufentanil 0.005, 0.02, or 0.08 mg/kg/day (0.03,0.1, or 0.4 times the human total procedural dose of 30 mcg/day based on body surface area, respectively) rom Gestation Day 16 through Lactation Day 21. Sufentanil reduced birth weights in the mid- and high-dose groups, decreased live fetuses in the high-dose group, and decreased pup survival in all groups in the presence of maternal toxicity (decreased weight gain and increased mortality in all groups).
8.2 Lactation
Risk Summary
The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for Sufentanil Citrate Injection and any potential adverse effects on the breastfed infant from Sufentanil Citrate Injection or from the underlying maternal condition.
Clinical Considerations
Infants exposed to Sufentanil Citrate Injection through breast milk should be monitored for excess sedation and respiratory depression. Withdrawal symptoms can occur in breastfed infants when maternal administration of an opioid analgesic is stopped, or when breastfeeding is stopped.
8.3 Females and Males of Reproductive Potential
Infertility
Chronic use of opioids may cause reduced fertility in females and males of reproductive potential. It is not known whether these effects on fertility are reversible [see Adverse Reactions (6.2)].
8.4 Pediatric Use
The safety and efficacy of intravenous sufentanil in pediatric patients as young as 1 day old undergoing cardiovascular surgery have been documented in a limited number of cases. The clearance of sufentanil in healthy neonates is approximately one-half that in adults and children. The clearance rate of sufentanil can be further reduced by up to a third in neonates with cardiovascular disease, resulting in an increase in the elimination half-life of the drug.
8.5 Geriatric Use
Elderly patients (aged 65 years or older) may have increased sensitivity to sufentanil. In general, use caution when selecting a dosage for an elderly patient, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy.
Respiratory depression is the chief risk for elderly patients treated with opioids, and has occurred after large initial doses were administered to patients who were not opioid-tolerant or when opioids were co-administered with other agents that depress respiration. Titrate the dosage of Sufentanil Citrate Injection slowly in geriatric patients and monitor closely for signs of central nervous system and respiratory depression [see Warnings and Precautions (5.6)].
8.6 Hepatic Impairment
Sufentanil Citrate Injection should be administered with caution to patients with liver dysfunction because of the extensive hepatic metabolism. Reduce the dosage as needed and monitor closely for signs of respiratory depression, sedation, and hypotension.
8.7 Renal Impairment
Sufentanil Citrate Injection should be administered with caution to patients with kidney dysfunction because of the renal excretion of sufentanil citrate and its metabolites. Reduce the dosage as needed and monitor for signs of respiratory depression, sedation, and hypotension.
9 DRUG ABUSE AND DEPENDENCE
9.1 Controlled Substance
Sufentanil Citrate Injection contains sufentanil, a Schedule II controlled substance.
9.2 Abuse
Sufentanil Citrate Injection contains sufentanil, a substance with a high potential for abuse similar to other opioids including hydrocodone, hydromorphone, methadone, morphine, oxycodone, oxymorphone, and tapentadol.. Sufentanil Citrate Injection can be abused and is subject to misuse, addiction, and criminal diversion [see Warnings and Precautions (5.1)]. Drug addiction is a cluster of behavioral, cognitive, and physiological phenomena that develop after repeated substance use and includes: a strong desire to take the drug, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to drug use than to other activities and obligations, increased tolerance, and sometimes a physical withdrawal.
Sufentanil Citrate Injection, like other opioids, can be diverted for non-medical use into illicit channels of distribution. Careful recordkeeping of prescribing information, including quantity, frequency, and renewal requests, as required by state and federal law, is strongly advised.
Risks Specific to Abuse of Sufentanil Citrate Injection
Abuse of Sufentanil Citrate Injection poses a risk of overdose and death. The risk is increased with concurrent use of Sufentanil Citrate Injection with alcohol and other central nervous system depressants. Parenteral drug abuse is commonly associated with transmission of infectious diseases such as hepatitis and HIV.
9.3 Dependence
Both tolerance and physical dependence can develop during chronic opioid therapy. Tolerance is the need for increasing doses of opioids to maintain a defined effect such as analgesia (in the absence of disease progression or other external factors). Tolerance may occur to both the desired and undesired effects of drugs, and may develop at different rates for different effects.
Physical dependence results in withdrawal symptoms after abrupt discontinuation or a significant dosage reduction of a drug. Withdrawal also may be precipitated through the administration of drugs with opioid antagonist activity (e.g., naloxone, nalmefene), mixed agonist/antagonist analgesics (pentazocine, butorphanol, nalbuphine), or partial agonists (buprenorphine). Physical dependence may not occur to a clinically significant degree until after several days to weeks of continued opioid usage.
10 OVERDOSAGE
Clinical Presentation
Acute overdose with Sufentanil Citrate Injection can be manifested by respiratory depression, somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, constricted pupils, and, in some cases, pulmonary edema, bradycardia, hypotension, partial or complete airway obstruction, atypical snoring, and death. Marked mydriasis rather than miosis may be seen with hypoxia in overdose situations [see Clinical Pharmacology (12.2)].
Treatment of Overdose
In case of overdose, priorities are the reestablishment of a patent and protected airway and institution of assisted or controlled ventilation, if needed. Employ other supportive measures (including oxygen and vasopressors) in the management of circulatory shock and pulmonary edema as indicated. Cardiac arrest or arrhythmias will require advanced life-support techniques. The opioid antagonists, naloxone or nalmefene, are specific antidotes to respiratory depression resulting from opioid overdose. For clinically significant respiratory or circulatory depression secondary to sufentanil overdose, administer an opioid antagonist. Opioid antagonists should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to sufentanil overdose.
Because the duration of opioid reversal is expected to be less than the duration of action of sufentanil in Sufentanil Citrate Injection, carefully monitor the patient until spontaneous respiration is reliably reestablished. If the response to an opioid antagonist is suboptimal or only brief in nature, administer additional antagonist as directed by the product's prescribing information. In an individual physically dependent on opioids, administration of the recommended usual dosage of the antagonist will precipitate an acute withdrawal syndrome. The severity of the withdrawal symptoms experienced will depend on the degree of physical dependence and the dose of the antagonist administered. If a decision is made to treat serious respiratory depression in the physically dependent patient, administration of the antagonist should be initiated with care and by titration with smaller than usual doses of the antagonist.
11 DESCRIPTION
Sufentanil Citrate Injection, USP is a sterile, nonpyrogenic solution of sufentanil citrate in water for injection. Sufentanil Citrate is a potent opioid analgesic which is administered either epidurally or by intravenous injection.
Each mL contains sufentanil citrate equivalent to 50 mcg of sufentanil. May contain sodium hydroxide and/or hydrochloric acid for pH adjustment. pH 4.2 (3.5 to 6.0).
The solution contains no bacteriostat, antimicrobial agent or added buffer and is intended for use only as a single-use injection. When smaller doses are required, the unused portion should be discarded in an appropriate manner.
Sufentanil Citrate, USP, occurs as a white crystalline powder and is chemically designated as N-[-4-(methyoxymethyl)-1-[2-(2-thienyl)ethyl]-4-piperidinyl]-N-phenylpropanamide 2-hydroxy-1,2,3-propanetricarboxylate (1:1).
The molecular formula of sufentanil citrate is C22H30N2O2S∙C6H8O7 and the molecular weight is 578.69. Sufentanil Citrate has the following structural formula:
Chemical Structure
12 CLINICAL PHARMACOLOGY
12.1 Mechanism of Action
Sufentanil is an opioid agonist. When used in balanced general anesthesia, sufentanil has been reported to be as much as 10 times as potent as fentanyl. When administered intravenously as a primary anesthetic agent with 100% oxygen, sufentanil is approximately 5 to 7 times as potent as fentanyl.
12.2 Pharmacodynamics
Effects on the Central Nervous System
Sufentanil produces respiratory depression by direct action on brain stem respiratory centers. The respiratory depression involves both a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation.
Sufentanil causes miosis, even in total darkness. Pinpoint pupils are a sign of opioid overdose but are not pathognomonic (e.g., pontine lesions of hemorrhagic or ischemic origins may produce similar findings). Marked mydriasis rather than miosis may be seen due to hypoxia in overdose situations.
Effects on the Gastrointestinal Tract and Other Smooth Muscle
Sufentanil causes a reduction in motility associated with an increase in smooth muscle tone in the antrum of the stomach and duodenum. Digestion of food in the small intestine is delayed and propulsive contractions are decreased. Propulsive peristaltic waves in the colon are decreased, while tone may be increased to the point of spasm resulting in constipation. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions, spasm of sphincter of Oddi, and transient elevations in serum amylase.
Effects on the Cardiovascular System
Sufentanil produces peripheral vasodilation which may result in orthostatic hypotension or syncope. Manifestations of histamine release and/or peripheral vasodilation may include pruritus, flushing, red eyes and sweating and/or orthostatic hypotension.
Effects on the Endocrine System
Opioids inhibit the secretion of adrenocorticotropic hormone (ACTH), cortisol, and luteinizing hormone (LH) in humans. They also stimulate prolactin, growth hormone (GH) secretion, and pancreatic secretion of insulin and glucagon [see Adverse Reactions (6.2)].
Chronic use of opioids may influence the hypothalamic-pituitary-gonadal axis, leading to androgen deficiency that may manifest as low libido, impotence, erectile dysfunction, amenorrhea, or infertility. The causal role of opioids in the clinical syndrome of hypogonadism is unknown because the various medical, physical, lifestyle, and psychological stressors that may influence gonadal hormone levels have not been adequately controlled for in studies conducted to date [see Adverse Reactions (6.2)].
Effects on the Immune System
Opioids have been shown to have a variety of effects on components of the immune system in in vitro and animal models. The clinical significance of these findings is unknown. Overall, the effects of opioids appear to be modestly immunosuppressive.
Concentration–Efficacy Relationships
The minimum effective analgesic concentration will vary widely among patients, especially among patients who have been previously treated with potent agonist opioids [see Dosage and Administration (2.1, 2.2)]. The minimum effective analgesic concentration of sufentanil for any individual patient may increase over time due to an increase in pain, the development of a new pain syndrome and/or the development of analgesic tolerance.
Concentration–Adverse Reaction Relationships
There is a relationship between increasing sufentanil plasma concentration and increasing frequency of dose-related opioid adverse reactions such as nausea, vomiting, CNS effects, and respiratory depression. In opioid-tolerant patients, the situation may be altered by the development of tolerance to opioid-related adverse reactions [see Dosage and Administration (2.1, 2.2, 2.3)].
12.3 Pharmacokinetics
Sufentanil Citrate Injection is administered by the intravenous or epidural route. The pharmacokinetics of intravenous sufentanil can be described as a three-compartment model.
Absorption
After epidural administration of incremental doses totaling 5 to 40 mcg sufentanil during labor and delivery, maternal and neonatal sufentanil plasma concentrations were at or near the 0.05 to 0.1 ng/mL limit of detection, and were slightly higher in mothers than in their infants.
Distribution
Plasma protein binding of sufentanil, related to the alpha acid glycoprotein concentration, was approximately 93% in healthy males, 91% in mothers and 79% in neonates. Sufentanil has a distribution time of 1.4 minutes and redistribution time of 17.1 minutes.
Elimination
The elimination half-life is 164 minutes in adults. The elimination half-life of sufentanil is shorter (e.g. 97 +/- 42 minutes) in infants and children, and longer in neonates (e.g. 434 +/- 160 minutes) compared to that of adolescents and adults.
Metabolism
The liver and small intestine are the major sites of biotransformation.
Excretion
Approximately 80% of the administered dose is excreted within 24 hours and only 2% of the dose is eliminated as unchanged drug.
13 NONCLINICAL TOXICOLOGY
13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility
Carcinogenesis
Long-term studies in animals to evaluate the carcinogenic potential of sufentanil have not been conducted.
Mutagenesis
Sufentanil was not genotoxic in the in vitro bacterial reverse mutation assay (Ames assay) or in the in vivo rat bone marrow micronucleous assay.
Impairment of Fertility
Fertility and early embryonic development studies were conducted in male and female rats treated with 0.005, 0.02 or 0.08 mg/kg sufentanil IV for 56 days and 14 days prior to mating through gestation respectively. Increased mortality was noted in all treatment groups. Lower pregnancy rated were noted following treatment of males at doses of 0.02 and 0.08 mg/kg (0.1 and 0.4 times the maximum human total procedural dose of 30 mcg/kg IV, based on a body surface area comparison), suggesting the potential for an adverse effect on fertility in males. Increased resorption of fetuses and reduced litter size was noted in the high dose females (0.4 times the maximum human total procedural dose of 30 mcg/kg IV, based on a body surface area comparison) suggesting the potential for fetotoxicity, likely due to maternal toxicity.
14 CLINICAL STUDIES
Epidural use in Labor and Delivery
Epidural sufentanil was tested in 340 patients in two (one single-center and one multicenter) double-blind, parallel studies. Doses ranged from 10 to 15 mcg sufentanil and were delivered in a 10 mL volume of 0.125% bupivacaine with and without epinephrine 1:200,000. In all cases sufentanil was administered following a dose of local anesthetic to test proper catheter placement. Since epidural opioids and local anesthetics potentiate each other, these results may not reflect the dose or efficacy of epidural sufentanil by itself.
Individual doses of 10 to 15 mcg sufentanil plus bupivacaine 0.125% with epinephrine provided analgesia during the first stage of labor with a duration of 1 to 2 hours. Onset was rapid (within 10 minutes). Subsequent doses (equal dose) tended to have shorter duration. Analgesia was profound (complete pain relief) in 80% to 100% of patients and a 25% incidence of pruritus was observed. The duration of initial doses of sufentanil plus bupivacaine with epinephrine is approximately 95 minutes, and of subsequent doses, 70 minutes.
There are insufficient data to critically evaluate neonatal neuromuscular and adaptive capacity following recommended doses of maternally administered epidural sufentanil with bupivacaine. However, if larger than recommended doses are used for combined local and systemic analgesia, e.g. after administration of a single dose of 50 mcg epidural sufentanil during delivery, then impaired neonatal adaption to sound and light can be detected for 1 to 4 hours and if a dose of 80 mcg is used impaired neuromuscular coordination can be detected for more than 4 hours.
16 HOW SUPPLIED/STORAGE AND HANDLING
Sufentanil Citrate Injection, USP equivalent to 50 mcg/mL sufentanil is supplied in the following single-use containers:
Unit of SaleConcentration
NDC 0409-3382-4950 mcg(50 mcg/mL)
Carton containing 10 Fliptop Vials
NDC 0409-3382-50100 mcg/2 mL(50 mcg/mL)
Carton containing 10 Fliptop Vials
NDC 0409-3382-51250 mcg/5 mL (50 mcg/mL)
Carton containing 10 Fliptop Vials
Protect from light. Retain in carton until time of use.
Store at 20 to 25°C (68 to 77°F). [See USP Controlled Room Temperature.]
Distributed by Hospira, Inc., Lake Forest, IL 60045 USA
Logo
Novaplus is a registered trademark of Vizient, Inc.
LAB-1125-2.0
Revised: 5/2018
Document Id: 1da45451-b797-41d8-91e3-5305c72b96cf
Set id: cd3dc1ac-47e6-4d2b-aa9d-6a1bacd2a0df
Version: 3
Effective Time: 20180510
Hospira, Inc.
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Indica’s Pain Relief Properties
Hey there, if you’re seeking natural alternatives for pain management, you’ve come to the right place. Indica strains have gained recognition for their potential to alleviate chronic pain, offering a potentially effective solution for those in need.
When it comes to pain relief, cannabis has shown promise in managing various types of discomfort. Indica strains, in particular, have analgesic and anti-inflammatory properties that make them a viable option for individuals seeking relief from conditions like nerve damage, inflammation, arthritis, migraines, and fibromyalgia. The cannabinoids found in Cannabis Indica, such as THC and CBD, interact with the body’s endocannabinoid system to modulate pain perception.
Key Takeaways:
• Indica strains are known for their potential to alleviate chronic pain.
• They have analgesic and anti-inflammatory properties.
• Indica may be effective for managing nerve damage, inflammation, arthritis, migraines, and fibromyalgia.
• The cannabinoids in Indica interact with the body’s endocannabinoid system to modulate pain perception.
• Further research is needed to establish specific strain recommendations and optimal dosing.
The Different Types of Cannabis
When it comes to cannabis, there are various types or strains available, each with its own unique characteristics and effects. The most common types of cannabis are Cannabis indica, Cannabis sativa, and hybrids.
Cannabis Indica
Cannabis indica is known for its distinct physical traits, such as broad, dark green leaves, a shorter stature, and dense buds. This type of cannabis is typically associated with a more relaxing and sedating effect on the body. It is often recommended for pain relief, insomnia, and nausea. Indica strains have analgesic and anti-inflammatory properties, making them a natural alternative to traditional pain medications.
Cannabis Sativa
On the other hand, Cannabis sativa is known for its energizing and uplifting effects. This type of cannabis is characterized by its taller stature, narrower leaves, and looser buds. Sativa strains are often used to improve mood, enhance creativity, and provide a more cerebral experience. They are generally recommended for daytime use.
Hybrids
Hybrid strains are a combination of both indica and sativa genetics. These strains are cultivated to create specific effects by crossing different strains. Hybrids can have a balanced blend of the characteristics of both indica and sativa, providing a combination of both physical relaxation and mental stimulation. The effects of hybrid strains can vary depending on the specific genetics and ratio of indica to sativa.
Overall, understanding the different types of cannabis is essential for finding the right strain that suits your needs and preferences. Whether you’re seeking pain relief, relaxation, focus, or creativity, there is a cannabis strain out there to cater to your individual desires.
Cannabis Indica for Pain Management
When it comes to finding natural alternatives for chronic pain relief, many individuals turn to cannabis, specifically Indica strains. Users have reported positive effects on pain management, making it a popular choice for those seeking alternative methods for pain relief.
In an online survey, participants indicated a preference for Indica strains for pain relief, sedation, and sleep. The analgesic and anti-inflammatory properties of Indica strains are believed to contribute to their effectiveness in reducing pain. However, it’s important to note that strain-specific recommendations are not medically proven, as there is limited research available on the use of specific cannabis strains for pain.
Individual variations in response to cannabis should also be taken into consideration. Further research is needed to explore the effects of different strains, dosages, and methods of delivery.
Benefits of Cannabis Indica for Pain Management Indica Strains
Effective in reducing pain Strain-specific recommendations are not medically proven
Preferred by users for pain relief, sedation, and sleep Individual variations in response to cannabis
Analgesic and anti-inflammatory properties Further research needed on different strains, dosages, and methods of delivery
“Cannabis Indica has been reported by users to have positive effects on pain management.”
While anecdotal evidence suggests the potential benefits of using Indica strains for pain relief, it is important to consult with a healthcare professional before incorporating cannabis into a pain management plan. This will help ensure personalized and safe use, taking into account individual medical history, current medications, and potential side effects.
Indica for Muscle Relaxation and Spasm Control
When it comes to finding natural remedies for muscle relaxation and spasm control, cannabis Indica strains may offer potential benefits. With their anti-inflammatory properties, Indica strains can help reduce inflammation in the muscles and joints, providing relief for conditions like multiple sclerosis and fibromyalgia. These strains have been reported to alleviate muscle spasms and stiffness associated with these conditions, promoting increased comfort and improved mobility.
Benefits of Indica for Muscle Relaxation:
• Reduces inflammation in muscles and joints
• Alleviates muscle spasms and stiffness
• Promotes comfort and improved mobility
By incorporating Indica strains into their wellness routines, individuals with muscle-related issues have the potential to experience relief from discomfort and enhanced relaxation. It is important, however, to consult with a healthcare professional and explore strain-specific recommendations for the most appropriate and effective use.
Using Indica strains for muscle relaxation has been a game-changer for me. I’ve noticed a significant reduction in muscle spasms and stiffness, allowing me to move more freely and comfortably. It’s a natural alternative that has made a positive impact on my daily life.
Indica Strain THC Content CBD Content Effects
Bubba Kush High Low Relaxation, pain relief, sedation
Purple Kush High Low Muscle relaxation, calming
Granddaddy Purple High Low Relaxation, sleep aid, pain relief
It is essential to note that individual experiences may vary, and further research is needed to fully understand the mechanisms and optimal use of Indica strains for muscle relaxation and spasm control. Nonetheless, the potential benefits of cannabis Indica make it an intriguing option for individuals seeking natural alternatives for muscle-related issues.
Indica for muscle relaxation
Indica for Anxiety and Stress Relief
When it comes to finding natural remedies for anxiety and stress relief, cannabis Indica strains offer a promising solution. The calming properties of Indica strains can help individuals relax and unwind, promoting a sense of tranquility in their daily lives. With their sedative effects, Indica strains can be a potential option for managing anxiety and stress without resorting to pharmaceuticals.
To achieve optimal results, it is important to choose Indica strains with higher CBD content and lower levels of THC, the psychoactive compound responsible for the “high” associated with cannabis. By selecting strains with higher CBD levels, individuals can experience the calming benefits of Indica without the strong psychoactive effects. This allows for relaxation and stress relief without impairing cognitive function or inducing excessive sedation.
While preliminary studies suggest positive outcomes, further research is needed to establish the effectiveness and optimal dosing of Indica for anxiety disorders. Despite the lack of comprehensive scientific evidence, many individuals report positive experiences using Indica strains for anxiety and stress relief. As with any alternative therapy, it is essential to consult with a healthcare professional before incorporating cannabis into your stress management routine.
The Benefits of Indica for Anxiety and Stress Relief:
• Promotes relaxation and calmness
• Reduces feelings of anxiety and stress
• Offers a natural alternative to pharmaceuticals
• Allows individuals to unwind and find tranquility
• Minimal cognitive impairment compared to high-THC strains
Discover the soothing effects of cannabis Indica strains for anxiety and stress relief. Incorporating Indica into your self-care routine may provide the relaxation and calmness you need to navigate through life’s challenges while minimizing the potential side effects of pharmaceutical interventions.
Indica for Sleep and Insomnia
Cannabis Indica has been recognized for its potential in alleviating sleep disorders and insomnia. The sedating effects of Indica strains can help calm the mind and promote relaxation, making it easier to fall asleep and achieve a restful night’s sleep. For individuals struggling with sleep issues, consuming Indica strains before bedtime may offer relief.
It is important to note that starting with low doses and gradually increasing as needed is crucial to avoid excessive sedation or cognitive impairment. Finding the right dosage for sleep benefits is a process of trial and error, as individual responses to cannabis can vary.
Research suggests that the cannabinoids in Cannabis Indica, particularly THC and CBD, interact with the body’s endocannabinoid system, which plays a role in regulating sleep-wake cycles. By modulating this system, Indica strains have the potential to promote a more balanced sleep pattern.
Indica for sleep disorders
However, it is important to consult with a healthcare professional before using Indica for sleep-related issues. They can provide guidance on appropriate strains, dosages, and methods of consumption, taking into account individual needs and any potential interactions with existing medications.
Benefits of Indica for Sleep and Insomnia Suggested Indica Strains
Enhanced relaxation and calmness Granddaddy Purple
Promotes a more balanced sleep pattern Northern Lights
Reduces sleep onset latency Bubba Kush
Alleviates sleep disturbances OG Kush
Indica strains have the potential to improve sleep quality and provide relief for individuals struggling with insomnia. However, further research is needed to understand the full effects and optimal usage of Indica for sleep-related issues.
Indica for Appetite Stimulation and Recreation
When it comes to Indica strains, their benefits extend beyond pain relief and relaxation. In fact, Indica strains are known for their ability to stimulate appetite. This makes them particularly valuable for individuals undergoing treatments like chemotherapy or those dealing with conditions such as HIV/AIDS or eating disorders. If you’re struggling to find your appetite, Indica might just be the solution you’ve been looking for.
But it’s not just the physical effects that make Indica strains popular. The recreational benefits of Indica are well-regarded among cannabis enthusiasts. When consumed, Indica can create a sense of tranquility and relaxation that is perfect for unwinding after a long day or simply enjoying some downtime. Many users also report enhanced sensory experiences, with intensified taste sensations and a heightened appreciation for music and nature. Indica strains can even spark creativity in some individuals, making it a versatile choice for recreational use.
As always, it’s important to be aware of local regulations and consumption guidelines when using Indica for recreational purposes. However, when used responsibly, Indica can offer a delightful and enjoyable experience, allowing you to tap into your senses and fully embrace the relaxation and euphoria it provides. So, whether you’re seeking appetite stimulation or looking to enhance your recreational experiences, Indica strains might just be the perfect choice for you.
FAQ
Can Cannabis Indica help alleviate chronic pain?
Yes, Cannabis Indica has been found to potentially alleviate certain types of chronic pain due to its analgesic and anti-inflammatory properties.
What are the different types of cannabis?
There are three main types of cannabis: Cannabis indica, Cannabis sativa, and hybrids.
Is Cannabis Indica effective for pain management?
Cannabis Indica has been reported by users to have positive effects on pain management, but more research is needed for medically proven strain-specific recommendations.
Can Cannabis Indica help with muscle relaxation and spasm control?
Yes, the anti-inflammatory properties of Cannabis Indica can help reduce inflammation in muscles and joints, providing relief for conditions like multiple sclerosis and fibromyalgia.
Does Cannabis Indica have calming effects for anxiety and stress relief?
Yes, Cannabis Indica has calming and soothing properties that may help with anxiety and stress relief. However, further research is needed to establish its effectiveness and optimal dosing.
Can Cannabis Indica help with sleep and insomnia?
Yes, the sedating properties of Cannabis Indica can help individuals relax and achieve restful sleep, making it potentially beneficial for sleep disorders and insomnia.
Is Cannabis Indica useful for appetite stimulation and recreational purposes?
Yes, Cannabis Indica can stimulate appetite and provide recreational experiences with enhanced sensory perceptions. However, it’s important to be mindful of local regulations and consumption guidelines.
Source Links
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9222580d47c553ea90dc0f5e416f8f3a
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Longevity
What Is Resveratrol?
What Is Resveratrol
Resveratrol Supplements
Resveratrol is a natural compound found in various plant species, including grapes, berries, and peanuts.
It has gained a lot of attention in recent years due to its potential health benefits, particularly its anti-inflammatory and antioxidant effects.
In this article, we'll explore the benefits of resveratrol supplements, their relationship to red wine, potential side effects, and what you need to know before taking them.
Benefits of Resveratrol
Resveratrol supplements have been studied for their potential to reduce inflammation, lower blood sugar levels, and improve heart health.
One study published in the Journal of the American College of Cardiology found that resveratrol improved arterial function and lowered blood pressure in adults with metabolic syndrome.
Another study published in the International Journal of Preventive Medicine found that resveratrol supplements reduced inflammation in adults with type 2 diabetes.
Resveratrol has also been studied for its potential to improve cognitive function, prevent cancer, and slow down the aging process.
However, more research is needed to determine the efficacy of resveratrol supplements in these areas.
Resveratrol and Red Wine
Red wine is often cited as a source of resveratrol, but it's important to note that the amount of resveratrol in red wine is relatively low.
Additionally, excessive alcohol consumption can have negative health effects, which may counteract any potential benefits of resveratrol.
Therefore, resveratrol supplements may be a more practical and effective way to obtain the benefits of this natural compound.
Side Effects
Resveratrol supplements are generally considered safe for most people when taken in recommended doses.
However, some people may experience mild side effects, such as digestive issues, headaches, or insomnia.
Additionally, resveratrol supplements may interact with certain medications, so it's important to talk to your healthcare provider before taking them.
The Bottom Line
Resveratrol supplements may offer several potential health benefits, including improved heart health, reduced inflammation, and lower blood sugar levels.
While red wine is often cited as a source of resveratrol, the amount of resveratrol in red wine is relatively low, and excessive alcohol consumption can have negative health effects.
As with any supplement, it's important to talk to your healthcare provider before taking resveratrol supplements to determine whether they're right for you.
But the studies on it are very promising for a number of factors.
Human Studies On Resveratrol
There have been numerous studies on the potential health benefits of resveratrol for humans.
Here are a few examples of some of the best studies on resveratrol:
1. A randomized controlled trial published in the Journal of the American College of Cardiology in 2015 found that resveratrol improved arterial function and lowered blood pressure in adults with metabolic syndrome.
2. A meta-analysis of randomized controlled trials published in the American Journal of Clinical Nutrition in 2014 found that resveratrol supplements significantly reduced systolic blood pressure in adults with hypertension.
3. A randomized controlled trial published in the International Journal of Preventive Medicine in 2013 found that resveratrol supplements reduced inflammation and improved glycemic control in adults with type 2 diabetes.
4. A randomized controlled trial published in the Journal of Clinical Endocrinology & Metabolism in 2014 found that resveratrol supplements improved insulin sensitivity and reduced liver fat in obese men.
5. A randomized controlled trial published in the Journal of Nutrition in 2015 found that resveratrol supplements improved cognitive function in older adults with mild cognitive impairment.
These studies suggest that resveratrol may have potential health benefits, including improving arterial function, reducing blood pressure, reducing inflammation, improving glycemic control, improving insulin sensitivity, reducing liver fat, and improving cognitive function.
The only lasting point with Resveratrol is the dose. While there is little concern for overdosing or taking too little, more studies are needed to find the optimal dose for each individual case.
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Written By Natasha Jordan
BHSc Nutritional Medicine, International health - University Of Queensland
Diploma In Dermal Science - AACDS
Daily Longevity Blend
A complete daily longevity routine with 18 ingredients, perfectly dosed and in their most bioavailable forms. Our all-in-one blend condenses the latest longevity research into one scoop.
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|
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b755ed28a90d11d590ef646404f4afc5
|
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