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no it can't tell you if you missed your period for 8 weeks
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Q: Will a pregnancy test tell you are pregnant if you have missed your period for 8 weeks?
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Can bacterial vaginosis mean your 3 weeks pregnant?
Bacterial vaginosis is not a sign of pregnancy. Signs of pregnancy are a missed period and a positive pregnancy test.
What pregnancy symptoms start showing at 5 weeks pregnant?
The most common pregnancy symptoms at five weeks are missed period, nausea, breast tenderness, and fatigue.
Missed period for almost 2 months now have light spotting for 2 weeks?
If you have missed your period for two months you may be pregnant. Take a pregnancy test to be sure. If you are not pregnant, stress may be the cause of your missed cycle.
Do you have to miss your period in order to find out that your pregnant?
No, you don't have to miss your period in order to find out that you're pregnant. A pregnancy test can be taken from two weeks after you've had sex, you don't have to wait for a missed period.
Missed period - are you pregnant?
A missed period is not always indicative of pregnancy. There are several reasons a period can be missed; however 20% of all pregnancies end in miscarriage (spontaneous abortion). Some females miss a period for weeks and then have what they think is a very heavy period when in fact it is a miscarriage.
Can you test 2 weeks before missed period?
Home pregnancy tests are designed to be used AFTER your missed period. Using it 2 weeks before a missed period could skew the results.
In how many weeks will i know if im pregnant?
you will have a missed period.
How many days until a missed period means your pregnant?
well when you take a pregnancy test and it come out positive you have to at least be 4 weeks pregnant for that test to positive
Could you have symptoms of pregnancy before your missed period?
yes. pregnancy begins 2 weeks before ovulation -- doctors calculate it as the first day of your last period. so even a week before your period is due, you are actually 3 weeks pregnant.
It has been 8 weeks since your last period Are you pregnant?
Maybe. Missed, irregular or late periods do not always indicate pregnancy, but if you are wondering, you should have a pregnancy test performed.
You have missed your period and had a positive pregnancy test but am not having pregnancy symptoms?
You don't need to have symptoms to be pregnant. Some people don't get symptoms for weeks. You're definitely pregnant. i would go to the doctor and get it checked
Could you be pregnant if you have missed your period but have no other pregnancy symptoms?
Yes you could. I didn't know I was pregnant till 16 weeks. No morning sickness with any of mine. Congrats if you are!!!
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-8,322,244,241,468,387,000 | [Skip to Content]
Cystic Fibrosis: Diet and Nutrition
What Is Cystic Fibrosis?
Cystic fibrosis (CF) is a genetic condition that affects the body's epithelial cells. These cells are found in many places, including the sweat glands, lungs, and pancreas.
An error in the cells causes problems with the body's balance of salt and water. The body responds by making thick mucus, which blocks the lungs and sometimes other ducts and passageways, causing infections and breathing problems.
How Does Cystic Fibrosis Affect Nutrition?
The sticky mucus from cystic fibrosis can block normal absorption of key nutrients and fat in the intestines, causing:
• poor digestion
• slow growth
• trouble gaining weight
• greasy bowel movements
Why Do Some Teens Need Enzymes?
CF often causes a condition called pancreatic insufficiency. This means the enzymes made in the pancreas that digest fat, carbohydrates, and protein don't pass into the intestines as they should. So the body can't digest food normally.
Teens with pancreatic insufficiency might have problems with growth and weight gain. They also might have frequent and bad-smelling bowel movements. They'll need to take prescribed enzymes with meals and snacks to help them digest food and keep a healthy weight. A CF doctor will work with a dietitian to prescribe enzymes based on weight, growth, and bathroom habits.
If you take pancreatic enzymes in pill form:
• Enzymes should be taken with all foods and drinks that have fat and protein.
• Enzymes should never be chewed or crushed. They must be swallowed whole.
• Enzymes are sensitive to temperature. Store in a cool, dry place. Avoid extremes in temperature, such as leaving enzymes in the car during the summer or winter months.
• Consider taking an extra enzyme cap for large meals or fast food meals that are extra fatty.
What's a Healthy Diet for Someone With CF?
In the past, a healthy diet for someone with cystic fibrosis was high-calorie, high-fat, and high-salt. But new therapies make weight gain easier and life expectancy longer. So the focus of a healthy diet is changing. It's becoming more important to consider how diet can keep you feeling healthy as you grow older. Healthy diet choices can help prevent other conditions, such as heart disease or cancer, while improving your quality of life.
Here are some basics of a healthy diet:
• Eat five servings per day of fruits and vegetables.
• Include protein with meals and snacks.
• Choose whole grains over refined grains.
• Avoid sugary drinks like juice, soda, sweet tea, lemonade, etc.
• Eat more homemade meals and less fast food or restaurant meals.
What's a Healthy Weight for Someone With CF?
A healthy weight for teens with cystic fibrosis is different for each person. Your CF team will talk a lot about body mass index (BMI). BMI is a way to measure if you are at a healthy weight (not underweight or overweight) by comparing your weight to your height. The goal for all teens with CF is to reach a healthy weight that supports healthy lungs. Talk to your CF doctor or dietitian if you have questions about your healthy weight goals.
What Extras Do Teens With Cystic Fibrosis Need?
Teens with CF have some specific nutritional needs:
Salt. Teens with CF lose more salt in their sweat than their peers. The dietitian may suggest adding extra salt to foods, eating salty snacks, and drinking sports drinks when teens exercise or spend time outdoors in hot weather.
Fat-soluble vitamins (vitamins A, D, E, and K). These vitamins are important for immune function, growth, and healing. They're absorbed along with fat. Most teens with CF have trouble digesting and absorbing fat, which means they may not absorb fat-soluble vitamins. Your fat-soluble vitamin levels will be checked once a year, and you might take a prescription CF-specific multivitamin.
Calcium. Teens with CF, especially those with pancreatic insufficiency, are at risk for osteopenia or osteoporosis (weak, brittle bones). Dairy products are good sources of calcium (and the full-fat varieties also are good sources of fat and calories). If you don't drink cow's milk, consider trying a milk alternative that is fortified with calcium.
Calories. Some teens with CF need extra calories to grow healthy and strong. The extra calories should come from a well-balanced, healthy diet.
How Can Teens Reach High-Calorie Needs?
Some teens with CF need more calories than their peers. The best way to meet these calorie needs is by eating a well-balanced diet, but adding extra calories with added fat. Here are some tricks for adding extra calories to your day:
• Add extra butter or oil to pasta, rice, potatoes, or cooked vegetables.
• Pair raw vegetables with salad dressing or hummus.
• Top salads and sandwiches with avocados or guacamole.
• Grill sandwiches in butter or margarine.
• Add a splash of heavy cream to milk, oatmeal, smoothies, or cream-based soups.
• Focus on high-calorie snacks. Try trail mix, peanut butter and banana sandwiches, full-fat yogurt with granola, or cheese crackers.
Why Do Some Teens Need Nutrition Supplements or Tube Feedings?
Some teens with CF may have trouble gaining weight from a high-calorie diet alone. A doctor or dietitian may recommend adding nutrition supplements to your diet. Nutrition supplements are calorie-rich drinks that also have protein, vitamins, and minerals. For some teens, this added source of calories is enough to improve weight gain.
If a high-calorie diet and nutrition supplements are not enough, a doctor or dietitian may recommend tube feedings. These feedings, done through a tube into the stomach, are often given at night for extra calories. These overnight feedings leave teens with CF free to enjoy normal meals and activities during the day.
Making the decision to get a feeding tube can be hard, but many teens and families express relief afterward. Tube feedings can help teens gain weight, while easing the stress and conflict around food and eating. Having a tube put in for the feedings usually is a simple procedure that doesn't need extensive surgery or a long hospital stay.
What Else Should I Know?
Meeting the unique nutrition needs of CF isn't always easy. Work with your team to set nutrition goals that you can reach. If talking about food or nutrition feels stressful, consider working with the psychologist on your CF team. They can help you manage the emotions linked to how you eat.
Besides the right diet, exercise can help support better lung health, mood, and quality of life. Talk to your doctor or the physical therapist on your CF team about the right kind of exercise for you.
Date reviewed: January 2020 | {
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More than shyness, this disorder causes intense fear about social interaction, often driven by irrational worries about humiliation (e.g. saying something stupid or not knowing what to say). Someone with social anxiety disorder may not take part in conversations, contribute to class discussions or offer their ideas, and may become isolated. Panic attacks are a common reaction to anticipated or forced social interaction.
Heredity, other biological factors, stressful life events, and thinking in a way that exaggerates relatively normal bodily reactions are all believed to play a role in the onset of panic disorder. Some research suggests panic attacks occur when a “suffocation alarm mechanism” in the brain is activated, falsely reporting that death is imminent. The exact cause or causes of panic disorder are unknown and are the subject of intense scientific investigation.
But some think that nature isn’t as much of an influence as nurture. People theorize that women tend to be socialized in a way that gives them permission to openly discuss emotion. So women may feel more comfortable admitting to feelings than men, who tend to be socialized to keep their feelings to themselves and are less likely to confess to emotional problems. Women may therefore get diagnosed with anxiety disorders more often than men. (9)
People with panic disorder have sudden and repeated attacks of fear that last for several minutes or longer. These are called panic attacks. Panic attacks are characterized by a fear of disaster or of losing control even when there is no real danger. A person may also have a strong physical reaction during a panic attack. It may feel like having a heart attack. Panic attacks can occur at any time, and many people with panic disorder worry about and dread the possibility of having another attack.
Nevertheless, if you are struggling with symptoms of an anxiety disorder it is not uncommon to feel alone and misunderstood. Because the fear that people with an anxiety disorder have is not experienced by others, they may not understand why, for example, being in a crowd of people, not being able to wash your hands after meeting a new person, or driving through the street where you got in a car accident can be really anxiety-provoking for someone with an anxiety disorder. People may comment that "there is no reason to worry about it" or that you "should just let it go".
Complementary and Alternative Therapies can be used in conjunction with conventional therapies to reduce the symptoms of anxiety. There is a growing interest in these types of alternative therapies, since they are non-invasive and can be useful to patients. They are typically not intended to replace conventional therapies but rather can be an adjunct therapy that can improve the overall quality of life of patients.
A large brief current is passed through a wire coil that is placed on the front of the head which is near the areas that regulate mood. The transient current creates a magnetic field that produces an electric current in the brain and stimulates nerve cells in the targeted region. The current typically only affects brain regions that are 5 centimeters deep into the brain which allows doctors to selectively target which brain regions to treat. Typical sessions lasts 30-60 minutes and do not require anesthesia. Sessions are administered 4-5 times a week for about 6 weeks. Although the procedure is painless, patients may experience a gentle tapping in the area of the head where the current is being administered. Neuromodulation has very few side effects but they may include headaches, slight tingling or discomfort in the area in which the coil is placed. rTMS may be administered alone or in combination with medication and/or psychotherapy.
Fear and anxiety are part of life. You may feel anxious before you take a test or walk down a dark street. This kind of anxiety is useful - it can make you more alert or careful. It usually ends soon after you are out of the situation that caused it. But for millions of people in the United States, the anxiety does not go away, and gets worse over time. They may have chest pains or nightmares. They may even be afraid to leave home. These people have anxiety disorders. Types include
Obsessive-compulsive Disorder (OCD): In OCD, a person becomes trapped in a pattern of repetitive thoughts and behaviors that are senseless and distressing but extremely difficult to overcome. Such rituals as counting, prolonged handwashing, and repeatedly checking for danger may occupy much of the person’s time and interfere with other activities. Like panic disorder, OCD can be treated effectively with medication and/or psychotherapy.
Guys, I am 23 and this might sound very stupid but i recently broke up with my boyfriend of 7 months(yes quite a less time to experience anxiety issues but yes..) One fine day he just comes over and says its done between us.. I have fell out of love and thats why I cant pretend to be with you. It happened on 17th of this month i.e. 17th july and for over a week i couldnt sleep, eat food and I was nauseaic and I am still in a bad state.. I am forcing myself to sleep, to not think about it but my attacks starts early in the morning and get suffocated and want to just run out of the space. I get urges to calling him, speak to him, tell him how much I love him and miss him but its all like I am speaking to a wall. And i dont trouble my parents with this problem. should i visit a counsellor or should I give myself some time to heal ?
Research upon adolescents who as infants had been highly apprehensive, vigilant, and fearful finds that their nucleus accumbens is more sensitive than that in other people when deciding to make an action that determined whether they received a reward.[56] This suggests a link between circuits responsible for fear and also reward in anxious people. As researchers note, "a sense of 'responsibility', or self-agency, in a context of uncertainty (probabilistic outcomes) drives the neural system underlying appetitive motivation (i.e., nucleus accumbens) more strongly in temperamentally inhibited than noninhibited adolescents".[56]
Panic disorder can be effectively treated with a variety of interventions, including psychological therapies and medication[9] with the strongest and most consistent evidence indicating that cognitive behavioral therapy has the most complete and longest duration of effect, followed by specific selective serotonin reuptake inhibitors.[37] Subsequent research by Barbara Milrod and her colleagues[38] suggests that psychoanalytic psychotherapy might be effective in relieving panic attacks, however, those results alone should be addressed with care. While the results obtained in joint treatments that include cognitive behavioral therapy and selective serotonin reuptake inhibitors are corroborated by many studies and meta-analysis, those obtained by Barbara Milrod are not. Scientific reliability of psychoanalytic psychotherapy for treating panic disorder has not yet been addressed. Specifically, the mechanisms by which psychoanalysis reduces panic are not understood; whereas cognitive-behavioral therapy has a clear conceptual basis that can be applied to panic. The term anxiolytic has become nearly synonymous with the benzodiazepines because these compounds have been, for almost 40 years, the drugs of choice for stress-related anxiety.
So I don’t know if I had a panic attack or anxiety attack. It happened last night after me and gf got into an argument and basically went to bed mad and angry. I woke up about 4am to her pushing the back of head to pulling towards her to give me a kiss. My heart was pounding really hard, I couldnt barely breath regularly like I should but couldn’t. I felt mildly nausea, and felt like throwing up but I never did and I was feeling a bit light-headed. This is my first time having this happen and I don’t thinks it’s happened before..at least not to my knowledge cause I never knew what the signs were for having an anxiety attack or a panic attack.
Post-traumatic stress disorder (PTSD) is an extreme anxiety disorder that can occur in the aftermath of a traumatic or life-threatening event. PTSD can be thought of as a panic attack that rarely, if ever, lets up. Symptoms of PTSD include flashbacks or nightmares about what happened, hypervigilance, startling easily, withdrawing from others, and avoiding situations that remind you of the event.
Obsessive-compulsive disorder (OCD) is characterized by unwanted thoughts or behaviors that seem impossible to stop or control. If you have OCD, you may be troubled by obsessions, such as a recurring worry that you forgot to turn off the oven or that you might hurt someone. You may also suffer from uncontrollable compulsions, such as washing your hands over and over.
To receive a diagnosis of panic disorder, the panic attacks must be unexpected and during the attack four or more of the above symptoms must occur. For panic attacks that are expected, meaning they might not be expected by the individual but are expected in relation to any phobia, anxiety or other mental health disorder, four or more symptoms must also occur.
Guided imagery is another relaxation strategy that can help reduce or prevent overwhelming anxiety. Guided imagery involves directed mental visualization to evoke relaxation. This could involve imagining your favorite beach or a peaceful garden that can distract you from your anxious state and allow your mind and body to focus on the positive thoughts and sensations of the imagery exercise.
Treatment of anxiety focuses on a two-pronged approach for most people, that focuses on using psychotherapy combined with occasional use of anti-anxiety medications on an as-needed basis. Most types of anxiety can be successfully treated with psychotherapy alone — cognitive-behavioral and behavioral techniques have been shown to be very effective. Anti-anxiety medications tend to be fast-acting and have a short-life, meaning they leave a person’s system fairly quickly (compared to other psychiatric medications, which can take weeks or even months to completely leave).
Several drugs can cause or worsen anxiety, whether in intoxication, withdrawal or from chronic use. These include alcohol, tobacco, cannabis, sedatives (including prescription benzodiazepines), opioids (including prescription pain killers and illicit drugs like heroin), stimulants (such as caffeine, cocaine and amphetamines), hallucinogens, and inhalants.[57] While many often report self-medicating anxiety with these substances, improvements in anxiety from drugs are usually short-lived (with worsening of anxiety in the long term, sometimes with acute anxiety as soon as the drug effects wear off) and tend to be exaggerated. Acute exposure to toxic levels of benzene may cause euphoria, anxiety, and irritability lasting up to 2 weeks after the exposure.[82]
So I don’t know if I had a panic attack or anxiety attack. It happened last night after me and gf got into an argument and basically went to bed mad and angry. I woke up about 4am to her pushing the back of head to pulling towards her to give me a kiss. My heart was pounding really hard, I couldnt barely breath regularly like I should but couldn’t. I felt mildly nausea, and felt like throwing up but I never did and I was feeling a bit light-headed. This is my first time having this happen and I don’t thinks it’s happened before..at least not to my knowledge cause I never knew what the signs were for having an anxiety attack or a panic attack.
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People generally can overcome panic attacks faster if they seek help after the first one or two, says psychologist Cheryl Carmin, PhD, director of clinical psychology training at the Wexner Medical Center and a professor at Ohio State University in Columbus. When you do seek help, your doctor or therapist will ask about your symptoms and the situations in which they arise, and might also recommend additional medical testing to rule out other health concerns.
In the past it might have taken months or years and lots of frustration before getting a proper diagnosis. Some people are afraid or embarrassed to tell anyone, including their doctors or loved ones about what they are experiencing for fear of being seen as a hypochondriac. Instead they suffer in silence, distancing themselves from friends, family, and others who could be helpful. Other people suffering from panic attacks don't know they have a real and highly treatable disorder. It is our hope that through increased education, people will feel more empowered to discuss their symptoms with a healthcare professional and seek appropriate treatment.
Psychotherapy is at least as important as medication treatment of panic disorder. In fact, research shows that psychotherapy alone or the combination of medication and psychotherapy treatment are more effective than medications alone in overcoming panic attacks. To address anxiety, cognitive behavioral therapy is widely accepted as an effective form of psychotherapy. This form of therapy seeks to help those with panic disorder identify and decrease the self-defeating thoughts and behaviors that reinforce panic symptoms. Behavioral techniques that are often used to decrease anxiety include relaxation and gradually increasing the panic sufferer's exposure to situations that may have previously caused anxiety. Helping the anxiety sufferer understand the emotional issues that may have contributed to developing symptoms is called panic-focused psychodynamic psychotherapy and has also been found to be effective.
Anxiety disorders are treated through medication and therapy. You might feel embarrassed talking about the things you are feeling and thinking, but talking about it, say experts, is the best treatment. A particular form of therapy is considered most effective: cognitive behavioral therapy, or CBT for short. Antidepressants — the types of medication most frequently used to treat depression — are the drugs that also work best for anxiety disorders.
Anxiety is an emotion characterized by an unpleasant state of inner turmoil, often accompanied by nervous behaviour such as pacing back and forth, somatic complaints, and rumination.[1] It is the subjectively unpleasant feelings of dread over anticipated events, such as the feeling of imminent death.[2][need quotation to verify] Anxiety is not the same as fear, which is a response to a real or perceived immediate threat,[3] whereas anxiety involves the expectation of future threat.[3] Anxiety is a feeling of uneasiness and worry, usually generalized and unfocused as an overreaction to a situation that is only subjectively seen as menacing.[4] It is often accompanied by muscular tension,[3] restlessness, fatigue and problems in concentration. Anxiety can be appropriate, but when experienced regularly the individual may suffer from an anxiety disorder.[3]
Almost everyone experiencing symptoms of a panic attack needs evaluation. Unless the person has a history of having panic attacks, is otherwise healthy, and is experiencing a typical attack, they must be evaluated promptly by a doctor. The level of evaluation depends on many factors. Err on the side of safety when deciding whether to go to a hospital's emergency department.
Learn how to control your breathing. Hyperventilation brings on many sensations (such as lightheadedness and tightness of the chest) that occur during a panic attack. Deep breathing, on the other hand, can relieve the symptoms of panic. By learning to control your breathing, you can calm yourself down when you begin to feel anxious. And if you know how to control your breathing, you’re also less likely to create the very sensations that you’re afraid of.
Cognitive therapy and exposure therapy are two CBT methods that are often used, together or by themselves, to treat social anxiety disorder. Cognitive therapy focuses on identifying, challenging, and then neutralizing unhelpful or distorted thoughts underlying anxiety disorders. Exposure therapy focuses on confronting the fears underlying an anxiety disorder to help people engage in activities they have been avoiding. Exposure therapy is sometimes used along with relaxation exercises and/or imagery.
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Dec
01
Shifting the Paradigm: Insight into the Germ Theory
Author // Jeanne Ohm, DC
Article Index
Shifting the Paradigm: Insight into the Germ Theory
Trusting the Process
All Pages
Since the founding of the germ theory of disease, scientists have offered a holistic perspective. At long last, their efforts are taking hold.
I grew up in a household afraid of germs. When my sister was born, my father had all guests put on surgical masks to protect her. We all had our tonsils taken out “just because,” and antibiotics were considered a miracle discovered by science. My generation was the one first introduced to fast food—we really believed it was food! Our mothers were sold the idea that formula could be better than breast milk. So began the modern, manipulated, misdirected generation.
Fortunately, before I had my kids, I was introduced to chiropractic. I discovered the body’s amazing intelligence and its innate ability to heal itself. I learned about nourishment, a healthy attitude and a functional nervous system. Among the many teachings of chiropractic’s founder, D.D. Palmer, and his son, B.J., I was most fascinated with B.J.’s comment, “If the ‘germ theory of disease’ were correct, there’d be no one living to believe it.”
Fortunately, my husband and I were able to live the “chiropractic lifestyle” with our kids. Years before the American Academy of Pediatrics recommended breastfeeding (yes, they finally did in the ’90s) we were strong advocates for it. Long before the allopathic healthcare system was recognizing the importance of nutrition, we as chiropractors were recommending and consuming good, wholesome, pesticide-free foods.
In 1951, again far ahead of the times, B.J. Palmer published a statement warning against the use of antibiotics. We knew that germs were not the cause of disease and we cautioned against the overuse of antibiotics decades before USA Today headlined their dangers in the 1990s. We also let our kids play in the sunshine (without toxic sunscreen) and in the backyard dirt, decades before the study came out saying exposure to animals and dirt is healthier than living in antimicrobial households. We insisted that symptoms should not be suppressed with drugs, but rather allowed to run their course while addressing the cause (which is actually the path of healing, not disease). When we questioned the use of vaccines (a practice rooted in mainstream, germ-phobic theories) we were further scorned for our blasphemous perspective.
We met other practitioners—naturopaths, homeopaths, midwives and herbalists, as well as parents who also understood these basic principles—and we rejoiced that there were others who were living from this logical but undermined paradigm. But we remained a marginalized group. Often ostracized, certainly ridiculed…and in some instances, violently opposed.
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Understanding the Paradigm
The germ theory proposes that microorganisms are the overriding cause of many diseases. It was initiated by Louis Pasteur in the 19th century when he examined humans and animals that showed signs of being sick and found that they had very high levels of bacteria and viruses compared to those who were not sick. He then made the assumption that germs infect our body and cause sickness and disease. Pasteur, along with German physician Robert Koch, is considered one of the fathers of the germ theory. The practice of allopathic, conventional medicine to this day is still based on this theory.
Less known is that several of Pasteur’s contemporaries refuted his idea that germs cause disease. Claude Bernard, a colleague and physiologist of that era, resolved that the health of the individual was determined by her internal environment. “The terrain is everything,” he wrote; “the germ is nothing.” Other scientists tested Bernard’s theory. Elie Metchnikoff, a Russian immunologist a generation younger than Bernard and Pasteur, suggested that a synergistic interaction exists between bacteria and its host. He, too, claimed that germs were not the problem. To prove it, he consumed cultures containing millions of cholera bacteria; he lived to write about it, and didn’t even get sick.
His contemporary, French chemist and biologist Antoine Bechamp, also believed that a healthy body would be immune to harmful bacteria, and only a weakened body could harbor harmful bacteria. His research contributed to this understanding when he discovered that there were living organisms in our bodies called microzymas, which essentially form into healthy cells in the healthy body and morph into unhealthy cells when the terrain is less than ideal. The conclusion: Germs do not invade us, but rather are “grown” within us when there is diseased tissue to live on.
Rudolf Virchow, another 19th-century scientist (dubbed the Father of Pathology), wrote, “If I could live my life over again, I would devote it to proving that germs seek their natural habitat—diseased tissue— rather than being the cause of diseased tissue; e.g. mosquitoes seek the stagnant water, but do not cause the pool to become stagnant.”
In this day and age, we have been taught that germs— bacteria and viruses—are bad, which ignores the vital functions they perform. They are designed to decompose dead and dying material. Germs are our planet’s recyclers; without them, life on earth couldn’t exist.
Out of the billions of bacteria and viruses we have in our bodies, most are considered “friendly germs.” Bacteria is essential for proper digestion and it scavenges dead cells in our body so they can be replaced by new healthy cells. When our body tissues become weak due to poor health management, normal bacteria and viruses start to multiply and scavenge our unhealthy, dying cells. Our immune system responds as a survival mechanism and we develop the symptoms of being “sick,” but the germs are just doing their job.
The question then becomes, what creates sickness and illness? Is it the germs or is it an unhealthy body? It has been said that on Pasteur’s deathbed, he admitted that Bernard was right and he, Pasteur, was wrong. Nonetheless, an era of antibiotic drugs, chemical pesticides and herbicides, vaccines and antibacterial soaps has ensued, resulting in a germphobic society and a pharmaceutical empire to lead the attack. But even worse, all of these weapons have interfered with the body’s natural microbiome and impaired our immunity.
Fast forward to June 2012, when the release of coordinated research from the Human Microbiome Project Consortium organized by the National Institutes of Health rocked the world. As The New York Times reported, “200 scientists at 80 institutions sequenced the genetic material of bacteria taken from 250 healthy people. They discovered more strains than they had ever imagined—as many as a thousand bacterial strains on each person. And each person’s collection of microbes was different from the next person’s. To the scientists’ surprise, they also found genetic signatures of diseasecausing bacteria lurking in everyone’s microbiome. But instead of making people ill, or even infectious, these disease-causing microbes simply live peacefully among their neighbors.”
Instead of the “one germ, one disease” theory that has dominated allopathic medicine for centuries, these findings imply that there is an entire ecosystem of bacteria symbiotically at work in the body, a concept understood by holistic practitioners for centuries. “This is a whole new way of looking at human biology and human disease,” says Dr. Phillip Tarr, a researcher and professor of pediatrics at the Washington University School of Medicine. “It’s awe-inspiring and it also offers incredible new opportunities.”
The following quote by Ronald J. Glasser, M.D., sums up the health crossroads we now face. This former assistant professor of pediatrics at the University of Minnesota writes, “It is the body that is the hero, not science, not antibiotics…not machines or new devices. The task of the physician today is what it has always been, to help the body do what it has learned so well to do on its own during its unending struggle for survival—to heal itself. It is the body, not medicine, that is the hero.” As more doctors realize the self-evident principles of supporting the terrain, perhaps the allopathic model of killing the “bad” germs to fight disease may finally shift to improving the terrain to support the friendly bacteria.
The body, like all of nature, exists by maintaining a state of balance. It is dependent upon an environment that nourishes and nurtures with interconnectivity and cooperation between whole systems, and an underlying recognition of intelligence and a respect for the natural processes and order. Therefore, the essentials for a healthy terrain can be broken into several general premises: Nourishing the Terrain, Coordinating the Function and Trusting the Process.
Nourishing the Terrain
When we think of nourishment, we naturally reflect on nutrition...the food necessary to establish a healthy terrain. After decades of propaganda leading us to believe that commercially produced “foods” are OK, we are coming to a rude awakening that we have deviated far from the natural, whole foods that truly nourish our bodies. Because this critical awareness is not upheld by all supporting systems in our society (agricultural, educational, economical, political, medical), only proactive individuals are making this difficult transition. We must be vigilant in selecting the foods we eat, how they are grown, how they are prepared and their consequent ability to nourish our cells. We know the importance of organically grown vegetables and fruits. Finding the best sources and preparations for our families may not be as convenient as we would like, but is certainly worth the extra effort. Our Nutrition section in this issue (page 42) offers a few important suggestions to incorporate nutrient-dense foods and eliminate those that overload us. Included are family-tested recipes that improve the terrain and enhance immune system function.
Coordinating the Function
The classic medical text Gray’s Anatomy tells us that the nervous system is the master control system of the body, determining the function of all systems, all functions and all organs. Newer to science is the profound interconnectivity between the nervous system and immune system. Once thought of as separate, these systems are now considered intertwined. It is now widely accepted that a healthy immune system supports nervous system function, and vice versa. This is very important for us to recognize if we want to create a healthy terrain.
The nervous and immune systems are interconnected in several known ways. Adrenal glands are one common link. Chemicals and hormones that are produced by cells of both systems are another connection. Additionally, research shows that the brain uses nerve cells to communicate directly with the immune system.
Chiropractic care was first linked to improved immunity during the deadly flu epidemic of 1917 and 1918, when chiropractic patients fared better than the general population. This observation spurred a study of the field. The data reported that flu victims under chiropractic care had an estimated .25 percent death rate, considerably less than the normal rate of 5 percent among flu victims who received no chiropractic care.
In 1936, pioneering endocrinologist Hans Selye began groundbreaking research on the effects of stress on our health. B.J. Palmer tells us:
Selye’s great contribution to science was this clear concept, that disease affects people according to their previously developed ability to adapt. The writer goes on to relate that the physician prefers to hear that you have had childhood diseases rather than avoided them. He knows that a bout of harmless chickenpox while you were a child, will probably immunize you for life, but that if you contract it first as an adult, it could run a very serious course. This is somewhat of a reversal to medical thinking in years past. This may seem strange, but the writer has this to say regarding antibiotics. “All too often, a patient will insist on a shot of glamorous penicillin or some newer antibiotic for a mild infection. The physician will explain that the drug is not necessary—that it is better for the body to use its own defenses—but the determined patient shops around until he finds someone who will administer it anyhow.” “The frequent result is that, although the individual’s own natural resistance would have conquered the infection, the antibiotic suddenly robs the body of the germs necessary to stimulate the antibody producing mechanism into action. And, a stubborn chronic disease takes hold, against which, antibiotics are now powerless.”
In chiropractic we understand that nerve system function can be interfered with by subluxations, which create interferences to the normal transmission of nerve impulses. When this occurs, any and all systems are affected. Certainly immune system function, dependent on proper functioning of the nervous system, can be impaired as well.
Since then, additional studies have supported chiropractic care to improve immunity. One study found that disease-fighting white blood cell counts were higher just 15 minutes after spinal adjustments. In a similar study, the immune system response in HIV-positive patients under regular care for six months showed a 48 percent increase in white blood cell counts. Conversely, the group that did not receive chiropractic adjustments experienced a 7.96 percent decrease in immunity cells. More research is certainly warranted. | {
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6,732,678,245,649,867,000 | Healing
Category
Subtype
Wound characteristics
Mechanical
Abrasions
Contusions
Lacerations
Incisions
Puncture wounds
Removal of superficial skin layer(s)
Disruption of blood vessels and extravasation of blood into tissue
Tissue disruption caused by blunt or sharp instrument, usually irregular
Tissue disruption caused by sharp instrument, usually linear
Penetration of sharp instrument or projectile into tissue
Thermal
Superficial
Partial thickness
Full thickness
Burns confined to epidermis
Burns involving papillary (superficial) or reticular (deep) dermis
Burns extending through dermis into subcutaneous tissue
Chemical
Alkali
Acid
Hydrocarbons
Fat saponification, cellular dehydration, and deep tissue penetration
Hard eschar, thermal injury, and electrolyte imbalances
Dissolution of cell membranes, typically superficial erythema & blistering
Electrical
Complex
Degrees of cutaneous and deep tissue injury associated with systemic complications
Radiation
Complex
Basal skin layer damage with short- and long-term sequelae
Chronic
Complex
Persistent inflammation and matrix degradation leading to nonhealing
Mechanical injuries take on a variety of forms. Abrasions are caused by a friction event such as scraping or rubbing and result in the removal of superficial skin layers. More severe forms of abrasions include avulsions, which involve detachment of skin and possibly underlying tissue. Degloving injuries are avulsions with compromised blood supply to the detached. Contusions, or bruises, are caused by blunt trauma and characteristically rupture blood vessels. Extravasation of blood into the affected tissue is evident by skin discoloration, which evolves over time as the hemoglobin degrades. Lacerations and incisions refer to tissue separation extending through the skin, with lacerations caused by accidental trauma and incisions caused by purposeful dissection. Puncture wounds result from sharp penetration through the skin by an instrument or a projectile. They may extend into deeper structures and/or produce a second wound at the exit site (through-and-through wounds).
In the mid twentieth century, Jackson described thermal injuries as demonstrating a characteristic cutaneous injury pattern, which is divided into three zones based on blood perfusion and tissue viability: zone of coagulation, zone of stasis, and zone of hyperemia. The innermost zone of coagulation represents the irreversibly damaged, necrotic tissue without perfusion. Surrounding the necrotic tissue is an area of moderately burned tissue that may survive or progress to coagulative necrosis depending on the wound environment. This so-called zone of stasis is characterized by increased capillary permeability and vascular damage. The final zone of hyperemia is an area of intense vasodilatation and inflammation that contains viable tissue and is not usually at risk of progression to necrosis [7, 8].
Electrical injuries produce a variety of cutaneous and extracutaneous damage that depend upon the strength (amperage), duration of contact, and path of transmission through the body. If the contact time is brief, damage is relatively restricted to the cell membrane and electrical mechanisms (e.g., heart arrhythmias), rather thermal mechanisms will dominate the injury pattern. With longer contact time, thermal injury dominates and the entire cell is affected. Higher amperage (charge per unit time) burns are associated with a greater degree of systemic complications such as ventricular fibrillation, rhabdomyolysis , compartment syndrome, and renal failure [9].
Chemical injuries are subdivided by causative agent into alkali and acid, with alkali burns generally considered the most severe. Alkali burns induce fat saponification (calcification) or liquefaction, profound cellular dehydration, and formation of alkaline proteinates (completely ionized proteins) that cause deeper tissue damage. Examples of alkalis include lime, cement, potassium hydroxide, and bleach. Acid injuries induce protein hydrolysis (tanning) and do not penetrate tissue as readily as alkalis. One notable acid burn results from hydrofluoric acid due to its unique mechanism of fluoride chelating calcium in the tissue and the risk of hypocalcemia; this is the only acid burn with a specific treatment with topical or systemic calcium. Finally , hydrocarbons such as organic solvents are capable of dissolving cell membranes and producing skin necrosis. Systemic absorption of hydrocarbons is associated with respiratory depression and hepatic toxicity [10].
Radiation with energy high enough to break up molecules is called ionizing radiation. Radiation injuries, which can be accidental or iatrogenic, are known to cause short- and long-term sequelae. Acute radiation syndrome describes the adverse effects of large doses of ionizing radiation on the skin. Basal skin layer damage results in inflammation, erythema, and desquamation. Blistering and ulceration may follow in days to weeks, and most wounds will heal normally, though larger doses may result in destruction of skin appendages, fibrosis, abnormal pigmentation, and ulceration or necrosis of exposed tissue. Acute ionizing radiation exposure is also associated with dysfunction of hematopoietic, gastrointestinal, and cerebrovascular, and systems [11].
32.3 Mechanisms of Wound Healing
Wound healing is classically divided into four phases: hemostasis, inflammation, proliferation, and remodeling. Considerable overlap exists between each phase, and a combination of biochemical and cellular events contributes to the natural continuum of tissue repair.
32.3.1 Hemostasis
The initial phase of wound healing is characterized by a coordinated effort between circulating platelets, soluble clotting factors, and vascular endothelium to stop hemorrhage by the formation of a clot. The key sequences of events are divided into (1) coagulation cascade and (2) platelet activation, although it is important to remember the fundamentally integrated nature of these processes.
Hemostasis is initiated by a chain reaction of soluble serum proteins to form an insoluble fibrin mesh. The coagulation cascade is grouped into the contact activation and tissue factor pathways (historically the intrinsic and extrinsic pathways, respectively). The initial reactions of the two enzyme cascades are unique with a final common pathway consisting of factors X, V, and thrombin. The primary pathway for blood coagulation is the tissue factor pathway, with the contact activation pathway playing a secondary role. The clotting cascade results in the generation of fibrin, which enhances platelet aggregation, and structurally reinforces the ensuing platelet plug [12]. Topical fibrin sealants promote hemostasis and skin graft adhesion in excised burn wounds [13].
Disruption of normal endothelium exposes subendothelial collagen and thrombogenic extracellular matrix molecules, most notably von Willebrand factor (vWF). Platelets adhere to vWF via the glycoprotein (GP) Ib receptor, which strengthens the interaction between platelets and underlying extracellular matrix. Patients with vWF deficiency or with mutations in the glycoprotein (GP) Ib receptor are known to have von Willebrand disease, which is the most common hereditary coagulation deficiency. Likewise, mutations in the GPIb receptor result in Bernard–Soulier syndrome. Both of these conditions result in bleeding tendencies because of altered platelet adhesion to exposed subendothelium [14].
Platelet adhesion leads to platelet activation, invoking the release of stored granule contents. Cues from the wound environment such as hypoxia and acidosis enhance platelet degranulation [15]. Alpha-granules store growth factors such as platelet factor-4 (PF4), platelet derived-growth factor, fibronectin, vWF, and fibrinogen [16]. Many of these substances enhance platelet adhesion or activation. PF4 binds with high affinity to endothelial-derived heparin, which inactivates the molecule and promotes coagulation. Antibodies bind to the PF4-heparin complex on platelet membranes in the syndrome of heparin-induced thrombocytopenia (HIT), which can lead to dangerously low levels of platelets with a paradoxical increase in thrombosis [17].
Dense granules harbor smaller molecules involved in platelet activation such as ADP, ATP, calcium, and serotonin. Release of these molecules into the platelet cytosol initiates a Gq-linked protein receptor cascade, which results in an increased cytosolic calcium concentration.
The platelet glycoprotein IIb-IIIa receptor deserves mention because of its relevance to cardiovascular medicine and disease. The natural ligand of GPIIb-IIIa is fibrinogen, which links the coagulation cascade with platelet activation. Platelet activation leads to increasing its affinity to bind fibrinogen, which enhances platelet aggregation and clotting factor-mediated coagulation. The activated platelets change shape from spherical to stellate, and the fibrinogen cross-links with glycoprotein IIb-IIIa receptors in neighboring platelets to promote aggregation and eventual clot formation [18]. The GPIIb-IIIA receptor is the target of several antiplatelet agents including abciximab, eptifibatide, and tirofiban. Similarly, the drug clopidogrel is known to inhibit ADP binding to the GPIIb-IIIA receptor, which results in a reduced ability of platelets to aggregate and consequently form clots.
32.3.2 Inflammation
Vasoconstriction occurs at the wound site immediately after injury, which is the beginning of the second event in wound healing: inflammation. Vasoconstriction is primarily mediated by catecholamines (epinephrine and norepinephrine), prostaglandin F, and thromboxane A2. The contraction of blood vessels aids platelet aggregation and hemostasis. Vasoconstriction is followed shortly by vasodilatation and increased vascular permeability, which allows access of inflammatory cells to the damaged tissue. Vasodilatation is mediated by prostaglandin E2, prostacyclin, histamine, serotonin, and kinins [16]. Inflammatory cells undergo a three-stage process of rolling along the vascular endothelium, integrin-mediated adhesion to endothelial cells, and transmigration into the extracellular space [19].
Neutrophils are the first inflammatory cell to arrive at the wound and play a primary role in the phagocytosis of bacteria and tissue debris. A huge array of molecular signals are chemoattractant agents for neutrophils, including products of platelet degranulation, formyl methionyl peptides cleaved from bacterial proteins, and the degradation products of matrix proteins. Neutrophils are a major source of early cytokines in the systemic response to injury, including tumor necrosis factor (TNF)-α [20].
Oxygen delivery influences all stages of wound healing. In addition to providing a substrate for ATP synthesis in aerobic cell metabolism, large quantities of oxygen are used by neutrophils for superoxide radical generation in oxidative killing. Furthermore, molecular oxygen itself is toxic to anaerobic microorganisms, and reactive oxygen species are used as chemotactic and extracellular signaling including phyagocyte recruitment in the healing wound bed [21]. Wound oxygenation is determined by blood perfusion, hemoglobin dissociation, local oxygen consumption, fraction of inspired oxygen, hemoglobin content, arterial oxygen tension, circulating blood volume, cardiac output, arterial inflow, and venous drainage [22].
Another early cell to infiltrate the wound site are monocytes, which undergo phenotypic changes into macrophages. Macrophages can be regarded as a “master cell” involved in wound healing because of their central role in phagocytosis, inflammatory cell recruitment, and systemic inflammation. Macrophages release a variety of growth factors such as transforming growth factor-β (TGF-β), platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF), which induce fibroblast proliferation and extracellular matrix production [23]. Macrophages express specific receptors for IgG (Fc receptor), complement C3b (CR1 and CR3), and fibronectin (integrins) that facilitate recognition and phagocytosis of opsonized pathogens. Importantly, macrophages also secrete cytokines such as IL-1 and TNF-α that modulate the systemic response to injury. Excessive production of TNF-α has been linked with multisystem organ failure as well as chronic non-healing ulcers [24]. As discussed later, both IL-1 and TNF-α appear to play crucial roles in early wound healing but may have an inhibitory effect on wound maturation if persistently elevated.
Emerging data suggest a role for nerve-derived neuropeptide in wound repair. Stimulation of efferent nerves is known to produce local vasodilation and plasma extravasation in skin, which contributes to the local inflammatory response. The neuropeptide substance P, released from terminal endings of sensory nerves in response to noxious stimuli, is known to influence inflammatory cell chemotaxis [25, 26], angiogenesis [27, 28], and keratinocyte proliferation [29]. We have previously suggested that the dysregulated neuroinflammation plays an important role in hypertrophic scarring, evident by increased levels of substance P and decreased levels of the regulating enzyme neutral endopeptidase [30], which is responsible for the exuberant matrix production, hyperemia, and pruritus seen in this condition [31].
A robust but appropriate inflammatory response is essential to prepare the wound bed for subsequent migration of proliferative cells. However, overzealous inflammation may inhibit the formation of granulation tissue and neovascularization. Experiments in mice constitutively expressing the chemotactic cytokine interferon-inducible protein 10 demonstrate that an intense inflammatory infiltrate inhibits angiogenesis and development of healthy granulation tissue [32]. Thus, as in all homeostatic systems, a careful balance of functionalized cellular and biochemical processes is essential to proper wound healing. Animal trials suggest a possible role for statins in wound healing in partial- and full-thickness burns. Whereas the combination of statins and angiotensin receptor antagonists have been demonstrated to reduce fibrosis in several organ systems, results in burn healing has been mixed. Atorvastatin has been shown to reduce inflammation and increase graft take in porcine wounds; however, in the same animal model, Losartan treatment resulted in decreased graft take, increased wound contraction and worse scarring [33, 34].
32.3.3 Proliferation
The proliferative phase is characterized by the formation of granulation tissue, which is a pink, soft, highly vascularized platform for tissue formation. Fibroblasts are evident at the wound site within 2–5 days and become the predominant cell type after the first week [35]. Macrophages drive the migration of fibroblasts by secreting a number of chemokines including TNF-α, PDGF, FGF, and TGF-β. Fibroblasts begin to deposit collagen and other extracellular matrix molecules that strengthen the wound bed. Macrophages stimulate fibroblasts to produce FGF-7 (keratinocyte growth factor) and IL-6, which promote keratinocyte migration and proliferation. IL-6 is also a potent stimulator of fibroblasts, which explains the decreased level found in aging fibroblasts and fetal wounds [36]. Unfortunately, granulation tissue also harbors high bacterial counts and proteolytic activity, so it may need to be excised before skin grafting. Granulation tissue in a burn wound prevents advancement of the epithelial tongue and epithelialization and likely leads to hypertrophic scar formation [37].
A number of other inflammatory cytokines may find clinical relevance in wound care. IL-8 secreted by macrophages and fibroblasts early in wound healing may have a stimulatory effect on keratinocytes and epithelialization. Topical application of IL-8 to human skin grafts in a chimeric mouse model enhanced keratinocyte proliferation and re-epithelialization [38]. Additionally, in both human and animal studies, topical application of PDGF improved wound strength and healing time [39]; unfortunately, clinical trials have demonstrated no significant difference in healing in chronic wounds [40].
TGF-β is expressed by platelets and fibroblasts in the wound bed and plays an important role in collagen deposition and turnover. TGF-β is the most potent known stimulator of fibroblast proliferation and can accelerate wound healing in steroid-treated and irradiated animals [41]. Overexpression of TGF-β mRNA has been found in keloid and hypertrophic scars, whereas fetal wounds contain relatively little TGF-β [42]. This contrast between the heavily fibrotic scars of keloid and the scarless repair observed in utero might underscore the importance of TGF-β in the fibrotic response to tissue injury. Gabriel [43] observed a similar phenomenon in burn injuries, where higher levels of TGF-β correlate with excessive wound contraction. Interestingly, exogenous application of TGF-β3 reduces monocyte and macrophage recruitment to the wound site, resulting in less deposition of collagen and fibronectin in the early stages of wound healing [44]. A formulation of TGF-β (Juvista) underwent phase III trials but failed to meet primary or secondary endpoints and was never widely released [45].
Coincident with fibroblast migration to the wound site is angiogenesis. Angiogenesis, or neovascularization, which has been thought to be a critical element of early wound healing for transport of metabolites to and from the regenerating tissue. More recent data suggest that normal healing can occur when angiogenesis is inhibited and that angiogenesis in the wound bed is not associated with increased blood flow to the wound. Vascular endothelial cells arise from both preexisting blood vessels and endothelial progenitor cells (EPCs) in bone marrow. The most important regulators of angiogenesis are vascular endothelial growth factor (VEGF) and FGF-2. Nissen et al. [46] observed a dose-dependent effect of both VEGF and FGF-2 in angiogenesis. VEGF is secreted as many different isoforms from a variety of stromal and mesenchymal cells, with the tyrosine kinase VEGF-receptor 2 emerging as the most preeminent in angiogenesis. VEGF/VEGFR2 signaling is involved in EPC migration from bone marrow, as well as promotion of endothelial cell proliferation and differentiation [47].
Hypoxia is a potent inducer of both angiogenesis and fibroblast proliferation. The major player in hypoxic gene expression is hypoxia-inducible factor 1 (HIF-1), a DNA-binding transcription factor that is known to alter gene transcription of a number of proteins involved in metabolism, angiogenesis, migration, and proliferation [48]. Cultured endothelial cells upregulate the expression of several pro-angiogenic molecules when cultured in hypoxia, including endothelin-1, VEGF, and PDGF-β chain [49]. Fibroblast replication and longevity are increased in low oxygen tension culture [50], as is TGF-β secretion [49]. These observations highlight the contribution of hypoxia in the wound bed in proliferative cell signaling.
Mechanotransduction or the translation of mechanical force into biochemical signaling represents one novel area of research [51]. Using matrix-integrin activation of signaling cascades, mechanical force is transmitted to targets including calcium-dependent signaling, nitric oxide signaling, mitogen-associated kinases, and Rho GTPases. The end product of these signals activate transcription factors that move to the nucleus and activate mechanoresponsive genes [51]. Silicone sheeting, a way of offloading skin tension in healing wounds, has shown promise in improving scaring. Further avenues to modulate the biochemical signaling and mechanotransduction networks have potential to reduce scar formation and promote skin regeneration [52, 53].
Recently, the role of immune cells, long ignored in wound healing research is under increased investigation. T cells migrate into the wound bed during the late proliferative and early remodeling phase. Mice deficient in T and B cells have a reduced capacity to scar [22], though contradictory reports exist concerning the beneficial effects of CD4+ and CD8+ lymphocytes on wound healing [54, 55]. Additionally, a unique type of T cell exists in the skin, known as dendritic epidermal T cells (DETC), which are thought to modulate many aspects of wound healing such as inflammation, host defense, and maintenance of tissue integrity. Mice lacking or defective in DETC show a delay in wound closure and a decrease in keratinocyte proliferation at the wound site [44, 56].
32.3.4 Epithelialization
Epithelialization is the third important response to cutaneous injury, critical because once the epithelial layer is regenerated the wound is often viewed as being “healed.” Keratinocytes migrate from wound edges and dermal appendages such as hair follicles, sweat glands, and sebaceous glands. The role of the epidermal appendages is especially evident in partial-thickness burns. Since the advancing epithelial tongue at the wound edge can migrate no more than ~1 cm, wounds depend on epidermal sources at the center of the wound. Full-thickness wounds larger than 2 cm rarely heal other than by contraction. Subsequent proliferation of these cells at the wound site provides a neo-epidermal covering. Keratinocyte migration and proliferation follow a discrete sequence of events: disassembly of hemidesmosomes and desmosomes , retraction of intracellular tonofilaments and keratin filaments, and formation of focal contacts and cytoplasmic actin filaments [57]. Martin [58] has extensively studied the interplay between laminin, matrix metalloproteinases (MMPs), integrins, and soluble growth factors in this process.
Renewal of keratinocytes during normal homeostasis and wound repair is a defining feature of re-epithelialization. The upper region of hair follicles below the sebaceous gland (known as the bulge) contains multipotent progenitor cells that contribute to maintenance and renewal of epithelium [59, 60]. Additionally, epidermal cells migrate from neighboring unwounded epidermis or from the infundibulum, the portion of the hair follicle between the epidermis and the sebaceous gland [61].
The relative contributions of the follicular stem cells and epidermal stem cells to re-epithelialization is debated, although genetic analyses have confirmed that the epidermis has intrinsic capacity for self-renewal and does not depend on follicle-derived multipotent progenitor cells [62, 63]. Further evidence for this notion comes from reports of de novo hair follicle generation in healing skin of adult mice [64]. This phenomenon, which has never been observed in humans, is contingent upon WNT-mediated signaling which is also involved in pattern formation and the epithelial–mesenchymal transformation during embryogenesis [65]. Elucidation of the overlapping pathways in wound repair, and development is a central principle of efforts toward scarless repair and skin regeneration.
32.3.5 Remodeling
Remodeling is the replacement of granulation tissue with scar over months after “healing.” A key feature of tissue remodeling that emerges during this stage of wound healing is the balance between extracellular matrix (ECM) synthesis and degradation. While fibrogenic growth factors such as PDGF and FGF stimulate fibroblast matrix deposition, resident cells induce continuous degradation by matrix metalloproteinases. MMPs are a family of zinc proteases that are capable of degrading a variety of ECM components such as collagen, fibronectin, proteoglycans, and laminin [66] which can improve wound healing through direct and indirect mechanisms [67].
Collagen composition of the wound appears to follow a similar pattern as embryogenesis. Granulation tissue is comprised of a large amount of collagen III, which is gradually replaced by collagen I. Collagen I provides a higher degree of tensile strength to the developing scar, although the final tensile strength approaches only 70% of uninjured skin [68]. A morphological change in fibroblasts ensues during wound contraction, in which fibroblasts begin to express alpha-smooth muscle actin and adapt functions of smooth muscle cells. The resulting cell is termed a myofibroblast and serves to enhance wound contraction.
32.3.6 Stem Cells
In addition to resident epidermal stem cells in the skin, bone marrow-derived stem cells may contribute substantially to cutaneous wound healing. Bone marrow contains both hematopoietic (CD34+) and non-hematopoietic (mesenchymal) stem cells which aid wound healing by direct contribution of cells as well as by paracrine signaling. A notable study, in which green fluorescent protein-labeled bone marrow stem cells were used to reconstitute the marrow of mice with cutaneous wounds, indicated that non-hematopoietic mesenchymal stem cells may contribute up to 15–20% of dermal fibroblasts in normal skin and healing cutaneous wounds. Fathke et al. [69] and Brittan et al. [70] have traced cells with a keratinocyte phenotype to bone marrow origin. Deng et al. [71] have shown evidence that bone marrow stem cells are involved in hair follicle regeneration. Bone marrow cells expand ex vivo to promote neovascularization [72], appendage regeneration [73], and accelerate wound closure [74].
Endothelial progenitor cells (EPCs) derive from CD34+ hematopoietic stem cells in the bone marrow and contribute some proportion of the endothelial cells to adult skin. Systemic transplantation of EPCs enhances wound healing in mice [75], as does topical application of EPCs to ischemic ulcers in diabetic mice [76]. The mechanism involves paracrine signaling from EPCs instead of direct contributions by endothelial cells [75].
Fibrocytes, a subpopulation of leukocytes that also arise in the bone marrow, were originally identified by their rapid recruitment from peripheral blood to wound sites in mice [77]. Fibrocytes are significantly increased in the blood of burned patients in comparison to normal individuals and appear to localize in the deeper papillary dermis [78]. These cells may contribute to the myofibroblast population in wounds and may be associated with hypertrophic scarring [79, 80].
32.4 Abnormal Wound Healing
32.4.1 Impaired Wound Healing
A variety of local and systemic factors are implicated in abnormal wound healing, which impair tissue regeneration by interrupting each of the stages of wound healing. Physical impediments (Table 32.2) to wound closure may delay or prevent healing, such as the presence of foreign bodies or neoplasms (for skin grafts, hematomas and seromas most commonly cause graft failure). Excessive tension on a wound or surrounding edema may compress the vascular supply and lead to ischemia; recent data also implicate mechanical tension as a leading cause for hypertrophic scar formation [81]. Therapeutic radiation and repetitive trauma are also well-known detriments to wound healing.
Table 32.2
Local and systemic factors that impair wound healing
Local factors
Systemic factors
Tension
Foreign bodies
Infection
Ischemia
Hematoma and seroma
Trauma
Edema
Irradiation
Connective tissue disorders
Hypothermia
Oxygen
Tobacco smoking
Malnutrition
Jaundice
Age
Diabetes mellitus
Uremia
Steroids
Chemotherapeutic agents
Adapted from [82]
A variety of insults can disturb wound healing by evoking hypoxia in the evolving wound. Disruption of vascular supply and depletion of oxygen can lead to wound hypoxia, which is associated with systemic diseases such as connective tissue disorders and microvascular disease in diabetes mellitus. Tobacco smoking produces similar effects through nicotine-induced vasoconstriction and displacement of oxygen on hemoglobin with carbon monoxide [83].
Infection is another classic adversary of proper wound healing. Wounds with bacterial counts that exceeding 105 organisms per gram of tissue will generally not heal by any means, including flap closure, skin graft placement, or primary intention [84]. The introduction of early excision and grafting for burn wounds has significantly reduced the prevalence of burn wound sepsis—which was historically a leading cause of burn mortality. Endotoxin produced by gram-negative bacteria stimulates phagocytosis and collagenase expression, which contributes to matrix degradation and destruction of normal tissue. Bacteria also accelerate protease production in macrophages (such as MMPs) while inhibiting protease inhibitor expression. This effect leads to increased matrix destruction and degradation of growth factors, which are characteristics of chronic nonhealing wounds [85].
Nutritional status has a profound effect on wound healing as well. Serum albumin is one of the most accurate predictors of surgical morbidity and mortality, with levels below 2.1 g/dL associated with poorer outcomes [86]. Protein replacement enhances wound healing [87], as does supplementation with the amino acids arginine, taurine, and glutamine [88, 89]. Whereas patients with large burns characteristically have albumin levels below 1.0 g/dL, exogenous albumen has never been demonstrated to improve outcomes. Early introduction of nutrition is a critical component of acute burn care and wound healing, with micronutrients playing an important role [90, 91]. Data suggest that the catabolic state can be modulated by propranolol in children [92] and oxandrolone in children and adults [93, 94]. Propranolol, a nonselective β-blocker, improved wound healing and perioperative hemodynamics in severely burned adults by increasing vascular resistance in the burn beds by leaving α-adrenergic receptors unopposed and decreasing blood loss during operative interventions [95].
Vitamin C (ascorbic acid) is an essential cofactor in proline and lysine hydroxylation during collagen synthesis, and supplementation of 100–1000 g per day may improve wound healing [89]. Vitamin A (retinoic acid) is required for wound re-epithelialization, maintenance of normal epithelium, proteoglycan synthesis, and normal immune function. Oral retinoid therapy counteracts the detrimental effects of corticosteroids on wound healing, possibly through promotion of TGF-β and IL-1 signaling [96]. Vitamin K deficiency impedes clot formation and hemostasis, while vitamin D is required for bone healing and calcium metabolism. Finally, vitamin E supplementation may serve an important role as an antioxidant in trauma patients. Early administration of vitamin E reduces the incidence of organ failure and the average length of ICU stay in critically ill surgical patients and may be relevant for burn patients [97].
The dietary minerals associated with wound healing include zinc and iron. Zinc is an essential cofactor in RNA and DNA polymerases. Deficiency inhibits granulation tissue formation [98] and delays wound healing [99]. Desneves et al. [88] report that zinc supplementation improves wound healing. Iron, another cofactor in DNA synthesis, is also key to proline and lysine hydroxylation. Although the role of iron in normal hematopoiesis is well established, chronically anemic patients do not appear to suffer from delayed wound healing [100]. Whereas selenium deficiency causes hair and skin abnormalities in humans and selenoproteins have been implicated in keratinocyte function and cutaneous morphogenesis [101], but selenium deficiency is yet to be associated with abnormal wound healing.
32.4.2 Hypertrophic Scars and Keloids
Hypertrophic scar and keloids represent fibroproliferative scars, which are characterized by excessive collagen deposition. These two morphological aberrations are difficult to differentiate: keloids are defined as scars that grow beyond the periphery of the original wounds and hypertrophic scars represent raised scars that remain confined to the boundaries of the original wound. Keloids rarely regress with time; hypertrophic scars frequently regress spontaneously. Both scar types appear to have a strong genetic component, with more prevalence in dark-skinned patients of African, Asian, Native American, or Latin American descent. Hypertrophic scars, the result of prolonged inflammation, are influenced by wound depth, skin tension, and delayed wound healing with increased inflammatory response and enhanced fibroblast activity [102]. Though theoretically preventable, hypertrophic scars tend to occur in pigmented individuals [103], young people, and rarely in the aged. Interestingly, they often develop in highly contractible body sites and rarely form on the scalp or the lower leg [104]. Proposed therapies to control hypertrophic scars act to reduce inflammation including steroid injections, radiotherapies, compression, and surgical methods to reduce skin tension [105]. The single nucleotide polymorphism p27kip1 decreases vascular restenosis due to fibrogenesis, but was not associated with hypertrophic scar severity [106]. Using a genome-wide association study of over 500 individuals with burn injuries, mutations in the CSMD1 gene have been associated with reduced hypertrophic scarring [107].
In light of its potent effect on fibroblast proliferation and collagen deposition, it is perhaps not surprising that TGF-β plays a central role in proliferative scarring. Colwell et al. [108] found increased levels of the TGF-β1 isoform in both keloids and hypertrophic scars. Likewise, antibodies to TGF-β isoforms reduce fibrosis in hypertrophic scars [109]. Novel therapies for hypertrophic and keloid scars are in development that target ECM synthesis and fibroblast proliferation [110].
32.4.3 Chronic Nonhealing Wounds
Dysfunction of normal wound healing processes leads to chronic wounds. In particular, chronic wounds appear to have sustained inflammation with less matrix production. Chronic wounds exhibit higher levels of cytokines such as IL-1, IL-6, and TNF-α, with reduced levels of essential growth factors such as EGF and PDGF. MMP-1, MMP-2, MMP-8, and MMP-9 are present at higher levels, with reduced levels of MMP inhibitors [111]. These nonhealing wounds are prone to developing squamous cell carcinoma, originally reported in burn wounds by Marjolin. Marjolin ulcers tend to be very aggressive and should be highly suspected with nonhealing burn wounds [112]. Therapy includes complete local extirpation of the cancer with negative margins and lymphatic mapping [113]. Other conditions such as osteomyelitis, pressure sores, venous stasis ulcers, and hidradenitis have also been associated with wound malignancies [114]; patients with impaired skin integrity due to burn injuries are at increased risk for decubitus ulcers, which constitute a closely monitored hospital acquired complication.
32.4.3.1 Wound Dressings
A variety of burn dressings and skin substitutes are employed in the treatments of burns and other wounds. One class of dressings is topical salves and ointments such as silver sulfadiazine, bacitracin, or mupirocin, which require daily dressing changes to minimize infection risks. Multi-day dressings such as Acticoat® (Smith & Nephew), or Mepilex® Ag (Molnlycke) can be used in wounds and partial-thickness burns, minimizing the need for dressing changes while having antimicrobial properties. Additionally, bioderived materials are being explored for wound healing properties as natural scaffolds including polysaccharide polymers such as cellulose, chitosan (similar to a glycosaminoglycan), and hyaluronic acid and natural proteins such as silk fibroin, fibrin glue, and collagen [115]. An ideal dressing should be antimicrobial, analgesic, long acting, easy to apply (transparent), and affordable. While no single product is a miracle cure, continued advancements and combinations show promise in complicated wound processes. Lupeol from the Cassia fistula fruit has shown some promise with antioxidative, antileukotriene, and antibacterial effects and can be released with a chitosan hydrogel mixture that may improve wound healing in some patients [116, 117]. Whereas the list of dressings and skin produces in Tables 32.3 and 32.4 is robust, it is by no means exhaustive, and new products are released regularly.
Nov 4, 2020 | Posted by in Aesthetic plastic surgery | Comments Off on Healing
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2,044,066,446,694,886,100 | Symptoms of stress
Stress, quite simply, is toxic. And, if you're paying attention, when you're stressed, you'll start noticing some physical cues your body's using to try and tell you to relax.
Pale Skin
Pasty skin
The problem: You look in the mirror and wonder where your rosy glow went.
Why it’s happening: Your body goes into survival mode when you are stressed. As a result, your body redirects blood flow from “unnecessary” organs, like your skin, to vital organs, like your heart and lungs. The reduced blood flow leads to poorer circulation, which in turn, rids you of your natural glow.
What you can do: To remove dead skin cells and revitalize skin, be sure to exfoliate regularly and make sure you’re eating a balanced diet of fruits and vegetables, which are full of antioxidants to counteract the negative effects of stress. And work on decreasing your stress levels to rid the root of your pasty skin.
Pimples
The problem: Whiteheads and blackheads are cropping up all over your face.
Why it’s happening: When you are stressed, your body releases androgen into your blood stream; this hormone ups the sebum, an oily substance, level in your body. The excess oil clogs pores, causing blemishes.
What you can do: Keep up with your skincare regime and use products to reduce the amount of oiliness on your skin. Also, take a warm bath and let the steam nourish your skin and help you relax.
Bleeding, sensitive gums
The problem: Your gums are so sensitive, flossing and brushing is almost unbearable.
Why it’s happening: Stress is an immune system killer, which means there’s less of a chance your body will be able to fight off bad bacteria that settles around your gum line. This buildup can cause inflammation, bleeding and pain.
What you can do: Keep up with your regime of regular brushing and flossing, but switch to brushes with softer bristles and add mouthwash to your routine to kill residual bacteria. Further, don’t take your stress out on your gums by brushing too vigorously; find other ways to vent your stress.
Exhaustion
The problem: No matter what you do, you can’t seem to rid yourself of the feeling you’re going to drop dead of fatigue.
Why it’s happening: Stress hormones can interfere with the feel-good hormones that gently lull you to sleep every night and can keep your brain “alert” even when it should be resting.
What you can do: If you have a steady stream of to-dos flowing through your head, write everything down before you hit the hay. Yoga and meditation will also help slow your brain down and allow you to de-stress.
Tummy troubles
The problem: You’re experiencing constipation or diarrhea.
Why it’s happening: When stress strikes, your sensitive intestinal lining gets doused in a series of negative hormones that are secreted by the body to, counterintuitively, protect it in times of duress. This can cause muscle spasms, cramping and fluctuations in the acid that’s secreted whenever you eat.
What you can do: Avoid foods that aggravate your intestinal tract (like fast food or anything greasy) and be sure to eat lots of fiber to cleanse your colon.
Itchy skin
The problem: You’ve developed itchy red bumps or hives all over your body.
Why it’s happening: According to researchers, one of the first physical signs you’re stressed may be itchy skin. This may happen because of histamine, a stress compound your body releases that’s directly linked to skin allergies.
What you can do: Hydrate by drinking lots of water and soothe upset skin with lotions containing aloe vera and calamine.
------------------------------
------------------------------
Đã đọc : 9142 lần
Liên hệ tư vấn
hỗ trợ trực tuyến
CHÚ Ý: AVS KHÔNG TƯ VẤN QUA CHAT
tư vấn qua điện thoại (3.000 đồng/phút): 1900 68 50 hoặc (04)1088 - 1 - 7
tư vấn trực tiếp: 2/15, phố Đào Duy Từ, phường Hàng Buồm, quận Hoàn Kiếm, Hà Nội
Lĩnh vực tư vấn:
- tư vấn tâm lý tình cảm, hôn nhân, gia đình
- tư vấn nuôi dạy trẻ
- tư vấn sức khỏe tình dục: xuất tinh sớm, lãnh cảm, nghệ thuật phòng the, bệnh tình dục....
- tư vấn sức khỏe sinh sản, giới tính
- tư vấn trị liệu tâm lý
- Các vấn đề tâm lý khác như ly hôn, stress
Gọi -1900 68 50 để đặt lich tư vấn trực tiếp
Biểu giá tư vấn tại đây
Khách hàng tư vấn trực tuyến xem hướng dẫn tư vấn tại đây | {
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-2,675,940,705,455,686,000 | PMCCPMCCPMCC
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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Trends Immunol. Author manuscript; available in PMC 2009 November 7.
Published in final edited form as:
PMCID: PMC2774448
NIHMSID: NIHMS153603
MHC class I assembly: out and about
Abstract
The assembly of major histocompatibility complex (MHC) class I molecules with peptides is orchestrated by several assembly factors including the transporter associated with antigen processing (TAP) and tapasin, the endoplasmic reticulum (ER) oxido-reductases ERp57 and protein disulfide isomerase (PDI), the lectin chaperones calnexin and calreticulin, and the ER aminopeptidase (ERAAP). Typically, MHC class I molecules present endogenous antigens to cytotoxic T lymphocytes (CTLs). However, the initiation of CD8+ T-cell responses against many pathogens and tumors also requires the presentation of exogenous antigens by MHC class I molecules. We discuss recent developments relating to interactions and mechanisms of function of the various assembly factors and pathways by which exogenous antigens access MHC class I molecules.
Introduction
The interaction between a T-cell receptor (TCR) on a cytotoxic T lymphocyte (CTL) and a major histocompatibility complex (MHC) class I peptide complex on an antigen presenting cell (APC) initiates many antiviral and antitumor immune responses. MHC class I molecules comprise a membrane-linked heavy chain, a soluble light chain [β2-microglobulin (β2m)] and a short peptide bound in a groove of the membrane-distal domains of the heavy chain. Complexes of MHC class I heavy chains, β2m and peptide are typically assembled in the endoplasmic reticulum (ER) of cells through a complex assembly pathway (reviewed in Ref. [1]). In the classical MHC class I assembly pathway, cytosol-derived proteins that are endogenous to cells are processed into peptides by the proteasome. The proteasome generates peptides optimized for MHC class I binding at the C terminus but extended at the N terminus relative to peptides bound to mature MHC class I molecules (reviewed in Ref. [2]). N-extended peptides are transported into the ER lumen by the transporter associated with antigen processing (TAP). In the ER, MHC class I heterodimers lacking peptides are recruited into complexes with the TAP transporter, in an interaction bridged by tapasin (Figure 1). ERp57, protein disulfide isomerase (PDI) and calreticulin also associate with the TAP-tapasin-MHC class I complex to form a large complex called the peptide loading complex (PLC) [1] (Figure 1; PDI not shown). Components of the PLC facilitate peptide binding to MHC class I molecules. ERAAP cleaves N-extended peptides at the N terminus, optimizing MHC class I peptide associations (reviewed in Ref. [2]). Peptide occupancy triggers dissociation of MHC class I from the PLC, exit from the ER and transit to the cell surface, where the MHC class I molecules become available for immune surveillance by T cells. This general pathway is relevant to the assembly of MHC class I peptide complexes in virally infected cells and tumor cells and to the subsequent immune recognition of such cells. Recent developments relating to this pathway will be reviewed in this article. Additionally, the initial priming of naïve CD8+ T cells into effector CTLs requires the processing of exogenous particulate and soluble antigens by dendritic cells (DCs) and presentation of such antigens via the MHC class I molecules of the DCs. This phenomenon is called cross-priming and is a key mechanistic step in the initial activation of CTL responses against tumor cells, viruses and other intracellular pathogens (reviewed in Ref. [3]). This review also summarizes recent information about cellular pathways used by antigen presenting cells (APCs) for the presentation of exogenous antigens to CD8+ T cells.
Figure 1
Components of the peptide-loading complex in the endoplasmic reticulum (ER). Major histocompatibility complex (MHC) class I heavy chains (green) and β2m (orange) are found in association with tapasin (red) and the TAP1-TAP2 (blue and yellow, respectively) ...
Transport of peptides for MHC class I antigen presentation
The role of TAP is to transport peptides from the cytosol into the ER. Two subunits, TAP1 and TAP2 (also known as ABCB2 and ABCB3, respectively; Figure 1), are required for peptide transport. TAP1 and TAP2 belong to the ATP binding cassette (ABC) family, transmembrane proteins that function in the ATP-dependent transport of various substrates across cellular membranes. TAP1 and TAP2 each contain a cytosolic nucleotide binding domain (NBD) and a transmembrane region with several predicted membrane-spanning segments (reviewed in Ref. [4]). Compared with other ABC transporters, TAP1 and TAP2 contain additional N-terminal transmembrane segments (Figure 1) that form the accessory domains for tapasin binding and MHC class I bridging [57]. Peptide translocation by TAP is preceded by peptide binding to TAP, and cytosol to ER translocation of peptides requires nucleotide hydrolysis (reviewed in Ref. [8]). Crystal structures of TAP1 NBD and of homologous ABC transporters have predicted that, at some point during the transport cycle, two ATP molecules are bound at the interface between TAP1 and TAP2 NBD dimers, [9,10], generating a ‘closed conformation‘ of the NBDs. The TAP1 nucleotide binding site contains naturally occurring modifications that attenuate its ATPase activity, and the TAP2 site is the main catalytically active site driving peptide transport [1013].
There is emerging consensus that substrate transport by ABC transporters might involve nucleotide-dependent reorganizations between two main conformational states [1416], as depicted in Figure 2 for peptide transport by TAP. The question of what molecular events initiate the catalytic cycle of ABC transporters and determine transitions between these two conformational states is of major interest to the field. The catalytic cycle of TAP is a target for immune evasion by different viruses. In addition to the well-known TAP inhibitors ICP47 and US6 encoded by herpes simplex viruses and human cytomegalovirus, respectively (reviewed in Ref. [4]), recent studies have revealed that the UL49.5 proteins of bovine herpesvirus 1, pseudorabies virus and equine herpesviruses 1 and 4 target different steps of the TAP catalytic cycle [17]. Additionally, the BNFL2a protein of Epstein Barr virus and homologous proteins of other viruses are also inhibitors of peptide and nucleotide binding by TAP [18]. A better understanding of the TAP catalytic cycle will allow further insights into mechanisms that viruses use to suppress the antigen shuttle pathway, and conversely, viral inhibitors of TAP may be useful reagents to further elucidate steps of the TAP catalytic cycle.
Figure 2
Model for the transporter associated with antigen processing (TAP) catalytic cycle deduced from structural and functional studies [916]. TAP1 is indicated in blue (dark), TAP2 in yellow (light), peptide in red, and the membrane in white. TAP ...
Stages of MHC class I assembly and formation of the PLC
A model for the assembly of MHC class I molecules involves the sequential interactions of (i) class I heavy chains with calnexin, (ii) class I heterodimers with calreticulin and (iii) class I heterodimers-calreticulin with TAP-tapasin-ERp57 (reviewed in Ref. [1]). However, the precise sequence of the MHC class I or the PLC assembly pathway is difficult to dissect unambiguously, because each component involved in MHC class I assembly and PLC formation can mediate multiple interactions. Tapasin uses its transmembrane and/or cytosolic domains for efficient TAP binding, and its ER luminal domains are able to interact with MHC class I and ERp57 [19,20]. Tapasin and ERp57 interact within the PLC via a disulfide bond between C95 of tapasin and C57 of ERp57 [1,20]. ERp57 can interact with both calreticulin and calnexin, and these complexes can bind and promote folding and assembly of MHC class I, tapasin and other partially folded glycoproteins via N-glycan and polypeptide-based binding interactions (reviewed in Ref. [21]). Finally, tapasin and peptide-receptive MHC class I molecules interact in the absence of other PLC components [2224].
Recent knockout mice–based experiments have been important to further dissect the role of ERp57 and calreticulin in PLC formation and function. In ERp57-deficient B cells, MHC class I molecules are recruited into complexes with TAP and tapasin but dissociate more rapidly [25]. Furthermore, the C95A mutant of tapasin that is unable to bind ERp57 is able to recruit MHC class I molecules into a complex with TAP when expressed in the human tapasin-deficient 721.220 cells [26]. Interactions between TAP, tapasin and MHC class I molecules are also observable in fibroblasts derived from calreticulin-deficient mouse embryos [27,28]. Thus, neither ERp57 nor calreticulin is essential for the TAP-tapasin-MHC class I interaction, although interactions within the PLC might be stabilized by ERp57 and/or calreticulin. However, MHC class I assembly and cell surface expression are negatively impacted in cells deficient in ERp57 or calreticulin, indicating that both factors are important for optimal function of the PLC [25,27,28]. Studies with mutant PLC components may provide further insights into the dynamics of the functional interactions within the PLC.
Redox chemistry and mechanisms of tapasin-assisted peptide loading
Tapasin stabilizes TAP and enhances peptide transport by TAP [19], a function shown to be crucial for enhancing peptide loading onto MHC class I molecules of tapasin-deficient mouse cells [29]. In the tapasin-deficient human melanoma cells (M553), interferon-γ (IFN-γ) increases TAP protein levels dramatically but has a small effect on induction of MHC class I surface expression in the absence of exogenous tapasin [30]. Thus, in some cells, tapasin-mediated enhancement in TAP activity may be insufficient to significantly induce cell surface MHC class I expression at least for some MHC class I allotypes. By what additional mechanisms could tapasin facilitate assembly and cell surface expression of MHC class I molecules? Early studies showed that soluble tapasin that was unable to bind or stabilize TAP was partially able to induce MHC class I cell surface expression [19]. Using purified soluble versions of MHC class I and tapasin, tapasin alone has no effect or only a small effect in enhancing peptide binding to MHC class I molecules [24,31], suggesting that the requirement for tapasin relates to the specifics of peptide loading in an intracellular environment. In studies that measured peptide binding by MHC class I molecules in lysates of tapasin-deficient 721.220 cells, reconstitution with soluble tapasin-ERp57 conjugates, but not soluble tapasin alone, significantly enhanced peptide loading of MHC class I molecules [32], coincident with enhanced stabilization of the heavy chain. The peptide binding groove of MHC class I heavy chains has a disulfide bond within its α2 domain (Figure 3). This disulfide bond is sensitive to reduction until the peptide binding groove becomes stably occupied with peptide [33], and reduction of the disulfide bond is expected to be unfavorable for peptide binding. Blockage of tapasin-ERp57 conjugate formation by the tapasin C95A mutation enhanced reduction of HLA-B*4402, coincident with enhanced ERp57 binding to HLA-B*4402, which led to the suggestion that the formation of tapasin-ERp57 conjugates might sequester the reductase activity of ERp57 away from the α2 domain disulfide bond [26]. Based on these results, one mechanism for tapasin-assisted peptide loading could involve the maintenance of the α2 domain disulfide bond in an oxidized form favorable for peptide loading [26]. The primary function of PDI was also suggested to relate to the maintenance of the α2 domain disulfide bond, based on analyses of MHC class I heavy chain oxidation state and cell surface expression in PDI-depleted cells [33]. Thus, important questions to be addressed include whether the functions of PDI and tapasin-ERp57 are linked or represent two independent mechanisms for maintenance of the α2 domain disulfide bond. It is alternatively possible that enhanced reduction of the HLA-B*4402 heavy chain that was observed in the presence of the tapasin C95A mutant [26] is secondary to the diminished functional activity of the tapasin C95A mutant in promoting MHC class I peptide loading. Further studies are needed to clarify mechanisms of ERp57 and PDI functions within the PLC and to better understand the effects of ERp57 on tapasin structure and functional activities.
Figure 3
Two crucial disulfide bonds in the peptide loading of major histocompatibility complex (MHC) class I molecules. Schematic representation of the peptide binding groove of a peptide-receptive MHC class I heavy chain (green), as viewed from the top, and ...
Tapasin and ERAAP as editors of the MHC class I peptide repertoire
Some studies suggest that tapasin edits the MHC class I peptide repertoire toward the binding of high-affinity peptides [32,34], although cellular evidence for a tapasin-induced MHC class I peptide repertoire that is high affinity or high stability has not been obtained [35,36]. The tapasin–MHC class I interaction is intrinsically peptide sensitive and dissociated by peptide binding [22,24,32]. More effective disengagement of tapasin–MHC class I complexes is induced by high-affinity peptides [24], and by this mechanism, tapasin could establish an affinity threshold for exit of peptide–MHC class I complexes from the ER. More direct editing might also occur; for instance, tethering of tapasin to MHC class I molecules via a fos-jun linkage enhanced dissociation rates of some peptide–MHC class I complexes [31]. In these studies, however, only a subset of the tested peptides was sensitive to tapasin during the dissociation reactions, and the magnitude of tapasin’s effect could not be predicted from the intrinsic dissociation rates of the peptide–MHC class I complexes, suggesting that other parameters are relevant to tapasin-mediated peptide selection [31]. ERAAP is also a key editor of the MHC class I peptide repertoire, and its peptidase activity generates optimal peptides from suboptimal N-extended sequences (reviewed in Ref. [2]). In ERAAP-deficient cells, despite the presence of tapasin, MHC class I molecules present many unstable and N-extended peptides to CD8+ T cells [37]. Thus, tapasin’s editing abilities might at best be restricted to some peptides or perhaps linked to the presence of ERAAP. Further studies are needed to address these possibilities.
Mechanisms and possible consequences of tapasin-dependent and independent MHC class I assembly
Recent studies have shown that HLA class I allotypes can differ dramatically in their intracellular assembly requirements [3840]. For example, HLA-B*4402 is highly tapasin dependent for its assembly, whereas HLA-B*4405 is relatively tapasin independent [39,40]. Mechanisms that govern these assembly differences and the functional effects of such differences are of considerable interest, because the assembly profile could impact the efficiency of the immune response to tumors and intracellular infections [41]. Kienast et al. [26] observed that, compared with HLA-B*4405, HLA-B*4402 was more susceptible to reduction of its α2 domain disulfide bond in the absence of tapasin and suggested that tapasin dependency reflected susceptibility to reduction of the α2 domain disulfide bond. However, as noted above, peptide occupancy influences the extent of reduction of the α2 domain disulfide bond [33], and we noted that the intrinsic peptide loading efficiency of HLA-B*4402 was lower than HLA-B*4405 when comparing binding of different peptide libraries [23]. Thus, it remains to be established whether reduction of the α2 domain disulfide is the cause or the effect of reduced peptide loading of HLA-B*4402 compared with HLA-B*4405 in the absence of tapasin.
Various genetic studies have elucidated the fact that the presence of particular HLA alleles can profoundly impact infectious disease and cancer outcomes. Not much is known about the impact of HLA-B*4402 versus HLA-B*4405 in disease outcomes, because HLA-B*4405 is a rare allele in population groups in which genetic studies were undertaken. However, other HLA class I associations with disease are well established. For example, HLA-B*57 and HLA-B*27 alleles are associated with slow AIDS progression, whereas certain HLA-B*35 alleles are associated with rapid AIDS progression (reviewed in Ref. [42]). A major cause of the strong influence of HLA allotypes on disease outcomes probably relates to differences in peptides presented by each HLA class I molecule. However, it is possible that another level of influence arises from the assembly phenotype of a HLA class I molecule. It has been shown that, compared with tapasin-independent allotypes, tapasin-dependent allotypes are more susceptible to inhibition by herpesviral factors that target TAP/tapasin [40,43]. Thus, in the context of infections that target ER assembly factors of the MHC class I pathway, a tapasin-dependent assembly profile may be disadvantageous for the CTL response. However, a tapasin-dependent assembly profile could benefit the immune response in other situations. For example, tapasin-dependent assembly, which seems to correlate with slow rates of ER-medial Golgi trafficking [23], could result in more consistent loading of antigen epitopes during infections with viruses that do not interfere with MHC class I assembly in the ER. More studies are needed to better understand the impact of MHC class I assembly characteristics on immune responses and disease outcomes in different infection models.
Mechanisms and pathways of antigen cross-presentation
Uptake of antigen
It has been well established that both soluble and cell-associated or particulate exogenous antigens can be taken up by APCs by the general mechanisms of endocytosis and phagocytosis and further processed for presentation by MHC class I molecules (reviewed in Refs. [3,44]). Additionally, some exogenous soluble proteins can directly traffic to the ER of DC during cross-presentation [45].
The physiologically relevant form of cross-presented antigen used for activation of a CD8 T-cell response is vigorously debated, and evidence supports a role for cellular proteins that are proteasome substrates [46,47] or preprocessed peptides [48], in particular those sequestered in complex with different heat-shock proteins (HSPs) [49]. Evidence suggests that high antigen stability might favor priming of CD8 T cells [46,47,50], probably by promoting steady-state antigen accumulation and persistence in multiple intracellular and extracellular environments encountered during cross-presentation. However, as with endogenous presentation (for example, Ref. [51]), interactions of less stable or partially degraded antigens with specific cellular chaperones and HSPs could enhance stability, inhibit premature degradation and promote cross-presentation. Additionally, HSP associations could assist with antigen uptake into APC via specific HSP receptors as previously suggested [49] and with antigen targeting into intracellular compartments favorable for cross-presentation. Although several HSP receptors have been defined (reviewed in Ref. [52]), the role of particular HSP receptors in actively promoting cross-presentation remains to be demonstrated.
Features of receptors and APCs used in cross-presentation
Use of specific receptor and/or adaptor systems during antigen uptake can indeed strongly dictate the intracellular localization of antigen [53] and the efficiency of cross-presentation [54]. Cross-presentation of soluble ovalbumin by mouse APCs was dependent on mannose receptor–mediated endocytosis, which directed ovalbumin into a stable early endosomal compartment. In the absence of the mannose receptor, scavenger receptor endocytosed or pinocytosed ovalbumin was rapidly transported to lysosomes, which resulted in efficient MHC class II presentation but severely compromised cross-presentation [54]. For phagocytosed antigens, variations in phagosome properties among different APCs can impact the cross-presentation efficiency of an APC. The increased efficiency of cross-presentation by mouse bone marrow–derived dendritic cells (BMDCs) compared with macrophages [55] was attributed to some unique DC traits. Compared with macrophages, the neutral pH and low proteolytic activity in BMDC phagosomes in the first few hours after phagocytosis is thought to favor cross-presentation by BMDCs [56]. The NADPH oxidase NOX2, which is significantly recruited to the BMDC phagosome, is thought to be important for maintaining a neutral pH in the BMDC phagosomal lumen and for inhibiting rapid degradation of antigens, which could destroy potential epitopes for cross-presentation [56].
Intracellular pathways of cross-presentation
Proposed pathways for cross-presentation fall into two main categories: those dependent on the TAP and proteasomal processing and those relatively independent of these factors. The latter, also termed the vacuolar pathway (Figure 4a, reviewed in [3,44]), involves proteolysis of endocytic antigens by cysteine proteases such as cathepsin S [57] and loading of recycling MHC class I within the same compartments. Because peptide loading in the vacuolar pathway is generally proteasome and TAP independent, the ability to use the vacuolar pathway might be restricted to a few select antigens that are appropriately cleavable within endosomes. A recent study showed that human plasmacytoid DCs (pDCs) displayed unusual accumulation of MHC class I molecules within recycling endosomes. Presentation of a matrix protein–derived peptide in the context of HLA-A2 occurred in a cathepsin-dependent and proteasome-independent manner [58], invoking a vacuolar pathway, as depicted in Figure 4a. However, other studies indicate that this mode of antigen presentation by pDCs might depend on particular antigens and/or MHC class I allotypes rather than being a general feature of pDC [59].
Figure 4
Proposed cellular pathways for antigen cross-presentation. (a) The transporter associated with antigen processing (TAP)-independent vacuolar pathway; endocytosed antigens are proteolytically processed by cysteine proteases such as cathepsin S. Peptide ...
Mechanisms of TAP and proteasome-dependent antigen cross-presentation
For TAP and proteasome-dependent presentation, antigens must reach the cytosol. Recent studies provide evidence for retro-transport of some antigens into the cytosol after their direct uptake into the ER of DCs [45]. The ER-associated degradation (ERAD) machinery, including Sec61, a putative translocon channel, is thought to function in ER to cytosol retro-transport [60,61] (Figure 4b). Antigen transport to the cytosol can also occur from phagocytic [62], endocytic [54,63] or macropinocytic [55,64,65] compartments. After a report that the phagosomal membranes are formed in part from the ER membrane [66], three laboratories described the observation of ERAD factors and components of the MHC class I peptide loading machinery within phagosomal membranes [6769] (Figure 4c). The presence of ERAD components on phagosomes provides an attractive mechanism for the translocation of phagosomal antigens to the cytosol for processing. However, the findings of ER components in phagosomal membranes were refuted in a subsequent report that described an inability to detect ER contribution to phagosome formation, based on various quantitative approaches [70]. Thus, the presence of ER components within phagosomal membranes remains controversial.
In related findings, a recent report suggests that TAP can be recruited to early endosomes in a TLR (Toll-like receptor) 4-MyD88–dependent manner [63]. A transferrin receptor–conjugated inhibitor of TAP, which localized to recycling endosomes, was found to inhibit cross-presentation of exogenous ovalbumin but not the presentation of endogenously expressed ovalbumin [63]. These results support a pathway in which soluble exogenous antigens are retro-translocated from endosomal compartments into the cytosol, followed by re-import of proteasomally processed peptides back into endosomes via endosomal TAP, where peptide loading of recycling MHC class I occurs (Figure 4d). Related mechanisms may determine endosomal and phagosomal localization of TAP, and thus, further understanding of the mechanisms by which TAP becomes endosomally localized, as well as additional quantitative demonstrations of the presence of other PLC and ER components in TAP-bearing endosomes may help resolve some of the current controversy surrounding the presence of ER components in phagosomal membranes. In this regard, it is also noteworthy that previous studies by Lizee et al. [71] have suggested the existence of an endo-lysosomal compartment for peptide loading of MHC class I molecules during cross-presentation and shown that a tyrosine-based targeting signal within the MHC class I cytoplasmic domain is important for routing MHC class I molecules through the endo-lysosomal compartments [71].
Conclusions
Thus, in many cases, the cytosol seems to be the main antigen processing site for both the endogenous and cross-presentation pathways, and TAP is a common crucial component to both pathways. Many aspects relating to TAP localization during cross-presentation remain to be clarified or further elucidated. Mechanisms by which phagosomal or endosomal antigens access the cytosol during cross-presentation remain an important area for further investigations, and why the cytosolic products of endosomally derived antigens might be preferentially retargeted into the endosome rather than the ER [63] (as may be predicted for a freely diffusing antigen) also remains to be addressed. Receptor systems that allow the best manipulations of cross-priming efficiencies remain to be fully defined and will be important toward vaccine studies. Structural and biochemical studies of PLC components and complexes will yield better insights into the specific functions of individual components of the PLC. Finally, research into novel pathogen-encoded mechanisms for evasion of the CTL responses will undoubtedly reveal new and unexpected details of the physiological assembly, trafficking and degradation pathways that are exploited by pathogens (see Refs. [17,33,72,73] for some recent examples).
Acknowledgments
The authors thank all our colleagues for numerous contributions that ensure that the field is thriving and generating debate and discussion. The authors also thank Yesung Park and Ben Schwartz for the artwork. Our contributions summarized here were supported by NIH Grants AI044115 and A1066131 (to M.R.).
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-5,079,003,090,936,195,000 | INTERNATIONAL ACADEMY OF AYURVED:Article:Draksa Mrdvika Raisins
Ayurveda and Neutraceuticals
Dr. Sunanda Ranade
Vice-Chairman
International Academy of Ayurved, Pune, India
(www.ayurved-int.com)
The terms Nutrition and Pharmaceuticals together denotes the Neutraceuticals. These are biological therapies for well being. The philosophy of this therapy focuses mainly on prevention. Greek physician Hippocrates (known as the father of medicine) said “let food be thy medicine and medicine be thy food”. Ayurveda also recommends using food as a medicine.
The name Neutraceuticals was given in 1989 by Stephen DeFelice, founder and chairman of the Foundation for Innovation in Medicine, in Cranford, New Jersey. Neutraceuticals is a specially treated food, vitamin, mineral, herb, etc. that you eat or drink in order to improve your health. It can be classified under food supplements, functional food, medicinal food and farma food.
A dietary supplement represents a product that contains Nutrients derived from food products are dietary supplements, and are often concentrated in liquid, capsule, powder or pill form. Functional food is a category which includes whole foods and fortified food substances. These reducing the risk of chronic disease and provide health-benefit. Medicinal food is formulated to be consumed or administered internally, under the supervision of a qualified physician. Farmaceuticals are valuable components obtained from agricultural crops and animals also. Neutraceuticals impose crucial roles in immune status and susceptibility to certain disease states.
Although the concept of Neutraceuticals is gaining more popularity its origin can be traced from ancient system of medicine Ayurveda. Rasayana is one of the branches of Ayurveda, which is used for achieving longevity. This can be obtained by using herbs, herbo-mineral substances or by specific foods. Aajasrik rasayana is specific type in which special foods can be used for increasing immunity, achieving health and longevity.
Concept of the health of a person is different in Ayurveda. Man is a miniature of the nature. Whatever present in the nature is also present in human being. Universe is made up of five great elements namely- earth, water, fire, air and ether. Therefore these five principles are present in the human being and food also. Health of a person depends on equilibrium of these five elements. Along with that balance in three Bioenergy namely Vata, Pitta , Kapha; seven tissues and proper function of digestion helps for maintenance of health.
Fresh organic food consumed according to agni (digestive power), constitution, at proper time maintain the health and reduces the risk of chronic diseases. According to Chhandogya Upnishad small part of digested food nourishes the mind also. Sattvic food has good impact on mind keeping the good health of mind and giving a person ability to think what is good for him and what is not.
Some examples of Ayurvedic Neutraceuticals are Chavanprash (Fruit jam of Amla or Indian gooseberry cooked with ghee, oil, sugar and various herbs). It is general health and preventive tonic for respiratory diseases. Rason Ksheerpak (Garlic cooked in milk is useful in arthritis). Kushmand pak (Winter melon or special type of white gourd, cooked with ghee and sugar-for debility, as geriatric tonic) Benefits of the food for health are mentioned long back. During the first Olympic Games the ancient Greeks used garlic as a performance-enhancing drug in 16th centuries. Lemon was used to prevent scurvy.
There is tradition in ancient villages to offer glass of water with jaggery to recover from tiredness after walking a long distance.
The stand, that food can be health promoting beyond its traditional nutritional value is gaining momentum amongst scientists, health professionals as well as consumers.
Functional foods and Neutraceuticals have obtained a middle ground between food and drug due to recognition of their role in health.
Ayurveda mentions special branch of treating simple diseases with the help of spices and other safe herbs that can be obtained anywhere. This branch is known as kitchen pharmacy or home remedies. There are many examples e.g.- Ginger + lemon juice in indigestion, Coffee with nutmeg in diarrhea. Cold infusion of cumin + coriander seeds for burning urination. Onion and garlic to reduce the cholesterol. Asafetida to reduce the pain in abdomen and Nutmeg in insomnia.
Curcuma is most favored spice. New research shows it is beneficial in preventing breast cancer. Also it is used for gargling in sour throat, and it is fast source of healing wounds.
Some of the food substances like curry leaves, sesame seeds, cheese, curd, soya, and cabbage give lot of calcium.Vegetables like yam, soya, curcuma contains Phyto -hormones useful in menopause.
Butter milk and yogurt in diarrhea works as Probiotic. One can use Carom (Ajowan) or Shunthi (Dry ginger ) in Irritable bowel syndrome. There are ample examples how the natural food can be helpful for maintenance of health and treating diseases.
Role of healthy food in treatment of different diseases has already been published in different journals.
In a nutshell, Neutraceuticals and functional foods consist of dietary supplements, energy drinks and bars, sport drinks, smoothies etc. These natural bioactive components have health promoting and disease preventing effects. The typical Indian everyday vegetarian diet consists of many types of fruit and leafy vegetables, spices, herbs, legumes and seeds that are rich in calcium, phytohormones, probiotics, phytonutrients, carotenoids, phenols, polyphenols, alkaloids, flavinoids, which impart favorable health related outcome in natural way.
Molecular level interactions between nutrients and other bioactive dietary molecules with the genome and the functional sequences in gene expression denotes the Neutrigenomics. This individualized approach through nutrigenomics goes very well with the Ayurvedic concept of dietary specifications according to individual’s prakriti, season of the year and time of the day. One has to take into consideration fresh, organic food in panchabhautik universe
Future Scope for Neutraceuticals and Ayurved
Without accepting wisdom of Ayurveda, one cannot turn back. Ayurveda and Neutraceuticals is a revolutionary step for health, fitness sector and prevention of diseases. The Neutraceuticals with traditional medicines will be the long standing consumer’s acceptance. Neutraceuticals may suppress the good old traces of Ayurveda. One has to take care for that. This indulgence should be designed in significant way to bring out best of both the sides.
Value of the food also depends on the region where it is grown. It differs from sandy desert, coastal area, middle part of the India and high up in the mountains of Himalaya. Environmental changes and change in quality of soil also makes lot of influence on food. Food cooked in proper pans adds more yield to the food. Stay away from coated pans, microwave, junk food and processed food. According to Ayurveda energetic principles of food depends on taste, potency, and its post digestive effect. (Rasa, Veerya, Veepak).
Broadly, such advanced nutritional products based on Ayurvedic principles may be aimed at providing cellular health support, Immune health support, Bio-chemical / neuro endocrine support, Nutritional support, through phytonutrients. Study of traditional and modern health science, Ayurvedic and modern nutritional science together, is beneficial for understanding of various metabolic processes and causative factors for diseases. It is possible to develop new products. . Yes we have proper pathway to take it forward and justify science behind the two. It will lead us to understand and formulate a conceptual basis for Ayurvedic Neutraceuticals of traditionally used products for better health outcomes that are aimed at providing basic nutrition for health and at the same time reducing disease risk.
Copyright (c) International Acedemy of ayurved. All rights reserved. Designed by: Shailani Software Solution LLP | {
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-5,711,847,675,487,842,000 | If I Have a Hysterectomy, Will I Go Through Menopause?
Undergoing a hysterectomy—surgery to remove all or part of the uterus—can raise many concerns, including the possibility of menopause. While it’s true that some women do enter menopause right after a hysterectomy, this depends on whether or not the ovaries are also removed during the procedure—a decision that hinges on the purpose of the surgery and your overall health. Knowing what to expect in either case can prepare you for this change, whenever it comes, and the symptoms you may experience.
Understanding Hysterectomy
A hysterectomy refers to the surgical removal of a woman’s uterus. It may be performed for a number of reasons, both benign (for example, uterine fibroids) and cancerous (such as uterine cancer).
Depending on the reason behind why a hysterectomy is being done, a doctor may also remove the ovaries and fallopian tubes (the tubes that connect a woman’s ovaries to her uterus).
With the removal of the ovaries, a premenopausal woman will immediately go into menopause, called surgical or induced menopause. Since she no longer has ovaries to produce estrogen, she may experience classic symptoms of estrogen depletion like hot flashes and/or vaginal dryness.
In addition to these symptoms, there are also health conditions associated with the low-estrogen state of menopause, like osteoporosis (when your bones weaken and become prone to breaking).
If you are premenopausal and your ovaries are not removed during a hysterectomy, your body will continue to produce estrogen. However, you will not have periods anymore, as there is no uterine lining to shed.
Surgical Menopause
There are a number of symptoms linked to both natural and surgical menopause; two of the most common ones include vaginal dryness and hot flashes.
Vaginal Dryness: With the loss of estrogen, the lining of a woman’s vagina becomes dry and itchy—a phenomenon called vaginal atrophy. This vaginal dryness, itching, and burning often make sex painful and, in turn, can lower a woman’s desire to have intercourse.
Hot Flashes: Estrogen deficiency throws off how a woman’s brain regulates body temperature, and this may lead to hot flashes. A hot flash is a sudden, intense feeling of heat or burning in the face, neck, and chest, often accompanied by redness.
A night sweat refers to a hot flash that occurs during sleep. Night sweats can negatively impact a woman’s sleep cycle, which may lead to tiredness during the day.
Other Symptoms of Surgical Menopause: There are a number of other symptoms of surgical menopause, although some of them are believed to also be caused by increasing age.
These symptoms include:
• Mood changes, like depression and anxiety
• Weight gain, especially around the waist
• Dry skin and hair loss
• Increased urinary problems, especially urinary tract infections and urinary incontinence (loss of urine without any control)
It’s important to note that for women who have undergone surgical removal of their ovaries, menopausal symptoms tend to be more intense than for a woman who experiences menopause naturally. Of course, this is not a hard-and-fast rule; menopausal symptoms vary widely and in degree from woman to woman.
Even so, this greater intensity of menopausal symptoms is attributed to the abrupt removal of the ovaries, which are a woman’s primary source of estrogen. In natural menopause, the ovaries gradually lose their ability to produce estrogen, so the body can (usually) adjust more easily.
Hysterectomy With Ovaries Left Intact
Women who have their ovaries intact, but without their uterus, won’t get their period anymore. You may, however, still experience premenstrual syndrome (PMS) or premenstrual dysphoric disorder (PMDD) because the hormones made by the ovaries will cause your body to continue to “cycle” monthly.
Occasionally, women whose ovaries were not removed during a hysterectomyexperience hot flashes and other menopausal symptoms. This is mostly due to the disturbance of the blood supply to the ovaries during surgery.
In addition, some women may undergo menopause a few years sooner than they normally would if they never underwent a hysterectomy (the average onset age for menopause is 51). | {
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7,742,506,875,084,722,000 |
Woman on Computer
How coaching can help women in menopause
Woman in menopause feeling happy
(This article was published on Life Coach Directory - https://www.lifecoach-directory.org.uk/memberarticles/how-coaching-can-help-women-in-menopause)
If you are a woman in your 50s, you are very likely to be in menopause.
Menopause occurs in every woman’s life. Regardless if they have had children or not, sooner or later women find themselves dealing with the end of their monthly period and, for the majority of them, that is a time when they face very disrupting symptoms. According to an imaginative theory by Zhao Xiao Lang, a Chinese medical doctor, when a woman is around 50 years old, the blood leaves her reproductive apparatus because she does not need it anymore. The blood then is redirected to the heart, providing it with nutrients and energy to enable her re-birth. I do not know whether this theory is scientifically acceptable, but I find it inspiring because I believe that middle-aged women need to look to this time of their life as the moment to take back control of their body, their time, their life. It can be an occasion to be born again.
Symptoms and psychological consequences
Menopause is not an easy ride. Only 20% of women who go through menopause do not experience any symptoms. The other 80% can experience hot flushes, night sweats, mood swings, low mood, muscle tension, joint pain, reduced libido and some more - varying from woman to woman - with significant physical and psychological consequences. And these symptoms may affect their overall wellbeing and productivity both in their personal and professional life.
Emotional challenges
Middle-aged women are the so-called “Sandwich generation”. They feel squeezed between ageing parents who need help and care and teen-age children who spend hours in their rooms with their door shut, keeping their closest family out of their life. Or they find themselves without purpose when their grown-up children go to University and leave the “nest”. And this is the time when a woman often stops feeling good in her own body. Fat starts accumulating around the waist; skin elasticity and radiance gradually reduce; the influence of gravity upon her body becomes visible. These external age signs are accompanied by emotional consequences: a sense of feeling invisible, not being able to trade on appearance anymore, seeing this point of life as the beginning of an inevitable decline.
What you can do
If you are in menopause and are experiencing the symptoms and/or the psychological consequences related to mid-life changes, a coach can help you take care of your body and implement a wellbeing programme that includes exercising regularly. Regular physical activity is important for many reasons:
• It can prevent weight gain, which also reduces the risk of cancer, heart disease, high blood pressure, and type 2 diabetes; it also strengthens the bones, reducing the risk of fractures and osteoporosis.
• It boosts mood, self-confidence and self-esteem and prevents cognitive decline and risk of depression.
• It helps control menopause symptoms such as hot flushes and insomnia: although there is no sufficient research in the subject, some experiments show that women in menopause may see a reduction in the severity and frequency of hot flushes and experience a better night sleep when doing daily physical activity.
1. With the support and guidance of a coach you will:
• Identify new wellness goals. They may regard losing weight or just achieving a sense of general wellbeing or getting rid of bad habits such as smoking or over-drinking.
• Design an action plan to maintain regular physical activity and develop healthy habits.
• Build a positive mindset to follow-through.
• Be held accountable: having to answer another person for your actions motivates you to stay on track with your goals
• Be supported in overcoming the obstacles that are stopping you from being consistent in your new behaviours.
2. A coach can also help you promote self-development actions that will serve as a confidence and self-esteem boost. You will learn how to replace negative thinking with new positive and growing-oriented beliefs. 3. On a spiritual side, a coach can encourage you to commit to regular mindfulness practice, which will significantly improve the overall level of your wellbeing. Mindfulness meditation and – in general – a mindful approach to life have proved to provide positive effects in boosting mood, controlling blood pressure, and reducing the level of stress and anxiety. Menopause cannot be avoided but we can embrace the change without fear and make this time of our life as a time of pride and an occasion for growing and learning. you are a woman in your 50s, you are very likely to be in menopause.
Menopause occurs in every woman’s life. Regardless they have had children or not, sooner or later women find themselves dealing with the end of their monthly period and, for the majority of them, that is a time when they face very disrupting symptoms.
SYMPTOMS AND PSYCHOLOGICAL CONSEQUENCES
Menopause is not an easy ride. Only 20% of women who go through menopause do not experience any symptoms. The other 80% can experience hot flushes, night sweats, mood swings, low mood, muscle tension, joint pain, reduced libido and some more - varying from woman to woman - with significant physical and psychological consequences. And these symptoms may affect their overall wellbeing and productivity both in their personal and professional life.
EMOTIONAL CHALLENGES
Middle-aged women are the so-called “Sandwich generation”, squeezed between ageing parents who need help and care and teen-age or grown-up children who think they do not need their care anymore. The weight of responsibilities towards their parents juxtaposes a sense of uselessness, due to the loss of identity as carers of their offspring.
External age signs (increased body weight, wrinkles, loss of skin elasticity) carry with them emotional distress such a sense of feeling invisible and the awareness of not being able to trade on appearance anymore. It feels like the first step to an inevitable decline.
WHAT YOU CAN DO
Menopausal woman going running
If you are in menopause and are experiencing the symptoms and/or the psychological consequences related to mid-life changes, a coach can help you take care of your body and implement a wellbeing programme that includes exercising regularly.
Regular physical activity is crucial for both physical and mental wellbeing because it helps prevent weight gain, control menopausal symptoms such as hot flushes and insomnia, and works as a confidence and self-esteem boost when you achieve your fitness goals.
With the support and guidance of a coach you will also identify new wellness goals; get rid of bad habits (smoking, drinking); implement a new healthy lifestyle; build a positive mindset; identify the limiting beliefs that are stopping you from achieving your desired outcomes.
Menopause cannot be avoided but we can embrace the change without fear and make this time of our life as a time of pride and an occasion for growing and learning.
#menopause #weightloss #coaching #menopausesymptoms #wellbeing #midlife #change #exercising #fitness
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Full Answer
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• Q:
What is vitamin B12 for?
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According to the National Institutes of Health, vitamin B12 helps the body maintain healthy nerves and blood cells and helps in the production of DNA. It also helps prevent a type of anemia called megaloblastic anemia that makes people tired and weak.
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WebMD indicates that vitamin B12 is mainly used for the treatment and prevention of vitamin B12 deficiency, diseases resulting from vitamin B12 deficiency and pernicious anemia. Additionally, this vitamin is used to reduce the risk of hyperhomocysteinemia, a heart condition, and to prevent age-related macular degeneration when taken with vitamin B6 and folic acid.
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714,545,680,884,920,000 | –Ashley, living with AHP
Resources
Stay informed with resources about AHP
There are a range of resources designed to help people understand acute hepatic porphyria (AHP) and handle the challenges of living with the disease. A great starting point is downloading a printable Doctor Discussion Guide. Once the Guide is downloaded, you can complete each section and then bring it to an upcoming doctor appointment. This can help start conversations about whether you should be tested for AHP.
Brochure with information about acute hepatic porphyria
ACUTE HEPATIC PORPHYRIA BROCHURE
This reader-friendly brochure takes you step by step through what AHP is, its signs and symptoms, diagnosis, and how to live with AHP.
Download PDF
LEARN ABOUT FAMILY GENETIC TESTING FOR AHP AND MAP YOUR FAMILY’S HISTORY
Knowledge of genetic risk of AHP may enable people to make informed decisions regarding lifestyle and medications with the intent to prevent attacks and complications of the disease. The following resources can help you learn more about the genetic risk of AHP, and how to talk with your family and doctor about genetic testing for AHP
Person diagnosed with acute hepatic porphyria
Alnylam Act®
Alnylam-sponsored third-party genetic testing for acute hepatic porphyria offered at no charge
The Alnylam Act® program was developed to reduce barriers to genetic testing to help people make more informed decisions about their health.
While Alnylam provides financial support for this program, tests and services are performed by independent third parties. Healthcare professionals must confirm that patients meet certain criteria to use the program. Alnylam receives de-identified patient data from this program, but at no time does Alnylam receive patient identifiable information. Alnylam receives contact information for healthcare professionals who use this program. Genetic testing is available in the US and Canada. Healthcare professionals who use this program have no obligation to recommend, purchase, order, prescribe, promote, administer, use, or support any Alnylam product.
Your doctor must sign up for the program and confirm that you meet certain criteria in order for you to receive genetic screening at no charge.
This helpful brochure offers a review of AHP, genetic testing, and the Alnylam Act® program.
Genetic testing
Download the Alnylam Act® Brochure | {
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988,769,685,456,302,300 | Does Maca Root Have Any Side Effects?
What are the side effects of Maca Root for health?
Peruvian Maca is an excellent health food and has fantastic health benefits. Still, in some cases, and like all herbal medicines, it can cause specific undesired harmful results, so it is important to know what these harmful effects are and when they can happen before using maca root.
Can Maca be noxious?
Is there any peril or side effects from consuming maca root? Let’s see this in this article.
If you are not one of the problems here, you can buy our quality Maca powder Lepidium peruvianum Chacon class without a doubt!
The dangers: an effect of dosage
it should note that it all depends on the dosage. Peruvian Maca is used in dry roots, pills, tablets, food sequels, spices, and fresh roots, and each state has a different concentration of active elements.
The powder, the dried, and fresh roots are usually for food use, and, aside from the contraindications and possible medication interactions stated below, they do not present any chance.
It is particularly capsules, tablets, and food additions that can cause complications if they are unnecessary doses. This process of taking refers to the directions for use and a medical examination.
What are the contraindications for Maca?
According to the National Agency for Food, Environmental, and Occupational Health Safety, it would be risky to consume maca root powder, without therapeutic discussion, in people:
• Suffering from hypertension
• Suffering from thyroid problems
• Cruciferous allergy victims
Metabolic syndrome
About thyroid difficulties, researches show that Maca may be helpful for some thyroid signs but may be dangerous to others, so seeing a physician is a must.
The metabolic type is a term for connecting a range of health problems with inferior body metabolism, such as low HDL-cholesterol, glucose intolerance, obesity, hypertriglyceridemia, type 2 diabetes, etc.
It is a so-called “emerging” sign, more common, which increases with age, but it is not a disease strictly speaking, but rather a grouping of chance factors. Discuss the guidance of a healthcare expert before taking Maca if you fall into one of these 4 classes.
What are the side effects of Maca root?
Maca is a portion of safe food, but over-consumption of the Peruvian root could, in extraordinary cases, have some unwanted effects. Take fildena or vidalista 40 to get rid of ED dilemmas. It is then better to reduce or even stop its consumption.
Here are the light known side effects of Maca, compared to its overuse:
• Raise in menstrual problems
• Reduced libido
• Hot flashes
• Weight gain
• Skin troubles
• Insomnia
Classic detoxification signs: diarrhea, dizziness, nausea, headache, stomach pain
To withdraw these side effects, it is desirable, to begin with, small doses and gradually progress to assess the body’s reply; this is called titration.
Maca throughout pregnancy, breastfeeding, and in children
No clinically examined researches have been made on Maca using throughout pregnancy or breastfeeding, so health experts advise maca consumption in this case.
It would help if you recognized that pregnant women had consumed Maca for thousands of years without any difficulties in Peru.
Likewise, no clinically tested examinations have been performed on Maca’s using in kids, but children in Peru consume it without any recognized care.
It is expedient to give it punctually and reduce the doses by 2 in older children and by 4 in more minor children.
Likely services between Maca and pills
To date, no drug interactions have been identified. If you are taking medication therapy, ask your doctor to get his authorization before starting a Maca course as a careful judgment.
What dosage should be followed?
There are lacking thoughts to give an exact dosage. Nutritionists usually suggest the following treatment: 2 to 3 g of Maca, about 3 level teaspoons per day split into 3 doses morning, noon, and evening, for a least 2-month remedy up to 3 months, with a week’s rest at the result of the first month.
This usually is the kind of cure served to take advantage of Maca’s aphrodisiac properties or use Maca to ease signs of menopause. For a flash cure, in case of research, sports game, recreation, moral test, etc., you can do this same cure for 1 week.
It would help if you understood that this dosage is much weaker than the regular eating of Peruvians of the hills, who use up to 50 g of fresh tuber per day, 365 days per year.
Advice reliable for most plants’ uses for medical goals: when you do a treatment, once the treatment is done, pause for a period about similar to the treatment before returning. You can use tadalista or vidalista 60 tadalafil goods for impotence. For example, you take a 2-week dose; then you take a rest of 1 to 2 weeks before likely resuming.
Conclusion
To conclude, it is ever necessary to recognize that just because a product is natural doesn’t mean you can do anything. The spices’ outcomes are trustworthy and valuable, which is why you must take care and inform yourself before beginning a cure.
Remember that food use, but in medication interaction or proven contraindication, does not work as a problem
Leave a Comment | {
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-7,795,915,137,341,548,000 | Pineal gland interface between the photoperiodic environment and the endocrine system
Research output: Contribution to journalReview articlepeer-review
203 Scopus citations
Abstract
The photoperiodic message that the pineal gland conveys to the organism is encoded in the circadian melatonin rhythm. Melatonin is a ubiquitously acting hormone that mediates seasonal changes in reproduction in nonhuman mammals and may have reproductive consequences in humans as well. Additionally, melatonin may relate to the function o f the immune system, hormone-responsive tumor growth, circadian rhythm disturbances, and a number of other processes.
Original languageEnglish (US)
Pages (from-to)13-19
Number of pages7
JournalTrends in Endocrinology and Metabolism
Volume2
Issue number1
DOIs
StatePublished - 1991
ASJC Scopus subject areas
• Endocrinology, Diabetes and Metabolism
• Endocrinology
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1.
Phytomedicine ; 80: 153382, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33113506
RESUMO
BACKGROUND: Although gastroprotective drugs have been used for peptic ulcer disease prevention and treatment, side effects have been observed. Finding a safe and effective treatment strategy is important. PURPOSE: Edible Trichodesma khasianum (T. khasianum) Clarke leaves are considered to protect against peptic ulcers. However, scientific evidence of this effect of T. khasianum Clarke leaves remains limited. STUDY DESIGN/METHODS: In this study, we aimed to evaluate the effect of T. khasianum Clarke leaves on ethanol-induced gastric injury and gut microbiota using RAW 264.7 cells, RGM-1 cells, and BALB/c mice, respectively. RESULT: The rosmarinic acid was identified as the major component of T. khasianum Clarke leaves extracted by 80% ethanol (80EETC). The results showed that 80EETC suppressed inflammatory mediator protein levels in LPS-induced RAW 264.7 cells. Additionally, heat shock protein expression, antiapoptotic ability, and wound healing migration capability were increased by 80EETC pretreatment in RGM-1 cells with the ethanol-induced injury. Remarkably, pretreatment with 80EETC (150 mg/kg b.w.) promoted gastric mucosal healing by decreasing oxidative stress, inflammatory response, proapoptotic protein expression, and gastric mucosa damage in ethanol-induced gastric injury in mice. Crucially, no liver or kidney toxicities were observed by 80EETC oral gavage. Moreover, 80EETC increased gut microbiota diversity and short-chain fatty acid production. CONCLUSION: Our results illustrated the remarkable gastroprotective effect by 80EETC treatment in vitro and in vivo. These findings are the first to demonstrate the powerful protective effect of T. khasianum Clarke leaves against gastric mucosal injury development.
Assuntos
Boraginaceae/química , Cinamatos/farmacologia , Depsídeos/farmacologia , Mucosa Gástrica/efeitos dos fármacos , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Administração Oral , Animais , Anti-Inflamatórios não Esteroides/química , Anti-Inflamatórios não Esteroides/farmacologia , Antioxidantes/metabolismo , Cinamatos/análise , Depsídeos/análise , Etanol/toxicidade , Ácidos Graxos Voláteis/metabolismo , Mucosa Gástrica/metabolismo , Mucosa Gástrica/patologia , Microbioma Gastrointestinal/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Estresse Oxidativo/efeitos dos fármacos , Úlcera Péptica/prevenção & controle , Extratos Vegetais/administração & dosagem , Extratos Vegetais/química , Folhas de Planta/química , Substâncias Protetoras/química , Células RAW 264.7
2.
Chem Biol Interact ; 331: 109233, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32991863
RESUMO
Cisplatin (cis-Dichlorodiammine platinum, CP), as the first-line chemotherapy drug of choice for many cancers such as urogenital system tumors and digestive tract tumors, also causes toxicity and side effects to the kidney. Previous studies have shown that Pulsatilla chinensis has significant anti-inflammatory and antioxidant activities, but the mechanism of cisplatin induced acute kidney injury (AKI) in vivo has not been thoroughly studied. The purpose of this study is to investigate the protective effect of pulchinenoside B4 (PB4), a representative and major component with a content of up to 10% in root of P. chinensis, on AKI induced by CP in mice. Our results indicated the significant protective effect of PB4 by evaluating renal function indicators, inflammatory factor levels and renal histopathological changes. In addition, PB4 may mainly act on NF-κB signaling pathway to reduce the levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in the kidney after CP exposure, thus exerting anti-inflammatory activity. Furthermore, PB4 regulated MAPK signaling pathway and its downstream apoptotic factors to inhibit the occurrence of apoptosis, such as Bax, Bcl-2, caspase 3 and caspase 9. Notably, the activations of caspase 3 induced by cisplatin were strikingly reduced in PB4-treated mice. Therefore, the above evidence suggested that PB4 is a potential renal protectant with significant anti-inflammatory and anti-apoptotic effects.
Assuntos
Lesão Renal Aguda/patologia , Apoptose/efeitos dos fármacos , Substâncias Protetoras/farmacologia , Transdução de Sinais/efeitos dos fármacos , Lesão Renal Aguda/induzido quimicamente , Lesão Renal Aguda/veterinária , Animais , Cisplatino/toxicidade , Modelos Animais de Doenças , Interleucina-1beta/metabolismo , Rim/efeitos dos fármacos , Rim/metabolismo , Rim/patologia , Masculino , Camundongos , Camundongos Endogâmicos ICR , Proteínas Quinases Ativadas por Mitógeno/metabolismo , NF-kappa B/metabolismo , Fosforilação , Substâncias Protetoras/química , Fator de Necrose Tumoral alfa/metabolismo
3.
PLoS One ; 15(9): e0238163, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32881885
RESUMO
OBJECTIVE: We evaluated the effects of grape juice (Vitis labrusca L.) on dyslipidemia, resistance to insulin, and left ventricular hypertrophy (LVH) in mice homozygous for the absence of the LDL receptor gene (LDLr -/-) under a hyperlipidemic diet. METHODOLOGY: We divided 30 male mice (3 months old) into three groups (n = 10); the HL group was fed a high-fat diet, the HLU group received a high-fat diet and 2 g/kg/day of grape juice, and the HLS group was fed a high-fat diet and simvastatin (20 mg/kg/day). We assessed the blood pressure profile of the mice. We also determined the levels of C-reactive protein (CRP) and lipid profile, glycemic and insulinemic profiles, and calculated the HOMA-IR. Cardiomyocyte hypertrophy, interstitial collagen deposit, and the expression of CD40 ligand (CD40L) and metalloproteinases 2 and 9 were assessed immunohistologically. RESULTS: After 60 days, the mice treated with grape juice showed similar results as those of the group treated with simvastatin. The use of grape fruit attenuated dyslipidemia and insulin resistance and significantly increased the levels of high cholesterol density lipoproteins (HDLc). The antioxidant potential of phenolic compounds associated with the increase in HDLc levels in the mice of the HLU group prevented the development of LVH and arterial hypertension since it inhibited the inflammatory response induced by the CD40 pathway and its ligand CD40L. Consequently, there was a lower expression of MMP-2 and MMP-9 and lower serum levels of CRP. CONCLUSION: Grape juice has a hypolipidemic and cardiac protective potential, presenting a similar effect as that of simvastatin through a direct antioxidant action of phenolic compounds, or indirectly, via antioxidant action and anti-inflammatory activity of the HDLc. These results suggest that grape juice is a functional food possessing a high potential to prevent cardiovascular diseases.
Assuntos
Dislipidemias/patologia , Sucos de Frutas e Vegetais , Hipertrofia Ventricular Esquerda/prevenção & controle , Vitis/química , Animais , Pressão Sanguínea/efeitos dos fármacos , Proteína C-Reativa/análise , Ligante de CD40/genética , Ligante de CD40/metabolismo , Colágeno/metabolismo , Dieta Hiperlipídica , Dislipidemias/tratamento farmacológico , Sucos de Frutas e Vegetais/análise , Ventrículos do Coração/patologia , Hipertrofia Ventricular Esquerda/patologia , Masculino , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 2 da Matriz/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Substâncias Protetoras/química , Substâncias Protetoras/uso terapêutico , Receptores de LDL/deficiência , Receptores de LDL/genética , Sinvastatina/uso terapêutico , Vitis/metabolismo
4.
J Cancer Res Clin Oncol ; 146(7): 1801-1811, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32435894
RESUMO
PURPOSE: Oral mucositis is a debilitating inflammatory disorder observed in patients undergoing active cancer treatment, particularly cancer of the head and neck region. A key pathway believed to be involved in the pathogenesis of oral mucositis is the formation of reactive oxygen species (ROS). The identification of compounds that can inhibit this pathway may therefore be of benefit in treating this disorder. The kava plant (Piper methysticum) contains various constituents, including flavokawain A (FKA), flavokawain B (FKB), yangonin, methysticin and kavain. These constituents are known to be biologically active and possess anti-oxidative properties. This study therefore focused on examining these constituents for their effect on ROS formation in an in vitro oral mucositis model. METHODS: Cell proliferation was assessed in normal oral keratinocytes (OKF6) treated with and without kava constituents, namely FKA, FKB, yangonin, methysticin and kavain using an MTS in vitro assay. Oxidative stress was assessed by co-treating and pre-treating OKF6 cells with H2O2. The effects were quantified by analysis of ROS production, using a CM-H2DCFDA assay. RESULTS: Pre-treatment of cells for 24 h with 2.5 µg/ml kavain and 5 µg/ml FKA demonstrated a significant protective anti-oxidative effect. Similarly, FKB at a concentration of 2.5 µg/ml, demonstrated a trend of ROS reduction but was observed to be cytotoxic at concentrations greater than 5 µg/ml. Reduction in ROS production by methysticin and yangonin was compromised by their cell cytotoxicity. CONCLUSION: This was the first study to identify the anti-oxidative effects and safety of FKA and kavain with regard to oral keratinocytes, highlighting their potential use in the development of a preventative treatment for oral mucositis.
Assuntos
Kava/química , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Antioxidantes/química , Antioxidantes/farmacologia , Linhagem Celular Tumoral , Células Cultivadas , Humanos , Peróxido de Hidrogênio/metabolismo , Queratinócitos/efeitos dos fármacos , Queratinócitos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/química , Substâncias Protetoras/química , Piranos/farmacologia , Pironas/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Estomatite/tratamento farmacológico , Estomatite/etiologia
5.
Food Chem ; 327: 127059, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32447138
RESUMO
The aim of this study was to purify and identify antioxidant peptides from watermelon seed protein hydrolysates (WSPHs-I: Mw < 1 kDa) and further evaluate their cytoprotective effects against H2O2-induced oxidative stress in HepG2 cells. After purification by Sephadex G-15 and semi-preparative reversed-phase high performance liquid chromatography (RP-HPLC), five peptides, RDPEER (P1), KELEEK (P2), DAAGRLQE (P3), LDDDGRL (P4), and GFAGDDAPRA (P5) were sequenced by LC-MS/MS and synthesized with solid-phase synthesis method. These peptides showed desirable 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging capacity (IC50: 0.216 ± 0.01-0.435 ± 0.03), 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging capacity (IC50: 0.54 ± 0.02-1.23 ± 0.03), and oxygen radical absorbance capacity (ORAC) (82.36 ± 1.2-130.67 ± 2.2 µM TE/mg). Among them, peptide P1 exhibited the strongest antioxidant capacity. Moreover, the results suggested that peptide P1 may protect HepG2 cells from H2O2-induced oxidative damage by significantly inhibiting reactive oxygen species (ROS), [Ca2+]i, malondialdehyde (MDA) levels and increasing antioxidative enzyme activities.
Assuntos
Citrullus/química , Peróxido de Hidrogênio/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Peptídeos/química , Hidrolisados de Proteína/química , Sequência de Aminoácidos , Antioxidantes/química , Antioxidantes/isolamento & purificação , Antioxidantes/farmacologia , Cromatografia Líquida de Alta Pressão , Citrullus/metabolismo , Células Hep G2 , Humanos , Oxirredução , Peptídeos/isolamento & purificação , Peptídeos/farmacologia , Proteínas de Plantas/metabolismo , Substâncias Protetoras/química , Substâncias Protetoras/isolamento & purificação , Substâncias Protetoras/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Sementes/química , Sementes/metabolismo , Relação Estrutura-Atividade , Espectrometria de Massas em Tandem
6.
Food Chem ; 322: 126742, 2020 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-32305872
RESUMO
Almond hulls, the main by-product of almond production, are considered a valuable source of bioactive phenolic compounds. This study aimed to characterize the phenolic composition, bioavailability of the phenolic-rich extracts from almond hulls (PEAH), and their protective effect on oxidative stressed Caco-2 cells induced by tert-butylhydroperoxide (t-BOOH). The ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS) analysis detected 11 phenolic compounds in the PEAH with high total phenolic content and antioxidant activity. Oxidative Caco-2 cell damage was reduced by PEAH, especially at 5 µg/mL, through scavenging reactive oxygen species (ROS), modulating the cellular endogenous antioxidant system and cell redox at a predictable status. Also, in vitro digestion influenced the phenolic compounds' composition and antioxidant power of PEAH. These results suggested that almond hulls, rich in phenolic compounds, can meliorate the oxidative stressed Caco-2 cells and restore its impaired redox balance, and ultimately improve health benefits.
Assuntos
Estresse Oxidativo/efeitos dos fármacos , Fenóis/química , Extratos Vegetais/química , Substâncias Protetoras/farmacologia , Prunus dulcis/química , Antioxidantes/química , Disponibilidade Biológica , Células CACO-2 , Cromatografia Líquida de Alta Pressão , Análise Discriminante , Meia-Vida , Humanos , Análise dos Mínimos Quadrados , Espectrometria de Massas , Oxirredução , Fenóis/farmacologia , Substâncias Protetoras/química , Substâncias Protetoras/farmacocinética , Prunus dulcis/metabolismo , Espécies Reativas de Oxigênio/química , terc-Butil Hidroperóxido/toxicidade
7.
J Food Sci ; 85(5): 1586-1595, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32267971
RESUMO
Radix Tetrastigma (RT) is a medicinal plant and functional food in China, distributed in various places in the south of China. Radix Tetrastigma extract (RTE) from different origins were collected and analyzed for their anti-inflammatory effects. Different RTEs showed different abilities to suppress shape deformation, decrease the nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in RAW 264.7 cells. Subsequently, their bioactive components were compared, and results showed RTEs are rich in flavonoid (85.25-436.70 mg RE/g DW), polysaccharides (100.45-349.26 mg glucose/g DW), phenolic (12.92-225.40 mg GAE/g DW) and protein contents (4.429-7.719 mg/g DW). Principal component analysis (PCA) and correlation studies indicated that anti-inflammatory capacity could be more associated with total flavonoid contents. High-performance liquid chromatography (HPLC) and Ultraperformance liquid chromatography-time-of flight mass spectrometry (UPLC-TOF/MS) analysis were conducted, and results showed that rutin, isoquercitrin, kaempferol-3-O-rutinoside and astragalin were main flavonoid compounds, among them astragalin exhibited a prior protective effect, suggesting it might be responsible for RTE's excellent anti-inflammatory capacity.
Assuntos
Anti-Inflamatórios/farmacologia , Lipopolissacarídeos/farmacologia , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Vitaceae/química , Animais , Anti-Inflamatórios/química , Cromatografia Líquida de Alta Pressão , Lipopolissacarídeos/efeitos adversos , Camundongos , Óxido Nítrico/imunologia , Óxido Nítrico Sintase Tipo II/imunologia , Extratos Vegetais/química , Substâncias Protetoras/química , Células RAW 264.7
8.
Nat Commun ; 11(1): 1608, 2020 03 30.
Artigo em Inglês | MEDLINE | ID: mdl-32231209
RESUMO
The emerging resistance of crop pathogens to fungicides poses a challenge to food security and compels discovery of new antifungal compounds. Here, we show that mono-alkyl lipophilic cations (MALCs) inhibit oxidative phosphorylation by affecting NADH oxidation in the plant pathogens Zymoseptoria tritici, Ustilago maydis and Magnaporthe oryzae. One of these MALCs, consisting of a dimethylsulfonium moiety and a long alkyl chain (C18-SMe2+), also induces production of reactive oxygen species at the level of respiratory complex I, thus triggering fungal apoptosis. In addition, C18-SMe2+ activates innate plant defense. This multiple activity effectively protects cereals against Septoria tritici blotch and rice blast disease. C18-SMe2+ has low toxicity in Daphnia magna, and is not mutagenic or phytotoxic. Thus, MALCs hold potential as effective and non-toxic crop fungicides.
Assuntos
Cátions/farmacologia , Produtos Agrícolas/efeitos dos fármacos , Fungicidas Industriais/farmacologia , Doenças das Plantas/prevenção & controle , Substâncias Protetoras/farmacologia , Animais , Ascomicetos/efeitos dos fármacos , Cátions/química , Daphnia/efeitos dos fármacos , Descoberta de Drogas , Grão Comestível/microbiologia , Fibroblastos/efeitos dos fármacos , Fungicidas Industriais/química , Humanos , Mitocôndrias/efeitos dos fármacos , Oryza/microbiologia , Doenças das Plantas/microbiologia , Substâncias Protetoras/química , Triticum/microbiologia , Ustilago/efeitos dos fármacos
9.
Carbohydr Polym ; 235: 115957, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-32122493
RESUMO
The present study aimed to investigate the protective effect of cultured Cordyceps sinensis polysaccharides (CSP) on cyclophosphamide (Cy)-induced intestinal mucosal immunosuppression and microbial dysbiosis in mice. Results showed that CSP stimulated cytokines secretion (IL-12, IFN-γ, IL-4, IL-13, IL-6, IL-17, IL-10, TGF-ß3, TNF-α, IL-2, IL-21) and transcription factors production (T-bet, GATA-3, RORγt, Foxp3). TLRs (TLR-2, TLR-4, TLR-6) and NF-κB pathway key proteins (p-IκB-α, NF-κB p65) were also upregulated after CSP administration. Moreover, CSP recovered SCFAs levels which decreased by Cy treatment. Furthermore, 16S rRNA sequencing of fecal samples was performed. α-diversity and ß-diversity analysis revealed CSP improved microbial community diversity and modulated the overall structure of gut microbiota. Taxonomic composition analysis found that CSP increased the abundance of probiotics (Lactobacillus, Bifidobacterium, Bacteroides) and decreased pathogenic bacteria (Clostridium, Flexispira). These findings suggested the potential of CSP as a prebiotics to reduce side effects of Cy on intestinal mucosal immunity and gut microbiota.
Assuntos
Cordyceps/química , Ciclofosfamida/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Imunidade nas Mucosas/efeitos dos fármacos , Intestinos/efeitos dos fármacos , Polissacarídeos/farmacologia , Substâncias Protetoras/farmacologia , Animais , Feminino , Intestinos/microbiologia , Camundongos , Camundongos Endogâmicos BALB C , Tamanho da Partícula , Polissacarídeos/química , Substâncias Protetoras/química , Propriedades de Superfície
10.
Sci Rep ; 10(1): 2056, 2020 02 06.
Artigo em Inglês | MEDLINE | ID: mdl-32029842
RESUMO
The lack of effective pharmacological treatments for acute kidney injury (AKI) remains a significant public health problem. Given the involvement of apoptosis and regulated necrosis in the initiation and progression of AKI, the inhibition of cell death may contribute to AKI prevention/recovery. Curcuminoids are a family of plant polyphenols that exhibit attractive biological properties that make them potentially suitable for AKI treatment. Now, in cultured tubular cells, we demonstrated that a crosslinked self-assembled star-shaped polyglutamate (PGA) conjugate of bisdemethoxycurcumin (St-PGA-CL-BDMC) inhibits apoptosis and necroptosis induced by Tweak/TNFα/IFNγ alone or concomitant to caspase inhibition. St-PGA-CL-BDMC also reduced NF-κB activation and subsequent gene transcription. In vivo, St-PGA-CL-BDMC prevented renal cell loss and preserved renal function in mice with folic acid-induced AKI. Mechanistically, St-PGA-CL-BDMC inhibited AKI-induced apoptosis and expression of ferroptosis markers and also decreased the kidney expression of genes involved in tubular damage and inflammation, while preserving the kidney expression of the protective factor, Klotho. Thus, due to renal accumulation and attractive pharmacological properties, the application of PGA-based therapeutics may improve nephroprotective properties of current AKI treatments.
Assuntos
Lesão Renal Aguda/tratamento farmacológico , Diarileptanoides/farmacologia , Túbulos Renais/efeitos dos fármacos , Ácido Poliglutâmico/farmacologia , Substâncias Protetoras/farmacologia , Lesão Renal Aguda/induzido quimicamente , Lesão Renal Aguda/imunologia , Lesão Renal Aguda/patologia , Animais , Apoptose/efeitos dos fármacos , Apoptose/imunologia , Linhagem Celular , Diarileptanoides/química , Diarileptanoides/uso terapêutico , Modelos Animais de Doenças , Avaliação Pré-Clínica de Medicamentos , Feminino , Ácido Fólico/toxicidade , Glucuronidase/metabolismo , Humanos , Túbulos Renais/patologia , Camundongos , Conformação Molecular , NF-kappa B/metabolismo , Necrose/tratamento farmacológico , Necrose/imunologia , Necrose/patologia , Ácido Poliglutâmico/química , Ácido Poliglutâmico/uso terapêutico , Substâncias Protetoras/química , Substâncias Protetoras/uso terapêutico , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/imunologia , Relação Estrutura-Atividade , Transcrição Genética/efeitos dos fármacos
11.
Mol Med Rep ; 21(3): 1633-1639, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32016475
RESUMO
The present study aimed to clarify the protective effects of pmethoxyphenyl morpholinophosphinodithioic acid (GYY4137), a watersoluble hydrogen sulfidereleasing molecule, on a rat model of intestinal ischemiareperfusion (IIR). A total of 40 healthy male Sprague Dawley (SD) rats were randomly divided into four groups (n=10/group): Group A, a shamsurgery group; Group B, the IIR group; group C, rats with IIR that were administered an abdominal injection of lowdose GYY4137 (40 mg/kg); and group D, rats with IIR that were administered highdose GYY4137 (80 mg/kg). Intestinal histomorphology was observed using hematoxylin and eosin staining, and the concentrations of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Apoptotic index (AI) was determined by terminal deoxynucleotidyltransferasemediated dUTP nick end labeling. Reverse transcriptionquantitative PCR analysis was performed to assess the expression levels of intestinal caspase3, Bax and Bcl2. Notably, disordered arrangement of intestinal villi and mucosal necrosis were detected in group B, which was substantially improved by GYY4137 treatment (groups C and D). MDA content (nmol/mg) was 2.83±0.36, 9.23±0.78, 4.97±0.45 and 3.51±1.05 nmol/mg in groups A, B, C and D, respectively. In addition, SOD concentration (U/mg) was 135.37±3.34, 76.45±1.39, 95.13±1.64 and 115.13±2.54 in groups A, B, C and D, respectively. Furthermore, AI in group B (21.73±1.17%) was markedly higher than that in group A (4.53±0.28%) and in the GYY4137 intervention groups (9.53±0.96 and 6.53±0.76% in groups C and D, respectively). Compared with in group A, the mRNA expression levels of Bax and caspase3 were markedly higher in group B (P<0.05), whereas the expression of Bcl2 was significantly lower (P<0.05). Furthermore, compared with in group B, Bcl2 expression was higher, and Bax and caspase3 expression was lower in groups C and D (P<0.05). In conclusion, GYY4137 may alleviate IIRinduced damage in SD rats.
Assuntos
Sulfeto de Hidrogênio/farmacologia , Intestinos/irrigação sanguínea , Intestinos/efeitos dos fármacos , Morfolinas/farmacologia , Compostos Organotiofosforados/farmacologia , Substâncias Protetoras/farmacologia , Traumatismo por Reperfusão/prevenção & controle , Animais , Apoptose/efeitos dos fármacos , Biomarcadores , Modelos Animais de Doenças , Expressão Gênica , Sulfeto de Hidrogênio/química , Imuno-Histoquímica , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologia , Intestinos/patologia , Masculino , Malondialdeído/metabolismo , Morfolinas/química , Compostos Organotiofosforados/química , Estresse Oxidativo/efeitos dos fármacos , Substâncias Protetoras/química , Ratos , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/etiologia , Traumatismo por Reperfusão/patologia , Superóxido Dismutase/metabolismo
12.
Biochim Biophys Acta Gen Subj ; 1864(5): 129543, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32007578
RESUMO
BACKGROUND: PYY (1-36) peptides from phylogenetically ancient fish, such as sea lamprey, have previously been shown to function as specific neuropeptide Y1 receptor (NPYR1) agonists. Although, sea lamprey PYY (1-36) is N-terminally stable, we reveal in this study that the peptide is subject to endopeptidase mediated C-terminal dipeptide degradation. In an attempt to prevent this, (d-Arg35)-sea lamprey PYY (1-36) was developed. METHODS: In vitro bioassays assessed enzymatic stability, insulinostatic activity as well as beta-cell anti-apoptotic actions of (d-Arg35)-sea lamprey PYY (1-36). Follow-up studies examined the impact of twice daily administration of sea lamprey PYY (1-36) or (d-Arg35)-sea lamprey PYY (1-36) in multiple low dose STZ-induced diabetic mice. RESULTS: (d-Arg35)-sea lamprey PYY (1-36) was fully resistant to plasma enzymatic degradation. The peptide possessed similar significant insulinostatic, as well as positive anti-apoptotic biological actions, as the parent peptide. Sea lamprey PYY (1-36) and (d-Arg35)-sea lamprey PYY (1-36) delayed diabetes progression in STZ mice. Both treatment interventions induced a significant decrease in body weight, food and fluid intake as well as glucose and glucagon concentrations. In addition, glucose tolerance, plasma and pancreatic insulin were partially normalised. (d-Arg35)-sea lamprey PYY (1-36) was significantly more effective than sea lamprey PYY (1-36) in terms of enhancing glucose-stimulate insulin release. Both treatments improved pancreatic islet morphology, linked to decreased apoptosis of beta-cells. CONCLUSION: We present (d-Arg35)-sea lamprey PYY (1-36) as the first-in-class N- and C-terminally stable PYY (1-36) peptide analogue. GENERAL SIGNIFICANCE: Enzymatically stable, long-acting PYY (1-36) peptides highlight the therapeutic benefits of sustained activation of NPYR1's in diabetes.
Assuntos
Diabetes Mellitus Experimental/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Peptídeos/uso terapêutico , Substâncias Protetoras/uso terapêutico , Receptores de Neuropeptídeo Y/agonistas , Animais , Linhagem Celular , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/prevenção & controle , Proteínas de Peixes/química , Proteínas de Peixes/uso terapêutico , Hipoglicemiantes/química , Insulina/metabolismo , Células Secretoras de Insulina/efeitos dos fármacos , Células Secretoras de Insulina/metabolismo , Masculino , Camundongos , Peptídeos/química , Petromyzon , Substâncias Protetoras/química , Receptores de Neuropeptídeo Y/metabolismo
13.
Molecules ; 25(5)2020 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-32106572
RESUMO
Alcoholic liver disease (ALD) threatens human health, so it is imperative that we find ways to prevent or treat it. In recent years, the study of polysaccharides has shown that they have different kinds of bioactivities. Among them are many biological effects that have been attributed to polysaccharide precursors. D-Isofloridoside (DIF) is one of the polysaccharide precursors from the marine red alga Laurencia undulata. This study evaluated the effect of DIF on alcohol-induced oxidative stress in human hepatoma cells (HepG2). As a result, DIF attenuated alcohol-induced cytotoxicity, reduced the amount of intracellular reactive oxygen species (ROS), and effectively reduced alcohol-induced DNA damage in HepG2 cells. In addition, a western blot showed that, after DIF treatment, the expression levels of glutathione (GSH), superoxide dismutase (SOD), and B-cell lymphoma-2 (bcl-2) increased, while the expression levels of γ-glutamyl transferase (GGT), BCL2-associated X (bax), cleaved caspase-3, and mitogen-activated protein kinase (p38 and c-Jun N-terminal kinase ) signal transduction proteins reduced. This showed that DIF may protect cells by reducing the amount of intracellular ROS and inhibiting intracellular oxidative stress and apoptotic processes. Finally, molecular docking demonstrated that DIF can bind to SOD, GGT, B-cell lymphoma-2, and bax proteins. These results indicated that DIF can protect HepG2 cells from alcohol-induced oxidative stress damage, making it an effective potential ingredient in functional foods.
Assuntos
Galactosídeos/farmacologia , Laurencia/química , Hepatopatias Alcoólicas/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Antioxidantes/química , Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Etanol/toxicidade , Galactosídeos/química , Regulação da Expressão Gênica/efeitos dos fármacos , Glutationa/genética , Células Hep G2 , Humanos , Hepatopatias Alcoólicas/patologia , Simulação de Acoplamento Molecular , Polissacarídeos/química , Polissacarídeos/farmacologia , Substâncias Protetoras/química , Substâncias Protetoras/farmacologia , Espécies Reativas de Oxigênio/química
14.
Molecules ; 25(5)2020 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-32106575
RESUMO
Anaphylactoid shock is a fatal hypersensitivity response caused by non-IgE mediated mast cell activation. These reactions are mediated by a family of G protein-coupled receptors (GPCRs) known as Mas related GPCRX2 (MRGPRX2). Several US FDA approved drugs which are used in day to day life have been reported to cause anaphylactoid shock. Surprisingly, no therapeutic drugs are available which can directly target MRGPRX2 for treatment of anaphylactoid shock. Genistein is a non-steroidal polyphenol known for its diverse physiological and pharmacological activities. In recent studies, Genistein has been reported for its anti-inflammatory activity on mast cells. However, the effects and mechanistic pathways of Genistein on anaphylactoid reaction remain unknown. In the present study, we designed a battery of in-vitro, in-silico and in-vivo experiments to evaluate the anti-anaphylactoid activity of Genistein in order to understand the possible molecular mechanisms of its action. The in-vitro results demonstrated the inhibitory activity of Genistein on MRGPRX2 activation. Further, a mouse model of anaphylactoid shock was used to evaluate the inhibitory activity of Genistein on blood vessel leakage and hind paw edema. Taken together, our findings have demonstrated a therapeutic potential of Genistein as a lead compound in the treatment of anaphylactoid shock via MRGPRX2.
Assuntos
Anafilaxia/tratamento farmacológico , Genisteína/farmacologia , Proteínas do Tecido Nervoso/antagonistas & inibidores , Substâncias Protetoras/farmacologia , Receptores Acoplados a Proteínas-G/antagonistas & inibidores , Receptores de Neuropeptídeos/antagonistas & inibidores , Anafilaxia/induzido quimicamente , Anafilaxia/genética , Anafilaxia/patologia , Animais , Degranulação Celular/efeitos dos fármacos , Modelos Animais de Doenças , Hipersensibilidade a Drogas/tratamento farmacológico , Hipersensibilidade a Drogas/genética , Genisteína/química , Humanos , Mastócitos/efeitos dos fármacos , Mastócitos/metabolismo , Mastócitos/patologia , Camundongos , Camundongos Knockout , Proteínas do Tecido Nervoso/genética , Substâncias Protetoras/química , Receptores Acoplados a Proteínas-G/genética , Receptores de Neuropeptídeos/genética , p-Metoxi-N-metilfenetilamina/toxicidade
15.
Chem Pharm Bull (Tokyo) ; 68(1): 46-57, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31902901
RESUMO
Over the past decade, a number of new 1,4-naphthoquinones have been isolated from natural sources and new 1,4-naphthoquinones with diverse structural features have been synthesized. Cardioprotective, anti-ischemic, hepatoprotective, neuroprotective and some other new properties were found for these compounds; their role in protecting against neurodegenerative diseases has been established. Their anti-inflammatory, antimicrobial and antitumor activities have been studied in more detail; new, previously unknown intracellular molecular targets and mechanisms of action have been discovered. Some compounds of this class are already being used as a medicinal drugs and some substances can be used as biochemical tools and probes for non-invasive detection of pathological areas in cells and tissues in myocardial infarction and neurodegenerative diseases using modern molecular imaging techniques.
Assuntos
Anti-Infecciosos/química , Anti-Inflamatórios/química , Naftoquinonas/química , Substâncias Protetoras/química , Anti-Infecciosos/farmacologia , Anti-Inflamatórios/farmacologia , Bactérias/efeitos dos fármacos , Citocinas/metabolismo , Humanos , Leucócitos Mononucleares/citologia , Leucócitos Mononucleares/efeitos dos fármacos , Leucócitos Mononucleares/metabolismo , Naftoquinonas/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Substâncias Protetoras/farmacologia , Trypanosoma/efeitos dos fármacos
16.
PLoS One ; 15(1): e0227308, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31910239
RESUMO
Seaweed polyphenols and polysaccharide plays a broad range of biological activity. The objective of the present study was to study and compare the skin protection activity of fucoidan rich polysaccharide extract (SPS) and polyphenol-rich extract (SPP) from the seaweed Sargassum vachellianum. The skin protection activity was analyzed based on their ability to scavenge free radicals such as hydrogen peroxide and hydroxyl radicals, UV absorption potential, tyrosinase inhibition, moisture preservation, and antibacterial activity. From the results, both SPP and SPS protects the skin from UV damage. SPP showed good free radical scavenging ability, antimicrobial activity against E.coli and S. aureus and effectively absorbed the UVB and UVA rays whereas SPS hardly absorbs the UVA and UVB rays and showed weak free radical scavenging ability and no antimicrobial activity. SPS showed considerable inhibition on tyrosinase (51.21%) and had better moisture absorption (52.1%) and retention (63.24%) abilities than SPP. The results specified that both SPS and SPP have balancing potential on skin protection and suitable combinations of both could act as an active ingredient in cosmetics.
Assuntos
Polifenóis/farmacologia , Polissacarídeos/farmacologia , Sargassum/química , Alga Marinha/química , Pele/efeitos dos fármacos , Anti-Infecciosos/química , Anti-Infecciosos/farmacologia , Antioxidantes/química , Antioxidantes/farmacologia , Escherichia coli/efeitos dos fármacos , Depuradores de Radicais Livres/toxicidade , Radicais Livres/toxicidade , Humanos , Peróxido de Hidrogênio/toxicidade , Radical Hidroxila/toxicidade , Monofenol Mono-Oxigenase/antagonistas & inibidores , Monofenol Mono-Oxigenase/metabolismo , Polifenóis/química , Polissacarídeos/química , Substâncias Protetoras/química , Substâncias Protetoras/farmacologia , Pele/patologia , Pele/efeitos da radiação , Espectroscopia de Infravermelho com Transformada de Fourier , Staphylococcus aureus/efeitos dos fármacos , Raios Ultravioleta/efeitos adversos
17.
Sci Rep ; 10(1): 195, 2020 01 13.
Artigo em Inglês | MEDLINE | ID: mdl-31932603
RESUMO
We recently reported that a butanol soluble fraction from the stem of Cassia occidentalis (CSE-Bu) consisting of osteogenic compounds mitigated methylprednisone (MP)-induced osteopenia in rats, albeit failed to afford complete protection thus leaving a substantial scope for further improvement. To this aim, we prepared an oral formulation that was a lipid-based self-nano emulsifying drug delivery system (CSE-BuF). The globule size of CSE-BuF was in the range of 100-180 nm of diluted emulsion and the zeta potential was -28 mV. CSE-BuF enhanced the circulating levels of five osteogenic compounds compared to CSE-Bu. CSE-BuF (50 mg/kg) promoted bone regeneration at the osteotomy site and completely prevented MP-induced loss of bone mass and strength by concomitant osteogenic and anti-resorptive mechanisms. The MP-induced downregulations of miR29a (the positive regulator of the osteoblast transcription factor, Runx2) and miR17 and miR20a (the negative regulators of the osteoclastogenic cytokine RANKL) in bone was prevented by CSE-BuF. In addition, CSE-BuF protected rats from the MP-induced sarcopenia and/or muscle atrophy by downregulating the skeletal muscle atrogenes, adverse changes in body weight and composition. CSE-BuF did not impact the anti-inflammatory effect of MP. Our preclinical study established CSE-BuF as a prophylactic agent against MP-induced osteopenia and muscle atrophy.
Assuntos
Doenças Ósseas Metabólicas/tratamento farmacológico , Sistemas de Liberação de Medicamentos , Glucocorticoides/toxicidade , Atrofia Muscular/tratamento farmacológico , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Senna (Planta)/química , Animais , Doenças Ósseas Metabólicas/induzido quimicamente , Doenças Ósseas Metabólicas/patologia , Butanóis/química , Emulsões , Masculino , Atrofia Muscular/induzido quimicamente , Atrofia Muscular/patologia , Fitoterapia , Extratos Vegetais/química , Caules de Planta/química , Substâncias Protetoras/química , Ratos , Ratos Sprague-Dawley
18.
Food Chem ; 314: 126166, 2020 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-31972406
RESUMO
The occurrence of the quercetin oxidation metabolite 2-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofuranone (BZF), whose antioxidant potency is notably higher than the antioxidant potency of quercetin, was investigated in twenty quercetin-rich plant foods. BZF was identified (HPLC-DAD-ESI-MS/MS) only in the dry outer scales of onions and shallots. Aqueous extracts of onions (OAE) and shallots (SAE) were evaluated for their antioxidant and cytoprotective properties. OAE, whose potency did not differ from SAE, protected ROS-exposed Caco2 cells against oxidative (78%) and cellular (90%) damage at a 3 µg/L concentration (corresponding to 0.03 nM of BZF). After chromatographic resolution of OAE, the BZF peak accounted fully and exclusively for its antioxidant effect. The antioxidant effects of OAE and of a pure BZF were described by two perfectly overlapping curves whose concentration-dependence was within the 3 × 10-4 to 102 nM BZF range. Such unprecedented low concentrations place BZF-containing plants on the frontier of the search for novel sources of antioxidants.
Assuntos
Antioxidantes/farmacologia , Benzofuranos/análise , Benzofuranos/farmacologia , Cebolas/química , Quercetina/metabolismo , Antioxidantes/química , Benzofuranos/metabolismo , Células CACO-2 , Cromatografia Líquida de Alta Pressão , Relação Dose-Resposta a Droga , Frutas/química , Humanos , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/química , Extratos Vegetais/farmacologia , Substâncias Protetoras/química , Substâncias Protetoras/farmacologia , Espectrometria de Massas em Tandem , Verduras/química
19.
Biomed Chromatogr ; 34(4): e4795, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31967660
RESUMO
In this study, we focused on studying the changes in urine metabolites in hyperlipidemic rats using ultra-performance liquid chromatography coupled with quadrupole time-of-fight mass spectrometry (UPLC-Q-TOF/MS) and metabolomics, as well as the effect of Citri Reticulatae Chachiensis Pericarpium (CRCP) on hyperlipidemia. These urine samples were examined by UPLC-Q-TOF/MS to obtain MS data. The MS data were analyzed by principal component analysis and partial least squares-discriminant analysis to identify the differential metabolites. CRCP reduced the body weight and levels of triglycerides, total cholesterol and low-density lipoprotein cholesterol and abnormally decreased high-density lipoprotein cholesterol in hyperlipidemic rats, which were significantly raised by a high-fat diet. Twenty-seven potential biomarkers were identified within the complex sample matrix of urine. Fourteen biomarkers increased in the hyperlipidemia rats compared with normal rats. Meanwhile, 13 biomarkers decreased. CRCP reversed abnormal changes in biomarkers, including 5-l-glutamyl-taurine, 5-aminopentanoic acid, cis-4-octenedioic acid and 2-octenedioic acid. These biomarkers show that hyperlipidemia is related to the metabolic pathways of taurine and hypotaurine metabolism, fatty acid biosynthesis, and arginine and proline metabolism. CRCP mainly prevents hyperlipidemia by intervening in these metabolic pathways.
Assuntos
Citrus/química , Dieta Hiperlipídica , Metaboloma/efeitos dos fármacos , Preparações de Plantas , Substâncias Protetoras , Animais , Biomarcadores/urina , Frutas/química , Masculino , Metabolômica , Preparações de Plantas/química , Preparações de Plantas/farmacologia , Substâncias Protetoras/química , Substâncias Protetoras/farmacologia , Ratos , Ratos Sprague-Dawley , Reprodutibilidade dos Testes
20.
Carbohydr Polym ; 230: 115567, 2020 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-31887913
RESUMO
Sulfated oligosaccharide of Gracilaria lemaneiformis (GLSO) was prepared from sulfated polysaccharides which possessed antiallergic activity by degradation with high temperature and pressure combined with vitamin C treatment. The present study demonstrated that GLSO could attenuate food anaphylaxis, and inhibit the production of immunoglobulin E, histamine, and related cytokines in both prevention and therapy ovalbumin-induced mice model. Additionally, the gut microbiota analysis revealed that GLSO markedly rescued OVA-induced changes in the Firmicutes to Bacteroidetes ratio. Following flow cytometry, GLSO was found to suppress the subpopulation of T helper 2 and B cells, and significantly up-regulate regulatory T cells (Tregs) differentiation. Furthermore, GLSO-mediated immunosuppression could be verified by co-culturing Tregs sorted from GLSO-treated mice and CD4+ T cells or mast cells. In a word, GLSO attenuated food anaphylaxis through the regulation of gut microbiota and induction of immunosuppression. GLSO had the potential to be used as a nutrient component against food allergy.
Assuntos
Antialérgicos/farmacologia , Hipersensibilidade Alimentar/tratamento farmacológico , Gracilaria/química , Oligossacarídeos/farmacologia , Substâncias Protetoras/farmacologia , Animais , Antialérgicos/química , Citocinas/metabolismo , Modelos Animais de Doenças , Hipersensibilidade Alimentar/imunologia , Hipersensibilidade Alimentar/prevenção & controle , Humanos , Imunossupressão , Mastócitos/efeitos dos fármacos , Camundongos , Oligossacarídeos/química , Oligossacarídeos/imunologia , Substâncias Protetoras/química , Sulfatos/química , Linfócitos T Reguladores/efeitos dos fármacos , Linfócitos T Reguladores/imunologia , Células Th2/efeitos dos fármacos , Células Th2/imunologia
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-3,186,597,911,763,113,500 | TY - JOUR AU - Rodríguez Velásquez, Javier Oswaldo AU - Cuesta Rivas, Joao AU - Correa Herrera, Sandra Catalina PY - 2022/08/24 Y2 - 2023/10/02 TI - Predictive methodology of the dynamics of the number of COVID-19 cases: application to China, Belgium, and South Korea JF - Revista Médica de Risaralda JA - Rev. Médica Risaralda VL - 28 IS - 1 SE - Artículo original DO - 10.22517/25395203.24932 UR - https://revistas.utp.edu.co/index.php/revistamedica/article/view/24932 SP - AB - <p><strong>Objectives:</strong> Multiple methodologies based on probability theory have been developed to establish predictions of dengue, malaria, HIV, obesity epidemics, among others. This research aimed to develop a new method for predicting the dynamics of the number of COVID-19 cases for China, Belgium, and South Korea based on the probability theory that allows the evaluation and comparison of their increment.</p><p><strong>Material and methods</strong>: Probability ranges of the number of COVID-19 cases were established, which were assigned to each of the daily number of COVID-19 cases reported by China, Belgium, and South Korea that were evaluated during 74, 50, and 50 days respectively. The frequency and probability of each daily range for each country was calculated. Their total probability and the probability of the dynamics in intervals of 8 consecutive days were calculated, and the values between countries were compared to evaluate their differences.</p><p><strong>Results</strong>: Probability values of 1.21E-30, 2.03E-22, and 3.15E-12 were established for China, Belgium, and South Korea, which allows the quantitative differentiation of the characteristics of their dynamics. The probability differences of the 8-day subspaces ranged from 0.003 to 1, allowing the temporal changes in the dynamics to be evaluated.</p><p><strong>Conclusion:</strong> The ranges established for the evaluation of the number of COVID-19 cases allow to differentiate the behavior of epidemics between countries and to stratify the severity of expansion. Highlighting an underlying mathematical order for this phenomenon permitted quantitatively predict its spatiotemporal dynamic and indirectly, the efficacy of public health politics implemented for each country.</p> ER - | {
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8,305,727,585,348,174,000 | Erythema infectiosum
Introduction
Slapped cheek syndrome (also called fifth disease or parvovirus B19) is a viral infection that's most common in children, although it can affect people of any age. It usually causes a bright red rash on the cheeks.
Although the rash can look alarming, slapped cheek syndrome is normally a mild infection that clears up by itself in one to three weeks. Once you've had the infection, you're usually immune to it for life.
However, slapped cheek syndrome can be more serious for some people. If you're pregnant, have a blood disorder or a weakened immune system and have been exposed to the virus, you should get medical advice.
This page covers:
Symptoms
When to get medical advice
What to do if you or your child has it
How you get it
Prevention
Symptoms of slapped cheek syndrome
Symptoms of slapped cheek syndrome usually develop 4-14 days after becoming infected, but sometimes may not appear for up to 21 days.
Initial symptoms
Some people with slapped cheek syndrome won't notice any early symptoms, but most people will have the following symptoms for a few days:
• a slightly high temperature (fever) of around 38C (100.4F)
• a runny nose
• sore throat
• a headache
• an upset stomach
• feeling generally unwell
The infection is most contagious during this initial period.
In adults, these symptoms are often accompanied by joint pain and stiffness, which may continue for several weeks or even months after the other symptoms have passed.
Slapped cheek rash
After a few days, a distinctive bright red rash on both cheeks (the so-called "slapped cheeks") normally appears, although adults may not get this.
By the time this rash develops, the condition is no longer contagious.
After another few days, a light pink rash may also appear on the chest, stomach, arms and thighs. This often has a raised, lace-like appearance and may be itchy.
The rashes will normally fade within a week or two, although occasionally the body rash may come and go for a few weeks after the infection has passed. This can be triggered by exercise, heat, anxiety or stress.
When to get medical advice
You don't usually need to see your GP if you think you or your child has slapped cheek syndrome, as the condition normally gets better on its own.
However, you should contact your GP, call NHS 111 or contact your local out-of-hours service if you have been exposed to anyone with slapped cheek or you have symptoms of the infection and:
In these cases, a blood test may be carried out to see if you're immune to the infection. If you're not immune, you'll be monitored carefully to check for any problems.
If you develop severe anaemia, it's likely that you'll need to be admitted to hospital and have a blood transfusion to replace your damaged blood cells.
What to do if you or your child has slapped cheek
Slapped cheek syndrome is usually mild and should clear up without specific treatment.
If you or your child is feeling unwell, you can try the following to ease the symptoms:
• rest and drink plenty of fluids – babies should continue their normal feeds
• for a fever, headaches or joint pain, you can take painkillers, such as paracetamol or ibuprofen – children under 16 shouldn't take aspirin
• to reduce itchiness, you can take antihistamines or use an emollient (moisturising lotion) – some antihistamines are not suitable for young children, so check with your pharmacist first
Unless you or your child is feeling unwell, there’s no need to stay away from school or work once the rash has developed, as the infection is no longer contagious by this point.
It's a good idea to notify your child's school about the infection, so children who develop early symptoms can be spotted quickly and vulnerable people can be made aware that they may need to get medical advice.
How do you get slapped cheek syndrome?
Slapped cheek syndrome is caused by a virus called parvovirus B19. This is found in the droplets in the coughs and sneezes of someone with the infection.
The virus is spread in a similar way to colds and flu. You can become infected by:
• inhaling droplets that are sneezed or coughed out by someone with the infection
• touching a contaminated surface or object and then touching your mouth or nose
Someone with slapped cheek syndrome is infectious during the period before the rash develops. Once the rash appears, the condition can no longer be passed on.
Preventing slapped cheek syndrome
It's very difficult to prevent slapped cheek syndrome, because people who have the infection are most contagious before they develop any obvious symptoms.
However, making sure that everyone in your household washes their hands frequently may help stop the infection from spreading.
There's currently no vaccine available to protect you against the condition.
020 8560 8971
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} | 6e3c8d3593f3f69280bb5502b214ab8e |
8,521,498,058,998,594,000 | Bodybuilding Advice That Will Help You Fill Out Your Clothes
by admin4
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Is building muscle your main aim? There are a lot of things that will help you achieve bigger muscles, and limit wastefulness in your workout efforts. If you want to be bigger and stronger, then this article can help you to attain those goals. Start using these tips to avoid wasting gym time.
Focus your weight-training regimen on squats, deadlifts, and bench presses. There is a good reason these exercises are thought of as the cornerstone of good bodybuilding. They have been proven over time to build up strength, increase your bulk and improve conditioning overall. Try to fit some form of these exercises into your workout.
Beginning your workout with warm-up exercises is crucial. Including ten or fifteen minute warm-ups can increase your blood flow and prepare your muscles for intense workouts. You’ll avoid injuries which could send you to the locker room.
If you’re just starting out with weight training, think about joining a gym. Your gym is likely to have a large variety of modern equipment, and they’ll have professionals available to help you learn how to use them correctly. You will have the chance to ask questions as needed.
Ask a local health food store about a protein powder which is all natural to help you supplement your diet. When mass-building muscle, your body needs more protein than when you are just exercising. Consuming the protein in shake or smoothie form can be quick and easy.
Keep a record of body fat while working to build muscles. Simply tracking your weight is not accurate since you may be gaining weight and muscle, but still losing fat. It is very easy to become discouraged when viewing your weight, but you should understand that your weight isn’t a good indicator of the amount of muscle you have.
Try learning your limits, but don’t stop exercising until you use everything at your disposal. Push yourself during each set until you are literally physically unable to complete another rep. If you start getting tired, shorten the lengths of the sets.
Always do compound exercises so you can have the most muscle growth possible. These moves incorporate many muscle groups at once, so they are efficient and effective. One example is the bench press, that works your chest, triceps and shoulders, all in one exercise.
If you want to increase your muscle mass, be sure to eat a diet rich in fresh fruit and whole grain foods. Avoid pre-packaged foods that come in boxes, which often contain chemicals, preservatives, and fillers that can hinder your body’s ability to heal itself. Healthy foods improve the strength and endurance of both your body and your immune system.
Do squats the smart way. Place your bar closer to the middle of your traps. By doing this, you place more load on the muscles of the lower body, including the thighs, buttocks and hips. Using these muscles will allow you to lift more weight.
A fantastic way to build motivation when you go to the gym is to workout with your friends. You and your friends can encourage each other, which will make it easier to push yourself harder during your workouts. This, in turn, will improve muscle growth.
Incorporate plyometric exercises into your muscle-building routine. This type of exercise develops the fast twitch fibers of your muscle, which stimulates muscle growth. Plyometrics are like ballistic moves because they require acceleration. For example, plyometric push-ups require you to propel your hands off the floor, pushing your body into the air.
Weight Machines
You want to mix up your routine to incorporate machine and free weights for the benefits each offers. Free weights are generally better for serious bodybuilding. On the other hand, beginners may prefer the safety of the weight machines. If you’re a rookie at muscle development, make sure that you use both in order to ensure that you don’t always use just weight machines.
Make sure that your form is good. If you are picking up weights without any type of form, you aren’t helping yourself and may suffer an injury. If you are adding a new lift to your routine, then practice it by the gym mirror until you are comfortable correcting your posture on your own.
Do not rely just on supplements. Supplements can help with many bodybuilding routines. However, they are not intended as a substitute for good nutrition. As their name states, they supplement a proper diet. It is recommended that supplements should be kept to a minimum.
The article you have just read provided you with ideas which can help you to attain your goals in short order. The tips offered here have provided you with a great place to start, as you work toward reaching your fitness goals. Apply this information today and start building up your muscles the way you want.
There are a number of ways exercising your muscles can improve your life, whether or not you have an interest in bulking up. It can increase strength in your body, lungs, joints and even self-esteem.
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-3,760,793,796,137,093,000 | Assessment of Stability and Discrimination Capacity of Radiomic Features on Apparent Diffusion Coefficient Images
Marco Bologna, Valentina D A Corino, Eros Montin, Antonella Messina, Giuseppina Calareso, Francesca G Greco, Silvana Sdao, Luca T Mainardi
Research output: Contribution to journalArticle
Abstract
The objectives of the study are to develop a new way to assess stability and discrimination capacity of radiomic features without the need of test-retest or multiple delineations and to use information obtained to perform a preliminary feature selection. Apparent diffusion coefficient (ADC) maps were computed from diffusion-weighted magnetic resonance images (DW-MRI) of two groups of patients: 18 with soft tissue sarcomas (STS) and 18 with oropharyngeal cancers (OPC). Sixty-nine radiomic features were computed, using three different histogram discretizations (16, 32, and 64 bins). Geometrical transformations (translations) of increasing entity were applied to the regions of interest (ROIs), and the intra-class correlation coefficient (ICC) was used to compare the features computed on the original and modified ROIs. The distribution of ICC values for minimal and maximal entity translations (ICC10 and ICC100, respectively) was used to adjust thresholds of ICC (ICCmin and ICCmax) used to discriminate between good, unstable (ICC10 < ICCmin), and non-discriminative features (ICC100 > ICCmax). Fifty-four and 59 radiomic features passed the stability-based selection for all the three histogram discretizations for the OPC and STS datasets, respectively. The excluded features were similar across the different histogram discretizations (Jaccard's index 0.77 ± 0.13 and 0.9 ± 0.1 for OPC and STS, respectively) but different between datasets (Jaccard's index 0.19 ± 0.02). The results suggest that the observed radiomic features are mainly stable and discriminative, but the stability depends on the region of the body under observation. The method provides a way to assess stability without the need of test-retest or multiple delineations.
Original languageEnglish
Pages (from-to)879-894
Number of pages16
JournalJournal of Digital Imaging
Volume31
Issue number6
DOIs
Publication statusPublished - Dec 2018
Fingerprint Dive into the research topics of 'Assessment of Stability and Discrimination Capacity of Radiomic Features on Apparent Diffusion Coefficient Images'. Together they form a unique fingerprint.
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-4,484,616,340,612,667,400 | RT Journal Article SR Electronic T1 Breathing Inhibited When Seizures Spread to the Amygdala and upon Amygdala Stimulation JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 10281 OP 10289 DO 10.1523/JNEUROSCI.0888-15.2015 VO 35 IS 28 A1 Brian J. Dlouhy A1 Brian K. Gehlbach A1 Collin J. Kreple A1 Hiroto Kawasaki A1 Hiroyuki Oya A1 Colin Buzza A1 Mark A. Granner A1 Michael J. Welsh A1 Matthew A. Howard A1 John A. Wemmie A1 George B. Richerson YR 2015 UL http://www.jneurosci.org/content/35/28/10281.abstract AB Sudden unexpected death in epilepsy (SUDEP) is increasingly recognized as a common and devastating problem. Because impaired breathing is thought to play a critical role in these deaths, we sought to identify forebrain sites underlying seizure-evoked hypoventilation in humans. We took advantage of an extraordinary clinical opportunity to study a research participant with medically intractable epilepsy who had extensive bilateral frontotemporal electrode coverage while breathing was monitored during seizures recorded by intracranial electrodes and mapped by high-resolution brain imaging. We found that central apnea and O2 desaturation occurred when seizures spread to the amygdala. In the same patient, localized electrical stimulation of the amygdala reproduced the apnea and O2 desaturation. Similar effects of amygdala stimulation were observed in two additional subjects, including one without a seizure disorder. The participants were completely unaware of the apnea evoked by stimulation and expressed no dyspnea, despite being awake and vigilant. In contrast, voluntary breath holding of similar duration caused severe dyspnea. These findings suggest a functional connection between the amygdala and medullary respiratory network in humans. Moreover, they suggest that seizure spread to the amygdala may cause loss of spontaneous breathing of which patients are unaware, and thus has potential to contribute to SUDEP.SIGNIFICANCE STATEMENT Sudden unexpected death in epilepsy (SUDEP) is the most common cause of death in patients with chronic refractory epilepsy. Impaired breathing during and after seizures is common and suspected to play a role in SUDEP. Understanding the cause of this peri-ictal hypoventilation may lead to preventative strategies. In epilepsy patients, we found that seizure invasion of the amygdala co-occurred with apnea and oxygen desaturation, and electrical stimulation of the amygdala reproduced these respiratory findings. Strikingly, the subjects were unaware of the apnea. These findings indicate a functional connection between the amygdala and brainstem respiratory network in humans and suggest that amygdala seizures may cause loss of spontaneous breathing of which patients are unaware—a combination that could be deadly. | {
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-3,277,318,441,363,159,600 | Managing Cancer Patients at Home
0
1309
views
cancer patient
Each patient has a plan to control and manage their pain. However, this plan should not only work for you but also your family. When people complain of distress, it usually means that they are either feeling the pain or feeling anxious due to their condition. Some may even find it hard to talk about their discomfort. However, treatment is only possible if you discuss your issues with your family and the medical team.
In this article, we will share some important tips to manage pain for cancer patients at home. Use the following tips to help your loved ones get through the most challenging and painful phase of their lives.
Tips to control pain
When someone you love is writhing in pain, you can help them alleviate their condition by providing them oral medication. Pain medicines work best if they are taken as per their schedule as instructed by their physician. You will want to treat pain as soon as it starts and follow a regular routine after that. You can also look for alternative methods to treat the pain such as homeopathy or natural treatments that can eventually do away the need for medications at all.
Improving quality of life
It is common for cancer patients to feel lethargic and exhausted due to cancer pain that often leaves them fatigued. Even though there is no way to fully eliminate the cancer pain, it can be made less severe and allow the patients to do more activities, living their lives normally. If your family members are involved in your care during cancer treatment, then you would be able to live a normal life to an extent and also make your pain less severe.
You and your family should also know how to deal with breakthrough pain that often creeps up between your doses. According to a Cancer Specialist in Mumbai, you can safely take pain medicines or homeopathy remedies in addition to your regular medicines to control the pain. However, always tell your doctors and people who are involved in your care about your situation so that your doses can be adjusted as per your needs.
Keep an eye out for these symptoms
• Recurring pain that subsides with medication but returns when your next medicine is due. This may indicate that your medication plan needs to be changed.
• If you find it hard to sleep
• Not feeling active or experience a lack of interest in things you usually enjoyed
• New areas where pain is experiences
• Inability to move around or do things
Things Cancer Patients Can Do
• Discuss with your cancer team: Tell them how the pain starts and how long it lasts. You should articulate how it makes you feel and how it is affecting your life.
• Inform the cancer team about pain medicine effectiveness: if you feel that your pain medicine is not as effective as it should be, then inform your cancer care team.
• Use a pain scale to rate the pain: Use a scale of 1-10 to express the pain you feel.
• Increase activity level gradually: Take your medication exactly as prescribed and once pain is relieved, you can gradually increase your level of activity.
• Don’t allow pain to get severe: Always take your medicine on time and don’t wait for the pain to increase. Don’t start or stop a medicine suddenly. Ask your cancer care team to do this.
Tips for Family Members
• Look for Signs of Pain: Family members should keep an eye out for pain signals and immediately administer pain medicine if patient is unable to move.
• Give them a warm bath: You can either give them warm baths or cool ice packs to help them relax. Also consider giving a gentle massage or pressure to relieve some kinds of pain.
• Look for signs of dizziness: This is especially important when you start a new medicine or change the dose. Help patients walk until they are confident they can do it on their own.
Caring for cancer patients requires immense amount of watchfulness. These tips will help you stay prepared in case of an adversity. | {
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-5,553,266,434,717,958,000 | In today’s world, whitening of teeth is a prevailing restorative procedure that is non-invasive and produces beautiful very attractive white teeth. When we begin to advance in age, it is logical for our teeth to darken and it is caused when the mineral structures in our teeth starts changing. Darkening of teeth also occurs from smoking, as well as f foods or liquids that have strong colors can have an effect on the total color of our teeth. Teeth may also darken as a result of some drugs.
Laser teeth whitening (power whitening) is one of the best and common way of solving the problem of discolored teeth. It is the use of light, combined with the peroxide bleaching gel to boost the speed and power of tooth whitening. It is a renowned procedure of teeth whitening because it is safe and it won’t cause damage to the patient’s gums or the structure of the tooth. It is now seen as the most effective whitening treatments. It leaves your teeth evidently whiter, sometimes more than 6 shades whiter.
Procedure of Laser Teeth Whitening
The procedure starts with removing of plaque and germs that have great effect in the teeth whitening process. Then, placing a rubber dam inside the mouth of the patient for the protection of the gum. After that, a bleaching gel is applied on the teeth. Then, a laser light is positioned over the teeth and activated which causes the whitening gel to turn to oxygen allowing it to penetrate the teeth discoloration. It takes about one hour and produces an ultra-fast whitening result.
Laser teeth whitening has been known to have a lot of advantages which includes:
1. Aesthetic appeal -laser teeth whitening is now being used to enhance beauty.
2. Safe and painless: It is painless and it’s the safest way of teeth whitening. It doesn’t cause any discomfort so anesthesia is not in consideration.
3. It is more convenient because the dentist does everything for you.
4. Unlike some teeth whitening methods, where have to wait for weeks and even months to see dramatic results, u get instant result.
5. Many clinics offer laser whitening making it accessible in every community.
Laser teeth whitening however some bit of setbacks which come in form of these has:
1. It is more expensive than most whitening treatments. The cost will be a major issue for the treatment.
2. Tooth sensitivity: Some patients may experience teeth sensitivity after the treatment but this is just temporary.
Laser teeth whitening is the most effective way if teeth whitening procedure but it is not recommended for everyone. It is not recommended for people who have receding gums, pregnant women, patients with sensitive teeth, patients below 16 years. It is also good to know that sometimes the teeth appear whiter than expected.
After the laser teeth whitening, the stains might resurface and could require another process of laser whitening. This leads to further expenses. You should also know that the term laser tooth whitening is a misnomer because no laser is used.
Getting A Wisdom Tooth Surgery in Singapore
Wisdom teeth are the third and final set of molars that most people get in their late teens or early twenties. Our mouth goes through many changes and the appearance of third molar i.e. wisdom tooth is a major landmark that usually takes place between the ages of 17...
Understanding Cosmetic Dentistry – Braces, Invisalign, Teeth Whitening & More
Some people still believe dentistry is just a case of filling and taking out teeth. In our society today, many people turn to cosmetic dentistry or aesthetic dentistry as a way of improving their appearance. Cosmetic dentistry is dentistry aimed at creating a positive...
Best Teeth Whitening Techniques
Tooth whitening also known as tooth bleaching when utilizing bleach is either the restoration of a natural tooth shade or whitening beyond the natural shade. Now there are various ways an individual can go about this and whiten his teeth to feel better about himself...
Laser Teeth Whitening Explained
In today’s world, whitening of teeth is a prevailing restorative procedure that is non-invasive and produces beautiful very attractive white teeth. When we begin to advance in age, it is logical for our teeth to darken and it is caused when the mineral structures in...
Getting a Tooth Extraction? Here’s What You Need To Know
Tooth extraction is the removal of a tooth from its socket in the bone. If a tooth has been broken or damaged by decay, a dentist will try to fix it with a filling, crown or other treatment. However, sometimes, there's too much damage for the tooth to be repaired. In...
Dental Pain Management
General medical practitioners are quickly called upon to manage acute dental pain in emergency situations, for example, domestically or in the rural areas, where it may not be possible for a dentist to provide immediate treatment. Common acute oral problems are...
Looking For The Cure To Dental Phobia?
Dental phobia can also be termed dental fear or odontophobia, dentophobia and dental anxiety. Dental phobia is the fear of dentistry and of receiving dental care. However a distinction has been made between dental anxiety, dental fear, and dental phobia. Dental...
Different Types Of Tooth Replacements Available.
In the past, it may not have mattered if people lost their teeth, especially those in the front. Never the less, attempts were made in the past to replace missing teeth, and archeological evidence suggests that indeed people in antiquity did wear “artificial” teeth,...
Getting Treatment for Your Smile
Smile treatment is a treatment for shorter teeth which may include reshaping and lengthening the two front central teeth with composite bonding or porcelain veneers. If you have a gummy smile, your cosmetic dentist may provide treatment to modify the gum line and...
Scaling And Polishing Of Teeth In Singapore
Even after regular brushing and flossing, there could still be the accumulation of tartar, plaque, and biofilm from both the tooth surface and underneath the gum line. Also, Tobacco, caffeine, wine and other such foods tend to stain teeth over time, and the counter...
Make an Appointment Today!
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5,546,623,446,016,190,000 | (37h) Adhesion and Translocation of Nanoparticles through Lipid Bilayers Studied By Mesoscale Simulations
Authors:
Burgess, S., Rutgers, The State University of New Jersey
Neimark, A. V., Rutgers, The State University of New Jersey
Vishnyakov, A., Rutgers, The State University of New Jersey
Understanding of the mechanisms of nanoparticle (NP) adhesion to lipid bilayer (LB) membranes, which constitute the foundation of cell membranes, is of paramount importance for the design of biomedical nanotechnologies, as well as for evaluating health threats related to nanoparticle manufacturing. NPs are employed as intracellular delivery vehicles for controlled release of genes and membrane impermeable chemicals. This process involves internalization, or intake of a drug containing NP, where the NP is first engulfed by the cell membrane, then transferred through the membrane into the cell. Since the NP adhesion is governed by multiple factors (NP size and shape, surface modification, hydrophobicity and charge) that cannot be easily varied in the experiments, the use of in silico modeling helps guide the experiments and optimize NP structure and surface properties. Despite the tremendous progress made recently in molecular simulations of biological systems, modeling of NP-lipid interactions is still difficult due to a complex interplay of distinct characteristic scales: LB thickness of ~5 nm, to NP size of 10-100 nm, to cell size of 5- 50 mm. Also, the dynamic processes of membrane rupture and NP trans-membrane transport involve metastable states and irreversible transformations, modeling of which requires non-trivial calculations of free energies and nucleation barriers.
The current study investigates the mechanisms of nanoparticle adhesion to and penetration through LB membranes. For this purpose, we construct a soft-core coarse-grained models of hydrophobic nanoparticle and 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) bilayer membrane maintained under constant surface tension conditions using a plank, to which a constant force is applied. In a series of dissipative particle dynamics simulations, we consider NP transport across the LB membrane. The free energy landscape of the NP in the bilayer vicinity is explored using the ghost field method that emulates a lab experiment performed with optical tweezers. Hydrophobic particles adsorb a self-assembled monolayer of lipid. As the NP approaches the LB, the latter deforms. The deformation is followed by a spontaneous fusion of the freestanding bilayer and the adsorbed monolayer and particle incorporation inside the hydrophobic inner space of LB. The encapsulation stage where NP is captured by LB corresponds to a free energy minimum. The transition between a free and encapsulated NP is associated with a free energy barrier. The barrier is insignificant when NP is smaller than LB width but increases rapidly with the NP diameter. NP escape from the LB membrane is also associated with deformation of the latter and a free energy penalty. The free energy barrier associated with NP escape decreases with the NP size, that is, shows a tendency opposite to the entry barrier.
This work was supported by NSF grant 1264702 | {
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Abstract
Wellens syndrome is usually diagnosed in asymptomatic patients with normal or only slightly elevated cardiac enzymes. There are two different ECG patterns (Type A and Type B) described in the literature. Earlier studies demonstrated that the appearance of the Wellens pattern had a specificity of 89% and a positive predictive value of 86% for severe stenosis of the left anterior descending artery (LAD) hence a timely recognition and therapeutic approach may prevent fatal outcomes in the patients. Here we are presenting a case of a 69-year-old gentleman with chest pain and Type A Wellens Syndrome pattern on ECG who was found to have LAD stenosis.
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6,328,150,724,545,075,000 | What is double vision?
If you see two of whatever you are looking at, you may have a condition known as double vision, also referred to as diplopia.
What causes double vision?
There are two possible causes of double vision. The first is a failure of both eyes to coordinate together, a condition referred to as “strabismus.” In normal single vision, both eyes can focus on the same object. The images seen by the two eyes are fused into a single picture by the brain. If the eyes do not point at the same object, the images seen by each eye are different and cannot be fused. The result is double vision, which may appear to the patient as blurry images, halos around an object or two distinct objects. The second cause of double vision may be uncorrected refractive error, that is, an object being viewed is split into two images by a defect in the eye’s optical system. Cataracts, uncorrected astigmatism or keratoconus may be the cause.
What are its implications?
Double vision can be extremely confusing. The brain acts to alleviate the visual discomfort by suppressing, or blanking out, one of the images. In young children, if this suppression of the vision persists over a continued length of time, it can lead to an impairment of the development of the visual system. The suppressed eye may get to the point where it is unable to see well, no matter which visual correction or appliance is used. This condition is called amblyopia, or lazy eye. Without immediate and proper intervention at an early age vision may never be restored.
How is it treated?
Treatment of double vision depends on the underlying cause. If the double vision is due to strabismus, it may consist of a program of vision therapy, surgical straightening of the eye or a combination of the two. Therapy is aimed at re-aligning the strabismic eye, where possible, without surgery and re-stimulating the part of the visual pathway to the brain that is not working correctly. If the double vision is due to the presence of cataracts, referral for possible cataract surgery will be undertaken. If it is secondary to astigmatism, corrective lenses will be prescribed to alleviate the double vision. | {
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-8,941,652,134,957,155,000 | Understanding CMC Arthritis and How Occupational Therapy Can Help
Carpometacarpal (CMC) arthritis, commonly known as thumb arthritis, is a condition that affects the base of the thumb, causing pain and limiting hand function. This blog will explore the causes, symptoms, and how occupational therapy can help manage CMC arthritis effectively.
What is CMC Arthritis?
CMC arthritis occurs at the carpometacarpal joint, where the thumb meets the wrist. This joint allows for a wide range of thumb movements that you make every day. In CMC arthritis, the cartilage that cushions the bones in this joint wears away, leading to bone-on-bone contact. This friction is what causes pain and inflammation in the hand.
Causes and Risk Factors
Several factors can contribute to the development of CMC arthritis. As we age, our bodies start to break down from repeated wear and tear. This condition is most common in people over 40 due to the natural repetitive movement of the joint. Genetics can also be a risk factor for those that are predisposed to arthritic conditions.
Like other forms of arthritis, previous injury can lead to CMC arthritis. Trauma or breaks in the joint lead to additional deterioration. And because we use our thumbs so frequently throughout the day, the continuous stress on the thumb joint can contribute to the development of arthritis.
Symptoms
The symptoms of CMC arthritis can vary in severity based on use and time with the condition. Some of the common symptoms include pain at the base of the thumb, swelling and inflammation around the joint, stiffness, weakness and reduced range of motion in the thumb and in severe cases, thumb deformity.
Occupational Therapy
Whether or not you have surgery to treat the condition, occupational therapy plays a crucial role in managing CMC arthritis. Here are some key strategies used in occupational therapy:
• Splinting: Custom splints can provide support to the thumb joint, reduce pain, and prevent further deformity. Splints can be worn during specific activities or continuously, depending on the severity of the condition.
• Heat and Cold Therapy: Applying heat can help relax muscles and improve circulation, while cold packs can reduce inflammation and numb the pain.
• Activity Modification: Teaching patients how to modify their activities to reduce stress on the thumb joint is essential. This includes using adaptive equipment or altering techniques for tasks like opening jars or turning keys. Educating patients on ergonomic principles can also help them set up their workstations and home environments to minimize strain on the thumb.
• Thumb Exercises: Specific exercises can help maintain or improve the strength and flexibility of the thumb. Comprehensive hand therapy programs tailored to individual needs can significantly enhance function and reduce symptoms.
CMC arthritis can be a debilitating condition, but with the right management strategies, individuals can lead fulfilling lives and continue to engage in their desired activities. Occupational therapy focuses on pain relief, joint protection, strengthening, and patient education. If you or someone you know is struggling with thumb arthritis, contact Motus to make a significant difference in managing this condition and improve quality of life.
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-1,130,659,976,881,572,000 | chairs for sciatic problems - Stop Your Sciatica ... Now!
siatica nerve sciatica symptoms sciatica treatment sciatic relief
Stop Your Sciatica ... Now!
Sciatica is back pain that then travels down your leg. I can be a "pain in the butt" to pain in your feet. The biggest fear you probably have is that it will get worse and you may end up needing surgery.
Apply electrical stimulation in the form of a Tens machine or Interferential. Apply ultrasound treatment. Operate on a slipped disk if neurological signs (nerve related symptoms) continue or worsen.
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chairs for sciatic problemsAyurveda is specialized in treating Sciatica with highest treatment success rate. It offers excellent Panchakarma therapies along with internal medicines for treating Sciatica.
Eliminate medical diseases such as Ankylosing Spondylitis.. Treat the cause as well as the symptoms. Prescribe anti-inflammatory medication (e.g. ibuprofen) and rest.
So... To stop your sciatica now you need to address the Piriformis muscle tightness and the lower joint issues. The pelvic imbalance needs correcting but this helps to stop your sciatica returning mainly, although it will also reduce your pain quickly.
Pain is usually relieved by lying down, often on one side. Pain is often better in the morning after a nights rest. Scoliosis or an S shaped or bent spine as seen from behind is often present with the patient bending away from the side of pain.
Lower back joint disruption also causes sciatica as the sciatic nerve is created by the lower joints. If these joints fail to move freely then the nerve at its source becomes irritated.
Sciatica Symptoms Acute low back pain. Pain radiating down the leg. This pain may be sharp and accompanied by pins and needles and / or numbness.
If pain persists for two to three months and the aforementioned treatments have not worked, surgery may be the most effective solution. Sufferers and their doctors must choose between two surgical procedures performed to relieved the pain of sciatica. These surgeries are elective and effective, relieving 75% to 95% of patients' pain.
One reason the sciatic nerve causes so much pain is because it is the longest nerve in the body! The nerve starts at the back of the pelvis and runs downward through the hip area and buttocks into each leg. Near the knee, the sciatic nerve divides into two nerves???the tibial and peroneal nerves. The tibial nerve runs behind the knee and the peroneal nerve runs along the side of the calf and ankle. Through the tibial and peroneal nerves, the sciatic nerve innervates ('stimulates') the action of many muscles in the lower legs and enables feeling in the thighs, legs, and feet.
Inflammation of the sacroiliac joints and associated ligaments are very common, especially following pregnancy where the hormone relaxing is released and this results in the relaxation of ligaments in preparation for childbirth. In most cases the causes of sacroiliitis are mechanical, however there may be other medical inflammatory conditions present such as Ankylosing Spondylitis as well as others which will need attention.
Areas of the lumbar spine may be tender and have poor mobility. Tight gluteal muscles and other muscles of the buttocks. What can I do? See a Physical Therapist who can identify the problems in the lower spine.
The pain may radiate out into your buttocks and low back and will often radiate to the front into the groin. Occasionally it is responsible for pain in the testicles among males.
Symptoms include: Pain located either to the left or right of your lower back. The pain can range from an ache to a sharp pain which can restrict movement.
They quite happily allow flexion and extension (bending forwards and backwards), lateral flexion (sideways movement) and twisting. However a combination of the two can put excess stress on the spine and damage the discs. This is particularly common in people who may lift heavy objects and twist with them for example unloading heavy boxes off the back of a lorry.
Sports massage will help relieve any soft tissue tension in the area. Use injection therapy. Advise Ice and cold therapy to reduce inflammation.
What other injuries are related or similar? Piriformis syndrome Sciatica Sacroiliac joint pain. The Sacroiliac joint Is? The Sacroiliac Joints are located at the bottom of the back. You have one either side of the spine. The Sacroiliac joints help make up the rear part of the pelvic girdle and sit between the sacrum and the ilia.
The best way to ease tension off the Piriformis muscle is to both stretch the muscle and to use Acupressure to reduce overall muscle tension. Stretching the muscle involves you lying on your back and pulling your knee towards your opposite shoulder. This stretches the Piriformis muscle; if you don't feel tightness in your buttock then you need to use a different stretch.
Depending on where the sciatic nerve is pinched will determine where you feel the pain which can radiate to the front of the knee or right down the back of the leg to the foot. The L5-S1 disc is the disc most commonly damaged and the L4-L5 disc the next most commonly damaged.
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Specific assessment tests: The Stork test - to assess weather the sacroiliac joint is moving correctly. Leg length difference measurements - both straight leg and bent leg assessments.
What are the similar or related injuries and conditions? Ankylosing Spondylitis Myofascial pain Low back pain Coping with Sciatica
Besides pain, other symptoms may accompany sciatica. These symptoms include sensations such as tingling, pins and needles, burning, numbness or muscle weakness. Such symptoms may be felt in the buttock, thigh, behind the knee, calf, ankle, and sometimes the foot.
A Pain deep in the cheeks of your bottom can be referred from the lower back. There does not necessarily have to be pain in the lower back as well for pain to be referred into the buttocks.
There may be muscle spasm in the lower back. Tenderness in the lower back when pressing in. Pain on the straight leg raise test which is not apparent when just stretching the hamstring only.
Piriformis tightness is a common cause as the sciatic nerve either runs through the muscle or next to it. If the muscle tightens the sciatica nerve becomes irritated and sciatica occurs.
The term "sciatica" refers to pain along a specific nerve - the sciatic nerve, which runs from your lower back down through each leg. It usually caused by a wayward vertebral disc, more commonly referred to as a pinched nerve or a herniated, ruptured, or slipped disc that has shifted from it's normal position in the vertebral column and is putting pressure on the radicular nerve (nerve root), which connects to the sciatic nerve.
Apply heat or a hot bath may help to relieve muscle spasm. Use a heat retainer or back brace can provide support in the early stages. See a sports injury specialist or doctor.
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Occasionally there may be referred pain into the lower limb which can be mistaken for sciatica. Classic symptoms are difficulty turning over in bed, struggling to put on shoes and socks and pain getting your legs in and out of the car.
Along with these therapies, Ayurveda has also described Sira vedana (Venesection) and Agni karma (Heat therapy) for treating Sciatica.
In four to six weeks, the majority of patients find their symptoms are relieved without surgery.
Sciatica is a general term for pain originating from the sciatic nerve. Sciatica is a symptom of a disorder that causes mild to sharp and sometimes excruciating pain. Patients have described sciatic pain as mildly disturbing to burning, aching, deep, and similar to a sudden bolt of lightning. Sciatic nerve pain travels from the buttock, down the back of the thigh, and into the leg. Leg pain is the classic hallmark of sciatica. Low back pain may accompany sciatica, and some patients experience sciatic pain extending into the foot. Another characteristic of sciatica is it usually affects either the lower left or right side of the body.
Stiffness in the lower back when getting up after sitting for long periods and when getting up from bed in the morning. Aching to one side of your lower back when driving long distances.
Pain is often triggered by a minor movement such bending over to pick something up. Pain may be worse by sitting, lifting, coughing or sneezing.
A prolapsed disc or slipped disc as it is sometimes known is not simply a disc that has 'slipped' out of place. Intervertibral discs separate the bones of the spine (or vertebrae) and their function is to act as shock absorbers or cushioning for the spine and allow movement.
Begin an exercise programme that will stretch and strengthen the muscles supporting the lumbar spine. Stretch the gluteal muscles and hip rotator muscles.
Physical therapy and chiropractic care ease the painful symptoms of sciatica and work as correctives to prevent future recurrences of the condition by helping to strengthen and tone the lower back.
Several low back conditions can cause sciatica, including: ??? Bulging disc or herniated disc: This is the most common cause of sciatica. When a disc bulges, the gel-like center (nucleus pulposus) pushes against the outer wall of the disc (annulus fibrosus). A herniated disc means that the nucleus pulposus breaks through the annulus fibrosus. With both bulging and herniated discs, the disc material can press on nerve roots, causing sciatica. The consequences of a herniated disc are worse than those of a bulging disc. The disc material that leaks out contains an acidic, chemical irritant (hyaluronic acid) that causes nerve inflammation. ??? Degenerative disc disease (DDD): Sciatica is a common result of the aging process that affects discs called degenerative disc disease. DDD is a change in the disc shape and function, and it can result in a bulging disc or a herniated disc and pain. ??? Piriformis syndrome: The piriformis muscle, located in the lower part of the spine, connects to the thighbone, and helps you rotate your hip. The sciatic nerve runs under the piriformis muscle, so muscle spasms can compress the sciatic nerve. It may be difficult to diagnose and treat as it is not easily identified by x-ray or MRI. ??? Pregnancy: The extra weight and pressure on your spine caused by pregnancy can cause compression of the sciatic nerve. The symptoms will usually go away after childbirth. ??? Spinal stenosis: Your nerves travel through passageways in your spine, and when this space narrows (stenosis), it can put pressure on the nerves in your low back. ??? Spinal tumors and spinal infections: Although very rare, tumors and infections can compress the sciatic nerve. ??? Spondylolisthesis: If a vertebra slips forward over the vertebra below it, it's called spondylolisthesis. This slip can pinch the nerve root and cause sciatica. ??? Trauma: You can develop sciatica because of direct nerve compression from an outside force. For example, you could be injured in a car accident, resulting in a pinched nerve in your low back.
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Begin extension exercises as soon as pain allows. What can a Physical Therapist or GP do? Determine the cause of the sciatic pain. Prescribe anti-inflammatory medication e.g. ibuprofen or muscle relaxants.
What are the symptoms of pain referred from the back? An aching in the buttocks that is difficult to pinpoint. The slump test may reproduce buttock pain which is eased when the neck is relaxed back (extended).
Treatment comprises of three approaches, Elimination (Sodhanam) of the accumulated toxic products of digestion, metabolism and the disease process, Pacification (Samanam) and correction of the entities responsible for altered functioning and Rasayanam (Rejuvenation) of the bodily tissue to regain and maintain natural strength and vitality.
Treatment in Ayurveda is aimed at restoring the equilibrium through correction of the underlying functional in-equilibrium. Ayurvedic treatments for Sciatica concentrate on bringing back the aggravated vata or vata kapha to the state of equilibrium and thereby to the state of health.
What can a Physical Therapist professional do? Manipulate and mobilize the segments of the lumbar spine. This is a good way of assessing whether the lumbar spine is a cause of buttock pain. If it is then symptoms will be relieved.
Ayurveda categorized Sciatica as one of diseases caused by vitiation Vata (one of the principle dosha in the body, responsible for the movement and functionality of the body). Sometimes even kapha (dosha responsible for lubrication and bodily fluids) vitiation along with vata (vata kaphaj) also causes sciatica.
Causes of Sciatica It's important to understand what conditions cause sciatica because remember, sciatica is not a condition ??? it's a medical term used to describe symptoms caused by other low back conditions.
The second stretch is to do the same as above but hold your ankle over your opposite knee with one hand and then use the other hand to pull your knee towards that opposite shoulder. This will create a greater stretch.
The intensity and duration of the pain varies with each person, and ranges from an infrequent and slightly irritating sensation to a constant, debilitating pain. It normally affects the lower back and one leg only, but pain may also extend to the feet and toes. Typical "flare-ups" last two weeks to a few months. During these episodes, sufferers have several options for sciatica pain relief.
Sciatica is a pain that starts in the back and radiates down one of the legs. It is quite a common complaint and is sciatica is caused by pressure on the sciatic nerve which runs down into the leg. The medical term is acute nerve root compression. The cause of pressure can be varied from a Slipped (Prolapsed) disk to muscle tension (Piriformis syndrome) or something less common such as a tumors, bony growths and infections.
The intervertebral discs are filled with a soft liquid in the middle called nucleus pullouts and when a disc prolapses this liquid squeezes out and puts pressure on the spinal cord compressing the nerve routes and causing pain.
The most common causes of sciatica are: pelvic imbalance, Piriformis muscle tightness, and lower back joint disruption. Pelvic imbalance causes the Sacro-Iliac joints to tighten which then allows the muscles in the buttock to go into spasm, leading to sciatica.
The strength of Ayurveda in the area of spine and joint treatments is globally appreciated. Since it addresses the root cause of the issue the results are fantastic. Therapies like Abyanga swedam, Pathrapotala swedam, Choornapinda swedam, Pizhichil, Shirodhara, Kadeevasthy, Navarakizhi, Vasti (the most important procedure in Ayurveda for curing Sciatica permanently) etc. are done as per the necessity and condition. These therapies are directed towards relieving the inflammatory changes and underlying causes of Sciatica, releasing the spasms and nerve compressions in the affected area, strengthening and nourishing entire spine & supporting tissues. Usually the treatment period is 3 - 5 weeks according to the severity of the disease.
These joints can often get stuck or in some cases one half of the pelvis can glide forwards or backwards, which is often referred to as a twisted pelvis. When this occurs it often irritates the Iliolumbar ligament which results in Inflammation. This is usually indicated by tenderness around the bony lumps which you can feel if you place your thumbs either side of your lower back.
Ilia rotation - this assesses weather the ilia is rotated on one side creating imbalance. What can a Physical Therapist or GP do? Use diagnostic tests to discover the cause of the problem.
You do not need to rub or press hard - just like jumper cabling a battery - you are just making a connection from one point to the next. And it is as simple as that...
The Acupressure technique is even simpler... A simple Acupressure point to reduce muscle tension is on the back of your knee. Just come in from the outside of your knee where your hamstring tendon is, the depression there is an Acupressure point for muscular tension. Simply hold this point on both knees at once and rest your hands there for at least 5 minutes. The longer you hold the point the more the tension will reduce.
Are you one of the over 80% of adults suffering from back pain? Then you need simple, valuable and expert advice. Dr Graeme Teague is an expert in the structural field, and has been in practice since 1991 - visit The Back Pain Advisor - http://www.back-pain-advisor.com for valuable and expert advice, tips and information on your back pain issues.
There are torsional or twisting forces applied to the pelvic girdle when the lower limbs are moved. These limbs act like long levers and without the sacroiliac joints and the pubic symphysis (at the front of the pelvis) which allow movement, the pelvis would very likely be subject to a fracture.
Use electrotherapy equipment to treat affected tissues. If indicated and safe to do, level the pelvis via manipulation. Articulate sacroiliac joint and restore normal function.
Use sports massage techniques to relax tight muscles. Gently apply mobilization techniques to the spine. Use traction or advise on the use of and Inversion Table.
In fact the majority of sciatica is simply fixed. Although disc injuries cause sciatica they are not the majority of sciatica cases. They only attribute approximately 10% of sciatica problems.
Ayurveda described sciatica as Gridhrasi (Gridhra means Eagle), as the gait of the affected person resembles that of an eagle's walk and the inflamed nerve appears like eagle's beak.
This is only a temporary fix for your back pain and sciatica, you still need to rebalance your pelvis (the most common cause of back pain), strengthen weak muscles, reduce muscle tension and correct all the joints not working correctly.
Deep tissue sports massage techniques can be applied to the lower back and buttocks to release muscle tension, particularly in chronic conditions. Acupuncture or dry needling can also help reduce chronic tension in muscles.
Sciatica treatment A Short Rest in bed if necessary in a position that is comfortable. A doctor may prescribe NSAID's (non steroidal anti inflammatory drugs) such as ibuprofen. Should always be taken under the direction of a doctor and do not if the patient has asthma.
If pain is severe, a patient may receive an epidural steroid injection. Steroids are injected directly into the painful area around the nerve and greatly reduce inflammation and pain. These injections are temporary and provide sciatic pain relief anywhere from one week to a year.
Sciatica can be simply fixed if you know how. Removing sciatica pain now is simple; stopping it returning is just as easy. You can actually lead a life without back pain ... just imagine all the activities you could do once again.
After the acute painful phase Restore pain free movement to the back through mobilization and stretching techniques. Ensure posture and correct lifting techniques are learned and maintained.
At-home remedies such as heat and ice packs often work wonders to alleviate pain and reduce inflammation. They should be used in twenty minute intervals every couple of hours for optimum effect. Over-the-counter or prescription medications such as acetaminophen (Tylenol) may also bring sciatica pain relief. Non-steroidal anti-inflammatory drugs (NSAIDs) can be particularly helpful in reducing inflammation, but can have painful side effects.
Sciatic pain can make life miserable. Walking, standing, bending over, driving a car, working at a computer, catching up on household chores, sneezing or coughing, and many other activities of daily living can cause sudden and intense pain. Patients who suffer sciatica, especially of a more acute nature, find the symptoms disrupt many aspects of their life.
Strengthen the core stabilizing muscles of the spine.
Terry O'Brien
http://www.BackTrouble.co.UK
Learn More about
Natural Sciatica Back Pain Treatments
There is a natural source of healing power in everyone. When this healing power is activated, it triggers a series of complicated internal processes producing a Healing Response. Pain or injury act to alert the body that damage control is needed, at which point the Healing Response begins and endorphins are generated to repair the affected area. This increases the heart rate and alters the blood...
Sciatic pain usually starts in the buttocks and extends down the rear of the thigh and lower leg to the sole of the foot and along the outer side of the lower leg to the top of the foot. Pain may also be present in the lower back. Sciatica refers to pain along the path of the sciatica nerve. It is usually caused by pressure on the sciatic nerve. Fortunately, most cases of sciatica are not...
Low back and leg pain are conditions that people from all walks of life and from all over the world oftentimes complain of ... regularly.The fact is that lower back pain can be debilitating for many individuals.?? Commonly, sciatica is the source of lower back pain in an individual.?? Through this article you are provided an overview of the basics of sciatica.?? By understanding sciatica you will...
I wanted to share with you the important sciatica stretches that you can do to help get rid of back pain. There are a lot of people out there that have back problems and most of these people would describe it as the greatest pain you ll ever experience. I think it s important to understand that it isn t a sharp pain that hits you in one spot; it s a sharp pain that spreads across your back. You...
It is pain in the butt quite literally. It can also be a pain in the hip, the thigh, the lower leg, or even the foot. In fact, the condition known as sciatica can send pain shooting anywhere in your lower body. What is causing all the commotion is the sciatic nerve, which is not one but a group of nerves bound together in a single sheath. The sciatica nerve runs from your lower back down each leg...
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J Appl Physiol (1985). 2000 Aug;89(2):549-56.
Pyruvate ingestion for 7 days does not improve aerobic performance in well-trained individuals.
Author information
1
Department of Human Biology and Nutritional Sciences, University of Guelph, Ontario, Canada.
2
U Guelph, Ontario, Canada
Abstract
The purposes of the present studies were to test the hypotheses that lower dosages of oral pyruvate ingestion would increase blood pyruvate concentration and that the ingestion of a commonly recommended dosage of pyruvate (7 g) for 7 days would enhance performance during intense aerobic exercise in well-trained individuals. Nine recreationally active subjects (8 women, 1 man) consumed 7, 15, and 25 g of pyruvate and were monitored for a 4-h period to determine whether blood metabolites were altered. Pyruvate consumption failed to significantly elevate blood pyruvate, and it had no effect on indexes of carbohydrate (blood glucose, lactate) or lipid metabolism (blood glycerol, plasma free fatty acids). As a follow-up, we administered 7 g/day of either placebo or pyruvate, for a 1-wk period to seven, well-trained male cyclists (maximal oxygen consumption, 62.3 +/- 3.0 ml. kg(-1). min(-1)) in a randomized, double-blind, crossover trial. Subjects cycled at 74-80% of their maximal oxygen consumption until exhaustion. There was no difference in performance times between the two trials (placebo, 91 +/- 9 min; pyruvate, 88 +/- 8 min). Measured blood parameters (insulin, peptide C, glucose, lactate, glycerol, free fatty acids) were also unaffected. Our results indicate that oral pyruvate supplementation does not increase blood pyruvate content and does not enhance performance during intense exercise in well-trained cyclists.
PMID:
10926637
DOI:
10.1152/jappl.2000.89.2.549
[Indexed for MEDLINE]
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-2,638,290,315,708,230,700 | top of page
Postural Stress Pain
According to The American Posture Institute, naturally aligned human beings have become the minority in our population, a true rarity. In today’s convenient and technologically developed world we seem to be missing the precious link with our own bodies, we are losing the capability of recognizing our wrong postures because they’ve become the new “right” and therefore getting sicker.
Most of us – technologically advanced human beings - are coping with some kind of postural stress. The most common symptom manifests as pain in the upper back, shoulders and neck region. Evolution hasn't prepared our bodies to the bio-mechanical stress of rounding our shoulders and leaning our heads forward while typing and texting for hours. The effects of poor posture are not just affecting adults later in life, rather they are affecting children of young ages as well.
Considering that human head weighs, on average, 12 lbs., any slight angle forward puts a strain on the muscles of your neck and upper back. The further you lean your head forward, and how long you keep that straining posture, determines how much extra work your neck and upper-back need to do. That will result in result in craniofascial pain, headaches, neck aches and shoulder pain, muscle stiffness, and decreased range of motion at the cervical area.
Another common postural stress effect of modern life will show up as pain and discomfort in the low back and it’s the result of prolonged periods of sitting. According to Cornell University Department of Ergonomics, up to 90% more pressure is put on your back when you sit versus. when you stand and, to make things worse, we habitually sit in ways that cause tension and imbalance. Again, the human body was designed to be kept in perpetual motion and not to be locked in a sitting position for long periods of time.
So, what can we do?
Some good advice just to get started:
Regular Massage Therapy preventing or treating stress postural pain through massage is a great way to be proactive by taking responsibility for your well-being. The idea that it’s a luxury approach has already been refuted, a monthly massage not only can be affordable but also, according to a myriad of studies, highly effective not only in treating muscle pain and spasm, but also preventing complications caused by muscle overuse, muscle weakness and muscle tightness.
Physical Activity - keep your body moving as it was designed for, try a new activity, yoga for example can be a very effective way of preventing and treating postural stress pain and it is a very low-risk activity. There's no excuse for not giving yoga a try.
Invest on a standing desk - standing, even for short periods throughout the working day, has been proven to help alleviate or prevent sitting-caused back pain.
Develop posture awareness - over our lifetime, unconscious habits form making it easy for us to miss when we're putting additional stresses on our bodies. Developing awareness of our own posture will help in regaining the natural ability of correctly positioning our bodies while standing, sitting, sleeping, working, driving, gradually replacing the old bad posture.
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2,648,587,718,800,662,000 | Does L-Tyrosine Break A Fast? What The Science Says
Some links in this article are affiliate links, which means we earn from qualifying purchases. Learn more.
With the popularity of supplements like L-Tyrosine, there’s confusion around what breaks a fast and what doesn’t.
As a dietitian, here’s my quick answer:
L-Tyrosine by itself blended with water will not break a fast because it is a free-form amino acid, which won’t kickstart insulin secretion.
However, L-Tyrosine mixed with sugary products or added to a flavored pre-workout supplement will likely break a fast (more on this below).
Key Takeaways
• Taking L-Tyrosine 30-60 minutes before exercise (or before a stressful event), whether in a fasted state or during a feeding window, can help with focus and concentration.
• L-Tyrosine is safe to take on an empty stomach, although some people might experience digestive upset, depending on the dose taken (no optimal dose has been established so far in the literature).
• Opt for a product that’s only ingredient is tyrosine to ensure you’re getting a higher quality product that won’t break a fast.
Will L-Tyrosine Break Your Fast?
Fasting is generally defined as abstaining from food and beverages that contain calories, with the purpose of avoiding an insulin response.
As L-tyrosine is an amino acid that does not contain a significant number of calories it will not break your fast.
That said, if you take a flavored L-Tyrosine supplement that contains additional ingredients (added sugar or sweeteners for example), and/or you mix it with a caloric drink, then it will break your fast.
Here are some examples of L-Tyrosine supplements:
• Pure, Unflavored L-Tyrosine. 100% L-Tyrosine Powder from MyProtein, only contains one ingredient (L-Tyrosine), and since the unflavored version has no caloric content from added sugars, nor sweeteners, it does not affect insulin secretion.
Therefore, taking this type of L-Tyrosine supplement (mixed with water) will not break your fast.
The active ingredients in this stack are caffeine, Beta-Alanine, Citrulline, and L-Tyrosine.
Even if a stack has been sweetened with artificial sweeteners (such as aspartame, saccharin, and sucralose that contain no calories), it might still impact your fast, since some studies have shown that zero-calorie sweeteners impact blood sugars and insulin secretion.
However, the research around zero-calorie sweeteners is inconclusive, since some evidence suggests that these cause a rise in blood sugars (despite not containing carbs and calories) and others suggest the contrary.
This is also a controversial topic for diabetes since some sweeteners are advertised as healthy alternatives for those managing diabetes.
Having said this, if you want to be sure not to break your fast, my advice would be to avoid taking flavored L-Tyrosine that might contain sweeteners.
Similarly, if you took pure L-Tyrosine and mixed it with juice or your usual whey protein shake, it would also break your fast, since the juice and protein shake used to mix it contains calories.
Is It Safe To Take L-Tyrosine on an Empty Stomach?
L-Tyrosine is safe to take on an empty stomach. Taking it on an empty stomach can actually help with its absorption as it is not competing with other nutrients for absorption.
However, some people may experience gastrointestinal discomfort, such as digestive upset when taking L-Tyrosine on an empty stomach but this depends on the dose and the individual’s digestive system.
To minimize the risk of gastrointestinal discomfort, it might be worth starting with a lower dose of L-Tyrosine and gradually increasing the dosage over time.
For example, 200 mg as the starting dose for a few days, and gradually moving up to 500 mg if 200 mg is tolerated.
If the above does not work, another option would be to wait until the feeding window to take L-Tyrosine, either with a small meal/snack or 30-60 minutes after a small meal/snack.
Should You Take L-Tyrosine When Fasting or During a Feeding Window?
The decision to take L-Tyrosine while fasting or during a feeding window depends on your goals and whether you tolerate it in a fasted state and on an empty stomach.
If your goal is to workout in a fasted state (e.g. if you train in the morning before your first meal), then taking the pure L-Tyrosine version will not interfere with your fast.
If you workout during your feeding window (e.g. if you train in the evening), then it may be beneficial to wait 2 hours after a meal/snack for better absorption.
For example, if you train at 7 pm, make sure you finish eating by 4:30 pm and you have your L-Tyrosine (unflavored, flavored, or in a stack) 30 minutes before your workout, at around 6:30 pm.
However, if you experience stomach upset on an empty stomach or in a fasted state, then you can take a serving of L-Tyrosine during a feeding window with a small snack.
For example, you could have a slice of white bread and jam 60 minutes before a workout, and take the supplement 30 minutes before a workout with a glass of juice.
How to Take L-Tyrosine Without Breaking a Fast
To avoid breaking a fast, ensure you have the unflavoured version of pure L-Tyrosine because the nutritional values of flavored versions vary and it’s unclear whether sweeteners will break your fast or not.
Additionally, to avoid breaking your fast I recommend mixing it with water (if taken in powder form) or taking it with water (if taken in pill form) rather than other beverages.
When it comes to dosage, the evidence is fairly limited for the optimal dose of L-Tyrosine, since the doses given in different studies range from 500 mg to 12 g daily (or up to 200 mg/kg daily).
For example, one study investigated the use of 100 mg/kg (i.e. if you weigh 55 kg or 121 lbs, this is 5.5 g) of tyrosine in human subjects during a 4.5 hour exposure to cold and hypoxia (a state in which oxygen is not sufficient).
Results showed that tyrosine significantly decreased symptoms, adverse moods, and performance impairments in those who were greatly impacted by these extreme conditions.
Despite these different ranges, a dose of 500mg – 1g daily might be enough to show some benefits in focus and alertness, even though its direct benefits on exercise performance remain inconclusive.
As a general guideline, add 500mg of unflavoured (pure) L-Tyrosine powder to water around 30-60 minutes before exercise. This will allow your body to metabolize it in time for your workout, without breaking your fast.
My personal favorite L-Tyrosine supplements are 100% L-Tyrosine powder from either Myprotein or BulkSupplements (for me, it just depends which one is cheaper at the time of purchasing).
Both offer a pure version that is free from additives (artificial sweeteners, flavorings, and preservatives) and easy to blend.
What Other Supplements Can Break a Fast?
About The Author
Giulia Rossetto
Giulia Rossetto is a qualified Dietitian and Nutritionist.
She holds a Masters in Human Nutrition (University of Sheffield, UK) and more recently graduated as a Dietitian (University of Malta).
Giulia aims to translate evidence-based science to the public through teaching and writing content. She has worked 4+ years in clinical settings and has also published articles in academic journals.
She is into running, swimming and weight lifting, and enjoys spending time in the mountains (she has a soft spot for hiking and skiing in the Italian Dolomites). | {
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-7,648,257,513,048,348,000 | %0 Journal Article %A Balocco, Angela Lucia %A López, Ana M %A Kesteloot, Cedric %A Horn, Jean-Louis %A Brichant, Jean-François %A Vandepitte, Catherine %A Hadzic, Admir %A Gautier, Philippe %T Quadratus lumborum block: an imaging study of three approaches %D 2021 %R 10.1136/rapm-2020-101554 %J Regional Anesthesia & Pain Medicine %P 35-40 %V 46 %N 1 %X Background and objectives Different injection techniques for the quadratus lumborum (QL) block have been described. Data in human cadavers suggest that the transverse oblique paramedian (TOP) QL3 may reach the thoracic paravertebral space more consistently than the QL1 and QL2. However, the distribution of injectate in cadavers may differ from that in patients. Hence, we assessed the distribution of the injectate after the QL1, QL2, and TOP QL3 techniques in patients.Materials and methods Thirty-four patients scheduled for abdominal surgery received QL blocks postoperatively; 26 patients received bilateral and 8 patients received unilateral blocks. Block injections were randomly allocated to QL1, QL2, or TOP QL3 techniques (20 blocks per each technique). The injections consisted of 18 mL of ropivacaine 0.375% with 2 mL of radiopaque contrast, injected lateral or posterior to the QL muscle for the QL1 and QL2 techniques, respectively. For the TOP QL3, the injection was into the plane between the QL and psoas muscles, proximal to the L2 transverse process. Two reviewers, blinded to the allocation, reviewed three-dimensional computed tomography (3D-CT) images to assess the distribution of injectate.Results and discussion The QL1 block spread in the transversus abdominis plane (TAP), QL2 in the TAP, and posterior aspect of the QL muscle, whereas TOP QL3 spread consistently in the anterior aspect of the QL muscle with occasional spread to the lumbar and thoracic paravertebral areas.Conclusions The spread of injectate after QL1, QL2, and QL3 blocks, resulted in different distribution patterns, primarily in the area of injection. The TOP QL3 did not result in consistent interfascial spread toward the thoracic paravertebral space. %U https://rapm.bmj.com/content/rapm/46/1/35.full.pdf | {
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-1,644,520,901,970,653,000 | Benzedrine side effects by duration, gender and age - a phase IV clinical study of FDA data
Summary:
Side effects are reported by people who take Benzedrine. Common side effects include aortic valve disease among females, and crohn's disease among males.
The phase IV clinical study is created by eHealthMe based on 12 reports from the FDA, and is updated regularly. You can use the study as a second opinion to make health care decisions.
Phase IV trials are used to detect adverse drug outcomes and monitor drug effectiveness in the real world. With medical big data and AI algorithms, eHealthMe is running millions of phase IV trials and makes the results available to the public. Our original studies have been referenced on 700+ medical publications including The Lancet, Mayo Clinic Proceedings, and Nature.
On Nov, 19, 2023
12 people who take Benzedrine and have side effects are studied.
What is Benzedrine?
Benzedrine has active ingredients of amphetamine sulfate. Currently, eHealthMe is studying from 27 Benzedrine users.
Number of Benzedrine reports submitted per year:
Benzedrine side effects.
Benzedrine side effects by gender *:
female:
1. Aortic valve disease
2. Asthenia (weakness)
3. Back pain
male:
1. Crohn's disease (condition that causes inflammation of the gastrointestinal tract)
2. Bronchitis (inflammation of the mucous membrane in the bronchial tubes)
3. Drug ineffective
Benzedrine side effects by age (0-1 to 60+) *:
0-1:
n/a
2-9:
n/a
10-19:
n/a
20-29:
n/a
30-39:
1. Bronchitis (inflammation of the mucous membrane in the bronchial tubes)
40-49:
n/a
50-59:
n/a
60+:
1. Crohn's disease (condition that causes inflammation of the gastrointestinal tract)
2. Asthenia (weakness)
3. Back pain
* Approximation only. Some reports may have incomplete information.
Do you take Benzedrine?
Personalize this study to your gender and age
How to use the study?
You can discuss the study with your doctor, to ensure that all drug risks and benefits are fully discussed and understood.
How the study uses the data?
The study is based on amphetamine sulfate (the active ingredients of Benzedrine) and Benzedrine (the brand name). Other drugs that have the same active ingredients (e.g. generic drugs) are not considered.
Related studies
Alternative drugs to, pros and cons of Benzedrine:
All Benzedrine side effects from A to Z:
a b c d e f g h i j k l m n o p q r s t u v w x y z
Who is eHealthMe?
With medical big data and proven AI algorithms, eHealthMe provides a platform for everyone to run phase IV clinical trials. We study millions of patients and 5,000 more each day. Results of our real-world drug study have been referenced on 700+ medical publications, including The Lancet, Mayo Clinic Proceedings, and Nature. Our analysis results are available to researchers, health care professionals, patients (testimonials), and software developers (open API).
WARNING, DISCLAIMER, USE FOR PUBLICATION
WARNING: Please DO NOT STOP MEDICATIONS without first consulting a physician since doing so could be hazardous to your health.
DISCLAIMER: All material available on eHealthMe.com is for informational purposes only, and is not a substitute for medical advice, diagnosis, or treatment provided by a qualified healthcare provider. All information is observation-only. Our phase IV clinical studies alone cannot establish cause-effect relationship. Different individuals may respond to medication in different ways. Every effort has been made to ensure that all information is accurate, up-to-date, and complete, but no guarantee is made to that effect. The use of the eHealthMe site and its content is at your own risk.
If you use this eHealthMe study on publication, please acknowledge it with a citation: study title, URL, accessed date.
Recent studies on eHealthMe: | {
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2,680,156,110,467,065,300 | Weight loss induced by Roux-en-Y gastric bypass but not laparoscopic adjustable gastric banding increases circulating bile acids
Rohit Kohli, David Bradley, Kenneth D. Setchell, J. Christopher Eagon, Nada Abumrad, Samuel Klein
Research output: Contribution to journalArticlepeer-review
227 Scopus citations
Abstract
Context: It has been hypothesized that increased plasma bile acids (BAs) contribute to metabolic improvements after Roux-en-Y gastric bypass (RYGB) surgery by the G protein-coupled receptor TGR5-mediated effects on glucagon-like peptide-1 secretion and thyroid hormones. Objective: The objective of this study was to evaluate the importance of bariatric surgery-induced alterations in BA physiology on factors that regulate glucose homeostasis (insulin secretion and sensitivity) and energy metabolism (resting energy expenditure and thyroid hormone axis). Design, Participants, Intervention, and Main Outcome Measure: Eighteen extremely obese subjects were studied before and after 20% weight loss, induced by either laparoscopic adjustable gastric banding (LAGB) (n = 10) or RYGB surgery (n = 8). Results: Plasma BAs more than doubled after RYGB [fasting: 1.08 (0.26-1.42) to 2.28 (1.59-3.28) μmol/L, P = .03; postprandial: 2.46 ± 1.59 to 6.00 ±2.75 μmol/L, P = .01] but were either lower or did not change after LAGB [fasting: 1.80 (1.49-2.19) to 0.92 (0.73-1.15) μmol/L, P = .02; postprandial: 3.71 ± 2.61 to 2.82 ± 1.75 μmol/L, P = .14]. Skeletal muscle expression of TGR5 targets, Kir6.2 and cyclooxygenase IV, increased after RYGB but not LAGB. Surgery-induced changes in BAs were associated with increased peak postprandial plasma glucagon-like peptide-1 (r2 = 0.509, P = .001) and decreased serum TSH (r 2 = 0.562, P < .001) but did not correlate with the change in insulin response to a meal (r2 = 0.013, P = .658), insulin sensitivity (assessed as insulin stimulated glucose disposal during a hyperinsulinemic-euglycemic clamp procedure) (r2 = 0.001, P = .995), or resting energy expenditure (r2 = 0.004, P = .807). Conclusions: Compared with LAGB, RYGB increases circulating BAs and TGR5 signaling, but this increase in BAs is not a significant predictor of changes in glucose homeostasis or energy metabolism.
Original languageEnglish (US)
Pages (from-to)E708-E712
JournalJournal of Clinical Endocrinology and Metabolism
Volume98
Issue number4
DOIs
StatePublished - Apr 2013
All Science Journal Classification (ASJC) codes
• Endocrinology, Diabetes and Metabolism
• Biochemistry
• Endocrinology
• Clinical Biochemistry
• Biochemistry, medical
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Dive into the research topics of 'Weight loss induced by Roux-en-Y gastric bypass but not laparoscopic adjustable gastric banding increases circulating bile acids'. Together they form a unique fingerprint.
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-1,946,288,437,155,945,700 | Fashion, Lifestyle & Parenting Blog
What is Body Sculpting?
Non-invasive body sculpting treatments are on the rise. They aim at whipping patients into shape without risky surgical procedures such as liposuction or the tiresome, endless sessions of sweating it out at the gym. In any case, the truth is that there are stubborn fat deposits that refuse to go away with exercise and diet. However, many people still have their doubts insofar as the effectiveness and the safety of these body sculpting techniques are concerned. What do these procedures involve? Are they safe? Below is a discussion of everything you need to know about Wildwood body sculpting.
What is Body Sculpting?
Body sculpting has to do with body treatments that seek to improve the shape of the body by destroying fat cells without making incisions in the skin. Some of the procedures make use of the energy generated by ultrasound, laser, or radio-frequency devices to destroy fat cells while others work by freezing the fat cells.
How do the Treatments Work?
All non-invasive body sculpting techniques work in an almost similar way. They simply get rid of stubborn fat deposits by simply destroying the fat cells in a given area. Then the cells and their contents are then flushed out of the body via the lymphatic system. Therefore, after treatment, the treated areas are unlikely to allow the accumulation of fats again. Thus, compared to dieting and exercise, body sculpting treatments can offer more lasting solutions.
What Treatments are Available?
As mentioned earlier, there are a number of techniques that your doctor can employ when it comes to non-surgical body sculpting. Some of the common ones include:
Laser Treatments
These ones usually use laser energy to generate heat that destroys the fat cells, which are then removed from the body through the lymphatic system.
Radio-frequency Treatments
This method also destroys fat cells by delivering energy that is then converted into heat. The treatments usually target the water found in the cells, and therefore, patients are advised to hydrate well before the procedure.
Ultrasound Treatments
These procedures use ultrasound vibrations to break down fat cells, which are then flushed out of the body through the lymphatic system.
Do the Treatments Hurt?
Most of the body sculpting procedures that involve hot or cold temperatures may involve some discomfort, including pain and burning or stinging sensation. The area that has been treated might also experience redness or swelling after the procedure. However, these side effects are mild, and they should not stop you from getting a more attractive body shape. In any case, non-invasive body sculpting procedures do not have any downtime, meaning that patients are able to get back to their day-to-day activities immediately after leaving the doctor’s office.
The Takeaway
Overall, it is apparent that body sculpting is an excellent procedure for people looking to get rid of stubborn fat deposits and improve their overall body shape. If you are looking for a reliable body sculpting services provider in Wildwood, NUWA WORLD is an excellent facility to visit. Feel free to contact them today for more information about their services. | {
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-3,031,034,282,715,769,300 | Ayurveda, Unani, Homeopathy, Allopathy
Ayurveda: The fundamental principle behind Ayurveda is to restore the imbalances caused due to the internal and external sources and restoring the system towards a perfect equilibrium.
Unani: The system of Unani was originated in Greece and was enriched by Arabs with their aptitude and practice. This requires the use of naturally occurring herbal medicines.
Homeopathy: This is a medical system aimed at the treatment of diseases by means of curing drugs that have the power of producing similar artificial systems to human beings.
Allopathy: It is a branch of medical science that deals with the treatment of diseases by means of medical remedies.
Ayurveda: In simple words Ayurveda stands for life science, here the science stands for the happy and the unhappy states of human life. Ayurveda basically has three branches that are Nara Ayurveda meaning dealing with human life and his diseases, Satva Ayurveda meaning dealing with Animal life and its diseases and the final one is Plant Ayurveda which means dealing with Plant Life and its diseases.
The main aim of Ayurveda is to achieve the following goals like:
1 Dharma
2 Artha
3 Kama
4 Moksha
A positive health deals with both a well-balanced metabolism and a happy state of mind.
The main goal of ayurvedic medicines is to promote good health and not to fight for diseases.
According to a study conducted by students of CAM therapy, everything living or dead is connected to the mind, body, and spirit. If any imbalance happens in this system it causes the body to fall ill. Apart from this, the many other factors that may affect your health maybe age, climate change, emotions and the people around you.
And those who practice Ayurveda believe in the 5 basic elements of life that are: apace, air, water, fire, and the earth.
Unani: It is a branch of science that deals with the various states of health and when not in health it deals with the reasons by which the health may be lost. In the case of unani the temperament is the main thing that is usually considered into consideration. It was originated in Greece and inherited by Arabs. This kind of system can be used for preventive and curative healthcare. This kind of system can be used for the treatment of all the organs of the body. This unani medical treatment has the capability to solve chronic diseases like skin and liver ailment or issues related to skin and liver.
According to the Indian history…this kind of medical treatment was practiced my Hakims and other practitioners.
Homeopathy
This is a branch of medical science which can be used for the holistic and complete treatment of the body. This medical treatment was found in Germany 200 years ago. It is dependent on two unconventional theories that are “Like Cures Like” and “Law of minimum dose”. This kind of medical treatment involves the use of drugs that are capable enough to develop real-time artificial systems.
ALLOPATHY
This is a modern way for the treatment of diseases some call this kind of a medical system as Western Medicine, Orthodox Medicine, BioMedicine, Mainstream medicine and conventional medicine. So basically its a modern way for the treatment of diseases.
Here the treatment is done by means of :
Medication
Surgery
Radiation
Other Therapies and Procedures
In the allopathic treatment of disease, doctors may use a range of treatments for the treatment of infection, illness, and disease. Allopathy was found in the 1800s and its main branch of the mainstream was found by the American College of Preventive Medicine. Some of the preventive care in allopathy includes vaccination for various immunes so as to prevent unwanted diseases.
One another type of treatment is there known as Osteopathy in which the bones and muscles of the body are treated properly. In the United States, Osteopathic doctors are well-defined doctors and surgeons.
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908,992,845,351,021,200 | Quick Answer: Does Hemp interact with medications?
The altered concentration, in turn, may lead to the medication not working, or an increased risk of side effects. Such drug interactions are usually hard to predict but can cause unpleasant and sometimes serious problems.
Does Hemp interact with other medications?
Initial studies show that CBD can definitely mess with medication levels in your system, even if you’re taking your prescribed dosage. But more research is needed to determine the severity of CBD interactions across different medications and to develop recommendations for taking them along with CBD.
Does Hemp oil interfere with blood pressure meds?
For some people, particularly those taking certain prescription medications, using CBD is risky. It has anticoagulant effects that can thin blood; it can also modestly lower blood pressure. These effects could be dangerous for people with certain medical conditions.
Does CBD interfere with statins?
In particular, research has found that CBD is a “potent inhibitor” of two enzymes (CYP3A4 and CYP2D6) that affect many common drugs, including antihistamines, benzodiazepines, certain antidepressants and statins.
IMPORTANT: How do you activate cannabinoid receptors?
Can you take CBD oil if you have high blood pressure?
Studies indicate that CBD may be able to help with high blood pressure. One recent study treated nine healthy men with one dose of 600 mg of CBD oil and found it reduced resting blood pressure, compared to a placebo.
Can CBD cause irregular heartbeat?
The cardiovascular effects of cannabis are not well known. Cannabis consumption has been shown to cause arrhythmia including ventricular tachycardia, and potentially sudden death, and to increase the risk of myocardial infarction (MI).
What are the negative side effects of hemp oil?
Though it’s often well-tolerated, CBD can cause side effects, such as dry mouth, diarrhea, reduced appetite, drowsiness and fatigue. CBD can also interact with other medications you’re taking, such as blood thinners. Another cause for concern is the unreliability of the purity and dosage of CBD in products.
Is hemp oil the same as CBD oil?
Hemp seed oil and CBD oil both derive from the cannabis plant. CBD oil comes from the flowers, leaves, and stems, while hemp seed oil uses extract from the seeds of the cannabis plant. Products containing hemp seed and CBD oils do not typically cause a high, since the levels of THC, if any, tend to be very low.
Does Hemp oil make you tired?
CBD does not have intoxicating properties like THC, so it won’t cause any negative effects like excessive sedation, drowsiness or feelings of fatigue.
Can CBD lower cholesterol?
CBD has been shown to improve cholesterol through its ability to regulate lipid uptake and blood pressure.
IMPORTANT: Your question: How long does hemp seed oil stay in your system?
Can you take CBD oil with cholesterol meds?
CBD-Statins Interactions
With long-term use, this could mean a risk to a patient’s health including more adverse side effects. While there is no conclusive evidence that combining CBD with statins is harmful, the aforementioned information suggests that it poses a possible health risk.
How long does it take for CBD oil to work for joint pain?
Effects may be felt within 15 to 45 minutes.
What medications does CBD interfere with?
CBD can alter the effects of other drugs
• a common blood thinner, warfarin.
• a heart rhythm medication, amiodarone.
• a thyroid medication, levothyroxine.
• several medications for seizure, including clobazam, lamotrigine, and valproate.
11.01.2021
What strain is good for high blood pressure?
Hypertension
• Hybrid. THC 27% Royal Wedding. aka Royal Wedding Cake. …
• Hybrid. THC 19% Orange Kush Breath. 4.2(11) …
• Hybrid. Terpwin Station. 4.2(13) hungry.
• Hybrid. Secret Recipe. 4.3(55) giggly.
• Indica. Gorilla OG. 4.7(3) …
• Sativa. Mountain Thunder. energetic.
• Hybrid. Copper Chem. talkative.
• Hybrid. Cherry Vanilla Cookies. 4.8(8)
How do you lower high blood pressure quickly?
Here are 17 effective ways to lower your blood pressure levels:
1. Increase activity and exercise more. …
2. Lose weight if you’re overweight. …
3. Cut back on sugar and refined carbohydrates. …
4. Eat more potassium and less sodium. …
5. Eat less processed food. …
6. Stop smoking. …
7. Reduce excess stress. …
8. Try meditation or yoga.
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} | 1a01aa77535b9ecfb87b9fc36adbcd2f |
4,064,273,053,458,413,000 | keyword
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hiv miRNA
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https://www.readbyqxmd.com/read/28489271/successful-treatment-of-kshv-inflammatory-cytokine-syndrome-kics-after-kidney-liver-transplant-correlations-with-hhv8-mirnome-and-specific-t-cell-response
#1
Alessandra Mularoni, Alessia Gallo, Giovanni Riva, Patrizia Barozzi, Monica Miele, Giovanni Cardinale, Giovanni Vizzini, Riccardo Volpes, Paolo Grossi, Daniele Di Carlo, Angelo Luca, Tommaso Trenti, Mario Luppi, Pier Giulio Conaldi
In post-transplant patients, HHV-8/KSHV infection is known to cause aggressive tumors, as well as severe non-neoplastic complications. These latter syndromes are driven by HHV-8/KSHV lytic reactivations and related hyper-inflammatory host responses, typically characterized by high viral loads, elevated levels of cytokines and other inflammation biomarkers, cytopenia, organ failure, high fever, and worsening conditions (with no evidence of B-cell neoplasias). These disorders are associated with a high mortality rate, often due to lack of prompt diagnosis, effective therapeutic approaches, and adequate follow up...
May 10, 2017: American Journal of Transplantation
https://www.readbyqxmd.com/read/28452924/genome-wide-analyses-of-microrna-profiling-in-interleukin-27-treated-monocyte-derived-human-dendritic-cells-using-deep-sequencing-a-pilot-study
#2
Xiaojun Hu, Qian Chen, Bharatwaj Sowrirajan, Marjorie Bosche, Tomozumi Imamichi, Brad T Sherman
MicroRNAs (miRNAs) regulate gene expression and thereby influence cell fate and function. Recent studies suggest that an abundant class of miRNAs play important roles in immune cells, such as T cells, natural killer (NK) cells, B cells, and dendritic cells (DCs). Interleukin (IL)-27 is a member of the IL-12 family of cytokines with broad anti-viral effects. It is a potent inhibitor of HIV-1 infection in CD4+ T cells and macrophages, as well as monocyte-derived immature dendritic cells (iDCs). This pilot study compared miRNA profiles between iDCs and IL-27-treated iDCs (27DCs) using deep sequencing methods and identified 46 known miRNAs that were significantly differentially expressed in 27DCs: 36 were upregulated and 10 downregulated by IL-27...
April 28, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28303346/high-throughput-sequencing-identifies-hiv-1-replication-and-latency-related-mirnas-in-cd4-t-cell-lines
#3
Xiangyun Lu, Jin Yang, Haibo Wu, Zongxing Yang, Changzhong Jin, Juan Wang, Linfang Cheng, Xiaorong Peng, Fumin Liu, Xiuming Peng, Sujing Ji, Huilin Ou, Tiansheng Xie, Hangping Yao, Nanping Wu
MicroRNAs are potent gene expression regulators involved in regulating various biological processes, including host-pathogen interactions. In this study, we used high-throughput sequencing to investigate cellular miRNA signatures related to HIV-1 replication and latent infection in CD4(+) T cell lines, which included HIV-1-replicating H9/HTLV-IIIB, HIV-1-latently-infected CEM-Bru cells, and their parental uninfected H9 and CEM-SS cells. Relatively few miRNAs were found to be modulated by HIV-1 replication or latent infection, while the cell-lineage-specific miRNA difference was more pronounced, irrespective of HIV-1 infection...
March 16, 2017: Archives of Virology
https://www.readbyqxmd.com/read/28273892/identifying-differentially-coexpressed-module-during-hiv-disease-progression-a-multiobjective-approach
#4
Sumanta Ray, Ujjwal Maulik
Microarray analysis based on gene coexpression is widely used to investigate the coregulation pattern of a group (or cluster) of genes in a specific phenotype condition. Recent approaches go one step beyond and look for differential coexpression pattern, wherein there exists a significant difference in coexpression pattern between two phenotype conditions. These changes of coexpression patterns generally arise due to significant change in regulatory mechanism across different conditions governed by natural progression of diseases...
December 2017: Scientific Reports
https://www.readbyqxmd.com/read/28250134/microrna-mir-126-5p-enhances-the-inflammatory-responses-of-monocytes-to-lipopolysaccharide-stimulation-by-suppressing-cylindromatosis-in-chronic-hiv-1-infection
#5
Jun Huang, Lingyan Zhu, Chao Qiu, Xuan Xu, Linxia Zhang, Xiangqing Ding, Qibin Liao, Jianqing Xu, Xiaoyan Zhang
Persistent immune activation during chronic human immunodeficiency virus type 1 (HIV-1) infection facilitates immune dysfunction and thereby fuels disease progression. The translocation of bacterial derivatives into blood and the hyperinflammatory responsiveness of monocytes have been considered important causative factors for persistent immune activation. Whether microRNAs (miRNAs) are involved in regulating monocyte-mediated inflammatory responses during chronic HIV-1 infection remains elusive. In this study, we show that miR-126-5p functions as a positive regulator of monocyte-mediated inflammatory responses...
May 15, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28236278/tat-mediated-induction-of-mirs-34a-138-promotes-astrocytic-activation-via-downregulation-of-sirt1-implications-for-aging-in-hand
#6
Guoku Hu, Ke Liao, Lu Yang, Gurudutt Pendyala, Yeonhee Kook, Howard S Fox, Shilpa Buch
Astrocyte activation is a hallmark of HIV infection and aging in the CNS. In chronically infected HIV patients, prolonged activation of astrocytes has been linked to accelerated aging including but not limited to neurocognitive impairment and frailty. The current study addresses the role of HIV protein Tat in inducing a set of small noncoding microRNAs (miRNA) that play critical role in astrogliosis. In our efforts to link astrocyte activation as an indicator of aging, we assessed the brains of both wild type and HIV transgenic rats for the expression of glial fibrillary acidic protein (GFAP)...
February 24, 2017: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/28222782/identification-of-mirna-mrna-crosstalk-in-cd4-t-cells-during-hiv-1-infection-by-integrating-transcriptome-analyses
#7
Qibin Liao, Jin Wang, Zenglin Pei, Jianqing Xu, Xiaoyan Zhang
BACKGROUND: HIV-1-infected long-term nonprogressors (LTNPs) are characterized by infection with HIV-1 more than 7-10 years, but keeping high CD4(+) T cell counts and low viral load in the absence of antiretroviral treatment, while loss of CD4(+) T cells and high viral load were observed in the most of HIV-1-infected individuals with chronic progressors (CPs) However, the mechanisms of different clinical outcomes in HIV-1 infection needs to be further resolved. METHODS: To identify microRNAs (miRNAs) and their target genes related to distinct clinical outcomes in HIV-1 infection, we performed the integrative transcriptome analyses in two series GSE24022 and GSE6740 by GEO2R, R, TargetScan, miRDB, and Cytoscape softwares...
February 21, 2017: Journal of Translational Medicine
https://www.readbyqxmd.com/read/28187417/a-machine-learning-approach-for-microrna-precursor-prediction-in-retro-transcribing-virus-genomes
#8
Müserref Duygu Saçar Demirci, Mustafa Toprak, Jens Allmer
Identification of microRNA (miRNA) precursors has seen increased efforts in recent years. The difficulty in experimental detection of pre-miRNAs increased the usage of computational approaches. Most of these approaches rely on machine learning especially classification. In order to achieve successful classification, many parameters need to be considered such as data quality, choice of classifier settings, and feature selection. For the latter one, we developed a distributed genetic algorithm on HTCondor to perform feature selection...
December 22, 2016: Journal of Integrative Bioinformatics
https://www.readbyqxmd.com/read/28132840/a-rapid-induction-mechanism-for-lin28a-in-trophic-responses
#9
Alexandra M Amen, Claudia R Ruiz-Garzon, Jay Shi, Megha Subramanian, Daniel L Pham, Mollie K Meffert
Environmental cues provoke rapid transitions in gene expression to support growth and cellular plasticity through incompletely understood mechanisms. Lin28 RNA-binding proteins have evolutionarily conserved roles in post-transcriptional coordination of pro-growth gene expression, but signaling pathways allowing trophic stimuli to induce Lin28 have remained uncharacterized. We find that Lin28a protein exhibits rapid basal turnover in neurons and that mitogen-activated protein kinase (MAPK)-dependent phosphorylation of the RNA-silencing factor HIV TAR-RNA-binding protein (TRBP) promotes binding and stabilization of Lin28a, but not Lin28b, with an accompanying reduction in Lin28-regulated miRNAs, downstream of brain-derived neurotrophic factor (BDNF)...
February 2, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28096489/induced-packaging-of-cellular-micrornas-into-hiv-1-virions-can-inhibit-infectivity
#10
Hal P Bogerd, Edward M Kennedy, Adam W Whisnant, Bryan R Cullen
Analysis of the incorporation of cellular microRNAs (miRNAs) into highly purified HIV-1 virions revealed that this largely, but not entirely, mirrored the level of miRNA expression in the producer CD4(+) T cells. Specifically, of the 58 cellular miRNAs detected at significant levels in the producer cells, only 5 were found in virions at a level 2- to 4-fold higher than that predicted on the basis of random cytoplasmic sampling. Of note, these included two miRNAs, miR-155 and miR-92a, that were reported previously to at least weakly bind HIV-1 transcripts...
January 17, 2017: MBio
https://www.readbyqxmd.com/read/28039100/utility-of-systematic-isolation-of-immune-cell-subsets-from-hiv-infected-individuals-for-mirna-profiling
#11
Manel E Bargalló, Alberto C Guardo, Maria J Maleno, Laia Miralles, Lander Egaña-Gorroño, Tuixent Escribà, Felipe García, Jose M Gatell, Mireia Arnedo, Montserrat Plana
INTRODUCTION: Peripheral blood mononuclear cells (PBMCs) are frequently used for genomic analyses, but several factors can affect the yield and integrity of nucleic acids, including the methods of cell collection and isolation. The goal of this work was to analyze the utility of systematic isolation of different immune cell subsets by immunomagnetic separation and the RNA integrity after isolated cells from samples of HIV-infected patients. METHODS: PBMC from Healthy Controls (HC, n=15), Elite Controllers (EC, n=15), Viremic Controllers (VC, n=15), Viremic Progressors (VP, n=15) and HIV-infected patients on therapy (ART, n=15) were isolated by Ficoll-Paque density gradient centrifugation...
December 27, 2016: Journal of Immunological Methods
https://www.readbyqxmd.com/read/28005686/transcriptome-analyses-identify-key-cellular-factors-associated-with-hiv-1-associated-neuropathogenesis-in-infected-men
#12
Narasimhan J Venkatachari, Siddhartha Jain, Leah Walker, Shalmali Bivalkar-Mehla, Ansuman Chattopadhyay, Ziv Bar-Joseph, Charles Rinaldo, Ann Ragin, Eric Seaberg, Andrew Levine, James Becker, Eileen Martin, Ned Sacktor, Velpandi Ayyavoo
OBJECTIVE: HIV-1 viral proteins and host inflammatory factors have a direct role in neuronal toxicity in vitro; however, the contribution of these factors in vivo in HIV-1-associated neurocognitive disorder (HAND) is not fully understood. We applied novel Systems Biology approaches to identify specific cellular and viral factors and their related pathways that are associated with different stages of HAND. DESIGN: A cross-sectional study of individuals enrolled in the Multicenter AIDS Cohort Study including HIV-1-seronegative (N = 36) and HIV-1-seropositive individuals without neurocognitive symptoms (N = 16) or with mild neurocognitive disorder (MND) (N = 8) or HIV-associated dementia (HAD) (N = 16)...
March 13, 2017: AIDS
https://www.readbyqxmd.com/read/28003477/argonaute-proteins-regulate-hiv-1-multiply-spliced-rna-and-viral-production-in-a-dicer-independent-manner
#13
Agathe Eckenfelder, Emmanuel Ségéral, Natalia Pinzón, Damien Ulveling, Céline Amadori, Marine Charpentier, Sabine Nidelet, Jean-Paul Concordet, Jean-François Zagury, Jean-Christophe Paillart, Clarisse Berlioz-Torrent, Hervé Seitz, Stéphane Emiliani, Sarah Gallois-Montbrun
Argonaute (Ago) proteins associate with microRNAs (miRNAs) to form the core of the RNA-induced silencing complex (RISC) that mediates post-transcriptional gene silencing of target mRNAs. As key players in anti-viral defense, Ago proteins are thought to have the ability to interact with human immunodeficiency virus type 1 (HIV-1) RNA. However, the role of this interaction in regulating HIV-1 replication has been debated. Here, we used high throughput sequencing of RNA isolated by cross-linking immunoprecipitation (HITS-CLIP) to explore the interaction between Ago2 and HIV-1 RNA in infected cells...
April 20, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/27993935/mirna-profiling-of-human-naive-cd4-t-cells-links-mir-34c-5p-to-cell-activation-and-hiv-replication
#14
Andreia J Amaral, Jorge Andrade, Russell B Foxall, Paula Matoso, Ana M Matos, Rui S Soares, Cheila Rocha, Christian G Ramos, Rita Tendeiro, Ana Serra-Caetano, José A Guerra-Assunção, Mariana Santa-Marta, João Gonçalves, Margarida Gama-Carvalho, Ana E Sousa
Cell activation is a vital step for T-cell memory/effector differentiation as well as for productive HIV infection. To identify novel regulators of this process, we used next-generation sequencing to profile changes in microRNA expression occurring in purified human naive CD4 T cells in response to TCR stimulation and/or HIV infection. Our results demonstrate, for the first time, the transcriptional up-regulation of miR-34c-5p in response to TCR stimulation in naive CD4 T cells. The induction of this miR was further consistently found to be reduced by both HIV-1 and HIV-2 infections...
February 1, 2017: EMBO Journal
https://www.readbyqxmd.com/read/27919232/microrna-27a-rs895819-is-associated-with-obesity-in-hiv-infected-preeclamptic-black-south-african-women-on-haart
#15
Niren Ray Maharaj, Prithiksha Ramkaran, Siddharthiya Pillay, Anil Amichund Chuturgoon
BACKGROUND: Preeclampsia (PE) and HIV/AIDS present a major health challenge globally. South Africa has the highest disease burden of both HIV/AIDS and PE in the world. Despite extensive research, the pathophysiology of these conditions is not completely understood, however a genetic predisposition in women may affect susceptibility. MiRNA-27a regulates adipogenesis and glucose metabolism. A single nucleotide polymorphism (SNP) in miRNA-27a (rs895819T > C) has shown to have disparate effects in various populations...
December 5, 2016: BMC Medical Genetics
https://www.readbyqxmd.com/read/27886048/interactions-between-the-hiv-1-unspliced-mrna-and-host-mrna-decay-machineries
#16
REVIEW
Daniela Toro-Ascuy, Bárbara Rojas-Araya, Fernando Valiente-Echeverría, Ricardo Soto-Rifo
The human immunodeficiency virus type-1 (HIV-1) unspliced transcript is used both as mRNA for the synthesis of structural proteins and as the packaged genome. Given the presence of retained introns and instability AU-rich sequences, this viral transcript is normally retained and degraded in the nucleus of host cells unless the viral protein REV is present. As such, the stability of the HIV-1 unspliced mRNA must be particularly controlled in the nucleus and the cytoplasm in order to ensure proper levels of this viral mRNA for translation and viral particle formation...
November 23, 2016: Viruses
https://www.readbyqxmd.com/read/27882942/emerging-roles-of-extracellular-vesicles-in-neurodegenerative-disorders-focus-on-hiv-associated-neurological-complications
#17
REVIEW
Guoku Hu, Lu Yang, Yu Cai, Fang Niu, Frank Mezzacappa, Shannon Callen, Howard S Fox, Shilpa Buch
Exosomes are membrane-enriched extracellular vesicles with a proposed diameter in the range of 30-100 nm. They are released during both normal homeostasis as well as under pathological conditions by most cell types. In recent years, there has been robust interest in the study of these vesicles as conduits for the delivery of information between cells in both analogous as well as disparate tissues. Their ability to transport specialized cargo including signaling mediators, proteins, messenger RNA and miRNAs characterizes these vesicles as primary facilitators of cell-to-cell communication and regulation...
November 24, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27852859/kaposi-s-sarcoma-associated-herpesvirus-micrornas-target-gadd45b-to-protect-infected-cells-from-cell-cycle-arrest-and-apoptosis
#18
Xiaoyan Liu, Christine Happel, Joseph M Ziegelbauer
Kaposi's sarcoma is one of the most common malignancies in HIV-infected individuals. The responsible agent, Kaposi's sarcoma-associated herpesvirus (KSHV; HHV8), expresses multiple microRNAs (miRNAs), but the targets and functions of these miRNAs are not completely understood. After infection in primary endothelial cells with KSHV, growth arrest DNA damage-inducible gene 45 beta (GADD45B) is one of the most repressed genes using genomic expression profiling. GADD45B was also repressed in mRNA expression profiling experiments when KSHV miRNAs were introduced to uninfected cells...
February 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/27761954/novel-insights-into-role-of-mir-320a-vdac1-axis-in-astrocyte-mediated-neuronal-damage-in-neuroaids
#19
Mahar Fatima, Bharat Prajapati, Kanza Saleem, Rina Kumari, Chitra Mohindar Singh Singal, Pankaj Seth
Astroglia are indispensable component of the tripartite synapse ensheathing innumerous soma and synapses. Its proximity to neurons aids the regulation of neuronal functions, health and survival through dynamic neuroglia crosstalk. Susceptibility of astrocyte to HIV-1 infection and subsequent latency culminates in compromised neuronal health. The viral protein HIV-1 transactivator of transcription (Tat) is neurotoxic. HIV-1 Tat is detected in brain of AIDS patients even in cases where viral load is non-detectable due to successful HAART therapy...
February 2017: Glia
https://www.readbyqxmd.com/read/27749601/microrna-210-microrna-331-and-microrna-7-are-differentially-regulated-in-treated-hiv-1-infected-individuals-and-are-associated-with-markers-of-systemic-inflammation
#20
Vibe Ballegaard, Ulrik Ralfkiaer, Karin K Pedersen, Malene Hove, Simon Koplev, Peter Brændstrup, Lars P Ryder, Hans O Madsen, Jan Gerstoft, Kirsten Grønbæk, Susanne D Nielsen
OBJECTIVE: Inflammation may contribute to increased risk of cardiovascular disease (CVD) in HIV-1 infection. MicroRNAs (miRNAs) are involved in the regulation of inflammation. In treated HIV-1-infected individuals, we aimed to identify differentially expressed miRNAs with known roles in inflammation and CVD risk, and to investigate associations between these and systemic inflammation. METHODS: In a screening cohort including 14 HIV-1-infected individuals and nine uninfected controls microarray profiling was performed using peripheral blood mononuclear cells (PBMC)...
October 3, 2016: Journal of Acquired Immune Deficiency Syndromes: JAIDS
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1,624,554,471,480,994,800 | MDMA (Molly/Ecstasy) Dosage
Research based information on MDMA (Molly/Ecstasy) dosage: read why you should take less than 120 mg of MDMA per session.
MDMA (Molly, Ecstasy) Dosage
This advice applies if you are determined to take MDMA. The safest option is to not use MDMA, the second safest option is to use MDMA responsibly, and the most dangerous option is to use MDMA irresponsibly.
Most important things to know about MDMA dosage
1. Guideline: your weight in kg, plus 50 = total dosage in milligrams for the session. (1.5 mg/kg with a 120 mg max may be more optimal, but the weight + 50 is a good rule of thumb). If you’re more cautious or want something a little less intense, perhaps weight in kg + 35-40.
2. If finger dipping powder: ideally switch to weighed doses, but if not that, use “crush, dab, wait.”
3. If using tablets and you haven’t taken a tablet from this exact batch before, start with half, or less.
4. Low doses may be particularly important for your first few uses, as you might unknowingly have a health condition like malignant hyperthermia that makes MDMA more dangerous. I believe your weight in kilograms + 20 is an appropriate and cautious first dosage.
5. A study found that MDMA desirable effects are maximized, and undesirable effects minimized, at doses between 81-100 mg.1
6. If you’re unwilling to use these dosage guidelines, please make extra sure your friends are aware of the signs of heat stroke and heat exhaustion, and pay extra attention to keeping cool.
7. “I think there’s no “safe” dose if you have a preexisting health condition contraindicated with MDMA.” For example, malignant hyperthermia, which you may have but be unaware of.
8. A small female died soon after consuming 500 mg of 91% pure MDMA. It is highly probable that they had a health condition that interacted dangerously with MDMA, but this shows why it’s important to pay attention to dosage.
9. This dosage advice is only relevant if you actually have MDMA! 87% of “Molly” analyzed by the DEA between 2009 and 2013 contained 0% MDMA, instead mostly containing substances like methylone and mephedrone.2 3 If these dosages seem low, remember that only 13% of “Molly” tested during that period contained any MDMA. Fake MDMA substances like methylone have weaker effects per milligram.
10. 46% of Ecstasy tablets analyzed in a study contained 0% MDMA.4
11. There’s a reasonable chance it may take a user 90 minutes to feel MDMA’s effects, and though rare it’s not unheard of for the effects to take 2-2.5 hours to kick in. Particularly if it’s one of your first 5 times using MDMA, please wait at least 2 hours before considering any redoses/booster doses, and avoid taking a booster dose at all if possible.
Dosage guideline: your weight in kg, plus 50 = total dosage in milligrams for the session.
We state the ‘kg + 50’ dosage guideline instead because of a great suggestion to optimize for helping the largest number of people the most - weight in kg + 50 easier and simpler to remember, and so may allow us to help more people, and with real MDMA, it’ll be a satisfying dose.1 The optimal method for harm-reduction if you’re willing is perhaps 1.5 mg/kg total during the session, with a 120 mg maximum even for heavy people.
Taking low doses may be particularly important for your first few uses, so that you can reduce the risk you have a health condition you’re unaware of that interacts dangerously with MDMA.
If you’re dosing by dipping your finger in the powder, ideally switch to weighed dosages, but if you can’t or won’t do that, follow the advice from UK group The Loop: crush crystals to a fine powder, lick your finger tip and dab the powder to consume a small amount, and then wait 1-2 hours before considering taking more.5 Crush, Dab, Wait. 🔨👇🕐
If using tablets: Look up your pill and see if you can figure out the dosage content. If you can’t, a good guideline is to take no more than 12 the pill, and then wait at least 1.5 hours before considering taking more.
If you’re unwilling to use these dosage guidelines, please make extra sure your friends are aware of the signs of heat stroke and heat exhaustion, and pay extra attention to keeping cool.
Consider 80 mg or less for your first roll
If it’s your first time, consider dosing of perhaps between 0.8 mg/kg - 1.2 mg/kg with a max of 80 mg. This allows you to make sure your product is high purity (you should still expect to feel some euphoria and empathy at 70 mg), and the other benefit for first time users is that it may reduce the risk of feeling “that no future MDMA sessions will ever be as good as my first time,” which is a somewhat common and often regrettable anecdotal sentiment.
75-120 mg if it’s not your first time
The best dosage of pure MDMA based on our current knowledge for maximum desirable effects, minimum undesirable effects, and safer use, is: your body weight in kg * 1.5 (or weight in lbs * 0.68), with a maximum of 120 mg, with no-redose or booster dose (Baggott).
So if you weigh 70kg/154lbs, you’d take 105 mg, with no redose/booster.
If you weigh 50kg/110lbs, you’d take 75 mg.
If you weigh 80kg/176lbs, you’d take 120 mg.
If you weigh 90kg/198lbs, you’d take 120 mg (120 mg maximum to reduce risk of neurotoxicity).
RollSafe knows that many people will choose not to follow this dosage advice. If you won’t do 1.5 mg/kg, we’d ask that you follow MDMA researcher Matthew Baggott’s advice to stay below 2 mg/kg MDMA in total (including re-doses) during a session.
Warnings:
• Your MDMA may not be pure, and you may be increasing your risk as a result. 87% of “Molly” analyzed by the DEA between 2009 and 2013 contained 0% MDMA, instead mostly containing “bath salts.”2 Terrible. 😠 Use a test kit to reduce some risks, but know that even test kits cannot guarantee purity. Read more on testing.
• Always re-set your dosage with a new source. It would be highly possible for someone to be used to taking ~250 mg of “Molly/MDMA” (that unknown to them) is fake/impure and actually methylone or similar, and then to get a new MDMA source, and then take 250 mg of what is now actually MDMA and put yourself at greater risk because MDMA has stronger effects at lower dosages than methylone.
Lower dosages help reduce neurotoxicity risk, help increase enjoyment, and help reduce the risk of serious adverse effects.6 7
From MDMA researcher Matthew Baggott:
“I trained in an MDMA neurotoxicity lab (Lewis Seiden’s) and then went on to do human studies (giving MDMA to volunteers to understand its emotional effects). I think MDMA may well be neurotoxic at the higher end of recreational doses. I wouldn’t personally take/give more than 1.5-1.7 mg/kg and would never take/give a booster dose, unless there was strong reason to think the person would have some clear benefit (as in MDMA-assisted psychotherapy) to offset the added risks. Just my opinion.”
“To the best of my understanding, doses around 1.5-1.7 mg/kg MDMA (roughly 100 to 125 mg MDMA) are unlikely to cause long-lasting serotonin changes. Studies by MAPS have looked for changes in mental abilities after people participated in their studies, with some participants receiving 125 mg followed by 62.5 mg, and have not found any changes.”
“In studies such as this, we sometimes see bigger effects on heart rate than I would want and people frequently say they feel close to maximal effects. As a result, I tend to think 1.5 mg/kg is high enough and I would worry that 120 mg is too high for many smaller people.
I do agree there are limits to mg/kg scaling. Mg/kg is correcting for the volume in your body that the drug dissolves into, with the idea that people will get similar blood (and then brain) concentrations. However, this volume doesn’t scale with weight perfectly because peoples’ bodies are different on the high and low ends of weight. So I would personally suggest 1.5 mg/kg up to a maximum of 120 mg. I don’t have strong evidence for a minimal dose from my studies, but if forced to choose I might use a minimum dose of 75mg.
Interestingly, MAPS is seeing preliminary evidence that lower doses might be more therapeutic, which is consistent with observations by therapist Leo Zeff that people want higher doses than they need.”
“I would discourage total doses over 2 mg/kg MDMA.” (During the entire session/night, including re-doses)
From the fantastic book Acid Test
“Since the MDMA dosage Ricaurte had tested was about three times the average therapeutic dose equivalent—1.7 milligrams per kilogram—Rick urged him to do another test at a lower dosage to determine if, at any point above the therapeutic dosage, MDMA would show no long-lasting effect on serotonin neurons anywhere in the brain.
That point came at 2.5 milligrams per kilogram, still 50 percent above the usual therapeutic dosage. Eight doses of that size were administered over four months (one dose every two weeks), after which there was no detectable damage to neurons. Rick was greatly relieved, since that would be the key to persuading the FDA that it would be safe enough to conduct human therapeutic trials.”8
How re-dosing (booster doses) is done in MDMA research
MAPS uses “80 or 120mg MDMA (plus supplemental half dose of 40 or 60mg unless contraindicated)”9
The re-dose of 12 of the initial dose is taken in MDMA PTSD research 1.5 to 2.5 hours after the first dose is ingested.10
If you do re-dose, you should follow this and take 12 of your initial dose just after you’ve peaked from the first dose, likely 2-2.5hrs after ingesting the first dose. Don’t redose before your first dose has reached peak effects, unless you’re using a dose and source that you’ve used many times before and therefore know exactly how strong the effects will be.
Before considering re-dosing, please note Matthew Baggott’s comments: “I wouldn’t personally take/give more than 1.5-1.7 mg/kg and would never take/give a booster dose, unless there was strong reason to think the person would have some clear benefit (as in MDMA-assisted psychotherapy) to offset the added risks. Just my opinion.”
There isn’t a good risk/benefit tradeoff of re-dosing except perhaps in therapeutic use (Baggott).
MDMA Dosage Safety
From private conversations with Emanuel Sferios of DanceSafe:
“I think there’s no “safe” dose if you have a preexisting health condition contraindicated with MDMA.” “Or if you are in a super hot environment.” “Or both.” “But it’s a relatively safe drug nonetheless.”
15-year-old Martha Fernback died three hours after consuming 500 mg of 91% pure MDMA. Some reports initially suspected the deadly adulterant PMA, but it was later reported after toxicology that she consumed 91% pure MDMA.
I would be unsurprised if many of the MDMA-related deaths occur in people with contraindicated health conditions, i.e. conditions that produce a susceptibility to heat stroke or cardiovascular disease. Though it is important to note that some people may have a contraindicated condition and not realize it.
Desirable effects are maximized between 81-100 mg
A study found that MDMA desirable effects are maximized, and undesirable effects minimized, at doses between 81-100 mg.1
If less than 120 mg sounds low to you, you may have been taking fake MDMA
Ask yourself: how certain are you of the purity levels, not just MDMA presence, of your MDMA? How do you know?
Are you aware that 87% of “Molly” analyzed by the DEA between 2009 and 2013 contained 0% MDMA, instead mostly containing substances like methylone and mephedrone (which, in higher dosages, can have some similar effects to MDMA)?2
And are you aware that 46% of Ecstasy tablets analyzed in a study contained 0% MDMA?4
Please buy a test kit if 120 mg sounds low to you. (Really, everyone should buy a test kit.)
Higher doses are less safe
Higher doses are more likely to cause neurotoxicity.11
Higher doses are more likely to lead to serious adverse effects, including the possibility of MDMA-related death. See this MDMA-related death after an individual consumed an estimated ~750 mg. Again: “I would be unsurprised if many of the MDMA-related deaths occur in people with contraindicated health conditions, i.e. conditions that produce a susceptibility to heat stroke or cardiovascular disease. Though it is important to note that some people may have a contraindicated condition and not realize it.”
People have died in MDMA-related deaths after consuming more than 125mg of pure MDMA (very few people, but more than zero). We have not heard of any deaths related to taking pure MDMA at a dosage of less than 125mg.
RollSafe does not support the Erowid dosage advice - it is too high for users that care about their health.
Measure your dosage
1. Don’t eyeball your doses, be safe.
2. Buy a 1 mg scale.
3. Use a playing card or similar - fold the card in half so it’s easier to pour later, put the card on the scale, then zero the scale.12
4. The scale should be at 0 mg.
5. Use a spoon or similar to put little bits of MDMA onto the playing card, until it reaches your (safe) dosage.
6. Put the folded edge of the card up to the capsule, and tap it until the MDMA is inside the capsule. This is why it helps if it is folded.
7. Done.
References
Recent Pages
More
What's in Molly? Learn The Ingredients in the Drug Molly
How often can you take MDMA (Molly/Ecstasy) and roll?
MDMA/Psychedelic Drug Testing Center
What are the best MDMA educational videos?
All Pages
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-7,280,765,193,889,163,000 | In the modern world, where screens and digital devices have become an integral part of our lives, maintaining optimal eye health is more crucial than ever. Our eyes are essential for experiencing the beauty of the world around us. This comprehensive guide will provide you with a wealth of information and practical tips to ensure your eye health remains at its best. From clear vision practices to eye-friendly habits, we’ll explore everything you need to know to keep your eyesight sharp and vibrant.
Eye Health Tips: Nurturing Visual Wellness
Our eyes are intricate and delicate organs that require proper care and attention. Nurturing their health is vital to maintain clear and sharp vision throughout your life.
Clear Vision Practices: Seeing the World Anew
Clear vision practices involve habits that enhance your ability to see the world in all its details. Regular eye exercises and relaxation techniques can significantly improve visual acuity.
Healthy Eyesight Suggestions: A Nutrient-Rich Diet
A well-balanced diet rich in vitamins and minerals is crucial for maintaining healthy eyesight. Foods like carrots, spinach, and citrus fruits provide essential nutrients that support optimal vision.
Visual Clarity Techniques: Focusing on Precision
Visual clarity techniques involve training your eyes to focus and perceive details accurately. These techniques can improve your ability to read fine print and notice subtle changes in your surroundings.
Maintaining Optic Wellness: Rest and Relaxation
Just like any other part of your body, your eyes need rest to stay healthy. Getting sufficient sleep and taking breaks during prolonged screen time can prevent eye strain and fatigue.
Vision Care Recommendations: Regular Check-ups
Regular eye check-ups with an optometrist are essential, even if you think your vision is perfect. These check-ups can detect issues early on and prevent potential complications.
Tips for Clear Eyes: Hydration and Comfort
Keeping your eyes well-hydrated and comfortable is essential. Remember to blink regularly, especially during extended screen time, to prevent dry eyes.
Eye-Friendly Habits: Balanced Screen Time
Excessive screen time can strain your eyes and lead to digital eye strain. Cultivate eye-friendly habits by taking breaks, adjusting screen settings, and maintaining proper lighting.
Enhancing Visual Health: UV Protection
Protecting your eyes from harmful ultraviolet (UV) rays is vital. Wearing sunglasses with UV protection when outdoors can prevent long-term damage to your eyes.
Eye Maintenance Guidelines: Cleanliness Matters
Practicing good eye hygiene by washing your hands before touching your eyes and properly cleaning contact lenses can prevent infections and maintain clear vision.
Practices for Sharp Vision: Active Lifestyle
Regular physical activity improves blood circulation, which in turn benefits your eyes. Engaging in regular exercise can contribute to better overall visual health.
Preserving Optical Clarity: Anti-Reflective Lenses
If you wear glasses, consider using lenses with anti-reflective coatings. These coatings reduce glare and reflections, improving your visual clarity.
Eyesight Boosting Tips: Mindful Habits
Mindfulness techniques, such as palming and focusing exercises, can relax your eye muscles and alleviate strain, ultimately boosting your eyesight.
Strategies for Healthy Vision: Long-Term Approach
Maintaining healthy vision is a lifelong commitment. By adopting specific strategies and habits, you can safeguard your eyesight for years to come.
Vision Preservation Methods: Blue Light Protection
Digital devices emit blue light that can potentially harm your eyes. Using blue light filters on screens and limiting screen time before bed can help preserve your vision.
Eye Wellness Advice: Hydration and Nutrition
Staying well-hydrated and consuming foods rich in omega-3 fatty acids, like fish, can support the health of the tiny blood vessels in your eyes.
Clear Eyesight Pointers: Adequate Lighting
Proper lighting is essential for clear vision. Ensure that your workspace is well-lit, and avoid glare or shadows that can strain your eyes.
Optimal Vision Habits: Ergonomic Setup
Maintaining an ergonomic workstation with the correct monitor height and distance can reduce eye strain and promote better posture, benefiting your overall visual health.
Techniques for Bright Vision: Contrast Enhancement
Adjusting the contrast and brightness settings on your devices can improve the clarity of what you see, making it easier to read and view images.
Caring for Your Eyes: Screen Breaks
The 20-20-20 rule is a helpful guideline: every 20 minutes, take a 20-second break, and focus on something 20 feet away to give your eyes a chance to relax.
Eye Hygiene Tips: Contact Lens Care
If you wear contact lenses, following proper hygiene and replacement schedules is essential to prevent infections and maintain optimal eye health.
Nurturing Visual Health: Regular Exercise
Physical activity improves blood circulation to the eyes, delivering essential nutrients and oxygen. Incorporating regular exercise into your routine can contribute to long-term visual health.
Keeping Vision Clear and Sharp: Regular Check-ups
Routine eye exams are crucial, even if your vision seems perfect. Conditions like glaucoma and macular degeneration often have no early symptoms, making early detection vital.
Eyesight Longevity Practices: Holistic Wellness
Adopting a holistic approach to wellness, including stress management, a balanced diet, and regular exercise, can significantly contribute to the longevity of your eyesight.
Frequently Asked Questions (FAQs)
Q: Can I improve my eyesight naturally?
A: While some natural practices and exercises might enhance visual acuity, it’s essential to consult an eye care professional for personalized advice.
Q: How often should I have my eyes checked?
A: It’s recommended to have a comprehensive eye exam every one to two years, even if you have no apparent vision problems.
Q: Are there specific foods that promote eye health?
A: Yes, foods rich in vitamins A, C, and E, as well as omega-3 fatty acids, can support eye health. These include carrots, spinach, citrus fruits, and fatty fish.
Q: Can digital screens damage my eyes?
A: Prolonged screen time can lead to digital eye strain, but using proper lighting, taking breaks, and using blue light filters can help mitigate potential damage.
Q: Is it necessary to wear sunglasses?
A: Yes, wearing sunglasses with UV protection is crucial to shield your eyes from harmful UV rays, which can lead to long-term damage.
Q: What’s the 20-20-20 rule?
A: The 20-20-20 rule suggests taking a 20-second break every 20 minutes of screen time and focusing on something 20 feet away to reduce eye strain.
Prioritizing your eye health is a long-term commitment that involves a combination of proper habits, regular check-ups, and a healthy lifestyle. By incorporating the practices and strategies outlined in this guide, you can enjoy clear and sharp vision throughout your life. Remember, your eyes are your windows to the world—take care of them, and they’ll continue to show you its beauty.
Tatum Eyecare is North Phoenix’s premier family eye care center. We’ve spared no expense to create the most pleasant, comfortable patient experience… including the finest furnishings, the best selection of prescription eyeglass frames, the most cutting-edge technology, and the most outstanding team of industry professionals. Come see why the choice for family eye care in the Valley has never been clearer. | {
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-3,558,078,784,500,119,600 | Can a Dental Splint or Mouthguard Really Help with TMJ Pain?
Can a Dental Splint or Mouthguard Really Help with TMJ Pain?
added on: March 31, 2024
Temporomandibular Joint Disorder (TMJ) is a condition that affects the jaw joint and the muscles surrounding it, leading to symptoms like pain, stiffness, headaches, and difficulty in jaw movement. Many individuals suffering from TMJ pain seek effective solutions to alleviate their discomfort, oftentimes without success. However, dental splints and mouthguards have gained popularity as potential treatments for TMJ pain and jaw discomfort, and may just be the right solution for you.
Understanding TMJ Pain
Before delving into the potential benefits of dental splints and mouthguards, it’s crucial to comprehend the nature of TMJ pain. The temporomandibular joint – or the TMJ – acts as a hinge connecting the jaw to the temporal bones of the skull. When this joint becomes misaligned or experiences excessive stress, it can result in TMJ pain. Common symptoms include jaw pain, difficulty chewing, clicking or popping sounds, and even headaches.
Are Dental Splints a Viable Solution for TMJ?
Dental splints for TMJ pain, also known as splint therapy or occlusal splints, are custom-made devices designed to fit over the teeth. They aim to stabilize the jaw joint and prevent excessive clenching or grinding, which are often associated with TMJ pain. These splints are typically worn during sleep, allowing the jaw muscles to relax and reducing strain on the temporomandibular joint.
In fact, research suggests that dental splints can be effective in managing TMJ pain by promoting proper jaw alignment and reducing the impact of habits like teeth grinding. However, the success of splint therapy varies among individuals, and it may not be a one-size-fits-all solution. It’s essential for individuals experiencing TMJ pain to consult with a dentist for a comprehensive assessment and personalized plan for TMJ treatment in Springfield.
Mouthguards for TMJ Pain Relief
Mouthguards, commonly associated with athletes for protecting teeth during sports activities, can also play a role in managing TMJ pain. These devices are worn over the teeth to prevent grinding and clenching. By creating a barrier between the upper and lower teeth, mouthguards help reduce the strain on the jaw joint and alleviate TMJ-related symptoms such as jaw pain or headaches.
TMJ Treatment
While dental splints and mouthguards can offer relief for some individuals, it’s crucial to recognize that they are just one component of a comprehensive TMJ treatment plan. Seeking professional guidance from a dentist experienced in TMJ disorders is essential for accurate diagnosis and personalized care.
If you’re looking for jaw pain or headache treatment in Springfield, you may just want to call your dentist, especially if nothing else has worked. Dental splints and mouthguards can be valuable tools in managing TMJ pain, but they are most effective when integrated into a comprehensive treatment plan. Always be open to talking with your dentist about any and all of your bodily symptoms, whether or not you think they’re related to dentistry. After all, they just may have the solution you’re looking for. | {
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-93,237,963,094,483,870 | Help with lossing weight and maintaining_Nutrition Dieting
Home Question and Answer Weight Loss Tips Common Sense To Lose Weight Weight Loss Recipes
Lose Weight > Question and Answer > Nutrition Dieting > Help with lossing weight and maintaining
Help with lossing weight and maintaining
8/17 9:17:46
Question
Hello Reverend, I am here to ask about how to loss 10 pounds without starving... and being extremly cranky lol. I am 5.4 in height 16 years old and 145 pounds and have meduim/large bone stamina(only "dumpy" child out of five lol). I have the extra weight around my lower belly and thighs and would like to take away my "pilsbury dough boy" roll and have my thighs thinner. I recinitly got an exercise bike from sears its a free spirit... works great but I seem to get sore legs when I use it(I put it on 2 or 3 and pedel relitivly slow)... is there a way to make my legs not get sore from doing this? I walk my two dogs daily... one by one(i've got two) and walk to the shops near by at the very lest every two days(sometimes twice a day), I don't like just sitting around. I hav dieted on and off for almost a year now... its getting anoying... when I come off the diets I eat too much and then in two weeks am over weight again and start over only to have history repete itself over and over. When I diet normaly I crach diet... 600/800 calroies a day, Slim & Trim diet pills(no enfedimen... only herbl green tea extract and gensing root... too boost matablizem), I also normaly do hundreds of sit ups a day during these crash diets and tons of light weight lifting arm curls/extream dance sesions and run with my dogs instead of walking them... it was its flaws.. I get very Sore, Crabby, irritable... snappy with other people and some times am very tired and rest when not doing my exercises... don't get me wrong these diets work but I hat ehtey way I act when I'm on there(hateful towards other...extremly). I want to lose the ten pounds because I'd like to fit better into my old pants and not feel so bad when I look at how wide my legs are at the thigh and not have to see that belly roll, I am hoping you can help me... I really don't want to go on a crash diet again and hgope to lose this weight very soon, I look forward to hearing from you,
ps; I could also use advice on maintaining weigh once dieting is over with,
Tara.
Answer
Tara,
Let's start with your 揹ieting? Your 揷rash diet?is very unhealthy. When you reduce calories to lose weight, you should not go below 1200-1500 calories a day. Reducing you total daily calories to 600-800 is a very bad idea. Your body will go into 搒tarvation mode??your metabolism will slow WAY down and you body will hold onto every calorie it can. When you stop your 揷rash diet?you will almost certainly gain weight. You are setting yourself up for failure with this type of diet. DON'T DO IT AGAIN! Taking diet pills to keep your metabolism up is not a good idea. Diet pills are just stimulants and probably add to your cranky, hateful mood. Also, if you read the fine print on the bottle or advertisement, it will say that weight loss should occur when taken with a healthy diet and regular exercise program. In my opinion, diet pills are not safe or effective enough to be used.
A healthy weight-loss diet will consist of a variety of healthy foods ?fruits, vegetables and whole grains. It will also avoid unhealthy foods ?high-fat meats, whole fat dairy products and foods with refined grains or added sugar (simple carbohydrates). You need to reduce your total calorie amount enough to begin to lose weight (but not below 1200-1500 calories a day). If you imagine your typical healthy meal (not a meal while you are 揹ieting?or binging) and cut the amount of food by 30%, that should be an appropriate sized meal. Call it the 70% meal ?you eat 70% of what you normally would. You won't be starving yourself, but you will be cutting some calories.
Your exercise routine should probably be more moderate also. You should not be exercising so hard or so long that you always have sore muscles. I like your pedaling speed of 搑elatively slow? and if done for 10, 15 or 20 minutes in the beginning, you shouldn't get sore legs. After a couple of weeks of 10-20 minutes most days, then you can increase the time by 5 minutes a day. Doing 揾undred of sit-ups a day?and 搕ons of weight lifting?is too extreme. Again, you are setting yourself up for failure by. Too much exercise at one time will certainly lead to sore muscles and this means you won't want to exercise or simply cannot continue exercising due to the pain.
Tara, you have a lot to learn about nutrition and exercise. I suggest you think about getting a couple of books to help you out. The American Heart Association's 揘o-Fad Diet?book is a great nutrition and weight loss book. The American College of Sports Medicine's 揂CSM Fitness Book?can help you learn about safe and effective exercise. Here are links to learn more about these books:
http://www.amazon.com/gp/product/1400051592/102-6044196-5931300?v=glance&n=28315...
http://www.amazon.com/gp/product/073604406X/ref=pd_sl_aw_alx-jeb-9-1_book_466035...
Lastly, at the young age of 16 years old, you need to be very careful about dieting. You are still growing and maturing and proper nutrition now is necessary to be healthy later in life. For example, your bone density as a mature adult is largely determined by your lifestyle today. Poor nutrition now can lead to poor bone healthy later in life. Also, your 揷rash diet?and obsession with weight loss means that you are at higher risk of developing an eating disorder. Eating disorders can damage your body for the rest of your life and leads to the deaths of many young adults. Please be very careful!
Moderation and persistence are the keys to success. Also, healthy diets, exercise routines and body weight are life-long habits. You cannot eat right occasionally or exercise occasionally and expect to maintain a healthy weight. Maintaining a healthy wieght means continuing with your healthy diet and regular exercise, except you can ease up just a little on your exercise and lower calorie diet.
Best of luck.
Todd
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2,613,196,166,655,853,000 | Fluoride Treatments
There's a new dental practice in Denver, CO
What are Fluoride Treatments?
A fluoride treatment can help to protect and strengthen your teeth. They are helpful when you’re prone to cavities and tooth decay, or if you already have a lot of fillings in your teeth. Fluoride treatments are especially beneficial for children, as they are more prone to developing tooth decay. These treatments can be done easily in our office and take just seconds to apply.
Why are Fluoride Treatments needed?
Fluoride is found in most dental products and public water sources. However, if you’re not getting enough fluoride, your dental health can suffer because of it. Likewise, if you’re more prone to cavities or have multiple fillings already, we may suggest fluoride treatments. Children often have these treatments automatically applied at their bi-annual checkup visits.
What Are Fluoride Treatments
Who Is A Candidate For Fluoride Treatments
Who is a candidate for Fluoride Treatments?
Any patient, regardless of age, is a candidate for fluoride treatments. Whether you want to protect your teeth further or are looking for a way to prevent the need for additional dental work, fluoride treatments are a suitable and easy option. Fluoride can even be applied to your teeth in conjunction with other procedures. This means you can have fluoride added to your teeth during an exam and cleaning.
What happens during the Fluoride Treatment process?
First, the teeth are cleaned and dried. The fluoride is then brushed onto the teeth and allowed to soak in. It will strengthen the teeth and prevent tooth decay. You will be told not to eat or drink for about 30 minutes following the procedure. It takes just seconds to apply the fluoride to your teeth, but you’ll find that it is incredibly helpful in protecting your smile. Fluoride is useful for both pediatric and adult teeth as a way to keep those beautiful smiles as protected as possible. We offer these treatments in our family-friendly office for both new and existing patients.
If you would like to learn more about fluoride treatments and our low wait-time office setting, call us today and we will be able to get you in for a convenient appointment. | {
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8,603,954,775,556,601,000 | What Happens When Your Heart Races: The Shocking Truth
When your heart beats too fast, it can lead to various symptoms such as dizziness, shortness of breath, and chest pain. The heart is a vital organ that pumps blood and circulates it throughout the body.
It beats at a specific rate, which is usually around 60-100 beats per minute at rest for most adults. However, sometimes the heart may beat faster than usual, known as tachycardia. This can occur due to various reasons such as stress, anxiety, strenuous physical activity, or medical conditions like atrial fibrillation.
When the heart beats too fast, it may not pump blood efficiently, leading to symptoms like palpitations, lightheadedness, and fainting. It is essential to understand the causes and symptoms of tachycardia to seek prompt medical attention and prevent any complications.
What Happens When Your Heart Races: The Shocking Truth
Credit: intermountainhealthcare.org
Contents
Understanding The Science Behind Your Racing Heartbeat
The anatomy of the heart involves several essential components. The heart pumps blood throughout the body, thanks to its four chambers, blood vessels, and valves. Electrical signals control heartbeat, with the sinoatrial node setting the pace. When your heart races, this is usually due to an increase in adrenaline or stimulants.
Symptoms of a racing heart can range from feeling anxious, dizzy, or faint to chest pain and difficulty breathing. Understanding the science behind your racing heartbeat can help you stay calm and take necessary steps to manage it. Keep an eye on your heart rate, and talk to a doctor if you are concerned.
Uncovering The Causes Of A Racing Heartbeat
A racing heartbeat can be caused by various factors such as stress and anxiety. Panic attacks can also trigger heart palpitations. Physical exertion can cause an increase in heart rate, but it is usually temporary. Certain medications can affect the heart rate and rhythm, causing palpitations.
Some medical conditions such as hyperthyroidism and atrial fibrillation can lead to a racing heartbeat. It’s important to identify the underlying cause of palpitations and seek medical attention if necessary. In some cases, lifestyle modifications such as reducing stress or avoiding caffeine and alcohol can help.
Regular exercise, a balanced diet, and getting enough sleep can also support overall heart health.
The Dangerous Consequences Of An Uncontrolled Racing Heartbeat
A racing heartbeat can lead to dangerous consequences such as hypertension and high blood pressure. This can lead to heart failure, an increased risk of stroke, and even cardiac arrest. It’s important to monitor your heart rate and seek medical attention if it consistently exceeds normal levels.
If left untreated, a racing heartbeat can cause damage to your heart and potentially be life-threatening. It’s essential to maintain a healthy lifestyle, including diet and exercise, to prevent any heart-related issues. Don’t wait until it’s too late, take care of your heart and live a long, healthy life.
Getting Diagnosed And Treated For A Racing Heartbeat
If your heart beats too fast, getting a proper diagnosis and treatment is crucial. Diagnostic tests such as an electrocardiogram and echocardiogram can help determine the cause of your racing heartbeat. Medications such as beta-blockers and calcium channel blockers can be prescribed by a healthcare professional for heart rate control.
Medical procedures such as catheter ablation and pacemaker implantation can also be done to regulate the heartbeat. Adopting lifestyle changes such as maintaining a healthy weight, quitting smoking, and reducing stress can improve overall heart health and prevent future instances of a racing heartbeat.
It’s important to seek medical attention if you experience symptoms such as dizziness, chest pain, or shortness of breath during a racing heartbeat.
Frequently Asked Questions On What Happens When Your Heart Beats Too Fast
What Causes Your Heart To Beat Too Fast?
Your heart can beat too fast due to several factors such as stress, anxiety, dehydration, caffeine, excessive alcohol consumption, or underlying health conditions such as arrhythmias, hyperthyroidism, and heart diseases.
What Are The Symptoms Of A Fast Heartbeat?
Symptoms of a fast heartbeat may include palpitations, rapid or irregular heartbeat, shortness of breath, chest discomfort, dizziness, lightheadedness, fainting, or sweating.
How Is A Fast Heartbeat Diagnosed?
A fast heartbeat can be diagnosed through various tests such as an electrocardiogram (ecg), holter monitor, echocardiogram, stress test, blood tests, and physical examination.
Can A Fast Heartbeat Be Treated?
Yes, a fast heartbeat can be treated based on the underlying cause. Treatment options may include lifestyle changes, medications, procedures, or surgeries. It is important to consult a healthcare professional for proper diagnosis and treatment.
How Can You Prevent A Fast Heartbeat?
You can prevent a fast heartbeat by adopting a healthy lifestyle such as regular exercise, balanced diet, stress management, hydration, limiting caffeine and alcohol consumption, and avoiding smoking. Regular medical checkups can also help detect and prevent potential health problems.
Conclusion
It’s important to understand the potential consequences of having a fast heart rate. From simple causes like dehydration and caffeine consumption to more serious underlying medical conditions like arrhythmia and heart disease, a fast heart rate should not be ignored.
As we’ve explored, the symptoms that may accompany a fast heart rate can greatly impact one’s quality of life. However, there are steps that can be taken to manage it. Lifestyle changes such as stress reduction, adequate hydration, and regular exercise have shown positive effects on heart rate.
In more severe cases, medical intervention may be necessary. It’s always recommended to consult with a healthcare professional to determine the appropriate course of action. With that being said, being mindful of your heart rate and understanding the potential causes and consequences can ultimately lead to a healthier and happier life.
Click Here to Leave a Comment Below 0 comments | {
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Tips for faster recovery from sprained ankle
Sprained ankle prevention, sprained ankle prevention tips, sprained ankle causes, sprained ankle
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Picture this: Your school football team has made it to the finales. You have to play in the big game tomorrow but you accidentally fall and sprain your ankle. Now before you stress out in such a situation, let us tell you some expert-approved ways on how to heal a sprained ankle as soon as possible.
A sprained ankle is a common occurrence among athletes and people who routinely exercise. It is also considerably easy to prevent common foot and ankle injuries
In this article, Dr Anuj Chawla, best foot and ankle specialist in Gurgaon discusses some top tips for the prevention of ankle injuries and how to manage them.
What is a sprained ankle?
A sprained ankle happens when you hurt the ligaments in your ankles. Ligaments are flexible tissues that hold two adjacent bones together. You can sprain your ankle when you are rolling or twist it by mistake.
Common symptoms of a sprained ankle include:
• Swelling and bruising of the ankle
• Limited range of motion
• Pain and Instability
• Tender ankle
• Popping sound at the time of injury
How to heal a sprained ankle?
Athletes would understand how recurring sprained ankles are. However, this injury can also be healed comfortably. The following remedies can be applied at home if a person suffers from an ankle sprain.
Tips on how to heal a sprained ankle-
1. R.I.C.E.
The R.I.C.E approach is very popular and beneficial for a swift recovery. It is a traditional tried and tested healing method. The acronym R.I.C.E. stands for – Rest, Ice, Compression and Elevation, respectively.
Rest: If you suffer from any injury at any body part, the primary step is to give proper rest to the affected area. You should not engage in any activity that could worsen the swelling or pain.
Ice: Applying ice to the sprain has also been proved favourable in most cases. You should place an ice pack to the ankle to reduce swelling and pain. If an ice pack is not available, you can simply wrap some ice cubes around in a towel and use it.
Compression: Doctors recommend compressing the sprained ankle by using an elastic or crepe bandage. This helps in reducing the swelling and alleviates pain. It is also helpful in maintaining joint stability. While the bandage should be wrapped around firmly, you should not bind it too tight. If the bandage is excessively tight, it can obstruct blood circulation and cause numbness.
Elevation: The last step of the R.I.C.E. is to elevate the sprained ankle. Elevating the ankle helps to avoid the buildup of fluid in the joints. It is suggested that you should support the ankle by placing a pillow under it while sleeping. You should keep the ankle at an elevated level from the heart to help reduce swelling.
2. Protection
In severe ankle sprains which limit the ability of the person to walk, some form of protection is helpful to prevent worsening of the injury. Protection and immobilization can be in the form of a cast, pneumatic walker boots or ankle brace. In fact, the acronym for healing acute ankle sprain has been changed by many from RICE to PRICE so as to include protection.
3. Medicines
Non Steroidal Anti Inflammatory Drugs (NSAIDS) like ibuprofen and Voveran (diclofenac) have been proven to be of significant benefit in early healing These medicines work by reducing the pain and swelling and hence hastening the recovery.
4. Physical therapy
Exercises and rehabilitation play a paramount role in preventing stiffness, early recovery and prevention of recurrence in future. Physical therapy after an ankle sprain should be started after a brief period of rest of 5-7 days or after the plaster is removed. The rehabilitation for acute ankle sprain can be divided into 3 phases:
1. Stretching and mobilization- Gentle mobilisation of the ankle and stretching of calf muscles is started first to combat the stiffness, promote blood circulation, reduce the swelling and hence boost the process of healing.
2. Strengthening– Once the movement of the ankle is restored close to normal, strengthening of the muscles around the ankle needs to be initiated. Strengthening primarily focuses on muscles on the outer side and the front of the ankle, namely evertors and dorsiflexors respectively but it has to be done all around the ankle
3. Proprioception training- The most neglected yet the most important part of rehabilitation after an ankle sprain is prevention of recurrence. Proprioception or balance training plays an important role in this. It helps in improving the coordination between the brain and ankle without involving the eyes. Simple exercises like single leg stance with eyes open and closed can be started to improve balance training as soon as one recovers from ankle sprain.
5. Massage
You can also go to a verified healthcare provider and choose for lightweight massage. You may also do a gentle massage at home yourself.
Sprained ankle prevention tips
Besides effective management, ankle sprains can also be prevented. Since such injuries are frequent events in sports. Athletes need to learn about the prevention of ankle injuries.
Here are some useful tips to prevent foot and ankle injuries:
1. Warm-up before any sports activity – Whether you are about to participate in a marathon or hit the gym, you should always do warm up in advance. Light stretching, jogging and more are considered good warm-ups to prepare the body for a workout.
2. Wear proper footwear – The idea of playing football in heels is most bizarre. There is a variety of footwear made for their specific purposes. While playing a sport, you should wear shoes specifically designed for sports. These shoes have the right arch support that helps to prevent foot and ankle injury.
3. Replace old shoes – Even if you have the right footwear, it is important to ensure that they constantly offer the right arch support. If your sports shoes have worn out, you should replace them for the prevention of ankle injuries.
4. Avoid uneven surfaces – Everyone likes an adventure but none likes a sprained ankle. If your physical activity involves running, jumping or walking, you should avoid going to uneven surfaces. Flat surfaces help you play better and avoid injuries. Even in outdoor sports such as hiking, while you cannot completely avoid rocks and steps, you should watch out for the ones that may pose danger.
5. Do ankle exercises – Particular exercises can help to prevent foot and ankle injuries. You should include these exercises in your regular workout schedule. Some of the common exercises for ankle include:
• Ankle circle: You simply have to sit on a flat surface with your legs outstretched and move your ankles in a circular motion.
• Heel raises: This exercise requires you to stand against a wall or another support. You are required to keep your legs a few inches apart. Slowly lift your heels and stand on your toes. Hold that position for a few seconds and repeat.
6. Prevent recurrent injuries – If you have suffered from a sprained ankle earlier, your chances of hurting your ankle, again, increases. To avoid ankle sprains, you can use a tape at the sight of the previous injury or wear an ankle brace during the sporting event.
7. Choose physical therapy – A certified physical therapist would be able to help with your ankle sprain and recovery. You can choose to go for physical therapy if you have suffered from a seriously sprained ankle that may affect your physical ability or strength.
When to consult a doctor in case of a sprained ankle?
If your pain does not alleviate after implementing these tips, you should instantly seek medical support. You should consult your healthcare provider if:
• Your pain is worsening
• You are unable to walk at all
• Your swelling does not reduce
The concluding note
A sprained ankle usually heals on its own without clinical intervention. The above-given tips can help you to encourage the healing process for a quicker recovery.
To learn more about muscle and joint injuries, consult Dr Anuj Chawla, best foot and ankle specialist at the CK Birla Hospital.
Also, read: 4 Types of foot pain one should not ignore
Do you have a question?
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-4,474,717,556,666,301,400 | Food-Intake Stability and Variability in Acutely Ill Older Adults Hospitalized in Internal Medicine Units
Research output: Contribution to journalArticle
Abstract
Aims: To identify the factors that has an impact on infected pressure ulcers healing among the elder outpatients. Methods: A retrospective study of data from elder outpatients with an infected pressure ulcer was conducted to identify factors that may affect their healing. Data from the elder outpatients between January 1, 2017, and December 31, 2017, in a general hospital in Shanghai, China, who had an infected pressure ulcer that was assessed using the Pressure Ulcer Scale for Healing (PUSH), were abstracted. The following variables were examined: demographic characteristics (gender, age, culture background, marriage status, medical insurance), health status and disease data (chronic diseases, vital signs, mobility, nutrition, diagnosis, medication), laboratory values (albumin, hemoglobin, blood glucose), and pressure ulcer characteristics (stage, location, healing status, duration). Results: One hundred and eleven (158) patient records were identified. Patient mean age was 81.29 ± 9.62 years, the maximum age is 105, and the minimum age is 60. Most ulcers (64; 40.5%) were Stage III and located in the sacral area (87; 16.4%). The incidence of wound infection in elder outpatients with pressure injury was 27.3%. The average score of PUSH was 10.41 ± 3.137. Logistic regression revealed that diabetes, edema and wound duration were risk factors of the wound infection in patients with pressure injury (P<0.05), and regular treatment was a protective factor (P<0.05). Conclusions: Wound infection is a common complication of patients with pressure injury. The elder outpatients with diabetes, edema and long lasting wounds (≥1 month) are at a high risk of wound infection and healing.
Original languageEnglish
Pages (from-to)490-491
Number of pages2
JournalInnovation in Aging
Volume2
Issue numbersuppl1
DOIs
StatePublished - 2018
Event21st International Association of Gerontology and Geriatrics (IAGG) World Congress - Moscone West San Francisco, San Francisco, United States
Duration: 23 Jul 201727 Jul 2017
https://www.geron.org/membership/27-meetings-events/821-iagg-2017-world-congress-of-gerontology-and-geriatrics
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A Doula Explains Why Eating the Placenta Is Beneficial to Moms
PHOTO BY Pixabay
• Taking placenta pills after giving birth has been a growing practice in the U.S. (and in the Philippines) because it is believed to help prevent postpartum depression and after-birth conditions. While doctors have said there is not enough scientific data available to back this up, it hasn't stopped moms like Paula Peralejo-Fernandez from ingesting placenta pills, which was prepared and made by her doula, Irina Otmakhova of Conscious Birth Manila, who also made placenta art for Paula.
SmartParenting.com.ph reached out to Otmakhova to get answers to the most common questions preggos and moms might have on placenta consumption, whether they're considering the practice or not. She studied placentophagy (consumption of the placenta) and placenta encapsulation methods with Placenta Benefits and International Association for Placenta and Postpartum (IPPA). She experienced its benefits first hand after giving birth in 2013.
When did the practice of consuming one’s placenta start?
Consuming the placenta is considered traditional medicine in China. According to Otmakhova, placenta consumption started gaining popularity around the same time the natural birth movement did when the decision-making authority when it came to childbirth was returned to mothers.
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What kind of benefits does placenta consumption offer?
"Most of the benefits of consuming the placenta are directly for the mother, but indirectly for the baby through mother's good energy level, abundant milk supply and mitigated postpartum mood swings," Otmakhova said. The iron in the placenta can help the mom fight anemia, increase her energy levels, and decrease fatigue and depression.
Placenta capsules are said to balance and even increase the production of certain hormones: estrogen, progesterone, and testosterone; prolactin; prostaglandin; Human Placental Lactogen (hPL); thyroid stimulating hormone; and oxytocin. All these hormones help to prepare the mother's body for lactation, enhances the bond between mother and child, regulates uterine cramping and help the woman's body to return to its pre-pregnant shape.
One hormone deserves particular attention: the Corticotropin Releasing Hormone (CRH), which helps reduce stress during pre-birth and actual labor. Otmakhova explains: "During the third trimester, the placenta functions as part of the endocrine system, pumping hormones, such as the iron-rich corticotropin-releasing hormone (CRH) into the [mother's] bloodstream. The placenta secretes so much CRH during the third trimester that scientists believe the hypothalamus stops producing it as a result."
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After the baby's birth, "[the new mom] loses not only the chemicals stored in the placenta but also the main hormone maker," she continues. Postpartum depression indicates low levels of CRH, and "it takes the hypothalamus about two weeks to reach rebirth levels of hormone output, hence consuming placenta packed with CRH helps in preventing postpartum depression," Otmakhova said.
How are placenta capsules made?
Otmakhova personally handles placenta encapsulation using the traditional Chinese method (TCM) for placenta encapsulation. She steams the placenta with heating herbs, dehydrate it for 10 hours, and put it into capsules. She says it's the safer method given our country's hot and humid climate.
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Another method of placenta encapsulation is the raw preparation method, which, Otmakhova believed, was used for the case that recently made headlines. She is referring to the baby who fell ill with Group B Streptococcus (GBS). According to the report by the U.S. Centers for Disease Control and Prevention (CDC), the unhygienic preparation of the placenta capsules, which the baby's mom took, likely caused the baby's bacterial infection.
"It did not involve heating through steaming but proceeds directly to dehydrating the raw slice of the placenta," she explained. "The enzymes contained in the placenta stayed intact, but there is a risk that not all bacteria has been dealt with during the preservation."
How does one take placenta pills?
In Otmakhova's practice, the dosage and number of placenta pills can range from taking one to two capsules twice a day to three capsules three times a day. "[A new mom] can always adjust the daily intake depending on [her] needs," she said. She prescribes dosage based on the following questions:
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• How are you feeling emotionally? Do you have any crying episodes or "baby blues?"
• How is breastfeeding going? Has the milk supply come in already?
• How is your energy level? Are you getting enough sleep?
• Are you eating enough?
• Do you feel any “after pains” or postpartum cramping?
Aside from taking placenta capsule during the first few weeks after giving birth, Otmakhova also advises new moms to set aside at least 10 to 20 pills to take during the onset of their first menstrual cycle after childbirth.
Since placenta capsules mostly help in hormone production, Otmakhova recommends that moms who have an overabundant supply of breast milk should never exceed taking nine capsules in 24 hours. Those who want to stop taking them should gradually reduce the number of pills they take in a day instead of quitting cold turkey.
Aside from placenta encapsulation, Irina Otmakhova of Conscious Birth Manila also makes placenta tincture, salve, and prints, as well as umbilical-cord keepsakes. Visit her website and Facebook page for inquiries.
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Open Access Article
This Open Access Article is licensed under a
Creative Commons Attribution 3.0 Unported Licence
A ratiometric fluorescent probe for imaging and quantifying anti-apoptotic effects of GSH under temperature stress
Xiaoyue Hanab, Xinyu Songa, Fabiao Yu*a and Lingxin Chen*a
aKey Laboratory of Coastal Environmental Processes and Ecological Remediation, Research Centre for Coastal Environmental Engineering and Technology, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, China. E-mail: lxchen@yic.ac.cn
bUniversity of Chinese Academy of Sciences, Beijing 100049, China
Received 30th June 2017 , Accepted 11th August 2017
First published on 11th August 2017
Hypothermia and hyperthermia are cell stressed states resulting from environmental temperature changes, which can abnormally decrease intracellular glutathione (GSH) concentrations and induce apoptosis. As the most abundant intracellular non-protein biothiol, GSH can protect cells from apoptosis. Considering the important roles of GSH in the anti-apoptotic process in cells and in vivo, we strive to develop a powerful chemical tool for the direct detection of GSH concentration changes under temperature stress. Herein, we report a ratiometric fluorescent probe (CyO-Dise) based on a selenium–sulfur exchange reaction for the qualitative and quantitative detection of GSH concentration fluctuations in cells and in vivo. The probe has been successfully used to assess the changes of GSH levels in HepG2 and HL-7702 cells using the stimulations of hypothermia and hyperthermia. In terms of the anti-apoptotic effect of GSH under hypothermic and hyperthermic conditions, human normal liver HL-7702 cells have stronger abilities to fight against temperature stress than human liver carcinoma HepG2 cells. Hypothermia and hyperthermia can also improve the drug resistance of cis-dichlorodiamineplatinum(II) (DDP)-resistant HepG2/DDP cells. The CyO-Dise probe has been employed to image GSH concentration changes in HepG2 and HepG2/DDP xenografts on nude mice. With the adjuvant therapy effects of hypothermia and hyperthermia, the chemotherapy drug DDP exhibits good ability for the treatment of HepG2 and HepG2/DDP xenografts. The above applications make our probe a potential new candidate for the accurate diagnosis of cancer and efficacy evaluation of treatment.
Introduction
The body temperature of mammals needs to be kept constant. Organisms often suffer from environmental temperature stress, including hyperthermia and hypothermia. Hyperthermia is a state within the temperature range of 39–50 °C,1 which invokes a series of cellular responses, involving metabolic pathways, inflammation reactions and apoptosis processes.2 Moreover, hyperthermia can induce the over-generation of intracellular reactive oxygen species (ROS), such as O2˙ and H2O2.3 The overproduced ROS will lead to oxidative damage to proteins, lipids, and nucleic acids. Therefore, hyperthermia can cause oxidative stress and result in cell apoptosis.4 To eliminate the excessive ROS, normal cells possess strong antioxidant defense systems, such as antioxidant enzymes, which produce reductive substances and antioxidant proteins. However, cancer cells lose most of the antioxidant capacity; they are more susceptible to heat injury than normal cells.5,6 The hypothermia state of an organism is usually within the range from 4–32 °C.7 Hypothermia affects the modulation of the cell cycle, metabolism, transcription, and translation.8 Hypothermia has been utilized to provide protection of nerve tissue from ischemia/reperfusion injury,9 however, long-term hypothermia will cause some complications, such as respiratory blockades, heart failure, and infection.10 Similar to hyperthermia, hypothermia can also induce the over-release of ROS, which is the main factor for cell apoptosis or necrosis.11,12 Although both hyperthermia and hypothermia can bring oxidation stress to an organism, the key point of ROS elimination has been attributed to the anti-oxidation of biothiols.13
Glutathione (GSH) is the most abundant intracellular non-protein thiol for cellular antioxidant defense systems. GSH serves as the key mediator in many cellular events, including the maintenance of intracellular redox activity, xenobiotic metabolism, intracellular signal transduction, and gene regulation.14 The overall concentration of GSH in cytosol ranges from 0.5 to 15 mM, depending on the cell type, with an overall ratio of GSH (reduced form)/GSSG (oxidized form) ranging from 30[thin space (1/6-em)]:[thin space (1/6-em)]1 to 100[thin space (1/6-em)]:[thin space (1/6-em)]1.15,16 Owing to the high concentrations and the irreplaceable performance of GSH in cells, we reason that GSH must play a vital role in the control of redox homoeostasis during the hypothermia or hyperthermia process. We strive to establish the relationship between the behaviour of GSH and the cell state when organism suffers from hypothermia or hyperthermia.
The traditional methods that have been developed to determine the intracellular GSH concentration in the hypothermia or hyperthermia process are the enzymatic recycling method and electrochemical method.13 However, these methods are time consuming and need tedious sample pre-treatments. It is challenging to achieve in situ and real-time detection in living cells. Fluorescent probes are indispensable tools for bioimaging and detection, because this technology directly allows non-invasive examination of biological living samples in situ and offers various parameters at the biomolecular level with high spatial and temporal resolution.17–20 Fluorescent probes based on small molecule dyes are of particular significance due to their small size, the possibility to finely tune their properties, and the ease of chemical modification.21–24 Fluorescent probes for the detection of GSH have been elegantly developed.25–27 These presented probes are mainly designed based on the strong nucleophilic properties of GSH, such as Michael addition28,29 and halogen nucleophilic substitution,30,31 as well as the cleavage of sulfonamide,32 sulfonate ester,33 nitroazo ether,34 the selenium–nitrogen bond,35,36 and disulfide.37 However, no fluorescent probe has been reported to quantify the fluctuation of GSH in living cells and in vivo under hyperthermic or hypothermic stress. Additionally, it is also required to explore new detection mechanisms for intracellular GSH. We now attempted to develop a fluorescent probe based on a new detection mechanism for the quantification and evaluation of the anti-apoptosis effect of GSH in cells and in vivo under hypothermic and hyperthermic conditions.
Herein, we designed and synthesized a ratiometric near-infrared (NIR) fluorescent probe, CyO-Dise, for direct qualitative and quantitative detection of GSH fluctuations during hyperthermia and hypothermia processes in living cells and in vivo (Scheme 1). The detection mechanism was inspired by the selenium–sulfur exchange reaction. The probe CyO-Dise was composed of three moieties. The ketone cyanine fluorophore (Keto-Cy) was modified with the response unit bis(2-hydroxyethyl) diselenide via an ester linkage and targeting moiety D-galactose through a click reaction. The intracellular GSH triggered the rearrangement of the π-conjugated system in the fluorophore, which resulted in a fast ratiometric fluorescence response. As far as we know, CyO-Dise is the first fluorescence tool for imaging and quantifying the anti-apoptosis effects of GSH in cells and in vivo under hypothermic and hyperthermic conditions.
image file: c7sc02888a-s1.tif
Scheme 1 The structure of CyO-Dise and proposed selenium–sulfur exchange reaction through an intramolecular cyclization reaction.
Results and discussion
Design and synthesis of the CyO-Dise
Intracellular GSH is maintained at millimolar concentrations (0.5–15 mM).38 The concentrations are generally higher than those of fluorescent probes (mainly ∼ μM) in living cells. Therefore, most of the reported fluorescent probes failed to qualitatively determine intracellular GSH. To accurately evaluate the fluctuations of GSH concentration during hypothermia and hyperthermia, we strived to develop a new fluorescent probe for the detection of GSH in cells. To qualitatively analyze GSH concentration at the millimolar level, the new probe should respond to changes of GSH levels with desirable reaction kinetics and thermodynamics. Taking the above factors into account, we were inspired by the selenium–sulfur exchange reaction.39 According to our previous work,40 we introduced a more reactive ester bridge instead of an amide junction in order to improve the reaction kinetics and thermodynamics of diselenide (R–Se–Se–R) towards GSH (Scheme 1). To verify this hypothesis, we computationally evaluated the detailed free energy barrier of the activation processes by GSH via molecular dynamics simulations and first-principles quantum mechanical/molecular mechanical free energy calculations. The calculation method is described in the ESI. The computational results clearly revealed the corresponding free energy profile of the exchange reaction through the intramolecular cyclization reaction (Scheme S2 and Fig. S3). From all of the molecules, the free energy barrier of the molecule containing a reactive ester bridge was calculated to be 49.6 kJ mol−1, while the molecule including an amide junction offered a high free energy barrier of 129.1 kJ mol−1. On the basis of the calculated free energy profiles, the reaction pathway of the ester bridge could be preferentially triggered by GSH. NIR absorption and emission profiles can maximize tissue penetration and minimize the absorbance of heme in hemoglobin and myoglobin, water, and lipids.41,42 Ratiometric probes can avoid various interference factors such as uneven loading or the inhomogeneous distribution of the fluorescent probes in cells.43 Integration of the response modulator into the NIR ketone cyanine scaffold could achieve a ratiometric fluorescence signal, which provides a precise and quantitative chemical tool with high sensitivity and inherent reliability.44 As shown in Scheme 1, the detection of GSH triggered the selenium–sulfur switch reaction, and the ester bridge accelerated the nucleophilic addition reactivation of the –SeH group, releasing the fluorophore. The rearranged polymethine π-electron system modulated a blue shift in the emission spectrum,45 which made our probe CyO-Dise a suitable chemical tool for quantifying the changes of GSH concentration in living cells. Taking advantage of the asialoglycoprotein receptor (ASGP-R), which specifically expresses on the plasma membrane of mammalian hepatocytes and selectively accepts the terminal galactose residues on desialylated glycoproteins,46–48 we introduced the galactose-terminated ligand here to obtain the targeting capability of CyO-Dise for hepatocytes in vivo.
The synthesis of the probe CyO-Dise is shown in Scheme S1. The fluorophore Keto-Cy was derived from heptamethine cyanine (Cy) in our lab.40 After integrating acetyl-D-galactopyranoside into the fluorophore via the click chemistry reaction, the obtained compound CyO-R′ was next treated with triphosgene. When the solvent was blow-dried in a nitrogen stream, bis(2-hydroxyethyl) diselenide was proportionally added to the reaction system. After hydrolyzing the acetyl, the probe CyO-Dise was finally yielded. All of the details of the synthesis are described in the ESI.
Spectral properties and selectivity of CyO-Dise
The spectroscopic properties of our probe CyO-Dise were investigated under simulated physiological conditions (10 mM HEPES, pH 7.4). Upon the addition of GSH, the maximum absorption wavelength shifted from 788 nm (ε788 nm = 2.1 × 104 M−1 cm−1) to 530 nm (ε530 nm = 2.19 × 104 M−1 cm−1) accompanied by a color change from green to red (Fig. S1a). The fluorescence spectrum displayed a remarkable blue-shift from 785 nm (Φ785 nm = 0.04) to 615 nm (Φ615 nm = 0.13) in maximum emission wavelength (Fig. S1b and c). The ratio of fluorescence intensity (F615 nm/F785 nm) was positively correlated with GSH concentration (Fig. S1d) and CyO-Dise could selectively detect GSH without interference by other species (Fig. S1f). As shown in Fig. S1–S5, our probe was a good candidate for the qualitative and quantitative detection of GSH in cells and in vivo.
Endogenous GSH changes under hypothermic and hyperthermic conditions
Since our probe CyO-Dise had exhibited good sensitivity and selectivity towards GSH, we further investigated the potential utilization of CyO-Dise for the detection of GSH level changes in living cells. To assess intracellular concentrations of GSH, a human normal liver cell line (HL-7702 cells) and human hepatocellular liver carcinoma cell line (HepG2 cells) were selected as cell models. Prior to cell tests, MTT assays were performed to check the cytotoxicity of CyO-Dise. The high cell viability of CyO-Dise indicated that the probe displayed low cytotoxicity to living cells (Fig. S7). Cell imaging experiments were performed using laser scanning confocal microscopy. All of the tested cells were incubated with 10 μM CyO-Dise for 5 min at 37 °C before imaging. The ratiometric fluorescence images was constructed via two fluorescence collection windows, channel 1 from 740 to 810 nm (λex = 635 nm), and channel 2 from 580 to 630 nm (λex = 515 nm). Pseudo-color ratio images were reconstructed to indicate the ratio of the emission intensity of channel 2 images and channel 1 images at the same time point. Before imaging, the cells were set at 4 °C and 30 °C for 30 min as severe and mild hypothermia states, respectively. Also, the cells were pretreated at 40 °C and 44 °C for 30 min as mild and severe hyperthermia states, respectively. As shown in Fig. 1a, either HepG2 or HL-7702 cells showed increased fluorescence intensity signal ratios after being kept in hypothermia and hyperthermia states. Under different temperature conditions, the signal intensities were obtained in the order: 4 °C > 44 °C > 30 °C > 42 °C > 37 °C. After calculations using the regression equation in Fig. S1d, we obtained concentrations of GSH in HL-7702 and HepG2 cells (Table S1). The results demonstrated that the cells could generate GSH in order to protect cells from temperature stress. Compared with HepG2 cells, HL-7702 cells displayed a higher ratio of fluorescence signal intensity under hypothermic or hyperthermic conditions (Fig. 1a). The results illustrated that different kinds of cells had different abilities to generate GSH. If the cells were pretreated with 5 mM N-ethylmaleimide (NEM) for 30 min in order to consume all of the GSH, almost no ratioed fluorescence signal was observed in HepG2 cells or HL-7702 cells (Fig. 1a). The results indicated that our probe could selectively image GSH fluctuations in hypothermia and hyperthermia states in living cells. Flow cytometry analysis, a kind of high-throughput assay technology, was performed to verify the above results. The results (Fig. 1b and Table S2) were consistent with the pseudo-color ratio images results (Fig. 1a and Table S1). The average fluorescence intensities of CyO-Dise under hypothermic and hyperthermic conditions in Fig. 1a and the corresponding mean ratio intensities in Fig. 1b were further shown in Fig. 1c and d. Additionally, the GSH concentrations were further measured using a Total Glutathione Assay Kit (Table S3). The testing results were consistent with each other. All of the results revealed that the probe CyO-Dise could be applied as a facilitative tool to directly image GSH fluctuations in hypothermia and hyperthermia states in living cells.
image file: c7sc02888a-f1.tif
Fig. 1 Real-time GSH quantification with CyO-Dise (10 μM) in HepG2 and HL-7702 cells under hypothermic (4 °C and 30 °C) and hyperthermic (42 °C and 44 °C) conditions for 30 min with or without 5 mM NEM treatment. (a) Pseudo-color ratio images. (b) Flow cytometry analysis. (c) Histograms of average ratio intensities in (a). (d) Corresponding mean ratio intensity in (b). The data are shown as mean (±s.d.) (n = 7).
Evaluation the anti-apoptotic effects of GSH
It has been reported that hypothermia and hyperthermia stimulations would induce cell apoptosis. Since our probe had been successfully applied to image the GSH concentration fluctuations during hypothermia (4 °C) and hyperthermia (44 °C), we tried to evaluate the anti-apoptotic effects of GSH in different types of cells during the hypothermia and hyperthermia processes. Cells were divided into five groups according to different treatments: 4 °C and 30 min; 4 °C and 2 h; 37 °C (as control); 44 °C and 30 min; 44 °C and 2 h. Compared with the control group, the cells in Fig. 2a at either 4 °C or 44 °C for 30 min displayed increased ratio-fluorescence signals, but those in the 2 h groups showed decreased ratio-fluorescence signals for the same kind of cell. The hyperthermic state offers higher ratio-fluorescence signals than those of hypothermia at the same time point. Upon comparison of HepG2 cells with HL-7702 cells, the ratio-fluorescence signals of HepG2 cell groups were weaker than those of HL-7702 cell whether at hypothermia or at hyperthermia (Fig. 2a). This result suggests the fact that normal cells (HL-7702 cells) could respond more to GSH changes than cancer cells (HepG2 cells) under the stresses of hypothermia and hyperthermia. The data that were obtained from laser scanning confocal microscopy were further verified using flow cytometry (Fig. 2i). We found that the concentrations of GSH first increased and then decreased during both stimulation processes. These changes of GSH concentration suggested that the intracellular GSH plays important roles in cell self-protection. Under short-term temperature stress (30 min), the mechanism of cell self-protection had a rapid response to changes in temperature stress. However, long-term stimulations (2 h) by hypothermia and hyperthermia were beyond the ability of cell self-protection. Upon incorporation into cells, cysteine is rapidly used to synthesize GSH. In order to further check the anti-apoptotic effects of GSH during hypothermia and hyperthermia, exogenous cysteine was added to increase intracellular GSH concentration. As shown in Fig. S14, the high concentrations of GSH could evidently reduce apoptosis when the test cells suffered from temperature stress. The results showed that GSH plays anti-apoptotic roles under hypothermic and hyperthermic conditions. Glutathione reductase (GR) is a key enzyme that catalyzes the reaction of oxidized glutathione (GSSG) to the reduced form (GSH), while the elimination of GSSG by GSH mainly relies on glutathione peroxidase (Gpx).49 We employed Western blot analysis to examine the levels of the two enzymes in the two different types of cell (Fig. 2k and S15). It was obvious that the HepG2 and HL-7702 cells that were treated at 4 °C or 44 °C for 30 min expressed much higher levels of GR than those cells that were treated for 2 h, while Gpx was upregulated after the 2 h treatment compared to those cells which were treated for 30 min. The enzymes within the five groups proved to have similar effects on the trends of the fluctuations of GSH concentration, which were highly consistent with the results measured with our probe.
image file: c7sc02888a-f2.tif
Fig. 2 Evaluation of the anti-apoptosis effects of GSH in cells during hypothermia (4 °C) and hyperthermia (44 °C) states at time points of 30 min and 2 h. (a and b) Pseudo-color ratio images. (c and d) Mitochondrial membrane potential (ΔΨm) analyzed using JC-1. (e and f) Apoptosis analysis by Annexin V/7-AAD: viable cells (Annexin V−/7-AAD−), early apoptosis (Annexin V+/7-AAD−), late apoptosis (Annexin V+/7-AAD+), and necrosis (Annexin V−/7-AAD+). (g and h) TEM observation (scale bars: 2 μm). (i) Flow cytometry analysis of GSH concentrations using CyO-Dise. (j) Ca2+ concentration analysis using Fluo 4-AM. (k) Western blot analysis of GR, Gpx, Hsp70, and pro-caspase 3. Relative molecular mass is indicated on the right. β-Actin was used as a loading control. The experiments were repeated seven times (n = 7 per test) and the data are shown as the mean (±s.d.).
We next confirmed the cell apoptosis that was caused by temperature stress via several apoptotic markers. Calcium ions (Ca2+) are one of the most important secondary messengers, and are involved in regulating many physiological processes in cells and tissues.50 In the apoptotic processes, the Ca2+ concentration of cytoplasm increased. We tried to assess the Ca2+ concentration with Fluo 4-AM via flow cytometry. As shown in Fig. 2j and S12, Ca2+ concentrations sharply increased after hypothermia and hyperthermia as compared with the control sample. Hyperthermia led to more release of Ca2+ than hypothermia at the same treatment time point. The elevation degrees were positively correlated with the stimulation time, and the increased concentration in the HepG2 cells was higher than that of the HL-7702 cells under the same conditions.
The results illustrated that the decrease of GSH concentration would induce the release of Ca2+ into the cytoplasm, which implies mitochondrial apoptosis. Mitochondrial membrane potential (ΔΨm) is another biomarker in the early apoptotic stage of cells. The efflux of mitochondrial Ca2+ can result in a collapse of ΔΨm, which directly reveals cell apoptosis. ΔΨm can be measured using the J-aggregate-forming lipophilic cation 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbo-cyanine iodide (JC-1) through flow cytometry.51 The changes of ΔΨm were detected via the red/green fluorescence ratio. As shown in Fig. 2c, the decreased red/green fluorescence intensity ratios were detected in all hypothermia and hyperthermia stimulation groups. As displayed in Fig. 2a and i, hyperthermia led to a greater decrease in fluorescence intensity ratios than hypothermia at the same treatment time point. The degrees of decrease in the ratios were proportional to the stimulation time. It was clear that HepG2 cells suffered a more severe decrease in fluorescence ratios than HL-7702 cells under the same conditions. The results were consistent with those received from Ca2+ analysis. Mitochondrial membrane potential collapse, which was caused by the efflux of Ca2+, resulted in the activation of apoptosis.
We also used an Annexin V/7-AAD Apoptosis Detection Kit to analyze the percentage of early apoptotic, late apoptotic, and necrotic cells. As shown in Fig. 2e, the percentage of early apoptotic and late apoptotic cells increased under hypothermic and hyperthermic conditions. However hyperthermia led to more severe cell apoptosis than hypothermia at the same treatment time point. Although the 2 h treatment resulted in more serious apoptotic damage than the 30 min treatment, HepG2 cells displayed remarkably more apoptosis and necrosis when compared to HL-7702 cells. The subcellular structure of the cells under hypothermic and hyperthermic conditions for 30 min and 2 h were observed using transmission electron microscopy (TEM). The mild swelling on the mitochondria (Fig. 2g) demonstrated that cell apoptosis occurred under hypothermia and hyperthermia conditions. Hsp70 (Heat Shock Protein 70) can protect cells from the adverse damage caused by hypothermia and hyperthermia. We analyzed the expression levels of Hsp70 in HL-7702 and HepG2 cells using Western blotting (Fig. 2k and S15c). After stimulating hypothermia and hyperthermia, the levels of Hsp70 in the two types of cells increased. Interestingly, hyperthermia induced greater Hsp70 expression than hypothermia under the same conditions. With the passage of time, the expression levels of Hsp70 increased. However, HepG2 cells expressed lower levels of Hsp70 than HL-7702 cells. The activation of an apoptotic executor, caspase 3, was assessed using the levels of pro-caspase 3 (Fig. 2k and S15d). Under the conditions of hypothermia and hyperthermia, the levels of pro-caspase 3 would decrease. Hyperthermia induced a greater reduction of pro-caspase 3 than hypothermia. The longer temperature stress was maintained for, the lower the level of pro-caspase 3, and the apoptosis degrees of liver cancer cells are more severe than normal liver cells. The results demonstrated caspase 3 could be activated when stimulated by hypothermia and hyperthermia. Additionally, hyperthermia was more effective on the induction of apoptosis to hepatocellular carcinoma cell lines.
Buthionine sulphoximine (BSO) is an inhibitor for gamma-glutamylcysteine synthetase (γ-GCS).52 The addition of BSO will reduce the cellular GSH concentrations. The faint ratio of the fluorescence signal in Fig. 2b suggested low levels of intracellular GSH. We also checked the changes of intracellular Ca2+ concentration, cellular ΔΨm, and cell apoptosis. The treatment with BSO could cause increase of Ca2+ concentrations (Fig. 2j). When compared with Fig. 2c, the cells in Fig. 2d provided lower red/green fluorescence ratios. The cells in Fig. 2f exhibited higher apoptosis and necrosis than the cells in Fig. 2e. The TEM images showed serious damage on cell membrane, organelles, and nuclear membrane (Fig. 2h). These findings confirmed that GSH was of critical importance for anti-apoptosis during hypothermia and hyperthermia. After comprehensively examining the above experimental results, we had reason to suggest that normal HL-7702 cells possessed a stronger ability to resist hypothermia and hyperthermia than HepG2 cancer cells.
Mechanism of the bio-effects of GSH in drug resistance
As one of the commonly used chemotherapeutic drugs, cis-dichlorodiamineplatinum(II) (DDP) can induce DNA intrastrand crosslinks and inhibit the replication and transcription of cancer cells.53 Unfortunately, long-term administration can result in DDP-resistance due to the GS-X pump on the cell membrane.54 The efflux of DDP relies on the formation of a GSH–Pt complex. Since hypothermia and hyperthermia could induce the decrease of GSH levels, we performed additional assays to inspect whether hypothermia and hyperthermia could reduce DDP-resistance via the changes of GSH level. We selected the resistant HepG2/DDP cell line as test model. The DDP-resistant HepG2/DDP cells were harvested via a 5 month simulation by DDP.55 The cell model was verified via MTT assay, and it has a much higher IC50 value (27.93 μg mL−1) compared with 1.93 μg mL−1 of the HepG2 cells (Fig. S16). We then identified the relationship between the GSH concentration and apoptosis of HepG2/DDP cells in the presence of DDP under the hypothermic and hyperthermic conditions. The apoptotic levels of HepG2/DDP cells in different therapeutic groups were measured using an Annexin V/7-AAD assay. As shown in Fig. 3b, both hypothermia and hyperthermia facilitated more apoptosis of HepG2/DDP cells than the group that was only treated with DDP. We then detected the changes of GSH in all experimental cell groups. As illustrated in Fig. 3a and e, the chemotherapeutic drug DDP hardly induced the changes of GSH concentration, while hypothermia and hyperthermia led to a significant decrease of intracellular GSH. It was noteworthy that the concentration of GSH in the cell group co-treated with DDP and hypothermia/hyperthermia presented a much lower ratio, which revealed severe apoptosis. However, exogenous cysteine treatments in Fig. S22 did not induce more apoptosis of HepG2/DDP cells than the control group, which was due to the higher GSH concentrations in the cysteine pre-treatment groups. This result indicated that the decrease of GSH resulting from hypothermia and hyperthermia could improve the DDP-resistance of HepG2/DDP cells. This mechanism of apoptosis induction was further validated in the following experiments.
image file: c7sc02888a-f3.tif
Fig. 3 The mechanism of the anti-apoptotic effect of GSH in HepG2/DDP cells under hypothermia and hyperthermia conditions. (a) Pseudo-color ratio images. (b) Apoptosis analysis using Annexin V/7-AAD: viable cells (Annexin V−/7-AAD−), early apoptosis (Annexin V+/7-AAD−), late apoptosis (Annexin V+/7-AAD+), and necrosis (Annexin V−/7-AAD+). (c) Mitochondrial membrane potential analyzed by JC-1. (d) Western blotting analysis of p-JNK, Bax, Bcl-2, cytochrome c, pro-caspase 3, cleaved-PARP, and Hsp70. (e) Flow cytometry analysis of GSH concentrations using CyO-Dise. (f) A statistical analysis of p-JNK protein expression. (g) A statistical analysis of the Bax to Bcl-2 protein expression ratio. (h) Ca2+ concentration analysis using Fluo 4-AM. (i) A statistical analysis of cytochrome c protein expression. (j) A statistical analysis of pro-caspase 3 protein expression. (k) A statistical analysis of cleaved-PARP protein expression. (l) A statistical analysis of Hsp70 protein expression. β-Actin was used as a loading control. (m) The mechanism of bio-effects of GSH in drug-resistant cells under stimulations of hypothermia and hyperthermia. The data are shown as means (±s.d.) (n = 7). The differences between the data were analyzed via two-way ANOVA. *P < 0.05, **P < 0.01.
As a dominant reductive species in cells, GSH protects the cells from oxidative stress in mitochondria. The changes of GSH concentration are involved in many pathological processes, such as cancer and inflammation. Therefore, hypothermia and hyperthermia have been applied to cancer adjuvant therapy. We hypothesized that the improvement of the DDP-resistance for HepG2/DDP cells benefited from the decrease of GSH concentration under the simulation of hypothermia or hyperthermia. As is known, p-JNK is a trigger of mitochondrial apoptosis, which leads to the increasing ratio of two downstream signal proteins: Bax and Bcl-2.56 Then Ca2+ stored in mitochondria effluxes into cytoplasm, which results in mitochondrial membrane potential collapse. Now the cells are becoming apoptotic. The expression of p-JNK, Bax, and Bcl-2 were examined using Western blot analysis. The changes of Ca2+ concentration and ΔΨm were investigated via flow cytometry analysis. The cell model groups were set as described in Fig. 3a. Compared with the control, there was no difference in the expression levels of p-JNK (DDP-treated group, Fig. 3d and f). p-JNK could be upregulated in the cell groups under the condition of hypothermia or hyperthermia. As expected, the synergic effects between DDP and hypothermia/hyperthermia significantly promoted the upregulation of p-JNK. Similarly, the ratio of Bax and Bcl-2 were at higher expression levels with the synergic effects between DDP and hypothermia/hyperthermia (Fig. 3d and g). In terms of downstream effects, higher Ca2+ concentrations were detected in cytoplasm with the co-stimulation of DDP and temperature stress (Fig. 3h). The red/green fluorescence ratio of ΔΨm in Fig. 3c continued to decrease with the degree of mitochondrial Ca2+ efflux. The results revealed that GSH concentration changes caused by temperature stress played decisive roles in improving the resistance of HepG2/DDP cells.
Moreover, cytochrome c is also a downstream effector for Bax and Bcl-2. Cytochrome c is a hydrogen carrier in the electron transport chain, which is located on the mitochondrial outer membrane.57 Once the mitochondrial membrane potential collapses, cytochrome c releases into cytoplasm from mitochondria, and is an apoptotic mediator to activate the apoptotic executor cleaved-caspase 3 and results in the cleavage of PARP (poly ADP ribose polymerase) in the nucleus.58,59 We next evaluated the expression levels of cytoplasmic cytochrome c, cleaved-caspase 3 and cleaved-PARP under the stimulating conditions. As shown in Fig. 3d and i, the level of cytochrome c in cytoplasm increased during hypothermia and hyperthermia. The addition of DDP would cause a substantial increase of cytoplasmic cytochrome c due to the synergy of hypothermia or hyperthermia. The cleaved-caspase 3 and cleaved-PARP were at higher levels in the synergy group, which is consistent with the apoptosis results tested via Annexin V/7-AAD assay (Fig. 3d, j and k). We also examined the Hsp70 expression in the above testing groups (Fig. 3d and l). We realized that the increase in Hsp70 levels is only dependent on the temperature stress factors, regardless of the utilization of DDP. The results might indicate that Hsp70 was activated to protect the cells from temperature stress when GSH concentrations began to decrease.
Herein, we emphasized that the stresses coming from hypothermia and hyperthermia would lead to the decrease of intracellular GSH. The mechanism of the bio-effects of GSH in drug-resistant cells during hypothermia and hyperthermia is shown in Fig. 3m. For those drug-resistant cells that are involved in the participation of GSH, such as HepG2/DDP cells, the low level of GSH would avoid the efflux of DDP. Therefore, the adjuvant therapy via hypothermia and hyperthermia would help to improve the cell resistance. For the mitochondrial apoptosis pathway, the low concentration of GSH triggered the increasing expression of p-JNK, which resulted in the increasing ratio of Bax/Bcl-2. Next, the efflux of Ca2+ in mitochondria resulted in mitochondrial membrane potential collapse. After cytochrome c was released into cytoplasm from mitochondria, the apoptotic executor cleaved-caspase 3 was activated. Finally, the cleavage of PARP occurred in the nucleus.
Therapy efficacies of hypothermia and hyperthermia for HepG2 xenografts
Encouraged by the results that the stimulations of hypothermia and hyperthermia could induce cancer cell apoptosis via decreasing the concentration of GSH, we next strived to investigate the adjuvant therapy efficacies of hypothermia/hyperthermia, as well as synergistic therapy efficacies of the chemotherapy drug and temperature stress. HepG2 xenografts were established in nude mice until the tumor volumes typically reached around 200 mm3. Then the tumor-bearing mice were divided into six groups (Fig. 4, for details, see ESI). The therapy groups were given 28 day chemotherapy, hypothermia/hyperthermia, and collaborative treatments, respectively. We first measured the GSH concentrations in different test groups using an in vivo imaging system in vivo and ex vivo. After intravenous injection for 30 min, our probe CyO-Dise dominantly accumulated at cancer lesions, displaying a good targeting capability of our probe for HepG2 tumors. As shown in Fig. 4a, b, f and g, hypothermia and hyperthermia led to a decrease of intracellular GSH levels. However, the synergistic therapy of the chemotherapy drug DDP and temperature stress definitely reduced the concentrations of intracellular GSH. The results indicated that hypothermia and hyperthermia could enhance the synergistic efficacies with DDP via lowering the concentrations of intracellular GSH.
image file: c7sc02888a-f4.tif
Fig. 4 The evaluation of GSH efficacy in HepG2 subcutaneous tumor xenografts. (a) In vivo imaging for 30 min after tail vein injection of a single-dose 0.2 mL of CyO-Dise (DMSO/saline 1[thin space (1/6-em)]:[thin space (1/6-em)]1/v/v) (n = 7 per group). (b) Ex vivo imaging of GSH in separated organs (lung, heart, liver, kidney, spleen) and tumors sacrificed from (a). (c) Representative slides of H&E-stained tumors sacrificed from (a). Magnification: ×400. (d) Immunofluorescence staining of proliferation markers Ki67 (red channel: λex/em = 635/670–770 nm) with anti-Ki67 mAb (Alexa Fluor 647 Conjugate) and nucleus (blue channel: λex/em = 405/410–490 nm) with DAPI of tumor sections. Scale bar: 50 μm. (e) TUNEL staining of tumor sections. Magnification: ×100. (f) Average ratio intensity values of (a). (g) Ratio analysis of corresponding organs in (b). (h) A statistical analysis of the data derived from (d). (i) A statistical analysis of the data derived from (e). (j) Tumor sizes, where the calculation of the volume followed the formula: volume = length × width2 × 0.5. (k) Tumors mean weights. The error bars shown in the figures represents the mean ± s.d. The differences between the data were analyzed via two-way ANOVA except for tumor sizes. *P < 0.05, **P < 0.01. The differences between tumor sizes were analyzed via one-way ANOVA. *P < 0.05, **P < 0.01 vs. control group. #P < 0.05, ##P < 0.01 vs. chemotherapy group.
The changes of pathological morphology were examined using H&E sections (Fig. 4c), Ki67 immunofluorescence (Fig. 4d), and TUNEL staining (Fig. 4e). H&E sections illustrated that the synergistic therapy with hyperthermia and DDP completely curbed the development of live cancer cells. Cancer cells began to differentiate, and the bile duct had already been observed. Ki67 is a cell proliferation antigen, and the positive rate of Ki67 represents the active level of cell proliferation. The inhibition of Ki67 expression in Fig. 4d and h implied that the synergistic therapy with temperature stress and DDP offered more satisfactory efficacies than other groups. TUNEL staining directly reflects the cleavage of DNA and it can be used to evaluate apoptosis. As shown in Fig. 4e and i, hypothermia and hyperthermia contribute to cell apoptosis during the chemotherapy treatment of cancer. The sizes of tumors and the body weights of mice were assessed every two days during a 28 day period (Fig. 4j and k). According to our experimental results, hypothermia and hyperthermia would lead to a decrease in intracellular GSH concentrations, and then induced cell apoptosis. Moreover, the physical therapy could effectively enhance the efficacies of chemotherapy drugs, such as DDP. However, in terms of the overall treatment efficacies and easy operation, we would give priority to hyperthermia as one of the cancer adjuvant therapies.
Therapy efficacies of hypothermia and hyperthermia for HepG2/DDP xenografts
In the course of cancer therapy, the resistance and heterogeneity of cancer cells are challengeable problems, which need to be urgently settled. The synergistic therapy of a chemotherapy drug and temperature stress had been proven to be successful for the inhibition of the resistant HepG2/DDP cell line (Fig. 3). The nude mice model bearing HepG2/DDP xenografts were divided into six groups for our experiments (for details, see the ESI). As shown in Fig. 5a, b, f and g, the testing groups of mice with hypothermia and hyperthermia showed a decrease in GSH concentrations. Although chemotherapy drug DDP seldom influenced the changes of the GSH levels, the co-therapy groups provided a more significant decrease of intracellular GSH, which was the pivotal point in the improvement of cancer resistance.
image file: c7sc02888a-f5.tif
Fig. 5 The evaluation of GSH efficacy in HepG2/DDP subcutaneous tumor xenografts. (a) In vivo imaging for 30 min after tail vein injection of a single-dose 0.2 mL of CyO-Dise (DMSO/saline 1[thin space (1/6-em)]:[thin space (1/6-em)]1/v/v) (n = 7 per group). (b) Ex vivo imaging of GSH in separated organs (lung, heart, liver, kidney, spleen) and tumors sacrificed from (a). (c) Representative slides of H&E-stained tumors sacrificed from (a). Magnification: ×400. (d) Immunofluorescence staining of proliferation markers Ki67 (red channel: λex/em = 635/670–770 nm) with anti-Ki67 mAb (Alexa Fluor 647 Conjugate) and nucleus (blue channel: λex/em = 405/410–490 nm) with DAPI of tumor sections. Scale bar: 50 μm. (e) TUNEL staining of tumor sections. Magnification: ×100. (f) Average ratio intensity values of (a). (g) Ratio analysis of corresponding organs in (b). (h) A statistical analysis of the data derived from (d). (i) A statistical analysis of the data derived from (e). (j) Tumor sizes, where the calculation of the volume followed the formula: volume = length × width2 × 0.5. (k) Tumor mean weights. The error bars shown in the figures represent the mean ± s.d. The differences between the data were analyzed via two-way ANOVA except for tumor sizes. *P < 0.05, **P < 0.01. The differences between tumor sizes were analyzed via one-way ANOVA. *P < 0.05, **P < 0.01 vs. control group. #P < 0.05, ##P < 0.01 vs. chemotherapy group.
The H&E sections, the expressions of Ki67 and the DNA cleavage of our testing groups were investigated. Pyknosis was observed in the synergistic therapy of hyperthermia and DDP indicated good therapeutic effects on HepG2/DDP-bearing nude mice (Fig. 5c). The immunofluorescence of Ki67 showed that the adoption of temperature stress or chemotherapy alone could not desirably inhibit the proliferations of HepG2/DDP, unless using synergistic therapies, especially with hyperthermia accompanying the administration of DDP (Fig. 5d and h). The TUNEL staining illustrated DNA cleavage with the adjuvant therapies of hypothermia and hyperthermia (Fig. 5e and f). The tumor sizes, body weights and tumor weights were also recorded (Fig. 5j and k). The results displayed that the growth of cancer lesions could be efficaciously inhibited by the synergistic therapies. The triple therapeutics (GSH + chemotherapy + hypothermia/hyperthermia treatment) showed higher GSH concentrations and unsatisfactory therapeutic effects (Fig. S23). In one word, when the cell suffered from hypothermia or hyperthermia, the decreased GSH concentration in HepG2/DDP cells would be beneficial to improving the drug resistance.
Conclusions
We have developed a NIR radiometric fluorescent probe CyO-Dise for the evaluation of the anti-apoptotic effects of GSH in living cells and in vivo. The probe is composed of fluorophore cyanine, response unit bis(2-hydroxyethyl) diselenide, and targeting moiety D-galactose. Based on the selenium–sulfur exchange reaction, CyO-Dise can detect GSH within 35 s. With the help of CyO-Dise, we find that intracellular GSH plays important roles in anti-apoptosis when HepG2 and HL-7702 cells are faced with hypothermia and hyperthermia. The short-term temperature stress can cause increase in cellular GSH concentrations, while the long-term temperature stress can result in an abnormal decrease in the levels of cellular GSH. HepG2 cells (human hepatocellular liver carcinoma cell line) have a lower ability to resist risks of temperature stress than that of HL-7702 cells (human normal liver cell line). Moreover, hypothermia and hyperthermia can be used to improve drug resistance of the HepG2/DDP cells via reducing drug efflux and activating the mitochondrial apoptosis pathway. The probe has been successfully used to image the GSH levels of HepG2 and HepG2/DDP xenografts in vivo. The adjuvant therapy effects of hypothermia and hyperthermia have been applied to the therapies of HepG2 and HepG2/DDP xenografts. The synergistic therapy of the chemotherapy drug and temperature stress had been proven to be efficacious for the inhibition of cancer growth. We believe that our proposed strategy can be of benefit for the development of new chemical tools in the accurate diagnosis of cancer and evaluation of the efficacy of treatment.
Conflicts of interest
There are no conflicts to declare.
Animal Testing Statement
All experimental procedures were conducted in conformity with institutional guidelines for the care and use of laboratory animals, and protocols were approved by the Institutional Animal Care and Use Committee in Binzhou Medical University, Yantai, China. Approval Number: No. BZ2014-102R.
Acknowledgements
We thank the National Nature Science Foundation of China (No. 21405172, No. 21775162 and No. 21575159), the program of Youth Innovation Promotion Association, CAS (Grant 2015170), and the State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, CAS (Grant KF2016-22).
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Footnote
Electronic supplementary information (ESI) available: Experimental detail procedures, synthetic procedures and characterization details, reaction kinetics and selectivity, and additional data. See DOI: 10.1039/c7sc02888a
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1,698,117,159,073,504,800 | R allergy immunotherapy 9 3
06.01.2020| Mandi Mayers| 2 comments
r allergy immunotherapy 9 3
An exciting announcement from MDedge. Click here for more information. Pollart Dellyse. Bright atriumhealth. The evidence-based answers to these and other questions will help you to update your knowledge of allergy immunotherapy. A Good-quality patient-oriented evidence Aloergy Inconsistent or limited-quality patient-oriented evidence C Consensus, usual practice, opinion, disease-oriented evidence, case series.
• PRACTICE RECOMMENDATIONS
• Allergy and immunotherapy. - Free Online Library
• Allergy immunotherapy: Who, what, when … and how safe? | MDedge Family Medicine
• References
• Allergen immunotherapy - Wikipedia
• Immunotherapy for mosquito allergy
• Redness, swelling, or irritation right around the site of the injection is normal. These symptoms should go away in 4 to 8 hours.
PRACTICE RECOMMENDATIONS
A lot depends on how many things you're allergic to and how severe your symptoms are. Generally, allergy shots work for allergies to ommunotherapy stingspollendust mitesmold, and pet dander. Get on the phone and go to the nearest emergency room if you have shortness of breath, a tight throat, or any other symptoms that worry you after getting your shot.
EAACI Guidelines on Allergen Immunotherapy: Allergic rhinoconjunctivitis. (9)Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College London, London, UK. (10)Section of Allergology, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The lrpd.lion-wolf.ru by: 3. Golden, David BK, et al. "Venom immunotherapy reduces large local reactions to insect stings." Journal of Allergy and Clinical Immunology (): 4. Ariano, R., and R. C. Panzani. "Efficacy and safety of specific immunotherapy to mosquito bites." European annals of allergy and clinical immunology (): 5. Apr 01, · Free Online Library: Allergy and immunotherapy.(Report) by "Townsend Letter"; Health, general Allergic reaction Care and treatment Immunoglobulin E Immunoglobulins Health aspects Immunotherapy Methods.
There is another type of immunotherapy: three under-the- tongue tablets that you can take at home. Called Grastek, Oralair, and Ragwitek, they treat hay fever and boost your tolerance of allergy triggers.
Allergy and immunotherapy. - Free Online Library
During the first part of the treatment, you get doses of the allergen every day instead of every few days. Your doctor will check on you closely, in case you have a bad reaction. In some cases, you may get medicine before you get the dose of the allergen, to help prevent a reaction. They may be more risky for people with heart or lung diseaseor who take certain medications.
Allergy immunotherapy: Who, what, when … and how safe? | MDedge Family Medicine
Tell your allergist about your health and any medicines you take, so you can decide if allergy shots are right for you. Meta-analyses have found that injections of allergens under the skin are effective in the treatment in allergic rhinitis in children [3] allergyy and in asthma.
Side effects during sublingual immunotherapy treatment are usually local immunogherapy mild and can often be eliminated allergy adjusting the dosage. Potential side effects related to subcutaneous immunotherapy treatment for asthma and allergic rhinoconjunctivitis include mild or moderate skin or respiratory reactions.
Discovered by Leonard Noon and John Freeman inallergen immunotherapy is the only medicine known to tackle not only the symptoms but also the immunoyherapy of respiratory allergies.
Subcutaneous immunotherapy, also known as allergy shots, is the historical route of administration and consists of injections of allergen extract, which must be performed immunotherapy a medical professional.
References
Subcutaneous immunotherapy protocols generally involve weekly injections during a build-up phase, followed by monthly a maintenance phase that consists of injections for a period of 3—5 years.
The length of the build-up phase is dependent upon how often injections are administered, but normally ranges from three to six months. Sublingual immunotherapy involves putting drops or a tablet of allergen extracts under the tongue, which are then absorbed through the lining of the mouth. Sublingual immunotherapy has been demonstrated to be effective against rhinoconjuctivitis and asthma symptoms. Sublingual immunotherapy is used to treat allergic rhinitis, often from seasonal allergies, and is typically given in several doses over a 12 week period.
While a number of side effects have been associated with sublingual immunotherapy, serious adverse effects are very rare about 1. Oral immunotherapy OIT involves feeding an allergic individual increasing amounts of a food allergen in order to raise the threshold which triggers a reaction.
In desensitization immunotherapy the aim is to induce or restore tolerance to the allergen by reducing its tendency to induce IgE production. People are desensitized through the administration allergy escalating doses of allergen that gradually decreases the IgE-dominated response. Immunotherapy immunotherapy also creates an increase in allergen-specific IgG4 antibodies and a decrease in allergen-specific IgE antibodies, as well as diminished mast cells and basophilstwo cell types that are large contributors to allergic reaction.
Reactivity is tested using oral food challenges or with skin prick tests. However, phase 3 can be done at home.
Allergen immunotherapy - Wikipedia
In the late 19th century and early 20th century, allergic conditions were immuontherapy attracting both medical attention as an emerging public health problem and immunoyherapy interest aided by progress in biochemical techniques and the immnuotherapy of molecular and pathogenic theories.
However, the many and varied treatment approaches were very unscientific. The British physicians Noon and Freeman were the first researchers to test pollen allergen immunotherapy in humans. After the groundbreaking work by Noon and Freeman in the UK and by Cooke and colleagues in the US, allergen immunotherapy was part of mainstream medical practice for hay fever treatment immunotherapy the s.
Later, sublingual formulations were found to be effective in symptom reduction in allergic rhinitis. Sublingual immunotherapy is also found to have a better safety profile than subcutaneous immunotherapy since the local side effects caused by sublingual immunotherapy contrasted with the possible systemic events that can occur with the subcutaneous immunotherapy.
Sublingual a,lergy drops are currently commercialized and used in most European and South American countries, and in Australia and Asian countries. In most European countries, national regulations allegy marketing of allergen products allervy "named patient preparations" NPPs.
In the United States, drop formulations have not yet received FDA approval, though off-label prescription is becoming common. The use of subcutaneous immunotherapy for treatment of environmental-based allergies and asthma is well supported by the majority of national and international allergy groups such as allergy World Allergy OrganizationCanadian Society of Allergy and Immunology, European Academy of Allergy and Clinical Immunologyand the American Academy of Allergy, Asthma and Immunology.
The cost for allergen immunotherapy varies by country and administration route. There is no clear and holistic transparency across therapy forms. As of [update]oral immunotherapy's balance of risk to benefit for food allergies was not well studied. Studies involving OIT have shown desensitization towards the allergen.
However, there are still questions about longevity of tolerance after the study has ended.
r allergy immunotherapy 9 3
One approach being studied is in altering the protein structure of the allergen to decrease alleergy response but still induce tolerance. Extensive heating of some foods can change the conformation of epitopes recognized by IgE antibodies.
Immunotherapy for mosquito allergy
In fact, studies show that regular consumption of heated food allergens can speed up allergy resolution. In one study, subjects allergic to milk were 16x more likely to develop complete milk tolerance compared to complete milk avoidance. Another approach regarding changes in protein is to change specific amino acids in the protein to decrease recognition of the allergen by immunothwrapy antibodies.
Allergy Shots (Immunotherapy): Effectiveness, Side-Effects & Risks
Another approach to improving oral immunotherapy is to change the immune environment to prevent T H 2 cells from responding to the allergens during treatment. For example, drugs that inhibit IgE-mediated signaling pathways can be used in addition to OIT to reduce immune response.
2 thoughts on “R allergy immunotherapy 9 3”
1. Rudolph Ruder:
I saw one reference in the European literature from but none since. I have attached some of the questions in the archives of Ask The Expert related to mosquito allergy. In general, the quality of the materials for testing and treatment are not standardized nor consistent making the efficacy for immunotherapy unpredictable.
2. Fritz Frisk:
Allergy shots help your body get used to allergens, the things that trigger an allergic reaction. During that time, your allergy symptoms will get better and may even go away.
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4,647,713,078,934,113,000 | Dizzy Riding In A Car At Night
Dizzy Riding In A Car At Night
Vertigo is often the sensation of the whole world, moving, spinning, or rocking instantly when a person is standing perfectly still. Some people also use the word vertigo to explain numerous signs and symptoms, ranging from dizziness to nausea or vomiting and equilibrium problems. The following therapy options are often made use of to deal with wooziness and also vertigo. Dizzy Riding In A Car At Night
If your wooziness or vertigo has been diagnosed as a result of any kind of underlying medical condition, you should consult your doctor right away prior to starting any type of exercises. Even if the symptoms you are experiencing are not because of a clinical condition, you should still see your doctor to make sure that your signs are not a result of something else. Your physician will likely advise several workouts or other procedures to treat your vertigo.
Dizzy Riding In A Car At Night
Dizziness as well as vertigo are triggered by physical elements. Nevertheless, some people are born with a slight difference in their inner ears, which can create them to really feel dizzy. This is most generally called sensorineural hearing loss or even more commonly described as lightheadedness. Various other physical variables include bad muscle mass tone, consisting of the muscle mass of the tongue and the face muscular tissues, and/or irregularities of vision. Some signs that are considered milder variations of wooziness are: the sensation of running out your body, a feeling that gravity is kicking you in the belly, lightheadedness, vomiting, supplanting the ears, feelings like you are mosting likely to lose consciousness, feeling removed from your body or globe, seeming like you are freaking out, or sensations that absolutely nothing makes good sense. Dizzy Riding In A Car At Night
vertigo is typically treated by several of the adhering to therapy options. Depending on your signs as well as the extent of your instance, therapy may range from straightforward to complex and needs the focus of a medical professional with experience dealing with dizziness. Several of these treatment options are talked about listed below.
No therapy is permanent or necessary. Wooziness will certainly resolve itself. If you continue to have signs after two days or if your wooziness lasts for greater than three days, you must check out a medical professional. The physician will do a series of examinations to identify the source of your symptoms. Some reasons for wooziness may be momentary problems such as sleep apnea or balance problems caused by a just recently identified illness. Some diseases such as diabetic issues, Parkinson’s disease, and hyperthyroidism can also bring about wooziness and also require to be evaluated as well as dealt with.
Vertigo is usually associated with vestibular payment. This is a condition that triggers the internal part of the mind to perceive head activities as exterior stimuli. It can be treated with medicine, workouts, or a mix of treatments. The therapy alternatives will differ according to the extent of your wooziness. Your doctor may suggest that you put on a vestibular assistance gadget, avoid abrupt movements, or change your workout regimens.
It is normally safe to assume that vertigo begins when you least expect it. When you depend on one foot and also feel lightheaded, opportunities are you are currently in a raised setting. It is crucial that you keep your head and torso right at all times. For those who are continuously on the go, there are tools that you can use to avoid this problem from occurring; they are normally called tilt table disks or magnetic dental braces.
Fortunately is that most individuals do not experience major dizziness signs when standing or sitting for three times longer than advised. Long term resting can in fact trigger significant problems such as carpal tunnel syndrome, weak point of the jaw muscles, and damages to the inner ear. The very best thing that you can do is to take your time when resting, and also stand up when required. This will certainly aid to minimize your risk of having wooziness signs. | {
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4,830,497,743,354,245,000 | The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.
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The use of oxalate to reduce dentin permeability under adhesive restorations.
PURPOSE: To test a novel approach to reducing dentin permeability that localizes occlusion of dentin tubules by calcium oxalate crystals to the subsurface without lowering resin bond strengths to oxalate-treated dentin surfaces. MATERIALS AND METHODS: Flat dentin surfaces of extracted human third molars were etched with a mass fraction of 32% phosphoric acid (Bisco) for 15 s and rinsed. Half of the surface was treated with a potassium oxalate gel (mass fraction of 3% monopotassium monohydrogen oxalate) for 2 mins. The entire surface was then moist bonded with either One Step (OS) or Scotchbond Multi-Purpose (SB) adhesive systems. A resin-based composite (Z-100) buildup was made over the entire surface. After storage for 24 hrs in distilled water, the teeth were longitudinally sectioned to separate the oxalate-treated half from the untreated (control) half. Each half was serially sectioned into several 0.7 mm thick slabs which were then trimmed to an hour-glass shape to reduce the bonded area to approximately 0.8 mm2 and tested in tension. Pre- and post-treatment hydraulic conductance (Lp) of dentin was determined using dentin discs with a standard protocol. SEM images were obtained to examine the effects of treatment both on the dentin surface and along the tubules beneath the surface. The bonded interface was also examined by SEM. RESULTS: Treating etched dentin discs with the oxalate gel caused significant reduction of the Lp of dentin (80% reduction, P < 0.05). There were no statistically significant differences between bond strengths of oxalate-treated and untreated surfaces for either adhesive system. OS resulted in a bond strength of 25.8 +/- 9.2 MPa to untreated and 27.8 +/- 8.9 MPa to oxalate treated surfaces (P > 0.05). SB showed bond strengths of 22.9 +/- 7.9 MPa and 22.9 +/- 9.6 MPa to untreated and treated surfaces, respectively (P > 0.05). SEM images showed that the application of potassium oxalate gel on etched dentin resulted in the formation of crystals inside the tubules rather than on the surface. Examination of the bonded interfaces demonstrated that the crystal formation inside the tubules did not compromise the formation of a typical hybrid layer on the top of dentin surfaces. Resin monomers penetrated into the tubules filling the spaces around the crystals forming resin tags with a jagged-like feature.[1]
References
1. The use of oxalate to reduce dentin permeability under adhesive restorations. Pashley, D.H., Carvalho, R.M., Pereira, J.C., Villanueva, R., Tay, F.R. American journal of dentistry. (2001) [Pubmed]
WikiGenes - Universities
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-3,233,092,445,623,030,000 | Vertigo refers to a sensation of dizziness or spinning. Cervical vertigo is a type of vertigo that results from a certain neck posture or movement.
Some experts use the term "cervicogenic dizziness" to more accurately describe this condition. Other names for it include proprioceptive vertigo, cervicogenic vertigo, and cervical dizziness.
Although the effects of gravity or the orientation of the head influence vertigo, cervical vertigo is not related to the orientation of the head.
There are a few different causes of cervical vertigo, such as trauma to the neck or poor posture. Treatment involves addressing any underlying muscular or medical issues, and there are also ways to help prevent some forms of cervical vertigo.
This article looks at the causes, treatments, and diagnosis of cervical vertigo, and it discusses when a person should see a doctor.
a woman feeling dizzy because of cervical vertigo Share on Pinterest
Loss of balance is one symptom of cervical vertigo.
Vertigo is the medical term for severe dizziness or feeling a spinning sensation in the body.
A person may feel as though the world is spinning around them. They may also feel as if they are spinning around, even as they stand still.
Anyone who has spun in circles and then stopped has felt a form of vertigo. Once they stop spinning, it feels as if the body keeps spinning.
Vertigo often comes about due to an inner ear problem or other condition, which may throw off the body's center of balance. With cervical vertigo, however, the cause of the dizziness is in the neck.
Cervical vertigo itself is generally a symptom of an underlying issue, such as a neck injury. A person will often experience symptoms of dizziness after a triggering event, typically from turning their head suddenly. This dizziness may last for a few minutes to a few hours.
A person with cervical vertigo may also experience symptoms such as:
Symptoms may be worse in some people after they exercise, or after minor things such as sneezing or getting up too fast.
a doctor examining a patients neck. Share on Pinterest
People with cervical vertigo often report having neck pain.
There are a few potential causes of cervical vertigo, many of which are related to traumatic injury to the neck or chronic, long term injuries.
The diagnosis itself is still somewhat controversial. In fact, a study in the journal Archives of Physiotherapynotes that health professionals do not fully understand the exact cause of symptoms, and that accurately diagnosing the condition is difficult.
There is currently no definitive test or resource for the condition, so doctors usually test for other things and eliminate them to find cervical vertigo.
A recent study in the journal Laryngoscope Investigative Otolaryngology found that people with cervical vertigo may appear to doctors as people with migraine who also have neck injuries, and 94% of people with cervical vertigo report having neck pain.
The muscles, nerves, and joints in the neck send signals, including signals about the body's orientation, to the lower brain and inner ear. This is part of the body's effort to stay balanced and coordinated.
The issues we list below may cause one or more signals to misfire, causing symptoms that include cervical vertigo:
Atherosclerosis
Blockages in the arteries of the neck may lead to injury in the area that could cause vertigo. This could be due to atherosclerosis, which is the thickening of the artery walls.
Injuries
Traumatic injuries, such as from a vehicle accident or other causes of whiplash, may cause damage in the head and neck, which may lead to cervical vertigo.
Surgeries to the neck may also cause cervical vertigo as a complication, especially if the site of the surgery was close to the brainstem or has damaged the arteries in the neck and head area.
Osteoarthritis
Advanced osteoarthritis in the area may lead to cervical spondylosis. This causes the vertebrae in the neck to wear down, which can put excess pressure on the nerves, arteries, or spinal cord itself. This could send inappropriate signals to the brain or block the flow of blood, causing vertigo.
A slipped disk
Slipped disks are more common in areas of the lower back, though they can occur anywhere in the spine.
A slipped disk, or herniated disk, occurs when the softer center of a spinal disk pushes out through a crack in the spine. In some cases, it causes no symptoms. In other cases, however, it may push into a nerve or artery and cause symptoms that can include cervical vertigo.
Poor posture
Poor posture may also contribute to cervical vertigo. Over time, the cervical spine may compress due to poor sitting posture or issues such as "text neck," wherein a person frequently bends their neck to look at electronic devices or books.
This can put extra pressure on the arteries in the neck and may cause some people to experience neck pain and vertigo.
After eliminating other causes of the issue and diagnosing cervical vertigo, a doctor will recommend a treatment depending on the specific underlying cause.
Treatment generally also includes symptom management, using one or more drugs to balance out the symptoms while doctors work to treat the underlying condition. This may include taking drugs to ease the dizziness, as well as medications to reduce pain and relax the muscles.
Most doctors will also recommend therapies such as physical therapy and posture training to help create space in the neck, increase range of motion, and build strength in the muscles. This alone may relive pressure in the area and help reduce symptoms.
Researchers still do not have a complete list of risk factors for cervical vertigo.
Age may be a risk factor, as general wear and tear may increase tension in the neck.
Atherosclerosis may also play a role, as reduced blood flow in the arteries may reduce blood flow to the areas of the brain and inner ear that control coordination and balance.
Poor posture also puts excess pressure on the head and neck, which may lead to the development of new symptoms or make existing symptoms worse.
Share on Pinterest
Practicing good posture when sitting may help prevent cervical vertigo.
Preventing cervical vertigo is not possible in every case, as some causes — such as vehicle accidents — may not be preventable. However, people can take a number of steps to help prevent other causes.
For example, exercising the muscles in the neck to keep them strong may help keep weight off the cervical disks and reduce pressure in the area.
When sitting, keeping the head, shoulders, and spine aligned may reduce pressure in the neck and avoid wear and tear on delicate structures.
Regularly stretching the neck, getting regular massages or chiropractic alignments, and using warm compresses to relax the area could also help.
In most cases, it is possible to treat and manage cervical vertigo. People with severe degeneration in their neck may have more difficulty treating the condition, though managing symptoms may be possible to help increase their quality of life.
Diagnosing cervical vertigo is tricky. It requires doctors to rule out many other conditions and serious issues before landing on cervical vertigo.
Anyone experiencing symptoms such as neck pain and dizziness after turning their neck should work with their doctor to diagnose and treat the underlying issue. | {
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Cognitive Behavioral Therapy
Cognitive Behavioral Therapy
If you have had therapy before, you likely have at least heard the term cognitive behavioural therapy. It is a form of therapy that treats the thoughts and evaluations that you have about yourself and the world around you. Cognitive behavioural therapy (CBT) is a very effective and useful form of therapy that can help you through many emotional and drug and alcohol addiction issues, so let’s take a look at it further, and you can see how CBT can help you.
How Does Cognitive Behavioral Therapy Work?
Cognitive Behavioral Therapy begins with the assumption that your thoughts control how you see the world, and how you feel about it. This form of therapy theorises that you learned, growing up, certain truths about the world, and internalised them as central beliefs about how things should be and how things are. Let’s look at an example to help understand this.
Imagine that you are sitting in your favourite coffee shop one afternoon, just sitting there reading a book. Without any warning, a stranger dumps a cup of coffee on your lap. You jump up and take care of yourself first, that’s just instinct. What happens next, however, is all based on those internal beliefs about life. Take a moment and ask yourself what you would feel and do? Would you be mad, and start yelling? Are you scared and looking for help? Or how about laughing at the absurdity of it all, maybe because it’s been such a hard day and this was just the final piece to an awful day that its ridiculous. Or perhaps any of a million other possible emotional combinations and reactions?
Thinking it through you can see that there are thousands of possible reactions that you could have, but what determines what you think and feel? Those internal beliefs and thoughts that happen so fast in your mind that you will not notice them without paying careful attention to what is going on inside your mind. That evaluation or thought will happen and colour how you see things and help you evaluate the situation. Following our example above, if you thought that people are threatening and the world is a dangerous place, you would probably be scared of the person who dumped coffee on you and look for help. If you had a belief structure that said that the only way to get what you want in life is to fight, you might jump up and punch the person without any question.
Cognitive behavioural therapy aims to identify and help you change those thoughts. It is a very focused and directed form of therapy which is used in alcohol rehabs that allows the therapist to work more and structure the sessions around your specific needs. Also, it is generally done as a brief form of therapy, with many lasting just 12-15 sessions, depending on individual need. Being short term, it is very focused, and will be centred on the present; very little time will be spent learning about how you grew up. Cognitive Behavioral Therapy centred treatment is about helping who you are now and helping you figure out what is helpful and healthy, and what you need to change. It is very useful in treating drug and alcohol addiction, anxiety and depression, with decades of research supporting its use as a treatment method for these conditions.
Additionally, dialectical behaviour therapy, a specialised form of Cognitive Behavioral Therapy, is evidence-based psychotherapy that uses traditional elements of CBT in partnership with other targeted approaches to treat addiction. Dialectical behaviour therapy teaches mindfulness, acceptance and distress tolerance, all skills which can be vastly beneficial during drug and alcohol recovery.
Cognitive Behavioral Therapy
One of the first things to accomplish in Cognitive Behavioral Therapy is to identify what your beliefs are about yourself and the world around you. The assessment is where the addiction therapist in the rehab will work with you to help you identify what your thoughts and beliefs are. While this sounds easy, you just talk about what you are thinking, but remember, these thoughts, these evaluations happen in a nanosecond, and you are not conscious of them. It takes time to identify what they are.
Cognitive Behavioral Therapy and Addiction Treatment
Many rehabilitation facilities incorporate CBT into an addiction treatment program. Using reframing and restructuring techniques, the addiction therapist will give you tools and activities to help first combat the unhelpful thoughts. It is a process, but changing your thoughts can be done. It involves slowing yourself down and evaluating each situation as it comes up. In other words, you act, you don’t react. The addiction therapist will teach you that by slowing down and asking yourself questions about the person, yourself, or the situation, you can often find other possible explanations, that are more in tune with reality, than the assumptions you typically make.
Cognitive Behavioral Therapy in rehab helps patients overcome drug addiction and alcoholism by:
• Helping to dismiss false beliefs and insecurities that lead to substance abuse
• Providing self-help tools to better their moods
• Teaching effective communication skills
Coping skills are another important aspect of Cognitive Behavioral Therapy. What is known about certain diseases like drug and alcohol addiction or depression, is that there are certain symptoms that just happen. They are biological in nature, and often are temporary, but require some help to get through them. That is where CBT comes in. CBT will teach you ways to cope and manage any types of distress that may happen to you. While it will be specific to you, there will be some general tips and helpful habits that they can give you so that you can start to live a healthier life overall.
Practice is also going to be a very vital part of Cognitive Behavioral Therapy as well. You can expect to have homework between sessions, as well as taking time during sessions to practice and review what you have done the past week. Change is never easy, and this kind of change takes time, effort, and most importantly, practice. Homework will be specific to you and the skills you are trying to learn. It will be practising, for example, how to come up with other possible reasons for why the person dumped coffee on your lap. Could it be an accident? Did this person think you were someone else? Were they having a seizure? It could be anything and slowing yourself down will let you see the reality of the situation and act appropriately.
Every person living under the weight of drug and alcohol addiction has unique circumstances which brought them there. Identifying and treating personal issues that prompt drug or alcohol abuse helps to reduce triggers and self-destructive behaviours.
Cognitive behavioural therapy in rehab is an amazing tool to use to learn more about yourself and why you react the way you do, and then learn to actually evaluate what you are doing to see if it fits with reality. It is well researched and can be used to treat a variety of diseases, including drug and alcohol addiction. CBT can give you back a meaningful and healthy life. Help and healing are out there for you with this.
If you know that you or a loved one is plagued with negative thoughts that fuel addictive tendencies, then CBT is a great option. However, the process of achieving freedom begins with contacting an expert to help point you in the right direction. You do not have to seek treatment alone or find a rehabilitation facility on your own. Contact us today to find a rehabilitation center near you. We can give you the key to unlock the door to a new path to life. Recovery is only a decision away.
==================================================================
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==================================================================
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-7,380,846,244,784,500,000 | Do you immediately gain weight when pregnant?
Most first-time moms don’t see an appreciable amount of weight gain until closer to 20 weeks. Second-time moms may see weight gain a little earlier, because they may not have as many issues with nausea and vomiting – or at least have more experience coping with it.
How quickly do you gain weight pregnant?
In general, you should gain about 2 to 4 pounds during the first three months you’re pregnant and 1 pound a week during the rest of your pregnancy. If you are expecting twins you should gain 35 to 45 pounds during your pregnancy.
Why am I putting on weight in early pregnancy?
This isn’t only due to the weight of the growing baby. Much of the weight gained is extra fluid (water) in the body. This is needed for things like the baby’s circulation, the placenta and the amniotic fluid. Medical guidelines used to be quite strict, with recommendations limiting weight gain to a few kilograms.
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Do you gain or lose weight in early pregnancy?
While the average weight gain during the first trimester is about 5 pounds, some women actually lose weight because of morning sickness and food aversions.
How much weight do you gain in the first month?
During their first month, most newborns gain weight at a rate of about 1 ounce (30 grams) per day. They generally grow in height about 1 to 1½ inches (2.54 to 3.81 centimeters) during the first month. Many newborns go through a period of rapid growth when they are 7 to 10 days old and again at 3 and 6 weeks.
How do you self check your stomach for pregnancy?
Walk your fingers up the side of her abdomen (Figure 10.1) until you feel the top of her abdomen under the skin. It will feel like a hard ball. You can feel the top by curving your fingers gently into the abdomen. Figure 10.1 With the woman lying on her back, begin by finding the top of the uterus with your fingers.
When do you start showing?
You’ll likely notice the first signs of a bump early in the second trimester, between weeks 12 and 16. You might start showing closer to 12 weeks if you are a person of lower weight with a smaller midsection, and closer to 16 weeks if you’re a person with more weight.
How can I avoid getting fat during pregnancy?
10 ways to avoid gaining too much pregnancy weight
1. Start pregnancy at a healthy weight if possible. …
2. Eat moderately and often. …
3. Drink up (water, that is) …
4. Make your cravings constructive. …
5. Make starches work harder. …
6. Start a simple walking regime. …
7. If you’re already moving, don’t stop. …
8. Have the occasional indulgence.
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Is early weight gain a sign of twins?
Twins or more: signs of a multiple pregnancy. A rapid and early weight gain during the first trimester often indicates you might be pregnant with multiples.
Do you get extra hungry in early pregnancy?
While feeling ravenous may be an early indicator of pregnancy, it’s unlikely for this to be your only symptom. In fact, many women find their appetite actually decreases in the first trimester, as morning sickness makes the sight and smell of food unappealing.
Can you still lose fat while pregnant?
But new research shows that obese women can safely exercise and diet to lose weight without any negative impact on their baby’s well-being. If you’re obese, you can still have a healthy pregnancy and delivery.
Can you lose weight during first trimester?
But losing weight in early pregnancy is actually pretty normal, especially if you’ve got a bad case of morning sickness. Here’s what to know about weight loss throughout your pregnancy if it should happen: RELATED: Secrets to Healthy Pregnancy Weight Gain.
Do you burn more calories when pregnant?
They also looked up data on the number of calories women burn while pregnant and lactating. A study from 2005 showed (paywall) they tend to burn roughly twice as many calories as normal.
How much weight did you gain by 20 weeks?
You may have gained around 8 to 10 pounds by this point.
How much weight did you gain first trimester?
While the majority of the pounds will make their appearance during the second and third trimester, there’s some initial weight gain that will happen in the first 12 weeks of pregnancy. In fact, on average, people gain 1 to 4 pounds in the first trimester — but it can vary.
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What trimester do you gain the most weight?
Third trimester weight gain is an important part of later pregnancy and is not usually a cause for concern. Many women will experience rapid weight gain during their third trimester. This is because the fetus typically gains the most weight in this time, according to the Office on Women’s Health (OWH).
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1,194,750,953,992,640,000 | Can cosmetic fillings become discolored?
Can cosmetic fillings become discolored is a question that had puzzled many people. Let's find the answer to this question! Trám răng thẩm mỹ khắc phục sâu răng hiệu quả Trám răng...
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Cosmetic filling - An effective tooth decay treatment
Cosmetic filling is a treatment to remedy tooth decay or tooth damage that is not too severe. Doctors will use the material to fill the cavities, protect the enamel, dentin,...
Cosmetic filling
According to Dr. Vo Van Nhan: Cosmetic fillings that resemble the natural tooth color can restore the shape, structure and even help cover some imperfection of the enamel. A composite...
What is Amalgam filling?
Nhan Tam Dental Clinic - Amalgam filling is a filling material that contains mercury with other metallic elements such as silver, copper, tin, etc., which help prevent tooth decay and...
Does tooth decay have to be treated with fillings? Why?
Question: Hello doctor! I have tooth decay and it seems to be more and more severe. Does decayed tooth need to be filled or what? Can it be restored like...
vo van nhan
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• 801-809 3/2 Street, Ward 7, District 10, Ho Chi Minh City, Vietnam
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• Mobile: (+84) 903 632 701 - (+84) 938 967 858 | {
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344,879,835,525,702,300 |
SHCDNi003-A
The cell line is not validated yet.
General#
Cell Line
hPSCreg Name
SHCDNi003-A
Cell line type Human induced pluripotent stem cell (hiPSC)
Last update 24th March 2021
User feedback
No feedback available yet.
Login to share your feedback, experiences or results with the research community.
Provider
Generator Shanghai Children's Hospital (SHCDN)
Owner Shanghai Children's Hospital (SHCDN)
Distributors
Derivation country China
External Databases
BioSamples SAMEA7044788
Cellosaurus CVCL_ZL96
CLO CLO_0102548
Wikidata Q98132503
General Information
Publications
* Is the cell line readily obtainable for third parties?
Yes
Research: allowed
Clinical: allowed
Commercial: allowed
Donor Information#
General Donor Information
Sex male
Age of donor (at collection) 10-14
Phenotype and Disease related information (Donor)
Diseases A disease was diagnosed.
Allan-Herndon-Dudley Syndrome
The donor is a carrier of a disease-associated mutation and affected.
Synonyms
• MCT8-Specific Thyroid Hormone Cell Membrane Transporter Deficiency
• Monocarboxylate Transporter 8 Deficiency
• Allan-Herndon-Dudley Syndrome
Genetic variants
X
NM_006517.4:c.1026+1G>A
Heterozygous
de novo
Family history None
Is the medical history available upon request? A one-year-old Chinese Han male infant with AHDS who presented with developmental delay, hypertonia, and often tilted his head back. Furthermore, he showed elevated serum FT3, decreased serum FT4 and T4.
Karyotyping (Donor)
Has the donor karyotype been analysed?
Yes
Karyotyping method: G-Banding
Other Genotyping (Donor)
Is there genome-wide genotyping or functional data available?
No
External Databases (Donor)
BioSamples SAMEA7044789
Ethics#
Has informed consent been obtained from the donor of the embryo/tissue from which the pluripotent stem cells have been derived? Yes
Was the consent voluntarily given? Yes
Has the donor been informed that participation will not directly influence their personal treatment? Yes
Can you provide us with a copy of the Donor Information Sheet provided to the donor? Yes
Do you (Depositor/Provider) hold the original Donor Consent Form? Yes
Please indicate whether the data associated with the donated material has been pseudonymised or anonymised. anonymised
Does consent explicitly allow the derivation of pluripotent stem cells? Yes
Does consent prevent CELLS DERIVED FROM THE DONATED BIOSAMPLE from being made available to researchers anywhere in the world? Yes
Does consent permit research by
an academic institution? Yes
a public organisation? Yes
a non-profit company? Yes
a for-profit corporation? Yes
Does consent expressly permit collection of genetic information? Yes
Does consent expressly permit storage of genetic information? Yes
Does consent prevent dissemination of genetic information? Yes
Has the donor been informed that their donated biosample or derived cells may be tested for the presence of microbiological agents / pathogens? Yes
Has the donor consented to receive information discovered during use of donated embryo/tissue that has significant health implications for the donor? Yes
How may genetic information associated with the cell line be accessed? Open Access
Will the donor expect to receive financial benefit, beyond reasonable expenses, in return for donating the biosample? No
Does the consent anticipate that the donor will be notified of results or outcomes of any research involving the donated samples or derived cells? Yes
Has a favourable opinion been obtained from a research ethics committee, or other ethics review panel, in relation to the Research Protocol including the consent provisions? Yes
Name of accrediting authority involved? Ethics Committee of Shanghai Children’s Hospital
Approval number REK 2017R021-F01
Has a favourable opinion been obtained from a research ethics committee, or other ethics review panel, in relation to the PROPOSED PROJECT, involving use of donated embryo/tissue or derived cells? Yes
Name of accrediting authority involved? Ethics Committee of Shanghai Children’s Hospital
Approval number REK 2017R021-F01
For generation of the cell line, who was the supplier of any recombined DNA vectors or commercial kits used?
hIPSC Derivation#
General
Source cell type
Autologous Peripheral Blood Mononuclear Cells
A preparation of autologous peripheral blood mononuclear cells (PBMCs).
Synonyms
• Autologous Peripheral Blood Mononuclear Cell
• Autologous PBMC
• Autologous PBMCs
• Autologous Peripheral Blood Mononuclear Cells
• Therapeutic PBMCs
show more synonyms
Age of donor (at collection) 10-14
Collected in 2019
Source cell line vendor Shanghai Children's Hospital
Passage number reprogrammed 10
Reprogramming method
Vector type Non-integrating
Vector Sendai virus
Genes
Is reprogramming vector detectable?
Yes
Methods used
PCR
Vector free reprogramming
Type of used vector free reprogramming factor(s)
Protein
Other
Selection criteria for clones cells are small and present a compact group
Derived under xeno-free conditions
Yes
Derived under GMP?
Yes
Available as clinical grade?
Unknown
Culture Conditions#
Surface coating Matrigel/Geltrex
Feeder cells
No
CO2 Concentration 5 %
Medium Essential 8™
Has Rock inhibitor (Y27632) been used at passage previously with this cell line?
Yes
Has Rock inhibitor (Y27632) been used at cryo previously with this cell line?
No
Has Rock inhibitor (Y27632) been used at thaw previously with this cell line?
Yes
Characterisation#
Analysis of Undifferentiated Cells
Marker Expressed Immunostaining RT-PCR FACS Enzymatic Assay Expression Profiles
SSEA-4
Yes
TRA 1-60
Yes
POU5F1 (OCT-4)
Yes
AFP
Yes
PAX6
Yes
Score:
Marker Present Absent
mCpG
OCT4
Morphology pictures
Microbiology / Virus Screening
Mycoplasma Negative
Certificate of Analysis
Is there a certificate of analysis available?
Yes
Passage:
Genotyping#
Karyotyping (Cell Line)
Has the cell line karyotype been analysed?
Yes
The result displays a normal karyotype(46, XY),without detectable abnormalities.
Karyotyping method: G-Banding
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While eating carbohydrates early in the day provides us with the energy needed to power through training sessions and complete our daily tasks, and the evening meal containing them helps us to replace lost glycogen from our final workout for the day, consuming carbohydrates after 6:00pm (or around this period) will only lead to an unnecessary output of insulin, an anabolic hormone responsible for, among other functions, increasing fat storage.
A new German study found that when you drink 17 ounces of water (about two glasses) within a certain time frame, your metabolic rate shoots up by about 30 percent. Using these results, they estimate that by increasing your current water intake by 1.5 liters a day, a person would burn an extra 17,400 calories a year, resulting in about a five-pound weight loss.
Calories play a vital role in how much weight you will be able to lose in 10 days. Calories are the fuel for your body and to lose weight, you have to eat fewer calories than you burn off through daily activity and exercise. According to ProHealth, one pound of fat is equal to 3,500 calories. This means you will need to reduce your diet by 500 or so calories a day to shed a single pound in a week. This means you can lose about one to three pounds in 10 days.
Thе mоѕt important part іѕ tо cut bасk on sugars and starches (carbs). Thеѕе аrе thе foods thаt stimulate secretion оf insulin thе most. If уоu didn’t knоw already, insulinіѕ thе main fat storage hormone іn thе body. Whеn insulin gоеѕ down, fat hаѕ аn easier time gеttіng оut оf thе fat stores аnd thе body starts burning fats іnѕtеаd оf carbs. Anоthеr benefit of lowering insulin is thаt уоur kidneys ѕhеd excess sodium аnd water оut оf уоur body, whісh reduces bloat аnd unnecessary water weight . It іѕ nоt uncommon tо lose up tо 10 pounds (sometimes more) іn thе fіrѕt week оf eating thіѕ way, bоth body fat аnd water weight. Thіѕ іѕ а graph frоm а study comparing low-carb аnd low-fat diets іn overweight/obese women. Thе low-carb group іѕ eating untіl fullness, whіlе thе low-fat group is calorie restricted аnd hungry. Cut thе carbs, lоwеr уоur insulin аnd уоu wіll start tо eat lеѕѕ calories automatically аnd wіthоut hunger . Put simply, lowering уоur insulin puts fat loss оn “autopilot.”
COMMENTSThe opinions expressed within this article are the personal opinions of the author. NDTV is not responsible for the accuracy, completeness, suitability, or validity of any information on this article. All information is provided on an as-is basis. The information, facts or opinions appearing in the article do not reflect the views of NDTV and NDTV does not assume any responsibility or liability for the same.
To cut calories and lose weight, you have to eat right. That means no empty calories from unhealthy foods, including chips, cakes and cookies. Skip foods that contain simple carbohydrates and eliminate soda altogether. By drinking water and avoiding breads, you may reduce your caloric intake enough to lose weight. If not, opt for vegetable dishes over meat-based ones and choose non-fat dairy when you can.
Instead of subjecting yourself to another endless workout, crank up the intensity and you’ll see results faster than you ever thought possible. The results of a study conducted at McMaster University in Ontario reveal that adult male study subjects who exercised intensely for a single minute had equivalent respiratory and metabolic changes to those who worked out at a slower pace for close to an hour, so if you want to burn through that belly fat, say so long to slow and steady.
“Research has shown that [drinking caffeine] before exercise can enhance athletic performance,” Jim White, RD, ACSM, dietitian, personal trainer, and owner of Jim White Fitness & Nutrition Studios tells us in What to Drink Before a Workout for Optimal Fat Loss. Plus, a study published in the journal Sports Medicine reveals that the natural energy source can help you train stronger for longer in workouts ranging from 60 seconds to even two hours. Just remember to skip the added sugar and creamer in your coffee to avoid packing pounds onto your frame.
If you’re looking to get lean, working out before you sit down to sunny-side-up eggs and toast may be your best bet. A study in the British Journal of Nutrition found that doing cardio on an empty stomach results in significantly higher fat oxidation, or fat loss, than exercise performed after you’ve eaten. Try hitting the elliptical or Stairmaster before breakfast, and make sure to bring a small snack with you to the gym to keep your blood sugar in check. To follow up your workout, check out these 16 Post-Workout Snacks Fitness Experts Swear By.
Speaking of intervals, high-intensity interval training (otherwise known as HIIT) has been shown to be incredibly effective for weight loss. Because the workouts are so intense, you don't need to put in an hour — or even 30 minutes — at the gym. According to the American College of Sports Medicine, seven minutes is all you need to get in the best shape of your life.
Steak with avocado, anyone? Whether you're on the keto diet or not, you may wanna try this super easy dinner! 🥩 🥑⠀ ⠀ Follow these👇 directions:⠀ ⠀ 1. Rub half of the oil and seasoning of your choice onto the beef. Heat a pan to medium and cook for 2-3 mins on each side or until done to your liking. Let the beef rest for a few minutes before slicing.⠀ 2. In the meantime, wash and dry the arugula, wash and slice the tomato, and peel and slice avocado. Assemble on a plate.⠀ 3. Drizzle remaining oil and vinegar on the salad and serve steak on top.
It has to do with your hormones leptin and ghrelin.[4] Your levels get all sort of messed up and it leads to them telling your body you're hungry when you're really just tired. And to top it off, when you're sleepy, you load up on sugar, grab take out for dinner because you're tired, and skip the gym for the same reason. That's three strikes right there.
That’s because it theoretically causes a mild ketosis (yep, the basis of the keto diet), which is a fat-burning state that should make you feel less hungry. The key in being successful with a low-carb diet (especially if you’re used to a more high-carb lifestyle) is to compensate for those lost carbs with protein-rich foods, says Dr. Cheskin. That way, your volume of food stays the same, but you’re doing it healthfully rather than in a way that exacerbates your weight gain.
2. When sitting down to a meal, it should be made up of at last half vegetables(lunch and dinner, usually more fruit at breakfast time). Eat the vegetables first along with the lean protein and THEN eat the carbohydrate portion of the meal, but only if you’re still hungry. If you’re not still hungry, then don’t eat it. The starch/carbohydrate usually contains more calories than the other components in the meal, so saving it till last helps to cut unnecessary calories as most people are not still hungry by the time they finish everything else.
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Retinopathy of Prematurity | Overview
Retinopathy of Prematurity in Humans
• Retinopathy of prematurity (ROP) is a major cause of blindness in children in the developing and developed world despite current surgical treatment in the late stage of the disease
• In the US ROP affects approximately 14 million infants and results in approximately 1,100-1,500 babies requiring treatment each year.
Causes of Retinopathy of Prematurity
• ROP is associated with excessive oxygen use shortly after birth. When human babies are born prematurely, they are often given supplemental oxygen to ensure adequate blood levels of oxygen. However, this can induce ROP. Human preterm infants with ROP show delayed development of the retinal vasculature, which can be associated with pathological neovascularization.
• The harmful neovascularization from ROP can damage the retina and lead to vision loss and blindness.
• Currently the two major risk factors for ROP appear to be low gestational weight of the baby and oxygen use, although elevated glucose may also play a role
Neovascularized vs Normal Retina
Above: A merged image of a hyperoxic mouse retina (left) with a normoxic retina (right) at P17. Note the neovascular tufts and vaso-obliteration on the left.
1. Silverman W (1980) Retrolental fibroplasia: a modern parable. Grune and Stratton, New York
2. http://www.aapos.org/terms/conditions/94
Oxygen-Induced Retinopathy in The Mouse
• Neonatal mice and their nursing mother are kept at room air from birth through postnatal day (P)7.
• From P7 to P12, the mice are exposed to 75% oxygen, which induces loss of immature retinal vessels and slows development of the normal retinal vasculature, leading to a central zone of vaso-obliteration (VO).
• The mice are returned to room air. At this point, the central avascular retina becomes hypoxic, triggering both normal vessel regrowth and a pathologic formation of extraretinal neovascularization (NV).
• Maximum severity of NV is reached at P17. Shortly thereafter, NV starts to regress and by P25 almost no VO or NV remains visible.
OIR Model Schematic
Above: A Representative Diagram of our model of OIR
We have found that VEGF, EPO and IGF-1 all contribute to the development of this harmful neovascularization (see Selected Publications). Our lab is currently investigating the role of the WNT, the JAK-STAT, and the FEVR pathways in the OIR model. Members of our lab have recently published papers investigating the role of SOCS3 and Cyp2C8 in our OIR model and we hope to use our knowledge of these pathways to develop treatments and therapies for ROP in humans. | {
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-7,252,485,337,881,488,000 | VetBact
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VetBact
Swedish University of Agricultural Sciences
Veterinary bacteriology: information about important bacteria
Veterinary bacteriology
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Matrix-Assisted Laser Desorption/Ionization Time Of Flight Mass Spectrometry (MALDI-TOF MS)
Matrix-Assisted Laser Desorption/Ionization Time Of Flight Mass Spectrometry (MALDI-TOF MS)The instrument in the image belongs to the Department of Biomedical Sciences and Veterinary Public Health at the Swedish University of Agriculture Science (SLU). Helena Ljung (018-672389) and Marina Falk are responsible for the equipment and it is possible to get isolates analyzed. - Click on the image to enlarge it.
Matrix-Assisted Laser Desorption/Ionization Time Of Flight Mass Spectrometry (MALDI-TOF MS)
Schematic description of the principle of MALDI-TOF MS. - Click on the image to enlarge it.
The principle of MALDI-TOF
Mass spectrometry based on the MALDI-TOF (or Maldi only) means that the bacterial isolate to be analyzed, is adsorbed to some type of carrier material (matrix). The isolate is then irradiated with laser UV light, so that the molecules in the bacteria are broken into positively charged fragments (ionization), which are thrown towards a detector. The time it takes for the fragment to reach the detector (time of flight) is measured. The time is dependent on fragment size and charge. Also very large molecules (proteins and nucleic acids) can be fragmented and ionized in this way. Large molecules give rise to many fragments and a characteristic mass spectrum, which can be used for identification.
The use of MALDI-TOF MS for identification of bacteria
One can perform these analyzes directly on bacterial colonies and the resulting mass spectrum is then compared with stored mass spectra of known bacterial species. Thus, you will get an analytical response within a minute and the method is considered to be very reliable. The more mass spectra of known bacteria you have to compare with, the safer the method will be.
MALDI-TOF MS is already used in some laboratories for veterinary bacteriology and many researchers believe that this technique will be tomorrow's routine method for identification of bacteria. The instrument is still very expensive, but material costs are low.
Score value
The software for the Maldi system contains a database with information about which fragments one can possibly get from a particular bacterium. This information can be used by the system to compare with unknown samples and calculate a score value for each sample. The score value is a measure of the probability that a particular isolate will represent a particular bacterial species/strain in the reference library. A score value between 0.000 and 1.699 means that identification is not possible since the peak of the unknown isolate does not represent any bacterium in the reference library. A score value between 1.700 and 1.999 are reliable only to the genus level, but a low confidence of identification at species level compared to reference peak list. . A score value between 2.000 and 3.000 are considered accurate of both genus- and species-level.
Updated: 2023-05-02.
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Swedish University of Agricultural Sciences | {
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Is A Low-Carb Diet Right For You?
Page 3 of 3
Zone Diet
What is it?
40, 30, 30. No, that's not a new type of zone defense. That's the breakdown of the Zone diet, which dictates that all meals be arranged according to the following ratio: 40% carbohydrates, 30% fat and 30% protein.
How much you eat total at each meal is a question of individual need. And how you arrange the meals works best with the aid of a nutritionist.
Like the Atkins diet, the Zone Diet seeks to limit carbs. However, the Zone differs in that it does not encourage ketosis (the process whereby the body burns fat reserves over carbohydrates), which many feel is not the ideal dietary state. The Zone is a regimented but balanced diet, not unlike certain dietary plans endorsed by The American Diabetes Association.
What do the critics say?
Criticism of the Zone Diet is much the same as that launched against all other low-carb diets, namely that the weight loss will not last and there's a risk of heart disease and increased cholesterol levels. It is for these reasons that the American Heart Association is critical of all low-carb diets.
That said, the Zone Diet probably allows for more carbs than any of the other low-carb routines. Whether or not that's a good thing, only time will tell.
Is it hard to stay on?
The Zone Diet is perhaps the most labor intensive of the three major low-carb diets. You're not just eating meals according to a new lifestyle choice; you're measuring food parts with great precision. This usually means relying on a dietitian, which can be costly and cumbersome (but a great resource nonetheless).
Although the Zone may be cumbersome, it isn't nearly as restrictive as Atkins. So if you're the kind of person who is likely to quit a diet if you feel deprived of something, this one might be your best bet.
lose weight the healthy way
There is a dizzying array of dieting options out there, and it's difficult to know which one to pick. But there are some certainties.
First, consulting your physician before starting a diet is always a good idea. Second, a moderate amount of daily exercise will always help you stay fit and healthy. Third, paying close attention to how you feel is as good an indicator as any when it comes to choosing a diet.
Remember; dieting is not a precise science. If it were, nobody would be carrying extra pounds. What works for one guy may not work for another. The secret is to find the right eating regimen for you.
Show comments
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5,011,628,341,612,041,000 | Immune thrombocytopenia (ITP)
Diagnosis
Your doctor will attempt to rule out other potential causes of bleeding and a low platelet count, such as an underlying illness or medications that you or your child may be taking, prior to the immune thrombocytopenia diagnosis.
The amounts of platelets can be determined via blood testing. Adults may infrequently require a bone marrow examination to rule out other issues.
Treatment
Mild immune thrombocytopenia patients might only require routine monitoring and platelet tests. Children typically get better on their own. Most individuals with ITP will require therapy at some point, as the condition frequently gets worse or is chronic.
Numerous methods of treatment are possible, such as taking drugs to increase your platelet count or having your spleen removed (splenectomy). Discuss the advantages and disadvantages of your treatment options with your doctor.
Medications
Your doctor will ask you about any over-the-counter drugs or dietary supplements you currently use to see whether you should stop using any that could impair platelet function. Aspirin, ibuprofen, and ginkgo biloba are some examples.
ITP medications include the following:
• Steroids. You’ll probably begin taking an oral corticosteroid like prednisone at the advice of your doctor. In accordance with your doctor’s instructions, you can gradually stop taking the medication after your platelet count has returned to a normal range. Because these drugs can raise your risk of infections, high blood sugar, and osteoporosis, prolonged use of them is not advised.
• Immune globulin. Your doctor might give you an injection of immune globulin if corticosteroids are ineffective. If you have serious bleeding or need to fast boost your blood count before surgery, this medication may also be utilized. Usually, the effect subsides after a few weeks.
• Medications that induce platelet production. Eltrombopag and romiplostim, two medications, assist your bone marrow in producing more platelets. These medications can make you more likely to develop blood clots.
• Other medications. By lowering the immune response that is destroying your platelets, rituximab helps you to have a higher platelet count. However, if you later decide to have surgery to remove your spleen, this medication may also lessen the effectiveness of any necessary immunizations.
Surgery
Your doctor may recommend to surgically remove the spleen due to the severity of the condition. Though it doesn’t work for everyone, this fast gets rid of your body’s primary cause of platelet destruction and raises your platelet count. Your vulnerability to infection is increased by living without a spleen.
Emergency treatment
ITP can occasionally cause serious bleeding, but this is unusual. Typically, platelet concentrate infusions are part of emergency care. Through a tube in a vein, steroids and immune globulin may also be administered. | {
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-7,122,459,584,740,216,000 | Short description
This respiratory disease is caused by the new coronavirus SARS-CoV-2, which was first identified in December 2019. COVID-19 can be almost asymptomatic or can run like a harmless cold. COVID-19 can lead to severe cases of pneumonia and acute lung failure, particularly in risk groups.
Detailed description
The viral infectious disease COVID-19 (= coronavirus disease-19) manifests itself as a respiratory disease with symptoms such as coughing, shortness of breath, fever or pneumonia. If the course of the disease is severe, it can lead to acute lung failure with fatal consequences. With increasing age and concomitant diseases, the risk of severe courses of the disease increases. The diagnosis is made using laboratory methods such as the RT-PCR test (reverse transcriptase polymerase chain reaction) developed by DZIF scientists, which can detect the presence of RNA of SARS-CoV-2 (= severe acute respiratory syndrome coronavirus-2) in patient samples. On January 30, 2020, the WHO initially declared a "public health emergency of international concern (PHEIC)" due to the worldwide spread of the virus. Since mid-March, COVID-19 has been classified as a pandemic. The lethality within the COVID-19 pandemic has not yet been conclusively clarified. Vaccines and antiviral drugs against COVID-19 are under development - also at DZIF.
You can find up-to-date information and behaviour rules concerning COVID-19/SARS-CoV-2 here:
Word Health Organization (WHO)
European Centre for Desease Prevention and Control (ECDC)
German Federal Government | {
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5,427,477,142,018,858,000 | Age, body mass index, race and other determinants of steroid hormone variability: The HERITAGE Family Study
O. Ukkola, J. Gagnon, T. Rankinen, P. A. Thompson, Y. Hong, A. S. Leon, D. C. Rao, J. S. Skinner, J. H. Wilmore, C. Bouchard
Research output: Contribution to journalArticlepeer-review
115 Scopus citations
Abstract
Objective and methods: To investigate from the HERITAGE Family Study database, 13 steroid hormones (androstane-3α, 17β-diol glucuronide, androsterone glucuronide, cortisol, dehydroepiandrosterone (DHEA), DHEA ester (DHEAE), DHEA sulfate (DHEAS), dihydrotestosterone (DHT), estradiol, 17-hydroxyprogesterone, progesterone, pregnenolone ester, sex hormone binding globulin (SHBG) and testosterone in each sex for their relationships with age, body mass index (BMI), race and key lifestyle variables. Sample sizes varied from 676 to 750 per hormone. Incremental regression methods were used to examine the contributions of the variables to steroid hormone variability. Results: Age was a major predictor for most steroid hormones. The greatest contribution of age was a negative relationship with DHEAS (R2 = 0.39). BMI was also associated with the variability of several steroid hormones, being the most important predictor of SHBG (R2 = 0.20) and of testosterone (R2 = 0.12) concentrations. When age and BMI were included, race still contributed significantly to the variations in cortisol (R2 = 0.02 for men and 0.04 for women), DHT (R2 = 0.02 for men and 0.03 for women), and progesterone (R2 = 0.03 for women). Nevertheless, race appeared to be less important than age and BMI. In addition, lifestyle indicators (food and nutrient intakes, smoking and physical activity) influenced steroid hormone variability. Their contributions, however, were minor in most cases once age, BMI and race had been taken into account. Conclusions: We conclude that age was the most important factor, followed by BMI, race and lifestyle factors in explaining steroid hormone variability.
Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalEuropean Journal of Endocrinology
Volume145
Issue number1
DOIs
StatePublished - 2001
Fingerprint
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-5,465,796,653,572,572,000 | Home » Frequently asked Questions on Health » How to treat fungal infection of the nails?
How to treat fungal infection of the nails?
Q: The nails of both my toes have turned black. The nail seems to be broken and also dead and when I look under my nail I can see some dead skin also. What should be done? My friends advised me to remove the whole nail and the nail can re grow. Can I just leave it as it is? I was planning to consult a dermatologist. Is he the right person to consult or should I go to some other doctor?
A:Fungal infection of nails is the common possibility one has to consider. I advise nail clipping for fungus examination. Oral anti fungal like griseofulvin or fluconozole can be considered. It has to be taken for a period of 12-18 weeks depending on the situation. Please consult a dermatologist who would be helpful in evaluating your case.
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1,745,303,794,446,299,600 | RxPharmacist
Common Checkpoint Inhibitors and Their Role in Cancer
Image: Unsplash.com
Background
Multiple medications have been discovered to target cell surface receptors. These are programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1). These receptors are specifically selected because they are important targets for cancer therapy. There are some similarities between these receptors, but there are differences to note. For example, the PD-1 receptor is expressed on T cells, B cells, monocytes, dendritic cells, natural killer T cells, and regulatory T cells. On the other hand, PD-L1 is expressed on T cells, B cells, dendritic cells, macrophages, bone marrow-derived mast cells, and a few non-immune cells.
T-cell exhaustion is commonly characterized by the presence of PD-1. PD-1 expression is found in cancers such as tumor infiltrating lymphocytes. PD-L1 is commonly overexpressed in many different types of tumors, such as tumor-associated macrophages.
To understand how PD-1 and PD-L1 work in the human body, it is best to look at each medication’s mechanism of action. The similarities between PD-1 and (PD-L1) medications are that they are monoclonal antibodies, (MAB) and are all available in an injection dosage form. The doses utilized are specific to the indication that the medication is being used for. Here, we will go into specifics to provide an overview of these medications that target cancer cells.
Medications
Nivolumab is a human IgG4 MAB and was approved by the FDA in 2014. This medication binds to the PD-1 and stops the PD-L1 and programmed death ligand-2 (PD-L2) from interacting with each other, which ultimately allows the PD-1 pathway inhibition to occur. Nivolumab is commonly indicated for:
• Melanoma
• Non-small cell lung cancer (NSCLC)
• Malignant pleural mesothelioma
• Renal cell carcinoma (RCC), hepatocellular carcinoma (HCC), and urothelial carcinoma
• Classical Hodgkin lymphoma (cHL)
• Squamous cell carcinoma of the head and neck (SCCHN)
• Esophageal, gastric, colorectal, and gastroesophageal junction cancer
• Esophageal adenocarcinoma
Nivolumab’s dose strengths are 40 mg/4 mL, 100 mg/10 mL, 120 mg/12 mL, and 240 mg/24 mL solution in a single-dose vial. The common dosages of this medication are 240 mg every two weeks and 480 mg every four weeks. It is important to be aware of the immune-mediated adverse reactions, infusion-related reactions, complications of allogeneic HSCT, and embryo-fetal toxicity associated with this medication. Multiple adverse reactions can occur such as fatigue, rash, musculoskeletal pain, nausea, vomiting, etc. Also, if it is being used with another agent, there are other adverse reactions to consider compared to when it’s being used as a single agent.
Pembrolizumab (approved by the FDA in 2014) is a human IgG4 kappa that targets the PD-1 receptor which is why it has a similar mechanism of action to nivolumab, as well as a similar adverse reaction profile. Pembrolizumab and nivolumab differ in their indications. Some pembrolizumab indications are:
• Melanoma
• NSCLC and (cHL)
• HCC, RCC, Merkel cell, cutaneous squamous cell, urothelial, and endometrial carcinoma
• Esophageal and gastric cancer
• Primary mediastinal large B-cell lymphoma (PMBCL)
• Head and neck squamous cell cancer (HNSCC)
• Microsatellite instability-high or mismatch repair deficient and colorectal cancer
• Cervical, tumor mutational burden-high (TMB-H), and triple-negative breast cancer
Typical doses in practice are 200 mg every 3 weeks or 400 mg every 6 weeks. The strengths of this medication offered are also 100 mg/4 mL (25 mg/mL) solution in a single-dose vial. The adverse effects profile is similar to nivolumab.
Atezolizumab was granted FDA approval in 2014 and is phage-derived human IgG1 MAB that blocks PDL1. This medication works by blocking the interaction between PD-1 and B7.1, but it doesn’t induce antibody-dependent cytotoxicity. Some of its indications are:
• Urothelial carcinoma
• NSCLC, SCLC, and HCC
• Melanoma
Some of the dosage forms available are 840 mg/14 mL (60 mg/mL) and 1200 mg/20 mL (60 mg/mL) solution in a single-dose vial. Routinely, doses of 840 mg every 2 weeks, 1200 mg every 3 weeks, or 1680 mg every 4 weeks are utilized in practice. It is important to be aware of the immune-mediated adverse reactions, infusion-related reactions, complications of allogeneic HSCT, and embryo-fetal toxicity which is similar to PD-1 precautions. The common adverse effects seen are fatigue, decreased appetite, nausea, and cough.
Avelumab is IgG1 human MAB anti-PD-L1. This medication was FDA approved in 2016, and is indicated for:
• Merkel cell carcinoma (MCC)
• Urothelial carcinoma (UC)
• RCC
This medication does warrant premedication and is used as needed thereafter. The common doses seen utilized are 800 mg every 2 weeks. The adverse effect profile is dependent on the indication that it is used for, but it is similar to what patients on atezolizumab experience. The common dosage form seen is 200 mg/10 mL (20 mg/mL) solution in single-dose vial.
Durvalumab is a human MAB that targets PD-L1 and was given FDA approval in 2017. Some of this medication’s indications are:
• Unresectable, Stage III NSCLC
• Extensive-stage small cell lung cancer (ES-SCLC)
• Locally advanced or metastatic biliary tract cancer (BTC)
Some of the injection dosage forms available are in a 500 mg/10 mL (50 mg/mL) and 120 mg/2.4 mL (50 mg/mL) solution in a single-dose vial. Commonly, patients receive either a weight-based dose that is dependent on their current weight, or a fixed dose of 1,500 mg every four weeks. The common adverse effects that patients experience are cough, fatigue, nausea, pneumonitis, and upper respiratory tract infections.
Table: PD-1 vs. PD-L1 Medications
Overall, when comparing PD-1 and PD-L1 medications, examining their different indications, dosage strengths, and side effect profiles can be useful in determining the right therapy for the right patient. The over-expression of PD-1 and PD-L1 in cancer cells is the reason why these receptors have been targeted in studies to identify new medication options for different cancer types. It is important to continue to stay up to date with the latest developments in literature because new and old medications are continuously being studied to find new indications and breakthrough therapies.
-Dagmara Zajac
RxPharmacist Team
References:
1. Tecentriq (atezolizumab) [prescribing information]. South San Francisco, CA: Genentech Inc; January 2022.
2. Bavencio (avelumab) [prescribing information]. Rockland, MA: EMD Serono Inc; July 2022.
3. Imfinzi (durvalumab) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; September 2022.
4. Opdivo (nivolumab) [prescribing information]. Princeton, NJ: Bristol-Myers Squibb Company; March 2022.
5. Keytruda (pembrolizumab) [prescribing information]. Whitehouse Station, NJ: Merck & Co Inc; March 2022.
6. Jiang Y, Chen M, Nie H, Yuan Y. PD-1 and PD-L1 in cancer immunotherapy: clinical implications and future considerations. Hum Vaccin Immunother. 2019;15(5):1111-1122. doi:10.1080/21645515.2019.1571892
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-8,202,442,109,276,462,000 | What is Dysphagia?
Dysphagia refers to difficulty in swallowing.
Our Speech Pathologists at Speech and Feeding Co are highly skilled therapists with a thorough understanding of swallowing disorders.
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Common conditions causing dysphagia include stroke, neurological disorders (e.g., Parkinson’s disease, dementia, head and neck cancers, and respiratory conditions like chronic obstructive pulmonary disease).
What are some signs or symptoms of dysphagia?
• Drooling
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Assessment:
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4,090,833,639,009,990,700 | Norwegian version of this page
Esguerra group
Dr. Esguerra´s research team is focused on exploring the fundamental mechanisms underlying brain function in health and disease.
Photo of a zebrafish
Photo:Thierry Marysael
Research focus
Using a combination of genetic and chemical approaches in zebrafish, the group seeks to elucidate the mechanisms of seizure generation, epileptogenesis and treatment resistance by probing the function of novel disease-associated gene variants involved in the etiology of pharmacoresistant epilepsies. The Esguerra Group is using engineered zebrafish mutants and transgenic reporter lines as well as pharmacological seizure models for carrying out in vivo chemical modifier screens to identify novel neuropharmacological tools and drug leads. These models and neuroactive small molecules will serve as valuable tools towards understanding the development, function, and diseases of the brain.
Aims:
1. Generate novel pharmacoresistant zebrafish epilepsy models
2. Functionally confirm disease-causative gene variants in vivo (genotype-phenotype correlation)
3. Identify bioactive small molecules with potential utility as anti-epileptic drug leads and pharmacological tools
4. Elucidate mechanisms of action of identified small molecules
Published Dec. 17, 2015 8:31 AM - Last modified July 1, 2021 3:49 PM | {
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1,661,814,651,585,603,600 | The term "neuropeptidases" refers to those enzymes that participate in the inactivation of synaptically released neuropeptides and therefore serve to turn off the generated peptide signal. In general, these enzymes are integral plasma membrane proteinases located as ectoenzymes. Some of the enzymes listed in the accompanying Tables are able to hydrolyze neuropeptides, but are present as cytosolic or secreted enzymes, or not present as ectoenzymes. Their physiological roles are therefore not fully established.
Only a relatively small group of CNS peptidases have been characterized as neuropeptide-inactivating ectoenzymes. The majority are zinc metalloenzymes for which specific and potent inhibitors have generally been developed. Some of these are found in abundance elsewhere, especially the renal and intestinal brush border membrane, but others appear to be more specific to the nervous system, e.g. pyroglutamyl aminopeptidase II. Neprilysin (NEP) is the prototype neuropeptidase originally discovered in the CNS as an enkephalin-degrading activity and subsequently as a substance P-hydrolyzing enzyme. It is appropriately located on neuronal membranes especially in the striatonigral pathway. Thus, it can act in an analogous manner to that of acetylcholinesterase at cholinergic terminals. Like several other neuropeptidases, it is also present in cells of the immune system where it may hydrolyze immunoregulatory peptides. In vivo, NEP is a broadly specific enzyme hydrolyzing a wide range of susceptible peptide substrates (enkephalins, substance P, atrial natriuretic peptide) as is its close homolog NEP II or secreted endopeptidase (SEP). Some other neuropeptidases appear to be much more substrate-specific. For example, pyroglutamyl amino-peptidase II appears to hydrolyze thyrotropin releasing hormone (TRH) exclusively. The unusual peptidase, glutamate carboxypeptidase II (GCP II) specifically inactivates the peptide neurotransmitter, N-acetylaspartylglutamate (NAAG) and GCP II inhibition can protect against some forms of neuronal death and may have applications in treatment of neuropathy.
Studies of changes in levels of neuropeptides in neurological disease have been limited in extent and no consistent pattern yet emerges. Likewise, factors regulating the expression of neuropeptidases both in the normal and the pathological state in the nervous system are little explored. Inhibitors of neuropeptidases are useful both as pharmacological tools in studies of neuropeptide physiology and also as potential therapeutic agents. Selective inhibitors of these enzymes have, to date, been obtained from natural products (e.g. phosphoramidon as NEP and endothelin converting enzyme 2 inhibitor) or designed (e.g. thiorphan selective for NEP) by analogy with similar enzymes from bacterial or other sources (e.g. thermolysin). Dual peptidase inhibitors (e.g. of NEP and angiotensin converting enzyme (ACE)) are increasingly finding favor as potential new therapeutics). Design of ACE, NEP and neurolysin inhibitors, in particular, will be aided by their recently solved three-dimensional structures.
A particular role for several neuropeptidases (especially NEP) has recently emerged in the turnover of the amyloidogenic Ab-peptide in Alzheimer's disease and age-dependent loss of NEP in the brain may contribute to the pathology. Strategies to up-regulate these CNS peptidases may therefore prove beneficial but raises some concerns with regard to potential side effects of their chronic inhibition.
Genome sequencing studies reveal that there are probably 8-10 NEP-like enzymes in the human genome and 24 in Drosophila. The Tables below describe the best characterized neuropeptidases. This includes a novel homolog of angiotensin converting enzyme (ACE2), not inhibited by classical ACE inhibitors, which appears to counterbalance the actions of ACE through its ability to convert angiotensin II to angiotensin-(1-7). Like several ectopeptidases, ACE2 serves serendipitously as a viral receptor, in this case for the severe acute respiratory syndrome (SARS) virus.
The Tables below contain accepted modulators and additional information. For a list of additional products, see the Materials section below.
Endopeptidases
Aminopeptidases
Carboxypeptidases
Abbreviations
AI: Angiotensin I
AII: Angiotensin II
AIII: Angiotensin III
AMC: 7-Amido-4-methyl coumarin
ANP: Atrial natriuretic peptide
BK: Bradykinin
CALLA: Common acute lymphoblastic leukemia antigen
CCK: Cholecystokinin
CD: Cluster differentiation antigen
CPE: Carboxy-phenyl ethyl
CPP: Carboxy-phenyl propyl
EDTA: Ethylenediaminetetraacetic acid
EC33: (S)-3-Amino-4-mercaptobutyl sulfonic acid
ET-I: Endothelin-1
ET-2: Endothelin-2
ET-3: Endothelin-3
GEMSA: Guanidinoethylmercaptosuccinic acid
Glp: Pyroglutamyl
GPI: Glycosylphosphatidylinositol
LHRH: Luteinizing hormone-releasing hormone
MGTA: 2-Mercaptomethyl-3-guanidinoethylthiopropranoic acid
MLN: (S,S)-2-[1-Carboxy-2-[3-(3,5-dichlorobenzyl)-3H-imidazol4-yl]-ethylamino]-4-methylpentanoic acid)
NAAG: N-Acetyl-L-aspartyl-L-glutamate
NAALA: N-Acetylated a-linked acidic dipeptidase
NKA: Neurokinin A
NKB: Neurokinin B
NPY: Neuropeptide Y
NT: Neurotensin
PC18: 2-Amino-4-methylsulfonyl butane thiol
PYY: Peptide YY
SARS: Severe acute respiratory syndrome
SP: Substance P
SRIF: Somatostatin
SS: Somatostatin
TRH: Thyrotropin releasing hormone
b: bovine
h: human
p: porcine
r: rat
s: salmon
sh: sheep
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Turner AJ, Hiscox JA, Hooper NM. 2004. ACE2: from vasopeptidase to SARS virus receptor. Trends in Pharmacological Sciences. 25(6):291-294. http://dx.doi.org/10.1016/j.tips.2004.04.001
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4,784,972,466,124,722,000 | Uncontrolled Asthma in Children: Topic Search Strategy
Topic Search Strategy: Uncontrolled Asthma in Children
Clinical Question
A PICOT question in nursing aids on the formulation of a clinical question and thus guide the search for evidence. Notably, according to Bethany (2019), PICOT is an acronym for the population (P), intervention (I), comparison (C), outcome (O), and time (T). The members in my team were focused on the identification and evaluation of various pieces of evidence guided by the PICOT on the issue of children with hospital admissions for uncontrolled asthma. Notably, the problem of uncontrolled asthma is a profound one, especially for neonates as well as the other children and teens. According to the Centers for Disease Control and Prevention (CDC) (2019), pediatric asthma affects 4-12 percent of women, especially those in their childbearing years. Additionally, asthma in children and adolescents who are aged between 5 and 17 years is responsible for a total loss of 10 million school days each year (CDC, 2019). Moreover, the costs of caretakers for pediatric asthma is $726.1 million per year due to work absence (Engelkes et al., 2015). For children, asthma is not only detrimental to the health and wellbeing of children but can also lead to fatalities.
My PICOT question in support of the group topic is: in children and teens aged between 0-17 years (Population/patient) what is the impact of asthma education (Intervention) to expectant mothers compared to medications (Comparison) on the prevention of hospital admissions for uncontrolled asthma (Outcomes) over a one-year period (Time). As such, the purpose of the paper is to investigate the impact of asthma education and self-management strategies to the application of medications in the prevention of hospital admissions for uncontrolled asthma among neonates and teens. The comparison of the two interventions helps in the determination of the most effective one and hence lead to evidence nursing practice. Additionally, it will help in the discovery of new ways in which uncontrolled asthma can be managed, especially in children and teens.
Levels of Evidence
The level of evidence required for addressing the question enables a researcher to search for the most appropriate and quality evidence. The type of question I am asking is which intervention is more effective between the provision of asthma education and self-management interventions to the pregnant mothers and the provision of asthma medications to children in the prevention of hospital admissions arising from the condition. As such, I am seeking to compare the two therapies and determine which one should be used. The best type of evidence which can be used to answer the question is the randomized controlled trial (RCT). RCT falls under level 1 of the level of evidence (LOE), which provides studies of good quality (Dang & Dearholt, 2017). Notably, a RCT is a comparative, prospective experiment that is conducted under controlled conditions (Bhide, Shah, & Acharya, 2018). The allocation of the interventions is done in a random approach to the comparison groups. Additionally, a RCT is effective in evaluating the relationship between an intervention and outcome. A RCT is a quantitative design which we used will tell whether the use of education outweighs the adoption of pharmacological therapies in the prevention of hospital admissions from uncontrolled asthma in newborns and teens.
Search Strategy
The search for the different articles and resources which I used to respond to the clinical question was done in different databases via the use of key terms and phrases. In specific, I used search terms such as “education in the management of neonate asthma,” “self-management interventions for pediatric asthma,” “pharmacological interventions of asthma in newborns,” “effectiveness of education of expectant women in the prevention of asthma in newborns,” “education versus medications in the prevention of asthma in children and teens.” One of the key databases that I used is the Agency for Healthcare Research & Quality (AHRQ). In specific, the AHRQ database uses various quality indicators in the determination of the standards of quality healthcare and whether healthcare facilities meet those standards. Additionally, Google Scholar was used in exploring the numerous studies which have been published on the subject matter of preventing hospital admissions from uncontrolled asthma in children and teens. The AHRQ will provide the provider-level indicators which should be monitored to ensure that avoidable hospitalizations are prevented.
I made various decisions in refinement to get the required articles down to a reasonable number for review. One of those was the inclusion and exclusion criteria. In specific, the studies had to deploy randomized controlled trials. Additionally, they had to be published less than ten years ago. Furthermore, they had to be relevant to the clinical issue. Using such limits ensured that the articles were filtered with the most relevant and recently published ones being used. Using the limits ensured that the only articles which came up were those that were of high quality and could provide relevant information about the clinical issue. In my next paper and the group’s work, two articles will provide guidance. One of those is Rice et al. (2015)’s “LEAP: A randomized–controlled trial of a lay-educator inpatient asthma education program.” The other article is “Management based on exhaled nitric oxide levels adjusted for atopy reduces asthma exacerbations in children: a dual centre randomized controlled trial” by Petsky et al. (2015). The choice of these two articles is based on their ability to conduct RCTs in evaluating whether education and medications are effective in the prevention of unavoidable hospitalizations of newborns with uncontrolled asthma.
Conclusion
Evidence-based practice allows for the use of interventions which have been proven and found effective in addressing various conditions. My team focused on the identification of the interventions which could be used to prevent avoidable hospitalizations of children and teens with uncontrolled asthma. I conducted a literature search of research studies which addressed my clinical questions, which is on addressing uncontrolled asthma. The articles which could help in the clinical question were RCTs, which fall under the level I of evidence. Using such a level of evidence helped in getting quality and relevant articles. The search used key terms/phrases and was done on the AHRQ and Google Scholar databases. Two articles were chosen, which were relevant and those which provided appropriate information for the clinical issue. The proposed study will provide evidence-based practice interventions for the prevention of avoidable hospitalizations of neonates and teens with uncontrolled asthma.
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2,358,272,959,534,679,000 |
Net carbs is simply total carbs minus fiber and non-digestible sugar alcohols, like erythritol. (This doesn’t apply to high glycemic sugar alcohols, like maltitol.) We don’t have to count fiber and certain sugar alcohols in net carbs, because they either don’t get broken down by our bodies, are not absorbed, or are absorbed but not metabolized. (Read more about sugar alcohols here.)
You’ll quickly find that salads are your friend when in ketosis, and for a good reason: they provide lots of food to fill you up, but they’re not going to bog you down. A bed of spinach with some red onion, bacon, a little tomato, and a hot sauce vinaigrette is quick and delicious. Add in some protein – perhaps that leftover salmon from day 1 – and you’ve got a complete, healthy lunch.
This is a wealth of information. My husband and I are starting the keto diet tomorrow and I knew nothing about it. When I sat down to look up information about it, I found this. Thank you! This is everything I need to know in one place. We are not as healthy as we’d like to be and I am optimistic this will help us obtain our goals, along with an exercise plan.
Advocates for the diet recommend that it be seriously considered after two medications have failed, as the chance of other drugs succeeding is only 10%.[9][31][32] The diet can be considered earlier for some epilepsy and genetic syndromes where it has shown particular usefulness. These include Dravet syndrome, infantile spasms, myoclonic-astatic epilepsy, and tuberous sclerosis complex.[9][33]
Hi Kelly, All packaged foods will have a nutrition label that list the macros per serving, including fat, protein and cabrohydrates. Net carbs, which is what most people look at for low carb and keto, are total carbs (the amount on the label) minus fiber and sugar alcohols, as explained in the article above. I have a low carb food list here that gives you a full list of all the foods you can eat, and the net carbs in each. You can also sign up above to be notified about the meal plans, which are a great way to get started.
Reduced hunger. Many people experience a marked reduction in hunger on a keto diet. This may be caused by an increased ability of the body to be fueled by its fat stores. Many people feel great when they eat just once or twice a day, and may automatically end up doing a form of intermittent fasting. This saves time and money, while also speeding up weight loss.
The transition process can be hard, especially when moving away from a diet that is normally carbohydrate heavy. This can sometimes bring on flu-like symptoms for a couple of days – ‘keto flu’ is a thing! Symptoms of the 'keto flu' include brain fog and fatigue, moodiness, migraines, and muscle cramping or tightness, which usually occur as a result of electrolyte changes or dehydration.
Hi 😀 yes I have a question, just starting this Keto diet, so we’re very new at this but my boyfriend had a heart attack 8 years ago so we need to be very careful to not get to high on fat with him. Can he still benefit from this diet. His Doctor said he needs to get some of his weight off he is having a hard time breathing. The Doctor said a low carb diet. But I, we would like to try the Keto diet.
The ketone bodies are possibly anticonvulsant; in animal models, acetoacetate and acetone protect against seizures. The ketogenic diet results in adaptive changes to brain energy metabolism that increase the energy reserves; ketone bodies are a more efficient fuel than glucose, and the number of mitochondria is increased. This may help the neurons to remain stable in the face of increased energy demand during a seizure, and may confer a neuroprotective effect.[56]
On a ketogenic diet, your entire body switches its fuel supply to run mostly on fat, burning fat 24-7. When insulin levels become very low, fat burning can increase dramatically. It becomes easier to access your fat stores to burn them off. This is great if you’re trying to lose weight, but there are also other less obvious benefits, such as less hunger and a steady supply of energy. This may help keep you alert and focused.
Many ketogenic dieters also swear by MCT oil. (MCT simply stands for medium chain triglycerides.) MCT's energy-sustaining powers can be explained as follows: When MCT oil is metabolized in the body, it behaves more like a carbohydrate than a fat. Unlike other fats, MCT oil does not go through the lymphatic system. Instead, it is transported directly to the liver where it is metabolized so it releases energy like a carbohydrate and creates lots of ketones (which can be used for fuel) in the process.
However, Kinobody also recommends that you try a “reverse pyramid” workout regimen. In this regimen, you start by doing a short set with the highest weight possible, and then you gradually work your way down to lighter weights and longer sets. Also, you can try another variant of the pyramid workout called the “triangle.” In this pyramid workout variant, you include some warmup sets, but these sets are not included in the counting structure of your pyramid workout.
The first signs of ketosis are known as the “keto flu” where headaches, brain fogginess, fatigue, and the like can really rile your body up. Make sure that you’re drinking plenty of waterand eating plenty of salt. The ketogenic diet is a natural diuretic and you’ll be peeing more than normal. Take into account that you’re peeing out electrolytes, and you can guess that you’ll be having a thumping headache in no time. Keeping your salt intake and water intake high enough is very important, allowing your body to re-hydrate and re-supply your electrolytes. Doing this will help with the headaches, if not get rid of them completely.
After years of developing his personal muscle building regimen and sharing it with others, Kinobody founder Greg O’Gallagher found that something was missing from his routine. He realized that he needed a way to maintain the exact bodyweight that most perfectly fit his needs, and from this realization, the Bodyweight Mastery Program was born. This program is offered at a discounted $49, and the exercises in the Bodyweight Mastery Program can be done anywhere. To explain the importance of bodyweight training, Greg invokes the example of James Bond.
Over time, Greg found that the number of times a client went to the gym didn’t seem to have much of an impact on their weight loss or muscle growth. He determined that exercise is actually a stressor, and that intense exercise should only be engaged in intermittently. Greg found that the body needs time to recover between training sessions, and from this discovery, MEGA minimal effort growth acceleration was born.
Hi, I’m still a bit skeptical, I have seen some of my friends do the keto diet, and have had good results. Though I am still not sure about the idea of the fats being eaten. They say they eat meat with the fat and must do so, is this correct? Also isn’t this not good for the body especially for the kidneys? Second, can a diabetic do this diet? There are many questions running through my head.
The ketogenic diet has been studied in at least 14 rodent animal models of seizures. It is protective in many of these models and has a different protection profile than any known anticonvulsant. Conversely, fenofibrate, not used clinically as an antiepileptic, exhibits experimental anticonvulsant properties in adult rats comparable to the ketogenic diet.[58] This, together with studies showing its efficacy in patients who have failed to achieve seizure control on half a dozen drugs, suggests a unique mechanism of action.[56]
Please Note: The author of this site is not engaged in rendering professional advice or services to the individual reader. The ideas, procedures, and suggestions contained within this work are not intended as a substitute for consulting with your physician. All matters regarding your health require medical supervision. The author shall not be liable or responsible for any loss or damage allegedly arising from any information or suggestions within this blog. You, as a reader of this website, are totally and completely responsible for your own health and healthcare.
I am trying to get back into keto. I did it before and I was so happy when I lost 10lbs (I did the keto for a month). I am ready to go back to this lifestyle. All this information is very helpful, I have written it all down so it can be easier for me to remember what is allowed and what is not. Looking forward to get back on this keto journey. Thank you for all the great info.
To figure out how many fat grams specifically you want, you would take the total number of calories it takes to maintain your body weight (normally around 14-16 calories per pound of body weight). Subtract your protein calories from that number and then divide by 9 (number of calories per gram of fat). This should give you how many total fat grams you need to eat per day.
Hi, my name is Kate and I would like to share my story. Up until about 2 years ago, I was 30 pounds overweight. Over the years I had followed many different diet plans, but failed every single time. I was "blessed" with a pear shaped body and no matter what i did, I always retained lots of stubborn fat in my lower body. Everything changed when I found the right diet program. Read my story here ==> http://bit.ly/mydietstory
We tried hard to find out more; in fact, there’s a section on the website called “how it works.” Unfortunately, there is very little information provided other than generic statements and promises. The site does say that it wants you to be as physically strong as possible to live up to the name “Superhero.” “Get ready to bench 300+ lbs, perform 100-lb pull ups and curl 75-lb dumbbells.”
In many developing countries, the ketogenic diet is expensive because dairy fats and meat are more expensive than grain, fruit and vegetables. The modified Atkins diet has been proposed as a lower-cost alternative for those countries; the slightly more expensive food bill can be offset by a reduction in pharmaceutical costs if the diet is successful. The modified Atkins diet is less complex to explain and prepare and requires less support from a dietitian.[55]
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-3,312,702,981,160,313,300 | About the Eye
The eyes are two of the most important parts of the human body. Understanding how they work can help promote knowledge about how to care for them and deal with the effects that can impact vision.
How the Eye Works
Sources: Video/video links - courtesy of geteyesmart.org; eye health information from the American Academy of Ophthalmology. | {
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-8,127,597,317,663,627,000 | Skip to content
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• Research article
• Open Access
The anteroposterior axis of the tibia is adjusted to approximately a right angle to the anterior pelvic plane in the standing position in patients with hip dysplasia similar to normal subjects: a cross-sectional study
• Norio Imai1, 2Email author,
• Dai Miyasaka2,
• Hayato Suzuki2,
• Kazuki Tsuchiya3,
• Tomoyuki Ito4,
• Izumi Minato5 and
• Naoto Endo2
Journal of Orthopaedic Surgery and Research201813:105
https://doi.org/10.1186/s13018-018-0816-z
Received: 21 January 2018
Accepted: 20 April 2018
Published: 2 May 2018
Abstract
Background
We previously described that the anteroposterior (AP) axis of the tibia is approximately perpendicular to the transverse axis of the anterior pelvic plane (APP) in the standing position in healthy subjects. The purpose of this study was to investigate the rotational alignment between the APP and clinical epicondylar axis and the AP axis of the tibia relative to pelvic coordination in the standing position in normal subjects and in women with developmental dysplasia of the hip (DDH) to aid decision making for surgeons in the alignment of implants in total hip or knee arthroplasty.
Methods
This study included 77 Japanese women. Twenty-nine in the DDH group underwent curved periacetabular osteotomy; 48 women without lumbago and knee pain were included in the normal group. Femoral neck anteversion (FNA), condylar twist angle, and knee rotation angle were measured in femoral coordination. The angle between the femoral neck axis and clinical epicondylar axis (CEA) was measured, the transverse axis of the APP was also measured, and the angle between the AP axis of the tibia and transverse axis of the APP was calculated.
Results
There was a moderate negative correlation between FNA and CEA relative to the APP. This finding indicated a trend towards greater FNA leading to more internal rotation. Knee rotation angle (KRA) relative to the APP was 1.65° ± 5.58° in the normal group and − 2.65° ± 7.57° in the DDH group. This finding indicated that the tibia AP axis was approximately perpendicular to the APP in the standing position both in the normal and DDH groups.
Conclusion
We found that the tibia AP axis was at approximately a right angle to the transverse axis of the APP in the standing position in both the normal and DDH groups, while the KRA was different in the normal and DDH groups. These findings may prove helpful for positional alignment investigations needed for implantation in total hip or knee arthroplasty and gait analysis.
Keywords
Anteroposterior axis of tibiaTibiofemoral rotationFemoral neck anteversionClinical epicondylar axisAnterior pelvic planeLower extremity alignment
Background
Spatial and geometrical malalignment between the femur and tibia such as tibiofemoral abnormal rotation is considered to cause some pathologies in the lower extremities, such as osteoarthritis of the knee and patellofemoral disorder including patellar dislocation, among others [17]. Moreover, Watanabe et al. [8] indicated that when preoperative rotational mismatch persisted, rotational mismatch could still occur after total knee arthroplasty, even if the components were placed in the correct position relative to anatomical landmark. Therefore, it is important to evaluate tibiofemoral rotation correctly.
Formerly, the alignment of the lower extremity was commonly evaluated with two-dimensional (2D) plain X-ray [7, 9, 10]. However, measurements with this 2D method are affected by the position of the pelvis and lower extremities of the subjects [11], and it is considered to produce measurement error and lead to reduced accuracy and reproducibility. Furthermore, the 2D method cannot assess rotational alignment such as tibiofemoral rotation.
Several reports have described that the anteroposterior (AP) axis of the tibia, which is defined by a line passing through the middle of the posterior cruciate ligament and the medial border of the patellar tendon attachment (so-called Akagi’s line), is at almost a right angle to the clinical epicondylar axis (CEA) [8, 12, 13].
We previously found that the CEA and the transverse axis of the anterior pelvic plane (APP) are approximately parallel in the standing position in healthy subjects [14]. Moreover, we also described that the AP axis of the tibia is approximately perpendicular to the transverse axis of the APP in the standing position in healthy subjects [15]. It is generally known that the proximal femur is more anteverted in patients with developmental dysplasia of the hip (DDH) [16, 17]. Consequently, it is speculated that the femur is more internally rotated during standing and walking in individuals with DDH compared to that in normal persons [18]. However, to our knowledge, no report has described the rotational alignment between the anterior pelvic plane (APP) and anteroposterior (AP) axis of the tibia in patients with DDH.
The purpose of this study was to investigate the rotational alignment between the APP and CEA, and the AP axis of the tibia relative to pelvic coordination in the standing position in normal subjects and women with DDH to aid surgeons in decision making for the alignment of implants in total hip or knee arthroplasty, as well as treatment for patellar dislocation and positional alignment investigations such as gait analysis.
Methods
Subjects
For this study, 77 Japanese women were enrolled because patients with DDH are reported to have a 9:1 female dominance [19]. Twenty-nine patients (29 legs) with bilateral DDH (mean age, 35.8 ± 8.8 years) from our institution who had undergone curved periacetabular osteotomy [20] for the early treatment of osteoarthritis of the hip joint due to acetabular dysplasia and whose center-edge angle of the hip joint was < 25°, as evaluated in the anteroposterior view on a plain radiograph of the hip, were enrolled in the DDH group. Patients with DDH who had previously undergone hip surgery or those with Crowe stages 2–4 of subluxation or Tönnis grades 2 and 3 of arthritic change according to plain radiographs of the hip bilaterally were excluded from this study. We also included 48 women (48 legs; mean age of women, 54.0 ± 10.8 years) without lumbago and knee pain and without any abnormal findings of the knee and spine on radiographic examination recruited from the family of outpatients and medical staff in the normal group. Computed tomography scans from all participants were examined to reconstruct a 3D bone model. With regard to the DDH group, computed tomography scans were examined before their operation to plan for osteotomy. This study was performed with the approval of the institutional research board of Niigata University Medical and Dental Hospital and written informed consent was obtained from the participants of the normal group. With regard to DDH group, the need for informed consent was waived because of the cross-sectional nature of this study that did not provide an intervention.
Radiographic examinations, including biplanar computed radiography images, were performed in the standing position, where each subject adopted a relaxed position with their knees fully extended and the toes aligned to the shoulders. Computed tomography from the pelvis to proximal tibia was also performed in the supine position with the knees fully extended.
Measurements
We used ZedHip® software (Lexi, Tokyo, Japan) to create three-dimensional (3D) digital bone models of the pelvis and femur and accurately reconstruct the spatial relationship between them [15, 21, 22]. We adjusted the 3D pelvis model to the APP [23], which contains both the anterior superior iliac spines and the pubic symphysis, which are the origin of this pelvis coordinate system. In the ZedHip® system, when the pelvis was adjusted to the APP, other bones such as the femur and tibia synchronously moved according to the pelvis position. With regard to the femoral coordinate system, the 3D model of the femur was positioned with the retrocondylar plane, which contains the bilateral posterior condyles and the most posterior point of the greater trochanter [24]. The femoral neck axis was defined as that in the method described by Sugano et al. [25] and measured in the plane just below the femoral head. Femoral neck anteversion (FNA) was measured as the angle between the femoral neck axis as above and the posterior condylar axis (PCA) (Fig. 1). Further, the CEA was defined as the line connecting the most prominent point of the medial epicondyle and the lateral epicondylar prominence. The condylar twist angle (CTA) was measured as the angle connecting the CEA and PCA (positive values indicate that the CEA is externally rotated relative to the PCA) (Fig. 2) [18]. The determination of the CEA and measurement of the CTA were also performed in the retrocondylar plane. The line through the midpoint of the lateral epicondylar prominence and the most prominent point of the medial epicondyle, and the line perpendicular to the CEA was defined as the femoral AP axis. With regard to the AP axis of the tibia, Akagi’s line [14] was selected. The knee rotation angle (KRA) was measured as the angle connecting the femoral AP axis and the AP axis of the tibia, projected onto the horizontal plane of the femoral coordinate system (Fig. 2). In the present study, negative values were defined as the internal rotation of the tibia relative to the femur and positive values as the external rotation.
Figure 1
Fig. 1
Measurement of the FNA. FNA (asterisk) is the angle between the femoral neck axis (a) and the PCA (b). FNA: femoral neck anteversion, PCA: positive external rotation
Figure 2
Fig. 2
Measurement of the CTA and knee rotation angle. CTA (dagger) is the angle between the PCA (b) and the CEA (c). KRA (number sign) is the angle between the tibial AP axis (d) and the line perpendicular to the femoral CEA (e). The solid lines represent the contour of the projected femoral condyle onto the femoral horizontal plane. The dotted lines represent the contour of the projected tibial condyle onto the femoral horizontal plane. CEA: clinical epicondylar axis, CTA: condylar twist angle, KRA: knee rotation angle, PCA: positive external rotation
FNA, CEA, and PCA relative to the APP were also measured in the standing position (APP-FNA, APP-CEA, and APP-PCA, respectively) using HipCAS® software (Lexi, Tokyo, Japan). The 3D digital bone models were projected onto the biplanar computed radiography images to match the contours of the 3D digital models with the computed radiography images for rotations and translations [15, 21, 22]. Kobayashi et al. [22] previously described the accuracy of HipCAS® in creating a 3D digital bone model that accurately reproduced the spatial relationship between the pelvis and the femur, and calculated the various alignment parameters within 1° and 1 mm of accuracy. Therefore, projection error and misalignment were estimated to be small in the current study. APP-FNA, APP-CEA, and APP-PCA were the angles that connected the FNA, CEA, and PCA projected onto the transverse plane of the pelvis and the APP was the line connecting both anterior superior iliac spines (Fig. 3).
Figure 3
Fig. 3
Measurement of the APP-FNA, APP-PCA, and APP-CEA. APP-FNA (white circle), APP-CEA (white square), and APP-PCA (white star) were defined as the angles connecting the FNA (a), PCA (b), and CEA (c), respectively, to the transverse axis APP (f). APP: anterior pelvic plane, CEA: clinical epicondylar axis, FNA: femoral neck anteversion, PCA: positive external rotation
Lastly, we calculated the estimated angle between the APP and AP axis of the tibia from the KRA in femoral coordination and APP-CEA with the formula: (AP axis of the tibia relative to the APP transverse axis) = (APP-CEA) − (KRA, the angle between the AP axis of the tibia and the line perpendicular to the CEA), as in our previous study [18] (Fig. 4).
Figure 4
Fig. 4
Calculation of the estimated AP axis of the tibia and the APP transverse axis. We calculated the estimated angle between the AP axis of the tibia (d) and the perpendicular line to the APP (g) from the KRA (number sign) and APP-CEA (white square) with the formula: (AP axis of the tibia relative to the APP transverse axis (white triangle)) = (APP-CEA) − (KRA). The solid lines represent the contour of the projected femoral condyle onto the femoral horizontal plane. The dotted lines represent the contour of the projected tibial condyle onto the femoral horizontal plane. AP: anteroposterior, APP: anterior pelvic plane, CEA: clinical epicondylar axis, KRA: knee rotation angle
Statistical analysis
We used SPSS statistical software (SPSS version 24, Inc., Chicago, IL, USA) to analyze the data. Regarding the FNA, CTA, KRA, APP-FNA, and APP-CEA, we used Pearson coefficients to determine the correlation coefficients. To evaluate variation, we calculated the mean absolute difference (MAD), variability (standard deviation), and intraobserver reliabilities with intraclass correlation coefficients (ICCs) and a two-sided 95% confidence interval. We measured intraobserver reliability with two measurements by one observer at at least 1-week intervals. Moreover, we also compared the measurements to assess the interobserver reliability by a single measurement with two observers. A p value < 0.05 was considered statistically significant.
Results
The details of the research subjects are demonstrated in Table 1. The FNA and KRA was significantly larger in the DDH group, while the CTA was almost the same (Table 2). There was a moderate positive correlation between the FNA and APP-FNA (regression equations: y = 0.32x + 5.57 in the normal group, y = 0.43x + 2.87 in the DDH group) and a negative correlation between the FNA and APP-CEA (regression equations: y = − 0.12x + 1.74 in the normal group, y = − 0.32x + 3.04 in the DDH group) (Table 3). This finding indicated a trend towards a greater FNA leading to more internal rotation. We also found a moderate positive correlation between the CTA and KRA in only the DDH group (regression equation: y = 1.51x − 9.57). This finding indicated a trend towards greater CTA leading to more external rotation of tibia relative to the femur in only the DDH group; there was no significant difference the between normal and DDH groups.
Table 1
Baseline characteristics of the participants
Normal group (n = 48)
DDH group (n = 29)
Age (years)
54.0 ± 10.8***
35.8 ± 8.8***
Body height (cm)
153.6 ± 5.8
159.4 ± 6.8
Body weight (kg)
52.6 ± 7.6
55.5 ± 7.5
BMI (kg/m2)
22.3 ± 2.7
21.9 ± 2.9
Values are mean ± standard deviation
BMI body mass index
*p < 0.05, **p < 0.01, ***p < 0.001
Table 2
Measurement of anatomical and positional angles
Normal group (n = 48)
DDH group (n = 29)
FNA (deg)
17.10 ± 9.16***
28.60 ± 12.69***
CTA (deg)
7.24 ± 1.89
7.37 ± 2.09
KRA (deg)
1.98 ± 6.86***
8.88 ± 7.02***
APP-FNA (deg)
10.73 ± 8.21*
16.71 ± 10.59*
APP-CEA (deg)
− 0.62 ± 4.24**
− 5.21 ± 8.55**
APP-tibia AP axis (deg)
1.65 ± 5.58*
− 2.65 ± 7.57*
Values are mean ± standard deviation
AP anteroposterior, APP anterior pelvic plane, APP-CEA clinical epicondylar axis relative to the APP, APP-FNA FNA relative to the APP, CTA condylar twist angle, FNA femoral neck anteversion, KRA knee rotation angle
*p < 0.05, **p < 0.01, ***p < 0.001
Table 3
Correlation coefficient between each parameter in the normal and DDH groups
FNA (deg)
CTA (deg)
KRA (deg)
APP-FNA (deg)
APP-CEA (deg)
APP-tibia AP axis (deg)
FNA (deg)
0.085
0.130
0.421*
− 0.352*
− 0.009
0.365
0.319
0.433*
− 0.451*
− 0.176
CTA (deg)
− 0.211
0.142
0.176
0.096
0.505*
0.205
− 0.042
0.338
KRA (deg)
0.086
− 0.218
− 0.214
0.107
− 0.181
0.266*
APP-FNA (deg)
− 0.396*
− 0.077
0.410*
0.226
APP-CEA (deg)
0.048
0.375*
Upper row: normal group; lower row: DDH group
AP anteroposterior, APP anterior pelvic plane, APP-CEA clinical epicondylar axis relative to APP, APP-FNA FNA relative to APP, CTA condylar twist angle, FNA femoral neck anteversion, KRA knee rotation angle
*p < 0.05
The KRA relative to the APP was 1.65° ± 5.58° in the normal group and − 2.65° ± 7.57° in the DDH group (Table 2). This finding indicated that the tibia AP axis was approximately perpendicular to the APP in the standing position.
Regarding validation, we obtained a high ICC for both intraobserver and interobserver reliability (Table 4).
Table 4
Intra- and interobserver reliabilities of each parameter
Intraobserver reliability
Interobserver reliability
MAD ± SD
ICC
MAD ± SD
ICC
FNA (deg)
1.28 ± 1.45
0.908
1.55 ± 1.82
0.858
CTA (deg)
0.64 ± 0.48
0.936
0.79 ± 0.57
0.918
KRA(deg)
1.47 ± 1.72
0.861
1.87 ± 1.84
0.829
APP-FNA (deg)
1.57 ± 1.86
0.818
1.78 ± 1.93
0.806
APP-CEA (deg)
0.73 ± 0.52
0.937
0.86 ± 0.77
0.914
APP-tibia AP axis (deg)
1.24 ± 0.92
0.868
1.58 ± 1.34
0.857
AP anteroposterior, APP anterior pelvic plane, APP-CEA clinical epicondylar axis relative to the APP, APP-FNA FNA relative to the APP, CTA condylar twist angle, FNA femoral neck anteversion, ICC interclass correlation coefficient, KRA knee rotation angle, MAD mean absolute difference, SD standard deviation
Discussion
In this current study, we evaluated the spatial relationship between the tibia AP axis and APP during standing in normal subjects and patients with DDH.
We found that the mean value of the KRA was 2.06° in the normal group. This value is similar to that obtained in previous reports for normal participants [1416]. Conversely, in patients with DDH, the KRA was 8.88°, indicating that the tibia AP axis was not nearly at a right angle to the CEA; instead, it was externally rotated relative to it. Nevertheless, the KRA relative to the APP was almost perpendicular to the APP in the standing position in both groups (1.65° in the normal group and − 2.65° in the DDH group).
Parikh et al. previously described that the medial rotation of the femur attributed to increased femoral anteversion leads to increased compensatory lateral rotation of the tibia, resulting in abnormal patellofemoral loads, and increased compression of the lateral patella facet and tension of the medial patellofemoral ligament; these biomechanical alterations consequently caused a tendency for anterior knee pain and/or lateral subluxation of the patella [26]. In patients with DDH, the femur is generally more anteverted and tibia is externally rotated relative to the femur; therefore, anterior knee pain and/or lateral subluxation of the patella may be more likely to occur than in normal persons. Moreover, surgeons should be mindful of mistracking, subluxation, and/or dislocation of patella in patients with DDH who undergo total knee arthroplasty.
We previously described that the CEA, considered as the functional flexion-extension axis of the knee [27, 28], was approximately parallel to the transverse axis of the APP plane in the standing position in normal subjects [14]. Moreover, we also reported that the AP axis of tibia was at approximately a right angle to the transverse axis of the APP plane in the standing position in normal subjects [18]. In our current study, we found that the tibia AP axis was approximately perpendicular to the APP, while the KRA was significantly larger in the DDH group. These results in our studies may be important to integrate these two axes with regard to not only the anatomical reference, but also the kinesiology. They may also prove helpful to decide the alignment of implants in total hip or knee arthroplasty, treatment for patellar dislocation, and positional alignment investigation such as gait analysis. However, further examination is required with regard to knee motion in patients with DDH because rotation between the tibia and femur during flexion and extension are the same in normal persons and patients with DDH.
The current study has several limitations. First, only a few subjects and only middle age people were enrolled in the normal group. Therefore, we cannot perform a power analysis. Second, the KRA was examined in the supine position, while the APP-FNA and APP-CEA were examined in the standing position. However, according to several reports, the difference in KRA between the supine and standing positions appears negligible [15, 16]. Kozanek et al. stated that the KRA was approximately 3° at contralateral toe-off, and nearly 0° from ipsilateral heel-rise to contralateral heel-strike, respectively, during the stance phase of treadmill gait [29]. Third, there was a difference in the plane of the measurement; the KRA was examined in femoral coordination, while the APP-FNA and APP-CEA were examined in pelvis coordination. Chen et al. reported that the tibia was internally rotated approximately 3° relative to the femur when the knee was flexed from 0° to 8° [30]. We preliminarily measured the femur in the 5° flexion and 3° adduction relative to the APP in the standing position on average and our computer simulation found that, with the lower extremity in this position, the expected difference of the angle was not more than 0.5°. Therefore, we believe that the position of the lower extremity did not affect the results of this study. Fourth, we examined only women in this study, because patients with DDH are reported to have a 9:1 female dominance [19]. In our institution, patients with DDH who had undergone curved periacetabular osteotomy were less than 15 in number over 8 years. Similar examination is required in male subjects in the future.
Conclusions
We found that the tibia AP axis was at approximately a right angle to the transverse axis of the APP in the standing position in both the normal and DDH groups, while the KRA was 8.88° in the DDH group. From our results, we believe that the femur is adjusted such that the anteroposterior axis of the tibia is approximately at a right angle to the anterior pelvic plane in the standing position not only in normal persons, but also in patients with hip dysplasia. These findings may prove helpful to decide the alignment of implants in total hip or knee arthroplasty, treatment for patellar dislocation, and positional alignment investigations such as gait analysis.
Abbreviations
AP:
Anteroposterior
APP:
Anterior pelvic plane
CEA:
Clinical epicondylar axis
CTA:
Condylar twist angle
FNA:
Femoral neck anteversion
ICC:
Intraclass correlation coefficient
KRA:
Knee rotation angle
MAD:
Mean absolute difference
PCA:
Posterior condylar axis
Declarations
Acknowledgements
We would like to thank Editage (http://www.editage.com/) for English language editing and publication support.
Funding
The author received no specific funding for this work.
Availability of data and materials
All data generated or analyzed during this study are included in this published article.
Authors’ contributions
NI, DM, HS, IM, and TI contributed to the conceptualization and formulation. NI and KT did the investigation and data collection. NI carried out the statistical analysis. The study was performed under supervision of DM and NE. All authors read and approved the final manuscript.
Ethics approval and consent to participate
This study was performed with the approval of the institutional research board of Niigata University Medical and Dental Hospital. Written informed consent was obtained from the participants of the normal group. With regard to DDH group, the need for informed consent was waived because of the cross-sectional nature of this study that did not provide an intervention.
Competing interests
The authors declare that they have no competing interests.
Publisher’s Note
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Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Authors’ Affiliations
(1)
Division of Comprehensive Geriatrics in Community, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
(2)
Department of Orthopedic Surgery, Niigata University Medical and Dental Hospital, Niigata, Japan
(3)
Division of Advanced Materials Science and Technology, Niigata University Graduate School of Science and Technology, Niigata, Japan
(4)
Department of Orthopedic Surgery, Saiseikai Niigata Daini Hospital, Niigata, Japan
(5)
Department of Orthopedic Surgery, Niigata Rinko Hospital, Niigata, Japan
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Copyright
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DNRS Interactive DVD Series & Seminars
The Importance of Breathing Patterns in CFS (and Fibromyalgia) Symptoms & Recovery
by Blake Graham, BSc, AACNEM
www.nutritional-healing.com.au
September 1, 2009
I have heard about the supposed importance of breathing in chronic fatigue syndrome (ME/CFS) for many years, and never took it very seriously. Then I read an article in Alternative and Complementary Therapies journal titled “Clinical Roundup: How Do You Treat Chronic Fatigue Syndrome in Your Practice?” In the article, eight integrative/alternative medicine experts described how they treat ME/CFS.
While they come from a variety of different backgrounds, four of the eight mentioned the importance of breathing. This inspired me to look into the role of breathing in more detail. After studying this topic, I have become completely convinced that this is a very important issue.
The issues discussed here are all heavily interrelated. These relate to:
- The rate and depth of breathing,
- Dysfunction of the autonomic nervous system (ANS), and - Stress.
These issues collectively constitute a very important [cycle] which contributes to, and perpetuates, ME/CFS. And the treatment I’ll discuss is designed to break the cycle of these three issues. Some people have a bias against 'low tech', mind-body or free treatments, assuming they are not as potent as other treatments, so please keep an open mind as you read through this.
One of the sources I read was the book Bursting With Energy, by Dr. Frank Shallenberger. In it, he describes “Breathing Right” as one of the “Eight Secrets for Improving Energy.” A brief summary of this chapter, explaining the difference between chest and diaphragmatic breathing, is found online HERE.
Improper Breathing Retards Metabolic Energy Production
While people with ME/CFS have normal blood oxygen, cellular oxygen levels are often inadequate. Optimal breathing improves cellular oxygen concentration. Mitochondrial function, a key issue for those with ME/CFS, is highly dependent on oxygen levels for energy production. Shallenberger cites a case study in his book in which a person increased his metabolic energy production 20% after just half an hour of breathing instruction.
Dr. Sarah Myhill, MD, a co-author of “Chronic Fatigue Syndrome and Mitochondrial Dysfunction,” discusses the importance of breathing in ME/CFS. (See “Hyperventilation – Makes you feel as if you can’t get your breath.”). She writes:
"Hyperventilation – the idea here is that for whatever reason, the patient over-breathes. One cannot increase the oxygen carrying capacity of the blood this way, so oxygen levels are not increased, but carbon dioxide is washed out. This changes the acidity of the blood in such a way that oxygen sticks more avidly to hemoglobin.
“So oxygen is not released to the mitochondria where it is required, and so mitochondria go slow - so cells go slow, and this results in fatigue."
Stress and Breathing
The link between stress and breathing goes both directions.
• Higher stress levels cause faster/deeper breathing,
• And faster breathing causes higher stress levels.
Read "Breathing Matters - Stress" by ear/nose/throat specialist Dr. Jim Bartley for an excellent article on the relationship between stress and breathing.
The Autonomic Nervous System and Breathing to Restore Balance
The autonomic nervous system (ANS) is the part of the nervous system which controls involuntary functions. It is composed of two sections, the parasympathetic nervous system (PNS) and the sympathetic nervous system (SNS).
• The SNS activates our stress response (the ‘fight or flight' response),
• And the PNS counteracts the stress response and is associated with relaxation, energy conservation, digestion, etc.
In many chronic illnesses, this autonomic balance is impaired with an excessive SNS response and under-active PNS response. Research on those with ME/CFS suggests the PNS relaxation response is under-active and SNS 'fight or flight' activity is either depressed, associated with exhaustion of the stress response system, or over-reactive. As the autonomic nervous system is one of the major regulatory systems in the body, this is a huge problem.
What does this have to do with breathing?
Well, it turns out that our breathing rate is a key signal to the autonomic nervous system that SNS activation is needed, and certain breathing practices can be used therapeutically to restore balance in the autonomic nervous system.
• Even if you feel mentally calm, if your breathing rate is overly fast, as it is for many people, this causes SNS activation.
• Slow breathing (also called 'paced respiration') tones and normalizes activity of both the SNS and PNS.
Read the fascinating article “The Science of Coherent Breathing” by Stephen Elliott for an in depth discussion of the link between breathing and autonomic nervous system balance.
It's also interesting to note that energy medicine practices such as qigong (which literally means ‘breathing exercise’) believe that slow abdominal breathing is critical for the balance and flow of energy in our system.
Using Coherent or Resonant Breathing - Daily Breath Training
While breathing experts don’t agree on everything, they all agree that we generally breathe too fast and too shallow - and that predominantly breathing through our nose is ideal.
While a typical person might have 15 to 20 breath cycles per minute, an ideal number is 5 to10 cycles per minute at rest. For example, five breath cycles per minute = one breath cycle per 12 seconds, or inhaling for six seconds and exhaling for 6 seconds.
While we can’t quickly take up these new habits permanently, what we can do is daily breath training. A person can listen to an audio track which has a sound cue every six seconds. You simply inhale or exhale at each interval using the track like a metronome. Breathing at this rate is referred to as coherent or resonant breathing.
What are the benefits of doing this?
• On an immediate basis, this is deeply relaxing for most people.
• Cumulative over several weeks, daily breath training has numerous benefits. It improves the function and balance of the autonomic nervous system, which carries with it a host of benefits. Our natural breathing rhythm gradually shifts in the direction of that during the training so we don’t just benefit during the breathing exercises.
Coherent breath training is one of the best ways to reduce levels of stress. You can order a ‘breathing pacemaker’ CD called 'Respire I' or download the audio tracks as MP3s (free audio samples are available). I enjoy track 2, which has Tibetan bells as the breath cue.
I recommend that people with ME/CFS do this breath exercise, combined with the practices described below, for 25 minutes twice daily.
1. Breathe through your nose and you should be able to feel your abdominal region expand with each inhalation. Breaths should be gentle and relaxed, not forceful or high volume.
2. While performing the breathing exercise, mentally scan your body and release any obvious areas of tension, e.g., in your jaw, shoulders and chest.
Throughout the day, periodically observe your breathing, slow your breathing rate and make sure you are breathing through your nose and abdominally. Also use this breathing technique, combined with Ujjayi (pronounced "oo-jai") breathing described below, in times of acute stress.
Ten minutes of Ujjayi breathing at five breaths per minute is an excellent stress buster!
Ujjayi Breathing for Calming Anxiety
In the excellent book How to Use Herbs, Nutrients, and Yoga in Mental Health Care, written by three psychiatrists affiliated with universities in New York, the authors recommend 'Respire I' from www.coherence.com, cited above. They also recommend combining this with a simple breathing technique called Ujjayi breathing (literally, 'loud breathing'), a yogic breathing technique. They write:
"Those who are able to learn Ujjayi breathing can be instructed to use the Respire I CD with Ujjayi for even greater effects. Ujjayi breathing creates a sound using contraction of laryngeal muscles with partial closure of the glottis, permitting fine regulation of the respiratory rate while increasing airway resistance, intrathoracic pressure, baroreceptor stimulation, HRV, RSA (Calabrese, Perrault, Dinh, Eberhard, & Benchetrit, 2000), and stimulation of somatosensory afferents in the pharynx, lungs, chest wall, and diaphragm. When done at a slow rate (2 to 6 breaths per minute) ... Ujjayi is physically and mentally calming.
"In clinical practice, the authors find that basic Ujjayi breathing is the single most rapidly effective breath intervention for anxiety symptoms in patients diagnosed with anxiety disorders... The patient who is taught Ujjayi breathing will usually experience a profound sense of physical and mental calmness within five to 10 minutes of doing this technique."
Type in “Ujjayi breath” at http://www.youtube.com to watch videos on this breathing technique. Incorporate Ujjayi breathing along with the coherent breathing for the duration that suits your body and complete the duration of the breathing time by simply breathing along to the sound cues.
You may need to start with just 5 minutes of Ujjayi breathing and build up over time as is comfortable. Make sure you keep your neck, throat, shoulders and chest relaxed as you breathe. It shouldn't feel strained or forceful, just relaxed and slow with a partial contraction of your throat muscles.
Complementary Practices – More Options for Banishing Stress
Start with the combination of coherent/resonant and Ujjayi breathing until it feels natural and easy. At this point, you can add aspects of other mind-body practices such as meditation or qigong for further benefit. A few options are as follows:
• Heart focus. Fascinating research from The Institute of HeartMath has found that focusing attention on the area of your heart improves the balance and tone of the autonomic nervous system. In the HeartMath coherence exercises, they instruct you to imagine your breath is flowing in and out of the area of your heart.
• Mantra based or breathing meditation. For example, focus attention on the flow of your breath.
• Qigong meditation. Qigong traditions believe the abdominal region between your navel and pelvic bone, called the lower dantian, is a key energy reservoir. Qigong practices often involve focusing attention, or meditating, on this area.
Related Articles:
Blake Graham, BSc, AACNEM, is a clinical nutritionist specializing in nutritional and environmental treatments for patients with ME/CFS, FM, and other chronic conditions. He is an Associate of the Australasian College of Nutritional and Environmental Medicine, directs the Nutritional Healing clinic in Perth (WA) http://www.nutritional-healing.com.au, and publishes a free Nutritional Healing e-Newsletter.
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61,053,757,831,555,090 | ELearning/Foundations/PhysicalBrain
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Before we discuss the physical basis of learning, we would do well to review the basic structure and functioning of the brain. This is a very abbreviated view and you are encouraged to explore further if this description interests or confuses you. We move from the macro to the micro.
Energy requirements
Human brains are expensive - metabolically speaking. It takes lot of energy to run our master organ. While making up about 2% of body weight, it consumes 20% of its energy. About two-thirds of the brain's energy budget is used to help nerve cells "fire" or send signals. The remaining third is used for "housekeeping," or cell-health maintenance (Swaminathan, 2008). Energy travels to the brain via blood vessels in the form of glucose, which is transported across the blood-brain barrier and used to produce adenosine triphosphate (ATP), the main currency of chemical energy within cells. Unlike how strenuous physical activity drains the body's energy much more intensely than sitting in a chair, high demand cognitive tasks (taking the SATs for example) increase energy consumption a tiny amount compared with the brain's gluttonous baseline intake (Jabr, 2012). Mental exhaustion, then, is much more a psychological phenomenon than a physical one.
Anatomy
There are about 100 trillion (100,000,000,000,000) connections between the 86 billion neurons in the brain. The average neuron makes about 1,000 synaptic connections with other neurons. Many of these connections occur with neighboring cells, but just as many occur with distance cells throughout the brain. It is a reality, then, that the brain is a complex, dense network of computational nodes communicating flexibly and along multiple pathways at nanosecond speeds. This interaction gives rise to our thoughts, feelings, and who we are. Truly amazing.
There are many ways in which to divide the brain. Here we begin with a simple three-part model.
1. Major brain regions
The hindbrain is the oldest part of the brain, from both evolutionary and growth perspectives. It includes the cerebellum, the pons and the medulla oblongata, which function collectively to support vital bodily processes. The medulla is joined to the spinal cord and controls unconscious body functions such as breathing, swallowing, blood circulation and muscle tone. Located above the medulla is the pons which serves as a bridge to connect the brainstem and the cerebellum. The pons receives information from visual areas to control eye and body movements and also plays a role in controlling patterns of sleep and arousal. Information is relayed from the pons to the cerebellum to control the coordination of muscular movements and maintain equilibrium. The cerebellum is always involved in learning that involves movement.
The midbrain sits between the forebrain and the hindbrain and forms a major part of the brainstem, which connects the spinal cord and the forebrain. It includes the tectum, cerebral penduncles, and the substantia nigra. These structures form connections between the cerebral cortex and the brainstem and spinal cord to control sensorymotor processes such as movement. Interestingly, the midbrain is the sole source of dopamine for the brain.
The forebrain is the largest part of the brain, most of which is made up of the cerebrum, or cerebral cortex. Other structures include components of the limbic system and basal nuclei (also called the basal ganglia), plus the corpus callosum connecting the hemispheres.
External lobes of the cerebral cortex Prefrontal cortices Limbic systemcomponents
2. External cortices of the brain 3. Prefrontal cortices 4. Limbic system components
Cerebral cortex
The cortex consists of six layers, each with different neuronal shapes, sizes and density as well as different organizations of nerve fibers. Each cortical hemisphere (Figure 2) is divided into lobes and subcortices: frontal or prefrontal (conscious thought), motor, somatosensory, parietal (integration of senses), occipital (sight), temporal (sound and smell), cingulate (also called the limbic cortex and cingulate gyrus (a gyrus is a rounded fold of the cortex, as see on the exposed brain), considered part of the limbic system), and the deeply buried insular cortex.
The sensory cortices contain both primary sensory areas, that receive lightly processed information from the sense organs, and accompanying association areas that integrate and recognize patterns such as objects, music, food, and odors. Interestingly, the association areas operate on a longer timescale (seconds) than sensory areas (milliseconds), thought to be due to the transient nature of our senses and the higher-level processing accomplished by the association areas (Runyan et al., 2017). Association areas, in turn, contribute to more complex cognitive and behavioral functions in the frontal cortex. It's interesting to note that 30% of the brain's neurons are devoted to the visual system, 8% for touch, 3% for hearing, and under 1% for taste and smell (Zhang, 2018).
The frontal lobes are further divided into premotor and prefrontal (abstract thought and analysis) cortices. The prefrontal cortex is again divided into multiple subcortices as we see in Figure 3. The cerebral cortex controls perception, memory, and all higher cognitive functions, including the ability to concentrate, reason and think in abstract form, with the subdivisions taking on their specific functions. The human cortex has historically been viewed as especially large in comparison to other animals, including the great apes. This size was thought to be the cause of our superior intelligence. Research (Barton & Venditti, 2012), however, demonstrates that the source of superior human intelligence lies in the distributed neural networks in human brains, and not on the size of its cerebrum. Given that intelligence depends on one's ability to integrate information, the networked brain makes perfect sense.
Situated beneath the cortex are the limbic system and the basal nuclei. Subcortical structures of the limbic system and basal nuclei consist of multiple neuronal clusters, or knots of neurons referred to as nuclei, that together perform the multiple functions of the structure.
Limbic system
The limbic system (Figure 4) includes, in both hemispheres, the hippocampus, fornix, dentate gyrus, amygdala, thalamus, hypothalamus, pituitary gland, mammillary body and olfactory bulb. Also known as the 'emotional brain', the limbic system is important in the formation of memories and in controlling emotions, decisions, motivation and learning.
The hippocampus is deeply involved in learning and memory. Among its functions are episodic memory (sequence of events), generalization, spatial navigation and memory, behavioral inhibition, as well as transference of short-term memory to long-term memory, recognition and recall. Partially wrapped with the hippocampus, the dentate gyrus is especially sensitive to pattern differences, allowing us to differentiate objects and ideas. It is also one of two structures that produces new neurons throughout our lives. The mammillary body is also involved in memory recall, and the fornix carries signals from the hippocampus to the mammillary body and thalamus.
The thalamus is considered the primary "relay station" between the senses and the forebrain, acting as an attentional screen determining the specific signals that get passed to different regions of the cortex, limbic system, and basal nuclei. It is also involved with the regulation of voluntary body movement, consciousness and sleep, arousal, and alertness. New research indicates that the thalamus is also the master "timekeeper" for actions requiring timing and coordination (Wang et al., 2017). The mechanism it uses is to increase or decrease neuron firing rates that send signals to the dorsomedial PFC and caudate nucleus (part of the basal nuclei) to match the requirements of the task. The hypothalamus regulates visceral functions, such as temperature, reproductive functions, eating, sleeping and the display of emotion. The amygdala is responsible for the integration of emotions, emotional behavior, and motivation. It receives input from all the senses as well as visceral inputs. It is essential to emotional and social learning, and thought to determine emotional intelligence. The amygdala is also involved in the expression and regulation of aggression and sexual behavior.
Basal Nuclei
5. Basal nuclei (purple)
Many sources include the basal nuclei (Figure 5) as part of the limbic system, but just as many do not. Located on both sides of the thalamus, the basal nuclei consist of the caudate nucleus and putamen (together called the ventral striatum), and the globus pallidus. Embodying a "go no-go system" the basal nuclei are involved in virtually all decision making. They receive information from and signals back to the cortex to regulate skeletal movement (initiating and terminating action, including timing and control of specific muscle movements) and other higher motor functions, reinforcing adaptive and suppressing maladaptive behaviors. Recent evidence indicates the same effect on cognition (Wessel et al., 2016). This go no-go system can be seen in action when we begin entering an elevator and suddenly realize another person is in front of us trying to leave the elevator, and also when we are reading and the phone rings. The cognitive cost of this action is that we forget what we've been reading immediately before the ringing phone (i.e., the contents of working memory are essentially erased). This new finding suggests a neural basis of distraction. The striatum is involved in most types of learning, especially behavioral conditioning and procedural learning. Habits and expertise, with their largely automatic and intuitive operation, are dependent upon the basal nuclei.
While this description suggests very distinct functions, in reality the structures form circuits of neural processing that meld into a wide array of emotional, cognitive, and physical responses.
Grey and white matter Axon bundles
6. Gray and white matter 7. The axon bundles of white matter
As we see in Figure 6, the entire cortex, as well as other parts of the nervous system, is made of "gray" matter and "white" matter. Gray matter consists of neural cell bodies, dendrites, unmyelinated (unprotected) axons for local communication, glial cells, and blood vessels. White matter is composed of bundles of myelinated axons (Figure 7) that connect various gray matter regions to each other and carry nerve impulses between neurons . White matter only contains the axons of the nerve cells, and not the cell bodies. They are the "transmission lines" of brain networks. Research indicates that white matter integrity abnormalities (e.g., reduced myelination, reduced axon fiber coherence) are strongly associated with major depression (Shen et al., 2017; Jung et al., 2010). Scientists hypothesize that this results in a lack of frontal cortical control over the limbic system and other structures involved in emotion processing.
Maturation generally proceeds from the back to the front of the brain, with the prefrontal cortex maturing the latest, during early adulthood.
Hemispheric differences
While research as debunked the myth of left-brain (logical), right-brain (intuitive) thinking, there are real differences behind the myth. Referred to as functional lateralization, specialization of some functions in the let and right hemispheres has been know to scientists for some time and is associated with improved cognitive, fine motor, and verbal and nonverbal communication ability (Gotts et al., 2013). The great majority of research has centered on the cerebral cortex, but lateralization within the limbic system and basal nuclei has also been found.
• Broca's (speech production) and Werneke's (language comprehension) areas are located predominantly in the temporal lobe of the left hemisphere (95% for right-handers and 70% for left-handers).
• The left hemisphere is more active in language and fine motor coordination, while the right hemisphere is more active in visuospatial and attentional processing.
• The left hemisphere shows a preference to interact exclusively with itself, while the right hemisphere interacts in a more integrated way with both hemispheres.
• The right hemisphere determines handedness.
• Language lateralization (favoring the left hemisphere) is most pronounced in right-handed males.
• The left hippocampus maintains bidirectional communication with other portions of the default mode network, indicating shared influence. The right hippocampus, on the other hand, maintains a one-direction communication, receiving signals but not sending them.
Individual differences
While the general structures of the brain are quite consistent among humans, there are individual differences that impact personality, learning, and other individual characteristics. We cite these to reinforce the idea that individual differences do indeed impact learning and that individualized teaching strategies may be necessary to accommodate them. Identified relationships:
• The brains of women are significantly more active in many more areas of the brain than men, especially in the prefrontal cortex, involved with focus and impulse control, and the limbic system, the emotional area of the brain involved with mood and anxiety. The visual and coordination centers of the brain were more active in men (Amen et al., 2017).
• There is greater variety in the size of men's brains than of women's. This could help explain why some psychiatric disorders such as ADHD and autism are more prevalent in boys (Wierenga et al., 2017).
• Reduced thickness of the anterior cingulate and dorsolateral cortices is predictive of sensation seeking and substance abuse (Holmes et al., 2016).
• Smaller volume (generally thickness and density) in the parietal cortex is associated with higher aversion to risk and increased sensitivity to physical and emotional pain (Datal, et al., 2014; Emerson, et al., 2014).
• Amygdala volume (size) correlates positively with both the number and complexity of individuals' social networks, as well as "reading" others' faces.
• Persons higher in "emotional empathy" (feeling emotion along with the other person) have higher-density insular cortices, while those higher in "cognitive empathy" (simply knowing what the other person is feeling and what they might be thinking) have higher-density in the midcingulate cortex (Eres et al., 2015).
• The right inferior gyrus (part of the ventral cortex) in "critical thinkers" is more highly activated when evaluating information than the less-critical. This region is associated with cognitive inhibition, in which the individual is able to stop or override certain mental processes (stop unwanted thoughts, weed out irrelevant information) while attending to new or contrary information (Lindeman et al., 2013).
• Different ways of experiencing the past are associated with distinct brain connectivity patterns that may be inherent to the individual and suggest a life-long 'memory trait'. Some people have richly detailed recollection of past experiences (episodic memory), while others tend to remember just the facts without details (semantic memory) (Sheldon, et al., 2016).
• With age, the hemisphere communicate bilaterally as a means of compensating for other negative aspects of aging, thus maintaining normal function. "Good roads make for efficient travel, and the brain is no different. By taking advantage of available pathways, aging brains may find an alternate route to complete the neural computations necessary for functioning" (Davis et al., 2017).
Developmental differences
Brain regions develop at roughly the same pace during normal brain maturation. An approach to measuring this coordinated development, called structural covariance, is being used to study neurodevelopmental disorders such as autism, ADHD, and conduct (antisocial) disorders. These findings support the hypothesis that these and other developmental disorders have neurodevelopmental origins.
Premature birth increases the chance of developing cognitive, motor and behavioural difficulties, problems that persist throughout school years (Allotey et al., 2017). "These results show children born prematurely have a higher risk of a number of developmental problems, including lower IQ and ADHD. It is important for the effect of a preterm birth on the neurodevelopment of children to be included in counselling for parents who expect or have had a preterm delivery. Likewise, any decision on the timing of delivery should take into consideration the long term effects of prematurity."
Gender The brains of men and women respond differently to prosocial and selfish behavior (Soutschek et al., 2017). The ventral striatum is responsible for the assessment of reward and is active whenever a decision is made. The striatum is more strongly activated in female brains during prosocial decisions (e.g., sharing found money) than selfish decisions (keeping the money for oneself). The opposite pattern is seen in male brains (higher activation during selfish decisons). Although the difference appears at the neurotransmitter level, the researchers speculate that cultural expectations account for the difference.
Autism The pace of development between cortical thickness in the inferior temporal and occipital lobes (called the fusiform gyrus) and amygdala volume are significantly out of sync in autistic persons when compared to normal subjects. The fusiform gyrus is key to social cognition and emotional awareness (Dziobeck, et al., 2010).
ADHD Attention deficit/hyperactivity disorder carries a number of neurological abnormalities. Children and teens with ADHD lag behind others of the same age in how quickly their brains develop (Jacobson et al., 2018) and form connections within, and between, key brain networks (Sripada, et al., 2014). Compared to matched (age, gender, etc.) normal controls, ADHD is marked by significant reductions in gray matter volume in the right insular cortex and right orbital prefrontal cortex, significantly decreased connectivity between the insular cortex and the right hippocampus, bilateral olfactory cortex, and caudate nucleus, and significantly increased activity between the insular cortex and the left middle temporal gyrus (Li et al., 2015). Further, Jacobson et al. (2018) found that the degree of volume deficit was correlated with the severity of symptoms.
Conduct disorders are separated into childhood-onset (CO-CD) and adolescence-onset (AO-CD). Examining the growth (in thickness) of the different cortical lobes (prefrontal, temporal, etc.), Fairchild et al. (2016) found an unusually high degree of uniform cortical lobe growth for CO-CD individuals, and an unusually low degree of uniformity of growth for AO-CD individuals. Growth of the different lobes for normal controls was somewhere in the middle.
Poverty is associated with tremendous differences in size, shape and functioning of children's brains, including less cortical volume, thickness and surface area, smaller hippocampus, and reduced plasticity (Noble, 2017). In general, children from disadvantaged homes tend to perform more poorly on tasks that test their language and memory skills, and the ability to exert self-control and avoid distraction. A study by Evans (2016) tracked 341 individuals over a 15-year period, beginning at age nine. Children in the study living in poverty had more psychological distress as adults, including more antisocial conduct like aggression and bullying and more helplessness behavior, than kids from middle-income backgrounds. Poor kids also had more chronic physiological stress and more deficits in short-term spatial memory.
Imagine how you might approach the same learning task for three different learners: one is risk-aversive, another highly sensitive to physical and psychic pain, and a third has difficulty focusing for more than a few minutes.
Blood supply
7. Blood supply to the brain
Although only 2% of the body's weight, the brain receives 20% of its blood supply. About two-thirds of this energy supports neuron firing with the remaining third committed to basic metabolism and maintenance functions (Swaminathan, 2008). The entire blood supply to the brain depends on two sets of branches from the dorsal aorta, the internal carotid arteries and the vertebral arteries. "Nerves and blood vessels lead intimately entwined lives. They grow up together, following similar cues as they spread throughout the body. Blood vessels supply nerves with oxygen and nutrients, while nerves control blood vessel dilation and heart rate. Studies have shown that when neurons work hard, blood flow increases to keep them nourished." (Dutchen, 2014). This intimate relationship is the basis of fMRI, which measures blood flow and not actual neuron activity.
The physiological demands served by the blood supply are particularly significant because neurons are more sensitive to oxygen deprivation than other kinds of cells with lower rates of metabolism. In addition, the brain is at risk from circulating toxins, and is specifically protected in this respect by the blood-brain barrier. As a result of the high metabolic rate of neurons, brain tissue deprived of oxygen and glucose is likely to sustain transient or permanent damage. Brief loss of blood supply (referred to as ischemia) can cause cellular changes, which, if not quickly reversed, can lead to cell death. Sustained loss of blood supply leads much more directly to death and degeneration of the deprived cells.
Very recent research shows that sensory stimulation during infancy results in richer, more complex neurovascular networks. The opposite is also true, with sensory deprivation resulting in shorter vessels and less branching. "The finding that neural activity is necessary and sufficient to trigger alterations of vascular networks reveals an important feature of neurovascular interactions" (Lacoste, 2014). This finding not only has implications for learning capacity, but also reveals the possibility for using sensory stimulation to generate new blood vessels in damaged areas of the brain. The research is described as "preliminary".
Neural networks and clusters
The brain's neural pathways Nodes of neural activity and their connecting pathways Dentate gyrus neurons within a mouse hippocampus
8. The brain's neural pathways 9. Concentrations of neural activity and their connecting pathways 10. A functional cluster of neurons (dentate gyrus) within a mouse hippocampus
The brain carries out its functions (including thinking, talking, listening) via neural networks and sub-networks, which connect the different structures within the brain so they can work seamlessly together to produce perception, thought, and action. These multi-part circuits respond together and regulate one another. They also vary in their connectivity according to the task at hand, increasing traffic here and silencing connections there. Physically, this means network member neurons are more densely connected to each other than to neurons of other networks. Consider how sidewalks provide preferred pathways between campus buildings. If the sidewalks don't provide the most convenient access, pedestrians create new pathways. And so it is with the brain. Mapping the networks and member neurons is referred to as the connectome, or the nervous system's wiring diagram.
Our previous understanding of these circuits likened the brain to a bowl of spaghetti with individual neurons reaching out to others in a more or less random fashion. However, imaging reveals a more organized pattern somewhat akin to the wiring in an office building where bundles of wires form the backbone of the system and smaller bundles radiate outward to specialized functions (Figure 8 above). As we move outward from the backbone, networks become smaller, as we see in Figure 9 above. Networks within larger networks operating at different oscillation bands (see brainwaves below).
Locally, neurons cluster to form anatomical structures, or nuclei (within the brain), with specialized functions. Figure 10 above is that of dentate gyrus neurons within a mouse hippocampus, which contributes to the formation of new episodic memories (Liu et al., 2012). Functional neural clusters don't only exist within the brain's structure, but also within sense organs and their neural pathways to the brain (referred to as ganglia). The eye and optic nerve separate incoming images into elements perceived by the brain. The olfactory bulb converts smells into signals for the brain to process. The ears are especially interesting in that the right ear is more geared toward speech and the left ear is attuned more to music. Children who have right-ear hearing impairment have more trouble in school than those with left-ear loss (vos Savant, 2014).
A 3-D view of the connectome
Individual neurons are constituents of multiple networks, and function in a manner consistent with one circuit for a particular function, and in another manner with a different circuit serving a different function (Figure 11 below). The neuron fires rhythmically in tune with one pathway for one function, and at another rate for a different function. Although a single neuron or group of neurons may represent a single phenomenon, such as angle of visual orientation, it participates in different memories associated with the particular visual angle. Similarly, a particular melody may trigger memories of multiple songs. This phenomenon helps explain the benefit of associating new material with that already learned, and the mixing of memories we can all attest to.
Neuronal participation in multiple circuits is demonstrated in research by Huth et. al (2012) in which they mapped neural activity as subjects viewed over 1,000 objects and actions. Two examples are seen below (Figures 12 and 13), with red representing high activity and blue low activity. Of special interest is the fact that similar concepts cluster in the same brain areas while very different concepts cluster further apart. This structure allows the brain to forego maintaining separate cells for each of the vast array of semantic concepts, a physical impossibility.
Individual neurons take part in multiple circuits Neural activity while viewing a photo of a planet Neural activity while viewing the word argue
11. Single neurons take part in multiple circuits 12. Neural activity while viewing a photo of a planet 13. Neural activity while viewing the word argue
A new video from Nature describes the brain's semantic map, or "brain dictionary". Also, see Huth et al., 2016.
The brain dictionary
Three learning networks
We previously discussed how the brain can be divided in numerous ways for different purposes. Here we take a look from a learning perspective (Figure 14). Three types of brain networks are especially important to learning: recognition, strategic and affective networks, all part of the forebrain (plus the cerebellum). These networks are named for their function and not their anatomical configuration, using brain imaging technologies while subjects performed different types of tasks and thinking.
14. Three Learning Networks
Recognition networks are specialized to sense and assign meaning to signals from within the body and the external environment. These networks assign meaning based on the patterns we perceive, allowing us to identify and understand information, ideas and concepts. Based in the back of the brain, recognition networks enable us to identify and interpret patterns of sound, light, taste, smell and touch. They enable us to recognize voices, faces and text, as well as more complex patterns like dance, justice and the structure of the atom.
Based in the frontal cortex and the cerebellum, strategic networks specialize in generating and overseeing mental and motor strategies. They enable us to plan, execute and monitor actions, tactics and strategies. These networks orchestrate virtually everything we do, from sweeping the floor, to composing an essay to executing a flight to the moon. They operate at the conscious level, as when we’re following travel directions, and subconsciously as our minds and bodies automatically carry out many aspects of walking or driving.
Affective networks, based in the subcortical and cortical portions of the limbic system, are specialized at evaluating recognition and strategic patterns and assigning them personal significance. Unpleasant stimuli are processed first via the more archaic subcortical region (recognizing danger) while pleasant stimuli are first processes through the cortical region (Paradiso el al., 1999). What we see is determined in large part by our internal state – a melting pot of emotions, needs, desires and memories. Whether we like it or not, everything we perceive and do is filtered through an affective screen made of, among others, our state of energy or fatigue, familiarity with and interest in aspects of the environment, our mood and personality.
At any instance, the many facets of the environment are competing for our attention. These demands require not only that we recognize them and formulate strategies, but that we also evaluate their significance and importance to ourselves. Think about it. Only affect answers the “why” of our lives.
Other important networks
Three important core networks are receiving considerable attention in explaining human behavior (McGrew, 2011):
The salience network is a controller or network switcher. Think of the salience network as the air traffic controller of the brain. Its job is to scan all information bombarding us from the outside world and from within our own brains. This controller decides which information is most urgent, task relevant, and which should receive priority, sending signals to areas of the brain for processing. This controlling network must suppress either the default or executive networks depending on the task at hand. It must suppress one, and activate the other. The salience network is centered in the anterior insular cortex and dorsal anterior cingulate, with connections to the thalamus, amygdala, orbitofrontal PFC, olfactory cortex, and the superior temporal cortex.
The default mode network (DMN) manages what your brain does when not engaged in specific tasks. It is the busy or active part of your brain when you are mentally passive. This network comprises an integrated system for autobiographical, self-monitoring and social cognitive functions. As such, it is especially important to our self-concept. The default mode network is also responsible for the spontaneous mind wandering and internal self-talk we engage in when not working on a specific task or, when carrying out a task that is so automatized (e.g., driving a car) that our mind starts to wander and generate spontaneous thoughts. The DMN is centered on the ventromedial PFC with connections with the orbitofrontal PFC, hypothalamus, amygdala, and a portion of the midbrain.
The central-executive network (CEN) produces higher-order cognition and attentional control. In other words, when you must engage your conscious brain to work on a problem, place information in your working memory as you think, focus your attention on a task or problem, etc., you are “thinking” and focusing your attention. The CEN is concentrated in the dorsolateral PFC and posterior parietal cortex.
There appears to be a direct, inverse relationship between the default mode network and the central executive network in that as one activates, the other largely deactivates (Chapman et al., 2017). The function of this relationship remains unsettled, with some experiments demonstrating high activity in the DMN and low activity in the CEN during creative tasks while others indicate the opposite.
The mirror neuron system is involved in understanding others' actions and their intentions behind them, and it underlies observational learning. There are two main networks of mirror neurons: one residing in the parietal lobe and the premotor cortex plus the posterior ventrolateral PFC (parietofrontal mirror system). This network is active when we carry out goal-directed behaviors and also when we observe the goal-directed behavior of others. In a sense, our brains are internally mimicing others' behavior in rehearsal for copying their actions. The other network, the limbic mirror system residing in the insula and posterior medial PFC, is devoted to the recognition of affective (emotional) behavior. This network is heavily involved in social reasoning and behavior.
Individual differences
The Human Connectome Project, launched in 2010 by several nations, is beginning to reveal new and interesting facts about the brain's wiring patterns that impact or reflect the human condition. Smith et al., (2015) compared regional brain connectivity (active communication) of 461 individuals in a resting state with multiple demographic and psychometric measures. Their major finding was that those with increased brain connectivity had higher life success factors like education and income levels, life satisfaction, and overall physical fitness. Hilger et al. (2017) found that higher interconnectivity between brain regions, especially when the anterior insula and the anterior cingulate cortex are more integrated with the larger network, to be associated with higher intelligence. On the other hand, they also identified brain regions (e.g., the junction area between temporal and parietal cortex) that are more strongly 'de-coupled' from the rest of the network in more intelligent people. This may result in better protection against distracting and irrelevant inputs.
Connectivity patterns between brain regions have been implicated in a variety of psychological and cognitive disorders. "In psychiatric disorders, functional connectivity, which is measured by temporal correlations between some brain regions, is too much increased or decreased compared to healthy control. It has been suggested that these abnormal connections cause the decrement of cognitive function" (Yamashita et al, 2017). The group has developed a technique called "connectivity neurofeedback training" to restore normal functioning. See ELearning/Brain enhancement for more on the technique.
Testing for creativity and connectivity, Durante and Dunson (2016) found high creativity to be significantly correlated with connectivity between the two hemispheres, especially in the frontal cortex. Beaty et al. (2017) found that highly creative people show three networks working in sync during creative tasks: the default mode, salience, and executive networks. Unlike normal people where these networks generally work in opposition to each other, the networks are activated simultaneously in highly creative people.
Neurons and neuroglia
NeuronEnglish.png Astrocyte, one type of neuroglia Differing voltages in axon branches
15. A prototypical neuron (nerve, nerve cell) 16. Astrocyte, one type of neuroglia (glia, glial cell) on a background of neural axons and dendrites 17. Neuron axon branches show electrical activity (voltage)
At its most fundamental level, the brain consists of specialized cells communicating with each other and maintaining brain health. Globally, there is an approximate 1 to 1 ratio (1:1) of neurons and glial cells in the brain, with the ratio varying significantly between regions (von Bartheld et al., 2016; Jabr, 2012). On one extreme, cortical white matter contains 15 glia for every neuron (15:1). The limbic system and basal nuclei contain about 11 glia for every one neuron (11:1). Cortical grey matter contains about 1.5 glia to each neuron (1.5:1). At the other extreme, the cerebellum contains about one glia for every four neurons (1:4). Both neurons and glial cells come in a variety of types. "There are hundreds, if not thousands, of types of brain cells that have different functions and behaviors" (Luo et al., 2017).
Neurons
The basic neuronal structure is seen in Figure 15. Remember that this is an illustration and neurons come in hundreds of configurations, all with the same basic parts.
Dendrites are the signal receiving protrusions branching from the cell body, and are the site of memory formation (Seibt et al., 2017). These protrusions grow and deconstruct as learning occurs, governed by specific proteins (Gao et al., 2017). Dendrite receptors, located on tiny spines protruding from the dendrite branches, come in different "families" even when they receive the same neurotransmitter. Each receptor type performs different functions for the neuron. Glutamate receptors, for example, include NMDA receptors, AMPA receptors, and kainate receptors, which perform different cellular functions like opening ion channels into the cell body, helping to build action potential. AMPA receptors are important to memory in that as these receptors fall into disuse, they fade away and with them specific memory traces (Migues et al., 2016). Further, some spines are responsive to different nuanced signals from the senses, such as particular angles in our field of vision (Wilson et al., 2016). Some respond only to vertical edges, others respond to only horizontal edges, while others respond to other angles. This constitutes a form of signal (information) processing that contributes to the perception of our world.
The central cell body is the largest part of a neuron and contains the neuron's nucleus, containing DNA, and other cell structures such as mitochondria and organelles. The nucleus encodes messenger RNA, which is transported to specific cites and builds proteins necessary for cell functions, including learning and memory. The cell body also integrates the multiple signals coming from other neurons, generates electrical impulses and propagates them down the axon, and maintains cellular health.
The axon carries nerve impulses away from the cell body. A neuron typically has one axon with multiple branches (see Figure 17) at the end that connect it with other neurons or with muscle or gland cells. Some axons may be quite long, reaching, for example, from the spinal cord down to a toe. Axons that extend to other brain and body regions are enclosed in a myelin sheath, which increases the speed of impulse transmission; some large axons may transmit impulses at speeds up to 300 feet (90 meters) per second. These axons make up the brain's "white matter". Short axons within grey matter that communicate locally are not generally myleanated.
Neuronal subtypes
Scientists have classified neurons into four main groups based on differences in shape (Jabr, 2012). Multipolar neurons are the most common neuron in the vertebrate nervous system and their structure most closely matches that of the model neuron: a cell body from which emerges a single long axon as well as a crown of many shorter branching dendrites. Unipolar neurons feature a single primary projection that functions as both axon and dendrites. Bipolar neurons usually inhabit sensory organs like the eye and nose. Their dendrites ferry signals from those organs to the cell body and their axons send signals from the cell body to the brain and spinal cord. Pseudo-unipolar neurons, a variant of bipolar neurons that sense pressure, touch and pain, have no true dendrites. Instead, a single axon emerges from the cell body and heads in two opposite directions, one end heading for the skin, joints and muscle and the other end travelling to the spinal cord.
Researchers also categorize neurons by function. Sensory neurons collect information from sensory organs—from the eyes, nose, tongue and skin, for example. Motor neurons carry signals from the brain and spinal cord to muscles. Interneurons (also called relay neurons) connect sensory and motor neurons of the peripheral nervous system with the central nervous system: the long axons of projection interneuons link distant brain regions to create and regulate networks; the shorter axons of local interneurons form smaller circuits between neighboring cells (Muñoz et al., 2017). A single type, parvalbumin-expressing neurons (PV cells), in the medial prefrontal cortex are essential to goal-driven attention (Kim et al., 2016) and can be activated using optogenetics. There are place cells within the hippocampus that record and track our physical location. There are mirror neurons that fire when we observe others' actions and also when we perform the same action.
These broad categories do not capture the true diversity of the nervous system. Not even close. In the cerebellum alone, there are nine subtypes of neurons (Jabr, 2012), and 21 in the frontal cortex (Luo et al., 2017). Neurolex.org includes a list of 310 neural subcategories.
In the past, it was thought that neurons were solely responsible for "brain work" while glial cells supported them by holding them in place, supplying them with nutrients and oxygen, insulating one neuron from another, and destroying and removing the carcasses of dead neurons (clean up). We now know that this picture is incomplete, and therefore inaccurate.
Neuroglia
18. Neuroglia: Astrocytes (green), Oligodendrocytes (blue); Microglia (deep red); Ependymal cells (pink).
While the support function of neuroglia have proven true, recent discoveries tell us that glia are also intimately involved in brain work. For example, glial cells are responsible for modulating the shape of nerve endings (Singhvi et al., 2016; Sakry, et al., 2014), affecting cognitive processing, sensory perception, and learning. "The glia release a specific protein fragment that influences neuronal cross-talk, most likely by binding to the synaptic contacts that neurons use for communication. Disruption of this information flow from the glia results in changes in the neural network, for example during learning processes." Tso et. al. (2017) have implicated astrocytes, a specialized glial cell, as the primary drivers of our internal clocks (circadian rhythms). Glia cells also play a pivotal role in the initial organization of the infant brain, coaxing neurons into specific pathways so that proper brain assembly can ensue (Rapti et al., 2017).
Glia subtypes
Glial cells maintain the brain's environment, regulate synapses and neurotransmitters, respond to injuries, and in certain cases can even become neurons (Yuhas, 2012). Five types of glia researchers have discovered so far:
Astrocytes (Figure 18, green) are the most common type of glial cell in the brain, and secrete GPC4 proteins into synapses affecting both axon terminals and dendrite receptors, enabling neuron-to-neuron communication (Farhy-Tselnicker, et al., 2017). They also take up neurotransmitters, cleaning up after neuronal activity. They wrap themselves around capillaries, forming the blood-brain barrier, and provide nutrition to nerve cells. During maturation of the chaotic young brain, astrocytes deactivate many synapses to create a more orderly network. The network remains relatively stable throughout adulthood, but astrocytes begin anew with their trimming function in elderly brains, especially in the hypothalamus and cerebellum, effectively reducing the number of synapses in the brain. This action is thought to cause or contribute to decreased metabolism and problems of physical coordination (Boisvert et al., 2018). Finally, astrocytes communicate with each other via calcium waves, similar to electrical/chemical brain waves in neurons. One function of this communication is the regulation of blood flow to the brain, and additional functions are postulated (Bazargani & Atwell, 2016).
Oligodendrocytes (blue) wrap the tips of their tentacles around axons in a fatty white coating called myelin (myelin sheath). Schwann cells in the peripheral nervous system function as both astrocytes and oligodendrocytes. Microglia (deep red) are the brain's rapid response team. Since the immune system's molecular machines can't cross the blood-brain barrier, microglia defend the brain from invaders. Finally, Ependymal cells (pink) produce cerebrospinal fluid and form the boundary of the brain's ventricles (cavities containing the fluid) and the central canal of the spinal cord.
Neuronal communication
Communication between nerve cells occurs at the synapse, a tiny gap between the end of one neuron and the top of another. Neurons communicate in one of two ways: The vast majority of neurons communicate chemically using neurotransmitters. A much smaller number communicate via electrical impulses. Neurons propagate their messages down the axon body and through the terminal branches via electrical pulses toward synapses with other cells.
In chemical synapses (Figure 19 below), this electrical pulse triggers the release of neurotransmitters from vesicles, essentially small sacs of neurotransmitter. The neurotransmitter receiving dendrites are populated with tiny mushroom-shaped buttons called dendritic spines. These spines play a major role in the strength and duration of neuronal communication. For example, in some instances, there are a large number of spines congregated together to receive incoming neurotransmitter while in other instances the number of spines is quite low (Kusters & Storm, 2014). Variation in the shape of spines also plays an important role, with some shapes creating more permanent memories and others temporary memories. We can also note that spine shapes can and do change in response to increased or decreased memory permanence. Chemical synapses communicate in one direction only.
In electrical synapses (Figure 20), neurons communicate via gap junctions. The gap junction contains a number of ion channels, allowing the flow of electricity between neurons in both directions. In this case, the gap between neurons is much smaller than chemical synapses. The most thoroughly studied electrical synapses occur between excitatory projection neurons of the inferior olivary nucleus (part of the medulla oblongata) and between inhibitory interneurons of the neocortex, hippocampus, and thalamus. These synapses require a special gap junction protein for robust coupling. Electrical synapses allow for quicker signal transmission, bidirectional communication, and they are thought to synchronize neural activity; a regulatory agent for other neurons.
Evidence (Qui et al., 2015; Fröhlich & McCormick, 2010) suggests there is a third form of transmission between neurons, with low amplitude electrical fields, starting with a single cell or group of cells, propagating wave transmissions through populations of cells, thus communicating without synaptic transmission. The electrical fields are thought to guide neocortical network activity within the brain, and wound healing in the body.
Chemical Synapse Electrical Synapse Click to view larger image
19. Chemical Synapse (credit Univ of Tokyo) 20. Electrical Synapse (credit Univ of Tokyo) 21. Hundreds of signals acting on a single neuron
Excitation and inhibition
Functionally, there is an important distinction between neurons important to learning: excitation and inhibition. Excititory neurons carry the information flow, promoting neuron firing in other cells both locally and long-range with other regions. Inhibitory nerves communicate locally to regulate the activity of excititory nerves. This action is considered to be the basis for single neurons participating in multiple pathways, with inhibitory nerves closing off some pathways and opening up others. Selective attention and the ability to screen out distractions, separating the "signal from the noise" is one manifestation of inhibitory nerves in action (Yang et al., 2016). During periods of focused learning, inhibitory neurons fire about half as often as normal (Kuhlman, 2013). About 80% of neurons are excititory and 20% inhibitory.
Signals from other neurons are received via the dendrites and travel down the axon to the terminal buttons, communicating with the dendrites of additional neurons. Key to this activity is action potential. Signals from other neurons do not necessarily result in the cell "firing". Figure 21 above shows the multitude of signals impinging on a single neuron, with excitatory signals in green and inhibitory signals in red (click Figure 21 to view full size). Each incoming signal adds to or decreases the action potential of the cell. Signal strength between neurons varies over two orders of magnitude, with a few strong connections among large numbers of weak ones (Cossell et al., 2015). Most of this difference comes from the size of the synapse, with larger ones including more vesicles of neurotransmitter released and uptook. Once potential passes a critical level, the cell fires and sends its message along to other neurons. Why do neurons share such a large number of weak connections? Cossell speculates that they may have significance for learning. "If neurons need to change their behavior, weak connections are already in place to be strengthened, perhaps ensuring rapid plasticity (thus learning) in the brain." As a result, the brain can quickly adapt to changes in the environment."
Uncoordinated signals of individual brain cells can be noisy, imprecise, and even contradictory - which means our brains cannot rely solely on the activity of single neurons to make accurate decisions about the world. Instead, during active cognition, the brain combines the activity of thousands to millions of neurons to ensure a more accurate message, which makes effective communication among large populations of neurons a central feature of the brain (Smith, G. et al., 2015).
Brainwaves
Activity in the brain is not constantly high or low, but rather organized in waves that come and go. Brain waves (technically called rhythmic neuronal oscillations) constitute patterns of electrical pulses from masses of neurons communicating with each other. In other words, groups of neurons fire together in wave-like patterns (fire-rest-fire-rest) that propagate through neural networks to carry information from one part of the brain to others. Your thoughts are literally carried on the waves of neuronal oscillations. Research tells us that brainwaves play an integral role in learning – they are the carriers of learning, and any other process involving communication between brain structures (Brincat & Mille, 2015). More on that in a minute. First, let's look at the phenomenon itself.
As we see in Figure 22, brain waves vary along two dimensions – frequency (Hertz: distance between peaks) and strength (amplitude: height of peaks and valleys). The higher the frequency, the lower the amplitude. This continuum is divided into “bands” and labeled as we see below (cps is short for cycles per second). Speedy gamma waves form a tight frenetic pattern while lazy delta waves are big and loopy. It happens that these patterns are closely associated with our state of mind, and also how we learn. Note that, while one wave pattern may dominate at any one time (e.g., "theta state"), depending on the current state of mind, all five patterns are generally present in the brain at all times.
Brainwaves.png
22. Brainwaves are patterns of neuron groups firing at different strengths and frequencies (Hertz and amplitude)
Wave patterns
Pseudo science has endowed particular wave patterns with magic-like properties and make recommendations based on them: “The Alpha-Theta border, from 7 to 8Hz, is the optimal range for visualization, mind programming and using the creative power of your mind.” While we know that electrical and magnetic stimulation, chemicals, biofeedback, the very recent neurofeedback, and meditation do change brainwave patterns, we have not attained that level of precision. Here, we use information from Cetin (2010) and Hermann (1997).
Gamma wave patterns are associated with the synchronous cooperation of various cell networks of the brain, associated with high-level perception and sense making – attuned to the present and also integrating the present with relevant memories. Recent research suggests it is associated with bursts of insight and high-level information processing, and the efficient formation of memories in the hippocampus. Debaters, professional athletes, theorists, programmers and others involved in intense cognitive and psychomotor effort would be in gamma. Interestingly, food-seeking behavior in humans and animals is also mediated by gamma wave patterns (Carus-Cadavieco et al., 2017). It's also known that activity in this frequency range is markedly reduced in Alzheimer patients.
Beta wave-like activity is characteristic of an engaged mind. A person in active conversation would be in beta. A person making a speech, or a teacher, or a talk show host would all be in beta when they are engaged in their work.
Alpha waves represent non-arousal, relaxation, and lack of focus. Consider sitting on a bench and looking out at the world with nothing particular in mind. The alpha state, then, is characteristic of mind-wandering, day dreaming, and lapses of attention. One can easily imagine how anyone listening to a lecture or driving on long stretches of isolated highways would oscillate between beta and alpha states.
Theta waves are important to the formation of memories, specifically emotional and contextual memories. Theta oscillations in the medial temporal lobe occur more often when someone is navigating an unfamiliar environment, and that the more quickly a person moves, the more theta oscillations take place—presumably to process incoming information faster. In an unexpected finding, theta oscillations were most prominent in a blind person who relied on a cane to move (Aghajan et al., 2017).
When dominant, theta waves constitute the border between sleep and wakefulness; a state of deep relaxation and a disengaged intellect. Meditation, biofeedback, hypnosis, and yoga all give rise to a theta state. Recent research suggests that the brain is reviewing and consolidating these memories during REM (rapid eye movement), or dream sleep when theta waves dominate among the hippocampus, amygdala, and the neocortex (Boyce et al., 2016).
Delta waves indicate deep dreamless sleep. Falling asleep, our brain waves calm, descending into slower and slower patterns, falling to less than one cycle per second. Humans dream in approximate 90 minute cycles, which grow longer through the night. Dreaming brings an increase in theta waves which again fall off into the delta band. Sleep spindles, the primary mechanism for transferring short-term memories, and perhaps other types of memories, emanating from the hippocampus to the prefrontal cortex, occur during dreamless sleep. For example, we know that deep sleep is critical to visual learning (Durkin, et. al., 2017).
The emerging picture, then, is of different types of memories being transferred to long-term memory during REM (theta band) and deep dreamless (delta band) sleep. In both cases, the hippocampus directs the cortex to replay and interpret important short-term memories and thus strengthen their presence in long-term memory, referred to as memory traces.
As mentioned above, neural networks operate at differing oscillations (bands) as we see below (Chennu et al., 2014). Subjects wore EEG caps while in relaxed eyes-open wakefulness, thus we see activity in the three lower bands only. Colors represent different networks. Thus, we see a multitude of networks functioning simultaneously, carrying on the many forms of brain work.
Alpha wave networks Theta wave networks Delta wave networks
23. Alpha wave networks 24. Theta wave networks 25. Delta wave networks
Brainwaves and brain work
Although the above descriptions of brainwaves are generally true, they fail to describe the utility of brainwaves in the more dynamic flow of daily life. Michalareas et al. (2016) have uncovered how bottom-up and top-down communication occurs between lower (i.e., sensory) and higher (i.e., cognitive) centers of the brain. Bottom-up communication occurs when lower brain areas, like when information enters through the eyes and flows from lower to higher visual areas, enlist higher areas to adopt their wave patterns in the gamma range and consciously perceive the visual field. Higher areas use past experience to organize and interpret the information, assign priority and direct the attention of lower areas, using alpha and beta bands, between 10 and 20 Hertz waves. We see, then, how the brain uses brain waves - rhythmic neuronal oscillations - to accomplish its work.
26. CA1 integrates past and present
Sense-making. Measuring brainwaves while subjects were involved in a variety of tasks, Colgin (2010) found the CA3 portion of the hippocampus (Figure 26), with its ability to recall past experience, and the medial temporal lobe, which deals with information about the present, communicating in the gamma band with a third region called CA1, also part of the hippocampus. Even more revealing, the temporal lobe communicated in the higher frequency portion of the gamma band while CA3 communicated in the lower frequency portion of the gamma band. CA1 rapidly and sporadically switched back and forth between the differing frequencies, apparently receiving signals from the two areas in turn and integrating their input.
Memory. Memory involves many structures within the brain, and their interconnectivity is key to both memory encoding and retrieval. Solomon et al. (2017) found that both encoding and retrieval are mediated with slow theta wave (3-8 Hz) network connectivity, thus synchronizing activity, essentially constituting parallel processing. On the other hand, fast gamma (30-100 Hz) network activity desynschronizes brain structures, creating asynchronous activity.
Learning. Explicit and implicit learning are accompanied by different patterns of brainwave activity (Loonis et al., 2017; Chafee & Crowe, 2017). During explicit learning tasks, correct choices are followed by an extended increase in alpha-beta waves (oscillating at 10-30 hertz) whereas incorrect choices lead to a brief increase in delta-theta waves (3-7 hertz). Incorrect choices also lead to neural spikes, indicative of high amplitude (high strength) neuronal firing. Further, alpha-beta waves decrease as learning progresses. Loonis speculates that alpha-beta waves may be indicative of the learner building a mental model of the task, which fades as the model is completed. In contrast, implicit learning increases delta-theta wave patterns only with correct responses, which fade as learning is consolidated. This pattern may reflect neural “rewiring” that encodes the implicit skill during learning. During explicit learning, wave activity is more pronounced in the hippocampus, prefrontal cortex, and medial temporal lobes. Pronounced activity is seen in the amygdala, striatum, motor cortex, and cerebellum during implicit learning.
Decision-making. Daniels et al. (2017) have uncovered the decision making process at the neuronal level (collective computation), recording neuron firing within the posterior prefrontal cortex of a macaque monkey. In very similar fashion to the recording below, the monkey is confronted with a decision. During initial processing, neurons fire in seemingly random fashion and, as the monkey approaches a decision, the neurons commence to firing at the same rate; from a multitude of firing patterns toward a synchronized gamma wave pattern. There is a slow(er) aggregation phase followed by a fast propagation phase. Daniels interprets this two-stage process as the central executive polling many sensory neurons for maximum input. "At first the 'neural voice' is heterogeneous and collective, but as the decision network gets close to the decision point, the 'neural voice' becomes homogeneous..." Further, they found that a lack of homogeneity during the propagation phase resulted in timid and poorly executed action following the decision point.
Pisauro et al. (2017) have identified a decision network in humans for perceptual-, value-, and reward-based decisions. The posterior medial frontal cortex maintains coupling with the ventromedial PFC and striatum (brain areas known to encode the subjective value of the decision alternatives) during the same process of evidence accumulation found by Daniels et al. above.
The following video (Figure 27) records the firing within a population of neurons of a mouse hippocampus as it searches for and finds food. The cells were modified so they would fluoresce when firing. Jennings et al. (2015) records neurons as they fire while the mouse searches for food (random firing; aggregation phase) until it comes upon and decides to eat the food (strong uniform pattern; propagation phase).
27. Active hippocampal neurons during a mouse's search for food.
Also inherent in decision making is the action that follows. Especially in the realm of visual-motor activity, such as walking down the street or playing basketball, the motor cortex prepares itself for multiple possibilities during the aggregation phase before a decision is made. In this way, the brain is prepared to execute motor commands whatever the decision. "The brain is continuously translating visual targets into possible actions that can be performed on those targets" (Gallivan et al., 2017).
Neurotransmitters
Neurotransmitters are the brain chemicals transferred across the synapse between neurons as they communicate. They can be broadly distributed throughout the central and peripheral nervous systems, constrained to specialized pathways, or anywhere in between. Most neurons make two or more neurotransmitters, which are released at different frequencies. More than fifty have been identified. We mention only the most common.
Excitatory neurotransmitters
Acetycholine was the first neurotransmitter to be identified, and is the most abundant in the nervous system. Its primary function is to excite the body's muscle structures.
Catecholamines dopamine, epinephrine, and norepinepherine are involved in reward-pleasure and learning. Dopamine is associated with alertness and energy, attention, and is the principle neurotransmitter involved in addiction due to its dominant role in the brain's reward and pleasure centers. Dopamine insufficiency is also associated with ADHD and schizophrenia.
Glutamate is considered to be the major mediator of excitatory signals in the central nervous system and is involved in most aspects of normal brain function including cognition, memory and learning. It not only mediates information processing, but also regulates brain development, cellular survival, differentiation and elimination as well as formation and elimination of synapses. It is located almost exclusively within cell bodies (99.99%) and remains inactive until expelled. Glial cells as well as neurons possess glutamate receptors, which uptake the substance rather than release it back into the synapse for reuptake. Glutamate is both essential and highly toxic at the same time, and very low levels must be maintained within the extracellular fluid.
Serotonin is broadly distributed in the brain and body and is involved in emotions, impulse control, sleep, dreaming, hunger, and arousal. Depletion of serotonin is known to be associated with depression, obsessions, and compulsions. Many biological clues suggest that serotonin, as well as other small molecules released from blood platelets when they are activated during clotting, play an integral role in cardiovascular disease. In addition, studies have shown that people who have suffered through major depression are more than four times more likely to have a heart attack.
Inhibitory neurotransmitters
GABA, gamma-aminobutyric acid, is the major inhibitory neurotransmitter in the central nervous center. It is involved in regulating anxiety and motor learning and may be related to eating and sleep disorders. GABA plays an outsized role in the infant brain, establishing the proper balance between excitatory and inhibitory synapses, laying the foundation for circuit formation (Oh et al., 2016). Reduced presence of GABA in adults manifests as poor attention and memory. "Higher brain functions depend on well-balanced neural activity within the underlying brain regions (McGarrity et al,, 2016)."
Endorphins, Enkephalins and Substance P. Endorphins and enkephalins are the body's natural opiates inducing feelings of wellbeing and reducing pain perception. They also depress physical functions like breathing and heartbeat. Substance P is the primary mediator of pain signals.
Purines adenine, guanine, hypoxanthine, and xanthine exist in both the central and peripheral nervous systems, and are implicated in learning and memory, locomotor and feeding behaviors, and sleep. Adenine and guanine also play crucial roles in DNA and RNA functions. A derivative of adenine, adenosine, is known to reduce the production of glutimate in the auditory thalamus (part of the thalamus), leading to reduced auditory learning ability in adults.
Endocannabinoids promote homeostasis throughout the body and are also involved in learning and memory, feeding, fear, and anxiety. They are believed to be synthesized by the body 'on-demand' rather than made and stored for later use. A recently uncovered function of endocannabinoids (CB2) is to increase and decrease the excitation (firing) threshold of neurons in the hippocampus, thus serving a regulatory function for hippocampus signaling to other parts of the brain (Stempel et al., 2016).
Genetics
27. Genes form a second level of organization within the brain.
On the frontier of brain research, the new field of genomics has revealed that the genes within our neurons constitute a second level of organization within the brain. Genomics examines the entire set of genetic information and activity contained within our cells. It reveals that the brain's genes are considerably more involved in regulating memory and behavior than ever imagined. Almost every cell in the body contains a complete set of DNA, each with about 25,000 genes. Genes are specific sequences of bases (DNA: A, T, G, C) that encode instructions for making proteins. We see in Figure 23 that genes are made of base pairs that together contain instructions for making proteins. These instructions vary in size from a couple hundred pairs to over two million.
A full 84% are active in the brain at any moment (Lein & Hawrylycz, 2014), with distinctive collections of genes at work in each major brain structure (and the rest of the body). The cortex, with its hemispheres and sub-cortices, is remarkably homogeneous in its genetic makeup. And, although there is individual variety, patterns of gene activity are quite consistent among humans.
Most genes do their work (are expressed) by being copied by short strands of transcription RNA, which in turn build specific proteins using amino acids. Genes, then, are essentially recipes for building proteins. Proteins, each consisting of between 1,000 and 10,000 molecules, have a large range of functions within the cell, including acting as antibodies to protect the cell from foreign invaders, enzymes that direct chemical reactions, messengers to transmit signals that coordinate biological processes, structural components of cell bodies, and the transport and storage of small molecules within the cell. With 42 million protein molecules within each cell, they are truly the workhorses of cell function.
An example of how genes impact learning and memory is the CREB gene, which encodes a protein that regulates the expression of other genes necessary for memory. CREB not only orchestrates memory formation, but also directs memory formation to brain cells containing the CREB protein (Silva, 2017). High concentrations of CREB are present in the young, which decreases with age. The CREB protein is key to linkages between memories; see Physical basis of memory for additional information.
Genes carry inherited behavior patterns, regulate the growth and number of dendrites (Molumby et al., 2016), determine which cells neurons communicate with and how (Paul et al., 2017), and influence learning abilities and disabilities. For example, genes synthesize new proteins to form memories (Rizzo et al., 2016), within dendrites of the neuron. Even though every cell in our body contains the same DNA, there is a surprising level of individuation within nerve cells that make each unique in structure and function (Erwin et al., 2016). This helps explain why identical twins can be so different.
Within the brain, repeated neural activity changes behavioral genes over time and these genes can eventually drive neural activity. Influence becomes a two-way street. Social anxiety, for example, may develop because of a series of embarrassing incidents. The initial response is driven by neural activity, but over time, long-term behavioral patterns emerge as a result of changes in gene expression, thus creating new and modified proteins that drive neural activity. We see, then, that personality is not a matter of nature or nurture, it is a matter of nature AND nurture. Thus, genetic changes within the brain's neurons reflect the accumulated experiences of the individual, forming a coherent perception of the world and behavioral patterns of the individual. Further, since genes are also the basic unit of heredity, the behavioral patterns can be passed on to offspring as much as physical characteristics.
The timing when different genes are first expressed appears to follow a strict pattern across the lifespan, a "genetic lifespan calendar" (Skene et al., 2017), taking place within the transcript RNA that copies DNA instructions to build proteins. The biggest changes occur during young adulthood, peaking around age 26, with most changes completed by middle age. This calendar is somewhat delayed in women, suggesting that the female brain ages more slowly than men.
Summary
The brain processes information in a hierarchy. As you are reading this page, the signal coming in through your eyes enters your brain through the thalamus, which temporally organizes it. That information then goes on to the primary visual cortex at the back of the brain, where populations of neurons respond to very specific basic properties. For instance, one set of neurons might fire up because the text on your screen is black and another set might activate because there are vertical lines. This population will then trigger a secondary set of neurons in the visual association cortex that respond to more complex shapes like circles, and so on until you have a complete picture of the physical properties of the text.. From there, signals move to the left temporal lobe, which comprehends the meaning of the words, and on to working memory in the prefrontal cortex, which comprehends the ideas and concepts being communicated. As the ideas are processed, other regions light up in response to perceived informational and emotional importance. If you react emotionally based on the information, the limbic system sends signals to the striatum, which initiates physical movement. If the information is new and makes an impression, it is temporally stored in the hippocampus until it is consolidated into long-term memory located throughout the cortex, based on the memory's components (faces, words, emotions).
Our look at the physical brain does not do justice to its elegance and complexity. We recommend you further your understanding by visiting websites on the subject. One place to begin is the Brainfacts.org website.
#top
Over to Processes supporting learning
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8,483,626,234,992,174,000 | Symptoms Of Eczema: Guiding You To A Diagnosis
Eczema is an inflammatory skin condition that worldwide has a lifetime prevalence of 12%. This means roughly one in eight people will experience the symptoms or visual signs of eczema at least once. The causes of eczema are multifactorial, but basically, it’s the manifestation of a hyperreactive immune system.
There are a number of ways to prevent and treat eczema but first, it’s important to identify whether your subjective symptoms and observable signs are in fact eczema.
What are the Symptoms of Eczema?
A symptom is a feeling that you have that you or your doctor cannot see. For example, when you get sick with the flu, the first symptom you experience might be fatigue or joint pains.
These are maladies that one cannot objectively measure from the outside. It requires your own interpretation to help guide the diagnosis of flu.
The most common symptom of eczema is itching but some people don’t have the urge to scratch and instead feel an irritated or raw sensation. It is possible to have the sensation of eczema without any visual skin lesions.
Patients can report feeling their skin stinging, burning, or itching without seeing any visual change in the appearance of the skin’s surface. This occurs especially early in the disease or in mild cases.
What is the Sign of Eczema?
A sign is a change that one can see. It is objective in that it can be measured or observed by the patient and doctor.
Going back to the flu example, a sign of the flu could be an elevated body temperature recorded by a thermometer or perspiration on the forehead.
If the flu leads to a secondary lung infection that can often be visualized with a chest x-ray. These are all signs used in diagnosis.
Signs of eczema can be wide-ranging. It may present as redness, scaling, or cracking. The skin lesions can weep fluid or be very dry.
Many of the signs of eczema are not caused by the inflammation itself –they are the result of scratching and rubbing secondary to the provoking symptoms.
The Signs and Symptoms Of Acute Eczema
1. Pruritus – itching sensation, the most common and often also the most intense of eczema symptoms. The itching can be worse at night, during the winter, or in any condition that leads to skin drying.
2. Erythema – redness
3. Vesiculation – eczema eruptions can have fluid-filled bubbles, appearing as blisters on the skin surface. This most often occurs during the initial, inflammatory stages of a lesion or lesions.
4. Stinging – if eczema is prompted by exposure to an irritant or allergen, the skin surface can begin burning, stinging, or smarting immediately. Alternatively, these sensations can be delayed for up to 24 hours.
The Signs And Symptoms Of Chronic Eczema
1. Pruritus – again, with chronic eczema a sensation of needing to itch is tantamount. Here, the repetitive rubbing and scratch lead to skin changes, oozing of fluid, and in some cases bleeding.
2. Xerosis (dry skin) – due to water loss through the outer layer of the skin, called the epidermis. Nearly every person with chronic eczema will display some degree of dry skin.
Unfortunately, dry skin can make it easier for allergens and irritants to penetrate the surface and then reactive the hyperimmune response—leading to a vicious cycle of eczema signs & symptoms.
3. Lichenification – the scratching and rubbing of chronic eczema produces a thickening of the skin, appearing at times almost leather-like. The skin markings are also more apparent in lichenification.
4. Fissures – cracks can develop in the skin, caused by repeated inflammation, dry skin, scar tissue from healing and aggravated by scratching and rubbing.
5. Hyperkeratosis – the coloring of the skin can change in chronic eczema, usually becoming darker from frequent rubbing.
Other Skin Conditions That Can Be Mistaken For Eczema:
Eczema can easily be mistaken for other skin conditions such as psoriasis, scabies, or seborrheic dermatitis. Use the chart below to help you differentiate between these common dermatologic conditions.
Skin Condition
Distribution
Signs
Symptoms
Additional
Info
Eczema
Wrists, ankles, feet, forehead, and around the eyes, hands, and fingers. Usually located on the flexing side of joints such as behind the knees or the front of elbows. Dry skin, reddened skin. Can have scales or ooze fluid. In later stages, the skin is thickened from continuous scratching and rubbing. Some appear as vesicles. Typically very pruritic/itchy. Can burn, tingle or sting. Symptoms are often worse in winter when the skin is drier. Associated with food and environmental allergies. Occurs in higher incidence in persons with asthma or allergic rhinitis (hay fever).
Psoriasis
Lesions appear on the extending side of joints such as the front of the knees or the back of the elbows. Thick, silvery, and scaly plaques that will bleed slightly when the scales are scratched or picked. Lesions are well-defined with clear borders. Itching is common but not definite and ranges depending on the case. Often accompanied by joint pain or nail changes, especially nail pitting. Crohn’s disease and ulcerative colitis are associated with higher rates of psoriasis.
Scabies
Most often found in skin webs found between the fingers, armpits, feet, thighs, elbows, male and female genitals, and any skin folds. Appears as small bumps with burrows where the mite has entered the skin. The bumps are reddened, inflamed, and crusty. Like eczema, scabies causes a great deal of itching. Itching increases at night, especially early in the infection. Caused by the human mite Sarcoptes scabiei. Contagious can be passed by bedding, sexual contact, clothes sharing, and even handshaking.
Seborrheic dermatitis.
(Commonly known as cradle cap or dandruff.)
Scalp, sides of the nose, chest, armpits, groin, ear canals, and eyebrows. Primarily occurs in oily skin areas. Yellowish, greasy scales. Skin can be reddened, but is not always. Can be pruritic (itchy) but not to the same degree as eczema. Thought is caused by a combination of a yeast called Malassezia and skin that overproduces oil.
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7,652,312,068,448,915,000 | Every species of Psilocybe has its own unique benefits and downsides. Despite that, many don’t know what species are the best for them. So, in this post we will talk about an uncommon species of mushrooms, Psilocybe cyanofibrillosa.
What Is Psilocybe Cyanofibrillosa?
Psilocybe cyanofibrillosa mushrooms are a little more potent and were said to have a more intense effect in users. These magic mushrooms can be found under many types of woods in different temperatures and humidity levels. They grow in Northern America, they are frequently found in British Columbia.
Psilocybe cyanofibrillosa, also known as rhododendron psilocybe, is a rare species from the Hymenogastraceae family. While it is also grown in other countries, these species have different chemical contents, and some can be deadly if consumed in large amounts. It’s essential to know which mushrooms you’re buying, even if you’re growing from spores.
EBSTL Mushroom Monotub Kit
Psilocybe Cyanofibrillosa Habitat
Psilocybe cyanofibrillosa grows on woody debris in conifer forests (pine needles), especially alongside trails where the needle litter has been compacted by foot traffic. Rhododendrons are its favorite spot too! The cyanofibrillosa fruits from September through December. It is widely distributed throughout western North America, from British Columbia to the coastal regions of Washington. They like to grow on dead wood, such as fallen trees and stumps.
See also: Psilocybe Stuntzii (Blue Ringer). How to Identify This Psilocybin Mushroom
How to Identify and Harvest the Cyanofibrillosa
The Psilocybe cyanofibrillosa is actually quite easy to identify because it has a very distinct shape. It often grows in clusters on dead hardwood trees or stumps, but it can also grow on living trees as well. The mushroom has a conical cap covered with brownish scales when wet (yellow or gray when dry), and underneath that cap there are gills that run down the stem; these gills are off-white at first but become brown (a bit of purple too) as they age.
The stem is white or brownish white and hollow throughout its length, and it is of medium length, depending on where the mushroom was growing when you found it.
QUTA Trippy Mushroom Stickers Pack
How Do You Grow Psilocybin Mushrooms?
Psilocybe cyanofibrillosa grows best in rich soil that has been fertilized with manure or compost. The best time to plant the spores is from October through December, when temperatures are between 50 degrees F and 70 degrees F.
Spores are best planted on soil or compost that has been sterilized for at least 24 hours before planting. You can also use a small amount of water from boiled potatoes as an alternative sterilization source if you don’t have access to electricity. Planting too many spores will result in poor growth because there won’t be enough nutrients available for each individual spore to grow into a mature shroom.
Microdosing
A microdose of psilocybin is a sub-perceptual dose that produces minor effects on the body and mind. The purpose is to gain insight into one’s own mental state, be it mental or spiritual. It can also be used to enhance creativity, though some artists have said that it doesn’t work for them.
See also: Panaeolus Cyanescens AKA Copelandia Cyanescens: Magic Mushroom
Dosage
Dosage can vary depending on how strong your mushrooms are, but as a general rule of thumb, start with 1g (0.03 oz). This is not an exact science, so start with a small dose and work your way up from there if you feel it’s necessary.
Neon Style Stickers Waterproof
Effects
The effects will last between 3-4 hours, depending on the strength of your mushrooms and your metabolism rate, so don’t expect to get high for the whole day. There are no side effects other than nausea if taken in excess (over 0.07 oz), so make sure you take care not to consume too much!
Potency
Psilocybe cyanofibrillosa potency depends on how active they are before harvesting, the temperature at which they were stored etc., however they tend to be relatively potent compared to other psychedelic shrooms.
Similar Posts: | {
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5,558,750,360,364,465,000 | Myths and Truths About Fiber | Chris Kresser
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Myths and Truths About Fiber
by
Last updated on
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For decades, fiber has been touted as an essential component of a healthy diet. The supposed benefits of a high-fiber diet have been drilled into us through recommendations by our doctors, government, and the food industry alike, yet many of these health claims have not been proven by research.
In fact, many studies have demonstrated that excess intake of fiber may actually be harmful, particularly for gut health.
The majority of the research supporting the benefits of dietary fiber come from epidemiological studies that link the consumption of fiber-rich fruits and vegetables with a lowered risk of certain diseases such as obesity, heart disease and cancer, particularly colon cancer.(1)
Yet when tested in the lab, controlled intervention trials that simply add fiber supplements to an otherwise consistent diet have not shown these protective effects. (2) (3) (4)
The Institute of Medicine recommends a daily fiber intake of 38 grams for men and 25 grams for women, which may come from dietary fibers, both soluble or insoluble, or the addition of “functional fibers” to the diet. The IOM defines functional fibers as non-digestible carbohydrates that have been isolated or extracted from a natural plant or animal source, or they may be manufactured or synthesized. Examples of functional fibers are psyllium husks, chitin from crustacean shells, fructooligosaccharides, polydextrose, and resistant dextrins. (6)
These functional fibers are often added to processed foods as a way to bulk up the fiber content for consumers looking to meet the IOM intake guidelines.
A recent report by NPR commented that despite the lack of significant evidence linking fiber intake to health outcomes such as reduced heart disease or cancer, many consumers are buying foods that are fortified with synthetic fiber additives under the guise of health promotion. (7) Three grams of added fiber is enough to allow these food products to claim to be a good source of fiber, and the food industry has used these fiber guidelines as a way to increase their sales of grain-based products in particular. (8)
Tan and Seow-Choen, in their 2007 editorial on fiber and colorectal disease, call insoluble fiber “the ultimate junk food”, as “it is neither digestible nor absorbable and therefore devoid of nutrition.” (9) Excess insoluble fiber can bind to minerals such as zinc, magnesium, calcium, and iron, preventing the absorption of these vital nutrients. (10) Large excesses of certain soluble fibers like pectin and guar may also inhibit pancreatic enzyme activity and protein digestion in the gut, leading to an anti-nutritive effect. (11)
The addition of insoluble and soluble fibers to processed foods may actually cause these foods to be even less nutritious than if they were not enriched with any fiber at all.
A high-fiber diet has also been described as a preventative strategy for the development of diverticulosis, a disease that is markedly more common in Western countries. However, when researchers tested the theory that a high-fiber diet prevented diverticulosis, they not only found that a high intake of fiber did not reduce the prevalence of diverticulosis, but that a high-fiber diet and greater number of bowel movements were independently associated with a higher prevalence of diverticula.(12) Interestingly, this study found no association between the presence of diverticulosis and red meat intake, fat intake, or physical activity, which are other factors commonly attributed to diverticulosis. Here is some more information on a diverticulitis diet and how to prevent it naturally.
The researchers hypothesized that one possible effect of a high-fiber diet in the development of diverticulosis could be the quantitative and qualitative changes in gut bacteria due to the excessive fiber intake. Both insoluble and soluble fibers are shown to alter gut bacteria in as little as two weeks. (13) It is possible that the high levels of excess fiber and overgrowth of intestinal bacteria may have contributed to the development of diverticular pouches in the colon.
This hypothesis brings up another side to the fiber debate: the effect of dietary fiber on beneficial gut bacteria, as well as the bacterial fermentation of undigested soluble fiber into short-chain fatty acids such as butyrate. When we eat the soluble fibers found in whole plant foods, the bacteria in our gut ferment these fibers into short-chain fatty acids like butyrate, proprionate, and acetate, and greater amounts of fiber consumed will lead to greater short-chain fatty acid production. (14) In this case, naturally occurring soluble fibers are very important for feeding the friendly bacteria that live in our guts.
One of the risks of long term very low-carbohydrate (VLC) diets, in my view, is the potentially harmful effect they can have on beneficial gut flora. VLC diets starve both bad and good gut bacteria, which means these diets can have therapeutic effects on gut infections in the short term, but may actually contribute to insufficiency of beneficial strains of gut bacteria over the long term.
Providing adequate levels of carbohydrate and soluble fiber to feed friendly bacteria is important for optimizing digestive health and maintaining the integrity of the gut lining through the production of short-chain fatty acids.
Stephan Guyenet has written an excellent blog post describing the benefits of butyrate and other short-chain fatty acids on the maintenance of healthy gut integrity. (15) Butyrate has anti-inflammatory effects, increases insulin sensitivity, and may delay the development of neurodegenerative diseases. It may also be helpful in the treatment of diseases of the colon such as Crohn’s, IBS or ulcerative colitis. (16)
Stephan believes that butyrate may play a significant role in healthy metabolic function, stress resistance, and the immune response. He also asserts that the epidemiologically observed benefits of a diet high in naturally occurring fiber are likely due to the higher butyrate production from these diets. In this case, a higher fiber diet could be protective and beneficial for health, particularly if the fiber is soluble.
So what does this mean for our own consumption of fiber?
Ideally, dietary fiber should be coming from whole food plant sources. Many foods in the Paleo diet are great sources of both soluble and insoluble fiber, such as yams and sweet potatoes, green leafy vegetables, carrots and other root vegetables, fruits with an edible peel (like apples and pears), berries, seeds, and nuts. Interestingly, butyrate itself is also found in high-fat dairy products such as butter and cheese, and can also be provided by the bacteria found in fermented foods.
Although I recommend that most people get fiber from whole foods, there are some people that may benefit from soluble fiber supplementation – including those that aren’t able to eat fruit or starch due to blood sugar issues or weight regulation, and those with severely compromised gut flora or gut dysbiosis. In these cases I’ve found soluble fiber and/or prebiotic supplements to be helpful.
For healthy people, including a variety of fibrous whole plant foods, fermented foods, and high-fat dairy as tolerated should eliminate the need to supplement with extra fiber, especially those insoluble fibers that are from sources high in anti-nutrients.
A Paleo diet with some level of attention paid to the quality and quantity of vegetables, fruits, and starchy tubers can provide adequate levels of soluble fiber to feed the friendly bacteria in the gut that convert these fibers into beneficial short-chain fats like butyrate.
Recommended supplements if needed:
Prebiotic: Klaire Labs Biotagen
Soluble fiber: Organic Acacia Fiber
Caution: it’s crucial to start with a very low dose of prebiotic or soluble fiber and build up slowly over time. This will minimize any potential adverse reaction that can occur with significant changes (even positive changes) to the gut microbiome. For Biotagen, start with 1/4 of 1/8 of a tsp (1/32 tsp.) and increase by 1/32 of a tsp every 4-5 days. For Organic Acacia Fiber, start with 1/4 of a tsp. once per day and build slowly from there.
115 Comments
Join the conversation
• Please watch my documentary earthlings free on YouTube, no cow, pigs or chickens wanna be murdered for your diet or your taste buds, they are not food they are a living being, shame on you author of this article.
1. scientists will provide you any outcome you pay for …. high fiber was a way for people for thousands of years before the invention of junk foods, supermarkets & others… now you poop 150-300 grams , when people had a high fiber diet, people poop many times more… american junk diet & lifestyle is to blame for all western diseases
2. I feel like a lot of people are critical of Chris’ research, however, seem to forget that he’s the one who has dedicated his life to academic research into functional health. I have personally tried everything and believe that there is no answer or one size fits all. HOWEVER, if you do have a compromised digestive system, putting anything into it that makes it work twice as hard is counterintuitive until it heals…which is fiber. Remove, heal then introduce again but not excessively. Fiber from natural foods exists for a reason….added fiber does not. Nature didn’t create fiber supplements. Simple.
3. Do not believe any of this. The problem with the American diet is that Americans do NOT consume enough fiber and the reason for the high incidence of colon cancer and other cancers of the gastric system.
With the American diet as it is, the amount of fiber in our diets is way too low compared to foreign countries where fiber is high on the list in their diets.
We eat too much processed foods that contain no fiber or very small amounts.
It is perfectly normal to have 2 or even 3 bowels movements a day. These bowel movements rid the body of toxins that we accumulate in our bodies. There are some people who have only 2 or 3 bowel movements a week! Sooner or later these people will come down with some kind of catastrophic illness in their gastric system, primarily colon cancer.
I don’t buy any of what Kresser has said here. The more fiber in your diet the better you will feel and your overall health will benefit from it.
• I’m convinced you didn’t read the entire article. Chris didn’t write “against” fiber intake. He shows that the effects (positive and negative) of fiber consumption on the digestive system need to be studied further, and scientific study has so far revealed that fiber itself isn’t a miracle food that does away with disease. It’s a fact that excessive fiber intake (especially insoluble fiber) can aggravate the intestines. Excessive amounts of any good thing, be it vitamin A or potassium or any other nutrient, has a negative effect on the body.
Chris actually recommends upping your fiber intake at the end of the article, but your statement that “the more fiber [you get] the better you will feel” is most certainly not true. Try eating a few servings of whole sunflower seeds and see how that feels.
• 2 or 3 bowls a day is healthy?
Is this guy healthier than me just because I only dump once every two days on average?
• You should be pooping several times a day. I didn’t start to have daily bowel movements until 6 months after starting changing my diet. I used to eat a bunch of processed crap like the typical american and I only pooped every other day. Now that I’m eating a bunch of fruits and vegetables and no processed food or refined sugar or dairy, I have 1-3 bowel movements a day. So in my experience, 2-3 bowel movements a day is healthier than pooping only once every couple of days.
Out of curiousity, what does your diet currently consist of?
• I just started eating a much healthier diet with more fruits and veggies. I’m only pooping once every 3 days which is scaring me. I’m thinking about taking fiber supplements to help things move along. Any recommendations?
• thats great you don’t eat dairy, but whole milk plain yogurt, sorry, but im not giving that up. There are a lot of great benefits and things to be said about whole-milk/fat dairy. Everyone is different, I think a lot of articles like this are generalized and they simply shouldn’t be….we all have different bodies and tolerances for things. I can tell you that fiber, sugar, nightshades, salt have no place in my body. They have ruined my health, amongst other things.
• The Japanese eat a relatively low fibre, high carbohydrate (white rice) diet and levels of colon cancer aren’t anywhere near as high as in the US.
• It is a myth that the Japanese subsist on large amounts of rice. They eat relatively small portions of rice supplemented with a very broad variety of vegetables and seafood. Modern Japanese diets are obviously changing, but please don’t assume the Japanese eat Sushi all day.
• Chris Kresser advocates eating a VERY high fiber DIET, that is, lots of fiber-rich FOODS which feed your healthy gut bacteria, and this article is just saying supplementation isn’t the same thing. He also advocates for fiber from veggie, rather than grain, sources. Listen to his RHR podcast episodes “Are High-Fat Diets Bad for the Microbiome?”, “Why You Need to Eat More Vegetables—And How to do it”, “Is a Disrupted Gut Microbiome at the Root of Modern Disease”, and “Are Vegetarian Diets Better for the Microbiome?” and you will hear really great and detailed information about how fiber is pretty much the most important thing to your health, since the you can’t be healthy without a healthy gut. He espouses eating small quantities of very high quality pasture-raised meats & organs, fatty fish, and raw pasture-raised dairy, but the rest (the vast majority) should be unprocessed, whole vegetables & some fruit, while avoiding grains, sugar (except what’s naturally occurring in WHOLE fruits), and industrial seed oils (which are high in inflammatory omega-6).
The big problem with the predominance of medical literature on fiber is that they fail to differentiate between fiber in grains (which is what most people think of and aim to increase consumption of) versus fiber in vegetables. Autoimmune and other chronic diseases of civilization generally respond very favorably to the omission of grains or, conversely, can be exacerbated by grain. If some people are eating fiber from something that makes them sicker (and their guts unhappy), that’s way different from subsisting on a diet comprised of spinach, broccoli, cucumbers, tomatoes, bell peppers, carrots, plantains, sweet potatoes, berries, and apples with a little high-quality protein thrown in. Eating a high-fiber wheat bran breakfast each day (processed food) with additional meals also made up of packaged, processed foods CANNOT compete with this in terms of health in the gut and bowel movements. Soon, we hope, there will be disambiguation research to put this point to rest. Meanwhile, uninformed people everywhere will continue to say the unqualified, nonspecific (and therefore inaccurate) statement, “more fiber is always better.”
4. I say soak and ferment all whole grains with saliva as culture for 24hrs or more before consumtion!:-)..
5. Can you actually propose A NUMBER?
I mean, the federal RDA for men is 38 grams fiber per day.
What is an unhealthily high fiber intake?
What would be your recommended upper limit?
• If you’re eating a Paleo diet heavy on vegetables, tubers, nuts, and seeds, you’re getting enough. Adjusting and monitoring your fiber intake is something you should do if your bowel movements are unhealthy. If everything is working fine, just keep eating real food while occasionally taking a probiotic with HSOs.
6. do you realize how many “may”s, could be, hopefully, are in this article? Nobody knows nothin.
• “may’s, could be, hopefully” words are for the lawyers whom are ready to pounce on any unsuspecting person to sue the crap out of them. (pun intended).
• Actually, they are the most accurate words that could be used.
Eating more vegetables may improve your health is far far more accurate than saying eating more vegetables will improve your health.
7. Maybe somebody can give me advice:
I can not tolerate fermented foods because of histamine intolerance. So I take a probiotic.
I suffer from a chronic procitits. At the beginning I felt little pain and had bloody stool, higher calprotectin. Through a Paleo diet (no gluten, low histamine, diary and egg free) I got rid of many symptoms like the bloody stool and most of the pain (was not much pain). But I still suffer from irregular motility and mood and energy swings which correlate with my bowel movements. This means:
I am often constipated for 2-3 days. Then I have either normal motility like I always had (2-3 per day) or I have one movement per day. When having my old motility back, I feel good energy. But the most time I feel like a little subdepressive and low energy…
When I had acute proctitis the first and only time, I could not tolerate anything but rice and potatoes. Sugar and diary gave me massive mood swings (anxiety). Had to eat rice and potatoes for a week with a probiotic to get normal again…
Since I suffer from proctitis I cannot tolerate any Gluten, or FOODMAPS. Foodmaps give me heavy brainfog and constipation (tried inulin)
I tried Bimuno (GOS) which my gut tolerated well, but I react allergic to it (I react to many things :-/)
So I ask myself if could use Lactulose as a prebiotic for a longer time. Is this an good alternative to inulin or FOS?
In my probiotic is FOS, but the bacteria eat it all up during the preactivation- phase (has to be diluted in water 25 minutes before drinking)
Or should I start with tiny amounts of FOS?! But even a tiny capsule of Inulin gaves me heavy brain fog for days last time I tried it. I have no idea where to go with there issues. There´s no Chris Kresser in Germany…:-/
Can anybody help me with this?
• Try to remove all vegges, dairy and eggs, and use only rice, almond milk, some steamed corn flakes, meat and fish with olive oil and a pick of salt, then reintroduce eggs and see how it go for a week.
Yes, is not completely paleo since i use some gluten free grains, but if i don’t i become so weak and my muscle so flat that i’m not able to stand still (i’m 58 kg and i lost about 35 kg after i get the sibo 3 years ago)..
If is ok and your constipation don’t worse then add dairy, and so on till you find what is bad for you. I immediately notice what foods cause pain since i get bloated, constipated with abdomin al pain (cause peristalsis increase) .
I can’t eat every kind of veggies for a long time, even zucchini, carrots and pumpkin cause pain. About fruits i eat sometimes an apple or papaya and i use filtered orange juice (homemade from oranges).
Veggies increses peristalsis and is very bad if you have a damaged gut. Bone broath sometimes cause cramps so i tend to avoid it and limit to 1-2 for week.
Sometimes i eat gluten free pasta (no preservatives) and white rice, and i’m ok, a bit of honey don’t hurt too. I need them or i feel very weak and bad.
There is no turn back once your gut is damaged, is our fault to consume refined craps, is our fault because we are ignorant to trust food lobbies and is our fault to use medications instead to fight the root of the cause, so is pratically something irreversible that we have to deal for the rest of your life, it mean low carbs and high fats/proteins because they are the only things that we can eat.
But i’m fine, i eat because is mandatory to our life, i don’t live for food anymore.
8. What about the fiber from vegetables like broccoli, cauliflower, bok choy, and lettuce? Do we need to be careful with those as well?
• Nope, everything about veggies is good and specially if eaten raw, as a snack, etc. Follow the greed diet and you will be just fine.
One of the things I noticed when reading the article is that it lacks real life cases about treating people with fiber, other than comments.
I have research the subject of fiber not only to be healthy but to control certain illnesses and disorders of the human body. Healthy people should ingest about 25 grams of fiber daily from food sources and “diabetic” people should ingest about 40 to 60 grams of fiber daily and this has been proved to be effective by a diabetes specialist doctor at the VA Hospital in Lexington, KY. He treated bad cases of diabetes with a heavy dosage of fiber and no medication and the results were excellent. Concerning diet, people should realize that it is not only fiber what the person should eat but also watch out for other things such as sugar, salt, cholesterol, fat, etc. However, for the digestive track natural fiber is the best. Some people cannot tolerate grains; however, there are some grains which those people will be ok eating such as Quinoa, the best grains of all, which can be cooked in a variety of ways and eaten at breakfast, lunch, and dinner. The best thing is to avoid any dairy products, sugar in all forms and from all sources, salt although sea salt is healthy in moderate amounts, fats from all sources, and foods containing cholesterol. Want to be healthy? Stay green in your diet!
• Bad grammar, very inaccurate information. With inflammatory bowel conditions you absolutely do need to limit your intake of gassy cruciferous vegetables like broccoli. Quinoa is not a grain. This person has no idea what they’re talking about and future readers should be warned not to listen to this garbage. It’s foolish.
• Vegetables best eaten raw…. avoid all dairy, salt, fat and food containing cholesterol…. Etc …..
You clearly don’t know enough about nutritional science. Better not giving advises to people again…
• High fiber foods does not necessarily mean it helps with blood glucose. The best method is to use a blood glucose meter after one and two hours after eating meals with carbs. I found black beans spiked my blood glucose.
• You Said, don’t eat “salt, fat and food containing cholesterol…. Etc …..”
You do realize that saturated fat is crucial to maintain a balance with your hormones? If not meat, at least some coconut. If you don’t eat cholesterol foods, then your body will just make the cholesterol from protein.
• I disagree with you and the doctor who gave 60 grams fiber. I myself did this to reverse type 2 and it worked BUT it caused me to become severely anemic and low minerals and has taken 4 years to get getter. Too mulch fiber binds to iron and mineral and vitamins and you never absorb them. It’s dangerous. I say rat your fiber in food not added supplements
9. Where does a product like PGX come in here. Some doctors recommend to use it at least once a day. What kind of fiber is it?
Thanks,
Pat
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8,154,479,837,571,149,000 | Skip to main content
[ "article:topic", "Orbits", "optic nerve", "Eyeballs", "Eyelids", "Nictitating Membrane", "Haw", "Eyelashes", "Conjunctiva", "Tear Glands", "sclera", "retina", "choroid", "White", "cornea", "iris", "pupil", "Rods", "Rod Cells", "Cone Cells", "fovea", "Blind Spot", "lens", "Anterior and Posterior Chambers", "Cataract", "Aqueous and Vitreous Humours", "Refraction", "authorname:lawsonr", "license:ccbysa", "showtoc:no" ]
Medicine LibreTexts
15.09: Sight
• Page ID
2861
• The eyes are the organs of sight. They consist of spherical eyeballs situated in deep depressions in the skull called the orbits. They are attached to the wall of the orbit by six muscles, which move the eyeball. Upper and lower eyelids cover the eyes during sleep and protect them from foreign objects or too much light, and spread the tears over their surface.
The nictitating membrane or haw is a transparent sheet that moves sideways across the eye from the inner corner, cleansing and moistening the cornea without shutting out the light. It is found in birds, crocodiles, frogs and fish as well as marsupials like the kangaroo. It is rare in mammals but can be seen in cats and dogs by gently opening the eye when it is asleep. Eyelashes also protect the eyes from the sun and foreign objects.
Structure of the Eye
Lining the eyelids and covering the front of the eyeball is a thin epithelium called the conjunctiva. Conjunctivitis is inflammation of this membrane. Tear glands that open just under the top eyelid secrete a salty solution that keeps the exposed part of the eye moist, washes away dust and contains an enzyme that destroys bacteria.
The wall of the eyeball is composed of three layers (see diagram 15.4). From the outside these are the sclera, the choroid and the retina.
Anatomy and physiology of animals Structure of the eye.jpg
Diagram 15.4 - The structure of the eye
The sclera is a tough fibrous layer that protects the eyeball and gives it rigidity. At the front of the eye the sclera is visible as the “white” of the eye, which is modified as the transparent cornea through which the light rays have to pass to enter the eye. The cornea helps focus light that enters the eye.
The choroid lies beneath the sclera. It contains a network of blood vessels that supply the eye with oxygen and nutrients. Its inner surface is highly pigmented and absorbs stray light rays. In nocturnal animals like the cat and possum this highly pigmented layer reflects light as a means of conserving light. This is what makes them shine when caught in car headlights.
At the front of the eye the choroid becomes the iris. This is the coloured part of the eye that controls the amount of light entering the pupil of the eye. In dim light the pupil is wide open so as much light as possible enters while in bright light the pupils contract to protect the retina from damage by excess light.
The pupil in most animals is circular but in many nocturnal animals it is a slit that can close completely. This helps protect the extra-sensitive light sensing tissues of animals like the cat and possum from bright sunlight.
The inner layer lining the inside of the eye is the retina. This contains the light sensing cells called rods and cones (see diagram 15.5).
The rod cells are long and fat and are sensitive to dim light but cannot detect colour. They contain large amounts of a pigment that changes when exposed to light. This pigment comes from vitamin A found in carrots etc. A deficiency of this vitamin causes night blindness. So your mother was right when she told you to eat your carrots as they would help you see in the dark!
The cone cells provide colour vision and allow animals to see details. Most are found in the centre of the retina and they are most densely concentrated in a small area called the fovea. This is the area of sharpest vision, where the words you are reading at this moment are focussed on your retina.
Anatomy and physiology of animals A rod and cone from the retina.jpg
Diagram 15.5 - A rod and cone from the retina
The nerve fibres from the cells of the retina join and leave the eye via the optic nerve. There are no rods or cones here and it is a blind spot. The optic nerve passes through the back of the orbit and enters the brain.
The lens is situated just behind the pupil and the iris. It is a crystalline structure with no blood vessels and is held in position by a ligament. This is attached to a muscle, which changes the shape of the lens so both near and distant objects can be focussed by the eye. This ability to change the focus of the lens is called accommodation. In many mammals the muscles that bring about accommodation are poorly developed, Rats, cows and dogs, for example, are thought to be unable to focus clearly on near objects.
In old age and certain diseases the lens may become cloudy resulting in blurred vision. This is called a cataract. Within the eyeball are two cavities, the anterior and posterior chambers, separated by the lens. They contain fluids the aqueous and vitreous humoursrespectively, that maintain the shape of the eyeball and help press the retina firmly against the choroid so clear images are seen.
How The Eye Sees
Eyes work quite like a camera. Light rays from an object enter the eye and are focused on the retina (the “film”) at the back of the eye. The cornea, the lens and the fluid within the eye all help to focus the light. They do this by bending the light rays so that light from the object falls on the retina. This bending of light is called refraction. The light stimulates the light sensitive cells of the retina and nerve impulses are produced that pass down the optic nerve to the brain (see diagram 15.6).
Anatomy and physiology of animals How light travels from the object to the retina of the eye.jpg
Diagram 15.6 - How the light travels from the object to the retina of the eye
Colour Vision In Animals
As mentioned before, the retina has two different kinds of cells that are stimulated by light - 'rods' and 'cones'. In humans and higher primates like baboons and gorillas the rods function in dim light and do not perceive colour, while the cones are stimulated by bright light and perceive details and colour.
Other mammals have very few cones in their retinas and it is believed that they see no or only a limited range of colour. It is, of course, difficult to find out exactly what animals do see. It is thought that deer, rats, and rabbits and nocturnal animals like the cat are colour-blind, and dogs probably see green and blue. Some fish and most birds seem to have better colour vision than humans and they use colour, often very vivid ones, for recognizing each other as well as for courtship and protection.
Binocular Vision
Animals like cats that hunt have eyes placed on the front of the head in such a way that both eyes see the same wide area but from slightly different angles (see diagram 15.7). This is called binocular vision. Its main advantage is that it enables the animals to estimate the distance to the prey so they can chase it and pounce accurately.
Anatomy and physiology of animals Well developed binocular vision.jpg
Diagram 15.7 - Well developed binocular vision in predator animals like the cat
In contrast plant-eating prey animals like the rabbit and deer need to have a wide panoramic view so they can see predators approaching. They therefore have eyes placed on the side of the head, each with its own field of vision (see diagram 15.8). They have only a very small area of binocular vision in front of the head but are extremely sensitive to movement.
Anatomy and physiology of animals Panaoramic monocular vision.jpg
Diagram 15.8 - Panoramic monocular vision in prey animals like the rabbit
Contributors
• Ruth Lawson (Otago Polytechnic; Dunedin, New Zealand) | {
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6,040,315,180,162,569,000 | Can hormones affect your weight?
Hormones are chemicals produced by glands in our body that act as regulators of vital bodily functions. These chemical messengers are responsible for our growth and development, mood, appetite, metabolism, and sexual function.
That’s why even a small disturbance in the hormonal levels- when your body releases too little or too much of a hormone — can significantly impact your health.
How do hormones influence weight?
Here’s a breakdown of the hormones that control hunger, fullness, metabolism, and fat distribution, all of which can influence body weight.
HORMONES THAT CONTROL APPETITE
HORMONES THAT AFFECT METABOLISM
HORMONES THAT AFFECT FAT DISTRIBUTION
Leptin
Ghrelin
Cholecystokinin
Insulin
Thyroid
Cortisol
Estrogen
Testosterone
HORMONES THAT CONTROL APPETITE
• Ghrelin “the hunger hormone”- Stimulates the hypothalamus (an area of the brain) indicating that your stomach is empty, and you need food.
• Leptin “the fullness hormone”-Leptin is a hormone secreted by fat cells of the body. It reduces your urge to eat by acting on the hypothalamus to indicate that you are ‘full’.
• Cholecystokinin (CCK)– CCK is a hormone released by the small intestine in response to food (especially fat and protein). It reduces food intake by stimulating ‘fullness’ centers in your brain, and it also increases the release of leptin.
Obesity is strongly associated with abnormalities in leptin (including elevated levels of leptin and leptin resistance) and low ghrelin levels. This may lead to overeating and weight gain.
HORMONES THAT AFFECT METABOLISM
Hormones that influence the number of calories your body burns (also called energy expenditure) play a significant role in weight management and obesity.
• Insulin “the storage hormone”– Insulin is produced by your pancreas. This hormone transfers glucose from food into your cells for either energy or storage (in your liver, muscle, and fat cells for later), depending on your body’s needs.
• Thyroid-The thyroid gland secretes hormones that are responsible for the regulation of metabolism. Hypothyroidism characterized by low thyroid hormone levels leads to less energy expenditure. This is why people with hypothyroidism may gain weight and are always tired and lethargic.
• Cortisol “the stress hormone”- Cortisol is produced by your adrenal glands that triggers an increase in heart rate and energy levels during times of stress. Cortisol redistributes fat to the abdominal region and increases appetite (especially a craving for foods rich in fat and sugar).
Elevated levels of insulin and insulin resistance (Diabetes) and elevated cortisol levels may lead to weight gain.
HORMONES THAT AFFECT FAT DISTRIBUTION
Fat storage in specific regions of our body is strictly regulated by certain hormones.
• Estrogen-Estrogen is responsible for regulating the female reproductive system. Estrogen levels change throughout the menstrual cycle as well as during pregnancy, nursing, and menopause. Individuals with low estrogen are more likely to gain body fat, especially in the midsection.
• Testosterone-Testosterone is the hormone responsible for the development of the male reproductive organs, sperm production, and libido. As a man gets older, these levels gradually decrease, and this leads to fat accumulation in the belly.
Low levels of sex hormones can affect your weight and health besides your libido and fertility.
The bottom line
Endocrinologists, who are doctors specializing in hormones and metabolism can evaluate and treat any disturbance in your hormonal balance and help you lead a healthy life. Call us on 1-347-384-5690 to get answers to your queries or pay us a visit at 1797 Pitkin Avenue, Brooklyn, New York 11212. We have the best endocrinologists and diabetes specialists to help you throughout the process. You can also visit our website at https://doralhw.org or contact us at info@doralhw.org if you have any queries. | {
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What to Eat (and Avoid) During a UTI
A burning sensation, abdominal pain, and cloudy urine are all signs of a potential urinary tract infection (UTI). This uncomfortable infection can affect any part of your urinary system—kidneys, ureters, bladder, and urethra—however, most UTIs involve the lower urinary tract (specifically, the bladder). The painful symptoms of a UTI are not only annoying, but they can also be dangerous—leading to serious consequences if the infection reaches the kidneys. The first step to feeling better is contacting a doctor, but there are some ways you may be able to relieve UTI symptoms in addition to following a professional care plan. Before we get into foods and drinks for UTIs, let’s cover some basics:
UTI Symptoms
Urinary tract infections (UTIs) are typically more common in women, but anyone can experience them. If you suspect you have a UTI, monitor for these symptoms:
• Strong, persistent urge to pee
• Burning sensation when urinating
• Passing frequent, small amounts of urine
• Nausea
• Cloudy urine
• Red, pink, or cola-colored urine (signs of blood in the urine)
• Foul-smelling urine
• Pain and pressure within the abdomen
• Pain during intercourse
• Fever and chills
• Pelvic pain, in women (around the center of the pelvis and around the pubic bone)
UTI Treatment
UTIs aren’t fun for anyone and the symptoms can worsen over time if left untreated. If you suspect you have a UTI and are experiencing any of the aforementioned symptoms, don’t suffer in silence. Reach out to a qualified medical provider like DispatchHealth as soon as possible to avoid any exacerbations.
In many cases, doctors will prescribe antibiotics to treat a UTI. In addition to following the care plan provided by your physician, sticking to a certain diet can help you manage those uncomfortable UTI symptoms and speed the healing process at home. With that in mind, DispatchHealth has put together a helpful guide on what to eat/drink (and what to avoid) with a UTI.
See if we service your area
What to Drink for a UTI
Can you treat a UTI by drinking cranberry juice? The answer behind the infamous cranberry juice cure is mixed. In some clinical studies (primarily with women), the consumption of pure cranberry juice, cranberry extracts, or cranberry supplements helped reduce the risk of repeated UTIs. In any case, however, the benefit to drinking cranberry juice for a UTI is small. So, what should you drink for a UTI instead? Water is by far the best beverage choice for someone with a UTI. Drinking at least 12 8-ounce cups of water each day while you have an infection will help flush the bacteria from your system and can speed up the healing process.
Foods to Eat for a UTI
In order to recover from a UTI as soon as possible, you may want to try consuming the following foods:
• Berries. Although researchers are still studying their effectiveness, it’s believed that eating cranberries, blueberries, and raspberries can help fight off a UTI. They contain proanthocyanidin, which has been shown to prevent infection-causing bacteria from adhering to the lining of the urinary tract.
• Probiotic-rich foods. Try incorporating foods like plain Greek yogurt, pickles, and sauerkraut into your diet, since they contain good bacteria that can help combat an infection.
• High-fiber foods. Foods that are high in fiber—such as bananas, beans, lentils, nuts, oats, and other whole grains—can help remove harmful bacteria from your body. They also encourage regular bowel movements, which can help relieve some bladder pressure.
• Salmon. Cold-water fish contain omega-3 fatty acids, which can help reduce inflammation caused by a UTI. Fish oil supplements are another great alternative for individuals who don’t eat fish; always consult your doctor before adding any supplements to your diet.
Things to Avoid: Sugar & UTIs
Adjusting your diet for a UTI involves more than introducing certain foods and drinks; it also means abstaining from things. Not sure where to start? Here’s a simple rule of thumb to follow: Avoid sugar for a UTI. Sugar is laced in an overwhelming amount of commercial foods and drinks these days. Unfortunately, it can also aggravate an infection. To cut back on these sugary delights and boost your care plan for a UTI, avoid:
• Carbohydrates
• Soda
• Alcohol (beer, wine, and liquor)
• Artificial sweeteners
Although there’s no evidence that artificial sweeteners can worsen a UTI, they have been shown to exacerbate bladder symptoms for individuals with chronic interstitial cystitis, so you may want to avoid them. Other foods and beverages to avoid with a UTI include:
• Spicy foods. Certain spicy foods can irritate the bladder. Instead, try sticking to a bland diet—like the “BRAT” diet—when you have a UTI.
• Citrus. Although they’re high in immunity-boosting vitamin C, highly acidic fruits like oranges, lemons, limes, and grapefruits can irritate your bladder and aggravate UTI symptoms.
• Caffeinated drinks. It’s important to stay hydrated when you have a UTI, but stay away from coffee and other caffeinated beverages. When in doubt, choose water!
At-Home Treatment for UTIs
Did you know that getting treatment for a UTI doesn’t have to require a visit to a doctor’s office or even an urgent care clinic? Thanks to DispatchHealth’s in-home service, you can receive the on-demand acute care you need without leaving the house. Within a few hours of requesting service, one of our teams will come directly to your home, perform an examination, and recommend an appropriate course of treatment, all for an affordable price. We’ve partnered with leading health insurance providers—including Medicare and Medicaid—to ensure that your care is covered under your current plan. And we also offer an affordable flat rate for individuals without insurance.
Contact DispatchHealth today to arrange a visit—you can do so over the phone, through our mobile app, or on our website. We look forward to providing you with the relief you need.
Sources
DispatchHealth relies only on authoritative sources, including medical associations, research institutions, and peer-reviewed medical studies.
Sources referenced in this article:
1. https://www.eehealth.org/blog/2019/05/what-to-eat-during-a-uti
2. https://www.everydayhealth.com/urinary-tract-infections-pictures/foods-and-drinks-that-may-irritate-your-bladder-1028.aspx
3. https://www.mayoclinic.org/diseases-conditions/urinary-tract-infection/symptoms-causes/syc-20353447
4. https://nortonhealthcare.com/news/5-power-foods-for-better-urinary-health/
5. https://www.yinovacenter.com/blog/eat-to-beat-urinary-tract-infection
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3,128,704,250,625,697,000 | Angelica Archangelica in homeopathy: properties, benefits and uses (all you need to know)
What is Angelica archangelica?
In classical homeopathy, angelica is not one of the preferred remedies; in modern homeopathy, however, the importance of Angelica has increased.
It is used for all kinds of digestive problems. The essential oils and bitter substances contained in the plant contribute to the formation of gastric acid and bile juices. The remedy helps with flatulence, loss of appetite and feeling of fullness, but also with exhaustion and anxiety.
Applied externally, Angelica archangelica is said to have an antirheumatic effect.
information about the agent
How do you recognize patients who need Angelica?
To date, there is no clear picture of the appearance or medicinal properties of Angelica archangelica. Patients who need the remedy are seen as fearful, lacking in self-confidence and attached to their homeland. They find changing places uncomfortable. In general, they lack flexibility. Darkness triggers intense feelings of fear. One often suffers from nightmares.
There are no observations of the child type of Angelica archangelica.
modalities
Angelica archangelica is indicated for all typical symptoms that improve or worsen with the following modalities:Improvement:
• Not known
Deterioration:
• Not known
What are typical uses for Angelica archangelica?
• fears
• exhaustion
• stomach pain
Areas of application in detail
fears
Fear of the dark and everything unknown
Dosage: 3 times a day 3 globules in the potency D6
Chest pain with cold and cough
Symptoms of pleurisy with shortness of breath, rattling breath sounds and cough.
Dosage: 3 times a day 3 globules in the potency D6
exhaustion/weakness
Deepest states of exhaustion, as also appear in glandular fever; nervous exhaustion with abdominal cramps
Dosage: 3 times a day 3 globules in the potency D6
Gastrointestinal complaints
Crampy stomach pain, stuck flatulence, feeling of fullness
Dosage: 3 times a day 3 globules in the potency D6
application information
Dosage form of Angelica archangelica
Globules are administered orally in low potencies up to 6X. Externally, the mother tincture is used for poultices.
Angelica archangelica dosage
Externally, compresses are made up to three times a day with the diluted mother tincture. For digestive problems, the remedy can be given three to five times a day with a dose of D6. In the case of chronic states of anxiety, homeopathic advice should be sought in order to be able to treat with higher potencies if necessary.
Angelica archangelica During pregnancy
Since the drug is said to have a menstrual-promoting effect, it is not advisable to give angelica during pregnancy.
Side effects of Angelica archangelica
The skin may temporarily become more sensitive to light. Caffeine, sugar, fatty foods and alcohol should be avoided during therapy with angelica. For pregnant women, the drug is only suitable to a limited extent and should not be administered independently. No other side effects are known.
Similar means
Arsenicum album
Angelica archangelica and Arsenicum album have a similar remedy in terms of exhaustion and indigestion, with Arsenicum album having more of a burning stomach pain in the foreground.
Typical potencies: Mother tincture, D1 to D6
fabric type: medicinal plant
Homeopathy
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2,260,080,841,614,437,600 | The effect of the timing of umbilical cord clamping on hemoglobin levels, neonatal outcomes and developmental status in infants at 4 months old
Soheila Nouraie, Sedigheh Amir Ali Akbari, Roshanak Vameghi, Alireza Akbarzade Baghban
Abstract
502
Objective:
Delayed umbilical cord clamping (DCC) increases blood transfer to newborns. Hence we investigated the effect of the timing of DCC on hemoglobin levels, neonatal outcomes and developmental status in infants at four months old
.
Materials & Methods:
This clinical trial examined infants born to 400 pregnant women immediately upon birth and at the age of four months. The newborns were randomly assigned to either the intervention group with a 90-120-second delay in umbilical cord clamping or the control group with a clamping delay of below 60 seconds, and blood samples were taken from their umbilical cords. The Ages and Stages Questionnaire was used to evaluate the infants’ developmental status.
Results:
Umbilical cord hemoglobin was found to be significantly higher in the intervention group compared to in the controls (P=0/024). No significant differences were observed between the two groups in terms of neonatal complications except neonatal jaundice was significantly more common in the intervention group (P=0/025), although the need for phototherapy was not different between the groups. Overall, no significant differences were observed between the two groups in terms of developmental status at four months old; however, the infants had better problem-solving skills in the delayed umbilical cord clamping group (P=0/015).
Conclusion:
The results obtained show that, despite elevating hemoglobin, delayed umbilical cord clamping but has no effects on infant development except in terms of problem-solving skills. Further studies are recommended on the effects of delayed umbilical cord clamping on infant development.
Keywords
Umbilical cord clamping, Hemoglobin, Child development.
Full Text:
PDF45
486
DOI: https://doi.org/10.22037/ijcn.v13i1.17662
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Copyright (c) 2018 Iranian Journal of Child Neurology | {
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1,199,451,661,086,531,000 | Skip to main content
Self-weighing among young adults: who weighs themselves and for whom does weighing affect mood? A cross-sectional study of a population-based sample
Abstract
Background
Self-weighing is widespread among young adults and is sometimes recommended by healthcare providers for weight management. The present study aims to deepen our understanding of who is frequently self-weighing among young adults, and to examine for whom self-weighing impacts mood based on weighing frequency and other eating and weight-related characteristics.
Methods
Survey data were collected from a large population-based sample of young adults (31.1 ± 1.6y) participating in Project EAT-IV (n = 1719). Cross-sectional data were stratified across sex and analyzed with chi-square, t-tests, and linear and logistic regressions controlling for age, ethnicity/race, education level, and income.
Results
Self-weighing frequency was higher among male and female young adults with a current eating disorder, those trying to lose weight or who endorsed any disordered eating behaviors or cognition, and females with higher BMI. Young adult females were significantly more likely than males to report that self-weighing impacted their mood (53% vs 27%, p < 0.05). Among both male and female young adults, there was a higher probability of participants reporting that self-weighing impacted their mood among those who were self-weighing more frequently, had higher BMI, were trying to lose weight, and endorsed disordered eating behaviors or cognitions.
Conclusion
Findings suggest that for many young adults, particularly females and those with weight-related concerns, self-weighing is a behavior that comes with emotional valence. The emotional consequences of self-weighing should be considered when making public health and clinical recommendations regarding the usefulness of self-weighing.
Plain English summary
Many young adults regularly weigh themselves, sometimes due to the recommendation of a healthcare professional. However, little is known about who weighs themselves and how weighing oneself impacts one’s mood. This study examines who tends to weigh themselves and for whom weighing themselves impacts their mood. Results from 1719 young adults from the general population showed that 53% of young women and 27% of young men reported that weighing themselves impacted their mood. Those with a current eating disorder, who had eating disorder symptoms, or had a higher BMI weighed themselves more frequently. Of concern, young adults who weighed themselves more frequently, had a higher BMI, or had eating disorder symptoms were also more likely to report that weighing themselves impacted their mood. These results suggest that for many young adults, weighing themselves has emotional consequences which could have further downstream health consequences such as engagement in disordered eating.
Background
Frequent self-weighing is often recommended in the context of weight management under the premise that self-weighing will increase awareness of how one’s behaviors affect weight, leading to behavior change, and ultimately to weight maintenance or loss [1,2,3]. However, there is a growing body of evidence suggesting that self-weighing may not always be helpful for weight maintenance and may actually be associated with harmful consequences. For example, longitudinal studies have found that adolescents and young adults who self-weighed more frequently at baseline experienced more weight gain over time [4, 5]. Further, longitudinal and experimental studies among adolescents and young adults have also found frequent self-weighing to be associated with decreased self-esteem, and increased anxiety and depression [6, 7]. Cross-sectional and longitudinal studies have also found that more frequent self-weighing is associated with increased likelihood of using unhealthy weight control behaviors [4, 5, 7,8,9]. Unhealthy weight control behaviors are of particular public health and clinical concern given associations between unhealthy weight control behaviors and numerous negative health consequences including the development of clinically significant eating disorders [10, 11], increased weight gain over time [12], and substance abuse [13, 14]. Because frequent self-weighing is a risk factor for unhealthy weight control behaviors, understanding who is engaging in frequent self-weighing is critical to developing relevant prevention strategies.
One mechanism by which self-weighing is thought to lead to unhealthy weight control behaviors is through self-weighing’s effect on mood. While self-weighing may be useful as a tool in weight regulation if it is received by the person as information, it may be harmful if the information leads to changes in mood, whether positively or negatively. Namely, mood changes due to self-weighing likely serve as a mediator between self-weighing and unhealthy weight control behaviors [7], as it is well established that both positive and negative or variable psychological states, including mood, are precursors to unhealthy weight control behaviors [11, 15,16,17]. Therefore, to understand for whom self-weighing may be most harmful, it is important to understand for whom self-weighing affects mood. Individuals more likely to be concerned with shape and weight (e.g. females, those of higher body mass index (BMI), those having experienced an eating disorder) may be at heightened risk for self-weighing impacting their mood, though little work has been done to examine these relationships [18, 19]. Understanding for whom self-weighing elicits an emotional response is an important first step in disentangling the complex cyclical relationships between thoughts, mood, behaviors, and weight [20].
It is also likely that the relationships between self-weighing and mood differ between males and females due to differences in societal pressure regarding weight. Among females, there is greater societal pressure to be thin and an increased likelihood of internalizing the thin ideal [21, 22], while among males there is a desire for leanness and simultaneous desire for increased muscularity [23]. The pressure for females to be lower weight specifically may result in females being less likely to view self-weighing objectively. Ultimately, less objectivity about weight may lead to females being more likely to have changes in mood due to self-weighing. Mintz et al. found that in a sample of female college students, approximately 70% weighed themselves and more than half reported that seeing the number on the scale impacted their mood [24]. However, because this sample was exclusively female college students, and was predominantly white, results may not hold true in the general population. Understanding who may be self-weighing and the factors that make an individual more likely to have their mood impacted by the practice of self-weighing will help inform future research to elucidate these relationships, as well as future public health and clinical recommendations regarding self-weighing.
The current study therefore aims to: 1) identify correlates of weighing frequency in a large population-based sample of young adult males and females; 2) determine whether self-weighing frequency is associated with reporting mood changes due to self-weighing among young adult males and females; and 3) examine whether certain eating and weight-related characteristics (lifetime eating disorder diagnosis history, weight management goals, engagement in disordered eating behaviors and cognitions, and BMI percentile) are associated with differing likelihood of mood changes due to self-weighing among young adult males and females.
Methods
Sample characteristics
Data for this cross-sectional analysis were collected as part of Project EAT (Eating and Activity in Teens and Young Adults)-IV, the fourth wave of a population-based study designed to examine dietary intake, physical activity, weight management behaviors, weight status, and associated factors in young adults. At the original assessment (1998–1999), a total of 4746 middle and senior high school students at 31 public schools in the Minneapolis-St. Paul metropolitan area of Minnesota completed surveys and anthropometric measures [25, 26]. Fifteen years later (2015–2016), original participants who had responded to at least one previous follow-up survey and could be contacted by mail (n = 2770) were mailed letters inviting them to complete the Project EAT-IV survey and a food frequency questionnaire. The selection of survey items for Project EAT-IV was guided by previous Project EAT surveys, formative focus groups with young adults, social cognitive theory and a life course perspective [27]. Scale psychometric properties were examined in the full EAT-IV survey sample and estimates of item test-retest reliability, reported below, were determined in a subgroup of 103 participants who completed the EAT-IV survey twice within a period of 1 to 4 weeks.
Complete EAT-IV survey data were collected online, by mail or by phone from 66.1% of those for whom correct contact information was available (n = 1830). Participants were excluded from the present analyses if they had missing data necessary to answer the stated research question for the present study. Specifically, participants were excluded from the current analysis if they were pregnant (n = 84), missing BMI measurement (n = 20) or missing responses to self-weighing measures including frequency of self-weighing or of self-weighing’s impact on mood (n = 7) for a final analytic sample of 1719 with a mean age of 31.0 years (SD = 1.6, range: 25–36). Individuals who were pregnant were excluded because we believed the relationships may differ based on pregnancy status [28]. Because attrition from the original school-based sample did not occur at random, in all analyses, the data were weighted using the response propensity method [29]. Response propensities (i.e., the probability of responding to the EAT-IV survey) were estimated using a logistic regression of response at 15-year follow-up on many predictor variables from the EAT-I baseline survey. The weighting method resulted in estimates representative of the demographic make-up of the original school-based sample, thereby allowing results to be more fully generalizable to the population who were middle- and high school students in the Minneapolis-St. Paul metropolitan area in 1998–1999. All study protocols were approved by the University of Minnesota’s Institutional Review Board Human Subjects Committee.
Self-weighing measures
Frequency of Self-Weighing was measured with the question: “How often do you weigh yourself?” (test-retest correlation: r = 0.91). This item had seven response options ranging from “less than once a month” to “more than once a day”. This question was adapted based on feedback received during a previous pilot study to include more response options examining the nuanced of more frequent self-weighing [30]. Self-weighing frequency was modeled as a 6-level categorical variable, with individuals who responded, “more than once a day” collapsed into the “every day” category, due to relatively small sizes in these categories.
Mood Changes Due to Self-Weighing was measured on a 4-level Likert scale anchored by “strongly disagree” and “strongly agree” with the statement: “When I weigh myself, the number I see on the scale impacts my mood” (test-retest correlation: r = 0.75). For these analyses, this variable was dichotomized to respondents who “agreed” or “strongly agreed” compared to respondents who “disagreed” or “strongly disagreed”, representing those who report experiencing mood changes due to self-weighing compared to those who do not.
Measures of other eating and weight-related characteristics
BMI percentile
Self-reported height (test-retest correlation: r = 0.98) and weight (test-retest correlation: r = 0.97) were used to calculate BMI. Height and weight measurements were also completed for a subsample as part of the third study wave and very high correlations with self-reported BMI were observed among both males (r = 0.95) and females (r = 0.98) [31, 32]. The following age and sex-specific BMI percentile cut-points were used: BMI < 15th percentile, 15th percentile ≤ BMI ≤ 85th percentile, BMI > 85th percentile. These cut-points were selected based on the work from Must, et al. [33].
Eating Disorder Diagnosis
Eating disorder diagnosis was measured with the question: “Do you currently or have you ever had an eating disorder?” (test-retest percent concordant: 98%). This item had three response options: “Yes, currently”, “Yes, recovered”, and “No, never”, and was modeled as a categorical exposure in regression models.
Weight Management Goal
Weight Management Goal was measured from participants’ response to the prompt, “Are you currently trying to: 1) lose weight, 2) stay the same weight, 3) gain weight, or 4) I am not trying to do anything about my weight” (test-retest percent concordant: 82%). Weight management goal was modeled as a categorical exposure in regression models, with “not trying to do anything about my weight” used as the reference category.
Fear of weight gain
Respondents who indicated they “strongly agree” with the statement: “I am worried about gaining weight” (test-retest correlation: r = 0.62) were categorized as having a fear of weight gain and all others were categorized as not being worried about gaining weight.
Weight/shape overvaluation
Respondents were categorized as having weight/shape overvaluation if they responded that either weight and shape were: “among the main things that affected how I felt about myself” or “were the most important things that affected how I felt about myself” to the prompt, “During the past six months, how important has your weight or shape been in how you feel about yourself?” (test-retest correlation: r = 0.71), or if the respondent was classified as low-weight or normal-weight but reported that they feel that they are: “somewhat overweight” or “very overweight” (test-retest correlation: r = 0.67). Questions were modeled after previously validated measures, and previous work in this population showing weight/shape concern to be important in the development of disordered eating behaviors [34, 35].
Binge eating
Respondents were categorized as engaging in binge eating if they responded “yes” to both of the following questions: “In the past year, have you ever eaten so much food in a short period of time that you would be embarrassed if others saw you? (binge eating)” (test-retest percent concordant: 90%) and “During the times when you ate this way, did you feel you couldn’t stop eating or control what or how much you were eating?” (test-retest percent concordant: 78%) [34].
Compensatory Behavior
Respondents who indicated that they “used laxatives” (test-retest percent concordant: 97%) or “made myself vomit” (test-retest percent concordant: 98%) to the prompt, “Have you done any of the following things in order to lose weight or keep from gaining weigh during the past year?” were classified as having engaged in compensatory behaviors [25, 36].
Sociodemographic characteristics
All covariates were assessed using self-reported measures. One question asked, “Are you…?” With responses of “Male” or “Female”. Age was calculated by subtracting the participants’ birthdays from date of survey completion. Participants were asked to identify their ethnic/racial background as any combination of: “White”, “Black or African American”, “Hispanic or Latino”, “Asian American”, “Native Hawaiian or Pacific Islander”, and/or “American Indian or Native American”, and categorized as follows: “White”, “African American”, “Hispanic”, “Asian”, and “Mixed or Other”. Education level ranged from “Middle school or junior high” to “Graduate or professional degree.” Total past-year pre-tax income was reported on a scale from “Less than $20,000” to “$100,000 or more”. It is important to assess both ethnicity/race and socio-economic status (as measured by education level and income) given the possibility that individuals from diverse ethnic/racial and low socio-economic backgrounds may be more likely to experience adverse health consequences due in part to racism and social inequities.
Statistical analyses
Based on expected differences in self-weighing related behavior and mood, it was determined a priori that all statistical analyses would be run separately for males and females [9]. Demographic characteristics and frequencies of each self-weighing variable and of the other eating and weight-related variables were compared between sexes using chi-square and t-tests. Associations between self-weighing frequency and the other eating and weight-related variables were modeled using linear regression. Self-weighing frequency was modeled as a square-root transformed continuous variable because this variable was heavily right skewed. Least square means and their 95% confidence intervals for self-weighing frequency by levels of the predictor variable were calculated from the models on the square-root scale and squared to convert them back to the weekly frequency scale.
Logistic regressions were used to test whether mood change due to self-weighing was associated with self-weighing frequency or the other eating and weight-related variables. Because a large proportion of participants reported changes in mood due to self-weighing (41%), the regression coefficients from the logistic model were used to generate estimated probabilities of reporting mood changes due to self-weighing [37, 38]. The linear and logistic regression models were adjusted for age, ethnic/racial categories, educational attainment, income, and BMI percentile. Statistical analyses were conducted using SAS version 9.4.
Results
Sample characteristics and prevalence of self-weighing and other eating and weight-related characteristics
Among this population-based sample of young adults (Table 1), self-weighing and changes in mood due to self-weighing were highly prevalent (Table 2). Over one third of female young adults (34.5%) and one quarter of male young adults (26.8%) reported weighing themselves at least once per week, 22.5% of female young adults and 17.0% of male young adults weighing themselves more than once per week, and 7.9% of female young adults and 7.0% of male young adults weigh once per day or more. Moreover, over half of female young adults (53.0%) and one quarter of male young adults (26.5%) reported mood changes due to self-weighing. Female young adults were significantly more likely than male young adults to report self-weighing once a month or more, mood changes due to self-weighing, current or past eating disorder diagnosis, trying to manage their weight, fear weight gain, weight/shape overvaluation, and use of binge eating and compensatory behaviors.
Table 1 Sociodemographic characteristics of sample statistics (n = 1719)
Table 2 Prevalence of self-weighing and other eating and weight-related characteristics
Correlations between eating and weight-related characteristics and frequency of self-weighing
Both female and male young adults who reported currently having an eating disorder weighed themselves more frequently than others, in analyses adjusted for sociodemographic characteristics and BMI (Table 3). Female young adults with a current eating disorder had a predicted average of weighing themselves 1.75 times per week (95% confidence interval (CI): 1.00, 2.69) as compared to 0.64 times per week (95% CI: 0.56, 0.71) for female young adults who never had an eating disorder, after adjusting for covariates. Female young adults with a BMI at or above the 85th percentile had a significantly higher predicted self-weighing frequency (0.79 times per week, 95% CI: 0.66, 0.93) compared to female young adults whose BMI was below the 15th percentile (0.35 times per week, 95% CI: 0.16, 0.60), though no other pairwise comparisons were statistically significant. We found no associations between BMI percentile category and predicted self-weighing frequency among male young adults. Among female young adults, predicted average weekly weighing frequency was higher among those who were trying to lose weight (0.85 times per week, 95% CI: 0.76, 0.96) and those trying to stay the same weight (0.56 times per week, 95% CI: 0.41, 0.73) compared to those not trying to do anything about their weight (0.23 times per week, 95% CI: 0.14, 0.35). Among male young adults, predicted average weekly weighing frequency was higher among those trying to lose weight (0.93 times per week, 95% CI: 0.80, 1.07) or gain weight (0.72 times per week, 95% CI: 0.46, 1.04) compared to those not trying to do anything about their weight (0.26 times per week, 95 CI: 0.18, 0.35). Both male and female young adults who reported any disordered eating behaviors or related cognitions (i.e., binge eating, compensatory behavior, fear of weight gain, or weight/shape overvaluation) had higher predicted self-weighing frequency as compared to those who did not report having the respective disordered eating cognitions or behaviors. For example, male young adults who used compensatory behaviors weighed themselves an average of 1.31 times per week (95% CI: 0.74, 2.05) compared to an average of 0.56 times per week (95% CI: 0.49, 0.63) among male young adults who did not report use of compensatory behaviors.
Table 3 Predicted average weekly self-weighing frequency by eating and weight-related characteristics (adjusted for BMI, age, ethnicity/race, sex, education and income)a
Associations between self-weighing frequency and mood changes due to self-weighing
Among females, more frequent self-weighing was consistently associated with increased likelihood of mood changes due to self-weighing (Table 4). Notably, 69% of females who weighed themselves a few times per week reported their mood was impacted by self-weighing (95% CI: 60%, 77%), as compared to 39% for females who weighed themselves less than once a month (95% CI: 34, 45%) after adjusting for covariates. Among males, a similar pattern was seen with males weighing themselves at least daily (probability = 47%, 95% CI: 35, 59%), a few times per week (probability = 34%, 95% CI: 25, 43%), and a few times per month (probability = 36%, 95% CI: 28%, 44%) being more likely to report self-weighing impacting mood compared to those who weighed less than once a month (probability = 20%, 95% CI: 16%, 24%) after adjusting for covariates.
Table 4 Predicted probability of mood changes due to self-weighing within levels of frequency of self-weighing, and other eating and weight-related characteristics (adjusted for BMI, age, ethnicity/race, educational attainment, and income)
Associations between other eating and weight-related characteristics and mood changes due to self-weighing
Males and females with a BMI at or above the 85th percentile were significantly more likely to have mood changes due to self-weighing compared to those with a BMI below the 85th percentile. Females in recovery from an eating disorder were also more likely to have mood changes due to self-weighing (Probability = 68%, 95% CI: 57%, 78%) compared to those with a current eating disorder (Probability = 59%, 95% CI: 33%, 80%) or who have never had an eating disorder (Probability = 50%, 95% CI: 46%, 54%). Among males, there were no associations between eating disorder diagnosis and mood changes due to self-weighing. Both males and females who were trying to lose weight, feared weight gain, had weight/shape overvaluation, or had binge eaten or used a compensatory behavior, were more likely to indicate mood changes due to self-weighing as compared to those who did not endorse the respective eating disorder behavior or cognition.
Discussion
This study examined the correlates of self-weighing frequency, and whether self-weighing frequency or other eating and weight-related measures (such as eating disorder diagnosis, BMI, weight management goals, and disordered eating behaviors and cognitions) are associated with mood changes due to self-weighing in a population-based sample of young adults. Self-weighing and reporting mood changes due to self-weighing were common among males and females, with over half of females and one quarter of males reported that their mood changed due to self-weighing. Male and female young adults with a current eating disorder diagnosis, those trying to lose weight, and those who reported disordered eating behaviors or cognitions weighed themselves more frequently than their counterparts, as did female young adults with higher BMI values. More frequent self-weighing was associated with increased likelihood of self-weighing affecting mood, particularly for females. Changes in mood due to self-weighing were more likely among those with a BMI above the 85th percentile, those trying to lose weight, or among those who reported any disordered eating behaviors or cognitions. Overall, these findings show that self-weighing is common, and that self-weighing affects mood for a large proportion of young adults, particularly those who are more likely to be weight-concerned.
Similar to prior work, we found self-weighing to be more frequent among those with eating disorders [39] and those with higher BMI [9, 40]. It is important to consider that there is likely overlap between these two groups, given that individuals with a higher BMI are more likely to have an eating disorder compared to individuals of lower BMI in population-based samples [41, 42]. Prior research has shown that mood changes due to self-weighing were common among a sample of predominantly Caucasian college females [24]. The present findings expand upon this research using a more socioeconomically and racially/ethnically diverse and older sample of young adults, corroborating a remarkably similar prevalence of mood changes due to self-weighing among females (53% in both population-based studies) [24]. Our results also demonstrate that a substantial proportion of males experience mood changes due to self-weighing, though a smaller proportion than females. The considerable prevalence of mood changes due to self-weighing among both males and females may be due in part to the prominence of appearance-based ideals for both males and females. However, self-weighing may be more likely to have an emotional impact on females because the ideal appearance for females is weight-centric, focusing on thinness, whereas the male appearance-ideal incorporates an increased desire for both muscularity and leanness, making weight less of a salient marker for body ideals among men [23, 43, 44]. Therefore, the number on the scale when self-weighing may be more indicative to appearance expectations for females rather than males, thereby causing weight to have more emotional valence for females.
Our results provide evidence that self-weighing may be most likely to cause mood changes for those with weight concerns. Females in recovery from an eating disorder were more likely to have mood changes due to self-weighing compared to those with no eating disorder history. Because both negative and positive emotions are a precursor for disordered eating [16, 45], our findings suggest that self-weighing may be particularly harmful for females working on recovery. Additionally, males and females with a higher BMI or who were trying to lose weight were more likely to report mood changes due to self-weighing. Current recommendations for weight loss among those with higher BMIs often include self-weighing [1]. While prior results suggest that mood may positively change if weight is lost [46], studies have found that self-weighing in the general public may actually contribute to weight gain [4, 5], thereby causing a negative change in mood. However, any direction of mood change may be construed as problematic, as the ability for the number on the scale to affect mood, irrespective of the direction, implies that there is a lack of objectivity to weight and that a sense of worth or identity is tied to weight for individuals whose mood is impacted. If the individual’s weight or direction of weight change is not in line with one’s ideals or goals, there may be a deterioration in mood and alternatively, an alignment between weight change and goals may lead to an improvement in mood. Because weight is highly variable short-term, body ideals are often unattainable and socially constructed, and long-term weight management is often unsuccessful, it stands to reason that having any emotional attachment to weight could be problematic long-term [47,48,49]. While counterintuitive, short-term positive changes in mood brought on by changes in weight could also be problematic. For example, in those with eating disorders who engaged in disordered eating and subsequently lost weight, their weight loss may lead to a positive change in mood, encouraging them to continue using disordered eating behaviors to pursue further weight loss and positive mood, thereby enforcing disordered eating patterns. Therefore, our results suggest that self-weighing may cause changes in mood in the populations for those who have weight concerns and those for whom self-weighing is often recommended: individuals with higher BMIs, and those trying to lose weight. Examining the types of mood changes in response to the scale in conjunction with expectancies and goals for weight, is an exciting direction for future research, as is examining the downstream consequences of mood changes due to self-weighing.
The community sample of young adults adds to the limited research on the potential consequences of self-weighing and for whom specifically frequent self-weighing may be problematic by causing changes in mood. Additionally, the large sample size allowed us to stratify analyses by sex, adding to the scant literature around self-weighing in males. However, this research is not without limitations, including the cross-sectional nature of the analysis, which does not allow for the determination of temporality of time-varying characteristics. Although Project EAT is a longitudinal study, mood changes due to self-weighing were only assessed in EAT-IV and thus we could not assess temporality of mood changes relative to the measures of eating and weight-related characteristics. Cognitive Behavioral theory has identified the reciprocal relationship between thoughts, mood and behaviors (e.g. eating behaviors, self-weighing behaviors) [20]. Due to research design, this study is not able to test the sequence or reciprocity of events but provides an important first step in understanding the complex relationships. Future research using ecological momentary assessment and randomized designs can better address the sequence of thoughts, mood, and behaviors, such as self-weighing. Additionally, our single item measure assessing the dichotomous impact of self-weighing on mood does not allow us to distinguish whether self-weighing negatively or positively impacts mood and if directionality of mood change differs across sub-populations, which is a promising direction for future research. There also may be heterogeneity in likelihood of weighing affecting mood among those that infrequently weigh, as there is likely a proportion of individuals who do not self-weigh as a form of body avoidance [50]. Items assessing weight/shape overvaluation and fear of weight gain were assessed using single item measures which may not fully capture these constructs; further research should examine the relationships between weight and shape overvaluation, fear of weight gain, and likelihood of self-weighing impacting mood, using more comprehensive scales. Due to stratification and sample size, we were also unable to examine gender minorities, which also warrants future examination. Future research should examine temporal relationships between self-weighing, mood, and behavior in young adults using longitudinal data at different time intervals (within a day, within a week, within a month, etc.), including ecological momentary assessment.
Conclusions
In a society where quantifying and tracking weight and weight-related behaviors is highly prevalent and likely increasing, it is important to identify potential consequences of weight-related self-monitoring [51,52,53]. In particular for self-weighing, individuals who are more likely to be concerned with their weight are more likely to weigh themselves frequently and are also more likely to be emotionally affected by self-weighing. While self-weighing is often promoted for weight management, and may be useful for those who can receive this information without emotional attachment, self-weighing may be harmful for a significant portion of the general young adult population and particularly those who have weight concerns, such as those with higher BMIs. Therefore, it is imperative to consider the potential negative emotional implications of self-weighing when considering future public health and clinical recommendations regarding self-weighing.
Availability of data and materials
Please contact the Principal Investigator, Dr. Dianne Neumark-Sztainer if interested in using Project EAT data.
Abbreviations
BMI:
Body mass index
EAT:
Eating and Activity in Teens and Young Adults
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Acknowledgements
Not applicable.
Funding
Data collection for the study was supported by Grant Number R01HL116892 from the National Heart, Lung, and Blood Institute (PI: Dianne Neumark-Sztainer). Additionally, the authors’ time to conduct the research and write this manuscript was supported by Grant Numbers: R35HL139853 from the National Heart, Lung, and Blood Institute (PI: Dianne Neumark-Sztainer), T32MH082761 from the National Institute of Mental Health (PI: Scott Crow), T32DK083250 from the National Institute of Diabetes and Digestive and Kidney Diseases (PI: Robert Jeffery), T32CA163184 from the National Cancer Institute (PI: Michele Allen), and K23HD090324–02 from the National Institute of Child Health and Human Development (PI: Katie Loth). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute, the National Institute of Mental Health, the National Institute of Diabetes and Digestive and Kidney Diseases, the National Cancer Institute, the National Institute of Child Health and Human Development, or the National Institutes of Health.
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SLH was the main writer of the paper, assisted with data interpretation, and gave final approval of this version to be published. CRP conceptualized the paper, wrote the initial draft of the paper, critically reviewed the paper, and gave final approval of this version to be published. KAL assisted in contextualizing the paper within the literature, critically reviewed the paper, and gave final approval of this version to be published. JM conducted the data analysis, critically reviewed the paper, and gave final approval of this version to be published. MEE assisted with conceptualization of the paper, critically reviewed the paper, and gave final approval of this version to be published. DNS is the principal investigator of the study, assisted in conceptualizing the paper and contributed to the design of the study. She also critically reviewed the paper, gave final approval of this version to be published,
Corresponding author
Correspondence to Samantha L. Hahn.
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Hahn, S.L., Pacanowski, C.R., Loth, K.A. et al. Self-weighing among young adults: who weighs themselves and for whom does weighing affect mood? A cross-sectional study of a population-based sample. J Eat Disord 9, 37 (2021). https://doi.org/10.1186/s40337-021-00391-y
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Keywords
• Self-weighing
• Self-monitoring
• Mood
• Young adults
• Weight management
• Eating disorders | {
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3,853,268,548,391,299,600 | Effect of dipeptidyl peptidase-4 inhibitors on plasma adiponectin: A systematic review and meta-analysis of randomized controlled trials
Amirhossein Sahebkar, V. Ponzo, S. Bo
Research output: Contribution to journalReview article
13 Citations (Scopus)
Abstract
© 2016 Bentham Science Publishers.Background/Objectives: The effect of dipeptidyl peptidase-4 (DPP-4) inhibitors on plasma concentrations of adiponectin, a fat-derived hormone with anti-atherogenic and anti-inflammatory properties, is uncertain. A systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to investigate this association in humans. Methods: RCTs investigating the impact of DPP-4 inhibitors on plasma adiponectin concentrations were identified after searching PubMed-Medline, SCOPUS, and Google Scholar databases (up to February 2015). As quantitative data synthesis methods, the random-effects model and the generic inverse variance method were applied. Standard methods of meta-regression, sensitivity analysis, and publication bias assessments were performed. Results: Eight RCTs with nine treatment-arms were included. Meta-analysis did not suggest a significant pooled effect of DDP-4 inhibitors on adiponectin values (weighed-mean-difference [WMD]: 0.19 μg/mL, 95%CI: -0.50, 0.88). However, a significant elevation of plasma adiponectin concentrations was observed in the subset of trials with vildagliptin (WMD: 0.55 μg/mL, 95%CI: 0.13, 0.98, p=0.010) but not sitagliptin (WMD: -0.06 μg/mL, 95%CI: -1.13, 1.00, p=0.907). There was a significant elevation of plasma adiponectin levels in the subset of trials comparing DPP-4 inhibitors versus placebo or no treatment (WMD: 0.74 μg/mL, 95%CI: 0.36, 1.12, p
Original languageEnglish
Pages (from-to)1356-1369
Number of pages14
JournalCurrent Medicinal Chemistry
Volume23
Issue number13
Publication statusPublished - 2016
Fingerprint Dive into the research topics of 'Effect of dipeptidyl peptidase-4 inhibitors on plasma adiponectin: A systematic review and meta-analysis of randomized controlled trials'. Together they form a unique fingerprint.
Cite this | {
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-2,172,812,451,262,764,800 | Skip to content
Sources of Vitamin B5: Unlocking the Power of this Essential Nutrient
Vitamin B5, also known as pantothenic acid, is an essential nutrient required for various bodily functions, including energy metabolism and organ function. In this article, we will be discussing the different sources of vitamin B5 and how they can be incorporated into one’s diet. Whether you are looking to maintain good overall health or alleviate specific health concerns, understanding the sources of vitamin B5 can help you make informed decisions about your diet and nutrition.
Understanding Vitamin B5
Vitamin B5, also known as pantothenic acid, is one of the essential B-complex vitamins. This water-soluble vitamin plays a vital role in energy metabolism, brain function, and the production of hormones and cholesterol. It is also essential for the proper functioning of the nervous system and aids in the synthesis of fatty acids.
Pantothenic acid is found in a wide range of foods, making it easy to incorporate into your diet. However, many people are not aware of the best sources of this essential nutrient. In this article, we will explore the top sources of vitamin B5 and how you can incorporate them into your diet.
Misconceptions About Vitamin B5
Before we dive into the sources of vitamin B5, it’s important to address some misconceptions about this essential nutrient. One of the most common misconceptions is that vitamin B5 is only found in animal products. While it’s true that animal products are a good source of vitamin B5, there are also plenty of plant-based sources.
Another misconception is that vitamin B5 supplements are necessary to meet your daily needs. While supplements can be helpful for those who have a deficiency, it’s best to get your vitamins from whole foods whenever possible.
See also How Essential Nutrients Improve Cognitive Function
Top Sources of Vitamin B5
1. Mushrooms
Mushrooms are an excellent source of vitamin B5, containing about 2.5 mg per cup. They are also low in calories and high in fiber, making them a great addition to any diet. Shiitake mushrooms are particularly high in vitamin B5, with over 5 mg per cup.
2. Avocado
Avocado is a nutrient-dense fruit that is rich in healthy fats, fiber, and a variety of vitamins and minerals. It is also a good source of vitamin B5, with one medium avocado containing around 2 mg.
3. Sweet Potatoes
Sweet potatoes are an excellent source of many vitamins and minerals, including vitamin B5. One medium sweet potato contains around 1 mg of vitamin B5.
4. Legumes
Legumes, such as lentils, chickpeas, and peas, are a great source of protein, fiber, and various vitamins and minerals, including vitamin B5. One cup of cooked lentils contains around 1 mg of vitamin B5.
5. Sunflower Seeds
Sunflower seeds are a delicious and nutritious snack that is rich in healthy fats, protein, and various vitamins and minerals, including vitamin B5. One ounce of roasted sunflower seeds contains around 1 mg of vitamin B5.
Incorporating Vitamin B5 into Your Diet
Now that we’ve covered the top sources of vitamin B5, let’s explore some ways to incorporate them into your diet. One of the easiest ways is to add mushrooms to your meals. They are versatile and can be added to soups, stir-fries, and salads.
Sweet potatoes are also easy to incorporate into your diet. You can roast them, mash them, or use them as a base for a healthy sweet potato bowl.
See also What is the Role of Magnesium in the Body?
Legumes are a great addition to salads, soups, and stews. They can also be used to make delicious dips, such as hummus.
Lastly, sunflower seeds make a great addition to oatmeal, yogurt, or smoothie bowls. You can also use them to add crunch to salads or roasted vegetables.
The Bottom Line
Vitamin B5 is an essential nutrient that plays a vital role in many bodily functions. While it’s easy to meet your daily needs through a healthy and balanced diet, many people are not aware of the best sources of this essential nutrient. By incorporating the top sources of vitamin B5 into your diet, you can ensure that you are getting all the benefits of this essential nutrient and supporting optimal health and well-being.
FAQs: Sources of Vitamin B5
What is vitamin B5?
Vitamin B5, also known as pantothenic acid, is a water-soluble vitamin that is part of the B vitamin family. It is essential for many bodily processes, including the production of energy, the metabolism of fats and carbohydrates, and the synthesis of hormones and cholesterol.
Why is vitamin B5 important?
Vitamin B5 plays a crucial role in keeping the body healthy and functioning properly. It supports the immune system, promotes healthy skin, and helps to regulate blood sugar levels. It is also essential for the proper functioning of the nervous system, and can help reduce stress and anxiety.
What are some food sources of vitamin B5?
There are many food sources of vitamin B5, including meat, fish, poultry, eggs, dairy products, and whole grains. Some of the best dietary sources of vitamin B5 include sunflower seeds, mushrooms, avocado, lentils, sweet potatoes, and broccoli.
See also Vitamin D Supplements for Bone Health
Can you get enough vitamin B5 from your diet alone?
Most people can get enough vitamin B5 from a balanced diet that includes a variety of foods. However, individuals who have a restricted or limited diet, such as vegans or vegetarians, may need to consider taking a vitamin B5 supplement to ensure they are getting enough of this important nutrient.
What are some signs of vitamin B5 deficiency?
A deficiency in vitamin B5 is rare but can lead to a number of health problems. Some signs of vitamin B5 deficiency include fatigue, muscle weakness, digestive problems, and numbness or tingling in the hands and feet. In severe cases, it can also lead to more serious health problems like anemia or nerve damage.
Are there any risks associated with taking vitamin B5 supplements?
Vitamin B5 is generally considered safe, and there are no known risks associated with taking vitamin B5 supplements. However, like with any supplement, it is important to speak with your healthcare provider before starting a new regimen, especially if you are currently taking any medications or have any underlying health conditions.
Leave a Reply
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-1,502,206,055,890,113,500 | Discover The Healing Power Of Turmeric
Turmeric is a member of the ginger family, derived from an asian plant called Curcuma longa. It has been used for thousands of years as a spice in food, dyes and in Ayurvedic (ancient Indian) and Chinese medicinal traditions. The medicinal properties and health benefits of the spice are attributed to: antioxidant, anti-inflammatory, anti-dyspepsia, anti-platelets, anti-viral, antifungal and antibacterial effects. It can be used for arthritis, psoriasis and other skin conditions. Chinese medicine has been using it for years, studies have shown it inhibits tumor cell growth and transformation of normal cells into cancer cells. Turmeric can even be used to prevent and slow the progression of Alzheimer’s disease. Usage of Turmeric dates back to ancient Greek where physician Dioscorides used it to stimulate appetite and cure indigestion. In India, Turmeric is one of the main ingredients for their cuisine, we can see why it is considered a valuable substance and was called the ”Indian saffron” in the middle ages.
Its significant effects on major diseases amazed scientists. With more than 4300 articles cited by PubMed on the subject of the different clinical uses of plant, curcumin or the Turmeric spice. This includes 1604 studies on cancer, 181 on Alzheimer’s, 151 on diabetes. Studies among the elderly populations in India, who consume Turmeric regularly, indicate low rate of occurrence of Alzheimer’s disease. In Alzheimer’s, Turmeric extract breaks up sticky polymers that usually fail to repair brain cells and their synapses. In the alleviation of arthritis, curcumin significantly inhibited inflammation of the joints and its destruction, thus it relieves pains experienced by patients. Its anticancer activities result to the death of various cancer cells in the skin, lower gastrointestinal tract and ovaries in laboratory trials. Another surprising health benefit is that those who regularly consumed Turmeric in food performed significantly better in examination than those who consumed it less frequently.
Curcumin, the active component in Turmeric, is extracted by first boiling the curcumin plant’s root and then dried and ground into a powder. Curcumin is then extracted by using a solvent and then, the solution is dried to recover the active component in powder form. Different extractions would result into Turmeric extracts of varying purity – tests conclude that the best concentration to achieve the clinical results against diseases is standardized at 95%.
While Turmeric can certainly be made part of one’s diet, some people might be put off by its bitter taste especially those who are not used to it. To make it easier for people to experience the health benefits brought by Turmeric extract consumption, laboratories have extracted and purified Turmeric into pills or capsules which would most probably have different concentrations of ingredients. When choosing Turmeric extract, it is strongly advised to choose one with curcumin that is standardized at 95%, the concentration where it would have the most effective antioxidant and anti-inflammatory activity.
To learn more Turmeric benefits, exactly how to properly use it for every situation, and all the tips and tricks for the fastest possible results, we highly recommend this fantastic eBook for all the effects and uses of turmeric: “Secrets of Turmeric”
Click here for Organifi Daily Turmeric Boost (Veggie Caps)
The Alkaline Diet can help with weight loss, physical energy and get your pH level to where it should be in order to help your body become more energized and resistant to sickness and disease. If you are always feeling tired or you just do not have the energy that you need to perform daily functions, the Alkaline Diet can help! The acid alkaline food chart is a very useful tool that can help you identify the healthy foods that can help improve your overall diet and get you on your way to enjoying a healthier and well balanced lifestyle.
Read previous post:
A Guide To Achieving Body Balance
Achieving balance in life is very important if you want to remain healthy and happy.
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-6,535,748,823,167,531,000 | Suitable for slimming your shape
Scientists have discovered that every woman belongs to a specific group of body shape (or silhouette). Of course this does not mean that we are all the same, but understanding the specific group of body shape we belong to is important for our lifestyle choices so we can improve certain aspects of our form and hide others.
Finding your ideal weight is not easy. And we turn to various diets in order to lose weight but, often, instead of losing weight, we end up gaining more weight. Not all diets are suitable for all women. To differentiate them we need to be aware of our metabolic structure and constitution. Here is a classification of the main types of female bodies with suggestions for when needed to lose weight
PEAR shaped
In the case of a pear shaped silhouette fat stores itself primarily on the outer side of the buttocks, hips and thighs. The upper body appears less pronounced than the lower one. Women who belong to this body shape take in weight more slowly than other shapes, but do this progressively.
APPLE shaped
In the case of the Apple shaped body the accumulation of fat is located primarily above the waist, stomach and chest, all this giving the body a stockylook. This silhouette is likea little harmonica because the upper part of the figure is wider than the lower one. Metabolism is slow enough, so your body burns calories more slowly. For this body shape we recommend complex carbohydrates and aerobic exercise.
Hourglass figure
In the case of the hourglass figure your upper body is proportionally relative in keeping with the lower one and the waistline remains proportionate and thin. Women with this silhouette are considered lucky in that they naturally have a harmonic body and even when gaining a few pounds this harmony won't disappear immediately. Although the hourglass can silhouette, can easily move into the danger zone, with an excessive diet and lack of exercise.
Rectangle shape
In the case of the rectangle shape your legs and arms are long, oval face and thin bones. Women who have this constitution tend to distribute excess fat evenly throughout the body, the waistline is always visible and the thighs remain relatively thin. Although women with this silhouette usually have a good metabolic, hormonal balance they too may gain weight as a result of an imbalanced diet.
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6,328,567,116,787,982,000 | Categories
Hair Loss
How To Diagnose And Treat Hair Loss with Homeopathy?
Who treats hair-related issues, and what is that person called?
Issues caused on skin, nails, and hair like rashes, wrinkles, Androgenic Alopecia, psoriasis, or melanoma to treat these problems A qualified and certified person is needed who can diagnose and treat the issues is known as a dermatologist and skin specialist.
To start diagnosing the causes of hair loss, dermatologists begin by asking questions about your situation, from how long you’ve been having hair loss symptoms. They start with gathering information.
Then they closely look at your scalp and gently pull out a hair which determines how weak your hair is and how easily it breaks out. After all this, dermatologists sometimes suggest tests performed related to the scalp, blood test or scalp biopsy to know more deeply about the condition to start treatment.
Is it possible to get hair to regrow?
Sometimes your hair regrows naturally as well if you recently Had a baby, Recovered from a significant illness or had surgery and Underwent cancer treatment, or Developed a mild case of a disease called alopecia areata, which causes your immune system to attack your hair follicles or naturally Got rid of psoriasis on your scalp then there are changes that your hairs might have a little hair growth.
How lifestyle impacts your hair loss?
Some hairstyles that pull can lead to hair loss, and other hair care products can lead to hair loss habits like not drying up the hair after a hair wash can lead to extreme hair loss if stopped or corrected immediately.
Which treatments are recommended by dermatologists?
If your hair does not regrow naturally and the dermatologist also tells you to have some treatment to start the hair growth, then they might suggest you some of these treatments:
Treatment for hair regrowth
Minoxidil is one of the most common medicines a dermatologist can suggest to an individual facing early hair loss. It helps in Stimulating hair growth and Prevents further hair loss. Minoxidil must be more effective when used along with some other treatment for hair loss as it is a result-oriented product. Use it according to the precipitation of your dermatologist.
Medical procedure to rejuvenate hair growth?
• Injections were given to the area of the scalp affected by alopecia areata. These injections have corticosteroids which help hair to regrow within 12 weeks. And individuals who have these injections have seen results in their hair regrowth.
• In the condition of extreme hair loss, a hair transplant is a solution for baldness in women and men as it is an easy and permanent solution for hair loss.
• If medications are not working, then you can consider low-level laser therapy, as it corrects the condition of Hereditary hair loss, Alopecia areata, and Hair loss due to chemotherapy and Also helps in Stimulating and healing scalp and hair growth after a hair transplant.
• Injecting plasma into the areas affected by baldness can help in rejuvenating the follicles, which helps in hair regrow after Follicular unit extraction (FUE) helps to grow the hair faster and more effectively.
How do vitamins, minerals, and other supplements promote hair growth?
Insufficient diet also promotes hair loss. Biotin, iron, or zinc are essential vitamins needed for healthy hair growth. To meet the need for sufficient minerals, dermatologists suggest protein-rich supplements. Also, recommend taking a multivitamin if supplements are not available.
During the life span, due to many hormonal changes, we sometimes have to go through the condition of hair loss. Some select to consult a dermatologist, and others choose the way of hair transplant. A hair transplant is one of the famous treatments individuals generally opt to deal with extreme hair loss.
A hair transplant is an easy way to get hair to regrow, but with all these factors, the essential element, hair transplant cost , is part of the discussion. After hearing about the hair transplant cost, many people drop their plans for hair transplant surgery. So they prefer going to a dermatologist to get hair to regrow naturally with the help of medications and advice.
Categories
Hair Loss Hair treatment
Is Homeopathy Suitable For Hair Regrowth Or Not?
Hair loss is one of the common hair problems faced by people around the globe. It has even made us not comb our hair out of fear of losing some hair strands. And the occurrence of dandruff aggravates the increase in hair fall and damage. These reasons have led many people to try out new techniques and methods of hair care.
Nowadays, people have even turned to homeopathy to find a cure for hair damage. You can see people flocking to the best Homeopathic Clinic in Mumbai to find a cure. But that brings up a big question, has homeopathy come up with a prescription for hair fall and damage?
Homeopathy, a cure used for ages, has been proven to have found treatment for almost all the diseases of the world. Fortunately, homeopathy has also found something for your hair care. But you should keep in mind that homeopathy works differently for different people. You must consult the best Homeopathic Doctor in Mumbai. Their expertise and knowledge in this field will help you in planning your hair care routine.
Homeopathy has various medicines for hair loss depending upon the cause of its problem. The best homeopathy doctor will assess your hair damage conditions in detail and find out its root cause. Then you will be prescribed a suitable prescription after their detailed assessment. These prescriptions are divided into two parts based on the grounds of hair fall.
Alopecia
Alopecia areata is an autoimmune disorder that mistakes your hair as a foreign object and attacks it, leading to hair fall. Hence here are the medicines for people suffering from this disease:
1. Fluoricum acidum: made out of hydrofluoric acid, this medicine is considered wonderful for hair loss, especially alopecia.
2. Calcarea Carbonica: also known as Calcarea carb, this medicine is prescribed for patients with hair loss, prematurely gray hair, brittle hair, and drying hair.
3. Vinca Minor: This medicine is prescribed for people battling alopecia and prematurely graying hair.
Baldness
Baldness is quite common in men. Although it is unheard of in women, they still end up losing a significant amount of hair in their 50s. There are some homeopathic medicines to combat baldness:
1.Silicea: It undergoes rigorous shaking (potentization) to cure baldness. Apart from that, Silicea is also used to combat eczema.
2.Baryta Carbonica: This medicine is used for patients having premature baldness, hair loss, premature graying, and dryness.
3. Lycopodium Cavatum: prepared from potentized club moss, this medicine tackles premature graying and baldness.
Dandruff
4.Psorinum: This medicine is used to combat dandruff. It reduces both dandruff and hair fall at the same time.
5. Mezereum: Made out of common salt through potentization, this medicine is used for post-childbirth hair fall amongst women.
6. Pulsatilla Pratensis: This medicine is also used by women post-childbirth. It is also used by women having trouble digesting fatty food and people having difficulty breathing.
Hence, these are the medicines you can use to deal with hair fall and hair loss. But you should consult the best doctor before using these medicines to ensure you take the proper medication.
Categories
Hair Loss
Homeopathic Approaches to Combat Hair Loss
Hair loss can be a frightening experience for all kinds of people. While there are different conventional treatments available, numerous people are changing to natural and holistic approaches to address this issue. Homeopathy, a delicate and powerful elective medication system, offers promising solutions for combating hair loss. In this blog, we will investigate how homeopathy can assist with re-establishing your hair’s health and vitality, all while thinking about the expertise of a Homeopathic Clinic and Homeopathic Doctor in Mumbai.
Understanding Homeopathic Treatments for Hair Loss:
Homeopathy depends on the rule of “like cures like.” It includes directing exceptionally diluted substances derived from natural sources to stimulate the body’s healing systems. Homeopathic remedies for hair loss center on the symptoms as well as recognizing and tending to the underlying causes.
Effective Homeopathic Remedies:
1. Thuja Occidentalis: This remedy is frequently suggested for hair loss brought about by dandruff or dry, brittle hair. It works on the hair’s surface and reinforces the hair follicles, advancing solid hair development.
2. Lycopodium Clavatum: Helpful for people encountering premature hair loss or balding, Lycopodium Clavatum resolves issues related to hormonal imbalance. It additionally helps with dealing with related symptoms like digestive issues and anxiety.
3. Silicea: When hair loss is assisted by sluggish hair growth and weak roots, Silicea can be helpful. It fortifies hair follicles and empowers the growth of thicker, better hair.
4. Phosphorus: People with hair loss because of scalp infections or alopecia areata can find relief with Phosphorus. This cure supports hair re-growth and overall hair health.
5. Natrum Muriaticum: Homeopathic specialists might suggest Natrum Muriaticum for hair loss resulting because of emotional stress or distress. It tends to address imbalance brought about by emotional factors, prompting further developed hair development.
Partnering with a Homeopathic Clinic:
For personalized and successful homeopathic treatments, counseling a certified Homeopathic Doctor is important. In Mumbai, you can find trustworthy Homeopathic Clinics with experienced professionals who spend significant time on hair loss and related concerns. By looking for proficient direction, you can get custom-fitted treatment plans and continuous help all through your journey to natural combat hair loss.
The Advantages of Homeopathy for Hair Loss:
1. Safety: Homeopathic remedies are natural, non-poisonous, and have no side impacts. They are safe for long-haul use, making them appropriate for people looking for manageable solutions for hair loss.
2. Holistic Approach: Homeopathy means to treat the person as a whole, considering physical, emotional, and mental viewpoints. This extensive approach helps address underlying imbalances and promote overall prosperity.
3. Personalized Treatment: Homeopathic remedies are recommended in view of an individual’s exceptional symptoms and qualities. This personalized approach ensures that the treatment focuses on the root cause of hair loss, expanding the possibilities of effective results.
Conclusion:
Homeopathic approaches offer a characteristic and holistic method for combatting hair loss. While looking for such treatments in Mumbai, counseling a respectable Homeopathic Clinic and experienced Homeopathic Doctor is essential.
Dr. Sonal’s Homoeopathic Clinic offers valuable insights and resources, making it a trusted homeopathic clinic in Mumbai for acquiring comprehensive knowledge in the field of healthcare.With their expertise, you can set out on a journey to re-establish your hair’s health and regain your morale, all in a protected and natural way.
Categories
Hair Loss Hair treatment homeopathy
How are hair fall and homeopathy treatment linked to one another?
Hair fall and homeopathy
The problem of hair fall is one of the common conditions that’s faced by individuals of different age groups. There’s a possibility that individuals lose 50 to 100 hair every day; that’s considered normal. But, if you lose more than that, then there’s a problem. If you have started losing hair that leads to baldness and hair fall spots, then you better get medical assistance at the earliest. Just make sure to get the right treatment plan by consulting the best hair loss Specialist In Mumbai.
What are the causes of hair fall?
Excessive hair loss can happen due to multiple reasons. There’s a possibility of losing hair after 3 to 4 months of having an illness or undergoing any surgery. In such a situation, hair loss can happen suddenly, making the situation even worse with time. If you are unsure about what’s the reason for hair loss and it’s getting worse with time, then you should get the supervision of the Homeopathic Doctor in Mumbai to handle the situation effectively. The possible causes of hair fall are mentioned-below and based on the same, the doctor will suggest the appropriate treatment plan:
• Hormonal problems happen with the thyroid gland. The problem can be underactive or overactive, which leads to hair fall.
• The intake of birth control pills and antidepressants can even create problems with hair health. If you start taking certain medication and notice hair fall, then you better get the doctor’s assistance right away & stop the medication.
• The most common reason behind baldness is male pattern baldness. There’s a possibility you have inherited the hair loss problem. In some cases, hair loss can occur at an early age.
• Another common hair loss pattern is alopecia areata, which means losing hair in patches. If you have any confusion in your mind, then make sure to get in touch with a homeopathic doctor.
As per the homeopathic doctor, you need to make your lifestyle habits all right and avoid the use of excessive junk food.
Please Note!
The homeopathic doctor will check your overall health and accordingly tell you what choice of treatment you need to follow.
Homeopathic tips to take care of your hair
Some of the homeopathic tips to take care of your hair health are:
• For the overall health of your hair, you need to keep yourself healthy from the inside out.
• Keep your diet plan healthy for hair well-being.
• Keep your diet plan balanced so that the body gets the mineral, vitamins, and other nutrients. So, make your hair shiny and strong with the right care.
• Never comb your hair too aggressively.
• You should never comb your hair when it’s too wet
Categories
Hair Loss
Guide on women’s health care: What to do if you gain weight in your 40s?
Weight gain in your 40s
Weight gain is a common concern among everyone. In this blog, the concern revolves around women who are in their 40s and face problems with their overall metabolism. And that’s the reason it’s essential to get in touch with the Women Health Care Specialist doctor in Mumbai to make an informed decision on what to do and what not.
Being mindful and careful towards every possible concern with the increase in age lets you know what’s best and if there’s something that should be changed in your daily life. The metabolism can go down in your mid-40s, leading to extreme decline in the hormones, loss of muscle mass, and weight gain. It’s a problem with disproportion that begins to create a lot of trouble for your overall well-being. So, be it perimenopause or menopause, getting the right care at the right time is essential. The expertise offered by the Homeopathic Doctor in Maharashtra helps you get closer to the natural and non-toxic approach to make everything much more manageable.
Tips for women’s health care after the 40s
Tip 1: Stay physically active
Make sure you are physically active, even in your 30s or 40s. A regular visit to the Homeopathic Clinic in Maharashtra to understand better the metabolic issues or any other health concerns. Suppose you have diabetes or thyroid, then ensure it is balanced.
Tip 2: Make sure the body gets IRON
You need to make your body move physically at least for 30 minutes every day. So, do the activities like aerobics, spinning, biking, Zumba, walking, running, or any other activity. With a regular exercise regime, your heart pumps blood, keeps your mood uplifted, reduces sex drive, and prevents osteoporosis.
You can even go yoga, which helps to strengthen the core and muscles. That’s not all the menopausal symptoms reduced like hot flashes, brain fog, and insomnia.
Tip 3: Keep a check over your food
When you do exercise, overall health does benefit. Other than that, you need to have a healthy meal every day. It’s all about being purposeful with your diet and incorporating the right kind of healthy food habits. The body needs the right nutritional value, and the right mix of healthy fruits and vegetables makes everything much better. So, keep the right track of everything, and you are good to go. Please do not have much of:
• Fried food
• Processed food
Tip 4: Acupuncture is good for health
There’s nothing like a quick-fix solution. You must be mindful about everything to keep everything at the right pace. Good and healthy lifestyle changes are the way to reduce the impact on health. Acupuncture can be a proven choice in your unhealthy life. The homeopathic doctor’s advice offers all the necessary and fruitful results that ultimately lead everything to the right approach.
Start the journey of healthy you with Homeopathy
If you want to know more, schedule an initial consultation with Dr. Sonal Jain to understand how to manage weight in your 40s.
Categories
Hair Loss Hair treatment
Are Homeopathic Medications The Perfect Solution To Treat Hair Fall?
There are many reasons why people tend to lose a lot of hair. Some common factors include hormonal imbalance, stress, or even genetics, which can lead to extreme hair loss in an individual. But with the help of a homeopathic doctor in Mumbai, you will be able to get rid of such issues without any complications.
Read more to learn!
Natural Substance Over Chemical
There are many people who are tired of trying out chemically infused products in their hair resulting in more hair loss. They want an alternative option that is more natural and organic which would work wonders for the hair. It will also help them to improve the curtail hair and even partially regrow the lost hair in some sections.
This is why we have seen a massive surplus of homeopathic medications for Hair Loss Treatment in Mumbai in recent times. It is one of the most hyped treatments available that provide the right therapy without any side effects.
Can You Stop Hair Loss Naturally?
According to the Homeopathic Doctor in Maharashtra, with the assistance of natural means, you will be able to reduce the risk of hair loss. Apart from that, we also know that diet plays a vital role in the overall health of the human body. Including raw vegetables and fresh herbs in your diet might help you a great deal to overcome the issue of hair loss within no time. It will also make your immunity stronger than ever before. For male or female pattern baldness, a change in the diet for the betterment will definitely help you a lot. You can also add protein and vitamin A to your diet for better results.
Another tactic you can adopt in your day-to-day life is Yoga, as it helps reduce the risk of stress-related hair fall. If you massage your scalp once a week, you will notice a drastic change in your scalp. They would be significantly more healthy as it will increase the blood flow to the area.
Which Homeopathic Medicine That Works For Hair Fall?
People now use different types of multiple natural supplements to strengthen the hair and promote regrowth. Some of the most common multiple natural supplements include fish oil supplements, especially those that have omega-three fatty acids, as they are famous for enhancing hair density due to the richness that we find in those oils. Other factors that fish oil contains are protein and antioxidants.
Another supplement that you can use for hair regrowth is aloe vera. It is a famous item that promotes scalp health while unclogging hair follicles.
The excess oil blocks the hair follicles, which prevents the promotion of hair regrowth. Many people also swear by the Ginseng supplements to help promote the stimulation of hair follicles.
For All Intents And Purposes
Contact Dr. Sonal Jain and get your homeopathic medication now for better hair growth.
Categories
Hair Loss Hair treatment homeopathy
Enlist the 6 superfood which is effective for strong and healthy hair
Healthy hair with a healthy diet
Almost everyone looks for a diet that benefits hair health. Indeed! The option you add to your plate should be nutritious enough that the hair locks get the right amount of nutrients. Additionally, the right kind of food makes scalp and hair health much better than it should be. No doubt, if you have excess hair loss, you must get the Hair Loss Treatment in Maharashtra on time and make everything much more manageable. The expertise of the homeopathic doctor is known to improve hair health and make hair loss much more manageable.
Superfood for healthy and strong hair
When you consult the Homeopathic Doctor in Mumbai, you must follow all necessary suggestions given by the doctor and even have the given food options added to your daily diet. Now, let’s understand which food options you should add to your daily food regime:
Option 1: Yogurt
Yogurt is one of the most loved dairy products that benefit overall health. It contains proteins that are known to control hair fall. Additionally, it has the right amount of Vitamin B5, which helps in hair breakage and thinning. As per your liking, you can have yogurt.
Option 2: Fatty fish
Fatty fish are effective options for trout, salmon, and mackerel with the right amount of omega-3 fatty acids and iron. All these nutrients play a vital role in hair loss and give necessary moisture. If you don’t eat non-veg, you should add walnuts and pumpkin seeds to your diet. If the problem does not get under control then visit the top-rated Homeopathic Clinic in Mumbai.
Option 3: Spinach
Spinach is one of the essential food options from the family of green vegetables. The spinach offers the hair goodness of Vitamin A, iron, and beta-carotene. Moreover, spinach accelerates the blood cell count. If you don’t eat non-veg, try to include spinach in your daily diet at least 1 or 2 times a week to counter hair loss.
Option 4: Eggs
Eggs are fruitful for hair health. The egg yolk is filled with the goodness of sulfur that boosts the health of hair follicles. So, to protect your hair against breakage and hair thinning, you should have eggs.
Option 5: Carrots
Carrots are a great choice because they contain antioxidants, beta-carotene, and Vitamin A. The combination boosts blood circulation to the scalp. If you dislike eating raw carrots, you should have fresh carrot juice.
Option 6: Almonds
Almonds are filled with the goodness of Vitamin A, D, E, B2, and B6. Moreover, it has mono fatty acids and magnesium that work wonders for hair health. To control your hair loss, make sure to have it in the right amount and empty stomach. Doing so lets your skin, nails, and hair be all healthy.
Categories
Hair Loss homeopathy
Homoeopathic Treatment For Different Types of Hair Loss And Its Causes
Hair loss is one of the most common problems we notice in all ages, gender, and ethnicity. It can be a very heartbreaking condition that takes a big toll on your self-confidence and aesthetics. In this cognition, the patient notices a portion of the head or any other part of the body to lose hair.
Most of the time, men are at the end of this scrutiny, where we see an effect on their scalp. Many scientists and researchers are still finding the real cause and the Hair Loss Treatment in Mumbai.
Causes Of Hair Loss
There are many reasons for hair loss. We have listed below some of the common causes:
1. Having family history (genetics)
2. Hormonal imbalances
3. Careless hair treatment
4. Experiencing a high level of stress
5. Abnormal immune system
6. Changes in lifestyle
7. Having side effects because of medication
Symptoms Of Hair Loss
Hair loss is basically a condition that starts out of nowhere and increases gradually and affects just the scalp area. In most cases, hair loss is a temporary issue, while in others, it can cause baldness. Some of the hair loss symptoms that you should be wary of are:
1. Patches or spots of hair loss on the scalp
2. Thinning of hair
3. Sudden hair loss because of anxiety and stress
4. Hair loss throughout the body
Homoeopathy And Hair Loss
We all know the efficacy of homeopathy and how it can help treat different types of hair loss. Yes! Hair loss!
With an ideology of a holistic approach, the Homoeopathic Doctor in Mumbai, with a personalized touch, treats hair loss. The specialist determines the treatment based on the actual cause and the extent of hair loss. Apart from that, they also keep an eye on the grade of baldness and the condition of the scalp and the hair.
Male pattern baldness or androgenic pattern is one of the main reasons for hair loss in men. This condition ends up with partial or complete baldness in some cases.
With homeopathy, you will be able to treat your hair loss symptoms along with its root cause, which can be an underlying health condition such as diabetes mellitus, thyroid disorder, or even in some cases, physical or emotional stress, without creating any complications.
Homeopathy For Male Pattern Baldness
It is one of the most common types of hair loss issues that we notice in men. Homeopathic medicines such as Thuja and Sabal can help you treat this condition easily. But make sure to take a prescription from the doctor first, as the real cause will help them determine the personalized remedy.
Based on the condition of the patient, the homeopath will give you the medications that are the natural inhibitors of Di-hydroxytestosterone, which is basically a derivative of the male hormone testosterone.
Homeopathy For Dry Hair
Because of the inadequate amount of moisture, there are chances for your hair to lose its shine and become dry. With the help of homeopathic medicines like lycopodium, natural mur, psorinum, and Sulphur, you can retain that moisture.
Categories
Hair Loss
Treat Your Hair Loss Issues With Homeopathic Medication In Mumbai
Hair fall is one of those problems that can hit anyone at any time. Especially in this era of toxic life and unhealthy lifestyle, it is very natural for one to suffer from such extensive hair fall.
Generally speaking, it is very standard for one to notice 50 to 100 hair strands falling daily. But in case it follows with a lot more hair, then it is a matter of concern, and you should not wait to get it treated under the guidance of a Homeopathic doctor.
You might wonder why homeopathic?
Well, in this blog, we will talk about why homeopathic remedies are the best option for hair fall treatment in Mumbai.
So without wasting any further, let’s get into it.
Why Choose Homeopathic Treatment For Hair Fall?
We have jotted down a list of reasons why you must select homeopathy for your hair fall issues.
• A natural remedy for a toxic lifestyle
Nowadays, it is tough to find a substitute that would provide a healthy and natural substance. This unhealthy lifestyle of eating junk food is living in pollution and exposure to harmful chemicals. It is no shock that you are noticing heavy hair fall. This is the reason why it is very vital for those people to choose something which is natural and provides high-quality treatment for hair loss.
• It is a safe and no-risk medication.
People vary from weird medication, especially for regulating their hormones. Hair loss treatment with conventional or traditional methods can bring up many side effects in the body, like acne, dark spots, and weight gain. But you would not have to worry about such a thing with homeopathic treatment in a homeopathic clinic in Mumbai.
So do not wait anymore and get treated with homeopathic medicines to avoid any side effects or risks while simultaneously getting rid of the root cause of hair loss.
• Cut the problem from the roots of the symptoms.
The ideology of homeopathy solely relies on “like cures like,” which loosely translates to curing the problem or the symptoms of hair fall with the help of its cause. What causes the problem will heal it. It is an absurd idea but one that works without any complication. Apart from that, unlike any other treatment, homeopathic medication not only works on curing the cause but also removing the symptoms of the problems for better results.
• It is a holistic approach.
When we talk about homeopathy, the first thing that strikes the mind is its holistic approach to treating any health condition, including hair fall. Its primary aspect is to regulate and stimulate the body, mind, and the soul together to form a better understanding of the concerns and treat it accordingly.
Contact Us Immediately
Dr. Sonal Jain homeopathic doctor in Mumbai works on providing better healthcare to their patients. If you have some doubts regarding hair fall treatment or any other issues, you can kindly contact us on:
Shop No. 22, Digamber Co-Operative Housing Society, Jerbai Wadia Road, Bhoiwada, Parel, Mumbai, Maharashtra 400012
Do you have a Query?
+91-9167007919
Do you have a Question?
drsonal013@gmail.com
Categories
Hair Loss
5 major causes of hair loss and homeopathy treatment to prevent it
Hair loss – One of the most nerve-wracking sights. Be it, men or women, both face the problem of hair loss. And losing hair locks in excess affects the person’s self-esteem and confidence. If you have been looking for Hair Fall treatment in Mumbai for a long time but cannot get yourself the effective treatment, then schedule an initial consultation with a homeopathic practitioner to improve your overall hair well-being.
The disruption in the hair cycle should be known to ensure you seek the most effective treatment plan. When you visit the Homeopathic Doctor in Maharashtra, the initial diagnosis is done to know the major root cause of the problem and see what can be next. The given blog will tell you about the major reasons behind hair loss so that the situation gets under control.
5 common reasons behind hair loss
Several reasons make hair health worse. But, some of the known ones who tell there’s a medical link between it and seeking homeopathic treatment will help to make it better:
Reason 1: Iron deficiency
When was the last time you got your iron deficiency checked? Iron is one of the biggest important factors in transporting oxygen to different body organs. If you lack iron, then the common reason is anemia. Moreover, it’s likely to trigger hair loss as the body is not functioning properly. So, the lack of oxygen to the hair follicles will affect hair health.
Reason 2: Less amount of protein in the diet
Does your diet have enough protein? If not, then the cycle of hair growth will get affected. Studies have shown such a state can make your hair get into the resting stage. Moreover, around 91% of vegetarians are diagnosed with protein deficiency. So, make sure to focus on your protein intake.
Reason 3: Excessive smoking or secondhand smoke
Someone who has the habit of smoking or even secondhand smoke has a higher chance of dealing with hair loss. This is because cigarette smoke contains harmful substances that are likely to affect hair health. One of the studies has shown that when you smoke in excess, the rate of DHT increases in the body, which triggers hair loss.
Reason 4: Vitamin D-3 deficiency
Another common reason is vitamin D3 deficiency, which triggers hair loss known by TE (Telogen Effluvium). Although, the hair loss that occurs with it is temporary. But, under this state, the hair gets into the resting phase, and then over time, there’s a factor of seeing an excessive amount of hair loss.
Reason 5: Health issue
If you had a health issue in the past, you are likely to have trouble keeping your hair healthy.
Are you looking for hair fall treatment?
Schedule your initial consultation with Dr. Sonal Jain to seek personalized and effective hair fall treatment. No matter what doubt you have in your mind, make sure to discuss the same. | {
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Genetics and Energy
By Mike Clark, PhD, MBA, JD, ABHRT, FAARM
“Any form of life that can’t generate its own energy is essentially dead. There is no life without energy.”
Our body needs energy to perform and to survive. How this energy is used and produced is essential to the health of our body and our children. For example, our brains alone use 20% of the energy generated by our internal systems.
Interesting fact: we may produce ten thousand times more energy (per gram) than the sun every second. See reference below.
The brain’ s primary function, processing and transmitting information through electrical signals, uses about 75% of this energy. Our nerve cells required tremendous energy to send out signals telling our cells how to act. (BrainFacts.org. Feb 1, 2019). And this is where we start to get into trouble.
When our signals are being interrupted or are not strong enough due to lack of enough energy, our minds slow down (or kick into hyper drive), we miss signals, we may engage in erratic behavior or suffer from a host of signaling issues including ADD, ADHD, dementia, Autism, depression, anxiety, addictions, poor sleep quality and many other conditions. For instance, imagine the frustration you experience when your cell phone is missing calls or has static.
So, what does this have to do with Genetics?
All of us have mutated genes, as many as 1.2 million! Most are benign. However, many can cause serious problems. The good news is that “genes are not our destiny” as one author states. The science of epigenetics tells us that we can modify how our genes act (called gene expression). How? By changing the environment which turns our genes on or off (like a light switch).
Through proper nourishment, a healthy lifestyle, and focused treatment through the knowledge obtained by genetic testing, we can help our mutated genes act in our best interest instead of against us. Also, using Nutrigenomics, the study of how our genes are affected by proper nourishment and our environment, is rapidly developing. It is providing us with more precise information on how to turn on our protective genes and turn off our harmful ones.
Methylation. When we are eating processed food and many of the over-the-counter supplements, we are consuming folic acid. Unfortunately, the body then needs to convert this folic to folate so it can use it to perform the approximately 250 processes involved in Methylation. If any or some of our 21 genes variations (referred to as mutations or Single-nucleotide Polymorphism -SNP) involved in methylation, are not working correctly, we are unable to provide fuel to our energy powerhouse, the mitochondria.
This also means we are not transporting key nutrients to the cells (simplified explanation) and our ability to heal and recover from any illness or trauma is compromised. Our ability to produce our No.1 antioxidant, Glutathione, is also compromised.
There are seven steps in this process and 21 gene SNPs that can affect the pathway. Testing all of them (not just the MTHFR gene) is necessary to ensure proper methylation treatment and to ensure fuel is getting to the Mitochondria so it can be used by the cells for energy production.
Did you know? Food sources of folate: Legumes, Asparagus, Eggs, Leafy Greens, Beets, Citrus Fruits, Brussels Sprouts, Broccoli. Avoid Folic acid which is in most processed foods.
Mitochondria. “They (Mitochondria) are organelles that act like a cellular digestive system that takes in nutrients , breaks them down, and creates energy for the cell.” (See Mitochondria and The Future of Medicine, at p12). The mitochondria are small organelles that are the powerhouses or our cells. Think Hoover Dam power and energy production! They are designed for maximum work. So why are we often tired? Why do we often seem to lack energy for any mundane tasks or complain that we wish we had more energy. Whyall of the Starbuck fixes? The energy drinks?
The genes that are instrumental to a properly functioning mitochondria may be mutated. If mutated, then without proper nourishment and lifestyle, you will lack energy. If you lack energy, your brain does not function at optimal levels. You may be depressed, anxious, lack enough brain power (energy) to perform daily activities. Signals from your brain are disrupted so cells do not act as they were meant to
act.
Genetic testing will provide focused information for better treatment options. Did you know? Moderate exercise creates more mitochondria. Strenuous exercise can create excess free radicals and damage the mitochondria.
Other information:
Approximately 60 to 70 percent of people in the United States have a genetic mutation that makes it challenging for their bodies to create enough 5-MTHF.
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7,897,118,854,726,911,000 | 2410 W. Jefferson St, Unit 108
Joliet, Illinois 60435Call us Today!(815) 745-5771
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Relieve Pain, Preserve Your Smile: Root Canals Explained at Dental Smiles of Joliet
At Dental Smiles of Joliet, we understand that experiencing tooth pain can be unsettling and disrupt your daily life. While the term "root canal" might evoke apprehension, it's a valuable procedure designed to save a damaged or infected tooth, alleviating pain and preserving your natural smile.
What is a Root Canal?
A root canal is a dental treatment that addresses the inner pulp of a tooth. The pulp contains nerves, blood vessels, and connective tissues. When this pulp becomes infected or severely damaged due to decay, trauma, or other factors, it can cause significant pain and discomfort.
Signs You Might Need a Root Canal
• Persistent toothache: This pain can be sharp, throbbing, or dull and may worsen with chewing or hot/cold sensitivity.
• Swollen or tender gums: Inflammation and redness around the affected tooth can indicate an infection.
• Visible pimple on the gums: In some cases, an abscess (pus-filled bump) may form near the infected tooth.
• Discoloration or darkening of the tooth: This can signify damage to the pulp or nerve tissue.
• Sensitivity to temperature changes: Pain upon exposure to hot or cold beverages/foods can be a sign of nerve irritation.
• Discomfort when biting or chewing: Pain while applying pressure to the tooth can indicate damage to the pulp or surrounding bone.
Benefits of Root Canal Therapy
• Pain relief: Root canals effectively eliminate the source of pain, allowing you to regain comfort and resume your daily activities.
• Preserves the natural tooth: By saving the tooth structure, root canals prevent the need for extraction and potential complications associated with missing teeth.
• Improved oral health: Removing the infection prevents further damage and spread to surrounding teeth and tissues.
• Maintains a natural appearance: Preserving the original tooth structure helps maintain a natural-looking smile.
Why Choose Dental Smiles of Joliet for Your Root Canal?
• Experienced and gentle dentists: Our team prioritizes your comfort and utilizes advanced techniques to ensure a smooth and efficient procedure.
• Patient-centered approach: We listen to your concerns and tailor the treatment plan to your specific needs and preferences.
• Modern technology: We utilize advanced equipment and techniques to ensure accurate diagnosis and efficient treatment.
• Relaxing environment: We strive to create a comfortable and welcoming environment for all our patients.
Don't let tooth pain control your life. Contact Dental Smiles of Joliet today to schedule a consultation and learn more about how root canal therapy can help you regain comfort and preserve your natural smile.
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Income-generation activities Home visits ↑ health knowledge, ↑ health care utilization, ↓ poverty ↑ nutrition and knowledge, ↓ anemia, ↓/NC night blindness, ↑ intake of vitamin A–rich foods, ↑/NC intake of vegetables, ↑ intake of ASF, ↓ underweight, ↑ health care utilization, ↓ poverty ↑ health knowledge, ↑ health care utilization, ↓ poverty
The mission of Student Health and Counseling Services is to enhance the physical and mental health of students in order to help them achieve academic success, personal development and lifelong wellness by providing an integrated program of quality, accessible, cost sensitive and confidential healthcare services, tailored to their unique and diverse needs and to assist the University community, through consultation and education, to develop a healthy campus environment consistent with UC Davis "Principles of Community".
According to researchers who recently reviewed the risks associated with coronary heart disease (CHD) in women, a poor diet was linked to 20 percent of all cases of heart disease. Factor in diet’s effect on other chronic diseases like diabetes and osteoporosis, and it’s obvious that good nutrition has huge women's health benefits. One way to immediately turn your health situation around is through the foods you choose to eat. Here are nine foods that you'll want to make part of your daily diet.
For girls and adult women, educational interventions are considered a powerful means of improving their health and nutritional status throughout their lives. Education level is often associated with maternal caregiving practices and the nutritional outcomes of their children (174, 175). Few studies, however, evaluated the impact of education as an intervention on women's nutrition outcomes. Instead, many studies used survey data and reported on associations between education and nutrition. For instance, in low- and middle-income countries, higher levels of education were associated with lower prevalence of underweight and higher prevalence of overweight among women (176, 177). However, this depended on the type of employment in which women participated (178, 179). In addition, in many high-income settings, the converse was true (177). Level of literacy was also associated with improved anthropometric measures. In southern Ethiopia, literate mothers were 25% less likely to be undernourished than were illiterate women (180). One econometric analysis suggested that doubling primary school attendance in settings with low school attendance was associated with a 20–25% decrease in food insecurity (181). Overall, though, these associations were limited in their ability to draw conclusions about causality and the effect of education interventions on nutrition outcomes.
Folate is most important for women of childbearing age. If you plan to have children some day, think of folate now. Folate is a B vitamin needed both before and during pregnancy and can help reduce risk of certain serious common neural tube birth defects (which affect the brain and spinal chord). Women ages 15-45 should include folate in their diet to reduce the risk for birth defects if one becomes pregnant, even if one is not planning a pregnancy.
Trying to balance the demands of family and work or school—and coping with media pressure to look and eat a certain way—can make it difficult for any woman to maintain a healthy diet. But the right food can not only support your mood, boost your energy, and help you maintain a healthy weight, it can also be a huge support through the different stages in a woman’s life. Healthy food can help reduce PMS, boost fertility, make pregnancy and nursing easier, ease symptoms of menopause, and keep your bones strong. Whatever your age or situation, committing to a healthy, nutritious diet will help you look and feel your best and get the most out of life.
To optimise women's control over pregnancy, it is essential that culturally appropriate contraceptive advice and means are widely, easily, and affordably available to anyone that is sexually active, including adolescents. In many parts of the world access to contraception and family planning services is very difficult or non existent and even in developed counties cultural and religious traditions can create barriers to access. Reported usage of adequate contraception by women has risen only slightly between 1990 and 2014, with considerable regional variability. Although global usage is around 55%, it may be as low as 25% in Africa. Worldwide 222 million women have no or limited access to contraception. Some caution is needed in interpreting available data, since contraceptive prevalence is often defined as "the percentage of women currently using any method of contraception among all women of reproductive age (i.e., those aged 15 to 49 years, unless otherwise stated) who are married or in a union. The “in-union” group includes women living with their partner in the same household and who are not married according to the marriage laws or customs of a country."[62] This definition is more suited to the more restrictive concept of family planning, but omits the contraceptive needs of all other women and girls who are or are likely to be sexually active, are at risk of pregnancy and are not married or "in-union".[37][63][58][59]
There are many well-documented challenges in disentangling empowerment interventions from other interventions with which they are delivered. Empowerment interventions are often integrated into income-generating activities and agricultural extension, and many empowerment approaches are retroactively classified as “nutrition-sensitive” despite a lack of nutrition components in the original intervention designs (5). In addition, many studies are limited in scope and their evaluation of nutrition outcomes (159), and it is difficult to evaluate which dimensions of women's empowerment matter most for nutrition (162). Notably, indicators to quantify women's empowerment are also not used consistently and vary widely between individual studies (158).
It takes a lot of discipline to turn down a cupcake or roll out of your warm bed for a cold morning run. To make staying on track easier, it's important to make a real connection with your motivation, says Tara Gidus, R.D., co-host of Emotional Mojo. So think less about fitting into your skinny jeans or spring break bikini and more about emotional ties to the people you love. “Your relationships will grow stronger when you are physically healthy and taking care of yourself,” she says.
After menopause. Lower levels of estrogen after menopause raise your risk for chronic diseases such as heart disease, stroke, and diabetes, and osteoporosis, a condition that causes your bones to become weak and break easily. What you eat also affects these chronic diseases. Talk to your doctor about healthy eating plans and whether you need more calcium and vitamin D to protect your bones. Read more about how very low estrogen levels affect your health in our Menopause section. Most women also need fewer calories as they age, because of less muscle and less physical activity. Find out how many calories you need based on your level of activity.
Income-generation interventions largely target adult women (women of reproductive age, women with young children, and older women). Many microfinance and loan programs are targeted to women because of their likelihood to pay back the loans, although women with lower education levels and smaller businesses do not benefit to the same degree as women who are educated or who have bigger businesses (165). There was limited evidence of such interventions targeting adolescent girls (169). In order to understand the potential impact of income-generating activities on adolescents, more information is needed about the pathways by which adolescents contribute to their own food security, the degree to which they rely on their caregivers to meet their nutritional needs, and how those dynamics change with the age of adolescents (169). Training, workshops, and extension activities were often delivered through community centers, community groups, and financial institutions (165). Other affiliated interventions, such as agricultural extension and nutrition education, were provided at the community level and at home visits (160, 173). These delivery platforms were effective at reaching women, including low-income women, particularly when they engaged with existing community groups (e.g., self-help, farmers’, and women's groups) (160, 161, 167, 169, 172, 173).
Despite these differences, the leading causes of death in the United States are remarkably similar for men and women, headed by heart disease, which accounts for a quarter of all deaths, followed by cancer, lung disease and stroke. While women have a lower incidence of death from unintentional injury (see below) and suicide, they have a higher incidence of dementia (Gronowski and Schindler, Table I).[6][19]
“Whole grains help with digestion and are excellent for your heart, regularity [because of the fiber content], and maintaining a steady level of blood sugar,” says Hincman. “They are also a great source of energy to power you throughout the day.” Whole grains, such as oats, also help improve cholesterol levels. While food manufacturers are adding fiber to all sorts of products, whole grains, like whole wheat, rye, and bran, need to be the first ingredient on the food label of packaged foods, she stresses. Watch your serving sizes, however. Current guidelines are for six one-ounce equivalent servings per day (five if you’re over 50). One ounce of whole-wheat pasta (weighed before cooking) is only one-half cup cooked.
Oils. When cooking try to use oils from plants instead of solid fats like butter, margarine, or coconut oil. See this list of oils and fats to see how healthy each type of cooking oil and solid fat is. Most women eat too much solid fat through packaged foods like chips or salad dressing, and not enough healthy fats like olive oil or the type of fat in seafood.
It's full of health, diet, fitness, and inspiring articles. My first issue was 142 pages of wonderfully educational and motivating articles with clear pictures. It's easy to highlight the articles to read. This magazine is ideal for people that are interested in women's health covering all kinds of topics ranging from nutrition to working out and from meditating to parenting. It also includes ads for the latest in skincare products, makeup, gear, and food, which I like so that I know what to shop for. When I need motivated and inspired or need to refocus, this is the magazine I choose!
It takes a lot of discipline to turn down a cupcake or roll out of your warm bed for a cold morning run. To make staying on track easier, it's important to make a real connection with your motivation, says Tara Gidus, R.D., co-host of Emotional Mojo. So think less about fitting into your skinny jeans or spring break bikini and more about emotional ties to the people you love. “Your relationships will grow stronger when you are physically healthy and taking care of yourself,” she says.
Integrated health care, which integrates curative and preventive interventions, can improve nutrition outcomes for women across the life course through improved access to counseling, vaccinations, and screening and treatment of illnesses (103–107). Access to primary health care positively contributed to the prevention, diagnosis, and management of both communicable and noncommunicable disease (108). Distribution of insecticide-treated bed nets, condoms, screening and testing for disease, and delivery of medical treatments were often associated with integrated health initiatives and improved health and nutrition outcomes (13, 109). Access to health care was associated with the delivery of nutrition-specific interventions to manage pregnancy-induced hypertension, diabetes, pre-eclampsia, and hemorrhage (106, 107, 110). However, some studies showed that integrated services increased knowledge, but did not result in changes in health or nutrition outcomes (103). In addition, in many settings, quality of care was inadequate (107) and incorrect diagnoses and treatments were common (111).
Nutrition-sensitive approaches are difficult to link to women's nutritional status (5, 102). This is due to limited measurement of benefits to program beneficiaries, families, households, and communities, limited timeframes to evaluate long-term impact, logistical and political realities that make implementation difficult, and different priorities of different stakeholders in multisectoral programs (102). Many nutrition-sensitive approaches, as will be described, thus focus on more distal measures of impact (e.g., coverage, knowledge) and not more proximal measures of women's nutritional status (e.g., BMI, anemia status, etc.).
A workout partner not only keeps you accountable, she also may help you clock more time at the gym and torch more fat. A British survey of 1,000 women found that those who exercise with others tend to train six minutes longer and burn an extra 41 calories per session compared to solo fitness fanatics. [Tweet this fact!] Women with Bikram buddies and CrossFit comrades said they push themselves harder and are more motivated than when they hit the gym alone.
Internationally, many United Nations agencies such as the World Health Organization (WHO), United Nations Population Fund (UNFPA)[171] and UNICEF[172] maintain specific programs on women's health, or maternal, sexual and reproductive health.[1][173] In addition the United Nations global goals address many issues related to women's health, both directly and indirectly. These include the 2000 Millennium Development Goals (MDG)[142][43] and their successor, the Sustainable Development Goals adopted in September 2015,[47] following the report on progress towards the MDGs (The Millennium Development Goals Report 2015).[174][37] For instance the eight MDG goals, eradicating extreme poverty and hunger, achieving universal primary education, promoting gender equality and empowering women, reducing child mortality rates, improving maternal health, combating HIV/AIDS malaria and other diseases, ensuring environmental sustainability, and developing a global partnership for development, all impact on women's health,[43][11] as do all seventeen SDG goals,[47] in addition to the specific SDG5: Achieve gender equality and empower all women and girls.[109][175]
The U.S. Department of Agriculture's (USDA) food pyramid system (www.mypyramid.gov) provides a good start by recommending that the bulk of your diet come from the grain group—this includes bread, cereal, rice and pasta— the vegetable group; and the fruit group. Select smaller amounts of foods from the milk group and the meat and beans group. Eat few—if any—foods that are high in fat and sugars and low in nutrients. The amount of food you should consume depends on your sex, age and level of activity.
The increasing focus on Women's Rights in the United States during the 1980s focused attention on the fact that many drugs being prescribed for women had never actually been tested in women of child-bearing potential, and that there was a relative paucity of basic research into women's health. In response to this the National Institutes of Health (NIH) created the Office of Research on Women's Health (ORWH)[154] in 1990 to address these inequities. In 1993 the National Institutes of Health Revitalisation Act officially reversed US policy by requiring NIH funded phase III clinical trials to include women.[119] This resulted in an increase in women recruited into research studies. The next phase was the specific funding of large scale epidemiology studies and clinical trials focussing on women's health such as the Women's Health Initiative (1991), the largest disease prevention study conducted in the US. Its role was to study the major causes of death, disability and frailty in older women.[155] Despite this apparent progress, women remain underepresented. In 2006 women accounted for less than 25% of clinical trials published in 2004,[156] A follow up study by the same authors five years later found little evidence of improvement.[157] Another study found between 10–47% of women in heart disease clinical trials, despite the prevalence of heart disease in women.[158] Lung cancer is the leading cause of cancer death amongst women, but while the number of women enrolled in lung cancer studies is increasing, they are still far less likely to be enrolled than men.[119]
Anemia can deplete your energy, leaving you feeling weak, exhausted, and out of breath after even minimal physical activity. Iron deficiency can also impact your mood, causing depression-like symptoms such as irritability and difficulty concentrating. While a simple blood test can tell your doctor if you have an iron deficiency, if you’re feeling tired and cranky all the time, it’s a good idea to examine the amount of iron in your diet.
Women also understand the relationship between working out and how it can affect everything they do in life. Most major health issues affecting women can be treated or improved by a simple workout plan. Weight loss and cardiovascular exercise help everything from stress and heart disease to diabetes. And don't forget the small, but important "fringe" benefits of fitness such as just feeling better about yourself, having more energy for your family and loved ones and living a life that begins every day by feeling good about getting up and getting moving.
Johnson, Paula A.; Therese Fitzgerald, Therese; Salganicoff, Alina; Wood, Susan F.; Goldstein, Jill M. (3 March 2014). Sex-Specific Medical Research Why Women's Health Can't Wait: A Report of the Mary Horrigan Connors Center for Women's Health & Gender Biology at Brigham and Women's Hospital (PDF). Boston MA: Mary Horrigan Connors Center for Women's Health & Gender Biology.
Systematically report and evaluate women's nutrition outcomes in research and program evaluation documents in low- and middle-income countries, including outcomes for adolescents, older women, and mothers (as opposed to reporting on women's nutrition as child nutrition outcomes alone). When possible, report and evaluate differences by setting (e.g., rural compared with urban) and socioeconomic status.
Interventions resulting in public infrastructure changes were found to be less effective than household-based interventions; however, both are important aspects of improved health outcomes for women (128, 130). Public water infrastructure requires regular maintenance and periodic replacement and water from these sources is often contaminated (130). However, even public water points that provide good-quality water have had minimal impacts on health outcomes (136). One review estimated that water-source interventions were associated with a 27% reduction in diarrhea risk at all ages, whereas household-based interventions were associated with a 43% reduction (128). This could be associated with bias and confounding, as measuring WASH outcomes is not a blinded process (128). The differential impact could also be related to practice. As compared with public water sources, home water connections were associated with greater odds of handwashing and fecal waste disposal (136). As a significant portion of diarrheal disease is a result of person-to-person transmission and poor hygiene, interventions that improve domestic hygiene behaviors can have a significant impact (136). Behavior change communication and resource provision, e.g., soap and point-of-use water treatment resources, were also important and sustainable aspects of WASH interventions (131, 137).
Poor nutrition may be one of the easiest conditions to self-diagnose. Look at the food pyramid and the suggested servings. Look at your diet. Are you getting the recommended daily amounts of fruits and vegetables? Enough calcium? Read the labels and compare what you eat to what you need. You may discover that even if your weight is ideal, you are not getting enough nutrition.
In addition to death occurring in pregnancy and childbirth, pregnancy can result in many non-fatal health problems including obstetrical fistulae, ectopic pregnancy, preterm labor, gestational diabetes, hyperemesis gravidarum, hypertensive states including preeclampsia, and anemia.[34] Globally, complications of pregnancy vastly outway maternal deaths, with an estimated 9.5 million cases of pregnancy-related illness and 1.4 million near-misses (survival from severe life-threatening complications). Complications of pregnancy may be physical, mental, economic and social. It is estimated that 10–20 million women will develop physical or mental disability every year, resulting from complications of pregnancy or inadequate care.[39] Consequently, international agencies have developed standards for obstetric care.[52]
It's full of health, diet, fitness, and inspiring articles. My first issue was 142 pages of wonderfully educational and motivating articles with clear pictures. It's easy to highlight the articles to read. This magazine is ideal for people that are interested in women's health covering all kinds of topics ranging from nutrition to working out and from meditating to parenting. It also includes ads for the latest in skincare products, makeup, gear, and food, which I like so that I know what to shop for. When I need motivated and inspired or need to refocus, this is the magazine I choose!
Delivery platforms for women across the life course. This Venn diagram represents the delivery platforms for different interventions by target population. The overlapping regions indicate delivery platforms that are shared by the target groups: adolescent girls, women of reproductive age, pregnant and lactating women, mothers of young children, and older women.
In the past, women have often tried to make up deficits in their diet though the use of vitamins and supplements. However, while supplements can be a useful safeguard against occasional nutrient shortfalls, they can’t compensate for an unbalanced or unhealthy diet. To ensure you get all the nutrients you need from the food you eat, try to aim for a diet rich in fruit, vegetables, quality protein, healthy fats, and low in processed, fried, and sugary foods.
Breast cancer is the second most common cancer in the world and the most common among women. It is also among the ten most common chronic diseases of women, and a substantial contributor to loss of quality of life (Gronowski and Schindler, Table IV).[6] Globally, it accounts for 25% of all cancers. In 2016, breast cancer is the most common cancer diagnosed among women in both developed and developing countries, accounting for nearly 30% of all cases, and worldwide accounts for one and a half million cases and over half a million deaths, being the fifth most common cause of cancer death overall and the second in developed regions. Geographic variation in incidence is the opposite of that of cervical cancer, being highest in Northern America and lowest in Eastern and Middle Africa, but mortality rates are relatively constant, resulting in a wide variance in case mortality, ranging from 25% in developed regions to 37% in developing regions, and with 62% of deaths occurring in developing countries.[17][122]
Much of the sugar we eat is added to other foods, such as regular soft drinks, fruit drinks, puddings, ice cream and baked goods, to name just a few. Soft drinks and other sugary beverages are the No. 1 offenders in American diets. A 12-ounce can of regular soda contains 8 teaspoons of sugar, exceeding the daily maximum amount recommended for women.
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Trimming some fat may eliminate some guilt, but be warned: Buying foods labeled “low-fat,” “non-fat,” or “fat-free” may encourage you to eat up to 50 percent more calories, according to three studies by Cornell University’s Food and Brand Lab. Fat’s not the issue when it comes your weight since most of these foods only have about 15 percent fewer calories than their regular counterparts. Go for the full-fat version and eat less—you probably will naturally since they taste better.
It's a cliché, to be sure, but a balanced diet is the key to good nutrition and good health. Following that diet, however, isn't always that easy. One challenge is that women often feel too busy to eat healthfully, and it's often easier to pick up fast food than to prepare a healthy meal at home. But fast food is usually high in fat and calories and low in other nutrients, which can seriously affect your health. At the other extreme, a multimillion dollar industry is focused on telling women that being fit means being thin and that dieting is part of good nutrition.
Native to East Asia, soybeans have been a major source of protein for people in Asia for more than 5,000 years. Soybeans are high in protein (more than any other legume) and fiber, low in carbohydrates and are nutrient-dense. Soybeans contain substances called phytoestrogens, which can significantly lower your "bad" LDL cholesterol and raise your "good" HDL cholesterol.
Adopting a plant-based diet could help tip the scales in your favor. A five-year study of 71,751 adults published in the Journal of the Academy of Nutrition and Dietetics found that vegetarians tend to be slimmer than meat-eaters even though both groups eat about the same number of calories daily. Researchers say it may be because carnivores consume more fatty acids and fewer weight-loss promoting nutrients, like fiber, than herbivores do. Go green to find out if it works for you.
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1,833,088,552,376,832,000 | What will mess up a urine test?
What will mess up a urine test?
Today’s drug tests can detect even trace amounts of alcohol, and for longer after exposure. So if you use anything with ethyl alcohol, your breath, blood, or urine sample might get flagged for possible signs of drinking. The same thing could happen even with alcohol-based hand sanitizers if you use them regularly.
What can cause a false negative urine drug test?
False-negatives can occur when the urine drug concentration is below the threshold level set by the laboratory performing the test. Dilute urine, the duration of time between ingestion of the drug and time of testing, and the quantity of the drug ingested may affect the occurrence of false-negatives.
Can urine test be false negative?
Another common reason for getting a false negative is not having enough hCG in the urine you test. In early pregnancy, you can dilute the hormone concentration in your urine if you drink a lot of water before testing. This is more likely to happen in very early pregnancy when you take the test later in the day.
How can I ruin a drug test?
This typically involves the addition of chemicals to a urine specimen to obstruct laboratory analysis of the specimen, or to mask or destroy the drug in the specimen. Common household chemicals used to adulterate a specimen include bleach, salt, vinegar, iodine, eye drops, and liquid hand soap.
Why can’t you wash your hands after a drug test?
“We are not allowed to frisk or search anyone in any way,” Claussen says. This part of the procedure makes it harder for people to smuggle in liquids or other materials that could be used to dilute the sample. – Next, you will be led into a bathroom, where you’ll have to wash your hands with soap.
How common is the hook effect?
The hook effect is uncommon. Researchers suggest that it occurs in 0.2–2% of immunoassays, which are medical laboratory tests that use antibodies to detect specific substances or analytes. Laboratory technicians often use sandwich assays .
How early can the hook effect happen?
“The variant hook effect occurs in women who are more than five weeks pregnant, but the devices were designed originally for supposedly early detection of pregnancy. | {
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-992,331,035,084,954,200 | Menu Close
Why knowing what black mamba venom does to the human body is crucial
Black mamba venom can be lethal. Photograph courtesy Thomas Birkenbach
Black mambas are extremely dangerous reptiles – in fact, many consider the species to be one of the world’s deadliest snakes. They are found in southern and eastern Africa, and are shy, evasive creatures. They won’t seek out human interaction. But if cornered or confronted, they will strike. And their venom is lethal.
Black mambas (don’t let the name fool you – they’re very rarely black, and are more usually a dark brown – it is the inside of the mouth which is black) probably cause the largest number of snake-related deaths in southern Africa. In a recent case, a South African judge died after being bitten by a black mamba while he was travelling in Zambia. But the data for the whole continent is limited, so the precise number isn’t known. This is chiefly because most of these deaths occur in rural parts of Africa with limited health infrastructure and other resources.
Sub-optimal mortuary facilities, inadequate professional manpower, poorly developed protocols and the lack of an efficient and reliable toxicology service means many of these deaths in Africa’s more rural areas are not properly diagnosed. It is most likely that these snakebite victims get buried without a thorough forensic pathological autopsy.
The black mamba is born with two to three drops of venom per fang. It is a front-fanged snake, with fangs up to 6.5 mm in length, located at the front of the upper jaw. An adult of the species has between 12 and 20 drops per fang. It takes just two drops of venom to kill an adult human. This means that even young black mambas are extremely dangerous.
Not much is known about the pathology of trauma of black mamba bites – that is, what the black mamba’s toxin does, physically, inside a victim’s system. We do know that the venom is neurotoxic and cardiotoxic. That means that it has a direct effect on the nerves and the heart.
The more we know, the better. If we know precisely what the toxin does, hospitals and clinics might be better prepared to treat those who’ve been bitten.
A recent case study
Recently my colleagues and I examined the case of a young man who was bitten by a black mamba in South Africa. He arrived at the hospital 20 minutes after being bitten and had already suffered cardiac arrest with accompanying hypoxic brain injury.
This was my third encounter with the victim of a black mamba bite. My first fatal encounter, in 2000, involved a 12-year-old girl who was bitten on the thigh by a black mamba. The second involved a British tourist who was accidentally bitten at a snake park, and who also died.
In this latest case, the co-workers of the young man who died were certain that the snake was a black mamba. This gave us, as forensic pathologists, an excellent opportunity to thoroughly investigate this matter. Oftentimes, the history is scant, with victims unable to properly identify the snake which bit them.
The forensic examination consists of a thorough macroscopic post mortem examination, followed by histological (microscopic) examination and blood tests.
A black mamba’s venom is complex. It interferes with transmission across the motor end-plate, which is where the nerves and muscles connect, so it will result in paralysis. The venom is also cardiotoxic, which means it may have a direct effect on the heart.
How to treat it
So what should you do if you or someone around you is bitten by a black mamba?
The first priority is to transport the victim to an appropriate medical facility as soon as possible. First-aid should focus on maintaining vital functions, such as respiratory support. Keep the victim still and try limit any unnecessary movement. Remove constricting items (for example rings and clothing), especially those close to the bite site.
The first-aid treatment of black mamba bites includes lymphatic retardation with the pressure immobilisation technique – in other words try and wrap a tight crepe bandage or tourniquet close to the bite site.
Medical management comprises continuous monitoring, making sure the airways are open, treating symptoms and the immediate administration of antivenom. The antivenom is injected intravenously because absorption is poor via the muscles. It’s also important not to inject into or around the bite site. In rare instances the victim may be put on extracorporeal membrane oxygenation, which is a way of providing prolonged cardiac and respiratory support to those whose heart and lungs are unable to provide oxygen to the body.
This combination of respiratory support and antivenom may save a person’s life. Over time, the antivenom will ease muscle paralysis and set the victim on the road to recovery.
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3,926,491,327,332,231,000 | How to Avoid Needing to See an Emergency Dentist
Stressed out by debilitating tooth pain? Or maybe an accident affected your teeth and mouth? In this case, consider emergency dental care. Today, most dentists provide this service. Early intervention can help dismiss the pain and prevent complications.
What constitutes a dental emergency? Are there any indicators and symptoms to watch for other than pain?
Let's see what dental emergencies are and how to stop them!
Without question, some dental issues require immediate attention. Since many dentists set aside time for emergencies, it should be easy to obtain treatment when needed. However, not every toothache is an emergency.
Severe injuries to the gums, teeth or face, grave infections or abscesses and loss of a filling or crown are considered dental emergencies. This group also includes:
• Lingering pain or bleeding that arises soon after dental therapy
• Wounds to the tongue, cheeks or lips
• Severe tooth pain brought on by accidents
• Tooth fractures
• Loss of a tooth
• Cracked or chipped teeth
• Facial discomfort
• Lost crowns
For instance, biting on a piece of food that is too firm may result in broken, cracked or knocked out teeth. Sports injuries, car accidents and falls are familiar culprits behind tooth loss. If any of these problems occur, contact a dentist immediately.
In the meantime, there are a few things that can lessen the damage and avoid complications. Let's say the tooth breaks or becomes loose. Leave the tooth inside the mouth until a dentist can examine it.
In the case of a knocked-out tooth, pick it up by the crown without handling its root. Rinse it carefully and position it back into its socket. If this isn't achievable, place it in a container. The dentist may be able to reinsert it and preserve its function.
If one or more teeth happen to become loose due to an injury or auto crash, try to place the teeth back into their original position. Apply a little pressure with the fingers. Visit the dentist on the same day.
Simple ways to prevent dental emergencies
Most dental emergencies are prevented with good hygiene. Simple things, such as brushing and flossing the teeth after every meal, will help keep the mouth healthy. If engaged in contact sports, wear a mouth guard to shield the teeth. Stay away from hard candy, popcorn kernels and other foods that may crack a tooth.
Don't use your teeth to open a bottle, break objects or cut items. Reduce sugar between meals. Purchase a new toothbrush every three months or so, and use mouthwash daily. Preferably, use toothpaste that contains fluoride. Chew sugar-free gum to clean teeth between meals.
If a tooth aches, do not take prescription drugs without consulting a dentist first. Certain medications can worsen symptoms and cause further complications.
Book an appointment with the dentist at least twice a year. Regular checkups can help spot any potential issues that affect tooth health.
Don't wait until a dental emergency to contact your dentist. Remember that prevention is better than treatment.
Request an appointment here: http://www.gatewaydental4u.com or call Gateway Dental at (703) 466-0568 for an appointment in our Ashburn office.
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8,379,383,905,790,904,000 | October 14, 2022,
What Causes Knee Pain?
The Bottom Line:
Did you know that one in four adults’ reports having joint pain? The knee is a commonly injured part of the body because it is a weight-bearing joint, making it is more susceptible to several acute and overuse injuries. This means that anyone can be affected by knee pain - whether you are an athlete who runs, a naturally aging older adult, or someone who walks frequently. But rather than focusing on the symptoms, how do you determine the actual cause of knee pain?
Why It Matters:
Knee pain can be caused by a lot of things, from a direct injury causing trauma to a biomechanical cause. Here are some common reasons people seek help for knee pain:
• Trauma - There is a wide range of ways knees can be injured, most having to do with a rapid movement where someone is twisting, bending, or even falling. These movements can lead to tearing of important stabilizing ligaments or disruption to the menisci. The most important thing to note about traumatic knee injuries is that getting it checked out as quickly as possible is key to preventing long-term complications.
• Overuse - Repetitive motions like walking long distances, climbing stairs, running, and jumping can cause overuse injuries in the knee. Overuse can lead to conditions like IT band syn-drome, patellar tendinitis, or strained ligaments - all causing pain. These conditions are equally as important to seek care for as sudden injuries because the pain in your knee often leads to poor movement patterns and misuse over time, which in turn can cause even more pain or make the problem worse!
• Other Causes - Other causes of knee pain are less common but just as severe and can include referred or radiating pain from the low back or a nerve entrapment near the knee joint. For these conditions, you must keep track of exactly where the pain is located and any other associated symptoms like numbness, weakness, or the feeling of pins and needles.
Next Steps:
Regardless of the type of knee pain you have, it is essential to seek treatment from a movement-based healthcare professional like us! After we determine the cause of your knee pain, we can create a complete treatment plan to help you get back to your favorite activities as quickly as possible.
Request Appointment
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6,521,016,244,172,416,000 | dvt
It is extremely dangerous to fly if you’ve been diagnosed with a DVT in any part of your leg or pelvic area.
In fact, you should never fly even if you have not been officially diagnosed but the suspicion is strong for a deep vein thrombosis.
• One leg has suddenly become swollen.
• It feels unusually warm to the touch in that area.
• It’s reddish or discolored.
• It hurts or feels very sore or crampy.
• These symptoms of a DVT usually occur in the lower leg, but a blood clot can also affect the upper leg, behind the knee and the pelvic region.
Avoid Flying at all Costs if You Have a DVT or Suspect One
“Someone with a known DVT should not fly,” says Walter Gaman, MD, FABFM, board certified in family medicine and the author of several award-winning books including “Age to Perfection: How to Thrive to 100, Happy, Healthy, and Wise.”
“A DVT in an extremity puts someone at risk for a serious and often deadly condition called a pulmonary embolism. That is when a blood clot travels to the lung.”
Here Is How that Works
• You’re sitting there on the plane, snoozing, listening to music, reading or talking.
• The DVT in your leg doesn’t give a hoot. If a piece of the blood clot, or the entire thing, feels like dislodging from the vein in your leg – it’s going to do so.
• Within seconds it travels to the lungs and gets into a pulmonary artery.
• Worse, if the fragmented DVT is big enough, it could block the point where the pulmonary arterial trunk splits off into each lung: a saddle embolism.
• If you get a saddle embolism while flying – you won’t survive it.
• If you get a non-saddle pulmonary embolism while in flight, you might survive it, but don’t bet the house and kids on that. Don’t even bet your child’s piggy bank.
pulmonary embolism
• Between the cabin pressure and the time it would take between landing the plane and getting to the nearest emergency room – suffering a pulmonary embolism while flying is a situation that would be tough to beat.
What About Flying After DVT Treatment?
“If you have been diagnosed and treated for a blood clot, it’s advisable that you not fly again for four to six weeks, once your healthcare provider has cleared you for flight,” says Dr. Gaman.
“Some providers may recommend that future flights only be taken while on prescribed blood thinners or aspirin as a precautionary measure.”
walter gaman, md
Dr. Gaman is a partner at Executive Medicine of Texas and is with the Staying Young Radio Show 2.0 podcast. | {
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7,735,383,091,454,083,000 | What Does the Nerve in the at the C5 and C6 Disc Control?
Answer
The cervical spine c5 and c6 discs control the nerve function of wrist extensors. These nerves are part of the peripheral nervous system, which is complex system used to control muscle and nerve function.
Q&A Related to "What Does the Nerve in the at the C5 and C6..."
Each of the eight cervical nerves controls certain reflexes in upper body. Damage to the C5/C6 nerves can hinder certain flexion and extension movements in the shoulders, arms, wrists
http://www.ehow.com/facts_5935827_c5_c6-nerve-dama...
Between the fith and sixth cervical vertibrae (neck bones) the cartilage disk between them is sticking out a bit to the left. This is most likely pinching the nerve root. This particular
http://wiki.answers.com/Q/What_is_a_small_central_...
The C6 nerve root;
http://www.chacha.com/question/which-cervical-nerv...
Bulges are normal, what you don't want is the bulge turning into a herniation. Even herniations are not that bad unless they impinge on your spinal cord causing numbness, tingling
http://answers.yahoo.com/question/index?qid=200607...
Explore this Topic
C5-C6 bulging discs are a very serious condition, as this can often pinch nerves in the spine. Symptoms can include pain in the neck. It can also lead to pain, ...
About - Privacy - AskEraser - Careers - Ask Blog - Mobile - Help - Feedback © 2014 Ask.com | {
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"rps_doc_openwebtext_importance_length_correction": -70.73676300048828,
"rps_doc_wikipedia_importance": -46.45110321044922,
"rps_doc_wikipedia_importance_length_correction": -42.6842155456543
},
"fasttext": {
"dclm": 0.2078816294670105,
"english": 0.8742220401763916,
"fineweb_edu_approx": 2.959885597229004,
"eai_general_math": 0.10845602303743362,
"eai_open_web_math": 0.4197389483451843,
"eai_web_code": 0.004551469814032316
}
} | {
"free_decimal_correspondence": {
"primary": {
"code": "612.82",
"labels": {
"level_1": "Industrial arts, Technology, and Engineering",
"level_2": "Medicine",
"level_3": "Physiology"
}
},
"secondary": {
"code": "617.1",
"labels": {
"level_1": "Industrial arts, Technology, and Engineering",
"level_2": "Medicine",
"level_3": "Surgery and Dentistry"
}
}
},
"bloom_cognitive_process": {
"primary": {
"code": "2",
"label": "Understand"
},
"secondary": {
"code": "3",
"label": "Apply"
}
},
"bloom_knowledge_domain": {
"primary": {
"code": "1",
"label": "Factual"
},
"secondary": {
"code": "2",
"label": "Conceptual"
}
},
"document_type_v1": {
"primary": {
"code": "3",
"label": "Reference/Encyclopedic/Educational"
},
"secondary": {
"code": "-1",
"label": "Abstain"
}
},
"extraction_artifacts": {
"primary": {
"code": "3",
"label": "Irrelevant Content"
},
"secondary": {
"code": "0",
"label": "No Artifacts"
}
},
"missing_content": {
"primary": {
"code": "1",
"label": "Truncated Snippets"
},
"secondary": {
"code": "4",
"label": "Missing Images or Figures"
}
},
"document_type_v2": {
"primary": {
"code": "18",
"label": "Q&A Forum"
},
"secondary": {
"code": "10",
"label": "Knowledge Article"
}
},
"reasoning_depth": {
"primary": {
"code": "2",
"label": "Basic Reasoning"
},
"secondary": {
"code": "1",
"label": "No Reasoning"
}
},
"technical_correctness": {
"primary": {
"code": "3",
"label": "Mostly Correct"
},
"secondary": {
"code": "2",
"label": "Partially Correct"
}
},
"education_level": {
"primary": {
"code": "1",
"label": "General Audience"
},
"secondary": {
"code": "2",
"label": "High School Level"
}
}
} | b755ed28a90d11d590ef646404f4afc5 |
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