Archive for the ‘Medicine’ Category
The proteins, lipids, and polysaccharides that make up most of the food we eat must be broken down into smaller molecules before our cells can use them either as a source of energy or as building blocks for other molecules. The breakdown processes must act on food taken in from outside, but not on the macromolecules inside our own cells. The enzymatic breakdown of food molecules is therefore digestion, which occurs either in our intestine outside cells, or in a specialized organelle within cells; the lysosome. A membrane that surrounds the lysosome keeps its digestive enzymes separated from the cytosol. In either case, the large polymeric molecules in food are broken down during digestion into their monomer subunits—proteins into amino acids, polysaccharides into sugars, and fats into fatty acids and glycerol through the action of enzymes. After digestion, the small organic molecules derived from food enter the cytosol of the cell, where their gradual oxidation begins. Oxidation occurs in two further stages of cellular catabolism. Stage 2 starts in the cytosol and ends in the major energy-converting organelle, the mitochondrion; stage 3 is entirely confined to the mitochondrion.
In stage 2 a chain of reactions called glycolysis converts each molecule of glucose into two smaller molecules of pyruvate. Sugars other than glucose are similarly converted to pyruvate after their conversion to one of the sugar intermediates in this glycolytic pathway. During pyruvate formation, two types of activated carrier molecules are produced; adenosine-5′-triphosphate and nicotinamide adenine dinucleotide. The pyruvate then passes from the cytosol into mitochondria. There, each pyruvate molecule is converted into carbon dioxide plus a two-carbon acetyl group; which becomes attached to coenzyme A, forming acetyl coenzyme A, another activated carrier molecule. Large amounts of acetyl coenzyme A are also produced by the stepwise breakdown and oxidation of fatty acids derived from fats, which are carried in the bloodstream, imported into cells as fatty acids, and then moved into mitochondria for acetyl coenzyme A production.
Stage 3 of the oxidative breakdown of food molecules takes place entirely in mitochondria. The acetyl group in acetyl coenzyme A is linked to coenzyme A through a high-energy linkage, and it is therefore easily transferable to other molecules. After its transfer to the four-carbon molecule oxaloacetate, the acetyl group enters a series of reactions called the citric acid cycle. The acetyl group is oxidized to carbon dioxide in these reactions, and large amounts of the electron carrier nicotinamide adenine dinucleotide are generated. Finally, the high-energy electrons from nicotinamide adenine dinucleotide are passed along an electron-transport chain within the mitochondrial inner membrane, where the energy released by their transfer is used to drive a process that produces adenosine-5′-triphosphate and consumes molecular oxygen. It is in these final steps that most of the energy released by oxidation is harnessed to produce most of the cell’s adenosine-5′-triphosphate.
Because the energy to drive adenosine-5′-triphosphate synthesis in mitochondria ultimately derives from the oxidative breakdown of food molecules, the phosphorylation of adenosine diphosphate to form adenosine-5′-triphosphate that is driven by electron transport in the mitochondrion is known as oxidative phosphorylation. Fascinating events occur within the mitochondrial inner membrane during oxidative phosphorylation. Through the production of adenosine-5′-triphosphate, the energy derived from the breakdown of sugars and fats is redistributed as packets of chemical energy in a form convenient for use elsewhere in the cell. Roughly, 109 molecules of adenosine-5′-triphosphate are in solution in a typical cell at any instant, and in many cells, all this adenosine-5′-triphosphate is turned over, that is, used up and replaced every 1–2 minutes.
In all, nearly half of the energy that could in theory be derived from the oxidation of glucose or fatty acids to water and carbon dioxide is captured and used to drive the energetically unfavorable reaction orthophosphate plus adenosine diphosphate giving adenosine-5′-triphosphate. By contrast, a typical combustion engine, such as a car engine, can convert no more than 20% of the available energy in its fuel into useful work. The rest of the energy is released by the cell as heat, making our bodies warm.
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Reduced sleep is linked with increase in body mass index in adolescents aged 14-18 years, particularly in heavier adolescents, according to a new study. Those who sleep an extra hour or more a night could lower their body mass index and so prevent overweight and obesity.
Physical inactivity and increased caloric intake explains the connection between short sleep and adolescent obesity. Short sleepers could be more exhausted during the daytime and spend less time being physically active. It is possible that short sleep add to total caloric intake due to more eating opportunities.
Short sleep affects hormones that regulate appetite and energy homeostasis. Such hormonal changes explain why there is an association between short sleep and adolescent obesity. An extra hour of sleep is associated with only a slight reduction in BMI at the 10th percentile. In comparison, greater reductions in BMI are observed at the 50th and 90th percentiles.
Increasing sleep from 8 to 10 hours per day at age 18 years result in a 4% reduction in the number of adolescents with a BMI higher than 25 kilograms per meter squared. The relationship between disturbed circadian rhythms and weight gain is well documented in animal models. However, it is not known if these findings in animals translate to humans, and thus more research is desirable to determine if staying awake at night and eating at night is associated with adolescent obesity.
Primary care physicians should advise adolescent patients to adopt good sleep hygiene practices, such as establish routine bed and wake times each day, associate the bedroom with sleep and not television viewing, and increase physical activity during the daytime.
Primary care physicians and other health care professionals could lend their support to changes in policies that would help support longer sleep duration among adolescents, for example, later high school start times and more physical education classes to increase daytime physical activity.
Achieving sufficient sleep needs should center on healthier eating, being more physically active, and creditability to the significance of sufficient sleep duration.
Credits: Dr Mitchell.
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You may think you know yourself like the back of your hand, but unless you’ve been DNA tested, there’s probably a lot you don’t know about yourself. Within each of the 50 trillion cells in your body rests the microscopic DNA that programs your entire being; your hair color, your height, your freckles or lack thereof, your likelihood of developing cancer and whether or not you can taste cilantro. Nevertheless, few people in their lifetime have actually unlocked this information via DNA mapping. For starters, it used to be quite expensive. Some might not even realize they have access to this information, while others simply might want to know what their DNA has in store for them as life unfolds.
Crushing these barriers is Anne Wojcicki’s 23andMe, a $99 DNA testing kit that requires just a few milliliters of spit. That’s it, no blood tests or pesky skin pricks. Eight weeks after mailing the kit back, you’ll receive a full genetic report that outlines your health risks and ancestry. During those two months, the scientists in 23andMe’s lab extract DNA from the cells in your spit and amplify the DNA so they have enough to work with. From there, the DNA is genotyped, yielding your unique report of what makes you, you. To get the full picture of their ancestry, though, women need to have their father or brother take the test; while everyone has mitochondrial DNA, paternal DNA is passed along through the Y chromosome, which women don’t have.
Thus far, more than 200,000 users have been genotyped via 23andMe, and 90% of those have opted to participate in the company’s research efforts. Each survey question counts as a data point, and to date, 23andMe has collected more than 100 million data points, with 2 million more coming each week. The company’s in-house research has studied life-threatening sarcomas, Parkinson’s disease and diabetes, as well as lighter topics; unibrows and why Shar-Pei dogs are so wrinkly.
With an eye toward revolutionizing health care, the company raised 50 million dollars last year to drop the price of the kits from $999 to $99 and dramatically grow its database. In her blog post about the price drop, Wojcicki writes, "This change is not just about a new price point for personal genetic testing. It is about an ambitious plan that could transform medicine for generations to come."
Would you do the test, if it revealed that you have an increased risk for Parkinson’s disease or lung cancer? People have strong opinions either way, but knowledge is power. It is very holistic to empower people with their genetic information. You, the individual, don’t have a voice in the system. You’re talked about as a human subject, with no agency in the health care system. You’re simply told what you’re going to get, and it’s often dictated by your insurance company.
The industry is filled with really, really good people who want to make a difference in health care, but the system is set up in such a way that we really don’t have optimal health care. Take Type 2 Diabetes, for example. It’s a preventable disease, but no one makes money until you actually develop diabetes and need to buy insulin and testing strips. The system is set up so they make tons of money once you’re diabetic, but if you don’t develop diabetes, no one makes money. This is a fundamental flaw in the system.
Because your genotype outlines your risks for developing various diseases and disorders, health care could one day focus on prevention. Patients would rather prevent a disease than treat it effectively, but in today’s system, doctors are taught how to treat various conditions, not prevent them altogether. Public should be empowered with their genetic information. It is really important information about your health, really fascinating information about your ancestry, and the aggregate data of having millions and millions of people together will create this incredibly powerful database that’s going to filter back to you and give you more information about you and make you healthier.
Interestingly, health care reform has piqued insurance companies’ interest in prevention, because understanding your genetics could keep you healthier and prevent complications and costly side effects. But while insurance companies may want this information, it is firmly protected by federal law, and that the information in essence, your identity, should be controlled by the individual at this point in time.
Though 23andMe has been around since 2006, its growth and database have skyrocketed since the $99 price point was introduced. With more people in the database, the company can provide a fuller user experience and tell you more about what your genes mean. What company is really focused on is growth right now. As the customer base grows, so too do the volume of emotional stories. 23andMe saved many lives and having your genetic information will revolutionize things for you.
Wojcicki has a degree in biology from Yale, her father is a particle physicist, and she grew up on Stanford’s campus, going to particle physics meetings and listening to people who want to challenge Einstein’s theories. The particle physicist community is a really fabulous community, and they’re really about the pursuit of science for the sake of science and pursuit of truth. It’s not a commercial entity, and I have a huge respect for them because they’re really passionate about what they do.
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Focusing on nutrition and lifestyle, Yale knows that the causes of the rise in obesity include the overconsumption of processed foods and sugar, too few nutrient-dense foods and too-large portion sizes, as well as stress, a sedentary lifestyle, sleep disturbances, not getting enough exercise, metabolic factors, and even environmental toxins. Now, a new study by scientists from Yale University School of Medicine has taken on the challenge to answer the question from a biological standpoint: Where does all that fat come from?
The results were published online in the journal Nature Cell Biology on Feb. 24. The National Institutes of Health funded the study.
Our body stores fat in adipose cells, which collect the fat from the foods we eat, making them available when we need energy. Surrounding our internal organs and found under the skin, adipose cells help cushion the body and keep it warm. When we consume more energy than we burn, adipose cells accumulate excess fat and increase in size.
Since lipid-laden mature adipocytes cannot divide, the increase in cell number in obesity must come from differentiation of precursor cells in the tissue. Using a process called differentiation, Rodeheffer and Ryan Berry isolated cells from fat and studied which ones could turn into fat cells. The scientists identified cells in mice with certain types of receptors on their surface that eventually transformed into white adipocytes, what most people recognize as fat.
The proliferation in recent decades of obesity and other related health problems, like type II diabetes, in the U.S. and other developed countries emphasizes the importance of determining how the body normally regulates fat mass is and how the process changes in obesity. Scientists will now be able study how these cells act under various conditions, such as during dieting, exercise or overeating.
Despite the high incidence of obesity and the health risks associated with it, our understanding of the basic biology of fat tissue is limited. According to Yale News, the scientists hope to discover what causes the precursors to make new fat cells in obesity and one day potentially block their creation. Yale School of Medicine scientists have answered a question millions regularly and plaintively ask themselves: Where did all that fat come from? The research paper, published online Feb. 24 in the journal Nature Cell Biology, identifies specific cell types that eventually transform into white adipocytes—the cells most people recognize as fat.
We can go back into the lab and ask how these cells are activated to actually make the fat says co-author Matthew Rodeheffer, assistant professor of comparative medicine and molecular, cellular, and developmental biology, and a researcher at the Yale Stem Cell Center. The increase of fat cells in obesity is particularly problematic because once established the cells are difficult to eliminate.
Scientists approached the dilemma by isolating cells from fat and studying which cells could turn into fat cells, by means of a process known as differentiation. They successfully identified cells with certain types of receptors that could in fact become fat cells. The new study in mice confirmed that cells with these specific receptors on their surface are the precursors that create fat cells in the body.
It is now possible to study how these cells behave under different conditions, such as exercise, dieting, or overeating. The scientists hope to discover what causes the precursors to make new fat cells in obesity and one day possibly in the future hinder their formation.
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Almost all women experience some nausea or vomiting when pregnant. Approximately one out of every hundred suffers from acute nausea during pregnancy called hyperemesis gravidarum and may need hospital treatment to restore hydration, electrolytes and vitamins intravenously.
English: Catherine, Duchess of Cambridge, on her first royal tour, visiting Ottawa for Canada Day celebrations. (Photo credit: Wikipedia)
At worst, women may die if they go untreated. “Many women find that the condition has an adverse effect on their work and family lives," says Åse Vikanes, senior researcher at the Norwegian Institute of Public Health and specialist in Gynecology and Obstetrics.
Making up for insufficient research activity Hyperemesis came under the spotlight earlier this winter when Kate, the Duchess of Cambridge, was hospitalized because of it. But research projects on this illness have been few and far between. When Dr Vikanes completed her doctoral degree in 2010 with funding from the Research Council of Norway, her thesis was the first in this field in Norway in 70 years.
Severe nausea during pregnancy is a relatively common affliction among women and even so it has been difficult to win understanding for the need for research. Not too many years ago, people sincerely believed that the cause could be the woman’s subconscious rejection of the child and the child’s father. The attitude in part has been that the pregnant woman needs to pull herself together. The real cause behind severe nausea during pregnancy remains unknown and looks to be complex. But there is little to support the idea that the explanation is psychological.
Both hormones and genetics involved. Several studies have shown that elevated levels of estrogen and the pregnancy hormone, human chorionic gonadotropin, may be involved. The likelihood is that hormonal, genetic and socio-economic factors all play a part. There is wide ethnic diversity in the occurrence of hyperemesis. In addition, the risk is higher among women whose mothers suffered from the syndrome. Non-smokers with a BMI that is higher or lower than the norm also show a higher tendency to experience severe nausea during pregnancy, whereas smoking appears to provide protection from the nausea. The occurrence of hyperemesis also varies with the mother’s age and the gender of the fetus, with younger mothers carrying baby girls at the greatest risk.
Dr Vikanes and her colleagues are now working to identify more risk factors linked to hyperemesis and to examine possible consequences of the condition on mother and child. Recent research has actually shown that the mother’s diet during pregnancy may be significant to the health of the child later in life.
Dr Vikanes is also involved in projects examining the impact of nutrition, physical activity and what can be referred to as "candidate genes". Candidate genes are genes that may cause an individual to be predisposed to illness – in this case, hyperemesis. We need to learn more about this so we can help women who suffer from this condition to get better treatment.
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