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While some research suggests that a diet high in omega-3 fatty acids can protect brain health, a large clinical trial by researchers at the National Institutes of Health found that omega-3 supplements did not slow cognitive decline in older persons. With 4,000 patients followed over a five-year period, the study is one of the largest and longest of its kind. It was published today in the Journal of the American Medical Association. “Contrary to popular belief, we didn’t see any benefit of omega-3 supplements for stopping cognitive decline,” said Emily Chew, M.D., . Dr. Chew leads the Age-Related Eye Disease Study (AREDS), which was designed to investigate a combination of nutritional supplements for slowing age-related macular degeneration (AMD), a major cause of vision loss among older Americans. That study established that daily high doses of certain antioxidants and minerals — called the AREDS formulation — can help slow the progression to advanced AMD. A later study, called AREDS2, tested the addition of omega-3 fatty acids to the AREDS formula. But the omega-3’s made no difference. Omega-3 fatty acids are made by marine algae and are concentrated in fish oils; they are believed to be responsible for the health benefits associated with regularly eating fish, such as salmon, tuna, and halibut.*Where studies have surveyed people on their dietary habits and health, they’ve found that regular consumption of fish is associated with lower rates of AMD, cardiovascular disease, and possibly dementia. “We’ve seen data that eating foods with omega-3 may have a benefit for eye, brain, and heart health,” Dr. Chew explained.
Link ID: 21340 - Posted: 08.26.2015
By Michelle Roberts Health editor, BBC News online People genetically prone to low vitamin-D levels are at increased risk of multiple sclerosis, a large study suggests. The findings, based on the DNA profiles of tens of thousands of people of European descent, add weight to the theory that the sunshine vitamin plays a role in MS. Scientists are already testing whether giving people extra vitamin D might prevent or ease MS. Experts say the jury is still out. It is likely that environmental and genetic factors are involved in this disease of the nerves in the brain and spinal cord, they say. And if you think you may not be getting sufficient vitamin D from sunlight or your diet, you should discuss this with your doctor. Taking too much vitamin D can also be dangerous. Research around the world already shows MS is more common in less sunny countries, further from the equator. But it is not clear if this relationship is causal - other factors might be at play. To better understand the association, investigators at McGill University in Canada compared the prevalence of MS in a large group of Europeans with and without a genetic predisposition to low vitamin D. © 2015 BBC.
Keyword: Multiple Sclerosis
Link ID: 21339 - Posted: 08.26.2015
By Laura Sanders By tweaking a single gene, scientists have turned average mice into supersmart daredevils. The findings are preliminary but hint at therapies that may one day ease the symptoms of such disorders as Alzheimer’s disease and schizophrenia, scientists report August 14 in Neuropsychopharmacology. The altered gene provides instructions for a protein called phosphodiesterase-4B, or PDE4B, which has been implicated in schizophrenia. It’s too early to say whether PDE4B will turn out to be a useful target for drugs that treat these disorders, cautions pharmacologist Ernesto Fedele of the University of Genoa in Italy. Nonetheless, the protein certainly deserves further investigation, he says. The genetic change interfered with PDE4B’s ability to do its job breaking down a molecular messenger called cAMP. Mice designed to have this disabled form of PDE4B showed a suite of curious behaviors, including signs of smarts, says study coauthor Alexander McGirr of the University of British Columbia. Compared with normal mice, these mice more quickly learned which objects in a cage had been moved to a new location, for instance, and could better recognize a familiar mouse after 24 hours. “The system is primed and ready to learn, and it doesn’t require the same kind of input as a normal mouse,” McGirr says. These mice also spent more time than usual exploring brightly lit spaces, spots that normal mice avoid. But this devil-may-care attitude sometimes made the “smart” mice blind to risky situations. The mice were happy to spend time poking around an area that had been sprinkled with bobcat urine. “Not being afraid of cat urine is not a good thing for a mouse,” McGirr says. © Society for Science & the Public 2000 - 2015
By Jessica Schmerler In the modern age of technology it is not uncommon to come home after a long day at work or school and blow off steam by reading an e-book or watching television. Lately, however, scientists have been cautioning against using light-emitting devices before bed. Why? The light from our devices is “short-wavelength-enriched,” meaning it has a higher concentration of blue light than natural light—and blue light affects levels of the sleep-inducing hormone melatonin more than any other wavelength. Changes in sleep patterns can in turn shift the body’s natural clock, known as its circadian rhythm. Recent studies have shown that shifts in this clock can have devastating health effects because it controls not only our wakefulness but also individual clocks that dictate function in the body’s organs. In other words, stressors that affect our circadian clocks, such as blue-light exposure, can have much more serious consequences than originally thought. How did you become interested in the effects of light on sleep? Brainard: I was interested in the effects of light on animals as a teenager. I never planned to be a scientist—I wanted to be a writer! So I learned more about the topic out of pure curiosity. When I began my career as a journalist, I interviewed researchers on the topic who encouraged me to pursue a career in science. So I returned to school to get my doctorate and studied the effects of different wavelengths and intensities of light on rodents. I have exclusively studied the effects of light on humans for the past 30 years. © 2015 Scientific American
A placebo can make you feel a little better – and now we know how to boost the effect. Drugs based on hormones that make us more cooperative seem to enhance the placebo effect. The finding could lead to changes in the way some trials are performed. Sometimes a sugar pill can be all you need, even when you know it doesn’t contain any medicine. We’re still not entirely sure why. The brain’s natural painkillers, such as dopamine and opioids, seem to be involved, but other factors may be at work too. Evidence that a compassionate, trustworthy carer can speed recovery suggests that there is also a social dimension to the placebo effect. “This interaction between the patient and care provider seems to be based on a more complex system,” says Luana Colloca at the University of Maryland in Baltimore. Hormones that modulate our social behaviour might play a role. Last year, a team led by Ulrike Bingel of the University Duisburg-Essen in Germany, found that oxytocin – the so-called “cuddle chemical” that is thought to help us trust, bond and form relationships – seems to boost the placebo effect, at least in men. In the study, Bingel’s team applied an inert ointment to the arms of male volunteers. Half of them were told that the cream would reduce the degree of pain caused by the painfully hot stimulus subsequently applied. Men who were told that they were receiving pain relief said that the heat was less painful than those who knew that the cream was inert. When oxytocin was squirted up volunteers’ noses, the men reported being in even less pain. The team didn’t test oxytocin in women. © Copyright Reed Business Information Ltd.
Aaron E. Carroll If there is one health myth that will not die, it is this: You should drink eight glasses of water a day. It’s just not true. There is no science behind it. And yet every summer we are inundated with news media reports warning that dehydration is dangerous and also ubiquitous. These reports work up a fear that otherwise healthy adults and children are walking around dehydrated, even that dehydration has reached epidemic proportions. Let’s put these claims under scrutiny. I was a co-author of a paper back in 2007 in the BMJ on medical myths. The first myth was that people should drink at least eight 8-ounce glasses of water a day. This paper got more media attention (even in The Times) than pretty much any other research I’ve ever done. It made no difference. When, two years later, we published a book on medical myths that once again debunked the idea that we need eight glasses of water a day, I thought it would persuade people to stop worrying. I was wrong again. Many people believe that the source of this myth was a 1945 Food and Nutrition Board recommendation that said people need about 2.5 liters of water a day. But they ignored the sentence that followed closely behind. It read, “Most of this quantity is contained in prepared foods.” Water is present in fruits and vegetables. It’s in juice, it’s in beer, it’s even in tea and coffee. Before anyone writes me to tell me that coffee is going to dehydrate you, research shows that’s not true either. Although I recommended water as the best beverage to consume, it’s certainly not your only source of hydration. You don’t have to consume all the water you need through drinks. You also don’t need to worry so much about never feeling thirsty. The human body is finely tuned to signal you to drink long before you are actually dehydrated. © 2015 The New York Times Company
Link ID: 21335 - Posted: 08.25.2015
By Esther Landhuis The birth of a child leaves its mark on the brain. Most investigations of these changes have focused on mothers, but scientists have recently begun looking more closely at fathers. Neural circuits that support parental behaviors appear more robust in moms a few weeks after the baby is born, whereas in dads the growth can take several months. A study in Social Neuroscience analyzed 16 dads several weeks after their baby's birth and again a few months later. At each check, the researchers administered a multiple-choice test to check for signs of depression and used MRI to image the brain. Compared with the earlier scans, MRI at three to four months postpartum showed growth in the hypothalamus, amygdala and other regions that regulate emotion, motivation and decision making. Furthermore, dads with more growth in these brain areas were less likely to show depressive symptoms, says first author Pilyoung Kim, who directs the Family and Child Neuroscience Lab at the University of Denver. Although some physiological brain changes are similar in new moms and dads, other changes seem different and could relate to the roles of each parent, says senior author James Swain, a psychiatrist at the University of Michigan (brain diagrams below). A 2014 behavioral study of expectant fathers showed that midpregnancy ultrasound imaging was a “magic moment” in the dads' emerging connection with their baby. Yet the emotional bond was different than it is in expectant moms. Instead of thinking about cuddling or feeding the baby, dads-to-be focused on the future: they imagined saving money for a college fund or walking down the aisle at their daughter's wedding. © 2015 Scientific American
By JOAN RAYMOND Rita Gunther McGrath, a Columbia Business School professor, is one of those business travelers who do not care about delays, cancellations or navigating a new location. What does concern her is the seeming inability to conquer jet lag, and the accompanying symptoms that leave her groggy, unfocused and feeling, she says, “like a dishrag.” “Jet lag has always been an issue for me,” says Ms. McGrath, who has been a business traveler for more than two decades and has dealt with itineraries that take her from New York to New Zealand to Helsinki to Hong Kong all within a matter of days. She has scoured the Internet for “jet lag cures,” and has tried preventing or dealing with the misery by avoiding alcohol, limiting light exposure or blasting her body with sunlight and “doing just about anything and everything that experts tell you to do,” Ms. McGrath said. “Jet lag is not conducive to the corporate environment,” she said. “There has to be some kind of help that actually works for those of us that travel a lot, but I sure can’t find it.” Although science is closer to understanding the basic biological mechanisms that make many travelers feel so miserable when crossing time zones, research has revealed that, at least for now, there is no one-size fits-all recommendation for preventing or dealing with the angst of jet lag. Recommendations to beat jet lag include adjusting sleep schedules, short-term use of medications to sleep or stay awake, melatonin supplements and light exposure timing, among others, said Col. Ian Wedmore, an emergency medicine specialist for the Army. © 2015 The New York Times Company
Keyword: Biological Rhythms
Link ID: 21333 - Posted: 08.25.2015
By Hanae Armitage The libido enhancement drug flibanserin (trade name Addyi) took center stage last week after winning long-sought approval from the U.S. Food and Drug Administration (FDA). The coverage from advocates and nonbelievers has run the gamut—advice, caution, and criticism likely to confuse undecided—but curious—onlookers. But exactly how Addyi drums up sex drive is still murky. The drug has a long backstory. It was originally investigated in 1995 by pharmacologist Franco Borsini and a team of researchers at Boehringer Ingelheim Italia in Milan as an antidepressant because of its ability to regulate neurotransmitters—the brain’s chemical-signaling molecules. In particular, the team suspected that the drug regulated three key neurotransmitters thought to influence mood: serotonin, dopamine, and norepinephrine. A clinical trial found it did little to alleviate depression, but did seem to have an effect on mood. It just wasn’t the mood the researchers were expecting. These early trials tipped clinicians to flibanserin’s more prominent role in sexual health, as female subjects had higher scores on the Arizona Sexual Experience Scale, a survey that asks participants to rate their satisfaction on a variety of sexual health topics, like how often participants felt sexual desire and how intense that desire was. A separate group of researchers, also at Boehringer Ingelheim, completed their first clinical trials to explore flibanserin as a libido-enhancer in 2008. They measured levels of desire through a journal-based evaluation in which subjects recorded their levels of sexual drive on a daily basis. But FDA twice concluded that the resulting increases in libido were not statistically significant, and regulators were wary of potentially dangerous side effects like dizziness, sleepiness, nausea, and fainting. © 2015 American Association for the Advancement of Science
Keyword: Sexual Behavior
Link ID: 21332 - Posted: 08.25.2015
By NINA STROHMINGER and SHAUN NICHOLS WHEN does the deterioration of your brain rob you of your identity, and when does it not? Alzheimer’s, the neurodegenerative disease that erodes old memories and the ability to form new ones, has a reputation as a ruthless plunderer of selfhood. People with the disease may no longer seem like themselves. Neurodegenerative diseases that target the motor system, like amyotrophic lateral sclerosis, can lead to equally devastating consequences: difficulty moving, walking, speaking and eventually, swallowing and breathing. Yet they do not seem to threaten the fabric of selfhood in quite the same way. Memory, it seems, is central to identity. And indeed, many philosophers and psychologists have supposed as much. This idea is intuitive enough, for what captures our personal trajectory through life better than the vault of our recollections? But maybe this conventional wisdom is wrong. After all, the array of cognitive faculties affected by neurodegenerative diseases is vast: language, emotion, visual processing, personality, intelligence, moral behavior. Perhaps some of these play a role in securing a person’s identity. The challenge in trying in determine what parts of the mind contribute to personal identity is that each neurodegenerative disease can affect many cognitive systems, with the exact constellation of symptoms manifesting differently from one patient to the next. For instance, some Alzheimer’s patients experience only memory loss, whereas others also experience personality change or impaired visual recognition. The only way to tease apart which changes render someone unrecognizable is to compare all such symptoms, across multiple diseases. And that’s just what we did, in a study published this month in Psychological Science. © 2015 The New York Times Company
Link ID: 21331 - Posted: 08.24.2015
Jon Hamilton More than 50 million adults in the U.S. have a disorder such as insomnia, restless leg syndrome or sleep apnea, according to an Institute of Medicine report. And it's now clear that a lack of sleep "not only increases the risk of errors and accidents, it also has adverse effects on the body and brain," according to Charles Czeisler, chief of the division of sleep and circadian disorders at Brigham and Women's hospital in Boston. Research in the past couple of decades has shown that a lack of sleep increases a person's risk for cardiovascular disease, diabetes, infections, and maybe even Alzheimer's disease. Yet most sleep disorders go untreated. Michael Arnott, of Cambridge, Massachusetts, says he used to have terrible trouble staying awake on long drives. Sleep specialists discovered he has obstructive sleep apnea, though not for the most common reasons — he isn't overweight, and doesn't smoke or take sedatives. "I would get groggy and feel like I've got to keep talking, open the window," Arnott says. His wife, Mary White, says being a passenger on those drives could be scary. "All of a sudden there'd be a change in the speed and I'd look over, and his eyes would be starting to close," she remembers. White thought her husband might have sleep apnea, which interferes with breathing. But Arnott was in denial. He figured he was free of most risk factors for apnea. He wasn't overweight, he didn't smoke or take sedatives, and he has always stayed in great shape. So his wife took the initiative. "I asked him to see a doctor and he wouldn't," she says. In 2012, though, White persuaded him to take part in a sleep research study that paid for his participation, and took place at a sleep lab in Boston –not too far from the couple's home in Cambridge. © 2015 NPR
Link ID: 21330 - Posted: 08.24.2015
Richard A. Friedman THANKS to Caitlyn Jenner, and the military’s changing policies, transgender people are gaining acceptance — and living in a bigger, more understanding spotlight than at any previous time. We’re learning to be more accepting of transgender individuals. And we’re learning more about gender identity, too. The prevailing narrative seems to be that gender is a social construct and that people can move between genders to arrive at their true identity. But if gender were nothing more than a social convention, why was it necessary for Caitlyn Jenner to undergo facial surgeries, take hormones and remove her body hair? The fact that some transgender individuals use hormone treatment and surgery to switch gender speaks to the inescapable biology at the heart of gender identity. This is not to suggest that gender identity is simply binary — male or female — or that gender identity is inflexible for everyone. Nor does it mean that conventional gender roles always feel right; the sheer number of people who experience varying degrees of mismatch between their preferred gender and their body makes this very clear. In fact, recent neuroscience research suggests that gender identity may exist on a spectrum and that gender dysphoria fits well within the range of human biological variation. For example, Georg S. Kranz at the Medical University of Vienna and colleagues elsewhere reported in a 2014 study in The Journal of Neuroscience that individuals who identified as transsexuals — those who wanted sex reassignment — had structural differences in their brains that were between their desired gender and their genetic sex. © 2015 The New York Times Company
Keyword: Sexual Behavior
Link ID: 21329 - Posted: 08.24.2015
By Kazi Stastna The U.S. approval of a pill to treat low libido in women has whipped up a whirlwind of debate and raised questions about whether the so-called female Viagra addresses the real reasons for lack of sexual desire. The U.S. Food and Drug Administration last week approved flibanserin, to be sold under the name Addyi starting in October, for the treatment of hypoactive sexual desire disorder (HSDD) among premenopausal women — some two decades after Viagra was approved for the treatment of male erectile dysfunction. Sprout Pharmaceuticals pitched flibanserin as a drug that would finally give women with sexual dysfunction similar treatment options to men and bused dozens of women to FDA hearings in Maryland to attest to its benefits and plead for its approval in what some saw as a heavy-handed and misleading public relations campaign. The FDA gave flibanserin the OK after twice rejecting it and despite concerns about its risks and modest efficacy because it said women suffering distress from low libido have an "unmet medical need." Days after it did, Canadian pharmaceutical company Valeant offered to buy Sprout for $1 billion US and said it will apply to get flibanserin approved in Canada and other countries. Although often likened to Viagra, flibanserin was created as an antidepressant and works on the brain while erectile dysfunction medications stimulate blood flow to the penis. Critics argue it's an ineffectual pharmacological solution for a problem better treated with relationship counselling, sex therapy and behavioural changes. "Their suffering is real, but the women who testified had a lot of different stories, and some of those stories were very good reasons for having low libido, including having six children, having a one-year-old, having had breast cancer treatment …," says Adriane Fugh-Berman, associate professor of pharmacology and physiology at Georgetown University in Washington, D.C., and director of PharmedOut, a pharmaceutical marketing watchdog group. ©2015 CBC/Radio-Canada.
Keyword: Sexual Behavior
Link ID: 21328 - Posted: 08.24.2015
Mo Costandi The human brain can be compared to something like a big, bustling city. It has workers, the neurons and glial cells which co-operate with each other to process information; it has offices, the clusters of cells that work together to achieve specific tasks; it has highways, the fibre bundles that transfer information across long distances; and it has centralised hubs, the densely interconnected nodes that integrate information from its distributed networks. Like any big city, the brain also produces large amounts of waste products, which have to be cleared away so that they do not clog up its delicate moving parts. Until very recently, though, we knew very little about how this happens. The brain’s waste disposal system has now been identified. We now know that it operates while we sleep at night, just like the waste collectors in most big cities, and the latest research suggests that certain sleeping positions might make it more efficient. Waste from the rest of the body is cleared away by the lymphatic system, which makes and transports a fluid called lymph. The lymphatic system is an important component of the immune system. Lymph contains white blood cells that can kill microbes and mop up their remains and other cellular debris. It is carried in branching vessels to every organ and body part, and passes through them, via the spaces between their cells, picking up waste materials. It is then drained, filtered, and recirculated. The brain was thought to lack lymphatic vessels altogether, and so its waste disposal system proved to be far more elusive. Several years ago, however, Maiken Nedergaard of the University of Rochester Medical Center and colleagues identified a system of hydraulic “pipes” running alongside blood vessels in the mouse brain. Using in vivo two-photon imaging to trace the movements of fluorescent markers, they showed that these vessels carry cerebrospinal fluid around the brain, and that the fluid enters inter-cellular spaces in the brain tissue, picking up waste on its way. © 2015 Guardian News and Media Limited
Link ID: 21327 - Posted: 08.22.2015
By Gretchen Vogel Researchers may have finally explained how an obesity-promoting gene variant induces some people to put on the pounds. Using state-of-the-art DNA editing tools, they have identified a genetic switch that helps govern the body’s metabolism. The switch controls whether common fat cells burn energy rather than store it as fat. The finding suggests the tantalizing prospect that doctors might someday offer a gene therapy to melt extra fat away. Along with calories and exercise, genes influence a person’s tendency to gain—and keep—extra pounds. One of the genes with the strongest link to obesity is called FTO. People with certain versions of the gene are several kilos heavier on average and significantly more likely to be obese. Despite years of study, no one had been able to figure out what the gene does in cells or how it influences weight. There was some evidence FTO helped control other genes, but it was unclear which ones. Some researchers had looked for activity of FTO in various tissues, without finding any clear signals. Melina Claussnitzer, Manolis Kellis, and their colleagues at Harvard University, Massachusetts Institute of Technology, and the Broad Institute in Cambridge, turned to data from the Roadmap Epigenomics Project, an 8-year effort that identified the chemical tags on DNA that influence the function of genes. The researchers used those epigenetic tags to look at whether FTO was turned on or off in 127 cell types. The gene seemed to be active in developing fat cells called adipocyte progenitor cells. © 2015 American Association for the Advancement of Science
Helen Thomson Genetic changes stemming from the trauma suffered by Holocaust survivors are capable of being passed on to their children, the clearest sign yet that one person’s life experience can affect subsequent generations. The conclusion from a research team at New York’s Mount Sinai hospital led by Rachel Yehuda stems from the genetic study of 32 Jewish men and women who had either been interned in a Nazi concentration camp, witnessed or experienced torture or who had had to hide during the second world war. They also analysed the genes of their children, who are known to have increased likelihood of stress disorders, and compared the results with Jewish families who were living outside of Europe during the war. “The gene changes in the children could only be attributed to Holocaust exposure in the parents,” said Yehuda. Her team’s work is the clearest example in humans of the transmission of trauma to a child via what is called “epigenetic inheritance” - the idea that environmental influences such as smoking, diet and stress can affect the genes of your children and possibly even grandchildren. The idea is controversial, as scientific convention states that genes contained in DNA are the only way to transmit biological information between generations. However, our genes are modified by the environment all the time, through chemical tags that attach themselves to our DNA, switching genes on and off. Recent studies suggest that some of these tags might somehow be passed through generations, meaning our environment could have and impact on our children’s health. © 2015 Guardian News and Media Limited
By Christian Jarrett If we’re being honest, most of us have at least some selfish aims – to make money, to win a promotion at work, and so on. But importantly, we pursue these goals while at the same time conforming to basic rules of decency. For example, if somebody helps us out, we’ll reciprocate, even if doing so costs us time or cash. Yet there is a minority of people out there who don’t play by these rules. These selfish individuals consider other people as mere tools to be leveraged in the pursuit of their aims. They think nothing of betrayal or backstabbing, and they basically believe everyone else is in it for themselves too. Psychologists call these people “Machiavellians,” and there’s a questionnaire that tests for this trait (one of the so-called “dark triad” of personality traits along with narcissism and psychopathy). People high in Machiavellianism are more likely to agree with statements like: It is wise to flatter important people and The best way to handle people is to tell them what they want to hear. Calling them Machiavellian is too kind. These people are basically jerks. Related Stories Inside the Brains of Happily Married Couples Lonely People’s Brains Work Differently Now a team of Hungarian researchers from the University of Pécs has scanned the brains of high scorers on Machiavellianism while they played a simple game of trust. Reporting their results in the journal Brain and Cognition, the researchers said they found that Machiavellians’ brains went into overdrive when they encountered a partner who exhibited signs of being fair and cooperative. Why? Tamas Bereczkei and his team say it’s because the Machiavellians are immediately figuring out how to exploit the situation for their own gain. The game involved four stages and the student participants — a mix of high and low scorers on Machiavellianism — played several times with different partners. First, the participants were given roughly $5 worth of Hungarian currency and had to decide how much to “invest” in their partner. Any money they invested was always tripled as it passed to their partner. © 2015, New York Media LLC.
Link ID: 21324 - Posted: 08.22.2015
By Catherine Saint Louis People who work 55 hours or more per week have a 33 percent greater risk of stroke and a 13 percent greater risk of coronary heart disease than those working standard hours, researchers reported on Wednesday in the Lancet. The new analysis includes data on more than 600,000 individuals in Europe, the United States and Australia, and is the largest study thus far of the relationship between working hours and cardiovascular health. But the analysis was not designed to draw conclusions about what caused the increased risk and could not account for all relevant confounding factors. “Earlier studies have pointed to heart attacks as a risk of long working hours, but not stroke,” said Dr. Urban Janlert, a professor of public health at Umea University in Sweden, who wrote an accompanying editorial. “That’s surprising.” Mika Kivimaki, a professor of epidemiology at University College London, and his colleagues combined the results of multiple studies and tried to account for factors that might skew the results. In addition to culling data from published studies, the researchers also compiled unpublished information from public databases and asked authors of previous work for additional data. Dr. Steven Nissen, the chief of cardiovascular medicine at the Cleveland Clinic, found the methodology unconvincing. “It’s based upon exclusively observational studies, many of which were unpublished,” and some never peer-reviewed, he said. Seventeen studies of stroke included 528,908 men and women who were tracked on average 7.2 years. Some 1,722 nonfatal and deadly strokes were recorded. After controlling for smoking, physical activity and high blood pressure and cholesterol, the researchers found a one-third greater risk of stroke among those workers who reported logging 55 or more hours weekly, compared with those who reported working the standard 35 to 40 hours. © 2015 The New York Times Company
Almost fully-formed brain grown in a lab. Woah: Scientists grow first nearly fully-formed human brain. Boffins raise five-week-old fetal human brain in the lab for experimentation. On Tuesday, all the above appeared as headlines for one particular story. What was it all about? Mini-brains 3 to 4 millimetres across have been grown in the lab before, but if a larger brain had been created – and the press release publicising the claim said it was the size of a pencil eraser – that would be a major breakthrough. New Scientist investigated the claims. The announcement was made by Rene Anand, a neuroscientist at Ohio State University in Columbus, at a military health research meeting in Florida. Anand says he has grown a brain – complete with a cortex, midbrain and brainstem – in a dish, comparable in maturity to that of a fetus aged 5 weeks. Anand and his colleague Susan McKay started with human skin cells, which they turned into induced pluripotent stem cells (iPSCs) using a tried-and-tested method. By applying an undisclosed technique, one that a patent has been applied for, the pair say they were able to encourage these stem cells to form a brain. “We are replicating normal development,” says Anand. He says they hope to be able to create miniature models of brains experiencing a range of diseases, such as Parkinson’s and Alzheimer’s. Inconclusive evidence But not everyone is convinced, especially as Anand hasn’t published his results. Scientists we sent Anand’s poster presentation to said that although the team has indeed grown some kind of miniature collection of cells, or “organoid”, in a dish, the structure isn’t much like a fetal brain. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 21322 - Posted: 08.22.2015
Tina Hesman Saey Researchers have discovered a “genetic switch” that determines whether people will burn extra calories or save them as fat. A genetic variant tightly linked to obesity causes fat-producing cells to become energy-storing white fat cells instead of energy-burning beige fat, researchers report online August 19 in the New England Journal of Medicine. Previously scientists thought that the variant, in a gene known as FTO (originally called fatso), worked in the brain to increase appetite. The new work shows that the FTO gene itself has nothing to do with obesity, says coauthor Manolis Kellis, a computational biologist at MIT and the Broad Institute. But the work may point to a new way to control body fat. In humans and many other organisms, genes are interrupted by stretches of DNA known as introns. Kellis and Melina Claussnitzer of Harvard Medical School and colleagues discovered that a genetic variant linked to increased risk of obesity affects one of the introns in the FTO gene. It does not change the protein produced from the FTO gene or change the gene’s activity. Instead, the variant doubles the activity of two genes, IRX3 and IRX5, which are involved in determining which kind of fat cells will be produced. FTO’s intron is an enhancer, a stretch of DNA needed to control activity of far-away genes, the researchers discovered. Normally, a protein called ARID5B squats on the enhancer and prevents it from dialing up activity of the fat-determining genes. In fat cells of people who have the obesity-risk variant, ARID5B can’t do its job and the IRX genes crank up production of energy-storing white fat. © Society for Science & the Public 2000 - 2015.