By Sandra G. Boodman, As the jet hurtled toward New York’s John F. Kennedy International Airport on New Year’s Day 2013, the clinical psychologist watched her 16-year-old daughter warily, praying there would be no recurrence of the girl’s inexplicable and bizarre behavior. The previous night, while walking down a street in Spain where the family had spent Christmas, the teenager suddenly began yelling that the traditional New Year’s Eve fireworks were actually bombs. On the flight home, the girl seemed entirely normal. Her mother thought the high school junior might have had a panic attack, stressed by her upcoming college search and impending wisdom teeth extraction. But the uneventful flight brought a short-lived relief. Five days later, the teenager was hospitalized for treatment of what appeared to be a severe psychotic break. And for the next six weeks, the news seemed to get worse as a more ominous diagnosis emerged — and with it the specter of death. “Every day seemed like a horror story,” said Carmen, a psychoanalyst who practices in New York and whose last name, along with that of her daughter, Mia, is being withheld at her request to protect her professional privacy. For Lara Marcuse, a neurologist at Mount Sinai Hospital in Manhattan who treated Mia during her hospitalization, those weeks were filled with tension and anxiety that deepened as she worried that the teenager might not survive her sudden illness. “If she was my age,” said Marcuse, who is 44, “Mia would either be dead, in a coma or in a state psychiatric center.” Instead Mia, now 18, has fully recovered. She recently had a part in her high school play, is anticipating graduation and looking forward to entering college in September. © 1996-2014 The Washington Post

Keyword: Schizophrenia
Link ID: 19548 - Posted: 04.29.2014

The hormone oxytocin appears to increase social behaviors in newborn rhesus monkeys, according to a study by researchers at the National Institutes of Health, the University of Parma in Italy, and the University of Massachusetts, Amherst. The findings indicate that oxytocin is a promising candidate for new treatments for developmental disorders affecting social skills and bonding. Oxytocin, a hormone produced by the pituitary gland, is involved in labor and birth and in the production of breast milk. Studies have shown that oxytocin also plays a role in parental bonding, mating, and in social dynamics. Because of its possible involvement in social encounters, many researchers have suggested that oxytocin might be useful as a treatment for conditions affecting social behaviors, such as autism spectrum disorders. Although oxytocin has been shown to increase certain social behaviors in adults, before the current study it had not been shown to do so in primate infants of any species. Working with infant rhesus monkeys, the NIH researchers found that oxytocin increased two facial gestures associated with social interactions— one used by the monkeys themselves in certain social situations, the other in imitation of their human caregivers. “It was important to test whether oxytocin would promote social behaviors in infants in the same respects as it appears to promote social interaction among adults,” said the study’s first author, Elizabeth A. Simpson, Ph.D., postdoctoral fellow of the University of Parma, conducting research in the Comparative Behavioral Genetics Section of the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development. “Our results indicate that oxytocin is a candidate for further studies on treating developmental disorders of social functioning.” The study was published online in Proceedings of the National Academy of Sciences.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 19547 - Posted: 04.29.2014

By JAN HOFFMAN How well can computers interact with humans? Certainly computers play a mean game of chess, which requires strategy and logic, and “Jeopardy!,” in which they must process language to understand the clues read by Alex Trebek (and buzz in with the correct question). But in recent years, scientists have striven for an even more complex goal: programming computers to read human facial expressions. We all know what it’s like to experience pain that makes our faces twist into a grimace. But can you tell if someone else’s face of pain is real or feigned? The practical applications could be profound. Computers could supplement or even replace lie detectors. They could be installed at border crossings and airport security checks. They could serve as diagnostic aids for doctors. Researchers at the University of California, San Diego, have written software that not only detected whether a person’s face revealed genuine or faked pain, but did so far more accurately than human observers. While other scientists have already refined a computer’s ability to identify nuances of smiles and grimaces, this may be the first time a computer has triumphed over humans at reading their own species. “A particular success like this has been elusive,” said Matthew A. Turk, a professor of computer science at the University of California, Santa Barbara. “It’s one of several recent examples of how the field is now producing useful technologies rather than research that only stays in the lab. We’re affecting the real world.” People generally excel at using nonverbal cues, including facial expressions, to deceive others (hence the poker face). They are good at mimicking pain, instinctively knowing how to contort their features to convey physical discomfort. © 2014 The New York Times Company

Keyword: Emotions; Robotics
Link ID: 19546 - Posted: 04.29.2014

By Lenny Bernstein FILE - In this Oct. 7, 2013 file photo, workers collect red grapes in the vineyards of the famed Chateau Haut Brion, a Premier Grand Cru des Graves, during the grape harvest in Pessac-Leognan, near Bordeaux, southwestern France. Global warming makes feeding the world harder and more expensive, a United Nations scientific panel said. A warmer world will push food prices higher, trigger Red wine gets all the good press for the cardiovascular benefits of the flavonoids it contains, but U.S. Department of Agriculture researchers are reporting that one white wine grape has the reds beat when it comes to slowing weight gain and lowering cholesterol, at least in laboratory animals. The researchers put hamsters on a high-fat diet supplemented by flour made from the seeds of grapes used for chardonnay, syrah and cabernet sauvignon wines. They found that the white grapes easily beat the reds in slowing the hamsters’ weight gain and limiting production of cholesterol. They believe the higher levels of flavonoids in the chardonnay grape seeds altered the work of genes related to fat metabolism. They also had an anti-inflammatory effect, according to a study the USDA scientists published in the Journal of Agricultural and Food Chemistry in February. In part, the researchers say in another paper yet to be published, the anti-oxidant compounds in the chardonnay grape seeds may work with bacteria in the gut to produce beneficial effects. The flour production also provides grape-growers a way to use seeds that currently are discarded and dumped during the chardonnay production. The Mayo Clinic has begun human trials to determine whether the same results can be achieved, said Wally Yokoyama, a research chemist for the USDA in Albany, Calif., and one of the authors of the two studies. The innovation is one of many in a new USDA report released this week. © 1996-2014 The Washington Post

Keyword: Obesity
Link ID: 19545 - Posted: 04.29.2014

By LAURENCE STEINBERG I’M not sure whether it’s a badge of honor or a mark of shame, but a paper I published a few years ago is now ranked No. 8 on a list of studies that other psychologists would most like to see replicated. Good news: People find the research interesting. Bad news: They don’t believe it. The paper in question, written with my former student Margo Gardner, appeared in the journal Developmental Psychology in July 2005. It described a study in which we randomly assigned subjects to play a video driving game, either alone or with two same-age friends watching them. The mere presence of peers made teenagers take more risks and crash more often, but no such effect was observed among adults. I find my colleagues’ skepticism surprising. Most people recall that as teenagers, they did far more reckless things when with their friends than when alone. Data from the Federal Bureau of Investigation indicate that many more juvenile crimes than adult crimes are committed in groups. And driving statistics conclusively show that having same-age passengers in the car substantially increases the risk of a teen driver’s crashing but has no similar impact when an adult is behind the wheel. Then again, I’m aware that our study challenged many psychologists’ beliefs about the nature of peer pressure, for it showed that the influence of peers on adolescent risk taking doesn’t rely solely on explicit encouragement to behave recklessly. Our findings also undercut the popular idea that the higher rate of real-world risk taking in adolescent peer groups is a result of reckless teenagers’ being more likely to surround themselves with like-minded others. My colleagues and I have replicated our original study of peer influences on adolescent risk taking several times since 2005. We have also shown that the reason teenagers take more chances when their peers are around is partly because of the impact of peers on the adolescent brain’s sensitivity to rewards. In a study of people playing our driving game, my colleague Jason Chein and I found that when teens were with people their own age, their brains’ reward centers became hyperactivated, which made them more easily aroused by the prospect of a potentially pleasurable experience. This, in turn, inclined teenagers to pay more attention to the possible benefits of a risky choice than to the likely costs, and to make risky decisions rather than play it safe. Peers had no such effect on adults’ reward centers, though. © 2014 The New York Times Company

Keyword: Attention; Emotions
Link ID: 19544 - Posted: 04.28.2014

One of our most mysterious and intriguing states of consciousness is the dream. We lose consciousness when we enter the deep waters of sleep, only to regain it as we emerge into a series of uncanny private realities. These air pockets of inner experience have been difficult for psychologists to study scientifically and, as a result, researchers have mostly resorted to measuring brain activity as the sleeper lies passive. But interest has recently returned to a technique that allows real-time communication from within the dream world. The rabbit hole between these worlds of consciousness turns out to be the lucid dream, where people become aware that they are dreaming and can influence what happens within their self-generated world. Studies suggest that the majority of people have had a lucid dream at some point in their life but that the experience is not common. As a result, there is now a minor industry in technologies and training techniques that claim to increase your chance of having a lucid dream although a recent scientific review estimated that the effect of any particular strategy is moderate at best. Some people, however, can reliably induce lucid dreams and it's these people who are allowing us to conduct experiments inside dreams. When trying to study an experience or behaviour, cognitive scientists usually combine subjective reports, what people describe about their experience, with behavioural experiments, to see what effect a particular state has on how people reason, act or remember. But both are difficult in dreamers, because they can't tell you much until they wake up and active participation in experiments is difficult when you are separated from the world by a blanket of sleep-induced paralysis. This paralysis is caused by neurons in the brainstem that block signals from the action-generating areas in the brain to the spinal nerves and muscles. The shutdown happens when Rapid Eye Movement or REM sleep starts, meaning that dreaming of even the most energetic actions results in no more than a slight twitch. One of the few actions that are not paralysed, however, is eye movement. This is where REM sleep gets its name from and this window of free action provides the lucid dreamer a way of signalling to the outside world. © 2014 Guardian News and Media Limited

Keyword: Sleep
Link ID: 19543 - Posted: 04.28.2014

By Julie Steenhuysen CHICAGO (Reuters) - International teams of researchers using advanced gene sequencing technology have uncovered a single genetic mutation responsible for a rare brain disorder that may have stricken families in Turkey for some 400 years. The discovery of this genetic disorder, reported in two papers in the journal Cell, demonstrates the growing power of new tools to uncover the causes of diseases that previously stumped doctors. Besides bringing relief to affected families, who can now go through prenatal genetic testing in order to have children without the disorder, the discovery helps lend insight into more common neurodegenerative disorders, such as ALS, also known as Lou Gehrig's disease, the researchers said. The reports come from two independent teams of scientists, one led by researchers at Baylor College of Medicine and the Austrian Academy of Sciences, and the other by Yale University, the University of California, San Diego, and the Academic Medical Center in the Netherlands. Both focused on families in Eastern Turkey where marriage between close relatives, such as first cousins, is common. Geneticists call these consanguineous marriages. In this population, the researchers focused specifically on families whose children had unexplained neurological disorders that likely resulted from genetic defects. Both teams identified a new neurological disorder arising from a single genetic variant called CLP1. Children born with this disorder inherit two defective copies of this gene, which plays a critical role in the health of nerve cells. Babies with the disorder have small and malformed brains, they develop progressive muscle weakness, they do not speak and they are increasingly prone to seizures.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 19542 - Posted: 04.28.2014

Epigenetics is one of the hottest fields in the life sciences. It’s a phenomenon with wide-ranging, powerful effects on many aspects of biology, and enormous potential in human medicine. As such, its ability to fill in some of the gaps in our scientific knowledge is mentioned everywhere from academic journals to the mainstream media to some of the less scientifically rigorous corners of the Internet. Epigenetics is essentially additional information layered on top of the sequence of letters (strings of molecules called A, C, G, and T) that makes up DNA. If you consider a DNA sequence as the text of an instruction manual that explains how to make a human body, epigenetics is as if someone's taken a pack of highlighters and used different colours to mark up different parts of the text in different ways. For example, someone might use a pink highlighter to mark parts of the text that need to be read the most carefully, and a blue highlighter to mark parts that aren't as important. There are different types of epigenetic marks, and each one tells the proteins in the cell to process those parts of the DNA in certain ways. For example, DNA can be tagged with tiny molecules called methyl groups that stick to some of its C letters. Other tags can be added to proteins called histones that are closely associated with DNA. There are proteins that specifically seek out and bind to these methylated areas, and shut it down so that the genes in that region are inactivated in that cell. So methylation is like a blue highlighter telling the cell "you don't need to know about this section right now." Methyl groups and other small molecular tags can attach to different locations on the histone proteins, each one having a different effect. Some tags in some locations loosen the attachment between the DNA and the histone, making the DNA more accessible to the proteins that are responsible for activating the genes in that region; this is like a pink highlighter telling the cell "hey, this part's important". © 2014 Guardian News and Media Limited

Keyword: Genes & Behavior; Development of the Brain
Link ID: 19541 - Posted: 04.28.2014

by Helen Thomson A 22-year-old man has been instantaneously transported to his family's pizzeria and his local railway station – by having his brain zapped. These fleeting visual hallucinations have helped researchers pinpoint places where the brain stores visual location information. Pierre Mégevand at the Feinstein Institute for Medical Research in Manhasset, New York, and his colleagues wanted to discover just where in the brain we store and retrieve information about locations and places. They sought the help of a 22-year-old man being treated for epilepsy, because the treatment involved implanting electrodes into his brain that would record his neural activity. Mégevand and his colleagues scanned the volunteer's brain using functional MRI while he looked at pictures of different objects and scenes. They then recorded activity from the implanted electrodes as he looked at a similar set of pictures. In both situations, a specific area of the cortex around the hippocampus responded to images of places, but not to images of other kinds of objects, such as body parts or tools. "There are these little spots of tissues that seem to care about houses and places more than any other class of object," says research team member Ashesh Mehta, also at the Feinstein Institute. Next, the team used the implanted electrodes to stimulate the brain in this area – a move that the volunteer said triggered a series complex visual hallucinations. First he described seeing a railway station in the neighbourhood where he lives. Stimulation of a nearby area elicited another hallucination, this time of a staircase and a blue closet in his home. When stimulation of these areas was repeated, the same scenes arose. © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory; Vision
Link ID: 19540 - Posted: 04.26.2014

by Laura Sanders When a baby cries at night, exhausted parents scramble to figure out why. He’s hungry. Wet. Cold. Lonely. But now, a Harvard scientist offers more sinister explanation: The baby who demands to be breastfed in the middle of the night is preventing his mom from getting pregnant again. This devious intention makes perfect sense, says evolutionary biologist David Haig, who describes his idea in Evolution, Medicine and Public Health. Another baby means having to share mom and dad, so babies are programmed to do all they can to thwart the meeting of sperm and egg, the theory goes. Since babies can’t force birth control pills on their mothers, they work with what they’ve got: Nighttime nursing liaisons keep women from other sorts of liaisons that might lead to another child. And beyond libido-killing interruptions and extreme fatigue, frequent night nursing also delays fertility in nursing women. Infant suckling can lead to hormone changes that put the kibosh on ovulation (though not reliably enough to be a fail-safe birth control method, as many gynecologists caution). Of course, babies don’t have the wherewithal to be interrupting their mothers’ fertility intentionally. It’s just that in our past, babies who cried to be nursed at night had a survival edge, Haig proposes. The timing of night crying seems particularly damning, Haig says. Breastfed babies seem to ramp up their nighttime demands around 6 months of age and then slowly improve — precisely the time when a baby would want to double down on its birth control efforts. © Society for Science & the Public 2000 - 2013

Keyword: Sexual Behavior; Evolution
Link ID: 19539 - Posted: 04.26.2014

By LAWRENCE K. ALTMAN Douglas L. Coleman, a Canadian-born scientist who upset scientific dogma by discovering that genes — not willpower, eating habits or other behaviors — could cause obesity in some people, died on April 16 at his home in Lamoine, Me. He was 82. The cause was aggressive basal cell cancer, said a spokeswoman for the Jackson Laboratory in Bar Harbor, Me., where Dr. Coleman spent his entire research career. Beginning in the 1960s, Dr. Coleman’s research showed that a blood-borne substance could curb hunger. In the 1990s, his findings led Dr. Jeffrey M. Friedman’s team at the Rockefeller University in Manhattan to identify the gene that produces the appetite suppressant leptin, which is released by fat cells. For their work, Dr. Coleman and Dr. Friedman shared the prestigious Lasker Award for basic medical research in 2010. Their discoveries upended the conventional wisdom that fat cells are simply energy storage bins, and demonstrated that fat tissue is an endocrine organ required for normal development. Scientists have learned from their research and others’ that fat produces a variety of hormones, cytokines and other chemicals in the body’s natural weight-control system. Douglas Leonard Coleman was born on Oct. 6, 1931, in Stratford, Ontario. Influenced by his father, Leonard, who repaired radios and refrigerators for a living, Douglas spent much of his youth investigating how things worked by taking them apart. He earned a chemistry degree from McMaster University in Hamilton, Ontario, and a doctorate in biochemistry from the University of Wisconsin. In 1958, facing poor employment prospects in academia or industry in Canada, he became a research scientist at the Jackson Laboratory, which studies mouse genetics to learn about human disease. He intended to spend a year or two there to gain experience in genetics and immunology, but stayed until he retired in 1991. After retiring, he turned a tract of land he owned into a nature preserve. © 2014 The New York Times Company

Keyword: Obesity; Genes & Behavior
Link ID: 19538 - Posted: 04.26.2014

Scientists have bioengineered, in neurons cultured from rats, an enhancement to a cutting edge technology that provides instant control over brain circuit activity with a flash of light. The research funded by the National Institutes of Health adds the same level of control over turning neurons off that, until now, had been limited to turning them on. “What had been working through a weak pump can now work through a highly responsive channel with many orders of magnitude more impact on cell function,” explained Karl Deisseroth, M.D., Ph.D., It is like going from a squirt to a gushing hose. Deisseroth and colleagues report on what is being hailed as a marvel of genetic engineering in the April 25, 2014 issue of the journal Science. Deisseroth’s team had pioneered the use of light pulses to control brain circuitry in animals genetically engineered to be light-responsive — optogenetics. Genes that allow the sun to control light-sensitive primitive organisms like algae, melded with genes that make fluorescent marker proteins, are fused with a deactivated virus that delivers them to specific types of neurons which they become part of — allowing pulses of light to similarly commandeer brain cells.

Keyword: Brain imaging
Link ID: 19537 - Posted: 04.26.2014

by Andy Coghlan HERE'S another reason to be fit and healthy. Staying free of "lifestyle diseases" and infections could put the brakes on Alzheimer's. The advice comes from teams that have pieced together how these bodily ailments create inflammation that ultimately spills over into the brain, sending its immune cells into a hyperactive, destructive state. "The idea is simple: monitoring and prompt treatment [of inflammation] could prevent the decline from Alzheimer's," said Hugh Perry of the University of Southampton, UK, as he presented the research at the Alzheimer's Research UK annual meeting in Oxford last month. As well as revealing step by step how disease and infection can aggravate and accelerate the early stages of Alzheimer's, Perry and his colleague Clive Holmes have begun a pioneering trial in 40 people to see if a drug that acts to dampen inflammation in the body can help delay the progress of the brain disease. Etanercept is already prescribed to people with rheumatoid arthritis, and works by sponging up a molecule that aggravates inflammation. According to Alzheimer's Disease International, 44 million people globally have dementia, of which Alzheimer's is the most common type. The beginnings of the disease are characterised by the appearance in the brain of plaques of amyloid proteins and tangles of tau proteins. They prompt the brain's native immune cells, the microglia, to multiply in a bid to dispose of the troublesome new debris. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers
Link ID: 19536 - Posted: 04.26.2014

By MATTHEW PERRONE WASHINGTON (AP) — The Food and Drug Administration announced Friday it will convene a public meeting in October to review the risks of psychiatric and behavioral side effects with Pfizer’s anti-smoking drug Chantix. The agency said in a federal notice it will convene its panel of psychiatric drug experts to discuss the pill’s risks and how to best manage them. Since 2009 Chantix has carried the government’s strongest safety warning — a ‘‘black box’’ label — because of links to hostility, agitation, depression and suicidal thoughts. The warning was added after the FDA received dozens of reports of suicide and hundreds of reports of suicidal behavior among patients taking the smoking-cessation drug. At that time, the FDA also required Pfizer to conduct additional studies to determine the extent of the side effects. A spokeswoman for Pfizer said Friday that the company recently submitted new data to the FDA comparing the drug’s psychiatric safety to placebo and other anti-smoking techniques. The FDA first began investigating potential side effects with Chantix in 2007, the year after the twice-a-day pill hit the market. The drug’s labeling tells patients to stop taking Chantix immediately if they experience agitation, depressed mood, suicidal thinking and other behavioral changes. Doctors are advised to weigh the drug’s risks against its potential benefits in helping patients quit smoking.

Keyword: Drug Abuse; Depression
Link ID: 19535 - Posted: 04.26.2014

Does reading faster mean reading better? That’s what speed-reading apps claim, promising to boost not just the number of words you read per minute, but also how well you understand a text. There’s just one problem: The same thing that speeds up reading actually gets in the way of comprehension, according to a new study. When you read at your natural pace, your eyes move back and forth across a sentence, rather than plowing straight through to the end. Apps like Spritz or the aptly named Speed Read are built around the idea that these eye movements, called saccades, are a redundant waste of time. It’s more efficient, their designers claim, to present words one at a time in a fixed spot on a screen, discouraging saccades and helping you get through a text more quickly. This method, called rapid serial visual presentation (RSVP), has been controversial since the 1980s, when tests showed it impaired comprehension, though researchers weren’t quite sure why. With a new crop of speed-reading products on the market, psychologists decided to dig a bit more and uncovered a simple explanation for RSVP’s flaw: Every so often, we need to scan backward and reread for a better grasp of the material. Researchers demonstrated that need by presenting 40 college students with ambiguous, unpunctuated sentences ("While the man drank the water that was clear and cold overflowed from the toilet”) while following their subjects’ gaze with an eye-tracking camera. Half the time, the team crossed out words participants had already read, preventing them from rereading (“xxxxx xxx xxx drank the water …”). Following up with basic yes-no questions about each sentence’s content, they found that comprehension dropped by about 25% in trials that blocked rereading versus those that didn’t, the researchers report online this month in Psychological Science. Crucially, the drop was about the same when subjects could, but simply hadn’t, reread parts of a sentence. Nor did the results differ much when using ambiguous sentences or their less confusing counterparts (“While the man slept the water …”). Turns out rereading isn’t a waste of time—it’s essential for understanding. © 2014 American Association for the Advancement of Science.

Keyword: Language; Attention
Link ID: 19534 - Posted: 04.26.2014

Regina Nuzzo Gene therapy delivered to the inner ear can help shrivelled auditory nerves to regrow — and in turn, improve bionic ear technology, researchers report today in Science Translational Medicine1. The work, conducted in guinea pigs, suggests a possible avenue for developing a new generation of hearing prosthetics that more closely mimics the richness and acuity of natural hearing. Sound travels from its source to ears, and eventually to the brain, through a chain of biological translations that convert air vibrations to nerve impulses. When hearing loss occurs, it’s usually because crucial links near the end of this chain — between the ear’s cochlear cells and the auditory nerve — are destroyed. Cochlear implants are designed to bridge this missing link in people with profound deafness by implanting an array of tiny electrodes that stimulate the auditory nerve. Although cochlear implants often work well in quiet situations, people who have them still struggle to understand music or follow conversations amid background noise. After long-term hearing loss, the ends of the auditory nerve bundles are often frayed and withered, so the electrode array implanted in the cochlea must blast a broad, strong signal to try to make a connection, instead of stimulating a more precise array of neurons corresponding to particular frequencies. The result is an ‘aural smearing’ that obliterates fine resolution of sound, akin to forcing a piano player to wear snow mittens or a portrait artist to use finger paints. To try to repair auditory nerve endings and help cochlear implants to send a sharper signal to the brain, researchers turned to gene therapy. Their method took advantage of the electrical impulses delivered by the cochlear-implant hardware, rather than viruses often used to carry genetic material, to temporarily turn inner-ear cells porous. This allowed DNA to slip in, says lead author Jeremy Pinyon, an auditory scientist at the University of New South Wales in Sydney, Australia. © 2014 Nature Publishing Group

Keyword: Hearing; Robotics
Link ID: 19533 - Posted: 04.24.2014

by Michael Slezak Could preventing the brain shrinkage associated with depression be as simple as blocking a protein? Post-mortem analysis of brain tissue has shown that the dendrites that relay messages between neurons are more shrivelled in people with severe depression than in people without the condition. This atrophy could be behind some of the symptoms of depression, such as the inability to feel pleasure. As a result, drugs that help repair the neuronal connections, like ketamine, are under investigation. But how this shrinkage occurs has remained a mystery, limiting researchers' ability to find ways of stopping it. Ronald Duman at Yale University wondered whether a protein called REDD1, which was recently shown to reduce myelin, the fatty material that protects neurons, was the key. To find out, his team bred rats unable to produce REDD1 and exposed them to a prolonged period of unpredictable stress. In normal rats, this stress resulted in depressive-like behaviour and brain shrinkage, but Duman's rats were unaffected. In contrast, rats engineered to overproduce REDD1 became depressed and had brain shrinkage, even without being stressed. What's more, injecting normal rats with a stress hormone boosted levels of REDD1 in the brain. Giving them a drug that blocked the production of stress hormones stopped them producing the protein, even when they were externally stressed. Taken together, the experiments show that REDD1 is necessary to produce the brain shrinkage seen in stressed rats, and that stress hormones are involved in its production – offering a possible way to prevent the shrinkage. © Copyright Reed Business Information Ltd

Keyword: Depression
Link ID: 19532 - Posted: 04.24.2014

Here to stay. The Y chromosome is small compared with the X, but is required to keep levels of some genes high enough for mammals to survive. The small, stumpy Y chromosome—possessed by male mammals but not females, and often shrugged off as doing little more than determining the sex of a developing fetus—may impact human biology in a big way. Two independent studies have concluded that the sex chromosome, which shrank millions of years ago, retains the handful of genes that it does not by chance, but because they are key to our survival. The findings may also explain differences in disease susceptibility between men and women. “The old textbook description says that once maleness is determined by a few Y chromosome genes and you have gonads, all other sex differences stem from there,” says geneticist Andrew Clark of Cornell University, who was not involved in either study. “These papers open up the door to a much richer and more complex way to think about the Y chromosome.” The sex chromosomes of mammals have evolved over millions of years, originating from two identical chromosomes. Now, males possess one X and one Y chromosome and females have two Xs. The presence or absence of the Y chromosome is what determines sex—the Y chromosome contains several genes key to testes formation. But while the X chromosome has remained large throughout evolution, with about 2000 genes, the Y chromosome lost most of its genetic material early in its evolution; it now retains less than 100 of those original genes. That’s led some scientists to hypothesize that the chromosome is largely indispensable and could shrink away entirely. © 2014 American Association for the Advancement of Science.

Keyword: Sexual Behavior
Link ID: 19531 - Posted: 04.24.2014

By Linda Carroll A college education may do a lot more than provide better job opportunities — it may also make brains more resilient to trauma, a new study suggests. The more years of education people have, the more likely they will recover from a traumatic brain injury, according to the study published Wednesday in Neurology. In fact, one year after a traumatic brain injury, people with a college education were nearly four times as likely as those who hadn’t finished high school to return to work or school with no disability. Earlier studies had shown that education might have a protective effect when it comes to degenerative brain diseases like Alzheimer’s. Scientists have theorized that education leads to greater “cognitive reserve,” which allows people to overcome or compensate for brain damage. So if there are two people with the same degree of damage from Alzheimer’s, the more highly educated one will show fewer symptoms. The assumption is that education changes and expands the brain, leaving it better able to cope with challenges. “Added capacity allows us to either work around the damaged areas or to adapt,” said Eric B. Schneider, an assistant professor of surgery at the Johns Hopkins School of Medicine. Schneider and his colleagues suspected that cognitive reserve might play an equally important role in helping people rehab from acute brain damage that results from falls, car crashes and other accidents as it does in Alzheimer’s disease.

Keyword: Brain Injury/Concussion; Learning & Memory
Link ID: 19530 - Posted: 04.24.2014

By Brady Dennis, The Food and Drug Administration will for the first time regulate the booming market of electronic cigarettes, as well as cigars, pipe tobacco and hookahs, under a proposal to be released Thursday. The move would begin to place restrictions on e-cigarettes, a nearly $2 billion industry that for years has operated outside the reach of federal regulators. If adopted, the government’s plan would force manufacturers to curb sales to minors, stop handing out free samples, place health warning labels on their products and disclose the ingredients. Makers of e-cigarettes also would be banned from making health-related claims without scientific evidence. The FDA’s proposal stops short of broader restrictions sought by many­ ­tobacco-control advocates. Regulators at this point are not seeking to halt online sales of e-cigarettes, curb television advertising, or ban the use of flavorings such as watermelon, grape soda and piña colada — all tactics that critics say are aimed at attracting young smokers and that have been banned for traditional cigarettes. Those restrictions might come eventually, FDA officials said, but not before more rigorous research can establish a scientific basis for tougher rules. “Right now, for something like e-cigarettes, there are far more questions than answers,” said Mitch Zeller, director of the FDA’s Center for Tobacco Products. Thursday’s action is about expanding FDA’s authority to products that have been “rapidly evolving with no regulation whatsoever,” in order to create a foundation for broader regulation in the future, he said. “It creates the framework. We’re calling this the first step. . . . For the first time, there will be a science-based, independent regulatory agency playing a vital gate-keeping function.” © 1996-2014 The Washington Post

Keyword: Drug Abuse
Link ID: 19529 - Posted: 04.24.2014