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Claudia Dreifus To Neil H. Shubin’s long résumé — paleontologist, molecular biologist, dean and professor of anatomy at the University of Chicago School of Medicine, best-selling author — can now be added “television host.” Dr. Shubin, 53, who helped discover the 375-million-year-old fish called Tiktaalik, hailed as a missing link between sea and land animals, will preside over “Your Inner Fish,” a three-part series on evolution (based on his book of the same title) that makes its debut Wednesday on PBS. We spoke in Chicago in February and in New York last month. What follows is an edited and condensed version of the conversations. Q. Where did you grow up? A. Suburban Philadelphia. My mom’s a retired nursing home administrator. My father, Seymour Shubin, is a fiction writer. He writes mysteries. My favorite is “The Captain”; it won an Edgar award. He’s an educated man, but science kind of scares him. So when I’m writing, my dad is my target audience. Whenever I hit a tricky scientific concept, I think, “How would I communicate this to him?” This is why my books are written, intentionally, without jargon, which can lead to some gyrations because jargon does have precision. The funny thing is, I’m not sure he always gets what I do. When I first started working on the book version of “Your Inner Fish,” he asked, “Neil, how did you become a scientist?” I thought, “All these years he’s seen me run off to the Arctic, but he’s never been quite sure what I do up there.” So let me ask you his question: How did you become a paleontologist? I was one of those kids with lots of hobbies: astronomy, dinosaurs, collecting rocks, collecting stamps. It all came together when I went to college in New York — Columbia — and volunteered at the American Museum of Natural History. That place was like a playground for me. © 2014 The New York Times Company

Keyword: Evolution
Link ID: 19466 - Posted: 04.10.2014

Jyoti Madhusoodanan Growing up in a stressful social environment leaves lasting marks on young chromosomes, a study of African American boys has revealed. Telomeres, repetitive DNA sequences that protect the ends of chromosomes from fraying over time, are shorter in children from poor and unstable homes than in children from more nurturing families. When researchers examined the DNA of 40 boys from major US cities at age 9, they found that the telomeres of children from harsh home environments were 19% shorter than those of children from advantaged backgrounds. The length of telomeres is often considered to be a biomarker of chronic stress. The study, published today in the Proceedings of the National Academy of Sciences1, brings researchers closer to understanding how social conditions in childhood can influence long-term health, says Elissa Epel, a health psychologist at the University of California, San Francisco, who was not involved in the research. Participants’ DNA samples and socio-economic data were collected as part of the Fragile Families and Child Wellbeing Study, an effort funded by the US National Institutes of Health to track nearly 5,000 children, the majority of whom were born to unmarried parents in large US cities in 1998–2000. Children's environments were rated on the basis of their mother's level of education; the ratio of a family’s income to needs; harsh parenting; and whether family structure was stable, says lead author Daniel Notterman, a molecular biologist at Pennsylvania State University in Hershey. © 2014 Nature Publishing Group

Keyword: Stress; Aggression
Link ID: 19465 - Posted: 04.09.2014

By By Stephanie Pappas, A little stress may be a good thing for teenagers learning to drive. In a new study, teens whose levels of the stress hormone cortisol increased more during times of stress got into fewer car crashes or near crashes in their first months of driving than their less-stress-responsive peers did. The study suggests that biological differences may affect how teens learn to respond to crises on the road, the researchers reported today (April 7) in the journal JAMA Pediatrics. Efforts to reduce teen car accidents include graduated driver licensing programs, safety messages and increased parental management, but these efforts seem to work better for some teens than others, the researchers said. Alternatives, such as in-vehicle technologies aimed at reducing accidents, may be especially useful for teens with a "neurological basis" for their increased risk of getting into an accident, they said. Automobile accidents are the No. 1 cause of death of teenagers in the United States, according to the Centers for Disease Control and Prevention. Car crashes also kill more 15- to 29-year-olds globally than any other cause, according to the World Health Organization.

Keyword: Stress; Aggression
Link ID: 19464 - Posted: 04.09.2014

|By Bret Stetka The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s. Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity. Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields. © 2014 Scientific American

Keyword: Parkinsons; Aggression
Link ID: 19463 - Posted: 04.09.2014

Julia Baird SYDNEY, Australia — PRETTY much the No. 1 question you are asked when you’re pregnant is: “Girl or boy?” If you choose not to find out, but to be deliciously surprised at birth, as I did, then you will be asked to guess: “What do you feel it is?” I used to scrunch up my eyes and try hard to draw on what people told me was an age-old female intuition: Which genitals were sprouting in my round belly? I could never tell, though. It is as though the entire world is trying to guess what, or who, is inside you. One oft-told tale is that girls steal your looks and make you fat, while boys just make your belly stick out straight. When I stood wearily bulging at one friend’s baby shower in Manhattan, a stylist confided that she thought our mutual friend was having a boy, because she looked so pretty. Then she looked me up and down: “I think you’re having a girl.” (I placed her in the same category as the neighbor who yelled, “Morning, Fatty!” over the side fence each day.) Why is whether a baby wears blue or pink the most pressing matter for adult acquaintances of a soon-to-be-born? Green is just fine, or white. But a 2007 Gallup poll found that most young Americans, and women under 50, would like to find out the sex of their baby before it is born. In some American fertility clinics, staff experts check the embryo’s sex before they implant it in the womb. So what will it do to our collective minds when forced to grasp that some people are neither gender? Not male, or female, but something else either encompassing, or rejecting, or just adapting from both? Last week, Australia had to grapple with just that after the High Court, in a historic decision, ruled that a person called Norrie May-Welby could register as “nonspecific” on official certificates. Now 52, Norrie was identified, physically, as male when she was born, in Scotland, but was drawn to the world of girls, playing with dolls at age 4 and tying her school tie around her head at night to create the illusion of long hair. She escaped into the library monitors’ group at school and made up adventures where she played six characters, five of whom were female: “I didn’t think there was any problem with this,” she says. “After all, just because I wasn’t really from Krypton, didn’t mean I couldn’t imagine being Supergirl.” © 2014 The New York Times Company

Keyword: Sexual Behavior
Link ID: 19462 - Posted: 04.09.2014

By: Larry Cahill, Ph.D. Early in 2013, the Food and Drug Administration (FDA) ordered the makers of the well-known sleep aid Ambien (zolpidem) to cut their recommended dose in half-but only for women. In essence, the FDA was acknowledging that despite extensive testing prior to the drug's release on the market, millions of women had been overdosing on Ambien for 20 years. On February 9, 2014, CBS's 60 Minutes highlighted this fact-and sex differences in general-by powerfully asking two questions: Why did this happen, and are men and women treated equally in research and medicine?1 The answer to the first question is that the biomedical community has long operated on what is increasingly being viewed as a false assumption: that biological sex matters little, if at all, in most areas of medicine. The answer to the second question is no, today's biomedical research establishment is not treating men and women equally. What are some of the key reasons for the biomedical community's false assumption, and why is this situation now finally changing? What are some of the seemingly endless controversies about sex differences in the brain generated by "anti-sex difference" investigators? And what lies at the root of the resistance to sex differences research in the human brain? For a long time, for most aspects of brain function, sex influences hardly mattered to the neuroscience mainstream. The only sex differences that concerned most neuroscientists involved brain regions (primarily a deep-brain structure called the hypothalamus) that regulate both sex hormones and sexual behaviors.2 Neuroscientists almost completely ignored possible sex influences on other areas of the brain, assuming that the sexes shared anything that was fundamental when it came to brain function. Conversely, the neuroscience mainstream viewed any apparent sex differences in the brain as not fundamental- something to be understood after they grasped the fundamental facts. By this logic, it was not a problem to study males almost exclusively, since doing so supposedly allowed researchers to understand all that was fundamental in females without having to consider the complicating aspects of female hormones. To this day, neuroscientists overwhelmingly study only male animals.3 © 2014 The Dana Foundation

Keyword: Sexual Behavior
Link ID: 19461 - Posted: 04.09.2014

If you know only one thing about violins, it is probably this: A 300-year-old Stradivarius supposedly possesses mysterious tonal qualities unmatched by modern instruments. However, even elite violinists cannot tell a Stradivarius from a top-quality modern violin, a new double-blind study suggests. Like the sound of coughing during the delicate second movement of Beethoven's violin concerto, the finding seems sure to annoy some people, especially dealers who broker the million-dollar sales of rare old Italian fiddles. But it may come as a relief to the many violinists who cannot afford such prices. "There is nothing magical [about old Italian violins], there is nothing that is impossible to reproduce," says Olivier Charlier, a soloist who participated in the study and who plays a fiddle made by Carlo Bergonzi (1683 to 1747). However, Yi-Jia Susanne Hou, a soloist who participated in the study and who until recently played a violin by Bartolomeo Giuseppe Antonio Guarneri "del Gesù" (1698 to 1744), questions whether the test was fair. "Whereas I believe that [the researchers] assembled some of the finest contemporary instruments, I am quite certain that they didn't have some of the finest old instruments that exist," she says. The study marks the latest round in debate over the "secret of Stradivarius." Some violinists, violinmakers, and scientists have thought that Antonio Stradivari (1644 to 1737) and his contemporaries in Cremona, Italy, possessed some secret—perhaps in the varnish or the wood they used—that enabled them to make instruments of unparalleled quality. Yet, for decades researchers have failed to identify a single physical characteristic that distinguishes the old Italians from other top-notch violins. The varnish is varnish; the wood (spruce and maple) isn't unusual. Moreover, for decades tests have shown that listeners cannot tell an old Italian from a modern violin. © 2014 American Association for the Advancement of Science

Keyword: Attention; Aggression
Link ID: 19460 - Posted: 04.08.2014

By BENEDICT CAREY Therapists who specialize in autism often use a child’s own interests, toys or obsessions as a way to connect, and sometimes to reward effort and progress on social skills. The more eye contact a child makes, for example, the more play time he or she gets with those precious maps or stuffed animals. But now a group of scientists and the author of a new book are suggesting that those favorite activities could be harnessed in a deeper, more organic way. If a child is fascinated with animated characters like Thomas the Tank Engine, why not use those characters to prompt and reinforce social development? Millions of parents do this routinely, if not systematically, flopping down on the floor with a socially distant child to playact the characters themselves. “We individualize therapy to each child already, so if the child has an affinity for certain animated characters, it’s absolutely worth studying a therapy that incorporates those characters meaningfully,” said Kevin Pelphrey, director of the child neuroscience laboratory at Yale. He and several other researchers, including John D. E. Gabrieli of M.I.T., Simon Baron-Cohen of the University of Cambridge and Pamela Ventola of Yale, are proposing a study to test the approach. The idea came from Ron Suskind, a former Wall Street Journal reporter whose new book “Life, Animated” describes his family’s experience reaching their autistic son, Owen, through his fascination with Disney movies like “The Little Mermaid” and “Beauty and the Beast.” It was Mr. Suskind’s story that first referred to ‘“affinity therapy.” He approached the researchers to put together a clinical trial based on the idea that some children can develop social and emotional instincts through the characters they love. Experts familiar with his story say the theory behind the therapy is plausible, given what’s known from years of studying the effects of other approaches. © 2014 The New York Times Company

Keyword: Autism
Link ID: 19459 - Posted: 04.08.2014

By Paul D. Thacker When the FDA denied Sprout Pharmaceutical’s bid last October to begin marketing flibanserin, a drug aimed at treating low sexual desire in women, women’s groups responded in anger. In January, representatives from eight different women’s groups, including the National Organization of Women, met with Janet Woodcock, the FDA’s head of pharmaceuticals, to protest the decision. Congress also got in on the act, with Reps. Debbie Wasserman Schultz, Chellie Pingree, Nita Lowey, and Louise Slaughter sending a letter to FDA Commissioner Margaret Hamburg to implore that, when evaluating drugs for female dysfunction (in medical terms Hypoactive Sexual Desire Disorder, or HSDD), Dr. Hamburg apply "the same standards of consideration given to the approved drugs for men in your risk/benefit evaluation." “We’ve now got 24 drugs for men for either testosterone replacement or erectile dysfunction,” Cindy Whitehead, Sprout’s chief operating officer told the Associated Press. “Yet there are zero drugs for the most common form of sexual dysfunction in women.” Anita H. Clayton, the interim chair of the department of psychiatry and neurobehavioral sciences at the University of Virginia School of Medicine, was more explicit, writing in a blistering column for the Huffington Post: “For the millions of women with HSDD, the FDA must overcome the problem of institutionalized sexism—unconscious and perhaps unintended, but damaging nonetheless.” The chorus was loud and clear: The FDA is sexist. The federal agency charged with approving drugs to protect and improve our health is now standing in the way of a woman’s right to have a satisfying sex life. This framing played out in numerous stories, with similar charges appearing in the American Prospect (“the FDA’s kinda sexist”), and the Washington Post (“Some critics say the agency—consciously or not—may be succumbing to society’s squeam­ishness about women’s sexual desires compared with those of men”). Not to be outdone with mere institutional sexism, a writer for the Wire mused whether “blatant, medieval sexism is also at play.” © 2014 The Slate Group LLC.

Keyword: Sexual Behavior
Link ID: 19458 - Posted: 04.08.2014

By JoNel Aleccia The engineer who drove a speeding commuter train off the rails in New York last year may have suffered from the most severe form of a dangerous sleep disorder, but health experts say he has plenty of company. As many as 22 million people in the U.S. — or up to 7 percent of the population — may suffer from obstructive sleep apnea, experts say. It’s a condition that causes airways to collapse during sleep, cutting off breathing dozens or sometimes hundreds of times a night, leaving them bleary-eyed and drowsy, even after a full night’s rest. William Rockefeller, 46, was diagnosed after the December 2013 crash that killed four and injured more than 70 with severe obstructive sleep apnea, documents released this week show. On a scale where as few as five sleep disruptions an hour can make someone sleepy, and 30 episodes are considered severe, Rockefeller logged about 66 arousals an hour, doctors said. “His sleep was really fragmented,” said Dr. Phyllis Zee, a sleep expert with the Northwestern Medicine Sleep and Circadian Rhythms Research Program. “Even if he were to sleep seven or eight hours, he would be sleep-deprived.” Zee and her colleagues suspected that Rockefeller might suffer from sleep deprivation. He was obese, records show, and there’s a certain fatigued look that she saw in news photos of the engineer. “That was one of my thoughts, ‘Oh my goodness, he has (OSA),’” she said.

Keyword: Sleep
Link ID: 19457 - Posted: 04.08.2014

By KENNETH CHANG This occasional column explores topics covered in Science Times 25 years ago to see what has changed — and what has not. The claim about babies was startling: A test administered to infants as young as 6 months could predict their score on an intelligence test years later, when they started school. “Why not test infants and find out which of them could take more in terms of stimulation?” Joseph F. Fagan III, the psychologist at Case Western Reserve University in Cleveland who developed the test, was quoted as saying in an article by Gina Kolata on April 4, 1989. “It’s not going to hurt anybody, that’s for sure.” In the test, the infant looks at a series of photographs — first a pair of identical faces, then the same face paired with one the baby hasn’t seen. The researchers measure how long the baby looks at the new face. “On the surface, it tests novelty preference,” said Douglas K. Detterman, a colleague of Dr. Fagan’s at Case Western. For reasons not quite understood, babies of below-average intelligence do not exhibit the same attraction to novelty. Dr. Fagan suggested that the test could be used to identify children with above-average intelligence in poorer families so they could be exposed to enrichment programs more readily available to wealthier families. But his primary motivation, said Cynthia R. Holland, his wife and longtime collaborator, was to look for babies at the other end of the intelligence curve, those who would fall behind as they grew up. “His hope was always was to identify early on, in the first year of life, kids who were at risk, cognitively, so we could focus our resources on them and help them out,” said Dr. Holland, a professor of psychology at Cuyahoga Community College. 25 YEARS LATER For the most part, the validity of the Fagan test holds up. Indeed, Dr. Fagan (who died last August) and Dr. Holland revisited infants they had tested in the 1980s, and found that the Fagan scores were predictive of the I.Q. and academic achievement two decades later when these babies turned 21. © 2014 The New York Times Company

Keyword: Intelligence; Aggression
Link ID: 19456 - Posted: 04.08.2014

By Sam Kean Kent Cochrane, the amnesiac known throughout the world of neuroscience and psychology as K.C., died last week at age 62 in his nursing home in Toronto, probably of a stroke or heart attack. Although not as celebrated as the late American amnesiac H.M., for my money K.C. taught us more important and poignant things about how memory works. He showed how we make memories personal and personally meaningful. He also had a heck of a life story. During a wild and extended adolescence, K.C. jammed in rock bands, partied at Mardi Gras, played cards till all hours, and got into fights in bars; he was also knocked unconscious twice, once in a dune-buggy accident, once when a bale of hay conked him on the head. In October 1981, at age 30, he skidded off an exit ramp on his motorcycle. He spent a month in intensive care and lost, among other brain structures, both his hippocampuses. As H.M.’s case demonstrated in the early 1950s, the hippocampus—you have one in each hemisphere of your brain—helps form and store new memories and retrieve old ones. Without a functioning hippocampus, names, dates, and other information falls straight through the mind like a sieve. At least that’s what supposed to happen. K.C. proved that that’s not quite true—memories can sometimes bypass the hippocampus. After the motorcycle accident, K.C. lost most of his past memories and could make almost no new memories. But a neuroscientist named Endel Tulving began studying K.C., and he determined that K.C. could remember certain things from his past life just fine. Oddly, though, everything K.C. remembered fell within one restricted category: It was all stuff you could look up in reference books, like the difference between stalactites and stalagmites or between spares and strikes in bowling. Tulving called these bare facts “semantic memories,” memories devoid of all context and emotion. © 2014 The Slate Group LLC

Keyword: Learning & Memory
Link ID: 19455 - Posted: 04.08.2014

By NICHOLAS BAKALAR A new study adds to the evidence that the use of antidepressants during pregnancy is associated with a higher risk of premature birth, though many factors most likely play a role and the relationship is complex. Researchers reviewed data from 41 studies, some of which controlled for factors like smoking, alcohol or coffee drinking, weight gain during pregnancy, and other behavioral and health issues. They found no increase in the risk of early birth with the use of antidepressants during the first trimester, a 53 percent higher risk over all and a 96 percent higher risk with antidepressant use late in pregnancy. Depression itself is a risk factor for premature births, and a few studies tried to account for this by using, as a control, a group of women with a diagnosis of depression who did not take antidepressants during their pregnancy. Generally, researchers still found a higher, though diminished, risk from taking antidepressants. The review was published in March in PLOS One. Does this mean that all pregnant women should avoid these drugs? No, said the senior author, Dr. Adam C. Urato, an assistant professor of maternal-fetal medicine at Tufts University. Risks and benefits have to be balanced, he said. “It’s very complex, and depends on the severity of the disease,” Dr. Urato added. “The point is that we have to get the right information out so that we can let pregnant women make an informed decision.” © 2014 The New York Times Company

Keyword: Depression; Aggression
Link ID: 19454 - Posted: 04.08.2014

By ANA GANTMAN and JAY VAN BAVEL TAKE a close look at your breakfast. Is that Jesus staring out at you from your toast? Such apparitions can be as lucrative as they are seemingly miraculous. In 2004, a Florida woman named Diane Duyser sold a decade-old grilled cheese sandwich that bore a striking resemblance to the Virgin Mary. She got $28,000 for it on eBay. The psychological phenomenon of seeing something significant in an ambiguous stimulus is called pareidolia. Virgin Mary grilled cheese sandwiches and other pareidolia remind us that almost any object is open to multiple interpretations. Less understood, however, is what drives some interpretations over others. In a forthcoming paper in the journal Cognition, we hope to shed some light on that question. In a series of experiments, we examined whether awareness of perceptually ambiguous stimuli was enhanced by the presence of moral content. We quickly flashed strings of letters on a computer screen and asked participants to indicate whether they believed each string formed a word or not. To ensure that the letter strings were perceptually ambiguous, we flashed them between approximately 40 and 70 milliseconds. (When they were presented for too long, people easily saw all the letter strings and demonstrated close to 100 percent accuracy. When they were presented too quickly, people were unable to see the words and performed “at chance,” around 50 percent accuracy.) Some of the strings of letters we flashed were words, others were not. Importantly, some of the words we flashed had moral content (virtue, steal, God) and others did not (virtual, steel, pet). Over the course of three experiments, we found that participants correctly identified strings of letters as words more often when they formed moral words (69 percent accuracy) than when they formed nonmoral words (65 percent accuracy). This suggested that moral content gave a “boost” to perceptually ambiguous stimuli — a shortcut to conscious awareness. We call this phenomenon the “moral pop-out effect.” © 2014 The New York Times Company

Keyword: Attention
Link ID: 19453 - Posted: 04.07.2014

By BARBARA EHRENREICH MY atheism is hard-core, rooted in family tradition rather than adolescent rebellion. According to family legend, one of my 19th-century ancestors, a dirt-poor Irish-American woman in Montana, expressed her disgust with the church by vehemently refusing last rites when she lay dying in childbirth. From then on, we were atheists and rationalists, a stance I perpetuated by opting, initially, for a career in science. How else to understand the world except as the interaction of tiny bits of matter and mathematically predictable forces? There were no gods or spirits, just our own minds pressing up against the unknown. But something happened when I was 17 that shook my safely rationalist worldview and left me with a lifelong puzzle. Years later, I learned that this sort of event is usually called a mystical experience, and I can see in retrospect that the circumstances had been propitious: Thanks to a severely underfunded and poorly planned skiing trip, I was sleep-deprived and probably hypoglycemic that morning in 1959 when I stepped out alone, walked into the streets of Lone Pine, Calif., and saw the world — the mountains, the sky, the low scattered buildings — suddenly flame into life. There were no visions, no prophetic voices or visits by totemic animals, just this blazing everywhere. Something poured into me and I poured out into it. This was not the passive beatific merger with “the All,” as promised by the Eastern mystics. It was a furious encounter with a living substance that was coming at me through all things at once, too vast and violent to hold on to, too heartbreakingly beautiful to let go of. It seemed to me that whether you start as a twig or a gorgeous tapestry, you will be recruited into the flame and made indistinguishable from the rest of the blaze. I felt ecstatic and somehow completed, but also shattered. © 2014 The New York Times Company

Keyword: Schizophrenia; Aggression
Link ID: 19452 - Posted: 04.07.2014

By GRETCHEN REYNOLDS Age-related vision loss is common and devastating. But new research suggests that physical activity might protect our eyes as we age. There have been suggestions that exercise might reduce the risk of macular degeneration, which occurs when neurons in the central part of the retina deteriorate. The disease robs millions of older Americans of clear vision. A 2009 study of more than 40,000 middle-aged distance runners, for instance, found that those covering the most miles had the least likelihood of developing the disease. But the study did not compare runners to non-runners, limiting its usefulness. It also did not try to explain how exercise might affect the incidence of an eye disease. So, more recently, researchers at Emory University in Atlanta and the Atlanta Veterans Administration Medical Center in Decatur, Ga., took up that question for a study published last month in The Journal of Neuroscience. Their interest was motivated in part by animal research at the V.A. medical center. That work had determined that exercise increases the levels of substances known as growth factors in the animals’ bloodstream and brains. These growth factors, especially one called brain-derived neurotrophic factor, or B.D.N.F., are known to contribute to the health and well-being of neurons and consequently, it is thought, to improvements in brain health and cognition after regular exercise. But the brain is not the only body part to contain neurons, as the researchers behind the new study knew. The retina does as well, and the researchers wondered whether exercise might raise levels of B.D.N.F. there, too, potentially affecting retinal health and vision. © 2014 The New York Times Company

Keyword: Vision
Link ID: 19451 - Posted: 04.07.2014

by Clare Wilson A genetic tweak can make light work of some nervous disorders. Using flashes of light to stimulate modified neurons can restore movement to paralysed muscles. A study demonstrating this, carried out in mice, lays the path for using such "optogenetic" approaches to treat nerve disorders ranging from spinal cord injury to epilepsy and motor neuron disease. Optogenetics has been hailed as one of the most significant recent developments in neuroscience. It involves genetically modifying neurons so they produce a light-sensitive protein, which makes them "fire", sending an electrical signal, when exposed to light. So far optogenetics has mainly been used to explore how the brain works, but some groups are exploring using it as therapy. One stumbling block has been fears about irreversibly genetically manipulating the brain. In the latest study, a team led by Linda Greensmith of University College London altered mouse stem cells in the lab before transplanting them into nerves in the leg – this means they would be easier to remove if something went wrong. "It's a very exciting approach that has a lot of potential," says Ziv Williams of Harvard Medical School in Boston. Greensmith's team inserted an algal gene that codes for a light-responsive protein into mouse embryonic stem cells. They then added signalling molecules to make the stem cells develop into motor neurons, the cells that carry signals to and from the spinal cord to the rest of the body. They implanted these into the sciatic nerve – which runs from the spinal cord to the lower limbs – of mice whose original nerves had been cut. © Copyright Reed Business Information Ltd.

Keyword: Movement Disorders
Link ID: 19450 - Posted: 04.05.2014

By Deborah Serani Sometimes I work with children and adults who can’t put words to their feelings and thoughts. It’s not that they don’t want to – it’s more that they don’t know how. The clinical term for this experience is alexithymia and is defined as the inability to recognize emotions and their subtleties and textures [1]. Alexithymia throws a monkey wrench into a person’s ability to know their own self-experience or understand the intricacies of what others feel and think. Here are a few examples those with alexithymia experience: Difficulty identifying different types of feelings Limited understanding of what causes feelings Difficulty expressing feelings Difficulty recognizing facial cues in others Limited or rigid imagination Constricted style of thinking Hypersensitive to physical sensations Detached or tentative connection to others Alexithymia was first mentioned as a psychological construct in 1976 and was viewed as a deficit in emotional awareness [2]. Research suggests that approximately 8% of males and 2% of females experience alexithymia, and that it can come in mild, moderate and severe intensities [3]. Studies also show that alexithymia has two dimensions – a cognitive dimension, where a child or adult struggles to identify, interpret and verbalize feelings (the “thinking” part of our emotional experience). And an affective dimension, where difficulties arise in reacting, expressing, feeling and imagining (the “experiencing” part of our emotional experience) [4]. © 2014 Scientific American

Keyword: Emotions; Aggression
Link ID: 19449 - Posted: 04.05.2014

By LISA SANDERS, M.D. On Thursday, we challenged Well readers to solve the mystery of a 23-year-old man with episodes of aggressive, manic behavior that couldn’t be controlled. Nearly 1,000 readers wrote in with their take on this terrifying case. More than 300 of you got the right class of disease, and 21 of you nailed the precise form of the disorder. Amazing! The correct diagnosis is … Variegate porphyria The first person with the correct answer was Francis Graziano, a 23-year-old recent graduate of the University of Michigan. His major in neuroscience really gave him a leg up on this case, he told me. He recalled a case he read of a young Vietnam veteran with symptoms of porphyria. He’s a surgical technician right now, waiting to hear where he’ll be going to medical school next year. Strong work, Dr.-to-be Graziano! The Diagnosis: The word porphyria comes from the ancient Greek word for purple, “porphyra,” because patients with this disease can have purplish-red urine, tears or saliva. The porphyrias are a group of rare genetic diseases that develop in patients born without the machinery to make certain essential body chemicals, including one of the most important parts of blood known as heme. This compound makes up the core of the blood component hemoglobin. (The presence of heme is why blood is red.) Patients who can’t make heme correctly end up with too much of its chemical precursors, known as porphyrins. The excess porphyrins injure tissues throughout the body, but especially in the nervous system. The disorder is characterized by frequent episodes of debilitating back or abdominal pain and is often accompanied by severe psychiatric symptoms. Patients with porphyria do not respond to most psychiatric medications. Indeed, many of these drugs make the symptoms of porphyria worse. © 2014 The New York Times Company

Keyword: Schizophrenia
Link ID: 19448 - Posted: 04.05.2014

David Adam The day the Brazilian racing driver Ayrton Senna died in a crash, I was stuck in the toilet of a Manchester swimming pool. The door was open, but my thoughts blocked the way out. It was May 1994. I was 22 and hungry. After swimming a few lengths of the pool, I had lifted myself from the water and headed for the locker rooms. Going down the steps, I had scraped the back of my heel on the sharp edge of the final step. It left a small graze through which blood bulged into a blob that hung from my broken skin. I transferred the drop to my finger and a second swelled to take its place. I pulled a paper towel from above the sink to press to my wet heel. The blood on my finger ran with the water as it dripped down my arm. My eyes followed the blood. And the anxiety, of course, rushed back, ahead even of the memory. My shoulders sagged. My stomach tightened. Four weeks earlier, I had pricked my finger on a screw that stuck out from a bus shelter's corrugated metal. It was a busy Saturday afternoon and there had been lots of people around. Any one of them, I thought, could easily have injured themselves in the way I had. What if one had been HIV positive? They could have left infected blood on the screw, which then pierced my skin. That would put the virus into my bloodstream. I knew the official line was that transmission was impossible this way – the virus couldn't survive outside the body – but I also knew that, when pressed for long enough, those in the know would weaken the odds to virtually impossible. They couldn't be absolutely sure. In fact, several had admitted to me there was a theoretical risk. © 2014 Guardian News and Media Limited

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 19447 - Posted: 04.05.2014