By Jessica Schmerler Young brains are plastic, meaning their circuitry can be easily rewired to promote learning. By adulthood, however, the brain has lost much of its plasticity and can no longer readily recover lost function after, say, a stroke. Now scientists have successfully restored full youthful plasticity in adult mice by transplanting young neurons into their brain—curing their severe visual impairments in the process. In a groundbreaking study published in May in Neuron, a team of neuroscientists led by Sunil Gandhi of the University of California, Irvine, transplanted embryonic mouse stem cells into the brains of other mice. The cells were primed to become inhibitory neurons, which tamp down brain activity. Prior to this study, “it was widely doubted that the adult brain would allow these cells to disperse, integrate and reactivate plasticity,” says Melissa Davis, first author of the study. Scientists have been attempting such a feat for years, refining their methods along the way, and the Irvine team finally saw success: the cells were integrated in the brain and caused large-scale rewiring, restoring the high-level plasticity of early development. In visually impaired mice, the transplant allowed for the restoration of normal vision, as demonstrated by tests of visual nerve signals and a swimming maze test. The scientists have not yet tested the transplanting technique for other neurological disorders, but they believe the technique has potential for many conditions and injuries depending on how, exactly, the new neurons restore plasticity. It is not yet known whether the proliferation of the transplanted cells accounts for the restored plasticity or if the new cells trigger plasticity in existing neurons. If the latter, the treatment could spur the rewiring and healing of the brain following traumatic brain injury or stroke. © 2015 Scientific American

Keyword: Vision; Stem Cells
Link ID: 21572 - Posted: 10.27.2015

By GINA KOLATA Three diseases, leading killers of Americans, often involve long periods of decline before death. Two of them — heart disease and cancer — usually require expensive drugs, surgeries and hospitalizations. The third, dementia, has no effective treatments to slow its course. So when a group of researchers asked which of these diseases involved the greatest health care costs in the last five years of life, the answer they found might seem surprising. The most expensive, by far, was dementia. The study looked at patients on Medicare. The average total cost of care for a person with dementia over those five years was $287,038. For a patient who died of heart disease it was $175,136. For a cancer patient it was $173,383. Medicare paid almost the same amount for patients with each of those diseases — close to $100,000 — but dementia patients had many more expenses that were not covered. On average, the out-of-pocket cost for a patient with dementia was $61,522 — more than 80 percent higher than the cost for someone with heart disease or cancer. The reason is that dementia patients need caregivers to watch them, help with basic activities like eating, dressing and bathing, and provide constant supervision to make sure they do not wander off or harm themselves. None of those costs were covered by Medicare. For many families, the cost of caring for a dementia patient often “consumed almost their entire household wealth,” said Dr. Amy S. Kelley, a geriatrician at Icahn School of Medicine at Mt. Sinai in New York and the lead author of the paper published on Monday in the Annals of Internal Medicine. © 2015 The New York Times Company

Keyword: Alzheimers
Link ID: 21571 - Posted: 10.27.2015

By Dina Fine Maron When powerful street drugs collectively known as synthetic pot are smoked, the resulting high mimics the effects of marijuana. Yet these man-made cannabinoids are not marijuana at all. The drugs, more commonly called spice, fake weed or K2, are made up of any number of dried, shredded plants sprayed with chemicals that live in a murky legality zone. They are highly dangerous—and their use is on the rise. Synthetic pot, which first hit the market in the early 2000s, has especially caught the attention of public health officials in the past couple of years, stemming from a surge in hospitalizations and violent episodes. Although the drugs act on the same brain pathway as weed's active ingredient, they can trigger harsher reactions, including heart attacks, strokes, kidney damage and delusions. Between June and early August usage of these drugs led to roughly 2,300 emergency room visits in New York State alone. Nationwide more than 6,000 incidents involving spice have been reported to U.S. poison-control centers this year—about double the number of calls in 2013. Ever changing recipes make it possible for spice sellers to elude the authorities. Each time an ingredient is banned, producers swap in another compound. The drugs are then sold on the Internet or at gas stations and convenience stores at prices lower than genuine marijuana. The changing formulations also pose a challenge for researchers trying to match the chemicals with their side effects or to develop tests to identify them in a user's system. “The drugs are present in blood for only a short period, so it's very difficult to detect them,” says Marilyn Huestis, chief of the Chemistry and Drug Metabolism Section at the National Institute on Drug Abuse. © 2015 Scientific American

Keyword: Drug Abuse
Link ID: 21570 - Posted: 10.27.2015

Bret Stetka Sometime around 1907, well before the modern randomized clinical trial was routine, American psychiatrist Henry Cotton began removing decaying teeth from his patients in hopes of curing their mental disorders. If that didn't work he moved on to more invasive excisions: tonsils, testicles, ovaries and, in some cases, colons. Cotton was the newly appointed director of the New Jersey State Hospital for the Insane and was acting on a theory proposed by influential Johns Hopkins psychiatrist Adolph Meyer, under whom Cotton had studied, that psychiatric illness is the result of chronic infection. Meyer's idea was based on observations that patients with high fevers sometimes experience delusions and hallucinations. In 1921 he published a well-received book on the theory called The Defective Delinquent and Insane: the Relation of Focal Infections to Their Causation, Treatment and Prevention. A few years later The New York Times wrote, "eminent physicians and surgeons testified that the New Jersey State Hospital for the Insane was the most progressive institution in the world for the care of the insane, and that the newer method of treating the insane by the removal of focal infection placed the institution in a unique position with respect to hospitals for the mentally ill." Eventually Cotton opened a hugely successful private practice, catering to the infected molars of Trenton, N.J., high society. © 2015 npr

Keyword: Depression; Neuroimmunology
Link ID: 21569 - Posted: 10.26.2015

By Dina Fine Maron Early-life exposure to anesthesia does not appear to lead to long-term cognitive problems, researchers announced today. New evidence from the first, randomized anesthesia trial in kids provides the strongest indication yet that exposing young children to anesthesia—at least for a brief time—will not saddle them with developmental deficits. The news comes just a couple of weeks after a medical advisory group reiterated its concerns about such exposures among children younger than four years. Previously, multiple animal and human studies have linked such exposure with cognitive impairment, but none of the information on humans came from a gold-standard, randomized study design that could help eliminate other reasons to explain such a connection. This is a “reassuring finding, but it is not the final answer,” says Dean Andropoulos, anesthesiologist in chief at Texas Children’s Hospital and an expert who was not involved in the work. The new study assesses only what happens to youngsters after a relatively brief bout with anesthetics, so it is possible that longer or repeated exposures to such chemicals may still cause neurodevelopmental issues. There may also be deficits in anesthesia-exposed children that are not measurable until later in life. The study followed more than 500 infants undergoing hernia repair across the U.S., Australia, the U.K., Canada, the Netherlands, New Zealand and Italy. The surgeries lasted an average of roughly an hour. About half of the children were randomly selected to be put under with general anesthesia, and the other half stayed awake during the surgery and received targeted anesthesic in a specific body region. The kids in the study were all younger than 60 weeks and were matched by where they had the surgery and whether they were born prematurely. © 2015 Scientific American

Keyword: Development of the Brain; Intelligence
Link ID: 21568 - Posted: 10.26.2015

Richard A. Friedman YOU can increase the size of your muscles by pumping iron and improve your stamina with aerobic training. Can you get smarter by exercising — or altering — your brain? Stories from Our Advertisers This is hardly an idle question considering that cognitive decline is a nearly universal feature of aging. Starting at age 55, our hippocampus, a brain region critical to memory, shrinks 1 to 2 percent every year, to say nothing of the fact that one in nine people age 65 and older has Alzheimer’s disease. The number afflicted is expected to grow rapidly as the baby boom generation ages. Given these grim statistics, it’s no wonder that Americans are a captive market for anything, from supposed smart drugs and supplements to brain training, that promises to boost normal mental functioning or to stem its all-too-common decline. The very notion of cognitive enhancement is seductive and plausible. After all, the brain is capable of change and learning at all ages. Our brain has remarkable neuroplasticity; that is, it can remodel and change itself in response to various experiences and injuries. So can it be trained to enhance its own cognitive prowess? The multibillion-dollar brain training industry certainly thinks so and claims that you can increase your memory, attention and reasoning just by playing various mental games. In other words, use your brain in the right way and you’ll get smarter. A few years back, a joint study by BBC and Cambridge University neuroscientists put brain training to the test. Their question was this: Do brain gymnastics actually make you smarter, or do they just make you better at doing a specific task? For example, playing the math puzzle KenKen will obviously make you better at KenKen. But does the effect transfer to another task you haven’t practiced, like a crossword puzzle? © 2015 The New York Times Company

Keyword: Learning & Memory; Intelligence
Link ID: 21567 - Posted: 10.26.2015

By Diana Kwon Microglia, the immune cells of the brain, have long been the underdogs of the glia world, passed over for other, flashier cousins, such as astrocytes. Although microglia are best known for being the brain’s primary defenders, scientists now realize that they play a role in the developing brain and may also be implicated in developmental and neurodegenerative disorders. The change in attitude is clear, as evidenced by the buzz around this topic at this year’s Society for Neuroscience (SfN) conference, which took place from October 17 to 21 in Chicago, where scientists discussed their role in both health and disease. Activated in the diseased brain, microglia find injured neurons and strip away the synapses, the connections between them. These cells make up around 10 percent of all the cells in the brain and appear during early development. For decades scientists focused on them as immune cells and thought that they were quiet and passive in the absence of an outside invader. That all changed in 2005, when experimenters found that microglia were actually the fastest-moving structures in a healthy adult brain. Later discoveries revealed that their branches were reaching out to surrounding neurons and contacting synapses. These findings suggested that these cellular scavengers were involved in functions beyond disease. The discovery that microglia were active in the healthy brain jump-started the exploration into their underlying mechanisms: Why do these cells hang around synapses? And what are they doing? © 2015 Scientific American

Keyword: Glia; Neuroimmunology
Link ID: 21566 - Posted: 10.26.2015

By ALEX HUTCHINSON WHEN marketing researchers at the University of Pennsylvania’s Wharton School rigged shopping carts at a major East Coast supermarket with motion-tracking radio-frequency tags, they unwittingly stumbled on a metaphor for our path through the aisles of life. Route data from more than 1,000 shoppers, matched to their purchases at checkout, revealed a clear pattern: Drop a bunch of kale into your cart and you’re more likely to head next to the ice cream or beer section. The more “virtuous” products you have in your basket, the stronger your temptation to succumb to vice. Such hedonic balancing acts are neither unpredictable — who, after all, hasn’t rewarded themselves with a piece of cake or an extra beer after a killer workout? — nor inherently bad. But an emerging body of research into what psychologists call the “licensing effect” suggests that this tit-for-tat tendency is deeply wired in us, operating even when we’re not aware of it. And in a world where we’re bombarded by pitches for an endless array of health-boosting products of dubious efficacy, that can be a problem. The key insight underlying the licensing effect, which was first described in 2006 by Uzma Khan, then a professor of marketing at Carnegie Mellon University, and Ravi Dhar of the Yale School of Management, is that our choices are contingent: Since we each have a fairly stable self-concept of how good/bad, healthy/unhealthy or selfish/altruistic we are, when one decision swings too far from this self-concept, we automatically take action to balance it out. © 2015 The New York Times Company

Keyword: Obesity; Attention
Link ID: 21565 - Posted: 10.26.2015

Dyscalculia is like dyslexia — but for those who have trouble with math instead of reading. But not enough people know about it, according to a neuroscientist. "There is a lack of awareness among teachers and educators," said Daniel Ansari, professor and Canada Research Chair in Developmental Cognitive Neuroscience at the University of Western Ontario. Individuals with dyscalculia have trouble with simple calculations. "If I ask you what is 1 + 3, you don't need to calculate. Four will pop in to your head, it is stored in your long-term memory," he said. But those with dyscalculia will have to use their hands to count. Scientists have known about dyscalculia since the 1940's but little research has been done on it, even though it is probably just as common as dyslexia, says Ansari. Currently, there is no existing universal form of testing for dyscalculia. But Ansari has come up with screening tests for children in kindergarten. He says it's important to diagnose dyscalculia early on, so individuals can learn to adapt and improve their skills before it's too late. "We don't just need math to be good in school but to function in society," said Ansari. He says research has shown poor math skills can lead to an increased chance of unemployment, imprisonment or mortgage default. ©2015 CBC/Radio-Canada.

Keyword: Attention
Link ID: 21564 - Posted: 10.26.2015

By Nicholas Bakalar A new study has found that sleep apnea is associated with an increased risk for gout, a painful disease of the big toe and other joints caused by elevated levels of uric acid in the blood. Observational studies have shown that people with sleep apnea have a higher prevalence of excess uric acid, but until now it has been unclear whether sleep apnea is associated with gout, and how strongly. Using records in a British health database, researchers studied 9,865 people, average age 54, with sleep apnea and matched them to 43,598 controls without the disorder. Because sleep apnea is associated with being overweight, the participants were matched for B.M.I., among many other characteristics. The study is in Arthritis & Rheumatology. After one year, compared with controls, people with sleep apnea were about 50 percent more likely to have had an attack of gout, and the increased risk was found without regard to sex, age or obesity. The conclusion suggests that treating sleep apnea would reduce gout attacks, but the lead author, Yuqing Zhang, a professor of medicine at Boston University, is cautious. “Our findings call for future studies to evaluate the effect of treating sleep apnea on serum uric acid levels and the risk of gout,” he said. © 2015 The New York Times Company

Keyword: Sleep
Link ID: 21563 - Posted: 10.26.2015

As we get older, most of us will experience some kind of brain degeneration. Typically, we lose the ability to make new neurons. Another problem is chronic, low-grade inflammation in the brain, which is implicated in many age-related brain disorders. To tackle both problems in one go, Ludwig Aigner at Paracelsus Medical University Salzburg in Austria and his colleagues targeted a set of receptors in the brain that, when activated, trigger inflammation. High numbers of these receptors are found in areas of the brain where neurons are born, suggesting they might also be involved in this process, too. A drug called montelukast (Singulair), regularly prescribed for asthma and allergic rhinitis, blocks these receptors, so Aigner and his colleagues tried it on young and old rats. The team used oral doses equivalent to those taken by people with asthma. The older animals were 20 months old – roughly equivalent to between 65 and 75 in human years. The younger rats were 4 months old – about 17 in human years. The animals were fed the drug daily for six weeks, while another set of young and old rats were left untreated. There were 20 young and 14 old rats in total. The rats took part in a range of learning and memory tests. One of these, for example, involved the rats being placed in a pool of water with a hidden escape platform. At the start of the study, untreated young rats learned to recognise landmarks and quickly find their way to the platform, while the untreated older animals struggled at the task. © Copyright Reed Business Information Ltd.

Keyword: Development of the Brain; Neurogenesis
Link ID: 21562 - Posted: 10.24.2015

By R. Douglas Fields “Why can’t you stop drinking?” This week at the Annual Meeting of the Society for Neuroscience in Chicago, researchers from the University of Chicago announced a new finding that provides a fresh answer to this persistent question that plagues people addicted to alcohol. The discovery offers an entirely new approach to treatment. Neuroscientist, Amy Lasek, at the Department of Psychiatry at the University of Illinois, Chicago, and colleagues, report that after binge drinking, neurons in brain circuits responsible for alcohol addiction become encased in a protein material, called a perineuronal net. The impenetrable coating cements neurons involved in alcohol addiction into a circuit that is extremely difficult to break. Current drugs for treating alcohol dependence work by modifying neurotransmitter signaling between neurons, but for many people these treatments cannot break the overwhelming compulsion to drink. Drugs that can break down the glue-like cement in perineuronal nets could offer a new approach to treatment. Lasek’s unusual approach into addiction research stems from her background as a molecular and cell biologist working in the field of cancer research. The root of cancer is changes in specific genes. Small molecules designed to target these aberrant genes is the approach used in cancer therapy. Lasek’s background made her think of finding molecularly targeted therapies for psychiatric disorders. Lasek and her colleagues began by studying fruit flies to search for gene variations that altered the fly’s behavior toward alcohol. She found several genes that had this effect, including an obscure one called ALK (anaplastic lymphoma kinase). Then she suppressed these genes in mice to see if the animal’s response to alcohol was altered. “I got hooked,” she says, “because to me the fact that you can manipulate a single gene in a single brain region and change behavior—like drinking or cocaine reward—was fascinating from a biological point of view!” © 2015 Scientific America

Keyword: Drug Abuse
Link ID: 21561 - Posted: 10.24.2015

By Carrie Arnold Most of the anorexia patients Dr. Joanna Steinglass sees in the inpatient eating-disorders unit at the New York State Psychiatric Institute have been to treatment before. While in the hospital or a residential treatment center, they generally gained weight and began to eat a wider variety of foods. But after they left, their old anorexic habits returned. They began skipping meals again or returning to their extreme exercise routines. All too soon, it seemed, the gains made in treatment and the hope for recovery that went along with it began to evaporate. According to the conventional wisdom around eating disorders, these relapses were really a misguided search for control. Or maybe the patients just weren’t ready for recovery yet. Or perhaps these were signs of self-control gone awry, spurred on by friends who marvel at their seemingly endless willpower. Interesting theories, and yet Steinglass disagreed. “Even when people show up at our hospital and want to make changes, they find it tough,” she said. Now a new study in Nature Neuroscience — which Steinglass co-authored — reveals why people with anorexia often struggle so much to integrate new ways of eating into their lives. In the brain, the behaviors associated with anorexia act a lot like habits, those daily decisions we make without thinking. And habits, according to both the scientific evidence and the colloquial wisdom, are phenomenally difficult to break. This new finding helps explain why anorexia has historically been so hard to treat: Anorexic patients are essentially fighting their own brains in an uphill battle for wellness. But more important, the new research may also point toward new and better ways to help those with the eating disorder overcome it. © 2015, New York Media LLC.

Keyword: Anorexia & Bulimia
Link ID: 21560 - Posted: 10.24.2015

Claire Cain Miller Boys are falling behind. They graduate from high school and attend college at lower rates than girls and are more likely to get in trouble, which can hurt them when they enter the job market. This gender gap exists across the United States, but it is far bigger for poor people and for black people. As society becomes more unequal, it seems, it hurts boys more. New research from social scientists offers one explanation: Boys are more sensitive than girls to disadvantage. Any disadvantage, like growing up in poverty, in a bad neighborhood or without a father, takes more of a toll on boys than on their sisters. That realization could be a starting point for educators, parents and policy makers who are trying to figure out how to help boys — particularly those from black, Latino and immigrant families. “It’s something about family disadvantage itself,” said David Figlio, a Northwestern University economist and co-author of a new paper, presented publicly for the first time on Thursday. “Black people in America are more disadvantaged than white people in America, and if we were to reduce the disadvantage, we may see a reduction in the relative gender gap as well.” Marianne Bertrand, an economist at University of Chicago who with Jessica Pan has studied the gender gap, also found that boys fare worse than girls in disadvantaged homes, and are more responsive than girls to parental time and resources. “Their findings were very consistent: Families that invest more in children are protective for boys,” she said. The reasons that boys react more negatively to disadvantage are varied and hard to pinpoint. Even in utero, boys are more sensitive to extreme stress than girls, and tend to have more unruly temperaments. Society discourages boys from showing vulnerability. Low-income families are often led by single mothers, which has been found to affect boys differently than girls. © 2015 The New York Times Company

Keyword: Development of the Brain; Sexual Behavior
Link ID: 21559 - Posted: 10.24.2015

By Bob Grant Scientists delving into the neurological underpinnings of traumatic brain injuries (TBI) are finding that there may be crucial differences in the long-term effects of the events that depend not only on the insult, but also on the victim. “No two brain injuries are identical,” University of Pennsylvania neuroscientist Akiva Cohen said during a press conference held at the Society for Neuroscience (SfN) annual meeting in Chicago on Monday (October 19). “Brain injury, like many pathologies these days, constitutes a spectrum.” In addition to a severity spectrum that spans mild to severe, brain injuries may differ in terms of how male and female animals respond to them, according to Ramesh Raghupathi, a neurobiologist at Drexel University. Raghupathi and his colleagues have found that young male mice suffer more depressive behaviors than female mice at both four and eight weeks after mild TBI, and females display more headache-like symptoms after similar insults, which can include concussion. “All of these animals at these times after injury are cognitively normal,” Raghupathi told reporters. “And they do not have any movement problems.” Raghupathi and his colleagues also found molecular differences that may underlie the sex differences in TBI response that they observed. “In the male mice,” he said, “there is a dramatic difference in dopamine transmission” compared to the uninjured mice.” Researchers have previously linked impaired dopamine signaling to depression. Raghupathi’s team tested for the lingering effects of TBI in mice by subjecting the animals to certain swimming tests—which are accepted as proxies for depression—and by using a thin filament to touch the faces of the rodents and recording their sensitivity as a measure of headache-like behaviors.

Keyword: Brain Injury/Concussion; Sexual Behavior
Link ID: 21558 - Posted: 10.24.2015

Elizabeth Blair The muppet Julia has not yet made her TV debut, but the wide-eyed little girl with a big smile is the star of her own "digital storybook" called "We're Amazing, 1,2,3." For over a year now, Sesame Street has been working with organizations such as Autism Speaks and Autism Self Advocacy to help reduce the stigma associated with autism spectrum disorder. As part of the campaign "See Amazing in All Children," the adorable muppet Abby Cadabby explains in one YouTube video, "Lots of kids have autism and that just means their brains work a little differently." Julia is not the first fictional media character with autism. But Michael Robb, Director of Research for Common Sense Media, an organization that rates and reviews media aimed at children, says Sesame Street's move is "pretty groundbreaking." "It can be difficult to start a conversation about children with disabilities. It's even harder when that difference isn't visible," he says. After looking through "We're Amazing, 1,2,3," Robb says the story could help children be more understanding of how Julia is different. "It's very real in terms of talking in simple language. It spells out these things in concrete ways that kids can understand. It shows ways she's just like other kids. It shows how making simple accommodations can help Julia." According to Dr. Jeanette Betancourt, Senior Vice President of U.S. Social Impact at Sesame Workshop, says Sesame Street producers are waiting to hear back from the autism community before introducing Julia to the show on TV. © 2015 npr

Keyword: Autism
Link ID: 21557 - Posted: 10.24.2015

Olivia Maynard It has been described as a ‘disruptive technology’ potentially capable of breaking our fatal relationship with tobacco. So the setting for a public debate on e-cigarettes - a museum part-funded by the tobacco industry, in a city home to the global headquarters of one of the largest tobacco manufacturers - was perhaps ironic. Yet on Wednesday evening, I found myself at the M-Shed in Bristol, watching just that: a debate about whether e-cigarettes could be part of the solution to the tobacco epidemic. To mark the launch of a new Integrative Cancer Epidemiology Programme, linked to the Medical Research Centre Integrative Epidemiology Unit at the University of Bristol, Professor Marcus Munafò (Professor of Biological Psychology at the University of Bristol) and Professor Linda Bauld (Professor of Health Policy at the University of Stirling), both collaborators of mine, discussed e-cigarettes. Professor Gabriel Scally (Public Health Doctor and former Regional Director of Public Health for the South West of England) chaired the discussion. Billed as a debate about whether e-cigarettes might be ‘the key to reducing smoking’, some in the audience may have expected a heated discussion. However, with this line-up of academics, influential in the fields of public health, tobacco and addiction, the discussion was evidence-based and measured. As for the motion of the debate, the panel was unanimous: e-cigarettes may not be the key to reducing smoking, but they are certainly an important part of the solution. © 2015 Guardian News and Media Limited

Keyword: Drug Abuse
Link ID: 21556 - Posted: 10.24.2015

Alzheimer's disease can be detected decades before onset, using a virtual reality test, a study suggests. People aged 18 to 30 were asked to navigate through a virtual maze to test the function of certain brain cells. Those with a high genetic risk of Alzheimer's could be identified by their performance, according to German neuroscientists. The findings could help future research, diagnosis and treatment, they report in the journal Science. The scientists, led by Lukas Kunz of the German Centre for Neurodegenerative Diseases in Bonn, say the high risk group navigated the maze differently and had reduced functioning of a type of brain cell involved in spatial navigation. The findings could give an insight into why people with dementia can find navigating the world around them challenging, they say. "Our results could provide a new basic framework for preclinical research on Alzheimer's disease and may provide a neurocognitive explanation of spatial disorientation in Alzheimer's disease," they report in Science. Although genes play a role in dementia, their effects are complex with many unknowns. Dr Laura Phipps of Alzheimer's Research, said the latest study focused on healthy younger people at higher genetic risk of Alzheimer's, suggesting they may already show alterations in spatial navigation several decades before the disease could start. © 2015 BBC.

Keyword: Alzheimers
Link ID: 21555 - Posted: 10.23.2015

By JAMES GORMAN No offense to tenors, but outside of opera, a high male voice is seldom, if ever, considered seductive. Scientific research has shown that women find deep male voices attractive, and the same is true in other species, like howler monkeys. Stories from Our Advertisers But evolution is often stingy in its gifts, and researchers investigating male competition to reproduce have discovered an intriguing trade-off in some species of howler monkeys: the deeper the call, the smaller the testicles. Jacob Dunn of Cambridge University, one of the leaders of the research, said that species evolved either to make lower-frequency sounds, or have larger testicles, but none had both a very low sound and very large testicles. “It’s a great study,” said Stuart Semple, an evolutionary anthropologist at the University of Roehampton in London who was not involved in the research. “It shows this really clear trade-off.” Dr. Dunn and other researchers, including W. Tecumseh Fitch, of the University of Vienna, and Leslie A. Knapp, of the University of Utah, studied the size of a bone in the vocal apparatus, which is directly related to how deep the calls are, and the size of testicles, to come up for averages in nine species of howlers. They had been intrigued by great variations in both the size of the howlers’ hyoid bones in museum collections and in the size of the monkeys’ testicles as seen in the field. Dr. Knapp said that some of them are large enough that they are quite obvious “when you look up into the trees.” They used the museum samples of the bone and living monkeys in zoos for testicle measurements, and reported their findings Thursday in the journal Current Biology. © 2015 The New York Times Company

Keyword: Sexual Behavior; Hearing
Link ID: 21554 - Posted: 10.23.2015

Jon Hamilton For a few days this week, a convention center in Chicago became the global epicenter of brain science. Nearly 30,000 scientists swarmed through the vast hallways of the McCormick Place convention center as part of the annual Society for Neuroscience meeting. Among them were Nobel Prize winners, the director of the National Institutes of Health, and scores of researchers regarded as the international rock stars of neuroscience. "It's amazing. I'm a bit overwhelmed," said Kara Furman, a graduate student from Yale who was attending her first Society for Neuroscience meeting. Furman was just one of several hundred neuroscientists I found standing in lines outside the center one afternoon, waiting for shuttle buses. She was pondering a presentation from a few hours earlier that she found "pretty mind-blowing." What was it about? "Using MRI techniques to access dopamine release at the molecular level," she told me, deadpan. Welcome to the five-day annual event that's become known simply as "The Neuro Meeting." It's where brain scientists from around the world come to present their own work and discover the "mind-blowing" research others are doing. And there are thousands of presentations to choose from. "I prepared an itinerary based on my interests and that ran into 20 pages," said Srinivas Bharath from the National Institute of Mental Health and Neurosciences in Bangalore, India. © 2015 npr

Keyword: Miscellaneous
Link ID: 21553 - Posted: 10.23.2015