Most Recent Links

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 61 - 80 of 19443

By Jen Christiansen I threw down a bit of a challenge last month at the Association of Medical Illustrators Conference in Minnesota. But first, I had to—somewhat unexpectedly—accept some challenges presented by others. And face the reality that some of us simply do not have the constitution of an anatomist. I love classic anatomical illustrations such as the vintage works of Andreas Vesalius and the more modern stylings of Frank Netter. And on that front, this conference definitely delivered. Talks by Daniel Garrison and Francine Netter were drool-worthy, and I snapped photos of quickly advancing slides presented by W. Bruce Fye on the history of the illustrated heart, so I could reverse-image search them later and spend more time checking out the details and context. Videos of Robert Beverly Hale’s Art Students League lectures on anatomy charmed me (as presented by Glen Hintz), as well as new videos of clean architectural microstructures like the inner ear, presented by Robert Acland. I had to make myself walk quickly by one vendor table to avoid blowing my book budget for the year (and then some) on an impulse buy of Vesalius’ 1543 De Humani Corporis Fabrica, newly translated to English. But I averted my gaze when surgeons presented on the topic of facial transplantation and skull reconstruction. Shoot, I couldn’t even look at the screen through the entirety of a fascinating talk by Elizabeth Weissbrod and Valerie Henry on creating and using virtual and prosthetic simulations for military emergency response training. I avoided the hands-on human cadaveric dissection workshop sessions, telling myself and others that my travel schedule would simply not allow me to get to the Mayo Clinic in Rochester, Minn., early enough to participate or observe. © 2014 Scientific American

Keyword: Brain imaging
Link ID: 19957 - Posted: 08.14.2014

The news of Robin Williams’s suicide has brought mental health into the spotlight this week. According to data from the Massachusetts Violent Death Reporting System at the department of public health, the number of deaths per year as a result of suicide in the state has increased 4 percent per year since 2003. The rate increased from 424 suicides in 2003 to a peak of 600 in 2010, before dropping back down to 588. That’s 8.9 suicides per 100,000, a total of 4,500 deaths for this preventable public health problem. There are many biological, sociological, and psychological risk factors that can increase an individual’s risk for committing suicide. But did you know that poor sleep could be a major factor pushing people over the edge, even if they aren’t depressed? We all know the feeling that when we’re under slept, we aren’t quite ourselves, but according to the Substance Abuse and Mental Health Services Administration, sleep complaints are actually one of the top 10 warning signs for suicide. A study published today in JAMA Psychiatry is the first research of its kind to draw a correlation between poor sleep habits and an increased risk for death by suicide by controlling for signs of depression. Stanford University School of Medicine researchers have found that over a 10 year observation period, people with poor sleep quality and no other depressive symptoms demonstrated a 1.2 times greater risk for death by suicide.

Keyword: Depression; Aggression
Link ID: 19956 - Posted: 08.14.2014

By NICHOLAS BAKALAR A new study reports that caffeine intake is associated with a reduced risk for tinnitus — ringing or buzzing in the ears. Researchers tracked caffeine use and incidents of tinnitus in 65,085 women in the Nurses’ Health Study II. They were 30 to 34 and without tinnitus at the start of the study. Over the next 18 years, 5,289 developed the disorder. The women recorded their use of soda, coffee and tea (caffeinated and not), as well as intake of candy and chocolate, which can contain caffeine. The results appear in the August issue of The American Journal of Medicine. Compared with women who consumed less than 150 milligrams of caffeine a day (roughly the amount in an eight-ounce cup of coffee), those who had 450 to 599 milligrams a day were 15 percent less likely to have tinnitus, and those who consumed 600 milligrams or more were 21 percent less likely. The association persisted after controlling for other hearing problems, hypertension, diabetes, use of anti-inflammatory Nsaid drugs, a history of depression and other factors. Decaffeinated coffee consumption had no effect on tinnitus risk. “We can’t conclude that caffeine is a cure for tinnitus,” said the lead author, Dr. Jordan T. Glicksman, a resident physician at the University of Western Ontario. “But our results should provide some assurance to people who do drink caffeine that it’s reasonable to continue doing so.” © 2014 The New York Times Company

Keyword: Hearing
Link ID: 19955 - Posted: 08.14.2014

by Catherine Brahic Think crayfish and you probably think supper, perhaps with mayo on the side. You probably don't think of their brains. Admittedly, crayfish aren't known for their grey matter, but that might be about to change: they can grow new brain cells from blood. Humans can make new neurons, but only from specialised stem cells. Crayfish, meanwhile, can convert blood to neurons that resupply their eyestalks and smell circuits. Although it's a long way from crayfish to humans, the discovery may one day help us to regenerate our own brain cells. Olfactory nerves are continuously exposed to damage and so naturally regenerate in many animals, from flies to humans, and crustaceans too. It makes sense that crayfish have a way to replenish these nerves. To do so, they utilise what amounts to a "nursery" for baby neurons, a little clump at the base of the brain called the niche. In crayfish, blood cells are attracted to the niche. On any given day, there are a hundred or so cells in this area. Each cell will split into two daughter cells, precursors to full neurons, both of which migrate out of the niche. Those that are destined to be part of the olfactory system head to two clumps of nerves in the brain called clusters 9 and 10. It's there that the final stage of producing new smell neurons is completed. © Copyright Reed Business Information Ltd.

Keyword: Neurogenesis; Aggression
Link ID: 19954 - Posted: 08.13.2014

|By Melinda Wenner Moyer For most people, “fat,” particularly the kind that bulges under the skin, is a four-letter word. It makes our thighs jiggle; it lingers despite our torturous attempts to eliminate it. Too much of it increases our risk for heart disease and type 2 diabetes (the most common form of the condition). For decades researchers have looked for ways to reduce our collective stores of fat because they seemed to do more harm than good. But biology is rarely that simple. In the late 2000s several research groups independently discovered something that shattered the consensus about the absolute dangers of body fat. Scientists had long known that humans produce at least two types of fat tissue—white and brown. Each white fat cell stores energy in the form of a single large, oily droplet but is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria. These organelles in turn burn up the droplets to generate heat. Babies, who have not yet developed the ability to shiver to maintain their body temperature, rely on thermogenic deposits of brown fat in the neck and around the shoulders to stay warm. Yet investigators assumed that all brown fat disappears during childhood. The new findings revealed otherwise. Adults have brown fat, too. Suddenly, people started throwing around terms like holy grail to describe the promise of brown fat to combat obesity. The idea was appealingly simple: if researchers could figure out how to incite the body to produce extra brown fat or somehow rev up existing brown fat, a larger number of calories would be converted into heat, reducing deposits of white fat in the process. © 2014 Scientific American

Keyword: Obesity
Link ID: 19953 - Posted: 08.13.2014

By GRETCHEN REYNOLDS Regular exercise may alter how a person experiences pain, according to a new study. The longer we continue to work out, the new findings suggest, the greater our tolerance for discomfort can grow. For some time, scientists have known that strenuous exercise briefly and acutely dulls pain. As muscles begin to ache during a prolonged workout, scientists have found, the body typically releases natural opiates, such as endorphins, and other substances that can slightly dampen the discomfort. This effect, which scientists refer to as exercise-induced hypoalgesia, usually begins during the workout and lingers for perhaps 20 or 30 minutes afterward. But whether exercise alters the body’s response to pain over the long term and, more pressing for most of us, whether such changes will develop if people engage in moderate, less draining workouts, have been unclear. So for the new study, which was published this month in Medicine & Science in Sports & Exercise, researchers at the University of New South Wales and Neuroscience Research Australia, both in Sydney, recruited 12 young and healthy but inactive adults who expressed interest in exercising, and another 12 who were similar in age and activity levels but preferred not to exercise. They then brought all of them into the lab to determine how they reacted to pain. Pain response is highly individual and depends on our pain threshold, which is the point at which we start to feel pain, and pain tolerance, or the amount of time that we can withstand the aching, before we cease doing whatever is causing it. © 2014 The New York Times Company

Keyword: Pain & Touch
Link ID: 19952 - Posted: 08.13.2014

|By Piercarlo Valdesolo In the summer of 2009 I tried to cure homemade sausages in my kitchen. One of the hazards of such a practice is preventing the growth of undesirable molds and diseases such as botulism. My wife was not on board with this plan, skeptical of my ability to safely execute the procedure. And so began many weeks of being peppered with warnings, relevant articles and concerned looks. When the time came for my first bite, nerves were high. My throat itched. My heart raced. My vision blurred. I had been botulized! Halfway through our walk to the hospital I regained my composure. Of course I had not been instantaneously struck by an incredibly rare disease that, by the way, takes at least 12 hours after consumption to manifest and does not share many symptoms with your garden variety anxiety attack. My experience had been shaped by my mindset. A decade of learning about the psychological power of expectations could not inoculate me from its effect. Psychologists know that beliefs about how experiences should affect us can bring about the expected outcomes. Though these “placebo effects” have primarily been studied in the context of pharmaceutical interventions (e.g. patients reporting pain relief after receiving saline they believed to be an analgesic), recent research has shown their strength in a variety of domains. Tell people that their job has exercise benefits and they will lose more weight than their coworkers who had no such belief. Convince people of a correlation between athleticism and visual acuity and they will show better vision after working out . Trick people into believing they are consuming caffeine and their vigilance and cognitive functioning increases. Some evidence shows that such interventions can even mitigate the negative effects of other experiences. For example, consuming placebo caffeine alleviates the cognitive consequences of sleep deprivation. © 2014 Scientific American

Keyword: Sleep; Aggression
Link ID: 19951 - Posted: 08.13.2014

By EDWARD LARKIN and IRENE HURFORD PHILADELPHIA — A FEW months ago, a patient came to our hospital, seeking help. One of us, Edward, was on the team that treated him. He was pleasant, if slightly withdrawn, and cogent. He was a college graduate in his 20s and had recently been fired from his job as a high school math teacher, because of unexpected absences. He had come to believe that government agents were conspiring against him, and he had taken to living out of a truck and sleeping in different parking lots. By the time he came to us, he was exhausted. A diagnosis became clear: he had schizophrenia. We admitted him to the hospital, and after a few days, with his symptoms under control, we released him. Unfortunately, we prescribed a medication for him that could cause significant, permanent harm, instead of an equally effective drug with milder side effects — all because he was uninsured. Schizophrenia, which affects 1 percent of the population and emerges in the late teens to early 20s, is deeply misunderstood. People who suffer from it are often suspected of being dangerous, but this is not usually the case, and antipsychotic drugs are very effective. Our patient was exactly the kind of person who, with the right treatment, could have weakened the stigma surrounding schizophrenia. Antipsychotic drugs fall into two classes: the older ones, like Haldol, and newer ones, like Abilify and Latuda. Both classes are equally effective at treating some of the worst symptoms of schizophrenia, specifically the hallucinations, delusions and paranoia that cause social alienation. (They’re not effective for treating “negative symptoms,” like low motivation.) But the older drugs can cause a multitude of serious side effects, including a potentially devastating one called tardive dyskinesia. This condition involves unsettling, animalistic smacking and wagging of the lips and tongue. At its extreme, it can affect the entire body. It occurs in 20 percent or more of patients who take the drugs long-term, and it tends to start so mildly that patients can’t identify it in time to stop taking the drugs. It is often irreversible. © 2014 The New York Times Company

Keyword: Schizophrenia
Link ID: 19950 - Posted: 08.13.2014

Sara Reardon When the states of Colorado and Washington voted to legalize marijuana in 2012, the abrupt and unprecedented policy switch sent the US National Institute on Drug Abuse (NIDA) into what its director Nora Volkow describes as “red alarm”. Although marijuana remained illegal for people under the age of 21, the drug’s increased availability and growing public acceptance suggested that teenagers might be more likely to try it (see ‘Highs and lows’). Almost nothing is known about whether or how marijuana affects the developing adolescent brain, especially when used with alcohol and other drugs. The new laws, along with advances in brain-imaging technology, convinced Volkow to accelerate the launch of an ambitious effort to follow 10,000 US adolescents for ten years in an attempt to determine whether marijuana, alcohol and nicotine use are associated with changes in brain function and behaviour. At a likely cost of more than US$300 million, it will be the largest longitudinal brain-imaging study of adolescents yet. Researchers are eager to study a poorly understood period of human development — but some question whether it is possible to design a programme that will provide useful information about the effects of drugs. “It’s definitely an idea that’s overdue,” says Deanna Barch, a psychologist at Washington University in St. Louis, Missouri. “The downside is it’s a lot of eggs in one basket.” © 2014 Nature Publishing Group,

Keyword: Development of the Brain; Aggression
Link ID: 19949 - Posted: 08.13.2014

By MICHAEL CIEPLY and BROOKS BARNES LOS ANGELES — Peering through his camera at Robin Williams in 2012, the cinematographer John Bailey thought he glimpsed something not previously evident in the comedian’s work. They were shooting the independent film “The Angriest Man in Brooklyn,” and Mr. Williams was playing a New York lawyer who, facing death, goes on a rant against the injustice and banality of life. His performance, Mr. Bailey said Tuesday, was a window into the “Swiftian darkness of Robin’s heart.” The actor, like his character, was raging against the storm. That defiance gave way on Monday to the personal demons that had long tormented Mr. Williams. With his suicide at age 63, Mr. Williams forever shut the window on a complicated soul that was rarely visible through the cracks of an astonishingly intact career. Given his well-publicized troubles with depression, addiction, alcoholism and a significant heart surgery in 2009, Mr. Williams should have had a résumé filled with mysterious gaps. Instead, he worked nonstop. At the very least — if his life had followed the familiar script of troubled actors — there would have been whispers of on-set antics: lateness, forgotten lines, the occasional flared temper. Not so with Mr. Williams. “He was ready to work, he was the first one on the set,” said Mr. Bailey, speaking of Mr. Williams’s contribution to “The Angriest Man in Brooklyn,” of which he was the star. “Robin was always 1,000 percent reliable,” said a senior movie agent, speaking on the condition of anonymity to conform to the wishes of Mr. Williams’s family. “He was almost impossibly high functioning.” As Hollywood struggled on Tuesday to understand how Mr. Williams — effervescent in the extreme — could take his own life, authorities released details of his death. A clothed Mr. Williams hanged himself with a belt from a door frame in his bedroom in Tiburon, Calif., according to Lt. Keith Boyd, assistant deputy chief coroner for Marin County. © 2014 The New York Times Company

Keyword: Depression
Link ID: 19948 - Posted: 08.13.2014

By Lenny Bernstein, Lena H. Sun and Sandhya Somashekhar Suicides are the 10th-leading cause of death in the United States and eighth among people in the 55- to 64-year-old age group. Comedian Robin Williams, who died Monday of an apparent suicide, was 63. In 2010, 38,364 people died this way. Many suicides are the result of undiagnosed or untreated depression, often masked by self-medicating behaviors such as alcohol and drug use. Though we don’t yet know the exact circumstances of Williams’s death, we do know that he long battled addictions to cocaine and alcohol and, according to his publicist, was struggling with “severe depression.” But unlike many people, Williams had the resources and the motivation to seek treatment, at least for his addictions. According to this report, he had undergone rehab at the famed Hazelden Addiction Treatment Center in Minnesota two months ago, and had sought treatment in 2006 when he began drinking again after 20 years of sobriety. How, then, do we explain the death of someone who appeared to recognize the danger he faced and was trying to address it? Here are some thoughts: • Suicides are often impulsive acts: People who kill themselves are not thinking clearly, have trouble solving problems and weigh risks differently from us, Jill Harkavy-Friedman, vice president of research for the American Foundation for Suicide Prevention, told To Your Health in March. If thwarted in their first attempt, they often do not try again immediately, she said.

Keyword: Depression; Aggression
Link ID: 19947 - Posted: 08.13.2014

Jia You Premature babies are more likely to produce piercing cries than their full-term peers are, researchers report online today in Biology Letters. Scientists have studied infant crying as a noninvasive way to assess how well a baby’s nervous system develops. Previous research of full-term babies indicates that an abnormally high pitch is associated with disturbances in an infant’s metabolism and neurological development. The team recorded spontaneous crying in preterm babies and full-term babies of the same age and compared the pitch of their sobs. They found that preterm babies whimper in a shriller voice, but not because they are smaller in size or grew at a slower rate in their mothers’ wombs. Instead, the researchers suspect the high pitch could reflect lower levels of activities in a premature baby’s vagal nerve, which extends from the brain stem to the abdomen. Vagal nerve activities are believed to decrease tension in the vocal cords, thus producing a lower pitch. Previous studies show that giving preterm babies massage therapies can stimulate their vagal activities, improve their ingestion, and help them gain weight. © 2014 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 19946 - Posted: 08.13.2014

James Gorman Deep in the mouse brain, scientists recently found that a very small network of cells, a few thousand at most, turns appetite on and off. They used the most sophisticated of modern techniques, but as has often happened in science — witness penicillin, Velcro and Viagra — the researchers discovered something they weren’t looking for. “This was an accidental discovery,” said David Anderson, of the California Institute of Technology, the senior scientist on the team that reported the finding, in Nature Neuroscience. The discovery may eventually lead to a better understanding and treatment of eating disorders. The surprise and drama of the finding are immediately clear, however, in lab videos. A mouse busily munches lab chow until a light signal is sent to its brain, and the mouse wanders off, no longer interested in food. His lab had previously studied this small group of neurons, in a part of the brain called the amygdala. That earlier research was on fear, an emotion strongly associated with the amygdala in both mice and humans. As a technique called optogenetics became more and more refined, he said, it seemed worth revisiting the neurons with this new tool. Optogenetics requires genetic manipulation of specific cells to make them sensitive to light in a certain wavelength, in this case blue light. Then fiber-optic cables are inserted into the brain, and when the light is turned on, neurons can be activated or turned off. Researchers in Dr. Anderson’s lab, including Haijiang Cai, a postdoctoral researcher and a co-author of the report, prepared the mice and conducted the experiment with the entirely unexpected result. © 2014 The New York Times Company

Keyword: Obesity
Link ID: 19945 - Posted: 08.12.2014

By Rachel Feltman Bioengineers have created the most realistic fake brain tissue ever – and it’s built like a jelly doughnut. The 3-D tissue, described in a paper published Monday in Proceedings of the National Academy of Sciences, is so structurally similar to a real rat brain (a common substitute for human brains in the lab) that it could help scientists answer longstanding questions about brain injuries and disease. Currently, the best way to study brain tissue is to grow neurons in a petri dish, but those neurons can only be grown flat. A real brain contains a complicated structure of 3-D tissue. Simply giving the neurons room to grow in three dimensions didn’t prove successful: While neurons will grow into more complicated structures in the right kind of gel, they don’t survive very long or mimic the structure of a real brain. Led by David Kaplan, the director of the Tissue Engineering Resource Center at Tufts University, researchers developed a new combination of materials to mimic the gray and white matter of the brain. The new model relies on a doughnut-shaped, spongy scaffold made of silk proteins with a collagen-based gel at the center. The outer scaffold layer, which is filled with rat neurons, acts as the grey matter of the brain. As the neurons grew networks throughout the scaffold, they sent branches out across the gel-filled center to connect with neurons on the other side. And that configuration is about as brain-like as lab-grown tissue can get. The basic structure can be reconfigured, too.

Keyword: Robotics; Aggression
Link ID: 19944 - Posted: 08.12.2014

By PAM BELLUCK The 40-year-old man showed up in Dr. Mary Malloy’s clinic with sadly disfiguring symptoms. His hands, elbows, ears and feet were blemished with protruding pustules and tuber-like welts, some so painful it was hard for him to walk. He suffered from a rare genetic condition called dysbetalipoproteinemia, which caused his cholesterol levels to soar so high that pools of fatty tissue seemed to bubble up under his skin. But there was something else about this patient. He was missing a gene that, when present in one form, greatly increases the risk of developing Alzheimer’s disease. Dr. Malloy, who co-directs the Adult Lipid Clinic at the University of California, San Francisco, and her colleagues saw an opportunity to answer an important neurological riddle: Does the absence of the gene — named apolipoprotein E, or APOE, after the protein it encodes — hurt the brain? If a person with this rare condition were found to be functioning normally, that would suggest support for a new direction in Alzheimer’s treatment. It would mean that efforts — already being explored by dementia experts — to prevent Alzheimer’s by reducing, eliminating or neutralizing the effects of the most dangerous version of APOE might succeed without causing other problems in the brain. The researchers, who reported their findings on Monday in the journal JAMA Neurology, discovered exactly that. They ran a battery of tests, including cognitive assessments, brain imaging and cerebrospinal fluid analyses. The man’s levels of beta-amyloid and tau proteins, which are markers of Alzheimer’s, gave no indication of neurological disease. His brain size was unaffected, and the white matter was healthy. His thinking and memory skills were generally normal. “This particular case tells us you can actually live without any APOE in the brain,” said Dr. Joachim Herz, a neuroscientist and molecular geneticist at University of Texas Southwestern Medical Center, who was not involved in the research. “So if they were to develop anti-APOE therapies for Alzheimer’s, we would not have to worry about serious neurological side effects.” © 2014 The New York Times Company

Keyword: Alzheimers
Link ID: 19943 - Posted: 08.12.2014

|By Nathan Collins Time zips by when you're having fun and passes slowly when you're not—except when you are depressed, in which case your time-gauging abilities are pretty accurate. Reporting in PLOS ONE, researchers in England and Ireland asked 39 students—18 with mild depression—to estimate the duration of tones lasting between two and 65 seconds and to produce tones of specified lengths of time. Happier students overestimated intervals by 16 percent and produced tones that were short by 13 percent, compared with depressed students' 3 percent underestimation and 8 percent overproduction. The results suggest that depressive realism, a phenomenon in which depressed people perceive themselves more accurately (and less positively) than typical individuals, may extend to aspects of thought beyond self-perception—in this case, time. They speculate that mindfulness treatments may be effective for depression, partly because they help depressed people focus on the moment, rather than its passing. © 2014 Scientific American

Keyword: Depression; Aggression
Link ID: 19942 - Posted: 08.12.2014

By NATALIE ANGIER SOUTH LUANGWA NATIONAL PARK, ZAMBIA — We saw the impala first, a young buck with a proud set of ridged and twisted horns, like helical rebar, bounding across the open plain at full, desperate gallop. But why? A moment later somebody in our vehicle gasped, and the answer became clear. Rising up behind the antelope, as though conjured on movie cue from the aubergine glow of the late afternoon, were six African wild dogs, running in single file. They moved with military grace and precision, their steps synchronized, their radio-dish ears cocked forward, their long, puppet-stick legs barely skimming the ground. Still, the impala had such a jump on them that the dogs couldn’t possibly catch up — could they? We gunned the engine and followed. The pace quickened. The dogs’ discipline held steady. They were closing the gap and oh, no, did I really want to watch the kill? To my embarrassed relief, the violence was taken off-screen, when prey and predators suddenly dashed up a hill and into obscuring bushes. By the time we reached the site, the dogs were well into their communal feast, their dark muzzles glazed with bright red blood, their white-tipped tails wagging in furious joy. “They are the most enthusiastic animals,” said Rosie Woodroffe of the Institute of Zoology in London, who has studied wild dogs for the last 20 years. “Other predators may be bigger and fiercer, but I would argue that there is nothing so enthusiastic as a wild dog,” she said. “They live the life domestic dogs wish they could live.” In 1997, while devising an action plan to help save the wild dog species, Lycaon pictus, Dr. Woodroffe felt anything but exuberant. Wild dogs were considered among the most endangered of Africa’s mammals; Dr. Woodroffe had yet to see one in the wild, and she feared she never would. © 2014 The New York Times Company

Keyword: Aggression; Aggression
Link ID: 19941 - Posted: 08.12.2014

Helen Shen Most people gradually recover from trauma, but a small fraction of individuals develop post-traumatic stress disorder (PTSD) — prompting scientists to look for the biological underpinnings of this extreme response to traumatic situations such as warfare, car accidents and natural disasters. Research published on 11 August in Proceedings of the National Academy of Sciences identifies up to 334 genes that may be involved in vulnerability to post-traumatic stress in rats1. Most animal studies of stress use intense stimuli such as electric shocks, designed to produce large, group differences between exposed and unexposed animals. But Nikolaos Daskalakis and his colleagues tried a subtler approach to elicit a wide range of individual responses in rats that had all experienced the same trauma — more closely mimicking the variability of human responses to disturbing events. "We wanted to capture the differences between a susceptible individual and one that is not susceptible to the same experience," says Daskalakis, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York. The researchers exposed around 100 rats to soiled cat litter — which evokes a feared predator — and tested the animals one week later for lingering effects of the trauma. About one-quarter of the exposed animals were classified as 'extreme' responders, showing high levels of anxiety and startling easily on hearing loud noises. Another quarter of the animals were 'minimal' responders, and exhibited anxiety levels similar to those of non-exposed rats. © 2014 Nature Publishing Group

Keyword: Stress; Aggression
Link ID: 19940 - Posted: 08.12.2014

By Gary Stix A gamma wave is a rapid, electrical oscillation in the brain. A scan of the academic literature shows that gamma waves may be involved with learning memory and attention—and, when perturbed, may play a part in schizophrenia, epilepsy Alzheimer’s, autism and ADHD. Quite a list and one of the reasons that these brainwaves, cycling at 25 to 80 times per second, persist as an object of fascination to neuroscientists. Despite lingering interest, much remains elusive when trying to figure out how gamma waves are produced by specific molecules within neurons—and what the oscillations do to facilitate communication along the brains’ trillions and trillions of connections. A group of researchers at the Salk Institute in La Jolla, California has looked beyond the preeminent brain cell—the neuron— to achieve new insights about gamma waves. At one time, neuroscience textbooks depicted astrocytes as a kind of pit crew for neurons, providing metabolic support and other functions for the brain’s rapid-firing information-processing components. In recent years, that picture has changed as new studies have found that astrocytes, like neurons, also have an alternate identity as information processors. This research demonstrates astrocytes’ ability to spritz chemicals known as neurotransmitters that communicate with other brain cells. Given that both neurons and astrocytes perform some of the same functions, it has been difficult to tease out what specifically astrocytes are up to. Hard evidence for what these nominal cellular support players might contribute in forming memories or focusing attention has been lacking. © 2014 Scientific American

Keyword: Attention; Aggression
Link ID: 19939 - Posted: 08.12.2014

By Smitha Mundasad Health reporter, BBC News Human brains grow most rapidly just after birth and reach half their adult size within three months, according to a study in JAMA Neurology. Using advanced scanning techniques, researchers found male brains grew more quickly than those of female infants. Areas involved in movement developed at the fastest pace. Those associated with memory grew more slowly. Scientists say collating this data may help them identify early signs of developmental disorders such as autism. For centuries doctors have estimated brain growth using measuring tape to chart a baby's head circumference over time. Any changes to normal growth patterns are monitored closely as they can suggest problems with development. But as head shapes vary, these tape measurements are not always accurate. Led by scientists at the University of California, researchers scanned the brains of 87 healthy babies from birth to three months. They saw the most rapid changes immediately after birth - newborn brains grew at an average rate of 1% a day. This slowed to 0.4% per day at the end of the 90-day period. Researchers say recording the normal growth trajectory of individual parts of the brain might help them better understand how early disorders arise. They found the cerebellum, an area of the brain involved in the control of movement, had the highest rate of growth - doubling in size over the 90-day period. BBC © 2014

Keyword: Development of the Brain; Aggression
Link ID: 19938 - Posted: 08.12.2014