By Mark Changizi The human fascination with color never ceases to amaze me. Our perceptual experience is filled with shapes and pitches and textures and timbres and depths and on and on, yet color seems to get the lion share of our excitement and philosophical attention. Color seems somehow more artistic than our other perceptual dimensions; it’s simply wonderful to behold, as evinced by the double rainbow guy; and we can’t resist wondering what it would be like to see dimensions of color beyond our own. In fact, RadioLab recently put out a great show on color that nicely conveys the romance we all have toward it. Question is: Why do we find color so enthralling? One of the reasons may be that the world can seem arbitrarily labeled in color, as if a painter dabbed over everything in order to make it beautiful… and that naturally makes us wonder what a different artist might do. What sort of splendor is a bird—who has an extra dimension of color beyond ours—treated to, for example? While I, too, feel the wonder of color, I don’t share this above intuition about color and its arbitrariness. It’s an unfortunate intuition, one that seeps its way not only into the minds of laymen, but into our “enhancement” products and even the hallowed halls of philosophy. In trying to explain what’s wrong with the intuition, let me begin with a thought experiment concerning a product that gives the wearer “shape enhancement” vision. “With our sunglasses’ shape-enhancement filter, you’ll see the world with more vibrant and interesting shapes. Round things will be rounder, regular polygons more muted…”

Keyword: Vision
Link ID: 17608 - Posted: 12.17.2012

By Jason G. Goldman While second nature to many of us, driving a car is actually a fairly complex process. At its most stripped down version, first you sit in the driver’s seat, then you start the engine, then you shift into gear, and then you must simultaneously steer while keeping your foot on the gas pedal. That doesn’t include things like adjusting your mirrors, verifying that you won’t drive into another person or car, and so on. In one sense, it is incredibly impressive that three dogs in New Zealand have learned – in a fairly rudimentary way – to drive a car. They sit in the driver’s seat, shift into gear, operate the steering wheel, and step on the accelerator. Those deserving the true accolades however are not the dogs, but the human trainers for their impressive patience and determination. The training that led man’s best friend to operate a car is no different from the kind of training behind the bird shows found at zoos all over the world, or the dolphin, killer whale, seal, or sea lion displays you might see at Sea World. It’s the same kind of training that scientists use to probe the emotional and cognitive lives of rats, mice, and the other critters that populate their laboratories. At the end of the day, it all comes down to a form of learning first described by Edward L. Thorndike at the beginning of the 1900s, which was later expanded and popularized by B.F. Skinner and taught to every student of Introductory Psychology: operant conditioning. While classical conditioning is a form of learning that binds external stimuli to reflexive, involuntary responses, operant conditioning involves voluntary behaviors, and is maintained over time by the consequences that follow those behaviors. In one experiment, Skinner placed pigeons individually into experimental chambers (sometimes referred to as “Skinner boxes”) that were designed to deliver food rewards at systematic intervals. He found that by rewarding a bird after it displayed a desired behavior, he could motivate the bird to increase the frequency of that particular behavior. © 2012 Scientific American

Keyword: Learning & Memory
Link ID: 17607 - Posted: 12.14.2012

by Kai Kupferschmidt Human beings tend to avoid places that smell of urine. But to mice, there is something positively addictive about the scent; they like to go back to a spot where they found the excretions again and again. Now, researchers have discovered that this behavior is triggered by a single protein in the urine of male mice. Mice use scent to mark their territory, advertise their social dominance, and convey information about their health and reproductive status. But these are usually volatile pheromones that disperse quickly, and it has remained unclear what exactly stimulates a female to be attracted to a specific male. Previous research had shown that female laboratory mice often return to a place where they have come across cage bedding soiled by males. Now, researchers at the University of Liverpool in the United Kingdom have confirmed this. Female mice spent five times as much time in a place where they had encountered a dish with male urine than at a place where they encountered water. Just 10 minutes of exposure to the urine was enough for the mice to show this place preference even after 14 days. However, if the mice were prevented from by a mesh screen touching the urine with their nose, the place seemed to lose its attractiveness. "That suggested that the story was not as simple as everybody assumed and volatile pheromones were not responsible," says behavioral ecologist Jane Hurst, one of the authors of the study. By separating the urine into different fractions, the scientists showed that a protein called darcin that they had identified in 2005—and which mice can only detect if their noses touch the urine—is responsible for the frequent visits. Pure darcin, produced in cell culture in the lab, elicited the same reaction, the authors report online today in Science. © 2010 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Sexual Behavior
Link ID: 17606 - Posted: 12.14.2012

By JAMES DAO Reviving a 20-year debate over illnesses of veterans of the 1991 Persian Gulf war, a new scientific paper presents evidence that nerve agents released by the bombing of Iraqi chemical weapons depots just before the ground war began could have carried downwind and fallen on American troops staged in Saudi Arabia. The paper, published in the journal Neuroepidemiology, tries to rebut the longstanding Pentagon position, supported by many scientists, that neurotoxins, particularly sarin gas, could not have carried far enough to sicken American forces. The authors are James J. Tuite and Dr. Robert Haley, who has written several papers asserting links between chemical exposures and gulf war illnesses. They assembled data from meteorological and intelligence reports to support their thesis that American bombs were powerful enough to propel sarin from depots in Muthanna and Falluja high into the atmosphere, where winds whisked it hundreds of miles south to the Saudi border. Once over the American encampments, the toxic plume could have stalled and fallen back to the surface because of weather conditions, the paper says. Though troops would have been exposed to low levels of the agent, the authors assert that the exposures may have continued for several days, increasing their impact. Though chemical weapons detectors sounded alarms in those encampments in the days after the January 1991 bombing raids, they were viewed as false by many troops, the authors report. © 2012 The New York Times Company

Keyword: Stress; Neurotoxins
Link ID: 17605 - Posted: 12.14.2012

A specific pattern of neuronal firing in a brain reward circuit instantly rendered mice vulnerable to depression-like behavior induced by acute severe stress, a study supported by the National Institutes of Health has found. When researchers used a high-tech method to mimic the pattern, previously resilient mice instantly succumbed to a depression-like syndrome of social withdrawal and reduced pleasure-seeking — they avoided other animals and lost their sweet tooth. When the firing pattern was inhibited in vulnerable mice, they instantly became resilient. "For the first time, we have shown that split-second control of specific brain circuitry can switch depression-related behavior on and off with flashes of an LED light," explained Ming-Hu Han, Ph.D. External Web Site Policy, of the Mount Sinai School of Medicine, New York City, a grantee of NIH’s National Institute of Mental Health (NIMH). "These results add to mounting clues about the mechanism of fast-acting antidepressant responses." Han, Eric Nestler, M.D., Ph.D. External Web Site Policy,of Mount Sinai, and colleagues, report on their study in the journal Nature. In a companion article, NIMH grantees Kay Tye, Ph.D. External Web Site Policy, of the Massachusetts Institute of Technology, Cambridge, Mass., and Karl Deisseroth, M.D., Ph.D. External Web Site Policy, of Stanford University, Stanford, Calif., used the same cutting-edge technique to control mouse brain activity in real time. Their study reveals that the same reward circuit neuronal activity pattern had the opposite effect when the depression-like behavior was induced by daily presentations of chronic, unpredictable mild physical stressors, instead of by shorter-term exposure to severe social stress.

Keyword: Stress; Depression
Link ID: 17604 - Posted: 12.14.2012

Gary Taubes. “It is better to know nothing,” wrote French physiologist Claude Bernard in An Introduction to the Study of Experimental Medicine (1865), “than to keep in mind fixed ideas based on theories whose confirmation we constantly seek.” Embracing a fixed idea is one of the main dangers in the evolution of any scientific discipline. Ideally, errors will be uncovered in the trial-by-fire of rigorous testing and the science will right itself. In rare cases, however, an entire discipline can be based on a fundamental flaw. As a science journalist turned science historian, I have written at length about how and why this may have happened in obesity research. I have suggested that the discipline may be a house of cards — as, by extension, may much research into the chronic diseases associated with obesity, such as diabetes. Before the Second World War, European investigators believed that obesity was a hormonal or regulatory disorder. Gustav von Bergmann, a German authority on internal medicine, proposed this hypothesis in the early 1900s. The theory evaporated with the war. After the lingua franca of science switched from German to English, the German-language literature on obesity was rarely cited. (Imagine the world today if physicists had chosen to ignore the thinking that emerged from Germany and Austria before the war.) Instead, physicians embraced the ideas of the University of Michigan physician Louis Newburgh, who argued that obese individuals had a “perverted appetite” that failed to match the calories that they consumed with their bodies' metabolic needs. “All obese persons are alike in one fundamental respect,” Newburgh insisted, “they literally overeat.” This paradigm of energy balance/overeating/gluttony/sloth became the conventional, unquestioned explanation for why we get fat. It is, as Bernard would say, the fixed idea. © 2012 Nature Publishing Group

Keyword: Obesity
Link ID: 17603 - Posted: 12.13.2012

by Peter Aldhous IT HAS been more than a decade in the works, but finally we know the main changes that will be introduced next May, when the American Psychiatric Association publishes the next edition of its Diagnostic and Statistical Manual of Mental Disorders, known as DSM-5. Those changes, which could influence the way millions are treated, include new definitions of autism and related conditions, and a shift in the criteria for depression to include some people grieving after bereavement. Debate over DSM-5 seems likely to rumble on. But now there is a deeper problem to ponder: while discoveries about the genes and brain circuits that underlie human behaviour are accumulating rapidly, they haven't led to major clinical advances. That's largely because these findings don't map well on to the constellation of conditions described in the DSM. When the last major revision was completed in 1994, its authors hoped that neurobiologists would soon home in on specific disruptions to brain circuitry involved in the main psychiatric disorders. "I was naive enough to think that it was just a matter of time," says Michael First of Columbia University in New York City. It hasn't worked out that way. Take schizophrenia: what was once considered to be a distinct psychotic disorder actually seems to cover a variety of disruptions to normal brain functioning. This suggests that many of psychiatry's diagnostic labels do not describe coherent conditions with common underlying causes. No wonder, then, that many conditions are so hard to treat. © Copyright Reed Business Information Ltd.

Keyword: Schizophrenia; Depression
Link ID: 17602 - Posted: 12.13.2012

By Laura Sanders Signs of depression can be turned on and off in mice with the flip of a switch. Activating or silencing the behavior of certain brain cells with laser light causes the animals to change their depressive behavior, two new studies find. Although the experiments were done in rodents, the results have direct relevance to human depression, says neurologist Helen Mayberg of the Emory University School of Medicine in Atlanta. The new work may point out places in the human brain that doctors can similarly stimulate to treat depression. The results, published online December 13 in Nature, took advantage of a technique called optogenetics, which allows scientists to control nerve cell behavior with a tiny fiber-optic light. In the studies, mice were genetically engineered to harbor nerve cell proteins that respond to light. The researchers could make certain nerve cells fire off messages by shining blue light, and quiet them by shining yellow light. These cells, which produce the chemical messenger dopamine, nestle in a brain region called the ventral tegmental area, a spot known for handling rewards. This system may be skewed in people with depression, since the disorder often keeps people from responding normally to things that used to be enjoyable. One tiny fiber-optic flash had an instant and profound effect on the mice’s behavior, says psychiatrist and neuroscientist Karl Deisseroth of Stanford University, who coauthored both papers. “That was pretty amazing for us.” © Society for Science & the Public 2000 - 2012

Keyword: Depression
Link ID: 17601 - Posted: 12.13.2012

By Ed Yong In a lab at Stanford University, a mouse is showing signs of depression. For around 10 weeks, it has experienced a series of irritations, from bouts without food or water, to erratic sleep patterns. Now, its motivation is low—when picked up by the tail, it makes few attempts to escape, and it doesn’t try to explore new spaces. It’s also less willing to sip from a sugary liquid– a sign that it gets less pleasure from normally pleasurable activities. It is never easy to assess the mental health of an animal, but this mouse is clearly showing some of the classic symptoms of depression. But not for long. Earlier, Kay Tye and Julie Mirzabekov altered the mouse so that a flash of light can activate a small part of its brain—the ventral tegmental area (VTA), near the bottom of the brain and close to the midline. A burst of light, and the mouse’s behaviour changes almost instantly. It struggles when held aloft, it explores open areas, and it regains its sweet tooth. A burst of light, and its symptoms disappear. But on the other side of the country, at the Mount Sinai School of Medicine, Dipesh Chaudhury and Jessica Walsh are doing the same thing to completely different effect. Their mice have been altered in a similar way, so that light can also switch on their VTA neurons. But these rodents have endured a shorter but more intense form of stress—10 days of being placed in cages with dominant, aggressive rivals. Because of the resulting attacks, some of them have developed depressive symptoms. Others are more resilient. But when Chaudhury and Walsh flashed the VTAs of these mice, resilient individuals transformed into susceptible ones.

Keyword: Depression
Link ID: 17600 - Posted: 12.13.2012

by Elizabeth Norton From a strictly Darwinian viewpoint, homosexuality shouldn't still be around. It isn't the best way to pass along one's genes, and to complicate the picture further, no "gay genes" have even been identified. According to a newly released hypothesis, the explanation may not lie in DNA itself. Instead, as an embryo develops, sex-related genes are turned on and off in response to fluctuating levels of hormones in the womb, produced by both mother and child. This tug of war benefits the unborn child, keeping male or female development on a steady course even amid spikes in hormones. But if these so-called epigenetic changes persist once the child is born and has children of its own, some of those offspring may be homosexual, the study proposes. Evolutionary geneticist William Rice of the University of California, Santa Barbara, felt there had to be a reason why homosexuality didn't just fade away down the generations. Research estimates that about 8% of the population is gay, and homosexuality is known to run in families. If one of a set of identical twins is gay, there's a 20% probability that the other will be, too. Furthermore, Rice notes, "homosexuality isn't just a human thing." Among California gulls, which he watches from his office window, about 14% of pairs are female-female. In Australian black swans, some 6% of pairs are male-male, and 8% of male sheep are attracted exclusively to male partners. But many genetic screens have failed to turn up genes that are responsible for sexual orientation. So to find out what makes homosexuality persist, Rice and colleagues began a comprehensive survey of the literature. © 2010 American Association for the Advancement of Science

Keyword: Sexual Behavior; Epigenetics
Link ID: 17599 - Posted: 12.13.2012

By KATIE THOMAS The drug maker Eli Lilly & Company said on Wednesday that it planned an additional study of an experimental Alzheimer’s drug that failed to improve the condition of people with the disease, saying that it remained hopeful about the drug’s prospects. The newest study is expected to get under way in the third quarter of 2013 and will focus on patients with mild Alzheimer’s disease. Lilly released results of two clinical trials in August that showed the drug, called solanezumab, did not significantly improve either the cognition or the daily functioning of people with mild and moderate forms of the disease. But despite that failure, the results also gave some reason for hope: when patients with mild Alzheimer’s were separated out, the drug was shown to significantly slow their decline in cognition. In a statement on Wednesday, the company said it decided not to pursue approval of the drug based on existing study results after it met with officials from the Food and Drug Administration. A Lilly executive said, however, that the company was still optimistic. “We remain encouraged and excited by the solanezumab data,” David Ricks, a senior vice president at Lilly and president of Lilly Bio-Medicines, said in the statement. “We are committed to working with the F.D.A. and other regulatory authorities to bring solanezumab to the millions of patients and caregivers suffering from this devastating disease who urgently need this potential treatment.” The Lilly drug is the second Alzheimer’s treatment to fail in clinical trials this year. Pfizer and Johnson & Johnson stopped development of a similar treatment, bapineuzumab, after it, too, was not shown to work. Both drugs target beta amyloid, a protein in the brain that is found in people with Alzheimer’s disease. © 2012 The New York Times Company

Keyword: Alzheimers
Link ID: 17598 - Posted: 12.13.2012

Posted by Heidi Ledford Just in time for the holidays, a team of MIT and Max Planck researchers has released EyeWire: an online game that allows users to trace neural connections through the retina. In the proud tradition of Foldit and other ‘citizen science’ endeavours, EyeWire aims to harness the power of the people to map the projections of retinal cells called JAM-B cells. JAM-B cells respond specifically to upward motion (which appears downward to the retina, because it receives inverted images), and were the first retinal ganglion cells distinguished on the basis of a molecular marker — a protein called ‘Junctional Adhesion Molecule B’ (JAM-B). Does the downward trajectory of the JAM-B cell projections relate to their function? The scientists behind EyeWire hope to find out. EyeWire, launched 10 December, is spearheaded by MIT’s Sebastian Seung, best known for taking the concept of mapping neural connections and turning it into the surprisingly digestible and well-read popular science book Connectomics: How the Brain’s Wiring Makes Us Who We Are. Seung and his colleagues chart the retinal connectome by taking serial electron micrographs of thin slices of tissue. They then trace individual neural projections through each slice and stitch it all together again into a three dimensional image. Seung’s team could use all the help it can get: in a review of Seung’s book, Caltech neuroscientist Christoph Koch estimated that to map a cubic millimetre of brain would require a billion images and a million working-years of analysis time for a trained technician. © 2012 Nature Publishing Group

Keyword: Brain imaging
Link ID: 17597 - Posted: 12.11.2012

Analysis by Emily Sohn Older people who remembered going hungry as children were slower to lose their mental sharpness as they reached old age. The new finding was only true for African-Americans, suggesting that the study hit on a particularly resilient group of people who thrived despite extreme childhood adversity. Even so, the study offers insight into how the experiences we have at very young ages can affect our health much later in life. "We know that the social experiences of African-Americans and Caucasians in this country have been very different, at least for people over age 65," said Lisa Barnes, a cognitive neuropsychologist at Rush University Medical Center in Chicago. "We wanted to measure that and see if it had any effect at all." In an effort to add to a growing interest in the long-term health influence of childhood adversity, Barnes and colleagues started by interviewing about 6,100 people who lived in Chicago and were enrolled in a study of Alzheimer's. All participants were at least 65 years old when the study began. The average starting age was 75. In the first interview, seniors answered questions about their childhoods, including details about health, the financial situations of their families and how often someone read books to them. They also took a cognitive exam that included tests of memory. © 2012 Discovery Communications, LLC.

Keyword: Alzheimers; Obesity
Link ID: 17596 - Posted: 12.11.2012

By SABRINA TAVERNISE PHILADELPHIA — After decades of rising childhood obesity rates, several American cities are reporting their first declines. The trend has emerged in big cities like New York and Los Angeles, as well as smaller places like Anchorage, Alaska, and Kearney, Neb. The state of Mississippi has also registered a drop, but only among white students. “It’s been nothing but bad news for 30 years, so the fact that we have any good news is a big story,” said Dr. Thomas Farley, the health commissioner in New York City, which reported a 5.5 percent decline in the number of obese schoolchildren from 2007 to 2011. The drops are small, just 5 percent here in Philadelphia and 3 percent in Los Angeles. But experts say they are significant because they offer the first indication that the obesity epidemic, one of the nation’s most intractable health problems, may actually be reversing course. The first dips — noted in a September report by the Robert Wood Johnson Foundation — were so surprising that some researchers did not believe them. Deanna M. Hoelscher, a researcher at the University of Texas, who in 2010 recorded one of the earliest declines — among mostly poor Hispanic fourth graders in the El Paso area — did a double-take. “We reran the numbers a couple of times,” she said. “I kept saying, ‘Will you please check that again for me?’ ” © 2012 The New York Times Company

Keyword: Obesity
Link ID: 17595 - Posted: 12.11.2012

A drug that works through the same brain mechanism as the fast-acting antidepressant ketamine briefly improved treatment-resistant patients' depression symptoms in minutes, with minimal untoward side effects, in a clinical trial conducted by the National Institutes of Health. The experimental agent, called AZD6765, acts through the brain's glutamate chemical messenger system. Existing antidepressants available through prescription, which work through the brain’s serotonin system, take a few weeks to work, imperiling severely depressed patients, who can be at high risk for suicide. Ketamine also works in hours, but its usefulness is limited by its potential for dissociative side-effects, including hallucinations. It is being studied mostly for clues to how it works. "Our findings serve as a proof of concept that we can tap into an important component of the glutamate pathway to develop a new generation of safe, rapid-acting practical treatments for depression," said Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health, which conducted the research. Zarate, and colleagues, reported on their results online Dec. 1, 2012 in the journal Biological Psychiatry. AZD6765, like ketamine, works by blocking glutamate binding to a protein on the surface of neurons, called the NMDA receptor. It is a less powerful blocker of the NMDA receptor, which may be a reason why it is better tolerated than ketamine.

Keyword: Depression
Link ID: 17594 - Posted: 12.11.2012

By BENEDICT CAREY They plotted a revolution, fell to debating among themselves, and in the end overturned very little except their own expectations. But the effort itself was a valuable guide for anyone who has received a psychiatric diagnosis, or anyone who might get one. This month, the American Psychiatric Association announced that its board of trustees had approved the fifth edition of the association’s influential diagnostic manual — the so-called bible of mental disorders — ending more than five years of sometimes acrimonious, and often very public, controversy. The committee of doctors appointed by the psychiatric association had attempted to execute a paradigm shift, changing how mental disorders are conceived and posting its proposals online for the public to comment. And comment it did: Patient advocacy groups sounded off, objecting to proposed changes in the definitions of depression and Asperger syndrome, among other diagnoses. Outside academic researchers did, too. A few committee members quit in protest. The final text, which won’t be fully available until publication this spring, has already gotten predictably mixed reviews. “Given the challenges in a field where objective lines are hard to draw, they did a solid job,” said Dr. Michael First, a psychiatrist at Columbia who edited a previous version of the manual and was a consultant on this one. Others disagreed. “This is the saddest moment in my 45-year career of practicing, studying and teaching psychiatry,” wrote Dr. Allen Frances, the chairman of a previous committee who has been one of the most vocal critics, in a blog post about the new manual, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, or DSM5. © 2012 The New York Times Company

Keyword: Depression; Autism
Link ID: 17593 - Posted: 12.11.2012

by Greg Miller A drug used for decades to treat high blood pressure and other conditions has shown promise in a small clinical trial for autism. The drug, bumetanide, reduced the overall severity of behavioral symptoms after 3 months of daily treatment. The researchers say that many parents of children who received the drug reported that their children were more "present" and engaged in social interactions after taking it. The new findings are among several recent signs that treatments to address the social deficits at the core of autism may be on the horizon. Several lines of evidence suggest that autism interferes with the neurotransmitter GABA, which typically puts a damper on neural activity. Bumetanide may enhance the inhibitory effects of GABA, and the drug has been used safely as a diuretic to treat a wide range of heart, lung, and kidney conditions. In the new study, researchers led by Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille, France, recruited 60 autistic children between the ages of 3 and 11 and randomly assigned them to receive either a daily pill of bumetanide or a placebo. (Neither the children's parents nor the researchers who assessed the children knew who received the actual drug.) As a group, those who got bumetanide improved by 5.6 points on a 60-point scale that's often used to assess behaviors related to autism, the researchers report today in Translational Psychiatry. That was enough to nudge the group average just under the cutoff for severe autism and into the mild to medium category. The study did not look directly at whether the drug improved all symptoms equally or some more than others. "We have some indications that the symptoms particularly ameliorated with bumetanide are the genuine core symptoms of autism, namely communication and social interactions," Ben-Ari says. More work will be needed to verify that impression. Ben-Ari says his team is now preparing for a larger, multicenter trial in Europe. © 2010 American Association for the Advancement of Science

Keyword: Autism
Link ID: 17592 - Posted: 12.11.2012

by Christian Jarrett, Ph.D in Brain Myths Back in the 1990s neuroscientists at the University of Parma identified cells in the premotor cortex of monkeys that had an unusual response pattern. They were activated when the monkeys performed a given action and, mirror-like, when they saw another individual perform that same movement. Since then, the precise function and influence of these neurons has become perhaps the most hyped topic in neuroscience. In 2000, Vilayanur Ramachandran, the charismatic neuroscientist, made a bold prediction: “mirror neurons will do for psychology what DNA did for biology.” He's at the forefront of a frenzy of excitement that has followed these cells ever since their discovery. For many, they have came to represent all that makes us human. Perhaps, in those early heady years, Ramachandran was just getting a little carried away? Not at all. For his 2011 book, The Tell-Tale Brain, Ramachandran took his claims further. In the chapter “The neurons that shaped civilisation”, he argues that mirror neurons underlie empathy, allow us to imitate other people, that they accelerated the evolution of the brain, that they help explain the origin of language, and most impressively of all, that they prompted the great leap forward in human culture that happened about 60,000 years ago. “We could say mirror neurons served the same role in early hominin evolution as the Internet, Wikipedia, and blogging do today,” he concludes. “Once the cascade was set in motion, there was no turning back from the path to humanity.” © Copyright 2002-2012 Sussex Directories, Inc

Keyword: Vision; Attention
Link ID: 17591 - Posted: 12.11.2012

By Scicurious I would like to start this post with a challenge. Can you get through this entire post WITHOUT feeling itchy? I know I couldn’t even write the first line. And I’m not alone. Itch is contagious. Watching someone else scratch can make you itch, and you should try to get through a lecture on a skin condition. I wonder how dermatologists can take it. What IS an itch? The clinical definition is that it’s an “unpleasant sensation associated with the urge to scratch”. Ok, then. Itching is a very important part of clinical diagnosis, from things like poison ivy to allergies to severe use of methamphetamine. In addition, there is a psychological disorder of severe itch which can be both disfiguring and incredibly distressing. But where does it come from and why do we itch? There’s an obvious evolutionary reason (OMG a spider on my arm getitoffgetitoffgetitioff!!!!), but what about social itch? We know about the neurobiological “itch matrix”, which involves areas of the brain associated with touch and somatosensory processing, the premotor areas (for scratching), the anterior insula, prefrontal cortex, thalamus, and cerebellum. From a combination of all of these areas (accompanied, of course, by other things like the visual areas to process seeing the spider on your hand), you get an itch and a scartching response, and other involved areas (like the insula and cingulate) may help make it unpleasant enough for you to want to deal with it. All of these areas are also associated with the processing of other stimuli, like touch and pain, which may contribute to the sensation of itch. © 2012 Scientific American,

Keyword: Pain & Touch; Attention
Link ID: 17590 - Posted: 12.11.2012

By WILLIAM J. BROAD When a hurricane forced the Nautilus to dive in Jules Verne’s “Twenty Thousand Leagues Under the Sea,” Captain Nemo took the submarine down to a depth of 25 fathoms, or 150 feet. There, to the amazement of the novel’s protagonist, Prof. Pierre Aronnax, no whisper of the howling turmoil could be heard. “What quiet, what silence, what peace!” he exclaimed. That was 1870. Today — to the dismay of whale lovers and friends of marine mammals, if not divers and submarine captains — the ocean depths have become a noisy place. The causes are human: the sonar blasts of military exercises, the booms from air guns used in oil and gas exploration, and the whine from fleets of commercial ships that relentlessly crisscross the global seas. Nature has its own undersea noises. But the new ones are loud and ubiquitous. Marine experts say the rising clamor is particularly dangerous to whales, which depend on their acute hearing to locate food and one another. To fight the din, the federal government is completing the first phase of what could become one of the world’s largest efforts to curb the noise pollution and return the sprawling ecosystem to a quieter state. The project, by the National Oceanic and Atmospheric Administration, seeks to document human-made noises in the ocean and transform the results into the world’s first large sound maps. The ocean visualizations use bright colors to symbolize the sounds radiating out through the oceanic depths, frequently over distances of hundreds of miles. © 2012 The New York Times Company

Keyword: Hearing
Link ID: 17589 - Posted: 12.11.2012