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Looking in a mirror at a reflection of their healthy hand could help people with persistent pain ease their symptoms and eventually overcome their problem, say scientists in the latest edition of the journal Clinical Medicine. The treatment, being developed by researchers from the University of Bath and the Royal National Hospital for Rheumatic Diseases (RNHRD), is based on a new theory about how people experience pain even when doctors can find no direct cause. This ‘cortical’ model of pain suggests that the brain’s image of the body can become faulty, resulting in a mismatch between the brain’s movement control systems and its sensory systems, causing a person to experience pain when they move a particular hand, foot or limb. Researchers believe that this kind of problem could be behind a host of pain-related disorders, such as complex regional pain syndrome and repetitive strain injury. In an investigation of whether this system can be corrected using mirrors to trick the brain, researchers asked a number of patients with complex regional pain syndrome (a chronic debilitating condition affecting 10,000 – 20,000 patients in the UK at any one time) to carry out routine exercises in front of a mirror. University of Bath © 2004
Keyword: Pain & Touch
Link ID: 8095 - Posted: 06.24.2010
Genetic variations that cause miscues in brain development may play an important role in dyslexia, according to new research presented last week at a meeting of the American Society of Human Genetics in Salt Lake City. People with dyslexia have reading impairments despite normal intelligence. The problem affects between 5% and 17% of the population. In the last few years, geneticists have begun to point the finger at particular genes (ScienceNOW, 22 February). However, little is known about how these genes might contribute to the condition. In one new study, a collaboration of 20 researchers led by Haiying Meng and Jeffrey Gruen of Yale University School of Medicine homed in on a region of chromosome 6 that has been implicated in previous dyslexia studies. Using DNA collected from 536 people with a dyslexic in their families, the researchers tracked 147 single-nucleotide polymorphisms (SNPs), places where the genetic code differs by one letter in different people. Searching for SNPs that tend to have one "spelling" in people with reading impairments and another spelling in normal readers, the researchers found that a disproportionate number of such SNPs showed up in a gene called DCDC2. © 2005 by the American Association for the Advancement of Science.
Keyword: Dyslexia; Genes & Behavior
Link ID: 8094 - Posted: 06.24.2010
Liars could be caught out by the reaction of their stomachs to telling untruths, suggests preliminary research from the University of Texas, US. The team believe that the early-stage technique could one day improve the accuracy of polygraph tests, which rely mostly on monitoring heart activity. “The heart is unreliable because it’s affected by not only by your brain, but by many other factors, such as hormones,” says Pankaj Pasricha, who is leading the team. “The gut has a mind of its own – literally. It has its own well-developed nervous system that acts independently of almost everything except your unconscious brain.” The test uses a device called an electrogastrogram (EGG) to determine when a person’s stomach “beats” speed up from the typical three per minute. Whereas heart beats can increase whether a person is lying or telling the truth, the group’s initial findings from 16 test subjects reveal that the stomach’s rate typically does not increase if a person is telling the truth, however nervous they may be. “This might very well be the case,” says Kevin Murphy, a psychologist at Penn State University, Pennsylvania, US, who recently headed a panel for the US National Academy of Sciences to analyse the science behind polygraph devices. “But polygraph detectors, whatever their ilk, measure stress and not lying. This new test might give more, potentially very useful, data. But it won’t give you the definitive truth.” © Copyright Reed Business Information Ltd.
Keyword: Stress
Link ID: 8093 - Posted: 06.24.2010
Roxanne Khamsi Mickey Mouse may have kept quiet during his early days on the silver screen, but his lab counterparts seem to have a penchant for song. That's the finding in an analysis of the ultrasonic sounds made by male mice wooing potential mates. For years, animal-behaviour experts have known that mice make vocalizations that are too high in pitch to be picked up by the human ear. Young mice, for example, make 'isolation calls' when cold or distressed. And male mice emit ultrasonic sounds in the presence of a potential mate or in response to chemical sex cues, called pheromones, in the urine of female mice. But until now, scientists had not examined these sounds for musical patterns. Thanks in part to a sophisticated computer program, Timothy Holy and Zhongsheng Guo of the Washington University School of Medicine in St Louis, Missouri, were able to tackle this challenge. Holy began by writing software that shifts the pitch of the male mouse's sounds, making the sounds deeper so that they can be heard by humans. "No one had ever pitch-shifted the mouse vocalization," he says. "The first time I played it back it was pretty surprising: it sounded so much like birdsong." ©2005 Nature Publishing Group
Keyword: Sexual Behavior; Language
Link ID: 8092 - Posted: 06.24.2010
Vulnerability to anxiety may be down to the size of a brain structure involved in fearful memories, say US scientists. People with a thicker ventromedial prefrontal cortex were better able to cope with stressful experiences. The findings may help explain why some people develop post-traumatic stress disorder (PTSD) while others bounce back after adversity, say the authors. The Massachusetts General Hospital study appears in Proceedings of the National Academy of Science. While it is normal to experience physical and psychological symptoms after an extremely stressful event, such as the recent London terrorist attacks, some people will continue to be consumed by overwhelming fear and may develop PTSD. A person with PTSD may experience unwanted flashbacks, poor sleep and depression, and avoidance certain situations that could trigger memories of the event. Studies in animals suggest that the ventromedial prefrontal cortex (vmPFC) is involved with helping the brain forget fearful events. Also, studies of have shown that people with PTSD have unusually inactive vmPFCs, again suggesting that this brain region is important in anxiety. In the current study, Dr Mohammed Milad and colleagues scanned the brains of 14 volunteers. (C)BBC
Keyword: Stress
Link ID: 8091 - Posted: 10.31.2005
By Shankar Vedantam, Washington Post Staff Writer For centuries, poets, philosophers and scientists have debated why humans spend as much as a third of their lives asleep. For Shakespeare, sleep was the "balm of hurt minds" -- denied to murderers such as Macbeth. For Sigmund Freud, sleep provided a platform for dreams, an outlet for the psyche to work out complex and dangerous feelings. Scientists today believe sleep consolidates learning and memory, and supports many essential mental and physical functions. The theorists have long disagreed about one another's ideas, but most agree on one thing: If nature makes people sleep away so much of their lives, the reason has to be something crucial. That seemed to be the only way to explain why sleep-deprived people crave sleep so badly that they doze off behind the wheel of a car going 60 mph, and why rats deprived of sleep die sooner than rats deprived of food. Yet a wealth of sleep research has regularly produced baffling paradoxes and conflicting lines of evidence about the uses, role and need for sleep. If sleep is primarily about providing mental rest, why do people's brains remain so active during sleep, as research in recent decades has found? © Copyright 1996-2005 The Washington Post Company
By PAUL COLLINS The moment I opened my eyes I knew something was wrong. The sun wasn't up yet, and a cry was forming in Morgan's throat. I padded over to his bed, puzzled. His darkened room was filled with battered brass instruments, playing cards, thick reference books - the inscrutable fascinations of an autistic 5-year-old. Morgan had always been in his own world, but it was a fairly happy one. In his waking hours he'd hum "In the Hall of the Mountain King" while shuffling through mysterious sequences of pinochle cards; lately he had become engrossed in an illustrated encyclopedia of electric guitars, squinting and smiling at the old pictures and names: Danelectro, Rickenbacker, Gretsch. Sometimes he'd brush past his baby brother and march up to me with a lump of Play-Doh. "Gibson ES-350," he'd demand. As I'd gamely fashion a fretboard and tuners out of clay, he'd grab his tarnished French horn, skip outside to the tree swing and blast out wobbling notes at the neighbors: borp, brap, boorp. I leaned farther over his bed. "Morgan?" Bam. I staggered back, smacking away another punch, yelling in surprise, "Go to your room!" - which didn't mean much since he was already in it. I retreated across the hall and snapped on the bathroom light. Blood was flowing from my nose. Behind me Morgan thrashed on his bed, pounding and kicking the bedroom wall, screaming. Copyright 2005 The New York Times Company
Keyword: Autism; Depression
Link ID: 8089 - Posted: 10.31.2005
By RANDY KENNEDY SITTING the other day in front of Picasso's rapturous "Girl Before a Mirror" at the Museum of Modern Art, Rueben Rosen wore the dyspeptic look of a man with little love for modern art. But the reason he gave for disliking the painting was not one you might expect to hear from an 88-year-old former real estate broker. Xanthe Alban-Davies discusses Picasso's "Girl Before a Mirror" with, from left, Rueben Rosen, Irene Brenton and Sheila Barnes at the Museum of Modern Art. "It's like he's trying to tell a story using words that don't exist," Mr. Rosen said. "It's like he's trying to tell a story using words that don't exist," Mr. Rosen said finally of Picasso, fixing the painter's work with a critic's stare. "He knows what he means, but we don't." This chasm of understanding is one that Mr. Rosen himself stares into every day. He has midstage Alzheimer's disease, as did the rest of the men and women who were sitting alongside him in a small semicircle at the museum, all of them staring up at the Picasso. It was a Tuesday, and the museum was closed, but if it had been open other visitors could have easily mistaken the group for any guided tour. Mr. Rosen and his friends did not wear the anxious, confused looks they had worn when they first arrived at the museum. They did not quarrel in the way that those suffering from Alzheimer's sometimes do. And when they talked about the paintings, they did not repeat themselves or lose the thread of the discussion, as they often do at the long-term care home where most of them live in Palisades, N.Y. Copyright 2005 The New York Times Company
Keyword: Alzheimers
Link ID: 8088 - Posted: 10.31.2005
Your brain is a time machine with three modes that control everything from instantaneous tasks such as moving, to maintaining long trains of thought and ultimately staying in synch with night and day. That's what scientists say. But they have no clue how most of it works. Focusing on the poorly understood middle time zone, where the brain does some of its best work, researchers at Duke University summarize this latest thinking in a new article in the journal Nature Reviews Neuroscience. Scientists have long understood human and animal brains to be governed in part by a circadian clock, which keeps us in synch with night and day. The rhythm of this 24-hour clock encourages nighttime sleep and allows many people to awaken with no help from a rooster. Another clock is thought to operate at the millisecond level, controlling movement and speech, among other vital functions that occur so quickly we don't really think about them. But in between, there must be a third timekeeper of the mind to aid all the functions that require seconds to minutes of attention. Nobody is sure about this, though. © 2005 Microsoft
Keyword: Miscellaneous; Biological Rhythms
Link ID: 8087 - Posted: 06.24.2010
By SANDRA BLAKESLEE One year after scientists discovered a gene whose flaw contributes to dyslexia, two more such genes have now been identified. The findings, described yesterday in Salt Lake City at a meeting of the American Society of Human Genetics, support the idea that many people deemed simply lazy or stupid because of their severe reading problems may instead have a genetic disorder that interfered with the wiring of their brains before birth. "I am ecstatic about this research," said Dr. Albert M. Galaburda of Harvard Medical School, a leading authority on developmental disorders who was not involved in the latest discoveries. The findings, added to last year's, mean that for the first time, "we have a link between genes, brain development and a complex behavioral syndrome," Dr. Galaburda said. As many as a dozen genes are probably involved in the disorder, he said, with each playing a role in the necessary migration of neurons as the brain's circuitry develops. Researchers said a genetic test for dyslexia should be available within a year or less. Children in families that have a history of the disorder could then be tested, with a cheek swab, before they are exposed to reading instruction. If children carry a genetic risk, they could be placed in early intervention programs. Copyright 2005 The New York Times Company
Keyword: Dyslexia; Genes & Behavior
Link ID: 8086 - Posted: 10.29.2005
By Robert Sanders BERKELEY – Picky female frogs in a tiny rainforest outpost of Australia have driven the evolution of a new species in 8,000 years or less, according to scientists from the University of Queensland, the University of California, Berkeley, and the Queensland Parks and Wildlife Service. "That's lightning-fast," said co-author Craig Moritz, professor of integrative biology at UC Berkeley and director of the Museum of Vertebrate Zoology. "To find a recently evolved species like this is exceptional, at least in my experience." When isolated populations of the green-eyed tree frog (gray and brown) met again 8,000 years ago, they found that each had changed in subtle ways. The calls of the male frogs were different, and more importantly, hybrid offspring were less viable. One population that was cut off from its southern kin (pink) found a way to ensure healthy young. Females, who choose mates based only on their call, began selecting mates with a the southern call type. Over thousands of years, this behavior exaggerated the pre-existing differences in call, lead to smaller body size in males of the "isolated southern population" and resulted in rapid speciation between the two populations of the southern lineage. The yet-to-be- named species arose after two isolated populations of the green-eyed tree frog reestablished contact less than 8,000 years ago and found that their hybrid offspring were less viable. To avoid hybridizing with the wrong frogs and ensure healthy offspring, one group of females preferentially chose mates from their own lineage. Over several thousand years, this behavior created a reproductively isolated population - essentially a new species - that is unable to mate with either of the original frog populations. Copyright UC Regents
Keyword: Sexual Behavior; Evolution
Link ID: 8085 - Posted: 06.24.2010
Researchers trying to crack one of medicine’s most perplexing unsolved mysteries can now keep abreast of late-breaking developments via the Schizophrenia Research Forum, a website launched this month with funding from the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH). Sponsored by NARSAD, The Mental Health Research Association, the site bills itself as a “virtual community” where researchers can link-up with colleagues and potential collaborators, learn about new findings, meetings and funding opportunities, and critique each other’s articles and ideas. “We’re hoping that the Forum will become a catalyst for creative thinking that will speed the pace of discovery,” said NIMH Director Thomas Insel, M.D. The site (www.schizophreniaforum.org) includes original news stories and interviews with leading scientists in the field. Among specific forums that invite contributions from the field, “Current Hypotheses” presents theory reviews, while an “Idea Lab” posts less formal treatments. Most features of the site are interactive and solicit comment. There will also be live chats with experts that will be archived for later viewing. For example, NIMH senior advisor Mayada Akil, M.D., who represents the Institute to the Forum, is tentatively scheduled to co-lead a discussion with Dr. Irving Gottesman, University of Virginia, on “Identifying Quantifiable Phenotypes in Schizophrenia Research.”
Keyword: Schizophrenia
Link ID: 8084 - Posted: 06.24.2010
Pediatric researchers at Yale School of Medicine have identified a gene on human chromosome 6 called DCDC2, which is linked to dyslexia, a reading disability affecting millions of children and adults. The researchers also found that a genetic alteration in DCDC2 leads to a disruption in the formation of brain circuits that make it possible to read. This genetic alteration is transmitted within families. "These promising results now have the potential to lead to improved diagnostic methods to identify dyslexia and deepens understanding of how the reading process works on a molecular level," said lead author Jeffrey R. Gruen, M.D., associate professor in the Pediatrics Department at Yale School of Medicine. The study will be published in a special issue of Proceedings of the National Academy of Sciences on October 28. Gruen and first author Haiying Meng will also present the findings that same day at the American Society of Human Genetics (ASHG) meeting in Salt Lake City, Utah. Gruen and co-authors used a statistical approach to study and compare specific DNA markers in 153 dyslexic families. "We now have strong statistical evidence that a large number of dyslexic cases--perhaps as many as 20 percent--are due to the DCDC2 gene," said Gruen. "The genetic alteration on this chromosome is a large deletion of a regulatory region. The gene itself is expressed in reading centers of the brain where it modulates migration of neurons. This very architecture of the brain circuitry is necessary for normal reading."
Keyword: Dyslexia; Genes & Behavior
Link ID: 8083 - Posted: 10.29.2005
The daily routines of one in ten American in Vermont, Alaska, Maine and other northern states will change for the worse on Oct. 30. The alterations start every year around October just after the end of daylight savings time. For most, the clock shift just adds an hour to the weekend -- but for sufferers of seasonal affective disorder, a syndrome involving recurring bouts of depression during fall and winter months, it marks the beginning of a difficult time of year when many forgo an after-work run for a nap, watch television instead of walk the dog, or sleep later in the morning. With this year's turning back of the clock, the 14.5 million Americans susceptible to SAD may begin feeling fatigued, worthless, disinterested, even suicidal. Many will receive treatment involving sitting in front of a light box for an hour or two a day in hopes that the white fluorescent or full-spectrum light will simulate sunlight and make them feel better. The treatment works reasonably well but is hard to stick with, so Kelly Rohan, a SAD expert and assistant professor of psychology at the University of Vermont, views it as more a quick fix than long-term solution.
Keyword: Depression; Biological Rhythms
Link ID: 8082 - Posted: 10.28.2005
By Jennifer Viegas, Discovery News — People pay more attention to body language than to facial expressions, even when observers are trying to focus on faces, according to a new study. The finding, published in this week's Proceedings of the National Academy of Sciences, suggests that interpretation of body language happens without conscious awareness. This instantaneous response also works like a silent alarm system in the brain whenever facial expressions do not match up properly to the individual's body language. The "alarm" is a message in the brain of the onlooker that something is not right with the other person. "The information from body language and its coherence with the facial expression are apprehended rapidly (along with) the assurance that we can trust our gut feeling when we feel somebody 'feels' funny," explained Beatrice de Gelder, one of the study's authors. © 2005 Discovery Communications Inc.
Keyword: Language
Link ID: 8081 - Posted: 06.24.2010
Tom Simonite "It's a small world," we say when a new acquaintance turns out to be linked to several other people we know. It happens surprisingly often. And it seems it happens even more to Scottish dolphins than it does to people. David Lusseau, from the University of Aberdeen, UK, has spent years researching the social world of dolphins, to find out who knows whom and how often they meet. For the 130-strong community living off the east coast of Scotland, he found, it takes an average of just 3.9 steps to link any two dolphins by the shortest possible route through mutual friends. Small-world networks, as mathematicians call them, have the property that any 'node', such as an individual person or dolphin, is connected to every other node through a limited number of steps. This is a result of the way that nodes are organised: most people, for example, have a cluster of close friends but also know a few people from different clusters. This means that connecting any two apparently widely separated people is surprising easy. Researchers have shown it takes about five-and-a-half steps, on average, to get between any two individuals in the world1. This fact is famous for inspiring the play Six Degrees of Separation, by John Guare, and the game 'six degrees of Kevin Bacon', which challenges players to link a given Hollywood actor to the star through a limited number of shared film appearances (see "My friend Flipper"). ©2005 Nature Publishing Group
Keyword: Miscellaneous
Link ID: 8080 - Posted: 06.24.2010
Roxanne Khamsi An injection that stimulates the growth of new brain cells can cause mice to lose more than 15% of their body weight, researchers say. Experts hope that the treatment, which lasts for weeks, could eventually be made into weight-loss drugs for humans. The discovery was inspired by the unexpected side effects of a drug that was tested in the 1990s as a treatment for amyotrophic lateral sclerosis (ALS), also called Lou Gehrig's disease. The drug, called Axokine, did not improve muscle control as much as expected, but trial participants did report a loss of appetite. Biologists wondered whether this appetite-suppression effect could be harnessed to fight obesity. "People tried to turn lemons into lemonade and ask what such drugs could do for weight control," explains Jeffrey Flier of the Harvard Medical School in Boston, Massachusetts. The effect with Axokine itself did not yield particularly promising results. Axokine's maker, Regeneron, conducted clinical trials for the drug against obesity in 2003, and then abandoned the idea. But researchers realized that similar drugs might re-wire the brain's desire for food. ©2005 Nature Publishing Grou
Keyword: Obesity
Link ID: 8079 - Posted: 06.24.2010
Scientists are one step closer to unraveling the complex mechanisms in the brain that regulate body weight. Working with mice — whose appetites are controlled by systems very similar to those in humans - they have identified a specific type of neuron that is essential for feeding behavior. Without these neurons, adult mice stop eating and undergo rapid weight loss. Remarkably, the researchers found that absence of these neurons only influenced eating behavior when they were removed from adult mice. If the neurons were eliminated in newborn mice, their developing brains found a way to compensate for the deficiency, and the mice grew up eating normally. The research, conducted by Serge Luquet at the University of Washington in the laboratory of Howard Hughes Medical Institute investigator Richard D. Palmiter, will be published in the October 28, 2005 issue of the journal Science. The task of sorting out the body's diverse and sometimes conflicting signals about hunger and satiety falls to a small cluster of about 5,000 cells in a region of the brain known as the arcuate nucleus. Hormones such as insulin, leptin, and ghrelin deliver information to the arcuate nucleus about whether the body has sufficient calories and nutrients. The brain, in turn, uses this information to decide whether to eat or expend energy. Two types of neurons that recognize and respond to these signals are found in the arcuate nucleus. The first of these, known as POMC (pro-opiomelanocortin) neurons, send signals to other parts of the brain to reduce appetite. Mice with defects in POMC neurons eat excessively and become obese. © 2005 Howard Hughes Medical Institute
Keyword: Obesity
Link ID: 8078 - Posted: 06.24.2010
EVANSTON, Ill. --- French neurologist Jean-Martin Charcot first described amyotrophic lateral sclerosis (ALS) in 1869, but, nearly 140 years later, little is known about the cause of the devastating neurodegenerative disease, and there is no cure. What is known about Lou Gehrig's disease, as it is commonly called, is that misfolded and damaged proteins clump together in cells to form aggregates and motor neurons die. But scientists have long debated whether or not the protein aggregates actually kill the cells. Now a research team at Northwestern University, using mammalian neurons and live-cell time-lapse spectroscopy, has become the first to clearly link the presence of the ALS-associated mutant SOD1 protein aggregates with neuronal cell death. This evidence could help explain the disease process and eventually lead to new therapeutics. In the study, published this month in the Journal of Cell Biology, the scientists looked one at a time at neuronal cells expressing the mutant SOD1 protein and found that in cells where the protein accumulated and aggregates formed, 90 percent of the cells went on to die. (They died between six and 24 hours after aggregates were visually detected.) Cells that did not form aggregates did not die.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 8077 - Posted: 10.27.2005
Is a bird in the hand really worth two in the bush? Depends whom you ask. A new study in monkeys suggests that decision-making in animals is more complex than previously thought. Patience is a puzzle. While it often pays to hold off just a bit longer, most animals will grab a small item of food rather than wait even a few seconds longer for a bigger one. But evolutionary theory predicts that all animals should do the smart thing and get the most out of the long term. So what's the hurry? Ecology can help answer the question. In a study published in April in Biology Letters, a team led by Jeff Stevens, a behavioral biologist at Harvard University in Cambridge, Massachusetts, demonstrated that marmosets will wait longer for a larger food reward than tamarins will. The researchers concluded that the explanation lies in the creatures' lifestyles: Marmosets chew on trees and wait patiently for sap to flow out, while tamarins impulsively grab insects. © 2005 by the American Association for the Advancement of Science.
Keyword: Learning & Memory; Drug Abuse
Link ID: 8076 - Posted: 06.24.2010


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