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Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders , it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.
The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.
Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can?t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.
Photo credit: Yoichi Araki, Ph.D.
By SINDYA N. BHANOO Learning can be traced back to individual neurons in the brain, according to a new study. “What we wanted to do was see if we could actually create a new association — a memory — and see if we would be able to see actual change in the neurons,” said Matias Ison, a neuroscientist at the University of Leicester in England and one of the study’s authors. He and his colleagues were able to monitor the brain activity of neurosurgical patients at UCLA Medical Center. The patients already had electrodes implanted in their medial temporal lobes for clinical reasons. The patients were first presented with images of notable people — like Jennifer Aniston, Clint Eastwood and Halle Berry. Then, they were shown images of the same people against different backdrops — like the Eiffel Tower, the Leaning Tower of Pisa and the Sydney Opera House. The same neurons that fired for the images of each of the actors also fired when patients were shown the associated landmark images. In other words, the researchers were able to watch as the patients’ neurons recorded a new memory — not just of a particular person, but of the person at a particular place. © 2015 The New York Times Company
Keyword: Learning & Memory
Link ID: 21126 - Posted: 07.02.2015
Jon Hamilton If you run into an old friend at the train station, your brain will probably form a memory of the experience. And that memory will forever link the person you saw with the place where you saw them. For the first time, researchers have been able to see that sort of link being created in people's brains, according to a study published Wednesday in the journal Neuron. The process involves neurons in one area of the brain that change their behavior as soon as someone associates a particular person with a specific place. "This type of study helps us understand the neural code that serves memory," says Itzhak Fried, an author of the paper and head of the Cognitive Neurophysiology Laboratory at UCLA. It also could help explain how diseases like Alzheimer's make it harder for people to form new memories, Fried says. The research is an extension of work that began more than a decade ago. That's when scientists discovered special neurons in the medial temporal lobe that respond only to a specific place, or a particular person, like the actress Jennifer Aniston. The experiment used a fake photo of actor Clint Eastwood and Pisa's leaning tower to test how the brain links person and place. More recently, researchers realized that some of these special neurons would respond to two people, but only if the people were connected somehow. For example, "a neuron that was responding to Jennifer Aniston was also responding to pictures of Lisa Kudrow," [another actress on the TV series Friends], says Matias Ison of the University of Leicester in the U.K. © 2015 NPR
By Gretchen Vogel The 2009 H1N1 influenza pandemic left a troubling legacy in Europe: More than 1300 people who received a vaccine to prevent the flu developed narcolepsy, an incurable, debilitating condition that causes overpowering daytime sleepiness, sometimes accompanied by a sudden muscle weakness in response to strong emotions such as laughter or anger. The manufacturer, GlaxoSmithKline (GSK), has acknowledged the link, and some patients and their families have already been awarded cpmpensation. But how the vaccine might have triggered the condition has been unclear. In a paper in Science Translational Medicine (STM) this week, researchers offer a possible explanation. They show that the vaccine, called Pandemrix, triggers antibodies that can also bind to a receptor in brain cells that help regulate sleepiness. The work strongly suggests that Pandemrix, which was given to more than 30 million Europeans, triggered an autoimmune re action that led to narcolepsy in some people who are genetically at risk. “They put together quite a convincing picture and provide a plausible explanation for what has happened,” says Pasi Penttinen, who heads the influenza program at the European Centre for Disease Prevention and Control in Stockholm. “It’s really the kind of work we’ve been waiting for for 5 years.” But the results still need to be confirmed in a larger study, the authors and other narcolepsy researchers say. A 2013 paper in STM by another group, documenting a different type of vaccine-triggered autoimmune re action, was retracted after the results proved irreproducible (Science, 1 August 2014, p. 498). © 2015 American Association for the Advancement of Science
by Andy Coghlan "I was completely revitalised," says Karen. "Suddenly, I could be sociable again. I would go to work, go home, eat dinner and feel restless." Karen (not her real name) experienced this relief from chronic fatigue syndrome while taking a drug that is usually used to treat the blood cancer lymphoma and rheumatoid arthritis (see "Karen's experience", below). She was one of 18 people with CFS who reported improvements after taking rituximab as part of a small trial in Bergen, Norway. The results could lead to new treatments for the condition, which can leave people exhausted and housebound. Finding a cause for CFS has been difficult. Four years ago, claims that a mouse virus was to blame proved to be unfounded, and some have suggested the disease is psychosomatic. The latest study implicates the immune system, at least in some cases. Rituximab wipes out most of the body's B-cells, which are the white blood cells that make antibodies. Øystein Fluge and Olav Mella of the Haukeland University Hospital in Bergen noticed its effect on CFS symptoms in 2004, when they used the drug to treat lymphoma in a person who happened to also have CFS. Several months later, the person's CFS symptoms had disappeared. A small, one-year trial in 2011 found that two-thirds of those who received rituximab experienced relief, compared with none of the control group. The latest study, involving 29 people with CFS, shows that repeated rituximab infusions can keep symptoms at bay for years. © Copyright Reed Business Information Ltd
Nancy Shute Powerful antipsychotic medications are being used to treat children and teenagers with ADHD, aggression and behavior problems, a study finds, even though safer treatments are available and should be used first. "There's been concern that these medications have been overused, particularly in young children," says Mark Olfson, a professor of psychiatry at Columbia University who led the study. It was published Wednesday in JAMA Psychiatry. "Guidelines and clinical wisdom suggest that you really should be using a high degree of caution and only using them when other treatments have failed, as a last resort." Olfson and his colleagues looked at prescription data from about 60 percent of the retail pharmacies in the United States in 2006, 2008 and 2010. That included almost 852,000 children, teenagers and young adults. Teens were most likely to be prescribed antipsychotics, with 1.19 percent getting the drugs in 2010, compared to 0.11 percent in younger children. Boys were more likely to be given the medications. Antipsychotic medications like clozapine and olanzapine are used to treat schizophrenia, bipolar disorder and some symptoms of autism. They have not been approved by the Food and Drug Administration to treat aggression and ADHD, but are prescribed off label to reduce disruptive behavior. FDA Debates Safety Of Antipsychotic Drugs In Kids Use of antipsychotics in children has been questioned because the drugs can have serious side effects, including tremors, weight gain, increased diabetes risk and elevated cholesterol. © 2015 NPR
Boys are more likely than girls to receive a prescription for antipsychotic medication regardless of age, researchers have found. Approximately 1.5 percent of boys ages 10-18 received an antipsychotic prescription in 2010, although the percentage falls by nearly half after age 19. Among antipsychotic users with mental disorder diagnoses, attention deficit hyperactivity disorder (ADHD) was the most common among youth ages 1-18, while depression was the most common diagnosis among young adults ages 19-24 receiving antipsychotics. Despite concerns over the rising use of antipsychotic drugs to treat young people, little has been known about trends and usage patterns in the United States before this latest research, which was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Mark OlfsonExternal Web Site Policy, M.D., M.P.H., of the Department of Psychiatry, College of Physicians and Surgeons and Columbia University and New York State Psychiatric Institute, New York City, and colleagues Marissa King, Ph.D., Yale, New Haven, Connecticut, and Michael Schoenbaum, Ph.D., NIMH, report their findings on July 1 in JAMA Psychiatry. “No prior study has had the data to look at age patterns in antipsychotic use among children the way we do here,” said co-author Michael Schoenbaum, Ph.D., senior advisor for mental health services, epidemiology and economics at NIMH. “What’s especially important is the finding that around 1.5 percent of boys aged 10-18 are on antipsychotics, and then this rate abruptly falls by half, as adolescents become young adults.” “Antipsychotics should be prescribed with care,” says Schoenbaum. “They can adversely affect both physical and neurological function and some of their adverse effects can persist even after the medication is stopped.”
by Michael Le Page It's good to be mixed-up. People whose parents are distantly related are, on average, taller, smarter and better educated than those whose parents are close relatives. Based on what we know about plants and animals, biologists have long suspected that people of mixed parentage have a genetic advantage. Now an extensive study may have confirmed the hunch. "It does imply that people who come from very different ancestry would be a bit taller and a bit more cognitively able," says team member Jim Wilson of the University of Edinburgh, UK. It has long been known that children are more likely to suffer from genetic diseases if their parents are close relatives, because they may inherit the same harmful gene variants from their mother and father. To probe the wider implications, Wilson and his colleagues analysed genome and life history data from 110 genome studies involving 350,000 people from Africa, Asia, Europe and North America. They were surprised to find no evidence of a link between having closely related parents and most of the traits they looked at, such as cholesterol levels, blood pressure and rates of diabetes. © Copyright Reed Business Information Ltd
By Ariel Sabar In televised remarks from the East Room of the White House on April 2, 2013, President Obama unveiled a scientific mission as grand as the Apollo program. The goal wasn’t outer space, but a frontier every bit as bewitching: the human brain. Obama challenged the nation’s “most imaginative and effective researchers” to map in real time the flickerings of all 100 billion nerve cells in the brain of a living person, a voyage deep into the neural cosmos never attempted at so fine a scale. A panoramic view of electric pulses pinballing across the brain could lead to major new understandings of how we think, remember and learn, and how ills from autism to Alzheimer’s rewire our mental circuitry. “We have a chance to improve the lives of not just millions,” the president said, “but billions of people on this planet.” The next month, six miles from the White House, a Harvard professor named Florian Engert grabbed a mic and, in front of the nation’s top neuroscientists, declared Obama’s effort essentially futile. “We have those data now,” said Engert, who, in a room full of professorial blazers and cardigans, was wearing a muscle shirt that afforded ample views of his bulging biceps. “We discovered they’re actually not all that useful.” (“I think whole-brain imaging is just a bunch of bull----,” is how he put it to me later.) To the other researchers, he must have sounded like a traitor. Engert, who is 48, was basically the first person on the planet to observe a brain in the wall-to-wall way Obama envisioned. He and his colleagues had done it with a sci-fi-worthy experiment that recorded every blip of brain activity in a transparent baby zebrafish, a landmark feat published just a year earlier in the marquee scientific journal Nature. For Engert to suggest that the president’s brain quest was bunk was a bit like John Glenn returning from orbit and telling JFK not to bother with a lunar landing.
Keyword: Brain imaging
Link ID: 21119 - Posted: 07.02.2015
By Erika Beras Marijuana is the drug of choice for people who drink alcohol. And people who use both are twice as likely to do so at the same time than to indulge in just one or the other. That’s according to a study in the journal Alcoholism: Clinical and Experimental Research. [Meenakshi S. Subbaraman and William C. Kerr, Simultaneous Versus Concurrent Use of Alcohol and Cannabis in the National Alcohol Survey The data came from self-reported answers that more than 8,600 people provided to what’s called the National Alcohol Surveys, done by phone in 2005 and 2010. People who used pot and alcohol were about twice as likely to drive drunk than those who just drank. And they doubled their chances of what are referred to as negative social consequences, such as arrests, fights and job problems. Meanwhile, another new study finds that if you’re chronically stoned, you’re more likely to remember things differently from how they happened, or not at all. Researchers showed a series of words to people who do not use marijuana and to regular pot users who had not partaken in a month. A few minutes later, all participants were shown the same list of words along with other words. The volunteers were then asked to identify only the original words. The pot smokers thought more of the new words were in the original list than did the nonusers. And brain scans revealed that the regular pot users showed less activity in brain regions associated with memory and cognitive resources than did the nonusers. The study is in the journal Molecular Psychiatry. [J. Riba et al, Telling true from false: cannabis users show increased susceptibility to false memories] © 2015 Scientific American
by Lisa Grossman Marriage for all, no gay gene required. For same-sex couples in the US, 26 June was a landmark date: the Supreme Court legalised marriage between two men or two women in all 50 states. "[Same-sex couples] ask for equal dignity in the eyes of the law," wrote Associate Justice Anthony Kennedy in the decision. "The Constitution grants them that right." But one thing the decision didn't do was declare sexual orientation a "suspect class" under the law, which would have given it the same protection as race. One of the criteria for this classification is that the trait must be immutable – an argument that the gay rights movement has internalised under the banner of "we're born this way". But although there is some evidence that sexual orientation has a genetic component, most scientists agree that it's not that simple. "There's significant consensus in the scientific community that there's enough different interacting causes for sexual orientation that two different individuals can be gay for different combinations of reasons," says sexuality researcher Lisa Diamond at the University of Utah. "I think all the evidence suggests that we're born with an underlying capacity and then that capacity interacts with a whole bunch of other influences," she says – whether they be prenatal, genetic or environmental. © Copyright Reed Business Information Ltd
Keyword: Sexual Behavior
Link ID: 21117 - Posted: 07.01.2015
By Dina Fine Maron The game is a contemporary of the original Nintendo but it still appeals to today’s teens and lab monkeys alike—which is a boon for neuroscientists. It offers no lifelike graphics. Nor does it boast a screen. Primate players—whether human or not—are simply required to pull levers and replicate patterns of flashing lights. Monkeys get a banana-flavored treat as a reward for good performance whereas kids get nickels. But the game's creators are not really in it for fun. It was created by toxicologists at the U.S. Food and Drug Administration in the 1980s to study how chronic exposure to marijuana smoke affects the brain. Players with trouble responding quickly and correctly to the game’s commands may have problems with short-term memory, attention or other cognitive issues. The game has since been adapted to address a different question: whether anesthetics used to knock pediatric patients unconscious during surgery and diagnostic tests could affect a youngster's long-term neural development and cognition. Despite 20 years’ worth of experiments in young rodents and monkeys, there have been few definitive answers. To date, numerous studies suggest that being put under with anesthesia early in life seems somehow related to future cognitive problems. But whether this association is causal or merely coincidence is unclear. Researchers do know that the young human brain is exceptionally sensitive. When kids are exposed to certain harmful chemicals in their formative years, that experience can fundamentally alter the brain’s architecture by misdirecting the physical connections between neurons or causing cell deaths. But unraveling whether anesthetics may fuel such long-term damage in humans remains a challenge. © 2015 Scientific American
by Colin Barras Men often lose their sex drive with age – and so, it seems do male Drosophila. Tsai-Feng Fu at the National Chi Nan University in Taiwan and his colleagues suspected that low levels of dopamine in the flies were to blame. Almost 300 neurones in the fruit-fly brain use dopamine. Comparing those linked to sexual function in elderly 40-day-old male flies and sprightly 10-day-old flies, Fu found the older neurones carried 10 times less dopamine. Boosting levels lengthened the time the older flies spent trying to mate. There are obviously big differences between a man's brain and that of a male Drosophila, but Fu says that the new results could provide a useful starting point for in-depth studies that may have clinical implications. For instance, that research might eventually identify ways to fine-tune dopamine levels in humans, perhaps to reverse age-related declines in sexual drive, or even to suppress an overactive libido. We already have therapies for treating male sexual dysfunction – notably the drug viagra. But probing the link between dopamine and sexual dysfunction is still important. For instance, dopamine-replacement therapy is one of the most effective treatments for Parkinson's disease – but the therapy can lead to harmful compulsive sexual behaviour. But Wendi Neckameyer at the Saint Louis University School of Medicine in Missouri isn't sure we should talk about potential implications for men just yet – it's enough to say that the researchers "have begun to tease out an incredibly complex neural circuit", she says. © Copyright Reed Business Information Ltd
Keyword: Sexual Behavior
Link ID: 21115 - Posted: 07.01.2015
Hannah Devlin Science correspondent Two licensed drugs have been shown to halt brain degeneration in mice, raising the prospect of a rapid acceleration in the search for a medicine to beat Alzheimer’s disease. The results, presented on Tuesday at the Alzheimer’s Society annual research conference in Manchester, have been hailed as “hugely promising” because they involve medicines that are already known to be safe and well-tolerated in people – potentially cutting years from the timeline for drugs to reach patients. Speaking ahead of her presentation, Giovanna Mallucci, professor of clinical neuroscience at the University of Cambridge, said: “It’s really exciting. They’re licensed drugs. This means you’d do a straightforward basic clinical trial on a small group of patients because these are not new compounds, they’re known drugs.” The scientists have chosen not to name the two drugs, which are currently used for conditions unrelated to dementia, to avoid the possibility of patients seeking to use them ahead of any clinical trial to prove their efficacy. The findings build on a landmark study two years ago, showing that brain cell death could be halted in mice by switching off a faulty signal in the brain that stops new proteins being produced. However, the breakthrough relied on a compound that had severe physical side-effects including weight loss and diabetes, making it unsuitable for use in humans. The two drugs were identified after Mallucci’s team screened hundreds of licensed compounds in search for something safe that had the same protective effects on the brain. Clare Walton, research manager at the Alzheimer’s Society, said: “The new results are hugely promising because the drugs are already given to people and we know they’re safe.” © 2015 Guardian News and Media Limited
Link ID: 21114 - Posted: 07.01.2015
Moheb Costandi Different immune cells regulate pain sensitization in male and female mice, according to research published on 29 June in Nature Neuroscience1. The surprising biological divide may explain why some clinical trials of pain drugs have failed, and highlights shortcomings in the way that many researchers design their experiments. The immune system has important roles in chronic pain, with cells called microglia being key players. Microglia express a protein called brain-derived neurotrophic factor (BDNF) to signal to spinal-cord neurons. When injury or inflammation occurs, this signal sensitizes the body to pain, so that even light touch hurts. Robert Sorge, a psychologist at the University of Alabama in Birmingham, and his colleagues induced persistent pain and inflammation in healthy male and female mice by severing two of the three sciatic nerve branches in their hind paws. Seven days later, they injected the animals with one of three drugs that inhibit microglial function. They found that all three drugs reversed pain sensitization in the male animals, as had been previously reported. But the treatments had no effect on the females, even though the animals had displayed equivalent levels of pain. The researchers also genetically engineered mice in which the BDNF gene could be deleted in microglia at any time during the animals' lives. At first, these animals exhibited normal responses to a nerve injury. Killing the microglia one week later extinguished that hypersensitivity in the male animals, but not in the females. This confirmed that in males, hypersensitivity to pain depends on BDNF signals from microglia, but that in females it is mediated by some other mechanism. © 2015 Nature Publishing Group,
By Christopher Intagliata Two decades ago, Swiss researchers had women smell the tee shirts that various men had slept in for two nights. Turned out that if women liked the aroma of a particular shirt, the guy who’d worn it was likely to have genetically coded immunity that was unlike the woman’s. Well the effect isn't just limited to sweaty shirts. Turns out we all smell things a little differently—you pick up a note of cloves, say, where I smell something more soapy—and that too gives clues to our degree of genetic similarity. Researchers tried that test with 89 people—having them sniff a couple dozen samples, and label each one using terms like lemony, coconut, fishy and floral. And each volunteer classified the scents differently enough that the researchers could single them out in subsequent tests, based on what they called each subject’s "olfactory fingerprint." Researchers then repeated that sniff test on another 130 subjects. But this time they did a blood test, too, to figure out each person's HLA type—an immune factor that determines whether you'll reject someone's organ, for example. They found that people who perceived smells similarly also had similar HLA types. Study author Lavi Secundo, a neuroscientist at the Weizmann Institute of Science in Israel, says the smell test could have real-world applications. "For organ donation you can think of this method as a quick, maybe a quick and dirty, method to sift between the best and the rest." He and his colleagues say it might even eliminate the need for 30 percent of the HLA tests done today. The work appears in the Proceedings of the National Academy of Sciences. [Lavi Secundo et al, Individual olfactory perception reveals meaningful nonolfactory genetic information] © 2015 Scientific American
By Jan Hoffman Guinea pigs do not judge. They do not bully. They are characteristically amiable, social and oh-so-tactile. They tuck comfortably into child-size laps and err on the side of the seriously cute. When playing with guinea pigs at school, children with autism spectrum disorders are more eager to attend, display more interactive social behavior and become less anxious, according to a series of studies, the most recent of which was just published in Developmental Psychobiology. In previous studies, researchers in Australia captured these results by surveying parents and teachers or asking independent observers to analyze videotapes of the children playing. In the new report, however, the researchers analyzed physiological data pointing to the animals’ calming effect on the children. The children played with two guinea pigs in groups of three — one child who was on the spectrum and two typically developing peers. All 99 children in the study, ages 5 to 12, wore wrist bands that monitored their arousal levels, measuring electric charges that race through the skin. Arousal levels can suggest whether a subject is feeling anxious or excited. The first time that typically developing children played with the guinea pigs, they reported feeling happy and registered higher levels of arousal. The researchers speculate that the children were excited by the novelty of the animals. Children with autism spectrum disorders also reported feeling elated, but the wrist band measurements suggested their arousal levels had declined. The animals seem to have lowered the children’s stress, the researchers concluded. © 2015 The New York Times Company
Link ID: 21111 - Posted: 06.30.2015
Henry Nicholls Andy Russell had entered the lecture hall late and stood at the back, listening to the close of a talk by Marta Manser, an evolutionary biologist at the University of Zurich who works on animal communication. Manser was explaining some basic concepts in linguistics to her audience, how humans use meaningless sounds or “phonemes” to generate a vast dictionary of meaningful words. In English, for instance, just 40 different phonemes can be resampled into a rich vocabulary of some 200,000 words. But, explained Manser, this linguistic trick of reorganising the meaningless to create new meaning had not been demonstrated in any non-human animal. This was back in 2012. Russell’s “Holy shit, man” excitement was because he was pretty sure he had evidence for phoneme structuring in the chestnut-crowned babbler, a bird he’s been studying in the semi-arid deserts of south-east Australia for almost a decade. After the talk, Russell (a behavioural ecologist at the University of Exeter) travelled to Zurich to present his evidence to Manser’s colleague Simon Townsend, whose research explores the links between animal communication systems and human language. The fruits of their collaboration are published today in PLoS Biology. One of Russell’s students Jodie Crane had been recording the calls of the chestnut-crowned babbler for her PhD. The PLoS Biology paper focuses on two of these calls, which appear to be made up of two identical elements, just arranged in a different way. © 2015 Guardian News and Media Limited
By Ariana Eunjung Cha One of the most heartbreaking things about Alzheimer's is that it has been impossible for doctors to predict who will get it before symptoms begin. And without early detection, researchers say, a treatment or cure may be impossible. Governments, drug companies and private foundations have poured huge amounts of money into trying to come up with novel ways to detect risk through cutting-edge technologies ranging from brain imaging, protein analysis of cerebrospinal fluid and DNA profiling. Now a new study, published in the journal Neurology, shows that perhaps something more old-fashioned could be the answer: a memory test. The researchers tracked 2,125 participants in four Chicago neighborhoods for 18 years, giving them tests of memory and thinking every three years. They found that those who scored lowest on the tests during the first year were 10 times more likely to be diagnosed with Alzheimer's down the road -- indicating that cognitive impairment may be affecting the brain "substantially earlier than previously established," the researchers wrote.
Allison Aubrey Bite into that bread before your main meal, and you'll spike your blood sugar and amp up your appetite. Waiting until the end of your dinner to nosh on bread can blunt those effects. Bite into that bread before your main meal, and you'll spike your blood sugar and amp up your appetite. Waiting until the end of your dinner to nosh on bread can blunt those effects. iStockphoto Ah, the bread basket. You sit down for a nice meal out, and there it appears: piping hot, giving off a waft of yeasty divinity. There's a reason this age-old tradition prevails. Even in the era of paleo and gluten-free, there are still hordes of us who will gladly nosh on crusty, chewy, soul-warming bread. But the downside may be more than just some extra calories. Turns out, eating all those carbs before a meal can amp up our appetites and spike our blood sugar. "The worst situation is having refined carbohydrates on an empty stomach, because there's nothing to slow down the digestion of that carbohydrate into sugar," explains David Ludwig, director of the Optimal Weight for Life Clinic at Boston Children's Hospital. © 2015 NPR
Link ID: 21108 - Posted: 06.30.2015
Emma Bowman In a small, sparse makeshift lab, Melissa Malzkuhn practices her range of motion in a black, full-body unitard dotted with light-reflecting nodes. She's strapped on a motion capture, or mocap, suit. Infrared cameras that line the room will capture her movement and translate it into a 3-D character, or avatar, on a computer. But she's not making a Disney animated film. Three-dimensional motion capture has developed quickly in the last few years, most notably as a Hollywood production tool for computer animation in films like Planet of the Apes and Avatar. Behind the scenes though, leaders in the deaf community are taking on the technology to create and improve bilingual learning tools in American Sign Language. Malzkuhn has suited up to record a simple nursery rhyme. Being deaf herself, she spoke with NPR through an interpreter. "I know in English there's just a wealth of nursery rhymes available, but we really don't see as much in ASL," she says. "So we're gonna be doing some original work here in developing nursery rhymes." That's because sound-based rhymes don't cross over well into the visual language of ASL. Malzkuhn heads the Motion Light Lab, or ML2. It's the newest hub of the National Science Foundation Science of Learning Center, Visual Language and Visual Learning (VL2) at Gallaudet University, the premier school for deaf and hard of hearing students. © 2015 NPR
Link ID: 21107 - Posted: 06.29.2015