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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.
Matt Kaplan Humans are among the very few animals that constitute a threat to elephants. Yet not all people are a danger — and elephants seem to know it. The giants have shown a remarkable ability to use sight and scent to distinguish between African ethnic groups that have a history of attacking them and groups that do not. Now a study reveals that they can even discern these differences from words spoken in the local tongues. Biologists Karen McComb and Graeme Shannon at the University of Sussex in Brighton, UK, guessed that African elephants (Loxodonta africana) might be able to listen to human speech and make use of what they heard. To tease out whether this was true, they recorded the voices of men from two Kenyan ethnic groups calmly saying, “Look, look over there, a group of elephants is coming,” in their native languages. One of these groups was the semi-nomadic Maasai, some of whom periodically kill elephants during fierce competition for water or cattle-grazing space. The other was the Kamba, a crop-farming group that rarely has violent encounters with elephants. The researchers played the recordings to 47 elephant family groups at Amboseli National Park in Kenya and monitored the animals' behaviour. The differences were remarkable. When the elephants heard the Maasai, they were much more likely to cautiously smell the air or huddle together than when they heard the Kamba. Indeed, the animals bunched together nearly twice as tightly when they heard the Maasai. “We knew elephants could distinguish the Maasai and Kamba by their clothes and smells, but that they can also do so by their voices alone is really interesting,” says Fritz Vollrath, a zoologist at the University of Oxford, UK (see video below). © 2014 Nature Publishing Group
Think women can’t do math? You’re wrong—but new research shows you might not change your mind, even if you get evidence to the contrary. A study of how both men and women perceive each other's mathematical ability finds that an unconscious bias against women could be skewing hiring decisions, widening the gender gap in mathematical professions like engineering. The inspiration for the experiment was a 2008 study published in Science that analyzed the results of a standardized test of math and verbal abilities taken by 15-year-olds around the world. The results challenged the pernicious stereotype that females are biologically inferior at mathematics. Although the female test-takers lagged behind males on the math portion of the test, the size of the gap closely tracked the degree of gender inequality in their countries, shrinking to nearly zero in emancipated countries like Sweden and Norway. That suggests that cultural biases rather than biology may be the better explanation for the math gender gap. To tease out the mechanism of discrimination, two of the authors of the 2008 study, Paola Sapienza and Luigi Zingales, economic researchers at Northwestern University’s Kellogg School of Management in Evanston, Illinois, and the University of Chicago Booth School of Business in Illinois, respectively, teamed up with Ernesto Reuben, an experimental psychologist at Columbia Business School in New York City, to design an experiment to test people's gender bias when it comes to judging mathematical ability. Study participants of both genders were divided into two groups: employers and job candidates. The job was simple: As accurately and quickly as possible, add up sets of two-digit numbers in a 4-minute math sprint. (The researchers did not tell the subjects, but it is already known that men and women perform equally well on this task.) © 2014 American Association for the Advancement of Science.
By Jessica Wright and SFARI.org It takes more mutations to trigger autism in women than in men, which may explain why men are four times more likely to have the disorder, according to a study published 26 February in the American Journal of Human Genetics. The study found that women with autism or developmental delay tend to have more large disruptions in their genomes than do men with the disorder. Inherited mutations are also more likely to be passed down from unaffected mothers than from fathers. Together, the results suggest that women are resistant to mutations that contribute to autism. “This strongly argues that females are protected from autism and developmental delay and require more mutational load, or more mutational hits that are severe, in order to push them over the threshold,” says lead researcher Evan Eichler, professor of genome sciences at the University of Washington in Seattle. “Males on the other hand are kind of the canary in the mineshaft, so to speak, and they are much less robust.” The findings bolster those from previous studies, but don't explain what confers protection against autism in women. The fact that autism is difficult to diagnose in girls may mean that studies enroll only those girls who are severely affected and who may therefore have the most mutations, researchers note. “The authors are geneticists, and the genetics is terrific,” says David Skuse, professor of behavioral and brain sciences at University College London, who was not involved in the study. “But the questions about ascertainment are not addressed adequately.” © 2014 Scientific American
By TARA PARKER-POPE For a $14.95 monthly membership, the website Lumosity promises to “train” your brain with games designed to stave off mental decline. Users view a quick succession of bird images and numbers to test attention span, for instance, or match increasingly complex tile patterns to challenge memory. While Lumosity is perhaps the best known of the brain-game websites, with 50 million subscribers in 180 countries, the cognitive training business is booming. Happy Neuron of Mountain View, Calif., promises “brain fitness for life.” Cogmed, owned by the British education company Pearson, says its training program will give students “improved attention and capacity for learning.” The Israeli firm Neuronix is developing a brain stimulation and cognitive training program that the company calls a “new hope for Alzheimer’s disease.” And last month, in a move that could significantly improve the financial prospects for brain-game developers, the Centers for Medicare and Medicaid Services began seeking comments on a proposal that would, in some cases, reimburse the cost of “memory fitness activities.” Much of the focus of the brain fitness business has been on helping children with attention-deficit problems, and on improving cognitive function and academic performance in healthy children and adults. An effective way to stave off memory loss or prevent Alzheimer’s — particularly if it were a simple website or video game — is the “holy grail” of neuroscience, said Dr. Murali Doraiswamy, director of the neurocognitive disorders program at Duke Institute for Brain Sciences. The problem, Dr. Doraiswamy added, is that the science of cognitive training has not kept up with the hype. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 19346 - Posted: 03.11.2014
by Kat Arney Feeling dopey? Refresh your "circadian eye" with a burst of orange light. Light is a powerful wake-up call, enhancing alertness and activity. Its effect is controlled by a group of photoreceptor cells in the eyeball that make the light-sensing pigment melanopsin. These cells, which work separately to the rods and cones needed for vision, are thought to help reset animals' body clocks - or circadian rhythms. Studies with people who are blind suggest this also happens in humans, although the evidence isn't conclusive. To find out how melanopsin wakes up the brain, Gilles Vandewalle at the University of Liege, Belgium, and his team gave 16 people a 10-minute blast of blue or orange light while they performed a memory test in an fMRI scanner. They were then blindfolded for 70 minutes, before being retested under a green light. People initially exposed to orange light had greater brain activity in several regions related to alertness and cognition when they were retested, compared with those pre-exposed to blue light. Light switch Vandewalle thinks that melanopsin is acting as a kind of switch, sending different signals to the brain depending on its state. Orange light, which has the longer wavelength, is known to make the pigment more light-sensitive, but blue light has the opposite effect. Green light lies somewhere in the middle. The findings suggest that pre-exposure to orange light pushes the balance towards the more light-sensitive form of melanopsin, enhancing the response in the brain. © Copyright Reed Business Information Ltd.
by Nathan Seppa MS patients who harbor low levels of vitamin D early in their disease fare worse over the next several years than patients with higher levels. Multiple sclerosis is marked by damage to the fatty sheaths coating nerve fibers in the brain. The result can be an off-and-on series of symptoms including loss of muscle control, numbness and problems thinking. Vitamin D, which the body makes from sun exposure, has shown promise in fighting a variety of diseases and may limit this MS onslaught (SN: 7/16/11, p. 22). In 2002, researchers studying the effect of the drug beta-interferon-1b against MS set aside blood samples from 465 patients. When researchers recently analyzed those samples, they found that patients who had blood levels of vitamin D exceeding 20 nanograms per milliliter at six and 12 months after the onset of MS had fewer symptom flare-ups during the rest of the five-year study than those with lower readings did. Some scientists think 20 nanograms per milliliter is a healthy level; others see 30 as a healthier minimum. MRI scans revealed that, after five years, those who had started out with low vitamin D levels had four times as much myelin damage as those who had higher levels. The results appear in the March JAMA Neurology. A. Ascherio et al. Vitamin D as an early predictor of multiple sclerosis activity and progression. JAMA Neurology. Vol. 71, March 2014, p. 306. doi:10.1001/jamaneurol.2013.5993. © Society for Science & the Public 2000 - 2013
By ALBERT SUN On a frigid night recently in Randolph, N.J., the Jersey Wildcats junior hockey team flew across the home rink during practice at Aspen Ice Arena, sending ice into the air. Hockey is known for its collisions, and concussions aren’t unusual, but the players didn’t seem particularly worried. On the backs of their heads were flashing green lights, signifying that all was well. “We’ll be behind the bench, and as soon as a player comes back we can look right down and it’ll be a nice light,” said the coach, Justin Stanlick. If the light changes color, “we can know that player needs to go see a trainer to get cleared.” The light is part of a head impact sensor called the Checklight, made by Reebok. The device is a black skullcap with an electronic strip and three lights on the back. It blinks green when a player has sustained no head impact on the ice, yellow after a moderate impact and red after a severe one. The Checklight relies on an accelerometer and a gyroscope to measure the force of an impact. The Checklight flashes green for no impact, yellow for a moderate blow, red for a severe one.Bryan Thomas for The New York Times The Checklight flashes green for no impact, yellow for a moderate blow, red for a severe one. Coaches and parents have only to look to see if a player has taken a serious blow. And because the sensors are objective, Reebok executives say, they may lessen the pressure on young athletes to project toughness and play through a concussion. Gage Malinowski, a 19-year-old defenseman for the Wildcats, recently returned to practice after suffering the latest in a series of concussions during a game in February. “There’s not a game where I don’t have at least 10 hits,” he said. © 2014 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 19343 - Posted: 03.11.2014
Why do some humans have lighter skin than others? Researchers have longed chalked up the difference to tens of thousands of years of evolution, with darker skin protecting those who live nearer to the equator from the sun’s intense radiation. But a new study of ancient DNA concludes that European skin color has continued to change over the past 5000 years, suggesting that additional factors, including diet and sexual attraction, may also be at play. Our species, Homo sapiens, first arose in Africa about 200,000 years ago, and researchers assume that its first members were as dark-skinned as Africans are today, because dark skin is advantageous in Africa. Dark skin stems from higher levels of the pigment melanin, which blocks UV light and protects against its dangers, such as DNA damage—which can lead to skin cancer—and the breakdown of vitamin B. On the other hand, skin cells need exposure to a certain amount of UV light in order to produce vitamin D. These competing pressures mean that as early humans moved away from the equator, it makes sense that their skin lightened. Recent research, however, has suggested that the picture is not so simple. For one thing, a number of genes control the synthesis of melanin (which itself comes in two different forms in humans), and each gene appears to have a different evolutionary history. Moreover, humans apparently did not begin to lighten up immediately after they migrated from Africa to Europe beginning about 40,000 years ago. In 2012, for example, a team led by Jorge Rocha, a geneticist at the University of Porto in Portugal, looked at variants of four pigmentation genes in modern Portuguese and African populations and calculated that at least three of them had only been strongly favored by evolution tens of thousands of years after humans left Africa. In January, another team, led by geneticist Carles Lalueza-Fox of the University of Barcelona in Spain, sequenced the genome of an 8000-year-old male hunter-gatherer skeleton from the site of La Braña-Arintero in Spain and found that he was dark rather than light-skinned—again suggesting that natural selection for light skin acted relatively late in prehistory. © 2014 American Association for the Advancement of Science
By RON SUSKIND In our first year in Washington, our son disappeared. Just shy of his 3rd birthday, an engaged, chatty child, full of typical speech — “I love you,” “Where are my Ninja Turtles?” “Let’s get ice cream!” — fell silent. He cried, inconsolably. Didn’t sleep. Wouldn’t make eye contact. His only word was “juice.” I had just started a job as The Wall Street Journal’s national affairs reporter. My wife, Cornelia, a former journalist, was home with him — a new story every day, a new horror. He could barely use a sippy cup, though he’d long ago graduated to a big-boy cup. He wove about like someone walking with his eyes shut. “It doesn’t make sense,” I’d say at night. “You don’t grow backward.” Had he been injured somehow when he was out of our sight, banged his head, swallowed something poisonous? It was like searching for clues to a kidnapping. After visits to several doctors, we first heard the word “autism.” Later, it would be fine-tuned to “regressive autism,” now affecting roughly a third of children with the disorder. Unlike the kids born with it, this group seems typical until somewhere between 18 and 36 months — then they vanish. Some never get their speech back. Families stop watching those early videos, their child waving to the camera. Too painful. That child’s gone. In the year since his diagnosis, Owen’s only activity with his brother, Walt, is something they did before the autism struck: watching Disney movies. “The Little Mermaid,” “Beauty and the Beast,” “Aladdin” — it was a boom time for Disney — and also the old classics: “Dumbo,” “Fantasia,” “Pinocchio,” “Bambi.” They watch on a television bracketed to the wall in a high corner of our smallish bedroom in Georgetown. It is hard to know all the things going through the mind of our 6-year-old, Walt, about how his little brother, now nearly 4, is changing. They pile up pillows on our bed and sit close, Walt often with his arm around Owen’s shoulders, trying to hold him — and the shifting world — in place. © 2014 The New York Times Company
Link ID: 19341 - Posted: 03.10.2014
Alison Abbott A simple blood test has the potential to predict whether a healthy person will develop symptoms of dementia within two or three years. If larger studies uphold the results, the test could fill a major gap in strategies to combat brain degeneration, which is thought to show symptoms only at a stage when it too late to treat effectively. The test was identified in a preliminary study involving 525 people aged over 70. The work identified a set of ten lipid metabolites in blood plasma that distinguished with 90% accuracy between people who would remain cognitively healthy from those who would go on to show signs of cognitive impairment. “These findings are potentially very exciting,” says Simon Lovestone, a neuroscientist at the University of Oxford, UK, and a cordinator of a major European public-private partnership seekimg biomarkers for Alzheimer's. But he points out that only 28 participants developed symptoms similar to those of Alzheimer's disease during the latest work. “So the findings need to be confirmed in independent and larger studies.” There is not yet a good treatment for Alzheimer’s disease, which affects 35 million people worldwide. Several promising therapies have been tested in clinical trials over the last few years, but all have failed. However, those trials involved people who had already developed symptoms. Many neuroscientists fear that any benefits of a treatment would be missed in such a study, because it could be impossible to halt the disease once it has manifested. “We desperately need biomarkers which would allow patients to be identified — and recruited into trials — before their symptoms begin,” says Lovestone. © 2014 Nature Publishing Group,
Link ID: 19340 - Posted: 03.10.2014
By INNA GAISLER-SALOMON WE intuitively understand, and scientific studies confirm, that if a woman experiences stress during her pregnancy, it can affect the health of her baby. But what about stress that a woman experiences before getting pregnant — perhaps long before? It may seem unlikely that the effects of such stress could be directly transmitted to the child. After all, stress experienced before pregnancy is not part of a mother’s DNA, nor does it overlap with the nine months of fetal development. Nonetheless, it is undeniable that stress experienced during a person’s lifetime is often correlated with stress-related problems in that person’s offspring — and even in the offspring’s offspring. Perhaps the best-studied example is that of the children and grandchildren of Holocaust survivors. Research shows that survivors’ children have greater-than-average chances of having stress-related psychiatric illnesses like post-traumatic stress disorder, even without being exposed to higher levels of stress in their own lives. Similar correlations are found in other populations. Studies suggest that genocides in Rwanda, Nigeria, Cambodia, Armenia and the former Yugoslavia have brought about distinct psychopathological symptoms in the offspring of survivors. What explains this pattern? Does trauma lead to suboptimal parenting, which leads to abnormal behavior in children, which later affects their own parenting style? Or can you biologically inherit the effects of your parents’ stress, after all? It may be the latter. In a study that I, together with my colleagues Hiba Zaidan and Micah Leshem, recently published in the journal Biological Psychiatry, we found that a relatively mild form of stress in female rats, before pregnancy, affected their offspring in a way that appeared to be unrelated to parental care. © 2014 The New York Times Company
Think you’ll always pick chocolate over a bag of chips? Don’t be so sure. Researchers have found that if they can get people to pay more attention to a particular type of junk food, they will begin to prefer it—even weeks or months after the experiment. The finding suggests a new way to manipulate our decisions and perhaps even encourage us to pick healthy foods. “This paper is provocative and very well done,” says Antonio Rangel, a neuroeconomist at the California Institute of Technology in Pasadena, who was not involved in the new study. “It is exciting because it’s a proof of concept that a relatively simple intervention can have this long-lasting effect.” Economists who study decision-making had previously found that, when deciding between multiple items, people tend to let their gaze linger on the things that they end up choosing. This observation has motivated companies to pursue flashy packaging to attract consumers’ eyes. Tom Schonberg, a neuroscientist at the University of Texas, Austin, wondered whether people’s preferences could be changed before being faced with such a decision by training their brains to pay more attention to certain items. His first task was figuring out what kind of junk food people preferred. He and his colleagues recruited more than 200 university students and set up an auction-style program that asked them how much they were willing to pay for 60 different kinds of snacks, from M&M’s to Fritos. Then, the participants went through a 30- to 50-minute computer training program that showed photos of foods that the participants had already rated. When some treats appeared on the screen, a short tone would play and signal the subject to press a button as fast as possible. When other treats popped up, the computer remained silent and the subject refrained from pressing the button. © 2014 American Association for the Advancement of Science
By BENEDICT CAREY Jack Belliveau, a Harvard scientist whose quest to capture the quicksilver flare of thought inside a living brain led to the first magnetic resonance image of human brain function, died on Feb. 14 in San Mateo, Calif. He was 55. The cause was complications of a gastrointestinal disorder, said his wife, Brigitte Poncelet-Belliveau, a researcher who worked with him at the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital. He lived in Boston. His wife said he died suddenly while visiting an uncle at his childhood home, which he owned. Dr. Belliveau was a 30-year-old graduate student at the Martinos Center when he hatched a scheme to “see” the neural trace of brain activity. Doctors had for decades been taking X-rays and other images of the brain to look for tumors and other lesions and to assess damage from brain injuries. Researchers had also mapped blood flow using positron emission tomography scans, but that required making and handling radioactive trace chemicals, whose signature vanished within minutes. Very few research centers had the technical knowledge or the machinery to pull it off. Dr. Belliveau tried a different approach. He had developed a technique to track blood flow, called dynamic susceptibility contrast, using an M.R.I. scanner that took split-second images, faster than was usual at the time. This would become a standard technique for assessing blood perfusion in stroke patients and others, but Dr. Belliveau thought he would try it to spy on a normal brain in the act of thinking or perceiving. “He went out to RadioShack and bought a strobe light, like you’d see in a disco,” said Dr. Bruce Rosen, director of the Martinos Center and one of Dr. Belliveau’s advisers at the time. “He thought the strobe would help image the visual areas of the brain, where there was a lot of interest.” © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19337 - Posted: 03.10.2014
Imagine that, after feeling unwell for a while, you visit your GP. "Ah," says the doctor decisively, "what you need is medication X. It's often pretty effective, though there can be side-effects. You may gain weight. Or feel drowsy. And you may develop tremors reminiscent of Parkinson's disease." Warily, you glance at the prescription on the doctor's desk, but she hasn't finished. "Some patients find that sex becomes a problem. Diabetes and heart problems are a risk. And in the long term the drug may actually shrink your brain … " This scenario may sound far-fetched, but it is precisely what faces people diagnosed with schizophrenia. Since the 1950s, the illness has generally been treated using antipsychotic drugs – which, as with so many medications, were discovered by chance. A French surgeon investigating treatments for surgical shock found that one of the drugs he tried – the antihistamine chlorpromazine – produced powerful psychological effects. This prompted the psychiatrist Pierre Deniker to give the drug to some of his most troubled patients. Their symptoms improved dramatically, and a major breakthrough in the treatment of psychosis seemed to have arrived. Many other antipsychotic drugs have followed in chlorpromazine's wake and today these medications comprise 10% of total NHS psychiatric prescriptions. They are costly items: the NHS spends more on these medications than it does for any other psychiatric drug, including antidepressants. Globally, around $14.5bn is estimated to be spent on antipsychotics each year. Since the 1950s the strategy of all too many NHS mental health teams has been a simple one. Assuming that psychosis is primarily a biological brain problem, clinicians prescribe an antipsychotic medication and everyone does their level best to get the patient to take it, often for long periods. There can be little doubt that these drugs make a positive difference, reducing delusions and hallucinations and making relapse less likely – provided, that is, the patient takes their medication. © 2014 Guardian News and Media Limited
Link ID: 19336 - Posted: 03.08.2014
|By Jason G. Goldman Most people don't spend much time pondering the diameter of their pupils. The fact is that we don't have much control over our pupils, the openings in the center of the irises that allow light into the eyes. Short of chemical interventions—such as the eyedrops ophthalmologists use to widen their patients' pupils for eye exams—the only way to dilate or shrink the pupils is by changing the amount of available light. Switch off the lamp, and your pupils will widen to take in more light. Step out into the sun, and your pupils will narrow. Mechanical though they may be, the workings of pupils are allowing researchers to explore the parallels between imagination and perception. In a recent series of experiments, University of Oslo cognitive neuroscientists Bruno Laeng and Unni Sulutvedt began by displaying triangles of varying brightness on a computer screen while monitoring the pupils of the study volunteers. The subjects' pupils widened for dark shapes and narrowed for bright ones, as expected. Next, participants were instructed to simply imagine the same triangles. Remarkably, their pupils constricted or dilated as if they had been staring at the actual shapes. Laeng and Sulutvedt saw the same pattern when they asked subjects to imagine more complex scenes, such as a sunny sky or a dark room. Imagination is usually thought of as “a private and subjective experience, which is not accompanied by strongly felt or visible physiological changes,” Laeng says. But the new findings, published in Psychological Science, challenge that idea. The study suggests that imagination and perception may rely on a similar set of neural processes: when you picture a dimly lit restaurant, your brain and body respond, at least to some degree, as if you were in that restaurant. © 2014 Scientific American
by Hal Hodson WHETHER striding ahead with pride or slouching sullenly, we all broadcast our emotions through body language. Now a computer has learned to interpret those unspoken cues as well as you or I. Antonio Camurri of the University of Genoa in Italy and colleagues have built a system which uses the depth-sensing, motion-capture camera in Microsoft's Kinect to determine the emotion conveyed by a person's body movements. Using computers to capture emotions has been done before, but typically focuses on facial analysis or voice recording. Reading someone's emotional state from the way they walk across a room or their posture as they sit at a desk means they don't have to speak or look into a camera. "It's a nice achievement," says Frank Pollick, professor of psychology at the University of Glasgow, UK. "Being able to use the Kinect for this is really useful." The system uses the Kinect camera to build a stick figure representation of a person that includes information on how their head, torso, hands and shoulders are moving. Software looks for body positions and movements widely recognised in psychology as indicative of certain emotional states. For example, if a person's head is bowed and their shoulders are drooping, that might indicate sadness or fear. Adding in the speed of movement – slow indicates sadness, while fast indicates fear – allows the software to determine how someone is feeling. In tests, the system correctly identified emotions in the stick figures 61.3 per cent of the time, compared with a 61.9 per cent success rate for 60 human volunteers (arXiv.org/1402.5047). Camurri is using the system to build games that teach children with autism to recognise and express emotions through full-body movements. Understanding how another person feels can be difficult for people with autism, and recognising fear is more difficult than happiness. © Copyright Reed Business Information Ltd.
A man blind since birth is taking up a surprising new hobby: photography. His newfound passion is thanks to a system that turns images into sequences of sound. The technology not only gives “sight” to the blind, but also challenges the way neurologists think the brain is organized. In 1992, Dutch engineer Peter Meijer created vOICe, an algorithm that converts simple grayscale images into musical soundscapes. (The capitalized middle letters sound out “Oh, I see!”). The system scans images from left to right, converting shapes in the image into sound as it sweeps, with higher positions in the image corresponding to higher sound frequencies. For instance, a diagonal line stretching upward from left to right becomes a series of ascending musical notes. While more complicated images, such as a person sitting on a lawn chair, at first seem like garbled noise, with enough training users can learn to “hear” everyday scenes. In 2007, neuroscientist Amir Amedi and his colleagues at the Hebrew University of Jerusalem began training subjects who were born blind to use vOICe. Despite having no visual reference points, after just 70 hours of training, the individuals went from “hearing” simple dots and lines to “seeing” whole images such as faces and street corners composed of 4500 pixels. (For comparison, Nintendo’s Mario was made up of just 192 pixels in his first video game appearance.) By attaching a head-mounted camera to a computer and headphones, the blind users were even able to navigate around a room by the sound cues alone. Every few steps the system snaps a photo and converts it into sound, giving the users their bearings as they traverse tables and trashcans. One patient even took up photography, using the head-mounted system to frame his snapshots. © 2014 American Association for the Advancement of Science.
by Bruce Bower Actor Philip Seymour Hoffman’s February death from a drug overdose triggered media reports blaming the terrible disease of addiction for claiming another life. But calling addiction a “disease” may be misguided, according to an alternative view with some scientific basis. Most people who are addicted to cigarette smoking, alcohol or other drugs manage to quit, usually on their own, after experiencing major attitude adjustments. Although relapses occur, successes ultimately outnumber fatalities. People can permanently walk away from addiction. Evidence that addiction is a solvable coping problem rather than a chronic, recurring disease seems like encouraging news. But it’s highly controversial. Neuroscientists and many clinicians regard drug addictions as brain illnesses best vanquished with the help of medications that fight cravings and withdrawal. From this perspective, drug-induced brain changes increase a person’s thirst for artificial highs and make quitting progressively more difficult. This conflict over addiction’s nature plays out in two lines of research: studies of remission and relapse among treated substance abusers and long-term studies of the general population. Follow-up investigations of people who attend treatment programs report that addicts never completely shake an urge to snort, inject, guzzle or otherwise consume their poisons of choice. Ongoing treatment in psychotherapy, rehab centers or 12-step groups encourages temporary runs of sobriety, but it’s easier to kick the bucket than to kick the habit. Surveys and long-term studies of the general population, however, observe that addicts typically spend their youth in a substance-induced haze but drastically cut back or quit using drugs altogether by early adulthood. Most of those who renounce the “high” life do so without formal treatment. © Society for Science & the Public 2000 - 2013.
Keyword: Drug Abuse
Link ID: 19332 - Posted: 03.08.2014
By SABRINA TAVERNISE Middle and high school students who used electronic cigarettes were more likely to smoke real cigarettes and less likely to quit than students who did not use the devices, a new study has found. They were also more likely to smoke heavily. But experts are divided about what the findings mean. The study’s lead author, Stanton Glantz, a professor of medicine at the University of California, San Francisco, who has been critical of the devices, said the results suggested that the use of e-cigarettes was leading to less quitting, not more. “The use of e-cigarettes does not discourage, and may encourage, conventional cigarette use among U.S. adolescents,” the study concluded. It was published online in the journal JAMA Pediatrics on Thursday. But other experts said the data did not support that interpretation. They said that just because e-cigarettes are being used by youths who smoke more and have a harder time quitting does not mean that the devices themselves are the cause of those problems. It is just as possible, they said, that young people who use the devices were heavier smokers to begin with, or would have become heavy smokers anyway. “The data in this study do not allow many of the broad conclusions that it draws,” said Thomas J. Glynn, a researcher at the American Cancer Society. The study is likely to stir the debate further over what electronic cigarettes mean for the nation’s 45 million smokers, about three million of whom are middle and high school students. Some experts worry that e-cigarettes are a gateway to smoking real cigarettes for young people, though most say the data is too skimpy to settle the issue. Others hope the devices could be a path to quitting. So far, the overwhelming majority of young people who use e-cigarettes also smoke real cigarettes, a large federal survey published last year found. Still, while e-cigarette use among youths doubled from 2011 to 2012, regular cigarette smoking for youths has continued to decline. The rate hit a record low in 2013 of 9.6 percent, down by two-thirds from its peak in 1997. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19331 - Posted: 03.08.2014
by Graham Lawton In August 2013, professional rugby union player Andy Hazell received a massive blow to the head while playing for his club Gloucester. Six "horrendous" months later he retired from the game, stricken by dizziness, mood swings and a sense of detachment. Hazell isn't the first rugby player to experience concussion during a game, and probably won't be the last to have to retire as a result. According to a campaign launched this week, rugby union players don't know enough about the risks of concussion – and the governing bodies aren't doing enough to prevent it. The problem isn't so much one-off blows like the one that ended Hazell's career, but long-term damage caused by repeated concussions over many years. Studies of boxers and American footballers have shown that these can lead to a degenerative brain disease called Chronic Traumatic Encephalopathy (CTE). CTE leads to memory problems, personality change and slowness of movement. It usually shows up in middle age, long after a sporting career is over. CTE has been an issue in American Football for years. Thousands of ex-professionals sued the National Football League alleging that it knew about the risks but covered them up. Last year the NFL offered a $765 million settlement package. Neurologists have long suspected that other contact sports might also lead to CTE – particularly rugby union because of its emphasis on high-speed "hits". Concussion is the fourth most common injury in the professional game. © Copyright Reed Business Information Ltd.
Keyword: Brain Injury/Concussion
Link ID: 19330 - Posted: 03.08.2014