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By Clare Wilson People who develop schizophrenia may have been born with brains with a different structure. The finding adds further support to the idea that genetics can play a key role in schizophrenia, which involves delusions and hallucinations and is often a lifelong condition once it develops. Schizophrenia has been the subject of a fierce nature-versus-nurture debate: childhood abuse is linked with a raised risk of the condition, but 108 genes have been implicated, too. Probing the biology of schizophrenia is difficult because brain tissue sampled from people with the condition is rarely available to study. Kristen Brennand of the Icahn School of Medicine at Mount Sinai in New York and her colleagues got around this by taking skin cells from 14 people with schizophrenia, and reprogramming them into stem cells and then nerve cells. They found that on average these nerve cells had lower levels of a signalling molecule called miR-9 than similar cells developed from people who do not have schizophrenia. A small string of nucleic acids, miR-9 can change the activity of certain genes and is known to play a role in how neurons develop in the fetus. In further experiments, Brennand’s team showed that miR-9 might also affect how neurons migrate from where they form, next to the fetal brain’s central cavities, out to their final resting place in the brain’s outer layers. © Copyright Reed Business Information Ltd.
By Patrick Monahan You might have seen a video from David Attenborough’s The Life of Birds series where a male superb lyrebird (Menura novaehollandiae) attempts to lure a mate by imitating a smorgasbord of bird calls and even chainsaws. As nature’s show-offs, male animals tend to have more elaborate colors and courtship behaviors than their female counterparts, so it’s typical that the male would get the public’s attention. The same is true in science: Plenty of female birds sing songs, but researchers have in the past often dismissed them as simply being evolutionary tag-alongs of the males’ “come hither” calls. Now, by recording the calls of female superb lyrebirds, researchers have found that they can keep up with the boys just fine. According to a study published this week in Frontiers in Ecology and Evolution, the females collectively imitated 19 other species of birds, and also sang lyrebird-specific songs. And they changed their songs depending on context, using more lyrebird-specific “whistle” calls when out foraging and vying for territory, but more mimicking calls when defending their nests (as in the audio file below). The fact that the females change their type of call depending on the context makes it likely that these songs evolved in their own right—and the males’ calls aren’t so special after all. Plus, that part about the chainsaw? It probably doesn’t even happen in the wild. © 2016 American Association for the Advancement of Science
By Emily Underwood Earlier this month, György Buzsáki of New York University (NYU) in New York City showed a slide that sent a murmur through an audience in the Grand Ballroom of New York’s Midtown Hilton during the annual meeting of the Cognitive Neuroscience Society. It wasn’t just the grisly image of a human cadaver with more than 200 electrodes inserted into its brain that set people whispering; it was what those electrodes detected—or rather, what they failed to detect. When Buzsáki and his colleague, Antal Berényi, of the University of Szeged in Hungary, mimicked an increasingly popular form of brain stimulation by applying alternating electrical current to the outside of the cadaver’s skull, the electrodes inside registered little. Hardly any current entered the brain. On closer study, the pair discovered that up to 90% of the current had been redirected by the skin covering the skull, which acted as a “shunt,” Buzsáki said. For many meeting attendees, the unusual study heightened serious doubts about the mechanism and effectiveness of transcranial direct current stimulation (tDCS), an experimental, noninvasive treatment that uses electrodes to deliver weak current to a person’s forehead, and the related tACS, which uses alternating current. Little is known about how these techniques might influence the brain. Yet many scientific papers have claimed that the techniques can boost mood, alleviate chronic pain, and even make people better at math by directly affecting neuronal activity. This has spawned a cottage industry of do-it-yourself gadgets promising to make people smarter and happier. © 2016 American Association for the Advancement of Science
Link ID: 22126 - Posted: 04.21.2016
Medical research and new drugs to treat human illness usually start with studies on mice and rats. But that type of research has been traditionally sexist — using far more male than female rodents. Scientists warn that has already led to drugs and treatments that are potentially dangerous for women and say the approach slows down the development of treatments and drugs that are safe and effective for everyone. Cara Tannenbaum, scientific director of the Institute of Gender and Health at the Canadian Institutes of Health Research, cited a couple of examples on CBC's The Current of cases where drug side-effects turned out to be far more harmful in women: A stomach drug called cisapride that was sold in the 1990s under the name Prepulsid was withdrawn by Health Canada in 2000 because it sometimes caused irregular heartbeat and sudden death "in women only," Tannenbaum said. Among the victims was the 15-year-old daughter of former Ontario MP Terence Young. "It's not clear that the drug was ever tested in female animals or minors," Tannenbaum added. Health Canada has issued a warning about sleeping pills containing the drug zolpiclone, also known as Ambien, Tannenbaum said. Women are recommended to take half the dose that is prescribed to men. "It was recently discovered that the level of the drug was 45 per cent higher in women the next day, which can lead to car accidents," Tannenbaum said. Jeffrey Mogil, a neuroscientist and pain specialist at McGill University, said there are lots of reasons to suspect men and women respond differently to many different kinds of drugs, but very little actual data. "We actually don't know the scope of the problem," he told The Current. ©2016 CBC/Radio-Canada.
By Esther Landhuis Peer inside the brain of someone with Alzheimer’s disease, and you’ll see some striking features: shriveled nerve cells and strange protein clumps. According to a leading theory, proteins called amyloid beta and tau build up in the brain and choke nerve cell communication, setting the disease in motion years before people suspect anything is wrong with their recall. Yet the Alzheimer’s brain has another curious aspect. Some of the clusters of toxic amyloid proteins are entangled with octopus-like immune cells called microglia, cells that live in the brain to clear unwanted clutter. By munching on amyloid plaques, microglia are thought to help keep the disease at bay. But these housekeeping cells have an additional role—they switch on inflammatory pathways. Inflammation is critically important when the immune system encounters infection or needs to repair tissue. If left unchecked, however, the inflammatory process churns out toxic substances that can kill surrounding cells, whose death triggers more inflammation and creates a vicious cycle. For years scientists have probed how neuroinflammation contributes to Alzheimer’s disease and other neurodegenerative ailments. Researchers face a number of immediate questions: Is neuroinflammation a driving force? Does it kick in when the disease is already underway and worsen the process? Could it be harnessed for good in the early stages? Those questions are far from settled, but research is starting to reveal a clearer picture. “It may not be the amyloid plaques themselves that directly damage neurons and the connections between them. Rather, it may be the immune reaction to the plaques that does the damage,” says Cynthia Lemere, a neuroscientist at Brigham and Women’s Hospital. Still, it is hard to say if microglia are good guys or bad, making it challenging to create therapeutics that target these cells. © 2016 Scientific American
By DAN LEVIN VANCOUVER, British Columbia — Dave Napio started doing heroin over four decades ago, at 11 years old. Like many addicts these days, he heads to Vancouver’s gritty Downtown Eastside neighborhood when he needs a fix. But instead of seeking out a dealer in a dark alley, Mr. Napio, 55, gets his three daily doses from a nurse at the Crosstown Clinic, the only medical facility in North America permitted to prescribe the narcotic at the center of an epidemic raging across the continent. And instead of robbing banks and jewelry stores to support his habit, Mr. Napio is spending time making gold and silver jewelry, hoping to soon turn his hobby into a profession. “My whole life is straightening out,” Mr. Napio, who spent 22 of his 55 years in prison, said during a recent interview in the clinic’s mirror-lined injection room. “I’m becoming the guy next door.” Mr. Napio is one of 110 chronic addicts with prescriptions for diacetylmorphine hydrochloride, the active ingredient in heroin, which he injects three times a day at Crosstown as part of a treatment known as heroin maintenance. The program has been so successful at keeping addicts out of jail and away from emergency rooms that its supporters are seeking to expand it across Canada. But they have been hindered by a tangle of red tape and a yearslong court battle reflecting a conflict between medicine and politics on how to address drug addiction. The clinic’s prescription program began as a clinical trial more than a decade ago. But it has garnered more interest recently as a plague of illicit heroin use and fatal overdoses of legal painkillers has swept across the United States, fueling frustration over ideological and legal obstacles to forms of treatment that studies show halt the spread of disease through needles and prevent deaths. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22123 - Posted: 04.21.2016
Nicola Davis The proportion of older people suffering from dementia has fallen by a fifth over the past two decades with the most likely explanation being because men are smoking less and living healthier lives, according to new scientific research. A team from three British universities concluded that as a result the number of new cases of dementia is lower than had been predicted in the 1990s, estimated at around 210,000 a year in the UK as opposed to 250,000. The findings are potentially significant because they suggest that it is possible to take preventative action, such as stopping smoking and reducing cholesterol, that could help avoid the condition. “Physical health and brain health are clearly highly linked,” said Carol Brayne of Cambridge University, who co-authored the study. Nick Fox, professor of neurology at University College, London, who was not involved in the study, agrees: “This does suggest that our risk, in any particular age in later life, can be reduced probably by what we do 10, 20 or 30 years before.” The scientists found that new cases of dementia had dropped from 20.1 in every 1,000 people per year in the first study conducted in the early 1990s to 17.7 in the second, which looked at new cases between 2008 and 2013. When sex and age differences were taken into account, the dementia rates were found to have dropped by 20%. The trend emerges from a dramatic drop in new cases for men across all age groups. In the 1990s study, for every 1,000 men aged 70-74, 12.9 went on to develop dementia within a year. In the second study, 20 years later, that figure had dropped to only 8.7 men. For men aged 65-69 the rate of new cases had more than halved between the two studies. © 2016 Guardian News and Media Limited
Link ID: 22122 - Posted: 04.20.2016
By Mitch Leslie The worst part of being sick isn’t always the muscle aches and coughing. It’s the foggy head, the crankiness, the apathy, and the fatigue—in short, what researchers call sickness behavior. A new study uncovers a molecular mechanism that explains why we feel so crummy when we’re under the weather. “It’s a nice study that’s covered a lot of ground,” says neuroimmunologist Colm Cunningham of Trinity College in Dublin who wasn’t connected to the research. “What they’ve found is very plausible.” Although sickness behavior is unpleasant, researchers think the symptoms we suffer during a viral or bacterial infection are beneficial, enabling us to divert our energy to fighting the pathogens that have invaded our bodies. For cancer patients and people with autoimmune diseases, however, sickness behavior can be an unwanted side effect of treatment with immune molecules known as interferons, which our cells naturally release when we have an infection. The condition has posed a puzzle for researchers because they assumed the blood-brain barrier, a protective system that excludes most pathogens and immune molecules from the brain, would block signals from the immune system. Although scientists have identified several mechanisms that allow such messages to cross the barrier and influence behavior, the question of how the immune system and brain communicate “has been only partially answered,” says immunophysiologist Keith Kelley of the University of Illinois, Urbana-Champaign, who wasn’t connected to the new study. © 2016 American Association for the Advancement of Science.
Link ID: 22121 - Posted: 04.20.2016
Melissa Davey Researchers have developed the world’s first blood test that can detect the abnormal metabolism of blood cells in people with Parkinson’s disease, which means the blood test could be used to diagnose the disorder. At present the only way to diagnose Parkinson’s disease, a degenerative neurological condition, is through ordering a range of tests and scans to rule out other disorders, combined with examining symptoms. Patients are often diagnosed only after they have developed symptoms and brain cells have already been destroyed. While there is no cure for Parkinson’s, early detection allows treatment with medication and physiotherapy to begin, which may slow the deterioration of motor functions in patients. Because diagnosing the disease is a process of elimination, and the symptoms mimic those of other neurological disorders, patients are also at risk being diagnosed and treated for the wrong disease. The group of Australian researchers from La Trobe University believe their blood test will enable doctors to detect Parkinson’s disease with unprecedented reliability and lead to earlier treatment. Their findings are under review by an international medical journal. © 2016 Guardian News and Media Limited
Link ID: 22120 - Posted: 04.20.2016
By Sarah Kaplan We know where the human story started: In Africa, millions of years ago, with diminutive people whose brains were just a third of the size of ours. And we know where it ended: with us. Yet a lot of what happened in between is still debated, including the question of how humans' bodies and noggins got so much bigger than our ancestors'. The traditional thinking is that the growth of both was spurred by the process of natural selection. The evolutionary advantages of a big body and a big brain are plentiful, so it seems reasonable to think that each developed independent of the other in response to the demands of survival in a hostile world. But a new study in the journal Current Anthropology suggests that, while our brains are certainly an advantageous adaptation, our imposing physiques (such as they are) are more of an evolutionary fluke. That's because the genes that determine brain and body size are the same, argues Mark Grabowski, a fellow at the American Museum of Natural History. So as humans evolved bigger and bigger brains, our bodies "just got pulled along." Grabowski acknowledges that it may seem like a counterintuitive conclusion — most of us learned in high school biology that evolution is about adapting to circumstances and that only the fittest survive. We're not used to thinking of traits as a product of happenstance. But evolutionary scientists know that lots of traits — even ultimately beneficial ones — are just the luck of the draw.
Link ID: 22119 - Posted: 04.20.2016
By JAMES GORMAN Bees find nectar and tell their hive-mates; flies evade the swatter; and cockroaches seem to do whatever they like wherever they like. But who would believe that insects are conscious, that they are aware of what’s going on, not just little biobots? Neuroscientists and philosophers apparently. As scientists lean increasingly toward recognizing that nonhuman animals are conscious in one way or another, the question becomes: Where does consciousness end? Andrew B. Barron, a cognitive scientist, and Colin Klein, a philosopher, at Macquarie University in Sydney, Australia, propose in Proceedings of the National Academy of Sciences that insects have the capacity for consciousness. This does not mean that a honeybee thinks, “Why am I not the queen?” or even, “Oh, I like that nectar.” But, Dr. Barron and Dr. Klein wrote in a scientific essay, the honeybee has the capacity to feel something. Their claim stops short of some others. Christof Koch, the president and chief scientific officer of the Allen Institute for Brain Science in Seattle, and Giulio Tononi, a neuroscientist and psychiatrist at the University of Wisconsin, have proposed that consciousness is nearly ubiquitous in different degrees, and can be present even in nonliving arrangements of matter, to varying degrees. They say that rather than wonder how consciousness arises, one should look at where we know it exists and go from there to where else it might exist. They conclude that it is an inherent property of physical systems in which information moves around in a certain way — and that could include some kinds of artificial intelligence and even naturally occurring nonliving matter. © 2016 The New York Times Company
Link ID: 22118 - Posted: 04.19.2016
Rachel Becker A highly contagious and deadly animal brain disorder has been detected in Europe for the first time. Scientists are now warning that the single case found in a wild reindeer might represent an unrecognized, widespread infection. Chronic wasting disease (CWD) was thought to be restricted to deer, elk (Cervus canadensis) and moose (Alces alces) in North America and South Korea, but on 4 April researchers announced that the disease had been discovered in a free-ranging reindeer (Rangifer tarandus tarandus) in Norway. This is both the first time that CWD has been found in Europe and the first time that it has been found in this species in the wild anywhere in the world. “It’s worrying — of course, especially for animals. It’s a nasty disease,” says Sylvie Benestad, an animal-disease researcher at the Norwegian Veterinary Institute in Oslo who, along with colleague Turid Vikøren, diagnosed the diseased reindeer. A key question now is whether this is a rare — even unique — case, or if the disease is widespread but so far undetected in Europe. “If it’s similar to our prion disease in the United States and Canada, the disease is subtle and it would be easy to miss,” says Christina Sigurdson, a pathologist at the University of California, San Diego, who has shown that reindeer can contract CWD in a laboratory environment1. © 2016 Nature Publishing Group,
Link ID: 22117 - Posted: 04.19.2016
Ian Sample Science editor The subtle impact of genetics on the age at which people lose their virginity has been teased apart by scientists and shown to have an effect on how well people fare at school. Though mostly driven by upbringing and peer behaviour, a person’s age when they first have sex is also shaped by biological factors where genes have a role to play. Researchers found that differences in DNA could account for a quarter of the variation in the age at which people lost their virginity, with other factors, among them religious beliefs, family background and peer pressure, making up the rest. Genes influence academic ability across all subjects, latest study shows Read more “We were able to calculate for the first time that there is a heritable component to age at first sex, and the heritability is about 25%, so one quarter nature, three quarters nurture,” said John Perry, an expert in reproductive ageing and related health conditions at Cambridge University. Among 38 sections of DNA found to affect the age at which people first had sex were genes that drive reproductive biology, such as the release of sex hormones and the age of puberty. Still others were found that appear to affect behaviour, personality and appearance. A variant of one of the genes, named CADM2, linked an early start to one’s sex life with risk-taking behaviour and having a large number of children. A version of another gene, MSRA, found in people who lost their virginity later than average, was linked to irritability. © 2016 Guardian News and Media Limited
Scientists believe injections of a natural protein may lessen the symptoms and progress of Alzheimer's dementia after promising early trials in mice. The treatment - IL 33 - appeared to improve memory and help clear and prevent brain deposits similar to those seen in people with Alzheimer's. Tentative human studies of the treatment will soon begin, but experts say it will take many years to know if it could help patients in real life. The work is published in PNAS journal. Interleukin 33, or IL 33 for short, is made by the body as part of its immune defence against infection and disease, particularly within the brain and spinal cord. And patients with Alzheimer's have been found to have lower amounts of IL 33 in their brains than healthy adults. The researchers from the University of Glasgow and the Hong Kong University of Science and Technology tested what effect a boost of IL 33 might have on mice bred to have brain changes akin to Alzheimer's. The rodents rapidly improved their memory and cognitive function to that of the age-matched normal mice within a week of having the injections. Prof Eddy Liew, who led the work at the University of Glasgow, is excited but cautious about his findings. "Exciting as it is, there is some distance between laboratory findings and clinical applications. There have been enough false 'breakthroughs' in the medical field to caution us not to hold our breath until rigorous clinical trials have been done." © 2016 BBC.
Link ID: 22115 - Posted: 04.19.2016
By Stephen L. Macknik, Susana Martinez-Conde The renowned Slydini holds up an empty box for all to see. It is not really a box—just four connected cloth-covered cardboard walls, forming a floppy parallelogram with no bottom or top. Yet when the magician sets it down on a table, it looks like an ordinary container. Now he begins to roll large yellow sheets of tissue paper into balls. He claps his hands—SMACK!—as he crumples each new ball in a fist and then straightens his arm, wordlessly compelling the audience to gaze after his closed hand. He opens it, and ... the ball is still there. Nothing happened. Huh. Slydini's hand closes once more around the tissue, and it starts snaking around, slowly and gracefully, like a belly dancer's. The performance is mesmerizing. With his free hand, he grabs an imaginary pinch of pixie dust from the box to sprinkle on top of the other hand. This time he opens his hand to reveal that the tissue is gone! Four balls disappear in this fashion. Then, for the finale, Slydini tips the box forward and shows the impossible: all four balls have mysteriously reappeared inside. Slydini famously performed this act on The Dick Cavett Show in 1978. It was one of his iconic tricks. Despite the prestidigitator's incredible showmanship, though, the sleight only works because your brain cannot multitask. © 2016 Scientific American,
Link ID: 22114 - Posted: 04.19.2016
By JEFFREY M. ZACKS and REBECCA TREIMAN OUR favorite Woody Allen joke is the one about taking a speed-reading course. “I read ‘War and Peace’ in 20 minutes,” he says. “It’s about Russia.” The promise of speed reading — to absorb text several times faster than normal, without any significant loss of comprehension — can indeed seem too good to be true. Nonetheless, it has long been an aspiration for many readers, as well as the entrepreneurs seeking to serve them. And as the production rate for new reading matter has increased, and people read on a growing array of devices, the lure of speed reading has only grown stronger. The first popular speed-reading course, introduced in 1959 by Evelyn Wood, was predicated on the idea that reading was slow because it was inefficient. The course focused on teaching people to make fewer back-and-forth eye movements across the page, taking in more information with each glance. Today, apps like SpeedRead With Spritz aim to minimize eye movement even further by having a digital device present you with a stream of single words one after the other at a rapid rate. Unfortunately, the scientific consensus suggests that such enterprises should be viewed with suspicion. In a recent article in Psychological Science in the Public Interest, one of us (Professor Treiman) and colleagues reviewed the empirical literature on reading and concluded that it’s extremely unlikely you can greatly improve your reading speed without missing out on a lot of meaning. Certainly, readers are capable of rapidly scanning a text to find a specific word or piece of information, or to pick up a general idea of what the text is about. But this is skimming, not reading. We can definitely skim, and it may be that speed-reading systems help people skim better. Some speed-reading systems, for example, instruct people to focus only on the beginnings of paragraphs and chapters. This is probably a good skimming strategy. Participants in a 2009 experiment read essays that had half the words covered up — either the beginning of the essay, the end of the essay, or the beginning or end of each individual paragraph. Reading half-paragraphs led to better performance on a test of memory for the passage’s meaning than did reading only the first or second half of the text, and it worked as well as skimming under time pressure. © 2016 The New York Times Company
For the first time, scientists have scanned the brains of subjects taking LSD, and found that the LSD state mimics that of infants. NPR's Rachel Martin speaks with researcher Robin Carhart-Harris. RACHEL MARTIN, HOST: Picture yourself in a boat on a river with tangerine trees and marmalade skies. Now picture yourself as a baby. You gaze up at your mother. She's got those kaleidoscope eyes. Pretty trippy, right? Turns out in a new study of brain scans, that the minds of people on LSD function in a similar way to babies' brains. Dr. Robin Carhart-Harris from Imperial College London's Center for Neuropsychopharmacology joins us from the studios of the BBC to talk about this study. So I understand this was the first time that brain scans like this have ever been done, looking specifically at the brains of people who have used LSD. How much LSD had your subjects taken? I mean, what were the prerequisites for a brain that you were going to scan? CARHART-HARRIS: Yeah, so they had to have had at least one experience with a psychedelic drug. So that includes LSD. It also includes magic mushrooms, other concoctions like ayahuasca, which is an Amazonian brew that has psychedelic properties. We gave them a moderate dose of LSD, roughly equivalent to what you might call a hit of LSD or one blotter of LSD if it was to be taken recreationally. MARTIN: So what kind of vetting did you have to do of the participants in your study because we should say different people respond to LSD in different ways? There are risks associated with this drug. CARHART-HARRIS: That's quite right. All drugs have risks, and LSD's no exception. One of the risks is that you might recruit someone who has a psychological vulnerability. So we're very, very careful when we recruit our volunteers to ensure that they have a solid mental health background. They don't have any personal or family history of any psychotic disorders - so those are things like schizophrenia. We have a psychiatrist assess them. We also evaluate their health. So they are very thoroughly screened. © 2016 npr
By Jillian Bell, CBC News New medical marijuana products produced by yeast could soon be on the market, the co-founder of a biotech company says. That could potentially lead to a wider range of cannabinoid-based drugs that proponents say could be more effective for treating certain medical conditions than medical marijuana itself. The appropriate use of medical marijuana has been a controversial topic, with many arguing that further research is needed to evaluate its efficacy as a treatment for a variety of ailments. In Canada, where the Liberal government has said it will legalize marijuana, medical marijuana is already used to treat a variety of conditions and symptoms, including lack of appetite in people with HIV/AIDS and nausea in those undergoing cancer treatment. The most well-known cannabinoid is tetrahydrolcannabinol, or THC, which is approved by the U.S. Food and Drug Administration to treat nausea and improve appetite. It's found in large amounts in marijuana plants, which is the reason why medical marijuana is often prescribed to treat nausea and increase appetite. But other cannabinoids, like cannabidiol (CBD) and cannabigerol (CBG) may have the potential to be potent treatments for other conditions as well. CBG also has its own medical properties. But it can also be easily chemically converted into other cannabinoids, including THC. ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 22111 - Posted: 04.18.2016
By David Shultz Mice supposedly don't speak, so they can't stutter. But by tinkering with a gene that appears to be involved in human speech, researchers have created transgenic mice whose pups produce altered vocalizations in a way that is similar to stuttering in humans. The mice could make a good model for understanding stuttering; they could also shed more light on how mutations in the gene, called Gnptab, cause the speech disorder. Stuttering is one of the most common speech disorders in the world, affecting nearly one out of 100 adults in the United States. But the cause of the stammering, fragmented speech patterns remains unclear. Several years ago, researchers discovered that stutterers often have mutations in a gene called Gnptab. Like a dispatcher directing garbage trucks, Gnptab encodes a protein that helps to direct enzymes into the lysosome—a compartment in animal cells that breaks down waste and recycles old cellular machinery. Mutations to other genes in this system are known to lead to the buildup of cellular waste products and often result in debilitating diseases, such as Tay-Sachs. How mutations in Gnptab causes stuttered speech remains a mystery, however. To get to the bottom of things, neuroscientist Terra Barnes and her team at Washington University in St. Louis in Missouri produced mice with mutation in the Gnptab gene and studied whether it affected the ultrasonic vocalizations that newly born mouse pups emit when separated from their mothers. Determining whether a mouse is stuttering is no easy task; as Barnes points out, it can even be difficult to tell whether people are stuttering if they’re speaking a foreign language. So the team designed a computer program that listens for stuttering vocalization patterns independent of language. © 2016 American Association for the Advancement of Science.
Link ID: 22110 - Posted: 04.16.2016
By Matthew Hutson Bad news for believers in clairvoyance. Our brains appear to rewrite history so that the choices we make after an event seem to precede it. In other words, we add loops to our mental timeline that let us feel we can predict things that in reality have already happened. Adam Bear and Paul Bloom at Yale University conducted some simple tests on volunteers. In one experiment, subjects looked at white circles and silently guessed which one would turn red. Once one circle had changed colour, they reported whether or not they had predicted correctly. Over many trials, their reported accuracy was significantly better than the 20 per cent expected by chance, indicating that the volunteers either had psychic abilities or had unwittingly played a mental trick on themselves. The researchers’ study design helped explain what was really going on. They placed different delays between the white circles’ appearance and one of the circles turning red, ranging from 50 milliseconds to one second. Participants’ reported accuracy was highest – surpassing 30 per cent – when the delays were shortest. That’s what you would expect if the appearance of the red circle was actually influencing decisions still in progress. This suggests it’s unlikely that the subjects were merely lying about their predictive abilities to impress the researchers. The mechanism behind this behaviour is still unclear. It’s possible, the researchers suggest, that we perceive the order of events correctly – one circle changes colour before we have actually made our prediction – but then we subconsciously swap the sequence in our memories so the prediction seems to come first. Such a switcheroo could be motivated by a desire to feel in control of our lives. © Copyright Reed Business Information Ltd.
Link ID: 22109 - Posted: 04.16.2016