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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 JAMES GORMAN Who’s a good dog? Well, that depends on whom you’re asking, of course. But new research suggests that the next time you look at your pup, whether Maltese or mastiff, you might want to choose your words carefully. “Both what we say and how we say it matters to dogs,” said Attila Andics, a research fellow at Eotvos Lorand University in Budapest. Dr. Andics, who studies language and behavior in dogs and humans, along with Adam Miklosi and several other colleagues, reported in a paper to be published in this week’s issue of the journal Science that different parts of dogs’ brains respond to the meaning of a word, and to how the word is said, much as human brains do. Photo A dog waiting for its brain activity to be measured in a magnetic resonance imaging machine for research reported in the journal Science. Credit Enik Kubinyi As with people’s brains, parts of dogs’ left hemisphere react to meaning and parts of the right hemisphere to intonation — the emotional content of a sound. And, perhaps most interesting to dog owners, only a word of praise said in a positive tone really made the reward system of a dog’s brain light up. The experiment itself was something of an achievement. Dr. Andics and his colleagues trained dogs to enter a magnetic resonance imaging machine and lie in a harness while the machine recorded their brain activity. A trainer spoke words in Hungarian — common words of praise used by dog owners like “good boy,” “super” and “well done.” The trainer also tried neutral words like “however” and “nevertheless.” Both the praise words and neutral words were offered in positive and neutral tones. The positive words spoken in a positive tone prompted strong activity in the brain’s reward centers. All the other conditions resulted in significantly less action, and all at the same level. © 2016 The New York Times Company
Laurel Hamers The brains of human ancestors didn’t just grow bigger over evolutionary time. They also amped up their metabolism, demanding more energy for a given volume, a new study suggests. Those increased energy demands might reflect changes in brain structure and organization as cognitive abilities increased, says physiologist Roger Seymour of the University of Adelaide in Australia, a coauthor of the report, published online August 31 in Royal Society Open Science. Blood vessels passing through bones leave behind holes in skulls; bigger holes correspond to bigger blood vessels. And since larger vessels carry more blood, scientists can use hole size to estimate blood flow in extinct hominids’ brains. Blood flow in turn indicates how much energy the brain consumed. (In modern humans, the brain eats up 20 to 25 percent of the energy the body generates when at rest.) Seymour and colleagues focused on the carotid arteries, the vessels that deliver the bulk of the brain’s blood. The team looked at nearly three dozen skulls from 12 hominid species from the last 3 million years, including Australopithecus africanus, Homo neanderthalensis and Homo erectus. In each, the researchers compared the brain’s overall volume with the diameter of the carotid artery’s tiny entrance hole at the base of the skull. “We expected to find that the rate of blood flow was proportional to the brain size,” Seymour says. “But we found that wasn’t the case.” Instead, bigger brains required more blood flow per unit volume than smaller brains. |© Society for Science & the Public 2000 - 2016.
Link ID: 22616 - Posted: 08.31.2016
By Alison F. Takemura | In mice, severely restricting caloric intake promotes the transformation of white fat into brown fat, which contains cells that burn energy faster, according to a study published today (August 25) in Cell Metabolism. The innate immune system, researchers from the University of Geneva, Switzerland, and their colleagues reported, mediates this fat cell-transforming effect. “The paper nicely characterizes this phenomenon,” said Ajay Chawla of the University of California, San Francisco, who was not involved in the work. “And it mechanistically seems to identify a pathway that we had identified.” Whereas the present study found diet induced a “beiging” phenotype—in which white adipose tissue starts to express more energy-expending brown fat cells—Chawla and colleagues had previously shown that cold temperatures, another extreme condition, can produce the same effect. Scientists are keenly interested in learning how to generate brown fat cells. A treatment could help stem the obesity epidemic. “Finding some mechanism to activate this response—ideally, in obese or diabetic individuals—is really attractive,” said postdoctoral researcher Salvatore Fabbiano of the University of Geneva who led the present study. Several conditions are already known to make white fat tissue more brown—cold temperatures, microbe loss, and gastric bypass surgery among them. Fabbiano and colleagues hypothesized that the common feature of all these experiences was an increased expenditure of calories compared to intake. © 1986-2016 The Scientist
Link ID: 22615 - Posted: 08.31.2016
By RACHEL RABKIN PEACHMAN New research shows that athletes who leave the game immediately after a concussion recover twice as fast as athletes who keep playing. Credit Fabrizio Costantini for The New York Times High school athletes who kept playing in the minutes after a concussion took nearly twice as long to recover as those who left the game immediately after the head trauma, a new study shows. The finding, published in the journal Pediatrics, is believed to be the first to focus on one of the most difficult social challenges of treating concussions: a pervasive sports culture that encourages young athletes to keep playing through pain. Medical guidelines call for benching the athlete immediately after the head injury to prevent long-term complications and the potentially devastating consequences of a second hit. “Kids are often reluctant to acknowledge a concussion,” said Dawon Dicks, a youth football coach with CoachUp in Andover, Mass. “The kid may want a scholarship and want to go to college, or it could be that ‘Dad or Coach wants me to play.’ That’s when they’re going to start to be a little dishonest in what they’re truly feeling.” The latest study tracked the neurological symptoms of 69 athletes who visited the University of Pittsburgh Medical Center Sports Medicine Concussion Program after suffering head trauma during a contact sport. The athletes, who ranged from 12 to 19 years old, came from football, soccer, ice hockey, volleyball, field hockey, basketball, wrestling and rugby. The sample included 35 athletes who were removed from games right after getting a concussion and compared their symptoms and recovery to 34 athletes who kept playing in the game or match after taking a hit. The study found that players who stayed in the game after head trauma took an average of 44 days to recover. By comparison, athletes who left a game immediately after signs of concussion took only an average of 22 days to recover. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 22614 - Posted: 08.30.2016
By Will Boggs MD NEW YORK (Reuters Health) - Most adults in the U.S. who screen positive for depression are not being treated for depression, according to results from Medical Expenditure Panel Surveys (MEPS). "With the recent increase in prescribing of antidepressant medications, many physicians might assume that undertreatment of depression is no longer a widespread problem," Dr. Mark Olfson from College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute in New York City told Reuters Health by email. "This study makes clear, however, that most American adults who screen positive for depression receive no treatment for their symptoms." Surveys from the early 2000s show that about half of U.S. adults with a lifetime medical history of major depressive disorder had never received treatment for depression. Still, little is known about the extent to which adults with depression in the U.S. receive depression care and the extent to which such patients are matched based on their illness severity to appropriate treatments and healthcare professionals. Dr. Olfson and colleagues used data from the 2012 and 2013 MEPS to examine the prevalence and treatment of adults with screen-positive depression (a Patient Health Questionnaire-2 score of 3 or less). They also assessed whether serious psychological distress was associated with more intensive treatment. © 2016 Scientific American
Link ID: 22613 - Posted: 08.30.2016
By STEVE SILBERMAN In the late 1930s, Charles Bradley, the director of a home for “troublesome” children in Rhode Island, had a problem. The field of neuroscience was still in its infancy, and one of the few techniques available to allow psychiatrists like Bradley to ponder the role of the brain in emotional disorders was a procedure that required replacing a volume of cerebrospinal fluid in the patient’s skull with air. This painstaking process allowed any irregularities to stand out clearly in X-ray images, but many patients suffered excruciating headaches that lasted for weeks afterward. Meanwhile, a pharmaceutical company called Smith, Kline & French was facing a different sort of problem. The firm had recently acquired the rights to sell a powerful stimulant then called “benzedrine sulfate” and was trying to create a market for it. Toward that end, the company made quantities of the drug available at no cost to doctors who volunteered to run studies on it. Bradley was a firm believer that struggling children needed more than a handful of pills to get better; they also needed psychosocial therapy and the calming and supportive environment that he provided at the home. But he took up the company’s offer, hoping that the drug might eliminate his patients’ headaches. It did not. But the Benzedrine did have an effect that was right in line with Smith, Kline & French’s aspirations for its new product: The drug seemed to boost the children’s eagerness to learn in the classroom while making them more amenable to following the rules. The drug seemed to calm the children’s mood swings, allowing them to become, in the words of their therapists, more “attentive” and “serious,” able to complete their schoolwork and behave. Bradley was amazed that Benzedrine, a forerunner of Ritalin and Adderall, was such a great normalizer, turning typically hard-to-manage kids into models of complicity and decorum. But even after marveling at the effects of the drug, he maintained that medication should be considered for children only in addition to other forms of therapy. © 2016 The New York Times Company
By Simon Oxenham It can seem like barely a week goes by without a new study linking the stage in a woman’s monthly cycle to her preferences in a sexual partner. Reportedly, when women are ovulating they are attracted to men who are healthier, more dominant, more masculine, have higher testosterone levels– the list goes on. But do women really exhibit such behavioural changes – and why are we so fascinated by the idea that they do? A popular theory in evolutionary psychology is that women seek out men with better genes while they are ovulating to have short term affairs with, so as to produce healthier babies. These men may not necessarily stick around for the long haul, but appear particularly attractive when a woman is in the fertile stage of her cycle. During the non-fertile phase, the theory goes that women seek out men who are more likely to make reliable long-term partners and good fathers. But something smells a bit fishy here. Are women really evolutionarily hard-wired to cuckold their partners? Or might the attraction of a salacious hypothesis – with slightly sexist overtones – be shaping some of this research? Masculine all month A review of these kinds of studies is now challenging this often-told story. Wendy Wood at the University of Southern California and her team have analysed 58 studies – some of which were never published – and found that this theory is largely unsupported by evidence. © Copyright Reed Business Information Ltd.
Laura Sanders Despite its name, the newly identified GluMI cell (pronounced “gloomy”) is no downer. It’s a nerve cell, spied in a mouse retina, that looks like one type of cell but behaves like another. Like neighboring retina nerve cells that subdue, or deaden, activity of other nerve cells, GluMI cells have a single arm extending from their body. But unlike those cells, GluMI cells actually seem to ramp up activity of nearby cells in a way that could aid vision. GLuMIs don’t seem to detect light firsthand, but they respond to it, Luca Della Santina of the University of Washington in Seattle and colleagues found. GluMIs are among a growing list of unexpected and mysterious cells found in the retinas of vertebrates, the researchers write August 8 in Current Biology. Citations L. Della Santina et al. Glutamatergic monopolar interneurons provide a novel pathway of excitation in the mouse retina. Current Biology. Vol. 26, August 8, 2016. doi:10.1016/j.cub.2016.06.016. |© Society for Science & the Public 2000 - 2016
Link ID: 22610 - Posted: 08.30.2016
By Daniel Engber In the spring of 2013, a 63-year-old social psychologist in Wurzburg, Germany, made a bold suggestion in a private email chain. For months, several dozen of his colleagues had been squabbling over how to double-check the scientific literature on “social priming,” the idea that even very subtle cues—the height of a chair, the temperature of a cup of coffee, the color of a printed word—can influence someone’s behavior or judgment. Now the skeptics in the group wanted volunteers: Who among the priming experts and believers would help them with a large-scale replication effort, in which a major finding would be tested in many different labs at once? Who—if anyone—would agree to put his research to this daunting test? The experts were reluctant to step forward. In recent months their field had fallen into scandal and uncertainty: An influential scholar had been outed as a fraud; certain bedrock studies—even so-called “instant classics”—had seemed to shrivel under scrutiny. But the rigidity of the replication process felt a bit like bullying. After all, their work on social priming was delicate by definition: It relied on lab manipulations that had been precisely calibrated to elicit tiny changes in behavior. Even slight adjustments to their setups, or small mistakes made by those with less experience, could set the data all askew. So let’s say another lab—or several other labs—tried and failed to copy their experiments. What would that really prove? Would it lead anyone to change their minds about the science?
Link ID: 22609 - Posted: 08.29.2016
Doctors describe 16-year-old Sebastian DeLeon as a walking miracle — he is only the fourth person in the U.S. to survive an infection from the so-called brain-eating amoeba. Infection from Naegleria fowleri is extremely rare but almost always fatal. Between 1962 and 2015, there were only 138 known infections due to the organism, according to the Centers for Disease Control and Prevention. Just three people survived. This summer, two young people, one in Florida and one in North Carolina, became infected after water recreation. Only one had a happy ending. DeLeon is a 16-year-old camp counselor. The Florida Department of Health thinks he got the infection while swimming in unsanitary water on private property in South Florida before his family came to visit Orlando's theme parks. So many things had to go right for DeLeon to survive. On a Friday, he had a bad headache. The next day, his parents decided this was way more than just a migraine and took him to the emergency room at Florida Hospital for Children. Doctors persuaded the family to do a spinal tap to rule out meningitis, even though he didn't have a stiff neck, the telltale symptom. Sheila Black, the lab coordinator, looked at the sample and assumed she saw white blood cells. But then she took a second, longer look. "We are all detectives," Black said. "We literally had to look at this and study it for a while and watch for the movement because the amoeba can look like a white cell. So unless you're actually visually looking for this and looking for the movement, you're going to miss it." © 2016 npr
Link ID: 22608 - Posted: 08.29.2016
By KATE MURPHY We’ve all seen them, those colorful images that show how our brains “light up” when we’re in love, playing a video game, craving chocolate, etc. Created using functional magnetic resonance imaging, or fM.R.I., these pictures are the basis of tens of thousands of scientific papers, the backdrop to TED talks and supporting evidence in best-selling books that tell us how to maintain healthy relationships, make decisions, market products and lose weight. But a study published last month in the Proceedings of the National Academy of Sciences uncovered flaws in the software researchers rely on to analyze fM.R.I. data. The glitch can cause false positives — suggesting brain activity where there is none — up to 70 percent of the time. This cued a chorus of “I told you so!” from critics who have long said fM.R.I. is nothing more than high-tech phrenology. Brain-imaging researchers protested that the software problems were not as bad nor as widespread as the study suggested. The dust-up has caused considerable angst in the fM.R.I. community, about not only the reliability of their pretty pictures but also how limited funding and the pressure to publish splashy results might have allowed such a mistake to go unnoticed for so long. The remedial measures some in the field are now proposing could be a model for the wider scientific community, which, despite breathtaking technological advances, often produces findings that don’t hold up over time. “We have entered an era where the kinds of data and the analyses that people run have gotten incredibly complicated,” said Martin Sereno, the chairman of the cognitive neuroimaging department at the University of California, San Diego. “So you have researchers using sophisticated software programs that they probably don’t understand but are generally accepted and everyone uses.” © 2016 The New York Times Company
Keyword: Brain imaging
Link ID: 22607 - Posted: 08.29.2016
By Usha Lee McFarling @ushamcfarling LOS ANGELES — A team of physicians and neuroscientists on Wednesday reported the successful use of ultrasound waves to “jump start” the brain of a 25-year-old man recovering from coma — and plan to launch a much broader test of the technique, in hopes of finding a way to help at least some of the tens of thousands of patients in vegetative states. The team, based at the University of California, Los Angeles, cautions that the evidence so far is thin: They have no way to know for sure whether the ultrasound stimulation made the difference for their young patient, or whether he spontaneously recovered by coincidence shortly after the therapy. But the region of the brain they targeted with the ultrasound — the thalamus — has previously been shown to be important in restoring consciousness. In 2007, a 38-year-old man who had been minimally conscious for six years regained some functions after electrodes were implanted in his brain to stimulate the thalamus. The ultrasound technique is a “good idea” that merits further study, said Dr. Nicholas Schiff, a pioneer in the field of using brain stimulation to restore consciousness who conducted the 2007 study. “It’s intriguing and it’s an interesting possibility,” said Schiff, a neuroscientist at Weill Cornell Medicine. The UCLA procedure used an experimental device, about the size of a teacup saucer, to focus ultrasonic waves on the thalamus, two walnut-sized bulbs in the center of the brain that serve as a critical hub for information flow and help regulate consciousness and sleep.
Link ID: 22606 - Posted: 08.27.2016
Laura Sanders Scientists have identified the “refrigerator” nerve cells that hum along in the brains of mice and keep the body cool. These cells kick on to drastically cool mice’s bodies and may prevent high fevers, scientists report online August 25 in Science. The results “are totally new and very important,” says physiologist Andrej Romanovsky of the Barrow Neurological Institute in Phoenix. "The implications are far-reaching." By illuminating how bodies stay at the right temperature, the discovery may offer insights into the relationship between body temperature and metabolism. Scientists had good reasons to think that nerve cells controlling body temperature are tucked into the hypothalamus, a small patch of neural tissue in the middle of the brain. Temperature fluctuations in a part of the hypothalamus called the preoptic area prompt the body to get back to baseline by conserving or throwing off heat. But the actual identify of the heat sensors remained mysterious. The new study reveals the cells to be those that possess a protein called TRPM2. “Overall, this is a major discovery in the field of thermoregulation,” says Shaun Morrison of Oregon Health & Science University in Portland. Jan Siemens, a neurobiologist at the University of Heidelberg in Germany, and colleagues tested an array of molecules called TRP channels, proteins that sit on cell membranes and help sense a variety of stimuli, including painful tear gas and cool menthol. In tests of nerve cells in lab dishes, one candidate, the protein TRPM2, seemed to respond to heat. |© Society for Science & the Public 2000 - 201
Keyword: Pain & Touch
Link ID: 22605 - Posted: 08.27.2016
By Amy Ellis Nutt Before iPhones and thumb drives, before Google docs and gigabytes of RAM, memory was more art than artifact. It wasn’t a tool or a byproduct of being human. It was essential to our character and therefore a powerful theme in both myth and literature. At the end of Book 2 of the “Divine Comedy,” with Paradise nearly in reach, Dante is dipped into the River Lethe, where the sins of the self are washed away in the waters of forgetfulness. To be truly cleansed of his memories, however, Dante must also drink from the river of oblivion. Only then will he be truly purified and the memories of his good deeds restored to him. Before we can truly remember, according to Dante, we must forget. In “Patient H.M.: A Story of Memory, Madness, and Family Secrets,” author Luke Dittrich seems to be saying that before we can forgive, we must remember. The terrible irony is that H.M., the real-life character around whom Dittrich’s book revolves, had no memory at all. In prose both elegant and intimate, and often thrilling, “Patient H.M.” is an important book about the wages not of sin but of science. It is deeply reported and surprisingly emotional, at times poignant, at others shocking. H.M., arguably the single most important research subject in the history of neuroscience, was once Henry Molaison, an ordinary New England boy. When Henry was 9 years old, he was hit by a bicyclist as he walked across the street in his home town, Hartford, Conn. © 1996-2016 The Washington Post
Keyword: Learning & Memory
Link ID: 22604 - Posted: 08.27.2016
By Kas Roussy, In a room at Sunnybrook Health Sciences Centre in Toronto, Brian Smith gives one last hug to his wife, Noreen. "You're doing really well, sweetheart," he says to her. Doctors have finished prepping the 76-year-old patient. She's clad in a blue hospital gown, her head has been shaved and metallic headgear is attached to her skull. Google's latest a spoon that steadies tremors New technology could help seniors stay independent longer She's ready to be wheeled into an MRI room, where she'll undergo a procedure that her doctors believe will revolutionize the way brain diseases are treated. Before that happens, Noreen leans into her husband for a kiss. "Best buddy," she whispers. Noreen Smith is among the three per cent of the Canadian population who suffer from a nervous system disorder called essential tremor. It causes uncontrollable shaking, most often in a person's hands. Smith noticed the first signs when she was 33. "It started developing in my dominant hand, which is my right hand," she said the day before her medical procedure from her home in Bobcaygeon, Ont. She went to a specialist who delivered the diagnosis: essential tremor. Media placeholder Smith ‘really, really excited’ about treatment’s potential0:48 Just as shocking was what he said next, alluding to a high-profile actor who had the condition. "This particular person wasn't terribly helpful because he said: 'Do you happen to know Katharine Hepburn? I'm going to give you some medication, and you can go home and get used to the idea that eventually you're going to end up looking like Katharine Hepburn.' I was devastated," says Smith. Medication helped for the first few years. But Smith's tremor was still severe and like others who suffer from this disorder, the shaking worsened with simple movements or everyday tasks like applying makeup or pouring a glass of water. ©2016 CBC/Radio-Canada.
Keyword: Movement Disorders
Link ID: 22603 - Posted: 08.25.2016
By Christie Aschwanden The Olympic stadium was quiet on Wednesday morning, and spectators in the sparsely filled stands seemed to pay little notice to South African runner Caster Semenya as she cruised to an easy win in her first-round heat of the 800 meters. But on Saturday evening, when Semenya will contest the 800-meter final, she’ll have the world’s eyes on her. “There is no more certain gold medal in the Rio Olympics than Semenya,” wrote Ross Tucker, an exercise scientist in South Africa, on his blog, The Science of Sport. “She could trip and fall, anywhere in the first lap, lose 20m, and still win the race.” If she does indeed dominate, some sports fans will be cheering Semenya, while others will be less inclined to celebrate, believing that she has an unfair advantage over her rivals. Semenya made headlines in 2009 amid rumors that track’s governing body, the International Association of Athletics Federations, had required her to undergo tests to confirm that she was female. Media accounts have reported that she has hyperandrogenism, a condition that causes higher-than-average testosterone levels — an allegation that neither Semenya nor the IAAF has publicly confirmed. Semenya’s case is the latest saga in sport’s checkered history of sex testing, a task that is purportedly aimed at creating an even playing field but — as I’ve discussed previously — raises serious questions about how athletics organizations treat women. Her muscular build, deep voice and remarkable results had raised suspicions among some of Semenya’s rivals about whether she was really a woman. “Just look at her,” said Mariya Savinova, a Russian runner now tangled in her country’s doping scandal.
By Sara Chodosh When a single neuron fires, it is an isolated chemical blip. When many fire together, they form a thought. How the brain bridges the gap between these two tiers of neural activity remains a great mystery, but a new kind of technology is edging us closer to solving it. The glowing splash of cyan in the photo above comes from a type of biosensor that can detect the release of very small amounts of neurotransmitters, the signaling molecules that brain cells use to communicate. These sensors, called CNiFERs (pronounced “sniffers”), for cell-based neurotransmitter fluorescent engineered reporters, are enabling scientists to examine the brain in action and up close. This newfound ability, developed as part of the White House BRAIN Initiative, could further our understanding of how brain function arises from the complex interplay of individual neurons, including how complex behaviors like addiction develop. Neuroscientist Paul Slesinger at Icahn School of Medicine at Mount Sinai, one of the senior researchers who spearheaded this research, presented the sensors Monday at the American Chemical Society’s 252nd National Meeting & Exposition. Current technologies have proved either too broad or too specific to track how tiny amounts of neurotransmitters in and around many cells might contribute to the transmission of a thought. Scientists have used functional magnetic resonance imaging to look at blood flow as a surrogate for brain activity over fairly long periods of time or have employed tracers to follow the release of a particular neurotransmitter from a small set of neurons for a few seconds. But CNiFERs make for a happy medium; they allow researchers to monitor multiple neurotransmitters in many cells over significant periods of time. © 2016 Scientific American
Keyword: Brain imaging
Link ID: 22600 - Posted: 08.25.2016
James Hamblin Like The Atlantic? Subscribe to the Daily, our free weekday email newsletter. Elite tennis players have an uncanny ability to clear their heads after making errors. They constantly move on and start fresh for the next point. They can’t afford to dwell on mistakes. Peter Strick is not a professional tennis player. He’s a distinguished professor and chair of the department of neurobiology at the University of Pittsburgh Brain Institute. He’s the sort of person to dwell on mistakes, however small. “My kids would tell me, dad, you ought to take up pilates. Do some yoga,” he said. “But I’d say, as far as I’m concerned, there's no scientific evidence that this is going to help me.” Still, the meticulous skeptic espoused more of a tennis approach to dealing with stressful situations: Just teach yourself to move on. Of course there is evidence that ties practicing yoga to good health, but not the sort that convinced Strick. Studies show correlations between the two, but he needed a physiological mechanism to explain the relationship. Vague conjecture that yoga “decreases stress” wasn’t sufficient. How? Simply by distracting the mind? The stress response in humans is facilitated by the adrenal glands, which sit on top of our kidneys and spit adrenaline into our blood whenever we’re in need of fight or flight. That stress response is crucial in dire circumstances. But little of modern life truly requires it (especially among academic scientists). Most of the time, our stress responses are operating as a sort of background hum, keeping us on edge. Turn that off, and we relax. © 2016 by The Atlantic Monthly Group
Link ID: 22599 - Posted: 08.25.2016
By Alice Callahan As new parents, Penn State researcher Doug Teti and his wife were co-sleepers, sharing their bed at night with all three of their children, now grown. So when Dr. Teti, a professor of human development and family studies, embarked on an usual study of co-sleeping, bringing cameras into the bedrooms of 139 Pennsylvania couples, he did not expect to see co-sleeping associated with family stress. But to his surprise, many of the parents in the study who co-slept with their children beyond 6 months of age, a group he called “persistent co-sleepers,” did show signs of stress, particularly the mothers. Dr. Teti emphasized that the research isn’t an indictment against co-sleeping, but does suggest that a number of factors, including cultural pressures and an unsupportive spouse, can make longer-term co-sleeping a more stressful experience for some families. “Co-sleeping is simply a practice, just like solitary sleep is a practice,” he said. “It is important for parents to be on the same page about whatever practices with their children they choose to put into effect.” The study, published this month in the journal Developmental Psychology, was unusual in that it tracked 139 couples, mostly married or living together, who generously allowed researchers to peek into their bedrooms with video cameras, recording nighttime interactions with their new babies at five time points in the first year of life. Co-sleeping — defined in this study as room-sharing or bed-sharing, often a mix of the two — was surprisingly common in early infancy. Nearly 75 percent of the parents co-slept with infants early on, and about half were still co-sleeping three months after the birth. But once the babies reached 6 months of age, only one in four babies continued to share a bed or a room with their parents. © 2016 The New York Times Company
Link ID: 22598 - Posted: 08.25.2016
Laura Sanders Brain scientists Eric Jonas and Konrad Kording had grown skeptical. They weren’t convinced that the sophisticated, big data experiments of neuroscience were actually accomplishing anything. So they devised a devilish experiment. Instead of studying the brain of a person, or a mouse, or even a lowly worm, the two used advanced neuroscience methods to scrutinize the inner workings of another information processor — a computer chip. The unorthodox experimental subject, the MOS 6502, is the same chip that dazzled early tech junkies and kids alike in the 1980s by powering Donkey Kong, Space Invaders and Pitfall, as well as the Apple I and II computers. Of course, these experiments were rigged. The scientists already knew everything about how the 6502 works. “The beauty of the microprocessor is that unlike anything in biology, we understand it on every level,” says Jonas, of the University of California, Berkeley. A barrel-hurling gorilla is the enemy in Donkey Kong, a video game powered by the MOS 6502 microprocessor. Along with Space Invaders and Pitfall, this game served as the “behavior” in a recent experiment. Using a simulation of MOS 6502, Jonas and Kording, of Northwestern University in Chicago, studied the behavior of electricity-moving transistors, along with aspects of the chip’s connections and its output, to reveal how it handles information. Since they already knew what the outcomes should be, they were actually testing the methods. By the end of their experiments, Jonas and Kording had discovered almost nothing. |© Society for Science & the Public 2000 - 2016
Keyword: Brain imaging
Link ID: 22597 - Posted: 08.24.2016