Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
ByAnna Vlasits The next revolution in medicine just might come from a new lab technique that makes neurons sensitive to light. The technique, called optogenetics, is one of the biggest breakthroughs in neuroscience in decades. It has the potential to cure blindness, treat Parkinson’s disease, and relieve chronic pain. Moreover, it’s become widely used to probe the workings of animals’ brains in the lab, leading to breakthroughs in scientists’ understanding of things like sleep, addiction, and sensation. So it’s not surprising that the two Americans hailed as inventors of optogenetics are rock stars in the science world. Karl Deisseroth at Stanford University and Ed Boyden at the Massachusetts Institute of Technology have collected tens of millions in grants and won millions in prize money in recent years. They’ve stocked their labs with the best equipment and the brightest minds. They’ve been lauded in the media and celebrated at conferences around the world. They’re considered all but certain to win a Nobel Prize. There’s only one problem with this story: It just may be that Zhuo-Hua Pan invented optogenetics first. Even many neuroscientists have never heard of Pan. Pan, 60, is a vision scientist at Wayne State University in Detroit who began his research career in his home country of China. He moved to the United States in the 1980s to pursue his PhD and never left. He wears wire-rimmed glasses over a broad nose framed by smile-lines in his cheeks. His colleagues describe him as a pure scientist: modest, dedicated, careful.
Keyword: Brain imaging
Link ID: 22625 - Posted: 09.03.2016
By LISA SANDERS, M.D. On Thursday, we challenged Well readers to take on the complicated case of a 50-year-old woman who felt feverish and couldn’t stop vomiting and who ended up losing a lot of weight. Like the doctors who saw her as she searched for a diagnosis, many of you focused on her recent journey to Kenya as the source of her symptoms. It was a completely reasonable approach, and one that was extensively explored by the doctors who cared for her. But ultimately it was incorrect. This was a really tough case. Indeed, only three of you got it right. The correct diagnosis was: Hyperthyroidism Thyroid hormone controls metabolism. The more of this hormone flowing in the body, the harder the body works. Because this hormone plays such an important role in how we function, the body tightly regulates how much of it is released and when. But just like every other system in the body, that regulatory mechanism can mess up, releasing either too little hormone (hypothyroidism) or, as in this case, too much. The usual symptoms of hyperthyroidism are pretty apparent: The heart races; patients are sweaty, shaky, itchy and sometimes feverish. The appetite increases, but because the entire body is revved up, there is often weight loss. Bowel movements become more frequent and sleep harder to come by. Frequent and uncontrolled vomiting is less common but has been reported. This patient had all of these symptoms. The most common cause of hyperthyroidism is an autoimmune disorder known as Graves’ disease, named after Dr. Robert Graves, a 19th-century Irish physician who wrote about the phenomenon of rapid and violent palpitations associated with an enlarged thyroid gland. In the 20th century it was discovered that the symptoms result when antibodies, the foot soldiers of the immune system, cause excess stimulation of the thyroid gland, resulting in the uncontrolled production and release of thyroid hormone. © 2016 The New York Times Company
Keyword: Hormones & Behavior
Link ID: 22624 - Posted: 09.03.2016
By Christof Koch Flies, birds, mice, dogs, monkeys and people all need to sleep. That is, they show daily periods of relative immobility and lack of response to external stimuli, such as light, sound or touch. This reduced sensitivity to external events distinguishes sleep from quiet resting, whereas the capacity to awaken from slumber distinguishes sleep from coma. Why sleep should be such a prominent feature of daily life across the animal kingdom, despite the fact that it leaves the sleeper unable to confront potential threats, remains mysterious. Still, much progress in characterizing the physiology and capabilities of the sleeping brain has occurred over the past century, driven by the ability to record electrical activity of the brain (via electroencephalography, or EEG, on the surface of the skull), of the eyes (via electrooculography, or EOG), and of facial or other muscles (via electromyography, or EMG). For scientists, it is this triad of simultaneous measurements that operationally defines the state of sleep, leading to both surprising and counterintuitive insights. Even without these tools, there are some basic things we do know about sleep. It is essential for our brain to function properly. Most of us have pulled all-nighters or have wanted to sleep but could not, unable to switch off our mind. The next day we are irritable, have trouble keeping our eyes open, and are terrible at tasks that demand sustained attention. Indeed, sleep deprivation causes many traffic accidents—the reason countries have laws that mandate a minimum rest period and maximum working hours for truck drivers. © 2016 Scientific American,
By JOHN P. GLUCK Albuquerque, N.M. — Five years ago, the National Institutes of Health all but ended biomedical and behavioral research on chimpanzees, concluding that, as the closest human relative, they deserved “special consideration and respect.” But chimpanzees were far from the only nonhuman primates used in research then, or now. About 70,000 other primates are still living their lives as research subjects in labs across the United States. On Wednesday, the N.I.H. will hold a workshop on “continued responsible research” with these animals. This sounds like a positive development. But as someone who spent decades working almost daily with macaque monkeys in primate research laboratories, I know firsthand that “responsible” research is not enough. What we really need to examine is the very moral ground of animal research itself. Like many researchers, I once believed that intermittent scientific gains justified methods that almost always did harm. As a graduate student in the late 1960s, I came to see that my natural recoil from intentionally harming animals was a hindrance to how I understood scientific progress. I told myself that we were being responsible by providing good nutrition, safe cages, skilled and caring caretakers and veterinarians for the animals — and, crucially, that what we stood to learn outweighed any momentary or prolonged anguish these animals might experience. The potential for a medical breakthrough, the excitement of research and discovering whether my hypotheses were correct — and let’s not leave out smoldering ambition — made my transition to a more “rigorous” stance easier than I could have imagined. One of my areas of study focused on the effects of early social deprivation on the intellectual abilities of rhesus monkeys. We kept young, intelligent monkeys separated from their families and others of their kind for many months in soundproof cages that remained lit 24 hours a day, then measured how their potential for complex social and intellectual lives unraveled. All the while, I comforted myself with the idea that these monkeys were my research partners, and that by creating developmental disorders in monkeys born in a lab, we could better understand these disorders in humans. © 2016 The New York Times Company
Keyword: Animal Migration
Link ID: 22622 - Posted: 09.03.2016
Laura Sanders An experimental drug swept sticky plaques from the brains of a small number of people with Alzheimer’s disease over the course of a year. And preliminary results hint that this cleanup may have staved off mental decline. News about the new drug, an antibody called aducanumab, led to excitement as it trickled out of recent scientific meetings. A paper published online August 31 in Nature offers a more comprehensive look at the drug’s effects. “Overall, this is the best news that we’ve had in my 25 years doing Alzheimer’s clinical research,” study coauthor Stephen Salloway of Brown University said August 30 at a news briefing. “It brings new hope for patients and families most affected by the disease.” The results are the most convincing evidence yet that an antibody can reduce amyloid in the brain, says Alzheimer’s researcherRachelle Doody of Baylor College of Medicine in Houston, who was not involved in the study. Still, experts caution that the results come from 165 people, a relatively small number. The seemingly beneficial effects could disappear in larger clinical trials, which are under way. “These new data are tantalizing, but they are not yet definitive,” says neuroscientist John Hardy of University College London. Like some other drug candidates for Alzheimer’s, aducanumab is an antibody that targets amyloid-beta, a sticky protein that accumulates in the brains of people with the disease. Delivered by intravenous injection, aducanumab appeared to get inside the brains of people with mild Alzheimer’s (average age about 73) and destroy A-beta plaques, the results suggest. After a year of exposure to the drug, A-beta levels had dropped. This reduction depended on the dose — the more drug, the bigger the decline in A-beta. In fact, people on the highest dose of the drug had almost no A-beta plaques in their brains after a year. |© Society for Science & the Public 2000 - 2016.
Link ID: 22621 - Posted: 09.01.2016
By Laurie McGinley The Food and Drug Administration, alarmed that increasing numbers of Americans are combining opioid painkillers and benzodiazepines, said Wednesday that it will require tough new warnings on the product labels that spell out the serious dangers of mixing the drugs. The agency said it will require “boxed warnings” — its strongest category — on 389 separate products and will mandate the warning on opioid-containing cough medications. The new language will list the hazards of using the medications in tandem, which include extreme sleepiness, respiratory depression, coma and even death. The agency noted that the misuse of opioids, powerful pain medications such as prescription oxycodone, hydrocodone and morphine, has “increased significantly” in the United States over the past two decades. Benzodiazepines are used to treat anxiety, insomnia and seizure disorders. Both classes of drugs depress the central nervous system and together can raise the risk of adverse outcomes. FDA officials said the number of patients prescribed both an opioid and a benzodiazepine increased by 41 percent — about 2.5 million people — between 2002 and 2014. From 2004 to 2011, the rate of emergency-department visits involving the non-medical use of both drug classes increased significantly and overdose deaths nearly tripled, the FDA said.
Merrit Kennedy More than 1,000 residents of a public housing complex in East Chicago, Ind., are now forced to relocate because of dangerously high lead levels in the area's soil. The West Calumet Housing Complex, which houses primarily low-income families, lies on the site of a former lead smelting company, as member station WBEZ reported. In July, the Environmental Protection Agency reported high lead levels in the soil in parts of the complex and notified the residents. The EPA advised parents to stop their kids from playing in the dirt, "to wash their children's toys regularly and to wash children's hands after they play outside." As WBEZ reported, the samples showed lead levels "three times higher than the federal safety standards and in some places even higher, much higher." After that, East Chicago Mayor Anthony Copeland "ordered the removal of 1,200 residents from the West Calumet housing project for safety concerns," according to the member station. The residents have now been informed that the 346-unit complex is set to be demolished. "Residents have been provided vouchers for temporary hotel living until their homes are done being cleaned. The residents will return to their homes for a few more months until vouchers for permanent housing are made available by the U.S. Department of Housing and Urban Development." © 2016 npr
By CATHERINE SAINT LOUIS In seven countries that recently experienced Zika outbreaks, there were also sharp increases in the numbers of people suffering from a form of temporary paralysis, researchers reported Wednesday. The analysis, published online in The New England Journal of Medicine, adds to substantial evidence that Zika infections — even asymptomatic ones — may bring on a paralysis called Guillain-Barré syndrome. The syndrome can be caused by a number of other factors, including infection with other viruses. Researchers studying the Zika epidemic in French Polynesia had estimated that roughly 1 in 4,000 people infected with the virus could develop the syndrome. The Centers for Disease Control and Prevention has said that the Zika virus is “strongly associated” with Guillain-Barré, but has stopped short of declaring it a cause of the condition. The new data suggest a telling pattern: Each country in the study saw unusual increases in Guillain-Barré that coincided with peaks in Zika infections, the researchers concluded. “It’s pretty obvious that in all seven sites there is a clear relationship,” said Dr. Marcos A. Espinal, the study’s lead author and the director of communicable diseases at the Pan American Health Organization, which collected data on confirmed and suspected cases of Zika infection and on the incidence of Guillain-Barré. “Something is going on.” In Venezuela, officials expected roughly 70 cases of Guillain-Barré from December 2015 to the end of March 2016, as mosquitoes were spreading the virus. Instead, there were 684 cases. Similarly, during five months in which the Zika virus was circulating in Colombia, officials recorded 320 cases of Guillain-Barré when there should have been about 100. From September 2015 to March 2016, while Zika infections peaked in El Salvador, cases of Guillain-Barré doubled to 184 from 92. © 2016 The New York Times Company
Keyword: Movement Disorders
Link ID: 22618 - Posted: 09.01.2016
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