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Fragment of rat brain simulated in supercomputer Moheb Costandi A controversial European neuroscience project that aims to simulate the human brain in a supercomputer has published its first major result: a digital imitation of circuitry in a sandgrain-sized chunk of rat brain. The work models some 31,000 virtual brain cells connected by roughly 37 million synapses. The goal of the Blue Brain Project, which launched in 2005 and is led by neurobiologist Henry Markram of the Swiss Federal Institute of Technology in Lausanne (EPFL), is to build a biologically-detailed computer simulation of the brain based on experimental data about neurons' 3D shapes, their electrical properties, and the ion channels and other proteins that different cell types typically produce (see ‘Brain in a box’). Such a simulation would provide deep insights into the way the brain works, says Markram. But other neuroscientists have argued that it will reveal no more about the brain’s workings than do simpler, more abstract simulations of neural circuitry — while sucking up a great deal of computing power and resources. The initiative has links with the Human Brain Project, a €1-billion (US$1.1-billion), decade-long initiative which Markram helped persuade the European Commission to fund, and which also aims to advance supercomputer brain simulation. It launched in 2013, with Markram as co-leader, although this March its leadership was switched and its scientific programme altered, after criticism of the way it was being managed. © 2015 Nature Publishing Group
Keyword: Brain imaging
Link ID: 21494 - Posted: 10.09.2015
Gay or straight? A saliva test can predict the answer, and get it right 67 per cent of the time – for male identical twins at least. The test, which uses clues from tiny modifications to a person’s genome, is the first that claims to detect sexual orientation. Many scientists have expressed caution over the results, while concerns over potential misuse of the test have led the study’s lead researcher to quit the project entirely. “The scientific benefit to understanding [why people vary in sexual orientation] is obvious to anyone with an iota of curiosity,” says Michael Bailey at Northwestern University in Evanston, Illinois. “The predictive test needs replication on larger samples in order to know how good it is, but in theory it’s quite interesting.” Over the last two decades, several studies have suggested that sexual orientation is, in part, down to our genes. Perhaps the biggest splash was made in 1993 by Dean Hamer’s team at the National Cancer Institute in Bethesda, Maryland, when they found that gay brothers tended to share a sequence of five genetic markers in a region of the X chromosome. The same region has been implicated in other studies of sexual orientation since, although researchers haven’t been able to single out “gay genes”. Other observations also suggest a genetic basis for sexual orientation, such as the mysterious fraternal birth order effect. For every male pregnancy a woman has, a subsequent son has a 33 per cent higher chance of being homosexual, although no one knows why. The overall chance is still low, however, rising from around 2 per cent to just 6 per cent for a third son. © Copyright Reed Business Information Ltd.
Elaine Korry Efforts to protect children in foster care from being inappropriately medicated with powerful antipsychotic drugs got a big boost forward on Tuesday, when California Gov. Jerry Brown signed three bills into law designed to reform prescribing. Overprescribing of psychiatric meds for foster youth is a persistent problem nationwide, with children given the drugs at double or triple the rate of those not in foster care. In 2011, the federal Government Accounting Office found nearly 1 in 4 children in foster care was taking psychotropic medications, which include antipsychotics, antidepressants, mood stabilizers and stimulants. Hundreds of children were found to be taking five or more psychotropic medications at a time, and thousands were prescribed doses that exceeded FDA-approved guidelines. According to the report, monitoring programs fell short of guidelines established by the American Academy of Child and Adolescent Psychiatry. Many of the medications have side effects that include lethargy, weight gain, diabetes and tremors. The California legislation, which covers 63,000 children and teens in foster care, will allow public health nurses access to medical records to monitor the foster children who are prescribed psychotropic drugs; identify the group homes that rely most on these medications and potentially require them to take corrective action; and provide child welfare workers with better training and oversight tools to spot dangerous prescribing practices. © 2015 NPR
By CATHERINE SAINT LOUIS Ever since the Food and Drug Administration approved the use of the narcotic painkiller OxyContin for certain children in August, it has faced unabated criticism from lawmakers and public officials who are wrestling with devastating rates of prescription opioid abuse in their communities. Last week, Hillary Rodham Clinton brought the issue to the presidential race, calling the agency’s action “absolutely incomprehensible.” The crux of the issue is whether the agency’s approval will lead to more prescriptions for OxyContin in young patients. For years, the powerful long-acting drug has been prescribed off-label to very sick children in severe pain from cancer or spinal-fusion surgery. (Doctors can prescribe an approved drug to anyone and for any use they see fit regardless of specifications on the label.) The agency’s approval means those doctors will finally have “information about how to do it appropriately,” like dosage recommendations, said Dr. Stephen Ostroff, the agency’s acting commissioner, in an interview. “We recognize this is a very nuanced issue,” said Dr. Ostroff, when asked about Mrs. Clinton’s recent comments. “It needs to be understood in the context of why this was done.” Dr. Kathleen A. Neville, a pediatric oncologist at Arkansas Children’s Hospital, routinely treats children with unremitting pain caused by cancer or sickle cell anemia. Her patients are the kind the F.D.A. envisioned would benefit from OxyContin, despite its “risks of addictions, abuse and misuse” as a warning on the new label says. Dr. Neville, who said she had no financial ties to makers of painkillers, applauded the agency’s approval. “Just because OxyContin has been abused or prescribed inappropriately doesn’t mean we should deprive the children who need the drug,” she said, adding it is “our obligation to have the best level of evidence for its use in children.” © 2015 The New York Times Company
A new drug for multiple sclerosis can cut relapses by almost 50% more than the current standard treatment, its manufacturer claims, raising the hopes of sufferers of the disease. The Swiss pharmaceutical giant Roche announced the headline results for its drug, ocrelizumab, but has not published the detailed outcome of its trials. The announcement was warmly welcomed by patients, not least because Roche claims the drug also has an impact on a form of the disease, called primary-progressive, which affects 10-15% of people with MS in the UK and for which there are no treatments. Roche claimed it cut disability in those patients by nearly a quarter. “These phase three trial results will provide a great deal of hope for people with primary-progressive MS, who currently don’t have any treatments available that can slow down the worsening of their condition,” said Nick Rijke, the MS Society’s executive director for policy and research. “Finding effective treatments for multiple sclerosis is our number one priority at the MS Society and this is a big moment. The drug was compared in the trials with Rebif, an established drug made by Merck that reduces relapses by about a third. Ocrelizumab – which does not yet have a brand name – was said to cut annual relapses by 46% and 47% compared with Rebif in the two trials. The biggest advantage, however, may be that it is claimed to cause fewer side effects than the established drug. © 2015 Guardian News and Media Limited
It can start with flashing lights, a tingling sensation and a feeling of unease, followed by excruciating pain. Migraines can be triggered by lack of food or too much stress but their underlying cause has remained a mystery. Now researchers have found that a migraine may be triggered by a protein deep in the brain that stimulates the neurons controlling facial sensations. The discovery creates a potential new target for safer migraine medicines and adds weight to the theory that neurons, not blood vessels, are responsible for migraine attacks. “Where a migraine starts is a key question,” says Debbie Hay at the University of Auckland in New Zealand. “There has been a great deal of debate around the mechanisms of migraine. If we can pin this down, we may have better chances of preventing it.” To investigate, Simon Akerman at New York University and Peter Goadsby at Kings College London, UK, studied two neuropeptides released by neurons thought to play a role in the pain associated with migraine. These protein-like molecules, called VIP and PACAP, first raised suspicion after they were found to be elevated in blood drained from the brains of people having a migraine attack. When researchers administered these peptides to volunteers, they found that they could cause a headache or migraine about two hours later. Both peptides widen blood vessels, which was thought to be significant in migraine. In fact, the only drugs specifically developed for migraine that are in use today – triptans – were designed to shrink blood vessels in the brain. As a result, they cannot be used by people with cardiovascular disorders. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 21489 - Posted: 10.08.2015
By Gretchen Reynolds We’ve probably all heard someone exclaim, “Ah, my endorphins are kicking in!” at the end of a good run. Endorphins are famous for supposedly producing “runner’s high,” that fleeting sense of calm and euphoria that engulfs many of us after a satisfying workout. But in fact, endorphins may be unfairly hogging the credit for making workouts enjoyable, according to an enlightening new experiment with animals. The findings suggest that endorphins have little to do with runner’s high. Instead, that euphoric feeling may be the product of a completely different but oddly familiar substance — the body’s own endocannabinoids, the chemicals that, like the cannabinoids in marijuana, lighten mood. Endorphins first became a household word in the 1980s, when researchers found that blood levels increased after prolonged exercise. This finding made sense. Exercise can cause discomfort or pain, and endorphins are the body’s self-produced opiates, with pain-relieving properties much like morphine. From that discovery, it was a short step to believing that endorphins must also produce the pleasurable mental sensations that many people feel after exercise. But there is a substantial problem with that idea, and it involves the substantial-ness of endorphins. They are large molecules, too big to pass through the blood-brain barrier. They might staunch pain in the muscles, but they wouldn’t have effects directly inside the brain, where any high would originate. So for the past decade or so, scientists have been looking for other substances that might be involved in making exercisers feel high, which led them, perhaps unsurprisingly, to endocannabinoids. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21488 - Posted: 10.08.2015
By Somer Bishop Subtle, significant. In a nutshell, these two words capture the symptoms of many girls with autism. Like many in my field, I’ve seen this subtlety firsthand. One 6-year-old girl I met several years ago seemed, at first, to have good social skills. She responded appropriately when I introduced myself, complimented my outfit, and politely answered all of my questions. It was only when I saw her again a few days later that I understood her family’s concerns: She made nearly identical overtures, as if our interaction were part of a play she had rehearsed. I also met a teenage girl with autism who was highly intelligent. Because she could not relate to the other girls at her high school, she began interacting exclusively with boys, whose social behaviors she found easier to imitate. She even went through a period of wanting to become a boy, reasoning that she might have more success navigating the social world as a male. The past several years have seen an explosion of studies aimed at backing up these one-off observations about how autism presents differently in girls than in boys. This is a welcome development, as understanding the unique presentation of autism in girls will help us to better identify and treat the disorder. Consistently recognizing autism in girls can be challenging, however. This is not only because girls with autism are as diverse as any other group of individuals with the disorder but also because most autism screening and diagnostic tools were developed based primarily on observations of behaviors in boys. © 2015 The Slate Group LLC.
by Sarah Schwartz People with multiple sclerosis who got less sun exposure and had higher body mass as young adults developed the disease sooner than those who spent more time in the sun and were a normal weight, a new study finds. In a study of over 1,100 Danish people with MS — a nervous system condition that causes muscle weakness and pain — patients who were overweight at age 20 developed multiple sclerosis an average of 1.5 years sooner than patients of normal weight. And subjects who reported spending time in the sun every summer’s day during adolescence developed the disease 1.8 years later, on average, than patients who got less sun exposure, Danish researchers report online October 7 in Neurology. The results echo earlier work that found a link between adolescent obesity and risk of MS. And sun exposure may increase patients’ levels of vitamin D, which has been shown to protect against the disease, the researchers say. © Society for Science & the Public 2000 - 2015
By Jessica Schmerler Many studies trumpet the positive effects of oxytocin. The hormone facilitates bonding, increases trust and promotes altruism. Such findings earned oxytocin its famous nickname, the “love hormone.” But more recent research has shown oxytocin has a darker side, too: it can increase aggression, risk taking and prejudice. A new analysis of this large body of work reveals that oxytocin's effects on our brain and behavior actually look a lot like another substance that can cut both ways: alcohol. As such, the hormone might point to new treatments for addiction. Researchers led by Ian Mitchell, a psychologist at the University of Birmingham in England, conducted the meta-analysis, which reveals that both oxytocin and alcohol reduce fear, anxiety and stress while increasing trust, generosity and altruism. Yet both also increase aggression, risk taking and “in-group” bias—favoring people similar to ourselves at the expense of others, according to the paper published in August in Neuroscience and Biobehavioral Reviews. The scientists posit that these similarities probably exist because oxytocin and alcohol act at different points in the same chemical pathway in the brain. Oxytocin stimulates release of the neurotransmitter GABA, which tends to reduce neural activity. Alcohol binds to GABA receptors and ramps up GABA activity. Oxytocin and alcohol therefore both have the general effect of tamping down brain activity—perhaps explaining why they both lower inhibitions. © 2015 Scientific American
Jo Marchant Most new painkiller drugs fail in clinical trials — but a growing placebo response may be to blame. Drug companies have a problem: they are finding it ever harder to get painkillers through clinical trials. But this isn't necessarily because the drugs are getting worse. An extensive analysis of trial data1 has found that responses to sham treatments have become stronger over time, making it harder to prove a drug’s advantage over placebo. The change in reponse to placebo treatments for pain, discovered by researchers in Canada, holds true only for US clinical trials. “We were absolutely floored when we found out,” says Jeffrey Mogil, who directs the pain-genetics lab at McGill University in Montreal and led the analysis. Simply being in a US trial and receiving sham treatment now seems to relieve pain almost as effectively as many promising new drugs. Mogil thinks that as US trials get longer, larger and more expensive, they may be enhancing participants’ expectations of their effectiveness. Stronger placebo responses have already been reported for trials of antidepressants and antipsychotics2, 3, triggering debate over whether growing placebo effects are seen in pain trials too. To find out, Mogil and his colleagues examined 84 clinical trials of drugs for the treatment of chronic neuropathic pain (pain which affects the nervous system) published between 1990 and 2013. © 2015 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 21484 - Posted: 10.07.2015
By Nicholas Bakalar There may be a link between later bedtimes and weight gain, new research suggests. Researchers studied 3,342 adolescents starting in 1996, following them through 2009. At three points over the years, all reported their normal bedtimes, as well as information on fast food consumption, exercise and television time. The scientists calculated body mass index at each interview. After controlling for age, sex, race, ethnicity and socioeconomic status, the researchers found that each hour later bedtime during the school or workweek was associated with about a two-point increase in B.M.I. The effect was apparent even among people who got a full eight hours of sleep, and neither TV time nor exercise contributed to the effect. But fast food consumption did. The study, in the October issue of Sleep, raises questions, said the lead author, Lauren D. Asarnow, a graduate student at the University of California, Berkeley. “First, what is driving this relationship?” she said. “Is it metabolic changes that happen when you stay up late? And second, if we change sleep patterns, can we change eating behavior and the course of weight change?” The scientists acknowledge that their study had limitations. Their sleep data depended on self-reports, and they did not have complete diet information. Also, they had no data on waist circumference, which, unlike B.M.I., can help distinguish between lean muscle and abdominal fat. © 2015 The New York Times Company
Laura Sanders Scribes usually have pretty good handwriting. That’s not the case for one prolific 13th century writer known to scholars only as the Tremulous Hand of Worcester. Now scientists suggest the writer suffered from a neurological condition called essential tremor. Neurologist Jane Alty and historical handwriting researcher Deborah Thorpe, both of the University of York in England, made the retrospective diagnosis August 31 in Brain after studying the spidery wiggles that pervade the scribe’s writing. Essential tremor can cause shaking of the hands, head and voice and is distinct from other tremor-causing conditions such as Parkinson’s disease. Here, the anonymous writer’s peculiar script is evident (lighter portion of text) in an early Middle English version of the Nicene Creed, a summary of the Christian faith. Buried in the manuscript are clues that helped the researchers conclude that essential tremor plagued the Tremulous Hand. The Tremulous Hand of Worcester’s writing appeared in more than 20 books, including the Nicene Creed, a summary of the Christian faith. The writer’s distinctive script is the lighter portion of the text, about a third of the way down the page. Several clues led researchers to diagnose the scribe with essential tremor (see following images). © Society for Science & the Public 2000 - 2015.
Keyword: Movement Disorders
Link ID: 21482 - Posted: 10.07.2015
By Virginia Morell How homing pigeons find their way home has long mystified scientists. Experiments have shown they rely on smells to create a mental map of their route and on the sun or Earth’s magnetic fields to navigate. But they also use vision, memorizing roads, railway lines, and rivers. To understand just how important pigeons’ visual memories are for homing, scientists trained 12 birds to fly to their home lofts while wearing patches covering one eye (as in the photo above). Each bird wore a GPS logging device and made 18 flights with the left or right eye blocked, followed by another 18 trips with the opposite eye covered. Unlike mammals, birds lack a key neural structure—the corpus callosum—that allows both hemispheres of the brain to access what an animal sees. The experiments revealed that this missing neural structure affects the pigeons’ homing abilities, the scientists report in today’s the Proceedings of the Royal Society B. Pigeons that learned their way home with a blocked left eye couldn’t repeat the same journey when they wore a patch over their right eye, and vice versa. Instead, they flew slightly off course, following more of a curve than a straight line. The new work proves that vision, too, plays a key role in how pigeons find their way home. © 2015 American Association for the Advancement of Science.
Susan Milius Bachelor prairie voles can’t tell females of their species apart. Yet the clueless fellows can change, forming pair-bonds for life with the opposite sex and even distinguishing between two female strangers. Bachelors aren’t blind or stupid; they recognize individual males among their fellow short-tailed Microtus ochrogaster rodents scurrying through old fields in the center of North America. And males are certainly interested in the interchangeable females. In lab tests, bachelors claw and bite at cage dividers between the sexes, says Alexander Ophir of Cornell University. Conquering the divide and mating with a female after just six hours of her company can form a lifelong pair-bond between voles. Only about 5 percent of mammal species live this socially monogamous lifestyle, and the voles have played starring roles in studies of the neurobiology of bonding. (Social monogamists, including both voles and some Homo sapiens, don’t entirely forgo extra-pair encounters.) A pair-bonded couple can crowd three litters of young into their roughly six to nine months of life in the wild, Ophir says. One aid to speeding through family life: Females can get pregnant as soon as they give birth. “You sometimes see pups being delivered as males are trying to copulate with the female,” he says. Pair-bonding requires recognizing at least one female. “It’s all well and good to fall in love, but if you don’t know who you fell in love with, it’s worthless,” Ophir says. And paired-up voles can go further. Tests show they notice the difference between two females they have never mated with, Ophir and former student Tomica Blocker report in the October Animal Behaviour. © Society for Science & the Public 2000 - 2015
By Miriam E. Tucker Before he got sick, Whitney Dafoe was an award-winning photographer and a world traveler. He’d helped build a nunnery in India, ridden a motorcycle in the Himalayas and visited all 50 American states. He also worked on Barack Obama’s 2008 presidential campaign, and although he was already ill by January 2009, pushed himself to travel to Washington from his California home to photograph the inauguration. But now, at 31, Whitney lies in bed in a darkened room in his parents’ home, unable to talk, walk or eat. He is fed intravenously and is barely able to tolerate light, sounds or being touched. His parents and the medical personnel who see him wear plain clothing when they enter his room because bright colors, shapes or any kind of print make him feel even worse, as does any movement that he’s not expecting. “It’s hard to explain how fragile he is,” says his mother, Janet Dafoe. This isn’t the picture that people imagine when they hear “chronic fatigue syndrome,” which is often viewed by the public and the health-care community as a trivial or primarily psychological complaint. In a February report, the Institute of Medicine gave the illness a new name — systemic exertion intolerance disease. Many patients have long criticized the name “chronic fatigue syndrome” for not reflecting the seriousness of the illness. The new name, some say, is not much of an improvement. Some patients call it by an older name, “myalgic encephalomyelitis.” Most official documents refer to it with a compromise term, “myalgic encephalomyelitis/chronic fatigue syndrome,” or ME/CFS.
Link ID: 21479 - Posted: 10.06.2015
By Erika Hayasaki For 40 years, Joel Dreyer was a respected psychiatrist who oversaw a clinic for troubled children, belonged to an exclusive country club, and doted on his four daughters and nine grandchildren. Then, suddenly, he became a major drug dealer. Why? In the 1980s, psychiatrist Joel Dreyer was a fixture on Detroit’s WXYZ Channel 7. His commercials promoting his treatment center, InnerVisions, which he named after the Stevie Wonder album, sometimes ran up to five times a day. In one ad, Dreyer blocks a bartender from serving a mug of beer to a patron and says, “Don’t let your marriage or your job suffer from alcohol or drugs.” In another, Dreyer, in a navy pinstriped suit with a white pocket square, looks into the camera, his expression concerned and sympathetic. “Don’t you want to talk to someone who will listen?” he asks. “Someone who won’t pass judgment? Someone who cares? Come talk to me.” InnerVisions, which was based in Southfield, a suburb northwest of Detroit, had a staff of 80 physicians, psychologists, and therapists and took up two floors of a high-rise. It had made Dreyer not only a public figure but also wealthy. He maintained a side career as an expert witness. Attorneys called on him because he was smart, charming, and persuasive. Dreyer mostly testified for the defense, and with each high-profile case, his celebrity grew. Between the clinic, trial work, and his private practice, he was earning as much as $450,000 a year. Dreyer loved to be the center of attention. He would sometimes ride to work on a motorcycle in a bejeweled Elvis outfit to entertain his colleagues.
By Kimberly G. Noble What if we could draw a line from key areas of a low-income child’s brain to a policy intervention that would dramatically reduce his or her chances of staying in poverty, dropping out of school and entering the criminal justice or social welfare system? Wouldn’t we want to make that policy prescription as widely available as any vaccination against childhood disease? Thanks to remarkable advances in neuroscience and the social sciences, we are closing in on this possibility. In a study published this year in Nature Neuroscience, several co-authors and I found that family income is significantly correlated with children’s brain size — specifically, the surface area of the cerebral cortex, which is the outer layer of the brain that does most of the cognitive heavy lifting. Further, we found that increases in income were associated with the greatest increases in brain surface area among the poorest children. Not surprisingly, our findings made many people uncomfortable. Some feared the study would be used to reinforce the notion that people remain in poverty because they are less capable than those with higher incomes. As neuroscientists, we interpret the results very differently. We know that the brain is most malleable in the early years of life and that experiences during that time have lifelong effects on the mind. Work by social scientists such as Sendhil Mullainathan at Harvard University and Eldar Shafir at Princeton University has shown that poverty depletes parents’ cognitive resources, leaving less capacity for making everyday decisions about parenting. These parents are also at far greater risk for depression and anxiety — poverty’s “mental tax.” All of this has important implications for children.
Archy de Berker and Sven Bestmann A great deal of excitement has been generated in recent weeks by a review paper examining the literature on the drug modafinil, which concluded that “modafinil may well deserve the title of the first well-validated pharmaceutical ‘nootropic’ [cognitive enhancing] agent”. Coverage in the Guardian, Telegraph, British Medical Journal, and the Independent all called attention to the work, with a press release from Oxford University trumpeting “Review of ‘smart drug’ shows modafinil does enhance cognition”. The paper in question is a well-written summary of the recent literature (although though it probably underestimates side effects, as pointed out in the British Medical Journal). A deeper problem is that reviews do not “show” anything. Reviews can be educational and informative, but that’s not the same as using all of the available data to test whether something works or not. Two different scientists can write reviews on the same topic and come to completely different conclusions. You can think of reviews as a watercolour painting of current knowledge. We sometimes forget that this is a far cry from a technical drawing, each element measured, quantified, and bearing a strict resemblance to reality. Scientists, and the public, trying to figure out what works face a tricky problem: there will often be many papers on a given topic, offering a variety of sometimes conflicting conclusions. Fortunately, we have a well-developed toolkit for assessing the state of the current literature and drawing conclusions from it. This procedure is called meta-analysis; it combines the available sources of data (e.g., published studies), and is extensively used to assess the efficacy of medical interventions. Initiatives such as the Cochrane Collaboration use meta-analyses to synthesize available evidence into a consensus on what works and what doesn’t. © 2015 Guardian News and Media Limited
By ANDREW POLLACK What could become the first gene therapy to win approval in the United States moved closer to market on Monday, when its developer announced that the medicine had succeeded in a late-stage clinical trial in treating an inherited eye disease that can cause blindness. The developer, Spark Therapeutics, said the treatment had allowed people with certain so-called inherited retinal dystrophies to more easily maneuver in dimmer light than they could before. The company said it planned to apply to the Food and Drug Administration next year for approval to sell the product. “We saw substantial restoration of vision in patients who were progressing toward complete blindness,” Dr. Albert M. Maguire, a professor of ophthalmology at the University of Pennsylvania and a lead researcher in the study, said in a news release being issued by Spark. Dr. Katherine High, Spark’s president and chief scientific officer, said this was the first successful randomized, controlled trial for any gene therapy aimed at an inherited disease. “I’ve been working in gene therapy for most of my career,” she said. “It’s been a long time coming, and I’m delighted.” Besides encouraging the once beleaguered field of gene therapy, the results — if interpreted positively by investors — could help lift biotechnology stocks, which have been battered recently by concerns over a backlash against high drug prices. Still, much remains unknown. Spark did not provide the actual trial data, saying only that the treatment achieved the main goal of the study as well as two out of three of its secondary goals. It is also unclear what the F.D.A. will deem sufficient for approval of the product. Spark’s stock had slumped in the last two months as it changed how it would measure the results of the trial. © 2015 The New York Times Company
Link ID: 21475 - Posted: 10.05.2015