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By Helen Thomson Take a walk while I look inside your brain. Scientists have developed the first wearable PET scanner – allowing them to capture the inner workings of the brain while a person is on the move. The team plans to use it to investigate the exceptional talents of savants, such as perfect memory or exceptional mathematical skill. All available techniques for scanning the deeper regions of our brains require a person to be perfectly still. This limits the kinds of activities we can observe the brain doing, but the new scanner will enable researchers to study brain behaviour in normal life, as well providing a better understanding of the tremors of Parkinson’s disease, and the effectiveness of treatments for stroke. Positron emission tomography scanners track radioactive tracers, injected into the blood, that typically bind to glucose, the molecule that our cells use for energy. In this way, the scanners build 3D images of our bodies, enabling us to see which brain areas are particularly active, or where tumours are guzzling glucose in the body. To adapt this technique for people who are moving around, Stan Majewski at West Virginia University in Morgantown and his colleagues have constructed a ring of 12 radiation detectors that can be placed around a person’s head. This scanner is attached to the ceiling by a bungee-cord contraption, so that the wearer doesn’t feel the extra weight of the scanner. © Copyright Reed Business Information Ltd
Keyword: Brain imaging
Link ID: 22557 - Posted: 08.13.2016
By Sunpreet Singh Every day people are exposed to hours of artificial light from a variety of sources – computers, video games, office lights and, for some, 24-hour lighting in hospitals and nursing homes. Now new research in animals shows that excessive exposure to “light pollution” may be worse for health than previously known, taking a toll on muscle and bone strength. Researchers at Leiden University Medical Center in the Netherlands tracked the health of rats exposed to six months of continuous light compared to a control group of rats living under normal light-dark conditions — 12 hours of light, followed by 12 hours of dark. During the study, the rats exposed to continuous light had less muscle strength and developed signs of early-stage osteoporosis. They also got fatter and had higher blood glucose levels. Several markers of immune system health also worsened, according to the report published in the medical journal Current Biology. While earlier research has suggested excessive light exposure could affect cognition, the new research was surprising in that it showed a pronounced effect on muscles and bones. While it’s not clear why constant light exposure took a toll on the motor functions of the animals, it is known that light and dark cues influence a body’s circadian rhythms, which regulate many of the body’s physiological processes. “The study is the first of its kind to show markers of negatively-affected muscle fibers, skeletal systems and motor performances due to the disruption of circadian clocks, remarkably in only a few months,” said Chris Colwell, a psychiatry professor and sleep specialist at the University of California, Los Angeles, who was not part of the study. “They found that not only did motor performance go down on tests, but the muscles themselves just atrophied, and mice physically became weaker under just two months under these conditions.” © 2016 The New York Times Company
Keyword: Biological Rhythms
Link ID: 22556 - Posted: 08.13.2016
David R. Jacobs, We all know that exercise improves our physical fitness, but staying in shape can also boost our brainpower. We are not entirely sure how, but evidence points to several explanations. First, to maintain normal cognitive function, the brain requires a constant supply of oxygen and other chemicals, delivered via its abundant blood vessels. Physical exercise—and even just simple activities such as washing dishes or vacuuming—helps to circulate nutrient-rich blood efficiently throughout the body and keeps the blood vessels healthy. Exercise increases the creation of mitochondria—the cellular structures that generate and maintain our energy—both in our muscles and in our brain, which may explain the mental edge we often experience after a workout. Studies also show that getting the heart rate up enhances neurogenesis—the ability to grow new brain cells—in adults. Regardless of the mechanism, mounting evidence is revealing a robust relation between physical fitness and cognitive function. In our 2014 study, published in Neurology, we found that physical activity has an extensive, long-lasting influence on cognitive performance. We followed 2,747 healthy people between the ages of 18 and 30 for 25 years. In 1985 we evaluated their physical fitness using a treadmill test: the participants walked up an incline that became increasingly steep every two minutes. On average, they walked for about 10 minutes, reaching 3.4 miles per hour at an 18 percent incline (a fairly steep hill). Low performers lasted for only seven minutes and high performers for about 13 minutes. A second treadmill test in 2005 revealed that our participants' fitness levels had declined with age, as would be expected, but those who were in better shape in 1985 were also more likely to be fit 20 years later. © 2016 Scientific American
Link ID: 22555 - Posted: 08.13.2016
Ramin Skibba Scientists and medical researchers in the United States have been studying the health benefits and risks of marijuana for decades. But despite the increasing availability of legal marijuana, scientists have been forced to obtain the drug from a single source — the University of Mississippi in Oxford, which grows pot for research on a campus farm under a contract with the National Institute on Drug Abuse (NIDA). Now, the university’s monopoly is coming to an end. In an unexpected move, the US Drug Enforcement Administration (DEA) announced on 11 August that it will allow any institution to apply for permission to grow marijuana for research. Nature explains how the policy could transform the study of marijuana. Why do researchers want to study pot — and how do they get it? Researchers have been extracting cannabinoids — chemical compounds found in cannabis — and developing strains of varying strength to test whether they could alleviate chronic pain and treat or mitigate the effects of ailments such as seizures and other neurological disorders. Approved medical-marijuana consumers may buy pot from dispensaries in more than half the country, and recreational marijuana use is permitted in a few states. But researchers are limited to the handful of strains grown by the University of Mississippi farm. © 2016 Macmillan Publishers Limited
Keyword: Drug Abuse
Link ID: 22554 - Posted: 08.13.2016
By THE EDITORIAL BOARD Supporters of a saner marijuana policy scored a small victory this week when the Obama administration said it would authorize more institutions to grow marijuana for medical research. But the government passed up an opportunity to make a more significant change. The Drug Enforcement Administration on Thursday turned down two petitions — one from the governors of Rhode Island and Washington and the other from a resident of New Mexico — requesting that marijuana be removed from Schedule 1 of the Controlled Substances Act. Drugs on that list, which include heroin and LSD, are deemed to have no medical use; possession is illegal under federal law, and researchers have to jump through many hoops to obtain permission to study them and obtain samples to study. Having marijuana on that list is deeply misguided since many scientists and President Obama have said that it is no more dangerous than alcohol. Over the years, Congress and attorneys general have deferred to the expertise of the D.E.A., which is the part of the Justice Department that enforces the nation’s drug laws. So the D.E.A. has amassed extensive control over drug policy making. It determines who gets to grow marijuana for research and which scholars are allowed to study it, for example. It has strongly resisted efforts by scientists, state officials and federal lawmakers to reclassify marijuana by rejecting or refusing to acknowledge evidence that marijuana is not nearly as harmful as federal law treats it. Since 1968, the University of Mississippi has been the only institution allowed to grow the plant for research. This has severely limited availability. The D.E.A. now says that because researchers are increasingly interested in studying marijuana, it will permit more universities to grow the cannabis plant and supply it to researchers who have been approved to conduct studies on it. This should make it easier for researchers to obtain varieties of marijuana with varying concentrations of different compounds. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22553 - Posted: 08.13.2016
Ed Yong At the age of seven, Henry Gustav Molaison was involved in an accident that left him with severe epilepsy. Twenty years later, a surgeon named William Scoville tried to cure him by removing parts of his brain. It worked, but the procedure left Molaison unable to make new long-term memories. Everyone he met, every conversation he had, everything that happened to him would just evaporate from his mind. These problems revolutionized our understanding of how memory works, and transformed Molaison into “Patient H.M.”—arguably the most famous and studied patient in the history of neuroscience. That’s the familiar version of the story, but the one presented in Luke Dittrich’s new book Patient H.M.: A Story of Memory, Madness, and Family Secrets is deeper and darker. As revealed through Dittrich’s extensive reporting and poetic prose, Molaison’s tale is one of ethical dilemmas that not only influenced his famous surgery but persisted well beyond his death in 2008. It’s a story about more than just the life of one man or the root of memory; it’s also about how far people are willing to go for scientific advancement, and the human cost of that progress. And Dittrich is uniquely placed to consider these issues. Scoville was his grandfather. Suzanne Corkin, the scientist who worked with Molaison most extensively after his surgery, was an old friend of his mother’s. I spoke to him about the book and the challenges of reporting a story that he was so deeply entwined in. Most of this interview was conducted on July 19th. Following a New York Times excerpt published on August 7th, and the book’s release two weeks later, many neuroscientists have expressed “outrage” at Dittrich’s portrayal of Corkin. The controversy culminated in a statement from MIT, where Corkin was based, rebutting three allegations in the book. Dittrich has himself responded to the rebuttals, and at the end of this interview, I talk to him about the debate. © 2016 by The Atlantic Monthly Group.
Keyword: Learning & Memory
Link ID: 22552 - Posted: 08.13.2016
Like many students of neuroscience, I first learned of patient HM in a college lecture. His case was so strange yet so illuminating, and I was immediately transfixed. HM was unable to form new memories, my professor explained, because a surgeon had removed a specific part of his brain. The surgery froze him in time. HM—or Henry Molaison, as his name was revealed to be after his death in 2008—might be the most famous patient in the history of brain research. He is now the subject of the new book, Patient HM: A Story of Memory, Madness, and Family Secrets. An excerpt from the book in the New York Times Magazine, which details MIT neuroscientist Sue Corkin’s custody fight over HM’s brain after his death, has since sparked a backlash. Should you wish to go down that particular rabbit hole, you can read MIT’s response, the book author’s response to the response, and summaries of the back and forth. Why HM’s brain was worth fighting over should be obvious; he was probably the most studied individual in neuroscience while alive. But in the seven years since scientists sectioned HM’s brain into 2,401 slices, it has yielded surprisingly little research. Only two papers examining his brain have come out, and so far, physical examinations have led to no major insights. HM’s scientific potential remains unfulfilled—thanks to delays from the custody fight and the limitations of current neuroscience itself. Corkin, who made her career studying HM, confronted her complicated emotions about his death in her own 2013 book. She describes being “ecstatic to see his brain removed expertly from his skull.” Corkin passed away earlier this year.
Keyword: Learning & Memory
Link ID: 22551 - Posted: 08.13.2016
Cassie Martin Understanding sea anemones’ exceptional healing abilities may help scientists figure out how to restore hearing. Proteins that the marine invertebrates use to repair damaged cells can also repair mice’s sound-sensing cells, a new study shows. The findings provide insights into the mechanics of hearing and could lead to future treatments for traumatic hearing loss, researchers report in the Aug. 1 Journal of Experimental Biology. “This is a preliminary step, but it’s a very useful step in looking at restoring the structure and function of these damaged cells,” says Lavinia Sheets, a hearing researcher at Harvard Medical School who was not involved in the study. Tentacles of starlet sea anemones (Nematostella vectensis) are covered in tiny hairlike cells that sense vibrations in the water from prey swimming nearby.The cells are similar to sound-sensing cells found in the ears of humans and other mammals. When loud noises damage or kill these hair cells, the result can range from temporary to permanent hearing loss. Anemones’ repair proteins restore their damaged hairlike cells, but landlubbing creatures aren’t as lucky. Glen Watson, a biologist at the University of Louisiana at Lafayette, wondered if anemones’ proteins — which have previously been shown to mend similar cells in blind cave fish — might also work in mammals. |© Society for Science & the Public 2000 - 2016.
Tim Radford Eight paraplegics – some of them paralysed for more than a decade by severe spinal cord injury – have been able to move their legs and feel sensation, after help from an artificial exoskeleton, sessions using virtual reality (VR) technology and a non-invasive system that links the brain with a computer. In effect, after just 10 months of what their Brazilian medical team call “brain training” they have been able to make a conscious decision to move and then get a response from muscles that have not been used for a decade. Of the octet, one has been able to leave her house and drive a car. Another has conceived and delivered a child, feeling the contractions as she did so. The extent of the improvements was unexpected. The scientists had intended to exploit advanced computing and robotic technology to help paraplegics recover a sense of control in their lives. But their patients recovered some feeling and direct command as well. The implication is that even apparently complete spinal cord injury might leave some connected nerve tissue that could be reawakened after years of inaction. The patients responded unevenly, but all have reported partial restoration of muscle movement or skin sensation. Some have even recovered visceral function and are now able to tell when they need the lavatory. And although none of them can walk unaided, one woman has been able to make walking movements with her legs, while suspended in a harness, and generate enough force to make a robot exoskeleton move. © 2016 Guardian News and Media Limited
Rachel Ehrenberg Pulling consecutive all-nighters makes some brain areas groggier than others. Regions involved with problem solving and concentration become especially sluggish when sleep-deprived, a new study using brain scans reveals. Other areas keep ticking along, appearing to be less affected by a mounting sleep debt. The results might lead to a better understanding of the rhythmic nature of symptoms in certain psychiatric or neurodegenerative disorders, says study coauthor Derk-Jan Dijk. People with dementia, for instance, can be afflicted with “sundowning,” which worsens their symptoms at the end of the day. More broadly, the findings, published August 12 in Science, document the brain’s response to too little shut-eye. “We’ve shown what shift workers already know,” says Dijk, of the University of Surrey in England. “Being awake at 6 a.m. after a night of no sleep, it isn’t easy. But what wasn’t known was the remarkably different response of these brain areas.” The research reveals the differing effects of the two major factors that influence when you conk out: the body’s roughly 24-hour circadian clock, which helps keep you awake in the daytime and put you to sleep when it’s dark, and the body’s drive to sleep, which steadily increases the longer you’re awake. Dijk and collaborators at the University of Liege in Belgium assessed the cognitive function of 33 young adults who went without sleep for 42 hours. Over the course of this sleepless period, the participants performed some simple tasks testing reaction time and memory. The sleepy subjects also underwent 12 brain scans during their ordeal and another scan after 12 hours of recovery sleep. Throughout the study, the researchers also measured participants’ levels of the sleep hormone melatonin, which served as a way to track the hands on their master circadian clocks. |© Society for Science & the Public 2000 - 2016
Link ID: 22548 - Posted: 08.12.2016
In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.
By Sharon Begley, The Massachusetts Institute of Technology brain sciences department and, separately, a group of some 200 neuroscientists from around the world have written letters to The New York Times claiming that a book excerpt in the newspaper’s Sunday magazine this week contains important errors, misinterpretations of scientific disputes, and unfair characterizations of an MIT neuroscientist who did groundbreaking research on human memory. In particular, the excerpt contains a 36-volley verbatim exchange between author Luke Dittrich and MIT’s Suzanne Corkin in which she says that key documents from historic experiments were “shredded.” “Most of it has gone, is in the trash, was shredded,” Corkin is quoted as telling Dittrich before she died in May, explaining, “there’s no place to preserve it.” Destroying files related to historic scientific research would raise eyebrows, but Corkin’s colleagues say it never happened. “We believe that no records were destroyed and, to the contrary, that professor Corkin worked in her final days to organize and preserve all records,” said the letter that Dr. James DiCarlo, head of the MIT Department of Brain and Cognitive Sciences, sent to the Times late Tuesday. Even as Corkin fought advanced liver cancer, he wrote, “she instructed her assistant to continue to organize, label, and maintain all records” related to the research, and “the records currently remain within our department.” © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22546 - Posted: 08.11.2016
Mo Costandi The human brain is often said to be the most complex object in the known universe, and there’s good reason to believe that it is. That lump of jelly inside your head contains at least 80 billion nerve cells, or neurons, and even more of the non-neuronal cells called glia. Between them, they form hundreds of trillions of precise synaptic connections; but they all have moveable parts, and these connections can change. Neurons can extend and retract their delicate fibres; some types of glial cells can crawl through the brain; and neurons and glia routinely work together to create new connections and eliminate old ones. These processes begin before we are born, and occur until we die, making the brain a highly dynamic organ that undergoes continuous change throughout life. At any given moment, many millions of them are being modified in one way or another, to reshape the brain’s circuitry in response to our daily experiences. Researchers at Yale University have now developed an imaging technique that enables them to visualise the density of synapses in the living human brain, and offers a promising new way of studying how the organ develops and functions, and also how it deteriorates in various neurological and psychiatric conditions. The new method, developed in Richard Carson’s lab at Yale’s School of Engineering and Applied Sciences, is based on positron emission tomography (PET), which detects the radiation emitted by radioactive ‘tracers’ that bind to specific proteins or other molecules after being injected into the body. Until now, the density of synapses in the human brain could only be determined by autopsy, using antibodies that bind to and stain specific synaptic proteins, or electron microscopy to examine the fine structure of the tissue. © 2016 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 22545 - Posted: 08.11.2016
By Andy Coghlan The switching-off of genes in the human brain has been watched live for the first time. By comparing this activity in different people’s brains, researchers are now on the hunt for abnormalities underlying disorders such as Alzheimer’s disease and schizophrenia. To see where genes are most and least active in the brain, Jacob Hooker at Harvard Medical School and his team developed a radioactive tracer chemical that binds to a type of enzyme called an HDAC. This enzyme deactivates genes inside our cells, stopping them from making the proteins they code for. When injected into people, brain scans can detect where this tracer has bound to an enzyme, and thus where the enzyme is switching off genes. Live epigenetics The switching-off of genes by HDACs is a form of epigenetics – physical changes to the structure of DNA that modify how active genes are without altering their code. Until now, the only way to examine such activity in the brain has been by looking at post-mortem brain tissue. In the image above from the study, genes are least active in the red regions, such as the bulb-shaped cerebellum area towards the bottom right. The black and blue areas show the highest levels of gene activity – where barely any HDACs are present – and the yellow and green areas fall in between. © Copyright Reed Business Information Ltd.
Nicola Davis Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain. Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not. Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease. The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins - variations that are present decades before the onset of the disease. Hope for Alzheimer's treatment as researchers find licensed drugs halt brain degeneration Read more “Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study. The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease. Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult. © 2016 Guardian News and Media Limited
By Effy Redman “There is no one who has not smiled at least once,” writes Marianne LaFrance, a Yale University psychology professor, in her 2011 book “Lip Service: Smiles in Life, Death, Trust, Lies, Work, Memory, Sex and Politics.” Her book explores how smiling unifies us. Like breath, the smile is universal. We smile to connect, to forgive, to love. A smile is beauty, human. But I have never smiled. Not once. I was born with Moebius syndrome — a rare form of facial paralysis that results from damage in the womb to the sixth and seventh cranial nerves, which control the muscles of the face. I was born in Britain, on the same day in 1982 the country’s first test-tube twins were born. But while science has created medical miracles like test-tube babies, there’s little that doctors can do for someone with Moebius syndrome. Decades later, I still cannot smile. Or frown. Or do any of the infinite subtle and not-so-subtle things with my face that I see others in the world around me doing every day. Doctors describe people with Moebius as having a “mask-like expression.” And that is what strangers must see. A frozen face, eyes unblinking. My mouth always open, motionless, the left corner of my lips slightly lower than the right. Walking down the street, I can feel the touch of casual observers’ eyes. A child’s very first “social smile” usually occurs six to eight weeks after birth, eagerly awaited by new parents. Because, as an infant, my face remained so expressionless, when I began laughing it took my mother a while to realize that the sound I was making was laughter. At what point, I wonder, did I begin to compensate for the absence of my smile. © 2016 The New York Times Company
Link ID: 22542 - Posted: 08.11.2016
By MIKE SACKS You’ve seen me. I know you have. I’m the guy wearing gloves on the subway in October. Or even into April. Perhaps I’m wearing just one glove, allowing my naked hand to turn the pages of a book. No big deal. Just another one-gloved commuter, heading home. If it’s crowded, you may have noticed me doing my best to “surf,” sans contact, until the car comes to a stop, in which case I may knock into a fellow passenger. Aboveground you may have seen me acting the gentleman, opening doors for others with a special paper towel I carry in my front left pocket for just such a momentous occasion. No? How about that guy walking quickly ahead of you, the one impishly avoiding sidewalk cracks? Or perhaps you’ve noticed a stranger who turns and makes eye contact with you for seemingly no reason. You may have asked, “You got a problem?” Oh, I definitely have a problem. But it has nothing to do with you, sir or madam. (And, yes, even in my thoughts I refer to you as “sir” and “madam.”) The problem here is what multiple doctors have diagnosed as obsessive-compulsive disorder. You may refer to it by its kicky abbreviation, O.C.D. I prefer to call it Da Beast. Da Beast is a creature I have lived with since I was 11, a typical age for O.C.D. to snarl into one’s life without invitation or warning. According to the International O.C.D. Foundation, roughly one in 100 adults suffers from the disorder. Each of us has his or her own obsessive thoughts and fears to contend with. My particular beast of burden is a fear of germs and sickness. It’s a popular one, perhaps the most common. © 2016 The New York Times Company
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 22541 - Posted: 08.11.2016
By Robert Lavine Just the briefest eye contact can heighten empathetic feelings, giving people a sense of being drawn together. But patients who suffer from autism, even in its most high-functioning forms, often have trouble establishing this sort of a social connection with other people. Researchers are delving into what’s going on behind the eyes when these magical moments occur, and the hormones and neural substrates involved may offer hope of helping people with autism. University of Cambridge neuroscientist Bonnie Auyeung and colleagues gave oxytocin—a compound commonly referred to as the “love hormone,” as it’s been found to play roles in maternal and romantic bonding—to both normal men and those with a high-functioning form of autism also called Asperger’s syndrome. The scientists then tracked the eye movements of the study subjects and found that, compared with controls, those who received oxytocin via nasal spray showed increases in the number of fixations—pauses of about 300 milliseconds—on the eye region of an interviewer’s face and in the fraction of time spent looking at this region during a brief interview (Translational Psychiatry, doi:10.1038/tp.2014.146, 2015). Oxytocin, a neuropeptide hormone secreted by the pituitary gland, has long been known to activate receptors in the uterus and mammary glands, facilitating labor and milk letdown. But research on the neural effects of oxytocin has been accelerated by the availability of a nasal spray formulation of the hormone, which can deliver it more directly to the brain, also rich with oxytocin receptors. Auyeung adds that her study used a unique experimental setup. “Other studies have shown that [oxytocin] increases looking at the eye region when presented with a picture of a face,” Auyeung says. “The new part is that we are using a live interaction.”
By CATHERINE SAINT LOUIS and MATT APUZZO The Obama administration is planning to remove a major roadblock to marijuana research, officials said Wednesday, potentially spurring broad scientific study of a drug that is being used to treat dozens of diseases in states across the nation despite little rigorous evidence of its effectiveness. The new policy is expected to sharply increase the supply of marijuana available to researchers. And in taking this step, the Obama administration is further relaxing the nation’s stance on marijuana. President Obama has said he views it as no more dangerous than alcohol, and the Justice Department has not stood in the way of states that have legalized the drug. For years, the University of Mississippi has been the only institution authorized to grow the drug for use in medical studies. This restriction has so limited the supply of marijuana federally approved for research purposes that scientists said it could often take years to obtain it and in some cases it was impossible to get. But soon the Drug Enforcement Administration will allow other universities to apply to grow marijuana, three government officials said. While 25 states have approved the medical use of marijuana for a growing list of conditions, including Parkinson’s, Crohn’s disease, Tourette’s syndrome, Alzheimer’s, lupus and rheumatoid arthritis, the research to back up many of those treatments is thin. The new policy could begin to change that. “It will create a supply of research-grade marijuana that is diverse, but more importantly, it will be competitive and you will have growers motivated to meet the demand of researchers,” said John Hudak, a senior fellow at the Brookings Institution. The new policy will be published as soon as Thursday in the federal register, according to the three officials, who have seen the policy but spoke on condition of anonymity because they were not authorized to discuss it. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22539 - Posted: 08.11.2016
By Virginia Morell Fourteen years ago, a bird named Betty stunned scientists with her humanlike ability to invent and use tools. Captured from the wild and shown a tiny basket of meat trapped in a plastic tube, the New Caledonian crow bent a straight piece of wire into a hook and retrieved the food. Researchers hailed the observation as evidence that these crows could invent new tools on the fly—a sign of complex, abstract thought that became regarded as one of the best demonstrations of this ability in an animal other than a human. But a new study casts doubt on at least some of Betty’s supposed intuition. Scientists have long agreed that New Caledonian crows (Corvus moneduloides), which are found only on the South Pacific island of the same name, are accomplished toolmakers. At the time of Betty’s feat, researchers knew that in the wild these crows could shape either stiff or flexible twigs into tools with a tiny, barblike hook at one end, which they used to lever grubs from rotting logs. They also make rakelike tools from the leaves of the screw pine (Pandanus) tree. But Betty appeared to take things to the next level. Not only did she fashion a hook from a material she’d never previously encountered—a behavior not observed in the wild—she seemed to know she needed this specific shape to solve her particular puzzle. © 2016 American Association for the Advancement of Science. A