Chapter 16. None
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By Jef Akst WIKIMEDIA COMMONS, GERRYSHAWThe deeper scientists probe into the complexity of the human brain, the more questions seem to arise. One of the most fundamental questions is how many different types of brain cells there are, and how to categorize individual cell types. That dilemma was discussed during a session yesterday (November 11) at the ongoing Society for Neuroscience (SfN) conference in San Diego, California. As Evan Macosko of the Broad Institute said, the human brain comprises billions of brain cells—about 170 billion, according to one recent estimate—and there is a “tremendous amount of diversity in their function.” Now, new tools are supporting the study of single-cell transcriptomes, and the number of brain cell subtypes is skyrocketing. “We saw even greater degrees of heterogeneity in these cell populations than had been appreciated before,” Macosko said of his own single-cell interrogations of the mouse brain. He and others continue to characterize more brain regions, clustering cell types based on differences in gene expression, and then creating subclusters to look for diversity within each cell population. Following Macosko’s talk, Bosiljka Tasic of the Allen Institute for Brain Science emphasized that categorizing cell types into subgroups based on gene expression is not enough. Researchers will need to combine such data with traditional metrics, such as morphology and electrophysiology to “ultimately come up with an integrative taxonomy of cell types,” Tasic said. “Multimodal data acquisition—it’s a big deal and I think it’s going to be a big focus of our future endeavors.” © 1986-2016 The Scientist
Keyword: Brain imaging
Link ID: 22886 - Posted: 11.19.2016
By Alice Klein Alzheimer’s disease can be prevented by stopping a crucial brain protein from turning rogue, a study in mice suggests. Tau protein has long been suspected to play a role in causing the condition. In healthy brains, tau is essential for normal cell functioning. But during Alzheimer’s disease, the protein goes haywire, clumping together to form twisted tangles and, it is thought, releasing toxic chemicals that harm the brain. Now Lars Ittner at the University of New South Wales, Australia, and his colleagues have pinpointed a crucial enzyme that controls how tau proteins behave in the brain. The enzyme, called p38γ kinase, helps keep tau in a healthy, tangle-free state, preventing the onset of memory loss and other symptoms in mice that have been bred to develop Alzheimer’s disease. The enzyme seems to block Alzheimer’s by interfering with the action of another problem protein, called beta-amyloid. Like tau, clumps of this protein accumulate in the brains of people with Alzheimer’s, making it another suspected cause of the disease. When beta-amyloid forms these sticky plaques, it can also modify the structure of tau proteins, causing them to form tangles and release toxic chemicals. But Ittner’s team found that p38γ kinase makes a different kind of structural change to tau. If this change is made first, it prevents beta-amyloid from being able to turn tau bad, and mice do not develop the disease. © Copyright Reed Business Information Ltd.
Link ID: 22883 - Posted: 11.18.2016
Hannah Devlin Science Correspondent Blind animals have had their vision partially restored using a revolutionary DNA editing technique that scientists say could in future be applied to a range of devastating genetic diseases. The study is the first to demonstrate that a gene editing tool, called Crispr, can be used to replace faulty genes with working versions in the cells of adults - in this case adult rats. Previously, the powerful procedure, in which strands of DNA are snipped out and replaced, had been used only in dividing cells - such as those in an embryo - and scientists had struggled to apply it to non-dividing cells that make up most adult tissue, including the brain, heart, kidneys and liver. The latest advance paves the way for Crispr to be used to treat a range of incurable illnesses, such as muscular dystrophy, haemophilia and cystic fibrosis, by overwriting aberrant genes with a healthy working version. Professor Juan Carlos Izpisua Belmonte, who led the work at the Salk Institute in California, said: “For the first time, we can enter into cells that do not divide and modify the DNA at will. The possible applications of this discovery are vast.” The technique could be trialled in humans in as little as one or two years, he predicted, adding that the team were already working on developing therapies for muscular dystrophy. Crispr, a tool sometimes referred to as “molecular scissors”, has already been hailed as a game-changer in genetics because it allows scientists to cut precise sections of DNA and replace them with synthetic, healthy replacements. © 2016 Guardian News and Media Limited
Link ID: 22882 - Posted: 11.17.2016
Laura Beil NEW ORLEANS — Popular heartburn drugs — already under investigation for possible links to dementia, kidney and heart problems (SN: 6/11/16, p. 8) — have a new health concern to add to the list. An analysis of almost 250,000 medical records in Denmark has found an association with stroke. Researchers from the Danish Heart Foundation in Copenhagen studied patients undergoing gastric endoscopy from 1997 to 2012. About 9,500 of all patients studied suffered from ischemic strokes, which occur when a blood clot blocks a blood vessel in the brain. Overall, the risk of stroke was 21 percent higher in patients taking a proton pump inhibitor, a drug that relieves heartburn, the researchers reported November 15 during the American Heart Association’s annual meeting. While those patients also tended to be older and sicker to start with, the level of risk was associated with dose, the researchers found. People taking the lowest drug doses (between 10 and 20 milligrams a day, depending on the drug) did not have a higher risk. At the highest doses, though, Prevacid (more than 60 mg/day) carried a 30 percent higher risk and Protonix (more than 80 mg/day) a 94 percent higher risk. For Prilosec and Nexium, stroke risk fell within that range. Introduced in the 1980s, proton pump inhibitors are available in both prescription and over-the-counter forms. While they are valuable drugs, “their use has been increasing rapidly,” says lead author Thomas Sehested, adding that people often take them for too long, or without a clear reason. Before taking them, he says, “patients need a conversation with their doctor to see if they really need these drugs.” |© Society for Science & the Public 2000 - 2016
Link ID: 22877 - Posted: 11.17.2016
By Clare Wilson It’s one of the boldest treatments in medicine: delivering an electrical current deep into the brain by implanting a long thin electrode through a hole in the skull. Such “deep brain stimulation” (DBS) works miracles on people with otherwise untreatable epilepsy or Parkinson’s disease – but drilling into someone’s head is an extreme step. In future, we may be able to get the same effects by using stimulators placed outside the head, an advance that could see DBS used to treat a much wider range of conditions. DBS is being investigated for depression, obesity and obsessive compulsive disorder, but this research is going slowly. Implanting an electrode requires brain surgery, and carries a risk of infection, so the approach is only considered for severe cases. But Nir Grossman of Imperial College London and his team have found a safer way to experiment with DBS – by stimulating the brain externally, with no need for surgery. The technique, unveiled at the Society for Neuroscience conference in San Diego, California, this week, places two electrical fields of different frequencies outside the head. The brain tissue where the fields overlap is stimulated, while the tissue under just one field is unaffected because the frequencies are too high. For instance, they may use one field at 10,000 hertz and another at 10,010 hertz. The affected nerve cells are stimulated at 10 hertz – the difference between the two frequencies. © Copyright Reed Business Information Ltd.
Link ID: 22875 - Posted: 11.16.2016
By GRETCHEN REYNOLDS Exercise may be an effective treatment for depression and might even help prevent us from becoming depressed in the first place, according to three timely new studies. The studies pool outcomes from past research involving more than a million men and women and, taken together, strongly suggest that regular exercise alters our bodies and brains in ways that make us resistant to despair. Scientists have long questioned whether and how physical activity affects mental health. While we know that exercise alters the body, how physical activity affects moods and emotions is less well understood. Past studies have sometimes muddied rather than clarified the body and mind connections. Some randomized controlled trials have found that exercise programs, often involving walking, ease symptoms in people with major depression. But many of these studies have been relatively small in scale or had other scientific deficiencies. A major 2013 review of studies related to exercise and depression concluded that, based on the evidence then available, it was impossible to say whether exercise improved the condition. Other past reviews similarly have questioned whether the evidence was strong enough to say that exercise could stave off depression. A group of global public-health researchers, however, suspected that newer studies and a more rigorous review of the statistical evidence might bolster the case for exercise as a treatment of and block against depression. So for the new analyses, they first gathered all of the most recent and best-designed studies about depression and exercise. © 2016 The New York Times Company
Link ID: 22874 - Posted: 11.16.2016
By Daniel Barron Neurobiology was the first class I shuffled into as a dopey freshman undergraduate student. Dr. Brown’s class began at 8AM. I wore that bowling jacket I bought from the Orem Deseret Industries, Utah’s version of Goodwill. I’d spent much of my childhood in lower-middle class neighborhoods of small towns: Middle and Junior High School in the Texas Hill Country; High School in rural Utah. In High School, I would jog through the countryside—down by the River Bottom’s road—and rehearse conversations and ideas that troubled me. I hadn’t learned the language of social justice or of science. I felt uneasy with many of the ideas I’d been taught but lacked the vocabulary to pinpoint why. Dr. Brown’s first lecture covered visual perception, ocular dominance columns, and the idea that brain structure and function were intertwined. To use my parlance at that age, this was a Revelation. The lecture outlined a completely novel way of thinking: the notion that between my ears, behind my forehead and nose was a collection of cells—of neurons, an organ—responsible for how I saw and perceived the world. I was young, I was a drug-free virgin, and this was without question the greatest catharsis I had ever experienced. Here wasn’t simply a foundation for my behavior, but for others’ as well. My theological leanings faded as I began to learn why I was Me. In response, I worked my ass off. © 2016 Scientific American,
Link ID: 22873 - Posted: 11.16.2016
Laura Beil NEW ORLEANS — Chronic sleep problems are associated with atrial fibrillation — a temporary but dangerous disruption of heart rhythm — even among people who don’t suffer from sleep apnea. An analysis of almost 14 million patient records has found that people suffering from insomnia, frequent waking and other sleep issues are more likely than sound sleepers to experience a condition in which the upper chambers of the heart quiver instead of rhythmically beating, allowing blood to briefly stagnate. “Even if you don’t have sleep apnea, is there something about sleep disruption that puts you at a higher risk of fibrillation,” said Gregory Marcus, a cardiologist at the University of California, San Francisco. “We should put a higher priority on studying sleep itself.” Marcus and Matthew Christensen, from the University of Michigan, presented their results November 14 at the annual meeting of the American Heart Association. People with atrial fibrillation have double the risk of having a heart attack, and up to five times the risk of stroke. Although the heart condition can be a consequence of aging, its prevalence is rising at about 4 percent per year for reasons that aren’t totally explained. In the United States, about 5 million people currently have the condition, and that number is expected to rise to 12 million by 2030. A large body of studies has found that sleep apnea, which occurs when a person stops breathing during the night, can lead to atrial fibrillation and a host of other health concerns. Identifying a risk of atrial fibrillation among people with no sleep apnea is unexpected, says Richard Becker, director of the University of Cincinnati Heart, Lung & Vascular Institute, who was not part of the study. |© Society for Science & the Public 2000 - 2016.
Link ID: 22872 - Posted: 11.16.2016
By Gary Stix Renowned neuroscientist Mu-Ming Poo is playing a key role in China’s contribution to the push by national and regional governments to set up gargantuan neuroscience research endeavors. The China Brain Project has yet to put forward funding specifics. But Poo, who directs the Institute of Neuroscience of the Chinese Academy of Sciences and has held multiple academic posts at U.S. universities, is helping to shape the project’s 15-year timeline. To circumvent the paucity of drugs for neurological illnesses, Poo’s own team wants to focus on finding solid evidence for video games and other behavioral training methods that might produce near-term cognitive benefits for China’s aging population. Poo talked to Scientific American recently about these plans. Can you tell us about the Chinese Brain Project? Its goal is similar to the brain projects that have been launched in other regions but I think we’ve put more emphasis on the brain disease aspect than the U.S. project has. The U.S. project is more concentrated on developing new technologies for observing and manipulating the activity of brain circuits. In China there is a particular urgency to solve problems related to brain diseases because of its large population and an aging society saddled with neurodegenerative diseases. If we don’t find a solution for Alzheimer's by 2050, the entire medical system is going broke. In China there is an estimate that there could be many tens of millions of Alzheimer's or Parkinson’s disease patients by 2050 if no cure is found, given the rate of increasing life expectancy. © 2016 Scientific American,
Link ID: 22870 - Posted: 11.16.2016
By Jessica Hamzelou Having an agile mind in your 90s might sound like wishful thinking, but some people manage to retain youthful memories until their dying days. Now post mortems have revealed that these “superagers” manage to do this even when their brains have the hallmarks of Alzheimer’s diseases. Superagers have the memory and cognition of the average person almost half their age, and manage to avoid Alzheimer’s symptoms. Aras Rezvanian at Northwestern University in Chicago, Illinois, and his colleagues have been looking at brain samples donated by such people to try to understand what their secret might be. The group looked at eight brains, all from people who had lived into their 90s, and had memory and cognition scores of the average 50-year-old until their final days. Specifically, the team studied two brain regions – the hippocampus, which is involved in memory, and the prefrontal cortex, which is key for cognition. They found that the brain samples of the superagers had plaques and tangles in them to varying degrees. These are sticky clumps and twisted fibres of protein that seem to be linked to the death of neurons, and are usually found in the brains of people with Alzheimer’s disease after they die. Of the eight superager samples, two had such a high density and distribution of these proteins that they resembled the most severe cases of Alzheimer’s. © Copyright Reed Business Information Ltd.
Link ID: 22868 - Posted: 11.15.2016
By Rachel Feltman and Sarah Kaplan Dear Science, I just got a new iPhone and can't decide what kind of headphones I should be using. I read somewhere that ear buds are worse for you than headphones that fit over your ear. Is that true? I don't want to damage my hearing by using the wrong thing. Here's what science has to say: At the end of the day, nothing really matters but volume. No pair of headphones is inherently “good” or “bad” for your hearing. But picking the right headphones can help you listen to your music more responsibly. The louder a sound is, the more quickly it can cause injury to your ears. If you're not careful, a powerful sound wave can actually tear right through your delicate eardrum, but that's unlikely to happen while blasting music. Most hearing loss is the result of nerve damage, and your smartphone is more than capable of wrecking your ears that way. You can be exposed to 85 decibels — the noise of busy city traffic — pretty much all day without causing nerve damage, but things quickly become dangerous once you get louder than that. At 115 decibels, which is about the noise level produced at a rock concert or by a chain saw, nerve damage can happen in less than a minute. You might not immediately notice significant hearing loss as the result of that nerve damage, but it will add up over time. Some smartphones can crank music to 120 decibels. If you listened to an entire album at that volume, you might have noticeable hearing loss by the time you took off your headphones. According to the World Health Organization, 1.1 billion teens and young adults globally are at risk of developing hearing loss because of these “personal audio devices.” You already know the solution, folks: Turn that music down. © 1996-2016 The Washington Post
Link ID: 22867 - Posted: 11.15.2016
By LISA FELDMAN BARRETT Bitterness. Hostility. Rage. The varieties of anger are endless. Some are mild, such as grumpiness, and others are powerful, such as wrath. Different angers vary not only in their intensity but also in their purpose. It’s normal to feel exasperated with your screaming infant and scornful of a political opponent, but scorn toward your baby would be bizarre. Anger is a large, diverse population of experiences and behaviors, as psychologists like myself who study emotion repeatedly discover. You can shout in anger, weep in anger, even smile in anger. You can throw a tantrum in anger with your heart pounding, or calmly plot your revenge. No single state of the face, body or brain defines anger. Variation is the norm. The Russian language has two distinct concepts within what Americans call “anger” — one that’s directed at a person, called “serditsia,” and another that’s felt for more abstract reasons such as the political situation, known as “zlitsia.” The ancient Greeks distinguished quick bursts of temper from long-lasting wrath. German has three distinct angers, Mandarin has five and biblical Hebrew has seven. In the past few weeks, many varieties of anger have been on vivid display. For starters, we now have an iconic angry man as the president-elect. Donald J. Trump is aggressive as he insists there’s something wrong with the country, and offensive when he’s provoked. He employs anger effectively to maintain his power and status. His anger is seen by his fans as strength and by his detractors as bombast. We’ve also seen Hillary Clinton’s more restrained anger, which she has directed against the divisiveness she perceived during the campaign. To her proponents, Mrs. Clinton’s anger fueled her resolve to push back against Mr. Trump’s most egregious statements. To her detractors, her anger made her a shrew. © 2016 The New York Times Company
By Arlene Karidis As a young teenager, Inshirah Aleem was sure she’d be heading to Harvard Law School in a few years. But the straight-A student went down another road. Within months of her 14th birthday, the quiet girl was telling outrageous lies, running away from home and stealing. She eventually landed in front of a judge and later was sent to foster care, where she lived in a basement, her belongings stuffed into a trash bag. It would be a year before Aleem, now a 38-year-old schoolteacher living in Greenbelt, was diagnosed with bipolar disorder. The brain condition is characterized by high (manic) moods and low (depressed) moods as well as by fluctuating energy levels. These unstable states are coupled with impaired judgment. The diagnosis explained her racing, disjointed thoughts and almost completely sleepless nights. And it explained her terrifying hallucinations, which were followed by a catatonic state where Aleem couldn’t move or talk. About 2.6 percent of adults and about 11.2 percent of 13- to-18-year-olds have bipolar disorder, according to the Substance Abuse and Mental Health Services Administration. The disorder can be hard to recognize and harder to treat. Combining medications often brings substantial improvement, but some patients experience side effects and show minimal improvement. Researchers, who have found that bipolar disorder is inherited more than 70 percent of the time, hope to identify drugs to target the 20 genetic variations known to be associated with the disorder. © 1996-2016 The Washington Post
Link ID: 22864 - Posted: 11.14.2016
By Jessica Hamzelou HB, who is paralysed by amyotrophic lateral sclerosis (ALS), has become the first woman to use a brain implant at home and in her daily life. She told New Scientist about her experiences using an eye-tracking device that takes about a minute to spell a word. What is your life like? All muscles are paralysed. I can only move my eyes. Why did you decide to try the implant? I want to contribute to possible improvements for people like me. What was the surgery like? The first surgery was no problem, but the second had a negative impact for my condition. Can you feel the implant at all? No. How easy is it to use? The hardware is easy to use. The software has been improved enormously by the UNP (Utrecht NeuroProsthesis) team. My part isn’t difficult anymore after these improvements. The most difficult part is timing the clicks. How has the implant changed your life? Now I can communicate outdoors when my eye track computer doesn’t work. I’m more confident and independent now outside. What are the best and worst things about it? The best is to go outside and be able to communicate. The worst were the false-positive clicks. But thanks to the UNP team that is fixed. Now that the study has been completed, would you like to keep the implant, or remove it? Of course I keep it. How do you feel about being the first person to have this implant? It’s special to be the first. Thinking ahead to the future, what else would you like to be able to do with the implant? I would like to change the television channel and my dream is to be able to drive my wheelchair. © Copyright Reed Business Information Ltd.
Amber Dance In a study published in Science in September, Cossart, a neurobiologist at the Institute of Neurobiology of the Mediterranean in Marseilles, France, opened up mouse brains to visualize their neural activity as the animals raced on treadmills and rested. As the mice ran, some 50 neurons in their hippocampi fired in sequence, possibly to help the animals measure the distance travelled. Later, when the mice were resting, certain subsets of those neurons turned on again1. This reactivation, Cossart suspects, has to do with encoding and retrieving memory — as if the mouse is recalling its earlier exercise. “The power of imaging is really to be able to see the cells, to see not only the active ones but also the silent ones and to map them on the anatomical structure of the brain,” she says. It has not yet provided proof for Cossart's hypothesis, but the microscope and neural-activity markers behind the techniques represent the very latest in methods to study brain connectivity. In the past, researchers studied just a few neurons at a time using electrodes implanted into the brain. But that gives a fairly crude picture of what is going on, like looking at a monitor with just a couple of functioning pixels, says Rafael Yuste, director of the NeuroTechnology Center at Columbia University in New York City. But new techniques are fleshing out the picture. Scientists can now watch neurons live and in colour, helping them to work out which cells work together. Methods such as Cossart's zoom in at the microscopic scale to catch individual neurons in the act; others provide a whole-brain, or mesoscopic, view. And although it is possible to perform these experiments with an off-the-shelf microscope, scientists have been customizing them to suit their specific purposes; these devices are in various stages of commercialization. © 2016 Macmillan Publishers Limited,
Keyword: Brain imaging
Link ID: 22861 - Posted: 11.12.2016
By STEPH YIN Researchers have designed a system that lets a patient with late-stage Lou Gehrig’s disease type words using brain signals alone. The patient, Hanneke De Bruijne, a doctor of internal medicine from the Netherlands, received a diagnosis of amyotrophic lateral sclerosis, also known as A.L.S. or Lou Gehrig’s disease, in 2008. The neurons controlling her voluntary muscles were dying, and eventually she developed a condition called locked-in syndrome. In this state, she is cognitively aware, but nearly all of her voluntary muscles, except for her eyes, are paralyzed, and she has lost the ability to speak. In 2015, a group of researchers offered an option to help her communicate. Their idea was to surgically implant a brain-computer interface, a system that picks up electrical signals in her brain and relays them to software she can use to type out words. “It’s like a remote control in the brain,” said Nick Ramsey, a professor of cognitive neuroscience at the University Medical Center Utrecht in the Netherlands and one of the researchers leading the study. On Saturday, the research team reported in The New England Journal of Medicine that Ms. De Bruijne independently controlled the computer typing program seven months after surgery. Using the system, she is able to spell two or three words a minute. “This is the world’s first totally implanted brain-computer interface system that someone has used in her daily life with some success,” said Dr. Jonathan R. Wolpaw, the director of the National Center for Adaptive Neurotechnologies in Albany. © 2016 The New York Times Company
David Cyranoski For more than a decade, neuroscientist Grégoire Courtine has been flying every few months from his lab at the Swiss Federal Institute of Technology in Lausanne to another lab in Beijing, China, where he conducts research on monkeys with the aim of treating spinal-cord injuries. The commute is exhausting — on occasion he has even flown to Beijing, done experiments, and returned the same night. But it is worth it, says Courtine, because working with monkeys in China is less burdened by regulation than it is in Europe and the United States. And this week, he and his team report1 the results of experiments in Beijing, in which a wireless brain implant — that stimulates electrodes in the leg by recreating signals recorded from the brain — has enabled monkeys with spinal-cord injuries to walk. “They have demonstrated that the animals can regain not only coordinated but also weight-bearing function, which is important for locomotion. This is great work,” says Gaurav Sharma, a neuroscientist who has worked on restoring arm movement in paralysed patients, at the non-profit research organization Battelle Memorial Institute in Columbus, Ohio. The treatment is a potential boon for immobile patients: Courtine has already started a trial in Switzerland, using a pared-down version of the technology in two people with spinal-cord injury. © 2016 Macmillan Publishers Limited
By Diana Kwon In people who suffer from pain disorders, painful feelings can severely worsen and spread to other regions of the body. Patients who develop chronic pain after surgery, for example, will often feel it coming from the area surrounding the initial injury and even in some parts of the body far from where it originates. New evidence suggests glia, non-neuronal cells in the brain, may be the culprits behind this effect. Glia were once thought to simply be passive, supporting cells for neurons. But scientists now know they are involved in everything from metabolism to neurodegeneration. A growing body of evidence points to their key role in pain. In a study published today in Science, researchers at the Medical University of Vienna report that glia are involved in long-term potentiation (LTP), or the strengthening of synapses, in pain pathways in the spinal cord. Neuroscientists Timothy Bliss and Terje Lømo first described LTP in the hippocampus, a brain area involved in memory, in the 1970s. Since then scientists have been meticulously studying the role this type of synaptic plasticity—the ability of synapses to change in strength—plays in learning and memory. More recently, researchers discovered that LTP could also amplify pain in areas where injuries or inflammation occur. “We sometimes call this a ‘memory trace of pain’ because the painful insult may lead to subsequent hypersensitivity to painful stimuli, and it was clear that synaptic plasticity can play a role here,” says study co-author Jürgen Sandkühler, a neuroscientist also at the Medical University of Vienna. But current models of how LTP works could not explain why discomfort sometimes becomes widespread or experienced in areas a person has never felt it before, he adds. © 2016 Scientific American
by Helen Thompson Narwhals use highly targeted beams of sound to scan their environment for threats and food. In fact, the so-called unicorns of the sea (for their iconic head tusks) may produce the most refined sonar of any living animal. A team of researchers set up 16 underwater microphones to eavesdrop on narwhal click vocalizations at 11 ice pack sites in Greenland’s Baffin Bay in 2013. The recordings show that narwhal clicks are extremely intense and directional — meaning they can widen and narrow the beam of sound to find prey over long and short distances. It’s the most directional sonar signal measured in a living species, the researchers report November 9 in PLOS ONE. The sound beams are also asymmetrically narrow on top. That minimizes clutter from echoes bouncing off the sea surface or ice pack. Finally, narwhals scan vertically as they dive, which could help them find patches of open water where they can surface and breathe amid sea ice cover. All this means that narwhals employ pretty sophisticated sonar. The audio data could help researchers tell the difference between narwhal vocalizations and those of neighboring beluga whales. It also provides a baseline for assessing the potential impact of noise pollution from increases in shipping traffic made possible by sea ice loss. |© Society for Science & the Public 2000 - 2016.
Link ID: 22856 - Posted: 11.12.2016
By John Bohannon When it comes to influential neuroscience research, University College London (UCL) has a lot to boast about. That's not the opinion of a human but rather the output of a computer program that has now parsed the content of 2.5 million neuroscience articles, mapped all of the citations between them, and calculated a score of each author's influence on the rest. Three of the top 10 most influential (see table below) neuroscientists hail from UCL: Karl Friston (1st), Raymond Dolan (2nd), and Chris Frith (7th). The secret of their success? "We got into human functional brain imaging very early," Frith says. Getting in early made it possible to "be first to do many of the obvious studies." The program, called Semantic Scholar, is an online tool built at the Allen Institute for Artificial Intelligence (AI2) in Seattle, Washington. When it debuted in April, it calculated the most influential computer scientists based on 2 million papers from that field. Since then, the AI2 team has expanded the corpus to 10 million papers, 25% of which are from neuroscience. They hope to expand that to all of the biomedical literature next year, over 20 million papers. When Semantic Scholar looks at a paper published online, what does it actually see? Much more than the typical academic search engine, says Oren Etzioni, CEO of AI2 who has led the project. "We are using machine learning, natural language processing, and [machine] vision to begin to delve into the semantics." © 2016 American Association for the Advancement of Science
Link ID: 22855 - Posted: 11.12.2016