Karen Ravn Birds of a feather may flock together, but do birds that flock together develop distinct cultures? Two studies published today in Science1, 2 find strong evidence that, at the very least, monkeys that troop together and whales that pod together do just that. And they manage it in the same way that humans do: by copying and learning from each other. A team led by Erica van de Waal, a primate psychologist at the University of St Andrews, UK, created two distinct cultures — 'blue' and 'pink' — among groups of wild vervet monkeys (Chlorocebus aethiops) in South Africa1. The researchers trained two sets of monkeys to eat maize (corn) dyed one of those two colours but eschew maize dyed the other colour. The scientists then waited to see how the groups behaved when newcomers — babies and migrating males — arrived. Both sets of newcomers seemed to follow social cues when selecting their snacks. Baby monkeys ate the same colour maize as their mothers. Seven of the ten males that migrated from one colour culture to another adopted the local colour preference the first time that they ate any maize. The trend was even stronger when they first fed with no higher-ranking monkey around, with nine of the ten males choosing the locally preferred variety. The only immigrant to buck this trend was a monkey who assumed the top rank in his new group as soon as he got there — and he may not have given a fig what anyone else ate. “The take-home message is that social learning — learning from others rather than through individual trial and error — is a more potent force in shaping wild animals’ behaviour than has been recognized so far,” says Andrew Whiten, an evolutionary and developmental psychologist at St Andrews and co-author of the paper. © 2013 Nature Publishing Group

Keyword: Learning & Memory; Aggression
Link ID: 18079 - Posted: 04.27.2013

Posted by Christy Ullrich Elephants may use a variety of subtle movements and gestures to communicate with one another, according to researchers who have studied the big mammals in the wild for decades. To the casual human observer, a curl of the trunk, a step backward, or a fold of the ear may not have meaning. But to an elephant—and scientists like Joyce Poole—these are signals that convey vital information to individual elephants and the overall herd. Biologist and conservationist Joyce Poole and her husband, Petter Granli, both of whom direct ElephantVoices, a charity they founded to research and advocate for conservation of elephants in various sanctuaries in Africa, have developed an online database decoding hundreds of distinct elephant signals and gestures. The postures and movements underscore the sophistication of elephant communication, they say. Poole and Granli have also deciphered the meaning of acoustic communication in elephants, interpreting the different rumbling, roaring, screaming, trumpeting, and other idiosyncratic sounds that elephants make in concert with postures such as the positioning and flapping of their ears. Poole has studied elephants in Africa for more than 37 years, but only began developing the online gestures database in the past decade. Some of her research and conservation work has been funded by the National Geographic Society. “I noticed that when I would take out guests visiting Amboseli [National Park in Kenya] and was narrating the elephants’ behavior, I got to the point where 90 percent of the time, I could predict what the elephant was about to do,” Poole said in an interview. “If they stood a certain way, they were afraid and were about to retreat, or [in another way] they were angry and were about to move toward and threaten another.” © 1996-2012 National Geographic Society.

Keyword: Language; Aggression
Link ID: 18078 - Posted: 04.27.2013

by Helen Thomson "I feel like I have been dropped into my body. I know this is my voice and these are my memories, but they don't feel like they belong to me." It happened out of the blue. Louise Airey was 8 years old, off sick from school, when suddenly she felt like she had been dropped into her own body. "It's just so difficult to verbalise what this feels like," she says. "All of a sudden you're hyper aware, and everything else in the world seems unreal, like a movie." She panicked, but told no one. The feeling soon passed but returned several times until, at the age of 19, a migraine triggered a sensation of being disconnected from the world that was to last 18 months. When she was in her 30s she was diagnosed with depersonalisation disorder – an altered sense of self with all-encompassing feelings of not occupying your own body, and detachment from your thoughts and actions. It has come and gone throughout her life, but since a traumatic pregnancy 20 months ago, these feelings have remained constant. "Other people seem like robots," Airey says. "It's like I'm watching a film, like I'm on my own in the centre of everything and nothing else is real. I'll be speaking to my children and I'll catch my voice talking and it seems really alien and foreign. It makes you feel very separated and lonely from everything, like you're the only person that is real." Depersonalisation disorder is not as rare as you might think, says Anthony David at King's College London and the Maudsley Hospital: it may affect almost 1 per cent of the British population (Social Psychiatry and Psychiatric Epidemiology, DOI: 10.1007/s00127-010-0327-7). We've all probably experienced mild versions of it at some point, in the unreal, spaced-out feeling you might get while severely jet-lagged or hung-over, for example. © Copyright Reed Business Information Ltd.

Keyword: Attention
Link ID: 18077 - Posted: 04.27.2013

David Adam David Kupfer is a modern-day heretic. A psychiatrist at the University of Pittsburgh in Pennsylvania, Kupfer, has spent the past six years directing the revision of a book commonly referred to as the bible of the psychiatric field. The work will reach a climax next month when the American Psychiatric Association (APA) unveils the fifth incarnation of the book, called the Diagnostic and Statistical Manual of Mental Disorders (DSM), which provides checklists of symptoms that psychiatrists around the world use to diagnose their patients. The DSM is so influential that just about the only suggestion of Kupfer's that did not meet with howls of protest during the revision process was to change its name from DSM-V to DSM-5. Although the title and wording of the manual are now settled, the debate that overshadowed the revision is not. The stark fact is that no one has yet agreed on how best to define and diagnose mental illnesses. DSM-5, like the two preceding editions, will place disorders in discrete categories such as major-depressive disorder, bipolar disorder, schizophrenia and obsessive–compulsive disorder (OCD). These categories, which have guided psychiatry since the early 1980s, are based largely on decades-old theory and subjective symptoms. The problem is that biologists have been unable to find any genetic or neuroscientific evidence to support the breakdown of complex mental disorders into separate categories. Many psychiatrists, meanwhile, already think outside the category boxes, because they see so many patients whose symptoms do not fit neatly into them. Kupfer and others wanted the latest DSM to move away from the category approach and towards one called 'dimensionality', in which mental illnesses overlap. According to this view, the disorders are the product of shared risk factors that lead to abnormalities in intersecting drives such as motivation and reward anticipation, which can be measured (hence 'dimension') and used to place people on one of several spectra. But the attempt to introduce this approach foundered, as other psychiatrists and psychologists protested that it was premature. © 2013 Nature Publishing Group

Keyword: Schizophrenia; Aggression
Link ID: 18073 - Posted: 04.25.2013

By Lucy Wallis BBC News Abby and Brittany Hensel are conjoined twins determined to live the normal, active life of outgoing 20-somethings anywhere. They have been to university, they travel, they have jobs. But how easy is it for two people to inhabit one body? Like most 23-year-olds Abby and Brittany Hensel love spending time with their friends, going on holiday, driving, playing sport such as volleyball and living life to the full. The identical, conjoined twins from Minnesota, in the United States, have graduated from Bethel University and are setting out on their career as primary school teachers with an emphasis on maths. Although they have two teaching licences, there is one practical difference when it comes to the finances. "Obviously right away we understand that we are going to get one salary because we're doing the job of one person," says Abby. "As maybe experience comes in we'd like to negotiate a little bit, considering we have two degrees and because we are able to give two different perspectives or teach in two different ways." "One can be teaching and one can be monitoring and answering questions," says Brittany. "So in that sense we can do more than one person." Their friend Cari Jo Hohncke has always admired the sisters' teamwork. "They are two different girls, but yet they are able to work together to do the basic functions that I do every day that I take for granted," says Hohncke. BBC © 2013

Keyword: Laterality
Link ID: 18072 - Posted: 04.25.2013

By PAM BELLUCK After most pregnancies, the placenta is thrown out, having done its job of nourishing and supporting the developing baby. But a new study raises the possibility that analyzing the placenta after birth may provide clues to a child’s risk for developing autism. The study, which analyzed placentas from 217 births, found that in families at high genetic risk for having an autistic child, placentas were significantly more likely to have abnormal folds and creases. “It’s quite stark,” said Dr. Cheryl K. Walker, an obstetrician-gynecologist at the Mind Institute at the University of California, Davis, and a co-author of the study, published in the journal Biological Psychiatry. “Placentas from babies at risk for autism, clearly there’s something quite different about them.” Researchers will not know until at least next year how many of the children, who are between 2 and 5, whose placentas were studied will be found to have autism. Experts said, however, that if researchers find that children with autism had more placental folds, called trophoblast inclusions, visible after birth, the condition could become an early indicator or biomarker for babies at high risk for the disorder. “It would be really exciting to have a real biomarker and especially one that you can get at birth,” said Dr. Tara Wenger, a researcher at the Center for Autism Research at Children’s Hospital of Philadelphia, who was not involved in the study. © 2013 The New York Times Company

Keyword: Autism; Aggression
Link ID: 18069 - Posted: 04.25.2013

By Stephen L. Macknik Why, oh why, would I order a plastic fork, costing $89 (on-sale), 5 months before its scheduled release? Because it promises to help me control my eating speed, which, I am now convinced, is indeed critical to controlling obesity and diabetes. The fork is essentially a Bluetooth device that communicates to your smartphone and counts how many bites you take each meal. More importantly, I believe it counts the amount of time between each bite and if you go too fast, it vibrates. [Insert vibrator to mouth joke here. Yes, I'm blonde.] The reason I think it will help me goes back to my gastric bypass two months ago. Before and after the surgery, patients of Dr. Robin Blackmore at the Scottsdale Healthcare Bariatric Surgery Unit must take a series of courses aimed at preparing patients for life after surgery. One of the main lessons is that patients must now eat each meal over a 20 minute period. No more, no less. As you might surmise, for patients like me, “no more” is ready to achieve, but “no less” than 20 minutes is surprisingly difficult. And they are well aware of how hard it is, demanding that you practice ahead of time. I don’t know about my fellow patients, but I didn’t practice at all and have paid the price numerous times since my surgery for eating too fast: let’s just say it sometimes leads to a temporary obstruction and leave it at that. Because the details are unbelievably disgusting. © 2013 Scientific American,

Keyword: Obesity
Link ID: 18068 - Posted: 04.24.2013

By R. Douglas Fields Scientists have speculated that it is a mild manifestation of pain or perhaps a malfunction of overly sensitive nerve endings stuck in a feedback loop. They have even wondered whether itching is mostly psychological (just think about bed bugs for a minute). Now a study rules out these possibilities by succeeding where past attempts have failed: a group of neuroscientists have finally isolated a unique type of nerve cell that makes us itch and only itch. In previous research, neuroscientists Liang Han and Xinzhong Dong of Johns Hopkins University and their colleagues determined that some sensory neurons with nerve endings in the skin have a unique protein receptor on them called MrgprA3. They observed under a microscope that chemicals known to create itching caused these neurons to generate electrical signals but that painful stimuli such as hot water or capsaicin, the potent substance in hot peppers, did not. In the new study published in Nature Neuroscience, the researchers used genetic engineering to selectively kill the entire population of MrgprA3 neurons in mice while leaving all the other sensory neurons intact. These mice no longer scratched themselves when exposed to itchy substances or allergens, but they showed no changes at all in responding to touch or pain-producing stimulation. The mice's behavior confirms that MrgprA3-containing neurons are essential for itch, but it does not rule out the possibility that these cells might respond to other sensations as well. To find out, the neuroscientists engineered a receptor that responds to capsaicin injected into the MrgprA3 neurons, in a type of mouse that lacks the capsaicin receptor in all its other cells. Now the only neurons that would be stimulated by capsaicin were the MrgprA3 neurons. If these cells are indeed itch-specific, injecting capsaicin into a tiny spot on the mouse's skin should make the rodent scratch instead of wincing in pain—which is exactly what happened. © 2013 Scientific American,

Keyword: Pain & Touch
Link ID: 18066 - Posted: 04.24.2013

By Scicurious Generally, I don’t think of being tickled as a particularly pleasurable or calming activity. Most people who are ticklish go immediately on the defensive and tense up, and I always got the impression that most people prefer NOT to be tickled rather than otherwise. However, that’s just us. And we’re not rats. And it turns out, you can calm a rat with tickling. Life is stressful. Whether it’s running from predators, meeting tight deadlines, or trying to keep fed, there’s a lot that seems to bring us down. What saves us from tearing our hair out? Well, the happy things in life. Tasty food, friends, hugs, puppies. You know, the good stuff. These things elicit positive feeling, and positive feeling have been linked to protecting us from stress. Of course, in humans, it’s easy to say that a positive outlook on life makes someone resistant to stress…but is it really true? They may co-occur, but do positive feelings really decrease stress? If you want to get at causes, one of the best ways is to use an animal model. But how do you come up with an animal model for…happiness? Well, you can tickle rats. As you can see in the video above, rats like to be tickled. They even respond with “laughter”! Of course, it’s not laughter as we know it, or even something we can hear. Instead, these are ultrasonic vocalizations at a specific frequency (50 kilohertz). Scientists figured they must be pleasure-sounds because rats make them when they play with other rats. And it turns out that rats make the same noise at the same frequency when they get tickled! © 2013 Scientific American

Keyword: Emotions; Aggression
Link ID: 18065 - Posted: 04.23.2013

By GREGORY COWLES When John Elder Robison was teaching his young son, Cubby, the finer points of etiquette almost two decades ago, he noted that in addition to “please” and “thank you,” it’s nice to include a salutation while making a request. “For example,” he said, “if you wanted me to get you milk, you could say: ‘Please, wondrous Dada, may I have some milk?’ ” The salutation never caught with Cubby. But by the last page of Mr. Robison’s engaging new memoir, readers may have no problem hailing the author that way. Part parenting guide, part courtroom drama, part catalog of the travails and surprising joys of life with the high-functioning form of autism called Asperger’s syndrome, this memoir will offer all parents — but particularly fathers — a lot to think about. That its author was almost 40 when he learned he had Asperger’s (a discovery he described in his first memoir, “Look Me in the Eye”), and that he eventually learned his son had the condition as well, make their story more remarkable, but do nothing to diminish its relevance even for readers with no personal experience of autism. Indeed, it can be hard to pinpoint what in the Robisons’ relationship is shaped by Asperger’s and what stems from their own idiosyncratic personalities. Cubby’s name, for instance: Mr. Robison tells us that when his wife (now ex) was pregnant, “I sensed that the best names were not in books at all. For example, if we ended up with a girl, I favored naming her Thugwena, because I knew a girl named Thugwena would be tough and not hassled by bullies.” For boys he liked Thugwald, or else “functional choices” like Kid or Boy. Is this an example of his deadpan humor, in evidence throughout, or is it his Asperger’s blinding him to how others might perceive his actions? Just when you conclude that his tongue is firmly in his cheek, he drops a passing reference to the family cat, Small Animal. © 2013 The New York Times Company

Keyword: Autism
Link ID: 18063 - Posted: 04.23.2013

Nathan J. Winograd People for the Ethical Treatment of Animals (PETA) is an organization that publicly claims to represent the best interest of animals -- indeed their "ethical treatment." Yet approximately 2,000 animals pass through PETA's front door every year and very few make it out alive. The vast majority -- 96 percent in 2011 -- exit the facility out the back door after they have been killed, when Pet Cremation Services of Tidewater stops by on their regular visits to pick up their remains. Between these visits, the bodies are stored in the giant walk-in freezer PETA installed for this very purpose. It is a freezer that cost $9,370 and, like the company which incinerates the bodies of PETA's victims, was paid for with the donations of animal lovers who could never have imagined that the money they donated to help animals would be used to end their lives instead. In fact, in the last 11 years, PETA has killed 29,426 dogs, cats, rabbits, and other domestic animals. Most animal lovers find this hard to believe. But seeing is believing. And if it is true that a picture speaks a thousand words, the following images speak volumes about who and what PETA really stands for. The PETA headquarters is on the aptly named Front Street. While claiming to be an animal rights organization, PETA does not believe animals have a right to live. Instead, it believes that people have a right to kill them, as long as the killing is done "humanely," which PETA interprets to mean poisoning them with an overdose of barbiturates, even if the animals are not suffering. In 2012, 733 dogs entered this building. They killed 602 of them. Only 12 were adopted. Also in 2012, they impounded 1,110 cats. 1,045 were put to death. Seven of them were adopted. They also took in 34 other companion animals, such as rabbits, of which 28 were put to death. Only four were adopted. © 2013 TheHuffingtonPost.com, Inc

Keyword: Animal Rights
Link ID: 18060 - Posted: 04.23.2013

Alison Abbott Activists occupied an animal facility at the University of Milan, Italy, at the weekend, releasing mice and rabbits and mixing up cage labels to confuse experimental protocols. Researchers at the university say that it will take years to recover their work. Many of the animals at the facility are genetic models for psychiatric disorders such as autism and schizophrenia. No arrests have been made following the 12-hour drama, which took place on Saturday, although the university says that it will press charges against the protesters. The activists took some of the animals and were told during negotiations that they would be permitted to come back later and take more. The attack was staged by the animal-rights group that calls itself Fermare Green Hill (or Stop Green Hill), in reference to the Green Hill dog-breeding facility near Brescia, Italy, which it targets for closure. Five activists entered laboratories in the university’s pharmacology department on Saturday morning. The lack of signs of a break-in suggests that the activists may have used an illegally acquired electronic card, says pharmacologist Francesca Guidobono-Cavalchini, who works there. They prised open the reinforced doors of the facility on the fourth floor, and two of them chained themselves by the neck to the main double doors such that any attempt to open the doors could have endangered their lives. © 2013 Nature Publishing Group

Keyword: Animal Rights
Link ID: 18059 - Posted: 04.23.2013

By Kate Wong Odds are you carry DNA from a Neandertal, Denisovan or some other archaic human. Just a few years ago such a statement would have been virtually unthinkable. For decades evidence from genetics seemed to support the theory that anatomically modern humans arose as a new species in a single locale in Africa and subsequently spread out from there, replacing archaic humans throughout the Old World without mating with them. But in recent years geneticists have determined that, contrary to that conventional view, anatomically modern Homo sapiens did in fact interbreed with archaic humans, and that their DNA persists in people today. In the May issue of Scientific American, Michael Hammer of the University of Arizona in Tucson examines the latest genetic findings and explores the possibility that DNA from these extinct relatives helped H. sapiens become the wildly successful species it is today. As Scientific American’s anthropology editor, I have an enduring interest in the rise of H. sapiens; and as longtime readers of this blog may know, I’m fascinated (you might even say obsessed) with Neandertals. So naturally I’ve been keen to find out how much, if any, Neandertal DNA I have in my own genome. Several consumer genetic testing companies now test for Neandertal genetic markers as part of their broader ancestry analysis, and after 23andMe lowered the price of their kit to $99 in December, I decided to take the plunge. As it happens, National Geographic’s Genographic Project had recently updated their own genetic test to look for Neandertal DNA, and they sent me a kit (retail price: $299) for editorial review, much as publishers do with new books. And so it was on a chilly Saturday in late January that I found myself spitting into a test tube for 23andMe and swabbing my cheek for the Genographic Project. © 2013 Scientific American

Keyword: Evolution; Aggression
Link ID: 18057 - Posted: 04.23.2013

By ELIZABETH WEIL According to Sonja Lyubomirsky, you have a happiness set point. It’s partly encoded in your genes. If something good happens, your sense of happiness rises; if something bad happens, it falls. But either way, before too long, your mood will creep back to its set point because of a really powerful and perverse phenomenon referred to in science as “hedonic adaptation.” You know, people get used to things. With her 2007 book, “The How of Happiness,” and this year’s follow-up, “The Myths of Happiness,” Dr. Lyubomirsky, a psychology professor at the University of California, Riverside, caused ripples in her field but also drew a wider audience, cementing her place in a long chain of happiness-industry stalwarts, from M. Scott Peck with “The Road Less Traveled” to Martin E. P. Seligman and “Learned Optimism” to Daniel Gilbert and his best-selling “Stumbling on Happiness.” Dr. Lyubomirsky’s findings can be provocative and, at times, counterintuitive. Renters are happier than homeowners, she says. Interrupting positive experiences makes them more enjoyable. Acts of kindness make people feel happier, but not if you are compelled to perform the same act too frequently. (Bring your lover breakfast in bed one day, and it feels great. Bring it every day, and it feels like a chore.) Dr. Lyubomirsky — 46, Russian and expecting to give birth to her fourth child this weekend — is an unlikely mood guru. “I really hate all the smiley faces and rainbows and kittens,” she said in her office. She doesn’t often count her blessings or write gratitude letters, both of which she thinks sound hokey even though her research suggests they make people happier. © 2013 The New York Times Company

Keyword: Emotions
Link ID: 18055 - Posted: 04.22.2013

By PAULA SPAN It was supposed to be a short stay. In 2006, Roger Anderson was to undergo surgery to relieve a painfully compressed spinal disk. His wife, Karen, figured the staff at the hospital, in Portland, Ore., would understand how to care for someone with Parkinson’s disease. It can be difficult. Parkinson’s patients like Mr. Anderson, for example, must take medications at precise intervals to replace the brain chemical dopamine, which is diminished by the disease. “You don’t have much of a window,” Mrs. Anderson said. “If you have to wait an hour, you have tremendous problems.” Without these medications, people may “freeze” and be unable to move, or develop uncontrolled movements called dyskinesia, and are prone to falls. But the nurses at the Portland hospital didn’t seem to grasp those imperatives. “You’d have to wait half an hour or an hour, and that’s not how it works for Parkinson’s patients,” Mrs. Anderson said. Nor did hospital rules, at the time, permit her to simply give her husband the Sinemet pills on her own. Surgery and anesthesia, the disrupted medications, an incision that subsequently became infected — all contributed to a tailspin that lasted nearly three months. Mr. Anderson developed delirium, rotated between rehab centers and hospitals, took a fall, lost 60 pounds. “People were telling me, ‘He’s never going to come home,’” Mrs. Anderson said. He did recover, and at 69 is doing well, his wife said, though his disease has progressed. But his wasn’t an unusual story, neurologists say. © 2013 The New York Times Company

Keyword: Parkinsons
Link ID: 18054 - Posted: 04.22.2013

By Susan Milius Zola the crow is about to face a test that has baffled animals from canaries to dogs. She’s a wild New Caledonian crow, and for the first time, she’s seeing a tidbit of meat dangling on a long string tied to a stick. She perches on the stick, bends down, grabs the string with her beak and pulls. But the string is too long. The meat still hangs out of reach. In similar tests, dogs, pigeons and many other species routinely falter. Some nibble at the string or keep tugging and dropping the same segment. Some pull at a string that’s not connected to food just as readily as a string that is. Eventually many get the hang of reeling in the tidbit, but they seem to learn by trial and error. Zola, however, does not fumble. On her first attempt, she anchors the first length of string by stepping on it and immediately bends down again for the next segment. With several more pulls and steps, Zola reels in the treat. Watching the crow, says Russell Gray, one of the researchers behind the string-pulling experiment, “people say, ‘Wow, it had a flash of insight.’ ” At first glance it seems Zola mentally worked through the problem as a human might, devising a solution in an aha moment. But Gray, of the University of Auckland in New Zealand, has had enough of such supposed animal geniuses. Asking whether the crow solves problems in the same way a human would isn’t a useful question, he says. He warns of a roller coaster that scientists and animal lovers alike can get stuck on: first getting excited and romanticizing a clever animal’s accomplishments, then crashing into disappointment when some killjoy comes up with a mundane explanation that’s not humanlike at all. © Society for Science & the Public 2000 - 2013

Keyword: Intelligence; Aggression
Link ID: 18051 - Posted: 04.20.2013

By STEPHEN CASTLE LONDON — British antitrust authorities on Friday accused the pharmaceuticals giant GlaxoSmithKline of paying three rivals to delay the introduction of a generic version of an antidepressant drug. It is the latest so-called pay-for-delay case drawing scrutiny from regulators on both sides of the Atlantic. The Office of Fair Trading in Britain contended that Glaxo had abused its dominant position in the market, kept prices artificially high and denied “significant cost savings” to Britain’s state-run health provider, the National Health Service. The British case centers on efforts by three companies, Alpharma, Generics (U.K.) and Norton Healthcare, to market an alternative to Seroxat, GlaxoSmithKline’s brand of paroxetine. The company sells it in the United States under the brand name Paxil. In recent years, regulators in Europe and the United States have paid greater attention to pay-for-delay deals, suspecting that they may allow pharmaceutical companies to make big profits by exploiting a brief but lucrative period of monopoly over the supply of a product. “These are blockbuster drugs,” said Farasat Bokhari, a senior lecturer in economics at the University of East Anglia, “so if they are on the market without generics challenging them then companies can maintain high, monopoly profits. “As soon as generic entry takes place,” Mr. Bokhari added, “prices drop significantly, sometimes by up to 70 to 80 percent.” GlaxoSmithKline, according to British authorities, warned the three companies that their generic equivalents would infringe a patent. To resolve the dispute, each of the rivals concluded one or more agreements with GlaxoSmithKline, the Office of Fair Trading said. © 2013 The New York Times Company

Keyword: Depression
Link ID: 18050 - Posted: 04.20.2013

By Puneet Kollipara Brain research has been on a lot of minds lately in the nation’s capital. After offering a brief shout-out to Alzheimer’s research in his February State of the Union address, President Barack Obama went a step further in April by announcing a decade-long effort to develop advanced tools for tracking human brain activity. The administration dubbed it the Brain Research through Advancing Innovative Neurotechnologies initiative, and proposed spending $100 million on the program in the 2014 fiscal year. Scientists have discussed such an endeavor for years, and pushed hard for it in the past few months. Writing March 15 in Science, researchers say the project would develop technologies to probe brain activity on a far greater scale and with higher resolution than is now possible. Current tools can monitor only small numbers of individual neurons at a time or capture blurry, bird’s-eye views of brain activity. The new tools would enable real-time mapping of how the thousands or millions of neurons in coordinated groups, known as circuits, work together. Brain functions — and, in many cases, dysfunctions — are thought to emerge from this still poorly described circuit level. “There’s no way to build a map until you develop the tools,” says Rafael Yuste, a neuroscientist at Columbia University’s Kavli Institute for Brain Science and one of the project’s proponents. Researchers call for developing three sets of tools to better understand brain circuits. One focus is on the creation of tools to measure the activities of all the individual neurons in a circuit. Another is on technologies to experimentally manipulate these neurons. The third tool set would store, analyze and make the data accessible to all researchers. © Society for Science & the Public 2000 - 2013

Keyword: Brain imaging
Link ID: 18046 - Posted: 04.20.2013

By Neuroskeptic A new paper could prompt a rethink of a technique that’s become very hot in neuroscience lately: Confounds in multivariate pattern analysis The authors are Princetonians Michael T. Todd and colleagues, and the method in question is multivariate pattern analysis (MVPA). I’ve written about this before and there’s a blog dedicated to it. MVPA searches for relatively subtle patterns of brain activity, most commonly in fMRI data. For example, a conventional fMRI study might compare activity when someone’s looking at a picture, compared to a blank screen, and would find increases of activity in the visual cortex. But MVPA might take two different pictures, and see if there’s a pattern of activity that’s unique to one picture over the other – even if overall activity in the visual cortex is the same. Neuroscientists have fallen in love with MVPA (and related methods) over the past 5 years, mainly I think because it’s promised to let us ‘read’ the brain: to not just see where in the brain things happen, but to glimpse what information is being represented. In the new paper, Todd et al make a very simple point: all MVPA really shows is that there are places where, in most people’s brain, activity differs when they’re doing one thing as opposed to another. But there infinite reasons why that might be the case, many of them rather trivial. The authors give the example of two very similar tasks, A and B. We’ll say these are imagining apples and imagining bananas. You scan some people doing A and B. You run a standard fMRI analysis, and find that nowhere in the brain shows a difference in activity, on average, between the two (as expected – they are similar.)

Keyword: Brain imaging
Link ID: 18045 - Posted: 04.20.2013

By David Brown, As a bioterrorism agent, ricin has the advantage of being easily made and highly potent. But there have been few fatal cases in the past 50 years, and there is little precise information about the substance’s effects on human beings. Ricin is not a microbe. It does not grow inside the body and can’t be passed from person to person. It is a toxin produced by the castor bean plant. When the beans are crushed for oil, the compound is left behind in the mashed material, of which more than a million tons is produced around the world each year. “It is a plant that grows wild throughout much of North America. You can buy the seeds online,” said Jennifer A. Oakes, a physician and expert in ricin poisoning at Albany Medical College. “It doesn’t take much to get a fatal dose. Somebody could do this in their house if they are motivated to.” Ricin’s best-known victim is Georgi Markov, a Bulgarian journalist who was stabbed by an umbrella on a London street in 1978. The umbrella’s tip injected a tiny metal capsule containing ricin into Markov’s leg. He died three days later. Apart from him, the only other ricin fatalities in the past 50 years have been a few suicides and accidental poisonings, usually after castor beans were eaten but at least once by injecting a crude extract. A person needs to take about 1,000 times as much ricin by mouth as by other routes to get a fatal dose. Unlike nerve agents and botulinum toxin, which disrupt nerve transmission and can cause death in minutes, ricin acts slowly. It stops the synthesis of proteins in cells, killing them over hours or days. A person dies of multi-organ failure as cells break down and fluid and essential electrolytes are lost. © 1996-2013 The Washington Post

Keyword: Neurotoxins
Link ID: 18043 - Posted: 04.18.2013