Chapter 16. None

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By Daisy Yuhas Greetings from Boston where the 21st annual meeting of the Cognitive Neuroscience Society is underway. Saturday and Sunday were packed with symposia, lectures and more than 400 posters. Here are just a few of the highlights. The bilingual brain has been a hot topic at the meeting this year, particularly as researchers grapple with the benefits and challenges of language learning. In news that will make many college language majors happy, a group of researchers led by Harriet Wood Bowden of the University of Tennessee-Knoxville have demonstrated that years of language study alter a person’s brain processing to be more like a native speaker’s brain. They found that native English speaking students with about seven semesters of study in Spanish show very similar brain activation to native speakers when processing spoken Spanish grammar. The study used electroencephalography, or EEG, in which electrodes are placed along the scalp to pick up and measure the electrical activity of neurons in the brain below. By contrast, students who have more recently begun studying Spanish show markedly different processing of these elements of the language. The study focused on the recognition of noun-adjective agreement, particularly in gender and number. Accents, however, can remain harder to master. Columbia University researchers worked with native Spanish speakers to study the difficulties encountered in hearing and reproducing English vowel sounds that are not used in Spanish. The research focused on the distinction between the extended o sound in “dock” and the soft u sound in “duck,” which is not part of spoken Spanish. The scientists used electroencephalograms to measure the brain responses to these vowel sounds in native-English and native-Spanish speakers. © 2014 Scientific American

Keyword: Language
Link ID: 19467 - Posted: 04.10.2014

Claudia Dreifus To Neil H. Shubin’s long résumé — paleontologist, molecular biologist, dean and professor of anatomy at the University of Chicago School of Medicine, best-selling author — can now be added “television host.” Dr. Shubin, 53, who helped discover the 375-million-year-old fish called Tiktaalik, hailed as a missing link between sea and land animals, will preside over “Your Inner Fish,” a three-part series on evolution (based on his book of the same title) that makes its debut Wednesday on PBS. We spoke in Chicago in February and in New York last month. What follows is an edited and condensed version of the conversations. Q. Where did you grow up? A. Suburban Philadelphia. My mom’s a retired nursing home administrator. My father, Seymour Shubin, is a fiction writer. He writes mysteries. My favorite is “The Captain”; it won an Edgar award. He’s an educated man, but science kind of scares him. So when I’m writing, my dad is my target audience. Whenever I hit a tricky scientific concept, I think, “How would I communicate this to him?” This is why my books are written, intentionally, without jargon, which can lead to some gyrations because jargon does have precision. The funny thing is, I’m not sure he always gets what I do. When I first started working on the book version of “Your Inner Fish,” he asked, “Neil, how did you become a scientist?” I thought, “All these years he’s seen me run off to the Arctic, but he’s never been quite sure what I do up there.” So let me ask you his question: How did you become a paleontologist? I was one of those kids with lots of hobbies: astronomy, dinosaurs, collecting rocks, collecting stamps. It all came together when I went to college in New York — Columbia — and volunteered at the American Museum of Natural History. That place was like a playground for me. © 2014 The New York Times Company

Keyword: Evolution
Link ID: 19466 - Posted: 04.10.2014

|By Bret Stetka The data confirm it: farmers are more prone to Parkinson’s than the general population. And pesticides could be to blame. Over a decade of evidence shows a clear association between pesticide exposure and a higher risk for the second most common neurodegenerative disease, after Alzheimer's. A new study published in Neurology proposes a potential mechanism by which at least some pesticides might contribute to Parkinson’s. Regardless of inciting factors — and there appear to be many — Parkinson’s ultimately claims dopamine-releasing neurons in a small, central arc of brain called the “substantia nigra pars compacta.” The nigra normally supplies dopamine to the neighboring striatum to help coordinate movement. Through a series of complex connections, striatal signals then find their way to the motor cortex and voila, we move. But when nigral neurons die, motor function goes haywire and the classic symptoms set in, including namely tremors, slowed movements, and rigidity. Pesticides first came under suspicion as potentially lethal to the nigra in the early 1980s following a tragic designer drug debacle straight out of Breaking Bad. Patients started showing up at Northern California ERs nearly unresponsive, rigid, and tremoring — in other words, severely Parkinsonian. Savvy detective work by neurologist Dr. William Langston and his colleagues, along with the Santa Clara County police, traced the mysterious outbreak to a rogue chemist and a bad batch. He’d been trying to synthesize a “synthetic heroin” — not the snow cone flavorings he claimed — however a powder sample from his garage lab contained traces of an impurity called MPTP. MPTP, it turned out, ravages dopaminergic neurons in the nigra and causes what looks like advanced Parkinson’s. All of the newly Parkinsonian patients were heroin users who had injected the tainted product. And MPTP, it also turned out, is awfully similar in structure to the widely used herbicide paraquat, leading some neurologists to turn their attention to farms and fields. © 2014 Scientific American

Keyword: Parkinsons; Aggression
Link ID: 19463 - Posted: 04.09.2014

Julia Baird SYDNEY, Australia — PRETTY much the No. 1 question you are asked when you’re pregnant is: “Girl or boy?” If you choose not to find out, but to be deliciously surprised at birth, as I did, then you will be asked to guess: “What do you feel it is?” I used to scrunch up my eyes and try hard to draw on what people told me was an age-old female intuition: Which genitals were sprouting in my round belly? I could never tell, though. It is as though the entire world is trying to guess what, or who, is inside you. One oft-told tale is that girls steal your looks and make you fat, while boys just make your belly stick out straight. When I stood wearily bulging at one friend’s baby shower in Manhattan, a stylist confided that she thought our mutual friend was having a boy, because she looked so pretty. Then she looked me up and down: “I think you’re having a girl.” (I placed her in the same category as the neighbor who yelled, “Morning, Fatty!” over the side fence each day.) Why is whether a baby wears blue or pink the most pressing matter for adult acquaintances of a soon-to-be-born? Green is just fine, or white. But a 2007 Gallup poll found that most young Americans, and women under 50, would like to find out the sex of their baby before it is born. In some American fertility clinics, staff experts check the embryo’s sex before they implant it in the womb. So what will it do to our collective minds when forced to grasp that some people are neither gender? Not male, or female, but something else either encompassing, or rejecting, or just adapting from both? Last week, Australia had to grapple with just that after the High Court, in a historic decision, ruled that a person called Norrie May-Welby could register as “nonspecific” on official certificates. Now 52, Norrie was identified, physically, as male when she was born, in Scotland, but was drawn to the world of girls, playing with dolls at age 4 and tying her school tie around her head at night to create the illusion of long hair. She escaped into the library monitors’ group at school and made up adventures where she played six characters, five of whom were female: “I didn’t think there was any problem with this,” she says. “After all, just because I wasn’t really from Krypton, didn’t mean I couldn’t imagine being Supergirl.” © 2014 The New York Times Company

Keyword: Sexual Behavior
Link ID: 19462 - Posted: 04.09.2014

By: Larry Cahill, Ph.D. Early in 2013, the Food and Drug Administration (FDA) ordered the makers of the well-known sleep aid Ambien (zolpidem) to cut their recommended dose in half-but only for women. In essence, the FDA was acknowledging that despite extensive testing prior to the drug's release on the market, millions of women had been overdosing on Ambien for 20 years. On February 9, 2014, CBS's 60 Minutes highlighted this fact-and sex differences in general-by powerfully asking two questions: Why did this happen, and are men and women treated equally in research and medicine?1 The answer to the first question is that the biomedical community has long operated on what is increasingly being viewed as a false assumption: that biological sex matters little, if at all, in most areas of medicine. The answer to the second question is no, today's biomedical research establishment is not treating men and women equally. What are some of the key reasons for the biomedical community's false assumption, and why is this situation now finally changing? What are some of the seemingly endless controversies about sex differences in the brain generated by "anti-sex difference" investigators? And what lies at the root of the resistance to sex differences research in the human brain? For a long time, for most aspects of brain function, sex influences hardly mattered to the neuroscience mainstream. The only sex differences that concerned most neuroscientists involved brain regions (primarily a deep-brain structure called the hypothalamus) that regulate both sex hormones and sexual behaviors.2 Neuroscientists almost completely ignored possible sex influences on other areas of the brain, assuming that the sexes shared anything that was fundamental when it came to brain function. Conversely, the neuroscience mainstream viewed any apparent sex differences in the brain as not fundamental- something to be understood after they grasped the fundamental facts. By this logic, it was not a problem to study males almost exclusively, since doing so supposedly allowed researchers to understand all that was fundamental in females without having to consider the complicating aspects of female hormones. To this day, neuroscientists overwhelmingly study only male animals.3 © 2014 The Dana Foundation

Keyword: Sexual Behavior
Link ID: 19461 - Posted: 04.09.2014

By BENEDICT CAREY Therapists who specialize in autism often use a child’s own interests, toys or obsessions as a way to connect, and sometimes to reward effort and progress on social skills. The more eye contact a child makes, for example, the more play time he or she gets with those precious maps or stuffed animals. But now a group of scientists and the author of a new book are suggesting that those favorite activities could be harnessed in a deeper, more organic way. If a child is fascinated with animated characters like Thomas the Tank Engine, why not use those characters to prompt and reinforce social development? Millions of parents do this routinely, if not systematically, flopping down on the floor with a socially distant child to playact the characters themselves. “We individualize therapy to each child already, so if the child has an affinity for certain animated characters, it’s absolutely worth studying a therapy that incorporates those characters meaningfully,” said Kevin Pelphrey, director of the child neuroscience laboratory at Yale. He and several other researchers, including John D. E. Gabrieli of M.I.T., Simon Baron-Cohen of the University of Cambridge and Pamela Ventola of Yale, are proposing a study to test the approach. The idea came from Ron Suskind, a former Wall Street Journal reporter whose new book “Life, Animated” describes his family’s experience reaching their autistic son, Owen, through his fascination with Disney movies like “The Little Mermaid” and “Beauty and the Beast.” It was Mr. Suskind’s story that first referred to ‘“affinity therapy.” He approached the researchers to put together a clinical trial based on the idea that some children can develop social and emotional instincts through the characters they love. Experts familiar with his story say the theory behind the therapy is plausible, given what’s known from years of studying the effects of other approaches. © 2014 The New York Times Company

Keyword: Autism
Link ID: 19459 - Posted: 04.08.2014

By Paul D. Thacker When the FDA denied Sprout Pharmaceutical’s bid last October to begin marketing flibanserin, a drug aimed at treating low sexual desire in women, women’s groups responded in anger. In January, representatives from eight different women’s groups, including the National Organization of Women, met with Janet Woodcock, the FDA’s head of pharmaceuticals, to protest the decision. Congress also got in on the act, with Reps. Debbie Wasserman Schultz, Chellie Pingree, Nita Lowey, and Louise Slaughter sending a letter to FDA Commissioner Margaret Hamburg to implore that, when evaluating drugs for female dysfunction (in medical terms Hypoactive Sexual Desire Disorder, or HSDD), Dr. Hamburg apply "the same standards of consideration given to the approved drugs for men in your risk/benefit evaluation." “We’ve now got 24 drugs for men for either testosterone replacement or erectile dysfunction,” Cindy Whitehead, Sprout’s chief operating officer told the Associated Press. “Yet there are zero drugs for the most common form of sexual dysfunction in women.” Anita H. Clayton, the interim chair of the department of psychiatry and neurobehavioral sciences at the University of Virginia School of Medicine, was more explicit, writing in a blistering column for the Huffington Post: “For the millions of women with HSDD, the FDA must overcome the problem of institutionalized sexism—unconscious and perhaps unintended, but damaging nonetheless.” The chorus was loud and clear: The FDA is sexist. The federal agency charged with approving drugs to protect and improve our health is now standing in the way of a woman’s right to have a satisfying sex life. This framing played out in numerous stories, with similar charges appearing in the American Prospect (“the FDA’s kinda sexist”), and the Washington Post (“Some critics say the agency—consciously or not—may be succumbing to society’s squeam­ishness about women’s sexual desires compared with those of men”). Not to be outdone with mere institutional sexism, a writer for the Wire mused whether “blatant, medieval sexism is also at play.” © 2014 The Slate Group LLC.

Keyword: Sexual Behavior
Link ID: 19458 - Posted: 04.08.2014

By JoNel Aleccia The engineer who drove a speeding commuter train off the rails in New York last year may have suffered from the most severe form of a dangerous sleep disorder, but health experts say he has plenty of company. As many as 22 million people in the U.S. — or up to 7 percent of the population — may suffer from obstructive sleep apnea, experts say. It’s a condition that causes airways to collapse during sleep, cutting off breathing dozens or sometimes hundreds of times a night, leaving them bleary-eyed and drowsy, even after a full night’s rest. William Rockefeller, 46, was diagnosed after the December 2013 crash that killed four and injured more than 70 with severe obstructive sleep apnea, documents released this week show. On a scale where as few as five sleep disruptions an hour can make someone sleepy, and 30 episodes are considered severe, Rockefeller logged about 66 arousals an hour, doctors said. “His sleep was really fragmented,” said Dr. Phyllis Zee, a sleep expert with the Northwestern Medicine Sleep and Circadian Rhythms Research Program. “Even if he were to sleep seven or eight hours, he would be sleep-deprived.” Zee and her colleagues suspected that Rockefeller might suffer from sleep deprivation. He was obese, records show, and there’s a certain fatigued look that she saw in news photos of the engineer. “That was one of my thoughts, ‘Oh my goodness, he has (OSA),’” she said.

Keyword: Sleep
Link ID: 19457 - Posted: 04.08.2014

By KENNETH CHANG This occasional column explores topics covered in Science Times 25 years ago to see what has changed — and what has not. The claim about babies was startling: A test administered to infants as young as 6 months could predict their score on an intelligence test years later, when they started school. “Why not test infants and find out which of them could take more in terms of stimulation?” Joseph F. Fagan III, the psychologist at Case Western Reserve University in Cleveland who developed the test, was quoted as saying in an article by Gina Kolata on April 4, 1989. “It’s not going to hurt anybody, that’s for sure.” In the test, the infant looks at a series of photographs — first a pair of identical faces, then the same face paired with one the baby hasn’t seen. The researchers measure how long the baby looks at the new face. “On the surface, it tests novelty preference,” said Douglas K. Detterman, a colleague of Dr. Fagan’s at Case Western. For reasons not quite understood, babies of below-average intelligence do not exhibit the same attraction to novelty. Dr. Fagan suggested that the test could be used to identify children with above-average intelligence in poorer families so they could be exposed to enrichment programs more readily available to wealthier families. But his primary motivation, said Cynthia R. Holland, his wife and longtime collaborator, was to look for babies at the other end of the intelligence curve, those who would fall behind as they grew up. “His hope was always was to identify early on, in the first year of life, kids who were at risk, cognitively, so we could focus our resources on them and help them out,” said Dr. Holland, a professor of psychology at Cuyahoga Community College. 25 YEARS LATER For the most part, the validity of the Fagan test holds up. Indeed, Dr. Fagan (who died last August) and Dr. Holland revisited infants they had tested in the 1980s, and found that the Fagan scores were predictive of the I.Q. and academic achievement two decades later when these babies turned 21. © 2014 The New York Times Company

Keyword: Intelligence; Aggression
Link ID: 19456 - Posted: 04.08.2014

By Sam Kean Kent Cochrane, the amnesiac known throughout the world of neuroscience and psychology as K.C., died last week at age 62 in his nursing home in Toronto, probably of a stroke or heart attack. Although not as celebrated as the late American amnesiac H.M., for my money K.C. taught us more important and poignant things about how memory works. He showed how we make memories personal and personally meaningful. He also had a heck of a life story. During a wild and extended adolescence, K.C. jammed in rock bands, partied at Mardi Gras, played cards till all hours, and got into fights in bars; he was also knocked unconscious twice, once in a dune-buggy accident, once when a bale of hay conked him on the head. In October 1981, at age 30, he skidded off an exit ramp on his motorcycle. He spent a month in intensive care and lost, among other brain structures, both his hippocampuses. As H.M.’s case demonstrated in the early 1950s, the hippocampus—you have one in each hemisphere of your brain—helps form and store new memories and retrieve old ones. Without a functioning hippocampus, names, dates, and other information falls straight through the mind like a sieve. At least that’s what supposed to happen. K.C. proved that that’s not quite true—memories can sometimes bypass the hippocampus. After the motorcycle accident, K.C. lost most of his past memories and could make almost no new memories. But a neuroscientist named Endel Tulving began studying K.C., and he determined that K.C. could remember certain things from his past life just fine. Oddly, though, everything K.C. remembered fell within one restricted category: It was all stuff you could look up in reference books, like the difference between stalactites and stalagmites or between spares and strikes in bowling. Tulving called these bare facts “semantic memories,” memories devoid of all context and emotion. © 2014 The Slate Group LLC

Keyword: Learning & Memory
Link ID: 19455 - Posted: 04.08.2014

By ANA GANTMAN and JAY VAN BAVEL TAKE a close look at your breakfast. Is that Jesus staring out at you from your toast? Such apparitions can be as lucrative as they are seemingly miraculous. In 2004, a Florida woman named Diane Duyser sold a decade-old grilled cheese sandwich that bore a striking resemblance to the Virgin Mary. She got $28,000 for it on eBay. The psychological phenomenon of seeing something significant in an ambiguous stimulus is called pareidolia. Virgin Mary grilled cheese sandwiches and other pareidolia remind us that almost any object is open to multiple interpretations. Less understood, however, is what drives some interpretations over others. In a forthcoming paper in the journal Cognition, we hope to shed some light on that question. In a series of experiments, we examined whether awareness of perceptually ambiguous stimuli was enhanced by the presence of moral content. We quickly flashed strings of letters on a computer screen and asked participants to indicate whether they believed each string formed a word or not. To ensure that the letter strings were perceptually ambiguous, we flashed them between approximately 40 and 70 milliseconds. (When they were presented for too long, people easily saw all the letter strings and demonstrated close to 100 percent accuracy. When they were presented too quickly, people were unable to see the words and performed “at chance,” around 50 percent accuracy.) Some of the strings of letters we flashed were words, others were not. Importantly, some of the words we flashed had moral content (virtue, steal, God) and others did not (virtual, steel, pet). Over the course of three experiments, we found that participants correctly identified strings of letters as words more often when they formed moral words (69 percent accuracy) than when they formed nonmoral words (65 percent accuracy). This suggested that moral content gave a “boost” to perceptually ambiguous stimuli — a shortcut to conscious awareness. We call this phenomenon the “moral pop-out effect.” © 2014 The New York Times Company

Keyword: Attention
Link ID: 19453 - Posted: 04.07.2014

By GRETCHEN REYNOLDS Age-related vision loss is common and devastating. But new research suggests that physical activity might protect our eyes as we age. There have been suggestions that exercise might reduce the risk of macular degeneration, which occurs when neurons in the central part of the retina deteriorate. The disease robs millions of older Americans of clear vision. A 2009 study of more than 40,000 middle-aged distance runners, for instance, found that those covering the most miles had the least likelihood of developing the disease. But the study did not compare runners to non-runners, limiting its usefulness. It also did not try to explain how exercise might affect the incidence of an eye disease. So, more recently, researchers at Emory University in Atlanta and the Atlanta Veterans Administration Medical Center in Decatur, Ga., took up that question for a study published last month in The Journal of Neuroscience. Their interest was motivated in part by animal research at the V.A. medical center. That work had determined that exercise increases the levels of substances known as growth factors in the animals’ bloodstream and brains. These growth factors, especially one called brain-derived neurotrophic factor, or B.D.N.F., are known to contribute to the health and well-being of neurons and consequently, it is thought, to improvements in brain health and cognition after regular exercise. But the brain is not the only body part to contain neurons, as the researchers behind the new study knew. The retina does as well, and the researchers wondered whether exercise might raise levels of B.D.N.F. there, too, potentially affecting retinal health and vision. © 2014 The New York Times Company

Keyword: Vision
Link ID: 19451 - Posted: 04.07.2014

by Clare Wilson A genetic tweak can make light work of some nervous disorders. Using flashes of light to stimulate modified neurons can restore movement to paralysed muscles. A study demonstrating this, carried out in mice, lays the path for using such "optogenetic" approaches to treat nerve disorders ranging from spinal cord injury to epilepsy and motor neuron disease. Optogenetics has been hailed as one of the most significant recent developments in neuroscience. It involves genetically modifying neurons so they produce a light-sensitive protein, which makes them "fire", sending an electrical signal, when exposed to light. So far optogenetics has mainly been used to explore how the brain works, but some groups are exploring using it as therapy. One stumbling block has been fears about irreversibly genetically manipulating the brain. In the latest study, a team led by Linda Greensmith of University College London altered mouse stem cells in the lab before transplanting them into nerves in the leg – this means they would be easier to remove if something went wrong. "It's a very exciting approach that has a lot of potential," says Ziv Williams of Harvard Medical School in Boston. Greensmith's team inserted an algal gene that codes for a light-responsive protein into mouse embryonic stem cells. They then added signalling molecules to make the stem cells develop into motor neurons, the cells that carry signals to and from the spinal cord to the rest of the body. They implanted these into the sciatic nerve – which runs from the spinal cord to the lower limbs – of mice whose original nerves had been cut. © Copyright Reed Business Information Ltd.

Keyword: Movement Disorders
Link ID: 19450 - Posted: 04.05.2014

By LISA SANDERS, M.D. On Thursday, we challenged Well readers to solve the mystery of a 23-year-old man with episodes of aggressive, manic behavior that couldn’t be controlled. Nearly 1,000 readers wrote in with their take on this terrifying case. More than 300 of you got the right class of disease, and 21 of you nailed the precise form of the disorder. Amazing! The correct diagnosis is … Variegate porphyria The first person with the correct answer was Francis Graziano, a 23-year-old recent graduate of the University of Michigan. His major in neuroscience really gave him a leg up on this case, he told me. He recalled a case he read of a young Vietnam veteran with symptoms of porphyria. He’s a surgical technician right now, waiting to hear where he’ll be going to medical school next year. Strong work, Dr.-to-be Graziano! The Diagnosis: The word porphyria comes from the ancient Greek word for purple, “porphyra,” because patients with this disease can have purplish-red urine, tears or saliva. The porphyrias are a group of rare genetic diseases that develop in patients born without the machinery to make certain essential body chemicals, including one of the most important parts of blood known as heme. This compound makes up the core of the blood component hemoglobin. (The presence of heme is why blood is red.) Patients who can’t make heme correctly end up with too much of its chemical precursors, known as porphyrins. The excess porphyrins injure tissues throughout the body, but especially in the nervous system. The disorder is characterized by frequent episodes of debilitating back or abdominal pain and is often accompanied by severe psychiatric symptoms. Patients with porphyria do not respond to most psychiatric medications. Indeed, many of these drugs make the symptoms of porphyria worse. © 2014 The New York Times Company

Keyword: Schizophrenia
Link ID: 19448 - Posted: 04.05.2014

Walking backward may seem a simple task, but researchers don’t know how the mind controls this behavior. A study published online today in Science provides the first glimpse of the brain circuit responsible—at least in fruit flies. Geneticists created 3500 strains of the insects, each with a temperature-controlled switch that turned random networks of neurons on when the flies entered an incubator. One mutant batch of fruit flies started strolling in reverse when exposed to warmth (video, right panel), which the team dubbed “moonwalkers,” in honor of Michael Jackson’s famous dance. Two neurons were responsible for the behavior. One lived in the brain and extended its connections to the end of the ventral nerve cord—the fly’s version of a spine, which runs along its belly. The other neuron had the opposite orientation—it started at the bottom of the nerve cord and sent its messaging cables—or axons—into the brain. The neuron in the brain acted like a reverse gear in a car; when turned on, it triggered reverse walking. The researchers say this neuron is possibly a command center that responds to environmental cues, such as, “Hey! I see a wall in front of me.” The second neuron functioned as the brakes for forward motion, but it couldn’t compel the fly to moonwalk. It may serve as a fail-safe that reflexively prevents moving ahead, such as when the fly accidentally steps onto a very cold floor. Using the two neurons as a starting point, the team will trace their links to sensory neurons for touch, sight, and smell, which feed into and control the moonwalking network. No word yet on the neurons responsible for the Macarena. © 2014 American Association for the Advancement of Science

Keyword: Movement Disorders
Link ID: 19445 - Posted: 04.05.2014

He was known in his many appearances in the scientific literature as simply K.C., an amnesiac who was unable to form new memories. But to the people who knew him, and the scientists who studied him for decades, he was Kent Cochrane, or just Kent. Cochrane, who suffered a traumatic brain injury in a motorcycle accident when he was 30 years old, helped to rewrite the understanding of how the brain forms new memories and whether learning can occur without that capacity. "From a scientific point of view, we've really learned a lot [from him], not just about memory itself but how memory contributes to other abilities," said Shayna Rosenbaum, a cognitive neuropsychologist at York University who started working with Cochrane in 1998 when she was a graduate student. Cochrane was 62 when he died late last week. The exact cause of death is unknown, but his sister, Karen Casswell, said it is believed he had a heart attack or stroke. He died in his room at an assisted living facility where he lived and the family opted not to authorize an autopsy. Few in the general public would know about Cochrane, though some may have seen or read media reports on the man whose life was like that of the lead character of the 2000 movie Memento. But anyone who works on the science of human memory would know K.C. Casswell and her mother, Ruth Cochrane, said the family was proud of the contribution Kent Cochrane made to science. Casswell noted her eldest daughter was in a psychology class at university when the professor started to lecture about the man the scientific literature knows as K.C. © CBC 2014

Keyword: Learning & Memory
Link ID: 19442 - Posted: 04.03.2014

Dr Nicola Davis The electronic nose in an instrument that attempts to mimic the human olfactory system. Humans and animals don't identify specific chemicals within odours; what they do is to recognise a smell based on a response pattern. You, as a human, will smell a strawberry and say "that's a strawberry". If you gave this to a traditional analytical piece of equipment, it might tell you what the 60-odd chemicals in the odour were - but that wouldn't tell you that it was a strawberry. How does it work? A traditional electronic nose has an array of chemical sensors, designed either to detect gases or vapours. These sensors are not tuned to a single chemical, but detect families of chemicals - [for example] alcohols. Each one of these sensors is different, so when they are presented to a complex odour formed of many chemicals, each sensor responds differently to that odour. This creates a pattern of sensor responses, which the machine can be taught [to recognise]. Can't we just use dogs? A dog is very, very sensitive. Special research teams work on training dogs to detect cancers as you would do explosives. What you we are trying to do with the electronic nose is create an artificial means of replicating what the dog does. Such machines have the advantage that they don't get tired, will work all day and you only need to feed them electricity. © 2014 Guardian News and Media Limited

Keyword: Chemical Senses (Smell & Taste); Aggression
Link ID: 19441 - Posted: 04.03.2014

Erika Check Hayden Monkeys on a reduced-calorie diet live longer than those that can eat as much as they want, a new study suggests. The findings add to a thread of studies on how a restricted diet prolongs life in a range of species, but they complicate the debate over whether the research applies to animals closely related to humans. In the study, which has been running since 1989 at the Wisconsin National Primate Research Center in Madison, 38 rhesus macaques (Macaca mulatta) that were allowed to eat whatever they wanted were nearly twice as likely to die at any age than were 38 monkeys whose calorie intakes were cut by 30%1. The same study reported2 in 2009 that calorie-restricted monkeys were less likely to die of age-related causes than control monkeys, but had similar overall mortality rates at all ages. “We set out to test the hypothesis: would calorie restriction delay ageing? And I think we've shown that it does,” says Rozalyn Anderson, a biochemist at the University of Wisconsin who led the study, which is published today in Nature Communications. She said it is not surprising that the 2009 paper did not find that the calorie-restricted monkeys lived longer, because at the time too few monkeys had died to prove the point. Eating a very low-calorie diet has been shown3 to prolong the lives of mice, leading to speculation that such a diet triggers a biochemical pathway that promotes survival. But what that pathway might be — and whether humans have it — has been a matter of hot debate. Eat to live In 2012, a study at the US National Institute on Aging (NIA) in Bethesda, Maryland, cast doubt on the idea, reporting4 that monkeys on low-calorie diets did not live longer than those that ate more food. But Anderson says that the Wisconsin findings are good news. © 2014 Nature Publishing Group

Keyword: Obesity
Link ID: 19439 - Posted: 04.02.2014

Neandertals and modern Europeans had something in common: They were fatheads of the same ilk. A new genetic analysis reveals that our brawny cousins had a number of distinct genes involved in the buildup of certain types of fat in their brains and other tissues—a trait shared by today’s Europeans, but not Asians. Because two-thirds of our brains are built of fatty acids, or lipids, the differences in fat composition between Europeans and Asians might have functional consequences, perhaps in helping them adapt to colder climates or causing metabolic diseases. “This is the first time we have seen differences in lipid concentrations between populations,” says evolutionary biologist Philipp Khaitovich of the CAS-MPG Partner Institute for Computational Biology in Shanghai, China, and the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, lead author of the new study. “How our brains are built differently of lipids might be due to Neandertal DNA.” Ever since researchers at the Max Planck sequenced the genome of Neandertals, including a super high-quality genome of a Neandertal from the Altai Mountains of Siberia in December, researchers have been comparing Neandertal DNA with that of living people. Neandertals, who went extinct 30,000 years ago, interbred with modern humans at least once in the past 60,000 years, probably somewhere in the Middle East. Because the interbreeding happened after moderns left Africa, today’s Africans did not inherit any Neandertal DNA. But living Europeans and Asians have inherited a small amount—1% to 4% on average. So far, scientists have found that different populations of living humans have inherited the Neandertal version of genes that cause diabetes, lupus, and Crohn’s disease; alter immune function; and affect the function of the protein keratin in skin, nails, and hair. © 2014 American Association for the Advancement of Science.

Keyword: Evolution; Aggression
Link ID: 19438 - Posted: 04.02.2014

By NATALIE ANGIER The “Iliad” may be a giant of Western literature, yet its plot hinges on a human impulse normally thought petty: spite. Achilles holds a festering grudge against Agamemnon (“He cheated me, wronged me ... He can go to hell...”) turning down gifts, homage, even the return of his stolen consort Briseis just to prolong the king’s suffering. Now, after decades of focusing on such staples of bad behavior as aggressiveness, selfishness, narcissism and greed, scientists have turned their attention to the subtler and often unsettling theme of spite — the urge to punish, hurt, humiliate or harass another, even when one gains no obvious benefit and may well pay a cost. Psychologists are exploring spitefulness in its customary role as a negative trait, a lapse that should be embarrassing but is often sublimated as righteousness, as when you take your own sour time pulling out of a parking space because you notice another car is waiting for it and you’ll show that vulture who’s boss here, even though you’re wasting your own time, too. Evolutionary theorists, by contrast, are studying what might be viewed as the brighter side of spite, and the role it may have played in the origin of admirable traits like a cooperative spirit and a sense of fair play. The new research on spite transcends older notions that we are savage, selfish brutes at heart, as well as more recent suggestions that humans are inherently affiliative creatures yearning to love and connect. Instead, it concludes that vice and virtue, like the two sides of a V, may be inextricably linked. “Spitefulness is such an intrinsically interesting subject, and it fits with so many people’s everyday experience, that I was surprised to see how little mention there was of it in the psychology literature,” said David K. Marcus, a psychologist at Washington State University. At the same time, he said, “I was thrilled to find something that people haven’t researched to exhaustion.” © 2014 The New York Times Company

Keyword: Emotions; Aggression
Link ID: 19436 - Posted: 04.01.2014