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Nell Greenfieldboyce The state of New Jersey has been trying to help jurors better assess the reliability of eyewitness testimony, but a recent study suggests that the effort may be having unintended consequences. That's because a new set of instructions read to jurors by a judge seems to make them skeptical of all eyewitness testimony — even testimony that should be considered reasonably reliable. Back in 2012, New Jersey's Supreme Court did something groundbreaking. It said that in cases that involve eyewitness testimony, judges must give jurors a special set of instructions. The instructions are basically a tutorial on what scientific research has learned about eyewitness testimony and the factors that can make it more dependable or less so. "The hope with this was that jurors would then be able to tell what eyewitness testimony was trustworthy, what sort wasn't, and at the end of the day it would lead to better decisions, better court outcomes, better justice," says psychologist David Yokum. Yokum was a graduate student at the University of Arizona, doing research on decision-making, when he and two colleagues, Athan Papailiou and Christopher Robertson, decided to test the effect of these new jury instructions, using videos of a mock trial that they showed to volunteers. © 2016 npr
Keyword: Learning & Memory
Link ID: 21828 - Posted: 01.27.2016
Jim Pfaus Self-labeled sex addicts often speak about their identities very clinically, as if they’re paralyzed by a scientific condition that functions the same way as drug and alcohol addiction. But sex and porn “addiction” are NOT the same as alcoholism or a cocaine habit. In fact, hypersexuality and porn obsessions are not addictions at all. They’re not included in the Diagnostic and Statistical Manual of Mental Disorders (DSM), and by definition, they don’t constitute what most researchers understand to be addiction. Here’s why: addicts withdraw. When you lock a dope fiend in a room without any dope, the lack of drugs will cause an immediate physiological response — some of which is visible, some of which we can only track from within the body. During withdrawal, the brains of addicts create junctions between nerve cells containing the neurotransmitter GABA. This process more or less inhibits the brain systems usually excited by drug-related cues — something we never see in the brains of so-called sex and porn addicts. A sex addict without sex is much more like a teenager without their smartphone. Imagine a kid playing Angry Birds. He seems obsessed, but once the game is off and it’s time for dinner, he unplugs. He might wish he was still playing, but he doesn’t get the shakes at the dinner table. There’s nothing going on in his brain that creates an uncontrollable imbalance.
By Jane E. Brody. About 15 years ago, I was invited to join a knitting group. My reluctant response — “When would I do that?” — was rejoined with “Monday afternoons at 4,” at a friend’s home not three minutes’ walk from my own. I agreed to give it a try. My mother had taught me to knit at 15, and I knitted in class throughout college and for a few years thereafter. Then decades passed without my touching a knitting needle. But within two Mondays in the group, I was hooked, not only on knitting but also on crocheting, and I was on my way to becoming a highly productive crafter. I’ve made countless afghans, baby blankets, sweaters, vests, shawls, scarves, hats, mittens, caps for newborns and two bedspreads. I take a yarn project with me everywhere, especially when I have to sit still and listen. As I’d discovered in college, when my hands are busy, my mind stays focused on the here and now. It seems, too, that I’m part of a national resurgence of interest in needle and other handicrafts, and not just among old grannies like me. The Craft Yarn Council reports that a third of women ages 25 to 35 now knit or crochet. Even men and schoolchildren are swelling the ranks, among them my friend’s three grandsons, ages 6, 7 and 9. Last April, the council created a “Stitch Away Stress” campaign in honor of National Stress Awareness Month. Dr. Herbert Benson, a pioneer in mind/body medicine and author of “The Relaxation Response,” says that the repetitive action of needlework can induce a relaxed state like that associated with meditation and yoga. Once you get beyond the initial learning curve, knitting and crocheting can lower heart rate and blood pressure and reduce harmful blood levels of the stress hormone cortisol. But unlike meditation, craft activities result in tangible and often useful products that can enhance self-esteem. I keep photos of my singular accomplishments on my cellphone to boost my spirits when needed. © 2016 The New York Times Company
Link ID: 21826 - Posted: 01.27.2016
James Gorman Spotted hyenas are the animals that got Sarah Benson-Amram thinking about how smart carnivores are and in what ways. Dr. Benson-Amram, a researcher at the University of Wyoming in Laramie, did research for her dissertation on hyenas in the wild under Kay E. Holekamp of Michigan State University. Hyenas have very complicated social structures and they require intelligence to function in their clans, or groups. But the researchers also tested the animals on a kind of intelligence very different from figuring out who ranks the highest: They put out metal boxes that the animals had to open by sliding a bolt in order to get at meat inside. Only 15 percent of the hyenas solved the problem in the wild, but in captivity, the animals showed a success rate of 80 percent. Dr. Benson-Amram and Dr. Holekamp decided to test other carnivores, comparing species and families. They and other researchers presented animals in several different zoos with a metal puzzle box with a treat inside and recorded the animals’ efforts. They tested 140 animals in 39 species that were part of nine families. They reported their findings on Monday in the Proceedings of the National Academy of Sciences. They compared the success rates of different families with absolute brain size, relative brain size, and the size of the social groups that the species form in the wild. Just having a bigger brain did not make difference, but the relative size of the brain, compared with the size of the body, was the best indication of which animals were able to solve the problem of opening the box. © 2016 The New York Times Company
Ian Sample Science editor Genetically modified (GM) monkeys that develop symptoms of autism have been created to help scientists discover treatments for the condition. The macaques carry a genetic fault that causes a rare disorder in humans called MeCP2 duplication syndrome. This produces a wide range of medical conditions, some of which mirror those seen in autism, such as difficulties with social interactions. Researchers say groups of the GM monkeys could be used to identify brain circuits involved in common autistic behaviours and to test new treatments designed to alleviate the symptoms. Because the monkeys pass the genetic defects on to their offspring, scientists can breed large populations of the animals for medical research. A group of 200 monkeys has been established at the scientists’ lab in China. The research, described in the journal Nature, paves the way for more varieties of GM monkeys that develop different mental and psychiatric problems which are almost impossible to study in other animals. “The first cohort of transgenic monkeys shows very similar behaviour to human autism, including increased anxiety, but most importantly, defects in social interactions,” said Zilong Qiu who led the research at the Institute of Neuroscience in Shanghai. © 2016 Guardian News and Media Limited or it
by Bethany Brookshire Unless you’re in the middle of biting into a delicious Reuben sandwich, you might forget that taste is one of the fundamental senses. “It’s required for our enjoyment of food,” explains Emily Liman, a taste researcher at the University of Southern California in Los Angeles. “Without taste … people stop eating. They don’t enjoy their food.” A life without the sweet jolt of sugar or the savory delights of umami seems, well, tasteless. When you put that mouthwatering combination of corned beef, Swiss cheese, Thousand Island dressing, sauerkraut and rye in your mouth, the chemicals in the sandwich stimulate taste buds on your tongue and soft palate. Those taste buds connect to the ends of nerve fibers extending delicately into the mouth. Those nerve fibers are the ends of cells located in the geniculate ganglion, a ball of cells nestled up against the ear canal on the side of your head. From there, taste sensations head toward the brain. Chemical messengers bridge the gap between the taste bud and the end of the nerve fiber. But what chemical is involved depends on the type of cell within the bud. There are three types of taste cells (imaginatively titled I, II and III). Type I is not well-understood, but it may be a kind of support cell for other taste cells. Type II, in contrast, is better known. These taste cells sense the slight bitterness of the rye seeds, the sweet edge of the Thousand Island dressing and the savory umami of the beef. They pass that delightful message on using the chemical ATP. © Society for Science & the Public 2000 - 2016
Alison Abbott For the second time in four months, researchers have reported autopsy results that suggest Alzheimer’s disease might occasionally be transmitted to people during certain medical treatments — although scientists say that neither set of findings is conclusive. The latest autopsies, described in the Swiss Medical Weekly1 on 26 January, were conducted on the brains of seven people who died of the rare, brain-wasting Creutzfeldt–Jakob disease (CJD). Decades before their deaths, the individuals had all received surgical grafts of dura mater — the membrane that covers the brain and spinal cord. These grafts had been prepared from human cadavers and were contaminated with the prion protein that causes CJD. But in addition to the damage caused by the prions, five of the brains displayed some of the pathological signs that are associated with Alzheimer’s disease, researchers from Switzerland and Austria report. Plaques formed from amyloid-β protein were discovered in the grey matter and blood vessels. The individuals, aged between 28 and 63, were unusually young to have developed such plaques. A set of 21 controls, who had not had surgical grafts of dura mater but died of sporadic CJD at similar ages, did not have this amyloid signature. According to the authors, it is possible that the transplanted dura mater was contaminated with small ‘seeds’ of amyloid-β protein — which some scientists think could be a trigger for Alzheimer’s — along with the prion protein that gave the recipients CJD. © 2016 Nature Publishing Group,
By Esther Landhuis Amid gloomy reports of an impending epidemic of Alzheimer’s and other dementias, emerging research offers a promising twist. Recent studies in North America, the U.K. and Europe suggest that dementia risk among seniors in some high-income countries has dropped steadily over the past 25 years. If the trend is driven by midlife factors such as building “brain reserve” and maintaining heart health, as some experts suspect, this could lend credence to staying mentally engaged and taking cholesterol-lowering drugs as preventive measures. At first glance, the overall message seems somewhat confusing. Higher life expectancy and falling birth rates are driving up the global elderly population. “And if there are more 85-year-olds, it’s almost certain there will be more cases of age-related diseases,” says Ken Langa, professor of internal medicine at the University of Michigan. According to the World Alzheimer Report 2015 (pdf), 46.8 million people around the globe suffered from dementia last year, and that number is expected to double every 20 years. Looking more closely, though, new epidemiological studies reveal a surprisingly hopeful trend. Analyses conducted over the last decade in the U.S., Canada, England, the Netherlands, Sweden and Denmark suggest that “a 75- to 85-year-old has a lower risk of having Alzheimer’s today than 15 or 20 years ago,” says Langa, who discussed the research on falling dementia rates in a 2015 Alzheimer’s Research & Therapy commentary (pdf). © 2016 Scientific America
Link ID: 21821 - Posted: 01.26.2016
by Graham McDougall, Jr., behavioral scientist at U. of Alabama Chemo brain is a mental cloudiness reported by about 30 percent of cancer patients who receive chemotherapy. Symptoms typically include impairments in attention, concentration, executive function, memory and visuospatial skills. Since the 1990s researchers have tried to understand this phenomenon, particularly in breast cancer patients. But the exact cause of chemo brain remains unclear. Some studies indicate that chemotherapy may trigger a variety of related neurological symptoms. One study, which examined the effects of chemotherapy in 42 breast cancer patients who underwent a neuropsychological evaluation before and after treatment, found that almost three times more patients displayed signs of cognitive dysfunction after treatment as compared with before (21 versus 61 percent). A 2012 review of 17 studies considering 807 breast cancer patients found that cognitive changes after chemotherapy were pervasive. Other research indicates that the degree of mental fogginess that a patient experiences may be directly related to how much chemotherapy that person receives: higher doses lead to greater dysfunction. There are several possible mechanisms to explain the cognitive changes associated with chemotherapy treatments. The drugs may have direct neurotoxic effects on the brain or may indirectly trigger immunological responses that may cause an inflammatory reaction in the brain. Chemotherapy, however, is not the only possible culprit. Research also shows that cancer itself may cause changes to the brain. In addition, it is possible that the observed cognitive decline may simply be part of the natural aging process, especially considering that many cancer patients are older than 50 years. © 2016 Scientific American,
Tash Reith-Banks I discovered Rob Newman’s comedy when I was 16. His shows were relentless: packed full of quotes, arguments, anger, history, philosophy and, above all, bladder-ruining laughs. Oil, urban angst, war, climate change and capitalism – Newman tore into all of these subject and more with verve, wit, and what must have been a well-used library card. Twenty years on his latest piece, The Brain Show, finds Newman on good form. He’s less angry young man, more genial, worried uncle. The laughs are still very much there, perhaps a shade gentler. One thing is still guaranteed: you’ll leave with a brain significantly fuller than before and a long reading list. The show itself majors on a sceptical look at neuroscience, especially what Newman sees as attempts to reduce the human brain to the status of a “wet computer”. He pours particular scorn on two experiments aimed at portioning the brain into neat, discrete emotional zones; he feels similarly about geneticists who think they can identify a homelessness gene, or one for low-voter turnout. Brian Cox gets a special mention for being a figurehead for lazily generalised science, with a wicked impression of Cox walking an audience through the growing and evolving human brain. Robert Newman: The Brain Show review – chewy neuro-comedy Dissing bad science, capitalists and Brian Cox, Robert Newman’s low-octane cabinet of neuroscientific curiosities has nonconformist bite As Newman later pointed out to me, citing Stephen Jay Gould: “the world we make, makes us. Cro-Magnon had the same brain as us, possibly slightly larger. Everything we’ve done since then has been the product of evolution on a brain of unvarying capacity.” © 2016 Guardian News and Media Limited
By Anne Pycha Future doctors may ask us to say more than “Ahhh.” Several groups of neuroscientists, psychiatrists and computer scientists are now investigating the extent to which patients' language use can provide diagnostic clues—before a single laboratory test is run. Increased computing power and new methods to measure the relation between behavior and brain activity have advanced such efforts. And although tests based on the spoken word may not be as accurate as gene sequencing or MRI scans, for diseases lacking clear biological indicators, language mining could help fill the gap. Psychiatrists at Columbia University interviewed 34 young adults at risk for psychosis, a common sign of schizophrenia that includes delusions and hallucinations. Two and a half years later five of the subjects had developed psychosis, and the remaining 29 remained free of the disorder. A specially designed algorithm combed the initial interviews collectively to look for language features that distinguished the two groups and found that psychosis correlated with shorter sentences, loss of flow in meaning from one sentence to the next and less frequent use of the words “that,” “what” and “which.” When later tested on each individual interview, the computer program predicted who did and who did not develop psychosis with 100 percent accuracy. The results were recently published in Schizophrenia, and a second round of testing with another group of at-risk subjects is now under way. Parkinson's Disease Twenty-seven subjects in a study at Favaloro University in Argentina listened to recorded sentences containing verbs associated with specific hand shapes (such as “applaud” or “punch”). As soon as they understood the sentence, participants pressed a button while keeping both hands in either a flat or clenched-fist position. © 2016 Scientific American
By SINDYA N. BHANOO Climate change may affect wood rats in the Mojave Desert in a most unusual way. A new study finds that warmer weather reduces their ability to tolerate toxins in the creosote bush, which they rely on for sustenance. The consequences may be dire for the wood rats. “There’s not much more they can eat out there,” said Patrice Kurnath, a biologist at the University of Utah and one of the study’s authors. She and her colleagues reported their findings in Proceedings of the Royal Society B: Biological Sciences. The leaves of the creosote bush contain a resin full of toxic compounds. They are known to cause kidney cysts and liver failure in laboratory rats. Wild wood rats, however, generally tolerate the poisons. Ms. Kurnath and her colleagues monitored the wood rats as they ate the leaves in warmer temperatures — around 83 degrees Fahrenheit. Although highs in the Mojave can reach the 80s and 90s during the summer, much of the year is cooler. The rats became less tolerant of the toxins and began to lose weight. The reason may have to do with how the liver functions in warmer weather, Ms. Kurnath said. The liver is the body’s primary detoxifying organ. When a mammalian liver is active, it increases internal body temperature. “In warmer weather, maybe you’re not producing huge amounts of heat and you’re not breaking down the toxins,” Ms. Kurnath said. © 2016 The New York Times Company
By Emily Underwood In 2008, in El Cajon, California, 30-year-old John Nicholas Gunther bludgeoned his mother to death with a metal pipe, and then stole $1378 in cash, her credit cards, a DVD/VCR player, and some prescription painkillers. At trial, Gunther admitted to the killing, but argued that his conviction should be reduced to second-degree murder because he had not acted with premeditation. A clinical psychologist and neuropsychologist testified that two previous head traumas—one the result of an assault, the other from a drug overdose—had damaged his brain’s frontal lobes, potentially reducing Gunther’s ability to plan the murder, and causing him to act impulsively. The jury didn’t buy Gunther’s defense, however; based on other evidence, such as the fact that Gunther had previously talked about killing his mother with friends, the court concluded that he was guilty of first-degree murder, and gave him a 25-years-to-life prison sentence. Gunther’s case represents a growing trend, a new analysis suggests. Between 2005 and 2012, more than 1585 U.S. published judicial opinions describe the use of neurobiological evidence by criminal defendants to shore up their defense, according to a study published last week in the Journal of Law and the Biosciences by legal scholar Nita Farahany of Duke University in Durham, North Carolina, and colleagues. In 2012 alone, for example, more than 250 opinions cited defendants’ arguments that their “brains made them do it”—more than double the number of similar claims made in 2007. © 2016 American Association for the Advancement of Science
Keyword: Drug Abuse
Link ID: 21816 - Posted: 01.23.2016
Richard A. Friedman WHO among us hasn’t wanted to let go of anxiety or forget about fear? Phobias, panic attacks and disorders like post-traumatic stress are extremely common: 29 percent of American adults will suffer from anxiety at some point in their lives. Sitting at the heart of much anxiety and fear is emotional memory — all the associations that you have between various stimuli and experiences and your emotional response to them. Whether it’s the fear of being embarrassed while talking to strangers (typical of social phobia) or the dread of being attacked while walking down a dark street after you’ve been assaulted (a symptom of PTSD), you have learned that a previously harmless situation predicts something dangerous. It has been an article of faith in neuroscience and psychiatry that, once formed, emotional memories are permanent. Afraid of heights or spiders? The best we could do was to get you to tolerate them, but we could never really rid you of your initial fear. Or so the thinking has gone. The current standard of treatment for such phobias revolves around exposure therapy. This involves repeatedly presenting the feared object or frightening memory in a safe setting, so that the patient acquires a new safe memory that resides in his brain alongside the bad memory. As long as the new memory has the upper hand, his fear is suppressed. But if he is re-traumatized or re-exposed with sufficient intensity to the original experience, his old fear will awaken with a vengeance. This is one of the limitations of exposure therapy, along with the fact that it generally works in only about half of the PTSD patients who try it. Many also find it upsetting or intolerable to relive memories of assaults and other traumatizing experiences. © 2016 The New York Times Company
Link ID: 21815 - Posted: 01.23.2016
By Diana Kwon Stories of cannabis’s abilities to alleviate seizures have been around for about 150 years but interest in medical marijuana has increased sharply in the last decade with the help of legalization campaigns. Credit: ©iStock Charlotte Figi, an eight-year-old girl from Colorado with Dravet syndrome, a rare and debilitating form of epilepsy, came into the public eye in 2013 when news broke that medical marijuana was able to do what other drugs could not: dramatically reduce her seizures. Now, new scientific research provides evidence that cannabis may be an effective treatment for a third of epilepsy patients who, like Charlotte, have a treatment-resistant form of the disease. Last month Orrin Devinsky, a neurologist at New York University Langone Medical Center, and his colleagues across multiple research centers published the results from the largest study to date of a cannabis-based drug for treatment-resistant epilepsy in The Lancet Neurology. The researchers treated 162 patients with an extract of 99 percent cannabidiol (CBD), a nonpsychoactive chemical in marijuana, and monitored them for 12 weeks. This treatment was given as an add-on to the patients’ existing medications and the trial was open-label (everyone knew what they were getting). The researchers reported the intervention reduced motor seizures at a rate similar to existing drugs (a median of 36.5 percent) and 2 percent of patients became completely seizure free. Additionally, 79 percent of patients reported adverse effects such as sleepiness, diarrhea and fatigue, although only 3 percent dropped out of the study due to adverse events. “I was a little surprised that the overall number of side effects was quite high but it seems like most of them were not enough that the patients had to come off the medication,” says Kevin Chapman, a neurology and pediatric professor at the University of Colorado School of Medicine who was not involved in the study. “I think that [this study] provides some good data to show that it's relatively safe—the adverse effects were mostly mild and [although] there were serious adverse effects, it's always hard to know in such a refractory population whether that would have occurred anyway.” © 2016 Scientific American,
By Brian Owens Guy Rouleau, the director of McGill University’s Montreal Neurological Institute (MNI) and Hospital in Canada, is frustrated with how slowly neuroscience research translates into treatments. “We’re doing a really shitty job,” he says. “It’s not because we’re not trying; it has to do with the complexity of the problem.” So he and his colleagues at the renowned institute decided to try a radical solution. Starting this year, any work done there will conform to the principles of the “open- science” movement—all results and data will be made freely available at the time of publication, for example, and the institute will not pursue patents on any of its discoveries. Although some large-scale initiatives like the government-funded Human Genome Project have made all data completely open, MNI will be the first scientific institute to follow that path, Rouleau says. “It’s an experiment; no one has ever done this before,” he says. The intent is that neuroscience research will become more efficient if duplication is reduced and data are shared more widely and earlier. Opening access to the tissue samples in MNI’s biobank and to its extensive databank of brain scans and other data will have a major impact, Rouleau hopes. “We think that it is a way to accelerate discovery and the application of neuroscience.” After a year of consultations among the institute’s staff, pretty much everyone—about 70 principal investigators and 600 other scientific faculty and staff—has agreed to take part, Rouleau says. Over the next 6 months, individual units will hash out the details of how each will ensure that its work lives up to guiding principles for openness that the institute has developed. They include freely providing all results, data, software, and algorithms; and requiring collaborators from other institutions to also follow the open principles. © 2016 American Association for the Advancement of Science.
Link ID: 21813 - Posted: 01.23.2016
Timothy Egan This weekend, I’m going to the Mojave Desert, deep into an arid wilderness of a half-million acres, for some stargazing, bouldering and January sunshine on my public lands. I won’t be out of contact. I checked. If Sarah Palin says something stupid on Donald Trump’s behalf — scratch that. When Sarah Palin says something stupid on Donald Trump’s behalf, I’ll get her speaking-in-tongues buffoonery in real time, along with the rest of the nation. The old me would have despised the new me for admitting such a thing. I’ve tried to go on digital diets, fasting from my screens. I was a friend’s guest at a spa in Arizona once and had so much trouble being “mindful” that they nearly kicked me out. Actually, I just wanted to make sure I didn’t miss the Seahawks game, mindful of Seattle’s woeful offensive line. In the information blur of last year, you may have overlooked news of our incredibly shrinking attention span. A survey of Canadian media consumption by Microsoft concluded that the average attention span had fallen to eight seconds, down from 12 in the year 2000. We now have a shorter attention span than goldfish, the study found. Attention span was defined as “the amount of concentrated time on a task without becoming distracted.” I tried to read the entire 54-page report, but well, you know. Still, a quote from Satya Nadella, the chief executive officer of Microsoft, jumped out at me. “The true scarce commodity” of the near future, he said, will be “human attention.” Putting aside Microsoft’s self-interest in promoting quick-flash digital ads with what may be junk science, there seems little doubt that our devices have rewired our brains. We think in McNugget time. The trash flows, unfiltered, along with the relevant stuff, in an eternal stream. And the last hit of dopamine only accelerates the need for another one. © 2016 The New York Times Company
Link ID: 21812 - Posted: 01.23.2016
Videos just discovered show the first people ever to be treated for the symptoms of Parkinson’s disease. The footage, hidden for half a century, shows Chilean miners with severe movement problems improving on daily doses of L-dopa. The videos were filmed by George Cotzias at Brookhaven National Laboratory in Upton, New York. In 1963, while studying the toxic effects of manganese in human tissues, Cotzias learned of four workers in the Corral del Quemado mine in Andacollo, Chile, who had developed a syndrome called manganism – which resembled Parkinson’s – through inhaling manganese dust. Cotzias travelled to Chile to include the miners in a trial of leva-dopa, a chemical building block that the body converts into dopamine, low levels of which cause uncontrolled movements in people with Parkinson’s. L-dopa was being tested in Parkinson’s patients around the same time but with little success – even small amounts caused adverse side-effects that prevented a high enough dose reaching the brain. The footage clearly shows the severe problems with walking and turning miners had before treatment. After several months of receiving a daily dose of L-dopa, they were able to feed themselves, shave, tie their shoelaces, and run. “It’s a very important part of the history of neurology,” says Marcelo Miranda, a researcher at Clinica Las Condes in Santiago, Chile, who found the footage, some of which was shown at a conference in the 1960s, but hasn’t been seen since. “It’s the only available document of that period that shows the first patients with Parkinson’s symptoms treated with L-dopa and their extraordinary response.” © Copyright Reed Business Information Ltd.
Link ID: 21811 - Posted: 01.23.2016
By Elizabeth Pennisi PACIFIC GROVE, CALIFORNIA—Bats have an uncanny ability to track and eat insects on the fly with incredible accuracy. But some moths make these agile mammals miss their mark. Tiger moths, for example, emit ultrasonic clicks that jam bat radar. Now, scientists have shown that hawk moths (above) and other species have also evolved this behavior. The nocturnal insects—which are toxic to bats—issue an ultrasonic “warning” whenever a bat is near. After a few nibbles, the bat learns to avoid the noxious species altogether. The researchers shot high-speed videos of bat chases in eight countries over 4 years. Their studies found that moths with an intact sound-producing apparatus—typically located at the tip of the genitals—were spared, whereas those silenced by the researchers were readily caught. As the video shows, when the moths hear the bat’s clicks intensifying as it homes in, they emit their own signal, causing the bat to veer off at the last second. It could be that, like the tiger moths, the hawk moths are jamming the bat’s signal. But, because most moth signals are not the right type to interfere with the bat’s, the researchers say it’s more likely that the bat recognizes the signal and avoids the target on its own. Presenting here last week at a meeting of the American Society of Naturalists, the researchers say this signaling ability has evolved three times in hawk moths and about a dozen more times overall among other moths. © 2016 American Association for the Advancement of Science
Link ID: 21810 - Posted: 01.23.2016
By Melissa Dahl It’s the fifth inning and the Tampa Bay Rays are beating the Cleveland Indians 6–2 when Cleveland’s relief pitcher Nick Hagadone steps in. Alas, Hagadone does little to turn around the Indians’ luck that day, closing out the long inning with a score of 10–2. Hagadone, apparently frustrated by his own lackluster performance, heads to the clubhouse and, on the way there, punches a door with his left fist — the fist that is, unfortunately, connected to his pitching arm. That momentary impulse would cost him dearly. Hagadone required surgery and eight months’ recovery time — and, to add insult to a literal injury, his team also relegated him to the minor leagues, a move that shrank his annual salary by more than 80 percent. When asked about what could possibly explain an action like this in a usually easy-going guy, the Indians’ team psychologist, Charlie Maher, could only offer variations on this: “He just snapped.” Unless you are also a relief pitcher in the major leagues, you will likely never be in exactly this situation. But how many times have you reacted aggressively, even violently, in a way that felt almost out of your control? You hurl your smartphone across the room, or you unleash a stream of expletives in a manner that would seem to a calmer, rational mind to be disproportionate to the situation at hand. “I just snapped” is how we explain it to ourselves and others, and then we move on. The phrase has become such a cliché that it’s easy to forget that it doesn’t really explain much of anything. What’s behind this impulsive, immediately regrettable behavior? R. Douglas Fields, a senior investigator at the National Institutes of Health, sought out an explanation in his new book, Why We Snap: Understanding the Rage Circuit in Your Brain, which includes the Hagadone story recounted above. © 2016, New York Media LLC