Chapter 13. Memory, Learning, and Development
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By BENEDICT CAREY Fourteen years ago, a leading drug maker published a study showing that the antidepressant Paxil was safe and effective for teenagers. On Wednesday, a major medical journal posted a new analysis of the same data concluding that the opposite is true. That study — featured prominently by the journal BMJ — is a clear break from scientific custom and reflects a new era in scientific publishing, some experts said, opening the way for journals to post multiple interpretations of the same experiment. It comes at a time of self-examination across science — retractions are at an all-time high; recent cases of fraud have shaken fields as diverse as anesthesia and political science; and earlier this month researchers reported that less than half of a sample of psychology papers held up. “This paper is alarming, but its existence is a good thing,” said Brian Nosek, a professor of psychology at the University of Virginia, who was not involved in either the original study or the reanalysis. “It signals that the community is waking up, checking its work and doing what science is supposed to do — self-correct.” The authors of the reanalysis said that many clinical studies had some of the same issues as the original Paxil study, and that data should be made freely available across clinical medicine, so that multiple parties could analyze them. The dispute itself is a long-running one: Questions surrounding the 2001 study played a central role in the so-called antidepressant wars of the early 2000s, which led to strong warnings on the labels of Paxil and similar drugs citing the potential suicide risk for children, adolescents and young adults. The drugs are considered beneficial and less risky for many adults over 25 with depression. © 2015 The New York Times Company
We all have our favourite movie moments, ones we love to watch again from time to time. Now it seems chimpanzees and bonobos, too, have the nous to recall thrilling scenes in movies they have previously seen and anticipate when they are about to come up. The results suggest apes can readily recall and anticipate significant recent events, just by watching those events once. Rather than use hidden food as a memory test, Japanese researchers made short movies and showed them to apes on two consecutive days. “We showed a movie instead, and asked whether they remember it when they only watch an event once, and an event totally new to them,” says Fumihiro Kano of Kyoto University in Japan. “Their anticipatory glances told us that they did.” Plot moment Kano and his colleague Satoshi Hirata made and starred in two short films. Another of the characters was a human dressed up as an ape in a King Kong costume who carried out attacks on people, providing the key plot moment in the first movie (see video). Both films were designed to contain memorable dramatic events, and the researchers deployed laser eye-tracking technology to see if the animals preferentially noticed and remembered these moments. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 21421 - Posted: 09.20.2015
Nancy Shute There have been suggestions that low levels of vitamin D might be a factor in cognitive decline and Alzheimer's disease, but there's no proof that the lack of D is actually causing the problems. A study published Monday doesn't prove that link, but it does find that people with low levels of vitamin D lost key thinking skills more quickly than people with enough. The study is notable because of the diversity of the participants: 62 percent were women, 30 percent were African-American, 25 percent Hispanic and 41 percent white. Most earlier studies looking at cognitive decline and vitamin D were in white people. The participants lived in California's Sacramento Valley and were mostly in their 70s when they entered the study. The researchers followed up with them for about five years, having them take annual neurological exams and neuropsychological testing at the University of California, Davis, Alzheimer's Disease Center. Most of the 382 people in the study were low on vitamin D, tested by measuring 25-hydroxyvitamin D in the blood. One-quarter of the participants were deficient in vitamin D, and 35 percent had levels deemed insufficient. That's not a surprise — most older people are below the "adequate" level of 20 to less than 50 ng/ml, often because they're not outside much. And most of the people in the study weren't getting the recommended three servings of dairy foods daily that could help. © 2015 NPR
By AMY HARMON Some neuroscientists believe it may be possible, within a century or so, for our minds to continue to function after death — in a computer or some other kind of simulation. Others say it’s theoretically impossible, or impossibly far off in the future. A lot of pieces have to fall into place before we can even begin to start thinking about testing the idea. But new high-tech efforts to understand the brain are also generating methods that make those pieces seem, if not exactly imminent, then at least a bit more plausible. Here’s a look at how close, and far, we are to some requirements for this version of “mind uploading.” The hope of mind uploading rests on the premise that much of the key information about who we are is stored in the unique pattern of connections between our neurons, the cells that carry electrical and chemical signals through living brains. You wouldn't know it from the outside, but there are more of those connections — individually called synapses, collectively known as the connectome — in a cubic centimeter of the human brain than there are stars in the Milky Way galaxy. The basic blueprint is dictated by our genes, but everything we do and experience alters it, creating a physical record of all the things that make us US — our habits, tastes, memories, and so on. It is exceedingly tricky to transition that pattern of connections, known as the connectome, into a state where it is both safe from decay and can be verified as intact. But in recent months, two sets of scientists said they had devised separate ways to do that for the brains of smaller mammals. If either is scaled up to work for human brains — still a big if — then theoretically your brain could sit on a shelf or in a freezer for centuries while scientists work on the rest of these steps. © 2015 The New York Times Company
By CLYDE HABERMAN Perhaps no crime staggers the mind, or turns the stomach, more than the murder of a baby, and so it is not a surprise when law enforcement comes down hard on the presumed killers. Often enough, these are men and women accused of having succumbed to sudden rage or simmering frustration and literally shaken the life out of a helpless infant who would not stop crying or would not fall asleep. Shaken baby syndrome has been a recognized diagnosis for several decades, though many medical professionals now prefer the term abusive head trauma. It is defined by a constellation of symptoms known as the triad: brain swelling, bleeding on the surface of the brain and bleeding behind the eyes. For years, those three symptoms by themselves were uniformly accepted as evidence that a crime had been committed, even in the absence of bruises, broken bones or other signs of abuse. While many doctors, maybe most, still swear by the diagnosis, a growing number have lost faith. Not that they doubt that some babies have been abused. But these skeptics assert that factors other than shaking, and having nothing to do with criminal behavior, may sometimes explain the triad. Has the syndrome been diagnosed too liberally? Are some innocent parents and other caretakers being wrongly sent to prison? Those questions, at the complex intersection of medicine and the law, can stir strong emotions among doctors, parents and prosecutors. They shape this first installment in a new series of Retro Report, video documentaries that explore major news stories of the past and their enduring consequences. The video’s starting point is a Massachusetts criminal case that introduced the concept of shaken baby syndrome to many Americans: the 1997 murder trial of Louise Woodward, an 18-year-old British au pair accused of having shaken an 8-month-old boy, Matthew Eappen, so aggressively that he died. Matthew also had injuries that may have predated Ms. Woodward’s joining the Eappen family in Newton, outside Boston. The focus, however, was on the triad of symptoms. To prosecution witnesses, they proved that the baby had been shaken violently, his head hitting some hard surface. © 2015 The New York Times Company
A study suggests that a chemical in dark chocolate and red wine can slow the progression of Alzheimer’s disease. But how conclusive is the data, and does this mean we should all drink more wine? New Scientist looks at the evidence. What is resveratrol? Found in grapes, red wine and dark chocolate, many claims have been made about resveratrol. It has been touted as a potential panacea for a range of age-related disorders, including cancer, diabetes and neurological problems, but so far most of the data supporting these claims has come from lab studies and work in animals. There have been only a few, small studies in humans. How might resveratrol protect us from age-related illness? Extremely calorie-restricted diets greatly reduce age-related diseases in lab animals. This is thought to happen through the activation of a group of enzymes called sirtuins, which seem to affect gene expression and protect against the effects of stress, including a poor diet. The hope is that resveratrol activates sirtuins to get the same benefits – like preventing the onset of age-related diseases, including Alzheimer’s – without having to stick to such a low-energy diet. But some experiments have suggested slowed ageing from caloric restriction may not be down to sirtuins after all. What does the latest study show? To see if resveratrol could delay the progression of Alzheimer’s disease in people , Scott Turner at Georgetown University Medical Centre in Washington DC and his team gave 119 people with mild to moderate symptoms of the disease either a gram of synthesised resveratrol twice a day in pills for a year, or a placebo. © Copyright Reed Business Information Ltd.
Link ID: 21404 - Posted: 09.14.2015
By Elizabeth Landau Ask a physician what the hormone vasopressin is good for, and she will explain that it regulates the volume of water in your body and also affects blood pressure. But since the 1990s, vasopressin has been a hot topic in a very different field: social behavior. And recently it has emerged as a possible target for treating autism spectrum disorders (ASD), which are characterized by social, behavioral and communication impairments. The research is still in early stages, however, and has yielded more questions than answers. Given that one out of 68 children in the U.S. has an autism spectrum disorder, researchers are scrambling to figure out what in the brain might be related to the symptoms, and how they might design an effective treatment. Vasopressin may be a key player in the disorder. But scientists do not yet know whether too much or too little of the hormone—or perhaps some combination of both—is tied to autism. New clinical trials may yield insights. “I think that the work is exciting and important” says Suma Jacob, who leads an autism research laboratory at the University of Minnesota. “I also think we still have a lot more work to do in this field as a whole.” Previous research has shown that vasopressin, like the hormone oxytocin, is associated with parenting behavior and social bonding, including falling in love. In fact, the two hormones are structurally very similar, and there are receptors in the brain that interact with both of them. But high levels of vasopressin are also associated with anxiety and aggression. Intriguingly, some animal studies have found that higher levels of vasopressin increased aggression specifically in males. © 2015 Scientific American
Alison Abbott Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed off the stage. But scientists have since shown that tissues can transmit symptoms of the disease between animals — and new results imply that humans, at least in one unusual circumstance, may not be an exception. The findings, published in this issue of Nature, emerged during autopsy studies of the brains of eight people who had died of the rare but deadly Creutzfeldt–Jakob disease (CJD; Z. Jaunmuktane et al. Nature 525, 247–250; 2015). They contracted it decades after treatment with contaminated batches of growth hormone that had been extracted from the pituitary glands of human cadavers. Six of the brains, in addition to the damage caused by CJD, harboured the tell-tale amyloid pathology that is associated with Alzheimer’s disease. “This is the first evidence of real-world transmission of amyloid pathology,” says molecular neuroscientist John Hardy of University College London (UCL). “It is potentially concerning.” If confirmed, the findings raise the spectre that tens of thousands of other people treated with the human growth-hormone (hGH) extracts might be at risk of Alzheimer’s. And although there is no suggestion that Alzheimer’s could be contracted through normal contact with patients, some scientists worry that the findings may have broader implications: that Alzheimer’s could be passed on by other routes through which CJD can be transmitted, such as blood transfusions or contaminated surgical instruments. © 2015 Nature Publishing Group
By Siri Carpenter Alex, age 10, bounds onto his bed to pose with his Aaron Rodgers poster, grinning as proudly as if he had recruited the Green Bay Packers’ quarterback himself. Continuing the tour of his suburban New York bedroom, he points out his Packers-themed alarm clock, his soccer trophy, his Boy Scout trophy, and then the big reveal: a homemade foam box in Packers green and gold. “Mmm, very nice,” I say. Alex grins—part shy, part sly—as he turns it around to show me the message on the back: “Jets stink.” Even though he seems to be an entirely ordinary boy, there’s something unusual about Alex: He once had autism, and now he does not. There was a time when Alex’s parents didn’t know if he would ever speak in full sentences, let alone joke around with a stranger. His autism, they suspected, might prevent any such future. Alex’s parents began to worry about him before he was even a year old. He wasn’t learning to sit, crawl, or stand as his fraternal twin brother was. Even more striking was how much less social he was than his brother. “Alex was an expressionless child,” says his mother, Amy. (Alex’s and Amy’s names have been changed to protect their privacy.) She remembers a friend trying in vain to get Alex to laugh—jumping up and down, gesturing wildly, making silly faces. “His brother would be in belly laughs, and Alex would be just glazed over,” Amy says. © 2015 The Slate Group LLC.
Link ID: 21393 - Posted: 09.10.2015
By Nicholas Bakalar Being obese at age 50 may be tied to an increased risk of developing Alzheimer’s disease at a younger age. Previous studies have shown that being overweight at midlife is associated with an increased risk of developing Alzheimer’s. Now researchers have found that it also predicts occurrence at a younger age. Scientists studied 1,394 cognitively normal people, average age around 60, following them for an average of 14 years. During the study, 142 developed Alzheimer’s. After controlling for age, race, level of education and cardiovascular risk factors, they found that each unit increase in B.M.I., or body mass index, at age 50 was associated with a 6.7-month decrease in the age of onset of Alzheimer’s. The study, in Molecular Psychiatry, also found an association of higher B.M.I. with larger deposits of neurofibrillary tangles on autopsy, one of the characteristics of brain damage in Alzheimer’s disease. “Age of onset is not as well studied as risk,” said the senior author, Dr. Madhav Thambisetty, a neurologist at the National Institute on Aging. “As we try to cure Alzheimer’s disease, we also want to delay the onset of symptoms. Until we know what factors accelerate onset, we won’t be able to test any potential interventions. And that is perhaps as important as the search for treatment.” © 2015 The New York Times Company
Mo Costandi In an infamous set of experiments performed in the 1960s, psychologist Walter Mischel sat pre-school kids at a table, one by one, and placed a sweet treat – a small marshmallow, a biscuit, or a pretzel – in front of them. Each of the young participants was told that they would be left alone in the room, and that if they could resist the temptation to eat the sweet on the table in front of them, they would be rewarded with more sweets when the experimenter returned. The so-called Marshmallow Test was designed to test self-control and delayed gratification. Mischel and his colleagues tracked some of the children as they grew up, and then claimed that those who managed to hold out for longer in the original experiment performed better at school, and went on to become more successful in life, than those who couldn’t resist the temptation to eat the treat before the researcher returned to the room. The ability to exercise willpower and inhibit impulsive behaviours is considered to be a core feature of the brain’s executive functions, a set of neural processes - including attention, reasoning, and working memory - which regulate our behaviour and thoughts, and enable us to adapt them according to the changing demands of the task at hand. Executive function is a rather vague term, and we still don’t know much about its underlying bran mechanisms, or about how different components of this control system are related to one another. New research shows that self-control and memory share, and compete with each other for, the same brain mechanisms, such that exercising willpower saps these common resources and impairs our ability to encode memories. © 2015 Guardian News and Media Limited
By Melinda Wenner Moyer A worrisome new study caught my eye last week as I perused the website of the journal Pediatrics. It was titled “Cognition and Brain Structure Following Early Childhood Surgery With Anesthesia.” Considering that my now 4-year-old underwent general anesthesia for a minor procedure when he was 2 and that my 14-month-old may be a candidate for ear tube surgery, my interest was immediately piqued. I clicked through and came face to face with a whole lot of yuck. The first sentence alone made me gasp: “Anesthetics induce widespread cell death, permanent neuronal deletion, and neurocognitive impairment in immature animals, raising substantial concerns about similar effects occurring in young children.” Wait, so anesthesia causes brain damage? Why didn’t anyone tell me? I thought. Obviously, I needed to know more. Considering that 6 million American children—including 1.5 million babies under the age of 1—undergo general anesthesia each year, this seemed like a pretty serious issue to delve into. Twenty studies and several phone calls later, I’m feeling a lot better about my kids’ brains. There are still many things scientists don’t know about how anesthesia affects the nervous system, in part because they can’t ethically do the types of experiments that would provide clear answers, like unnecessarily exposing kids to anesthesia. But based on the research that does exist, there’s really no need for parents to freak out. If “going under” has an effect on the developing brain, it’s likely to be very small. Even Andreas Loepke, the pediatric anesthesiologist at Cincinnati Children’s Hospital Medical Center who co-authored the Pediatrics paper, was reassuring to me over the phone. “These are theoretical concerns,” he said. © 2015 The Slate Group LLC.
In 1938, an Austrian pediatrician named Hans Asperger gave the first public talk on autism in history. Asperger was speaking to an audience of Nazis, and he feared that his patients — children who fell onto what we now call the autism spectrum — were in danger of being sent to Nazi extermination camps. As Asperger spoke, he highlighted his "most promising" patients, a notion that would stick with the autistic spectrum for decades to come. "That is where the idea of so-called high-functioning versus low-functioning autistic people comes from really — it comes from Asperger's attempt to save the lives of the children in his clinic," science writer Steve Silberman tells Fresh Air's Terry Gross. Silberman chronicles the history of autism and examines some of the myths surrounding our current understanding of the condition in his new book, NeuroTribes. Along the way, he revisits Asperger's calculated efforts to save his patients. Steve Silberman's articles have been published in Wired, The New Yorker, Nature and Salon. Silberman shies away from using the terms high-functioning and low-functioning, because "both of those terms can be off base," he says. But he praises Asperger's courage in speaking to the Nazis. "I would literally weep while I was writing that chapter," he says. NeuroTribes also explores how a 1987 expansion of the medical definition of autism (which was previously much narrower and led to less frequent diagnoses) contributed to the perception that there was an autism epidemic. © 2015 NPR
Link ID: 21378 - Posted: 09.03.2015
By Jennifer Couzin-Frankel Some rare diseases pull researchers in and don’t let them go, and the unusual bone condition called fibrodysplasia ossificans progressiva (FOP) has long had its hooks in Aris Economides. “The minute you experience it it’s impossible to step back and forget it,” says the functional geneticist who runs the skeletal disease program at Regeneron Pharmaceuticals in Tarrytown, New York. “It’s devastating in the most profound way.” The few thousand or so people with FOP worldwide live with grueling uncertainty: Some of their muscles or other soft tissues periodically, and abruptly, transform into new bone that permanently immobilizes parts of their bodies. Joints such as elbows or ankles may become frozen in place; jaw motion can be impeded and the rib cage fixed, making eating or even breathing difficult. Twenty years after he first stumbled on FOP, Economides and his colleagues report today that the gene mutation shared by 97% of people with the disease can trigger its symptoms in a manner different than had been assumed—through a single molecule not previously eyed as a suspect. And by sheer chance, Regeneron had a treatment for this particular target in its freezers. The company tested that potential therapy, a type of protein known as a monoclonal antibody, on mice with their own form of FOP and lo and behold, they stopped growing unwelcome new bone. © 2015 American Association for the Advancement of Science.
Aftab Ali People who were born prematurely are less intelligent later on in life and earn less money as a result, according to a new study by the University of Warwick. Researchers at the Coventry-based institution said they found a link which connects pre-term birth with low reading and, in particular, maths skills which affect the amount of wealth accumulated as adults. Funded by the Nuffield Foundation, the researchers examined data from two other large studies, following children born more than a decade apart, with one group from 1958 and the other from 1970. In total, more than 15,000 individuals were surveyed – which recruited all children born in a single week in England, Scotland, and Wales. Data were examined for all individuals who were born at between 28 and 42 weeks gestational age, and who had available wealth information at the age of 42. Those participants who were born pre-term – at less than 37 weeks – were compared with those who were born full-term to find both groups’ mathematical ability in childhood had a direct effect on how much they earned as an adult, regardless of later educational qualifications. In order to measure adult wealth, the researchers looked at factors including: family income and social class, housing and employment status, and their own perceptions of their financial situation. In regards to academic abilities, they examined: validated measures for mathematics, reading, and intelligence, along with ratings from teachers and parents. © independent.co.uk
By Gretchen Reynolds At the age of 93, Olga Kotelko — one of the most successful and acclaimed nonagenarian track-and-field athletes in history — traveled to the University of Illinois to let scientists study her brain. Ms. Kotelko held a number of world records and had won hundreds of gold medals in masters events. But she was of particular interest to the scientific community because she hadn’t begun serious athletic training until age 77. So scanning her brain could potentially show scientists what late-life exercise might do for brains. Ms. Kotelko died last year at the age of 95, but the results of that summer brain scan were published last month in Neurocase. And indeed, Ms. Kotelko’s brain looked quite different from those of other volunteers aged 90-plus who participated in the study, the scans showed. The white matter of her brain — the cells that connect neurons and help to transmit messages from one part of the brain to another — showed fewer abnormalities than the brains of other people her age. And her hippocampus, a portion of the brain involved in memory, was larger than that of similarly aged volunteers (although it was somewhat shrunken in comparison to the brains of volunteers decades younger than her). Over all, her brain seemed younger than her age. But because the scientists didn’t have a scan showing Ms. Kotelko’s brain before she began training, it’s impossible to know whether becoming an athlete late in life improved her brain’s health or whether her naturally healthy brain allowed her to become a stellar masters athlete. © 2015 The New York Times Company
By SINDYA N. BHANOO The human eye has a blind spot, though few of us realize it. Now, a new study suggests that it is possible to reduce the spot with training. The optic nerve, which carries visual signals to the brain, passes through the retina, a light-sensitive layer of tissue. There are no so-called photoreceptors at the point where the optic nerve intersects the retina. The right eye generally compensates for the left eye’s blind spot and vice versa, so the spot is hardly noticed. Researchers trained 10 people using a computer monitor and an eye patch. The participants were shown a waveform in the visual field of their blind spot day after day. After 20 days of this repeated stimulation, the blind spot shrunk by about 10 percent. The researchers believe that neurons at the periphery of the blind spot became more responsive, effectively reducing the extent of functional blindness. The findings add to a growing body of research suggesting that the human eye can be trained, said Paul Miller, a psychologist at the University of Queensland in Australia and an author of the study, which appeared in the journal Current Biology. This kind of training may help researchers develop better treatments for visual impairments like macular degeneration. “This is the leading cause of blindness in the western world,” Mr. Miller said. © 2015 The New York Times Company
An experimental gene therapy reduces the rate at which nerve cells in the brains of Alzheimer’s patients degenerate and die, according to new results from a small clinical trial, published in the current issue of the journal JAMA Neurology. Targeted injection of the Nerve Growth Factor gene into the patients’ brains rescued dying cells around the injection site, enhancing their growth and inducing them to sprout new fibres. In some cases, these beneficial effects persisted for 10 years after the therapy was first delivered. Alzheimer’s is the world’s leading form of dementia, affecting an estimated 47 million people worldwide. This figure is predicted to almost double every 20 years, with much of this increase is likely to be in the developing world. And despite the huge amounts of time, effort, and money devoted to developing an effective cure, the vast majority of new drugs have failed in clinical trials. The new results are preliminary findings from the very first human trials designed to test the potential benefits of nerve growth factor (NGF) gene therapy for Alzheimer’s patients. NGF was discovered in the 1940s by Rita Levi-Montalcini, who convincingly demonstrated that the small protein promotes the survival of certain sub-types of sensory neurons during development of the nervous system. Since then, others have shown that it also promotes the survival of acetylcholine-producing cells in the basal forebrain, which die off in Alzheimer’s. © 2015 Guardian News and Media Limited
We all have days when we feel like our brain is going at a snail’s pace, when our neurons forgot to get out of bed. And psychologists have shown that IQ can fluctuate day to day. So if we’re in good health and don’t have a sleep deficit from last night’s shenanigans to blame, what’s the explanation? Sophie von Stumm, a psychologist at Goldsmiths University, London, set about finding out. In particular, she wanted to know whether mood might explain the brain’s dimmer switch. Although it seems intuitively obvious that feeling low could compromise intellectual performance, von Stumm says research to date has been inconclusive, with some studies finding an effect and others not. “On bad mood days, we tend to feel that our brains are lame and work or study is particularly challenging. But scientists still don’t really know if our brains work better when we are happy compared to when we are sad.” To see if she could pin down mood’s effect on IQ more convincingly, von Stumm recruited 98 participants. Over five consecutive days they completed questionnaires to assess their mood, as well as tests to measure cognitive functions, such as short-term memory, working memory and processing speed. Surprisingly, being in a bad mood didn’t translate into worse cognitive performance. However, when people reported feeling positive, von Stumm saw a modest boost in their processing speed. © Copyright Reed Business Information Ltd.
By Dina Fine Maron Whenever the fictional character Popeye the Sailor Man managed to down a can of spinach, the results were almost instantaneous: he gained superhuman strength. Devouring any solid object similarly did the trick for one of the X-Men. As we age and begin to struggle with memory problems, many of us would love to reach for an edible mental fix. Sadly, such supernatural effects remain fantastical. Yet making the right food choices may well yield more modest gains. A growing body of evidence suggests that adopting the Mediterranean diet, or one much like it, can help slow memory loss as people age. The diet's hallmarks include lots of fruits and vegetables and whole grains (as opposed to ultrarefined ones) and a moderate intake of fish, poultry and red wine. Dining mainly on single ingredients, such as pumpkin seeds or blueberries, however, will not do the trick. What is more, this diet approach appears to reap brain benefits even when adopted later in life—sometimes aiding cognition in as little as two years. “You will not be Superman or Superwoman,” says Miguel A. Martínez González, chair of the department of preventive medicine at the University of Navarra in Barcelona. “You can keep your cognitive abilities or even improve them slightly, but diet is not magic.” Those small gains, however, can be meaningful in day-to-day life. Scientists long believed that altering diet could not improve memory. But evidence to the contrary started to emerge about 10 years ago. © 2015 Scientific American
Link ID: 21350 - Posted: 08.28.2015