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A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American

Keyword: Robotics
Link ID: 22222 - Posted: 05.17.2016

By JONATHAN BALCOMBE Washington — IN March, two marine biologists published a study of giant manta rays responding to their reflections in a large mirror installed in their aquarium in the Bahamas. The two captive rays circled in front of the mirror, blew bubbles and performed unusual body movements as if checking their reflection. They made no obvious attempt to interact socially with their reflections, suggesting that they did not mistake what they saw as other rays. The scientists concluded that the mantas seemed to be recognizing their reflections as themselves. Mirror self-recognition is a big deal. It indicates self-awareness, a mental attribute previously known only among creatures of noted intelligence like great apes, dolphins, elephants and magpies. We don’t usually think of fishes as smart, let alone self-aware. As a biologist who specializes in animal behavior and emotions, I’ve spent the past four years exploring the science on the inner lives of fishes. What I’ve uncovered indicates that we grossly underestimate these fabulously diverse marine vertebrates. The accumulating evidence leads to an inescapable conclusion: Fishes think and feel. Because fishes inhabit vast, obscure habitats, science has only begun to explore below the surface of their private lives. They are not instinct-driven or machinelike. Their minds respond flexibly to different situations. They are not just things; they are sentient beings with lives that matter to them. A fish has a biography, not just a biology. Those giant manta rays have the largest brains of any fish, and their relative brain-to-body size is comparable to that of some mammals. So, an exception? Then you haven’t met the frillfin goby. © 2016 The New York Times Company

Keyword: Intelligence; Evolution
Link ID: 22221 - Posted: 05.16.2016

Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o

Keyword: Huntingtons; Movement Disorders
Link ID: 22220 - Posted: 05.16.2016

By CLYDE HABERMAN At respected research centers in the United States and other countries, scientists have spent much of their professional lives in drug rehabilitation. It is not because they themselves struggle with addiction. What they are trying to rehabilitate are the drugs. Their focus is on mind-altering compounds that fell far from grace nearly half a century ago, LSD prominent among them. Along with other psychedelics, it was outlawed by the federal government, damned as bearing a high potential for abuse and offering no accepted medical benefit. But in recent years, researchers have sought to rescue hallucinogens from exile by examining their efficacy in treating certain disorders of the mind, and perhaps even in understanding the nature of consciousness and spirituality. The work of these scientists now draws the attention of Retro Report, a series of video documentaries that examine major news stories of the past and their enduring significance. Psychoactive substances, often derived from mushrooms, have been part of human cultures from Central and South America to the Sahara for thousands of years. But there is no need to look that far back; 1938 will do. That was when Albert Hofmann, a Swiss chemist searching for a drug to combat circulatory ailments, happened to synthesize lysergic acid diethylamide: LSD or, more familiarly, acid. Five years later, Dr. Hofmann, who died in 2008 at age 102, accidentally ingested a small dose of his creation and discovered its mind-blowing potential as he embarked on the first known acid trip. Many more such journeys would follow, for him and for countless others. © 2016 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 22219 - Posted: 05.16.2016

By Julia Shaw You see a crime take place. You are interviewed about it. You give a statement about what you saw. Do you think that at a later date you would be able to detect whether someone had tampered with your statement? Or re-written parts of it? This is currently a hot topic in the UK, where a very recently published inquiry into the so-called Hillsborough disaster, in which 96 people were crushed to death during a soccer match in 1989, found that testimonies had been deliberately altered by police. Research published earlier this year by the false memory dream team at the University of California, looked directly into the implications of such police (mis)conduct. They found that it is possible that changed statements can go unnoticed by the person who gave the original testimony, and may even develop into a false memory that accommodates the false account. To describe this effect, the researchers came up with the term "memory blindness"—the phenomenon of failing to recognize our own memories. The term was intended to mirror the ‘choice blindness’ literature. Choice blindness is forgetting choices that we have made. The researchers wanted to know “Can choice blindness have lasting effects on eyewitness memory?” To examine this, PhD Student Kevin Cochran and his colleagues conducted two experiments. © 2016 Scientific American

Keyword: Learning & Memory
Link ID: 22218 - Posted: 05.16.2016

Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr

Keyword: Movement Disorders; Neuroimmunology
Link ID: 22217 - Posted: 05.16.2016

By John Horgan Speakers at the 2016 Tucson consciousness conference suggested that “temporal nonlocality” or other quantum effects in the brain could account for free will. But what happens when the brain is immersed in a hot tub? This is the second of four posts on “The Science of Consciousness” in Tucson, Arizona, which lasted from April 26 to April 30. (See Further Reading for links to other posts.) Once again, I’m trying to answer the question: What is it like to be a skeptical journalist at a consciousness conference? -- John Horgan DAY 2, THURSDAY, APRIL 28. HOT TUBS AND QUANTUM INCOHERENCE Breakfast on the patio with Stuart Kauffman, who has training in… almost everything. Philosophy, medicine, science. We’ve bumped heads in the past, but we’re friendly now. In his mid-70s, Stu is still obsessed with--and hacking away at--the biggest mysteries. We talk about… almost everything. Quantum mechanics, the origin of life, materialism, free will, God, the birth and death of his daughter, the death of his wife, his re-marriage, predictability versus possibility. As Stu speaks, his magnificent, weathered face looks happy/sad, arrogant/anxious. Superposition of emotions. He tells me about his brand-new book, Humanity in a Creative Universe, in which he outlines a perspective that can help lift us out of our spiritual crisis. Who saves the savior? I scoot to a morning session, “Consciousness and Free Will.” I hope it will supply me with ammo for my defenses of free will. I can do without God, but not free will. © 2016 Scientific American, a Division of Nature America, Inc.

Keyword: Consciousness
Link ID: 22216 - Posted: 05.16.2016

By Adam Gopnik On a bitter, soul-shivering, damp, biting gray February day in Cleveland—that is to say, on a February day in Cleveland—a handless man is handling a nonexistent ball. Igor Spetic lost his right hand when his forearm was pulped in an industrial accident six years ago and had to be amputated. In an operation four years ago, a team of surgeons implanted a set of small translucent “interfaces” into the neural circuits of his upper arm. This afternoon, in a basement lab at a Veterans Administration hospital, the wires are hooked up directly to a prosthetic hand—plastic, flesh-colored, five-fingered, and articulated—that is affixed to what remains of his arm. The hand has more than a dozen pressure sensors within it, and their signals can be transformed by a computer into electric waves like those natural to the nervous system. The sensors in the prosthetic hand feed information from the world into the wires in Spetic’s arm. Since, from the brain’s point of view, his hand is still there, it needs only to be recalled to life. Now it is. With the “stimulation” turned on—the electronic feed coursing from the sensors—Spetic feels nineteen distinct sensations in his artificial hand. Above all, he can feel pressure as he would with a living hand. “We don’t appreciate how much of our behavior is governed by our intense sensitivity to pressure,” Dustin Tyler, the fresh-faced principal investigator on the Cleveland project, says, observing Spetic closely. “We think of hot and cold, or of textures, silk and cotton. But some of the most important sensing we do with our fingers is to register incredibly minute differences in pressure, of the kinds that are necessary to perform tasks, which we grasp in a microsecond from the feel of the outer shell of the thing. We know instantly, just by touching, whether to gently squeeze the toothpaste or crush the can.”

Keyword: Pain & Touch
Link ID: 22215 - Posted: 05.14.2016

By JONAH BROMWICH It’s relatively easy to determine when someone is too drunk to drive. If a driver’s blood-alcohol level is 0.08 percent or higher, that person is considered legally impaired. But a study says that measuring the effects of marijuana on drivers is far trickier, and that blood tests are an unreliable indication of impairment by cannabis. As more states consider legalizing the substance, that presents a challenge to legislators seeking to create laws on driving while impaired by marijuana. The study, commissioned by the AAA Foundation for Traffic Safety, found that laws in six states that legally assess impairment by measuring how much THC (the active ingredient in marijuana) is in a person’s blood are not supported by science. “There is no concentration of the drug that allows us to reliably predict that someone is impaired behind the wheel in the way that we can with alcohol,” said Jake Nelson, AAA’s director of traffic safety advocacy and research. Lawmakers in those states looked to policies on drunken driving for cues on how to legislate against driving while high. But the body absorbs alcohol and cannabis in different ways, the study said. While drunkenness directly correlates to alcohol in the bloodstream, cannabis impairment takes place only when THC makes its way into the fatty tissue of the brain. Regular marijuana users, including those who take the drug medicinally, often show no signs of impairment after using, according to Jolene Forman, a staff lawyer for the Drug Policy Alliance, a drug-reform advocacy group. She also said that marijuana can stay in the blood for hours, days and even weeks after its effects wear off. © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 22214 - Posted: 05.14.2016

Bret Stetka Last year, in an operating room at the University of Toronto, a 63-year-old women with Alzheimer's disease experienced something she hadn't for 55 years: a memory of her 8-year-old self playing with her siblings on their family farm in Scotland. The woman is a patient of Dr. Andres Lozano, a neurosurgeon who is among a growing number of researchers studying the potential of deep brain stimulation to treat Alzheimer's and other forms of dementia. If the approach pans out it could provide options for patients with fading cognition and retrieve vanished memories. Right now, deep brain stimulation is used primarily to treat Parkinson's disease and tremor, for which it's approve by the Food and Drug Administration. DBS involves delivering electrical impulses to specific areas of the brain through implanted electrodes. The technique is also approved for obsessive-compulsive disorder and is being looked at for a number of other brain disorders, including depression, chronic pain and, as in Lozano's work, dementia. In 2008 Lozano's group published a study in which an obese patient was treated with deep brain stimulation of the hypothalamus. Though no bigger than a pea, the hypothalamus is a crucial bit of brain involved in appetite regulation and other bodily essentials such as temperature control, sleep and circadian rhythms. It seemed like a reasonable target in trying to suppress excessive hunger. To the researcher's surprise, following stimulation the patient reported a sensation of deja vu. He also perceived feeling 20 years younger and recalled a memory of being in a park with friends, including an old girlfriend. With increasing voltages his memories became more vivid. He remembered their clothes. © 2016 npr

Keyword: Learning & Memory
Link ID: 22213 - Posted: 05.14.2016

By Nicholas Bakalar Exposure to pesticides may increase the risk for amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, a new study has found. The study, in JAMA Neurology, included 156 patients with A.L.S. and 128 controls. All participants completed questionnaires providing information on age, sex, ethnicity, education, marital status, residential history, occupational history, smoking and military service. The researchers used the information on residence and occupation to estimate long-term exposure to pesticides, and then took blood samples to determine serum levels of 122 persistent environmental pollutants. The scientists divided exposure into four time periods: ever exposed, exposed in the last 10 years, exposed 10 to 30 years ago, and exposed more than 30 years ago. Exposure to pesticides at any time was associated with a fivefold increased relative risk for A.L.S. compared to no exposure. Even exposure more than 30 years ago tripled the risk. Military service was associated with double the risk, confirming findings of previous studies. “This is an association, not causality,” cautioned the senior author, Dr. Eva L. Feldman, a professor of neurology at the University of Michigan. “We found that people with A.L.S. were five times more likely to have been exposed to pesticides, but we don’t want people to conclude that pesticides cause A.L.S.” © 2016 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Neurotoxins
Link ID: 22212 - Posted: 05.14.2016

Laura Sanders Brain waves during REM sleep solidify memories in mice, scientists report in the May 13 Science. Scientists suspected that the eye-twitchy, dream-packed slumber known as rapid eye movement sleep was important for memory. But REM sleep’s influence on memory has been hard to study, in part because scientists often resorted to waking people or animals up — a stressful experience that might influence memory in different ways. Richard Boyce of McGill University in Montreal and colleagues interrupted REM sleep in mice in a more delicate way. Using a technique called optogenetics, the researchers blocked a brain oscillation called theta waves in the hippocampus, a brain structure involved in memory, during REM sleep. This light touch meant that the mice stayed asleep but had fewer REM-related theta waves in their hippocampi. Usually, post-learning sleep helps strengthen memories. But mice with disturbed REM sleep had memory trouble, the researchers found. Curious mice will spend more time checking out an object that’s been moved to a new spot than an unmoved object. But after the sleep treatment, the mice seemed to not remember objects’ earlier positions, spending equal time exploring an unmoved object as one in a new place. These mice also showed fewer signs of fear in a place where they had previously suffered shocks. Interfering with theta waves during other stages of sleep didn’t seem to cause memory trouble, suggesting that something special happens during REM sleep. R. Boyce et al. Causal evidence for the role of REM sleep theta rhythm in contextual memory consolidation. Science. Vol. 352, p. 812, May 13, 2016. doi: 10.1126/science.aad5252. © Society for Science & the Public 2000 - 2016.

Keyword: Sleep; Learning & Memory
Link ID: 22211 - Posted: 05.14.2016

By Emily Underwood One of the telltale signs of Alzheimer’s disease (AD) is sticky plaques of ß-amyloid protein, which form around neurons and are thought by a large number of scientists to bog down information processing and kill cells. For more than a decade, however, other researchers have fingered a second protein called tau, found inside brain cells, as a possible culprit. Now, a new imaging study of 10 people with mild AD suggests that tau deposits—not amyloid—are closely linked to symptoms such as memory loss and dementia. Although this evidence won’t itself resolve the amyloid-tau debate, the finding could spur more research into new, tau-targeting treatments and lead to better diagnostic tools, researchers say. Scientists have long used an imaging technique called positron emission tomography (PET) to visualize ß-amyloid deposits marked by radioactive chemical tags in the brains of people with AD. Combined with postmortem analyses of brain tissue, these studies have demonstrated that people with AD have far more ß-amyloid plaques in their brains than healthy people, at least as a general rule. But they have also revealed a puzzle: Roughly 30% of people without any signs of dementia have brains “chock-full” of ß-amyloid at autopsy, says neurologist Beau Ances at Washington University in St. Louis in Missouri. That mystery has inspired many in the AD field to ask whether a second misfolded protein, tau, is the real driver of the condition’s neurodegeneration and symptoms, or at least an important accomplice. Until recently, the only ways to test that hypothesis were to measure tau in brain tissue after a person died, or in a sample of cerebrospinal fluid (CSF) extracted from a living person by needle. But in the past several years, researchers have developed PET imaging agents that can harmlessly bind to tau in the living brain. The more tau deposits found in the temporal lobe, a brain region associated with memory, the more likely a person was to show deficits on a battery of memory and attention tests, the team reports today in Science Translational Medicine. © 2016 American Association for the Advancement of Science.

Keyword: Alzheimers; Brain imaging
Link ID: 22210 - Posted: 05.12.2016

Erika Check Hayden The largest-ever genetics study in the social sciences has turned up dozens of DNA markers that are linked to the number of years of formal education an individual completes. The work, reported this week in Nature, analysed genetic material from around 300,000 people. “This is good news,” says Stephen Hsu, a theoretical physicist at Michigan State University in East Lansing, who studies the genetics of intelligence. “It shows that if you have enough statistical power you can find genetic variants that are associated with cognitive ability.” Yet the study’s authors estimate that the 74 genetic markers they uncovered comprise just 0.43% of the total genetic contribution to educational achievement (A. Okbay et al. Nature http://dx.doi.org/10.1038/nature17671; 2016). By themselves, the markers cannot predict a person’s performance at school. And because the work examined only people of European ancestry, it is unclear whether the results apply to those with roots in other regions, such as Africa or Asia. The findings have proved divisive. Some researchers hope that the work will aid studies of biology, medicine and social policy, but others say that the emphasis on genetics obscures factors that have a much larger impact on individual attainment, such as health, parenting and quality of schooling. © 2016 Nature Publishing Group

Keyword: Genes & Behavior; Learning & Memory
Link ID: 22209 - Posted: 05.12.2016

Laura Glynn, Pregnancy brain typically refers to lapses in attention and memory. About 80 percent of new mothers report difficulties remembering things that once came naturally, and although not all studies support this, the weight of the evidence shows that during pregnancy, women exhibit measurable declines in important cognitive skills. But it's not all bad news. The maternal brain also features important enhancements. Mother rats score higher in tests of attention, foraging and planning than peers who have never given birth. These gains most likely render them better able to defend and provide for their pups. The benefits for human moms are less clear, but data are emerging that suggest human pregnancies initiate neural restructuring. A 2010 study found that in the first few months after giving birth, human females show changes in several key brain regions. Specifically, they often exhibit increased volume in the hypothalamus, striatum and amygdala—areas essential for emotional regulation and parental motivation—as well as in regions governing decision making and protective instincts. We can glean further evidence from behavioral changes during pregnancy. Many women exhibit blunted physiological and psychological responses to stress, which may afford mother and fetus protection from the potentially adverse effects of taxing situations. And in the postpartum period, the hormones that sustain breast-feeding maintain these dampened stress responses. © 2016 Scientific American

Keyword: Hormones & Behavior; Learning & Memory
Link ID: 22208 - Posted: 05.12.2016

By Lisa Damour Parents of teenagers face a confounding crosscurrent. While the legalization of marijuana in several American states now bolsters the common belief among adolescents that the drug is safe for recreational use, research documenting marijuana’s diffuse and possibly permanent harm to the teenage brain continues to pile up. Normally developing teenagers question authority and are likely to be skeptical of adults bearing bad news about a widely used party drug. So how do we have successful conversations about the hazards of marijuana use? An open-ended exchange that credits the adolescent’s own observations may do more good than a single sit-down or lecture. Beyond that, we might consider how the facts are often received by adolescents. With all the talk about cannabis legalization, parents may feel compelled to remind their teenagers that recreational marijuana is still banned for most American adults and for anyone under 21. Adolescents who use marijuana risk immediate legal consequences and, in districts with zero-tolerance policies, may be barred from organized school activities, suspended or expelled. They may also face long-term penalties affecting some jobs, internships, colleges and travel visas. But the repercussions of being caught with marijuana don’t faze all teenagers. Most adolescents can name celebrities, famous athletes and classmates who use marijuana regularly, even flagrantly, without running into trouble. Teenagers tend to bristle at rules that seem arbitrary, such as the state-by-state regulations for marijuana and the fact that alcohol, which has a lot in common with pot, is legal. Further, adolescents can be understandably cynical about laws that aren’t applied evenly to everyone: While African-Americans and whites use the drug at similar rates, African-Americans are nearly four times as likely to be arrested for marijuana possession. However real and lasting the penalties for pot use may be, parents often run into resistance when trying to make this case to teenagers. © 2016 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 22207 - Posted: 05.12.2016

Sara Reardon As a medical student in Paris in the 1980s, Eric Vilain found himself pondering the differences between men and women. What causes them to develop differently, and what happens when the process goes awry? At the time, he was encountering babies that defied simple classification as a boy or girl. Born with disorders of sex development (DSDs), many had intermediate genitalia — an overlarge clitoris, an undersized penis or features of both sexes. Then, as now, the usual practice was to operate. And the decision of whether a child would be left with male or female genitalia was often made not on scientific evidence, says Vilain, but on practicality: an oft-repeated, if insensitive, line has it that “it's easier to dig a hole than build a pole”. Vilain found the approach disturbing. “I was fascinated and shocked by how the medical team was making decisions.” Vilain has spent the better part of his career studying the ambiguities of sex. Now a paediatrician and geneticist at the University of California, Los Angeles (UCLA), he is one of the world's foremost experts on the genetic determinants of DSDs. He has worked closely with intersex advocacy groups that campaign for recognition and better medical treatment — a movement that has recently gained momentum. And in 2011, he established a major longitudinal study to track the psychological and medical well-being of hundreds of children with DSDs. © 2016 Nature Publishing Group

Keyword: Sexual Behavior; Development of the Brain
Link ID: 22206 - Posted: 05.11.2016

By Hazem Zohny Here is a picture of the nine-dot problem. The task seems simple enough: connect all nine dots with four straight lines, but, do so without lifting the pen from the paper or retracing any line. If you don’t already know the solution, give it a try – although your chances of figuring it out within a few minutes hover around 0 percent. In fact, even if I were to give you a hint like “think outside of the box,” you are unlikely to crack this deceptively (and annoyingly!) simple puzzle. And yet, if we were to pass a weak electric current through your brain (specifically your anterior temporal lobe, which sits somewhere between the top of your ear and temple), your chances of solving it may increase substantially. That, at least, was the finding from a study where 40 percent of people who couldn’t initially solve this problem managed to crack it after 10 minutes of transcranial direct current stimulation (tDCS) – a technique for delivering a painlessly weak electric current to the brain through electrodes on the scalp. How to explain this? It is an instance of the alleged power of tDCS and similar neurostimulation techniques. These are increasingly touted as methods that can “overclock” the brain in order to boost cognition, improve our moods, make us stronger, and even alter our moral dispositions. The claims are not completely unfounded: there is evidence that some people become slightly better at holding and manipulating information in their minds after a bout of tDCS. It also appears to reduce some people’s likelihood of formulating false memories, and seems to have a lasting improvement on some people’s ability to work with numbers. It can even appear to boost creativity, enhancing the ability of some to make abstract connections between words to come up with creative analogies. But it goes further, with some evidence that it can help people control their urges as well improve their mood. And beyond these psychological effects, tDCS of the part of the brain responsible for movement seems to improve muscular endurance and reduce fatigue. © 2016 Scientific American

Keyword: Learning & Memory
Link ID: 22205 - Posted: 05.11.2016

By Daniel Barron No matter where we call home, where we were raised, or what we ate for breakfast, our brains process information pretty much the same as anyone else in the world. Which makes sense—our genomes are 99.6-99.9% identical, which makes our brains nearly so. Look at a landscape or cityscape and comparable computations occur in your brain as in someone from another background or country. Zhangjiajie National Forest Park, China. Credit: Chensiyuan, via Wikimedia Commons under GFDL Consider my recent walk through China’s Zhangjiajie National Forest Park, an inspiration for James Cameron’s Avatar. Some of our first steps into the park involved a 1,070 foot ascent in the Bailong elevator, the world’s tallest outdoor elevator. Crammed within the carriage were travelers from Japan, India, China, the U.S.A., and Korea. No matter our origin, the Wulingyuan landscape didn’t disappoint: the towering red and green rock formations stretched towards the sky as they defied gravity. Gasps and awes were our linguistic currency while our visual cortices gleefully fired away. The approximately 3000 quartzite sandstone pillars, with their unusual red and green contrasts, mesmerized our visual centers, demanding our attention. One of the brain’s earliest visual processing centers, V1, lies at the middle of the back of our head. V1 identifies simple forms like vertical, horizontal, and diagonal edges of contrasting intensities, or lines. Look at a vertical line, and neurons that are sensitive to vertical lines will fire more quickly; look at a horizontal line, and our horizontal neurons buzz away. © 2016 Scientific American

Keyword: Attention; Vision
Link ID: 22204 - Posted: 05.11.2016

By PAM BELLUCK BALTIMORE — Leave it to the youngest person in the lab to think of the Big Idea. Xuyu Qian, 23, a third-year graduate student at Johns Hopkins, was chatting in late January with Hongjun Song, a neurologist. Dr. Song was wondering how to test their three-dimensional model of a brain — well, not a brain, exactly, but an “organoid,” essentially a tiny ball of brain cells, grown from stem cells and mimicking early brain development. “We need a disease,” Dr. Song said. Mr. Qian tossed out something he’d seen in the headlines: “Why don’t we check out this Zika virus?” Within a few weeks — a nanosecond compared with typical scientific research time — that suggestion led to one of the most significant findings in efforts to answer a central question: How does the Zika virus cause brain damage, including the abnormally small heads in babies born to infected mothers? The answer could spur discoveries to prevent such devastating neurological problems. And time is of the essence. One year after the virus was first confirmed in Latin America, with the raging crisis likely to reach the United States this summer, no treatment or vaccine exists. “We can’t wait,” said Dr. Song, at the university’s Institute for Cell Engineering, where he and his wife and research partner, Dr. Guo-Li Ming, provided a pipette-and-petri-dish-level tour. “To translate our work for the clinic, to the public, normally it takes years. This is a case where we can make a difference right away.” The laboratory’s initial breakthrough, published in March with researchers at two other universities, showed that the Zika virus attacked and killed so-called neural progenitor cells, which form early in fetal development and generate neurons in the brain. © 2016 The New York Times Company

Keyword: Development of the Brain; Neurogenesis
Link ID: 22203 - Posted: 05.11.2016