Chapter 16. None

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By Kensy Cooperrider, Rafael Núñez “What is the difference between yesterday and tomorrow?” The Yupno man we were interviewing, Danda, paused to consider his answer. A group of us sat on a hillside in the Yupno Valley, a remote nook high in the mountains of Papua New Guinea. Only days earlier we had arrived on a single-engine plane. After a steep hike from the grass airstrip, we found ourselves in the village of Gua, one of about 20 Yupno villages dotting the rugged terrain. We came all the way here because we are interested in time—in how Yupno people understand concepts such as past, present and future. Are these ideas universal, or are they products of our language, our culture and our environment? As we interviewed Danda and others in the village, we listened to what they said about time, but we paid even closer attention to what they did with their hands as they spoke. Gestures can be revealing. Ask English speakers about the difference between yesterday and tomorrow, and they might thrust a hand over the shoulder when referring to the past and then forward when referring to the future. Such unreflective movements reveal a fundamental way of thinking in which the past is at our backs, something that we “leave behind,” and the future is in front of us, something to “look forward” to. Would a Yupno speaker do the same? Danda was making just the kinds of gestures we were hoping for. As he explained the Yupno word for “yesterday,” his hand swept backward; as he mentioned “tomorrow,” it leaped forward. We all sat looking up a steep slope toward a jagged ridge, but as the light faded, we changed the camera angle, spinning around so that we and Danda faced in the opposite direction, downhill. With our backs now to the ridge, we looked over the Yupno River meandering toward the Bismarck Sea. “Let's go over that one more time,” we suggested. © 2016 Scientific American,

Keyword: Attention
Link ID: 22778 - Posted: 10.22.2016

By Laura Wright, Researchers have the clearest-ever picture of the receptor that gives humans the 'high' from marijuana, which could lead to a better understanding of how the drug affects humans. Scientists have long known that molecules from THC, the psychoactive component of marijuana, bind to and activate the receptor known as CB1. But now they know that it has a three-dimensional crystal structure. The authors of the paper, which was published Thursday in the journal Cell, say this information is crucial to improve our understanding of this receptor as marijuana use becomes widespread and, in many places, legalized. Now that they know the shape of the receptor, they can get a better idea of how different molecules bind to it, which is what causes reactions in humans. "What is important is to understand how different molecules bind to the receptor, how they control the receptor function, and how this can affect different people," said Raymond Stevens, co-author of the study. Dr. Mark Ware, the executive director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research at the Alan Edwards pain management unit at the McGill University Health Centre, called the discovery a "breakthrough." "Suddenly we've been given the design of the building," he explained. "We can work out ways to get in the building, we know where the windows and doors and stairs are, and we know kind of how the building is structured now." They both said that knowing the receptor's design can lead to better drug design. K2 synthetic pot It's also a key step to understanding the differences between natural cannabinoids, found in the marijuana plant, and synthetic cannabinoids, made in labs. ©2016 CBC/Radio-Canada.

Keyword: Drug Abuse
Link ID: 22776 - Posted: 10.22.2016

By Agata Blaszczak-Boxe Some rodents have a sweet tooth. And sometimes, you need to get crafty to reach your sugar fix. Rats have been filmed for the first time using hooked tools to get chocolate cereal – a manifestation of their critter intelligence. Akane Nagano and Kenjiro Aoyama, of Doshisha University in Kyotanabe, Japan, placed eight brown rats in a transparent box and trained them to pull small hooked tools to obtain the cereal that was otherwise beyond their reach. In one experiment they gave them two similar hooked tools, one of which worked well for the food retrieval task, and the other did not. The rats quickly learned to choose the correct tool for the job, selecting it 95 per cent of the time. The experiments showed that the rats understood the spatial arrangement between the food and the tool. The team’s study is the first to demonstrate that rats are able to use tools, says Nagano. The rats did get a little confused in the final experiment. When the team gave them a rake that looked the part but with a bottom was too soft and flimsy to move the cereal, they still tried to use it as much as the working tool that was also available. But, says Nagano, it is possible their eyesight was simply not good enough for them to tell that the flimsy tool wasn’t up to the task. The rodents’ crafty feat places them in the ever-growing club of known tool-using animals such as chimps, bearded capuchin monkeys, New Caledonian crows, alligators and even some fish. © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory; Intelligence
Link ID: 22774 - Posted: 10.22.2016

By Catherine Caruso Imagine you are faced with the classic thought experiment dilemma: You can take a pile of money now or wait and get an even bigger stash of cash later on. Which option do you choose? Your level of self-control, researchers have found, may have to do with a region of the brain that lets us take the perspective of others—including that of our future self. A study, published today in Science Advances, found that when scientists used noninvasive brain stimulation to disrupt a brain region called the temporoparietal junction (TPJ), people appeared less able to see things from the point of view of their future selves or of another person, and consequently were less likely to share money with others and more inclined to opt for immediate cash instead of waiting for a larger bounty at a later date. The TPJ, which is located where the temporal and parietal lobes meet, plays an important role in social functioning, particularly in our ability to understand situations from the perspectives of other people. However, according to Alexander Soutschek, an economist at the University of Zurich and lead author on the study, previous research on self-control and delayed gratification has focused instead on the prefrontal brain regions involved in impulse control. “When you have a closer look at the literature, you sometimes find in the neuroimaging data that the TPJ is also active during delay of gratification,” Soutschek says, “but it's never interpreted.” © 2016 Scientific American

Keyword: Attention
Link ID: 22772 - Posted: 10.20.2016

Hannah Devlin Science correspondent Monkeys have been observed producing sharp stone flakes that closely resemble the earliest known tools made by our ancient relatives, proving that this ability is not uniquely human. Previously, modifying stones to create razor-edged fragments was thought to be an activity confined to hominins, the family including early humans and their more primitive cousins. The latest observations re-write this view, showing that monkeys unintentionally produce almost identical artefacts simply by smashing stones together. The findings put archaeologists on alert that they can no longer assume that stone flakes they discover are linked to the deliberate crafting of tools by early humans as their brains became more sophisticated. Tomos Proffitt, an archaeologist at the University of Oxford and the study’s lead author, said: “At a very fundamental level - if you’re looking at a very simple flake - if you had a capuchin flake and a human flake they would be the same. It raises really important questions about what level of cognitive complexity is required to produce a sophisticated cutting tool.” Unlike early humans, the flakes produced by the capuchins were the unintentional byproduct of hammering stones - an activity that the monkeys pursued decisively, but the purpose of which was not clear. Originally scientists thought the behaviour was a flamboyant display of aggression in response to an intruder, but after more extensive observations the monkeys appeared to be seeking out the quartz dust produced by smashing the rocks, possibly because it has a nutritional benefit. © 2016 Guardian News and Media Limited

Keyword: Evolution
Link ID: 22771 - Posted: 10.20.2016

Tina Hesman Saey VANCOUVER — Zika virus’s tricks for interfering with human brain cell development may also be the virus’s undoing. Zika infection interferes with DNA replication and repair machinery and also prevents production of some proteins needed for proper brain growth, geneticist Feiran Zhang of Emory University in Atlanta reported October 19 at the annual meeting of the American Society of Human Genetics. Levels of a protein called p53, which helps control cell growth and death, shot up by 80 percent in human brain cells infected with the Asian Zika virus strain responsible for the Zika epidemic in the Americas, Zhang said. The lab dish results are also reported in the Oct. 14 Nucleic Acids Research. Increased levels of the protein stop developing brain cells from growing and may cause the cells to commit suicide. A drug that inactivates p53 stopped brain cells from dying, Zhang said. Such p53 inhibitors could help protect developing brains in babies infected with Zika. But researchers would need to be careful giving such drugs because too little p53 can lead to cancer. Zika also makes small RNA molecules that interfere with production of proteins needed for DNA replication, cell growth and brain development, Zhang said. In particular, a small viral RNA called vsRNA-21 reduced the amount of microcephalin 1 protein made in human brain cells in lab dishes. The researchers confirmed the results in mouse experiments. That protein is needed for brain growth; not enough leads to the small heads seen in babies with microcephaly. Inhibitors of the viral RNAs might also be used in therapies, Zhang suggested. |© Society for Science & the Public 2000 - 2016

Keyword: Development of the Brain
Link ID: 22770 - Posted: 10.20.2016

By Meredith Knight In June, international diabetes organizations endorsed provocative new guidelines suggesting physicians should consider gastric bypass surgery for a greatly expanded number of diabetics—those with a body mass index of 30 and above as opposed to just those with a BMI of 40 or more. Research has shown that the surgery helps people lose more weight, maintain the loss longer and achieve better blood glucose levels than those who slim down by changing diet and exercise habits. Now a study in mice suggests the effectiveness of bariatric surgery may stem in part from changes it causes in the brain. According to the study, published in the International Journal of Obesity, gastric bypass surgery causes the hyperactivation of a neural pathway that leads from stomach-sensing neurons in the brain stem to the lateral parabrachial nucleus, an area in the midbrain that receives sensory information from the body, and then to the amygdala, the brain's emotion- and fear-processing center. The obese mice underwent so-called Roux-en-Y bypass surgery, in which surgeons detach most of the stomach, leaving only a tiny pouch connected to the small intestine. Shortly after the surgery, the mice begin to show increased activation in this neural pathway, along with reduced meal size and a preference for less fatty food. They also begin to secrete higher levels of satiety hormones. Similar behavioral and hormonal patterns are found in humans after bypass surgery, suggesting that the brain changes may also be similar—but the authors say looking at this particular circuit in humans with brain imaging is difficult because the resolution is not up to the task. © 2016 Scientific American,

Keyword: Obesity
Link ID: 22768 - Posted: 10.19.2016

By MARC SANTORA The morning after Christine Grounds gave birth to her son Nicholas, she awoke to find a neurologist examining her baby. It was summer 2006, and Nicholas was her first child. There had been no indication that anything was wrong during her pregnancy, but it was soon clear that there was a problem. “Did you know he has microcephaly?” she remembers the doctor asking matter-of-factly. Confused, she replied, “What is microcephaly?” This was before the Zika virus had spread from Brazil across South and Central America and the Caribbean and reached Florida. It was before doctors had determined that the virus could cause microcephaly, a birth defect in which children have malformed heads and severely stunted brain development. And it was before people had seen the devastating pictures of scores of newborns with the condition in Brazil and elsewhere that shocked the world this year. Ms. Grounds, a 45-year-old psychotherapist, and her husband, Jon Mir, who live in Manhattan, had no idea what microcephaly would mean for them or for their child. “We had a diagnosis but no prognosis,” recalled Mr. Mir, 44, who works in finance. The doctors could offer few answers. “We don’t know if he will walk,” the couple recalled being told. “We don’t know if he will talk. He might be in a vegetative state.” But the truth was, even the doctors did not know. As mosquito season draws to a close in much of the country, taking with it the major risk of new Zika infections, there are still more than 2,600 pregnant women who have tested positive for the virus in the United States and its territories, according to the Centers for Disease Control and Prevention. They, and thousands more around the world, face the prospect of giving birth to a child with microcephaly. © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22766 - Posted: 10.19.2016

By Meredith Wadman The second century C.E. Greek physician and philosopher Galen advised patients suffering from disorders of the spirit to bathe in and drink hot spring water. Modern day brain scientists have posited that Galen’s prescription delivered more than a placebo effect. Lithium has for decades been recognized as an effective mood stabilizer in bipolar disease, and lithium salts may have been present in the springs Galen knew. Yet exactly how lithium soothes the mind has been less than clear. Now, a team led by Ben Cheyette, a neuroscientist at the University of California in San Francisco (UCSF), has linked its success to influence over dendritic spines, tiny projections where excitatory neurons form connections, or synapses, with other nerve cells. Lithium treatment restored healthy numbers of dendritic spines in mice engineered to carry a genetic mutation that is more common in people with autism, schizophrenia, and bipolar disorder than in unaffected people, they report today in Molecular Psychiatry. The lithium also reversed symptoms in these mutant mice—lack of interest in social interactions, decreased motivation, and increased anxiety—that mimic those in the human diseases. “They showed there’s a correlation between the ability of lithium to reverse not only the behavioral abnormalities in the mice, but also the [dendritic] spine abnormalities,” says Scott Soderling, a neuroscientist at Duke University in Durham, North Carolina, who studies how dysfunctions in signaling at brain synapses and lead to psychiatric disorders. Soderling adds that the work also sheds light on the roots of these diseases. “It gives further credence to this idea that these spine abnormalities are functionally linked to the behavioral disorders.” © 2016 American Association for the Advancement of Science.

Keyword: Schizophrenia
Link ID: 22764 - Posted: 10.18.2016

Laura Sanders When the body’s internal sense of time doesn’t match up with outside cues, people can suffer, and not just from a lack of sleep. Such ailments are similar in a way to motion sickness — the queasiness caused when body sensations of movement don’t match the external world. So scientists propose calling time-related troubles, which can afflict time-zone hoppers and people who work at night, “circadian-time sickness.” This malady can be described, these scientists say, with a certain type of math. The idea, to be published in Trends in Neurosciences, is “intriguing and thought-provoking,” says neuroscientist Samer Hattar of Johns Hopkins University. “They really came up with an interesting idea of how to explain the mismatch.” Neuroscientist Raymond van Ee of Radboud University in the Netherlands and colleagues knew that many studies had turned up ill effects from an out-of-whack circadian clock. Depression, metabolic syndromes and memory troubles have been found alongside altered daily rhythms. But despite these results, scientists don’t have a good understanding of how body clocks work, van Ee says. Van Ee and colleagues offer a new perspective by using a type of math called Bayesian inference to describe the circadian trouble. Bayesian inference can be used to describe how the brain makes and refines predictions about the world. This guesswork relies on the combination of previous knowledge and incoming sensory information (SN: 5/28/16, p. 18). In the case of circadian-time sickness, these two cues don’t match up, the researchers propose. |© Society for Science & the Public 2000 - 2016

Keyword: Sleep
Link ID: 22763 - Posted: 10.18.2016

By PERRI KLASS, M.D. It’s a classic which-came-first question: Is the child not getting enough sleep because of problem behaviors, especially at bedtime, or is the child behaving problematically because of not getting enough sleep? The answers are most likely yes and yes, and the back-and-forth currents can drag a child down developmentally. In an editorial in JAMA Pediatrics in 2015, Michelle M. Garrison, a research assistant professor at the University of Washington in the division of child and adolescent psychiatry, described this intersection of sleep and behavior problems in early childhood as a “feedback whirlpool.” Dr. Garrison was commenting on a longitudinal study of more than 32,000 Norwegian mothers and their children who were followed from birth to age 5; the children with sleep problems at 18 months, including short sleep duration (sleeping 10 hours or less) or frequent nocturnal awakenings (three times a night or more) had more emotional and behavioral problems at the age of 5. This held true even when the researchers adjusted for emotional and behavioral problems already present in the 18-month-olds; compared to children at the same behavioral baseline, the kids with sleep problems ran into more difficulties as they developed. “Sleep really does drive behavior problems and behavior problems are driving sleep problems, it really is bidirectional,” Dr. Garrison said. “A child can start having problems with emotional regulation, melting down more, and that makes it more difficult for the family to do all the things they have to do so the child can get good sleep. Sleep gets worse; behavior gets worse. It can really be an awful cycle for the kid and the family both.” Dr. Oskar Jenni, a professor of developmental pediatrics at Zurich University Children’s Hospital, said that there is a great deal of variation in the individual sleep needs of children at any given age. Parents need to understand their children’s sleep needs and rhythms, since behavior problems can also arise when children are compelled to spend more time in bed than they actually need. “My main message is adjusting bedtime to the needs of the children in both directions,” he said. © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22762 - Posted: 10.18.2016

By Michael Price When you’re smiling, it may feel like the whole world is smiling with you, but a new study suggests that some facial expressions may not be so universal. In fact, several expressions commonly understood in the West—including one for fear—have very different meanings to one indigenous, isolated society in Papua New Guinea. The new findings call into question some widely held tenets of emotional theory, and they may undercut emerging technologies, like robots and artificial intelligence programs tasked with reading people’s emotions. For more than a century, scientists have wondered whether all humans experience the same basic range of emotions—and if they do, whether they express them in the same way. In the 1870s, it was the central question Charles Darwin explored in The Expression of the Emotions in Man and Animals. By the 1960s, emeritus psychologist Paul Ekman, then at the University of California (UC) in San Francisco, had come up with an accepted methodology to explore this question. He showed pictures of Westerners with different facial expressions to people living in isolated cultures, including in Papua New Guinea, and then asked them what emotion was being conveyed. Ekman’s early experiments appeared conclusive. From anger to happiness to sadness to surprise, facial expressions seemed to be universally understood around the world, a biologically innate response to emotion. That conclusion went virtually unchallenged for 50 years, and it still features prominently in many psychology and anthropology textbooks, says James Russell, a psychologist at Boston College and corresponding author of the recent study. But over the last few decades, scientists have begun questioning the methodologies and assumptions of the earlier studies. © 2016 American Association for the Advancement of Science.

Keyword: Emotions
Link ID: 22761 - Posted: 10.18.2016

Bruce Bower Scientists, politicians, clinicians, police officers and medical workers agree on one thing: The U.S. mental health system needs a big fix. Too few people get the help they need for mental ailments and emotional turmoil that can destroy livelihoods and lives. A report in the October JAMA Internal Medicine, for instance, concludes that more than 70 percent of U.S. adults who experience depression don’t receive treatment for it. Much attention focuses on developing better psychiatric medications and talk therapies. But those tactics may not be enough. New research suggests that the longstanding but understudied problem of stigma leaves many of those suffering mental ailments feeling alone, often unwilling to seek help and frustrated with treatment when they do. “Stigma about mental illness is widespread,” says sociologist Bernice Pescosolido of Indiana University in Bloomington. And the current emphasis on mental ills as diseases of individuals can unintentionally inflame that sense of shame. An effective mental health care system needs to address stigma’s suffocating social grip, investigators say. “If we want to explain problems such as depression and suicide, we have to see them in a social context, not just as individual issues,” Pescosolido says. |© Society for Science & the Public 2000 - 2016

Keyword: Depression
Link ID: 22758 - Posted: 10.15.2016

Analysis of a trial that used the drug canagliflozin found that as people lost weight, their appetite increased proportionately, leading to consumption of more calories and weight loss plateau (leveling off). The findings provide the first measurement in people of how strongly appetite counters weight loss as part of the body’s feedback control system regulating weight. Results are currently available on BioRxiv (link is external) and will publish in Obesity during Obesity Week 2016. A team led by the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) analyzed data from a year-long, placebo-controlled, double-blind trial in people with type 2 diabetes who could eat and drink without restriction by the study. Of the 242 participants, 153 received canagliflozin, a drug that caused a substantial increase in the amount of glucose excreted in their urine. Those people were not directly aware of that calorie loss, which caused a gradual decrease in weight averaging about eight pounds. The team used a validated math model to calculate the changes in the amount of calories consumed during the study. They found no long-term calorie intake changes in the 89 people who got a placebo. However, for every pound of lost weight, the people treated with canagliflozin consumed about 50 calories per day more than they were eating before the study. This increase in appetite and calorie intake led to slowing of weight loss after about six months. The measurements are consistent with the researchers’ analysis of data from a separate trial on a commercial weight loss program not involving canagliflozin. In the weight loss program trial, despite the dieters’ consistent efforts to reduce calorie intake, their increased appetite resulted in a progressive increase in calorie intake — three times stronger than the changes in caloric expenditure that typically accompany weight loss — and weight loss plateau. Findings from the analyses suggest that persistent effort is required to avoid weight regain.

Keyword: Obesity
Link ID: 22756 - Posted: 10.15.2016

By Jessica Boddy You’d probably never notice a jumping spider across your living room, but it would surely notice you. The arachnids are known for their brilliant eyesight, and a new study shows they have even greater sensory prowess than we thought: Jumping spiders can hear sounds even though they don’t have ears—or even eardrums. To find this out, researchers implanted tiny electrodes in a region of spiders’ brains that would show whether sound was being processed. Then they placed the spiders on a specially designed box to eliminate any vibrations from below—most spiders sense their surroundings through vibrations—and scared the heck out of them with a speaker-produced buzz of one of their predators, the mud dauber wasp. An out-of-earshot, high-frequency buzz and a silent control elicited no response from the spiders. But the 80-hertz wasp buzz made them freeze and look around, startled, just as they would do in the wild. What’s more, data from the electrodes showed a spike in brain activity with each buzz, revealing that spiders actually hear sounds, from a swooping mud dauber wasp to you crunching potato chips on your couch. The researchers, who publish their work today in Current Biology, say further study is needed to see exactly how spiders receive sounds without eardrums, but they believe sensitive hairs on their legs play a part. © 2016 American Association for the Advancement of Science.

Keyword: Hearing
Link ID: 22755 - Posted: 10.15.2016

By Smitha Mundasad Health reporter People who experience frequent drops in blood pressure or dizziness when suddenly standing up are at increased risk of dementia, scientists say. Writing in Plos Medicine they suggest that less blood reaches the brain during these moments, leading to brain cell damage over time. Dementia experts say this is a "robust study" and "plausible explanation" that needs further investigation. Charities point out that factors such as smoking carry higher risks. But they say the work adds to growing evidence that changes in blood pressure have an impact on the brain. Previous studies have linked high blood pressure to types of dementia. But in this paper scientists focused on transient periods of low blood pressure - also known as postural hypotension - which become more common in older age. These episodes can sometimes leave people feeling dizzy or give them "head rushes" when standing up suddenly. Researchers from the Erasmus Medical Center, in the Netherlands, tracked 6,000 people for an average of 15 years. They found those who suffered repeated periods of low blood pressure on standing were more likely to develop dementia in the years that followed. Researcher Dr Arfan Ikram said: "Even though the effect can be seen as subtle - with an increased risk of about 4% for people with postural hypotension compared to those without it - so many people suffer from postural hypotension as they get older that it could have a significant impact on the burden of dementia across the world." He told the BBC: "If people experience frequent episodes of dizziness on standing, particularly as they get older, they should see their GPs for advice." © 2016 BBC

Keyword: Alzheimers
Link ID: 22753 - Posted: 10.13.2016

Lauren Silverman It's been a wild ride for kratom lately. Since Aug. 31, when the Drug Enforcement Administration announced its intention to classify the plant as a Schedule I substance, a group of kratom vendors filed a lawsuit against the government to block the move, angry advocates took to social media in protest and scientists questioned whether they would be able to continue kratom research. Now, the DEA is withdrawing its notice of intent to put kratom in the most restrictive category of controlled substances, with drugs like LSD and heroin. The DEA says it will instead open an official public comment period — to last until Dec. 1, 2016 — for people to share their experiences using kratom as a medical treatment. It has also requested that the Food and Drug Administration expedite scientific research. DEA spokesman Russ Baer says the DEA received more than 2,000 phone calls since August, mostly in opposition to the plan to classify kratom as Schedule I. "So in a spirit of transparency, and to open this up to public dialogue, we withdrew our notice to temporarily schedule kratom," Baer says. "We will then give full consideration to those comments before we move forward with any action." Kratom is derived from the leaves of a tree native to Southeast Asia. It is a relative of the coffee plant. According to David Kroll, a pharmacologist and medical writer, farmers and indigenous people have used it for hundreds of years as both a stimulant to increase work output and also as a way to relax. © 2016 npr

Keyword: Drug Abuse
Link ID: 22752 - Posted: 10.13.2016

By MIKE IVES HONG KONG — President Rodrigo Duterte of the Philippines was elected in May after pledging to kill 100,000 criminals in his first six months in office, vowing that fish in Manila, the capital, would grow fat from eating the bodies of drug dealers and other “do nothings.” In Mr. Duterte’s first three months as president, his bloody campaign led to the killing of about 1,400 drug suspects by the police and hundreds of others by extrajudicial means, according to official estimates. He has also publicly accused thousands of government officials of being involved in the drug trade, in some cases offering no evidence. The campaign has taken particular aim at people who use or sell shabu, a cheap form of methamphetamine that has caused grave health and social problems across the country. Mr. Duterte has likened shabu addicts to zombies and claimed — absent evidence — that many are “no longer viable for rehabilitation” because abusing the drug shrinks their brains. What is methamphetamine? Methamphetamine is an addictive stimulant that can be made from ephedrine and other readily available chemicals. It typically comes in either tablets, called yaba in parts of Asia, or crystalline form. The first variety is common in mainland Southeast Asia, and the second — known as shabu, ice or crystal meth, among other names — is more popular in the Philippines and many other countries. It also tends to be more potent and more deeply intertwined with international drug manufacturing and smuggling networks, according to a report by the United Nations Office on Drugs and Crime. How does the drug affect people who use it? Smoking, snorting, ingesting or injecting methamphetamine can cause aggression, memory loss and a range of other health complications, including heart attack or sudden death. Links between methamphetamine abuse and crime, disease transmission and other social problems have also been documented. A study by the RAND Corporation found that the effects of methamphetamine abuse, including the burden of addiction and treatment, cost the United States $23.4 billion in 2005. © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 22751 - Posted: 10.13.2016

By peering into the eyes of mice and tracking their ocular movements, researchers made an unexpected discovery: the visual cortex — a region of the brain known to process sensory information — plays a key role in promoting the plasticity of innate, spontaneous eye movements. The study, published in Nature, was led by researchers at the University of California, San Diego (UCSD) and the University of California, San Francisco (UCSF) and funded by the National Eye Institute (NEI), part of the National Institutes of Health. “This study elegantly shows how analysis of eye movement sheds more light on brain plasticity — an ability that is at the core of the brain’s capacity to adapt and function. More specifically, it shows how the visual cortex continues to surprise and to awe,” said Houmam Araj, Ph.D., a program director at NEI. Without our being aware of it, our eyes are in constant motion. As we rotate our heads and as the world around us moves, two ocular reflexes kick in to offset this movement and stabilize images projected onto our retinas, the light-sensitive tissue at the back of our eyes. The optokinetic reflex causes eyes to drift horizontally from side-to-side — for example, as we watch the scenery through a window of a moving train. The vestibulo-ocular reflex adjusts our eye position to offset head movements. Both reflexes are crucial to survival. These mechanisms allow us to see traffic while driving down a bumpy road, or a hawk in flight to see a mouse scurrying for cover.

Keyword: Vision
Link ID: 22750 - Posted: 10.13.2016

By Elizabeth Pennisi Although it has a face—and body—that only a mother could love, the naked mole rat has a lot to offer biomedical science. It lives 10 times longer than a mouse, almost never gets cancer, and doesn’t feel pain from injury and inflammation. Now, researchers say they’ve figured out how the rodents keep this pain away. “It’s an amazing result,” says Harold Zakon, an evolutionary neurobiologist at the University of Texas, Austin, who was not involved with the work. “This study points us to important areas … that might be targeted to reduce this type of pain.” Naked mole rats are just plain weird. They live almost totally underground in colonies structured like honey bee hives, with hundreds of workers servicing a single queen and her few consorts. To survive, they dig kilometers of tunnels in search of large underground tubers for food. It’s such a tough life that—to conserve energy—this member of the rodent family gave up regulating its temperature, and they are able to thrive in a low-oxygen, high–carbon dioxide environment that would suffocate or be very painful to humans. “They might as well be from another planet,” says Thomas Park, a neuroscientist at the University of Illinois, Chicago. Gary Lewin, a neuroscientist at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Berlin, began working with naked mole rats because a friend in Chicago was finding that the rodent's pain fibers were not the same as other mammals'. In 2008, the studies led to the finding that naked mole rats didn’t feel pain when they came into contact with acid and didn’t get more sensitive to heat or touch when injured, like we and other mammals do. Lewin was hooked and has been raising the rodents in his lab ever since. They are a little more challenging than rats or mice, he notes, because with just one female per colony producing young, he never really has quite enough individuals for his studies. © 2016 American Association for the Advancement of Science

Keyword: Pain & Touch; Evolution
Link ID: 22749 - Posted: 10.12.2016