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Sara Reardon Annie is lying down when she answers the phone; she is trying to recover from a rare trip out of the house. Moving around for an extended period leaves the 56-year-old exhausted and with excruciating pain shooting up her back to her shoulders. “It's really awful,” she says. “You never get comfortable.” In 2011, Annie, whose name has been changed at the request of her lawyer, slipped and fell on a wet floor in a restaurant, injuring her back and head. The pain has never eased, and forced her to leave her job in retail. Annie sued the restaurant, which has denied liability, for several hundred thousand dollars to cover medical bills and lost income. To bolster her case that she is in pain and not just malingering, Annie's lawyer suggested that she enlist the services of Millennium Magnetic Technologies (MMT), a Connecticut-based neuroimaging company that has a centre in Birmingham, Alabama, where Annie lives. MMT says that it can detect pain's signature using functional magnetic resonance imaging (fMRI), which measures and maps blood flow in the brain as a proxy for neural activity. The scan is not cheap — about US$4,500 — but Steven Levy, MMT's chief executive, says that it is a worthwhile investment: the company has had ten or so customers since it began offering the service in 2013, and all have settled out of court, he says. If the scans are admitted to Annie's trial, which is expected to take place early this year, it could establish a legal precedent in Alabama. Most personal-injury cases settle out of court, so it is impossible to document how often brain scans for pain are being used in civil law. But the practice seems to be getting more common, at least in the United States, where health care is not covered by the government and personal-injury cases are frequent. Several companies have cropped up, and at least one university has offered the service. © 2015 Nature Publishing Group

Keyword: Pain & Touch; Brain imaging
Link ID: 20615 - Posted: 02.25.2015

By KATIE THOMAS The retired tennis player Monica Seles spent this month making the rounds of television talk shows, appearing on everything from “Good Morning America” to “The Dr. Oz Show” to share her personal struggle with binge eating. “It took a while until I felt comfortable talking about it,” she said in a People magazine interview, explaining that she secretly devoured food for years while she was a professional athlete. “That’s one of the reasons I decided to do this campaign: to raise awareness that binge eating is a real medical condition.” But that is not the only reason. Ms. Seles is a paid spokeswoman for Shire, which late last month won approval to market its top-selling drug, Vyvanse, to treat binge-eating disorder, a condition that once existed in the shadow of better-known disorders like anorexia and bulimia but was officially recognized as its own disorder in 2013 by the American Psychiatric Association. As Shire introduces an ambitious campaign to promote Vyvanse but also to raise awareness about the disorder, some are saying the company is going too far to market a drug, a type of amphetamine, that is classified by the federal government as having a high potential for abuse. Shire’s track record is adding to the worry: The company helped put another once-stigmatized condition — attention deficit hyperactivity disorder — on the medical map and made billions of dollars from the sale of drugs, like Vyvanse and Adderall, to treat it. In recent years, federal officials have cited the company for inappropriately marketing Vyvanse and other A.D.H.D. drugs. In addition, some drug safety experts questioned why the Food and Drug Administration so swiftly approved the drug for binge eating — seeking little outside input — despite the fact that, for decades, amphetamines, which suppress the appetite, were widely abused as a treatment for obesity. © 2015 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 20614 - Posted: 02.25.2015

Helen Shen Repeated head injuries in American football have been linked to a degenerative brain disorder later in life. Dave Duerson suspected that something was wrong with his brain. By 2011, 18 years after the former American football player had retired from the Phoenix Cardinals, he experienced frequent headaches, memory problems and an increasingly short temper. Before he killed himself, he asked that his brain be donated for study. Researchers who examined it found signs of chronic traumatic encephalopathy (CTE), a degenerative condition linked to repeated head injuries. At least 69 cases have been reported in the literature since 2000, many in former boxers and American football players (P. H. Montenigro et al. Alz. Res. Ther. 6, 68; 2014) — heightening public concern about concussions during contact sports. Yet much about CTE is unknown, from its frequency to its precise risk factors and even whether its pathology is unique. Researchers now hope to take a major step towards answering those questions. At Boston University in Massachusetts on 25–27 February, neuroscientists will convene to examine the characteristics of CTE in brain tissue from post-mortem examinations. They hope to agree on a set of diagnostic criteria for the disease, and to assess whether it is distinct from other brain disorders, such as Alzheimer’s disease. The effort is sorely needed, says Walter Koroshetz, acting director of the US National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, which is organizing the meeting. “The definition is the important piece that lets you do the rest of the research,” he says. And the stakes are high. CTE is associated with memory loss, irritability, depression and explosive anger, which are thought to appear and worsen years after repeated head trauma. © 2015 Nature Publishing Group

Keyword: Brain Injury/Concussion
Link ID: 20613 - Posted: 02.25.2015

By Michelle Roberts Health editor, BBC News online Scientists have proposed a new idea for detecting brain conditions including Alzheimer's - a skin test. Their work, which is at an early stage, found the same abnormal proteins that accumulate in the brain in such disorders can also be found in skin. Early diagnosis is key to preventing the loss of brain tissue in dementia, which can go undetected for years. But experts said even more advanced tests, including ones of spinal fluid, were still not ready for clinic. If they were, then doctors could treatment at the earliest stages, before irreversible brain damage or mental decline has taken place. Brain biomarker Investigators have been hunting for suitable biomarkers in the body - molecules in blood or exhaled breath, for example, that can be measured to accurately and reliably signal if a disease or disorder is present. Dr Ildefonso Rodriguez-Leyva and colleagues from the University of San Luis Potosi, Mexico, believe skin is a good candidate for uncovering hidden brain disorders. Skin has the same origin as brain tissue in the developing embryo and might, therefore, be a good window to what's going on in the mind in later life - at least at a molecular level - they reasoned. Post-mortem studies of people with Parkinson's also reveal that the same protein deposits which occur in the brain with this condition also accumulate in the skin. To test if the same was true in life as after death, the researchers recruited 65 volunteers - 12 who were healthy controls and the remaining 53 who had either Parkinson's disease, Alzheimer's or another type of dementia. They took a small skin biopsy from behind the ear of each volunteer to test in their laboratory for any telltale signs of disease. Specifically, they looked for the presence of two proteins - tau and alpha-synuclein. © 2015 BBC.

Keyword: Alzheimers; Parkinsons
Link ID: 20612 - Posted: 02.25.2015

By Sandhya Sekar It’s stressful being a low-ranking hyena—so stressful that even their chromosomes feel it. Researchers have discovered that the challenges of African savanna hyena society shorten underdogs’ telomeres, stretches of DNA that bookend chromosomes and protect them from wear and tear during cell replication. The stress may come from the top hyenas getting the best meat, whereas lower ranking individuals have to travel long distances—sometimes to the edges of the group territory—to fend for themselves. With increased stress, higher amounts of stress hormones and cellular byproducts like oxygen ions and peroxides are produced, both of which have been shown to shorten telomeres in other species. When telomeres fall below a certain length, cells go into damage-control mode and kick off biochemical pathways that can result in cell death. The study, the team reports online today in Biology Letters, is the first to show that the stress of social hierarchy can shorten telomeres in a wild species. © 2015 American Association for the Advancement of Science.

Keyword: Stress
Link ID: 20611 - Posted: 02.25.2015

by Penny Sarchet An injection and a dash of exercise could be the secret to keeping trim. These rainbow mice, imaged in infrared to reveal how much energy they are burning while on a treadmill, are revealing how a shot can boost a muscle's ability to burn calories. Red body parts show where lots of energy is being used. The mouse on the right has a red patch on its left hind leg, which corresponds to the spot where it received an injection of a substance developed by Denice Hodgson-Zingman from the University of Iowa and colleagues. The substance is a type of morpholino, a compound that can be designed to target specific genes, in this case to alter proteins responsible for storing energy. The disruption causes muscles to burn more energy even during mild exercise, such as a gentle trot on a treadmill. In contrast, the untreated mouse on the left, which is doing the same amount of exercise, is using less energy in the same spot, as illustrated by the colder green colour. The researchers hope the injection will help people who want to burn more calories do so through routine everyday activities, eliminating the need for intense exercise. Journal reference: Molecular Therapy, DOI: 10.1038/mt.2015.2141 © Copyright Reed Business Information Ltd.

Keyword: Obesity
Link ID: 20610 - Posted: 02.24.2015

By Barron H. Lerner, M.D. I can’t stand it when someone behind me at a movie chews popcorn with his or her mouth open. I mean, I really can’t stand it. I have misophonia, a condition with which certain sounds can drive someone into a burst of rage or disgust. Although only identified and named in the last 20 years, misophonia has been enthusiastically embraced, with websites, Facebook pages and conferences drawing small armies of frustrated visitors. As a primary care physician, I find that misophonia can present some special challenges: At times, my patients can be the source of annoying sounds. At other times, the condition can be a source of special bonding if I realize that a patient is a fellow sufferer. But some experts question whether misophonia really exists. By naming it, are we giving too much credence to a series of symptoms that are no big deal? Coined by the married researchers Margaret and Pawel Jastreboff of Emory University in 2002, misophonia (“hatred of sound”) is sometimes referred to as selective sound sensitivity syndrome. Like me, those with the disorder identify a series of specific sounds that bother them. A2013 study by Arjan Schröder and his colleagues at the University of Amsterdam identified the most common irritants as eating sounds, including lip smacking and swallowing; breathing sounds, such as nostril noises and sneezing; and hand sounds, such as typing and pen clicking. The range of responses to these noises is broad, from irritation to disgust to anger. Some sufferers even respond with verbal or physical aggression to those making the noises. One woman reported wanting to strangle her boyfriend in response to his chewing. © 2015 The New York Times Company

Keyword: Hearing; Emotions
Link ID: 20609 - Posted: 02.24.2015

By Emily Underwood Infants born prematurely are more than twice as likely to have difficulty hearing and processing words than those carried to full-term, likely because brain regions that process sounds aren’t sufficiently developed at the time of delivery. Now, an unusual study with 40 preemies suggests that recreating a womblike environment with recordings of a mother's heartbeat and voice could potentially correct these deficits. "This is the kind of study where you think ‘Yes, I can believe these results,’ " because they fit well with what scientists know about fetal brain development, says cognitive scientist Karin Stromswold of Rutgers University, New Brunswick, in New Jersey. A fetus starts to hear at about 24 weeks of gestation, as neurons migrate to—and form connections in—the auditory cortex, a brain region that processes sound, Stromswold explains. Once the auditory cortex starts to function, a fetus normally hears mostly low-frequency sounds—its mother’s heartbeat, for example, and the melody and rhythm of her voice. Higher frequency tones made outside of the mother's body, such as consonants, are largely drowned out. Researchers believe that this introduction to the melody and rhythm of speech, prior to hearing individual words, may be a key part of early language acquisition that gets disrupted when a baby is born too soon. In addition to being bombarded with the bright lights, chemical smells, and shrill sounds of a hospital’s intensive care unit, preemies are largely deprived of the sensations they'd get in the womb, such as their mother's heartbeat and voice, says Amir Lahav, a neuroscientist at Harvard Medical School in Boston. Although mothers are sometimes allowed to hold premature newborns for short periods of time, the infants are often considered too fragile to leave their temperature- and humidity-controlled incubators, he says. Preemies often have their eyes covered to block out light, and previous studies have shown that reducing overall levels of high-frequency noise in a neonatal intensive care unit—by lowering the number of incubators in a unit, for example, or giving preemies earplugs—can improve premature babies' outcomes. Few studies have actively simulated a womblike environment, however, he says. © 2015 American Association for the Advancement of Science.

Keyword: Development of the Brain; Hearing
Link ID: 20608 - Posted: 02.24.2015

By Aleksandra Sagan, CBC News Photos of emaciated women proudly displaying their protruding hips and ribs, as well as thinspirational quotes "fat-shaming" those who dare to eat, continue to thrive on social media, despite the best attempts by sites like Instagram to temper the reach of the pro-eating disorder community. Some girls gain thousands of followers posting pictures of "thigh gaps" and "bikini bridges," as well as underweight celebrities and thinspirational quotes like model Kate Moss's mantra: "nothing tastes as good as skinny feels." "It just provides a lot of positivity for them, just in a very maladaptive way," says Edward Selby, of the more visual outlet that sites like Instagram provide. An assistant professor of clinical psychology at Rutgers University in New Jersey, Selby is the director of a lab there that studies what makes people more likely to develop anorexia (self-starvation), bulimia (binge-eating and purging) and other eating disorders. About one in 20 young women in Canada has an eating disorder, according to the Toronto-based National Initiative for Eating Disorders. And people suffering from these diseases often feel good after exercising, purging, swallowing a laxative or doing other things that contribute to their illness, Selby says. They get caught in a "cyclic feedback loop," with the positive emotions pushing them to engage more in these risky behaviours. Online pro-anorexia and bulimia communities simply add to that loop by celebrating a person's unhealthy achievements, he says. "Finally under 130! Woohoo!" writes one user with a photo of her feet on a scale. "Yay congrats," reads a response. Another girl posts a screen grab from an app claiming that she's been fasting for more than a day. It receives 32 likes and a "great job" among the comments. ©2015 CBC/Radio-Canada

Keyword: Anorexia & Bulimia
Link ID: 20607 - Posted: 02.24.2015

By JON PALFREMAN EUGENE, Ore. — FOUR years ago, I was told I had Parkinson’s disease, a condition that affects about one million Americans. The disease is relentlessly progressive; often starting with a tremor in one limb on one side of the body, it spreads. The patient’s muscles become more rigid, frequently leading to a stooped posture, and movements slow down and get smaller and less fluid. As the disease advances — usually over a number of years — the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment. Can Parkinson’s be slowed, stopped or even reversed? Can the disease be prevented before it starts, like polio and smallpox? More than at any time in history, success seems possible. Having sequenced the human genome, biomedical researchers have now set their sights on the ultimate frontier — the human brain. The formidable puzzle is to figure out how a three-pound lump of mostly fatty matter enables us to perform a seemingly endless number of tasks, like walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing ... and why those awesome abilities break down with neurological disease. Many scientists view Parkinson’s as a so-called pathfinder. If they can figure out what causes Parkinson’s, it may open the door to understanding a host of other neurodegenerative diseases — and to making sense of an organ of incredible complexity. In Parkinson’s, the circuitry in a tiny region of the brain called the basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally acts as a kind of adviser that helps people learn adaptive skills by classic conditioning — rewarding good results with dopamine bursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to deploy their muscles to reach, grab, babble and crawl, and later to accomplish many complex tasks without thinking. For example, when a tennis player practices a stroke over and over again, the basal ganglia circuitry both rewards and “learns” the correct sequence of activities to produce, say, a good backhand drive automatically. © 2015 The New York Times Company

Keyword: Parkinsons
Link ID: 20606 - Posted: 02.24.2015

By Sandra G. Boodman Catherine Cutter’s voice was her livelihood. A professor of food science at Penn State University, the microbiologist routinely lectured to large classes about food safety in the meat and poultry industries. But in 2008, after Cutter’s strong alto voice deteriorated into a raspy whisper, she feared her academic career might be over.How could she teach if her students could barely hear her? The classroom wasn’t the only area of Cutter’s life affected by her voicelessness. The mother of two teenagers, Cutter, now 52, recalls that she “couldn’t yell — or even talk” to her kids and would have to knock on a wall or countertop to get their attention. Social situations became increasingly difficult as well, and going to a restaurant was a chore. Using the drive-through at her bank or dry cleaner was out of the question because she couldn’t be heard. “I just retreated,” said Cutter, who sought assistance from nearly two dozen specialists for her baffling condition. The remedies doctors prescribed — when they worked at all — resulted in improvement that was temporary at best. For two years Cutter searched in vain for help. It arrived in the form of a neurosurgeon she consulted for a second opinion about potentially risky surgery to correct a different condition. He suggested a disorder that had never been mentioned, a diagnosis that proved to be correct — and correctable. Until then, “everyone had been looking in the wrong place,” Cutter said.

Keyword: Movement Disorders
Link ID: 20605 - Posted: 02.24.2015

by Michael Slezak If you want to counteract the effects of getting drunk, a big dose of the so-called "cuddle-chemical" oxytocin might be the answer. Oxytocin has important roles in sexual behaviour and social bonding, and has previously been investigated as a way to help wean alcoholics off drink. While studying this effect in rats, Michael Bowen from the University of Sydney noticed something strange. Rats that had been given oxytocin didn't seem to get drunk. "Those that had the oxytocin were up and moving about as if they hadn't had any alcohol at all, whereas the ones that didn't have oxytocin were quite heavily sedated," Bowen says. This effect was confirmed in a second experiment, in which half the rats were given an injection of oxytocin straight into the brain, at a level about 150,000 times what would normally be found there. They were then given alcohol, after which researchers tested their motor control and reaction times. Oxytocin seemed to completely counteract the effects of the booze – even when a rat had consumed what would be equivalent to about one and a half bottles of wine in humans. "The rats that had received oxytocin, as well as the alcohol, were virtually indistinguishable from the rats that hadn't received any alcohol at all," says Bowen. This could be thanks to the brain's GABA receptors, where alcohol is thought to exert its intoxicating effects. Bowen's team found that oxytocin was binding to two parts of these receptors, blocking alcohol from getting there. "It was actually preventing alcohol affecting these sites in the brain that make you intoxicated." © Copyright Reed Business Information Ltd

Keyword: Drug Abuse; Hormones & Behavior
Link ID: 20604 - Posted: 02.24.2015

Charles F. Zorumski It is indeed possible for a person to get intoxicated and not remember what she or he did. This state is called a “blackout” or, more precisely, a “memory blackout.” During a blackout a person is intoxicated but awake and interacting with the environment in seemingly meaningful ways, such as holding a conversation or driving a car. After the period of intoxication, usually the next day, the person has no or, at best, vague recall for events that occurred while inebriated. At times, being in this state can have disastrous consequences, such as waking up in an unknown or unsafe place, losing personal possessions or participating in risky behaviors. On the neural level, a blackout is a period of anterograde amnesia. That is, a person's ability to form new memories becomes impaired. Although a person does not lose previously learned information, he or she may also find it more difficult to recall certain facts while intoxicated. Yet once a person sobers up, his or her memory and ability to learn new information are not permanently affected. How alcohol, or ethanol, produces a memory blackout is not completely understood. It is clear, however, that alcohol can impair a process in brain cells called long-term potentiation (LTP), a cellular mechanism thought to underlie memory formation, particularly in the hippocampus. © 2015 Scientific American

Keyword: Drug Abuse; Learning & Memory
Link ID: 20603 - Posted: 02.24.2015

A dozen university students have been treated at Connecticut hospitals after overdosing on "Molly" or MDMA, a popular synthetic party drug. Police are investigating after the overdoses were reported late Sunday on the campus of Wesleyan University in Middletown, Connecticut. By Monday, eight remained in hospital and two were in critical condition. It was unclear whether the students had been together or where the drugs had come from. Middletown Police Chief William McKenna said that their "first and foremost goal is to obtain information on the batch of Molly that was distributed to the students on the campus," adding, "this information is critical in ensuring the recovery of those students affected." A pure and more powerful form of MDMA often sold as "Molly" can cause liver, kidney, cardiovascular failure, or death. In a campus-wide statement, Wesleyan president Michael S Roth urged students to "please, please stay away from illegal substances, the use of which can put you in extreme danger. One mistake can change your life forever". Dean Michael Whaley, vice president of student affairs at Wesleyan University, sent a letter to the school body on Sunday recommending students to check on their friends. Ten of the 12 people were Wesleyan students. In 2013, Molly-related deaths and illnesses forced the Electric Zoo Festival in New York to shut down early after two young people died and four were confined to hospital.

Keyword: Drug Abuse
Link ID: 20602 - Posted: 02.24.2015

|By Roni Jacobson Several pharmaceutical drugs promise to help addicts quit, and many people embrace the ease of popping a pill. Yet research continues to show that although medication can help, support networks and therapy targeting the underlying behaviors are still the best available ways to kick addiction over the long term. In addition, some of these medications come with scary side effects—hundreds of people have reportedly committed suicide while on the smoking-cessation drug Chantix, for example. Read on for short profiles of the addiction drugs currently on the market, as well as a few compounds that may hit shelves soon. © 2015 Scientific American,

Keyword: Drug Abuse
Link ID: 20601 - Posted: 02.24.2015

By ABIGAIL ZUGER, M.D. On an early summer night in 1944, on the wooded shoulder of a rural Massachusetts highway, a man in a rumpled brown suit wandered in the shadows. Whenever a car passed, he dropped to the ground and lay flat. His hair was matted, his face smeared with mud. He was a respectable Boston doctor on the lam, hungry, lost and ill. He was Mimi Baird’s father, Dr. Perry Baird, a Texas-born, Harvard-trained physician whose severe bipolar disease ultimately destroyed his life and scarred his family with the usual wide-ranging cruelties of mental illness. Dr. Baird vanished from Ms. Baird’s life when she was a little girl. She saw him once, briefly, when she was a teenager, then never again. He died in his mid-50s, in 1959. More than 30 years later, when Ms. Baird herself was in her 50s, a large package arrived on her doorstep and her father re-entered her world. The box contained a manuscript long forgotten in a relative’s garage, written in smudged pencil on onionskin paper, a memoir her father had composed of five terrible months in his life. The story began the very day Dr. Baird said goodbye to 5-year-old Mimi and her sister, and permanently left the household. Stunned and bereft all over again, Ms. Baird then spent two decades chasing down the rest of the story, talking to neighbors, colleagues and relatives about long-ago events and obtaining her father’s medical records. Now in her late 70s, a retired medical administrator, she has, with the help of a co-author, woven all this material into “He Wanted the Moon,” an extraordinary Möbius strip of a book. (Read an excerpt.) Its core is the full text of her father’s manuscript, deftly annotated and explained. Around it she layers the voices of caretakers, friends, relatives and medical authorities. Events are revisited and reframed, turned inside out, then right side up again. The book is autobiography, biography, science, history and literature all in one, as instructive as any textbook and utterly impossible to put down. © 2015 The New York Times Company

Keyword: Schizophrenia
Link ID: 20600 - Posted: 02.24.2015

By Nathan Seppa Ask anybody — stress is bad news. The negative view of stress has been expressed so consistently that the concept is now built into our vernacular, which is spiced with advice on avoiding it: Take it easy. Calm down. Chill. Of course, a good case of stress comes in handy during an encounter with a grizzly bear on a hiking trail. In that situation, a stress reaction delivers a burst of hormones that revs up the heart and sharpens attention. This automatic response has served humans well throughout evolution, improving our odds of seeing another day. Problems arise, however, when stress becomes a feature of daily life. Chronic stress is the kind that comes from recurring pain, post-traumatic memories, unemployment, family tension, poverty, childhood abuse, caring for a sick spouse or just living in a sketchy neighborhood. Nonstop, low-grade stress contributes directly to physical deterioration, adding to the risk of heart attack, stroke, infection and asthma. Even recovery from cancer becomes harder. Scientists have now identified many of the biological factors linking stress to these medical problems. The evidence centers on nagging inflammation and genetic twists that steer cells off a healthy course, resulting in immune changes that allow ailments to take hold or worsen. Despite the bad rap stress has acquired throughout history, researchers have only recently been able to convince others that it’s dangerous. “It’s taken much more seriously now,” says Janice Kiecolt-Glaser, a clinical psychologist at Ohio State University in Columbus. “In the 1980s, we were still in the dark ages on this stuff.” © Society for Science & the Public 2000 - 2015

Keyword: Stress; Neuroimmunology
Link ID: 20599 - Posted: 02.21.2015

By Elizabeth Pennisi Researchers have increased the size of mouse brains by giving the rodents a piece of human DNA that controls gene activity. The work provides some of the strongest genetic evidence yet for how the human intellect surpassed those of all other apes. "[The DNA] could easily be a huge component in how the human brain expanded," says Mary Ann Raghanti, a biological anthropologist at Kent State University in Ohio, who was not involved with the work. "It opens up a whole world of possibilities about brain evolution." For centuries, biologists have wondered what made humans human. Once the human and chimp genomes were deciphered about a decade ago, they realized they could now begin to pinpoint the molecular underpinnings of our big brain, bipedalism, varied diet, and other traits that have made our species so successful. By 2008, almost two dozen computerized comparisons of human and ape genomes had come up with hundreds of pieces of DNA that might be important. But rarely have researchers taken the next steps to try to prove that a piece of DNA really made a difference in human evolution. "You could imagine [their roles], but they were just sort of 'just so' stories,” says Greg Wray, an evolutionary biologist at Duke University in Durham, North Carolina. Wray is particularly interested in DNA segments called enhancers, which control the activity of genes nearby. He and Duke graduate student Lomax Boyd scanned the genomic databases and combed the scientific literature for enhancers that were different between humans and chimps and that were near genes that play a role in the brain. Out of more than 100 candidates, they and Duke developmental neurobiologist Debra Silver tested a half-dozen. They first inserted each enhancer into embryonic mice to learn whether it really did turn genes on. Then for HARE5, the most active enhancer in an area of the brain called the cortex, they made minigenes containing either the chimp or human version of the enhancer linked to a “reporter” gene that caused the developing mouse embryo to turn blue wherever the enhancer turned the gene on. Embryos’ developing brains turned blue sooner and over a broader expanse if they carried the human version of the enhancer, Silver, Wray, and their colleagues report online today in Current Biology. © 2015 American Association for the Advancement of Science

Keyword: Development of the Brain; Genes & Behavior
Link ID: 20598 - Posted: 02.21.2015

by Sarah Zielinski No one would be shocked to find play behavior in a mammal species. Humans love to play — as do our cats and dogs. It’s not such a leap to believe that, say, a red kangaroo would engage in mock fights. But somehow that behavior seems unlikely in animals other than mammals. It shouldn’t, though. Researchers have documented play behavior in an astonishing range of animals, from insects to birds to mammals. The purpose of such activities isn’t always clear — and not all scientists are convinced that play even exists — but play may help creatures establish social bonds or learn new skills. Here are five non-mammals you may be surprised to find hard at play: Crocodilians Alligators and crocodiles might seem more interested in lurking near the water and chomping on their latest meal, but these frightening reptiles engage in play, Vladimir Dinets of the University of Tennessee in Knoxville reports in the February Animal Behavior and Cognition. Dinets combined 3,000 hours of observations of wild and captive crocodilians with published reports and information gathered from other people who work with the animals. He found examples of all three types of play: Locomotor play: This is movement without any apparent reason or stimulus. Young, captive American alligators, for instance, have been spotted sliding down slopes of water over and over. And a 2.5-meter-long crocodile was seen surfing the waves near a beach in Australia. Object play: Animals like toys, too. A Cuban crocodile at a Miami zoo picked up and pushed around flowers floating in its pool for several days of observation. And like a cat playing with a mouse, a Nile crocodile was photographed as it repeatedly threw a dead hippo into the air. Object play is recognized as so important to crocodilian life “that many zoo caretakers now provide various objects as toys for crocodilians as part of habitat enrichment programs,” Dinets notes. © Society for Science & the Public 2000 - 2015.

Keyword: Development of the Brain
Link ID: 20597 - Posted: 02.21.2015

Maanvi Singh Your tongue doubtless knows the difference between a high-fat food and the low-fat alternative. Full-fat ice cream and cream cheese feel silkier and more sumptuous. Burgers made with fatty meat are typically juicer than burgers made with lean meat. OK, so, we've long known fat gives food a desirable texture. But some scientists are now making the case that we should also think of fat as the sixth primary taste, along with sweet, salt, sour, bitter and umami. Early in February, researchers from Deakin University in Australia published a paper in the journal Flavour arguing that "the next 5 to 10 years should reveal, conclusively, whether fat can be classified as the sixth taste." So what would it take for fat to become an official taste? "Strictly speaking, taste is a chemical function," Russell Keast, a sensory scientist at Deakin and lead author of the paper, tells The Salt. He says that when a chemical substance – a salt or sugar crystal, for example — comes into contact with sensory cells in our mouths, it triggers a series of reactions. The cells in our mouths tell other nerve cells that they're perceiving something sweet or salty and those nerve cells eventually pass this information on to the brain. According to the paper, there are five criteria that need to be met to call something a primary taste. It starts with a chemical stimuli (like sugar or salt), which then trigger specific receptors on our taste buds. Then, there has to be a viable a pathway between these receptors and our brains, and we've got to be able to perceive and process the taste in the brain. And finally, this whole process has to trigger downstream effects in the body. © 2015 NPR

Keyword: Chemical Senses (Smell & Taste)
Link ID: 20596 - Posted: 02.21.2015