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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.
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
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.
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
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
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
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
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
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
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
By Christie Aschwanden Paul Offit likes to tell a story about how his wife, pediatrician Bonnie Offit, was about to give a child a vaccination when the kid was struck by a seizure. Had she given the injection a minute sooner, Paul Offit says, it would surely have appeared as though the vaccine had caused the seizure and probably no study in the world would have convinced the parent otherwise. (The Offits have such studies at the ready — Paul is the director of the Vaccine Education Center at the Children’s Hospital of Philadelphia and author of “Deadly Choices: How the Anti-Vaccine Movement Threatens Us All.”) Indeed, famous anti-vaxxer Jenny McCarthy has said her son’s autism and seizures are linked to “so many shots” because vaccinations preceded his symptoms. But, as Offit’s story suggests, the fact that a child became sick after a vaccine is not strong evidence that the immunization was to blame. Psychologists have a name for the cognitive bias that makes us prone to assigning a causal relationship to two events simply because they happened one after the other: the “illusion of causality.” A study recently published in the British Journal of Psychology investigates how this illusion influences the way we process new information. Its finding: Causal illusions don’t just cement erroneous ideas in the mind; they can also prevent new information from correcting them. Helena Matute, a psychologist at Deusto University in Bilbao, Spain, and her colleagues enlisted 147 college students to take part in a computer-based task in which they each played a doctor who specializes in a fictitious rare disease and assessed whether new medications could cure it. ©2015 ESPN Internet Ventures.
Tom Stafford Trusting your instincts may help you to make better decisions than thinking hard, a study suggests. It is a common misconception that we know our own minds. As I move around the world, walking and talking, I experience myself thinking thoughts. "What shall I have for lunch?", I ask myself. Or I think, "I wonder why she did that?" and try and figure it out. It is natural to assume that this experience of myself is a complete report of my mind. It is natural, but wrong. There's an under-mind, all psychologists agree – an unconscious which does a lot of the heavy lifting in the process of thinking. If I ask myself what is the capital of France the answer just comes to mind – Paris! If I decide to wiggle my fingers, they move back and forth in a complex pattern that I didn't consciously prepare, but which was delivered for my use by the unconscious. The big debate in psychology is exactly what is done by the unconscious, and what requires conscious thought. Or to use the title of a notable paper on the topic, 'Is the unconscious smart or dumb?' One popular view is that the unconscious can prepare simple stimulus-response actions, deliver basic facts, recognise objects and carry out practised movements. Complex cognition involving planning, logical reasoning and combining ideas, on the other hand, requires conscious thought. A recent experiment by a team from Israel scores points against this position. Ran Hassin and colleagues used a neat visual trick called Continuous Flash Suppression to put information into participants’ minds without them becoming consciously aware of it.
Link ID: 20594 - Posted: 02.19.2015
by Catherine Lawson Over the last six years Adam Gazzaley's research has undergone a transformation. He's moved from studying how the brain works, to studying the brain as it ages, then into the domain of applying methodology he's developed to improve the brain's functions. At WIRED Health 2015 he'll outline his vision of the future, one where "we're thinking about software and hardware as medicine". In particular, Gazzaley plans to talk to the WIRED Health audience about video games "that are custom-designed to challenge the brain in a very particular way". Gazzaley's team at University of California, San Francisco previously demonstrated that a custom-designed video game can be highly effective in treating a specific cognitive deficit. They developed NeuroRacer, a driving game aimed at improving multi-tasking skills in older people. The success of NeuroRacer propelled Gazzaley into new partnerships, giving him access to resources that further advance his games development program into areas like motion capture and virtual reality. He's excited about coupling his games with mobile devices that will allow them to function outside the lab. Gazzaley will talk about four new games he's working on, in particular a meditation-inspired one. Meditrain is the product of his collaboration with Buddhist author and teacher Jack Kornfield. Developed for the iPad, he hopes to demonstrate part of it at WIRED Health.
Keyword: Learning & Memory
Link ID: 20593 - Posted: 02.19.2015
Boer Deng Smoking marijuana may stoke a yearning for crisps, but understanding how it affects hunger is relevant not just to those who indulge in it. The drug has yielded a ripe target for scientists who seek to stimulate or suppress appetite: the receptor CB1, found in cells throughout the body. When activated by the anti-nausea drug dronabinol — which is also a component of marijuana (Cannabis sativa) — CB1 prompts the release of hunger-promoting hormones1. And suppressing its activity is thought to aid in weight loss2. But the mechanism by which the receptor kills or kindles appetite is not entirely understood. Now neuroscientist Tamas Horvath, of Yale University in New Haven, and colleagues report in Nature that nerve cells called pro-opiomelanocortin (POMC) neurons play a key role in this process3. POMC had generally been thought to promote satiation, but Horvath's team found that POMC neurons in the brain release not just a hunger-suppressing hormone, but also one that promotes appetite. Which hormone is secreted is regulated by a protein in the cells' mitochondria, structures that regulate energy levels. When the CB1 receptor is activated, this mitochondrial protein induces POMC to switch from secreting the substance that suppresses gorging to one that encourages it. The finding is intriguing, says Uberto Pagotto, a neuroscientist at the University of Bologna who has studied cannabinoids for many years. “It gives us a different starting point to look at CB1 receptors and the mitochondria,” he says. © 2015 Nature Publishing Group
Catherine Brahic THE nature versus nurture debate is getting a facelift this week, with the publication of a genetic map that promises to tell us which bits of us are set in stone by our DNA, and which bits we can affect by how we live our lives. The new "epigenomic" map doesn't just look at genes, but also the instructions that govern them. Compiled by a consortium of biologists and computer scientists, this information will allow doctors to pinpoint precisely which cells in the body are responsible for various diseases. It might also reveal how to adjust your lifestyle to counter a genetic predisposition to a particular disease. "The epigenome is the additional information our cells have on top of genetic information," says lead researcher Manolis Kellis of the Massachusetts Institute of Technology. It is made of chemical tags that are attached to DNA and its packaging. These tags act like genetic controllers, influencing whether a gene is switched on or off, and play an instrumental role in shaping our bodies and disease. Researchers are still figuring out exactly how and when epigenetic tags are added to our DNA, but the process appears to depend on environmental cues. We inherit some tags from our parents, but what a mother eats during pregnancy, for instance, might also change her baby's epigenome. Others tags relate to the environment we are exposed to as children and adults. "The epigenome sits in a very special place between nature and nurture," says Kellis. Each cell type in our body has a different epigenome – in fact, the DNA tags are the reason why our cells come in such different shapes and sizes despite having exactly the same DNA. So for its map, the Roadmap Epigenomics Consortium collected thousands of cells from different adult and embryonic tissues, and meticulously analysed all the tags. © Copyright Reed Business Information Ltd.