The organizers of today's Pro-Test rally at the University of California, Los Angeles, say it succeeded beyond their hopes. Hundreds of people—many of them students and postdocs—came out to show their support for biomedical research. U.S. scientists who use animals in their research have been under attack from animal rights extremists in recent years, and UCLA has been the epicenter. Many scientists have been reluctant to speak up in defense of their work for fear of provoking further harassment. But today that changed. "I'm amazed," UCLA neuroscientist David Jentsch said of the turnout (campus police put the crowd at about 700). Jentsch organized the rally after waking up one night last month to find his car in flames. Animal rights activists later claimed responsibility. Jentsch modeled today's rally on protests at the University of Oxford that helped turn the tide of public opinion against animal rights extremists who opposed construction of a research lab there. Despite the time and effort it took away from his research and the hate e-mail he endured, Jentsch says the rally was worth it. "I think putting our faces on what we do humanizes the effort and makes it harder to write obscene things in the middle of the night and to brutalize people." Pro-testers gathered on the edge of the UCLA campus as a counter protest staged by animal rights groups was winding down across the street. The anti-vivisection rally, part of the annual World Week for Animals in Laboratories, attracted fewer people—several dozen—and at times there seemed to be almost as many journalists as protesters. The media, including CNN and several local television stations, had turned out perhaps hoping to see a confrontation. There wasn't one. The visible police presence may have helped, but everyone on both sides appeared to be on their best behavior. © 2008 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 12796 - Posted: 06.24.2010

A study has found that painkillers such as ibuprofen cannot prevent Alzheimer's disease - but does not rule out that they may delay its onset. Work had raised hope that non-steroidal anti-inflammatory drugs (NSAIDs) might have a preventative effect. But the latest 12-year study found the risk of dementia was 66% higher in people with heavy NSAID use, compared with those with little or no use. The University of Washington study features in the journal Neurology. A US study published last year and based on data from almost 250,000 veterans showed those who used ibuprofen for more than five years were more than 40% less likely to develop Alzheimer's. The latest research focused on 2,736 people with an average age of 75 at the start of the study. Lead researcher Dr Eric Larson said: "Although we hoped to find a protective effect, there was none. "Thus, for this age group, there's no basis for taking NSAIDs to prevent Alzheimer's disease." His colleague Dr John Breitner said a key difference between the latest study and previous work was that the participants were older. He said: "It has been argued for some time that NSAID use delays the onset of Alzheimer's disease. It would follow that studies looking at younger people who use NSAIDs would show fewer cases of Alzheimer's, while in groups of older people there might be more cases, including those that would have occurred earlier if they had not been delayed. We must not ignore the fundamental finding, which is an increase in the risk of dementia in the NSAID users. We need further research to understand that result more clearly." Rebecca Wood, of the Alzheimer's Research Trust, said there were no clear evidence pinning down the effect of NSAIDs - if any - on dementia. (C)BBC

Keyword: Alzheimers
Link ID: 12795 - Posted: 04.23.2009

By LAURAN NEERGAARD WASHINGTON -- Food hijacked Dr. David Kessler's brain. Not apples or carrots. The scientist who once led the government's attack on addictive cigarettes can't wander through part of San Francisco without craving a local shop's chocolate-covered pretzels. Stop at one cookie? Rarely. It's not an addiction but it's similar, and he's far from alone. Kessler's research suggests millions share what he calls "conditioned hypereating" _ a willpower-sapping drive to eat high-fat, high-sugar foods even when they're not hungry. In a book being published next week, the former Food and Drug Administration chief brings to consumers the disturbing conclusion of numerous brain studies: Some people really do have a harder time resisting bad foods. It's a new way of looking at the obesity epidemic that could help spur fledgling movements to reveal calories on restaurant menus or rein in portion sizes. "The food industry has figured out what works. They know what drives people to keep on eating," Kessler tells The Associated Press. "It's the next great public health campaign, of changing how we view food, and the food industry has to be part of it." He calls the culprits foods "layered and loaded" with combinations of fat, sugar and salt _ and often so processed that you don't even have to chew much. Overeaters must take responsibility, too, and basically retrain their brains to resist the lure, he cautions. © 2009 The Associated Press

Keyword: Obesity; Drug Abuse
Link ID: 12794 - Posted: 06.24.2010

By Alice Park The promise of energy drinks is pretty irresistible — push your body, work hard, sweat buckets, and if you need an extra boost, down a bottle or two of liquid fuel to drive you through the rest of your workout. Makes sense, since the drinks provide your body with carbohydrates in the form of sugars — the fuel that cells and tissues like muscle need to keep working. But exercise experts say that despite what you may think, energy drinks have no effect at all on your tired muscles. Instead, when your energy is petering out, a swig of an energy drink works on the brain to keep you inspired and motivated to push on. Researchers at the University of Birmingham and Manchester Metropolitan University report in the Journal of Physiology that sugary energy drinks activate reward and pleasure regions in the brain, a boost that can translate to better performance — and one that does not occur with other artificially sweetened beverages. In the study, volunteers who got sugary energy drinks were able to complete a physical-training session 2% faster than those who got artificially sweetened drinks, and improved their mean power output as well. "What we are suggesting is a central-governor model," says Ed Chambers, one of the study's co-authors and a researcher at the School of Sport and Exercise Sciences at the University of Birmingham. "Ultimately, the brain controls exercise performance by controlling the neural outflow to the exercising muscles." © 2009 Time Inc.

Keyword: Drug Abuse
Link ID: 12793 - Posted: 06.24.2010

By Nicole Branan Forming a grammatically correct sentence may seem to require advanced cognitive skills, but it turns out that our creative language capacity might rely on a less sophisticated system than is commonly thought. A recent study suggests that our ability to construct sentences may arise from procedural memory—the same simple memory system that lets our dogs learn to sit on command. Scientists distinguish between procedural memory, which is relevant for learning skills such as how to swim, and declarative memory, which stores knowledge, including facts and memories of events, such as one’s birthday, says Victor S. Ferreira of the University of California, San Diego. To find out which system is at work when we form sentences, Ferreira and his team exploited a phenomenon called syntactic persistence—speakers tend to use the same grammatical pattern they have used or heard in previous sentences. The researchers tested four healthy individuals and four amnesic patients. The amnesiacs’ procedural memory was intact, meaning that they could learn skills with repetitive practice, but their declarative memory abilities were damaged, leaving them unable to memorize new facts. First, all participants heard and repeated a sentence. Then they saw an unrelated picture and had to describe it. Finally, participants heard another sentence that was either identical to the original sentence or subtly changed in its meaning or grammatical structure, or both. © 1996-2009 Scientific American Inc.

Keyword: Language
Link ID: 12792 - Posted: 06.24.2010

by Linda Geddes A GROWING appreciation of the links between anorexia and autism spectrum disorders has uncovered new opportunities for treating the eating disorder. Mental health professionals are now attempting to train the brains of people with anorexia to be more flexible and to see the big picture as well as fine details. In doing so, they hope patients will be less inclined to obsess about body weight and calories and be better equipped to overcome their eating disorder in the long term, as well as gaining weight more immediately. Last month, the international Academy for Eating Disorders published a paper calling for eating disorders (EDs) such as anorexia and bulimia to receive the same degree of healthcare as other biologically based mental illnesses such as schizophrenia, bipolar disorder and obsessive compulsive disorder (OCD) (International Journal of Eating Disorders, DOI: 10.1002/eat.20589). Other groups are even calling for anorexia to be placed in the same diagnostic category as autism spectrum disorders (ASD). The main reason for this change is a growing understanding of the biological basis of EDs. Twin studies suggest that between 50 and 83 per cent of EDs have a genetic basis. Now, evidence suggests that people with anorexia have cognitive traits associated with ASD. "Eating disorders and autism spectrum disorders are obviously not the same thing, but they do have some things in common," says Janet Treasure of the Institute of Psychiatry in London. © Copyright Reed Business Information Ltd

Keyword: Autism; Anorexia & Bulimia
Link ID: 12791 - Posted: 06.24.2010

by Dan Jones DAYBREAK, and a group of apes are dancing around a rectangular monolith so dark it seems to suck light in. Inspired by this mysterious object, one of them grabs a bone and begins to wield it as a tool - then as a weapon. The armed ape goes hunting, makes a kill and eats flesh for the first time. Next day, he drives a rival group of apes from a watering hole and murders their leader. This, according to Stanley Kubrick's sci-fi masterpiece 2001: A space odyssey, is the dawn of humankind. If only it were that simple. Anyone trying to understand our origins soon realises that no one thing pushed our ape ancestors across the threshold of humanity. It is difficult to pin down what makes us human anyway. We walk upright on two legs, with disproportionately large brains held high, communicating in spoken languages, navigating the complexity of human social life, producing sophisticated tools and artefacts, and creating culture. The story of how we became human is woven from many strands. Attempts to unravel that tale have until recently relied on the hard evidence of fossilised bones. This has allowed us to make inferences about certain aspects of our ancestors: how big they were, how they moved and their cranial capacity. But there is a limit to what you can learn from bones. In particular, they tell us little about our ancestors' less tangible traits, such as how fast they grew, their age at weaning and sexual maturity, and how many offspring they had. They also tell us almost nothing about thought and behaviour. This is a problem, says Robin Dunbar of the University of Oxford, because such factors are important in human evolution. "They're all part of the big story." © Copyright Reed Business Information Ltd

Keyword: Evolution
Link ID: 12790 - Posted: 06.24.2010

By Bruce Bower Predicting whether patients with mental disorders will become violent is a dicey business, and one the legal system has thrust upon mental-health workers. A new study encouragingly suggests that swift swings in the intensity of symptoms can often peg which psychiatric patients are on the verge of threatening or hurting others. Employing a statistical technique called dynamic systems modeling, the new work shows that among psychiatric patients with documented histories of committing violent acts, those whose symptoms of emotional distress rapidly and repeatedly fluctuated from mild to severe during a 26-week period were particularly apt to assault others or to threaten them with a weapon, say psychologist Candice Odgers of the University of California, Irvine and her colleagues. In cases of rapid symptom fluctuation, patients went from peaks to valleys of emotional health about every two to four weeks, the team reports in a paper published online April 15 and slated to appear in the American Journal of Psychiatry. Violence occurred less frequently among patients whose symptoms fluctuated from high to low points over longer stretches, which often lasted about 10 weeks. Overall, patients whose symptoms rapidly ebbed and flowed were almost three times as likely to become violent than those whose symptoms oscillated slowly. Patients who displayed rapidly fluctuating psychiatric symptoms that also worsened during the study were especially likely to commit two or more violent acts during the study period. © Society for Science & the Public 2000 - 2009

Keyword: Emotions; Aggression
Link ID: 12789 - Posted: 06.24.2010

By Claire Thomas In 1989, The Lancet carried a curious report on a dog that kept licking a mole on her owner's leg. The mole turned out to be a malignant melanoma. Since then, scientists have observed similar "disease sniffing" abilities in mice and rats, which tend to avoid sickly members of their own species. Now researchers think they have figured out how these animals do it. Scientists have previously identified a number of mouse smell receptors, cell-surface proteins in the animals' noses that pick up everything from the fragrance of food to the scent of fear (ScienceNOW, 21 August 2008). Neurogeneticist Ivan Rodriguez of the University of Geneva in Switzerland and colleagues wondered whether there might be additional such receptors that respond to a disease "scent," perhaps by detecting chemicals associated with bacteria and inflammation. The researchers scoured the already deciphered mouse genome, looking for genes that might encode additional receptor proteins in its olfactory system, the sensory cells that connect the nose to the brain. They found genes for five new receptors, all of which belong to a known family of proteins called formyl peptide receptors (FPRs). The known FPRs include two immune system receptors that detect chemicals given off by pathogens in the blood, helping immune cells track down and attack foreign bodies. Could the newly identified ones on olfactory cells do the same, detecting pathogens but those outside the body on another animal? Rodriguez's team exposed olfactory mouse neurons in the lab to disease-causing bacteria and the urine of sick mice. Sure enough, some of the chemicals sparked a "smell response" in the neurons, as reflected by electrical changes in the cells, the researchers report online today in Nature. © 2009 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 12788 - Posted: 06.24.2010

By Tina Hesman Saey Rubbernecking neurons don’t do an injured brain any good. Newborn neurons rush to the scene of the damage but don’t pitch in to help heal the wound, a new study shows. Scientists have had great hopes that new neurons produced in the brain after a stroke or other insult could migrate to the wounded area and replace damaged cells. Previous research has shown that the newborns are attracted to injury sites, but a new study that appears in the April 22 Journal of Neuroscience shows that those neurons don’t form replacements for the majority of cells. The results indicate that simply boosting neuron production may not help heal the brain. Zhengang Yang of Fudan University in Shanghai and colleagues induced strokes in a part of rats’ brains called the striatum, which controls movement, and marked new neurons so the cells could be traced as they migrated through the brain. The researchers examined the cells for certain proteins that are hallmarks of different neuron types, to see which kind of neuron the cells differentiated into. Previous research has shown that new neurons are born in the adult brain in two places — the hippocampus and the subventricular zone, or SVZ. Neurons born in the SVZ usually migrate to the olfactory bulb. But after a stroke, some of the new SVZ neurons flock to the wound site. Yang and his colleagues show in the new study that the new SVZ neurons don’t form medium-sized spiny neurons, the type of cell most common in the striatum. Only neurons producing calretinin and Sp8, two markers of olfactory bulb neurons, migrate into the wounded striatum. There, the neurons form the same type that they would in the olfactory bulb, if they survive at all. © Society for Science & the Public 2000 - 2009

Keyword: Neurogenesis; Regeneration
Link ID: 12787 - Posted: 06.24.2010

This week’s New Yorker has a fascinating article about the growing use of “neuro-enhancing” drugs by college students and others to improve focus, reduce sleep needs and lengthen study time and work hours. Drugs like Adderall and Ritalin, typically prescribed to improve focus of people with attention deficit problems, now are being taken by people with healthy brains to help them boost achievement. One doctor has even coined a term for the practice: cosmetic neurology. Author Margaret Talbot writes: A young man I’ll call Alex recently graduated from Harvard. As a history major, Alex wrote about a dozen papers a semester. He also ran a student organization, for which he often worked more than forty hours a week; when he wasn’t on the job, he had classes. Weeknights were devoted to all the schoolwork that he couldn’t finish during the day, and weekend nights were spent drinking with friends and going to dance parties. …Since, in essence, this life was impossible, Alex began taking Adderall to make it possible. Adderall, a stimulant composed of mixed amphetamine salts, is commonly prescribed for children and adults who have been given a diagnosis of attention-deficit hyperactivity disorder. But in recent years Adderall and Ritalin, another stimulant, have been adopted as cognitive enhancers: drugs that high-functioning, overcommitted people take to become higher-functioning and more overcommitted…. College campuses have become laboratories for experimentation with neuroenhancement. Copyright 2009 The New York Times Company

Keyword: Drug Abuse; ADHD
Link ID: 12786 - Posted: 06.24.2010

by Margaret Talbot A young man I’ll call Alex recently graduated from Harvard. As a history major, Alex wrote about a dozen papers a semester. He also ran a student organization, for which he often worked more than forty hours a week; when he wasn’t on the job, he had classes. Weeknights were devoted to all the schoolwork that he couldn’t finish during the day, and weekend nights were spent drinking with friends and going to dance parties. “Trite as it sounds,” he told me, it seemed important to “maybe appreciate my own youth.” Since, in essence, this life was impossible, Alex began taking Adderall to make it possible. Adderall, a stimulant composed of mixed amphetamine salts, is commonly prescribed for children and adults who have been given a diagnosis of attention-deficit hyperactivity disorder. But in recent years Adderall and Ritalin, another stimulant, have been adopted as cognitive enhancers: drugs that high-functioning, overcommitted people take to become higher-functioning and more overcommitted. (Such use is “off label,” meaning that it does not have the approval of either the drug’s manufacturer or the Food and Drug Administration.) College campuses have become laboratories for experimentation with neuroenhancement, and Alex was an ingenious experimenter. His brother had received a diagnosis of A.D.H.D., and in his freshman year Alex obtained an Adderall prescription for himself by describing to a doctor symptoms that he knew were typical of the disorder. During his college years, Alex took fifteen milligrams of Adderall most evenings, usually after dinner, guaranteeing that he would maintain intense focus while losing “any ability to sleep for approximately eight to ten hours.” In his sophomore year, he persuaded the doctor to add a thirty-milligram “extended release” capsule to his daily regimen.

Keyword: Drug Abuse; ADHD
Link ID: 12785 - Posted: 06.24.2010

Children resuscitated at birth are more likely to have a low IQ by the age of eight, even if they appear healthy as babies, research has suggested. The study compared babies who were resuscitated at birth - some needing further care, but others not - with those who had a problem-free delivery. It suggests even mild problems around delivery may be enough to cause subtle damage to the brain. The study, by Bristol's Southmead Hospital, appears in the Lancet. It is based on children who were part in a long-term research project known as the Children of the 90s study. The researchers defined a low IQ as being less than 80. They found that children who were resuscitated, but required no further treatment, had a 65% increased risk of a low IQ compared with those who were not. The risk of a low IQ for children who were resuscitated and also required further treatment for signs of brain damage, known as encephalopathy, was six times higher than babies delivered without any problem. Damage caused during labour is due to the brain being starved of oxygen, a phenomenon known as hypoxia. Overall the risk of a low IQ for any of the children was still relatively low. But writing in The Lancet, the researchers said: "Infants who needed resuscitation, even if they did not develop encephalopathy in the neonatal period, had a substantially increased risk of a low full-scale IQ score. "The data suggest that mild perinatal physiological compromise might be sufficient to cause subtle neuronal or synaptic (nerve cell junction) damage, and thereby affect cognition in childhood and potentially in adulthood." (C)BBC

Keyword: Development of the Brain; Intelligence
Link ID: 12784 - Posted: 04.23.2009

By RONI CARYN RABIN It may be hard to fathom, but in the haystack of government health statistics that track cancer, car accidents, twin births to women over 40, fat teenagers and people who quit smoking, there has been no reliable estimate of the number of Americans affected by paralysis. Until now. A study to be released on Tuesday by the Christopher and Dana Reeve Foundation reports that far more Americans than previously estimated are paralyzed to some degree: 5.6 million people, representing 1.9 percent of the population, or roughly 1 in 50 Americans. Previous estimates — or “guesstimates,” as some have called them — hovered around 4 million at most, and some were as low as 1.4 million. “Nobody had any idea what the numbers were, because no one ever tried to find out,” said Joseph Canose, vice president for quality of life at the Reeve Foundation’s Paralysis Resource Center, who led the study. “There were many different ways of counting it, and there was no common definition, and the numbers were all over the place.” But the figures, which could have enormous implications for public policy, research financing and health care, are already causing controversy, because the estimates for paralysis caused by certain diseases and conditions differ drastically from long-accepted numbers. Copyright 2009 The New York Times Company

Keyword: Movement Disorders
Link ID: 12783 - Posted: 06.24.2010

Dr. Michael Stein treats ordinary ailments such as heart failure and headaches, and cares for people in the throes of addiction. Stein is also a novelist and Brown University professor of medicine and community health. His latest work combines those pursuits in the true story of one woman's fight to live the life she lost to addiction. Lucy Fields is the name he gives to a 29-year-old patient addicted to the painkiller Vicodin. The drug is the most-prescribed medication in the United States, 20 times more common than Prozac or penicillin. "The Addict: One Patient, One Doctor, One Year" is a portrait of her battle to kick the drug. Here is an edited version of a recent conversation with Stein. Q. Why do you treat addicts? A. People who are addicted in general are young and physically healthy, so if you can help them, the satisfaction is a rarity for an internist. I typically deal with chronic illnesses that are slow to get better or never get better, whereas people who are addicts can really dramatically change. Q. Does that make you an optimist? A. All doctors are optimists. We want our patients to get better. With addicts, you are literally trying to change someone's mind. Their brains need to be helped to rid themselves of this problem. That is a difficult, long-lasting process that requires patience and optimism. © 2009 NY Times Co

Keyword: Drug Abuse
Link ID: 12782 - Posted: 06.24.2010

By SALLY SATEL, M.D. Last fall, British television broadcast a reality program called “How Mad Are You?” The plot was simple: 10 volunteers lived together for a week in a castle in the Kent countryside and took part in a series of challenges. The twist was the lack of a prize. Five of the volunteers had a history of a serious mental illness, like obsessive compulsive disorder and bipolar disorder, and five did not. The challenges, meant to elicit latent symptoms, included mucking out a cowshed, performing stand-up comedy and taking psychological tests. But the real test came at the end of the week. Could a panel of experts — a psychiatrist, psychologist and a psychiatric nurse — tell them apart? They could not. After watching hours of videotape, the experts correctly identified only two of the five people with a history of mental illness. And they misidentified two of the healthy people as having a mental illness. The point was made: even trained professionals cannot reliably determine mental illness by appearances alone. “Having a mental illness doesn’t have to become your defining characteristic,” wrote the producer, Rob Liddell, in describing the program. “It shouldn’t set you apart in society.” The leading mental health advocacy group in England and Wales, MIND, praised the program for encouraging viewers “to re-examine their preconceptions.” Copyright 2009 The New York Times Company

Keyword: Schizophrenia; OCD - Obsessive Compulsive Disorder
Link ID: 12781 - Posted: 06.24.2010

By Claire Thomas An intense scouring of the X chromosome has turned up nine new genes tied to X-linked mental retardation, a group of conditions marked by severe cognitive impairment. The study also surprisingly indicates that more than 1% of the estimated 800 genes on the X chromosome have no function in the body. "[The work] sets the stage for the next frontier in human and medical genetics," says Han Brunner, an expert in congenital conditions at the University of Nijmegen in the Netherlands who was not involved in the research. Mental retardation afflicts 2% to 3% of the general population, and researchers have linked a small proportion of these cases to a faulty X chromosome. In addition to cognitive problems, patients with X-linked mental retardation (XLMR)--which includes fragile x syndrome (ScienceNOW, 24 May 2007)--may also suffer from epilepsy, macrocephaly (an enlarged head), and reproductive defects. XLMR is far more common in boys, as they only inherit one X chromosome and thus don't have the backup copy that girls do. Traditional genetic methods, such as looking at family trees and sequencing individual genes, have linked defects in 80 genes on the X chromosome to XLMR, but the discovery rate has slowed, suggesting that those techniques have reached their limit. So, in the current study, 18 research teams from the United States, the United Kingdom, Australia, France, and Germany turned to a new computer program called AutoCSA, which ramps up the amount of DNA that can be sequenced at one time. The researchers sequenced 720 out of about 800 genes on the X chromosome, comparing 208 individuals with XLMR with unaffected family members. In all, the effort took 6 years and would have been "unthinkable" using traditional methods, says Patrick Tarpey, a molecular geneticist at the Sanger Institute in Cambridge, U.K., who was part of the collaboration. © 2009 American Association for the Advancement of Science

Keyword: Development of the Brain; Genes & Behavior
Link ID: 12780 - Posted: 06.24.2010

by Joyce Gramza It’s been 20 years since the discovery of the gene that causes the most common type of Muscular Dystrophy — Duchenne MD — and patients are still waiting for a cure. "The mutation causes muscle fibers to pull away from each other and with progressive use of your muscles in these patients it eventually leads to muscle damage, severe muscle damage," explains Dean Burkin, assistant professor of pharmacology at the University of Nevada, Reno School of Medicine. Gene therapy to replace the faulty dystrophin gene might be a solution, but Burkin and his colleagues are excited about a simpler and potentially safer approach based on work they are publishing in this week’s Proceedings of the National Academy of Sciences. "This could be an IV drug for the patients if the work in the mouse models that we’ve been using translates to human studies," Burkin says. "That would allow a fair ease of treatment for the patients…. We’ve obviously got to do some safety tests and there’s still a few studies that we need to do. But in the field there are a number of drugs including ours that are being developed. "These patients, especially, have been waiting a long time for new therapies to come about and I think we’re at the cusp now." ©2009 ScienCentral

Keyword: Movement Disorders; Muscles
Link ID: 12779 - Posted: 06.24.2010

By LEE DYE So after looking for years you finally found your perfect mate. Was it good judgment on your part, helped along by a lot of romance, or was it just a case of cold genetics? It may well be that your genes, not your superior taste when it comes to the opposite sex, made the choice for you. But even your genes can get it wrong. At least if you are a fruit fly. A team of scientists at Cornell University in Ithaca, N.Y., and the University of Queensland in Brisbane, Australia, have been trying for a number of years to figure out the role genes play in mate selection. Of course, they would prefer to study the same thing in humans, but there seems to be an ethical problem with having people mate with strangers to produce children for scientific research. So for now, fruit flies will have to do. These amazing creatures share many genes with higher life forms, including humans, and they go through so many generations in such a short period of time that they are very useful for research. And they're cheap, fortunately, because their lifespan is only a couple of weeks. In their latest experiment, the researchers used two different strains of fruit flies that have lived in separate and controlled environments in their lab for 15 years. © 2009 ABCNews Internet Ventures

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 12778 - Posted: 06.24.2010

By Jonah Lehrer One of the first tricks in Penn and Teller's Las Vegas show begins when Teller—the short, quiet one—strolls onstage with a lit cigarette, inhales, drops it to the floor, and stamps it out. Then he takes another cigarette from his suit pocket and lights it. No magic there, right? But then Teller pivots so the audience can see him from the other side. He goes through the same set of motions, except this time everything is different: Much of what just transpired, the audience now perceives, was a charade, a carefully orchestrated stack of lies. He doesn't stamp out the first cigarette—he palms it, then puts it in his ear. There is no second cigarette; it's a pencil stub. The smoke from the first butt is real, but the lighter used on the pencil is actually a flashlight. Yet the illusion is executed so perfectly that every step looks real, even when you're shown that it is not. Penn and Teller demonstrate the seven basic principles of magic. The trick is called Looks Simple, and the point is that even a puff on a cigarette, closely examined, can disintegrate into smoke and mirrors. "People take reality for granted," Teller says shortly before stepping onstage. "Reality seems so simple. We just open our eyes and there it is. But that doesn't mean it is simple." For Teller (that's his full legal name), magic is more than entertainment. He wants his tricks to reveal the everyday fraud of perception so that people become aware of the tension between what is and what seems to be. Our brains don't see everything—the world is too big, too full of stimuli. So the brain takes shortcuts, constructing a picture of reality with relatively simple algorithms for what things are supposed to look like. Magicians capitalize on those rules. Wired.com © 2009 Condé Nast Digital

Keyword: Attention; Vision
Link ID: 12777 - Posted: 06.24.2010