by David Wolman MICHELLE Dawson can't handle crowded bus journeys, and she struggles to order a cup of coffee in a restaurant because contact with strangers makes her feel panicky. Yet over the past few years, Dawson has been making a name for herself as a researcher at the Rivière-des-Prairies hospital, part of the University of Montreal in Canada. Dawson's field of research is the cognitive abilities of people with autism - people such as herself. She is one of a cadre of scientists who say that current definitions of this condition rely on findings that are outdated, if not downright misleading, and that the nature of autism has been fundamentally misunderstood for the past 70 years. Medical textbooks tell us that autism is a developmental disability diagnosed by a classic "triad of impairments": in communication, imagination and social interaction. While the condition varies in severity, about three-quarters of people with autism are classed, in the official language of psychiatrists, as mentally retarded. Over the past decade or so, a growing autistic pride movement has been pushing the idea that people with autism aren't disabled, they just think differently to "neurotypicals". Now, research by Dawson and others has carried this concept a step further. They say that auties, as some people with autism call themselves, don't merely think differently: in certain ways they think better. Call it the autie advantage. © Copyright Reed Business Information Ltd.

Keyword: Autism
Link ID: 14047 - Posted: 06.24.2010

People who get less than six hours sleep per night have an increased risk of dying prematurely, researchers said on Wednesday. Those who slumbered for less than that amount of time were 12 percent more likely to die early, though researchers also found a link between sleeping more than nine hours and premature death. "If you sleep little, you can develop diabetes, obesity, hypertension and high cholesterol," Francesco Cappuccio, who led research on the subject at Britain's University of Warwick, told AFP. The study, conducted with the Federico II University in Naples, Italy, aggregated decade-long studies from around the world involving more than 1.3 million people and found "unequivocal evidence of the direct link" between lack of sleep and premature death. "We think that the relation between little sleep and illness is due to a series of hormonal and metabolical mechanisms," Cappuccio said. The findings of the study were published in the Sleep journal. Cappuccio believes the duration of sleep is a public health issue and should be considered as a behavioral risk factor by doctors. "Society pushes us to sleep less and less," Cappuccio said, adding that about 20 percent of the population in the United States and Britain sleeps less than five hours. © 2010 Discovery Communications, LLC.

Keyword: Sleep
Link ID: 14046 - Posted: 06.24.2010

by Linda Geddes GENE hunters looking for the causes of strokes and other common diseases may have been looking in the wrong place. It seems that common mutations in the DNA of mitochondria, tiny structures that form the energy powerhouses of cells, may protect people against strokes, and play a role in Parkinson's and other complex diseases. Until now mitochondrial DNA has only been associated with a few, rare disorders: catastrophic mutations can cause diseases such as MELAS, which results in muscle weakness and seizures. But recent studies have hinted that less problematic - but far more common - mitochondrial mutations might also be implicated in diseases with no obvious link to energy demand, including strokes. Mitochondrial DNA varies from person to person, but humans can generally be divided into broad "haplogroups" on the basis of the combinations of mutations they possess. Patrick Chinnery at the University of Newcastle, UK, and his colleagues assigned haplogroups to 950 people who'd had strokes, 340 people with heart disease symptoms, and 2939 healthy volunteers, all of whom live in Oxfordshire, UK. They found that among those people who'd had strokes, half as many belonged to haplogroup "K" as would be expected in the general population. The researchers conclude that K - which accounts for around 9 per cent of people of European ancestry - decreases the risk of stroke by 50 per cent compared with the other haplogroups. This makes it one of the best predictors of stroke risk identified so far - on a par with aggressively lowering blood pressure (The Lancet Neurology, DOI: 10.1016/S1474-4422(10)70083-1). © Copyright Reed Business Information Ltd.

Keyword: Stroke; Genes & Behavior
Link ID: 14045 - Posted: 06.24.2010

by Greg Miller People with Tourette syndrome are plagued by unwanted movements and verbal tics that run the gamut from extra eye blinks and grimaces to involuntary grunts or even cursing. Although the disorder tends to run in families, little is known about its genetic basis. Now researchers have found a mutated gene that appears to cause the disorder in one extremely unusual family with nine afflicted individuals. Although this mutation is not the cause of the vast majority of Tourette syndrome cases, it may push researchers to investigate a mechanism—and potential treatments—they otherwise would not have considered. Since the French neurologist Georges Gilles de la Tourette first described his namesake condition 125 years ago, scientists have puzzled over the cause. Much recent attention has focused on a brain region called the basal ganglia that is involved in repetitive behaviors and on the neurotransmitter dopamine. In 2005, a team led by child psychiatrist and geneticist Matthew State of Yale University School of Medicine, reported one of the first genetic clues to the disorder, a mutation in a gene called SLITRK1 that seems to be responsible for a rare handful of cases. But the function of SLITRK1 and its contribution to Tourette syndrome are still largely a mystery. In the new study, State and colleagues examined a family in which the father and all eight offspring (six sons and two daughters) have the syndrome. Extensive genetic detective work led them to a mutation in a gene called HDC, which encodes L-histidine decarboxylase, an enzyme involved in the production of histamine, a signaling molecule with a wide variety of roles throughout the body. The same mutation was present in all members of the family who had Tourette but was absent in thousands of DNA samples from control subjects, who included unrelated people with similar ethnic backgrounds as well as a group of 720 Tourette patients, the researchers report today in The New England Journal of Medicine. The mutated version of the HDC gene likely results in a truncated version of the enzyme, which would result in reduced histamine levels, State says. © 2010 American Association for the Advancement of Science

Keyword: Tourettes; Genes & Behavior
Link ID: 14044 - Posted: 06.24.2010

by Mark Buchanan FROM outside economist Ernst Fehr's office at the University of Zurich in Switzerland you would have no idea that he had been tipped to win a Nobel economics prize. For one thing, the name on the door looks as if it has been dashed off on the cheapest of departmental printers. But Fehr himself seems to fit the bill. Smiling broadly, he extends a hand, eager to talk about his experiences, whether favourable, amusing or confounding. Ironically, he says, it was one of the latter that led to his current success. In reality, it all started with failure. Twenty years ago, Fehr had a seemingly sensible idea - that a deep-seated human preference for fairness might play an important role in economics. He thought it might explain why companies - even in countries without a minimum wage - don't offer jobs paying wages far below the standard, despite research showing plenty of unemployed people would willingly take the work. It doesn't happen, he suggested, because companies know that workers hired at a lower wage feel they are being cheated, causing them to grow disgruntled and work less hard. Fehr wrote a paper on the idea that fairness matters, which was promptly rejected by every prestigious economic journal he sent it to on the grounds that people only care about how much they get for themselves, not how that compares to what others might receive. "Most economists would be deeply unhappy if paid less than what they consider to be fair, so I thought I had a convincing answer," Fehr says. "But I found out that in theoretical economics, fairness just doesn't count." © Copyright Reed Business Information Ltd.

Keyword: Emotions; Evolution
Link ID: 14043 - Posted: 06.24.2010

By STEPHANIE NANO NEW YORK - Researchers are reporting the first scientific evidence that a hormone banned in sports can boost athletic performance. The improvement from human growth hormone was modest, and only in sprinting. It didn't increase strength or fitness. Athletes likely to benefit are those in sprint events like running or swimming that require a burst of energy, and where a split second can decide the winner, the Australian researchers said. Human growth hormone, or HGH, is one of many substances banned by the Olympics and other sports even though there hasn't been any good proof that it can enhance performance. Previous studies in athletes have been small and brief. Story continues below ↓advertisement | your ad here The new research tested it in about 100 recreational athletes for two months. "This is the first demonstration that growth hormone improves performance and justifies its ban in sport," said Dr. Ken Ho, who led the study at the Garvan Institute of Medical Research in Sydney. Human growth hormone is made by the pituitary gland and promotes growth of bone and other tissue. A manufactured version is available, but its use is restricted to certain conditions in children and adults, including short stature, growth hormone deficiency and wasting from AIDS. Copyright 2010 The Associated Press

Keyword: Hormones & Behavior
Link ID: 14042 - Posted: 05.04.2010

The risk of suicide or suicide attempts by adults who start taking antidepressants does not seem to vary by the type of medication, a new study finds. Study author Dr. Sebastian Schneeweiss of Brigham and Women's Hospital and Harvard Medical School and his co-authors aimed to find out whether the risk of suicide is equal across different classes of antidepressants or whether some classes offer safety advantages in adults. "There was no clinically meaningful difference in risk among individuals taking different classes of medications," the researchers concluded in the May issue of the journal Archives of General Psychiatry. The researchers analyzed pharmacy and hospital records of 87,543 adults in British Columbia who started taking antidepressants between 1997 and 2005. During the first year of antidepressant use, 751 people attempted suicide and 104 committed suicide, according to a review of hospital records and death certificates. Most of the suicides and suicide attempts occurred in the first six months after starting treatment. The researchers found no clinically meaningful difference in risk among those taking different classes of antidepressants such as: © CBC 2010

Keyword: Depression
Link ID: 14041 - Posted: 06.24.2010

By JOHN TIERNEY The human ego has never been quite the same since the day in 1960 that Jane Goodall observed a chimpanzee feasting on termites near Lake Tanganyika. After carefully trimming a blade of grass, the chimpanzee poked it into a passage in the termite mound to extract his meal. No longer could humans claim to be the only tool-making species. The deflating news was summarized by Ms. Goodall’s mentor, Louis Leakey: “Now we must redefine tool, redefine Man, or accept chimpanzees as human.” So what have we actually done now that we’ve had a half-century to pout? In a 50th anniversary essay in the journal Science, the primatologist William C. McGrew begins by hailing the progression of chimpanzee studies from field notes to “theory-driven, hypothesis-testing ethnology.” He tactfully waits until the third paragraph — journalists call this “burying the lead” — to deliver the most devastating blow yet to human self-esteem. After noting that chimpanzees’ “tool kits” are now known to include 20 items, Dr. McGrew casually mentions that they’re used for “various functions in daily life, including subsistence, sociality, sex, and self-maintenance.” Sex? Chimpanzees have tools for sex? No way. If ever there was an intrinsically human behavior, it had to be the manufacture of sex toys. Considering all that evolution had done to make sex second nature, or maybe first nature, I would have expected creatures without access to the Internet to leave well enough alone. Copyright 2010 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 14040 - Posted: 06.24.2010

By Sandy Fritz Old age brings with it a host of physical woes, and among the most common is hearing loss. Forty percent of Americans older than 65 suffer from hearing loss, and by 2030 some 65 million Americans will be hard of hearing. Now joint work by researchers at the universities of Wisconsin, Florida, Washington and Tokyo has uncovered the mechanism behind age-related hearing loss, and with the help of simple chemicals, they have managed to keep old mice hearing as well as young pups. The team investigated a molecular mechanism that has been implicated in many age-related maladies but had not yet been tied to hearing loss. Our bodies are constantly exposed to short-lived organic molecules known as free radicals, which harm cells in a process called oxidation. When cells are stressed by oxi­dative damage, they release a protein called Bak, which triggers a cascade of events culminating in cell suicide. To test whether this mechanism was responsible for age-related hearing loss, the researchers compared normal mice with genetically engineered mice that do not have the gene necessary to make Bak. These Bak-deficient mice failed to develop hearing problems as they aged, but the ordinary mice, subjected to the same oxidative stress, became hard of hearing. Although most cells in the body are replaced with new cells after they die, the inner ear’s sensory nerve cells and ganglion neurons do not regenerate, so hearing loss is permanent. © 2010 Scientific American

Keyword: Hearing; Apoptosis
Link ID: 14039 - Posted: 06.24.2010

By Katherine Harmon The immune system's cells work hard to fight off infections. But new research is uncovering their important role in cognition, and a study published online May 3 in The Journal of Experimental Medicine reveals how the immune system's T cells, which aren't present in the brain, can impact learning and memory. Inflammation around the brain can hamper thinking, and attacks by inflammatory immune cells have been linked to declines in cognitive ability in patients who have, for example, multiple sclerosis or dementia. "Unexpectedly, however, T cells were recently shown to support learning and memory, though the underlying mechanism was unclear," wrote the study's authors, led by Noël Derecki of the Department of Neuroscience at the University of Virginia in Charlottesville. To uncover the mechanisms at work, Dereki and colleagues set out to determine why mice deficient in T cells performed poorly in maze learning tests even though T cells themselves are not normally found in the brain and are generally involved with inflammatory responses. The answer lay in a series of interactions that involves the meninges, or the membranes that surround the central nervous system, where T cells have been shown to congregate after maze training in mice. Of particular interest to researchers were T cells that make the immune protein IL-4, a cytokine that inhibits other compounds that encourage swelling. When these T cells had been knocked out of mice, the area around the brain and central nervous system had more myeloid cells, which seem to spur inflammation and impair learning. © 2010 Scientific American

Keyword: Learning & Memory; Neuroimmunology
Link ID: 14038 - Posted: 06.24.2010

By Nathan Seppa People with post-traumatic stress disorder seem to accumulate an array of genetic changes different from those found in healthy people, researchers report online May 3 in the Proceedings of the National Academy of Sciences. The new findings, while showing differences between people with and without PTSD, don't shed light on whether these differences might play a role in PTSD, says study coauthor Sandro Galea, a physician and epidemiologist at Columbia University in New York City. Only a fraction of people who witness a traumatic event develop PTSD. In an attempt to identify what makes people who develop PTSD biologically different from those who don’t, Galea and his colleagues obtained blood samples from 100 people in the Detroit area. All had been exposed to at least one potentially traumatic event, and 23 were diagnosed with PTSD. The scientists tested 14,000 genes in these blood samples for chemical changes to DNA that can affect gene activity without altering the genetic information itself. The researchers focused on the methylation of genes, a process in which a methyl molecule is added to DNA, typically turning off a gene and inhibiting production of the protein that the gene encodes. If people with PTSD have more or less methylation in specific genes, that might somehow contribute to PTSD, Galea says. © Society for Science & the Public 2000 - 2010

Keyword: Stress; Genes & Behavior
Link ID: 14037 - Posted: 06.24.2010

by Kathleen McGowan There is an art to removing the brain from a human cadaver. The donor should be lying faceup, and you should stand just behind the crown of the head. Carefully cut through the skin to expose the skull. Using a neurosurgery drill with a guard plate, cut the bone all the way around the head, above the ears. (It might help to pretend you are a barber giving a monk his tonsure.) This process, called fenestration, is more precise than using a saw. Out of respect for the donor, you do not want to damage the brain. Remove the top of the skull. With a small scalpel, carefully detach the cranial nerves, which emerge from the brain and thread their way through the skull to the face. As you gently lift the brain away from the skull with your left hand, cut the spinal cord with your right, releasing the brain from the skull. Once the organ is loose in your hand, you must be exceedingly gentle: At this stage it has the consistency of a ripe peach. Weigh it, then treat it with fixatives to preserve the tissue. Such is the art practiced by Jacopo Annese, a neuroanatomist at the University of California at San Diego. Annese is one of the world’s few experts in dissecting and slicing entire human brains; he has been practicing this craft since 1994. His dream is to create the world’s most complete open-access neuroanatomy library, featuring high-resolution digital images of whole human brain slices. Because of his expertise and this ambition, Annese was chosen by a group of researchers to cut, archive, and curate the most famous brain in neuroscience, that of Henry Molaison—better known to students and researchers worldwide as the legendary amnesiac patient “H. M.”

Keyword: Learning & Memory
Link ID: 14036 - Posted: 06.24.2010

By Katherine Harmon The benefits of breast milk for babies are numerous. Lower rates of childhood obesity, decreased incidence of asthma and even better brain development are all linked with drinking more of mother's milk in infancy, and despite decades of research and promising marketing claims, the formula industry has not caught up to mother nature in the milk department. But even if technicians could develop a better food for infants, researchers are now realizing that skipping the lactation phase would be problematic for mothers' health. In fact, not breastfeeding after giving birth seems to put women at higher risk for breast and ovarian cancer, diabetes, cardiovascular disease and many other serious health conditions. The mechanisms behind these increased risks are still being sorted out, but researchers think that by not engaging in the process that the body prepares for during pregnancy, many crucial systems can go out of whack. And the effects can last for decades after children are weaned. "The normal physiology is breastfeeding after pregnancy," says Alison Stuebe, an assistant professor in the Division of Maternal Fetal Medicine at the University of North Carolina in Chapel Hill, who describes breastfeeding as the fourth trimester of pregnancy. When women cannot or choose not to breastfeed, "there are myriad consequences, and we're just figuring them out," she says. © 2010 Scientific American,

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 14035 - Posted: 06.24.2010

It is a common experience for many men: A girlfriend or wife starts crying out of nowhere and suddenly the guys are being accused of being insensitive. Women are whizzes at reading, and even predicting, emotion in others. And they often expect their partners to be, too. Scientists, however, have joined the men's side, saying such expectations are unreasonable for the male kind. A nasal spray that works like a performance enhancer for empathy brain circuits could render the bickering unnecessary, a new study suggests. Its key ingredient is oxytocin, a hormone known to promote social bonding. Men and women both have endogenous levels of oxytocin naturally created by the body — it likely helps them fall in love, spurs parenting instincts and makes orgasms, well, more orgasmic. But women tend to have a special relationship with the hormone. It reaches particular highs during pregnancy and lactation, cementing the mother-infant bond. It might also help women be so adept at reading social cues. To see whether men could acquire this same emotional expertise, the researchers gave 48 men and 26 women two empathy tests. One required using social cues (happy, angry or neutral facial expressions) to figure out the right answers in a game. The second test used pictures of various scenarios and asked subjects to rate how much the scene emotionally moved him or her (considered a test of "emotional empathy"). Participants were also asked to name the primary emotion of the main character in the scene (a test of "cognitive empathy"). © 2010 LiveScience.com.

Keyword: Emotions; Hormones & Behavior
Link ID: 14034 - Posted: 06.24.2010

By GARDINER HARRIS An experimental drug succeeded in a small clinical trial in bringing about what the researchers called substantial improvements in the behaviors associated with retardation and autism in people with fragile X syndrome, the most common inherited cause of these mental disabilities. The surprising results, disclosed in an interview this week by Novartis, the Swiss pharmaceutical giant that makes the drug, grew out of three decades of painstaking genetic research, leaps in the understanding of how the brain works, the advocacy of families who refused to give up, and a chance meeting between two scientists who mistakenly showed up at the same conference. “Just three years ago, I would have said that mental retardation is a disability needing rehab, not a disorder needing medication,” said Dr. Thomas R. Insel, director of the National Institute of Mental Health, who was told of the Novartis trial results. “Any positive results from clinical trials will be amazingly hopeful.” Dr. Mark C. Fishman, president of the Novartis Institutes for BioMedical Research, cautioned against too much optimism. The trial involved only a few dozen patients, only some of whom benefited from treatment. The drug is likely to be years away from being commercially available and could fail in further clinical trials, he said. “We have been reluctant to make this public because we still need to do more experiments, do them correctly and in a bigger way,” Dr. Fishman said. “But our group feels pretty good about the data.” Copyright 2010 The New York Times Company

Keyword: Genes & Behavior; Intelligence
Link ID: 14033 - Posted: 06.24.2010

By TARA PARKER-POPE After we hit 40, many of us begin to worry about our aging brains. Will we spend our middle years searching for car keys and forgetting names? The new book “The Secret Life of the Grown-Up Brain: The Surprising Talents of the Middle-Aged Mind,” by Barbara Strauch, has the answers, and the news is surprisingly upbeat. Sure, brains can get forgetful as they get old, but they can also get better with age, reports Ms. Strauch, who is also the health editor at The New York Times. Ms. Strauch, who previously tackled teenage brains in her book “The Primal Teen,” spoke with me this week about aging brains and the people who have them. Here’s our conversation: Q. After exploring the teenage brain, why did you decide to write a book about grown-ups? A. Well, I have a middle-aged brain, for one thing. When I would go give talks about “The Primal Teen,” I’d be driven to the airport or back by a middle-aged person, and they’d turn to me and say: “You should do something about my brain. My brain is suddenly horrible. I can’t remember names.” That’s why I started looking into it. I had my own middle-aged issues like going into an elevator and seeing somebody and thinking, “Who are you?” Q. So what’s the bad news about the middle-aged brain? A. Obviously, there are issues with short-term memory. There are declines in processing speed and in neurotransmitters, the chemicals in our brain. But as it turns out, modern middle age is from 40 to 65. During this long time in the middle, if we’re relatively healthy our brains may have a few issues, but on balance they’re better than ever during that period. Copyright 2010 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 14032 - Posted: 06.24.2010

by Dave Munger Across the animal kingdom, the decision of whether or not to be faithful to a mate often comes down to Darwinian considerations. Dear Darwin, I’m seeking the ideal mate, and I just don’t know what to do. I could mate with the biggest, strongest male in my niche, but all the other females are just as interested in him as I am, and I’m worried he won’t give our offspring and me the attention we deserve. I could have a less-attractive male all to myself, but then I run the risk of having inferior offspring. I’m half-tempted to pair up with a runt, but then mate with the hunk on the side. What do you think? Is monogamy all it’s cracked up to be? — Evolving in Evanston Dear Evolving, You said it, sister! True monogamy is actually quite rare among animals. Take birds, for example. While there are lots of socially monogamous birds, pairing up for a season or even for life, true loyalty is much more rare. As Jeremy Yoder, a graduate student who studies symbiosis in moths and Joshua trees notes on his blog, as many as 90 percent of bird species “cheat” on their mates, and about 11 percent of chicks aren’t fathered by the bird the mother has paired with. ©2005-2009 Seed Media Group LLC.

Keyword: Sexual Behavior
Link ID: 14031 - Posted: 06.24.2010

By Nikhil Swaminathan The argument over whether intelligence is innate or environmentally influenced has raged for more than a century. One of the most recent issues in the nature versus nurture debate is the effect of breast-feeding on IQ. Research shows that the fatty acids in human milk may influence brain development. Using that data as a springboard, a group of scientists, led by a team at the King's College London Institute of Psychiatry, set out to determine how the makeup of infants interacts with their mothers' milk to affect intelligence. Their findings, published in Proceedings of the National Academy of Science USA: breastfeeding can boost a baby's intelligence quotient if the newborn has a certain version of a gene, called FADS2 (fatty acid desaturase 2), which affects how fatty acids are processed. "We were searching for an empirical example that would allow us to show scientists that it is possible to use the environment as a tool, to uncover novel genes that are important for human outcomes—including diseases," says study co-author Terrie Moffitt, a psychiatry professor of at King's College. "Our chain of logic from environment to genetic marker allowed us to discover for the first time the link between the FADS2 gene and the IQ, an important child health outcome." The genetic marker that Moffitt refers to is located in the FADS2 gene, which has two primary variations. The new study, based on 1,000 New Zealander children (a portion of whom were breast-fed) in the early 1970s as well as on more than 2,000 breast-fed kids who lived in the U.K. in the mid 1990s, showed that 90 percent of the subjects had at least one copy of the more common version of FADS2 and 50 percent of them had two copies. © 2010 Scientific American,

Keyword: Development of the Brain; Intelligence
Link ID: 14030 - Posted: 06.24.2010

By Yoshiaki Kikuchi and Madoka Noriuchi It’s probably not surprising that mothers excel at recognizing and interpreting the moods and emotions of their infants. Although infants can’t speak, mothers seem to know what their babies are thinking: they smile when their baby smiles and they frown when their baby is upset. Research suggests that the mother’s ability to understand the needs of her infant is very important for establishing a secure mother-infant relationship. However, the neural mechanisms that underlie these behaviors are poorly understood. Such knowledge is crucial for understanding normal as well as abusive and neglectful mothering. In recent years, several studies have been carried out using functional magnetic resonance imaging (fMRI) to better understand how a mother’s brain responds to her own child’s cues. The most recent, led by neuroscientist Lane Strathearn and colleagues at Baylor College of Medicine, investigated what happens inside the brain of a mother when she looks at the facial expressions of her own infant. In the study, 28 first-time mothers were shown pictures of their seven-month old child that they had never seen before. (The pictures were taken when the mother was not present.) The pictures spanned a wide range of human emotion and included images of the child making happy, sad or neutral faces. These pictures were then matched with images of an unknown infant. The central finding was that seeing the happy face of the mother’s own infant activated all of the key areas in the brain associated with reward processing. These regions include the ventral tegmental area, substantia nigra and the striatum. This finding suggests that for mothers the sight of their smiling baby is a potent reward and represents a uniquely pleasurable experience. Furthermore, this neural response was graded, so that happy faces led to more activation than neutral faces. Sad faces generated the least activation. In other words, the response of mothers in their reward areas seemed to directly mirror the emotions the infant displayed. © 2010 Scientific American,

Keyword: Sexual Behavior; Emotions
Link ID: 14029 - Posted: 06.24.2010

by Shaoni Bhattacharya CAN'T find a mate? Try parthenogenesis. The type of asexual reproduction may be part of an extreme survival strategy for sharks. In parthenogenesis, females' eggs start dividing without being fertilised. This produces daughters that are genetically similar to the mother. It was first observed in a captive hammerhead shark in 2001, but this was an isolated incident, and the shark pup died after three days, making it difficult to say much about its evolutionary significance. Kevin Feldheim at the Field Museum in Chicago, and an international team of colleagues, have now shown that the incident was not exceptional and sharks born from a virgin mother can survive for many years (Journal of Heredity, vol 101, p 374). The team were inspired by the 2001 birth to keep eggs produced by a captive white-spotted bamboo shark at the Belle Isle Aquarium of the Detroit Zoological Institute. The female had never encountered a male during her adult life and biologists had assumed the eggs were infertile. To their surprise seven incubated eggs produced two pups that survived five years before they were transferred to another facility. Genetic analysis confirmed that they were parthenogens. "This suggests that parthenogenesis is a viable shark survival strategy," says Paulo Prodöhl of Queen's University Belfast, UK, who is investigating a possible case of virgin birth in the whitetip reef shark. © Copyright Reed Business Information Ltd.

Keyword: Sexual Behavior; Evolution
Link ID: 14028 - Posted: 06.24.2010