By Fayana Richards Can't stand today's music? Neither can tune-deaf people. In fact, the disorder makes listening to any music unenjoyable, because the brain can't organize the sounds into a comprehensible melody. New research indicates that the problem lies somewhere in the conscious mind: The brains of tune-deaf individuals know when a sour note has been played, but the people themselves are unaware of it. Two percent to 4% of the U.S. population is tune deaf. People with the disorder, also known as tone deafness, have trouble telling the difference between a good melody and a bad one. Tune deafness is highly heritable, yet biologists know little about what goes wrong in the brain. The normal process of detecting bad notes has been much better described: A device that measures brain activity, called an electroencephalograph, registers two signals, known as mismatch negativity (MMN) and P300. Neuroscientist Allen Braun and colleagues at the U.S. National Institute on Deafness and Other Communication Disorders in Bethesda, Maryland, wondered if the same signals would turn up in the brains of tune-deaf people as they listened to a botched melody. The researchers had seven tune-deaf and 10 non-tune-deaf people listen to a variety of familiar tunes such as "Mary Had a Little Lamb" and "The Star-Spangled Banner" while an electroencephalograph measured their brain activity. As expected, these subjects did not have the typical MMN response to poorly played tunes, the team reports today in PLoS One. But to their surprise, the researchers did detect the P300 response to the incorrect notes. Braun believes these results show that the brain can detect the differences even though tune-deaf people aren't aware. © 2008 American Association for the Advancement of Science.

Keyword: Hearing
Link ID: 11706 - Posted: 06.24.2010

In a classic “Seinfeld” dilemma, Jerry draws a blank on his new girlfriend’s name, and the relationship has become too intimate for him just to ask. Throughout the half hour episode, Jerry’s various ploys to jog his memory bear no fruit, and the denouement comes too late to salvage the nascent romance. By the end of the show, the girlfriend has discovered his predicament, become irate, and stormed out of his apartment. And that’s when it hits him: Dolores. Now, two psychologists from McMaster University are shedding light on the cause of Jerry’s mental block. According to a new study by Amy Beth Warriner and Karin Humphreys, the longer you try to come up with the word that’s on the tip of your tongue, the more likely you’ll be to get stuck on that word in the future. For years, Humphreys herself endured a Seinfeld-like struggle with the word 'obsidian,' the term for black, shiny volcanic glass. Instead of saying 'obsidian,' Humphreys would think, “It’s like oblong, but no, it’s not oblong. I know that it’s not oblong but that’s the only word coming to mind,” she says. But out of this protracted mental battle came an idea: maybe by straining her memory on that stubborn vocabulary word, she was making it even harder to remember the answer later on. To test out this hypothesis, she and Warriner brought 30 undergraduates into the psychology laboratory. Through their experiment, they found that “by actually getting into a tip of the tongue state, I’ve actually dug myself into a hole, and I’ve made this wrong learning. And the next time I go to do that, I’m going to get into this wrong state again,” says Humphreys. © ScienCentral, 2000-2008.

Keyword: Learning & Memory
Link ID: 11705 - Posted: 06.24.2010

Ewen Callaway You might call it our circadian eye. A handful of retina cells sense light, not for vision, but instead to reset our body clocks each day. Killing off these cells in mice leaves their sight unharmed, but throws their clocks out of whack, two new studies show. Jolting these cells back into action might offer salvation to insomniacs, whose circadian cycles are slightly off, says Satchidananda Panda, a molecular biologist at the Salk Institute in San Diego, who led one study. Natural degeneration of these cells could also explain why insomnia often strikes the elderly. "Maybe we can develop an eye drug to reset your clock," he says. Alternatively, triggering the cells with extra-pale blue light – the wavelengths they're most sensitive to – could do the same trick, says Samer Hattar, a neuroscientist at Johns Hopkins University in Baltimore. Hattar's team identified the same role for the cells, which produce a recently-discovered light sensor called melanopsin. The first evidence for our circadian eye came in the 1920s, when an American physician noticed that congenitally blind mice can still dilate their pupils – a sign of light detection – despite lacking rods and cones, the photosensors that transform light to vision. © Copyright Reed Business Information Ltd.

Keyword: Biological Rhythms; Vision
Link ID: 11703 - Posted: 06.24.2010

Katharine Sanderson Have you ever felt your heart wrench when selling your beaten-up old car, or offered up a formerly prized possession to the voracious hordes on eBay with a hint of sadness? If so, you have experienced the 'endowment effect' – in which people value a something more once they possess it. Exactly why this happens is not known. It could be because humans overvalue the positive and ignore the negative associations, or it could be that the thought of losing something is just too much to bear. Now, psychologists led by Brian Knutson at Stanford University in Palo Alto, California, have imaged the brain as it struggles with this effect — and have shown that parting with our possessions really does hurt1. "Selling something you like is painful,” says Scott Rick, who studies emotional responses at the University of Pennsylvania, Philadelphia, and is co-author of the paper, published in the journal Neuron. Their findings suggest that the endowment effect is due to simple anxiety over losing our possessions, rather than any tendency to overvalue it. © 2008 Nature Publishing Group

Keyword: Emotions
Link ID: 11702 - Posted: 06.24.2010

Smoking and obesity could both cause permanent hearing damage, say scientists. Either could threaten blood flow to the ear, they say, with damage levels clearly linked to the level of obesity or the length of a smoking habit. However, the Antwerp University-led study found that high levels of work noise remained the biggest risk. In a separate study, smoking in middle age was linked to worse memory, which could hasten the arrival of dementia. A link between smoking and hearing problems has been suggested by others, but the conclusions of the latest research, involving more than 4,000 men and women aged between 53 and 67, offer the most convincing evidence to date. All the study participants were given a hearing test, then asked about their lifestyle and where they worked. Dr Erik Fransen, of the University of Antwerp in Belgium, one of the lead researchers, said that the ability to pick out high frequency sounds was damaged in smokers and the obese, although to not as great an extent as those exposed to very loud noise in the workplace. He said: "The hearing loss is proportional to how much you smoke and your body mass index (BMI). "It starts getting worse once you have smoked regularly for more than one year." He said that, unlike some parts of the body, once damage had occurred, there was no prospect of recovery. "Once the damage is done, it's done. It does not repair." The theory behind the hearing damage is similar to the reason smoking and obesity can harm other organs. Both can disrupt the flow of blood around the body, and Dr Fransen suggested that the resulting lack of oxygen, coupled with the failure to remove toxic waste from the ear, can be damaging. (C)BBC

Keyword: Drug Abuse; Hearing
Link ID: 11701 - Posted: 06.10.2008

By Lisa Conti Splenda is not satisfying—at least according to the brain. A new study found that even when the palate cannot distinguish between the artificial sweetener and sugar, our brain knows the difference. At the University of California, San Diego, 12 women underwent functional MRI while sipping water sweetened with either real sugar (sucrose) or Splenda (sucralose). Sweeteners, real or artificial, bind to and stimulate receptors on the taste buds, which then signal the brain via the cranial nerve. Although both sugar and Splenda initiate the same taste and pleasure pathways in the brain—and the subjects could not tell the solutions apart—the sugar activated pleasure-related brain regions more extensively than the Splenda did. In particular, “the real thing, the sugar, elicits a much greater response in the insula,” says the study’s lead author, psych­ia­trist Guido Frank, now at the Univer­sity of Colorado at Denver. The insula, involved with taste, also plays a role in enjoyment by connecting regions in the reward system that encode the sens­a­tion of pleasantness. Although Splenda elicits less overall activity within the brain, the researchers were surprised to find that the artificial sweetener seems to inspire more communication between these regions. “Looking at the connection between the taste areas, Splenda is stronger,” Frank says. He suggests that when we taste Splenda, the reward system becomes activated but not satiated. “Our hypoth­esis is that Splenda has less of a feedback mechanism to stop the craving, to get satisfied.” © 1996-2008 Scientific American Inc.

Keyword: Obesity
Link ID: 11700 - Posted: 06.24.2010

By Nikhil Swaminathan Stacey Gayle used to love music. Listening to it and performing it was a big part of her life. She had stacks of CDs in her car, went to concerts of artists like Sean Paul, and would go to parties where hot songs would blare. She was also an active member of the choir at her church: Solid Rock Church of the Nazarene. Then she started having seizures. The first one happened while she slept in her bedroom in Rosedale, Queens in New York City on the night of March 3, 2005. She had just turned 22. Her mother rushed her to the emergency room, where doctors stabilized her. Several brain scans and blood tests gave no clue as to why she seized. Soon after, she had another, this time at a friend's barbecue. She blacked out, fell down and started to shake like crazy as her brain cells went out of whack, firing electrical signals without pause. At first, the seizures seemed to occur randomly. In the spring of 2006, however, she noticed a pattern. At the time, Sean Paul's "Temperature" was sitting at the top of the Billboard Hot 100 singles chart, continually being played on urban radio stations. It was playing at nearly every barbecue and party she went to. That was a problem: "Every time it would go on, I would pass out and go into a seizure," she recalls. © 1996-2008 Scientific American Inc.

Keyword: Epilepsy; Hearing
Link ID: 11699 - Posted: 06.24.2010

By BENEDICT CAREY Staring at a pattern meant to evoke an optical illusion is usually an act of idle curiosity, akin to palm reading or astrology. The dot disappears, or it doesn’t. The silhouette of the dancer spins clockwise or counterclockwise. The three-dimensional face materializes or not, and the explanation always seems to have something to do with the eye or creativity or even personality. The radiating lines trick the brain into perceiving motion forward, so the center appears to bulge. That’s the usual cue to nod and feign renewed absorption in the pattern. In fact, scientists have investigated such illusions for hundreds of years, looking for clues to how the brain constructs a seamless whole from the bouncing kaleidoscope of light coming through the eyes. Brain researchers today call the illusions perceptual, not optical, because the entire visual system is involved, and their theories about what is occurring can sound as exotic as anyone’s. In the current issue of the journal Cognitive Science, researchers at the California Institute of Technology and the University of Sussex argue that the brain’s adaptive ability to see into the near future creates many common illusions. “It takes time for the brain to process visual information, so it has to anticipate the future to perceive the present,” said Mark Changizi, the lead author of the paper, who is now at Rensselaer Polytechnic Institute. “One common functional mechanism can explain many of these seemingly unrelated illusions.” His co-authors were Andrew Hsieh, Romi Nijhawan, Ryota Kanai and Shinsuke Shimojo. Copyright 2008 The New York Times Company

Keyword: Vision
Link ID: 11698 - Posted: 06.24.2010

By Elsa Youngsteadt Sometimes seizures become a nightmare without end. Roughly 15% of epileptics will, at some point, experience status epilepticus, a medical emergency in which convulsions can only be stopped with strong anesthetics. Now researchers have found a piece of cellular machinery--an acid-activated ion channel-- that helps bring seizures under control. They hope the discovery will lead to new drugs that could stop these deadly events. For decades, researchers have suspected a link between brain acidity and seizures. In 1929, doctors noted that patients breathing CO2 had shorter seizures; the gas boosts the acidity of blood reaching the brain. Even without intervention, brain pH can drop during a seizure due to changes in breathing and metabolism. John Wemmie, a psychiatrist at the University of Iowa in Iowa City and colleagues wondered if an ion channel called ASIC1a might play a role, as it is known to activate neurons by pumping calcium and sodium across the cell membrane when the brain becomes acidic. Wemmie's team compared normal mice with those that were genetically engineered to lack the channel. When they injected these knockouts and controls with chemicals that cause epilepsy-like seizures, the normal mice fared much better than the ones without ASIC1a. A compound called kainate produced serious whole-body convulsions in all seven knockout mice, whereas the six normal mice had only minor seizures in their heads and fore-limbs. A second group of knockouts injected with a different drug, PTZ, had longer seizures than control mice--and those seizures were several times more likely to become deadly tonic-clonic whole-brain seizures (formerly known as "grand mal" seizures). In contrast, mice genetically engineered to have double the normal number of ASIC1a channels had shorter and less severe seizures than wild-type mice, the team reports online this week in Nature Neuroscience. © 2008 American Association for the Advancement of Science

Keyword: Epilepsy
Link ID: 11697 - Posted: 06.24.2010

-- Relentless evolution towards more intelligent species may have been driven not just by progressively larger brains but by the increasingly complex way in which they were wired, reports a study released Sunday. Scientists in Britain probing the origins of the human brain focused on the role of synapses, the junctions between nerves which transfer electrical signals -- and information -- from one brain cell to the next via a series of biochemical switches. Most research to date has assumed that synapses, made of proteins, are essentially the same in all animals, ranging from the lowly earthworm all the way up the evolutionary ladder to humans. What makes some species more intelligent than others, according to this prevailing wisdom, is sheer mass -- more neurons equals greater data-processing capacity. "The view that 'more nerves' is sufficient to explain 'more brain power' is simply not supported by our study," said lead researcher Seth Grant, who heads the Genes to Cognition Program at the Wellcome Trust Sanger Institute in Britain. Looking at the density and molecular makeup of synapses, the study, published in Nature Neuroscience, found dramatic differences between species. © 2008 Discovery Communications, LLC

Keyword: Evolution; Intelligence
Link ID: 11696 - Posted: 06.24.2010

Colin Barras The brain region responsible for one of humankind's neatest mental tricks may have been identified. We think nothing of singling out one person's voice at a party buzzing with people chatting. But researchers have struggled to understand just how the human brain manages to filter out a single thread of conversation from a tangle of similar background noises. The phenomenon was labelled the "cocktail party effect" in the 1950s by Colin Cherry, a British cognitive scientist. Now, if we don't know exactly how, at least we may know where. Researchers conducting brain scans of people listening to multiple sounds, say that the secondary auditory cortex – located in the temporal lobe at the side of the head – does much of the work. Hidden tone Alexander Gutschalk at the Ruprecht-Karl University of Heidelberg in Germany and his team decided to study brain activity during this "informational masking". They hooked volunteers up to a Magnetoencephalography (MEG) imager and played them a sound file containing a large number of randomly repeating tones across a range of frequencies. © Copyright Reed Business Information Ltd

Keyword: Hearing
Link ID: 11695 - Posted: 06.24.2010

By Susan Gaidos To the brain, remembering the past and visualizing the future look surprisingly similar When Alice climbs through the looking glass, she encounters a topsy-turvy world. People are punished before committing a crime, and sometimes fingers bleed before a pinprick occurs. Those strange events reflect a memory that works both ways in that world, allowing people to remember things before they happen. As the Queen explains to Alice: “It’s a poor sort of memory that only works backwards.” Now, back in this world, scientists are discovering that human memory does indeed work forward. A growing number of studies show that the mental machinery for reliving your past performs another—perhaps more vital—task: envisioning your future. Other studies show that total amnesiacs report a “blank” when asked about their personal futures. And severely depressed patients, who tend to think about both the past and future in a nonspecific manner, have difficulty visualizing positive future events. Such findings have stimulated scientists to rethink the role of memory. Rather than viewing it as a mere storehouse of facts and autobiographical data, researchers are beginning to recognize that memory also constructs, simulates and predicts possible future events in an ever-changing environment. Perhaps, some say, this kind of autobiographical memory exists precisely for this purpose. © Society for Science & the Public 2000 - 2008

Keyword: Learning & Memory
Link ID: 11694 - Posted: 06.24.2010

By Lauren Cahoon Call it the chicken-and-egg debate of the addiction world: Cocaine addicts are known for being frenetic, but which came first, the behavior or the habit? New research indicates that, at least in rats, it's the behavior that begets addiction. What's more, the study has pinpointed the character trait--impulsiveness--that is responsible for developing true drug dependence. Experts believe that the findings may lead to new approaches for treating addiction. Scientists who study drug addiction have a common problem: The individuals they deal with are already addicted, so it's hard to tell what, if any, behaviors led to the initial dependence. What they do know is that two traits--impulsiveness and thrill-seeking--tend to define most drug addicts. Although the behaviors are similar, scientists have been able to parse them in the lab: Highly impulsive rats jump the gun on simple tasks--pushing a button, for example, before they are signaled to do so; thrill-seeking rats, meanwhile, will rapidly explore any new environment--immediately sniffing various objects in a new cage, for example--whereas normal rats would wait until they felt comfortable in their surroundings. In hopes of discovering if either of these two traits might be a catalyst for drug addiction, psychologists David Belin and Barry Everitt, both of the University of Cambridge in the U.K., hooked up the sensation-seeking rats and the impulsive rats to a device that dispensed cocaine directly into the rats' brains. The rats could control the dispenser, so they could take the cocaine whenever they wanted. As the team reports in today's issue of Science, the thrill seekers tried the cocaine immediately, taking it in sky-high doses. The impulsive rats weren't as quick to turn to the drug, however, and when they did, they took it in smaller amounts. © 2008 American Association for the Advancement of Science.

Keyword: Drug Abuse
Link ID: 11693 - Posted: 06.24.2010

Daniel Cressey Controlling your anger and reacting sensibly when someone treats you badly can be a problem. And if you have low levels of serotonin, it can be even more of a problem, a new study has found. Molly Crockett at the University of Cambridge, UK, and her colleagues gave volunteers a drink that temporarily lowered their levels of serotonin, a brain 'neurotransmitter' linked to happy mood. They then had them play ‘the Ultimatum Game’, which involves accepting or rejecting offers of money. Those with lower serotonin levels showed increased retaliation to offers that they perceived to be unfair. “We’ve suspected for years that there’s a link between serotonin and impulsive aggression and emotional regulation,” says Crockett. “Until this study it wasn’t clear whether serotonin was playing a causal role.” It has long been known that low serotonin levels are associated with groups of people prone to impulsiveness and problems with emotional control, such as alcoholics, violent criminals and suicide attempters. Low serotonin is also found in clinical conditions such as depression and anxiety. “We’ve known for 30 years that low serotonin is associated with impulsivity, inwardly directed aggression and outwardly directed aggression,” says David Nutt, head of the Psychopharmacology Unit at the University of Bristol’s Faculty of Medicine and Dentistry, who was not involved in the new study. “What we are doing now is externally manipulating it. We need to study it in a more controlled environment.” © 2008 Nature Publishing Group

Keyword: Emotions; Aggression
Link ID: 11692 - Posted: 06.24.2010

An active social life appears to delay memory loss as we age, a new study shows. The finding, which appears in the July issue of The American Journal of Public Health, suggests that strong social ties, through friends, family and community groups, can preserve our brain health as we age and that social isolation may be an important risk factor for cognitive decline in the elderly. Researchers at the Harvard School of Public Health used data gathered from 1998 to 2004 from the Health and Retirement Study, a large, nationally representative population of American adults ages 50 and older. Participants took memory tests at two-year intervals during the study period. Testers read a list of 10 common nouns to survey respondents, who were then asked to recall as many words as possible immediately and again after a five-minute delay. The researchers also measured social integration based on marital status, volunteer activities, and contact with parents, children and neighbors. The results showed that individuals who in their 50s and 60s engaged in a lot of social activity also had the slowest rate of memory decline. In fact, compared to those who were the least socially active, study subjects who had the highest social integration scores had less than half the rate of memory loss. The researchers controlled for variables like age, gender, race and health status. Those who had the fewest years of formal education appeared to have the most to gain from an active social life as they aged. The study showed that the protective effect of social integration was greatest among individuals with fewer than 12 years of education. Copyright 2008 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 11691 - Posted: 06.05.2008

By Seth Borenstein WASHINGTON - A little strategically placed makeup quickly turns the wimpiest of male barn swallows into chick magnets, amping up their testosterone and even trimming their weight, new research shows. It's a "clothes make the man" lesson that — with some caveats — also applies to human males, researchers say. Using a $5.99 marker, scientists darkened the rust-colored breast feathers of male New Jersey barn swallows, turning lighter birds to the level of those naturally darkest. They had already found, in a test three years ago, that the marked-up males were more attractive to females and mated more often. This time they found out that the more attractive appearance, at least in the bird world, triggered changes to the animals' body chemistry, increasing testosterone. "Other females might be looking at them as being a little more sexy, and the birds might be feeling better about themselves in response to that," said study co-author Kevin McGraw, an evolutionary biology professor at Arizona State University. © 2008 The Associated Press.

Keyword: Sexual Behavior; Evolution
Link ID: 11690 - Posted: 06.24.2010

By John Bohannon Today's couch potato lifestyle has been blamed for skyrocketing rates of obesity, but the cause of this trend may have more to do with the potato than the couch. An analysis of 20 years of published data on people's daily energy expenditure indicates that overeating, rather than a sedentary existence, is the major cause of the industrial world's obesity epidemic. What is certain about obesity is that it is ultimately caused by an imbalance in people's energy budgets. When you take in more calories than you burn, your body squirrels the excess away as fat. The imbalance can stem from too much food, too little physical activity, or a combination of the two. Studies of self-reported exercise and eating habits have suggested that daily physical activity has decreased in recent decades, while daily caloric intake has remained steady. But people's accounting of their own behaviors is notoriously inaccurate. To get more reliable data, biologists Klaas Westerterp of Maastricht University in the Netherlands and John Speakman of the University of Aberdeen in the U.K. turned to a technique called the doubly labeled water (DLW) method. Over 2 weeks, subjects are given trace amounts of water molecules whose hydrogen or oxygen atoms contain extra neutrons. The body draws on the oxygen atoms for metabolism, expelling some of them in carbon dioxide. By tracking the ratio of heavy hydrogen and oxygen in the urine, researchers can estimate a person's overall rate of metabolism. © 2008 American Association for the Advancement of Science

Keyword: Obesity; Genes & Behavior
Link ID: 11689 - Posted: 06.24.2010

If you're a sucker for sweets, it might be in your genes. Researchers at the University of Toronto discovered a genetic difference in people who consume extra sugar in their diet. "Certainly environmental factors can influence the foods that we like and dislike," says nutrigenomics researcher Ahmed El-Sohemy. “But what this line of research demonstrates is that there is also a biological or a genetic basis for some of our likes and dislikes of foods." El-Sohemy and his colleagues studied two large groups of volunteers, who completed detailed records of their daily diet. Analyzing blood samples, they found that people with a different form of a gene called GLUT 2 had consistently higher daily sugar intakes. “Initially what we were interested in finding is why some people show a more dramatic rise in blood sugar after a meal,” El-Sohemy explains. “The reason we focused on this particular gene is because it’s known to function primarily in the pancreas. That’s the organ that’s responsible for sensing changes in blood sugar and producing insulin in response to clear it. We found there was no difference in how quickly individuals with the two versions of the gene cleared glucose from their blood, but surprisingly, those who had a particular version of this gene just consumed more sugar... the fat intake was the same, protein was the same, other types of carbohydrates was the same. So it seemed to be very specific to sugar.” © ScienCentral, 2000-2008.

Keyword: Genes & Behavior; Chemical Senses (Smell & Taste)
Link ID: 11688 - Posted: 06.24.2010

-- It doesn't pay to be smart and ignorance really is bliss if you want a long life -- at least if you're a fly, according to new research by a Swiss university. Scientists Tadeusz Kawecki and Joep Burger at the University of Lausanne said Wednesday they had discovered a "negative correlation between an improvement in a fly's mental capacity and its longevity". As part of their research project, the results of which are published in the journal Evolution, they divided into two a group of flies from the Basel region of northwestern Switzerland. One half was left in a natural state while the other had its intelligence boosted by Pavlovian methods, such as associating smell and taste with particular food or experiences. Over 30 to 40 generations, these methods led to flies which clearly learned better and remembered things for longer. The flipside was that the flies left in their natural state lived longer on average than their "cleverer" counterparts, with a lifespan of 80-85 days rather than the normal 50-60.. © 2008 Discovery Communications, LLC

Keyword: Learning & Memory; Evolution
Link ID: 11687 - Posted: 06.24.2010

Katharine Sanderson Human stem cells have been used to correct abnormal brain development in mice with fatal brain disorders, offering hope for treating a range of neurological disorders including some deadly childhood genetic diseases. Those behind the new treatment hope that human clinical trials could be just a few years away. The treatment uses human glial progenitor cells — cells that can differentiate into the glial cells that, among other things, make up myelin. Myelin, a protein that insulates the long 'arms' of nerve cells, called axons, helps the conduction of neural signals throughout the nervous system. A team led by Steven Goldman, at the University of Rochester in New York, took the progenitor cells from white matter in the fetal human brain and injected them into the spinal cords of mutant shiverer mice shortly after their birth. The mice, which shiver and shake as their name suggests, have severe neurological defects caused by a genetic mutation that stops them producing myelin. Without myelin, neural signals get stuck, causing potentially fatal disease. “There’s no way we’d be able to conduct a [neural] signal very far if it weren’t for myelin,” Goldman explains. As they develop, shiverer mice become unable to walk forwards, have increasing numbers of seizures, and typically die at just 18–21 weeks of age. © 2008 Nature Publishing Group

Keyword: Multiple Sclerosis; Glia
Link ID: 11686 - Posted: 06.24.2010