Ben Harder When John D. Abramson was practicing family medicine in Hamilton, Mass., he prided himself on how conscientiously he selected the drugs that he prescribed. He closely followed pharmaceutical research. He kept track of the latest medical guidelines. And he maintained his distance when company salespeople, with promotional pitches at the ready, appeared at the practice that Abramson shared with several colleagues during the 1980s and 1990s. He typically didn't speak to pharmaceutical sales agents, although he did let them leave behind free samples of drugs that their companies sold. Abramson knew that the companies wanted him and his colleagues to prescribe new and often expensive drugs rather than their older, less costly alternatives. But he saw no harm in stockpiling the freebies and handing them out to patients who were without health insurance and unable to buy drugs on their own. "I thought I was being Robin Hood," Abramson says. Before long, however, he grew so familiar with administering the free drugs that he found himself writing prescriptions for the same substances for insured patients, whose coverage would then pay for the medications. For pharmaceutical companies, Abramson's behavior meant new customers. "That's what they wanted," he says. "They were playing me like a violin." Abramson left medical practice nearly 4 years ago to write Overdo$ed America: The Broken Promise of American Medicine (2004, New York: Harper Collins), which trains a critical eye on pharmaceutical companies' influence on medical research and practice. Copyright ©2005 Science Service.

Keyword: Depression
Link ID: 7710 - Posted: 06.24.2010

By Jennifer Viegas, Discovery News — Most animals, including many humans, investigate only a handful of potential mates before selecting a partner, but scientists have just determined that certain California crabs may check out 106 males or more before mating. The finding, published in the current Animal Behavior, means that these female fiddler crabs, Uca crenulata, are the choosiest known animals on Earth. "As far as I know, no other species has been observed sampling nearly as many candidates as the California fiddler crab," said Catherine deRivera, lead author of the study. DeRivera, who is a research biologist at the University of California, San Diego, told Discovery News, "Most invertebrates, some mammals, amphibians and reptiles mate with neighbors or the first candidate that comes along, or at least the first that correctly performs the courtship ritual." DeRivera and her team observed a population located at an open tidal area of the Sweetwater River estuary in Chula Vista, Calif. Male crabs have bachelor pad burrows. The males stand in groups near their burrows and wave to females with their large claw in a motion that deRivera said looks just like a human beckoning "come here." Copyright © 2005 Discovery Communications Inc.

Keyword: Sexual Behavior; Evolution
Link ID: 7709 - Posted: 06.24.2010

By Cory Hatch People who suffer from brain or spinal cord trauma often have few options beyond physical therapy and hope; injuries to the central nervous system rarely heal and often worsen over time. But recently, researchers from Helsinki, Finland, found a tiny chunk of protein that not only keeps these cells alive but also encourages new cells to grow. The protein—called KDI tri-peptide (KDI)—could someday lead to new treatment options for people suffering from a wide range of neurological problems from spinal cord injury to Alzheimer's disease, says researcher Päivi Liesi. In earlier studies, Liesi and her colleagues found that rats with damaged spinal cords could walk again after three months when they injected KDI near the injury. The protein also shows promise for human cells, at least in the petri dish. How does KDI work? Liesi's most recent research, which appeared July 25 on the Journal of Neuroscience Research website, found that the KDI protein prevents cell death by blocking a substance called glutamate. Normally, glutamate helps cells communicate with one another for learning and memory. However, glutamate is toxic to injured neural cells, causing the cells to take in too much calcium and die. This cell death by glutamate occurs in many different types of nervous system injuries and diseases, including Alzheimer's disease, Lou Gehrig's disease, and spinal cord injuries. Copyright © 2005 U.S.News & World Report

Keyword: Regeneration; Alzheimers
Link ID: 7708 - Posted: 06.24.2010

New research shows that we have a hard time letting go of fears associated with members of a different race. This apparent predisposition was reduced in those who had been involved in interracial dating. The basic experiment paired mild electric shocks with pictures of male faces, as well as various animals. When the shocks were removed, the subjects continued to react fearfully to the faces of a different race. “What was most surprising for me was that the responses were equal for black and white participants,” said Elizabeth Phelps from New York University. “In our culture, we have certain stereotypes, which might make you expect a white person to hold onto negative associations with black males. But black persons had a similar reaction toward white males.” Phelps and her colleagues measured a fear response by increased sweating in their adult subjects. As previous experiments have shown, images of snakes and spiders elicited a response even after the shocks stopped, while the negative emotional reaction to birds and butterflies quickly subsided. This bias toward different animals is thought to be inherent as opposed to learned. Humans who were born wary of snakes and spiders had a better chance to survive. An evolutionary basis is supported by other research with primates. Lab monkeys, who had never seen a real snake in their life, showed persistent fear of a toy snake, but not a toy bunny. © 2005 MSNBC.com © 2005 Microsoft

Keyword: Emotions; Learning & Memory
Link ID: 7707 - Posted: 06.24.2010

With many of us constantly fighting the bulge we often turn to low-calorie foods and artificial sweeteners in hopes of satisfying those sweet cravings without the added calories. But it's pretty clear that most of those sweeteners don't taste exactly like sugar. Now, life might get a whole lot sweeter, and healthier, based on discoveries by a researcher, whose name happens to mean "sugar" in German. "My last name is Zuker, which means sugar. So I guess that indeed it was just meant to be," jokes Charles Zuker, a Howard Hughes Medical Institute investigator at the University of California, San Diego. Zuker, a professor of biology and neurosciences, has been working to try to understand how our brains encode and decode information from our five senses — in this case how it perceives tastes. "How does the brain know what you just tasted? How does it know whether it's good or bad? Well before we can know what the brain knows, we need to know what the tongue knows," Zuker explains. Zucker and his colleagues discovered, four years ago, that all sweet things, no matter their structure or chemical composition, are identified as tasting sweet when they bind to only a couple of sweet receptors — the molecule in the taste cells of the tongue. Unlike any other receptor in the body, they have more than one region that can be activated by different molecule — different kinds of sweet stuff. © ScienCentral, 2000-2005.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 7706 - Posted: 06.24.2010

BOSTON-- Researchers from Harvard Medical School have found a molecule that is unexpectedly involved in dopamine signaling, and in a manner that supports the potential of dopamine as an alternative target for treating depression. The results provide evidence that there is a molecular link between impaired dopamine signaling and depression, which affects 16 percent of the adult population in the United States. The research appears in the July 29 issue of Cell. Li-Huei Tsai, Harvard Medical School (HMS) professor of pathology, HMS research fellow Sang Ki Park, and colleagues worked with mice and found a novel function for the molecule Par-4 (prostate apoptosis response 4)--as a binding partner for dopamine receptor D2. When mice deficient in Par-4 were subjected to stress, they showed depression-like behaviors, proposing Par-4–as a molecular link between dopamine signaling and depression. Par-4 was previously implicated as a proapoptotic factor in neurodegenerative diseases such as Alzheimer's disease. These new findings reveal an unexpected role for Par-4 in the dopamine system and present a rare glimpse of molecular mechanisms behind clinical depression. "Current antidepression therapies are mostly based on the deficiency or imbalance of the serotonin and noradrenaline systems. Our study highlights the importance of the dopamine system, a less appreciated target in the current antidepression therapies," said Tsai, also a Howard Hughes Medical Institute investigator.

Keyword: Depression
Link ID: 7705 - Posted: 06.24.2010

Andreas von Bubnoff A bird that lives in the Ecuadorian rain forest attracts mates by striking its wing feathers together behind its back, researchers say. Birds and other vertebrates usually court partners by expelling air to produce sound. But the male club-winged manakin (Machaeropterus deliciosus) is the first found to use purely mechanical means to produce its 'songs'. "This is completely unprecedented in the vertebrate world," says Kimberly Bostwick of Cornell University in Ithaca, New York, the lead author of the study, which appears in this week's Science1. The technique is more common in insects such as crickets. Only the male manakins have been spotted making noise this way. Their songs sound like two sharp clicks followed by a sustained, violin-like note. That much has been known for a long time: Charles Darwin wrote about the strange manakin sounds2 in 1871. He also noted that the male birds had some feather shafts with thickened ends. ©2005 Nature Publishing Group

Keyword: Sexual Behavior
Link ID: 7704 - Posted: 06.24.2010

Durham, N.C. – Duke University Medical Center researchers have discovered a new mechanism by which chronically high levels of the neurotransmitter dopamine exert their effects on the brain. Normally associated with triggering feelings of pleasure, excess concentrations of dopamine underlie schizophrenia, attention deficit hyperactivity disorder and other psychiatric conditions. The findings therefore provide new research avenues to understand and potentially manage such dopamine-related human disorders, the researchers said. "We've thought that neurotransmitters relay messages to the brain in two speeds: fast and slow," said lead author of the study Jean-Martin Beaulieu, Ph.D. of Duke. "However, our new findings reveal that brain receptors that respond to dopamine actually have two slow modes: one that takes place over a period of minutes and a second -- newly discovered -- that lasts for hours. In fact, it may be that this effect continues for as long as dopamine remains in the system." This sustained action of dopamine may be particularly important for understanding psychiatric conditions, which are characterized by persistently high levels of the brain messenger, Beaulieu said. The researchers report their findings in the July 29, 2005, issue of Cell. "This mechanism appears to be more important than those earlier described for prolonged stimulation by dopamine, as would be the case in those with psychiatric conditions," said senior author Marc Caron, Ph.D., of Duke. "The new pathway can now be evaluated for potential new inhibitors that might be better at controlling particular psychotic behaviors." Caron is a professor of cell biology at Duke and faculty member at the Duke Institute for Genome Sciences & Policy. © 2001-2005 Duke University Medical Center

Keyword: Schizophrenia
Link ID: 7703 - Posted: 06.24.2010

Researchers have discovered a regulatory molecule that links faulty dopamine signaling in the brain to the neural machinery that breaks down in people who suffer from depression. The findings may explain why commonly prescribed antidepressants can take weeks to work and why the drugs are ineffective for some people. The researchers said their findings could open the way for the development of antidepressant drugs with improved efficacy. The researchers, led by Howard Hughes Medical Institute investigator Li-Huei Tsai at Harvard Medical School, published their findings in the July 29, 2005, issue of the journal Cell. According to Tsai, one of the longstanding puzzles in the treatment of depression has been the long lag time that it takes before antidepressants begin to work. These drugs ameliorate depression by increasing levels of the neurotransmitters serotonin and/or noradrenaline in the brain. Since the clinical effects of these drugs are usually significantly delayed, it is now believed that their efficacy depends on changes to later events in the signaling pathway resulting from adaptation to chronic treatment, said Tsai. Neurotransmitters such as serotonin and dopamine are molecular “messengers” that neurons fire at protein receptors on the surface of neighboring neurons. Drugs that influence the levels of these neurotransmitters are central to treating a wide range of neurological disorders. © 2005 Howard Hughes Medical Institute

Keyword: Depression
Link ID: 7702 - Posted: 06.24.2010

Overview Combining partially differentiated stem cells with gene therapy can promote the growth of new "insulation" around nerve fibers in the damaged spinal cords of rats, a new study shows. The treatment, which mimics the activity of two nerve growth factors, also improves the animals' motor function and electrical conduction from the brain to the leg muscles. The finding may eventually lead to new ways of treating spinal cord injury in humans. Combining partially differentiated stem cells with gene therapy can promote the growth of new "insulation" around nerve fibers in the damaged spinal cords of rats, a new study shows. The treatment, which mimics the activity of two nerve growth factors, also improves the animals' motor function and electrical conduction from the brain to the leg muscles. The finding may eventually lead to new ways of treating spinal cord injury in humans. The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. The new study provides the best demonstration to date that producing a nerve-insulating substance called myelin can lead to functional improvements in animals with spinal cord injury. Previous studies have shown that the loss of myelin around nerve fibers contributes to the impaired function after a spinal cord injury. However, until now it has not been clear whether promoting new myelin growth in the spinal cord can reverse this damage, says Scott R. Whittemore, Ph.D., of the University of Louisville in Kentucky, who led the new study. "Many other investigators have suggested that remyelination is a possible approach to repair the spinal cord, but this is the first study to show unequivocally that it works," says Dr. Whittemore. "It is a proof of principle." Although the finding is promising, much work remains before such a technique could be used in humans. The study appears in the July 27, 2005, issue of the Journal of Neuroscience .*

Keyword: Regeneration; Glia
Link ID: 7701 - Posted: 07.29.2005

By SANDRA BLAKESLEE The Department of Agriculture is investigating another possible case of mad cow disease in a domestic cow, its chief veterinarian said yesterday. The department would not say where the farm was, other than to say it was remote. The veterinarian, Dr. John Clifford, said that the 12-year-old cow died in April but that its brain tissue was not tested until last week. Because the initial results were ambiguous, scientists at the National Veterinary Services Laboratory in Ames, Iowa, are conducting more tests to determine whether the cow was infected. Although the brain tissue was collected in April, the veterinarian forgot to send it in, Dr. Clifford said. "While that time lag is not optimal, it has no implications in terms of the risk to human health," he said. The carcass was destroyed, Dr. Clifford said, "and therefore there is absolutely no risk to human or animal health from this animal." Samples are also being sent to an international mad cow laboratory in Weybridge, England. Scientists there have a wide variety of methods for finding the misfolded proteins, or prions, that cause the brain-wasting mad cow disease. Two cases of mad cow disease have been confirmed in the United States. The first, involving a cow born in Canada, was discovered in Washington State in December 2003. The second was a Texas cow that died in November but whose brain was not tested for the disease until last month. British scientists made the diagnosis after American scientists missed it because of using incomplete testing methods. Copyright 2005 The New York Times Company

Keyword: Prions
Link ID: 7700 - Posted: 07.28.2005

Men and women seem to perceive pain in different ways. That may mean they sometimes need different pain-relief drugs MALES and females respond to pain differently, even as children. In most places, boys are expected to show a stiff upper lip when they get hurt, while in girls wailing is, well, girlie. In part, this difference is learnt—or, at least, reinforced by learning. But partly, it is innate. It is hard, for instance, to blame upbringing for the finding that boy and girl babies show different responses to pain six hours after birth, or that male rats are more long-suffering than females. It is also life-long. Ed Keogh of the University of Bath, in England, and his colleagues have found that women report feeling pain in more bodily areas than men, and also feel it more often over the course of their lives. Many researchers are therefore concluding that genetics underpins at least some of the difference, and that females really do feel pain more than males. Indeed, some go further. They think that the way men and women experience pain is not only quantitatively different, but qualitatively different, too. In other words, men's and women's brains process pain using different circuits. Some pain scientists therefore think it is only a matter of time before painkillers are formulated differently for men and women in order to account for this difference. Jeffrey Mogil, director of the pain genetics laboratory at McGill University in Montreal, is one of the leading advocates of such “pink and blue” painkillers. Pick a disease at random, he says, and the chances are that females and males will handle the pain associated with it differently. That seems to be true in mice, at least. When new mouse “models” of human disease are created by genetic engineers, Dr Mogil and his colleagues are often asked to test the engineered mice for their responses to pain. They consistently find differences in the way the mutant, diseased mice and their non-mutation-carrying brethren respond to painful stimuli. But, generally, those differences are seen more strongly in one sex than the other. Copyright © The Economist Newspaper Limited 2005.

Keyword: Pain & Touch; Sexual Behavior
Link ID: 7699 - Posted: 06.24.2010

MONTREAL--Scientists at the MUHC have made progress in understanding what causes migraines. The research, published in the new issue of the Proceedings of National Academy of Sciences (PNAS), reveals how gene mutations known to cause a form of inherited migraine--the kind that cause debilitating headaches and light flashes known as auras--target a cellular process involved in brain cell communication. "A number of mutations have been shown to result in familial migraines," says Dr. Rhoda Blostein--a medical scientist at the Research Institute of the MUHC, professor in the Department of Medicine and Biochemistry at McGill University, and author of the new study. "Discovering genetic mutations that cause disease is important, but in order to develop treatments we must understand what these mutations do." By engineering several genetic mutations known to cause inherited migraines (type 2), and incorporating them into human cells, Dr. Blostein and her team showed several genotypes damage the operation of a tiny cellular mechanism commonly known as the Sodium Pump (Sodium/Potassium ATPase enzyme). "Much of what happens in your brain--from memory to basic movement--is the result of the transmission of electrical impulses along nerve cells," says Dr. Blostein. "This is a basic process by which our brain cells communicate." By expelling sodium from the cell, and drawing potassium from outside, the sodium pump maintains a gradient of potassium, which is critical for the propagation of electrical signals along nerve cells. Like an air conditioner in the heat of summer, the sodium pump is a massive energy hog, consuming around 30% of the energy produced by the cell in order to perform this vital cellular process.

Keyword: Pain & Touch
Link ID: 7698 - Posted: 07.28.2005

Working with mice, University of Iowa scientists and colleagues from Okayama University, Japan, have shown that it is possible to cure a certain type of hereditary deafness by silencing a gene that causes hearing loss. Richard Smith, M.D., the Sterba Hearing Research Professor in Otolaryngology at the UI Roy J. and Lucille A. Carver College of Medicine, described the study as a proof-of-principle experiment, but added that the success may point the way to new treatments for deafness in humans. "We gave a genetically-deafened mouse interfering RNA that specifically prevents a gene from being expressed that would otherwise cause deafness. By preventing its expression, we prevented the deafness," said Smith who was senior author of the study. "Even though this is in the early stages, it is really exciting because it points to other options for people who have hearing loss other than hearing aids or cochlear implants." The gene-silencing technique used by the UI team is called RNA interference (RNAi) and works specifically against genetic conditions caused by a so-called dominant negative mechanism -- when a single copy of the mutant gene is sufficient to cause disease because the protein from the faulty gene has a dominant adverse effect over the protein from the normal gene. Although many of the most common deafness genes do not work through this mechanism, several human forms of inherited deafness, including the one mimicked by the UI mouse model, are caused by a dominant negative mechanism.

Keyword: Hearing; Genes & Behavior
Link ID: 7697 - Posted: 07.28.2005

In the exquisitely regulated networks of the brain, hundreds of channels, receptors, and other specialized proteins work together to control communication at the synapses, or junctions between neurons. Working with mice, scientists have found that a single molecule, known as Nova, helps control the production of a large, closely related set of these specialized proteins. The 49 proteins regulated by Nova all play some role at the synapse - as neurotransmitter receptors, ion channels, adhesion molecules, and scaffold proteins - or in guiding the development of axons, the long projections of the nerve cell body. According to the researchers, Nova's role in controlling the production of these related proteins represents a means by which the entire set can be regulated as a group. “What we found is that Nova regulates a very refined, restricted piece of biology, and it regulates it in a very multi-tiered and complicated way,” said Robert B. Darnell, a Howard Hughes Medical Institute investigator at The Rockefeller University and senior author on the study. Darnell's colleagues at Rockefeller and scientists from the University of Amsterdam, Affymetrix, Inc., and the National Cancer Institute also contributed to the work, which was published in the August issue of the journal Nature Genetics. Like all cells in the body, brain cells must rely on the same limited set of genes - about 20,000 to 30,000 - as the blueprint for the unique assortment of proteins they need to carry out their function. One way cells achieve this diversity is by modifying messenger RNA molecules - the intermediary material in the conversion of gene to protein. Regulatory molecules like Nova oversee the cutting and pasting of the RNA - including and excising different bits and pieces in a process known as alternative splicing - to produce an assortment of proteins from the same gene. © 2005 Howard Hughes Medical Institute.

Keyword: Development of the Brain
Link ID: 7696 - Posted: 06.24.2010

A particularly aggressive form of brain tumor called a glioma may be vulnerable to a drug currently used to treat Crohn's disease, according to a new study in mice. The finding is good news to scientists looking for better treatment options for a cancer that is almost always fatal. The drug exploits a weakness of glioma cells. While most cells take in a necessary amino acid called cystine through a variety of pathways, a team led by Harald Sontheimer, a neuroscientist with the University of Alabama at Birmingham, has discovered that glioma cells have only one mechanism for grabbing the amino acid. Earlier studies elsewhere found that cystine intake in leukemia cells is impaired by sulfasalazine, a drug used to treat diseases such as Crohn's, which causes inflammation of the intestinal tract. So, Sontheimer and colleagues wondered if the drug would cut off the cystine supply to glioma tumors. To test the theory, the researchers first injected mice with malignant human glial tissue. After the tissue developed into tumors, the team divided the mice into three groups. Two groups got sulfasalazine for either 1 or 3 weeks, and a control group received saline. Within 48 hours of receiving the drug, mice in the sulfasalazine group showed biochemical signs that glioma cells were affected. And within a matter of weeks, the size of their tumors had shrunk dramatically. The drug also increased the animals' survival rate. Mice in the control group showed no improvement, the team reports 27 July in the Journal of Neuroscience. Copyright © 2005 by the American Association for the Advancement of Science

Keyword: Glia
Link ID: 7695 - Posted: 06.24.2010

New Haven, Conn.--Patients who are delirious during hospitalization one year later had 13 percent fewer days of survival during the following year when compared to patients without delirium, according to a study published this month in the Archives of Internal Medicine. Delirium is a frequent problem for hospitalized older patients with consequences ranging from increased morbidity and mortality, persistent functional decline and increased and costlier hospital stay to higher rates of nursing home placement, increased caregiver burden, and overall higher health care costs, the researchers said. Previous studies demonstrated an increased risk of mortality associated with delirium, but little was known about the mortality time course. The objective of this study was to estimate the fraction of a year of life lost associated with delirium at a one-year follow up. The study included 919 patients 70 and older who participated in an earlier study on delirium prevention intervention. Of these patients, 115 had delirium during their hospital stay. "Patients with delirium survived 274 days on average compared with 321 days for patients without delirium, representing a difference of 13 percent a year," said Douglas Leslie, assistant professor of psychiatry at Yale School of Medicine.

Keyword: Miscellaneous
Link ID: 7694 - Posted: 07.28.2005

Michael Hopkin Humans can learn skills without remembering what they have done, according to a study of patients with severe amnesia. Such learning is seen in monkeys, but experts were unsure whether humans retained this ability, because of our tendency to think consciously about whatever we are learning. Most people gather information and abilities through a process of 'declarative' learning, in which they remember the act of learning as well as the new skill or knowledge itself. Hopefully, you'll recall reading this article, as well as remembering the nuggets of information it contains. This process of explicit thought offers a fast route to learning, but requires sophisticated mental machinery. Declarative learning is centred on a brain region called the medial temporal lobe, which is thought to coordinate the storage of memories in the brain. Other animals, which lack our cognitive powers, use a slower, more primitive method called habit learning. If one item in a pair of objects is designated the 'correct' item, monkeys can learn to select this particular item by simple trial and error. Without realizing they are doing it, they gradually acquire the habit of picking the right option. ©2005 Nature Publishing Group

Keyword: Learning & Memory
Link ID: 7693 - Posted: 06.24.2010

How did University of Alberta researchers discover that animals zig when they were only supposed to zag? A little birdie told them. In studying the spatial memory of wild-caught mountain chickadees, University of Alberta researchers were surprised to discover the birds contradicting prior research that showed how animals navigate. This study is the first to reveal a different pattern. Previously, only animals that had been raised in human-made enclosures had been tested. The findings are published in the July issue of Biology Letters. To get their bearings, humans and other animals are often guided by the geometrical shape of their environment. For example, humans have an easy time distinguishing the door located at the ends of a hallway from those located in the middle, but may confuse doors at the two ends, such as when they re-enter a hallway in a hotel. "This has been observed in every species tested, even when landmarks alone could be used, suggesting that animals are predisposed to go by geometry," said co-author Dr. Chris Sturdy, a professor of psychology and member of the Centre for Neuroscience at the University of Alberta.

Keyword: Animal Migration
Link ID: 7692 - Posted: 07.27.2005

By Ishani Ganguli An improved ability to distinguish the bitter taste of natural toxins in foods may have made a difference in the survival of early humans as they radiated out of Africa, according to a genetic analysis by researchers led by a group at University College London, appearing in the July 26 issue of Current Biology. The new study suggests that a particular allele for the G protein-coupled taste receptor TAS2R16-which mediates the response to bitter cyanogenic glycosides found in many food plants-has been favored by human evolution. "There is a general understanding that higher primates and humans in particular are losing some of their sensory capabilities because we have replaced sensory perception with other means of protecting ourselves-cooking food, for instance, or even changing diet," said coauthor Nicole Soranzo. However, these results suggest that there is more to the evolutionary story, said John Glendinning, of Barnard College in New York, who did not participate in the study. "This is the first study that's really looked seriously at the functional consequences of one of these [receptors] as it relates to bitter taste ecology," Glendinning told The Scientist. The authors sequenced the entire coding region and part of the 5' and 3' untranslated regions of the TAS2R16 gene in nearly 1000 individuals representing 60 populations worldwide. Out of the 17 variable sites, they focused on amino acid site 172, which tends to be lysine (K) or asparagine (N) and lies in an extracellular loop domain of the receptor. Based on comparisons with nonhuman primate sequences, they estimated that the K allele was ancestral and that the N allele emerged between 77,751 and 685,380 years ago, just before early humans were leaving Africa. © 2005 The Scientist,

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 7691 - Posted: 06.24.2010