Most Recent Links

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 22361 - 22380 of 29511

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

Irvine, Calif., --A research team led by UC Irvine neuroscientists has identified how the brain processes and stores emotional experiences as long-term memories. The research, performed on rats, could help neuroscientists better understand why emotionally arousing events are remembered over longer periods than emotionally neutral events, and may ultimately find application in treatments for conditions such as post-traumatic stress disorder. The study shows that emotionally arousing events activate the brain's amygdala, the almond-shaped portion of the brain involved in emotional learning and memory, which then increases a protein called "Arc" in the neurons in the hippocampus, a part of the brain involved in processing and enabling the storage of lasting memories. The researchers believe that Arc helps store these memories by strengthening the synapses, the connections between neurons. The study will appear in today's issue of the Proceedings of the National Academy of Sciences. "Emotionally neutral events generally are not stored as long-term memories," said Christa McIntyre, the first author of the paper. "On the other hand, emotionally arousing events, such as those of September 11, tend to be well-remembered after a single experience because they activate the amygdala."

Keyword: Stress; Emotions
Link ID: 7690 - Posted: 07.27.2005

Happy, sad, angry, scared: Some of us are good at hiding these everyday emotions, while others are unable to disguise them. Whether subtle or intense, facial expressions are the key to how we identify human emotion. Most studies of how we recognize facial expressions have used static models of intense expressions. But new research indicates that facial motion—seeing the range of movement in the arching of an eyebrow or the curve of a smile—is in fact an extremely important part of what makes subtle facial expressions identifiable. A recent study by Zara Ambadar and Jeffrey F. Cohn of the University of Pittsburgh and Jonathan W. Schooler of the University of British Columbia, examined how motion affects people's judgment of subtle facial expressions. Their report, "Deciphering the Enigmatic Face: The Importance of Facial Dynamics in Interpreting Subtle Facial Expressions," is in the May 2005 issue of Psychological Science, a journal of the American Psychological Society. Two experiments demonstrated robust effects of motion in facilitating the perception of subtle facial expressions depicting six emotions, anger, disgust, fear, happiness, sadness and surprise. For the initial experiment, participants viewed a series of subtle facial expressions, displayed by faces on a computer screen. The faces varied in the way they were displayed; in the single static display, only the final expression was shown, while the dynamic displays showed the emergence of a subtle expression through several images, ending at the identical final expression.

Keyword: Emotions
Link ID: 7689 - Posted: 06.24.2010

How alike are you and your husband or wife — or, you and your best friend? Probably more alike than you realize. A study of twins shows that people's spouses and best friends are much more similar to them than was previously recognized — about as close as brothers and sisters. The research also suggested that the preference for partners who are similar to us is partly due to our genes. The research was conducted by J. Philippe Rushton and Trudy Ann Bons of the University of Western Ontario. Their findings are reported in "Mate Choice and Friendship in Twins: Evidence for Genetic Similarity," published in the July 2005 issue of Psychological Science, a journal of the American Psychological Society. Several hundred pairs of identical and fraternal twins, their spouses, and their best friends were sent a 130-item questionnaire that measured social background, personality, and attitudes. Twins turned out to be as similar to their spouses and friends as they were to their fraternal twins, though not as similar as they were to identical twins. The spouses of identical twins (who share 100 percent of their genes) were also more similar to each other than were the spouses of fraternal twins (who only share 50 percent of their genes); the same was true of twins' best friends.

Keyword: Genes & Behavior
Link ID: 7688 - Posted: 06.24.2010

By LAURA TANGLEY These days, it seems, even the moral values of birds are subject to scrutiny. To investigate the spousal fidelity of eastern imperial eagles, large raptors native to central Asia, a team of surreptitious scientists collected feathers the birds had shed near their nests in northern Kazakhstan. Extracting and analyzing DNA from the feathers confirmed that not a single eagle had strayed from its mate during the course of the six-year study - a degree of monogamy unusual among birds. Biologists once believed that most, if not all, bird species were monogamous. But over the past decade, that presumption, based on observations of apparently faithful male-female pairs building nests and raising young together, has been overturned by genetic "paternity tests" of blood samples from the birds. In more than 75 percent of avian species looked at so far, researchers have discovered broods that have two or more fathers. Because obtaining their blood is so difficult, however, large raptors like eagles remain largely untested. Biologists suspect that raptors, unlike smaller songbirds, may indeed be monogamous, in part because they are long-lived species in which males invest considerable energy caring for their offspring and mates. In addition, raptors are "large, ferocious birds of prey equipped with talons and sharp curved beaks," said Andrew DeWoody, an associate professor of genetics at Purdue and a co-author of the eagle study, published online this month in Molecular Ecology. "If a bird gets caught cheating, the repercussions could be severe." Copyright 2005 The New York Times Company

Keyword: Sexual Behavior
Link ID: 7687 - Posted: 07.26.2005

Durham, N.C. – Plant toxins in the diets of early humans drove the evolution of a bitter taste receptor better able to detect them, suggests new genetic research by scientists at University College London, Duke University Medical Center, and the German Institute of Human Nutrition. The ability to discern bitter flavors likely offered a survival advantage by protecting ancient people from poisonous fare, the researchers concluded. Today, however, the same sensory sensitivity may have adverse consequences for human health, they added, by causing an aversion to bitter-tasting nutrients, some of which might lower the risk of cancer and heart disease. In their study, the researchers examined the sequence of one gene encoding the bitter taste receptor TAS2R16 in 60 human populations from all over the world. By reconstructing the history of the gene, the researchers found evidence of evolutionary selection. Specifically, they found that particular derived variants of the taste receptor rapidly rose to high frequency many thousands of years ago, before the expansion of early humans out of Africa. Through further analyses they showed that one of the selected gene variants confers an increased sensitivity to particular toxins, including five that release cyanide when digested. The receptor variant also is more sensitive to certain beneficial compounds, they showed. The team reported its findings in the July 26, 2005, issue of Current Biology. The researchers included senior author David Goldstein, Ph.D., of the Duke Institute for Genome Sciences & Policy (IGSP) and lead author Nicole Soranzo, Ph.D., of the University College London. © 2001-2005 Duke University Medical Center.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 7686 - Posted: 06.24.2010

The brain is bombarded by information about the physical proportions of our bodies. The most familiar sensations, such as a puff of wind or the brush of our own shirt sleeve, serve to constantly remind the brain of the body's outer bounds, creating a sense of what is known as proprioception. In a new study, researchers report this week that the brain's ability to interpret external signals and update its sense of bodily self is more dynamic than had been previously thought and that such updates can happen very quickly, altering within a matter of seconds how body parts and individual touch sensations are perceived. The information that is integrated in the course of proprioception comes from several different senses, including touch, pain, vision, information from muscles, and so on. The brain must combine all these information inputs to accurately perceive the external world through our body's interaction with it and also to produce a coherent sense of self. Because all these signals carry such different kinds of information, the brain must perform a constant juggling act in order to make sense of the body and the world. In the new study, the research team used a method called tendon vibration to induce a distortion of healthy volunteers' sense of their own bodies. When the biceps tendon of the right arm was vibrated, the subjects in the experiments felt within seconds that their right elbow was rotating away from the body, even though the arm was actually quite still. If subjects held their left index finger with their right hand while this happened, they felt their left index finger getting longer as they felt their arm move.

Keyword: Pain & Touch
Link ID: 7685 - Posted: 07.26.2005

CHICAGO – A testosterone patch may produce modest increases in sexual desire and frequency of satisfying sexual experiences in women who develop distressful, low sexual desire following hysterectomy and removal of the fallopian tubes and ovaries, according to a study in the July 25 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. Diminished sexual desire has been reported by 30 to 50 percent of women who undergo surgical menopause (menopause induced by the surgical removal of both ovaries), according to background information in the article. In one form of female sexual dysfunction, hypoactive sexual desire disorder, a chronic absence of desire for sexual activity results in personal distress. When the ovaries are removed (oophorectomy), blood levels of sex hormones, including testosterone, drop. Although some women see improvements in sexual functioning with estrogen therapy alone, previous studies suggest that the combination of estrogen and testosterone is more effective in preserving sexual desire. Glenn D. Braunstein, M.D., of Cedars-Sinai Medical Center, Los Angeles, and colleagues conducted a 24-week, randomized, double blind, multicenter clinical trial in women who developed distressful low sexual desire after surgical menopause and were receiving oral estrogen therapy. The 447 women (aged 24 to 70 years) were randomized to receive placebo or testosterone patches twice weekly in one of three progressively higher doses. Testosterone levels were checked at baseline, 12 and 24 weeks. Changes in sexual desire and frequency of satisfying sexual activity were determined on the basis of a woman's reports on standardized questionnaire and sexual function activity log.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 7684 - Posted: 06.24.2010

Two recent studies suggest that multiple rare mutations within a single gene may increase risk for autism, according to investigators with the Vanderbilt Center for Molecular Neuroscience and the Vanderbilt Kennedy Center for Research on Human Development While debate still rages over the 'cause' of autism, mounting evidence suggests that genetic factors play a major role in the disease. Two recent studies suggest that multiple rare mutations within a single gene may increase risk for autism. Their findings also may point to new therapeutic options for this devastating disorder. In this pair of studies, the researchers identify and characterize a number of mutations in the gene that regulate brain levels of serotonin, a neurotransmitter involved in many biological processes including breathing, digestion, sleep, appetite, blood vessel constriction, mood and impulsivity. About 25 percent of people with autism have elevated levels of serotonin in their blood. Selective serotonin reuptake inhibitors (SSRIs), drugs used to treat depression, anxiety and obsessive-compulsive disorders, also improve some of the symptoms of the disorder. These findings have led scientists to propose that serotonin plays an important role in autism. In the August issue of the American Journal of Human Genetics, Sutcliffe, Blakely and colleagues report that several mutations within the serotonin transporter (SERT) gene, which regulates serotonin levels in the brain, may be risk factors for autism.

Keyword: Autism
Link ID: 7683 - Posted: 07.26.2005

Jim Giles Why doesn't the world go dark when we blink? Because a critical part of the brain switches off and fails to detect the blackness behind closed eyes, says a team of neuroscientists. We blink about ten times a minute without noticing any change in what we see. Researchers had suspected that this is because the visual system is inactivated during blinking, but were not able to prove this. A team at University College London have cracked the problem by inserting an optical fibre into the mouths of people wearing black-out goggles. The fibre illuminated the back of the subjects' retinas, so that they saw a light at all times, even when they blinked. This allowed the researchers, who publish their results in Current Biology1, to distinguish between the effects of the act of blinking and the darkness that it causes. Using magnetic resonance imaging (fMRI) brains scans, Davina Bristow and colleagues revealed that activity in a part of the visual system known as V3 was suppressed in subjects when they blinked. V3 is one of a series of brain areas that handle signals sent from the eyes. With it out of action, the blink goes unnoticed. "It's not that the visual gap is filled in," says Bristow. "It's that you're not aware of it." ©2005 Nature Publishing Group

Keyword: Vision
Link ID: 7682 - Posted: 06.24.2010

Scientists say they have discovered a protein that could be injected to repair damaged nerves and brain cells. The protein, KDI tripeptide, works by blocking the harmful effects of a substance present in degenerative brain diseases and spinal cord injuries. By blocking this substance, called glutamate, KDI prevents permanent cell death and helps the body heal itself. The Finnish work from the University of Helsinki will be published online by the Journal of Neuroscience Research. So far the researchers have tested KDI in the lab on animals and nerve cells from humans. The findings have been promising and they hope to be able to begin treating people with nerve and degenerative brain diseases, such as Alzheimer's and Parkinson's disease, using KDI injections within a year. Since KDI occurs naturally in some form in the body, researchers do not believe it will have major toxic side effects. None have been noted during their work to date. Lead researcher Dr Päivi Liesi said: "We have had such good results with animals that I think it is totally feasible we would be ready to start human clinical trials within a year." Currently, KDI has to be injected as a solution directly to the damaged area. However, in the future it might be possible to make the treatment as an oral drug or an intravenous injection, said Dr Liesi. Her work builds on that of Dr George Martin from the National Institute on Ageing, at the US National Institutes of Health, who first discovered the molecule that KDI is derived from. Dr Martin said: "This represents a new approach and one with considerable promise. (C)BBC

Keyword: Regeneration
Link ID: 7681 - Posted: 07.25.2005