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October 15, 2006, 7:15 PM CT

Same Gene For Cleft Lip And Skin Biology

Same Gene For Cleft Lip And Skin Biology
Following up on an earlier discovery that a gene called IRF6 is involved in the common birth defect cleft lip and palate, scientists at the University of Iowa Roy J. and Lucille A. Carver College of Medicine and their colleagues have identified the function of the gene. Their latest findings, published online Oct. 15 in Nature Genetics, reveal an unexpected role for IRF6 in the growth and development of skin cells, a discovery that may have implications for wound healing and cancer research.

In 2002, Brian Schutte, Ph.D., UI associate professor of pediatrics and nursing, and Jeff Murray, M.D., UI professor of pediatrics, pediatric dentistry and biological sciences, and the Roy J. Carver Chair in Perinatal Health, led a study showing that mutations in IRF6 cause Van der Woude syndrome (VWS), a rare, dominantly inherited form of cleft lip and palate. Subsequently, the scientists observed that this gene also is mutated in 10 to 15 percent of the more common, so-called non-syndromic cases of cleft lip and palate. Cleft lip and palate, where the lip or both the lip and palate (roof of the mouth) fail to close, occurs in approximately one of every 1,000 babies.

In order to determine the function of this gene, the scientists created mice that lacked IRF6. These mice had very abnormal skin as well as a cleft palate. Detailed analysis of the mice revealed that IRF6 regulates the proliferation and differentiation of keratinocytes -- the main cell type in the epidermis or outer layer of skin. Keratinocytes also provide a protective barrier around the mouth, gut, liver, lung, kidney and other internal organs.........

Posted by: JoAnn      Permalink         Source


October 15, 2006, 6:27 PM CT

Potential New Treatments For Birth Defects

Potential New Treatments For Birth Defects
May be after a while those babies need not be born with cleft lip and palate. New research is paving way for therapy of these birth defects while they are still in womb.

University of Manchester scientists have uncovered the causes behind two genetic conditions that lead to facial anomalies including clefts, where the lip and often the roof of the mouth, or palate, fail to form properly.

Working with colleagues at the University of Iowa, Manchester husband and wife team Mike and Jill Dixon together with researcher Rebecca Richardson, have identified the role of a gene called IRF6.

"We had previously shown that a mutation in the IRF6 gene causes Van der Woude syndrome a rare inherited form of cleft lip and palate," said Professor Mike Dixon, a dentist based in the Faculty of Life Sciences.

"It has also been observed that defects in this gene are responsible for a significant number of other cleft lip and palate disorders that are not correlation to any particular syndrome".

The team established that mice missing the gene developed abnormal skin as well as cleft palate. Further analysis revealed that IRF6 controls the development of keratinocytes the main type of cells in the outer layers of the skin, known as the epidermis.

"Put simply, mutations of IRF6 in Van de Woude syndrome make the skin cells too sticky, so they stick to each other and other types of cell much sooner than they should resulting in these facial anomalies," said Professor Dixon.........

Posted by: JoAnn      Permalink         Source


October 15, 2006, 6:20 PM CT

Commonplace Sugar Controls Seizures

Commonplace Sugar Controls Seizures
This sugar has been in clinical use for decades, but now it is finding new uses, a potential cure for epilepsy.

2-deoxy-glucose, or 2DG, has long been used in radio labeling, medical scanning and cancer imaging studies in humans. But now, scientists at the University of Wisconsin-Madison have found the substance also blocks the onset of epileptic seizures in laboratory rats.

Published in the journal Nature Neuroscience, the findings have potentially huge implications for up to half of all epileptic patients who currently have no access to therapy, says senior author Avtar Roopra, a UW-Madison assistant professor of neurology.

"We pumped the rats full [of 2DG] and still saw no side effects," says Roopra, who estimates that the compound may be available for human use within five years. "I see 2DG as an epilepsy management therapy much like insulin is used to treat diabetes."

"All the available epilepsy therapys have focused on suppressing seizures," says co-author and renowned epilepsy expert Tom Sutula, a UW-Madison professor of neurology. "There has been hope that [new drugs] will not only suppress seizures, but modify their consequences. [2DG] appears to be a novel therapy that offers great promise to achieve that vision."

About 1 percent of the world's population suffers from epilepsy, a neurological condition that makes people susceptible to seizures. Researchers think that seizures, of which there are a number of kinds, occur due to sudden changes in how brain cells send electrical signals to each other. In about 30 to 50 percent of epilepsy patients, available therapys - including the removal of parts of the brain's temporal lobe - are largely ineffective.........

Posted by: Daniel      Permalink         Source


October 13, 2006, 4:53 AM CT

Studying Pediatric AIDS Vaccine

Studying Pediatric AIDS Vaccine
Researchers at Makerere University, in Kampala, Uganda, along with researchers from Johns Hopkins and other institutions worldwide, have begun the first clinical safety trial in Africa of a vaccine to prevent mother-to-child transmission of HIV through breastfeeding. Breast milk is a leading route of infection in the developing world, as per the United Nations World Health Organization, which estimates that each day 1,800 newborns are infected with the AIDS virus, 30 percent to 40 percent by virus carried in their mother's milk.

Enrollment of the first newborn took place at Mulago Hospital in Kampala. The so-called phase I study is designed to test the safety of injecting newborns with the vaccine, formally known as ALVAC-HIV (vCP1521). If the vaccine is found to be safe in this study, and if it is later shown to be effective in reducing the chance of infants' becoming infected during breastfeeding, scientists estimate that it could potentially stop up to 8,000 of Uganda's 22,000 infections a year in children. Initial results are expected by mid-2007.

"A vaccine is the easiest way to help prevent mother-to-child transmission of the disease, as healthy alternatives to breastfeeding, such as infant formula, are not available or affordable to most new mothers in the developing world, a number of of whom do not know they are HIV positive," says study protocol chair and pediatric infectious disease specialist Laura Guay, M.D., who will lead Hopkins' efforts.........

Posted by: Mark      Permalink         Source


October 12, 2006, 10:15 PM CT

Leading Reason For Corneal Transplants

Leading Reason For Corneal Transplants
Guided by families with an unusual number of cases, researchers at Johns Hopkins have discovered the genetic origins of at least one form of Fuchs corneal dystrophy, FCD, the leading reason for corneal transplantation in the United States.

In one form or another, FCD's trademark deterioration of the cells covering the clear, outermost lens of the eye affects more than 4 percent of the population over 40. Late in life, the dystrophy causes swelling of the cornea and can severely affect vision, making it impossible to see well even with glasses or contact lenses. It's believed that various forms of FCD are due to multiple gene mutations.

In a report in the recent issue of Investigative Ophthalmology, a team led by Hopkins ophthalmologist John Gottsch, M.D., says they were able to map a common form of Fuchs, found most often in women, to chromosome 18.

"Finding this chromosomal locus is putting us in the right neighborhood to find culprit genes," says Gottsch. "Now we have to start knocking on every door".

Gottsch is heartened by success with earlier Fuchs gene-hunting studies. The Hopkins group tracked down its first FCD-related gene in a Virginia family with multiple, early onset cases. That gene, labeled COL8A2, was mapped to chromosome 1.........

Posted by: Mike      Permalink         Source


October 12, 2006, 4:42 AM CT

Refocusing On Patients With HIV, Hepatitis

Refocusing On Patients With HIV, Hepatitis
As HIV patients live longer thanks to advanced therapies, scientists are looking for better ways to treat accompanying maladies such as hepatitis that traditionally were not emphasized.

"People are living longer with HIV now, but then we see people developing complications from liver disease due to hepatitis," said Dr. Mamta Jain, assistant professor of internal medicine at UT Southwestern Medical Center. "Before we had effective HIV treatment, there was no interest in treating hepatitis C because the thought was the patient would die of AIDS. Well, they're not dying of AIDS, so we are making an effort to try to treat more patients for hepatitis C".

Other diseases, such as cirrhosis or hepatocellular cancers, progress faster in co-infected HIV and hepatitis patients. As a result, health-care providers are trying to intervene as early as possible, said Dr. Jain, who specializes in infectious diseases.

Dr. Jain oversees a co-infection clinic at Parkland Memorial Hospital where patients are reviewed for hepatitis and HIV and can participate in clinical trials. Generally, co-infection rates range from 10 percent to 33 percent of HIV patients. Rates run at about 25 percent at the clinic in Parkland, which is the teaching hospital for UT Southwestern.

UT Southwestern has several ongoing clinical trials for which doctors are recruiting potential patients. The latest study involves whether giving hepatitis C, or HCV, medications early on during HIV disease speeds recovery or improves hepatitis therapies.........

Posted by: Mark      Permalink         Source


October 11, 2006, 5:18 AM CT

Hiv Gets A Makeover

Hiv Gets A Makeover Tweaking HIV. A newly engineered version of the AIDS virus, dubbed stHIV, replicates robustly in rhesus monkey cells.
The slow pace of AIDS research can be pinned, in no small part, on something akin to the square-peg-round-hole conundrum. The HIV-1 virus won't replicate in monkey cells, so scientists use a monkey virus - known as SIVmac, or the macaque version of simian immunodeficiency virus - to test potential therapies and vaccines in animals. But therapies and vaccines that are effective on SIV don't necessarily translate into human success. Now, using a combination of genetic engineering and forced adaptation, scientists at Rockefeller and the Aaron Diamond AIDS Research Center have created a version of the AIDS virus that replicates vigorously in both human and monkey cells - an advance that has the potential to revolutionize vaccine research.

In a paper published in today's issue of Science, Paul Bieniasz, associate professor and head of the Laboratory of Retrovirology, describes how he and colleagues maneuvered around the intrinsic immunity of primate cells by replacing just a few parts of the human virus - the ones responsible for blocking replication in monkey cells - with components from SIV. "Overall, the virus is a mixture of engineering and forced evolution," Bieniasz says. "It sounds simple, in theory, but it took us two years to do".

Bieniasz and Theodora Hatziioannou, a research scientist in the lab and the paper's first author, had to overcome two major obstacles: the first was a protein called TRIM5 that, in monkeys, recognizes the outer shell or "capsid" of HIV-1 but not that of SIV. By swapping out the capsid region of the HIV-1 genome for that of the monkey virus, and then selectively growing the viruses that replicated most robustly, over several generations Hatziioannou created an HIV-1 mutant that could evade the monkey cells' TRIM5 recognition.........

Posted by: Mark      Permalink         Source


October 10, 2006, 9:56 PM CT

Material That Stops Bleeding In Seconds

Material That Stops Bleeding In Seconds
MIT and Hong Kong University scientists have shown that some simple biodegradable liquids can stop bleeding in wounded rodents within seconds, a development that could significantly impact medicine.

When the liquid, composed of protein fragments called peptides, is applied to open wounds, the peptides self-assemble into a nanoscale protective barrier gel that seals the wound and halts bleeding. Once the injury heals, the nontoxic gel is broken down into molecules that cells can use as building blocks for tissue repair.

"We have found a way to stop bleeding, in less than 15 seconds, that could revolutionize bleeding control," said Rutledge Ellis-Behnke, research scientist in the MIT Department of Brain and Cognitive Sciences.

This study, which will appear in the online edition of the journal Nanomedicine on Oct. 10, marks the first time that nanotechnology has been used to achieve complete hemostasis, the process of halting bleeding from a damaged blood vessel.

Doctors currently have few effective methods to stop bleeding without causing other damage. More than 57 million Americans undergo nonelective surgery each year, and as much as 50 percent of surgical time is spent working to control bleeding. Current tools used to stop bleeding include clamps, pressure, cauterization, vasoconstriction and sponges.........

Posted by: Scott      Permalink         Source


October 9, 2006, 9:27 PM CT

Celiac Disease And Cognitive Decline

Celiac Disease And Cognitive Decline Image courtesy of celiacdisease.net
Mayo Clinic scientists have uncovered a new link between celiac disease, a digestive condition triggered by consumption of gluten, and dementia or other forms of cognitive decline. The investigators' case series analysis -- an examination of medical histories of a group of patients with a common problem -- of 13 patients would be reported in the recent issue of Archives of Neurology.

"There has been very little known about this correlation between celiac disease and cognitive decline until now," says Keith Josephs, M.D., Mayo Clinic neurologist and study investigator. "This is the largest case series to date of patients demonstrating cognitive decline within two years of the onset of celiac disease symptom onset or worsening."

Says Joseph Murray, M.D., Mayo Clinic gastroenterologist and study investigator, "There has been a fair amount written before about celiac disease and neurological issues like peripheral neuropathy (nerve problems causing numbness or pain) or balance problems, but this degree of brain problem -- the cognitive decline we've found here -- has not been recognized before. I was not expecting there would be so a number of celiac disease patients with cognitive decline."

The next step in the research will be to investigate the measure and nature of the correlation between the two conditions.........

Posted by: Sue      Permalink         Source


October 9, 2006, 9:13 PM CT

Progress In HIV Research

Progress In HIV Research
How a harmless virus called GB Virus type C (GBV-C) protects against HIV infection is now better understood. Scientists at the Department of Veterans Affairs (VA) Iowa City Health Care System and the University of Iowa have identified a protein segment that strongly inhibits HIV from growing in cell models.

The team observed that an 85-amino acid segment within a GBV-C viral protein called NS5A greatly slows down HIV from replicating in cells grown in labs. The study results will appear online this week in the Proceedings of the National Academy of Sciences.

The finding builds on earlier VA and UI work showing that people with HIV who also are infected GBV-C live longer than those infected only with HIV, said Jinhua Xiang, M.D., a VA research health scientific specialist, UI researcher and the current study's principal author.

GBV-C and its role in HIV infection have been studied for nearly a decade by Xiang, along with another study author Jack Stapleton, M.D., staff doctor and researcher at the VA Iowa City Health Care System and professor of internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine.

"Identifying a specific protein made by GBV-C that inhibits HIV growth in cell culture strengthens the argument that GBV-C is responsible for the prolonged survival observed in several studies of HIV-positive people," Xiang said. "Understanding how the protein works may allow us to develop target-specific therapies that can mimic these effects and inhibit HIV.........

Posted by: Mark      Permalink         Source



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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell.

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