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Latest News
Genetic Link to Heart Failure

A team of researchers, at Washington University School of Medicine, St Louis, has identified a group of 12 genetic variants in the HSPB7 gene that is associated with heart failure in humans. The research is reported in the Journal of Clinical Investigation. The team, led by Gerald Dorn, used an approach they have recently developed that allows ultra-high-throughput targeted DNA sequencing to identify genetic variation in four genes with biological relevance to heart failure. They identified in a large group of Caucasian individuals with heart failure, 129 separate genetic variants in the four genes, including 23 that seemed to be novel. Further analysis of 1117 Caucasian individuals with heart failure and 625 nonaffected Caucasians indicated that a block of 12 genetic variants in the HSPB7 gene was associated with heart failure. Confirmation of this association was provided by analysis of an independent group of individuals. The authors hope to use the same approach to identify further genetic variants associated with heart failure, a disease that is influenced by multiple genetic factors.

Biofilms: Researchers Discover New Ways to Treat Chronic Infections

Researchers at Binghamton University, State University of New York, have identified three key regulators required for the formation and development of biofilms. The discovery could lead to new ways of treating chronic infections. Biofilms -- communities of bacteria in self-produced slime -- may be found almost anywhere that solids and liquids meet, whether in nature, in hospitals or in industrial settings. Biofilms are implicated in more than 80 percent of chronic inflammatory and infectious diseases caused by bacteria, including ear infections, gastrointestinal ulcers, urinary tract infections and pulmonary infections in cystic fibrosis patients, according to the Centers for Disease Control. Biofilms are difficult to eradicate with conventional antimicrobial treatments since they can be nearly 1,500-fold more resistant to antibiotics than planktonic, free-floating cells. Biofilms also pose a persistent problem in many industrial processes, including drinking water distribution networks and manufacturing.

Keeping Hepatitis C Virus at Bay After a Liver Transplant

One of the most common reasons for needing a liver transplant is liver failure or liver cancer caused by liver cell infection with hepatitis C virus (HCV). However, in nearly all patients the new liver becomes infected with HCV almost immediately. But now, Hideki Ohdan, Kazuaki Chayama, and colleagues, at Hiroshima University, Japan, have developed an approach that transiently keeps HCV levels down in most treated HCV-infected patients receiving a new liver. The researchers report their findings in the Journal of Clinical Investigation. Specifically, the team took immune cells known as lymphocytes from the donor livers before they were transplanted into the HCV-infected patients, activated them in vitro, and then injected them into the patients three days after they had received their liver transplants. Importantly, these infused cells were able to keep the HCV at bay even though the patients were taking immunosuppressive drugs to prevent their immune systems from rejecting the new livers. Despite showing clear clinical effects, the authors are planning further studies in which they will modify the protocol in an attempt to find a way to keep HCV levels down for longer and in all patients.

Looking Back in Time 12 Billion Years With New Instruments on Herschel Space Observatory

An instrument package developed in part by the University of Colorado at Boulder for the $2.2 billion orbiting Herschel Space Observatory launched in May by the European Space Agency has provided one of the most detailed views yet of space up to 12 billion years back in time. The December images have revealed thousands of newly discovered galaxies in their early stages of formation, said CU-Boulder Associate Professor Jason Glenn, a co-investigator on the Spectral and Photometric Imaging Receiver, or SPIRE instrument, riding aboard Herschel. The new images are being analyzed as part of the Herschel Multi-tiered Extragalactic Survey, or HerMES, which involves more than 100 astronomers from six countries. Equipped with three cameras including SPIRE, the Herschel Space Observatory was launched in May 2009 from Europe's Spaceport in French Guiana. The spacecraft -- about one and one-half times the diameter of the Hubble Space Telescope -- is orbiting nearly 1 million miles from Earth. Herschel is the first space observatory to make high-resolution images at submillimeter wavelengths, which are longer than visible and infrared light waves and shorter than radio waves. SPIRE was designed to look for emissions from clouds and dust linked to star-forming regions in the Milky Way and beyond, said Glenn. The most recent observations were made in the constellation Ursa Major, which includes the Big Dipper.

Pancreas Alpha-Cells Can Convert to Insulin-Producing Beta-Cells

In a mouse model, scientists have discovered that alpha-cells in the pancreas, which do not produce insulin, can convert into insulin-producing beta-cells, advancing the prospect of regenerating beta-cells as a cure for type 1 diabetes. The research team, led by senior author Dr. Pedro L. Herrera of the University of Geneva, demonstrated that beta-cells will spontaneously regenerate after near-total beta-cell destruction in mice and the majority of the regenerated beta-cells are derived from alpha-cells that had been reprogrammed, or converted, into beta-cells. Using a unique model of diabetes in mice, in which nearly all of the beta-cells are rapidly destroyed, the researchers found that if the mice were maintained on insulin therapy, beta-cells were slowly and spontaneously restored, eventually eliminating the need for insulin replacement. Alpha-cells normally reside alongside beta-cells in the pancreas and secrete a hormone called glucagon, which works in opposition to insulin to regulate the levels of sugar in the blood. Alpha-cells are not attacked by the autoimmune processes that destroy beta-cells and cause type 1 diabetes. Dr. Andrew Rakeman, the Juvenile Diabetes Research Foundation (JDRF) Program Manager in Beta-Cell Therapies and who was not involved in the research, said that the breakthrough in Dr. Herrera's work is the demonstration that alpha-to-beta-cell reprogramming can be a natural, spontaneous process. "If we can understand the signals that are triggering this conversion, it will open a whole new potential strategy for regenerating beta-cells in people with type 1 diabetes," he said. "It appears that the body can restore beta-cell function either through reprogramming alpha-cells to become beta-cells or, as previously shown by others, by increasing growth of existing beta cells. This path may be particularly useful in individuals who have had the disease for a long time and have no, or very few, remaining beta cells." Interestingly, the researchers pointed out that the critical factor in sparking the alpha-to-beta-cell reprogramming was removing (or ablating) nearly all the original insulin-producing cells in the mice. In mice where the loss of beta cells was more modest, the researchers either found no evidence of beta cell regeneration (when only half the cells were destroyed) or less alpha cell reprogramming (when less than 95 percent of cells were destroyed). "The amount of beta-cell destruction thus appears to determine whether regeneration occurs. Moreover, it influences the degree of cell plasticity and regenerative resources of the pancreas in adult organisms," said Dr. Herrera. This work was published online on April 4, 2010 in Nature. The image shows three lightly stained islets of Langerhans.

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