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Archive - Nov 7, 2012

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Stem Cells and Nanofibers Yield Promising Nerve Research

Every week in his clinic at the University of Michigan, neurologist Joseph Corey, M.D., Ph.D., treats patients whose nerves are dying or shrinking due to disease or injury. He sees the pain, the loss of ability, and the other effects that nerve-destroying conditions cause – and wishes he could give patients more effective treatments than what's available, or regenerate their nerves. Then he heads to his research lab at the VA Ann Arbor Healthcare System (VAAAHS), where his team is working toward that exact goal. In new research published in several recent papers, Dr. Corey and his colleagues from the U-M Medical School, VAAAHS, and the University of California, San Francisco (UCSF) report success in developing polymer nanofiber technologies for understanding how nerves form, why they don't reconnect after injury, and what can be done to prevent or slow damage. Using polymer nanofibers thinner than human hairs as scaffolds, researchers coaxed a particular type of brain cell to wrap around nanofibers that mimic the shape and size of nerves found in the body. They've even managed to encourage the process of myelination – the formation of a protective coating that guards larger nerve fibers from damage. They began to see multiple concentric layers of the protective substance called myelin start to form, just as they do in the body. Together with the laboratory team of their collaborator Dr. Jonah Chan at UCSF, the authors reported their findings in Nature Methods online on July 15, 2012. The research involves oligodendrocytes, which are the supporting actors to neurons -- the "stars" of the central nervous system. Without oligodendrocytes, central nervous system neurons can't effectively transmit the electrical signals that control everything from muscle movement to brain function.

New Drug Target Found for Cystic Fibrosis

Vancouver researchers have discovered the cellular pathway that causes lung-damaging inflammation in cystic fibrosis (CF), and determined that reducing the pathway’s activity also decreases inflammation. The finding offers a potential new drug target for treating CF lung disease, which is a major cause of illness and death for people with CF. “Developing new drugs that target lung inflammation would be a big step forward,” says Dr. Stuart Turvey, who led the research. Dr. Turvey is the director of clinical research and senior clinician scientist at the Child & Family Research Institute and a pediatric immunologist at BC Children’s Hospital. He is an associate professor in the Department of Pediatrics at the University of British Columbia. The research was published online on October 26, 2012 in the Journal of Immunology. For the study, researchers compared the immune response of normal lung cells with that of CF lung cells after exposing both types of cells to bacteria in the lab. In healthy cells, exposure to bacteria triggers the cell to secrete special molecules that attract immune cells to fight the infection. In CF lung cells, the researchers discovered that a series of molecular events called the unfolded protein response is more highly activated. It causes the CF lung cells to secrete more molecules that attract an excessive amount of immune cells, which leads to increased inflammation. They also found that treating the CF cells with a special chemical normalized the unfolded protein response and stabilized the cells’ immune response. CF is the most common genetic disease affecting young Canadians. One in every 3,600 children born in Canada has CF. There is no cure.

High SFRP4 Protein Reveals Diabetes Risk Many Years in Advance

When a patient is diagnosed with type 2 diabetes, the disease has usually already progressed over several years and damage to areas such as blood vessels and eyes has already taken place. To find a test that indicates who is at risk at an early stage would be valuable, as it would enable preventive treatment to be put in place. Researchers at Lund University in Sweden, together with colleagues, have now identified a promising candidate for a test of this kind. The findings were published in the November 7, 2012 issue of Cell Metabolism. "We have shown that individuals who have above-average levels of a protein called SFRP4 in the blood are five times more likely to develop diabetes in the next few years than those with below-average levels", says Dr. Anders Rosengren, a researcher at the Lund University Diabetes Centre (LUDC), who has led the work on the risk marker. It is the first time a link has been established between the protein SFRP4, which plays a role in inflammatory processes in the body, and the risk of type 2 diabetes. Studies at the LUDC, in which donated insulin-producing beta cells from diabetic individuals and non-diabetic individuals have been compared, show that cells from diabetics have significantly higher levels of the protein. It is also the first time the link between inflammation in beta cells and diabetes has been proven. "The theory has been that low-grade chronic inflammation weakens the beta cells so that they are no longer able to secrete sufficient insulin. There are no doubt multiple reasons for the weakness, but the SFRP4 protein is one of them", says Dr. Taman Mahdi, main author of the study and one of the researchers in Dr. Rosengren's group. The level of the protein SFRP4 in the blood of non-diabetics was measured three times at intervals of three years.