Science (August 15, 2011)
new way of dealing with the ignition uses molecules called polymers to wipe the remnants of damaged cells before the immune system becomes overly active, researchers from Duke University Medical Center reports. This discovery, published Aug. 15 in the magazine
Proceedings of the National Academy of Sciences, offers a promising new approach to the treatment of inflammatory autoimmune diseases such as lupus and multiple sclerosis, which are marked by overactive immune response. Depending on the disease, cells that were damaged disk or perpetuate immune response, said Bruce A. Sullenger, Ph.D., Director, Duke Translational Research Institute and lead author of the study. We showed that we can prevent this process. Sullenger said that the idea of a new approach follows from earlier findings of scientists Prince and others dying, and diseased cells shedding nucleic acids - the building blocks of life, including DNA and RNA - which then turn to high levels. While DNA and RNA within the cell regulate important functions such as growth and lasix 120 mg division, outside the cells in the blood, these nucleic acids are powerful signals to the immune system that something is amiss. After activation of the immune system begins to attack the fight that cause cell damage, regardless of infection or toxic substances. Under normal circumstances, this inflammatory reaction eventually restores order. In some cases, however, the inflammatory reaction is stable and out of control, leading to tissue damage and causes symptoms such as fever and pain. Chronic inflammation has been involved in lupus, multiple sclerosis, obesity, psoriasis, irritable bowel syndrome, arthritis and many other diseases. The Duke scientists working to break this cycle, focusing on a set of molecules called nucleic acid binding polymers that have been designed to penetrate the nucleic acid inside the cells and deactivate specific immune triggers. Then we had a "Eureka moment," said Sullenger. Because inflammatory nucleic acids outside cells, while DNA and RNA function in cells, we realized that polymers can communicate with the outside of nucleic acids without disrupting the intracellular function of DNA and RNA. It was a simple mop-up approach, and it worked as planned, in experiments on mice: We could use polymers as molecular scavengers - sponges, to walk and absorb and neutralize inflammatory nucleic acids, so that the immune system does not recognize and keep overdrive inflammation, Sullenger said. David S. Pisetskyy, MD, Ph.D., Duke rheumatologist and co-author, said anti-inflammatory approach has many potential applications, not only for autoimmune disorders, but also for acute tissue damage severe bacterial and viral infections, bruises and injuries . One option is to assess the impact of polymers include acute events such as trauma, when it may be easier to measure the presence of nucleic acids in the blood and the effect of polymer binding Pisetskyy, adding that long-term safety of new anti-inflammatory approach in humans remains unknown. Sullenger said patents were filed for the opening and the team moves forward in developing treatments. At some level, we opened this huge box features, and now we have to figure out which way to go, he said. In addition to the Sullenger and Pisetskyy, study co-authors include: Jaewoo Lee, Jang Wook Sohn; Ying Chang and Kam W. Leong. Research partially funded by the National Heart, Lung and Blood. The researchers reported no conflicts of interest.

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and Google +1: Other Bookmark and collaboration: History Source: above story with materials provided. Note: materials may be edited for content and length. For more information, please contact the source listed above. Journal Links Jaewoo Lee
Chan Wook Son,
Ying Zhang,
Kam W. Leong, David Pisetskyy
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, and Bruce A. Sullenger. Nucleic acid binding polymers as anti-inflammatory agent. PNAS, August 15, 2011 DOI:
Warning: This article is not intended for medical advice, diagnosis or treatment. The views expressed here do not necessarily reflect the views of science and its employees. .

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