Study has implications for prevention of brain damage after exposure
Later this fall, emergency-medicine physicians enter into what they call the "CO season" – a time when faulty furnaces and other mechanical mishaps lead to a spike in cases of carbon monoxide (CO) poisoning. CO poisoning is the leading cause of injury and death by poisoning worldwide, with about 40,000 people treated in the U.S. annually. Brain damage occurs – days to weeks later – in half of the patients with a serious case of CO poisoning.
The physiological causes of this delayed decline were not well understood until now. A team led by Stephen R. Thom, MD, PhD, Professor of Emergency Medicine and Chief of Hyperbaric Medicine, at the University of Pennsylvania School of Medicine, report this week online in the Proceedings of the National Academies of Sciences, that CO causes profound changes in myelin basic protein (MBP) – a major protein constituent of myelin, the protective sheath surrounding neurons. Using an animal model, they showed that the CO-induced changes in MBP set into motion an autoimmune response in which lymphocytes, triggered to eliminate altered MBP, continue to attack normal MBP.
Karen Kreeger | EurekAlert!
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Enzymes behave differently in a test tube compared with the molecular scrum of a living cell. Chemists from the University of Basel have now been able to simulate these confined natural conditions in artificial vesicles for the first time. As reported in the academic journal Small, the results are offering better insight into the development of nanoreactors and artificial organelles.
Enzymes behave differently in a test tube compared with the molecular scrum of a living cell. Chemists from the University of Basel have now been able to...
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