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PRODID:-//Virginia Tech//VT Calendar//EN
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DTSTAMP:20150319T150000Z
UID:1425679195048@events.msu.edu
CATEGORIES:Conferences / Seminars / Lectures
DTSTART:20150319T150000Z
DTEND:20150320T045900Z
SUMMARY:Physiology Seminar
DESCRIPTION:
 "The Role of Mitochondrial Dysfunction in Ischemia/Reperfusion 
 Injury" - Dr. Jason Bazil\n
 \n
 Ischemia/reperfusion 
 (I/R) injury is the most 
 significant cause of cell death resulting from 
 a heart attack or stroke. How tissues respond 
 to ischemia followed by reperfusion determines 
 the outcome of critical events ranging 
 from cardiopulmonary bypass surgery to hemorrhagic 
 shock. And the primary pathway initiating 
 cell death in high energy-demand tissues 
 such as the heart, brain, and kidney centers 
 on mitochondria. In all of these organs, an ischemic 
 insult directly affects cellular and 
 mitochondrial energetics, calcium handling, and 
 free radical homeostasis. The subsequent reperfusion 
 ultimately initiates apoptotic signaling 
 cascades through mitochondrial dependent 
 pathways triggered by calcium and reactive 
 oxygen species. These consequences underlie 
 certain clinical practices-for example, the use 
 of cold cardioplegia used to metabolically 
 arrest the heart prior to transplantation. Yet 
 we lack an understanding of the relevant metabolic 
 and signaling processes that is detailed 
 enough to explain experimental observations, 
 predict differential outcomes, and help 
 guide therapeutics. A systems approach, using 
 experiments to inform computational models and 
 models to interpret and design relevant experiments, 
 is necessary to expand our understanding 
 of the biochemistry and physiology that 
 underpin mitochondrial reperfusion injury. 
 Using this approach, investigation of mitochondrial 
 calcium fluxes and sequestration reveals 
 a novel mechanism responsible for the protective 
 effect of adenine nucleotides during mitochondrial 
 calcium loading. Furthermore, systems 
 analysis identifies the mechanism by which 
 succinate accumulates in ischemic tissue 
 and leads to the burst of free radicals observed 
 during reperfusion.\n\n
 Price: free\n
 Sponsor: Dept. of Physiology\n
 Sponsor's Homepage: http://www.psl.msu.edu/\n
 Contact name: Chris Shaltry\n
 Contact phone: 884-5034\n
 Contact email: shaltryc@cns.msu.edu\n
 for more info visit the web at:\n 
 http://www.psl.msu.edu/\n
LOCATION:1425 Biomedical and Physical Sciences Bldg
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