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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Nathan Frederick Chiappa
PhD Proposal Presentation
Date: Monday, August 1st, 2016
Time: 1:00 PM
Location: Petit Institute Suddath Room (1128)
Committee Members:
Edward A. Botchwey, PhD (BME, Advisor)
Clinton H. Joiner, MD, PhD (Emory University School of Medicine)
Wilbur A. Lam, MD, PhD (BME)
Alfred H. Merrill, PhD (Chemistry and Biochemistry)
Mark P. Styczynski , PhD (ChBE)
Eberhard O. Voit, PhD (BME)
Evaluation of the Dysfunction of Sphingolipid Metabolism in Sickle Cell Disease Using Lipidomics and Computational Systems Biology
Sickle cell disease is a genetic disease affecting approximately 100,000 Americans. People with this disease experience a number of problems including chronic inflammation, organ damage, and painful vaso-occlusive crises. Research has identified several pathways involved in the disease pathology, though definitive cause and effect relationships have made development of therapies difficult. Recently, sphingolipids have been shown to play roles in many aspects of red blood cell biology. We have previously shown significant alterations in the levels of many sphingolipids in sickle red blood cells compared to normal red blood cells. However, what causes these differences and what the functional significance is remain unclear. The overall hypothesis of this proposed research is that changes in the activities of sphingolipid-metabolizing enzymes in sickle red blood cells disrupt sphingolipid levels both at steady-state and in response to hypoxia. First, we will quantify differences in the activities of sphingolipid-metabolizing enzymes in normal and sickle red blood cells. Second, we will evaluate the differences in the response of sphingolipid levels in sickle and normal red blood cells to changes in oxygen levels. Finally, we will use computational modeling to predict targets for counteracting the changes in sphingolipids in sickle cell disease.
