Ischemic events of even a very short duration are not tolerated Ill in humans. The human cost of ischemia, when looked at as combined cardiovascular disease, dwarfs all other causes of death in the United States. Annually, CVD kills as many people in the US as does cancer, chronic lower respiratory disease, accidents, and diabetes mellitus combined. In 2005 (the latest year for which final statistics are available), CVD was responsible for 864,480 deaths or 35.3 percent of total deaths for the year. In my study, I have used the nematode Caenorhabditis elegans to determine genetic and environmental modulators of oxygen deprivation a key component of ischemia. I have found that animals with mutations in insulin like signaling pathways, neuronal function, electron transport chain components, germline function, and animals that are preconditioned by being raised on a diet of E. coli HT115 bacteria at 25°C have an enhanced ability to survive long-term (>72 hours) anoxia (<.005 kPa O2) at 20°C. The enhanced anoxia survival phenotype partially correlates with increased levels of carbohydrate stores in the nematodes. Suppression of this enhanced anoxia survival phenotype is possible by altering expression of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase, the FOXO transcription factor DAF-16, and 5’-AMP kinase.
Identifer | oai:union.ndltd.org:unt.edu/info:ark/67531/metadc103350 |
Date | 08 1900 |
Creators | LaRue, Bobby Lee, Jr. |
Contributors | Padilla, Pamela A., Benjamin, Robert C., Dzialowski, Edward M. (Edward Michael), Hynds, DiAnna, Schwark, Harris D. |
Publisher | University of North Texas |
Source Sets | University of North Texas |
Language | English |
Detected Language | English |
Type | Thesis or Dissertation |
Format | Text |
Rights | Public, LaRue, Bobby Lee, Jr., Copyright, Copyright is held by the author, unless otherwise noted. All rights |
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