CHED 948 |
| Cigarette smoking accounts for the development of about 80% of the lung cancer cases. Other than correlated lung cancer development in smokers, significant inflammation has also been noted. Prior research on human lung fibroblasts has shown a significant inflammatory response to cigarette smoke toxicants. This lab has previously focused on prostaglandin mediated inflammation and toxicity in cells exposed to cigarette smoke. Previous research however, has shown that there are multiple pathways that seem to be operating in tandem with the prostaglandin pathway. In this study we have monitored the effects of mainstream toxicants on the nitric oxide pathway and specifically looked at the stimulation and inhibition of the endothelial nitric oxide synthase (eNOS) system. More specifically, this research targets further understanding of eNOS modulation by the AKT signal transduction pathway after fibroblast exposure to cigarette smoke extracts. |
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Undergraduate Research Poster Session: Biochemistry
2:00 PM-4:00 PM, Monday, March 26, 2007 Hyatt Regency Chicago -- Riverside Center, Poster
Division of Chemical Education |