Complement is activated following ischemia/reperfusion and periods of oxidative stress. My research team of post-doctoral fellows, research assistant(s), and myself investigate the molecular mechanisms involved in complement activation at the cellular level, particularly the role of endothelial cells. We have shown that normal endothelial cells activate complement following oxidative stress. The mechanism of complement-induced tissue injury is not completely characterized. Another focus of our research investigates the mechanism of complement-induced tissue injury and the specific contributions of the various biologically active complement components involved, namely: C5a, C3b, iC3b, and C5b-9. Additionally, the specific pathways (i.e., classical, lectin, and alternative) involved in complement activation are investigated by use of genetically altered mice, as well as developing novel specific inhibitors to the key components.Our laboratory uses an integrated approach to investigate these research areas. We use molecular, biochemical, pharmacological, cellular, organ, and whole animal models to investigate the mechanisms involved. Using this approach, we can quickly ascertain the mechanisms involved, identify potential therapeutic targets, and validate the in vitro findings in animal models. Current projects in the laboratory investigate acute hyperglycemia, coagulation and vascular function and the interaction of complement in these clinically relevant conditions.I am currently wrapping up my studies to take early retirement for health reasons. My wife and I will relocate to the Coral Coast of Fiji to take up local missionary missions to help those in the local villages and relax for retirement.Specialties: Skilled cardiovascular physiologist that is able to work from DNA to the whole animal. Ability to translate bench work to clinic. Experienced with startup biotech companies and assisting with the movement from preclinical to clinical trials.When not in Fiji, i am busy doing research on honeybees in Ohio.