307 University Boulevard Medical Science Building 3030 Department of Physiology Mobile, AL 36688

Phone 251-460-6838 Fax 251-460-6967 E-mail amd304@jaguar1.usouthal.edu

Amanda Davis

Education	1997-2000 Auburn University Auburn, AL 2000-2002 Southern Union State Community College Opelika, AL Associate of Science 2002 - 2005 University of South Alabama Mobile, AL Bachelor of Science § Major: Biology § Minor: Chemistry 2005- Present University of South Alabama Mobile, AL Graduate Student College of Medicine Basic Medical Science PhD Program § Department of Physiology
Professional experience	May- August 2005 University of South Alabama College of Medicine Mobile, AL Laboratory Technician Microbiology Helicobacter pylori
Publications and presentations	Articles 1. Philipp S, Yang XM, Davis AM, Downey JM, Cohen, MV. Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade. Cardiovascular Research 2006. 70:308-14 2. Downey JM, Davis AM, Cohen MV. Signaling pathways in ischemic preconditioning. Heart Failure Reviews. 2007. 12: 181-188 Abstracts 1. Davis AM, Cohen MV, Downey JM. Brief Exposure to Intracoronary Bradykinin at Reperfusion Limits Infarct Size in Isolated Rabbit Hearts by a Mechanism That Involves Both Free Radical Production and PKC. USA College of Medicine Research Forum. University of South Alabama. Mobile, AL. October 19 2007. 2. Yang XM, Davis A, Downey JM, Cohen MV. PMA administered just before reperfusion salvages ischemic myocardium by an adenosine A2b-dependent mechanism. Journal of Molecular and Cellular Cardiology. 40 (2006):869. Poster Presentations 1. Davis AM, Cohen MV, Downey JM. Brief Exposure to Intracoronary Bradykinin at Reperfusion Limits Infarct Size in Isolated Rabbit Hearts by a Mechanism That Involves Both Free Radical Production and PKC. USA College of Medicine Research Forum. University of South Alabama. Mobile, AL. October 19 2007.
Professional memberships	American Heart Association 2006-present American Physiological Society 2006-present American Society for Microbiology 2005-present American Association for the Advancement of Science 2002-present
Leadership experience	University of South Alabama Basic Medical Sciences Student Organization Class representative 2005-2006 Departmental representative 2006-2007 Vice President 2007-2008
Awards received	Phi Kappa Delta Honor Society Membership 2006-present (invitation only)
Research Interests	Myocardial damage incurred during coronary thrombosis (blockage of coronary artery) is due to decreased flow of blood, termed ischemia, which results in a lack of nutrition to the tissue. Prolonged lack of nutrition leads to tissue death, termed infarction. The ultimate goal when treating myocardial infarction (MI) is to return blood flow to the occluded area as soon as possible so as to salvage as much of the affected tissue as possible. Finding a way to render the heart resistant to ischemia and or to reduce reperfusion injury could further decrease cell death related to MI. In 1986 a way to render the myocardium less susceptible to ischemia-induced infarction was found. Protection of the myocardium was produced by subjecting a canine heart to several brief periods of ischemia prior to the extended period of ischemia. Preconditioning the myocardium with ischemia resulted in infarct sizes that were approximately 25% of those observed in control hearts that had not been preconditioned. In 2000, an overview of preconditioning’s mechanism was proposed. The hypothesis was that receptor stimulation led to the opening of mitochondrial ATP sensitive potassium channels (mitoKATP), causing free radicals to be made by the mitochondria. This pathway became known as the trigger phase. The ROS produced during the trigger phase then somehow activate protein kinase C (PKC) which leads to protection of the myocardium. In 2002, it was shown that brief cycles of ischemia/reperfusion during early reperfusion, termed post-conditioning, reduced infarct size in dog hearts as much as did ischemic preconditioning. Subsequent findings showed that some parts of the signaling pathway involved were similar to those in ischemic preconditioning. Several agents were shown to have the ability to protect the myocardium when given at reperfusion. These agents included insulin, AMP579, an adenosine A1/A 2 agonist, transforming growth factor beta-1 (TGF-β1), urocortin, cardiotrophin-1, CGX1051, a peptide derived from Conus snail venom, NECA, bradykinin, and erythropoietin. Post-conditioning and substances that confer protection to the myocardium when administered at reperfusion, such as bradykinin and NECA, could be important in treating MI. My research looks at protection provided by bradykinin administered at reperfusion and the signal transduction pathway that is triggered by bradykinin. I hypothesize that the signaling pathway of this pharmacological post-conditioning is the same as the signal pathway of bradykinin in classical preconditioning. Several elements of the bradykinin post-conditioning pathway have already been identified and indeed do seem to be the same as in preconditioning. In order to carry out my research, I am using a rabbit model. I employ both in situ and isolated organ models in which the end point is typically infarct size; additionally I obtain biopsies of the heart for use in protein studies.
Current Research	Previously others in the lab have shown PI3 kinase, eNOS, and ERK to be components in the signal transduction pathway activated by bradykinin given at reperfusion. I have identified several additional components of the signaling pathway including PKC and reactive oxygen species (ROS). I plan to continue studying this pathway and work to identify other components that are involved. I have also determined that the minimum time required for bradykinin to be present in the myocardium to protect is 15 minutes in the isolated rabbit heart.