Our lab studies aspects of molecular and cellular pharmacology related to multiple disease processes. Our goals focus on investigating mechanisms of cellular communication and cellular proliferation. Studies have included aspects of blood cell proliferation, cancer cell proliferation, bacterial cell proliferation, endothelial cell proliferation, vascular smooth muscle cell proliferation, and cardiomyocyte communication.
Medical Education Research
Undergraduate medical education is continually changing to meet the demands and needs of our future health care practitioners. We are interested in developing and assessing methods of disseminating medical knowledge in order to identify the best practices for educating our future health care providers. Currently we are investigating the impact of using medical simulators on student learning in both the didactic and clinical components of medical training.
Moffit, JA, MK Henry, KC Welliver, AJ Jepson, and ER Garnett. Hindlimb unloading results in increased predisposition to cardia arrhythmias and alters left ventricular connexin43 expression. Am J Physiol Regul Integr Comp Physiol 304: R362-R373, 2013
Wilson, WA, MK Henry G Ewing, J Rehmann, CA Canby, JT Gray and EP Finnerty. A pre-matriculation intervention to improve the adjustment of students to medical school. Teaching & Learning in Medicine; 23(3): 256-262., 2011
Hamadmad S, Henry MK, and Hohl RJ. Erythropoietin receptor signal transduction requires protein geranylgeranylation. J Pharmacol Exp Ther; 316(1):403-409., 2006
Chakravarti P., Henry MK, Quelle FQ. Prolactin and heregulin override DNA damage-induced growth arrest and promote phosphatidylinositol-3 kinase-dependent proliferation in breast cancer cells. Int J Oncol; 26: 509-514., 2005
Henry MK, Nimbalkar D, Hohl RJ, and Quelle FW. Cytokine induced phosphoinositide 3-kinase activity promotes Cdk2 activation in factor-dependent hematopoietic cells. Exp Cell Res; 299: 257-266, 2004
Nimbalkar D, Henry MK, and Quelle FW. Cytokine activation of phosphoinositide 3-kinase sensitizes hematopoietic cells to cisplatin-induced death. Cancer Res; 63: 1034-1039. , 2003
Eapen AK, Henry MK, Quelle DE, and Quelle FW. DNA damage-induced G1 arrest in hematopoietic cells is overridden following PI-3 kinase dependent activation of cdk2. Mol Cell Biol; 21: 6113-6121. , 2001
Henry MK, Lynch JT, and Quelle FW. DNA damage-induced cell cycle arrest of hematopoietic cells is overridden by activation of the PI-3Kinase/Akt signaling pathway. Blood; 98: 834-841., 2001
Henry MK, Unsworth BR, Sychev V, Guryeva TS, Dadasheva OA, Piert SJ, Lagel KE, Dubrovin LC, Jahns GC, Boda K, Sabo V, Samet MM, and Lelkes PI. Investigator: Lelkes PI. Launch conditions might affect the formation of blood vessels in the quail chorioallantoic membrane. Folia Vet; 42 Suppl: S25-31. , 1998