José Jalife, M.D., completed his M.D. at the Universidad Nacional Autónoma de México in 1972. After clinical training in Spain, he returned to Mexico to conduct research in cardiovascular pharmacology and physiology at the Universidad Nacional and the National Institute of Cardiology. In 1973, he moved to the United States to work as a postdoctoral fellow the Upstate Medical Center in Syracuse, NY, and the Masonic Medical Research Laboratory in Utica, NY. He joined the Department of Pharmacology, Upstate Medical University, as a member of the faculty in 1980 and became its Chairman in 1988. In 2008, he was recruited by the University of Michigan to his present position as an endowed professor and co-director of the Center for Arrhythmia Research.
Dr. Jalife is a leader in his field of research, which focuses on using sophisticated mathematical and biophysical concepts to increase understanding of the mechanisms of life-threatening cardiac arrhythmias, from the molecule to the bedside. He has published more than 258 original papers and review articles, and has edited/authored thirteen books, including the internationally acclaimed Cardiac Electrophysiology: From Cell to Bedside, now in its fifth edition. Dr. Jalife has been a member of the Research Committee A of NHLBI, and has served on the Cardiology Advisory Committee, as a member in the Cardiovascular Study Section, (CVA, 1997-2001) and the more recently established ESTA Study Section, as well as in various site visit committees and the Executive Committee of the Basic Science Council of AHA.
In 2001 Dr. Jalife was awarded the Distinguished Scientist Award of the American College of Cardiology. Other accolades include the Lucian Award for Research in Circulatory Diseases from McGill University, the President's Award for Research at SUNY Upstate Medical University, the Professor Pierre Rijlant Award from the Académie Royale de Médecine de Belgique in Brussels, Belgium, and the 2002 State University of New York Chancellor's Award for Excellence in Scholarship and Creative Activities. In 2008 Dr. Jalife was elected Vice-President of the Cardiac Electrophysiology Society.
My research is focused on bringing sophisticated mathematical and biophysical concepts to increase the understanding of the mechanisms of life-threatening cardiac arrhythmias, from the molecule to the bedside. We investigate the molecular mechanisms and nonlinear dynamics of heart rhythm and conduction disturbances including atrial and ventricular arrhythmias. The techniques that we employ in this endeavour include single myocyte patch clamp, single cell molecular imaging, high resolution laser scanning confocal microscopy, whole heart optical mapping and whole animal in vivo physiological monitoring. Recently we have started to explore the utility of using patient specific stem cells to gain insight into cardiac arrhythmia mechanisms on an individual basis.
High-rate pacing-induced atrial fibrillation effectively reveals properties of spontaneously occurring paroxysmal atrial fibrillation in humans. Calvo D, Atienza F, Jalife J, MartÌ_nez-Alzamora N, Bravo L, Almendral J, GonzÌÁlez-Torrecilla E, Arenal A, Bermejo J, FernÌÁndez-AvilÌ©s F, Berenfeld O. Europace. 2012 Jun 13
Simultaneous voltage and calcium mapping of genetically purified human induced pluripotent stem cell-derived cardiac myocyte monolayers. Lee P, Klos M, Bollensdorff C, Hou L, Ewart P, Kamp TJ, Zhang J, Bizy A, Guerrero-Serna G, Kohl P, Jalife J, Herron TJ. Circ Res. 2012 Jun 8;110(12):1556-63.
Dynamic reciprocity of sodium and potassium channel expression in a macromolecular complex controls cardiac excitability and arrhythmia. Milstein ML, Musa H, Balbuena DP, Anumonwo JM, Auerbach DS, Furspan PB, Hou L, Hu B, Schumacher SM, Vaidyanathan R, Martens JR, Jalife J. Proc Natl Acad Sci U S A. 2012 Apr 16.
Chloroquine terminates stretch-induced atrial fibrillation more effectively than flecainide in the sheep heart. Filgueiras-Rama D, Martins RP, Mironov S, Yamazaki M, Calvo CJ, Ennis SR, Bandaru K, Noujaim SF, Kalifa J, Berenfeld O, Jalife J. Circ Arrhythm Electrophysiol. 2012 Jun 1;5(3):561-70.
A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heart. Noujaim SF, Kaur K, Milstein M, Jones JM, Furspan P, Jiang D, Auerbach DS, Herron T, Meisler MH, Jalife J. FASEB J. 2012 Jan;26(1):63-72