A central goal of Dr. Salama's laboratory is to elucidate the mechanisms responsible for the initiation and termination of cardiac arrhythmias. To achieve this, they have developed the use of voltage-sensitive dyes and high temporal and spatial resolution optical techniques to map patterns of action potential (AP) propagation and repolarization. These novel methods are used to elucidate of the mechanisms that generate spatial heterogeneities of AP durations and the interplay between dispersion of repolarization (DOR) and anisotropic conduction velocities (CV). Animal models for cardiac arrhythmias include: acute ischemia in the guinea pig heart and 2 rabbit models of the long QT syndrome (LQTS). A number of mechanisms are being investigated as factors that promote arrhythmias in the LQTS: elevation of extracellular K+, sympathetic stimulation, and the role of spontaneous Ca2+ oscillation from the sarcoplasmic reticulum. Mapping spatial heterogeneities of intracellular Ca2+ transients in mammalian hearts using Ca2+ indicator dyes and imaging techniques. Once the normal heterogeneities of Ca2+ are determined, changes in Ca2+ transients will be analyzed in a wide range of physiological conditions to determined parameter that modulate Ca2+ transients. This laboratory has been at the forefront of the investigation of the role of sulfhydryl oxidation-reduction as a mechanisms to regulate Ca2+ release from the sarcoplasmic reticulum (SR). They are continuing this line of work in very exciting direction.
- BS, City College of New York, 1970
- MS, University of Pennsylvania, 1972
- PhD, University of Pennsylvania, 1977
- Postdoctoral, University of Pennsylvania, 1979
Education & Training
Henry BL, Gabris B, Li Q, Martin B, Giannini M, Parikh A, Patel D, Haney J, Schwartzman DS, Shroff SG, Salama G. Relaxin suppresses atrial fibrillation in aged rats by reversing fibrosis and upregulating Na(+) channels. Heart Rhythm. 2016; 13(4) PMID 26711798: 983-91.
Nemec J, Kim JJ, Salama G. The link between abnormal calcium handling and electrical instability in acquired long QT syndrome - Does calcium precipitate arrhythmic storms?. Prog Biophys Mol Biol. 2016; 120(1-3): 210-21.
Kim JJ, Nemec J, Li Q, Salama G. Synchronous systolic subcellular Ca2+-elevations underlie ventricular arrhythmia in drug-induced long QT type 2. Circ Arrhythm Electrophysiol. 2015; 8(3): 703-12.
Kim JJ, Yang L, Lin B, Zhu X, Sun B, Kaplan AD, Bett GC, Rasmusson RL, London B, Salama G. Mechanism of automaticity in cardiomyocytes derived from human induced pluripotent stem cells. J Mol Cell Cardiol. 2015; 81 (Apr): 81-93.
Tanha M, Chakraborty SK, Gabris B, Waggoner AS, Salama G, Yaron D. Computational and experimental characterization of a fluorescent dye for detection of potassium ion concentration. J Phys Chem A. 2014; 118(42): 9837-43.
Tchao J, Kim JJ, Lin B, Salama G, Lo CW, Yang L, Tobita K. Engineered Human Muscle Tissue from Skeletal Muscle Derived Stem Cells and Induced Pluripotent Stem Cell Derived Cardiac Cells. Int J Tissue Eng. 2013; Sep 28
Lu TY, Lin B, Kim J, Sullivan M, Tobita K, Salama G, Yang L. Repopulation of decellularized mouse heart with human induced pluripotent stem cell-derived cardiovascular progenitor cells. Nat Commun. 2013; 4(2307)
Parikh A, Patel D, McTiernan CF, Xiang W, Haney J, Yang L, Lin B, Kaplan AD, Bett GC, Rasmusson RL, Shroff SG, Schwartzman D, Salama G. Relaxin suppresses atrial fibrillation by reversing fibrosis and myocyte hypertrophy and increasing conduction velocity and sodium current in spontaneously hypertensive rat hearts. Circ Res. 2013; 113(3): 313-21.
Kim JJ, Nemec J, Papp R, Strongin R, Abramson JJ, Salama G. Bradycardia alters Ca(2+) dynamics enhancing dispersion of repolarization and arrhythmia risk. Am J Physiol Heart Circ Physiol. 2013; 304(6): H848-60.
