Principal Research Scientist – Experimental Cardiology 

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Areas Of Interest

  • Cardiac Excitation-Contraction Coupling
  • Cardiac & Neuronal Cellular Electrophysiology
  • Molecular Gene Therapy Development
  • Differentiation of Human iPS cells for Disease/Mutation Models and Drug Development

Professional Membership

  • Biophysical Society
  • Heart Rhythm Society
  • American Heart Association
  • American Physiological Society

Research Statement

My most recent research projects have focused on investigating the aberrant physiology of cardiac myocytes due to dysregulated calcium handling, particularly in relation to its propensity to cause arrhythmias (e.g., atrial fibrillation).  Abnormal calcium handling in cardiac myocytes (heart muscle cells) can arise consequent to intrinsic defect(s) in excitation-contraction coupling (cellular basis for the electrical-mechanical transduction of the heart beat) and/or via defects in extrinsic elements that modulate myocyte extrinsically, such as the autonomic nervous system (‘fight-or-flight’ and ‘rest-and-digest’ responses) and the renin-angiotensin-aldosterone system (controls blood pressure and electrolyte balance).  Problems in extrinsic calcium regulation can cause problems in intrinsic calcium regulation, and vice versa, and is often the root cause of cardiac arrhythmias, cardiomyopathies and heart failure.  Both intrinsic and extrinsic mediation of aberrant calcium handling in myocytes is ultimately the result of defects at the molecular level, which can be due to mutations in genes (molecular ‘architects’) that then produce faulty proteins (molecular ‘work-horses’), or consequent changes invoked by ‘stresses’ (e.g., oxidative stress, chronic illness, toxins, etc.).