Investigator, BC Children’s Hospital
Professor of Biomedical Physiology and Kinesiology, Simon Fraser University (SFU)
Canada Research Chair in Molecular Cardiac Physiology
Associate Member of Molecular Biology and Biochemistry, SFU
Adjunct Professor of Cellular and Physiological Sciences, University of British Columbia (UBC)
Adjunct Professor of Pathology and Laboratory Medicine, UBC
Adjunct Professor of Pharmaceutical Sciences, UBC
- PDF, Niigata Yakka Daigaku, Niigata, JP. 1980
- MSc, PhD, UCLA, Los Angeles, CA. 1979
- B.Ed, McGill University, Montréal, QC. 1970
- Myocardial excitation – contraction coupling: ontogeny and phylogeny
Although the neonate heart is completely responsible for delivering blood to the body, it is still immature in many respects. This is particularly true of the cardiac contractile system and its regulatory mechanisms. The strength of cardiac contraction is determined by the amount of calcium (Ca2+) delivered to the contractile element. Thus the levels of Ca2+ inside each cell (or cardiomyocyte) rise and fall each beat, and peak value can vary substantially in response to physiological needs and/or hormones such as adrenaline. How this is achieved in the neonate heart, although poorly understood, is quite different from the adult heart. This has clinical implications; for example, in children with congenital heart disease (present in 1% of live births), the heart must often be arrested during surgical correction. However, these techniques are largely derived from our understanding of the adult heart. We hope to improve the success rate of surgical correction, and better understand “normal” heart development and the deviations that occur in congenital heart diseases.
Molecular mechanisms of electrogenesis in the neonate heart
CIHR funded project focusing on the molecular and cellular mechansms of junctional ectopic tachycardia (JET). JET is an arrhythmia that occurs with relatively high frequency in neonates after open heart surgery. The etiology of JET is poorly understood and as a consequence existing treatments are non-specific and often lack efficacy.
Ontogeny of myocardial excitation- contraction coupling mechanisms
CIHR funded project with the objectives of determining the molecular and cellular changes in cardiomyocytes from the earliest stages post-partum until adulthood with an eye to understanding certain congenital heart diseases.
Regulation of cardiac myofilament sensitivity to calcium
Heart and Stroke Foundation funded project that addresses the structure function relationship of troponin C and its ability to bind Ca2+, a primary determinant of cardiac contractility. The research involves making mutations of troponin C and understanding how the structural changes that result affect Ca2+ binding to the regulatory domain of the molecule. Information from this project will be directed to the development of a novel class of Ca2+-senstizing drugs which may be used to treat heart failure.