Simon M. Harrison, PhD
Simon Harrison, PhD, carried out his doctoral work in the Department of Physiology at Glasgow University working with Dr. David Miller. His research focused on the mechanisms of relaxation of ventricular muscle. He was awarded his Doctor of Philosophy (PhD) degree in July of 1986, and then moved to the University of California to further his research interests. He was awarded three consecutive American Heart Association Fellowships (1986-1989) working in the laboratory of Professor Donald Bers. In 1989, he returned to the United Kingdom to take up a post-doctoral position at the University of Leeds, collaborating with Professor Mark Boyett. In 1992, he was awarded a prestigious Wellcome Trust Fellowship and at its end, a Lectureship in the Department of Physiology at the University of Leeds. In 1999, he was promoted to Senior Lecturer and continued his research into mechanisms of cardiac excitation-contraction coupling in health and various disease states. His work has been supported by research grants from the British Heart Foundation, the Medical Research Council, The British Journal of Anesthesia, and the Welcome Trust, and he has worked with and trained many graduate students and post-doctoral fellows. He has presented his work at meetings around the world and published 55 full, peer-reviewed research papers in international journals. Dr Harrison also undertook a variety of administrative roles during his tenure at the University of Leeds. These included being Deputy Head of School, Program Leader, Examinations Officer, Post-Graduate Tutor, and Faculty Director of Student Education with oversight of all undergraduate and postgraduate programs in the Faculty of Biological Sciences while simultaneously building a reputation of excellence in student education and support. After 24 years at Leeds, he joined Ross University School of Medicine in 2015 as a Professor in the Department of Physiology.
- 1982–1985 - Postgraduate Student, Glasgow University, UK. Supervisor: David J. Miller. PhD Thesis entitled "The involvement of mitochondria in the intracellular control of contraction in cardiac muscle.”
- 1979–1982 - BSc Leeds University. Graduated with IIi Honours in Physiology.
- 1972–1979 - Royal Grammar School, Guildford, Surrey, UK 7 'O' levels and 3 'A' levels.
Research grants awarded (2005–date):
- *2007–2010 - The British Heart Foundation Project grant, £140,958
Collaborators: Hopkins and Steele
Mechanisms underlying Ca2+ dysregulation in experimental sepsis
- =2007–2009 - Association of Anaesthetists grant, £14,800
Changes in gene expression in models of sepsis.
- *2005–2006 - FBS research support fund, £5000
Array studies of physiological and pathological hypertrophy
- *2004-2007- White Rose Consortium Studentship, £38,000.
Collaborator: Prof P Hopkins
Mechanisms of sepsis in ventricular muscle.
- *2003-2006 - The British Heart Foundation Project grant, PG/02/151, £123,996
Mechanisms underlying the inhibitory effects of volatile anaesthetics on
Ca2+ handling and contractility in ventricular muscle.
>1.8 M GBP (total research grant income)
(* denotes as PI; = denotes as a co-investigator)
- The Physiological Society
- Fellow of the Higher Education Academy (UK)
Dr. Harrison’s research focussed predominately on the regulation of surface membrane and sarcoplasmic reticulum (SR) membrane channels and receptors and how these are affected in health (e.g., in voluntary exercise) as well as in a variety of disease states including experimental sepsis and hypertrophy. Another strand of his research related to the impact of volatile anaesthetic agents on the regulation of Ca2+ and contractility as a result of effects on surface membrane channels, ion exchangers, and SR membrane targets. He has regularly published his research in internationally recognised journals (24 papers since 2001) and maintained a continuous record of research funding from 1987 to 2010. In August of 2010, he was appointed to the role of Faculty Director of Undergraduate Student Education (FDUSE) at the University of Leeds, resulting in a change in his career focus away from bench research and more toward academic administration, enhancing the student’s academic experience, and student support and mentoring.
- Ansell, L., Hardy, M.E.L., Duke, A., Steele, D.S. & Harrison, S.M. Histones H3 and H4 induce Ca2+ overload and necrosis in rat ventricular myocytes (in preparation for submission).
- Duncan, D.J., Yank, Z., Hopkins, P.M., Steele, D.S. and Harrison, S.M. (2010). TNF-α and IL-1β increase Ca2+ leak from the sarcoplasmic reticulum and susceptibility to arrhythmia in rat ventricular myocytes. Cell Calcium 47, 378-386.
- Stones R, Billeter, R., Zhang, H, Harrison, S.M. & White, E. (2009). The role of transient outward K+ current in electrical remodelling induced by voluntary exercise in female rat hearts. Basic Research in Cardiology 104, 643-652.
- Zhang, H., Tao, T., Kharche, S., Harrision, S.M. (2009) Modelling changes in transmural propagation and susceptibility to arrhythmia induced by volatile anaesthetics in ventricular tissue. Journal of Theoretical Biology 257, 279-291.
- Stones R, Natali, A., Billeter, R., Harrison, S.M. & White, E. (2008). Voluntary exercise-induced changes in β2-adrenoceptor signalling in rat ventricular myocytes. Experimental Physiology 93, 1065-1075.
- Stones R, Calaghan, S.C., Billeter, R., Harrison, S.M. & White, E. (2007). Transmural variations in gene expression of stretch-modulated proteins in the rat left ventricle. Pflugers Archiv 454, 545-549.
- Fowler, M.R., Naz, J.R, Graham, M.D. Orchard, C.H. & Harrison, S.M. (2007). Age and hypertrophy alter the contribution of sarcoplasmic reticulum and Na+/Ca2+ exchange to Ca2+ removal in rat left ventricular myocytes. Journal of Molecular and Cellular Cardiology 42, 582-589.
- Duncan, D.J., Hopkins, P.M. and Harrison, S.M. (2007). Negative inotropic effects of tumour necrosis factor-α and interleukin-1β are ameliorated by alfentanil in rat ventricular myocytes. British Journal of Pharmacology 150, 720-726.
- Fowler, M.R., Orchard, C.H. & Harrison, S.M. (2007). Cellular distribution of calcium current is unaltered during compensated hypertrophy in the spontaneously hypertensive rat. Pflugers Archiv. 453, 463-469.
- Graham, M., Hopkins, P.M. and Harrison, S.M. (2006). Antagonistic actions of halothane and sevoflurane on spontaneous Ca2+ release in rat ventricular myocytes. Anesthesiology, 105, 58-64.
- Bru-Mercier, G., Hopkins, P.M. & Harrison, S.M. (2005). Halothane and sevoflurane inhibit Na/Ca exchange current in rat ventricular myocytes. British Journal of Anaesthesia 95, 305-309.
- Stones R, Billeter, R., Harrison, S.M. & White, E. (2005). Heterogenic contractile response of rat left ventricular myocytes to β1-adrenoreceptor stimulation. European Journal of Pharmacology 512, 117-120.
- Fowler, M.R., Naz, J.R, Graham, M.D., Bru-Mercier, G., Harrison, S.M. & Orchard, C.H. (2005). Decreased Ca extrusion via Na/Ca exchange in epicardial left ventricular myocytes during compensated hypertrophy. American Journal of Physiology Heart; 288 H2431-H2438.
- Graham, M.D., Bru-Mercier, G., Hopkins, P.M. Harrison, S.M. (2005). Transient and sustained changes in myofilament Ca2+ sensitivity contribute to the inotropic effects of sevoflurane. British Journal of Anaesthesia 94, 279-286.
- Yang, Z., Harrison, S.M. & Steele, D.S. (2005). ATP-dependent effects of halothane on SR Ca2+ regulation in permeabilized atrial myocytes. Cardiovascular Research 65, 167-176.