100th Anniversary Seminar Series

Friday 13th, January, 2012

‘Physical Inactivity: The Biggest Public Health Problem of the 21st Century’

Time: 11:00 a.m.

Place: Room 2/36, Strathcona Anatomy and Dentistry Building, 3640 University Street

Guest Speaker: Steven Blair

Recipient, Bloomberg-Manulife Prize for Promotion of Active Health
Professor, Departments of Exercise Science and Epidemiology/Biostatistics,
University of South Carolina

Friday 17th, February, 2012

 "The remarkable dexterity of the human hand: how does the brain do it?"

Time: 12:30-1:30 pm

Location: Room M1, Strathcona Anatomy & Dentistry Bldg, 3640 University St.

Guest Speaker: Randy Flanagan, Ph.D., Queen’s University

Background: Dr. Flanagan completed with M.A. and Ph.D. in the Department of Kinesiology & Physical Education (1986) and the Department of Psychology at McGill University, respectively.

Abstract: Although scientists have invented chess computer programs that can rival grand-masters, we have yet to design a robot that can manipulate a chess piece with anything like the dexterity of a 5-year old child. The remarkable manipulative skill of the human hand is not the result of rapid sensorimotor processes, nor of fast or powerful effector mechanisms. Rather, the secret lies in the way manual tasks are organized and controlled by the nervous system. In this talk I will discuss what we have learned about the sensorimotor control processes that support dexterous object manipulation.

Friday 30th, March, 2012

"Cardiac Contraction and Sudden Cardiac Death: The Role of Troponin"

Time: 11:00 am

Location: Room M1, Strathcona Anatomy & Dentistry Bldg, 3640 University St.

Guest Speaker:  Professor Glen Tibbits,  Canada Research Chair in Cardiac Molecular Physiology, Simon Fraser University

Abstract:  Troponin which is located on the thin filament of the cardiac contractile apparatus is a critical initiator of the contractile process. This protein is made up of three critical components: troponin C (cTnC), troponin I (cTnI) and troponin T (cTnT) which act in a concerted manner to activate cardiac contraction in response to its physiological trigger rising cytosolic Ca2+ levels. These proteins are relatively highly conserved in nature over a span of 400 million years from fish to humans. However mutations in troponin proteins can be associated with the disease hypertrophic cardiomyopathy which is the leading cause of sudden cardiac death in young athletes. The talk will explore the evolution of troponin as well describe its potential role in sudden cardiac death.

Friday 13th, April, 2012

“Exercise mimetics" as potential therapeutic agents for Duchenne muscular dystrophy: How basic biology can lead to clinical trials"

Time: 11:00 am

Location: Arts Building, W-215, 853 rue Sherbrooke Ouest Montreal H3A 0G5 Quebec Canada

Guest Speaker: Dr. Bernard Jasmin, Professor, Department of Cellular and Molecular Medicine, Vice-Dean of Research, Faculty of Medicine, University of Ottawa.

Abstract: Duchenne muscular dystrophy (DMD) is a common inherited neuromuscular disorder. The disease is severe since children display motor deficits in their early childhood, become wheelchair-bound by adolescence, and usually die in their second or third decade of life. DMD results from mutations/deletions in the X-linked dystrophin gene which prevents production of full-length dystrophin. Although the genetic defect was identified more than 20 years ago, there is still no effective cure to counteract the relentless progression of DMD. Several therapeutic avenues including gene therapy and cell transfer, are currently being examined in a number of laboratories.

An alternative strategy consists in utilizing a protein normally expressed in dystrophic muscle which, once expressed at appropriate levels and at the correct subcellular location, could compensate for the lack of dystrophin. An ideal candidate for such a role is utrophin. Therefore, it becomes important to decipher the mechanisms involved in controlling expression of utrophin in attempt to identify key regulatory events, signaling cascades and cellular targets. The central idea is to then develop pharmacological therapies to increase expression of utrophin in DMD muscle fibers via manipulations of these specific cellular targets and pathways with appropriate drugs/small molecules.

Our work over the past decade has identified a number of pathways that control utrophin expression in muscle fibers. Using this knowledge, we have recently initiated a series of pre-clinical studies using several molecules including the so-called "exercise mimetics", that activate these pathways causing an increase in utrophin expression and a clear attenuation of the dystrophic phenotype. As we forge ahead with these basic biological experiments and pre-clinical studies, we are also developing clinical trials for DMD since some of these compounds are either already FDA-approved or in clinical trials for other, unrelated diseases. Such an approach could accelerate considerably the development and implementation of novel pharmacological therapies for DMD.