[BIC-announce] FW: Special Lecture - Monday, June 8, 4:00 p.m. - Rajiv R. Ratan - Twists and Turns (Non Helical) on the Transcriptional Road to Cell Death: Implications for Brain Protection and Repair

Jennifer Chew, Ms. jennifer.chew at mcgill.ca
Mon Jun 8 08:53:30 EDT 2009


PLEASE DISCARD IF THIS IS A DUPLICATE.  THANK YOU.  JENNIFER     
 

 
________________________________

From: MNISTAFF - Montreal Neurological Institute Staff [mailto:MNISTAFF at LISTS.MCGILL.CA] On Behalf Of Grace Flynn, Ms.
Sent: Friday, June 05, 2009 3:20 PM
To: MNISTAFF at LISTS.MCGILL.CA
Subject: Special Lecture - Monday, June 8, 4:00 p.m. - Rajiv R. Ratan - Twists and Turns (Non Helical) on the Transcriptional Road to Cell Death: Implications for Brain Protection and Repair



*****REMINDER*****


Special Lecture:
 
Speaker:       Rajiv R. Ratan, Burke Professor of Neurology and Neuroscience, Weill Medical College of Cornell University
                       Burke-Cornell Medical Research Institute 

Title:              Twists and Turns (Non Helical) on the Transcriptional Road to Cell Death: Implications for Brain Protection and Repair 

Time/ Date:      4:00 p.m. - Monday, June 8, 2009

Place:               de Grandpré Communications  Centre

Hosted by:      David R. Colman, PhD
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  Research July 1992 -  present   
  Nervous  system diseases are among the leading causes of handicaps in  non-institutionalized people in the United States. Traditional goals of  neurorehabilitation have focused on decreasing handicaps of patients by  improving function at the level of disability. However, responsible  rehabilitation begins by promoting preventative measures.  Among the preventative measures  that might improve recovery after nervous system injuries such as stroke  includes pharmacological prevention of delayed cell death. Several  converging lines of inquiry suggest that free radicals may be important  mediators of primary and secondary neuronal injury and consequent  disability in acute and chronic neurodegenerative states. However,  antioxidants have been disappointing as neurological therapeutics. These  limitations derive, in part, from inadequate understanding of markers of  oxidative stress in neurons, mechanisms of defense against oxidants; how  these endogenous mechanisms of defense can be augmented to therapeutic  advantage and the role of free radicals in normal cell function. We have  used the experimental leverage of an in vitro model of neuronal oxidative  stress to demonstrate: a) that free radicals can inappropriately unleash a  protein synthesis-dependent suicide death pathway in neurons. b.) to  identify transcription factors such as NF-kB and hypoxia-inducible  factor-1, which are targets for antioxidants in abrogating cell death; and  c.) to purify a contaminating and multipotent anti-apoptotic activity from  a bovine liver catalase preparation and to identify it as arginase. These  studies have identified novel strategies for limiting neuronal apoptosis  and potential markers for antioxidant treatment in the central nervous  system. In  accomplishing these research goals, I have participated in training  undergraduates, graduate students and post-doctoral fellows. I have also  taught a seminar course at Harvard Medical School on the "Transcriptional  regulation of survival and death in neurons".  The course attempts, by using  distinct transcription factors as case studies, to outline how  transcription factors may regulate homeostatic responses and how small  molecules that emulate these transcriptional responses might be useful in  decreasing disability associated with neurological disease.   The  overall goal of these research and teaching activities is to impact at the  hospital bedside, neurological disability by developing small molecules  that prevent neuronal death. In keeping with these goals I have been  participating in the evaluation and care of patients on the neurology ward  who are in need of rehabilitation.                            

 
 
 







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