Talent Expansion in Quantitative Biology

The Jay Boland Seminar Series

March 27, 2008      Dr. King Jordan, Georgia Tech University

March 31, 2008      Dr. Hannah Callendar, Postdoctoral Associate, Institute for Mathematics and its Applications, University of Minnesota

Title:                  Math + Biology = Infinite Possibilities

 

Abstract:                             The growing field of mathematical biology poses interesting and important problems to researchers of all levels.  My goal in this presentation is not only to give students a taste of the most basic concepts involved in modeling real-world, biological systems, but also to encourage them to investigate the infinite number of possibilities biomath provides. This talk will consist of three main parts.  First, I will review some of the basic mathematical tools used in a wide variety of biological applications.  Next I will give some examples of elementary mathematical models of population dynamics and disease propagation.  Finally, I will present some of my own research in the area of mathematical modeling of cellular signaling pathways, which are part of a complex system of communication that governs basic cellular activities and coordinates cell actions.

 

April 14, 2008          Dr. Dorea Vierling-Claassen, Joint post-doctoral research fellow at Mass. General Hospital (Harvard Medical School) and Boston University

Title:                                    Modeling cortical rhythms in schizophrenia: using math to bridge the gap between physiology and function in human disease

Abstract:                             A major challenge in the study of any neurological illness is to determine what impact physiological alterations, which are often studied post-mortem tissue, might have on the working human brain.  This is particularly true for diseases, such as Schizophrenia (a mental illness affecting about 1.1% of the adult population), that have no widely accepted animal model.  Many physiological and structural brain alterations have been identified in schizophrenia, including alterations in blood vessel size, size and shape of deep brain structures, cortical thickness, and quantity of certain neurotransmitters.  However, it is extremely difficult to link these changes to any impact they might have on the working human brain, let alone how they may contribute to symptoms.  Computational modeling provides a unique way to bridge this gap.  In this talk, I will present recent work using differential equations modeling to link evidence of changes in cortical inhibitory cells to altered auditory processing in schizophrenia. 

References:

1.            Lewis, D.A., T. Hashimoto, and D.W. Volk, Cortical inhibitory neurons and schizophrenia. Nat Rev Neurosci, 2005. 6(4): p. 312-24.

2.            Vierling-Claassen, D., et al., Modeling GABA alterations in schizophrenia: a link between impaired inhibition and altered gamma and beta range auditory entrainment. J Neurophysiol, 2008, in press.