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2007 Summer Program in Systems Physiology Each summer the MBI hosts a 3-week education program. The first week is spent in a tutorial, which combines morning lectures with active learning laboratories in the afternoon. The following 2 weeks are spent working on guided team projects and participating in a miniconference to share project results. The program is meant primarily for graduate students; college instructors and qualified undergraduates will also be considered. The 2007 Summer Program dates are July 23 - August 10: July 23-27, 2007 In these lectures Keener will give an introduction to mathematical models of cellular physiological processes, based on material found in Keener and Sneyd, Mathematical Physiology. Included will be discussion of enzyme kinetics and biochemical reaction networks, cellular transport processes (channels, transporters, ATPases), membrane excitability, calcium signaling, cell regulatory processes, bursting and secretion, cellular communication and coupling, and waves in continuous and discrete media. The lectures will assume familiarity with ordinary and partial differential equations, and some understanding of stochastic processes (Markov processes).
July 30 - August 10, 2007
Group presentation: PDF An adult dermal wound heals with the formation of scar tissue. An important factor in determining the quality of the healed tissue is the ratio between different kinds of collagen fibers. The project will develop a mathematical model of the scarred tissues, and compare it with healthy tissue. The model will involve a system of ODEs.
When grown in vitro, cells are frequently seeded into
biological gels, such as collagen. The mechanical properties of the gel
(such as stiffness, alignment of fibre in the microstructure, etc.)
affect the architecture of the tissues formed by the cells. These
cell-gel interactions are currently being investigated by a
multidisciplinary team led by Dr Keith Gooch in the Department of
Biomedical Engineering. In this project, we will investigate hypotheses
for how cells can compact the surrounding gel, and how the fibrous gel
microstructure may affect this process. Our models will be validated
against experimental results from Dr Gooch's lab, and data from the
literature.
Tuberculosis is a major health problem causing more than 2 million deaths annually. The current vaccine, BCG is the most widely used vaccine in the world, but it provides only partial protection against the disease (estimates of protection range from 0-80%) and in particular in the high endemic regions BCG has failed to control TB. Therefore, a new vaccine is needed that can prevent new cases of tuberculosis, estimated at 8-10 million a year. One approach to increase the efficacy of BCG could be to add genes from M. tuberculosis encoding proteins (ESAT-6, Ag85A, and Ag85B) known to mediate protection as subunit vaccines. It has been shown that a vaccination with a fusion protein consisting of Ag85B and ESAT-6 promoted strong immune response, which was highly protective against TB in the mouse and non-human primate models. We aim to model these two vaccine strategies mathematically via a set of ordinary differential equations and to compare the results with real data. References: J. Dietrich, C.V. Lundberg, and P. Andersen, TB vaccine strategies - What is needed to solve a complex problem?, Tuberculosis, Vol. 86, 2006.
Group presentation: PDF Apoptosis, or programmed cell death, is triggered either by extrinsic factors (e.g. certain cytokines that dock on cell membrane receptors) or intrinsic factors (e.g. cytochrome c released from mitochondria due to intracellular stress). Both types of death factors induce the activation of caspases -- proteolytic enzymes that chew up proteins. The aims of this project are: (1) to integrate the extrinsic and intrinsic pathways of apoptosis into a comprehensive network model, and (2) to develop a computer program to solve the dynamical equations of the model and explore the regions of parameter space where all-or-none decisions of cell death are taken, and, if possible, determine analytic expressions involving a set of key parameters that controls cell death decision. [Reference: Legewie E, et al. (2006) PLoS Computational Biology 2(9): e120., and Refs.(103)-(105) cited at the end of this paper.]
Group presentation: PDF The purpose of the project is to use mathematics to study some aspects of
cell metabolism, in particular the methionine metabolism.
Group presentation: PPT This project focuses on tumor immunology and, in particular, the dynamics of the interaction of cytotoxic T-lymphocytes (a special type of white blood cell) with specific types of tumor cells. The aim of the project is to develop predictive mathematical models describing the attack of tumor cells by lymphocytes in a small, multicellular tumor, without necrosis and at some stage prior to tumor-induced angiogenesis. Attention will be focused upon the well-documented phenomenon of cancer dormancy and the m echanisms by which tumors escape immune defenses. |
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