Seminar - Engineering for Quantitative Cell Biology
Date: April 18, 2008
Time: 4:00 PM
Location: Matheson Hall, Room: 109
Speaker(s):
Bahrad A. Sokhansanj, Ph.D.
Assistant Professor
Details:
The concept of using quantitative biology to bridge the gap between the molecular world of cells and human health and complex systemic disease ("molecular health engineering"), followed by a discussion of recent results from our laboratory. This includes 3 main areas: (1) modeling and experiments to predict the impact of individual genetic variation in the human DNA base excision repair pathway, (2) developing nano-tools for measuring variant DNA repair protein activity, and (3) a hybrid modeling and experimental approach to understand the impact of changing a cell's oxidative stress environment on the regulation of stress response, with applications to chronic inflammatory disease.
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Biosketch:
Biosketch:
Our research philosophy is that the bridge between basic molecular biology and medicine will be built with bioengineering, through quantitative measurements and modeling. Our focus is a systems approach to a critical problem in chronic disease, including cancer: the impact of chronic inflammation on cell repair, apoptosis and death.
Our approach is to blend modern experimental methods with mathematical modeling and computer simulation to analyze the complex systemic response of a cell to the environmental stresses and intercellular signals of chronic inflammation.
The current focus of our research is the regulation of DNA base excision repair (BER) under pro-inflammatory conditions. BER is the major cellular process responsible for the repair of oxidative DNA damage, which can result from the elevated levels of oxidative stress during inflammation. If a cell cannot repair damage, then normally it should proceed to apoptosis, a regulated form of cell death that is anti-inflammatory. If the balance between repair and cell death is dysregulated, then cells may proliferate abnormally - or if the repair pathway is overwhelmed, then they may be damaged, dysfunctional, and potentially even mutagenic.
While our work may be generally applicable for chronic inflammation (i.e., diabetes, ulcerative colitis, autoimmune disorders, inflammatory pain, etc.) we are focusing on processes relevant for COPD, chronic obstructive pulmonary disease.
Education:
Ph.D. 2002, Engineering-Applied Science, University of California, Davis
M.S. 2000, Applied Science, University of California, Davis
B.S. 1998, Engineering Physics, University of Saskatchewan
Active Research Projects:
1. The role of DNA damage and repair phenotypes in modulating the predisposition to apoptosis as an outcome of cell stress.
2. Characterizing the role of oxidative stress response (apoptosis vs. necrosis/proliferation) in the progression of COPD - specifically the diminished tolerance of acute infections in chronically ill patients.
3. Development of experimental, analytical, and modeling methods for quantitative biology.
Publications:
1. *Sokhansanj BA, Lim, DC, Atkins AJ, Zhao H. Quantifying repair and apoptosis under oxidative stress and mitochondrial disruption. Manuscript in prep., 2006.
2. Sokhansanj, BA, Lim DC. The role of non-apoptotic cell response to stress in acute exacerbations of chronic obstructive pulmonary disease (COPD). Manuscript in preparation, 2006.
3. *Zhao H, Sokhansanj BA. Application-oriented modeling of cellular microtubule dynamics. Manuscript submitted to Biophys Chem, 2006.
4. *Datta S, Sokhansanj BA. Accelerated Search for biomolecular network models to interpret high-throughput experimental data. Manuscript submitted to BMC Bioinformatics, 2006.
5. Hu X, Sokhansanj B, Wu D, Tang Y. A novel approach for mining and fuzzy simulation of sub-networks from large biomolecular networks. IEEE Trans Fuzzy Syst, in press, 2006 (to appear 2007).
6. Kriete A, Sokhansanj BA, Coppock DL, West GB. Systems approaches to the networks of aging. Ageing Res Rev, 5(4): 434-448, Nov 2006.
7. *Sokhansanj BA, Wilson DM 3rd. Estimating the impact of human base excision repair protein variants on the repair of oxidative DNA base damage. Cancer Epidemiol. Biomarkers Prev., 15(5): 1000-1008, May 2006.
8. Motin VL, Georgescu AM, Fitch JP, Gu PP, Nelson DO, Mabery SL, Garnham JB, Sokhansanj BA, Ott LL, Coleman MA, Elliott JM, Kegelmeyer LM, Wyrobek AJ, Slezak TR, Brubaker RR, Garcia E*. Temporal global changes in gene expression during temperature transition in Yersinia pestis. J. Bacteriol., 186(18): 6298-6305, Sep. 2004.
9. *Sokhansanj BA, Fitch, JP, Quong, JN, Quong, AA. Linear fuzzy gene networks obtained from microarray data by exhaustive search. BMC Bioinformatics, 5(1): 108, Aug. 2004.
10. *Sokhansanj BA, Wilson DM 3rd. Oxidative DNA damage background estimated by a system model of base excision repair. Free Radic. Biol. Med., 37(3): 422-427, Aug. 1, 2004.
11. Quong, AA, Kercher, JR, McCready, PM, Quong JN, Sokhansanj BA, Fitch, JP*. An indexed modeling and experimental strategy for biosignatures of pathogen and host. J. Franklin Inst., 341, 157-174, 341(1-2): 157-174, Jan.-Mar., 2004.
12. Sokhansanj BA, Rodrigue, GR, Fitch JP, Wilson DM 3rd. A quantitative model of human DNA base excision repair. I. Mechanistic insights. Nucleic Acids Res., 30(8): 1817-1825, Apr. 15, 2002.
13. Motin VL, Georgescu AM, Elliott JM, Hu P, Worsham PL, Ott LL, Slezak TR, Sokhansanj BA, Regala WM, Brubaker RR, Garcia E. Genetic variability of Yersinia pestis isolates as predicted by PCR-based IS100 genotyping and analysis of structural genes encoding glycerol-3-phosphate dehydrogenase (glpD). J. Bacteriol., 184(4): 1019-1027, Feb. 2002.
14. Fitch JP, Sokhansanj B. Genomic engineering: moving beyond DNA sequence to function. Proc. IEEE, 88(12): 1949-1971, Dec. 2000.
Directions:
Matheson Hall is located at 32nd and Market Streets.
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