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Program in Toxicology


Postdoctoral Fellows


Post-doctoral fellows are supported by a National Institute of Environmental Health Sciences training grant as well as by research grants. Consult Dr. B. Paige Lawrence about the current availability of these positions or a more general listing of positions at this medical center.
Stephen M. Bauer
B.A. 1998 (St. John Fisher College); Ph.D. 2007 (University of Rochester)
E-Mail: Stephen_Bauer@urmc.rochester.edu

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Neonatal oxygen supplementation and its effects on the immune response to respiratory viral infections.

Asthma is a chronic disease of the lungs with hallmark signs of airway inflammation. Bisphenol A (BPA) is a common environmental estrogen found in food can linings, dental fillings, plastic bottles, and some paper receipts. Asthma prevalence has dramatically increased since industrialization, a period when bisphenol A usage has also significantly increased. This suggests an environmental influence on the rise in asthma.
      Using a murine model, I am examining the effects of maternal bisphenol A exposure on asthma. We hypothesize that maternal bisphenol A exposure will enhance the severity/ development of asthma in our model. We also wish to investigate the mechanism by which bisphenol A may act to cause its affects on asthma. Developmental exposure to BPA likely contributes to other human diseases and our work with asthma may help elucidate common mechanisms of BPA action.

Advisor: B. Paige Lawrence, Ph.D.

Jae-woong Hwang 
B.S. 2000; Ph.D. 2008 (Seoul National University, South Korea).
E-Mail: jae-woong_hwang@URMC.rochester.edu

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Role of SIRT1 in cigarette smoke-induced autophagy.

Human sirtuin (SIRT1) is essential for maintaining silent chromatin via the deacetylation of proteins including non-histones and histones. SIRT1 plays an important role in a wide variety of processes, including stress resistance, metabolism, apoptosis, senescence, differentiation, and aging. SIRT1 regulates cigarette smoke-induced inflammation, and cigarette smoke causes oxidative stress which is now known to be responsible for triggering inflammatory events and apoptosis in the lungs of smokers/COPD patients.
     Oxidative stress is implicated in autophagy and SIRT1 has a role in regulation of autophagy. Autophagy is a general term for the degradation of cytoplasmic components within lysosomes and is important for various physiological and pathophysiological processes. My research interest is to study the role of SIRT1 in role of cigarette smoke-induced autophagic cell death in lung cells, and its relevance to human COPD.
Advisor: Irfan Rahman, Ph.D.

Hiromi Ishitobi, Ph.D. 
Ph.D. 2008 (University of Tokyo, Japan).
E-Mail: Hiromi_Ishitobi@URMC.rochester.edu

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Effects of prenatal exposure to chemical and non-chemical stressors on brain functions.

The stress response, mediated by the hypothalamus-pituitary-adrenal (HPA) axis, is critical to survival, whereas excessive stress can have permanent deleterious health effects. Prenatal stress can result in epigenetic re-programming of HPA axis function with lifelong health consequences. Among those include psychiatric disorders such as depression and anxiety and altered cognition, social behavior and response to later stress challenge.
     HPA axis reactivity and cognitive functions are also altered permanently by developmental exposure to environmental contaminants, such as lead (Pb), methylmercury (MeHg) and arsenic (As). Therefore, our hypothesis is that non-chemical stressors that produce the same (common) adverse outcomes, or act on the same biological system/substrates as a chemical exposure have the potential to produce additive or greater effects when combined with that chemical. We test this hypothesis with a focus on effects on locomotor activity and operant behaviors, and .
Advisor: Deborah A. Cory-Slechta, Ph.D.

Guangbi Jin
B.S. 1987 (Bethune Medical University, Changchun, China); Ph.D. 2003 (University of Tokyo)
E-Mail: guangbi_jin@urmc.rochester.edu

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Role of aryl hydrocarbon receptor (AhR) activation in antigen-presenting cell function.

My research interest is the role of aryl hydrocarbon receptor (AhR) activation in antigen-presenting cell function that results in diminished clonal expansion and differentiation of influenza virus-specific CD8+ T cells. AhR is a ligand-activated transcription factor that is expressed in cells of the immune system. The pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin) is the most potent AhR agonist known, and is also a well known immune suppressant. However, the precise molecular mechanism remains unclear.
      We have previously shown that AhR activation by TCDD suppresses the proliferation and differentiation of influenza virus-specific CD8+ T cells. However, TCDD does not affect CD8+ T cells directly, suggesting that defects in other cells essential for activating CD8+ T cells are affected by AhR activation. I am currently testing the hypothesis that exposure to TCDD will affect the functions of dendritic cells.
Advisor: B. Paige Lawrence, Ph.D.

Isaac Kirubakaran Sundar
B.Sc. 2000 (University of Madras, India); M.Sc. 2002, (Periyar University, India); Ph.D. 2007 (Pondicherry University, India) E-Mail: isaac_sundar@urmc.rochester.edu

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Epigenetic regulation of lung inflammation.

Epigenetics is the term used to describe heritable changes in gene expression that are not coded in the DNA sequence itself but by post-translational modifications in DNA and histone proteins. These modifications include histone acetylation, deacetylation and methylation. Aging, diet, environmental exposures and other stresses can cause epigenetic alterations, resulting in cancer or other chronic inflammatory diseases, such as COPD, asthma, and pulmonary fibrosis.
     The aim of our research is to determine the molecular mechanisms of epigenetic alterations via IKKalpha and MAP kinase pathways in response to environmental oxidants, such as cigarette smoke (CS). Understanding the intracellular signaling pathways involved in epigenetic regulation of lung inflammation will allow us to identify therapeutic targets for many chronic inflammatory lung diseases and cancer.
Advisor: Irfan Rahman, Ph.D.
Revised January 19, 2012 (vgl)