Annual Meeting Program - Society of Toxicology

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Society of Toxicology 2008 Program Description (Continued) Monday Monday Morning, March 17 7:30 AM to 2:00 PM Room 3A MONDAY MORNING Undergraduate Education Program Chairperson(s): Vicente Santa Cruz, CDI chair, Chevron Phillips Chemical Company, LP, The Woodlands, TX, and Mari Stavanja, RTR Tobacco Company, Winston-Salem, NC Sponsored by: Committee for Diversity Initiatives This event is for undergraduate students and advisors receiving MARC and SOT travel funding, and SOT program volunteers. 7:30 AM–8:10 AM Meeting for Students, Advisors, Peer Mentors, and SOT Hosts 8:15 AM–9:15 AM Plenary Lecture (Exhibit Hall 4F) 9:30 AM–11:15 AM Poster Session for Visiting Students (Exhibit Hall) 11:15 AM–12:15 PM Selected Scientific Sessions 12:15 PM–1:30 PM In Vitro Luncheon: Development of In Vitro Screening Tools to Test for Drug-Induced Mitochondrial Toxicities, Yvonne Will, Pfizer, Inc., San Diego, CA 1:30 PM–2:00 PM Closing Session (Room 3A) Monday Morning, March 17 8:15 AM to 9:15 AM Exhibit Hall 4F Plenary Opening Lecture: Perspectives on Science in the 21 st Century Lecturer: Nobel Laureate Lee Hartwell, Fred Hutchinson Cancer Research Center, Seattle, WA Dr. Lee Hartwell didn’t realize as a boy that his youthful predilection for chasing butterflies hinted at his future as a geneticist. Nor did his teen-age tinkering on auto engines give him a clue that he would win a Nobel Prize. But today, his career’s work in cell genetics has changed the way we think about life itself. Early in his research career, Hartwell set out to find an organism simple enough to experiment on, yet complex enough to provide insight into humans. He made a risky choice: to use yeast, the same single-celled fungus that makes bread dough rise. At the time, most scientists thought yeast was not a good model for understanding the complexity of human cells. Hartwell persisted, and a series of experiments over several years led to a landmark discovery. He discovered the genes that control cell divisiongenes that turned out to be the universal machinery for cell growth in organisms from fungi to frogs to humans. This discovery in yeast not only showed the unity of all life, it also had practical applications for human health. By identifying “checkpoint” genes that determine whether a cell is dividing normally, Hartwell provided important clues to cancer, which arises from abnormal, uncontrolled cell growth. Hartwell’s discoveries have led him and other scientists to explore ways to stop abnormal cells from dividing. Researchers hope this work will lead to new and better ways to prevent, diagnose, and treat cancer. For his insightful discoveries, Hartwell received the 2001 Nobel Prize in Physiology or Medicine. Monday Morning, March 17 9:30 AM to 11:15 AM Exhibit Hall Poster Session for Visiting Students Chairperson(s): Vicente Santa Cruz, CDI Chair, Chevron Phillips Chemicals International N.V., Brussels, Belgium, and Mari Stavanja, RJR Tobacco Company, Winston Salem, NC Sponsored by: Committee for Diversity Initiatives This poster session is part of the Undergraduate Education Program. All are welcome to view the specially selected presentations which provide an overview of research in toxicology and demonstrate the diversity within the discipline. up-to-date information at www.toxicology.org 87
47 th Annual Meeting & ToxExpo Monday Program Description (Continued) Abstract # Abstract # Monday Morning, March 17 9:30 AM to 12:15 PM Room 6A Monday Morning, March 17 9:30 AM to 12:15 PM Room 605 SYMPOSIUM SESSION: METALS, MICROGLIA, AND NEUROINFLAMMATION Chairperson(s): David Lawrence, Wadsworth Center, Albany, NY and Michael Aschner, Vanderbilt University Medical Center, Nashville, TN. Endorsed by: Metals Specialty Section* Neurotoxicology Specialty Section The major immune cell that permanently resides within the brain parenchyma is the microglial cell. Current consensus suggests that microglia are derived from the hematopoietic monocyte lineage and that blood monocytes differentiate into perivascular macrophages which develop into microglia as they traffic into multiple brain regions. Another hematopoietic cell residing in the brain is the mast cell. Most other immune cells only transiently migrate through the brain. A major question that continues to be debated is whether neurotoxic metals directly activated immune cells within the brain that subsequently induce neuronal damage or whether metal toxicants induce neuronal damage, which subsequently activates the immune cells (mainly microglia) leading to exacerbated neuronal damage. An alternative hypothesis is that microglia are neuroprotective but metals cause loss of microglial protective factors because of microglial degeneration and/or elevated production of potential cytotoxicants. Numerous cytokines have been implicated in the neuroinflammation and neurodegeneration, but their cellular sources have not been fully delineated. The various neuroimmune mechanisms posited to regulate neuroinflammation, neuroprotection, and neuronal degeneration will be discussed. #13 9:30 METALS, MICROGLIA, AND NEUROINFLAMMATION. D. Lawrence. Wadsworth Center, Albany, NY. #14 9:40 ROLE OF MICROGLIA IN METAL NEUROTOXICITY. M. Aschner. Pediatrics, Vanderbilt University Medical Center, Nashville, TN. #15 10:15 POTENTIAL ROLE OF MICROGLIA IN MANGANESE NEUROTOXICITY. N. M. Filipov, P. L. Crittenden and S. Lee. CEHS, Basic Sciences, Mississippi State University, Mississippi State, MS. #16 10:50 LEAD AND MERCURY INDUCED NEUROIMMUNE CHANGES IN THE BRAIN. D. Lawrence 1 , J. Kasten-Jolly 1 , D. Gao 1 , T. Mondal 1 and C. Hudson 2 . 1 Wadsworth Center, Albany, NY and 2 SUNY Upstate Medical University, Syracuse, NY. #17 11:25 MICROGLIAL ACTIVATION OR MICROGLIAL DEGENERATION? W. J. Streit. Neuroscience, University of Florida, Gainesville, FL. Sponsor: D. Lawrence. 12:00 QUESTIONS FROM THE AUDIENCE. SYMPOSIUM SESSION: MOLECULAR BASIS FOR SUSCEPTIBILITY TO CHEMICAL TOXICITY AND DISEASE Chairperson(s): Ronald Hines, Medical College of Wisconsin, Milwaukee, WI and Jim MacGregor, Toxicology Consulting Services, Arnold, MD. Endorsed by: Mechanisms Specialty Section Molecular Biology Specialty Section Regulatory and Safety Evaluation Specialty Section* Risk Assessment Specialty Section The completion of the Human Genome Project in 2003, and more recently, the first phase of the International HapMap project, have provided valuable tools which we are still learning how to use effectively in our goal to improve human health and prevent disease. For example, the cost-effective and rigorous ability to perform whole genome association studies for complex diseases has only been achieved within this past year. Although exciting and of clear utility in identifying multiple genetic loci whose variability will contribute to disease risk, such association studies still must be followed-up with more detailed analyses to understand the causative variants that contribute to differential susceptibility. Further, there now is widespread acceptance that most if not all complex disease arises because of an interaction between our genome and the environment. Thus, a careful assessment and definition of phenotype, including environmental exposure, is critical. We also now have clear examples wherein epigenetic changes caused by environmental factors, including transgenerational epigenetics changes, can also have a significant impact on disease risk. This symposium will provide state-of-the-art updates on our understanding of the molecular basis for individual differences in susceptibility to chemical toxicity and disease. Topics to be covered include how regulatory polymorphisms resulting in variation in gene expression can impact risk, chemical-induced epigenetic changes and their impact on susceptibility, the use of genetic variation to predict risk and efficacy during drug development and the use of pathway analyses to understand complex disease risk using Parkinson’s disease as an example. Thus, this symposium will span from fundamental, mechanistic studies, to translational investigations and clinical applications, demonstrating the strengths of an interdisciplinary approach to environmental health issues. #18 9:30 MOLECULAR BASIS FOR SUSCEPTIBILITY TO CHEMICAL TOXICITY AND DISEASE. R. Hines. Medical College of Wisconsin & Children’s Research Institute, Milwaukee, WI. #19 9:35 REGULATORY POLYMORPHISMS AND THEIR IMPACT ON SUSCEPTIBILITY. R. N. Hines. Pediatrics, Medical College of Wisconsin & Children’s Research Institute, Milwaukee, WI. #20 10:15 EPIGENETICS AND ITS IMPORTANCE IN TOXICOLOGY. R. L. Jirtle. Radiation Oncology, Duke University Medical Center, Durham, NC. #21 10:55 THE USE OF GENETIC VARIATION TO PREDICT RISK AND EFFICACY DURING DRUG DEVELOPMENT. A. D. Roses. Joseph and Kathleen Bryan Alzheimer’s Disease Research Center, Durham, NC. Sponsor: R. Hines. #22 11:35 A GENOMIC PATHWAY APPROACH TO COMPLEX DISEASES: PROMISE, PITFALLS, AND REMEDIES. D. Maraganore. Mayo Clinic College of Medicine, Rochester, MN. Sponsor: R. Hines. 88 SOT’s 47 th Annual Meeting
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Annual Meeting Program - Society of Toxicology

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