Program - Society of Toxicology

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50 th Anniversary Annual Meeting and ToxExpo Program Description (Continued) Tuesday Abstract # Abstract # #1702 1:30 DOES THE CLOCK MAKE THE POISON? INFLUENCE OF THE CIRCADIAN CLOCK ON TOXICOLOGICAL MECHANISMS AND OUTCOMES. H. Zarbl 1 and L. A. Hooven 2 . 1 Environmental and Occupational Health Sciences Institiute, Robert Wood Johnson Medical School, Piscataway, NJ and 2 Department of Zoology, Oregon State University, Portland, OR. 1:30 INTRODUCTION. Helmut Zarbl #1703 1:35 ENVIRONMENTAL INFLUENCES UNCOUPLE PERIPHERAL CLOCKS FROM SCN CLOCKS. U. Schibler. Molecular Biology, University of Geneva, Geneva, Switzerland. Sponsor: H. Zarbl. #1704 2:00 TICK-TOXICOLOGY: CLOCK GENE EXPRESSION AND INTERACTIONS BETWEEN THE MOLECULAR PATHWAYS FOR THE REGULATION OF CIRCADIAN RHYTHMS, AND TOXIN METABOLISM. D. J. Earnest. Neuroscience and Experimental Therapeutics, Texas A&M Health Sciences Center, College Station, TX. Sponsor: H. Zarbl. #1705 2:25 THE HEPATOCYTE AUTONOMOUS CLOCK MODULATES THE CHRONOTOXICITY OF ACETAMINOPHEN. C. A. Bradfield 1 , J. A. Walisser 1 , B. P. Johnson 1 , Y. Liu 1 , A. Shen 1 , E. L. McDearmon 1 , B. McIntosh 1 , A. Vollrath 1 , A. C. Schook 2 and J. S. Takahashi 2 . 1 The McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI and 2 Northwestern Univeristy, Evanston, IL. #1706 2:50 CIRCADIAN EXPRESSION OF DRUG PROCESSING GENES IN MICE. C. D. Klaassen. Pharmacology, University of Kansas Medical Center, Kansas City, KS. #1707 3:15 RELEVANCE OF CIRCADIAN DISRUPTION AND CIRCADIAN INDUCTION FOR CANCER CONTROL. F. Levi. Rhythmes Biologiques et Cancer, INSERM, Villejuif, France. Sponsor: H. Zarbl. #1708 3:40 METHYLSELENOCYSTEINE RESETS THE RHYTHMIC EXPRESSION OF CIRCADIAN AND GROWTH REGULATORY GENES DISRUPTED BY NITROSOMETHYLUREA IN VIVO. M. Fang and H. Zarbl. Environmental and Occupational Health Sciences Institiute, Robert Wood Johnson Medical School, Piscataway, NJ. 4:05 PANEL DISCUSSION/Q&A. Tuesday Afternoon, March 8 1:30 PM to 4:15 PM Room 143 Symposium Session: Macrophages: Regulators of Toxicity and Disease Pathogenesis Chairperson(s): Debra Laskin, Rutgers University, Piscataway, NJ, and Andrew Gow, Rutgers University, Piscataway, NJ. Sponsor: Toxicologic and Exploratory Pathology Specialty Section Endorsed by: Immunotoxicology Specialty Section Mechanisms Specialty Section Nanotoxicology Specialty Section Macrophages function as control switches of the immune system, providing a balance between pro- and anti-inflammatory responses. To accomplish this, they develop into different subsets: classically (M1) or alternatively (M2) activated macrophages. Whereas M1 macrophages display a cytotoxic, proinflammatory phenotype, M2 macrophages, suppress immune and inflammatory responses and participate in wound repair and angiogenesis. Critical to the actions of these divergent or polarized macrophage subpopulations is the regulated release of inflammatory mediators. When properly controlled, classically activated M1 macrophages effectively destroy invading pathogens, tumor cells, and foreign materials. However, when M1 activation becomes uncontrolled, these cells release excessive quantities of cytotoxic mediators that contribute to disease pathogenesis. The activity of M1 macrophages is countered by alternatively activated M2 macrophages which release mediators that down regulate M1 cells, and stimulate growth, extracellular matrix turnover, and tissue repair. Aberrant functioning of M2 macrophages can lead to fibrosis and tumor metastasis and progression. Ultimately, it is the balance in the production of mediators by these two cell types that determines the outcome of the tissue response to chemical toxicants and disease progression. These different models will be presented to illustrate this divergent role of macrophages in disease pathogenesis and toxicity. #1709 1:30 MACROPHAGES: REGULATORS OF TOXICITY AND DISEASE PATHOGENESIS. D. Laskin and A. Gow. Pharmacology and Toxicology, Rutgers University, Piscataway, NJ. 1:30 INTRODUCTION. Debra Laskin #1710 1:35 MACROPHAGES AND HEPATOTOXICITY: A BATTLE OF FORCES. D. Laskin 1 , C. Gardner 1 , Y. Liu 1 and J. Laskin 2 . 1 Pharmacology and Toxicology, Rutgers University, Piscataway, NJ and 2 UMDNJ-RWJ Medical School, Piscataway, NJ. #1711 2:05 LUNG MACROPHAGE RESPONSES TO BIOACTIVE ENGINEERED NANOMATERIALS (ENM) INVOLVES ACTIVATION OF THE NLRP3 INFLAMMASOME. A. Holian and C. Migliaccio. Center for Environmental Health Sciences, University of Montana, Missoula, MT. #1712 2:35 MACROPHAGE DIVERSITY AND POLARIZATION IN IMMUNOPATHOLOGY. A. Mantovani. Istituto Clinico Humanitas IRCCS, University of Milan, Milan, Italy. Sponsor: D. Laskin. #1713 3:05 MECHANISMS OF MICROGLIAL ACTIVATION IN RESPONSE TO TOXICANTS. A. Gow. Pharmacology and Toxicology, Rutgers University, Piscataway, NJ. Sponsor: D. Laskin. 264 Education-Career Development Sessions Exhibitor Hosted Sessions Featured Sessions Historical Highlights Informational Sessions Platform Sessions
Society of Toxicology 2011 Program Description (Continued) Abstract # #1714 3:35 MACROPHAGE DIVERSITY PROMOTES TUMOR PROGRESSION AND METASTASIS. J. W. Pollard. Department of Developmental and Molecular Biology, Albert Einstein College of Medicine Yeshiva University, New York. Sponsor: D. Laskin. 4:05 PANEL DISCUSSION/Q&A. Tuesday Afternoon, March 8 1:30 PM to 4:15 PM Room 147 Integration of Toxicological and Epidemiological Evidence to Understand Human Risk Symposium Session: When Is Exposure Not Exposure? Defining the Dose-Response Region between “Effect” and “Adverse Effect” Implications for Human Health Risk Assessment Chairperson(s): Caroline English, NSF International, Ann Arbor, MI, and Edward Ohanian, U.S. EPA, Washington, D.C. Sponsor: Risk Assessment Specialty Section Endorsed by: Molecular Biology Specialty Section ‘Omics technologies demonstrate global changes in gene regulation and expression following chemical exposure, causing toxicologists to revisit the question, what is an adverse effect and what isn’t. Dose-dependent transitions in genomic and related responses reflect the levels of exposure that cause detectable perturbations to the biological system under study. We will focus on two transitions, having both dose and temporal dimensions, which are advanced as being pivotal to understanding mode of action and prediction of toxicity. The first transition is from no-detectable-effect on the biological system relative to unexposed controls, to the first-perceptibleeffect at the global genome level; observed as up- and down-regulation of genes that regulate adaptive responses. The second transition is from the adaptive response region to the first adverse response or critical effect region of the dose-response relationship. We will explore if and how ‘omic phenomena elicited by chemical exposures translate into useful information for risk assessors. Consideration of the adaptive capacity of the biological system and severity of the effect might further inform our definition of the term adverse and inform the magnitude of traditional uncertainty factors used. Understanding dose-dependent transitions combined with dosimetry models that characterize the exposure-tissue concentration relationship might permit risk assessors to define exposures delimited by safe and adverse boundaries. We will conclude by describing emerging advances in high-throughput quantitative ‘omic technologies, and findings from studies with endogenous and exogenous compounds and nanoparticulates, to address how we move from the vast array of ‘omic data generated to practical risk assessment applications. #1715 1:30 WHEN IS EXPOSURE NOT EXPOSURE? DEFINING THE DOSE-RESPONSE REGION BETWEEN “EFFECT” AND “ADVERSE EFFECT” IMPLICATIONS FOR HUMAN HEALTH RISK ASSESSMENT. C. English. NSF International, Ann Arbor, MI. 1:30 INTRODUCTION. Caroline English #1716 1:39 USE OF THE HIERARCHICAL OXIDATIVE STRESS PARADIGM FOR HAZARD AND RISK ASSESSMENT IN RESPONSE TO AMBIENT ULTRAFINE AND ENGINEERED NANOPARTICLE TOXICITY. A. E. Nel. Medicine, University of California Los Angeles, Los Angeles, CA. Sponsor: A. Nel. Abstract # #1717 2:05 HUMAN EXPOSURE CONTEXT FOR NANOPARTICLE TOXICITY ASSESSMENT BY BIOLOGICAL PATHWAY BASED DOSE- RESPONSE MODELING. J. G. Teeguarden 1 , M. N. Costa 2 , K. M. Waters 2 and J. E. McDermott 2 . 1 Biological Monitoring and Modeling, Pacific Northwest National Laboratory, Richland, WA and 2 Computational Biology and Bioinformatics, Pacific Northwest National Laboratory, Richland, WA. #1718 2:31 TIME-DEPENDENT CHANGES IN THE TRANSCRIPTOME: AN APPROACH FOR IDENTIFYING TRANSCRIPTIONAL PROFILES ASSOCIATED WITH THE ONSET OF CHRONIC PHENOTYPIC CHANGES. D. C. Wolf. NHEERL/ORD, U. S. EPA, Research Triangle Park, NC. #1719 2:57 FORMALDEHYDE: DOSE-DEPENDENT TRANSITIONS FOR AN ENDOGENOUS COMPOUND WITH HIGH DOSE CARCINOGENICITY. M. E. Andersen. Computational Biology, The Hamner Institutes for Health Sciences, Research Triangle Park, NC. #1720 3:23 ENVIRONMENTAL EPIGENOMICS AND RISK ASSESSMENT: WHAT CONSTITUTES AN ADVERSE EFFECT AND ISSUES OF NONLINEARITY. D. C. Dolinoy. Environmental Health Sciences, University of Michigan, Ann Arbor, MI. #1721 3:49 INTERPRETING DOSE-RESPONSE INFORMATION ON INTERMEDIATE STAGES OF CAUSAL CASCADES IN TOXICITY MODE OF ACTION. L. R. Rhomberg. Gradient, Cambridge, MA. Tuesday Afternoon, March 8 1:30 PM to 4:15 PM Room 150 Workshop Session: Nonclinical to Clinical Abuse Liability Assessment of Drugs: Current Practices, Challenges, and Impact of Recent Regulatory Guidance Chairperson(s): Brian Gemzik, Bristol-Myers Squibb, Princeton, NJ, and Carrie Markgraf, Merck, Lafayette, NJ. Sponsor: Regulatory and Safety Evaluation Specialty Section Endorsed by: Drug Discovery Toxicology Specialty Section Neurotoxicology Specialty Section An increased level of attention has been focused on the assessment of abuse liability for drugs that affect the central nervous system as a consequence of recent regulatory guidances from the EMEA, ICH, as part of M3(R2), and U.S. FDA (draft). It is therefore critical to understand the current issues facing the pharmaceutical research and regulatory communities in the evaluation of new drug candidates for abuse and dependence potential. Nonclinical and clinical evaluations each contribute to the assessment of a drug for class scheduling, and to the information in the product label. Animal models for the study of drugs with pharmacologic mechanisms known to be associated with abuse are well characterized, and clinical trial protocols enrolling experienced users of abused drugs have been widely utilized in risk assessment. However, unique challenges are encountered in both nonclinical and clinical discovery and development settings when evaluating drugs with novel mechanisms of action. In recognition of the need for a broad and integrated understanding in the toxicology community, this symposium will blend current topics in this field of growing interest, Tuesday Poster Sessions Regional Interest Session Roundtable Sessions Symposium Sessions Thematic Sessions Workshop Sessions 265
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50 th Anniversary Annual Meeting &
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Scientific Program Overview A page
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9:00 AM-12:30 PM POSTER SESSionS
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March 6-10, 2011 Walter E. Washingt
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Celebration Activities Historical H
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of the Society Regional Chapter Yea
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SOT Presidents 1961-2011 1966 1967
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The SOT Council Thanks and Recogniz
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of the Past 50 Years 2003 Michael D
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SOT Job Bank YOUR RECRUITMENT AND E
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Society of Toxicology 2011 Author I
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Society of Toxicology 2011 2010-201
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