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stressors can be modified by behavior and can have dramatic impact on vulnerability. Additionally, nonchemical stressors can modify the response to exposure or modify the level of exposure. Many would call inclusion of all these factors important to cumulative risk assessment. Environmental exposures are rarely to single chemical stressors and often this convergence occurs during critical windows of development. The need to expand single substance risk assessments to complex environmental mixtures remains a challenge. This challenge can be addressed with improved problem formulation of the health risk of concern. The reality in assessing children’s health risk is that there is often a paucity of data for children’s exposures and hazards. In addition, the lack of data in developing animals for non food use pesticides limits extrapolation and risk estimation in humans. This lack of data creates a dependence on default safety and/or uncertainty factors. The contemporary challenge is how can critical data gaps be filled efficiently and effectively with new technologies that reduce uncertainty and reliance on cumbersome and expensive animal testing. (This abstract does not reflect EPA policy). 657 WHERE DO I GO NOW? RATIONAL CAREER DEVELOPMENT PLANNING FOR EARLY-CAREER SCIENTISTS. B. J. Lew 1 and A. Wang 2 . 1 Environmental Medicine, University of Rochester, Rochester, NY and 2 National Center for Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, NC. Toxicology training during graduate school and postdoctoral fellowships provides early-career scientists with a wide array of transferable skills that can be used in many job sectors, but navigating the all of the possible career options can be a daunting task. Additionally, finding and preparing for a career path that is right for yourself is not always easy, particularly when it differs from that of your mentor or is non-traditional. The majority of students and postdocs are trained in academic institutions with resources that prepare them for a career in academia. However, a recent National Postdoctoral Association survey indicated that even though 45% of the postdocs plan on being a tenure-track faculty member, less than 20% will obtain this position. Therefore, it is important for early-career scientists to gather ample information and diverse experiences to better prepare them for multiple career paths. The first step in this process is to identify transferable skills and translate them into realistic paths towards a rewarding job. With broad coverage of non-traditional career paths in toxicology, this session will provide early-career scientists with insight on how to map a career path that fits their passion and skills. Using an interactive format, speakers will identify tools to utilize in pursuit to navigating different paths. Discussions will include identifying marketable skills, rational career planning, networking, and improving marketability. Grant preparation will also be discussed during a presentation on writing a successful career transition grant application. Specifically, the K99/R00 grant program, which has no citizenship restrictions, provides support to an individual postdoctoral fellow transitioning to an independent faculty position. 658 HOW TO IDENTIFY YOUR SKILLS AND PASSIONS. K. Keefe. Pharmacology and Toxicology, University of Utah, Salt Lake City, UT. Sponsor: B. Lew. Socrates is quoted as saying, “The unexamined life is not worth living”. It’s probably safe to say that at some point even Socrates stopped and wondered whether he had made the right career choice or whether he should be doing something else. Although used here out of context, Socrates’ words offer instruction to us as scientists in identifying our skills and passions. That instruction is “examine”. Identifying our passions involves examining our values and interests and deciding which of those will form the basis on which we make decisions about various matters, including our career, at any particular point in time. This presentation will discuss the need for continual examination of ones values and interests, and will provide reference to resources that individuals can use to help them conduct such examination. Identifying one’s skills also requires examination; that is, examination of one’s training and acquired skills, as well as one’s inherent strengths and weaknesses. Furthermore, the identification of one’s skills requires one to think broadly about the capabilities developed to date. This presentation will provide a broad perspective on the transferable skills of PhD-level scientists that should be examined, and will highlight resources available to participants so that they can fully examine their skill set and improve their ability to market those skills to employers in a wide range of career settings. The insight derived from such examination should allow one to make career choices consistent with one’s skills and passions; in turn leading to a life that one feels is worth living. 659 CAREER PLANNING AND DEVELOPMENT FOR EARLY- CAREER SCIENTISTS. D. C. Wolf. ORD/NHEERL, U. S. EPA, Research Triangle Park, NC. Early career development can be looked at as being of two major phases. The first phase is the formal educational process leading to an awarded degree, postdoctoral training, and potentially formal certification in a scientific discipline. The second phase is the informal education of becoming successful in the business of science. During both phases of your early career it is important to prepare yourself educationally to capitalize on an opportunity when it presents itself. Since you cannot predict what the opportunity might be, having a broad understanding of the scientific disciplines with which you will be interacting during your early career is essential. There is plenty of time in your life to become highly specialized, but doing that too early can be too limiting. To maximize your training and early career development it is important to develop good relationships with multiple mentors. These mentoring relationships do not, and should not, always be formal but include people who can provide you with insights and accumulated wisdom from a variety of perspectives. A critical attribute of all successful individuals is their ability to know and understand themselves so that they can honestly assess what strengths and weaknesses they have that could influence their own career development. For some people having a formal Individual Development Plan that provides specific training activities and career goals is effective. The most important thing to remember is that you must take control of your career; you need to seek out mentors as well as mentor others, ask for training in areas you desire to understand, and say yes to opportunities as they arise. [This abstract of a proposed presentation does not represent the views or policies of the U. S. EPA.] 660 IMPROVING NETWORKING AND COMMUNICATION SKILLS. L. Conlan. Office of Intramural Training & Education, NIH, Bethesda, MD. Sponsor: B. Law. Networking is a communication skill that every scientist can, and should, develop. Networking helps you in the job market, can foster collaborations, and builds friendships. Learn how to network using the Internet, departmental seminars, professional meetings, and everyday life. Gain confidence in your ability to create and maintain lasting scientific and personal relationships. Special emphasis will be provided on strategies to help you navigate networking at a large meetings, such as Society of Toxicology, and smaller meetings you may be attending. 661 MAKING YOURSELF MORE MARKETABLE IN PRIVATE INDUSTRY. J. A. Popp. Stratoxon, Lancaster, PA. Numerous and very diverse employment opportunities for toxicologists are available in private industry. These opportunities are located in various industrial sectors such as pharmaceutical, medical devices, chemical, agrochemical and consumer products. Job functions are also very diverse and include “bench” based scientists, safety assessment scientists, management of toxicology programs and risk assessment specialists. The hiring process is generally rigorous with the applicant being interviewed by individuals with extremely varied backgrounds and interests. While scientific expertise is highly regarded, it is strongly considered within the companies needs. Interests and experience outside of immediate specialty training will be highly regarded. Consideration of whether the applicant is likely to fit the “corporate culture” will be considered. Of course the applicant should also be making the same assessment. The hiring manager(s) will be evaluating personal characteristic including interest in working in a team environment, ability to adapt to changing scenarios and openness to new approaches. Demonstration of self confidence, minus arrogance, will certainly have an impact on the hiring decision. Industrial positions should be considered for the opportunities provided and not as a second career choice. Most notably, industrial positions provide the opportunity to “make a difference” and to see the results or impact of the contribution made. 662 THE NIH PATHWAYS TO INDEPENDENCE AWARD: A TRANSITION TO AN ACADEMIC CAREER. C. Shreffler. Division of Extramural Research and Training, NIEHS, Research Triangle Park, NC. Sponsor: S. Nadadur. The NIH Pathways to Independence Award (K99/R00) is the ideal grant mechanism for individuals in a postdoctoral position who wish to pursue an academic career since it provides research grant funding to jump start the research program at 140 SOT 2010 ANNUAL MEETING
the beginning of the academic career. The award is unique among NIH training and career development awards in that it is open to both U. S. Citizens and noncitizens who have postdoctoral appointments at U. S. Institutions. Individuals apply for the K99/R00 while still in the postdoctoral appointment and the award allows the candidate to receive both mentored and independent research support from the same award. Although the research program must have a unifying hypothesis, logical sequence of specific aims to test the hypothesis, and be continuous in time, the application is essentially a composite of two different types of programs, one which is a mentored program and the other which is an independent research effort. This session focuses on the K99/R00 grant program, its provisions and review, and presents tips to address the “hybrid” nature of the application. 663 A POLYMORPHISM IN THE AH-RECEPTOR GENE IS RELATED TO HYPERTENSION AND ENDOTHELIUM- DEPENDENT VASODILATION. L. Lind 1 and M. P. Lind 2, 3 . 1 Acute and Internal Medicine, Department of Medical Sciences, Uppsala University Hospital, Uppsala University, Uppsala, Sweden, 2 Occupational and Environmental Medicine, Department of Medical Sciences, Uppsala University, Uppsala, Sweden and 3 Institute of Environmental Medicine, Karolinska institutet, Stockholm, Sweden. Objectives: Since we previously have shown that a dioxin-like agonist for the aryl hydrocarbon receptor (AHR, Ah- receptor, Dioxin receptor) increases blood pressure, we here examined the relations between single nucleotide polymorphisms (SNPs) in the AHR gene and prevalence of hypertension in a population-based sample. For SNPs related to hypertension, we also evaluated the relation to endothelium-dependent vasodilation (EDV) as a secondary aim. Material: Blood pressure was measured in 1016 men and women, aged 70 in the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study. Hypertension was defined to be prevalent in individuals on antihypertensive treatment or with blood pressure >140/90 mmHg. EDV was measured by acetylcholine infusion in the forearm and venous occlusion plethysmography. Twenty SNPs in the AhR gene were chosen according to data from the HapMap project and they were genotyped using the Illumina Golden Gate assay. Results: Of the 20 SNPs analysed, six showed an association with hypertension with a p-value < 0.05. The strongest association signal was found for the SNPs rs17137566 (p=0.0038 following gender-adjustment), where a dose-response for the number of A alleles and the prevalence of hypertension was seen, with the rare allele being protective against hypertension. This genotype was also related to EDV in the expected way (p= 0.018 following gender-adjustment). Conclusion: The present study showed that genetic variation in the AHR gene is related to hypertension, as well as to endothelium-dependent vasodilatation in resistance vessels, suggesting that the AHR could be involved in blood pressure and resistance vessel regulation. 664 BIOMARKERS AND ONSET OF NON-SPECIFIC BUILDING RELATED SYMPTOMS IN THE DWELLING. A COHORT STUDY FROM 1992 TO 2002. B. G. Sahlberg 1 , D. Norbäck 1 , G. Weslander 1 and C. Janson 2 . 1 Department of Medical Sciences, Occupational and Environmental Medicine, Uppsala, Sweden and 2 Department of Medical Sciences, Respiratory Medicine & Allergology, Uppsala, Sweden. There are many studies on non specific building related symptoms and indoor environment. Most of them are cross-sectional and several deals with occupational environments only a few of them comprise domestic exposures. Our study is based on data from one centre, Uppsala of the European Community Respiratory Health Survey (ECRHS). The ECRHS was a multi-centre population study carried out on subjects aged 20- 44 years in 1992. A smaller random and symptomatic sample of subjects who had completed the screening questionnaire was invited to attend for a more detailed interview-led questionnaire, blood tests for the measurement of total and specific IgE, a skin-prick test, spirometry and methacholine challenge. A follow-up study ECRHS II was carried out in 2000 (N=627). The aim was to investigate changes of symptoms during the follow-up period, also to investigate changes of different types of indoor exposures at home (dampness/mould, painting, ETS and wall to wall carpet) and relate them to symptoms in a population sample of adults from Uppsala, Sweden. We also wanted to investigate relations of biomarkers and indoor exposures at home and new onset of symptoms. Biomarkers study at base line was ECP(eosinophil cationic protein) with a median (M) value of 12.10 μg/l and a inter quartile range(IQR) of 8.36 μg/l – 18.40 μg/l and EOS(eosinophil counts) 150 μg/l (90 - 231) and in the follow-up hsCRP(High-Sensitivity C- Reactive Protein) 1.04ml/l (0.47 - 2.42)and IL-6(Interleukin-6) 8.62 ng/l (5.58 - 10.94). The total levels of serum immunoglobulin E (IgE) was measured at both occasion. The M and IQR was 28.45 IE/ml (11.70 - 80.90) and 35.80 IE/ml (17.40 - 98.60). Our finding provide evidence of an association between biomarkers, dampness in the dwelling and new onset of mucosal membrane symptoms. 665 EPIDEMIOLOGIC EVIDENCE FOR FORMALDEHYDE- INDUCED LYMPHOHEMATOPOIETIC MALIGNANCIES. B. Sonawane, T. Bateson, J. Whalan and D. DeVoney. National Center for Environmental Assessment, U.S. Environmental Protection Agency, Washington, DC. Epidemiologic studies indicate an association between formaldehyde exposure and lymphohematopoietic (LHP) malignancies in a range of occupational cohorts as well as in case-control studies. Early studies reported the strongest associations for all leukemia and for myeloid leukemia as a specific subtype. There has been considerable debate on the biological plausibility of formaldehyde-induced leukemia, specifically for myeloid leukemia. Therefore, available data were analyzed by etiologically-related subtypes in an effort to better understand which disease, or disease groupings, are consistently associated with formaldehyde exposure, thereby providing a better basis for judging biological plausibility. Data from two published cohorts were available for subtype analysis; a study of garment workers (Hayes et al., 1990) and the NCI study of industrial workers (Beane-Freeman et al., 2009). Unadjusted odds ratios for two novel disease groupings are presented for each study: 1) all LHP, less myeloid leukemia (ICD 8 codes 200-204, 206-209), and 2) solid tumors of lymphoid origin (ICD 8 codes 200- 203). For both cohorts, associations between formaldehyde exposure and LHP malignancies (ORs 1.39(1.05- 1.84) and 1.36(1.04-1.78) were retained without myeloid leukemia (ORs of 1.35(0.99-1.85) and 1.30(0.97-1.74) in garment workers and the peak exposure group in the NCI industrial cohort respectively. Similar associations were also found when considering only solid tumors (OR 1.24(0.84-1.84) and 1.32(0.92- 1.89)). These data suggest that observed associations of increased LHP are not due solely to increases in myeloid leukemia as was previously believed. The finding of positive association for the lymphoid subtypes, especially Hodgkin’s Disease, multiple myeloma and other diseases which arise from mature lymphocytes, reframes the debate on the biological plausibility of formaldehyde-induced LHP malignancies. Disclaimer: This abstract does not necessarily reflect EPA policy. 666 ASSOCIATION OF LOW-LEVEL BLOOD LEAD AND BLOOD PRESSURE IN THE NHANES 1999–2006. F. Scinicariello, H. Abadin and E. Murray. Division Tox and Env.Med., ATSDR/CDC, Atlanta, GA. Sponsor: B. Fowler. Background: A relationship between blood pressure (BP) and high level blood lead concentrations has been reported and this relationship appeared to be influenced by the sex and/ or race of the participants. The objective of this study was to evaluate whether low blood-lead levels (BLLs ≤10 μg/dL) were associated with BP among adults aged 20 years and older in the U.S. population. Methods: We analyzed data from NHANES 1999–2006 participants aged 20 years or older who were white non-Hispanic or black non-Hispanic with BLLs ≤10 μg/dL. Outcome variables were systolic and diastolic BP measurements and hypertension status. Results: In multiple regression analyses, BLLs were significantly correlated with higher systolic BP among black men and women, but not white, participants. The change in systolic BP associated with a two-fold increase of blood lead concentration was 1.59 mmHg in black men, and 1.66 mmHg in black women. BLLs were significantly associated with higher diastolic BPs among white men and women and black men, but not among black women. Black men with BLLs between 5.01 and 10 μg/dL had an adjusted prevalence odds ratio of 1.98 (95% CI: 1.11–3.50) to have hypertension compared with black men with BLL
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The Toxicologist Supplement to Toxi
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The Toxicologist Supplement to Toxi
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1 BIOLOGICAL PATHWAY ANALYSIS: AN I
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11 ICH INITIATIVES FOR CONDUCTING P
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models. Experimental approaches and
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30 SILICA AND ASBESTOS IMMUNOTOXICI
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40 NONCANCER TOXICITY POTENTIAL AT
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ased products for patient administr
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nase regulates Hsp27-induced reorga
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exposure resulted in splenomegaly.
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We investigated the effect of imati
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well plate prevented free cell move
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98 DERIVING SIGNATURES OF IN VIVO T
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sulfate, cinnamic aldehyde, 2,4-din
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The final product will be a system
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mercially available STP brands by m
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for six weeks, with 10 mg/kg azoxym
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eceived RES post-TCDD exposure when
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morigenesis. Knocking down of JARID
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163 MICROPET IMAGING OF [18F]-DFNSH
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These results are comparable to tha
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activity as assessed by lever press
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for measured physico-chemical param
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199 DEVELOPMENT OF A MULTIPARAMETER
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To cause PLD, a drug needs to enter
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In contrast to the parent PBDEs and
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transiently transfected HEK 293 cel
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TCDD exposure, 24 h prior to a 20 %
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244 NON-ADDITIVE EFFECTS OF PCB153
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253 COMPARISON OF MIXTURE TOXICITY
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two cerium oxide nanoparticles of v
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271 SIZE-DEPENDENT EFFECTS OF TUNGS
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adigms such as Tox 21 and Toxcast,
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QDs with emission maximum at 800nm
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Cleveland, while others were found
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without the need of animal testing.
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Conclusions: These results are cons
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ing oxime reactivation and organoph
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335 A NON-OXIME IMPROVES SURVIVAL I
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alties suffer from permanent lung i
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ies have established inflammatory b
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363 GENETIC VARIATION IN ISOGENIC M
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372 EVALUATING THE BIOLOGICAL INTER
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dose of 1/20 LD50 (400 mg/kg.bwt) f
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median CR-adjusted isoflavone conce
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data indicate that AhR deletion pro
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Page 95 and 96: tal neurotoxicity (DNT) test (OECD
Page 97 and 98: of selected microorganisms that are
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Page 101 and 102: 446 MOLECULAR CLONING AND CHARACTER
Page 103 and 104: portant in predicting risk. CYPs 1A
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Page 109 and 110: 482 TYPE III DEIODINASE (D3) IS PRO
Page 111 and 112: tancy evaluation and ranking of bat
Page 113 and 114: 501 CHARACTERIZATION OF ESTERASE, G
Page 115 and 116: 510 REDOX CYCLING BY ENDOGENOUS 2-
Page 117 and 118: prostate cancer cells. All 8 BEL de
Page 119 and 120: metallic nickel nanoparticles. Acti
Page 121 and 122: variety of more or less reactive ch
Page 123 and 124: 550 QUALIFICATION STRATEGIES-GENOTO
Page 125 and 126: ferentiation, and 3) how mixtures o
Page 127 and 128: 572 LOW-CHRONIC ARSENIC EXPOSURE: E
Page 129 and 130: 582 IDENTIFICATION OF SENSITIVE URI
Page 131 and 132: duced by the genetic outcross of fe
Page 133 and 134: fects of new compounds are equally
Page 135 and 136: acterize the current state of the s
Page 137 and 138: 620 CHARACTERIZATION OF POTENTIAL I
Page 139 and 140: ways. Moreover, both MAP kinase and
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Page 143: studies such as the NCS, consider h
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Page 153 and 154: 699 PROMUTAGEN ACTIVATION AND P450
Page 155 and 156: oxodG in bone marrow, spleen, kidne
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Page 159 and 160: ment were 18.0 and 4.5 nM for BEAS-
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Page 165 and 166: screening of cell migration. High-c
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Page 169 and 170: mice; the decrease was more pronoun
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Page 173 and 174: 793 PULMONARY RESPONSE, OXIDATIVE S
Page 175 and 176: cilitate clinical and industrial ap
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Page 179 and 180: 821 KIDNEY INJURY MOLECULE-2 GENE D
Page 181 and 182: commercial applications, and have b
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Page 187 and 188: etate (immunotoxicity). 2,4-D was t
Page 189 and 190: 867 MELATONIN AMELIORATES CYCLOPHOS
Page 191 and 192: pharmacokinetic (PBPK) models. Ten
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893 UNVEILING ASSOCIATIONS BETWEEN
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using area under the concentration
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912 COMMERCIAL FISH DIETS INDUCE VI
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922 A STUDY OF PHOTOTOXICITY FOLLOW
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from 0.1 to 2.9 g/L (saturated vapo
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vasive method for assessing several
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950 ARSENITE DOWN-REGULATES THE CAR
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inflammatory signaling is altered b
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treated wood. Seventy-five of 132 w
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ergy homeostasis and raising levels
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treated with mercury and then with
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997 IN VIVO CORRELATES OF THE MANGA
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of the panel. The panel was compris
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sponse, location, and severity scor
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tant source of n-3 fatty acids such
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old for serious, irreversible or es
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1045 SUBCHRONIC TOXICITY EVALUATION
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sites collected 3 days after inject
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1063 MOLECULAR MECHANISM OF OLANZAP
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esponses, and can be available for
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hence more physiologically relevant
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thesized apoproteins, so we tested
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vate CYP3A5 but could be released b
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1108 STYRENE-INDUCED TOXIC EFFECTS
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1118 THE PRESENCE OF DIETHYL FUMARA
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zebrafish cells were first exposed
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utene-1,4-dial, which has been show
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groups, largely due to lower non-HD
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Exposure to gluten in individuals w
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contrast to VGSC activators such as
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1175 70% HYDROFLUORIC ACID (HF) CUT
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axis. An increase in hyaline drople
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1194 esiRNA AND siRNA HIGH-THROUGHP
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1203 ARYL HYDROCARBON RECEPTOR-DNA
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permeability (calcein), mitochondri
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olytic caspase activation, caspase-
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teristics of a human T-type voltage
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80% of the activity from the yellow
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1251 DEVELOPMENTAL EXPOSURE TO DELT
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1260 MANEB ENHANCES MPP + -INDUCED
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demonstrated by knockdown of beclin
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1278 PINK1 AND MITOCHONDRIAL DYNAMI
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treatment for number of live worms.
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1297 INVESTIGATION OF THE NEUROTOXI
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1306 DEVELOPMENT OF AN IN VITRO ASS
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1315 EVALUATION OF 3- AND 1-METHYLH
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prior to kainic acid-induced seizur
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1334 AFFECT OF GENETIC VARIATION ON
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1346 THE OTHER WORLD OF THE TRANSCR
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strate, leading to excess microvesi
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1368 OVERVIEW OF THERAPEUTIC VACCIN
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to a bovine adrenal cortical epithe
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DOTC had no effects. These results
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1398 PULMONARY TOXICITY OF CERIUM D
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PPARα, LXR, ER, AR and AhR activit
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1417 MECHANISM OF GENDER-DIVERGENT
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els, they disrupt homeostatic contr
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were to characterize exposure of th
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1448 ADVERSE OUTCOME PATHWAYS AND E
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the level in urine was 25% of the m
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1;akt-2 double mutant and pdk-1 mut
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jury effects when compared to contr
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tude than equivalent oral doses. Af
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cells; and increased iNOS and MCP-1
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B6.Cg-Kit W-sh mice. These findings
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1511 STATIN-TREATMENT EFFECTIVELY R
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1520 EFFECT OF INHALATION EXPOSURE
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numbers of IFN-γ producing cells w
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These data indicate that TCDD treat
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esponse to allogenic cells, where P
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larly suppressed LPS-induced TNF-α
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1565 INFLUENCE OF EXPOSURE ROUTE AN
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veloping animals to adverse effects
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the observed CL values were 0.07 L/
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which is most relevant for potentia
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tive impairment, suggesting that ox
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1611 AN IN VITRO METABOLOMICS APPRO
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Expression of the β6 integrin (Itg
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ats (10 μg/kg TCDD). Here we repor
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at liver slices and how the metabon
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with gender differences in AUC and
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oxetine (30 mg/kg reduced to 15 mg/
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eleased from necrotic cells where i
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plants, they are present in surface
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ferentiation (quantitative in-cell
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control for macrophage activation).
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to 0.5μg/ml. Minimal inhibitory co
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lines tested. Given that dex and AT
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tion in the absence of an immune re
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treated rats had lower calcium load
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1740 PROFILING COMPOUNDS WITH CARDI
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dothelial cells confirmed caveolin-
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1758 GINKGO BILOBA EXTRACT INDUCES
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arin-induced suppression of MDR1 ex
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1780 ANTIANDROGENIC AND ANTIPROLIFE
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included in the evaluation, most of
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1799 GUIDANCE ON THE APPLICATION OF
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However, substances with EC3 values
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1816 CD-INDUCED EGFR TRANSACTIVATIO
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1826 KERATIN 7 EXPRESSION IN INDEPE
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centa were collected at the time of
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1845 SYSTEMATIC SCREENING OF YEAST
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underlying the development of co-mo
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eing measured in experimental roden
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ufactured in the US for more than 3
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nine (N7-THB-Gua) and N7-hydroxyphe
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1892 EFFECT OF LAMBDA-CYHALOTHRIN O
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22 in Phase I. Antimicrobial pestic
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kinetic and dynamic differences, an
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iphenyl, saccharin and melamine was
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1930 DEVELOPMENT OF A RELATIVE SOUR
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1939 MODE OF ACTION FOR THE CANCER
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human was about 1.5-fold lower (60
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Disruption of BDEC integrity in alp
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1968 A HUMAN HEPG2 LUCIFERASE ASSAY
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in the offspring during tumor devel
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een developed to investigate perfus
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to 131.73 μg/mL for KLH-specific I
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cell lines (ATCC) were cultured in
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flammation and xenobiotic metabolis
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vide many contributions: with its g
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to-metal joint replacement. For exa
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to be addressed or negotiated. Deci
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especially with anti-TNF therapies.
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genic line Tg(are:eGFP) was created
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2074 COMPUTATIONAL ASSESSMENT OF TH
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2084 INHIBITION OF 11β-HSD1 DECREA
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(T) and express several enzymes inv
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2101 GENISTEIN MODULATION OF BLOOD
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males per group were dosed orally o
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ate the feasibility of assessing re
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changed. Hepatic protein carbonyl l
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sought to examine alterations in he
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2147 A SINGLE AMINO ACID CONTROLS T
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Gstm7) was independent of both CAR
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ility of tungsten trioxide (WO3), t
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ured by real-time PCR array and rel
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glucose, and creatinine levels, and
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Several studies have reported suppr
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exposure between TCDD-exposed labor
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Furthermore, with increasing number
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Society of Toxicology 2010 Author I
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Society of Toxicology 2010 Abstract
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49 th Annual Meeting and ToxExpo A
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The Official Journal of the Society
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