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and 1.2 LD50 exposure groups displayed robust signs of nerve agent intoxication and also had cardiac lesions; animals at the 0.6 or 0.8 X LD50 doses showed mild or no signs of intoxication and were free of cardiac damage. Next, rats were challenged with 1.2 X LD50 soman, and different groups of animals were euthanized at progressively longer delays following agent challenge. Plasma obtained at the time of euthanasia was assayed for norepinephrine, epinephrine and troponin, and the heart tissue was prepared with Masson’s trichrome to detect cardiac lesions. The results showed that 15-30 min after nerve agent exposure there were significant increases in epinephrine and norepinephrine levels, but no changes in cardiac troponin levels. At 2-4 hr after intoxication, cardiac troponin levels increased and elevations persisted at least 24 hr after exposure. The differential timing of the catecholamine and troponin increases supports the hypothesis that the release of catecholamines triggers the subsequent cardiac damage. This may result from a direct overstimulation of the sympathetic nervous system by the high levels of acetylcholine. The elicitation of convulsive activity by the nerve agent may be contributory, since only animals that developed pronounced convulsions developed cardiac lesions, whereas animals that displayed no or only minor signs of intoxication all had normal cardiac tissue. 2016 CENTRALLY ACTING THERAPEUTIC ADJUNCTS FOR NERVE AGENT INTOXICATION. I. Koplovitz*, J. H. McDonough and T. Shih. Research Division, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD. The brain is a major target for the toxic action of organophosphorus nerve agents (NA). Two therapeutic approaches were conducted to assess the ability of centrally active therapies to improve treatment outcomes following lethal NA intoxication. One approach was to investigate tertiary oxime (MINA) that can readily penetrate into the brain to determine whether reactivation of central AChE inhibited by NA will increase survival and terminate seizures. The other approach was to evaluate the survival benefit of adding scopolamine (SCP) to current treatment regimens. All studies were conducted in male Hartley guinea pigs exposed s.c. to lethal and seizure-inducing doses of various NA. In reactivation studies, the tertiary oxime was administered 15 min after 1 x LD50 of sarin, soman, cyclosarin, or VR; peripheral tissue, blood and regional brain oxime dose-dependent AChE activity was determined 45 min later. Oxime doses from these studies were used as treatments 1 min after NA with or without atropine (ATS) and/or 2-PAM to assess the influence on 24-hr survival. Various oxime doses were evaluated for antizeizure activity when administered at the time of and up to 40 min after seizure onset. SCP studies were conducted to determine its survival benefit as an adjunct to ATS plus quaternary oxime (2-PAM or MMB-4) treatment administered 1 min after 2 x LD50 of various NAs with or without pyridostigmine (PB) pretreatment. Human relevant doses of SCP, ATS, 2-PAM, and PB were evaluated. Tertiary oxime resulted in dose-dependent increases in AChE activity in the brain, improved survival and terminated seizures. Seizures could be terminated even when the tertiary oxime was administered 40 min after seizure onset. SCP increased survival at 24 hr, which appeared to be dependent on recovery/restoration of AChE activity either through oxime reactivation or decarbamlyation of PB-protected AChE. Both centrally acting oxime and SCP appear to be viable therapeutic approaches as adjunct treatments to mitigate the toxic effects of NA and improve treatment outcomes. 2017 RICIN TOXICITY IN BALB/C 3T3 CELLS: DOSE DEPENDENT PROTEIN EXPRESSION DETERMINED BY MASS SPECTROMETRY BASED PROTEOMICS. V. H. Bevilacqua 1 , S. Deshpande 2 , J. S. Madren-Whalley 3 , R. Jabbour 4 , K. Jones 5 , L. M. Reilly 6 and J. S. Rice 7 . 1 Point Detection Branch, Edgewood Chemical Biological Center, Aberdeen Proving Ground, MD, 2 STC, Edgewood, MD, 3 Biotechnology Branch, Edgewood Chemical Biological Center, Aberdeen Proving Ground, MD, 4 SAIC, Gunpowder, MD, 5 NuSep, Bogart, GA, 6 Physical Science Department, Bethany College, Bethany, WV and 7 Elona Biotechnologies, Inc., Greenwood, IN. Sponsor: J. Sekowski. Ricin has remained a significant potential biological threat agent due in part to its wide availability and ease of extraction from the castor bean. It is a glycoprotein made up of A- and B-chains with the B-chain facilitating transport of the lectin into the cell. Once inside, it kills the cell by inhibiting protein synthesis. Ricin is considered extremely toxic to man by multiple routes of exposure. Proteomics based on mass spectrometry (MS) data can yield biomarker and relative protein expression information for interrogation of physiological changes in toxin-dosed cells. We have analyzed trypsinized cellular protein extracts from BALB/c 3T3 murine fibroblasts dosed with three concentrations of ricin (IC 20 , IC 50 , IC 80 ) and a vehicle control by liquid chromatography tandem MS. Nine hundred proteins were characterized employing bioinformatics methods including in-house (ABOID, Edgewood Chemical Biological Center) and external (ProteoIQ, NuSep) software. Approximately 5% of the observed proteins were common to all dose levels, indi- 432 SOT 2011 ANNUAL MEETING cating that ricin did not affect relative expression of these proteins, while more than 10% of observed proteins were unique to each specific dose level. These results indicate a dose-dependent response of relative protein expression to ricin exposure by 3T3 cells. Ongoing pathway analysis may reveal the survival mechanism for cells dosed at low levels, which in turn will provide insight into the related 3T3 physiological changes required to overcome ricin dosing. Funding: The Edgewood Chemical Biological Center In-House Laboratory Independent Research Program. 2018 ASSESSMENT OF PRO-2-PRALIDOXIME (PRO-2-PAM) THERAPY FOR EXPOSURE TO ORGANOPHOSPHATE AGENTS IN GUINEA PIGS. J. C. DeMar 1 , S. M. Somerville 1 , R. H. Ratcliffe 1 , T. C. Ku 1 , N. M. Nur 1 , B. M. Ursic 1 , S. M. Schulz 2 , K. H. Smith 2 , E. D. Clarkson 2 and R. K. Gordon 1 . 1 Regulated Laboratories, Walter Reed Army Institute of Research, Silver Spring, MD and 2 Medical Toxicology Branch, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD. Novel therapeutics to overcome neuro-toxic effects of organophosphate (OP) agents are needed due to past use in combat and terrorism. Standard exposure therapy includes pralidoxime chloride (2-PAM), which restores OP-inhibited PNS acetylcholinesterase (AChE) activity. Since 2-PAM is charged, it cannot cross into the brain to restore CNS AChE. In guinea pigs, we evaluated the ability of pro-2- PAM, a non-polar pro-drug of 2-PAM, to protect the brain after OP-agent exposure. First, animals were pre-treated with pyridostigmine bromide and then subcutaneously given 1 × LD 50 of the OP-agent diisopropylfluorophosphate (DFP) and treated with pro-2-PAM and PNS acting atropine methyl bromide. Seizure (by EEG radiotelemetry) was alleviated, brain AChE activity (by enzyme assay) was increased, and hippocampal cell death (by histopathology at 24 h post-exposure) was prevented. In contrast, 2-PAM did not afford this protection. Pro-2-PAM reduced DFP-induced brain damage with treatment delays up to 60 min and at recoveries to 7 days. Next, we evaluated pro-2-PAM therapy to the chemical warfare OP-agents soman (GD), VR, and VX. In pyridostigmine pre-treated animals cutaneously exposed to GD, VR, or VX and treated with pro-2-PAM and CNS active atropine sulfate, there was reduced hippocampal damage to 10, 3, and 3 × LD 50 , respectively, at 24 h. Brain AChE activity also increased compared to exposed non-treated controls. 2-PAM, however, did not show similar CNS-protection. In conclusion, pro-2-PAM is a promising therapeutic for treating the detrimental effects of OPagent poisoning in the brain. Support: CounterACT NINDS U01 NS058166-01 and DTRA 1.E0033_07_WR_C. Opinions or assertions contained herein are private views of the authors, and are not to be construed as official or as reflecting views of the NIH, US Army, or DoD. 2019 SULFUR MUSTARD-INDUCED RESPONSES OF AIRWAY AND SKIN IN VITRO. J. Seagrave, W. Weber and G. Grotendorst. Lovelace Respiratory Research Institute, Albuquerque, NM. Sulfur mustard (SM) is a vesicant that has been used in warfare and is a potential threat to civilians either from acts of terrorism or through accidental exposure to abandoned military caches of the chemical. Exposure of the skin produces blisters and slow-healing wounds resulting in scarring, while exposure of the lung causes short-term sloughing of the epithelium and longer term fibrotic responses. Inflammatory responses are also involved. Currently, few useful therapeutic agents are available to ameliorate the adverse reactions to this agent. In vitro models of human tissues could provide faster and more cost-effective screening prior to definitive testing in an animal model. As preliminary model development, we exposed human full thickness models of the skin and airway epithelium (EpiDerm and EpiAirway cultures; MatTek Corp.) to SM vapor or to air. Half of the cultures were then transferred to the appropriate medium and the others were transferred to medium containing approximately 10 million freshly isolated human peripheral blood leukocytes. The cultures were returned to the incubator. After 24 h, the medium was harvested for analysis of matrix metalloproteinase (MMP) activity and cytokines. The cell layers were cut into two parts: one was fixed for histopathology and the other was frozen in lysis buffer. Epithelial sloughing (airway) and microblister formation (dermal) was observed in the SM-exposed cultures. The results showed upregulation of several key cytokines, with some modulation of the responses in cultures with leukocytes during the post-exposure incubations. In many cases, the responses closely mirrored responses in the lungs of rats exposed to SM vapors. MMP activity was increased in the medium as well as the cell lysates of the dermal model. These results provide preliminary information for further development of a relevant model for testing potential therapeutics.
This work was supported by Cooperative Agreement from the National Institute of Neurological Diseases and Stroke, National Institutes of Health [grant number 5U54NS058185-03]. 2020 PREGABALIN REDUCES THE DURATION OF ACUTE SEIZURES INDUCED BY SOMAN EXPOSURE. M. Furtado 1 , F. Rossetti 1 , L. Lumley 2 , M. Addis 1 , M. Moffett 2 , B. Robertson 1 , K. Bailey 1 , S. Chanda 1 , N. Kelley 2 , M. Stone 2 , T. Pak 1 , S. Lichtenstein 1 and D. Yourick 1 . 1 Walter Reed Army Institute of Research, Silver Spring, MD and 2 U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Edgewood, MD. Organophosporous (OP) compounds are acetylcholinesterase inhibitors that constitute a hazard and exposure induces status epilepticus (SE), brain injury and spontaneous recurrent seizures (SRS). Long-term pregabalin treatment delays the occurrence of SRS in the lithium-pilocarpine model, protecting piriform and entorhinal cortex. Pregabalin is also used for the treatment of partial-onset seizures in patients that are nonresponsive to conventional treatments. In this study we tested if pregabalin, in combination with diazepam is effective against OP-induced seizures. Male Sprague-Dawley rats had EEG recorded through telemetry (Data Sciences International) 24 hours/day. Animals were pretreated with HI-6 (125 mg/kg, i.p.) 30 min prior to exposure to soman (110 μg/kg, s.c.) at USAMRICD. Rats were injected with atropine (2 mg/kg, i.m.) one min after exposure and diazepam (10 mg/kg, s.c.) was injected 30 min post SE onset in conjunction with pregabalin (200, 100 and 50 mg/kg i.p.) or vehicle. Animals were euthanized 15 days after exposure and brains were processed for nissl, silver and fluorojade B staining. Electrographic seizures were estimated through the use of a customized MATLAB toolbox (Mathworks, Vers. 7) and confirmed by visual screening. The preliminary findings indicated that animals treated with 200, 100 or 50 mg/kg of pregabalin had termination of initial SE earlier than the control rats (One Way ANOVA, p
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The Toxicologist Supplement to Toxi
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The Toxicologist Supplement to Toxi
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1 BIODEGRADABLE MATERIALS FOR TISSU
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that genetic toxicology data are ge
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well-orchestrated lung inflammation
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scribed in the literature. We have
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years ago). We will illustrate how
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involved in the biodegradation proc
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stem cells but rather a treatment i
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additional compound showed agreemen
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82 COMPARISON OF 3H-THYMIDINE INCOR
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irritants. While in practice these
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alleles are especially vulnerable t
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109 CD4+ T CELL INTRINSIC TNF RECEP
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118 TO STUDY THE SIGNAL TRANSDUCTIO
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PAHs, such as dioxins, are prevalen
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containing substituents and/or hydr
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146 COMPUTATIONAL MODELING FOR QT P
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suggest that the combination of too
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164 TRANSLOCATOR PROTEIN (18 KDA) (
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function as a metal binding protein
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laboratory has demonstrated that NR
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known. The aim of this study was to
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from 5 to 28 days in duration) in e
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positive cells, caspase-3 activatio
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creased level in the 46 kDa preproe
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invasiveness at concentrations repr
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thracene (DMBA,50 μg in acetone, a
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247 CO-CARCINOGENESIS OF N, N- DIET
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sponds to the endosomal dsRNA that
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ODD in both WT (maximum 177% of con
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Lastly, using p53siRNA cells, p53 w
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its receptor Mpl to exert its funct
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294 LOW LEVEL OF LEAD CAN INDUCE PH
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lunar surface presented potential h
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lar about cellular export mechanism
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DNA in the kidney medulla, grandula
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5.00 and 7.50 mg/kg/day by oral gav
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events and carcinogenesis. Here we
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tinization of cells of the hair fol
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358 CHARACTERIZATION OF GENOME-WIDE
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RNAi were also performed to identif
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376 A FUNCTIONAL CROSSTALK BETWEEN
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UGT1A gene induction, while this re
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tivity, specifically peroxisome pro
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and cytotoxic effects; however, its
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histone deacetylase that is necessa
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ment. Paradoxically, buthionine sul
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drug leflunomide and its major (A77
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442 GENE EXPRESSION AND MORPHOLOGIC
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451 INHIBITION OF THE MITOCHONDRIAL
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460 SULFORAPHANE PREVENTS ACETAMINO
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drophilic/lipophilic balance. Other
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pharmacokinetic and toxicological p
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489 USE OF ‘OMICS DATA TO IMPROVE
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498 APPLICATION OF AGE-SPECIFIC ADJ
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507 A DOSE VOLUME TOLERABILITY STUD
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involved the use of an acute inflam
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sorption in the gastrointestinal (G
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(ABC) transporters actively transpo
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545 BEHAVIORAL EFFECTS OF REPIN IN
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a blood pressure phenotype that res
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and inhalation exposure system that
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and lethality associated with these
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position, on vascular reactivity an
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therefore more accurate and reprodu
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commercial chrysotile product that
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elative to their controls. ST-depre
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ats. The majority of the studies fo
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in the China Jintan Child Cohort St
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corneum thickness, cellular epiderm
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645 EVALUATION OF THE IN VITRO EPIS
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654 TCDD ADSORBED ONTO NATURAL AND
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tion revealed no test article-relat
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671 INFLAMMATION AND TISSUE DAMAGE
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model, ethanol was found to inhibit
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689 ENHANCED SUPPRESSIVE FUNCTION O
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NAC + LPS yielded different levels
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707 LIFE-STAGE PBPK MODELS FOR MULT
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downstream of the apical endpoint o
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726 UPDATED ALUMINUM PHARMACOKINETI
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global parameter sensitivity analys
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and renal inflammation induced by 2
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754 PLASMA, URINE, AND TISSUE CONCE
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cently characterized transporter OA
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exposure system was developed from
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lood cell mass and decrease in urin
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practical alternatives to MC in non
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imals dosed with 167 mg/kg THU alon
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and organ weights, clinical signs a
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yet is induced in most bladder and
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830 RISK ASSESSMENT OF THE SPILL: C
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knowledgebase creation. Results are
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852 UNDERSTANDING STRUCTURAL AND PH
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for integrating epidemiology and an
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motor activity, including age of th
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y partial purification of urine (fr
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pacity for self-renewal and may dif
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sue. The depth of our analysis led
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910 IMPLEMENTING CALIFORNIA’S GRE
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concentrations in six tissues and b
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934 THE FDA’S LIVER TOXICITY KNOW
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943 GENOME-WIDE DNA METHYLATION DIF
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membrane localization and subsequen
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trols, respectively. Subtoxic and t
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survival using both smoking regimes
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as non-, weak, moderate, or strong
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988 NNK-INDUCED CYTOKINE ALTERATION
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group (one-way ANOVA, p90 % viabili
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ered as an organ involved in xenobi
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Transport of CPZ across the Caco-2
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estrous cycle and sexual behavior d
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mRNA expression levels. Collectivel
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1043 THE EFFECTS OF ENDOCRINE DISRU
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1052 MONO-2-ETHYLHEXYL PHTHALATE IN
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Results: MC was variable within and
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UtSMCs. Phosphorylation of FoxO1 wa
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nonpregnant and pregnant diabetic m
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1089 PFOA-INDUCED LIVER EFFECTS IN
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events in the liver. AZD9056 was ev
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The peppermint oil caused a concent
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OA did not affect food consumption.
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1126 PERSISTENT DEVELOPMENTAL ARYLH
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1135 BACH2 BINDING TO Prdm1 AS A ME
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The purpose of this project was to
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one marrow. Since Chk1 is an attrac
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1163 THE MRNA AND MIRNA PROFILE OF
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have now compared the IC50 values b
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1181 ELUCIDATION OF FACTORS DETERMI
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enced by pre-exposure to cigarette
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if abnormal PF was associated with
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weight (P=0.016) and small for gest
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portant cause of death, compared to
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posure groups. However, the differe
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Naphthalene is routinely analyzed i
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1245 SEASONAL CHARACTERIZATION OF H
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1255 URINARY T, T MUCONIC ACID LEVE
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modating a reliable data evaluation
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enzoquinone generate ROS and arylat
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teins (e.g. C3, 4, and 5, APOB, VDB
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1293 TRANSFORMING GROWTH FACTOR BET
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mation was decreased to the same le
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1312 EVALUATION OF THE SENSITIVITY
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luted OFR and CRL. Culture media ex
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urinary TCPy levels, blood and brai
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activity. The dose-response curves
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mice, each with 4 dose groups. One
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exposure to both ATR and DACT has a
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third tetratricopeptide repeats (TP
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7d. 28d after TMT injury there was
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subunits. Each cell type was treate
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1394 COMPARATIVE EFFECTS OF METHYLM
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1403 GENOTOXICITY AND PRE-NEOPLASTI
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vated only in high-dose-treated ani
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1421 DOSE-RESPONSE OF NAPHTHALENE-I
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cisplatin; 1.2-, 1.9- and 2.9-fold
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Day 11 and started to recover on Da
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1448 DEVELOPMENT OF A METHOD FOR QU
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1457 GLOBAL GENE PROFILING REVEALS
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cluding mouse and human macrophage,
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model of lung inflammation and host
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1484 NANOTOXICOLOGY AND NANOHEALTH
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throughput in vitro approach was us
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1502 IMMUNOLOGICAL ASPECTS OF AN AN
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(CIA) and the Streptococcal cell wa
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sitizers were 100% concordant among
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1530 MINIMAL RISK LEVELS FOR STYREN
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ical groups in the field of regulat
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vitro with this potentially insect-
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their performance on toxicological
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need for a better understanding of
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1577 AN IN VITRO MODEL SYSTEM FOR A
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gene expression post-transcriptiona
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1595 GENE EXPRESSION PROFILE OF RAT
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to confirm a hepatotoxic property o
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1613 AN INVESTIGATION OF THE CLEARA
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its nuclear translocation was reduc
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were collected from TK animals at d
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egulated targets were selected for
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U/L after tetracycline. Minocycline
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peri-pubertal FasL-/- mice show a d
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showed similar levels of apoptosis
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1676 TWO BIOMARKERS FOR EVALUATION
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motifs selected. This system was ap
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1693 VOC SERUM LEVELS IN THE GENERA
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1702 DOES THE CLOCK MAKE THE POISON
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those with high nickel content are
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isk assessment. However, unique cha
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model of APAP metabolism and glutat
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logically & morphologically similar
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posure, blood chemistry was analyze
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elated to oxidative stress by measu
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Page 435: 2011 IDENTIFICATION OF A NOVEL VX M
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2249 INTERACTION BETWEEN DIETARY SE
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2258 PHARMACOKINETICS, EXCRETION BA
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2267 SENSITIVE AND SPECIFIC FLUORES
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2276 METABOLISM AND DISPOSITION OF
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ment of hypertension in companion a
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for the propyl series can be used f
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2304 IN VITRO EXPOSURE AND EVALUATI
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2313 THE SYNERGISTIC EFFECT OF SODI
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genes that play a crucial role in M
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2330 THE ROLE OF TRANSFORMING GROWT
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ined following up to 96 h continuou
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effect doses obtained with the rat
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diated transcriptional response of
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docrine disruptor activities of EDC
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individuals. Week 6 results were qu
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functionality of photosystem II and
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wild mice (Mus musculus) from areas
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2406 TOXICITY AND BIOACCUMULATION O
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Isocitric acid is the acid in the h
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2425 EFFECTS OF FUMONISINS IN ETHAN
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centration(μg/g) were: 5.1-95.3; 2
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2445 AUTOPHAGY IN DEVELOPMENT: A LI
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sures to inhaled Mn in dust. Nevert
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2466 CRITICAL EVALUATION OF ANIMAL
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elationships predict that resting r
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2489 COMPARATIVE TOXICITY OF BIODIE
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2497 TRANSCRIPTIONAL REGULATION OF
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2506 TOXICOLOGICAL CONSIDERATIONS O
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launched with the aim of developing
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forms mRNA expression levels were a
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2534 CUTANEOUS WOUND HEALING IN THE
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wells (0, 1, 5, 10, 25, 50, 100, an
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2553 AN ORGANOTYPIC MICROLIVER PLAT
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serum-free media. At 24 hrs, the gr
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2572 INCREASED ARSENIC BIOACCESSIBI
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nology to develop improved methods.
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tuna, swordfish, or mako shark (3.5
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nificantly reduce circulating thyro
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grouped into 9 observation periods
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histopathological or biochemical ev
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exhibited a hyperactive phenotype,
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the search of effective drugs for e
Page 571 and 572:
2644 COVALENT BINDING OF 14 C 2-MET
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aries targeting all transcription f
Page 575 and 576:
(p 9 weeks) and CSC phenotype acqui
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2673 IMMUNE-MEDIATED VASCULAR INJUR
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for risk identification and charact
Page 581 and 582:
to control toxicant delivery in tob
Page 583 and 584:
Author Index (Continued) The numera
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Page 587 and 588:
Page 589 and 590:
Page 591 and 592:
Page 593 and 594:
Page 595 and 596:
Page 597 and 598:
Page 599 and 600:
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Page 605 and 606:
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Page 609 and 610:
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Keyword Index (Continued) Arsenite
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Keyword Index (Continued) Covalent
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Keyword Index (Continued) flow cyto
Page 617 and 618:
Keyword Index (Continued) innate im
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Keyword Index (Continued) nanoparti
Page 621 and 622:
Keyword Index (Continued) preservat
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Keyword Index (Continued) Thrombocy
Page 625 and 626:
Toxicological Sciences The Official
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The Toxicologist - Society of Toxicology

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