The Toxicologist - Society of Toxicology

More documents

Recommendations

Info

As a result, single exposure of 0.0125%, 0.0375%, and 0.0625% PHMG-Ph induced inflammatory response with increased proinflammatory cytokines and immune cell infiltration to the lungs, and interestingly, this inflammation did not resolved till the end of the experiments (14 days after instillation). The histopathology showed the both inflammation and pulmonary fibrosis exacerbated at day 14 after exposure in dose-dependent manner. Also PHMG-Ph decreased the total cell number and the CD4+/CD8+ cell proportion in thymus and induced severe medulla reduction based on histopathology data. These observations demonstrated that PHMG-Ph exposed to lung lead to pulmonary inflammation and fibrosis as well as to thymic atrophy. 211 Inhalation of a Spot Welding Aerosol Using an Adhesive Increased Airway Resistance but Not Lung Inflammation. J. M. Antonini, A. Afshari, J. A. Thompson, J. S. Fedan, W. McKinney, T. G. Meighan, M. C. Jackson, B. T. Chen, D. Schwegler-Berry, A. Erdely, D. Frazer and P. C. Zeidler-Erdely. NIOSH, Morgantown, WV. Spot welding (SW) is used in the automotive and aircraft industries where high speed repetitive welding is needed and relatively thin metal sections are welded. Epoxy adhesives are applied as sealers to the seams of the metals that are joined. SW produces complex aerosols composed of both metal and volatile compounds which may cause bronchitis and asthma in workers. The goal was to assess the effect of SW fumes on lung function and toxicity. Male Sprague-Dawley rats were exposed by inhalation to 20 mg/m 3 of SW aerosol in the presence of an adhesive for 4 hr/d x 8 d. Controls were exposed to air. Size distribution of the aerosol as determined by a MOUDI particle impactor was tri-modal with a MMAD of 1.66 μm in the largefine mode, 0.30 μm in the small-fine mode, and 0.01-0.05 μm in the ultrafine mode. Two distinct particle morphologies were observed- a brownish metal particle that predominated in the small-fine particle fraction and a black, glue-like particle that was in the large-fine fraction. The metal fraction was found to be >90% Fe. Significant amounts of volatiles (e.g., benzene, toluene, others) were present, likely produced from the vaporization of the adhesive. At different times after exposure, bronchoalveolar lavage (BAL) was performed to assess lung toxicity. Lung resistance (R L ) was evaluated in a separate set of animals before and after challenge with inhaled methacholine (MCh). Immediately after exposure, baseline R L was significantly elevated in the group exposed to the SW fumes. Basal R L returned to control level by 1 d after exposure. Reactivity to MCh was not affected at any time point after fume exposure. No significant increase in lung inflammation (neutrophil influx) or injury (cytotoxicity and lung epithelial permeability) was observed in BAL fluid at 1 and 5 d after exposure to SW fume. Acute inhalation of SW fumes at occupationally-relevant concentrations may act as an irritant as evidenced by the increased R L but had little effect on toxicity. 212 Cardiopulmonary Health Effects of Traffic-Related Air Pollutants in a Healthy Population. J. E. Mirowsky 1 , R. Peltier 2 , M. Lippmann 1 , L. Griffith 1 , J. Carter 3 , D. Diaz- Sanchez 3 , W. Cascio 3 and T. Gordon 1 . 1 Environmental Medicine, New York University, Tuxedo, NY; 2 Environmental Health Science, University of Massachusetts, Amherst, MA; 3 US EPA, Research Triangle Park, NC. There is emerging evidence that inhaling certain components of ambient particulate matter, specifically traffic pollutants, is associated with adverse health effects. We hypothesized that exposure to air pollution components of diesel exhaust-rich traffic, compared to cars-only traffic, produces greater adverse cardiopulmonary effects. In this case-crossover study, 23 participants were recruited to measure pulmonary function, exhaled NO, blood cytokines, heart rate variability, and blood pressure prior to, immediately after, and 24 hours after intermittent walking along 3 diverse roadways. Exposures lasted for 1.5 hours between June and September in 2011 and 2012, and personal exposures to pollutants were collected. The 3 locations differed by traffic type: the George Washington Bridge (GWB) carries truck and car traffic, the Garden State Parkway (GSP) carries only car traffic, and Sterling Forest, NY (SF) acted as a control location. Levels of PM2.5, PM10, black carbon, elemental carbon, and organic carbon were found to be highest at GWB and lowest at SF for all pollutants measured. The traffic count was similar between GSP and GWB. Using a repeated measures 2-way ANOVA, p-values were generated for time, location, and interactions between time and location. Location was a significant factor for FVC (p = 0.04) and FEV1 (p = 0.05); a significant interaction term for pulse pressure was also observed (p < 0.01). Upon further analysis, systolic and pulse pressures varied significantly amongst locations when comparing the baseline and 24 hr-post measurement, while IL-1β varied amongst locations between the baseline and immediately after exposure. A trend of increasing eNO at the GWB was seen immediately after exposure, but did not reach significance (p = 0.06). These results suggest that acute effects of traffic-related pollution are observed in a small, healthy population; these effects differed by traffic type. 44 SOT 2013 ANNUAL MEETING 213 Ventricular Transcriptional Data Provide Mechanistic Insights into Diesel Exhaust-Induced Attenuation of Cardiac Contractile Response and Blood Pressure. U. P. Kodavanti, V. L. Bass, J. Crooks, B. Vallanat, H. Ren, M. C. Schladweiler, R. F. Thomas, T. Krantz, C. King, C. J. Gordon and A. D. Ledbetter. EPHD/NHEERL/ORD, US EPA, Research Triangle Park, NC. Human exposure to diesel exhaust (DE) has been associated with cardiovascular impairments however the mechanisms and the role of hypertension are not well understood. We have shown that DE reduces blood pressure (BP) and cardiac contractility in healthy normotensive Wistar Kyoto (WKY) rats. We hypothesized that DE would induce differential myocardial gene expression changes that modulate contractility in WKY and spontaneously hypertensive (SH) rats, and that lowering BP in WKY and SH with hydralazine (HYD) would increase this effect of DE. Male WKY and SH rats were treated with HYD (150 mg/L) in drinking water for 10 days prior to exposure and until necropsy. All rats were exposed to clean air or freshly-generated whole DE (1500 μg/m3), 5-hrs/day for 2-days. Systolic BP was monitored using the tail-cuff method on days -10, 0, and 2. Left ventricular genome-wide expression was analyzed using Illumina RatRef-12 BeadChips. As expected, WKY and SH rat’s ventricular gene expression patterns differed markedly. Surprisingly, DE exposure caused differential expression of 256 genes in WKY but none in SH rats. In WKY rats, the effect of HYD on expression patterns were nearly identical to changes induced by DE (same genes with same directional change); while HYD was without effect on expression changes in SH rats despite lowering BP. Genes inhibited by DE or HYD in WKY were induced at baseline in SH and vice versa. These genes inhibited by DE and HYD were related to sequestration of oxidants, inhibition of proteases, and membrane stability. The genes upregulated by DE and HYD in WKY included those involved in decreasing BP and muscle contraction as well as calcium homeostasis and apoptosis. In conclusion, acute DE exposure caused gene expression changes only in normotensive WKY rats; these changes mimicked those induced by HYD and are associated with decreased cardiac contractility and BP in healthy rats. (Abstract does not reflect USEPA policy) 214 Comparative Cardiopulmonary Toxicity of Soy Biofuel and Diesel Exhausts in Healthy and Hypertensive Rats. M. C. Schladweiler 1 , V. L. Bass 1 , R. F. Thomas 1 , J. E. Richards 1 , D. Johnson 2 , D. L. Andrews 4 , A. Nyska 3 , T. Krantz 1 , C. King 1 and U. P. Kodavanti 1 . 1 EPHD/NHEERL/ORD, US EPA, Research Triangle Park, NC; 2 Curriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC; 3 Tel Aviv University, Tel Aviv, Israel; 4 RCU/NHEERL/ORD, US EPA, Research Triangle Park, NC. Increased use of renewable energy sources raise concerns about health effects of emissions from such sources. We conducted a comprehensive analysis of relative cardiopulmonary health effects of exhausts from 1) 100% soy biofuel (B100), 2) 20% soy biofuel + 80% low sulfur petroleum diesel (B20), and 3) 100% petroleum diesel (B0) in rats. Normotensive Wistar Kyoto and spontaneously hypertensive rats were exposed to these 3 exhausts at 0, 50, 150 and 500 μg/m3, 4 h/day for either 2d or 4 wk (5 d/wk) to mimic near environmental concentrations. Additionally, WKY rats were exposed for 1d and responses were analyzed 0 hr, 1d or 4d later for time course analysis. Hematological parameters, in vitro platelet aggregation, bronchoalveolar lavage fluid (BALF) markers of pulmonary injury and inflammation, ex-vivo aortic ring constriction, heart and aorta mRNA markers of atherogenesis, and serum biomarkers of acute cardiac injury as well as cytokines were analyzed. The presence of pigmented macrophages in the lung alveoli was clearly evident with all 3 exhaust exposures. Overall, exposure to all 3 exhausts produced only modest effects in most endpoints analyzed in both rat strains. BALF γglutamyl transferase (GGT) activity was the most consistent marker shown to be increased in both strains with all 3 fuels (B0>B100>B20) without increases in BALF neutrophils. Small inconsistent changes in aorta mRNA markers of inflammation, vasoconstriction and thrombosis, and those of serum biomarkers need to be interpreted cautiously. Our comparative evaluations show modest cardiovascular and pulmonary effects at low concentrations of all exhausts. Additionally, our study highlights the value of BALF levels of GGT activity as the most sensitive biomarker in low level inhalation studies. (This abstract does not represent USEPA policy).
215 Acute and Delayed Effects of Intermittant Ozone on Cardiovascular and Thermoregulatory Responses of Young and Aged Rats. A. F. Johnstone 1 , R. C. MacPhail 1 , C. Aydin 2 and C. J. Gordon 1 . 1 TAD, NHEERL, US EPA, Research Triangle Park, NC; 2 Physiology, University of Uludag, Bursa, Turkey. Ozone (O3) is associated with cardiovascular and respiratory diseases. The aged population is considered to be more sensitive to air pollutants but relatively few studies have demonstrated increased susceptibility in animal models of aging. To study the acute and delayed physiological responses to O3, core temperature (Tc) and heart rate (HR) monitored by telemetry in adult (12 m) and senescent (24 m) Brown Norway rats exposed to intermittent O3 (1.0 ppm, 6 hr/d for 2 consecutive d for 12 wk). Tc and HR dropped precipitously in both age groups during the 1st bout of O3 exposure; Tc decreased from ~38 to ~35 °C while HR decreased from ~300 to ~175 b/min. These acute responses were attenuated during the 2nd day of O3. As O3 exposures continued, the acute Tc and HR responses abated but the aged animals were consistently less affected than the young adults throughout the 12 wk exposure period. During 5 d of recovery in home cages, both young and senescent rats displayed a fever-like ~0.5 °C elevation in daytime Tc. HR was also elevated in the young adults during recovery. The rise in Tc persisted for 2-3 d after O3. The O3-induced fever was marked following the 1st exposure, abated by the 3rd exposure week but then gained in magnitude throughout the remainder of the study. We postulate that inflammatory responses of the respiratory system to O3 are exacerbated in younger animals, leading to accentuated acute physiological responses compared to that of senescent rats. This is an abstract of a proposed presentation and does not reflect US EPA policy. 216 Dose and Effect of Inhaled Ozone in Resting versus Exercising Human Subjects: Comparison with Resting Rats. G. E. Hatch, J. McKee, J. S. Brown, B. McDonnell, E. Seal, J. Soukup, R. Slade, K. Crissman and R. B. Devlin. Environmental Public Health Division, US EPA, Research Triangle Park, NC. Rationale: Human controlled exposure studies have generally focused on subjects exposed to ozone (O 3 ) while exercising. We exposed resting subjects to labeled O 3 ( 18 O 3 , 0.4 ppm, for 2 hr) and compared O 3 dose and effects with our previously published study of exercising subjects. Methods: We measured O 3 dose as the concentration of 18 O in cells and extracellular material of nasal, bronchial and bronchoalveolar lavage fluid (BALF) immediately post exposure and related these measurements to O 3 effects on inflammation, epithelial permeability and phagocytosis in the same fluids and to breathing parameters measured during the 18 O 3 exposure. A parallel study of resting subjects examined FEV 1 changes during and immediately following a 2 hr exposure to 0.18, 0.25, 0.3 and 0.4 ppm O 3 . Results: Subjects exposed while resting had 18 O concentrations in BALF and nasal lavage that were proportional to the amount of air breathed during exposure. Significant but small changes were observed in BALF total cells and neutrophils and in BALF cell phagocytosis following resting O 3 , however, most indicators of O 3 effects that were observable in exercising subjects (including increased BALF supernatant protein, lactate dehydrogenase, interleukin-6 and low molecular weight antioxidants) were not observed in resting subjects. The 18 O incorporation into BALF of resting humans was similar to that of similarly exposed resting F344 rats. FEV 1 changes in resting human subjects showed a much attenuated response compared to exercising subjects. Conclusions: Quantitative measures of alveolar O 3 dose and toxicity that were observed previously in exercising subjects were greatly reduced or non-observable in O 3 exposed resting subjects. Resting rats and resting humans have similar alveolar O 3 dose. Disclaimer: This abstract does not represent E.P.A. policy. 217 Biological Responses in Rats Exposed to Mainstream Smoke from a Heated Cigarette Compared to a Conventional Reference Cigarette. H. Fujimoto 1 , H. Tsuji 1 , I. Fukuda 1 , T. Nishino 1 , M. K. Lee 2 , R. Renne 3 and H. Yoshimura 1 . 1 R&D Group, Japan Tobacco Inc., Yokohama, Japan; 2 Scientific and Regulatory Affairs, Japan Tobacco International S.A, Geneva, Swaziland; 3 Roger Renne ToxPath Consulting, Sumner, WA. The heated cigarette (HC) generates mainstream smoke (MS) primarily by vaporizing the components of the tobacco rod using a carbon heat source at the cigarette tip. Consequently, MS of HC contains markedly less chemical constituents compared to conventional (combusted) cigarettes. In this study, MS from a non-ventilated HC (nvHC) was generated under a modified Canadian Intense Regimen (CIR) and its biological activities were compared to those of Reference (3R4F) cigarettes, using nose-only inhalation studies. In a 5-week inhalation study, female SD rats were exposed to MS of either cigarette at 600 or 1000 μg wet total particulate matter (WTPM) /L for 1 hr, 2 times/day, 7 days/week for 5 weeks. Pulmonary inflammation was significantly weaker in nvHC groups compared to 3R4F groups, based on the neutrophil counts and deviation enzyme levels in bronchoalveolar lavage fluid (BALF). After a 4-week recovery, BALF parameters of nvHC groups were similar to the air-exposed Sham group, while those of 3R4F groups remained elevated. In a 13-week inhalation study, male and female SD rats were exposed to MS from each cigarette at 200, 600, or 1000 WTPM μg/L for 1 hr/day, 7 days/week for 13 weeks. Histopathological changes in the respiratory tract were significantly lower in incidence/severity for nvHC groups, especially in respiratory epithelial hyperplasia and accumulation of pigmented macrophages in alveoli. After a 13-week recovery, the lesions were completely or partially regressed, except for accumulation of pigmented macrophages in alveoli, in both nvHC and 3R4F groups. In conclusion, nvHC demonstrated clearly and significantly lower biological activities compared to 3R4F, based on the BALF parameters and histopathology. 218 A Cross-Regulatory T Cell Response in Pulmonary Hypertension. G. Grunig, W. Chen, C. Hoffman, T. Gordon and S. Park. NYU Medical Center, Tuxedo, NY. Exposure to urban air pollution (fuel emissions, particulate matter) has been associated with the exacerbation of autoimmune diseases. Our studies are focused on the mechanism of immune response induced pulmonary hypertension. We have shown that co-exposure of mice to inhaled antigen and urban particulate matter (PM) exacerbates pulmonary arterial remodeling and induces pulmonary hypertension. The current studies were performed with neutralizing anti-cytokine antibodies to identify the critical mediators for pulmonary hypertension and the interactions in the mediator-network. Sensitized mice were intranasally challenged with either antigen (Ovalbumin) combined with urban PM2.5 (collected in New York City), or given saline. Groups of mice were injected with neutralizing anti-Interleukin (IL)-13, or anti-IL-17A/F antibodies alone or in combination, or control antibody. Right ventricular systolic pressures and immune response markers in the lungs were measured. Intranasal challenge with antigen and urban PM significantly increased right ventricular systolic pressures. Only combined, but not single, injections with IL-13and IL-17A/F-blockers significantly reduced this outcome. Surprisingly, injections with single neutralizing antibodies not only significantly reduced the inflammatory markers known to be regulated by IL-13 or IL-17A/F, but also revealed cross-inhibition of these markers. For example, the increased expression of the antigen presentation molecule, major histocompatibility class II (MHCII), by airway dendritic cells was inhibited by the IL-13 blocker given alone or in combination, while the IL-17A/F blocker lead to an increase in MHCII expression. Conversely, infiltration of the airways with neutrophils was inhibited by the administration of the IL- 17A/F blocker given alone or in combination, while injections with the IL-13 blocker increased neutrophil influx. In conclusion, exposure to antigen and urban PM induced pulmonary hypertension by elaborating a mixed immune response that has at least two, crossregulatory arms that are controlled by IL-13 and IL-17A/F, respectively. 219 Capsule-Based Aerosol Generator (CBAG)—Validation in a Rat Model of LPS-Induced Nonallergic Pulmonary Inflammation. S. Jordan, S. Moore and R. Armstrong. Huntingdon Life Sciences, Huntingdon, United Kingdom. Sponsor: E. Moore. Intratracheal (IT) insufflation is the principal method of delivery of inhaled drug substances to conscious non-clinical species in early drug development; however, this achieves particulate deposition dissimilar to conscious inhaled delivery and can produce artefactual toxicological and pharmacological results. The CBAG was developed(1) as an alternative to IT insufflation whilst providing representative inhalation exposure by demonstrating the effectiveness of the CBAG in the rat model of LPS-induced non-allergic airway inflammation. Rats were exposed to 0.01, 0.1 or 1.0 mg/kg of inhaled fluticasone propionate (FP) over a 20-minute period using nominally 1 mg filled hydroxypropyl methyl cellulose size 2 capsules at blend strengths of 1, 10 and 100% w/w of FP respectively. Two concurrent control groups were exposed to lactose only using the same regime. Twenty minutes after the end of the inhalation exposure the animals were challenged with either aerosolised LPS (0.1 mg/mL) for the FP groups and one control group or 0.9% w/v saline (second control group) for 30 minutes. Rats were euthanized 4hrs following the challenge SOT 2013 ANNUAL MEETING 45
Page 1 and 2: The Toxicologist Supplement to Toxi
Page 3 and 4: The Toxicologist Supplement to Toxi
Page 5 and 6: 1 A Refresher of Immunoglobulin and
Page 7 and 8: 12 Understanding Toxic Neuropathy i
Page 9 and 10: SWCNTs (raw FeSWCNT or purified cSW
Page 11 and 12: 34 Computational Systems Biology Mo
Page 13 and 14: driving allergic airway response, c
Page 15 and 16: E100, E0 vapors caused no overt mat
Page 17 and 18: in heart rate, blood pressure, brea
Page 19 and 20: hearts showed a coronary artery dis
Page 21 and 22: inducible NADPH oxidase dependent m
Page 23 and 24: 93 Simulated Metabolism in the Lang
Page 25 and 26: (female pubertal assay, OPPTS 890.1
Page 27 and 28: 112 Endocrine Disruption Potential
Page 29 and 30: The incorporation of in vitro data
Page 31 and 32: was validated by the following resu
Page 33 and 34: 139 A Systematic Analysis of ToxCas
Page 35 and 36: 148 Mucosa-Associated Enteropathoge
Page 37 and 38: 158 The Cannabinoid WIN 55, 212-2 D
Page 39 and 40: signaling. ARNT is expressed as two
Page 41 and 42: 177 Modifying Effect of Glycidol Fa
Page 43 and 44: 24 and 72 hours post treatment. We
Page 45 and 46: line and the effects of the haploty
Page 47: organ weight, gross findings, or hi
Page 51 and 52: 224 Interaction of Human Bronchial
Page 53 and 54: espiratory and olfactory mucosal le
Page 55 and 56: hyperresponsiveness to MCh aerosol
Page 57 and 58: shown that the collagen content is
Page 59 and 60: fect is consistently higher in male
Page 61 and 62: surrogate) in the presence or absen
Page 63 and 64: of field controls were 46.3 ± 5 μ
Page 65 and 66: 290 Interpretation of Multiroute Da
Page 67 and 68: 18.8 ml/min/kg) were more similar t
Page 69 and 70: Urinary excretion at 72 h post admi
Page 71 and 72: into a physiologically based pharma
Page 73 and 74: 327 Cytochrome P450 Gene Transcript
Page 75 and 76: (LD50 = 25 μM). Both pre- and post
Page 77 and 78: 345 Prediction of Human Equivalent
Page 79 and 80: only remnants, including utriculi a
Page 81 and 82: 363 MicroRNA Microarray Analysis of
Page 83 and 84: 371 Mechanisms of Vesicating Agent
Page 85 and 86: 381 Effect of Asbestos Exposure on
Page 87 and 88: PCB126 at doses of 0.1; 1 or 10μg/
Page 89 and 90: 399 Immunotoxicity of the Nasal Ass
Page 91 and 92: 407 The Dermal Exposure to Silica N
Page 93 and 94: 416 Exposure to Triclosan Augments
Page 95 and 96: ventilation. Two independent method
Page 97 and 98: the German Federal Ministry of Educ
Page 99 and 100:
443 Sonolytic Degradation of Pluron
Page 101 and 102:
mice were anesthetized and lungs an
Page 103 and 104:
mulations propelled the development
Page 105 and 106:
fluorophore was removed by ultrafil
Page 107 and 108:
The objective of this study was: (1
Page 109 and 110:
489 Preliminary Toxicokinetics of N
Page 111 and 112:
were twice as much susceptible to d
Page 113 and 114:
improve the fit to the available in
Page 115 and 116:
lead to i) a significant reduction
Page 117 and 118:
(CYP1A1). Induction of this enzyme
Page 119 and 120:
We have described a role for miRNAs
Page 121 and 122:
individual treatment. Both compound
Page 123 and 124:
554 Toxicogenomic Analysis of Envir
Page 125 and 126:
563 Global Gene Expression Changes
Page 127 and 128:
572 Preliminary Steps in a Whole Mi
Page 129 and 130:
581 Chemical Characterization of Co
Page 131 and 132:
fungicides. Studies indicated that
Page 133 and 134:
of the used soil. Mortality and som
Page 135 and 136:
from repeated doses, and the utilit
Page 137 and 138:
618 Use of a Physiologically-Based
Page 139 and 140:
emained as such through 24 hours po
Page 141 and 142:
number of hepatic neutrophils remai
Page 143 and 144:
human PRL (150 ng/ml) or human PL (
Page 145 and 146:
time and Nrf2 -dependent increase i
Page 147 and 148:
664 Hepatic Flavin-Containing Monoo
Page 149 and 150:
673 Hypoxia Perturbs PCB-Induced Ar
Page 151 and 152:
factor tool predicted the activatio
Page 153 and 154:
to 50 μM Cd for 4 or 8 hours. Glob
Page 155 and 156:
701 Reprogramming of the HepG2 Geno
Page 157 and 158:
a process that was tested using di(
Page 159 and 160:
a. Integrated Mode-of-Action (MoA)
Page 161 and 162:
MitoPark mice also showed a dramati
Page 163 and 164:
738 Human Antibodies Can Cross Guin
Page 165 and 166:
Based on an initial 2 day dose-resp
Page 167 and 168:
non-invasive methodology to measure
Page 169 and 170:
768 Air Quality Impacts of Natural
Page 171 and 172:
pathology by disrupting the normal
Page 173 and 174:
pathways. Through these activities
Page 175 and 176:
Approval of the Medical Research Et
Page 177 and 178:
ile duct hyperplasia and hepatocell
Page 179 and 180:
degradation enzymes, matrix metallo
Page 181 and 182:
825 Image-Derived Models of Subcell
Page 183 and 184:
used a number of strategies to mani
Page 185 and 186:
ange of the population. It is gener
Page 187 and 188:
858 Flexible and Transparent Comput
Page 189 and 190:
available tool that provides a foun
Page 191 and 192:
876 Web-Based Benchmark Dose Modeli
Page 193 and 194:
885 A Mechanistic Approach to Under
Page 195 and 196:
observed pharmacokinetic difference
Page 197 and 198:
Funding: EU-FP7 (ENFIRO; grant agre
Page 199 and 200:
913 Protective Role of Carnosine Ag
Page 201 and 202:
measurable neurobehavioral endpoint
Page 203 and 204:
For the TLDA- derived PCR data, a m
Page 205 and 206:
samples within each group, strongly
Page 207 and 208:
950 Smoking-Induced microRNA Change
Page 209 and 210:
IL-1α. This approach has been adva
Page 211 and 212:
969 Collaborative Project in JCIA f
Page 213 and 214:
977 Predicting Eye Irritation of Ag
Page 215 and 216:
organophosphates, organochlorines,
Page 217 and 218:
996 Does the Barker Hypothesis Appl
Page 219 and 220:
1005 Effects of Di(2-Ethylhexyl)-Ph
Page 221 and 222:
compared to single housing. In conc
Page 223 and 224:
1023 Hyperactivity of Rat and Mouse
Page 225 and 226:
1 and Rho kinase inhibitor (HA1077)
Page 227 and 228:
and subcutaneous and/or dermal infl
Page 229 and 230:
inding in the liver, which involves
Page 231 and 232:
tion, glycolysis, and amino acid me
Page 233 and 234:
was isolated from frozen samples, a
Page 235 and 236:
1079 MicroRNA Regulation of Alcohol
Page 237 and 238:
an inducer of hyperglycemia) to cha
Page 239 and 240:
1097 Deletion of Hepatocyte Nuclear
Page 241 and 242:
study, we validated this short-term
Page 243 and 244:
ferentiation and glucose metabolism
Page 245 and 246:
tients treated with desipramine, th
Page 247 and 248:
from mesenteric and uterine vascula
Page 249 and 250:
Akt2 function preservation. For mec
Page 251 and 252:
1152 Serum and Hepatic Alkaline Pho
Page 253 and 254:
fold) with a dissociation constant
Page 255 and 256:
1171 Fin Whale Cells Are More Resis
Page 257 and 258:
develop analytical means to measure
Page 259 and 260:
and location of ROS, and 2) cell an
Page 261 and 262:
25% of patients receiving Imatinib
Page 263 and 264:
lesions originate from is not clear
Page 265 and 266:
Our analysis detected and corrected
Page 267 and 268:
and APC. Results: Etirinotecan pego
Page 269 and 270:
to the amount of fecal contaminatio
Page 271 and 272:
1243 A High-Throughput Analytical M
Page 273 and 274:
1252 Using Doubly-Labeled Water Ene
Page 275 and 276:
implying that BPA is toxic to human
Page 277 and 278:
1271 The Aryl Hydrocarbon Receptor
Page 279 and 280:
1280 Aryl Hydrocarbon Receptor (AhR
Page 281 and 282:
genes, suggesting a role for AHRRa
Page 283 and 284:
and cellular proliferation. Underst
Page 285 and 286:
1307 Toxicological Evaluation of th
Page 287 and 288:
in blood as confirmed by a componen
Page 289 and 290:
activation of scavenger receptor B
Page 291 and 292:
AgNPs in dilutions of an environmen
Page 293 and 294:
after dosing for TEM analysis. Imag
Page 295 and 296:
various cell-lines. However, the da
Page 297 and 298:
and the presence of leukocytes and
Page 299 and 300:
1374 PCB 95 and IFN-gamma Exert Opp
Page 301 and 302:
on estrogens. It is not known how t
Page 303 and 304:
cell number, was reduced at PND10,
Page 305 and 306:
1402 Repeated Exposure to Paraquat
Page 307 and 308:
weeks (3 injections/week). We recor
Page 309 and 310:
1421 Differential Antagonism of Tet
Page 311 and 312:
of the syringe suggesting loss due
Page 313 and 314:
1439 Interleukin 17 Responses Induc
Page 315 and 316:
strains were exposed in triplicate
Page 317 and 318:
1458 An In Vitro Placental Model Us
Page 319 and 320:
Phagotest® (Glycotope Biotechnolog
Page 321 and 322:
1477 Use of An In Vitro Flow Cytome
Page 323 and 324:
1487 Evaluation of Genotoxicity of
Page 325 and 326:
commonly used in textile industry.
Page 327 and 328:
under hamster S9-activated and non-
Page 329 and 330:
neutrophilic to eosinophilic respon
Page 331 and 332:
1524 The Palmitoylation of Meh1, a
Page 333 and 334:
for Dark, Pb afforded 0.607 mg/kg f
Page 335 and 336:
to 5.4 or 54.1 mg/m3, respectively)
Page 337 and 338:
1552 Body-Residue Based Environment
Page 339 and 340:
1561 Identifying No Observed Effect
Page 341 and 342:
studies/endpoints led by academic i
Page 343 and 344:
1580 In Vitro Episkin Skin Corrosio
Page 345 and 346:
RXR, opening the possibility that t
Page 347 and 348:
1601 Enhanced Susceptibility of Fat
Page 349 and 350:
potential to impact the safety asse
Page 351 and 352:
A dataset of over 200 compounds cov
Page 353 and 354:
that link in vivo outcomes (includi
Page 355 and 356:
in humans, occurring in eight newbo
Page 357 and 358:
novel mechanisms of action where th
Page 359 and 360:
their homes, learn about historic a
Page 361 and 362:
toxicology where Tox-21c could have
Page 363 and 364:
compounds and Colcemide as an aneug
Page 365 and 366:
dose dependent increases (p< 0.05)
Page 367 and 368:
1707 Dose Response and Temporality
Page 369 and 370:
several cells, including cancer cel
Page 371 and 372:
1727 Characterization of Cigarette
Page 373 and 374:
1736 Coating Nanoporous Alumina: Ce
Page 375 and 376:
1745 Comparison of Toxicity of Bare
Page 377 and 378:
using microscopy, cytotoxicity test
Page 379 and 380:
ona, and 1.8 folds lower than the d
Page 381 and 382:
RESULTS: Electronic microscopy stud
Page 383 and 384:
effect of its flavonolignans. Becau
Page 385 and 386:
These results suggest that mollugin
Page 387 and 388:
m266.2 were not different from thos
Page 389 and 390:
and associated drug accumulation, w
Page 391 and 392:
1820 Application of Canine Kidney T
Page 393 and 394:
1829 Effect of Body-Weight Loading
Page 395 and 396:
mechanisms of cell death, we invest
Page 397 and 398:
post-translational modifications of
Page 399 and 400:
as oxidative stress, Ca2+ dysregula
Page 401 and 402:
studies assessing cognitive and mot
Page 403 and 404:
spine density of hippocampal pyrami
Page 405 and 406:
individually or in combinations, in
Page 407 and 408:
1893 A Comparative Study on Renal T
Page 409 and 410:
same hand and between washed and no
Page 411 and 412:
1911 Molecular, Cellular, and Histo
Page 413 and 414:
1920 Endocrine Modulatory Effects o
Page 415 and 416:
CYP19 mRNA levels were observed wit
Page 417 and 418:
males and females. In efforts to bl
Page 419 and 420:
worker’s capacity to adapt to hea
Page 421 and 422:
from different studies indicates th
Page 423 and 424:
1966 Associations between Carcinoge
Page 425 and 426:
1975 Assessment of the Impacts of C
Page 427 and 428:
For this analysis, nine PCBs with d
Page 429 and 430:
1993 PBDE-100 Induces Mitochondrial
Page 431 and 432:
2002 Cyp1b1-Deficiency Alters Struc
Page 433 and 434:
enzymes and xenobiotic transporters
Page 435 and 436:
protected against p-aminophenol (PA
Page 437 and 438:
status has shown much promise. Howe
Page 439 and 440:
esidues in proteins. The significan
Page 441 and 442:
where no peak (same action througho
Page 443 and 444:
were exposed to ethyl-alcohol via t
Page 445 and 446:
2066 Validation of a 7-Color Flow C
Page 447 and 448:
tive and detoxification genes. In a
Page 449 and 450:
activated B cells and BCL-6, a tran
Page 451 and 452:
later time points. Therefore, BPA e
Page 453 and 454:
2102 Brominated Diphenyl Ether-47 I
Page 455 and 456:
distribution and excretion or other
Page 457 and 458:
serum Inhibin B was never changed.
Page 459 and 460:
2130 Structural Changes in Various
Page 461 and 462:
Methods: Adult male Fisher 344 rats
Page 463 and 464:
asked what genes are involved in Me
Page 465 and 466:
study examined whether combined Pb+
Page 467 and 468:
elated to dried blood spots and mas
Page 469 and 470:
15(R) D2 increased by 3.3 / 2.3-fol
Page 471 and 472:
otic transcription factors nuclear
Page 473 and 474:
genes. On the other hand, the creat
Page 475 and 476:
2203 Resistance to Dioxin-Induced H
Page 477 and 478:
data because the human data were no
Page 479 and 480:
odent cancer bioassay of MTBE in dr
Page 481 and 482:
(BMCL) estimates were extrapolated
Page 483 and 484:
outcomes which differ from those ou
Page 485 and 486:
2250 Validation of the Yeast Estrog
Page 487 and 488:
in cell index, indicative of cytoto
Page 489 and 490:
platform maybe most appropriate for
Page 491 and 492:
200, 1000, or 2000 parts per billio
Page 493 and 494:
2288 Paradoxical Effects of Ongoing
Page 495 and 496:
for intracellular tracking of GR us
Page 497 and 498:
2306 Evaluating Arsenic Speciation
Page 499 and 500:
2316 Integrative Toxicopathological
Page 501 and 502:
improve food safety is to reduce ex
Page 503 and 504:
ased on human oral challenge studie
Page 505 and 506:
2344 The Global Burden of Disease C
Page 507 and 508:
HDACs had opposite effects, suggest
Page 509 and 510:
useful in human health risk assessm
Page 511 and 512:
1.7% in mucosal side. These results
Page 513 and 514:
2381 Silica Nanoparticles Induce Ac
Page 515 and 516:
have been well-demonstrated to be o
Page 517 and 518:
2400 Fibrinogen: A New Kid on the B
Page 519 and 520:
all critical factors. Vital organ s
Page 521 and 522:
identifying QSARs that are applicab
Page 523 and 524:
after the training, and the percent
Page 525 and 526:
sham control group was included to
Page 527 and 528:
after 15 min incubation with the C8
Page 529 and 530:
2462 Nonhuman Primate Sexual Maturi
Page 531 and 532:
2472 Modeling Human Genetic Variabi
Page 533 and 534:
two subgroups, hippocampus were dis
Page 535 and 536:
2495 Physiologically-Based Pharmaco
Page 537 and 538:
plexes with important functional gr
Page 539 and 540:
Notes SOT 2013 AnnuAl MeeTing 535
Page 541 and 542:
Author Index (Continued) B Baan, R
Page 543 and 544:
Author Index (Continued) Cassis, L
Page 545 and 546:
Author Index (Continued) Dodmane, P
Page 547 and 548:
Author Index (Continued) Gilpin, S
Page 549 and 550:
Author Index (Continued) Huh, G 18
Page 551 and 552:
Author Index (Continued) Krantz, Q
Page 553 and 554:
Author Index (Continued) Martin, S
Page 555 and 556:
Author Index (Continued) Niklas, J
Page 557 and 558:
Author Index (Continued) Rana, P 2
Page 559 and 560:
Author Index (Continued) Shin, K 6
Page 561 and 562:
Author Index (Continued) Touissant,
Page 563 and 564:
Author Index (Continued) Wormser, U
Page 565 and 566:
Abstract Keyword Index (Continued)
Page 567 and 568:
Page 569 and 570:
Page 571 and 572:
Page 573 and 574:
Page 575 and 576:
Page 577 and 578:
Page 579 and 580:
e O cial Journal of the Society of
show all

The Toxicologist - Society of Toxicology

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?