@article{judson_houck_martin_richard_knudsen_shah_little_wambaugh_setzer_kothya_et al._2016, title={Analysis of the effects of cell stress and cytotoxicity on in vitro assay activity across a diverse chemical and assay space}, volume={152}, number={2}, journal={Toxicological Sciences}, author={Judson, R. and Houck, K. and Martin, M. and Richard, A. M. and Knudsen, T. B. and Shah, I. and Little, S. and Wambaugh, J. and Setzer, R. W. and Kothya, P. and et al.}, year={2016}, pages={323–339} }
 @article{watson_planchart_mattingly_winkler_reif_kullman_2016, title={From the Cover: Embryonic Exposure to TCDD Impacts Osteogenesis of the Axial Skeleton in Japanese medaka,Oryzias latipes}, volume={155}, ISSN={1096-6080 1096-0929}, url={http://dx.doi.org/10.1093/toxsci/kfw229}, DOI={10.1093/toxsci/kfw229}, abstractNote={Recent studies from mammalian, fish, and in vitro models have identified bone and cartilage development as sensitive targets for dioxins and other aryl hydrocarbon receptor ligands. In this study, we assess how embryonic 2,3,7,8-tetrachlorochlorodibenzo-p-dioxin (TCDD) exposure impacts axial osteogenesis in Japanese medaka (Oryzias latipes), a vertebrate model of human bone development. Embryos from inbred wild-type Orange-red Hd-dR and 3 transgenic medaka lines (twist:EGFP, osx/sp7:mCherry, col10a1:nlGFP) were exposed to 0.15 nM and 0.3 nM TCDD and reared until 20 dpf. Individuals were stained for mineralized bone and imaged using confocal microscopy to assess skeletal alterations in medial vertebrae in combination with a qualitative spatial analysis of osteoblast and osteoblast progenitor cell populations. Exposure to TCDD resulted in an overall attenuation of vertebral ossification characterized by truncated centra, and reduced neural and hemal arch lengths. Effects on mineralization were consistent with modifications in cell number and cell localization of transgene-labeled osteoblast and osteoblast progenitor cells. Endogenous expression of osteogenic regulators runt-related transcription factor 2 (runx2) and osterix (osx/sp7), and extracellular matrix genes osteopontin (spp1), collagen type I alpha I (col1), collagen type X alpha I (col10a1), and osteocalcin (bglap/osc) was significantly diminished at 20 dpf following TCDD exposure as compared with controls. Through global transcriptomic analysis more than 590 differentially expressed genes were identified and mapped to select pathological states including inflammatory disease, connective tissue disorders, and skeletal and muscular disorders. Taken together, results from this study suggest that TCDD exposure inhibits axial bone formation through dysregulation of osteoblast differentiation. This approach highlights the advantages and sensitivity of using small fish models to investigate how xenobiotic exposure may impact skeletal development.}, number={2}, journal={Toxicological Sciences}, publisher={Oxford University Press (OUP)}, author={Watson, AtLee T. D. and Planchart, Antonio and Mattingly, Carolyn J. and Winkler, Christoph and Reif, David M. and Kullman, Seth W.}, year={2016}, month={Nov}, pages={485–496} }
 @article{ducharme_reif_gustafsson_bondesson_2015, title={Comparison of toxicity values across zebrafish early life stages and mammalian studies: Implications for chemical testing}, volume={55}, journal={Reproductive Toxicology (Elmsford, N.Y.)}, author={Ducharme, N. A. and Reif, D. M. and Gustafsson, J. A. and Bondesson, M.}, year={2015}, pages={3–10} }
 @article{rebuli_camacho_adonay_reif_aylor_patisaul_2015, title={Impact of Low-Dose Oral Exposure to Bisphenol A (BPA) on Juvenile and Adult Rat Exploratory and Anxiety Behavior: A CLARITY-BPA Consortium Study}, volume={148}, ISSN={["1096-0929"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84952932385&partnerID=MN8TOARS}, DOI={10.1093/toxsci/kfv163}, abstractNote={Bisphenol A (BPA) is a high volume production chemical and has been identified as an endocrine disruptor, prompting concern that developmental exposure could impact brain development and behavior. Rodent and human studies suggest that early life BPA exposure may result in an anxious, hyperactive phenotype but results are conflicting and data from studies using multiple doses below the no-observed-adverse-effect level are limited. To address this, the present studies were conducted as part of the CLARITY-BPA (Consortium Linking Academic and Regulatory Insights on BPA Toxicity) program. The impact of perinatal BPA exposure (2.5, 25, or 2500 µg/kg body weight (bw)/day) on behaviors related to anxiety and exploratory activity was assessed in juvenile (prepubertal) and adult NCTR Sprague-Dawley rats of both sexes. Ethinyl estradiol (0.5 µg/kg bw/day) was used as a reference estrogen. Exposure spanned gestation and lactation with dams gavaged from gestational day 6 until birth and then the offspring gavaged directly through weaning (n = 12/sex/group). Behavioral assessments included open field, elevated plus maze, and zero maze. Anticipated sex differences in behavior were statistically identified or suggested in most cases. No consistent effects of BPA were observed for any endpoint, in either sex, at either age compared to vehicle controls; however, significant differences between BPA-exposed and ethinyl estradiol-exposed groups were identified for some endpoints. Limitations of this study are discussed and include suboptimal statistical power and low concordance across behavioral tasks. These data do not indicate BPA-related effects on anxiety or exploratory activity in these developmentally exposed rats.}, number={2}, journal={TOXICOLOGICAL SCIENCES}, author={Rebuli, Meghan E. and Camacho, Luisa and Adonay, Maria E. and Reif, David M. and Aylor, David L. and Patisaul, Heather B.}, year={2015}, month={Dec}, pages={341–354} }
 @article{kollitz_zhang_hawkins_whitfield_reif_kullman_2015, title={Molecular Cloning, Functional Characterization, and Evolutionary Analysis of Vitamin D Receptors Isolated from Basal Vertebrates}, volume={10}, ISSN={["1932-6203"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84929469049&partnerID=MN8TOARS}, DOI={10.1371/journal.pone.0122853}, abstractNote={The vertebrate genome is a result of two rapid and successive rounds of whole genome duplication, referred to as 1R and 2R. Furthermore, teleost fish have undergone a third whole genome duplication (3R) specific to their lineage, resulting in the retention of multiple gene paralogs. The more recent 3R event in teleosts provides a unique opportunity to gain insight into how genes evolve through specific evolutionary processes. In this study we compare molecular activities of vitamin D receptors (VDR) from basal species that diverged at key points in vertebrate evolution in order to infer derived and ancestral VDR functions of teleost paralogs. Species include the sea lamprey (Petromyzon marinus), a 1R jawless fish; the little skate (Leucoraja erinacea), a cartilaginous fish that diverged after the 2R event; and the Senegal bichir (Polypterus senegalus), a primitive 2R ray-finned fish. Saturation binding assays and gel mobility shift assays demonstrate high affinity ligand binding and classic DNA binding characteristics of VDR has been conserved across vertebrate evolution. Concentration response curves in transient transfection assays reveal EC50 values in the low nanomolar range, however maximum transactivational efficacy varies significantly between receptor orthologs. Protein-protein interactions were investigated using co-transfection, mammalian 2-hybrid assays, and mutations of coregulator activation domains. We then combined these results with our previous study of VDR paralogs from 3R teleosts into a bioinformatics analysis. Our results suggest that 1, 25D3 acts as a partial agonist in basal species. Furthermore, our bioinformatics analysis suggests that functional differences between VDR orthologs and paralogs are influenced by differential protein interactions with essential coregulator proteins. We speculate that we may be observing a change in the pharmacodynamics relationship between VDR and 1, 25D3 throughout vertebrate evolution that may have been driven by changes in protein-protein interactions between VDR and essential coregulators.}, number={4}, journal={PLOS ONE}, author={Kollitz, Erin M. and Zhang, Guozhu and Hawkins, Mary Beth and Whitfield, G. Kerr and Reif, David M. and Kullman, Seth W.}, year={2015}, month={Apr} }
 @article{rovida_asakura_daneshian_hofman-huether_leist_meunier_reif_rossi_schmutz_valentin_et al._2015, title={Toxicity testing in the 21st century beyond environmental chemicals}, volume={32}, number={3}, journal={Altex-alternatives to Animal Experimentation}, author={Rovida, C. and Asakura, S. and Daneshian, M. and Hofman-Huether, H. and Leist, M. and Meunier, L. and Reif, D. and Rossi, A. and Schmutz, M. and Valentin, J. P. and et al.}, year={2015}, pages={171–181} }
 @article{wilson_reif_reich_2014, title={Hierarchical Dose-Response Modeling for High-Throughput Toxicity Screening of Environmental Chemicals}, volume={70}, ISSN={["1541-0420"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84895891991&partnerID=MN8TOARS}, DOI={10.1111/biom.12114}, abstractNote={Summary}, number={1}, journal={BIOMETRICS}, publisher={Wiley-Blackwell}, author={Wilson, Ander and Reif, David M. and Reich, Brian J.}, year={2014}, month={Mar}, pages={237–246} }
 @article{truong_reif_st mary_geier_truong_tanguay_2014, title={Multidimensional In Vivo Hazard Assessment Using Zebrafish}, volume={137}, number={1}, journal={Toxicological Sciences}, author={Truong, L. and Reif, D. M. and St Mary, L. and Geier, M. C. and Truong, H. D. and Tanguay, R. L.}, year={2014}, pages={212–233} }
 @article{filer_patisaul_schug_reif_thayer_2014, title={Test driving ToxCast: endocrine profiling for 1858 chemicals included in phase II}, volume={19}, ISSN={["1471-4973"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84908151070&partnerID=MN8TOARS}, DOI={10.1016/j.coph.2014.09.021}, abstractNote={Identifying chemicals, beyond those already implicated, to test for potential endocrine disruption is a challenge and high throughput approaches have emerged as a potential tool for this type of screening. This review focused the Environmental Protection Agency's (EPA) ToxCast(TM) high throughput in vitro screening (HTS) program. Utility for identifying compounds was assessed and reviewed by using it to run the recently expanded chemical library (from 309 compounds to 1858) through the ToxPi(TM) prioritization scheme for endocrine disruption. The analysis included metabolic and neuroendocrine targets. This investigative approach simultaneously assessed the utility of ToxCast, and helped identify novel chemicals which may have endocrine activity. Results from this exercise suggest the spectrum of environmental chemicals with potential endocrine activity is much broader than indicated, and that some aspects of endocrine disruption are not fully covered in ToxCast.}, journal={CURRENT OPINION IN PHARMACOLOGY}, author={Filer, Dayne and Patisaul, Heather B. and Schug, Thaddeus and Reif, David and Thayer, Kristina}, year={2014}, month={Dec}, pages={145–152} }
 @article{motsinger-reif_reif_fanelli_ritchie_2009, title={A Comparison of Analytical Methods for Genetic Association Studies (vol 32, pg 767, 2008)}, volume={33}, ISSN={["0741-0395"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-71249125696&partnerID=MN8TOARS}, DOI={10.1002/gepi.20420}, abstractNote={Genetic EpidemiologyVolume 33, Issue 8 p. 751-751 ErratumFree Access A comparison of analytical methods for genetic association studies Alison A. Motsinger-Reif, Alison A. Motsinger-Reif Bioinformatics Research Center, Department of Statistics, North Carolina State University, Raleigh, North CarolinaSearch for more papers by this authorDavid M. Reif, David M. Reif National Center for Computational Toxicology, US Environmental Protection Agency, Research Triangle Park, North CarolinaSearch for more papers by this authorTheresa J. Fanelli, Theresa J. Fanelli Center for Human Genetics Research and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, TennesseeSearch for more papers by this authorMarylyn D. Ritchie, Marylyn D. Ritchie Center for Human Genetics Research and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, TennesseeSearch for more papers by this author Alison A. Motsinger-Reif, Alison A. Motsinger-Reif Bioinformatics Research Center, Department of Statistics, North Carolina State University, Raleigh, North CarolinaSearch for more papers by this authorDavid M. Reif, David M. Reif National Center for Computational Toxicology, US Environmental Protection Agency, Research Triangle Park, North CarolinaSearch for more papers by this authorTheresa J. Fanelli, Theresa J. Fanelli Center for Human Genetics Research and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, TennesseeSearch for more papers by this authorMarylyn D. Ritchie, Marylyn D. Ritchie Center for Human Genetics Research and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, TennesseeSearch for more papers by this author First published: 17 March 2009 https://doi.org/10.1002/gepi.20420AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume33, Issue8December 2009Pages 751-751 RelatedInformation}, number={8}, journal={GENETIC EPIDEMIOLOGY}, publisher={Wiley-Blackwell}, author={Motsinger-Reif, Alison A. and Reif, David M. and Fanelli, Theresa J. and Ritchie, Marylyn D.}, year={2009}, month={Dec}, pages={751–751} }
 @article{motsinger-reif_reif_fanelli_ritchie_2008, title={A Comparison of Analytical Methods for Genetic Association Studies}, volume={32}, ISSN={["1098-2272"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-58149346724&partnerID=MN8TOARS}, DOI={10.1002/gepi.20345}, abstractNote={Abstract}, number={8}, journal={GENETIC EPIDEMIOLOGY}, publisher={Wiley-Blackwell}, author={Motsinger-Reif, Alison A. and Reif, David M. and Fanelli, Theresa J. and Ritchie, Marylyn D.}, year={2008}, month={Dec}, pages={767–778} }
 @misc{motsinger_ritchie_reif_2007, title={Novel methods for detecting epistasis in pharmacogenomics studies}, volume={8}, number={9}, journal={Pharmacogenomics}, author={Motsinger, A. A. and Ritchie, M. D. and Reif, D. M.}, year={2007}, pages={1229–1241} }