Research Topics
Species | N J WalkerSummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
Unraveling the complexities of the mechanism of action of dioxinsNigel J Walker
National Institute of Environmental Health Sciences, National Institutes of Health, PO Box 12233, MD EC-34, 111 T. W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 95:297-9. 2007
Absolute estimation of initial concentrations of amplicon in a real-time RT-PCR processMarjo V Smith
Constella Group, Suite 200, 2605 Meridian Pky, Durham, NC, USA
BMC Bioinformatics 8:409. 2007..The more elaborate mechanistic models require many more parameters than can be fit from a single amplification, while the empirical models provide little insight and are difficult to tailor to specific reactants...- Tech.Sight. A technique whose time has comeNigel J Walker
Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Science 296:557-9. 2002 
A 21st century paradigm for evaluating the health hazards of nanoscale materials?Nigel J Walker
National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 110:251-4. 2009....- Comparison of chronic toxicity and carcinogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in 2-year bioassays in female Sprague-Dawley ratsNigel J Walker
Environmental Toxicology Program, National Institute of Environmental Health Sciences, Natinal Institutes of Health, Research Triangle Park, NC 27709, USA
Mol Nutr Food Res 50:934-44. 2006..This may result from differences in the experimental protocols as well as divergence in the biological behavior of the different stocks of Sprague-Dawley rat strains used... - Real-time and quantitative PCR: applications to mechanism-based toxicologyN J Walker
Molecular Epidemiology and Dosimetry Section, Laboratory of Computational Biology and Risk Analysis, NIEHS, 111 Alexander Drive, PO Box 12233, MD D4 01, Research Triangle Park, NC 27709, USA
J Biochem Mol Toxicol 15:121-7. 2001..The aim of this review is to provide the reader with an overview of this technology and to highlight specific applications of this technology to some key areas of molecular toxicology... - Pulmonary lesions in female Harlan Sprague-Dawley rats following two-year oral treatment with dioxin-like compoundsNigel J Walker
National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 35:880-9. 2007..Potential mechanisms leading to altered differentiation and/or proliferation of bronchiolar and alveolar epithelia may be through CYP1A1 induction or disruption of retinoid metabolism... - Hepatocarcinogenesis in female Sprague-Dawley rats following discontinuous treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxinN J Walker
Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 54:330-7. 2000.... - Characterization of the dose-response of CYP1B1, CYP1A1, and CYP1A2 in the liver of female Sprague-Dawley rats following chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxinN J Walker
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
Toxicol Appl Pharmacol 154:279-86. 1999.... - Differences in kinetics of induction and reversibility of TCDD-induced changes in cell proliferation and CYP1A1 expression in female Sprague-Dawley rat liverN J Walker
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Carcinogenesis 19:1427-35. 1998.... - Dose-additive carcinogenicity of a defined mixture of "dioxin-like compounds"Nigel J Walker
National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27705, USA
Environ Health Perspect 113:43-8. 2005..These data support the use of the TEF approach for dioxin cancer risk assessments... - Physiological modeling of a proposed mechanism of enzyme induction by TCDDM C Kohn
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
Toxicology 162:193-208. 2001..Predicted induction at low doses was found to vary widely with the assumptions used in the construction of a model. More detailed descriptions of biological processes might provide more reliable predictions of enzyme induction... - Regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced tumor promotion by 17 beta-estradiol in female Sprague--Dawley ratsM E Wyde
National Institute of Environmental Health Sciences, Environmental Toxicology Program, Research Triangle Park, North Carolina 22709, USA
Toxicol Appl Pharmacol 173:7-17. 2001.... - Induction of hepatic 8-oxo-deoxyguanosine adducts by 2,3,7,8-tetrachlorodibenzo-p-dioxin in Sprague-Dawley rats is female-specific and estrogen-dependentM E Wyde
National Institute of Environmental Health Sciences, Environmental Toxicology Program, Research Triangle Park, North Carolina 27709, USA
Chem Res Toxicol 14:849-55. 2001..These studies provide strong evidence that the induction of 8-oxo-dG by TCDD occurs via a chronic, sex-specific, estrogen-dependent mechanism... - Animal models of human response to dioxinsJ A Grassman
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
Environ Health Perspect 106:761-75. 1998..The information gained from animal models is important for developing mechanistic models of dioxin toxicity and critical for assessing the risks to human populations under different circumstances of exposure... - Differential toxicogenomic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin in malignant and nonmalignant human airway epithelial cellsJeanelle M Martinez
National Institute of Environmental Health Sciences, Rall Building 101, 111 Alexander Drive, Research Triangle Park, NC 27709, USA
Toxicol Sci 69:409-23. 2002..In addition, TCDD altered specific immunomodulatory genes in the HPL1A cells. These data show that TCDD alters multiple integrated networks of signaling pathways associated with pulmonary disease, particularly that of lung cancer... - Gingival carcinogenicity in female Harlan Sprague-Dawley rats following two-year oral treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like compoundsKatsuhiko Yoshizawa
Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 83:64-77. 2005..These results indicate that dioxin and DLCs target the gingiva of the oral cavity, in particular the junctional epithelium of molars... - Isolation and characterization of a novel gene induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liverO Selmin
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Carcinogenesis 17:2609-15. 1996.... - Promotion of altered hepatic foci by 2,3,7,8-tetrachlorodibenzo-p-dioxin and 17beta-estradiol in male Sprague-Dawley ratsMichael E Wyde
National Institute of Environmental Health Sciences, Environmental Toxicology Program, 111 Alexander Drive, Building 101, Room D452, MD4-01, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 68:295-303. 2002..The weaker potency of tumor promotion and lack of induction of cell replication and DNA damage in male rats likely explain the female-specific hepatocarcinogenicity of TCDD in chronic bioassays... - Olfactory epithelial metaplasia and hyperplasia in female Harlan Sprague-Dawley rats following chronic treatment with polychlorinated biphenylsAbraham Nyska
Laboratory of Experimental Pathology National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 9998, USA
Toxicol Pathol 33:371-7. 2005..Variable amounts of acute inflammatory exudate appeared within the lumen of the nasal cavity, overlying the affected epithelium. Occasionally, the inflammation eroded through the skull and into the adjacent olfactory bulbs... - Incidences of selected lesions in control female Harlan Sprague-Dawley rats from two-year studies performed by the National Toxicology ProgramAmy E Brix
Experimental Pathology Laboratories, PO Box 12766, Research Triangle Park, NC 27709, USA
Toxicol Pathol 33:477-83. 2005..2%). Squamous metaplasia is not a lesion commonly observed in NTP control Fischer rats. The Harlan SD rats had a very low incidence of mononuclear cell leukemia (0.5%), compared with an incidence of 24% in female Fischer rats... - Exocrine pancreatic pathology in female Harlan Sprague-Dawley rats after chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like compoundsAbraham Nyska
Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, National Institutes of Health DHHS, PO Box 12233, Research Triangle Park, NC 27709, USA
Environ Health Perspect 112:903-9. 2004..These results indicate that the pancreatic acini are target tissues for dioxin and certain dioxin-like compounds. Key words: carcinogenesis, dioxin, furans, inflammation, pancreas, polychlorinated biphenyls... - Classification of proliferative hepatocellular lesions in harlan sprague-dawley rats chronically exposed to dioxin-like compoundsJames R Hailey
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 33:165-74. 2005..This paper describes the morphology of these lesions, as well as the diagnostic approach taken in this series of studies... - EGR1 is a novel target for AhR agonists in human lung epithelial cellsJeanelle M Martinez
Laboratory of Computational Biology and Risk Analysis, NIEHS, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 82:429-35. 2004..Increased expression of a transcription factor EGR1 with tumorigenic and other biological activities could contribute to the deleterious pulmonary effects of exposure to these environmental agents... - Oral and dermal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces cutaneous papillomas and squamous cell carcinomas in female hemizygous Tg.AC transgenic miceMichael E Wyde
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Toxicol Sci 82:34-45. 2004..Differences in response between the routes of exposure may reflect pharmacokinetic differences in the delivery of TCDD to the skin over the duration of the study... - Gene interaction network suggests dioxin induces a significant linkage between aryl hydrocarbon receptor and retinoic acid receptor betaHiroyoshi Toyoshiba
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Environ Health Perspect 112:1217-24. 2004..Simulation studies demonstrated the method works well, even for small samples... - Evaluation of toxic equivalency factors for induction of cytochromes P450 CYP1A1 and CYP1A2 enzyme activity by dioxin-like compoundsHiroyoshi Toyoshiba
National Institute of Environmental Health Sciences, 27709, Durham, NC, USA
Toxicol Appl Pharmacol 194:156-68. 2004..These results indicate that for some biological responses, the use of a single relative potency factor (RPF) is not appropriate for the comparison of the dose response behavior of different dioxin-like congeners... - The putative tumor suppressor Tsc-22 is downregulated early in chemically induced hepatocarcinogenesis and may be a suppressor of Gadd45bMari Iida
Laboratory of Molecular Carcinogenesis, Toxicology Operations Branch, Environmental Toxicology Program, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
Toxicol Sci 99:43-50. 2007..These data provide evidence that Tsc-22 is a suppressor of Gadd45b expression, which may contribute to an early antiapoptotic response... - Mechanisms of exocrine pancreatic toxicity induced by oral treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin in female Harlan Sprague-Dawley RatsKatsuhiko Yoshizawa
Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Sci 85:594-606. 2005..Changes in the expression of CYP or CCKAR may have induced the acinar-cell tumors by initiating proliferation... - Follicular epithelial cell hypertrophy induced by chronic oral administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin in female Harlan Sprague-Dawley ratsYoshiro Tani
Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 32:41-9. 2004..These results indicate that the follicular cell response was hypertrophic and reversible. This information should contribute to diagnosis of nonneoplastic thyroid follicular lesions in rats... - Characterization of bronchiolar metaplasia of the alveolar epithelium in female Sprague-Dawley rats exposed to 3,3',4,4',5-pentachlorobiphenyl (PCB126)Amy E Brix
Experimental Pathology Laboratories, Inc, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 32:333-7. 2004.... 
Predicting the hepatocarcinogenic potential of alkenylbenzene flavoring agents using toxicogenomics and machine learningScott S Auerbach
National Toxicology Program, National Institute of Environmental Health Sciences, NIH, RTP, NC 27709, USA
Toxicol Appl Pharmacol 243:300-14. 2010..Furthermore, we find that exposure duration is a critical variable in the success or failure of such an approach, particularly when evaluating chemicals with unknown carcinogenic potency...- Drug-induced expression of nonsteroidal anti-inflammatory drug-activated gene/macrophage inhibitory cytokine-1/prostate-derived factor, a putative tumor suppressor, inhibits tumor growthJeanelle M Martinez
Laboratories of Molecular Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
J Pharmacol Exp Ther 318:899-906. 2006..Drugs that target NAG-1 could lead to a unique strategy for the development of chemotherapeutic and chemopreventive agents... - Effects of TCDD upon IkappaB and IKK subunits localized in microsomes by proteomicsMaribel E Bruno
Proteomics Group, National Center for Toxicogenomics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Arch Biochem Biophys 406:153-64. 2002..Overall, proteomic analysis indicated the presence of NF-kappaB pathway members in microsomes, selectively altered by dioxin, which may influence immune and inflammatory responses within the liver... - Area under the curve as a dose metric for promotional responses following 2,3,7,8-tetrachlorodibenzo-p-dioxin exposureAmy H Kim
University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Toxicol Appl Pharmacol 191:12-21. 2003..74 versus 0.20%, respectively. These findings suggest that the peak magnitude of TCDD in liver rather than AUC may play a significant role in the induction of complex biological responses by TCDD... - Increase in cardiovascular pathology in female Sprague-Dawley rats following chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3,3',4,4',5-pentachlorobiphenylMicheal P Jokinen
Pathology Associates, Durham, NC, USA
Cardiovasc Toxicol 3:299-310. 2003..The authors' investigations indicate that the rat cardiovascular system is a target for dioxin toxicity, which increases the incidence of spontaneous cardiomyopathy and arteritis... - Accumulation of M1dG DNA adducts after chronic exposure to PCBs, but not from acute exposure to polychlorinated aromatic hydrocarbonsYo Chan Jeong
Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, NC 27599, USA
Free Radic Biol Med 45:585-91. 2008..In summary, the results from the present study support the hypothesis that oxidative DNA damage plays a key role in toxicity and carcinogenicity following long-term PCB exposure... - Respiratory tract lesions in noninhalation studiesDonald M Sells
Battelle Columbus Laboratories, Columbus, OH 43201, USA
Toxicol Pathol 35:170-7. 2007..The presence of respiratory tract lesions in noninhalation studies emphasizes the need for a thorough examination of the respiratory tract including nasal passages, regardless of the route of administration... - A critical comparison of murine pathology and epidemiological data of TCDD, PCB126, and PeCDFKatsuhiko Yoshizawa
Toxicologic Pathology, Drug Safety Research Laboratories, Astellas Pharma Inc, Yodogawa, Osaka, Japan
Toxicol Pathol 35:865-79. 2007.... - Subchronic exposure to TCDD, PeCDF, PCB126, and PCB153: effect on hepatic gene expressionChad M Vezina
University of Wisconsin-Madison, School of Pharmacy, Madison, Wisconsin, USA
Environ Health Perspect 112:1636-44. 2004..Together, these findings may help to elucidate some of the fundamental features of dioxin toxicity and may further clarify the biologic role of the AhR signaling pathway... - Development of a refined database of mammalian relative potency estimates for dioxin-like compoundsLaurie C Haws
ChemRisk, 8024 Mesa Dr, 126, Austin, Texas 78731, USA
Toxicol Sci 89:4-30. 2006.... - Migration of intradermally injected quantum dots to sentinel organs in miceNeera V Gopee
National Center for Toxicological Research, U S Food and Drug Administration, Jefferson, Arkansas 72079, USA
Toxicol Sci 98:249-57. 2007.... - Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) enhances triggered afterdepolarizations in rat ventricular myocytesAn Xie
Department of Basic Pharmaceutical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, SC, USA
Cardiovasc Toxicol 6:99-110. 2006..These effects may lead to clinically relevant ventricular arrhythmia especially when susceptible individuals are under elevated sympathetic stress or suffering from other myocardiopathies coincided with Ca2+-overload... - Impact of physiologically based pharmacokinetic modeling on benchmark dose calculations for TCDD-induced biochemical responsesAmy H Kim
Curriculum in Toxicology, University of North Carolina at Chapel Hill, 509 Mary Ellen Jones Building, CB#7270, 27599, USA
Regul Toxicol Pharmacol 36:287-96. 2002..BB(01) and BB(10) values from both methods were within two orders of magnitude of current human general population exposure to all dioxin-like compounds... - Safe handling of nanotechnologyAndrew D Maynard
Woodrow Wilson International Center for Scholars, USA
Nature 444:267-9. 2006 - Research strategies for safety evaluation of nanomaterials, part II: toxicological and safety evaluation of nanomaterials, current challenges and data needsMichael P Holsapple
ILSI Health and Environmental Sciences Institute, One Thomas Circle, NW, 9th Floor, Washington, District of Columbia 20005, USA
Toxicol Sci 88:12-7. 2005....