Research Topics
| James F DillmanSummaryAffiliation: Walter Reed Army Medical Center Country: USA Publications
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Detail Information
Publications
Sulfur mustard induces the formation of keratin aggregates in human epidermal keratinocytesJames F Dillman
Applied Pharmacology Branch, U S Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010 5400, USA
Toxicol Appl Pharmacol 193:228-36. 2003..These studies demonstrate that sulfur mustard induces keratin aggregation in keratinocytes and support further investigation into the role of keratin aggregation in sulfur mustard-induced vesication...
An inhibitor of p38 MAP kinase downregulates cytokine release induced by sulfur mustard exposure in human epidermal keratinocytesJames F Dillman
Applied Pharmacology Branch, US Army Medical Research Institute of Chemical Defense, 3100 Ricketts Point Road, MCMR U, Aberdeen Proving Ground, MD 21010 5400, USA
Toxicol In Vitro 18:593-9. 2004..These results show that p38 MAP kinase plays a role in SM-induced cytokine production in HEK and suggest that inhibiting this pathway may alleviate the profound inflammatory response elicited by cutaneous SM exposure...
Genomic analysis of rodent pulmonary tissue following bis-(2-chloroethyl) sulfide exposureJames F Dillman
Applied Pharmacology and Neurotoxicology Branches, U S Army Medical Research Institute of Chemical Defense, 3100 Ricketts Point Road, Aberdeen Proving Ground, Maryland 21010 5400, USA
Chem Res Toxicol 18:28-34. 2005..Thus, SM exposure induces transcriptional changes that reveal the cellular response to this potent alkylating agent...
Comparison of non-human primate and human whole blood tissue gene expression profilesJames F Dillman
Applied Pharmacology Branch, U S Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland 21010 5400, USA
Toxicol Sci 87:306-14. 2005..These results show that human genechips can be used for expression profiling of NHP samples and provide a foundation for the development of tools for comparing human and NHP gene expression profiles...
Transcriptional responses of the nerve agent-sensitive brain regions amygdala, hippocampus, piriform cortex, septum, and thalamus following exposure to the organophosphonate anticholinesterase sarinKimberly D Spradling
Cell and Molecular Biology Branch, US Army Medical Research Institute of Chemical Defense USAMRICD, 3100 Ricketts Point Road, Aberdeen Proving Ground, MD 21010 5400, USA
J Neuroinflammation 8:84. 2011....
Microarray analysis of mouse ear tissue exposed to bis-(2-chloroethyl) sulfide: gene expression profiles correlate with treatment efficacy and an established clinical endpointJames F Dillman
Cell and Molecular Biology Branch, United States Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010 5400, USA
J Pharmacol Exp Ther 317:76-87. 2006..These data provide a basis for elucidating the mechanisms of response to SM and drug treatment and also provide a basis for developing strategies to accelerate development of effective SM medical countermeasures...
Bifunctional alkylating agent-induced p53 and nonclassical nuclear factor kappaB responses and cell death are altered by caffeic acid phenethyl ester: a potential role for antioxidant/electrophilic response-element signalingGary D Minsavage
Cell and Molecular Biology Branch, U S Army Medical Research Institute of Chemical Defense, 3100 Ricketts Point Road, Aberdeen Proving Ground, MD 21010 5400, USA
J Pharmacol Exp Ther 321:202-12. 2007....
Genomic analysis of murine pulmonary tissue following carbonyl chloride inhalationAlfred M Sciuto
Pharmacology Division, U S Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland 21010 5400, USA
Chem Res Toxicol 18:1654-60. 2005..We are also investigating other pathways that are responsive to phosgene exposure to identify mechanisms of toxicity and potential therapeutic targets...
Transcriptional analysis of rat piriform cortex following exposure to the organophosphonate anticholinesterase sarin and induction of seizuresKimberly D Spradling
Cell and Molecular Biology Branch, US Army Medical Research Institute of Chemical Defense USAMRICD, 3100 Ricketts Point Road, Aberdeen Proving Ground, MD 21010 5400, USA
J Neuroinflammation 8:83. 2011..Therefore, there is a need to discover drug treatments that are effective when administered after the onset of seizures and secondary responses that lead to brain injury...
Global gene expression in rat brain and liver after oral exposure to the explosive hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX)Desmond I Bannon
Directorate of Toxicology, US Army Center for Health Promotion and Preventive Medicine CHPPM, Aberdeen Proving Ground, Maryland 21010 5403, USA
Chem Res Toxicol 22:620-5. 2009....
Sulfur mustard induced cytokine production and cell death: investigating the potential roles of the p38, p53, and NF-kappaB signaling pathways with RNA interferenceAlbert L Ruff
Cell and Molecular Biology Branch, Research Division, U S Army Medical Research Institute of Chemical Defense, 3100 Ricketts Point Road, Aberdeen Proving Ground, MD 21010 5400, USA
J Biochem Mol Toxicol 24:155-64. 2010..Interestingly, inhibition of p53 by RNAi potentiated SM-induced cell death, suggesting that the role of p53 in SM injury, may be complex and not simply prodeath...
Genomics and proteomics in chemical warfare agent research: recent studies and future applicationsPatrick A Everley
Research Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010, USA
Toxicol Lett 198:297-303. 2010..Here we present an overview of how genomics and proteomics technologies have been applied to CWA research and also provide a series of questions focused on how these techniques could further our understanding of CWA toxicity...
A large-scale quantitative proteomic approach to identifying sulfur mustard-induced protein phosphorylation cascadesPatrick A Everley
Research Division, United States Army Medical Research Institute of Chemical Defense, 3100 Ricketts Point Road, Aberdeen Proving Ground, Maryland 21010, USA
Chem Res Toxicol 23:20-5. 2010..Further de novo analysis of these phosphoproteins using interaction mapping software revealed both known and novel pathways that may serve as future therapeutic targets of SM exposure...
Gene expression profiling of rat hippocampus following exposure to the acetylcholinesterase inhibitor somanJames F Dillman
Cell and Molecular Biology Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Maryland 21010 5400, USA
Chem Res Toxicol 22:633-8. 2009..These data provide important insights into the molecular pathways involved in soman-induced neuropathology and a basis for generating hypotheses about the mechanism of soman-induced neurodegeneration...
A system-based approach to interpret dose- and time-dependent microarray data: quantitative integration of gene ontology analysis for risk assessmentXiaozhong Yu
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, 98105, USA
Toxicol Sci 92:560-77. 2006....
