The mission of the Center for Environmental Exposure and Disease (CEED) is to improve human health by performing transdisciplinary research to elucidate how the total environment, the genome and the epigenome interact to mitigate the risk of disease. CEED research focuses on: 1) assessing and modeling exposures, 2) discovering and applying biological response indicators which link exposures to mechanisms of pathogenesis, 3) developing and implementing targeted prevention, intervention, and treatment strategies, 4) reducing exposures by influencing public policy, planning and regulation, and 5) engaging and informing stakeholders. By analogy with Precision Medicine, CEED envisions that the integration of data from exposure biology, genomics, epigenetics and microbiomics to assess exposures, biological responses, mechanisms of pathogenesis and disease prevention will significantly impact the future of environmental health. The CEED vision is to lead the development of precision environmental health research through the integration of clinical, basic, and population-based studies, using the acquired information to prevent and/or treat environmental disease. The strategy is to combine the Center's long-standing breadth and depth of expertise in environmental health research with new capabilities in exposure biology, epigenomics, and microbiomics.
The Specific Aims are:
Aim 1 : Move basic, clinical and population research toward precision environmental health by: i) fostering a collaborative, transdisciplinary research environment, ii) supporting innovative research and emerging science through Pilot grant funding, and iii) providing cost-effective access to Facility Cores that maintain state-of-the-art technologies and expertise.
Aim 2 : Provide training and mentoring opportunities to junior investigators and established researchers in innovative and emerging environmental health research through: i) mentoring committees and a structured mentoring curriculum, ii) collaborative research, iii) Career Development Awards and Pilot Project grants, and iv) opportunities for expanded training with other NIEHS Centers.
Aim 3 : Strengthen and expand existing relationships with community partners by: i) facilitating bidirectional interactions among CEED researchers and community partners to identify environmental concerns and desired outcomes, ii) developing research programs that address community health needs, and iii) providing research results, educational materials and expertise to communities and health professionals, enabling them to minimize exposures and influence public health policy.
Aim 4 : Translate research findings to stakeholders in local, state and federal government agencies to provide guidance on mitigation of risk, to influence public policy, and to support legislation that reduces exposure and improve environmental health.
The mission of the CEED is to improve human health by performing transdisciplinary research to elucidate how the total environment interacts with host factors to mitigate the risk of disease. To accomplish the mission, CEED researchers focuses on: 1) assessing and modeling exposures;2) discovering and applying biological response indicators which link exposures to mechanisms of pathogenesis;3) developing and implementing targeted prevention, intervention, and treatment strategies;4) reducing exposures by influencing public policy, planning and regulation;and 5) engaging and informing stakeholders. CEED envisions that the integration of data from exposure biology, genomics, epigenetics and microbiomics to assess exposures, biological responses, mechanisms of pathogenesis and disease prevention, will significantly impact the future of environmental health.
|Venosa, Alessandro; Gow, James G; Hall, LeRoy et al. (2017) Regulation of Nitrogen Mustard-Induced Lung Macrophage Activation by Valproic Acid, a Histone Deacetylase Inhibitor. Toxicol Sci 157:222-234|
|Yang, Jennifer A; Stires, Hillary; Belden, William J et al. (2017) The Arcuate Estrogen-Regulated Transcriptome: Estrogen Response Element-Dependent and -Independent Signaling of ER? in Female Mice. Endocrinology 158:612-626|
|Hamm, Jon; Sullivan, Kristie; Clippinger, Amy J et al. (2017) Alternative approaches for identifying acute systemic toxicity: Moving from research to regulatory testing. Toxicol In Vitro 41:245-259|
|Fang, Mingzhu; Ohman Strickland, Pamela A; Kang, Hwan-Goo et al. (2017) Uncoupling genotoxic stress responses from circadian control increases susceptibility to mammary carcinogenesis. Oncotarget 8:32752-32768|
|Russo, Daniel P; Kim, Marlene T; Wang, Wenyi et al. (2017) CIIPro: a new read-across portal to fill data gaps using public large-scale chemical and biological data. Bioinformatics 33:464-466|
|Bak, Min Ji; Das Gupta, Soumyasri; Wahler, Joseph et al. (2017) Inhibitory Effects of ?- and ?-Tocopherols on Estrogen-Stimulated Breast Cancer In Vitro and In Vivo. Cancer Prev Res (Phila) 10:188-197|
|George, Blessy; You, Dahea; Joy, Melanie S et al. (2017) Xenobiotic transporters and kidney injury. Adv Drug Deliv Rev 116:73-91|
|Joseph, Laurie B; Composto, Gabriella M; Perez, Roberto M et al. (2017) Sulfur mustard induced mast cell degranulation in mouse skin is inhibited by a novel anti-inflammatory and anticholinergic bifunctional prodrug. Toxicol Lett :|
|Garbuzenko, Olga B; Ivanova, Vera; Kholodovych, Vladislav et al. (2017) Combinatorial treatment of idiopathic pulmonary fibrosis using nanoparticles with prostaglandin E and siRNA(s). Nanomedicine 13:1983-1992|
|Sobolewski, Marissa; Weiss, Bernard; Martin, Melanie et al. (2017) Toxicoanthropology: Phthalate exposure in relation to market access in a remote forager-horticulturalist population. Int J Hyg Environ Health 220:799-809|
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