The purpose of the Research Translation Core is to make research outcomes available to governmental organizations responsible for protecting the health of local communities, to the scientific community in general, and to other SRPs in particular. This is in addition to organizations engaged with the BU SRP through the Community Engagement Core. The principal goal is to provide knowledge of exposure and health effects useful in risk assessment needed for consequential decision-making. This proposal builds on our previous work and includes new partners who can use the SRP and Project results for assessment, regulation and reduction of contaminants found at hazardous waste sites.
Specific Aim 1 : Coordinate communication of research within BU SRP, in New England, and the larger NIEHS SRP community to improve application of findings, provide access to data, consolidate resources and increase productivity and collaboration.
Specific Aim 2 : Develop and. maintain partnerships with governmental environmental and public health agencies and provide them with data and expertise that might improve risk assessment-based decisions, particularly with respect to developmental and reproductive effects of environmental chemicals.
Specific Aim 3 : Effect technology transfer by identifying potential end-users of technologies, assays and resources developed by BU SRP projects and facilitate their application.
Specific Aim 4 : Pursue, initiate and implement Center-specific research translation activities (i.e., emanating from the BU SRP), working with the Community Engagement and Training Cores to have a broader impact.

Public Health Relevance

Our emphasis on open access and the willingness of our investigators to share reagents, new analytic methods, risk assessment techniques, and software, have contributed to the confidence in our partners of our commitment to make our work available to agencies and individuals who must make difficult decisions each day to improve public health and protect the lives of residents living in proximity to hazardous waste sites.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
3P42ES007381-18S1
Application #
8908680
Study Section
Special Emphasis Panel (ZES1-JAB-J)
Program Officer
Henry, Heather F
Project Start
Project End
Budget Start
2014-04-01
Budget End
2015-03-31
Support Year
18
Fiscal Year
2014
Total Cost
$4,867
Indirect Cost
$1,894
Name
Boston University
Department
Type
DUNS #
604483045
City
Boston
State
MA
Country
United States
Zip Code
02118
Aschengrau, Ann; Gallagher, Lisa G; Winter, Michael et al. (2018) Modeled exposure to tetrachloroethylene-contaminated drinking water and the occurrence of birth defects: a case-control study from Massachusetts and Rhode Island. Environ Health 17:75
Weisskopf, Marc G; Seals, Ryan M; Webster, Thomas F (2018) Bias Amplification in Epidemiologic Analysis of Exposure to Mixtures. Environ Health Perspect 126:047003
Narasimhan, Supraja; Stanford Zulick, Elizabeth; Novikov, Olga et al. (2018) Towards Resolving the Pro- and Anti-Tumor Effects of the Aryl Hydrocarbon Receptor. Int J Mol Sci 19:
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Lille-Langøy, Roger; Karlsen, Odd André; Myklebust, Line Merethe et al. (2018) Sequence variations in pxr (nr1i2) from zebrafish (Danio rerio) strains affect nuclear receptor function. Toxicol Sci :
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Eide, Marta; Rydbeck, Halfdan; Tørresen, Ole K et al. (2018) Independent losses of a xenobiotic receptor across teleost evolution. Sci Rep 8:10404
Watt, James; Baker, Amelia H; Meeks, Brett et al. (2018) Tributyltin induces distinct effects on cortical and trabecular bone in female C57Bl/6J mice. J Cell Physiol 233:7007-7021
Aschengrau, Ann; Gallagher, Lisa G; Winter, Michael et al. (2018) Modeled exposure to tetrachloroethylene-contaminated drinking water and the risk of placenta-related stillbirths: a case-control study from Massachusetts and Rhode Island. Environ Health 17:58
Kim, Stephanie; Li, Amy; Monti, Stefano et al. (2018) Tributyltin induces a transcriptional response without a brite adipocyte signature in adipocyte models. Arch Toxicol 92:2859-2874

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