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Daniel R. Prows

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  66
Citations -  3099

Daniel R. Prows is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Lung injury & Quantitative trait locus. The author has an hindex of 26, co-authored 65 publications receiving 2906 citations. Previous affiliations of Daniel R. Prows include University of Cincinnati & University of Cincinnati Academic Health Center.

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The Collaborative Cross, a community resource for the genetic analysis of complex traits

Gary A. Churchill, +113 more
- 01 Nov 2004 - 
TL;DR: The Collaborative Cross will provide a common reference panel specifically designed for the integrative analysis of complex systems and will change the way the authors approach human health and disease.
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Acute lung injury: functional genomics and genetic susceptibility.

TL;DR: In this paper, the sensitivity of inbred mouse strains was investigated following acute lung injury that was induced by fine nickel sulfate aerosol, and the temporal expression of genes and expressed sequence tags was assessed by complementary DNA microarray analysis.
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Liver fatty acid-binding protein expression in transfected fibroblasts stimulates fatty acid uptake and metabolism.

TL;DR: Results show in detail for the first time using an intact cell culture system that L-FABP expression not only stimulated fatty acid uptake, but also increased intracellular esterification of exogenously supplied fatty acids.
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Genetic analysis of ozone-induced acute lung injury in sensitive and resistant strains of mice

TL;DR: The findings implicate various genetic and epigenetic factors in individual susceptibility to air pollution in inbred mice and suggest that genetic determinants may control predisposition to the harmful effects of ozone.
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Intestinal and liver fatty acid binding proteins differentially affect fatty acid uptake and esterification in L-cells

TL;DR: Data show for the first time that distinct FABP differentially affect both fatty acid uptake and intracellular esterification.