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Thomas M. Badger

Researcher at University of Arkansas for Medical Sciences

Publications -  305
Citations -  13313

Thomas M. Badger is an academic researcher from University of Arkansas for Medical Sciences. The author has contributed to research in topics: Soy protein & Offspring. The author has an hindex of 63, co-authored 299 publications receiving 12304 citations. Previous affiliations of Thomas M. Badger include University of Arkansas & United States Department of Agriculture.

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Uterine phenotype of young adult rats exposed to dietary soy or genistein during development.

TL;DR: It is suggested that lifetime dietary exposure to soy foods does not alter uterine cell phenotype in young adult rats, while GEN, by enhancing uterine endometrial glandular apoptosis in vivo and in vitro, may confer protection against uterine carcinoma.
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Concentrations of Purine Metabolites Are Elevated in Fluids from Adults and Infants and in Livers from Mice Fed Diets Depleted of Bovine Milk Exosomes and their RNA Cargos

TL;DR: Diets depleted of bovine-milk exosomes and RNA cargos caused increases in hepatic purine metabolites in mice, and in plasma and urine from human adults and infants, compared with exosome-sufficient controls.
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Fetal programing of colon cancer in adult rats: correlations with altered neonatal growth trajectory, circulating IGF-I and IGF binding proteins, and testosterone

TL;DR: Results indicate an effect of dietary protein type during pregnancy on colon tumor multiplicity and colon tissue gene expression, and serum IGF-I and testosterone in progeny rats as later adults.
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Effects of enteral nutrition and ethanol on cytochrome P450 distribution in small intestine of male rats

TL;DR: The P450 isozymes examined displayed differing intestinal distributions, responded to dietary manipulations, and were affected by ethanol treatment in a fashion not coordinated with that observed for hepatic isoz enzymes.
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Differential effects of short term feeding of a soy protein isolate diet and estrogen treatment on bone in the pre-pubertal rat.

TL;DR: SPI increased while E2 decreased bone turnover compared to CAS, and both treatments decreased serum sclerostin levels, suggesting SPI and E2 have different effects on bone turnover prior to puberty.