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Barbara D. Abbott

Researcher at Research Triangle Park

Publications -  79
Citations -  6142

Barbara D. Abbott is an academic researcher from Research Triangle Park. The author has contributed to research in topics: Developmental toxicity & Receptor. The author has an hindex of 40, co-authored 79 publications receiving 5600 citations. Previous affiliations of Barbara D. Abbott include United States Environmental Protection Agency.

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The Plasticizer Diethylhexyl Phthalate Induces Malformations by Decreasing Fetal Testosterone Synthesis during Sexual Differentiation in the Male Rat

TL;DR: Data indicate that DEHP disrupts male rat sexual differentiation by reducing T to female levels in the fetal male rat during a critical stage of reproductive tract differentiation.
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ARNT-deficient mice and placental differentiation.

TL;DR: The primary cause of lethality appears to be failure of the embryonic component of the placenta to vascularize and form the labyrinthine spongiotrophoblast, which may be related to ARNT's known role in hypoxic induction of angiogenesis.
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Activation of Mouse and Human Peroxisome Proliferator–Activated Receptors (α, β/δ, γ) by Perfluorooctanoic Acid and Perfluorooctane Sulfonate

TL;DR: In this article, the potential for perfluorooctanoic acid (PFOA) and PFOS to activate peroxisome proliferator-activated receptors (PPARs), using a transient transfection cell assay, was evaluated.
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Activation of Mouse and Human Peroxisome Proliferator−Activated Receptor Alpha by Perfluoroalkyl Acids of Different Functional Groups and Chain Lengths

TL;DR: It is concluded that PFAAs of increasing carbon backbone chain lengths induce increasing activity of the mouse and human PPARalpha with a few exceptions, and PFAA carboxylates are stronger activators of mouse andhuman PPAR alpha than PFAA sulfonates.
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Perfluorooctanoic Acid–Induced Developmental Toxicity in the Mouse is Dependent on Expression of Peroxisome Proliferator–Activated Receptor-alpha

TL;DR: Early pregnancy loss was independent of PPARalpha expression and PFOA induced postnatal lethality and expression of one copy of the gene was sufficient to mediate this effect, although other mechanisms may contribute.