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Patrick E. Chappell

Researcher at Oregon State University

Publications -  35
Citations -  1774

Patrick E. Chappell is an academic researcher from Oregon State University. The author has contributed to research in topics: Gonadotropin-releasing hormone & Circadian rhythm. The author has an hindex of 18, co-authored 31 publications receiving 1600 citations. Previous affiliations of Patrick E. Chappell include Northwestern University & University of California, San Diego.

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The Circadian Clock Protein BMAL1 Is Necessary for Fertility and Proper Testosterone Production in Mice

TL;DR: The reproductive capacity of mice lacking Bmal1 (Arntl, Mop3), one of the central circadian clock genes, is investigated, and expression of the steroidogenic acute regulatory protein (StAR) gene and protein, which regulates the rate-limiting step of steroidogenesis, was decreased in testes from B mal1 KO mice.
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Stimulation of Gonadotropin-Releasing Hormone Surges by Estrogen. I. Role of Hypothalamic Progesterone Receptors

TL;DR: Findings provide direct support for the hypothesis that activation of PRs, specifically those in hypothalamic regions including the AVPV, is an obligatory event in the stimulation of GnRH surges by E2.
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Endocrine defects in mice carrying a null mutation for the progesterone receptor gene

TL;DR: Serum LH levels in PRKO mice were found to be elevated by approximately 2-fold over basal (metestrus) values in WT mice, and progesterone levels were likewise similar in the two groups, as were hypothalamic LHRH concentrations.
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Circadian gene expression regulates pulsatile gonadotropin-releasing hormone (GnRH) secretory patterns in the hypothalamic GnRH-secreting GT1-7 cell line.

TL;DR: The GT1-7 mouse hypothalamic cell line is used as a model for GnRH secretion and it is demonstrated that oscillations of these components can be induced by stimuli such as serum and the adenylyl cyclase activator forskolin, similar to effects observed in fibroblasts.
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Absence of gonadotropin surges and gonadotropin-releasing hormone self-priming in ovariectomized (OVX), estrogen (E2)-treated, progesterone receptor knockout (PRKO) mice.

TL;DR: It is demonstrated that the presence of PR is an absolute requirement for the transmission of E2-induced signals leading to gonadotropin surges, and that PR activation is obligatory for expression of the GnRH self-priming effect as well as for generation of E1-induced LH and FSH surges.