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Peter J. O'Shaughnessy

Researcher at University of Glasgow

Publications -  107
Citations -  5929

Peter J. O'Shaughnessy is an academic researcher from University of Glasgow. The author has contributed to research in topics: Leydig cell & Sertoli cell. The author has an hindex of 47, co-authored 107 publications receiving 5328 citations. Previous affiliations of Peter J. O'Shaughnessy include University of Oulu & Medical Research Council.

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Fetal Development of Leydig Cell Activity in the Mouse Is Independent of Pituitary Gonadotroph Function

TL;DR: Examination of the development of fetal pituitary LH levels and Leydig cell function in normal mice and in hypogonadal mice that lack GnRH and, thus, circulating gonadotropins shows that pituitsary LH synthesis can start in the absence of GnRH but is dependent on LH for a normal level of synthesis and secretion.
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Changes in Leydig Cell Gene Expression During Development in the Mouse

TL;DR: Developmental changes in the expression of 18 Leydig cell-specific mRNA species were measured by real-time polymerase chain reaction to partially characterize the developmental phenotype of the cells in the mouse and to identify markers of adult Leydigs cell differentiation.
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Hormonal control of germ cell development and spermatogenesis.

TL;DR: Regulation of spermatogenesis in primates appears to be similar to that in rodents although the role of FSH may be greater and understanding of the mechanisms by which these hormones act to regulate this process is still lacking.
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Impact of endocrine-disrupting compounds (EDCs) on female reproductive health.

TL;DR: The evidence for EC, including EDC, involvement in female reproductive dysfunction is summarised, potential mechanisms of EC action in the female are highlighted and the need for further research into EC effects on female development and reproductive function is emphasised.
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Regulation of Sertoli Cell Number and Activity by Follicle-Stimulating Hormone and Androgen during Postnatal Development in the Mouse

TL;DR: The results show that testosterone, but not FSH, is required for Sertoli cell proliferation during fetal and early neonatal life; FSH and testosterone both regulate the late stages of Sertolis cell proliferation.