Thesis (Ph. D.)--University of Wisconsin, 1965. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph.D.) OGI School of Science & Engineering at OHSU, December 2006. / Abstract: leaves xviii-xix. Includes bibliographical references (leaves 112-132).

Progesterone is essential for the maintenance of pregnancy in cattle. Recent trends in decreased reproductive efficiency in dairy cattle have led researchers to believe that increased catabolism and decreased peripheral concentrations of progesterone are at fault. The objective of this study was to determine if the induction of an accessory corpus luteum (CL), via human chorionic gonadotropin (hCG), alters blood perfusion of CL, peripheral concentrations of progesterone, or hepatic steroid inactivating enzymes. We hypothesized that the induction of an accessory CL would decrease blood perfusion of the CL, decrease peripheral concentrations of progesterone, and increase clearance of progesterone in the liver. Total blood perfusion of the CL was increased in cows with 2 CL compared to cows with 1 CL, but concentrations of progesterone and hepatic enzymes did not differ. Overall, the increased blood perfusion in cows with 2 CL did not alter concentrations of progesterone or progesterone clearance.

Thesis (doctoral)--Utrecht, 1981.

Call number: LD2668 .T4 1964 C77 / Master of Science

Exogenous prostaglandins (PGs) have been reported to suppress or to promote the function of the primate corpus luteum in vitro and in vivo, but the role of endogenous ovarian prostaglandins in regulating luteal function during the menstrual cycle is unknown. Infusion (via osmotic pump) of the prostaglandin-synthesis inhibitor sodium meclofenamate into the corpus luteum, but not via the jugular vein, during the midluteal phase of the menstrual cycle resulted in a decline in progesterone levels and premature menses in rhesus monkeys (Macaca mulatta). These results suggest that meclofenamate suppresses the production of an obligatory luteotropic prostaglandin or other metabolite of arachidonic acid. We were unable to confirm that ovarian prostaglandin synthesis was diminished during treatment, since we could not consistently measure a gradient in PGE or PGF₂(α) across the ovary. Dispersed cells from the macaque corpus luteum produced PGF₂(α) in vitro. Production was stimulated by exposure to arachidonic acid and was inhibited by meclofenamate and another prostaglandin-synthesis inhibitor, flurbiprofen. Although the two drugs were potent inhibitors of prostaglandin synthesis in vitro, intraluteal infusion of flurbiprofen in monkeys did not mimic the luteolytic effects of meclofenamate. These studies provide the first evidence of an obligatory luteotropic role for a metabolite of arachidonic acid during the primate luteal phase. However the data suggest that the luteolytic effect of meclofenamate in vivo is not mediated entirely by the inhibition of local prostaglandin synthesis. Further studies are needed to determine the mechanism(s) of meclofenamate-induced luteolysis and to identify the putative obligatory luteotropin.

No description available.

The involvement of clock genes in the temporal regulation of the function and lifespan of the corpus luteum (CL) has not been investigated in detail. Immunohistochemistry and real-time quantitative PCR techniques were used to examine the expression of the canonical clock genes: period1, period2, period3, cryptochrome1, cryptochrome2, clock and bmal1, at protein and mRNA levels respectively. The expression of the clock genes was examined in the human CL, cultured luteinised granulosa cells, cultured luteal fibroblast-like cells and the ovine CL. The main findings were that clock genes are expressed in the human and ovine CL; that this expression is manifest at mRNA and protein level in all discernible cell types within the human and ovine CL, and that the pattern of mRNA expression differs between the early luteal phase compared to the late luteal phase. The circadian expression of the clock genes was established in the ovine CL during the late luteal phase and could not be determined in the human CL, although indications from cultured luteinised granulosa cells and luteal fibroblast-like cells suggest that this may also be the case in humans. With the exception of per2, the circadian pattern of clock gene expression emerged in the late luteal phase CL when the early luteal phase CL did not demonstrate circadian clock gene expression. This emergence later in the lifespan of the CL was akin to that observed in embryonic development, where the clock genes are initially non-rhythmic but then acquire circadian rhythmicity with age. In this case, the clock genes have been proposed to perform a non-classical circadian timing role in the timing of embryonic development. The per2 gene was also found to be special, in its loss rather than gain of rhythmic gene expression across the luteal lifespan and in its protein localisation in the cytoplasm of some granulosa-lutein cells. The exceptional behaviour of per2 is consistent with a growing body of evidence supporting its role as a unique clock gene in many respects, able to maintain circadian protein levels in the absence of circadian gene expression, integrating peripheral clock inputs and outputs and acting as a tumour suppressor gene. The CL was also found to be a potential target of melatonin regulation, based on its possession of melatonin MT1 receptors and the timing of circadian cry1 gene expression in the late luteal phase. The expression of cry1 is known to be directly melatonin-induced in the PT and appeared to be similarly activated, downstream of a melatonin signal, in the CL. This supports the evolving view of a hierarchical organisation of the central and peripheral clocks, which are integrated in order to establish information feedback loops that maintain circadian homeostasis, and which can regulate seasonal physiology.

Graduation date: 1991

Thesis (M.S.)--West Virginia University, 2001. / Title from document title page. Document formatted into pages; contains vii, 60 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 57-60).