Thesis (M.S.) in Animal Sciences--University of Maine, 2003. / Includes vita. Includes bibliographical references (leaves 59-62).

Thesis (M.S.) in Animal Sciences--University of Maine, 2005. / Includes vita. Includes bibliographical references (leaves 44-59).

No description available.

Production of hormones in the ovary is controlled by endocrine, paracrine, autocrine and intracrine influences. Similar controls may exist in the placenta. I wished to investigate the involvement of second messengers in the action of hormones in control of hormonogenesis in rat ovary and human placenta. The second messengers involved in the action of gonadotropin-releasing hormone (GnRH) and prostaglandin (PG) F₂[formula omitted] were investigated in rat granulosa and luteal cells. As well, the endocrine role of GnRH in the placenta and the possible second messengers involved were investigated. Monolayer cultures of rat granulosa and luteal cells and human placental cells were prepared. Rat granulosa cells were mechanically dispersed; rat luteal cells were enzymatically dispersed with collagenase and DNase. Rat granulosa cells were treated during the first 24 hours in culture; rat luteal cells were treated up to 3 days after dispersion. Radioimmunoassay of medium was used to determine the effect of treatments on hormone production. Studies which examined the effect of hormones on the intracellular free calcium concentration ([Ca²⁺]i) in single cells using the calcium sensitive fluorescent dye, Fura-2, were done in monolayer rat granulosa and luteal cell cultures. Human placental cells, from first trimester and term placentae, were dispersed using trypsin-DNase or collagenase-DNase. Cells were cultured for 2 days prior to treatment. The effects of treatments on production of steroid (progesterone and estrogen), glycoprotein (human chorionic gonadotropin; hCG) and protein (human placental lactogen; hPL) hormones were determined by radioimmunoassay of the medium. In rat granulosa and luteal cell cultures, I examined the effect of a number of hormones and second messengers. Effects of follicle-stimulating hormone (FSH), luteinizing hormone (LH), cyclic adenosine monophosphate (cAMP), GnRH and PGF₂[formula omitted] on ovarian hormonogenesis have been previously reported. Changes in cytosolic free calcium concentrations ([Ca²⁺]i) in response to PGF₂[formula omitted] were measured in single rat granulosa and luteal cells. I found that in 34% of granulosa cells, and 53% of luteal cells, there was a 3 to 4 fold increase in resting [Ca²⁺]i within 30 seconds of administration of PGF₂[formula omitted]. Many cells which responded to PGF₂[formula omitted] also responded to GnRH (39% of granulosa cells; 67% of luteal cells). The immediate source of the increased [Ca²⁺]i appeared to be common intracellular stores. No change in hormone production in response to GnRH in placental cell cultures was seen. Trypsin dispersion may have damaged cell surface receptors, therefore the effect of second messengers on hormone production in these cultures was examined. In term and first trimester trophoblast cultures, I observed the following effects with 8-bromo-cyclic adenosine monophosphate (8-br-cAMP): inhibited estrogen production from the supplied androgen precursors; stimulated hCG production; stimulated hPL production in first trimester placental cell cultures (hPL was not measured in enough term cultures to determine the effect of 8-br-cAMP), and stimulated progesterone production. I also investigated the effects of activators and inhibitors of the phosphoinositide (PtdIns(4,5)P₂) breakdown second messenger pathway (TPA, A23187, arachidonic acid); no effects of these agents were seen. Other hormones suspected of having endocrine, paracrine or autocrine effects in the placenta were tested without effect. I conclude that GnRH and PGF₂[formula omitted] cause increases in [Ca²]i in rat ovarian cells, from common intracellular stores of calcium, and that the production of hormones by the human placenta may be under regulation of an agent or agents which induce production of cAMP. / Medicine, Faculty of / Obstetrics and Gynaecology, Department of / Graduate

No description available.

Thesis (Ph. D.)--University of Hawaii at Manoa, 1995. / Includes bibliographical references (leaves 116-131). / Microfiche. / xvi, 131 leaves, bound ill. (some col.) 29 cm

Thesis (M.Sc (Biochemistry))--Mahidol University, 1982.

Intrauterine crowding and placental insufficiency are main reasons for prenatal losses in swine. Two studies were conducted to examine: 1) conceptus development and in vitro steroidogenic capability of three regions of the placenta (middle, inner, polar) at d 30, 50, 70, and 90 of gestation; and 2) the effects of intrauterine position and fetal sex on conceptus development and in vitro steroidogenic activity of the placenta and endometrium at d 40, 60, 80, and 100 of gestation. All variables were examined in gilts that were uterine intact before hysterectomy (n=19) and in gilts unilaterally hysterectomized-ovariectomized (UHOX) before breeding (n=17) to induce intrauterine crowding. Placentas were combined according to the sex of the fetus associated with the placental unit (except at d 30). Placentas were sectioned into middle, inner and polar regions. Placental tissues were incubated, and release of progesterone (P₄) and estrone (E₁) was determined. Fetal survival rate was greater (P< .01, .05, .001 at d 50, 70 and 90, respectively) from intact versus UHOX gilts. Placental length and weight, fetal length and weight, and allantoic fluid volume were greater in intact compared to UHOX gilts. The polar region of the placenta released less P₄ than the other regions at d 50, 70 and 90. Uterine status (P< .005) affected P₄ release only at d 90. Sex of the fetus did not affect placental P₄ release. Region of the placenta affected E₁, release at d 30 (P< .01) and d 50 (P< .06). Uterine status did not affect E₁ release. Sex of the fetus affected (P< .001) E₁ release only at d 50. In the second study, a total of 45 gilts was used. Placentas and endometrium were combined based upon the intrauterine position of the associated fetus. Placental and endometrial tissues were incubated and release of P₄ and E₁ was determined. Uterine status (intact or UHOX) did not affect the variables measured. Intrauterine position affected fetal and placental weights (P< .02 and .01, respectively) at d 40 of gestation. No significant effect of intrauterine position was detected on placental and endometrial P₄ release. At d 100 of gestation, placentas associated with fetuses bordered in utero by fetuses of the same sex released more (P< .01) E₁ compared to placentas associated with fetuses bordered by fetuses of the opposite sex. Estrone release by the endometrium was not significantly affected by intrauterine position. Only trace amounts of testosterone and dehydroepiandrosterone sulfate were measured in the fetal fluids at all days of gestation. Intrauterine position had no effect on P₄, E₁ or androstenedione concentrations in fetal fluids. Collectively, the results indicated a) a differential release of P₄ and E₁ by the three regions of the placenta at certain days of gestation, b) no compensatory increase in placental steroidogenic activity per unit of tissue when total placental mass was reduced, and c) a limited effect of intrauterine position on placental and endometrial steroidogenesis at various days of gestation. / Ph. D.