published_or_final_version / Anatomy / Master / Master of Philosophy

Thesis (M. Phil.)--University of Hong Kong, 1994. / Includes bibliographical references (leaves 186-201).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1964. / Typescript. Vita. Includes bibliographical references (leaves 59-68).

Thesis (M.S.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on October 31, 2007) Includes bibliographical references.

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Thesis (Ph. D.)--University of Wisconsin--Madison, 1964. / Typescript. Vita. Includes summaries reprinted from Science, vol. 137, no. 3533 (Sept. 14, 1962), p. 860-861 and from American Zoologist, vol. 2, no. 4 (Nov. 1962), p. 219. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Missouri, 1936. / Plates printed on both sides. Biography. Bibliography: p. 86-88.

Superovulatory treatment with exogenous gonadotrophins adversely affects the uterus through the disruption of the delicate balance of ovarian steroid (estrogens, progestins, androgens) secretion rates. To examine the uterine effects of this treatment, 189 animals were given 4, 20 or 40 IU pregnant mare serum gonadotrophin (PMSG) at 28 days of age and sacrificed every 24 h until day 10 (D10) post injection. To study the long term uterine effects, 12 rats were treated with 4 or 40 IU PMSG and killed on D30. The morphological and histological changes of control (4 IU) uteri mimicked those of the adult on a comparable time course from D2 to D5. Administration of superovulatory doses (2 0, 4 0 IU) of PMSG produced stromal hypertrophy by D2 and focal papillary hyperplasia of the luminal epithelia by D3. It is suggested that previous exposure to high levels of estrogen and androgens, secondary to superovulation, are possible causes for this pathology. Levels of 17B-estradiol following 2 0 and 40 IU PMSG treatment were significantly (p<0.005, p<0.05) elevated above those of controls from DI to early D3 and at D2, respectively. Androgen levels of both groups (20 IU, 40 IU) significantly (p<0.05, p<0.005) increased from baseline at DI to maxima by D2 and D3, respectively. In the 20 IU PMSG group, the hyperplasia gradually regressed after D3 and was absent by D10. The hyperplasia in the 40 IU PMSG group, however, had diffused by D6. It is suspected that preceding elevated levels of estrogen may be responsible for this progressive change. At D4, levels of 17B-estradiol reached a maximum, which was significantly (p<0.001) greater than those of controls and 20 IU PMSG treated rats. Between D6 and D10, the hyperplasia partially regressed. Examination of uteri from D30 revealed no evidence of pathology. In addition to these structural effects, superovulation induced secretion of a mucinous substance in both 20 IU and 40 IU PMSG groups at D5-D6 and D6-D7, respectively. These results suggest that abnormal changes in the uterine histology and metabolism may result following administration of superovulatory doses of PMSG. Although these dose-dependent alterations appear reversible, they may interfere with preparations associated with implantation and thus require further investigation. / Medicine, Faculty of / Obstetrics and Gynaecology, Department of / Graduate

Call number: LD2668 .T4 1936 P48