Thesis (Ph. D.)--University of Wisconsin--Madison, 1962. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 70-73).

Thesis--Wisconsin. / Vita. Includes bibliographical references (leaves 196-226).

Thesis (M.S.)--University of Wisconsin--Madison, 1981. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 49-53).

Thesis (M.S.)--University of Wisconsin--Madison, 1981. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 53-59).

Lau Man Tat. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 95-126). / Abstracts in English and Chinese. / Abstract (in English) --- p.i / Abstract (in Chinese) --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Figures --- p.xi / List of Tables --- p.xiii / Symbols and Abbreviations --- p.xiv / Scientific Names --- p.xvii / Chapter Chapter 1 --- General Introduction / Chapter 1.1 --- Gonadotropins / Chapter 1.1.1 --- Structure --- p.2 / Chapter 1.1.2 --- Function --- p.6 / Chapter 1.1.3 --- Regulation --- p.9 / Chapter 1.1.3.1 --- Hypothalamic regulators (GnRH) --- p.9 / Chapter 1.1.3.2 --- Endocrine regulators from gonads (steroids) --- p.12 / Chapter 1.1.3.3 --- Paracrine regulators (activin) --- p.14 / Chapter 1.2 --- Activin Family of Growth Factors / Chapter 1.2.1 --- Activin / Chapter 1.2.1.1 --- Structure --- p.14 / Chapter 1.2.1.2 --- Function --- p.14 / Chapter 1.2.1.3 --- Signaling --- p.18 / Chapter 1.2.2 --- Follistatin / Chapter 1.2.2.1 --- Structure --- p.21 / Chapter 1.2.2.2 --- Function --- p.21 / Chapter 1.3 --- Transcriptional regulation of pituitary gonadotropin subunit genes at the promoter level --- p.22 / Chapter 1.4 --- The project objectives and long-term significance --- p.26 / Chapter Chapter 2 --- "Cloning of Smad2, Smad3, Smad4 and Smad7 from the Goldfish Pituitary and Their Involvement in the FSHβ Transcription in LβT2 cells" / Chapter 2.1 --- Introduction --- p.28 / Chapter 2.2 --- Materials and Methods / Chapter 2.2.1 --- Chemicals --- p.31 / Chapter 2.2.2 --- Animals --- p.32 / Chapter 2.2.3 --- Isolation of total RNA --- p.32 / Chapter 2.2.4 --- "Cloning of cDNA fragments of Smad 2, 3, 4 and 7 from the goldfish pituitary" --- p.32 / Chapter 2.2.5 --- Rapid amplification of 5'-cDNA ends (5'-RACE) and full-length cDNA(3'-RACE) --- p.33 / Chapter 2.2.6 --- Primary pituitary cell culture --- p.34 / Chapter 2.2.7 --- "Validation of semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) assays for goldfish Smad 2, 3, 4 and7" --- p.35 / Chapter 2.2.8 --- Construction of the reporter plasmid containing the goldfish FSHβ promoter --- p.36 / Chapter 2.2.9 --- Construction of expression plasmids --- p.37 / Chapter 2.2.10 --- Cell culture and transient transfection --- p.38 / Chapter 2.2.11 --- SEAP reporter gene assay --- p.39 / Chapter 2.2.12 --- β-galactosidase reporter gene assay --- p.40 / Chapter 2.2.13 --- Data analysis --- p.40 / Chapter 2.3 --- Results / Chapter 2.3.1 --- "Cloning and sequence characterization of goldfish Smad 2, 3,4 and7" --- p.41 / Chapter 2.3.2 --- "Tissue distribution of Smad 2，3, 4 and 7 expression" --- p.42 / Chapter 2.3.3 --- "Validation of semi-quantitative RT-PCR assays for Smad 2, 3,4 and7" --- p.43 / Chapter 2.3.4 --- Activin regulation of Smad 2，3，4 and 7 expression in cultured goldfish pituitary cells --- p.44 / Chapter 2.3.5 --- "Smad 2, 3 and 7 regulate basal and activin-induced FSHβ transcription in LβT2 cells" --- p.44 / Chapter 2.3.6 --- Autocrine regulation of the gfFSHβ transcription by activin in LβT2 cells --- p.45 / Chapter 2.4. --- Discussion --- p.47 / Chapter Chapter 3 --- Promoter Analysis for the Smad Responsive Element (SRE) in the Goldfish Follicle Stimulating Hormone β(FSHβGene / Chapter 3.1 --- Introduction --- p.71 / Chapter 3.2 --- Materials and Methods / Chapter 3.2.1 --- Chemicals --- p.74 / Chapter 3.2.2 --- Construction of expression plasmids --- p.74 / Chapter 3.2.3 --- Construction of SEAP reporter plasmids containing different lengths of gfFSHβ promoter --- p.74 / Chapter 3.2.4 --- Cell culture and transient transfection --- p.75 / Chapter 3.2.5 --- Reporter gene assays for SEAP and β-Gal --- p.75 / Chapter 3.2.6 --- Data Analyses --- p.76 / Chapter 3.3 --- Results / Chapter 3.3.1 --- Localization of the proximal Smad-responsive Element (SRE) in the gfFHSβ promoter --- p.76 / Chapter 3.4 --- Discussion --- p.78 / Chapter Chapter 4 --- General Discussion / Chapter 4.1 --- Overview --- p.89 / Chapter 4.2 --- Contribution of the present research / Chapter 4.2.1 --- Cloning and characterization of Smad proteins from the goldfish pituitary --- p.90 / Chapter 4.2.2 --- Regulation of Smads in primary pituitary cell culture --- p.90 / Chapter 4.2.3 --- Identification of the Smad responsive element (SRE) on the gfFSHβ promoter --- p.91 / Chapter 4.3 --- Future research direction --- p.93 / References --- p.95

Thesis (M.S.)--West Virginia University, 2009. / Title from document title page. Document formatted into pages; contains vi, 56 p. : ill. Includes abstract. Includes bibliographical references (p. 45-56).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1969. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Call number: LD2668 .T4 1984 G58 / Master of Science

In the ewe, one to three antral follicles emerge or grow from a pool of small antral follicles (1 to 3 mm in diameter) every 3 to 5 days and reach diameters of ¡Ý5 mm before regression or ovulation. Each follicular wave is triggered by a peak in serum concentrations of FSH. It is not clear what characteristics of an FSH peak cause follicular wave emergence and what aspects of development of a follicular wave are regulated by its preceding FSH peak.<p> In Experiment 1, we found that the amplitude of FSH peaks decreased, while basal serum FSH concentrations increased across the inter-ovulatory interval (P < 0.05). However, there were no associated changes in the growth, static or regression phases of follicular waves or the number and size of follicles in a wave. In Experiment 2, using computer-assisted quantitative echotextural analysis, we found that the numerical pixel value (NPV) for the wall of anovulatory follicles emerging in the third wave of the cycle was significantly higher than for waves 1 and 2 at the time of wave emergence but it decreased as follicles reached maximum follicular diameter (P < 0.05). A tendency for a similar pattern for the wall of follicles in the last wave of the cycle was also observed (P = 0.07).<p> In Experiment 3, treatment with ovine FSH (oFSH) increased the amplitude of an FSH peak by 5 to 6 fold. This treatment increased estradiol production (P < 0.05) but had little effect on other characteristics of the subsequent follicular wave. Daily injections of oFSH (Experiment 4) for four days, resulted in the occurrence of 4 discrete peaks in serum FSH concentrations. Each injection of oFSH resulted in the emergence of a new follicular wave.<p> In Experiment 5, six cyclic ewes received oFSH (0.1 ¦Ìg/kg, sc) every 6 h for 42 h, to try to give a gradual increase in the leading slope of an FSH peak. Serum FSH concentrations increased in oFSH treated ewes (P < 0.05) resulting in an additional peak between two endogenously driven FSH peaks and therefore, did not give the planned gradual leading slope to an FSH peak. Ovine FSH treatment occurred in the early growth phase of wave 1 of the inter-ovulatory interval and increased the growth rate of growing follicles in that wave, compared to control ewes (P < 0.05). This apparently induced dominance in follicles in wave 1, causing them to suppress wave emergence in response to the injected FSH. In Experiment 6, oFSH was infused constantly (1.98 ¦Ìg/ewe/h, iv, n = 6) for 60 h. Infusion of oFSH maintained serum FSH concentrations at a level similar to the zenith of a peak. This resulted in a superstimulatory effect with a peak in the mean number of large follicles on Day 2 after the start of FSH infusion (P < 0.001).<p> A hormonal milieu similar to low serum progesterone concentrations was created by treatment of ewes with prostaglandin and medroxyprogesterone acetate (MAP) sponges (Experiment 7). This treatment delayed regression of the penultimate follicular wave of a cycle. However, the delayed follicular atresia was accompanied by a greater degree of apoptosis in somatic cells of follicles growing in the penultimate wave compared to those in the final wave of the cycle, when collected one day before expected ovulation.<p> In conclusion, trends in basal serum concentrations of FSH and peaks in serum FSH concentrations, across the estrous cycle, are associated with changes in the image attributes of follicles emerging later in the estrous cycle, perhaps reflecting a greater readiness of those follicles for ovulation and formation of CL. The ovine ovary can respond to discrete peaks in serum FSH concentrations with the emergence of new follicular waves on a daily basis. This led us to conclude that follicular dominance is not evident in the ewe and peaks in serum FSH concentrations are likely to be driven by some endogenous rhythm that is unrelated to ovarian follicular secretory products. However, direct dominance can be induced by giving supplemented FSH during the growth phase of a follicle. Extended exposure of ovine ovaries to the serum concentrations of FSH found at the zenith of a peak overrides the mechanisms that recruit follicles into a wave and induces a superovulatory response in cyclic ewes. Finally, an increase in the incidence of apoptosis occurs in antral follicles in sheep that have an extended lifespan, prior to any morphological changes detectable by ultrasonography. This would seem to cause decreased follicular viability and lowered fertility of the oocytes that the follicles contain.

In the ewe, one to three antral follicles emerge or grow from a pool of small antral follicles (1 to 3 mm in diameter) every 3 to 5 days and reach diameters of ¡Ý5 mm before regression or ovulation. Each follicular wave is triggered by a peak in serum concentrations of FSH. It is not clear what characteristics of an FSH peak cause follicular wave emergence and what aspects of development of a follicular wave are regulated by its preceding FSH peak.<p> In Experiment 1, we found that the amplitude of FSH peaks decreased, while basal serum FSH concentrations increased across the inter-ovulatory interval (P < 0.05). However, there were no associated changes in the growth, static or regression phases of follicular waves or the number and size of follicles in a wave. In Experiment 2, using computer-assisted quantitative echotextural analysis, we found that the numerical pixel value (NPV) for the wall of anovulatory follicles emerging in the third wave of the cycle was significantly higher than for waves 1 and 2 at the time of wave emergence but it decreased as follicles reached maximum follicular diameter (P < 0.05). A tendency for a similar pattern for the wall of follicles in the last wave of the cycle was also observed (P = 0.07).<p> In Experiment 3, treatment with ovine FSH (oFSH) increased the amplitude of an FSH peak by 5 to 6 fold. This treatment increased estradiol production (P < 0.05) but had little effect on other characteristics of the subsequent follicular wave. Daily injections of oFSH (Experiment 4) for four days, resulted in the occurrence of 4 discrete peaks in serum FSH concentrations. Each injection of oFSH resulted in the emergence of a new follicular wave.<p> In Experiment 5, six cyclic ewes received oFSH (0.1 ¦Ìg/kg, sc) every 6 h for 42 h, to try to give a gradual increase in the leading slope of an FSH peak. Serum FSH concentrations increased in oFSH treated ewes (P < 0.05) resulting in an additional peak between two endogenously driven FSH peaks and therefore, did not give the planned gradual leading slope to an FSH peak. Ovine FSH treatment occurred in the early growth phase of wave 1 of the inter-ovulatory interval and increased the growth rate of growing follicles in that wave, compared to control ewes (P < 0.05). This apparently induced dominance in follicles in wave 1, causing them to suppress wave emergence in response to the injected FSH. In Experiment 6, oFSH was infused constantly (1.98 ¦Ìg/ewe/h, iv, n = 6) for 60 h. Infusion of oFSH maintained serum FSH concentrations at a level similar to the zenith of a peak. This resulted in a superstimulatory effect with a peak in the mean number of large follicles on Day 2 after the start of FSH infusion (P < 0.001).<p> A hormonal milieu similar to low serum progesterone concentrations was created by treatment of ewes with prostaglandin and medroxyprogesterone acetate (MAP) sponges (Experiment 7). This treatment delayed regression of the penultimate follicular wave of a cycle. However, the delayed follicular atresia was accompanied by a greater degree of apoptosis in somatic cells of follicles growing in the penultimate wave compared to those in the final wave of the cycle, when collected one day before expected ovulation.<p> In conclusion, trends in basal serum concentrations of FSH and peaks in serum FSH concentrations, across the estrous cycle, are associated with changes in the image attributes of follicles emerging later in the estrous cycle, perhaps reflecting a greater readiness of those follicles for ovulation and formation of CL. The ovine ovary can respond to discrete peaks in serum FSH concentrations with the emergence of new follicular waves on a daily basis. This led us to conclude that follicular dominance is not evident in the ewe and peaks in serum FSH concentrations are likely to be driven by some endogenous rhythm that is unrelated to ovarian follicular secretory products. However, direct dominance can be induced by giving supplemented FSH during the growth phase of a follicle. Extended exposure of ovine ovaries to the serum concentrations of FSH found at the zenith of a peak overrides the mechanisms that recruit follicles into a wave and induces a superovulatory response in cyclic ewes. Finally, an increase in the incidence of apoptosis occurs in antral follicles in sheep that have an extended lifespan, prior to any morphological changes detectable by ultrasonography. This would seem to cause decreased follicular viability and lowered fertility of the oocytes that the follicles contain.