The suppressor of cytokine signaling ( SOCS ) proteins have been identified as important regulators of cytokine signaling. SOCS - 3 has been identified as being essential for normal fetal growth and survival, with the null mutation of the socs - 3 gene resulting in embryo death. The specific role of SOCS - 3 in fetal development, however, has yet to be characterized. Therefore, the overall aim of this thesis was to identify and quantify SOCS - 3 mRNA in a range of fetal tissues in the sheep. After identification of SOCS - 3 expression in fetal tissues, we then aimed to determine the ontogenic profile of SOCS - 3 in three key fetal tissues ; the liver, adipose tissue and adrenal gland, and whether SOCS - 3 expression in these tissues was altered after withdrawal and stimulation of prolactin ( PRL ). SOCS - 3 mRNA was found to be differentially expressed in a range of fetal tissues in late gestation and was higher in the fetal liver than in the pancreas, spleen and kidney. SOCS - 3 expression increased throughout gestation in the fetal liver, however, its expression decreased in the fetal adipose tissue and adrenal in late gestation. The pituitary hormone PRL has previously been implicated as a fetal growth factor. In the sheep fetus, PRL receptors are expressed in the fetal liver, adipose tissue and adrenal. We aimed to determine whether PRL plays a role in the maintenance of SOCS - 3 expression in the liver, adipose tissue and adrenal gland in late gestation, and whether SOCS - 3 expression can be regulated by acute PRL stimulation. We have demonstrated that PRL withdrawal suppressed SOCS - 3 expression in the liver, whereas acute PRL stimulation upregulated SOCS - 3 expression in the adrenal. Neither PRL withdrawal nor stimulation had an effect on SOCS - 3 expression in the adipose tissue. In summary, the data presented in this thesis would suggest that SOCS - 3 has tissue specific functions in late gestation. Furthermore, its expression is regulated in a tissue specific manner in response to the withdrawal or acute stimulation by PRL This provides the first evidence to suggest that the fetal liver and adrenal are both sensitive to either chronic or acute changes in plasma PRL concentrations, measured as the suppression or upregulation of SOCS - 3. We speculate that changes in SOCS - 3 mRNA expression relates to the regulation of growth and functional maturation of fetal tissues throughout gestation, and that PRL may represent an important factor which acts to alter SOCS - 3 expression in key fetal tissues. / Thesis (Ph.D.)--School of Molecular and Biomedical Science, 2006.

Bibliography: leaves 161-189. / xx, 189 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / The aim of the series of experiments described in this thesis was to investigate the functional characteristics of the subpopulations of the corticotrophs in the fetal pituitary during normal development and after chronic intrauterine stress. / Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biomedical Sciences, Discipline of Physiology, 2004

Errata pasted onto back end-paper. Bibliography: leaves 213-246. Describes the interactions among pituitary-derived peptides, intra-adrenal exposure to glucocorticoids and the local adrenal and endocrine IGF axes in the growth and functional activation of the ovine fetal adrenal gland before birth. Also considers the involvement of these systems in the fetal response to chronic stess and intra-uterine growth restriction. Proposes and develops several conceptual models of the control of adrenal growth and function in late-gestation.

Bibliography: 161-199. / [xxvi], 199, [151] leaves, [7] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Characterises the normal otogeny of the cellular composition and structure of placentomes in sheep, their relationship to the macroscopic parameters of placentome size and morphology, and the effect of experimental and natural restriction of implantation on the growth and development of placentomes between mid and late gestation. / Thesis (Ph.D.)--University of Adelaide, Dept. of Obstetrics and Gynaecology, 1995

Errata pasted onto back end-paper. / Bibliography: leaves 213-246. / xix, 246, [30] leaves : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Describes the interactions among pituitary-derived peptides, intra-adrenal exposure to glucocorticoids and the local adrenal and endocrine IGF axes in the growth and functional activation of the ovine fetal adrenal gland before birth. Also considers the involvement of these systems in the fetal response to chronic stess and intra-uterine growth restriction. Proposes and develops several conceptual models of the control of adrenal growth and function in late-gestation. / Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2000

Abstract not available

Abstract not available

"March 2003" / Includes bibliographical references (leaves 237-297) / ix, 297 leaves : ill. (some col.), plates (col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, School of Agriculture and Wine, Discipline of Animal Science, 2005

Includes bibliographical references. / 1 v. (various foliations) : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Indicates that retarded fetal growth in sheep, associated with restricted supply of substrates to the fetus, is accompanied by reduced concentrations of insulin-like growth factor I in fetal blood and its decreased production in several major fetal tissues. / Thesis (Ph.D.)--University of Adelaide, Dept. of Obstetrics and Gynaecology, 1995

[Truncated abstract] In obstetric practice, pregnant women at risk of pre-term delivery between 24 and 34 weeks of gestation are administered synthetic glucocorticoids (betamethasone or dexamethasone) to induce fetal organ maturation. During this gestational period, the fetal kidney is undergoing a phase of rapid organogenesis with an increase in renal growth and active nephrogenesis occurring. The studies comprising this thesis examine the effects of prenatal betamethasone exposure on the fetal and adult ovine kidney. The central hypothesis of these studies was that exposure of the fetal kidney to betamethasone in late gestation would change renal structure and induce long-term alterations in the expression of glucocorticoid-sensitive genes and proteins. In the fetal studies, pregnant Merino ewes bearing single fetuses received single or repeated-weekly intra-muscular (i.m.) injections of betamethasone (0.5 mg/kg body weight) or saline commencing on day 104 of gestation (term is 150 days). Kidneys were collected from fetuses at 109, 116, 121 and 146 days of gestation (d). Using gold standard unbiased stereological techniques, the physical disector/fractionator method, total glomerular (nephron) number and glomerular volume were determined in 146 d fetal kidneys exposed to repeated maternal saline or betamethasone administration. In the adult study, kidneys were collected from 3.5-year-old sheep that had been exposed to ... In this thesis I have demonstrated that renal growth restriction as a result of betamethasone exposure is associated with a reduction in fetal nephron endowment. Although betamethasone does not appear to consistently alter nephron number or glomerular size, it may indirectly affect total nephron endowment through effects on renal growth. I have also provided evidence which suggests that lategestation betamethasone exposure in sheep does not program permanent alterations in the renal expression of genes or proteins involved in glucocorticoid hormone action or components of the renin-angiotensin system. Therefore, exposure of the fetal kidney to betamethasone during nephrogenesis may alter renal structure if kidney growth is perturbed; however, there are no persistent alterations in the expression of glucocorticoid-sensitive genes. These findings are consistent with the preservation of normal basal blood pressure in the adult sheep I studied and with the limited results from human studies of late-gestation maternal glucocorticoid administration.