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No description available.

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.

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No description available.

No description available.

A maioria das perdas auditivas adquiridas ou congênitas decorre de dano ou perda das células ciliares da cóclea ou dos seus neurônios associados. A irreversibilidade da surdez em mamíferos ocorre devido à incapacidade de substituição das células perdidas, seja por divisão celular ou por regeneração de células endógenas no epitélio da orelha interna. Com isso o objetivo deste trabalho foi obtenção de linhagens de células progenitoras do epitélio coclear de fetos de cães com 40 dias de gestação, colaborando com futuras pesquisas relacionadas a trabalhos de tratamento para surdez neurossensorial. Foram utilizados oito fetos caninos com idade compreendidos a 40 dias de gestação, nos quais, foi realizada uma dissecação no crânio, expondo a cóclea para a retirada do epitélio coclear, visando sua analise morfológica, e obtenção de suas células. Para analise morfológica do tecido colear realizou-se as técnicas macroscópica, microscópica e de imunohistoquímica. As células obtidas da cóclea foram fotodocumentadas, e submetidas às analises de método colorimétrico MTT (3-(4,5-Dimethylthiazol-2-уl)-2,5-Diphenyltetrazolium Bromide), análise do ciclo celular, análise da imunofenotipagem e da diferenciação celular. Em cultivo as células apresentaram formato fibroblastóide. Na caracterização imunofenotipica apresentaram marcação positiva para marcadores de células-tronco mesenquimais e de pluripotência e marcação negativa para células hematopoiéticas. Apresentaram ainda a capacidade de diferenciação para linhagens celulares osteogênicas, adipogênicas e condrogênicas. Essas análises sugeriram resultados satisfatórios na obtenção, quantificação e caracterização dessas células, as quais foram adquiridas a partir de células do epitélio coclear de feto de cão, as quais poderão constituir fontes de células a serem utilizadas na terapia celular da espécie canina destinada ao tratamento de surdez causada por lesões ou danos do epitélio coclear / Most acquired or congenital hearing loss results from damage or loss of hair cells of the cochlea or their associated neurons. The irreversibility of deafness in mammals is due to the lost cells replacement inability, either by cell division or by regeneration of endogenous cells in the epithelium of the inner ear. Therefore, the objective of this work was to increase knowledge about getting progenitor cell lines of the cochlear epithelium from dogs’ fetuses with 40 days of gestation, collaborating with future research related to treatment work for sensorineural deafness. Eight canine fetuses were used aged as mentioned above, in which, a dissection was performed in the skull, exposing the cochlea to the withdrawal of the cochlear epithelium, for their morphological analysis and cells obtainment. For morphological analysis of the cochlear tissue was held the macroscopic techniques, microscopy and immunohistochemistry. The cochlea cells obtained were photo documented and analyzed for the colorimetric method MTT ( 3- ( 4,5- dimethylthiazol -2- уl ) -2,5 - Diphenyltetrazolium Bromide), cell cycle analysis, immunophenotyping analysis and cell differentiation. In culture, the cells showed fibroblast format. In immunophenotype characterization, they presented positive staining for mesenchymal stem cell markers and pluripotency and negative marking for hematopoietic cells. They also exhibit the differentiation capacity for cell osteogenic lineages, adipogenic and chondrogenic. These analyzes suggested satisfactory results in obtainment, quantification and characterization of these cells, which were acquired from the dog fetal cells’ cochlear epithelium, which may be cells of fonts to be used in cellular therapy of canine species for the treatment of deafness caused by injury or damage to the cochlear epithelium

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / Anencefalia é o defeito do tubo neural mais severo. A morfologia do ureter de fetos anencéfalos é desconhecida. O objetivo deste trabalho é analisar a estrutura do ureter de fetos humanos normais e anencéfalos (FHA). Nós estudamos 16 ureteres de 8 fetos sem anomalias congênitas (4 masculinos e 4 femininos) com idades entre 16 e 27 semanas pós concepção (SPC) e 14 ureteres de 7 FHA (4 masculinos e 3 femininos) com idades entre 19 e 33 SPC. Os ureteres foram dissecados e emblocados em parafina. Foram feitos cortes com 5 m e depois corados com Tricrômico de Masson, para quantificação das células de músculo liso (CML) e determinação da área da a luz do ureter, espessura e diâmetro. As amostras também foram coradas com Resorcina Fucsina de Weigert ( para observação das fibras elásticas) e Vermelho de Picro Sirius com polarização e análise imunohistoquímica das fibras do colágeno tipo III. Os dados da quantificação do músculo foram expressos em densidade volumétrica (Vv-%). As imagens foram capturadas com microscópio Olympus BX51 e câmera Olympus DP70. A análise morfológica da área do lúmen, espessura e diâmetro foram feitas usando o software Image J. As médias foram comparadas usando o teste t não pareado (p<0.05). O epitélio do ureter estava bem preservado em ambos os grupos, e não houve diferença entre os grupos. Não observamos fibras do sistema elástico em qualquer ureter analisados. Concentração de músculo liso (Vv) não diferiram significativamente (p = 0,4413) em FHA (12% 1,628) e grupo controle (13,51% 0,9231). A área de luz ureteral foi significativamente menor (p = 0,0341) em FHA (6365&#956;m 1,282), quando comparado ao grupo controle (20,170 5,480 mM). O diâmetro ureteral foi significativamente menor (p = 0,0294) em FHA (166.7&#956;m 10,99) quando comparado ao grupo controle (240 26,6 mM). A espessura ureteral foi significativamente menor (p = 0,0448) em FHA (30.57&#956;m 2,034), quando comparado ao grupo controle (7,453 47.49&#956;m). Colágeno tipo III foi observado em maior quantidade nos ureteres da FHA. Alterações estruturais ureterais nos fetos anencéfalos foram significativas em nosso estudo. O ureter de fetos com anencefalia mostraram mais concentração de colágeno tipo III, menor diâmetro, área e espessura. Nervos ureterais em FHA podem ser modificados devido a lesão cerebral com consequente dano no controle dos nervos ureterais. Isto pode levar a alterações estruturais no ureter de fetos anencéfalos. / Anencephaly is the most severe neural tube defect. Morphology of the ureter in anencephalic fetuses is unknown. The objective of this paper is to analyze the structure of the ureter in normal and anencephalic human fetuses (AHF). We studied 16 ureters from 8 fetuses without congenital anomalies (4 male and 4 female) aged 16 to 27 weeks post-conception (WPC) and 14 ureters from 7 AFH (4 male and 3 female) aged 19 to 33 WPC. The ureters were dissected and embedded in paraffin, from which 5m thick sections were obtained and stained in Masson trichrome, to quantify smooth muscle cells (SMC) and to determine the ureteral lumen area, thickness and diameter. The samples were also stained in Weigert Resorcin Fucsin (to observe elastic fibers) and Picro-Sirius Red with polarization and immunohistochemistry analysis of the collagen type III fibers to observe collagen. Stereological analysis of SMC was performed in sections. Data were expressed as volumetric density (Vv-%). The images were captured with Olympus BX51 microscopy and Olympus DP70 camera. The stereological analysis and the ureteral lumen area, thickness and diameter were done using the software Image Pro and Image J. Means were statistically compared using the unpaired t-test (p < 0.05). The ureteral epithelium was well preserved in the anencephalic and control groups without differences in the two groups. We did not observe elastic system fibers in any ureter analyzed. Smooth muscle concentration (Vv) did not differ significantly (p=0.4413) in AFH (12% 1.628) and control group (13.51% 0.9231). The ureteral lumen area was significantly smaller (p=0.0341) in AFH (6365m 1282) when compared to control group (20170 m 5480). The ureteral diameter was significantly smaller (p=0.0294) in AFH (166.7m 10.99) when compared to control group (240 m 26.6). The ureteral thickness was significantly smaller (p=0.0448) in AFH (30.57m 2.034) when compared to control group (47.49m 7.453). Type III collagen was observed in a higher quantity in ureters of AFH. Structural ureteral alterations in AFH were significant in our study. The ureter in fetuses with anencephalia showed more type III collagen concentration, smaller diameter, area and thickness. Ureteral nerves in AFH could be modified due to cerebral lesions with consequent brain control damage in ureteral nerves. This could lead to structural alterations in anencephalic ureter fetuses.