A series of six experiments was conducted on female cattle and guinea-pigs to investigate the effects of some anabolic compounds on both growth and reproductive functions in the two species. The results indicate that trenbolone acetate increased significantly, the live-weight gains of heifers and improved the efficiency of food conversion. Zeranol and oestradiol-17 treatments had no effect on growth performance. Trenbolone acetate inhibited or delayed ovulation and resulted in elevation of plasma oestradiol-17 concentrations. Zeranol and oestradiol-17 had no effect on estrous cycle occurrence nor ovulation as determined by plasma progesterone concentrations. It is concluded from studies investigating the response to gonadotrophin releasing hormone (Gn-RH), oestradiol benzoate (OE2-B) and pregnant mares' serum gonadotrophins (PMSG) that trenbolone acetate acts (1) on the pituitary gland to decrease the sensitivity to Gn-RH, (2) on the ovary to decrease the sensitivity of the ovarian follicles to gonadotrophins and (3) acts on the pituitary gland and/or the hypothalamus to block the positive feedback effect of oestrogen to release the LH-surge. In the guinea-pig, trenbolone acetate at dose levels of 2 and 10 mg/kg body-weight inhibited ovulation. At a dose level of 0.4 mg/kg body weight, trenbolone acetate prolonged the length of the oestrous cycle. When trenbolone and testosterone, at dose levels of 3.1 and 15.7 mmol/l each, were compared, trenbolone was shown to have more general promoting activity than testosterone. The high dose of both hormones inhibited ovulation and increased the rate of occurrence of atretic follicles. However, only testosterone at the higher dose decreased the weight of the ovaries and lowered the number of follicles. From studies measuring the response to follicles stimulating hormone (FSH) and human chorionic gonadotrophin (HCG), it is concluded that, in the female guinea-pig, trenbolone acetate had no effect on LH-surge mechanism, but it may act on the pituitary gland to block the release of FSH.

Les travaux de cette thèse ont porté sur le contrôle des neurones à GHRH dans des conditions physiologiques et pathologiques. Le but étant de caractériser les mécanismes cellulaires et moléculaires impliqués dans le fonctionnement ou dérégulations du réseau de neurones à GHRH. Ces neurones sont les principaux stimulateurs de la libération de l’hormone de croissance (GH). Nous avons d’abord montré que l’axe de la croissance et de l’appétit peuvent être régulés indépendamment au niveau de l’hypothamus. En effet, la ghréline, seule hormone produite par le tractus gastro-intestinal et connue pour stimuler la libération de GH en agissant principalement sur les neurones GHRH, stimule ces derniers de manière uniquement directe. Ces effets sont indépendants de ceux qu’elle exerce sur les neurones voisins à NPY, orexigéniques. De plus, la ghréline et les GHS (agonistes sélectifs du récepteur de la ghréline) ne changent pas le mode de décharge électrique des neurones à GHRH ni ne les synchronise. Enfin, ces effets ne présentent pas de dimorphisme sexuel. Dans un second temps, la somatostatine, principal inhibiteur de l’axe GH, induit un rythme d’activité électrique des neurones à GHRH médié par les récepteurs de sous-type SST1 et SST2. Ces effets sont donc temps-dépendants, et aussi sexuellement dimorphiques. Ils sont probablement impliqués dans la modulation de la pulsatilité ultradienne de la libération de GH. Enfin, après un traumatisme crânien, nous observons un déficit de la libération de GH qui apparaît tôt et est soutenu, comme ceux observés chez l’humain. Aucune inflammation ni changement histologique n’a été observe dans l’hypophyse. Cependant, l’inflammation, impliquant une réaction tanycytaire, microgliale, astrocytaire, est présente dans le noyau arqué et l’éminence médiane (EM), ou sont respectivement présents les corps cellulaires et terminaisons des neurones à GHRH. Ceci est lié à des changements morpho-fonctionnels de l’EM (augmentation perméabilité, rupture des barrières tanycytaires). Aucun changement n’a été observé dans le noyau périventriculaire, où sont localisés les neurones à somatostatine. Enfin, les propriétés électriques passives des neurones à GHRH ne sont pas modifiées. En conclusion, une dérégulation de leur activité au niveau des terminaisons nerveuses doit expliquer les défauts posttraumatiques de libération de GH. / The works of this thesis were interested in the control of the hypothalamic GHRH neurons in physiological and pathological conditions. The goal was to clarify the molecular and cellular mechanisms involved in the control or impairments of GHR neuronal network functions. These neurons are the main stimulators of the GH release. We first showed that the hypothalamic growth axis could be regulated independently from the feeding network. Indeed, GHRH neurons are directly stimulated by ghrelin, which is the only hormone produced by the gastrointestinal tract known to stimulate the GH release through acting mainly on GHRH neurons. These effects are independent from its orexigenic effects exerted on the neighbourings NPY neurons. In addition, ghrelin and GHS (synthetic ghrelin receptor agonists) don’t change neither the firing rate of GHRH neurons, nor synchronize them. These effects are not gender-dependant; by contrast, Somatostatin, the major GH axis inhibitor, generates a sexual dimorphic and rhythmic inhibition of the GHRH neurons electrical activity mediated by its SST1 and SST2 receptors subtypes. These effects are so time-dependant direct and indirect effects and can probably be involved in the generation of the ultradian rhythm of the GH release. After a traumatic brain injury, we found an early and sustained deficiency of the GH release, like those observed in human. No pathological changes are visible in the pituitary gland. Inflammation occurs at the arcuate nucleus, and mainly at the median eminence levels; it involves a strong astrocyte reaction, tanycytes, and microglial and (or) infiltrated immune cells activations. These changes elicit morpho-functional impairments of the median eminence, permeability and leakage of the tanycyte barrier between the blood, CSF and Arc; at the opposite, nothing occur at the periventricular level, where are located SST neurons. Neither the number of GHRH neurons, neither their passive electrophysiological properties changed. Impairments of the activities of the GHRH nerve terminals, maybe associated to impairments of their regulated activity, must explain a GH deficiency.

No description available.

Heart transplantation has enjoyed a spectacular success over the past 25 years. Prior to 1980 less than 350 operations were carried out with an overall one year survival of less than 60%. In 1995 more than 3,000 transplants were performed with a one year survival of 83%. However, growth and improved survival have both plateaued over the last few years; the former because of the falling donor supply and the latter, in part, because of the use of less suitable donors in an effort to offset the problem of supply. Much attention has been focused on the drama of the surgery and the intricacies of immunological manipulation whilst little effort has been devoted to the area of donor management, despite the fact that primary graft failure is responsible for as many post transplant deaths as either infection or rejection. Optimum preservation of the donor heart has also provided a difficult challenge, such that, despite a considerable scientific effort little advance has been achieved to extend the 4 hour safe storage limit which has remained in place over the past 20 years. In this dissertation the problem has been approached by combining laboratory based preservation models with an objective regime of donor management. A sensitive isolated small animal working heart model was developed and used to characterise cardioplegic induction. Subsequently, the model was used to examine the interaction of oxygen content with the mode of delivery, during preservation. Finally, a number of representative solutions were combined with the most promising oxygen delivery method. These studies served to illustrate the utility of controlled laboratory studies and offer the prospect of more than doubling post storage function. The development of a rigorous donor management regime was also shown to be capable of reducing the variance in haemodynamic parameters by up to 44% whilst safely increasing the donor pool by approximately 30%. It is the contention of this thesis that the only prospect of improving the current impasse with the supply of donor hearts in sufficient quantity and of acceptable quality, is by the combination of appropriate laboratory models with controlled clinical trials.

Wang, Yanfei. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 135-148). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

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

Congenital hypothyroidism (CH), a pediatric endocrine condition that results in early thyroid hormone (TH) insufficiency, is associated with visuospatial dysfunction suggestive of selective dorsal visual stream impairment. However, the ventral visual stream has not been adequately investigated in this population and so the effect of early TH insufficiency on development of the two streams had not been clearly established. This thesis used a comprehensive set of neuropsychological and experimental tests to assess higher-order visual functions in children and adolescents with CH compared with typically developing individuals. The results show that while CH is associated with poorer performance on tasks tapping into dorsal stream functions such as judgment of line orientation, spatial localization, three-dimensional block and two-dimensional mental construction, judgment of object location, and mental rotation, performance on typical ventral stream tasks such as identity discrimination, including abstract shapes, faces, and buildings, is relatively unimpaired. Thus this thesis establishes that the dorsal visual stream is selectively vulnerable to TH insufficiency. In addition to the investigating the nature of the higher-order visual problems in CH, this thesis explores the mechanism underlying these problems and assesses whether they result from organizational effects by early TH or activational effects by current TH levels. The data support the organizational mechanism and suggest that prenatal TH insufficiency results in irreversible changes to the dorsal visual stream due to the timing of dorsal stream development, which occurs earlier than ventral stream development and is thus more vulnerable to insult.

Congenital hypothyroidism (CH), a pediatric endocrine condition that results in early thyroid hormone (TH) insufficiency, is associated with visuospatial dysfunction suggestive of selective dorsal visual stream impairment. However, the ventral visual stream has not been adequately investigated in this population and so the effect of early TH insufficiency on development of the two streams had not been clearly established. This thesis used a comprehensive set of neuropsychological and experimental tests to assess higher-order visual functions in children and adolescents with CH compared with typically developing individuals. The results show that while CH is associated with poorer performance on tasks tapping into dorsal stream functions such as judgment of line orientation, spatial localization, three-dimensional block and two-dimensional mental construction, judgment of object location, and mental rotation, performance on typical ventral stream tasks such as identity discrimination, including abstract shapes, faces, and buildings, is relatively unimpaired. Thus this thesis establishes that the dorsal visual stream is selectively vulnerable to TH insufficiency. In addition to the investigating the nature of the higher-order visual problems in CH, this thesis explores the mechanism underlying these problems and assesses whether they result from organizational effects by early TH or activational effects by current TH levels. The data support the organizational mechanism and suggest that prenatal TH insufficiency results in irreversible changes to the dorsal visual stream due to the timing of dorsal stream development, which occurs earlier than ventral stream development and is thus more vulnerable to insult.

Reproduction de : Thèse d'exercice : Médecine : Nancy 1 : 2003. / Titre provenant de l'écran-titre.

Thesis (Ph. D.)--University of Missouri-Columbia, 2003. / Typescript. Vita. Includes bibliographical references (leaves 91-102). Also available on the Internet.