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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

A micro-capon assay method for androgens and its application to human blood

Johnston, Carter Dupuy, January 1945 (has links)
Thesis (Ph. D.)--University of Chicago, 1942. / Reproduced from type-written copy. "Literature cited": p. 17-18.
2

Mechanisms Underlying Sex Differences In Impulsivity

January 2019 (has links)
archives@tulane.edu / The current set of experiments aimed to explore mechanisms underlying sex differences in impulsive behavior in adult rats and sex differences in structures involved in impulse control. Preliminary studies demonstrated sex differences in adult impulsive action and prepubertal impulsive choice with males making more impulsive responses than females. In our studies, neither prepubertal nor adult gonadectomy, and subsequently a loss of gonadal hormone exposure, had any effect on a sex difference in impulsive action. Neonatal exposure of gonadal hormones in females led to a masculinization of impulsive responding in adulthood and eliminated an observed sex difference. This result demonstrates neonatal gonadal hormones to be an organizing mediator of an adult sex difference in impulsive action. No sex difference was seen in adult impulsive choice across hormone conditions. Analysis of myelin protein levels within the orbitofrontal cortex (OFC), a region important for inhibiting impulsive behavior, revealed adult females to exhibit greater levels of myelin basic protein (MBP) than males. This adult sex difference was revealed to be mediated by organizing effects of pubertal gonadal hormone exposure. Inactivation of indirect pathway projecting striatal neurons, neurons important for inhibition of motor output, via designer receptors exclusively activated by designer drug (DREADD) technology, led to a decrease in impulsive responding in adult males and females, eliminating an observed sex difference. Collectively, these results demonstrate for the first time periods of gonadal hormone driven organization of brain morphology and behavior with implications for sex differences in decision making and impulse control. / 1 / Jeffrey Scott Darling
3

Réentraînement à l'effort chez des sujets atteints du syndrome métabolique : impact sur les réponses hormonales et la qualité de vie / Exercise Training in men with metabolic syndrome : the effects on hormones and quality of life

Baillot, Aurélie 13 December 2010 (has links)
Le syndrome métabolique (Smet) désigne une combinaison d'anomalies métaboliques (obésité, insulinorésistance, dyslipidémie et hypertension) reliées entre elles, dont l‘origine n‘est pas encore définie. D‘après la littérature, les personnes atteintes du Smet présentent des altérations hormonales et de la qualité de vie, mais ce concept étant relativement récent, peu d‘études se sont intéressées aux effets de l‘activité physique régulière sur ces paramètres. Notre travail se divise en deux parties. Dans un premier temps, nous avons étudié la corrélation entre les concentrations hormonales surrénaliennes plasmatiques et salivaires au repos et à l‘exercice chez les hommes atteints du Smet. Il apparait que la corrélation obtenue au repos n‘est pas altérée de manière significative à l‘exercice. Dans un second temps, nous avons étudié les effets d‘une activité physique régulière contrôlée de 8 semaines sur les réponses hypophysaires, surrénaliennes et androgéniques, ainsi que sur les capacités physiques et la qualité de vie chez des hommes atteints du Smet. Nos résultats montrent qu‘un entraînement aérobie de courte durée ne provoque pas de changement anthropométrique mais induit une diminution significative du cortisol salivaire au repos sans modifier les autres concentrations hormonales. Par ailleurs, les capacités physiques et la dimension psycho-sociale de la qualité de vie sont significativement améliorées. Ces données confirment l‘effet bénéfique de l‘activité physique régulière sur les capacités physiques et la qualité de vie, tout en laissant supposer que le cortisol salivaire serait un marqueur précoce signant l‘amélioration des capacités physiques chez les sujets atteints du Smet. D‘autres études, incluant des cohortes plus larges et des durées de réentraînement à l‘effort plus importantes, seraient nécessaires pour compléter ce travail. / The metabolic syndrome (Mets) is a cluster of metabolically related abnormalities (abdominal obesity insulin resistance, dyslipidemia and hypertension), with no obvious defined cause. In the literature, individuals with Mets seem to have hormonal and quality of life alterations, but this concept is relatively recent and few studies have investigated the effects of regular physical activity on these parameters. Our work divides into two parts. First, we studied the correlation between plasmatic and saliva adrenocortical hormonal at rest and during exercise in men with Mets. It appears that the correlation obtained at rest is maintained during exercise. Secondly, we studied the effects of 8 weeks of controlled regular physical activity on the pituitary, adrenocortical and androgenic hormones, physical capacity and quality of life in men with Mets. Our results show that aerobic exercise training does not induce anthropometric modifications but decreases significantly basal saliva cortisol without any other hormonal change. In parallel, physical capacity and psychosocial impact dimension of quality of life are significantly improved. These data confirm the beneficial effect of regular physical activity on physical capacity and quality of life. It is tempting to suggest that saliva cortisol could be an early marker reflecting improvement of physical capacities in individuals with Mets. Further works with larger cohort and longer training programs are required to complete this work.
4

The role of pituitary adenylate cyclase-activating polypeptide (PACAP) in cell cycle exit, differentiation and apoptosis during early chick brain development

Erhardt, Nola Marlene 12 April 2017 (has links)
Regulated survival, proliferation and differentiation of cells in the nervous system is crucial for development. Much of regulation is controlled by hormones. There is abundant evidence that a member of the glucagon superfamily, pituitary adenylate cyclase-activating polypeptide (PACAP), is important in this process. PACAP functions have been described in the peripheral and central nervous systems of many species. Although the primary function of PACAP is not known, its high conservation and presence in all species examined to date suggest it is vital to normal development. My thesis objective was to determine the response of early CNS neuroblasts to PACAP, in conjunction with another glucagon superfamily member, growth hormone releasing hormone (GHRH). GHRH is best known for causing release of growth hormone from the pituitary, but it also has functions in nervous system development. Because PACAP and GHRH are encoded on the same gene in non-mammalian vertebrates, it is possible that they have similar or coordinated functions. PACAP affects development by altering levels of proliferation and differentiation and decreasing apoptosis. For these reasons, I focused my research in these areas. Using neuroblast-enriched cultures from embryonic day 3.5 chick, my first goal was to show that PACAP and GHRH affected these cells. Radioimmunoassays for cAMP revealed that all but one form of PACAP, and only one form of GHRH, caused an increase in cAMP relative to controls. As to the former, comparison of differing PACAP structures suggested that conservation at the amino terminus was important in binding the hormone to the receptor. The fact that PACAP, but not GHRH, increased cAMP, indicated that evolution of PACAP and GHRH had altered their functions. Chick neuroblasts were also shown to produce PACAP and its primary receptor, suggesting an autocrine/paracrine role for PACAP. My next goal was to examine the nature of the downstream effects of increased cAMP. To study cell cycle, I developed a protocol using proliferating cell nuclear antigen (PCNA) and propidium iodide (PI), in fixed cell populations. PCNA is present in low amounts in non-cycling cells, but rises sharply in actively proliferating cells. The PI helped delineate cell cycle compartments, because in permeabilized cells it binds to and quantifies DNA. Changes in G0, G1, S and G2/M were recorded using flow cytometry. Because the cells were producing PACAP and most were cycling, rather than add more PACAP I chose to block the PACAP receptor. This caused cell cycle exit. I also blocked the cell cycle at two points, and showed that exogenous PACAP could release some cells from the block, and return them to cycling. PACAP affected apoptosis also, but because the protocol was not designed to measure this, I adopted another protocol using flow cytometry. With live cells, and fluorescein diacetate, which is retained and fluoresces in healthy cells, and PI, which enters only cells with damaged membranes, I used the characteristic of apoptotic cells to die with membranes intact to confirm increased apoptosis when the PACAP receptor was blocked. This left the question of whether PACAP affected differentiation. The cell cycle protocol had shown some cells were still quiescent, not dying, at 24 h, so I hypothesized that they might be differentiating. I used proteomics to test this. With isotope-coded affinity tagged (ICAT) analysis, I measured changes in protein content in cells that had been treated with the receptor blocker, compared to control. This confirmed previous work and my hypothesis that some cells were differentiating. Because this technique is not commonly used in molecular biology, I also evaluated the effectiveness of the technique. My work showed that endogenous PACAP keeps chick neuroblasts alive and cycling, but will allow some to differentiate rather than die, when the hormone is withdrawn. Obviously, PACAP plays a crucial role in early chick brain development. / Graduate
5

Adrenal secretion, estrus, and ovarian activity in bovine treated with corticosteroids

Cook, James Francis, 1949- January 1972 (has links)
No description available.
6

Plasma corticoids and progestins in postpartum dairy cows

Okerberg, Carlin Vance, 1947- January 1972 (has links)
No description available.
7

Hormonal influences on sex-linked sexual attitudes

Charles, Nora 15 May 2009 (has links)
Previous studies of non-human animals and humans with endocrine abnormalities have demonstrated that higher prenatal androgen levels promote more male-typical behavior, including cognitive abilities and sexual behavior. Research on normal hormonal fluctuations (e.g. menstrual cycle studies) has shown additional effects of circulating sex hormones in postnatal life on the expression of a number of sex-linked cognitive and sexual behaviors. This research was designed to replicate previously reported sex differences in a variety of domains and to extend prior findings of an association between low (male-typical) 2nd to 4th digit (2D:4D) ratio, enhanced (maletypical) mental rotation ability, and more liberal (male-typical) sexual attitudes and behavior in women. This is also the first study to examine the effects of hormonal factors and other sex-linked variables on sociosexuality in men. As part of this study, participants (n = 127) completed a battery of gender role measures, sex-linked cognitive tasks, and a sexual attitudes questionnaire. Prenatal androgen levels were indirectly measured by means of the index to ring finger (2D:4D) ratio, and testosterone and progesterone levels were obtained from saliva samples collected at each session from participants who were not using hormonal contraceptives. Results replicate previously reported sex differences in sexual attitudes, sex-linked behaviors and personality traits. More importantly, results provide the first evidence for both pre- and postnatal contributions to sexual attitudes. Men with lower (more male-typical) 2D:4D ratios reported less restricted (more male-typical) sexual attitudes, suggesting that prenatal hormone levels may influence sexual attitudes in adulthood, at least in men. Additionally, the tendency for women who were not using hormonal contraceptives to report less restricted sexual attitudes during the mid-luteal phase of their cycle than during the menstrual phase suggests that changes in circulating sex hormone levels in adulthood, such as those during the menstrual cycle, may influence sexual attitudes in women.
8

Loss of DACH2 is an Early Event in Breast and Ovarian Carcinogenesis

Chehade, Rania 18 February 2014 (has links)
Mechanistic insights into how enduring menstrual cycle hormonal signaling promotes tumorigenesis are emerging. We performed a genome-wide screen in primary epithelial cells to identify hormonally-regulated candidates that initiate pro-tumorigenic phenotypes in normal cells. One candidate, DACH2, has been described as part of a network that regulates organogenesis during development. In vitro, we find that DACH2 expression is regulated by estrogen and progesterone in a dosage dependent manner. Lentiviral-mediated shRNA silencing of DACH2 in hormonally responsive tissues promotes expansion of cells with progenitor characteristics. Within gene expression profiles of fallopian tubes, DACH2 is a member of a minimal gene classifier that distinguishes follicular versus luteal phases. Decreased DACH2 is characteristic of luteal-phase tubal cells and the majority of ovarian serous carcinomas. These studies suggest that DACH2 may orchestrate a physiological program that, when deregulated, locks cells in a progenitor-state, induces uncontrolled proliferation, and predisposes cells for breast and ovarian carcinogenesis.
9

Loss of DACH2 is an Early Event in Breast and Ovarian Carcinogenesis

Chehade, Rania 18 February 2014 (has links)
Mechanistic insights into how enduring menstrual cycle hormonal signaling promotes tumorigenesis are emerging. We performed a genome-wide screen in primary epithelial cells to identify hormonally-regulated candidates that initiate pro-tumorigenic phenotypes in normal cells. One candidate, DACH2, has been described as part of a network that regulates organogenesis during development. In vitro, we find that DACH2 expression is regulated by estrogen and progesterone in a dosage dependent manner. Lentiviral-mediated shRNA silencing of DACH2 in hormonally responsive tissues promotes expansion of cells with progenitor characteristics. Within gene expression profiles of fallopian tubes, DACH2 is a member of a minimal gene classifier that distinguishes follicular versus luteal phases. Decreased DACH2 is characteristic of luteal-phase tubal cells and the majority of ovarian serous carcinomas. These studies suggest that DACH2 may orchestrate a physiological program that, when deregulated, locks cells in a progenitor-state, induces uncontrolled proliferation, and predisposes cells for breast and ovarian carcinogenesis.
10

Antisense peptides and protein structure

侯嘉俊, Hau, Ka-chun. January 2002 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

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