Thesis (Ph. D.)--University of Wisconsin--Madison, 1955. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 83-87).

Thesis (Ph. D.)--University of Hong Kong, 1996. / Includes bibliographical references (leaf 140-157).

Thesis (Ph. D.)--University of Virginia, 2000. / Spine title: Role of REGL in glucose repression. Includes bibliographical references (p. 194-220). Also available online through Digital Dissertations.

Thesis (M. Phil.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 112-131) Also available online.

Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 133-144).

Thesis (Ph.D.) - University of Queensland, 2003. / Includes bibliography.

Thesis (Ph. D.)--Ohio State University, 2005. / Available online via OhioLINK's ETD Center; full text release delayed at author's request until 2006 Nov 30

Thesis (Ph.D)--Boston University / The purpose of the research was to investigate the action of prostatic acid phosphatase on a spectrum of physiologically significant phosphate esters under varying environmental conditions. The effects of varying pH, substrate concentration, and enzyme concentration, the influence of inhibitors, and the influence of time on enzymatic hydrolysis were studied with each substrate. The enzymes extracted from both normal and cancerous prostatic tissue were used in an attempt to discover any differences existing between enzymes. A survey of the literature was made. A historical review of the history of acid phosphatase, its distribution in animal tissues and the influence of experimental conditions on enzyme activity is included in the body of the dissertation. Little work has been done to investigate the action of acid phosphatases on physiologically significant substrates, and the comparison of normal and cancerous enzyme preparations from human tissues has attracted the attention of only several investigators. [TRUNCATED]

The response of Pseudomonas aeruginosa to phosphate starvation and subsequent refeeding was studied by following changes in turbidity, cell count and chemical composition on incubation in phosphate deficient medium. In shaken, phosphate deficient cultures, the turbidity and viable cell count were shown to increase significantly, with the latter reaching a maximum level at 24 hours under the conditions employed. A linear response of phosphate starved cells to low levels of phosphate supplied exogenously was evident from turbidity measurements, and a threshold requirement for phosphate analogous to the "energy of maintenance" (McGrew and Mallette, 1962) was not detected. In still, phosphate deficient cultures, the turbidity and total cell count increased and the viable cell count decreased slightly at 24 hours. The levels of protein and deoxyribonucleic acid (DNA) per ml of culture increased during this period, and the amount of ribonucleic acid (RNA) decreased. Extensive ribosomal degradation was apparent from sucrose density gradient centrifugation patterns. An enzyme having an alkaline pH optimum and displaying activity against a wide variety of phosphomonoesters was demonstrated in phosphate-starved cells. The enzyme was inhibited by inorganic phosphate, and was considered to be the counterpart of the repressible phosphomono-esterase reported in other microorganisms and studied in detail in Escherichia coli (Torriani, i960; Garen and Levinthal, I960; Heppel, Harkness and Hilmoe, 1962). The enzyme activity of cell free extracts of P. aeruginosa was shown to be associated mainly with the ribosomal fraction. / Land and Food Systems, Faculty of / Graduate

L’obésité, liée à la résistance à l’insuline, au diabète de type 2 et aux maladies cardiovasculaires, est un problème de santé majeur de notre société. Nous avons démontré que la protéine tyrosine phosphatase Shp1, dont l’expression est significativement augmentée dans les tissus cibles de l’insuline chez les souris obèses, est un régulateur de l’homéostasie du glucose dans le foie et le muscle. Shp1 est impliqué dans la modulation de l’expression et de l’activité du récepteur nucléaire PPARγ dans le foie. Nos recherches ont porté sur la caractérisation de Shp1 dans les adipocytes, la signalisation de l’insuline et le transport du glucose soit en sous-exprimant ou en exprimant de façon constitutive Shp1 dans les cellules adipeuses 3T3-L1. L’état physiologique des cellules a été caractérisé par la mesure de la coloration Oil-Red-O, des triglycérides, de l’expression de PPARγ et de ses gènes cibles et de leurs protéines, de la réponse à l’insuline par le transport du glucose ainsi que l’expression et de la phosphorylation des protéines impliquées dans la signalisation de l’insuline. La diminution de l’expression de Shp1 a entraîné un délai lors du début de la différenciation mesurée par l’expression retardée de PPARγ et certains de ses gènes cibles, mais n’a pas beaucoup affecté le phénotype des cellules complètement différenciées. Bien que la réduction de Shp1 ait augmenté la phosphorylation d’Akt stimulée par l’insuline, le transport de glucose n’a pas été modifié dans ces cellules, et l’expression de glut4 a légèrement diminué. L’expression constitutive de Shp1 a entraîné une forte diminution des niveaux de PPARγ, inhibant totalement la différenciation, l’expression de glut4 et le transport du glucose. Nos données suggèrent que Shp1 joue un rôle important dans les adipocytes comme régulateur de l’adipogenèse par la modulation de l’expression et l’activité de PPARγ et par la régulation de la signalisation de l’insuline. / Obesity, which is causally linked to the development of insulin resistance, type 2 diabetes (T2D) and cardiovascular disease (CVD), is a major health issue in our society. We have demonstrated that the protein tyrosine phosphatase Shp1, whose expression is significantly increased in insulin target tissues of obese mice, is a regulator of glucose homeostasis in liver and muscle. Shp1 is implicated in the modulation of expression and activity of the nuclear receptor PPARγ in liver. Here, we describe the characterization of Shp1 in adipocytes by analyzing its role in adipocyte differentiation, insulin signaling and glucose transport by either knocking-down or constitutively expressing Shp1 in 3T3-L1 adipose cells. The physiological state of the cells was characterized by measuring Oil-Red-O staining, triglyceride content, expression of PPARγ and its target genes and their proteins, insulin response by glucose uptake and the expression and phosphorylation of proteins involved in insulin signaling. Knockdown of Shp1 led to a retardation in the onset of differentiation as measured by delayed expression of PPARγ and some of its target genes, but did not much affect the phenotype of fully differentiated cells. Although reducing Shp1 increased insulin-stimulated Akt-phosphorylation, glucose transport was not changed in these cells, and glut4 expression was slightly decreased. Constitutive expression of Shp1, resulted in a strong decrease of PPARγ levels thereby totally inhibiting differentiation, glut4 expression and glucose transport. Our data suggest that Shp1 plays an important role in adipocytes both by acting as a regulator of adipogenesis through modulation of the expression and activity of PPARγ and by regulating the insulin signaling pathway.