Thesis (Ph. D.)--University of Texas at Austin, 2000. / Vita. Includes bibliographical references (leaves 261-290). Available also in a digital version from Dissertation Abstracts.

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My studies have investigated the possible involvement of the plasminogen activator/plasmin system in glomerular physiology and pathology. Urokinase plasminogen activator and its cellular receptor are not found immunocytochemically within the normal or diseased glomerulus in vivo. Plasminogen activator inhibitor-1, an inhibitor of urokinase plasminogen activator was, however, identified in crescents from cases of crescentic glomerulonephritis, but not within the glomerular tuft proper. Culture of human glomerular cells initially revealed urokinase plasminogen activator and plasminogen activator-1 proteins within the supernatant of epithelial cells and mesangial cells, as measured by ELISA. However, immunocytochemical characterisation of each of the cell cultures showed that there was contamination of some of the mesangial cell cultures by epithelial cells. Pure cultures of both types of cell produced plasminogen activator inhibitor-1. However, measurement of urokinase plasminogen activator activity by zymography confirmed that this molecule was not present within supernatants obtained from pure mesangial cell cultures. Furthermore, the use of combined non-isotopic in situ hybridisation and immunocytochemistry allowed identification of urokinase plasminogen activator mRNA only within human cultured glomerular epithelial cells and not within mesangial cells. This finding proved that contaminating epithelial cells were responsible for urokinase plasminogen activator production in cultures thought to be made up of pure mesangial cells. Thus there is excellent evidence for synthesis of this molecule only by epithelial cells. Non-isotopic and radioactive in situ hybridisation were unsuccessful in identifying urokinase plasminogen activator within human kidney sections and the difficulties involved in the methodology of this technique, and the implications of the culture cell work for the role of the plasminogen activator/plasmin system in the glomerulus, are discussed.

Chronic renal failure (CRF) is associated with loss of lean body mass, a high incidence of malnutrition, and with insulin resistance. CRF is often complicated by metabolic acidosis. Metabolic acidosis is known to alter both protein and carbohydrate metabolism. A series of studies have been undertaken to investigate the effect of metabolic acidosis on protein metabolism in both normal and CRF human subjects, and to study whether metabolic acidosis in CRF affects insulin sensitivity. Protein turnover was studied using the technique of primed constant infusions of L-[1-¹³C]leucine. Normal subjects were studied before and after ammonium chloride induced metabolic acidosis. Acidosis was associated with increased protein turnover and amino acid oxidation. In CRF subjects, correction of acidosis with sodium bicarbonate decreased protein turnover and amino acid oxidation. The effect of acidosis in CRF on insulin mediated carbohydrate metabolism was studied using the technique of the hyperinsulinaemic euglycaemic clamp. Insulin sensitivity increased with correction of acidosis. By combining L-[1-¹³C]leucine infusions with hyperinsulinaemic euglycaemic clamps, the response of protein metabolism to hyperinsulinaemia was measured before and after correction of acidosis. The presence of acidosis did not impair the ability of insulin to modulate protein metabolism. There is therefore, dissociation between the effects of acidosis in CRF on insulin mediated carbohydrate metabolism and insulin mediated protein metabolism. In summary, metabolic acidosis increases protein catabolism in both normal and CRF man and may contribute to the loss of lean body mass characteristic of CRF. Insulin resistance in CRF improves with correction of acidosis. However the effects of acidosis on protein metabolism are not mediated via alterations in insulin sensitivity.

Thesis (M. Med. Sc.)--University of Hong Kong, 2008. / Includes bibliographical references (p. 58-63)

Thesis (Ph. D.)--Ohio State University, 2003. / Title from first page of PDF file. Document formatted into pages; contains xiv, 254 p.; also includes graphics Includes bibliographical references. Available online via OhioLINK's ETD Center

Thesis--University of Wisconsin--Madison. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 146-168).

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Thesis (Ph.D.)--York University, 2006. Graduate Programme in Economics. / Typescript. Includes bibliographical references (leaves 141-151). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://proquest.umi.com/pqdweb?index=0&did=1251858901&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1195140742&clientId=5220

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences