Bibliography: leaves 105-151. / xi, 151, [47] leaves, [3] leaves of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis examines the effect of remodelling HDL on the metabolism of apo A-I. The major focus is on the effects of CETP and LCAT in the regulation of apo A-I concentration in DHL. The effects of incubation of HDL with CETP in the presence of VLDL and/or LDL on apo A-I concentration in HDL are examined. The characterization of the dissociated apo A-I from HDL is presented. The studies demonstrate that the dissociation of apo A-I from HDL mediated by CETP is preventable and reversible in a process dependent on LCAT activity. The mechanism by which HDL apo A-I content is increased is also explored. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1997?

Bibliography: leaves 105-151. / xi, 151, [47] leaves, [3] leaves of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis examines the effect of remodelling HDL on the metabolism of apo A-I. The major focus is on the effects of CETP and LCAT in the regulation of apo A-I concentration in DHL. The effects of incubation of HDL with CETP in the presence of VLDL and/or LDL on apo A-I concentration in HDL are examined. The characterization of the dissociated apo A-I from HDL is presented. The studies demonstrate that the dissociation of apo A-I from HDL mediated by CETP is preventable and reversible in a process dependent on LCAT activity. The mechanism by which HDL apo A-I content is increased is also explored. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1997?

Thesis (Ph. D.)--Oregon State University, 2008. / Printout. Includes bibliographical references (leaves 124-133). Also available on the World Wide Web.

Thesis (Ph.D.)--Duquesne University, 2005. / Title from document title page. Abstract included in electronic submission form. Includes bibliographical references (p. 156-171) and index.

Thesis (Ph. D.)--University of Hong Kong, 1993.

Thesis (Ph. D.)--University of Hong Kong, 1998. / Includes bibliographical references (leaves 170-195).

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

Thesis (Ph. D.)--University of Texas at Austin, 2005. / Vita. Includes bibliographical references.

This thesis examined aspects of production and utilization of acetate in humans via measurements of plasma concentrations in different circumstances with particular attention to changes in diabetes. Circulating plasma acetate was measured by a modified acetate kinase-based enzymatic spectrophotometric method with adequate sensitivity and specificity for levels encountered in human plasma. Fasting plasma acetate was increased in diabetics and correlated with glucose and indices of glucose disposal. Levels increased further when they were fed different high- fibre diets. The rise in acetate levels after lactulose ingestion correlated with changing breath hydrogen excretion in subjects with suspected malabsorption. Plasma acetate levels increased during fat infusion, and conversely, fell with suppression of fatty acid levels during euglycaemic clamping. Insulin appeared to promote acetate production from glucose by enhancing glycolysis and acetyl CoA availability, although its activity in reducing lipolysis had an opposite effect. The hepatic formation of acetate from ethanol did not appear influenced by prior chlorpropamide intake. Glucose tolerance was unaffected by a 150mmol/hr acetate load, but acetate tolerance was impaired when glucose was simultaneously available. Adipose tissue lipolysis was suppressed during acetate infusions as evident from reduced levels of glycerol and non-esterifled fatty acids. Blood 'ketone body' levels were increased, suggesting direct conversion from acetate. Possibly as a result, fat oxidation assessed from gaseous exchange, was reduced with infused acetate. Acetate utilization was impaired in diabetic patients from higher fasting plasma levels and slower metabolic clearance. The defect in diabetes was probably due to both over-production and under-utilization, and could be related to the enhanced lipolysis, hyperglycaemia and a reportedly reduced hepatic activity of acetyl CoA synthetase. It was concluded that acetate is derived from both colonic fermentation and endogenous catabolism of glucose and fatty acids and appears rapidly metabolisable in humans. Some areas of further interest in human acetate metabolism were highlighted.

A novel plasma cell-restricted E2A-containing ~-tE2-binding species, designated P-E2A, which forms during the mature B- to plasma cell transition has recently been detected (Jacobs, 1993). In order to elucidate the molecular components of P-E2A, a human plasma cell eDNA library was constructed from the ARH-77 cell line, and the yeast two-hybrid system was employed to search for E2A-interacting plasma cell factors. A hybrid vector that expresses the bHLH region of E4 7 was constructed and utilized as bait to detect E2A-interacting clones. Three clones were isolated that represent possible candidates for in vivo E2A interactions. To improve the specificity and sensitivity of the system, we devised an alternative strategy to the yeast two-hybrid system for the in vivo detection ofE-box-binding E2A-interacting proteins.