A newly discovered activity in human serum protects porcine aortic endothelial cells in culture from injury by very low density lipoproteins (VLDL). This factor, toxicity-preventing activity (TxPA), was measured in 29 relatively young men (43 ± 8 years) who had undergone coronary angiography. The level of TxPA was found to be significantly reduced (P < 0.001) in men who demonstrated more than 15% narrowing of their coronary arteries. Men (n = 18) who had 15% or less narrowing were found to have 104 ± 48 units of TxPA while men (n = 11) with coronary artery disease had 48 ± 24 units of TxPA. A value derived from the product of TxPA and the high density lipoprotein cholesterol (HDL-C) level divided by the non-HDL-C (total cholesterol-HDL-C) accurately separated 97% of the men into 2 groups. TxPA thus appears to be a new protective factor in coronary artery disease, which, when combined with total cholesterol and high density lipoprotein cholesterol values, provides an accurate classification of established coronary artery disease in these subjects.

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / toc / Zoology / Master / Master of Philosophy

published_or_final_version / abstract / Chemistry / Doctoral / Doctor of Philosophy

No description available.

Includes bibliographical references (leaves 198-223) Examines the metabolism of plasma lipoprotein triacylglyceride in sheep (Ovis aries) under normal fed conditions, fasting and alloxan diabetes.

Reduced high-density lipoprotein cholesterol (HDL-C) concentrations are a major risk factor for cardiovascular disease. Intense interest recently has been in identifying the genetic factors that contribute to an aberrant HDL-C phenotype. Finding genetic factors associated with low HDL-C concentrations in New Zealanders was the major aim of this study, with a similar analysis aimed at finding factors associated with high HDL-C concentrations included. The study began with an investigation of a New Zealand family with HDL-C deficiency. The proband had virtually no HDL-C, and was homozygous for an R1068H mutation in the ABCA1 gene. Nineteen relatives were recruited into the study, and an analysis aimed at finding the underlying cause for the disparate HDL-C phenotypes amongst H1068 carriers initiated. A further investigation into HDL-C levels aimed to find other genetic factors that contribute to HDL-C in New Zealanders. Subjects were selected from those taking part in the Otago Vascular Disease study, and placed into three groups based on their HDL-C lipid measurement: low (n=154), mid (n=105), and high (n=102) HDL-C. Mutations in ABCAI and the apolipoprotein AI gene (APOAI) were identified in subjects with low HDL-C. Polymorphisms in ABCA1 and APOAI were also investigated as contributors to HDL-C concentrations. Seventeen SNPs in functionally relevant regions were genotyped in the three HDL-C groups. Five single polymorphisms and one polymorphism haplotype showed a statistically significant association with HDL-C concentrations. The final analysis investigated plasma lipoprotein compositions in individuals with low HDL-C to identify if other lipoprotein abnormalities concurred. Individuals with HDL-C below 0.65 mmol/L were almost invariably associated with triglyceride-rich VLDL and/or triglyceride-rich LDL. This finding may have relevance for an increased atherosclerotic risk for those with low HDL-C.

"September 2004" / Bibliography: leaves 236-262. / xxxi, 262 leaves : ill., plates (col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 2004

Thesis (Ph. D.)--University of Oregon, 2006. / Typescript. Includes vita and abstract. Includes bibliographical references (leaves 93-99). Also available for download via the World Wide Web; free to University of Oregon users.

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.