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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.
101

Record linkage : applied to a clinical trial and cohort study

MacLeod, Margaret Catriona Morag January 1995 (has links)
No description available.
102

Manipulation of the fatty acid composition of porcine tissues with respect to the human diet

Leskanich, Christian O'Neil January 1995 (has links)
No description available.
103

Oligo/amenorrhoea : endocrine profiles, ovarian ultrasound, insulin resistan and anthropometric factors; relationships between insulin resistance and ovarian function

Al-Naser Al Zekri, Huda M. January 1997 (has links)
No description available.
104

A systematic overview of lipid-lowering agents

Conroy, Clare January 1996 (has links)
No description available.
105

The effect of exercise and alcohol ingestion on blood coagulation, fibrinolysis and lipid profiles

Lin, Xia January 1997 (has links)
No description available.
106

The health and well-being of individuals before and after coronary artery bypass surgery

Lindsay, Grace M. January 1999 (has links)
No description available.
107

Reductive metabolism of aliphatic tertiary amine n-oxides

Tien, Pamela January 1999 (has links)
This study is based on a proposal concerning the feasibility of using aliphatic tertiary amine N-oxides as antiarrhythmic agent prodrugs. Lignocaine was selected as a candidate for prodrug development, because the N-oxide is a non-active, polar derivative of lignocaine and the drug of choice for ventricular arrhythmia, a symptom associated with ischaemic episodes leading to regions of transiently hypoxic heart tissue. An HPLC analytical method was developed to study the metabolism of lignocaine N-oxide. The rapid and sensitive analysis of lignocaine and its metabolites was demonstrated with good reproducibility, stability and high recovery. In this study, it was identified that lignocaine N-oxide can be reduced to its active parent compound, lignocaine with no other metabolites detected in the absence of oxygen. Under anaerobic conditions, no further metabolism of lignocaine was demonstrated in rat liver microsomes and heart S9 fractions suggesting no secondary metabolites were formed. The reduction of lignocaine N-oxide has been shown to be both enzymic and non-enzymic, NADPH dependent, oxygen sensitive and can be suppressed by CO, CN- and protein denaturation. Under anaerobic conditions, in vitro lignocaine N-oxide reduction was found to occur in NADPH supplemented rat liver homogenates, microsomal suspensions; rat heart homogenates, cytosolic solutions; human phenotyped cytochrome P450 isoforms; purified enzymes- cytochrome P450 reductase, xanthine oxidase, deoxymyoglobin and NADPHI ascorbate reduced protohaem (haemin). This reaction can be suppressed through the chemically mediated decrease ofP450 and bs levels in rat liver microsomes. Previous studies demonstrated that lignocaine N-oxide was non-active in aerobic rat heart in vivo and was potent under ischaemic conditions. In this study, high recovery of lignocaine N-oxide was found in the urine of normal rats suggesting low metabolism of the prodrug in oxic tissues. However, in hypoxic isolated rat hearts, lignocaine N-oxide was found to be reduced to lignocaine. The data presented suggested that the bioactivation of lignocaine N-oxide could be regulated by the prevailing oxygen tension in the ischaemic arrhythmic heart. Essentially the pro drug activation of lignocaine N-oxide may be triggered by the ischaemic state of the heart and terminated as the oxygen content in the heart returns to a more normal level. A controlled release and site-specific active drug delivery of lignocaine N-oxide, a hypoxia-mediated antiarrhythmic agent, may thus be achieved.
108

Prediction of initial involvement of first grade Greek school children in an out-of-school, organized, community physical activity programme : an application of the theory of planned behaviour

Atsalakis, Mihalis January 1994 (has links)
No description available.
109

The acute effects of exercise and diet on the composition and distribution of human plasma lipoproteins

Griffin, Bruce Arthur January 1988 (has links)
It has been proposed that exercise may confer protection against coronary heart disease by inducing changes in plasma lipoproteins and especially high density lipoprotein (HDL) subfractions that are associated with a reduced incidence of this condition. This thesis examines the effects of different forms of exercise and dietary variation on HDL, to determine whether exercise-induced changes in HDL subfractions are consistent with their role in providing protection against coronary heart disease. No changes were observed in the concentration of low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), HDL-cholesterol (HDL-C) or HDL particle size after acute bouts of exercise. However, a significant increase in the concentration of HDL3-C and a significant decrease in HDL2-C was evident following a 21 km and a 42 km race. In a series of prolonged walks on different diets, progressive and significant increases in the concentration of HDL-C (HDL2) occurred during walking on mixed and high-fat diets. These changes were accompanied by significant reductions in the concentration of VLDL-C and increases in the particle size of HDL. In contrast, walking on a high-carbohydrate diet was followed by a significant decrease in the concentration of HDL-C and increase in the concentration of VLDL-C and VLDL-triglyceride (VLDL-TG). In the absence of exercise, a similar but less pronounced response was observed during and after the high-fat diet, whereas a greater decrease in the concentration of HDL-C occurred during the high-carbohydrate diet. Under each set of experimental conditions, changes in the proportion of apoprotein E-rich HDL, a subfraction of HDL that has been implicated in a direct mechanism of coronary protection, appeared to be unrelated to increases in HDL-C and HDL particle size. These results therefore indicated that variation in diet can profoundly influence the effects of exercise upon HDL subfractions and suggest that prolonged walking may, in part, confer health benefit through HDL facilitating the clearance of TG-rich lipoproteins.
110

Regulation of human endothelial ICAM-1, E-selectin and VCAM-1 by polyunsaturated fatty acids and antioxidants

Collie-Duguid, Elaina S. R. January 1997 (has links)
The 3 PUFA, EPA and DHA, down-regulated human endothelial adhesion molecules in the presence of an inflammatory stimulus, DHA exerted more pronounced effects than EPA. The 6 PUFA, in contrast, exerted limited control over endothelial adhesion molecule expression under the conditions employed in this study. This indicates that the specific structure of the 3 PUFA, possibly combined with their degree of unsaturation, may be critical to their regulation of endothelial function. The antioxidant, quercetin, down-regulated some cytokine-induced endothelial adhesion molecules. In addition, quercetin acted synergistically with EPA and AA to decrease TNF--induced ICAM-1 or E-selectin protein, respectively. This may reflect regulation of eicosanoid production from these PUFA by quercetin, since this antioxidant inhibits enzymes critical to these metabolic pathways (i.e. cyclooxygenase and lipoxygenase). Hence, quercetin may mediate its inhibitory effects independently of its antioxidant properties. In contrast, -tocopheryl acetate up-regulated IL-1-induced E-selectin proteins levels. This antioxidant also, at least partially, blocked most of the inhibitory actions of the PUFA investigated. Recent data in the literature indicate that PUFA may exert their inhibitory effects on endothelial function through their oxidised derivatives. This provides a putative pathway via which -tocopheryl acetate may block the PUFA effects. The strength and type of inflammatory stimulus determined the sensitivity of the activated endothelial cells to each of the agents investigated. Inhibition of leukocyte adhesion to activated HUVEC, in response to EPA, DHA, or AA in the presence of quercetin, demonstrated a direct effect of these combined agents on endothelial function. The individual agents did not significantly reduce leukocyte adhesion.

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