M.Tech. (Homoeopathy) / Please refer to full text to view abstract

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by Ying Tat Mak. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 178-198). / Title --- p.1 / Abstract --- p.2 / Acknowledgments --- p.5 / Contents --- p.6 / Abbreviations --- p.9 / List of Tables --- p.11 / List of Figures --- p.13 / Chapter Chapter 1: --- Introduction / Chapter 1.1 --- Cholesterol Metabolism and Atherosclerosis --- p.15 / Chapter 1.1.1 --- Cholesterol and Cholesterol Metabolism --- p.17 / Chapter 1.1.2 --- Cholesterol Transport: Apolipoprotein and Lipoprotein --- p.23 / Chapter 1.1.3 --- Cholesterol and Atherosclerosis --- p.26 / Chapter 1.2 --- Hyperlipidaemia --- p.30 / Chapter 1.2.1 --- Primary and Secondary Hyperlipidaemia --- p.31 / Chapter 1.2.2 --- Mutations leading to Primary Hypercholesterolaemia --- p.36 / Chapter 1.3 --- Familial Hypercholesterolaemia --- p.38 / Chapter 1.3.1 --- Historical Aspects --- p.38 / Chapter 1.3.2 --- Clinical Features - Diagnosis and Consequences --- p.39 / Chapter 1.3.3 --- Population Prevalence --- p.40 / Chapter 1.3.4 --- Mutations in the Low Density Lipoprotein Receptor Gene --- p.41 / Chapter 1.4 --- Methods for Detecting Mutations in LDL Receptor Gene --- p.51 / Chapter 1.4.1 --- Southern Blotting Based Methods --- p.51 / Chapter 1.4.2 --- Polymerase Chain Reaction Based Methods --- p.52 / Chapter 1.4.3 --- Screening Methods for Unknown Mutations in LDL Receptor Gene --- p.56 / Chapter 1.5 --- Mutations of the LDL receptor gene in Chinese --- p.58 / Chapter Chapter 2: --- Objectives --- p.63 / Chapter Chapter 3: --- Materials and Methods / Chapter 3.1 --- Subjects / Chapter 3.1.1 --- Familial Hypercholesterolaemia Patients --- p.65 / Chapter 3.1.2 --- Normocholesterolaemia Subjects --- p.67 / Chapter 3.2 --- Materials / Chapter 3.2.1 --- Enzymes --- p.67 / Chapter 3.2.2 --- DNA Markers --- p.68 / Chapter 3.2.3 --- Reagents Kits --- p.68 / Chapter 3.2.4 --- Primers for PCR --- p.68 / Chapter 3.2.5 --- Chemicals and Reagents --- p.69 / Chapter 3.2.6 --- Radioisotopes --- p.70 / Chapter 3.2.7 --- Solutions and Buffers --- p.70 / Chapter 3.3 --- Methods / Chapter 3.3.1 --- Blood Collection --- p.71 / Chapter 3.3.2 --- General Biochemistry Tests --- p.72 / Chapter 3.3.3 --- DNA Extraction --- p.72 / Chapter 3.3.4 --- RNA Extraction --- p.73 / Chapter 3.3.5 --- Polymerase Chain Reaction --- p.74 / Chapter 3.3.6 --- Agarose Gel Electrophoresis --- p.76 / Chapter 3.3.7 --- Polyacrylamide Gel Electrophoresis --- p.78 / Chapter 3.3.8 --- Single Strand Conformation Polymorphism --- p.79 / Chapter 3.3.9 --- Reverse Transcription - Polymerase Chain Reaction --- p.79 / Chapter 3.3.10 --- Direct DNA Sequencing --- p.81 / Chapter 3.3.11 --- Haplotyping of the LDL receptor gene --- p.83 / Chapter 3.3.12 --- Restriction Enzyme Digestion --- p.84 / Chapter Chapter 4: --- Results / Chapter 4.1 --- Patients Investigations --- p.88 / Chapter 4.1.1 --- Normal Control Subjects --- p.88 / Chapter 4.1.2 --- Patients --- p.88 / Chapter 4.2 --- PCR-SSCP Analysis of LDL Receptor Gene --- p.90 / Chapter 4.3 --- Summary of Mutations Identified --- p.92 / Chapter 4.4 --- Novel Mutations --- p.94 / Chapter 4.5 --- Previously Reported Mutations --- p.97 / Chapter 4.6 --- Polymorphisms and Silent Mutation --- p.100 / Chapter 4.6.1 --- New Polymorphism --- p.100 / Chapter 4.6.2 --- New Silent Mutation --- p.102 / Chapter 4.6.3 --- Reported Polymorphisms --- p.103 / Chapter 4.7 --- Southern Blotting --- p.103 / Chapter 4.8 --- Haplotypes --- p.104 / (All Figures for Chapter 4) --- p.106 / Chapter Chapter 5: --- Discussions / Chapter 5.1 --- Use of SSCP in Screening for Mutations and Polymorphisms --- p.158 / Chapter 5.2 --- Novel and Reported Mutations --- p.160 / Chapter 5.3 --- Novel Polymorphism and Silent Mutation --- p.170 / Chapter 5.4 --- Common Polymorphisms --- p.171 / Chapter 5.5 --- Possible Common Mutations of the LDL Receptor Gene in Chinese --- p.172 / Chapter 5.6 --- Pattern of LDL Receptor Gene Mutations in Chinese --- p.173 / References --- p.178

Most research on hypercholesterolemia concerns the association of cholesterol to stress, with very few references to psychotherapeutic interventions, which are on small and motivated samples. Especially in Greece, no research has been done either on the association of cholesterol to psychological factors or the treatment of cholesterol by psychological interventions. The present study examined the effectiveness of a brief psychological intervention in decreasing high or borderline cholesterol levels. Fifty-eight hypercholesterolemic individuals were recruited for the study. This sample was a part of a group of 6,000 Athenian adults used in a long-term prospective study of cardiovascular diseases and their risk factors. Participants were partially randomised for age, sex and cholesterol into an intervention and a control group. A brief group psychological intervention was used which focused on the realisation of sources of stress and the expression of "unacceptable" thoughts and feelings. The theoretical background was psychodynamic and systemic. Intervention groups met weekly for 1 /2 hour sessions, while the control groups were invited to come to the hospital once a month for the first 3 months. The treatment outcome was assessed using blood tests of cholesterol, high density lipoproteines (HDL), low density lipoproteines (LDL), psychological tests and a questionnaire evaluating the group intervention. Participants were followed up for 1 year and were assessed at 3- month, 6-month and 1-year intervals. A statistically significant difference was found in the intervention group between the first and the second measurements of cholesterol, HDL and LDL. Also, the intervention group was found to have significantly greater decrease in cholesterol and LDL than the control group when the change scores between the initial and first follow-up measurements were compared. Significant changes were found in cholesterol, HDL and LDL in the third follow-up in the control group, which is difficult to vii explain since no association was found with any psychological or lifestyle parameters examined. No significant differences between the intervention and the control group were found on the psychological measures used in the study. However, correlations were found between decrease in cholesterol at the 1" follow-up and patients' satisfaction with the group process. The group process was analysed as well as case studies of two group members who responded well to the intervention and two who did not. These analyses suggested that participants were confronting a struggle between strong moral, social and familial obligations and their own attitudes towards life, which created strong feelings of guilt, anger and tension. Their unfamiliarity with psychotherapy and their motivation to obtain symptom relief seemed to influence the outcome of the intervention. A combination of health education and brief group psychotherapy is suggested. However, further evidence is required to support the effectiveness of brief psychological intervention in the decrease in cholesterol as well as the finding of the significant decrease in cholesterol in the control group at the 1- year follow-up.

Lan Wei. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 260-301). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Photocopy. Ann Arbor, Mich. : UMI Dissertation Services, 2002. xx, 301 p. : ill. ; 22 cm. / Abstracts in English and Chinese.

Abstract To facilitate the diagnosis of hypercholesterolemia, we wanted to create a simple and rapid method for diagnosing familial hypercholesterolemia in a homogenous population. The PCR method for the FH-Helsinki mutation detected 25 FH-Helsinki positive patients, two of whom had no clinical signs of FH, but had a positive family history for the disease. The method is exceptionally useful in Northern Finland, where 62% of the FH patients carry the FH-Helsinki mutation. The role of polymorphisms and mutations of the apo B particle as etiologic factors of hypercholesterolemia was studied in a population of moderately hypercholesterolemic individuals. The catabolism of the patients' own LDL was compared to that of a healthy and normocholesterolemic donor, and no major differences were observed. However, the presence of the XbaI cutting site was associated with elevated cholesterol values and a slightly lowered LDL catabolic rate. Patients homozygous for the EcoRI cutting site also had a slow LDL catabolic rate and slightly elevated cholesterol values. The MspI and Ins/del polymorphisms of the apo B particle were not associated with variations in LDL catabolism. The e 4 allele of apolipoprotein E was slightly more frequent in our hypercholesterolemic population than in the average population. The lipid values did not differ significantly between the apo E phenotypes in moderately hypercholesterolemic individuals, nor could we detect any differences in the catabolic rates of their LDL according to the apo E phenotype (individuals with the phenotype apo E 2/2 were excluded from the study). In our population of CAD patients, the frequency of the e 4 allele was lower than in CAD populations from Southern Finland (0.23 vs. 0.32), suggesting that apo E 4 is not so strongly associated with coronary disease in Northern Finland as in other populations. The E 4 phenotype was associated with slightly smaller LDL cholesterol reductions by colestipol and lovastatin treatment compared with patients with the phenotype 2/3. The lipid risk factors of male and female CAD patients were studied in a group of patients admitted to one ward of the Oulu University Hospital. We found the males to have the typical high LDL cholesterol and low HDL cholesterol lipid pattern, but women with two- or three-vessel CAD had high LDL and low HDL cholesterol associated with high VLDL lipids, and hypertension, diabetes or smoking. Pharmacological treatment of hypercholesterolemia was studied by comparing lovastatin to colestipol, and in a separate study where a new drug, enprostil was used. Enprostil, whose main effect is on the gastrointestinal tract, would be a useful alternative for long-term treatment of hypercholesterolemia. Unfortunately, however, gastrointestinal side-effects limit its long-term use. Colestipol reduced plasma LDL cholesterol and elevated plasma HDL cholesterol and triglycerides, but it, too, caused gastrointestinal side-effects. Lovastatin proved to be the most effective cholesterol-lowering drug with the least side-effects, and statins have now been established as the most widely used hypocholesterolemic drugs.

A research report submitted to the Faculty of Health Sciences, University of the Witwatersrand in fulfilment of the requirements for the Degree of Master of Medicine in the branch of Internal Medicine / Untreated patients with heterozygous familial hypercholesterolaemia (hFH) are at increased risk for atherosclerosis. Surrogate markers to predict atheroma include the presence of endothelial dysfunction (ED) as well as increased levels of inflammatory markers / IT2018

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Thesis (M.S.)--University of Michigan, 1997. / Includes bibliographical references.