Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol inst., 2003. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 4 uppsatser.

Diss. (sammanfattning) Uppsala : Univ., 2004. / Härtill 4 uppsatser.

No description available.

FUNDAMENTOS: A reestenose após intervenção coronária percutânea é maior nos pacientes com vasos de pequeno calibre em comparação aos vasos grandes. Os stents com sirolimus demonstraram importante redução da reestenose em vasos maiores que 3,0mm. O desempenho destes stents nos vasos pequenos deve ser investigado. MATERAIS E MÉTODOS: O propósito deste estudo foi avaliar a redução do volume de hiperplasia intimal após angioplastia com stents com sirolimus (Cypher®) comparados com os stents não recobertos de estrutura metálica fina (Pixel®), em pacientes com vasos pequenos. Oitenta pacientes com doença arterial coronária foram prospectivamente incluídos em duas séries consecutivas de tratamento, sendo a primeira empregando stents com sirolimus (50) e a segunda stents não recobertos de estrutura metálica fina (30). Os resultados foram: menor porcentual de obstrução da prótese através da análise volumétrica do ultrasom intracoronário [5,0% (EP=0,77) versus 39,0% (EP=4,72), p<0,001], menor perda tardia intra-stent [0,25mm (EP=0,03) versus 1,11mm (EP=0,13), p<0,001] e no segmento do vaso-alvo [0,30mm (EP=0,04) versus 0,83mm (EP=0,11), p<0,001], e também menor reestenose intra-stent (0% versus 33,3%, p<0,001) e no segmento do vaso (4% versus 36,7%, p<0,001) com os stents com sirolimus. A sobrevivência livre de eventos aos oito meses de evolução foi de 96% com os stents com sirolimus versus 86,7% com os stents não recobertos (p=0,190). CONCLUSÃO: Os pacientes com vasos de pequeno calibre após o implante de stents com sirolimus evoluem com menor hiperplasia intimal (menor porcentual de obstrução intra-stent e menor perda tardia) do que quando são utilizados stents não recobertos de estrutura metálica fina. Isto resulta em redução significativa da reestenose angiográfica aos oito meses de evolução / BACKGROUND: Patients with small vessels treated with percutaneous coronary interventions are at high risk of restenosis. Sirolimus-eluting stents has proved safety and effectiveness in reducing restenosis in large vessels. The outcomes after sirolimus-eluting stents in small vessels have not been adequately investigated. METHODS: We conducted a prospective study in 80 patients with small vessels treated with percutaneous intervention with sirolimus-eluting stents (Cypher(TM)) compared to thin-strut-thickness stents (Pixel(TM)). The primary end point was the reduction in intimal hyperplasia volume after coronary stenting accessed by intravascular ultrasound. OUTCOMES: the use of sirolimus-eluting stents compared with the use of the thin-strut-thickness stents reduced in-stent obstruction as a percent of volume [5,0% (EP=0,77) versus 39,0% (EP=4,72), p<0,001], in-stent lateloss [0,25mm (EP=0,03) versus 1,11mm (EP=0,13), p<0,001], in-segment late-loss [0,30mm (EP=0,04) versus 0,83mm (EP=0,11), p<0,001], and instent and in-segment restenosis [0% versus 33,3%, (p<0,001); 4% versus 36,7%, p<0,001), respectively]. The event-free-survival at 8 months was 96% for sirolimus-eluting stents and 86,7% for the thin-strut-thickness stents (p=0,190). CONCLUSIONS: In this study, the use of sirolimus eluting stents in patients with small vessels reduce intimal hyperplasia, in-stent and insegment late-loss, and in-stent and in-segment restenosis in comparison to thin-strut-thickness stents

by Choi Ka Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 113-128). / Abstract and appendix in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Abstract (Chinese version) --- p.iv / Table of Contents --- p.vi / List of Tables --- p.xi / List of Figures --- p.xiv / List of Abbreviations --- p.xv / Chapter CHAPTER ONE: --- BACKGROUND AND LITERATURE REVIEW / Chapter 1.1 --- Coronary Heart Disease: a global health problem --- p.1 / Chapter 1.2 --- Risk Factors of Coronary Heart Disease --- p.3 / Chapter 1.2.1 --- Age --- p.3 / Chapter 1.2.2 --- Gender --- p.4 / Chapter 1.2.3 --- Family History of Cardiovascular Disease --- p.5 / Chapter 1.2.4 --- Hypercholesterolemia --- p.7 / Chapter 1.2.5 --- Unhealthy Dietary Habits --- p.11 / Chapter 1.2.6 --- Obesity --- p.14 / Chapter 1.2.7 --- Physical Inactivity --- p.20 / Chapter 1.3 --- Clustering of Risk Factors --- p.24 / Chapter 1.4 --- Risk Factors in Children: Atherosclerosis Begins Early in Life --- p.26 / Chapter CHAPTER TWO: --- RESEARCH IN HONG KONG AND PURPOSES OF THIS STUDY / Chapter 2.1 --- Nutrition Transition --- p.27 / Chapter 2.2 --- CHD Mortality Trends in Hong Kong --- p.28 / Chapter 2.3 --- Serum Total Cholesterol and Obesity in Hong Kong Adults --- p.29 / Chapter 2.4 --- "Obesity, Serum Total Cholesterol, Dietary Habits and Physical Activity of Hong Kong Children and Adolescents" --- p.31 / Chapter 2.5 --- Study Purpose and Objectives --- p.35 / Chapter CHAPTER THREE: --- SURVEY DESIGN / Chapter 3.1 --- Sample Selection --- p.39 / Chapter 3.2 --- "Blood Total Blood Cholesterol, Triglyceride and Anthropometric Measurements" --- p.40 / Chapter 3.2.1 --- Total Blood Cholesterol and Triglyceride --- p.40 / Chapter 3.2.2 --- Anthropometry Measures --- p.42 / Chapter 3.3 --- Questionnaire --- p.45 / Chapter 3.3.1 --- Questionnaire Design and Pre-testing --- p.45 / Chapter 3.3.2 --- General Health and Socio-demographic Questionnaire --- p.47 / Chapter 3.3.3 --- Physical Activity Questionnaire --- p.47 / Chapter 3.3.4 --- Dietary Questionnaire --- p.48 / Chapter 3.4 --- Data Management --- p.49 / Chapter 3.5 --- Statistics --- p.49 / Chapter 3.6 --- Data Analysis --- p.50 / Chapter 3.6.1 --- Blood Total Cholesterol and Triglyceride --- p.50 / Chapter 3.6.2 --- Obesity and Fat Distribution --- p.50 / Chapter 3.6.3 --- Diet --- p.51 / Chapter 3.6.4 --- Physical Activity Patterns --- p.51 / Chapter 3.6.5 --- Body Mass Index of Parent and Family History of Diseases --- p.52 / Chapter CHAPTER FOUR: --- RESULTS / Chapter 4.1 --- Sample Size and the Characteristics of the Students in the Two Schools --- p.54 / Chapter 4.2 --- Gender and Age Distribution --- p.55 / Chapter 4.3 --- Blood Total Cholesterol and Triglyceride --- p.56 / Chapter 4.4 --- Anthropometry Measures --- p.58 / Chapter 4.5 --- Dietary Habits --- p.60 / Chapter 4.5.1 --- Dietary Composition of 3-day Dietary Record --- p.60 / Chapter 4.5.2 --- Eating Behaviors --- p.65 / Chapter 4.6 --- Physical Activity --- p.68 / Chapter 4.7 --- Family History of Diseases --- p.70 / Chapter 4.8 --- Parents' Anthropometry --- p.71 / Chapter 4.9 --- Demographic Data --- p.71 / Chapter 4.10 --- Inter-relationships --- p.75 / Chapter 4.10.1 --- Blood Total Cholesterol and Triglyceride --- p.75 / Chapter a. --- "Blood Total Cholesterol, Triglyceride and Body Fatness" --- p.75 / Chapter b. --- "Blood Total Cholesterol, Triglyceride and Diet" --- p.75 / Chapter c. --- "Blood Total Cholesterol, Triglyceride and Physical Activity Patterns" --- p.77 / Chapter d. --- Blood Total Cholesterol，Triglyceride and Family History of Hypercholesterolemia --- p.78 / Chapter e. --- Relative Importance of the Key Factors in Predicting Blood Total Cholesterol levels --- p.79 / Chapter 4.10.2 --- Obesity and Body Fatness --- p.79 / Chapter a. --- "Obesity, Body Fatness and Physical Activity Patterns" --- p.79 / Chapter b. --- "Obesity, Body Fatness and Diets" --- p.82 / Chapter c. --- Body Fatness and Genetics --- p.84 / Chapter 4.10.3 --- Diet and Physical Activity --- p.86 / Chapter 4.10.4 --- "Blood Total Cholesterol, Triglyceride, Obesity and Other Demographic or Economic Characteristics" --- p.87 / Chapter 4.11 --- Clustering of Risk Factors among Obese children --- p.87 / Chapter CHAPTER FIVE: --- DISCUSSION / Chapter 5.1 --- Implication of Research Findings --- p.89 / Chapter 5.2 --- Limitations --- p.108 / Chapter CHAPTER SIX: --- CONCLUSIONS AND RECOMMENDATIONS --- p.111 / References --- p.113 / Appendices / Chapter I --- Questionnaire (English version) --- p.129 / Chapter II --- Questionnaire (Chinese version) --- p.139 / Chapter III --- Introductory letter (English version) --- p.152 / Chapter V --- Introductory letter (Chinese version) --- p.153 / Chapter V --- Consent form (English version) --- p.154 / Chapter VI --- Consent form (Chinese version) --- p.155 / Chapter VII --- Photos of the standard household measures given to children for estimation of portion size (English version) --- p.156 / Chapter VIII --- Photos of the standard household measures given to children for estimation of portion size (Chinese version) --- p.157 / Chapter IX --- Responses from the children to the food frequency questionnaire --- p.158 / Chapter X --- The frequency of the reported food items liked or disliked by the children --- p.160

by Frankie Kar-Ming Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 101-107). / Acknowledgements --- p.IV / Abstract --- p.V / Abbreviations --- p.VI / Chapter Chapter 1 --- Introduction to Lipoprotein and Apolipoprotein --- p.1 / Chapter 1.1 --- Lipoprotein structure and classification --- p.1 / Chapter 1.2 --- Apolipoprotein A-I and B100 --- p.1 / Chapter 1.2.1 --- Apolipoprotein A-I (apoA-I) --- p.1 / Chapter 1.2.2 --- Apolipoprotein B100 (apoB100) --- p.3 / Chapter 1.2.3 --- Biological functions of apolipoprotein --- p.4 / Chapter 1.3 --- Evidence linking apoA-I and B100 with atherosclerosis --- p.4 / Chapter 1.4 --- The roles of apoA-I and B100 in the development of atherosclerosis --- p.6 / Chapter 1.5 --- Measurement of human serum lipoproteins as an assessment of risk for coronary heart disease (CHD) --- p.8 / Chapter 1.6 --- Aims of this study --- p.10 / Chapter Chapter 2 --- Purification of ApoA-I and B100 and Production of Polyclonal Antibodies --- p.12 / Chapter 2.1 --- Introduction --- p.12 / Chapter 2.1.1 --- Purification of apoA-I and B100 from human serum --- p.12 / Chapter 2.1.2 --- Immunization for polyclonal antibodies production against apoA-I and B100 --- p.14 / Chapter 2.1.3 --- Antibody purification --- p.15 / Chapter 2.1.3.1 --- Ammonium sulfate precipitation --- p.17 / Chapter 2.1.3.2 --- DEAE and QEAE Sepharose --- p.17 / Chapter 2.1.3.3 --- Protein A and Protein G --- p.17 / Chapter 2.1.3.4 --- Affinity chromatography --- p.18 / Chapter 2.2 --- Methods --- p.20 / Chapter 2.2.1 --- Purification of HDL and LDL --- p.20 / Chapter 2.2.2 --- Purification of apolipoproteins --- p.22 / Chapter 2.2.3 --- Immunization of rabbit with apoA-I and B100 --- p.23 / Chapter 2.2.4 --- Enzyme-linked immunosorbent assay (ELISA) --- p.24 / Chapter 2.2.5 --- Purification of lipoprotein specific immunoglobulin from antisera --- p.25 / Chapter 2.2.5.1 --- Salt fractionation --- p.25 / Chapter 2.2.5.2 --- Purification of immunoglobulin by Protein A affinity chromatography --- p.25 / Chapter 2.2.5.3 --- Isolation of specific antibody by lipoprotein-coupled affinity chromatography --- p.26 / Chapter 2.3 --- Results --- p.27 / Chapter 2.3.1 --- Purification of apoA-I and B100 --- p.27 / Chapter 2.3.2 --- Purification of immunoglobulins from rabbit anti-apolipoprotein sera --- p.32 / Chapter 2.4 --- Discussion --- p.38 / Chapter Chapter 3 --- Production of monoclonal antibodies against apoA-I and B100 --- p.48 / Chapter 3.1 --- Introduction --- p.48 / Chapter 3.1.1 --- What is monoclonal antibody? --- p.48 / Chapter 3.1.2 --- The basic methodology --- p.49 / Chapter 3.1.2.1 --- Immunization of host --- p.49 / Chapter 3.1.2.2 --- Cell lines required for fusion --- p.49 / Chapter 3.1.2.3 --- Fusion --- p.51 / Chapter 3.1.2.4 --- Selection of hybrids --- p.52 / Chapter 3.1.2.5 --- Screening assay --- p.54 / Chapter 3.1.2.6 --- Cloning --- p.54 / Chapter 3.1.2.7 --- Bulk production of monoclonal antibody --- p.55 / Chapter 3.1.2.8 --- Monoclonal antibody purification --- p.55 / Chapter 3.2 --- Methods --- p.55 / Chapter 3.2.1 --- Immunization of mice with apoA-I and apoB100 --- p.55 / Chapter 3.2.2 --- Preparation before fusion --- p.58 / Chapter 3.2.2.1 --- Preparation of tissue culture working solutions --- p.58 / Chapter 3.2.2.2 --- Preparation of spleen cells --- p.59 / Chapter 3.2.2.3 --- Preparation of myeloma cells --- p.60 / Chapter 3.2.3 --- Fusion --- p.60 / Chapter 3.2.4 --- Screening assay for positive clones --- p.61 / Chapter 3.2.5 --- Limiting dilution cloning --- p.61 / Chapter 3.2.6 --- Determination of isotype --- p.62 / Chapter 3.2.7 --- Cryopreservation of myeloma and established hybridoma cell lines --- p.62 / Chapter 3.2.7.1 --- Freezing cells --- p.62 / Chapter 3.2.7.2 --- Thawing cells --- p.63 / Chapter 3.2.8 --- Bulk production of monoclonal antibodies from ascites --- p.63 / Chapter 3.2.9 --- Purification of monoclonal antibodies from ascites --- p.63 / Chapter 3.2.10 --- Western blot analyses of the monoclonal antibodies --- p.64 / Chapter 3.2.11 --- Iodination of apolipoproteins --- p.64 / Chapter 3.2.12 --- Binding of the monoclonal antibody to iodinated apolipoprotein --- p.65 / Chapter 3.2.13 --- Competitive displacement analyses --- p.65 / Chapter 3.3 --- Results --- p.66 / Chapter 3.3.1 --- Development of monoclonal antibodies --- p.66 / Chapter 3.3.2 --- Purification of monoclonal antibody from ascites --- p.69 / Chapter 3.3.3 --- Western blotting analyses of AB6 and BE8 --- p.69 / Chapter 3.3.4 --- Monoclonal antibody titration curve for apolipoproteins by radioimmunoassays --- p.75 / Chapter 3.3.5 --- Competitive displacement analysis of AB6 and BE8 --- p.75 / Chapter 3.4 --- Discussion --- p.79 / Chapter Chapter 4 --- Enzyme-linked immunosorbent assay (ELISA) for ApoA-I --- p.84 / Chapter 4.1 --- Introduction --- p.84 / Chapter 4.1.1 --- Alkaline phosphatase (ALP) --- p.84 / Chapter 4.1.2 --- Conjugation methods --- p.85 / Chapter 4.1.3 --- Design of the immunoassay format --- p.87 / Chapter 4.1.4 --- Modified solid-phase: Protein A antibody-capture ELISA (PACE) --- p.87 / Chapter 4.2 --- Materials and Methods --- p.90 / Chapter 4.2.1 --- Conjugation of AB6 with maleimide activated alkaline phosphatase --- p.90 / Chapter 4.2.2 --- Titration curve of AB6-ALP conjugate --- p.90 / Chapter 4.2.3 --- Calibration curve of apoA-I sandwich ELISA --- p.91 / Chapter 4.2.4 --- Measurement of apoA-I by Protein A antibody-capture ELISA --- p.91 / Chapter 4.3 --- Results --- p.92 / Chapter 4.3.1 --- Characterization of AB6-ALP conjugate --- p.92 / Chapter 4.3.2 --- Calibration curve for the measurement of apoA-I --- p.92 / Chapter 4.4 --- Discussion --- p.95 / Chapter Chapter 5 --- General Conclusions --- p.99 / References --- p.101

by Chan Chi Fai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 119-137). / Chapter SECTION 1 --- INTRODUCTION / Chapter 1.1 --- Overview on lipids --- p.2 / Chapter 1.1.1 --- Definition and Classification of Lipids --- p.2 / Chapter 1.1.2 --- Lipoproteins and Apolipoproteins --- p.4 / Chapter 1.1.3 --- Outline of Lipoprotein Metabolism --- p.9 / Chapter 1.1.4 --- LDL Metabolism --- p.12 / Chapter 1.2 --- Dyslipidaemia and Cardiovascular Disease (CVD) --- p.16 / Chapter 1.2.1 --- Definition --- p.16 / Chapter 1.2.2 --- Dyslipidaemia and CAD --- p.16 / Chapter 1.2.3 --- Dyslipidaemia in Non-Insulin Dependent Diabetes Millitus Patients --- p.18 / Chapter 1.2.4 --- Claasification of Dyslipidaemia --- p.24 / Chapter 1.2.5 --- Causes of Hyperlipidaemia --- p.26 / Chapter 1.3 --- Dyslipidaemia and Atherosclerosis --- p.29 / Chapter 1.3.1 --- Pathogenesis of Atherosclerosis --- p.29 / Chapter 1.3.2 --- Mechanism of Atherogenesis --- p.31 / Chapter 1.3.3 --- Intrinsic Roles of LDL in Atherogenesis --- p.33 / Chapter (1) --- LDL Oxidizability --- p.33 / Chapter (2) --- LDL Particle Size Heterogeneity --- p.39 / Chapter 1.4 --- Management of Dyslipidaemia --- p.42 / Chapter 1.5 --- Aims of This Study --- p.49 / Chapter SECTION 2 --- MATERIALS AND METHODS / Chapter 2.1 --- Materials --- p.52 / Chapter 2.1.1 --- Patients and Controls --- p.52 / Chapter 2.1.2 --- Drug Administration Trials --- p.54 / Chapter 2.1.3 --- Blood Samples --- p.55 / Chapter 2.1.4 --- Biochemicals --- p.56 / Chapter 2.1.5 --- Solutions and Buffers --- p.56 / Chapter 2.1.6 --- Apparatus and Equipment --- p.60 / Chapter 2.2 --- Methods --- p.62 / Chapter 2.2.1 --- General Clinical Biochemistry Tests --- p.62 / Chapter 2.2.2 --- Apolipoprotein Assays --- p.62 / Chapter 2.2.3 --- Ultracentrifugation of LDL Fraction --- p.63 / Chapter 2.2.4 --- De-Salting of LDL Fraction --- p.64 / Chapter 2.2.5 --- Qualitative Determination of LDL-Cholesterol and Protein Fractions --- p.64 / Chapter 2.2.6 --- In Vitro Assessment of LDL Oxidizability --- p.65 / Chapter 2.2.7 --- Electrophoretic Gel Pattern of LDL Fraction During In Vitro Oxidizability --- p.65 / Chapter 2.2.8 --- Study of LDL Particle Size --- p.66 / Chapter 2.2.9 --- Statistical Analysis --- p.67 / Chapter SECTION 3 --- RESULTS / Chapter 3.1 --- Quantitative Determination and Standardization of LDL Fractions --- p.69 / Chapter 3.2 --- In Vitro Assessment of LDL Oxidizability --- p.72 / Chapter 3.3 --- Electrophoretic Patterns of LDL during In Vitro Oxidizability --- p.72 / Chapter 3.4 --- LDL Sizing --- p.73 / Chapter 3.5 --- "Correlations of Triglycerides Concentration, LDL Particle Size and Oxidizability" --- p.76 / Chapter 3.6 --- Diabetes Millitus --- p.83 / Chapter 3.6.1 --- NIDDM Patients & Controls --- p.83 / Chapter 3.6.2 --- Effect of Drug Treatment on Serum Lipid-Lipoprotein- Apolipoprotein Profile --- p.86 / Chapter 3.7 --- Hypertriglyceridaemic Patients --- p.90 / Chapter 3.7.1 --- Patients & Controls --- p.90 / Chapter 3.7.2 --- Bezafibrate Treatment --- p.91 / Chapter 3.8 --- CAD Patients --- p.97 / Chapter 3.8.1 --- CAD Patients & Controls --- p.97 / Chapter SECTION 4 --- DISCUSSION / Chapter 4.1 --- Patients and Controls --- p.101 / Chapter 4.2 --- Ultracentrifugation of LDL Fractions --- p.102 / Chapter 4.3 --- In Vitro LDL Oxidizability --- p.103 / Chapter 4.4 --- "Association of TG, LDL Oxidizability and Particle Size" --- p.105 / Chapter 4.5 --- LDL Sizing --- p.106 / Chapter 4.6 --- Comparsion of Patients and Controls in Lipid-Lipoprotein- Apolipoprotein Profiles --- p.107 / Chapter 4.7 --- The Effect of Lovastatin and Acipimox on NIDDM Patients --- p.111 / Chapter 4.8 --- The Effect of Bezafibrate on Hypertriglyceridaemic Patients --- p.114 / Chapter SECTION 5 --- CONCLUSION --- p.116 / References --- p.119 / Appendices --- p.138