Conclusions: In the same number of people treated, the number of CVD events avoided for the overall risk approach is always larger than that of the blood pressure approach. The additional benefits of overall risk approach compared with the blood pressure approach decreases as the percentage of people from the total population is increased. If the current practice and hypertension guidelines in China are shifted to the overall risk approach, many more CVD events could be avoided with the same resources used. / Methods: The sample used in the analyses includes a subsample of 38,673 persons from the 2002 China National Nutrition and Health Survey, who were 30-74 years old, without previous CVD, and had data on all major CVD risk factors. CVD risks of the patients selected by each approach are predicted using suitable risk prediction equation. The RRR of anti-hypertensive drug treatment derived from meta-analyses of RCTs. The difference in the absolute effectiveness between the two approaches is used to quantify how many more CVD events can be prevented in 1000 people treated by the ORA as compared to the BPA. / Objective: To estimate and compare the number of major cardiovascular events that could be avoided by shifting the blood pressure approach to the overall risk approach if the same percentage of people in a large, representative Chinese population is treated with anti-hypertensive drugs. / Results: When 2.5%, 5.5%, 10.1%, 15.5%, 20.7%, 25.7% or 33.0% of the 38,673 subjects were treated by anti-hypertensive drugs by using the two approaches respectively, 22 (95%CI: 17∼28), 13 (11∼16), 9 (8∼10), 7 (6∼8), 6 (5∼7), 5 (4∼6), or 4 (3∼4) more CVD events could be avoided in every 1000 people treated if the blood pressure approach is shifted to the overall risk approach, which is in general a 15% to 25% increase in CVD events prevented. / Qin, Ying. / Adviser: Jin Ling Tang. / Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 116-121). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Xiang Hai Liao. / "July 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 180-200). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Frontal lobe atrophy (FLA) is associated with late-life depression and cognitive impairment, although the pathogenesis of FLA in stroke is unclear. In an aim to ascertain whether FLA is affected by WMLs, we analyzed the MRIs of 471 Chinese ischemic stroke patients. Lobar atrophy was defined by a widely-used visual rating scale. WML severity was rated using the Fazekas scale. There was no correlation between PVH and DWMH and temporal and parietal atrophy. The results of this study suggest that FLA in ischemic stroke may be associated with SVD. / Poststroke depression (PSD) is the most common form of poststroke psychiatric morbidity. Small subcortical infarcts (SSIs) can result from small vessel disease (SVD) and large artery disease (LAD). No study has yet explored PSD in different etiological types of SSIs. To address this gap, 127 patients with SSIs resulting from LAD or SVD were examined. PSD was evaluated with the Geriatric Depression Scale (GDS) three months after stroke. The LAD group had a significantly higher frequency of PSD, and LAD was found to be a significant independent risk factor for PSD. This study suggests that cerebral blood perfusion may play an important role in PSD. / Post-stroke emotional lability (PSEL) is a distressing and embarrassing complaint among stroke survivors. Lesions located in various cortical and subcortical areas are thought to be involved in the pathophysiology of PSEL.The clinical significance of microbleeds (MBs) in the development of psychiatric conditions following stroke is unknown. We carried out a study to examine the association between PSEL and MBs in 519 Chinese patients with acute ischemic stroke admitted consecutively. PSEL was evaluated three months after the index stroke, and the number and location of MBs were evaluated with MRI. According to Kim's criteria, 74 (14.3%) of the patients had PSEL. Our results suggest that MBs in the thalamus may play a role in the development of PSEL. The importance of MBs in PSEL and other psychiatric conditions in stroke survivors warrants further investigation. / The first study reported in this thesis involved 328 Chinese ischemic stroke patients who were administered a series of neuropsychological tests covering seven domains three months after stroke. Two hundred and fifty-six of these patients were followed-up for one year. Volumetry of the infarcts, WMLs, and hippocampus atrophy on magnetic resonance imaging (MRI) was conducted. The prevalence of cognitive impairment was 54.9% at baseline and 52.4% at the one-year follow-up, although most of the patients (85.5%) remained cognitively stable. The evolution of cognitive impairment no dementia (CIND) at the one-year follow-up was bidirectional, with 11.2% progressing to dementia and 21.0% reverting to cognitive intact. WMLs volume rather than hippocampal volume was a significant predictor of cognitive impairment, cognitive decline, and delayed dementia. WMLs also had an independent effect on executive function, attention, visual memory, visuoconstruction, and visuomotor speed. / This thesis investigates the clinical and imaging characterization of cognitive impairment and psychiatric morbidity in Chinese stroke patients. The conclusions of the studies reported herein can be summarized as follows. (1) The prevalence of cognitive impairment is high among Chinese poststroke patients, but most remain cognitively stable at one year after stroke; WMLs rather than hippocampal atrophy predict cognitive impairment, longitudinal cognitive decline, and delayed dementia; (2) DLPFC atrophy is correlated with poor verbal fluency in elderly women with stroke, but not in their male counterparts; (3) LAD may be associated with PSD in patients with small subcortical infarcts; (4) MBs in the thalamus are associated with PSEL; (5) frontal lobe infarction and diabetes may be risk factors of insomnia symptoms in stroke patients; and (6) FLA in ischemic stroke may be associated with SVD. (Abstract shortened by UMI.) / Chen, Yangkun. / Adviser: Wai Kwong Tang. / Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 217-238). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Ho Sin Ka Janice. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 105-119). / Abstracts in English and Chinese. / Chapter CHAPTER 1. --- Introduction / Chapter 1.1. --- Epidemiology of Type 2 Diabetes --- p.1 / Chapter 1.2. --- Risk factors contributing to Type 2 Diabetes --- p.3 / Chapter 1.2.1. --- Environmental and physiological factors --- p.3 / Chapter 1.2.2. --- Genetic factors --- p.3 / Chapter 1.3. --- Disruption of energy homeostasis in the pathogenesis of type 2 diabetes --- p.6 / Chapter 1.3.1. --- Clinical spectrum of diabetes --- p.6 / Chapter 1.3.2. --- Insulin as a key regulator of energy homeostasis --- p.7 / Chapter 1.3.3. --- Insulin secretion and glucose metabolism --- p.8 / Chapter 1.3.4. --- Insulin action and lipid metabolism --- p.9 / Chapter 1.3.5. --- Lipotoxicity and glucotoxicity --- p.12 / Chapter 1.3.6. --- Role of transcription factors as metabolic switch --- p.13 / Chapter 1.4. --- Candidate genes implicated in type 2 diabetes susceptibility --- p.15 / Chapter 1.4.1. --- Candidate genes involved in insulin secretion pathway --- p.15 / Chapter 1.4.1.1. --- HNF4A --- p.15 / Chapter 1.4.1.2. --- HNF1A --- p.16 / Chapter 1.4.1.3. --- PDX1/PBX1 --- p.17 / Chapter 1.4.1.4. --- NEUROD1 --- p.17 / Chapter 1.4.1.5. --- GCK --- p.17 / Chapter 1.4.1.6. --- KCNJ11/ABCC8 --- p.18 / Chapter 1.4.2 --- Candidate genes involved in insulin action pathway --- p.19 / Chapter 1.4.2.1. --- PPARG --- p.19 / Chapter 1.4.2.2. --- PPARA --- p.20 / Chapter 1.4.2.3. --- PPARGC1A --- p.20 / Chapter 1.4.2.4. --- ADIP0Q --- p.21 / Chapter 1.4.2.5. --- LPL --- p.21 / Chapter 1.4.2.6. --- UPC --- p.22 / Chapter 1.5. --- Hypothesis and objectives of the study --- p.23 / Chapter CHAPTER 2. --- Materials and methods / Chapter 2.1. --- Study design --- p.25 / Chapter 2.1.1. --- Two-stage candidate gene association design --- p.25 / Chapter 2.1.2. --- Power calculation --- p.27 / Chapter 2.2. --- Study cohort --- p.29 / Chapter 2.2.1. --- Subject recruitment --- p.29 / Chapter 2.2.2. --- Clinical and biochemical measurements --- p.30 / Chapter 2.2.3. --- Clinical definitions --- p.31 / Chapter 2.3. --- Genetic study --- p.32 / Chapter 2.3.1. --- Candidate gene selection --- p.32 / Chapter 2.3.2. --- SNP selection --- p.32 / Chapter 2.3.3. --- DNA sample preparation --- p.35 / Chapter 2.3.4. --- Genotyping methods --- p.36 / Chapter 2.3.4.1. --- Allele specific Tm shift assay --- p.36 / Chapter 2.3.4.2. --- Mass spectrometry assay --- p.40 / Chapter 2.4. --- Data quality control --- p.42 / Chapter 2.4.1. --- Stage 1 --- p.42 / Chapter 2.4.2. --- Stage 2 --- p.42 / Chapter 2.5. --- Statistical analysis --- p.45 / Chapter 2.5.1. --- Stage 1 analysis --- p.45 / Chapter 2.5.2. --- Stage 2 analysis --- p.45 / Chapter 2.5.3. --- Stage 1 and 2 combined analysis --- p.46 / Chapter CHAPTER 3. --- Results / Chapter 3.1. --- Clinical characteristics of subjects in stages 1 and 2 studies --- p.48 / Chapter 3.2. --- Case-control associations in stage 1 --- p.51 / Chapter 3.2.1. --- Association with T2D --- p.51 / Chapter 3.2.2. --- Association with T2D subset by metabolic syndrome --- p.54 / Chapter 3.3. --- Case-control associations in stage 2 --- p.60 / Chapter 3.3.1. --- SNP selection for genotyping --- p.60 / Chapter 3.3.2. --- Association with T2D --- p.63 / Chapter 3.3.3. --- Association with T2D subset by metabolic syndrome --- p.64 / Chapter 3.4. --- Case-control associations in combined stages 1 and 2 --- p.66 / Chapter 3.4.1. --- Association with T2D --- p.66 / Chapter 3.4.2. --- Association with T2D subset by metabolic syndrome --- p.70 / Chapter 3.4.3. --- Association with T2D subset by age at diagnosis --- p.74 / Chapter 3.4.4. --- Association with T2D subset by gender --- p.76 / Chapter 3.4.5. --- Genetic epistasis for T2D association --- p.79 / Chapter 3.5. --- Metabolic traits associations in control subjects in combined stages 1 and 2 studies --- p.83 / Chapter CHAPTER 4. --- Discussion --- p.86 / Chapter 4.1. --- Role of insulin secretion genes in type 2 diabetes --- p.87 / Chapter 4.2. --- Role of insulin action genes in type 2 diabetes --- p.92 / Chapter 4.3. --- Combined genetic effects on risk for type 2 diabetes --- p.97 / Chapter 4.4. --- Summary --- p.98 / Chapter 4.5. --- Limitation of this study and future direction --- p.101 / REFERENCES --- p.104 / APPENDICES --- p.119 / Chapter Appendix 1: --- Gene structure and linkage disequilibrium of genotyped SNPs of candidate genes --- p.119 / Chapter Appendix 2: --- Information of SNPs genotyped in stage 1 --- p.130 / Chapter Appendix 3: --- T2D association results (additive model) of 152 SNPs for stage 1 case- control samples --- p.137 / Chapter Appendix 4: --- T2D association results (additive model) of 152 SNPs for stage 1 case- control samples subset by metabolic syndrome status in cases --- p.144 / Chapter Appendix 5: --- T2D association results (additive model) of 22 SNPs for stage 2 case- control samples --- p.151 / Chapter Appendix 6: --- T2D association results (additive model) of 22 SNPs for stage 2 case- control samples subset by metabolic syndrome status in cases --- p.153

Wong, Ling Yee. / Thesis submitted in: August 2007. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 110-127). / Abstracts in English and Chinese. / Thesis Abstract --- p.i / 論文摘要 --- p.iv / Acknowledgements --- p.vi / Abbreviations --- p.vii / Thesis Content --- p.xii / List of Figures --- p.xv / List of Tables --- p.xvii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter Chapter 2 --- Literature Review --- p.3 / Chapter 2.1. --- Multiple Myeloma (MM) --- p.3 / Chapter 2.1.1 --- Epidemiology --- p.4 / Chapter 2.1.2 --- Cause and Risk Factors --- p.5 / Chapter 2.1.3 --- Pathophysiology --- p.5 / Chapter 2.1.4 --- Diagnosis and Clinical Presentation --- p.6 / Chapter 2.1.5 --- Classification of Plasma Cell Disorders --- p.6 / Chapter 2.1.5.1 --- Monoclonal Gammopathy of Undetermined Significance (MGUS) --- p.6 / Chapter 2.1.5.2 --- Asymptomatic (Smouldering) MM --- p.7 / Chapter 2.1.5.3 --- Indolent MM --- p.7 / Chapter 2.1.5.4 --- Symptomatic MM --- p.8 / Chapter 2.1.6 --- Staging --- p.9 / Chapter 2.1.7 --- Treatment --- p.11 / Chapter 2.1.8 --- Molecular Abnormality --- p.12 / Chapter 2.2 --- DNA Microarray Analysis in MM --- p.13 / Chapter 2.2.1 --- MM Pathogenesis --- p.15 / Chapter 2.2.2 --- Molecular Classification of MM --- p.18 / Chapter 2.2.3 --- Anti-MM Drug Studies --- p.22 / Chapter 2.3 --- Cancer Treatment Response Prediction --- p.24 / Chapter 2.3.1 --- MP Treatment --- p.24 / Chapter 2.3.1.1 --- Melphalan --- p.25 / Chapter 2.3.1.2 --- Prednisone --- p.27 / Chapter 2.3.1.3 --- MP Treatment Response Prediction in MM --- p.29 / Chapter 2.3.2 --- Cancer Prognosis using DNA Microarray --- p.31 / Chapter Chapter 3 --- Materials and Methods --- p.36 / Chapter 3.1. --- Patient Specimens for Gene Expression Profiling and Quantitative Real-time PCR --- p.36 / Chapter 3.2. --- Magnetic Cell Sorting of CD138-positive Plasma Cells --- p.37 / Chapter 3.2.1 --- Density Gradient Centrifugation --- p.37 / Chapter 3.2.2 --- Positive Selection of CD138-positive Cells --- p.37 / Chapter 3.3 --- Generation of Gene Expression Profiles --- p.39 / Chapter 3.3.1 --- RNA Extraction --- p.39 / Chapter 3.3.2 --- RNA Assessment --- p.40 / Chapter 3.3.3 --- Synthesis and Purification of Double-strand cDNA --- p.40 / Chapter 3.3.4 --- In vitro Transcription (IVT) and Recovery of Biotin-labeled cRNA --- p.41 / Chapter 3.3.5 --- cRNA Fragmentation and Hybridization Reaction Mixture Preparation --- p.41 / Chapter 3.3.6 --- Hybridization --- p.42 / Chapter 3.3.7 --- Post-hybridization Wash --- p.42 / Chapter 3.3.8 --- Detection with Streptavidin-dye Conjugate --- p.43 / Chapter 3.3.9 --- Bioarray Scanning and Spot Signal Quantitation --- p.43 / Chapter 3.4 --- Microarray Data Analysis --- p.45 / Chapter 3.4.1 --- Normalization and Filtering --- p.45 / Chapter 3.4.2 --- Unsupervised Clustering Analysis --- p.45 / Chapter 3.4.3 --- Supervised Class Comparison Analysis --- p.46 / Chapter 3.5 --- Microarray Verification and Candidate Gene Validation --- p.47 / Chapter 3.5.1 --- RNA Extraction --- p.47 / Chapter 3.5.2 --- Reverse Transcription PCR --- p.47 / Chapter 3.5.3 --- Quantitative Real-time PCR --- p.48 / Chapter 3.6 --- Predictive Value Calculation --- p.49 / Chapter 3.7 --- Experimental Flow --- p.49 / Chapter Chapter 4 --- Results --- p.53 / Chapter 4.1 --- Gene Expression Profiling of Chinese MM --- p.53 / Chapter 4.1.1 --- Unsupervised Clustering Analysis --- p.53 / Chapter 4.1.1.1 --- Hierarchical Clustering --- p.53 / Chapter 4.1.1.2 --- Principal Component Analysis (PCA) --- p.54 / Chapter 4.1.2 --- Identification of Statistically Differentially Expressed Genes --- p.58 / Chapter 4.1.2.1 --- Two-Sample t-statistics --- p.58 / Chapter 4.1.2.2 --- Significance Analysis of Microarrays (SAM) --- p.58 / Chapter 4.1.2.3 --- Microarray Verification --- p.66 / Chapter 4.2 --- Development of MP Treatment Response Biomarker in MM --- p.70 / Chapter 4.2.1 --- Unsupervised Clustering Analysis --- p.70 / Chapter 4.2.1.1 --- Hierarchical Clustering --- p.70 / Chapter 4.2.1.2 --- PCA --- p.70 / Chapter 4.2.2 --- Identification of Statistically Differentially Expressed Genes --- p.74 / Chapter 4.2.2.1 --- Two sample t-statistics --- p.74 / Chapter 4.2.2.2 --- SAM --- p.74 / Chapter 4.2.3 --- Verification of Candidate Gene CYB5D1 --- p.76 / Chapter Chapter 5 --- Discussion --- p.79 / Chapter 5.1 --- Global Gene Expression Profiling: DNA Microarray --- p.79 / Chapter 5.2 --- Microarray Data Normalization and Gene Filtering --- p.81 / Chapter 5.3 --- Microarray Data Analysis --- p.83 / Chapter 5.3.1 --- Unsupervised Clustering Analysis --- p.83 / Chapter 5.3.1.1 --- Hierarchical Clustering --- p.83 / Chapter 5.3.1.2 --- PCA --- p.85 / Chapter 5.3.2 --- Identification of Statistically Differentially Expressed Genes --- p.86 / Chapter 5.4 --- Verification of Candidate Genes by Quantitative Real-time PCR --- p.89 / Chapter 5.5 --- Gene Expression Profiling of Chinese MM --- p.90 / Chapter 5.5.1 --- Comparison of Gene Expression Patterns of MM and Normal Plasma Cells --- p.90 / Chapter 5.5.2 --- Differentially Expressed Genes between MM and Normal Plasma Cells..… --- p.91 / Chapter 5.5.2.1 --- Common Differentially Expressed Genes with Previous Studies --- p.94 / Chapter 5.5.2.2 --- Potential Tumor Suppressor Genes in Differentially Expressed Genes..… --- p.96 / Chapter 5.5.2.3 --- Verified Differentially Expressed Genes --- p.98 / Chapter 5.5.3 --- Future Studies --- p.101 / Chapter 5.6 --- Development of MP Treatment Response Biomarker in MM --- p.103 / Chapter 5.6.1 --- Comparison of Gene Expression Patterns of MP Good Responders (GR) and Poor Responders (PR) --- p.103 / Chapter 5.6.2 --- Differentially Expressed Gene between MP GR and PR: CYB5D1 --- p.104 / Chapter 5.6.3 --- Possible Role of CYB5D1 in MP Resistance in MM Cells --- p.104 / Chapter 5.6.4 --- Potential Clinical Application of CYB5D1 in MP Treatment Response Prediction in MM --- p.106 / Chapter 5.6.5 --- Future Studies --- p.106 / Chapter Chapter 6 --- Conclusion --- p.108 / Chapter 6.1 --- Gene Expression Profiling of Chinese MM --- p.108 / Chapter 6.2 --- Development of MP Treatment Response Biomarker in MM --- p.108 / References --- p.110 / Appendix --- p.128

Acute coronary syndrome (ACS), a term used to cover a group of clinical symptoms compatible with acute myocardial ischemia, represents a high-risk group of patients with coronary heart disease (CHD). To improve quality of care, international guidelines for the management of ACS have been established and are updated regularly. In the era of evidence based medicine, adherence to therapeutic guidelines is essential for optimal care of ACS patients. However, most data on ACS epidemiology, treatment and outcomes are derived from western population. There are limited data in Chinese population in terms of prevalence, presentation, response to treatment and clinical outcome. / Among 624 patients finished Short Form (SF)-36 questionnaires, health related quality of life (HRQoL) were compared between patients underwent PCI versus those treated conservatively across 3 age groups (<60, 60-79 and ≥80 years). PCI was performed in 73.6%,55.7% and 21.3% in patients aged <60,60-79 and older than 80 years, respectively (p<0.01). Elderly patients were more likely to be female (16.9 vs. 35.4 vs. 54.6%, p<0.01) and had more co-morbidities (p<0.01). Older patients were less likely to undergo angiography (84.8 vs. 65.2 vs. 24.8%, p<0.01). Baseline HRQoL decreased with advancing age (p<0.01). However, elderly patients who underwent PCI-experienced the most improvement in physical health than younger age groups. PCI was an independent predictor (OR, 1.79,95% CI: 1.10-2.92) of better physical health status at 6 months. In conclusion, elderly ACS patients who underwent PCI experienced the most improvement in physical health compared to younger patients. Our findings suggest that age per se should not deter against revascularization because of potential benefits in HRQOL. / In summary, this is the first registry which described patients' characteristics, treatment and management practices, and hospital outcomes over the whole spectrum of ACS in Hong Kong. The study identified gaps between guideline and clinical practice as well as the reasons of these gaps, and measured the impact of such gaps on the outcomes of patients with ACS. Compared with internationally reported data, Hong Kong patients are different in terms of age and risk factors distribution. Treatment gaps exist between international therapeutic guideline recommendations and clinical practice, especially among the high risk population, the elderly and female patients. Better understanding and narrowing these gaps between guideline and practice will lead to improvement in quality of care and clinical outcomes. Increase use ofrisk stratification models and health status assessments may improve decision making in the management of ACS. / Patients with ACS were divided into low- and high-predicted risk of mortality at 6 months using the GRACE risk score (≥142.5 was defined as high-risk). We evaluated the use of in-hospital angiography, revascularization, anti-platelet, angiotensin converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB), beta-blockers and statins therapy between high and low-risk patients. There were 259 patients in the high- and 742 in the low-risk groups. Paradoxically, high-risk compared to low-risk patients were less likely to underwent coronary angiography and/or revascularization during the index hospitalization (33% vs. 64% and 25% vs. 50%, both p<0.01). Hospital initiated pharmacotherapies are also lower in high-risk patients (24% vs. 55% for c1opidogrel, 49% vs. 58% for ACEI/ARBs, 54% vs. 69% for beta-blockers and 56% vs. 77% for statins; all p<0.01). After adjustment, high-risk patients remained less likely to undergo revascularization (adjusted odds ratio [OR], 0.47; 95% CI, 0.33-0.73, p<0.001) than low-risk patients. Advanced age, increased creatinine level and higher GRACE score were independent predictors for failure to administer evidence-based therapies. Thus, patients with ACS at high risk of mortality were paradoxically less likely to undergo revascularization or receive medications according to guidelines. Better adherence to evidence-based therapies in high-risk patients may improve clinical outcome and quality of health care. / The Hong Kong ACS registry was designed to investigate epidemiology, treatment and outcome of ACS patients under current medical care system, it was conducted in a university affiliated teaching hospital from February 2006 to December 2009. Clinical characteristics and treatment data were collected at baseline, 30 days and 6 months after onset in a standard defined case report form. SF-36 questionnaire was completed after admission and at 6 months. Outcomes were evaluated mortality and morbidity in clinical aspect and quality of life in aspect of health status. / The Main findings were as followed: Totally 1001 patients admitted with ACS were recruited. Among all patients enrolled, 31.7% were diagnosed with ST-segment elevation myocardial infarction, 42.7% with non-S'T-segrnent myocardial infarction and 21.6% with unstable angina. The median age was 72 (interquartile range 61-79) years; 77.2% were >60 years old, and 31.5% were women. / Women presented more often with NSTE-ACS than men (77.3% of women vs. 63.2% of men, p<0.001). Despite having greater cornorbidities including hypertension, diabetes, hypercholesterolemia, renal impairment and history of heart failure etc., women were observed to have higher GRACE (global registry of acute coronaryevents) score than men (128+/-32 vs. 118+/-37, p score than men (128+/-32 vs. 118+/-37, p<0.01). Women were less likely to be assigned invasive procedures (43.3% vs. 62.9%, p<0.001) as well as pharmacotherapies such as clopidogrel (41.1% vs. 58.8%, p<0.001), glycoprotein (GP) IIb/IIIa antagonists (5.3% vs. 11.6%, p=0.001) and statins (64.1% vs. 77.2%, p<0.01) et al. than men. For in-hospital mortality, the adjusted odds ratio for men compared to women was similar (odds ratio [OR]: 1.32, 95% CI: 0.62-2.83, p=0.47). The higher 6 month mortality and major cardiac events rate in women were not significant after adjusting for differences in clinical characteristics and percutaneous coronary intervention (PCI) (OR=1.02; 95% CI 0.62 to 1.68; p=0.95). In summary, there were differences in baseline characteristics and in the management of women and men admitted for ACS. Advanced age and high comorbidities prevalence could explain most of the difference between genders suggesting that decision making bias in clinical practice is anti-age but not anti-female. Overall, in-hospital and 6 months mortality was similar for women and men after adjustments. / Li, Rujie. / "December 2010." / Adviser: Cheuk-Man Yu. / Source: Dissertation Abstracts International, Volume: 73-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 145-166). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

A convenience sample of 184 first-time childbearing women was recruited from two public hospitals with one hospital randomly selected as the experimental group. The experimental group (n = 92) received the childbirth psychoeducation programme and routine childbirth education. The comparison group (n = 92) received the routine childbirth education only. / Outcomes on learned resourcefulness, maternal role competence and perinatal depression were measured by C-SCS, C-PSOC (Efficacy Subscale) and Edinburgh Postnatal Depression Scale (EPDS), respectively, at baseline, immediately post-intervention, six weeks and six months postpartum. Maternal role satisfaction was assessed at six weeks and six months postpartum using C-PSOC (Satisfaction Subscale). Doubly multivariate analysis of covariance was performed to compare the effects of childbirth psychoeducation programme between the experimental and comparison groups. In addition, 16 participants in the experimental group were interviewed at six weeks postpartum to explore their perceived impacts of childbirth psychoeducation programme in helping them cope with the experience of new motherhood. Content analysis was used to analyze the interview data. / Results of the phase I study indicated good psychometric properties of C-SCS and C-PSOC in Chinese childbearing women. Results in the phase II study revealed significant improvement in learned resourcefulness at six weeks postpartum (p = 0.004), and overall reduction in depressive symptoms (p = 0.01) for women receiving the childbirth psychoeducation programme compared with the routine childbirth education group after adjusting for baseline group differences on age and social support. No significant change was detected on maternal role competence. However, women receiving the childbirth psychoeducation programl1'l;e had significantly higher level of satisfaction in the maternal role at six weeks postpartum (p = 0.01). / The crisis nature of early motherhood, the frequent feeling of incompetence in the maternal role, the increasing evidence of postpartum depression in the Chinese population, coupled with the changing nature of socio-cultural environment challenge midwives to make continued refinement of childbirth education to enhance women's adjustment during the transition to motherhood. Learned resourcefulness has been identified as an important coping repertoire that promotes healthy adjustment in the perinatal period. The aim of this study was to determine the effectiveness of a childbirth psychoeducation programme based on the concept of learned resourcefulness. / The qualitative interviews revealed that the experimental group perceived the childbirth psychoeducation programme to be helpful in increasing their confidence in the maternal role, improving their emotional well-being and fostering the development of learned resourcefulness skills. The findings of this study support the effectiveness of childbirth psychoeducation programme based on the concept of learned resourcefulness for reducing depressive symptoms in first-time Chinese childbearing women, and highlight the contributions midwives can make to continue improving the quality of childbirth education in Chinese society. / The study had two phases. The first phase aimed at establishing the psychometric properties of the Chinese versions of Self-Control Schedule (C-SCS) and Parenting Sense of Competence Scale (C-PSOC), which were used as outcome measures in the second phase. The second phase adopted a pretest-posttest, control group quasi-experimental design to examine the effects of a childbirth psychoeducation programme on learned resourcefulness, maternal role competence and satisfaction, and perinatal depression. / Ngai Fei Wan. / Adviser: W. Y. Ip. / Source: Dissertation Abstracts International, Volume: 72-11, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 259-300). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese; some appendices in Chinese.

Conclusions. The growing epidemic of type 2 diabetes and its cardiorenal complications place a major burden on our health care system. Diabetic kidney disease is of particular importance in Asian populations including Chinese. In this series of studies, using a large prospective cohort established since 1995, I confirmed the powerful predictive value of albuminuria on cardio-renal complications. Inhibition of the RAAS interacted with both modifiable and genetic factors, notably the ACE I/D polymorphism, on the development of cardio-renal complications. In addition, it was found that CKD predicts CVD independent of albuminuria. Based on two prospective studies, I confirmed the effectiveness of global risk-factor control using structured care protocol to prevent these devastating complications. (Abstract shortened by UMI.) / I then examined the possible independent and interactive effects of CKD and albuminuria on cardio-renal outcomes in the original cohort of 5,004 patients. Glomerular filtration rate was estimated (eGFR) by the Modification of Diet in Renal Disease equation. The frequency of CKD as defined by eGFR <60ml/min/1.73m 2 was 15.8% in the cohort at baseline, when 6% of patients had serum creatinine ≥150mumol/L. / In collaboration with colleagues, I have conducted a series of studies to examine the prognostic factors for cardio-renal complications in Chinese type 2 diabetic patients. The modulating effects of RAAS inhibition and the effectiveness of rnuitidisciplinary care to prevent ESRD are also examined. / Research Hypotheses. (1) Albuminuria is a prognostic factor on cardio-renal outcomes in type 2 diabetes patients; (2) Chronic Kidney Disease is associated with other metabolic risk factors and phenotypes and is a prognostic factor on cardio-renal outcomes in type 2 diabetes patients; (3) Angiotensin-converting-enzyme insertion/deletion polymorphism is a prognostic factor on cardio-renal outcomes in type 2 diabetes patients, and has an effect on treatment responses with RAAS blockage with ACE inhibitors; (4) Structured care models by risk stratification using various prognostic factors and adherence to care protocol can improve cardio-renal outcome in type 2 diabetes patients. / Results. In a prospective cohort of 5,004 patients, I examined the effect of albuminuria and ACE inhibition on survival and cardio-renal outcomes in 3,773 patients who had been observed for at least 6 months with a mean follow up period of 35.8 months. / Taken together, measurement of serum creatinine alone without GFR estimation may underestimate the frequency of CKD in Chinese type 2 diabetic patients. Estimated GFR was inversely associated wit-29h an increasing frequency of micro- and macrovascular complications cross-sectionally and an increased risk of all-cause mortality prospectively, independent of albuminuria and metabolic control. / So Wing Yee. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3422. / Thesis (M.D.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 203-243). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / School code: 1307.

Although the clinical efficacy of statins has been well established, there is a wide inter-individual variation in the lipid responses to statins. Pharmacogenetic studies have identified some genetic differences that contribute to the variation, but overall the results have been disappointing. The studies described in this thesis were performed to examine whether certain genetic variants predicted the lipid responses to rosuvastatin in Chinese patients. Over 400 Chinese patients with increased risk of cardiovascular disease (CVD) who were treated with rosuvastatin 10 mg daily for at least 4 weeks (more than 97% of patients had at least 6 weeks treatment) were studied, including 166 having familial hypercholesterolaemia (FH) and 36 having rheumatoid arthritis (RA). They were genotyped for 135 polymorphisms in 62 candidate genes/loci potentially related to pharmacokinetics or pharmacodynamics of statins and lipid metabolism. Associations between genetic polymorphisms and the lipid responses to rosuvastatin were analyzed in 386 patients with good compliance. The associations between genetic polymorphisms and some risk factors for CVD including baseline lipid levels, high-sensitivity C-reactive protein (hsCRP), uric acid and bilirubin levels were also analyzed. / Some novel genetic determinants of the LDL-C response to rosuvastatin treatment have been identified in this study. The responses in HDL-C and triglycerides were related more closely to the baseline levels of these lipids than to any of the polymorphisms examined. Genetic associations with baseline lipid parameters, hsCRP, uric acid and bilirubin were identified and generally correspond with some of the previous reports of studies in Chinese and other ethnic groups. / The key findings of the study are as follows: 1. The polymorphisms most highly associated with the low-density lipoprotein cholesterol (LDL-C) response were 421C>A in the ATP-binding cassette G2 (ABCG2) gene (P=9.2x10 -7), followed by 18281G>A (V257M) in the flavin-containing monooxygenase 3 (FMO3) gene (P=0.0002), 1421C>G in the lipoprotein lipase (LPL) gene (P=0.002), and rs4420638 in the apolipoprotein E/C-I/C-IV/C-II (APOE/C1/C4/C2) gene cluster (P=0.004). These genetic polymorphisms and having FH totally explained 13.6% of the variance in percentage change in LDL-C in response to rosuvastatin. The greater percentage reduction in LDL-C in patients with the ABCG2 421AA genotype compared to those with the ABCG2 421CC genotype was equivalent to at least doubling the dose of rosuvastatin. 2. Three SNPs (glucokinase regulator [ GCKR] rs1260326, apolipoprotein AS [APOA5] -1131T>C and the solute carrier organic anion transporter 1B1 [SLCO1B1] 521T>C) tended to be associated with percentage changes in high-density lipoprotein cholesterol (HDL-C) (P<0.05), but none of these reached the overall significance level. In multivariate stepwise regression analysis, baseline HDL-C (P=1.6x10 -6), having diabetes (P=0.0004) or RA (P=0.002) and the SLCO1B1 521T>C polymorphism (P=0.03) were determinants of HDL-C responses, contributing 9.9% of the variance in percentage change in HDL-C, but the genetic factors only contributed to 0.8% of the variance. 3. The triglyceride response to rosuvastatin was highly variable and was strongly related to baseline levels. The diacylglycerol acyltransferase-2 (DGAT2) rs10899113 C>T polymorphism tended to be associated with reduced triglyceride response in a gene-dose dependent manner. However, in multivariate stepwise regression analysis, baseline triglyceride level was the only factor that strongly related to the triglyceride response, explaining 14.4% of the variance. 4. This study has also analyzed relationships between on-treatment plasma hsCRP concentrations and cardiovascular risk factors and 14 single nucleotide polymorphisms in CRP and other candidate genes, which showed that central obesity, low HDL-C and CRP polymorphisms are major determinants of higher hsCRP levels in Chinese patients on treatment with rosuvastatin. 5. The association between genetic polymorphisms and lipid traits were analyzed in FH and non-FH patients separately due to their different lipid profiles. The analysis has shown that there were different genetic predictors of lipid levels in patients with and without FH and that more genetic factors appeared to affect the baseline lipid levels in patients with FH compared to non-FH patients, suggesting complex interactions between genetic and environmental factors and plasma cholesterol levels in patients with and without FH. 6. The SLC2A9 (solute carrier family 2, member 9) rs1014290 T>C was significantly associated with plasma uric acid levels in a gene-dose dependent manner (P=1.0x10-5) and the relationship was more pronounced in women or in patients without hypertension than in men or patients with hypertension. The ABCG2 421 C>A did not show a significant effect on uric acid levels. 7. The UGT1A1 (uridine diphosphate glucuronosyltransferases family, polypeptide A1) variants *28 (P=1.5x10 -9) and *6 (P=2.2x10-7) were independently associated with increased baseline bilirubin levels. Polymorphisms in SLCO1B1 did not appear to affect bilirubin levels in this study. / Hu, Miao. / Adviser: Brian Tomlinson. / Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 230-264). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Jiang, Jieying. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 170-186). / Abstract also in Chinese. / ACKNOWLEDGEMENT --- p.II / ABBREVIATIONS --- p.III / ABSTRACT OF THESIS ENTITLED: --- p.VI / 摘要 --- p.IX / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Individual variations of blood sex steroid levels and their determinants --- p.1 / Chapter 1.1.1 --- Introduction to Sex steroids --- p.1 / Chapter 1.1.2 --- Androgens --- p.1 / Chapter 1.1.2.1 --- Types of androgens --- p.1 / Chapter 1.1.2.2 --- Androgens plasma concentration and relative biological potencies --- p.2 / Chapter 1.1.2.3 --- Androgen biosynthesis and metabolism --- p.3 / Chapter 1.1.2.4 --- Testosterone transportation in plasma --- p.6 / Chapter 1.1.2.5 --- Measurement of free testosterone --- p.7 / Chapter 1.1.2.6 --- The hypothalamus-pituitary-testicular axis and testosterone secretion --- p.8 / Chapter 1.1.2.7 --- Androgen action --- p.10 / Chapter 1.1.2.8 --- Androgen biological function and diseases in men --- p.11 / Chapter 1.1.3 --- Estrogen biological function and diseases in men --- p.12 / Chapter 1.1.4 --- Factors influencing circulating sex steroid levels --- p.13 / Chapter 1.1.4.1 --- Genetic determinants affecting sex steroid levels --- p.15 / Chapter 1.2 --- Genetic variants in sex steroid metabolic pathway and hepatocellular carcinoma (HCC) --- p.18 / Chapter 1.2.1 --- Epidemiology of HCC --- p.18 / Chapter 1.2.2 --- Etiological factors of HCC --- p.22 / Chapter 1.2.3 --- The male predominance in HCC --- p.24 / Chapter 1.2.4 --- Genetic predisposition to HCC --- p.26 / Chapter CHAPTER 2 --- PART A STUDY: GENETIC VARIATIONS IN SEX STEROID METABOLIC PATHWAY AND ASSOCIATION WITH SEX STEROID LEVELS --- p.28 / Chapter 2.1 --- Introduction --- p.28 / Chapter 2.1.1 --- Candidate genes association with sex steroid levels --- p.28 / Chapter 2.1.2 --- Genes involved in androgen metabolism --- p.29 / Chapter 2.1.2.1 --- SRD5A --- p.29 / Chapter 2.1.2.2 --- HSD3B1 --- p.30 / Chapter 2.1.2.3 --- HSD17B2 --- p.31 / Chapter 2.1.2.4 --- AKR1C3 and AKRlC4 --- p.31 / Chapter 2.1.2.5 --- AKR1D1 --- p.32 / Chapter 2.1.3 --- Genes involved in estrogen metabolism --- p.32 / Chapter 2.1.3.1 --- CYP19A1 --- p.32 / Chapter 2.1.3.2 --- Other genes involved in estrogen metabolism --- p.33 / Chapter 2.1.4 --- Association of sex steroid related genes and blood concentrations of sex steroid levels --- p.33 / Chapter 2.1.4.1 --- Genes involved in androgen metabolic pathway and association with sex steroid levels --- p.33 / Chapter 2.1.4.2 --- Genes involved in estrogen metabolic pathway and association with sex steroid levels --- p.36 / Chapter 2.1.5 --- Aims of the study (Part A) --- p.37 / Chapter 2.2 --- Materials and methods --- p.38 / Chapter 2.2.1 --- Study subjects and biological samples --- p.38 / Chapter 2.2.2 --- TagSNP selection --- p.39 / Chapter 2.2.3 --- Genotyping of tagging SNPs --- p.41 / Chapter 2.2.4 --- Genotyping methods comparison --- p.52 / Chapter 2.2.5 --- Statistics --- p.53 / Chapter 2.3 --- Results --- p.54 / Chapter 2.3.1 --- Characteristics of study population --- p.54 / Chapter 2.3.2 --- Replication study for the association of CYP19A1 --- p.55 / Chapter 2.3.2.1 --- Association of the SNP rs2470152 and rs2899470 with serum estrogen and testosterone levels --- p.55 / Chapter 2.3.2.2 --- Halotype analysis and haplotype association in the tertile groups --- p.61 / Chapter 2.3.2.3 --- Haplotype construction of 3 SNPs --- p.63 / Chapter 2.3.3 --- SRD5A1 --- p.65 / Chapter 2.3.3.1 --- Association of SRD5A1 and sex steroid levels --- p.65 / Chapter 2.3.3.2 --- Haplotype analysis and haplotype association in the tertile groups --- p.71 / Chapter 2.3.4 --- SRD5A2 --- p.72 / Chapter 2.3.4.1 --- Association of SRD5A2 and sex steroid levels --- p.72 / Chapter 2.3.4.2 --- Haplotype association analysis of SRD5A2 in tertile groups --- p.76 / Chapter 2.3.5 --- HSD3B1 --- p.77 / Chapter 2.3.5.1 --- Association of HSD3B1 and sex steroid levels --- p.77 / Chapter 2.3.6 --- HSD17B2 --- p.80 / Chapter 2.3.6.1 --- Association of HSD17B2 and sex steroid levels --- p.80 / Chapter 2.3.6.2 --- Halotype association analysis of HSD17B2 in the tertile groups --- p.87 / Chapter 2.3.7 --- AKR1C4 --- p.89 / Chapter 2.3.7.1 --- Association of AKR1C4 and sex steroid levels --- p.89 / Chapter 2.3.7.2 --- Halotype association analysis of AKR1C4 in the tertile groups --- p.93 / Chapter 2.3.8 --- AKR1D1 --- p.94 / Chapter 2.3.8.1 --- Association of AKR1D1 and sex steroid levels --- p.94 / Chapter 2.3.8.2 --- Haplotype association analysis of AKR1D1 in the tertile groups --- p.99 / Chapter 2.3.9 --- AKR1C3 --- p.100 / Chapter 2.3.9.1 --- Association of AKR1C3 and sex steroid levels --- p.100 / Chapter 2.3.9.2 --- Haplotype association analysis of AKR1C3 in the tertile groups --- p.104 / Chapter 2.3.10 --- Overall association of polymorphisms in sex steroid metabolism genes and metabolites levels in blood --- p.105 / Chapter 2.4 --- Discussion --- p.106 / Chapter 2.4.1 --- SRD5A and sex steroid levels --- p.106 / Chapter 2.4.2 --- HSD17B2 and sex steroid levels --- p.110 / Chapter 2.4.3 --- "AKR1D1, AKR1C4, AKR1C3 and catabolic intermediates of sex steroids" --- p.112 / Chapter 2.4.4 --- HSD3B1 and sex steroid levels --- p.114 / Chapter 2.4.4 --- CYP19A1 and sex steroid levels --- p.114 / Chapter CHAPTER 3 --- PART B STUDY: GENETIC VARIATIONS IN SEX STEROID METABOLIC PATHWAY AND ASSOCIATION WITH HCC --- p.119 / Chapter 3.1 --- Introduction --- p.119 / Chapter 3.1.1 --- Previous genetic association studies of HCC on sex steroid metabolic pathways --- p.119 / Chapter 3.1.2 --- Previous genetic association studies of HCC in other pathways --- p.120 / Chapter 3.1.3 --- "Association of sex steroid related genes and other cancers, like prostate cancer" --- p.121 / Chapter 3.1.4 --- Aims of the study (Part B) --- p.123 / Chapter 3.2 --- Materials and method --- p.125 / Chapter 3.2.1 --- "Study subjects, Genomic DNA extraction" --- p.125 / Chapter 3.2.2 --- Tissue specimen and cell lines --- p.125 / Chapter 3.2.3 --- TagSNP selection --- p.126 / Chapter 3.2.4 --- Genotyping of tagging SNPs --- p.126 / Chapter 3.2.5 --- Statistics --- p.127 / Chapter 3.2.6 --- Extraction of RNA and Reverse-Transcription-PCR --- p.128 / Chapter 3.3 --- Results --- p.130 / Chapter 3.3.1 --- SRD5A1 --- p.130 / Chapter 3.3.1.1 --- SRD5A1 polymorphisms and risk of HCC --- p.130 / Chapter 3.3.2 --- SRD5A2 --- p.134 / Chapter 3.3.2.1 --- SRD5A2 polymorphisms and risk of HCC --- p.134 / Chapter 3.3.2.2 --- Haplotype analysis --- p.136 / Chapter 3.3.3 --- HSD3B1 --- p.137 / Chapter 3.3.3.1 --- HSD3B1 polymorphisms and risk of HCC --- p.137 / Chapter 3.3.3.2 --- Haplotype analysis --- p.139 / Chapter 3.3.4 --- HSD17B2 --- p.140 / Chapter 3.3.4.1 --- HSD17B2 polymorphisms and risk of HCC --- p.140 / Chapter 3.3.4.2 --- Haplotype analysis --- p.143 / Chapter 3.3.5 --- CYP19A1 --- p.144 / Chapter 3.3.5.1 --- CYP19A1 polymorphisms and risk of HCC --- p.144 / Chapter 3.3.5.2 --- Haplotype analysis --- p.146 / Chapter 3.3.6 --- AKR1C4 --- p.147 / Chapter 3.3.6.1 --- AKR1C4 polymorphisms and risk of HCC --- p.147 / Chapter 3.3.6.2 --- Haplotype analysis --- p.148 / Chapter 3.3.7 --- AKR1D1 --- p.149 / Chapter 3.3.7.1 --- AKR1D1 polymorphisms and risk of HCC --- p.149 / Chapter 3.3.7.2 --- Haplotype analysis --- p.150 / Chapter 3.3.8 --- AKR1C3 --- p.151 / Chapter 3.3.8.1 --- AKR1C3 polymorphisms and risk of HCC --- p.151 / Chapter 3.3.8.2 --- Haplotype analysis --- p.152 / Chapter 3.3.9 --- mRNA expression study of the 5 α -reductase isoforms --- p.153 / Chapter 3.3.9.1 --- Expression of SRD5A1 and SRD5A2 mRNAin HCC patients --- p.153 / Chapter 3.3.9.2 --- Expression of SRD5A1 and SRD5A2 mRNAin prostate and HCC cell lines --- p.154 / Chapter 3.3.10 --- Overall association of polymorphisms in sex steroid metabolism genes and risk of HCC --- p.154 / Chapter 3.3.11 --- GMDR analysis --- p.156 / Chapter 3.4 --- Discussion --- p.159 / Chapter 3.4.1 --- 5 α-reductase and risk of HCC --- p.159 / Chapter 3.4.1.1 --- SRD5A2 --- p.160 / Chapter 3.4.1.2 --- SRD5A1 --- p.161 / Chapter 3.4.2 --- Other genes and association with HCC --- p.162 / Chapter 3.4.2.1 --- HSD17B2 and risk of HCC --- p.162 / Chapter 3.4.2.2 --- "HSD3B1, AKR1C3, AKR1C4, AKR1D1 and risk of HCC" --- p.163 / Chapter 3.4.2.3 --- CYP19A1 and risk of HCC --- p.164 / Chapter 3.4.3 --- Gene-Gene interactions associated with HCC --- p.165 / Chapter CHAPTER 4 --- CONCLUSIONS AND PROSPECT FOR FUTURE WORK --- p.166 / Chapter 4.1 --- Conclusion --- p.166 / Chapter 4.2 --- Future works and prospect --- p.169 / REFERENCES --- p.170