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Lau Siu Wai Maggie. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 236-245). / List of Figures --- p.i / List of Tables --- p.viii / List of Abbreviations --- p.x / Abstract --- p.xii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Postulated Pathophysiology of Essential Hypertension --- p.1 / Chapter 1.2 --- Measurement of Cardiac Output (CO) by Transthoracic Electrical Bioimpedance (TEB) and Other Methodologies --- p.6 / Chapter 1.3 --- Measurement of Blood Pressure --- p.10 / Chapter 1.4 --- Use of Antihypertensive Agents in Essential Hypertension --- p.12 / Chapter Chapter 2. --- The Method of Transthoracic Electrical Bioimpedance --- p.15 / Chapter 2.1 --- Introduction --- p.15 / Chapter 2.2 --- Development of Theory --- p.18 / Chapter 2.3 --- Measurements of Haemodynamic Parameters --- p.24 / Chapter 2.4 --- Literature Review - Validity of the Technique --- p.30 / Chapter Chapter 3 --- A Study on Reproducibility of Thoracic Electrical Bioimpedance in Healthy Subjects --- p.39 / Chapter 3.1 --- Objectives --- p.39 / Chapter 3.2 --- Methodology --- p.39 / Chapter 3.2.1 --- Subjects --- p.39 / Chapter 3.2.2 --- Study design --- p.41 / Chapter 3.2.3 --- Non-invasive haemodynamic monitoring --- p.41 / Chapter 3.2.4 --- Blood Pressure Measurement --- p.43 / Chapter 3.2.5 --- Isometric Exercise --- p.43 / Chapter 3.2.6 --- Data analysis --- p.44 / Chapter 3.2.7 --- Statistical analysis --- p.46 / Chapter 3.3 --- Results --- p.50 / Chapter 3.3.1 --- Systolic blood pressure --- p.50 / Chapter 3.3.2 --- Diastolic blood pressure --- p.52 / Chapter 3.3.3 --- Mean arterial pressure --- p.54 / Chapter 3.3.4 --- Heart rate --- p.55 / Chapter 3.3.5 --- Thoracic fluid index --- p.58 / Chapter 3.3.6 --- Stroke index --- p.60 / Chapter 3.3.7 --- Cardiac index --- p.62 / Chapter 3.3.8 --- Systemic vascular resistance index --- p.65 / Chapter 3.4 --- Discussion --- p.70 / Chapter Chapter 4 --- Literature Review --- p.73 / Chapter 4.1 --- Atenolol: Beta-adrenoceptor antagonists with β1-selectivity --- p.73 / Chapter 4.2 --- Pindolol: Beta-adrenoceptor antagonists with ISA --- p.78 / Chapter 4.3 --- Alpha1-adrenoceptor antagonists --- p.81 / Chapter 4.4 --- Angiotensin Converting Enzyme Inhibitors --- p.84 / Chapter 4.5 --- Calcium Channel Blockers --- p.87 / Chapter 4.6 --- Central Alpha Agonist --- p.91 / Chapter 4.7 --- Thiazide Diuretics --- p.94 / Chapter Chapter 5 --- The Integrated Hypertension Study --- p.97 / Chapter 5.1 --- Objectives --- p.97 / Chapter 5.2 --- Methodology --- p.97 / Chapter 5.2.1 --- Subjects --- p.97 / Chapter 5.2.2 --- Study design --- p.109 / Chapter 5.2.3 --- Non-invasive haemodynamic monitoring --- p.110 / Chapter 5.2 4 --- Blood Pressure Measurement --- p.111 / Chapter 5.2.5 --- Isometric Exercise --- p.111 / Chapter 5.2.6 --- Data analysis --- p.111 / Chapter 5.2.7 --- Statistical analysis --- p.112 / Chapter 5.2.8 --- Limitations of the study --- p.113 / Chapter 5.3 --- Results --- p.117 / Chapter 5.3.1 --- Atenolol --- p.117 / Chapter 5.3.2 --- Pindolol --- p.125 / Chapter 5.3.3 --- Doxazosin --- p.132 / Chapter 5.3.4 --- Enalapril --- p.138 / Chapter 5.3.5 --- Nifedipine Retard --- p.145 / Chapter 5.3.6 --- Methyldopa --- p.152 / Chapter 5.3.7 --- Cyclopenthiazide --- p.160 / Chapter 5.4 --- Comparisons of the anti-hypertensive drugs studied --- p.167 / Chapter 5.4.1 --- Baseline values --- p.167 / Chapter 5.4.2 --- Percentage changes after active treatment --- p.170 / Chapter 5.5 --- Discussion --- p.196 / Chapter 5.5.1 --- Atenolol --- p.196 / Chapter 5.5.2 --- Pindolol --- p.199 / Chapter 5.5.3 --- Doxazosin --- p.200 / Chapter 5.5.4 --- Enalapril --- p.202 / Chapter 5.5.5 --- Nifedipine Retard --- p.203 / Chapter 5.5.6 --- Methyldopa --- p.204 / Chapter 5.5.7 --- Cyclopenthiazide --- p.205 / Chapter 5.5.8 --- Comparison of the anti-hypertensive drugs studied --- p.206 / Chapter Chapter 6 --- Acute haemodynamic effects of Atenolol and Pindolol --- p.208 / Chapter 6.1 --- Objectives --- p.208 / Chapter 6.2 --- Methodology --- p.208 / Chapter 6.2.1 --- Subjects --- p.208 / Chapter 6.2.2 --- Study Design --- p.209 / Chapter 6.2.3 --- Statistical analysis --- p.209 / Chapter 6.3 --- Results --- p.211 / Chapter 6.3.1 --- Acute haemodynamic changes of atenolol --- p.211 / Chapter 6.3.2 --- Acute and short-term haemodynamic changes of atenolol --- p.219 / Chapter 6.3.3 --- Acute haemodymmic changes of pindolol --- p.221 / Chapter 6.3.4 --- Acute and short-term haemodymmic changes of pindolol --- p.222 / Chapter 6.3.5 --- Comparison of the acute haemodymmic effects of atenolol and pindolol --- p.226 / Chapter 6.4 --- Discussion --- p.230 / Chapter Chapter 7 --- Conclusion --- p.232 / References --- p.236 / Acknowledgements

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Background. Hypertension carries a high risk of cardiovascular complications. Patient medication non-compliance has been identified to be an major factor for suboptimal blood pressure control in clinical practice. Different strategies have been proposed to improve patient medication compliance but their effects on clinical outcomes were inconsistent. Methods . A telephone survey was conducted to examine patient medication compliance with anti-hypertensive drugs in Hong Kong. I then established a Pharmacist-managed Compliance Clinic in a public out-patient setting and provided individualized patient education to non-compliant patients identified by physicians. A telephone follow-up was arranged at 4-week after intervention followed by a more in-depth reassessment on subsequent physician clinic visit day. The immediate endpoint was patient compliance rate. Intermediate endpoint was systolic and diastolic blood pressure control. Other outcome measures were control of other cardiovascular risk factors and level of healthcare resources utilization. / Conclusion. Pharmacist-managed Compliance Clinic is effective in improving patient medication compliance and has positive impact on clinical outcomes. (Abstract shortened by UMI.) / Results. A total of 853 patients were successfully contacted and completed the patient survey. According to our definition, 80.4% of patients interviewed were considered to be compliant. Factors associated with medication compliance included multiple drug therapy, presence of drug adverse effects, patient's awareness of preventive nature of medication, rapport between patient and physician, and full-time working status. A causal model was successfully established with latent factors identified for medication non-compliance. The factors included patient's functional status, provision of health advice and concern from physician, and patient's knowledge regarding reasons for drug taking. Another two hundreds hypertensive patients were followed at the Pharmacist-managed Compliance Clinic. On average, each patient attended 1.3 pharmacist visits. The non-compliance rate fell from 100% to 20% after a single pharmacist intervention. Significant improvement was observed in patients' mean blood pressures readings as well as the diabetic and lipid control. Positive impacts on healthcare resources utilization were also observed. / Chan Man Chi Grace. / "June 2005." / Adviser: Juliana C.N. Chan. / Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3730. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 126-151). / 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. / Abstract in English and Chinese. / School code: 1307.

Lee Kwing Chin, Kenneth. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (p. 298-357). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

The current recommendations by the American Heart Association for health promotion are that all persons should partake in regular physical activity in order to reduce the risk of cardiovascular disease. Regular physical exercise reduces blood pressure and is an important component of the management of hypertension. It is therefore important that patients with hypertension participate in habitual physical exercise. Many hypertensive patients who exercise will require anti-hypertensive medication. However, some antihypertensive agents cause fatigue during exercise. In order for patients to gain the full benefits of an active lifestyle, it is important that the prescribed antihypertensive agent does not prevent them performing and enjoying sustained exercise. It has been well documented that β-blockers cause premature fatigue during physical exercise. The effects on exercise performance of other first line antihypertensive medications, such as calcium channel antagonists have not been extensively investigated. In particular, the effects of these agents on prolonged submaximal exercise endurance have not been well studied. The object of this thesis was to compare the effects of isradipine, a dihydropyridine calcium channel antagonist, to those of atenolol, a β₁-selective antagonist, on maximal and submaximal exercise performance and on short duration high-intensity exercise in physically active hypertensive patients. The study design was a crossover trial where drug treatments were double blinded and randomised. Physically active volunteers with mild to moderate hypertension were recruited. 11 subjects performed i) progressive exercise to exhaustion for determination of maximal oxygen consumption (VO₂max), maximal work load and cardiorespiratory responses to maximal exercise, ii) prolonged submaximal exercise for determination of exercise endurance, cardiorespiratory responses and ratings of perceived exertion (APE), and iii) short duration, high intensity exercise consisting of a 30 second maximal exercise test (Wingate test) to determine skeletal muscle power output, following 4 weeks ingestion of isradipine (2.5mg bd), atenolol (50mg bd) or placebo. Diastolic blood pressure at rest was reduced by both atenolol and isradipine, but was lowered to a greater extent by atenolol (83.3 vs 89.0 vs 96.1 mmHg, atenolol vs isradipine vs placebo, p<.0005). Systolic blood pressure at rest tended to be similarly reduced by both agents, but was significantly reduced during maximal and submaximal exercise by atenolol only (p<.001, atenolol vs isradipine, placebo). Heart rate at rest and during maximal and submaximal exercise was decreased by atenolol only (p<.0005, atenolol vs isradipine, placebo). Maximal exercise performance was reduced after atenolol ingestion compared to placebo but not after isradipine ingestion. Peak workload achieved during the maximal exercise test was decreased after atenolol but unchanged after isradipine ingestion (214 vs 243 W, atenolol vs placebo, p<.01). Similarly, VO₂max was reduced after atenolol compared to placebo but was unchanged after isradipine ingestion (33.6 vs 36.4, 33.6 vs 36.1 mlO₂/kg/min, atenolol vs placebo, atenolol vs isradipine, p<.05). Both atenolol and isradipine ingestion reduced submaximal endurance time compared to placebo (27.8 vs 46.4, 34.4 vs 46.4 min, atenolol vs placebo, isradipine vs placebo, p<.005), and increased rating of perceived exertion (APE) after 30 min of submaximal exercise (p<.05). Submaximal oxygen consumption (VO₂), ventilation, respiratory exchange ratio (REA) and blood lactate, glucose and free fatty acid concentrations were not altered after the ingestion of either agent. Neither agent influenced peak skeletal muscle power, total work done, or rate of fatigue during the Wingate test compared to placebo. The results of these studies indicate that impaired performance and increased RPE during submaximal exercise after ingestion of either atenolol or isradipine is not due to alterations of ventilation, VO₂, RER, or blood lactate, glucose and free fatty acid concentrations during prolonged submaximal exercise. Similarly, reduced submaximal exercise performance after atenolol or isradipine ingestion is not due to factors which would also limit the ability of skeletal muscle to perform short duration, high intensity exercise before a bout of prolonged exercise. This study demonstrates that prolonged submaximal exercise testing can reveal an impairment in exercise performance after ingestion of antihypertensive medication which is not evident during maximal exercise testing. This finding is important as prolonged submaximal exercise is the form of exercise which most hypertensive patients actually perform. Further research is required on the effects of anti-hypertensive medications on submaximal exercise performance before firm recommendations can be made regarding medications most suitable for the physically active hypertensive patient. The results of these and other studies indicate that it is not yet possible to make claims that the calcium channel antagonist agents are without effect on physical exercise performance in physically active hypertensive patients.

Lim Sze Nee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 165-176). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract (Chinese Version) --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Tables --- p.xi / List of Figures --- p.xiii / List of Abbreviation --- p.xvii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1. --- General Introduction --- p.1 / Chapter 1.1 --- Classification of algae --- p.2 / Chapter 1.2 --- Chemical and mineral composition of marine macroalgae --- p.4 / Chapter 1.3 --- Uses of marine macroalgae --- p.7 / Chapter 1.3.1 --- Food --- p.7 / Chapter 1.3.2 --- Industrial uses --- p.8 / Chapter 1.3.3 --- Agricultural uses --- p.9 / Chapter 1.3.3.1 --- Fertilizer --- p.9 / Chapter 1.3.3.2 --- Fodder --- p.9 / Chapter 1.3.4 --- Medicinal properties --- p.10 / Chapter 1.4 --- Pharmacological effects of marine macroalgae --- p.11 / Chapter 1.4.1 --- Antioxidant activity --- p.11 / Chapter 1.4.2 --- Hypotensive activity --- p.11 / Chapter 1.4.3 --- Antiviral activity --- p.12 / Chapter 1.4.4 --- Antimicrobial activity --- p.12 / Chapter 1.4.5 --- Antitumor activity --- p.13 / Chapter 1.4.6 --- Hypocholesterolemic activity --- p.14 / Chapter 1.5 --- Objectives --- p.14 / Chapter CHAPTER 2 --- Free Radical Scavenging and Antioxidative Activities of Marine Macroalgae --- p.16 / Chapter 2.1 --- Introduction --- p.16 / Chapter 2.1.1 --- Free radicals: definition and sources --- p.16 / Chapter 2.1.2 --- Free radical-induced damage --- p.16 / Chapter 2.1.2.1 --- Biological lipid peroxidation --- p.16 / Chapter 2.1.2.2 --- Lipid oxidation of foods --- p.18 / Chapter 2.1.3 --- Antioxidants --- p.19 / Chapter 2.1.3.1 --- Antioxidants --- p.19 / Chapter 2.1.3.2 --- Antioxidant mechanisms --- p.20 / Chapter 2.1.4 --- Synthetic antioxidants --- p.21 / Chapter 2.1.5 --- Natural antioxidants --- p.24 / Chapter 2.1.6 --- Objectives --- p.27 / Chapter 2.2 --- Methods and Materials --- p.28 / Chapter 2.2.1 --- Preparation of algae extracts --- p.28 / Chapter 2.2.2 --- Determination of free radical scavenging activities --- p.32 / Chapter 2.2.2.1 --- Superoxide anions scavenging activity --- p.32 / Chapter 2.2.3 --- Antioxidative activity using hemolysis assay --- p.33 / Chapter 2.2.3.1 --- Preparation of red blood cell (RBC) --- p.33 / Chapter 2.2.3.2 --- Hemolysis assay --- p.33 / Chapter 2.2.4 --- Lipid peroxidation assay --- p.34 / Chapter 2.2.4.1 --- Preparation of rat brain homogenates --- p.34 / Chapter 2.2.4.2 --- Measurement of lipid peroxidation --- p.34 / Chapter 2.2.5 --- Statistics --- p.35 / Chapter 2.3 --- Results --- p.36 / Chapter 2.3.1 --- Superoxide radical scavenging activity of algal extracts --- p.36 / Chapter 2.3.2 --- Effects of algae extracts on hemolysis assay --- p.41 / Chapter 2.3.3 --- Effects of algae extracts on lipid peroxidation --- p.44 / Chapter 2.4 --- Discussion --- p.50 / Chapter CHAPTER 3 --- Isolation of Antioxidative Phenolic Compounds from Sargassum siliquastrum --- p.60 / Chapter 3.1 --- Introduction --- p.60 / Chapter 3.1.1 --- Phenolic compounds --- p.60 / Chapter 3.1.2 --- Major classes of phenolic compounds --- p.60 / Chapter 3.1.3 --- Functional aspects of phenolic compounds --- p.61 / Chapter 3.1.3.1 --- Functions of phenolic compounds in plants --- p.61 / Chapter 3.1.3.2 --- Biological and pharmacological activities --- p.64 / Chapter 3.1.3.3 --- Food industry --- p.65 / Chapter 3.1.4 --- Polyphenolic compounds in brown algae --- p.66 / Chapter 3.1.5 --- Objectives --- p.68 / Chapter 3.2 --- Methods and Materials --- p.69 / Chapter 3.2.1 --- Extraction and isolation of antioxidant components from S siliquastrum --- p.69 / Chapter 3.2.2 --- Thin-Layer chromatography --- p.70 / Chapter 3.2.3 --- Antioxidant activity --- p.71 / Chapter 3.2.4 --- Determination of total phenolics --- p.71 / Chapter 3.2.5 --- Infrared spectra --- p.72 / Chapter 3.2.6 --- Ultra-violet and visible (UV-vis) spectrophotometry --- p.72 / Chapter 3.2.7 --- Statistics --- p.73 / Chapter 3.3 --- Results --- p.73 / Chapter 3.3.1 --- Identification of phenolic compounds from various solvent extracts of S. siliquastrum --- p.73 / Chapter 3.3.2 --- Isolation of dichloromethane fraction by liquid chromatography --- p.81 / Chapter 3.3.3 --- Phenolic content of isolated compounds --- p.86 / Chapter 3.3.4 --- IR and UV-vis spectra --- p.86 / Chapter 3.4 --- Discussion --- p.92 / Chapter 3.4.1 --- Antioxidative activities --- p.92 / Chapter 3.4.2 --- Relationship between phenolic contents and antioxidant activity --- p.95 / Chapter 3.4.3 --- Identification of antioxidant compounds --- p.97 / Chapter CHAPTER 4 --- Hypotensive Activities of Marine Algae in the Rat --- p.102 / Chapter 4.1 --- Introduction --- p.102 / Chapter 4.1.1 --- Basic principles of cardiovascular system --- p.102 / Chapter 4.1.2 --- Regulation of arterial pressure --- p.105 / Chapter 4.1.2.1 --- Short-term regulation of arterial pressure --- p.105 / Chapter 4.1.2.2 --- Long-term regulation of arterial pressure --- p.107 / Chapter 4.1.3 --- Hypertension --- p.108 / Chapter 4.1.3.1 --- Causes of hypertension --- p.109 / Chapter 4.1.3.2 --- Where do antihypertensive or hypotensive agents act? --- p.114 / Chapter 4.1.3.2.1 --- Sympathetic nervous system inhibitors --- p.115 / Chapter 4.1.3.2.2 --- Diuretics --- p.120 / Chapter 4.1.3.2.3 --- Vasodilators --- p.121 / Chapter 4.1.3.2.4 --- Calcium antagonist (Calcium channel blockers) --- p.121 / Chapter 4.1.3.2.5 --- Angiotensin-converting enzyme (ACE) inhibitors --- p.122 / Chapter 4.1.3.2.6 --- Antihypertensive drug combination --- p.122 / Chapter 4.1.4 --- The relationship between hypertension and free radicals --- p.123 / Chapter 4.1.5 --- Development of new antihypertensive agenrs --- p.124 / Chapter 4.2 --- Materials and methods --- p.125 / Chapter 4.2.1 --- Animal care --- p.125 / Chapter 4.2.2 --- Preparation of the blood pressure measurement in rats --- p.125 / Chapter 4.2.2.1 --- Effects of seaweed extracts on arterial blood pressure of rat --- p.126 / Chapter 4.2.2.1.1 --- Single-dose response curve --- p.126 / Chapter 4.2.2.1.2 --- Cumulative-dose response curve --- p.126 / Chapter 4.2.2.2 --- Pharmacological blocker studies --- p.128 / Chapter 4.2.3 --- Statistics --- p.131 / Chapter 4.3 --- Results --- p.131 / Chapter 4.3.1 --- Hypotensive effects of marine algal extracts --- p.131 / Chapter 4.3.2 --- Effects of pharmacological blockers on MAP --- p.135 / Chapter 4.4 --- Discussion --- p.150 / Chapter 4.4.1 --- Hypotensive effects of the marine algal extracts --- p.150 / Chapter 4.4.2 --- Pharmacological action of marine algal extracts --- p.152 / Chapter CHAPTER 5 --- Conclusion --- p.160 / REFERENCES --- p.165 / RELATED PUBLICATIONS --- p.177

Fung Yin Lee, Annie. / "January 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 132-146). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Conclusions. Regardless the method the information on benefit was provided, the maximum amount of money which people are willing to pay for antihypertensive varied substantially. Using relative risk to present the benefit would distort the viewpoint of the public regarding the importance of drug treatment. Residents were much more conservative in antihypertensive drugs than physicians. Most hypertensive patients in China would probably not accept drugs treatment for primary prevention if they are adequately informed. Rural residents were on average, less willing to take antihypertensive drugs than urban residents. Residents had a poor perception of their cardiovascular risk due to hypertension and the benefit of drug treatment. Most physicians in our study did not have good knowledge on overall risk approach and Chinese national guidelines. They had also very poor knowledge and skills related to evidence based medicine. (Abstract shortened by UMI.) / Objective. To assess the maximum amount of money residents are willing to pay for antihypertensive drugs given the actual benefit of treatment. To decide the minimum benefit (expressed in NNT) above which people are willing to pay for antihypertensive drugs at the current cost. To determine the minimum risk of cardiovascular disease (CVD) above which people would be willing to pay for antihypertensive at the current cost. To assess whether reporting of study results by using relative risk reduction and NNT affects people's willingness to pay for and physicians' willingness to prescribe antihypertensive drugs. To evaluate patients' and physicians' perception of perceived CVD risk due to hypertension and benefit of treatment. To assess knowledge, attitude and perception of the public and physicians regarding antihypertensive drugs and physicians' knowledge and skills on evidence based medicine. / Results. The response rate for residents was 91%. 95% of respondents reported that they would be willing to take antihypertensive drugs if they found to have high blood pressure. The majority of residents did not know the ultimate goal of blood pressure lowering was to reduce the risk of CVD. 91% said that they had not enough knowledge and information to make drug-taking decisions. The perceived 5-year baseline risk in the absence of treatment, absolute risk reduction and relative risk reduction was 70%, 40% and 60% respectively. Rural residents tended to over-rate their risk and benefit more than urban residents. Overall, 2%, 3% and 47% of residents were not willing to pay anything for antihypertensive drugs when information on benefit of treatment was described in general, with RRR and with NNT respectively. The median cost the residents were willing to pay was $500, $700 and $100 respectively for responding three ways of describing the benefit. / The response rate for physicians was 95%. The perceived 5-year baseline risk, absolute risk reduction and relative risk reduction was 40%, 20% and 39% respectively. Internists tended to give a slightly higher estimate of the 5-year risk (40% vs 30%, p&lt;0.05) and of the RRR (39 vs 29, p&lt;0.05). Overall, physicians were more likely to prescribe antihypertensive drugs when the benefit information was expressed in RRR than when it was expressed in NNT (p&lt;0.001). The median minimum NNT and the 5-year CVD risk above which physicians are willing to prescribe was 200 and 1.5% respectively. / Wang Weizhong. / "November 2006." / Adviser: Jinling Tang. / Source: Dissertation Abstracts International, Volume: 68-08, Section: B, page: 5119. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 105-114) / 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. / Electronic reproduction. Ann Arbor, MI : ProQuest dissertations and theses, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.