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Chan Wai-Hon. / "September 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 137-156). / 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.

Tingan Chen. / "March 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 100-142). / 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.

A xerostomia é um efeito adverso comum e frequentemente irreversível decorrente da radioterapia de neoplasias malignas da região de cabeça e pescoço, afetando, sobremaneira, a qualidade de vida dos pacientes. Diferentes métodos para solucionar tal problema são propostos, de resultados, todavia questionáveis. Este estudo avaliou a eficácia clínica da acupuntura como método de tratamento preventivo e curativo de tais condições. Os pacientes foram distribuídos, aleatoriamente, em três grupos: grupo preventivo, constituído de 12 indivíduos, sem queixa de secura bucal, tratados com 12 a 16 sessões de acupuntura, antes e durante a radioterapia; grupo curativo, constituído de 12 indivíduos, diagnosticados, clinicamente, com xerostomia severa, tratados com 12 aplicações de acupuntura após concluído o tratamento oncológico, e grupo controle, formado pelos mesmos indivíduos do grupo curativo no momento da primeira consulta, precedente à terapêutica com acupuntura. O tratamento foi conduzido de acordo com os princípios da medicina tradicional chinesa e medicina ocidental ortodoxa, realizado de forma padronizada para todos os pacientes, duas vezes por semana, por um período de 20 minutos cada sessão. A avaliação da eficácia terapêutica fundamentou-se na mensuração da xerostomia, conduzida sob duas formas: objetiva, através da sialometria, com o registro quantitativo dos índices de fluxo salivar em repouso e estimulado (IFSR e IFSE), e subjetiva, por intermédio dos questionários Xerostomia Inventory (XI) modificado, Escala Visual Analógica (EVA) e Treatment Emergent Symptom Scale (TESS), mensurando o grau de severidade dos sintomas. Os resultados obtidos no grupo preventivo foram estatisticamente significativos quanto as avaliações objetivas e subjetivas, evidenciados por índices de fluxo salivar mais elevados tanto para o IFSR (P<0.001) como para o IFSE (P<0.001) e pela menor intensidade dos sintomas (P<0.001), quando comparadas ao controle. Para o grupo curativo, resultados também significativos foram constatados em ambas as avaliações, demonstrados pelo aumento dos IFSR (P<0.05) e IFSE (P<0.05) e redução da sintomatologia (P<0.05), comparados aos valores iniciais. Constatamos também que houve efeito de grupo e os pacientes que se beneficiaram do método preventivo, obtiveram médias estatisticamente mais significativas (P<0.001), para ambas as respostas clínicas, objetivas e subjetivas. É lícito concluir que a acupuntura mostrou-se um importante método de tratamento de xerostomia decorrente da radioterapia, visto ter alcançado uma confiabilidade significativa de eficácia, que nos faz indicá-la e sugerir a disponibilização do método preventivo nos centros de tratamento. / Xerostomia is a common and usually irreversible radiotherapy side effect in patients with head and neck cancer, affecting the patients’ quality of life. Many attempts have been suggested to manage this condition nevertheless of questionable results. This study evaluated the acupuncture treatment efficacy as a preventive and curative method for radiation-induced xerostomia. The patients were randomly assigned in three groups: preventive, composed of 12 individuals, without complaints of dry mouth, treated with 12-16 acupuncture sessions, before and concomitant radiotherapy; curative, composed by 12 individuals, diagnosed with severe xerostomia, treated with 12 acupuncture sessions after radiation therapy, and control, comprised of the curative’s group patients at the moment of the first visit, preceding this therapy. Acupuncture treatment, according to traditional Chinese medicine and occidental orthodox medicine concepts was performed twice a week, lasting 20 minutes each session, following standardize techniques for all patients. Acupuncture efficacy was evaluated, based upon objective and subjective methods of xerostomia measurements, performed by sialometry, measuring the resting and stimulated salivary flow rates (RSFR and SSFR), and by means of questionnaires such as Xerostomia Inventory (XI) modified, Visual Analog Scale (VAS) and Treatment Emergent Symptom Scale (TESS), which evaluated referred symptoms. Results obtained in preventive group, evidenced RSFR (P<0.001) and SSFR (P<0.001) significantly increased, and improvement of symptoms (P<0.001), compared with control. Within curative group, after acupuncture treatment, the results showed statistically significant improved for both resting and stimulated salivary flow rates (P<0.05) and reduces of referred symptoms (P<0.05). There were statistically differences between groups, being the patients in preventive group those who evidenced the most significant improved of values (P<0.001) for objective and subjective evaluations. We concluded that acupuncture plays an important role in xerostomia’s treatment, as shown by the results, reaching a significant confiability of efficacy, indicating and suggesting the preventive method at oncology centers.

Ng Kenway. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 169-189). / Abstracts in English and Chinese ; questionnaire also in Chinese. / ABSTRACT --- p.I / 摘要 --- p.IV / ACKNOWLEDGEMENT --- p.V / TABLE OF CONTENTS --- p.VII / ABBREVIATION --- p.XI / LIST OF TABLES --- p.XIII / LIST OF FIGURES --- p.XIV / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter CHAPTER 2 --- LITERATURE REVIEW --- p.4 / Chapter 2.1 --- SIDE EFFECTS OF RADIATION THERAPY IN HEAD & NECK CACNER PATIENTS --- p.6 / Chapter 2.2 --- NUTRITIONAL ALTERATIONS IN CANCER PATIENTS --- p.9 / Chapter 2.3 --- FACTORS INFLUENCING ALTERATION IN CALORIE INTAKE IN CANCER PATIENTS --- p.12 / Chapter 2.3.1 --- Evidence for impaired calorie intake in cancer patients --- p.12 / Chapter 2.3.2 --- Anorexia --- p.13 / Chapter 2.3.2.1 --- Mucositis of upper food passage --- p.13 / Chapter 2.3.2.2 --- "Change in saliva and taste, food aversions" --- p.14 / Chapter 2.3.2.3 --- Psychological and emotional factors --- p.14 / Chapter 2.3.2.4 --- Cytokines --- p.15 / Chapter 2.4 --- FACTORS INFLUENCING ENERGY EXPENDITURE IN CANCER PATIETNS --- p.17 / Chapter 2.4.1 --- Introduction --- p.17 / Chapter 2.4.2 --- Components of total energy expenditure --- p.22 / Chapter 2.4.2.1 --- Measurement of Basal metabolic rate --- p.22 / Chapter 2.4.2.2 --- Energy cost of physical activity --- p.25 / Chapter 2.4.2.3 --- Thermic effect of food (TEF) --- p.26 / Chapter 2.5 --- METHODS FOR NUTRITIONAL ASSESSMENT --- p.27 / Chapter 2.5.1 --- Body weight and body composition --- p.27 / Chapter 2.5.2 --- Dietary intake --- p.30 / Chapter 2.6 --- METHODS FOR ENERGY EXPENDITURE MEASUREMENT --- p.35 / Chapter 2.7 --- CYTOKINES AND LEPTIN CHANGES IN CANCER PATIENTS --- p.40 / Chapter 2.7.1 --- Cytokines --- p.40 / Chapter 2.7.1.1 --- Tumor necrosis factor --- p.40 / Chapter 2.7.1.2 --- Interleukin 1 and interleukin 6 --- p.44 / Chapter 2.7.2 --- Leptin --- p.45 / Chapter 2.8 --- THE IMPACT OF MALNUTRITION ON CANCER SURVIVAL --- p.49 / Chapter CHAPTER 3 --- OBJECTIVES OF STUDY --- p.53 / Chapter CHAPTER 4 --- METHODS --- p.55 / Chapter 4.1 --- RETROSPECTIVE STUDY --- p.56 / Chapter 4.1.1 --- Patients --- p.56 / Chapter 4.1.2 --- Cancer staging --- p.56 / Chapter 4.1.3 --- Cancer treatment --- p.57 / Chapter 4.1.4 --- Outcome endpoints --- p.57 / Chapter 4.1.5 --- Determinants --- p.58 / Chapter 4.1.6 --- Statistical analysis --- p.58 / Chapter 4.2 --- PROSPECTIVE STUDY --- p.59 / Chapter 4.2.1 --- "Patients, oncological treatment, and assessment time points" --- p.59 / Chapter 4.2.2 --- Assessment of nutritional intake by food record --- p.60 / Chapter 4.2.3 --- Assessment of radiotherapy-induced symptoms --- p.61 / Chapter 4.2.4 --- Assessment of Basal metabolic rate --- p.62 / Chapter 4.2.5 --- Assessment of total energy expenditure and energy balance --- p.63 / Chapter 4.2.6 --- Assessment of body composition --- p.65 / Chapter 4.2.7 --- Measurement of cytokines --- p.68 / Chapter 4.2.7.1 --- Serum TNF-α --- p.69 / Chapter 4.2.7.2 --- Serum Human Leptin --- p.72 / Chapter CHAPTER 5 --- RESULTS --- p.80 / Chapter 5.1 --- RETROSPECTIVE STUDY --- p.81 / Chapter 5.1.1 --- The 5-year profile of bodyweight change during and after the end of radiotherapy --- p.81 / Chapter 5.1.2 --- Analysis on relation between weight loss and survival --- p.82 / Chapter 5.1.2.1 --- Patient and cancer stage --- p.82 / Chapter 5.1.2.2 --- Percentage of patients with weight loss at end of radiotherapy --- p.82 / Chapter 5.1.2.3 --- Cancer treatment outcome --- p.82 / Chapter 5.1.2.4 --- Univariate analysis --- p.82 / Chapter 5.1.2.5 --- Multivariate analysis --- p.83 / Chapter 5.2 --- PROSPECTIVE STUDY --- p.84 / Chapter 5.2.1 --- The profile of nutritional measurements during radiotherapy --- p.84 / Chapter 5.2.1.1 --- Bodyweight and body composition before and during RT --- p.84 / Chapter 5.2.1.2 --- Calorie intake before and during RT --- p.85 / Chapter 5.2.1.3 --- Energy expenditure before and during RT --- p.86 / Chapter 5.2.1.4 --- Energy balance before and during RT --- p.88 / Chapter 5.2.2 --- The profile of nutritional measurements during the 6-month period after radiotherapy --- p.88 / Chapter 5.2.2.1 --- Body weight and body composition during the 6 months after radiotherpay --- p.88 / Chapter 5.2.2.2 --- Calorie intake during the 6 months after radiotherapy --- p.90 / Chapter 5.2.2.3 --- Energy expenditure during the 6 months after radiotherapy --- p.91 / Chapter 5.2.2.4 --- Energy balance during the 6 months after radiotherapy --- p.92 / Chapter 5.2.3 --- Radiotherapy-induced Symptoms --- p.92 / Chapter 5.2.3.1 --- Profile of symptoms after RT --- p.92 / Chapter 5.2.3.2 --- Detailed profile of symptoms during RT --- p.95 / Chapter 5.2.4 --- The profile of cytokines during and after completion of RT --- p.95 / Chapter 5.2.4.1 --- SerumTNF-α --- p.96 / Chapter 5.2.5.2 --- Serum leptin --- p.96 / Chapter CHAPTER 6 --- DISCUSSION --- p.144 / Chapter 6.1 --- RETROSPECTIVE STUDY --- p.145 / Chapter 6.2 --- PROSPECTIVE STUDY --- p.147 / Chapter 6.2.1 --- The magnitude of the problem --- p.147 / Chapter 6.2.2 --- The potential determinants of weight loss --- p.147 / Chapter 6.2 3 --- Is weight loss due to the cancer or due to its treatment? --- p.148 / Chapter 6.2.4 --- "Is the weight loss influenced by pre-treatment factors, i. e. anthropometrical data?" --- p.148 / Chapter 6.2.5 --- "Is the pattern weight loss compatible with the model of calorie-protein malnutrition, similar to a starvation state?" --- p.149 / Chapter 6.2.6 --- Is the weight loss due to increased energy expenditure? --- p.150 / Chapter 6.2.7 --- Is the weight loss due to reduced calorie intake? --- p.151 / Chapter 6.2.8 --- Is weight loss during radiotherapy due to negative energy balance? --- p.151 / Chapter 6.2.9 --- What causes reduced calorie intake: Are radiotherapy-induced symptoms contributive? --- p.152 / Chapter 6.2.10 --- What are the observations on and implications of cytokine changes? --- p.155 / Chapter 6.2.11 --- What determines the recovery of body weight during 6 months after end of radiotherapy? --- p.158 / Chapter 6.2.12 --- Is the weight loss in the post RT recovery period due to negative energy balance? --- p.159 / Chapter 6.2.13 --- What are the implications on nutritional intervention? --- p.159 / Chapter 6.2.14 --- Limitations and future studies --- p.164 / Chapter CHAPTER 7 --- CONCLUSIONS --- p.166 / REFERENCES --- p.169 / APPENDIX 1 CONSENT FORM I (IN ENGLISH) --- p.190 / APPENDIX 2 CONSENT FORM I (IN CHINESE) --- p.193 / APPENDIX 3 CONSENT FORM II (IN ENGLISH) --- p.196 / APPENDIX 4 CONSENT FORM II (IN CHINESE) --- p.199 / APPENDIX 5 3-DAY DIET RECORD --- p.202 / APPENDIX 6 24-HOUR DIETARY RECALL --- p.206 / APPENDIX 7 SUBJECTIVE NUTRITIONAL ASSESSMENT --- p.208 / APPENDIX 8 PHYSICAL ACTIVITY QUESTIONNAIRE --- p.210 / APPENDIX 9 BONE SCAN REPORT --- p.215

Tang Wan-yee. / "July 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 192-212). / 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.

Cheung Mei-chun. / "January 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (p. 66-94). / 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.

by Jing Xian Li. / Thesis (Ph.D.)--Chinese university of Hong Kong, 1998. / Includes bibliographical references (p. 137-151). / 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.

Yang, Chao. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 137-146). / Abstracts in English and Chinese. / Thesis Committee --- p.i / Acknowledgements --- p.ii / Contents --- p.iii / Declaration --- p.vii / Abstract --- p.viii / 摘要 --- p.xi / Abbreviations --- p.xiii / Chapter CHAPTER ONE: --- INTRODUCTION / Chapter 1.1 --- Occurrence and Structure of Phytosterols in Plants --- p.P.1 / Chapter 1.2 --- Biological Effects of Phytosterols / Chapter 1.2.1 --- Cholesterol-lowering Effect of Phytosterols --- p.P.3 / Chapter 1.2.2 --- Anti-cancer Effect of Phytosterols --- p.P.5 / Chapter 1.2.3 --- Anti-proliferative Effect of Phytosterols --- p.P.5 / Chapter 1.3 --- Intake and Absorption of Phytosterols in Human Beings --- p.P.6 / Chapter 1.4 --- Occurrence and Physiological Levels of Phytosterol Oxidation Products (POPs) / Chapter 1.4.1 --- Occurrence of POPs --- p.P.8 / Chapter 1.4.2 --- Physiological Levels of POPs --- p.P.8 / Chapter 1.5 --- Endothelium and the Vascular Tone / Chapter 1.5.1 --- Role of Endothelium in the Control of Vascular Tone --- p.P.11 / Chapter 1.5.2 --- "Endothelial Dysfunction, Cholesterol Oxidation Products (COPs) and Phytosterol Oxidation Products (POPs)" --- p.P.12 / Chapter 1.6 --- Calcium Homeostasis in the Vascular Smooth Muscle Cells (VSMCs) / Chapter 1.6.1 --- Modes of Ca2+ Entry in VSMCs --- p.P.15 / Chapter 1.6.2 --- Modes of Ca2+ Efflux in VSMCs --- p.P.18 / Chapter 1.7 --- Objectives of the Study --- p.P.19 / Chapter CHAPTER TWO: --- β-SITOSTEROL OXIDATION PRODUCTS ATTENUATE VASORELAXATION BY INCREASING REACTIVE OXYGEN SPECIES AND CYCLOOXYGENASE-2 / Chapter 2.1 --- Introduction --- p.P.21 / Chapter 2.2 --- Materials and Methods / Chapter 2.2.1 --- Preparation of SOPs --- p.P.24 / Chapter 2.2.2 --- Gas Chromatography -mass Spectrometry (GC-MS) Identification of SOPs --- p.P.24 / Chapter 2.2.3 --- Analysis of SOPs --- p.P.25 / Chapter 2.2.4 --- Vessel Preparation --- p.P.25 / Chapter 2.2.5 --- Isometric Force Measurement --- p.P.26 / Chapter 2.2.6 --- Western Blotting --- p.P.27 / Chapter 2.2.7 --- Primary Culture of Rat Aortic Endothelial Cell --- p.P.28 / Chapter 2.2.8 --- Measurement of SOPs-induced Intracellular Oxidative Stress --- p.P.29 / Chapter 2.2.9 --- Drugs --- p.P.30 / Chapter 2.2.10 --- Data Analysis --- p.P.30 / Chapter 2.3 --- Results / Chapter 2.3.1 --- GC-MS Identification of SOPs --- p.P.32 / Chapter 2.3.2 --- Analysis of SOPs --- p.P.34 / Chapter 2.3.3 --- SOPs But Not β-Sitosterol Impaired ACh- and A23187-induced relaxations --- p.P.36 / Chapter 2.3.4 --- Inhibition of COX Pathway Reversed SOPs-induced Impairment in Relaxation --- p.P.39 / Chapter 2.3.5 --- SOPs Elevated Endothelial COX-2 Expression --- p.P.42 / Chapter 2.3.6 --- SOPs Increased COX-2 Expression via An Oxidative Stress-sensitive Pathway --- p.P.45 / Chapter 2.4 --- Discussion --- p.P.52 / Chapter 2.5 --- Conclusion --- p.P.56 / Chapter CHAPTER THREE: --- β-SITOSTEROL OXIDATION PRODUCTS POSSESS POTENTIAL VOCC BLOCKING EFFECT IN VSMCs / Chapter 3.1 --- Introduction / Chapter 3.1.1 --- 2+ Modes of Ca Entry and Efflux in Vascular Smooth Muscle Cells (VSMCs) --- p.P.57 / Chapter 3.1.2 --- Effect of Cholesterol and COPs on VSMCs --- p.P.57 / Chapter 3.2 --- Methodology and Materials / Chapter 3.2.1 --- Vessel Preparation --- p.P.59 / Chapter 3.2.2 --- Isometric Force Measurement iv --- p.P.59 / Chapter 3.2.3 --- Drugs --- p.P.60 / Chapter 3.2.4 --- Data Analysis --- p.P.61 / Chapter 3.3 --- Results / Chapter 3.3.1 --- SOPs but not β-Sitosterol Induced Relaxation in 60 mM K+ -preconstricted Endothelium-denuded Aorta --- p.P.62 / Chapter 3.3.2 --- Both SOPs and β-Sitosterol did not Relax U46619-preconstricted Endothelium-denuded Aorta --- p.P.64 / Chapter 3.3.3 --- Both SOPs and β-Sitosterol did not Relax PDA -preconstricted Endothelium-denuded Aorta --- p.P.66 / Chapter 3.3.4 --- SOPs Attenuated 60 mM K+-induced Contraction --- p.P.68 / Chapter 3.3.5 --- SOPs Attenuated Phenylephrine-induced Contraction --- p.P.70 / Chapter 3.3.6 --- Effect of SOPs on Concentration-dependent Responses to U46619 --- p.P.72 / Chapter 3.3.7 --- Preincubation with Bay K 8644 Abolished SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.74 / Chapter 3.3.8 --- Preincubation with Thapsigargin did not Affect SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.76 / Chapter 3.3.9 --- Preincubation with Ouabain did not Affect SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.78 / Chapter 3.3.10 --- Preincubation with Nickel Potentiated SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.80 / Chapter 3.4 --- Discussion --- p.P.84 / Chapter 3.5 --- Conclusion and Future Work --- p.P.88 / Chapter CHAPTER FOUR: --- INVOLEMENT OF NITRIC OXIDE IN THE PROTECTIVE EFFECTS OF PHYTOSTEROLS AGAINST HOMOCYSTEINE-INDUCED IMPAIRMENT OF ENDOTHELIUM-DEPENDENT RELAXATIONS OF RAT AORTA / Chapter 4.1 --- Introduction --- p.P.89 / Chapter 4.2 --- Materials and Method / Chapter 4.2.1 --- Vessel Preparation --- p.P.93 / Chapter 4.2.2 --- Isometric Force Measurement --- p.P.93 / Chapter 4.2.3 --- Western Blotting --- p.P.94 / Chapter 4.2.4 --- "1,1 -diphenyl-2-picrylhydrazyl (DPPH) Radical Scavenging Capacity" --- p.P.96 / Chapter 4.2.5 --- Primary Culture of Rat Aortic Endothelial Cells V --- p.P.96 / Chapter 4.2.6 --- Measurement Intracellular Oxidative Stress --- p.P.97 / Chapter 4.2.7 --- Nitric Oxide (NO) Measurement --- p.P.97 / Chapter 4.2.8 --- Drugs --- p.P.98 / Chapter 4.2.9 --- Data Analysis --- p.P.99 / Chapter 4.3 --- Results / Chapter 4.3.1 --- Impairment of Endothelium-dependent Relaxation by HC was Reversed by ROS Scavenger --- p.P.100 / Chapter 4.3.2 --- Brassicasterol Reversed HC-induced Endothelial Dysfunction In a Dose-dependent Manner --- p.P.102 / Chapter 4.3.3 --- β-Sitosterol and Stigmasterol Reversed HC-induced Endothelial Dysfunction --- p.P.104 / Chapter 4.3.4 --- Effects of β-Sitosterol Oxidation Products (SOPs) on HC-induced Endothelial Dysfunction --- p.P.106 / Chapter 4.3.5 --- Effects of Brassicasterol and β-Sitosterol on H2O2-induced Impairment of Endothelium-dependent Relaxation --- p.P.108 / Chapter 4.3.6 --- Phytosterols did not Directly Scavenge Free Radicals --- p.P.110 / Chapter 4.3.7 --- "HC and Brassicasterol did not Affect the Expression of SOD-1, SOD-2, eNOS, COX-1 and COX-2 in Aorta" --- p.P.112 / Chapter 4.3.8 --- HC Increased ROS Production in Primary Rat Aortic Endotelial Cells --- p.P.116 / Chapter 4.3.9 --- Brassicasterol did not Reverse the ROS Production by HC treatment In the Endothelial Cells --- p.P.120 / Chapter 4.3.10 --- Effect of L-NAME on Reversing the Effect of Brassicasterol on ACh-induced Relaxation --- p.P.123 / Chapter 4.3.11 --- Brassicasterol Reversed the Inhibitory Effect of HC on ACh-induced NO Production in Endothelial Cells --- p.P.125 / Chapter 4.4 --- Discussion --- p.P.128 / Chapter 4.5 --- Conclusion and Future Work --- p.P.132 / Chapter CHAPTER FIVE: --- CONCLUSIONS AND FUTURE WORK --- p.P.134 / Chapter CHAPTER SIX: --- REFERENCES --- p.P.137

Cheung Kwok Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 123-136). / ABSTRACT (English) --- p.i / ACKNOWLEDGMENTS --- p.1 / LIST OF FIGURES --- p.3 / LIST OF TABLES --- p.5 / LIST OF ABBREVIATIONS --- p.7 / Chapter I. --- INTRODUCTION AND OBJECTIVES --- p.8 / Chapter II. --- LITERATURE REVIEWS --- p.11 / Chapter II.A. --- Maternal Serum Alpha-fetoprotein Screeningin Singleton Pregnancies --- p.11 / Chapter II.A.1. --- Physiology of Alpha-fetoprotein --- p.12 / Chapter II.A.2. --- Historical Background of Screening by Alpha- fetoprotein --- p.12 / Chapter II.A.3. --- Factors that Influence Maternal Serum Alpha- fetoprotein Concentration --- p.13 / Chapter ILA.4. --- Elevated Maternal Serum Alpha-fetoprotein Concentration and Adverse Pregnancy Outcomes and Complications --- p.14 / Chapter II.A.4.a. --- Low Birth Weight --- p.16 / Chapter II.A.4.b. --- Fetal Loss --- p.17 / Chapter II.A.4.c. --- Pregnancy Induced Hypertension --- p.18 / Chapter II.B. --- Maternal Serum Human Chorionic Gonadotrophin Screening in Singleton Pregnancies --- p.18 / Chapter II.B.1. --- Physiology of Human Chorionic Gonadotrophin --- p.18 / Chapter II.B.2. --- Historical Background of Screening by Human Chorionic Gonadotrophin --- p.20 / Chapter II.B.3. --- Factors that Influence Maternal Serum Human Chorionic Gonadotrophin --- p.21 / Chapter II.B.4. --- Elevated Maternal Serum Human Chorionic Gonadotrophin Concentration and Pregnancy Complications --- p.21 / Chapter II.B.5. --- Maternal Serum AFP and hCG Concentrations and Adverse Outcomes or Complications in Twin Pregnancies --- p.23 / Chapter II.C. --- Mechanism for the Association between Adverse Outcomes and Elevated Maternal Serum Alpha- fetoprotein and Human Chorionic Gonadotrophin --- p.25 / Chapter III. --- METHODS --- p.28 / Chapter III.A. --- Study Population --- p.28 / Chapter III.B. --- Sample Collection and Analysis --- p.29 / Chapter III.C. --- Clinical Information --- p.30 / Chapter III.D. --- Microparticle Enzyme Immunoassay --- p.30 / Chapter III.D.1. --- Principles --- p.30 / Chapter III.D.1.a. --- Reaction Process --- p.31 / Chapter III.D.1.b. --- MEIA Assembly --- p.33 / Chapter III.D.1.c. --- Operation --- p.34 / Chapter III.D.2. --- AFP Assay --- p.34 / Chapter III.D.2.a. --- AFP Reagents --- p.34 / Chapter III.D.2.b. --- Sample Dilution --- p.36 / Chapter III.D.3. --- Total p-hCG Assay --- p.37 / Chapter III.D.3.a. --- Total p-hCG Reagents --- p.37 / Chapter III.D.3.b. --- Sample Dilution --- p.39 / Chapter III.D.4. --- Intra- and Inter-assay Variation --- p.39 / Chapter III.E. --- Data Handling --- p.42 / Chapter III.F. --- Statistical Analysis --- p.42 / Chapter III.F.1. --- Calculations of Median Values of Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin Concentrations --- p.42 / Chapter III.F.2. --- Analysis for Adverse Outcomes or Complications --- p.43 / Chapter III.F.3. --- Adjustment of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Gestational Age and Maternal Weight --- p.46 / Chapter IV. --- RESULTS --- p.48 / Chapter IV.A. --- Median Values of Maternal Serum Alpha-fetoprotein Human Chorionic Gonadotrophin --- p.48 / Chapter IV.B. --- Prediction of Adverse Outcomes by Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin --- p.60 / Chapter IV.B. l. --- Preterm Delivery --- p.60 / Chapter IV.B.2. --- Spontaneous Preterm Delivery --- p.64 / Chapter IV.B.3. --- Premature Delivery --- p.68 / Chapter IV.B.4. --- Spontaneous Premature Delivery --- p.68 / Chapter IV.B.5. --- Other Outcomes or Complications --- p.72 / Chapter IV.B.6. --- Single Predictor for Most Adverse Outcomes --- p.74 / Chapter IV.C. --- Adjustment of Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin for Maternal Weight and Gestational Age --- p.75 / Chapter IV.C.1. --- Distribution of Alpha-fetoprotein and Human Chorionic Gonadotrophin during Mid-trimester --- p.76 / Chapter IV.C.2. --- Adjustment of Alpha-fetoprotein for Maternal Weight and Gestational Age --- p.79 / Chapter IV.C.3. --- Adjustment of Human Chorionic Gonadotrophin for Maternal Weight and Gestational Age --- p.80 / Chapter IV.D. --- Predictiveness of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Adverse Outcomes after Adjusted for Maternal Weight and Gestational Age --- p.83 / Chapter IV.D.l. --- Preterm Delivery --- p.86 / Chapter IV.D.2. --- Spontaneous Preterm Delivery --- p.86 / Chapter IV.D.3. --- Premature Delivery --- p.92 / Chapter IV.D.4. --- Spontaneous Premature Delivery --- p.92 / Chapter IV.D.5. --- Other Adverse Outcomes or Complications --- p.98 / Chapter IV.D.6. --- Single Predictor for Most Adverse Outcomes --- p.98 / Chapter V. --- DISCUSSIONS --- p.100 / Chapter V.A. --- Median Values of Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadtrophin --- p.100 / Chapter V.B. --- Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin Screening for Adverse Outcomes --- p.103 / Chapter V.C. --- Adjustment of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Maternal Weight and Gestational Age --- p.109 / Chapter V.D. --- Predictiveness of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Adverse Outcomes after Maternal Weight and Gestational Age Adjustment --- p.112 / Chapter V.E. --- Conclusions --- p.113 / Chapter V.F. --- Future Directions --- p.116 / APPENDIX 1 DATA BASE OF CLINICAL INFORMATION --- p.117 / APPENDIX 2 SEVERITY AND CLASSIFICATION OF PREGNANCY INDUCED HYPERTENSION --- p.122 / REFERENCES --- p.123