Wang Ya-Ping. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 152-161). / 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.

Fan Boli. / "January 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 219-248). / 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.

Hypoxia is a common patho-physiological phenomenon in many types of diseases, including tumors, myocardial infarction and cerebral ischemia. It is believed that hypoxia not only affects the cellular regulation pathways, but also interferes genome, transcriptome and proteome inside tumor, eventually enhances tumor development by increasing malignancy and metastatic potential, induction of resistance towards radiotherapy and chemotherapy, activation of angiogenic mechanism, etc. One of the major biological events for hypoxia is induction of apoptosis, which is believed to provide a selective pressure for tumor progression. However, the mechanism of hypoxia induced apoptosis is not well established. In the present study, the molecular mechanism of hypoxia induced apoptosis was investigated and was found to be different in human squamous carcinoma A431 cells and human hepatocellular carcinoma HepG2 cells. In HepG2 cells, the conventional intrinsic apoptotic pathway that involved the activation of caspase-9 and -3 was found to be triggered by hypoxia through a newly identified p53 - Bnip-3 shunt. On the other hand, caspase-4 and -10 were found to be activated under hypoxia and may be related to hypoxia induced DNA fragmentation in A431 cells. Reoxygenation prior to hypoxia is the event after blood reperfusion in tumor vasculature. It is demonstrated in this study that reoxygenation is a distinctive stress from hypoxia, and it is very likely to be induced by reactive oxygen species. Apart from apoptosis, the mechanism for the development of drug resistance after hypoxia is also not yet clearly identified. In this study, resistance towards several common chemotherapeutic drugs after cells were subjected to hypoxia/reoxygenation cycles were demonstrated. Among them, the possible role of the genes related to methotrexate and cisplatin resistance were also investigated. / Ho Yiu Fung. / "August 2006." / Adviser: Tim-Tak Kwok. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1393. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 159-176). / 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. / Abstracts in English and Chinese. / School code: 1307.

Yim, Po Yee Annie. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 166-219). / Abstracts in English and Chinese. / Acknowledgements --- p.ii / Abstract --- p.iv / Abbreviations --- p.xi / Table of Content --- p.xiii / List of Figures --- p.xviii / List of Tables --- p.xxi / Major Conference Presentations --- p.xxiii / Publication in Preparation --- p.xxvi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General Overview of Adolescent Idiopathic Scoliosis (AIS) --- p.2 / Chapter 1.2 --- Natural History --- p.3 / Chapter 1.3 --- Current Treatments --- p.5 / Chapter 1.3.1 --- Non-operative Treatments --- p.5 / Chapter 1.3.2 --- Surgical Treatments --- p.6 / Chapter 1.4 --- Current Hypothesis on the Etiology of AIS --- p.8 / Chapter 1.4.1 --- Genetic Factors --- p.8 / Chapter 1.4.2 --- Neuromuscular Impairment --- p.10 / Chapter 1.4.3 --- Abnormalities in Skeletal Development --- p.11 / Chapter 1.4.4 --- Metabolic Dysfunction --- p.12 / Chapter 1.4.4.1 --- Lower Bone Mineral Density --- p.12 / Chapter 1.4.4.2 --- Delayed Sexual Maturity --- p.14 / Chapter 1.4.4.3 --- Hormonal Dysfunction --- p.14 / Chapter 1.5 --- Skeletal arid Spinal Growth in AIS --- p.16 / Chapter 1.5.1 --- Abnormal Growth during Puberty --- p.16 / Chapter 1.5.2 --- Growth Pattern --- p.17 / Chapter 1.5.3 --- Disproportional Growth in AIS --- p.18 / Chapter 1.5.4 --- Asymmetric Growth --- p.20 / Chapter 1.6 --- Melatonin and its Receptor --- p.22 / Chapter 1.6.1 --- Introduction --- p.22 / Chapter 1.6.2 --- Melatonin Receptor --- p.24 / Chapter 1.6.3 --- Melatonin's Role in t h e Skeletal System --- p.25 / Chapter 1.6.4 --- Melatonin-Deficient Scoliotic Animal Model --- p.27 / Chapter 1.6.5 --- Melatonin and AIS --- p.29 / Chapter 1.6.5.1 --- Melatonin Level in AIS --- p.30 / Chapter 1.6.5.2 --- Melatonin Receptor in AIS --- p.30 / Chapter Chapter 2 --- Hypothesis and Objectives --- p.39 / Chapter 2.1 --- Study Hypothesis --- p.40 / Chapter 2.2 --- Objectives --- p.41 / Chapter Chapter 3 --- Abnormal skeletal growth patterns in adolescent idiopathic scoliosis - A longitudinal study till skeletal maturity --- p.42 / Chapter 3.1 --- Introduction --- p.43 / Chapter 3.2 --- Methodology --- p.44 / Chapter 3.2.1 --- Recruitments of Subjects --- p.44 / Chapter 3.2.1.1 --- Patients with AIS --- p.44 / Chapter 3.2.1.2 --- Normal Controls --- p.44 / Chapter 3.2.1.3 --- Patients Consents --- p.45 / Chapter 3.2.2 --- Anthropometric Measurements --- p.45 / Chapter 3.2.3 --- Data Analysis --- p.46 / Chapter 3.2.3.1 --- Cross-sectional Study --- p.46 / Chapter 3.2.3.2 --- Longitudinal Study --- p.46 / Chapter 3.3 --- Results --- p.47 / Chapter 3.3.1 --- Cross-sectional Study of Anthropometric Measurements --- p.47 / Chapter 3.3.2 --- Longitudinal Study of Anthropometric Measurements --- p.48 / Chapter 3.3.2.1 --- Comparison Adjusted for Chronological Age --- p.49 / Chapter 3.3.2.2 --- Comparison Along Year Since Menarche (YSM) --- p.49 / Chapter 3.4 --- Discussion --- p.51 / Chapter Chapter 4 --- Establishment of a Melatonin-Deficierit Induced Scoliotic Model with Locally Bred Chicken --- p.63 / Chapter 4.1 --- Introduction --- p.64 / Chapter 4.2 --- Methodology --- p.67 / Chapter 4.2.1 --- Animals --- p.67 / Chapter 4.2.2 --- Materials and Reagents --- p.67 / Chapter 4.2.3 --- Pinealectomy --- p.68 / Chapter 4.2.4 --- Confirmation of Pineal Gland Removal --- p.69 / Chapter 4.2.5 --- Development of Scoliosis --- p.69 / Chapter 4.2.6 --- Measurement of Long Bone Growth --- p.70 / Chapter 4.2.7 --- Measurement of Weight --- p.71 / Chapter 4.2.8 --- Measurement of Bone Mineral Density (BMD) --- p.71 / Chapter 4.2.8.1 --- Micro Computed Tomography (MicroCT) --- p.71 / Chapter 4.2.8.2 --- Image Processing and Evaluation of BMD --- p.71 / Chapter 4.2.9 --- Data Analysis --- p.72 / Chapter 4.2.9.1 --- Measurements of Long Bone Growth and Weight --- p.72 / Chapter 4.2.9.2 --- Bone Mineral Density --- p.72 / Chapter 4.3 --- Results --- p.73 / Chapter 4.3.1 --- Confirmation of Pineal Gland Removal --- p.73 / Chapter 4.3.2 --- Occurrence of Scoliosis --- p.73 / Chapter 4.3.3 --- Measurements of Long Bone and Weight --- p.74 / Chapter 4.3.4 --- Measurement of Bone Mineral Density --- p.75 / Chapter 4.4 --- Discussion --- p.76 / Chapter Chapter 5 --- Expression of Melatonin Receptor in AIS and Control --- p.102 / Chapter 5.1 --- Introduction --- p.103 / Chapter 5.2 --- Methodology --- p.105 / Chapter 5.2.1 --- Subjects Recruitments --- p.105 / Chapter 5.2.2 --- Cell Isolation --- p.106 / Chapter 5.2.2.1 --- Bone Biopsies for Osteoblasts Isolation --- p.106 / Chapter 5.2.2.2 --- Materials and Reagents --- p.106 / Chapter 5.2.2.3 --- Isolation of Osteoblasts from Bone Biopsies --- p.107 / Chapter 5.2.3 --- Expression Level and Pattern of Melatonin Receptors 1A and IB --- p.108 / Chapter 5.2.3.1 --- Materials and Reagents --- p.108 / Chapter 5.2.3.2 --- Validation of Specificities of Antibodies by Co-immunoprecipitation --- p.113 / Chapter 5.2.3.3 --- Quantification of Protein Expression of Melatonin Receptors in Osteoblasts --- p.115 / Chapter 5.2.3.4 --- Quantification of mRNA Expression of Melatonin Receptor in Osteoblast --- p.117 / Chapter 5.2.3.5 --- Localization of Melatonin Receptor 1A and IB by Immunofluorescence Staining --- p.119 / Chapter 5.2.4 --- Evaluation and Correlation of Clinical Phenotypes with Melatonin Receptor Expression --- p.120 / Chapter 5.2.5 --- Data Analysis --- p.120 / Chapter 5.3 --- Results --- p.121 / Chapter 5.3.1 --- Protein Expression of Melatonin Receptor 1A and IB --- p.121 / Chapter 5.3.2 --- mRNA Expression of Melatonin Receptor 1A and IB --- p.121 / Chapter 5.3.3 --- Localization of Melatonin Receptors 1A and IB --- p.122 / Chapter 5.3.4 --- Evaluation and Correlation of Clinical Phenotypes with Melatonin Receptor Expression --- p.123 / Chapter 5.4 --- Discussion --- p.124 / Chapter Chapter 6 --- Summary and Overall Discussion --- p.152 / Chapter 6.1 --- Study Flowchart --- p.153 / Chapter 6.2 --- Summary and Discussion --- p.159 / Chapter 6.3 --- Limitations and Further Studies --- p.163 / Bibliography --- p.166

Zhu, Ranxu. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 123-142). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Xu Li. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 204-242). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

No description available.

Bibliography: leaves [280]-301

Hyperhomocysteinemia is a risk factor for cardiovascular disease and stroke. Nutritional and/or genetic disruptions in homocysteine metabolism can cause hyperhomocysteinemia. Mild methylenetetrahydrofolate reductase (MTHFR) deficiency due to the 677C → T mutation in the MTHFR gene is the most common genetic cause of hyperhomocysteinemia. The 677C → T variant is associated with an increased risk for neural tube defects, pregnancy complications, schizophrenia and Down syndrome, and with a decreased risk for colon cancer and leukemia. This variant is also a potential risk factor for vascular disease. Severe MTHFR deficiency results in homocystinuria, an inborn error of metabolism with neurological and vascular complications. We have generated mice with a knockout of the Mthfr gene. The Mthfr-deficient mice exhibit hyperhomocysteinemia and decreased methylation capacity. The Mthfr+/- mice appear normal, whereas the Mthfr-/- mice are smaller and have reduced survival. Abnormal external granule neuron development associated with increased cell death in the cerebellum was observed in the Mthfr-/- mice. / Evidence for cardiovascular pathology was obtained in several ways. Impaired aortic relaxation response to acetylcholine was seen in the Mthfr +/- mice fed a high methionine diet. Both Mthfr+/- and Mthfr-/- mice fed a low folate high methionine diet developed myocardial fibrosis in the left ventricle. Abnormal lipid deposition in the proximal portion of the aorta was observed in older Mthfr+/- and Mthfr-/- mice. After crossing Mthfr -deficient mice with apoE-null mice, we demonstrated that MTHFR deficiency promoted atherogenesis and its progression in the apoE-null mice. / Gene expression in brain of Mthfr-deficient mice was investigated via microarray analysis. Five genes with altered expression in the brain of Mthfr-/- mouse were validated by RT-PCR. In biochemical studies of human MTHFR, both FAD and folate were shown to stabilize the purified recombinant wild type and mutant MTHFRs from the baculovirus expression system against heat inactivation. The effect of folate appeared to be secondary to that of FAD, and S-adenosylmethionine (SAM) inhibited purified wild type and mutant MTHFRs with similar efficiency. / This dissertation will significantly contribute to our understanding of the role of MTHFR in human disease.

A prospective study was conducted on a group of 160 students from 9 to 14 years of age with learning disabilities to predict neuropsychological outcome using perinatal information as predictors. Perinatal information was obtained from the Maternal Perinatal Scale (MPS) (Dean & Gray, 1985). Subjects' neuropsychological functioning was assessed by the Short Neuropsychological Screening Device (SNSD) (Reitan & Herring, 1985). Information concerning subjects' intelligence was obtained from the Wechsler Intelligence Scale for Children-III (WISC-III) administered within the past two years. Hollingshead's Four Factor Index of Social Status was employed to determine subjects' socioeconomic status. A stepwise multiple regression analysis yielded a regression model that contained a subset of 7 perinatal risk factors, involving: (1) Obstetric History; (2) Gestational Age; (3) Psychosocial Events; (4) Delivery; (5) Intrauterine Stress; (6) Teratogenic Stress; and (7) Fetal Oxygenation. A hierarchical regression analysis was further performed to examine if adding socioeconomic and intellectual information to the regression model could increase the prediction of neuropsychological outcome. Results showed that up to 82% of the variability in the neuropsychological outcome was explained by the linear composite of the 7 risk factors. When socioeconomic and intellectual information were added to the regression model, the prediction of neuropsychological outcome was significantly improved. About 201 of the students with learning disabilities in the present study were found to display symptoms similar to minimal brain damage (MBD) relating to poor visual-motor integration, underdeveloped language skills, and aphasic conditions. The results support the theory of a "continuum of reproductive casualty" proposed by Pasamanick et al. (1956). The importance of detecting early indicators of neuropsychological deficits in at risk children was further suggested by the present study. / Department of Educational Psychology