submitted by Chair Siu Fan. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 75-83). / Chapter 1 --- INTRODUCTION --- p.1 / Chapter 2 --- LITERATIRE REVIEW --- p.3 / Chapter 2.1 --- Causes and clinical syndromes in MPS --- p.3 / Chapter 2.1.1 --- MPS --- p.4 / Chapter 2.1.2 --- Classification of MPS --- p.4 / Chapter 2.1.2.1 --- MPS I (Hurler's syndrome) --- p.5 / Chapter 2.1.2.2 --- MPS IS (Scheie syndrome) --- p.5 / Chapter 2 .1.2.3 --- MPS II (Hunter's disease) --- p.6 / Chapter 2.1.2.4 --- MPS Type III (The Sanfilippo diseases) --- p.6 / Chapter 2.1.2.5 --- MPS Type IV (Morquio's disease) --- p.6 / Chapter 2.1.2.6 --- MPS Type VI (Maroteaux 一 Lamy syndrome) --- p.7 / Chapter 2.1.2.7 --- MPS Type VII (Sly syndrome) --- p.8 / Chapter 2.1.3 --- Treatment and prospects for MPS --- p.8 / Chapter 2.1.3.1 --- To manage the handicaps and disabilities --- p.8 / Chapter 2.1.3.2 --- Enzyme replacement --- p.9 / Chapter 2.1.3.3 --- Bone marrow transplantation --- p.10 / Chapter 2.2 --- Basic aspects of GAG --- p.10 / Chapter 2.2.1 --- Distributions of GAG --- p.12 / Chapter 2.2.2 --- Functions and Roles of GAG --- p.12 / Chapter 2.2.3 --- Stepwise degradation of GAGs --- p.12 / Chapter 2.2.4 --- Source of urinary GAG --- p.13 / Chapter 2.2.5 --- Common features of GAGS --- p.14 / Chapter 2.2.6 --- Factors affecting the excretion pattern ot GAG --- p.16 / Chapter 2.3 --- Methods for MPS Diagnosis --- p.16 / Chapter 2.3.1 --- Qualitative urine methods for screening and typing --- p.16 / Chapter 2.3.1.1 --- Spot tests --- p.16 / Chapter 2.3.1.2 --- Precipitation methods --- p.16 / Chapter 2.3.1.3 --- One-dimensional electrophoresis --- p.17 / Chapter 2.3.1.4 --- Two-dimensional electrophoresis --- p.17 / Chapter 2.3.1.5 --- Thin layer chromatography --- p.17 / Chapter 2.3.2 --- Quantitative methods for urinary GAG --- p.17 / Chapter 2.3.2.1 --- Measurement of hexuronic acid --- p.18 / Chapter 2.3.2.2 --- HPLC or Column chromatography --- p.18 / Chapter 2.3.2.3 --- Dye-binding methods --- p.19 / Chapter 2.3.3 --- Cytological studies --- p.19 / Chapter 2.3.4 --- Tissue culture --- p.20 / Chapter 2.3.5 --- Tissue biopsy --- p.20 / Chapter 2.3.6 --- Prenatal diagnosis of the MPS --- p.21 / Chapter 2.4 --- Bacterial GAG hydrolytic enzymes --- p.23 / Chapter 2.5 --- Summary of Literature Review --- p.25 / Chapter 3. --- AIMS OF STUDY --- p.26 / Chapter 4. --- MATERIALS AND METHODS --- p.26 / Chapter 4.1 --- Sample collection --- p.26 / Chapter 4.2 --- Materials &-Equipment --- p.26 / Chapter 4.3 --- Preparation of Reagents and Standards --- p.27 / Chapter 4.3.1 --- Stock DMB reagent solutions --- p.27 / Chapter 4.3.2 --- Working DMB solution --- p.27 / Chapter 4.3.3 --- GAG standards --- p.27 / Chapter 4.3.4 --- Reagents for electrophoresis --- p.27 / Chapter 4.3.4.1 --- 0.1M barium acetate solution --- p.27 / Chapter 4.3.4.2 --- 15% ethanolic barium acetate --- p.28 / Chapter 4.3.4.3 --- 50% ethanolic barium acetate --- p.28 / Chapter 4.3.4.4 --- Alcian blue working solution --- p.28 / Chapter 4.3.4.5 --- 0.1M Tris Buffer --- p.28 / Chapter 4.3.4.6 --- CTB Tris solution --- p.28 / Chapter 4.3.4.7 --- 2.0M lithium chloride --- p.28 / Chapter 4.3.5 --- Reagents for enzymatic degradation --- p.28 / Chapter 4.3.5.1 --- Reconstitution of CSE enzyme --- p.28 / Chapter 4.3.5.2 --- Reconstitution of DSE enzyme --- p.29 / Chapter 4.3.5.3 --- Reconstitution ofHSE I enzyme --- p.29 / Chapter 4.4 --- Methods --- p.31 / Chapter 4.4.1 --- Cobas Bio DMB method --- p.31 / Chapter 4.4.2 --- Cobas Fara DMB method --- p.31 / Chapter 4.4.3 --- Evaluation of methods --- p.31 / Chapter 4.4.3.1 --- To study the matrix effect --- p.31 / Chapter 4.4.3.2 --- Calibration --- p.31 / Chapter 4.4.3.3 --- Precision performance --- p.34 / Chapter 4.4.3.4 --- Linearity check --- p.34 / Chapter 4.4.3.5 --- Detection Limit --- p.34 / Chapter 4.4.3.6 --- Recovery study --- p.35 / Chapter 4.4.3.7 --- Correlation with Cobas Bio to develop the reference range --- p.35 / Chapter 4.4.4 --- Electrophoresis method --- p.36 / Chapter 4.4.4.1 --- Sample preparation --- p.36 / Chapter 4.4.4.2 --- Electrophoresis procedure --- p.36 / Chapter 4.4.5 --- Enzymatic degradation method --- p.37 / Chapter 4.4.5.1 --- Digestion of GAG in aqueous and urine matrix --- p.37 / Chapter 4.4.5.2 --- To optimize the amount of enzyme used to degrade GAG --- p.38 / Chapter 4.4.5.3 --- To study the specificity of GAG degrading enzyme --- p.39 / Chapter 4.4.5.4 --- To study the interaction of GAG --- p.40 / Chapter 4.4.5.5 --- To study the stability of enzyme CSE and DSE --- p.40 / Chapter 4.4.5.6 --- Study MPS patient sample --- p.41 / Chapter 5 --- Results --- p.42 / Chapter 5.1 --- Performance characteristics of the DMB method --- p.42 / Chapter 5.1.1 --- Matrix effect --- p.42 / Chapter 5.1.2 --- Calibration --- p.42 / Chapter 5.1.3 --- Precision performance --- p.42 / Chapter 5.1.4 --- Linearity Range --- p.42 / Chapter 5.1.5 --- Detection limit --- p.42 / Chapter 5.1.6 --- Recovery --- p.47 / Chapter 5.1.7 --- Correlation of Cobas Fara with Cobas Bio --- p.47 / Chapter 5.2 --- Results of GAG enzymatic degradation --- p.50 / Chapter 5.2.2 --- To optimise the amount of enzyme for GAG degradation --- p.57 / Chapter 5.2.3 --- The specificity of GAG degrading enzymes --- p.57 / Chapter 5.2.4 --- The interaction of GAG --- p.57 / Chapter 5.2.5 --- The stability of enzymes --- p.57 / Chapter 5.2.6 --- MPS patient study --- p.57 / Chapter 5.2.6.1 --- Type I/II/VI/VII --- p.57 / Chapter 5.2.6.2 --- MPS Type III patient 1 --- p.64 / Chapter 5.2.6.3 --- MPS Type IIIC patient 2 --- p.64 / Chapter 6. --- DISCUSSION --- p.67 / Chapter 6.1 --- Automated DMB method on Cobas Fara --- p.67 / Chapter 6 2 --- GAG specific degradation enzymes --- p.70 / Chapter 7. --- CONCLUSION & SUGGESTION FOR FUTURE STUDIES --- p.73 / Chapter 8. --- REFERENCES --- p.75

by Fok Ho Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 114-120). / Abstracts in English and Chinese. / Acknowledgements --- p.ii / Abstract --- p.iii / 槪論 --- p.v / List of Abbreviations --- p.vi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter Chapter 2 --- Toxicological studies on the effect of Ilex latifolia extract and its saponin-enriched Fraction --- p.19 / Chapter Chapter 3 --- Hypoglycemic effect of Ilex latifolia extract and its saponin-enriched fraction --- p.51 / Chapter Chapter 4 --- Hypolipidemic effect of Ilex latifolia extract and its saponin-enriched fraction --- p.78 / Chapter Chapter 5 --- Conclusion --- p.109 / References --- p.114

Liu, Yanan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 87-98). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts also in Chinese.

Ong Chik Ying Rose. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 181-195). / Abstracts in English and Chinese. / Acknoledgements --- p.i / List of Abbreviations --- p.ii / Abstract --- p.iii / Abstract in Chinese --- p.v / List of Publications and Abstracts --- p.vii / List of Figures --- p.viii / List of Tables --- p.xi / Contents --- p.xii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Saponins --- p.3 / Chapter 1.1.1 --- Structure of saponins --- p.3 / Chapter 1.1.2 --- Occurrence of saponins --- p.7 / Chapter 1.1.3 --- Bioactivities of saponins --- p.8 / Chapter 1.2 --- Paris Polyphylla --- p.9 / Chapter 1.2.1 --- Chonglou --- p.11 / Chapter 1.3 --- Polyphyllin D --- p.12 / Chapter 1.4 --- Apoptosis --- p.15 / Chapter 1.4.1 --- Apoptosis and necrosis --- p.16 / Chapter 1.4.2 --- Initiation phase of apoptosis --- p.16 / Chapter 1.4.2.1 --- Extrinsic apoptotic pathway --- p.18 / Chapter 1.4.2.2 --- Intrinsic apoptotic pathway --- p.19 / Chapter 1.4.3 --- Execution phase of apoptosis --- p.19 / Chapter 1.4.4 --- Termination phase of apoptosis --- p.20 / Chapter 1.5 --- Multi-drug resistance (MDR) --- p.21 / Chapter 1.5.1 --- MDR mediated by decreased drug accumulation --- p.21 / Chapter 1.5.2 --- MDR mediated by enhanced anti-oxidant enzyme activities --- p.25 / Chapter 1.5.3 --- MDR mediated by enhanced detoxification of drugs --- p.25 / Chapter 1.5.4 --- MDR mediated by enhanced DNA repair system --- p.26 / Chapter 1.5.5 --- MDR mediated by altered apoptotic pathway --- p.26 / Chapter 1.5.6 --- Current strategies for overcoming multidrug resistance in cancer --- p.27 / Chapter 1.6 --- Hepatocellular carcinoma (HCC) --- p.30 / Chapter 1.7 --- Objectives of project --- p.32 / Chapter Chapter 2 --- Materials and Methods --- p.33 / Chapter 2.1 --- Materials --- p.34 / Chapter 2.1.1 --- Culture of Cells --- p.34 / Chapter 2.1.1.1 --- Cell lines --- p.34 / Chapter 2.1.1.2 --- Preservation of Cells --- p.35 / Chapter 2.1.2 --- Culture Media --- p.36 / Chapter 2.1.2.1 --- RPMI 1640 (Phenol Red Medium) --- p.36 / Chapter 2.1.2.2 --- RPMI 1640 (Phenol Red-free Medium) --- p.36 / Chapter 2.1.3 --- Buffers and Reagents --- p.37 / Chapter 2.1.3.1 --- Buffer for Common Use --- p.37 / Chapter 2.1.3.2 --- Reagents for Annexin-V-FITC/PI Assay --- p.37 / Chapter 2.1.3.3 --- Reagents for Western Blotting Analysis --- p.37 / Chapter 2.1.4 --- Chemicals --- p.40 / Chapter 2.1.4.1 --- Fluorescence Dyes --- p.40 / Chapter 2.1.4.2 --- Antibodies --- p.41 / Chapter 2.1.4.3 --- Other Chemicals --- p.42 / Chapter 2.1.5 --- Summary of chemicals used in this study --- p.43 / Chapter 2.2 --- Methods --- p.48 / Chapter 2.2.1 --- In vitro Cell Cytotoxicity Assay --- p.48 / Chapter 2.2.1.1 --- AlamarBlue Assay --- p.48 / Chapter 2.2.2 --- Flow Cytometry --- p.50 / Chapter 2.2.2.1 --- Analysis by Flow Cytometry --- p.50 / Chapter 2.2.2.2 --- Determination of Apoptotic and Late Apoptotic/Necrotic Cells with Annexin-V-FITC/PI Cytometric Analysis --- p.50 / Chapter 2.2.2.3 --- Determination of Mitochondrial Membrane Potential in cells --- p.51 / Chapter 2.2.2.4 --- Determination of Hydrogen Peroxide (H2O2) Release in cells --- p.52 / Chapter 2.2.2.5 --- Measurement of doxorubicin accumulation in cells --- p.53 / Chapter 2.2.2.6 --- Determination of P-glycoprotein expression level in cells --- p.54 / Chapter 2.2.2.7 --- Determination of mitochondrial depolarization and swellingin isolated mitochondria --- p.54 / Chapter 2.2.3 --- Methods involved in DNA sequencing of MDRl promoter --- p.56 / Chapter 2.2.3.1 --- DNA extraction --- p.56 / Chapter 2.2.3.2 --- DNA and Gel Band Purification --- p.56 / Chapter 2.2.3.3 --- Assessment of DNA amount --- p.57 / Chapter 2.2.3.4 --- Polymerase Chain Reaction --- p.57 / Chapter 2.2.3.5 --- Agarose Gel Electrophoresis --- p.59 / Chapter 2.2.3.6 --- Preparation for DNA sequencing --- p.59 / Chapter 2.2.4 --- Western Blotting Analysis --- p.61 / Chapter 2.2.4.1 --- Preparation of Proteins from Cells --- p.61 / Chapter 2.2.4.2 --- Preparation of proteins from isolated mitochondria --- p.63 / Chapter 2.2.4.3 --- Protein analysis with Western analysis --- p.63 / Chapter 2.2.5 --- Confocal laser scanning microscopy (Confocal microscopy) --- p.66 / Chapter 2.2.5.1 --- Analysis with confocal microscopy --- p.66 / Chapter 2.2.5.2 --- Determination of mitochondrial changes in cells by confocal microscopy --- p.66 / Chapter 2.2.5.3 --- Determination of lysosomal rupture in cells by confocal microscopy --- p.67 / Chapter 2.2.6 --- Mitochondrial isolation --- p.68 / Chapter Chapter 3 --- Results 一 Resistance Mechanisms in RHepG2 cells --- p.69 / Chapter 3.1 --- Resistance of RHepG2 cells towards various chemical agents --- p.70 / Chapter 3.1.1 --- RHepG2 cells are resistant to doxorubicin --- p.70 / Chapter 3.1.2 --- RHepG2 cells are resistant to taxol --- p.72 / Chapter 3.1.3 --- RHepG2 cells are resistant to valinomycin --- p.74 / Chapter 3.2 --- Resistance mechanism in RHepG2 cells --- p.76 / Chapter 3.2.1 --- Reduced doxorubicin accumulation is observed in RHepG2 cells --- p.76 / Chapter 3.2.2 --- More P-glycoproteins on the cell surface was observed in RHepG2 cells --- p.80 / Chapter 3.2.3 --- Inhibition of P-glycoprotein activity increased doxorubicin accumulation in RHepG2 cells --- p.82 / Chapter 3.2.4 --- HepG2 and RHepG2 cells contain the same P-glycoprotein promoter region --- p.86 / Chapter 3.2.5 --- RHepG2 over-expressed Bcl-2 --- p.91 / Chapter 3.2.6 --- HepG2 and RHepG2 cells had the same level of Bax protein --- p.93 / Chapter Chapter 4 --- Results - Effects of Polyphyllin D in HepG2 and RHepG2 cells --- p.95 / Chapter 4.1 --- Cytotoxicity of Polyphyllin D in HepG2 and RHepG2 cells --- p.96 / Chapter 4.1.1 --- Polyphyllin D exhibited cytotoxic effect in both HepG2 and RHepG2 cells --- p.96 / Chapter 4.2 --- Apoptotic mechanism caused by Polyphyllin D in HepG2 and RHepG2 cells --- p.93 / Chapter 4.2.1 --- Polyphyllin D caused apoptosis in HepG2 and RHepG2 cells --- p.98 / Chapter 4.2.2 --- Polyphyllin D did not activate caspase8 --- p.103 / Chapter 4.2.3 --- Polyphyllin D did not concentrate on the plasma membrane of cells --- p.106 / Chapter 4.2.4 --- Polyphyllin D did not change Bcl-2 level in HepG2 and RHepG2 cells --- p.109 / Chapter 4.2.5 --- Polyphyllin D treatment enhanced Bax protein expression in both HepG2 and RHepG2 cells --- p.111 / Chapter 4.2.6 --- Polyphyllin D caused cytochrome c and AIF release in HepG2 and RHepG2 cells --- p.113 / Chapter 4.2.7 --- Polyphyllin D induced mitochondrial membrane depolarization in HepG2 and RHepG2 cells --- p.118 / Chapter 4.2.8 --- Polyphyllin D caused mitochondrial swelling in HepG2 and clustering of mitochondriain RHepG2 cells --- p.122 / Chapter 4.2.9 --- "Polyphyllin D caused H202 release in HepG2 and RHepG2 cells, and the cytotoxic effects of Polyphyllin D could be reduced by NAC" --- p.127 / Chapter 4.2.10 --- Polyphyllin D caused permeabilization of lysosomes --- p.132 / Chapter 4.3 --- Site of action of Polyphyllin D in cells --- p.135 / Chapter 4.3.1 --- Purity of isolated mitochondria --- p.135 / Chapter 4.3.2 --- Polyphyllin D caused cytochrome c release from the HepG2 and RHepG2 isolated mitochondria --- p.137 / Chapter 4.3.3 --- Polyphyllin D induced mitochondrial depolarization in HepG2 and RHepG2 isolated mitochondria --- p.139 / Chapter 4.3.4 --- Polyphyllin D caused mitochondrial swelling in HepG2 and RHepG2 isolated mitochondria --- p.142 / Chapter 4.4 --- Resistance reversal effects of Polyphyllin D in RHepG2 cells --- p.144 / Chapter 4.4.1 --- Polyphyllin D increased doxorubicin accumulation in RHepG2 cells --- p.144 / Chapter 4.4.2 --- P-glycoprotein expression was not down-regulated after Polyphyllin D treatment --- p.146 / Chapter 4.4.3 --- Co-treatment of doxorubicin with Polyphyllin D had enhanced cytotoxic effect --- p.148 / Chapter Chapter 5 --- Discussion - Resistance mechanisms in RHepG2 cells --- p.150 / Chapter 5.1 --- Resistance of RHepG2 cells towards various chemical reagents --- p.151 / Chapter 5.2 --- Resistance mechanisms in RHepG2 cells --- p.154 / Chapter Chapter 6 --- Discussion - Effects of Polyphyllin D in HepG2and RHepG2 cells --- p.159 / Chapter 6.1 --- Cytotoxicity of Polyphyllin D in HepG2 and RHepG2 cells --- p.160 / Chapter 6.2 --- Apoptotic mechanisms caused by Polyphyllin D in HepG2 and RHepG2 cells --- p.162 / Chapter 6.3 --- Site of action of Polyphyllin D in HepG2 andRHepG2 cells --- p.172 / Chapter 6.4 --- Resistance reversal effects of Polyphyllin D in RHepG2 cells --- p.175 / Chapter Chapter 7 --- Future Perspectives --- p.177 / Chapter Chapter 8 --- Conclusion --- p.179 / References

Chan Wai Sing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 199-210). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABBREVIATIONS --- p.ii / ABSTRACT --- p.vi / CHINESE ABSTRACT --- p.x / TABLE OF CONTENTS --- p.xiii / Chapter CHAPTER 1: --- GENERAL INTRODUCTION / Chapter 1.1 --- What is hematopoiesis? --- p.1 / Chapter 1.1.1 --- The development of hematopoietic progenitor cells --- p.1 / Chapter 1.1.2 --- The regulation of hematopoiesis by environmental factors --- p.4 / Chapter 1.1.3 --- The regulation of hematopoiesis by transcription factors --- p.7 / Chapter 1.2 --- Leukemia --- p.9 / Chapter 1.2.1 --- Classification of leukemia --- p.11 / Chapter 1.2.2 --- Pathology and etiology of leukemia --- p.15 / Chapter 1.2.2.1 --- Inheritance --- p.15 / Chapter 1.2.2.2 --- Environmental factors --- p.16 / Chapter 1.2.2.3 --- Virus infection --- p.17 / Chapter 1.2.3 --- Genetics of leukemia --- p.17 / Chapter 1.2.3.1 --- Point mutations --- p.17 / Chapter 1.2.3.2 --- Translocations --- p.18 / Chapter 1.2.3.3 --- Gene and chromosomal deletions --- p.18 / Chapter 1.2.3.4 --- Chromosomal duplication or gene amplification --- p.18 / Chapter 1.2.4 --- Current therapeutic strategies for leukemia --- p.20 / Chapter 1.2.4.1 --- Chemotherapy --- p.20 / Chapter 1.2.4.2 --- Stem cell transplantation --- p.21 / Chapter 1.2.4.3 --- Immunotherapy --- p.22 / Chapter 1.2.4.4 --- Gene therapy --- p.23 / Chapter 1.2.5 --- Novel approaches for the treatment of leukemia --- p.23 / Chapter 1.2.5.1 --- Differentiation therapy of leukemia --- p.24 / Chapter 1.2.5.2 --- Induction of apoptosis in the treatment of leukemia --- p.25 / Chapter 1.3 --- Topoisomerase-targeting agents --- p.27 / Chapter 1.3.1 --- What is topoisomerase? --- p.27 / Chapter 1.3.2 --- Structures and action mechanisms of Top I- and Top II-targeting agents --- p.28 / Chapter 1.3.3 --- Anti-tumor activities of topoisomerase-targeting agents --- p.37 / Chapter 1.4 --- Aims and scopes of this investigation --- p.39 / Chapter CHAPTER 2: --- MATERIALS AND METHODS / Chapter 2.1 --- Materials --- p.42 / Chapter 2.1.1 --- Mice --- p.42 / Chapter 2.1.2 --- Cell lines --- p.42 / Chapter 2.1.3 --- "Cell culture medium, buffers and other reagents" --- p.43 / Chapter 2.1.4 --- Radioisotope and scintillation fluid --- p.47 / Chapter 2.1.5 --- Reagents and buffers for flow cytometry --- p.48 / Chapter 2.1.6 --- Antibodies for flow cytometry --- p.50 / Chapter 2.1.7 --- Recombinant cytokines --- p.51 / Chapter 2.1.8 --- Reagents for DNA extraction --- p.52 / Chapter 2.1.9 --- Reagents for total RNA isolation --- p.53 / Chapter 2.1.10 --- Reagents and buffers for RT-PCR --- p.54 / Chapter 2.1.11 --- Reagents and buffers for gel electrophoresis --- p.58 / Chapter 2.1.12 --- Reagents and buffers for Western blot analysis --- p.59 / Chapter 2.1.13 --- Reagents for measuring caspase activity --- p.64 / Chapter 2.2 --- Methods --- p.67 / Chapter 2.2.1 --- Culture of the leukemia cell lines --- p.67 / Chapter 2.2.2 --- Isolation and preparation of normal hematopoietic cells --- p.67 / Chapter 2.2.3 --- [3 H]-TdR proliferation assay --- p.68 / Chapter 2.2.4 --- Determination of cell viability --- p.69 / Chapter 2.2.5 --- Assay for anti-leukemic activity in vivo --- p.70 / Chapter 2.2.6 --- Assessment of differentiation-associated characteristics --- p.71 / Chapter 2.2.7 --- Assays for apoptosis --- p.73 / Chapter 2.2.8 --- Cell cycle analysis (DNA content evaluation) --- p.75 / Chapter 2.2.9 --- Gene expression study --- p.75 / Chapter 2.2.10 --- Protein expression study --- p.79 / Chapter 2.2.11 --- Measurement of caspase activity --- p.82 / Chapter 2.2.12 --- Statistical analysis 一 --- p.83 / Chapter CHAPTER 3: --- STUDIES ON THE ANTI-PROLIFERATIVE EFFECT OF TOPOISOMERASE-TARGETING AGENTS ON LEUKEMIA CELLS / Chapter 3.1 --- Introduction --- p.84 / Chapter 3.2 --- Results --- p.86 / Chapter 3.2.1 --- The anti-proliferative effect of topoisomerase-targeting agents on human and murine leukemia cells in vitro --- p.86 / Chapter 3.2.2 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the clonogenicity of the murine myeloid leukemia WEHI-3B JCS cells in vitro --- p.105 / Chapter 3.2.3 --- Effects of 10-hydroxy-camptothecin and etoposide phosphate on the tumorigenicity and proliferation of the murine myeloid leukemia WEHI-3B JCS cells invivo --- p.106 / Chapter 3.2.4 --- Cytotoxic effect of 10-hydroxy-camptothecin and etoposide phosphate on normal hematopoietic cells and WEHI-3B JCS cells in vitro --- p.109 / Chapter 3.2.5 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the cell cycle kinetics of WEHI-3B JCS cells --- p.114 / Chapter 3.2.6 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the expression of cell cycle-regulatory genes in the murine myeloid leukemia WEHI-3B JCS cells --- p.116 / Chapter 3.2.7 --- Combination effect of 10-hydroxy-camptothecin or etoposide phosphate with cytokines on the proliferation of the murine myeloid leukemia WEHI-3B JCS cells --- p.123 / Chapter 3.3 --- Discussion --- p.127 / Chapter CHAPTER 4: --- STUDIES ON THE DIFFERENTIATION-INDUCING EFFECT OF 10-HYDROXY-CAMPTOTHECIN AND ETOPOSIDE PHOSPHATE ON THE MURINE MYELOID LEUKEMIA WEHI-3B JCS CELLS / Chapter 4.1 --- Introduction --- p.132 / Chapter 4.2 --- Results --- p.134 / Chapter 4.2.1 --- Morphological changes in the murine myeloid leukemia WEHI-3B JCS cells treated with 10-hydroxy-camptothecin and etoposide phosphate --- p.134 / Chapter 4.2.2 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the size and granularity of the murine myeloid leukemia WEHI-3B JCS cells --- p.138 / Chapter 4.2.3 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the plastic adhering property of the murine myeloid leukemia WEHI-3B JCS cells --- p.140 / Chapter 4.2.4 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the NBT-reducing activity of the murine myeloid leukemia WEHI-3B JCS cells --- p.142 / Chapter 4.2.5 --- Surface antigen immunophenotyping of the murine myeloid leukemia WEHI-3B JCS cells treated with 10-hydroxy- camptothecin and etoposide phosphate --- p.145 / Chapter 4.2.6 --- Induction of non-specific esterase activity in the murine myeloid leukemia WEHI-3B JCS cells by 10-hydroxy- camptothecin and etoposide phosphate --- p.152 / Chapter 4.3 --- Discussion --- p.154 / Chapter CHAPTER 5: --- STUDIES ON THE APOPTOSIS-INDUCING EFFECT OF 10-HYDROXY-CAMPTOTHECIN AND ETOPOSIDE PHOSPHATE ON THE MURINE MYELOID LEUKEMIA WEHI-3B JCS CELLS / Chapter 5.1 --- Introduction --- p.157 / Chapter 5.2 --- Results --- p.160 / Chapter 5.2.1 --- Induction of nuclear disintegration in the murine myeloid leukemia WEHI-3B JCS cells by 10-hydroxy-camptothecin and etoposide phosphate --- p.160 / Chapter 5.2.2 --- Induction of DNA fragmentation in the murine myeloid leukemia WEHI-3B JCS cells by 10-hydroxy-camptothecin and etoposide phosphate --- p.162 / Chapter 5.2.3 --- Induction of phosphatidylserine translocation in murine myeloid leukemia WEHI-3B JCS cells by 10-hydroxy- camptothecin and etoposide phosphate --- p.167 / Chapter 5.2.4 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the expression of apoptosis-regulatory genes in the murine myeloid leukemia WEHI-3B JCS cells --- p.171 / Chapter 5.2.5 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on the expression of apoptosis-regulatory proteins in the murine myeloid leukemia WEHI-3B JCS cells --- p.177 / Chapter 5.2.6 --- Induction of mitochondrial membrane depolarization in the murine myeloid leukemia WEHI-3B JCS cells by 10-hydroxy- camptothecin and etoposide phosphate --- p.179 / Chapter 5.2.7 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate on caspase activity in the murine myeloid leukemia WEHI-3B JCS cells --- p.181 / Chapter 5.2.8 --- Effect of 10-hydroxy-camptothecin and etoposide phosphate intracellular Ca2+ level in the murine myeloid leukemia WEHI-3B JCS cells --- p.186 / Chapter 5.3 --- Discussion --- p.189 / Chapter CHAPTER 6: --- CONCLUSIONS AND FUTURE PERSPECTIVES --- p.192 / REFERENCES --- p.199

Chu Ka-wing, Kevin. / "June 2001." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 194-215) / 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.

Christopher John Haines. / Thesis (M.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 239-279). / LIST OF TABLES --- p.xviii / LIST OF FIGURES --- p.xxi / LIST OF ABBREVIATIONS --- p.xxii / Chapter CHAPTER1 --- INTRODUCTION --- p.1 / Problems related to the menopause / Research plan / Chapter CHAPTER2 --- OVERVIEW --- p.15 / Introduction / Atherosclerosis and the lipid profile / Coronary artery disease and lipid abnormalities in women / "Exogenous oestrogens, progestogens and coronary artery disease " / Lipoprotein (a) / Chapter CHAPTER3 --- GENERAL METHODOLOGY --- p.134 / Recruitment of cases / Pharmacokinetics / Data collection and analysis of samples / Ethical considerations / Chapter CHAPTER4 --- STUDY I -THE SHORT TERM EFFECTS OF ORAL OESTROGEN --- p.157 / Crossover analysis of effects of oral oestrogen on lipoprotein (a) and other lipoproteins / Relationship between lipoprotein (a) and other lipids and lipoproteins / Chapter CHAPTER5 --- STUDY II -THE SUSTAINED EFFECTS OF ORAL OESTROGEN --- p.186 / Analysis of prolonged effects of oral oestrogen on lipoprotein (a) and other lipids and lipoproteins / Chapter CHAPTER6 --- STUDY III -THE EFFECTS OF COMBINED CYCLICAL HORMONE REPLACEMENT THERAPY --- p.196 / Analysis of effect of combined cyclical hormone replacement therapy on lipoprotein (a) and other lipids and lipoproteins / Comparison between sampling during oestrogen alone and combined phase of treatment / Chapter CHAPTER7 --- STUDY IV -THE EFFECTS OF PERCUTANEOUS OESTROGEN --- p.214 / Analysis of effect of percutaneous on lipoprotein (a) and other lipids and lipoproteins / Chapter CHAPTER8 --- SUMMARY AND CONCLUSIONS --- p.228 / BIBLIOGRAPHY --- p.239

by Shen Tai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 84-92). / Chapter CHAPTER1 --- INTRODUCTION --- p.2 / Chapter CHAPTER2 --- LITERATURE REVIEW / Chapter 2.1 --- Fibronectin --- p.4 / Chapter 2.1a --- Functions and basic molecular structure --- p.4 / Chapter 2.1b --- Polymorphism and alternative splicing --- p.5 / Chapter 2.1c --- Primary classification --- p.6 / Chapter 2.2 --- Oncofetal fibronectin --- p.7 / Chapter 2.2a --- Introduction --- p.7 / Chapter 2.2b --- Recognition by FDC-6 monoclonal antibody --- p.7 / Chapter 2.2c --- Specificity of FDC-6 antibody --- p.8 / Chapter 2.2d --- Glycosylation of fetal fibronectin molecule --- p.9 / Chapter 2.2e --- Fibronectin and human pregnancy --- p.9 / Chapter 2.2f --- Regulation of fetal fibronectin synthesis --- p.11 / Chapter 2.2g. --- Possible mechanism of fetal fibronectin release --- p.12 / Chapter 2.3 --- The uterine cervix in human labour --- p.13 / Chapter 2.3a --- Introduction --- p.14 / Chapter 2.3b --- Physiological cervical ripening --- p.14 / Chapter 2.3c --- Role of prostaglandins --- p.16 / Chapter 2.3d --- Fibronectin and degradation of cervical matrix --- p.16 / Chapter 2.4 --- Evaluation of cervical status --- p.17 / Chapter 2.4a --- Bishop score --- p.17 / Chapter 2.4b --- Intravaginal ultrasound evaluation of cervix --- p.18 / Chapter 2.4c --- Fibronectin as a tool for evaluation of cervical status --- p.19 / Chapter 2.5 --- Pre-induction cervical ripening with PGE2 --- p.20 / Chapter 2.5a --- Introduction --- p.20 / Chapter 2.5b --- Route of delivery --- p.21 / Chapter 2.5c --- Indications for cervical ripening with prostaglandins --- p.21 / Chapter 2.5d --- Possible Mechanism --- p.22 / Chapter 2.5e --- PGE2 effectiveness and potential risks --- p.23 / Chapter 2.5f --- Other cervical ripening techniques and agents --- p.25 / Chapter 2.5g --- Prediction for outcomes of induction and pre- induction cervical ripening with PGE2 --- p.26 / Chapter 2.6 --- Application of fibronectin in Obstetrics --- p.29 / Chapter 2.6a --- Prediction of preterm delivery --- p.29 / Chapter 2.6b --- Evaluation of cervical status --- p.31 / Chapter 2.6c --- Prediction of prolonged pregnancy --- p.32 / Chapter 2.6d --- Prediction for outcomes of induced labor --- p.32 / Chapter CHAPTER3 --- METHODOLOGY / Chapter 3.1 --- Introduction --- p.36 / Chapter 3.2. --- Study population and recruitment --- p.36 / Chapter 3.2a --- Inclusive criterion --- p.36 / Chapter 3.2b --- Exclusive criterion --- p.36 / Chapter 3 3 --- Measurement of Fetal Fibronectin --- p.38 / Chapter 3.3.1 --- Fetal Fibronectin Membrane Immunoassay --- p.39 / Chapter 3.3.1a --- Principle of the test --- p.39 / Chapter 3.3.1b --- Reagent and materials --- p.39 / Chapter 3.3.1c --- Specimen collection --- p.40 / Chapter 3.3.1d --- Assay procedure and interpretation of results --- p.40 / Chapter 3.3.2 --- Fetal Fibronectin Enzyme Immunoassay --- p.40 / Chapter 3.3.2a --- Principle of the test --- p.40 / Chapter 3.3.2b --- Materials --- p.41 / Chapter 3.3.2c --- Specimen collection --- p.42 / Chapter 3.3.2d --- Assay procedure and interpretation of results --- p.43 / Chapter 3.4 --- Cervical status determination --- p.44 / Chapter Chapter4 --- RESULT --- p.47 / Chapter Chapter5 --- DISCUSSION --- p.80 / REFERENCES --- p.83

Liu, Xiaozhuo. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 156-169). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract in Chinese (摘要） --- p.iv / Acknowledgments --- p.vi / List of Abbreviations --- p.vii / Table of Contents --- p.xiv / Chapter Chapter One: --- General Introduction / Chapter 1.1 --- Hematopoiesis and Leukemia --- p.1 / Chapter 1.1.1 --- An Overview on Hematopoiesis --- p.1 / Chapter 1.1.2 --- Leukemia --- p.6 / Chapter 1.1.2.1 --- An Overview of Leukemia --- p.6 / Chapter 1.1.2.2 --- Classification and Epidemiology of Leukemia --- p.8 / Chapter 1.1.2.3 --- Conventional Approaches to Leukemia Therapy --- p.12 / Chapter 1.1.2.4 --- Novel Approaches to Leukemia Therapy --- p.15 / Chapter 1.2 --- Sophoraflavanone G: A Bioactive Compound Isolated from Kushen --- p.18 / Chapter 1.2.1 --- An Overview of Kushen: A Traditional Chinese Medicine --- p.19 / Chapter 1.2.2 --- An Overview of Lavandulyl Flavanones --- p.22 / Chapter 1.2.3 --- Historical Development and Occurrence of Sophoraflavanone G --- p.24 / Chapter 1.2.4 --- Biological Activities of Sophoraflavanone G --- p.25 / Chapter 1.2.4.1 --- Anti-microbial and Insecticidal Activities --- p.25 / Chapter 1.2.4.2 --- Anti-tumor Activities --- p.26 / Chapter 1.2.4.3 --- Pharmacodynamics of Sophoraflavanone G --- p.27 / Chapter 1.3 --- Objectives and Scopes of the Present Study --- p.30 / Chapter Chapter Two: --- Materials and Methods / Chapter 2.1 --- Materials --- p.32 / Chapter 2.1.1 --- Animals --- p.32 / Chapter 2.1.2 --- Cell lines --- p.32 / Chapter 2.1.3 --- "Cell Culture Medium, Buffers and Other Reagents" --- p.34 / Chapter 2.1.4 --- Reagents and Buffers for Flow Cytometry --- p.37 / Chapter 2.1.5 --- Reagents for DNA Extraction --- p.39 / Chapter 2.1.6 --- Reagents for Measuring Caspase Activity --- p.40 / Chapter 2.1.7 --- "Reagents, Buffers and Materials for Western Blotting" --- p.43 / Chapter 2.2 --- Methods --- p.48 / Chapter 2.2.1 --- Extraction and Isolation of Sophoraflavanone G from Kushen --- p.48 / Chapter 2.2.2 --- Culture of Tumor Cell Lines --- p.49 / Chapter 2.2.3 --- "Isolation, Preparation and Culturing of Human Peripheral Blood Leukocytes and Murine Bone Marrow Cells" --- p.50 / Chapter 2.2.4 --- Assays for Anti-proliferation and Cytotoxicity --- p.51 / Chapter 2.2.5 --- Determination of Anti-leukemic Activity In Vivo (In Vivo Tumorigenicity Assay) --- p.52 / Chapter 2.2.6 --- Cell Cycle Analysis by Flow Cytometry --- p.53 / Chapter 2.2.7 --- Measurement of Apoptosis-induced Activities --- p.54 / Chapter 2.2.8 --- Protein Expression Study --- p.59 / Chapter 2.2.9 --- Assessment of Differentiation-associated Characteristics --- p.64 / Chapter 2.2.10 --- Statistical Analysis --- p.65 / Chapter Chapter Three: --- Studies on the Anti-proliferative Effect of Sophoraflavanone G on Human Myeloid Leukemia Cells / Chapter 3.1 --- Introduction --- p.66 / Chapter 3.2 --- Results --- p.69 / Chapter 3.2.1 --- Structure Identification of Sophoraflavanone G Isolated from Sophora flavescens --- p.69 / Chapter 3.2.2 --- Anti-proliferative Activity of Sophoraflavanone G on Various Myeloid Leukemia Cell Lines --- p.72 / Chapter 3.2.3 --- Effect of Sophoraflavanone G on the Viability of the Human Promyelocytic Leukemia HL-60 Cells --- p.80 / Chapter 3.2.4 --- Cytotoxic Effect of Sophoraflavanone G on Primary Normal Cells In Vitro --- p.83 / Chapter 3.2.5 --- Kinetic and Reversibility Studies of the Anti-proliferative Effect of Sophoraflavanone G on the Human Promyelocytic Leukemia HL-60 Cells --- p.85 / Chapter 3.2.6 --- Effect of Sophoraflavanone G on the In Vivo Tumorigenicity of the HL-60 Cells --- p.88 / Chapter 3.2.7 --- Effect of Sophoraflavanone G on the Cell Cycle Profile of the HL-60 cells In Vitro --- p.90 / Chapter 3.2.8 --- Effect of Sophoraflavanone G on the Expression of Cell Cycle-regulatory Proteins in the HL-60 Cells --- p.93 / Chapter 3.2.9 --- Anti-proliferative Effect of Sophoraflavanone G on Multidrug-resistant (MDR) Leukemia Cell Line HL-60/MX2 Cells --- p.95 / Chapter 3.3 --- Discussion --- p.101 / Chapter Chapter Four: --- Studies on the Apoptosis- and Differentiation-inducing Activities of Sophoraflavanone G on Human Myeloid Leukemia Cells / Chapter 4.1 --- Introduction --- p.109 / Chapter 4.2 --- Results --- p.114 / Chapter 4.2.1 --- Induction of DNA Fragmentation in the Human Promyelocytic Leukemia HL-60 Cells by Sophoraflavanone G --- p.114 / Chapter 4.2.2 --- Induction of Phosphatidylserine Externalization in the Human Promyelocytic Leukemia HL-60 Cells by Sophoraflavanone G as Detected by Annexin V-GFP and PI Double Staining Method --- p.116 / Chapter 4.2.3 --- Effects of Sophoraflavanone G on the Caspase Activities in the Human Promyelocytic Leukemia HL-60 Cells --- p.119 / Chapter 4.2.4 --- Induction of Mitochondrial Membrane Depolarization in the Human Promyelocytic Leukemia HL-60 Cells by Sophoraflavanone G --- p.124 / Chapter 4.2.5 --- Involvement of Bcl-2 Family Members in Sophoraflavanone G-induced Apoptosis in the Human Promyelocytic Leukemia HL-60 Cells --- p.128 / Chapter 4.2.6 --- Effects of Sophoraflavanone G on the Induction of Reactive Oxygen Species in the Human Promyelocytic Leukemia HL-60 Cells --- p.131 / Chapter 4.2.7 --- Effect of Sophoraflavanone G on the Intracellular Ca2+ Level in the Human Promyelocytic Leukemia HL-60 Cells --- p.134 / Chapter 4.2.8 --- Morphological Studies on the Sophoraflavanone G-treated Human Promyelocytic Leukemia HL-60 Cells --- p.136 / Chapter 4.2.9 --- Effect of Sophoraflavanone G on the NBT Reducing Activity of the Human Promyelocytic Leukemia HL-60 Cells --- p.138 / Chapter 4.3 --- Discussion --- p.140 / Chapter Chapter Five: --- Conclusions and Future Perspectives --- p.148 / References --- p.156

Skin cancer incidence is increasing while the rates of other cancers is declining. The purpose of this quantitative study was to determine whether health self-efficacy predicted skin cancer protective behaviors. The theory of health self-efficacy provided the framework for the study. Secondary data were collected from the 2008 and 2014 Health Information National Trends Surveys. The study sample included women 18-34 years of age because this population is especially vulnerable to skin cancer. Results of logistic regression analyses indicated that higher levels of health self-efficacy predicted greater sunscreen use, but higher health self-efficacy levels did not predict avoidance of tanning bed or booth use. No significant changes were found in sunscreen use and tanning bed and booth use between 2008 and 2014. Findings may be used to develop educational programs and medical interventions to decrease the incidence of skin cancer.