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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
171

Actions of tumour necrosis factor: in vitro cytotoxicity and in vivo toxicity.

January 1988 (has links)
by Wong Wah Yau. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1988. / Bibliography: leaves 219-228.
172

Expression of a major surface antigen of Toxoplasma gondii (P30) in Escherichia coli and Arabidopsis thaliana.

January 2000 (has links)
Chi-shing Lo. / Thesis submitted in: November 1999. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 119-138). / Abstracts in English and Chinese. / Statement --- p.iii / Acknowledgments --- p.iv / Abbreviations --- p.v / Abstract --- p.vii / Abstract (Chinese version) --- p.ix / Table of contents --- p.xi / List of Figure --- p.xvii / List of Table --- p.xix / Chapter Chapter 1: --- General Introduction --- p.1 / Chapter 1.1 --- BIOLOGY OF TOXOPLASMA GONDII --- p.1 / Chapter 1.1.1 --- Life cycle of Toxoplasma gondii --- p.2 / Chapter (a) --- Tachyzoite --- p.3 / Chapter (b) --- Bradyzoite --- p.3 / Chapter 1.1.2 --- Genetics of Toxoplasma gondii --- p.4 / Chapter (a) --- Population genetics --- p.4 / Chapter (b) --- Molecular genetics --- p.5 / Chapter (c) --- Genome analysis --- p.7 / Chapter 1.1.3 --- Invasion --- p.8 / Chapter 1.1.4 --- Surface of Toxoplasma gondii --- p.9 / Chapter (a) --- Tachyzoite surface --- p.9 / Chapter (b) --- Bradyzoite surface --- p.11 / Chapter (c) --- Sporozite surface --- p.11 / Chapter (d) --- Glycoprotein antigens --- p.12 / Chapter 1.2 --- TREATMENT OF TOXOPLASMOSIS --- p.13 / Chapter 1.2.1 --- Chemotherapy --- p.13 / Chapter (a) --- Drug against metabolism and protein synthesis on nuclear genome --- p.13 / Chapter (b) --- Drug against other organelles --- p.14 / Chapter (c) --- Drug resistance --- p.15 / Chapter 1.2.2 --- Toxoplasma vaccine --- p.16 / Chapter (a) --- Mutant strains of Toxoplasma gondii as vaccine --- p.17 / Chapter (b) --- Subunit vaccine --- p.19 / Chapter (c) --- P30 as subunit vaccine --- p.20 / Chapter 1.3 --- AIM OF THE STUDY --- p.22 / Chapter Chapter 2 --- : Expression of P30 in Escherichia coli --- p.23 / Chapter 2.1 --- INTRODUCTION --- p.23 / Chapter 2.1.1 --- Why Escherichia coli? --- p.23 / Chapter 2.1.2 --- protein folding --- p.24 / Chapter 2.1.3 --- T7-based gene expression system --- p.25 / Chapter (a) --- Biology of T7 RNA polymerase --- p.26 / Chapter (b) --- pET translational vector --- p.26 / Chapter (c) --- Hislidine-tagged protein --- p.27 / Chapter (d) --- Host strain for expression --- p.28 / Chapter 2.2 --- MATERIALS --- p.29 / Chapter 2.2.1 --- Bactcrial strains --- p.29 / Chapter 2.2.2 --- Mouse strain --- p.29 / Chapter 2.2.3 --- Chemicals --- p.29 / Chapter 2.2.4 --- Nucleic acids --- p.30 / Chapter 2.2.5 --- Kit and reagents --- p.31 / Chapter 2.2.6 --- Antibodies --- p.31 / Chapter 2.2.7 --- Solutions --- p.32 / Chapter 2.2.8 --- Enzymes --- p.33 / Chapter 2.2.9 --- Sequencing primers --- p.33 / Chapter 2.3 --- METHODS --- p.34 / Chapter 2.3.1 --- Modification of P30 gene --- p.34 / Chapter (a) --- Preparation of recombinant plasmids,pBV220-ASP30PI and pBV220- SP30hisAPI --- p.36 / Chapter (b) --- Digestion of pBV220-ASP30PI and pBV220-SP30hisAPI with DraII and EcoRI --- p.37 / Chapter (c) --- Purification of DNA fragments from agarose gel --- p.37 / Chapter (d) --- Ligation of fragments of pBV220-ΔSP30PI and pBV220-SP30hisAPI --- p.38 / Chapter (e) --- Preparation of DH5α competent cells --- p.38 / Chapter (f) --- Transformation of recombinant pBV220-ΔSP30hisAPI --- p.38 / Chapter (g) --- Plasmid preparation of putative pBV220-ΔSP30API --- p.39 / Chapter (h) --- Plasmid preparation of pET-ΔSP30API --- p.39 / Chapter (i) --- Cycle sequencing reaction on putative plasmid pET-ASP30API --- p.40 / Chapter 2.3.2 --- Expression and Purification of his-tag P30 --- p.41 / Chapter (a) --- Expression profile of his-tag P30 production by IPTG induction --- p.41 / Chapter (b) --- SDS-polyacrylamide gel electrophoresis (SDS-PAGE) --- p.41 / Chapter (c) --- Purification of his-tag P30 --- p.43 / Chapter (d) --- Bradford Protein Microassay (Bio-Rad) --- p.43 / Chapter 2.3.3 --- Characterization of his-tag P30 --- p.44 / Chapter (a) --- Western blot of induced bacterial lysate by monoclonal anti-his-tag antibody --- p.44 / Chapter (b) --- Western blot of his-tag with seropositive sera of mice,rabbit and human --- p.46 / Chapter (c) --- Enterokinase digestion of his-tag P30 --- p.46 / Chapter (d) --- N'terminal amino acid sequencing of pure and enterokinase-cut his-tag --- p.47 / Chapter (e) --- Western blot of T. gondii lysate with antiserum against his-tag P30 --- p.47 / Chapter 2.4 --- RESULTS --- p.49 / Chapter 2.4.1 --- Modification of P30 gene --- p.49 / Chapter 2.4.2 --- "Expression, purification and characteriziation of his-tag P30 in bacteria" --- p.54 / Chapter 2.5 --- DISCUSSIONS --- p.64 / Chapter 2.5.1 --- Modification of P30 gene --- p.64 / Chapter 2.5.2 --- Expression and purification of his-tag P30 --- p.66 / Chapter 2.5.3 --- Characterization of his-tag P30 --- p.67 / Chapter Chapter 3 --- : Expression of P30 in Arabidopsis thalina --- p.69 / Chapter 3.1 --- INTRODUCTION --- p.69 / Chapter 3.1.1 --- Why Arabidopsis thalina? --- p.69 / Chapter 3.1.2 --- In planta transformation --- p.70 / Chapter 3.1.3 --- Transgenic plants as vacine production systems --- p.72 / Chapter (a) --- Stable expression of E. coli heat-liable enterotoxin B subunit and cholera-toxin B subunit --- p.73 / Chapter (b) --- Stable expression of Hepatitis B surface antigen (HBsAg) --- p.74 / Chapter (c) --- Stable expression of Norwalk virus capsid protein --- p.75 / Chapter (d) --- Transient expression by tobacco mosaic virus --- p.75 / Chapter (e) --- Transient expression by Cowpea mosaic virus capsid protein fusion --- p.76 / Chapter 3.2 --- MATERIALS --- p.77 / Chapter 3.2.1 --- Bacterial strains --- p.77 / Chapter 3.2.2 --- Arabidopsis strains --- p.77 / Chapter 3.2.3 --- Chemicals --- p.77 / Chapter 3.2.4 --- Nucleic acids --- p.78 / Chapter 3.2.5 --- Kit and reagents --- p.78 / Chapter 3.2.6 --- Solutions --- p.79 / Chapter 3.2.7 --- Enzymes and buffers --- p.81 / Chapter 3.2.8 --- PCR and Sequencing primers --- p.81 / Chapter 3.3 --- METHODS --- p.82 / Chapter 3.3.1 --- Construction of V7-ASP30API --- p.82 / Chapter 3.3.2 --- Agrobacterium-mediated transformation of Arabidopsis by vacuum infiltration --- p.83 / Chapter (a) --- Preparation of electro-competent Agrobacterium --- p.83 / Chapter (b) --- Transformation of electro-competent Agrobacterium with V7- ASP30API --- p.84 / Chapter (c) --- Plasmid preparation of V7-ASP30API from transformed Agrobacterium --- p.84 / Chapter (d) --- Vacuum infiltration --- p.85 / Chapter 3.3.3 --- Screening of homozygous transgenic plants --- p.86 / Chapter 3.3.4 --- Detecton of transgene P30 in genomic DNA of transgenic plants --- p.87 / Chapter (a) --- Preparation of DIG-labelled probe --- p.87 / Chapter (b) --- Estimation the yield of DIG-labelled probe --- p.88 / Chapter (c) --- Extraction of genomic DNA from transgenic plants --- p.88 / Chapter (d) --- Restriction digestion of genomic DNA with EcoRI and HindIII --- p.89 / Chapter (e) --- DNA transfer from gel to nylon membrane --- p.89 / Chapter (f) --- Detection of hybridized DIG-labelled probe on membrane/ blot --- p.90 / Chapter (g) --- PCR on genomic DNA of transgenic plants with specific primers --- p.91 / Chapter 3.3.5 --- Analysis of transgene RNA expression in transgenic plants --- p.91 / Chapter (a) --- Extraction of total RNA from plants --- p.91 / Chapter (b) --- Northern blot on RNA of F2 transgenic plants --- p.92 / Chapter (c) --- RT-PCR on RNA of F3 transgenic plants --- p.93 / Chapter 3.3.6 --- Detection of his-tag P30 protein in F3 transgenic plants --- p.93 / Chapter 3.4 --- RESULTS --- p.95 / Chapter 3.4.1 --- Construction of V7-ASP30API --- p.95 / Chapter 3.4.2 --- Screening of homozygous transgenic plants --- p.99 / Chapter 3.4.3 --- Molecular analysis of transgene P30 in transgenic plants --- p.101 / Chapter 3.5 --- DISCUSSIONS --- p.108 / Chapter 3.5.1 --- Construction and optimization of expression construct --- p.108 / Chapter 3.5.2 --- Screening and selection of homozyous transgenic plants --- p.109 / Chapter 3.5.3 --- Analysis of transgenic plants --- p.110 / Chapter Chapter 4 : --- General Discussions --- p.112 / Chapter 4.1 --- Significances of studying Toxoplasma gondii --- p.112 / Chapter 4.2 --- Expression of recombinant P30 in prokaryotic systems --- p.113 / Chapter 4.2 --- Expression of recombinant P30 in eukaryotic systems --- p.115 / Reference --- p.119
173

Investigation into the mechanism of action of corticosteroids to antagonise cisplatin- and motion-induced emesis.

January 2000 (has links)
Sam Sze Wing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 156-184). / Abstracts in English and Chinese. / Publications based on work in this thesis --- p.ii / Abstract --- p.iii / Acknowledgements --- p.vii / Chapter 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Corticosteroids --- p.2 / Chapter 1.1.1 --- Chemical Structure of Steroids --- p.3 / Chapter 1.1.2 --- Biosynthesis of Endogenous Corticosteroids --- p.3 / Chapter 1.1.2.1 --- Regulation of Cortisol synthesis and negative feedback system --- p.4 / Chapter 1.1.3 --- Biological Significance of Corticosteroids --- p.5 / Chapter 1.1.3.1 --- Involvement of corticosteroids as anti-inflammatory drugs --- p.6 / Chapter 1.1.3.2 --- Eicosanoid biosynthesis --- p.7 / Chapter 1.1.3.3 --- Lipoxygenase pathway --- p.9 / Chapter 1.1.3.4 --- Side-effects of prolonged use of corticosteroids --- p.9 / Chapter 1.2 --- Organisation of the Emetic Reflex --- p.11 / Chapter 1.2.1 --- Motor Pathway of Emetic Reflex --- p.12 / Chapter 1.2.1.1 --- Retching and vomiting --- p.12 / Chapter 1.2.1.2 --- Nausea --- p.13 / Chapter 1.2.2 --- Components of the Emetic Reflex --- p.14 / Chapter 1.2.2.1 --- The vomiting centre (VC) --- p.15 / Chapter 1.2.2.2 --- Area postrema (AP) / Chemoreceptor trigger zone (CTZ) --- p.15 / Chapter 1.2.2.3 --- The nucleus tractus solitarius (NTS) --- p.17 / Chapter 1.2.2.4 --- Gastrointestinal tract and vagus nerves --- p.17 / Chapter 1.2.2.5 --- Neurotransmitter receptors --- p.18 / Chapter 1.3 --- Chemotherapy-Induced Emesis --- p.19 / Chapter 1.3.1 --- Cancer as a cause of mortality in Man --- p.20 / Chapter 1.3.2 --- Chemotherapeutic Agents --- p.20 / Chapter 1.3.2.1 --- Different classes --- p.20 / Chapter 1.3.2.2 --- Emetogenic potential --- p.21 / Chapter 1.3.3 --- Cisplatin-Induced Emesis --- p.23 / Chapter 1.3.3.1 --- Unfavourable effects associated with chemotherapy-induced nausea and emesis --- p.24 / Chapter 1.3.3.2 --- Anticipatory nausea and vomiting --- p.24 / Chapter 1.3.3.3 --- Profile of cisplatin-induced emesis --- p.25 / Chapter 1.3.4 --- Animal Models of Cisplatin-Induced Acute and Delayed Emesis --- p.26 / Chapter 1.3.5 --- Mechanisms and Pathways Involves in Chemotherapy-Induced Emesis --- p.28 / Chapter 1.3.6 --- Anti-Emetic Drugs for the Treatment of Chemotherapy-Induced Emesis --- p.31 / Chapter 1.3.6.1 --- 5-HT3 receptor antagonists --- p.31 / Chapter 1.3.6.2 --- Dopamine receptor antagonists --- p.33 / Chapter 1.3.6.3 --- Benzodiazepines --- p.35 / Chapter 1.3.6.4 --- Cannabinoids --- p.35 / Chapter 1.3.6.5 --- Antihistamines and anticholinergics --- p.35 / Chapter 1.3.6.6 --- NK1 receptor antagonists --- p.37 / Chapter 1.3.6.7 --- Corticosteroids --- p.38 / Chapter 1.3.6.8 --- Multi-agent anti-emetic regimens --- p.39 / Chapter 1.4 --- Motion-Induced Emesis --- p.41 / Chapter 1.4.1 --- Incidence --- p.42 / Chapter 1.4.2 --- Mechanisms and Pathways Involved in Motion Sickness --- p.43 / Chapter 1.4.2.1 --- Importance of the vestibular apparatus --- p.44 / Chapter 1.4.2.2 --- Importance of the area postrema --- p.45 / Chapter 1.4.2.3 --- The nucleus tractus solitarius --- p.46 / Chapter 1.4.2.4 --- Hormone and neurotransmitters --- p.46 / Chapter 1.4.3 --- Animal models in Motion-Induced Emesis --- p.47 / Chapter 1.4.4 --- Anti-Emetic Drugs for the Treatment of Motion Sickness --- p.48 / Chapter 1.4.4.1 --- Anticholinergics --- p.49 / Chapter 1.4.4.2 --- Antihistamines --- p.49 / Chapter 1.4.4.3 --- Non-selective muscarinic and histamine receptor antagonists --- p.51 / Chapter 1.4.4.4 --- Sympathomimetics --- p.51 / Chapter 1.4.4.5 --- NK1i receptor antagonists --- p.51 / Chapter 1.4.4.6 --- 5-HT1A agonists --- p.52 / Chapter 1.4.4.7 --- 5-HT2 receptor agonist --- p.52 / Chapter 1.4.4.8 --- Arginine vasopressin (AVP) antagonists --- p.53 / Chapter 1.4.4.9 --- Opioid receptor agonists --- p.53 / Chapter 1.4.4.10 --- Dexamethasone and hormone levels --- p.54 / Chapter 1.4.4.11 --- Other anti-emetic drugs --- p.55 / Chapter 1.5 --- Aims of the Studies --- p.56 / Chapter 2 --- Methods --- p.59 / Chapter 2.1 --- Cisplatin-Induced Emesis Studies --- p.60 / Chapter 2.1.1 --- Animals --- p.60 / Chapter 2.1.2 --- Induction and Measurement of Emesis --- p.60 / Chapter 2.1.3 --- The Effects of Corticosteroids on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.63 / Chapter 2.1.4 --- "The Effects of Dexamethasone (1 mg/kg, i.p.) Administered as an Intervention Treatment on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.63 / Chapter 2.1.5 --- The Effects of Cortrosyn Depot (Tetracosactrin) on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.63 / Chapter 2.1.6 --- The Effects of Metyrapone on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.64 / Chapter 2.1.7 --- The Effects of Indomethacin on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.64 / Chapter 2.1.8 --- "The Effects of DFU and L-745,337 Administered as an Intervention Treatments on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.64 / Chapter 2.1.9 --- "The Effects of MK-886 (L-663,536) on Cisplatin-Induced Acute and Delayed Retching and Vomiting" --- p.65 / Chapter 2.1.10 --- The Effects of a Combination of Indomethacin and MK-886 on Cisplatin- Induced Acute and Delayed Retching and Vomiting --- p.65 / Chapter 2.1.11 --- Statistical Analysis --- p.66 / Chapter 2.2 --- Motion-Induced Emesis Studies --- p.67 / Chapter 2.2.1 --- Animals --- p.67 / Chapter 2.2.2 --- Measurement of Emesis --- p.67 / Chapter 2.2.3 --- Induction of Emesis in Motion-Naive Suncus murinus: Effects of Glucocorticoids --- p.68 / Chapter 2.2.4 --- Induction of Emesis in Motion-Sensitive Suncus murinus: Effects of Dexamethasone --- p.70 / Chapter 2.2.5 --- Preparation of Serum --- p.72 / Chapter 2.2.6 --- Measurement of Serum Cortisol by Enzyme-Linked Immunoassay (ELISA) --- p.72 / Chapter 2.2.6.1 --- Immunoassay kit --- p.72 / Chapter 2.2.6.2 --- Assay procedures --- p.73 / Chapter 2.2.7 --- Measurement of Serum Adrenocorticotrophin (ACTH) by Radioimmunoassay (RIA) --- p.75 / Chapter 2.2.7.1 --- Immunoassay kit --- p.75 / Chapter 2.2.7.2 --- Assay procedures --- p.76 / Chapter 2.2.8 --- Statistical Analysis --- p.79 / Chapter 3 --- Results --- p.81 / Chapter 3.1 --- Cisplatin-Induced Emesis --- p.82 / Chapter 3.1.1 --- General Profile of Emesis Induced by Cisplatin --- p.82 / Chapter 3.1.2 --- Antagonism of Cisplatin-Induced Emesis by Corticosteroids --- p.82 / Chapter 3.1.3 --- "The Effect of Dexamethasone (1 mg/kg, i.p.) Administered as an Intervention Treatment on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.84 / Chapter 3.1.4 --- The Effect of Cortrosyn Depot (Tetracosactrin) on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.85 / Chapter 3.1.5 --- The Effect of Metyrapone on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.85 / Chapter 3.1.6 --- "The Effect of Indomethacin, DFU and L-745,337 on Cisplatin-Induced Acute and Delayed Retching and Vomiting" --- p.86 / Chapter 3.1.7 --- The Effect of MK-886 on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.88 / Chapter 3.1.8 --- The Effect of Combination of Indomethacin and MK-886 on Cisplatin- Induced Acute and Delayed Retching and Vomiting --- p.89 / Chapter 3.2 --- Motion-Induced Emesis --- p.91 / Chapter 3.2.1 --- General Effect of Motion on Serum Cortisol and ACTH Levelsin Motion Naive Suncus murinus --- p.91 / Chapter 3.2.2 --- The Effect of Glucocorticoids on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion-Naive Male Suncus murinus --- p.92 / Chapter 3.2.2.1 --- Effect of dexamethasone --- p.92 / Chapter 3.2.2.2 --- Effect of betamethasone --- p.93 / Chapter 3.2.2.3 --- Effect of methylprednisolone --- p.93 / Chapter 3.2.3 --- The Effect of Glucocorticoids on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion Naive Female Suncus murinus --- p.94 / Chapter 3.2.3.1 --- Effect of dexamethasone --- p.94 / Chapter 3.2.3.2 --- Effect of betamethasone --- p.95 / Chapter 3.2.3.3 --- Effect of methylprednisolone --- p.95 / Chapter 3.2.4 --- The Effect of Dexamethasone on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion-Sensitive Suncus murinus --- p.96 / Chapter 3.2.4.1 --- Effect of dexamethasone on male motion-sensitive animals --- p.97 / Chapter 3.2.4.2 --- Effect of dexamethasone on female motion-sensitive animals --- p.97 / Chapter 4 --- Discussion --- p.131 / Chapter 4.1 --- "Cisplatin (5 mg/kg, i.p.)-Induced Emesis in Control Animals" --- p.132 / Chapter 4.2 --- Anti-Emetic Action of Corticosteroids in the Ferret --- p.133 / Chapter 4.3 --- Metyrapone Study --- p.138 / Chapter 4.4 --- Cortrosyn Depot Study --- p.139 / Chapter 4.5 --- Role of Cycloxygenase --- p.141 / Chapter 4.6 --- Role of 5-Lipoxygenase --- p.143 / Chapter 4.7 --- Duel Inhibition of Cycloxygenase and 5-Lipoxygenase --- p.144 / Chapter 4.8 --- Anti-Emetic Potential of Glucocorticoids in Suncus murinus --- p.145 / Chapter 4.9 --- General Summary --- p.149 / Appendix I --- p.152 / Appendix II --- p.154 / References --- p.156
174

Studies on antiulcer effects of Hippophae rhamnoides.

January 1999 (has links)
Song Jing-mei. / Thesis submitted in: December 1998. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 141-156). / Abstract also in Chinese. / Title page --- p.i / Acknowledgments --- p.ii / Table of contents --- p.iii / Abbreviations --- p.viii / Abstract --- p.x / 摘要 --- p.xii / Chapter Chapter1 --- Introduction --- p.1 / Chapter Chapter2 --- Evaluation of Antiulcer Effect Exhibited by Hippophae rhamnoides Using Different Ulcer Models / Chapter 2.1 --- Introduction --- p.20 / Chapter 2.1.1 --- Ethanol-induced gastric lesions --- p.24 / Chapter 2.1.2 --- NSAID-induced gastric lesions --- p.24 / Chapter 2.1.3 --- Stress-induced gastric lesions --- p.25 / Chapter 2.1.4 --- Pylorus ligation-induced gastric lesions --- p.25 / Chapter 2.1.5 --- Acetic acid-induced chronic gastric ulcer --- p.26 / Chapter 2.1.6 --- Necrotizing agent-induced lesion model --- p.27 / Chapter 2.2 --- Materials and Methods / Chapter 2.2.1 --- Plant materials --- p.28 / Chapter 2.2.2 --- Identification of the plant --- p.28 / Chapter 2.2.3 --- Preparation of crude extract for animal studies --- p.28 / Chapter 2.2.4 --- Experimental animals --- p.31 / Chapter 2.2.5 --- Ethanol-induced gastric mucosal lesions --- p.31 / Chapter 2.2.6 --- Acidified aspirin-induced gastric lesions --- p.32 / Chapter 2.2.7 --- Water immersion plus restraint-induced stress lesion model --- p.32 / Chapter 2.2.8 --- Pylorus ligation-induced gastric lesions --- p.32 / Chapter 2.2.9 --- Acetic acid-induced chronic gastric ulcer --- p.34 / Chapter 2.2.10 --- Necrotizing agent-induced gastric lesions --- p.34 / Chapter 2.2.11 --- Test of acute toxicity of Hippophae --- p.35 / Chapter 2.2.12 --- Statistical analysis --- p.35 / Chapter 2.3 --- Results / Chapter 2.3.1 --- Effect of Hr extract on ethanol-induced gastric lesions --- p.36 / Chapter 2.3.2 --- Effect of Hr extract on aspirin-induced gastric damage --- p.39 / Chapter 2.3.3 --- Effect of Hr extract on stress-induced gastric lesions --- p.40 / Chapter 2.3.4 --- Effect of Hr extract on pylorus ligation-induced gastric injury --- p.43 / Chapter 2.3.5 --- Effect of Hr extract on acetic acid-induced chronic ulcer --- p.48 / Chapter 2.3.6 --- Effect of Hr extract on necrotizing agent-induced gastric damage --- p.54 / Chapter 2.3.7 --- Test of acute toxicity of Hr --- p.55 / Chapter 2.4 --- Discussion / Chapter 2.4.1 --- Cytoprotective effect of Hr against ethanol-induced lesions --- p.56 / Chapter 2.4.2 --- Preventive effect of Hr on NSAIDs-induced gastric lesions --- p.57 / Chapter 2.4.3 --- Inhibitory effect of Hr on stress-induced lesions --- p.58 / Chapter 2.4.4 --- Inhibitory effect of Hr extract on pylorus ligation-induced gastric lesions --- p.59 / Chapter 2.4.5 --- Healing effect of Hr extract on acetic acid-induced gastric ulcer --- p.60 / Chapter 2.4.6 --- Protective effect of Hr extract on necrotizing agent-induced gastric damage --- p.61 / Chapter 2.4.7 --- Summary --- p.61 / Chapter Chapter3 --- Study on Cytoprotective Effect of Hippophae rhamnoides on Ethanol-induced Gastric Damage / Chapter 3.1 --- Introduction --- p.63 / Chapter 3.2 --- Materials and Methods --- p.65 / Chapter 3.2.1 --- Chemicals and Instruments --- p.65 / Chapter 3.2.2 --- Test on effect of different concentrations of ethanol on gastric mucosa --- p.67 / Chapter 3.2.3 --- Examination of the gastric protective effect of Hr extract by different routes of administration --- p.68 / Chapter 3.2.4 --- Study on relationship between gastric protective effect of Hr extract and endogenous PGs --- p.68 / Chapter 3.2.5 --- Measurement of gastric mucosal blood flow (GMBF) --- p.69 / Chapter 3.2.6 --- Measurement of gastric secretion and acidity in gastric juice --- p.70 / Chapter 3.2.7 --- Measurement of gastric gastric emptying rate --- p.70 / Chapter 3.2.8 --- Measurement of pepsin content in gastric juice --- p.71 / Chapter 3.2.9 --- Measurement of protein content in gastric juice --- p.73 / Chapter 3.2.10 --- Measurement of mucus content on gastric wall --- p.75 / Chapter 3.2.11 --- Measurement of GSH content in gastric mucosa --- p.77 / Chapter 3.2.12 --- Measurement of PGE2 content in gastric mucosa --- p.79 / Chapter 3.2.13 --- Determination of protein content in gastric mucosa --- p.81 / Chapter 3.3 --- Results / Chapter 3.3.1 --- Test on gastric lesions induced by different concentrations of ethanol --- p.83 / Chapter 3.3.2 --- Effect of Hr extract on ethanol-induced gastric damage by different routes of administration --- p.83 / Chapter 3.3.3 --- Effect of Hr extract on GMBF and output of gastric acid --- p.85 / Chapter 3.3.4 --- Effect of Hr extract on gastric emptying rate --- p.87 / Chapter 3.3.5 --- Effect of Hr extract on gastric mucus --- p.88 / Chapter 3.3.6 --- Effect of Hr extract on gastric GSH content --- p.89 / Chapter 3.3.7 --- Influence of Hr extract on endogenous prostanglandin-E2 --- p.90 / Chapter 3.3.8 --- Antagonistic effect of indomethacin on the gastric protection of Hr extract --- p.91 / Chapter 3.4 --- Discussion / Chapter 3.4.1 --- Formation of gastric lesions induced by ethanol at different concentrations --- p.92 / Chapter 3.4.2 --- Different routes of administration --- p.92 / Chapter 3.4.3 --- "Role of GMBF, gastric acidity and acid output in the formation of gastric lesions" --- p.93 / Chapter 3.4.4 --- Effect of Hr extract on gastric motility --- p.95 / Chapter 3.4.5 --- Effect of Hr extract on gastric mucus --- p.96 / Chapter 3.4.6 --- Effect of Hr extract on gastric GSH content --- p.96 / Chapter 3.4.7 --- Effect of Hr extract on endogenous prostaglandins --- p.98 / Chapter 3.4.8 --- Summary --- p.99 / Chapter Chapter 4 --- Study on plant constituents of Hippophae rhamnoides / Chapter 4.1 --- Introduction --- p.100 / Chapter 4.2 --- Materials and Methods --- p.100 / Chapter 4.2.1 --- Plant Materials --- p.100 / Chapter 4.2.2 --- Plant Extraction --- p.101 / Chapter 4.2.3 --- Fractionation of hexane-extract by column chromatography --- p.103 / Chapter 4.2.4 --- Phytochemical identification and analyses of vitamin content in Hr extract --- p.104 / Chapter 4.2.4.1 --- Identification of vitamin A and vitamin C in the Hr extract by TLC --- p.104 / Chapter 4.2.4.2 --- Identification of α-tocopherol and γ-tocopherol by HPLC --- p.105 / Chapter 4.2.4.3 --- Analyses of the content of α-tocopherol in the Hr extract --- p.108 / Chapter 4.2.4.4 --- Identification and analysis of fatty acid in the Hr fractions --- p.111 / Chapter 4.2.4.4.1 --- Esterification of fatty acids --- p.111 / Chapter 4.2.4.4.2 --- Isolation and identification of FAME by GC-MS --- p.111 / Chapter 4.2.4.5 --- Quantitative analysis of composition and relative content of fatty acid in the Hr fractions --- p.112 / Chapter 4.3 --- Results / Chapter 4.3.1 --- Phytochemical analysis and identification --- p.114 / Chapter 4.3.1.1 --- Identification of vitamin A --- p.114 / Chapter 4.3.1.2 --- Identification of vitamin C --- p.115 / Chapter 4.3.1.3 --- Identification of α-tocopherol and γ-tocopherol --- p.116 / Chapter 4.3.1.4 --- Quantitative analysis of α-tocopherol content in the Hr extract --- p.117 / Chapter 4.3.1.5 --- Identification of fatty acid composition --- p.117 / Chapter 4.3.1.6 --- Analysis of relative content of fatty acids in the Hr extract --- p.122 / Chapter 4.3.1.7 --- Study on phytosterols of Hr --- p.124 / Chapter 4.3.2 --- Examination of antiulcer effect of Hr fractions against ethanol-induced gastric lesions --- p.124 / Chapter 4.3.2.1 --- Effect of different extracts of Hr seed on ethanol-induced gastric lesions --- p.125 / Chapter 4.3.2.2 --- Effect of fractions of hexane-extract of Hr on gastric lesions induced by ethanol --- p.126 / Chapter 4.3.2.3 --- Effect of Hr components on gastric lesions induced by different ulcer models --- p.127 / Chapter 4.3.2.3.1 --- Effect of Hr components on ethanol-induced lesions --- p.127 / Chapter 4.3.2.3.2 --- Effect of Hr components against stress-induced gastric lesions --- p.128 / Chapter 4.3.2.3.3 --- Effect of β-sitosterol against gastric lesions induced by pylorus ligation --- p.129 / Chapter 4.4 --- Discussion / Chapter 4.4.1 --- Role of fatty acids in the stomach protection --- p.130 / Chapter 4.4.2 --- Role of vitamins in the gastric protection --- p.133 / Chapter 4.4.3 --- Role of plant terpenoids in the stomach --- p.134 / Chapter 4.4.4 --- Summary --- p.135 / Chapter Chapter 5 --- General discussion --- p.136 / References --- p.141
175

Studies on the mechanisms and anti-tumor activities of green tea epicatechin isomers.

January 2000 (has links)
by Ip Wai-Ki. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 213-233). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABBREVIATIONS --- p.ii / ABSTRACT --- p.vi / 撮要 --- p.x / TABLE OF CONTENTS --- p.xiv / Chapter CHAPTER 1: --- GENERAL INTRODUCTION / Chapter 1.1 --- Hematopoiesis --- p.1 / Chapter 1.1.1 --- Introduction to Hematopoiesis --- p.1 / Chapter 1.1.2 --- Cytokines in Hematopoiesis --- p.4 / Chapter 1.2 --- Leukemia --- p.6 / Chapter 1.2.1 --- Leukemia: Abnormalities in Blood Cell Formation --- p.6 / Chapter 1.2.2 --- Classification of Leukemia --- p.8 / Chapter 1.2.3 --- The Causes and Molecular Basis of Leukemia --- p.8 / Chapter 1.2.4 --- Therapy of Leukemia --- p.11 / Chapter 1.2.5 --- Control of Leukemia by Hematopoietic Growth Factors and Other Compounds --- p.12 / Chapter 1.2.6 --- Molecular Control of Apoptosis and Cell Cycle in Leukemia --- p.13 / Chapter 1.2.6.1 --- Regulation of Cell Cycle and Apoptosis by Genes and Regulatory Proteins --- p.14 / Chapter 1.2.6.1.1 --- Cell Cycle --- p.14 / Chapter 1.2.6.1.2 --- Apoptosis --- p.15 / Chapter 1.2.6.2 --- Role of Apoptosis and Cell Cycle in the Development of Leukemia --- p.17 / Chapter 1.3 --- Green Tea --- p.19 / Chapter 1.3.1 --- Origin and Cultivation of Tea Plants --- p.19 / Chapter 1.3.2 --- Classification and Manufacturing of Tea --- p.21 / Chapter 1.3.3 --- The Chemistry of Tea --- p.22 / Chapter 1.3.3.1 --- Chemical Composition of Tea --- p.22 / Chapter 1.3.3.2 --- Separation and Purification of Green Tea Polyphenols --- p.27 / Chapter 1.3.3.3 --- The Chemical Properties of Green Tea Polyphenols --- p.28 / Chapter 1.3.4 --- Bioavailability and Pharmacokinetic of Green Tea Epicatechins --- p.28 / Chapter 1.3.4.1 --- Human Studies --- p.29 / Chapter 1.3.4.2 --- Animal Studies --- p.30 / Chapter 1.3.5 --- Physiological and Pharmacological Activities of Green Tea Catechins --- p.31 / Chapter 1.3.5.1 --- Anti-oxidative Activity --- p.32 / Chapter 1.3.5.2 --- Hypocholesterolemic and Hypolipidemic Activity --- p.33 / Chapter 1.3.5.3 --- Anti-inflammatory Activity --- p.34 / Chapter 1.3.5.4 --- Anti-microbial Activity --- p.35 / Chapter 1.3.5.5 --- Anti-mutagenic Activity --- p.36 / Chapter 1.3.5.6 --- Anti-carcinogenesis --- p.37 / Chapter 1.3.5.7 --- Direct Anti-tumor Activity --- p.41 / Chapter 1.3.5.8 --- Modulating Activity in Endocrine System --- p.43 / Chapter 1.3.5.9 --- Other Biological Activities --- p.43 / Chapter 1.3.6 --- Possible Anti-cancer Mechanisms of Green Tea Epicatechins --- p.44 / Chapter 1.3.6.1 --- Modulation of Anti-tumor Immunity --- p.44 / Chapter 1.3.6.2 --- Direct Growth Inhibition by Controlling the Signal Transduction Pathways --- p.45 / Chapter 1.3.6.3 --- Induction of Apoptosis and Cell Cycle Arrest --- p.46 / Chapter 1.3.6.4 --- Inhibition of Tumor Metastasis --- p.47 / Chapter 1.4 --- Aims and Scopes of This Investigation --- p.48 / Chapter CHAPTER 2: --- MATERIALS AND METHODS / Chapter 2.1 --- Materials --- p.50 / Chapter 2.1.1 --- Animals --- p.50 / Chapter 2.1.2 --- Cell Lines --- p.50 / Chapter 2.1.3 --- Sheep Red Blood Cells (SRBC) --- p.52 / Chapter 2.1.4 --- "Cell Culture Medium, Buffers and Reagents" --- p.52 / Chapter 2.1.5 --- Tea Extracts and Green Tea Epicatechins --- p.56 / Chapter 2.1.6 --- Recombinant Cytokines --- p.57 / Chapter 2.1.7 --- Vitamin Analogs --- p.59 / Chapter 2.1.8 --- Taxol (Baccatin III N-benzoyl-β-phenyllisoserine ester) --- p.59 / Chapter 2.1.9 --- 18β-Glycyrrhetinic Acid (18β-GA) --- p.60 / Chapter 2.1.10 --- [methyl-3H] Thymidine (3H-TdR) --- p.60 / Chapter 2.1.11 --- Liquid Scintillation Cocktail --- p.60 / Chapter 2.1.12 --- Reagents and Buffers for Flow Cytometery --- p.61 / Chapter 2.1.13 --- Reagents for DNA Extraction --- p.62 / Chapter 2.1.14 --- Reagents for Total RNA Isolation --- p.63 / Chapter 2.1.15 --- Reagents and Buffers for RT-PCR Study --- p.64 / Chapter 2.1.16 --- Reagents and Buffers for Gel Electrophoresis --- p.67 / Chapter 2.1.17 --- Reagents and Buffers for Western Blot Analysis --- p.68 / Chapter 2.2 --- Methods --- p.77 / Chapter 2.2.1 --- Culture of the Leukemic Cell Lines --- p.77 / Chapter 2.2.2 --- "Isolation, Preparation and Culture of Primary Mouse Cells" --- p.77 / Chapter 2.2.3 --- Determination of Cell Viability --- p.78 / Chapter 2.2.4 --- [3H]-TdR Incorporation Assay --- p.79 / Chapter 2.2.5 --- Cell Morphology Study --- p.79 / Chapter 2.2.6 --- Apoptosis Study --- p.80 / Chapter 2.2.7 --- Animal Studies --- p.81 / Chapter 2.2.8 --- Gene Expression Study --- p.82 / Chapter 2.2.9 --- Protein Expression Study --- p.85 / Chapter 2.2.10 --- Statistical Analysis --- p.88 / Chapter CHAPTER 3: --- THE ANTI-TUMOR ACTIVITIES OF TEA EXTRACTS AND PURIFIED GREEN TEA EPICATECHIN ISOMERS ON VARIOUS LEUKEMIC CELL LINES / Chapter 3.1 --- Introduction --- p.89 / Chapter 3.2 --- Results --- p.91 / Chapter 3.2.1 --- The Effects of Tea Extracts on Various Leukemia Cells --- p.91 / Chapter 3.2.1.1 --- Differential Anti-proliferative Effect of Different Tea Extracts on Various Leukemic Cell Lines In Vitro --- p.91 / Chapter 3.2.1.2 --- Differential Cytotoxic Effect of Different Tea Extracts on the Murine Lymphocytic Leukemia L1210 Cells In Vitro --- p.92 / Chapter 3.2.1.3 --- Induction of Apoptosis in HL-60 Cells by Different Tea Extracts In Vitro --- p.92 / Chapter 3.2.2 --- The Effects of Purified Green Tea Epicatechin Isomers on Various Leukemic Cell Lines --- p.101 / Chapter 3.2.2.1 --- In Vitro Anti-proliferative Effect of Green Tea Epicatechin Isomers on Various Human and Murine Leukemic Cell Lines --- p.101 / Chapter 3.2.2.2 --- In Vitro Cytotoxic Effect of Green Tea Epicatechin Isomers on Various Human and Murine Leukemic Cell Lines --- p.117 / Chapter 3.2.2.3 --- Effects of Green Tea Epicatechin Isomers on the Differentiation of Myeloid Leukemia Cells --- p.131 / Chapter 3.2.2.4 --- Apoptosis-Inducing Effect of Different Green Tea Epicatechin Isomers on HL-60 and JCS Cells --- p.134 / Chapter 3.2.2.5 --- Effect of EGCG on the In Vivo Tumorigenicity of Leukemia JCS and L1210 Cells --- p.142 / Chapter 3.3 --- Discussion --- p.144 / Chapter CHAPTER 4: --- MECHANISTIC STUDIES ON THE ANTI PROLIFERATIVE AND APOPTOSIS-INDUCING ACTIVITIES OF GREEN TEA EPICATECHIN ISOMERS ON LEUKEMIA CELLS / Chapter 4.1 --- Introduction --- p.149 / Chapter 4.2 --- Results --- p.152 / Chapter 4.2.1 --- Combining Effect of EGCG and Physiological Differentiation Inducers on the Proliferation of HL-60 and JCS Cells --- p.152 / Chapter 4.2.2 --- Combining Effect of EGCG and Cytokines on the Proliferation of JCS Cells --- p.155 / Chapter 4.2.3 --- Combining Effect ofEGCG and Other Phytochemicals on the Proliferation of HL-60 and JCS Cells --- p.161 / Chapter 4.2.4 --- Modulatory Effect of EGCG on the Expression of Apoptosis-regulatory Genes in HL-60 Cells --- p.168 / Chapter 4.2.5 --- Modulatory Effect of EGCG on the Expression of Growth-related and Apoptosis-regulatory Proteins in HL-60 Cells --- p.170 / Chapter 4.3 --- Discussion --- p.177 / Chapter CHAPTER 5: --- EFFECTS OF GREEN TEA EPICATECHIN ISOMERS ON THE GROWTH AND DIFFERENTIATION OF MURINE HEMATOPOIETIC CELLS / Chapter 5.1 --- Introduction --- p.184 / Chapter 5.2 --- Results --- p.186 / Chapter 5.2.1 --- In Vitro Effects of EGCG on Murine Lymphocytes --- p.186 / Chapter 5.2.1.1 --- In Vitro Effect of EGCG on the Proliferation of Murine Splenocytes --- p.186 / Chapter 5.2.1.2 --- In Vitro Effect of EGCG on the Mitogen-induced Proliferation of Murine Splenocytes --- p.186 / Chapter 5.2.1.3 --- Cytotoxic Effect of EGCG on Murine Lymphocytes --- p.189 / Chapter 5.2.2 --- Primary Humoral Immune Response to SRBCin EGCG-treated Mice --- p.191 / Chapter 5.2.3 --- In Vitro Studies of the Effects of EGCG on Murine Bone Marrow Cells --- p.192 / Chapter 5.2.3.1 --- Effects of EGCG on the In Vitro Proliferation of Murine Bone Marrow Cells --- p.192 / Chapter 5.2.3.2 --- The Combining Effect of EGCG and Growth Factors on the In Vitro Proliferation of Murine Bone Marrow Cells --- p.192 / Chapter 5.2.3.3 --- In Vitro Cytotoxic Effect of EGCG on Murine Bone Marrow Cells --- p.196 / Chapter 5.2.4 --- Effect of EGCG on the Differentiation of Murine Bone Marrow Cells --- p.199 / Chapter 5.2.5 --- Combining Effects of EGCG and Growth Factors on the Morphology of Murine Bone Marrow Cells --- p.199 / Chapter 5.3 --- Discussion --- p.204 / Chapter CHAPTER 6: --- CONCLUSIONS AND FUTURE PERSPECTIVES --- p.207 / REFERENCES --- p.213
176

Clinical application of adriamycin resistance screening and the in vitro effect of adriamycin on osteosarcoma cells.

January 1998 (has links)
by To Siu Hang. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 84-92). / Abstract also in Chinese. / Declaration --- p.i / Abstract --- p.ii / Acknowledgement --- p.vi / Abbreviations --- p.vii / List of Figures --- p.viii / List of Tables --- p.xii / Content --- p.xiv / Chapter 1. --- INTRODUCTION --- p.1 / Chapter 1.1. --- Osteosarcoma --- p.1 / Chapter 1.1.1. --- Incidence / Chapter 1.1.2. --- Age and Sex Distribution / Chapter 1.1.3. --- Clinical Features / Chapter 1.1.4. --- Treatment / Chapter 1.2. --- Adriamycin --- p.9 / Chapter 1.2.1. --- Drug Action / Chapter 1.2.2. --- Pharmacology / Chapter 1.3. --- Multidrug Resistance --- p.11 / Chapter 1.4. --- P-glycoprotein --- p.13 / Chapter 1.4.1. --- Nature / Chapter 1.4.2. --- Tissue Distribution / Chapter 1.4.3. --- Relation with MDR / Chapter 1.5 --- Multidrug Resistance Protein --- p.16 / Chapter 1.6. --- Reactive Oxygen Species --- p.17 / Chapter 1.6.1. --- Problems Arising from ROS / Chapter 1.6.2. --- Oxidative Stress and Diseases / Chapter 1.6.3. --- Defense System / Chapter 1.6.4. --- Antioxidative Enzymes / Chapter 1.6.5. --- Relation with MDR / Chapter 1.7. --- Topoisomerase II --- p.22 / Chapter 1.8. --- Methods to Detect MDR --- p.24 / Chapter 1.8.1. --- P-glycoprotein Immunohistochemistry / Chapter 1.8.2. --- Adriamycin Binding Assay / Chapter 1.9. --- Aims of Study --- p.25 / Chapter 2. --- MATERIALS AND METHODS --- p.27 / Chapter 2.1. --- Clinical Study --- p.27 / Chapter 2.1.1. --- Patients Recruitment / Chapter 2.1.2. --- Adriamycin Binding Assay / Chapter 2.1.3. --- P-glycoprotein Immunohistochemistry / Chapter 2.1.3.1. --- Sample and Control Preparation / Chapter 2.1.3.2. --- Immunohistochemical Procedure / Chapter 2.1.4. --- Tumour Necrosis Assessment / Chapter 2.2. --- Effect of Adriamycin on Osteosarcoma Cells --- p.32 / Chapter 2.2.1. --- Establishment of Adriamycin Adapted Osteosarcoma Cells / Chapter 2.2.1.1. --- Maintenance and Subculture of SaOS-2 Cell Line / Chapter 2.2.1.2. --- Storage of Cell Line / Chapter 2.2.1.3. --- Adriamycin Treatment / Chapter 2.2.2. --- KB-V1 Cell Culture / Chapter 2.2.3. --- Adriamycin Binding Assay / Chapter 2.2.4. --- P-glycoprotein Immunohistochemistry / Chapter 2.2.4.1. --- Sample and Control Preparation / Chapter 2.2.4.2. --- Immunohistochemical Procedures / Chapter 2.2.5. --- Thymidine Incorporation Assay / Chapter 2.2.5.1. --- Assay Procedures / Chapter 2.2.6. --- Catalase Assay / Chapter 2.2.6.1. --- Assay Procedures / Chapter 2.2.6.2. --- Unit Calculation / Chapter 2.2.7. --- Glutathione Peroxidase Assay / Chapter 2.2.7.1. --- Assay Procedures / Chapter 2.2.7.2. --- Unit Calculation / Chapter 2.2.8. --- Protein Determination / Chapter 2.3. --- Statistical Analysis --- p.45 / Chapter 3. --- RESULTS --- p.46 / Chapter 3.1. --- Clinical Study --- p.46 / Chapter 3.1.1. --- Patients Recruitment / Chapter 3.1.2. --- Correlation of Adriamycin Sensitivity to Tumour Necrosis / Chapter 3.1.3. --- Correlation of P-glycoprotein Expression to Tumour Necrosis / Chapter 3.1.4. --- Correlation of P-glycoprotein Expression to Adriamycin Sensitivity / Chapter 3.2. --- Effect of Adriamycin on Osteosarcoma Cells --- p.63 / Chapter 3.2.1. --- Adriamycin Sensitivity and P-glycoprotein Expression / Chapter 3.2.2. --- Thymidine Incorporation Rate / Chapter 3.2.3. --- Intracellular Concentration of Catalase / Chapter 3.2.4. --- Intracellular Concentration of Glutathione Peroxidase / Chapter 4. --- DISCUSSIONS --- p.71 / Chapter 4.1. --- Clinical Study --- p.71 / Chapter 4.1.1. --- Patients Recruitment / Chapter 4.1.2. --- Correlation between Adriamycin Sensitivity and Tumour Necrosis / Chapter 4.1.3. --- Correlation between P-glycoprotein Expression and Tumour Necrosis / Chapter 4.1.3.1. --- P-glycoprotein Is Induced During Chemotherapy / Chapter 4.1.3.2. --- P-glycoprotein Cannot Serve As a Prognostic Factor / Chapter 4.1.4. --- Correlation Between Adriamycin Sensitivity and P-glycoprotein Expression / Chapter 4.2. --- Effect of Adriamycin on Osteosarcoma Cells --- p.76 / Chapter 4.2.1. --- Adriamycin Sensitivity and P-glycoprotein Expression / Chapter 4.2.2. --- Proliferation Rate / Chapter 4.2.3. --- Antioxidative Enzymes Activities / Chapter 5. --- CONCLUSION --- p.82 / Chapter 6. --- FURTHER STUDY --- p.83 / Chapter 7. --- BIBLIOGRAPHY --- p.84 / Chapter 8. --- APPENDIX - SOLUTIONS PREPARATION --- p.93
177

Low density lipoprotein as a targeted carrier for anti-tumour drugs.

January 2001 (has links)
by Lo Hoi Ka Elka. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 172-181). / Abstracts in English and Chinese. / ABSTRACT --- p.i / 摘要 --- p.iv / LIST OF TABLES AND FIGURES --- p.viii / ABBREVIATIONS --- p.xiv / Chapter CHAPTER 1 : --- INTRODUCTION / Chapter 1.1. --- DIFFERENT TREATMENTS OF THE CANCER THERAPY --- p.1 / Chapter 1.2. --- THE SIDE EFFECTS OF CANCER TREATMENT / Chapter 1.2.1. --- Surgery --- p.1 / Chapter 1.2.2. --- Radiotherapy --- p.2 / Chapter 1.2.3. --- Chemotherapy --- p.2 / Chapter 1.3. --- THE CHARACTERISTICS OF DOXORUBICIN (DOX) / Chapter 1.3.1. --- The structure of Dox --- p.6 / Chapter 1.3.2. --- The actions of Dox --- p.8 / Chapter 1.3.3. --- The adverse side effect of Dox --- p.8 / Chapter 1.4. --- THE RATIONALE OF USING LOW DENSITY LIPOPROTEIN (LDL) AS A TARGET CARRIER IN CANCER THERAPY / Chapter 1.4.1. --- The correlation between cholesterol and cancer --- p.9 / Chapter 1.4.2. --- Low density lipoprotein (LDL) as a target carrier --- p.11 / Chapter 1.4.3. --- The down and up regulation of LDL receptors --- p.14 / Chapter 1.4.4. --- The characteristics of Fuctus Craegus (FC) --- p.15 / Chapter 1.5. --- DIFFERENT METHODS OF THE PREPARATION OF THE LOW DENSITY LIPOPROTEIN-DRUG (LDL- DRUG) --- p.18 / Chapter 1.6. --- THE CHARACTERISTICS OF LOW DENSITY LIPOPROTEIN (LDL) / Chapter 1.6.1. --- The structure of LDL --- p.20 / Chapter 1.6.2. --- The metabolic pathway of LDL in human bodies --- p.23 / Chapter 1.7. --- THE MULTIDRUGS RESISTANCE IN TUMOR CELLS --- p.25 / Chapter 1.7.1. --- The mechanism of multidrug resistance --- p.27 / Chapter 1.7.2. --- The structure of P-glycoprotein --- p.27 / Chapter 1.7.3. --- The mechanism of P-glycoprotein --- p.30 / Chapter 1.8. --- COMBINED TREATMENT WITH HYPERTHERMIA --- p.31 / Chapter 1.9. --- AIM OF THE STUDY --- p.33 / Chapter CHAPTER 2 : --- MATERIALS AND METHODS / Chapter 2.1. --- MATERIALS / Chapter 2.1.1. --- Animals --- p.34 / Chapter 2.1.2. --- Buffers --- p.34 / Chapter 2.1.3. --- Cell culture reagents --- p.36 / Chapter 2.1.4. --- Chemicals --- p.38 / Chapter 2.1.5. --- Culture of cells --- p.40 / Chapter 2.2. --- METHODS / Chapter 2.2.1. --- In vitro studies / Chapter 2.2.1.1. --- "LDL, doxorubicin complex formation" --- p.41 / Chapter 2.2.1.2. --- Determination of the concentration of LDL-Dox --- p.42 / Chapter 2.2.1.3. --- In vitro cytotoxicity --- p.43 / Chapter 2.2.1.4. --- The cytotoxicity of the combined treatment with anticancer drugs --- p.44 / Chapter 2.2.1.5. --- The preparation of Fructus Crataegus (FC) --- p.46 / Chapter 2.2.1.6. --- Western blot --- p.47 / Chapter 2.2.1.7. --- Flow cytometry --- p.49 / Chapter 2.2.1.8. --- Confocal laser scanning microscopy --- p.52 / Chapter 2.2.2. --- In vivo studies / Chapter 2.2.2.1. --- Subcutaneous injection of R-HepG2 cells in nude mouse --- p.55 / Chapter 2.2.2.2. --- Treatment schedules --- p.55 / Chapter 2.2.2.3. --- Assay of investigating of the myocardial injury --- p.56 / Chapter 2.2.2.4. --- Tissue preparation procedure for light microscope (LM) --- p.57 / Chapter 2.2.3. --- Statistical analysis in our research --- p.59 / Chapter CHAPTER 3 : --- RESULTS / Chapter 3.1. --- in vitro STUDIES / Chapter 3.1.1. --- The preparation of low density lipoprotein-doxorubicin (LDL-Dox) --- p.60 / Chapter 3.1.2. --- Studies on human hepatoma cells line (HepG2 cells) / Chapter 3.1.2.1. --- The comparison of Dox and LDL-Dox accumulated in HepG2 cells --- p.63 / Chapter 3.1.2.2. --- Confocal laser scanning microscopic (CLSM) studies on the accumulation of Dox and LDL-Dox in HepG2 cells --- p.65 / Chapter 3.1.2.3. --- The comparsion of the cytotoxicity of Dox and LDL-Dox on HepG2 cells --- p.67 / Chapter 3.1.2.4. --- The comparison of the cytotoxicty of Dox and LDL-Dox with and without hyperthermia on HepG2 cells --- p.73 / Chapter 3.1.2.5. --- The comparison of accumulation of Dox and LDL-Dox in HepG2 cells treated with and without combination of with hyperthermia --- p.77 / Chapter 3.1.2.6. --- Confocal laser scanning microscopic (CLSM) studies on the accumulation of Dox and LDL-Dox in HepG2 treated cells with and without hyperthermia --- p.80 / Chapter 3.1.2.7. --- Modulation of LDL receptors on HepG2 cells------Up- regulation of LDL receptors by Fructus Craegtus (FC) / Chapter 3.1.2.7.1. --- The comparsion of LDL receptor expression on HepG2 cells after Fructus Craegtus (FC) pre-treatment --- p.83 / Chapter 3.1.2.7.2. --- The comparison of accumulation of LDL-Dox accumulated in HepG2 cells pre-treated with and without Fructus Craegtus (FC) --- p.85 / Chapter 3.1.2.7.3. --- Confocal laser scanning microscopic (CLSM) studies on the accumulation of LDL-Doxin HepG2 cells after Fructus Craegtus (FC) pre- treatment --- p.88 / Chapter 3.1.2.7.4. --- Cytotoxicity of combined treatment with LDL-Dox and Fructus Craegtus (FC) --- p.91 / Chapter 3.1.3. --- Studies on multidrug human resistant hepatoma cell line (R-HepG2 cells) / Chapter 3.1.3.1. --- The overexpression level of P-glycoprotein in resistant cell line R-HepG2 --- p.93 / Chapter 3.1.3.2. --- The comparison of Dox and LDL-Dox accumulated in R- HepG2 cells --- p.95 / Chapter 3.1.3.3. --- Confocal laser scanning microscopic (CLSM) studies on the accumulation of Dox and LDL-Dox in R-HepG2 cells --- p.97 / Chapter 3.1.3.4. --- The comparsion of the cytotoxicity of Dox and LDL-Dox on R-HepG2 cells --- p.99 / Chapter 3.1.3.5. --- The comparison of the cytotoxicty of Dox and LDL-Dox with and without hyperthermia on R-HepG2 cells --- p.109 / Chapter 3.1.3.6. --- The comparison of the accumulation of Dox and LDL- Dox in R-HepG2 cells treated in combination with hyperthermia --- p.113 / Chapter 3.1.3.7. --- Confocal laser scanning microscopic (CLSM) studies on the accumulation of Dox and LDL-Dox in R-HepG2 cells with and without hyperthermia --- p.117 / Chapter 3.1.3.8. --- Modulation of LDL receptors on R-HepG2 cells ------ Up-regulation of LDL receptors by Fructus Craegtus (FC) / Chapter 3.1.3.8.1. --- The comparsion of LDL receptor expression on R-HepG2 cells after Fructus Craegtus (FC) pre-treatment --- p.120 / Chapter 3.1.3.8.2. --- The comparsion of the accumulation of LDL- Dox in R-HepG2 cells after Fructus Craegtus (FC) pre-treatment --- p.122 / Chapter 3.1.3.8.3. --- Confocal laser scanning microscopic (CLSM) studies in the accumulation of LDL-Dox by Fructus Craegtus pre-treatment in R-HepG2 cells --- p.125 / Chapter 3.1.3.8.4. --- The comparison of cytotoxicity of combined treatment with LDL-Dox and Fructus Craegtus (FC) in R-HepG2 cells --- p.128 / Chapter 3.2. --- in vivo STUDIES / Chapter 3.2.1. --- The comparison of Dox and LDL-Dox on reducing the tumor sizes and weight in nude mice bearing R-HepG2 cells / Chapter 3.2.1.1. --- The comparison of Dox and LDL-Dox on reducing the tumor size in nude mice bearing R-HepG2 cells --- p.130 / Chapter 3.2.1.2. --- The comparison of Dox and LDL-Dox on reducing the tumor weight in nude mice bearing R-HepG2 cells --- p.138 / Chapter 3.2.2. --- Myocardial injury measured by Lactate dehydrogenase (LDH) activity in nude mice bearing R-HepG2 cells treated with Dox and LDL-Dox --- p.140 / Chapter 3.2.3. --- Myocardial injury measured by Creatine kinase (CK) activity in nude mice bearing R-HepG2 cells treated with Dox and LDL-Dox --- p.143 / Chapter 3.2.4. --- Histological studies of heart of nude mice bearing R-HepG2 cells treated with Dox and LDL-Dox / Chapter 3.2.4.1. --- Heart section of nude mice --- p.146 / Chapter 3.2.4.2. --- Heart section of nude mice bearing R-HepG2 cells --- p.148 / Chapter 3.2.4.3. --- Heart section of lmg/kg Dox treated nude mice bearing R- HepG2 cells --- p.150 / Chapter 3.2.4.4. --- Heart section of 2mg/kg Dox treated nude mice bearing R- HepG2 cells --- p.152 / Chapter 3.2.4.5. --- Heart section of lmg/kg LDL-Dox treated nude mice bearing R-HepG2 cells --- p.154 / Chapter CHAPTER 4 --- : DISCUSSION / Chapter 4.1. --- in vitro STUDIES / Chapter 4.1.1. --- The cytotoxicity of Dox and LDL-Dox on HepG2 cells and R- HepG2 cells --- p.156 / Chapter 4.1.2. --- The combined treatment on HepG2 cells and R-HepG2 cells --- p.157 / Chapter 4.1.3. --- The modulation of LDL-R expression --- p.159 / Chapter 4.2. --- in vivo STUDIES --- p.162 / Chapter CHAPTER 5 --- : CONCLUSION / Chapter 5.1. --- CONCLUSION / Chapter 5.1.1. --- In vitro studies --- p.167 / Chapter 5.1.2. --- In vivo studies --- p.169 / Chapter 5.2. --- FUTURE PROSPECTIVE --- p.170 / REFERENCES --- p.172
178

The signaling pathway mediating the proliferative action of TNF-α in C6 glioma cells.

January 2001 (has links)
by Ho Wai Fong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 207-243). / Abstracts in English and Chinese. / Title --- p.i / Abstract --- p.ii / 摘要 --- p.v / Acknowledgements --- p.viii / Table of Contents --- p.x / List of Abbreviations --- p.xviii / List of Figures --- p.xxiv / List of Tables --- p.xxix / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Traumatic brain injury --- p.1 / Chapter 1.2 --- Ceils of the nervous system: glia --- p.1 / Chapter 1.2.1 --- Astroglia - / Chapter 1.2.1.1 --- Molecular markers of astroglia --- p.3 / Chapter 1.2.1.2 --- Functions of astroglia --- p.3 / Chapter 1.2.2 --- Oligodendrocyte --- p.5 / Chapter 1.2.2.1 --- Molecular markers of oligodendrocyte --- p.6 / Chapter 1.2.2.2 --- Functions of oligodendrocyte --- p.6 / Chapter 1.2.3 --- Microglia --- p.7 / Chapter 1.2.3.1 --- Molecular markers of microglia --- p.7 / Chapter 1.2.3.2 --- Functions of microglia --- p.8 / Chapter 1.3 --- Cytokine and brain injury --- p.8 / Chapter 1.4 --- Tumor necrosis factor alpha (TNF-α) --- p.9 / Chapter 1.5 --- TNF-α receptor --- p.10 / Chapter 1.6 --- Biological activities of TNF-α --- p.11 / Chapter 1.7 --- Signaling mechanism --- p.13 / Chapter 1.7.1 --- Protein kinase C --- p.13 / Chapter 1.7.2 --- Protein kinase A --- p.14 / Chapter 1.7.3 --- p38 mitogen-activated protein kinase (p38 MAPK) --- p.15 / Chapter 1.7.3.1 --- Biological activities of p38 MAPK --- p.18 / Chapter 1.7.4 --- Inducible nitric oxide synthase (iNOS) --- p.20 / Chapter 1.7.5 --- cAMP responsive element binding protein (CREB) --- p.21 / Chapter 1.7.6 --- Transcription factor c-fos --- p.23 / Chapter 1.7.7 --- Nuclear factor kappa-B (NF-kB) --- p.24 / Chapter 1.8 --- "Brain injury, astrogliosis and scar formation" --- p.26 / Chapter 1.9 --- β-adrenergic receptor (β-AR) --- p.28 / Chapter 1.9.1 --- Functions of β-AR in astrocytes --- p.29 / Chapter 1.10 --- Why do we use C6 glioma cell? --- p.31 / Chapter 1.11 --- Fluorescent differential display (FDD) --- p.34 / Chapter 1.12 --- Aims and Scopes of this project --- p.36 / Chapter Chapter 2 --- MATERIALS AND METHODS / Chapter 2.1 --- Material --- p.40 / Chapter 2.1.1 --- Cell line --- p.40 / Chapter 2.1.2 --- Cell culture reagents --- p.40 / Chapter 2.1.2.1 --- Complete Dulbecco's modified Eagle medium (CDMEM) --- p.40 / Chapter 2.1.2.2 --- Rosewell Park Memorial Institute (RPMI) medium --- p.41 / Chapter 2.1.2.3 --- Phosphate buffered saline (PBS) --- p.41 / Chapter 2.1.3 --- Recombinant cytokines --- p.41 / Chapter 2.1.4 --- Chemicals for signal transduction study --- p.42 / Chapter 2.1.4.1 --- Modulators of p38 mitogen-activated protein kinase (p38 MAPK) --- p.42 / Chapter 2.1.4.2 --- Modulators of protein kinase C (PKC) --- p.42 / Chapter 2.1.4.3 --- Modulators of protein kinase A (PKA) --- p.42 / Chapter 2.1.4.4 --- β-Adrenergic agonist and antagonist --- p.43 / Chapter 2.1.5 --- Antibodies --- p.44 / Chapter 2.1.5.1 --- Anti-p38 mitogen-activated protein kinase (p38 MAPK) antibody --- p.44 / Chapter 2.1.5.2 --- Anti-phosporylation p38 mitogen-activated protein kinase (p-p38 MAPK) antibody --- p.44 / Chapter 2.1.5.3 --- Antibody conjugates --- p.44 / Chapter 2.1.6 --- Reagents for RNA isolation --- p.45 / Chapter 2.1.7 --- Reagents for DNase I treatment --- p.45 / Chapter 2.1.8 --- Reagents for reverse transcription of mRNA and fluorescent PCR amplification --- p.45 / Chapter 2.1.9 --- Reagents for fluorescent differential display --- p.46 / Chapter 2.1.10 --- Materials for excision of differentially expressed cDNA fragments --- p.46 / Chapter 2.1.11 --- Reagents for reamplification of differentially expressed cDNA fragments --- p.46 / Chapter 2.1.12 --- Reagents for subcloning of reamplified cDNA fragments --- p.47 / Chapter 2.1.13 --- Reagents for purification of plasmid DNA from recombinant clones --- p.47 / Chapter 2.1.14 --- Reagents for DNA sequencing of differentially expressed cDNA fragments --- p.47 / Chapter 2.1.15 --- Reagents for reverse transcription-polymerase chain reaction (RT-PCR) --- p.48 / Chapter 2.1.16 --- Reagents for electrophoresis --- p.50 / Chapter 2.1.17 --- Reagents and buffers for Western blot --- p.50 / Chapter 2.1.18 --- Other chemicals and reagents --- p.50 / Chapter 2.2 --- Maintenance of rat C6 glioma cell line --- p.51 / Chapter 2.3 --- RNA isolation --- p.52 / Chapter 2.3.1 --- Measurement of RNA yield --- p.53 / Chapter 2.4 --- DNase I treatment --- p.53 / Chapter 2.5 --- Reverse transcription of mRNA and fluorescent PCR amplification --- p.54 / Chapter 2.6 --- Fluorescent differentia display --- p.55 / Chapter 2.7 --- Excision of differentially expressed cDNA fragments --- p.59 / Chapter 2.8 --- Reamplification of differentially expressed cDNA fragments --- p.59 / Chapter 2.9 --- Subcloning of reamplified cDNA fragments --- p.60 / Chapter 2.10 --- Purification of plasmid DNA from recombinant clones --- p.63 / Chapter 2.11 --- DNA sequencing of differentially expressed cDNA fragments --- p.64 / Chapter 2.12 --- Reverse transcription-polymerase chain reaction (RT-PCR) --- p.66 / Chapter 2.13 --- Western bolt analysis --- p.67 / Chapter Chapter 3 --- RESULTS / Chapter 3.1 --- DNase I treatment --- p.71 / Chapter 3.2 --- FDD RT-PCR and band excision --- p.71 / Chapter 3.3 --- Reamplification of excised cDNA fragments --- p.74 / Chapter 3.4 --- Subcloning of reamplified cDNA fragments --- p.77 / Chapter 3.5 --- DNA sequencing of subcloned cDNA fragments --- p.77 / Chapter 3.6 --- Confirmation of the differentially expressed cDNA fragments by RT-PCR and Western blotting --- p.84 / Chapter 3.6.1 --- Effects of TNF-α on p38a mitogen protein kinase (p38 α MAPK) --- p.84 / Chapter 3.6.2 --- Effects of TNF-α on p38 a MAPK and p-p38 α MAPK protein level --- p.86 / Chapter 3.7 --- Effects of TNF-α on p38 MAPK --- p.88 / Chapter 3.7.1 --- "Effects of TNF-α on p38 α, β,γ andδ MAPK" --- p.88 / Chapter 3.7.2 --- Role of TNF-receptor (TNF-R) subtype in the TNF-α-induced p3 8 MAPK expression in C6 cells --- p.89 / Chapter 3.7.3 --- The signaling system mediating TNF-α-induced p38 a MAPK expression in C6 cells --- p.92 / Chapter 3.7.3.1 --- The involvement of PKC in TNF-α-induced p38 MAPK expression in C6 cells --- p.92 / Chapter 3.7.3.2 --- The involvement of PKC in TNF-α-induced p38 MAPK expression in C6 cells --- p.98 / Chapter 3.7.4 --- The relationship between p38 MAPK and β-adrenergic mechanisms in C6 cells --- p.99 / Chapter 3.7.4.1 --- Effects of isoproterenol and propanol on p38 MAPK mRNA levels in C6 cells --- p.103 / Chapter 3.7.4.2 --- Effects of β1-agonist and -antagonist on p38 MAPK mRNA levels in C6 cells --- p.106 / Chapter 3.7.4.3 --- Effects of β2-agonist and -antagonist on p38 MAPK mRNA levels in C6 cells --- p.107 / Chapter 3.8 --- The relationship between p3 8 MAPK and inducible nitric oxide synthase (iNOS) expression --- p.113 / Chapter 3.8.1 --- Effects of TNF-α on the iNOS expression in C6 cells --- p.113 / Chapter 3.8.2 --- Role of TNF-receptors (TNF-R) subtypes in the TNF-α- induced iNOS expression in C6 cells --- p.115 / Chapter 3.8.3 --- The signaling system mediating TNF-α-induced iNOS expression in C6 cells --- p.115 / Chapter 3.8.3.1 --- The involvement of p38 MAPK in the TNF-α-induced iNOS expression in C6 cells --- p.117 / Chapter 3.8.3.2 --- The involvement of PKA in the TNF-α-induced iNOS expression in C6 cells --- p.119 / Chapter 3.9 --- The relationship between p38 MAPK and cAMP-responsive element binding protein (CREB) expression --- p.120 / Chapter 3.9.1 --- Effects of TNF-α on the CREB expression in C6 cells --- p.120 / Chapter 3.9.2 --- Role of TNF-receptors (TNF-R) subtypes in the TNF-α- induced CREB expression in C6 cells --- p.124 / Chapter 3.9.3 --- The signaling system mediating TNF-α-induced CREB expression in C6 cells --- p.126 / Chapter 3.9.3.1 --- The involvement of p38 MAPK in the TNF-α-induced CREB expression in C6 cells --- p.126 / Chapter 3.9.3.2 --- The involvement of PKC in the TNF-α-induced CREB expression in C6 cells --- p.128 / Chapter 3.9.3.3 --- The involvement of PKA in TNF-α-induced CREB expression in C6 cells --- p.129 / Chapter 3.9.4 --- The relationship between CREB and β-adrenergic mechanisms in C6 cells --- p.136 / Chapter 3.9.4.1 --- Effects of isoproterenol and propanol on CREB mRNA levels in C6 cells --- p.136 / Chapter 3.9.4.2 --- Effects of β1-agonist and -antagonist on CREB mRNA levels in C6 cells --- p.139 / Chapter 3.9.4.3 --- Effects of (32-agonist and -antagonist on CREB mRNA levels in C6 cells --- p.142 / Chapter 3.10 --- The relationship between p38 MAPK and transcription factor c-fos expression --- p.146 / Chapter 3.10.1 --- Effects of TNF-α on the c-fos expression in C6 cells --- p.146 / Chapter 3.10.2 --- Role of TNF-receptors (TNF-R) subtypes in the TNF-α- induced c-fos expression in C6 cells --- p.146 / Chapter 3.10.3 --- The signaling system mediating TNF-α-induced c-fos expression in C6 cells --- p.149 / Chapter 3.10.3.1 --- The involvement of p38 MAPK in the TNF-α-induced c-fos expression in C6 cells --- p.149 / Chapter 3.10.3.2 --- The involvement of PKC in the TNF-α-induced c-fos expression in C6 cells --- p.151 / Chapter 3.10.3.3 --- The involvement of PKA in TNF-α-induced c-fos expression in C6 cells --- p.154 / Chapter 3.10.4 --- The relationship between c-fos and β-adrenergic mechanisms in C6 cells --- p.157 / Chapter 3.10.4.1 --- Effects of isoproterenol and propanolol on c-fos mRNA levels in C6 cells --- p.157 / Chapter 3.10.4.2 --- Effects of β1-agonist and -antagonist on c-fos mRNA levels in C6 cells --- p.160 / Chapter 3.10.4.3 --- Effects of β2-agonist and -antagonist on c-fos mRNA levels in C6 cells --- p.164 / Chapter 3.11 --- The relationship between p38 MAPK and transcription factor NF-kB expression --- p.168 / Chapter 3.11.1 --- Effects of TNF-α on the NF-kB expression in C6 cells --- p.168 / Chapter 3.11.2 --- Role of TNF-receptors (TNF-R) subtypes in the TNF-α- induced NF-kB expression in C6 cells --- p.168 / Chapter 3.11.3 --- The signaling system mediating TNF-α-induced NF-kB expression in C6 cells --- p.171 / Chapter 3.11.3.1 --- The involvement of p38 MAPK in the TNF-α-induced NF-kB expression in C6 cells --- p.171 / Chapter 3.11.3.2 --- The involvement of PKC in the TNF-α-induced NF-kB expression in C6 cells --- p.173 / Chapter Chapter 4 --- DISCUSSION AND CONCLUSION / Chapter 4.1 --- Effects of tumor-necrosis factor-alpha (TNF-α) on C6 cell proliferations --- p.176 / Chapter 4.2 --- The Signaling System Involved in TNF-α-Induced p38 MAPK Expression in C6 cells --- p.178 / Chapter 4.3 --- The Signaling System Involved in TNF-α-Induced iNOS Expression in C6 cells --- p.184 / Chapter 4.4 --- The Signaling System Involved in TNF-α-Induced CREB Expression in C6 cells --- p.186 / Chapter 4.5 --- The Signaling System Involved in TNF-α-Induced c-fos Expressionin in C6 cells --- p.190 / Chapter 4.6 --- The Signaling System Involved in TNF-α-Induced NF-kB Expression in C6 cells --- p.193 / Chapter 4.7 --- Conclusions --- p.195 / Chapter 4.8 --- Possible application / References
179

Effect of antisense oligonucleotides against glucose transporters on CACO-2 colon adenocarcinoma cells.

January 2000 (has links)
by Lai Mei Yi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 130-136). / Abstracts in English and Chinese. / Acknowledgment --- p.i / Abstract --- p.ii / 論文撮耍 --- p.v / List of Figures --- p.viii / List of Tables --- p.xi / Abbreviations --- p.xii / Table of content --- p.xiii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Facilitative glucose transporters --- p.1 / Chapter 1.1.1 --- Predicted Secondary structure of Glutl --- p.1 / Chapter 1.1.2 --- The tissue-specific distribution of glucose transporters --- p.2 / Chapter 1.2 --- Increase of glucose uptake in cancer cells --- p.5 / Chapter 1.3 --- Antisense oligonucleotide therapeutics --- p.7 / Chapter 1.3.1 --- Chemical modifications of oligonucleotides --- p.7 / Chapter 1.3.2 --- Cellular Uptake of Oligonucleotide --- p.11 / Chapter 1.3.3 --- Mechanism of action --- p.13 / Antisense-mediated RNA Cleavage --- p.14 / """Occupancy-only"" mediated mechanism" --- p.15 / Chapter 1.3.4 --- Antisense treatment in vivo --- p.17 / Chapter 1.4.5 --- Human Studies of Antisense Treatment --- p.18 / Chapter Chapter 2 --- Materials & Methods --- p.20 / Chapter 2.1 --- Materials --- p.20 / Chapter 2.2 --- Cell Culture --- p.21 / Chapter 2.2.1 --- Human colon adenocarcinoma cell Line (Caco-2) --- p.21 / Chapter 2.3 --- General Methodology for treatment of cells with antisense oligonucleotides --- p.22 / Chapter 2.3.1 --- Treatment of cells with oligonucleotides --- p.22 / Chapter 2.4 --- Cytotoxicity Assay --- p.23 / Chapter 2.4.1 --- MTT assay --- p.23 / Chapter 2.4.2 --- 3H-thymidine incorporation --- p.23 / Chapter 2.5 --- RNA extraction --- p.24 / Chapter 2.6 --- Competitive Reverse-transcription polymerase chain reaction (RT-PCR) of glucose transporters --- p.25 / Chapter 2.7 --- Measurement of 2-deoxy-D-glucose and Fructose transport --- p.27 / Chapter 2.8 --- Western blotting --- p.28 / Chapter 2.9 --- Flow cytometry --- p.30 / Chapter 2.9.1 --- Measurement of cellular accumulation of fluorophore-labeled oligonucleotide --- p.30 / Chapter 2.10 --- Design of antisense oligonucleotide --- p.31 / Chapter 2.11 --- ATP assay --- p.34 / Chapter 2.12 --- Animals studies --- p.35 / Chapter Chapter 3 --- Optimization of phosphorothioate antisense oligonucleotide delivery by Lipofectin --- p.36 / Chapter 3.1 --- Introduction --- p.36 / Chapter 3.2 --- Measurement of oligonucleotide uptake --- p.38 / Chapter 3.2.1 --- Lipofectin as a delivery system for the oligonucleotide uptake --- p.39 / Chapter 3.2.2 --- Effect of Lipofectin ratio on the oligonucleotide uptake --- p.41 / Chapter 3.2.3 --- Effect of oligonucleotide concentration on the oligonucleotide uptake --- p.41 / Chapter 3.2.4 --- Effect of incubation time on the oligonucleotide uptake --- p.44 / Chapter 3.2.5 --- Effect of oligonucleotide length on cellular uptake --- p.44 / Chapter 3.3 --- Effect of Lipofectin on cell viability --- p.47 / Chapter Chapter 4 --- In vitro effect of Antisense Oligonucleotides against glucose transporters on Caco-2 Cell --- p.49 / Chapter 4.1 --- Introduction --- p.49 / Chapter 4.2 --- Design of Antisense Oligonucleotides against Glucose Transporters gene --- p.50 / Chapter 4.3. --- Antisense effect of different regions of antisense oligonucleotide --- p.52 / Chapter 4.4 --- Antisense and Sense effect of oligonucleotide against start codon (G5 7015) on Caco-2 cells --- p.59 / Chapter 4.4.1 --- Effect of oligonucleotide to Lipofectin ratio on cell viability --- p.59 / Chapter 4.4.2 --- Dose-Response Study: effect of concentration of antisense - oligonucleotide on cell viability --- p.61 / Chapter 4.4.3 --- Effect of length´ؤof oligonucleotide on cell viability --- p.61 / Chapter 4.4.4 --- Time-Response Study: effect of antisense oligonucleotide on cell viability --- p.66 / Chapter 4.5 --- "The effect of antisense oligonucleotide against Glut1, Glut3 and Glut5 on cell viability of Caco-2 cells" --- p.70 / Chapter 4.6 --- Analysis of ATP content in Caco-2 cells by using antisense oligonucleotide flanking start codon (G5 7015) --- p.72 / Chapter 4.7 --- Effect of G5 7015 on HepG2 cells --- p.72 / Chapter Chapter 5 --- Effect of antisense oligonucleotides against Glut5 on mRNA and Protein levels of Glut5 gene --- p.76 / Chapter 5.1 --- Introduction --- p.76 / Chapter 5.2 --- RT-PCR of Glut isoform in Caco-2 cells --- p.77 / Chapter 5.3 --- Effect of antisense oligonucleotides against Glut 5 on mRNA level in Caco-2 cells --- p.77 / Chapter 5.3.1 --- Effect of oligonucleotides targeted different region of Glut5 gene on Glut5 message level --- p.77 / Chapter 5.3.2 --- Reduction in expression of mRNA level of Glut5 by using antisense oligonucleotides targeting start codon (G5 7015) --- p.81 / Chapter 5.3.3 --- Study of the dose and time dependence on inhibition of mRNA expression in G5 7015 treated Caco-2 cells --- p.83 / Chapter 5.3.4 --- Cross-Inhibition of antisense targeting glucose transporter isoforms --- p.83 / Chapter 5.4 --- Reduction in Glut5 protein level using G5 7015 antisense oligonucleotide --- p.86 / Chapter 5.5 --- Inhibition of Glut5 activity using G57015 oligonucleotide --- p.88 / Chapter 5.6 --- Inhibition of Glut5 mRNA level in vivo --- p.93 / Chapter Chapter 6 --- The possible role for Glucose Transporters in the Modification of Multidrug Resistance in Tumor cells --- p.95 / Chapter 6.1 --- Introduction --- p.95 / Chapter 6.2 --- Materials & Methods --- p.97 / Chapter 6.2.1 --- Cell culture --- p.97 / Chapter 6.2.2 --- Chemicals --- p.98 / Chapter 6.2.3 --- Measurement of doxorubicin uptake --- p.99 / Chapter 6.3 --- The expression of P-glycoprotein and Doxorubicin resistance of R-HepG2 cells --- p.99 / Chapter 6.4 --- Comparison of H3-2-deoxyglucose uptake between HepG2 and R-HepG2 cells --- p.99 / Chapter 6.5 --- Quantification of Glut1 and Glut3 expression by RT-PCR --- p.102 / Chapter 6.6 --- Comparison of doxorubicin between HepG2 and R-HepG2 cells cultured accumulation in glucose free medium --- p.104 / Chapter 6.7 --- The time course of doxorubicin accumulation in R-HepG2 cells culturing in glucose free medium --- p.106 / Chapter 6.8 --- "Cell viability of R-HepG2 cells after treatment of glucose transporter inhibitors, phloretin (PT), cytochalasin B (CB) and mitochondrial inhibitor,2,4-Dinitrophenol (DNP)" --- p.106 / Chapter 6.9 --- "Effect of glucose transporter inhibitors (PT, CB) and mitochondrial inhibitor (DNP) on doxorubicin accumulationin R-HepG2" --- p.110 / Chapter 6.10 --- Effect of antisense oligonucleotide against Glutl on doxorubicin accumulation in R-HepG2 cell --- p.113 / Chapter 6.11 --- "Analysis of ATP content and 3H-2-deoxy-D-glucose uptakein R-HepG2 after treatments of PT, CB and DNP" --- p.115 / Chapter Chapter 7 --- Discussion --- p.117 / Chapter 7.1 --- Antisense oligonucleotide against glucose transportersin Caco-2 cell --- p.117 / Chapter 7.2 --- Cellular uptake of oligonucleotide --- p.119 / Chapter 7.3 --- In vitro study of using antisense oligonucleotide against Glut5 --- p.121 / Chapter 7.4 --- In vivo study of using antisense oligonucleotide against Glut5 --- p.126 / Chapter 7.5 --- Possible role of inhibition of glucose transport in reversing P- gp --- p.127 / Chapter Chapter 8 --- References --- p.130
180

The anti-tumor effects of arsenic trioxide on human breast adenocarcinoma cell line, MCF-7.

January 2002 (has links)
by Chow Ka Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 203-221). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Abstract in Chinese --- p.iv / List of Abbreviations --- p.vi / Table of Contents --- p.xi / List of Figures --- p.xviii / List of Tables --- p.xxii / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- The Characteristics of Arsenic Trioxide (AS2O3) --- p.2 / Chapter 1.2 --- The Therapeutic Applications of Arsenic Trioxide (As203) --- p.5 / Chapter 1.3 --- Acute Promyelocytic Leukemia (APL) --- p.6 / Chapter 1.3.1 --- Pathologies of APL --- p.7 / Chapter 1.3.2 --- All Trans Retinoic Acid (ATRA) Treatment of APL Patients --- p.7 / Chapter 1.3.3 --- Clinical Trials of Arsenic Trioxide (As203) on APL Patients --- p.9 / Chapter 1.3.4 --- In Vitro and In Vivo Studies of Arsenic Trioxide (As203) in the Treatment of APL --- p.10 / Chapter 1.3.4.1 --- Induction of Apoptosis --- p.11 / Chapter 1.3.4.2 --- Induction of Cell Differentiation --- p.11 / Chapter 1.3.5 --- General Toxicity and Side Effects of Arsenic Trioxide (AS2O3) on APL Patients --- p.12 / Chapter 1.4 --- Effects of Arsenic Trioxide (As203) on Other Primary Cancer Cells and Cancer Cell Lines --- p.12 / Chapter 1.5 --- Epidemiology of Breast Cancer --- p.14 / Chapter 1.6 --- Classification of Breast Cancer --- p.17 / Chapter 1.7 --- Etiology of Breast Cancer --- p.17 / Chapter 1.8 --- Hormones and Breast Cancer --- p.18 / Chapter 1.9 --- Estrogen Receptors (ER) --- p.20 / Chapter 1.9.1 --- Structures of Estrogen Receptors (ER) --- p.21 / Chapter 1.9.2 --- Estrogen Receptors (ER) Mediated Signaling Pathway --- p.22 / Chapter 1.9.2.1 --- Ligand Dependent Pathway --- p.22 / Chapter 1.9.2.2 --- Ligand Independent Pathway --- p.22 / Chapter 1.9.2.3 --- Estrogen Response Element (ERE)-Independent Pathway --- p.23 / Chapter 1.9.2.4 --- Non-Genomic Pathway --- p.23 / Chapter 1.9.3 --- Estrogen Receptors (ER) Regulated Gene Expression --- p.25 / Chapter 1.10 --- Current Therapy of Breast Cancer --- p.26 / Chapter 1.10.1 --- Hormonal Therapy (Anti-Estrogenicity) --- p.26 / Chapter 1.10.1.1 --- Tamoxifen --- p.26 / Chapter 1.10.1.2 --- Other Pure Anti-Estrogens --- p.28 / Chapter 1.10.2 --- Regulation of Estrogen Receptors (ER) and Transcription Coregulators --- p.29 / Chapter 1.10.3 --- Apoptosis Induction --- p.29 / Chapter 1.11 --- Aims of Study --- p.30 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.32 / Chapter 2.1 --- Materials --- p.33 / Chapter 2.1.1 --- Cell Lines and Culture Media --- p.33 / Chapter 2.1.1.1 --- Cell Lines --- p.33 / Chapter 2.1.1.2 --- Culture Media --- p.34 / Chapter 2.1.2 --- Chemicals --- p.35 / Chapter 2.1.3 --- Reagents and Buffers --- p.36 / Chapter 2.1.3.1 --- Reagents for MTT Assay --- p.36 / Chapter 2.1.3.2 --- Reagents for [methyl-3H] Thymidine Incorporation into DNA --- p.37 / Chapter 2.1.3.3 --- Reagents for Trypan Blue Exclusion Assay --- p.37 / Chapter 2.1.3.4 --- Reagents and Buffers for Western Blot Analysis --- p.37 / Chapter 2.1.3.5 --- Reagents and Buffers for Flow Cytometry --- p.40 / Chapter 2.1.3.6 --- Reagents and Buffers Reverse Transcription Polymerase Chain Reaction (RT-PCR) --- p.40 / Chapter 2.1.3.7 --- Reagents for Transfection and Luciferase Reporter Assay --- p.41 / Chapter 2.1.3.8 --- Reagents and Buffers for In Vivo Studies --- p.42 / Chapter 2.2 --- Methods --- p.42 / Chapter 2.2.1 --- In Vitro Studies --- p.42 / Chapter 2.2.1.1 --- Cell Treatment --- p.42 / Chapter 2.2.1.2 --- Drug Preparation --- p.43 / Chapter 2.2.1.3 --- MTT Assay --- p.43 / Chapter 2.2.14 --- Trypan Blue Exclusion Assay --- p.44 / Chapter 2.2.1.5 --- [methyl-3H] Thymidine Incorporation into DNA --- p.45 / Chapter 2.2.1.6 --- Detection of DNA Fragmentation --- p.45 / Chapter 2.2.1.7 --- ERα Competitive Binding Assay --- p.47 / Chapter 2.2.1.8 --- Cell Cycle Analysis by Flow Cytometry with Propidium Iodide (PI) Staining --- p.48 / Chapter 2.2.1.9 --- Cell Cycle Analysis by Flow Cytometry with Annexin V-PI Staining --- p.48 / Chapter 2.2.1.10 --- Cell Cycle Analysis by Flow Cytometry with JC-1 Staining --- p.49 / Chapter 2.2.1.11 --- Cell Cycle Analysis by Flow Cytometry with Hydroethidine (HE) Staining --- p.50 / Chapter 2.2.1.12 --- Western Blot Analysis of Proteins --- p.50 / Chapter 2.2.1.13 --- Assessment of the Transcriptional Activity of ERα --- p.55 / Chapter 3.2.1.14 --- Reverse Transcription Polymerase Chain Reaction (RT-PCR) --- p.57 / Chapter 2.2.2 --- In Vivo Studies --- p.61 / Chapter 2.2.2.1 --- Animal Models --- p.61 / Chapter 2.2.2.2 --- Treatment Schedules --- p.61 / Chapter 2.2.2.3 --- Sacrifice of Nude Mice --- p.61 / Chapter 2.2.2.4 --- Enzymatic Assays --- p.62 / Chapter 2.2.2.4.1 --- Aspartate Transaminase (AST) --- p.63 / Chapter 2.2.2.4.2 --- Alanine Transaminase (ALT) --- p.64 / Chapter 2.2.2.4.3 --- Creatine Kinase (CK) --- p.65 / Chapter 2.2.2.4.4 --- Lactate Dehydrogenase (LDH) --- p.66 / Chapter CHAPTER 3 --- "Effects of Arsenic Trioxide (As203) on Human Breast Adenocarcinoma Cell Line, MCF-7 Cell Line" --- p.68 / Chapter 3.1 --- Introduction --- p.69 / Chapter 3.2 --- Effect of As203 on Cell Survival of MCF-7 cells by MTT Assay --- p.70 / Chapter 3.3 --- Cytotoxicity of As203 on MCF-7 Cells by Trypan Blue Exclusion Assay --- p.72 / Chapter 3.4 --- Effect of As203 on DNA Synthesis and Cell Proliferation of MCF-7 cells by [methyl-3H] Thymidine Incorporation into DNA --- p.76 / Chapter 3.5 --- Comparison of Cytotoxicity of AS2O3 on MCF-7 Cells with that of Tamoxifen --- p.79 / Chapter 3.6 --- Summary --- p.82 / Chapter CHAPTER 4 --- Effects of Arsenic Trioxide (As203) on 17β Estradiol Stimulated MCF-7 cells --- p.83 / Chapter 4.1 --- Introduction --- p.84 / Chapter 4.2 --- Effect of 17β estradiol on Cell Viability of MCF-7 Cells by MTT Assay --- p.86 / Chapter 4.3 --- Effect of As203 and 17β Estradiol on Cell Survival of MCF-7 Cells by MTT Assay --- p.88 / Chapter 4.4 --- Cytotoxicity of As203 on 17β Estradiol Stimulated MCF-7 cells by Cell Number Counting with Hemacytometer --- p.92 / Chapter 4.5 --- Growth Inhibitory Effect of As203 on 17β Estradiol stimulated MCF-7 cells by [methyl-3H] Thymidine Incorporation into DNA --- p.94 / Chapter 4.6 --- "Effect of As203 on Cell Survival of Hormone Independent Breast Cancer Cell Line, MDA-MB-231 Cells" --- p.96 / Chapter 4.7 --- Summary --- p.100 / Chapter CHAPTER 5 --- Effects of Arsenic Trioxide (As203) on Normal Cells --- p.102 / Chapter 5.1 --- Introduction --- p.103 / Chapter 5.2 --- "Effect of As203 on Normal Human Fibroblast Cell Line, Hs68" --- p.104 / Chapter 5.3 --- Effects of As203 on the Normal Cells of Nude Mice --- p.106 / Chapter 5.3.1 --- Effect of AS2O3 on Aspartate Transaminase (AST) Activity of Nude Mice --- p.107 / Chapter 5.3.2 --- Effect of As203 on Alanine Transaminase (ALT) Activity of Nude Mice --- p.109 / Chapter 5.3.3 --- Effect of As203 on Creatine Kinase (CK) Activity of Nude Mice TABLE OF CONTENTS --- p.111 / Chapter 5.3.4 --- Effect of As203 on Lactate Dehydrogenase (LDH) Activity of Nude Mice --- p.113 / Chapter 5.4 --- Summary --- p.115 / Chapter CHAPTER 6 --- Action Mechanisms underlying the Survival Inhibitory Effects of Arsenic Trioxide (As203) on MCF-7 cells --- p.116 / Chapter 6.1 --- Introduction --- p.117 / Chapter 6.2 --- Detection of Apoptosis --- p.119 / Chapter 6.2.1 --- Detection of DNA Fragmentation --- p.119 / Chapter 6.2.2 --- Phosphatidylserine (PS) Externalization Detected by Flow Cytometry with Annexin V-PI Staining --- p.124 / Chapter 6.2.2.1 --- The Principle --- p.124 / Chapter 6.2.2.2 --- PS Externalization upon AS2O3 Treatment --- p.126 / Chapter 6.3 --- Analysis of Cell Cycle Distribution of MCF-7 Cells --- p.130 / Chapter 6.3.1 --- The Principle --- p.130 / Chapter 6.3.2 --- Regulation of Cell Cycle Distribution of MCF-7 Cells upon As2O3 Treatment --- p.131 / Chapter 6.4 --- The Action Mechanisms Underlying As203 Induced Apoptosis or Cell Cycle Arrest --- p.137 / Chapter 6.4.1 --- Effect of As203 on Mitochondrial Membrane Potential of MCF-7 Cells --- p.137 / Chapter 6.4.2 --- Regulation of Free Oxidative Species (ROS) Production in MCF-7 Cells upon AS2O3 Treatment --- p.140 / Chapter 6.4.2.1 --- Analysis of Superoxide Production in MCF-7 Cells upon AS2O3 Treatment by Flow Cytometry with Hydroethidine (HE) Staining --- p.140 / Chapter 6.4.2.2 --- Effect of As203 on Cell Survival of MCF-7 Cells Co-treated with N-Acteyl-L-Cysteine (NAC) by MTT Assay --- p.143 / Chapter 6.4.3 --- Regulation of Bcl-2 Protein Level in MCF-7 Cells upon As2O3 Treatment --- p.145 / Chapter 6.4.4 --- Regulation of p53 Protein Level in MCF-7 Cells upon AS2O3 Treatment --- p.147 / Chapter 6.5 --- Summary --- p.149 / Chapter CHAPTER 7 --- Effects of Arsenic Trioxide (As203) on Estrogen Receptor a (ERα) Mediated Signaling Pathway in MCF-7 cells --- p.150 / Chapter 7.1 --- Introduction --- p.151 / Chapter 7.2 --- Effect of As203 on Estrogen Binding to Estrogen Receptor a (ERα) by ERα Competitive Binding Assay --- p.152 / Chapter 7.3 --- Regulation of Estrogen Receptor a (ERα) mRNA Level upon As2O3 Treatment by RT-PCR --- p.156 / Chapter 7.4 --- Regulation of Estrogen Receptor a (ERα) Protein Level upon As2O3 Treatment --- p.159 / Chapter 7.5 --- Regulation of Estrogen Receptor a (ERα) Transcriptional Activity upon AS2O3 treatment --- p.161 / Chapter 7.6 --- "Regulation of Estrogen Target Gene, c-myc, Protein Level upon As2O3 Treatment" --- p.164 / Chapter 7.7 --- Effects of As203 on Cell Cycle Distribution of MCF-7 Cells under Estrogens Stimulation --- p.167 / Chapter 7.8 --- Summary --- p.173 / Chapter CHAPTER 8 --- Discussion --- p.174 / Chapter 8.1 --- The Anti-Tumor Effects of As203 on MCF-7 Cells --- p.175 / Chapter 8.2 --- Cytotoxicity of As203 on MCF-7 Cells --- p.175 / Chapter 8.2.1 --- Induction of Apoptosis in MCF-7 Cells upon As2〇3 Treatment --- p.176 / Chapter 8.2.2 --- Action Mechanisms Underlying the Induction of Apoptosis by As2〇3 --- p.178 / Chapter 8.3 --- Growth Inhibition of As203 on MCF-7 Cells --- p.182 / Chapter 8.3.1 --- Cell Cycle Regulation of MCF-7 Cells upon As203 Treatment --- p.182 / Chapter 8.4 --- Growth Inhibitory Effects of As203 on Estrogen Stimulated MCF-7 Cells --- p.186 / Chapter 8.4.1 --- Regulation of Estrogen Receptor a (ERα) Signaling Pathway in MCF-7 cells upon as2o3 Treatment --- p.188 / Chapter 8.5 --- Cross Talk of ERα Signaling Pathway and Apoptosis in Mediating the Anti-Tumor Effects of As203 on MCF-7 Cells --- p.195 / Chapter 8.6 --- Toxicity of AS2O3 towards Normal Tissues --- p.197 / Chapter CHAPTER 9 --- Conclusion and Future Perspectives --- p.200 / Chapter 9.1 --- Conclusion --- p.200 / Chapter 9.2 --- Future Perspectives --- p.202 / References --- p.203

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