Dissertations / Theses on the topic 'Fatty Liver – Hong Kong'

There are a number of existing staging systems for patients with hepatocellular carcinoma (HCC). Yet, Barcelona Clinic Liver Cancer (BCLC) staging classification is the only one which suggests treatment guidance. Although BCLC staging is widely used in Western countries, it may not fit in the management of HCC patients in Hong Kong as they mostly have different etiologies and have more aggressive treatment strategy when compared with their counterparts in Western countries. It is aimed in this thesis to develop a new prognostic staging system in conjunction with treatment guidelines for HCC patients in Hong Kong. Three thousand eight hundred and fifty six adult HCC patients presented to the Department of Surgery, Queen Mary Hospital between January 1995 and December 2008 were included. The patient data were randomly separated into a training set and a test set for scheme development and performance assessment respectively. Four established prognostic factors which have determinative roles in treatment, namely Eastern Cooperative Oncology Group performance status, Child-Pugh grade, tumor status, and presence of extrahepatic vascular invasion/metastasis, were selected in building the scheme. Cox proportional hazards regression on overall survival was used to derive a relative coefficient for each category of these four factors. Clinical knowledge in addition to the relative coefficients was involved in the proposal of the prognostic stages. Then a classification and regression tree analysis was performed to elicit a set of simple clinical decision rules given the factors. This tree-structured classifier was adjusted with clinical judgment and reconciled with the proposed prognostic staging system for treatment guidelines. This Hong Kong Combined Liver Cancer (HKCLC) prognostic classification scheme stratifies patients to stages I to V with distinct overall survival outcomes. Its performance was compared to BCLC scheme for their discriminatory ability as staging systems and effectiveness of treatment guidelines. The former used receiver operating characteristics (ROC) analysis and concordance index as measures of the ability to distinguish patients with different prognosis for overall survival. HKCLC staging had significantly larger 1-year, 3-year and 5-year area under ROC curve values and higher concordance index vis-a-vis BCLC staging. The latter compared the overall survival of patients who received different treatments. The overall survival of patients with the same BCLC stage and the same HKCLC stage but received HKCLC recommended treatments were compared with those received BCLC recommended treatments by Kaplan-Meier plots and log-rank test. HKCLC treatment guidelines had wider indications for more aggressive treatments than the BCLC treatment schedule, and demonstrated significant survival benefit in our patients.
published_or_final_version
Surgery
Master
Master of Philosophy

 This study primarily aimed to evaluate the usefulness of fatty acids (FAs) in revealing trophic relationships in Hong Kong wetlands, through a combination of field studies and laboratory experiments. A field-based study in Mai Po mangroves involved FA profiling of basal food sources (i.e., leaf litter from three mangrove species, diatoms and macroalgae, and sediments) and consumers (particularly crabs). FA composition of all mangroves was similar, and lacked some polyunsaturated FAs present in diatoms and macroalgae. Uca and Sesarma crabs, with different feeding mechanisms, had divergent FA profiles: Uca arcuata FAs reflected a diet of macroalgae and diatoms, while FAs of Sesarma spp. were typical of mangrove leaves. Temporal changes in consumer FA profiles between 2001 and 2007 appeared attributable to increased sedimentation at Mai Po and shifts in organic content of the substratum. A second field-based study was conducted at Luk Keng marsh where a salinity gradient (0 to 30?) allowed investigation of the effects of salinity changes in FA profiles and stable isotope (carbon and nitrogen) signatures of the consumers and their foods. Basal food sources were leaf litter, including a fungal biomarker of decomposition (ergosterol), fine particulate organic matter (FPOM) and periphyton. Both FPOM and periphyton (but not leaf litter) contained 20:4 and 20:5 FAs, but their concentrations were affected by salinity. FA 20:4 occurred at higher levels in samples from fresh water, whilst FA 20:5 exhibited the opposite pattern and was more abundant under saline conditions, and thus the ratio of FA 20:4 to FA 20:5 decreased with increasing salinity. Combined application of FA biomarkers and isotopic signatures were able to elucidate trophic relationships between consumers and their food at Luk Keng confirming that FA 20:4 as a useful biomarker in the freshwater portion and FA 20:5 in the more saline area. FA 20:4 was particularly associated with predatory freshwater insects that had high δ15N values, but was scarce in primary consumers (snails, detritivorous beetles) with low δ15N values. Two laboratory experiments were undertaken to investigate: 1) the effect of diet on FA profiles in the apple snail, Pomacea canaliculata, and 2) interacting effects of diet and salinity on FA profiles of the Indian medaka fish, Oryzias melastigma. The results of the apple snail study showed that dietary-mediated changes in FA profiles were only reflected in the snail tissues after at least three months, and FA profiles of digestive tissues and neutral lipids were first to respond to the dietary change. The results of the medaka study demonstrated that the ratio of FA 20:4 to FA 20:5 was affected by both diet and salinity, reflecting a similar finding in the Luk Keng field study, although diet had a stronger effect on this ratio. The results of both field studies supported the use of FA profiles as food web tracers in wetlands and were complemented by laboratory results that yielded insights which will allow refinement of FA biomarker applications in food-web studies.
published_or_final_version
Biological Sciences
Doctoral
Doctor of Philosophy

Background: Liver transplantation is a curative method for end-stage liver diseases, small unresectable hepatocellular carcinoma and acute liver failure. The discovery of immunosuppressive drugs increases the survival rate of liver transplanted recipients by reducing the incidence of graft rejection. Several complications such as renal dysfunction and increase risk of malignancy result from life-long treatment of transplanted recipients with immunosuppressant. If recipients are over-immunosuppressed, the risk of infection might be increased. On the other hands, if recipients are under-immunosuppressed, the risk of rejection would be increased. It should be useful if a test or a bio-marker that could predict and differentiate infection and rejection in transplanted recipients. Therefore, patients could be treated before adverse conditions. Although therapeutic drug monitoring has been performed as a routine test, it is mainly targeted for minimizing drug toxicity but little help in predicting infection and rejection. A new assay named Cylex? Immuknow? assay is designed to measure global cell mediated immunity of immunosuppressed population, by quantifying the amount of ATP synthesis by CD4+ T cells in response to PHA stimulation. It is undergoing evaluation in assessing the immune status of patients in order to predict the risk of infection and rejection, and also other conditions. (1, 2) Objectives: In this pilot study, we would like to evaluate ImmuKnow for predicting the risk of infection and rejection in liver transplanted recipients in Hong Kong. Methods: Blood samples were collected from liver transplanted recipients at different time intervals. The immune cell response of these patients was measured by Immuknow assay. Patients with low immune response might have a high risk of infection, patients with high immune response might have a high risk of rejection, and patients with moderate immune response should be clinically stable. Results and conclusion: Twenty-six blood samples were collected from eight transplanted recipients. The average Immuknow assay value for the post-transplant samples was 304.6 ng/mL ATP which represented moderate immune cell response according to the interpretation table. (Table 3) This was reasonable as the subjects were all clinically stable by well-controlled immunosuppression. The result was consistent with other studies. (1, 3) However, the association between low immune cell response and infection, and the association between high immune cell response and graft rejection could not be investigated as both of these conditions were not found in this pilot study. A larger study including episodes of infection and rejection should be conducted in order to evaluate the value of Immuknow assay more completely.
published_or_final_version
Pathology
Master
Master of Medical Sciences

Among NAFLD patients without known diabetes or high fasting plasma glucose at or above 7.0 mmol/I, 21% had undiagnosed diabetes and 29% had impaired glucose tolerance. In this population, post-challenge hyperglycemia was associated with NASH and liver fibrosis. Oral glucose tolerance test should be considered in the evaluation of NAFLD patients.
NAFLD is closely related to metabolic syndrome. Using the ethnic-specific IDF criteria, 70% of NAFLD patients had metabolic syndrome, compared to 7% of the general population. A significant proportion of NAFLD patients had body mass index between 23 and 25 kg/m2. The diagnosis of NAFLD may predate the development of different components of metabolic syndrome.
NAFLD patients have lower serum adiponectin level than healthy controls. NASH patients have higher serum tumor necrosis factor alpha (TNF-alpha) level than those with simple steatosis. The differences in adipokines remained significant after adjustment for traditional metabolic risk factors. These suggest that abnormalities in adipokines may be involved in the pathogenesis of NAFLD and NASH. On the other hand, genetic polymorphisms of the adiponectin and TNF-alpha genes are not associated with histological severity.
Since advanced fibrosis is less common in Chinese NAFLD patients, performing liver biopsies on every NAFLD patient for disease staging does not appear to be essential or cost-effective. Recently, the NAFLD fibrosis score is developed using 6 clinical parameters including age, BMI, impaired fasting glucose or diabetes, AST/ALT ratio, platelet count and albumin. The score had high negative predictive value of 91% in excluding advanced fibrosis in Chinese NAFLD patients. It may also reduce the burden of liver biopsies in the majority of cases.
Through a series of clinical studies in Chinese nonalcoholic fatty liver disease (NAFLD) patients in Hong Kong, we demonstrated that nonalcoholic steatohepatitis (NASH) and advanced fibrosis do occur in Chinese, with around 10% of NAFLD patients having advanced fibrosis, and 80% having necroinflammation. Importantly, up to half of the patients had progression of liver fibrosis upon long-term follow-up.
by Wong Wai Sun.
Adviser: Lik Yuen Henry Chan.
Source: Dissertation Abstracts International, Volume: 70-09, Section: B, page: .
Thesis submitted in: May 2008.
Thesis (M.D.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references (leaves 219-263).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
School code: 1307.

by Yim-kam Kwong.
Thesis (M.Phil.)--Chinese University of Hong Kong, 1993.
Includes bibliographical references (leaves 119-133).
ACKNOWLEDGEMENT --- p.vii
LIST OF TABLES --- p.viii
LIST OF FIGURES --- p.x
ABSTRACT --- p.1
SECTION
Chapter 1. --- INTRODUCTION --- p.3
Chapter 2. --- LITERATURE REVIEW --- p.6
Chapter 3. --- MATERIALS AND METHODS --- p.39
Chapter 4. --- RESULTS --- p.61
Chapter 5. --- DISCUSSION --- p.103
Chapter 6. --- CONCLUSION --- p.116
REFERENCES --- p.119
APPENDIX --- p.134
Chapter SECTION 1 --- INTRODUCTION --- p.3
Chapter SECTION 2 --- LITERATURE REVIEW --- p.6
Chapter 2.1 --- IRON --- p.6
Chapter 2.1.1 --- CHEMISTRY --- p.6
Chapter 2.1.2 --- METABOLISM --- p.6
Chapter 2.1.2.1 --- Homeostasis --- p.6
Chapter 2.1.2.2 --- Absorption --- p.8
Chapter 2.1.2.3 --- Transportation - Role of transferrin in iron transport --- p.9
Chapter 2.1.2.4 --- Storage --- p.10
Ferritin --- p.11
Haemosiderin --- p.13
Chapter 2.2 --- IRON OVERLOAD --- p.14
Chapter 2.2.1 --- AETIOLOGY --- p.14
Chapter 2.2.2 --- PREVALENCE --- p.15
Chapter 2.2.3 --- MECHANISM --- p.16
Chapter 2.2.4 --- PATHOLOGY OF IRON OVERLOAD --- p.17
Chapter 2.2.4.1 --- Increased absorption of iron from the diet --- p.18
Chapter 2.2.4.2 --- Parenteral administration of excess iron --- p.21
Chapter 2.2.4.3 --- Increased iron absorption combined with transfusional overload --- p.22
Chapter 2.2.4.4 --- Miscellaneous conditions --- p.23
Chapter 2.2.5 --- CLINICAL PRESENTATION --- p.24
Chapter 2.2.6 --- EFFECT OF IRON OVERLOAD --- p.25
Chapter 2.2.6.1 --- Role of iron in lipid peroxidation --- p.25
Chapter 2.2.6.2 --- Iron and neoplasia --- p.26
Chapter 2.3 --- ASSESSMENT OF IRON OVERLOAD --- p.26
Chapter 2.3.1 --- NON-SERUM PARAMETER --- p.26
Chapter 2.3.1.1 --- Localization of stored iron --- p.27
Chapter 2.3.1.2 --- Morphometric assessment of hepatic iron in liver biopsy --- p.30
Chapter 2.3.1.3 --- Hepatic iron concentration --- p.31
Chapter 2.3.1.4 --- Atomic absorption spectrophotometry --- p.32
Chapter 2.3.1.5 --- Hepatic imaging studies --- p.33
Chapter 2.3.2 --- SERUM PARAMETERS --- p.34
Chapter 2.3.2.1 --- Serum ferritin measurement --- p.34
Chapter 2.3.2.2 --- Serum iron --- p.36
Chapter 2.3.2.4 --- Transferrin saturation --- p.37
Chapter SECTION 3 --- MATERIALS AND METHOD --- p.39
Chapter 3.1 --- SUBJECTS --- p.39
Chapter 3.1.1 --- SOURCE OF TISSUE SAMPLES AND CASE SELECTION --- p.39
Chapter 3.1.1.1 --- The controls --- p.39
Chapter 3.1.1.2 --- The transfusion group --- p.39
Chapter 3.1.1.3 --- The non-transfusion group --- p.40
Chapter 3.1.1.4 --- The total group --- p.40
Chapter 3.2 --- METHODS --- p.40
Chapter 3.2.1. --- HISTOLOGICAL METHOD --- p.44
Chapter 3.2.1.1 --- Haematoxylin and Eosin Stain --- p.47
Chapter 3.2.1.2 --- Perls' Prussian Blue Method --- p.49
Chapter 3.2.1.3 --- The Rowe's Method of Iron Deposition --- p.47
Chapter 3.2.1.4 --- Method 1 --- p.48
Chapter 3.2.1.5 --- Method2 Estimation and grouping of % area --- p.49
Chapter 3.2.1.6 --- "Comparison of Rowe's method, and the two histological iron grading methods" --- p.54
Chapter 3.2.2 --- CHEMICAL MEASUREMENT --- p.55
Chapter 3.2.2.1 --- Sectioning of paraffin liver blocks for chemical measurement --- p.55
Chapter 3.2.2.2 --- Paraffin removal --- p.56
Chapter SECTION 4 --- RESULTS --- p.61
Chapter 4.1 --- HISTOLOGICAL ASSESSMENT --- p.61
Chapter 4.1.1 --- HISTOLOGICAL STUDY --- p.61
Chapter 4.1.2 --- SEX DISTRIBUTION --- p.65
Chapter 4.1.3 --- AGE DISTRIBUTION --- p.65
Chapter 4.2 --- CHEMICAL MEASUREMENT --- p.81
Chapter 4.2.1 --- EVALUATION OF ANALYTICAL PRECISION --- p.84
Chapter 4.2.2 --- RESULT OF CHEMICAL MEASUREMENTS --- p.81
Chapter 4.2.3 --- ASSOCIATED CONDITIONS IN PATIENTS WITH LIVER TISSUE IRON > 50 μMOL/G --- p.86
Chapter 4.3 --- CORRELATION OF HISTOLOGICAL ASSESSMENT WITH CHEMICAL MEASUREMENT --- p.88
Chapter 4.3.1 --- CORRELATION OF HISTOLOGICAL ASSESSMENT WITH CHEMICAL MEASUREMENT BY METHOD 1 --- p.88
Chapter 4.3.2 --- CORRELATION OF ASSESSMENT WITH CHEMICAL MEASUREMENT BY METHOD 2 --- p.89
Chapter 4.3.2.1 --- Percentage area --- p.95
Chapter 4.3.2.2 --- Score --- p.96
Chapter 4.4 --- PANCREATIC AND MYOCARDIAC HAEMOSIDEROSIS --- p.100
Chapter 4.4.1 --- METHOD 2 --- p.100
Chapter SECTION 5 --- DISCUSSIONS --- p.103
Chapter SECTION 6 --- CONCLUSIONS --- p.116
REFERENCES --- p.119
APPENDIX --- p.134

by Peng Xiu Hong.
Thesis (M.Phil.)--Chinese University of Hong Kong, 1998.
Includes bibliographical references (leaves 63-81).
Abstract also in Chinese.
Acknowledgment --- p.i
List of abbreviations --- p.v
List of Tables --- p.vii
Legend for figures --- p.x
Abstract (English) --- p.xi
(Chinese) --- p.xiv
Chapter PART ONE. --- INTRODUCTION AND METHODOLOGY --- p.1
Chapter Chapter 1. --- Introduction and aim of study --- p.2
Chapter Chapter 2. --- Biological background --- p.7
Chapter Chapter 3. --- Literature reviews on serum fatty acids studies --- p.16
Chapter Chapter 4. --- Subjects and methods --- p.25
Chapter PART TWO. --- RESULTS AND DISCUSSION --- p.34
Chapter Chapter 5. --- Omnivore adults --- p.35
Chapter 5.1. --- Results --- p.37
Chapter 5.1.1 --- Results on serum fatty acid composition in different groups --- p.37
Chapter 5.1.2 --- Results on correlation of serum fatty acid composition with serum lipids and diet --- p.38
Chapter 5.2. --- Discussion --- p.41
Chapter Chapter 6. --- Omnivore children --- p.46
Chapter 6.1. --- Results --- p.48
Chapter 6.1.1 --- "Results on serum fatty acid composition, lipids and body fatness in the omnivore children" --- p.48
Chapter 6.1.2 --- Results on correlation of serum fatty acids with blood lipids and body fatness --- p.49
Chapter 6.2. --- Discussion --- p.50
Chapter Chapter 7. --- Vegetarians --- p.52
Chapter 7.1. --- Results --- p.53
Chapter 7.1.1 --- Results on serum fatty acid composition in vegetarian adults and children --- p.54
Chapter 7.1.2 --- Results on comparison of serum fatty acids in vegetarians to omnivores --- p.54
Chapter 7.1.3 --- "Results on dietary intake, blood lipids and their correlation with serum lipids in vegetarian adults" --- p.53
Chapter 7.2 --- Discussion --- p.57
Chapter Chapter 8. --- Conclusion --- p.61
References --- p.63
Tables and figures --- p.81
Appendix: Distribution of serum fatty acids analyzed by Gas-Liquid Chromatography --- p.118

Ho Kar Fai, William.
Thesis submitted in: July 2002.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2003.
Includes bibliographical references (leaves 121-129).
Abstracts in English and Chinese.
Abstract --- p.I
Acknowledgement --- p.V
Table of Contents --- p.VI
Abbreviations --- p.VIII
Chapter Chapter 1 --- Introduction --- p.1
Chapter 1.1 --- The recent situation of hepatitis B infection and HBV-induced HCC in Hong Kong
Chapter 1.2 --- Natural history of HBV infection in human
Chapter 1.3 --- The genomic organization of HBV
Chapter 1.4 --- Potential oncogenic mechanism of HBV-induced hepatocarcinogenesis
Chapter 1.5 --- Aim of the present study
Chapter Chapter 2 --- Materials and methods --- p.16
Chapter 2.1 --- Transformation in E.coli for subtracted normal-counterpart library
Chapter 2.2 --- PCR amplification of subtracted clones
Chapter 2.3 --- Sequencing of subtracted clones with dye-terminator cycle sequencing technology
Chapter 2.4 --- Sequence analysis and database construction
Chapter 2.5 --- Molecular cloning and characterization of novel gene
Chapter 2.6 --- In silico structural and functional analysis of Z313
Chapter 2.7 --- Cloning and sequencing analysis of zinc finger protein 313 (Z313)
Chapter 2.7.1 --- PCR amplification of target gene -Z313
Chapter 2.7.2 --- Mini-preparation of plasmid DNA
Chapter 2.7.3 --- Cycle sequencing of cloned cDNA -Z313 with dye-primer technology
Chapter 2.8 --- Multiple Tissue Northern (MTN) blot hybridisation
Chapter 2.9 --- RT-PCR analysis of Z313
Chapter 2.10 --- Subcellular localization study of Z313 by Green Fluorescent Protein (GFP)
Chapter 2.10.1 --- Directional cloning of Z313 into pEGFP-Cl
Chapter 2.10.2 --- Mini-preparation of plasmid DNA
Chapter 2.10.3 --- Transient transfection of plasmids in different cell lines
Chapter 2.10.4 --- Microscope observation of GFP transfected cells
Chapter Chapter 3 --- Results --- p.49
Chapter 3.1 --- PCR selection of subtracted clones for sequencing analysis
Chapter 3.2 --- Partial sequencing of selected subtracted clones
Chapter 3.3 --- DNA homology searching using program - BLASTN
Chapter 3.4 --- Catalogue of the 467 ESTs from the subtracted normal-counterpart library
Chapter 3.5 --- Classification and frequency of the subtracted normal-counterpart cDNA clones
Chapter 3.6 --- Identification of putative differentially expressed genes in HCC surrounding normal liver
Chapter 3.7 --- Categorization of ESTs exclusively appeared in the subtracted normal- counterpart library
Chapter 3.8 --- In silico structural and functional analysis of zinc finger protein313 (Z313)
Chapter 3.9 --- Molecular cloning of zinc finger protein 313 (Z313)
Chapter 3.10 --- Northern analysis of zinc finger protein 313 (Z313)
Chapter 3.11 --- RT-PCR analysis of zinc finger protein 313 (Z313)
Chapter 3.12 --- Subcellular localization study of zinc finger protein 313 (Z313)
Chapter Chapter 4 --- Discussion --- p.104
Chapter 4.1 --- EST analysis on the subtracted normal-counterpart cDNA clones
Chapter 4.1.1 --- Characterization of ESTs generated from the subtracted normal-counterpart library
Chapter 4.1.2 --- Putative differentially expressed genes in HCC surrounding normal liver related to hepatocellular carcinoma
Chapter 4.2 --- Molecular cloning and characterization of zinc finger protein313 (Z313)
Chapter 4.3 --- Future aspects
References --- p.121

Wong Chun-kwan.
Thesis submitted in: December 1999.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2000.
Includes bibliographical references (leaves 127-137).
Abstracts in English and Chinese.
Abstract --- p.i
Acknowledgments --- p.viii
Tables of Contents --- p.ix
List of Figures --- p.xv
List of Tables --- p.xxvi
Chapter Chapter 1: --- INTRODUCTION --- p.1
Chapter Chapter 2: --- LITERATURE REVIEW --- p.8
Chapter 2.1 --- Toxicology --- p.8
Chapter 2.1.1 --- Acute toxicity test --- p.8
Chapter 2.1.2 --- Biochemical Analysis --- p.9
Chapter 2.1.3 --- Organ weights --- p.10
Chapter 2.2 --- Histology --- p.11
Chapter 2.2.1 --- Light Microscope --- p.11
Chapter 2.2.2 --- Electron Microscopy --- p.11
Chapter 2.3 --- Tissue injury --- p.12
Chapter 2.3.1 --- Free-radical mechanisms --- p.12
Chapter 2.3.2 --- Lipid peroxidation --- p.13
Chapter 2.4 --- Carbon tetrachloride (CC14) --- p.14
Chapter 2.4.1 --- Mechanisms of carbon tetrachloride toxicity --- p.15
Chapter 2.5 --- Trichloroethylene (TCE) --- p.18
Chapter 2.5.1 --- Mechanisms of trichloroethylene toxicity --- p.21
Chapter 2.6 --- Dimethyl sulfoxide (DMSO) --- p.25
Chapter 2.7 --- N-acetylcysteine (NAC) --- p.27
Chapter Chapter 3: --- MATERIALS AND METHODS --- p.28
Chapter 3.1 --- Materials --- p.28
Chapter 3.2 --- Methods --- p.31
Chapter 3.2.1 --- Acute hepatotoxicity test on aqueous seaweed extracts --- p.31
Chapter 3.2.1.1 --- Preparation of aqueous extracts of seaweed --- p.31
Chapter 3.2.1.2 --- Experimental protocol --- p.31
Chapter 3.2.1.3 --- Biochemical assays --- p.32
Chapter 3.2.1.4 --- Organ weights --- p.36
Chapter 3.2.1.5 --- Histopathological examination --- p.36
Chapter 3.2.1.6 --- Statistical analysis --- p.36
Chapter 3.2.2 --- Curative and preventive tests of seaweed aqueous extracts against the CCl4-induced hepatotoxicity --- p.37
Chapter 3.2.2.1 --- Preparation of aqueous extracts of seaweed --- p.37
Chapter 3.2.2.2 --- Experimental protocol --- p.37
Chapter 3.2.2.3 --- Biochemical assays --- p.39
Chapter 3.2.2.4 --- Organ weights --- p.39
Chapter 3.2.2.5 --- Histopathological examination --- p.40
Chapter 3.2.2.6 --- Statistical analysis --- p.41
Chapter 3.2.3 --- Acute hepatotoxicity test of TCE in rats by oral and intraperitoneal routes --- p.42
Chapter 3.2.3.1 --- Experimental protocol --- p.42
Chapter 3.2.3.2 --- Biochemical assays --- p.43
Chapter 3.2.3.3 --- Organ weights --- p.43
Chapter 3.2.3.4 --- Histopathological examination --- p.44
Chapter 3.2.3.5 --- Statistical analysis --- p.44
Chapter 3.2.4 --- Curative and preventive tests of seaweed aqueous extracts against the TCE effective dose-induced toxicity --- p.44
Chapter 3.2.4.1 --- Preparation of aqueous extracts of seaweed --- p.44
Chapter 3.2.4.2 --- Experimental protocol --- p.45
Chapter 3.2.4.3 --- Biochemical assays --- p.46
Chapter 3.2.4.4 --- Organ weights --- p.46
Chapter 3.2.4.5 --- Histopathological examination --- p.46
Chapter 3.2.5 --- Antidotal effects of dimethyl sulfoxide (DMSO) and N-acetylcysteine (NAC) against CC14- and TCE- induced poisoning in rats --- p.47
Chapter 3.2.5.1 --- Experimental protocol --- p.47
Chapter 3.2.5.2 --- Biochemical assays --- p.48
Chapter 3.2.5.3 --- Organ weights --- p.48
Chapter 3.2.5.4 --- Histopathological examination --- p.49
Chapter 3.2.6 --- Hepatoprotective effect of seaweeds' methanol extract against CC14- and TCE-induced poisoning in rats --- p.49
Chapter 3.2.6.1 --- Preparation of methanol extracts of seaweed --- p.49
Chapter 3.2.6.2 --- Experimental protocol --- p.50
Chapter 3.2.6.3 --- Biochemical assays --- p.52
Chapter 3.2.6.4 --- Organ weights --- p.52
Chapter 3.2.6.5 --- Histopathological examination --- p.53
Chapter Chapter 4 --- RESULTS --- p.54
Chapter 4.1 --- Acute hepatotoxicity test on aqueous seaweed extracts --- p.54
Chapter 4.1.1 --- The biochemical assays of the serum transaminase activity --- p.54
Chapter 4.1.2 --- The organ weight (Aqueous seaweed crude extracts) --- p.56
Chapter 4.2 --- Curative and preventive tests of seaweed aqueous extracts against the CCl4-induced hepatotoxicity --- p.58
Chapter 4.2.1 --- The biochemical assays of the serum transaminase activity (Curative) --- p.58
Chapter 4.2.2 --- The organ weight (Curative) --- p.60
Chapter 4.2.3 --- The biochemical assays of the serum transaminase activity (Preventive) --- p.62
Chapter 4.2.4 --- The organ weight (Preventive) --- p.64
Chapter 4.3 --- Acute hepatotoxicity test of TCE in rats by oral and intraperitoneal routes --- p.66
Chapter 4.3.1 --- Oral route --- p.66
Chapter 4.3.1.1 --- One-time oral route --- p.66
Chapter 4.3.1.2 --- Two-time oral route --- p.66
Chapter 4.3.2 --- Intraperitoneal route --- p.66
Chapter 4.3.3 --- Time course of the effective dose of 20% TCE in i.p. route --- p.67
Chapter 4.4 --- Curative and preventive tests of seaweed aqueous extracts against the TCE effective dose-induced toxicity --- p.12
Chapter 4.4.1 --- The biochemical assays of the serum transaminase activity (Curative) --- p.72
Chapter 4.4.2 --- The organ weight (Curative) --- p.74
Chapter 4.4.3 --- The biochemical assays of the serum transaminase activity (Preventive) --- p.76
Chapter 4.4.4 --- The organ weight (Preventive) --- p.78
Chapter 4.5 --- Antidotal effects of dimethyl sulfoxide (DMSO) and N-acetylcysteine (NAC) against CC14- and TCE-induced poisoning in rats --- p.80
Chapter 4.5.1 --- The biochemical assays of the serum transaminase activity (Curative) --- p.80
Chapter 4.5.2 --- The organ weight (Curative) --- p.82
Chapter 4.5.3 --- The biochemical assays of the serum transaminase activity (Preventive) --- p.84
Chapter 4.5.4 --- The organ weight (Preventive) --- p.86
Chapter 4.6 --- Hepatoprotective effect of methanol extract of seaweed against CC14- and TCE-induced poisoning in rats --- p.88
Chapter 4.6.1 --- The biochemical assays of the serum transaminase activity (Curative) --- p.88
Chapter 4.6.2 --- The organ weight (Curative) --- p.89
Chapter 4.7 --- Histopathological examinations --- p.90
Chapter 4.7.1 --- Acute hepatotoxicity test on aqueous seaweed extracts --- p.91
Chapter 4.7.2 --- Curative and preventive tests of seaweed aqueous extracts against the CC14-induced hepatotoxicity --- p.92
Chapter 4.7.3 --- Acute hepatotoxicity test of TCE in rats by oral and intraperitoneal routes --- p.99
Chapter 4.7.4 --- Curative and preventive tests of seaweed aqueous extracts against the TCE effective dose-induced toxicity --- p.100
Chapter 4.7.5 --- Antidotal effects of dimethyl sulfoxide (DMSO) and N-acetylcysteine (NAC) against CC14- and TCE-induced poisoning in rats --- p.100
Chapter 4.7.6 --- Hepatoprotective effect of methanol extract of seaweed against CC14- and TCE-induced poisoning in rats --- p.102
Chapter Chapter 5 --- DISCUSSION --- p.106
Chapter Chapter 6 --- CONCLUSION --- p.124
REFERENCES --- p.127
APPENDIX --- p.138

submitted by Liu Dan.
Thesis (M.Sc.)--Chinese University of Hong Kong, 1998.
Includes bibliographical references (leaves 66-80).
Abstract also in Chinese.
CONTENTS --- p.i
LIST OF TABLES --- p.iii
LIST OF FIGURES --- p.iv
LIST OF ABBREVIATIONS --- p.v
ACKNOWLEDGEMENTS --- p.vi
ABSTRACT --- p.vii
Chapter Chapter 1 --- INTRODUCTION --- p.1
Chapter 1.1 --- History --- p.1
Chapter 1.2 --- Immunoglobulins --- p.3
Chapter 1.2.1 --- Structure --- p.3
Chapter 1.2.2 --- Properties of immunoglobulins --- p.7
Chapter 1.3 --- Monoclonal proteins and monoclonal gammopathies --- p.12
Chapter 1.3.1 --- Monoclonal proteins --- p.12
Chapter 1.3.2 --- Monoclonal gammopathies --- p.14
Chapter 1.4 --- Laboratory investigation of monoclonal immunoglobulin --- p.17
Chapter 1.4.1 --- The current procedure of investigation in laboratory --- p.17
Chapter 1.4.2 --- Problems in identifying monoclonal immunolgobuin --- p.19
Chapter 1.5 --- Comparison of different techniques --- p.20
Chapter 1.5.1 --- Immunoelectrophoresis --- p.20
Chapter 1.5.2 --- Immunofixation electrophoresis --- p.22
Chapter 1.5.3 --- Isoelectric focusing and immunoisoelectric focusing --- p.24
Chapter 1.6 --- Aim of the present study --- p.27
Chapter 1.7 --- Design of experiment --- p.27
Chapter Chapter 2 --- MATERIALS AND METHODS --- p.30
Chapter 2.1 --- Study subjects --- p.30
Chapter 2.2 --- Apparatus --- p.30
Chapter 2.2 --- Apparatus --- p.30
Chapter 2.3 --- Reagents and materials --- p.32
Chapter 2.4 --- Preparation of gels --- p.35
Chapter 2.5 --- Isoelectric focusing procedure --- p.36
Chapter 2.6 --- Acid fixation and staining --- p.37
Chapter 2.7 --- Technical factors affecting results --- p.38
Chapter Chapter 3 --- RESULTS --- p.40
Chapter 3.1 --- Interpretation of results in isoelectric focusing --- p.40
Chapter 3.2 --- Affecting factors --- p.47
Chapter 3.3 --- Comparison of the results between IEF and IFE --- p.53
Chapter Chapter 4 --- DISCUSSION --- p.59
Chapter Chapter 5 --- CONCLUSION --- p.65
References --- p.66