When the research, which forms the basis of this thesis was started in 1979, the theoretically attractive situation of transient focal cerebral ischaemia simulating a cerebral vessel occlusion followed by re-vascularization, had not been specifically investigated with barbiturate treatment. Cerebral infarction is progressive and evolves over hours, proceeding from ischaemia and functional loss to cell death. Sundt et al (1969), Crowell et al (1970), Hayakawa and Waltz (1975). Complete recovery is possible if re-vascularization is instituted in time. This time interval depends on the regional cerebral bloodflow during the period of the vessel occlusion and this bloodflow is provided by the collateral circulation. Thus, whether infarction results and the extent of it, becomes a factor of the period of ischaemia and the collateral circulation present. Dujovny et al (1976), Morawetz et al (1978), Ojeman et al (1979), Kieck and Crowell (1979), Jones et al (1981). This ischaemic period may vary tremendously from less than an hour to as much as 5 hours and occlusion times of up to an hour can be tolerated without infarction at very low regional cerebral bloodflow levels. Morawetz et al (1978), Kieck and Crowell (1979), Jones et al (1981). In the clinical situation there would be an obligatory delay from the onset of ischaemia to the institution of barbiturate treatment and completion of re-vascularization. Treatment during this period would thus be a major contribution if it could afford protection so as to allow restitution of cerebral bloodflow before irreversible infarction took place. The South African Vervet monkey was chosen for the investigation of the effect of barbiturate treatment on transient focal cerebral ischaemia in a model simulating the clinical event. In this experiment pentobarbital therapy would be delayed for 1 hour to provide for the expected delay that would occur from the onset of ischaemia to the institution of treatment. Similarly, ischaemia was to last 4 hours to allow for a minimum time interval necessary to complete the re-vascularization. It was also borne in mind that many stroke patients would be older people; the barbiturate dose of 30mg/kg would be such as to induce prolonged coma but not major cardiovascular disturbances with a fall in blood pressure and/or cardiac arrest.

by Lee Hon Kit. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 80-89). / Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- Lipids and Lipoproteins --- p.1 / Chapter 1.1.1 --- Chemistry and Classification of Lipids --- p.1 / Chapter 1.1.2 --- Lipoprotein and Apolipoprotein --- p.3 / Chapter 1.1.2.1 --- Lipoprotein: Structure and Classification --- p.3 / Chapter 1.1.2.2 --- Apolipoprotein: Structure and Function --- p.5 / Chapter 1.1.2.3 --- Lipoprotein (a) and Apolipoprotein (a) --- p.8 / Chapter 1.1.3 --- Outline of Lipid and Lipoprotein Metabolism --- p.10 / Chapter 1.1.3.1 --- Exogenous Lipid Metabolism --- p.10 / Chapter 1.1.3.2 --- Endogenous Lipid Pathway --- p.13 / Chapter 1.2 --- "Dyslipidaemia: Definition, Classification and Coronary Heart Disease" --- p.20 / Chapter 1.2.1 --- Definition --- p.20 / Chapter 1.2.2 --- Classification of Dyslipidaemia --- p.21 / Chapter 1.2.3 --- Dyslipidaemia and CHD --- p.24 / Chapter 1.3 --- Dyslipoproteinaemia and Atherogenesis --- p.25 / Chapter 1.3.1 --- Pathology and Pathogenesis --- p.25 / Chapter 1.3.2 --- Central Role of Oxidised LDL in Atherogenesis --- p.29 / Chapter 1.3.3 --- LDL Heterogeneity and Atherogenesis --- p.37 / Chapter 1.4 --- Management of Dyslipidaemia --- p.41 / Chapter 1.4.1 --- Drug therapy --- p.43 / Chapter 1.4.1.1 --- Triglyceride Lowering Drugs --- p.43 / Chapter 1.4.1.2 --- Cholesterol Lowering Drugs --- p.45 / Chapter 1.4.1.3 --- Combination Drug Therapy --- p.46 / Chapter 1.5 --- Aims of this study --- p.49 / Chapter 2. --- Materials and Methods --- p.50 / Chapter 2.1 --- Materials --- p.50 / Chapter 2.1.1 --- Patients and Controls --- p.50 / Chapter 2.1.2 --- Drug Administration Trials --- p.51 / Chapter 2.1.3 --- Blood Samples --- p.52 / Chapter 2.1.4 --- Chemicals and Solutions --- p.52 / Chapter 2.1.5 --- Apparatus and Equipments --- p.52 / Chapter 2.2 --- Methods --- p.54 / Chapter 2.2.1 --- "Serum Cholesterol, Triglyceride and High Density Lipoprotein cholesterol" --- p.54 / Chapter 2.2.2 --- "Apolipoprotein AI, B-100 and Lipoprotein (a) Assays" --- p.54 / Chapter 2.2.3 --- Ultracentrifugation of LDL Fraction --- p.55 / Chapter 2.2.4 --- In Vitro Assessment of LDL Oxidisability --- p.55 / Chapter 2.2.4.1 --- De-Salting of LDL Fraction --- p.55 / Chapter 2.2.4.2 --- Continuously Diene Formation Monitoring --- p.56 / Chapter 2.2.5 --- LDL Particle Size --- p.56 / Chapter 2.2.6 --- Statistical Analysis --- p.57 / Chapter 3. --- Results --- p.59 / Chapter 3.1 --- Quantitative Measurement of apo B-100 --- p.59 / Chapter 3.2 --- "Associations between Serum Triglyceride, LDL Particle Size and LDL Oxidisability" --- p.60 / Chapter 3.3 --- "Effect of single drug and combination drug therapy on lipids, lipoproteins and apolipoproteins" --- p.64 / Chapter 3.3.1 --- Quantitative Changes of Lipids and Lipoproteins --- p.64 / Chapter 3.3.2 --- Qualitative changes of LDL particles --- p.65 / Chapter 4. --- Discussion --- p.74 / Chapter 4.1 --- "Associations between Triglyceride concentration, HDL Cholesterol concentration, LDL oxidisability and Particle Size" --- p.74 / Chapter 4.2 --- Effects of Fluvastatin and Gemfibrozil on Combined Hyperlipidaemic Patients --- p.76

Lee Kwing Chin, Kenneth. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (p. 298-357). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

This study investigates the impact of the scale-up of antiretroviral treatment (ART) on the health system in South Africa. It looks at the positive and negative effects of treatment scale-up on human resources and staff morale, on HIV prevention programmes, and on other health system programmes, looking specifically at the integration of programmes and the use of infrastructure. There is much debate as to the place of treatment as a response to the epidemic because it has been found to be less cost-effective than prevention interventions. However this study argues that it is difficult to accurately assess cost effectiveness because it does not take into account other ways in which treatment may be effective, such as its impact on other aspects of health care, most notably on staff morale and on prevention. Thus this study investigates the impact of treatment intervention on the health system as a whole in order to determine the effectiveness of treatment as a policy response. This research uses data collected in 2006 at two sites in South Africa: the Ilembe district in KwaZulu-Natal province and the Cape Winelands Region in the Western Cape province. Twenty-one health care professionals were interviewed across the two sites in order to determine their perspectives on the impacts of ART scale-up on these aspects of the health care system. Interviews were conducted at hospitals, clinics and on hospice where ART was being administered ART scale-up, as predicted, was having a mixed impact on the health system as a whole. For the most part, the programmes were not having negative impacts on the rest of the health system in the form of taking infrastructure, funding, or human resources from other departments. The programmes, on separate budgets, were not directly taking resources from other departments, although there were some instances of borrowing space, staff, or equipment when necessary. The treatment programmes were reported to be adding further strain to an already resource-limited health care system, which was most notable in the issues of space and staff shortages. In addition, the treatment programmes did not appear to be bringing in additional funding, staff development, or infrastructure to benefit the health system as a whole.The major positive impact of the ART rollout on the health system was creating positive staff morale and a sense of hope throughout the health system. The health system was now able to address HIVIAIDS and was able to provide treatment whereas prior to rollout there was little apart from palliative care that could be done for people living with HIVIAIDS. In addition, treatment was adding to prevention efforts by raising awareness in the community about HIV/AIDS and by increasing uptake of voluntary counseling and testing. There is a need to address the resource limitations in the health care system, most notably human resource shortages. The success of treatment programmes was dependent on having motivated and dedicated staff. It is necessary to further attract and retain health care professionals to the field in order to ensure the sustainable success of ART rollout. Funding also needs to be addressed to ensure that sustainable resources are available to support the ever-growing needs of the treatment programmes. / Thesis (M.A.)-University of KwaZulu-Natal, Durban, 2008.

A!dissertation submitted to the Faculty of Science, University of the Witwatersrand, Johannesburg, in the fulfillment of the requirements for the degree of Master of Science. 2013. / Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease affecting in excess of 26.6 million individuals globally. The neuropathological features of AD include extracellular deposition of amyloid beta (Aβ) plaques and intracellular neurofibrillary tangle formation. The cellular prion protein (PrPC) regulates the amyloidogenic cleavage pathway involved in Aβ shedding and interacts with the Aβ peptide. Given these interactions, the aim of this study was to investigate the influence of the 37kDa/67kDa laminin receptor (LRP/LR)- the cellular receptor for prion proteins- on Aβ shedding. Transfection of HEK293 cells with short hairpin RNAs (shRNAs) directed against LRP mRNA significantly decreased LRP levels in addition to Aβ shedding. Flow cytometric analysis revealed unchanged cell surface levels of the amyloid precursor protein (APP), β-secretase and γ-secretase after transfection of cells with shRNAs, suggesting a role of LRP/LR in Aβ shedding via a mechanism independent of gene-expression modulation of these key proteins. LRPshRNA treatment significantly reduced sAPPβ expression, implicating LRP/LR in APP processing specifically via augmenting the activity of β-secretase. Colocalisation of LRP/LR with APP, β- and γ-secretase, respectively, alludes to a possible interaction between said proteins. Therefore, LRP-shRNAs are suggested as alternative therapeutic tools for AD treatment.

Thesis (M. Pharm.)--University of the Witwatersrand, Faculty of Health Sciences, 2013. / Ocular diseases of the anterior segment are ubiquitous, especially among elderly patients. The development of novel drug delivery systems on the journey for improved treatment is therefore imperative. Aside from anatomical and physiological barriers of the eye, the actual dosage form plays a crucial role. Although liquid eye drops are the first-choice dosage form, the shortcomings do not go unnoticed. In an attempt to circumvent these drawbacks, a novel instantly soluble eye drop device was developed. The system aimed to provide an easier administration form, comfort for the patient and improve drug bioavailability to anterior chamber. This was a steer toward attaining patient-convenience and compliance which are critically challenging factors. Preformulatory studies allowed for the screening and selection of candidate components and key processing conditions. Hydrophilic polymers and excipients were selected for attainment of small, rapid disintegrating yet robust matrices via lyophilization of solutions. Design of experiments generated formulations by means of a Face centred central composite design (FCCCD) that underwent thorough physicochemical and mechanical assessment. Overall, robust rapidly disintegrating solid eye drops were produced. Fastest disintegration time was noted to be 0.200s. Drug content ranged from 79-96%. An improved permeation of formulations compared to a pure drug dispersion was seen. Mathematical modeling was conducted for better insight into the behavior of the device on the eye surface. Statistical analysis through constraint optimization yielded a single optimal formulation. Thermal and molecular transition analysis showed congruent findings with no incompatibility between components. Combinatory surface morphology and porositometric studies confirmed the presence of interconnecting pores across the matrix surface. Drug release kinetic evaluation predicted that best model fit was first-order release. Ocular irritancy studies by means of the HET-CAM test indicated that both drug-loaded and drug-free eye drops had an irritation score of 0 with the inference of good tolerability. Ex vivo permeation across excised rabbit cornea showed an improved steady state drug flux (0.00052mg.cm-2.min-1) and permeability co-efficient (1.7x10-4cm.min-1) for the optimized device compared to pure drug and a marketed eye drop preparation. In vivo analysis was conducted on the rabbit model with insertion of the device into the ocular cul-de-sac. Subsequently, ultra performance liquid chromatography (UPLC) analysis of the aspirated aqueous humour for model drug timolol maleate detection was conducted. The device demonstrated improved drug levels (Cmax = 3ug/mL) in comparison to commercial eye drops (Cmax = 1.97ug/mL) and was well tolerated. Level A point-to-point IVIVC plots indicated a R2 value of 0.84. This served to imply that the in vitro dissolution data can be compared to and may serve as a surrogate to that of in vivo pK data. Histopathological assessment on the enucleated eye ball confirmed the lack of noxious effects of the device on ocular tissue. From this study, the solid eye drop device was concluded to be safe as a drug delivery system for the anterior eye. Looking toward innovative trends and modifications, a bi-layered solid eye drop system with enhanced permeability capabilities employing low molecular weight chitosan was further fabricated for preliminary investigation.

Wong Suk-kwan, Amy. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1988. / Bibliography: leaves 184-206.

Lau Siu Wai Maggie. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 236-245). / List of Figures --- p.i / List of Tables --- p.viii / List of Abbreviations --- p.x / Abstract --- p.xii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Postulated Pathophysiology of Essential Hypertension --- p.1 / Chapter 1.2 --- Measurement of Cardiac Output (CO) by Transthoracic Electrical Bioimpedance (TEB) and Other Methodologies --- p.6 / Chapter 1.3 --- Measurement of Blood Pressure --- p.10 / Chapter 1.4 --- Use of Antihypertensive Agents in Essential Hypertension --- p.12 / Chapter Chapter 2. --- The Method of Transthoracic Electrical Bioimpedance --- p.15 / Chapter 2.1 --- Introduction --- p.15 / Chapter 2.2 --- Development of Theory --- p.18 / Chapter 2.3 --- Measurements of Haemodynamic Parameters --- p.24 / Chapter 2.4 --- Literature Review - Validity of the Technique --- p.30 / Chapter Chapter 3 --- A Study on Reproducibility of Thoracic Electrical Bioimpedance in Healthy Subjects --- p.39 / Chapter 3.1 --- Objectives --- p.39 / Chapter 3.2 --- Methodology --- p.39 / Chapter 3.2.1 --- Subjects --- p.39 / Chapter 3.2.2 --- Study design --- p.41 / Chapter 3.2.3 --- Non-invasive haemodynamic monitoring --- p.41 / Chapter 3.2.4 --- Blood Pressure Measurement --- p.43 / Chapter 3.2.5 --- Isometric Exercise --- p.43 / Chapter 3.2.6 --- Data analysis --- p.44 / Chapter 3.2.7 --- Statistical analysis --- p.46 / Chapter 3.3 --- Results --- p.50 / Chapter 3.3.1 --- Systolic blood pressure --- p.50 / Chapter 3.3.2 --- Diastolic blood pressure --- p.52 / Chapter 3.3.3 --- Mean arterial pressure --- p.54 / Chapter 3.3.4 --- Heart rate --- p.55 / Chapter 3.3.5 --- Thoracic fluid index --- p.58 / Chapter 3.3.6 --- Stroke index --- p.60 / Chapter 3.3.7 --- Cardiac index --- p.62 / Chapter 3.3.8 --- Systemic vascular resistance index --- p.65 / Chapter 3.4 --- Discussion --- p.70 / Chapter Chapter 4 --- Literature Review --- p.73 / Chapter 4.1 --- Atenolol: Beta-adrenoceptor antagonists with β1-selectivity --- p.73 / Chapter 4.2 --- Pindolol: Beta-adrenoceptor antagonists with ISA --- p.78 / Chapter 4.3 --- Alpha1-adrenoceptor antagonists --- p.81 / Chapter 4.4 --- Angiotensin Converting Enzyme Inhibitors --- p.84 / Chapter 4.5 --- Calcium Channel Blockers --- p.87 / Chapter 4.6 --- Central Alpha Agonist --- p.91 / Chapter 4.7 --- Thiazide Diuretics --- p.94 / Chapter Chapter 5 --- The Integrated Hypertension Study --- p.97 / Chapter 5.1 --- Objectives --- p.97 / Chapter 5.2 --- Methodology --- p.97 / Chapter 5.2.1 --- Subjects --- p.97 / Chapter 5.2.2 --- Study design --- p.109 / Chapter 5.2.3 --- Non-invasive haemodynamic monitoring --- p.110 / Chapter 5.2 4 --- Blood Pressure Measurement --- p.111 / Chapter 5.2.5 --- Isometric Exercise --- p.111 / Chapter 5.2.6 --- Data analysis --- p.111 / Chapter 5.2.7 --- Statistical analysis --- p.112 / Chapter 5.2.8 --- Limitations of the study --- p.113 / Chapter 5.3 --- Results --- p.117 / Chapter 5.3.1 --- Atenolol --- p.117 / Chapter 5.3.2 --- Pindolol --- p.125 / Chapter 5.3.3 --- Doxazosin --- p.132 / Chapter 5.3.4 --- Enalapril --- p.138 / Chapter 5.3.5 --- Nifedipine Retard --- p.145 / Chapter 5.3.6 --- Methyldopa --- p.152 / Chapter 5.3.7 --- Cyclopenthiazide --- p.160 / Chapter 5.4 --- Comparisons of the anti-hypertensive drugs studied --- p.167 / Chapter 5.4.1 --- Baseline values --- p.167 / Chapter 5.4.2 --- Percentage changes after active treatment --- p.170 / Chapter 5.5 --- Discussion --- p.196 / Chapter 5.5.1 --- Atenolol --- p.196 / Chapter 5.5.2 --- Pindolol --- p.199 / Chapter 5.5.3 --- Doxazosin --- p.200 / Chapter 5.5.4 --- Enalapril --- p.202 / Chapter 5.5.5 --- Nifedipine Retard --- p.203 / Chapter 5.5.6 --- Methyldopa --- p.204 / Chapter 5.5.7 --- Cyclopenthiazide --- p.205 / Chapter 5.5.8 --- Comparison of the anti-hypertensive drugs studied --- p.206 / Chapter Chapter 6 --- Acute haemodynamic effects of Atenolol and Pindolol --- p.208 / Chapter 6.1 --- Objectives --- p.208 / Chapter 6.2 --- Methodology --- p.208 / Chapter 6.2.1 --- Subjects --- p.208 / Chapter 6.2.2 --- Study Design --- p.209 / Chapter 6.2.3 --- Statistical analysis --- p.209 / Chapter 6.3 --- Results --- p.211 / Chapter 6.3.1 --- Acute haemodynamic changes of atenolol --- p.211 / Chapter 6.3.2 --- Acute and short-term haemodynamic changes of atenolol --- p.219 / Chapter 6.3.3 --- Acute haemodymmic changes of pindolol --- p.221 / Chapter 6.3.4 --- Acute and short-term haemodymmic changes of pindolol --- p.222 / Chapter 6.3.5 --- Comparison of the acute haemodymmic effects of atenolol and pindolol --- p.226 / Chapter 6.4 --- Discussion --- p.230 / Chapter Chapter 7 --- Conclusion --- p.232 / References --- p.236 / Acknowledgements

by Cheung Wah. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 64-68). / Tuberculosis in the Elderly : Presentation and Therapeutic Problems -a Clinical and Pharmacological Study / Contents / Chapter 1. --- Summary --- p.6 / Chapter 2. --- Introduction --- p.7 / Chapter 3. --- Aims of the Study --- p.11 / Chapter 4. --- Subjects and Methods --- p.12 / Chapter 5. --- Results --- p.36 / Chapter 6. --- Discussion --- p.55 / Chapter 7. --- Conclusion --- p.61 / Chapter 8. --- Acknowledgement --- p.63 / Chapter 9. --- References --- p.64

by King Yeung Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 143-148). / Abstracts in English and Chinese. / Title Page --- p.i / Acknowledgement --- p.ii / List of Abbreviations --- p.iii / Table of contents --- p.v / Abstract --- p.viii / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Liver diseases --- p.1 / Chapter 1.2 --- Current treatments of liver diseases --- p.3 / Chapter 1.3 --- Schizandrae --- p.5 / Chapter 1.3.1 --- Chemistry of Schizandrae (Wuweizi) --- p.6 / Chapter 1.3.2 --- Pharmacology of Wuweizi --- p.8 / Chapter 1.3.2.1 --- Hepato-protective effect of Wuweizi --- p.9 / Chapter 1.3.3 --- Toxicology and side-effects of Wuweizi --- p.11 / Chapter 1.4 --- Carbon tetrachloride (CC14) intoxication --- p.12 / Chapter 1.5 --- Hepatic drug metabolism: essential factors --- p.13 / Chapter 1.6 --- Aim --- p.14 / Chapter 2 --- Phase I metabolism --- p.15 / Chapter 2.1 --- Introduction --- p.15 / Chapter 2.2 --- Materials and Methods --- p.18 / Chapter 2.2.1 --- Animals --- p.18 / Chapter 2.2.2 --- Chemicals --- p.18 / Chapter 2.2.3 --- Instruments --- p.19 / Chapter 2.2.4 --- Preparation of Schizandra seed extract --- p.19 / Chapter 2.2.5 --- Animal model of liver damages --- p.20 / Chapter 2.2.6 --- Evaluation of protective effect of Schizandra extract --- p.22 / Chapter 2.2.7 --- Evaluation of healing effect of Schizandra extract --- p.24 / Chapter 2.2.8 --- Extraction of antipyrine from blood and urine --- p.26 / Chapter 2.2.9 --- TLC method for quantitative analysis of antipyrine --- p.26 / Chapter 2.2.10 --- Analysis of pharmacokinetic parameters of antipyrine --- p.27 / Chapter 2.2.11 --- Statistical analysis --- p.28 / Chapter 2.3 --- Results --- p.30 / Chapter 2.3.1 --- Effect of CCI4 and Schizandra seed extract on antipyrine metabolism --- p.30 / Chapter 2.4 --- Discussion --- p.41 / Chapter 3 --- Phase II metabolism --- p.44 / Chapter 3.1 --- Introduction --- p.44 / Chapter 3.2 --- Materials and Methods --- p.46 / Chapter 3.2.1 --- Chemicals --- p.46 / Chapter 3.2.2 --- Preparation of Schizandra extract --- p.46 / Chapter 3.2.3 --- Preparation of Salicylamide solution (for injection) --- p.47 / Chapter 3.2.4 --- Preparation of 2，4-dinitrophenylhydrazine solution --- p.47 / Chapter 3.2.5 --- Animal groups --- p.47 / Chapter 3.2.6 --- Animal model of liver damage --- p.48 / Chapter 3.2.7 --- Evaluation of the hepato-protective effect of Schizandra extract --- p.49 / Chapter 3.2.8 --- Determination of serum glutamate pyruvate transaminase (SGPT/ALT) and serum glutamate oxaloacetate transaminase (SGOT/AST) --- p.50 / Chapter 3.2.9 --- Salicylamide adminstration and plasma collection --- p.51 / Chapter 3.2.10 --- Procession of plasma and urine samples --- p.52 / Chapter 3.2.11 --- HPLC Analysis --- p.54 / Chapter 3.2.12 --- Preparation of liver microsomes --- p.55 / Chapter 3.2.13 --- Determination of cytochrome P450 --- p.56 / Chapter 3.2.14 --- Determination of protein content of the liver microsomes --- p.57 / Chapter 3.2.15 --- Data Analysis --- p.58 / Chapter 3.2.16 --- Statistical Analysis --- p.58 / Chapter 3.3 --- Results --- p.60 / Chapter 3.3.1 --- Liver enzyme levels --- p.60 / Chapter 3.3.2 --- Phase II metabolism profile of salicylamide --- p.61 / Chapter 3.3.3 --- Cytochrome P450 content of liver --- p.64 / Chapter 3.4 --- Discussion --- p.65 / Chapter 3.4.1 --- Liver enzyme assay --- p.65 / Chapter 3.4.2 --- Cytochrome P450 activity --- p.67 / Chapter 3.4.3 --- Hepatic metabolism of salicylamide --- p.68 / Chapter 3.4.4 --- Effect of CC14 intoxication on Phase II metabolism --- p.71 / Chapter 3.4.5 --- Wuweizi actions on Phase II metabolism --- p.73 / Chapter 4 --- Protein binding --- p.102 / Chapter 4.1 --- Introduction --- p.102 / Chapter 4.2 --- Materials and Methods --- p.104 / Chapter 4.2.1 --- Chemicals --- p.104 / Chapter 4.2.2 --- Instruments --- p.105 / Chapter 4.2.3 --- Preparation of Warfarin sodium solution --- p.105 / Chapter 4.2.4 --- Animal groups --- p.106 / Chapter 4.2.5 --- Equilibrium dialysis --- p.106 / Chapter 4.2.5.1 --- Equilibration time --- p.106 / Chapter 4.2.5.2 --- Equilibrium dialysis of different warfarin concentration --- p.107 / Chapter 4.2.6 --- High performance liquid chromatography analysis of warfarin --- p.108 / Chapter 4.2.7 --- Calibration curve --- p.109 / Chapter 4.3 --- Results --- p.111 / Chapter 4.3.1 --- Equilibriation time --- p.111 / Chapter 4.3.2 --- Calibration curve --- p.111 / Chapter 4.3.3 --- Free concentration of warfarin --- p.112 / Chapter 4.4 --- Discussion --- p.114 / Chapter 4.4.1 --- Effect of CCl4 intoxication on free percentage of warfarin --- p.114 / Chapter 4.4.2 --- Effcct of wuweizi cxtract on free percentage of warfarin --- p.115 / Chapter 4.4.2.1 --- Depletion of plasma albumin concentration --- p.116 / Chapter 4.4.2.2 --- Displacement of warfarin by WWZ extract --- p.117 / Chapter 4.4.3 --- Concentration dependent protein binding --- p.118 / Chapter 5 --- Hepatic blood flow --- p.124 / Chapter 5.1 --- Introduction --- p.124 / Chapter 5.2 --- Materials and Methods --- p.126 / Chapter 5.2.1 --- Chemicals....: --- p.126 / Chapter 5.2.2 --- Instruments --- p.126 / Chapter 5.2.3 --- Preparation of indocyanine green (ICG) solution --- p.126 / Chapter 5.2.4 --- Preparation of Schizandra seed extract --- p.127 / Chapter 5.2.5 --- Animals groups --- p.127 / Chapter 5.2.6 --- Animal model of liver damage --- p.128 / Chapter 5.2.7 --- Evaluation of hepato-protective effect of Schizandra extract --- p.129 / Chapter 5.2.8 --- Evaluation of healing effect of Schizandra extract --- p.129 / Chapter 5.2.9 --- Quantitative analysis of ICG in plasma by UV spectroscopy --- p.130 / Chapter 5.2.10 --- Analysis of pharmacokinetic parameters of ICG --- p.131 / Chapter 5.2.11 --- Statistical analysis --- p.132 / Chapter 5.3 --- Results --- p.133 / Chapter 5.4 --- Discussion --- p.135 / Chapter 5.4.1 --- Effect of CCl4 intoxication on hepatic blood flow --- p.135 / Chapter 5.4.2 --- Effect of WWZ pretreatment on hepatic blood flow --- p.135 / Chapter 5.4.3 --- Effect of WWZ healing on hepatic blood flow --- p.136 / Chapter 6 --- General conclusion --- p.139 / Significance of the study --- p.141 / References --- p.143