Asthma has long been considered as one of the most common health problems in the world. In Hong Kong, the prevalence of childhood asthma has increased from 4.8% in 1989, to 10.2% in 2002. In spite of the popularity of using Chinese herbs to treat asthma in Hong Kong, evidence on the effectiveness of herbal treatments is lacking. The Chinese herbal formula CUF2 is an innovative formula developed in the Institute of Chinese Medicine, The Chinese University of Hong Kong and it is composed of 5 commonly used Chinese herbs: Radix astragali, Cordyceps sinesis, Radix Scutellaria, Bulbus fritillariae cirrhosae and Radix stemonae. These herbs are chosen because of their well-known effects on either reducing coughing and sputum production, or anti-inflammatory and immunomodulatory activities. Based on the theoretical benefits of CUF2, we conducted a series of animal, in vitro and clinical studies to explore the efficacy, safety and mechanism of action of CUF2. / Following the establishment of the animal model, we have investigated the effect of CUF2 using this model of asthma. We found that 28 days pretreatment with CUF2 could reduce total cell number and eosinophilia in bronchoalveolar lavage fluid (BALF), prevent the eosinophil infiltration of airways, decrease pulmonary inflammatory cells, and reduce mucus and goblet cell hyperplasia. Especially in the reduction of goblet cell hyperplasia, we demonstrated that there was no significant difference between the effects of high dose CUF2 and dexamethasone (DEX). The eosinophilic immune-inflammatory responses in the airways in OA-sensitized/challenged rats were completely blocked by DEX returning to almost the same as those in normal rats, but the loss of thymus index and body weight were also observed. In contrast to the overall immunosuppressive effects of DEX, decreased production of inflammatory cytokines and chemokines [interleukin (IL)-4, tumor necrosis factor (TNF)-alpha, macrophage inflammatory protein (MIP)-2 and monocyte chemotactic protein-1 (MCP-1)], increased production of IL-10 and interferon-gamma (IFN-gamma) in BALF and no suppression of body weight and thymus index were demonstrated in the CUF2-treated groups. There was a dose-response relationship with more prominent effects seen with higher doses of CUF2. These findings indicate that the CUF2 has anti-airway inflammatory activity and exhibits immunomodulatory effect on Th1/Th2 responses in ovalbumin sensitized rats after allergen challenge, and this may imply its potential application to patients with allergic asthma. / In order to evaluate the clinical efficacy and safety, we conducted a multicenter, randomized, double blind, parallel and placebo controlled clinical trial. The same Chinese herbal formula was used in this clinical trial in 85 children aged 7-15 years with mild to moderate perennial asthma as an adjuvant therapy for 6 months. The primary outcome measure was the steroid dosage reduction. Other outcome measures included changes in disease severity score (DSS), lung function, serum concentrations of total IgE and the levels of some key allergy and inflammatory markers in peripheral blood, fractional exhaled nitric oxide (FENO), frequency of asthma attacks and quality of life (QOL). To assess safety, we did urinalysis, complete blood count, liver function and renal function at baseline and the end of the study. Drug compliance and adverse effects were also checked at each monthly visit. All patients were maintained on inhaled corticosteroid at their usual dose and dosing interval, and continued to receive short-acting, inhaled beta2-agonists as needed. There were no serious adverse events reported in the 6-month study period by any of the subjects. Hematological (except eosinophils count) and biochemical profiles (including renal function and liver function) remained within normal limits in the CUF2 group and placebo group at the end of the study. CUF2 was well tolerated in asthmatic children. Both CUF2 group and placebo group showed an improvement in most of clinical parameters. The dosage of inhaled corticosteroid was successfully reduced in both groups. Both groups had similar decrease in DSS, improved QOL and improved lung function parameter PEFR (L/min). Although these parameters showed no statistically significant difference between two groups, the percentage of eosinophils and lymphocytes were significantly decreased in CUF2 group as compared with the placebo group. The CUF2 group also showed improved diary symptom score, reduced expression of TNF-alpha and slight increase in anti-inflammation cytokine IL-18 in the blood. A trend of greater improvement in frequency of upper respiratory infection (URI) in CUF2 group was noted, but no statistical significance was attained. The changes in lung function parameter FEV1%, FENO, frequency of asthma attacks and serum concentrations of total IgE, IgE HDM, IgE cat, cockroach, TARC, LTB4 and LTC4D4E4 showed no statistically significant difference CUF2 group and placebo group. Overall, our data demonstrated that CUF2 treatment had some immunomodulatory effect in childhood asthma. Our findings should support further investigations of Chinese herbal medicine in the area of asthma without steroid therapy. / In the animal study, firstly we attempted to establish a novel murine model of asthma. We adopted a modified sensitization procedure using 10-point subcutaneous and intraperitoneal injections of Ovalbumin (OA) with freshly prepared Al(OH)3 and successfully induced severe airway allergic reactions in young Sprague Dawley (SD) rats. In this SD rat model, allergen exposure triggered accumulation of inflammation cells and eosinophils in the airway submucosa and goblet cells hyperplasia in mucosa, lung function test revealed obstructive lung function changes that included increase of lung resistance (RL) and decrease of dynamic lung compliance (Cdyn). Cytokine and chemokine assays showed that there was a change of the TH1/Th2 balance as illustrated by the high Th2 (interleukin-4)/Th1 (interferon-gamma) ratio. These results demonstrated the feasibility and validity of the SD rat model for studying allergic asthma. This SD model is much cheaper and readily available than the Brown Norway rat model and may facilitate further drug trial in asthma. / In the in vitro study, we investigated the effect of CUF2 on the release of cytokines and/or gene expression using human mast cell line HMC-1, human bronchial epithelial cell line BEAS-2B, peripheral blood mononuclear cells (PBMCs) from healthy subjects and airway cells present in induced sputum from asthmatic patients. We have shown (1) the CUF2 had no cytotoxic effects in final working concentration; (2) CUF2 had inhibitory effects on IL-6, TNF-alpha and granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion from HMC-1 in a dose-dependent manner. However, no reduction of IL-8 production in HMC-1 was demonstrated. (3) In addition, study of the effect of CUF2 on the expression of cytokine gene from HMC-1 showed that IL-4, IL-6 and GM-CSF mRNA expressions were down regulated at 24 hours, 24 hours, 16 hours and 24 hours of time points, respectively. No effects on IL-8 and TNF-alpha mRNA expression was observed. (4) Furthermore, CUF2 also significantly inhibited in vitro IL-6 and GM-CSF secretion in TNF-alpha stimulated BEAS-2B cell and reduced GM-CSF production in airway cells present in induced sputum from asthmatic children. (5) We observed that CUF2 enhanced TNF-alpha and IL-6 production but did not alter the levels of GM-CSF and IL-8 in mitogen-stimulated PBMCs from health subject. These findings suggest that pharmacological activities of the CUF2 may be mediated by regulating the production of cytokines in human mast cell, bronchial epithelial cell, airway cell and PBMCs. / In this study, a novel animal asthma model has been established. This model has extensively characterized and exhibited several inflammatory, immunological features that resemble those of human asthma and may facilitate further drug trial in asthma. CUF2 showed its efficacy treating the animal model of allergic asthma. In vitro study also provided evidence of its beneficial dichotomous effects on cytokine and chemokine production in HMC-1, PBMCs and airway cells. A multi-center, randomized, double blind, placebo controlled clinical trial showed that CUF2 had a certain degree of clinical efficacy. Furthermore, the use of CUF2, with the study dose and treatment period, was safe. The efficacy of individual ingredient and the mechanism of CUF2 have not been clarified and further investigations are warranted. In conclusion, our results provided evidence of the potential beneficial effect of CUF2 on immune system functions and supported the potential use of TCM as therapeutic drugs for allergic inflammatory diseases. / by Wong Yeuk Oi. / "September 2005." / Advisers: Yn Tz Sung; Kowk Pui Fung. / Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6296. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 330-349). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

For the development of a G6PD-deficient mouse model, we introduced the mutant Gpdxa-m1Neu allele (a severe ENU-induced mutation that results in 13-15% G6PD activities of wild type littermates) into the C57L/J background (a strain that constitutively exhibits low G6PD activity) through a breeding program. Of significance is that 78% of the F2 generation had G6PD activities <2 U/g Hb, levels similar to those of severe G6PD deficiency in human. The efficacy of this model was preliminary verified by the known haemolytic agent, naphthalene, as demonstrated by the decrease of GSH/GSSG ratio by 24.6% (P=0.032) and increase of methaemoglobin by 4.5 fold (P=0.8) when compared with the respective control without treatment. / Genetic analysis of 14 mutation hotpots was performed on 98 hemi-/homozygous and 17 heterozygous G6PD-deficient human subjects. We developed a novel Multiplex Primer Extension Reaction (MPER) assay and detected seven specific mutations in 97 subjects: c.1376G>T (33.7%), c.1388G>A (29.6%), c.871G>A + c.1311C>T (12.3%), c.95A>G (9.2%), c.392G>T (7.1%), c.1024C>T (6.2%) and c.1360C>T (1.0%). For the genotyping of 15 heterozygous female, all mutations were identified as follows: c.1376G>T/Normal (33.3%), c.1388G>A/Normal (26.7%), c.871G>A/Normal + c.1311C>T/Normal (20.0%), c.95A>G/Normal (13.3%) and c.392G>T./Normal (6.7%). The c.871G>A and 'silent' mutation c.1311 C>T was newly found to coexist in a high proportion of genotype in our population. / Glucose-6-phosphate dehydrogenase (G6PD)-deficient subjects are vulnerable to chemical-induced haemolysis if exposed to oxidative agents. Little is known, however, of the haemolytic effects of Chinese herbal medicine on G6PD-deficient subjects. Only one case study has reported that a G6PD-deficient newborn developed severe haemolysis after ingestion of Rhizoma Coptidis. Besides, recent studies reported that green tea and its constituents exerted pro-oxidative effects on cellular systems in culture. / Glucose-6-phosphate dehydrogenase deficiency is a genetic disorder inherited in the X-linked manner. The condition is prevalent in the Mediterranean region, Africa and Southeast Asia. In Hong Kong, the frequency of G6PD deficiency is around 4.5% in males and 0.3% in females. Over 140 specific mutations of the X-linked gene for G6PD have been characterized in various geographic regions. However, the local mutation pattern has not been clearly determined. / In conclusion, some Chinese herbal medicine, tea and tea polyphenols significantly altered the oxidative status of G6PD-deficient erythrocytes in vitro. Their in vivo effects on G6PD-deficient individuals would be further investigated by the novel G6PD-dificient mouse model. / In this study, we aim (1) to investigate effects of (a) a panel of Chinese Herbal Medicine (CHM), (b) tea and its constituents, on the oxidative status of human G6PD-deficient erythrocytes in vitro ; (2) to characterize the genotype of G6PD-deficiency in the Chinese population and their specific response to oxidative stress; (3) to develop a novel strain of mice as a model for study of chemicals agents on G6PD-deficient red cell in vivo. / Our results showed that six of eighteen CHM significantly reduced GSH levels in the G6PD-deficient erythrocytes (p<0.05, n=10). After exposure to 1 mg/mL of Rhizoma Coptidis, GSH levels in G6PD-deficient erythrocytes was decreased by 48.9 +/- 5.4% (P<0.001, n=10). At 5 mg/mL of Cortex Moutan, Radix Rehmanniae, Radix Bupleuri, Rhizoma Polygoni Cuspidati and Flos Chimonanthi, GSH levels were decreased significantly (P=0.001 to 0.004) by 51.8 +/- 7.6%, 25.9 +/- 6.7%, 21.0 +/- 6.9%, 17.5 $ 6.7% and 8.7 +/- 6.8% respectively. There were noticeable increases in levels of methaemoglobin by 2.8 fold (5 mg/mL, P=0.012) and 3.4 fold (10 mg/mL, P=0.016) in the presence of Rhizoma Coptidis and Cortex Moutan, respectively, in G6PD-deficient erythrocytes. / We also investigated the pro-oxidative effect of tea and its polyphenolic components on G6PD erythrocytes from G6PD-deficient (n=8) and normal adult (n=8) subjects. The tea extracts significantly reduced GSH and increased GSSG levels in G6PD-deficient erythrocytes in a dose-dependent manner (0.5-10 mg/mL), but not in normal erythrocytes. Similar dose-dependent responses to (-)-Epigallocatechin (EGC) and (-)-Epigallocatechin-3gallate (EGCG), but not to the other polyphenols, were observed. In G6PD-deficient cells, GSH was reduced by 43.3% (EGC at 0.05 mg/mL) and 33.3% (EGCG at 0.5 mg/mL), compared with pre-challenged levels. The concentration of methaemoglobin was increased significantly when these cells were challenged with tea extracts, and EGC. Plasma haemoglobin levels were higher in G6PD-deficient samples after exposure to tea extracts, EGCG, EGC and gallic acid, compared with those in normal blood. / Ko Chun Kay. / "August 2006." / Advisers: Tai Fai Fok; Kwai Har Karen Li. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1577. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. xxii-xliii). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Tong, Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 66-78). / Abstracts in English and Chinese; includes Chinese. / Acknowledgements --- p.i / Conferences & Academic Awards --- p.ii / Table of contents --- p.iii / List of figures --- p.vii / List of tables --- p.viii / List of abbreviations --- p.ix / Abstract --- p.x / Abstract (Chinese) / Chapter Chapter I --- Background of diabetes mellitus and DM complicating pregnancy …… --- p.1 / Chapter 1.1 --- Definitions and clinical manifestations of Diabetes Mellitus --- p.1 / Chapter 1.2 --- Diagnostic criteria of DM --- p.1 / Chapter 1.3 --- Classification of DM --- p.1 / Chapter 1.4 --- Prevalence of DM --- p.2 / Chapter 1.5 --- Aetiology and Pathogenesis of DM --- p.3 / Chapter 1.6 --- Treatment of DM --- p.3 / Chapter 1.7 --- Complications of DM --- p.4 / Chapter 1.8 --- DM complicating pregnancy --- p.4 / Chapter 1.8.1 --- Implications of DM complicating pregnancy --- p.4 / Chapter 1.8.2 --- Diabetic Embryopathy --- p.5 / Chapter 1.8.3 --- Incidences of the major congenital anomalies --- p.5 / Chapter 1.8.4 --- Possible pathogenesis of congenital anomalies in DM complicating pregnancy --- p.6 / Chapter 1.8.4.1 --- Apoptosis --- p.6 / Chapter 1.8.4.2 --- Oxidative stress --- p.7 / Chapter 1.8.4.3 --- Arachidonic acid and PGE2 --- p.7 / Chapter 1.8.5 --- Clinical management of DM complicating pregnancy --- p.8 / Chapter 1.8.5.1 --- Pre-pregnancy care --- p.8 / Chapter 1.8.5.2 --- Antenatal management of DM complicating pregnancy --- p.9 / Chapter Chapter II --- Background of Traditional Chinese Medicine in treatment of DM --- p.10 / Chapter 2.1 --- Definition and manifestations of DM in TCM theory --- p.10 / Chapter 2.2 --- Historical context of DM in TCM --- p.10 / Chapter 2.2.1 --- "Spring and Autumn Period and Warring States Period (770 B.C.一8 A.D.): The first nomenclature of ""Wasting Thirst""" --- p.10 / Chapter 2.2.2 --- "Han Dynasty (9 A.D.-280 A.D.)： monograph on ""Wasting Thirst""" --- p.11 / Chapter 2.2.3 --- "Sui and Tang Dynasty (581 A.D.-960 A.D.)： the diagnosing marker of ""Wasting Thirst""" --- p.11 / Chapter 2.2.4 --- Song Dynasty (960 A.D.-1270 A.D.): the Golden Time of developing the treatment on DM --- p.12 / Chapter 2.2.5 --- Ming and Qing Dynasty (1270 A.D. - 1911 A.D.): the integration period of TCM theory on DM --- p.15 / Chapter 2.3 --- Aetiology of DM in TCM theory --- p.15 / Chapter 2.3.1 --- Congenital weakness --- p.16 / Chapter 2.3.2 --- Improper diet --- p.16 / Chapter 2.3.3 --- Emotional disorders and overstrain --- p.17 / Chapter 2.3.4 --- Excessive sexual activities --- p.17 / Chapter 2.4 --- Pathogenesis of DM in TCM theory --- p.17 / Chapter 2.5 --- Prognosis of DM in TCM theory --- p.19 / Chapter 2.5.1 --- """Dual Qi-Yin Deficiency"" and ""Dual Yin-Yang Deficiency""" --- p.19 / Chapter 2.5.2 --- "Multi-systemic malfunction of ""Zang Fu""" --- p.19 / Chapter 2.6 --- Principle of treatment --- p.20 / Chapter 2.7 --- Commonly used herbal remedies and recent experimental studies --- p.20 / Chapter 2.8 --- TCM on relieving DM complications --- p.21 / Chapter 2.9 --- "Dwarf Lilyturf Tuber (Ophiopogonis Radix, Mai Dong,麥冬）" --- p.21 / Chapter 2.10 --- Objectives and hypothesis --- p.22 / Chapter 2.10.1 --- Objectives --- p.22 / Chapter 2.10.2 --- Hypotheses --- p.23 / Chapter Chapter III --- Methodology and Results --- p.24 / Chapter 3.1 --- Set up of mouse embryos --- p.24 / Chapter 3.1.1 --- Mouse strain --- p.24 / Chapter 3.1.2 --- Research animal ethnics and care guidelines --- p.24 / Chapter 3.1.3 --- Mouse sacrifice and embryo dissection --- p.24 / Chapter 3.1.4 --- Grouping of embryos --- p.25 / Chapter 3.2 --- Preparations of D-glucose --- p.25 / Chapter 3.3 --- Chinese medicine quality controls and preparations --- p.25 / Chapter 3.4 --- Whole mouse embryo culture --- p.26 / Chapter 3.5 --- Morphological scoring on mouse embryos and statistical analysis --- p.27 / Chapter 3.6 --- Establishment of cranial NTD by D-glucose --- p.28 / Chapter 3.6.1 --- Dosage of D-glucose to induce cranial NTD --- p.29 / Chapter 3.6.2 --- Result --- p.30 / Chapter 3.7 --- Experimental designs --- p.31 / Chapter 3.8 --- Part I: Efficacy and dose-response effects of Maidong extract --- p.32 / Chapter 3.8.1 --- Safety dose of Maidong extract on non-diabetic mouse embryos --- p.32 / Chapter 3.8.1.1 --- Dosage --- p.32 / Chapter 3.8.1.2 --- Result --- p.35 / Chapter 3.8.2 --- Efficacy and dose-effect response of Maidong extract on non-diabetic mouse embryos --- p.36 / Chapter 3.8.2.1 --- Dosage and grouping --- p.37 / Chapter 3.8.2.2 --- Result --- p.38 / Chapter 3.9 --- Part II: Efficacy and dose-response effects of serum from Maidong extract-treated rat serum --- p.40 / Chapter 3.9.1 --- Preparation of Maidong treated non-diabetic full rat serum --- p.41 / Chapter 3.9.1.1 --- Rats --- p.41 / Chapter 3.9.1.2 --- Dosage for feeding --- p.41 / Chapter 3.9.1.3 --- Administration --- p.42 / Chapter 3.9.1.4 --- Termination of rats and preparation of rat serum --- p.42 / Chapter 3.9.2 --- Safety dose of Maidong treated non-diabetic full rat serum non-diabetic mouse embryos --- p.43 / Chapter 3.9.2.1 --- Dosage --- p.43 / Chapter 3.9.2.2 --- Result --- p.44 / Chapter 3.9.3 --- Protective Effect of Maidong extract-treated full rat serum --- p.46 / Chapter 3.9.3.1 --- Dosage and grouping --- p.46 / Chapter 3.9.3.2 --- Result --- p.47 / Chapter 3.10 --- "Part III: Efficacy and dose-response effects of Ophiopogonin D, a major chemical component of Maidong in preventing hyperglycemia-induced cranial neural tube defect" --- p.49 / Chapter 3.10.1 --- Safety dose of Ophiopogonin D --- p.50 / Chapter 3.10.1.1 --- Preparation of Ophiopogonin D --- p.50 / Chapter 3.10.1.2 --- Dosage --- p.50 / Chapter 3.10.1.3 --- Results --- p.52 / Chapter 3.10.2 --- Efficacy and dose-response effects of Ophiopogonin D --- p.53 / Chapter 3.10.2.1 --- Dosage and grouping --- p.53 / Chapter 3.10.2.2 --- Results --- p.55 / Chapter Chapter IV --- Discussion --- p.58 / Chapter 4.1 --- Whole embryo culture system --- p.58 / Chapter 4.2 --- Quality control of Maidong extract --- p.58 / Chapter 4.3 --- "Therapeutic effect of single herb, formula and chemical components" --- p.59 / Chapter 4.4 --- Dosage of D-glucose to induce cranial NTD --- p.60 / Chapter 4.5 --- Dosage and efficacy of Maidong extract and Ophiopogonin D --- p.60 / Chapter 4.6 --- Administration of Maidong extract to non-diabetic female rats --- p.61 / Chapter Chapter V --- Conclusions --- p.63 / Chapter Chapter VI --- Future Study --- p.64 / References --- p.66

Wong, Ka Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 177-189). / Abstracts in English and Chinese; includes Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vii / List of Appendices --- p.xi / List of Tables --- p.xii / List of Figures --- p.xiv / Abbreviations --- p.xvi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General Introduction --- p.1 / Chapter 1.2 --- Background to the study --- p.2 / Chapter 1.2.1 --- Epidemiology of cancer --- p.2 / Chapter 1.2.1.1 --- Incidence and mortality in the World --- p.2 / Chapter 1.2.1.2 --- Incidence and mortality in Hong Kong --- p.4 / Chapter 1.2.2 --- Prevalence of Traditional Chinese Medicine (TCM) --- p.5 / Chapter 1.2.3 --- Prevalence of Traditional Chinese Medicine (TCM) in cancer --- p.6 / Chapter 1.2.4 --- Development of TCM in Hong Kong --- p.7 / Chapter 1.3 --- Theoretical rationale of the study --- p.8 / Chapter 1.4 --- Significance of the study --- p.11 / Chapter Chapter 2 --- Literature Review --- p.13 / Chapter 2.1 --- Introduction --- p.13 / Chapter 2.2 --- The concept of Advanced Cancer --- p.13 / Chapter 2.2.1 --- Pathology of Advanced Cancer --- p.14 / Chapter 2.2.1.1 --- Metastatic Cancer --- p.14 / Chapter 2.2.2 --- Sign and Symptoms of Advanced Cancer --- p.19 / Chapter 2.2.3 --- Diagnosis of Advanced Cancer --- p.19 / Chapter 2.2.4 --- Current Treatment for Advanced Cancer --- p.21 / Chapter 2.2.5 --- Limitation of Current Treatments --- p.24 / Chapter 2.3 --- Diagnosis and Treatment by TCM of Advanced Cancer --- p.26 / Chapter 2.3.1 --- (Advanced) Cancer from the TCM perspectives --- p.26 / Chapter 2.3.2 --- Diagnosis by TCM of Advanced Cancer --- p.27 / Chapter 2.3.3 --- Treatment by TCM of Advanced Cancer --- p.28 / Chapter 2.4 --- Current Evidences about the Clinical Effectiveness of TCM on Cancer Patients --- p.29 / Chapter 2.5 --- The concept of Health-related Quality of Life (HRQOL) --- p.35 / Chapter 2.5.1 --- The importance of HRQOL to cancer patients --- p.35 / Chapter 2.5.2 --- HRQOL instruments --- p.37 / Chapter 2.5.2.1 --- EORTC QLQ-C30 --- p.38 / Chapter 2.5.2.2 --- SF-36 --- p.39 / Chapter 2.6 --- Summary of Literature Review --- p.40 / Chapter 2.7 --- The research questions --- p.41 / Chapter 2.8 --- Research Hypotheses --- p.42 / Chapter 2.9 --- The design of TCM protocol --- p.42 / Chapter Chapter 3 --- Methodology --- p.45 / Chapter 3.1 --- Introduction --- p.45 / Chapter 3.2 --- Protocol --- p.45 / Chapter 3.2.1 --- Study Design --- p.46 / Chapter 3.2.2 --- Selection of Participants --- p.46 / Chapter 3.2.2.1 --- Inclusion criteria --- p.48 / Chapter 3.2.2.2 --- Exclusion criteria --- p.49 / Chapter 3.2.3 --- Sample size calculation --- p.50 / Chapter 3.2.4 --- Setting --- p.51 / Chapter 3.2.5 --- Interventions --- p.51 / Chapter 3.2.5.1 --- Treatment --- p.51 / Chapter 3.2.5.2 --- Medication and dose/dosage --- p.52 / Chapter 3.2.5.3 --- Treatment Assignment --- p.55 / Chapter 3.2.5.4 --- Concurrent Medications --- p.56 / Chapter 3.2.6 --- Procedure and Methods --- p.56 / Chapter 3.2.6.1 --- Informed Consent --- p.56 / Chapter 3.2.6.2 --- Documentation --- p.57 / Chapter 3.2.6.3 --- Assessment Procedure --- p.57 / Chapter 3.2.7 --- Outcome Measurements --- p.62 / Chapter 3.2.7.1 --- Survey Questionnaire --- p.62 / Chapter 3.2.7.2 --- Quality of life (QOL) instruments --- p.62 / Chapter 3.2.7.3 --- Global Ratings --- p.64 / Chapter 3.2.7.4 --- Physical Examination and Laboratory tests --- p.65 / Chapter 3.2.8 --- Safety Considerations --- p.66 / Chapter 3.2.8.1 --- Adverse Events (AE) --- p.66 / Chapter 3.2.8.2 --- Serious Adverse Event (SAE) --- p.66 / Chapter 3.2.8.3 --- Causality Assessment --- p.67 / Chapter 3.2.9 --- Ethical consideration --- p.68 / Chapter 3.2.10 --- Data Collection --- p.69 / Chapter 3.3 --- Data analysis --- p.69 / Chapter 3.4 --- Expected Outcomes of Study --- p.71 / Chapter Chapter 4 --- Results --- p.72 / Chapter 4.1 --- Study Progress --- p.72 / Chapter 4.2 --- The Participants --- p.72 / Chapter 4.3 --- Clinical characteristics and Socio-demographics of Participants --- p.75 / Chapter 4.4 --- Main Outcome - Quality of Life --- p.78 / Chapter 4.4.1 --- QLQ-C30 --- p.79 / Chapter 4.4.1.1 --- Scoring and Transforming of items into scales --- p.79 / Chapter 4.4.1.2 --- Changes of Individual Scale at Different Visits --- p.80 / Chapter 4.4.1.3 --- Clinical significance of Scales --- p.98 / Chapter 4.4.2 --- SF-36 --- p.104 / Chapter 4.4.2.1 --- Scoring and Transforming of items into scales --- p.104 / Chapter 4.4.2.2 --- Changes of Individual Scale at Different Visits --- p.104 / Chapter 4.4.2.3 --- SF-36 Summary Scales --- p.113 / Chapter 4.4.3 --- Correlation of QLQ-C30 and SF-36 --- p.115 / Chapter 4.5 --- Measurement of Physical examination --- p.117 / Chapter 4.5.1 --- Body Weight --- p.117 / Chapter 4.6 --- Measurement of Laboratory Blood tests --- p.118 / Chapter 4.6.1 --- "Comparison of CBC, RFT, LFT and LD" --- p.118 / Chapter 4.6.2 --- Tumor Markers --- p.120 / Chapter 4.7 --- Adverse Events and Serious Adverse Events --- p.121 / Chapter 4.8 --- Global Ratings --- p.123 / Chapter 4.8.1 --- Global Rating 1 - Severity of Disease --- p.123 / Chapter 4.8.2 --- Global Rating 2 - Global Disease Status --- p.124 / Chapter 4.8.2.1 --- Change in Global Disease Status --- p.125 / Chapter 4.8.2.2 --- Agreement between RCMP and clinician --- p.125 / Chapter 4.8.2.3 --- Patients' perception after treatment --- p.126 / Chapter 4.9 --- Distribution of TCM patterns and Chinese herbal medicines --- p.127 / Chapter 4.10 --- Survival Rate --- p.132 / Chapter 4.11 --- Conclusion --- p.133 / Chapter Chapter 5 --- Discussion --- p.135 / Chapter 5.1 --- Conclusion on findings --- p.135 / Chapter 5.2 --- Baseline profile of participants --- p.137 / Chapter 5.3 --- Feasibility of TCM on advanced cancer patients --- p.139 / Chapter 5.3.1 --- Recruitment of Participants --- p.139 / Chapter 5.3.2 --- Compliance of participants to the study schedule --- p.140 / Chapter 5.4 --- Health-related Quality of Life --- p.142 / Chapter 5.5 --- Safety of TCM --- p.149 / Chapter 5.6 --- Chinese medicine practitioner vs Western medicine doctor --- p.150 / Chapter 5.7 --- TCM pattern differentiation and treatment --- p.151 / Chapter 5.8 --- Implication of study --- p.154 / Chapter 5.8.1 --- Clinical implication --- p.154 / Chapter 5.8.2 --- Policy implication --- p.154 / Chapter 5.9 --- Limitations of the study --- p.155 / Chapter 5.10 --- Recommendations for further studies --- p.157 / Chapter 5.11 --- Overall Conclusion --- p.158 / Appendices --- p.160 / References --- p.177

Yu, Siu Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 117-124). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Chinese Abstract --- p.iv / Table of Contents --- p.v / List of Figures --- p.viii / List of Tables --- p.x / List of Abbreviations --- p.xi / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General introduction of sleep --- p.1 / Chapter 1.1.1 --- Sleep disorders --- p.1 / Chapter 1.1.2 --- Classification systems for sleep disorders --- p.2 / Chapter 1.2 --- Insomnia --- p.4 / Chapter 1.2.1 --- Definition --- p.4 / Chapter 1.2.2 --- Consequences of insomnia --- p.6 / Chapter 1.2.3 --- Prevalence --- p.8 / Chapter 1.2.4 --- Subtypes of insomnia --- p.9 / Chapter 1.2.5 --- Causes --- p.12 / Chapter 1.2.6 --- Treatment of insomnia --- p.13 / Chapter 1.2.6.1 --- Cognitive-behavioral therapy for insomnia --- p.14 / Chapter 1.2.6.2 --- Pharmacological treatment for insomnia --- p.17 / Chapter 1.3 --- Traditional Chinese medicine and herbs in SD formula --- p.22 / Chapter 1.4 --- Drosophila model for studying sleep --- p.25 / Chapter 1.4.1 --- Drosophila as a disease model --- p.25 / Chapter 1.4.2 --- Drosophila Sleep --- p.26 / Chapter 1.4.3 --- Similarity of Drosophila and mammalian sleep --- p.26 / Chapter 1.4.4 --- Methods for measuring Drosophila sleep --- p.29 / Chapter 1.4.4.1 --- Surrogate measurement of sleep in Drosophila --- p.31 / Chapter 1.5 --- Objectives of study --- p.33 / Chapter 2 --- Materials and Methods --- p.35 / Chapter 2.1 --- Preparation of the Sleep Disorder (SD) extract --- p.35 / Chapter 2.2 --- Establishment of the Drosophila sleep model --- p.38 / Chapter 2.2.1 --- Drosophila culture --- p.38 / Chapter 2.2.1.1 --- Fly stock --- p.38 / Chapter 2.2.1.2 --- Fly food --- p.38 / Chapter 2.2.1.3 --- Culture environment --- p.38 / Chapter 2.2.2 --- Preparation of flies for experiments --- p.39 / Chapter 2.2.3 --- Agar food and drug preparation --- p.39 / Chapter 2.2.4 --- Measurement of activity and sleep in fly --- p.40 / Chapter 2.2.5 --- Determining the effects of SD extract on Drosophila sleep --- p.40 / Chapter 2.2.5.1 --- Data analysis --- p.41 / Chapter 2.2.6 --- Test of amount of food intake for different dosages of SD using food dye --- p.41 / Chapter 2.2.7 --- Survival test --- p.42 / Chapter 2.3 --- Establishment of the Drosophila caffeine-induced insomnia model --- p.43 / Chapter 2.3.1 --- Determining the effects of caffeine on the Drosophila sleep --- p.43 / Chapter 2.3.2 --- Determining the effects of SD extract on the Drosophila caffeine-induced insomnia model --- p.43 / Chapter 2.3.2.1 --- HPLC determination of caffeine intake in Drosophila --- p.44 / Chapter 2.3.2.2 --- "Spectrophotometric measurement of caffeine, SD and caffeine-SD solutions" --- p.45 / Chapter 2.4 --- "Expression of Cyp6a8, Djun and Dfos in drug-treated Drosophila heads" --- p.46 / Chapter 2.4.1 --- Drug treatment and collection of fly head samples --- p.46 / Chapter 2.4.2 --- Total RNA extraction from fly heads --- p.46 / Chapter 2.4.3 --- Real-time polymerase chain reaction analysis --- p.48 / Chapter 2.5 --- Determining the effects of SD formula on short-sleep mutants --- p.51 / Chapter 2.5.1 --- Fly stocks --- p.51 / Chapter 2.5.2 --- Experimental design --- p.51 / Chapter 3. --- Results --- p.53 / Chapter 3.1 --- Establishment of the Drosophila sleep model --- p.53 / Chapter 3.1.1 --- Baseline activity and sleep --- p.53 / Chapter 3.1.2 --- Effect of SD on Drosophila sleep --- p.55 / Chapter 3.1.3 --- Amount of food intake for different dosages of SD --- p.57 / Chapter 3.1.4 --- Effect of SD on the survival of wide-type (CSI) flies --- p.59 / Chapter 3.2 --- Establishment of the caffeine-induced insomnia model in Drosophila --- p.61 / Chapter 3.2.1 --- Effect of Caffeine on Drosophila sleep --- p.61 / Chapter 3.2.2 --- Effect of the SD on the caffeine-induced wakefulness --- p.64 / Chapter 3.2.3 --- Validation of caffeine intake by HPLC --- p.68 / Chapter 3.2.4 --- "Spectra of caffeine, SD and caffeine-SD solutions" --- p.72 / Chapter 3.3 --- Effect of SD on the sleep of short-sleep mutants --- p.74 / Chapter 3.3.1 --- fumin mutant --- p.74 / Chapter 3.3.2 --- minisleep mutant --- p.78 / Chapter 3.3.3 --- HkY fly --- p.82 / Chapter 3.4 --- Effect of the SD and caffeine on gene expression --- p.86 / Chapter 3.4.1 --- Effect of the SD and caffeine on Cyp6a8 mRNA expression --- p.86 / Chapter 3.4.2 --- Effect of the SD and caffeine on Djun mRNA expression --- p.89 / Chapter 3.4.3 --- Effect of the SD and caffeine on Dfos mRNA expression --- p.91 / Chapter 4. --- Discussion --- p.93 / Chapter 4.1 --- Rationales for evaluating the effect of SD formula in Drosophila model --- p.94 / Chapter 4.2 --- Establishment of the Drosophila Sleep model --- p.96 / Chapter 4.2.1 --- Hypnotic effect of SD in Drosophila --- p.97 / Chapter 4.2.2 --- Toxicity of SD extract in fly --- p.98 / Chapter 4.3 --- Effect of SD on Drosophila caffeine-induced insomnia model --- p.100 / Chapter 4.3.1 --- Drug administration in Drosophila --- p.102 / Chapter 4.4 --- Effect of SD on Short-sleep mutant --- p.105 / Chapter 4.5 --- Study of gene expression by SD --- p.108 / Chapter 4.6 --- Limitations of the model --- p.112 / Chapter 5. --- Conclusion and Future Prospects --- p.115 / Chapter 5.1 --- Conclusion --- p.115 / Chapter 5.2 --- Future prospects --- p.115 / References --- p.117

Wong Kin Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 151-166). / Abstracts in English and Chinese. / Chapter (I) --- ABSTRACT (IN ENGLISH) --- p.i / Chapter (II) --- Abstract (in Chinese) --- p.iv / Chapter (III) --- ACKNOWLEDGEMENTS --- p.vii / Chapter (IV) --- PERSONAL CONTRIBUTION TO THE WORK --- p.ix / Chapter (V) --- PUBLICATIONS --- p.x / Chapter (VI) --- TABLE OF CONTENTS --- p.xi / Chapter (VII) --- List of Abbreviations --- p.xvi / Chapter (VIII) --- LIST OF FIGURES --- p.xx / Chapter (IX) --- LIST OF TABLES --- p.xxii / Chapter Section 1: --- GENERAL INTRODUCTION / Chapter CHAPTER 1 --- General Introduction of Atopic Dermatitis --- p.1-8 / Chapter 1.1. --- Definition of Atopic Dermatitis --- p.1 / Chapter 1.2. --- Epidemiology and Classification --- p.3 / Chapter 1.3. --- Factors Provoking Flares of AD / Chapter 1.3.1. --- Genetics --- p.5 / Chapter 1.3.2. --- "Allergens-Food Allergens, Aeroallergens and Autoallergens" --- p.6 / Chapter 1.3.3. --- Microbial Colonization: Staphylococcus Aureus (S. aureus) --- p.7 / Chapter CHAPTER 2 --- Measurements of AD Severity and Quality of Life Impairment --- p.9-14 / Chapter 2.1. --- Scoring of Atopic Dermatitis severity and the SCORing Atopic Dermatitis (SCORAD) Index --- p.9 / Chapter 2.2. --- Quality of life Measurement --- p.10 / Chapter 2.3. --- The Children's Dermatology Life Quality Index --- p.11 / Chapter CHAPTER 3 --- Management of AD --- p.15-19 / Chapter 3.1. --- Current Management of AD and Their Drawbacks --- p.15 / Chapter 3.2. --- Traditional Chinese Herbal Medicne (TCHM) / Chapter 3.2.1. --- General Principle of TCHM --- p.17 / Chapter 3.2.2. --- Side Effects of Using TCHM --- p.18 / Chapter 3.2.3. --- Literature Reviews of TCHM Use in Treating AD --- p.18 / Chapter CHAPTER 4 --- The Pentaherbs Formula for AD Treatment --- p.20-26 / Chapter 4.1. --- Pilot study: Pentaherbs Capsule as Treatment Option of AD Children --- p.20 / Chapter 4.2. --- Literature Review: Nature of Five Herbs / Chapter 4.2.1. --- PHF as Treatment Option of AD under TCHM Concepts --- p.22 / Chapter 4.2.2. --- PHF as Treatment Option of AD from Modern Research Literature --- p.22 / Chapter CHAPTER 5 --- Pathobiology of Atopic Dermatitis --- p.27-40 / Chapter 5.1. --- Nature of Complexity of Pathogenesis --- p.27 / Chapter 5.2. --- Skin barrier-impairment of epidermal barrier --- p.28 / Chapter 5.3. --- Biphasic T cell response in skin of AD --- p.29 / Chapter 5.4. --- Nature of Immunoglobulin-E and its Role in Atopic Dermatitis --- p.32 / Chapter 5.5. --- Innate Immunity Defect in AD --- p.33 / Chapter 5.6. --- Role of Superantigen in Pathogenesis of AD --- p.35 / Chapter 5.7. --- "Cytokines, Chemokines and Inflammatory Mediators in Pathogenesis of Atopic Dermatitis" / Chapter 5.7.1. --- Proinflammatory Cytokines --- p.37 / Chapter 5.7.2. --- Th1/Th2 Cytokines --- p.37 / Chapter 5.7.3. --- Chemokines --- p.38 / Chapter 5.7.4. --- Pruritus Mediators --- p.39 / Chapter Section 2: --- CLINICAL TRIAL OF PENTAHERBS / Chapter CHAPTER 1 --- Objective --- p.41 / Chapter CHAPTER 2 --- Materials and Methods (RCT) --- p.42-51 / Chapter 2.1. --- Materials / Chapter 2.1.1. --- SCORAD worksheet --- p.42 / Chapter 2.1.2. --- CDLQI questionnaire --- p.42 / Chapter 2.1.3. --- Allergic Rhinitis Score (ARS) --- p.43 / Chapter 2.1.4. --- ELISA Assay Kits --- p.43 / Chapter 2.1.5. --- EDTA blood collestion tubes --- p.43 / Chapter 2.2. --- Methods / Chapter 2.2.1. --- Design --- p.45 / Chapter 2.2.2. --- Intervention --- p.45 / Chapter 2.2.3. --- Treatment / Chapter 2.2.3.1 --- The Pentaherbs Formula --- p.45 / Chapter 2.2.3.2 --- Randomization --- p.48 / Chapter 2.2.3.3 --- Concomitant Treatment in Study Period --- p.48 / Chapter 2.2.4. --- Participants --- p.49 / Chapter 2.2.5. --- Outcome Measures --- p.50 / Chapter 2.2.6. --- Statistical Analysis --- p.50 / Chapter CHAPTER 3 --- Results (RCT) --- p.52-67 / Chapter 3.1. --- Demographics --- p.52 / Chapter 3.2. --- Drug Compliance --- p.55 / Chapter 3.3. --- Efficacy / Chapter 3.3.1. --- SCORAD Score --- p.56 / Chapter 3.3.2. --- Quality of Life Score --- p.56 / Chapter 3.3.3. --- Duration and Amount of CS Usage --- p.59 / Chapter 3.3.4. --- Amount of Antihistamine Usage --- p.61 / Chapter 3.3.5. --- Allergic Rhinitis Score --- p.61 / Chapter 3.3.6. --- Blood chemistry and Haematology --- p.63 / Chapter 3.3.7. --- Plasma TARC and BDNF level --- p.63 / Chapter 3.4. --- Tolerability --- p.65 / Chapter Section 3: --- IN VITRO STUDY OF PENTAHERBS / Chapter CHAPTER 1 --- Objectives and Study Design --- p.68 / Chapter CHAPTER 2 --- Materials and Methods (In vitro Study) --- p.69-86 / Chapter 2.1. --- Materials for in vitro study / Chapter 2.1.1. --- Preparation of the Water Extracts of PHF Capsules --- p.69 / Chapter 2.1.2. --- Endotoxin Assay --- p.69 / Chapter 2.1.3. --- Cell isolation and culture ofPBMC / Chapter 2.1.3.1 . --- Cell Isolation from Human Peripheral Blood --- p.70 / Chapter 2.1.3.2. --- Culture of Peripheral Blood Mononuclear Cells --- p.70 / Chapter 2.1.4. --- Trypan Blue Exclusion Assay --- p.72 / Chapter 2.1.5. --- [3H]-Thymidine incorporation Assay --- p.72 / Chapter 2.1.6. --- Supernatant Collection and ELISA --- p.72 / Chapter 2.1.7. --- RNA Extraction and RT-PCR / Chapter 2.1.7.1. --- Reagents for RNA Extraction --- p.73 / Chapter 2.1.7.2. --- Reagents for Reverse Transcription --- p.73 / Chapter 2.1.7.3. --- Reagents for Polymerase Chain Reaction --- p.74 / Chapter 2.1.7.4. --- Reagents for Gel Electrophoresis --- p.74 / Chapter 2.2. --- Methods / Chapter 2.2.1. --- Isolation and Culture PBMC / Chapter 2.2.1.1. --- Isolation of PBMC --- p.76 / Chapter 2.2.1.2. --- Culture of Isolated PBMC --- p.76 / Chapter 2.2.1.3. --- PHA/SEB Treatment --- p.77 / Chapter 2.2.2. --- Preparation of PHF Water Extracts and Endotoxin Level / Chapter 2.2.2.1. --- Hot Water Extraction --- p.78 / Chapter 2.2.2.2. --- Limulus Amebocyte Lysate Assay --- p.78 / Chapter 2.2.3. --- Study on the Cytotoxic and Mitogenic Effects of PHF on PBMC / Chapter 2.2.3.1. --- Trypan Blue Exclusion Assay --- p.80 / Chapter 2.2.3.2. --- [3H]-Thymidine Incorporation Assay --- p.80 / Chapter 2.2.4. --- Study on the Effect of PHF on PBMC Inflammatory Mediator Production / Chapter 2.2.4.1. --- Determination of Inflammatory Mediator Expression Levels by ELISA --- p.82 / Chapter 2.2.4.2. --- Semi-quantification of Inflammatory Mediator mRNA Levels by RT-PCR --- p.83 / Chapter 2.2.5. --- Statistical Analysis --- p.86 / Chapter CHAPTER 3 --- Results(In vitro) --- p.87-114 / Chapter 3.1. --- preparation of PHF Water Extracts and Endotxin Level --- p.87 / Chapter 3.2. --- Cytotoxicity Effect of PHF on PBMC --- p.88 / Chapter 3.3. --- Mitogenicity Effect of PHF on PBMC --- p.93 / Chapter 3.4. --- Effects of PHF on Expression of Inflammatory Mediators from PBMC Following Mitogen (PHA) Stimulation / Chapter 3.4.1. --- Effects of PHF on mRNA Expression of Inflammatory Mediators from PHA-stimulated PBMC --- p.98 / Chapter 3.4.2. --- Effects of PHF on Secretion of Inflammatory Mediators from PHA-stimulated PBMC --- p.101 / Chapter 3.5 --- Effects of PHF on Expression of Inflammatory Mediators from SEB-stimulated PBMC / Chapter 3.5.1. --- Effects of PHF on mRNA Expression of Inflammatory --- p.106 / Chapter 3.5.2. --- Effescts of PHF on secretion of inflammatory Mediatorsfrom SEM-Stimulated PBMC --- p.109 / Chapter 3.6. --- Summarization of Effects of PHF on Expression of Inflammatory Mediators from PHA- and SEB-stimulated PBMC / Chapter 3.6.1. --- Mitogen (PHA) Stimulation --- p.114 / Chapter 3.6.2. --- Superantigen (SEB) Stimulation --- p.114 / Chapter Section 4: --- DISCUSSIONS / Chapter CHAPTER 1 --- Discussions on RCT of PHF --- p.115-122 / Chapter 1.1. --- Clinical Efficacy and Tolerability of PHF for Treatment of Children AD: a RCT study / Chapter 1.2. --- Efficacy of PHF for Treatment of Children with AD --- p.117 / Chapter 1.3. --- Safety and Tolerability of PHF Use for Treatment of Children with AD --- p.119 / Chapter 1.4. --- Rounding up --- p.121 / Chapter CHAPTER 2 --- Discussions on In vitro Immunomodulatory Activities of PHF --- p.123-130 / Chapter 2.1. --- General Effects of PHF on PBMC --- p.123 / Chapter 2.2. --- Effects of PHF on Inflammatory Mediators Expression in PBMC --- p.124 / Chapter CHAPTER 3 --- Limitations of the Present Study --- p.131-132 / Chapter Section 5: --- CONCLUSIONS AND FUTURE PROSPECTS / Chapter CHAPTER 1 --- Conclusions --- p.133 / Chapter CHAPTER 2 --- Future Prospects --- p.134-135 / Chapter Section 6: --- APPENDICES / Appendix1 --- p.137 / Appendix2 --- p.142 / Appendix3 --- p.149 / Chapter Section 7: --- BIBLIOGRAPHY --- p.151-166

published_or_final_version / Architecture / Master / Master of Architecture

M. Tech. Entrepreneurship / The purpose of this study is to develop a consumer profile of traditional Chinese medicine consumption in South Africa. The research was based upon a nomethetic survey, a total sample size of 321 respondents was selected according to the convenience sampling technique to participate in the research. Descriptive data analysis was performed indicating that behaviour control and social impact norms primarily influencing the purchase of traditional Chinese medicine.

The Best M.Phil Thesis in the Faculties of Dentistry, Engineering, Medicine and Science (University of Hong Kong), Li Ka Shing Prize,1995-1997 / published_or_final_version / Chemistry / Master / Master of Philosophy

published_or_final_version / Chinese Medicine / Master / Master of Philosophy