Apart from associated genes, a candidate causative gene NTF4 was screened and two novel putative mutations (Gly157Ala and Ala182Val) detected, likely accounting for 0.29% of POAG. In the exploration of new POAG genes, two functional candidates CNTF and SPARC were screened and excluded. / Differential association profiles were found for SNPs in/near CAV1, CAV2, CYP46A1, LMX1B, PLXDC2, TLR4, TMTC2, ZP4 and 2p16.3. SNPs at CAV1, CAV2, TLR4 and 2p16.3 were associated with POAG, whilst SNPs around other genes were unlikely to be risk factors for the disease, at least in Chinese. TLR4 rs7037117 was associated with HTG in southern Chinese (P=0.0016, OR=2.72, recessive model). SNP rs1533428 at 2p16.3 showed an age-specific association of with late-onset POAG (age at diagnosis >60 years; P=1.14x10-5, OR=2.02, dominant model) but not with juvenile- and adult-onset POAG. Moreover, rs1533428 formed a joint effect with rs7037117 to confer stronger risk to HTG (P=2.8x10 -4, OR=4.53). Besides, rs4236601 near the CAV1 and CAV2 genes was confirmed as a risk factor for POAG and another two protective SNPs rs6975771 and rs959173 were identified; moreover, that the risk and protective alleles were located in different haplotypes suggested multiple roles of the genes. / Glaucoma is a group of degenerative optic neuropathies and the leading cause of irreversible blindness worldwide. Primary open-angle glaucoma (POAG) is a major type of glaucoma in most populations. It is classified into high-tension glaucoma (HTG) and normal-tension glaucoma (NTG) according to the level of intraocular pressure. POAG has complex etiology. It could be monogenic or caused by multiple risk factors. At least 22 linkage loci have been mapped, with 3 genes (MYOC, OPTN, and WDR36 ) identified. Also, more than 30 susceptibility genes have been reported, many of which, however, remain unverified. / In the mapping of the causal gene at GLC1N, a truncation mutation c.1090delT in the MEGF11 gene was found to be cosegregated with glaucoma in the GLC1N-linked pedigree. Subsequent identification of c.1090delT in an unrelated JOAG patient supported that it is a disease-causing mutation. The identification of four splice-site mutations (IVS17+2insT, IVS17-4C>G, IVS17-2A>G and c.2472A>C) exclusively in patients provided further evidence supporting MEGF11 as a causative gene for POAG. Mutations in this gene likely account for approximately 1% of POAG or 2% of JOAG. / This thesis describes our work on the identification of new POAG genes by using a 3-tiered strategy: (1) to identify new genetic profiles of variants around the CAV1, CAV2, CYP46A1, LMX1B, NTF4, PLXDC2, TLR4, TMTC2, ZP4 genes and the 2p16.3 locus; (2) to evaluate CNTF and SPARC as disease genes for POAG; and (3) to map the causal gene at the GLC1N locus for juvenile-onset POAG (JOAG). / Totally 1645 unrelated participants were enrolled, including a Hong Kong cohort of 281 HTG, 311 NTG and 248 controls, a Shantou cohort of 102 HTG, 28 NTG and 298 controls and, a Beijing cohort of 177 HTG and 200 controls. Also involved were members of the GLC1M-linked Philippine pedigree and the GLC1N-linked Hong Kong pedigree with JOAG, which have been previously described. / Chen, Lijia. / Adviser: Chi Pui Pang. / Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 185-210). / 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, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

In the study of alphaA-crystallin (CRYAA), G98R CRYAA was cloned into a mammalian expression vector pcDNA6-His/myc version B and the sequence was confirmed by direct sequencing. Following lipophilic transfection to lens epithelial B3 cells, the recombinant mutated CRYAA protein was highly insoluble upon 0.5% Triton X-100 (Tx) extraction. It was retained and formed aggregation, and distributed in the endoplasmic reticulum (ER) along with the ER resident protein (protein disulfide isomerise). The wild-type (WT) CRYAA was found to be soluble and diffusely distributed in the cytoplasm. The accumulation of G98R mutant induced ER stress, and the affected cells were prone to apoptosis. After treatment with a small chemical molecule, the natural osmolyte trimethylamine N oxide (TMAO), the Tx insolubility of mutant protein was reduced in dose- and time-dependent manners. It was also prone to be degraded via ubiquitin proteasome pathway (UPP). In mutant-expressing cells, the mutant protein aggregation was decreased after treatment. The ER stress and the rate of apoptosis were also alleviated, probably mediated by heat shock response, as demonstrated by the effect of TMAO on heat shock protein 70 expression. / The third eye gene model was myocilin (MYOC ), the first identified gene responsible for primary open angle glaucoma. The aim of this study was to investigate if glaucoma-causing MYOC variants, including D384N MYOC, could be correctable. D384N MYOC was identified in a Chinese family diagnosed with high tension juvenile-onset primary open-angle glaucoma. Disease causing mutations in MYOC (R82C, C245Y, Q368X P370L, T377M, D380A, D384N, R422C, R422H, C433R, Y437H, I477N, I477S and N480K) were cloned into mammalian expression vector p3XFLAG-myc-CMV"-25 and the sequences confirmed by direct sequencing. Following lipophilic transfection to human trabecular meshwork (HTM) cells, the Tx solubility and secretion of MYOC and cell apoptosis were examined in the presence or not with small chemical treatments. 4-PBA, TMAO and deuterium oxide (D2O), reduced the portion of insoluble fractions to various extents in the mutant proteins. The osmolytes TMAO and D2O were more effective than 4-PBA in improving MYOC solubility. TMAO was further shown to improve the secretion and ER-Golgi trafficking of D384N MYOC, thereby reducing the ER stress and rescuing cells from apoptosis. (Abstract shortened by UMI.) / The truncated G165fsX8 gammaD-crystallin ( CRYGD) variant was studied to further examine the effects of small chemical-assisted protein rescue of a CRYGD mutant that causes congenital cataract. G165fsX8 CRYGD was identified in a Chinese family with nuclear type of congenital cataract. The mutation was cloned into a mammalian expression vector p3XFLAG-myc-CMV"-25 and sequence was confirmed by direct sequencing. Following lipophilic transfection to COS-7 cells, the G165fsX8 CRYGD mutant protein was significantly insoluble upon 0.5% Tx extraction and was mistrafficked to the nuclear envelope with co-localization with nuclear lamins, whereas WT protein was Tx soluble and nuclear located. Treatment with small chemical sodium 4-phenylbutyrate (4-PBA) substantially reduced the Tx insolubility and reversed the mutant protein to nuclear localization. This correction has resulted in better cell survival, probably via a heat-shock response, as demonstrated by heat-shock protein 70 up-regulation. / To date, many genes and mutations are identified to cause various ocular diseases. Some of them result in a disruption of protein folding, an important cause of disease pathogenesis and progression. In my laboratory, novel mutations of crystallins and myocilin have been identified to segregate with congenital cataract and primary open-angle glaucoma, respectively. In this thesis, I reported molecular investigations of the resultant protein variants and their altered cellular functions in relation to the clinical phenotypes that contributed to new understanding of the roles of these genes in ocular tissues. / Gong, Bo. / Adviser: Chi-Pui Pang. / Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 163-188). / 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, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Mak, Keng Hou. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 77-91). / Abstracts in English and Chinese. / Thesis Committee --- p.2 / Declaration --- p.3 / Table of Contents --- p.4 / List of Abbreviations --- p.6 / List of Figures --- p.8 / Abstract --- p.10 / Chapter Chapter 1 --- Introduction --- p.12 / Chapter 1.1 --- Background --- p.12 / Chapter 1.1.1 --- Overview of apoptosis --- p.12 / Chapter 1.1.2 --- Synopsis of the apoptotic pathway --- p.13 / Chapter 1.1.3 --- Defining apoptosis --- p.14 / Chapter 1.1.4 --- Interaction between pro- and anti-apoptotic factors determines cell fate --- p.14 / Chapter 1.1.5 --- DNA fragmentation during the execution phase --- p.15 / Chapter 1.1.6 --- Current understanding of the point of commitment in apoptosis --- p.16 / Chapter 1.1.7 --- Previous studies and hypotheses related to the reversibility of late-state apoptosis --- p.16 / Chapter 1.1.8 --- Unanswered questions --- p.19 / Chapter 1.2 --- "Hypothesis and objectives, Study models and Significance" --- p.19 / Chapter 1.2.1 --- Hypothesis and objectives --- p.19 / Chapter 1.2.2 --- Study models --- p.20 / Chapter 1.2.3 --- Significance --- p.20 / Chapter Chapter 2 --- Materials and Methods --- p.22 / Chapter Chapter 3 --- Results --- p.30 / Chapter 3.1 --- Dying cells reversed execution stage of apoptosis after removal of apoptotic stimuli --- p.30 / Chapter 3.2 --- Dying cells reversed apoptosis after DNA damage --- p.37 / Chapter 3.3 --- Genetic alterations and transformation occurred after reversal of apoptosis --- p.43 / Chapter 3.4 --- Investigating molecular mechanism driving reversal of apoptosis --- p.50 / Chapter 3.4.1 --- Preparation and characterization of samples for microarray --- p.50 / Chapter 3.4.2 --- Gene ontology enrichment analysis of the expression profile during reversal of apoptosis --- p.52 / Chapter 3.4.3 --- Interfering stress response or anti-apoptotic factors during the reversal of apoptosis drove cells to terminal death --- p.56 / Chapter Chapter 4 --- Discussion --- p.62 / Chapter 4.1 --- "Reversal of apoptosis in ""normal cells"" was observed" --- p.62 / Chapter 4.2 --- Cells surviving apoptosis had their genomes damaged and altered --- p.63 / Chapter 4.3 --- Transformation occurred after reversal of apoptosis --- p.65 / Chapter 4.4 --- Investigating molecular mechanism driving reversal of apoptosis --- p.65 / Chapter 4.5 --- Summary --- p.68 / Chapter Chapter 5 --- Perspectives --- p.70 / Chapter 5.1 --- Could reversal of apoptosis be evolutionarily advantageous? --- p.70 / Chapter 5.2 --- "Reversal of apoptosis as an ""individualistic"" behavior against organismal integrity" --- p.71 / Chapter 5.3 --- Proposed studies --- p.72 / Chapter 5.3.1 --- Other apoptotic targets that may leave persistent effects --- p.72 / Chapter 5.3.2 --- Post- caspase activation regulation of apoptosis --- p.74 / Chapter 5.3.3 --- Identifying correlation between reversal of apoptosis and cancer --- p.74 / Chapter 5.3.4 --- Single cell methods and cell tracking system for further studies --- p.75 / Chapter 5.3.5 --- Notes on studying reversal of apoptosis in relation to phagocytosis --- p.76 / References --- p.77

前言：間充質幹細胞容易擴增並且能分化為成骨細胞、軟骨細胞和脂肪細胞，並且能對炎症、感染和損傷做出反應，並且遷移到相應的組織部位。這些特性使間充質幹細胞成為骨骼組織工程學中非常重要的細胞來源。外周血間充質幹細胞是一種存在於血液中的間充質幹細胞，而主要的間充質幹細胞存在與骨髓中，被稱之為骨髓間充質幹細胞。在我們實驗室之前的研究中通過DNA微陣列發現外周血間充質幹細胞中很多基因的表達與骨髓間充質幹細胞有很大區別。這其中的一些基因可能參與調控間充質幹細胞的分化和歸巢，我們從中挑選了三個變化比較明顯的基因--CRBP1, N-cadherin和 SOX11做進一步研究。本研究的目的在於研究CRBP1, N-cadherin和 SOX11在骨髓間充質幹細胞分化和遷移中的作用及相關機理。 / 方法：培養的骨髓間充質幹細胞來源於6-8周大小的SD大鼠。細胞的表型經過多分化潛能測試（成骨分化，成脂分化和成軟骨分化）和流式細胞儀檢驗。克隆大鼠的CRBP1, N-cadherin和SOX11基因到慢病毒載體。而且還設計了針對CRBP1和 N-cadherin的shRNA及非特異性對照shRNA。慢病毒由暫態轉染293FT細胞產生。細胞遷移實驗採用了BD Falcon的細胞遷移系統（cell culture insert）。實驗採用了定量PCR、免疫共沉澱、western雜交和雙螢光報告檢驗。對於體內實驗，細胞經感染帶有不同基因的病毒後，種植到Si-TCP材料並移植到裸鼠皮下。8周後，收集樣品進行組織學和免疫組織學分析。最後，我們建立了大鼠的股骨開放式骨折模型，並在4天后將SOX11基因修飾的間充質幹細胞通過心臟注射打到大鼠體內。4周後，收集股骨骨折樣品並進行microCT、力學測試和組織學分析。 / 結果：CRBP1過表達能夠促進骨髓間充質幹細胞的成骨分化潛能，並能抑制其成脂分化。進一步的機理研究表明CRBP1可以通過與RXRα的蛋白相互作用抑制RXRα誘導的β-catenin降解，從而維持β-catenin和磷酸化-ERK1/2在較高的水準，導致間充質幹細胞成骨能力增強；N-cadherin過表達可以促進間充質幹細胞的遷移，但是卻通過下調β-catenin和磷酸化ERK1/2抑制其成骨分化。過表達SOX11可以通過增強BMP信號通路促進三系分化。SOX11還可以通過啟動CXCR4的表達來促進細胞遷移。最後，在大鼠的股骨開放骨折模型上通過系統注射，我們證明穩定過表達SOX11的間充質幹細胞遷移到骨折部位的數量明顯增加。這些細胞到達骨折部位以後可以起始骨痂的鈣化，促進骨折的修復。 / 結論：本研究證明CRBP1, N-cadherin 和SOX11具有調節骨髓間充質幹細胞遷移和/或分化的功能。這些基因也許會成為幹細胞治療的新靶點。系統注射SOX11基因修飾的骨髓間充質幹細胞對於骨折修復可能具有較好的療效。本研究初步研究了CRBP1, N-cadherin 和SOX11在間充質幹細胞中的作用，為探討以間充質幹細胞為基礎的組織工程的某些新臨床應用提供了一些線索。 / Introduction: Mesenchymal stem cells (MSCs) can be easily harvested, expanded, and have the capability of differentiating into osteoblasts, chondrocytes and adipocytes, and they can home to various tissues in response to stimuli such as inflammation, infection and injuries. MSCs are therefore valuable cell source for musculoskeletal tissue engineering. Peripheral blood-derived MSCs (PB-MSCs) are one kind of MSCs that reside in peripheral blood, whereas the main source of MSCs is bone marrow-derived MSCs (BM-MSCs). In our previous study, we found many genes were differentially expressed in the PB-MSCs compared to their counterpart BM-MSCs demonstrated by microarray analysis, among which the effects of CRBP1, SOX11 and N-cadherin on MSCs in terms of migration and differentiation are studied. / Methods: BM-MSCs and PB-MSCs were cultured from 6-8 weeks SD rats. The phenotypes of MSCs were characterized by tri-lineage (adipo-, osteo- and chondrogenic) differentiation and flow cytometry analysis. The genes encoding rat CRBP1, SOX11 and N-cadherin were cloned into lentiviral vectors respectively. shRNAs targeting CRBP1, N-cadherin, and one nonspecific shRNA were designed. Pseudo-lentivirus was produced by transient transfection of 293FT cells. Cell migration was examined using transwell insert culture system. Quantitative RT-PCR, CO-IP, western blot and dual-luciferase assay were employed in the studies. For in vivo study, MSCs transduced with different genes were seeded on Si-TCP scaffolds and implanted subcutaneously in nude mice. 8 weeks later, the samples were collected for histological and immunohistological analysis. Finally, an open femoral fracture model was established in 8-week old SD rats, SOX11-modified MSCs were injected at four days after fracture. At 4-week after MSCs injection, the femurs were collected for microCT, mechanical test and histological analysis. / Results: For CRBP1gene, our results showed that CRBP1 overexpression promoted osteogenic differentiation of BM-MSCs, while inhibited their adipogenic differentiation. We demonstrated that CRBP1 promoted osteogenic differentiation by inhibiting RXRα-induced β-catenin degradation through physical interactions, and maintaining β-catenin and pERK1/2 at higher levels. For N-cadherin gene, we found that N-cadherin overexpression promoted MSCs migration, and suppressed osteogenic potential of MSCs through inhibiting ERK and β-catenin signaling pathways. For SOX11 gene, we demonstrated that SOX11 overexpression enhanced the adipo-, osteo- and chondrogenic differentiation of BM-MSCs, through enhancing BMP signaling pathways. The migration capacity of BM-MSCs was also enhanced when Sox-11 was overexpressed, through activating CXCR4 expression. Finally, in the open femur fracture model we demonstrated that a larger number of SOX11-overexpressing BM-MSCs migrated to the fracture site, initiated earlier callus ossification and improved bone fracture healing quality. / Conclusions: This study demonstrated that CRBP1, N-cadherin and SOX11 gene can regulate the migration and/or differentiation potentials of BM-MSCs. These genes may become new therapeutic targets in stem cell therapy applications. Systemic administration of genetically modified SOX11-overexpressing BM-MSCs may be useful in promoting fracture healing. Overall, this study defined some unknown functions of CRBP1, N-cadherin and SOX11 in MSCs and shed the lights on some novel therapeutic implications for MSCs-based tissue engineering. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Xu, Liangliang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 128-144). / Abstract also in Chinese. / Declaration --- p.i / Abstract --- p.ii / 摘要 --- p.v / Acknowledgements --- p.vii / Chapter 1 --- p.1 / Introduction --- p.1 / Chapter 1.1 --- Mesenchymal stem cells --- p.2 / Chapter 1.1.1 --- Characteristics of mesenchymal stem cells --- p.2 / Chapter 1.1.2 --- Bone marrow- and peripheral blood-derived MSCs --- p.4 / Chapter 1.1.3 --- Other tissue-derived MSCs --- p.5 / Chapter 1.2 --- Adipogenesis of MSCs --- p.6 / Chapter 1.3 --- Chondrogenesis of MSCs --- p.7 / Chapter 1.4 --- Osteogenesis of MSCs --- p.8 / Chapter 1.4.1 --- Regulators of osteogenesis --- p.9 / Chapter 1.4.2 --- Stratergies for improving bone tissue engineering --- p.11 / Chapter 1.5 --- Signaling pathways involved in osteogenesis --- p.13 / Chapter 1.5.1 --- ERK signaling pathway --- p.14 / Chapter 1.5.2 --- Wnt signaling pathway --- p.15 / Chapter 1.5.3 --- BMP signaling pathway --- p.17 / Chapter 1.6 --- Migration of MSCs --- p.20 / Chapter 1.7 --- Fracture healing --- p.22 / Chapter 1.8 --- Clinical application of MSCs --- p.23 / Chapter 1.8.1 --- BM-MSCs vs. PB-MSCs --- p.24 / Chapter 1.8.2 --- Autologous vs. Allogeneic MSCs transplantation --- p.25 / Chapter 1.9 --- Scope of the present study --- p.26 / Chapter 1.9.1 --- CRBP1 --- p.26 / Chapter 1.9.2 --- N-cadherin --- p.27 / Chapter 1.9.3 --- SOX11 --- p.27 / Chapter 1.10 --- Experimental scheme --- p.29 / Chapter 2 --- p.31 / Comparison between PB-MSCs and BM-MSCs --- p.31 / Chapter 2.1 --- Chapter introduction --- p.32 / Chapter 2.2 --- Materials and methods --- p.33 / Chapter 2.2.1 --- Cell culture --- p.33 / Chapter 2.2.2 --- Flow cytometry --- p.33 / Chapter 2.2.3 --- Adipogenic differentiation --- p.34 / Chapter 2.2.4 --- Osteogenic differentiation --- p.34 / Chapter 2.2.5 --- RNA Extraction and Real-time PCR --- p.34 / Chapter 2.3 --- Results --- p.35 / Chapter 2.3.1 --- Morphology of PB-MSCs --- p.35 / Chapter 2.3.2 --- Cellular surface markers of BM-MSCs and PB-MSCs --- p.36 / Chapter 2.3.3 --- Multi-differentiation potential of BM-MSCs and PB-MSCs --- p.38 / Chapter 2.3.4 --- Target genes expression in BM-MSCs and PB-MSCs --- p.39 / Chapter 2.4 --- Discussion and future work --- p.40 / Chapter 3 --- p.41 / Role of CRBP1 in Differentiation and Migration of MSCs --- p.41 / Chapter 3.1 --- Chapter introduction --- p.42 / Chapter 3.2 --- Materials and methods --- p.46 / Chapter 3.2.1 --- Chemicals --- p.46 / Chapter 3.2.2 --- Isolation and culture of BM-MSCs --- p.46 / Chapter 3.2.3 --- RNA Extraction and Real-time PCR --- p.47 / Chapter 3.2.4 --- Plasmid construction, transfection, production of lentivirus and infection --- p.48 / Chapter 3.2.5 --- Osteogenic differentiation --- p.50 / Chapter 3.2.6 --- Adipogenic differentiation --- p.50 / Chapter 3.2.7 --- Western blot --- p.51 / Chapter 3.2.8 --- Immunofluorescence labeling and fluorescence microscopy --- p.52 / Chapter 3.2.9 --- Cell migration assay --- p.52 / Chapter 3.2.10 --- Ectopic bone formation assay --- p.52 / Chapter 3.2.11 --- Statistical analysis --- p.53 / Chapter 3.3 --- Results --- p.53 / Chapter 3.3.1 --- Transducing BM-MSCs with lentivirus carrying CRBP1 or shRNAs --- p.53 / Chapter 3.3.2 --- CRBP1 accelerates osteogenesis of BM-MSCs via enhancing ERK1/2 and β-catenin pathways --- p.56 / Chapter 3.3.3 --- CRBP1 stabilizes β-catenin by inhibiting RXRα-induced degradation --- p.58 / Chapter 3.3.4 --- CRBP1 inhibits adipogenesis of BM-MSCs --- p.61 / Chapter 3.3.5 --- CRBP1 overexpression has no effect on MSCs migration potential --- p.63 / Chapter 3.3.6 --- CRBP1 promotes ectopic bone formation in vivo --- p.64 / Chapter 3.4 --- Discussion --- p.66 / Chapter 3.5 --- Future work --- p.73 / Chapter 4 --- p.74 / Role of N-cadherin in Differentiation and Migration of MSCs --- p.74 / Chapter 4.1 --- Chapter introduction --- p.75 / Chapter 4.2 --- Materials and methods --- p.78 / Chapter 4.2.1 --- Chemicals --- p.78 / Chapter 4.2.2 --- Isolation and culture of BM-MSCs --- p.78 / Chapter 4.2.3 --- Plasmid construction, transfection, production of lentivirus and infection --- p.79 / Chapter 4.2.4 --- Osteogenic differentiation and ALP activity assay --- p.81 / Chapter 4.2.5 --- Western blot --- p.81 / Chapter 4.2.6 --- Ectopic bone formation assay --- p.82 / Chapter 4.2.7 --- Statistical analysis --- p.82 / Chapter 4.3 --- Results --- p.83 / Chapter 4.3.1 --- Expression of N-cadherin during osteogenesis in MSCs --- p.83 / Chapter 4.3.2 --- N-cadherin overexpression inhibits osteogenesis through suppressing β-catein and ERK1/2 signaling pathways --- p.84 / Chapter 4.3.3 --- N-cadherin silencing increases osteogenesis through enhancing β-catenin and ERK1/2 signaling pathways --- p.86 / Chapter 4.3.4 --- N-cadherin promotes migration of MSCs --- p.87 / Chapter 4.3.5 --- Cellular surface markers of SV40-immortalized MSCs --- p.89 / Chapter 4.3.6 --- N-cadherin inhibits ectopic bone formation in vivo --- p.89 / Chapter 4.4 --- Discussion --- p.91 / Chapter 4.5 --- Future work --- p.94 / Chapter 5 --- p.96 / Role of SOX11 in Differentiation and Migration of MSCs --- p.96 / Chapter 5.1 --- Chapter introduction --- p.97 / Chapter 5.2 --- Materials and methods --- p.105 / Chapter 5.2.1 --- Plasmid construction, transfection, production of lentivirus and infection --- p.105 / Chapter 5.2.2 --- Cell culture --- p.106 / Chapter 5.2.3 --- Luciferase reporter gene assay --- p.106 / Chapter 5.2.4 --- Osteogenic differentiation and ALP activity assay --- p.106 / Chapter 5.2.5 --- Adipogenic differentiation --- p.107 / Chapter 5.2.5 --- Chondrogenic diffferentiation --- p.107 / Chapter 5.2.6 --- Western blot --- p.108 / Chapter 5.2.7 --- RNA Extraction and Real-time PCR --- p.108 / Chapter 5.2.8 --- Cell migration --- p.110 / Chapter 5.2.9 --- Ectopic bone formation --- p.110 / Chapter 5.2.10 --- Fracture healing model and analysis --- p.111 / Chapter 5.2.11 --- Statistical Analysis --- p.112 / Chapter 5.3 --- Results --- p.112 / Chapter 5.3.1 --- SOX11 is upregulated during osteogenesis of BM-MSCs --- p.112 / Chapter 5.3.2 --- SOX11 promotes adipogenesis in BM-MSCs --- p.113 / Chapter 5.3.3 --- SOX11 promotes migration of BM-MSCs --- p.114 / Chapter 5.3.4 --- SOX11 promotes osteogenesis in BM-MSCs --- p.115 / Chapter 5.3.5 --- SOX11 promotes chondrogenesis of MSCs --- p.117 / Chapter 5.3.6 --- Mechanisms of how SOX11 regulates differentiation and migration of MSCs --- p.118 / Chapter 5.3.7 --- SOX11-modified MSCs promote bone fracture healing in an open femur fracture rat model --- p.122 / Chapter 5.4 --- Discussion --- p.126 / Chapter 5.5 --- Future work --- p.131 / Appendix --- p.153

Xue, Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 95-102). / Abstract also in Chinese. / Thesis committe --- p.2 / Statement --- p.3 / Abstract --- p.4 / Acknowledgement --- p.8 / General abbreviations --- p.10 / Abbreviations of chemicals --- p.13 / List of figures --- p.15 / List of tables --- p.16 / Table of contents --- p.17 / Chapter Chapter 1 --- General Introduction / Chapter 1.1 --- Impact of bacterial blight on rice production --- p.25 / Chapter 1.2 --- The plant immune system --- p.25 / Chapter 1.2.1 --- Preformed resistance --- p.25 / Chapter 1.2.2 --- PAMP triggered immunity (PTI) --- p.26 / Chapter 1.2.3 --- Effecter triggered immunity (ETI) --- p.27 / Chapter 1.2.3.1 --- R genes --- p.27 / Chapter 1.2.3.2 --- Hypersensitive responses (HR) --- p.27 / Chapter 1.2.3.3 --- Systemic acquired resistance (SAR) --- p.28 / Chapter 1.2.3.3.1 --- Salicylic acid is required for SAR establishment --- p.28 / Chapter 1.2.3.3.2 --- Involvement of lipid-based molecules in SAR signaling --- p.28 / Chapter 1.2.3.3.3 --- NPR1: the master regulator of SAR --- p.29 / Chapter 1.2.3.3.4 --- Expression of pathogenesis related (PR) genes --- p.29 / Chapter 1.2.4 --- Interaction between SA and JA --- p.29 / Chapter 1.2.5 --- Other important signaling components in plant defense responses --- p.30 / Chapter 1.2.5.1 --- G proteins --- p.30 / Chapter 1.2.5.2 --- G proteins in defense responses --- p.30 / Chapter 1.3 --- OsGAPl is a C2 (protein kinase C conserved region 2) domain harboring GTPase activating protein --- p.32 / Chapter 1.4 --- OsYchFl is a GTPase and an interacting partner of OsGAPl --- p.32 / Chapter 1.5 --- Hypothesis and objectives of this research --- p.33 / Chapter Chapter 2 --- materials and methods / Chapter 2.1 --- Materials --- p.35 / Chapter 2.1.1 --- Chemicals and reagents --- p.39 / Chapter 2.1.2 --- Commercial kits --- p.40 / Chapter 2.1.3 --- Primers used --- p.41 / Chapter 2.1.4 --- Equipment and facilities used: --- p.47 / Chapter 2.1.5 --- "Buffer, solution, gel and medium:" --- p.47 / Chapter 2.2 --- Methods: --- p.51 / Chapter 2.2.1 --- Culture of bacterial strains --- p.51 / Chapter 2.2.2 --- Composition of medium used in this work for cultivating bacterial strains: --- p.51 / Chapter 2.2.3 --- Plant growth and treatment --- p.52 / Chapter 2.2.3.1 --- Surface sterilization of Arabidopsis thaliana seeds --- p.52 / Chapter 2.2.3.2 --- Seed germination and Arabidopsis plant growth --- p.52 / Chapter 2.2.4 --- Generation of transgenic Arabidopsis --- p.53 / Chapter 2.2.4.1 --- Agrobacterium-mediated Arabidopsis transformation --- p.53 / Chapter 2.2.5 --- Pathogen inoculation test --- p.54 / Chapter 2.2.6 --- Molecular cloning --- p.54 / Chapter 2.2.6.1 --- DNA sequencing: --- p.55 / Chapter 2.2.6.2 --- Transformation of E. coli strains: --- p.55 / Chapter 2.2.6.3 --- Transformation of Agrobacteria by electroporation --- p.55 / Chapter 2.2.7 --- DNA and RNA extraction --- p.56 / Chapter 2.2.7.1 --- Plasmid DNA extraction from bacterial cells --- p.56 / Chapter 2.2.7.2 --- Genomic DNA extraction from plant tissues --- p.56 / Chapter 2.2.7.3 --- RNA extraction from plant tissues --- p.56 / Chapter 2.2.8 --- Northern blot --- p.57 / Chapter 2.2.9 --- Subcellular localization studies --- p.58 / Chapter 2.2.9.1 --- Transformation of tobacco BY-2 cells --- p.58 / Chapter 2.2.9.2 --- Maintenance of transgenic tobacco BY-2 cells --- p.59 / Chapter 2.2.9.3 --- Confocal microscopy --- p.59 / Chapter 2.2.9.4 --- Electron microscopy --- p.59 / Chapter 2.2.10 --- Bimolecular fluorescence complementation studies (BiFC) --- p.60 / Chapter 2.2.10.1 --- Construct making --- p.61 / Chapter 2.2.10.2 --- Preparation of rice protoplasts --- p.61 / Chapter 2.2.10.3 --- PEG-mediated transfection --- p.62 / Chapter 2.2.10.4 --- Detection of protein-protein interaction --- p.62 / Chapter Chapter 3 --- Results / Chapter 3.1 --- OsGAPl interacts with OsYchFl in vivo --- p.63 / Chapter 3.1.1 --- Construction of vectors for BiFC transient assay in rice protoplasts --- p.64 / Chapter 3.1.2 --- BiFC assay in rice protoplasts revealed in vivo interaction between the OsGAPl and the OsYchFl proteins --- p.66 / Chapter 3.2.1 --- Subcellular localization of OsGAPl --- p.68 / Chapter 3.2.2 --- Localization of OsGAPl and OsYchFl in rice leaves revealed by electron microscopy --- p.70 / Chapter 3.3 --- Functional characterization of OsYchFl / Chapter 3.3.1 --- Characterization of Arabidopsis YchF1 knockdown mutant --- p.75 / Chapter 3.3.2 --- Complementation of AtYchF1 knockdown Arabidopsis --- p.77 / Chapter 3.3.3.1 --- Pathogen inoculation test --- p.80 / Chapter Chapter 4 --- Discussion / Chapter 4.1 --- Significance of the project --- p.85 / Chapter 4.2 --- In vivo interaction between OsGAPl and OsYchFl --- p.86 / Chapter 4.3 --- OsGAPl is located either inside the cytosol or on the plasma membrane in transgenic tobacco BY-2 cells --- p.87 / Chapter 4.4 --- Study of wounding effect on the subcellular localization of OsGAPl and OsYchFl at whole plant level by EM --- p.88 / Chapter 4.5 --- OsYchFl functions as a negative regulator of defense responses in A.thaliana --- p.90 / Chapter 4.6 --- Conclusion --- p.92 / References --- p.95 / Appendix --- p.103

Lam, Hilary. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 182-191). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.I / ABSTRACT --- p.III / TABLE OF CONTENTS --- p.V / LIST OF FIGURES --- p.X / LIST OF TABLES --- p.XIX / LIST OF ABBREVIATIONS --- p.XXII / Chapter Chapter 1: --- LITERATURE REVIEW --- p.1 / Chapter 1. --- Aristolochia --- p.1 / Chapter 1.1 --- "Aristolochia, as a plant" --- p.1 / Chapter 1.2 --- The chemicals in Aristolochia --- p.1 / Chapter 1.3 --- "Aristolochia, as herbal remedies" --- p.3 / Chapter 1.4 --- The Aristolochia poisoning cases --- p.4 / Chapter 1.5 --- The mechanism of AAs --- p.6 / Chapter 1.6 --- Renaming CHN to AAN --- p.6 / Chapter 1.7 --- Banning Aristolochia herbs --- p.7 / Chapter 1.8 --- The possible cause of ANN --- p.8 / Chapter 1.8.1 --- Misuse of Chinese Medicine --- p.8 / Chapter 1.8.2 --- Substitution --- p.9 / Chapter 1.8.3 --- The complexities of the herbal nomenclature --- p.9 / Chapter 1.8.4 --- Adulteration --- p.11 / Chapter 1.9 --- Methods for authenication --- p.12 / Chapter 1.9.1 --- Traditional methods for authentication --- p.12 / Chapter 1.9.2 --- The advantage of using molecular methods --- p.13 / Chapter 1.9.2.1 --- DNA fingerprinting --- p.13 / Chapter 1.9.2.2 --- DNA sequencing --- p.15 / Chapter 1.10 --- Method selection rationale --- p.15 / Chapter 1.11 --- The need for molecular authentication of six medicinal herbs --- p.17 / Chapter 1.11.1 --- The herb Mutong --- p.17 / Chapter 1.11.1.1 --- The poisoning cases reported --- p.19 / Chapter 1.11.1.2 --- Other authentication studies of Mutong --- p.19 / Chapter 1.11.2 --- The herb Muxiang --- p.20 / Chapter 1.11.2.1 --- Chemical profile --- p.21 / Chapter 1.11.2.2 --- Other authentication studies of Muxiang --- p.21 / Chapter 1.11.3 --- The herb Baiying --- p.22 / Chapter 1.11.3.1 --- The poisoning cases reported --- p.23 / Chapter 1.11.3.2 --- Other authentication studies of Baiying --- p.24 / Chapter 1.11.4 --- The herb Fangj --- p.i 24 / Chapter 1.11.4.1 --- Chemical profile --- p.25 / Chapter 1.11.4.2 --- The poisoning cases reported --- p.26 / Chapter 1.11.5 --- The herb Madouling --- p.26 / Chapter 1.11.6 --- The herb Zhushalian --- p.27 / Chapter 1.12 --- Aristolochia specific markers --- p.28 / Chapter 1.13 --- Significance of the research --- p.29 / Chapter Chapter 2: --- OBJECTIVE --- p.30 / Chapter Chapter 3: --- MATERIALS AND METHODS --- p.31 / Chapter 3.1 --- Samples source --- p.31 / Chapter 3.2 --- Total DNA extraction --- p.39 / Chapter 3.2.1 --- Cetyltriethylammonium bromide extraction --- p.39 / Chapter 3.2.2 --- Commercial kit extraction --- p.40 / Chapter 3.3 --- DNA amplification --- p.42 / Chapter 3.4 --- DNA fingerprinting --- p.43 / Chapter 3.4.1 --- DNA concentration determination --- p.43 / Chapter 3.4.2 --- ISSR fingerprinting --- p.44 / Chapter 3.5 --- Agarose gel electrophoresis --- p.45 / Chapter 3.6 --- Purification of PCR product --- p.46 / Chapter 3.7 --- Cloning of PCR product --- p.47 / Chapter 3.7.1 --- Ligation --- p.47 / Chapter 3.7.2 --- Transformation --- p.48 / Chapter 3.7.3 --- Cell cultivation --- p.48 / Chapter 3.7.4 --- Plasmid extraction --- p.49 / Chapter 3.7.5 --- Insert confirmation --- p.49 / Chapter 3.8 --- DNA sequencing --- p.50 / Chapter 3.8.1 --- Cycle sequencing --- p.50 / Chapter 3.8.2 --- Purification of cycle sequencing product --- p.51 / Chapter 3.8.3 --- DNA analysis --- p.51 / Chapter 3.9 --- Sequence analysis --- p.52 / Chapter Chapter 4: --- AUTHENICATION OF MUTONG --- p.53 / Chapter 4.1 --- Results --- p.53 / Chapter 4.1.1 --- Sequence alignment --- p.54 / Chapter 4.1.1.1 --- trnL-trnF sequences --- p.54 / Chapter 4.1.1.2 --- psbA-trnH sequences --- p.55 / Chapter 4.1.2 --- Percentage similarity analysis --- p.64 / Chapter 4.1.3 --- Dendrogram analysis --- p.67 / Chapter 4.2 --- Discussion --- p.73 / Chapter 4.2.1 --- Evaluation of chloroplast trnL-trnF region in differentiation of Mutong --- p.73 / Chapter 4.2.2 --- Evaluation of chloroplast psbA-trnH region in differentiation of Mutong --- p.74 / Chapter 4.2.3 --- Evaluation of using DNA sequencing in differentiation of Mutong --- p.75 / Chapter 4.3 --- Conclusion --- p.77 / Chapter Chapter 5: --- AUTHENICATION OF MUXIANG --- p.78 / Chapter 5.1 --- Results --- p.78 / Chapter 5.1.1 --- Sequence alignment --- p.79 / Chapter 5.1.1.1 --- trnL-trnF sequences --- p.79 / Chapter 5.1.1.2 --- psbA-trnH sequences --- p.80 / Chapter 5.1.2 --- Percentage similarity analysis --- p.88 / Chapter 5.1.3 --- Dendrogram study --- p.91 / Chapter 5.2 --- Discussion --- p.97 / Chapter 5.2.1 --- Evaluation of chloroplast trnL-trnF region in differentiation of Muxiang --- p.97 / Chapter 5.2.2 --- Evaluation of chloroplast psbA-trnH region in differentiation of Muxiang --- p.99 / Chapter 5.3 --- Conclusion --- p.100 / Chapter Chapter 6: --- AUTHENICATION OF BAIYING --- p.102 / Chapter 6.1 --- Results --- p.102 / Chapter 6.1.1 --- Sequence alignment --- p.103 / Chapter 6.1.2 --- Percentage similarity analysis --- p.107 / Chapter 6.1.3 --- Dendrogram analysis --- p.107 / Chapter 6.2 --- Discussion --- p.109 / Chapter 6.2.1 --- Evaluation of chloroplast psbA-trnH region in differentiation of Solarium and Aristolochia --- p.109 / Chapter 6.2.2 --- Molecular authentication of Baiying --- p.112 / Chapter 6.3 --- Conclusion --- p.113 / Chapter Chapter 7: --- AUTHENICATION OF FANGJI --- p.114 / Chapter 7.1 --- Results --- p.114 / Chapter 7.1.1 --- Sequence alignment --- p.115 / Chapter 7.1.1.1 --- trnL-trnF sequence --- p.115 / Chapter 7.1.1.2 --- psbA-trnH sequence --- p.116 / Chapter 7.1.2 --- Percentage similarity analysis --- p.123 / Chapter 7.1.3 --- Dendrogram study --- p.126 / Chapter 7.2 --- Discussion --- p.132 / Chapter 7.2.1 --- Evaluation of chloroplast trnL-trnF region in differentiation of Fangji --- p.132 / Chapter 7.2.2 --- Evaluation of chloroplast psbA-trnH region in differentiation of Fangji --- p.133 / Chapter 7.3 --- Conclusion --- p.133 / Chapter Chapter 8: --- AUTHENICATION OF MADOULING --- p.135 / Chapter 8.1 --- Results --- p.135 / Chapter 8.1.1 --- Sequence alignment --- p.136 / Chapter 8.1.1.1 --- trnL-trnF sequence --- p.136 / Chapter 8.1.1.2 --- psbA-trnH sequence --- p.136 / Chapter 8.1.2 --- Percentage similarity analysis --- p.143 / Chapter 8.1.3 --- Dendrogram study --- p.146 / Chapter 8.2 --- Discussion --- p.152 / Chapter 8.2.1 --- Evaluation of chloroplast trnL-trnF region in differentiation of Madouling --- p.152 / Chapter 8.2.2 --- Evaluation of chloroplast psbA-trnH region in differentiation of Madouling --- p.153 / Chapter 8.3 --- Conclusion --- p.153 / Chapter Chapter 9: --- AUTHENICATION OF ZHUSHALIAN --- p.155 / Chapter 9.1 --- Results --- p.155 / Chapter 9.1.1 --- Sequence alignment --- p.156 / Chapter 9.1.1.1 --- trnL-trnF sequence --- p.156 / Chapter 9.1.1.2 --- psbA-trnH sequence --- p.157 / Chapter 9.1.2 --- Percentage similarity analysis --- p.157 / Chapter 9.1.3 --- Dendrogram study --- p.162 / Chapter 9.2 --- Discussion --- p.166 / Chapter 9.2.1 --- Evaluation of chloroplast trnL-trnF region in differentiation of Zhushalian --- p.166 / Chapter 9.2.2 --- Evaluation of chloroplast psbA-trnH region in differentiation of Zhushalian --- p.171 / Chapter 9.3 --- Conclusion --- p.171 / Chapter Chapter 10: --- ARISTOLOCHIA SPECIFIC MARKER --- p.172 / Chapter 10.1 --- ISSR fingerprinting --- p.172 / Chapter 10.2 --- Discussion --- p.178 / Chapter Chapter 11: --- CONCLUSION --- p.180 / BIBLIOGRAPHY --- p.182 / APPENDIX - MATERIALS PREPARATION --- p.192

Tam, Oi Sin Pancy. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 101-128). / Abstracts in English and Chinese. / Table of Contents / Title page --- p.i / Abstract --- p.iii / 摘要 --- p.vi / Acknowledgements --- p.viii / Table of Contents --- p.ix / List of Figures --- p.xiii / List of Tables --- p.xv / Abbreviations --- p.xvii / Publications related to the work of this thesis --- p.xx / Conference Presentations related to this thesis --- p.xxi / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- AMD --- p.1 / Chapter 1.2 --- Epidemiology --- p.4 / Chapter 1.3 --- Classification --- p.5 / Chapter 1.3.1 --- Dry AMD --- p.6 / Chapter 1.3.2 --- Wet/Exudative AMD --- p.9 / Chapter 1.4 --- Etiology and risk factors of AMD --- p.10 / Chapter 1.4.1 --- Gender and Ethnicity --- p.10 / Chapter 1.4.2 --- Smoking and vascular factors --- p.11 / Chapter 1.4.3 --- Genetic Factor --- p.11 / Chapter 1.5 --- Molecular Genetics of AMD --- p.12 / Chapter 1.5.1 --- Linkage studies --- p.12 / Chapter 1.5.2 --- Candidate genes search --- p.15 / Chapter 1.5.3 --- Genome-Wide Association --- p.18 / Chapter 1.5.3.1 --- Complement Factor H --- p.20 / Chapter 1.5.3.2 --- LOC387715 --- p.22 / Chapter 1.6 --- Statistical Analysis --- p.23 / Chapter 1.6.1 --- Genotyping --- p.23 / Chapter 1.6.2 --- Quality Assessment of Genetic Data --- p.24 / Chapter 1.6.3 --- Association Analysis --- p.26 / Chapter 1.6.4 --- Population Stratification --- p.26 / Chapter 1.6.5 --- Haplotype Analysis of Multiple SNPs --- p.26 / Chapter 1.6.6 --- Population Attributable Risk --- p.27 / Chapter 1.6.7 --- Interaction analysis --- p.28 / Chapter 1.7 --- Objectives --- p.28 / Chapter Chapter 2 --- Materials and Method --- p.30 / Chapter 2.1. --- Materials --- p.30 / Chapter 2.1.1. --- Proteins --- p.30 / Chapter 2.1.2. --- Chemicals --- p.30 / Chapter 2.1.3. --- Solutions and Buffers --- p.31 / Chapter 2.1.4. --- Reagents and Kits --- p.31 / Chapter 2.1.5. --- Apparatus --- p.32 / Chapter 2.1.6. --- Softwares --- p.32 / Chapter 2.2. --- Methods --- p.32 / Chapter 2.2.1. --- Study Subjects --- p.33 / Chapter 2.2.2. --- AMD atients --- p.33 / Chapter 2.2.3. --- Control Subjects --- p.34 / Chapter 2.2.4. --- DNA Extraction and Quantification --- p.34 / Chapter 2.2.5. --- Whole genome wide SNP scanning --- p.34 / Chapter 2.2.6. --- HTRA1 Genotyping --- p.38 / Chapter 2.2.6.1. --- Serial Polymerase Chain Reactions --- p.38 / Chapter 2.2.6.2. --- Cycle sequencing --- p.40 / Chapter 2.3. --- Statistical analysis --- p.40 / Chapter 2.3.1. --- Hardy-Weinberg Equilibrium Test --- p.40 / Chapter 2.3.2. --- Association Analysis: Linkage disequilibrium --- p.42 / Chapter 2.3.3. --- Haplotype Analysis --- p.43 / Chapter 2.3.4. --- Interaction Analysis --- p.43 / Chapter Chapter 3 --- Results --- p.46 / Chapter 3.1. --- Genome-wide Association Study of Exudative AMD --- p.46 / Chapter 3.1.1. --- Genotyping and Association Analysis --- p.46 / Chapter 3.1.2. --- Haplotype Analysis --- p.50 / Chapter 3.2. --- HTRA1 Genotyping --- p.57 / Chapter 3.2.1. --- Association Analysis --- p.57 / Chapter 3.2.2. --- Haplotype Analysis --- p.68 / Chapter 3.2.3. --- rsl 1200638 - Smoking Interaction --- p.68 / Chapter 3.2.4. --- rsl 1200638 - rs800292 Interaction --- p.74 / Chapter Chapter 4 --- Discussion --- p.79 / Chapter 4.1. --- Genome-wide Association Study of Exudative AMD --- p.79 / Chapter 4.1.1. --- Limitations and Concerns of Genome-Wide Association Study --- p.84 / Chapter 4.2. --- HTRA1 Genotyping --- p.85 / Chapter 4.2.1 --- Association and Haplotype Analysis --- p.85 / Chapter 4.2.2. --- HTRA1 --- p.87 / Chapter 4.2.3. --- Gene-Environment Interaction --- p.93 / Chapter 4.2.4. --- Gene-Gene Ineraction --- p.94 / Conclusions and Future Aspects --- p.97 / Electronic-Database Information --- p.100 / References --- p.101

Zhong, Lan. / Thesis Ph.D. Chinese University of Hong Kong 2014. / Includes bibliographical references (leaves 122-154). / Abstracts also in Chinese. / Title from PDF title page (viewed on 24, October, 2016). / Zhong, Lan.

Yu, Jing. / "November 2011." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 161-172). / Abstracts in English and Chinese. / Abstract --- p.I / 摘要 --- p.III / Acknowledgements --- p.V / Contents --- p.VI / List of Figures --- p.VIII / List of Tables --- p.X / Abbreviations and Symbols --- p.XII / Chapter CHAPTER 1 --- Introduction --- p.1 / Chapter 1.1 --- Phylogenetic study of Hedyotis --- p.2 / Chapter 1.1.1 --- Rubiaceae --- p.2 / Chapter 1.1.2 --- Controversial taxonomic issues --- p.9 / Chapter 1.2 --- Traditional Chinese medicine (TCM) --- p.19 / Chapter 1.2.1 --- Introduction --- p.19 / Chapter 1.2.2 --- Baihuasheshecao --- p.20 / Chapter 1.2.3 --- Authentication of Baihuasheshecao --- p.23 / Chapter 1.3 --- Icefishes in the Hong Kong market --- p.23 / Chapter 1.3.1 --- Introduction --- p.23 / Chapter 1.4 --- Molecular approach --- p.25 / Chapter 1.4.1 --- Introduction to molecular phylogeny --- p.25 / Chapter 1.4.2 --- FINS (Forensically Informative Nucleotide Sequencing) for species identification --- p.27 / Chapter 1.4.3 --- DNA sequence markers --- p.28 / Chapter 1.5 --- Objectives --- p.38 / Chapter CHAPTER 2 --- MATERIALS AND METHODOLOGY --- p.41 / Chapter 2.1 --- Materials --- p.42 / Chapter 2.2 --- DNA extraction --- p.50 / Chapter 2.3 --- Polymerase chain reaction (PCR) method --- p.51 / Chapter 2.4 --- Gel electrophoresis --- p.54 / Chapter 2.5 --- PCR production purification --- p.54 / Chapter 2.6 --- Ligation and transformation and transformation of PCR product --- p.56 / Chapter 2.7 --- DNA sequencing and sequence analyses --- p.58 / Chapter CHAPTER 3 --- USING FORENSICALLY INFORMATIVE NUCLEOTIDE SEQUENCING (FINS) TECHNOLOGY FOR SPECIES IDENTIFICATION --- p.64 / Chapter 3.1 --- Authentication of Baihuasheshecao by FINS Analysis --- p.65 / Chapter 3.1.1 --- Authentication using FINS technology --- p.65 / Chapter 3.1.2 --- Relative effectiveness of DNA regions for FINS analysis --- p.70 / Chapter 3.1.3 --- Phylogenetic interpretation --- p.72 / Chapter 3.2 --- Authentication of Salangids (Icefishes) by FINS Analysis --- p.74 / Chapter 3.2.1 --- Analysis based on mitochondrial ribosome DNA region --- p.74 / Chapter 3.2.2 --- Analysis based on mitochondrial 16S rRNA --- p.77 / Chapter 3.2.3 --- Analysis based on combined regions --- p.79 / Chapter 3.2.4 --- Phylogenetic analysis --- p.81 / Chapter 3.2.5 --- Discussion --- p.85 / Chapter 3.3 --- Conclusions --- p.88 / Chapter CHAPTER 4 --- PHYLOGENTIC STUDY OF HEDYOTIS IN CHINA AND THEIR POSITION IN SPERMACOCEAE --- p.89 / Chapter 4.1 --- Phylogentic study of Hedyotis species in Chinese --- p.90 / Chapter 4.1.1 --- Nuclear ITS region --- p.90 / Chapter 4.1.2 --- Plastid trnL intron and trnL-V intergenic spacer region --- p.94 / Chapter 4.1.3 --- Plastid trnH-psbA intergenic spacer region --- p.98 / Chapter 4.1.4 --- Plastid rbcL region --- p.102 / Chapter 4.1.5 --- Plastid matK region --- p.106 / Chapter 4.1.7 --- Combined analysis --- p.114 / Chapter 4.2 --- The phylogenetic position of Hedyotis (species in China) in the tribe of Spermacoceae s.1 --- p.121 / Chapter 4.2.1 --- Plastid trnL - F intergenic spacer region --- p.121 / Chapter 4.2.2 --- Plastid rbcL region --- p.133 / Chapter 4.2.3 --- Plastid rps16 region --- p.141 / Chapter 4.3 --- Discussion --- p.153 / Chapter 4.3.1 --- Comparison of phylogenetic utility of the six DNA regions --- p.153 / Chapter 4.3.2 --- Diplophragma section --- p.154 / Chapter 4.3.3 --- "Hedyotis, Dimetia, Euoldendandia and Gonotheca sections" --- p.156 / Chapter 4.3.4 --- The position of Hedyotis (species in China) in Spermacoceae --- p.158 / Chapter 4.4 --- Conclusions --- p.160 / REFERENCES --- p.161 / APPENDIX --- p.173

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