by Yeung, Sai-mo, Simon. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1989. / Bibliography: leaves 189-207.

by Fong Wing-ping. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1987. / Bibliography: leaves 186-198.

Rowlands Dewi Kenneth. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 113-121). / Abstract --- p.i / Acknowledgements --- p.iii / Publications --- p.iv / Abbreviations --- p.v / Contents --- p.vii / Chapter Chapter 1 --- Prostaglandins --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.2 --- Prostanoid biosynthesis and metabolism --- p.1 / Chapter 1.3 --- Prostaglandin receptors --- p.3 / Chapter 1.3.1 --- DP-receptors --- p.3 / Chapter 1.3.2 --- EP1-receptors --- p.4 / Chapter 1.3.3 --- EP2-receptors --- p.4 / Chapter 1.3.4 --- EP3-receptors --- p.5 / Chapter 1.3.5 --- EP4-receptors --- p.6 / Chapter 1.3.6 --- FP-receptors --- p.7 / Chapter 1.3.7 --- IP-receptors --- p.8 / Chapter 1.3.8 --- TP-receptors --- p.11 / Chapter 1.4 --- Agonists and antagonists --- p.11 / Chapter Chapter 2 --- Role of prostacyclin in pain modulation --- p.14 / Chapter 2.1 --- Pain --- p.14 / Chapter 2.2 --- Prostaglandins and pain --- p.15 / Chapter 2.3 --- Prostacyclin and pain --- p.16 / Chapter 2.3.1 --- [3H]-Iloprost binding sites --- p.16 / Chapter 2.3.2 --- IP-receptor mRNA --- p.17 / Chapter 2.3.3 --- IP-receptor knockout mice --- p.17 / Chapter 2.3.4 --- Direct nociceptive action of prostacyclin --- p.18 / Chapter 2.4 --- Treatment of prostanoid-induced pain --- p.19 / Chapter Chapter 3 --- Dorsal root ganglion cells --- p.21 / Chapter 3.1 --- In vitro model of pain --- p.21 / Chapter 3.2 --- Characteristics of cultured DRG cells --- p.22 / Chapter 3.2.1 --- Size and distribution --- p.22 / Chapter 3.2.2 --- Biochemical and physiological characteristics --- p.22 / Chapter 3.2.2.1 --- Gapsaicin-sensitive neurones --- p.23 / Chapter 3.2.2.2 --- Neuropeptide content --- p.23 / Chapter 3.2.2.3 --- Elevation of [Ca2+］i --- p.24 / Chapter 3.3 --- Effect of nerve growth factor --- p.24 / Chapter Chapter 4 --- Materials and solutions --- p.26 / Chapter 4.1 --- Materials --- p.26 / Chapter 4.2 --- Solutions --- p.30 / Chapter 4.2.1 --- Culture medium --- p.30 / Chapter 4.2.2 --- Buffers --- p.31 / Chapter 4.2.3 --- Solutions --- p.32 / Chapter Chapter 5 --- Development of dorsal root ganglion cell preparation --- p.33 / Chapter 5.1 --- Introduction --- p.33 / Chapter 5.2 --- Methods --- p.34 / Chapter 5.2.1 --- Dissection of dorsal root ganglia --- p.34 / Chapter 5.2.2 --- Preparation of a single-cell suspension --- p.34 / Chapter 5.2.2.1 --- Effect of trimming dorsal root ganglia --- p.34 / Chapter 5.2.2.2 --- Enzymatic dissociation --- p.35 / Chapter 5.2.2.3 --- Mechanical dissociation --- p.36 / Chapter 5.2.3 --- Neuronal cell enrichment --- p.36 / Chapter 5.2.3.1 --- Differential adhesion --- p.36 / Chapter 5.2.3.2 --- BSA gradient --- p.37 / Chapter 5.2.3.3 --- Combination of BSA gradient and differential adhesion --- p.37 / Chapter 5.2.4 --- Cell counting --- p.37 / Chapter 5.2.5 --- Culture conditions --- p.38 / Chapter 5.2.6 --- Size distribution of DRG cells --- p.39 / Chapter 5.2.7 --- Immunocytochemistry --- p.39 / Chapter 5.3 --- Results and discussion --- p.40 / Chapter 5.3.1 --- Preparation of single-cell suspension --- p.40 / Chapter 5.3.2 --- Neuronal cell enrichment --- p.42 / Chapter 5.3.3 --- Size distribution of DRG cells --- p.32 / Chapter 5.3.4 --- Effects of mitotic inhibitors and NGF --- p.45 / Chapter 5.3.5 --- Immunocytochemistry --- p.48 / Chapter 5.4 --- Conclusions --- p.48 / Chapter Chapter 6 --- Methods --- p.53 / Chapter 6.1 --- Dorsal root ganglion cell preparation --- p.53 / Chapter 6.1.1 --- Preparation of tissue culture plates and coverslips --- p.54 / Chapter 6.1.2 --- Preparation of Pasteur pipettes --- p.54 / Chapter 6.2 --- Measurement of adenylate cyclase activity --- p.55 / Chapter 6.2.1 --- Introduction --- p.55 / Chapter 6.2.2 --- Preparation of columns --- p.55 / Chapter 6.2.3 --- Measurement of [3H]-cyclic AMP production --- p.56 / Chapter 6.2.4 --- Data analysis --- p.57 / Chapter 6.3 --- Measurement of phospholipase C activity --- p.58 / Chapter 6.3.1 --- Introduction --- p.58 / Chapter 6.3.2 --- Preparation of columns --- p.58 / Chapter 6.3.3 --- Measurement of [3H]-inositol phosphate production --- p.59 / Chapter 6.3.4 --- Data analysis --- p.60 / Chapter 6.4 --- Measurement of [Ca2+]i --- p.60 / Chapter 6.4.1 --- Introduction --- p.60 / Chapter 6.4.2 --- Preparations of cells --- p.61 / Chapter 6.4.3 --- Measurement of Fura-2 fluorescence --- p.62 / Chapter 6.5 --- Measurement of neuropeptides --- p.62 / Chapter 6.5.1 --- Introduction --- p.62 / Chapter 6.5.2 --- Preparation of cells --- p.63 / Chapter 6.5.3 --- CGRP assay --- p.64 / Chapter 6.5.4 --- Substance P assay --- p.64 / Chapter 6.5.5 --- Purification of samples using Sep-Pak cartridges --- p.65 / Chapter Chapter 7 --- Characterisation of prostacyclin receptors on adult rat dorsal root ganglion cells --- p.66 / Chapter 7.1 --- Stimulation of adenylate cyclase --- p.66 / Chapter 7.1.1 --- Introduction --- p.66 / Chapter 7.1.2 --- Agonist concentration-response curves --- p.67 / Chapter 7.1.3 --- Cross-desensitisation experiments --- p.72 / Chapter 7.1.4 --- Evidence for EP3-receptors --- p.77 / Chapter 7.1.5 --- G-protein coupling of the IP-receptor --- p.77 / Chapter 7.1.6 --- Discussion --- p.78 / Chapter 7.1.7 --- Conclusions --- p.82 / Chapter 7.2 --- Stimulation of phospholipase C --- p.82 / Chapter 7.2.1 --- Introduction --- p.82 / Chapter 7.2.2 --- Agonist concentration-response curves --- p.83 / Chapter 7.2.3 --- G-protein coupling --- p.83 / Chapter 7.2.4 --- Discussion and Conclusions --- p.84 / Chapter 7.3 --- Stimulation of changes in [Ca2+]i --- p.87 / Chapter 7.3.1 --- Introduction --- p.87 / Chapter 7.3.2 --- Preliminary results --- p.87 / Chapter 7.3.3 --- Discussion and conclusions --- p.89 / Chapter Chapter 8 --- Neuropeptide release by adult rat dorsal root ganglion cells --- p.90 / Chapter 8.1 --- Introduction --- p.90 / Chapter 8.2 --- Methods and Results --- p.91 / Chapter 8.3 --- Discussion --- p.91 / Chapter 8.4 --- Conclusions --- p.92 / Chapter Chapter 9 --- Regulation of prostacyclin receptors on adult rat DRG cells --- p.93 / Chapter 9.1 --- Introduction --- p.93 / Chapter 9.2 --- Contribution of non-neuronal cells --- p.93 / Chapter 9.3 --- Effect of DRG cell density --- p.94 / Chapter 9.4 --- Effect of indomethacin --- p.99 / Chapter 9.5 --- Contribution of endogenously-produced non-prostanoid ligands --- p.100 / Chapter 9.6 --- Effect of PKC activation --- p.102 / Chapter 9.7 --- Discussion --- p.104 / Chapter 9.8 --- Conclusions --- p.106 / Chapter Chapter 10 --- General Discussion and Conclusions --- p.107 / Chapter 10.1 --- Development of DRG cell preparation --- p.107 / Chapter 10.2 --- Effect of prostanoid mimetics on intracellular messengers --- p.108 / Chapter 10.3 --- Regulation of prostacyclin receptors --- p.109 / Chapter 10.4 --- Role of prostacyclin in pain modulation --- p.111 / References --- p.113

Kwan Hon Pong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 115-156). / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iii / Abbreviations --- p.v / Acknowledgment --- p.vii / Chapter 1. --- Introduction / Chapter 1.1 --- Diabetes mellitus - general introduction --- p.1 / Chapter 1.1.1 --- Animal models of diabetes --- p.5 / Chapter 1.1.2 --- Streptozotocin-induced diabetes (SID) --- p.6 / Chapter 1.1.2.1 --- Mechanism of the diabetogenic effect of STZ --- p.7 / Chapter 1.1.2.2 --- Administration of STZ --- p.9 / Chapter 1.2 --- Impairment of cognitive function in diabetes mellitus --- p.9 / Chapter 1.3 --- Common mechanisms suggested in diabetic neuropathy --- p.15 / Chapter 1.3.1 --- Polyol pathway activation --- p.15 / Chapter 1.3.2 --- Redox potential alterations --- p.16 / Chapter 1.3.3 --- Nonenzymatic glycation --- p.17 / Chapter 1.3.4 --- PKC alteration --- p.18 / Chapter 1.4 --- Do the common mechanisms of neuropathy induced the cognitive impairment in diabetes --- p.18 / Chapter 1.5 --- Structure and function of the hippocampus --- p.20 / Chapter 1.6 --- The definition and mechanism of learning and memory --- p.21 / Chapter 1.7 --- The mechanisms underlying the early and late phases of LTP in hippocampus --- p.23 / Chapter 1.7.1 --- Perforant and schaffer collaterals pathways --- p.23 / Chapter 1.7.2 --- Mossy fibre pathway --- p.24 / Chapter 1.7.3 --- Late phase of LTP in hippocampus --- p.25 / Chapter 1.8 --- GABAergic interaction in hippocampal plasticity --- p.25 / Chapter 1.9 --- The objective of the project --- p.27 / Chapter 1.10 --- Hypothesis --- p.27 / Chapter 1.10.1 --- The initial role of glutamate receptors --- p.28 / Chapter 1.10.2 --- Involvement of putative retrograde messengers --- p.30 / Chapter 1.10.3 --- The role of GABA receptors --- p.37 / Chapter 1.10.4 --- The role of the CREB --- p.40 / Chapter 2. --- Materials and methods / Chapter 2.1 --- Animals --- p.43 / Chapter 2.1.1 --- Induction of diabetes mellitus --- p.43 / Chapter 2.1.2 --- Insulin therapy --- p.45 / Chapter 2.1.3 --- Sample collection --- p.46 / Chapter 2.2 --- Isolation of total RNA --- p.47 / Chapter 2.3 --- Quantitation of total RNA --- p.51 / Chapter 2.4 --- Reverse transcription --- p.53 / Chapter 2.5 --- PCR --- p.54 / Chapter 2.5.1 --- Preparation of PCR --- p.54 / Chapter 2.5.2 --- Purification of PCR product --- p.60 / Chapter 2.5.3 --- Confirmation of PCR products by DNA sequencing --- p.61 / Chapter 2.5.4 --- PCR analysis --- p.62 / Chapter 2.5.4.1 --- Quantitation of cDNA --- p.62 / Chapter 2.5.4.2 --- Radioactive PCR --- p.65 / Chapter 2.5.4.3 --- cDNA gel electrophoresis --- p.66 / Chapter 3. --- Results / Chapter 3.1 --- Ionotropic glutamate receptor subtypes --- p.72 / Chapter 3.1.1 --- Non-NMDA receptors --- p.72 / Chapter 3.1.1.1 --- AMPA receptors --- p.72 / Chapter 3.1.1.2 --- Kainate receptors --- p.72 / Chapter 3.1.2 --- NMDA receptors --- p.76 / Chapter 3.2 --- Metabotropic glutamate receptor subtypes --- p.79 / Chapter 3.2.1 --- Group I subtype --- p.79 / Chapter 3.2.2 --- Group II subtypes --- p.79 / Chapter 3.3 --- Synthases of retrograde messengers --- p.79 / Chapter 3.4 --- Calcium-related receptors --- p.82 / Chapter 3.5 --- "GABA receptor subtypes (Aαl-4,BRla)" --- p.85 / Chapter 3.6 --- Glutamic acid decarboxylase (GAD) --- p.88 / Chapter 3.7 --- Enzyme genes related to CREB dephosphorylation --- p.88 / Chapter 3.8 --- Effect of insulin therapy on ionotropic glutamate receptor subtypes --- p.91 / Chapter 3.9 --- Effect of insulin therapy on metabotropic glutamate receptor subtypes --- p.91 / Chapter 3.10 --- Effect of insulin therapy on synthases of retrograde messenger --- p.91 / Chapter 3.11 --- Effect of insulin therapy on GAB A receptor subtype --- p.91 / Chapter 4. --- Discussion / Chapter 4.1 --- SID on Glutamate receptor subtypes --- p.96 / Chapter 4.2 --- SID on Calcium-related receptors --- p.105 / Chapter 4.3 --- SID on Synthases of retrograde messengers --- p.106 / Chapter 4.4 --- SID on GABA receptor subtypes --- p.109 / Chapter 4.5 --- SID on enzyme genes related to dephosphorylation of CREB --- p.111 / Chapter 4.6 --- Effect on insulin therapy on gene expression in hippocampus --- p.113 / Chapter 5. --- References --- p.115

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Typescript (photocopy). / Digitized by Kansas Correctional Industries

Financial authorities have traditionally relied on fines, suspensions, and bars to discipline misconduct in financial markets and, in that way, protect public investors and promote financial development. In theory, these sanctions should be sufficiently high to internalize the social cost of wrongdoing and deter future misbehavior. In practice, however, public firms are often criticized for being under-punished. This concern has motivated a line of research, especially in the United States, to examine whether enforcement actions initiated by public authorities generate negative indirect effects for the firms accused of misbehavior and, therefore, whether those effects supplement the regulatory sanction. In general, the answer to this question is positive under certain circumstances. Whether or not firms also suffer collateral effects in emerging financial markets, however, is a question that has received little attention in the literature. The purpose of this work is therefore to make a first step to fill this gap. Addressing this gap is important because emerging markets are smaller, less liquid, and more concentrated than the United States' financial market, which might neutralize the side financial effects of enforcement that prior studies have documented. As a result, the policy recommendations proposed in the prior literature are not necessarily applicable to emerging economies. This work focuses on three specific types of collateral effects: the effect of enforcement on (1) the defendant's stock price, (2) the defendant's operating performance, and (3) the cost of external financing. In terms of types of violations and sample countries, this work focuses on enforcement actions triggered by securities regulation violations in the five countries that form the MSCI-EC-LATAM index (Morgan Stanley Capital International Emerging Markets Index - Latin America). The results indicate that the stock price and operating performance of firms whose insiders were sanctioned for insider trading decline significantly after the imposition of the sanction. These results have various implications for the regulation of official penalties as a tool to promote financial development.

Introduction: Poultry workers have an increased risk of respiratory symptoms associated with various irritant and allergenic exposures causing airway inflammation. This study investigated the levels of (1-3)-β-D glucan exposure in several poultry farming processes. The objectives involved categorising the different tasks undertaken in the poultry industry. After which a method was established and validated to detect and quantify the levels of (1-3)-β-D glucan using the Glucatell assay. This assay was used to measure the amount of (1-3)-β-D glucan poultry farm workers were exposed to using personal sampling. Thereafter, general respiratory symptoms were described briefly via the administration of a respiratory questionnaire. Method: A total of 308 personal air samples were collected from several poultry farming processes (rearing, laying, hatchery, broilers, catching) of a large poultry farm in the North West Province. A walkthrough checklist was used to obtain information on various exposure determinants such as farm size, number of chickens, ventilation system, bedding material used and poultry feed used. The Glucatell assay (Associates of Cape Cod, East Falmouth, MA, USA) was used to quantify the concentration of (1-3)-β-D glucans in the air samples. Results: The geometric mean concentrations of (1-3)-β-D glucans ranged from 24.38 to 645.98 ng/m3 across the various poultry farming processes investigated. Workers in the broiler farms were exposed to two times higher levels of (1-3)-β-D glucans compared to those in the breeding farms. The sizes of the broiler farm houses as well as the age of the chickens were among the main determinants of exposure. The larger broiler farm houses (GM=5.2 ng/m3, GSD=3.74) had significantly (p<0.05) lower levels than the smaller broiler farm houses (GM=6.4 ng/m3, GSD=2.14) whilst houses with older chickens had higher (1-3)-β-D glucan levels (G=5.8 ng/m3,

The computer to pupil ratio has changed drastically in the past decades, from 125:1 in 1983 to less than 2:1 in 2009 (Gray, Thomas, and Lewis, 2010), allowing for teachers and students to integrate technology throughout the educational experience. The area of educational assessment has adapted to the increased use of technology. Trends in assessment and technology include a movement from paper-based to computer-based testing for all types of assessments, from large-scale assessments to teacher-created classroom tests. Computer-based testing comes with many benefits when compared to paper-based testing, but it is necessary to determine if results are comparable, especially in situations where computer-based and paper-based tests can be used interchangeably. The main purpose of this study was to expand upon the base of research comparing paper-based and computer-based testing, specifically with elementary students and mathematical fluency. The study was designed to answer the following research questions: (1) Are there differences in fluency-based performance on math computation problems presented on paper versus on the computer? (2) Are there differential mode effects on computer-based tests based on sex, grade level, or ability level? A mixed-factorial design with both within- and between-subject variables was used to investigate the differences between performance on paper-based and computer-based tests of mathematical fluency. Participants completed both paper- and computer-based tests, as well as the Group Math Assessment and Diagnostic Evaluation as a measure of general math ability. Overall findings indicate that performance on paper- and computer-based tests of mathematical fluency are not comparable and student grade-level may be a contributing factor in that difference.