by Lui Chi Pang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 265-281). / Acknowledgements --- p.i / Abbreviations --- p.ii / Abstract --- p.iii / Table of contents --- p.vii / Introduction / Review of Literature --- p.2 / Chapter I. --- Cellular response of hyperthermia --- p.3 / Chapter A) --- Effects on macromolecules synthesis --- p.3 / Chapter B) --- Effects on glycolysis and respiration --- p.5 / Chapter C) --- "Effects on plasma membrane, intracellular ionic level and intracellular pH" --- p.6 / Chapter II. --- Physical aspects --- p.11 / Chapter A) --- Survival curves --- p.11 / Chapter B) --- Concept of thermal dose --- p.13 / Chapter III. --- Clinical thermal theraphy --- p.21 / Chapter A) --- Hyperthermia in vivo --- p.21 / Chapter B) --- Combination of hyperthermia and radiotheraphy --- p.29 / Chapter C) --- Combination of hyperthermia and chemotherapy --- p.37 / Chapter IV. --- Thermotolerance --- p.48 / Scope of study --- p.54 / Materials and Methods / Chapter I. --- Cytotoxicity tests of cells in vitro --- p.59 / Chapter II. --- Whole body hyperthermia on Ehrlich ascite tumour (EAT)-bearing mice --- p.63 / Chapter III. --- Combination of hyperthermia and drugs --- p.66 / Chapter IV. --- Measurement of intracellular pH --- p.68 / Chapter V. --- Assay for sialic acids in the plasma membrane --- p.72 / Chapter VI. --- Assays of nucleolar proteins --- p.76 / Chapter VII. --- Acetylation of nuclear proteins --- p.80 / Chapter VIII. --- Detection of 72-kD heat shock protein --- p.93 / Results and Discussion / Chapter I. --- Cytotoxicity of hyperthermia in vitro --- p.102 / Chapter II. --- Hyperthermia on EAT cells in vivo --- p.131 / Chapter III. --- Cytotoxicity of combination of hyperthermia and drugs --- p.148 / Chapter IV. --- Intracellular pH changes during hyperthermia --- p.162 / Chapter V. --- Modification of sialic acid level in plasma membrane --- p.180 / Chapter VI. --- Conformational changes of nucleolar proteins --- p.193 / Chapter VII. --- Hyperthermic effect on acetylation of nuclear proteins --- p.209 / Chapter VIII. --- Induction of 72-kD heat shock protein --- p.223 / General Discussion / Chapter A. --- Hyperthermic cytotoxicity --- p.249 / Chapter B. --- Effects on plasma membrane and control of intracellular pH --- p.253 / Chapter C. --- Effects on the nuclear proteins --- p.256 / Chapter D. --- Conclusion --- p.263 / Bibliography --- p.264

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 110-128).

No description available.

Thesis (M.S.)--University of Michigan, 1960.

No description available.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 5 uppsatser.

Introdução: O Reiki está entre as terapias baseadas em energia mais frequentes. Estudar terapias com bases em mecanismos holísticos complexos e dinâmicos, influenciados por diferentes fatores individuais e ambientais exige uma série de avaliações em diferentes modelos experimentais. Neste contexto, o estudo in vitro permite o controle dos fatores externos às células, evita a alta variabilidade individual, propiciando resultados em menor tempo. Dentre os leucócitos, os neutrófilos são aqueles que estão presentes em maior quantidade no sangue periférico, atuando de maneira importante nas fases iniciais das reações inflamatórias, como mecanismo de defesa, estando no rol das primeiras células do sistema imune que se deslocam dos vasos para os tecidos. Objetivo: Avaliar o efeito do Reiki sobre a viabilidade celular e a atividade da enzima mieloperoxidase de neutrófilos humanos in vitro. Método: É um estudo laboratorial, experimental, duplo cego, com abordagem quantitativa. Foi realizado no Laboratório de Fisiologia Celular e Biologia Molecular da Universidade Cruzeiro do Sul - Campus Anália Franco São Paulo SP. A amostra de sangue humano foi obtida de cinco voluntários saudáveis. O ensaio necessitou de 20mL de sangue obtido por punção venosa periférica. Critério de inclusão: adulto, do sexo masculino, saudável na faixa dos 20 aos 40 anos. Critérios de exclusão: problema de saúde referido, uso de medicamentos, uso de terapia complementar (como terapias energéticas, fitoterapia, meditação e outras). O grupo experimental recebeu aplicação de Reiki, em temperatura ambiente, por meio da imposição de mãos, a 15 cm de distância por 15 minutos. A aplicação de Reiki foi realizada uma vez ao dia, durante três dias consecutivos, em sessões a cada 24 horas. O grupo controle permaneceu pelo mesmo tempo e nas mesmas condições ambientais do grupo de intervenção, sem a aplicação da técnica de biocampo. As células foram avaliadas pela técnica de exclusão do corante azul de Tripan, que permite diferenciar células vivas e mortas, pela exclusão do corante pelas células viáveis, e contadas em câmara de Neubauer. A atividade da enzima mieloperoxidase (MPO) foi avaliada por meio do ensaio de quimiluminescência. A análise da viabilidade celular foi feita em triplicata utilizando-se como resultado a média. Análise de dados. Medidas de variabilidade e tendência central, modelo de equações de estimação generalizadas para distribuição binomial nos dados de viabilidade para comparar os grupos longitudinalmente e um modelo de ANOVA para medidas repetidas não paramétrico para o MPO, ao nível de significância de 5%. Resultados: As médias da viabilidade celular foram superiores no grupo experimental, quando observadas a média dos cinco ensaios para cada momento de aferição segundo o grupo estudado, com diferença estatisticamente significante (p = 0,0040). A atividade da MPO, expressa em Unidades Relativas de Luminescência foi superior no grupo experimental (p = 0,0020). Conclusão: Houve aumento tanto da viabilidade celular, quanto da atividade da enzima mieloperoxidase dos neutrófilos in vitro pertencentes ao grupo experimental quando comparados ao grupo controle. / Introduction: Reiki is within as more frequent energy-based therapies. Studying therapies based on complex and dynamic holistic mechanisms, influenced by different individuals and environmental factors, requires a series of assessments in different experimental models. In this context, in vitro studies allow the control of cells external factors, avoiding the high individual variability, providing results in a shorter time. Among leukocytes, neutrophils are those present in greater amounts in the peripheral blood, acting in the main role in the early stages of inflammatory reactions, as a defense mechanism, being in the rank of the first cells of the immune system that move from the vessels to the tissues. Objective: Evaluate the effect of Reiki on cell viability and myeloperoxidase activity of human neutrophils in vitro. Method: It is an experimental, double-blind, laboratory study with a quantitative approach. It was done at Laboratory of Cellular Physiology and Molecular Biology of Cruzeiro do Sul University - Anália Franco Campus - São Paulo - SP. The human blood samples were obtained from five healthy volunteers. The test required 20mL of blood obtained by peripheral venous puncture. Inclusion criteria: adult, male, between the ages of 20 and 40 years. Exclusion criteria: volunteers reporting health problems, use of medications and use of complementary therapy (as energy therapies, phytotherapy, meditation and others). The experimental group received the Reiki application, at room temperature, by means of the laying on of hands to 15 cm of distance by 15 minutes. A Reiki application was performed once a day, for three consecutive days, in sessions every 24 hours. The control group remained at the same period and at the same environmental conditions as the intervention group, but without any application of the biofield technique. The cells were evaluated through the technique of the Trypan blue exclusion test, that allows to differentiate alive and dead cells, through dye exclusion by viable cells, and counted in Neubauers chamber. The activity of the myeloperoxidase (MPO) enzyme was evaluated by chemiluminescence assay. The analysis of cell viability was done in triplicate using as the result the measures average. Data analysis. Measurements of variability and central tendency, generalized estimation equation model equations for binomial distribution of cell viability data for a longitudinal comparison of groups and ANOVA model for non-parametric repeated measures for MPO, at a significance level of 5%. Results: The cellular viability means were higher in the experimental group when evaluated the mean of the five experimental assays in each measurement moment according to the group studied, with a statistically significant difference (p = 0.0040). MPO activity, expressed in Relative Luminescence Units, was higher in the experimental group, except in the fifth assay, and with an exacerbation of enzyme activity in the third assay, with a statistically significant difference (p = 0.0020). Conclusion: There was an increase in both cell viability and myeloperoxidase enzyme in vitro neutrophils from experimental group when compared to the control group, both with statistically significant differences.

5‐羟色胺（5-HT）是一种强有力的血管活性神经递质，被广泛的应用在调节血管张力。当5‐HT 被释放后，会被单胺氧化酶（MAOs）催化的酶促反应代谢，从而产生不同的代谢产物，比如5‐HIAA，5‐HTOL 和过氧化氢（H₂O₂）。然而，5‐HT对于内皮细胞活性氧物种（ROS）的产生作用以及5‐HT 转运体，5‐HT 受体，MAOs和ROS 的产生伴随着细胞内钙变化是否参与了其中的信号传导尚未被阐明。所以，这个研究最初的目的是考查外源性加入的5‐HT 对于脐静脉内皮细胞中ROS产生的影响以及其潜在的生物机理。 / 数据清楚的显示在没有L‐NAME（一种抑制一氧化氮（NO）产生的抑制剂）预处理的情况下，5‐HT 并不能在脐静脉内皮细胞内产生显著性的ROS。然而，在L‐NAME 预处理的情况下，NO 的产生被完全抑制，我们观察到明显的显著性的线粒体内的ROS 产生。5‐HT 产生的线粒体ROS 可以被clorgyline（一种MAO‐A 抑制剂），indatraline（一种5‐HT 转运体阻断剂），LY272015（一种5‐HT‐2B 受体拮抗剂），ketanserin（一种5‐HT2A 受体拮抗剂），XeC（一种IP3 受体拮抗剂），Gd³⁺（一种非选择性TRP 通道阻断剂），BAPTA（一种强效钙离子螯合剂），PEG‐Catalase，U73122（一种选择性PLC 抑制剂）以及没有钙离子的培养基所阻止。同时，5‐HT介导的胞内钙离子变化被XeC, Gd³⁺, BAPTA, U73122, ketanserin, LY272015 以及没有钙离子的培养基所阻止。另外，MAO‐A 基因敲除抑制了5‐HT 导致的线粒体ROS的产生却对5‐HT 介导的胞内钙离子变化没有影响。基于以上所述的结果，我们可以得出结论，通过5‐HT 转运体，5‐HT 被摄取入细胞内，然后通过MAO‐A 介导的酶促代谢反应，产生钙离子依赖性的线粒体内ROS 的产生，这一结论对于解释血小板聚集而引起的内皮细胞功能性障碍起到非常重要的作用。 / 根据前人所述，内皮细胞内产生的ROS 对于内皮细胞通透性变化有着重要的作用，但是5‐HT 诱导的脐静脉内皮细胞ROS 的增加是否会对内皮通透性有所影响并没有被说明。在这项研究中，我们设计了实验旨在测试平面细胞表面积（ PCSA ）， 跨内皮电阻（ TER ）， 细胞高度， 肌球蛋白轻链磷酸化（MLCphosphorylation）和肌动蛋白细胞骨架（F‐actin cytoskeleton）水平的变化。此外，b‐catenin 在ROS 引起的F‐actin cytoskeleton 重组中的作用也在我们的讨论范围之内。 / 数据表明，在L‐NAME 预处理的情况下，5-HT 降低了脐静脉内皮的PCSA，TER 以及细胞高度，却增加了MLCP 和与b‐catenin 表达负相关的F‐actincytoskeleton 的水平。这些作用明显被PEG‐Catalase 预处理和MAO‐A 基因敲除减弱，证明了5‐HT 通过MAO‐A 介导产生的H₂O₂ 可以增加内皮细胞的通透性。 / 据文献报道，不论内源性还是外源性的低浓度的H₂O₂ 都可以激活导致血管生成的信号通路。文献进一步表明5‐HT 可以通过特定的5‐HT 受体亚型促进各种类型的内皮细胞的血管生成。然而，5‐HT 诱导的H₂O₂ 对于脐静脉内皮的血管生成作用并没有被报道。我们通过最初的实验先验证5‐HT 对于内皮细胞增殖和迁移的影响，然后我们才去验证H₂O₂ 在其中的作用及其潜在的机理。 / 实验结果表明，在L‐NAME 预处理的情况下，不论是急性（30 分钟）还是慢性（24 小时）的5‐HT 的处理都可以导致脐静脉内皮细胞的迁移，而这个作用会被5‐HT‐2 受体拮抗剂ketanserin，LY272015，ROS 清除剂PEG‐Catalase 以及PI3K的抑制剂wortmannin 所抑制。同时，在L‐NAME 预处理下，5‐HT 增加了cortactin,p‐Akt 和 p‐eNOS 的蛋白表达量而并没有影响Akt, eNOS 和p‐cortactin 的蛋白表达量。而5‐HT 增加的p‐Akt 和p‐eNOS 的蛋白表达被wortmannin 和PEG‐Catalase所抑制。不论是在Cyuant 细胞增殖检测还是在BrdU 细胞增殖检测中，5‐HT 诱导了一种非显著性的DNA 合成的增加，并且再BrdU 细胞增殖检测中，增加了的DNA 合成被PEG‐Catalase 显著性降低。总结以上实验结果，我们可以得出结论，通过一种5‐HT‐2 受体介导的PI3K 依赖性通路，而不是cortactin 磷酸化依赖性的信号通，路5‐HT 可以引导内皮细胞迁移。 / 除此之外，ROS 也被印证可以加剧内皮细胞的炎症反应和加速内皮细胞的老化。因此，我们也观察了5‐HT 对于粘附蛋白比如ICAM‐1 和VCAM‐1 以及抗老化因子SIRT‐1 的表达是否有影响。数据表明，在L‐NAME 预处理的情况下，30 分钟的5‐HT 处理显著的增加了ICAM‐1，SIRT‐1 而不是VCAM‐1 的表达。同时，这些作用均可以被PEG‐Catalase 所抑制表明了5‐HT 通过诱导H₂O₂ 的产生来形式其促进炎症反应和抗衰老的作用。 / 最后，总结以上，通过抑制NO 的产生，5‐HT 可以通过MAO‐A 介导的酶促代谢反应在人体脐静脉内皮细胞线粒体诱导ROS 的产生。同时，5‐HT 诱导的H₂O₂参与了改变内皮细胞通透性，促进血管生成（内皮迁移）及炎症反应的过程。 / 5-Hydroxytryptamine (5-HT), a potent vasoactive neurotransmitter, is involved in the regulation of vascular tone. After its release, 5-HT is terminated at the nerve terminals via enzymatic metabolism catalyzed by monoamine oxidases (MAOs), resulting in the generation of different metabolites (e.g. 5-HIAA, 5-HTOL and H₂O₂). Our lab demonstrates for the first time that 5-HT-induced ROS production indeed occurs and therefore, the aim of this study is to investigate exogenously added 5-HT on ROS generation in human umbilical vein endothelial cells (HUVECs), in order to understand the mechanisms involved in 5-HT-induced ROS production. / Our results clearly demonstrated that in the absence of L-NAME(a NO production inhibitor), there wasno apparent ROS production induced by 5-HT. However, after the inhibition of NO synthesis by L-NAME, 5-HT caused a significant increase in mitochondrial H₂O₂ production. The 5-HT-induced mitochondrial H₂O₂ generation was sensitive to clorgyline (a MAO-A inhibitor), indatraline (a 5-HT transporter blocker), LY272015 (a 5-HT2B antagonist) and ketanserin (a 5-HT2A antagonist), Xextospongin C（XeC，a IP3 receptor antagonist), Gd³⁺ (a non-selective TRP channel blocker), BAPTA (a potent Ca²⁺ ions chelator), PEG-Catalase, U73122 (a selective PLC inhibitor), and in [Ca²⁺]o-free medium. Concurrently, 5-HT-mediated [Ca²⁺]i changes were sensitive to XeC, Gd³⁺, BAPTA, U73122, ketanserin, LY272015, and in [Ca²⁺]o-free conditions. In addition, gene knockdown of MAO-A suppressed 5-HT-elicited H₂O₂ production with no effects on [Ca²⁺]i changes. Based on all the results above, we can conclude that 5-HT caused a Ca²⁺-dependent mitochondrial H₂O₂ generation via MAO-A-mediated metabolism with the pre-requisite uptake of 5-HT into HUVECs through 5-HT transporter. / ROS derived from endothelial cells have been implicated in changes in endothelial permeability, but whether 5-HT-induced H₂O₂ generation could alter endothelial cells permeability has as yet not been demonstrated. Here, we measured the planar cell surface area (PCSA), transendothelial electrical resistance (TER), cell height, myosin light chain phosphorylation and F-actin cytoskeleton level in response to 5-HT challenge to investigate the change of endothelial permeability. Moreover, the participation of β-catenin in regulation of F-actin cytoskeleton remodeling in ROS-modulated alteration in endothelial permeability was also investigated. Results indicated that in the presence of L-NAME, 5-HT reduced the PCSA, TER and cell height in HUVECs. In contrast, 5-HT (with L-NAME) increased myosin light chain phosphorylation (MLCP) expression and F-actin cytoskeleton level, which are negatively associated with β-catenin expression. All of these effects were ameliorated by pre-treatment of PEG-Catalase or gene knockdown of MAO-A, implying 5-HT can consistently elicit the increase in endothelial permeability via MAO-A mediated H₂O₂ generation. / Low dose of ROS from exogenous or endogenous source can activate signaling pathway that lead to angiogenesis.5-HT can promote endothelial angiogenesis through specific 5-HT receptor subtype in various endothelial cell types, but the concomitant ROS generation had not previously been indicated to play a role in the process. In this study, we seek to test out the effects of 5-HT on endothelial cells migration, and should there be a functional role for ROS in the process. / Our results revealed that in the presence of L-NAME, both acute (30 min) and chronic (24 hr) treatment of 5-HT caused HUVECs migration, the effects of which were reversed by pre-incubation of 5-HT-2 receptor antagonists, ketanserin, LY272015, ROS scavenger PEG-Catalase or selective PI3K inhibitor wortmannin. With L-NAME, 5-HT consistently increased cortactin, p-Akt and p-eNOS expression without affecting total Akt, eNOS and p-cortactin protein expression whereas the increased p-Akt and p-eNOS expression are suppressed by pre-treatment of wortmanin or PEG-Catalase. Both in Cyuant cell proliferation assay and BrdU assay, 5-HT caused a trend but non-significant increase in DNA synthesis whereas the pre-treatment of PEG-Catalase significantly suppressed cell proliferation in the BrdU assay. Based on these results, we can conclude that 5-HT elicits endothelial migration via 5-HT-2 receptor-mediated H₂O₂ generation in a PI3K-dependent pathway. Under this circumstance, cortactin phosphorylation-dependent pathway was excluded. / Besides, ROS is notorious for effects like aggravation of inflammation and acceleration aging processes. The investigation extends to looking at alterations ofexpression of adhesion protein including ICAM-1 and VCAM-1 in the inflammatory response pathway and also to looking at the major aging parameter SIRT-1 in the presence of 5-HT in endothelium. Our data showed that in the presence of L-NAME, 30 min treatment of 5-HT significantly increased ICAM-1 and SIRT-1 expression without altering VCAM-1 expression and the up-regulation of ICAM-1 and SIRT-1 expression was prevented by PEG-Catalase. / In conclusion, with the eradication of the influence of NO, 5-HT induced mitochondrial H₂O₂ production via MAO-A-mediated metabolism in HUVECs. At the same time, 5-HT-induced H₂O₂ generation was involved in increasing endothelial permeability, inflammation and angiogenesis (cell migration). / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Zhang, Qian. / Thesis (Ph.D.) Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 326-450). / Abstracts also in Chinese. / Zhang, Qian.

by Chang Chuen Chung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves 125-140). / Acknowledgement --- p.4 / List of Abbreviations --- p.5 / Abstract --- p.7 / Chapter CHAPTER I --- INTRODUCTION --- p.10 / Chapter 1.1 --- Astrocytes in the Central Nervous System --- p.10 / Chapter 1.1.1 --- Characteristics of astrocytes --- p.10 / Chapter 1.1.2 --- Functional roles of astrocytes --- p.11 / Chapter 1.1.2.1 --- General functions of astrocytes --- p.11 / Chapter 1.1.2.2 --- Volume regulation of astrocytes in CNS injuries --- p.12 / Chapter 1.1.2.3 --- Immunological functions of astrocytes --- p.13 / Chapter 1.2 --- Taurine in the CNS --- p.15 / Chapter 1.2.1 --- The biochemistry and distribution of taurine --- p.15 / Chapter 1.2.2 --- Physiological functions of taurine in the CNS --- p.19 / Chapter 1.2.3 --- Uptake and release of taurine by cultured astrocytes --- p.20 / Chapter 1.2.3.1 --- Taurine uptake in astrocytes --- p.21 / Chapter 1.2.3.2 --- Taurine release in astrocytes --- p.22 / Chapter 1.3 --- Tumor necrosis factor in the CNS --- p.23 / Chapter 1.3.1 --- Characteristics of tumor necrosis factor --- p.23 / Chapter 1.3.2 --- Sources of TNF in the CNS --- p.25 / Chapter 1.3.3 --- Functions of TNF in the CNS --- p.26 / Chapter 1.3.4 --- TNF and signal transduction --- p.27 / Chapter 1.4 --- cGMP second messenger system in astrocyte --- p.29 / Chapter 1.4.1 --- cGMP as second messenger in astrocytes --- p.29 / Chapter 1.4.2 --- Post cGMP cascade effects --- p.30 / Chapter 1.5 --- The aims of this project --- p.30 / Chapter CHAPTER II --- METHODS --- p.34 / Chapter 2.1 --- Primary astrocytes culture --- p.34 / Chapter 2.1.1 --- Primary rat astrocytes culture --- p.34 / Chapter 2.1.2 --- Primary mouse astrocytes culture --- p.36 / Chapter 2.1.3 --- Culture of rat C6 glioma cell line --- p.36 / Chapter 2.1.4 --- Subculture of astrocytes in different media --- p.37 / Chapter 2.2 --- Taurine uptake and release assay --- p.39 / Chapter 2.2.1 --- Taurine uptake assay --- p.39 / Chapter 2.2.2 --- Taurine release assay --- p.41 / Chapter 2.3 --- The effects of TNF on taurine transport --- p.42 / Chapter 2.4 --- The effects of TNF on cell volume in astrocytes --- p.43 / Chapter 2.5 --- "The effects of TNF on amino acids, glucose and neurotransmitters uptake" --- p.43 / Chapter 2.5.1 --- The effects of TNF on amino acids uptake --- p.43 / Chapter 2.5.2 --- The effects of TNF on glucose uptake --- p.44 / Chapter 2.5.3 --- The effects of TNF on neurotransmitters uptake --- p.45 / Chapter 2.6 --- The effects of LPS on taurine uptake in astrocytes --- p.46 / Chapter 2.7 --- The effects of IFN-¡’ on taurine uptake in astrocytes --- p.46 / Chapter 2.8 --- The effects of PMA on taurine uptake in astrocytes --- p.47 / Chapter 2.9 --- "The effects of TNF on thymidine, uridine and leucine incorporation in astrocytes" --- p.47 / Chapter 2.10 --- The effects of TNF on basal level of cGMP in astrocytes --- p.48 / Chapter 2.11 --- The effects of TNF on protein phosphorylation in astrocytes --- p.49 / Chapter 2.12 --- The effects of TNF on calcium uptake in astrocytes --- p.50 / Chapter CHAPTER III --- RESULTS --- p.51 / Chapter 3.1 --- The effects of TNF on taurine transport in cultured rat astrocytes --- p.51 / Chapter 3.1.1 --- The effects of TNF on [3H]-taurine uptake -time course study --- p.52 / Chapter 3.1.2 --- The effects of TNF on the kinetic parameters of the taurine uptake system --- p.54 / Chapter 3.1.3 --- The effects of TNF concentration on taurine uptake --- p.63 / Chapter 3.1.4 --- The effects of TNF exposure time on taurine uptake --- p.65 / Chapter 3.1.5 --- The effects of TNF on cell volume change in astrocytes --- p.67 / Chapter 3.1.6 --- "Comparison of the effects of TNF on taurine uptake amongst cultured primary rat astrocytes, primary mouse astrocytes and C6 glioma cell line" --- p.69 / Chapter 3.1.7 --- The effects of TNF on taurine release --- p.71 / Chapter 3.1.8 --- The specificity of the effects of TNF on taurine uptake --- p.74 / Chapter 3.1.8.1 --- The effects of TNF on the uptake of amino acids and glucose in primary rat astrocytes --- p.79 / Chapter 3.1.8.2 --- The effects of TNF on neurotransmitters uptake --- p.87 / Chapter 3.1.9 --- The effects of LPS on taurine uptake in astrocytes --- p.92 / Chapter 3.1.10 --- The effects of IFN-¡’ on taurine uptake in astrocytes --- p.97 / Chapter 3.1.11 --- The effects of PMA on taurine uptake --- p.99 / Chapter 3.2 --- The effects of TNF on cell metabolism in rat astrocytes --- p.102 / Chapter 3.2.1 --- The effects of TNF on astrocyte proliferation --- p.102 / Chapter 3.2.2 --- The effects of TNF on RNA synthesis --- p.103 / Chapter 3.2.3 --- The effects of TNF on protein synthesis --- p.106 / Chapter 3.2.4 --- The effects of TNF on basal level of cGMP --- p.108 / Chapter 3.2.5 --- The effects of TNF on protein phosphorylation --- p.111 / Chapter 3.2.6 --- The effects of TNF on calcium uptake --- p.113 / Chapter Chapter IV --- DISCUSSION AND CONCLUSION --- p.116 / References --- p.125

by Poon Yam Kau. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 174-183). / Abstract --- p.1 / Chapter Chapter 1 --- General Introduction / Chapter 1.1 --- Discovery of melatonin --- p.4 / Chapter 1.2 --- Biosynthesis of melatonin --- p.4 / Chapter 1.3 --- Physiology of melatonin and other pineal indoles --- p.5 / Chapter 1.4 --- Relationship between pineal indoles and cancers --- p.6 / Chapter 1.5 --- Macrophages --- p.9 / Chapter 1.6 --- Lymphocytes --- p.11 / Chapter Chapter 2 --- Effects of different light/dark cycles on serum melatonin level in mice and effect of melatonin-feeding on serum glutamate-oxaloacetate transaminase (GOT) activity in mice / Chapter 2.1 --- Introduction --- p.14 / Chapter 2.2 --- Materials and methods --- p.15 / Chapter 2.3 --- Results --- p.22 / Chapter 2.4 --- Discussion --- p.23 / Chapter Chapter 3 --- Actions of endogenous and exogenous melatonin on murine peritoneal macrophages / Chapter 3.1 --- Introduction --- p.27 / Chapter 3.2 --- Materials and methods --- p.28 / Chapter 3.3 --- Results --- p.33 / Chapter 3.4 --- Discussion --- p.36 / Chapter Chapter 4 --- Actions of endogenous and exogenous melatonin on murine splenic lymphocytes / Chapter 4.1 --- Introduction --- p.55 / Chapter 4.2 --- Materials and methods --- p.56 / Chapter 4.3 --- Results --- p.62 / Chapter 4.4 --- Discussion --- p.69 / Chapter Chapter 5 --- In vitro effects of melatonin on murine peritoneal macrophages and splenic lymphocytes / Chapter 5.1 --- Introduction --- p.105 / Chapter 5.2 --- Materials and methods --- p.106 / Chapter 5.3 --- Results --- p.109 / Chapter 5.4 --- Discussion --- p.113 / Chapter Chapter 6 --- Effects of methoxytryptamine on murine peritoneal macrophages and splenic lymphocytes / Chapter 6.1 --- Introduction --- p.125 / Chapter 6.2 --- Materials and methods --- p.126 / Chapter 6.3 --- Results --- p.129 / Chapter 6.4 --- Discussion --- p.132 / Chapter Chapter 7 --- In vitro effects of pineal indoles on cultured tumor cell lines / Chapter 7.1 --- Introduction --- p.145 / Chapter 7.2 --- Materials and methods --- p.146 / Chapter 7.3 --- Results --- p.148 / Chapter 7.4 --- Discussion --- p.152 / Chapter Chapter 8 --- General Discussion --- p.170 / References --- p.174