by Yueming Qian. / Publication date from spine. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 209-244). / ABSTRACT --- p.i / ACKNOWLEDGEMENTS --- p.iii / PUBLICATIONS --- p.iv / Chapter CHAPTER 1 --- General Introduction --- p.1 / Chapter CHAPTER 2 --- Methodology --- p.53 / Chapter CHAPTER 3 --- Characterisation of Vascular EP-Receptors --- p.76 / Chapter PART 1 --- EP-receptors on the human isolated pulmonary artery --- p.77 / Chapter PART 2 --- EP-receptors on the guinea-pig isolated aorta --- p.100 / Chapter CHAPTER 4 --- Neuronal IP-Receptors in the Rat Colon --- p.130 / Chapter CHAPTER 5 --- Differential Effects of Non-Prostanoid Prostacyclin Mimetics on Human Pulmonary Artery and Rat Colon --- p.173 / Chapter CHAPTER 6 --- General Discussion and Perspective --- p.200 / REFERENCES --- p.209

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The possible role of the prostaglandins (PGs) in the regulation of protein turnover was investigated, firstly in hypertrophying rat skeletal muscle at 20 hours, 3 days and 7 days after synergist tenotomy, and secondly, in various tissues of the rainbow trout (Salmo gairdneri, Richardson) following re-feeding. An inhibitor of PG synthesis was used in both cases (fenbufen and indomethacin, respectively). 1) Fenbufen (at a dose of 1200mg/kg of diet) did not inhibit the hypertrophy of the soleus and plantaris muscles although there appeared to be an initial reduction in muscle RNA content. 2) Muscle growth was generally increased in fenbufen fed rats by 7 days after synergist tenotomy (10 days on fenbufen diet). 3) The fractional rate of protein synthesis in both control and overloaded muscles was reduced by fenbufen at this time (in 86g rats). The calculated rates of protein breakdown were also reduced in these muscles but to a greater extent than synthesis. This inhibition of protein degradation was most marked in the overloaded soleus and plantaris muscles. 4) The tenotomised gastrocnemius muscle experienced a true atrophy in the fenbufen-treated rats by 7 days. This atrophy involved greatly elevated rates of protein degradation when compared to the tenotomised muscle from rats fed a normal diet. In 6 day fasted rainbow trout, tissue protein synthesis was measured at 3 hours, 6 hours and 12 hours after re-feeding. The rapidity of the stimulation of protein synthesis by re-feeding and the nature of the response was tissue-specific. The administration of indomethacin (at a dose of 2mg/100g body weight) one hour prior to the meal, partially blocked the re-feeding response of protein synthesis in the gill at 6 hours after the meal, but stimulated protein synthesis in the liver and white muscle at this time.

by Zhi-Hui Xie. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 214-244). / Abstract --- p.i / Acknowledgments --- p.iv / Publications --- p.v / Abbreviations --- p.vi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Neutrophils --- p.1 / Chapter 1.1.1 --- General --- p.1 / Chapter 1.1.2 --- HL-60 cells as model of neutrophils --- p.3 / Chapter 1.1.3 --- Physiological role --- p.6 / Chapter 1.1.4 --- Intracellular signalling --- p.12 / Chapter 1.1.4.1 --- General --- p.12 / Chapter 1.1.4.2 --- Intracellular signalling linked by FMLP receptors --- p.13 / Chapter 1.1.4.3 --- Intracellular signalling of neutrophil functions --- p.17 / Chapter 1.2 --- Neutrophil aggregation --- p.21 / Chapter 1.2.1 --- General --- p.21 / Chapter 1.2.2 --- Measurement of aggregation --- p.24 / Chapter 1.3 --- Prostaglandins/Prostanoids --- p.25 / Chapter 1.3.1 --- General --- p.25 / Chapter 1.3.2 --- Prostanoid receptors --- p.27 / Chapter 1.3.2.1 --- Agonists and antagonists --- p.28 / Chapter 1.3.2.2 --- EP1 receptors --- p.32 / Chapter 1.3.2.3 --- EP2 receptors --- p.33 / Chapter 1.3.2.4 --- EP3 receptors --- p.34 / Chapter 1.3.2.5 --- EP4 receptors --- p.37 / Chapter 1.3.2.6 --- DP receptors --- p.38 / Chapter 1.3.2.7 --- IP receptors --- p.39 / Chapter 1.3.2.8 --- TP receptors --- p.40 / Chapter 1.3.2.9 --- FP receptors --- p.40 / Chapter 1.4 --- Regulation of neutrophil functions by prostanoids --- p.42 / Chapter 1.4.1 --- Inhibition --- p.42 / Chapter 1.4.2 --- Activation --- p.46 / Chapter 1.4.3 --- Role of cyclic AMP --- p.48 / Chapter 1.5 --- Aim of this study --- p.51 / Chapter Chapter 2 --- Materials and methods --- p.53 / Chapter 2.1 --- Materials and solutions --- p.53 / Chapter 2.1.1 --- Materials --- p.53 / Chapter 2.1.2 --- "Buffers, solutions and cell culture medium" --- p.62 / Chapter 2.2 --- Methods --- p.64 / Chapter 2.2.1 --- Culture of HL-60 cells --- p.64 / Chapter 2.2.2 --- Differentiation of HL-60 cells --- p.65 / Chapter 2.2.3 --- Preparation of neutrophils --- p.65 / Chapter 2.2.4 --- Measurement of neutrophil aggregation --- p.67 / Chapter 2.2.5 --- Measurement of [Ca2+]i --- p.69 / Chapter 2.2.6 --- Microscopic observation --- p.70 / Chapter 2.2.7 --- Measurement of [3H]-cyclic AMP accumulation --- p.72 / Chapter 2.2.8 --- Measurement of [3H]-PGE2 receptor binding --- p.73 / Chapter 2.3 --- Data analysis --- p.76 / Chapter Chapter 3 --- Differentiation of HL-60 cells --- p.77 / Chapter 3.1 --- Introduction --- p.77 / Chapter 3.2 --- Results and discussion --- p.78 / Chapter 3.2.1 --- The observation of cell proliferation and morphology --- p.78 / Chapter 3.2.2 --- The response of HL-60 cells to FMLP --- p.80 / Chapter 3.2.3 --- The response of HL-60 cells to ATP --- p.83 / Chapter 3.3 --- Conclusion --- p.84 / Chapter Chapter 4 --- Activation of dHL-60 cells by PGE2 --- p.90 / Chapter 4.1 --- Effect of PGE2 on cell aggregation and [Ca2+]i --- p.90 / Chapter 4.1.1 --- Introduction --- p.90 / Chapter 4.1.2 --- Results --- p.90 / Chapter 4.1.2.1 --- Effect of PGE2 on cell aggregation --- p.90 / Chapter 4.1.2.2 --- Effect of PGE2 on [Ca2+]i --- p.91 / Chapter 4.1.2.3 --- Effect of PGE2 on human neutrophils --- p.93 / Chapter 4.1.2.4 --- Do PGE2 and PGE1 act at the same receptor? --- p.94 / Chapter 4.1.3 --- Discussion --- p.95 / Chapter 4.1.3.1 --- Activation of dHL-60 cells by PGE2 --- p.95 / Chapter 4.1.3.2 --- Effect of PGE2 on human neutrophils --- p.99 / Chapter 4.2 --- What does the aggregation response mean? --- p.101 / Chapter 4.2.1 --- Introduction --- p.101 / Chapter 4.2.2 --- Results --- p.101 / Chapter 4.2.2.1 --- Observation by light microscopy --- p.101 / Chapter 4.2.2.2 --- Observation by Scanning Electron Microscope --- p.102 / Chapter 4.2.3 --- Discussion --- p.103 / Chapter 4.3 --- Conclusion --- p.106 / Chapter Chapter 5 --- Characterisation of prostanoid receptors on dHL-60 cells --- p.121 / Chapter 5.1 --- Introduction --- p.121 / Chapter 5.2 --- Results --- p.121 / Chapter 5.2.1 --- Effect of prostanoid receptor agonists and antagonists on cell aggregation --- p.121 / Chapter 5.2.2 --- Effect of prostanoid receptor agonists on [Ca2+]i --- p.122 / Chapter 5.3 --- Discussion --- p.123 / Chapter 5.3.1 --- Involvement of prostanoid receptors --- p.123 / Chapter 5.3.2 --- Involvement of EP receptors --- p.126 / Chapter 5.4 --- Conclusion --- p.130 / Chapter Chapter 6 --- Binding studies of [3H]-PGE2 on rat neutrophils and dHL-60 cells --- p.137 / Chapter 6.1 --- Introduction --- p.137 / Chapter 6.2 --- Results --- p.138 / Chapter 6.3 --- Discussion --- p.140 / Chapter Chapter 7 --- The mechanism of action of PGE2 in activating dHL-60 cells --- p.146 / Chapter 7.1 --- Introduction --- p.146 / Chapter 7.2 --- Methods --- p.147 / Chapter 7.2.1 --- Pretreatment with enzyme inhibitors --- p.147 / Chapter 7.2.2 --- Pretreatment with toxins --- p.148 / Chapter 7.2.3 --- Pretreatment with PMA --- p.148 / Chapter 7.3 --- Results and discussion --- p.148 / Chapter 7.3.1 --- The role of Ca2+ --- p.149 / Chapter 7.3.2 --- The role of cyclic AMP --- p.152 / Chapter 7.3.3 --- The role of PI3-kinase --- p.159 / Chapter 7.3.4 --- The role of PLD --- p.165 / Chapter 7.3.5 --- The role of PLA2 --- p.169 / Chapter 7.3.6 --- The role of tyrosine kinase --- p.171 / Chapter 7.3.7 --- The role of PKC --- p.173 / Chapter 7.3.8 --- The role of G protein --- p.180 / Chapter 7.3.9 --- The role of cyclic GMP --- p.185 / Chapter 7.3.10 --- The role of KATP channels --- p.186 / Chapter 7.4 --- Conclusion --- p.187 / Chapter Chapter 8 --- General discussion and conclusion --- p.209 / References --- p.214

published_or_final_version / abstract / toc / Medicine / Master / Doctor of Medicine

Thesis (Ph. D.)--University of Virginia, 1997. / Includes bibliographical references (93-107). Also available online through Digital Dissertations.

Tübingen, Univ., Diss., 2005.