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by Chan Chun-wai, Francis. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves 105-116). / Abstract --- p.I / Acknowledgments --- p.III / Abbreviations --- p.IV / Objectives --- p.VI / Content --- p.VII / Chapter Section 1 --- Introduction / Chapter I. --- Preamble --- p.1 / Chapter II. --- Characteristics of Cell Death Process --- p.1 / Chapter II.1. --- Necrosis --- p.1 / Chapter II.2. --- Apoptosis-Programmed Cell Death --- p.5 / Chapter III. --- Triggering of Programmed Cell Death --- p.10 / Chapter IV. --- DNA Fragmentation and Activation of Endogenous Endonuclease --- p.12 / Chapter V. --- Signal Transduction Leading to Programmed Cell Death --- p.14 / Chapter V.1. --- Role of Calcium Ion --- p.14 / Chapter V.2. --- Role of Protein Kinase C --- p.15 / Chapter V.3. --- Protein Dephosphorylation by Phosphatases --- p.16 / Chapter V.4. --- Role of Adenosine 3':5'-cyclic Monophosphate --- p.17 / Chapter V.5. --- Other Signaling Mechanisms --- p.17 / Chapter VI. --- Gene Regulation in Programmed Cell Death --- p.19 / Chapter VI. 1. --- Gene Expression in Programmed cell death --- p.19 / Chapter VI. 1.1 . --- Tissue Transglutaminase --- p.19 / Chapter VI. 1.2. --- Poly (ADP-ribose) Polymerase --- p.20 / Chapter VI. 1.3. --- Testosterone-Repressed Prostate Message-2 Gene --- p.20 / Chapter VI. 1.4. --- Other Programmed Cell Death Associated Gene Expressions --- p.21 / Chapter VI.2. --- Protooncogene Regulation in Programmed Cell Death --- p.22 / Chapter VI.2.1. --- bcl-2 Expression --- p.22 / Chapter VI.2.2. --- c-myc Expression --- p.23 / Chapter VII. --- Concanavalin A and succinylated Concanavalin A --- p.25 / Chapter VII. 1. --- Physiochemical Characterization --- p.25 / Chapter VII.2. --- Cellular Response to Concanavalin A --- p.29 / Chapter VIII. --- Features of Murine Macrophage Cell Line PU5-1.8 and Normal Macrophages --- p.32 / Chapter Section 2 --- Materials and Methods / Chapter I. --- Materials --- p.33 / Chapter II. --- Cell Culture --- p.33 / Chapter III. --- [Methyl-3H]-Thymidine Incorporation Assay --- p.34 / Chapter IV. --- [Methyl-3H]-Thymidine Release Assay --- p.34 / Chapter V. --- "3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT ) Cell Death Assay" --- p.35 / Chapter VI. --- Identification of Cell Death using DNA Chelating Fluorescence Probes´ؤFluorescent Microscopy and Confocal Laser Microscopy --- p.35 / Chapter VII. --- Analysis of DNA Fragmentation --- p.37 / Chapter VIII. --- Determination of Fluxes by Confocal Laser Microscopy --- p.38 / Chapter IX. --- Determination of PKC Activation by Western Blotting and Immunocytochemistry --- p.39 / Chapter X. --- Statistical Analysis --- p.41 / Chapter Section 3 --- Results / Chapter I. --- Concanavalin A was a Cell Death Causing Agent in PU5-1.8 cells --- p.42 / Chapter I.1 --- Con A Reduced the Cell Proliferation in PU5-1.8 cells --- p.42 / Chapter I.2. --- Con A Exhibited Cytotoxic Effect to PU5-1.8 cells --- p.44 / Chapter I.3. --- Con A Exhibited Cytotoxic Effect on Normal Peritoneal Macrophages --- p.46 / Chapter I.4. --- Succinylated Concanavalin A Showed a Weaker Cytotoxic Effect in the PU5-1.8 cells --- p.46 / Chapter I.5. --- α-D-Methylmannopyranoside Inhibited the Cytotoxic Effect of Con A in PU5-1.8 cells --- p.50 / Chapter I.6. --- FCS Inhibited the Con A-induced cell death of PU5-1.8 cells --- p.52 / Chapter II. --- Concanavalin A was an Apoptosis Causing Agentin PU5-1.8 cells --- p.57 / Chapter II. 1. --- Con A Induced Apoptosis in PU5-1.8 cells --- p.57 / Chapter II. 2. --- Con A Enhanced the Release of DNA in PU5-1.8 cell --- p.63 / Chapter II. 3. --- Con A Induced DNA fragmentation in PU5-1.8 cells --- p.63 / Chapter II.4. --- Cycloheximide Inhibited the Con A-Induced Cell Death in PU5-1.8 cells --- p.67 / Chapter II.5. --- Nicotinamide Inhibited the Con A-Induced Cell Death in PU5-1.8 cells --- p.71 / Chapter III. --- Signaling elicited by Concanavalin A --- p.74 / Chapter III.1. --- Con A Increased Intracellular Free Calcium Ion Concentration of PU5-1.8 cells --- p.74 / Chapter III. 1.1. --- Con A Induced Ca2+ Mobilization in PU5-1.8 cells --- p.74 / Chapter III. 1.2. --- Con A Induced the Ca2+ Influx and Intracellular Ca2+ Mobilization --- p.78 / Chapter III. 1.3. --- BAPTA-AM Inhibited the Ca2+ Mobilization in PU5-1.8 cells Stimulated by Con A --- p.80 / Chapter III.2. --- Role of Protein kinase C --- p.86 / Chapter III.2.1. --- Con A Increased the amount of PKC in PU5-1.8 cells --- p.86 / Chapter III.2.2. --- Con A translocated the Protein Kinase C from Cytosol into Subnuclear Region --- p.86 / Chapter III.2.3. --- The Cell Death Induced by Con A Is Partially Inhibited by PKC Depletion But not by Staurosporine --- p.89 / Chapter Section 4 --- Discussions / Chapter I. --- PU5-1.8 cells as a Model for the Study of Cell Deathin Macrophages --- p.94 / Chapter II. --- Concanavalin A caused Cell Death in PU5-1.8 cells --- p.95 / Chapter III. --- Concanavalin A induced Programmed Cell Death in PU5-1.8 cells --- p.97 / Chapter IV. --- Increase in Intracellular Calcium was not Required in Con A-induced Cell Death --- p.100 / Chapter V. --- Activation of Protein Kinase C was Partially Required for Con A-induced Cell Death --- p.101 / Chapter VI. --- General Discussions --- p.102 / Chapter Section 5 --- Bibliography --- p.104 / Reference --- p.104

by Wei-Zai Shen. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (p. 170-193) / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

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Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.