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BCL-2 family in retinal degeneration in ischemia/reperfusion injury and in the RCS rats.January 1998 (has links)
Chiu Kin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 100-116). / Abstract also in Chinese. / TABLE OF CONTENTS --- p.I / ACKNOWLEDGEMENTS --- p.V / LIST OF FIGURES --- p.VI / LIST OF ABBREVIATIONS --- p.VIII / ABSTRACT --- p.1 / Chapter 1. --- INTRODUCTION --- p.5 / Chapter 2. --- LITERATURE REVIEW --- p.7 / Chapter 2.1 --- RETINAL ISCHEMIA --- p.7 / Chapter 2.1.1 --- INDUCTION OF RETINAL ISCHEMIA --- p.7 / Chapter 2.1.2 --- MECHANISMS OF RETINAL ISCHEMIA/REPERFUSION DAMAGE --- p.8 / Chapter 2.1.2.1. --- Free radical --- p.8 / Chapter 2.1.2.2 --- Excitotoxicity --- p.9 / Chapter 2.1.3 --- APOPTOSIS IN RETINAL ISCHEMIA/REPERFUSION INJURY --- p.10 / Chapter 2.2 --- RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEONS (RCS) RAT --- p.15 / Chapter 2.3 --- BCL-2 FAMILY MEMBERS --- p.16 / Chapter 2.3.1 --- FAMILY MEMBERS AND THEIR INTERACTIONS --- p.16 / Chapter 2.3.2 --- SUBCELLULAR LOCALIZATION --- p.18 / Chapter 2.3.3 --- PHYSICAL STRUCTURE AND PORE FORMATION --- p.19 / Chapter 2.3.4 --- BIOLOGICAL EFFECTS OF BCL-2 --- p.20 / Chapter 3. --- OBJECTIVES --- p.24 / Chapter 4. --- MATERIALS AND METHODS --- p.27 / Chapter 4.1. --- RETINAL ISCHEMIA AND REPERFUSION INDUCED LOSS OF INNER RETINAL ELEMENTS --- p.27 / Chapter 4.1.1. --- TISSUE RESPONSES IN THE RAT RETINAS AFTER TRANSIENT ELEVATED INTRAOCULAR PRESSURE INDUCED RETINAL ISCHEMIA/REPERFUSION INSULT --- p.27 / Chapter 4.1.1.1. --- Induction of retinal ischemia/reperfusion insult with transient elevated intraocular pressure (IOP) --- p.27 / Chapter 4.1.1.2. --- Animal experiments --- p.28 / Chapter 4.1.1.3. --- Histopathology and measurement of inner retinal thickness (IRT) --- p.28 / Chapter 4.1.1.4. --- Flat preparation of the retinas and retinal ganglion cell counts (RGCCs) --- p.29 / Chapter 4.1.2. --- INTERNUCLEOSOMAL DNA FRAGMENTATION AND IN SITU NICKED DNA DETECTIONS AT DIFFERENT TIME AFTER REPERFUSION IN THE RAT RETINAS --- p.30 / Chapter 4.1.2.1. --- Enzyme-linked immunosorbent assay (ELISA) of mono- and oligonucleosomes --- p.30 / Chapter 4.1.2.2. --- In-situ terminal deoxynucleotidyl transferase (TdT)-mediated biotin- dUTP nicked end labelling (TUNEL) --- p.31 / Chapter 4.1.3. --- "IMMUNOHISTOCHEMISTRY OF BCL-2, BAX AND P53" --- p.32 / Chapter 4.1.4. --- "DOUBLE LABELLING OF BCL-2, BAX AND TUNEL" --- p.33 / Chapter 4.1.5. --- IN-SITU REVERSE TRANSCRIPTASE - POLYMERASE CHAIN REACTION OF BCL-2 AND BAX --- p.34 / Chapter 4.1.5.1. --- Primers design and specificity test --- p.34 / Chapter 4.1.5.2. --- In-situ RT-PCR --- p.36 / Chapter 4.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEONS (RCS) RATS --- p.38 / Chapter 4.2.1. --- HISTOPATHOLOGY --- p.38 / Chapter 4.2.2 --- MORPHOMETRY OF CELLS IN THE RETINAL GANGLION CELL LAYER (RGCL) AND THE INNER NUCLEAR LAYER (INL) --- p.39 / Chapter 4.2.3. --- IMMUNOHISTOCHEMISTRY OF BCL-2 AND BAX --- p.39 / Chapter 5. --- RESULTS --- p.40 / Chapter 5.1. --- RETINAL ISCHEMIA AND REPERFUSION INDUCED LOSS OF INNER RETINAL ELEMENTS --- p.40 / Chapter 5.1.1. --- TISSUE RESPONSES IN THE RAT RETINAS AFTER TRANSIENT ELEVATED INTRAOCULAR PRESSURE INDUCED ISCHEMIA/ REPERFUSION INSULT --- p.40 / Chapter 5.1.1.1. --- Histopathology --- p.40 / Chapter 5.1.1.2. --- Morphometry of inner retinal thickness --- p.40 / Chapter 5.1.1.3. --- Retinal ganglion cell counts (RGCCs) --- p.41 / Chapter 5.1.2. --- INTERNUCLEOSOMAL DNA FRAGMENTATION AND IN SITU NICKED DNA DETECTION AT DIFFERENT TIME AFTER REPERFUSION IN THE RAT RETINAS --- p.41 / Chapter 5.1.2.1. --- Enzyme-linked immunosorbent assay (ELISA) of mono- and oligonucleosomes --- p.42 / Chapter 5.1.2.2. --- In situ TUNEL --- p.42 / Chapter 5.1.3. --- BCL-2 AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.42 / Chapter 5.1.3.1. --- Immunohistochemistry of Bcl-2 --- p.42 / Chapter 5.1.3.2. --- Double labelling of Bcl-2 and TUNEL --- p.43 / Chapter 5.1.3.3. --- In situ RT-PCR for bcl-2 mRNA --- p.43 / Chapter 5.1.4. --- BAX AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.44 / Chapter 5.1.4.1. --- Immunohistochemistry of Bax --- p.44 / Chapter 5.1.4.2. --- Double labelling of Bax and TUNEL --- p.45 / Chapter 5.1.4.3. --- In situ RT-PCR for bax mRNA --- p.45 / Chapter 5.1.5. --- P53 IMMUNOREACTIVITY AT VARIOUS TIME AFTER REPERFUSION --- p.46 / Chapter 5.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEON (RCS) RATS --- p.47 / Chapter 5.2.1. --- HISTOPATHOLOGY --- p.47 / Chapter 5.2.2. --- MORPHOMETRY OF CELLS IN THE RGCL AND INL --- p.47 / Chapter 5.2.3. --- IMMUNOHISTOCHEMISTRY OF BCL-2 AND BAX --- p.47 / Chapter 5.2.3.1. --- Bcl-2 --- p.47 / Chapter 5.2.3.2. --- Bax --- p.48 / Chapter 6. --- DISCUSSION --- p.49 / Chapter 6.1. --- RETINA ISCHEMIA AND REPERFUSION INDUCED LOSS OF RETINAL ELEMENTS --- p.51 / Chapter 6.1.1 --- REPERFUSION TIME DEPENDENT TISSUE RESPONSES IN RAT RETINAS --- p.51 / Chapter 6.1.2 --- ISCHEMIA/REPERFUSION INDUCED APOPTOSIS IN RAT RETINAS --- p.52 / Chapter 6.1.3 --- BCL-2 AND RETINAL ISCHEMIA/REPERFUSION INSULT --- p.53 / Chapter 6.1.4 --- BAX AND RETINAL ISCHEMIA/REPERFUSION INSULT --- p.58 / Chapter 6.1.5 --- P53 AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.60 / Chapter 6.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEON (RCS) RAT --- p.61 / Chapter 6.2.1. --- HISTOPATHOLOGY AND MORPHOMETRY --- p.62 / Chapter 6.2.2. --- BCL-2 --- p.63 / Chapter 6.2.3. --- BAX --- p.64 / Chapter 7. --- CONCLUSION --- p.65 / APPENDIX A FIGURES --- p.66 / APPENDIX B REFERENCES --- p.100
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Pathogenetic mechanisms of the retinal degeneration: neuronal degeneration in retinitis pigmentosa. / CUHK electronic theses & dissertations collectionJanuary 1999 (has links)
by Zhang Chun. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (p. 154-197). / 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. / Abstract in Chinese and English.
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