Kwong Man Kwong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 83-99). / TABLE OF CONTENTS --- p.i / ACKNOWLEDGEMENTS --- p.vi / LIST OF FIGURES --- p.vii / LIST OF ABBREVIATIONS --- p.ix / Chapter I. --- ABSTRACT --- p.1 / Chapter II. --- INTRODUCTION --- p.4 / Chapter III. --- LITERATURE REVIEW --- p.6 / Chapter A. --- EXCITATORY AMINO ACIDS AND EXCITOTOXICITY --- p.6 / Chapter 1. --- GLUTAMATE RECEPTORS --- p.7 / Chapter 2. --- NMDA RECEPTOR --- p.9 / Chapter 3. --- EXCITOTOXICITY --- p.10 / Chapter a. --- ACUTE PHASE --- p.10 / Chapter b. --- DELAYED PHASE --- p.11 / Chapter c. --- MECHANISM --- p.11 / Chapter i) --- Inhibition of Na+，K+-ATPase --- p.12 / Chapter ii) --- Impaired Mitochondrial Calcium Buffering --- p.12 / Chapter iii) --- Perturbation of Cytoskeletal Organisation --- p.13 / Chapter iv) --- Phospholipase Activation --- p.14 / Chapter v) --- Endonuclease Activation --- p.15 / Chapter vi) --- Protein Kinase C Activation --- p.15 / Chapter vii) --- Xanthine Oxidase Activation --- p.16 / Chapter viii) --- Nitric Oxidase Synthase Activation --- p.16 / Chapter B. --- APOPTOSIS --- p.19 / Chapter 1. --- MORPHOLOGICAL CHANGES --- p.19 / Chapter 2. --- BIOCHEMICAL AND MOLECULAR CHANGES --- p.20 / Chapter 3. --- APOPTOTIC MEDIATORS --- p.21 / Chapter a. --- INTERLEUKIN-1β CONVERTING ENZYME (ICE) --- p.21 / Chapter b. --- ENDONUCLEASE --- p.22 / Chapter c. --- NITRIC OXIDE SYNTHASE (NOS) --- p.23 / Chapter d. --- POLY(ADP-RIBOSE) POLYMERASE (PARP) --- p.24 / Chapter e. --- CALPAINS --- p.25 / Chapter IV. --- NMDA INDUCED APOPTOSIS IN RAT RETINA --- p.27 / Chapter A. --- RATIONALE --- p.27 / Chapter B. --- MATERIALS AND METHODS --- p.31 / Chapter 1. --- NMDA INDUCED EXCITOTOXICITY --- p.31 / Chapter a. --- INTRAVITREAL INJECTIONS --- p.31 / Chapter b. --- RETINAL GANGLION CELL COUNTS (RGCC) --- p.32 / Chapter i) --- Flat Preparation of Rat Retina --- p.33 / Chapter ii) --- RGCC --- p.33 / Chapter d. --- INNER RETINAL THICKNESS (IRT) --- p.34 / Chapter i. --- Preparation of Epoxyl Specimens --- p.34 / Chapter ii. --- Measurement of IRT --- p.36 / Chapter 2. --- DOSE RESPONSE STUDY OF NMDA --- p.36 / Chapter 3. --- NMDA INDUCED APOPTOSIS IN RAT RETINA --- p.37 / Chapter a. --- GEL ELECTROPHORESIS OF RETINAL DNA --- p.37 / Chapter b. --- HISTOPATHOLOGICAL STUDIES --- p.39 / Chapter i) --- Light Microscopy --- p.39 / Chapter ii) --- Terminal Deoxynucleotidyl Transferase-mediated dUTP-biotin Nick End Labelling (TUNEL) --- p.40 / Chapter iii) --- Electron Microscopy (EM) --- p.41 / Chapter c. --- MORPHOMETRY --- p.41 / Chapter i) --- TUNEL Positive Nuclei --- p.41 / Chapter ii) --- RGCC and IRT --- p.42 / Chapter 4. --- STUDY OF ENZYME INHIBITORS --- p.42 / Chapter C. --- RESULTS --- p.43 / Chapter 1. --- EXCITOTOXICITY IN RAT RETINA --- p.43 / Chapter a. --- RGCC --- p.43 / Chapter b. --- IRT --- p.44 / Chapter 2. --- DOSE DEPENDENT TISSUE RESPONSES AND REGIONAL RESPONSES --- p.44 / Chapter a. --- RGCC --- p.44 / Chapter b. --- IRT --- p.45 / Chapter 3. --- NMDA INDUCED APOPTOSIS IN RAT RETINA --- p.45 / Chapter a. --- RETINAL DNA GEL ELECTROPHORESIS --- p.46 / Chapter b. --- HISTOPATHOLOGY AND TUNEL --- p.46 / Chapter c. --- MORPHOMETRY OF TUNEL AT THE RGCL AND INL --- p.47 / Chapter d. --- TISSUE RESPONSES AT 7 DAYS AFTER INJECTION --- p.48 / Chapter e. --- EM --- p.48 / Chapter i) --- RGCL --- p.48 / Chapter ii) --- INL --- p.48 / Chapter 4. --- ENZYME INHIBITOR STUDY IN NMDA INDUCED EXCITOTOXICITY --- p.49 / Chapter a. --- EFFECT OF VARIOUS ENZYME INHIBITORS ON RGCC --- p.49 / Chapter b. --- EFFECT OF VARIOUS ENZYME INHIBITORS ON IRT --- p.50 / Chapter D. --- DISCUSSION --- p.51 / Chapter 1. --- NMDA INDUCED EXCITOTOXICITY IN RAT RETINA --- p.51 / Chapter 2. --- DOSE DEPENDENT RESPONSES AND REGIONAL RESPONSES --- p.55 / Chapter 3. --- NMDA INDUCED APOPTOSIS IN RAT RETINA --- p.58 / Chapter 4. --- INHIBITOR STUDY --- p.62 / Chapter a. --- ICE --- p.63 / Chapter b. --- ENDONUCLEASE --- p.65 / Chapter c. --- NOS --- p.67 / Chapter d. --- PARP --- p.69 / Chapter e. --- CALPAIN --- p.70 / Chapter V. --- NMDA INDUCED APOPTOSIS IN RABBIT RETINA --- p.72 / Chapter A. --- RATIONALE --- p.72 / Chapter B. --- MATERIALS AND METHODS --- p.73 / Chapter 1. --- INTRAVITREAL INJECTION OF NMDA --- p.73 / Chapter 2. --- HISTOPATHOLOGY AND TUNEL --- p.74 / Chapter 3. --- MORPHOMETRY OF TUNEL --- p.74 / Chapter 4. --- TISSUE RESPONSES AT 7 DAYS AFTER INJECTION --- p.74 / Chapter a. --- RGCC --- p.74 / Chapter b. --- IRT --- p.74 / Chapter 5. --- EM --- p.75 / Chapter C. --- RESULTS --- p.76 / Chapter 1. --- HISTOPATHOLOGY AND TUNEL --- p.76 / Chapter 2. --- MORPHOMETRY OF TUNEL --- p.77 / Chapter 3. --- TISSUE RESPONSES AT 7 DAYS POST INJECTION --- p.78 / Chapter a. --- RGCC --- p.78 / Chapter b. --- IRT --- p.78 / Chapter 4. --- EM --- p.79 / Chapter a. --- RGCL --- p.79 / Chapter b. --- INL --- p.79 / Chapter B. --- DISCUSSION --- p.80 / Chapter VI. --- CONCLUSION --- p.82 / Chapter VII. --- REFERENCES --- p.83 / Chapter VIII. --- FIGURES --- p.100

Thesis (Ph. D.)--University of Hong Kong, 2007. / Also available online.

Thesis (Ph. D.)--University of Hong Kong, 2007. / Title proper from title frame. Also available in printed format.

Thesis (Ph. D.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 110-132).

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

It has been known that light input can affect the emotions of a person. The depressive syndrome Seasonal Affective Disorder (SAD) is an effective example of the power of light in changing the mood of a person. Patients with SAD have recurring depressive episodes that follow seasonal changes, which is due to the changing daylight hours. This phenomenon suggests that there would be receptors in the retina that would not simply be responsible for vision, but also for the regulation of non-visual signals such as emotion. In many animals, projections have been found from the retina to the dorsal raphe nucleus (DRN). This brain region is a serotonergic area and has been found to be involved in the occurrence of depression. As such, the cells in the retina which were found to have projections to the DRN have a high possibility to be involved in emotion regulation. Retinal Ganglion Cells (RGCs) are classified into many types. A specific type known as an alpha cell is suspected to be the DRN-projecting subtype. This study uses Lycium Barbarum Polysaccharide (LBP) as a treatment in protecting the large RGCs from corticosterone (CORT) -induced damage. The aim is to observe if LBP will provide neuroprotection to large sized RGCs damaged by 40mg/kg or 50mg/kg CORT, and hence if LBP can be further investigated as a possible anti-depressant drug. This study observed that although LBP did not reduce large cell deaths, it reduced cell atrophy of the RGCs under high dosage of CORT (50mg/kg). For the same number of cells counted, treatment groups with a high dose CORT injection found more cells over 300μm2 in area than cells under 300μm2. Also, it was found that the temporal quadrants were more sensitive to cell size change than the nasal quadrants, paving way for more in-depth research of the spatial sensitivity to CORT or to LBP. The findings in this study indicate that LBP does indeed have a neuroprotective effect on large RGCs, although this effect is limited and as of yet seems conditional, as this study ignores the effect of CORT and LBP on other large cell properties such as the dendritic field size and the amount of synapses. Further studies are needed to determine the mechanism of the neuroprotective effect of LBP and to determine the exact site of action LBP works on. / published_or_final_version / Anatomy / Master / Master of Medical Sciences

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / abstract / toc / Botany / Master / Master of Philosophy

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

Introduction: Hirschsprung’s Disease (HD) is the congenital absence of ganglion cells (GCs) within the distal intestine. Our objectives are to determine if apoptosis of myenteric GCs occurs during human development and to determine if myenteric GC apoptosis or injury contributes to HD. Materials and Methods: Apoptosis of myenteric GCs was assessed in archived fetal intestinal tissue (n = 4; 15-41 weeks gestational age) and in HD at the transition zone (TZ) (n = 6) using anti-cleaved caspase-3. Immunohistochemistry for GFAP, CD68, HLA-DR and APP was used to assess the presence of enteric reactive changes. Results: No activated caspase-3 expression was present in the myenteric GCs of the developing human intestine or the TZ of HD. No significant increase in GFAP, CD68, HLA-DR or APP expression was present. Conclusions: Apoptosis does not appear to occur during the development of the human myenteric plexus or, in conjunction with GC injury, in HD.