published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / Anatomy / Doctoral / Doctor of Philosophy

A practical model is proposed for predicting the detectability of targets at arbitrary locations in the visual field, in arbitrary gray-scale backgrounds, and under photopic viewing conditions. The major factors incorporated into the model include: (i) the optical point spread function of the eye, (ii) local luminance gain control (Weber's law), (iii) the sampling array of retinal ganglion cells, (iv) orientation and spatial-frequency dependent contrast masking, (iv) broadband contrast masking, (vi) and efficient response pooling. The model is tested against previously reported threshold measurements on uniform backgrounds (the ModelFest data set and data from Foley et al. 2007), and against new measurements reported here for several ModelFest targets presented on uniform, 1/f noise, and natural backgrounds, at retinal eccentricities ranging from 0 to 10 deg. Although the model has few free parameters, it is able to account quite well for all the threshold measurements. / text

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal.

Nesta pesquisa, os aspectos macroestruturais, microestruturas e histoquímicos do complexo ganglionar celíaco foram investigados em 6 cães domésticos saudáveis e 6 cães domésticos acometidos pela diabetes mellitus, com o objetivo de identificar possíveis diferenças estruturais, morfométricas e quantitativas nos neurônios ganglionares celíacos. desta forma, observamos o gânglio celíaco esquerdo originou-se junto à origem da artéria celíaca esquerda e apresentava um formato irregular, seu aspecto era nodular, caracterizando um complexo ganglionar. Em relação a histoquímica, foram encontrados neurônios NADPH-diaphorase positivos, apresentando reação visível. A positividade da reação permitiu-nos concluir que há neurônios potencialmente nitrérgicos no gânglio celíaco de animais sadios e diabéticos. No entanto, não podemos afirmar se estes neurônios são efetivamente nitrérgicos, porque exige a combinação de outras reações imunohistoquímicas. O tamanho do corpo celular do neurônio do gânglio celíaco, representado pela sua área seccional, aumentou significativamente nos animais do grupo diabético quando comparado aos do grupo controle, tendo um fator de aumento de 1,3x. O aumento na área seccional do núcleo no grupo diabético foi de 1,39x maior que no grupo controle, sendo este aumento significativo. Em termos práticos isto significa que nos animais diabéticos, o núcleo e o corpo celular neuronal aumentam em proporções muito próximas. / In this research, the macrostructural, microstructural and histochemical aspects were investigated in 6 clinacally health dogs and 6 diabetic dogs aiming to identify the possible alterations on the strucutre, morphometric and qualitative parameteres of neurons of the celiac ganglionar complex. Our observations revealed that the celiac ganglion was originated close to the origin of the celiac artery and showed a irregular aspect, being caractherized as a complex. Histochemically, neurons NADPH-diaphorase reactives were identified. This positive reaction, on both health and diabetic animals, led us to conclude this neurons were potentially nitrergic, besides, to confirm the nitrergic aspect for this neurons it is necessary to combine immunohistochemical method. Neurons celular body size of the celiac ganglion, represented by its sectional area, increased significantly, at 1.3x rate, on the diabetic animals when compared to the health animals. The increase on the nuclear sectional area of the diabetic animals were significant, at 1.39x rate larger than the other group. These results mean that on the diabetic animals, nuclear and neuronal body celular raise rate increases proportionally.

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