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Trabajo de Investigación Requisito para optar al Título de Cirujano Dentista / Autor no autoriza el acceso a texto completo de su tesis en el Portal de Tesis Electrónicas / Introducción: La Periodontitis Apical Asintomática (PAA) corresponde a una patología inflamatoria causada por microorganismos que invaden los canales radiculares del diente. Se caracteriza por la destrucción de los tejidos periapicales en presencia de varios mediadores inflamatorios. La metaloproteinasa de matriz extracelular-12 (MMP-12), expresada en varias patologías inflamatorias crónicas, tiene la capacidad de degradar varios componentes de la matriz extracelular (MEC) tales como elastina, fibronectina y colágeno. También es capaz de activar a otras MMPs con actividad gelatinasa y colagenasa, y dada su función, podría estar involucrada en la patogénesis de la PAA. El objetivo de nuestro trabajo fue determinar la localización tisular de MMP-12 en biopsias de quistes radiculares inflamatorios (QRI), granulomas periapicales (GPA) y en tejido periapical sano You are using demo version Please purchase full version from www.technocomsolutions.com Materiales y Métodos: En este estudio descriptivo se incluyeron 10 sujetos con diagnóstico clínico de PAA e indicación de extracción y 5 sujetos con diagnóstico clínico de Ligamento Periodontal Sano (LS) e indicación de extracción por ortodoncia, con diagnóstico anátomo-patológico de GPA (n=5), QRI (n=5) y LS (n=5). Posteriormente se analizó la inmunolocalización de la MMP-12 mediante inmunohistoquímica para su posterior observación por microscopía óptica. Resultados: De un total de 15 muestras, la MMP-12 se detectó en los 5 QRI y 5 GPA estudiados, mientras que no se detectó en las muestras de LS. En ambos tipos de lesiones periapicales, MMP-12 fue inmunolocalizada principalmente en el infiltrado inflamatorio. En GPA, se observó inmunopositividad en células compatibles con macrófagos, mastocitos, y plasmocitos; mientras que en QRI, MMP-12 se inmunolocalizó en el revestimiento epitelial e infiltrado inflamatorio, particularmente en plasmocitos. Conclusiones: MMP-12 se inmunolocaliza en el infiltrado inflamatorio de GPA y QRI, mientras que no se identificó en LS y por tanto, podría estar involucrada en la patogénesis de la PAA en asociación con el proceso inflamatorio periapical.

MSc (Med), University of the Witwatersrand, Faculty of Health Sciences / Background: Males have a higher prevalence of cardiovascular diseases compared to premenopausal women. However, postmenopausal women are at equal risk to men. It has therefore been suggested that estrogen is cardioprotective. Although the exact mechanisms of the purported cardioprotective effects of estrogen are unknown, estrogen administration has been reported to suppress beta-adrenergic receptor up-regulation in ovariectomized female rats. As beta-adrenergic activation induces cardiomyocyte apoptosis and necrosis, and hence adverse cardiac remodelling and heart failure, I aimed to determine whether the extent of beta-adrenergic induced apoptosis and necrosis differs between males and females. Methods: 27 male Wistar rats were assigned to one of two groups: ISO M (n=14) receiving a beta-adrenergic receptor agonist, isoproterenol (0.02mg/kg) and CON M (n=13) receiving vehicle (saline, 0.2ml). 29 female Wistar rats were assigned to one of two groups: ISO F (n=15) receiving a beta-adrenergic receptor agonist, isoproterenol (0.02mg/kg) and CON F (n=14) receiving vehicle. Isoproterenol and saline were administered by means of daily subcutaneous injections for 5 days. On the 5th day, cardiac geometry and function were assessed before and after ISO or saline administration using echocardiography. Rats were then terminated under anaesthesia within 30 minutes of ISO (or vehicle) administration and blood samples collected for the determination of serum estrogen concentration (ELISA). Female rats were terminated in proestrus which corresponds to peak estrogen concentrations. Cardiac myocyte apoptosis was assessed histologically using the DeadEndTM Colorimetric TUNEL system (Promega, Madison, WI, USA). The number of apoptotic cardiomyocyte nuclei was expressed as a percentage of the total number of cardiomyocyte nuclei per slide (heamotoxylin and eosin stain). Necrosis and fibrosis (pathological score) were assessed by assigning a pathological score to sections stained for fibrosis (van Gieson). Groups were iii compared using two-way (gender and regimen; and including repeated measures for echocardiography data) ANOVA followed by the Tukey-Kramer post hoc test. Results: As expected estrogen concentrations were higher in female compared to male rats (mean±SEM, pg.ml-1; ISO M: 7.04±1.41; CON M: 7.14±0.53; ISO F: 23.00±3.47; CON F: 19.31±3.66; p<0.01). Five days of ISO or saline administration had no effect on cardiac function or geometry in either the male or the female rats. Inotropic effects (increased heart rate and cardiac function) were observed in response to acute ISO administration in both male and female rats. The female rats had slower heart rates (p<0.05) and showed a greater heart rate response to acute ISO administration than the male rats (p<0.05). But the acute ISO induced increments in cardiac function were similar between genders. Five days of ISO administration induced cardiomyocyte apoptosis in male rats but not in female rats (mean±SEM, % ; ISO M: 0.086±0.013; CON M: 0.030±0.004; ISO F: 0.053±0.004; CON F: 0.041±0.007; p<0.05). Furthermore, 5 days of ISO administration induced cardiomyocyte necrosis in male rats but not in female rats (mean±SEM, pathological score; ISO M: 1.21±0.21, CON M: 0.46±0.14, ISO F: 0.50±0.11, CON F: 0.68±0.12, p<0.01). Conclusion: Male rats are more susceptible than female rats to beta-adrenergic induced cardiomyocyte apoptosis and necrosis. The protective effects of estrogen against the adverse effects of beta-adrenergic activation on the heart, may explain the lower risk of cardiovascular disease in premenopausal women compare to men; however, the possible role of progesterone cannot be ignored.

University of Macau / Institute of Chinese Medical Sciences

Entre los receptores de muerte celular, se describe al receptor Fas en células linfoides como un receptor que activa tanto apoptosis como necrosis. Recientemente se ha asociado la inducción de apoptosis con la salida de ATP vía hemicanales formados por panexina-1 en linfocitos. Por otra parte, muchas evidencias señalan al ATP extracelular como mediador de muerte celular, tanto por necrosis como por apoptosis, identificándose al receptor purinérgico P2X7 como receptor de muerte, el que tiene como único ligando biológico al ATP. En este contexto, en esta Tesis, se determinó que las células A20 (derivadas de linfocitos B de ratón) y Jurkat (derivadas de linfocitos T humanos), pero no Ramos, Raji (derivadas de linfocitos B humanos) y A20R (derivadas de linfocitos B de ratón) son sensibles a FasL. En células Jurkat el tipo de muerte celular que predominó fue la apoptosis, en cambio en A20 fue la necrosis. Solo las células Jurkat liberaron ATP en forma significativa de manera tiempo dependiente en respuesta a estimulación con FasL y no se obtuvo evidencia de daño en la membrana plasmática. En estas células la liberación de ATP fue inhibida por zVAD (inhibidor general de caspasas) y z-IETD (inhibidor de caspasa 8), pero no por zDEVD (inhibidor de caspasa 3). Además, la pre-incubación con inhibidores de hemicanales formados por panexinas (carbenoxolona y probenecid), pero no de hemicanales formados por conexinas (heptanol) también inhibió la liberación de ATP en respuesta a FasL. Por otra parte, en las células Jurkat los inhibidores de los receptores P2X7, oATP y BBG, inhibieron la muerte celular por apoptosis, en cambio los inhibidores de esfingomielinasas (miriocina, imipramina y GW4869) no protegieron a estas células al estimularlas con FasL. En células A20, oATP y el inhibidor de esfingomielinasa neutra (GW4869) mostraron un efecto protector al inhibir la muerte por necrosis inducida por FasL. Además, se apreció un efecto protector en la muerte por apoptosis al pre-tratar estas células con suramina. En ambos tipos celulares el tratamiento con N-acetilcisteína bloqueó la generación de especies reactivas de oxígeno (ROS) inducidas por FasL. Estos resultados representan la primera evidencia de que se produce una cooperación entre dos receptores de muerte celular, Fas y P2X7, en la ejecución de la muerte celular en células linfoides. Frente al mismo estímulo en células A20 y Jurkat, el tipo de muerte celular y los mecanismos involucrados son en parte distintos. En células A20, FasL gatilla muerte celular por necrosis, que podría involucrar la participación de otros receptores P2X distintos a P2X7. En cambio, en las células Jurkat la activación del receptor Fas por FasL lleva, por una parte a la activación de caspasa-8 y posteriormente, a la activación de la caspasa-3. Por otro lado, la liberación de ATP activada por caspasa-8 sería mediada por hemicanales formados por panexina-1. Esto a su vez llevaría a la activación del receptor P2X7, que gatillaría la muerte celular por apoptosis en un mecanismo que podría involucrar la participación de ROS. Esto es un hallazgo importante, ya que en las células Jurkat, que son células tipo II, además de tBID, liberan ATP vía hemicanales formados por panexina-1 lo que también contribuiría a la amplificación de la vía intrínseca de la apoptosis mediante la activación del receptor P2X7.

by Chun-kwok Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1990. / Bibliography: leaves 181-196. / ABSTRACT --- p.i / ACKNOWLEDGEMENTS --- p.iii / ABBREVIATIONS --- p.iv / CHAPTER / Chapter 1. --- INTRODUCTION : An overview of Tumor Necrosis Factor ( TNF) / Chapter 1. --- The discovery of tumor necrosis factor (TNF) --- p.1 / Chapter 2. --- Production of tumor necrosis factor --- p.3 / Chapter 3. --- Physiochemical properties of TNF --- p.5 / Chapter 4. --- Biological activities of TNF on various cells in the mammal --- p.8 / Chapter 5. --- Mechanisms of anti-tumor action of TNF --- p.12 / Chapter 6. --- Clinical studies of Hr-TNF --- p.19 / Chapter 2. --- AIM OF INVESTIGATION --- p.23 / Chapter 3. --- MATERIALS AND METHODS / Chapter A. --- MATERIALS --- p.26 / Chapter B. --- METHODS / Chapter 1. --- Preparation of Reagents --- p.30 / Chapter 2. --- Cell Culture --- p.31 / Chapter 3. --- Lymphocytes proliferation --- p.32 / Chapter 4. --- In vitro production of tumor necrosis factor (TNF) by peritoneal macrophages of ICR mice --- p.33 / Chapter 5. --- Production of TNF in animals --- p.34 / Chapter 6. --- Determination of TNF titre --- p.35 / Chapter 7. --- Determination of TNF containing serum titre on EAT in vitro --- p.35 / Chapter 8. --- Mortality determination of mice --- p.36 / Chapter 9. --- "3H-Thymidine, 3H-uridine, 14C-leucine incorporation" --- p.36 / Chapter 10. --- Glucose uptake determination --- p.37 / Chapter 11. --- Whole body hyperthermic treatment of EAT bearing mice --- p.37 / Chapter 12. --- Lipolysis assay --- p.38 / Chapter 13. --- Statistical analysis --- p.39 / Chapter 4. --- IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR USING ZYMOSAN AND LIPOPOLYSACCHARIDE / INTRODUCTION --- p.40 / EXPERIMENTAL --- p.43 / RESULTS --- p.45 / DISCUSSION --- p.65 / Chapter 5. --- SIDE EFFECTS DURING IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR IN EHRLICH ASCITES TUMOR BEARING MICE / INTRODUCTION --- p.70 / EXPERIMENTAL --- p.72 / RESULTS --- p.74 / DISCUSSION --- p.93 / Chapter 6. --- MODIFIED PROCEDURE FOR THE IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR FOR THE TREATMENT OF EHRLICH ASCITES TUMOR BEARING MICE / INTRODUCTION --- p.98 / EXPERIMENTAL --- p.99 / RESULTS --- p.100 / DISCUSSION --- p.108 / Chapter 7. --- "COMBINED TREATMENTS OF IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR (TNF) WITH HYPERTHERMIA, METHOTREXATE (MTX), POLYRIBOINOSINIC-POLYRIBOCYTIDYLIC ACID (POLY I.C), N-(PHOSPHONACETYL)-L-ASPARTATE (PALA) ON EAT BEARING MICE" / INTRODUCTION --- p.111 / EXPERIMENTAL --- p.116 / RESULTS --- p.118 / DISCUSSION --- p.133 / Chapter 8. --- EFFECTS OF IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR ON EHRLICH ASCITES TUMOR CELLS CYTOTOXICITY / INTRODUCTION --- p.138 / EXPERIMENTAL --- p.140 / RESULTS --- p.142 / DISCUSSION --- p.151 / Chapter 9. --- SIDE EFFECTS OF TUMOR NECROSIS FACTOR AND LIPOPOLYSACCHARIDE ON RAT IN VITRO AND IN VIVO / INTRODUCTION --- p.154 / EXPERIMENTAL --- p.157 / RESULTS --- p.159 / DISCUSSION --- p.170 / Chapter 10. --- CONCLUSION AND OUTLOOK --- p.174 / BIBLIOGRAPHY --- p.181

by Chung-Pui Cheng. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1987. / Bibliography: leaves 142-163.

Wong, Chi Bun. / Thesis submitted in: Nov 2006. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 116-127). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / 摘要 --- p.v / Abbreviations --- p.vii / List of Table and Figures --- p.ix / Table of Contents --- p.x / Chapter Chapter 1 --- p.1 / Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- Identification of the proteins regulated by BRE when BRE was over-expressed or silencedin C2C12 and D122 --- p.1 / Chapter 1.1.1 --- What is BRE? --- p.1 / Chapter 1.1.2 --- BRE gene is Highly Conserved --- p.2 / Chapter 1.1.3 --- BRE binds to the Intracellular Domain of TNFR1 and Fas --- p.3 / Chapter 1.1.4 --- BRE Suppresses Apoptosis --- p.4 / Chapter 1.1.5 --- "BRE forms a Holoenzyme Complex with BRCA1, BARD1 and BRCC36" --- p.4 / Chapter 1.16 --- Roles of the Differentially Expressed Proteins Identified in the siRNA knockdown Experiments --- p.5 / Chapter 1.1.6.1 --- Akt3 --- p.5 / Chapter 1.1.6.2 --- Mdm2/4 --- p.6 / Chapter 1.1.6.3 --- Prohibitin --- p.7 / Chapter 1.1.6.4 --- Carbonic Anhydrase III --- p.8 / Chapter 1.1.6.5 --- 26S Proteasome --- p.8 / Chapter 1.2 --- The Role of BRE in Liver: a morphological approach --- p.9 / Chapter 1.2.1 --- The General Structure of the Liver. --- p.9 / Chapter 1.2.2 --- The Essential Functions of the Liver --- p.11 / Chapter 1.2.3 --- Inflammation of the Liver --- p.11 / Chapter 1.2.3.1 --- Hepatitis --- p.11 / Chapter 1.2.3.2 --- Acute Hepatitis --- p.12 / Chapter 1.2.3.3 --- Chronic Hepatitis --- p.12 / Chapter 1.2.4 --- Necrosis and Apoptosis --- p.13 / Chapter 1.2.5 --- The Apoptotic Pathway --- p.14 / Chapter 1.2.6 --- Hepatic Necrosis is Divided into Different Zones --- p.16 / Chapter 1.2.6.1 --- Hepatitis Necrosis is Categorized into 3 Zones --- p.16 / Chapter 1.2.7 --- Carbon Tetrachloride (CCL4) --- p.16 / Chapter 1.2.8 --- TNFa is a Pleiotropic Cytokine --- p.17 / Chapter 1.3 --- The Objectives of This Project --- p.20 / Chapter Chapter 2 --- p.21 / Chapter 2. --- Materials and Methods --- p.21 / Chapter 2.1 --- Animals --- p.21 / Chapter 2.2 --- Adminstration of Carbon Tetrachloride and Corn Oil --- p.21 / Chapter 2.3 --- Cell Cultures --- p.22 / Chapter 2.4 --- Cell Culturing --- p.22 / Chapter 2.5 --- Gene Silencing with Small Interfering RNA (siRNA) --- p.23 / Chapter 2.5.1 --- Transfection with BRE siRNA --- p.24 / Chapter 2.6 --- Cell Proliferation Assays --- p.24 / Chapter 2.7 --- In-Situ Hybridization of BRE Sense and Antisense Probes --- p.25 / Chapter 2.8 --- Immunohistological Staining --- p.26 / Chapter 2.9 --- Semi-Quantitative RT-PCR --- p.28 / Chapter 2.10 --- Comparative Proteomics --- p.29 / Chapter 2.10.1 --- Sample Preparation for Two Dimensional Gel Electrophoresis --- p.29 / Chapter 2.10.2 --- Two Dimensional Polyacrylamide Gel Electrophoresis --- p.30 / Chapter 2.10.3 --- In-Gel Digestion and MALDI-TOF Analysis --- p.31 / Chapter 2.11 --- Western Blotting --- p.32 / Chapter 2.12 --- Flow Cytometry --- p.34 / Chapter 2.13 --- Haematoxylin and Eosin Staining (H&E) --- p.34 / Chapter Chapter 3 --- p.36 / Chapter 3. --- Results --- p.36 / Chapter 3.1 --- BRE expression in C2C12 cells --- p.36 / Chapter 3.2 --- Comparative Proteomic Profile of BRE silenced C2C12 cells --- p.41 / Chapter 3.3 --- Effect of Silencing BRE on C2C12 cell Proliferation --- p.49 / Chapter 3.4 --- Effects of BRE over-expression in D122 cells --- p.54 / Chapter 3.5 --- BRE Expression in the Liver --- p.62 / Chapter 3.5.1 --- Histological Analysis of Liver Sections after 24 hours of CCL4 Insult --- p.62 / Chapter 3.5.2 --- BRE Expression in the Liver --- p.62 / Chapter 3.6 --- Histological Study of Liver Treated with CCL4 --- p.67 / Chapter 3.7 --- BRE Expression in Experimental Liver --- p.76 / Chapter Chapter 4 --- p.92 / Chapter 4. --- Discussion --- p.92 / Chapter 4.1 --- Expression of BRE in C2C12 --- p.92 / Chapter 4.2 --- The Regulatory Function of BRE --- p.96 / Chapter 4.3 --- The Relationship Between BRE and p53 --- p.98 / Chapter 4.4 --- The Relationship Between BRE and NFkB --- p.104 / Chapter 4.5 --- BRE Expression in Normal Control and CCL4 Treated Livers --- p.105 / Chapter 4.6 --- A Possible Explanation for the Necrosis Pattern Observed --- p.107 / Chapter 4.7 --- The Relationship Between BRE and the TNF Receptors --- p.109 / Chapter Chapter 5 --- p.112 / Chapter 5. --- Conclusion and Future Prospects --- p.112 / References --- p.116

Ko Samuel. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 230-252). / 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. / Abstracts in English and Chinese.

Thesis (Ph. D.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.