Thesis (M.A.)--Boston University / In spite of the rapid development of the study of plant viruses and virus diseases there is still no generally accepted definition of a virus. Cook (1946) divided the history of plant virus study into three periods. The first dated from 1576, with the first published description of a virus disease, the breaking of tulips by Carolus Clusius and ended in 1868 with a description of the variegation of Abutilon striatum Dicks..The second began in 1882 with Mayer's work on tobacco mosaic. The third started in 1906 when the study of plant viruses was really beginning. Smith (1948) suggested adding a fourth period commencing in 1935 with Stanley's crystallization of the tobacco mosaic virus as a definite entity. Since then the physicist, the biochemist, and the serologist have joined in the research. Estimates of losses due to plant virus diseases are difficult to make because of varying conditions. Bawden (1950) stated that the one thing common to all plant viruses is that they are nucleoproteins containing a ribose nucleic acid. [TRUNCATED]

Memoria para optar al Título Profesional de Médico Veterinario / El polimetilmetacrilato (PMMA) es uno de los materiales más comúnmente utilizados como barra conectora en fijadores externos en Medicina Veterinaria, la polimerización de este material es un proceso exotérmico, que puede llegar a temperaturas sobre los 100 °C. Este calor se puede transmitir a través de las agujas de fijación ósea, presentándose como un peligro para el éxito de la cirugía, ya que se sabe que la temperatura de necrosis ósea es de 56 °C. La alternativa que se propone, es el uso de la masa epóxica (MEp), la cual se polimeriza a menos de 60 °C y posee similares características biomecánicas. En éste estudio se esperaba determinar la transferencia de calor desde el polímero a la aguja de fijación ósea. Para esto se realizaron mediciones en la masa con termocuplas, y en las agujas de fijación ósea con un termómetro infrarrojo. Se pudo confirmar que, la MEp polimeriza a temperaturas significativamente menores que el PMMA. Sin embargo, el sistema de medición en las agujas de fijación no fue eficiente. A pesar de esto, si se pudo determinar que existe un efecto disipador de las agujas de mayor calibre sobre las temperaturas alcanzadas por las masas de mayor volumen y además se puede concluir que MEp es un material adecuado y más seguro para ser utilizado como barra conectora con el fin de evitar producir necrosis ósea.

Objetivo: Determinar si existe asociación entre las variables clínico laboratoriales de ingreso con la severidad de necrosis pancreática en pacientes del servicio de cirugía páncreas del HNERM en el periodo 2006- 2007. Metodología: Estudio analítico observacional de tipo transversal, se revisa la historia clínica de 67 pacientes que cumplen con los criterios de selección y según la ficha de recolección de datos clínico laboratoriales, luego se realiza el análisis estadístico con el paquete SPSS v.22.0. Y se realiza la prueba chi cuadrado de variables independientes para determinar la asociación y luego la prueba de OR para ver si constituyen un factor de riesgo o de protección estas variables Resultados: Se incluyeron 67 pacientes (M: 42, F: 25) con pancreatitis aguda grave, edad promedio de 49,87 años. La prueba chi cuadrado con un p<0.05 y con 2 grados de libertad para el análisis derrame pleural vs grado de severidad de necrosis obtuvo un valor 0 de 0,502, no fue significativo, tampoco al análisis hipoalbuminemia vs grado de severidad de necrosis, se obtuvo un valor p de 0,433, no hubo diferencia significativa. Para las variables leucocitosis (p=0.006), hiperbilirrubinemia directa p=0.004) y hematocrito (0,025) se obtuvo asociación así como OR significativo (10,125), (16,5) y (0,144) respectivamente Conclusiones: existe asociación entre la leucocitosis e hiperbilirrubinemia directa con la severidad de necrosis pancreática en pacientes del servicio de cirugía páncreas del HNERM en el periodo 2006-2007, además el nivel bajo de hematocrito constituye un factor de menor riesgo de tener IST grave. Palabras clave: derrame pleural, hipoalbuminemia, necrosis pancreática, IST, leucocitosis, hiperbilirrubinemia, hematocrito. / --- Objective: To determinate the association between the clinical laboratory variables entrance to the severity of pancreatic necrosis in patients from the pancreatic surgery HNERM in 2006-2007. Methodology: Analytical observational cross-sectional study, the medical records of 67 patients who meet the selection criteria and according to the data-gathering clinical laboratory data were reviewed, then the statistical analysis with SPSS v.22.0 package is performed. and chi square test is performed independent variables to determine the association and then test to see if OR constitute a risk factor or protective these variables Results: acute with severe pancreatitis, average age of 49.87 years 67 patients (: 42, F 25 F) were included. The chi-square test with p <0.05 and 2 degrees of freedom for analysis pleural effusion vs severity of necrosis obtained a value 0 of 0.502, was not significant, not to hypoalbuminemia analysis vs severity of necrosis was obtein ap of 0.433, no significant difference value. For leukocytosis variables (p = 0.006), direct hyperbilirubinemia p = 0.004) and hematocrit (0.025) as well as a significant association OR (10,125) it was obtained, (16.5) and (0.144), respectively Conclusions: the association between leukocytosis and direct hyperbilirubinemia with the severity of pancreatic necrosis in patients from the pancreatic surgery HNERM in 2006-2007, plus low hematocrit level is a factor less risk of grave IST. Keywords: pleural effusion, hypoalbuminemia, pancreatic necrosis, IST, leukocytosis, hyperbilirubinemia, hematocrit. / Tesis

Previous studies have suggested that T cell contact‐dependent signaling of macrophages (MΦ) is mediated by membrane tumor necrosis factor‐α (memTNF‐α), based on the observation that anti‐TNF‐α could inhibit T cell‐mediated MΦ activation. The current report confirms that anti‐TNF‐α does inhibit activation of interferon‐γ (IFN‐γ)‐primed MΦ by paraformaldehyde‐fixed activated T cells. However, the involvement of membrane molecules other than memTNF‐α in the contact‐dependent signaling is suggested by two lines of evidence. First, the TH2 clone, AK8, displayed neither secreted TNF‐α/β nor memTNF‐α/β detectable by bioassay or immunofluorescence. Nonetheless, AK8 cells were equally effective, on a per cell basis, in contact‐dependent signaling of MΦ activation as TH2 and TH1 cells which do express memTNF‐α. Second, the expression of memTNF‐α by the TH clone, D10.G4, is maximal 24 h after activation, whereas the ability of this clone to activate MΦ is maximal at 6–8 h of activation and declines thereafter. Since TNF‐α is known to play a critical role in activation of MΦ effector function, it was hypothesized that T cell membrane components other than memTNF‐α might signal MΦ production of TNF‐α, thus allowing autocrine TNF‐α stimulation of MΦ effector function. In support of this, it is demonstrated that paraformaldehyde‐fixed activated TH2 cells can induce de novo production and release of TNF‐α by MΦ. This effect was not an artifactual result of paraformaldehyde fixation since paraformaldehyde‐fixed resting T cells did not induce TNF‐α gene expression. Previous studies have demonstrated a role for autocrine TNF‐α stimulation in LPS induction of effector function in recombinant IFN‐γ‐primed MΦ. The current study confirms that TNF‐α plays a critical role in T cell contact‐dependent signaling of MΦ but indicates that memTNF on the T cells may not be a sine qua non factor for contact‐dependent signaling. The data suggest that other T cell membrane molecules contribute to activation of MΦ effector function by stimulation of MΦ TNF‐α production.

Bovine parvovirus (BPV) is a helper-independent parvovirus. It has a small icosahedral capsid with a single stranded DNA genome. It is a highly stable virus with a narrow host range. It causes acute gastroenteritis in calves. It is considered to be a cytolytic virus because it kills the host cells. However, the mechanism by which the virus causes cell death is not known. The work described in this thesis assessed different parameters of cell death in BPV infected embryonic bovine tracheal (EBTr) cells. There are several ways for viruses to induce cell death. Viruses can induce apoptosis in the infected cell. They can also kill the host cell by necrosis. Several approaches were used in this work to look for evidence of apoptosis and necrosis. Cells undergoing apoptosis exhibit cardinal signs that distinguish them from other dying cells. Among these signs are the exposure of phosphatidylserine to the outer surface of the plasma membrane, DNA fragmentation into non-random DNA sections that are multimers of 180bp, nuclear morphology changes and caspase activation. These signs were studied in this research and data collected from these experiments did not show any positive sign of apoptosis in infected cells due to virus infection. Cells undergoing a necrotic cell death have a different pattern. The cells swell then burst releasing their cytoplasmic contents. The DNA is fragmented in a random fashion. Cellular morphology was studied in this research and the data suggested that BPV infected cells swell, then shrink and detach from the surface of the culture vessel. Moreover, formation of apoptotic bodies was not detected in dying infected cells. Release of cytoplasmic contents was also assessed by looking at concentrations of LDH enzyme, viral haemagglutinin, and the number of infectious viral particles in the media of infected cells. Data from the different approaches employed in this study do not support the hypothesis that BPV kills the infected EBTr cell by apoptosis, rather, infected cells in culture become necrotic, swell, release their cytoplasmic contents, and detach.

La necrosis bacteriana de la vid, causada por la bacteria de cuarentena Xylophilus ampelinus, es una enfermedad de difícil control químico y que ha causado en España importantes pérdidas económicas. Actualmente, es endémica en distintas zonas de Aragón y Galicia y se han identificado focos aislados en La Rioja. Ante la carencia de métodos sensibles y específicos de detección de esta bacteria que se puedan utilizar para el análisis rutinario, se ha puesto a punto un método de extracción y un protocolo de detección serológica de X. ampelinus. El método de extracción se basa en el lavado interno a presión de los sarmientos a analizar. El protocolo de detección se basa en la técnica ELISA-DASI, utilizando anticuerpos monoclonales específicos. Ambos hacen posible la detección de esta bacteria de cuarentena en material vegetal durante cualquier época del año. También se ha puesto a punto la detección mediante inmunoimpresión en membrana de nitrocelulosa, que puede ser utilizada para detección rápida o para confirmación de sintomatologías dudosas. Se ha realizado una prospección en las denominaciones de origen Campo de Borja y Somontano, utilizando el lavado interno de los sarmientos y la técnica ELISA-DASI. Se detectó la bacteria en el 4'7% y 0'9% de los sarmientos analizados, siendo la primera vez que mediante dicha técnica se detecta la enfermedad en sarmientos asintomáticos y en la zona de Somontano. En la prospección se observó una distribución irregular de X. ampelinus en las cepas analizadas. La distribución de la bacteria en las plantas de una parcela naturalmente infectada fue al azar. Se realizó un estudio de sensibilidad a la necrosis bacteriana en plantas de 19 variedades españolas injertadas en los patrones Rupestris de Lot, R-110 y 41-B. Se observó que el primer patrón confería mayor sensibilidad a las variedades injertadas y que todas las variedades ensayadas se mostraron sensibles a X. ampelinus. Entre ellas, las variedades Merseguera, Palomino, Airén, Bobal, Juan Ibáñez y Granegro se comportaron como muy sensibles y Mazuela, Tinto basto y Garnacha peluda mostraron baja sensibilidad. / Cambra Alvarez, M. (1997). La necrosis bacteriana de la vid, causada por xylophilus ampelinus. Detección serológica, distribución en Aragón y sensibilidad varietal [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/10952

by Ko Samuel. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 209-227). / Abstract also in Chinese. / Acknowledgements --- p.i / Abbreviations --- p.ii / Abstract --- p.vii / Abstract in Chinese --- p.x / List of Figures --- p.xiii / List of Tables --- p.xx / Publication --- p.xxi / Contents --- p.xxii / Chapter Chapter 1. --- General Introduction --- p.1 / Chapter 1.1 --- Tumor Necrosis Factor --- p.2 / Chapter 1.1.1 --- History of Tumor Necrosis Factor --- p.2 / Chapter 1.1.2 --- TNF Subtypes and Their Purification --- p.3 / Chapter 1.1.3 --- Release of TNF --- p.9 / Chapter 1.1.4 --- Biological Actions of TNF --- p.9 / Chapter 1.2 --- Tumor Necrosis Factor Receptor --- p.11 / Chapter 1.2.1 --- Purification of TNF Receptor --- p.11 / Chapter 1.2.2 --- Regulation of TNF Receptor --- p.14 / Chapter 1.2.3 --- "Functions of TNF Receptor 1,Receptor 2 and Soluble TNF Receptors" --- p.15 / Chapter 1.3 --- Possible Signal Transductions of Tumor Necrosis Factor-Alpha --- p.17 / Chapter 1.3.1 --- Activation of Phospholipase A2 Cascade --- p.18 / Chapter 1.3.2 --- Activation of Phospho lipase C Pathway --- p.19 / Chapter 1.3.3 --- Activation of Sphingomyelin Pathway --- p.20 / Chapter 1.3.4 --- Activation of Protein Kinase --- p.22 / Chapter 1.3.5 --- Activation of the Cascade of Death Domain --- p.23 / Chapter 1.4 --- Induction of Both Necrosis and Apoptosis by Tumor Necrosis Factor-Alpha --- p.25 / Chapter 1.4.1 --- Apoptosis Versus Necrosis --- p.25 / Chapter 1.4.2 --- TNF Can Induce Both Apoptosis and Necrosis --- p.27 / Chapter 1.5 --- Possible Mechanisms of Tumor Necrosis Factor-Alpha- Mediated Cytotoxicity --- p.27 / Chapter 1.5.1 --- Release of Reactive Oxygen Species --- p.28 / Chapter 1.5.2 --- Release of Intracellular Calcium --- p.31 / Chapter 1.5.3 --- Miscellaneous Mechanisms --- p.36 / Chapter 1.6 --- Objective of Studies --- p.37 / Chapter Chapter 2. --- Materials and Methods --- p.39 / Chapter 2.1 --- Materials --- p.40 / Chapter 2.1.1 --- Buffer --- p.40 / Chapter 2.1.2 --- Culture Media --- p.45 / Chapter 2.1.3 --- Chemicals --- p.46 / Chapter 2.1.4 --- Culture of Cells --- p.49 / Chapter 2.1.4.1 --- "Tumor Necrosis Factor-Alpha-Sensitive Cell Line, L929" --- p.49 / Chapter 2.1.4.2 --- "Tumor Necrosis Factor-Alpha-Resistant Cell Line, rL929, rL929-l IE and rL929-4F" --- p.50 / Chapter 2.2 --- Methods --- p.50 / Chapter 2.2.1 --- Agarose Gel Electrophoresis --- p.50 / Chapter 2.2.2 --- Cytotoxicity Assay --- p.52 / Chapter 2.2.3 --- Confocal Laser Scanning Microscopy --- p.53 / Chapter 2.2.4 --- Flow Cytometry --- p.57 / Chapter Chapter 3. --- Results --- p.65 / Chapter 3.1 --- Induction of Apoptosis in Tumor Necrosis Factor-Alpha- Treated L929 Cell --- p.66 / Chapter 3.1.1 --- Introduction --- p.66 / Chapter 3.1.2 --- TNF Induced DNA Fragmentation in L929 Cells --- p.67 / Chapter 3.2 --- Effect of Tumor Necrosis Factor-Alpha on Cell Cycle --- p.73 / Chapter 3.2.1 --- Introduction --- p.73 / Chapter 3.2.2 --- Effect of TNF on Cell Cycle --- p.75 / Chapter 3.3 --- Release of Reactive Oxygen Species in Tumor Necrosis Factor-Alpha Treatment --- p.79 / Chapter 3.3.1 --- Introduction --- p.79 / Chapter 3.3.2 --- Release of Reactive Oxygen Species in TNF- Treated L929 Cells is Time Dependent --- p.81 / Chapter 3.3.3 --- Effect of Antioxidants on TNF-Mediated Cytotoxicity --- p.93 / Chapter 3.3.4 --- Effect of Mitochondrial Inhibitors on TNF-Mediated Cytotoxicity --- p.96 / Chapter 3.4 --- The Role of Calcium in Tumor Necrosis Factor-Alpha Treatment --- p.112 / Chapter 3.4.1 --- Introduction --- p.112 / Chapter 3.4.2 --- Release of Intracellular Calcium in TNF-Treated L929 Cells --- p.113 / Chapter 3.4.3 --- Effect of Calcium-Inducing Agents on TNF-Treated L929Cells --- p.127 / Chapter 3.5 --- Relationship between Reactive Oxygen Species and Calcium in Tumor Necrosis Factor-Alpha-Mediated Cytotoxicity --- p.133 / Chapter 3.5.1 --- Introduction --- p.133 / Chapter 3.5.2 --- Effect of Intracellular Calcium Chelator on TNF- Mediated ROS Release and Cytotoxicity --- p.133 / Chapter 3.5.3 --- Effect of Mitochondrial Calcium on TNF-Mediated ROS Release and Cytotoxicity --- p.147 / Chapter 3.6 --- Effect of Tumor Necrosis Factor-Alpha on pH --- p.162 / Chapter 3.6.1 --- Introduction --- p.162 / Chapter 3.6.2 --- Effect of TNF on pH --- p.162 / Chapter 3.7 --- Effect of Tumor Necrosis Factor-Alpha on Mitochondrial Membrane Potential --- p.165 / Chapter 3.7.1 --- Introduction --- p.165 / Chapter 3.7.2 --- Effect of TNF and Some Drugs on Mitochondrial Membrane Potential --- p.165 / Chapter 3.8 --- "Comparison of Effects of Tumor Necrosis Factor-Alpha on Susceptible Cell Line, L929 and Resistant Cell Line, rL929, rL929-11E and rL929-4F" --- p.169 / Chapter 3.8.1 --- Introduction --- p.169 / Chapter 3.8.2 --- Effect of TNF on the Cytotoxicity of Resistant Cell Lines --- p.170 / Chapter 3.8.3 --- Effect of TNF on the Release of ROS in Resistant Cell Lines --- p.170 / Chapter 3.8.4 --- Effect of TNF on the Release of Calcium in Resistant Cell Lines --- p.178 / Chapter 3.8.5 --- Effect of TNF on Cell Cycle in Resistant Cell Lines --- p.185 / Chapter Chapter 4. --- General Discussion --- p.187 / Chapter 4.1 --- Tumor Necrosis Factor Induced Apoptosis in L929 Cells --- p.188 / Chapter 4.2 --- Tumor Necrosis Factor Increased the Release of Reactive Oxygen Species in L929 Cells --- p.189 / Chapter 4.3 --- Tumor Necrosis Factor Increased the Release of Calcium in L929 Cells --- p.194 / Chapter 4.4 --- Calcium Induced Reactive Oxygen Species Release in TNF- Treated L929 Cells --- p.197 / Chapter 4.5 --- Tumor Necrosis Factor Did Not Change the pH and Mitochondrial Membrane Potential in TNF-Treated L929 Cells --- p.198 / Chapter 4.6 --- Tumor Necrosis Factor Did Not Increase the Release of Reactive Oxygen Species or Calcium in Resistant Cell Lines --- p.201 / Chapter Chapter 5. --- Future Perspective --- p.204 / Chapter 5.1 --- The Relationship Between Tumor Necrosis Factor and Cytochrome c --- p.205 / Chapter 5.2 --- The Relationship Between Tumor Necrosis Factor and Mitochondrial DNA Damage --- p.206 / Chapter 5.3 --- Clinical studies with Tumor Necrosis Factor --- p.206 / References --- p.208

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published_or_final_version / Physiology / Master / Master of Philosophy

published_or_final_version / abstract / Pathology / Doctoral / Doctor of Philosophy