544 resultados para Perforación aórtica tardía
Resumo:
La lesión traumática de la aorta descendente, causada por el extremo filoso de una fractura costal izquierda, es una inusual, y altamente mortal, complicación del trauma torácico cerrado. En este artículo se presenta el caso de una paciente adulta, hospitalizada por trauma torácico cerrado, que fallece repentinamente luego de un cambio postural días después de la admisión. En la autopsia se evidenciaron perforaciones aórticas coincidentes con segmentos de fracturas de los arcos costales posteriores izquierdos 5 y 7. El estudio histopatológico mostró que las lesiones estaban en proceso de reparación. Este caso demuestra que ante una muerte inesperada asociada a trauma torácico con fracturas costales es fundamental la realización de una autopsia médico-legal a fin de reconocer las perforaciones tardías de la aorta torácica.
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En la localidad de Posoltega, Nicaragua se realizó un estudio sobre la competencia de malezas en el cultivo de Soya (Glyxine max L.) sembrado en fecha tardía después del 15 de Agosto con el objetivo de conocer el comportamiento de las malezas y su efecto sobre el desarrollo y rendimiento del cultivo de soya en esa época del año. El experimento se estableción en el Centro Experimental del Algodón en un diseño de Bloques completos el Azar con diez tratamientos y cuatro repeticiones y se sembró la variedad “Cristalina”. Durante el estudio se presentaron especies como kallstroamia máxima, Portulaco oleracese, Euporbia hetterophylla Denmodium canun Cyperus rotundus, Sorghum hapalense entre otros siendo las especies de hoja ancha las más prediminantes. Respecto al desarrollo y rendimiento de la soya estos fueron afectados sensiblemente por el fotoperiodo, además que la competencia de malezas redujo los rendimientos hasta en un 65.8 % para los tratamientos que sufrieron mayor tiempo de enmalezamiento. Finalmente, se recomienda mantener el cultivo limpio en sus primeras fases de desarrollo y repetir el ensayo evaluando el efecto retardado de las malezas.
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Resumen: Se estudia, en adultos de ambos sexos, la asociación entre la depresión y la presencia simultánea de calcificación en las arterias coronarias y la raíz aórtica por un lado, y entre la depresión y la presencia de calcificación coronaria, por otro lado. Estudio transversal. Participaron mayores de 21 años, asintomáticos, sin antecedentes coronarios, que se realizaron una angiotomografía cardíaca por indicación del médico tratante y que fueron evaluados para la depresión. La presencia de calcificación se evaluó mediante angiotomografía cardíaca. La depresión se evaluó mediante un test psicológico. Resultados: 60 adultos, 30 hombres y 30 mujeres, media de 51 ± 5 años. Encontramos una asociación de mayor fortaleza entre la depresión y la calcificación en dos ubicaciones (calcificación coronaria y aórtica) que en un solo lugar (calcificación coronaria). Las personas con calcificación coronaria y aórtica puntuaron más alto en las pruebas de depresión que las personas con calcificación coronaria únicamente. El presente estudio tiene limitaciones debido al tamaño de la muestra y el diseño utilizado. Sin embargo, los resultados sugieren que podría ser interesante estudiar una muestra más grande, con un diseño prospectivo, teniendo en cuenta otras variables intervinientes. Los resultados del presente trabajo confirmaron la presencia simultánea de la depresión y las lesiones ateroscleróticas. Se sugieren dos preguntas: si el tratamiento de la depresión podría modificar el proceso de evolución de las lesiones, y viceversa, y si una intervención terapéutica en ambos (enfermedad aterosclerótica y la depresión), sería más acertada que sólo realizar el tratamiento de la enfermedad aterosclerótica.
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Integran este número de la revista ponencias presentadas en Studia Hispanica Medievalia VIII: Actas de las IX Jornadas Internacionales de Literatura Española Medieval, 2008, y de Homenaje al Quinto Centenario de Amadis de Gaula.
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[ES] Este trabajo ofrece una introducción a uno de los más ricos epistolarios latinos conservados de la Antigüedad. San Jerónimo revitaliza el género epistolar en poco más de 150 cartas, algunas de ellas muy extensas, escritas entre los años 374 y 419/20 d.C., con una constante y abierta predilección por un despliegue de su profunda formación intelectual y exegética.
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414 p.: graf.
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A menopausa e a hipertensão podem alterar o remodelamento cardiovascular, porém pouco se sabe sobre sua associação no remodelamento ventricular esquerdo e na aorta. As ratas foram separadas em quatro grupos com seis animais cada: grupo Sham, OVX (ratas ooforectomizadas), 2K1C (ratas com dois rins, um clipe), e grupo 2K1C+OVX com período experimental de 11 semanas. O ventrículo esquerdo (VE) e a aorta torácica foram removidos e analisados (microscopia de luz, imuno-histoquímica e estereologia). A citologia vaginal mostrou que os animais dos grupos Sham e 2K1C ciclaram normalmente, entretanto, os animais dos grupos OVX e OVK+2K1C permaneceram na fase do diestro ou proestro. Comparado ao grupo Sham, a pressão arterial aumentou 12% no grupo OVX e 35% maior nos grupos 2K1C e OVX+2K1C. A relação massa do VE/comprimento da tíbia e a área seccional média de cardiomiócitos aumentaram em todos os grupos com exceção do grupo Sham. A vascularização intramiocárdica foi reduzida cerca de 30% em relação ao grupo Sham, não havendo diferença significativa entre os grupos OVX, 2K1C e OVX+2K1C. O tecido conjuntivo cardíaco teve um aumento superior a 45% nos grupos 2K1C e OVX+2K1C comparados ao grupo Sham, sem diferença entre o os animais do grupo Sham e OVX. O número de núcleos de cardiomiócitos do VE foi gradualmente menor nos grupos OVX, 2K1C e OVX+2K1C, sem diferença entre os dois últimos grupos. Imuno-histoquímica positiva para receptor AT1 da Ang II nas células musculares lisas da túnica média da aorta foi observado em todos os grupos. Estes resultados indicam que a ooforectomia e a hipertensão renovascular agem aumentando a pressão arterial independentemente, com conseqüente remodelamento cardíaco adverso, com estímulo maior da hipertensão renovascular que da menopausa induzida cirurgicamente.
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Temperature effect on the pathogenicity of selected Edwardsiella tarda V-1 strain to Japanese eel, Anguilla japonica was investigated. To evaluate the effects of both pathogen incubation temperature and fish cultivation temperature on pathogen pathogenicity a two-factor design was conducted. E. tarda was incubated at 15, 20, 25, 30 and 37±1°C, and the fish (mean weight: 100g) were reared at 15, 20, 25 and 28±1°C respectively. The fish reared at different temperatures were infected with the E. tarda incubated at different temperatures. The results of a 4-day LD50 test showed that temperature significantly affected the pathogenicity of E. tarda (p<0.01) and the interaction between the two factors was also significant (p<0.01). For fish reared at 20°C the pathogenicity of E. tarda was the highest at 30°C of pathogen incubation. When the fish rearing temperature was raised to 25 and 28°C, the pathogenicity of E. tarda incubated at all temperatures increased. Isolation testing demonstrated results similar to those of LD50. The selected isolate was virulent to eel, but pathogenicity varied with temperature.
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The occurrence of diseases is a significant setback for successful aquafarming. One of the common fish bacterial disease syndromes, Edwardsiellosis is caused by Edwardsiella tarda, a gram-negative, rod shaped bacterium associated with several diseases of marine and fresh water fish. In this study, an attempt was made to observe and analyze the onset of clinical symptoms and certain haematological parameters in Koi Carp, Cyprinus carpio L., following artificial infection with Edwardsiella tarda. The disease progress was observed and the clinical symptoms were monitored over a period of 15 days following infection. Fish were sampled at three day intervals to analyse the haematological parameters: total erythrocyte counts (RBC), total leucocyte counts (WBC), haemoglobin content and differential leucocyte count. Clinical symptoms observed included: erratic swimming behaviour, loss of appetite, haemorrhages, dropsy and exophthalmia. There was a significant decrease in the total RBC and haemoglobin levels by the 3rd and 6th day post infection, and an increase thereafter. WBC counts were higher in all infected groups in comparison to the control group. A significant increase in the number of neutrophils was found in the infected group up to the 9th day and a decrease thereafter. The lymphocyte number was significantly less up to the 12th day while the monocyte counts were significantly higher up to the 12th day post infection. The results showed that the bacterium, E. tarda, is pathogenic to Koi Carp. The hematological changes and clinical signs in infected fish reported in this paper will be helpful in the identification and the control of this infection.
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Aim: To investigate the effect of copper on the virulence of Edwardsiella tarda. Methods and Results: The pathogenic Edw. tarda strain TX5 was cultured under copper-stressed conditions and examined for any potential alteration in capacities that are associated with pathogenicity. The results showed that compared to untreated TX5, Cu-treated TX5 exhibits reduced planktonic and biofilm growth, an impaired ability to adhere to host mucus, modulation of host immune response, and dissemination in host blood and liver. Consistent with these observations, the overall bacterial virulence of Cu-treated TX5 is significantly attenuated. SDS-PAGE analyses of whole cell protein production showed that Cu-treated TX5 differs from the untreated TX5 in its production of at least one protein. Quantitative real time reverse transcriptase PCR analyses showed that copper treatment decreased the expression of virulence-associated genes encoding components of the type III and type VI secretion systems, the Eth haemolysin system, and the LuxS/AI-2 quorum-sensing system. Conclusions: Prolonged exposure to copper has multiple effects on TX5 and results in significant attenuation of bacterial virulence. Significance and Impact of the Study: The results of this study demonstrate that copper treatment has a broad and profound effect on the virulence-associated capacities of TX5, which is exerted at least in part at the transcription level. These findings provide new insights to the antimicrobial mechanism of copper.
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Edwardsiella tarda is an important Gram-negative enteric pathogen affecting both animals and humans. It possesses a type III secretion system (T3SS) essential for pathogenesis. EseB, EseC and EseD have been shown to form a translocon complex after secretion, while EscC functions as a T3SS chaperone for EseB and EseD. In this paper we identify EscA, a protein required for accumulation and proper secretion of another translocon component, EseC. The escA gene is located upstream of eseC and the EscA protein has the characteristics of T3SS chaperones. Cell fractionation experiments indicated that EscA is located in the cytoplasm and on the cytoplasmic membrane. Mutation with in-frame deletion of escA greatly decreased the secretion of EseC, while complementation of escA restored the wild-type secretion phenotype. The stabilization and accumulation of EseC in the cytoplasm were also affected in the absence of EscA. Mutation of escA did not affect the transcription of eseC but reduced the accumulation level of EseC as measured by using an EseC-LacZ fusion protein in Ed. tarda. Co-purification and co-immunoprecipitation studies demonstrated a specific interaction between EscA and EseC. Further analysis showed that residues 31-137 of EseC are required for EseC-EscA interaction, Mutation of EseC residues 31-137 reduced the secretion and accumulation of EseC in Ed. tarda. Finally, infection experiments showed that mutations of EscA and residues 31-137 of EseC increased the LD50 by approximately 10-fold in blue gourami fish. These results indicated that EscA functions as a specific chaperone for EseC and contributes to the virulence of Ed. tarda.
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Edwardsiella tarda is a gram-negative pathogen with a broad host range that includes humans, animals, and fish. Recent studies have shown that the LuxS/autoinducer type 2 (AI-2) quorum sensing system is involved in the virulence of E. tarda. In the present study, it was found that the E. tarda LuxS mutants bearing deletions of the catalytic site (C site) and the tyrosine kinase phosphorylation site, respectively, are functionally inactive and that these dysfunctional mutants can interfere with the activity of the wild-type LuxS. Two small peptides, 5411 and 5906, which share sequence identities with the C site of LuxS, were identified. 5411 and 5906 proved to be inhibitors of AI-2 activity and could vitiate the infectivity of the pathogenic E. tarda strain TX1. The inhibitory effect of 5411 and 5906 on AI-2 activity is exerted on LuxS, with which these peptides specifically interact. The expression of 5411 and 5906 in TX1 has multiple effects (altering biofilm production and the expression of certain virulence-associated genes), which are similar to those caused by interruption of luxS expression. Further study found that it is very likely that 5411 and 5906 can be released from the strains expressing them and, should TX1 be in the vicinity, captured by TX1. Based on this observation, a constitutive 5411 producer (Pseudomonas sp. strain FP3/pT5411) was constructed in the form of a fish commensal isolate that expresses 5411 from a plasmid source. The presence of FP3/pT5411 in fish attenuates the virulence of TX1. Finally, it was demonstrated that fish expressing 5411 directly from tissues exhibit enhanced resistance against TX1 infection.
Resumo:
Edwardsiella tarda is a gram-negative pathogen with a broad host range that includes humans, animals, and fish. Recent studies have shown that the LuxS/autoinducer type 2 (AI-2) quorum sensing system is involved in the virulence of E. tarda. In the present study, it was found that the E. tarda LuxS mutants bearing deletions of the catalytic site (C site) and the tyrosine kinase phosphorylation site, respectively, are functionally inactive and that these dysfunctional mutants can interfere with the activity of the wild-type LuxS. Two small peptides, 5411 and 5906, which share sequence identities with the C site of LuxS, were identified. 5411 and 5906 proved to be inhibitors of AI-2 activity and could vitiate the infectivity of the pathogenic E. tarda strain TX1. The inhibitory effect of 5411 and 5906 on AI-2 activity is exerted on LuxS, with which these peptides specifically interact. The expression of 5411 and 5906 in TX1 has multiple effects (altering biofilm production and the expression of certain virulence-associated genes), which are similar to those caused by interruption of luxS expression. Further study found that it is very likely that 5411 and 5906 can be released from the strains expressing them and, should TX1 be in the vicinity, captured by TX1. Based on this observation, a constitutive 5411 producer (Pseudomonas sp. strain FP3/pT5411) was constructed in the form of a fish commensal isolate that expresses 5411 from a plasmid source. The presence of FP3/pT5411 in fish attenuates the virulence of TX1. Finally, it was demonstrated that fish expressing 5411 directly from tissues exhibit enhanced resistance against TX1 infection.
Regulation of autoinducer 2 production and luxS expression in a pathogenic Edwardsiella tarda strain
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Edwardsiella tarda is a bacterial pathogen that can infect both humans and animals. TX1, an Ed. tarda strain isolated from diseased fish, was found to produce autoinducer 2 (Al-2)-like activity that was growth phase dependent and modulated by growth conditions. The gene coding for the Al-2 synthase was cloned from TX1 and designated luxS(Et). LuxS(Et) was able to complement the Al-2 mutant phenotype of Escherichia coli strain DH5 alpha. Expression Of luxS(Et) correlated with Al-2 activity and was increased by glucose and decreased by elevated temperature. The effect of glucose was shown to be mediated through the cAMP-CRP complex, which repressed luxS(Et) expression. Overexpression of luxS(Et) enhanced Al-2 activity in TX1, whereas disruption of luxS(Et) expression by antisense RNA interference (i) reduced the level of Al-2 activity, (ii) impaired bacterial growth under various conditions, (iii) weakened the expression of genes associated with the type III secretion system and biofilm formation, and (iv) attenuated bacterial virulence. Addition of exogenous Al-2 was able to complement the deficiencies in the expression of TTSS genes and biofilm production but failed to rescue the growth defects. Our results (i) demonstrated that the Al-2 activity in TX1 is controlled at least in part at the level of luxS(Et) expression, which in turn is regulated by growth conditions, and that the temporal expression of luxS(Et) is essential for optimal bacterial infection and survival; and (ii) suggested the existence in Ed. tarda of a LuxS/Al-2-mediated signal transduction pathway that regulates the production of virulence-associated elements.