7 resultados para Juste peine
em Archivo Digital para la Docencia y la Investigación - Repositorio Institucional de la Universidad del País Vasco
Resumo:
Nivel educativo: Grado. Duración (en horas): Más de 50 horas
Resumo:
[ES]A lo largo de este artículo se pasan revista a cinco cuentiones que muestran la evolución de la pena de muerte en la Corona de Castilla a lo largo de la Edad Media. En primer lugar, se presta atención al paso de la ejecución privada de la justicia a la pública y en qué casos se mantuvo la venganza, aunque con la autorización judicial. En segundo lugar, se pasa revista a las formas de aplicar la pena de muerte, privilegiando los siguientes tipos: el ahorcamiento por los pies, el asaeteamiento, el empozamiento y el encubamiento. En tercer lugar, se expone el ritual de ejecución de las penas capitales desde que el reo sale de la cárcel y es conducido al cadalso, hasta que el cuerpo es sepultado o queda expuesto a perpetuidad. En cuarto lugar, se reflexiona sobre la incidencia de la rebeldía o contumacia del acusado ante los requerimientos de la justicia en la imposición de la pena de muerte. En quinto y último lugar, se analizan las circunstancias que llevaron a la Corona de Castilla, a partir del último tercio del siglo XV, a relegar la pena de muerte entre el elenco punitivo y preferir castigos que tuvieran utilidad pública.
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[ES]La pena de cárcel, como única respuesta al delito, no constituye ninguna solución para el hecho delincuencial. No es solución para la víctima porque queda en el más profundo de los desamparos. No es solución para el infractor porque la cárcel no sólo no rehabilita sino que puede generar más delincuencia, como lo acredita el alto índice de reincidencia. Finalmente, no es una solución para la Comunidad por los altos costes, no sólo penitenciarios. Sólo integrada con otras respuestas no carcelarias, la respuesta prisional permite un abordaje sensato de la delincuencia. Se aboga, por ello, por una justicia que reconozca la existencia de otras instancias reparadoras como: la mediación, el arbitraje, el diálogo víctima - agresor, etc.
Resumo:
Papillomaviruses (PVs) are widespread pathogens. However, the extent of PV infections in bats remains largely unknown. This work represents the first comprehensive study of PVs in Iberian bats. We identified four novel PVs in the mucosa of free-ranging Eptesicus serotinus (EserPV1, EserPV2, and EserPV3) and Rhinolophus ferrumequinum (RferPV1) individuals and analyzed their phylogenetic relationships within the viral family. We further assessed their prevalence in different populations of E. serotinus and its close relative E. isabellinus. Although it is frequent to read that PVs co-evolve with their host, that PVs are highly species-specific, and that PVs do not usually recombine, our results suggest otherwise. First, strict virus-host co-evolution is rejected by the existence of five, distantly related bat PV lineages and by the lack of congruence between bats and bat PVs phylogenies. Second, the ability of EserPV2 and EserPV3 to infect two different bat species (E. serotinus and E. isabellinus) argues against strict host specificity. Finally, the description of a second noncoding region in the RferPV1 genome reinforces the view of an increased susceptibility to recombination in the E2-L2 genomic region. These findings prompt the question of whether the prevailing paradigms regarding PVs evolution should be reconsidered.
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Background: Sporadic Creutzfeldt-Jakob disease (sCJD) is a rare neurodegenerative disorder in humans included in the group of Transmissible Spongiform Encephalopathies or prion diseases. The vast majority of sCJD cases are molecularly classified according to the abnormal prion protein (PrPSc) conformations along with polymorphism of codon 129 of the PRNP gene. Recently, a novel human disease, termed "protease-sensitive prionopathy", has been described. This disease shows a distinct clinical and neuropathological phenotype and it is associated to an abnormal prion protein more sensitive to protease digestion. Case presentation: We report the case of a 75-year-old-man who developed a clinical course and presented pathologic lesions compatible with sporadic Creutzfeldt-Jakob disease, and biochemical findings reminiscent of "protease-sensitive prionopathy". Neuropathological examinations revealed spongiform change mainly affecting the cerebral cortex, putamen/globus pallidus and thalamus, accompanied by mild astrocytosis and microgliosis, with slight involvement of the cerebellum. Confluent vacuoles were absent. Diffuse synaptic PrP deposits in these regions were largely removed following proteinase treatment. PrP deposition, as revealed with 3F4 and 1E4 antibodies, was markedly sensitive to pre-treatment with proteinase K. Molecular analysis of PrPSc showed an abnormal prion protein more sensitive to proteinase K digestion, with a five-band pattern of 28, 24, 21, 19, and 16 kDa, and three aglycosylated isoforms of 19, 16 and 6 kDa. This PrPSc was estimated to be 80% susceptible to digestion while the pathogenic prion protein associated with classical forms of sporadic Creutzfeldt-Jakob disease were only 2% (type VV2) and 23% (type MM1) susceptible. No mutations in the PRNP gene were found and genotype for codon 129 was heterozygous methionine/valine. Conclusions: A novel form of human disease with abnormal prion protein sensitive to protease and MV at codon 129 was described. Although clinical signs were compatible with sporadic Creutzfeldt-Jakob disease, the molecular subtype with the abnormal prion protein isoforms showing enhanced protease sensitivity was reminiscent of the "protease-sensitive prionopathy". It remains to be established whether the differences found between the latter and this case are due to the polymorphism at codon 129. Different degrees of proteinase K susceptibility were easily determined with the chemical polymer detection system which could help to detect proteinase-susceptible pathologic prion protein in diseases other than the classical ones.
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681 p.
Resumo:
Papillomaviruses (PVs) are widespread pathogens. However, the extent of PV infections in bats remains largely unknown. This work represents the first comprehensive study of PVs in Iberian bats. We identified four novel PVs in the mucosa of free-ranging Eptesicus serotinus (EserPV1, EserPV2, and EserPV3) and Rhinolophus ferrumequinum (RferPV1) individuals and analyzed their phylogenetic relationships within the viral family. We further assessed their prevalence in different populations of E. serotinus and its close relative E. isabellinus. Although it is frequent to read that PVs co-evolve with their host, that PVs are highly species-specific, and that PVs do not usually recombine, our results suggest otherwise. First, strict virus-host co-evolution is rejected by the existence of five, distantly related bat PV lineages and by the lack of congruence between bats and bat PVs phylogenies. Second, the ability of EserPV2 and EserPV3 to infect two different bat species (E. serotinus and E. isabellinus) argues against strict host specificity. Finally, the description of a second noncoding region in the RferPV1 genome reinforces the view of an increased susceptibility to recombination in the E2-L2 genomic region. These findings prompt the question of whether the prevailing paradigms regarding PVs evolution should be reconsidered.