925 resultados para Repression


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O contrabando é uma actividade comercial ilícita que não tem uma origem definida, uma vez que, ultrapassa todas as fronteiras espaciais e temporais. No entanto, a partir do século XIX e ao longo do período da Primeira Guerra Mundial, o tema constitui uma das principais preocupações dos países Aliados. Nas Conferências de Haia (1899 e 1907) e Londres (1908-09), o conceito é discutido e são promulgadas listas com as mercadorias consideradas contrabando de guerra. Durante a Primeira Guerra Mundial é criado o bloqueio económico com o intuito de reprimir o contrabando e a circulação de mercadorias com destino ao inimigo. Esta dissertação de mestrado tem como principal objectivo compreender o significado, a importância e o impacto do contrabando num contexto local e inserido numa conjuntura de guerra e pós-guerra. Destacando os actores, as dinâmicas de resistência e repressão, assim como as relações entre o poder central, poder local e contrabandistas.

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Dissertação (mestrado)—Universidade de Brasília, Instituto de Ciências Sociais, Departamento de Sociologia, 2016.

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[ES]El siglo XX fue caracterizado por un desarrollo de las dictaduras, que, a través de un marco legal, realizaron políticas de exclusión y de represión contra aquellos que se mostraban opuestos al régimen. A partir de una definición de los “enemigos” como “peligrosos”, y a través de una lucha por la defensa de la comunidad, los gobiernos totalitarios crearon una legislación en base a estos términos, que propició el control social y en última instancia, el holocausto. El presente Trabajo tratará de abordar los orígenes de este Derecho, tanto en la dictadura nacionalsocialista, como en la franquista, la teoría y dogmática que las fundó y las políticas que se llevaron a cabo. Se realizará un análisis del mismo y una perspectiva actual a raíz de estos hechos.

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The neural crest is a group of migratory, multipotent stem cells that play a crucial role in many aspects of embryonic development. This uniquely vertebrate cell population forms within the dorsal neural tube but then emigrates out and migrates long distances to different regions of the body. These cells contribute to formation of many structures such as the peripheral nervous system, craniofacial skeleton, and pigmentation of the skin. Why some neural tube cells undergo a change from neural to neural crest cell fate is unknown as is the timing of both onset and cessation of their emigration from the neural tube. In recent years, growing evidence supports an important role for epigenetic regulation as a new mechanism for controlling aspects of neural crest development. In this thesis, I dissect the roles of the de novo DNA methyltransferases (DNMTs) 3A and 3B in neural crest specification, migration and differentiation. First, I show that DNMT3A limits the spatial boundary between neural crest versus neural tube progenitors within the neuroepithelium. DNMT3A promotes neural crest specification by directly mediating repression of neural genes, like Sox2 and Sox3. Its knockdown causes ectopic Sox2 and Sox3 expression at the expense of neural crest territory. Thus, DNMT3A functions as a molecular switch, repressing neural to favor neural crest cell fate. Second, I find that DNMT3B restricts the temporal window during which the neural crest cells emigrate from the dorsal neural tube. Knockdown of DNMT3B causes an excess of neural crest emigration, by extending the time that the neural tube is competent to generate emigrating neural crest cells. In older embryos, this resulted in premature neuronal differentiation. Thus, DNMT3B regulates the duration of neural crest production by the neural tube and the timing of their differentiation. My results in avian embryos suggest that de novo DNA methylation, exerted by both DNMT3A and DNMT3B, plays a dual role in neural crest development, with each individual paralogue apparently functioning during a distinct temporal window. The results suggest that de novo DNA methylation is a critical epigenetic mark used for cell fate restriction of progenitor cells during neural crest cell fate specification. Our discovery provides important insights into the mechanisms that determine whether a cell becomes part of the central nervous system or peripheral cell lineages.

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Doutoramento em Engenharia Agronómica - Instituto Superior de Agronomia - UL

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O Policiamento de Proximidade é o modelo de policiamento atual em Portugal, privilegiando uma postura preventiva e dando relevo à pró-atividade das forças policiais. À Guarda Nacional Republicana, enquanto força policial, cabe-lhe zelar pelos direitos, liberdades e garantias dos cidadãos, constitucionalmente protegidos, através dessa atuação preventiva, procurando intensificar pró-ativamente a sua presença no seio da sociedade. Contudo, por vezes é necessário recorrer a uma intervenção de caráter repressivo, a fim de repor a ordem e visando uma prevenção futura, evitando os comportamentos antissociais. Torna-se assim pertinente estudar de que forma se articulam a atuação preventiva e repressiva da GNR, de modo a perceber se é possível existir um equilíbrio entre elas, ou se, por alguma razão, existem limitações no seu emprego. O Destacamento Territorial de Coimbra constitui o estudo de caso. Esta investigação para além de descrever a articulação entre ambas as formas de atuação, pretende ainda identificar aquilo que as caracteriza bem como as suas potencialidades e vulnerabilidades. De forma a recolher a informação pretendida, foram privilegiadas a análise documental, entrevistas ao Comandante de Destacamento Territorial de Coimbra e aos respetivos Comandantes dos Postos Territoriais, bem como questionários aos militares do destacamento responsáveis por exercerem o patrulhamento. Seguidamente procedeu-se à análise de conteúdo dos dados recolhidos. Das conclusões retiradas, salienta-se que a falta de recursos principalmente humanos, corresponde a um problema do destacamento, que dificulta uma ação de patrulhamento contínuo junto do cidadão e que contribui para o Policiamento de Proximidade. Denota-se também a intensa fiscalização rodoviária que, apesar de ter uma natureza preventiva, é interpretada pela população com uma imagem de repressão.

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The apparent simplicity of viruses hides the complexity of their interactions with their hosts. Viruses are masters at circumventing host defenses and manipulating the cellular environment for their own benefit. The replication of the largest known family of single-stranded DNA viruses, Geminiviridae, is impaired by DNA methylation and Arabidopsis mutants affected in cytosine methylation are hypersusceptible to geminivirus infection. This implies that plants might use methylation as a defense against geminiviruses and that the viral genome is a target for plant DNA methyltransferases. We have found a novel counter-defense strategy used by geminiviruses, that reduces the expression of the plant maintenance DNA methyltransferases, MET1 and CMT3, in both, locally and systemically infected tissues. Furthermore, we demonstrated that the virus-mediated repression of these two maintenance DNA methyltransferases is widely spread among different geminivirus species. Additionally, we identified Rep as the geminiviral protein responsible for the repression of MET1 and CMT3, and another viral protein, C4, as an ancillary player in MET1 downregulation. The presence of Rep, suppresses TGS of an Arabidopsis transgene and of host loci whose expression is strongly controlled by CG methylation. Bisulfite sequencing analyses showed that the expression of Rep caused a substantial reduction in the levels of DNA methylation at CG sites. Our findings suggest that Rep, the only viral protein essential for geminiviral replication, displays TGS suppressor activity through a mechanism distinct from the one thus far described for geminiviruses.

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Streptococcus suis is an emerging zoonotic pathogen. With the lack of an effective vaccine, antibiotics remain the main tool to fight infections caused by this pathogen. We have previously observed a reserpine-sensitive fluoroquinolone (FQ) efflux phenotype in this species. Here, SatAB and SmrA, two pumps belonging to the ATP binding cassette (ABC) and the major facilitator superfamily (MFS), respectively, have been analyzed in the fluoroquinolone-resistant clinical isolate BB1013. Genes encoding these pumps were overexpressed either constitutively or in the presence of ciprofloxacin in this strain. These genes could not be cloned in plasmids in Escherichia coli despite strong expression repression. Finally, site-directed insertion of smrA and satAB in the amy locus of the Bacillus subtilis chromosome using ligated PCR amplicons allowed for the functional expression and study of both pumps. Results showed that SatAB is a narrow-spectrum fluoroquinolone exporter (norfloxacin and ciprofloxacin), susceptible to reserpine, whereas SmrA was not involved in fluoroquinolone resistance. Chromosomal integration in Bacillus is a novel method for studying efflux pumps from Gram-positive bacteria, which enabled us to demonstrate the possible role of SatAB, and not SmrA, in fluoroquinolone efflux in S. suis.

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Culture, history, and biology are inseparable. Cultural manifestations are necessarily immersed in a context, originate in the embodied minds that create them, and are directed to the embodied minds that receive them and recreate them within their contexts (individual and collective). The novel and the film of historical memory in Spain aim to connect their audiences with a problem that has not been solved, as the Civil War, the postwar, and the pact of forgetfulness left a wide sector of the Spanish society voiceless. During the last few years, a series of initiatives coming from the arts, as well as other realms such as the legal, have sought to reexamine the unhealed wound that still haunts Spanish subjects. La voz dormida [The Sleeping Voice] is one of those initiatives. It begins as testimony, develops into a hybrid and intertextual novel, and later becomes a film. It constitutes an inclusive project, one of offering an alternative version to the “official history”, while incorporating the marginal voices of women that had been left out of the memory of the war and the dictatorship. Objective and Results By examining both the literary and the cinematic versions of Chacón’s work I aimed to evidence the connections that exist between the artistic portrayal of the postwar repression (particularly how it affects women) and the current movement of recovery of historical memory in Spain. Specifically, I was interested in showing how both the novel and the film employ a series of narrative strategies that emphasize the body and intentionality, with the purpose of creating in readers and spectators an empathetic response that may lead to prosocial behavior. In order to carry out this interdisciplinary study, which relates fiction, mind, and socio-historical context, I draw on cognitive theories of literature and film, as well as theories from social and developmental psychology, such as the Richard Gerrig’s theory of narrative experience, Keith Oatley’s psychology of fiction, Suzanne Keen’s theory of narrative empathy, and the empathy-altruism hypothesis, derived form the ideas of Jean Decety, among others...

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Power flow calculations are one of the most important tools for power system planning and operation. The need to account for uncertainties when performing power flow studies led, among others methods, to the development of the fuzzy power flow (FPF). This kind of models is especially interesting when a scarcity of information exists, which is a common situation in liberalized power systems (where generation and commercialization of electricity are market activities). In this framework, the symmetric/constrained fuzzy power flow (SFPF/CFPF) was proposed in order to avoid some of the problems of the original FPF model. The SFPF/CFPF models are suitable to quantify the adequacy of transmission network to satisfy “reasonable demands for the transmission of electricity” as defined, for instance, in the European Directive 2009/72/EC. In this work it is illustrated how the SFPF/CFPF may be used to evaluate the impact on the adequacy of a transmission system originated by specific investments on new network elements

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This paper extends the symmetric/constrained fuzzy powerflow models by including the potential correlations between nodal injections. Therefore, the extension of the model allows the specification of fuzzy generation and load values and of potential correlations between nodal injections. The enhanced version of the symmetric/constrained fuzzy powerflow model is applied to the 30-bus IEEE test system. The results prove the importance of the inclusion of data correlations in the analysis of transmission system adequacy.

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In restructured power systems, generation and commercialization activities became market activities, while transmission and distribution activities continue as regulated monopolies. As a result, the adequacy of transmission network should be evaluated independent of generation system. After introducing the constrained fuzzy power flow (CFPF) as a suitable tool to quantify the adequacy of transmission network to satisfy 'reasonable demands for the transmission of electricity' (as stated, for instance, at European Directive 2009/72/EC), the aim is now showing how this approach can be used in conjunction with probabilistic criteria in security analysis. In classical security analysis models of power systems are considered the composite system (generation plus transmission). The state of system components is usually modeled with probabilities and loads (and generation) are modeled by crisp numbers, probability distributions or fuzzy numbers. In the case of CFPF the component’s failure of the transmission network have been investigated. In this framework, probabilistic methods are used for failures modeling of the transmission system components and possibility models are used to deal with 'reasonable demands'. The enhanced version of the CFPF model is applied to an illustrative case.

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In contemporary times family business research has been dominated by three theoretical perspectives; principal-agent theory, stewardship theory, and resource-based view theory (Siebels 2012) but at the same time scholars argue that what still needs further attention is how underlying processes and phenomena can be explained (Melin, Nordqvist & Sharma  2014). In order to understand themes such as repression or relations of asymmetry the suggestion in this chapter is to move towards a critical stance of thinking which involves problematizing the obvious issues in family firms (Alvesson & Deetz 2000) and moreover allowing the critical perspective to destabilize assumptions made within earlier research (Freire, 1974). By discussing critical theory in general but foremost the Freirean  (1970, 1974) critical pedagogy specifically, the arguments in the chapter revolves around how critical pedagogy can open up for a more novel view on family business. The purpose is via critical pedagogy discuss family business from a limited situation perspective, and to argue for a Freirean (1970) dialogue as means of developing a critical consciousness for family members in the family business context. The chapter concludes with some recommendations on platforms or common grounds in which dialogue and raising of consciousness can occur in which the concept can open up possibilities for interesting learning transfer and bring multidimensional knowledge into the family firm.

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Résumé : c-Myc est un facteur de transcription (FT) dont les niveaux cellulaires sont dérégulés dans la majorité des cancers chez l’homme. En hétérodimère avec son partenaire obligatoire Max, c-Myc lie préférentiellement les séquences E-Box (CACGTG) et cause l’expression de gènes impliqués dans la biosynthèse des protéines et des ARNs, dans le métabolisme et dans la prolifération cellulaire. Il est maintenant bien connu que c-Myc exerce aussi son potentiel mitogène en liant et inhibant différents FTs impliqués dans l’expression de gènes cytostatiques. Entre autres, c-Myc est en mesure d’inhiber Miz-1, un FT comportant 13 doigts de zinc de type Cys2-His2 (ZFs) impliqué dans l’expression de plusieurs gènes régulateurs du cycle cellulaire comprenant les inhibiteurs de CDK p15[indice supérieur INK4], p21[indice supérieur CIP1] et p57[indice supérieur KIP2]. Plus récemment, il fut démontré qu’en contrepartie, Miz-1 est aussi en mesure de renverser les fonctions activatrices de c-Myc et de prévenir la prolifération de cellules cancéreuses dépendantes de c-Myc. Ces différentes observations ont mené à la suggestion de l’hypothèse intéressante que la balance des niveaux de Miz-1 et c-Myc pourrait dicter le destin de la cellule et a permis d’établir Miz-1 comme nouvelle cible potentielle pour le développement d’agents anti-cancéreux. Malgré le fait que ces deux protéines semblent centrales à la régulation du cycle cellulaire, les mécanismes moléculaires leur permettant de s’inhiber mutuellement ainsi que les déterminants moléculaires permettant leur association spécifique demeurent assez peu documentés pour le moment. De plus, la biologie structurale de Miz-1 demeure à être explorée puisque qu’aucune structure de ses 13 ZFs, essentiels à sa liaison à l’ADN, n’a été déterminée pour l’instant. Les travaux réalisés dans le cadre cette thèse visent la caractérisation structurale et biophysique de Miz-1 dans le contexte de la répression génique causée par le complexe c-Myc/Miz-1. Nous présentons des résultats d’éxpériences in vitro démontrant que Miz-1 interagit avec c-Myc via un domaine contenu entre ses ZFs 12 et 13. De plus, nous démontrons que Miz-1 et Max sont en compétition pour la liaison de c-Myc. Ces résultats suggèrent pour la permière fois que Miz-1 inhibe les activités de c-Myc en prévenant son interaction avec son partenaire obligatoire Max. De plus, ils laissent présager que que Miz-1 pourrait servir de référence pour le développement d’inhibiteurs peptidiques de c-Myc. Finalement, nous avons réalisé la caractérisation structurale et dynamique des ZFs 1 à 4 et 8 à 10 de Miz-1 et avons évalué leur potentiel de liaison à l’ADN. Les résultats obtenus, couplés à des analyses bio-informatiques, nous permettent de suggérer un modèle détaillé pour la liaison spécifique de Miz-1 à son ADN consensus récemment identifié.

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Résumé : Les maladies cardiovasculaires représentent la principale cause de mortalité mondiale, soit le tiers des décès annuels selon l’Organisation mondiale de la Santé. L’hypercholestérolémie, caractérisée par une élévation des niveaux plasmatiques de lipoprotéines de faible densité (LDL), est l’un des facteurs de risque majeur pour les maladies cardiovasculaires. La proprotéine convertase subtilisine/kexine type 9 (PCSK9) joue un rôle essentiel dans l’homéostasie du cholestérol sanguin par la régulation des niveaux protéiques du récepteur LDL (LDLR). PCSK9 est capable de se lier au LDLR et favorise l’internalisation et la dégradation du récepteur dans les lysosomes. L’inhibition de PCSK9 s’avère une cible thérapeutique validée pour le traitement de l’hypercholestérolémie et la prévention des maladies cardiovasculaires. Par contre, plusieurs mécanismes responsables de la régulation et la dégradation du complexe PCSK9-LDLR n’ont pas encore été complètement caractérisés comme la régulation par la protéine annexin A2 (AnxA2), un inhibiteur endogène de PCSK9. De plus, plusieurs évidences suggèrent la présence d’une ou plusieurs protéines, encore inconnues, impliquées dans le mécanisme d’action de PCSK9. Celles-ci pourraient réguler l’internalisation et le transport du complexe PCSK9-LDLR vers les lysosomes. Les objectifs de cette thèse sont de mieux définir le rôle et l’impact de l’AnxA2 sur la protéine PCSK9 en plus d’identifier de nouveaux partenaires d’interactions de PCSK9 pour mieux caractériser son mécanisme d’action sur la régulation des niveaux de LDLR. Nous avons démontré que l’inhibition de PCSK9 par l’AnxA2 extracellulaire s’effectue via sa liaison aux domaines M1+M2 de la région C-terminale de PCSK9 et nous avons mis en évidence les premières preuves d’un contrôle intracellulaire de l’AnxA2 sur la traduction de l’ARNm de PCSK9. Nos résultats révèlent une liaison de l’AnxA2 à l’ARN messager de PCSK9 qui cause une répression traductionnelle. Nous avons également identifié la protéine glypican-3 (GPC3) comme un nouveau partenaire d’interaction extracellulaire avec le PCSK9 et intracellulaire avec le complexe PCSK9-LDLR dans le réticulum endoplasmique des cellules HepG2 et Huh7. Nos études démontrent que GPC3 réduit l’activité extracellulaire de PCSK9 en agissant comme un compétiteur du LDLR pour la liaison avec PCSK9. Une meilleure compréhension des mécanismes de régulation et de dégradation du complexe PCKS9-LDLR permettra de mieux évaluer l’impact et l’efficacité des inhibiteurs de la protéine PCSK9.