A chamada hermenêutica tradicional tem se mostrado impotente desde a Constituição de Weimar em acompanhar e explicar a transformação por que passaram as Constituições no século XX. Por outro lado, a moderna metodologia de interpretação da Constituição ampliou demasiadamente a importância do fator político, empobrecendo a consistência jurídica da Constituição, conduzindo a sua concretização a um estado de crise. Porém, não é possível desprezar as novas metodologias, especialmente naqueles países onde a democracia está longe de resolver as questões sociais. A Metódica Estruturante de Friedrich Müller, inserindo-se no rol das novas metodologias, intenta superar a deficiência verificada nas modernas teorias, assim como nas teorias tradicionais. Desenvolveu-se ela com base na experiência constitucional alemã e tratou de inúmeros temas da teoria jurídica, aproveitando o presente trabalho apenas o núcleo metodológico principal dessa teoria, a sua metódica jurídica, que consiste precisamente em uma particular concepção de estrutura da norma, que se revela num processo de concreção normativa. Pretende-se realizar o estudo dessa metódica, aplicando-a às decisões proferidas pelo Supremo Tribunal Federal no âmbito da ordem econômica, de modo a verificar conclusivamente a conformidade ou não dessa teoria com o modo como os magistrados da Corte Suprema estruturam seus votos. Assim, o objeto de trabalho da análise é a argumentação jurídica e a pergunta que se fará é, por um lado, em que medida a metódica estruturante descreve a organização argumentativa das decisões do STF e, de outro lado, em que medida apresenta-se estruturada a argumentação jurídica das decisões do STF à luz da metódica. Ao final, conclui-se que as decisões proferidas pelo Supremo não adotam um padrão de organização que siga um modelo estruturado como aquele erigido pela Metódica Estruturante / Since the Weimar Constitution, the so called Traditional Hermeneutics has been incapable of dealing with the changes occurred in the XX century constitutions. On the other hand, the modern theories have excessively enlarged the boundaries of interpretation, leading to a critical situation in this sector. Friedrich Müller theory, in spite of being a modern theory, intends to overcome these mentioned deficiencies. It was developed within the German constitutional experience and only the main core of it, the law methodic, will be important for the purposes of this work. Therefore, the objective of this work is to apply Müllers law methodic to the decisions taken by the Brazilian Supreme Court in the field of constitutional economic order. At the end, the work concluded that the Brazilian Supreme Court decisions, in the field of the constitutional economic order, do not comply with a structural model of decisions like the one developed by Friedrich Müller.

La dystrophine Dp71, issue du gène DMD impliqué dans la dystrophie musculaire de Duchenne intervient dans le maintien de l'homéostasie rétinienne et de la barrière hémato-rétinienne. Nous avons mis en évidence une localisation rétinienne jusque-là méconnue de la Dp71 au sein des astrocytes rétiniens. Nous avons également étudié l'effet in vivo de l'absence de Dp71, sur le développement vasculaire et observé une plus faible densité et une morphologie astrocytaire différente comparativement aux souris contrôles, à l'origine d'un développement vasculaire retardé. Compte tenu de la spécificité du réseau vasculaire rétinien dont l'étanchéité des parois est maintenue en partie par les pieds des CGM et des astrocytes, nous avons émis l'hypothèse, étant donné l'implication de la Dp71 dans la stabilisation de ces cellules, d'une altération de cette protéine dans les phénomènes de rupture de la BHR. Ainsi dans un modèle transitoire de rupture de la BHR in vivo relativement " pur ", sans ischémie ni injection de VEGF, nous avons observé une diminution de l'expression de la dystrophine Dp71 ainsi que du canal aqueux AQP4 et une délocalisation du canal potassique Kir4.1 dans les CGM. L'injection intra-vitréenne de Dexaméthasone dans ce modèle a permis de prévenir les modifications d'expression et de localisation de ces protéines. / Dp71, a dystrophin produced from DMD gene, is involved in retinal homeostasis and maintenance of blood retinal barrier. We have previously shown that Dp71, part of a complex called Dystrophin associated protein, is involved in the localization of aqueous and potassic channels in Muller glial cell (MGC), particularly around blood vessels, allowing maintenance of retinal homeostasis. Based on the knowledge that growing retinal vessels migrate on an astrocyte template during development, we highlighted the expression of Dp71 in retinal astrocytes. In absence of Dp71, in vivo, we observed a lower density and a different morphology of retinal astrocytes compared to control retina in mice, responsible for a delayed vascular development. Due to the role of barrier of the retinal vascular network, insured also by astrocytes, we studied a model of post surgical BRB breakdown and found a decreased of Dp71 protein expression associated with Kir4.1 delocalization and AQP4 decrease in MGC. Intravitreal Dexamethasone prevents these protein expression changes. We suggest here that the membrane associated cytoskeletal protein, Dp71, expressed in astrocytes is involved in the maintenance of astrocytes density and morphology necessary as a template for retinal vascular development. This protein insure also a key role in retinal homeostasis by localizing and maintaining aqueous and potassic channels in MGC. Moreover when this protein is altered, Dexamethasone seems to be capable to promote Dp71 expression which could have wide clinical implications in retinal diseases treatment and the target for retinal neuroprotection under pathological conditions seems to be the macroglial cells.

This thesis describes about theoretical design and practical realization of self-contained module for intensity and absorbed dose measuring of X-Radiation from High Voltage X-RAY industrial sources. In the first part, thesis is focused on ways and solutions of radiation protection and principles of measuring absorbed dose and intensity of radiation and possibilities of sending measured data through sensor networks. In the second part, the complete schematic of measuring module is solved, critical blocks are tested and design of PCB is done. Detection circuit, blocks for optical and acoustic signaling, power management and control of the entire device are designed. Detection circuit uses a GM Tube. Next, main box of whole device is designed and made by 3D printing technology. The next step is putting hardware into operation and writing test firmware included verification of wireless communication through WiFi.

The topic of the thesis is the mechanisms of cellular volume regulation in the rat retina. Müller cells as main macroglial cells of the retina are supposed to play important roles in the regulation of the retinal ion- and osmohomeostasis and, thus, in the regulation of the extracellular space volume. In the first part of the thesis, signaling pathways were determined which are involved in the regulation of the volume of Müller glial cells and bipolar cells, the main second-order cells of the retina, in the healthy rat retina. The topic of the second part of the thesis is the evaluation of gliotic alterations of Müller cells in a transgenic rat model of retinal degeneration (CMV-PKD21/703 HA rats), in order to obtain indications for a pathogenic role of reactive glial cells in the development of retinal degeneration and edema. Various methods were used including immunohistochemical stainings, real-time RT-PCR, patch-clamp recordings, and cell swelling experiments. The data suggest that both neurons and reactive Müller cells may contribute to formation of retinal edema. In contrast to Müller cells, bipolar cells are apparently not capable to regulate the extracellular space volume in the healthy retina. However, reactive Müller cells are impaired in their capability to regulate retinal water and ion homeostasis. Impaired regulation of the extracellular space volume may result in neuronal hyperexcitation and degeneration.

Focusing on novels by three contemporary German authors and one multi-author theater text, “A Multidirectional Europe” investigates how their writing responds to post-1989 memory paradigms in which post-socialist memory, in relation to the Holocaust and Second World War, has received asymmetrical attention. Conceived as an interdisciplinary and comparative study, this dissertation analyzes how narrative texts by Herta Müller (1953-), Nino Haratischwili (1983-), Saša Stanišić (1978-) and the play Ein europäisches Abendmahl [2017] frame the memory of socialism in relation to the Holocaust, considering the ways in which these authors challenge the larger post- or transnational discourse of a supposedly “unified Europe.” Having migrated from Romania, Georgia, and Bosnia respectively, these authors, I argue, integrate post-socialist memories into German, and European, memory discourses through their play with genre, narrative structure, figurative language, and intertextuality. Although sociohistorical context is crucial in my readings for questions of memory, this dissertation seeks to transcend bounded definitions of memory, embracing a dynamic approach that is more inclusive in terms of the (hi)stories that are told and that contribute to the imagination of a heterogenous continent. Combining cultural studies, literary analysis, and memory theory, I move away from reading these works under the lens of autobiographical trauma, seeking instead to examine the negotiation of post-socialist memory through attending to generic and formal elements of the literary texts. My literary close readings methodologically draw on individual texts, while reflecting how literature is in exchange with other media and also present in the public sphere. Rather than a homogeneous entity, I show, the invoked Europe constitutes a multidirectional network. Through my focus on contexts beyond East Germany and its experience of state socialism, I address the intersections of migration and memory and their relevance for contemporary and future Germany and Europe, while counteracting approaches that traditionally center West Central Europe in discussions of the continent. In dialogue with Michael Rothberg’s conceptualization of multidirectional memory, I furthermore contribute to ongoing debates on different histories of violence, such as the current discussion about the relation or interaction between the memories of colonialism and the Holocaust.

”vivid and fiery”
  Carolina Müller as phenomenon at the Royal Theatre Carolina Müller is identical with the Royal Theatre and she was the first professional female opera singer in Sweden. The audience’s perception of her stage personality and her agency in her portrayal of the title role in C. W. Gluck’s opera Alceste at the Stockholm opera in 1781 will throw light on her quality; her singing and acting style according to the affect she created on stage linked to the age of sensibility. Carolina Müller’s agency constitutes a gap in Swedish theatre history which will be examined in order to reach a better understanding of the structures behind her position. Willmar Sauter’s concept of the theatrical event, but with a feministic perspective on the role of the actress, is used to analyze her performativity, which I characterize as both passionate and sentimental. I use historical descriptive sources to understand her stage personality, and I will look into her performance of Alceste from the perspective of late eighteenth century acting. Secondly, I look into the prescriptive sources linked to Alceste, to examine how her stage personality affected the production, she had a great impact on the creation of the opera characters written for her after her Alceste. Finally, I highlight how the European exchange allowed her to emerge as a phenomenon. Telling her story is a contribution to the history of the prima donnas of the north, and thereby to the field of feminist historiography.  Carolina Müller, Gluck, Alceste, actress, Royal Theatre, phenomenon, stage personality, agency, theatrical event, performativity, sensibility, gaze

No description available.

Anti-müllerian hormone (AMH) is expressed in male embryos and represses development of müllerian ducts during testis differentiation in mammals, birds and reptiles. Amh orthologues have been identified in teleosts despite them lacking müllerian ducts. Previously we found sexually dimorphic aromatase activity in tilapia brains before ovarian differentiation. This prompted us to search for further dimorphisms in tilapia brains during sex differentiation and see whether amh is expressed. We cloned the tilapia amh gene and found that it contains 7 exons but no spliced forms. The putative protein presents highest homologies with Amh proteins of pejerrey and medaka as compared to other Perciformes. We analysed amh expression in adult tissues and found elevated levels in testes, ovary and brain. Amh expression was dimorphic with higher levels in XY male brains at 10–15 dpf, when the gonads were still undifferentiated and gonadal amh was not dimorphic. Male brains had 2.7-fold higher amh expression than gonads. Thereafter, amh levels decreased in the brain while they were up-regulated in differentiating testes. Our study indicates that amh is transcribed in male brains already at 10 dpf, suggesting that sexual differentiation may be occurring earlier in tilapia brain than in gonads. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

Les cellules gliales sont essentielles au fonctionnement du système nerveux. Dans la rétine, les cellules gliales de Müller assurent à la fois l’homéostasie du tissu et la protection des neurones, notamment celle des cellules ganglionnaires de la rétine (CGRs). L’hypothèse principale de la thèse est que les cellules de Müller joueraient un rôle primordial dans la survie neuronale tant au plan de la signalisation des neurotrophines/proneurotrophines par suite d’une blessure que lors des mécanismes d’excitotoxicité. Contrairement au brain-derived neurotrophic factor (BDNF), le nerve growth factor (NGF) n’est pas en mesure d’induire la survie des CGRs après une section du nerf optique. Le premier objectif de la thèse a donc été de localiser les récepteurs p75NTR et TrkA du NGF dans la rétine adulte et d’établir leur fonction respective en utilisant des ligands peptidomimétiques agonistes ou antagonistes spécifiques pour chacun des récepteurs. Nos résultats ont démontré que TrkA est surexprimé par les CGRs après l’axotomie, tandis que p75NTR est spécifiquement exprimé par les cellules de Müller. Alors que NGF n’est pas en mesure d’induire la survie des CGRs, l’activation spécifique de TrkA par des ligands peptidomimétique est nettement neuroprotectrice. De façon surprenante, le blocage sélectif de p75NTR ou l’absence de celui-ci protège les CGRs de la mort induite par l’axotomie. De plus, la combinaison de NGF avec l’antagoniste de p75NTR agit de façon synergique sur la survie des CGRS. Ces résultats révèlent un nouveau mécanisme par lequel le récepteur p75NTR exprimé par les cellules gliales de Müller peut grandement influencer la survie neuronale. Ensuite, nous avons voulu déterminer l’effet des proneurotrophines dans la rétine adulte. Nous avons démontré que l’injection de proNGF induit la mort des CGRs chez le rat et la souris par un mécanisme dépendant de p75NTR. L’expression de p75NTR étant exclusive aux cellules de Müller, nous avons testé l’hypothèse que le proNGF active une signalisation cellulaire non-autonome qui aboutit à la mort des CGRs. En suivant cette idée, nous avons montré que le proNGF induit une forte expression du tumor necrosis factor α (TNFα) dans les cellules de Müller et que l’inhibition du TNF bloque la mort neuronale induite par le proNGF. L’utilisation de souris knock-out pour la protéine p75NTR, son co-récepteur sortiline, ou la protéine adaptatrice NRAGE a permis de montrer que la production de TNF par les cellules gliales était dépendante de ces protéines. Le proNGF semble activer une signalisation cellulaire non-autonome qui cause la mort des neurones de façon dépendante du TNF in vivo. L’hypothèse centrale de l’excitotoxicité est que la stimulation excessive des récepteurs du glutamate sensibles au N-Methyl-D-Aspartate (NMDA) est dommageable pour les neurones et contribue à plusieurs maladies neurodégénératives. Les cellules gliales sont soupçonnées de contribuer à la mort neuronale par excitotoxicité, mais leur rôle précis est encore méconnu. Le dernier objectif de ma thèse était d’établir le rôle des cellules de Müller dans cette mort neuronale. Nos résultats ont démontré que l’injection de NMDA induit une activation du nuclear factor κB (NF-κB) dans les cellules de Müller, mais pas dans les CGRs, et que l’utilisation d’inhibiteurs du NF-κB empêche la mort des CGRs. De plus, nous avons montré que les cellules de Müller en réaction à l’activation du NF-κB produisent la protéine TNFα laquelle semble être directement impliquée dans la mort des CGRs par excitotoxicité. Cette mort cellulaire se produit principalement par l’augmentation à la surface des neurones des récepteurs AMPA perméables au Ca2+, un phénomène dépendant du TNFα. Ces donnés révèlent un nouveau mécanisme cellululaire non-autonome par lequel les cellules gliales peuvent exacerber la mort neuronale lors de la mise en jeu de mécanismes excitotoxiques. / Glial cells are essential for the functioning of the nervous system. In the retina, the Müller glial cells ensure the homeostasis of this tissue as well as the protection of neurons including the retinal ganglion cells (RGCs). The main hypothesis of this thesis is that Müller cells play a predominant role in neuronal survival both at the levels of neurotrophin/proneurotrophin signaling following injury and excitotoxic mechanisms. Unlike the brain-derived neurotrophic factor (BDNF), the nerve growth factor (NGF) is unable to induce RGCs survival following optic nerve transection. The first objective of the thesis was therefore to describe the expression of the two receptors of NGF, p75NTR and TrkA, in the adult retina and to address their functional role by using peptidomimetic agonistic or antagonistic ligands specific for each receptor. Our results showed that TrkA is overexpressed by RGCs following axotomy, whereas p75NTR is specifically expressed by Müller cells. While NGF by itself does not promote RGC survival, selective activation of TrkA receptors using peptidomimetic ligands is markedly neuroprotective. Surprisingly, selective blockers of p75NTR, or the absence of p75NTR, protect RGCs from axotomy-induced death. Moreover, combination of NGF or TrkA agonists with p75NTR antagonists functions synergistically to enhance RGC survival. These results reveal a new mechanism by which p75NTR expression by Müller glia may profoundly influence neuronal survival. Next, we wanted to address the effect of proneurotrophins in the adult retina. We showed that injection of proNGF induces the death of RGCs in rats and mice by a p75NTR-dependent signaling mechanism. Expression of p75NTR in the adult retina being confined to Müller glial cells, we tested the hypothesis that proNGF activates a non-cell autonomous signaling pathway to induce RGC death. Consistent with this notion, we showed that proNGF induced a robust expression of tumor necrosis factor α (TNFα) in Müller cells, and that genetic or biochemical ablation of TNFα blocked proNGF-induced death of retinal neurons. Mice rendered null for p75NTR, its co-receptor sortilin, or the adaptor protein NRAGE were defective in proNGF-induced glial TNFα production and did not undergo proNGF-induced retinal ganglion cell death. We concluded that proNGF activates a non-cell autonomous signaling pathway that causes TNFα-dependent death of retinal neurons in vivo. The central hypothesis of excitotoxicity is that excessive stimulation of neuronal N-Methyl-D-Aspartate (NMDA)-sensitive glutamate receptors is harmful to neurons and contributes to a variety of neurological disorders. Glial cells have been proposed to participate in excitotoxic neuronal loss, but their precise role is poorly defined. In this in vivo study, we showed that NMDA induces a strong NF-κB activation in Müller glia, but not in retinal neurons. Intriguingly, NMDA-induced death of retinal neurons was effectively blocked by inhibitors of NF-κB activity. We demonstrated that TNFα protein produced in Müller glial cells via an NMDA-induced NF-κB dependent pathway plays a crucial role in the excitotoxic loss of retinal neurons. This cell loss occurs mainly through a TNFα-dependent increase in Ca2+-permeable AMPA receptors on susceptible neurons. Thus, our data reveal a novel non-cell-autonomous mechanism by which glial cells can profoundly exacerbate neuronal death following excitotoxic injury.

Keywords: GDR literature, historical drama, postdramatic theatre, history, memory, Heiner Müller, Walter Benjamin, Bertolt Brecht, Lehrstück Abstract: The aim of this thesis is to analyse the representation of the German history and its relation with the reality of the GDR in selected dramas by Heiner Müller (1929-1995): Germania Death in Berlin, Germania 3 Ghosts at Dead Man, Life of Gundling Frederick of Prussia Lessing's Dream Sleep Scream, The Battle, The Horatian and The Hamletmachine. The main focus of interest is also the approach of the playwright to selected literary and theatrical genres as historical drama, Lehrstück and postdramatic theatre. The philosophical background of the analysis is based mainly on Walter Benjamin's essay On the Concept of History and his description of the painting Angelus Novus by Paul Klee. Furthermore, the thesis examines the methods of dramatization in Heiner Müller's plays.