La institución del genio : en torno al teatro épico.

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Teaching and live performances : applied theatre in universities and schools

This article compares the classroom process of school teachers and university lecturers to the activity of theatrical performance. In doing so, it probes the potential of live performance as an educational instrument. It concludes by tracing some of the history of applications of theatre to education, from the time of Brecht to the present day.

A arte de conduzir-se pelo ensino de teatro: realidades e ficções de alunos-diretores em Camarão

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

O teatro político de rua praticado pelos coletivos ALMA e Dolores: estéticas de combate e semeadura

Pós-graduação em Artes - IA

Pequenas criaturas e o efeito de real: a estética da crueldade em Rubem Fonseca

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

A estrutura dialógica nos contos de Llanson: entre o lírico e o dramático

Pós-graduação em Letras - IBILCE

O cinema de Manoel de Oliveira: um caso singular

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Teatro, cinema e literatura: confluências

Esta coletânea traz 14 estudos apresentados durante dois encontros acadêmicos realizados na Faculdade de Ciências e Letras da Unesp, em Araraquara, em 2011. Os artigos, produzidos por especialistas de diversas áreas, tiveram como foco principal, o tema proposto para os eventos: as confluências entre teatro, cinema e literatura. Na primeira parte do livro, os estudos têm por denominador comum as relações entre peças de teatro, obras cinematográficas e textos literários. Entre os artigos, há uma análise comparativa das características literárias-políticas do alemão Bertold Brecht, a partir de duas de suas peças, e de um filme, de cujo roteiro foi autor, além de uma reflexão sobre o peta e romancista francês Jules Romains, com foco naquilo que o poeta tomou de empréstimo à arte do cinematógrafo, e um texto sobre a técnica cinematográfica do close-up no filme Vagas estrelas da Ursa, de Luchino Visconti, que tem a personagem principal baseada em Electra. “Ato II – Peças, pessoas, personagens”, a segunda parte do livro, tem seu foco no teatro. Entre os artigos, estão uma análise de duas coletâneas de ensaios do crítico teatral Décio de Almeida Prado, um estudo sobre a peça Esperando Godot, de Samuel Beckett, que aborda uma estética do absurdo, modernamente trágica, uma representação critica da ideologia norte-americana em peças de Tennessee Wiliams e uma discussão sobre a religiosidade católica na peça A Revolução dos Beatos, de Dias Gomes.

Futebol, poesia e drama: o espetáculo

O que seria necessário para que se pudesse dizer que uma partida de futebol semelha de alguma forma a um espetáculo teatral, poético, emocional? O artigo propõe um passeio livre pela história dos diferentes tipos de teatro e pelas mudanças sofridas ao longo dos anos. A autora lembra que existe, da metade do século passado para cá, uma nítida divisão que colocou em campos opostos o teatro dramático e o teatro épico, o drama rigoroso contra o texto quase absolutamente livre, Aristóteles contra Brecht. E volta a apresentar as razões pela qual se pode afirmar que existem certos momentos no futebol que o aproximam ainda mais do espetáculo teatral, da dança, da comédia e do drama

Toxicity of clopidogrel and ticlopidine on human myeloid progenitor cells: importance of metabolites

Ticlopidine and clopidogrel are thienopyridine derivatives used for inhibition of platelet aggregation. Not only hepatotoxicity, but also bone marrow toxicity may limit their use. Aims of the study were to find out whether non-metabolized drug and/or metabolites are responsible for myelotoxicity and whether the inactive clopidogrel metabolite clopidogrel carboxylate contributes to myelotoxicity. We used myeloid progenitor cells isolated from human umbilical cord blood in a colony-forming unit assay to assess cytotoxicity. Degradation of clopidogrel, clopidogrel carboxylate or ticlopidine (studied at 10 and 100 μM) was monitored using LC/MS. Clopidogrel and ticlopidine were both dose-dependently cytotoxic starting at 10 μM. This was not the case for the major clopidogrel metabolite clopidogrel carboxylate. Pre-incubation with recombinant human CYP3A4 not only caused degradation of clopidogrel and ticlopidine, but also increased cytotoxicity. In contrast, clopidogrel carboxylate was not metabolized by recombinant human CYP3A4. Pre-incubation with freshly isolated human granulocytes was not only associated with a myeloperoxidase-dependent degradation of clopidogrel, clopidogrel carboxylate and ticlopidine, but also with dose-dependent cytotoxicity of these compounds starting at 10 μM. In conclusion, both non-metabolized clopidogrel and ticlopidine as well as metabolites of these compounds are toxic towards myeloid progenitor cells. Taking exposure data in humans into account, the myelotoxic element of clopidogrel therapy is likely to be secondary to the formation of metabolites from clopidogrel carboxylate by myeloperoxidase. Concerning ticlopidine, both the parent compound and metabolites formed by myeloperoxidase may be myelotoxic in vivo. The molecular mechanisms of cytotoxicity have to be investigated in further studies.

Hepatocellular toxicity of clopidogrel: Mechanisms and risk factors

Clopidogrel is a prodrug used widely as a platelet aggregation inhibitor. After intestinal absorption, approximately 90% is converted to inactive clopidogrel carboxylate and 10% via a two-step procedure to the active metabolite containing a mercapto group. Hepatotoxicity is a rare but potentially serious adverse reaction associated with clopidogrel. The aim of this study was to find out the mechanisms and susceptibility factors for clopidogrel-associated hepatotoxicity. In primary human hepatocytes, clopidogrel (10 and 100μM) was cytotoxic only after cytochrome P450 (CYP) induction by rifampicin. Clopidogrel (10 and 100μM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt). Clopidogrel (100μM) decreased the cellular glutathione content in HepG2/CYP3A4 supersome and triggered an oxidative stress reaction (10 and 100µM) in HepG2/CYP3A4, but not in HepG2/wt. Glutathione depletion significantly increased the cytotoxicity of clopidogrel (10 and 100µM) in HepG2/CYP3A4 supersome. Co-incubation with 1μM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. HepG2/CYP3A4 incubated with 100μM clopidogrel showed mitochondrial damage and cytochrome c release, eventually promoting apoptosis and/or necrosis. In contrast to clopidogrel, clopidogrel carboxylate was not toxic for HepG2/wt or HepG2/CYP3A4 up to 100µM. In conclusion, clopidogrel incubated with CYP3A4 is associated with the formation of metabolites that are toxic for hepatocytes and can be trapped by glutathione. High CYP3A4 activity and low cellular glutathione stores may be risk factors for clopidogrel-associated hepatocellular toxicity.

Toxicity of thienopyridines on human neutrophil granulocytes and lymphocytes

Thienopyridines can cause neutropenia and agranulocytosis. The aim of the current investigations was to compare cytotoxicity of ticlopidine, clopidogrel, clopidogrel carboxylate and prasugrel for human neutrophil granulocytes with the toxicity for lymphocytes and to investigate underlying mechanisms. For granulocytes, clopidogrel, ticlopidine, clopidogrel carboxylate and prasugrel were concentration-dependently toxic starting at 10μM. Cytotoxicity could be prevented by the myeloperoxidase inhibitor rutin, but not by the cytochrome P450 inhibitor ketoconazole. All compounds were also toxic for lymphocytes, but cytotoxicity started at 100μM and could not be prevented by rutin or ketoconazole. Granulocytes metabolized ticlopidine, clopidogrel, clopidogrel carboxylate and prasugrel, and metabolization was inhibited by rutin, but not by ketoconazole. Metabolism of these compounds by lymphocytes was much slower and could not be inhibited by ketoconazole or rutin. In neutrophils, all compounds investigated decreased the electrical potential across the inner mitochondrial membrane, were associated with cellular accumulation of ROS, mitochondrial loss of cytochrome c and induction of apoptosis starting at 10μM. All of these effects could be inhibited by rutin, but not by ketoconazole. Similar findings were obtained in lymphocytes; but compared to neutrophils, the effects were detectable only at higher concentrations and were not inhibited by rutin. In conclusion, ticlopidine, clopidogrel, clopidogrel carboxylate and prasugrel are toxic for both granulocytes and lymphocytes. In granulocytes, cytotoxicity is more accentuated than in lymphocytes and depends on metabolization by myeloperoxidase. These findings suggest a mitochondrial mechanism for cytotoxicity for both myeloperoxidase-associated metabolites and, at higher concentrations, also for the parent compounds.