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„Wer das Leben liebt, liest nicht. Und geht erst recht nicht ins Kino."[3] Wer mit sich selbst und seinem Leben zufrieden ist, schreibt keine Romane. So lautet die lapidare Einsicht, die der französische Erfolgsautor Michel Houellebecq seiner Studie über den Außenseiter Howard Phillips Lovecraft aus dem Jahr 1991 programmatisch voranstellt. Die Lektüre und das Empfinden einer gleichsam existenziellen Notwendigkeit zu schreiben erweisen die Leser und den Autor als Komplizen, als geheime Bundesgenossen in einer Wendung „gegen das Leben, gegen die Welt", wie der Untertitel jener ersten Monographie Houellebecqs über den wahlverwandten Autor Howard Phillips Lovecraft, den die Zeitgenossen als ‚Einsiedler von Providence' bezeichnet haben, programmatisch lautet. Autor und Leser erfahren sich überraschend als Verbündete, die sich gegen die wahrgenommene Trivialität des Daseins verschworen haben. Sie sind, vielleicht ohne es selbst zu ahnen, verbunden im poetischen Widerstand gegen die Monotonie und Banalität einer meist langweiligen empirischen Wirklichkeit, deren erdrückender Wirkung durch Ausflüge in die Phantasie und ins Gedankenexperiment oder durch gewagte Zukunftsprojektionen, sei es in der wissenschaftlichen Hypothesenbildung oder im genetischen Laborversuch, immer nur zeitweilig zu entrinnen ist.
O objetivo deste artigo é analisar os elementos centrais da crítica realizada por Axel Honneth ao pensamento de Michel Foucault, em Crítica do Poder, articulando-a com sua análise da obra do chamado "círculo interno" da Escola de Frankfurt, principalmente Adorno e Horkheimer. Dessa maneira, entende-se que Honneth opera uma aproximação do pensamento foucaultiano à tradição crítica frankfurtiana, com ênfase em deficiências comuns que apontam para uma filiação entre os autores e, ao mesmo tempo, para sua insuficiência na análise da sociedade contemporânea. Tal leitura, contudo, em que pese sua inovação em pôr lado a lado Foucault e Habermas enquanto desenvolvimentos rivais da Teoria Crítica, é limitada tanto cronologicamente, por não levar em consideração a reorientação realizada por Foucault, a partir de 1978, quanto por identificar problematicamente as noções de poder e dominação. Essa limitação não inviabiliza, entretanto, manter o gesto de convergência entre o pensamento foucaultiano e a Escola de Frankfurt, pensando-o através de uma via positiva, que não se restrinja às limitações das suas ferramentas críticas, mas que, ao contrário, ao focalizar a radicalidade de tal crítica, torne possível destacar a sua atualidade.
Michael Stolleis – notice
(2016)
Der Jurist Michael Stolleis (geb. 1941) gilt als einer der international führenden Rechtshistoriker auf dem Gebiet des öffentlichen Rechts. Bis zu seiner Emeritierung 2006 lehrte er als Professor für Öffentliches Recht und Rechtsgeschichte an der Johann Wolfgang Goethe-Universität Frankfurt am Main. Von 1991 bis Ende 2009 leitete er das Max-Planck-Institut für europäische Rechtsgeschichte. Michael Stolleis ist Mitglied zahlreicher Akademien der Wissenschaften in verschiedenen Ländern und ist Teil des Redaktionsgremiums mehrerer Fachzeitschriften und Reihen. Seine Hauptarbeitsgebiete liegen in den Bereichen Öffentliches Recht (Sozialrecht), Juristische Zeitgeschichte und Neuere Rechtsgeschichte (insbesondere Wissenschaftsgeschichte des öffentlichen Rechts).
Michael Jary wurde am 24.9.1906 in Laurahütte/Siemianowice (bei Kattowitz in Oberschlesien, heute in Polen) geboren. Jarys Vater war Werkmeister in der Königshütte, die Mutter, die das musische Interesse des Jungen früh erkannte, Schneiderin. Der kleine Jary sollte Missionar werden und wurde darum auf die Klosterschule Heiselgenkreuz der Steyler Missionare (in der Nähe von Neiße) geschickt. Dort entdeckte er seine Liebe zur Musik. Mit 18 Jahren verließ Jary das Kloster und besuchte das Konservatorium in Beuthen. Er leitete einen Kirchen- und Arbeiterchor und schrieb erste Kammermusikwerke, die der Sender Gleiwitz kurz nach seiner Gründung ausstrahlte. Das Stadttheater von Neiße und Plauen engagierte ihn schließlich als zweiten Kapellmeister. 1929 wurde Jary in die Staatlich-Akademische Musikhochschule zu Berlin aufgenommen, studierte dort Kompositionstechnik und Dirigieren. Als Mitglied der Meisterklasse begegnete er Musikern wie Arnold Schönberg und Igor Stravinsky. 1931 wurde ihm der Beethoven-Preises der Stadt Berlin verliehen.
Este artigo tem por objetivo investigar a correlação de pensamento entre três importantes nomes da segunda metade do século XIX – Friedrich Nietzsche, Sigmund Freud e Hugo von Hofmannsthal – que se debruçaram sobre as crises da identidade masculina frente ao retorno do matriarcado. Tendo a Viena fin-de-siècle como cenário, o feminino é apresentado aqui por intermédio de Electra, que no texto homônimo de Hofmannsthal representa não só o fortalecimento como a própria destruição da mulher.
NKG2D is a potent activating immunoreceptor expressed on nearly all cytotoxic lymphocytes promoting their cytotoxicity against self-cells expressing NKG2D ligands (NKG2DLs). NKG2DLs are MHC class I-like glycoproteins that usually are not expressed on “healthy” cells. Rather, their surface expression is induced by various forms of cellular stress, viral infection, or malignant transformation. Hence, cell surface NKG2DLs mark “dangerous” cells for elimination by cytotoxic lymphocytes and therefore can be considered as “kill-me” signals. In addition, NKG2DLs are up-regulated on activated leukocytes, which facilitates containment of immune responses. While the NKG2D receptor is conserved among mammals, NKG2DL genes have rapidly diversified during mammalian speciation, likely due to strong selective pressures exerted by species-specific pathogens. Consequently, NKG2DL genes are not conserved in man and mice, although their NKG2D-binding domains maintained structural homology. Human NKG2DLs comprise two members of the MIC (MICA/MICB) and six members of the ULBP family of glycoproteins (ULBP1–6) with MICA representing the best-studied human NKG2DLs by far. Many of these studies implicate a role of MICA in various malignant, infectious, or autoimmune diseases. However, conclusions from these studies often were limited in default of supporting in vivo experiments. Here, we report a MICA transgenic (MICAgen) mouse model that replicates central features of human MICA expression and function and, therefore, constitutes a novel tool to critically assess and extend conclusions from previous in vitro studies on MICA. Similarly to humans, MICA transcripts are broadly present in organs of MICAgen mice, while MICA glycoproteins are barely detectable. Upon activation, hematopoietic cells up-regulate and proteolytically shed surface MICA. Shed soluble MICA (sMICA) is also present in plasma of MICAgen mice but affects neither surface NKG2D expression of circulating NK cells nor their functional recognition of MICA-expressing tumor cells. Accordingly, MICAgen mice also show a delayed growth of MICA-expressing B16F10 tumors, not accompanied by an emergence of MICA-specific antibodies. Such immunotolerance for the xenoantigen MICA ideally suits MICAgen mice for anti-MICA-based immunotherapies. Altogether, MICAgen mice represent a valuable model to study regulation, function, disease relevance, and therapeutic targeting of MICA in vivo.
Mitochondrial cristae are connected to the inner boundary membrane via crista junctions which are implicated in the regulation of oxidative phosphorylation, apoptosis, and import of lipids and proteins. The MICOS complex determines formation of crista junctions. We performed complexome profiling and identified Mic13, also termed Qil1, as a subunit of the MICOS complex. We show that MIC13 is an inner membrane protein physically interacting with MIC60, a central subunit of the MICOS complex. Using the CRISPR/Cas method we generated the first cell line deleted for MIC13. These knockout cells show a complete loss of crista junctions demonstrating that MIC13 is strictly required for the formation of crista junctions. MIC13 is required for the assembly of MIC10, MIC26, and MIC27 into the MICOS complex. However, it is not needed for the formation of the MIC60/MIC19/MIC25 subcomplex suggesting that the latter is not sufficient for crista junction formation. MIC13 is also dispensable for assembly of respiratory chain complexes and for maintaining mitochondrial network morphology. Still, lack of MIC13 resulted in a moderate reduction of mitochondrial respiration. In summary, we show that MIC13 has a fundamental role in crista junction formation and that assembly of respiratory chain supercomplexes is independent of mitochondrial cristae shape.
Experimental results are presented for 180 in silico designed octapeptide sequences and their stabilizing effects on the major histocompatibility class I molecule H-2Kb. Peptide sequence design was accomplished by a combination of an ant colony optimization algorithm with artificial neural network classifiers. Experimental tests yielded nine H-2Kb stabilizing and 171 nonstabilizing peptides. 28 among the nonstabilizing octapeptides contain canonical motif residues known to be favorable for MHC I stabilization. For characterization of the area covered by stabilizing and non-stabilizing octapeptides in sequence space, we visualized the distribution of 100,603 octapeptides using a self-organizing map. The experimental results present evidence that the canonical sequence motives of the SYFPEITHI database on their own are insufficient for predicting MHC I protein stabilization.