26 research outputs found

    Die Hörspiele von Wolfgang Ambros, Josef Prokopetz und M.O. Tauchen

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    Der österreichische SĂ€nger und Songschreiber Wolfgang Ambros hat zwischen 1973 und 1981 vier Hörspiele veröffentlicht. Verfasst hat er sie gemeinsam mit Josef Prokopetz und M.O. Tauchen. Die vorliegende Dissertation setzt diese Werke, popularkulturelle Sozialsatiren, in Bezug zum Wiener Volkstheater. Der Autor wollte beweisen, dass die Ambros-Hörspiele FĂ€ustling, Der Watzmann ruft, Schaffnerlos und Augustin in der Tradition des Wiener Volkstheaters stehen. Das bedeutet aber nicht, dass von den UrsprĂŒngen der Wiener Volkskomödie eine durchgĂ€ngige Traditionslinie von Joseph Anton Stranitzky ĂŒber Johann Nestroy bis zu Wolfgang Ambros und der Musikbewegung Austropop verfolgt wurde, sondern, dass VersatzstĂŒcke des Wiener Volkstheaters in den untersuchten Hörspielen ausfindig gemacht, analysiert und interpretiert wurden. In diesem Kontext wurde auch ein großes Augenmerk darauf gelegt die literarische QualitĂ€t der Hörspiele von Ambros, Prokopetz und Tauchen herauszuarbeiten um ihnen auf diesem Weg den ihnen gebĂŒhrenden Rang in der österreichischen Hörspiel- und Literaturgeschichte zu geben. DarĂŒberhinaus wurde auch auf die zum Teil hohe QualitĂ€t zahlreicher anderer Songtexte von Wolfgang Ambros, Josef Prokopetz und vor allem jenen von Georg Danzer hingewiesen. Austropop ist nicht nur ein Teil österreichischer Musik-, sondern auch Literaturgeschichte. Dieses Faktum in der Forschung zu etablieren ist eines der Hauptanliegen der vorliegenden Doktorarbeit. Die vier untersuchten Hörspiele sind in ihrem sozialsatirischen Impetus und durch ihre mannigfaltige kĂŒnstlerische Gestaltung als Prototypen der traditionsbrechenden Haltung des Austropop anzusehen und das, weil beziehungsweise obwohl sie aus der Tradition mit der Tradition, in diesem Falle, der des Wiener Volkstheaters, arbeiten. Dieses Oszillieren zwischen Traditionsbruch und Weiterleben der Tradition möchte der Verfasser mit seiner Dissertation versuchen aufzuzeigen.The Austrian singer and songwriter Wolfgang Ambros published between 1973 and 1981 four radio plays. He wrote them together with Josef Prokopetz and M.O. Tauchen. This dissertation examines the reference of these works to the Viennese Volkstheater. The Ambros-radio-plays, the author calls them “popular-cultural social satires”, FĂ€ustling, Der Watzmann ruft, Schaffnerlos and Augustin keep the tradition of the Viennese Volkstheater. That doesn’t mean, that there is a continous and incessant tradition from Joseph Anton Stranitzky to Johann Nestroy and from Johann Nestroy to Wolfgang Ambros and the musical movement called “Austropop” - it means, that rudiments and elements of the Viennese Volkstheater live on in the radio plays of Ambros, Tauchen and Prokopetz. In this context the author also investigated and analysed the partially high literary quality of Ambros’ radio plays, his and the songs of Georg Danzer. The lyrics of Ambros, Prokopetz and primarily Danzer and also the examined radio plays are part of the Austrian history of literature and history of radio plays. This doctoral thesis wants to treat these radio plays and songs with the kind of due respect the Austrian history of literature and radio plays has been ignoring until today. FĂ€ustling, Der Watzmann ruft, Schaffnerlos and Augustin are classic examples for Austropop, a movement which breakes with (musical) traditions and social taboos even though the protagonists of Austropop work with traditional elements, in this case with elements of the Viennese Volkstheater. The radio plays of Ambros, Prokopetz and Tauchen oscillate between destruction, disruption, mutation, metamorphosis and preservation of tradition. To work out this fact is the purpose of the dissertation Die Hörspiele von Wolfgang Ambros, Josef Prokopetz und M.O. Tauchen. Popularkulturelle Sozialsatiren in der Tradition des Wiener Volkstheaters

    Bile acids reduce endocytosis of high-density lipoprotein (HDL) in HepG2 cells.

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    High-density lipoprotein (HDL) transports lipids to hepatic cells and the majority of HDL-associated cholesterol is destined for biliary excretion. Cholesterol is excreted into the bile directly or after conversion to bile acids, which are also present in the plasma as they are effectively reabsorbed through the enterohepatic cycle. Here, we provide evidence that bile acids affect HDL endocytosis. Using fluorescent and radiolabeled HDL, we show that HDL endocytosis was reduced in the presence of high concentrations of taurocholate, a natural non-cell-permeable bile acid, in human hepatic HepG2 and HuH7 cells. In contrast, selective cholesteryl-ester (CE) uptake was increased. Taurocholate exerted these effects extracellularly and independently of HDL modification, cell membrane perturbation or blocking of endocytic trafficking. Instead, this reduction of endocytosis and increase in selective uptake was dependent on SR-BI. In addition, cell-permeable bile acids reduced HDL endocytosis by farnesoid X receptor (FXR) activation: chenodeoxycholate and the non-steroidal FXR agonist GW4064 reduced HDL endocytosis, whereas selective CE uptake was unaltered. Reduced HDL endocytosis by FXR activation was independent of SR-BI and was likely mediated by impaired expression of the scavenger receptor cluster of differentiation 36 (CD36). Taken together we have shown that bile acids reduce HDL endocytosis by transcriptional and non-transcriptional mechanisms. Further, we suggest that HDL endocytosis and selective lipid uptake are not necessarily tightly linked to each other

    GW4064 and CDCA reduce CD36 expression and function.

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    <p>(a) HepG2 cells were treated with the indicated concentrations of GW4064 or chenodeoxycholate (CDCA) in media containing lipoprotein-deficient serum (lpds) for 24 hours and gene expression was analyzed by qRT-PCR (n = 3). (b) Cells were incubated with 10 ”M GW4064 or 100 ”M CDCA in media containing lpds for 24 hrs and protein expression was determined by western blot analysis and results were quantitated by densitometry (n = 3). (c) Fatty-acid uptake was determined after treatment with 10 ”M GW4064 or 100 ”M CDCA as described in the methods section (n = 3).</p

    Taurocholate reduces HDL endocytosis SR-BI-dependently.

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    <p>(a) HepG2 cells were incubated with or without 1 mM taurocholate and ATP hydrolysis was measured as a decrease in extracellular ATP. One representative experiment out of three independent experiments is shown. (b) SR-BI knockdown efficiency in HepG2 cells transfected with scrambled shRNA and HepG2 cells transfected with SR-BI shRNA (n = 3). Selective lipid uptake analysis using double labeled <sup>125</sup>I/<sup>3</sup>H-CE-HDL in scrambled control (c) or SR-BI knockdown (d) HepG2 cells (n = 3). Selective cholesteryl-ester uptake was calculated by subtracting <sup>125</sup>I-HDL uptake from <sup>3</sup>H-CE-HDL uptake.</p

    Bile acids and a non-steroidal FXR agonist reduce HDL endocytosis.

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    <p>(a) HepG2 cells were treated with the indicated concentrations of GW4064 or chenodeoxycholate (CDCA) in media containing lipoprotein-deficient serum (lpds) for 24 hours. Gene expression was analyzed by qRT-PCR and expression levels were normalized to GAPDH expression (n = 2). The increase in SHP mRNA indicates FXR activation. (b) HepG2 cells were incubated with 10 ”M GW4064 or 100 ”M CDCA in media containing lpds for 24 hours. Cells were then incubated with 50 ”g/ml HDL-Alexa<sup>488</sup> for 1 hour. Cells were fixed, counterstained with DAPI and imaged. Green: HDL; blue: nucleus; bar = 10 ”m. (c) Quantification of fluorescence intensities of (b). (d) HepG2 cells were incubated with 10 ”M GW4064 or 100 ”M CDCA in media containing lpds for 24 hours. Cells were then incubated with 20 ”g/ml <sup>125</sup>I-HDL for 1 hour. Uptake was determined after displacing cell surface bound HDL by a 100-fold excess at 4°C for 1 hour (n = 3).</p

    Integrated Biological Control of the Sugar Beet Weevil <i>Asproparthenis punctiventris</i> with the Fungus <i>Metarhizium brunneum</i>: New Application Approaches

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    The mass occurrence of the sugar beet weevil (Asproparthenis punctiventris, previously Bothynoderes punctiventris) has been endangering sugar beet cultivation in Austria for centuries. Exacerbated by climatic and political changes (warmer, drier spring and limited access to chemical pesticides), new approaches are needed to counter the problem. The aim of our work was to test whether the bioinsecticide Metarhizium brunneum Ma 43 (formerly M. anisopliae var. anisopliae BIPESCO 5/F52) can be used as a sustainable plant protection product against the sugar beet weevil. Our goal was to control the pest in all its development stages through multiple applications. Therefore, GranMetTM-P, a granular formulation of M. brunneum Ma 43, was applied in spring to establish the fungus in the soil, whereas GranMetTM-WP, a liquid formulation of the production strain, was used in early summer on trap ditches and leaves to target the adult weevils. Soil and plant samples as well as weevils were collected during the planting season from the trial sites to evaluate the development of the fungus and the mycosis of the treated weevils. In addition, data on hibernating weevils and their emigration from untreated field sites was collected. In all field sites, the Metarhizium spp. abundance increased above the background level (−1 soil dry weight) after application of the product. With an increasing number of treatments per plot, and thus an increased contact possibility between pest and the fungus, a rise in the mycosis rate was observed. In conclusion, the various Metarhizium application strategies, which are already available or in testing, must be implemented to ensure control in both old and new sugar beet fields. Metarhizium is a further asset in the successful control of this sugar beet pest

    Taurocholate neither exerts cytotoxic effects, nor inhibits transferrin or LDL endocytosis in HepG2 cells.

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    <p>(a) Cells were incubated with the indicated concentrations of taurocholate for 1 hour. No release of LDH into the cell culture supernatant was detected. 0.1% Triton-X100 was used as a positive control. (b) Cells were incubated with 20 ”g/ml transferrin-Alexa<sup>488</sup> (b) or 50 ”g/ml LDL-Alexa<sup>568</sup> (c) with or without 1 mM taurocholate at 37°C for 1 hour. Cells were fixed, counterstained with DAPI and imaged. Green: transferrin; red: LDL; blue: nucleus; bar = 10 ”m. Neither transferrin nor LDL uptake were altered. Quantifications of fluorescent signals are depicted next to the images. (d) Cells were incubated with or without 1 mM taurocholate for 1 hour. Cells were fixed, stained with Filipin and imaged. Bar = 10 ”m. Representative images of 3 independent experiments are shown.</p

    GW4064 and CDCA reduce HDL endocytosis independently of SR-BI.

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    <p>(a) HepG2 cells were treated with the indicated concentrations of GW4064 or chenodeoxycholate (CDCA) in media containing lipoprotein-deficient serum (lpds) for 24 hours and gene expression was analyzed by qRT-PCR (n = 3). (b) Cells were incubated with 10 ”M GW4064 or 100 ”M CDCA in media containing lpds for 24 hrs and protein expression was determined by western blot analysis and results were quantitated by densitometry (n = 3). HepG2 cells transfected with scrambled shRNA (c) or SR-BI shRNA (d) were incubated with 10 ”M GW4064 or 100 ”M CDCA in media containing lpds for 24 hours. Cells were then incubated with 20 ”g/ml double labeled <sup>125</sup>I/<sup>3</sup>H-CE-HDL for 1 hr. Selective cholesteryl-ester uptake was calculated by subtracting <sup>125</sup>I-HDL uptake from <sup>3</sup>H-CE-HDL uptake (n = 3).</p

    Modification of HDL by taurocholate does not alter endocytosis.

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    <p>(a) HDL was incubated with or without 1 mM taurocholate in media in the absence of cells for 1 hour. HDL size was then analyzed by size exclusion chromatography. HDL incubated with taurocholate is eluted earlier, indicating increased size. (b) HDL-Alexa<sup>488</sup> was incubated with or without 1 mM taurocholate in media in the absence of cells for 1 hour. Free taurocholate was then removed using gel filtration and HepG2 cells were incubated with this modified HDL-Alexa<sup>488</sup> for 1 hour. Cells were fixed, counterstained with DAPI and imaged. (c) Quantification of fluorescence intensities from (b); n = 3. Green: HDL; blue: nucleus; bar = 10 ”m.</p
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