989 resultados para 29-278A


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Aufsätze auf der Grundlage der Vorträge IX 28, ausgearbeitet vom Institut für Sozialforschung; veröffentlicht in der Reihe "Frankfurter Beiträge zur Soziologie", Frankfurt, 1956; "Zum Begriff der Soziologie". Typoskript mit handschriftlichen Korrekturen, 20 Blatt; "Gesellschaft". Typoskript mit handschriftlichen Korrekturen, 30 Blatt; "Individuuen". Typsokript mit handschriftlichen Korrekturen, 26 Blatt; "Gruppe". Typoskript mit handschriftlichen Korrekturen, 25 Blatt; "Die Masse". Typsokript mit handschriftlichen Korrekturen, 23 Blatt; "Kultur und Zivilisation". Typoskript mit handschriftlichen Korrekturen, 20 Blatt; "Kunst- und Musiksoziologie". Typoskript mit handschriftlichen Korrekturen, 22 Blatt; "Vorurteil". Typoskript mit handschriftlichen Korrekturen, 16 Blatt; "Ideologie". Typoskript mit handschriftlichen Korrekturen, 31 Blatt; Pollock, Friedrich: 10 Briefe an Theodor W. Ardono, Zürich, 1955; 7 Briefe mit Unterschrift von Theodor W. Adorno, Frankfurt, 1955; 27 Blatt; Hirzel, Johannes: 2 Briefe mit Unterschrift an Friedrich Pollock und Beilagen, Frankfurt, 1955; 4 Blatt; Adorno, Theodor W. : 2 Briefe mit Unterschrift an Max Horkheimer, ohne Ort, 1955; 2 Blatt; Kux, Ernst: 1 Brief an Max Horkheimer und Beilagen, Zürich, 07.01.1954; 8 Blatt; Literaturverzeichnis; 20 Blatt; Pollock, Friedrich: Memoranden und Notizen zur Bearbeitung und Herausgabe der "Soziologischen Exkurse"; Maus, Heinz: Memorandum zur Bearbeitung der Vorträge; Typoskript, 2 Blatt; siehe auch VIII 42.3-4 und XIII 22;

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"Einleitung in die Philosophie", Wintersemester 1932/33, eigenhändige Notizen, 1 Heft, 12 Blatt, davon 5 leer, und 8 zusätzliche Blätter; Zwei Aufsätze vor 1933 (enthält: "Über Kants Philosophie", Typoskript mit eigenhändigen Korrekturen, 8 Blatt. Mit 1 Blatt von Theodor W. Adorno an Max Horkheimer, 29.04.1954 (GS 11, S. 202-208; "Nicolai Hartmann", ca 1931, Typoskript mit eigenhändigen Korrekturen, 6 Blatt (GS 2, S. 172-176)); "Zur Emanzipation der Philosophie von der Wissenschaft" (GS 10, S. 334-419). Über Empiriokritizismus (Mach), Neukantianismus (Cohen), Phänomenologie (Husserlm Scheler), Lebensphilosophie (Bergson), nach 1927 - vor 1933; a) Typoskript mit eigenhändigen Korrekturen, gebunden, 114 Blatt, b) Typoskript mit handschriftlichen Korrekturen, 109 Blatt; Über Erkenntnistheorie und Gestalttheorie (GS 11, S. 22-69), Manuskript, in 2 Heften (Heft 1, 96 Blatt; Heft 2, 32 Blatt);

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208 Briefe zwischen Margot von Mendelssohn und Max Horkheimer; 1 Brief von Max Horkheimer und Arthur Gagliotti, 23.09.1948; 1 Brief an Robert Alexander (Arzt) von Margot von Mendelssohn, 15.06.1948; 3 Briefe zwischen Margot von Mendelssohn und Frederick Pollock, Januar 1946; 1 Brief an U. S. Attorney (Los Angeles) von Max Horkheimer, [1946]; 1 Brief von Hilda Kahn an Margot von Mendelssohn, 27.01.1944;

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208 Briefe zwischen Margot von Mendelssohn und Max Horkheimer; 1 Brief von Max Horkheimer an H. L. Byram, 01.05.1954; 1 Brief an Margot von Mendelssohn von Edgar E. Walden, 16.04.1954; 1 Brief von Robert S. Butts an Margot von Mendelssohn, [1954];

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Vorbesitzer: Johann Hartmann Beyer

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c-Src, a protein tyrosine kinase (PTK) the specific activity of which is increased $>$20-fold in $\sim$80% of colon tumors and colon tumor cell lines, plays a role in both growth regulation and tumorigenicity of colon tumor cells. To examine the effect of increased c-Src specific activity on colon tumor cells, coumarin-derived tyrosine analog PTK inhibitors were assessed in a standard colon tumor cell line, HT-29. Of the nine compounds tested for inhibiting c-Src activity in a standard immune complex kinase assay from c-Src precipitated from HT-29 cells, the 7,8-dihydroxy-containing compounds daphnetin and fraxetin were most effective, with IC$\sb{50}$s of 0.6 $\pm$ 0.2 mM and 0.6 $\pm$ 0.3 mM, respectively. Treatment of HT-29 cells with daphnetin resulted in inhibition of cell growth in a dose-dependent manner. In contrast, scopoletin, a relatively poor Src inhibitor in vitro, did not inhibit HT-29 cell growth in the concentration range tested. In daphnetin treated cells, a dose-dependent decrease of c-Src activity paralleling cell growth inhibition was also observed; the IC$\sb{50}$ was 0.3 $\pm$ 0.1 mM for c-Src autophosphorylation. In contrast, the IC$\sb{50}$ for c-Src protein level was $>$ 0.6 mM, indicating that the effects of daphnetin were primarily an enzymatic activity of c-Src, rather than protein level in HT-29 cells. These results are the first to demonstrate that c-Src specific activity regulates colon tumor cell growth.^ To elucidate the signaling pathways activated by c-Src in colon tumor cells, the Src family substrate FAK, which has been shown to play a role in both extracellular matrix-dependent cell growth and survival, was examined. Coprecipitation assays showed Src-FAK association in detergent insoluble fractions of both attached and detached HT-29 cells, indicating that Src-FAK association in HT-29 cells is stable and, unlike untransformed cells, not dependent on cell-substratum contact. FAK also coprecipitated with Grb2, an adaptor protein also playing a role in cell proliferation and survival, in both attached and detached HT-29 cells, suggesting that a Src-FAK-Grb2-mediated signaling pathway(s) in HT-29 cells is/are constitutively activated.^ FAK was also analyzed in c-src antisense HT-29 clones AS15 and AS33 in which c-Src is specifically reduced by transfection of an antisense expression vector. FAK protein level is unexpectedly decreased in both AS15 and AS33 cells by 5-fold and 1.5-fold compared to HT-29, respectively, corresponding with the decreased expression of c-Src observed in these cells. FAK protein level was not decreased compared to parental in the c-src "sense" clone S8. Northern blot analyses showed decreased FAK mRNA levels compared to parental in AS15 and AS33, correlating with decreased FAK protein level, indicating that FAK activity in the antisense cells is regulated, at least in part, by altering FAK expression, and that this regulation is Src dependent. Because FAK has been implicated in anoikis, the ability of c-src antisense cells to survive in the absence of cell-substratum contact was examined. Decreased cell survival is seen in both AS15 and AS33, correlating with the decreases in c-Src and FAK levels and tumorigenicity in these cells. These results suggest that at least one mechanism by which activation of c-Src contributes to tumorigenic phenotype of colon tumor cells is by aberrantly promoting a survival signal through unregulated Src-FAK-Grb2 complexes. (Abstract shortened by UMI.) ^

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