995 resultados para 04081205 TM-53
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Welsch (Projektbearbeiter): Bekanntgabe der in der Vorversammlung gewählten Kandidaten des 53. Berliner Urwahlbezirks
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Mo. L. Fochs
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Vorbesitzer: Philipp III. von Kronberg; Anastasia von Westerburg; Johann Maximilian zum Jungen
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Vorbesitzer: Petrus Lupolt; Dominikanerkloster Frankfurt am Main
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22 Briefe zwischen Robert M. MacIver und Max Horkheimer, 1941-1947; 4 Briefe und Beilage zwischen Julius B. Maller vom Amercian Jewish Committee und Max Horkheimer, 1945-1946; 3 Briefe zwischen Eric Mann und Max Horkheimer, 1947; 13 Briefe und Beilagen zwischen Ludwig Marcuse und Max Horkheimer, 1941-1948 sowie 1 Manuskript von Ludwig Marcuse: War Guilt and Peace Aims, dazu von Max Horkheimer Gutachten und Entwürfe; 8 Briefe zwischen Siegfried Marck und Max Horkheimer, 1945-1950; 7 Briefe zwischen Claire Marck vom American Jewish Committee und Max Horkheimer, 1945-1946; 4 Briefe zwischen Alfred von Martin und Max Horkheimer, 1948-1949; 2 Briefe und Beilage zwischen Hugo Marx und Max Horkheimer, 1945; 44 Briefe und Beilage zwische Julius Marx und Max Horkheimer, 1945-1949; 2 Briefe und Beilage zwischen Heinrich Meng und Max Horkheimer, 10.07.1942, 29.10.1942; 5 Briefe zwischen Karl Menges und Max Horkheimer, 1943-1944; 8 Briefe und Beilage Karl A. Menninger, William C. Menninger und Max Horkheimer, 1941-1949; 23 und Beilage Joseph Messinger und Max Horkheimer, 1945-1949; 2 Briefe zwischen Robert K. Merton und Max Horkheimer, 1949; 1 Brief von Fritz Merz an Max Horkheimer, 1949; 9 Briefe zwischen Fred Mielke und Max Horkheimer, 1948-1950 siehe auch Alexander Mitscherlich; 1 Brief von Max Horkheimer bzw. Theodor W. Adorno an George Mintzer, ca. 1944; 5 Briefe zwischen Walter G. Muelder und Max Horkheimer, 1942-1943; 21 Briefe und Beilage zwischen Dorothy Mulgrave und Max Horkheimer, 1941-1948; 2 Briefe zwischen Arthur E. Murphy und Max Horkheimer, 1947;
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u.a.: Lieferprobleme bei Brockhaus; Privatbibliothek Schopenhauers; Vergleich der Philosophie Schopenhauers mit der slawischen Mythologie; Sexualität; Georg Wilhelm Friedrich Hegel; Russalki;
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Flucht 1866, Hilfs-Fond von Freunden, Abrechnung
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Trägerband: Inc. gr. fol. 3 Bd. 3; Vorbesitzer: Dominikanerkloster Frankfurt am Main
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Vorbesitzer: Abraham Merzbacher;
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comp. H. Henkel
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Vorbesitzer: Martin Hermann; Marcus Alstad; David Herckenrath;
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The epidermal growth factor receptor (EGFR) and its ligands are overexpressed in many human tumors, including bladder and pancreas, correlating with a more aggressive tumor phenotype and poor patient prognosis. We initiated the present study to characterize the heterogeneity of gefitinib responsiveness in a panel of human bladder and pancreatic cancer cell lines in order to identify the biological characteristics of EGFR-dependent proliferation that could be used to prospectively identify drug-sensitive tumors. A second objective was to elucidate how to best exploit these results by utilizing gefitinib in combination therapy. To these ends, we examined the effects of the EGFR antagonist gefitinib on proliferation and apoptosis in a panel of 18 human bladder cancer cell lines and 9 human pancreatic cancer cell lines. Our data confirmed the existence of marked heterogeneity in Iressa responsiveness with less than half of the cell lines displaying significant growth inhibition by clinically relevant concentrations of the drug. Gefitinib responsiveness was found to be p27 kip1 dependent as DNA synthesis was restored following exposure to p27siRNA. Unfortunately, Iressa responsiveness was not closely linked to surface EGFR or TGF-α expression in the bladder cancer cells, however, cellular TGF-α expression correlated directly with Iressa sensitivity in the pancreatic cancer cell lines. These findings provide the potential for prospectively identifying patients with drug-sensitive tumors. ^ Further studies aimed at exploiting gefitinib-mediated cell cycle effects led us to investigate if gefitinib-mediated TRAIL sensitization correlated with increased p27kip1 accumulation. We observed that increased TRAIL sensitivity following gefitinib exposure was not dependent on p27 kip1 expression. Additional studies initiated to examine the role(s) of Akt and Erk signaling demonstrated that exposure to PI3K or MEK inhibitors significantly enhanced TRAIL-induced apoptosis at concentrations that block target phosphorylation. Furthermore, combinations of TRAIL and the PI3K or MEK inhibitors increased procaspase-8 processing above levels observed with TRAIL alone, indicating that the effects were exerted at the level of caspase-8 activation, considered the earliest step in the TRAIL pathway. ^