Fragm. lat. VI 42 - Graduale (Fer.V in Coena Domini, Parasc.; Juliana)

Trägerbände: Inc. qu. 801; Inc. oct. 276; Inc. oct. 310; Vorbesitzer: Dominikanerkloster Frankfurt am Main

Na 1 Nachlass Max Horkheimer, 599 - Korrespondenzen u.a. mit Friedrich Pollock und Karl August Wittfogel (p. VI 42, 1-210)

Briefwechsel zwischen Max Horkheimer, Frederick Pollock und Karl August und Olga Wittfogel; 1 Brief von Karl August Wittfogel an Stephen Duggan, 02.08.1936; 2 Briefe an Max Horkheimer von Karl August Wittfogel, November 1937; 1 Brief von Karl August Wittfogel an Carter, 16.07.1936; 1 Brief an den American Consul General (Tientein, China) von Max Horkheimer, 03.04.1936; 1 Brief von Max Horkheimer an Owen Lattimore, 28.12.1935;

Na 1 Nachlass Max Horkheimer, 600 - Korrespondenzen u.a. mit Friedrich Pollock (p. VI 42, 211-386)

Briefwechsel zwischen Max Horkheimer, Frederick Pollock und Karl August und Olga Wittfogel; 2 Briefe zwischen Edith B. Bernett und Max Horkheimer, April 1940; 2 Briefe zwischen Max Horkheimer und Philip Vaudrin, Juli 1939; 3 Briefe an David H. Stevens von Max Horkheimer, 26.03.1938; 1 Brief von A. Radcliffe an Frederick Pollock, 18.11.1937; 3 Briefe an Max Horkheimer von der Columbia University Faculty of Political Science (New York), November 1937; 2 Briefe von der Columbia University Department of History (New York) an Max Horkheimer, November 1937; 1 Brief an Max Horkheimer von Sharon Beard, 27.11.1937; 1 Brief von Ruth Benedict an Max Horkheimer, 19.11.1937; 1 Brief an Max Horkheimer von Franz Boas, 19.11.1937; 1 Brief von R. E. Chaddock an Max Horkheimer, 21.11.1937; 1 Brief an Max Horkheimer von Ch'ao-ting Chi, 19.11.1937; 1 Brief von J. M. Clark an Max Horkheimer, 22.11.1937; 1 Brief an Dr. Wertheimer von Morris R. Cohen, 29.11.1937; 1 Brief von Alfred E. Cohn an Max Horkheimer, 26.11.1937; 1 Brief an Max Horkheimer von John J. Coss, 22.11.1937; 1 Brief von George S. Counts an Max Horkheimer, 24.11.1937; 1 Brief an Max Horkheimer von A. P. Evans, 22.11.1937; 3 Briefe von Gertrude Stewart an Max Horkheimer, 20. - 24.11.1937; 1 Brief an Max Horkheimer von L. C. Goodrich, 22.11.1937; 1 Brief von John W. Innes an Max Horkheimer, 20.11.1937; 1 Brief an Max Horkheimer von Philip C. Jessup, 24.11.1937; 1 Brief von John A. Krout an Max Horkheimer, 23.11.1937; 1 Brief an Max Horkheimer von Bruno Lasker, 20.11.1937; 1 Brief von Samuel McCune Lindsay an Max Horkheimer, 24.11.1937; 1 Brief an Max Horkheimer von K. N. Llewellyn, 26.11.1937; 1 Brief von R. S. Lynd an Max Horkheimer, [November 1937]; 1 Brief an Max Horkheimer von R. M. MacIver, 19.11.1937; 1 Brief von Julian W. Mack an Max Horkheimer, 24.11.1937; 1 Brief an Max Horkheimer von Arthur Maxmahon, 20.11.1937; 1 Brief von Jerome Michael an Max Horkheimer, 26.11.1937; 1 Brief an Max Horkheimer von Wesley C. Mitchell, 22.11.1937; 1 Brief von der Columbia University School of Business (New York) an Max Horkheimer, 22.11.1937; 2 Briefe zwischen Max Horkheimer und der John Simon Guggenheim Memorial Foundation (New York), November 1937; 2 Briefe von der Columbia University Department of Psychology (New York) an Max Horkheimer, November 1937; 1 Brief an Max Horkheimer von Goodwin Watson, 23.11.1937; 1 Brief von Otto Nathan an Max Horkheimer, 26.11.937; 1 Brief an Max Horkheimer von John K. Norton, 23.11.1937; 1 Brief von der Columbia University Department of Chinese (New York) an Max Horkheimer, 23.11.1937; 1 Brief an Max Horkheimer von Gerold Tanquary Robinson, 19.11.1937; 1 Brief von der Columbia University Department of Public Law and Government (New York) an Max Horkheimer, 22.11.1937; 1 Brief an Max Horkheimer von R. C. Sailer, 20.11.1937; 1 Brief von Herbert W. Schneider an Max Horkheimer, 22.11.1937; 1 Brief an Max Horkheimer von R. L. Schuyler, 20.11.1937; 1 Brief von Pauline Steorns an Max Horkheimer, 22.11.1937; 1 Brief an Max Horkheimer von Frank Tannenbaum, 19.11.1937; 1 Brief von Alfred Vagés an Max Horkheimer, 26.11.1937;

Tumor heterogeneity dictates sensitivity to gefitinib (Iressa(TM)/ZD1839) in solid tumor models

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. ^

Description and chemical composition of ferromanganese encrustations and deposits in the Atlantic Ocean from R/V Atlantis II cruises 20, 42, 60, 85; R/V Chain cruise 35; R/V Knorr cruise 61 and RRS Shackleton cruise 75/1 stations

Chemical and mineralogical compositions of ferromanganese oxide coatings on rocks dredged from the New England Seamounts, the Sierra Leone Rise and the Mid-Atlantic Ridge near the Equator have been determined in an investigation of regional differences in Atlantic ferromanganese deposits. Most encrustations are clearly of hydrogenous origin, consisting mainly of todorokite and delta MnO2, but several recovered from the equatorial fracture zones may be hydrothermal accumulations. Differences in the chemistry of the water column and in growth rates of the ferromanganese coatings may be important in producing this regional contrast in composition. Fine-scale changes in element abundances within the encrustations indicate that the nature of the substrate has little influence on compositional variations.