Mitteilungen

Hugo Bergmann

Zündet Lichter an!

J. Bergmann

Na 1 Nachlass Max Horkheimer, 493 - Korrespondenzen mit Mitarbeitern (u.a. Gerhard Brand, Ludwig von Friedeburg und Jürgen Habermas) aus dem Institut für Sozialforschung (p. V 193, 1 - 212)

Briefe zwischen Mitarbeitern des Instituts für Sozialforschung und Max Horkheimer, 1964-1973; 13 Briefe und Beilagen zwischen dem Verwaltungsleiter IfS Siegfried Geissler und Max Horkheimer, 1968-1973; 9 Briefe zwischen Klaus Körber (Institut für Sozialforschung) und Max Horkheimer, 1971-1973; 2 Briefe zwischen dem Professor Rudolf Gunzert und Max Horkheimer, 1972; 2 Briefe zwischen Dr. Joachim Bergmann (Institut für Sozialforschung) und Max Horkheimer, 1971; 2 Briefe zwischen dem Professor Gerhard Brandt und Max Horkheimer, 1971; 6 Briefe zwischen Herbert Ludwig (Institut für Sozialforschung) und Max Horkheimer, 1966-1967; 3 Briefe von Max Horkheimer an Professor Franz Böhm, 1966; Briefe zwischen den Mitarbeitern des Instituts für Sozialforschung und Max Horkheimer, 1955-1959; 4 Briefe von Jürgen Habermas an Max Horkheimer, Frankfurt, 1957-1959; 3 Briefe zwischen Christoph Oehler und Max Horkheimer, 1959; 13 Briefe zwischen Ludwig von Friedeburg und Max Horkheimer, 1955-1959; 1 Brief von Werner Wilkening an Max Horkheimer, 1958; 1 Brief von Gerhard Brandt an Max Horkheimer, 1958; 1 Brief von Max Horkheimer an den Dekan Helmut Viebrock, 1958; 2 Briefe von Egon Becker mit Helge Pross und Ludwig Friedeburg an Max Horkheimer, Frankfurt, 1958-1959; 2 Briefe von Helge Pross mit Egon Becker und Ludwig Friedeburg an Max Horkheimer, Frankfurt, 1958-1959; 1 Brief von Dieter Arenz an Max Horkheimer, Frankfurt, 1956; Briefe vom und an das Institut für Sozialforschung (Advisory Board of the Institute of Social Research), 1940-1947; Briefe und Briefentwürfe an und von Mitgliedern des Advisory Board betreffend die Zusendung von Max Horkheimer "Eclipse of Reason" und Karl August Wittvogel/Olga Lang, "Chinese Family and Society"; vom Institut für Sozialforschung, 1946-1947; 1 Brief von Edwin Borchard vom Institut für Sozialforschung, 1947; 1 Brief von Friedrich Pollock an Alfred E. Cohn, Los Angeles, 1947; 1 Brief von Friedrich Pollock an Stephan Duggan, Los Angeles, 1947; 2 Briefe zwischen Lloyd K. Garrison und Friedrich. Pollock, 1947; 1 Brief von Friedrich Pollock an Calvin B. Hoover, Los Angeles, 1947; 1 Brief von Friedrich Pollock an Philip C. Jessup, Los Angeles, 1947; 1 Brief von Friedrich Pollock an Wesley C. Mitchell, Los Angeles, 1947; 1 Brief von Friedrich Pollock an William A. Neilson, Los Angeles, 1947; 1 Brief von Friedrich Pollock an Frederick M. Padelford, Los Angeles, 1947; 1 Brief von Friedrich Pollock an Thorsten Sellin, Los Angeles, 1947; 3 Briefe zwischen John Whyte und Friedrich Pollock, 1947; 2 Briefe zwischen Louis Wirth und Friedrich Pollock, 1947; 1 Brief von Friedrich Pollock an Howard Woolston, Los Angeles, 1947; 1 Brief von George H. Sabine an das Institut für Sozialforschung, Ithaca, New York, 1946; Briefe und Briefentwürfe an und von Mitgliedern des Advisory Board betreffend den Druck eines neuen Briefkopfs des Instituts, 1940; 1 Brief von Leo Löwenthal, Pacific Palisades an Margot von Mendelssohn, 1942; 1 Brief von Leo Löwenthal an Margot von Mendelssohn, Pacific Palisades, 1942; 1 Brief von Max Horkheimer an K. Pilser, 1942; 2 Briefe zwischen Charles A. Beard und Max Horkheimer, 1940; 2 Briefe zwischen Edwin M. Borchard und Max Horkheimer, 1940; 3 Briefe zwischen Henry Sloane Coffin und Max Horkheimer, 1940; 2 Briefe zwischen Morris R. Cohen und Max Horkheimer, 1940; 2 Briefe zwischen Alfred E. Cohn und Max Horkheimer, 1940; 2 Briefe zwischen Stephen Duggan und Max Horkheimer, 1940; 2 Briefe zwischen dem Soziologen Henry Pratt Fairchild und Max Horkheimer, 1940; 2 Briefe zwischen Sidney B. Fay und Max Horkheimer, 1940; 2 Briefe zwischen Lloyd K. Garrison und Max Horkheimer, 1940; 1 Brief von Max Horkheimer an Calvin B. Hoover, 1940; 2 Briefe zwischen Robert M. Hutchins und Max Horkheimer, 1940; 2 Briefe zwischen Philip C. Jessup und Max Horkheimer, 1940; 2 Briefe zwischen Lewis L. Lorwin und Max Horkheimer, 1940; 2 Briefe zwischen Robert S. Lynd und Max Horkheimer, 1940; 2 Briefe zwischen Robert M. MacIver und Max Horkheimer, 1940; 2 Briefe von Max Horkheimer an Charles H. McIlwain, 1940; 2 Briefe zwischen Charles E. Merriam und Max Horkheimer, 1940; 2 Briefe zwischen Wesley C. Mitchell und Max Horkheimer, 1940; 2 Briefe zwischen William A. Nielson und Max Horkheimer, 1940; 5 Briefe zwischen Howard W. Odum und Max Horkheimer, 1940; 3 Briefe zwischen Frederick M. Padelford und Max Horkheimer, 1940; 3 Briefe von Max Horkheimer an Max Radin, 1940; 2 Briefe zwischen George H. Sabine und Max Horkheimer, 1940; 2 Briefe zwischen Thorsten Sellin und Max Horkheimer, 1940; 2 Briefe zwischen James T. Shotwell und Max Horkheimer, 1940; 1 Brief von dem Soziologen Louis Wirth an Franz Neumann, Chicago, 1940; 1 Brief von Louis Wirth an Franz L. Neumann, Chicago, 1940; 3 Briefe zwischen Howard Woolston und Max Horkheimer, 1940;

Frankfurter Universitätszeitung : mit amtlichen Mitteilungen der Universität

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Elucidating the role of mesenchymal stem cell participation in the tumor microenvironment

To meet the requirements for rapid tumor growth, a complex array of non-neoplastic vascular, fibroblastic, and immune cells are recruited to the tumor microenvironment. Understanding the origin, composition, and mechanism(s) for recruitment of these stromal components will help identify areas for therapeutic intervention. Previous findings have suggested that ex-vivo expanded bone marrow-derived MSC home to the sites of tumor development, responding to inflammatory signals and can serve as effective drug delivery vehicles. Therefore, we first sought to fully assess conditions under which MSC migrate to and incorporate into inflammatory microenvironments and the consequences of modulated inflammation. MSC delivered to animals bearing inflammatory insults were monitored by bioluminescence imaging and displayed specific tropism and selective incorporation into all tumor and wound sites. These findings were consistent across routes of tumor establishment, MSC administration, and immunocompetence. MSC were then used as drug delivery vehicles, transporting Interferon β to sites of pancreatic tumors. This therapy was effective at inhibiting pancreatic tumor growth under homeostatic conditions, but inhibition was lost when inflammation was decreased with CDDO-Me combination treatment. Next, to examine the endogenous tumor microenvironment, a series of tissue transplant experiments were carried out in which tissues were genetically labeled and engrafted in recipients prior to tumor establishment. Tumors were then analyzed for markers of tumor associated fibroblasts (TAF): α-smooth muscle actin (α-SMA), nerve glia antigen 2 (NG2), fibroblast activation protein (FAP), and fibroblast specific protein (FSP) as well as endothelial marker CD31 and macrophage marker F4/80. We determined the majority of α-SMA+, NG2+ and CD31+ cells were non-bone marrow derived, while most FAP+, FSP+, and F4/80+ cells were recruited from the bone marrow. In accord, transplants of prospectively isolated BM MSC prior to tumor development indicated that these cells were recruited to the tumor microenvironment and co-expressed FAP and FSP. In contrast, fat transplant experiments revealed recruited fat derived cells co-expressed α-SMA, NG2, and CD31. These results indicate TAF are a heterogeneous population composed of subpopulations with distinct tissues of origin. These models have provided a platform upon which further investigation into tumor microenvironment composition and tests for candidate drugs can be performed. ^

NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS

Secondary metabolites are produced by numerous organisms and can either be benign to humans or harmful. Genes involved in the synthesis and transport of these secondary metabolites are frequently found in gene clusters, which are often located in subtelomeric regions of the chromosome. These clusters are often coordinately regulated, being almost exclusively dependent on transcription factors that are located within the clusters themselves. Secondary metabolites are also regulated by a variety of factors, including nutritional factors, environmental factors and developmental processes. Gliotoxin, which is produced by a variety of Aspergillus species, Trichoderma species, and Penicillium species, exhibits immunosuppressive properties and has therefore been the subject of research for many laboratories. There have been a few proteins shown to regulate the gliotoxin cluster, most notably GliZ, a Zn2Cys6 binuclear finger transcription factor that lies within the cluster, and LaeA, a putative methyltransferase that globally regulates secondary metabolism clusters within numerous fungal organisms, although no study has demonstrated the direct binding of any protein to a promoter region in the gliotoxin cluster. I report here two novel proteins, GipA, a C2H2 transcription factor and GipB, a hybrid sensor kinase, which are involved in regulating the gliotoxin biosynthetic cluster. GipA plays an important role in gliotoxin production, as high-copy expression of gipA induces gliotoxin biosynthesis and loss of gipA reduces gliotoxin biosynthesis by 50%. GipB is also involved in regulating gliotoxin production, as high-copy expression of gipB induces gliotoxin biosynthesis, but only during certain stages of asexual development. Furthermore, loss of gipB reduces gliotoxin biosynthesis by 10%. Based on data obtained from this project, I propose a model for the regulation of gliA, the efflux pump of the gliotoxin cluster, which involves GipB signaling through both GliZ and GipA. I propose that GliZ and GipA are interdependent, as mutation of the GipA DNA binding site in the gliA promoter negatively affects both GliZ-mediated and GipA-mediated induction of gliA. This is further supported by the fact that GliZ cannot fully induce gliA in the absence of GipA and vice versa. This is the first time that anyone has shown evidence of a protein directly binding to the gliotoxin cluster. Even though biosynthetic clusters are often coordinately regulated, my model raises the possibility that gliA is independently regulated, as the layout of the binding site in the gliA promoter is not present upstream of any other genes in the gliotoxin cluster, except for gliZ.