Hs. Rothschild 2° 63 - Sammlung von Costümblättern

Vorbesitzer: Freiherrlich Carl von Rothschild'sche Bibliothek Frankfurt am Main; Akzessionsnummer: x18722

Die Sammlung Erich von Goldschmidt Rothschild

eingel. von L. Schnorr von Carolsfeld. Beschrieben von L. Schnorr von Carolsfeld und H. Huth

Na 1 Nachlass Max Horkheimer, 38 - Korrespondenzen u.a. mit Arthur E. Nadel (p. I 19, 1-102)

40 Briefe zwischen Arthur E. Nadel und Max Horkheimer, 1934-1939; 1 Brief von Arthur E. Nadel an Armin Hodler, 02.02.1939; 18 Briefe zwischen Otto Nathan und Max Horkheimer, 1934-1940; 1 Brief von Friedrich Pollock an Paul Tillich, 12.11.1938; 5 Briefe zwischen dem National Council of Jewish Women New York Section und Max Horkheimer, 1937-1939; 1 Brief vom National Council of Parent Education Poughkeepsie, New York an Max Horkheimer, 17.06.1940; 1 Brief vom National Research Council Washington an Max Horkheimer, 15.02.1941; 2 Briefe zwischen dem National Roster of Scientific and Specialized Personnel Washington und Max Horkheimer, 1940; 2 Briefe zwischen Lisel Nädele und Max Horkheimer, 11.12.1939, 22.01.1940; 1 Brief von Benjamin Nathaniel Nelson an Max Horkheimer, 20.04.1938 sowie Briefwechsel mit der C.R.B. Educational Foundation, New York; 2 Briefe zwischen der C.R.B. Educational Foundation, New York und Max Horkheimer, 16.12.1937; 1 Brief von Max Horkheimer an Neumann, 08.07.1934; 3 Briefe und Beilage zwischen Fritz Neumark, Jenny Neumark und Max Horkheimer, 08.08.1939 sowie Briefwechsel mit Otto Strauß; 2 Briefe zwischen Otto Strauß vom Selfhelp for German Emigree New York und Max Horkheimer, 01.08.1939, 04.08.1939;

Das Haus Rothschild : seine Geschichte und seine Geschäfte ; Aufschlüsse und Enthüllungen zur Geschichte des Jahrhunderts, insbesondere des Staatsfinanz- und Börsenwesens ; zum erstenmale dargestellt

[Friedrich Arnold Steinmann]

Rothschild-Literatur : Sammlung von Zeitungsausschnitten, die sich auf das Haus Rothschild beziehen

Fingierter Hauptsachtitel. Digitalisat der Original-Zeitungsausschnitte der Universitätsbibliothek Frankfurt am Main

Rothschild-Rosen

Anonym

Ms.Ff.F.Stoltze 3. 398 - Brief von Friedrich Stoltze an Caroline Rothschild

Sein Hund und dessen Bellen

Hs. Rothschild 8° 63 - Hertzog Ernst von Bayern. Abschrift der Herzog Ernst-Handschrift D in Gotha

Vorbesitzer: Freiherrlich Carl von Rothschild'sche Bibliothek Frankfurt am Main (Bibliothek für Neuere Sprachen und Musik)

Ms. germ. oct. 350 - Geometrischer Grundriss der dem Freiherrn C. M. von Rothschild, in Bornheimer Gemarkung, zustehenden Guenthersburg nebst den dazu gehörenden Gärten und deren nächsten Umgebung.

Vorbesitzer: Freiherrlich Carl von Rothschild'sche Bibliothek Frankfurt am Main; alte Signatur: Gs 215/300; Akzessionsnummer: 19195

M. Carl von Rothschild, Brustbild

Signatur des Originals: S 36/G02086

Dictionnaire hébreu-français : contenant 1. La nomenclature et la traduction de tous les mots hébreux et chaldéens contenus dans la bible et dans le rituel des prières journalières ...

N. Ph. Sander et I. Trenel

Gender differences in colorectal cancer screening and incidence in large nationwide, population-based cohorts

Background. A few studies have reported gender differences along the colorectal cancer (CRC) continuum but none has done so longitudinally to compare a cancer and a non-cancer populations.^ Objectives and Methods. To examine gender differences in colorectal cancer screening (CRCS); to examine trends in gender differences in CRC screening among two groups of patients (Medicare beneficiaries with and without cancer); to examine gender differences in CRC incidence; and to examine for any differences over time. In Paper 1, the study population consisted of men and women, ages 67–89 years, with CRC (73,666) or without any cancer (39,006), residing in 12 U.S. Surveillance Epidemiology and End-Results (SEER) regions. Crude and age-adjusted percentages and odds ratios of receiving fecal occult blood test (FOBT), sigmoidoscopy (SIG), or colonoscopy (COL) were calculated. Multivariable logistic regression was used to assess gender on the odds of receiving CRC screening over time.^ In Paper 2, age-adjusted incidence rates and proportions over time were reported across race, CRC subsite, CRC stage and SEER region for 373,956 patients, ages 40+ years, residing in 9 SEER regions and diagnosed with malignant CRC. ^ Results. Overall, women had higher CRC screening rates than men and screening rates in general were higher in the SEER sample of persons with CRC diagnosis. Significant temporal divergence in FOBT screening was observed between men and women in both cohorts. Although the largest temporal increases in screening rates were found for COL, especially among the cohort with CRC, little change in the gender gap was observed over time. Receipt of FOBT was significantly associated with female gender especially in the period of full Medicare coverage. Receipt of COL was also significantly associated with male gender, especially in the period of limited Medicare coverage.^ Overall, approximately equal numbers of men (187,973) and women (185,983) were diagnosed with malignant CRC. Men had significantly higher age-adjusted CRC incidence rates than women across all categories of age, race, subsite, stage and SEER region even though rates declined in all categories over time. Significant moderate increases in rate difference occurred among 40-59 year olds; significant reductions occurred among patients age 70+, within subsite rectum, unstaged and distant stage CRC, and eastern and western SEER regions. ^ Conclusions. Persistent gender differences in CRC incidence across time may have implications for gender-based interventions that take age into consideration. A shift toward proximal cancer was observed over time for both genders, but the high proportion of men who develop rectal cancer suggests that a greater proportion of men may need to be targeted with newer screening methods such as fecal DNA or COL. Although previous reports have documented higher CRC screening among men, higher incidence of CRC observed among men suggests that higher risk categories of men are probably not being reached. FOBT utilization rates among women have increased over time and the gender gap has widened between 1998 and 2005. COL utilization is associated with male gender but the differences over time are small.^

MUTATIONS IN STAT3 ASSOCIATED WITH HUMAN HYPER IgE SYNDROME ENHANCE NFκB AND MAPK-MEDIATED GENE EXPRESSION

Hyper IgE syndrome (HIES) is a multisystem disorder resulting in bone and immune system abnormalities. It is associated with mutations in STAT3, which disrupt protein domains responsible for transcriptional function. Patients with HIES display osteoporosis and enhanced inflammatory cytokine production similar to hematopoietic Stat3-deficient mice. Since osteoclast and inflammatory cytokine genes are NFκB targets, these observations indicate a possible deregulation of NFκB signaling in both mice and humans with STAT3-deficiency. Here, we sought to examine the role of STAT3 in the regulation of NFκB-mediated gene expression through analysis of three HIES STAT3 point mutations in both hematopoietic and non- hematopoietic cells. We found that IL-6-induced tyrosine phosphorylation of STAT3 was partially or completely abrogated by HIES mutations in the transactivation domain (V713L) or SH2 domain (V637M), respectively, in both hematopoietic and non- hematopoietic cells. By contrast, IL-6-induced tyrosine phosphorylation of an HIES mutant in the STAT3 DNA-binding domain (R382W) was intact. The R382W and V713L mutants significantly reduced IL-6-dependent STAT3 transcriptional activity in reporter gene assays. Moreover, the R382W and V637M mutants significantly diminished IL-6-responsive expression of the endogenous STAT3 target gene, Socs3, as assessed by quantitative real-time PCR (qPCR) in the RAW macrophage cell line. These observations indicate the HIES mutants dominantly suppress the transcriptional activity of wild type STAT3, albeit to varying degrees. All three HIES mutants enhanced LPS-induced expression of the NFκB target genes IL6 (IL-6), Cxcl10 (IP- 10), and Tnf (TNFα) in RAW cells, as indicated by qPCR. Furthermore, overexpression of wild type STAT3 in Stat3-deficient murine embryonic fibroblasts significantlyreduced LPS-stimulated expression of IL6, Cxcl10, and IL12p35. In addition, in aprimary murine osteoclast differentiation assay, a STAT3-specific SH2 domain inhibitor led to significantly increased levels of osteoclast-specific gene expression. These results suggest that STAT3 serves as a negative regulator of NFκB-mediated gene expression, and furthermore imply that STAT3 mutations associated with HIES contribute to the osteopenia and inflammation observed in HIES patients.