Heil den Bayreuther Festspielen : Verachtet mir die Meister nicht und ehret ihre Kunst!

Signatur des Originals: S 36/F07053

Scenenbilder aus Parsifal : Ihr schönen Kinder, musst' ich sie nicht schlagen? Zu euch Holden ja wehrten sie mir den Weg.

Signatur des Originals: S 36/F10470

{[N.N.], Szenenfoto, Gruppenbildnis, in: Hurra, mir erwe, Mainz: Stadttheater, 1932/33

Signatur des Originals: S 36/F11331

Die Zauberflöte : Königin d. Nacht: Ich bin zu Gram und Leid erkohren, Man raubte meine Tochter mir.

Signatur des Originals: S 36/G00157

Maria Wilhelmine von Hasselt-Barth als Carlo Broschi, Alexander Reichart als Rafael, Opernszene, Doppelbildnis, in: Daniel-François-Esprit Auber: Des Teufels Antheil : Rafael: "Mir die Ehre!- Dir das Geld!"

Signatur des Originals: S 36/G13784

"Fremd bin ich bei Euch und heimisch, gebt mir Besitz, meinen Todten zu begraben." : Predigt am Sabbath: חיי שרה [Ḥaye Śarah] im neuen Isr. Tempel in Hamburg

von Schwabacher

THE p63 ISOFORM ∆Np63α INHIBITS EPITHELIAL – MESENCHYMAL TRANSITION BY PROMOTING THE EXPRESSION OF MIR-205 IN HUMAN BLADDER CANCER CELLS

p63, a p53 family member, is a transcription factor that has complex roles in cancer. This study focuses on the role of the ∆Np63α isoform in bladder cancer (BC). Epithelial – mesenchymal transition (EMT) is a physiological process that plays an important part in metastasis and drug resistance. At the molecular level, EMT is characterized by the loss of the epithelial marker E-cadherin, and the acquisition of the transcriptional repressors of E-cadherin (ZEB1, ZEB2, TWIST, SNAI1 and SNAI2). Recent publications highlight the role of microRNAs belonging to the miR-200 family and miR-205 in preventing EMT through suppression of ZEB1 and ZEB2. p53, the homologue of p63, is implicated in regulating EMT by modulating the expression of miR-200c; however, the mechanisms underlying miR-205 control remain unclear. Here we show that ∆Np63α regulates the transcription of miR-205 and controls EMT in human BC cells. We observed a strong correlation between the expression of ∆Np63α, miR-205 and E-cadherin in a panel of BC cell lines (n=28) and also in bladder primary tumors from a cohort of patients (n=98). A remarkably inverse correlation is observed between ∆Np63α and ZEB1/2 in cell lines. Stable knockdown (KD) ∆Np63α in UC6, an “epithelial” BC cell line, decreased the expression of miR-205 and induced ZEB1/2 expression, the effects that were reversed by expression of exogenous miR-205. Moreover, overexpressing ∆Np63α in UC3, a “messenchymal” BC cell line, brought about opposite results, an increase in miR-205 expression and a reduction in ZEB1/2 expression. Modulation of ∆Np63α expression resulted in a parallel change in the expression of miR-205 and miR-205 “host” gene (miR-205HG). Nuclear run-on and chromatin immunoprecipitation experiments demonstrated that ∆Np63α regulates the transcription of miR-205 through controlling the recruitment of RNA Polymerase II to the promoter of miR-205HG. Interestingly, high miR-205 expression correlated with poor clinical outcome in BC patients, consistent with our recent publication highlighting the enrichment of ∆Np63 in a lethal subset of muscle invasive BC. In summary, our data present the important roles of ∆Np63α in preventing EMT mediated by miR-205. Our study also identifies miR-205 as a potential molecular marker to predict clinical outcome in BC patients.

ROLE OF MIR-19A RELEASED BY INFLAMMATORY BREAST CANCER CELLS IN THE REGULATION OF DENDRITIC CELL FUNCTIONS: IN VITRO MODEL OF CROSSTALK IN THE TUMOR MICROENVIRONMENT OF INFLAMMATORY BREAST CANCER

Inflammatory breast cancer (IBC) is a rare but very aggressive form of locally advanced breast cancer (1-6% of total breast cancer patients in United States), with a 5-year overall survival rate of only 40.5%, compared with 85% of the non-IBC patients. So far, a unique molecular signature for IBC able to explain the dramatic differences in the tumor biology between IBC and non-IBC has not been identified. As immune cells in the tumor microenvironment plays an important role in regulating tumor progression, we hypothesized that tumor-associated dendritic cells (TADC) may be responsible for regulating the development of the aggressive characteristics of IBC. MiRNAs can be released into the extracellular space and mediate the intercellular communication by regulating target gene expression beyond their cells of origin. We hypothesized that miRNAs released by IBC cells can induce an increased activation status, secretion of pro-inflammatory cytokines and migration ability of TADC. In an in vitro model of IBC tumor microenvironment, we found that the co-cultured of the IBC cell line SUM-149 with immature dendritic cells (iDCSUM-149) induced a higher degree of activation and maturation of iDCSUM-149 upon stimulation with lipopolysaccharide (LPS) compared with iDCs co-cultured with the non-IBC cell line SUM-159 (iDCSUM-159), resulting in: increased expression of the costimulatory and activation markers; higher production of pro-inflammatory cytokines (TNF-a, IL-6); and 3) higher migratory ability. These differences were due to the exosome-mediated transfer of miR-19a and miR-146a from SUM-149 and SUM-159, respectively, to iDCs, causing the downregulation of the miR-19a target genes PTEN, SOCS-1 and the miR-146a target genes IRAK1, TRAF6. PTEN, SOCS-1 and IRAK1, TRAF6 are important negative and positive regulator of cytokine- and TLR-mediated activation/maturation signaling pathway in DCs. Increased levels of IL-6 induced the upregulation of miR-19a synthesis in SUM-149 cells that was associated with the induction of CD44+CD24-ALDH1+ cancer stem cells (CSCs) with epithelial-to-mesenchymal transition (EMT) characteristics. In conclusion, in IBC tumor microenvironment IL-6/miR-19a axis can represent a self-sustaining loop able to maintain a pro-inflammatory status of DCs, leading to the development of tumor cells with high metastatic potential (EMT CSCs) responsible of the poor prognosis in IBC patients.

Torsiones y distorsiones de la imagen : Beltenebros de Antonio Muñoz Molina y de Pilar Miró

La transposición del discurso literario al cinematográfico plantea una operación sumamente productiva que no consiste en una mera traducción o copia, sino que implica una versión y una interpretación posible (entre muchas otras) que el director o el guionista realizan del texto literario. No se puede hablar, por lo tanto, de fidelidades o infidelidades, sino de los procedimientos a partir de los cuales un texto literario se resignifica y se transfigura en su versión fílmica. En España, durante la década del 80, se dio gran impulso a la industria cinematográfica y muchas novelas de la literatura española contemporánea fueron llevadas a la pantalla grande. Este impulso se extendió durante las décadas siguientes de modo que la transposición de la literatura al cine se convirtió en un fenómeno frecuente. En este contexto, es que la novela Beltenebros de Antonio Muñoz Molina fue llevada al cine por Pilar Miró. Este trabajo se propone indagar cómo se produce la transposición en este caso, analizando tanto los planos estructural y semántico como los recursos propiamente cinematográficos, con el objetivo de ensayar una posible interpretación acerca de las diferencias de ideología y actitud ante lo narrado que distinguen al texto literario de su versión fílmica.