Dieter Kranz et Friedrich Luft : la critique théâtrale radiophonique dans le Berlin (Est et Ouest)d’après-guerre

« Le théâtre chante, nous nous en faisons l’écho ». De 1946 à 1990, le critique Friedrich Luft partagea sa passion du théâtre avec les auditeurs de la station de radio ouest-berlinoise RIAS, en animant hebdomadairement une émission de quinze minutes, Stimme der Kritik [Voix de la critique], dans laquelle il présentait les mises en scène qui lui avaient plu. Outre ce format, il avait également conçu en 1951 une émission mensuelle d’environ trois quarts d’heure, Wir gehen ins Theater [Nous allons au théâtre], qui faisait entendre des extraits de pièces du répertoire berlinois de l’époque. De l’autre côté de la frontière, une dizaine d’années après, un autre critique de théâtre, Dieter Kranz, avait créé à Berlin-Est une émission symétrique de quinze minutes Atelier und Bühne [Atelier et Scène] qui fut diffusée de 1956 à 1991. Il dirigea ensuite, de 1961 à 1991, une émission mensuelle de quarante-cinq minutes, Berlin - Weltstadt des Theaters [Berlin, capitale mondiale du théâtre], dans laquelle, ayant obtenu des théâtres le droit d’enregistrer les répétitions générales, il introduisait des interviews avec l’auteur, le metteur en scène, le scénographe ou certains des comédiens. De ces œuvres radiophoniques restent des centaines d’heures de pur plaisir acoustique qui donnent un aperçu étonnant du théâtre dans le Berlin d’après-guerre. Le présent article révèle l’activité de ces deux critiques de théâtre berlinois et les resitue dans leur contexte historique et politique.« The theatre sings; we echo it ». From 1946 to 1990, the critic Friedrich Luft shared his passion for the theatre with the listeners of the West Berlin radio station RIAS in presenting a weekly fifteen-minute broadcast, Stimme der Kritik [Voices of criticism] during which he introduced to the productions which had appealed to him. Beyond this format, in 1951, he had also conceived a monthly broadcast of about forty-five minutes, Wir gehen ins Theater [We go to the theatre] in which excerpts from the Berlin repertoire of the time were heard. Across the border, some ten years later in East Berlin, another theatre critic, Dieter Kranz, had created a symmetrical fifteen-minute broadcast, Atelier und Bühne [Workshop and stage], which was heard from 1956 to 1991. Then, from 1961 to 1991 he managed a monthly forty-five-minute broadcast, Berlin-Weltstadt des Theaters [Berlin – world capital of the theatre] during which, having obtained from the theatres the right to record dress rehearsals, he introduced to interviews with the playwright, the producer, the scenographer, or some of the comedians. Of all these radio works are left hundreds of hours of pure acoustic pleasure which leave a stunning account of the theatre in postwar Berlin. The present article reveals these two Berlin theatre critics’ activities and put them back in their historical and political context

Struktur-Funktionsanalyse des Transkriptionsfaktors Sox10 und Aspekte der Evolution

The invention of neural crest (NC) cells and oligodendrocytes played an important role in the emergence of the vertebrate phylum during evolution. In humans, mutations of the transcription factor SOX10 affect the development of these cell types and result in a wide range of neurocristopathies and demyelinating diseases. A direct link between SOX10 mutations and the severity of the disease has been proposed. However the exact mode of action of different mutations and more generally the importance of the different domains of the Sox10 protein on developmental processes have not been studied in detail. The first aim of this study was therefore to better characterize the functional importance of different Sox10 domains and the influence of SOX10 mutations on early NC development. Using overexpression in the chicken neural tube, I showed that Sox10 functions during early NC development rely on its DNA binding and transactivation abilities. My results moreover argue that truncated SOX10 proteins which result from nonsense mutations in exon 4 of the SOX10 gene behave as dominant negatives but that production of these proteins is prevented in human patients by nonsense mediated decay. Different mutations within the SOX10 protein can furthermore influence oligodendrocytes and NC-derived lineages differentially. This last conclusion was also confirmed in a knock-in mouse mutant where wild-type Sox10 was replaced by a mutant version without cooperative binding capabilities. In these mice, development of most NC-derived-cell types was severely impaired whereas oligodendrocyte development was not. The second aim of this study was to understand how Sox10 acquired its essential functions in oligodendrocytes and NC cells during evolution. For that purpose I analyzed the capability of Sox100B from Drosophila melanogaster to perform Sox10 specific functions in vivo. Sox100B was overexpressed in the chicken neural tube and a mutant mouse line was established where the Sox10 allele was replaced by the Sox100B open reading frame. Anaysis of these animals showed that Sox100B can take over the functions of Sox10 during early NC, Schwann cell and oligodendrocyte development arguing that an ancestral SoxE gene could have easily integrated into the gene regulatory networks that control the development of these cell types following its co-option. However, later developmental defects in several NC derived lineages in mice homozygous for the Sox100B replacement allele indicate that some degree of functional specialization and adaptation of SoxE protein properties have taken place later on.Die Entstehung von Neuralleistenzellen und Oligodendrozyten war ein wichtiger Schritt in der Evolution der Wirbeltiere. Mutationen des Transkriptionfaktors SOX10 beeinträchtigen die Entwicklung dieser Zelltypen im Menschen und verursachen Neurocristopathien und demyelinisierende Schädigungen. Es wird angenommen, dass die Art und die Position der Mutationen einen direkten Einfluß auf den Schweregrad der Krankheit haben. Die genaue Wirkungsweise der verschiedenen Mutationen, sowie die Bedeutung von verschiedenen Domänen des Sox10 Proteins für Entwicklungprozesse wurden bisher allerdings nicht genau analysiert. Im Rahmen dieser Arbeit wurden die funktionelle Bedeutung von verschiedenen SOX10 Domänen und der Einfluß von SOX10 Mutationen auf die frühe Entwicklung der Neuralleistenzellen untersucht. Die Überexpression von SOX10 im Neuralrohr von Hühner-Embryonen zeigte, dass die Funktion in der frühen Entwicklung der Neuralleistenzellen auf der DNA-Bindefähigkeit und Transaktivierungsfähigkeit des Proteins beruht. Außerdem zeigen meine Ergebnisse, dass verkürzte SOX10 Proteine, die aufgrund von Nonsense-Mutationen innerhalb des vierten Exons des SOX10 Gens produziert wurden, sich dominant negativ verhalten, dass aber die Herstellung solcher Proteine im Menschen durch „nonsense mediated decay“ vermieden wird. Verschiedene Mutationen des SOX10 Proteins hatten weiterhin unterschiedlichen Einfluß auf Oligodendrozyten und verschiedene Neuralleistenderivate. Diese Aussage wurde mittels einer knock-in Mausvariante bestätigt, in der das Wildtyp Sox10 Protein durch eine Mutante ohne kooperative DNA-Bindefähigkeit ersetzt wurde. Die Entwicklung von Neuralleistenderivaten war in diesen Mäusen stark beeinträchtigt, wohingegen die Oligodendrozytenentwicklung normal war. Im zweiten Teil dieser Arbeit sollte analysiert werden, wie Sox10 während der Evolution seine essentiellen Funktionen in Oligodendrozyten und Neuralleistenzellen erwarb. Zu diesem Zweck untersuchte ich, ob das Sox100B Protein aus Drosophila melanogaster die spezifischen Funktionen von Sox10 in vivo ausführen kann. Es wurde Sox100B im Neuralrohr von Hühner-Embryonen überexprimiert und eine Mauslinie generiert, in der das Sox10 Allel durch den offenen Leserahmen von Sox100B ersetzt wurde. Die Analyse dieser Tiere zeigte, dass Sox100B die Funktionen von Sox10 in der frühen Neuralleisten-, Schwannzellen- und Oligodendrozytenentwicklung übernehmen kann. Diese Ergebnisse beweisen, dass eine Funktionsübernahme der ursprünglichen Eigenschaften (Ko-Option) eines anzestralen SoxE Gens in das genregulatorische Netzwerk stattgefunden hat, das die Entwicklung dieser Zelltypen kontrolliert. Spätere Entwicklungsdefekte in verschiedenen Neuralleistenderivaten in Sox10Sox100B/Sox100B Mäusen zeigten aber, dass gewisse funktionelle Spezialisierungen und Adaptationen der SoxE Proteinwirkungen im Nachhinein erfolgt sind

Morphologic Basis for Developing Diverticular Disease, Diverticulitis, and Diverticular Bleeding

Diverticula of the colon are pseudodiverticula defined by multiple outpouchings of the mucosal and submucosal layers penetrating through weak spots of the muscle coat along intramural blood vessels. A complete prolapse consists of a diverticular opening, a narrowed neck, and a thinned diverticular dome underneath the serosal covering. The susceptibility of diverticula to inflammation is explained by local ischemia, translocation of pathogens due to retained stool, stercoral trauma by fecaliths, and microperforations. Local inflammation may lead to phlegmonous diverticulitis, paracolic/mesocolic abscess, bowel perforation, peritonitis, fistula formation, and stenotic strictures. Diverticular bleeding is due to an asymmetric rupture of distended vasa recta at the diverticular dome and not primarily linked to inflammation. Structural and functional changes of the bowel wall in diverticular disease comprise: i) Altered amount, composition, and metabolism of connective tissue; ii) Enteric myopathy with muscular thickening, deranged architecture, and altered myofilament composition; iii) Enteric neuropathy with hypoganglionosis, neurotransmitter imbalance, deficiency of neurotrophic factors and nerve fiber remodeling; and iv) Disturbed intestinal motility both in vivo (increased intraluminal pressure, motility index, high-amplitude propagated contractions) and in vitro (altered spontaneous and pharmacologically triggered contractility). Besides established etiologic factors, recent studies suggest that novel pathophysiologic concepts should be considered in the pathogenesis of diverticular disease

Anti-Inflammatory Properties of the SGLT2 Inhibitor Empagliflozin in Activated Primary Microglia

Sodium-glucose cotransporter 2 (SGLT2) inhibitors, including empagliflozin, are routinely used as antidiabetic drugs. Recent studies indicate that beside its beneficial effects on blood glucose level, empagliflozin may also exert vascular anti-inflammatory and neuroprotective properties. In the brain, microglia are crucial mediators of inflammation, and neuroinflammation plays a key role in neurodegenerative disorders. Dampening microglia-mediated inflammation may slow down disease progression. In this context, we investigated the immunomodulatory effect of empagliflozin on activated primary microglia. As a validated experimental model, rat primary microglial cells were activated into a pro-inflammatory state by stimulation with LPS. The influence of empagliflozin on the expression of pro-inflammatory mediators (NO, Nos2, IL6, TNF, IL1B) and on the anti-inflammatory mediator IL10 was assessed using quantitative PCR and ELISA. Further, we investigated changes in the activation of the ERK1/2 cascade by Western blot and NFkB translocation by immunostaining. We observed that empagliflozin reduces the expression of pro- and anti-inflammatory mediators in LPS-activated primary microglia. These effects might be mediated by NHE-1, rather than by SGLT2, and by the further inhibition of the ERK1/2 and NFkB pathways. Our results support putative anti-inflammatory effects of empagliflozin on microglia and suggest that SGLT2 inhibitors may exert beneficial effects in neurodegenerative disorders

Impaired Expression of Neuregulin 1 and Nicotinic Acetylcholine Receptor β4 Subunit in Diverticular Disease

Neuregulin 1 (NRG1) regulates the expression of the nicotinic acetylcholine receptor (nAChR) and is suggested to promote the survival and maintenance of the enteric nervous system (ENS), since deficiency of its corresponding receptor complex ErbB2/ErbB3 leads to postnatal colonic aganglionosis. As diverticular disease (DD) is associated with intestinal hypoganglionosis, the NRG1-ErbB2/ErbB3 system and the nAChR were studied in patients with DD and controls. Samples of tunica muscularis of the sigmoid colon from patients with DD (n = 8) and controls (n = 11) were assessed for mRNA expression of NRG1, ErbB2, and ErbB3 and the nAChR subunits α3, α5, α7, β2, and β4. Site-specific gene expression levels of the NRG1-ErbB2/3 system were determined in myenteric ganglia harvested by laser microdissection (LMD). Localization studies were performed by immunohistochemistry for the NRG1-ErbB2/3 system and nAChR subunit β4. Rat enteric nerve cell cultures were stimulated with NRG1 or glial-cell line derived neurotrophic factor (GDNF) for 6 days and mRNA expression of the aforementioned nAchR was measured. NRG1, ErbB3, and nAChR subunit β4 expression was significantly down-regulated in both the tunica muscularis and myenteric ganglia of patients with DD compared to controls, whereas mRNA expression of ErbB3 and nAChR subunits β2, α3, α5, and α7 remained unaltered. NRG1, ErbB3, and nAChR subunit β4 immunoreactive signals were reduced in neuronal somata and the neuropil of myenteric ganglia from patients with DD compared to control. nAChR subunit β4 exhibited also weaker immunoreactive signals in the tunica muscularis of patients with DD. NRG1 treatment but not GDNF treatment of enteric nerve cell cultures significantly enhanced mRNA expression of nAchR β4. The down-regulation of NRG1 and ErbB3 in myenteric ganglia of patients with DD supports the hypothesis that intestinal hypoganglionosis observed in DD may be attributed to a lack of neurotrophic factors. Regulation of nAChR subunit β4 by NRG1 and decreased nAChR β4 in patients with DD provide evidence that a lack of NRG1 may affect the composition of enteric neurotransmitter receptor subunits thus contributing to the intestinal motility disorders previously reported in DD

Replacement of mouse Sox10 by the Drosophila ortholog Sox100B provides evidence for co-option of SoxE proteins into vertebrate-specific gene-regulatory networks through altered expression

AbstractNeural crest cells and oligodendrocytes as the myelinating glia of the central nervous system exist only in vertebrates. Their development is regulated by complex regulatory networks, of which the SoxE-type high-mobility-group domain transcription factors Sox8, Sox9 and Sox10 are essential components. Here we analyzed by in ovo electroporation in chicken and by gene replacement in the mouse whether the Drosophila ortholog Sox100B can functionally substitute for vertebrate SoxE proteins. Sox100B overexpression in the chicken neural tube led to the induction of neural crest cells as previously observed for vertebrate SoxE proteins. Furthermore, many aspects of neural crest and oligodendrocyte development were surprisingly normal in mice in which the Sox10 coding information was replaced by Sox100B arguing that Sox100B integrates well into the gene-regulatory networks that drive these processes. Our results therefore provide strong evidence for a model in which SoxE proteins were co-opted to these gene-regulatory networks mainly through the acquisition of novel expression patterns. However, later developmental defects in several neural crest derived lineages in mice homozygous for the Sox100B replacement allele indicate that some degree of functional specialization and adaptation of SoxE protein properties have taken place in addition to the co-option event

Effects of different ischemic preconditioning strategies on physiological and cellular mechanisms of intestinal ischemia/reperfusion injury: Implication from an isolated perfused rat small intestine model

Background Intestinal ischemia/reperfusion (I/R)-injury often results in sepsis and organ failure and is of major importance in the clinic. A potential strategy to reduce I/R-injury is the application of ischemic preconditioning (IPC) during which repeated, brief episodes of I/R are applied. The aim of this study was to evaluate physiological and cellular effects of intestinal I/R-injury and to compare the influence of in-vivo IPC (iIPC) with ex-vivo IPC (eIPC), in which blood derived factors and nerval regulations are excluded. Results I/R-injury decreased intestinal galactose uptake (iIPC group: p<0.001), increased vascular perfusion pressure (iIPC group: p<0.001; eIPC group: p<0.01) and attenuated venous flow (iIPC group: p<0.05) while lactate-to-pyruvate ratio (iIPC group, eIPC group: p<0.001), luminal flow (iIPC group: p<0.001; eIPC group: p<0.05), goblet cell ratio (iIPC group, eIPC group: p<0.001) and apoptosis (iIPC group, eIPC group: p<0.05) were all increased. Application of iIPC prior to I/R increased vascular galactose uptake (P<0.05) while eIPC had no significant impact on parameters of I/R-injury. On cellular level, I/R-injury resulted in a reduction of the phosphorylation of several MAPK signaling molecules. Application of iIPC prior to I/R increased phosphorylation of JNK2 and p38δ while eIPC enhanced CREB and GSK-3α/β phosphorylation. Conclusion Intestinal I/R-injury is associated with major physiological and cellular changes. However, the overall influence of the two different IPC strategies on the acute phase of intestinal I/R-injury is rather limited

Rapid multi-generational acclimation of coralline algal reproductive structures to ocean acidification

The future of coral reef ecosystems is under threat because vital reef-accreting species such as coralline algae are highly susceptible to ocean acidification. Although ocean acidification is known to reduce coralline algal growth rates, its direct effects on the development of coralline algal reproductive structures (conceptacles) is largely unknown. Furthermore, the long-term, multi-generational response of coralline algae to ocean acidification is extremely understudied. Here, we investigate how mean pH, pH variability and the pH regime experienced in their natural habitat affect coralline algal conceptacle abundance and size across six generations of exposure. We show that second-generation coralline algae exposed to ocean acidification treatments had conceptacle abundances 60% lower than those kept in present-day conditions, suggesting that conceptacle development is initially highly sensitive to ocean acidification. However, this negative effect of ocean acidification on conceptacle abundance disappears after three generations of exposure. Moreover, we show that this transgenerational acclimation of conceptacle development is not facilitated by a trade-off with reduced investment in growth, as higher conceptacle abundances are associated with crusts with faster growth rates. These results indicate that the potential reproductive output of coralline algae may be sustained under future ocean acidification.journal articl