Das Buch in der nationalsozialistischen Propagandapolitik

Diese Studie untersucht die Buchpolitik der NS-Zeit im Kontext der modernen Massenmedien. Gestützt auf zahlreiche veröffentlichte und unveröffentlichte Quellen, rekonstruiert sie die Buchförderungspolitik im Spannungsfeld von politischen Interessen und langfristig wirksamen Traditionsbindungen, von ideologischen Imperativen und marktwirtschaftlichen Konditionen, von totalitären Ansprüchen und einer modernen, ausdifferenzierten Gesellschaft. Zugleich dokumentiert die Analyse die Auswirkungen dieser Spannungen in den z.T. widersprüchlichen literaturpolitischen Diskursen über das auch zwischen 1933 und 1945 diversifizierte literarische Feld

Literary translation from Flemish into German during the Nazi regime

. During the Nazi regime and, more specifically, the Second World War, literary translation was eyed with suspicion by the controlling instances as it inevitably involved the import of foreign thought as well as economic exchange with foreign states. Against this backdrop, Flanders represents an interesting case. On the one hand, since it was considered a ‘kindred’ source-language nation, the translation of Flemish literature into German was encouraged within the constraints of the totalitarian system. On the other hand, persisting literary traditions, the private market logic, the agency of mediators, and the prevailing Catholic tone and idyllic nature of much Flemish literature caused significant disparities between translation policy and practice. Starting from the publishing figures of translated Flemish literature in Nazi Germany and their evolution during the twelve-year period, this article confronts official attitudes and discourses regarding Flemish translated fiction with the actual situation within the translated fiction market

Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The pathogenesis of viral myocarditis is conceptually a multiphase process, initiated by the infection of cardiomyocytes, followed by activation of the immune system, and resulting in myocardial fibrosis and left ventricular dysfunction. In parallel to the direct infection of the heart, CVB3 replicates in lymphatic organs such as the pancreas. Due to infection of the pancreas, the model of experimental CVB3-induced myocarditis is estimated as a severe burden for the challenged animals. Application of analgesics in frame of the animal welfare act (European directive 2010/63/EU) is more and more becoming a matter of debate. For this purpose, we summarized published studies for 13 different opioids and discussed their potential impact on CVB3-induced myocarditis. In addition, with this summary we also want to provide guidance for researchers beyond the myocarditis field to estimate the impact of opioids on the immune system for their specific model. In the literature, both immunosuppressive as well as immune-activating effects of opioids have been described, but examinations in experimental CVB3-induced myocarditis have still not been reported so far. Based on the existing publications, administration of opioids in experimental CVB3-induced myocarditis might result in more severe disease progression, including higher mortality, or a less pronounced myocarditis model, failing to be used for the establishment of new treatment options. Taken together, the applicability of opioids in experimental CVB3-induced myocarditis and in inflammatory models in general needs to be carefully evaluated and further investigated

A Toolbox of Potential Immune-Related Therapies for Inflammatory Cardiomyopathy

Myocarditis is a multifactorial disorder, characterized by an inflammatory reaction in the myocardium, predominantly triggered by infectious agents, but also by antigen mimicry or autoimmunity in susceptible individuals. Unless spontaneously resolved, a chronic inflammatory course concludes with cardiac muscle dysfunction portrayed by ventricular dilatation, clinically termed inflammatory cardiomyopathy (Infl-CM). Treatment strategies aim to resolve chronic inflammation and preserve cardiac function. Beside standard heart failure treatments, which only play a supportive role in this condition, systemic immunosuppressants are used to diminish inflammatory cell function at the cost of noxious side effects. To date, the treatment protocols are expert-based without large clinical evidence. This review describes concept and contemporary strategies to alleviate myocardial inflammation and sheds light on potential inflammatory targets in an evidence-based order

Cardiac Extracellular Vesicles (EVs) Released in the Presence or Absence of Inflammatory Cues Support Angiogenesis in Different Manners

Cells release extracellular vesicles (EVs) to communicate in a paracrine manner with other cells, and thereby influence processes, such as angiogenesis. The conditioned medium of human cardiac-derived adherent proliferating (CardAP) cells was recently shown to enhance angiogenesis. To elucidate whether their released EVs are involved, we isolated them by differential centrifugation from the conditioned medium derived either in the presence or absence of a pro-inflammatory cytokine cocktail. Murine recipient cells internalized CardAP-EVs as determined by an intracellular detection of human proteins, such as CD63, by a novel flow cytometry method for studying EV-cell interaction. Moreover, endothelial cells treated for 24 h with either unstimulated or cytokine stimulated CardAP-EVs exhibited a higher tube formation capability on Matrigel. Interestingly, unstimulated CardAP-EVs caused endothelial cells to release significantly more vascular endothelial growth factor and interleukin (IL)-6, while cytokine stimulated CardAP-EVs significantly enhanced the release of IL-6 and IL-8. By nCounter® miRNA expression assay (NanoString Technologies) we identified microRNA 302d-3p to be enhanced in unstimulated CardAP-EVs compared to their cytokine stimulated counterparts, which was verified by quantitative polymerase chain reaction. This study demonstrates that both CardAP-EVs are pro-angiogenic by inducing different factors from endothelial cells. This would allow to select potent targets for a safe and efficient therapeutic application

Mesenchymal Stem Cells and Inflammatory Cardiomyopathy: Cardiac Homing and Beyond

Under conventional heart failure therapy, inflammatory cardiomyopathy usually has a progressive course, merging for alternative interventional strategies. There is accumulating support for the application of cellular transplantation as a strategy to improve myocardial function. Mesenchymal stem cells (MSCs) have the advantage over other stem cells that they possess immunomodulatory features, making them attractive candidates for the treatment of inflammatory cardiomyopathy. Studies in experimental models of inflammatory cardiomyopathy have consistently demonstrated the potential of MSCs to reduce cardiac injury and to improve cardiac function. This paper gives an overview about how inflammation triggers the functionality of MSCs and how it induces cardiac homing. Finally, the potential of intravenous application of MSCs by inflammatory cardiomyopathy is discussed