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Het gedachtegoed van de 'Identitäre Bewegung' in de 'Partij voor de Vrijheid' (PVV), 'Forum voor Democratie' (FvD) en de 'Alternative für Deutschland' (AfD)
Diese Masterarbeit befasst sich mit der Frage nach Überschneidungen und Differenzen zwischen dem Gedankengut der 'Identitären Bewegung' und den Positionen der 'Partij voor de Vrijheid' (PVV), des 'Forum voor Democratie' (FvD) und der 'Alternative für Deutschland' (AfD). Während personelle Verbindungen oft Beachtung finden, bleibt die Untersuchung der inhaltlichen Überlappungen weitgehend unerforscht. Ziel der Studie ist es, Gemeinsamkeiten und Unterschiede zwischen den Ideologien dieser rechtspopulistischen Parteien und der 'Identitären Bewegung' zu identifizieren. Die Analyse konzentriert sich auf drei Aspekte des identitären Gedankenguts: Ethnopluralismus, Genderpolitik und Europa. Es wird eine qualitative Analyse der Wahlprogramme und Debattenbeiträge der PVV, des FvD und der AfD im Zeitraum von 2016 bis 2021 durchgeführt. Die Ergebnisse liefern wertvolle Einblicke in die ideologischen Überschneidungen und Differenzen dieser Parteien und der 'Identitären Bewegung'.In deze masterscriptie worden de raakvlakken en verschillen onderzocht tussen het gedachtegoed van de 'Identitäre Bewegung' en de posities van de 'Partij voor de Vrijheid' (PVV), 'Forum voor Democratie' (FvD) en de 'Alternative für Deutschland' (AfD). Hoewel persoonlijke connecties vaak de aandacht trekken, blijft de inhoudelijke overlap grotendeels onderbelicht. Deze studie heeft als doel om de overeenkomsten en verschillen tussen de ideologieën van deze rechtspopulistische partijen en de 'Identitäre Bewegung' in kaart te brengen, met een focus op etnopluralisme, genderpolitiek en Europa. Er wordt een kwalitatieve analyse uitgevoerd van de verkiezingsprogramma's en debatbijdragen van deze partijen tussen 2016 en 2021. De resultaten bieden waardevolle inzichten in de ideologische raakvlakken en verschillen tussen deze rechtspopulistische partijen en de 'Identitäre Bewegung'
Host-pathogen interaction: Enterobacter cloacae exerts different adhesion and invasion capacities against different host cell types
New antibiotics are urgently needed due to the huge increase of multidrug-resistant bacteria. The underexplored gram-negative bacterium 'Enterobacter cloacae' is known to cause severe urinary tract and lung infections (UTIs). The pathogenicity of 'E. cloacae' in UTI has only been studied at the bioinformatic level, but until now not within systematic 'in vitro' investigations. The present study assesses different human cell lines for monitoring the early steps of host-pathogen interaction regarding bacterial adhesion to and invasion into different host cells by flow cytometric adhesion assay, classical cell counting assay, gentamicin invasion assay, and confocal laser scanning microscopy. To our knowledge, this is the first report in which 'E. cloacae' has been investigated for its interaction with human bladder, kidney, skin, and lung cell lines under in vitro conditions. Data indicate that 'E. cloacae' exerts strong adhesion to urinary tract (bladder and kidney) and lung cells, a finding which correlates with the clinical relevance of the bacterium for induction of urinary tract and lung infections. Furthermore, 'E. cloacae' ATCC 13047 barely adheres to skin cells (A-431) and shows no relevant interaction with intestinal cells (Caco-2, HT-29), even in the presence of mucin (HT29 MTX). In contrast, invasion assays and confocal laser scanning microscopy demonstrate that 'E. cloacae' internalizes in all tested host cells, but to a different extent. Especially, bladder and kidney cells are being invaded to the highest extent. Defective mutants of fimH and fimA abolished the adhesion of 'E. cloacae' to T24 cells, while csgA deletion had no influence on adhesion. These results indicate that 'E. cloacae' has different pattern for adhesion and invasion depending on the target tissue, which again correlates with the clinical relevance of the pathogen. For detailed investigation of the early host-pathogen interaction T24 bladder cells comprise a suitable assay system for evaluation the bacterial adhesion and invasion
Hypercontractile cardiac phenotype in mice overexpressing the regulatory subunit PR72 of protein phosphatase 2A
Background: The activity, localization, and substrate specificity of the protein phosphatase 2A (PP2A) heterotrimer are controlled by various regulatory B subunits. PR72 belongs to the B'' gene family and has been shown to be upregulated in human heart failure. However, little is known about the functions of PR72 in the myocardium. Methods: To address this issue, we generated a transgenic mouse model with heart-specific overexpression of PP2A-PR72. Biochemical and physiological methods were used to determine contractility, Ca2+ cycling parameters, and protein phosphorylation. Results: A 2.5-fold increase in PR72 expression resulted in moderate cardiac hypertrophy. Maximal ventricular pressure was increased in catheterized transgenic mice (TG) compared to wild-type (WT) littermates. This was accompanied by an increased shortening of sarcomere length and faster relaxation at the single-cell level in TG. In parallel with these findings, the peak amplitude of Ca2+ transients was increased, and the decay in intracellular Ca2+ levels was shortened in TG compared to WT. The changes in Ca2+ cycling in TG were also evident from an increase in the full duration and width at half maximum of Ca2+ sparks. Consistent with the contractile data, phosphorylation of phospholamban at threonine-17 was higher in TG hearts. The lower expression of the Na+/Ca2+ exchanger may also contribute to the hypercontractile state in transgenic myocardium. Conclusion: Our results suggest that PP2A-PR72 plays an important role in regulating cardiac contractile function and Ca2+ cycling, indicating that the upregulation of PR72 in heart failure is an attempt to compensate functionally
The roles of toll-like receptor 4, CD33, CD68, CD69, or CD147/EMMPRIN for monocyte activation by the DAMP S100A8/S100A9
The S100A8/A9 heterocomplex is an abundant damage-associated molecular pattern and mainly expressed by monocytes, inflammatory activated keratinocytes and neutrophilic granulocytes. The heterocomplex as well as the heterotetramer are involved in a variety of diseases and tumorous processes. However, their detailed mode of action and especially which receptors are involved hereby remains to be fully revealed. Several cell surface receptors are reported to interact with S100A8 and/or S100A9, the best studied being the pattern recognition receptor TLR4. RAGE, CD33, CD68, CD69, and CD147, all of them are involved as receptors in various inflammatory processes, are also among these putative binding partners for S100A8 and S100A9. Interactions between S100 proteins and these receptors described so far come from a wide variety of cell culture systems but their biological relevance in vivo for the inflammatory response of myeloid immune cells is not yet clear. In this study, we compared the effect of CRISPR/Cas9 mediated targeted deletion of CD33, CD68, CD69, and CD147 in ER-Hoxb8 monocytes on S100A8 or S100A9 induced cytokine release with TLR4 knockout monocytes. Whereas deletion of TLR4 abolished the S100-induced inflammatory response in monocyte stimulation experiments with both S100A8 and S100A9, knockouts of CD33, CD68, CD69, or CD147 revealed no effect on the cytokine response in monocytes. Thus, TLR4 is the dominant receptor for S100-triggered inflammatory activation of monocytes
Unraveling the blue shift in porphyrin fluorescence in glioma: The 620 nm peak and its potential significance in tumor biology
In glioma surgery, the low-density infiltration zone of tumors is difficult to detect by any means. While, for instance, 5-aminolevulinic acid (5-ALA)-induced fluorescence is a well-established surgical procedure for maximizing resection of malignant gliomas, a cell density in tumor tissue of 20–30% is needed to observe visual fluorescence. Hyperspectral imaging is a powerful technique for the optical characterization of brain tissue, which accommodates the complex spectral properties of gliomas. Thereby, knowledge about the signal source is essential to generate specific separation (unmixing) procedures for the different spectral characteristics of analytes and estimate compound abundances. It was stated that protoporphyrin IX (PpIX) fluorescence consists mainly of emission peaks at 634 nm (PpIX634) and 620 nm (PpIX620). However, other members of the substance group of porphyrins fluoresce similarly to PpIX due to their common tetrapyrrole core structure. While the PpIX634 signal has reliably been assigned to PpIX, it has not yet been analyzed if PpIX620 might result from a different porphyrin rather than being a second photo state of PpIX. We thus reviewed more than 200,000 spectra from various tumors measured in almost 600 biopsies of 130 patients. Insufficient consideration of autofluorescence led to artificial inflation of the PpIX620 peak in the past. Recently, five basis spectra (PpIX634, PpIX620, flavin, lipofuscin, and NADH) were described and incorporated into the analysis algorithm, which allowed more accurate unmixing of spectral abundances. We used the improved algorithm to investigate the PpIX620 signal more precisely and investigated coproporphyrin III (CpIII) fluorescence phantoms for spectral unmixing. Our findings show that the PpIX634 peak was the primary source of the 5-ALA-induced fluorescence. CpIII had a similar spectral characteristic to PpIX620. The supplementation of 5-ALA may trigger the increased production of porphyrins other than PpIX within the heme biosynthesis pathway, including that of CpIII. It is essential to correctly separate autofluorescence from the main PpIX634 peak to analyze the fluorescence signal. This article highlights the need for a comprehensive understanding of the spectral complexity in gliomas and suggests less significance of the 620 nm fluorescence peak for PpIX analysis and visualization