Für wen gebe ich mein Urteil ab? Der systematische Einfluss des Fragebogenadressaten auf Kausalattributionsgewichtungen bei geschlossenen Antwortformaten

Die Fragebogenforschung belegt, dass Respondenten durch Kontextinformationen eines Fragebogens systematisch in ihrem Antwortverhalten beeinflusst werden. So zeigten Norenzayan und Schwarz (1999), dass Probanden bei freier Antwortmöglichkeit eher persönlichkeitsbezogene Ursachen zur Erklärung von Straftaten nennen, wenn der Fragebogen scheinbar von einem Institut für Persönlichkeitsforschung (verglichen mit einem Institut für Sozialforschung) erstellt wurde. Hierzu diskutierte Erklärungen sind einerseits Konversationsmaximen, die einen Bezug zwischen Adressat und Gesagtem induzieren, andererseits kognitive Primings, die selektive kognitive Aktivierungen und damit Verfügbarkeiten bedingen sollen. Die vorliegende Studie untersucht diese Erklärungsalternativen, indem sie erstmals in einem analogen Studiendesign persönlichkeitsbezogene und soziale Gründe in geschlossenen Antwortformaten vorgibt und gewichten lässt. Mögliche Gewichtungsunterschiede sind somit nicht mittels kognitiver Verfügbarkeit erklärbar. Eine Kovarianzanalyse (Alter, Geschlecht und die Big-Five-Persönlichkeitsdimensionen als Kovariaten) belegt im Einklang mit den Konversationsmaximen eine signifikant stärkere Bedeutungszuschreibung für persönlichkeitsbezogene Ursachen unter der Bedingung „Institut für Persönlichkeitsforschung“ im Vergleich zu „Institut für Sozialforschung“ und einer Kontrollbedingung („Institut für Kriminologie“)

Press Release. EU Funded Project "Fostering Queer Feminist Intersectional Resistances against Transnational Anti-Gender Politics (RESIST)" Launches

Anti-gender politics pose a grave threat to modern democratic formations because they challenge people's everyday survival, bodily integrity, and self-determination. Anti-gender spans the political spectrum and manifests not only in illiberal and authoritarian regimes but also in democracies that are considered liberal and inclusive. Taking a transnational and intersectional approach, RESIST analyses anti-gender formations in their complexity and contradictions and explores the effects of anti-gender politics on the everyday lives of those vulnerable to it and on democracies on the whole. RESIST engages with heterogeneous manifestations of anti-gender across the EU, Europe, and beyond through eight national case studies (Belarus, France, Germany, Greece, Ireland, Poland, Spain, Switzerland) and a transnational case study of people living in exile as a result of anti-gender persecution. RESIST pursues a mixed methods approach to analyse the production and circulation of gender-equality repressive strategies and discourses and their effects on lived experiences and resistances. RESIST innovates methodologically to engender democracy by fostering collaboration between academia and civil society organisations (CSOs), especially amongst people who come to be targets of anti-gender, including women and lesbian, gay, bisexual, transgender, and intersex (LGBTI+) persons. If those social groups whose fundamental rights are most at risk of violation by anti-gender are empowered to resist, then entire democratic societies benefit. RESIST centres feminist agency and collaborative knowledge production in (a) the research contents and results, (b) the methodological design, and (c) the social impact by generating new responsive feminist theories and practical solutions. At a time of increasing political disillusionment, RESIST creates hopeful, imaginative futures, transformative theories, and more inclusive worlds

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes