Individual and Contextual Variation in EU issue Voting: the Role of Political Information

Publication based on research carried out in the framework of the European Union Democracy Observatory (EUDO) of the Robert Schuman Centre for Advanced Studies, European University Institute.The journal issue has been produced in the framework of the PIREDEU Project, one of the projects carried out by the EUDO Public Opinion Observatory.Increasing politicization in EU member states about European issues can be expected to strengthen the impact of attitudes towards Europe on vote choice in European Parliament (EP) elections. At the same time this impact is likely to vary between voters and contexts as a function of political information. This study explores the role of political information in explaining individual and contextual heterogeneity in the degree of EU issue voting. Using a two-step hierarchical estimation procedure to explore both individual and contextual variation, we show that while EU issue voting in the 2009 EP elections is only slightly more pronounced among the politically sophisticated, it is clearly more extensive in contexts that provide higher levels of political information on European matters.1. Introduction 2. Explaning EP vote choice: the second-order model & the EU issue voting model 3. Individual and contextual heterogeneity in EU issue voting 4. Data, methods and operationalizations 5. Empirical results 6. Conclusion Acknowledgements App

Not all news sources are equally informative : a cross-national analysis of political knowledge in Europe

Across a sample of twenty-seven European nations, we examine variation in the level of factual political knowledge in relation to self-reported exposure to news programs aired by public or commercial channels, and to broadsheet or tabloid newspapers. Unlike previous studies, we estimate the effects of exposure to these news outlets while controlling for self-selection into the audience. Our results show that the positive effects of exposure to broadsheets and public broadcasting on knowledge remain robust. Finally, we show that only exposure to broadsheets (and not to public broadcasting) narrows the knowledge gap within nations; relatively apathetic individuals who read broadsheet newspapers are able to “catch up” with their more attentive counterparts

Recombinant Human IgA1 and IgA2 Autoantibodies to Type VII Collagen Induce Subepidermal Blistering Ex Vivo

Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody-mediated diseases. In epidermolysis bullosa acquisita (EBA), an autoimmune disease with severe and chronic skin blistering, autoantibodies are directed against type VII collagen. IgG is the predominant autoantibody isotype of EBA, the pathogenicity of which has been demonstrated in a variety of in vivo and ex vivo disease models. In contrast, there is not much evidence for the pathogenicity of IgA, which may appear as the only autoantibody isotype in some EBA patients. To investigate the pathogenic potential of IgA autoantibodies, we generated chimeric V gene-matched human IgA1, IgA2, and control IgG1 autoantibodies directed against type VII collagen. Immobilized immune complexes containing the rIgA1 and rIgA2 autoantibodies induced the dose-dependent release of reactive oxygen species from neutrophil granulocytes, a precondition for blister formation. Moreover, both rIgA1 and rIgA2 induced leukocyte-dependent dermal-epidermal separation in cryosections of human skin. In contrast with rIgG1, neither rIgA1 nor rIgA2 was capable of inducing complement deposition at the dermal-epidermal junction. Because complement activation is a prerequisite for blister induction, this lack of function compared with IgG1 may be compensated for by the stronger activation of neutrophil granulocytes by both IgA1 and IgA2. For IgG-mediated AIBD, immunoadsorption therapy is a convenient treatment modality for the removal of pathogenic autoantibodies, particularly in treatment-resistant cases. The results of this study show the pathogenic potential of IgA autoantibodies and support the development of adsorber matrices for IgA-mediated AIBD