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  1. Book ; Article ; Online: Perceived income positions and attitudes towards EU inequality

    Bublitz, Elisabeth / Wang, Hequn / Jäger, Julian / Beblo, Miriam / Lohmann, Henning

    A cross-country survey experiment

    2022  

    Abstract: We examine the relationship between perceived income positions and attitudes towards inequality at a supranational-level. Conducting a survey in four EU Member States (Germany, Italy, Poland, and Sweden), we confirm that their citizens misperceive their ... ...

    Abstract We examine the relationship between perceived income positions and attitudes towards inequality at a supranational-level. Conducting a survey in four EU Member States (Germany, Italy, Poland, and Sweden), we confirm that their citizens misperceive their own income position in the EU. Once we account for these misperceptions, we find that those with a lower income rank assess EU income differences as more unjust and are more supportive of an EU minimum wage. When we inform a randomized subsample about their actual income position in the EU, those who learn to be richer than they initially thought assess EU income differences as less unjust. Respondents in Italy, Poland, and to a lesser extent Sweden drive these results whereas income misperceptions of German respondents have opposing effects.
    Keywords ddc:330 ; D31 ; D63 ; F55 ; Income ; Misperceptions ; Inequality ; EU Minimum Wage ; European Union ; Survey Experiment
    Subject code 331
    Language English
    Publisher Hamburg: Universität Hamburg, Fakultät für Wirtschafts- und Sozialwissenschaften, WiSo-Forschungslabor
    Publishing country de
    Document type Book ; Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Humanized mutant FUS drives progressive motor neuron degeneration without aggregation in 'FUSDelta14' knockin mice.

    Devoy, Anny / Kalmar, Bernadett / Stewart, Michelle / Park, Heesoon / Burke, Beverley / Noy, Suzanna J / Redhead, Yushi / Humphrey, Jack / Lo, Kitty / Jaeger, Julian / Mejia Maza, Alan / Sivakumar, Prasanth / Bertolin, Cinzia / Soraru, Gianni / Plagnol, Vincent / Greensmith, Linda / Acevedo Arozena, Abraham / Isaacs, Adrian M / Davies, Benjamin /
    Fratta, Pietro / Fisher, Elizabeth M C

    Brain : a journal of neurology

    2017  Volume 140, Issue 11, Page(s) 2797–2805

    Abstract: Mutations in FUS are causative for amyotrophic lateral sclerosis with a dominant mode of inheritance. In trying to model FUS-amyotrophic lateral sclerosis (ALS) in mouse it is clear that FUS is dosage-sensitive and effects arise from overexpression per ... ...

    Abstract Mutations in FUS are causative for amyotrophic lateral sclerosis with a dominant mode of inheritance. In trying to model FUS-amyotrophic lateral sclerosis (ALS) in mouse it is clear that FUS is dosage-sensitive and effects arise from overexpression per se in transgenic strains. Novel models are required that maintain physiological levels of FUS expression and that recapitulate the human disease-with progressive loss of motor neurons in heterozygous animals. Here, we describe a new humanized FUS-ALS mouse with a frameshift mutation, which fulfils both criteria: the FUS Delta14 mouse. Heterozygous animals express mutant humanized FUS protein at physiological levels and have adult onset progressive motor neuron loss and denervation of neuromuscular junctions. Additionally, we generated a novel antibody to the unique human frameshift peptide epitope, allowing specific identification of mutant FUS only. Using our new FUSDelta14 ALS mouse-antibody system we show that neurodegeneration occurs in the absence of FUS protein aggregation. FUS mislocalization increases as disease progresses, and mutant FUS accumulates at the rough endoplasmic reticulum. Further, transcriptomic analyses show progressive changes in ribosomal protein levels and mitochondrial function as early disease stages are initiated. Thus, our new physiological mouse model has provided novel insight into the early pathogenesis of FUS-ALS.
    MeSH term(s) Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Disease Models, Animal ; Endoplasmic Reticulum, Rough/metabolism ; Frameshift Mutation ; Gene Dosage ; Gene Expression Profiling ; Gene Knock-In Techniques ; Heterozygote ; Humans ; Mice ; Mitochondria/metabolism ; Motor Neurons/metabolism ; Neuromuscular Junction/metabolism ; Protein Aggregation, Pathological/genetics ; Protein Aggregation, Pathological/metabolism ; RNA-Binding Protein FUS/genetics ; RNA-Binding Protein FUS/metabolism ; Ribosomal Proteins/genetics
    Chemical Substances RNA-Binding Protein FUS ; Ribosomal Proteins
    Language English
    Publishing date 2017-10-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awx248
    Database MEDical Literature Analysis and Retrieval System OnLINE

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