25 research outputs found

    Relative commutants of strongly self-absorbing C*-algebras

    Get PDF
    The relative commutant AAUA'\cap A^{\mathcal{U}} of a strongly self-absorbing algebra AA is indistinguishable from its ultrapower AUA^{\mathcal{U}}. This applies both to the case when AA is the hyperfinite II1_1 factor and to the case when it is a strongly self-absorbing C*-algebra. In the latter case we prove analogous results for (A)/c0(A)\ell_\infty(A)/c_0(A) and reduced powers corresponding to other filters on N\bf N. Examples of algebras with approximately inner flip and approximately inner half-flip are provided, showing the optimality of our results. We also prove that strongly self-absorbing algebras are smoothly classifiable, unlike the algebras with approximately inner half-flip.Comment: Some minor correction

    Some Calkin algebras have outer automorphisms

    No full text

    THE ISOMORPHISM RELATION FOR SEPARABLE C*-ALGEBRAS

    No full text
    Abstract. We prove that the isomorphism relation for separable C ∗-algebras, and also the relations of complete and n-isometry for operator spaces and systems, are Borel reducible to the orbit equivalence relation of a Polish group action on a standard Borel space. 1

    Glial Fibrillary Acidic Protein Autoimmunity After Aseptic Meningitis: A Report of 2 Cases

    No full text
    Bien C, Büttner T, Reichen I, et al. Glial Fibrillary Acidic Protein Autoimmunity After Aseptic Meningitis: A Report of 2 Cases. Neurology: Neuroimmunology & Neuroinflammation. 2024;11(1): e200180.OBJECTIVES: We describe 2 patients with glial fibrillary acidic protein (GFAP) autoimmunity secondary to aseptic viral meningitis or meningoencephalomyelitis.; METHODS: This study involved a retrospective chart review.; RESULTS: Two female patients, 45 and 55 years of age, developed aseptic meningoencephalomyelitis or meningitis; in one patient, it was likely caused by herpes simplex virus 2. The patients were recovering from the infectious condition when they, 51 and 5 days after onset, had new symptoms with detection of GFAP antibodies in the CSF; CSF and serum samples from the initial lumbar punctures had been negative for GFAP antibodies. Both patients recovered with steroid treatment (in one case, plus rituximab; in the other, plus azathioprine) including resolution of MRI and CSF abnormalities.; DISCUSSION: These 2 patients had GFAP autoimmunity secondary to viral meningoencephalomyelitis or meningitis. This suggests that GFAP astrocytopathy might not always be a primary disease entity; it may follow another brain injury that triggers this autoimmune response. Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology

    NR1H3 p.Arg415Gln is not associated to multiple sclerosis risk

    Full text link
    A recent study by Wang et al. (2016a) claims that the low-frequency variant NR1H3 p.Arg415Gln is sufficient to cause multiple sclerosis in certain individuals and determines a patient's likelihood of primary progressive disease. We sought to replicate this finding in the International MS Genetics Consortium (IMSGC) patient collection, which is 13-fold larger than the collection of Wang et al. (2016a), but we find no evidence that this variant is associated with either MS or disease subtype. Wang et al. (2016a) also report a common variant association in the region, which we show captures the association the IMSGC reported in 2013. Therefore, we conclude that the reported low-frequency association is a false positive, likely generated by insufficient sample size. The claim of NR1H3 mutations describing a Mendelian form of MS-of which no examples exist-can therefore not be substantiated by data. This Matters Arising paper is in response to Wang et al. (2016a), published in Neuron. See also the related Matters Arising paper by Minikel and MacArthur (2016) and the response by Wang et al. (2016b), published in this issue
    corecore