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               <dc:title>14-3-3 protein in the CSF as prognostic marker in early multiple sclerosis</dc:title>
               <dc:creator>Martínez Yélamos, Antonio</dc:creator>
               <dc:creator>Saiz Hinarejos, Albert</dc:creator>
               <dc:creator>Sánchez del Valle Díaz, Raquel</dc:creator>
               <dc:creator>Casado Ruiz, Virginia</dc:creator>
               <dc:creator>Ramon Torrell, Josep M. (Josep Maria)</dc:creator>
               <dc:creator>Graus Ribas, Francesc</dc:creator>
               <dc:creator>Arbizu Urdiain, Txomin</dc:creator>
               <dc:subject>Líquid cefalorraquidi</dc:subject>
               <dc:subject>Esclerosi múltiple</dc:subject>
               <dc:subject>Proteïna-tirosina-fosfatasa</dc:subject>
               <dc:subject>Cerebrospinal fluid</dc:subject>
               <dc:subject>Multiple sclerosis</dc:subject>
               <dc:subject>Protein-tyrosine phosphatase</dc:subject>
               <dc:description>Axonal damage probably occurs early in the evolution of MS. Five of 38 (13%) patients had a positive assay for the neuronal 14-3-3 protein in the CSF obtained at the first clinically isolated syndrome suggestive of MS. A positive 14-3-3 assay was the only independent predictor for a shorter time to conversion to clinical definite MS (risk ratio 4.1; 95% CI 1.1 to 15) and to reach an Expanded Disability Status Scale (EDSS) > or =2 at the end of follow-up (odds ratio 14.8; 95% CI 2.86 to 76.8). The detection of the 14-3-3 protein in the CSF at the first neurologic event suggestive of MS may be a useful predictor of short-term evolution.</dc:description>
               <dc:date>2020-04-24T11:17:43Z</dc:date>
               <dc:date>2020-04-24T11:17:43Z</dc:date>
               <dc:date>2001-08-28</dc:date>
               <dc:date>2020-04-24T11:17:43Z</dc:date>
               <dc:type>info:eu-repo/semantics/article</dc:type>
               <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
               <dc:relation>Reproducció del document publicat a: https://doi.org/10.1212/wnl.57.4.722</dc:relation>
               <dc:relation>Neurology, 2001, vol. 57, num. 4, p. 722-724</dc:relation>
               <dc:relation>https://doi.org/10.1212/wnl.57.4.722</dc:relation>
               <dc:rights>(c) American Academy of Neurology, 2001</dc:rights>
               <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
               <dc:publisher>Lippincott, Williams &amp; Wilkins. Wolters Kluwer Health</dc:publisher>
               <dc:source>Articles publicats en revistes (Ciències Clíniques)</dc:source>
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