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Takako Matsuoka

Researcher at Kindai University

Publications -  9
Citations -  1057

Takako Matsuoka is an academic researcher from Kindai University. The author has contributed to research in topics: Tocilizumab & Neuromyelitis optica. The author has an hindex of 5, co-authored 8 publications receiving 860 citations.

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Dysbiosis in the gut microbiota of patients with multiple sclerosis, with a striking depletion of species belonging to clostridia XIVa and IV clusters

TL;DR: Analysis of the bacterial 16S ribosomal RNA (rRNA) gene by using a high-throughput culture-independent pyrosequencing method provided evidence of a moderate dysbiosis in the structure of gut microbiota in patients with MS, and phylogenetic tree analysis revealed that many of the clostridial species associated with MS might be distinct from those broadly associated with autoimmune conditions.
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Efficacy of the anti–IL-6 receptor antibody tocilizumab in neuromyelitis optica A pilot study

TL;DR: This study provides Class IV evidence that in patients with NMO, TCZ reduces relapse rate, neuropathic pain, and fatigue, and Class III evidence that Interleukin-6 receptor blockade is a promising therapeutic option for NMO.
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Clinical improvement in a patient with neuromyelitis optica following therapy with the anti-IL-6 receptor monoclonal antibody tocilizumab

TL;DR: A case with NMO who responded to monthly administration of the anti-IL-6 receptor antibody tocilizumab and the treatment rapidly reduced the elevated numbers of plasmablasts and anti-AQP4 autoantibodies in the patient.
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Plasmablasts as Migratory IgG-Producing Cells in the Pathogenesis of Neuromyelitis Optica

TL;DR: It is demonstrated that CD138+HLA-DR+ plasmablasts, a subset of IgG-producing cells, are increased in the peripheral blood and are enriched among the cerebrospinal fluid (CSF) lymphocytes during the relapse of neuromyelitis optica.
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Differential effects of fingolimod on B-cell populations in multiple sclerosis.

TL;DR: The frequencies of each B-cell population in peripheral blood mononuclear cells (PBMC) were greatly reduced 2 weeks after starting fingolimod treatment, and a significant reduction in activated memory B cells (CD38int-high), particularly those expressing Ki-67, a marker of cell proliferation.