Publications by authors named "K Tsuburaya"

Over-drainage after a ventriculoperitoneal (VP) shunt can often lead to chronic subdural hematoma; however, the treatment is unclear. Hematoma drainage is performed after physically stopping the shunt function, such as by ligating or removing the shunt system. However, shunt reconstruction is required after the subdural hematoma improves.

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Isolated abducens nerve palsy (IANP), caused by secondary communicating hydrocephalus, has been rarely documented; in addition, its mechanism and appropriate treatment are not understood well. This study presents a case of bilateral IANP with hydrocephalus in a 62-year-old man who was successfully treated with cerebrospinal fluid (CSF) diversion to correct an enlarged retroclival space during the follow-up of recurrent brain tumor in the right parieto-occipital lobe. The patient was treated with three resections, temozolomide, and irradiation before developing IANP.

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As a candidate microRNA antifibrotic effector in skin wounds, miR-146b-5p was upregulated by basic FGF, and PDGFRα was identified as a direct target of miR-146b-5p in fibroblasts. The treatment of fibroblasts with a miR-146b-5p mimic markedly downregulated the expression of PDGFRα and collagen type I. miR-146b-5p mimic transfection in wounds markedly attenuated cutaneous fibrosis, whereas a miR-146b-5p inhibitor strongly promoted fibrosis, with increases in PDGFRα and collagen I levels.

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Endogenous neural stem/progenitor cells (NPCs) can migrate toward sites of injury, but the migration activity of NPCs is insufficient to regenerate damaged brain tissue. In this study, we showed that p38 MAP kinase (p38) is expressed in doublecortin-positive adult NPCs. Experiments using the p38 inhibitor SB203580 revealed that endogenous p38 participates in NPC migration.

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Aims: Sporadic amyotrophic lateral sclerosis (SALS) seems to be a multifactorial disease, the pathogenesis of which may involve both genetic and environmental factors. The present study aims at identifying a possible genetic change that confers risk for SALS.

Methods: We performed whole-genome screening of a copy-number variation (CNV) using a CNV beadchip, followed by real-time quantitative polymerase chain reaction (qPCR) and region-targeted high-density oligonucleotide tiling microarray.

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