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Yoshinori Taniguchi

Researcher at Kōchi University

Publications -  118
Citations -  1770

Yoshinori Taniguchi is an academic researcher from Kōchi University. The author has contributed to research in topics: Medicine & Kidney disease. The author has an hindex of 20, co-authored 102 publications receiving 1364 citations. Previous affiliations of Yoshinori Taniguchi include University of Washington.

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Ixekizumab, an interleukin-17A antagonist in the treatment of ankylosing spondylitis or radiographic axial spondyloarthritis in patients previously untreated with biological disease-modifying anti-rheumatic drugs (COAST-V): 16 week results of a phase 3 randomised, double-blind, active-controlled and placebo-controlled trial

Désirée van der Heijde, +90 more
- 08 Dec 2018 - 
TL;DR: Each dosing regimen of ixekizumab was superior to placebo for improving radiographic axial spondyloarthritis signs and symptoms in patients not previously treated with bDMARDs; the safety profile was consistent with previous indications of IXekzumab.
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Sestrin-2 and BNIP3 regulate autophagy and mitophagy in renal tubular cells in acute kidney injury.

TL;DR: Observations demonstrate that autophagy is induced in renal tubules by at least two independent pathways involving p53-sestrin-2 and HIF-1α-BNIP3, which may be activated by different types of stress to protect the renal tubule during AKI.
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Ixekizumab for patients with non-radiographic axial spondyloarthritis (COAST-X): a randomised, placebo-controlled trial

Atul Deodhar, +117 more
- 04 Jan 2020 - 
TL;DR: Ixekizumab was superior to placebo for improving signs and symptoms in patients with non-radiographic axial spondyloarthritis and no new safety signals were identified.
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Cisplatin-induced macroautophagy occurs prior to apoptosis in proximal tubules in vivo

TL;DR: The data suggest that autophagy is a kind of cell damage index and that cells with activated Autophagy will be scavenged by apoptosis, and is involved in cell death in renal tubular injury.
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Retinoids augment the expression of podocyte proteins by glomerular parietal epithelial cells in experimental glomerular disease.

TL;DR: ATRA statistically significantly increased the number of glomerular epithelial transition cells in experimental proteinuricglomerular diseases and may provide a useful pharmacologic approach to decipher the mechanisms underlying the possible progenitor role of parietal epithelial cells.