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Yuji Naito
Researcher at Kyoto Prefectural University of Medicine
Publications - 861
Citations - 23341
Yuji Naito is an academic researcher from Kyoto Prefectural University of Medicine. The author has contributed to research in topics: Medicine & Gastric mucosa. The author has an hindex of 65, co-authored 810 publications receiving 19381 citations. Previous affiliations of Yuji Naito include Kyoto Prefectural University.
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Gut microbiota in the pathogenesis of inflammatory bowel disease
TL;DR: Clinical and experimental data suggest dysbiosis may play a pivotal role in the pathogenesis of IBD, and the therapeutic options for manipulating the altered gut microbiota, such as probiotics and fecal microbiota transplantation are reviewed.
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Midterm clinical result of tissue-engineered vascular autografts seeded with autologous bone marrow cells.
Toshiharu Shinoka,Goki Matsumura,Narutoshi Hibino,Yuji Naito,Manabu Watanabe,Takeshi Konuma,Takahiko Sakamoto,Masayoshi Nagatsu,Hiromi Kurosawa +8 more
TL;DR: Biodegradable conduits or patches seeded with autologous bone marrow cells showed normal function and the tissue-engineering approach may provide an important alternative to the use of prosthetic materials in the field of pediatric cardiovascular surgery.
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Silver nanoparticles as a safe preservative for use in cosmetics
TL;DR: Ag nanoparticles were found to be very stable, showed sufficient preservation efficacy against mixed bacteria and mixed fungi, and did not penetrate normal human skin, suggesting that Ag nanoparticles may have potential for use as a preservative in cosmetics.
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Role of active oxygen, lipid peroxidation, and antioxidants in the pathogenesis of gastric mucosal injury induced by indomethacin in rats.
Toshikazu Yoshikawa,Yuji Naito,A Kishi,Takashi Tomii,Toshiro Kaneko,Iinuma S,Hiroshi Ichikawa,Mitsunori Yasuda,S Takahashi,Kondo M +9 more
TL;DR: It is suggested that active oxygen species and lipid peroxidation play an important part in the pathogenesis of gastric mucosal injury induced by indomethacin, and that the decreased glutathione peroxidase activity aggravated the injury due to accelerated accumulation of hydrogen peroxide and lipidperoxides in the gastricucosal cell.
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Heme oxygenase-1 and anti-inflammatory M2 macrophages.
TL;DR: The present current evidence indicates that HO-1 induction mediated by multiple pathways can drive the phenotypic shift to M2 macrophages and suggests that HO -1 induction in macrophage is a potential therapeutic approach to immunomodulation in widely diverse human diseases.