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Nobuhiro Fujii
Researcher at Sapporo Medical University
Publications - 203
Citations - 6887
Nobuhiro Fujii is an academic researcher from Sapporo Medical University. The author has contributed to research in topics: Interferon & Gene. The author has an hindex of 43, co-authored 202 publications receiving 6438 citations. Previous affiliations of Nobuhiro Fujii include Health Sciences University of Hokkaido.
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Journal ArticleDOI
Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Diseases
Nobuyuki Sasaki,Ryo Fukatsu,Kayo Tsuzuki,Yorihide Hayashi,Taku Yoshida,Nobuhiro Fujii,Takao Koike,Ikuro Wakayama,Richard Yanagihara,Ralph A. Garruto,Naoji Amano,Zenji Makita +11 more
TL;DR: The results suggest that AGE may contribute to eventual neuronal dysfunction and death as an important factor in the progression of various neurodegenerative diseases, including Alzheimer's disease.
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Inactivation of SARS Coronavirus by Means of Povidone-Iodine, Physical Conditions and Chemical Reagents
TL;DR: The efficacy of several povidone-iodine (PVP-I) products, a number of other chemical agents and various physical conditions were evaluated for their ability to inactivate the severe acute respiratory syndrome coronavirus (SARS-CoV).
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Induction of Suppressor of Cytokine Signaling-3 by Herpes Simplex Virus Type 1 Contributes to Inhibition of the Interferon Signaling Pathway
Shin-ichi Yokota,Noriko Yokosawa,Tamaki Okabayashi,Tatsuo Suzutani,Shunsuke Miura,Kowichi Jimbow,Nobuhiro Fujii +6 more
TL;DR: The SOCS3 protein appears to be mainly responsible for the suppression of IFN signaling and IFN production that occurs during HSV-1 infection.
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Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.
Tamaki Okabayashi,Hiroaki Kariwa,Shin-ichi Yokota,Shigeo Iki,Tomokazu Indoh,Noriko Yokosawa,Ikuo Takashima,Hiroyuki Tsutsumi,Nobuhiro Fujii +8 more
TL;DR: Overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS.
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Measles virus suppresses interferon-α signaling pathway: suppression of Jak1 phosphorylation and association of viral accessory proteins, C and V, with interferon-α receptor complex
TL;DR: It is suggested that functional disorder of the type I IFN receptor complex is due to “freezing” of the receptor through its association with the C and/or V proteins of MeV.