R
R. Yanagihara
Researcher at National Institutes of Health
Publications - 52
Citations - 1654
R. Yanagihara is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Scrapie & Virus. The author has an hindex of 26, co-authored 52 publications receiving 1629 citations.
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Complete nucleotide sequence of a highly divergent human T-cell leukemia (lymphotropic) virus type I (HTLV-I) variant from melanesia: genetic and phylogenetic relationship to HTLV-I strains from other geographical regions.
TL;DR: The complete nucleotide sequence of an HTLV-I isolate from the Solomon Islands is reported, suggesting it could not have arisen from a reocmbinational event involvingHTLV-II but rather might be an example of independent viral evolution in this remote population.
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Heightened expression of tumor necrosis factor alpha, interleukin 1 alpha, and glial fibrillary acidic protein in experimental Creutzfeldt-Jakob disease in mice
TL;DR: The collective findings of T NF-alpha overexpression during the course of clinical disease suggest that TNF-alpha may mediate the myelin sheath vacuolation observed in experimental CJD.
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New haemorrhagic fever with renal syndrome-related virus in indigenous wild rodents in united states
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Characterization of a variant of human T-lymphotropic virus type I isolated from a healthy member of a remote, recently contacted group in Papua New Guinea.
R. Yanagihara,Vivek R. Nerurkar,Ralph M. Garruto,Mark A. Miller,M E Leon-Monzon,C L Jenkins,R C Sanders,Pawel P. Liberski,Michael P. Alpers,D. C. Gajdusek +9 more
TL;DR: A variant of human T-lymphotropic virus type I (HTLV-I) isolated from an interleukin 2-dependent, CD8+ T-cell line derived from peripheral blood mononuclear cells of a healthy member of a remote, recently contacted hunter-horticulturalist group in Madang province of Papua New Guinea is characterized.
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White matter ultrastructural pathology of experimental Creutzfeldt-Jakob disease in mice
TL;DR: The data indicate that the damage to myelinated axons in the panencephalopathic type of CJD is accomplished primarily by active degradation of myelin by macrophages and astrocytes and by formation of intra-axonal and intra-myelin vacuoles.