N
Naomi Sugimori
Researcher at Kanazawa University
Publications - 31
Citations - 684
Naomi Sugimori is an academic researcher from Kanazawa University. The author has contributed to research in topics: Aplastic anemia & Bone marrow. The author has an hindex of 14, co-authored 31 publications receiving 636 citations. Previous affiliations of Naomi Sugimori include Ehime University.
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Journal ArticleDOI
Characterization of T-cell repertoire of the bone marrow in immune-mediated aplastic anemia: evidence for the involvement of antigen-driven T-cell response in cyclosporine-dependent aplastic anemia
Weihua Zeng,Shinji Nakao,Hideyuki Takamatsu,Akihiro Yachie,Akiyoshi Takami,Yukio Kondo,Naomi Sugimori,Hirohito Yamazaki,Yuji Miura,Shintaro Shiobara,Tamotsu Matsuda +10 more
TL;DR: Findings indicate that antigen-driven expansion of T cells is involved in the pathogenesis of AA characterized by CyA-dependent recovery of hematopoiesis, with high homology of the amino acid sequence of the CDR3 between two different patients.
Journal ArticleDOI
Isolation of a T-Cell Clone Showing HLA-DRB1*0405-Restricted Cytotoxicity for Hematopoietic Cells in a Patient With Aplastic Anemia
Shinji Nakao,Akiyoshi Takami,Akiyoshi Takami,Hideyuki Takamatsu,Hideyuki Takamatsu,Weihua Zeng,Weihua Zeng,Naomi Sugimori,Naomi Sugimori,H Yamazaki,H Yamazaki,Yuji Miura,Yuji Miura,Mikio Ueda,Mikio Ueda,Shintaro Shiobara,Shintaro Shiobara,Takeshi Yoshioka,Takeshi Yoshioka,Toshihiko Kaneshige,Toshihiko Kaneshige,Masaki Yasukawa,Masaki Yasukawa,Tamotsu Matsuda,Tamotsu Matsuda +24 more
TL;DR: The results indicate that the AA patient has T cells capable of killing hematopoietic cells in an HLA-DRB1*0405-restricted manner and that such cytotoxic T cells may contribute to the pathogenesis of AA.
Journal ArticleDOI
Origin and fate of blood cells deficient in glycosylphosphatidylinositol-anchored protein among patients with bone marrow failure.
Chiharu Sugimori,Kanako Mochizuki,Zhirong Qi,Naomi Sugimori,Ken Ishiyama,Yukio Kondo,Hirohito Yamazaki,Akiyoshi Takami,Hirokazu Okumura,Shinji Nakao +9 more
TL;DR: The findings suggest that the PNH‐type cells in patients with BM failure are derived from single PIGA mutant haematopoietic stem cells even when their percentages are <1% and their fate depends on the proliferation and self‐maintenance properties of the individual PIG a mutants.
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Favorable outcome of patients who have 13q deletion: a suggestion for revision of the WHO ‘MDS-U’ designation
Kohei Hosokawa,Takamasa Katagiri,Naomi Sugimori,Ken Ishiyama,Yumi Sasaki,Yu Seiki,Aiko Sato-Otsubo,Masashi Sanada,Seishi Ogawa,Shinji Nakao +9 more
TL;DR: It is suggested that myelodysplastic syndrome-unclassified with del(13q) is a benign bone marrow failure subset characterized by good response to immunosuppressive therapy and a high prevalence of increased glycosylphosphatidylinositol-anchored protein-deficient cells, and should not be considered an intermediate-risk chromosomal abnormality.
Journal ArticleDOI
Aberrant increase in the immature platelet fraction in patients with myelodysplastic syndrome: a marker of karyotypic abnormalities associated with poor prognosis
Naomi Sugimori,Yukio Kondo,Masami Shibayama,Mika Omote,Akiyoshi Takami,Chiharu Sugimori,Ken Ishiyama,Hirohito Yamazaki,Shinji Nakao +8 more
TL;DR: Some patients with myelodysplastic syndrome show a marked increase in the percentage of immature platelet fraction (IPF%) despite the absence of severe thrombocytopenia, and this investigation investigated the IPF% and other laboratory findings of 51 patients recently diagnosed with MDS.