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Yoshiko Sato

Researcher at Shinshu University

Publications -  25
Citations -  2877

Yoshiko Sato is an academic researcher from Shinshu University. The author has contributed to research in topics: Induced pluripotent stem cell & Medicine. The author has an hindex of 10, co-authored 20 publications receiving 2422 citations. Previous affiliations of Yoshiko Sato include Kyoto University.

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A more efficient method to generate integration-free human iPS cells

TL;DR: A simple method is reported, using p53 suppression and nontransforming L-Myc, to generate human induced pluripotent stem cells (iPSCs) with episomal plasmid vectors, which may provide iPSCs suitable for autologous and allologous stem-cell therapy in the future.
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An Efficient Nonviral Method to Generate Integration-Free Human-Induced Pluripotent Stem Cells from Cord Blood and Peripheral Blood Cells†‡§

TL;DR: A modified protocol enabling efficient iPSC induction from CD34+ cord blood cells and from peripheral blood isolated from healthy donors using these plasmid vectors is reported, which enabled the establishment of blood‐derived iPSCs from seven healthy donors ranging in age from their 20s to their 60s.
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Differentiation-defective phenotypes revealed by large-scale analyses of human pluripotent stem cells.

TL;DR: Comparisons of the in vitro neural differentiation of 40 hiPSCs and 10 human embryonic stem cells showed that seven hiPSC clones retained a significant number of undifferentiated cells even after neural differentiation culture and formed teratoma when transplanted into mouse brains.
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Overview: an iPS cell stock at CiRA.

TL;DR: The iPSC stock is recruited from healthy, consenting HLA-type homozygous donors and is made with peripheral blood-derived mononuclear cells or umbilical cord blood and is intended to be offered not only to Japanese centers but also overseas medical institutions and companies.
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Essential role of gastric gland mucin in preventing gastric cancer in mice

TL;DR: In this article, the authors showed that the absence of αGlcNAc triggers gastric tumorigenesis through inflammation-associated pathways in vivo, and they also observed significantly reduced αGlncNAc in human gastric adenocarcinoma and adenoma.