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大島弘子 제주대학교 1984 논문집 Vol.17 No.1
Ⅰ. 主節의 述語가 現在形인 경우 「PQ」는 P節의 事態가 成立하면 즉시 自然發生的으로, Q節이 成立한다는 意味를 文章이며, Q節에 話者의 主觀的인 態度(特히, 相對方에의 作用을 포함해서)를 나타내는 形式이 오기 어려우며, 個別假定性(未來의 어느 한時點을 假定하는 用法)이 弱하다. 「PQ」는 P節과 Q節의 關係가 必然的인 點에서 「PQ」의 文型과는 重複되지만, Q節의 mood의 制約은 「PQ」보다 부드러우며, 따라서 個別假定性은 「PQ」보다 강하다. 「PQ」는 Q節에 mood의 制約이 없고 P節과 Q節의 關係가 偶然的이다. 따라서 個別假定性이 가장 강하다. Q節이 成立하기 위해선 P節의 完了가 條件이 된다. 「PQ」는 P節을 假定, 그 成立을 前提로하여 話者가 취해야 할 態度 (判斷, 意志, 決意, 要求, 命令등)을 나타낸다. 따라서 Q節은 그러한 形式을 취해야 한다. 또 對話의 서두에 「PQ」의 文章이 오는일은 없다. Ⅱ. 主節의 述語가 過去形인 경우 「PQ」는 Q節에 動作完了를 나타내는 過去形이 오는 일은 없다. 過去의 事實에 反對되는 假想, 確認, 過去의 狀態가 오는 일은 있다. 「PQ」는 對話를 시작할때의 態度 (判斷등)을 나타내는 것이기 때문. 過去形이 오는 일이 없다. 「PQ」는 前半의 P節과 後半의 Q節이 偶然히 同時에, 또는 近接해서 일어나는 일을 말한다. P節과 Q節의 接績에 主體(話者)의 意志는 나타나 있지 않다. 「PQ」는 P節과 Q節의 接續에 意志가 나타나 있거나 나타나 있지 않거나 간에, 同時性, 近接性 繼起性을 가진 두개의 事態를 단지 漠然하게 이어준다. Ⅰ에서 P節과 Q節이 가지고 있던 必然的인 接續관계는 Ⅱ의 경우에는 없다. 「」의 本質的인 機能은 條件表現이 아니고, 이와같이 漠然한 接續關係에 있다고 생각한다.
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Han, Tae-Su,Voon, Dominic Chih-Cheng,Oshima, Hiroko,Nakayama, Mizuho,Echizen, Kanae,Sakai, Eri,Yong, Zachary Wei Ern,Murakami, Kazuhiro,Yu, Liang,Minamoto, Toshinari,Ock, Chan-Young,Jenkins, Brendan J Elsevier 2019 Gastroenterology Vol.156 No.4
<P><B>Background & Aims</B></P> <P>Gastritis is associated with development of stomach cancer, but little is known about changes in microRNA expression patterns during gastric inflammation. Specific changes in gene expression in epithelial cells are difficult to monitor because of the heterogeneity of the tissue. We investigated epithelial cell-specific changes in microRNA expression during gastric inflammation and gastritis-associated carcinogenesis in mice.</P> <P><B>Methods</B></P> <P>We used laser microdissection to enrich epithelial cells from K19-C2mE transgenic mice, which spontaneously develop gastritis-associated hyperplasia, and Gan mice, which express activated prostaglandin E2 and Wnt in the gastric mucosa and develop gastric tumors. We measured expression of epithelial cell-enriched microRNAs and used bioinformatics analyses to integrate data from different systems to identify inflammation-associated microRNAs. We validated our findings in gastric tissues from mice and evaluated protein functions in gastric cell lines (SNU-719, SNU-601, SNU-638, AGS, and GIF-14) and knockout mice. Organoids were cultured from gastric corpus tissues of wild-type and miR-135b–knockout C57BL/6 mice. We measured levels of microRNAs in pairs of gastric tumors and nontumor mucosa from 28 patients in Japan.</P> <P><B>Results</B></P> <P>We found microRNA 135b (miR-135B) to be the most overexpressed microRNA in gastric tissues from K19-C2mE and Gan mice: levels increased during the early stages of gastritis-associated carcinogenesis. Levels of miR-135B were also increased in gastric tumor tissues from <I>gp130</I> <SUP> <I>F/F</I> </SUP> mice and patients compared with nontumor tissues. In gastric organoids and immortalized cell lines, expression of miR-135B was induced by interleukin 1 signaling. K19-C2mE mice with disruption of <I>Mir-135b</I> developed hyperplastic lesions that were 50% smaller than mice without <I>Mir-135b</I> disruption and had significant reductions in cell proliferation. Expression of miR-135B in gastric cancer cell lines increased their colony formation, migration, and sphere formation. We identified <I>FOXN3</I> and <I>RECK</I> messenger RNAs (mRNAs) as targets of miR-135B; their knockdown reduced migration of gastric cancer cell lines. Levels of <I>FOXN3</I> and <I>RECK</I> mRNAs correlated inversely with levels of miR-135B in human gastric tumors and in inflamed mucosa from K19-C2mE mice.</P> <P><B>Conclusions</B></P> <P>We found expression of miR-135B to be up-regulated by interleukin L1 signaling in gastric cancer cells and organoids. miR-135B promotes invasiveness and stem-cell features of gastric cancer cells in culture by reducing <I>FOXN3</I> and <I>RECK</I> messenger RNAs. Levels of these messenger RNA targets, which encode tumor suppressor, are reduced in human gastric tumors.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Nakayama Mizuho,Wang Dong,Kok Sau Yee,Hiroko Oshima,Oshima Masanobu 대한암예방학회 2022 Journal of cancer prevention Vol.27 No.1
Comprehensive genome analyses have identified frequently mutated genes in human colorectal cancers (CRC). These include APC, KRAS, SMAD4, TP53, and FBXW7. The biological functions of the respective gene products in cell proliferation and homeostasis have been intensively examined by in vitro experiments. However, how each gene mutation or combinations of specific mutations drive malignant progression of CRC in vivo has not been fully understood. Based on the genomic information, we generated mouse models that carry multiple mutations of CRC driver genes in various combinations, and we performed comprehensive histological analyses to link genetic alteration(s) and tumor phenotypes, including liver metastasis. In this review article, we summarize the phenotypes of the respective genetic models carrying major driver mutations and discuss a possible mechanism of mutations underlying malignant progression.
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Xiao Ma,Satoshi Tsuda,Xin Yang,Ning Gu,Hiroko Tanabe,Rieko Oshima,Tetsuya Matsushita,Tatsuro Egawa,Ai-Jun Dong,Bei-Wei Zhu,Tatsuya Hayashi 한국식품영양과학회 2013 Journal of medicinal food Vol.16 No.3
Skeletal muscle is a major organ that is important for whole-body glucose metabolism. We found that when isolated rat epitrochlearis muscle was incubated with a Pu-erh tea hot-water extract (PTE) for 30 min, the rate of 3-O-methyl-D-glucose (3MG) transport increased in the absence of insulin. This activation was associated with an increase in Ser473 phosphorylation of Akt, a signaling intermediary leading to insulin-dependent glucose transport, but not Tyr458 phosphorylation of phosphoinositide 3-kinase p85, an upstream molecule of Akt. PTE-stimulated 3MG transport was also not accompanied by Thr172 phosphorylation of the catalytic α-subunit of 5′-AMP-activated protein kinase (AMPK). Gallic acid, a water-soluble ingredient in Pu-erh tea, stimulated Akt phosphorylation, but not AMPK phosphorylation. These results suggest that Pu-erh tea potentially promotes skeletal muscle glucose transport at least in part by activating Akt.
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