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著者 平井 陽至|
発行日 2012-03-23
出版物タイトル
資料タイプ 学位論文
著者 永井 祐介|
発行日 2012-03-23
出版物タイトル
資料タイプ 学位論文
著者 岩室 雅也|
発行日 2012-03-23
出版物タイトル
資料タイプ 学位論文
著者 増田 紘子|
発行日 2012-03-23
出版物タイトル
資料タイプ 学位論文
著者 濱田 博喜|
発行日 2012-04
出版物タイトル 岡山実験動物研究会報
28巻
資料タイプ その他
著者 安井 金也|
発行日 2012-04
出版物タイトル 岡山実験動物研究会報
28巻
資料タイプ その他
著者 Miyoshi, Shin-ichi| Abe, Yuki| Senoh, Mitsutoshi| Mizuno, Tamaki| Maehara, Yoko| Nakao, Hiroshi|
発行日 2011-05
出版物タイトル Toxicon
57巻
6号
資料タイプ 学術雑誌論文
著者 Wajima, Takeaki| Sabui, Subrata| Fukumoto, Megumi| Kano, Shigeyuki| Ramamurthy, Thandavarayan| Chatterjee, Nabendu Sekhar| Hamabata, Takashi|
発行日 2011-10
出版物タイトル Microbial Pathogenesis
51巻
4号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/48262
フルテキストURL 66_2_119.pdf.pdf
著者 Oka, Hiroaki| Ouchida, Mamoru| Kondo, Takuya| Morita, Fumio| Shimizu, Kenji|
抄録 Human lymphoblastoid TK6 and WTK-1 cells are widely used to detect mutagens in vitro. TK6 cells have wild-type TP53 alleles, while WTK-1 cells have one allele of mutated TP53. Both cells were treated with 5-fluorouracil (5-FU), and gene mutation assay and micronucleus assay were performed to clarify the differential response related to the TP53 gene status. The effects of 5-FU on gene expression were assessed by microarray and quantitative RT-PCR analyses. In WTK-1 cells, 5-FU increased the frequency of cells with micronucleus and mutation. In TK6 cells, frequency of cells with micronucleus was increased but the mutation frequency was not. The cytotoxicity induced by 5-FU was more prominent in TK6 cells than in WTK-1 cells. Analysis of gene expression showed that the genes involved in the TP53 pathway were up-regulated in TK6 cells but not in WTK-1 cells. The differential responses to 5-FU between these cell lines appeared to be due to the difference in the TP53 gene status, thus providing a molecular basis for the bioassays using these cell lines in the toxicology field. Our results indicate that the clinical efficacy of 5-FU chemotherapy may depend on the TP53 genotype.
キーワード 5-fluorouracil TP53 Tk mutation assays microarray analysis
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2012-04
66巻
2号
出版者 Okayama University Medical School
開始ページ 119
終了ページ 129
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2012 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22525470
Web of Science KeyUT 000303175300005
JaLCDOI 10.18926/AMO/48261
フルテキストURL 66_2_111.pdf.pdf
著者 Shinomiya, Misae| Kawamura, Kenji| Tanida, Emiko| Nagoshi, Megumi| Motoda, Hirotoshi| Kasanami, Yoshiko| Hiragami, Fukumi| Kano, Yoshio|
抄録 We studied the effects of natural essential oil on neurite outgrowth in PC12m3 neuronal cells to elucidate the mechanism underlying the action of the oils used in aromatherapy. Neurite outgrowth can be induced by nerve growth factor (NGF), where ERK and p38 MAPK among MAPK pathways play important roles in activating intracellular signal transduction. In this study, we investigated whether d-limonene, the major component of essential oils from oranges, can promote neurite outgrowth in PC12m3 cells, in which neurite outgrowth can be induced by various physical stimulations. We also examined by which pathways, the ERK, p38 MAPK or JNK pathway, d-limonene acts on PC12m3 cells. Our results showed that neurite outgrowth can be induced when the cells are treated with d-limonene. After treatment with d-limonene, we observed that p38 MAPK is strongly activated in PC12m3 cells, while ERK is weakly activated. In contrast, JNK shows little activity. A study using an inhibitor of p38 MAPK revealed that neurite outgrowth in PC12m3 cells is induced via the activation of p38 MAPK by d-limonene. The results thus indicate that d-limonene may promote neural cell differentiation mainly via activation of the p38 MAPK pathway.
キーワード essential oil d-limonene p38 MAP kinase PC12 mutant cells
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2012-04
66巻
2号
出版者 Okayama University Medical School
開始ページ 111
終了ページ 118
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2012 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22525469
Web of Science KeyUT 000303175300004
JaLCDOI 10.18926/AMO/48258
フルテキストURL 66_2_83.pdf.pdf
著者 Kuroda, Shinji| Urata, Yasuo| Fujiwara, Toshiyoshi|
抄録 Radiotherapy plays a central part in cancer treatment, and use of radiosensitizing agents can greatly enhance this modality. Although studies have shown that several chemotherapeutic agents have the potential to increase the radiosensitivity of tumor cells, investigators have also studied a number of molecularly targeted agents as radiosensitizers in clinical trials based on reasonably promising preclinical data. Recent intense research into the DNA damage-signaling pathway revealed that ataxia-telangiectasia mutated (ATM) and the Mre11-Rad50-NBS1 (MRN) complex play central roles in DNA repair and cell cycle checkpoints and that these molecules are promising targets for radiosensitization. Researchers recently developed three ATM inhibitors (KU-55933, CGK733, and CP466722) and an MRN complex inhibitor (mirin) and showed that they have great potential as radiosensitizers of tumors in preclinical studies. Additionally, we showed that a telomerase-dependent oncolytic adenovirus that we developed (OBP-301 [telomelysin]) produces profound radiosensitizing effects by inhibiting the MRN complex via the adenoviral E1B55kDa protein. A recent Phase I trial in the United States determined that telomelysin was safe and well tolerated in humans, and this agent is about to be tested in combination with radiotherapy in a clinical trial based on intriguing preclinical data demonstrating that telomelysin and ionizing radiation can potentiate each other. In this review, we highlight the great potential of ATM and MRN complex inhibitors, including telomelysin, as radiosensitizing agents.
キーワード ATM (ataxia-telangiectasia mutated) MRN (Mre11-Rad50-NBS1) complex radiosensitization adenovirus E1B55kDa
Amo Type Review
出版物タイトル Acta Medica Okayama
発行日 2012-04
66巻
2号
出版者 Okayama University Medical School
開始ページ 83
終了ページ 92
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2012 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22525466
Web of Science KeyUT 000303175300001
著者 田中 弘之|
発行日 2012-04-01
出版物タイトル 岡山医学会雑誌
124巻
1号
資料タイプ 学術雑誌論文
著者 西崎 正彦| 藤原 康宏| 丁田 泰宏| 金澤 卓| 二宮 基樹| 藤原 俊義|
発行日 2012-04-01
出版物タイトル 岡山医学会雑誌
124巻
1号
資料タイプ 学術雑誌論文
著者 王 英正|
発行日 2012-04-01
出版物タイトル 岡山医学会雑誌
124巻
1号
資料タイプ 学術雑誌論文
著者 万倉 三正| 野田 泰子| 森 昭胤|
発行日 2012-04-01
出版物タイトル 岡山医学会雑誌
124巻
1号
資料タイプ 学術雑誌論文
著者 朝倉 昇司| 橋本 大吾| 高嶋 秀一郎| 杉山 暖子| 前田 嘉信| 赤司 浩一| 谷本 光音| 豊嶋 崇徳|
発行日 2012-04-01
出版物タイトル 岡山医学会雑誌
124巻
1号
資料タイプ 学術雑誌論文
著者 別宮 洋子| 二宮 善文| 大橋 俊孝|
発行日 2012-04-01
出版物タイトル 岡山医学会雑誌
124巻
1号
資料タイプ 学術雑誌論文
著者 Ichiyama, Kenji| Mitsuzumi, Hitoshi| Zhong, Ming| Tai, Akihiro| Tsuchioka, Akihiro| Kawai, Saeko| Yamamoto, Itaru| Gohda, Eiichi|
発行日 2009-02-21
出版物タイトル Immunology Letters
122巻
2号
資料タイプ 学術雑誌論文