2022/12/01 更新

写真a

オオサワ マミ
大澤 まみ
OSAWA Mami
所属
教育研究院 医歯学系 保健学系列 助教
医学部 保健学科 検査技術科学専攻 助教
職名
助教
外部リンク

学位

  • 博士(医学) ( 2021年3月   新潟大学 )

  • 修士(医科学) ( 2015年3月   新潟大学 )

  • 学士(保健学) ( 2013年3月   新潟大学 )

研究キーワード

  • アポトーシス

  • 代償性増殖

  • エクソソーム

  • 臨床化学

  • 脂質

  • 薬剤耐性

研究分野

  • ライフサイエンス / 分子生物学

  • ライフサイエンス / 医化学

経歴(researchmap)

  • 新潟大学   医学部保健学科検査技術科学   助教

    2022年4月 - 現在

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  • 新潟大学医歯学総合病院   臨床検査技師

    2015年4月 - 2022年3月

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経歴

  • 新潟大学   教育研究院 医歯学系 保健学系列   助教

    2022年4月 - 現在

  • 新潟大学   医学部 保健学科 検査技術科学専攻   助教

    2022年4月 - 現在

学歴

  • 新潟大学医歯学総合研究科   分子細胞医学専攻   医学博士

    2016年4月 - 2021年3月

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  • 新潟大学医歯学総合研究科医科学専攻   医科学専攻   医学修士

    2013年4月 - 2015年3月

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  • 新潟大学   医学部保健学科   検査技術科学専攻

    2009年4月 - 2013年3月

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所属学協会

委員歴

  • 一般社団法人新潟県臨床検査技師会   新潟支部幹事 生涯教育  

    2017年4月 - 2019年3月   

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論文

  • Exosomal p38 Mitogen-activated Protein Kinase Promotes Tumour Repopulation in TP53-mutated Bile Duct Cancer Cells. 査読 国際誌

    Mami Osawa, Yasunobu Matsuda, Jun Sakata, Toshifumi Wakai

    Anticancer research   42 ( 2 )   745 - 757   2022年2月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND/AIM: Tumour repopulation is a major obstacle for successful cancer treatment. This study investigated whether anticancer agents contribute to tumour repopulation in TP53-mutated bile duct cancer cells. MATERIALS AND METHODS: TP53-mutated HuCCT1 and HuH28 cells were exposed to anticancer agents, and recipient cells were exposed to their conditioned media or exosomes. The effect of inhibitors and siRNA-mediated gene silencing of p38 mitogen-activated protein kinase (MAPK) and of TP53 was analyzed by cell proliferation assays and western blotting. RESULTS: Conditioned media from genotoxic agent-treated cells promoted proliferation of recipient cells (p<0.05), and this effect was abrogated by exosome inhibitors. Exosomes from gemcitabine- or cisplatin-treated cells increased cell proliferation by 1.6- to 2.2-fold (p<0.05) through p38 MAPK signalling. These effects of exosomes were inhibited by inhibition/silencing of p38 MAPK but not by TP53 silencing. CONCLUSION: Exosomal p38 MAPK plays a pivotal role in tumour repopulation in a TP53-independent manner.

    DOI: 10.21873/anticanres.15533

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  • Urokinase-type Plasminogen Activator Is a Therapeutic Target for Overcoming Sorafenib Resistance in Hepatoma Cells. 査読 国際誌

    Mami Osawa, Yasunobu Matsuda, Yoshiaki Kinoshita, Toshifumi Wakai

    Anticancer Research   41 ( 2 )   645 - 660   2021年2月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND/AIM: Sorafenib is a multikinase inhibitor approved as a first-line therapy for hepatocellular carcinoma. This study examined the sorafenib resistance mechanism. MATERIALS AND METHODS: Hepatoma HepG2 cells were exposed to sorafenib, and the biological activity of the conditioned media was analyzed using cell proliferation/apoptosis assays, multiplex immunoassays, ELISA, and western blot analyses. The effect of urokinase-type plasminogen activator (uPA) inhibitors or siRNA-mediated gene silencing was examined in culture experiments and a mouse xenograft tumor model. RESULTS: Sorafenib increased uPA secretion, which was abrogated by an Akt inhibitor. The growth-inhibitory effect of sorafenib was significantly enhanced by the uPA inhibitors UK122 and amiloride. Sorafenib-induced apoptosis was increased 2.4-fold in uPA siRNA-transduced cells (p<0.05). Combined therapy with sorafenib and amiloride significantly decreased tumor volumes [mean volume: 759 mm3 (sorafenib) vs. 283 mm3 (sorafenib plus amiloride), p<0.05]. CONCLUSION: uPA may play a critical role in sorafenib resistance.

    DOI: 10.21873/anticanres.14816

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  • Epidermal growth factor receptor/heme oxygenase-1 axis is involved in chemoresistance to cisplatin and pirarubicin in HepG2 cell lines and hepatoblastoma specimens. 査読 国際誌

    Takashi Kobayashi, Masayuki Kubota, Yoshiaki Kinoshita, Yuhki Arai, Toshiyuki Oyama, Naoki Yokota, Koichi Saito, Yasunobu Matsuda, Mami Osawa

    Pediatric Surgery International   35 ( 12 )   1369 - 1378   2019年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    PURPOSE: To investigate the possibility that the antioxidant stress protein Heme oxygenase-1 (HO-1) is involved in the acquisition of chemoresistance in cisplatin and pirarubicin (CITA) therapy. METHODS: Human hepatoblastoma-derived cell line (HepG2) was used to generate a knockdown cell line of HO-1 by small interfering RNA (siRNA). Expression of HO-1, epidermal growth factor receptor (EGFR), Akt, and extracellular signal-regulated kinase1/2 (ERK1/2) was examined by Western blot. The cytotoxic effect of cisplatin, pirarubicin, and EGFR inhibitor was examined by trypan blue staining. In human hepatoblastoma specimens (n = 5), changes of HO-1 expression were examined immunohistochemically before and after CITA therapy. RESULTS: HO-1 expression in HepG2 cells was increased by the treatment of cisplatin (CDDP) and pirarubicin (THP) dose-dependently. In HO-1 knockdown HepG2 cells, the HO-1 was not expressed and the percentage of trypan blue-positive cells (dead cells) was significantly increased after treatment of CDDP and THP. The EGFR inhibitor decreased the levels of HO-1, phospho-Akt and phospho-ERK1/2 in HepG2 cells. Combination treatment of EGFR inhibitor with CDDP and THP increased the cytotoxic effect in HepG2 cells. In human hepatoblastoma specimens, 4 of the 5 patients (80%) showed HO-1 expression changed much stronger in the viable tumor cells after CITA therapy. CONCLUSION: The cytotoxic effects of CDDP and THP were both enhanced under HO-1 knockdown conditions as well as under conditions that inhibit the activation pathway of HO-1 by EGFR inhibitors. EGFR/HO-1 axis may be involved in acquiring chemoresistance in HepG2 cell lines as well as in human hepatoblastoma.

    DOI: 10.1007/s00383-019-04563-5

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  • 肝がん細胞株におけるオーロラキナーゼ阻害剤・ソラフェニブ併用療法の解析 査読

    大澤 まみ, 松田 康伸, 若井 俊文, 廣瀬 雄己, 永橋 昌幸, 坂田 純, 小林 隆, 藤巻 隼, 窪田 正幸

    新潟大学保健学雑誌   12 ( 1 )   57 - 63   2015年9月

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    担当区分:筆頭著者   記述言語:日本語   出版者・発行元:新潟大学医学部保健学科  

    【目的】肝細胞癌(肝がん)は、化学療法の効果が乏しい予後不良な悪性疾患である。本研究では、新規の分子標的薬オーロラキナーゼ阻害剤の肝がんに対する作用機序を解析した。【方法】肝がん細胞株HepG2にオーロラキナーゼ阻害剤AZD1152を添加し、細胞シグナルをウエスタン・ブロットで解析した。また分子標的薬ソラフェニブをAZD1152と併用して、アポトーシス誘導率や細胞増殖を観察した。【結果】AZD1152単剤は、がん細胞の増殖は抑制するものの、細胞殺傷効果は認められなかった。AZD1152添加後のがん細胞では、ストレスキナーゼERKが著明に活性化しており、ERK阻害剤やソラフェニブを併用するとアポトーシス細胞数がAZD1152単剤に比べ約20倍に増加した(p<0.01)。【総括】AZD1152は肝がんに対する殺傷効果が極めて弱く、ERK活性化がその原因であることが示唆された。ソラフェニブはERK阻害作用を有しており、有意にオーロラキナーゼ阻害剤の効果を増強した。(著者抄録)

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  • 代償性増殖 細胞死に伴う細胞調節 の分子機構 査読

    大澤 まみ, 松田 康伸, 若井 俊文, 廣瀬 雄己, 坂田 純, 小林 隆, 藤巻 隼, 窪田 正幸

    新潟大学保健学雑誌   11 ( 1 )   1 - 6   2014年3月

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    担当区分:筆頭著者   記述言語:日本語   出版者・発行元:新潟大学医学部保健学科  

    近年、アポトーシス細胞が周囲の細胞に生存・増殖を促す「代償性増殖作用」をもつことが明らかとなったが、そのメカニズムについては未だ不明な点が多い。最近の研究報告により、アポトーシスを進行させる因子であるカスパーゼが、ストレスキナーゼJNKやプロスタグランジンE2を介して、細胞増殖を誘導させる作用を併せ持つことが明らかになった。また酸化ストレスに関与するインターロイキン-11も、代償性増殖に関与する可能性が報告されており、本機構が多彩な因子によって調節されている可能性が推測されている。今後、さらなる研究の発展により、代償性増殖を利用した医療の発展に期待がもたれる。(著者抄録)

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    その他リンク: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2014&ichushi_jid=J06421&link_issn=&doc_id=20140728400001&doc_link_id=http%3A%2F%2Fhdl.handle.net%2F10191%2F38938&url=http%3A%2F%2Fhdl.handle.net%2F10191%2F38938&type=%90V%8A%83%91%E5%8Aw%81F%90V%8A%83%91%E5%8Aw%8Aw%8Fp%83%8A%83%7C%83W%83g%83%8A_Nuar&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F80230_3.gif

  • 非アルコール性脂肪肝炎関連肝細胞がんにおける活性型p70S6キナーゼの解析 査読

    松田 康伸, 若井 俊文, 廣瀬 雄己, 坂田 純, 小林 隆, 大澤 まみ, 藤巻 隼, 窪田 正幸

    新潟大学保健学雑誌   11 ( 1 )   51 - 56   2014年3月

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    記述言語:日本語   出版者・発行元:新潟大学医学部保健学科  

    【目的】非アルコール性脂肪肝炎(NASH)は、近年急速に増加している原因不明の肝疾患である。本研究では、肝がん治療に有効とされる分子標的薬ラパマイシンの標的シグナルp70S6キナーゼが、NASH肝がんの病態に関与している可能性について検討した。【方法】根治的外科手術療法を施行したNASH肝がん22例の病変組織に対して、リン酸化型(活性型)p70S6キナーゼの免疫組織化学染色を行い、臨床因子・予後の比較検討を行った。【結果】NASH肝がん22例中12例(54.5%)がリン酸化型p70S6キナーゼを高発現しており、組織未分化度と相関した(p=0.047)。リン酸化型P70S6キナーゼ高発現群は、外科切除後3年以内再発率が有意に増加していた(p=0.045)。【総括】p70S6キナーゼを高発現しているNASH肝がんは、再発頻度が高い傾向がある。同シグナルを阻害する分子標的薬ラパマイシンは、本疾患の再発防止に有効である可能性が示唆された。(著者抄録)

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  • Valproic acid overcomes transforming growth factor-beta-mediated sorafenib resistance in hepatocellular carcinoma 査読

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Yuki Hirose, Jun Sakata, Takashi Kobayashi, Shun Fujimaki, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi

    International Journal of Clinical and Experimental Pathology   7 ( 4 )   1299 - 1313   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Hepatitis B virus X stimulates redox signaling through activation of ataxia telangiectasia mutated kinase 査読

    Yasunobu Matsuda, Ayumi Sanpei, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Yuki Hirose, Jun Sakata, Takashi Kobayashi, Shun Fujimaki, Masaaki Takamura, Satoshi Yamagiwa, Masahiko Yano, Shogo Ohkoshi, Yutaka Aoyagi

    International Journal of Clinical and Experimental Pathology   7 ( 5 )   2032 - 2043   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:E-CENTURY PUBLISHING CORP  

    Hepatitis B virus X (HBX) protein plays a crucial role in carcinogenesis, but its mechanism is unclear. The involvement of ataxia telangiectasia mutated (ATM) kinase in the enhanced redox system was investigated by examining the phosphorylation level of ATM in HBX gene-transfected cells and in transgenic mice following redox system manipulation by treatment with hydrogen peroxide (H2O2) or antioxidant. Western blotting and immunostaining showed that phospho-ATM was significantly increased by HBX both in vitro (3.2-fold; p&lt;0.05) and in vivo (4-fold; p&lt;0.05), and this effect was abrogated by antioxidant treatment. The level of PKC-delta in HBX-expressing cells was increased 3.5-fold compared to controls. Nuclear localized NF-E2-related factor 2 (Nrf2) was increased in HBX-expressing cells exposed to H2O2, but remained at lower levels after the treatment with rottlerin, KU55933, or caffeine. The levels of anti-oxidant molecules were increased in HBX expressing cells and in transgenic mice, indicating that HBX stimulates the Nrf2-mediated redox system. The levels of intracellular reactive oxygen species (ROS) were significantly increased in HBX-expressing cells treated with hydrogen peroxide in the presence of ATM inhibitor KU55933 or caffeine. Treatment of HBX-expressing cells with KU55933 or caffeine before the exposure to H2O2 increased the ratio of cell apoptosis to 33 +/- 4% (p&lt;0.05) and 22 +/- 4% (p&lt;0.05), respectively. Collectively, HBX stimulates the ATM-mediated PKC-delta/Nrf2 pathway, and maintains the enhanced activity of the redox system. Therefore, manipulating ATM kinase activity might be a useful strategy for treating HBX-induced carcinogenesis.

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  • Clinical significance of cell cycle inhibitors in hepatocellular carcinoma. 査読

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi, Mami Osawa, Shun Fujimaki, Ayumi Sanpei, Takuya Genda, Takafumi Ichida

    Medical Molecular Morphology   46 ( 4 )   185 - 192   2013年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    It is well accepted that cell cycle regulators are strongly implicated in the progression of cancer development. p16 and p27 are potent cyclin-dependent kinase (CDK) inhibitors involved in G1 phase progression, and are regarded as adverse prognostic biomarkers for various types of cancers. It has been reported that the main mechanism for p16 inactivation is aberrant DNA methylation, while p27 is exclusively inactivated by proteasome-mediated protein degradation. We have found that p27 is decreased in around half of hepatocellular carcinomas (HCCs), and in some cases p27 is inactivated by inappropriate interaction with cyclin D1/CDK4 complexes. In such cases, p16 is concomitantly inactivated through DNA methylation. Taking into consideration the complex interaction between p16 and p27, a comprehensive analysis including p16 and p27 would be useful for predicting the prognosis of HCC patients.

    DOI: 10.1007/s00795-013-0047-7

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  • p27 Is a Critical Prognostic Biomarker in Non-Alcoholic Steatohepatitis-Related Hepatocellular Carcinoma 査読

    Yasunobu Matsuda, Toshifumi Wakai, Yuki Hirose, Mami Osawa, Shun Fujimaki, Masayuki Kubota

    International Journal of Molecular Sciences   14 ( 12 )   23499 - 23515   2013年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MDPI AG  

    Non-alcoholic steatohepatitis (NASH) is a recently identified chronic liver disease, which progresses to liver cirrhosis and hepatocellular carcinoma (HCC). As the number of patients studied to date has been limited, clinically useful prognostic biomarkers of NASH-related HCC have not been available. In this study, we investigated the status of a cell-cycle regulator, p27, in NASH-related HCC. p27 has been regarded as a prognostic factor in various types of cancer patients. A total of 22 cases with NASH-related HCC were analyzed for p27 protein expression, and phosphorylation at threonine 157 (T157) and serine 10 (S10) by immunohistochemical analysis. The correlation of p27 with tumor characteristics, disease-free survival (DFS), and overall survival was analyzed. p27 expression was decreased in 13 HCCs (59%), and was significantly correlated with enlarged tumor size (p = 0.01) and increased cell proliferation (p &lt; 0.01). Phospho-p27 at T157 and S10 was detected in four (18%) and seven (32%) cases, respectively, and patients positive for phospho-p27 (S10) showed reduced DFS (hazard ratio 7.623, p = 0.016) by univariate analysis. Further studies with more patients are required to verify the usefulness of p27 as a biomarker for predicting tumor recurrence in NASH patients.

    DOI: 10.3390/ijms141223499

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  • Effects of rapamycin on granulation formation in response to centrally doubled coiled stents as a tracheal substitute 査読

    Masayuki Kubota, Yasunobu Matsuda, Shun Fujimaki, Mami Osawa, Toshifumi Wakai, Kengo Nakaya

    Journal of Pediatric Surgery   48 ( 12 )   2416 - 2424   2013年12月

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    記述言語:英語   掲載種別:研究論文(国際会議プロシーディングス)  

    Introduction: In experiments involving tracheal wall defects in rabbits, metallic coil stents inevitably induce granulation formation in the defects. We examined the involvement of the mammalian target of rapamycin (mTOR) signaling pathway in granulation formation and examined the effects of rapamycin. Methods: The anterior half of the tracheal wall was removed for a longitudinal length of six tracheal rings. Metallic coils were placed into the tracheal lumen through a wall defect. The rabbits were sacrificed two months after undergoing an endoscopic examination, and the granulation tissue in the tracheal defects was removed for a Western blot analysis and immunohistochemical analysis. Rapamycin (0.5 mg kg- 1 day- 1) was administered three times per week intramuscularly. The data were expressed as the relative expression versus the expression of actin. Results: The level of mTOR phosphorylation in the resected trachea was 0.72 ± 0.45, and it significantly increased in the granulation tissue to 11.6 ± 5.2, with concomitant increases in the phosphorylation levels of p70S6K and S6RP in all five rabbits. Although the systemic administration of rapamycin significantly decreased the levels of phosphorylated mTOR to 4.0 ± 2.4 in the five treated rabbits, the clinical outcomes were unsatisfactory. Three of the five treated rabbits exhibited signs of wound complications, and wet granulation tissue that caused respiratory symptoms was found inside and outside of the coils in four rabbits. Conclusions: Although rapamycin effectively reduced the mTOR activity in the granulation tissue, the granulation formation process seemed to be disturbed, most likely owing to the immunosuppressive effects of rapamycin. © 2013 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.jpedsurg.2013.08.013

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  • P21-activated kinase-2 is a critical mediator of transforming growth factor-beta-induced hepatoma cell migration. 査読

    Munehiro Sato, Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Shun Fujimaki, Ayumi Sanpei, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi

    Journal of Gastroenterology and Hepatology   28 ( 6 )   1047 - 1055   2013年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND AND AIM: Transforming growth factor-beta (TGF-beta) has been shown to play a central role in the promotion of cell motility, but its functional mechanism has remained unclear. With the aim of investigating the diagnostic and treatment modalities for patients with hepatocellular carcinoma (HCC), the signaling pathway that may contribute to TGF-beta-mediated cell invasion in hepatoma cells was evaluated. METHODS: Three hepatoma cell lines, HepG2, PLC/PRF/5, and HLF, were treated with TGF-beta, and the involvement of the non-canonical TGF-beta pathway was analyzed by cell migration assays. HepG2 cells were treated with a p21-activated kinase-2 (PAK2)-targeting small interfering RNA and analyzed for their cell motility. The relationships between the PAK2 status and the clinicopathological characteristics of 62 HCC patients were also analyzed. RESULTS: The cell migration assays showed that Akt is a critical regulator of TGF-beta-mediated cell migration. Western blotting analyses showed that TGF-beta stimulated Akt and PAK2 in all three hepatoma cell lines, and phosphorylated PAK2 was blocked by Akt inhibitor. Suppression of PAK2 expression by small interfering RNA resulted

    DOI: 10.1111/jgh.12150

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  • Mycotoxins are conventional and novel risk biomarkers for hepatocellular carcinoma. 査読

    Yasunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Ayumi Sanpei, Shun Fujimaki

    World Journal of Gastroenterology   19 ( 17 )   2587 - 2590   2013年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Hepatocellular carcinoma (HCC) is a common malignant disease with poor prognosis. To improve the clinical outcome, early diagnosis of HCC arising from nonviral agents and hepatitis virus is important. Among several etiological factors, mycotoxins defined as carcinogens by the International Agency for Research in Cancer (IARC) might be one of the critical risk factors for nonviral HCC. Aflatoxin B1 is the most well-known carcinogenic mycotoxin for HCC, but the role of the other types of mycotoxin remains unclear. Several studies have reported that a chromatographic separation technique based on high-performance liquid chromatography can successfully detect the concentration of mycotoxins in plasma. Recently, serum level of ochratoxin A (OTA), a widely distributed mycotoxin classified as Group 2B by IARC, was evaluated in HCC patients in Egypt. The results suggested that serum OTA levels might be a good biomarker for HCC. In this article, we review recent studies of OTA, and discuss its possible significance as a biomarker of HCC.

    DOI: 10.3748/wjg.v19.i17.2587

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  • DNA damage sensor γ -H2AX is increased in preneoplastic lesions of hepatocellular carcinoma. 査読

    Yaunobu Matsuda, Toshifumi Wakai, Masayuki Kubota, Mami Osawa, Masaaki Takamura, Satoshi Yamagiwa, Yutaka Aoyagi, Ayumi Sanpei, Shun Fujimaki

    The Scientific World Journal   2013   597095 - 597095   2013年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Phosphorylated histone H2AX ( gamma -H2AX) is a potential regulator of DNA repair and is a useful tool for detecting DNA damage. To evaluate the clinical usefulness of gamma -H2AX in hepatocellular carcinoma (HCC), we measured the level of gamma -H2AX in HCC, dysplastic nodule, and nontumorous liver diseases. METHODS: The level of gamma -H2AX was measured by immunohistochemistry in fifty-eight HCC, 18 chronic hepatitis, 22 liver cirrhosis, and 19 dysplastic nodules. Appropriate cases were also examined by fluorescence analysis and western blotting. results: All cases with chronic liver disease showed increased levels of gamma -H2AX expression. In 40 (69.9%) of 58 cases with HCC, the labeling index (LI) of gamma -H2AX was above 50% and was inversely correlated with the histological grade. Mean gamma -H2AX LI was the highest in dysplastic nodule (74.1 +/- 22.1%), which was significantly higher than HCC (P &lt; 0.005). Moreover, gamma -H2AX was significantly increased in nontumorous tissues of HCC as compared with liver cirrhosis without HCC (62.5 +/- 24.7%, from 5.1 to 96.0%, P &lt; 0.005). CONCLUSIONS: gamma -H2AX was increased in the preneoplastic lesions of HCC and

    DOI: 10.1155/2013/597095

    PubMed

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MISC

  • IFCC標準化に対応した4社の乳酸脱水素酵素(LD)活性測定試薬の性能評価

    松田 将門, 大澤 まみ, 星山 良樹, 成田 一衛

    医療検査と自動化   45 ( 4 )   396 - 396   2020年8月

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    記述言語:日本語   出版者・発行元:(一社)日本医療検査科学会  

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  • 私が国立大学病院を職場に選んだ理由 -若手技師からみた検査部-

    大澤まみ

    全国国立臨床検査技師会会誌   2018年6月

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    担当区分:筆頭著者  

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  • 家兎における代用気管としての中心部二重コイルと周囲肉芽形成に対するラパマイシンの効果

    窪田 正幸, 松田 康信, 藤巻 隼, 大澤 まみ, 若井 俊文, 仲谷 健吾

    日本小児外科学会雑誌   51 ( 2 )   300 - 300   2015年4月

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    記述言語:日本語   出版者・発行元:(NPO)日本小児外科学会  

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  • Blockade of CD26 Augments the Therapeutic Potential of Marrow Stem Cells in the Liver

    MATSUDA Yasunobu, WAKAI Toshifumi, HIROSE Yuki, Sakata Jun, Kobayashi Takashi, Osawa Mami, Fujimaki Shun, Kubota Masayuki

    新潟大学保健学雑誌 = Journal of health sciences of Niigata University   11 ( 1 )   39 - 49   2014年3月

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    記述言語:英語   出版者・発行元:新潟大学医学部保健学科  

    Background & Aims: The therapeutic potential of marrow stem cells for liver disease is currently unclear. The aim of this study was to investigate whether potentiating the chemotaxis ability of stromal cell-derived factor 1 could augment the engraftment of marrow stem cells and ameliorate tissue damage. Methods: Female mice reconstructed with β-galactosidase-positive male marrow cells were repeatedly injected with carbon tetrachloride to induce liver cirrhosis. The statuses of stromal cell-derived factor 1 and its inhibitor CD26 were examined by immunohistochemical staining, enzyme-linked immunosorbent assays and colorimetric assays. Recipients were treated with an inhibitory peptide for CD26(Diprotin A)together with granulocyte colony-stimulating factor, and the marrow-derived cells were tracked through the β-galactosidase activity or sex-determining region on the Y chromosome. Results: Stromal cell-derived factor 1 expression and CD26 activity were both significantly increased and marrow-derived hepatocytes were not observed in liver cirrhosis, suggesting that the potential of stem cell homing is impaired by liver damage. Granulocyte colony-stimulating factor only induced a few cell clusters comprising 2-6 marrow-derived hepatocytes at a late stage of liver cirrhosis. In contrast, when animals with liver cirrhosis were treated with Diprotin A after granulocyte colonystimulating factor-induced stem cell mobilization, marrow-derived hepatocytes increased to 2-4% of the total hepatocytes and both the serum albumin and hepatic hydroxyproline contents were ameliorated(p < .05). Conclusions: Maintaining the chemotaxis ability of stromal cell-derived factor 1 may represent an effective strategy for validating stem cell therapy.

    CiNii Article

    CiNii Books

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    その他リンク: http://hdl.handle.net/10191/38942

講演・口頭発表等

  • 乳酸脱水素酵素(LD)活性測定におけるJSCC勧告法とIFCC推奨法の比較 4社の試薬を用いた検討

    大澤 まみ, 松田 将門, 星山 良樹, 成田 一衛

    医療検査と自動化  2020年8月 

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  • CK測定における混濁血清処理剤フリーゲンIIの影響の評価 CK低値の血清、血漿検体における検討.

    大澤 まみ, 松田 将門, 星山 良樹

    日本医学検査学会  2018年5月 

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    記述言語:日本語  

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  • 混濁血清処理剤フリーゲンIIを用いた乳び検体のCK測定手順の検討

    大澤 まみ, 松田将門, 星山良樹

    北日本支部医学検査学会  2017年10月 

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  • Urokinase-Type Plasminogen Activator/FGF-2 Pathway Is A Critical Target For Sorafenib Resistance In Hepatoma Cells

    大澤 まみ, 松田 康伸, 窪田 正幸, 若井 俊文

    日本癌学会総会記事  2017年9月 

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    記述言語:英語  

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  • Hepatoma Cells Acquire Sorafenib Resistance through Akt-Fibroblast Growth Factor Signaling

    大澤 まみ, 松田 康伸, 若井 俊文, 窪田 正幸

    日本癌学会総会記事  2014年9月 

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    記述言語:英語  

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  • Chemotherapy-Induced Apoptotic Hepatoma Cells Stimulate Compensatory Proliferation

    Mami Osawa, Yasunobu Matsuda, Shun Fujimaki, Toshifumi Wakai, Masayuki Kubota

    21st United European Gastroenterology Week  2013年10月 

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  • 肝がん細胞株における抗がん剤誘導性代償性増殖の解析

    大澤 まみ, 松田康伸, 藤巻隼, 若井俊文, 窪田正幸

    日本臨床分子形態学会総会  2013年9月 

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受賞

  • Travel grant award

    2013年10月   21st United European Gastroenterology Week Berlin 2013   Chemotherapy-Induced Apoptotic Hepatoma Cells Stimulate Compensatory Proliferation

    Mami Osawa, Yasunobu Matsuda, Shun Fujimaki, Wakai Toshifumi, Kubota Masayuki

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共同研究・競争的資金等の研究

  • 「恥ずかしくない学校トイレ」環境の開発~児童ウェル・ビーイングを目指して~

    2022年8月 - 2023年3月

    令和4年度 新潟大学U-goグラント 

    大澤まみ, 中島伸子, 亀岡雅紀

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    担当区分:研究代表者 

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  • 血清乳びの定量化によるインスリン抵抗性糖尿病の新規検出法の確立

    研究課題/領域番号:22H04387  2022年4月 - 2023年3月

    日本学術振興会  科学研究費助成事業 奨励研究  奨励研究

    大澤 まみ

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    配分額:410000円 ( 直接経費:410000円 )

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  • リポ蛋白リパーゼを用いた新しい乳び検体処理法の開発

    2019年4月 - 2020年3月

    日本学術振興会  科学研究費助成事業  奨励研究

    大澤 まみ

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    担当区分:研究代表者  資金種別:競争的資金

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  • DNA傷害細胞由来エキソソームを用いた再生治療法の開発

    2014年4月 - 2015年3月

    協和会  医学研究助成金 

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担当経験のある授業科目

  • 医学検査管理総論

    2022年
    -
    現在
    機関名:新潟大学

  • 臨床検査実習

    2022年
    -
    現在
    機関名:新潟大学

  • スタディスキルズ (検査)

    2022年
    -
    現在
    機関名:新潟大学

  • 血液検査科学実習

    2022年
    -
    現在
    機関名:新潟大学

  • 保健学総合

    2022年
    -
    現在
    機関名:新潟大学

 

学術貢献活動

  • 実践で活きる精度管理の考え方~不確かさの活用を例に~

    役割:パネル司会・セッションチェア等

    第20回生物試料分析科学会信越支部総会  2022年7月

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    種別:学会・研究会等 

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