2021/12/22 更新

写真a

マツカワ アキヒロ
松川 昭博
MATSUKAWA Akihiro
所属
医歯薬学域 教授
職名
教授
外部リンク

学位

  • 博士(医学) ( 熊本大学 )

研究キーワード

  • サイトカイン・ケモカイン

  • シグナル伝達

  • 自然免疫

  • 炎症とがん

  • 炎症

研究分野

  • ライフサイエンス / 実験病理学

  • ライフサイエンス / 免疫学

学歴

  • 熊本大学    

    1989年4月 - 1993年3月

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    国名: 日本国

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  • 熊本大学   Faculty of Medicine   Medical School

    1981年4月 - 1987年3月

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経歴

  • 岡山大学医学部長補佐

    2019年4月 - 2021年3月

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  • 岡山大学医学部副学部長

    2017年4月 - 2019年3月

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  • 岡山大学全学教育・学生支援機構副機構長

    2017年4月 - 2018年3月

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  • 岡山大学大学改革のためのプロジェクト副リーダー

    2017年4月 - 2018年3月

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  • 岡山大学高等教育開発推進室副室長

    2016年4月 - 2018年3月

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  • 岡山大学副理事(大学改革担当)

    2016年4月 - 2017年3月

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  • 岡山大学   Medical School, Faculty of Medicine

    2015年4月 - 2017年3月

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  • 岡山大学高等教育開発推進機構副機構長

    2014年10月 - 2016年3月

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  • 岡山大学学長補佐

    2014年4月 - 2016年3月

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  • 岡山大学高等教育開発推進機構設置準備室室長

    2014年4月 - 2014年9月

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  • 岡山大学医歯薬学総合研究科医学教育リノベーションセンター長

    2012年4月 - 2018年3月

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  • 岡山大学医学部副学部長

    2011年4月 - 2015年3月

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  • 岡山大学医学部医学科教務委員長

    2009年4月 - 2015年3月

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  • 岡山大学動物実験委員会委員長

    2006年4月 - 現在

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  • 岡山大学自然生命科学研究支援センター動物資源部門長

    2006年4月 - 現在

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  • 岡山大学医歯薬学総合研究科 教授

    2005年10月 - 現在

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  • 熊本大学大学院医学薬学研究科 助教授

    2004年1月 - 2005年9月

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  • 熊本大学大学院医学薬学研究科 講師

    2003年1月 - 2004年1月

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  • ミシガン大学医学部病理学研究員

    1998年7月 - 1999年4月

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  • ミシガン大学医学部病理学主任研究員

    1998年5月 - 2001年2月

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  • 熊本大学医学部 助手(第一病理)

    1993年11月 - 2002年12月

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  • 熊本大学医学部附属病院 医員(整形外科)

    1993年4月 - 1993年10月

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  • 菊水町立病院研修医(整形外科)

    1988年7月 - 1989年3月

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  • 熊本大学   University Hospital

    1987年6月 - 1988年6月

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▼全件表示

所属学協会

▼全件表示

委員歴

  • Nature Group   Scientific reports, associate editor  

    2015年4月 - 現在   

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    団体区分:その他

  • 日本病理学会   Pathology International 常任刊行委員  

    2014年4月 - 現在   

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    団体区分:学協会

  • 日本炎症再生学会   Editorial Board Member of Inflammation and Regeneration  

    2011年4月 - 現在   

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    団体区分:学協会

 

論文

  • Crosstalk between Cancer Cells and Fibroblasts for the Production of Monocyte Chemoattractant Protein-1 in the Murine 4T1 Breast Cancer. 国際誌

    Mayu Imamura, Tiantian Li, Chunning Li, Masayoshi Fujisawa, Naofumi Mukaida, Akihiro Matsukawa, Teizo Yoshimura

    Current issues in molecular biology   43 ( 3 )   1726 - 1740   2021年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2) is shown to promote the progression of breast cancer. We previously identified cancer cell-derived granulocyte-macrophage colony-stimulating factor (GM-CSF) as a potential regulator of MCP-1 production in the murine 4T1 breast cancer, but it played a minimum role in overall MCP-1 production. Here, we evaluated the crosstalk between 4T1 cells and fibroblasts. When fibroblasts were co-cultured with 4T1 cells or stimulated with the culture supernatants of 4T1 cells (4T1-sup), MCP-1 production by fibroblasts markedly increased. 4T1 cells expressed mRNA for platelet-derived growth factor (PDGF)-a, b and c, and the PDGF receptor inhibitor crenolanib almost completely inhibited 4T1-sup-induced MCP-1 production by fibroblasts. However, PDGF receptor antagonists failed to reduce MCP-1 production in tumor-bearing mice. Histologically, 4T1 tumors contained a small number of αSMA-positive fibroblasts, and Mcp-1 mRNA was mainly associated with macrophages, especially those surrounding necrotic lesions on day 14, by in situ hybridization. Thus, although cancer cells have the capacity to crosstalk with fibroblasts via PDGFs, this crosstalk does not play a major role in MCP-1 production or cancer progression in this model. Unraveling complex crosstalk between cancer cells and stromal cells will help us identify new targets to help treat breast cancer patients.

    DOI: 10.3390/cimb43030122

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  • Protective effects of anti-HMGB1 monoclonal antibody on lung ischemia reperfusion injury in mice. 国際誌

    Kentaro Nakata, Mikio Okazaki, Dai Shimizu, Ken Suzawa, Kazuhiko Shien, Kentaroh Miyoshi, Shinji Otani, Hiromasa Yamamoto, Seiichiro Sugimoto, Masaomi Yamane, Daiki Ousaka, Toshiaki Ohara, Akihiro Matsukawa, Masahiro Nishibori, Shinichi Toyooka

    Biochemical and biophysical research communications   573   164 - 170   2021年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    During ischemia reperfusion (IR) injury, high mobility group box 1 (HMGB1), a chromatin binding protein, is released from necrotic cells and triggers inflammatory responses. We assessed the therapeutic effect of a neutralizing anti-HMGB1 monoclonal antibody (mAb) on lung IR injury. A murine hilar clamp model of IR was used, where mice were divided into sham and IR groups with intravenous administration of anti-HMGB 1 mAb or control mAb. We analyzed the effect of anti-HMGB1 mAb against IR injury by assessing lung oxygenation, lung injury score, neutrophil infiltration, expression of proinflammatory cytokines and chemokines, levels of mitogen-activated protein kinase (MAPK) signaling, and measurement of apoptotic cells. Anti-HMGB1 mAb significantly decreased the plasma level of HMGB1 elevated by IR. The severity of IR injury represented by oxygenation capacity, lung injury score, and neutrophil infiltration was significantly improved by anti-HMGB1 mAb treatment. The expression of proinflammatory factors, including IL-1β, IL-6, IL-12, TNF-α, CXCL-1, and CXCL-2, and phosphorylation of p38 MAPK were both significantly reduced by anti-HMGB1 mAb treatment. Furthermore, anti-HMGB1 mAb treatment suppressed apoptosis, as determined through TUNEL assays. Overall, anti-HMGB1 mAb ameliorated lung IR injury by reducing inflammatory responses and apoptosis. Our findings indicate that anti-HMGB1 mAb has potential for use as a therapeutic to improve IR injury symptoms during lung transplantation.

    DOI: 10.1016/j.bbrc.2021.08.015

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  • PolyI:C suppresses TGF-β1-induced Akt phosphorylation and reduces the motility of A549 lung carcinoma cells. 国際誌

    Takahiro Yamaguchi, Teizo Yoshimura, Toshiaki Ohara, Masayoshi Fujisawa, Gao Tong, Akihiro Matsukawa

    Molecular biology reports   48 ( 9 )   6313 - 6321   2021年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUNDS: Epithelial mesenchymal transition (EMT) is a critical process involved in the invasion and metastasis of cancer, including lung cancer (LC). Transforming growth factor (TGF)-β is one of factors capable of inducing EMT. Polyinosinic-polycytidylic acid (polyI:C), a synthetic agonist for toll-like receptor (TLR) 3, can enhance immune responses and has been used as an adjuvant for cancer vaccines; however, it remains unclear whether it influences other process, such as EMT. In the present study, we examined the effects of polyI:C on TGF-β-treated A549 human LC cells. METHODS AND RESULTS: By in vitro cell proliferation assay, polyI:C showed no effect on the growth of A549 cells treated with TGF-β1 at the concentration range up to 10 μg/ml; however, it markedly suppressed the motility in a cell scratch and a cell invasion assay. By Western blotting, polyI:C dramatically decreased TGF-β1-induced Ak strain transforming (Akt) phosphorylation and increased phosphatase and tensin homologue (PTEN) expression without affecting the Son of mothers against decapentaplegic (Smad) 3 phosphorylation or the expression level of E-cadherin, N-cadherin or Snail, indicating that polyI:C suppressed cell motility independently of the 'cadherin switching'. The Akt inhibitor perifosine inhibited TGF-β1-induced cell invasion, and the PTEN-specific inhibitor VO-OHpic appeared to reverse the inhibitory effect of polyI:C. CONCLUSION: PolyI:C has a novel function to suppress the motility of LC cells undergoing EMT by targeting the phosphatidylinositol 3-kinase/Akt pathway partly via PTEN and may prevent or reduce the metastasis of LC cells.

    DOI: 10.1007/s11033-021-06625-1

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  • In Silico and In Cell Hybrid Selection of Nonrapalog Ligands to Allosterically Inhibit the Kinase Activity of mTORC1. 国際誌

    Raef Shams, Akihiro Matsukawa, Yukari Ochi, Yoshihiro Ito, Hideyuki Miyatake

    Journal of medicinal chemistry   2021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)  

    Cancer-specific metabolic alterations hyperactivate the kinase activity of the mammalian/mechanistic target of rapamycin (mTOR) for overcoming stressful environments. Rapalogs, which allosterically inhibit mTOR complex 1 (mTORC1), have been approved as anticancer agents. However, the immunosuppressive side effect of these compounds results in the promotion of tumor metastasis, thereby limiting their therapeutic efficacy. We first report a nonrapalog inhibitor, WRX606, identified by a hybrid strategy of in silico and in cell selections. Our studies showed that WRX606 formed a ternary complex with FK506-binding protein-12 (FKBP12) and FKBP-rapamycin-binding (FRB) domain of mTOR, resulting in the allosteric inhibition of mTORC1. WRX606 inhibited the phosphorylation of not only the ribosomal protein S6 kinase 1 (S6K1) but also eIF4E-binding protein-1 (4E-BP1). Hence, WRX606 efficiently suppressed tumor growth in mice without promotion of metastasis. These results suggest that WRX606 is a potent lead compound for developing anticancer drugs discovered by in silico and in cell methods.

    DOI: 10.1021/acs.jmedchem.1c00536

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  • Spred2 controls the severity of Concanavalin A-induced liver damage by limiting interferon-gamma production by CD4+ and CD8+ T cells 査読

    Sun C, Fujisawa M, Ohara T, Liu Q, Cao C, Yang X, Yoshimura T, Kunkel SL, Matsukawa A

    Journal of Advanced Research   online   2021年4月

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    担当区分:最終著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Nanog is a promising chemo-resistant stemness marker and therapeutic target by iron chelators for esophageal cancer. 国際誌

    Toru Narusaka, Toshiaki Ohara, Kazuhiro Noma, Noriyuki Nishiwaki, Yuki Katsura, Takuya Kato, Hiroaki Sato, Yasuko Tomono, Satoru Kikuchi, Hiroshi Tazawa, Yasuhiro Shirakawa, Akihiro Matsukawa, Toshiyoshi Fujiwara

    International journal of cancer   149 ( 2 )   347 - 357   2021年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Esophageal cancer is a disease showing poor prognosis. Although combination chemotherapy using cisplatin and 5-fluorouracil is standard for unresectable esophageal cancer, the response rate is 35%. Cancer stem cells (CSCs) and inflammation are reportedly responsible for the poor prognosis of esophageal cancer. However, comprehensive analyses have not been conducted and proposals for progress remain lacking. Iron is known to be a key factor in the stemness of CSCs. This study focused on the therapeutic potential of iron control using iron chelators for CSCs in esophageal cancer. Among 134 immunohistochemically analyzed cases, Nanog expression was high in 98 cases and low in 36 cases. High Nanog expression correlated with low overall and disease-free survivals. The iron chelators deferasirox (DFX) and SP10 suppressed the proliferation and expression of stemness markers in TE8 and OE33 cells. DFX and SP10 did not induce compensatory interleukin (IL)-6 secretion, although cisplatin did result in high induction. Moreover, BBI608 and SSZ, as other CSC-targeting drugs, could not suppress the expression of stemness markers. Together, Nanog expression appears related to poor prognosis in esophageal cancer patients, and inhibition of stemness and compensatory IL-6 secretion by iron chelators may offer a novel therapeutic strategy for esophageal cancer.

    DOI: 10.1002/ijc.33544

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  • Utility of gastric biopsy in diagnosing IgG4-related gastrointestinal disease. 国際誌

    Kaori Uchino, Kenji Notohara, Takeshi Uehara, Yasuhiro Kuraishi, Junya Itakura, Akihiro Matsukawa

    Pathology international   71 ( 2 )   124 - 134   2021年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The utility of gastric biopsy for diagnosing immunoglobulin (Ig)G4-related gastrointestinal disease (IgG4-GID) remains unclear. Bottom-heavy plasmacytosis (BHP) is a distinct feature of IgG4-GID. To clarify the feasibility of using gastric biopsies to diagnose BHP in IgG4-GID, we analyzed the histological features and immunostaining of gastric biopsy specimens from 31 known IgG4-related disease (IgG4-RD) patients and we assessed the presence of BHP in 1696 consecutive routine gastric biopsies. Cases with both >10 IgG4-positive plasma cells per high-power field and an IgG4/IgG-positive ratio >40% were defined as IgG4-high. Ten of the 31 IgG4-RD patients were concluded to have IgG4-GID, in which IgG4-positive plasma cells were notably detected at the deeper part of the mucosa. Six cases displayed BHP whereas the remaining four cases showed transmural infiltration with concomitant Helicobacter pylori-associated gastritis. In addition to BHP, we identified two unique histologic features for IgG4-GID: plasmacytic aggregation in the muscularis mucosae and permeative plasmacytic infiltration between fundic glands in the non-atrophic mucosa. Six of the routine cases (0.35%) displayed BHP, including a case with IgG4-RD. IgG4-GID can be suspected by the presence of gastric biopsy specimens with characteristic histological features. Such cases are recommended to undergo further examinations to determine whether IgG4-RD is present.

    DOI: 10.1111/pin.13059

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  • Expression of Spred2 in the urothelial tumorigenesis of the urinary bladder. 国際誌

    Shinsuke Oda, Masayoshi Fujisawa, Li Chunning, Toshihiro Ito, Takahiro Yamaguchi, Teizo Yoshimura, Akihiro Matsukawa

    PloS one   16 ( 11 )   e0254289   2021年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Aberrant activation of the Ras/Raf/ERK (extracellular-signal-regulated kinase)-MAPK (mitogen-activated protein kinase) pathway is involved in the progression of cancer, including urothelial carcinoma; but the negative regulation remains unclear. In the present study, we investigated pathological expression of Spred2 (Sprouty-related EVH1 domain-containing protein 2), a negative regulator of the Ras/Raf/ERK-MAPK pathway, and the relation to ERK activation and Ki67 index in various categories of 275 urothelial tumors obtained from clinical patients. In situ hybridization demonstrated that Spred2 mRNA was highly expressed in high-grade non-invasive papillary urothelial carcinoma (HGPUC), and the expression was decreased in carcinoma in situ (CIS) and infiltrating urothelial carcinoma (IUC). Immunohistochemically, membranous Spred2 expression, important to interact with Ras/Raf, was preferentially found in HGPUC. Interestingly, membranous Spred2 expression was decreased in CIS and IUC relative to HGPUC, while ERK activation and the expression of the cell proliferation marker Ki67 index were increased. HGPUC with membranous Spred2 expression correlated significantly with lower levels of ERK activation and Ki67 index as compared to those with negative Spred2 expression. Thus, our pathological findings suggest that Spred2 counters cancer progression in non-invasive papillary carcinoma possibly through inhibiting the Ras/Raf/ERK-MAPK pathway, but this regulatory mechanism is lost in cancers with high malignancy. Spred2 appears to be a key regulator in the progression of non-invasive bladder carcinoma.

    DOI: 10.1371/journal.pone.0254289

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  • Spred2-deficiency enhances the proliferation of lung epithelial cells and alleviates pulmonary fibrosis induced by bleomycin. 国際誌

    Akina Kawara, Ryo Mizuta, Masayoshi Fujisawa, Toshihiro Ito, Chunning Li, Kaoru Nakamura, Cuiming Sun, Masaki Kuwabara, Masahiro Kitabatake, Teizo Yoshimura, Akihiro Matsukawa

    Scientific reports   10 ( 1 )   16490 - 16490   2020年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The mitogen-activated protein kinase (MAPK) pathways are involved in many cellular processes, including the development of fibrosis. Here, we examined the role of Sprouty-related EVH-1-domain-containing protein (Spred) 2, a negative regulator of the MAPK-ERK pathway, in the development of bleomycin (BLM)-induced pulmonary fibrosis (PF). Compared to WT mice, Spred2-/- mice developed milder PF with increased proliferation of bronchial epithelial cells. Spred2-/- lung epithelial cells or MLE-12 cells treated with spred2 siRNA proliferated faster than control cells in vitro. Spred2-/- and WT macrophages produced similar levels of TNFα and MCP-1 in response to BLM or lipopolysaccharide and myeloid cell-specific deletion of Spred2 in mice had no effect. Spred2-/- fibroblasts proliferated faster and produced similar levels of MCP-1 compared to WT fibroblasts. Spred2 mRNA was almost exclusively detected in bronchial epithelial cells of naïve WT mice and it accumulated in approximately 50% of cells with a characteristic of Clara cells, 14 days after BLM treatment. These results suggest that Spred2 is involved in the regulation of tissue repair after BLM-induced lung injury and increased proliferation of lung bronchial cells in Spred2-/- mice may contribute to faster tissue repair. Thus, Spred2 may present a new therapeutic target for the treatment of PF.

    DOI: 10.1038/s41598-020-73752-3

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  • Elastin and collagen IV double staining: A refined method to detect blood vessel invasion in breast cancer. 国際誌

    Masayoshi Fujisawa, Masako Omori, Hiroyoshi Doihara, Ye-Min Than, Hnin Wint Wint Swe, Teizo Yoshimura, Akihiro Matsukawa

    Pathology international   70 ( 9 )   612 - 623   2020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)  

    Blood vessel invasion (BVI) is a prognostic indicator in various cancers. Elastic stain, which highlights blood vessel walls, is commonly used to detect BVI. In the breast, however, its diagnostic usefulness is limited because it also highlights some intraductal carcinoma components, which often mimic BVI. In this study, we aimed to improve BVI detection in breast cancer and developed a double staining: Victoria blue for elastin and immunohistochemistry for collagen IV. Collagen IV fibers were retained along the basement membranes of intraductal carcinoma components, whereas they were rearranged or lost in BVI. From these observations, we defined BVI as the presence of tumor cells inside an elastic ring with a rearrangement or loss of collagen IV fibers. Using these criteria, we found BVI in 148 cases (49%) among 304 cases of primary operable invasive breast carcinoma, and the presence of BVI correlated significantly with poor prognosis. By contrast, we detected BVI in 94 cases (31%) or 14 cases (5%) by elastic van Gieson or CD31 immunostaining among the same cases, respectively, with no statistically significant association with prognosis. Thus, elastin and collagen IV double staining facilitates the detection of BVI in breast cancer and is useful to predict prognosis.

    DOI: 10.1111/pin.12971

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  • Decreased miR-200b-3p in cancer cells leads to angiogenesis in HCC by enhancing endothelial ERG expression. 査読 国際誌

    Aye Moh-Moh-Aung, Masayoshi Fujisawa, Sachio Ito, Hiroshi Katayama, Toshiaki Ohara, Yoko Ota, Teizo Yoshimura, Akihiro Matsukawa

    Scientific reports   10 ( 1 )   10418 - 10418   2020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)  

    Transcription factor ERG (erythroblast transformation-specific (ETS)-related gene) is essential in endothelial differentiation and angiogenesis, in which microRNA (miR)-200b-3p targeting site is expected by miRNA target prediction database. miR-200b is known decreased in hepatocellular carcinoma (HCC), however, the functional relation between ERG and miR-200b-3p, originating from pre-miR-200b, in HCC angiogenesis remains unclear. We investigated whether hepatocyte-derived miR-200b-3p governs angiogenesis in HCC by targeting endothelial ERG. Levels of miR-200b-3p in HCC tissues were significantly lower than those in adjacent non-HCC tissues. Poorly differentiated HCC cell line expressed lower level of miR-200b-3p compared to well-differentiated HCC cell lines. The numbers of ERG-positive endothelial cells were higher in HCC tissues than in adjacent non-HCC tissues. There was a negative correlation between the number of ERG-positive cells and miR-200b-3p expression in HCC tissues. Culture supernatants of HCC cell lines with miR-200b-3p-overexpression reduced cell migration, proliferation and tube forming capacity in endothelial cells relative to the control, while those with miR-200b-3p-inhibition augmented the responses. Exosomes isolated from HCC culture supernatants with miR-200b-3p overexpression suppressed endothelial ERG expression. These results suggest that exosomal miR-200b-3p from hepatocytes suppresses endothelial ERG expression, and decreased miR-200b-3p in cancer cells promotes angiogenesis in HCC tissues by enhancing endothelial ERG expression.

    DOI: 10.1038/s41598-020-67425-4

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  • Development of self-adhesive pulp-capping agents containing a novel hydrophilic and highly polymerizable acrylamide monomer. 国際誌

    Kumiko Yoshihara, Noriyuki Nagaoka, Takumi Okihara, Masao Irie, Akihiro Matsukawa, Mariano Simón Pedano, Yukinori Maruo, Yasuhiro Yoshida, Bart Van Meerbeek

    Journal of materials chemistry. B   8 ( 24 )   5320 - 5329   2020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)  

    Several studies have shown the clinical success of hydraulic calcium-silicate cements (hCSCs) for direct and indirect pulp capping and root repair. However, hCSCs have various drawbacks, including long setting time, poor mechanical properties, low bond strength to dentin, and relatively poor handling characteristics. To overcome these limitations, a light-curable, resin-based hCSC (Theracal LC, Bisco) was commercially introduced; however, it did not exhibit much improvement in bond strength. We developed a light-curable self-adhesive pulp-capping material that contains the novel acrylamide monomer N,N'-{[(2-acrylamido-2-[(3-acrylamidopropoxy)methyl]propane-1,3-diyl)bis(oxy)]bis(propane-1,3-diyl)}diacrylamide (FAM-401) and the functional monomer 4-methacryloxyethyl trimellitate anhydride (4-MET). Two experimental resin-based hCSCs containing different calcium sources (portlandite: Exp_Pl; tricalcium silicate cement: Exp_TCS) were prepared, and the commercial hCSCs Theracal LC and resin-free hCSC Biodentine served as controls. The performance of each cement was evaluated based on parameters relevant for vital pulp therapy, such as curing degree on a wet surface, mechanical strength, as determined using a three-point bending test, shear bond strength to dentin, cytotoxicity, as determined using an MTT assay, and the amount of calcium released, as determined using inductively coupled plasma atomic emission spectrometry. Both experimental cements cured on wet surfaces and showed relatively low cytotoxicity. Furthermore, their flexural and shear bond strength to dentin were significantly higher than those of the commercial references. High calcium release was observed for both Exp_Pl and Biodentine. Thus, Exp_Pl as a new self-adhesive pulp-capping agent performed better than the commercial resin-based pulp-capping agent in terms of mechanical strength, bond strength, and calcium release.

    DOI: 10.1039/d0tb00079e

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  • Juvenile Granulosa Cell Tumor with an Unusual Clinical Course: A Late-onset and Late Recurrent Case.

    Thar Htet San, Yoko Ota, Soichiro Fushimi, Masayoshi Fujisawa, Hiroyuki Yanai, Hiroko Toda, Tadayoshi Kunitomo, Keisuke Kodama, Akihiro Matsukawa

    Acta medica Okayama   74 ( 2 )   159 - 163   2020年4月

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    記述言語:英語  

    Juvenile granulosa cell tumors (JGCTs) are rare ovarian tumors with overall good prognoses. They differ from adult granulosa cell tumors (AGCTs), which are well known for late recurrence. Most JGCTs (~97%) occur in individuals <30 years old. We report a recurrent JGCT in a 40-year-old woman 5 years after initial presentation. The histological appearance and lack of 402C>G missense point mutation of FOXL2 gene (characteristic of AGCT but absent in JGCT) allowed differentiation from AGCT. This is the first comprehensive report of JGCT with late recurrence. Although rare, late recurrence of JGCT can occur; long-term surveillance is suggested.

    DOI: 10.18926/AMO/58275

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  • A Promising New Anti-Cancer Strategy: Iron Chelators Targeting CSCs. 査読

    Yuehua Chen, Toshiaki Ohara, Boyi Xing, Jiping Qi, Kazuhiro Noma, Akihiro Matsukawa

    Acta medica Okayama   74 ( 1 )   1 - 6   2020年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Iron is a trace but vital element in the human body and is necessary for a multitude of crucial processes in life. However, iron overload is known to induce carcinogenesis via oxidative stress. Cancer cells require large amounts of iron for their rapid division and cell growth. Iron was recently found to play a role in cancer stem cells (CSCs); it maintains stemness during development. Iron also plays an important role in stemness by moderating reactive oxygen species. Thus, iron metabolism in CSCs is a promising therapeutic target. In this review, we summarize the roles of iron in cancer cells and CSCs. We also summarize anti-cancer therapeutic studies with iron chelators and describe our expectation of a new therapeutic strategy for CSCs on the basis of our findings.

    DOI: 10.18926/AMO/57946

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  • A Surgical Instructor Training Course for the Next Generation. 査読

    Masaomi Yamane, Yasuhiro Mandai, Hideo Ino, Akihiro Matsukawa, Shinichi Toyooka

    Acta medica Okayama   74 ( 1 )   73 - 76   2020年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    In 2016, Gunma University Hospital's Medical Accident Investigation Committee released a report reiterating the necessity of medical education and the need for surgeons to master non-technical skills. We designed a 17-h training course for surgical instructors, designed to teach participants how to sufficiently educate surgeon trainees and encourage their professional identity formation. A post-training survey showed that participants improved their awareness, and their behavioral changes led to favorable team performances. We then began offering a 3-h workshop focusing on the participants' experiences. We propose that the training course using participant narratives is required and effective to establish surgeons' self-reflection and professional identity as surgeons.

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  • Cancer Cell-Derived Granulocyte-Macrophage Colony-Stimulating Factor Is Dispensable for the Progression of 4T1 Murine Breast Cancer. 国際誌

    Teizo Yoshimura, Kaoru Nakamura, Chunning Li, Masayoshi Fujisawa, Tsuyoshi Shiina, Mayu Imamura, Tiantian Li, Naofumi Mukaida, Akihiro Matsukawa

    International journal of molecular sciences   20 ( 24 )   2019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)  

    We previously reported that 4T1 murine breast cancer cells produce GM-CSF that up-regulates macrophage expression of several cancer promoting genes, including Mcp-1/Ccl2, Ccl17 and Rankl, suggesting a critical role of cancer cell-derived GM-CSF in cancer progression. Here, we attempted to define whether 4T1 cell-derived GM-CSF contributes to the expression of these genes by 4T1tumors, and their subsequent progression. Intraperitoneal injection of anti-GM-CSF neutralizing antibody did not decrease the expression of Mcp-1, Ccl17 or Rankl mRNA by 4T1 tumors. To further examine the role of cancer cell-derived GM-CSF, we generated GM-CSF-deficient 4T1 cells by using the Crisper-Cas9 system. As previously demonstrated, 4T1 cells are a mixture of cells and cloning of cells by itself significantly reduced tumor growth and lung metastasis. By contrast, GM-CSF-deficiency did not affect tumor growth, lung metastasis or the expression of these chemokine and cytokine genes in tumor tissues. By in-situ hybridization, the expression of Mcp-1 mRNA was detected in both F4/80-expressing and non-expressing cells in tumors of GM-CSF-deficient cells. These results indicate that cancer cell-derived GM-CSF is dispensable for the tuning of the 4T1 tumor microenvironment and the production of MCP-1, CCL17 or RANKL in the 4T1 tumor microenvironment is likely regulated by redundant mechanisms.

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  • Multipotent Neurotrophic Effects of Hepatocyte Growth Factor in Spinal Cord Injury. 国際誌

    Kentaro Yamane, Haruo Misawa, Tomoyuki Takigawa, Yoshihiro Ito, Toshifumi Ozaki, Akihiro Matsukawa

    International journal of molecular sciences   20 ( 23 )   2019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)  

    Spinal cord injury (SCI) results in neural tissue loss and so far untreatable functional impairment. In addition, at the initial injury site, inflammation induces secondary damage, and glial scar formation occurs to limit inflammation-mediated tissue damage. Consequently, it obstructs neural regeneration. Many studies have been conducted in the field of SCI; however, no satisfactory treatment has been established to date. Hepatocyte growth factor (HGF) is one of the neurotrophic growth factors and has been listed as a candidate medicine for SCI treatment. The highlighted effects of HGF on neural regeneration are associated with its anti-inflammatory and anti-fibrotic activities. Moreover, HGF exerts positive effects on transplanted stem cell differentiation into neurons. This paper reviews the mechanisms underlying the therapeutic effects of HGF in SCI recovery, and introduces recent advances in the clinical applications of HGF therapy.

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  • Negative impact of recipient SPRED2 deficiency on transplanted lung in a mouse model. 査読 国際誌

    Hashimoto K, Yamane M, Sugimoto S, Hirano Y, Kurosaki T, Otani S, Miyoshi K, Ohara T, Okazaki M, Yoshimura T, Oto T, Matsukawa A, Toyooka S

    Transplant immunology   57   101242 - 101242   2019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)  

    DOI: 10.1016/j.trim.2019.101242

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  • Rechargeable anti-microbial adhesive formulation containing cetylpyridinium chloride montmorillonite. 国際誌

    Kenya Matsuo, Kumiko Yoshihara, Noriyuki Nagaoka, Yoji Makita, Hideki Obika, Takumi Okihara, Akihiro Matsukawa, Yasuhiro Yoshida, Bart Van Meerbeek

    Acta biomaterialia   100   388 - 397   2019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)  

    Long-term anti-bacterial effect is a desired ability of any dental material in combating tooth caries as one of the most common and widespread persistent diseases today. Among several cationic quaternary ammonium compounds with antiseptic properties, cetylpyridinium chloride (CPC) is often used in mouthrinses and toothpastes. In this study, we incorporated CPC in a soft phyllosilicate mineral (clay), referred to as montmorillonite (Mont), to enable gradual CPC release with rechargeability. Besides measuring CPC release and recharge, we examined the anti-bacterial effect, cytotoxicity and bonding effectiveness of five experimental adhesive formulations, prepared by adding 1 and 3 wt% CPC_Mont, 3 wt% Mont (without CPC), and 1 and 3 wt% CPC (without Mont) to the commercial adhesive Clearfil S3 Bond ND Quick ('C-S3B'; Kuraray Noritake). Strong inhibition of Streptococcus mutans biofilm formation by CPC_Mont adhesives was confirmed by optical density and SEM. CPC release from CPC_Mont adhesives was higher and lasted longer than from CPC adhesives, while CPC_Mont adhesives could also be recharged with CPC upon immersion in 2 wt% CPC. In conclusion, CPC_Mont technology rendered adhesives anti-bacterial properties with recharge ability, this without reducing its bonding potential, neither increasing its cytotoxicity. STATEMENT OF SIGNIFICANCE: Dental caries is one of the most prevalent chronic diseases in the population worldwide and is the major cause of tooth loss. In this study, we developed cetylpyridinium chloride (CPC) loaded montmorillonite (CPC-Mont) with a long-term antibacterial efficacy to prevent caries. CPC is an antibacterial agent approved by FDA, used as an OTC drug and contained in oral hygiene aids. CPC-Mont was incorporated in a dental adhesive to gradually release CPC. CPC_Mont technology rendered adhesives anti-bacterial properties with rechargeability, this without reducing its bonding potential, neither increasing its cytotoxicity.

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  • The relationship between the PD-L1 expression of surgically resected and fine-needle aspiration specimens for patients with pancreatic cancer. 査読

    Matsumoto K, Ohara T, Fujisawa M, Takaki A, Takahara M, Tanaka N, Kato H, Horiguchi S, Yoshida R, Umeda Y, Fushimi S, Yagi T, Matsukawa A, Okada H

    Journal of gastroenterology   54 ( 11 )   1019 - 1028   2019年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/s00535-019-01586-6

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  • Prolonged warm ischemia exacerbated acute rejection after lung transplantation from donation after cardiac death in a mouse. 査読

    Hirano Y, Sugimoto S, Yamamoto S, Okada M, Otani S, Ohara T, Yamane M, Matsukawa A, Oto T, Toyooka S

    General thoracic and cardiovascular surgery   68 ( 1 )   57 - 62   2019年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/s11748-019-01181-9

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  • SOCS3 overexpression in T cells ameliorates chronic airway obstruction in a murine heterotopic tracheal transplantation model. 査読

    Mesaki K, Yamane M, Sugimoto S, Fujisawa M, Yoshimura T, Kurosaki T, Otani S, Miyoshi S, Oto T, Matsukawa A, Toyooka S

    Surgery today   49 ( 5 )   443 - 450   2019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)  

    DOI: 10.1007/s00595-018-1753-5

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  • Combined effect of anti-high-mobility group box-1 monoclonal antibody and peramivir against influenza A virus-induced pneumonia in mice. 国際誌

    Kazuki Hatayama, Nobuyuki Nosaka, Mutsuko Yamada, Masato Yashiro, Yosuke Fujii, Hirokazu Tsukahara, Keyue Liu, Masahiro Nishibori, Akihiro Matsukawa, Tsuneo Morishima

    Journal of medical virology   91 ( 3 )   361 - 369   2019年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Human pandemic H1N1 2009 influenza virus causes significant morbidity and mortality with severe acute lung injury due to the excessive inflammatory reaction, even with neuraminidase inhibitor use. The anti-inflammatory effect of anti-high-mobility group box-1 (HMGB1) monoclonal antibody (mAb) against influenza pneumonia has been reported. In this study, we evaluated the combined effect of anti-HMGB1 mAb and peramivir against pneumonia induced by influenza A (H1N1) virus in mice. Nine-week-old male C57BL/6 mice were inoculated with H1N1 and treated with intramuscularly administered peramivir at 2 and 3 days post-infection (dpi). The anti-HMGB1 mAb or a control mAb was administered at 2, 3, and 4 dpi. Survival rates were assessed, and lung lavage and pathological analyses were conducted at 5 and 7 dpi. The combination of peramivir with the anti-HMGB1 mAb significantly improved survival rate whereas the anti-HMGB1 mAb alone did not affect virus proliferation in the lungs. This combination therapy also significantly ameliorated histopathological changes, neutrophil infiltration, and macrophage aggregation by inhibiting HMGB1, inflammatory cytokines, and oxidative stress. Fluorescence immunostaining showed that the anti-HMGB1 mAb inhibited HMGB1 translocation from type I alveolar epithelial cells. In summary, combining anti-HMGB1 with conventional anti-influenza therapy might be useful against severe influenza virus infection.

    DOI: 10.1002/jmv.25330

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  • A Novel Combination Cancer Therapy with Iron Chelator Targeting Cancer Stem Cells via Suppressing Stemness. 査読 国際誌

    Yuki Katsura, Toshiaki Ohara, Kazuhiro Noma, Takayuki Ninomiya, Hajime Kashima, Takuya Kato, Hiroaki Sato, Satoshi Komoto, Toru Narusaka, Yasuko Tomono, Boyi Xing, Yuehua Chen, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Tomonari Kasai, Masaharu Seno, Akihiro Matsukawa, Toshiyoshi Fujiwara

    Cancers   11 ( 2 )   2019年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Excess iron causes cancer and is thought to be related to carcinogenesis and cancer progression including stemness, but the details remain unclear. Here, we hypothesized that stemness in cancer is related to iron metabolism and that regulating iron metabolism in cancer stem cells (CSCs) may be a novel therapy. In this study, we used murine induced pluripotent stem cells that expressed specific stem cell genes such as Nanog, Oct3/4, Sox2, Klf4, and c-Myc, and two human cancer cell lines with similar stem cell gene expression. Deferasirox, an orally available iron chelator, suppressed expression of stemness markers and spherogenesis of cells with high stemness status in vitro. Combination therapy had a marked antitumor effect compared with deferasirox or cisplatin alone. Iron metabolism appears important for maintenance of stemness in CSCs. An iron chelator combined with chemotherapy may be a novel approach via suppressing stemness for CSC targeted therapy.

    DOI: 10.3390/cancers11020177

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  • Abrogated Caveolin-1 expression via histone modification enzyme Setdb2 regulates brain edema in a mouse model of influenza-associated encephalopathy. 査読 国際誌

    Imakita N, Kitabatake M, Ouji-Sageshima N, Hara A, Morita-Takemura S, Kasahara K, Matsukawa A, Wanaka A, Mikasa K, Ito T

    Scientific reports   9 ( 1 )   284 - 284   2019年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41598-018-36489-8

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  • Spred2 Regulates High Fat Diet-Induced Adipose Tissue Inflammation, and Metabolic Abnormalities in Mice. 査読 国際誌

    Takahiro Ohkura, Teizo Yoshimura, Masayoshi Fujisawa, Toshiaki Ohara, Rie Marutani, Kaya Usami, Akihiro Matsukawa

    Frontiers in immunology   10   17 - 17   2019年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Chronic low-grade inflammation in visceral adipose tissues triggers the development of obesity-related insulin resistance, leading to the metabolic syndrome, a serious health condition with higher risk of cardiovascular disease, diabetes, and stroke. In the present study, we investigated whether Sprouty-related EVH1-domain-containing protein 2 (Spred2), a negative regulator of the Ras/Raf/ERK/MAPK pathway, plays a role in the development of high fat diet (HFD)-induced obesity, adipose tissue inflammation, metabolic abnormalities, and insulin resistance. Spred2 knockout (KO) mice, fed with HFD, exhibited an augmented body weight gain, which was associated with enhanced adipocyte hypertrophy in mesenteric white adipose tissue (mWAT) and deteriorated dyslipidemia, compared with wild-type (WT) controls. The number of infiltrating macrophages with a M1 phenotype, and the crown-like structures, composed of macrophages surrounding dead or dying adipocytes, were more abundant in Spred2 KO-mWAT compared to in WT-mWAT. Exacerbated adipose tissue inflammation in Spred2 KO mice led to aggravated insulin resistance and fatty liver disease. To analyze the mechanism(s) that caused adipose tissue inflammation, cytokine response in mWAT was investigated. Stromal vascular fraction that contained macrophages from Spred2 KO-mWAT showed elevated levels of tumor necrosis factor α (TNFα) and monocyte chemoattractant protein-1 (MCP-1/CCL2) compared with those from WT-mWAT. Upon stimulation with palmitate acid (PA), bone marrow-derived macrophages (BMDMs) derived from Spred2 KO mice secreted higher levels of TNFα and MCP-1 than those from WT mice with enhanced ERK activation. U0126, a MEK inhibitor, reduced the PA-induced cytokine response. Taken together, these results suggested that Spred2, in macrophages, negatively regulates high fat diet-induced obesity, adipose tissue inflammation, metabolic abnormalities, and insulin resistance by inhibiting the ERK/MAPK pathway. Thus, Spred2 represents a potential therapeutic tool for the prevention of insulin resistance and resultant metabolic syndrome.

    DOI: 10.3389/fimmu.2019.00017

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  • SPRED2 deficiency may lead to lung ischemia-reperfusion injury via ERK1/2 signaling pathway activation. 査読

    Okada M, Yamane M, Yamamoto S, Otani S, Miyoshi K, Sugimoto S, Matsukawa A, Toyooka S, Oto T, Miyoshi S

    Surgery today   48 ( 12 )   1089 - 1095   2018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)  

    DOI: 10.1007/s00595-018-1696-x

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  • A novel, nontoxic iron chelator, super-polyphenol, effectively induces apoptosis in human cancer cell lines. 査読 国際誌

    Toshiaki Ohara, Yasuko Tomono, Xing Boyi, Sun Yingfu, Kazuhiro Omori, Akihiro Matsukawa

    Oncotarget   9 ( 67 )   32751 - 32760   2018年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Iron chelation therapy is the main treatment for iron overload disease. Iron chelators were recently reported to be useful for cancer therapy; however, they cause side effects that make them difficult to use in some cancer patients. Thus, a novel oral iron chelator, super-polyphenol (SP), was developed for cancer therapy to decrease the side effects. SP is either water soluble or insoluble, and has different isoforms according to the number of side chains. Of these isoforms, water-soluble SP6 and SP10 appear to be the best candidates, as they have the strongest chelating abilities. In this study, we focused on the usefulness and safety of SP6 and SP10 as anti-cancer drugs, and examined their anti-cancer effects and toxicity. The results showed that SP6 and SP10 inhibited cancer cell proliferation by inducing apoptosis in HCT116, HSC-2, A549, and MCF-7 cancer cells. SP10 also inhibited tumor growth in an HCT116 xenograft model. SP6 and SP10 had no acute toxicities. An intravenous injection test revealed that SP6 and SP10 had better safety profiles than the iron chelator deferoxamine. In conclusion, SP is a novel oral iron chelator with anti-cancer effects and few adverse side effects. This is the first report of SP in the literature.

    DOI: 10.18632/oncotarget.25973

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  • miRNA-133a-5p Inhibits the Expression of Osteoblast Differentiation-Associated Markers by Targeting the 3' UTR of RUNX2. 国際誌

    Wei Zhang, Yonggang Wu, Yasuyuki Shiozaki, Yoshihisa Sugimoto, Tomoyuki Takigawa, Masato Tanaka, Akihiro Matsukawa, Toshifumi Ozaki

    DNA and cell biology   37 ( 3 )   199 - 209   2018年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Recent studies have recognized the involvement of microRNAs (miRNAs) in the development of osteoporosis, which regulate the balance between osteogenesis and osteoclasis. In this study, we investigated the regulation by miRNA-133a-5p on the osteoblast differentiation-associated markers in the mouse osteoblast-like MC3T3-E1 cells by RUNX2. First, we manipulated the miRNA-133a level in the MC3T3-E1 cells with 20 or 40 nM miR-133a-5p mimics, miR-133a-5p inhibitor, or scramble miRNA. Then, we quantified with real-time polymerase chain reaction (qRT-PCR) the expression of Collagen I, osteocalcin (OCN), and osteopontin (OPN) in the miR-133a-5p-manipulated MC3T3-E1 cells. And the confocal microscopy was also utilized to confirm the regulation by miR-133a-5p on the expression of the three molecules. We also investigated the extracellular matrix (ECM) mineralization and the alkaline phosphatase (ALP) activity in the miR-133a-5p-manipulated MC3T3-E1 cells. In addition, we explored the possible targeting by miR-133a-5p on RUNX2, which was a well-recognized promoter to osteoblast differentiation, with luciferase reporter, qRT-PCR, and Western blotting assay. Results demonstrated that the miRNA-133a-5p mimics markedly reduced, whereas the miRNA-133a-5p inhibitor significantly promoted the expression of Collagen I, OCN, and OPN, the ECM mineralization, and the ALP activity in MC3T3-E1 cells. The alignment analysis demonstrated a high homology between miRNA-133a-5p and the 3' UTR of RUNX2. Moreover, the luciferase reporter assay demonstrated that miRNA-133a-5p targeted the 3' UTR of RUNX2, and inhibited the expression of RUNX2 in both mRNA and protein levels. In conclusion, we identified the inhibition by miRNA-133a-5p to the expression of osteoblast differentiation markers, to the ECM mineralization, and to the ALP activity in MC3T3-E1 cells, by targeting the 3' UTR of RUNX2. Our study suggests that miRNA-133a-5p might be an important target to inhibit osteoblast differentiation in osteoporosis.

    DOI: 10.1089/dna.2017.3936

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  • Spred2 Deficiency Exacerbates D-Galactosamine/Lipopolysaccharide -induced Acute Liver Injury in Mice via Increased Production of TNFα. 査読 国際誌

    Xu Yang, Masayoshi Fujisawa, Teizo Yoshimura, Toshiaki Ohara, Miwa Sato, Megumi Mino, Thar Htet San, Tong Gao, Steven L Kunkel, Akihiro Matsukawa

    Scientific reports   8 ( 1 )   188 - 188   2018年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Acute liver injury (ALI) is characterized by hepatocyte damage and inflammation. In the present study, we examined whether the absence of Sprouty-related EVH1-domain-containing protein 2 (Spred2), a negative regulator of the Ras/Raf/ERK/MAPK pathway, influences ALI induced by D-galactosamine (D-GalN) and lipopolysaccharide (LPS). Compared to wild-type mice, Spred2-/- mice developed exacerbated liver injury represented by enhanced hepatocyte damage and inflammation. Enhanced ERK activation was observed in Spred2-/--livers, and the MEK/ERK inhibitor U0126 ameliorated ALI. Hepatic tumour necrosis factor α (TNFα) and interleukin (IL)-1β levels were increased in Spred-2-/--livers, and the neutralization of TNFα dramatically ameliorated ALI, which was associated with decreased levels of endogenous TNFα and IL-1β. When mice were challenged with D-GalN and TNFα, much severer ALI was observed in Spred2-/- mice with significant increases in endogenous TNFα and IL-1β in the livers. Immunohistochemically, Kupffer cells were found to produce TNFα, and isolated Kupffer cells from Spred2-/- mice produced significantly higher levels of TNFα than those from wild-type mice after LPS stimulation, which was significantly decreased by U0126. These results suggest that Spred2 negatively regulates D-GalN/LPS-induced ALI under the control of TNFα in Kupffer cells. Spred2 may present a therapeutic target for the treatment of ALI.

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  • Collagen-Binding Hepatocyte Growth Factor (HGF) alone or with a Gelatin- furfurylamine Hydrogel Enhances Functional Recovery in Mice after Spinal Cord Injury. 査読 国際誌

    Yamane K, Mazaki T, Shiozaki Y, Yoshida A, Shinohara K, Nakamura M, Yoshida Y, Zhou D, Kitajima T, Tanaka M, Ito Y, Ozaki T, Matsukawa A

    Scientific reports   8 ( 1 )   917 - 917   2018年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41598-018-19316-y

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  • 鉄キレート剤の幹細胞性制御による新規癌治療法の確立

    大原利章, 大原利章, 桂佑貴, 野間和広, 鳴坂徹, 二宮卓之, 友野靖子, 田澤大, 香川俊輔, 白川靖博, 松川昭博, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   29th   2018年

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  • ラットにおけるチタン結合性BMPの骨形成促進効果についての検討

    内野崇彦, 塩崎泰之, 吉田晶, 宇川諒, 池田吉宏, 村岡聡介, 辻寛謙, 伊藤嘉浩, 松川昭博, 尾崎敏文

    移植(Web)   53 ( 6 )   2018年

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  • ラット脊椎固定モデルにおけるrhBMP2添加リン酸化プルランフィルムの有用性の検討

    宇川諒, 塩崎泰之, 村岡聡介, 吉田晶, 瀧川朋亨, 三澤治夫, 尾崎敏文, 松川昭博

    Journal of Spine Research   9 ( 3 )   2018年

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  • Ovarian stromal cells as a source of cancer-associated fibroblasts in human epithelial ovarian cancer: A histopathological study. 国際誌

    Masayoshi Fujisawa, Aye Moh-Moh-Aung, Zheng Zeng, Teizo Yoshimura, Yoji Wani, Akihiro Matsukawa

    PloS one   13 ( 10 )   e0205494   2018年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Fibroblasts are a major component of cancer tissue and known to contribute to cancer progression. However, it remains unknown whether they are derived from local fibroblasts or of other origin. This study was designed to identify the contribution of local stromal cells to cancer stroma in human epithelial ovarian cancer. Seventy-six cases of surgically resected primary ovarian carcinoma (48 cases confined to the ovaries and 28 cases with distant metastases) and 17 cases of secondary ovarian tumor (e.g. colon cancer metastasized to the ovary) were enrolled in this study. The tissues were immunostained for forkhead box protein L2 (FOXL2), a transcription factor crucial for ovarian development and function, and markers for cancer-associated fibroblasts (CAFs) and inflammatory cells. Under normal condition, FOXL2 expression was restricted to ovarian stromal cells and some other types of cells in female genital tracts and never found in other sites of the body. FOXL2-positive cells were found in all primary and secondary tumors in the ovary, and were the dominant stromal cells in most cases. In contrast, only a few FOXL2-positive cells were found in peritoneal seeding sites of four serous carcinoma cases, and all the other tumors at extraovarian sites had no FOXL2-positive cells. FOXL2-positive cells in the ovarian lesion variably expressed CAFs markers, such as alpha-smooth muscle actin and fibroblast activating protein, as determined by double immunostaining. Background inflammation, but not histological subtype or origin of the neoplasm seemed to correlate with the proportion of FOXL2-positive cells. These results suggest that ovarian stromal cells are the main source of cancer stroma in the ovary but do not seem to move to distant sites via circulation together with tumor cells. Our results also support the hypothesis that cancer-associated fibroblasts may originate locally, which was previously demonstrated using animal models.

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  • Spred-2 protects mice from ConA-induced liver injury

    Cuiming Sun, Teizo Yoshimura, Masatoshi Fujisawa, Toshiaki Ohara, Xu Yang, Akihiro Matsukawa

    CYTOKINE   100   120 - 120   2017年12月

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    記述言語:英語   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

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  • Spred-2 deficiency exacerbates lipopolysaccharide (LPS)/D-galactosamine (D-GalN) induced acute liver injury

    Yang Xu, Teizo Yoshimura, Masayoshi Fujisawa, Toshiaki Ohara, Cuiming Sun, Akihiro Matsukawa

    CYTOKINE   100   137 - 137   2017年12月

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    記述言語:英語   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

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  • Iron depletion is a novel therapeutic strategy to target cancer stem cells. 国際誌

    Takayuki Ninomiya, Toshiaki Ohara, Kazuhiro Noma, Yuki Katsura, Ryoichi Katsube, Hajime Kashima, Takuya Kato, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Fumiaki Kimura, Ling Chen, Tomonari Kasai, Masaharu Seno, Akihiro Matsukawa, Toshiyoshi Fujiwara

    Oncotarget   8 ( 58 )   98405 - 98416   2017年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Adequate iron levels are essential for human health. However, iron overload can act as catalyst for the formation of free radicals, which may cause cancer. Cancer stem cells (CSCs), which maintain the hallmark stem cell characteristics of self-renewal and differentiation capacity, have been proposed as a driving force of tumorigenesis and metastases. In the present study, we investigated the role of iron in the proliferation and stemness of CSCs, using the miPS-LLCcm cell model. Although the anti-cancer agents fluorouracil and cisplatin suppressed the proliferation of miPS-LLCcm cells, these drugs did not alter the expression of stemness markers, including Nanog, SOX2, c-Myc, Oct3/4 and Klf4. In contrast, iron depletion by the iron chelators deferasirox and deferoxamine suppressed the proliferation of miPS-LLCcm cells and the expression of stemness markers. In an allograft model, deferasirox inhibited the growth of miPS-LLCcm implants, which was associated with decreased expression of Nanog and Sox2. Altogether, iron appears to be crucial for the proliferation and maintenance of stemness of CSCs, and iron depletion may be a novel therapeutic strategy to target CSCs.

    DOI: 10.18632/oncotarget.21846

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  • Spred2-deficiecy Protects Mice from Polymicrobial Septic Peritonitis by Enhancing Inflammation and Bacterial Clearance 国際誌

    Junya Itakura, Miwa Sato, Toshihiro Ito, Megumi Mino, Soichiro Fushimi, Sakuma Takahashi, Teizo Yoshimura, Akihiro Matsukawa

    SCIENTIFIC REPORTS   7 ( 1 )   87 - 92   2017年10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:NATURE PUBLISHING GROUP  

    Sepsis is an infection-induced systemic inflammatory syndrome and a major cause of death for critically ill patients. Here, we examined whether the absence of Sprouty-related EVH1-domain-containing protein 2 (Spred2), a negative regulator of the Ras/Raf/ERK/MAPK pathway, influences host defense against polymicrobial sepsis (PMS) induced by cecal ligation and puncture (CLP). Compared to wildtype mice, Spred2(-)/(-) mice exhibited higher survival rates with increased level of leukocyte infiltration and local chemokine production and reduced plasma and peritoneal bacterial loads after CLP. The MEK inhibitor U0126 significantly reduced LPS-induced chemokine production by Spred2(-)/(-) resident macrophages in vitro, and decreased CLP-induced leukocyte infiltration in vivo. Spred2(-)/(-)resident macrophages, but not neutrophils or elicited macrophages, exhibited increased phagocytic activity. Interestingly, surface expression of complement receptor 1/2 (CR1/2) was increased in Spred2(-)/(-) resident macrophages in response to lipopolysaccharide in a manner dependent on the ERK/MAPK pathway, and blocking CR1/2 in vivo resulted in reduced leukocyte infiltration and increased bacterial loads after CLP. Taken together, our results indicate that Spred2-deficiency protects mice from PMS via increased activation of the ERK/MAPK pathway and subsequent increase in innate immune responses. Thus, inhibiting Spred2 may present a novel means to prevent the development of PMS.

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  • The STAT4/MLL1 Epigenetic Axis Regulates the Antimicrobial Functions of Murine Macrophages 国際誌

    William F. Carson, Karen A. Cavassani, Elyara M. Soares, Soichiro Hirai, Nicolai A. Kittan, Matthew A. Schaller, Melissa M. Scola, Amrita Joshi, Akihiro Matsukawa, David M. Aronoff, Craig N. Johnson, Yali Dou, Katherine A. Gallagher, Steven L. Kunkel

    JOURNAL OF IMMUNOLOGY   199 ( 5 )   1865 - 1874   2017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)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Macrophages are critical immune cells for the clearance of microbial pathogens and cellular debris from peripheral tissues. Macrophage inflammatory responses are governed by gene expression patterns, and these patterns are often subject to epigenetic control. Chromatin modifications, such as histone methylation, regulate gene accessibility in macrophages, and macrophage polarization is governed in part by the expression and function of chromatin-modifying enzymes. The histone methyltransferase mixed-lineage leukemia 1 (MLL1) preferentially modifies lysine residue 4 on the unstructured protein tail of histone H3. MLL1 expression and function have been shown to be governed by signal transduction pathways that are activated by inflammatory stimuli, such as NF-kappa B. Therefore, we sought to investigate the role of MLL1 in mediating macrophage inflammatory responses. Bone marrow-derived macrophages from mice with a targeted MLL1 gene knockout (Lys2-Cre(+/-) MLL1(fx/fx)) exhibited decreased proinflammatory gene expression with concurrent decreases in activating histone methylation. However, MLL1-deficient macrophages also exhibited increased phagocytic and bacterial killing activity in vitro. RNA profiling of MLL1-knockout macrophages identified numerous genes involved with inflammatory responses whose expression was altered in response to TLR ligands or proinflammatory cytokines, including STAT4. STAT4-dependent cytokines, such as type I IFNs were able to drive MLL1 expression in macrophages, and MLL1-knockout macrophages exhibited decreased activating histone methylation in the STAT4 promoter. These results implicate an important role for MLL1-dependent epigenetic regulation of macrophage antimicrobial functions.

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  • 学生が作成するハンドブックを用いた臨床実習教育プロジェクトPOCCE

    日高 啓介, 大塚 勇輝, 飯田 淳義, 万代 康弘, 三好 智子, 山根 正修, 松川 昭博

    医学教育   48 ( Suppl. )   160 - 160   2017年8月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • Molecular Subtypes of Breast Cancers from Myanmar Women: A Study of 91 Cases at Two Pathology Centers 国際誌

    Thar Htet San, Masayoshi Fujisawa, Soichiro Fushimi, Lamin Soe, Ngu Wah Min, Teizo Yoshimura, Toshiaki Ohara, Myint Myint Yee, Shinsuke Oda, Akihiro Matsukawa

    Asian Pacific journal of cancer prevention : APJCP   18 ( 6 )   1617 - 1621   2017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: Breast cancer is the most common cancer in Myanmar women. Revealing the hormonal receptor
    status, human epidermal growth factor receptor 2 (HER2) and Ki-67 expression is useful for estimating patient
    prognosis as well as determination of treatment strategy. However, immunohistochemical features and classification of
    molecular subtypes in breast cancers from Myanmar remain unknown. Methods: The clinicopathological features of
    91 breast cancers from Myanmar women were examined. Immunohistochemistry was performed on tissue specimens
    with antibodies to estrogen receptor (ER), progesterone receptor (PgR), HER2, Ki-67, cytokeratin (CK)5/6 and CK14.
    Immunohistochemistry-based molecular subtyping was conducted. Results: Breast cancers in Myanmar women were
    relatively large, high grade with frequent metastatic lymph nodes. Of the 91 patients, tumors with ER positive, PgR
    positive, and HER2 positive were 57.1%, 37.4%, and 28.6%, respectively. The most prevalent subtype was luminal B
    (HER2-) (39.6%), followed by HER2 (22.0%), triple negative (TN)-basal-like (12.1%), luminal A (11.0%), TN-null
    (8.8%) and luminal B (HER2+) (6.6%). The mean Ki-67 expression of 91 cases was 33.9% (33.9% ± 19.2%) and the
    median was 28% (range; 4%-90%). The mean Ki-67 expression of luminal A, luminal B, HER2 and TN-basal-like/
    null was 7%, 30%, 40%, and 57%/43%, respectively. A higher Ki-67 expression significantly correlated with a higher
    grade, larger size and higher stage of malignancy. Conclusions: We, for the first time, investigated the histopathological
    features of breast cancers from Myanmar women. Myanmar breast cancers appeared to be aggressive in nature, as
    evidenced by high frequency of poor-prognosis subtypes with high level of Ki-67 expression.

    DOI: 10.22034/APJCP.2017.18.6.1617

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  • Low prevalence of human mammary tumor virus (HMTV) in breast cancer patients from Myanmar 国際誌

    Thar Htet San, Masayoshi Fujisawa, Soichiro Fushimi, Teizo Yoshimura, Toshiaki Ohara, Lamin Soe, Ngu Wah Min, Ohnmar Kyaw, Xu Yang, Akihiro Matsukawa

    INFECTIOUS AGENTS AND CANCER   12 ( 1 )   60 - 66   2017年4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:BIOMED CENTRAL LTD  

    Background: Human mammary tumor virus (HMTV) is 90-95% homologous to mouse mammary tumor virus (MMTV), one of the causal agents of murine mammary tumors. HMTV (MMTV-like) sequences were reported to be present in human breast cancers from several populations with a prevalence range of 0-78%; however, the prevalence of HMTV in breast cancers from Myanmar remains unknown.
    Methods: Fifty-eight breast cancer samples from Myanmar women were examined in this study. DNA was isolated from formalin-fixed paraffin-embedded specimens, and HMTV envelope sequences were detected by semi-nested PCR. The sequence of the PCR products was also confirmed.
    Results: Only 1.7% (1 of 58) of the breast cancers were positive for HMTV, and the sequence of PCR products was 98.9% identical to the reference HMTV sequence (GenBank accession No. AF243039). The tumor with HMTV was grade III invasive ductal carcinoma, 7.0 cm in size with lymph node metastasis (T3, N1, M0).
    Conclusions: We, for the first time, investigated the presence of HMTV in Myanmar breast cancer patients. In accordance with other Asian studies, the prevalence of HMTV in Myanmar was quite low, supporting the hypothesis that Asian breast cancers have different etiologies than in Western countries, where HMTV is more prevalent.

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  • Spred-2欠損はGalN/LPS誘導性の急性肝障害を悪化させる(Spred-2 deficiency exacerbated GalN/LPS induced acute liver injury) 査読

    楊 旭, 吉村 禎造, 藤澤 真義, 大原 利章, 佐藤 美和, 美野 愛, 松川 昭博

    日本病理学会会誌   106 ( 1 )   446 - 446   2017年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • polyI:CによるAktリン酸化抑制を介した腫瘍細胞の転移抑制機構(Poly I:C suppress migration of carcinoma cells by inhibiting Akt phosphorylation)

    山口 隆廣, 吉村 禎造, 大原 利章, 藤澤 真義, 松川 昭博

    日本病理学会会誌   106 ( 1 )   282 - 282   2017年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 除鉄はマウスiPS細胞の腫瘍化を未分化マーカーの発現制御を介して抑制する(Tumorigenesis of miPS cells is prevented from suppressing the stemness by iron depletion treatment) 査読

    大原 利章, Xing Boyi, 桂 佑貴, 松川 昭博

    日本病理学会会誌   106 ( 1 )   405 - 405   2017年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 前頭葉に発生し,てんかん原性を示した髄膜腫合併髄膜血管腫症の1例

    河原明奈, 伏見聡一郎, 板倉淳哉, 藤澤真義, 小林勝弘, 林裕美子, 伊達勲, 上利崇, 柳井広之, 松川昭博

    診断病理   34 ( 1 )   46 - 50   2017年

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  • 緑内障手術のサイエンス - 濾過手術とサイトカインを中心に

    井上俊洋, 谷原秀信, 布田龍佑, 福島美紀子, 伊藤康裕, 川路隆博, 岩尾圭一郎, 高橋枝里, 藤本智和, 井上みゆき, 岩尾美奈子, 笠岡奈々子, 原竜平, 正林耕平, 榮木大輔, 大平さおり, 後藤章子, 小島祥, 芳賀彰, 黒田詩子, 中島圭一, 平川沙織, 福島亜矢子, 松村理世, 徳永瞳, 川畑和幸, 北村文香, 西澤麻保, 二口亜希子, 松本桃佳, 吉村長久, 亀田隆範, 吉田晃敏, 川井基史, 川井尚子, 木下茂, 上田真由美, 古賀彩加, 稲谷大, 瀧原祐史, 本庄恵, 石井優, 菊田順一, 古家雅之, 松川昭博, 猿渡淳二, 田賀哲也, 鹿川哲史

    日本眼科学会雑誌   121 ( 3 )   314 - 335   2017年

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  • ラット脊椎固定モデルにおけるrhBMP2添加リン酸化プルランフィルムの有用性の検討

    宇川諒, 塩崎泰之, 村岡聡介, 池田吉弘, 内野崇彦, 小田孔明, 吉村将秀, 吉田晶, 瀧川朋亨, 三澤治夫, 尾崎敏文, 松川昭博

    移植   52 ( 6 )   582 - 582   2017年

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  • Tumor-Associated Macrophages in the Development of 4-Nitroquinoline-1-Oxide-Induced Tongue Squamous Cell Carcinoma in a Mouse Model 国際誌

    Kentaro Miki, Yorihisa Orita, Yuka Gion, Soshi Takao, Kyotaro Ohno, Mai Takeuchi, Toshihiro Ito, Akira Minoura, Tomoyasu Tachibana, Hidenori Marunaka, Takuma Makino, Akihiro Matsukawa, Kazunori Nishizaki, Tadashi Yoshino, Yasuharu Sato

    ONCOLOGY   93 ( 3 )   204 - 212   2017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:KARGER  

    Objective: We aimed to determine the distribution of tumor-associated macrophages (TAMs) in the development of tongue squamous cell carcinoma (SCC) and to elucidate the role of TAMs in the progression of tongue SCC. Methods: The expression of the macrophage markers nitric oxide synthase, Retnla, and mannose receptor 1 in the development of tongue SCC was longitudinally observed using real-time quantitative polymerase chain reaction. Additionally, an immunohistochemical study using an anti-mannose receptor (MR) antibody was performed. Results: The numbers of both of M1 and M2 macrophages in the tongues of mice treated with 4-nitroquinoline-1-oxide (4NQO) were significantly lower compared with those of normal tongues. The cyclo-oxygenase-2 (COX-2) inhibitor did not prevent cancer progression and did not affect the total number of macrophages in the tongues of 4NQO-treated mice. In the immunohistochemical studies, MR staining was observed in lymphangio-endothelium in the subepithelial area of the tongues. The staining intensity of the MR was significantly stronger in the 4NQO-treated mice compared with that in control mice and 4NQO-treated mice treated with the COX-2 inhibitor. Conclusion: TAMs may not contribute to the development of 4NQO-induced tongue SCC. MR expression is associated with the progression of 4NQO-induced tongue SCC. (C) 2017 S. Karger AG, Basel

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  • 多忙生嚢胞性変化を呈した輪状細管を伴う性策腫瘍(SCAT)の一例

    太田陽子, 伏見聡一郎, 堀田真智子, タテサン, 内野かおり, 藤澤真義, 和仁洋治, 松川昭博

    診断病理   34 ( 3 )   231 - 235   2017年

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  • 超音波内視鏡下穿刺吸引術(EUS-FNA)で得られたgangliocytic paragangliomaの細胞像の検討

    河合 穂高, 伏見 聡一郎, 板倉 淳哉, 井上 博文, 藤井 昌江, 武部 祐一郎, 松川 昭博

    日本臨床細胞学会雑誌   55 ( 6 )   376 - 381   2016年11月

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    記述言語:日本語   出版者・発行元:(公社)日本臨床細胞学会  

    背景:Gangliocytic paraganglioma(GP)は、十二指腸乳頭部に好発するまれな腫瘍で、主として粘膜下に存在するため、生検による確定診断は困難なことが多い。EUS-FNAは術前診断の有効な方法として期待されるが、その報告は少ない。症例:60歳代、男性。タール便を主訴に上部消化管内視鏡が施行された。生検では十二指腸粘膜のみしか得られなかった。EUS-FNA検体では、細顆粒状クロマチンを有する短紡錘形〜類円形の核をもつ紡錘形細胞に加え、少数ながら核小体の目立つ大型細胞も認められた。多彩な細胞像を呈し、核所見などから神経内分泌系の腫瘍が疑われた。膵十二指腸切除検体では十二指腸乳頭部の近傍に粘膜下腫瘍が認められた。組織学的に腫瘍は、Zellballen配列をとる上皮様細胞、明瞭な核小体をもつ神経節細胞様細胞、束状の紡錘形細胞(支持細胞)の3成分から構成されていた。最終的にGPと病理診断された。結論:EUS-FNA検体では必ずしも3成分の細胞が採取されない可能性がある。しかし、3成分の細胞が正しく採取され、さらにセルブロックの免疫組織化学的検討を加えれば、診断は可能と思われた。(著者抄録)

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  • A Novel Role of Spred2 in the Colonic Epithelial Cell Homeostasis and Inflammation 国際誌

    Sakuma Takahashi, Teizo Yoshimura, Takahiro Ohkura, Masayoshi Fujisawa, Soichiro Fushimi, Toshihiro Ito, Junya Itakura, Sakiko Hiraoka, Hiroyuki Okada, Kazuhide Yamamoto, Akihiro Matsukawa

    SCIENTIFIC REPORTS   6   37531 - 37531   2016年11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:NATURE PUBLISHING GROUP  

    Rapid and adequate mucosal healing is important for a remission of ulcerative colitis (UC) patients. Here, we examined whether Spred2, a member of the Sprouty-related EVH1-domain-containing proteins that inhibit the Ras/Raf/ERK pathway, plays a role in colonic mucosal homeostasis and inflammation by using Spred2 knockout (KO) mice. We first detected increased epithelial cell proliferation and cadherin 1 expression in the colon of naive Spred2 KO mice compared to wild-type mice. Interestingly, Spred2 KO mice were resistant to dextran sulfate sodium (DSS)-induced acute colitis as indicated by lower levels of body weight loss and disease activity index. Histologically, epithelial cell injury and inflammation were milder in the colonic mucosa of Spred2 KO mice on day 3 and almost undetectable by day 8. Experiments with bone chimeric mice indicated that Spred2 deficiency in non-hematopoietic cells was responsible for the reduced sensitivity to DSS. Finally, Spred2 KO mice developed significantly fewer tumors in response to azoxymethane plus DSS. Taken together, our results demonstrate, for the first time, that Spred2 plays an important role in the regulation of colonic epithelial cell proliferation and inflammation by potentially down-regulating the activation of ERK. Thus, Spred2 may be a new therapeutic target for the treatment of UC.

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  • Regulatory T cells function at the early stage of tumor progression in a mouse model of tongue squamous cell carcinoma 国際誌

    Kentaro Miki, Yorihisa Orita, Yuka Gion, Soshi Takao, Kyotaro Ohno, Mai Takeuchi, Toshihiro Ito, Hiroyuki Hanakawa, Tomoyasu Tachibana, Hidenori Marunaka, Takuma Makino, Akira Minoura, Akihiro Matsukawa, Kazunori Nishizaki, Tadashi Yoshino, Yasuharu Sato

    CANCER IMMUNOLOGY IMMUNOTHERAPY   65 ( 11 )   1401 - 1410   2016年11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:SPRINGER  

    The objective of this study was to observe the distribution of regulatory T cells (Tregs) in the development of tongue squamous cell carcinoma (SCC) and to determine the role of Tregs in the progression of tongue SCC. A mouse model of 4-nitroquinoline-1-oxide (4NQO)-induced-tongue SCC was established. The expression of Forkhead box P3 (Foxp3), interleukin 10, transforming growth factor-beta, chemokine CC motif ligands 17, 20, and CC chemokine receptor 4 was determined using real-time quantitative polymerase chain reaction. Foxp3 expression was also analyzed using immunohistochemistry. The results were compared with those of control mice and of 4NQO-treated mice treated with a cyclooxygenase-2 (COX-2) inhibitor. Well to moderately differentiated tongue SCC was induced in all of the experimental mice. The amount of Tregs of the experimental mice was over 10 times as much as control mice at the early stage of tumor progression. COX-2 inhibitor did not prevent the progression of tongue SCC and did not reduce the total amount of Tregs. Tregs function at the early stage of the development of tongue SCC, and it may be effective to suppress Tregs at the early stage of tumor progression for the treatment and/or prevention of tongue SCC.

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  • 多糖複合体を基材とした感染制御能と生体吸収性を有する抗菌薬含有骨セメントの開発

    渡邉典行, 香川洋平, 張偉, 吉村将秀, 吉田晶, 田中雅人, 吉田靖弘, 松川昭博, 尾崎敏文

    日本整形外科学会雑誌   90 ( 8 )   S1819   2016年8月

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    記述言語:日本語  

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  • Sprouty-Related Ena/Vasodilator-Stimulated Phosphoprotein Homology 1-Domain-Containing Protein-2 Critically Regulates Influenza A Virus-Induced Pneumonia 国際誌

    Toshihiro Ito, Junya Itakura, Sakuma Takahashi, Miwa Sato, Megumi Mino, Soichiro Fushimi, Masao Yamada, Tuneo Morishima, Steven L. Kunkel, Akihiro Matsukawa

    CRITICAL CARE MEDICINE   44 ( 7 )   E530 - E543   2016年7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:LIPPINCOTT WILLIAMS & WILKINS  

    Objectives: Influenza A virus causes acute respiratory infections that induce annual epidemics and occasional pandemics. Although a number of studies indicated that the virus-induced intracellular signaling events are important in combating influenza virus infection, the mechanism how specific molecule plays a critical role among various intracellular signaling events remains unknown. Raf/MEK/extracellular signal-regulated kinase cascade is one of the key signaling pathways during influenza virus infection, and the Sprouty-related Ena/vasodilator-stimulated phos-phoprotein homology 1-domain-containing protein has recently been identified as a negative regulator of Raf-dependent extracellular signal-regulated kinase activation. Here, we examined the role of Raf/MEK/extracellular signal-regulated kinase cascade through sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein in influenza A viral infection because the expression of sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein was significantly enhanced in human influenza viral-induced pneumonia autopsy samples.
    Design: Prospective animal trial.
    Setting: Research laboratory.
    Subjects: Wild-type and sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 knockout mice inoculated with influenza A.
    Interventions: Wild-type or sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 knockout mice were infected by intranasal inoculation of influenza A (A/PR/8). An equal volume of phosphate-buffered saline was inoculated intranasally into mock-infected mice.
    Measurements and Main Results: Influenza A infection of sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 knockout mice led to higher mortality with greater viral load, excessive inflammation, and enhanced cytokine production than wild-type mice. Administration of MEK inhibitor, U0126, improved mortality and reduced both viral load and cytokine levels. Furthermore, bone marrow chimeras indicated that influenza A-induced lung pathology was most severe when sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 expression was lacking in nonimmune cell populations. Furthermore, microarray analysis revealed knockdown of sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 led to enhanced phosphatidylinositol 3-kinase signaling pathway, resulting that viral clearance was regulated by sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 expression through the phosphatidylinositol 3-kinase signaling pathway in murine lung epithelial cells.
    Conclusions: These data support an important function of sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 in controlling influenza virus-induced pneumonia and viral replication. Sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein-2 may be a novel therapeutic target for controlling the immune response against influenza influenza A virus infection.

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  • 臨床実習前に行う医療シミュレーション教育コースの取り組み

    万代 康弘, 山根 正修, 飯田 淳義, 三好 智子, 松川 昭博, 谷本 光音

    医学教育   47 ( Suppl. )   119 - 119   2016年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • Spred-2欠損はGalN/LPS誘導性の急性腎障害を悪化させる(Spred-2 deficiency exacerbates D-Galactosamine/lipopolysaccharide -induced acute liver injury) 査読

    楊 旭, 吉村 禎造, 藤澤 真義, 大原 利章, 山口 隆廣, サン・タ・テ, 小田 晋輔, 佐藤 美和, 美野 愛, 松川 昭博

    日本病理学会会誌   105 ( 1 )   449 - 450   2016年4月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 臨床病態に近い不均一性とがん幹細胞性を備えた新規腫瘍モデルの開発 査読

    大原 利章, 友野 靖子, 吉村 禎造, 藤澤 真義, 松川 昭博

    日本病理学会会誌   105 ( 1 )   365 - 365   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 膀胱腫瘍におけるRas-Raf-ERK経路とその制御因子Spred-2の解析 査読

    小田 晋輔, 藤澤 真義, 吉村 禎造, 大原 利章, 河原 明奈, 山口 隆廣, 太田 陽子, 松川 昭博

    日本病理学会会誌   105 ( 1 )   464 - 464   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • ミャンマーの乳がんの組織学的側面(Histologic Profile of Breast Cancer in Myanmar) 査読

    サン・タ・テ, 藤澤 真義, 伏見 聡一郎, イー・ミント・ミント, Yang Xu, Aye Moh Moh Aung, 渡邉 治之, 荒嶋 康晴, 大原 利章, 松川 昭博

    日本病理学会会誌   105 ( 1 )   566 - 566   2016年4月

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  • Induction of Monocyte Chemoattractant Proteins in Macrophages via the Production of Granulocyte/Macrophage ColonyStimulating Factor by Breast Cancer Cells 国際誌

    Teizo Yoshimura, Tomozumi Imamichi, Jonathan M. Weiss, Miwa Sato, Liangzhu Li, Akihiro Matsukawa, Ji Ming Wang

    FRONTIERS IN IMMUNOLOGY   7 ( JAN )   1524 - 1524   2016年1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:FRONTIERS MEDIA SA  

    Monocyte chemoattractant protein-1 (MCP-1)/CCL2 plays an important role in the initiation and progression of cancer. We previously reported that in 4T1 murine breast cancer, non-tumor stromal cells, including macrophages, were the major source of MCP-1. In the present study, we analyzed the potential mechanisms by which MCP-1 is upregulated in macrophages infiltrating 4T1 tumors. We found that cell free culture supernatants of 4T1 cells (4T1-sup) markedly upregulated MCP-1 production by peritoneal inflammatory macrophages. 4T1-sup also upregulated other MCPs, such as MCP-3/CCL7 and MCP-5/CCL12, but modestly upregulated neutrophil chemotactic chemokines, such as KC/CXCL1 or MIP-2/CXCL2. Physicochemical analysis indicated that an approximately 2-3 kDa 4T1 cell product was responsible for the capacity of 4T1-sup to upregulate MCP-1 expression by macrophages. A neutralizing antibody against granulocyte/macrophage colony stimulating factor (GM-CSF), but not macrophage CSF, almost completely abrogated MCP-1-inducing activity of 4T1-sup, and recombinant GM-CSF potently upregulated MCP-1 production by macrophages. The expression levels of GM-CSF in 4T1 tumors in vivo were higher than other tumors, such as Lewis lung carcinoma. Treatment of mice with anti-GM-CSF antibody significantly reduced the growth of 4T1 tumors at the injection sites but did not reduce MCP-1 production or lung metastasis in tumor-bearing mice. These results indicate that 4T1 cells have the capacity to directly upregulate MCP-1 production by macrophages by releasing GM-CSF; however, other mechanisms are also involved in increased MCP-1 levels in the 4T1 tumor microenvironment.

    DOI: 10.3389/fimmu.2016.00002

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  • Iron depletion enhances the effect of sorafenib in hepatocarcinoma 国際誌

    Shinichi Urano, Toshiaki Ohara, Kazuhiro Noma, Ryoichi Katsube, Takayuki Ninomiya, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Fumiaki Kimura, Kazuhiro Nouso, Akihiro Matsukawa, Kazuhide Yamamoto, Toshiyoshi Fujiwara

    CANCER BIOLOGY & THERAPY   17 ( 6 )   648 - 656   2016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:TAYLOR & FRANCIS INC  

    Human hepatocellular carcinoma (HCC) is known to have a poor prognosis. Sorafenib, a molecular targeted drug, is most commonly used for HCC treatment. However, its effect on HCC is limited in clinical use and therefore new strategies regarding sorafenib treatment are required. Iron overload is known to be associated with progression of chronic hepatitis and increased risk of HCC. We previously reported that iron depletion inhibited cancer cell proliferation and conversely induced angiogenesis. Indeed iron depletion therapy including iron chelator needs to be combined with anti-angiogenic drug for its anti-cancer effect. Since sorafenib has an anti-angiogenic effect by its inhibitory targeting VEGFR, we hypothesized that sorafenib could complement the anti-cancer effect of iron depletion. We retrospectively analyzed the relationship between the efficacy of sorafenib and serum iron-related markers in clinical HCC patients. In clinical cases, overall survival was prolonged in total iron binding capacity (TIBC) high- and ferritin low-patients. This result suggested that the low iron-pooled patients, who could have a potential of more angiogenic properties in/around HCC tumors, could be adequate for sorafenib treatment. We determined the effect of sorafenib (Nexavar (R)) and/or deferasirox (EXJADE (R)) on cancer cell viability, and on cell signaling of human hepatocarcinoma HepG2 and HLE cells. Both iron depletion by deferasirox and sorafenib revealed insufficient cytotoxic effect by each monotherapy, however, on the basis of increased angiogenesis by iron depletion, the addition of deferasirox enhanced anti-proliferative effect of sorafenib. Deferasirox was confirmed to increase vascular endothelial growth factor (VEGF) secretion into cellular supernatants by ELISA analysis. In in vivo study sorafenib combined with deferasirox also enhanced sorafenib-induced apoptosis. These results suggested that sorafenib combined with deferasirox could be a novel combination chemotherapy for HCC.

    DOI: 10.1080/15384047.2016.1177677

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  • 可視光硬化型ゼラチンとコラーゲン結合性肝細胞増殖因子を用いた脊髄損傷治療

    山根健太郎, 吉田晶, 松川昭博, 伊藤嘉浩, 尾崎敏文

    移植   51 ( 6 )   517 - 517   2016年

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  • Bone engineering by phosphorylated-pullulan and β-TCP composite 国際誌

    Xu Y, Ito T, Fushimi S, Takahashi S, Itakura J, Kimura R, Sato M, Mino M, Yoshimura A, Matsukawa A

    Biomedical Materials   10 ( 6 )   065009 - 065009   2015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)  

    DOI: 10.1088/1748-6041/10/6/065009

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  • Early Growth Response-1 Plays an Important Role in Ischemia-Reperfusion Injury in Lung Transplants by Regulating Polymorphonuclear Neutrophil Infiltration. 査読 国際誌

    Yamamoto S, Yamane M, Yoshida O, Waki N, Okazaki M, Matsukawa A, Oto T, Miyoshi S

    Transplantation   99 ( 11 )   2285 - 2293   2015年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1097/TP.0000000000000783

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  • 新規生体吸収性骨セメントの細胞動態の検討

    ZHANG W, 吉田晶, 山根健太郎, 香川洋平, 篠原健介, 吉田靖弘, 松川昭博, 尾崎敏文

    日本整形外科学会雑誌   89 ( 8 )   S1575   2015年9月

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  • 臨床実習1年後のOSCE手術室清潔操作・患者安全シナリオの実践

    万代 康弘, 山根 正修, 松川 昭博, 芝 直基, 三好 智子, 谷本 光音

    医学教育   46 ( Suppl. )   125 - 125   2015年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 5年次OSCEの導入に当たり 医学部でのOSCEの位置づけ

    三好 智子, 山根 正修, 芝 直基, 万代 康弘, 松川 昭博, 谷本 光音

    医学教育   46 ( Suppl. )   125 - 125   2015年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • Anti-high mobility group box-1 monoclonal antibody treatment provides protection against influenza A virus (H1N1)-induced pneumonia in mice 国際誌

    Nobuyuki Nosaka, Masato Yashiro, Mutsuko Yamada, Yosuke Fujii, Hirokazu Tsukahara, Keyue Liu, Masahiro Nishibori, Akihiro Matsukawa, Tsuneo Morishima

    CRITICAL CARE   19 ( 249 )   s13054-0 - 249   2015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)   出版者・発行元:BIOMED CENTRAL LTD  

    Introduction: Provision for the emergence of an influenza pandemic is an urgent issue. The discovery of a novel anti-influenza therapeutic approach would increase the effectiveness of traditional virus-based strategies. This study was undertaken to evaluate the therapeutic effects of anti-high mobility group box-1 (HMGB1) monoclonal antibody (mAb) treatment on influenza A virus (H1N1)-induced pneumonia in mice.
    Methods: Nine-week-old male C57BL/6 mice were inoculated with H1N1, then anti HMGB1 mAb or control mAb were administered intravenously at 1, 24 and 48 hours after H1N1 inoculation and the survival rate was analyzed. Lung lavage and histopathological analysis were performed on days 3, 5, 7 and 10 after inoculation.
    Results: Anti-HMGB1 mAb significantly improved the survival rate of H1N1-inoculated mice (1 out of 15 versus 8 out of 15 deaths in the anti-HMGB1 mAb-treated group versus the control mAb-treated group, p &lt; 0.01), although the treatment did not affect virus propagation in the lungs. The treatment also significantly attenuated histological changes and neutrophil infiltration in the lungs of H1N1-inoculated mice. This was associated with inhibition of HMGB1 and suppression of inflammatory cytokine/chemokine expression and oxidative stress enhancement, which were observed in H1N1-inoculated mice. The expression of receptor for advanced glycation end products and nuclear factor kappa B was attenuated by the treatment.
    Conclusions: Anti-HMGB1 mAb may provide a novel and effective pharmacological strategy for severe influenza virus infection in humans by reducing the inflammatory responses induced by HMGB1.

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  • 鉄コントロールを用いた新規がん幹細胞治療法の基礎的検討 査読

    大原 利章, 伏見 総一郎, 松川 昭博

    日本病理学会会誌   104 ( 1 )   283 - 283   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 限局性皮質異形成と皮質結節(結節性硬化症)との鑑別が問題になった一例

    太田陽子, 山口隆廣, 小田晋輔, 河原明奈, 板倉淳哉, 伏見聡一郎, 大原俊章, 平麻美, 宮田元, 松川昭博

    日本病理学会会誌   104 ( 1 )   2015年

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  • The anabolic effect of plasma-mediated ablation on the intervertebral disc: stimulation of proteoglycan and interleukin-8 production. 国際誌

    Fabrice A Kuelling, Kevin T Foley, Jane J Liu, Ellen Liebenberg, Anthony H Sin, Akihiro Matsukawa, Jeffrey C Lotz

    The spine journal : official journal of the North American Spine Society   14 ( 10 )   2479 - 87   2014年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND CONTEXT: Plasma-mediated radiofrequency-based ablation (coblation) is an electrosurgical technique currently used for tissue removal in a wide range of surgical applications, including lumbar microdiscectomy. In vitro and in vivo studies have shown the technique to alter the expression of inflammatory cytokines in the disc, increasing the levels of interleukin-8 (IL-8), which may promote maturation and remodeling of the disc matrix. PURPOSE: To better understand the effect of coblation treatment, this study characterizes the temporal and spatial pattern of healing after stab injury to the rabbit intervertebral disc, with and without plasma-mediated radiofrequency treatment. PATIENT SAMPLE: A total of 23 New Zealand white rabbits. STUDY DESIGN: Annular and nuclear stab injuries. OUTCOME MEASURES: Sandwich enzyme-linked immunosorbent assay evaluated the concentrations of cytokines tumor necrosis factor-α, IL-1β, and IL-8. Histopathologic evaluations were performed on whole discs and end plates. Tissue sections were stained with Safranin-O to evaluate nucleus pulposus and annulus fibrosus proteoglycan content and with Alcian blue for extracellular proteoglycan content. Intradiscal leakage pressure was evaluated by injecting methylene blue dye into the nucleus. METHODS: Animals underwent annular and nuclear stab injuries on three consecutive lumbar discs (L2-L3 to L4-L5). The three levels were randomly assigned into one of the three groups for treatment with a plasma-mediated radiofrequency ablation device (TOPAZ; ArthroCare Corp., Austin, TX, USA): active treatment of the nucleus only (SN); active treatment of both nucleus and annulus (SNA); sham treatment. Unstabbed/untreated discs from L5-L6 (n=5) served as normal controls. Animals were euthanized at 4, 8, and 28 days postsurgery. RESULTS: Tumor necrosis factor-α was detected in sham discs at 4 and 8 days, but not in coblation groups (SN or SNA); IL-1β was below detection in all three treatment groups. Interleukin-8 levels increased in all treatment groups at 4 and 8 days compared with normal control, peaking at 4th day for sham and SN groups and 8th day (p>.3) for the SNA group (a 2.5-fold increase). Pressure measurements revealed higher leakage in the SN group, but no statistically significant differences. Histopathology showed higher proteoglycan production by 28 days in the SNA and SN groups compared with sham. All three treatment groups showed ruptured annular fibers from the stab injury, but maintained the overall architecture. Remnants of notochordal tissue within the nucleus were evident in all treatment groups at 4 and 8 days, but were only found in sham group by 28 days. At this time, unlike the normal or sham controls, the nucleus of SN and SNA discs had fibrocartilaginous tissue with chondrocyte-like cells. Significant differences in the disc architecture grade were only noted when comparing normal controls with other groups by 28 days (p<.001). CONCLUSIONS: Plasma-mediated radiofrequency ablation appears to have an anabolic effect on disc cells, stimulating proteoglycan and IL-8 production and maintaining annulus architecture. Coblation treatment appears to reduce cellular response to proinflammatory stimuli and restore overall disc architecture that may prove beneficial in a number of degenerative disc paradigms. Further studies are encouraged to investigate the therapeutic effect of the technique.

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  • Metastasis of 4T1 murine breast cancer cells to the lung is dependent on the chemokine CCL2/MCP-1 produced by stromal cells in the primary tumor

    Teizo Yoshimura, O. M. Zack Howard, Toshihiro Ito, Masaki Kuwabara, Akihiro Matsukawa, Keqiang Chen, Ying Liu, Mingyong Liu, Ji Ming Wang

    CANCER RESEARCH   74 ( 19 )   2014年10月

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    記述言語:英語   出版者・発行元:AMER ASSOC CANCER RESEARCH  

    DOI: 10.1158/1538-7445.AM2014-3585

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  • Spred-2 Deficiency Exacerbates Lipopolysaccharide-Induced Acute Lung Inflammation in Mice 国際誌

    Yang Xu, Toshihiro Ito, Soichiro Fushimi, Sakuma Takahashi, Junya Itakura, Ryojiro Kimura, Miwa Sato, Megumi Mino, Akihiko Yoshimura, Akihiro Matsukawa

    PLOS ONE   9 ( 10 )   e108914   2014年10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:PUBLIC LIBRARY SCIENCE  

    Background: Acute respiratory distress syndrome (ARDS) is a severe and life-threatening acute lung injury (ALI) that is caused by noxious stimuli and pathogens. ALI is characterized by marked acute inflammation with elevated alveolar cytokine levels. Mitogen-activated protein kinase (MAPK) pathways are involved in cytokine production, but the mechanisms that regulate these pathways remain poorly characterized. Here, we focused on the role of Sprouty-related EVH1-domain-containing protein (Spred)-2, a negative regulator of the Ras-Raf-extracellular signal-regulated kinase (ERK)-MAPK pathway, in lipopolysaccharide (LPS)-induced acute lung inflammation.
    Methods: Wild-type (WT) mice and Spred-2(-/-) mice were exposed to intratracheal LPS (50 mu g in 50 mu L PBS) to induce pulmonary inflammation. After LPS-injection, the lungs were harvested to assess leukocyte infiltration, cytokine and chemokine production, ERK-MAPK activation and immunopathology. For ex vivo experiments, alveolar macrophages were harvested from untreated WT and Spred-2(-/-) mice and stimulated with LPS. In in vitro experiments, specific knock down of Spred-2 by siRNA or overexpression of Spred-2 by transfection with a plasmid encoding the Spred-2 sense sequence was introduced into murine RAW264.7 macrophage cells or MLE-12 lung epithelial cells.
    Results: LPS- induced acute lung inflammation was significantly exacerbated in Spred-2(-/-) mice compared with WT mice, as indicated by the numbers of infiltrating leukocytes, levels of alveolar TNF-alpha, CXCL2 and CCL2 in a later phase, and lung pathology. U0126, a selective MEK/ERK inhibitor, reduced the augmented LPS-induced inflammation in Spred-2(-/-) mice. Specific knock down of Spred-2 augmented LPS-induced cytokine and chemokine responses in RAW264.7 cells and MLE-12 cells, whereas Spred-2 overexpression decreased this response in RAW264.7 cells.
    Conclusions: The ERK-MAPK pathway is involved in LPS-induced acute lung inflammation. Spred-2 controls the development of LPS-induced lung inflammation by negatively regulating the ERK-MAPK pathway. Thus, Spred-2 may represent a therapeutic target for the treatment of ALI.

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  • 新しい可視光硬化ゼラチンを用いた家兎骨軟骨欠損モデルにおける組織修復効果

    馬崎哲朗, 山根健太郎, 吉田晶, 松川昭博, 中村真理子, 吉田靖弘, 北嶋隆, 伊藤嘉浩, 尾崎敏文

    日本整形外科学会雑誌   88 ( 8 )   S1587   2014年8月

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  • Chemokine Receptor CCR8 Is Required for Lipopolysaccharide-Triggered Cytokine Production in Mouse Peritoneal Macrophages 査読 国際誌

    Tomoyuki Oshio, Rei Kawashima, Yuki I. Kawamura, Teruki Hagiwara, Noriko Mizutani, Toshihiko Okada, Takeshi Otsubo, Kyoko Inagaki-Ohara, Akihiro Matsukawa, Tatsuya Haga, Shigeru Kakuta, Yoichiro Iwakura, Seijiro Hosokawa, Taeko Dohi

    PLOS ONE   9 ( 4 )   e94445   2014年4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:PUBLIC LIBRARY SCIENCE  

    Chemokine (C-C motif) receptor 8 (CCR8), the chemokine receptor for chemokine (C-C motif) ligand 1 (CCL1), is expressed in T-helper type-2 lymphocytes and peritoneal macrophages (PM phi) and is involved in various pathological conditions, including peritoneal adhesions. However, the role of CCR8 in inflammatory responses is not fully elucidated. To investigate the function of CCR8 in macrophages, we compared cytokine secretion from mouse PM phi or bone marrow-derived macrophages (BMM phi) stimulated with various Toll-like receptor (TLR) ligands in CCR8 deficient (CCR8(-/-)) and wild-type (WT) mice. We found that CCR8(-/-) PM phi demonstrated attenuated secretion of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-10 when stimulated with lipopolysaccharide (LPS). In particular, LPS-induced IL-10 production absolutely required CCR8. CCR8-dependent cytokine secretion was characteristic of PM phi but not BMM phi. To further investigate this result, we selected the small molecule compound R243 from a library of compounds with CCR8-antagonistic effects on CCL1-induced Ca2+ flux and CCL1-driven PM phi aggregation. Similar to CCR8(-/-) PM phi, R243 attenuated secretion of TNF-alpha, IL-6, and most strikingly IL-10 from WT PM phi, but not BMM phi. CCR8(-/-)PM phi and R243-treated WT PM phi both showed suppressed c-jun N-terminal kinase activity and nuclear factor-kappa B signaling after LPS treatment when compared with WT PM phi. A c-Jun signaling pathway inhibitor also produced an inhibitory effect on LPS-induced cytokine secretion that was similar to that of CCR8 deficiency or R243 treatment. As seen in CCR8(-/-) mice, administration of R243 attenuated peritoneal adhesions in vivo. R243 also prevented hapten-induced colitis. These results are indicative of cross talk between signaling pathways downstream of CCR8 and TLR-4 that induces cytokine production by PMQ. Through use of CCR8(-/-) mice and the new CCR8 inhibitor, R243, we identified a novel macrophage innate immune response pathway that involves a chemokine receptor.

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  • A novel, visible light-induced, rapidly cross-linkable gelatin scaffold for osteochondral tissue engineering 国際誌

    Tetsuro Mazaki, Yasuyuki Shiozaki, Kentaro Yamane, Aki Yoshida, Mariko Nakamura, Yasuhiro Yoshida, Di Zhou, Takashi Kitajima, Masato Tanaka, Yoshihiro Ito, Toshifumi Ozaki, Akihiro Matsukawa

    SCIENTIFIC REPORTS   4   4457 - 302   2014年3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:NATURE PUBLISHING GROUP  

    Osteochondral injuries remain difficult to repair. We developed a novel photo-cross-linkable furfurylamine-conjugated gelatin (gelatin-FA). Gelatin-FA was rapidly cross-linked by visible light with Rose Bengal, a light sensitizer, and was kept gelled for 3 weeks submerged in saline at 37 degrees C. When bone marrow-derived stromal cells (BMSCs) were suspended in gelatin-FA with 0.05% Rose Bengal, approximately 87% of the cells were viable in the hydrogel at 24 h after photo-cross-linking, and the chondrogenic differentiation of BMSCs was maintained for up to 3 weeks. BMP4 fusion protein with a collagen binding domain (CBD) was retained in the hydrogels at higher levels than unmodified BMP4. Gelatin-FA was subsequently employed as a scaffold for BMSCs and CBD-BMP4 in a rabbit osteochondral defect model. In both cases, the defect was repaired with articular cartilage-like tissue and regenerated subchondral bone. This novel, photo-cross-linkable gelatin appears to be a promising scaffold for the treatment of osteochondral injury.

    DOI: 10.1038/srep04457

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  • In vitro and in vivo enhanced osteogenesis by kaempferol found by a high-throughput assay using human mesenchymal stromal cells 査読

    Tetsuro Mazaki, Takashi Kitajima, Yasuyuki Shiozaki, Miwa Sato, Megumi Mino, Aki Yoshida, Mariko Nakamura, Yasuhiro Yoshida, Masato Tanaka, Toshifumi Ozaki, Akihiro Matsukawa, Yoshihiro Ito

    JOURNAL OF FUNCTIONAL FOODS   6   241 - 247   2014年1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:ELSEVIER SCIENCE BV  

    High-throughput screening was performed as a phenotypic screening on clinically relevant human mesenchymal stem cells to identify small molecules that affect stem cell fate. From a library of pharmacologically active small molecules, we identified kaempferol, which is a natural flavonol, with a high osteogenic activity. Kaempferol achieved the highest levels of bone-specific markers among the chemicals tested in vitro. The osteogenic activity of kaempferol was the same as that of ipriflavone, which is a synthetic isoflavone, in ovariectomized mouse experiments. Considering that kaempferol is present in various foods such as vegetables and fruits, it will be useful as a new preventive medicine for osteoporosis. (C) 2013 Elsevier Ltd. All rights reserved.

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  • Galectin-9 prolongs the survival of septic mice by expanding tim-3-expressing natural killer T cells and PDCA-1+ CD11c+ macrophages. 査読 国際誌

    KADOWAKI Takeshi, MORISHITA Asahiro, NIKI Toshiro, HARA Junko, SATO Miwa, TANI Jyoji, MIYOSHI Hisaaki, YONEYAMA Hirohito, MASAKI Tsutomu, HATTORI Toshio, MATSUKAWA Akihiro, HIRASHIMA Mitsuomi

    Crit Care.   17 ( 6 )   R284   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)  

    Introduction: Galectin-9 ameliorates various inflammatory conditions including autoimmune diseases by regulating T cell and macrophage/dendritic cell (DC) functions. However, the effect of galectin-9 on polymicrobial sepsis has not been assessed.Methods: We induced polymicrobial sepsis by cecal ligation and puncture (CLP) in mice. The survival rate was compared between galectin-9- and PBS-treated CLP mice. An ELISA was used to compare the levels of various cytokines in the plasma and culture supernatants. Fluorescence-activated cell sorting analysis was further performed to compare the frequencies of subpopulations of spleen cells.Results: Galectin-9 exhibited a protective effect in polymicrobial sepsis as demonstrated in galetin-9 transgenic mice and therapeutic galectin-9 administration. In contrast, such effect was not observed in nude mice, indicating the involvement of T cells in galectin-9-mediated survival prolongation. Galectin-9 decreased TNFα, IL-6, IL-10 and, high mobility group box 1 (HMGB1) and increased IL-15 and IL-17 plasma and spleen levels. Galectin-9 increased the frequencies of natural killer T (NKT) cells and PDCA-1+ CD11c+ macrophages (pDC-like macrophages) but did not change the frequency of CD4 or CD8 T cells, γδT cells or conventional DC. As expected, galectin-9 decreased the frequency of Tim-3+ CD4 T cells, most likely Th1 and Th17 cells. Intriguingly, many spleen NK1.1+ NKT cells and pDC-like macrophages expressed Tim-3. Galectin-9 increased the frequency of Tim-3-expressing NK1.1+ NKT cells and pDC-like macrophages. Galectin-9 further increased IL-17+ NK1.1+ NKT cells.Conclusion: These data suggest that galectin-9 exerts therapeutic effects on polymicrobial sepsis, possibly by expanding NKT cells and pDC-like macrophages and by modulating the production of early and late proinflammatory cytokines. © 2013 Kadowaki et al.; licensee BioMed Central Ltd.

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  • Oxaliplatin-induced liver injury mimicking metastatic tumor on images: a case report. 国際誌

    Kaori Uchino, Masayoshi Fujisawa, Takanori Watanabe, Yoshikatsu Endo, Tetsuji Nobuhisa, Yusuke Matsumoto, Kyohei Kai, Shiso Sato, Kenji Notohara, Akihiro Matsukawa

    Japanese journal of clinical oncology   43 ( 10 )   1034 - 8   2013年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Oxaliplatin-based chemotherapy is widely used for advanced colorectal cancer treatment, but it occasionally induces liver injury that is characterized histologically by sinusoidal dilatation, hepatic plate atrophy and/or venular obstruction. Most of the patients do not reveal apparent radiological abnormalities, however. Here, we report the case of a 47-year-old man with a radiologically detectable mass-forming oxaliplatin-induced sinusoidal injury that mimicked multiple liver tumors. These mass lesions were found on computed tomography images after the administration of six cycles of folinic acid, fluorouracil and oxaliplatin therapy as adjuvant chemotherapy for Stage III rectal cancer. The patient had to undergo liver resection because imaging studies could not exclude metastases. The histological examination revealed that a resected mass lesion was composed of severe sinusoidal dilatation. Milder dilatation was also seen in the surrounding parenchyma. We diagnosed the patient as having an oxaliplatin-induced sinusoidal injury with severe deviation. As oxaliplatin is a standard agent in colorectal cancer therapy today, all clinicians and pathologists should be aware of such non-neoplastic lesions as one of the rare differential diagnoses of metastatic liver tumor, to prevent overtreatment.

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  • In reply. 国際誌

    Yoshimasa Takeda, Hiroshi Hashimoto, Koji Fumoto, Tetsuya Danura, Hiromichi Naito, Naoki Morimoto, Hiroshi Katayama, Soichiro Fushimi, Akihiro Matsukawa, Aiji Ohtsuka, Kiyoshi Morita

    Anesthesiology   118 ( 2 )   469 - 70   2013年2月

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  • Redox-active protein Thioredoxin-1 administration ameliorates influenza a virus (H1N1)-induced acute lung injury in mice 国際誌

    Masato Yashiro, Hirokazu Tsukahara, Akihiro Matsukawa, Mutsuko Yamada, Yosuke Fujii, Yoshiharu Nagaoka, Mitsuru Tsuge, Nobuko Yamashita, Toshihiro Ito, Masao Yamada, Hiroshi Masutani, Junji Yodoi, Tsuneo Morishima

    Critical Care Medicine   41 ( 1 )   171 - 181   2013年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    OBJECTIVES:: Influenza virus infections can cause severe acute lung injury leading to significant morbidity and mortality. Thioredoxin-1 is a redox-active defensive protein induced in response to stress conditions. Animal experiments have revealed that thioredoxin-1 has protective effects against various severe disorders. This study was undertaken to evaluate the protective effects of recombinant human thioredoxin-1 administration on influenza A virus (H1N1)-induced acute lung injury in mice. DESIGN:: Prospective animal trial. SETTING:: Research laboratory. SUBJECTS:: Nine-week-old male C57BL/6 mice inoculated with H1N1. INTERVENTION:: The mice were divided into a vehicle-treated group and recombinant human thioredoxin-1-treated group. For survival rate analysis, the vehicle or recombinant human thioredoxin-1 was administered intraperitoneally every second day from day-1 to day 13. For lung lavage and pathological analyses, vehicle or recombinant human thioredoxin-1 was administered intraperitoneally on days-1, 1, and 3. MEASUREMENTS AND MAIN RESULTS:: Lung lavage and pathological analyses were performed at 24, 72, and 120 hrs after inoculation. The recombinant human thioredoxin-1 treatment significantly improved the survival rate of H1N1-inoculated mice, although the treatment did not affect virus propagation in the lung. The treatment significantly attenuated the histological changes and neutrophil infiltration in the lung of H1N1-inoculated mice. The treatment significantly attenuated the production of tumor necrosis factor-α and chemokine (C-X-C motif) ligand 1 in the lung and oxidative stress enhancement, which were observed in H1N1-inoculated mice. H1N1 induced expressions of tumor necrosis factor-α and chemokine (C-X-C motif) ligand 1 in murine lung epithelial cells MLE-12, which were inhibited by the addition of recombinant human thioredoxin-1. The recombinant human thioredoxin-1 treatment started 30 mins after H1N1 inoculation also significantly improved the survival of the mice. CONCLUSIONS:: Exogenous administration of recombinant human thioredoxin-1 significantly improved the survival rate and attenuated lung histological changes in the murine model of influenza pneumonia. The protective mechanism of thioredoxin-1 might be explained by its potent antioxidative and anti-inflammatory actions. Consequently, recombinant human thioredoxin-1 might be a possible pharmacological strategy for severe influenza virus infection in humans. © 2013 by the Society of Critical Care Medicine and Lippincott Williams &amp
    Wilkins.

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  • Enhanced in vivo osteogenesis by nanocarrier-fused bone morphogenetic protein-4. 国際誌

    Yasuyuki Shiozaki, Takashi Kitajima, Tetsuro Mazaki, Aki Yoshida, Masato Tanaka, Akihiro Umezawa, Mariko Nakamura, Yasuhiro Yoshida, Yoshihiro Ito, Toshifumi Ozaki, Akihiro Matsukawa

    International journal of nanomedicine   8   1349 - 60   2013年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    PURPOSE: Bone defects and nonunions are major clinical skeletal problems. Growth factors are commonly used to promote bone regeneration; however, the clinical impact is limited because the factors do not last long at a given site. The introduction of tissue engineering aimed to deter the diffusion of these factors is a promising therapeutic strategy. The purpose of the present study was to evaluate the in vivo osteogenic capability of an engineered bone morphogenetic protein-4 (BMP4) fusion protein. METHODS: BMP4 was fused with a nanosized carrier, collagen-binding domain (CBD), derived from fibronectin. The stability of the CBD-BMP4 fusion protein was examined in vitro and in vivo. Osteogenic effects of CBD-BMP4 were evaluated by computer tomography after intramedullary injection without a collagen-sponge scaffold. Recombinant BMP-4, CBD, or vehicle were used as controls. Expressions of bone-related genes and growth factors were compared among the groups. Osteogenesis induced by CBD-BMP4, BMP4, and CBD was also assessed in a bone-defect model. RESULTS: In vitro, CBD-BMP4 was retained in a collagen gel for at least 7 days while BMP4 alone was released within 3 hours. In vivo, CBD-BMP4 remained at the given site for at least 2 weeks, both with or without a collagen-sponge scaffold, while BMP4 disappeared from the site within 3 days after injection. CBD-BMP4 induced better bone formation than BMP4 did alone, CBD alone, and vehicle after the intramedullary injection into the mouse femur. Bone-related genes and growth factors were expressed at higher levels in CBD-BMP4-treated mice than in all other groups, including BMP4-treated mice. Finally, CBD-BMP4 potentiated more bone formation than did controls, including BMP4 alone, when applied to cranial bone defects without a collagen scaffold. CONCLUSION: Altogether, nanocarrier-CBD enhanced the retention of BMP4 in the bone, thereby promoting augmented osteogenic responses in the absence of a scaffold. These results suggest that CBD-BMP4 may be clinically useful in facilitating bone formation.

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  • マウスインフルエンザ肺炎におけるレドックス制御蛋白チオレドキシン(TRX-1)の治療的効果

    八代将登, 塚原宏一, 松川昭博, 山田睦子, 藤井洋輔, 長岡義晴, 津下充, 山下信子, 伊藤利洋, 山田雅夫, 増谷弘, 淀井淳司, 森島恒雄

    岡山医学会雑誌   125 ( 2 )   109-112 (J-STAGE)   2013年

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    記述言語:日本語  

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  • Monocyte chemoattractant protein-1/CCL2 produced by stromal cells promotes lung metastasis of 4T1 murine breast cancer cells. 査読 国際誌

    Yoshimura T, Howard OM, Ito T, Kuwabara M, Matsukawa A, Chen K, Liu Y, Liu M, Oppenheim JJ, Wang JM

    PloS one   8 ( 3 )   e58791   2013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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  • The linkage of innate and adaptive immune response during granulomatous development. 査読 国際誌

    Ito T, Connett JM, Kunkel SL, Matsukawa A

    Frontiers in immunology   4   10 - 10   2013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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  • Occult Compression Fracture of Metacarpal Head without Evidence of Avascular Necrosis.

    Keiichiro Nishida, Hiroyuki Hashizume, Akihiro Matsukawa, Kenzo Hashizume, Yasunori Shimamura, Yasuyuki Torigoe, Toshifumi Ozaki

    Acta medica Okayama   67 ( 5 )   311 - 7   2013年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    We report a case of 4th metacarpal head collapse of a 19-year-old healthy man. MRI revealed T1 low and T2 high regions in the collapsed 4th metacarpal head, as well as in the right 3rd and left 4th metacarpal head. Our initial diagnosis was occult compression fracture due to avascular necrosis, known as Dieterich's disease. However, pathological findings of surgically resected right 4th metacarpal head were compatible with transient osteoporosis and metacarpal head fracture followed by active tissue repair. The autologous osteochondral transplants from costchondral junction survived and maintained their size and shape even at 10-year follow-up.

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  • Elevated Levels of Monocyte Chemoattractant Protein-1 in the Aqueous Humor after Phacoemulsification 国際誌

    Motofumi Kawai, Toshihiro Inoue, Masaru Inatani, Naoko Tsuboi, Kohei Shobayashi, Akihiro Matsukawa, Akitoshi Yoshida, Hidenobu Tanihara

    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE   53 ( 13 )   7951 - 7960   2012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:ASSOC RESEARCH VISION OPHTHALMOLOGY INC  

    PURPOSE. To elucidate the impact of phacoemulsification on aqueous monocyte chemoattractant protein-1 (MCP-1) levels, and identify its cell origin.
    METHODS. For clinical study, aqueous humor samples were collected before and after surgery (17.0 +/- 4.0 months postoperatively) from 21 cataract cases that underwent phacoemulsification and intraocular lens (IOL) implantation. Aqueous MCP-1 levels were determined using a multiplex immunoassay. For animal experiments, rabbits underwent phacoemulsification (+/- IOL). Aqueous humor samples were collected from nonoperated eyes and operated eyes, and immunoassays were performed. Eyes were analyzed by reverse transcription-polymerase chain reaction and immunohistochemical studies.
    RESULTS. In the clinical study, mean (+/- SD) aqueous MCP-1 levels were higher postoperatively (1773.5 +/- 321.2 pg/mL) than preoperatively (796.9 +/- 211.3 pg/mL; P &lt; 0.0001). In animal experiments, mean aqueous MCP-1 levels (pg/mL) were higher in postoperative eyes on day 30 (207.1 +/- 62.9) than in nonoperated eyes (31.2 +/- 12.5; P = 0.018). IOL implantation did not affect the changes in MCP-1 levels. After phacoemulsification, MCP-1 mRNA expression was increased in the cornea, iris, ciliary body, and capsular bag. Expression of MCP-1 mRNA in the capsular bag, but not the other tissues, increased from day 30 to 90. Immunohistochemical studies showed positive immunoreactivity for MCP-1 in cells of the posterior capsule after phacoemulsification.
    CONCLUSIONS. Aqueous MCP-1 levels were elevated in both human and animal eyes after phacoemulsification. Proliferated lens epithelial cells on the capsule might be the major cell origin for prolonged MCP-1 production after phacoemulsification. (http://www.umin.ac.jp/number, UMIN000005788.) (Invest Ophthalmol Vis Sci. 2012;53:7951-7960) DOI: 10.1167/iovs.12-10231

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  • Spred-2 deficiency exacerbates acetaminophen–induced hepatotoxicity in mice. 国際誌

    Wakabayashi H, Ito T, Fushimi S, Nakashima Y, Itakura J, Qiuying L, Min Min Win, Cuiming S, Chen C, Sato M, Mino M, Ogino T, Makino H, Yoshimura A, Matsukawa A

    Clin Immunol.   144 ( 3 )   272 - 282   2012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)  

    DOI: 10.1016/j.clim.2012.07.002

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  • Notch system in the linkage of innate and adaptive immunity. 査読 国際誌

    Ito T, Connett JM, Kunkel SL, Matsukawa A

    Journal of leukocyte biology   92 ( 1 )   59 - 65   2012年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1189/jlb.1011529

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  • Effects of Pharyngeal Cooling on Brain Temperature in Primates and Humans A Study for Proof of Principle 国際誌

    Yoshimasa Takeda, Hiroshi Hashimoto, Koji Fumoto, Tetsuya Danura, Hiromichi Naito, Naoki Morimoto, Hiroshi Katayama, Soichiro Fushimi, Akihiro Matsukawa, Aiji Ohtsuka, Kiyoshi Morita

    ANESTHESIOLOGY   117 ( 1 )   117 - 125   2012年7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:LIPPINCOTT WILLIAMS & WILKINS  

    Background: Pharyngeal cooling decreases brain temperature by cooling carotid arteries. This study was designed to evaluate the principle of pharyngeal cooling in monkeys and humans.
    Methods: Monkeys (n = 10) were resuscitated following 12 min of cardiac arrest. Pharyngeal cooling (n = 5), in which cold saline (5 degrees C) was perfused into the cuff at the rate of 500 ml/min, was initiated simultaneously with the onset of resuscitation for 30 min. Patients (n = 3) who were in an intensive care unit were subjected to 30 min of pharyngeal cooling under propofol anesthesia.
    Results: In the animal study, core brain temperature was significantly decreased compared with that in the control group by 1.9 degrees C (SD = 0.8, P &lt; 0.001) and 3.1 degrees C (SD = 1.0, P &lt; 0.001) at 10 ruin and 30 min after the onset of cooling, respectively. The cooling effect was more evident in an animal with low postresuscitation blood pressure. Total dose of epinephrine, number of direct current shocks, and recovery of blood pressure were not different between the two groups. The pharyngeal epithelium was microscopically intact on day 5. In the clinical study, insertion of the cuff and start of perfusion did not affect heart rate or blood pressure. Tympanic temperature was decreased by 0.6 +/- 0.1 degrees C/30 min without affecting bladder temperature. The pharynx was macroscopically intact for 3 days.
    Conclusions: Pharyngeal cooling rapidly and selectively decreased brain temperature in primates and tympanic temperature in humans and did not have adverse effects on return of spontaneous circulation, even when initiated during cardiac arrest in primates.

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  • Egr1: a novel target for ameliorating acute allograft rejection in an experimental lung transplant model 国際誌

    Naohisa Waki, Masaomi Yamane, Sumiharu Yamamoto, Mikio Okazaki, Seiichiro Sugimoto, Akihiro Matsukawa, Takahiro Oto, Shinichiro Miyoshi

    EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY   41 ( 3 )   669 - 675   2012年3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:OXFORD UNIV PRESS INC  

    Acute allograft rejection is one of the significant complications occurring in lung transplant recipients. Early growth response-1 (Egr-1), zinc-finger-type transcription factor, is known as a master switch regulator of diverse chemical mediators. We used an orthotopic mouse model of left lung transplant to elucidate the function of Egr-1 in acute pulmonary rejection.
    Left lung grafts retrieved from C57BL/6 wild mice or C57BL/6 Egr-1-null mice were orthotopically transplanted into BALB/c mice; the lungs were harvested at day 1, 3, 5 or 7 after lung transplantation. The grade of acute rejection was histopathologically evaluated. The intragraft gene expression levels of Egr-1 and downstream target mediators were quantitatively measured by real-time polymerase chain reaction. Immunohistochemical analysis was used to determine the location and distribution of the Egr-1 protein in the pulmonary graft.
    Severe acute rejection was observed in allografts from wild-type mice at 5 days after transplantation. Only minimal rejection was seen in the lung graft from Egr-1-null donor mice at 5 days after transplantation. Strong upregulation of Egr-1 mRNA transcripts was observed at day 1, which then decreased during the next 5 days. The mRNA of Egr-1 target mediators [interleukin-1-beta (IL-1 beta), monocyte chemotactic protein-1 (MCP-1) and plasminogen activator inhibitor-1] reached maximal levels at day 5. Egr-1-null allografts exhibited significantly lower expressions of IL-1 beta and MCP-1 mRNA (P &lt; 0.05).
    Our study showed that deletion of Egr-1 in lung allografts ameliorates severe acute rejection with the reduction of expression levels of chemical mediators, implying a new possible strategy for treating acute pulmonary allograft rejection.

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  • Prostatic stromal tumor of uncertain malignant potential (STUMP) with unrecognized growth pattern 国際誌

    Soichiro Fushimi, Tetsuya Ogino, Ken Aoki, Junya Itakura, Toshihiro Ito, Tadashi Oeda, Hiroyuki Yanai, Akihiro Matsukawa

    PATHOLOGY INTERNATIONAL   62 ( 1 )   69 - 71   2012年1月

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    記述言語:英語   出版者・発行元:WILEY-BLACKWELL  

    DOI: 10.1111/j.1440-1827.2011.02741.x

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  • Local effects of intra-articular injection of anti-rabbit tumor necrosis factor alpha monoclonal antibody in antigen-induced arthritis of the rabbit temporomandibular joint 国際誌

    Taishi Ohtani, Manabu Habu, Amit Khanal, Izumi Yoshioka, Akihiro Matsukawa, Kazuhiro Tominaga

    JOURNAL OF ORAL PATHOLOGY & MEDICINE   41 ( 1 )   96 - 105   2012年1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:WILEY-BLACKWELL  

    BACKGROUND: Local effects of intra-articular (IA) injection of anti-rabbit tumor necrosis factor alpha monoclonal antibody (anti-TNF alpha mAb) for antigen-induced mono-arthritis (AIA) of the rabbit temporomandibular joint (TMJ) and its systemic influences were evaluated.
    METHODS: Biochemical analysis of synovial fluid (SF), clinical and histopathological analyses of TMJ, and serum analysis were performed after inducing AIA in bilateral TMJs of 40 New Zealand White rabbits. IA injection of anti-TNF alpha mAb in unilateral TMJ (TNF blockade side; n = 12) and IgG (n = 12) was performed while saline injected on the contralateral side. TNF alpha and IL-1 beta in SF was analyzed at Days 1, 3, 7, and 21. Joint swelling and head withdrawal reflex threshold (WRT) over TMJs were evaluated in TNF blockade side (n = 12) with histopathological analysis at Days 3, 7, and 21. In remaining four animals with TNF blockade, TNF alpha and anti- TNF alpha mAb in serum were analyzed.
    RESULTS: Tumor necrosis factor alpha in SF was significantly lower in TNF blockade side on all days but IL-1 beta was lower only on Day 3. WRT was significantly higher at all times in the blockade side. Less inflammatory reactions and degenerative changes of cartilage were observed on Days 7 and 21 in the blockade side. TNF alpha and anti- TNF alpha mAb were under detection level in serum at all times.
    CONCLUSIONS: Intra-articular injection of anti- rabbit TNF alpha mAb in mono-arthritis model was effective to control local inflammation and degenerative joint changes. Further, low-dose IA injection of antibody may not have systemic side effects. J Oral Pathol Med (2012) 41: 96105

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  • Correlation of neutrophil and monocyte derived interleukin-1 receptor antagonist and interleukin-8 with colitis severity in the rabbit 国際誌

    Kenta Kaneda, Fumio Saitoh, Hirom Shibusawa, Hidetaka Maegawa, Abbi R. Saniabadi, Nobuhito Kashiwagi, Akihiro Matsukawa

    CYTOKINE   56 ( 2 )   508 - 514   2011年11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:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    Activated neutrophils and monocytes produce interleukin (IL)-8, a pro-inflammatory chemokine, but also IL-1 receptor antagonist (IL-1ra), which is an anti-inflammatory cytokine. We were interested to see the profiles of IL-8 and IL-1ra in the colonic tissue and in the peripheral blood leukocytes (PBL) during the development of immune complex induced colitis in rabbits. IL-1ra and IL-8 in PBL were measured in 26 rabbits at time 0 h, 24 h, and 48 h after induction of colitis. The colons were removed at 48 h for measuring myeloperoxidase (MPO), ulcer area, IL-1ra and IL-8. Epithelial damage, crypt abscess formation and leukocyte infiltration of the colonic tissue were major features of this colitis model. During the development of colitis, there was an increase in circulating neutrophils and monocytes (P &lt; 0.0001), but not lymphocytes. Likewise, elevated amounts of IL-Ira (P = 0.0001) and IL-8 (P = 0.0219) production by PBL were observed following induction of colitis. Flow cytometry revealed major source of IL-1ra was monocytes, while the main sources of IL-8 were neutrophils and monocytes. There was correlation between MPO and ulcer area (R(s) = 0.6327, P &lt; 0.0001). At 24 h, PBL from MPO(High) group (n = 11) showed increased IL-1ra (P = 0.027) and IL-8 (P = 0.0128) levels vs MPO(Low) group (n = 15). IL-8 production by PBL showed correlation with tissue MPO (R(s) = 0.4273, P = 0.0295). The colitis in this model was associated with an increase in circulating monocytes and neutrophils, which released increased amounts of IL-8 and IL-1ra. Further, IL-8 and IL-1ra showed correlation with the severity of colitis. These observations should significantly further understandings on the role of neutrophils and monocytes in the immunopathogenesis of ulcerative colitis. (C) 2011 Elsevier Ltd. All rights reserved.

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  • The Critical Role of Notch Ligand Delta-like 1 in the Pathogenesis of Influenza A Virus (H1N1) Infection 国際誌

    Toshihiro Ito, Ronald M. Allen, William F. Carson, Matthew Schaller, Karen A. Cavassani, Cory M. Hogaboam, Nicholas W. Lukacs, Akihiro Matsukawa, Steven L. Kunkel

    PLOS PATHOGENS   7 ( 11 )   e1002341   2011年11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:PUBLIC LIBRARY SCIENCE  

    Influenza A viral infections have been identified as the etiologic agents for historic pandemics, and contribute to the annual mortality associated with acute viral pneumonia. While both innate and acquired immunity are important in combating influenza virus infection, the mechanism connecting these arms of the immune system remains unknown. Recent data have indicated that the Notch system is an important bridge between antigen-presenting cells (APCs) and T cell communication circuits and plays a central role in driving the immune system to overcome disease. In the present study, we examine the role of Notch signaling during influenza H1N1 virus infection, focusing on APCs. We demonstrate here that macrophages, but not dendritic cells (DCs), increased Notch ligand Delta-like 1 (Dll1) expression following influenza virus challenge. Dll1 expression on macrophages was dependent on retinoic acid-inducible gene-I (RIG-I) induced type-I IFN pathway, and not on the TLR3-TRIF pathway. We also found that IFN alpha-Receptor knockout mice failed to induce Dll1 expression on lung macrophages and had enhanced mortality during influenza virus infection. Our results further showed that specific neutralization of Dll1 during influenza virus challenge induced higher mortality, impaired viral clearance, and decreased levels of IFN-gamma. In addition, we blocked Notch signaling by using gamma-secretase inhibitor (GSI), a Notch signaling inhibitor. Intranasal administration of GSI during influenza infection also led to higher mortality, and higher virus load with excessive inflammation and an impaired production of IFN-gamma in lungs. Moreover, Dll1 expression on macrophages specifically regulates IFN-gamma levels from CD4(+) and CD8(+) T cells, which are important for anti-viral immunity. Together, the results of this study show that Dll1 positively influences the development of anti-viral immunity, and may provide mechanistic approaches for modifying and controlling the immune response against influenza H1N1 virus infection.

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  • 黒色真菌Exophiala. jeanselmeiによる左手背皮下膿瘍を呈したフェオヒフォミコーシスの1例

    森三郎, 平谷恵子, 井上さおり, 川上直明, 藤野寿幸, 松川昭博

    尾道市立病院医学雑誌   27 ( 1 )   55 - 58   2011年

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  • Oxidative stress enhances granulocytic differentiation in HL60 cells, an acute promyelocytic cell line 国際誌

    Arikawa T, Saita N, Oomizu S, Ueno M, Matsukawa A, Katoh S, Kojima K, Nagahara K, Miyake M, Yamauchi A, Kohrogi H, Hirashima M

    Free Radic Res   44 ( 11 )   1328 - 1337   2010年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.3109/10715762.2010.503757

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  • Galectin-9 ameliorates immune complex-induced arthritis by regulating FcγR expression on macrophages. 国際誌

    Arikawa T, Watanabe K, Seki M, Matsukawa A, Oomizu S, Sakata K, Sakata A, Ueno M, Saita N, Niki T, Yamauchi A, Hirashima M

    CLINICAL IMMUNOLOGY   133 ( 3 )   382 - 392   2009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)  

    DOI: 10.1016/j.clim.2009.09.004

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  • Forced expression of suppressor of cytokine signaling 3 in T cells protects the development of concanavalin A-induced hepatitis in mice 国際誌

    Soichiro Fushimi, Tetsuya Ogino, Junko Hara, Tomohiro Takahata, Hiroshi Wakabayashi, Haruyuki Watanabe, Yasuharu Arashima, Masato Kubo, Akihiro Matsukawa

    CLINICAL IMMUNOLOGY   133 ( 3 )   437 - 446   2009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:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    T cells play central rotes in liver diseases, but the regulatory mechanism by cytokine signaling is not well understood. In the present study, we explored the role of SOCS3 in T cells in concanavalin A (ConA)-induced hepatitis. Mice with T-cell-specific overexpression of SOCS3 (SOCS3-cTg) showed reduced hepatic damage and improved mice survival relative to the control, an event that was associated with decreased apoptotic signals Fas and pStat1. Expression of Th1-cytokines/chemokines was decreased in SCCS3-cTg liver with reduced expression of T-bet, a Th1-transcription factor. Flow cytometric analysis of the liver lymphocytes demonstrated that activated CD4(+) T cells, cytotoxic T cells and. natural killer T cells were significantly decreased in SOCS3-cTg liver with decreased expression of perforin and granzyme 8, injurious molecules for hepatocyte damage. These results suggest that forced expression of SOCS3 in T cells prevents ConA-induced liver injury by inhibiting several phases of Th1 responses. (C) 2009 Elsevier Inc. All rights reserved.

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  • Increased CCL2 Expression and Macrophage/Monocyte Migration During Microbicide-Induced Vaginal Irritation 国際誌

    Carsten Alt, Travis Harrison, Linda Dousman, Nahoko Fujita, Ken Shew, Thanh-Thuy Tran, Sara Shayesteh, Akihiro Matsukawa, Jon Mirsalis, Annalisa D&apos;Andrea

    CURRENT HIV RESEARCH   7 ( 6 )   639 - 649   2009年11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:BENTHAM SCIENCE PUBL LTD  

    Despite availability of successful prevention strategies, HIV continues to spread at alarming rates, especially among women in developing countries. Vaginal microbicides offer a promising approach for blocking transmission of HIV when condom use cannot be negotiated with male partners. A major problem in the development of vaginal microbicides is chemically induced vaginal irritation, which can enhance the risk of HIV transmission. Evaluation of vaginal irritation prior to clinical trials typically uses an expensive and animal-intensive rabbit vaginal irritation model, which could be supplemented by measuring additional inflammatory biomarkers. We studied several immunological parameters as potential biomarkers of vaginal irritation, using the spermicides nonoxynol-9 and benzalkonium chloride as test microbicides. We measured amounts of cytokines, as well as inflammatory cells, in vaginal tissue lysates and on the vaginal surface. We observed that treatment with the selected microbicides increases quantities of the inflammatory cytokines interleukin-1, CXCL8, and CCL2 in the vaginal tissue parenchyma, and of CCL2 on the vaginal surface. This observation was correlated with increases in macrophages in the vaginal parenchyma. We suggest that measurements of CCL2 and macrophages can serve as new inflammatory biomarkers to evaluate the safety of promising novel microbicides for prevention of HIV.

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  • Successful steroid pulse therapy for brain lesion caused by Shiga toxin 2 in rabbits (vol 46, pg 179, 2009)

    Jun Fujii, Yoshimasa Kinoshita, Akihiro Matsukawa, Sharon Y. A. M. Villanueva, Takashi Yutsudo, Shin-ichi Yoshida

    MICROBIAL PATHOGENESIS   46 ( 6 )   345 - 345   2009年6月

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    記述言語:英語   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    DOI: 10.1016/j.micpath.2009.04.001

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  • Galectin-9 accelerates transforming growth factor beta 3-induced differentiation of human mesenchymal stem cells to chondrocytes 国際誌

    Tomohiro Arikawa, Akihiro Matsukawa, Kota Watanabe, Ken-mei Sakata, Masako Seki, Megumi Nagayama, Keisuke Takeshita, Kanako Ito, Toshiro Niki, Souichi Oomizu, Rika Shinonaga, Naoki Saita, Mitsuomi Hirashima

    BONE   44 ( 5 )   849 - 857   2009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)   出版者・発行元:ELSEVIER SCIENCE INC  

    Galectin-9 (Gal-9), a beta-galactoside binding lectin, plays a crucial role in innate and adaptive immunity. in the rat collagen-induced arthritis model, administration of Gal-9 induced repair of existing cartilage injury even when joints were already swollen with cartilage destruction. We thus attempted to explore the role of Gal-9 in chondrocyte differentiation utilizing human mesenchymal stem cell (MSC) pellet Cultures. During chondrogenesis induced by transforming growth factor beta 3 (TGF beta 3), MSCs strongly expressed endogenous Gal-9. Expression of Gal-9 peaked on day 14 and the neutralization of endogenous Gal-9 resulted in the reduced chondrogenesis, indicating possible involvement of Gal-9 in TGF beta-mediated chondrogenesis. In pellets, addition of Gal-9 significantly enhanced TGF beta 3-induced chondrogenesis. as evidenced by increasing proteoglycan content, but not cell proliferation. In the absence of Gal-9, collagen expression by MSCs switched from type I to type II on 28 days after stimulation with TGR beta 3. When MSCs were co-stimulated with Gal-9, the class switch occurred on day 21. In addition, Gal-9 synergistically enhanced TGF beta 3-induced phosphorylation of Smad2, though Gal-9 did not itself induce detectable Smad2 phosphorylation. These results Suggest that Gal-9 has a beneficial effect on cartilage repair in injured joints by induction of differentiation of MSCs into chondrocytes. (C) 2009 Elsevier Inc. All rights reserved.

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  • Successful steroid pulse therapy for brain lesion caused by Shiga toxin 2 in rabbits 国際誌

    Jun Fujii, Yoshirnasa Kinoshita, Akihiro Matsukawa, Sharon Y. A. M. Villanueva, Takashi Yutsudo, Shin-ichi Yoshida

    MICROBIAL PATHOGENESIS   46 ( 4 )   179 - 184   2009年4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:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    Betamethasone sodium phosphate (BSP) is usually used as a steroid therapy for human brain edema. High doses of BSP (36 mg/kg) twice a day for two days statistically reduced the mortality rate and improved the survival period of Stx2 (1.4 mu g/kg: 1.6LD(50))-toxemic rabbits. We made evaluations on three kinds of magnetic resonance images (MRI) including T1-weighted, T2-weighted, and enhanced MRI using gadopentetate dimeglumine (Gd-DTPA) to detect brain lesion induced by an intravenous injection of Stx2 in rabbits. Enhanced T1-weighted MRI was the most sensitive tool to find leakage of Gd-DTPA suggesting impairment of the blood brain barrier caused by Stx2. Enhanced MRI revealed that BSP treatment inhibited the leakage of Gd-DTPA, as directly evidenced by the protective effect of BSP against brain edema induced by intravenous injection of Stx2. Interleukin 1 beta was not induced after Stx2 treatment in brain primary mixed cell culture. Crown Copyright (C) 2009 Published by Elsevier Ltd. All rights reserved.

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  • Activation of c-Jun N-terminal kinase is essential for oxidative stress-induced Jurkat cell apoptosis by monochloramine 国際誌

    Tetsuya Ogino, Michitaka Ozaki, Mutsumi Hosako, Masako Omori, Shigeru Okada, Akihiro Matsukawa

    LEUKEMIA RESEARCH   33 ( 1 )   151 - 158   2009年1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:PERGAMON-ELSEVIER SCIENCE LTD  

    Leukemic cell apoptosis may be enhanced by appropriate oxidative stress. We report here the mechanism of Jurkat cell apoptosis by monochloramine (NH(2)Cl), a neutrophil-derived oxidant. NH(2)Cl induced caspase-dependent apoptosis, which was preceded by cytochrome c and Smac/Diablo release from mitochondfia. Within 10 min of NH(2)Cl treatment, c-Jun N-terminal kinase (JNK) activation and elevation of cytosolic Ca(2+) were observed. JNK inhibitors (SP600125 or JNK inhibitor VIII) significantly suppressed the apoptosis as well as caspase cleavage and cytochrome c release. In contrast, Ca(2+) chelation by EGTA + acetoxymethyl-EGTA had no effects on apoptosis. Our results indicated that JNK activation contributed most importantly to the NH(2)Cl-induced apoptosis. (C) 2008 Elsevier Ltd. All fights reserved.

    DOI: 10.1016/j.leukres.2008.07.009

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  • Pathophysiology of sepsis and recent patents on the diagnosis, treatment and prophylaxis for sepsis 国際誌

    Yasumasa Okazaki, Akihiro Matsukawa

    Recent Patents on Inflammation and Allergy Drug Discovery   3 ( 1 )   26 - 32   2009年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Despite advances in the development of powerful antibiotics and intensive care unit, sepsis is still life threatening and the mortality rate remains unchanged for the past three decades. Recent prospective trials with biological response modifiers have shown a modest clinical benefit. The pathological basis of sepsis is initially an excessive inflammatory response against invading pathogens, leading to systemic inflammatory response syndrome (SIRS). Evidence reveals that a variety of inflammatory mediators orchestrate the intense inflammation through complicated cellular interactions. More recent data indicate that most septic patients survive this stage and then subjected to an immunoparalysis phase, termed compensatory anti-inflammatory response syndrome (CARS), which is more fatal than the initial phase. Sepsis is a complicated clinical syndrome with multiple physiologic and immunologic abnormalities. In this review, we summarize the recent understandings of the pathophysiology of sepsis, and introduce recent patents on diagnosis, treatment and prophylaxis for sepsis. © 2009 Bentham Science Publishers Ltd.

    DOI: 10.2174/187221309787158416

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  • Invasion of atheromatous plaques into tunica media causes coronary outward remodeling in WHHLMI rabbits 国際誌

    Masashi Shiomi, Satoshi Yamada, Akihiro Matsukawa, Hiroyuki Itabe, Takashi Ito

    ATHEROSCLEROSIS   198 ( 2 )   287 - 293   2008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)   出版者・発行元:ELSEVIER IRELAND LTD  

    To clarify the mechanism of coronary outward remodeling, we examined atherosclerotic coronary arteries morphologically using WHHLMI rabbits that develop coronary atherosclerosis spontaneously. Perfusion-fixed coronary segments of WHHLMI rabbits were prepared at 500 mu m intervals. After immunohistochemical staining and histopathological staining, the areas and lengths of the arterial wall and the lesions were measured. Obvious outward remodeling was observed in coronary sections with greater than 40% cross-sectional narrowing. In coronary sections with greater than 40% cross-sectional narrowing, the tunica media was thick at the shoulder of atheromatous plaque and was thin beneath the atheromatous plaques. Macrophages infiltrated those attenuated tunica media expressed matrix metalloproteinases and oxidized LDL was accumulated in those areas. In those areas, collagen fibers and the internal elastic lamina had disappeared partly and apoptotic smooth muscle cells were observed. Proliferation of smooth muscle cells was observed at the attenuated tunica media and adjacent adventitia. The present results suggest that invasion of atheromatous plaques into the tunica media causes coronary outward remodeling. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

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  • Galectin-9 suppresses the generation of Th17, promotes the induction of regulatory T cells, and regulates experimental autoimmune arthritis 国際誌

    Masako Seki, Souichi Oomizu, Ken-mei Sakata, Atsuko Sakata, Tomohiro Arikawa, Kota Watanabe, Kanako Ito, Keisuke Takeshita, Toshiro Niki, Naoki Saita, Nozomu Nishi, Akira Yamauchi, Shigeki Katoh, Akihiro Matsukawa, Vijay Kuchroo, Mitsuomi Hirashima

    CLINICAL IMMUNOLOGY   127 ( 1 )   78 - 88   2008年4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:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    The effects of galectin-9 on a mouse collagen-induced arthritis (CIA) model were assessed to clarify whether galectin-9 suppresses CIA by regulating T cell. immune responses. Galectin-9 suppressed CIA in a dose-dependent manner, and such suppression was observed even when treatment was started on 7 days after the booster, indicating its preventive and therapeutic effects. Galectin-9 induced the decreased levels of pro-inflammatory cytokines, IL-17, IL-12, and IFN gamma in the joint. Gatectin-9 induced the decreased number of CD4(+) TIM-3(+) T cells in peripheral blood. Galectin-9-deficient mice became susceptible to CIA may be by increased number of CD4(+) TIM-3(+) T cells and decreased number of Treg cells. We further found that galectin-9 induces differentiation of naive T cells to Treg cells, and it suppresses differentiation to Th17 cells in vitro. The present results suggested that galectin-9 ameliorates CIA by suppressing the generation of Th17, promoting the induction of regulatory T cells. (C) 2008 Elsevier Inc. All rights reserved.

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  • 悪性中皮腫の1剖検例

    尾関孝二, 三輪栄子, 筑田絵理, 原田美由紀, 松川昭博

    日本臨床細胞学会岡山支部会誌   26   37 - 38   2008年

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  • 乳腺血管肉腫の1例.

    松岡博美, 井上博文, 今井みどり, 藤田勝, 森下由美子, 大森昌子, 市村浩一, 柳井広之, 大原信哉, 松川昭博

    日本臨床細胞学会岡山支部会誌   27   34 - 35   2008年

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  • 悪性転化を示したnuclear palisadingを伴う隆起性皮膚線維肉腫の一例.

    大森昌子, 柳井広之, 荻野哲也, 松川昭博, 吉野正

    診断病理   25 ( 2 )   72 - 76   2008年

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  • STAT proteins in innate immunity during sepsis: Lessons from gene knockout mice

    Akihiro Matsukawa

    ACTA MEDICA OKAYAMA   61 ( 5 )   239 - 245   2007年10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:OKAYAMA UNIV MED SCHOOL  

    The innate immune system provides immediate defense against infection and serves as the first line of host defense during infection. In innate immunity, leukocytes such as neutrophils; and macrophages recognize and respond to pathogens in a non-specific manner. Therefore, the recruitment and activation of leukocytes are essential in innate immunity, and are governed by a variety of chemical mediators including cytokines. Cytokines are generally divided into 2 types, termed type-1 and type-2 cytokines. Type-1 cytokines are important in local host defense, while type-2 cytokines play a protective role when inflammatory response spreads to the body. These cytokines exert their biological functions through the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. STAT1/3/4/6 are transcription factors that mediate IFN gamma/IL-10/IL-12/IL-13 cytokine signaling, respectively. Evidence indicates that STAT proteins have a significant impact on innate immunity during sepsis. This review focuses on recent understandings in the regulation of innate immunity by STAT proteins during sepsis and septic shock. The suppressor of cytokine signaling (SOCS) proteins are a family of SH2 domain-containing cytoplasmic proteins that complete a negative feedback loop to attenuate signal transduction from cytokines that act through the JAK/STAT pathway. The participation of SOCS proteins in sepsis is also discussed.

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  • CCL2/monocyte-chemoattractant protein-1 as a novel biomarker for the safety evaluation of microbicide-induced vaginal irritation

    Carsten Alt, Travis Harrison, Nahoko Fujita, Kenneth Shew, Thuy Tran, Akihiro Matsukawa, Charles Litterst, Jon Mirsalis, Annalisa D'Andrea

    CYTOKINE   39 ( 1 )   1 - 2   2007年7月

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    記述言語:英語   出版者・発行元:ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD  

    DOI: 10.1016/j.cyto.2007.07.009

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  • Inhibition of CCL1-CCR8 interaction prevents aggregation of macrophages and development of peritoneal adhesions 国際誌

    Akiyoshi Hoshino, Yuki I. Kawamura, Masato Yasuhara, Noriko Toyama-Sorimachi, Kenji Yamamoto, Akihiro Matsukawa, Sergio A. Lira, Taeko Dohi

    JOURNAL OF IMMUNOLOGY   178 ( 8 )   5296 - 5304   2007年4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:AMER ASSOC IMMUNOLOGISTS  

    Peritoneal adhesions are a significant complication of surgery and visceral inflammation; however, the mechanism has not been fully elucidated. The aim of this study was to clarify the mechanism of peritoneal adhesions by focusing on the cell trafficking and immune system in the peritoneal cavity. We investigated the specific recruitment of peritoneal macrophages (PM phi) and their expression of chemokine receptors in murine models of postoperative and postinflammatory peritoneal adhesions. PM phi aggregated at the site of injured peritoneum in these murine models of peritoneal adhesions. The chemokine receptor CCR8 was up-regulated in the aggregating PN phi when compared with naive PM phi. The up-regulation of CCR8 was also observed in PM phi, but not in bone marrow-derived M phi, treated with inflammatory stimulants including bacterial components and cytokines. Importantly, CCL1, the ligand for CCR8, a product of both PM phi and peritoneal mesothelial cells (PMCs) following inflammatory stimulation, was a potent enhancer of CCR8 expression. Cell aggregation involving PM phi and PMCs was induced in vitro in the presence of CCL1. CCL1 also up-regulated mRNA levels of plasminogen activator inhibitor-1 in both PM phi and PMCs. CCR8 gene-deficient mice or mice treated with anti-CCL1-neutralizing Ab exhibited significantly reduced postoperational peritoneal-adhesion. Our study now establishes a unique autocrine activation system in PM phi and the mechanism for recruitment of PM phi together with PMCs via CCL1/CCR8, as immune responses of peritoneal cavity, which triggers peritoneal adhesions.

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  • Sudden death of a young woman due to aortic dissection caused by Turner’s syndrome 国際誌

    Mimasaka S, Ohtsu Y, Tsunenari S, Matsukawa A, Hashiyada M, Takahashi S, Funayama M

    Pathol Int   57 ( 4 )   219 - 223   2007年4月

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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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  • Overexpression of suppressor of cytokine signaling-3 in T cells exacerbates acetaminophen-induced hepatotoxicity 国際誌

    Kosuke Numata, Masato Kubo, Hiroyuki Watanabe, Katsumasa Takagi, Hiroshi Mizuta, Seiji Okada, Steven L. Kunkel, Takaaki Ito, Akihiro Matsukawa

    JOURNAL OF IMMUNOLOGY   178 ( 6 )   3777 - 3785   2007年3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:AMER ASSOC IMMUNOLOGISTS  

    Cytokines have been implicated in the progression of acetaminophen (APAP)-induced acute liver injury. Suppressors of cytokine signaling (SOCS) proteins are negative regulators of cytokine signaling by inhibiting the JAK-STAT pathway, but their role in APAP hepatotoxicity is unknown. In this present study, we attempted to explore the role of SOCS3 in T cells in APAP-induced liver injury. Mice with a cell-specific overexpression of SOCS3 in T cells (SOCS3Tg, in which Tg is transgenic) exhibited exaggerated hepatic injury after APAP challenge, as evidenced by increased serum alanine aminotransferase levels, augmented hepatic necrosis, and decreased survival relative to the wild-type mice. Adaptive transfer of SOCS3Tg-CD4(+) T cells into T and B cell-deficient RAG-2(-/-) mice resulted in an exacerbated liver injury relative to the control. In SOCS3Tg mice, hepatocyte apoptosis was enhanced with decreased expression of antiapoptotic protein bcl-2, whereas hepatocyte proliferation was reduced with altered cell cycle-regulatory proteins. Levels of IFN-gamma and TNF-alpha in the circulation were augmented in SOCS3Tg mice relative to the control. Studies using neutralizing Abs indicated that elevated IFN-gamma and TNF-alpha were responsible for the exacerbated hepatotoxicity in SOCS3Tg mice. Activation of STATl that is harmful in liver injury was augmented in SOCS3Tg hepatocytes. Alternatively, hepatoprotective STAT3 activation was decreased in SOCS3Tg hepatocytes, an event that was associated with augmented SOCS3 expression in the hepatocytes. Altogether, these results suggest that forced expression of SOCS3 in T cells is deleterious in APAP hepatotoxicity by increasing STAT1 activation while decreasing STAT3 activation in hepatocytes, possibly through elevated IFN-gamma and TNF-alpha.

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  • 非定型奇形腫様/ラブドイド腫瘍 atypical teratoid/rhabdoid tumor (AT/RT)の1例

    大森昌子, 柳井広之, 荻野哲也, 井上智, 市川智継, 松川昭博, 吉野正

    診断病理   24;115-120   2007年

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  • Overexpression of suppressor of cytokine signaling-5 in T cells augments innate immunity during septic peritonitis 国際誌

    Hiroyuki Watanabe, Masato Kubo, Kosuke Numata, Katsumasa Takagi, Hiroshi Mizuta, Seiji Okada, Takaaki Ito, Akihiro Matsukawa

    JOURNAL OF IMMUNOLOGY   177 ( 12 )   8650 - 8657   2006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:AMER ASSOC IMMUNOLOGISTS  

    Suppressors of cytokine signaling (SOCS) proteins are negative regulators of cytokine signaling by inhibiting the JAK-STAT signal transduction pathway, but their role in innate immunity remains to be investigated. In the present study, we demonstrate that overexpression of SOCS5 in T cells augments innate immunity during septic peritonitis induced by cecal ligation and puncture (CLP). Mice with a cell-specific overexpression of SOCS5 in T cells (SOCS5 transgenic (Tg)) were resistant to the lethality relative to the wild-type (WT) mice. This was most likely due to the enhanced innate immunity in SOCS5Tg mice, as bacterial burden in SOCS5Tg mice was significantly lower than WT mice. Accumulation of neutrophils and macrophages was augmented in SOCS5Tg mice, an event that was accompanied by increased peritoneal levels of IL-12, IFN-gamma, and TNF-alpha. In vitro bactericidal activities of macrophages and neutrophils were enhanced in SOCS5Tg mice. Both neutrophils and macrophages from WT mice adopted enhanced bacterial killing activity when cocultured with CD4(+) T cells from SOCS5Tg mice, relative to CD4(+) T cells from WT mice. Adoptive transfer of SOCS5Tg-CD4(+) T cells into T- and B cell-deficient RAG-2(-/-) mice resulted in augmented leukocyte infiltration and increased peritoneal levels of IL-12, IFN-gamma, and TNF-alpha after CLP, as compared with the controls. Furthermore, CLP-induced bacterial burden in RAG2(-/-) mice harboring SOCS5Tg-CD4(+) T cells was significantly reduced relative to the controls. These findings provide evidence that intervention of SOCS5 expression in T cells affects innate immunity, which highlight a novel role of T cells during sepsis.

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  • The neuropeptide neuromedin U promotes IL-6 production from macrophages and endotoxin shock 国際誌

    M Moriyama, A Matsukawa, S Kudoh, T Takahashi, T Sato, T Kano, A Yoshimura, M Kojima

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   341 ( 4 )   1149 - 1154   2006年3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:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Neuromedin U (NMU) is a neuropeptide involved in appetite, circadian rhythm, and pronociception. However, the NMU receptor NMU-R1 has been shown to be expressed in immune cells and NMU promotes mast cell-dependent inflammation. In this study, we demonstrated that NMU plays an important role in IL-6 production in macrophages. NMU-deficient mice were resistant against cecal ligation puncture- as well as LPS-induced septic shock. IL-6 but not TNF-alpha levels were markedly reduced in LPS-treated NMU-deficient mice compared with wild type mice. Both NMU and NMU-R1 were expressed in wild type peritoneal macrophages, and treatment with LPS resulted in up-regulation of NMU but down-regulation of NMU-RI expression, however, no down-regulation of NMU-RI was observed in NMU-deficient macrophages where LPS-induced IL-6 production was severely reduced. These data suggest that LPS-induced IL-6 expression is partly dependent on autocrine/paracrine activation of the NMU-NMU-R1 signals in macrophages. (c) 2006 Elsevier Inc. All rights reserved.

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  • Relationship between TNF-alpha and TUNEL-positive chondrocytes in antigen-induced arthritis of the rabbit temporomandibular joint 国際誌

    Y Hirota, M Habu, K Tominaga, M Sukedai, A Matsukawa, T Nishihara, J Fukuda

    JOURNAL OF ORAL PATHOLOGY & MEDICINE   35 ( 2 )   91 - 98   2006年2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:BLACKWELL PUBLISHING  

    BACKGROUND: Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end-labeling (TUNEL) staining is a widely accepted method for the detection of DNA fragmentation in nuclei of apoptotic cells. Tumor necrosis factor (TNF)-alpha is closely associated with changes in condylar cartilage and modulates apoptosis in various tissues including cartilage. The aim of this study was to investigate the relationship between apoptotic chondrocytes and TNF-alpha in a rabbit model of arthritis.
    METHOD: Unilateral temporomandibular joint (TMJ) arthritis was induced in 20 adult New Zealand White rabbits. From 1 day to 6 weeks after the induction of arthritis, immunohistochemical analysis for TNF-alpha and TUNEL was performed.
    RESULTS: In condylar cartilage, TNF-alpha-positive cells and TUNEL-positive cells were localized together. TNF-alpha-positive chondrocytes seemed to precede TUNEL-positive cells.
    CONCLUSIONS: The results of the present study suggest that TNF-alpha may be involved in apoptosis and/or apoptotic necrosis of chondrocytes as TMJ arthritis progresses from the acute to chronic stage.

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  • Absence of CC chemokine receptor 8 enhances innate immunity during septic peritonitis 国際誌

    Akihiro Matsukawa, Shinji Kudoh, Gen-ichiro Sano, Takako Maeda, Takaaki Ito, Nicholas W. Lukacs, Cory M. Hogaboam, Steven L. Kunkel, Sergio A. Lira

    FASEB JOURNAL   20 ( 2 )   302 - 304   2006年2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:FEDERATION AMER SOC EXP BIOL  

    An effective clearance of microbes is crucial in host defense during infection. In the present study, we demonstrate that CC chemokine receptor 8 (CCR8) skews innate immune response during septic peritonitis induced by cecal ligation and puncture (CLP). CCR8 was expressed in resident peritoneal macrophages and elicited leukocytes during CLP in the wild-type CCR8+/+ mice. CCR8-/- mice were resistant to CLP-induced lethality relative to CCR8+/+ mice, and this resistance was associated with an augmented bacterial clearance in CCR8-/- mice. In vitro, peritoneal macrophages from CCR8-/- mice, but not neutrophils, exhibited enhanced bactericidal activities relative to those from CCR8+/+ mice. Upon stimulation with the bacterial component LPS, elevated levels of superoxide generation, lysosomal enzyme release, and nitric oxide generation, effector molecules for bacterial killing were detected in CCR8-/- macrophages relative to CCR8+/+ macrophages. In addition, CCR8-/- macrophages produced significantly higher levels than CCR8+/+ macrophages of several cytokines and chemokines known to augment bactericidal activities of leukocytes that include TNF-alpha, IL-12, macrophage-derived chemokine (MDC/CCL22), macrophage inflammatory protein (MIP)-2, and KC. Altogether, these results indicate that CCR8 may have a negative impact on host defense during septic peritonitis, providing a new paradigm for the role of CCR8 in innate immunity.

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  • Inhibitory effects of dimethylacetyl-beta-cyclodextrin on lipopolysaccharide-induced macrophage activation and endotoxin shock in mice 国際誌

    H Arima, K Motoyama, A Matsukawa, Y Nishimoto, F Hirayama, K Uekama

    BIOCHEMICAL PHARMACOLOGY   70 ( 10 )   1506 - 1517   2005年11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:PERGAMON-ELSEVIER SCIENCE LTD  

    The potential use of hydrophilic cycloclextrins (CyDs) as an inhibitor for lipopolysaccharide (LPS) was examined. Of the five CyDs used in this study, dimethylacetyl-beta-cyclodextrin (DMA7-beta-CyD) had greater inhibitory activity than other CyDs against the production of nitric oxide (NO) and various proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) in murine macrophages stimulated with two serotypes of LPS and lipid A. The inhibitory effect of DMA7-beta-CyD on NO production was also observed in macrophages stimulated with lipoteichoic acid (LTA), but not peptidoglycan (PGN), polyinosinic-polycytidylic acid (poly I:C) or CpG oligonucleotide (CpG-ODN). Several studies have suggested that the inhibitory effects of DMA7-beta-CyD could be ascribed to the interaction with LPS. Simultaneous administration of DMA7-beta-CyD not only intraperitoneally but also intravenously and intraperitoneal injection of aqueous solution containing LPS and D-galactosamine in murine endotoxin shock model suppressed fatality. Also, DMA7-beta-CyD decreased blood level of TNF-alpha as well as serum levels of aspartate transaminase (AST) and alanine transaminase (ALT) in mice. In conclusion, DMA7-beta-CyD may have promise as a new therapeutic agent for endotoxin shock induced by LPS. (c) 2005 Elsevier Inc. All rights reserved.

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  • Effects of denervation on neuromuscular junctions in the thyroarytenoid muscle 国際誌

    Y Kumai, T Ito, A Matsukawa, E Yumoto

    LARYNGOSCOPE   115 ( 10 )   1869 - 1872   2005年10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:WILEY  

    Objectives/Hypothesis. To evaluate the effects of denervation on muscle fibers and neuromuscular junctions (NMJ) of the rat thyroarytenoid (TA) muscle with a histochemical method to monitor the status of degenerative NMJ. Study Design: Quantitative assessment to monitor the status of degenerative muscle fibers and NMJ in the TA muscle. Methods: Wistar rats were killed at 6, 12, 18, and 24 hours and at 2, 4, and 10 weeks after left recurrent laryngeal nerve (RLN) transection. Hematoxylin-eosin stain was used to evaluate the atrophic changes of the TA muscle. The pre- and postsynaptic structures of the NMJ were detected histochemically. These changes were evaluated by comparing the results between the treated (T) and untreated (U) sides (T/U ratio) in the same section. Results. The atrophic changes in the TA muscle progressed gradually, and at 10 weeks, the T/U ratios of the entire muscle area and of the muscle fiber size decreased to 53.2 +/- 10.7% and 55.5 +/- 6.8%, respectively (P &lt; .01). The number of nerve terminals decreased significantly at 18 hours (P &lt; .01), and they disappeared completely by 24 hours. In contrast, at 10 weeks, 70.5 +/- 12.4% (P &lt; .01) of acetylcholine receptors (AchRs) were preserved. Conclusions: In the rat TA muscle, denervation. influences the presynaptic nerve terminals more than the postsynaptic AchRs and the muscle fibers. The results could be a basis for understanding the mechanism of laryngeal denervation and reinnervation processes in animal models.

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  • Stat3 in resident macrophages inflammatory response 国際誌

    A Matsukawa, S Kudo, T Maeda, K Numata, H Watanabe, K Takeda, S Akira, T Ito

    JOURNAL OF IMMUNOLOGY   175 ( 5 )   3354 - 3359   2005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)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Inflammation is counterbalanced by anti-inflammatory cytokines such as IL-10, in which Stat3 mediates the signaling pathway. In this study, we demonstrate that resident macrophages, but not other cell types, are important targets of IL-10 in a murine model of acute peritonitis. Injection of thioglycollate i.p. induced a considerable number of neutrophils and macrophages in the peritoneum, which was significantly augmented in mice with a cell-type specific disruption of the Stat3 gene in macrophages and neutrophils (LysMcre/Stat3flox(/-) mice). The augmented leukocyte infiltration was accompanied by increased peritoneal levels of TNF-alpha, MIP-2, KC chemokine (KC), and MCP-1/CCL2. Stat3 was tyrosine phosphorylated in peritoneal resident macrophages as well as infiltrating leukocytes in the littermate controls, suggesting that Stat3 in either or both of these cells might play a regulatory role in inflammation. The peritoneal levels of TNF-alpha, MIP-2, KC, and MCP-1 were similarly elevated in LysMcre/Stat3(flox/)-mice rendered leukopenic by cyclophosphamide treatment as compared with the controls. Adoptive transfer of resident macrophages from LysMcre/Stat3(flox/-) mice into the control littermates resulted in increases in the peritoneal level of TNF-alpha, MIP-2, KC, and MCP-1 after i.p. injection of thioglycollate. Under these conditions, control littermates harboring LysMcre/Stat3(flox/-) macrophages exhibited an augmented leukocyte infiltration relative to those received control macrophages. Taken together, these data provide evidence that resident macrophages, but not other cell types, play a regulatory role in inflammation through a Stat3 signaling pathway. Stat3 in resident macrophages appears to function as a repressor protein in this model of acute inflammation.

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  • Intervertebral disc cells produce tumor necrosis factor alpha, interleukin-1 beta, and monocyte chemoattractant protein-1 immediately after herniation: An experimental study using a new hernia model 国際誌

    M Yoshida, T Nakamura, A Sei, T Kikuchi, K Takagi, A Matsukawa

    SPINE   30 ( 1 )   55 - 61   2005年1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:LIPPINCOTT WILLIAMS & WILKINS  

    Study Design. A new hernia model that simulates human disc herniations was developed in rabbits. The herniated discs were examined by gross appearance and histology and production of tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 was investigated.
    Objectives. To clarify the early mechanism of spontaneous herniated disc resorption.
    Summary of Background Data. Macrophage infiltration in herniated discs is essential for disc resorption. However, surgically removed human herniated disc tissues and existing animal hernia models are not suitable for analyzing the mechanism of macrophage infiltration. Recently, we have demonstrated that intervertebral disc cells are capable of producing monocyte chemoattractant protein-1, a potent macrophage chemoattractant, after stimulation with tumor necrosis factor alpha and interleukin-1beta.
    Methods. Intervertebral disc herniations were surgically developed in rabbits using a new technique. The herniated discs were excised at appropriate time intervals after the surgery, and the size and histologic findings were examined. Expressions of tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 in herniated discs were investigated immunohistochemically.
    Results. A new rabbit model of disc herniation was established. The herniated discs spontaneously reduced in size by 12 weeks postsurgery. Infiltrating cells, mainly composed of macrophages, were observed from day 3. Immunohistochemically, intervertebral disc cells in the herniated discs produced tumor necrosis factor alpha and interleukin-1beta on day 1, followed by monocyte chemoattractant protein-1 on day 3.
    Conclusions. The new hernia model appears to be very useful for studying herniated disc resorption. Intervertebral disc cells may produce inflammatory cytokines/chemokine immediately after the onset of disc herniation, possibly triggering subsequent macrophage infiltration that leads to disc resorption.

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  • Chief cell hyperplasia with structural and nuclear atypia: a variant of fundic gland polyp 国際誌

    A Matsukawa, R Kurano, T Takemoto, M Kagayama, T Ito

    PATHOLOGY RESEARCH AND PRACTICE   200 ( 11-12 )   817 - 821   2005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:URBAN & FISCHER VERLAG  

    A case of an unusual variant of fundic gland polyp (FGP) composed of chief cell hyperplasia with structural and nuclear atypia in an 87-year-old woman is presented. Gastrointestinal endoscopy revealed a sessile polyp in the cardia/corpus transition zone and a polypoid lesion in the fundus. Histologically, the polyp in the cardia/corpus showed a typical appearance of FGP, while that in fundus demonstrated a tumorous lesion composed of irregular branched tubules with nuclear stratification. Despite the structural distortion and nuclear atypia, mitotic figures were absent and MIB-1 positive cells were less than 3%. Immunohistochemically, the cytoplasms of the tubules were negative for gastric mucin and Muc-5AC glycoprotein, but mostly positive for pepsinogen-I, indicating that the proliferated glands consisted mainly of chief cells, not mucous cells. Parietal cells were occasionally found in the glands. At the periphery of the lesion, microcysts composed of parietal cells, chief cells, and mucous cells had developed. Altogether, the polyp in the fundus was diagnosed as an unusual variant of FGP with chief cell hyperplasia. This FGP should be differentiated from tubular adenocarcinoma. Proliferation of chief cells with occasional parietal cells is critical for the differential diagnosis. (c) 2004 Elsevier GmbH. All rights reserved.

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  • Innate immune response in Th1- and Th2-dominant mouse strains 国際誌

    H Watanabe, K Numata, T Ito, K Takagi, A Matsukawa

    SHOCK   22 ( 5 )   460 - 466   2004年11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:LIPPINCOTT WILLIAMS & WILKINS  

    C57BL/6 and BALB/c mice are prototypical Th1- and Th2-type mouse strains, respectively. In the present study, we attempted to characterize the innate immune response of macrophages from these mouse strains. Macrophages from C57BL/6 mice produced higher levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-12 than those from BALB/c mice after stimulation with macrophage-activating lipopeptide-2 (MALP-2, a synthetic TLR-2 ligand) or lipopolysaccharide (LPS, a TLR-4 ligand). The augmented IL-12 production by C57BL/6 macrophages increased interferon-gamma and, in contrast, decreased IL-13 production by CD4+ T cells. On stimulation with MALP-2 or LIPS, C57BL/6 macrophages produced lysosomal enzyme and nitric oxide, effector molecules for bacterial killing, whereas BALB/c macrophages did not. Bactericidal activity of BALB/c macrophages was impaired relative to C57BL/6 macrophages when cells were infected with live bacteria in vitro. In a murine model of septic peritonitis induced by cecal ligation and puncture (CLP), BALB/c mice failed to facilitate bacterial clearance relative to C57BL/6 mice despite an augmented peritoneal leukocyte infiltration that was associated with increased peritoneal levels of cytokines/chemokines. BALB/c mice exhibited increased plasma and hepatic levels of cytokines/chemokines, resulting in an exaggerated systemic inflammation as determined by acute-phase proteins. Finally, BALB/c mice were vulnerable to CILP-induced lethality relative to C57BL/6 mice. Altogether, innate immune response of macrophages is different between these mouse strains, which may affect the development of Th1 and Th2 adaptive immunity in these strains. Reduced systemic inflammatory response in C57BL/6 mice that may result from an eminent local response appears to be beneficial during sepsis.

    DOI: 10.1097/01.shk.0000142249.08135.e9

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  • Role of CC chemokine CCL6/C10 as a monocyte chemoattractant in a murine acute peritonitis 国際誌

    AM LaFleur, NW Lukacs, SL Kunkel, A Matsukawa

    MEDIATORS OF INFLAMMATION   13 ( 5-6 )   349 - 355   2004年10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:CARFAX PUBLISHING  

    THE aim of this study was to determine the role of CC chemokine CCL6/C10 in acute inflammation. Intraperitoneal injection of thioglycollate increased peritoneal CCL6, which peaked at 4 h and remained elevated at 48 h. Neutralization of CCL6 significantly inhibited the macrophage infiltration (34-48% reduction), but not other cell types, without decreasing the other CC chemokines known to attract monocytes/macrophages. CCL6 was expressed in peripheral eosinophils and elicited macrophages, but not in elicited neutrophils. Peritoneal CCL6 level was not decreased in granulocyte-depleted mice where eosinophil influx was significantly impaired. Thus, CCL6 appears to contribute to the macrophage infiltration that is independent of other CC chemokines. Eosinophils pre-store CCL6, but do not release CCL6 in the peritoneum in this model of inflammation.

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  • Role of CCR4 ligands, CCL17 and CCL22, during Schistosoma mansoni egg-induced pulmonary granuloma formation in mice 国際誌

    C Jakubzick, HT Wen, A Matsukawa, M Keller, SL Kunkel, CM Hogaboam

    AMERICAN JOURNAL OF PATHOLOGY   165 ( 4 )   1211 - 1221   2004年10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:AMER SOC INVESTIGATIVE PATHOLOGY, INC  

    Controversy persists pertaining to the role of CCR4 ligands, namely CCL17 (or thymus and activation regulated chemokine; TARC) and CCL22 (or macrophage-derived chemokine; MDC), in Th2-type cytokine-dominated responses in the lung. Accordingly, the present study addressed the relative role of each of these CC chemokines during an evolving pulmonary granulomatous response elicited by the intrapulmonary embolization of live Schistosoma mansoni eggs into S. mansoni-sensitized mice. CCL22 protein expression peaked at day 4, but CCL17 levels were not increased significantly at any time after egg challenge. CCR4 transcript and protein expression were highest at day 8 after egg embolization and CCR4 protein was prominently expressed in macrophages surrounding S. mansoni eggs. Systemic immunoneutralization of CCL22 from the time of egg injection into S. mansoni-sensitized mice for 8 days significantly decreased CCR4 protein expression, the eosinophil content, the overall size of the egg granuloma, and its hydroxyproline content. Whole lung levels of interferon-gamma were also significantly increased at day 8 in anti-CCL22-treated mice. The systemic immunoneutralization of CCL17 had a lesser effect on all of the granuloma parameters listed above, but this antibody treatment significantly decreased granuloma hydroxyproline content to a greater extent than the anti-CCL22 antibody treatment. In addition, the immunoneutralization of CCL17 significantly increased whole lung levels of interleukin (IL)-4, IL-5, IL-13, transforming growth factor-beta, ILL-12, and tumor necrosis factor-a at day 8 after egg infusion. Thus, these studies demonstrate a major role for CCL22 and a lesser role for CCL17 during an evolving S. mansoni egg granuloma in the lung.

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  • Wall shear modulation of cytokines in early vein grafts 国際誌

    ZH Jiang, SA Berceli, CL Pfahnl, LZ Wu, D Goldman, M Tao, M Kagayama, A Matsukawa, CK Ozaki

    JOURNAL OF VASCULAR SURGERY   40 ( 2 )   345 - 350   2004年8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:MOSBY, INC  

    Objective: Pro-inflammatory cytokine-driven mechanisms have been implicated in vein graft failure, though little is known about the effect of hemodynamic factors and anti-inflammatory counter-regulatory mechanisms. We hypothesized that early temporal expression of the pro-inflammatory cytokine interleukin (IL)-1beta and the anti-inflammatory cytokine IL-10 proceeds by way of wall shear stress-dependent pathways in the arterializing vein graft.
    Methods. Rabbits (n = 27) underwent bilateral jugular vein carotid interposition grafts, and simultaneous unilateral distal carotid branch ligation, to produce both low-flow and high-flow grafts in the same animal. Vein grafts were harvested at 1, 3, 7, 14, and 28 days and were assessed for architecture, wall shear stress, and cytokine messenger RNA levels (quantitative real-time two-step reverse transcription polymerase chain reaction).
    Results. The model resulted in an immediate 90% flow reduction (P &lt; .001, paired t test) in the vein graft on the ligated side, and a 36% increase (P = .01) in contralateral graft flow. This persisted as similar to15-fold flow differential throughout the 28-day period. The construction yielded a 15-fold differential in wall shear stress between low-flow and high-flow vein grafts (P &lt; .001, two-way repeated measures analysis of variance). Intimal hyperplasia began by day 3, and was 6-fold more in low wall shear grafts by 28 days (230.6 +/- 35.4 mum intimal thickness vs 36.1 +/- 17.6 mum for low shear versus high shear grafts; P = .001). For both cytokines time independently affected mRNA expression (P &lt; .001, global analysis of variance). Exposure of vein grafts to the arterial circulation markedly up-regulated IL-10 at 1 day, with significantly more induction in the low shear setting (P =.002). IL-1beta protein localized to the developing neointima at days 1 and 3. Conversely, IL-10 slowly increased until day 14, with significantly more expression in the high shear grafts (P &lt; .001).
    Conclusions. Vein graft adaptation induces early pro-inflammatory cytokine IL-1beta expression and delayed protective IL-10 expression (most notable under high shear conditions), both of which are modulated by wall shear. These differential temporal windows offer strategies for appropriately timed pro-inflammatory or anti-inflammatory therapies to interrupt pathologic vein graft adaptations. (J Vasc Surg 2004;40:345-50.)
    Clinical Relevance: Neointimal hyperplasia continues to limit the durability of vein bypass grafts. Emerging evidence suggests that inflammatory mechanisms drive the neointimal hyperplasic response. This study demonstrates that specific hemodynamic forces (altered wall shear stress) differentially affect early pro-inflammatory interleukin (IL)-1beta and delayed anti-inflammatory IL-10 signaling. These distinct temporal windows for IL-1beta and IL-10 cytokine expression offer strategies for appropriately timed pro-inflammatory and anti-inflammatory therapies to interrupt pathologic vein graft adaptations.

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  • Up-regulated expression and activation of the orphan chemokine receptor, CCRL2, in rheumatoid arthritis. 国際誌

    Carole L Galligan, Wataru Matsuyama, Akihiro Matsukawa, Hiroshi Mizuta, David R Hodge, O M Zack Howard, Teizo Yoshimura

    Arthritis and rheumatism   50 ( 6 )   1806 - 14   2004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)  

    OBJECTIVE: Rheumatoid arthritis (RA) is a chronic inflammatory condition characterized by a cellular influx and destruction of the joint architecture. Chemokines characteristically regulate leukocyte recruitment and activation. Chemokine (CC motif) receptor-like 2 (CCRL2) is an orphan receptor with homology to other CC chemokine receptors. We undertook this study to examine CCRL2 expression in RA, cytokine regulation of expression, and the source of a putative ligand in an attempt to determine the role of this receptor during inflammation. METHODS: Expression of CCRL2 on joint-infiltrating leukocytes was examined by immunocytochemistry. In vitro studies evaluated CCRL2 expression in primary neutrophils using Northern and Western blotting and reverse transcriptase-polymerase chain reaction. HEK 293 cells expressing two splice variants of CCRL2 (HEK/CCRL2A or HEK/CCRL2B) were generated with a retroviral expression system, and their migration in response to fractions of synovial fluid (SF) from RA patients was examined using a 48-well chamber. RESULTS: CCRL2 expression was observed on all infiltrating neutrophils and on some macrophages obtained from the SF of 5 RA patients. In vitro studies of primary neutrophils revealed that CCRL2 messenger RNA (mRNA) was rapidly up-regulated following stimulation with lipopolysaccharide (1 microg/ml) or tumor necrosis factor (5 ng/ml). The mRNA for both CCRL2A and CCRL2B were expressed in cytokine-stimulated neutrophils. Cells expressing either of these splice variants migrated in response to a fraction of RA SF. CONCLUSION: CCRL2 expression is up-regulated on synovial neutrophils of RA patients. Inflammatory products present in the SF activate this receptor, indicating that CCRL2 is a functional receptor that may be involved in the pathogenesis of RA.

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  • Upregulated expression and activation of the orphan chemokine receptor, CCRL2, in rheumatoid arthritis

    C Galligan, W Matsuyama, A Matsukawa, H Mizuta, DR Hodge, OMZ Howard, T Yoshimura

    FASEB JOURNAL   18 ( 4 )   A469 - A469   2004年3月

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    記述言語:英語   出版者・発行元:FEDERATION AMER SOC EXP BIOL  

    DOI: 10.1002/art.20275

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  • Involvement of tumor necrosis factor-α and interleukin-8 in antigen-induced arthritis of the rabbit temporomandibular joint. 国際誌

    Sukedai M, Tominaga K, Habu M, Matsukawa A, Nishihara T, Fukuda J

    J. Oral Pathol. Med   33 ( 2 )   102 - 110   2004年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/j.1600-0714.2004.00008.x

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  • Aberrant inflammation and lethality to septic peritonitis in mice lacking STAT3 in macrophages and neutrophils 国際誌

    A Matsukawa, K Takeda, S Kudo, T Maeda, M Kagayama, S Akira

    JOURNAL OF IMMUNOLOGY   171 ( 11 )   6198 - 6205   2003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:AMER ASSOC IMMUNOLOGISTS  

    Stat3 is a transcription factor mediating anti-inflammatory properties of IL-10. In the present study, we demonstrate a pivotal role of Stat3 expressed in innate immune cells during septic peritonitis induced by cecal ligation and puncture (CLP). Mice with targeted disruption of Stat3 in macrophages and neutrophils were succumbed to septic peritonitis induced by CLP. The mice displayed an excessive local and systemic inflammation relative to the control mice, an event that was accompanied by substantial increases in the level of multiple cytokines. Hepatic and renal injury was significantly exacerbated in mice with Stat3 deficiency. Despite enhanced inflammatory responses, the mice failed to facilitate bacterial clearance as compared with the control mice. In addition, the mice exhibited an increased lethality after i.p. inoculation of live bacteria recovered from CLP-mice. In vitro, resident peritoneal macrophages from mice with Stat3 deficiency impaired bactericidal activity relative to the control whereas productions of inflammatory cytokines were significantly augmented when cells were stimulated with a synthetic lipopeptide, macrophage-activating lipopeptide-2 and LPS. Elicited macrophages and neutrophils with Stat3 deficiency also impaired bactericidal activity as compared with those with Stat3. Lysosomal enzyme release, an effector molecule for bacterial clearance, was significantly decreased in elicited leukocytes with Stat3 deficiency while increasing the production of inflammatory cytokines. Altogether, these results suggest that macrophage/neutrophil-specific STAT3 is crucial in not only modulating multiple organ failure associated with systemic inflammation but also intensifying the bactericidal activity, which highlight the significance of cell-specific Stat3 in the protective immunity during sepsis.

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  • Detection of neutrophils and possible involvement of interleukin-8 in diffuse lamellar keratitis after laser in situ keratomileusis 国際誌

    N Asano-Kato, Toda, I, S Shimmura, T Noda-Tsuruya, K Fukagawa, M Yoshinaga, A Matsukawa, K Tsubota

    JOURNAL OF CATARACT AND REFRACTIVE SURGERY   29 ( 10 )   1996 - 2000   2003年10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:ELSEVIER SCIENCE INC  

    Purpose: To investigate the cell populations in diffuse lamellar keratitis (DLK) infiltration after laser in situ keratomileusis and the possible mechanism underlying the infiltration.
    Setting: Department of Ophthalmology, Tokyo Dental College, Chiba, Japan.
    Methods: To develop DLK in rabbit eyes, 25 muL of lipopolysaccharide (LPS) solution at a concentration of 50 mug/mL was applied to the stromal bed beneath corneal flaps. For control rabbits, phosphate-buffered saline was applied. Postoperative examination by slitlamp microscopy was performed for 3 days after surgery. Rabbit eyes were excised and examined for histopathology with hematoxylin and eosin staining. Immunohistochemical analysis for interleukin (IL)-8 was performed.
    Results: Diffuse lamellar keratitis-like inflammation composed mainly of neutrophils was reproduced by LIDS instillation in rabbit eyes. In eyes with severe inflammation, IL-8 immunoreactivity was found in the stromal keratocytes and infiltrating neutrophils.
    Conclusions: The major cell type in the DLK infiltration induced by LPS instillation in rabbit eyes was the neutrophil. Interleukin-8, a prototype of CXC chemokine produced by keratocytes and neutrophils, may contribute to the development of DLK. (C) 2003 ASCRS and ESCRS

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  • Tumor necrosis factor-α inhibition reduces CXCL-8 levels but fails to prevent fibrin generation and does not improve outcome in a rabbit model of endotoxic shock. 国際誌

    Rodriguez-Wilhelmi P, Montes R, Matsukawa A, Nariuchi H, Hurtado V, Montes M, Hermida J, Rocha E

    J. Lab. Clin. Med.   141 ( 4 )   257 - 264   2003年4月

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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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  • Interleukin (IL)-8 and growth related oncogene-a in severe endotoxemia and the effects of a tumor necrosis factor-α/IL-1β inhibitor on these chemokines 国際誌

    Rodriguez-Wilhelmi P, Montes R, Matsukawa A, Hurtado V, Montes M, Hermida J, Rocha E

    Exp. Mol. Pathol   73 ( 3 )   220 - 229   2002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)  

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  • Expression of monocyte chemoattractant protein-1 in primary cultures of rabbit intervertebral disc cells 国際誌

    M Yoshida, T Nakamura, T Kikuchi, K Takagi, A Matsukawa

    JOURNAL OF ORTHOPAEDIC RESEARCH   20 ( 6 )   1298 - 1304   2002年11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:ELSEVIER SCI LTD  

    Macrophages are considered essential for herniated disc resorption, and chemokines may play a role in their recruitment. Here we demonstrate that intervertebral disc cells are capable of producing monocyte chemoattractant protem-1 (MCP-1), a CC chemokine that is chemotactic for macrophages. Nucleus pulposus cells and anulus fibrosus cells were harvested from intervertebral discs of healthy rabbits, and the cells were stimulated with either interleukin (IL)-1beta or tumor necrosis factor (TNF)alpha. Reverse transcriptase polymerase chain reaction demonstrated that IL-1beta and TNFalpha induced mRNA expression for MCP-1 in nucleus pulposus and anulus fibrosus cells. Protein concentrations of MCP-1 in the culture supernatants were quantitated by fluoroimmunoassay, which showed that nucleus pulposus and anulus fibrosus cells dose- and time-dependently produced MCP-1 after IL-1beta- and TNFalpha-stimulation, an event that was completely abrogated by IL-1 receptor antagonist and anti-TNFalpha monoclonal antibody, respectively. Nucleus pulposus cells produced significantly higher levels of MCP-1 than did anulus fibrosus cells. Immunohistochemically, the intensity of MCP-1 positive cells in nucleus pulposus cells was stronger than that in anulus fibrosus cells. Altogether, our data clearly demonstrated the production of MCP-1 in intervertebral disc cells, suggesting the possible involvement of disc cells in an early stage of macrophage infiltration. (C) 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.

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  • The endotoxin-induced plasminogen activator inhibitor-1 increase in rabbits is not tumor necrosis factor-α dependent and can occur in the absence of interleukin-1β 国際誌

    Montes R, Rodriguez-Wilhelmi P, Hurtado V, Matsukawa A, Montes M, Hermida J, Rocha E

    Thromb. Haemost   88 ( 4 )   639 - 643   2002年10月

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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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  • Involvement of CXC chemokine growth-related oncogene-alpha in monosodium urate crystal-induced arthritis in rabbits 国際誌

    K Fujiwara, S Ohkawara, K Takagi, M Yoshinaga, A Matsukawa

    LABORATORY INVESTIGATION   82 ( 10 )   1297 - 1304   2002年10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:LIPPINCOTT WILLIAMS & WILKINS  

    Accumulation of neutrophils is a prominent feature of gouty arthritis in which CXC chemokines may play a role. Recently, we have shown that IL-8 (CXCL8) contributes to neutrophil influx in a rabbit model of gouty arthritis. Here, we demonstrate that growth-related oncogene-a (GROalpha) (CXCL1), a prototype of CXC chemokine, is also involved in this process. GROalpha level in the joints peaked at 2 hours after intra-articular injection of monosodium urate crystals, at a time before the neutrophil influx reached the maximal level (9 hours). Once decreased, the level increased and reached the second peak at 9 hours. The kinetics was comparable to that of IL-8. Administration of anti-GROalpha mAb attenuated the neutrophil influx at the same level as did the anti-IL-8 IgG, and combination of these antibodies enhanced the inhibition, resulting in a 33% reduction. Interaction of GROalpha with TNFalpha, IL-1beta, and IL-8 was next investigated by injecting antibodies or receptor antagonist with monosodium urate crystals. Administration of anti-TNFalpha mAb did not alter GROalpha level at 2 hours, but inhibited the levels 9 hours after the injection. Treatment with either IL-1 receptor antagonist or anti-IL-8 IgG resulted in decreased levels of GROalpha at 2 and 9 hours. Neutralization of GROalpha with anti-GROalpha mAb did not alter TNFalpha, IL-1beta, and IL-8 levels at their peak (2 hours), but decreased the second peak of IL-1beta (9 hours) and IL-8 (12 hours). These results provide evidence that GROalpha as well as IL-8 are involved ad eundem in the neutrophil infiltration in this model. IL-1 and IL-8, but not TNFalpha, are responsible in part for the initial phase of GROalpha, whereas these cytokines induce GROalpha in a late phase. GROalpha does not seem to initiate TNFalpha, IL-1beta, and IL-8, in an early phase, but induces IL-1beta and IL-8 in a late phase.

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  • Mice genetically lacking endothelial selectins are resistant to the lethality in septic peritonitis 国際誌

    A Matsukawa, NW Lukacs, CM Hogaboam, RN Knibbs, DC Bullard, SL Kunkel, LM Stoolman

    EXPERIMENTAL AND MOLECULAR PATHOLOGY   72 ( 1 )   68 - 76   2002年2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:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Leukocyte interactions with vascular endothelium are an initial step for leukocyte entry into infectious foci where endothelial selectins may play a key role. Infiltrating leukocyte is essential for bacterial clearance, suggesting that endothelial selectins would be important in host defense against microorganisms. To address this, E-, P-, and E/P-selectiti-deficient mice (E-/-, P-/-, E/P-/-) and wild-type (WT) mice underwent cecal ligation and puncture (CLP). Neither leukocyte infiltration nor bacterial load in the peritoneum was altered in E-/-, P-/- and E/P-/- mice compared to WT mice. However, E-/-, P-/- and E/P-/- mice were resistant to the lethality induced by CLP. At the mechanistic level, E-/-, P-/-, and E/P-/- mice did not develop renal dysfunction, a possible cause of death during sepsis. The serum level of interleukin-13 in E`, P-/-, and E/P-/- mice that had undergone CLP was higher than that in WT mice, whereas levels of macrophage inflammatory protein-2, KC in serum, and KC in kidney were lower than those in WT mice. These experiments demonstrate that endothelial selectin-mediated leukocyte rolling is not required for leukocyte entry in septic peritonitis and that endothelial selectins may affect mice survival during sepsis by influencing the cytokine profiles. (C) 2002 Elsevier Science.

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  • Local overexpression of monocyte chemoattractant protein-1 at vessel wall induces infiltration of macrophages and formation of atherosclerotic lesion - Synergism with hypercholesterolemia 国際誌

    M Namiki, S Kawashima, T Yamashita, M Ozaki, T Hirase, T Ishida, N Inoue, K Hirata, A Matsukawa, R Morishita, Y Kaneda, M Yokoyama

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   22 ( 1 )   115 - 120   2002年1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:LIPPINCOTT WILLIAMS & WILKINS  

    Monocyte/macrophage infiltration to the arterial wall is an initial step in atherosclerosis, and monocyte chemoattractant protein-1 (MCP-1) is thought to play a central role in the recruitment of these cells. In the present study, we examined the role of local expression of MCP-1 at the vessel wall in the initiation and development of atherosclerosis. We transfected the cDNA encoding rat MCP-1 into the vessel wall of the rabbit carotid artery with the use of the hemagglutinating virus of Japan (HVJ)-liposome method. The rabbits were divided into the following groups: (1) those fed normal chow and transfected with MCP-1-HVJ, (2) those fed a high cholesterol diet (1% cholesterol) and transfected with MCP-1-HVJ, and (3) those fed a high cholesterol diet and transfected with control-HVJ. Prescribed diets were started 2 weeks before transfection and were continued for another 2 weeks. In group I, vascular lesion formation was not found, and anti-rabbit monocyte/macrophage antibody (RAM-11) staining for monocytes/macrophages was negative, although anti-rat MCP-1 antibody (R-17) staining for rat MCP-1 was positive mainly in endothelial cells. Cholesterol feeding increased plasma cholesterol levels to 1801+/-444 mg/dL in group 2. In group 2, all rabbits displayed neointimal formation with infiltration of RAM-11-positive cells, and a part of the lesion was also positive for Sudan III lipid staining. In group 3, hypercholesterolemia did not induce the infiltration of monocytes/ macrophages and subsequent lesion formation in the vessel wall despite definite upregulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on the endothelium. To initiate atherosclerotic changes, local MCP-1 overexpression at the vessel is not sufficient, and activation of other factors induced by hypercholesterolemia is required.

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  • Functional distinction between CXC chemokines, interleukin-8 (IL-8), and growth related oncogene (GRO) α in neutrophil infiltration 国際誌

    Fujiwara K, Matsukawa A, Ohkawara S, Takagi K, Yoshinaga M

    Lab. Invest   82 ( 1 )   15 - 23   2002年1月

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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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  • Effect of methylprednisolone on phospholipase A(2) activity and lung surfactant degradation in acute lung injury in rabbits

    K Kuwabara, S Furue, Y Tomita, M Ueno, T Ono, A Matsukawa, M Yoshinaga, K Mikawa, K Nishina, M Shiga, H Obara, Y Hori

    EUROPEAN JOURNAL OF PHARMACOLOGY   433 ( 2-3 )   209 - 216   2001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:ELSEVIER SCIENCE BV  

    Glucocorticoids are the most potent and widely used anti-inflammatory agents, but they are not particularly effective against early phase of acute respiratory distress syndrome. We investigated whether methylprednisolone, a synthetic glucocorticoid, could inhibit increase of phospholipase A(2) activity in the lung and lead to protection against a model of acute respiratory distress syndrome in rabbits. Infusion of oleic acid (0.1 ml/kg/h, i.v. for 2 h) provoked pulmonary hemorrhage and edema, protein leakage and massive neutrophil infiltration, resulted in severe hypoxemia and impaired lung compliance, accompanying the increase of phospholipase A(2) activity and interleukin-8, and degradation of surfactant in the bronchoalveolar lavage fluid. Infusion of methylprednisolone (60 mg/kg/h, i.v. for 30 min before the oleic acid and then 0.5 mg/kg/h, i.v, for 6 h) did not improve the above described lung injury induced by oleic acid, nor did it suppress phospholipase A(2) activity and degradation of surfactant in bronchoalveolar lavage fluid, while it strongly reduced interleukin-8 levels in both plasma and bronchoalveolar lavage fluid. We conclude that methylprednisolone did not attenuate oleic acid-induced acute lung injury and this can be explained partly by its failure to reduce the increase of phospholipase A(2) activity and the surfactant degradation in the lung, which might also account for its clinical ineffectiveness against early acute respiratory distress syndrome. (C) 2001 Elsevier Science B.V All rights reserved.

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  • Interleukin-1β in antigen-induced arthritis of the rabbit temporomandibular joint.

    Tominaga K, Alstergren P, Kurita H, Matsukawa A, Fukuda J, Kopp S

    Arch Oral Biol   46 ( 6 )   539 - 544   2001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)  

    DOI: 10.1016/S0003-9969(01)00009-7

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  • III. Chemokines and other mediators, 8. Chemokines and their receptors in cell-mediated immune responses in the lung

    A Matsukawa, NW Lukacs, CM Hogaboam, SW Chensue, SL Kunkel

    MICROSCOPY RESEARCH AND TECHNIQUE   53 ( 4 )   298 - 306   2001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)   出版者・発行元:WILEY-LISS  

    Chemokines constitute a large family of chemotactic cytokines that belong to a super-gene family of 8-10 kDa proteins. The chemokines are considered to be primarily beneficial in host defense against invading pathogens. However, the reactions induced by chemokines can be occasionally excessive, resulting in a harmful response to the host. Recent studies in chemokine biology have elucidated that chemokines are involved in the initiation, development, and maintenance of numbers of diseases including lung diseases. In addition to its chemotactic activity, evidence suggests that chemokines can modify the outcome of the cell-mediated immune responses by altering the Th1/Th2 cytokine profile. Chemokines are also capable of dictating the direction of specific immune responses. Chemokine action is mediated by a large super-family of G-protein coupled receptors, and the receptors are preferentially expressed on Th1/Th2 cells. Certain chemokine receptors are constitutively expressed in immune surveying cells such as dendritic cells and naive T cells. The corresponding chemokines are present in normal lymphoid tissues, suggesting a role of chemokines/receptors in cell homing and cell-cell communication in lymphoid tissue that can be an initial step for immune recognition. Thus, comprehension of the chemokine biology in immune responses appears to be fundamental for understanding the pathogenesis of T cell-mediated immune responses. The following review will highlight the current insight into the role of chemokines and their receptors in the cell-mediated immune response, with a special focus on lung diseases. (C) 2001 Wiley-Liss, Inc.

    DOI: 10.1002/jemt.1096

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  • Therapeutic time-window of a group IIA phospholipase A(2) inhibitor in rabbit acute lung injury: Correlation with lung surfactant protection

    S Furue, K Mikawa, K Nishina, M Shiga, M Ueno, Y Tomita, K Kuwabara, Teshirogi, I, T Ono, Y Hori, A Matsukawa, M Yoshinaga, H Obara

    CRITICAL CARE MEDICINE   29 ( 4 )   719 - 727   2001年4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:LIPPINCOTT WILLIAMS & WILKINS  

    Objective: We attempted to determine whether group IIA secretory phospholipase A(2) (sPLA(2)-IIA) blockade after the onset of lung injury exerted therapeutic efficacy in the treatment of oleic acid (OA)-induced acute lung injury by using S-5920/LY315920Na, a novel specific inhibitor of sPLA(2)-IIA, with special interest in the changes of lung surfactant.
    Design:Prospective animal study.
    Setting: University laboratory.
    Subjects: Forty Japanese white rabbits.
    Interventions: The rabbits, under anesthesia, were endotracheally intubated and mechanically ventilated and then were divided into the following groups: OA + vehicle groups, intravenous infusion of OA for the first 2 hrs (0.1 mL . kg(-1). hr(-1)) with the addition of vehicle (1 or 2 hrs after OA administration, each n = 9, total 18 rabbits); OA + S-59201/Y315920Na groups, treated identically to the OA control with the addition of S-5920/LY315920Na (1 mg/kg bolus followed by infusion at 0.5 mg . kg(-1). hr(-1)) after OA (1 or 2 hrs after OA administration, each n = 9, total 18 rabbits); saline control groups, treated with saline instead of OA with the addition of vehicle (1 hr after OA administration, 4 rabbits). Arterial blood gas, lung mechanics, lung inflammation, lung surfactant phospholipids, and production of inflammatory mediators in the lung were measured.
    Measurements and Main Results:Treatment with S-5920/ LY315920Na 1 hr after OA infusion, but not 2 hrs after infusion, significantly attenuated the lung injury, as estimated by hypoxemia, decreased lung compliance, pulmonary edema, and vascular permeability. The therapeutic efficacy was similar to that found in our previous pretreatment study. The treatment after 1 hr dramatically inhibited OA-induced surfactant degradation in the bronchoalveolar lavage fluid (BALF), without affecting the concentrations of thromboxane A(2), leukotriene B-4, and interleukin-8 in BALF. The degree of surfactant degradation in BALF paralleled well with the severity of the lung injury. Furthermore, recombinant human sPLA(2)-IIA reproduced the similar hydrolysis pattern of isolated surfactant in vitro, which was inhibited by S-5920/ LY315920Na.
    Conclusions:Our results indicate that therapeutic blockade of sPLA(2)-IIA ameliorated lung dysfunction via protection of surfactant degradation in an animal model of acute lung injury, and they suggest a new strategy in treating clinical acute lung injury.

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  • Erythromycin attenuates an experimental model of chronic bronchiolitis via augmenting monocyte chemoattractant protein-1

    T Takahashi, M Suga, A Matsukawa, K Sato, T Okamoto, H Ichiyasu, S Ohkawara, M Yoshinaga, M Ando

    EUROPEAN RESPIRATORY JOURNAL   17 ( 3 )   360 - 367   2001年3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:EUROPEAN RESPIRATORY SOC JOURNALS LTD  

    The mechanisms underlying the therapeutic efficacy of erythromycin (EM) in diffuse panbronchiolitis (DPB) was investigated. For this purpose, an experimental rabbit model of DPB induced by Pseudomonas aeruginosa inoculation was employed. Daily administration of EM (3 mg(.)kg(.)day(-1)) led to an increase in the number of macrophages in bronchoalveolar lavage fluid (BALF) at an early phase, while reducing the size of granulomatous lesions at the late phase without affecting the number of viable bacteria recovered from the infected lung.
    Reverse transcriptase polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and immunohistochemical studies showed that monocyte chemoattractant protein (MCP)-1 was produced in both BALF and infected lung. EM treatment resulted in a significant increase in the level of MCP-1 in BALF, while reducing that of tumour necrosis factor (TNF)-alpha, interleukin (IL)-beta and IL-beta. EM also increased MCP-1 messenger ribonucleic acid (mRNA) and protein expression in the infected lung. MCP-1 blockade abolished the protective effect of EM, as neutralization of MCP-I with anti-MCP-l antibodies reduced the E;CZ-induced increase in the number of macrophages in BALF, and augmented size of the granulomatous lesions, as compared to control.
    The results of the present study suggest that erythromycin attenuates the pulmonary granuloma formation, at least in part, by increasing the production of monocyte chemoattractant protein-1.

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  • Pivotal role of signal transducer and activator of transcription (Stat)4 and Stat6 in the innate immune response during sepsis

    A Matsukawa, MH Kaplan, CM Hogaboam, NW Lukacs, SL Kunkel

    JOURNAL OF EXPERIMENTAL MEDICINE   193 ( 6 )   679 - 688   2001年3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:ROCKEFELLER UNIV PRESS  

    Signal transducer and activator of transcription (Stat)4 and Stat6 are transcription factors that provide type 1 and type 2 response, respectively. Here, we explored the role of Stat4 and Stat6 in innate immunity during septic peritonitis. Stat4(-/-) and Stat6(-/-) mice were resistant to the lethality compared with wild-type (WT) mice. At the mechanistic level, bacterial levels in Stat6(-/-) mice were much lower than in WT mice, which was associated with increased peritoneal levels of interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, macrophage-derived chemokine (MDC), and C10, known to enhance bacterial clearance, In Stat4-/- mice, hepatic inflammation and injury during sepsis were significantly ameliorated without affecting local responses. This event was associated with increased hepatic levels of IL-10 and IL-13, while decreasing those of macrophage inflammatory protein (MIP)-2 and KC. Sepsis-induced renal injury was also abrogated in Stat4(-/-) mice, which was accompanied by decreased renal levels of MIP-2 and KC without altering IL-10 and IL-13 levels. Thus, Stat6(-/-) and Stat(4-/-) mice appeared to be resistant to septic peritonitis by enhancing local bacterial clearance and modulating systemic organ damage, respectively, via balancing cytokine responses. These results clearly highlight an important role of local type 1 and systemic type 2 cytokine response ill protective immunity during sepsis, which can be regulated by Stat proteins.

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  • Early recruitment of neutrophils determines subsequent T1/T2 host responses in a murine model of Legionella pneumophila pneumonia

    K Tateda, TA Moore, JC Deng, MW Newstead, XY Zeng, A Matsukawa, MS Swanson, K Yamaguchi, TJ Standiford

    JOURNAL OF IMMUNOLOGY   166 ( 5 )   3355 - 3361   2001年3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:AMER ASSOC IMMUNOLOGISTS  

    The contribution of neutrophils to lethal sensitivity and cytokine balance governing T1 and T2 host responses was assessed in a murine model of Legionella pneumophila pneumonia, Neutrophil depletion by administration of granulocyte-specific mAb RB6-8C5 at 1 day before infection rendered mice - 100-fold more susceptible to lethal pneumonia induced by L, pneumophila. However, this treatment did not alter early bacterial clearance, despite a substantial decrease in neutrophil influx at this time point. Cytokine profiles in the lungs of control mice demonstrated strong T1 responses, characterized by an increase of IFN-gamma and IL-12, In contrast, neutrophil-depleted mice exhibited significantly lower levels of IFN-gamma and IL-12, and elevation of T2 cytokines, IL-4 and IL-10, Immunohistochemistry of bronchoalveolar lavage cells demonstrated the presence of IL-12 in neutrophils, but not alveolar macrophages, Moreover, IL-12 was detected in lavage cell lysates by ELISA, which was paralleled to neutrophil number. However, intratracheal administration of recombinant murine IL-12 did not restore resistance, whereas reconstitution of IFN-gamma drastically improved bacterial clearance and survival in neutrophil-depleted mice. Taken together, these data demonstrated that neutrophils play crucial roles in primary L, pneumophila infection, not via direct killing but more immunomodulatory effects. Our results suggest that the early recruitment of neutrophils may contribute to T1 polarization in a murine model of L. pneumophila pneumonia.

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  • 緑膿菌誘発家兎びまん性汎細気管支炎におけるエリスロマイシンの効果-MCP-1産生増加による肉芽腫様病変の改善

    高橋利弘, 菅守隆, 佐藤圭創, 岡本龍哉, 一安秀範, 松川昭博, 大河原進, 吉永秀, 安藤正幸

    Jpn. J. Antibiot   2001年

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  • Neutrophil infiltration as a crucial step for monocyte chemoattractant protein (MCP)-1 to attract monocytes in lipopolysaccharide-induced arthritis in rabbits

    S Miyazaki, A Matsukawa, S Ohkawara, K Takagi, M Yoshinaga

    INFLAMMATION RESEARCH   49 ( 12 )   673 - 678   2000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:BIRKHAUSER VERLAG AG  

    Objective and Design: To evaluate the mechanism whereby monocyte chemoattractant protein (MCP)-1 attracts monocytes in vivo.
    Subjects: New Zealand white rabbits (175 rabbits) were used.
    Treatment: LPS, MCP-1 or IL-8 was injected into knee joints. Antibodies against various cytokines or IL-1 receptor antagonist were injected to neutralize cytokine activities.
    Methods: The numbers of leukocyte populations, levels of cytokines in joints were estimated.
    Results: Partial inhibition of neutrophil influx with anti-IL-8 IgG (10 mug) suppressed LPS-induced macrophage influx by 43 +/- 8.5% (p&lt;0.05) without affecting the MCP-I level. Intraarticular injection of MCP-1 (1-30 &lt;mu&gt;g) induced macrophage influx. The event was accompanied by a small number of neutrophils in an early phase. Go-injection of IL-8 (1.0 mug) enhanced the MCP-1-induced macrophage infiltration (p&lt;0.01). In neutrophil-depleted rabbits, LPS failed to induce macrophage influx even though the MCP-1 level was maintained, and macrophage influx following exogenously administered MCP-1 was also dramatically inhibited.
    Conclusions: Early events associated with neutrophil infiltration appear to be important for MCP-1 to induce a later macrophage influx in LPS-arthritis.

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  • Chemokine C10 promotes disease resolution and survival in an experimental model of bacterial sepsis

    ML Steinhauser, CM Hogaboam, A Matsukawa, NW Lukacs, RM Strieter, SL Kunkel

    INFECTION AND IMMUNITY   68 ( 11 )   6108 - 6114   2000年11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:AMER SOC MICROBIOLOGY  

    Previous studies have suggested that the C-C chemokine C10 is involved in the chronic stages of host defense reactions. The present study addressed the role of C10 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Unlike other C-C chemokines, C10 levels in the peritoneal wash were increased approximately 30-fold above baseline levels at 48 h after CLP surgery. Immunoneutralization of peritoneal C10 Levels with polyclonal anti-C10 antiserum during CLP-induced peritonitis negatively impacted mouse survival over 4 days. In contrast,,when 500 ng of recombinant murine C10 was administered immediately after CLP surgery, the ii-day survival rate increased from 20% to over 60%. The C10 therapy appeared to facilitate a rapid and significant enhancement of the Levels of tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-I) and a later increase in interleukin-13 (IL-13) levels in the peritoneal cavity. In vitro studies showed that the combination of IL-1 beta and C10 markedly augmented TNF-alpha synthesis by peritoneal macrophages and that C10 synthesis was induced in these cells following their exposure to IL-13, At 24 h after CLP surgery, only 25% of C10-treated mice were bacteremic versus 85% of the control group that exhibited dissemination of bacteria into the circulation, The Lack of bacteremia in C10-treated mice appeared to be related, in part, to in vitro evidence that C10 significantly enhanced the bacterial phagocytic activity of peritoneal macrophages. In addition, in vivo evidence suggested that C10 therapy significantly reduced the amount of material that leaked from the damaged gut. Taken together, the results of this study demonstrate that the C10 chemokine rapidly promotes disease resolution in the CLP model through its direct effects on the cellular events critically involved in host defense during septic peritonitis.

    DOI: 10.1128/IAI.68.11.6108-6114.2000

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  • Acute effects of smoke exposure on the cellular and cytokine profile in isolated perfused lungs

    M Kyi, Y Miyazaki, T Inoue, S Miyake, A Matsukawa, Y Yoshizawa

    RESPIRATION PHYSIOLOGY   123 ( 1-2 )   143 - 151   2000年10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:ELSEVIER SCIENCE BV  

    The aim of this study was to assess the acute effects of cigarette smoke exposure on cellular and cytokine profile in BAL fluids in an isolated perfused rabbit assay. The experimental animals were categorized into four groups: (1) unexposed controls and (2) cigarette smoke-exposed animals perfused with autologous whole blood; (3) unexposed controls and cigarette smoke-exposed; (4) cigarette smoke-exposed animals perfused with Krebs' Ringer solution containing 5% bovine serum albumin and glucose. Cigarette smoke induced an increase in total cell numbers (mainly alveolar macrophages in BAL fluids) and an increase in the permeability index of BAL. Levels of interleukin 8 were also significantly decreased in BAL fluids due to acute effects of cigarette smoke exposure. The most likely explanation for cigarette smoke-induced increase of inflammatory cells in BAL in lungs is because of the release of pre-existing cells from reservoirs within the lungs. The acute effects of cigarette smoke-induced increase of pulmonary epithelial permeability may also play an important role in the cellular recruitment into airspaces from the lung reservoirs. (C) 2000 Elsevier Science B.V. All rights reserved.

    DOI: 10.1016/S0034-5687(00)00147-X

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  • Pivotal role of the CC chemokine, macrophage-derived chemokine, in the innate immune response

    A Matsukawa, CM Hogaboam, NW Lukacs, PM Lincoln, HL Evanoff, SL Kunkel

    JOURNAL OF IMMUNOLOGY   164 ( 10 )   5362 - 5368   2000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)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Macrophage-derived chemokine (MDC), a recently identified CC chemokine, has been regarded to be involved in chronic inflammation and dendritic cell and lymphocyte homing, In this study, we demonstrate a pivotal role for MDC during experimental sepsis induced by cecal ligation and puncture (CLP), Intraperitoneal administration of MDC (1 mu g/mouse) protected mice from CLP-induced lethality. The survival was accompanied by increased number of peritoneal macrophages and decreased recovery of viable bacteria from the peritoneum and peripheral blood. In addition, mice treated with an i.p. injection of MDC cleared bacteria more effectively than those in the control when 3 x 10(8) CFU live Escherichia coli was i.p. inoculated. Endogenous MDC was detected in the peritoneum after CLP, and neutralization of the MDC with anti-MDC Abs decreased CLP-induced recruitment of peritoneal macrophages and increased the recovery of viable bacteria from the peritoneum and peripheral blood. MDC blockade was deleterious in the survival of mice after CLP. In vitro, MDC enhanced the phagocytic and killing activities of peritoneal macrophages to E, coli and induced both a respiratory burst and the release of lysozomal enzyme from macrophages, Furthermore, MDC dramatically ameliorated CLP-induced systemic tissue inflammation as well as tissue dysfunction, which were associated in part with decreased levels of TNF-alpha, macrophage inflammatory proteins-1 alpha and -2, and KC in specific tissues. Collectively, these results indicate novel regulatory activities of MDC in innate immunity during sepsis and suggest that MDC may aid in an adjunct therapy in sepsis.

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  • Therapeutic use of chemokines

    CM Hogaboam, C Bone-Larson, A Matsukawa, ML Steinhauser, K Blease, NW Lukacs, SL Kunkel

    CURRENT PHARMACEUTICAL DESIGN   6 ( 6 )   651 - 663   2000年4月

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    記述言語:英語   出版者・発行元:BENTHAM SCIENCE PUBL BV  

    Chemokines are involved in a number of pathological processes, and therefore represent important targets. However, it has also become apparent that chemokines have exciting therapeutic applications in inflammatory, infectious and cancer-related diseases. The following review will highlight the application of novel therapies including viral-encoded, recombinant, and genetically engineered chemokines to a number of diseases or disorders. Advances in the application of novel chemokine delivery procedures both at the research bench and the clinical bedside will also be discussed. Overall, the utilization of chemokines to prevent and treat disease has tremendous potential.

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  • Endogenous MCP-1 influences systemic cytokine balance in a murine model of acute septic peritonitis

    A Matsukawa, CM Hogaboam, NW Lukacs, PM Lincoln, RM Strieter, SL Kunkel

    EXPERIMENTAL AND MOLECULAR PATHOLOGY   68 ( 2 )   77 - 84   2000年4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:ACADEMIC PRESS INC  

    Sepsis and septic syndrome represent an intense systemic response with multiple physiologic and immunologic abnormalities, leading to multiple organ failure. Recent investigations suggest that the critical conditions are balanced by endogenous cytokines. In the present study, we examined the involvement of endogenous monocyte chemoattractant protein (MCP)-1 in the regulation of cytokine production in tissue/organs in a murine model of acute septic peritonitis induced by cecal ligation and puncture (CLP). Initial studies showed that CLP induced elevated levels of MCP-1 in tissues, such as liver, lung, and kidney. To neutralize endogenous MCP-1, either anti-MCP-1 antibodies or control antibodies were intraperitoneally administered 2 h prior to CLP. Administration of anti-MCP-1 antibodies resulted in a decrease in the level of interleukin (IL)-13 in tissues, while increasing the level of tumor necrosis factor-alpha, compared to control. In addition, anti-MCP-1 treatment decreased the level of IL-12 and, in contrast, increased the level of IL-10 in specific tissues. These findings suggest that endogenous MCP-1 influences the cytokine balance in tissues in favor of antiinflammatory and immune-enhancing cytokines, probably protecting the host from tissue/organ damage during sepsis. (C) 2000 Academic Press.

    DOI: 10.1006/exmp.1999.2296

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  • Exaggerated hepatic injury due to acetaminophen challenge in mice lacking C-C chemokine receptor 2

    CM Hogaboam, CL Bone-Larson, ML Steinhauser, A Matsukawa, J Gosling, L Boring, IF Charo, KJ Simpson, NW Lukacs, SL Kunkel

    AMERICAN JOURNAL OF PATHOLOGY   156 ( 4 )   1245 - 1252   2000年4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:AMER SOC INVESTIGATIVE PATHOLOGY, INC  

    Monocyte chemoattractant protein-1 is one of the major C-C chemokines that has been implicated in liver injury. The C-C chemokine receptor, CCR2, has been identified as the primary receptor that mediates monocyte chemoattractant protein-1 (MCP-1) responses in the mouse. Accordingly, the present study addressed the role of CCR2 in mice acutely challenged with acetaminophen (APAP). Mice genetically deficient in CCR2 (CCR2(-/-)) and their wild-type counterparts (CCR2(+/+)) were fasted for 10 hours before receiving an intraperitoneal injection of APAP (300 mg/kg), Liver and serum samples were removed from both groups of mice before and at 24 and 48 hours post APAP, Significantly elevated levels of MCP-1 were detected in liver samples from CCR2(+/+) and CCR2(-/-) mice at 24 hours post-APAP. Although CCR2(+/+) mice exhibited no liver injury at any time after receiving APAP, CCR2(-/-) mice exhibited marked evidence of necrotic and TUNEL-positive cells in the liver, particularly at 24 hours post-APAP, Enzyme-linked immunosorbent assay analysis of liver homogenates from both groups of mice at the 24 hours time point revealed that liver tissue from CCR2(-/-) mice contained significantly greater amounts of immunoreactive IFN-gamma and TNF-alpha. The in vivo immunoneutralization of IFN-gamma or TNF-alpha significantly attenuated APAP-induced liver injury in CCR2(-/-) mice and increased hepatic IL-13 levels. Taken together, these findings demonstrate that CCR2 expression in the liver provides a hepatoprotective effect through its regulation of cytokine generation during APAP challenge.

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  • Lazaroid reduces production of IL-8 and IL-1 receptor antagonist in ischemic spinal cord injury

    T Kunihara, S Sasaki, N Shiiya, H Ishikura, Y Kawarada, A Matsukawa, K Yasuda

    ANNALS OF THORACIC SURGERY   69 ( 3 )   792 - 798   2000年3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:ELSEVIER SCIENCE INC  

    Background. 21-aminosteroids (lazaroids) have demonstrated the protective effect against cerebral ischemic injury through the inhibition of lipid peroxidation. We examined whether lazaroids affected the production of proinflammatory and antiinflammatory cytokines in ischemic spinal cord injury model.
    Materials. Anesthetized New Zealand white rabbits underwent a 20-minute infrarenal aortic cross-clamping (AXC) with pretreatment of either an intravenous 3 mg/kg lazaroid U74389G (group L; n = 10) or the same volume saline (group P; n = 10), Sham operation group (group S; n = 6) underwent only exposure of the aorta. Plasma concentrations of interleukin (IL)-8, -1 beta, -1 receptor antagonist (IL-1ra) and tumor necrosis factor (TNF)-alpha were measured at four time points. Functional assessment with Tarlov score at 24 and 48 hours after pretreatment, pathologic assessment of the spinal cord, and measurements of cytokine levels in the spinal cord were performed.
    Results, The maximum elevation of plasma IL-8 and -1ra levels occurred at 1 hour after declamping in four measurement points, Plasma IL-8 and -1ra levels in group L were significantly lower than those in group P (*p &lt; 0.05), Plasma TNF alpha peaked at 5 minutes after declamping, but decreased afterwards. Plasma TNF alpha levels were not different among three groups, Spinal IL-8 levels in group L (0.98 +/- 0.34 ng/g tissue) were lower than those in group P (7.26 +/- 2.26 ng/g tissue) (*p &lt; 0.05), Spinal IL-1ra and TNF alpha were not significantly different Tarlov scare and pathologic assessment were better in group L,
    Conclusions. Lazaroid U-74389G reduced the production of systemic IL-8 and -1ra and spinal IL-8 when AXC. caused spinal cord injury. These results indicate that lazaroids may attenuate ischemic endothelial cell injury or activation of leukocytes,
    (C) 2000 by The Society of Thoracic Surgeons.

    DOI: 10.1016/S0003-4975(99)01413-7

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  • Expression and contribution of endogenous IL-13 in an experimental model of sepsis

    A Matsukawa, CM Hogaboam, NW Lukacs, PM Lincoln, HL Evanoff, RM Strieter, SL Kunkel

    JOURNAL OF IMMUNOLOGY   164 ( 5 )   2738 - 2744   2000年3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:AMER ASSOC IMMUNOLOGISTS  

    IL-13 has been shown to exert potent anti-inflammatory properties. In this study, we elucidated the functional role of endogenous IL-13 in a murine model of septic peritonitis induced by cecal ligation and puncture (CLP). Initial studies demonstrated that the level of IL-13 increased in tissues including liver, lung, and kidney, whereas no considerable increase was found int either peritoneal fluid or serum after CLP, Immunohistochemically, IL-13-positive cells were Kupffer cells in liver, alveolar macrophages in lung, and epithelial cells of urinary tubules in kidney. IL-13 blockade with anti-IL-13 Abs significantly decreased the survival rate of mice after CLP from 53% to 14% on day 7 compared with control, To determine the potential mechanisms whereby IL-13 exerted a protective role in this model, the effects of anti-IL-13 Abs on both local and systemic inflammation were investigated, Administration of anti-IL-13 Abs did not alter the leukocyte infiltration and bacterial load in the peritoneum after CLP hut dramatically increased the neutrophil influx in tissues after CLP, an effect that was accompanied by significant increases in the serum levels of aspartate transaminase, alanine transaminase, blood urea nitrogen, and creatinine, Tissue injury caused by IL-13 blockade was associated with increases in mRNA and the protein levels of CXC chemokines macrophage inflammatory protein-2 and KC as web as the CC chemokine macrophage inflammatory protein-1 alpha and the proinflammatory cytokine TNF-alpha. Collectively, these results suggest that endogenous IL-13 protected mice from CLP-induced lethality by modulating inflammatory responses via suppression of overzealous production of inflammatory cytokines/chemokines in tissues.

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  • CXC chemokine GRO is essential for neutrophil infiltration in LPS-induced uveitis in rabbits

    JS Mo, A Matsukawa, S Ohkawara, M Yoshinaga

    EXPERIMENTAL EYE RESEARCH   70 ( 2 )   221 - 226   2000年2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:ACADEMIC PRESS LTD  

    The purpose of this study was to investigate the role and regulation of the CXC chemokine GRO and the interaction between GRO and IL-8 in LPS-induced uveitis in rabbits. Uveitis was induced by intravitreal injection of 100 ng of LPS in rabbits. After the LPS injection, GRO was produced in aqueous humor and peaked at 24 hr. Immunohistochemistry showed that ciliary epithelial cells were responsible for production of GRO. Blocking the activity of GRO by anti-GRO serum reduced LPS-induced aqueous neutrophil counts by 80%, but did not reduce the mononuclear cell counts or protein levels or IL-8 levels. Regulation of GRO production by TNF alpha, IL-1 and IL-8 was studied. Anti-TNF alpha mAb alone did not inhibit the 24 hr LPS induced GRO levels, whereas rrIL-1Ra inhibited the GRO production by 58%. The combination of anti-TNF alpha mAb and rrIL-1Ra inhibited 93 % of GRO production. Although treatment with anti-IL-8 IgG inhibited the neutrophil infiltration by 66%, treatment with this antibody did not inhibit GRO production.
    Taken together, our results suggest that GRO is an essential mediator for neutrophil infiltration in LPS-induced uveitis in rabbits. Most of GRO production is mediated by TNF alpha and IL-1. GRO and IL-8 act in concert to mediate neutrophil infiltration. (C) 2000 Academic Press.

    DOI: 10.1006/exer.1999.0778

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  • Adenoviral-mediated overexpression of monocyte chemoattractant protein-1 differentially alters the development of Th1 and Th2 type responses in vivo

    A Matsukawa, NW Lukacs, TJ Standiford, SW Chensue, SL Kunkel

    JOURNAL OF IMMUNOLOGY   164 ( 4 )   1699 - 1704   2000年2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:AMER ASSOC IMMUNOLOGISTS  

    The expression of chemokines during an immune response may participate in determining the intensity and type of the developing immune response. In the present study, we have examined the effect of overexpressing monocyte chemoattractant protein (MCP)-1 at the site of immunization during different stages of Th1- and Th2-type granulomatous responses. The overexpression of MCP-1 by MCP-1 adenovirus during the sensitization phase of the purified protein derivative Th1-type model significantly reduced the elicitation of the granulomatous response. In contrast, the overexpression of MCP-1 during the sensitization phase of the schistosome egg Ag Th2 response led to an enhanced granulomatous reaction. When cytokines were examined upon restimulation of splenocytes ex vivo, an altered cytokine profile was observed, as compared with control mice. IFN-gamma and IL-12 were significantly reduced in the purified protein derivative Th1-type response, whereas IL-10 and IL-13 were up-regulated in the schistosome egg Ag Th2-type response. The regulation of the immune response was further examined by using the MCP-1 adenovirus at later time points during the elicitation phase. When MCP-1 was overexpressed during the elicitation phase of the responses, neither the Th1-type nor the Th2-type granuloma was altered. Likewise, the cytokine profiles after restimulation of splenocytes ex vivo were unchanged, Thus, the function of MCP-1 may depend on the stage and type of immune response.

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  • Chemokines and innate immunity

    Matsukawa A, Hogaboam CM, Lukacs NW, Kunkel SL

    Rev. Immunogenetics   2: 339-358   2000年

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  • A case of juvenile hyaline fibromatosis

    Honda Y, Ohkawara S, Iyama K, Matsukawa A, Yoshinaga M

    Jpn J Diagn Pathol   17 ( 2 )   190 - 192   2000年

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  • 若年性多発性硝子化線維腫症の1症例

    本田由美, 大河原 進, 猪山賢一, 松川昭博, 吉永 秀

    診断病理   17 ( 2 )   190 - 192   2000年

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  • 緑膿菌誘発家兎慢性細気管支炎モデルにおけるエリスロマイシンの効果-アポトーシスに対する作用

    高橋利弘, 菅守隆, 佐藤圭創, 岡本龍哉, 一安秀範, 松川昭博, 大河原進, 吉永秀, 安藤正幸

    Jpn. J. Antibiot   2000年

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  • Galectin-9 expands immunosuppressive macrophages to ameliorate T-cell-mediated lung inflammation 国際誌

    Arikawa, T, N. Saita, S. Oomizu, M. Ueno, A. Matsukawa, S. Katoh, K. Kojima, K. Nagahara, M. Miyake, A. Yamauchi, H. Kohrogi, M. Hirashima

    Eur J Immunol   40 ( 2 )   548 - 558   1999年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1002/eji.200939886

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  • Functional roles of MCP-1 in Propionibacterium acnes-induced, T cell-mediated pulmonary granulomatosis in rabbits.

    Ichiyasu H, Suga M, Matsukawa A, Iyonaga K, Mizobe T, Takahashi T, Ando M

    Journal of leukocyte biology   65 ( 4 )   482 - 91   1999年

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  • Crucial role of group IIA phospholipase A2 in oleic acid-induced acute lung injury in rabbits.

    Furue S, Kuwabara K, Mikawa K, Nishina K, Shiga M, Maekawa N, Ueno M, Chikazawa Y, Ono T, Hori Y, Matsukawa A, Yoshinaga M, Obara H

    Am. J. Respir. Crit. Care Med   160   1292 - 1302   1999年

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  • Role and regulation of IL-8 and MCP-1 in LPS-induced uveitis in rabbits.

    Mo JS, Matsukawa A, Ohkawara S, Yoshinaga M

    Exp. Eye Res.   68   333 - 340   1999年

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  • Endogenous monocyte chemoattractant protein-1 (MCP-1) protects mice in a model of acute septic peritonitis: cross-talk between MCP-1 and leukotriene B4.

    Matsukawa A, Hogaboam CM, Lukacs NW, Lincoln PM, Strieter RM, Kunkel SL

    J. Immunol.   163   6148 - 6154   1999年

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  • Increased interleukin-1 (IL-1) and imbalance between IL-1 and IL-1 receptor antagonist during acute inflammation in experimental shigellosis

    Arondel J, Singer M, Matsukawa A, Zychlinsky A, Sansonetti PJ

    Infect. Immun.   67   6056 - 6066   1999年

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  • Involvement of growth-related protein in lipopolysaccharide-induced rabbit arthritis: cooperation between growth-related protein and IL-8, and interrelated regulation among TNFa, IL-1, IL-1 receptor antagonist, IL-8, and growth-related protein.

    Matsukawa A, Yoshimura T, Fujiwara K, Maeda T, Ohkawara S, Yoshinaga M

    Lab. Invest.   79   591 - 600   1999年

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  • Interleukin-8 as an essential factor in the human chorionic gonadotropin-induced rabbit ovulatory process: interleukin-8 induces neutrophil accumulation and activation in ovulation.

    Ujioka T, Matsukawa A, Tanaka N, Matsuura K, Yoshinaga M, Okamura H

    Biol. Reprod   58   526 - 530   1998年

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  • Analysis of the cytokine network among tumor necrosis factor a, interleukin-1b, interleukin-8, and interleukin-1 receptor antagonist in monosodium urate crystal-induced rabbit arthritis.

    Matsukawa A, Yoshimura T, Maeda T, Takahashi T, Ohkawara S, Yoshinaga M

    Lab. Invest.   78   559 - 569   1998年

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  • Analysis of the cytokine interaction among interleukin-1b, interleukin-8, and interleukin-1 receptor antagonist in the rabbit ovulatory process.

    Ujioka T, Matsukawa A, Tanaka N, Matsuura K, Yoshinaga M, Okamura H

    Fertil. Steril   70   759 - 765   1998年

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  • Production and regulation of monocyte chemoattractant protein-1 in lipopolysaccharide- or monosodium urate crystal-induced arthritis in rabbits: roles of tumor necrosis factor a, interleukin-1, and interleukin-8.

    Matsukawa A, Miyazaki S, Maeda T, Tanase S, Feng L, Ohkawara S, Yoshinaga M, Yoshimura T

    Lab. Invest.   78   973 - 985   1998年

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  • Involvement of TNFa, IL-1b and IL-1 receptor antagonist in LPS-induced rabbit uveitis.

    Mo JS, Matsukawa A, Ohkawara S, Yoshinaga M

    Exp. Eye Res   66   547 - 557   1998年

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  • IL-8 is an essential mediator of the increased delayed-phase vascular permeability in LPS-induced rabbit pleurisy.

    Fukumoto T, Matsukawa A, Yoshimura T, Edamitsu S, Ohkawara S, Takagi K, Yoshinaga M

    J. Leukoc. Biol.   63   584 - 590   1998年

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  • Propionibacterium acnesによる実験的肺肉芽腫形成について

    一安 秀範, 菅 守隆, 溝部 孝則, 彌永 和宏, 山中 徹, 山本 太郎, 高橋 利弘, 松川 昭博, 吉永 秀, 安藤 正幸

    日本サルコイドーシス学会雑誌   16   21 - 22   1997年3月

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    記述言語:日本語   出版者・発行元:日本サルコイドーシス  

    DOI: 10.14830/jssog1987.16.21

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  • Blocking of TNFa and IL-1 inhibits leukocyte infiltration at early, but not at late stage of S. aureus-induced arthritis and the concomitant cartilage destruction in rabbits.

    Kimura M, Matsukawa A, Ohkawara S, Takagi K, Yoshinaga M

    Clin. Immunol. Immunopathol   82   18 - 25   1997年

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  • Detection and characterization of IL-1 receptor antagonist in tissues from healthy rabbits: IL-1 receptor antagonist is probably involved in health.

    Matsukawa A, Fukumoto T, Maeda T, Ohkawara S, Yoshinaga M

    Cytokine   9   307 - 315   1997年

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  • IL-8 is involved in homologous TNFa-, but not in IL-1b-induced neutrophil infiltration in rabbits.

    Miyamoto K, Matsukawa A, Ohkawara S, Takagi K, Yoshinaga M

    Inflamm. Res.   46   472 - 477   1997年

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  • Involvement of tumor necrosis factor-a, interleukin-1b, interleukin-8, and interleukin-1 receptor antagonist in acute lung injury caused by local shwartzman reaction.

    Imamura S, Matsukawa A, Ohkawara S, Kagayama M, Yoshinaga M

    Pathol. Int.   47   16 - 24   1997年

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  • Analysis of the inflammatory cytokine network among TNFa, IL-1b, IL-1 receptor antagonist, and IL-8 in LPS-induced rabbit arthritis.

    Matsukawa A, Yoshimura T, Miyamoto K, Ohkawara S, Yoshinaga M

    Lab. Invest.   76   629 - 638   1997年

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  • Interleukin-1 receptor antagonist: characterisation of its gene expression in rabbit tissues and large-scale expression in eucaryotic cells using a baculovirus expression system 査読

    Apostolopoulos J, Ross S, Davenport P, Matsukawa A, Yoshinaga M, Tipping PG

    J. Immunol. Methods   199   27 - 35   1996年

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  • Administration of neutralizing antibody against rabbit IL-1 receptor antagonist exacerbates lipopolysaccharide-induced arthritis in rabbits 査読

    Fukumoto T, Matsukawa A, Ohkawara S, Takagi K, Yoshinaga M

    Inflamm. Res   45   479 - 485   1996年

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  • Cytokine generation in rabbits during extracorporeal lung assist with a mini hollow fiber lung 査読

    Yanagi F, Terasaki H, Matsukawa A, Ohkawara S, Morioka T, Yoshinaga M

    Artif. Organs   20   209 - 217   1996年

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  • Suppressive effect of a neutrophil elastase inhibitor on the development of collagen-induced arthritis.

    Kakimoto K, Matsukawa A, Yoshinaga M, and Nakamura H

    165   269 - 32   1995年

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  • Role of TNFa, IL-1, and IL-1ra in the mediation of leukocyte infiltration and increased vascular permeability in rabbits with LPS-induced pleurisy 査読

    Edamitsu S, Matsukawa A, Ohkawara S, Takagi K, Nariuchi H, Yoshinaga M

    Clin. Immunol. Immunopathol.   75   68 - 74   1995年

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  • Neutrophil accumulation and activation by homologous IL-8 in rabbits. IL-8 induces destruction of cartilage and production of IL-1 and IL-1 receptor antagonist in vivo 査読

    Matsukawa A, Yoshimura T, Maeda T, Ohkawara S, Takagi K, Yoshinaga M

    J. Immunol   154   5418 - 5425   1995年

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  • Development of a neutralizing monoclonal antibody against rabbit IL-1 receptor antagonist and utilization for ELISA and measurement of masked IL-1 activity in biological materials.

    Matsukawa A, Furukawa S, Ohkawara S, Takagi K, and Yoshinaga M

    23   129 - 142   1994年

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  • Production of IL-1 and IL-1 receptor antagonist and the pathological significance in lipopolysaccharide-induced arthritis in rabbits.

    Matsukawa A, Ohkawara S, Maeda T, Takagi K, and Yoshinaga M

    Clin. Exp. Immunol.   93   206 - 211   1993年

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  • Lipoma arborescens with hemarthrosis of the knee. A case report

    Edamitsu S, Mizuta H, Kubota K, Matsukawa A, and Takagi K

    Acta Orthop. Scand.   64   601 - 602   1993年

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  • Production, purification and characterization of a rabbit recombinant IL-1 receptor antagonist 査読

    Matsukawa A, Mori S, Ohkawara S, Maeda T, Tanase S, Edamitsu S, Yanagi F, and Yoshinaga M

    Biomed. Res. 13:269-277   13   269 - 277   1992年

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▼全件表示

書籍等出版物

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    医歯薬出版株式会社  2013年 

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    南山堂  2012年 

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    2011年 

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    朝倉出版  2009年 

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    医歯薬出版  2009年 

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  • 感染とサイトカイン・サイトカイン情報伝達

    医歯薬出版社  2009年 

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  • 図説分子病態学4版

    中外医学社  2008年 

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  • Master of Medicine:Systemic pathology

    2007年 

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  • 炎症とサイトカイン・シグナル伝達

    岡山医学会誌  2006年 

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  • 自然免疫/炎症とサイトカイン・シグナル伝達

    岡山医学会誌  2006年 

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  • Monthly Book Derma 75

    全日本病院出版会  2003年 

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  • 動物モデルにおける尿酸結晶誘発関節炎−サイトカイン・ケモカインの産生とそのネットワ−ク−

    メディカルレビュ-社  2003年 

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  • The biological response to planned and unplanned injuries: Cellular, molecular and genetic aspects

    Elsevier  2003年 

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  • Chemokines in the lung

    Marcel Dekker  2003年 

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  • 図説分子病態学

    中外医学社  2003年 

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  • Helicobacter meets inflammatory bowel disease

    Medical Tribune Inc  2002年 

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▼全件表示

MISC

  • コロナ禍における医学科1年次行動科学I〜社会におけるコミュニケーション〜の実施とアウトカム

    三好 智子, 小崎 吉訓, 越智 可奈子, 吉田 登志子, 山根 正修, 赤穂 宗一郎, 伊野 英男, 大塚 愛二, 松川 昭博

    医学教育   52 ( Suppl. )   122 - 122   2021年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 医学科1年生における行動科学授業「コロナ禍での医学生生活を考える」 コロナ禍での入学の現状と課題

    越智 可奈子, 三好 智子, 小崎 吉訓, 赤穂 宗一郎, 吉田 登志子, 山根 正修, 伊野 英男, 大塚 愛二, 松川 昭博

    医学教育   52 ( Suppl. )   147 - 147   2021年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • Spred2はHCCで幹細胞性をmiR-506-3pによって一部負に抑制する(Spred2 down-regulates stemness in HCC partly through targeting miR-506-3p)

    高 桐, 藤澤 真義, Aye Moh Moh Aung, 大原 利章, 吉村 禎造, 王 天一, 伊藤 佐智夫, 松川 昭博

    日本病理学会会誌   110 ( 1 )   225 - 225   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 乳癌における傍導管浸潤(periductal invasion)の臨床病理学的意義

    藤澤 真義, 大森 昌子, 松川 昭博

    日本病理学会会誌   110 ( 1 )   322 - 322   2021年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • IgG4関連消化器病変の診断における胃生検の有用性(Utility of gastric biopsy in diagnosing IgG4-related gastrointestinal disease)

    内野 かおり, 能登原 憲司, 上原 剛, 倉石 康弘, 板倉 淳哉, 松川 昭博

    日本病理学会会誌   110 ( 1 )   300 - 300   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 肺腺癌におけるSpred2の発現と増殖、浸潤との関連の検討

    太田 陽子, 藤澤 真義, 吉村 禎造, スマルディカ・イワヤン, 枝園 和彦, 阪口 政清, 豊岡 伸一, 松川 昭博

    日本病理学会会誌   110 ( 1 )   291 - 291   2021年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 4T1乳癌モデルにおいてMCP-1産生を促す癌細胞・線維芽細胞間のクロストーク(Crosstalk between cancer cells and fibroblasts for MCP: production of MCP-1 in 4T1 breast cancer)

    吉村 禎造, 今村 真悠, り・てぃあんてぃあん, てぃあん・みあお, 李 春寧, 藤澤 真義, 松川 昭博

    日本病理学会会誌   110 ( 1 )   231 - 231   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 異なる亜集団の腫瘍細胞から放出されたエクソソームWnt7aによリ4T1細胞の転移は促進される(4T1 cells promote tumor metastasis by exosomal Wnt7a released from distinct subpopulations)

    李 春寧, 大原 利章, 藤澤 真義, 阪口 政清, 山本 健一, 田 ミャオ, 王 宇沢, 吉村 禎造, 松川 昭博

    日本病理学会会誌   110 ( 1 )   231 - 231   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 腫瘍環境のSpred2欠損は4T1乳がん細胞の増殖と転移を抑制する(Spred2 deficiency in cancer microenvironment inhibits progression of 4T1 breast cancer cells in mice)

    Tian Miao, 吉村 禎造, 李 春寧, 大原 利章, 藤澤 真義, 松川 昭博

    日本病理学会会誌   110 ( 1 )   324 - 324   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 癌関連線維芽細胞に対する鉄キレート剤の効果(Effects of Iron Chelators on Cancer-associated Fibroblasts)

    王 宇沢, 大原 利章, 李 春寧, 田 ミャオ, 小槙 志保, 吉村 禎造, 藤澤 真義, 松川 昭博

    日本病理学会会誌   110 ( 1 )   324 - 324   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • HCC細胞のオートファジーにおけるSpred2の役割とERK活性化との関係(Role of Spred2 in autophagy in HCC cells and its relation to ERK activation)

    王 天一, 藤澤 真義, 大原 利章, 吉村 禎造, 高 桐, 松川 昭博

    日本病理学会会誌   110 ( 1 )   314 - 314   2021年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 胎児期に一過性骨髄異常増殖症を発症し、胎盤にfetal vascular malperfusionを伴ったダウン症候群の1剖検例

    濱崎 友洋, 藤澤 真義, 宮原 宏幸, 伏見 聡一郎, 堀田 真智子, 和仁 洋治, 松川 昭博

    診断病理   37 ( 4 )   428 - 434   2020年10月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

    胎児期に一過性骨髄異常増殖症(transient abnormal myelopoiesis:TAM)を発症し、生後4日で死亡したダウン症候群の新生児の1剖検例を経験した。母体は20代の経産婦で、妊娠31週5日に胎児機能不全を認め緊急帝王切開となった。患児は新生児仮死の状態であった。出生直後の末梢血は白血球数が異常高値で、塗抹標本で多数の巨核球系の芽球を認めた。染色体検査で21トリソミーと判明したため、TAMと診断した。組織学的に、胎盤では絨毛の血管が消失した領域が認められ、fetal vascular malperfusion(FVM)と考えた。腫瘍細胞が絨毛内の血管内腔に充満し、血栓形成を伴っている像を認め、TAMがFVMの一因であることが推測された。(著者抄録)

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  • 留学報告会は学生の留学指向を高める

    前田 雛乃, 久保 卓也, 松川 昭博

    医学教育   51 ( Suppl. )   149 - 149   2020年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 岡山大学医療教育学生会 学生会はなぜ続くのか

    久保 卓也, 橋本 千名津, 松川 昭博

    医学教育   51 ( Suppl. )   219 - 219   2020年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 岡山大学医療教育学生会の活動 学生の満足・不満調査の結果と合わせて

    荒木 さくら, 橋本 千名津, 高瀬 ミキ, 瀬尾 里奈, 久保 卓也, 片岡 仁美, 松川 昭博

    医学教育   51 ( Suppl. )   218 - 218   2020年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 先輩から後輩へ 臨床実習は怖くない

    久保 卓也, 池内 綾介, 窪 征宣, 三好 智子, 松川 昭博

    医学教育   51 ( Suppl. )   126 - 126   2020年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 医学科における国際バカロレア教育修了者の強み 医学科1年次の行動科学における評価より

    三好 智子, 山根 正修, 小崎 吉訓, 佐藤 明香, 万代 康弘, 吉田 登志子, Sabina Mahmood, 伊野 英男, 大塚 愛二, 松川 昭博

    医学教育   51 ( Suppl. )   114 - 114   2020年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 【パンデミック下の医学教育-現在進行形の実践報告-】オンライン授業 COVID-19によるパンデミック下での医学科5年生に対するオンラインを用いたプロフェッショナリズム・行動科学教育

    三好 智子, 山根 正修, 小崎 吉訓, 片岡 仁美, 横田 雄也, 光田 栄子, 越智 可奈子, 小比賀 美香子, 伊野 英男, 松川 昭博, 大塚 愛二

    医学教育   51 ( 3 )   279 - 281   2020年6月

  • 乳癌における血管浸潤の検索法 新規法(Elastin and collagen 4 double staining)と従来法との比較検討

    藤澤 真義, 大森 昌子, 松川 昭博

    日本病理学会会誌   109 ( 1 )   311 - 311   2020年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred2は腫瘍幹細胞性の維持に関与しHepG2 HCCの悪性度を低下させる(Spred2 involved in tumor stemness maintenance down-regulates malignant potential of HepG2 HCC)

    高 桐, 吉村 禎造, 大原 利章, 藤澤 真義, 松川 昭博

    日本病理学会会誌   109 ( 1 )   348 - 348   2020年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • Spred2欠損はコンカナバリンA誘発性肝傷害をCXCL9/10を介したT細胞の誘引により悪化させる(Spred2 deficiency exacerbated Concanavalin A-induced liver injury by attracting T cells via CXCL9/10)

    孫 翠明, 吉村 禎造, 藤澤 真義, 大原 利章, 松川 昭博

    日本病理学会会誌   109 ( 1 )   346 - 347   2020年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 食道癌の幹細胞性を制御する鉄キレート療法の開発(Stemness control by iron chelator is a novel therapeutic strategy for esophageal cancer)

    大原 利章, 鳴坂 徹, Xing Boyi, Wang Yuze, 松川 昭博

    日本病理学会会誌   109 ( 1 )   338 - 339   2020年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 癌転移は,エキソソームの異なる細胞亜群からの放出によって調節される(Cancer metastasis is regulated via exosomes released from distinct cell subpopulation)

    李 春寧, 吉村 禎造, 田 ミョウ, 大原 利章, 藤澤 真義, 松川 昭博

    日本病理学会会誌   109 ( 1 )   358 - 358   2020年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 急激な経過をたどりdiffuse alveolar hemorrhageにて死亡したSLEの一例

    河原 明奈, 藤澤 真義, 松川 昭博

    日本病理学会会誌   109 ( 1 )   484 - 484   2020年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • ラット頭蓋骨欠損モデルに対する間葉系幹細胞と凍結乾燥リン酸化プルランの有用性

    村岡聡介, 三澤治夫, 瀧川朋亨, 山根健太郎, 池田吉宏, 辻寛謙, 高尾真一郎, 松川昭博, 尾崎敏文

    日本整形外科学会雑誌   94 ( 8 )   2020年

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  • 膵癌におけるFNA検体と切除検体とのPD-L1発現の検討 査読

    松本 和幸, 高木 章乃夫, 大原 利章, 藤澤 真義, 高原 政宏, 加藤 博也, 吉田 龍一, 楳田 祐三, 八木 孝仁, 松川 昭博, 岡田 裕之

    日本消化器病学会雑誌   116 ( 臨増大会 )   A826 - A826   2019年11月

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    記述言語:日本語   出版者・発行元:(一財)日本消化器病学会  

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  • 膵癌におけるFNA検体と切除検体とのPD-L1発現の検討

    松本 和幸, 高木 章乃夫, 大原 利章, 藤澤 真義, 高原 政宏, 加藤 博也, 吉田 龍一, 楳田 祐三, 八木 孝仁, 松川 昭博, 岡田 裕之

    日本消化器病学会雑誌   116 ( 臨増大会 )   A826 - A826   2019年11月

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    記述言語:日本語   出版者・発行元:(一財)日本消化器病学会  

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  • ラットにおけるチタン結合性BMPの骨形成促進効果についての検討

    内野 崇彦, 塩崎 泰之, 吉田 晶, 宇川 諒, 池田 吉宏, 村岡 聡介, 辻 寛謙, 伊藤 嘉浩, 松川 昭博, 尾崎 敏文

    日本整形外科学会雑誌   93 ( 8 )   S1941 - S1941   2019年9月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 学生による留学オリエンテーションのすすめ

    久保 卓也, 今村 真悠, 住田 まどか, 中村 薫, 松川 昭博

    医学教育   50 ( Suppl. )   177 - 177   2019年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 行動科学におけるらせん型カリキュラムの必要性

    三好 智子, 山根 正修, 飯田 淳義, 万代 康弘, 吉田 登志子, 伊野 英男, 那須 保友, 松川 昭博

    医学教育   50 ( Suppl. )   229 - 229   2019年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 学生による留学オリエンテーションのいろは

    久保 卓也, 今村 真悠, 住田 まどか, 中村 薫, 松川 昭博

    医学教育   50 ( Suppl. )   242 - 242   2019年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 行動科学におけるらせん型カリキュラムの必要性

    三好 智子, 山根 正修, 飯田 淳義, 万代 康弘, 吉田 登志子, 伊野 英男, 那須 保友, 松川 昭博

    医学教育   50 ( Suppl. )   229 - 229   2019年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 簡略化した外科指導者養成講習会の実施

    山根 正修, 松川 昭博

    医学教育   50 ( Suppl. )   194 - 194   2019年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • THE RELATIONSHIP BETWEEN THE PD-L1 EXPRESSION OF SURGICAL RESECTED AND FINE-NEEDLE ASPIRATION SPECIMENS FOR PATIENTS WITH PANCREATIC CANCER 査読

    Matsumoto Kazuyuki, Ohara Toshiaki, Fujisawa Masayoshi, Takaki Akinobu, Takahara Masahiro, Kato Hironari, Horiguchi Shigeru, Matsukawa Akihiro, Okada Hiroyuki

    GASTROENTEROLOGY   156 ( 6 )   S758   2019年5月

  • 乳癌における静脈浸潤の新規検索法

    藤澤 真義, モウモウアウン・エイ, 柳井 広之, 大森 昌子, 松川 昭博

    日本病理学会会誌   108 ( 1 )   289 - 289   2019年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred2はINF gamma生産を調節することによりマウスのConA誘発肝障害を予防する(Spred2 protects mice from ConA-induced liver injury by regulating IFN gamma production) 査読

    孫 翠明, 藤澤 真義, 大原 利章, 吉村 禎造, 松川 昭博

    日本病理学会会誌   108 ( 1 )   382 - 382   2019年4月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • HepG2細胞におけるSpred2遺伝子の不活化はERK経路を活性化して細胞増殖、移動および浸潤を促進する(Spred2 deletion accelerates growth, migration and invasion in HepG2 cells by activating ERK pathway) 査読

    高 桐, 楊 旭, 藤澤 真義, 大原 利章, 吉村 禎造, 松川 昭博

    日本病理学会会誌   108 ( 1 )   382 - 382   2019年4月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 食道癌の幹細胞性を制御する鉄キレート療法の開発(Stemness control by iron chelator can be a novel therapeutic strategy for esophageal cancer) 査読

    大原 利章, 鳴坂 徹, Xing Boyi, Chen Yuehua, 松川 昭博

    日本病理学会会誌   108 ( 1 )   318 - 318   2019年4月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 異なる細胞亜集団に由来するエキソソームによって癌の進行が制御される可能性(Cancer progression can be regulated by exosomes from distinct cell subpopulation) 査読

    李 春寧, 田 ミョウ, 大原 利章, 藤澤 真義, 吉村 禎造, 松川 昭博

    日本病理学会会誌   108 ( 1 )   394 - 394   2019年4月

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  • 非腫瘍細胞におけるFpr2欠損は4T1マウス乳癌細胞の肺転移を抑制する(Fpr2-deficiency in Non-tumor Cells Decreases Lung Metastasis of 4T1 Murine Breast Cancer Cells)

    吉村 禎造, Weiss Jonathan M., Li Chunning, Li Tiantian, Gong Wanghua, 松川 昭博, Wang Ji MIng

    日本病理学会会誌   108 ( 1 )   290 - 290   2019年4月

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  • miR-200b-3p発現低下は転写因子ERGを標的として肝細胞癌の血管新生に関与する(Downregulated miR-200b-3p plays a role in angiogenesis of hepatocellular carcinoma by targeting ERG)

    エイ・モウモウ・アウン, 藤澤 真義, 吉村 禎造, 松川 昭博

    日本病理学会会誌   108 ( 1 )   329 - 329   2019年4月

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  • 癌細胞が産生するGM-CSFは、癌の進展・転移に関わるか? マウス4T1乳癌モデルでの検討

    中村 薫, Li Chunning, Li Tiantian, 藤澤 真義, 松川 昭博, 向田 直史, 吉村 禎造

    日本病理学会会誌   108 ( 1 )   464 - 464   2019年4月

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  • マウス4T1乳癌モデルにおける新たなMCP-1産生機序の同定 腫瘍細胞・線維芽細胞間のクロストーク

    今村 真悠, 藤澤 真義, Li Tiantian, 河原 明奈, 松川 昭博, 吉村 禎造

    日本病理学会会誌   108 ( 1 )   461 - 461   2019年4月

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  • 高齢発症で再発を繰り返し、致死的な経過をたどった若年性顆粒膜細胞腫の一例(Juvenile granulosa cell tumor with unusual clinical course: a late-onset and late recurrent case)

    太田 陽子, タテ・サン, 伏見 聡一郎, 藤澤 真義, 柳井 広之, 戸田 博子, 大森 昌子, 國友 忠義, 松川 昭博

    日本病理学会会誌   108 ( 1 )   408 - 408   2019年4月

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  • 肺線維芽細胞の増殖におけるSpred2の役割

    河原 明奈, 水田 亮, 藤澤 真義, 吉村 禎造, 松川 昭博

    日本病理学会会誌   108 ( 1 )   353 - 353   2019年4月

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  • ラットにおけるチタン結合性BMPの骨形成促進効果についての検討

    内野 崇彦, 塩崎 泰之, 吉田 晶, 宇川 諒, 池田 吉宏, 村岡 聡介, 辻 寛謙, 伊藤 嘉浩, 松川 昭博, 尾崎 敏文

    移植   53 ( 6 )   382 - 382   2019年3月

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  • 新規多糖誘導体リン酸化プルランフィルムとBMP-2の併用はラット脊椎固定モデルにおいて骨癒合を促進する

    宇川 諒, 塩崎 泰之, 村岡 聡介, 池田 吉宏, 辻 寛謙, 吉田 晶, 吉原 久美子, 瀧川 朋亨, 三澤 治夫, 尾崎 敏文, 松川 昭博

    Journal of Spine Research   10 ( 3 )   683 - 683   2019年3月

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    記述言語:日本語   出版者・発行元:(一社)日本脊椎脊髄病学会  

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  • 膵癌におけるFNA検体と切除検体とのPD-L1発現の検討

    松本和幸, 高木章乃夫, 大原利章, 藤澤真義, 高原政宏, 加藤博也, 吉田龍一, 楳田祐三, 八木孝仁, 松川昭博, 岡田裕之

    日本消化器病学会雑誌(Web)   116   2019年

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  • 骨形成促進のための整形外科バイオマテリアル ラットにおけるチタン結合性BMPの骨形成促進効果についての検討

    内野 崇彦, 塩崎 泰之, 吉田 晶, 宇川 諒, 池田 吉宏, 村岡 聡介, 辻 寛謙, 野田 知之, 伊藤 嘉浩, 尾崎 敏文, 松川 昭博

    日本整形外科学会雑誌   92 ( 8 )   S1933 - S1933   2018年8月

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  • 学生企画によるアクティブ・ラーニング型研究オリエンテーション・報告会の実践報告

    久保 卓也, 今村 真悠, 住田 まどか, 林田 慎太郎, 松川 昭博

    医学教育   49 ( Suppl. )   118 - 118   2018年7月

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  • 学生が医学研究インターンシップにおける研究室(学内・国内・海外)選択で考慮する要因

    今村 真悠, 久保 卓也, 住田 まどか, 林田 慎太郎, 松川 昭博

    医学教育   49 ( Suppl. )   131 - 131   2018年7月

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  • 学生が研究を通して自らの成長に期待すること

    住田 まどか, 久保 卓也, 今村 真悠, 林田 慎太郎, 松川 昭博

    医学教育   49 ( Suppl. )   130 - 130   2018年7月

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  • 免疫病理学の新展開 Ras-Raf-ERK/MAPK経路とその制御因子Spred-2による炎症・がんの制御

    松川 昭博

    日本病理学会会誌   107 ( 1 )   208 - 208   2018年4月

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  • microRNA 200b-3pはERGを標的とすることで肝細胞癌の血管新生に関与している可能性がある(MicroRNA 200b-3p May Play a Role in Angiogenesis of Hepatocellular Carcinoma by Targeting ERG)

    エイ・モゥモゥ・アウン, 藤澤 真義, 吉村 禎造, 松川 昭博

    日本病理学会会誌   107 ( 1 )   369 - 369   2018年4月

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  • 4T1マウス乳癌の進展におけるがん細胞由来GM-CSFの果たす役割(The role of tumor cell-derived GM-CSF in the progression of 4T1 murine breast cancer)

    吉村 禎造, 中村 薫, 佐藤 美和, 李 春寧, 藤澤 真義, 向田 直史, 松川 昭博

    日本病理学会会誌   107 ( 1 )   341 - 341   2018年4月

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  • 胎児期に一過性骨髄異常増殖症を発症し胎盤にfetal thrombotic vasculopathyを伴ったダウン症の1例

    濱崎 友洋, 藤澤 真義, 伏見 聡一郎, 堀田 真智子, 苗村 智, 和仁 洋治, 吉村 禎造, 松川 昭博

    日本病理学会会誌   107 ( 1 )   530 - 530   2018年4月

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  • Spred2欠損は内臓脂肪織炎、インスリン抵抗性を増悪させる 査読

    大倉 隆宏, 丸谷 梨栄, 吉村 禎造, 藤澤 真義, 大原 利章, 松川 昭博

    日本病理学会会誌   107 ( 1 )   347 - 347   2018年4月

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  • 除鉄による癌幹細胞の幹細胞性マーカーと機能は制御される(Iron depletion suppress the stemness markers and functions of cancer stem cells) 査読

    大原 利章, Sun Yingfu, 友野 靖子, 松川 昭博

    日本病理学会会誌   107 ( 1 )   299 - 299   2018年4月

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  • 肺腺がんにおけるSpred2の役割の解明

    太田 陽子, 藤澤 真義, 吉村 禎造, スマルディカ・イワヤン, 枝園 和彦, 阪口 政清, 豊岡 伸一, 松川 昭博

    日本病理学会会誌   107 ( 1 )   414 - 414   2018年4月

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  • ブレオマイシン肺線維症モデルにおけるSpred-2の役割

    河原 明奈, 水田 亮, 藤澤 真義, 吉村 禎造, 松川 昭博

    日本病理学会会誌   107 ( 1 )   413 - 413   2018年4月

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  • ヒト卵巣癌における線維芽細胞の由来

    藤澤 真義, 柳井 広之, 和仁 洋治, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   107 ( 1 )   389 - 389   2018年4月

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  • Sarcomatoid changeがみられたclear cell RCC with unusual papillary configurationの一例

    河原 明奈, 藤澤 真義, 黒田 直人, 松川 昭博

    日本病理学会会誌   106 ( 2 )   93 - 93   2017年9月

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  • 5年次OSCEの意義について

    高尾 賢一朗, 万代 康弘, 三好 智子, 飯田 淳義, 山根 正彦, 松川 昭博

    医学教育   48 ( Suppl. )   261 - 261   2017年8月

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  • 医学教育学生会のこれまでの歩みと今後の展望

    河野 和馬, 川口 満理奈, 大塚 勇輝, 今村 竜太, 中村 薫, 山根 正修, 松川 昭博

    医学教育   48 ( Suppl. )   157 - 157   2017年8月

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  • 医学科1年次に導入した行動科学がもたらしたもの

    三好 智子, 山根 正修, 飯田 淳義, 万代 康弘, 小比賀 美香子, 片岡 仁美, 那須 保友, 松川 昭博

    医学教育   48 ( Suppl. )   145 - 145   2017年8月

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  • 多糖複合体を担体とした抗菌薬伝達システムの開発

    渡邉 典行, 吉田 晶, 田中 雅人, 松川 昭博, 尾崎 敏文

    日本整形外科学会雑誌   91 ( 8 )   S1661 - S1661   2017年8月

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  • 一年次社会コミュニケーション(行動科学科目)を受講して

    林田 慎太郎, 大塚 勇輝, 日高 啓介, 山根 正修, 松川 昭博, 三好 智子, 飯田 淳義, 万代 康弘

    医学教育   48 ( Suppl. )   266 - 266   2017年8月

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  • ヒト卵巣癌における線維芽細胞の由来

    藤澤 真義, 柳井 広之, 和仁 洋治, 松川 昭博

    日本病理学会会誌   106 ( 1 )   318 - 318   2017年3月

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  • 著明な偽血管肉腫様構造を示した乳腺化生癌の1例

    大森 昌子, 能島 舞, 田中 顕之, 柳井 広之, 松川 昭博, 吉野 正

    日本病理学会会誌   106 ( 1 )   491 - 491   2017年3月

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  • ラブドイド形質を呈した低分化大腸癌の一例

    太田 陽子, 伏見 聡一郎, 堀田 真智子, 河田 卓也, 板倉 淳哉, 藤澤 真義, 和仁 洋治, 松川 昭博

    日本病理学会会誌   106 ( 1 )   381 - 382   2017年3月

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  • 間質性肺炎モデルにおけるSpred-2の役割

    河原 明奈, 藤澤 真義, 吉村 禎造, 松川 昭博

    日本病理学会会誌   106 ( 1 )   330 - 330   2017年3月

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  • 膀胱腫瘍におけるRas-ERK経路とその制御因子Spred-2の解析

    小田 晋輔, 藤澤 真義, 吉村 禎造, 大原 利章, 河原 明奈, 山口 隆廣, 太田 陽子, 松川 昭博

    日本病理学会会誌   106 ( 1 )   326 - 326   2017年3月

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  • 医学部6年次生は二次救命処置のリーダーができるか

    飯田 淳義, 万代 康弘, 芝 直基, 塚原 紘平, 内藤 宏道, 寺戸 通久, 佐藤 圭路, 鵜川 豊世武, 中尾 篤典, 松川 昭博, 那須 保友

    日本救急医学会雑誌   27 ( 9 )   444 - 444   2016年9月

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  • 新規生体材料リン酸化プルランによるインプラントコーティング技術の開発

    香川 洋平, 渡邉 典行, 張 偉, 吉村 将秀, 吉田 晶, 吉田 靖弘, 尾崎 敏文, 松川 昭博

    日本整形外科学会雑誌   90 ( 8 )   S1813 - S1813   2016年8月

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  • 5年次SDによるワクチン予防接種 臨床実習プログラムとしての評価

    大塚 勇輝, 山根 正修, 日高 啓介, 飯田 淳義, 万代 康弘, 三好 智子, 松川 昭博

    医学教育   47 ( Suppl. )   112 - 112   2016年7月

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  • 医学部の前臨床2年次での英語PBLグループへの参加(Joining the English PBL group as a Pre-clinical Second Year Medical Student)

    佐武 秀紀, 佐々並 三紗, 松川 昭博, Mahmood Sabina

    医学教育   47 ( Suppl. )   281 - 281   2016年7月

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    記述言語:英語   出版者・発行元:(一社)日本医学教育学会  

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  • 学生主体による医学英語学習グループがどのように医学英語教育に関わっているか(How a Medical English learning group managed by students can contribute to medical English education)

    池田 礼奈, Mahmood Sabina, 松川 昭博

    医学教育   47 ( Suppl. )   281 - 281   2016年7月

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    記述言語:英語   出版者・発行元:(一社)日本医学教育学会  

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  • 臨床実習に臨み学生が修得すべき事 学生の考え、指導医の考え

    川野 香, 難波 満理奈, 山根 正修, 飯田 淳義, 万代 康弘, 三好 智子, 片岡 仁美, 松川 昭博

    医学教育   47 ( Suppl. )   276 - 276   2016年7月

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  • 患者アンケートからみた臨床実習の評価

    難波 満里奈, 川野 香, 山根 正修, 飯田 淳義, 万代 康弘, 三好 智子, 片岡 仁美, 松川 昭博

    医学教育   47 ( Suppl. )   276 - 276   2016年7月

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  • 全臨床系教室を対象とした個別の学内FDの取り組み

    山根 正修, 松川 昭博

    医学教育   47 ( Suppl. )   217 - 217   2016年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 医学生による予防接種実践コースのカリキュラム作成

    山根 正修, 松川 昭博, 万代 康弘, 飯田 淳義, 三好 智子

    医学教育   47 ( Suppl. )   216 - 216   2016年7月

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  • 学生アンケートに基づく漢方教育への提言

    日高 啓介, 松川 昭博, 大塚 勇輝, 飯田 淳義, 万代 康弘, 三好 智子, 山根 正修

    医学教育   47 ( Suppl. )   136 - 136   2016年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • てんかんの原因となった、髄膜腫を併存した髄膜血管腫症の1例

    河原 明奈, 伏見 聡一郎, 板倉 淳哉, 小田 晋輔, 太田 陽子, 堀田 真智子, 藤澤 真義, 柳井 広之, 松川 昭博

    日本病理学会会誌   105 ( 1 )   562 - 562   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 多房性嚢胞性変化を呈したsex cord tumor with annular tubules(SCTAT)の一例

    太田 陽子, 伏見 聡一郎, 堀田 真智子, 河田 卓也, サン・タ・テ, 内野 かおり, 藤澤 真義, 和仁 洋治, 松川 昭博

    日本病理学会会誌   105 ( 1 )   400 - 400   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 乳癌細胞によるGM-CSF産生を介したマクロファージにおけるMCP-1/CCL2の誘導(Induction of MCP-1/CCL2 in macrophages via GM-CSF production by breast cancer cells)

    吉村 禎造, Imamichi Tomozumi, Weiss Jonathan M., 佐藤 美和, Li Liangzhu, 松川 昭博, Wang Ji Ming

    日本病理学会会誌   105 ( 1 )   326 - 326   2016年4月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 遺伝子組換えから病態へのアプローチ Spred-2による炎症の制御

    松川 昭博

    日本病理学会会誌   105 ( 1 )   265 - 265   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred-2欠損によるシスプラチン腎障害増悪における好中球の関与

    藤井 裕生, 何 佳利, 吉村 禎造, 藤澤 真義, 佐藤 美和, 楊 旭, 松川 昭博

    日本病理学会会誌   105 ( 1 )   592 - 592   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 濾胞性リンパ腫の経過中にT細胞性リンパ腫を合併した2症例

    藤澤 真義, 和仁 洋治, 伏見 聡一郎, 佐藤 康晴, 山鳥 一郎, 松川 昭博

    日本病理学会会誌   105 ( 1 )   560 - 560   2016年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 新規生体材料によるインプラントコーティング

    香川 洋平, 山根 健太郎, 篠原 健介, 渡邉 典行, 張 偉, 吉田 晶, 吉田 靖弘, 尾崎 敏文, 松川 昭博

    日本整形外科学会雑誌   89 ( 8 )   S1576 - S1576   2015年9月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 脊髄損傷治療におけるコラーゲン結合性ドメイン連結肝細胞増殖因子の有用性

    山根 健太郎, 吉田 晶, 篠原 健介, 張 偉, 香川 洋平, 渡邉 典行, 伊藤 嘉浩, 田中 雅人, 松川 昭博, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 8 )   S1622 - S1622   2015年9月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 多糖複合体リン酸化プルランを用いた抗菌薬含有骨セメントの開発

    渡邉 典行, 山根 健太郎, 香川 洋平, 篠原 健介, 張 偉, 吉田 晶, 松川 昭博, 吉田 靖弘, 田中 雅人, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 8 )   S1577 - S1577   2015年9月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • シミュレーションセンター運用の現状と問題点 将来に向けて シミュレーションセンター運営におけるシミュレーションスペシャリストの重要性

    万代 康弘, 三好 智子, 香西 佳美, 伊野 英男, 片岡 仁美, 松川 昭博, 谷本 光音

    医学教育   46 ( Suppl. )   72 - 72   2015年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • SD(Student Doctor)による予防接種の導入

    原田 洸, 山根 正修, 三好 智子, 松川 昭博

    医学教育   46 ( Suppl. )   190 - 190   2015年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 診療参加型臨床実習における評価の改善

    山根 正修, 松川 昭博

    医学教育   46 ( Suppl. )   183 - 183   2015年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 外科系医師のための指導者養成講習会の開催

    山根 正修, 万代 康弘, 伊野 英男, 松川 昭博

    医学教育   46 ( Suppl. )   138 - 138   2015年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 脊髄損傷急性期における肝細胞増殖因子の抗炎症効果について コラーゲン結合性改変HGFを用いた検討

    山根 健太郎, 篠原 健介, 伊藤 嘉浩, 杉本 佳久, 田中 雅人, 松川 昭博, 尾崎 敏文

    Journal of Spine Research   6 ( 3 )   585 - 585   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本脊椎脊髄病学会  

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  • ミャンマーの乳がんの症例におけるマウス乳腺腫瘍ウイルス(MMTV)のenv様配列の検出(Detection of Mouse Mammary Tumor Virus(MMTV) env-like sequence in breast cancer cases in Myanmar)

    サン・タテ, ミント・イーイー, ミント・アイアイ, モン・ミャット, イーミン・トミント, ソー・ラミン, 板倉 淳哉, 伏見 聡一郎, 伊藤 利洋, 松川 昭博

    日本病理学会会誌   104 ( 1 )   425 - 425   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 創傷治癒はSpred-2欠損で短縮する

    河原 明奈, 板倉 淳哉, 小田 晋輔, 伏見 聡一郎, 伊藤 利博, 松川 昭博

    日本病理学会会誌   104 ( 1 )   392 - 392   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 病理と基礎生命科学との接点(第12回) 免疫応答と疾患

    松川 昭博

    病理と臨床   33 ( 3 )   311 - 316   2015年3月

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    記述言語:日本語   出版者・発行元:(株)文光堂  

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  • 仙骨部にPlemorphic hyalinaizing angiectatic tumor(PHAT)様の腫瘍を認めた一例

    山口 隆廣, 河原 明奈, 太田 陽子, 小田 晋輔, 板倉 淳哉, 伏見 聡一郎, サン・タテ, 松川 昭博, 豊田 博

    日本病理学会会誌   104 ( 1 )   364 - 364   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 非典型的な組織像を示した膵solid-pseudopapillary neoplasm(SPN)の一例

    小田 晋輔, 河原 明奈, 伏見 聡一郎, 太田 陽子, 山口 隆廣, サン・タテ, 板倉 淳哉, 大原 俊章, 平 麻美, 松川 昭博

    日本病理学会会誌   104 ( 1 )   355 - 355   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred-2の欠損はリポポリサッカライドに誘発される急性肺炎を増悪させる(Spred-2 Deficiency Exacerbates Lipopolysaccharide-induced Acute Lung Inflammation)

    楊 旭, 伊藤 利洋, 伏見 聡一郎, 高橋 索真, 板倉 淳哉, 佐藤 美和, 美野 愛, 松川 昭博

    日本病理学会会誌   104 ( 1 )   284 - 284   2015年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • IgG4関連疾患の診断病理 その進歩と問題点 1型自己免疫性膵炎の病理所見 CD163陽性マクロファージの意義

    内野 かおり, 能登原 憲司, 松川 昭博

    日本病理学会会誌   104 ( 1 )   191 - 191   2015年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 膀胱粘膜下傍神経節腫の2例

    小田 晋輔, 伏見 聡一郎, 山口 隆廣, 伊藤 利洋, 大枝 忠史, 市川 孝治, 柳井 広之, 國友 忠義, 中本 周, 松川 昭博

    鳥取医学雑誌   42 ( 3-4 )   147 - 152   2014年12月

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    記述言語:日本語   出版者・発行元:(公社)鳥取県医師会  

    われわれは膀胱に発生した傍神経節腫の2例を経験した。症例1は90歳代女性。血尿の精査中、膀胱鏡で右壁に3cm大の粘膜下腫瘍が認められ、経尿道的膀胱腫瘍切除術(transurethral resection of bladder tumor:TURBT)を施行された。症例2は70歳代男性。胸部大動脈瘤術後の経過観察中に、Computed tomography(CT)検査にて膀胱腫瘍を指摘され、膀胱鏡を行ったところ新たに別の粘膜下腫瘍が認められTURBTを施行された。2例とも病理組織学的に傍神経節腫と診断された。膀胱に発生する傍神経節腫はまれであり、文献的考察を加えて報告する。(著者抄録)

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  • 新規生体材料によるインプラントコーティング技術

    香川 洋平, 馬崎 哲朗, 山根 健太郎, 篠原 健介, 吉田 晶, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    日本整形外科学会雑誌   88 ( 8 )   S1501 - S1501   2014年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • QCM-Dによる様々な細胞種の接着と伸展の観察

    竹下 裕治, 張本 乾一, 玉井 美保, 南 隆之, 荻 博次, 長岡 紀幸, 松川 昭博, 吉田 靖弘, 田川 陽一

    日本生物工学会大会講演要旨集   平成26年度   154 - 154   2014年8月

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    記述言語:日本語   出版者・発行元:(公社)日本生物工学会  

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  • 脊髄損傷急性期における肝細胞増殖因子の抗炎症効果の検討

    山根 健太郎, 馬崎 哲朗, 吉田 晶, 香川 洋平, 篠原 健介, 北嶋 隆, 伊藤 嘉浩, 松川 昭博, 田中 雅人, 尾崎 敏文

    日本整形外科学会雑誌   88 ( 8 )   S1510 - S1510   2014年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 臨床実習前の医療教育シミュレーションコース

    山根 正修, 芝 直基, 三好 智子, 内海 方嗣, 万代 康弘, 松川 昭博, 岡山大学医学部医学科教務委員会

    医学教育   45 ( Suppl. )   136 - 136   2014年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • Ras-Raf-ERK経路からみたA型インフルエンザ(H1N1)感染

    松川 昭博, 伊藤 利洋

    NEUROINFECTION   19 ( 1 )   40 - 42   2014年7月

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    記述言語:日本語   出版者・発行元:日本神経感染症学会  

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  • CPC解説(第59回) シュウ酸カルシウム結晶沈着を伴ったAspergillus nigerによる侵襲性肺アスペルギルス症の1例

    板倉 淳哉, 伏見 聡一郎, 荻野 哲也, 伊藤 利洋, 小田 晋輔, 河原 明奈, 萩谷 英大, 桑原 宏子, 松川 昭博

    病理と臨床   32 ( 6 )   669 - 675   2014年6月

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    記述言語:日本語   出版者・発行元:(株)文光堂  

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  • 家兎骨軟骨欠損モデルにおける可視光硬化ゼラチンおよび骨髄間質細胞の組織修復効果

    馬崎 哲朗, 塩崎 泰之, 山根 健太郎, 吉田 晶, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    移植   49 ( 1 )   178 - 178   2014年5月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 可視光硬化型ゼラチンとコラーゲン結合性肝細胞増殖因子を用いた脊髄損傷治療

    山根健太郎, 馬崎哲朗, 篠原健介, 吉田晶, 松川昭博, 中村真理子, 吉田靖弘, 北嶋隆, 伊藤嘉浩, 田中雅人, 尾崎敏文

    J Spine Res   5 ( 3 )   473   2014年3月

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    記述言語:日本語  

    J-GLOBAL

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  • 骨髄移植後の皮膚GVHDの経過中にVZV肝炎を発症した1例

    河原 明奈, 伊藤 利洋, 伏見 聡一郎, 板倉 淳哉, 小田 晋輔, 松川 昭博

    日本病理学会会誌   103 ( 1 )   303 - 303   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Exophiala dermatitidis感染による肺出血および多発脳梗塞を認めた急性骨髄性白血病の一剖検例

    伏見 聡一郎, 伊藤 利洋, 片瀬 直樹, 玉村 亮, サン・タテ, 板倉 淳哉, 河原 明奈, 小田 晋輔, 松川 昭博

    日本病理学会会誌   103 ( 1 )   293 - 293   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred2欠損マウスにおける敗血症抵抗性のメカニズム

    板倉 淳哉, 小田 晋輔, 河原 明奈, 佐藤 美和, 美野 愛, 伏見 聡一郎, 伊藤 利洋, 松川 昭博

    日本病理学会会誌   103 ( 1 )   248 - 248   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • インフルエンザウィルス(H1N1)感染症ならびに二次性細菌性肺炎のエピジェネティクス解析

    伊藤 利洋, 板倉 淳哉, 河原 明奈, 小田 晋輔, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   103 ( 1 )   224 - 224   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Ras/ERK系と大腸粘膜治癒 Ras/ERK系の阻害因子Spred-2の解析を通じて

    高橋 索真, 平岡 佐規子, 伏見 聡一郎, 伊藤 利洋, 板倉 淳哉, 木村 亮二朗, 楊 旭, 篠倉 美理, 中川 裕貴, 住居 優一, 竹井 大介, 井口 俊博, 半井 明日香, 森藤 由記, 秋田 光洋, 原田 馨太, 岡田 裕之, 松川 昭博, 山本 和秀

    消化器と免疫   ( 50 )   66 - 68   2014年3月

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    記述言語:日本語   出版者・発行元:日本消化器免疫学会  

    【目的】Ras/ERK系を抑制するSpred-2のIBDへの関与を検討する。【方法】Spred-2 KOマウスおよびWTマウスにDSS腸炎を誘導し、症状変化・組織像・大腸粘膜の細胞増殖を評価した。【結果】Spred-2 KOマウスではWTマウスより腸炎の症状が軽く、腸管上皮の再生が速やかであった。また、腸管上皮中のBrdU陽性細胞の比率が有意に高かった。【結論】Spred-2はIBDにおける粘膜治癒を抑制している可能性がある。(著者抄録)

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  • 家兎骨軟骨欠損モデルにおける可視光硬化ゼラチンおよび結合性改変成長因子CBD-BMP4による組織修復効果

    馬崎 哲朗, 山根 健太郎, 吉田 晶, 松川 昭博, 伊藤 嘉浩, 尾崎 敏文

    中部日本整形外科災害外科学会雑誌   57 ( 春季学会 )   124 - 124   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)中部日本整形外科災害外科学会  

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  • 間質性肺炎モデルにおけるSpred-2の役割

    水田 亮, 伊藤 利洋, 板倉 淳哉, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   103 ( 1 )   392 - 392   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • モノクロラミンによる酸化ストレスとK562細胞の分化誘導

    荻野 哲也, 松川 昭博

    日本病理学会会誌   103 ( 1 )   357 - 357   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 帝王切開中に発見・切除された子宮perivascular epithelioid cell tumor(PEComa)の一例

    小田 晋輔, 内野 かおり, 和仁 洋治, 松川 昭博

    日本病理学会会誌   103 ( 1 )   342 - 342   2014年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 家兎骨軟骨欠損モデルにおける可視光硬化ゼラチンおよび骨髄間質細胞の組織修復効果

    馬崎哲朗, 塩崎泰之, 山根健太郎, 吉田晶, 松川昭博, 中村真理子, 吉田靖弘, 北嶋隆, 伊藤嘉浩, 尾崎敏文

    移植(Web)   49 ( 1 )   178(J-STAGE)   2014年

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    記述言語:日本語  

    J-GLOBAL

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  • 多糖誘導体リン酸化プルランをキーマテリアルとした多目的硬組織接着剤の開発

    吉田靖弘, 松川昭博, 高柴正悟, 沖原巧, 伊東孝

    医科学応用研究財団研究報告   31   23 - 27   2014年

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  • 固形癌に対する除鉄誘導による血管新生阻害薬併用療法の確立

    大原利章, 木村文昭, 浦野真一, 二宮卓之, 勝部亮一, 野間和広, 友野靖子, 藤原俊義, 松川昭博

    日本鉄バイオサイエンス学会学術集会プログラム・抄録集   38th   2014年

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  • 十二指腸乳頭部に発生したgangliocytic paragangliomaの細胞像と組織像の検討

    伏見 聡一郎, 井上 博文, 小田 晋輔, 河原 明奈, 板倉 淳哉, 平 麻美, 伊藤 利洋, 松川 昭博, 加藤 博也, 市村 浩一, 柳井 広之

    日本臨床細胞学会岡山支部会誌   32   36 - 36   2013年12月

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    記述言語:日本語   出版者・発行元:岡山県臨床細胞学会  

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  • Ras-Raf-ERK経路からみたA型インフルエンザ(H1N1)感染

    松川 昭博

    NEUROINFECTION   18 ( 2 )   120 - 120   2013年9月

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    記述言語:日本語   出版者・発行元:日本神経感染症学会  

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  • 可視光硬化型ゼラチンとコラーゲン結合性ドメイン連結成長因子を用いた脊髄損傷治療

    篠原 健介, 馬崎 哲朗, 塩崎 泰之, 吉田 晶, 松川 昭博, 尾崎 敏文

    日本整形外科学会雑誌   87 ( 8 )   S1440 - S1440   2013年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 家兎骨軟骨欠損モデルにおける可視光硬化ゼラチンおよび骨髄間質細胞の組織修復効果

    香川 洋平, 馬崎 哲朗, 塩崎 泰之, 山根 健太郎, 吉田 晶, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    日本整形外科学会雑誌   87 ( 8 )   S1405 - S1405   2013年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • ケンフェロールが骨粗鬆症モデルマウスの骨吸収と骨組織に与える影響

    吉田 晶, 塩崎 泰之, 馬場 哲朗, 山根 健太郎, 松川 昭博, 北嶋 隆, 伊藤 嘉浩, 美野 愛, 佐藤 美和, 尾崎 敏文

    日本整形外科学会雑誌   87 ( 8 )   S1380 - S1380   2013年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 可視光硬化ゼラチンとcollagen binding domain(CBD)-BMP4の併用による家兎骨軟骨組織修復効果

    馬崎 哲朗, 塩崎 泰之, 山根 健太郎, 香川 洋平, 篠原 健介, 吉田 晶, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    日本整形外科学会雑誌   87 ( 8 )   S1606 - S1606   2013年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 医学生の臨床実習充実化のために研修医が果たす役割 岡山大学病院初期研修医の学生教育に対する意識調査

    三好 智子, 片岡 仁美, 小比賀 美香子, 渡辺 文恵, 別府 治恵, 森 祐子, 山根 正修, 松川 昭博, 尾崎 敏文, 谷本 光音

    医学教育   44 ( Suppl. )   112 - 112   2013年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 臨床実習における臨床技術認定制度の導入 名札に張って分かる技術認定シールを作成

    山根 正修, 松川 昭博, 岡山大学医学部臨床系教育企画委員会

    医学教育   44 ( Suppl. )   144 - 144   2013年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 炎症・免疫機構の新基軸と疾病の病理 A型インフルエンザウイルス(H1N1)感染とMAPK経路

    松川 昭博, 伊藤 利洋

    日本病理学会会誌   102 ( 1 )   185 - 185   2013年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred-2発現ベクターの作製とその応用

    篠倉 美理, 木村 亮二朗, 伊藤 利洋, 松川 昭博

    日本病理学会会誌   102 ( 1 )   503 - 503   2013年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 1型自己免疫性膵炎におけるマクロファージの分布の検討

    内野 かおり, 能登原 憲司, 藤澤 真義, 和仁 洋治, 松川 昭博

    日本病理学会会誌   102 ( 1 )   439 - 439   2013年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Spred2欠損マウスは敗血症性抵抗性を示す

    板倉 淳哉, 伊藤 利洋, 佐藤 美和, 美野 愛, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   102 ( 1 )   433 - 433   2013年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 多彩な組織像を示す乳腺腺様嚢胞癌の3例

    大森 昌子, 豊田 博, 柳井 広之, 高田 尚良, 松川 昭博, 吉野 正

    日本病理学会会誌   102 ( 1 )   370 - 370   2013年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • T細胞Suppressor of Cytokine Signaling 5(SOCS5)の過剰発現はLPSトレランス効果を増強する

    伊藤 利洋, 板倉 淳哉, 佐藤 美和, 美野 愛, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   102 ( 1 )   326 - 326   2013年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 小腸腸間膜嚢胞腺癌の1例

    宇田 征史, 吉岡 貴裕, 伏見 卓郎, 佐々木 洸太, 松本 朝子, 村田 年弘, 松川 昭博

    日本臨床外科学会雑誌   74 ( 4 )   968 - 972   2013年4月

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    記述言語:日本語   出版者・発行元:日本臨床外科学会  

    症例は80歳,男性.直腸S状部癌の精査目的CT検査,MRI検査にて回腸腸間膜に長径12cmの一部に石灰化を伴い造影効果のある充実性成分を伴う嚢胞性腫瘤を認めた.小腸腸間膜嚢胞腺癌,重複腸管,変性したGIST等を鑑別診断とし手術を行った.腫瘤は回腸末端から40から50cmの腸間膜に位置し浸潤傾向はなく腸管切除することなく核出術にて完全切除を行えた.摘出した腫瘤は13×6×5cm,256gで病理検査にて充実性腫瘤部に癌細胞を認め他部位の嚢胞壁には正常の円柱上皮,高円柱状異型細胞への移行像を認め嚢胞腺癌と診断された.腸間膜嚢胞に発生する腸間膜嚢胞腺癌は極めてまれな疾患であるが,今回われわれは直腸S状部癌の術前精査にて偶然発見された小腸腸間膜嚢胞腺癌の1例を経験したので若干の文献的考察を加え報告する.(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=2013&ichushi_jid=J03156&link_issn=&doc_id=20130507160021&doc_link_id=10.3919%2Fjjsa.74.968&url=https%3A%2F%2Fdoi.org%2F10.3919%2Fjjsa.74.968&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

  • 硬組織接着性多糖誘導体リン酸化プルランの骨再生能の検討

    山根 健太郎, 塩崎 泰之, 馬崎 哲朗, 杉本 佳久, 瀧川 朋亨, 田中 雅人, 松川 昭博, 尾崎 敏文

    Journal of Spine Research   4 ( 3 )   575 - 575   2013年3月

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    記述言語:日本語   出版者・発行元:(一社)日本脊椎脊髄病学会  

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  • 妊娠中に発症し高度のネフローゼを呈した急性糸球体腎炎の生検例

    伏見 聡一郎, 桑本 聡史, 野坂 加苗, 徳安 祐輔, 中本 周, 上浦 望, 尾田 高志, 城 謙輔, 松川 昭博

    診断病理   30 ( 1 )   66 - 70   2013年1月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

    症例は妊娠中の20代女性。高度のネフローゼ症候群を呈し、腎生検が行われた。組織学的に糸球体の腫大と管内への炎症細胞浸潤を認めた。免疫染色では有意な所見は得られなかったが、組織化学的に糸球体でplasmin活性が認められ、溶連菌感染後急性糸球体腎炎と考えられた。本例の鑑別診断においてplasmin活性の酵素組織化学的所見が意義あると考えられた。文献的考察も加えて報告する。(著者抄録)

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  • マウスにおける改変型成長因子Collagen binding domain BMP4の効果

    塩崎 泰之, 馬崎 哲朗, 吉田 晶, 山根 健太郎, 田中 雅人, 松川 昭博, 尾崎 敏文

    移植   47 ( 6 )   498 - 498   2012年12月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • コラーゲン結合性骨形成蛋白質BMP4の骨芽細胞に対する影響

    吉田 晶, 古松 毅之, 塩崎 泰之, 馬崎 哲朗, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    移植   47 ( 6 )   498 - 498   2012年12月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • マウスを用いた遺伝子改変成長因子Collagen binding domain BMP4の効果

    塩崎 泰之, 馬崎 哲郎, 山根 健太郎, 吉田 靖弘, 中村 真理子, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文, 松川 昭博

    日本バイオマテリアル学会大会予稿集   シンポジウム2012   269 - 269   2012年11月

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    記述言語:日本語   出版者・発行元:日本バイオマテリアル学会  

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  • 家兎骨軟骨欠損モデルにおける可視光硬化ゼラチンの骨軟骨組織修復の効果

    馬崎 哲朗, 塩崎 泰之, 吉田 晶, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    日本バイオマテリアル学会大会予稿集   シンポジウム2012   325 - 325   2012年11月

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    記述言語:日本語   出版者・発行元:日本バイオマテリアル学会  

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  • ウサギの骨欠損モデルにおいてコラーゲン結合性骨形成蛋白質は骨形成を促進する

    吉田 晶, 塩崎 泰之, 馬崎 哲朗, 古松 毅之, 松川 昭博, 中村 真理子, 吉田 靖弘, 北島 隆, 伊藤 嘉浩, 尾崎 敏文

    日本バイオマテリアル学会大会予稿集   シンポジウム2012   270 - 270   2012年11月

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    記述言語:日本語   出版者・発行元:日本バイオマテリアル学会  

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  • 炎症の発現・制御におけるサイトカインシグナル伝達

    松川 昭博

    小児感染免疫   24 ( 3 )   303 - 307   2012年10月

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    記述言語:日本語   出版者・発行元:日本小児感染症学会  

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  • ウサギの骨欠損モデルにおけるコラーゲン結合性骨形成蛋白質の有効性

    馬崎 哲朗, 塩崎 泰之, 吉田 晶, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    日本整形外科学会雑誌   86 ( 8 )   S1071 - S1071   2012年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • ウサギ尺骨骨欠損モデルを用いたリン酸化プルランの骨再生能の検討

    山根 健太郎, 塩崎 泰之, 馬崎 哲朗, 吉田 晶, 杉本 佳久, 瀧川 朋亨, 田中 雅人, 松川 昭博, 尾崎 敏文

    日本整形外科学会雑誌   86 ( 8 )   S1349 - S1349   2012年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • コラーゲン結合型BMP4の骨芽細胞に対する影響

    吉田 晶, 馬崎 哲朗, 塩崎 泰之, 古松 毅之, 松川 昭博, 中村 真理子, 吉田 靖弘, 北嶋 隆, 伊藤 嘉浩, 尾崎 敏文

    日本整形外科学会雑誌   86 ( 8 )   S1343 - S1343   2012年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 「患者から学ぶ」臨床実習のための授業 私たち学習者ができること

    光田 栄子, 徳増 一樹, 小林 宏紀, 中村 千華, 松谷 歩, 後藤 良子, 清水 大, 松本 聖, 松川 昭博, 松岡 賢市, 久本 晃子

    医学教育   43 ( Suppl. )   157 - 157   2012年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 岡山大学医学部医学科クリニカルクラークシップハンドブック

    徳増 一樹, 光田 栄子, 小林 宏紀, 中村 千華, 清水 大, 大西 康博, 羽田 佑, 後藤 良子, 和泉 誠人, 碓井 喜明, 波戸本 理絵, 高橋 達也, 多屋 彗, 松谷 歩, 松川 昭博

    医学教育   43 ( Suppl. )   158 - 158   2012年7月

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    記述言語:日本語   出版者・発行元:(一社)日本医学教育学会  

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  • 抗酸菌性肉芽腫形成時の混合型白血病(MLL)の病理学的役割(Pathological role of mixed lineage leukemia (MLL) during mycobacterial granuloma formation)

    伊藤 利洋, 板倉 淳哉, 伏見 聡一郎, 荻野 哲也, Kunkel Steven, 松川 昭博

    日本病理学会会誌   101 ( 1 )   279 - 279   2012年3月

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    記述言語:英語   出版者・発行元:(一社)日本病理学会  

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  • 炎症の発現・制御におけるサイトカインシグナル伝達

    松川 昭博

    日本病理学会会誌   101 ( 1 )   175 - 175   2012年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 大腸癌における組織中のCD204陽性M2マクロファージの浸潤様式の検討

    松本 正樹, 左村 和磨, 加藤 恵美, 伏見 聡一郎, 板倉 淳哉, 伊藤 利洋, 荻野 哲也, 松川 昭博

    日本病理学会会誌   101 ( 1 )   441 - 441   2012年3月

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  • リンパ節生検でKaposi肉腫と多中心型Castleman病と診断したAIDSの1例

    伏見 聡一郎, 能登原 憲司, 板倉 淳哉, 伊藤 利洋, 荻野 哲也, 松川 昭博, 石川 典由, 中本 周

    日本病理学会会誌   101 ( 1 )   378 - 378   2012年3月

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  • 酸化ストレスによる白血病細胞の分化とERKのリン酸化の修飾

    荻野 哲也, 平 麻美, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   101 ( 1 )   374 - 374   2012年3月

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  • Intratarsal keratinous cyst of the Meibomian glandの2例

    内野 かおり, 藤澤 真義, 松川 昭博

    日本病理学会会誌   101 ( 1 )   296 - 296   2012年3月

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  • インフルエンザ感染におけるThioredoxin binding protein 2(TBP-2)の役割

    八代 将登, 山田 睦子, 藤井 洋輔, 斉藤 有希恵, 長岡 義晴, 津下 充, 山下 信子, 塚原 宏一, 松川 昭博, 森島 恒雄

    日本小児科学会雑誌   116 ( 2 )   240 - 240   2012年2月

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  • 肝RFA後に広範な肉芽組織を形成した1例

    原田 聡介, 郷原 英夫, 芝本 健太郎, 井石 龍比古, 金澤 右, 内海 方嗣, 松田 浩明, 八木 孝仁, 中村 進一郎, 伏見 聡一郎, 松川 昭博

    Japanese Journal of Radiology   30 ( Suppl.I )   69 - 69   2012年2月

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    記述言語:日本語   出版者・発行元:(公社)日本医学放射線学会  

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  • 虚血再灌流肺障害にはMAPK経路の活性化が関与する

    岡田真典, 山根正修, 伊賀徳周, 原田昌明, 西川仁士, 平山伸, 山本澄治, 脇直久, 三好健太郎, 大谷真二, 杉本誠一郎, 宗淳一, 豊岡伸一, 大藤剛宏, 松川昭博, 三好新一郎

    日本肺および心肺移植研究会プログラム・抄録集   28th   15   2012年

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    記述言語:日本語  

    J-GLOBAL

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  • 赤白血病細胞株K562における細胞分化のレドックス制御

    荻野 哲也, 平 麻美, 松川 昭博

    日本病理学会会誌   100 ( 1 )   372 - 372   2011年3月

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  • Concanavalin A肝炎におけるCD4+T細胞SOCS1の役割

    岡 浩介, 高須賀 裕樹, 伏見 聡一郎, 松川 昭博

    日本病理学会会誌   100 ( 1 )   495 - 495   2011年3月

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  • 管周囲性の増殖パターンを示す前立腺low grade stromal sarcomaの一例

    伏見 聡一郎, 板倉 淳哉, 伊藤 利洋, 平 麻美, 荻野 哲也, 柳井 広之, 松川 昭博

    日本病理学会会誌   100 ( 1 )   438 - 438   2011年3月

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  • 画像上多発肝腫瘤と認識された大腸癌化学療法中の肝類洞病変

    内野 かおり, 藤澤 真義, 能登原 憲司, 松川 昭博

    日本病理学会会誌   100 ( 1 )   382 - 382   2011年3月

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  • 【Th17細胞分化の誘導と抑制】Th17細胞のSOCSによる制御

    松川 昭博

    臨床免疫・アレルギー科   54 ( 4 )   418 - 423   2010年10月

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    記述言語:日本語   出版者・発行元:(有)科学評論社  

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  • 肝移植後早期合併症 移植後真菌感染症で特異な臨床症状のみられた劇症肝不全の1例

    岡島 英明, 岩崎 寛智, 須田 博子, 林田 信太郎, 井田 智, 武市 卒之, 上野 美佳子, 阿曽沼 克弘, 松川 昭博, 猪山 賢一, 猪股 裕紀洋

    臨牀と研究   87 ( 9 )   1316 - 1317   2010年9月

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    記述言語:日本語   出版者・発行元:大道学館出版部  

    38歳男。高度の黄疸を伴った肝機能異常を認め、肝性昏睡が出現したため持続血液濾過透析、血漿交換を行うも改善なく、弟をドナーとした緊急肝移植を行った。術後早期にAST、ALT、T-Bilの上昇を認め、急性拒絶反応と考えてステロイドパルスを行った。術後38日目にCRPが上昇し、胸部X線で両肺野に浸潤影がみられた。腹水からカンジダ陽性、サイトメガロウイルス早期抗原陽性細胞を認め、免疫抑制剤を中止し、抗菌療法、抗真菌療法、抗ウイルス療法を行った。術後70日には感染は改善したが、AST、ALT、T-Bilが再上昇し、免疫抑制剤を再開した。術後121日目に痙攣を伴った意識消失が出現し、ショック状態に陥り、頭部CTで多数の低吸収域を認め、心電図では完全房室ブロックで、緊急ペースメーカーを挿入した。しかし、心不全状態は持続し、多臓器不全に陥り術後126日目に死亡した。剖検所見で脳および心筋に真菌塊による塞栓形成を認めた。

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  • T細胞特異的SOCS5過剰発現はマウス抗II型コラーゲン抗体関節炎において関節炎を遷延させる

    高畑 智宏, 松川 昭博, 西田 圭一郎, 尾崎 敏文

    日本整形外科学会雑誌   84 ( 8 )   S1145 - S1145   2010年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • Choroid plexus carcinomaの2例

    安藤 翠, 市村 浩一, 田中 健大, 柳井 広之, 松川 昭博, 吉野 正

    日本病理学会会誌   99 ( 1 )   354 - 354   2010年3月

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  • セルブロック法併用で診断しえた膵腫瘍の2症例 転移性膵腫瘍と原発性膵内分泌腫瘍

    井上 博文, 藤田 勝, 松岡 博美, 今井 みどり, 那須 篤子, 市村 浩一, 田中 健大, 柳井 広之, 大原 信哉, 松川 昭博

    日本臨床細胞学会雑誌   49 ( Suppl.1 )   276 - 276   2010年3月

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  • 著明な細胞外粘液とsignet ring cell carcinomaからなる結節を形成したinvasive lobular carcinomaの一例

    大森 昌子, 柳井 広之, 豊田 博, 松川 昭博

    日本病理学会会誌   99 ( 1 )   341 - 341   2010年3月

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  • 酸化ストレスによる白血病細胞の分化誘導修飾

    荻野 哲也, 平 麻美, 松川 昭博

    日本病理学会会誌   99 ( 1 )   274 - 274   2010年3月

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  • マクロファージのシグナル伝達 ガレクチン9によるマクロファージのFcgレセプター発現制御とコラーゲン抗体誘導関節炎への効果(Galectin-9 ameliorates immune complex-induced arthritis by regulating FcgR expression on macrophages)

    有川 智博, 渡邊 浩大, 松川 昭博, 大水 総一, 仁木 敏朗, 山内 清明, 平島 光臣

    日本免疫学会総会・学術集会記録   39   105 - 105   2009年11月

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    記述言語:英語   出版者・発行元:(NPO)日本免疫学会  

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  • 子宮頸癌の最近の知見と細胞診 腺系病変を中心に 子宮頸部の神経内分泌腫瘍 組織分類と細胞像

    柳井 広之, 藤田 勝, 田中 正純, 戸井 紳二, 吉野 正, 松川 昭博

    日本臨床細胞学会雑誌   48 ( Suppl.2 )   433 - 433   2009年9月

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  • 妊娠期にみられた乳腺血管肉腫の1例

    松岡 博美, 藤田 勝, 今井 みどり, 井上 博文, 森下 由美子, 那須 篤子, 大森 昌子, 市村 浩一, 柳井 広之, 松川 昭博

    日本臨床細胞学会雑誌   48 ( Suppl.2 )   559 - 559   2009年9月

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  • マウス抗II型コラーゲン抗体関節炎におけるTh1/2反応とSOCS3・SOCS5による制御

    高畑 智宏, 松川 昭博, 西田 圭一郎, 尾崎 敏文

    日本整形外科学会雑誌   83 ( 8 )   S1120 - S1120   2009年8月

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  • 当院における子宮内膜細胞診の疑陽性判定症例の再検討

    井上 博文, 藤田 勝, 松岡 博美, 今井 みどり, 那須 篤子, 森下 由美子, 市村 浩一, 大森 昌子, 大原 信哉, 柳井 広之, 松川 昭博, 則松 良明

    日本臨床細胞学会中国四国連合会会報   ( 24 )   31 - 31   2009年7月

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    記述言語:日本語   出版者・発行元:日本臨床細胞学会-中国四国連合会  

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  • 超音波内視鏡下膵穿刺吸引細胞診における検体の取り扱いとその有用性(第二報)

    井上 博文, 藤田 勝, 松岡 博美, 今井 みどり, 那須 篤子, 森下 由美子, 市村 浩一, 大森 昌子, 大原 信哉, 柳井 広之, 松川 昭博, 越川 卓

    日本臨床細胞学会中国四国連合会会報   ( 24 )   39 - 39   2009年7月

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    記述言語:日本語   出版者・発行元:日本臨床細胞学会-中国四国連合会  

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  • 免疫学 感染とサイトカイン・サイトカイン情報伝達

    松川 昭博

    医学のあゆみ   229 ( 12 )   1157 - 1158   2009年6月

  • TTF-1陽性を示したgliosarcomaの一例

    伏見 聡一郎, 宮田 元, 中本 周, 荻野 哲也, 松川 昭博, 大浜 栄作

    日本病理学会会誌   98 ( 1 )   296 - 296   2009年3月

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  • 動脈瘤破裂で緊急入院し敗血症ショックで死亡した神経線維腫症I型(Neurofibromatosis 1:NF1)の一例

    岡崎 泰昌, 飛田 陽, 板倉 淳哉, 荻野 哲也, 松川 昭博

    日本病理学会会誌   98 ( 1 )   290 - 290   2009年3月

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  • モノクロラミン誘発性アポトーシスにおけるinhibitor of apoptosis proteinおよびp53AIP1の変化

    荻野 哲也, 大森 昌子, 松川 昭博

    日本病理学会会誌   98 ( 1 )   279 - 279   2009年3月

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  • 膀胱内進展により自然尿中に腫瘍細胞を認めた乳房外Paget病の1例

    藤田 勝, 松岡 博美, 井上 博文, 今井 みどり, 森下 由美子, 那須 篤子, 市村 浩一, 柳井 広之, 松川 昭博

    日本臨床細胞学会雑誌   48 ( Suppl.1 )   267 - 267   2009年3月

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  • T細胞SOCSとエンドトキシン(LPS)トレランス

    小畠 千晶, 若林 宏, 伏見 聡一郎, 原 淳子, 松川 昭博

    日本病理学会会誌   98 ( 1 )   398 - 398   2009年3月

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  • 組織球性絨毛間腔炎の3例

    柳井 広之, 江口 香, 吉野 正, 松川 昭博

    日本病理学会会誌   98 ( 1 )   373 - 373   2009年3月

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  • T細胞SOCS3過剰発現による敗血症免疫調節

    松川 昭博, 原 淳子, 渡辺 治之, 荒嶋 康晴, 伏見 聡一郎

    日本病理学会会誌   98 ( 1 )   365 - 365   2009年3月

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  • マウス抗II型コラーゲン抗体関節炎におけるTh1/2反応とSOCS3・SOCS5による制御

    高畑 智宏, 松川 昭博, 西田 圭一郎, 尾崎 敏文

    日本整形外科学会雑誌   82 ( 8 )   S1244 - S1244   2008年8月

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  • バルプロ酸は骨折治癒を促進する マウス骨折モデルを用いた検討

    久慈 怜, 高畑 智宏, 松川 昭博, 古松 毅之, 野田 知之, 尾崎 敏文

    日本整形外科学会雑誌   82 ( 8 )   S1260 - S1260   2008年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • ガレクチン9は敗血症抵抗性に働く

    松川 昭博, 原 淳子, 飛田 陽, 平島 光臣

    Inflammation and Regeneration   28 ( 4 )   361 - 361   2008年7月

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    記述言語:日本語   出版者・発行元:(一社)日本炎症・再生医学会  

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  • ガレクチン-9はC5aの産生阻害により抗コラーゲン抗体誘導関節炎を抑制する

    渡邊 浩大, 有川 智博, 坂田 研明, 坂田 敦子, 仁木 敏郎, 松川 昭博, 平島 光臣

    日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集   52回・17回   264 - 264   2008年4月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • マウス抗II型コラーゲン抗体関節炎におけるTh1/2/17反応とSOCS3・SOCS5による制御

    高畑 智宏, 松川 昭博, 西田 圭一郎, 尾崎 敏文

    日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集   52回・17回   385 - 385   2008年4月

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  • 病理解剖を行われたリウマチ性疾患患者14症例の検討

    若林 宏, 山中 龍太郎, 三宅 剛平, 高杉 幸司, 杉山 晃一, 山下 美鈴, 矢野 隆介, 相田 哲史, 槇野 博史, 松川 昭博

    日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集   52回・17回   286 - 286   2008年4月

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  • Tリンパ球依存性ConA肝炎におけるT細胞SOCS3の役割解明

    伏見 聡一郎, 高畑 智宏, 若林 宏, 荻野 哲也, 松川 昭博

    日本病理学会会誌   97 ( 1 )   255 - 255   2008年3月

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  • 炎症研究の新しい展開 炎症制御とSOCS(Suppressors of cytokine signaling)

    松川 昭博

    日本病理学会会誌   97 ( 1 )   141 - 141   2008年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 唾液腺腺房細胞癌の二症例

    今井 みどり, 藤田 勝, 井上 博文, 松岡 博美, 森下 由美子, 岡崎 泰昌, 大森 昌子, 柳井 広之, 松川 昭博, 吉野 正

    日本臨床細胞学会雑誌   47 ( Suppl.1 )   183 - 183   2008年3月

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    記述言語:日本語   出版者・発行元:(公社)日本臨床細胞学会  

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  • 胃癌術後化学療法中、蓚酸カルシウムの著明な沈着を伴うアスペルギルス肺炎で死亡した1例

    板倉 淳哉, 伏見 聡一郎, 荻野 哲也, 大森 昌子, 松川 昭博

    日本病理学会会誌   97 ( 1 )   398 - 398   2008年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 気管支腺上皮性乳頭腫の一例

    大森 昌子, 柳井 広之, 荻野 哲也, 松川 昭博, 吉野 正

    日本病理学会会誌   97 ( 1 )   375 - 375   2008年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • T細胞性白血病細胞株Jurkat細胞におけるモノクロラミン誘発性アポトーシスのメカニズム

    荻野 哲也, 大森 昌子, 松川 昭博

    日本病理学会会誌   97 ( 1 )   310 - 310   2008年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 腹水中に腫瘍細胞を認めた乳腺小葉癌の1例.

    藤田勝, 松岡博美, 井上博文, 今井みどり, 森下由美子, 大森昌子, 市村浩一, 柳井広之, 大原信哉, 松川昭博

    日本臨床細胞学会岡山支部会誌   27   36 - 37   2008年

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  • 超音波内視鏡下戦死吸引細胞診が有用であった膵内分泌腫瘍の二例

    井上博文, 藤田勝, 松岡博美, 今井みどり, 森下由美子, 市村浩一, 大森昌子, 大原伸哉, 柳井広之, 松川昭博

    日本臨床細胞学会雑誌   47   512   2008年

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  • 酸化ストレス 細胞・臓器機能への影響とその制御 好中球由来のオキシダントによる細胞の機能修飾

    荻野 哲也, Tin Aung Than, 大森 昌子, 寳迫 睦美, 平松 万尚, 尾崎 倫孝, 松川 昭博, 岡田 茂

    Organ Biology   14 ( 3 )   213 - 213   2007年10月

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    記述言語:日本語   出版者・発行元:(一社)日本臓器保存生物医学会  

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  • T細胞SOCS3によるマウス敗血症モデルの自然免疫調節

    松川 昭博, 伏見 聡一郎, 若林 宏, 渡辺 弘之

    Inflammation and Regeneration   27 ( 4 )   420 - 420   2007年7月

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    記述言語:日本語   出版者・発行元:(一社)日本炎症・再生医学会  

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  • T細胞SOCS3過剰発現は薬剤誘発性劇症肝炎を悪化させる

    松川 昭博, 沼田 亨祐, 伊藤 隆明

    日本病理学会会誌   96 ( 1 )   171 - 171   2007年2月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • Nuclear palisadingを伴うDFSPから発生したfibrosarcomaの一例

    大森 昌子, 柳井 広之, 荻野 哲也, 松川 昭博, 吉野 正

    日本病理学会会誌   96 ( 1 )   337 - 337   2007年2月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 肺塞栓症にて死亡した上大静脈原発の血管肉腫の一剖検例

    伏見 聡一郎, 荻野 哲也, 平松 万尚, 大森 昌子, 柳井 広之, 松川 昭博

    日本病理学会会誌   96 ( 1 )   316 - 316   2007年2月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • モノクロラミンによるカルシウム輸送の修飾

    荻野 哲也, 大森 昌子, 松川 昭博

    日本病理学会会誌   96 ( 1 )   289 - 289   2007年2月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 関節リウマチ〜臨床解析と新治療 安定性ガレクチン-9は慢性関節リウマチのラット/マウスモデルを抑制する(Stable Galectin-9 suppresses rat/murine models of rheumatoid arthritis)

    Sakata Ken-mei, Seki Masako, Takashita Keisuke, Ito Kanako, Arikawa Tomohiro, Matsukawa Akihiro, Sakata Atsuko, Hirashima Mitsuomi

    日本免疫学会総会・学術集会記録   36   290 - 290   2006年11月

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    記述言語:英語   出版者・発行元:(NPO)日本免疫学会  

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  • 急性大動脈解離の破裂により死亡した若年女性の1例

    美作 宗太郎, 大津 由紀, 幸松 宏恵, 是枝 亜子, 米満 孝聖, 恒成 茂行, 松川 昭博, 橋谷田 真樹, 舟山 眞人

    日本法医学雑誌   60 ( 2 )   197 - 197   2006年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本法医学会  

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  • 動脈硬化による冠動脈のリモデリングに及ぼす中膜の拡大と脆弱化の影響

    塩見 雅志, 山田 悟士, 板部 洋之, 松川 昭博, 伊藤 隆

    日本動脈硬化学会総会プログラム・抄録集   38回   238 - 238   2006年7月

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    記述言語:日本語   出版者・発行元:(一社)日本動脈硬化学会  

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  • Atypical teratoid rhabdoid tumor(AT/RT)の一例

    大森 昌子, 柳井 広之, 荻野 哲也, 井上 智, 松川 昭博, 吉野 正

    日本病理学会会誌   95 ( 1 )   312 - 312   2006年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 摂食抑制ペプチド,ニューロメジンUの炎症における役割の解明

    森山 麻衣子, 井上 博雅, 松川 昭博, 佐藤 貴弘, 加納 龍彦, 吉村 昭彦, 児島 将康

    日本内分泌学会雑誌   82 ( 1 )   95 - 95   2006年4月

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    記述言語:日本語   出版者・発行元:(一社)日本内分泌学会  

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  • ジメチルアセチル-β-シクロデキストリンによるエンドトキシンショック抑制の機構解明

    本山 敬一, 有馬 英俊, 松川 昭博, 平山 文俊, 上釜 兼人

    日本薬学会年会要旨集   126年会 ( 3 )   139 - 139   2006年3月

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    記述言語:日本語   出版者・発行元:(公社)日本薬学会  

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  • 自然免疫/炎症とサイトカインシグナル伝達.

    松川昭博

    岡山医誌   118,109-112   2006年

  • 炎症とサイトカインシグナル伝達.

    松川昭博

    岡山医誌   118,185-186   2006年

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  • 安定化ガレクチン9はコラーゲン関節炎重症度を軽減させる

    積 正子, 竹下 慶亮, 坂田 研明, 山中 徹, 松川 昭博, 坂田 敦子, 平島 光臣

    日本免疫学会総会・学術集会記録   35   253 - 253   2005年11月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • 関節リウマチ滑膜組織におけるガレクチン9発現と滑膜細胞アポトーシス誘導

    坂田 研明, 積 正子, 山中 徹, 松川 昭博, 坂田 敦子, 平島 光臣

    日本免疫学会総会・学術集会記録   35   253 - 253   2005年11月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • 悪性腱鞘巨細胞腫と鑑別を要した手に発生した平滑筋肉腫の一例

    川添 泰弘, 薬師寺 俊剛, 岩本 克也, 佐藤 広生, 前川 剛士, 林田 実, 松川 昭博

    整形外科と災害外科   54 ( 3 )   595 - 599   2005年9月

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    記述言語:日本語   出版者・発行元:西日本整形・災害外科学会  

    58歳男.近医にて1年前に右手掌軟部腫瘤に対して摘出術が施行され,4ヵ月前に局所再発に対して再度摘出術が施行され,平滑筋肉腫である腱鞘巨細胞腫と診断された.今回,再び局所に腫瘤が出現したため紹介来院となった.臨床経過・局所所見・MRI所見などより腱鞘巨細胞腫と診断し摘出術を施行した.摘出標本の病理組織学的所見と平滑筋肉腫との鑑別目的の免疫染色結果から悪性腱鞘巨細胞腫と診断された.CTによる全身検索にて肺野に多発性結節性病変を認め,肺転移と診断し化学療法を開始した.悪性腱鞘巨細胞腫と平滑筋肉腫の鑑別には免疫組織化学的検索が有用であった.手に悪性腫瘍が発生することは比較的稀であるが,術前の良性・悪性の鑑別は慎重に行うべきであるものと考えられた

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    その他リンク: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2005&ichushi_jid=J00766&link_issn=&doc_id=20050927120047&doc_link_id=10.5035%2Fnishiseisai.54.595&url=https%3A%2F%2Fdoi.org%2F10.5035%2Fnishiseisai.54.595&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

  • 安定化ガレクチン9による関節リウマチ滑膜細胞死誘導と関節炎モデル治療の試み

    坂田 研明, 積 正子, 伊藤 佳奈子, 有川 智博, 税田 直樹, 山中 徹, 松川 昭博, 坂田 敦子, 平島 光臣

    アレルギー   54 ( 8-9 )   1087 - 1087   2005年9月

  • 薬剤誘発性劇症肝炎におけるSOCS3の分子基盤 治療分子標的としての可能性

    松川 昭博, 沼田 亨祐, 渡辺 弘之, 伊藤 隆明, 久保 允人

    炎症・再生   25 ( 4 )   394 - 394   2005年7月

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    記述言語:日本語   出版者・発行元:(一社)日本炎症・再生医学会  

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  • 肺におけるPML蛋白質,SUMO-1の発現

    伊藤 隆明, 宇高 直子, 松川 昭博

    日本病理学会会誌   94 ( 1 )   295 - 295   2005年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 肺癌細胞株におけるSTATの発現

    宇高 直子, 松川 昭博, 伊藤 隆明

    日本病理学会会誌   94 ( 1 )   202 - 202   2005年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • ガレクチン9による抗腫瘍効果

    松川 昭博, 伊藤 隆明, 平島 光臣

    日本病理学会会誌   94 ( 1 )   234 - 234   2005年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • SOCS3による薬剤誘発性劇症肝炎の調節機構の解明

    沼田 亨祐, 渡辺 弘之, 伊藤 隆明, 松川 昭博

    日本病理学会会誌   94 ( 1 )   229 - 229   2005年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • マウス敗血症モデルを用いたSOCS5による自然免疫調節機構の解析

    渡辺 弘之, 沼田 亨祐, 伊藤 隆明, 松川 昭博

    日本病理学会会誌   94 ( 1 )   227 - 227   2005年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • エンドトキシンショックに対するジメチルアセチル-β-シクロデキストリンの抑制効果

    本山 敬一, 有馬 英俊, 松川 昭博, 三宅 健介, 西本 洋志, 平山 文俊, 上釜 兼人

    薬剤学: 生命とくすり   65 ( Suppl. )   118 - 118   2005年3月

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    記述言語:日本語   出版者・発行元:(公社)日本薬剤学会  

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  • 自然免疫/炎症の発現・制御に関わるサイトカインとシグナル伝達因子の機能解明

    松川 昭博

    日本病理学会会誌   93 ( 2 )   13 - 13   2004年10月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • マクロファージ・好中球特異的Stat3欠損マウスにみる獲得免疫反応

    松川 昭博, 伊藤 隆明

    炎症・再生   24 ( 4 )   515 - 515   2004年7月

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    記述言語:日本語   出版者・発行元:(一社)日本炎症・再生医学会  

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  • 肺転移をきたした悪性腱鞘巨細胞腫の1例

    川添 泰弘, 薬師寺 俊剛, 松川 昭博, 佐藤 広生, 高木 克公

    日本整形外科学会雑誌   78 ( 6 )   S713 - S713   2004年6月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • マクロファージ・好中球に発現するStat3によるTh1・Th2型獲得免疫制御

    松川 昭博, 伊藤 隆明

    日本病理学会会誌   93 ( 1 )   225 - 225   2004年5月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 生体肝移植術後の真菌感染症による感染性完全房室ブロック

    岡島 英明, 吉元 和彦, 小寺 厚志, 武市 卒之, 上野 美佳子, 阿曽沼 克弘, 河野 宏明, 松川 昭博, 猪山 賢一, 猪股 裕紀洋

    日本外科学会雑誌   105 ( 臨増 )   594 - 594   2004年3月

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    記述言語:日本語   出版者・発行元:(一社)日本外科学会  

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  • 腹腔常在マクロファージに発現するStat3による急性炎症制御作用

    松川 昭博, 竹田 潔, 審良 静男

    日本免疫学会総会・学術集会記録   33   135 - 135   2003年11月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • 敗血性腹膜炎モデルにおけるCCケモカインリセプター8の機能解析

    松川 昭博, 佐野 元市郎, 前田 貴子, Kunkel Steven, Lira Sergio

    炎症・再生   23 ( 6 )   473 - 473   2003年11月

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    記述言語:日本語   出版者・発行元:(一社)日本炎症・再生医学会  

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  • 【痛風・高尿酸血症とサイトカイン】痛風関節炎のメカニズムとサイトカイン 動物モデルにおける尿酸結晶誘発関節炎 サイトカイン・ケモカインの産生とそのネットワーク

    松川 昭博

    高尿酸血症と痛風   11 ( 2 )   147 - 151   2003年9月

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    記述言語:日本語   出版者・発行元:(株)メディカルレビュー社  

    痛風関節炎は,高尿酸血症を背景に関節周囲に沈着した尿酸結晶(MSU結晶)が関節内に遊離して起こる急性関節炎であり,局所に浸潤した白血球,特に好中球がMSU結晶の貪食と消化に働く.この炎症反応は,MSU結晶の刺激によってホストが産生する種々の炎症メディエーターによって起こるが,近年のin vitro及びin vivoの研究から,関節炎発症におけるサイトカインの役割が明らかになってきた.そこで,ウサギ尿酸結晶誘発関節炎を用いた著者等の解析を中心に,関節炎誘発に関わるサイトカイン・ケモカインとそのネットワークについて最近の知見を交えて述べた

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  • 椎間板細胞はヘルニア発生早期に炎症性サイトカインを発現する 新たな椎間板ヘルニアモデルを用いて

    吉田 正一, 中村 孝文, 松川 昭博, 瀬井 章, 菊池 太朗, 水溜 正也, 高木 克公

    日本整形外科学会雑誌   77 ( 8 )   S956 - S956   2003年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 【好中球と皮膚疾患】好中球と炎症

    松川 昭博

    Derma.   ( 75 )   1 - 7   2003年6月

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    記述言語:日本語   出版者・発行元:(株)全日本病院出版会  

    生体に微生物の侵入などの異変がおこると,好中球はただちに内皮細胞間隙を割り込んで血管外へ遊出し,局所に浸潤する.浸潤した好中球は微生物を認識・貪食し,その酸素依存性及び非依存性の殺菌機構により消化する.即ち,好中球浸潤は炎症反応で最も顕著な細胞反応であり,浸潤した好中球は一次生体防御系の上で中心的な役割を担っている.しかし,活性化された好中球から放出される種々の因子は必然的に正常なホストの組織傷害をも伴う.このように,本来は防御系に働く炎症反応が自己組織の傷害を量的・時間的に過剰に引き起こす場合,医学的には病的現象としての「炎症」ととらえられ,治療の対象となる

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  • CXCケモカインIL-8とGROの異なるin vivo作用

    藤原 一徳, 松川 昭博, 大河原 進, 吉永 秀

    日本免疫学会総会・学術集会記録   31   306 - 306   2001年12月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • 急性肝障害時にみられるmacrophage-derived chemokine(MDC,CCL22)の抗炎症作用

    松川 昭博, Lukacs Nicholas, Kunkel Steven, 吉永 秀

    日本免疫学会総会・学術集会記録   31   312 - 312   2001年12月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • 若年性多発性硝子化線維腫症(Juvenile hyaline fibromatosis)の1症例

    本田由美, 大河原進, 猪山賢一, 松川昭博, 吉永秀

    日本病理学会雑誌   2000年

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  • 【高尿酸血症と痛風】重要性を増した合併症の治療と対策 痛風関節炎のメカニズム

    松川 昭博

    Medical Practice   16 ( 7 )   1113 - 1116   1999年7月

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    記述言語:日本語   出版者・発行元:(株)文光堂  

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  • 大腿骨後顆に高度なosteolysisをきたしたTKAの1例

    桑原 公倫, 白石 稔, 水田 博志, 中村 英一, 高木 克公, 吉田 正一, 松川 昭博

    整形外科と災害外科   48 ( 2 )   383 - 390   1999年3月

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    記述言語:日本語   出版者・発行元:西日本整形・災害外科学会  

    66歳女,変形性膝関節症にてMg-II,セメントレス人工膝関節置換術を施行し,4年後より膝関節腫脹と疼痛を来し,X線像で大腿骨後顆にosteolysisを認めた.再置換術を施行した際,大腿骨内側顆後方と外側顆後方に各30×20×15mm,15×15×10mm大の骨欠損と,滑膜増生,metallosis,膝蓋骨面のHDP及びtibia surfaceの磨耗を認めた

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    その他リンク: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=1999&ichushi_jid=J00766&link_issn=&doc_id=19990330030010&doc_link_id=%2Fdl8ortra%2F1999%2F004802%2F010%2F0383-0390%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fdl8ortra%2F1999%2F004802%2F010%2F0383-0390%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • Propionibacterium acnesによる実験的肺肉芽腫形成と単球/マクロファージ・リンパ球集簇に関するMCP-1の役割

    一安 秀範, 菅 守隆, 彌永 和宏, 山本 太郎, 高橋 利弘, 松川 昭博, 吉永 秀, 安藤 正幸

    日本サルコイドーシス学会雑誌   18 ( 1 )   33 - 33   1998年11月

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    記述言語:日本語   出版者・発行元:日本サルコイドーシス  

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  • 痛風治療剤コルヒチンの作用機序 モデル動物を用いてのサイトカイン産生及び白血球機能評価

    松川 昭博

    リウマチ   38 ( 2 )   343 - 343   1998年4月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • ウサギ尿酸結晶誘発関節炎におけるTNFα,IL-1β,IL-8の産生とそのネットワーク

    松川 昭博, 吉永 秀

    プリン・ピリミジン代謝   21 ( 2 )   180 - 183   1997年12月

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    記述言語:日本語   出版者・発行元:(一社)日本痛風・尿酸核酸学会  

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  • 痛風・高尿酸血症の病態 尿酸塩による関節炎の病態

    松川 昭博, 吉永 秀

    Mebio   14 ( 9 )   56 - 62   1997年9月

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    記述言語:日本語   出版者・発行元:(株)メジカルビュー社  

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  • ウサギ尿酸結晶誘発関節炎におけるMCP-1の発現動態

    松川 昭博

    リウマチ   37 ( 2 )   261 - 261   1997年4月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • 実験関節炎におけるIL-1raの動態と役割

    松川 昭博, 福本 巧, 吉永 秀

    日本整形外科学会雑誌   70 ( 11 )   751 - 758   1996年11月

  • 尿酸結晶関節炎におけるIL-8の産生動態とその局在

    松川 昭博

    リウマチ   36 ( 2 )   247 - 247   1996年4月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • 抑制基調サーボ機構として機能する正常臓器内のIL-1 receptor antagonist

    松川 昭博

    日本病理学会会誌   85 ( 1 )   181 - 181   1996年3月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 好中球,マクロファージの活性化と組織障害:Interleukin-8, Monocyte Chemoattractant Protein-1の役割

    吉村 禎造, 松川 昭博, 山城 重雄

    化学療法の領域   12 ( 2 )   222 - 227   1996年1月

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    記述言語:日本語   出版者・発行元:(株)医薬ジャーナル社  

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  • 内因性IL-1 receptor antagonist(IL-1ra)は炎症自己制御因子として機能する

    福本 巧, 松川 昭博, 木村 真

    日本整形外科学会雑誌   69 ( 8 )   s1440 - s1440   1995年8月

  • 実験関節炎におけるIL-1raの動態と役割

    吉永 秀, 松川 昭博

    日本整形外科学会雑誌   69 ( 8 )   s1557 - s1557   1995年8月

  • in vivoにおけるONO-5046の好中球エラスターゼ活性抑制効果 LPSおよびIL-8誘導関節炎を用いて

    松川 昭博

    リウマチ   35 ( 2 )   356 - 356   1995年4月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • 黄色ブドウ球菌加熱死菌関節炎におけるTumor necrosis factor-α(TNF-α),Interleukin-1(IL-1)の役割

    木村 真, 松川 昭博, 枝光 淳

    日本整形外科学会雑誌   68 ( 8 )   s1497 - s1497   1994年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 炎症局所におけるIL-1receptor antagonist(IL-1ra)の意義

    松川 昭博

    リウマチ   34 ( 2 )   453 - 453   1994年4月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • LPS関節炎における軟骨破壊のメカニズム

    松川 昭博

    リウマチ   33 ( 6 )   710 - 710   1993年12月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • 抗ウサギIL-1レセプターアンタゴニスト・モノクローナル中和抗体の開発とこれを用いたIL-1活性の再検討

    松川 昭博, 大河原 進, 枝光 淳, 高本 克公, 吉永 秀

    日本免疫学会総会・学術集会記録   23   352 - 352   1993年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • ウサギLPS胸膜炎に伴う細胞浸潤と血管透過性亢進の誘導におけるIL-1、TNF-αの役割

    枝光 淳, 大河原 進, 松川 昭博, 高木 克公, 吉永 秀

    日本免疫学会総会・学術集会記録   23   353 - 353   1993年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本免疫学会  

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  • インターロイキンと病態 インターロイキン1,TNF

    松川 昭博, 大河原 進

    BIO medica   8 ( 9 )   703 - 707   1993年8月

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    記述言語:日本語   出版者・発行元:(株)北隆館  

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  • 尿酸結晶関節炎におけるIL-1,TNFαの関与

    松川 昭博

    日本整形外科学会雑誌   67 ( 8 )   s1271 - s1271   1993年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • IL-1レセプターアンタゴニスト

    松川 昭博, 吉永 秀

    Annual Review免疫   1993   110 - 117   1993年1月

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    記述言語:日本語   出版者・発行元:(株)中外医学社  

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  • ウサギLPS誘発関節炎におけるInterleukin-1 (IL-1)の役割 ウサギIL-1receptor antagonist (IL-1ra)を用いての炎症の解析

    松川 昭博

    リウマチ   32 ( 6 )   778 - 778   1992年12月

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    記述言語:日本語   出版者・発行元:(一社)日本リウマチ学会  

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  • 炎症局所で見出したIL-1抑制因子の構造と機能

    大河原 進, 松川 昭博

    病態生理   11 ( 12 )   962 - 966   1992年12月

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    記述言語:日本語   出版者・発行元:(株)永井書店  

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  • ウサギLipopolysaccharide (LPS)関節炎におけるInterleukin-1,Tumor necrosis factor-α (TNF-α)の役割

    松川 昭博

    日本整形外科学会雑誌   66 ( 8 )   S1356 - S1356   1992年8月

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    記述言語:日本語   出版者・発行元:(公社)日本整形外科学会  

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  • 炎症の場における好中球の蛋白合成能 特にIL-1,IL-1raの産生

    大河原 進, 松川 昭博, 吉永 秀

    月刊細胞   24 ( 6 )   220 - 224   1992年5月

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    記述言語:日本語   出版者・発行元:(株)ニュー・サイエンス社  

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  • 最近注目されている各種インヒビター IL-1レセプター・アンタゴニスト

    大河原 進, 松川 昭博, 枝光 淳

    臨床免疫   24 ( 5 )   607 - 618   1992年5月

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    記述言語:日本語   出版者・発行元:(有)科学評論社  

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  • LPS関節炎におけるInterleukin-1の役割

    松川 昭博

    日本病理学会会誌   81 ( 1 )   170 - 170   1992年4月

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    記述言語:日本語   出版者・発行元:(一社)日本病理学会  

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  • 侵襲と生体反応

    松川 昭博, 相良 孝昭, 吉永 秀

    外科と代謝・栄養   24 ( 4 )   457 - 464   1990年9月

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    記述言語:日本語   出版者・発行元:日本外科代謝栄養学会  

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  • 炎症とIL1

    大河原 進, 相良 孝昭, 松川 昭博

    自律神経   27 ( 4 )   369 - 374   1990年8月

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    記述言語:日本語   出版者・発行元:日本自律神経学会  

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  • タンパク合成能に依存した多核白血球の新しい機能

    相良 孝昭, 松川 昭博, 後藤 文正

    病態生理   9 ( 7 )   582 - 585   1990年7月

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    記述言語:日本語   出版者・発行元:(株)永井書店  

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  • 反復性膝蓋骨脱臼における大腿骨顆部骨性形態のレ線的検討

    松川 昭博, 水田 博志, 久保田 健治

    整形外科と災害外科   38 ( 4 )   1684 - 1687   1990年3月

  • 炎症から免疫応答へのシナップスとしてのサイトカイン

    後藤 久美子, 後藤 文正, 松川 昭博

    臨床免疫   22 ( 3 )   422 - 432   1990年3月

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    記述言語:日本語   出版者・発行元:(有)科学評論社  

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  • スポーツ選手における第2ケーラー病について

    松川 昭博, 水田 博志, 久保田 健治

    日本足の外科研究会雑誌   10   149 - 152   1989年7月

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    記述言語:日本語   出版者・発行元:(一社)日本足の外科学会  

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  • スポーツによる両膝前十字靱帯損傷の3例

    松川 昭博, 水田 博志, 久保田 健治

    臨床スポーツ医学   6 ( 別冊 )   278 - 280   1989年6月

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    記述言語:日本語   出版者・発行元:(株)文光堂  

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▼全件表示

講演・口頭発表等

  • Spred2 regulates cancer stemness in HCC cells, targeting on miR-506-3p and its downstream KLF4

    Tong Gao, Aye Moh Moh Aung, Masahiro Fujisawa, Toshiaki Ohara, Teizo Yoshimura, Sachio Ito, Akihiro Matsukawa

    第50回日本免疫学会総会 

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    開催年月日: 2021年12月8日 - 2021年12月10日

    会議種別:ポスター発表  

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  • Distinct subpopulations of the murine 4T1 breast cancer cells cooperate with cancer metastasis through Wnt/β-catenin signaling pathway by exosomal Wnt7a

    Chunning Li, Teizo Yoshimura, Akihiro Matsukawa

    第50回日本免疫学会総会 

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    開催年月日: 2021年12月8日 - 2021年12月10日

    会議種別:ポスター発表  

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  • コロナ禍における医学科1年次行動科学I~社会におけるコミュニケーション~の実施とアウトカム

    三好智子, 小崎吉訓, 越智可奈子, 吉田登志子, 山根正修, 赤穂宗一郎, 伊野英男, 大塚愛二, 松川昭博

    第53回日本医学教育学会大会 

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    開催年月日: 2021年7月30日 - 2021年7月31日

    会議種別:口頭発表(一般)  

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  • 医学科1年生における行動科学授業 「コロナ禍での医学生生活を考える」-コロナ禍での入学の現状と課題

    越智 可奈子, 三好 智子, 小崎 吉訓, 赤穂 宗一郎, 吉田 登志子, 山根 正修, 伊野 英男, 大塚 愛二, 松川 昭博

    第53回日本医学教育学会大会 

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    開催年月日: 2021年7月30日 - 2021年7月31日

    会議種別:口頭発表(一般)  

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  • 4T1乳癌モデルにおいてMCP-1産生を促す癌細胞・線維芽細胞間のクロストーク

    吉村禎造, 今村真悠, Tiantian Li, 田ミャオ, 李春寧, 藤澤真義, 松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:口頭発表(一般)  

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  • 乳癌における傍導管浸潤(periductal invasion)の臨床病理学的意義

    藤澤真義, 大森昌子, 松川昭博

    第110回日本病理学会総会 

     詳細を見る

    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:ポスター発表  

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  • 肺腺癌におけるSpred2の発現の検討と増殖、浸潤との関連

    太田陽子, 藤澤真義, 吉村禎造, IWayan S, ん和彦, 阪口政清, 豊岡伸一, 松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:ポスター発表  

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  • 癌関連線維芽細胞に対する鉄キレート剤の効果

    王宇沢, 大原利章, 李春寧, 田ミャオ, 小槙志保, 吉村禎造, 藤澤真義, 松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:ポスター発表  

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  • Spred2はHCCで幹細胞性をmiR-506-3pによって一部負に抑制する

    高桐、藤澤真義、大原利章、吉村禎造、王天一、伊藤佐智夫、松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:口頭発表(一般)  

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  • 異なる亜集団の腫瘍細胞から放出されたエクソソームWnt7aにより4T1細胞の転移は促進される

    李春寧、大原利章、藤澤真義、阪口政清、山本健一、田ミャオ、王宇沢、吉村禎造、松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:口頭発表(一般)  

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  • IgG4関連消化器病変の診断における胃生検の有用性

    内野かおり, 能登原憲司, 上原剛, 倉石康弘, 板倉淳哉, 松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:ポスター発表  

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  • HCC細胞のオートファジーにおけるSpred2の役割とERK活性化との関係

    王天一, 藤澤真義, 大原利章, 吉村禎造, 高桐, 松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:ポスター発表  

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  • 腫瘍環境のSpred2欠損は4T1乳がん細胞の増殖と転移を抑制する

    Miao Tian, 吉村禎造, 李春寧, 大原利章, 藤澤真義, 松川昭博

    第110回日本病理学会総会 

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    開催年月日: 2021年4月22日 - 2021年4月24日

    会議種別:ポスター発表  

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  • 先輩から後輩へ〜臨床実習は怖くない〜

    久保卓也, 池内綾介, 窪征宣, 三好智子, 松川昭博

    第52回日本医学教育学会 

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    開催年月日: 2020年7月17日 - 2020年7月18日

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  • 医学科における国際バカロレア教育修了者の強み〜医学科1年次の行動科学における評価より〜

    三好智子, 山根正修, 小崎吉訓, 佐藤明香, 万代康弘, 吉田登志子, Mahmood Sabina, 伊野英男, 大塚愛二, 松川昭博

    第52回日本医学教育学会 

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    開催年月日: 2020年7月17日 - 2020年7月18日

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  • 岡山大学医療教育学生会

    久保卓也, 橋本千名津, 松川昭博

    第52回日本医学教育学会 

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    開催年月日: 2020年7月17日 - 2020年7月18日

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  • 急激な経過をたどりdiffuse alveolar hemorrhageにて死亡したSLEの一例

    河原明奈, 藤澤真義, 松川昭博

    第108回日本病理学会総会 

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    開催年月日: 2020年4月16日 - 2020年4月18日

    会議種別:ポスター発表  

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  • 癌転移は,エキソソームの異なる細胞亜群からの放出によって調節される

    李春寧, 吉村禎造, 田ミョウ, 大原利章, 藤澤真義, 松川昭博

    第108回日本病理学会総会 

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    開催年月日: 2020年4月16日 - 2020年4月18日

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  • Spred2 deficiency exacerbated Concanavalin A-induced liver injury by attracting T cells via CXCL9/10

    孫翠明, 吉村禎造, 藤澤真義, 大原利章, 松川昭博

    第108回日本病理学会総会 

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    開催年月日: 2020年4月16日 - 2020年4月18日

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  • 食道癌の幹細胞性を制御する鉄キレート療法の開発

    大原利章, 鳴坂徹, Boyi Xing, Yuze Wang, 松川 昭博

    第108回日本病理学会総会 

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    開催年月日: 2020年4月16日 - 2020年4月18日

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  • Spred2 involved in tumor stemness maintenance down-regulates malignant potential of HepG2 HCC

    高桐, 吉村禎造, 大原利章, 藤澤真義, 松川昭博

    第108回日本病理学会総会 

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    開催年月日: 2020年4月16日 - 2020年4月18日

    会議種別:ポスター発表  

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  • 乳癌における血管浸潤の検索法:新規法(Elastin and collagen 4 double staining)と従来法との比較検討

    藤澤真義, 大森昌子, 松川昭博

    第108回日本病理学会総会 

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    開催年月日: 2020年4月16日 - 2020年4月18日

    会議種別:ポスター発表  

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  • Granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent and independent production of the chemokine monocyte chemoattractant protein -1 (MCP-1) by macrophages in the 4T1 murine breast cancer.

    Yoshimura T, Mukaida N, Matsukawa A

    第48回日本免疫学会総会 

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    開催年月日: 2019年12月11日

    会議種別:ポスター発表  

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  • 悪性症候群後に発症し、20年以上の経過後死亡した小脳性運動失調症の一剖検例

    千葉陽一, 吉井りつ, 野中和香子, 松川昭博, 佐藤明, 上野正樹

    第10回日本神経病理学会中国四国地方会 

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    開催年月日: 2019年11月23日 - 2019年11月24日

    会議種別:口頭発表(一般)  

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  • 簡略化した外科指導者養成講習会の実施

    山根正修, 松川昭博

    第51回日本医学教育学会 

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    開催年月日: 2019年7月26日 - 2019年7月27日

    会議種別:口頭発表(一般)  

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  • 学生による留学オリエンテーションのいろは

    久保卓也, 今村真悠, 住田まどか, 中村薫, 松川昭博

    第51回日本医学教育学会 

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    開催年月日: 2019年7月26日 - 2019年7月27日

    会議種別:口頭発表(一般)  

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  • 行動科学におけるらせん型カリキュラムの必要性

    三好智子, 山根正修, 飯田淳義, 万代康弘, 吉田登志子, 伊野英男, 那須保友, 松川昭博

    第51回日本医学教育学会 

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    開催年月日: 2019年7月26日 - 2019年7月27日

    会議種別:口頭発表(一般)  

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  • Fpr2-deficiency in Non-tumor Cells Decreases Lung Metastasis of 4T1 Murine Breast Cancer Cells

    吉村 禎造, Weiss Jonathan M, Li Chunning、Li Tiantian, Gong Wanghua, 松川 昭博, Wang Ji Ming

    第108回日本病理学会総会 

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    開催年月日: 2019年5月9日 - 2019年5月11日

    会議種別:口頭発表(一般)  

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  • マウス4T1乳癌モデルにおける新たなMCP-1産生機序の同定―腫瘍細胞・線維芽細胞間のクロストーク

    今村 真悠, 藤澤 真, Li Tiantian, 河原 明奈, 松川 昭博, 吉村 禎造

    第108回日本病理学会総会 

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    開催年月日: 2019年5月9日 - 2019年5月11日

    会議種別:ポスター発表  

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  • Downregulated miR-200b-3p plays a role in angiogenesis of hepatocellular carcinoma by targeting ERG

    モウモウアウン エイ, 藤澤 真義, 吉村 禎造, 松川 昭博

    第108回日本病理学会総会 

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    開催年月日: 2019年5月9日 - 2019年5月11日

    会議種別:口頭発表(一般)  

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  • 癌細胞が産生するGM-CSFは、癌の進展・転移に関わるか? マウス4T1乳癌モデルでの検討

    中村 薫, Li Chunning, Li Tiantian, 藤澤 真義, 松川 昭博, 向田 直史, 吉村 禎造

    第108回日本病理学会総会 

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    開催年月日: 2019年5月9日 - 2019年5月11日

    会議種別:ポスター発表  

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  • Spred2 deletion accelerates growth, migration and invasion in HepG2 cells by activating ERK pathway

    高 桐, 楊 旭, 藤澤 真義, 大原 利章, 吉村 禎造, 松川 昭博

    第108回日本病理学会総会 

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    開催年月日: 2019年5月9日 - 2019年5月11日

    会議種別:ポスター発表  

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  • Cancer progression can be regulated by exosomes from distinct cell subpopulation

    李 春寧, 田 ミョウ, 大原 利章, 藤澤 真義, 吉村 禎造, 松川 昭博

    第108回日本病理学会総会 

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    開催年月日: 2019年5月9日