徳島大学 / 教育研究者総覧 --- 河野弘

専門分野

研究テーマ

著書・論文

著書:

1.	河野弘, 西岡安彦 : 膠原病の肺病変, 南江堂, 2019年4月.
2.	岸潤, 河野弘, 西岡安彦 : 強皮症, 2014年9月.

学術論文(審査論文):

1.	Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Kojin Murakami, Takeshi Imakura, Yuya Yamashita, Kozo Kagawa, Hiroshi Kawano, Eiji Hara and Yasuhiko Nishioka : A novel BRD4 degrader, ARV-825, attenuates lung fibrosis through senolysis and antifibrotic effect., Respiratory Investigation, Vol.61, No.6, 781-792, 2023. (要約) For senescent cells, ARV825 induced the expression of an apoptosis marker while reducing the expression of BRD4 and senescence markers. On the other hand, for early passage pre-senescent cells, ARV825 reduced the expression of collagen type 1 and α-smooth muscle actin. In an experimental mouse model of lung fibrosis, ARV825 attenuated lung fibrosis and improved lung function. Immunohistochemical staining revealed a significant decrease in the number of senescent alveolar type 2 cells in lung tissue due to ARV825 treatment. (キーワード) Humans / Mice / Animals / Nuclear Proteins / Senotherapeutics / Transcription Factors / Lung / Idiopathic Pulmonary Fibrosis / Bleomycin / Collagen / Mice, Inbred C57BL / Cell Cycle Proteins (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.resinv.2023.08.003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37741093 ● Search Scopus @ Elsevier (PMID): 37741093 ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2023.08.003 (DOI: 10.1016/j.resinv.2023.08.003, PubMed: 37741093)
2.	Takeshi Imakura, Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Takahiro Niimura, Kojin Murakami, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : A polo-like kinase inhibitor identified by computational repositioning attenuates pulmonary fibrosis., Respiratory Research, Vol.24, No.1, 148, 2023. (要約) These findings suggest that targeting PLK1 may be a novel therapeutic approach for pulmonary fibrosis by inhibiting lung fibroblast proliferation without affecting lung epithelial cells. In addition, while in silico screening is useful, it is essential to fully determine the biological activities of candidates by wet-lab validation studies. (キーワード) Mice / Animals / Drug Repositioning / Thiophenes / Benzimidazoles / Lung / Idiopathic Pulmonary Fibrosis / Fibroblasts / Bleomycin (徳島大学機関リポジトリ) ● Metadata: 119057 (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s12931-023-02446-x (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37269004 ● Search Scopus @ Elsevier (PMID): 37269004 ● Search Scopus @ Elsevier (DOI): 10.1186/s12931-023-02446-x (徳島大学機関リポジトリ: 119057, DOI: 10.1186/s12931-023-02446-x, PubMed: 37269004)
3.	Kozo Kagawa, Seidai Satou, Kazuya Koyama, Takeshi Imakura, Kojin Murakami, Yuya Yamashita, Nobuhito Naito, Hirohisa Ogawa, Hiroshi Kawano and Yasuhiko Nishioka : The lymphocyte-specific protein tyrosine kinase-specific inhibitor A-770041 attenuates lung fibrosis via the suppression of TGF-β production in regulatory T-cells., PLoS ONE, Vol.17, No.10, e0275987, 2022. (要約) These results suggest that Lck inhibition attenuated lung fibrosis by suppressing TGF-β production in Tregs and support the role of Tregs in the pathogenesis of lung fibrosis. (キーワード) Mice / Animals / 肺線維症 (pulmonary fibrosis) / T-Lymphocytes, Regulatory / Transforming Growth Factor beta1 / Bleomycin / Transforming Growth Factor beta / Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / Mice, Inbred C57BL (徳島大学機関リポジトリ) ● Metadata: 118786 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0275987 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36301948 ● Search Scopus @ Elsevier (PMID): 36301948 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0275987 (徳島大学機関リポジトリ: 118786, DOI: 10.1371/journal.pone.0275987, PubMed: 36301948)
4.	Hitoshi Nishijima, Mizuki Sugita, Natsuka Umezawa, Naoki Kimura, Hirokazu Sasaki, Hiroshi Kawano, Yasuhiko Nishioka, Minoru Matsumoto, Takeshi Oya, Koichi Tsuneyama, Junko Morimoto and Mitsuru Matsumoto : Development of organ-specific autoimmunity by dysregulated Aire expression., Immunology and Cell Biology, Vol.100, No.5, 371-377, 2022. (要約) Deficiency for AIRE/Aire in both humans and mice results in the development of organ-specific autoimmune disease. We tested whether augmented and/or dysregulated AIRE/Aire expression might be also prone to the breakdown of self-tolerance. To define the effect of augmented Aire expression on the development of autoimmunity, antigen-specific clonal deletion and production of clonotypic regulatory T cells (Tregs) in the thymus were examined using mice expressing two additional copies of Aire in a heterozygous state (3xAire-knockin mice: 3xAire-KI). We found that both clonal deletion of autoreactive T cells and production of clonotypic Tregs in the thymus from 3xAire-KI were impaired in a T-cell receptor-transgenic system. Furthermore, 3xAire-KI females showed higher scores of experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein than wild-type littermates, suggesting that augmented Aire expression exacerbates organ-specific autoimmunity under disease-prone conditions. In humans, we found that one patient with amyopathic dermatomyositis showed CD3 (キーワード) Animals / 自己免疫 (autoimmunity) / Clonal Deletion / Encephalomyelitis, Autoimmune, Experimental / 女性 (female) / Humans / Immune Tolerance / Mice / Myelin-Oligodendrocyte Glycoprotein / Thymus Gland (徳島大学機関リポジトリ) ● Metadata: 117817 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/imcb.12546 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35313042 ● Search Scopus @ Elsevier (PMID): 35313042 ● Search Scopus @ Elsevier (DOI): 10.1111/imcb.12546 (徳島大学機関リポジトリ: 117817, DOI: 10.1111/imcb.12546, PubMed: 35313042)
5.	Tamotsu Tanaka, Kazuya Koyama, Naoko Takahashi, Katsuya Morito, Hanif Ali, Momoyo Azuma, Kozo Kagawa, Hiroshi Kawano, Rumana Yesmin, Mutsumi Aihara and Yasuhiko Nishioka : Lysophosphatidic acid, ceramide 1-phosphate and sphingosine 1-phosphate in peripheral blood of patients with idiophathic pulmonary fibrosis, The Journal of Medical Investigation : JMI, Vol.69, No.3.4, 196-203, 2022. (要約) Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial pneumonias. Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are signaling lipids that evoke growth factor-like responses to many cells. Recent studies revealed the involvement of LPA and S1P in the pathology of IPF. In this study, we determined LPA, S1P and ceramide 1-phosphate (C1P) in peripheral blood plasma of IPF patients, and examined correlation to the vital capacity of lung (VC), an indicator of development of fibrosis. Blood plasma samples were taken from eleven patients with IPF and seven healthy volunteers. The lipids of the sample were extracted and subjected to liquid chromatography-tandem mass spectrometry for analysis. Results showed that there is a significant negative correlation between VC and plasma LPA levels, indicating that IPF patients with advanced fibrosis had higher concentration of LPA in their plasma. Average of S1P levels were significantly higher in IPF patients than those in healthy subjects. Although it is not statistically significant, a similar correlation trend that observed in LPA levels also found between VC and S1P levels. These results indicated that plasma LPA and S1P may be associated with deterioration of pulmonary function of IPF patients. J. Med. Invest. 69 : 196-203, August, 2022. (キーワード) Ceramides / Fibrosis / Humans / Idiopathic Pulmonary Fibrosis / Lysophospholipids / Sphingosine (徳島大学機関リポジトリ) ● Metadata: 117621 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.69.196 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244770 ● Search Scopus @ Elsevier (PMID): 36244770 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.196 (徳島大学機関リポジトリ: 117621, DOI: 10.2152/jmi.69.196, PubMed: 36244770)
6.	Hirokazu Ogino, Makoto Tobiume, Kozo Kagawa, Hiroshi Kawano, Satoshi Sakaguchi, Atsuro Saijo, Daisuke Matsumoto, Hiromitsu Takizawa, Yuriko Morikawa, Yoshimi Bando, Hisatsugu Goto, Hiroshi Nokihara and Yasuhiko Nishioka : A Case of Radiation-associated Angiosarcoma Presenting as Massive Pleural Effusion., Internal Medicine, Vol.61, No.9, 1393-1397, 2021. (要約) A 67-year-old man was admitted to our hospital for massive pleural effusion. He had a history of mandibular gingival carcinoma treated with radiation therapy (RT). Based on the cytology findings of pleural effusion and a thoracoscopic pleural biopsy, we finally diagnosed him with radiation-associated angiosarcoma. Retrospective cell-block immunocytochemistry with pleural effusion also showed potential utility for the diagnosis. This case highlights the importance of considering the possibility of radiation-associated secondary cancer in patients with pleural effusion who have a history of RT. (キーワード) Aged / Biopsy / Hemangiosarcoma / Humans / 男性 (male) / Pleural Effusion / Retrospective Studies / Thoracoscopy (徳島大学機関リポジトリ) ● Metadata: 118013 (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.8195-21 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34645765 ● Search Scopus @ Elsevier (PMID): 34645765 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.8195-21 (徳島大学機関リポジトリ: 118013, DOI: 10.2169/internalmedicine.8195-21, PubMed: 34645765)
7.	Takeshi Imakura, Seidai Satou, Tetsu Tomonari, Kojin Murakami, Naoki Takahashi, Nobuhito Naito, Masato Mima, Kozo Kagawa, Kazuya Koyama, Haruka Nishimura, Hiroshi Kawano, Hiroshi Nokihara, Masahiko Azuma, Tetsuji Takayama and Yasuhiko Nishioka : Lenvatinib-induced Interstitial Pneumonia in a Patient with Hepatocellular Carcinoma., Internal Medicine, Vol.61, No.8, 1211-1217, 2021. (要約) Lenvatinib is a multi-targeted tyrosine kinase inhibitor available for the treatment of unresectable hepatocellular carcinoma (HCC). We herein report an 84-year-old-man with interstitial pneumonia caused by lenvatinib. Four months after the start of lenvatinib administration for HCC, chest computed tomography revealed bilateral ground-glass opacity. However, he continued to take lenvatinib for four more months until he complained of dyspnea on exertion. This is a case of lenvatinib-induced interstitial pneumonia that progressed relatively slowly with a long asymptomatic period despite the appearance of pneumonia on image findings. (キーワード) Aged, 80 and over / Carcinoma, Hepatocellular / Humans / Liver Neoplasms / Lung Diseases, Interstitial / 男性 (male) / Phenylurea Compounds / Quinolines (徳島大学機関リポジトリ) ● Metadata: 118011 (出版サイトへのリンク) ● Publication site (DOI): 10.2169/internalmedicine.7300-21 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34544944 ● Search Scopus @ Elsevier (PMID): 34544944 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.7300-21 (徳島大学機関リポジトリ: 118011, DOI: 10.2169/internalmedicine.7300-21, PubMed: 34544944)
8.	Hiroshi Kawano, Kazuya Koyama, Haruka Nishimura, Yuko Toyoda, Kozo Kagawa, Seidai Satou, Nobuhito Naito, Hisatsugu Goto, Yutaka Inagaki and Yasuhiko Nishioka : Development of improved method to identify and analyze lung fibrocytes with flow cytometry in a reporter mouse strain., Immunity, Inflammation and Disease, Vol.9, No.1, 120-127, 2020. (要約) cells. (徳島大学機関リポジトリ) ● Metadata: 116531 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/iid3.361 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33369271 ● Search Scopus @ Elsevier (PMID): 33369271 ● Search Scopus @ Elsevier (DOI): 10.1002/iid3.361 (徳島大学機関リポジトリ: 116531, DOI: 10.1002/iid3.361, PubMed: 33369271)
9.	Nobuhito Naito, Hiroshi Kawano, Yuya Yamashita, Mayo Kondou, Shotaro Haji, Ryosuke Miyamoto, Yuko Toyoda, Yasuhisa Kanematsu, Yuishin Izumi, Yoshimi Bando and Yasuhiko Nishioka : Neuropsychiatric systemic lupus erythematosus with cerebellar vasculitis and obstructive hydrocephalus requiring decompressive craniectomy., Modern Rheumatology Case Reports, Vol.5, No.1, 52-57, 2020. (要約) A 36-year-old woman who had been diagnosed with systemic lupus erythematosus (SLE) was admitted to our hospital due to increasing disease SLE activity. Despite the intensification of immunosuppressive treatment, headache newly developed and worsened. Magnetic resonance imaging (MRI) revealed spreading of a high-intensity area along the sulci of the bilateral cerebellar hemispheres. She was diagnosed with neuropsychiatric SLE and methylprednisolone (mPSL) pulse therapy was started. However, consciousness disorder due to cerebellar oedema with obstructive hydrocephalus appeared and required decompressive craniectomy. The histological findings of the biopsy specimens from cerebellar vermis were compatible with features of vasculitis. She was successfully treated adding intravenous cyclophosphamide therapy. (出版サイトへのリンク) ● Publication site (DOI): 10.1080/24725625.2020.1826626 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33021438 ● Search Scopus @ Elsevier (PMID): 33021438 ● Search Scopus @ Elsevier (DOI): 10.1080/24725625.2020.1826626 (DOI: 10.1080/24725625.2020.1826626, PubMed: 33021438)
10.	Shun Morizumi, Seidai Satou, Kazuya Koyama, Hiroyasu Okazaki, Yajuan Chen, Hisatsugu Goto, Kozo Kagawa, Hirohisa Ogawa, Haruka Nishimura, Hiroshi Kawano, Yuko Toyoda, Hisanori Uehara and Yasuhiko Nishioka : Blockade of Pan-Fibroblast Growth Factor Receptors Mediates Bidirectional Effects in Lung Fibrosis., American Journal of Respiratory Cell and Molecular Biology, Vol.63, No.3, 317-326, 2020. (要約) H]thymidine incorporation assays. The expression of FGFR was analyzed using IB or flow cytometry. We also investigated the effect of BGJ398 on pulmonary fibrosis induced by bleomycin in mice. Both lung fibroblasts and AECs expressed FGFRs. BGJ398 significantly inhibited the proliferation and migration of lung fibroblasts stimulated with FGF2. BGJ398 also reduced the proliferation of AECs in response to FGF2. Although the administration of BGJ398 ameliorated pulmonary fibrosis in bleomycin-treated mice, it increased mortality resulting from alveolar injury and inhibition of AEC regeneration. These data suggest that the total inhibition of FGFR signaling can suppress lung fibrosis by inhibiting fibroblast activities, although alveolar injury is simultaneously caused. (キーワード) Alveolar Epithelial Cells / Animals / Bleomycin / Fibroblasts / Humans / Idiopathic Pulmonary Fibrosis / Indoles / Lung / Mice / リン酸化 (phosphorylation) / Receptors, Fibroblast Growth Factor / シグナル伝達 (signal transduction) (徳島大学機関リポジトリ) ● Metadata: 115073 (出版サイトへのリンク) ● Publication site (DOI): 10.1165/rcmb.2019-0090OC (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32338990 ● Search Scopus @ Elsevier (PMID): 32338990 ● Search Scopus @ Elsevier (DOI): 10.1165/rcmb.2019-0090OC (徳島大学機関リポジトリ: 115073, DOI: 10.1165/rcmb.2019-0090OC, PubMed: 32338990)
11.	Shuichi Abe, Seidai Satou, Yoshinori Aono, Momoyo Azuma, Masami Kishi, Koyama Kazuya, Takahashi Naoki, Kozo Kagawa, Hiroshi Kawano and Yasuhiko Nishioka : Functional analysis of human fibrocytes derived from monocytes reveals their profibrotic phenotype through paracrine effects, The Journal of Medical Investigation : JMI, Vol.67, No.1.2, 102-112, 2020. (要約) Fibrocytes, which are bone marrow-derived collagen-producing cells, were reported to play a role in the pathogenesis of pulmonary fibrosis. However, their function in pulmonary fibrosis is unclear. We analyzed their function compared with that of monocytes and localization in fibrotic tissues in patients with idiopathic pulmonary fibrosis (IPF). We compared the gene expression profile of monocyte-derived fibrocytes with that of monocytes by microarray analysis. Proliferation and differentiation into myofibroblasts were examined by 3H-thymidine incorporation assay and Western blotting. We measured the level of growth factors in the culture supernatant of fibrocytes by ELISA. The localization of fibrocytes in lung tissues of patients with IPF was determined by immunofluorescence staining. Compared with monocytes, fibrocytes had higher expression of extracellular matrix- and growth factor-encoding genes, including PDGF-B, FGF-2 and VEGF-B. Although fibrocytes did not proliferate in response to PDGF, co-culture of fibrocytes stimulated the growth of lung fibroblasts through the production of PDGF-BB. In the lung of IPF patients, CD45+Collagen-I+FSP-1+ cells, which have a similar phenotype to fibrocytes, were detected and co-stained with anti-PDGF antibody. This study suggested that fibrocytes function in pulmonary fibrosis partly by producing PDGF in the lungs of IPF patients. J. Med. Invest. 67 : 102-112, February, 2020. (徳島大学機関リポジトリ) ● Metadata: 114734 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.67.102 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378592 ● Search Scopus @ Elsevier (PMID): 32378592 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.102 (徳島大学機関リポジトリ: 114734, DOI: 10.2152/jmi.67.102, PubMed: 32378592)
12.	Takeshi Imakura, Yuko Toyoda, Seidai Satou, Kazuya Koyama, Haruka Nishimura, Kozo Kagawa, Naoki Takahashi, Nobuhito Naito, Kojin Murakami, Hiroshi Kawano, Masahiko Azuma, Tsutomu Shinohara and Yasuhiko Nishioka : Distinct improvement of pulmonary function, ground-glass opacity, hypoxia and physical findings in an idiopathic pulmonary fibrosis patient after pirfenidone treatment : a case report with a review of the literature., The Journal of Medical Investigation : JMI, Vol.67, No.3.4, 358-361, 2020. (要約) Background : Pirfenidone (PFD), an anti-fibrosis drug for idiopathic pulmonary fibrosis (IPF), suppresses disease progression and delays decline of forced vital capacity. However, this drug rarely makes marked improvement of pulmonary function, chest high-resolution computed tomography (HRCT) findings and hypoxia. Case presentation : A 59 year-old-man, who was a former smoker and had a history of alcoholic liver cirrhosis, developed exertional dyspnea and was referred to our hospital. HRCT showed honeycomb changes with surrounding ground-glass opacity (GGO) in a predominantly basal and subpleural distribution. He was diagnosed with IPF and the treatment with PFD was started. At 16 months after the start of treatment, the predicted forced vital capacity value markedly improved from 82.9% to 98.6%. His resting-state partial pressure of arterial oxygen while breathing room air increased from a minimum of 54.7 mmHg (at 2 months treatment) to 72.5 mmHg. The GGO observed at diagnosis disappeared in HRCT. But after 32 months of treatment, his general condition got worse gradually, and he died from chronic progression of IPF after 48 months of treatment. Conclusion : Our case suggests that a complication of chronic liver disease and the existence of GGO may be characteristics of super-responder to PFD treatment for IPF patients. J. Med. Invest. 67 : 358-361, August, 2020. (徳島大学機関リポジトリ) ● Metadata: 115454 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.67.358 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33148916 ● Search Scopus @ Elsevier (PMID): 33148916 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.67.358 (徳島大学機関リポジトリ: 115454, DOI: 10.2152/jmi.67.358, PubMed: 33148916)
13.	Hiroyasu Okazaki, Seidai Satou, Kazuya Koyama, Shun Morizumi, Shuichi Abe, Momoyo Azuma, Yajuan Chen, Hisatsugu Goto, Yoshinori Aono, Hirohisa Ogawa, Kozo Kagawa, Haruka Nishimura, Hiroshi Kawano, Yuko Toyoda, Hisanori Uehara, Hiroyuki Kouji and Yasuhiko Nishioka : The novel inhibitor PRI-724 for Wnt/β-catenin/CBP signaling ameliorates bleomycin-induced pulmonary fibrosis in mice., Experimental Lung Research, Vol.45, No.7, 188-199, 2019. (要約) These results suggest that the β-catenin/CBP inhibitor PRI-724 is a potent antifibrotic agent that acts by modulating the activity of macrophages in the lungs. (徳島大学機関リポジトリ) ● Metadata: 113984 (出版サイトへのリンク) ● Publication site (DOI): 10.1080/01902148.2019.1638466 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31298961 ● Summary page in Scopus @ Elsevier: 2-s2.0-85068899202 (徳島大学機関リポジトリ: 113984, DOI: 10.1080/01902148.2019.1638466, PubMed: 31298961, Elsevier: Scopus)
14.	Yuko Toyoda, Kazuya Koyama, Hiroshi Kawano, Haruka Nishimura, Kozo Kagawa, Shun Morizumi, Nobuhito Naito, Seidai Satou, Yuya Yamashita, Naoki Takahashi, Hisatsugu Goto, Masahiko Azuma and Yasuhiko Nishioka : Clinical features of interstitial pneumonia associated with systemic lupus erythematosus., Respiratory Investigation, Vol.57, No.5, 435-443, 2019. (要約) In SLE cases, IP primarily occurred in male and elderly patients. In addition to the NSIP pattern, the UIP pattern was evident on HRCT scans of IP-related SLE. The survival of SLE patients was unrelated to IP. (キーワード) Adult / Age of Onset / Aged / Disease Progression / Female / Humans / Incidence / Lung Diseases, Interstitial / Lupus Erythematosus, Systemic / Male / Middle Aged / Retrospective Studies / Sex Factors / Tomography, X-Ray Computed / Young Adult (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.resinv.2019.04.005 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31235450 ● Search Scopus @ Elsevier (PMID): 31235450 ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2019.04.005 (DOI: 10.1016/j.resinv.2019.04.005, PubMed: 31235450)
15.	Masaki Hanibuchi, Akira Kanoh, Takuya Kuramoto, Tatsuro Saito, Makoto Tobiume, Atsuro Saijo, Hiroyuki Kozai, Mayo Kondou, Shun Morizumi, Hiroto Yoneda, Kozo Kagawa, Hirokazu Ogino, Seidai Satou, Hiroshi Kawano, Kenji Otsuka, Yuko Toyoda, Hiroshi Nokihara, Hisatsugu Goto and Yasuhiko Nishioka : Development, validation, and comparison of gene analysis methods for detecting mutation from non-small cell lung cancer patients-derived circulating free DNA., Oncotarget, Vol.10, No.38, 3654-3666, 2019. (徳島大学機関リポジトリ) ● Metadata: 115668 (出版サイトへのリンク) ● Publication site (DOI): 10.18632/oncotarget.26951 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31217900 ● Search Scopus @ Elsevier (PMID): 31217900 ● Search Scopus @ Elsevier (DOI): 10.18632/oncotarget.26951 (徳島大学機関リポジトリ: 115668, DOI: 10.18632/oncotarget.26951, PubMed: 31217900)
16.	Kazuya Koyama, Hisatsugu Goto, Shun Morizumi, Kozo Kagawa, Haruka Nishimura, Seidai Satou, Hiroshi Kawano, Yuko Toyoda, Hirohisa Ogawa, Sakae Homma and Yasuhiko Nishioka : The Tyrosine Kinase Inhibitor TAS-115 Attenuates Bleomycin-induced Lung Fibrosis in Mice., American Journal of Respiratory Cell and Molecular Biology, Vol.60, No.4, 478-487, 2019. (要約) The signaling pathways of growth factors, including platelet-derived growth factor, can be considered specific targets for overcoming the poor prognosis of idiopathic pulmonary fibrosis. Nintedanib, the recently approved multiple kinase inhibitor, has shown promising antifibrotic effects in patients with idiopathic pulmonary fibrosis; however, its efficacy is still limited, and in some cases, treatment discontinuation is necessary owing to toxicities such as gastrointestinal disorders. Therefore, more effective agents with less toxicity are still needed. TAS-115 is a novel multiple tyrosine kinase inhibitor that preferably targets platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor receptor, and c-FMS in addition to other molecules. In this study, we evaluated the antifibrotic effect of TAS-115 on pulmonary fibrosis in vitro and in vivo. TAS-115 inhibited the phosphorylation of PDGFR on human lung fibroblast cell line MRC-5 cells and suppressed their platelet-derived growth factor-induced proliferation and migration. Furthermore, TAS-115 inhibited the phosphorylation of c-FMS, a receptor of macrophage colony-stimulating factor, in murine bone marrow-derived macrophages and decreased the production of CCL2, another key molecule for inducing pulmonary fibrosis, under the stimulation of macrophage colony-stimulating factor. Importantly, the inhibitory effects of TAS-115 on both PDGFR and c-FMS were 3- to 10-fold higher than those of nintedanib. In a mouse model of bleomycin-induced pulmonary fibrosis, TAS-115 significantly inhibited the development of pulmonary fibrosis and the collagen deposition in bleomycin-treated lungs. These data suggest that strong inhibition of PDGFR and c-FMS by TAS-115 may be a promising strategy for overcoming the intractable pathogenesis of pulmonary fibrosis. (キーワード) Animals / Bleomycin / Cell Line / Cell Movement / Cell Proliferation / Humans / Male / Mice / Mice, Inbred C57BL / Phosphorylation / Protein Kinase Inhibitors / Pulmonary Fibrosis / Quinolines / Receptor, Macrophage Colony-Stimulating Factor / Receptors, Platelet-Derived Growth Factor / Receptors, Vascular Endothelial Growth Factor / Thiourea (出版サイトへのリンク) ● Publication site (DOI): 10.1165/rcmb.2018-0098OC (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30540913 ● Search Scopus @ Elsevier (PMID): 30540913 ● Search Scopus @ Elsevier (DOI): 10.1165/rcmb.2018-0098OC (DOI: 10.1165/rcmb.2018-0098OC, PubMed: 30540913)
17.	Hirokazu Ogino, Masaki Hanibuchi, Satoshi Sakaguchi, Yuko Toyoda, Toshifumi Tezuka, Hiroshi Kawano, Soji Kakiuchi, Kenji Otsuka, Atsuro Saijo, Masahiko Azuma, Hiroshi Nokihara, Hisatsugu Goto and Yasuhiko Nishioka : The clinical features of older patients with lung cancer in comparison with their younger counterparts., Respiratory Investigation, Vol.57, No.1, 40-48, 2019. (要約) We should positively consider standard treatments for older patients. However, not only their shorter life expectancy but also their poor PS and multiple comorbidities that sometimes render patients unable to receive standard treatments and several chemotherapy regimens, make their prognosis poor. The standard treatments for older patients, especially in locally advanced stages, require modification. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.resinv.2018.10.003 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30448243 ● Search Scopus @ Elsevier (PMID): 30448243 ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2018.10.003 (DOI: 10.1016/j.resinv.2018.10.003, PubMed: 30448243)
18.	Masami Kishi, Yoshinori Aono, Seidai Satou, Kazuya Koyama, Momoyo Azuma, Shuichi Abe, Hiroshi Kawano, Jun Kishi, Yuko Toyoda, Hiroyasu Okazaki, Hirohisa Ogawa, Hisanori Uehara and Yasuhiko Nishioka : Blockade of platelet-derived growth factor receptor-β, not receptor-α ameliorates bleomycin-induced pulmonary fibrosis in mice., PLoS ONE, Vol.13, No.12, 2018. (要約) Platelet-derived growth factor (PDGF) has been implicated in the pathogenesis of pulmonary fibrosis. Nintedanib, a multi-kinase inhibitor that targets several tyrosine kinases, including PDGF receptor (PDGFR), was recently approved as an anti-fibrotic agent to reduce the deterioration of FVC in patients with idiopathic pulmonary fibrosis (IPF). However, the effects of PDGFR-α or -β on pulmonary fibrosis remain unclear. In an attempt to clarify their effects, we herein used blocking antibodies specific for PDGFR-α (APA5) and -β (APB5) in a bleomycin (BLM)-induced pulmonary fibrosis mouse model. The effects of these treatments on the growth of lung fibroblasts were examined using the 3H-thymidine incorporation assay in vitro. The anti-fibrotic effects of these antibodies were investigated with the Ashcroft score and collagen content of lungs treated with BLM. Their effects on inflammatory cells in the lungs were also analyzed using bronchoalveolar lavage fluid. We investigated damage to epithelial cells and the proliferation of fibroblasts in the lungs. APA5 and APB5 inhibited the phosphorylation of PDGFR-α and -β as well as the proliferation of lung fibroblasts induced by PDGF-AA and BB. The administration of APB5, but not APA5 effectively inhibited BLM-induced pulmonary fibrosis in mice. Apoptosis and the proliferation of epithelial cells and fibroblasts were significantly decreased by the treatment with APB5, but not by APA5. The late treatment with APB5 also ameliorated fibrosis in lungs treated with BLM. These results suggest that PDGFR-α and -β exert different effects on BLM-induced pulmonary fibrosis in mice. A specific approach using the blocking antibody for PDGFR-β may be useful for the treatment of pulmonary fibrosis. (徳島大学機関リポジトリ) ● Metadata: 113268 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0209786 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30596712 ● Search Scopus @ Elsevier (PMID): 30596712 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0209786 (徳島大学機関リポジトリ: 113268, DOI: 10.1371/journal.pone.0209786, PubMed: 30596712)
19.	Masaki Hanibuchi, Soji Kakiuchi, Shinji Atagi, Fumitaka Ogushi, Eiji Shimizu, Takashi Haku, Yuko Toyoda, Masahiko Azuma, Mayo Kondo, Hiroshi Kawano, Kenji Otsuka, Satoshi Sakaguchi, Hiroshi Nokihara, Hisatsugu Goto and Yasuhiko Nishioka : A multicenter, open-label, phase II trial of S-1 plus carboplatin in advanced non-small cell lung cancer patients with interstitial lung disease., Lung Cancer, Vol.125, 93-99, 2018. (要約) A total of 33 advanced or recurrent NSCLC patients with ILD were prospectively enrolled in this multicenter, open-label, phase II study. Every 4 weeks, CBDCA at a dose of AUC 5 on day 1 and S-1 at a dose of 80 mg/m (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.lungcan.2018.09.007 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30429044 ● Search Scopus @ Elsevier (PMID): 30429044 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lungcan.2018.09.007 (DOI: 10.1016/j.lungcan.2018.09.007, PubMed: 30429044)
20.	Hiroyuki Kozai, Yuko Toyoda, Hisatsugu Goto, Jun Kishi, Makoto Tobiume, Yuya Yamashita, Haruka Nishimura, Mayo Kondou, Hiroshi Kawano and Yasuhiko Nishioka : A case of interstitial pneumonia associated with anti-PL-7 antibody in a patient with rheumatoid arthritis., The Journal of Medical Investigation : JMI, Vol.65, No.1,2, 147-150, 2018. (要約) A 65-year-old female had been treated rheumatoid arthritis (RA), interstitial pneumonia (IP) and nephrotic syndrome with prednisolone and cyclosporine. She was emergently admitted to our hospital due to the worsening exertional dyspnea and severe hypoxemia. Chest computed tomography (CT) showed new diffuse ground-glass opacities (GGOs) with slight consolidations along with bronchovascular bundle were observed in addition to pre-existing reticular shadows in both lungs with lower lobe-predominance. An acute exacerbation (AE) of pre-existing IP triggered by an infection was suspected, and the treatment with antibiotics and corticosteroid pulse therapy improved her general condition and chest radiological findings. Because some auto-antibodies associated with acute/subacute onset IP have recently become available in clinic, we examined those including anti-aminoacyl tRNA synthetase (ARS) antibodies, and found that she was positive for anti-PL-7 antibody. We diagnosed her anti-synthetase syndrome (ASS) without symptom of myositis, and her IP was considered to be ASS-related. The careful consideration is necessary to precisely diagnose and treat the patients with RA-associated interstitial lung diseases as the several etiologies may be overlapped in the same patient. J. Med. Invest. 65:147-150, February, 2018. (キーワード) Aged / Amino Acyl-tRNA Synthetases / Arthritis, Rheumatoid / Autoantibodies / 女性 (female) / Humans / Lung Diseases, Interstitial (徳島大学機関リポジトリ) ● Metadata: 111454 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.65.147 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29593187 ● CiNii @ 国立情報学研究所 (CRID): 1390282679224622464 ● Summary page in Scopus @ Elsevier: 2-s2.0-85044475211 (徳島大学機関リポジトリ: 111454, DOI: 10.2152/jmi.65.147, PubMed: 29593187, CiNii: 1390282679224622464, Elsevier: Scopus)
21.	Hitoshi Nishijima, Tatsuya Kajimoto, Yoshiki Matsuoka, Yasuhiro Mouri, Junko Morimoto, Minoru Matsumoto, Hiroshi Kawano, Yasuhiko Nishioka, Hisanori Uehara, Keisuke Izumi, Koichi Tsuneyama, Il-mi Okazaki, Taku Okazaki, Kazuyoshi Hosomichi, Ayako Shiraki, Makoto Shibutani, Kunitoshi Mitsumori and Mitsuru Matsumoto : Paradoxical development of polymyositis-like autoimmunity through augmented expression of autoimmune regulator (AIRE)., Journal of Autoimmunity, Vol.86, 75-92, 2018. (要約) Autoimmunity is prevented by the function of the autoimmune regulator [AIRE (Aire in mice)], which promotes the expression of a wide variety of tissue-restricted antigens (TRAs) from medullary thymic epithelial cells (mTECs) and from a subset of peripheral antigen-presenting cells (APCs). We examined the effect of additive expression of human AIRE (huAIRE) in a model of autoimmune diabetes in NOD mice. Unexpectedly, we observed that mice expressing augmented AIRE/Aire developed muscle-specific autoimmunity associated with incomplete maturation of mTECs together with impaired expression of Aire-dependent TRAs. This led to failure of deletion of autoreactive T cells together with dramatically reduced production of regulatory T cells in the thymus. In peripheral APCs, expression of costimulatory molecules was augmented. We suggest that levels of Aire expression need to be tightly controlled for maintenance of immunological tolerance. Our results also highlight the importance of coordinated action between central tolerance and peripheral tolerance under the common control of Aire. (徳島大学機関リポジトリ) ● Metadata: 112347 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jaut.2017.09.006 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28931462 ● Search Scopus @ Elsevier (PMID): 28931462 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jaut.2017.09.006 (徳島大学機関リポジトリ: 112347, DOI: 10.1016/j.jaut.2017.09.006, PubMed: 28931462)
22.	Seidai Satou, Shinohara Shintaro, Hayashi Shinya, Morizumi Shun, Abe Shuichi, Okazaki Hiroyasu, Chen Yanjuan, Hisatsugu Goto, Yoshinori Aono, Hirohisa Ogawa, Koyama Kazuya, Nishimura Haruka, Hiroshi Kawano, Yuko Toyoda, Hisanori Uehara and Yasuhiko Nishioka : Anti-fibrotic efficacy of nintedanib in pulmonary fibrosis via the inhibition of fibrocyte activity., Respiratory Research, Vol.18, No.1, 172, 2017. (要約) Nintedanib, a tyrosine kinase inhibitor that is specific for platelet-derived growth factor receptors (PDGFR), fibroblast growth factor receptors (FGFR), and vascular endothelial growth factor receptors (VEGFR), has recently been approved for idiopathic pulmonary fibrosis. Fibrocytes are bone marrow-derived progenitor cells that produce growth factors and contribute to fibrogenesis in the lungs. However, the effects of nintedanib on the functions of fibrocytes remain unclear. Human monocytes were isolated from the peripheral blood of healthy volunteers. The expression of growth factors and their receptors in fibrocytes was analyzed using ELISA and Western blotting. The effects of nintedanib on the ability of fibrocytes to stimulate lung fibroblasts were examined in terms of their proliferation. The direct effects of nintedanib on the differentiation and migration of fibrocytes were also assessed. We investigated whether nintedanib affected the accumulation of fibrocytes in mouse lungs treated with bleomycin. Human fibrocytes produced PDGF, FGF2, and VEGF-A. Nintedanib and specific inhibitors for each growth factor receptor significantly inhibited the proliferation of lung fibroblasts stimulated by the supernatant of fibrocytes. Nintedanib inhibited the migration and differentiation of fibrocytes induced by growth factors in vitro. The number of fibrocytes in the bleomycin-induced lung fibrosis model was reduced by the administration of nintedanib, and this was associated with anti-fibrotic effects. These results support the role of fibrocytes as producers of and responders to growth factors, and suggest that the anti-fibrotic effects of nintedanib are at least partly mediated by suppression of fibrocyte function. (キーワード) Animals / Cell Movement / Cells, Cultured / Dose-Response Relationship, Drug / Fibroblasts / Humans / Indoles / Male / Mice / Mice, Inbred C57BL / Pulmonary Fibrosis / Treatment Outcome / Vascular Endothelial Growth Factor A (徳島大学機関リポジトリ) ● Metadata: 114546 (出版サイトへのリンク) ● Publication site (DOI): 10.1186/s12931-017-0654-2 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28915889 ● Summary page in Scopus @ Elsevier: 2-s2.0-85029541214 (徳島大学機関リポジトリ: 114546, DOI: 10.1186/s12931-017-0654-2, PubMed: 28915889, Elsevier: Scopus)
23.	Soji Kakiuchi, Masaki Hanibuchi, Toshifumi Tezuka, Atsuro Saijo, Kenji Otsuka, Satoshi Sakaguchi, Yuko Toyoda, Hisatsugu Goto, Hiroshi Kawano, Masahiko Azuma, Fumitaka Ogushi and Yasuhiko Nishioka : Analysis of acute exacerbation of interstitial lung disease associated with chemotherapy in patients with lung cancer: A feasibility of S-1., Respiratory Investigation, Vol.55, No.2, 145-152, 2016. (要約) Although this was a small retrospective study, its findings showed that S-1 and etoposide may be relatively safe options for the treatment of patients with lung cancer and concomitant ILD. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.resinv.2016.10.008 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28274530 ● Search Scopus @ Elsevier (PMID): 28274530 ● Search Scopus @ Elsevier (DOI): 10.1016/j.resinv.2016.10.008 (DOI: 10.1016/j.resinv.2016.10.008, PubMed: 28274530)
24.	Yuko Toyoda, Masaki Hanibuchi, Jun Kishi, Hiroshi Kawano, Shun Morizumi, Seidai Satou, M Kondo, Terumi Takikura, Toshifumi Tezuka, Hisatsugu Goto and Yasuhiko Nishioka : Clinical features and outcome of acute exacerbation of interstitial pneumonia associated with connective tissue disease., The Journal of Medical Investigation : JMI, Vol.63, No.3,4, 294-299, 2016. (要約) Acute exacerbation (AE) of interstitial lung disease is reported to be developed in not only idiopathic pulmonary fibrosis but also connective tissue disease-associated interstitial pneumonia (CTD-IP). As the significance of AE of CTD-IP has not been so widely recognized, its clinical feature is not fully elucidated. In the present study, we investigated the incidence, clinical features and outcome of AE of CTD-IP. We retrospectively reviewed admitted cases in our department with medical record from 2011 to 2015. Among 155 patients with CTD-IP, 10 (6.5%) cases developed AE (6 rheumatoid arthritis, 2 polymyositis/dermatomyositis, 1 systemic lupus erythematosus, 1 Sjögren syndrome), and one died of AE within 30 days. Median survival time after the onset of AE was 169 days in all 10 patients. The treatment with immunosuppressant just before AE onset might improve the prognosis of AE. The median survival time after the onset of AE was significantly longer in patients showing good response to corticosteroid compared with those with poor response to corticosteroid (805 days and 45 days, respectively) (p <0.05), suggesting that there are some cases in CTD-IP, showing the good response to corticosteroid even when AE was complicated. J. Med. Invest. 63: 294-299, August, 2016. (徳島大学機関リポジトリ) ● Metadata: 111197 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.63.294 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27644575 ● Summary page in Scopus @ Elsevier: 2-s2.0-84987881651 (徳島大学機関リポジトリ: 111197, DOI: 10.2152/jmi.63.294, PubMed: 27644575, Elsevier: Scopus)
25.	Hiroshi Kawano, Hitoshi Nishijima, Junko Morimoto, Fumiko Hirota, Ryoko Morita, Yasuhiro Mouri, Yasuhiko Nishioka and Mitsuru Matsumoto : Aire expression is inherent to most medullary thymic epithelial cells during their differentiation program., The Journal of Immunology, Vol.195, No.11, 5149-5158, 2015. (要約) Aire in medullary thymic epithelial cells (mTECs) plays an important role in the establishment of self-tolerance. Because Aire+ mTECs appear to be a limited subset, they may constitute a unique lineage(s) among mTECs. An alternative possibility is that all mTECs are committed to express Aire in principle, but Aire expression by individual mTECs is conditional. To investigate this issue, we established a novel Aire reporter strain in which endogenous Aire is replaced by the human AIRE-GFP-Flag tag (Aire/hAGF-knockin) fusion gene. The hAGF reporter protein was produced and retained very efficiently within mTECs as authentic Aire nuclear dot protein. Remarkably, snapshot analysis revealed that mTECs expressing hAGF accounted for >95% of mature mTECs, suggesting that Aire expression does not represent a particular mTEC lineage(s). We confirmed this by generating Aire/diphtheria toxin receptor knockin mice in which long-term ablation of Aire+ mTECs by diphtheria toxin treatment resulted in the loss of most mature mTECs beyond the proportion of those apparently expressing Aire. These results suggest that Aire expression is inherent to all mTECs but may occur at particular stage(s) and/or cellular states during their differentiation, thus accounting for the broad impact of Aire on the promiscuous gene expression of mTECs. (徳島大学機関リポジトリ) ● Metadata: 109688 (出版サイトへのリンク) ● Publication site (DOI): 10.4049/jimmunol.1501000 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26503950 ● Search Scopus @ Elsevier (PMID): 26503950 ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1501000 (徳島大学機関リポジトリ: 109688, DOI: 10.4049/jimmunol.1501000, PubMed: 26503950)
26.	Hitoshi Nishijima, Satsuki Kitano, Hitoshi Miyachi, Junko Morimoto, Hiroshi Kawano, Fumiko Hirota, Ryoko Morita, Yasuhiro Mouri, Kiyoshi Masuda, Issei Imoto, Koichi Ikuta and Mitsuru Matsumoto : Ectopic Aire expression in the thymic cortex reveals inherent properties of Aire as a tolerogenic factor within the medulla., The Journal of Immunology, Vol.195, No.10, 4641-4649, 2015. (要約) Cortical thymic epithelial cells (cTECs) and medullary thymic epithelial cells (mTECs) play essential roles in the positive and negative selection of developing thymocytes, respectively. Aire in mTECs plays an essential role in the latter process through expression of broad arrays of tissue-restricted Ags. To determine whether the location of Aire within the medulla is absolutely essential or whether Aire could also function within the cortex for establishment of self-tolerance, we used bacterial artificial chromosome technology to establish a semiknockin strain of NOD-background (β5t/Aire-transgenic) mice expressing Aire under control of the promoter of β5t, a thymoproteasome expressed exclusively in the cortex. Although Aire was expressed in cTECs as typical nuclear dot protein in β5t/Aire-Tg mice, cTECs expressing Aire ectopically did not confer transcriptional expression of either Aire-dependent or Aire-independent tissue-restricted Ag genes. We then crossed β5t/Aire-Tg mice with Aire-deficient NOD mice, generating a strain in which Aire expression was confined to cTECs. Despite the presence of Aire(+) cTECs, these mice succumbed to autoimmunity, as did Aire-deficient NOD mice. The thymic microenvironment harboring Aire(+) cTECs, within which many Aire-activated genes were present, also showed no obvious alteration of positive selection, suggesting that Aire's unique property of generating a self-tolerant T cell repertoire is functional only in mTECs. (出版サイトへのリンク) ● Publication site (DOI): 10.4049/jimmunol.1501026 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26453754 ● Summary page in Scopus @ Elsevier: 2-s2.0-84951861488 (DOI: 10.4049/jimmunol.1501026, PubMed: 26453754, Elsevier: Scopus)
27.	Hiroshi Kawano, Masaki Hanibuchi, Yoshijima Terumi, Yuko Toyoda, Jun Kishi, Toshifumi Tezuka and Yasuhiko Nishioka : A case of atypical Takayasu arteritis initially presenting with peripheral artery disease, Case Reports in Clinical Pathology, Vol.2, No.2, 34-40, 2015. (出版サイトへのリンク) ● Publication site (DOI): 10.5430/crcp.v2n2p34 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.5430/crcp.v2n2p34 (DOI: 10.5430/crcp.v2n2p34)
28.	Seidai Satou, Masaki Hanibuchi, Makoto Tobiume, Jun Kishi, Yuko Toyoda, Hiroshi Kawano, Mikiko Takahashi, Yuh Fukuda and Yasuhiko Nishioka : A case of IgG4-related interstitial lung disease showing usual interstitial pneumonia pattern: Unusual case for histological features with pathological proof, Case Reports in Clinical Pathology, Vol.2, No.1, 6-11, 2015. (出版サイトへのリンク) ● Publication site (DOI): 10.5430/crcp.v2n1p6 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.5430/crcp.v2n1p6 (DOI: 10.5430/crcp.v2n1p6)
29.	佐藤正大, 後東久嗣, 阿部秀一, 竹﨑彰夫, 河野弘, 青野純典, 西岡安彦 : ヒトfibrocyte分化における遺伝子発現解析と分子標的治療薬による分化制御の検討, 分子呼吸器病, Vol.19, No.1, 135-139, 2015年. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520854804901101056 (CiNii: 1520854804901101056)
30.	Yoshinori Aono, Masami Kishi, Yuki Yokota, Momoyo Azuma, Katsuhiro Kinoshita, Akio Takezaki, Seidai Sato, Hiroshi Kawano, Jun Kishi, Hisatsugu Goto, Hisanori Uehara, Keisuke Izumi and Yasuhiko Nishioka : Role of PDGF/PDGFR axis in the trafficking of circulating fibrocytes in pulmonary fibrosis, American Journal of Respiratory Cell and Molecular Biology, Vol.51, No.6, 793-801, 2014. (要約) Circulating fibrocytes have been reported to migrate into the injured lungs, and contribute to fibrogenesis via CXCL12-CXCR4 axis. In contrast, we report that imatinib mesylate prevented bleomycin (BLM)-induced pulmonary fibrosis in mice by inhibiting platelet-derived growth factor receptor (PDGFR), even when it was administered only in the early phase. The goal of this study was to test the hypothesis that platelet-derived growth factor (PDGF) might directly contribute to the migration of fibrocytes to the injured lungs. PDGFR expression in fibrocytes was examined by flow cytometry and RT-PCR. The migration of fibrocytes was evaluated by using a chemotaxis assay for human fibrocytes isolated from peripheral blood. The numbers of fibrocytes triple-stained for CD45, collagen-1, and CXCR4 were also examined in lung digests of BLM-treated mice. PDGFR mRNA levels in fibrocytes isolated from patients with idiopathic pulmonary fibrosis were investigated by real-time PCR. Fibrocytes expressed both PDGFR-α and -β, and migrated in response to PDGFs. PDGFR inhibitors (imatinib, PDGFR-blocking antibodies) suppressed fibrocyte migration in vitro, and reduced the number of fibrocytes in the lungs of BLM-treated mice. PDGF-BB was a stronger chemoattractant than the other PDGFs in vitro, and anti-PDGFR-β-blocking antibody decreased the numbers of fibrocytes in the lungs compared with anti-PDGFR-α antibody in vivo. Marked expression of PDGFR-β was observed in fibrocytes from patients with idiopathic pulmonary fibrosis compared with healthy subjects. These results suggest that PDGF directly functions as a strong chemoattractant for fibrocytes. In particular, the PDGF-BB-PDGFR-β biological axis might play a critical role in fibrocyte migration into the fibrotic lungs. (キーワード) Animals / Benzamides / Case-Control Studies / Chemotaxis / Drug Evaluation, Preclinical / Female / Humans / Injections, Intraperitoneal / Mice, Inbred C57BL / Piperazines / Platelet-Derived Growth Factor / 肺線維症 (pulmonary fibrosis) / Pyrimidines / Receptor, Platelet-Derived Growth Factor beta / Receptors, CXCR4 / シグナル伝達 (signal transduction) (出版サイトへのリンク) ● Publication site (DOI): 10.1165/rcmb.2013-0455OC (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24885373 ● Summary page in Scopus @ Elsevier: 2-s2.0-84918792291 (DOI: 10.1165/rcmb.2013-0455OC, PubMed: 24885373, Elsevier: Scopus)
31.	Yuko Toyoda, Sho Tabata, Jun Kishi, Takuya Kuramoto, Atsushi Mitsuhashi, Atsuro Saijo, Hiroshi Kawano, Hisatsugu Goto, Yoshinori Aono, Masaki Hanibuchi, Hideaki Horikawa, Toshihiro Nakajima, Tatsuhiko Furukawa, Saburo Sone, Shin-ichi Akiyama and Yasuhiko Nishioka : Thymidine Phosphorylase Regulates the Expression of CXCL10 in Rheumatoid Arthritis Fibroblast-like Synoviocytes, Arthritis & Rheumatology, Vol.66, No.3, 560-568, 2014. (要約) Thymidine phosphorylase (TP) in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) is induced by tumor necrosis factor α (TNFα) and other cytokines that have been reported to be major inflammation mediators in RA. We previously demonstrated that TP plays an important role in angiogenesis and tumor growth, invasion, and metastasis. The aim of this study was to investigate whether the role of TP in the pathogenesis of RA is similar to its role in tumors. In FLS obtained from 2 patients with RA, the expression of TP, interferon-γ (IFNγ)-inducible protein 10 (CXCL10), and other cytokines was measured by quantitative real-time polymerase chain reaction, immunoblotting, and enzyme-linked immunosorbent assays. Microarray analysis was performed using FLS transfected with TYMP complementary DNA and treated with a TP inhibitor. The expression of TP in FLS was up-regulated by TNFα, interleukin-1β (IL-1β), IL-17, IFNγ, and lipopolysaccharide. Microarray analysis of FLS overexpressing TP identified CXCL10 as a thymidine phosphorylase-related gene. The expression of CXCL10 was induced by TNFα, and this induction was suppressed by TYMP small interfering RNA and TP inhibitor. Furthermore, the combination of TNFα and IFNγ synergistically augmented the expression of TP and CXCL10. TP-induced CXCL10 expression was suppressed by the antioxidant EUK-8. In the synovial tissue of patients with RA, TP levels were significantly correlated with CXCL10 expression. The combination of TNFα and IFNγ strongly induced the expression of thymidine phosphorylase in RA FLS. The induction of thymidine phosphorylase enhanced the expression of CXCL10, which may contribute to the Th1 phenotype and bone destruction observed in RA. (キーワード) Arthritis, Rheumatoid / Cells, Cultured / Chemokine CXCL10 / Cytokines / Humans / Interferon-gamma / Synovial Membrane / Thymidine Phosphorylase / Tumor Necrosis Factor-alpha (徳島大学機関リポジトリ) ● Metadata: 106062 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/art.38263 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24574215 ● Summary page in Scopus @ Elsevier: 2-s2.0-84896289470 (徳島大学機関リポジトリ: 106062, DOI: 10.1002/art.38263, PubMed: 24574215, Elsevier: Scopus)
32.	矢野祖, 西條敦郎, 近藤真代, 河野弘, 豊田優子, 柿内聡司, 岸潤, 埴淵昌毅, 古川貴大, 藤田浩司, 西岡安彦 : 神経根障害で発症した神経サルコイドーシスの一例, 四国医学雑誌, Vol.68, No.3,4, 153-158, 2012年. (要約) A52-year-old woman was referred to our hospital for further examination of thoracolumbarpain. As dysesthesia at Th4level was seen in neurological examination, thoracic radiculopathy ormyelopathy was suspected. Blood examination showed elevated level of serum ACE and lysozyme.Lymphadenopathy was evident in bilateral hila and mediastina with marked FDG and Galliumaccumulation in FDG-PET-CT and Gallium scintigraphy, respectively. The number of lymphocytesand the CD4/CD8ratio were increased in the BALF. Histological findings of specimens obtainedfrom the lung and the skin lesion revealed noncaseating epithelioid granuloma, which yielded thediagnosis of sarcoidosis. The cerebrospinal fluid examinations showed elevated level of cell counts,proteins and β2-microglobulin. Taken together, she was diagnosed as neurosarcoidosis with thoracicradiculopathy. Her symptoms were improved with oral administration of prednisolone, butthey were exacerbated when prednisolone dose was tapered to20mg/day. Combined therapy ofmethotrexate and prednisolone was initiated, thereafter her symptoms disappeared completely. (キーワード) neurosarcoidosis / radiculopathy / prednisolone / methotrexate (徳島大学機関リポジトリ) ● Metadata: 102837 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050845763842119680 (徳島大学機関リポジトリ: 102837, CiNii: 1050845763842119680)

総説・解説:

1.	河野弘, 西岡安彦 : グッドパスチャー症候群, 日本医師会雑誌, Vol.149, No.2, 244-246, 2020年10月.
2.	豊田優子, 佐藤正大, 河野弘, 西岡安彦 : 関節リウマチ治療薬と肺病変, 呼吸器内科, Vol.36, No.6, 618-626, 2019年12月. (キーワード) rheumatoid arthritis (RA) / drug-induced pneumonia / methotrexate (MTX) / biological drug / disease modifying antirheumatic drugs (DMARDs) (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1523388080905010944 (CiNii: 1523388080905010944)
3.	河野弘, 西岡安彦 : 間質性肺炎・慢性閉塞性肺疾患, 薬局, Vol.70, No.5, 85-90, 2019年4月.
4.	森住俊, 河野弘, 豊田優子, 小山壱也, 西村春佳, 香川耕造, 後東久嗣, 西岡安彦 : ブレオマイシン肺線維症モデルにおける線維芽細胞増殖因子受容体阻害薬の抗線維化効果の検討, 分子呼吸器病, Vol.22, No.1, 96-98, 2018年3月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520573330524696832 (CiNii: 1520573330524696832)
5.	河野弘, 西岡安彦 : 膠原病における肺病変へのアプローチ, リウマチ科, Vol.55, No.4, 345-352, 2016年4月.
6.	豊田優子, 河野弘, 西岡安彦 : 間質性肺炎の免疫療法は有効か?, 呼吸器内科, Vol.28, No.6, 451-455, 2015年.

国際会議:

1.	Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Murakami Kojin, Yuya Yamashita, Danzan NandinErdene, Bando Hiroki, Keiko Haji, Nobuhito Naito, Hiroshi Kawano, Eiji Hara and Yasuhiko Nishioka : A novel senolytic drug, ARV-825, ameliorates experimental lung fibrosis, ERS International Congress 2023, Milano, Sep. 2023.
2.	Hiroki Bando, Seidai Satou, Hirohisa Ogawa, Kazuya Koyama, Murakami Kojin, Yuya Yamashita, Danzan Nandin-Erdene, Keiko Haji, Nobuhito Naito, Hiroshi Kawano and Yasuhiko Nishioka : Anamorelin, a ghrelin receptor agonist, inhibited the allergic airway inflammation in mice, ERS International Congress 2023, Milano, Sep. 2023.
3.	Murakami Kojin, Nishimura Haruka, Hiroshi Kawano, Danzan Nandin-Erdene, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kazuya Koyama, Seidai Satou and Yasuhiko Nishioka : Analysis of the Anti-fibrotic Potential of JAK Inhibitors in a Bleomycin-induced Pulmonary Fibrosis Model, ATS 2023, Washington, DC, May 2023.
4.	Kazuya Koyama, Seidai Satou, Hiroshi Kawano, Hiroshi Kawano, Atsushi Mitsuhashi, Murakami Kojin, Yuya Yamashita, Keiko Haji, Kozo Kagawa, Hirohisa Ogawa and Yasuhiko Nishioka : Evaluation of fibrocytes in silica-induced and bleomycin-induced pulmonary fibrosis model in mice by single cell RNA-seq analysis, APSR 2022, Seoul, Nov. 2022.
5.	Imakura Takeshi, Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Takahiro Niimura, Murakami Kojin, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : Computational drug repositioning and wet-lab validation approach identifies polo-like kinase inhibitors as potential therapeutics for pulmonary fibrosis, ERS International Congress 2022, Barcelona, Sep. 2022.
6.	Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Kojin Murakami, Takeshi Imakura, Yuya Yamashita, Keiko Haji, Kozo Kagawa, Hiroshi Kawano, Eiji Hara and Yasuhiko Nishioka : A Novel Senolytic Agent, ARV-825, Ameliorates Bleomycin-InducedPulmonary Fibrosis in Mice, ATS 2022 International Conference, San Francisco, May 2022.
7.	Takeshi Imakura, Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Takahiro Niimura, Kojin Murakami, Yuya Yamashita, Keiko Haji, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : Computational Drug Repositioning Approach Identifies Polo-Like KinaseInhibitors as Potential Therapeutics for Pulmonary Fibrosis, ATS 2022 International Conference, San Francisco, May 2022.
8.	Kazuya Koyama, Hiroshi Kawano, Atsushi Mitsuhashi, Kojin Murakami, Takeshi Imakura, Yuya Yamashita, Keiko Haji, Kozo Kagawa, Seidai Satou, Hirohisa Ogawa and Yasuhiko Nishioka : Single Cell RNA-seq Analysis of Fibrocytes in Silica Induced Mouse Pulmonary Fibrosis Model, ATS 2022 International Conference, San Francisco, May 2022.
9.	Imakura Takeshi, Seidai Satou, Kazuya Koyama, Takahiro Niimura, Kohjin Murakami, Yuya Yamashita, Takahashi Naoki, Nobuhito Naito, Kozo Kagawa, Hiroshi Kawano, Yoshito Zamami, Keisuke Ishizawa and Yasuhiko Nishioka : Polo-like kinase inhibitors identified by computational repositioning attenuates bleomycin-induced pulmonary fibrosis in mice, APSR 2021, Kyoto and online, Nov. 2021.
10.	Kohjin Murakami, Takahashi Naoki, Seidai Satou, Imakura Takeshi, Yuya Yamashita, Kozo Kagawa, Kazuya Koyama, Hiroshi Kawano, Tanigawara Kazuaki, Toriumi Wataru and Yasuhiko Nishioka : Therapeutic effect of oligonucleotide therapeutics PK-7010 in mouse model of bleomycin-induced lung fibrosis, APSR 2021, Kyoto and online, Nov. 2021.
11.	Nobuhito Naito, Hiroshi Kawano, Imakura Takeshi, Yuya Yamashita, Kohjin Murakami, Kozo Kagawa, Kazuya Koyama, Seidai Satou, Hiroshi Nokihara, Inagaki Yutaka and Yasuhiko Nishioka : Development of improved method to identify and analyze lung fibrocytes with flow cytometry in a reporter mouse strain, APSR 2021, Kyoto and online, Nov. 2021.
12.	Kozo Kagawa, Kazuya Koyama, Seidai Satou, Imakura Takeshi, Kohjin Murakami, Yuya Yamashita, Takahashi Naoki, Nobuhito Naito, Hiroshi Kawano and Yasuhiko Nishioka : A Lck-specific inhibitor, A-770041, attenuates pulmonary fibrosis via the suppression of TGF-b production in regulatory T cells, APSR 2021, Kyoto and online, Nov. 2021. (出版サイトへのリンク) ● Publication site (DOI): 10.1111/resp.14150_945 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1111/resp.14150_945 (DOI: 10.1111/resp.14150_945)
13.	Hiroshi Kawano, Nishimura Haruka, Imakura Takeshi, Yuya Yamashita, Kohjin Murakami, Nobuhito Naito, Kozo Kagawa, Kazuya Koyama, Seidai Satou, Hiroshi Nokihara and Yasuhiko Nishioka : Analysis of anti-fibrotic potential of JAK inhibitors in bleomycin-induced pulmonary fibrosis model, APSR 2021, Kyoto and online, Nov. 2021. (出版サイトへのリンク) ● Publication site (DOI): 10.1111/resp.14150_915 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1111/resp.14150_915 (DOI: 10.1111/resp.14150_915)
14.	Kozo Kagawa, Kazuya Koyama, Seidai Satou, Imakura Takeshi, Kohjin Murakami, Takahashi Naoki, Nobuhito Naito, Nishimura Haruka, Hiroshi Kawano and Yasuhiko Nishioka : Anti-fibrotic efficacy of Lck inhibitor via the suppression of TGF-β production in regulatory T cells, ERS International Congress 2021, WEB, Sep. 2021. (出版サイトへのリンク) ● Publication site (DOI): 10.1183/13993003.congress-2021.PA3285 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1183/13993003.congress-2021.PA3285 (DOI: 10.1183/13993003.congress-2021.PA3285)
15.	Takahashi Naoki, Seidai Satou, Imakura Takeshi, Kohjin Murakami, Nobuhito Naito, Kozo Kagawa, Kazuya Koyama, Hiroshi Kawano, Tanigawara Kazuaki, Toriumi Wataru and Yasuhiko Nishioka : Oligonucleotide therapeutics PK-7010 in combination with nintedanib ameliorates bleomycin-induced pulmonary fibrosis in mice, ATS 2021, 米国(WEB), May 2021. (出版サイトへのリンク) ● Publication site (DOI): 10.1164/ajrccm-conference.2021.203.1_MeetingAbstracts.A4444 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1164/ajrccm-conference.2021.203.1_MeetingAbstracts.A4444 (DOI: 10.1164/ajrccm-conference.2021.203.1_MeetingAbstracts.A4444)
16.	Kazuya Koyama, Hiroshi Kawano, Yuya Yamashita, Imakura Takeshi, Takahashi Naoki, Nobuhito Naito, Seidai Satou and Yasuhiko Nishioka : Clinical Features of the Acute Exacerbation of Rheumatoid Arthritis-Associated Interstitial Lung Disease, ATS 2021, 米国(WEB), May 2021.
17.	Takahashi Naoki, Seidai Satou, Imakura Takeshi, Murakami Kojin, Nobuhito Naito, Kozo Kagawa, Kazuya Koyama, Hiroshi Kawano, Tanigawara Kazuaki, Toriumi Wataru and Yasuhiko Nishioka : The novel oligonucleotide therapeutics PK-7010 for TGF-β1 ameliorates bleomycin-induced pulmonary fibrosis in micen, ERS International Congress 2020 Virtual, WEB, Sep. 2020. (出版サイトへのリンク) ● Publication site (DOI): 10.1183/13993003.congress-2020.3373 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1183/13993003.congress-2020.3373 (DOI: 10.1183/13993003.congress-2020.3373)
18.	Seidai Satou, Yamamoto Takushi, Waki Kana, Morimoto Yuki, Imakura Takeshi, Murakami Kojin, Takahashi Naoki, Nobuhito Naito, Kozo Kagawa, Kazuya Koyama, Hiroshi Kawano, Koichi Tsuneyama and Yasuhiko Nishioka : Analysis of localization of nintedanib and cyclophosphamide in pulmonary fibrosisusing the iMScope TRIOS, ERS International Congress 2020 Virtual, WEB, Sep. 2020. (出版サイトへのリンク) ● Publication site (DOI): 10.1183/13993003.congress-2020.3385 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1183/13993003.congress-2020.3385 (DOI: 10.1183/13993003.congress-2020.3385)
19.	Kozo Kagawa, Koyama Kazuya, Seidai Satou, Takahashi Naoki, Nishimura Haruka, Nobuhito Naito, Hiroshi Kawano, Yuko Toyoda and Yasuhiko Nishioka : Antifibrotic effects of Lck inhibition on bleomycin-induced pulmonary fibrosis in mice., ERS International Congress 2019, Madrid, Oct. 2019. (出版サイトへのリンク) ● Publication site (DOI): 10.1183/13993003.congress-2019.PA5372 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1183/13993003.congress-2019.PA5372 (DOI: 10.1183/13993003.congress-2019.PA5372)
20.	Koyama Kazyua, Nobuhito Naito, Kozo Kagawa, Nishimura Haruka, Hiroshi Kawano, Yuko Toyoda, Hisatsugu Goto, Masahiko Azuma and Yasuhiko Nishioka : Acute Respiratory Failure in Patients with Rheumatoid Arthritis Associated Interstitial Lung Disease, ATS 2019 International Conference, Dallas, May 2019. (出版サイトへのリンク) ● Publication site (DOI): 10.1164/ajrccm-conference.2019.199.1_MeetingAbstracts.A1445 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.1164/ajrccm-conference.2019.199.1_MeetingAbstracts.A1445 (DOI: 10.1164/ajrccm-conference.2019.199.1_MeetingAbstracts.A1445)
21.	Hiroshi Kawano, Koyama Kazuya, Nishimura Haruka, Yuko Toyoda, Kagawa Kozo, Seidai Satou, Naito Nobuhito, Hisatsugu Goto, Inagaki Yutaka and Yasuhiko Nishioka : Development of improved method to identify and analyze lung fibrocytes with flow cytometry in a reporter mouse strain, ERS International Congress, Paris, Sep. 2018.
22.	Koyama Kazuya, Kagawa Kozo, Nishimura Haruka, Hiroshi Kawano, Yuko Toyoda, Hisatsugu Goto, Hirohisa Ogawa, Hisanori Uehara and Yasuhiko Nishioka : Novel Multi-tyrosine Kinase Inhibitor TAS-115 Attenuates Bleomycin-induced Pulmonary Fibrosis In Mice., ATS 2018 International Conference, San Diego, May 2018.
23.	Yuko Toyoda, Morizumi Shun, Seidai Satou, Okazaki Hiroyasu, Chen Yanjuan, Hisatsugu Goto, Hirohisa Ogawa, Nishimura Haruka, Koyama Kazuya, Hiroshi Kawano, Yoshinori Aono, Hisanori Uehara and Yasuhiko Nishioka : Role of Fibroblast Growth Factor/Fibroblast Growth Factor Receptor Signal in Bleomycin-Induced Pulmonary Fibrosis in Mice., ATS 2017 International Conference, Washington, D.C., May 2017.
24.	Seidai Satou, Hisatsugu Goto, Shun Morizumi, Hiroyasu Okazaki, Yajuan Chen, Hiroshi Kawano, Yuko Toyoda, Masaki Hanibuchi, Masahiko Azuma and Yasuhiko Nishioka : Effect of blockade of fibroblast growth factor receptor signaling in experimental pulmonary fibrosis in mice, ATS 2016 International Conference, May 2016.
25.	Hiroshi Kawano, Hitoshi Nishijima, Junko Morimoto, Yasuhiro Mouri and Mitsuru Matsumoto : Aire expression is inherent to all medullary thymic epithelial cells during their differentiation program, The 4th European Congress of Immunology, Vienna, Austria, Sep. 2015.
26.	Katsuhiro Kinoshita, Yoshinori Aono, Hisatsugu Goto, Momoyo Azuma, Takezaki Akio, Yoshijima Terumi, Kishi Masami, Jun Kishi, Yuko Toyoda, Hiroshi Kawano, Abe Shuichi, Toshifumi Tezuka, Hisanori Uehara, Keisuke Izumi and Yasuhiko Nishioka : Antifibrotic effects of focal adhesion kinase inhibitor in bleomycin-induced pulmonary fibrosis in mice., 18th Congress of the Asian Pacific Society of Respirology, Yokohama, Nov. 2013.

国内講演発表:

1.	坂東紀子, 坂東弘基, 土師恵子, 美馬正人, 福家麻美, 内藤伸仁, 尾崎領彦, 荻野広和, 佐藤正大, 河野弘, 坂口暁, 埴淵昌毅, 西岡安彦 : 当科における重症喘息に対する生物学的製剤の治療効果の検討, 第268回徳島医学会学術集会, 2024年3月.
2.	山本浩生, 坂東弘基, 土師恵子, 山下雄也, 内藤伸仁, 佐藤正大, 河野弘, 埴淵昌毅, 西岡安彦 : ステロイド抵抗性の気道病変に対してシクロホスファミドが著効した再発性多発軟骨炎の1例, 第129回日本内科学会四国地方会, 2023年12月.
3.	河野弘, 青井優, 安宅克博, 村上行人, 山下雄也, 内藤伸仁, 荻野広和, 佐藤正大, 西岡安彦 : 顕微鏡的多発血管炎の診断時にEBVの再活性化を呈し，リツキシマブにて寛解導入療法を行った1例, 第34回日本リウマチ学会中国・四国支部学術集会, 2023年12月.
4.	青井優, 河野弘, 安宅克博, 村上行人, 山下雄也, 内藤伸仁, 荻野広和, 佐藤正大, 西岡安彦 : 胸膜炎，間質性肺疾患を先行し，発熱性好中球減少症と肺病変の増悪で発症したSLEの1例, 第34回日本リウマチ学会中国・四国支部学術集会, 2023年12月.
5.	坂東弘基, 佐藤正大, 村上行人, 山下雄也, 内藤伸仁, 小山壱也, 河野弘, 小川博久, 西岡安彦 : グレリン受容体作動薬アナモレリンのアレルギー性気道炎症モデルマウスにおける検討, 第72回日本アレルギー学会学術大会, 2023年10月.
6.	佐藤正大, 小川博久, 村上行人, 山下雄也, 土師恵子, 河野弘, 原英二, 西岡安彦 : BRD4 阻害剤 ARV825 の線維化関連遺伝子の発現抑制と老化細胞除去を介した抗線維化効果の検討, 第3回日本びまん性肺疾患研究会, 2023年9月.
7.	土師恵子, 佐藤正大, 小川博久, 村上行人, 山下雄也, 小山壱也, 河野弘, 小林克利, 諸星俊郎, 西岡安彦 : オートタキシン阻害作用を有する 2ccPA の肺線維症における有効性の検討, 第3回日本びまん性肺疾患研究会, 2023年9月.
8.	寺澤翠, 坂東弘基, 土師恵子, 小路貴俊, 米田浩人, 佐藤正大, 河野弘, 埴淵昌毅, 西岡安彦 : シクロスポリンが有効であった血清IL-18高値の重症成人発症スティル病の1例, 第128回日本内科学会四国地方会, 2023年7月.
9.	坂東弘基, 佐藤正大, 村上行人, 山下雄也, 内藤伸仁, 小山壱也, 河野弘, 小川博久, 西岡安彦 : グレリン受容体作動薬アナモレリンのアレルギー性気道炎症モデルマウスにおける検討, 第63回日本呼吸器学会学術講演会, 2023年4月.
10.	村上行人, 佐藤正大, 山下雄也, 土師恵子, 坂東弘基, 内藤伸仁, 小山壱也, 河野弘, 稲村典昭, 蓮見惠司, 西岡安彦 : 新規可溶性エポキシヒドロラーゼ阻害薬SMTP-44Dの肺線維症に対する有効性の検討, 第63回日本呼吸器学会学術講演会, 2023年4月.
11.	河野弘, 小路貴俊, 安宅克博, 村上行人, 山下雄也, 内藤伸仁, 荻野広和, 佐藤正大, 西岡安彦 : リンパ球特異的チロシンキナーゼ阻害薬A-770041は制御性T細胞によるTGF-βs産生抑制を介して肺線維症を改善する, 第67回日本リウマチ学会総会・学術集会, 2023年4月.
12.	新居香織, 土師恵子, 青井優, 山下雄也, 内藤伸仁, 荻野広和, 河野弘, 佐藤正大, 埴淵昌毅, 西岡安彦 : 関節炎を呈したACTH 単独欠損症の1例, 第127回日本内科学会四国地方会, 2022年12月.
13.	寺澤翠, 土師恵子, 市原聖也, 山下雄也, 福家麻美, 内藤伸仁, 米田浩人, 香川耕造, 荻野広和, 河野弘, 佐藤正大, 埴淵昌毅, 西岡安彦 : 抗PD-L1抗体投与後に顕在化した抗ARS抗体陽性間質性肺炎の1例, 第67回日本呼吸器学会中国・四国地方会, 2022年12月.
14.	小路貴俊, 内藤伸仁, 河野弘, 村上行人, 山下雄也, 美馬正人, 荻野広和, 佐藤正大, 西岡安彦 : 両側声帯麻痺を呈した多発血管炎性肉芽腫症に伴う肥厚性硬膜炎の1例, 第33回日本リウマチ学会中国・四国支部学術集会, 2022年12月.
15.	安宅克博, 河野弘, 小路貴俊, 村上行人, 山下雄也, 美馬正人, 内藤伸仁, 荻野広和, 佐藤正大, 西岡安彦 : 劇症1型糖尿病と同時期に発症した両側特発性外眼筋炎の1例, 第33回日本リウマチ学会中国・四国支部学術集会, 2022年12月.
16.	内藤伸仁, 西村春佳, 山下雄也, 村上行人, 土師恵子, 小山壱也, 荻野広和, 佐藤正大, 河野弘, 埴淵昌毅, 西岡安彦 : ブレオマイシン誘発肺線維症モデルマウスを用いたJAK阻害薬の抗線維化効果についての検討, 第50回日本臨床免疫学会総会, 2022年10月.
17.	土師恵子, 矢葺洋平, 美馬正人, 米田浩人, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : MET阻害薬が著効したMET遺伝子 exon14 skipping 変異陽性肺扁平上皮癌の1例, 第126回日本内科学会四国地方会, 2022年6月.
18.	高橋啓輝, 矢葺洋平, 市原聖也, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 重度の嚥下障害を合併した抗Ro52抗体陽性皮膚筋炎の1例, 第126回日本内科学会四国地方会, 2022年6月.
19.	河野弘, 今倉健, 山下雄也, 村上行人, 内藤伸仁, 佐藤正大, 西岡安彦 : ブレオマイシン誘発肺線維症モデルマウスにおけるJAK阻害薬の抗線維化効果に関する検討, 第66回日本リウマチ学会総会・学術集会, 2022年4月.
20.	Seidai Satou, Kazuya Koyama, Hirohisa Ogawa, Kojin Murakami, Takeshi Imakura, Yuya Yamashita, Hiroshi Kawano, Eiji Hara and Yasuhiko Nishioka : Antifibrotic and senolytic activity of novel BRD4 degrader ARV825 in experimental model of lung fibrosis, The 62nd Annual Meeting of the Japanese Respiratory Society, Apr. 2022.
21.	美馬正人, 佐藤正大, 原田紗希, 鈴江涼子, 山下雄也, 尾崎領彦, 土師恵子, 内藤伸仁, 河野弘, 軒原浩, 西岡安彦 : 抗ARS抗体陽性間質性肺疾患の胸部画像所見の検討, 第62回日本呼吸器学会学術講演会, 2022年4月.
22.	小山壱也, 三橋惇志, 今倉健, 村上行人, 香川耕造, 佐藤正大, 河野弘, 小川博久, 西岡安彦 : シングルセル解析を用いた肺線維症マウスモデルにおけるfibrocyteの検討, 第62回日本呼吸器学会学術講演会, 2022年4月.
23.	河野弘, 今倉健, 村上行人, 内藤伸仁, 香川耕造, 小山壱也, 佐藤正大, 軒原浩, 西岡安彦 : レポーターマウスを用いた肺線維細胞の新規同定法, 第62回日本呼吸器学会学術講演会, 2022年4月.
24.	今倉健, 佐藤正大, 小山壱也, 新村貴博, 村上行人, 山下雄也, 土師恵子, 香川耕造, 河野弘, 座間味義人, 石澤啓介, 西岡安彦 : In silico解析により同定されたPLK阻害剤のブレオマイシン誘発肺線維症モデルマウスにおける効果の検討, 第62回日本呼吸器学会学術講演会, 2022年4月.
25.	石田卓也, 河野弘, 今倉健, 村上行人, 山下雄也, 美馬正人, 内藤伸仁, 荻野広和, 佐藤正大, 西岡安彦 : 当院における膠原病関連間質性肺疾患に対するニンテダニブの使用経験, 第32回日本リウマチ学会中国・四国支部学術集会, 2021年12月.
26.	市原聖也, 河野弘, 今倉健, 村上行人, 山下雄也, 美馬正人, 内藤伸仁, 荻野広和, 佐藤正大, 西岡安彦 : 再発性多発軟骨炎治療中の不明熱精査でUBA1遺伝子解析により診断したVEXAS症候群の1例, 第32回日本リウマチ学会中国・四国支部学術集会, 2021年12月.
27.	市原聖也, 矢葺洋平, 村上行人, 香川耕造, 米田浩人, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 亜急性に進行し，蜂巣肺様の所見を呈した薬剤性肺障害の1例, 第125回日本内科学会四国地方会, 2021年12月.
28.	石田卓也, 矢葺洋平, 香川耕造, 山下雄也, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 成人Still病との鑑別を要した家族性地中海熱非典型例の1例, 第125回日本内科学会四国地方会, 2021年12月.
29.	村上尚哉, 矢葺洋平, 尾崎領彦, 香川耕造, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : Sitafloxacinが奏効した肺Mycobacterium abscessus subsp. massiliense 症の1例, 第72回日本結核・非結核性抗酸菌症学会中国四国支部会, 2021年12月.
30.	高丸利加子, 矢葺洋平, 磯村祐太, 香川耕造, 小山壱也, 大塚憲司, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 自然退縮を認めた気管支原発唾液腺型腫瘍の1例, 第30回日本呼吸器内視鏡学会中国四国支部会, 2021年12月.
31.	小川瑛, 矢葺洋平, 青井優, 香川耕造, 小山壱也, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 両側肺に多発する斑状影を呈した自己免疫性肺胞蛋白症の1例, 第65回日本呼吸器学会中国・四国地方会, 2021年12月.
32.	原田祥子, 矢葺洋平, 美馬正人, 尾崎領彦, 香川耕造, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 非結核性抗酸菌症との鑑別を要し，amikacin + minocyclineが奏効した肺ノカルジア, 第65回日本呼吸器学会中国・四国地方会, 2021年12月.
33.	小山壱也, 河野弘, 西岡安彦 : 肺線維化におけるシングルセル解析, 第1回日本びまん性肺疾患研究会(基礎研究特別講演), 2021年10月.
34.	村上行人, 高橋直希, 佐藤正大, 今倉健, 山下雄也, 香川耕造, 小山壱也, 河野弘, 谷川原万顕, 鳥海亙, 西岡安彦 : ブレオマイシン誘発肺線維症モデルマウスにおける新規核酸医薬の有効性の検討, 第1回日本びまん性肺疾患研究会, 2021年10月.
35.	坂口暁, 矢葺洋平, 今倉健, 米田浩人, 村上行人, 小山壱也, 香川耕造, 小川瑛, 荻野広和, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 索状の小葉間隔壁の肥厚を認め胸腔鏡下肺生検にて診断した間質性肺炎の1例, 第63回日本呼吸器学会中国・四国地方会, 2021年8月.
36.	高丸利加子, 内藤伸仁, 原田紗希, 山下雄也, 尾崎領彦, 高橋直希, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 当科における全身性エリテマトーデスに対するベリムマブの使用経験, 第124回日本内科学会四国地方会, 2021年5月.
37.	石田卓也, 内藤伸仁, 今倉健, 香川耕造, 佐藤正大, 河野弘, 軒原浩, 高山哲治, 西岡安彦 : レンバチニブによる薬剤性肺障害の1例, 第124回日本内科学会四国地方会, 2021年5月.
38.	山下雄也, 今倉健, 高橋直希, 内藤伸仁, 佐藤正大, 河野弘, 西岡安彦 : 関節リウマチに伴う間質性肺炎急性増悪の臨床的特徴 ∼特発性肺線維症急性増悪との比較検討∼, 第65回日本リウマチ学会総会・学術集会, 2021年4月.
39.	村上行人, 佐藤正大, 今倉健, 西村春佳, 高橋直希, 内藤伸仁, 香川耕造, 小山壱也, 河野弘, 吾妻雅彦, 軒原浩, 西岡安彦 : 抗線維化薬2剤を切り替えて使用した特発性肺線維症症例の後方視的検討, 第61回日本呼吸器学会学術講演会, 2021年4月.
40.	西村春佳, 佐藤正大, 今倉健, 村上行人, 内藤伸仁, 香川耕造, 小山壱也, 河野弘, 軒原浩, 西岡安彦 : ブレオマイシン誘発肺線維症モデルマウスにおけるJAK阻害剤の効果に関する検討, 第61回日本呼吸器学会学術講演会, 2021年4月.
41.	高橋直希, 佐藤正大, 今倉健, 村上行人, 内藤伸仁, 香川耕造, 小山壱也, 河野弘, 軒原浩, 谷川原万顕, 鳥海亙, 西岡安彦 : ブレオマイシン誘発肺線維症モデルマウスにおける核酸医薬PK-7010とnintedanibの併用効果の検討, 第61回日本呼吸器学会学術講演会, 2021年4月.
42.	今倉健, 内藤伸仁, 山下雄也, 原田紗希, 香川耕造, 米田浩人, 佐藤正大, 河野弘, 長谷加容子, 軒原浩, 西岡安彦 : 当科における成人発症スティル病症例の検討, 第262回徳島医学会学術集会, 2021年3月.
43.	青井優, 内藤伸仁, 今倉健, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : Atezolizumab投与後に著明な血小板減少症をきたした1例, 第262回徳島医学会学術集会, 2021年3月.
44.	美馬正人, 内藤伸仁, 原田紗希, 今倉健, 山下雄也, 髙橋直希, 佐藤正大, 河野弘, 西岡安彦 : 当科における抗ARS抗体陽性症例の検討, 第31回日本リウマチ学会中国・四国支部学術集会, 2020年12月.
45.	山下雄也, 内藤伸仁, 原田紗希, 今倉健, 髙橋直希, 佐藤正大, 河野弘, 西岡安彦 : ST合剤による無菌性髄膜炎を呈したシェーグレン症候群の一例, 第31回日本リウマチ学会中国・四国支部学術集会, 2020年12月.
46.	原田紗希, 内藤伸仁, 岡本悠里, 香川耕造, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 不明熱の精査でMEFV遺伝子解析により診断した家族性地中海熱の1例, 第123回日本内科学会四国地方会, 2020年11月.
47.	阿部あかね, 内藤伸仁, 大塚憲司, 川上行奎, 藤井志朗, 岩本誠司, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 非小細胞肺癌に合併した後天性血友病Aの1例, 第123回日本内科学会四国地方会, 2020年11月.
48.	米田浩人, 内藤伸仁, 香西博之, 大塚憲司, 佐藤正大, 河野弘, 軒原浩, 吾妻雅彦, 西岡安彦 : 当科における悪性胸膜中皮腫に対するnivolumab投与症例の検討, 第123回日本内科学会四国地方会, 2020年11月.
49.	折野逸人, 内藤伸仁, 内藤仁美, 髙橋直希, 田中宏典, 佐藤正大, 河野弘, 上原久典, 軒原浩, 高山哲治, 西岡安彦 : 肝肺症候群に進展したサルコイドーシスの1例, 第64回日本呼吸器学会中国・四国地方会, 2020年11月.
50.	磯村祐太, 内藤伸仁, 山下雄也, 福家麻美, 小山壱也, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 当科における胸水貯留を呈した膠原病および類縁疾患症例の検討, 第64回日本呼吸器学会中国・四国地方会, 2020年11月.
51.	梶本達也, 内藤伸仁, 内藤仁美, 佐藤正大, 河野弘, 軒原浩, 吾妻雅彦, 西岡安彦 : 全身性強皮症に伴う間質性肺炎の増悪との鑑別を要した鳥関連過敏性肺炎の1例, 第29回日本呼吸器内視鏡学会中国四国支部会, 2020年11月.
52.	國重道大, 内藤伸仁, 原田紗季, 山下雄也, 高橋直希, 美馬正人, 香西博之, 佐藤正大, 河野弘, 西庄俊彦, 浜田大輔, 軒原浩, 松浦哲也, 西良浩一, 西岡安彦 : 当科における骨・関節病変を呈した非結核性抗酸菌症の検討, 第71回日本結核・非結核性抗酸菌症学会中国四国支部会, 2020年11月.
53.	河野弘, 山下雄也, 内藤伸仁, 佐藤正大, 門田宗之, 伊勢孝之, 八木秀介, 佐田政隆, 軒原浩, 西岡安彦 : 高安動脈炎による難治性皮膚潰瘍に対してべペルミノゲンペルプラスミド(ヒト肝細胞増殖因子プラスミドベクター)投与が奏効した1例, 第48回日本臨床免疫学会総会, 2020年10月.
54.	髙橋直希, 佐藤正大, 小山壱也, 香川耕造, 内藤伸仁, 今倉健, 豊田優子, 河野弘, 谷川原万顕, 鳥海亙, 西岡安彦 : ブレオマイシン誘発肺線維症モデルマウスにおける核酸医薬PK-7010の抗線維化効果の検討, 第60回日本呼吸器学会学術講演会, 2020年9月.
55.	香川耕造, 小山壱也, 佐藤正大, 髙橋直希, 西村春佳, 河野弘, 豊田優子, 篠原勉, 西岡安彦 : ブレオマイシン肺線維症マウスモデルにおけるLck阻害の抗線維化効果, 第60回日本呼吸器学会学術講演会, 2020年9月.
56.	西岡安彦, 小山壱也, 三橋惇志, Afroj Tania, 河野弘 : 肺線維症モデルにおけるscRNA-Seqを用いた線維細胞の解析, 第60回日本呼吸器学会学術講演会(シンポジウム), 2020年9月.
57.	河野弘, 内藤伸仁, 安宅克博, 今倉健, 山下雄也, 高橋直希, 近藤真代, 佐藤正大, 豊田優子, 西岡安彦 : 当院における進行性線維化を伴う膠原病関連間質性肺疾患の検討, 第64回日本リウマチ学会総会・学術集会, 2020年8月.
58.	佐藤正大, 村上行人, 豊田優子, 小山壱也, 西村春佳, 香川耕造, 髙橋直希, 河野弘, 吾妻雅彦, 西岡安彦 : 2剤の抗線維化薬を使用した特発性肺線維症症例の検討, 第117回日本内科学会講演会, 2020年8月.
59.	青井優, 香川耕造, 内藤伸仁, 佐藤正大, 河野弘, 三好人正, 松浦朋美, 柏原秀也, 吉川幸造, 豊田優子, 坂東良美, 軒原浩, 高山哲治, 島田光生, 西岡安彦 : 好酸球性多発血管炎性肉芽腫症の治療中に回腸出血をきたし，血管炎との鑑別が困難であったCMV腸炎の1例, 第260回徳島医学会学術集会, 2020年2月.
60.	安宅克博, 河野弘, 今倉健, 内藤伸仁, 近藤真代, 佐藤正大, 豊田優子, 西岡安彦 : 蛋白濾出性胃腸症，クリオグロブリン血症を伴ったMCTDの1例, 第30回日本リウマチ学会中国・四国支部学術集会, 2019年12月.
61.	内藤伸仁, 河野弘, 今倉健, 近藤真代, 佐藤正大, 豊田優子, 西岡安彦 : 当科におけるANCA陽性間質性肺炎症例の検討, 第30回日本リウマチ学会中国・四国支部学術集会, 2019年12月.
62.	石田卓也, 香川耕造, 米田浩人, 西村賢二, 山本遥平, 佐藤正大, 河野弘, 軒原浩, 西岡安彦 : 顕微鏡的多発血管炎の治療中に重症筋無力症クリーゼを発症した1例, 第121回日本内科学会四国地方会, 2019年12月.
63.	石田卓也, 香川耕造, 米田浩人, 坂東紀子, 内藤伸仁, 荻野広和, 佐藤正大, 河野弘, 西村賢二, 山本遥平, 豊田優子, 軒原浩, 西岡安彦 : 顕微鏡的多発血管炎の治療中に重症筋無力症クリーゼを発症した1例, 第259回徳島医学会学術集会, 2019年8月.
64.	香川耕造, 小山壱也, 佐藤正大, 高橋直希, 西村春佳, 内藤伸仁, 河野弘, 豊田優子, 西岡安彦 : ブレオマイシン肺線維症マウスモデルにおけるLck阻害の抗線維化効果, 第61回日本呼吸器学会中国・四国地方会, 2019年7月.
65.	内藤仁美, 香川耕造, 近藤真代, 佐藤正大, 内藤伸仁, 河野弘, 豊田優子, 吾妻雅彦, 軒原浩, 西岡安彦 : 関節リウマチで治療中に抗MDA5抗体陽性をみとめ，無筋症性皮膚筋炎と診断された間質性肺炎の2例, 第61回日本呼吸器学会中国・四国地方会, 2019年7月.
66.	福家麻美, 豊田優子, 荻野広和, 河野弘, 後東久嗣, 軒原浩, 吾妻雅彦, 西岡安彦 : Stevens-Johnson症候群後に合併した閉塞性細気管支炎にステロイドおよびタクロリムスが有効であった1例, 第6回日本呼吸ケア・リハビリテーション学会中国・四国支部学術集会, 2019年6月.
67.	髙橋直希, 内藤伸仁, 近藤真代, 荻野広和, 河野弘, 豊田優子, 三木浩和, 吾妻雅彦, 軒原浩, 西岡安彦 : 治療抵抗性のSLEに伴う赤芽球癆にシクロホスファミドパルス療法が著効した1例, 第120回日本内科学会四国地方会, 2019年5月.
68.	内藤伸仁, 河野弘, 近藤真代, 荻野広和, 佐藤正大, 豊田優子, 後東久嗣, 西岡安彦 : 間質性肺炎合併関節リウマチに対するJAK阻害薬の使用経験, 第63回日本リウマチ学会総会・学術集会, 2019年4月.
69.	岡﨑弘泰, 佐藤正大, 森住俊, 小山壱也, 小川博久, 香川耕造, 西村春佳, Yajuan Chen, 青野純典, 阿部秀一, 東桃代, 後東久嗣, 河野弘, 豊田優子, 上原久典, 小路弘行, 西岡安彦 : ブレオマイシン肺線維症マウスモデルにおけるWnt/B-カテニン/CBPシグナル阻害薬PRI-724による抗線維化効果の検討, 第59回日本呼吸器学会学術講演会, 2019年4月.
70.	Hiroshi Nokihara, Masaki Hanibuchi, Souji Kakiuchi, Atagi Shinji, Ogushi Fumitaka, Shimizu Eiji, Haku Takashi, Yuko Toyoda, Masahiko Azuma, Mayo Kondou, Hiroshi Kawano, Kenji Otsuka, Satoshi Sakaguchi, Hisatsugu Goto and Yasuhiko Nishioka : A multicenter, open-label, phase II trial of S-1 plus carboplatin in advanced NSCLC patients with interstitial lung disease, The 59th Annual Meeting of the Japanese Respiratory Society, Apr. 2019.
71.	小山壱也, 内藤伸仁, 香川耕造, 西村春佳, 佐藤正大, 河野弘, 豊田優子, 後東久嗣, 吾妻雅彦, 西岡安彦 : 関節リウマチ合併間質性肺炎患者の急性呼吸不全の臨床的検討, 第59回日本呼吸器学会学術講演会, 2019年4月.
72.	小山壱也, 内藤伸仁, 香川耕造, 近藤真代, 西村春佳, 佐藤正大, 河野弘, 豊田優子, 吾妻雅彦, 後東久嗣, 西岡安彦 : マウス肺線維症モデルにおける新規multi-tyrosine kinase inhibitor TAS-115の抗線維化効果の検討, 第258回徳島医学会学術集会, 2019年2月.
73.	坂東紀子, 近藤真代, 河野弘, 藤野泰輝, 岡久稔也, 豊田優子, 軒原浩, 吾妻雅彦, 後東久嗣, 高山哲治, 西岡安彦 : 潰瘍性大腸炎加療中に発症し，治療に難渋したニューモシスチス肺炎の一例, 第60回日本呼吸器学会中国・四国地方会, 2018年12月.
74.	原田紗希, 近藤真代, 西村春佳, 内藤伸仁, 河野弘, 大崎裕亮, 坂東良美, 髙橋直希, 香川耕造, 西岡安彦, 荻野広和, 飛梅亮, 西條敦郎, 軒原浩, 豊田優子, 吾妻雅彦, 後東久嗣, 上原久典, 西岡安彦 : 傍腫瘍性神経症候群を合併した小細胞肺癌の一例, 第60回日本呼吸器学会中国・四国地方会, 2018年12月.
75.	坂東弘基, 近藤真代, 宮城亮, 荻野広和, 飛梅亮, 尾矢剛志, 小川博久, 河野弘, 豊田優子, 軒原浩, 吾妻雅彦, 後東久嗣, 西良浩一, 西岡安彦 : エイの刺創後に発症した皮膚Mycobacterium massiliense症の一例, 第69回日本結核病学会中国四国支部会, 2018年12月.
76.	佐藤正大, 豊田優子, 内藤伸仁, 米田浩人, 香川耕造, 西村春佳, 近藤真代, 小山壱也, 河野弘, 後東久嗣, 西岡安彦 : 気管支肺胞洗浄液中fibrocyteにおけるmiR-21発現の疾患別差異に関する検討, 第27回日本呼吸器内視鏡学会中国四国支部会, 2018年12月.
77.	宮本憲哉, 近藤真代, 内藤伸仁, 山崎博輝, 豊田優子, 荻野広和, 河野弘, 後東久嗣, 梶龍兒, 西岡安彦 : 免疫介在性壊死性ミオパチーの1例, 第119回日本内科学会四国地方会, 2018年12月.
78.	山下雄也, 河野弘, 今倉健, 内藤伸仁, 近藤真代, 荻野広和, 佐藤正大, 豊田優子, 後東久嗣, 西岡安彦 : TAFRO症候群の1例, 第29回日本リウマチ学会中国・四国支部学術集会, 2018年12月.
79.	内藤伸仁, 河野弘, 近藤真代, 荻野広和, 佐藤正大, 豊田優子, 後東久嗣, 西岡安彦 : EBウイルス再活性化を反復した高疾患活動性関節リウマチに対してアバタセプトが有効であった1例, 第29回日本リウマチ学会中国・四国支部学術集会, 2018年11月.
80.	米田浩人, 荻野広和, 豊田優子, 河野弘, 大塚憲司, 西條敦郎, 軒原浩, 後東久嗣, 西岡安彦 : 高齢肺癌患者の若年者と比較した臨床的特徴, 第56回日本癌治療学会学術集会, 2018年10月.
81.	森戸克弥, 清水良多, 高橋尚子, 下澤伸行, 東桃代, 河野弘, 西岡安彦, 福田達也, 小暮健太朗, 田中保 : ヒト血漿中セラミド及びセラミド1-リン酸の分子種組成と細胞への取り込み, 第91回日本生化学会大会, 2018年9月.
82.	森あずさ, 内藤伸仁, 山﨑博輝, 林理恵, 坂東紀子, 原田沙希, 河野弘, 豊田優子, 後東久嗣, 梶龍兒, 久保宜明, 西岡安彦 : 免疫介在性壊死性ミオパチーの1例, 第257回徳島医学会学術集会, 2018年8月.
83.	國重道大, 米田浩人, 河野弘, 西條敦郎, 飛梅亮, 近藤真代, 坂東弘基, 小川博久, 軒原浩, 後東久嗣, 西岡安彦 : 腸型肺腺癌の1例, 第57回日本肺癌学会中国・四国支部学術集会, 2018年7月.
84.	坂東紀子, 豊田優子, 河野弘, 佐藤正大, 小山壱也, 西村春佳, 香川耕造, 内藤伸仁, 吾妻雅彦, 西岡安彦 : 当科で経験した抗MDA5抗体陽性皮膚筋炎合併間質性肺炎の臨床像の検討, 第59回日本呼吸器学会中国・四国地方会, 2018年7月.
85.	内藤伸仁, 森田優, 香川耕造, 近藤真代, 西村春佳, 河野弘, 豊田優子, 岸潤, 後東久嗣, 西岡安彦 : Tocilizumab が有効であった重症成人発症スティル病の1例, 第118回日本内科学会四国地方会, 2018年6月.
86.	小山壱也, 豊田優子, 西村春佳, 香川耕造, 森住俊, 河野弘, 後東久嗣, 西岡安彦 : マウス肺線維症モデルにおけるmulti-tyrosine kinase inhibitor TAS-115の抗線維化効果の検討．, 第58回日本呼吸器学会学術講演会., 2018年4月.
87.	西村春佳, 森住俊, 豊田優子, 鈴江涼子, 小山壱也, 香川耕造, 内藤伸仁, 河野弘, 後東久嗣, 西岡安彦 : 当院における特発性肺線維症に対するNintedanibの治療症例の検討．, 第58回日本呼吸器学会学術講演会, 2018年4月.
88.	内藤伸仁, 河野弘, 山下雄也, 近藤真代, 荻野広和, 豊田優子, 岸潤, 後東久嗣, 西岡安彦 : アザチオプリン併用療法が有効であった間質性肺炎合併抗MDA5抗体陽性皮膚筋炎の3例．, 第62回日本リウマチ学会総会・学術集会, 2018年4月.
89.	内藤伸仁, 森田優, 大塚憲司, 河野弘, 豊田優子, 岸潤, 後東久嗣, 西岡安彦 : Tocilizumabが有効であった重症成人発症スティル病の1例．, 第256回徳島医学会学術集会, 2018年2月.
90.	辻本賀美, 内藤伸仁, 近藤真代, 香西博之, 河野弘, 大塚憲司, 後東久嗣, 岸潤, 吾妻雅彦, 西岡安彦 : 多発単神経炎を合併した好酸球性多発血管炎性肉芽腫症(EGPA)において免疫グロブリン大量療法(IVIG)が有効であった3例, 第117回日本内科学会四国地方会, 2017年12月.
91.	山下雄也, 河野弘, 岸潤, 内藤伸仁, 荻野広和, 近藤真代, 森住俊, 豊田優子, 後東久嗣, 吾妻雅彦, 西岡安彦 : 全身性強皮症を背景にposterior reversible encephalopathy syndromeを発症した一例, 第28回日本リウマチ学会中国・四国支部学術集会, 2017年11月.
92.	今倉健, 内藤伸仁, 山下雄也, 荻野広和, 岸潤, 河野弘, 近藤真代, 森住俊, 豊田優子, 後東久嗣, 吾妻雅彦, 西岡安彦 : ループス心筋炎の2例, 第28回日本リウマチ学会中国・四国支部学術集会, 2017年11月.
93.	河野弘, 松本満, 西岡安彦 : ほぼすべての胸腺髄質上皮細胞が成熟過程でAireを発現する機能を備えている, 第28回日本リウマチ学会中国・四国支部学術集会, 2017年11月.
94.	荻野広和, 豊田優子, 河野弘, 岸潤, 近藤真代, 森住俊, 山下雄也, 後東久嗣, 吾妻雅彦, 西岡安彦 : 当院における肺病変合併全身性エリテマトーデス症例の臨床的検討, 第28回日本リウマチ学会中国・四国支部学術集会, 2017年11月.
95.	鈴江涼子, 西村春佳, 荻野広和, 大塚憲司, 飛梅亮, 河野弘, 福家麻美, 山下雄也, 後東久嗣, 西岡安彦 : 心タンポナーデをきたした結核性心膜炎の1例, 第68回日本結核病学会中国四国支部会, 2017年10月.
96.	鈴江涼子, 森住俊, 大塚憲司, 豊田優子, 河野弘, 小山壱也, 香西博之, 西村春佳, 後東久嗣, 西岡安彦 : 特発性肺線維症に対するnintedanibの使用経験, 第57回日本呼吸器学会中国・四国地方会, 2017年7月.
97.	西村春佳, 手塚敏史, 西條敦郎, 河野弘, 後東久嗣, 岸潤, 軒原浩, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 肺扁平上皮癌治療後の空洞病変に認めた肺アスペルギルス症の1例, 第116回日本内科学会四国地方会, 2017年5月.
98.	近藤真代, 手塚敏史, 河野弘, 後東久嗣, 岸潤, 埴淵昌毅, 吾妻雅彦, 土師正太郎, 梶龍兒, 西岡安彦 : 小脳浮腫および水頭症を認め開頭減圧術を要したNPSLEの1例, 第116回日本内科学会四国地方会, 2017年5月.
99.	豊田優子, 岸潤, 河野弘, 森住俊, 小山壱也, 西村春佳, 香川耕造, 手塚敏史, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 当院における全身性エリテマトーデス合併間質性肺炎の臨床的検討, 第57回日本呼吸器学会学術講演会, 2017年4月.
100.	Shun Morizumi, Seidai Satou, Hirokazu Ogino, Koyama Kazuya, Haruka Nishimura, Yuko Toyoda, Hiroshi Kawano and Yasuhiko Nishioka : Inhibition of pan-fibroblast growth factor receptor signaling in bleomycin-induced pulmonary fibrosis in mice, The 57th Annual Meeting of the Japanese Respiratory Society, Apr. 2017.
101.	河野弘, 豊田優子, 岸潤, 森住俊, 近藤真代, 山下雄也, 手塚敏史, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 当院における間質性肺炎合併全身性エリテマトーデス症例の臨床的検討, 第61回日本リウマチ学会総会・学術集会, 2017年4月.
102.	髙島拓也, 手塚敏史, 近藤真代, 飛梅亮, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 : Exon19とexon21の遺伝子変異を同時に認めた肺腺癌の1例, 第56回日本呼吸器学会中国・四国地方会, 2016年12月.
103.	菊地高史, 手塚敏史, 近藤真代, 荻野広和, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 : Stevens-Johnson 症候群後に発症した閉塞性細気管支炎にステロイドおよびタクロリムスが有効であった1例, 第56回日本呼吸器学会中国・四国地方会.岡山.2016年12月23, 2016年12月.
104.	杉峯優人, 手塚敏史, 香川耕造, 米田浩人, 大塚憲司, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 : EBUS-TBNA後に縦隔炎を発症した縦隔原発セミノーマの1例, 第25回日本呼吸器内視鏡学会中国四国支部会, 2016年12月.
105.	原倫世, 手塚敏史, 近藤真代, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 : EBによる末梢神経障害を呈した結核性胸膜炎の1例, 第67回日本結核病学会中国四国支部会, 2016年12月.
106.	豊田優子, 山下雄也, 森住俊, 近藤真代, 荻野広和, 河野弘, 手塚敏史, 岸潤, 後東久嗣, 埴淵昌毅, 埴淵昌毅, 西岡安彦 : 当院における膠原病関連間質性肺炎の急性憎悪の臨床的検討, 第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月.
107.	荻野広和, 岸潤, 河野弘, 手塚敏史, 豊田優子, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 関節リウマチの薬物療法における栄養状態の変化の検討, 第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月.
108.	山下雄也, 豊田優子, 荻野広和, 河野弘, 手塚敏史, 岸潤, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 当院におけるループス腎炎に対するIVCYとMMFの治療経験, 第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月.
109.	田中こころ, 荻野広和, 宮田淳也, 山下雄也, 森住俊, 近藤真代, 河野弘, 手塚敏史, 豊田優子, 岸潤, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 15年前より認める慢性腎機能障害に対してステロイド加療が奏功した腎サルコイドーシスの1例, 第27回日本リウマチ学会中国・四国支部学術集会, 2016年12月.
110.	米田浩人, 手塚敏史, 山下雄也, 西條敦郎, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 : 多発性胃十二指腸潰瘍を伴ったMTX関連リンパ増殖性疾患の1例, 第115回日本内科学会四国地方会, 2016年11月.
111.	香西博之, 手塚敏史, 山下雄也, 西條敦郎, 河野弘, 後東久嗣, 岸潤, 吾妻雅彦, 埴淵昌毅, 西岡安彦 : Gefitinib投与中にAchromobacter Xylosoxidansによる菌血症を発症した肺腺癌の1例, 第115回日本内科学会四国地方会, 2016年11月.
112.	森住俊, 佐藤正大, 荻野広和, 河野弘, 坂口暁, 後東久嗣, 岸潤, 埴淵昌毅, 吾妻雅彦, 西岡安彦 : 当院におけるニンテダニブの特発性肺線維症に対する使用経験, 第114回日本内科学会四国地方会, 2016年5月.
113.	河野弘, 近藤真代, 西條敦郎, 豊田優子, 岸潤, 西岡安彦 : 当院における膠原病に合併した肺癌の検討, 第60回日本リウマチ学会総会・学術集会, 2016年4月.
114.	豊田優子, 佐藤正大, 岸潤, 河野弘, 森住俊, 岸昌美, 手塚敏史, 坂口暁, 後東久嗣, 埴淵昌毅, 西岡安彦 : 当院における膠原病関連間質性肺炎の急性増悪に関する臨床的検討, 第56回日本呼吸器学会学術講演会, 2016年4月.
115.	手塚敏史, 小川博久, 近藤真代, 吾妻雅彦, 豊田優子, 佐藤正大, 岡崎弘泰, 河野弘, 岸潤, 後東久嗣, 埴淵昌毅, 西岡安彦 : RAS阻害剤 (XRP44X) を用いた喘息モデルマウスにおける検討, 第56回日本呼吸器学会学術講演会, 2016年4月.
116.	曽我部洋平, 佐藤正大, 西條敦郎, 中野万有里, 河野弘, 坂口暁, 豊田優子, 後東久嗣, 岸潤, 埴淵昌毅, 西岡安彦 : 癌性髄膜炎に対しアファチニブが奏効した2例, 第54回日本呼吸器学会中国・四国地方会, 2015年12月.
117.	山下雄也, 荻野広和, 岸潤, 豊田優子, 森住俊, 近藤真代, 瀧倉輝実, 佐藤正大, 河野弘, 手塚敏史, 後東久嗣, 埴淵昌毅, 西岡安彦 : 強膜炎，ネフローゼ症候群および僧房弁腱索断裂による重症僧房弁閉鎖不全症を呈した全身性エリテマトーデスの1例, 第26回日本リウマチ学会中国・四国支部学術集会, 2015年12月.
118.	Junko Morimoto, Yumiko Nishikawa, Hiroshi Kawano, Yasuhiro Mouri, Hitoshi Nishijima and Mitsuru Matsumoto : A novel Aire-dependent subset of medullary thymic epithelial cells that express Ly6 family protein, 第44回日本免疫学会学術集会, Nov. 2015.
119.	Hitoshi Nishijima, Yasuhiro Mouri, Junko Morimoto, Hiroshi Kawano and Mitsuru Matsumoto : Paradoxical development of polymyositis-like autoimmunity by the additive expression of AIRE, 第44回日本免疫学会学術集会, Nov. 2015.
120.	武井美貴子, 近藤真代, 佐藤正大, 河野弘, 豊田優子, 埴淵昌毅, 西岡安彦, 三木浩和, 田中久美子, 高山哲治 : 好酸球性胆管炎を合併した全身性エリテマトーデスの1例, 第112回日本内科学会四国地方会, 2015年6月.
121.	豊田優子, 瀧倉輝実, 近藤真代, 佐藤正大, 尾崎領彦, 岸潤, 手塚敏史, 河野弘, 後東久嗣, 埴淵昌毅, 西岡安彦 : 膠原病に合併した血球貪食性リンパ組織球症の4症例, 第59回日本リウマチ学会総会・学術集会, 2015年4月.
122.	Hitoshi Nishijima, Junko Morimoto, Yasuhiro Mouri, Hiroshi Kawano, Koichi Ikuta and Mitsuru Matsumoto : Approaches to identify Aire-regulated non-tissue-restricted antigen genes by the ectopic expression of Aire in thymic cortex, 第43回日本免疫学会学術集会, Dec. 2014.
123.	Hiroshi Kawano, Junko Morimoto, Yasuhiro Mouri, Hitoshi Nishijima, Yasuhiko Nishioka and Mitsuru Matsumoto : Unexpected disturbance of the development of medullary thymic epithelial cells at immature stages by the long-term ablation of mature Aire-expressing cells, 第43回日本免疫学会学術集会, Dec. 2014.
124.	近藤真代, 佐藤正大, 豊田優子, 岸潤, 手塚敏史, 吉嶋輝実, 岸昌美, 河野弘, 後東久嗣, 埴淵昌毅, 西岡安彦 : 血小板減少を契機として診断された高齢者のSLEの2例, 第25回日本リウマチ学会中国・四国支部学術集会, 2014年12月.
125.	松本康平, 尾崎領彦, 豊田優子, 中野万有里, 森住俊, 河野弘, 岸潤, 柿内聡司, 埴淵昌毅, 西岡安彦 : 高Ca血症にて発症した多臓器サルコイドーシスの1例, 第51回日本呼吸器学会中国・四国地方会, 2014年7月.
126.	豊田優子, 岸潤, 河野弘, 後東久嗣, 埴淵昌毅, 中島利博, 西岡安彦 : 関節リウマチ患者由来の線維芽細胞様滑膜細胞において thymidine phosphorylaseはCXCL10 を制御する, 第58回日本リウマチ学会総会学術集会, 2014年4月.
127.	山本聖子, 埴淵昌毅, 森住俊, 岸昌美, 木下勝弘, 河野弘, 竹﨑彰夫, 豊田優子, 東桃代, 後東久嗣, 岸潤, 西岡安彦 : 左上葉無気肺を呈したアレルギー性気管支肺アスペルギルス症の一例, 第248回徳島医学会, 2014年2月.
128.	猪子未希, 西條敦郎, 岸昌美, 埴淵昌毅, 青野純典, 豊田優子, 木下勝弘, 手塚敏史, 吉嶋輝実, 河野弘, 岸潤, 西岡安彦, 池田真由美, 吉田光輝, 先山正二, 福田悠 : 肺多発浸潤影と胸膜炎を初発症状とした多発性筋炎の1例, 第247回徳島医学会学術集会, 2013年8月.
129.	長瀬紗季, 豊田優子, 阿部秀一, 岸潤, 河野弘, 手塚敏史, 埴淵昌毅, 池田真由美, 先山正二, 西岡安彦 : サルコイドーシスの経過観察中に肺腺癌を合併した1例, 第49回日本呼吸器学会中国・四国地方会, 2013年7月.
130.	森住俊, 大塚憲司, 豊田優子, 河野弘, 岸潤, 手塚敏史, 吉嶋輝実, 柿内聡司, 埴淵昌毅, 西岡安彦 : 脳炎と腹部大動脈瘤を合併した多発血管炎性肉芽腫症の1例, 第108回日本内科学会四国地方会, 2013年6月.
131.	吉嶋輝実, 河野弘, 手塚敏史, 豊田優子, 岸潤, 西岡安彦 : 原因不明の末梢閉塞性動脈疾患加療中に冠動脈瘤が発覚し高安動脈炎と診断した1例., 第57回日本リウマチ学会総会・学術集会, 2013年4月.
132.	吉嶋輝実, 埴淵昌毅, 東桃代, 豊田優子, 河野弘, 岸潤, 竹﨑彰夫, 岡﨑弘泰, 長尾多美子, 鈴木麗子, 高開登茂子, 先山正二, 西岡安彦 : 徳島大学病院職員における潜在性結核感染症の現状, 第63回日本結核病学会中国四国支部会, 2013年2月.
133.	河野弘, 豊田優子, 岸潤, 埴淵昌毅, 西岡安彦 : 抗CCP抗体高値を呈し関節炎を伴わずに発症したステロイド抵抗性器質化肺炎の1例, 第23回日本リウマチ学会中国・四国支部学術集会, 2012年10月.
134.	近藤真代, 豊田優子, 阿部秀一, 河野弘, 岸昌美, 竹﨑彰夫, 東桃代, 柿内聡司, 後東久嗣, 青野純典, 埴淵昌毅, 西岡安彦 : 病勢に関連してCA19-9の変動を認めた非結核性抗酸菌症の1例, 第20回日本呼吸器内視鏡学会中国四国支部会, 2012年3月.
135.	矢野祖, 近藤真代, 河野弘, 西條敦郎, 豊田優子, 柿内聡司, 岸潤, 埴淵昌毅, 西岡安彦, 古川貴大, 藤田浩司 : 神経サルコイドーシスの1例, 第244回徳島医学会学術集会, 2012年2月.
136.	岡崎弘泰, 豊田優子, 岸潤, 河野弘, 柿内聡司, 後東久嗣, 埴淵昌毅, 吾妻雅彦, 榊美佳, 西岡安彦 : 組織診断が得られた肝サルコイドーシスの2症例, 第22回日本リウマチ学会中国・四国支部学術集会, 2011年12月.
137.	近藤真代, 河野弘, 柿内聡司, 岸潤, 埴淵昌毅, 吾妻雅彦, 近藤絵里, 合田正和, 石丸直澄, 西岡安彦 : IgG4関連下垂体炎の1例, 第105回日本内科学会四国地方会, 2011年11月.

その他・研究会:

1.	西嶋仁, 梶本達也, 松岡慶樹, 毛利安宏, 森本純子, 河野弘, 松本満 : NOD系統特異的に多発性筋炎様症状をもたらすゲノム領域の解析, 第14回四国免疫フォーラム, 2015年6月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

肺微小環境内リゾリン脂質制御に基づく抗線維化療法の開発 (研究課題/領域番号: 24K11578 )
一細胞遺伝子発現解析を用いた新規線維化促進細胞集団の同定と分子標的薬開発への応用 (研究課題/領域番号: 19K08652 )
線維細胞の遊走を標的とした新たな膠原病肺治療法の開発 (研究課題/領域番号: 16K21197 )
研究者番号（30771571）による検索

特任准教授 : 河野弘

研究活動

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

総説・解説:

国際会議:

国内講演発表:

その他・研究会:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

特任准教授 : 河野 弘

研究活動

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

総説・解説:

国際会議:

国内講演発表:

その他・研究会:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

特任准教授 : 河野弘