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田中 創始タナカ ハジメ

所属部署医学研究科地域医療教育学分野
職名講師
メールアドレスhajimetngmail.com
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Last Updated :2019/09/19

研究者基本情報

基本情報

    プロフィール:2010 名古屋市立大学医学部医学科学位 博士(医学)
    1996 岐阜大学医学部卒業

    2017 名古屋市立大学総合内科・総合診療科(地域医療教育学分野)病院講師
    2016 名古屋市立大学総合内科・総合診療科(地域医療教育学分野)助教
    2014 知多厚生病院第2消化器内科部長
    2011-2014 University of California at Davis, Visiting assistant professor
    2010 愛知医科大学消化器内科講師
    2009 愛知医科大学消化器内科助教
    2005 名古屋市立大学臨床機能内科臨床研究医
    2003 春日井市民病院消化器内科
    2000 国立療養所恵那病院(現:市立恵那病院)内科
    1999 名古屋市立大学第一内科臨床研究医
    1997 名古屋市立城北病院(現:名古屋市立西部医療センター)泌尿器科
    1996 名古屋市立大学病院泌尿器科

    専門:胆膵内科
    研究分野:消化器(自己免疫疾患と発がん;膵臓・大腸)
    科研費研究者番号:30433220

学歴

  • 2010年03月 - 現在, 名古屋市立大学医学部医学科学位 博士(医学)
  • 1996年03月 - 現在, 岐阜大学医学部卒業

学位

  • 医学博士, 名古屋市立大学

経歴

  •   2017年07月 - 現在, 名古屋市立大学病院, 総合診療科(地域医療教育学分野), 病院講師
  •   2016年07月 - 2017年06月, 名古屋市立大学病院, 総合診療科(地域医療教育学分野), 助教
  •   2014年04月 - 2016年06月, 愛知厚生連知多厚生病院, 第2消化器内科, 部長
  •   2011年08月 - 2014年03月, University of California at Davis, Visiting assistant professor
  •   2010年04月 - 2011年06月, 愛知医科大学病院, 消化器内科, 講師
  •   2009年10月 - 2010年04月, 愛知医科大学病院, 消化器内科, 助教
  •   2005年10月 - 2009年09月, 名古屋市立大学病院, 消化器・代謝内科, 臨床研究医
  •   2003年04月 - 2005年09月, 春日井市民病院, 消化器内科
  •   2000年07月 - 2003年03月, 国立療養所恵那病院(現:市立恵那病院), 内科
  •   1999年04月 - 2000年06月, 名古屋市立大学病院, 第一内科(現:消化器・代謝内科), 臨床研究医
  •   1997年04月 - 1999年03月, 名古屋市立城北病院(現:名古屋市立西部医療センター), 泌尿器科
  •   1996年04月 - 1997年03月, 名古屋市立大学病院, 泌尿器科, 臨床研修医

研究活動情報

論文

  • The modulation of co-stimulatory molecules by circulating exosomes in primary biliary cirrhosis, Takashi Tomiyama, Guo Xiang Yang, Ming Zhao, Weici Zhang, Hajime Tanaka, Hajime Tanaka, Jing Wang, Patrick S.C. Leung, Kazuichi Okazaki, Xiao Song He, Qianjin Lu, Ross L. Coppel, Christopher L. Bowlus, M. Eric Gershwin, Cellular and Molecular Immunology, 14, 276 - 284,   2017年03月, © 2017 CSI and USTC. All rights reserved. Exosomes are nanoparticles of endocytic origin, secreted by a myriad of cell populations that are attracting increased attention by virtue of their ability to modulate cell-to-cell communications. They are also attracting attention in a variety of immunological issues, including autoimmunity and, in particular, their ability to regulate cytokine and chemokine activation. Primary biliary cirrhosis (PBC) is considered a model autoimmune disease, which has a highly focused cytotoxic response against biliary epithelial cells. We have isolated exosomes from plasma from 29 patients with PBC and 30 healthy controls (HCs), and studied the effect of these exosomes on co-stimulatory molecule expression and cytokine production in mononuclear cell populations using an ex vivo system. We also identified the microRNA (miRNA) populations in PBC compared to HC exosomes. We report herein that although exosomes do not change cytokine production, they do significantly alter co-stimulatory molecule expression on antigen-presenting populations. Further, we demonstrated that CD86 up-regulated expression on CD14 + monocytes, whereas CD40 up-regulated on CD11c + dendritic cells by exosomes from patients with PBC. In addition, there were differences of miRNA expression of circulating exosomes in patients with PBC. These data have significant importance based on observations that co-stimulatory molecules play a differential role in the regulation of T-cell activation. Our observation indicated that aberrant exosomes from PBC selectively induce expression of co-stimulatory molecules in different subset of antigen-presenting cells. These alterations may involve in pathogenesis of autoimmune liver disease.
  • Immunological potential of cytotoxic T lymphocyte antigen 4 immunoglobulin in murine autoimmune cholangitis, H. Tanaka, G. X. Yang, T. Tomiyama, T. Tomiyama, K. Tsuneyama, K. Tsuneyama, W. Zhang, P. S C Leung, R. L. Coppel, T. Joh, S. G. Nadler, A. A. Ansari, C. Bowlus, M. E. Gershwin, Clinical and Experimental Immunology, 180, (3) 371 - 382,   2015年01月, © 2015 British Society for Immunology. Cytotoxic T lymphocyte antigen 4 (CTLA-4) immunoglobulin (Ig) is an important regulator of T cell activation and a fusion protein directed at CD80 and CD86; it blocks co-stimulatory signalling and T cell activation. We have taken advantage of a murine model of human primary biliary cirrhosis (PBC), mice expressing a transforming growth factor (TGF)-β receptor II dominant negative (dnTGF-βRII) transgene to address the potential therapeutic efficacy of CTLA-4 Ig. To mimic patients with PBC at different stages or duration of disease, we treated mice with either CTLA-4 Ig or control IgG three times weekly from 3 to 12 or 24 weeks of age, or from 12 to 24 weeks of age. CTLA-4 Ig treatment from 3 weeks of age significantly reduced liver inflammation to 12 weeks of age. Treatment initiated at 12 weeks of age also ameliorated the autoimmune cholangitis at 24 weeks of age. However, in mice treated at 3 weeks of age, suppression of liver inflammation was not sustained and colitis was aggravated when treatment was extended to 24 weeks of age. Our data indicate that, in dnTGF-βRII mice, CTLA-4 Ig treatment has short-term beneficial effects on autoimmune cholangitis, but the effect varies according to duration of treatment and the time in which therapy was initiated. Further dissection of the events that lead to the reduction in therapeutic effectiveness of CTLA-4 Ig will be critical to determining whether such efforts can be applied to human PBC.
  • Successful immunotherapy of autoimmune cholangitis by adoptive transfer of forkhead box protein 3+ regulatory T cells, H. Tanaka, W. Zhang, G. X. Yang, Y. Ando, T. Tomiyama, T. Tomiyama, K. Tsuneyama, P. Leung, R. L. Coppel, A. A. Ansari, Z. X. Lian, W. M. Ridgway, T. Joh, M. E. Gershwin, Clinical and Experimental Immunology, 178, (2) 253 - 261,   2014年01月, © 2014 British Society for Immunology. Summary: Treatment of primary biliary cirrhosis (PBC) has lagged behind that of other autoimmune diseases. In this study we have addressed the potential utility of immunotherapy using regulatory T cells (T reg ) to treat murine autoimmune cholangitis. In particular, we have taken advantage of our ability to produce portal inflammation and bile duct cell loss by transfer of CD8 + T cells from the dominant negative form of transforming growth factor beta receptor type II (dnTGF-βRII) mice to recombination-activating gene (Rag)1 -/- recipients. We then used this robust established adoptive transfer system and co-transferred CD8 + T cells from dnTGF-βRII mice with either C57BL/6 or dnTGF-βRII forkhead box protein 3 (FoxP3 + ) T cells. Recipient mice were monitored for histology, including portal inflammation and intralobular biliary cell damage, and also included a study of the phenotypical changes in recipient lymphoid populations and local and systemic cytokine production. Importantly, we report herein that adoptive transfer of T reg from C57BL/6 but not dnTGF-βRII mice significantly reduced the pathology of autoimmune cholangitis, including decreased portal inflammation and bile duct damage as well as down-regulation of the secondary inflammatory response. Further, to define the mechanism of action that explains the differential ability of C57BL/6 T reg versusdnTGF-βRII T reg on the ability to down-regulate autoimmune cholangitis, we noted significant differential expression of glycoprotein A repetitions predominant (GARP), CD73, CD101 and CD103 and a functionally significant increase in interleukin (IL)-10 in T reg from C57BL/6 compared to dnTGF-βRII mice. Our data reflect the therapeutic potential of wild-type CD4 + FoxP3 + T reg in reducing the excessive T cell responses of autoimmune cholangitis, which has significance for the potential immunotherapy of PBC.
  • Anti-CD40 ligand monoclonal antibody delays the progression of murine autoimmune cholangitis, H. Tanaka, G. X. Yang, N. Iwakoshi, S. J. Knechtle, K. Kawata, K. Tsuneyama, K. Tsuneyama, P. Leung, R. L. Coppel, A. A. Ansari, T. Joh, C. Bowlus, M. E. Gershwin, Clinical and Experimental Immunology, 174, (3) 364 - 371,   2013年12月, Summary: While there have been significant advances in our understanding of the autoimmune responses and the molecular nature of the target autoantigens in primary biliary cirrhosis (PBC), unfortunately these data have yet to be translated into new therapeutic agents. We have taken advantage of a unique murine model of autoimmune cholangitis in which mice expressing a dominant negative form of transforming growth factor β receptor II (dnTGFβRII), under the control of the CD4 promoter, develop an intense autoimmune cholangitis associated with serological features similar to human PBC. CD40-CD40 ligand (CD40L) is a major receptor-ligand pair that provides key signals between cells of the adaptive immune system, prompting us to determine the therapeutic potential of treating autoimmune cholangitis with anti-CD40L antibody (anti-CD40L; MR-1). Four-week-old dnTGFβRII mice were injected intraperitoneally with either anti-CD40L or control immunoglobulin (Ig)G at days 0, 2, 4 and 7 and then weekly until 12 or 24 weeks of age and monitored for the progress of serological and histological features of PBC, including rigorous definition of liver cellular infiltrates and cytokine production. Administration of anti-CD40L reduced liver inflammation significantly to 12 weeks of age. In addition, anti-CD40L initially lowered the levels of anti-mitochondrial autoantibodies (AMA), but these reductions were not sustained. These data indicate that anti-CD40L delays autoimmune cholangitis, but the effect wanes over time. Further dissection of the mechanisms involved, and defining the events that lead to the reduction in therapeutic effectiveness will be critical to determining whether such efforts can be applied to PBC. © 2013 British Society for Immunology.
  • Identification of Potential Cytokine Pathways for Therapeutic Intervention in Murine Primary Biliary Cirrhosis, Kazuhito Kawata, Masanobu Tsuda, Masanobu Tsuda, Guo Xiang Yang, Weici Zhang, Hajime Tanaka, Koichi Tsuneyama, Koichi Tsuneyama, Patrick Leung, Xiao Song He, Stuart Knechtle, Aftab A. Ansari, Ross L. Coppel, M. Eric Gershwin, PLoS ONE, 8, (9) ,   2013年09月, Primary biliary cirrhosis (PBC) is considered a model autoimmune disease, with the most highly directed and specific autoantibody in both murine and human autoimmunity, the anti-mitochondrial autoantibody (AMA). However, therapeutic advances in this disease have lagged behind. Herein we have taken advantage of our unique model of murine PBC in which mice immunized with 2-octynoic acid coupled to BSA (2OA-BSA), a compound identified by quantitative structure activity relationships (QSAR) of human AMA binding, develop an intense inflammatory cholangitis with striking similarities to humans with PBC. In particular, we have constructed several unique gene-deleted mice, including mice deleted of IL-12p40, IL-12p35, IFN-γ, IL-23p19, IL-17A, IL-17F and IL-22, immunized these animals with 2OA-BSA and followed the natural history of immunopathology to identify key pathways that might provide clues for successful therapy. Our data indicate that whereas both IL-12/Th1 and IL-23/Th17 are involved in cholangitis, it is the IL-12/Th1 signaling pathway that elicits pathology. In fact, deletion of IFN-γ prevents disease and suppresses autoantibodies. Importantly, deletion of the Th17 cytokines IL-17A and IL-22, but not IL-17F, reduces biliary damage; IL-17A-knockout mice have reduced levels of anti-mitochondrial antibody. We further demonstrate that the production of IFN-γ is significantly decreased in the liver of IL-23p19 -/- , IL-17A -/- and IL-22 -/- mice compared with controls. However, the ability of T cells to produce IFN-γ was not affected in Th17 cytokine-deficient mice. Our data indicate that a deficient Th17 pathway suppresses the accumulation of IFN-γ producing cells in liver during the early phase of cholangitis. In conclusion, whereas IFN-γ has a pivotal role in the early events involved in the pathogenesis of autoimmune cholangitis induced by 2OA-BSA, the IL-23/Th17 pathway potentiates the effects of IL-12/IFN-γ-mediated immunopathology. © 2013 Kawata et al.
  • Clonality, activated antigen-specific CD8+ T cells, and development of autoimmune cholangitis in dnTGFβRII mice, Kazuhito Kawata, Guo Xiang Yang, Yugo Ando, Hajime Tanaka, Weici Zhang, Yoshimasa Kobayashi, Koichi Tsuneyama, Koichi Tsuneyama, Patrick S C Leung, Zhe Xiong Lian, Zhe Xiong Lian, William M. Ridgway, Aftab A. Ansari, Xiao Song He, M. Eric Gershwin, Hepatology, 58, (3) 1094 - 1104,   2013年09月, There are several murine models described with features similar to human primary biliary cirrhosis (PBC). Among these models, the one which has the closest serologic features to PBC is a mouse with a T-cell-restricted expression of the dominant negative transforming growth factor β receptor type II (dnTGFβRII). Our work has demonstrated that CD8 + T cells from dnTGFβRII mice transfer autoimmune cholangitis to Rag1 -/- recipients. However, it remained unclear whether the autoimmune cholangitis was secondary to an intrinsic function within CD8 + T cells or due to the abnormal TGFβR environment within which CD8 + T cells were generated. To address this mechanistic issue, we used our dnTGFβRII, OT-I/Rag1 -/- , OT-II/Rag1 -/- mice and in addition generated OT-I/dnTGFβRII/Rag1 -/- , and OT-II/dnTGFβRII/Rag1 -/- mice in which the entire T-cell repertoire was replaced with ovalbumin (OVA)-specific CD8 + or CD4 + T cells, respectively. Importantly, neither the parental OT-I/dnTGFβRII/Rag1 -/- mice and/or OT-II/dnTGFβRII/Rag1 -/- mice developed cholangitis. However, adoptive transfer demonstrated that only transfer of CD8 + T cells from dnTGFβRII mice but not CD8 + T cells from OT-I/Rag1 -/- mice or from OT-I/dnTGFβRII/Rag1 -/- mice transferred disease. These data were not secondary to an absence of CD4 + T cell help since a combination of CD8 + T cells from OT-I/dnTGFβRII/Rag1 -/- and CD4 + T cells from OT II/dnTGFβRII/Rag1 -/- or CD8 + T cells from OT-I/dnTGFβRII/Rag1 -/- with CD4 + T cells from OT-II/Rag1 -/- mice failed to transfer disease. Conclusion: Defective TGFβRII signaling, in addition to clonal CD8 + T cells that target biliary cells, are required for induction of autoimmune cholangitis. (Hepatology 2013;53:1094-1104). © 2013 by the American Association for the Study of Liver Diseases.
  • Twenty-one proteins up-regulated in human H-ras oncogene transgenic rat pancreas cancers are up-regulated in human pancreas cancer, Setsuko Yabushita, Setsuko Yabushita, Katsumi Fukamachi, Fumitake Kikuchi, Fumitake Kikuchi, Masakazu Ozaki, Kaori Miyata, Tokuo Sukata, Yoshihito Deguchi, Hajime Tanaka, Anna Kakehashi, Satoshi Kawamura, Satoshi Uwagawa, Hideki Wanibuchi, Masumi Suzui, David B. Alexander, David B. Alexander, Hiroyuki Tsuda, Pancreas, 42, (6) 1034 - 1039,   2013年08月01日, OBJECTIVES: We have established rat models of pancreatic ductal adenocarcinoma (PDAC) in which expression of a human H-ras G12V or K-ras G12V oncogene regulated by the Cre/lox system drives pancreatic carcinogenesis. Pancreatic ductal adenocarcinoma which develops in H-ras G12V and K-ras G12V transgenic rats is cytogenetically and histopathologically similar to human PDAC. The present study was designed to determine the feasibility of using the commercially available H-ras G12V transgenic rat to find diagnostic protein biomarkers for human pancreatic cancer. METHODS: For an animal model to be useful for searching for protein biomarkers for a disease, it is essential that proteins that are up-regulated in the model are also up-regulated in humans. We used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to compare H-ras G12V transgenic rat PDAC with surrounding normal pancreas tissue. RESULTS: We identified 30 up-regulated proteins in the H-ras G12V transgenic rat PDAC lesions; importantly, 21 human homologs of these 30 rat proteins are up-regulated in human pancreatic cancer patients. CONCLUSIONS: These results indicate that numerous proteins that are up-regulated in H-ras G12V transgenic rat PDAC are also up-regulated in human pancreatic cancer; therefore, this rat model can be used to search for diagnostic biomarkers for this disease. Copyright © 2013 by Lippincott Williams & Wilkins.
  • Metabolomic and transcriptomic profiling of human K-ras oncogene transgenic rats with pancreatic ductal adenocarcinomas, Setsuko Yabushita, Katsumi Fukamachi, Hajime Tanaka, Takako Fukuda, Kayo Sumida, Yoshihito Deguchi, Kazuki Mikata, Kazuhiko Nishioka, Satoshi Kawamura, Satoshi Uwagawa, Masumi Suzui, David B. Alexander, David B. Alexander, Hiroyuki Tsuda, Carcinogenesis, 34, (6) 1251 - 1259,   2013年06月01日, Pancreatic ductal adenocarcinoma (PDAC) is one of the most debilitating malignancies in humans, and one of the reasons for this is the inability to diagnose this disease early in its development. To search for biomarkers that can be used for early diagnosis of PDAC, we established a rat model of human PDAC in wh ich expression of a human K-rasG12V oncogene and induction of PDAC are regulated by the Cre/lox system. In the present study, transgenic rats bearing PDAC and control transgenic rats with normal pancreatic tissues were used for metabolomic analysis of serum and pancreatic tissue by non-targeted and targeted gas chromatography-mass spectrometry and transcriptomic analysis of pancreatic tissue by microarray. Comparison of the metabolic profiles of the serum and pancreatic tissue of PDAC-bearing and control rats identified palmitoleic acid as a metabolite, which was significantly decreased in the serum of PDAC-bearing animals. Transcriptomic analysis indicated that several transcripts involved in anaerobic glycolysis and nucleotide degradation were increased and transcripts involved in the trichloroacetic acid cycle were decreased. Other transcripts that were changed in PDACbearing rats were adenosine triphosphate citrate lyase (decreased: fatty acid biosynthesis), fatty acid synthase (increased: fatty acid biosynthesis) and arachidonate 5-lipoxygenase activating protein (increased: arachidonic acid metabolism). Overall, our results suggest that the decreased serum levels of palmitoleic acid in rats with PDAC was likely due to its decrease in pancreatic tissue and that palmitoleic acid should be investigated in human samples to assess its diagnostic significance as a serum biomarker for human PDAC. © The Author 2013. Published by Oxford University Press. All rights reserved.
  • A novel reporter rat strain that expresses LacZ upon Cre-mediated recombination, Katsumi Fukamachi, Hajime Tanaka, Yuto Sakai, Yuto Sakai, David B. Alexander, Mitsuru Futakuchi, Hiroyuki Tsuda, Masumi Suzui, Genesis, 51, (4) 268 - 274,   2013年04月01日, The recent widespread application of Cre/loxP technology has resulted in a new generation of conditional animal models that can better recapitulate many salient features of human disease. These models benefit from the ability to monitor the expression and functionality of Cre protein. We have generated a conditional (Cre/loxP dependent) LacZ reporter rat (termed the LacZ541 rat) to monitor Cre in transgenic rats. When LacZ541 rats were bred with another transgenic rat line expressing Cre recombinase under the control of the CAG promoter, LacZ/Cre double transgenic embryos displayed ubiquitous expression of LacZ, and when LacZ541 rats were bred with transgenic rats expressing Cre/loxP-dependent oncogenic H- or K-ras, LacZ was expressed in the lesions resulting from the activation of the oncogene. The LacZ541 rat enables evaluation of the performance of Cre-expressing systems which are based upon transgenic rats or somatic gene transfer vectors and provides efficient and simple lineage marking. © 2013 Wiley Periodicals, Inc.
  • Immunological orchestration of liver fibrosis., Tanaka H, Leung PS, Kenny TP, Gershwin ME, Bowlus CL, Clinical reviews in allergy & immunology, 43, (3) 220 - 229,   2012年12月, 査読有り
  • Circulating microRNAs in serum of human K-ras oncogene transgenic rats with pancreatic ductal adenocarcinomas., Yabushita S, Fukamachi K, Tanaka H, Sumida K, Deguchi Y, Sukata T, Kawamura S, Uwagawa S, Suzui M, Tsuda H, Pancreas, 41, (7) 1013 - 1018,   2012年10月, 査読有り
  • A case of obstructive jaundice due to limy bile treated with Endoscopic Papillary Balloon Dilatation (EPBD) in young patient, Kazunori Adachi, Hajime Tanaka, Yuji Kobayashi, Nobuhiko Hayashi, Norimitsu Ishii, Tamotsu Kanazawa, Makoto Sasaki, Haruhisa Nakao, Kunio Kasugai, Masashi Yoneda, Gastroenterological Endoscopy, 54, (3) 466 - 473,   2012年03月01日, A 27-year-old woman consulted our hospital with epigastric pain. Since obstructive jaundice caused by limy bile in the common bile duct was diagnosed based on blood tests and imaging studies, emergency endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic balloon dilatation (EBD) were performed to remove limy bile and stones in the common bile duct. The drainage was assumed effective, because a massive volume of limy bile flowed from the common bile duct ; however, jaundice was exacerbated due to EBD stent obstruction on the following day, Endoscopic papillary balloon dilatation (EPBD) and lithotripsy were carried out. Endoscopic nasobiliary drainage (ENBD) was performed after removal of the common bile duct stones. The limy bile was subsequently removed completely from the common bile duct. After improvement of the jaundice, laparoscopic cholecystectomy was performed for the gallstones. EPBD and lithotripsy were effective for obstructive jaundice due to limy bile in a young patient.
  • A case of pancreatic glucagonoma with erythema., Yoshida M, Hayashi K, Ohara H, Miyabe K, Okumura F, Naitoh I, Tanaka H, Ando T, Nakazawa T, Takahashi S, Joh T, Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology, 107, (6) 930 - 936,   2010年06月, 査読有り
  • Mature acinar cells are refractory to carcinoma development by targeted activation of Ras oncogene in adult rats., Tanaka H, Fukamachi K, Futakuchi M, Alexander DB, Long N, Tamamushi S, Minami K, Seino S, Ohara H, Joh T, Tsuda H, Cancer science, 101, (2) 341 - 346,   2010年02月, 査読有り
  • Clinical significance of extrapancreatic lesions in autoimmune pancreatitis., Naitoh I, Nakazawa T, Ohara H, Ando T, Hayashi K, Tanaka H, Okumura F, Miyabe K, Yoshida M, Sano H, Takada H, Joh T, Pancreas, 39, (1) e1 - 5,   2010年01月, 査読有り
  • An animal model of preclinical diagnosis of pancreatic ductal adenocarcinomas., Fukamachi K, Tanaka H, Hagiwara Y, Ohara H, Joh T, Iigo M, Alexander DB, Xu J, Long N, Takigahira M, Yanagihara K, Hino O, Saito I, Tsuda H, Biochemical and biophysical research communications, 390, (3) 636 - 641,   2009年12月, 査読有り
  • [A case of peritoneal dissemination from mucinous carcinoma of the duodenum, which was associated with tumor thrombosis in the accessory pancreatic duct and successfully treated by chemotherapy]., Okumura F, Senoo K, Yoshida M, Miyabe K, Naito I, Tanaka H, Hayashi K, Ando T, Nakazawa T, Ohara H, Hamaguchi K, Kanai M, Ito K, Joh T, Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology, 106, (12) 1736 - 1743,   2009年12月, 査読有り
  • Metastasis-induced acute pancreatitis in a patient with small cell carcinoma of the lungs., Tanaka H, Nakazawa T, Yoshida M, Miyabe K, Okumura F, Naitoh I, Hayashi K, Ando T, Ohara H, Joh T, JOP : Journal of the pancreas, 10, (5) 557 - 561,   2009年09月, 査読有り
  • IgG4-related hepatic inflammatory pseudotumor with sclerosing cholangitis: a case report and review of the literature., Naitoh I, Nakazawa T, Ohara H, Ando T, Hayashi K, Tanaka H, Okumura F, Sano H, Joh T, Cases journal, 2,   2009年06月, 査読有り
  • Clinical course and indications for steroid therapy of sclerosing cholangitis associated with autoimmune pancreatitis., Nakazawa T, Ohara H, Ando T, Hayashi K, Naitoh I, Okumura F, Tanaka H, Sano H, Joh T, Hepato-gastroenterology, 56, (91-92) 584 - 588,   2009年05月, 査読有り
  • Role of osteopontin in calcification in autoimmune pancreatitis., Takada H, Nakazawa T, Ohara H, Ando T, Hayashi K, Naito I, Okumura F, Tanaka H, Yamada T, Takahashi S, Joh T, Digestive diseases and sciences, 54, (4) 793 - 801,   2009年04月, 査読有り
  • Autoimmune pancreatitis associated with various extrapancreatic lesions during a long-term clinical course successfully treated with azathioprine and corticosteroid maintenance therapy., Naitoh I, Nakazawa T, Ohara H, Sano H, Ando T, Hayashi K, Tanaka H, Okumura F, Miyabe K, Yoshida M, Takahashi S, Joh T, Internal medicine (Tokyo, Japan), 48, (23) 2003 - 2007,   2009年, 査読有り
  • Endoscopic transpapillary intraductal ultrasonography and biopsy in the diagnosis of IgG4-related sclerosing cholangitis., Naitoh I, Nakazawa T, Ohara H, Ando T, Hayashi K, Tanaka H, Okumura F, Takahashi S, Joh T, Journal of gastroenterology, 44, (11) 1147 - 1155,   2009年, 査読有り
  • [Case of duodenal stenosis due to hematoma after rupture of the inferior pancreaticoduodenal artery aneurysm treated by coil embolization]., Hayashi K, Ohara H, Naito I, Okumura F, Ogawa K, Tanaka H, Wada T, Ando T, Nakazawa T, Joh T, Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology, 105, (12) 1766 - 1774,   2008年12月, 査読有り
  • Liver atrophy and portal stenosis in two cases of sclerosing cholangitis associated with autoimmune pancreatitis., Hirano A, Nakazawa T, Ohara H, Ando T, Hayashi K, Tanaka H, Naito I, Okumura F, Yokoyama Y, Joh T, Internal medicine (Tokyo, Japan), 47, (19) 1689 - 1694,   2008年, 査読有り
  • Autoimmune sclerosing cholangiopancreatitis with little pancreatic involvements by imaging findings., Hayashi K, Nakazawa T, Ohara H, Ando T, Takada H, Tanaka H, Sasaki M, Kataoka H, Nakao H, Joh T, Hepato-gastroenterology, 54, (79) 2146 - 2151,   2007年10月, 査読有り
  • Usefulness of transpapillary bile duct brushing cytology and forceps biopsy for improved diagnosis in patients with biliary strictures., Kitajima Y, Ohara H, Nakazawa T, Ando T, Hayashi K, Takada H, Tanaka H, Ogawa K, Sano H, Togawa S, Naito I, Hirai M, Ueno K, Ban T, Miyabe K, Yamashita H, Yoshimura N, Akita S, Gotoh K, Joh T, Journal of gastroenterology and hepatology, 22, (10) 1615 - 1620,   2007年10月, 査読有り
  • Effects of eicosapentaenoic acid on urinary calcium excretion in calcium stone formers., Yasui T, Tanaka H, Fujita K, Iguchi M, Kohri K, European urology, 39, (5) 580 - 585,   2001年05月, 査読有り


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