K Nakata

Summary

Affiliation: International Medical Center of Japan
Country: Japan

Publications

  1. ncbi request reprint [Tuberculosis and the human immunodeficiency virus infection]
    K Nakata
    Department of Respiratory Diseases, International Medical Center of Japan
    Nihon Hansenbyo Gakkai Zasshi 69:87-92. 2000
  2. ncbi request reprint [The mechanism of HIV replication at the site of inflammation coinfected with HIV and M. tuberculosis]
    Koh Nakata
    Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, 1 21 1, Toyama, Shinjuku ku, Tokyo 162 8655, Japan
    Kekkaku 77:687-92. 2002
  3. ncbi request reprint Dihydroheptaprenyl and dihydrodecaprenyl monophosphates induce apoptosis mediated by activation of caspase-3-like protease
    E Yasugi
    Division of Biochemistry and Nutrition, Research Institute, International Medical Center of Japan, Tokyo
    Biochim Biophys Acta 1389:132-40. 1998
  4. ncbi request reprint Mechanisms of polymorphonuclear neutrophil-mediated induction of HIV-1 replication in macrophages during pulmonary tuberculosis
    Yoshihiko Hoshino
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA
    J Infect Dis 195:1303-10. 2007
  5. pmc Maximal HIV-1 replication in alveolar macrophages during tuberculosis requires both lymphocyte contact and cytokines
    Yoshihiko Hoshino
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    J Exp Med 195:495-505. 2002
  6. ncbi request reprint Why does the autoantibody against granulocyte-macrophage colony-stimulating factor cause lesions only in the lung?
    Koh Nakata
    Bioscience and Medical Research Center, Niigata University Medical and Dental Hospital, Asahimachi Dohri, Niigata, Japan
    Respirology 11:S65-9. 2006
  7. ncbi request reprint Granulocyte-macrophage colony-stimulating factor inhalation therapy for patients with idiopathic pulmonary alveolar proteinosis: a pilot study; and long-term treatment with aerosolized granulocyte-macrophage colony-stimulating factor: a case report
    Ryushi Tazawa
    Respiratory Medicine and Translational Research Clinic, Tohoku University Hospital, Seiryomachi, Sendai, Japan
    Respirology 11:S61-4. 2006
  8. ncbi request reprint Granulocyte-macrophage colony-stimulating factor and lung immunity in pulmonary alveolar proteinosis
    Ryushi Tazawa
    Institute of Development, Aging, and Cancer, Tohoku University Department of Hematology and Immunology, Tohoku University Hospital, Japan
    Am J Respir Crit Care Med 171:1142-9. 2005
  9. ncbi request reprint [Molecular pathogenesis in tuberculosis complicated with AIDS]
    Koh Nakata
    Bioscience Medical Research Center, Niigata Medical Dental Hospital, Niigata, Japan
    Kekkaku 79:659-67. 2004
  10. ncbi request reprint Pulmonary alveolar proteinosis
    Jeffrey J Presneill
    Intensive Care Unit, Royal Melbourne Hospital, Grattan Street, Parkville 3050, Victoria, Australia
    Clin Chest Med 25:593-613, viii. 2004

Collaborators

  • Hideaki Nagai
  • Naoto Keicho
  • T Dohi
  • E Yasugi
  • Y Hoshino
  • Ryushi Tazawa
  • Katsushi Kurosu
  • Yoshikazu Inoue
  • Kanji Uchida
  • Bruce C Trapnell
  • Haruko Iwabuchi
  • Toshihiro Nukiwa
  • Emi Hamano
  • Ikuo Ishige
  • Yoshinobu Eishi
  • John F Seymour
  • Jeffrey J Presneill
  • Koichiro Tatsumi
  • Yuichi Takiguchi
  • Norio Yumoto
  • William N Rom
  • Michael D Weiden
  • Makoto Naito
  • Takashi Kawasaki
  • Makoto Uchiyama
  • Takashi Yamamoto
  • Koichi Hagiwara
  • Toru Arai
  • Miki Takeshita
  • Junichi Saito
  • Hiromitsu Ohta
  • Osamu Ishimoto
  • Yasuhiko Hirabayashi
  • Masato Watanabe
  • Masahito Ebina
  • Ikumi Matsushita
  • Ayako Mikami
  • Jagirdar Jaishree
  • Masayoshi Oh-eda
  • Takayuki Kuriyama
  • Atsuo Mikata
  • Yoshitsugu Yamada
  • Takayuki Kitamura
  • Takahiro Terakawa
  • Yasunori Kasahara
  • Nobuhiro Tanabe
  • Kazuo Hanaoka
  • Jeffrey A Whitsett
  • Takatyuki Kuriyama
  • Jagirdai Jaishree
  • Aatsuo Mikata

Detail Information

Publications15

  1. ncbi request reprint [Tuberculosis and the human immunodeficiency virus infection]
    K Nakata
    Department of Respiratory Diseases, International Medical Center of Japan
    Nihon Hansenbyo Gakkai Zasshi 69:87-92. 2000
    ..The promotion of HIV-1 production is not only due to activated translocation of a nuclear factor. NF-kB, but also due to reduced inhibitory factor, C/EBPb 16 kD which binds to HIV LTR and represses the transcription of HIV-1...
  2. ncbi request reprint [The mechanism of HIV replication at the site of inflammation coinfected with HIV and M. tuberculosis]
    Koh Nakata
    Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, 1 21 1, Toyama, Shinjuku ku, Tokyo 162 8655, Japan
    Kekkaku 77:687-92. 2002
    ..Contact between activated lymphocytes and macrophages is necessary to down-regulate inhibitory C/EBP beta, thereby derepressing the HIV-1 LTR. Lymphocyte derived soluble factor(s) activate NF-kappa B, further enhancing the HIV-LTR...
  3. ncbi request reprint Dihydroheptaprenyl and dihydrodecaprenyl monophosphates induce apoptosis mediated by activation of caspase-3-like protease
    E Yasugi
    Division of Biochemistry and Nutrition, Research Institute, International Medical Center of Japan, Tokyo
    Biochim Biophys Acta 1389:132-40. 1998
    ..We interpret these results to mean that dihydroprenyl phosphates with more than seven isoprene units have apoptosis-inducing activity and that their signal is mediated by caspase-3-like activation...
  4. ncbi request reprint Mechanisms of polymorphonuclear neutrophil-mediated induction of HIV-1 replication in macrophages during pulmonary tuberculosis
    Yoshihiko Hoshino
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA
    J Infect Dis 195:1303-10. 2007
    ....
  5. pmc Maximal HIV-1 replication in alveolar macrophages during tuberculosis requires both lymphocyte contact and cytokines
    Yoshihiko Hoshino
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    J Exp Med 195:495-505. 2002
    ..Contact between activated lymphocytes and macrophages is necessary to down-regulate inhibitory C/EBPbeta, thereby derepressing the HIV-1 LTR. Lymphocyte-derived cytokines activate NF-kappaB, further enhancing the HIV-1 LTR...
  6. ncbi request reprint Why does the autoantibody against granulocyte-macrophage colony-stimulating factor cause lesions only in the lung?
    Koh Nakata
    Bioscience and Medical Research Center, Niigata University Medical and Dental Hospital, Asahimachi Dohri, Niigata, Japan
    Respirology 11:S65-9. 2006
    ..However, this finding posed the question as to why the autoantibody against GM-CSF caused lesions only in the lung...
  7. ncbi request reprint Granulocyte-macrophage colony-stimulating factor inhalation therapy for patients with idiopathic pulmonary alveolar proteinosis: a pilot study; and long-term treatment with aerosolized granulocyte-macrophage colony-stimulating factor: a case report
    Ryushi Tazawa
    Respiratory Medicine and Translational Research Clinic, Tohoku University Hospital, Seiryomachi, Sendai, Japan
    Respirology 11:S61-4. 2006
    ..The results suggest that the efficacy of GM-CSF inhalation therapy might be related to the drug preparation mode, choice of nebulizer, and duration of treatment...
  8. ncbi request reprint Granulocyte-macrophage colony-stimulating factor and lung immunity in pulmonary alveolar proteinosis
    Ryushi Tazawa
    Institute of Development, Aging, and Cancer, Tohoku University Department of Hematology and Immunology, Tohoku University Hospital, Japan
    Am J Respir Crit Care Med 171:1142-9. 2005
    ..Our study shows that GM-CSF administration engenders a decrease in the neutralizing capacity against the protein in the lungs. Thereby, it facilitates restoration of the normal function of alveolar macrophages...
  9. ncbi request reprint [Molecular pathogenesis in tuberculosis complicated with AIDS]
    Koh Nakata
    Bioscience Medical Research Center, Niigata Medical Dental Hospital, Niigata, Japan
    Kekkaku 79:659-67. 2004
    ..Contact between activated lymphocytes and macrophages is necessary to downregulate inhibitory C/EBP beta, thereby derepressing the HIV-1 LTR. Lymphocyte derived soluble factor(s) activate NF-kappaB, further enhancing the HIV-1 LTR...
  10. ncbi request reprint Pulmonary alveolar proteinosis
    Jeffrey J Presneill
    Intensive Care Unit, Royal Melbourne Hospital, Grattan Street, Parkville 3050, Victoria, Australia
    Clin Chest Med 25:593-613, viii. 2004
    ..The last decade has brought new advances in laboratory and clinical research that are lifting a veil not only on PAP but also on general aspects of pulmonary surfactant biology and innate immune defense...
  11. ncbi request reprint BCL-6 mutations in pulmonary lymphoproliferative disorders: demonstration of an aberrant immunological reaction in HIV-related lymphoid interstitial pneumonia
    Katsushi Kurosu
    Department of Respirology B2, Graduate School of Medicine, Chiba University, Chiba, Japan
    J Immunol 172:7116-22. 2004
    ....
  12. ncbi request reprint Pulmonary alveolar proteinosis
    Bruce C Trapnell
    Division of Pulmonary Biology, Children s Hospital Medical Center, Cincinnati, OH 45229, USA
    N Engl J Med 349:2527-39. 2003
  13. ncbi request reprint High-affinity autoantibodies specifically eliminate granulocyte-macrophage colony-stimulating factor activity in the lungs of patients with idiopathic pulmonary alveolar proteinosis
    Kanji Uchida
    Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, 1 21 1 Toyama, Shinjuku City, Tokyo 162 8655, Japan
    Blood 103:1089-98. 2004
    ..Our data strengthen the evidence associating anti-GM-CSF autoantibodies with the pathogenesis of this disease...
  14. ncbi request reprint Oligoclonal T cell expansions in pulmonary lymphoproliferative disorders: demonstration of the frequent occurrence of oligoclonal T cells in human immunodeficiency virus-related lymphoid interstitial pneumonia
    Katsushi Kurosu
    Department of Respirology, School of Medicine, Chiba University, Chiba, Japan
    Am J Respir Crit Care Med 165:254-9. 2002
    ....
  15. ncbi request reprint Expression of PU.1 and terminal differentiation of alveolar macrophages in newborn rats
    Haruko Iwabuchi
    Division of Cellular and Molecular Pathology, Department of Cellular Function, Niigata University Graduate School of Medical and Dental Sciences, Asahimachi 1 757, Niigata 951 8510, Japan
    Cell Tissue Res 329:71-9. 2007
    ..These results suggest that AMs are initially immature, and that their terminal differentiation starts after birth concomitantly with an increased expression of PU.1...