Chubachi, Shotaro

写真a

Affiliation

School of Medicine, Department of Internal Medicine (Pulmonary Medicine) (Shinanomachi)

Position

Instructor

Career 【 Display / hide

  • 2015.04
    -
    Present

    内科学教室、呼吸器内科, 助教

Academic Background 【 Display / hide

  • 2005.03

    昭和大学, 医学部

    University

Academic Degrees 【 Display / hide

  • 博士(医学), 慶應義塾大学, Dissertation

    Polymorphism of LRP5 gene and emphysema severity are associated with osteoporosis in Japanese patients with or at risk for COPD.

 

Research Areas 【 Display / hide

  • Respiratory organ internal medicine

Research Themes 【 Display / hide

  • COPD, 

    2009.04
    -
    Present

  • 肺癌, 

    2009.04
    -
    Present

  • COPD, 

    2009.04
    -
    Present

 

Books 【 Display / hide

  • 呼吸器内科

    Chubachi Shotaro, 科学評論社, 2013.06

    Scope: 【COPDの併存症とその治療】 COPDと骨粗鬆症

  • Medical Practice

    Chubachi Shotaro, 文光堂, 2012.04

    Scope: 【気管支喘息・実地診療の最前線】 セミナー/病態に基づく実地診療のポイント 喘息とCOPDの関連性と鑑別 診療上の相違点

  • 呼吸器内科

    Chubachi Shotaro, 科学評論社, 2011.09

    Scope: COPDのバイオマーカー(解説)

Papers 【 Display / hide

  • Intermittent Exposure to Cigarette Smoke Increases Lung Tumors and the Severity of Emphysema More than Continuous Exposure

    Kameyama, N., Chubachi, S., Hegab, A. E., Yasuda, H., Kagawa, S., Tsutsumi, A., Fukunaga, K., Shimoda, M., Kanai, Y., Soejima, K. and Betsuyaku, T.

    Am J Respir Cell Mol Biol 59 ( 2 ) 179 - 188 2018.08

    Research paper (scientific journal), Joint Work,  ISSN  1535-4989

     View Summary

    Lung cancer and chronic obstructive pulmonary disease are leading causes of morbidity and mortality worldwide, and cigarette smoking is a main risk factor for both. The presence of emphysema, an irreversible lung disease, further raises the risk of lung cancer in patients with chronic obstructive pulmonary disease. The mechanisms involved in smoke-induced tumorigenesis and emphysema are not fully understood, attributable to a lack of appropriate animal models. Here, we optimized a model of cigarette smoke (CS)-induced lung cancer and emphysema in A/J mice treated with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, a potent carcinogen. We investigated whether variations in CS exposure patterns with the same total amount and duration of exposure affect tumorigenesis and/or development of emphysema. Continuous CS exposure for 3 months significantly suppressed 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced development of adenomas and adenocarcinomas; however, emphysema independently developed during this period. Surprisingly, intermittent CS exposure increased the severity of emphysema and resulted in a higher incidence of adenocarcinomas. Furthermore, intermittent CS exposure elicited a marked increase in M2-polarized macrophages within and near the developed tumors. By employing a CS exposure protocol with repeated cycles of cessation and relapse, we provide evidence that intermittent CS exposure enhances tumorigenesis and emphysema progression more than that of continuous CS exposure.

  • Development of Necrotizing Myopathy Following Interstitial Lung Disease with Anti-signal Recognition Particle Antibody

    Kusumoto, T., Okamori, S., Masuzawa, K., Asakura, T., Nishina, N., Chubachi, S., Naoki, K., Fukunaga, K. and Betsuyaku, T.

    Intern Med 57 ( 14 ) 2045 - 2049 2018.07

    Research paper (scientific journal), Joint Work,  ISSN  1349-7235

     View Summary

    A 72-year-old man was admitted due to dyspnea on exertion with interstitial shadows and elevated serum creatinine kinase (CK). Despite a close examination, which included magnetic resonance imaging (MRI), we could not diagnose myopathy. Prednisolone was administered and gradually tapered. One year later, anti-signal recognition particle (SRP) antibody was confirmed and he was re-admitted for hypoxemia with elevated CK. MRI revealed muscle edema and a histopathological examination of a muscle biopsy specimen showed necrotizing myopathy. Prednisolone, cyclosporine, and intravenous immunoglobulin were administered. Physicians should carefully monitor muscle symptoms and serum CK levels in cases of interstitial lung disease with anti-SRP antibodies.

  • Plasma sE-cadherin and the plasma sE-cadherin/sVE-cadherin ratio are potential biomarkers for chronic obstructive pulmonary disease

    Shirahata, T., Nakamura, H., Nakajima, T., Nakamura, M., Chubachi, S., Yoshida, S., Tsuduki, K., Mashimo, S., Takahashi, S., Minematsu, N., Tateno, H., Asano, K., Fujishima, S. and Betsuyaku, T.

    Biomarkers 23 ( 5 ) 414 - 421 2018.07

    Research paper (scientific journal), Joint Work,  ISSN  1366-5804

     View Summary

    BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by airway inflammation with endothelial dysfunction. Cadherins are adhesion molecules on epithelial (E-) and vascular endothelial (VE-) cells. Soluble (s) cadherin is released from the cell surface by the effects of proteases including matrix metalloproteinases (MMPs). OBJECTIVE: The aim of this study was to examine the associations of sE-/sVE-cadherin levels in plasma with the development of COPD. METHODS: Plasma sE-/VE-cadherin levels were measured by an enzyme-linked immunosorbent assay in 115 patients with COPD, 36 symptomatic smokers (SS), 63 healthy smokers (HS) and 78 healthy non-smokers (HN). sE-cadherin and MMP-7 levels in epithelial lining fluid (ELF) were measured in 24 patients (12 COPD and 12 control). RESULTS: Plasma sE-cadherin levels and sE-cadherin/sVE-cadherin ratios were significantly higher in COPD and SS than in HS and HN groups, while plasma sVE-cadherin levels were lower in COPD than in HS and HN groups (p < 0.0001). sE-cadherin levels paralleled the severity of airflow limitation in both plasma (p < 0.01) and ELF (p < 0.05), while plasma sVE-cadherin levels were inversely correlated with the extent of emphysema (p < 0.05). MMP-7 levels were correlated with sE-cadherin levels in ELF. CONCLUSIONS: Plasma sE-cadherin levels and sE-cadherin/sVE-cadherin ratios are potential biomarkers for COPD.

  • Clinical utility of blood neutrophil-lymphocyte ratio in Japanese COPD patients

    Sakurai, K., Chubachi, S., Irie, H., Tsutsumi, A., Kameyama, N., Kamatani, T., Koh, H., Terashima, T., Nakamura, H., Asano, K. and Betsuyaku, T.

    BMC Pulm Med 18 ( 1 ) 65 2018.05

    Research paper (scientific journal), Joint Work,  ISSN  1471-2466

     View Summary

    BACKGROUND: Neutrophil-to-lymphocyte ratio (NLR) is a biomarker of inflammation in chronic obstructive pulmonary disease (COPD) patients. But, a meaningful threshold and the longitudinal changes are unknown. We aimed to investigate the association between NLR and the clinical characteristics of COPD patients and to determine a meaningful threshold and the longitudinal changes for NLR. METHODS: Keio University and its affiliate hospitals conducted an observational COPD cohort study over 3 years. We performed a blood examination and a pulmonary function test. Blood examination was completed at baseline and annually thereafter, at a time when the disease was stable. Two hundred seventy-four patients who had at least 3 blood examinations over 3 years were included. RESULTS: Baseline NLR was correlated with baseline C-reactive protein (CRP) (r = 0.18, p = 0.003) and SAA (r = 0.34, p < 0.001). We defined an NLR score of 2.7 as the arbitrary cut-off value based on upper quartile points. COPD patients with NLR >/= 2.7 were older (p = 0.037), had a lower BMI (p = 0.005) and a lower %FEV1 (p = 0.0003) compared to patients with NLR < 2.7. Receiver-operating-characteristic (ROC) curves showed the optimal cutoff for the baseline NLR in the predicting moderate/severe exacerbation to be 2.7, which was same as the upper quartile points. Follow-up analysis over 3 years revealed that the differences in the trends of NLR among the three groups based on the categories of exacerbations (moderate or severe, mild, no exacerbation) were significant (p = 0.006). CONCLUSIONS: NLR is associated with COPD severity and exacerbations. For predicting exacerbations, we estimated the threshold of NLR to be 2.7 at baseline. TRIAL REGISTRATION: Clinical trial registered with the University Hospital Medication Information Network ( UMIN000003470 , April 10, 2010).

  • Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema

    Sasaki, M., Chubachi, S., Kameyama, N., Sato, M., Haraguchi, M., Miyazaki, M., Takahashi, S., Nakano, T., Kuroda, Y., Betsuyaku, T. and Matsuo, K.

    PLoS One 13 ( 1 ) e0191611 2018

    Research paper (scientific journal), Joint Work,  ISSN  1932-6203

     View Summary

    Smoking is a common risk factor for both chronic obstructive pulmonary disease (COPD) and osteoporosis. In patients with COPD, severe emphysema is a risk factor for vertebral fracture; however, the effects of smoking or emphysema on bone health remain largely unknown. We report bone deterioration in a mouse model of emphysema induced by nose-only cigarette smoke (CS) exposure. Unexpectedly, short-term exposure for 4-weeks decreased bone turnover and increased bone volume in mice. However, prolonged exposure for 20- and 40-weeks reversed the effects from suppression to promotion of bone resorption. This long-term CS exposure increased osteoclast number and impaired bone growth, while it increased bone volume. Strikingly, long-term CS exposure deteriorated bone quality of the lumbar vertebrae as illustrated by disorientation of collagen fibers and the biological apatite c-axis. This animal model may provide a better understanding of the mechanisms underlying the deterioration of bone quality in pulmonary emphysema caused by smoking.

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Presentations 【 Display / hide

  • COPDと間質性肺炎に合併する肺癌の臨床

    Chubachi Shotaro

    第37回日本画像医学会, 2018.02, Symposium, Workshop, Panelist (public offering)

  • Radiological features of structural basis where cancer develops in COPD lungs

    Chubachi Shotaro

    American Thoracic Society 2017 International Conference, 2017.05, Oral Presentation(general)

  • COPDコホート研究追跡期間に新規に発症した肺癌の発症前CTの画像的特徴

    Chubachi Shotaro

    第57回日本呼吸器学会学術講演会, 2017.04, Symposium, Workshop, Panelist (public offering)

  • Cluster Analysis Based on Comorbidities for Japanese COPD Patients

    Chubachi Shotaro

    American Thoracic Society 2016 International Conference, 2016.05, Oral Presentation(general)

  • 全身併存症クラスター解析を用いた日本人COPD患者のフェノタイプ分類

    Chubachi Shotaro

    第56回日本呼吸器学会学術講演会, 2016.04, Symposium, Workshop, Panelist (public offering)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 肺気腫及び肺気腫合併肺癌の新規予防薬の探索

    2019.04
    -
    2022.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 中鉢 正太郎, Grant-in-Aid for Scientific Research (C), Principal Investigator

  • 喫煙誘導マウスモデルにおける肺がん発生機序

    2017.04
    -
    2019.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 中鉢 正太郎, Grant-in-Aid for Young Scientists (B), Principal Investigator

Awards 【 Display / hide

  • 日本呼吸器学会学術部会賞 優秀賞 

    2017.04, 日本呼吸器学会

  • 昭和大学 上條旗が丘賞

    2005.03, 昭和大学

     View Description

    課外活動で本学の名を宣揚せしめ、かつ人物、学業ともに優秀と認められた学生を卒業時に表彰。

  • 昭和大学 上條賞

    2005.03, 昭和大学

     View Description

    最終学年において、人物が優秀で学業成績が抜群の学生を卒業時に表彰。

 

Courses Taught 【 Display / hide

  • LECTURE SERIES, INTERNAL MEDICINE (PULMONOLOGY)

    2019

  • CLINICAL TRAINING IN DIAGNOSIS

    2019

  • CASE STUDIES OF INTERNAL MEDICINE

    2019

Courses Previously Taught 【 Display / hide

  • 内科学呼吸器 急性呼吸窮迫症候群と急性呼吸不全の管理

    Keio University, 2018, Autumn Semester, Major subject, Lecture, Within own faculty

  • 診断学実習 ケーススタディー

    Keio University, 2018, Autumn Semester, Major subject, Lecture, Within own faculty

  • 診断学実習 血液ガス分析

    Keio University, 2018, Autumn Semester, Major subject, Lecture, Within own faculty