Updated on 2022/03/22

写真a

 
SAKAMOTO Koji
 
Organization
Nagoya University Hospital Respiratory Medicine Assistant professor of hospital
Title
Assistant professor of hospital
Contact information
メールアドレス

Degree 1

  1. 博士(医学) ( 2012.7   名古屋大学 ) 

Research Areas 1

  1. Life Science / Respiratory medicine

Current Research Project and SDGs 1

  1. 細胞外微粒子の呼吸器への影響

Education 2

  1. Nagoya University   Graduate School, Division of Medical Sciences

    - 2012.3

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    Country: Japan

  2. Nagoya University   Graduate School, Division of Medical Sciences

    - 2012.3

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    Country: Japan

Professional Memberships 4

  1. 日本呼吸器学会

  2. 日本アレルギー学会

  3. American Thoracic Society

  4. 日本内科学会

Awards 3

  1. International Session Award

    2017  

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    Award type:Award from international society, conference, symposium, etc.  Country:Japan

  2. The I.M. Rosenzweig Junior Investigator Award

    2016   Pulmonary Fibrosis Foundation  

    Koji Sakamoto

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    Award type:Award from publisher, newspaper, foundation, etc.  Country:United States

  3. Scientific Abstract Award

    2014   American Thoracic Society  

    Koji Sakamoto

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    Award type:Award from international society, conference, symposium, etc.  Country:United States

 

Papers 71

  1. Size and surface modification of silica nanoparticles affect the severity of lung toxicity by modulating endosomal ROS generation in macrophages Reviewed International journal

    Inoue Masahide, Sakamoto Koji, Suzuki Atsushi, Nakai Shinya, Ando Akira, Shiraki Yukihiko, Nakahara Yoshio, Omura Mika, Enomoto Atsushi, Nakase Ikuhiko, Sawada Makoto, Hashimoto Naozumi

    PARTICLE AND FIBRE TOXICOLOGY   Vol. 18 ( 1 ) page: 21   2021.6

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Particle and Fibre Toxicology  

    Background: As the application of silica nanomaterials continues to expand, increasing chances of its exposure to the human body and potential harm are anticipated. Although the toxicity of silica nanomaterials is assumed to be affected by their physio-chemical properties, including size and surface functionalization, its molecular mechanisms remain unclear. We hypothesized that analysis of intracellular localization of the particles and subsequent intracellular signaling could reveal a novel determinant of inflammatory response against silica particles with different physico-chemical properties. Results: We employed a murine intratracheal instillation model of amorphous silica nanoparticles (NPs) exposure to compare their in vivo toxicities in the respiratory system. Pristine silica-NPs of 50 nm diameters (50 nm-plain) induced airway-centered lung injury with marked neutrophilic infiltration. By contrast, instillation of pristine silica particles of a larger diameter (3 μm; 3 μm-plain) significantly reduced the severity of lung injury and neutrophilic infiltration, possibly through attenuated induction of neutrophil chemotactic chemokines including MIP2. Ex vivo analysis of alveolar macrophages as well as in vitro assessment using RAW264.7 cells revealed a remarkably lower cellular uptake of 3 μm-plain particles compared with 50 nm-plain, which is assumed to be the underlying mechanism of attenuated immune response. The severity of lung injury and neutrophilic infiltration was also significantly reduced after intratracheal instillation of silica NPs with an amine surface modification (50 nm-NH2) when compared with 50 nm-plain. Despite unchanged efficacy in cellular uptake, treatment with 50 nm-NH2 induced a significantly attenuated immune response in RAW264.7 cells. Assessment of intracellular redox signaling revealed increased reactive oxygen species (ROS) in endosomal compartments of RAW264.7 cells treated with 50 nm-plain when compared with vehicle-treated control. In contrast, augmentation of endosomal ROS signals in cells treated with 50 nm-NH2 was significantly lower. Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Conclusions: Our murine model suggested that the pulmonary toxicity of silica NPs depended on their physico-chemical properties through distinct mechanisms. Cellular uptake of larger particles by macrophages decreased, while surface amine modification modulated endosomal ROS signaling via NOX2, both of which are assumed to be involved in mitigating immune response in macrophages and resulting lung injury.

    DOI: 10.1186/s12989-021-00415-0

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  2. Prognostic Impact and Risk Factors of Immune-Related Pneumonitis in Patients With Non-Small-Cell Lung Cancer Who Received Programmed Death 1 Inhibitors. Reviewed International journal

    Jun Fukihara, Koji Sakamoto, Junji Koyama, Takayasu Ito, Shingo Iwano, Masahiro Morise, Masahiro Ogawa, Yasuhiro Kondoh, Tomoki Kimura, Naozumi Hashimoto, Yoshinori Hasegawa

    Clinical lung cancer   Vol. 20 ( 6 ) page: 442 - +   2019.11

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    INTRODUCTION: Pneumonitis is one of the immune-related adverse events of programmed death 1 (PD-1) inhibitors that sometimes cause lethal outcomes. Although some recent reports have described PD-1 inhibitors as more effective in non-small-cell lung cancer (NSCLC) patients with immune-related adverse events than in those without, few data are available on the prognosis of those treated with PD-1 inhibitors who developed immune-related pneumonitis (IRP). Additionally, the robust risk factors of IRP have not been well elucidated. PATIENTS AND METHODS: A retrospective review of patients with recurrent or advanced NSCLC who took a PD-1 inhibitor (nivolumab or pembrolizumab monotherapy) between January 2016 and March 2018 was undertaken. Radiologic findings such as unilateral infiltration were also defined as IRP as long as they were deemed relevant to PD-1 inhibitors. RESULTS: Twenty-seven (16%) of 170 patients developed IRP. Although 22 (81%) of 27 patients with IRP recovered with drug cessation with or without corticosteroid therapy, 8-week landmark analysis showed the overall survival after administration of the PD-1 inhibitor was significantly shorter in patients with IRP than in those without (8.7 vs. 23.0 months, P = .015). Patients with IRP tended to not receive next-line treatment and choose best supportive care after cessation of PD-1 inhibitor therapy. In the multivariate analysis, pembrolizumab (vs. nivolumab) and low serum albumin were independent risk factors for IRP. CONCLUSION: Development of IRP was correlated with poor prognosis in patients with NSCLC. Further study is necessary for establishing the best prediction and management strategies for IRP.

    DOI: 10.1016/j.cllc.2019.07.006

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  3. COVID-19-Triggered Acute Exacerbation of IPF, an Underdiagnosed Clinical Entity With Two-Peaked Respiratory Failure: A Case Report and Literature Review Reviewed International journal

    Goto Yosuke, Sakamoto Koji, Fukihara Jun, Suzuki Atsushi, Omote Norihito, Ando Akira, Shindo Yuichiro, Hashimoto Naozumi

    FRONTIERS IN MEDICINE   Vol. 9   page: 815924   2022.2

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Frontiers in Medicine  

    Because severe coronavirus disease 2019 (COVID-19) affects the respiratory system and develops into respiratory failure, patients with pre-existing chronic lung disorders, such as idiopathic pulmonary fibrosis (IPF), are thought to be at high risk of death. Patients with IPF often suffer from a lethal complication, acute exacerbation (AE), a significant part of which is assumed to be triggered by respiratory viral infection. However, whether mild to moderate COVID-19 can trigger AE in patients with IPF remains unknown. This is the case report of a 60-year-old man with a 4-year history of IPF who successfully recovered from moderate COVID-19 but subsequently developed more severe respiratory failure, which was considered to be a COVID-19-triggered acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF). It is important to be aware of the risk of AE-IPF after COVID-19 and to properly manage this deadly complication of IPF. Recent literature reporting cases with chronic interstitial lung diseases which developed respiratory failure by complications with COVID-19 is also reviewed and discussed.

    DOI: 10.3389/fmed.2022.815924

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  4. Overexpression of bone morphogenetic protein receptor type 2 suppresses transforming growth factor beta-induced profibrotic responses in lung fibroblasts Reviewed International coauthorship International journal

    Fukihara Jun, Maiolo Suzanne, Kovac Jessica, Sakamoto Koji, Wakahara Keiko, Hashimoto Naozumi, Reynolds Paul N.

    EXPERIMENTAL LUNG RESEARCH   Vol. 48 ( 1 ) page: 35 - 51   2022.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Experimental Lung Research  

    Purpose of the study: Idiopathic pulmonary fibrosis (IPF) is a progressive disease with a poor prognosis. As the efficacy of currently available antifibrotics is limited, development of new therapies is warranted. Transforming growth factor (TGF)-β plays a central role in the pathogenesis of IPF through mechanisms such as promoting the production of extracellular matrix by fibroblasts. Conversely, bone morphogenetic proteins (BMPs) are known to be antifibrotic and may counterbalance TGF-β signaling via BMP receptor type 2 (BMPR2). However, little is known about the expression status of BMPR2 and its function in pulmonary fibrosis, and manipulation of BMPR2 expression has never been attempted. In this study, we aimed at evaluating the effectiveness of BMPR2 upregulation for modulating the imbalance of the TGF-β/BMP axis and reduce the profibrotic changes in lung fibroblasts. Materials and Methods: We investigated BMPR2 expression in pulmonary fibrosis and TGF-β/BMP signaling in lung fibroblasts. Then we evaluated the impact of BMPR2 upregulation using adenoviral transduction on TGF-β-induced Smad2/3 phosphorylation and fibronectin production in lung fibroblasts. Results: BMPR2 was distributed in airway epithelium and alveolar walls in rat lungs. BMPR2 expression was decreased in fibrotic lesions in the lungs of rats with bleomycin-induced pulmonary fibrosis and in human lung fibroblasts (HLFs) stimulated with TGF-β. Although Smad2/3 phosphorylation and fibronectin production were not suppressed solely by BMPs, phosphorylated Smad2/3 was decreased in BMPR2-transduced cells even without BMP stimulation. Fibronectin was decreased only when BMPR2-transduced HLFs were stimulated with BMP7 (but not BMP4). Similar results were also observed in IPF patient HLFs and rat lung fibroblasts. Conclusions: BMPR2 expression was reduced in fibrotic lungs and lung fibroblasts stimulated with TGF-β. BMPR2 transduction to lung fibroblasts reduced Smad2/3 phosphorylation, and reduced fibronectin production when treated with BMP7. Upregulation of BMPR2 may be a possible strategy for treating pulmonary fibrosis.

    DOI: 10.1080/01902148.2021.2024301

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  5. Successful Treatment with High-dose Steroids for Acute Exacerbation of Idiopathic Pulmonary Fibrosis Triggered by COVID-19

    Omote Norihito, Kanemitsu Yoshihiro, Inoue Takahiro, Yonezawa Toshiyuki, Ichihashi Takuji, Shindo Yuichiro, Sakamoto Koji, Ando Akira, Suzuki Atsushi, Niimi Akio, Ito Satoru, Imaizumi Kazuyoshi, Hashimoto Naozumi

    Internal Medicine   Vol. 61 ( 2 ) page: 233 - 236   2022

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:The Japanese Society of Internal Medicine  

    <p>We herein report a case of acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) triggered by COVID-19. An 87-year-old woman tested positive for COVID-19 on a polymerase chain reaction test, and computed tomography revealed ground-glass opacity (GGO) superimposed on a background pattern consistent with usual interstitial pneumonia. Considering these data, we diagnosed her with AE-IPF. She experienced worsening of dyspnea and expansion of the GGO. Therefore, we introduced high-dose steroids (methylprednisolone 250 mg/day for 3 days). After the treatment, the pulmonary infiltrates improved. She was discharged from our hospital without severe disability. High-dose steroids can be a viable treatment option for AE-IPF triggered by COVID-19. </p>

    DOI: 10.2169/internalmedicine.8163-21

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  6. Fibroblasts positive for meflin have anti-fibrotic property in pulmonary fibrosis. Reviewed International coauthorship International journal

    Yoshio Nakahara, Naozumi Hashimoto, Koji Sakamoto, Atsushi Enomoto, Taylor S Adams, Toyoharu Yokoi, Norihito Omote, Sergio Poli, Akira Ando, Keiko Wakahara, Atsushi Suzuki, Masahide Inoue, Akitoshi Hara, Yasuyuki Mizutani, Kazuyoshi Imaizumi, Tsutomu Kawabe, Ivan O Rosas, Masahide Takahashi, Naftali Kaminski, Yoshinori Hasegawa

    The European respiratory journal   Vol. 58 ( 6 )   2021.12

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    The prognosis of elderly individuals with idiopathic pulmonary fibrosis (IPF) remains poor. Fibroblastic foci, in which aggregates of proliferating fibroblasts and myofibroblasts are involved, are the pathological hallmark lesions in IPF to represent focal areas of active fibrogenesis. Fibroblast heterogeneity in fibrotic lesions hampers the discovery of the pathogenesis of pulmonary fibrosis. Therefore, to determine of the pathogenesis of IPF, identification of functional fibroblasts is warranted. This study was aimed to determine the role of fibroblasts positive for meflin, identified as a potential marker for mesenchymal stromal cells, during the development of pulmonary fibrosis. We characterised meflin-positive cells in a single cell atlas established by single-cell RNA sequencing (scRNA-seq)-based profiling of 243 472 cells from 32 IPF lungs and 29 normal lung samples. scRNA-seq combined with in situ RNA hybridisation identified proliferating fibroblasts positive for meflin in fibroblastic foci, not dense fibrosis, of fibrotic lungs in IPF patients. We determined the role of fibroblasts positive for meflin using bleomycin (BLM)-induced pulmonary fibrosis. A BLM-induced lung fibrosis model for meflin-deficient mice showed that fibroblasts positive for meflin had anti-fibrotic property to prevent pulmonary fibrosis. Although transforming growth factor-β-induced fibrogenesis and cell senescence with senescence-associated secretory phenotype were exacerbated in fibroblasts via the repression or lack of meflin, these were inhibited in meflin-deficient fibroblasts with meflin reconstitution. These findings provide evidence to show the biological importance of meflin expression on fibroblasts and myofibroblasts in the active fibrotic region of pulmonary fibrosis.

    DOI: 10.1183/13993003.03397-2020

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  7. The Effect of Pirfenidone on the Prescription of Antibiotics and Antitussive Drugs in Patients With Idiopathic Pulmonary Fibrosis: A Post Hoc Exploratory Analysis of Phase III Clinical Trial. Reviewed International journal

    Suzuki A, Sakaguchi H, Sakamoto K, Ebina M, Azuma A, Ogura T, Taguchi Y, Suga M, Takahashi H, Sugiyama Y, Kudoh S, Nukiwa T, Miyazawa S, Kondoh Y

    Chest   Vol. 160 ( 4 ) page: 1372 - 1376   2021.10

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    DOI: 10.1016/j.chest.2021.05.058

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  8. Impact of post-capillary pulmonary hypertension on mortality in interstitial lung disease. Reviewed International journal

    Ryo Teramachi, Hiroyuki Taniguchi, Yasuhiro Kondoh, Tomoki Kimura, Kensuke Kataoka, Toshiki Yokoyama, Taiki Furukawa, Mitsuaki Yagi, Koji Sakamoto, Naozumi Hashimoto, Yoshinori Hasegawa

    Respiratory investigation   Vol. 59 ( 3 ) page: 342 - 349   2021.5

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    BACKGROUND: Pulmonary hypertension (PH) influences mortality in patients with interstitial lung disease (ILD). Almost all studies on patients with ILD, have focused on the clinical impact of pre-capillary PH on survival. Therefore, little is known about the influence of post-capillary PH. We aimed to assess the prevalence of post-capillary PH and its clinical impact on survival in patients with ILD, followed by comparison with pre-capillary PH. METHODS: This retrospective study enrolled 1152 patients with ILD who were diagnosed with PH using right heart catheterization between May 2007 and December 2015. We analyzed the demographics and composite outcomes (defined as death from any cause or lung transplantation) of patients with post-capillary PH and compared them with patients with pre-capillary PH. RESULTS: Thirty-two (20%) of the 157 patients with ILD-PH were diagnosed with post-capillary PH. Patients with post-capillary PH had significantly lower modified Medical Research Council scores, higher diffusion capacity for carbon monoxide, higher resting PaO2, lower pulmonary vascular resistance (PVR), and higher lowest oxygen saturation during the 6-min walk test compared to those with pre-capillary PH. Cardiovascular diseases were associated with a higher risk of mortality in patients with post-capillary PH. Multivariate Cox proportional hazards analysis demonstrated no significant difference between the composite outcomes in pre-capillary and post-capillary PH, while PVR and the ILD Gender-Age-Physiology Index were significantly associated with the composite outcome. CONCLUSIONS: We found that approximately one-fifth of patients with ILD-PH were diagnosed with post-capillary PH, and that PVR and not post-capillary PH was associated with mortality.

    DOI: 10.1016/j.resinv.2020.12.010

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  9. The Importance of Appropriate Diagnosis in the Practical Management of Chronic Obstructive Pulmonary Disease Reviewed

    Hashimoto Naozumi, Wakahara Keiko, Sakamoto Koji

    DIAGNOSTICS   Vol. 11 ( 4 )   2021.4

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    Chronic obstructive pulmonary disease (COPD) is projected to continue to contribute to an increase in the overall worldwide burden of disease until 2030. Therefore, an accurate assessment of the risk of airway obstruction in patients with COPD has become vitally important. Although the Global Initiative for Chronic Obstructive Lung Disease (GOLD), the American Thoracic Society (ATS) and European Respiratory Society (ERS), and the Japanese Respiratory Society (JRS) provide the criteria by which to diagnose COPD, many studies suggest that it is in fact underdiagnosed. Its prevalence increases, while the impact of COPD-related systemic comorbidities is also increasingly recognized in clinical aspects of COPD. Although a recent report suggests that spirometry should not be used to screen for airflow limitation in individuals without respiratory symptoms, the early detection of COPD in patients with no, or few, symptoms is an opportunity to provide appropriate management based on COPD guidelines. Clinical advances have been made in pharmacotherapeutic approaches to COPD. This article provides a current understanding of the importance of an appropriate diagnosis in the real-world management of COPD.

    DOI: 10.3390/diagnostics11040618

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  10. Long noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state Reviewed International coauthorship International journal

    Omote Norihito, Sakamoto Koji, Li Qin, Schupp Jonas C., Adams Taylor, Ahangari Farida, Chioccioli Maurizio, DeIuliis Giuseppe, Hashimoto Naozumi, Hasegawa Yoshinori, Kaminski Naftali

    PHYSIOLOGICAL REPORTS   Vol. 9 ( 3 ) page: e14727   2021.2

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    DOI: 10.14814/phy2.14727

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  11. Serum mitochondrial DNA predicts the risk of acute exacerbation and progression of IPF. Reviewed International coauthorship International journal

    Koji Sakamoto, Taiki Furukawa, Yasuhiko Yamano, Kensuke Kataoka, Ryo Teramachi, Anjali Walia, Atsushi Suzuki, Masahide Inoue, Yoshio Nakahara, Changwan Ryu, Naozumi Hashimoto, Yasuhiro Kondoh

    The European respiratory journal   Vol. 57 ( 1 )   2021.1

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    DOI: 10.1183/13993003.01346-2020

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  12. Supplemental oxygen improves exercise capacity in IPF patients with exertional desaturation. Reviewed International journal

    Shinichi Arizono, Taiki Furukawa, Hiroyuki Taniguchi, Koji Sakamoto, Tomoki Kimura, Kensuke Kataoka, Tomoya Ogawa, Fumiko Watanabe, Yasuhiro Kondoh

    Respirology (Carlton, Vic.)   Vol. 25 ( 11 ) page: 1152 - 1159   2020.11

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    BACKGROUND AND OBJECTIVE: The efficacy of supplemental oxygen during exercise remains unclear for patients with IPF, as there have been conflicting results from recent prospective studies with small sample sizes. METHODS: This prospective, single-blind, randomized, crossover trial evaluated the efficacy of supplemental oxygen compared with placebo air during exercise in consecutive patients with IPF without resting hypoxaemia at initial evaluation. Patients with <90% SpO2 in a 6MWT using room air were randomly assigned to a CWRET at 80% of peak work rate with oxygen or placebo air gas via nasal cannula at 4 L/min. The primary endpoint was the effect of supplemental oxygen on endurance time. RESULTS: We recruited 72 consecutive patients (median age: 66.5 years, % FVC: 84.6%, % DLCO : 61.4%). Supplemental oxygen significantly increased the endurance time (340-424 s; P < 0.001) and minimum SpO2 (88.0-94.0%; P < 0.001) compared with placebo air. Furthermore, supplemental oxygen significantly improved dyspnoea and leg fatigue. In a multivariate linear regression analysis, the endurance time on air was an independent explanatory variable of the improvement rate of endurance time (P = 0.02). CONCLUSION: In mild-moderate IPF with exercise-induced hypoxaemia even without resting hypoxaemia, supplemental oxygen during exercise improved the endurance time, desaturation and subjective symptoms. Patients with shorter endurance times with placebo air showed better improvement with supplemental oxygen.

    DOI: 10.1111/resp.13829

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  13. Clinical burden of immune checkpoint inhibitor-induced pneumonitis. Invited Reviewed International journal

    Koji Sakamoto, Jun Fukihara, Masahiro Morise, Naozumi Hashimoto

    Respiratory investigation   Vol. 58 ( 5 ) page: 305 - 319   2020.9

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    Immune checkpoint inhibitors (ICIs) have been a breakthrough in medical oncology. However, many patients experience a novel type of adverse drug reaction that has a unique clinical presentation, called immune-related adverse events (irAEs). A breakdown of self-tolerance and an exaggerated autoimmune reaction by the host are assumed to be the underlying mechanisms. Therefore, special attention to the optimal diagnosis and management is required. Among the various effects of irAE, pneumonitis has been recognized as an important manifestation because of its high morbidity and mortality. As the application of ICIs is expanding to a wider variety of tumor types, as well as its use with cytotoxic agents and radiation, clinicians are highly likely to encounter this complication. In this review, we will summarize the current understanding of the underlying mechanisms, incidence, risk factors, optimal diagnostic workup, and management of ICI-related pneumonitis (IRP). We will also review fundamental information on drug-induced lung toxicity in the oncology setting. In addition, research perspectives focused on better risk stratification and management to avoid serious complications in the future are presented.

    DOI: 10.1016/j.resinv.2020.05.008

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  14. Acute Exacerbation of Pleuroparenchymal Fibroelastosis Secondary to Allogenic Hematopoietic Stem Cell Transplantation.

    Murakami Y, Sakamoto K, Okumura Y, Suzuki A, Mii S, Sato M, Yokoi T, Hashimoto N, Hasegawa Y

    Internal medicine (Tokyo, Japan)     2020.7

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    DOI: 10.2169/internalmedicine.4995-20

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  15. High-flow nasal cannula therapy for acute respiratory failure in patients with interstitial Pneumonia: A retrospective observational study Reviewed International journal

    Omote N.

    Nagoya Journal of Medical Science   Vol. 82 ( 2 ) page: 301 - 313   2020.5

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Nagoya Journal of Medical Science  

    DOI: 10.18999/nagjms.82.2.301

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  16. Reply to "Prognostic Impact and Risk Factors of Immune-Related Pneumonitis in Patients With Non-Small-Cell Lung Cancer Who Received Programmed Death-1 Inhibitors". Reviewed International journal

    Jun Fukihara, Koji Sakamoto, Junji Koyama, Takayasu Ito, Shingo Iwano, Masahiro Morise, Masahiro Ogawa, Yasuhiro Kondoh, Tomoki Kimura, Naozumi Hashimoto, Yoshinori Hasegawa

    Clinical lung cancer   Vol. 21 ( 3 ) page: E205 - E205   2020.5

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    DOI: 10.1016/j.cllc.2019.11.013

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  17. Acute exacerbations of fibrotic interstitial lung diseases. Reviewed International journal

    Suzuki A, Kondoh Y, Brown KK, Johkoh T, Kataoka K, Fukuoka J, Kimura T, Matsuda T, Yokoyama T, Fukihara J, Ando M, Tanaka T, Hashimoto N, Sakamoto K, Hasegawa Y

    Respirology (Carlton, Vic.)   Vol. 25 ( 5 ) page: 525 - 534   2020.5

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    DOI: 10.1111/resp.13682

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  18. <Editors' Choice> Renewed Japanese spirometric reference variables and risk stratification for postoperative outcomes in COPD patients with resected lung cancer. Reviewed International journal

    Yu Okada, Naozumi Hashimoto, Shingo Iwano, Koji Kawaguchi, Takayuki Fukui, Koji Sakamoto, Kenji Wakai, Kohei Yokoi, Yoshinori Hasegawa

    Nagoya journal of medical science   Vol. 81 ( 3 ) page: 427 - 438   2019.8

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    Although the lower limit of normal (LLN) of FEV1/FVC detects at-risk patients for postoperative outcomes among Japanese chronic obstructive pulmonary disease (COPD) patients with resected lung cancer, there was a lack of a Japanese reference equation to calculate the LLN of FEV1/FVC. Renewed Japanese spirometric reference variables might enable us to verify clinical impact of the LLN of FEV1/FVC among the Japanese population. To evaluate the clinical impact of the LLN of FEV1/FVC by using this renewed reference, data were retrospectively analyzed from 609 newly diagnosed lung cancer patients who had undergone thoracic surgery between 2006 and 2011. The combined assessment of the 0.70 fixed ratio and the LLN of the FEV1/FVC ratio classified the 609 subjects into the COPD (214 subjects), non-COPD (337 subjects), and in-between (58 subjects) groups, respectively. All of the relative odds ratios (ORs) of postoperative outcomes for the comparison between the in-between and non-COPD groups did not show significant confidence intervals (CIs). On the other hand, the adjusted ORs of postoperative outcomes for the COPD group versus the non-COPD group were 2.840 (95% CI: 1.824-4.421) for prolonged oxygen therapy (POT), 1.836 (95% CI: 1.166-2.890) for prolonged postoperative stays, and 1.637 (95% CI: 1.007-2.663) for combined complications. Adjusted comparisons of POT between the in-between and COPD groups also showed a significant relative OR of 2.984 (95% CI: 1.447-6.153). A standardized assessment of the LLN of FEV1/FVC by a renewed Japanese spirometric reference provides risk stratification for postoperative outcomes in the population.

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  19. Repressive role of stabilized hypoxia inducible factor 1α expression on transforming growth factor β-induced extracellular matrix production in lung cancer cells. Reviewed International journal

    Ando A, Hashimoto N, Sakamoto K, Omote N, Miyazaki S, Nakahara Y, Imaizumi K, Kawabe T, Hasegawa Y

    Cancer science   Vol. 110 ( 6 ) page: 1959 - 1973   2019.6

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    DOI: 10.1111/cas.14027

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  20. Performance of the COPD Assessment Test in patients with connective tissue disease-associated interstitial lung disease

    Suzuki Atsushi, Kondoh Yasuhiro, Swigris Jeffrey James, Matsuda Toshiaki, Kimura Tomoki, Kataoka Kensuke, Ando Masahiko, Hashimoto Naozumi, Sakamoto Koji, Hasegawa Yoshinori

    RESPIRATORY MEDICINE   Vol. 150   page: 15-20   2019.4

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    DOI: 10.1016/j.rmed.2019.01.017

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  21. Multidimensional improvement in connective tissue disease-associated interstitial lung disease: Two courses of pulse dose methylprednisolone followed by low-dose prednisone and tacrolimus. Reviewed International journal

    Yamano Y, Taniguchi H, Kondoh Y, Ando M, Kataoka K, Furukawa T, Johkoh T, Fukuoka J, Sakamoto K, Hasegawa Y

    Respirology (Carlton, Vic.)   Vol. 23 ( 11 ) page: 1041 - 1048   2018.11

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    DOI: 10.1111/resp.13365

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  22. Outcomes with newly proposed classification of acute respiratory deterioration in idiopathic pulmonary fibrosis

    Teramachi Ryo, Kondoh Yasuhiro, Kataoka Kensuke, Taniguchi Hiroyuki, Matsuda Toshiaki, Kimura Tomoki, Yokoyama Toshiki, Yamano Yasuhiko, Furukawa Taiki, Sakamoto Koji, Hashimoto Naozumi, Hasegawa Yoshinori

    RESPIRATORY MEDICINE   Vol. 143   page: 147-152   2018.10

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    DOI: 10.1016/j.rmed.2018.09.011

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  23. Performance of the St George's Respiratory Questionnaire in patients with connective tissue disease-associated interstitial lung disease. Reviewed International journal

    Suzuki A, Kondoh Y, Swigris JJ, Ando M, Kimura T, Kataoka K, Yamano Y, Furukawa T, Numata M, Sakamoto K, Hasegawa Y

    Respirology (Carlton, Vic.)   Vol. 23 ( 9 ) page: 851 - 859   2018.9

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    DOI: 10.1111/resp.13293

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  24. Prognostic evaluation by oxygenation with positive end-expiratory pressure in acute exacerbation of idiopathic pulmonary fibrosis: A retrospective cohort study.

    Suzuki A, Taniguchi H, Ando M, Kondoh Y, Kimura T, Kataoka K, Matsuda T, Yokoyama T, Sakamoto K, Hasegawa Y

    The clinical respiratory journal   Vol. 12 ( 3 ) page: 895 - 903   2018.3

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    DOI: 10.1111/crj.12602

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  25. Thin-section computed tomography-determined usual interstitial pneumonia pattern affects the decision-making process for resection in newly diagnosed lung cancer patients: a retrospective study Reviewed

    Hashimoto N, Ando A, Iwano S, Sakamoto K, Okachi S, Matsuzaki A, Okada Y, Wakai K, Yokoi K, Hasegawa Y

    BMC Pulm Med   Vol. 18 ( 1 ) page: 2   2018.1

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    DOI: 10.1186/s12890-017-0565-5

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  26. A scoring system to predict the elevation of mean pulmonary arterial pressure in idiopathic pulmonary fibrosis

    Furukawa Taiki, Kondoh Yasuhiro, Taniguchi Hiroyuki, Yagi Mitsuaki, Matsuda Toshiaki, Kimura Tomoki, Kataoka Kensuke, Johkoh Takeshi, Ando Masahiko, Hashimoto Naozumi, Sakamoto Koji, Hasegawa Yoshinori

    EUROPEAN RESPIRATORY JOURNAL   Vol. 51 ( 1 )   2018.1

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    DOI: 10.1183/13993003.01311-2017

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  27. Pirfenidone as salvage treatment for refractory bleomycin-induced lung injury: a case report of seminoma Reviewed International journal

    Koji Sakamoto, Satoru Ito, Naozumi Hashimoto, Yoshinori Hasegawa

    BMC CANCER   Vol. 17 ( 1 ) page: 526   2017.8

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    Background: Bleomycin-induced lung injury, a major complication of chemotherapy for germ cell tumors, occasionally fails to respond to the standard treatment with corticosteroids and develops into severe respiratory insufficiency. Little is known about salvage treatment for refractory cases.
    Case presentation: A 63-year-old man who had been diagnosed with stage I seminoma and undergone a high orchiectomy 1 year previously developed swelling of his left iliac lymph node and was diagnosed with a recurrence of the seminoma. He was administered a standard chemotherapy regimen of cisplatin, etoposide, and bleomycin. At the end of second cycle, he developed a dry cough and fever that was accompanied by newly-identified bilateral infiltrates on chest X-ray. Despite initiation of oral prednisolone, his exertional dyspnea and decline in pulmonary functions continued to be aggravated. High-dose pulse treatment with methylprednisolone was introduced and improved his symptoms and radiologic findings. However, the maintenance dose of oral prednisolone allowed reactivation of the disease with evidence of newly-developed bilateral lung opacities on high-resolution CT scans. Considering his glucose intolerance and cataracts as complications of corticosteroid treatment, administration of pirfenidone was initiated with the patient's consent. Pirfenidone at 1800 mg/day was well tolerated, and resolved his symptoms and abnormal opacities on a chest CT scan. Subsequently, the dose of prednisolone was gradually tapered without worsening of the disease. At the most recent follow-up, he was still in complete remission of seminoma with a successfully tapered combination dose of prednisolone and pirfenidone.
    Conclusions: Pirfenidone, a novel oral agent with anti-inflammatory and -fibrotic properties, should be considered as a salvage drug for refractory cases of bleomycin-induced lung injury.

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  28. Aging Impairs Alveolar Macrophage Phagocytosis and Increases Influenza-Induced Mortality in Mice Reviewed International journal

    Christine K. Wong, Candice A. Smith, Koji Sakamoto, Naftali Kaminski, Jonathan L. Koff, Daniel R. Goldstein

    JOURNAL OF IMMUNOLOGY   Vol. 199 ( 3 ) page: 1060 - 1068   2017.8

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    Influenza viral infections often lead to increased mortality in older people. However, the mechanisms by which aging impacts immunity to influenza lung infection remain unclear. We employed a murine model of influenza infection to identify these mechanisms. With aging, we found reduced numbers of alveolar macrophages, cells essential for lung homeostasis. We also determined that these macrophages are critical for influenza-induced mortality with aging. Furthermore, aging vastly alters the transcriptional profile and specifically downregulates cell cycling pathways in alveolar macrophages. Aging impairs the ability of alveolar macrophages to limit lung damage during influenza infection. Moreover, aging decreases alveolar macrophage phagocytosis of apoptotic neutrophils, downregulates the scavenging receptor CD204, and induces retention of neutrophils during influenza infection. Thus, aging induces defective phagocytosis by alveolar macrophages and increases lung damage. These findings indicate that therapies that enhance the function of alveolar macrophages may improve outcomes in older people infected with respiratory viruses.

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  29. Modified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model Reviewed International journal

    Luai Huleihel, Jacobo Sellares, Nayra Cardenes, Diana Alvarez, Rosa Faner, Koji Sakamoto, Guoying Yu, Maria G. Kapetanaki, Naftali Kaminski, Mauricio Rojas

    AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY   Vol. 313 ( 1 ) page: L92 - L103   2017.7

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    Although different preclinical models have demonstrated a favorable role for bone marrow-derived mesenchymal stem cells (B-MSC) in preventing fibrosis, this protective effect is not observed with late administration of these cells, when fibrotic changes are consolidated. We sought to investigate whether the late administration of B-MSCs overexpressing microRNAs (miRNAs) let-7d (antifibrotic) or miR-154 (profibrotic) could alter lung fibrosis in a murine bleomycin model. Using lentiviral vectors, we transduced miRNAs (let-7d or miR-154) or a control sequence into human B-MSCs. Overexpression of let-7d or miR-154 was associated with changes in the mesenchymal properties of B-MSCs and in their cytokine expression. Modified B-MSCs were intravenously administered to mice at day 7 after bleomycin instillation, and the mice were euthanized at day 14. Bleomycin-injured animals that were treated with let-7d cells were found to recover quicker from the initial weight loss compared with the other treatment groups. Interestingly, animals treated with miR-154 cells had the lowest survival rate. Although a slight reduction in collagen mRNA levels was observed in lung tissue from let-7d mice, no significant differences were observed in Ashcroft score and OH-proline. However, the distinctive expression in cytokines and CD45-positive cells in the lung suggests that the differential effects observed in both miRNA mice groups were related to an effect on the immunomodulation function. Our results establish the use of miRNA-modified mesenchymal stem cells as a potential future research in lung fibrosis.

    DOI: 10.1152/ajplung.00323.2016

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  30. Progression of mean pulmonary arterial pressure in idiopathic pulmonary fibrosis with mild to moderate restriction Reviewed International journal

    Ryo Teramachi, Hiroyuki Taniguchi, Yasuhiro Kondoh, Masahiko Ando, Tomoki Kimura, Kensuke Kataoka, Atsushi Suzuki, Taiki Furukawa, Koji Sakamoto, Yoshinori Hasegawa

    RESPIROLOGY   Vol. 22 ( 5 ) page: 986 - 990   2017.7

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    Background and objectiveElevation of mean pulmonary arterial pressure (MPAP) is associated with poor prognosis in patients with idiopathic pulmonary fibrosis (IPF), yet the progression of MPAP in patients with IPF has not been sufficiently elucidated. We evaluated serial changes in MPAP and its determinants in patients with IPF with mild to moderate restriction.
    MethodsWe retrospectively reviewed patients with IPF who underwent initial evaluations including right heart catheterization (RHC) in our institute from May 2007 to December 2013 with follow-up RHC at least 1year later. Patients with forced vital capacity (FVC)&lt;50% predicted or those with pulmonary artery wedge pressure&gt;15mm Hg were excluded.
    ResultsA total of 95 patients were included. Median follow-up time of second RHC was 1.8years. MPAP increased significantly at follow-up (from 16.8 to 20.2mm Hg; P&lt;0.001), and annual change in MPAP (MPAP) was 1.8mm Hg/year. In multiple regression analysis, the lowest oxygen saturation (SpO(2) ) at 6-min walk test (6MWT) was an independent predictor of MPAP. When adjusted for age, sex, baseline MPAP and FVC % predicted, MPAP was a significant predictor of mortality (hazard ratio: 1.21; P=0.001).
    ConclusionMPAP was significantly associated with desaturation in the 6MWT, and with increased mortality in patients with IPF with mild to moderate restriction.
    We reviewed patients with idiopathic pulmonary fibrosis with mild to moderate restriction and showed that mean pulmonary arterial pressure (MPAP) was progressive. The lowest oxygen saturation (SpO(2) ) in the 6-min walk test at baseline was an independent predictor of annual change in MPAP.

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  31. COPD Assessment Test for measurement of health status in patients with idiopathic pulmonary fibrosis: A cross-sectional study. Reviewed

    Matsuda T, Taniguchi H, Ando M, Kondoh Y, Kimura T, Kataoka K, Sakamoto K, Suzuki A, Furukawa T, Hasegawa Y

    Respirology (Carlton, Vic.)   Vol. 22 ( 4 ) page: 721-727   2017.5

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    DOI: 10.1111/resp.12936

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  32. Soluble thrombomodulin in bronchoalveolar lavage fluid is an independent predictor of severe drug-induced lung injury Reviewed International journal

    Atsushi Suzuki, Hiroyuki Taniguchi, Yasuhiro Kondoh, Masahiko Ando, Naohiro Watanabe, Tomoki Kimura, Kensuke Kataoka, Toshiki Yokoyama, Koji Sakamoto, Yoshinori Hasegawa

    RESPIROLOGY   Vol. 22 ( 4 ) page: 744 - 749   2017.5

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    Background and objectiveDrug-induced lung injury (DLI) can result from a vast number of agents, and sometimes presents findings similar to those of acute respiratory distress syndrome (ARDS). Previous studies have reported that circulating levels of soluble thrombomodulin (TM) reflect endothelial injuries, which play key roles in the development of ARDS. We hypothesized that endothelial injuries are an important aspect of pathogenesis in severe DLI. The primary aim of this study was to examine the associations between soluble TM and disease severity in DLI patients.
    MethodsOf the 2580 patients who underwent a bronchoalveolar lavage (BAL) procedure at Tosei General Hospital between May 2007 and February 2015, we retrospectively analysed the data of 68 DLI patients. Soluble TM in plasma and BAL fluid (BALF), and other biomarkers were included in our analysis.
    ResultsAt the time of diagnosis, 39 patients (57%) had respiratory failure (partial pressure of oxygen/inspiratory oxygen fraction ratio, PaO2 /FiO(2) ratio&lt;300). There was a significant negative linear correlation between the PaO2 /FiO(2) ratio and soluble TM in BALF (r=-0.448, P&lt;0.001). In a stepwise multiple regression analysis, soluble TM in BALF and surfactant protein D (SP-D) were the only independent determinants of the PaO2 /FiO(2) ratio. Additionally, in a multivariate logistic regression model, soluble TM in BALF (adjusted OR (aOR): 7.48, 95% CI: 1.60-34.98) and SP-D (aOR: 5.31, 95% CI: 1.40-20.15) was an independent predictor of respiratory failure (PaO2 /FiO(2) ratio&lt;300).
    ConclusionSoluble TM in BALF is an independent predictor of severe DLI. These findings underscore the importance of pulmonary endothelial injuries in the pathogenesis of severe DLI.
    Soluble thrombomodulin in bronchoalveolar lavage is an independent predictor of severe drug-induced lung injury (DLI). Pulmonary endothelial injuries are an important aspect of pathogenesis in severe DLI.

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  33. Validation of the prognostic value of MMP-7 in idiopathic pulmonary fibrosis Reviewed International journal

    Argyris Tzouvelekis, Jose D. Herazo-Maya, Martin Slade, Jen-Hwa Chu, Giuseppe Deiuliis, Changwan Ryu, Qin Li, Koji Sakamoto, Gabriel Ibarra, Hongyi Pan, Mridu Gulati, Danielle Antin-Ozerkis, Erica L. Herzog, Naftali Kaminski

    RESPIROLOGY   Vol. 22 ( 3 ) page: 486 - 493   2017.4

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    Background and objective: Idiopathic pulmonary fibrosis (IPF) is a progressive disease with poor prognosis and variable clinical course. Although matrix metalloproteinase-7 (MMP-7) is emerging as an important IPF biomarker, reproducibility across studies is unclear. We aimed to determine whether a previously reported prognostic threshold for MMP-7 was predictive of mortality in an independent cohort of IPF patients.
    Methods: MMP-7 concentrations obtained from heparinized plasma samples were determined by ELISA in 97 patients with IPF and 41 healthy controls. The association of the previously published heparin plasma MMP-7 threshold of 12.1 ng/mL with all-cause mortality or transplant-free survival (TFS) was determined, either as an independent biomarker or as part of the modified personal clinical and molecular mortality index (m-PCMI).
    Results: MMP-7 plasma concentrations were significantly higher in IPF patients compared to healthy controls (14.40 +/- 6.55 ng/mL vs 6.03 +/- 2.51 ng/mL, P &lt; 0.001). The plasma MMP-7 threshold of 12.1 ng/mL was significantly associated with both all-cause mortality and TFS (unadjusted Cox proportional hazard ratio (HR) = 25.85 and 15.49, 95% CI: 10.91-61.23 and 5.41-44.34, respectively, P &lt; 0.001). MMP-7 concentrations, split by 12.1 ng/mL, were significantly (P &lt; 0.05) predictive of mortality and TFS after adjusting for age, gender, smoking and baseline pulmonary function parameters, in a multivariate Cox proportional hazards model. MMP-7 concentrations were negatively correlated with diffusing lung capacity of carbon monoxide (DLCO) (r = -0.21, P = 0.02), and positively with a mortality risk scoring system (GAP) that combines age, gender, forced vital capacity (FVC) and DLCO (r = 0.32, P = 0.001).
    Conclusion: This study confirms that MMP-7 concentrations could be used to accurately predict outcomes across cohorts and centres, when similar collection protocols are applied.

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  34. SH2 Domain-Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis Reviewed International coauthorship International journal

    Argyrios Tzouvelekis, Guoying Yu, Christian L. Lino Cardenas, Jose D. Herazo-Maya, Rong Wang, Tony Woolard, Yi Zhang, Koji Sakamotol, Hojin Lee, Jae-Sung Yi, Giuseppe Deluliis, Nikolaos Xylourgidis, Farida Ahangari, Patty J. Lee, Vassilis Aidinis, Erica L. Herzog, Robert Homer, Anton M. Bennett, Naftali Kaminski

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   Vol. 195 ( 4 ) page: 500 - 514   2017.2

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    Rationale: Idiopathic pulmonary fibrosis (IPF) is a chronic fatal lung disease with dismal prognosis and no cure. The potential role of the ubiquitously expressed SH2 domain-containing tyrosine phosphatase-2 (SHP2) as a therapeutic target has not been studied in IPF.
    Objectives: To determine the expression, mechanistic role, and potential therapeutic usefulness of SHP2 in pulmonary fibrosis.
    Methods: The effects of SHP2 overexpression and inhibition on fibroblast response to profibrotic stimuli were analyzed in vitro in primary human and mouse lung fibroblasts. In vivo therapeutic effects were assessed in the bleomycin model of lung fibrosis by SHP2-lentiviral administration and transgenic mice carrying a constitutively active SHP2 mutation.
    Measurements and Main Results: SHP2 was down-regulated in lungs and lung fibroblasts obtained from patients with IPF. Immunolocalization studies revealed that SHP2 was absent within fibroblastic foci. Loss of SHP2 expression or activity was sufficient to induce fibroblast-to-myofibroblast differentiation in primary human lung fibroblasts. Overexpression of constitutively active SHP2 reduced the responsiveness offibroblasts to profibrotic stimuli, including significant reductions in cell survival and myofibroblast differentiation. SHP2 effects were mediated through deactivation of fibrosis-relevant tyrosine kinase and serine/threonine kinase signaling pathways. Mice carrying the Noonan syndrome-associated gain-of-function SHP2 mutation (SHP2(D61G/+)) were resistant to bleomycin-induced pulmonary fibrosis. Restoration of SHP2 levels in vivo through lentiviral delivery blunted bleomycin-induced pulmonary fibrosis.
    Conclusions: Our data suggest that SHP2 is an important regulator of fibroblast differentiation, and its loss as observed in IPF facilitates profibrotic phenotypic changes. Augmentation of SHP2 activity or expression should be investigated as a novel therapeutic strategy for IPF.

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  35. Hemosiderin-laden macrophages are an independent factor correlated with pulmonary vascular resistance in idiopathic pulmonary fibrosis: a case control study Reviewed International journal

    Jun Fukihara, Hiroyuki Taniguchi, Masahiko Ando, Yasuhiro Kondoh, Tomoki Kimura, Kensuke Kataoka, Taiki Furukawa, Takeshi Johkoh, Junya Fukuoka, Koji Sakamoto, Yoshinori Hasegawa

    BMC PULMONARY MEDICINE   Vol. 17 ( 1 ) page: 30   2017.2

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    Background: Increases in hemosiderin-laden macrophages (HLM) are reported to be observed in idiopathic pulmonary fibrosis (IPF). According to a recent study, significant correlation between hemosiderin deposition in the lung tissue of IPF and pulmonary hypertension evaluated by echocardiography has been suspected. In this study, we aimed to evaluate whether HLM in bronchoalveolar lavage fluid (BALF) is a factor correlated with pulmonary hemodynamic parameters evaluated by right heart catheterization in patients with IPF.
    Methods: Initial data from 103 consecutive patients with IPF who underwent surgical lung biopsy between November 2007 and March 2014 were retrospectively analyzed. The "HLM score" of BALF was established by dividing the number of Perls' Prussian blue stain positive macrophages by the total number of macrophages counted.
    Results: BALF showed an elevated HLM score (38.2%). Right heart catheterization revealed mean pulmonary arterial pressure (mPAP) of 16.3 mmHg and pulmonary vascular resistance (PVR) of 1.55 Wood units. HLM score was positively correlated with mPAP (rho = 0.204; rho = 0.038) and PVR (rho = 0.349, rho &lt; 0.001). In multivariate analysis, 6-min walk distance (standardized partial regression coefficient [beta], -0.391; p &lt; 0.001), minimum oxygen saturation during 6-min walk distance (beta, -0.294; rho = 0.001) and HLM score (beta, 0.265; rho = 0.002) were independently correlated with PVR.
    Conclusions: HLM score in BALF is an independent factor correlated with PVR in patients with IPF.

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  36. The St. George's Respiratory Questionnaire as a prognostic factor in IPF Reviewed International journal

    Taiki Furukawa, Hiroyuki Taniguchi, Masahiko Ando, Yasuhiro Kondoh, Kensuke Kataoka, Osamu Nishiyama, Takeshi Johkoh, Junya Fukuoka, Koji Sakamoto, Yoshinori Hasegawa

    RESPIRATORY RESEARCH   Vol. 18 ( 1 ) page: 18   2017.1

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    Background: It is unclear whether health related quality of life (HRQL) may have a predictive value for mortality in idiopathic pulmonary fibrosis (IPF). We investigated the relationship between HRQL assessed using the St. George's Respiratory Questionnaire (SGRQ) and survival time in patients with IPF, and tried to determine a clinical meaningful cut off value to predict poorer survival rates.
    Methods: We retrospectively analyzed consecutive patients with IPF who underwent an initial evaluation from May 2007 to December 2012. The diagnosis of IPF was made according to the 2011 international consensus guidelines. We used Cox proportional hazard models to identify independent predictors for mortality rate in patients with IPF.
    Results: We examined 182 eligible cases, average age was 66 years old, and 86% were male. Mean levels of percent predicted FVC, DLco, six-minute-walk test distance, and the SGRQ total score were around 80%, 58%, 580 m, and 34 points. On multivariate analysis, the SGRQ total score (hazard ratio [HR], 1.012; 95% confidence interval [CI] 1.001-1.023; P = .029) and percent predicted FVC (HR, 0.957; 95% CI 0.944-0.971, P &lt; .001) were independent predictors for mortality rate. Moreover, a score higher than 30 points in the SGRQ total score showed higher mortality rate (HR, 2.047; 95% CI, 1.329-3.153; P = .001).
    Conclusions: The SGRQ total score was one of independent prognostic factors in patients with IPF. Total scores higher than 30 points were associated with higher mortality rates.

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  37. Exercise hypoxaemia as a predictor of pulmonary hypertension in COPD patients without severe resting hypoxaemia. Reviewed

    Nakahara Y, Taniguchi H, Kimura T, Kondoh Y, Arizono S, Nishimura K, Sakamoto K, Ito S, Ando M, Hasegawa Y

    Respirology (Carlton, Vic.)   Vol. 22 ( 1 ) page: 120-125   2017.1

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    DOI: 10.1111/resp.12863

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  38. Exogenous induction of unphosphorylated PTEN reduces TGFβ-induced extracellular matrix expressions in lung fibroblasts. Reviewed

      Vol. 25 ( 1 ) page: 86-97   2017.1

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    DOI: 10.1111/wrr.12506

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  39. Depression Is Significantly Associated with the Health Status in Patients with Idiopathic Pulmonary Fibrosis. Reviewed

    Matsuda T, Taniguchi H, Ando M, Kondoh Y, Kimura T, Kataoka K, Nishimura K, Nishiyama O, Sakamoto K, Hasegawa Y

    Internal medicine (Tokyo, Japan)   Vol. 56 ( 13 ) page: 1637-1644   2017

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    DOI: 10.2169/internalmedicine.56.7019

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  40. Impact of mild to moderate COPD on feasibility and prognosis in non-small cell lung cancer patients who received chemotherapy

    Omote Norihito, Hashimoto Naozumi, Morise Masahiro, Sakamoto Koji, Miyazaki Shinichi, Ando Akira, Nakahara Yoshio, Hasegawa Yoshinori

    INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE   Vol. 12   page: 3541 - 3547   2017

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    DOI: 10.2147/COPD.S149456

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  41. PULMONARY REHABILITATION IN PATIENTS WITH IDIOPATHIC PULMONARY FIBROSIS: COMPARISON WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE

    Arizono Shinichi, Taniguchi Hiroyuki, Sakamoto Koji, Kondoh Yasuhiro, Kimura Tomoki, Kataoka Kensuke, Ogawa Tomoya, Watanabe Fumiko, Tabira Kazuyuki, Kozu Ryo

    SARCOIDOSIS VASCULITIS AND DIFFUSE LUNG DISEASES   Vol. 34 ( 4 ) page: 283-289   2017

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  42. Pulmonary rehabilitation in patients with idiopathic pulmonary fibrosis: comparison with chronic obstructive pulmonary disease. Reviewed International journal

    Arizono S, Taniguchi H, Sakamoto K, Kondoh Y, Kimura T, Kataoka K, Ogawa T, Watanabe F, Tabira K, Kozu R

    Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG   Vol. 34 ( 4 ) page: 283 - 289   2017

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    DOI: 10.36141/svdld.v34i4.5549

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  43. Pulmonary rehabilitation in patients with idiopathic pulmonary fibrosis: Comparison with chronic obstructive pulmonary disease

    Arizono S., Taniguchi H., Sakamoto K., Kondoh Y., Kimura T., Kataoka K., Ogawa T., Watanabe F., Tabira K., Kozu R.

    Sarcoidosis Vasculitis and Diffuse Lung Diseases   Vol. 34 ( 4 ) page: 283 - 289   2017

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    Background: While the efficacy of pulmonary rehabilitation (PR) in chronic obstructive pulmonary disease (COPD) has been well established, emerging evidence also suggests its benefit in idiopathic pulmonary fibrosis (IPF). However, the differences and similarities between how PR affects diseases with different physiologies remain unknown. Objective: This study aimed to compare the efficacy of PR in COPD and IPF patients by performing multifactorial evaluation with various exercise capacity measurements, and dyspnea and health-related quality of life (QoL) assessment. Methods: Twenty-two IPF patients (%vital capacity: 72%) and 27 COPD patients (%forced expiratory volume1: 43%) were recruited. Subjects who completed a 10-week outpatient PR program were analyzed. We assessed five exercise capacity indicators (6-minute walking distance, incremental shuttle walking distance, endurance time, peak work rate, and peak values for oxygen uptake [peak VO2]), dyspnea (Baseline Dyspnea Index: BDI), and health-related QoL (St. George's Respiratory Questionnaire: SGRQ) at baseline and immediately following completion of the PR program. Results: After 10 weeks of PR, all exercise capacity measurements, except VO2, as well as BDI and SGRQ score improved significantly (p<0.05) in both disease groups. The magnitude of the observed changes in each outcome, assessed by the effect size, was comparable between IPF and COPD patients. This was also true for endurance time, the measurement most responsive to PR, with a large effect size. Conclusions: PR can result in comparable improvements in exercise capacity, including endurance time, and dyspnea and HRQoL in both IPF and COPD patients after 10 weeks of exercise training.

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  44. Impact of Thin-Section Computed Tomography-Determined Combined Pulmonary Fibrosis and Emphysema on Outcomes Among Patients With Resected Lung Cancer. Reviewed

    Hashimoto N, Iwano S, Kawaguchi K, Fukui T, Fukumoto K, Nakamura S, Mori S, Sakamoto K, Wakai K, Yokoi K, Hasegawa Y

    The Annals of thoracic surgery   Vol. 102 ( 2 ) page: 440-7   2016.8

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  45. Mean pulmonary arterial pressure as a prognostic indicator in connective tissue disease associated with interstitial lung disease: a retrospective cohort study. Reviewed

    Takahashi K, Taniguchi H, Ando M, Sakamoto K, Kondoh Y, Watanabe N, Kimura T, Kataoka K, Suzuki A, Ito S, Hasegawa Y

    BMC pulmonary medicine   Vol. 16 ( 1 ) page: 55   2016.4

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    DOI: 10.1186/s12890-016-0207-3

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  46. Hypoxia-induced modulation of PTEN activity and EMT phenotypes in lung cancers. Reviewed

    Kohnoh T, Hashimoto N, Ando A, Sakamoto K, Miyazaki S, Aoyama D, Kusunose M, Kimura M, Omote N, Imaizumi K, Kawabe T, Hasegawa Y

    Cancer cell international   Vol. 16   page: 33   2016

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    DOI: 10.1186/s12935-016-0308-3

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  47. Biomarkers in the Evaluation and Management of Idiopathic Pulmonary Fibrosis. Reviewed

    Tzouvelekis A, Herazo-Maya J, Sakamoto K, Bouros D

    Current topics in medicinal chemistry   Vol. 16 ( 14 ) page: 1587-98   2016

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  48. Lung-Dominant Connective Tissue Disease: Clinical, Radiologic, and Histologic Features. Reviewed

    Omote N, Taniguchi H, Kondoh Y, Watanabe N, Sakamoto K, Kimura T, Kataoka K, Johkoh T, Fujimoto K, Fukuoka J, Otani K, Nishiyama O, Hasegawa Y

    Chest   Vol. 148 ( 6 ) page: 1438-1446   2015.12

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    DOI: 10.1378/chest.14-3174

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  49. Direct regulation of transforming growth factor β-induced epithelial-mesenchymal transition by the protein phosphatase activity of unphosphorylated PTEN in lung cancer cells. Reviewed

      Vol. 106 ( 12 ) page: 1693-704   2015.12

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    DOI: 10.1111/cas.12831

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  50. Recombinant Human Thrombomodulin in Acute Exacerbation of Idiopathic Pulmonary Fibrosis. Reviewed

    Kataoka K, Taniguchi H, Kondoh Y, Nishiyama O, Kimura T, Matsuda T, Yokoyama T, Sakamoto K, Ando M

    Chest   Vol. 148 ( 2 ) page: 436-443   2015.8

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    DOI: 10.1378/chest.14-2746

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  51. Risk stratification by the lower limit of normal of FEV1/FVC for postoperative outcomes in patients with COPD undergoing thoracic surgery. Reviewed

    Osuka S, Hashimoto N, Sakamoto K, Wakai K, Yokoi K, Hasegawa Y

    Respiratory investigation   Vol. 53 ( 3 ) page: 117-23   2015.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.resinv.2015.01.005

    PubMed

  52. Broader criteria of undifferentiated connective tissue disease in idiopathic interstitial pneumonias. Reviewed

    Kondoh Y, Johkoh T, Fukuoka J, Arakawa H, Tanaka T, Watanabe N, Sakamoto K, Kataoka K, Kimura T, Taniguchi H

    Respiratory medicine   Vol. 109 ( 3 ) page: 389-96   2015.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.rmed.2015.01.009

    PubMed

  53. Endurance time is the most responsive exercise measurement in idiopathic pulmonary fibrosis. Reviewed

    Arizono S, Taniguchi H, Sakamoto K, Kondoh Y, Kimura T, Kataoka K, Ogawa T, Watanabe F, Nishiyama O, Nishimura K, Kozu R, Tabira K

    Respiratory care   Vol. 59 ( 7 ) page: 1108-15   2014.7

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.4187/respcare.02674

    PubMed

  54. Let-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts. Reviewed

    Huleihel L, Ben-Yehudah A, Milosevic J, Yu G, Pandit K, Sakamoto K, Yousef H, LeJeune M, Coon TA, Redinger CJ, Chensny L, Manor E, Schatten G, Kaminski N

    American journal of physiology. Lung cellular and molecular physiology   Vol. 306 ( 6 ) page: L534-42   2014.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1152/ajplung.00149.2013

    PubMed

  55. Crizotinib-induced acute interstitial lung disease in a patient with EML4-ALK positive non-small cell lung cancer and chronic interstitial pneumonia. Reviewed

    Watanabe N, Nakahara Y, Taniguchi H, Kimura T, Kondoh Y, Kataoka K, Sakamoto K

    Acta oncologica (Stockholm, Sweden)   Vol. 53 ( 1 ) page: 158-60   2014.1

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.3109/0284186X.2013.802838

    PubMed

  56. Efficacy of combined therapy with cyclosporin and low-dose prednisolone in interstitial pneumonia associated with connective tissue disease. Reviewed

    Watanabe N, Sakamoto K, Taniguchi H, Kondoh Y, Kimura T, Kataoka K, Ono K, Fukuoka J, Nishiyama O, Hasegawa Y

    Respiration; international review of thoracic diseases   Vol. 87 ( 6 ) page: 469-77   2014

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1159/000358098

    PubMed

  57. Significance of pulmonary arterial pressure as a prognostic indicator in lung-dominant connective tissue disease. Reviewed

    Suzuki A, Taniguchi H, Watanabe N, Kondoh Y, Kimura T, Kataoka K, Matsuda T, Yokoyama T, Sakamoto K, Nishiyama O, Hasegawa Y

    PloS one   Vol. 9 ( 9 ) page: e108339   2014

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1371/journal.pone.0108339

    PubMed

  58. Endobronchial ultrasound transbronchial needle aspiration in older people. Reviewed

    Okachi S, Imai N, Imaizumi K, Hase T, Shindo Y, Sakamoto K, Aso H, Wakahara K, Hashimoto I, Ito S, Hashimoto N, Sato M, Kondo M, Hasegawa Y

    Geriatrics & gerontology international   Vol. 13 ( 4 ) page: 986-92   2013.10

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/ggi.12043

    PubMed

  59. Quadriceps weakness contributes to exercise capacity in nonspecific interstitial pneumonia. Reviewed

    Watanabe F, Taniguchi H, Sakamoto K, Kondoh Y, Kimura T, Kataoka K, Ogawa T, Arizono S, Nishiyama O, Hasegawa Y

    Respiratory medicine   Vol. 107 ( 4 ) page: 622-8   2013.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.rmed.2012.12.013

    PubMed

  60. Pulmonary hypertension as a prognostic indicator at the initial evaluation in idiopathic pulmonary fibrosis. Reviewed

    Kimura M, Taniguchi H, Kondoh Y, Kimura T, Kataoka K, Nishiyama O, Aso H, Sakamoto K, Hasegawa Y

    Respiration; international review of thoracic diseases   Vol. 85 ( 6 ) page: 456-63   2013

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1159/000345221

    PubMed

  61. Involvement of TGFβ-induced phosphorylation of the PTEN C-terminus on TGFβ-induced acquisition of malignant phenotypes in lung cancer cells. Reviewed

      Vol. 8 ( 11 ) page: e81133   2013

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1371/journal.pone.0081133

    PubMed

  62. Predictors of the need to initiate noninvasive ventilation in stable outpatients with acute exacerbation of chronic obstructive pulmonary disease. Reviewed

    Taga S, Taniguchi H, Watanabe N, Kondoh Y, Kimura T, Kataoka K, Aso H, Sakamoto K, Hasegawa Y

    Internal medicine (Tokyo, Japan)   Vol. 52 ( 16 ) page: 1781-6   2013

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    PubMed

  63. Differential modulation of surfactant protein D under acute and persistent hypoxia in acute lung injury. Reviewed

    Sakamoto K, Hashimoto N, Kondoh Y, Imaizumi K, Aoyama D, Kohnoh T, Kusunose M, Kimura M, Kawabe T, Taniguchi H, Hasegawa Y

    Am J Physiol Lung Cell Mol Physiol.   Vol. 303 ( 1 ) page: L43-53   2012.7

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  64. Acute exacerbation of IPF following diagnostic bronchoalveolar lavage procedures.

    Sakamoto K, Taniguchi H, Kondoh Y, Wakai K, Kimura T, Kataoka K, Hashimoto N, Nishiyama O, Hasegawa Y.

    Respir Med   Vol. 106 ( 3 ) page: 436-42   2012

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  65. Involvement of the transcription factor twist in phenotype alteration through epithelial-mesenchymal transition in lung cancer cells.

    Nakashima H, Hashimoto N, Aoyama D, Kohnoh T, Sakamoto K, Kusunose M, Imaizumi K, Takeyama Y, Sato M, Kawabe T, Hasegawa Y.

    Mol Carcinog   Vol. 51   page: 400-410   2012

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  66. Risk factors of acute exacerbation of idiopathic pulmonary fibrosis. Reviewed

    Kondoh Y, Taniguchi H, Katsuta T, Kataoka K, Kimura T, Nishiyama O, Sakamoto K, Johkoh T, Nishimura M, Ono K, Kitaichi M.

    Sarcoidosis Vasc Diffuse Lung Dis   Vol. 27   page: 103-110   2010

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  67. Serum KL-6 in fibrotic NSIP: Correlations with physiologic and radiologic parameters.

    Sakamoto K, Taniguchi H, Kondoh Y, Johkoh T, Sumikawa H, Kimura T, Nishiyama O, Kato K, Kataoka K, Ono K, Kitaichi M, Hasegawa Y.

    Respir Med   Vol. 104   page: 127-133   2009

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  68. Acute exacerbation of idiopathic pulmonary fibrosis as the initial presentation of the disease.

    Sakamoto K, Taniguchi H, Kondoh Y, Ono K, Hasegawa Y, Kitaichi M.

    Eur Respir Rev   Vol. 18   page: 129-132.   2009

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  69. 原発性肺クリプトコッカス症の臨床的検討 Reviewed

    阪本 考司, 麻生 裕紀, 横山 俊樹, 加藤 景介, 西山 理, 木村 智樹, 近藤 康博, 谷口 博之

    感染症学雑誌   Vol. 4   page: 403-407   2007.7

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  70. びまん性肺疾患に対する外科的肺生検の検討 合併症、診断効率と早期死亡について

    阪本 考司, 横山 俊樹, 麻生 裕紀, 岩木 舞, 野間 聖, 加藤 景介, 西山 理, 木村 智樹, 近藤 康博, 谷口 博之

    日本呼吸器学会雑誌   Vol. 44 ( 10 ) page: 675-680   2006.10

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  71. 化学療法を施行したIV期非小細胞肺癌におけるQuality of Life

    西山 理, 谷口 博之, 近藤 康博, 木村 智樹, 加藤 景介, 野間 聖, 岩木 舞, 麻生 裕紀, 阪本 考司, 清水 淳市

    日本呼吸器学会雑誌   Vol. 44 ( 5 ) page: 368-373   2006.5

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MISC 5

  1. Risk Factor Evaluation of Programmed Death 1 Inhibitor Related Pneumonitis in Patients with Non-Small Cell Lung Cancer

    Fukihara J., Sakamoto K., Iwano S., Morise M., Hashimoto N., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   Vol. 197   2018

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  2. Risk Stratification For Airflow Obstruction-Related Outcomes Based On A Renewed Japanese Spirometric Reference By Using The Lambda-Mu-Sigma Method

    Hashimoto N., Okada Y., Sakamoto K., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   Vol. 195   2017

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  3. Unphosphorylated Pten Inhibits Tgf beta-Induced Aberrant Cell Motility In Epithelial Cells Via Differential Phosphatase Activities

    Hashimoto N., Sakamoto K., Miyazaki S., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   Vol. 195   2017

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  4. The Impact Of CT-Detected Usual Interstitial Pneumonia Pattern As The Decision-Making Factor For Treatment Of Lung Cancer

    Ando A., Hashimoto N., Sakamoto K., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   Vol. 195   2017

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  5. Single Cell Rna-Sequencing Reveals Distinct Effects Of Inhibition Of Fendrr, A Long Non-Coding Rna Implicated In Fibroblast To Myofibroblast Differentiation

    Adams T., Sakamoto K., Ahangari F., Munivar A., Kaminski N.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   Vol. 195   2017

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Presentations 30

  1. Assessment of Circulating Mitochondrial DNA as a Liquid Biomarker in Acute Exacerbation of Idiopathic Pulmonary Fibrosis International conference

    Sakamoto K., Furukawa T., Yamano Y., Teramachi R., Kataoka K., Hashimoto N., Kondoh Y., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 

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    Event date: 2019

    Language:English   Presentation type:Poster presentation  

  2. Possible UIP Pattern with Traction Bronchiectasis on HRCT: Prognostic Impact in IIP International conference

    Fukihara J., Kondoh Y., Kimura T., Kataoka K., Matsuda T., Yokoyama T., Furukawa T., Johkoh T., Fukuoka J., Sakamoto K., Hashimoto N., Hasegawa Y., Brown K. K.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 

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    Event date: 2018

    Language:English   Presentation type:Poster presentation  

  3. Lung Epithelium Overexpressed Noncoding Rna (leon): A Potential Regulator Of Epithelial Gene Expression In Idiopathic Pulmonary Fibrosis International conference

    Guardela B. Juan, Herazo-Maya J. D., Sakamoto K., Li Q., Deluliis G., Yan X., Prasse A., Kaminski N.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 

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    Event date: 2017

    Language:English   Presentation type:Poster presentation  

  4. Performance Of The Saint George's Respiratory Questionnaire (sgrq) In Patients With Connective Tissue Disease-Associated Interstitial Lung Disease (ctd-Ild) International conference

    Suzuki A., Taniguchi H., Kondoh Y., Swigris J. J., Yamano Y., Furukawa T., Numata-Nakamura M., Sakamoto K., Ando M., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 

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    Event date: 2017

    Language:English   Presentation type:Poster presentation  

  5. Transduction of PTEN with mutated its C-terminal phosphorylation sites inhibits TGFb- induced phe notype alterations through epithelial-mesenchymal transition International conference

    K. Sakamoto, N. Hashimoto, D. Aoyama, M. Kusunose, M. Kimura, T. Kohnoh, K. Imaizumi, Y. Hasegawa.

    American Thoracic Society 2012 International Conference 

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    Event date: 2012

    Language:English   Presentation type:Poster presentation  

    Country:United States  

  6. Acute Exacerbation of IPF Following Bronchoalveolar Lavage Procedures International conference

    K. Sakamoto, H. Taniguchi, Y. Kondoh, K. Wakai, T. Kimura, K. Kataoka, N. Hashimoto, O. Nishiyama, Y. Hasegawa.

    Chest 2011 Annual Congress 

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    Event date: 2011

    Language:English   Presentation type:Oral presentation (general)  

    Country:United States  

  7. Modulated Expression Of Surfactant Protein D In Acute Lung Injury Might Be Associated With Epithelial-Mesenchymal Transition In Epithelial Cells International conference

    K. Sakamoto, N. Hashimoto, K. Imaizumi, H. Taniguchi, Y. Kondoh, T. Kohnoh, D. Aoyama, T. Ogawa, Y. Hasegawa.

    American Thoracic Society 2011 International Conference 

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    Event date: 2011

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  8. Modulated expression of surfactant protein D in acute lung injury might be associated with epithelial-mesenchymal transition in epithelial cells. International conference

    K. Sakamoto, N. Hashimoto, Y. Hasegawa.

    FASEB Summer Research Conferences 2010 

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    Event date: 2010

    Language:English   Presentation type:Poster presentation  

    Country:United States  

  9. EMT-Related Gene, Twist, for Phenotype Change in Lung Cancer Cells International conference

    K. Sakamoto, N. Hashimoto, K. Imaizumi, H. Nakashima, T. Kohnoh, D. Aoyama, T. Ogawa, Y. Hasegawa.

    American Thoracic Society 2010 International Conference 

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    Event date: 2010

    Language:English   Presentation type:Poster presentation  

    Country:United States  

  10. Assessment of Circulating Mitochondrial DNA as a Liquid Biomarker in Acute Exacerbation of Idiopathic Pulmonary Fibrosis

    Sakamoto K, Furukawa T, Yamano Y, Teramachi R, Kataoka K, Hashimoto N, Kondoh Y, Hasegawa Y

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2019 

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  11. TINCR, a Long Intergenic Noncoding RNA Decreased in IPF, Is a Novel Regulator of Airway Epithelial Cell Differentiation International coauthorship International conference

    Omote N., Sakamoto K., Li Q., Schupp J. C., Adams T., Ahangari F., Chioccioli M., Xylourgidis N., DeIuliis G., Hashimoto N., Hasegawa Y., Kaminski N.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2019 

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  12. The Role of Meflin Expression in Fibroblasts During Development of Pulmonary Fibrosis International conference

    Hashimoto N., Nakahara Y., Sakamoto K., Enomoto A., Yokoi T., Suzuki A., Inoue M., Wakahara K., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2020 

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  13. The new-defined mesenchymal stromal/stem cell marker has a protective role in the development of acute lung injury International conference

    Nakahara Yoshio, Hashimoto Naozumi, Sakamoto Koji, Ando Akira, Inoue Masahide, Suzuki Atsushi, Enomoto Atsushi, Hasegawa Yoshinori

    EUROPEAN RESPIRATORY JOURNAL  2019.9.28 

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  14. The hypoxia-inducible factor 1a protein stabilizers inhibit transforming growth factor beta-induced extracellular matrix proteins in epithelial cells and fibroblasts International conference

    Ando Akira, Hashimoto Naozumi, Sakamoto Koji, Hasegawa Yoshinori

    EUROPEAN RESPIRATORY JOURNAL  2018.9.15 

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  15. Single-Cell RNAseq of Aging Mouse Lungs Reveals Global and Cell-Specific Inflammatory Aberrations International coauthorship International conference

    Cosme C. Jr., McDonough J. E., Adams T., Schupp J. C., Omote N., Ahangari F., Deluliis G., Sakamoto K., Kaminski N.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2020 

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  16. Silica Nanoparticle Induced Lung Injury in Mice: Dissecting Relative Contribution of Its Size and Surface Modification International coauthorship International conference

    Inoue M., Sakamoto K., Suzuki A., Nakahara Y., Hashimoto N., Hasegawa Y., Sawada M.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2020 

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  17. Serum CRP Decrease Has Predictive Value for LongTerm Disease Control by PD-1/ PD-L1 Inhibitors in Patients with NSCLC International conference

    Matsuzawa R., Morise M., Tanaka I., Koyama J., Kimura T., Kondoh Y., Hase T., Sakamoto K., Hashimoto N., Hasegawa Y.

    JOURNAL OF THORACIC ONCOLOGY  2019.10 

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  18. Recurrent Acute Exacerbations of Fibrotic Interstitial Lung Diseases International conference

    Suzuki A., Kondoh Y., Brown K. K., Kimura T., Kataoka K., Matsuda T., Yokoyama T., Ando M., Hashimoto N., Sakamoto K., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2019 

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  19. Possible UIP Pattern with Traction Bronchiectasis on HRCT: Prognostic Impact in IIP International coauthorship International conference

    Fukihara J, Kondoh Y, Kimura T, Kataoka K, Matsuda T, Yokoyama T, Furukawa T, Johkoh T, Fukuoka J, Sakamoto K, Hashimoto N, Hasegawa Y, Brown K. K

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2018 

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  20. Pirfenidone Delays the Prescription of Concomitant Drugs in Patients with Idiopathic Pulmonary Fibrosis: Post-Hoc Analysis of Japanese Phase III Clinical Trial International conference

    Suzuki A., Sakaguchi H., Ebina M., Azuma A., Ogura T., Taguchi Y., Suga M., Takahashi H., Sugiyama Y., Kudoh S., Nukiwa T., Miyazawa S., Sakamoto K., Kondoh Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2020 

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  21. Performance Of The Saint George's Respiratory Questionnaire (sgrq) In Patients With Connective Tissue Disease-Associated Interstitial Lung Disease (ctd-Ild) International conference

    Suzuki A, Taniguchi H, Kondoh Y, Swigris J. J, Yamano Y, Furukawa T, Numata-Nakamura M, Sakamoto K, Ando M, Hasegawa Y

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2017 

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    Language:English   Presentation type:Poster presentation  

  22. Lung Epithelium Overexpressed Noncoding Rna (leon): A Potential Regulator Of Epithelial Gene Expression In Idiopathic Pulmonary Fibrosis International conference

    Guardela B. Juan, Herazo-Maya J. D, Sakamoto K, Li Q, Deluliis G, Yan X, Prasse A, Kaminski N

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2017 

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    Language:English   Presentation type:Poster presentation  

  23. Loss of lncRNA FENDRR Induces Senescence in Adult Mouse Lungs International coauthorship International conference

    Xylourgidis N., Sakamoto K., Schupp J. C., Adams T., DeIuliis G., Omote N., Hashimoto N., Hasegawa Y., Kaminski N.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2019 

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    Language:English   Presentation type:Poster presentation  

  24. Long Non-Coding RNA TINCR Is a Novel Regulator of Human Bronchial Epithelial Cell Differentiation International coauthorship International conference

    Omote N., Sakamoto K., Li Q., Schupp J. C., Adams T., Ahangari F., Chioccioli M., Hashimoto N., Hasegawa Y., Kaminski N.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2020 

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  25. Increased Circulating Mitochondrial DNA Content Predicts Fatal Complication and Worse Prognosis in Idiopathic Pulmonary Fibrosis International conference

    Sakamoto K., Furukawa T., Yamano Y., Teramachi R., Suzuki A., Nakahara Y., Inoue M., Kataoka K., Hashimoto N., Kondoh Y., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2020 

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  26. Exogenous Induction Of Unphosphorylated Tumor Suppressor Phosphatase And Tensin Homolog Deleted On Chromosome 10 Modulates Transforming Growth Factor beta-Induced Extracellular Matrix Expression In Lung Fibroblasts International conference

    Omote N., Hashimoto N., Kimura M., Miyazaki S., Ando A., Sakamoto K., Hasegawa Y.

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE  2017 

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  27. Exogenous induction of unphosphorylated PTEN reduces TGF beta-induced extracellular matrix expressions in lung fibroblasts International conference

    Motohiro Kimura, Naozumi Hashimoto, Masaaki Kusunose, Daisuke Aoyama, Koji Sakamoto, Shinichi Miyazaki, Akira Ando, Norihiro Omote, Kazuyoshi Imaizumi, Tsutomu Kawabe, Yoshinori Hasegawa

    WOUND REPAIR AND REGENERATION  2017  WILEY

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    Transforming growth factor beta (TGF beta) plays an important role in regulating aberrant extracellular matrix (ECM) production from alveolar/epithelial cells (AECs) and fibroblasts in pulmonary fibrosis. Although the tumor suppressor gene phosphatase and tensin homologue deleted from chromosome 10 (PTEN) can negatively control many TGF beta-activated signaling pathways via the phosphatase activity, hyperactivation of the TGF beta-related signaling pathways is often observed in fibrosis. Loss of PTEN expression might cause TGF beta-induced ECM production. In addition, TGF beta was recently shown to induce loss of PTEN enzymatic activity by phosphorylating the PTEN C-terminus. Therefore, we hypothesized that exogenous transfer of unphosphorylated PTEN (PTEN4A) might lead to reduce TGF beta-induced ECM expression in not only epithelial cells but also fibroblasts. Adenovirus-based exogenous PTEN4A induction successfully reduced TGF beta-induced fibronectin expression and retained beta-catenin at the cell membrane in human epithelial cells. Exogenous unphosphorylated PTEN also attenuated TGF beta-induced ECM production and inhibited TGF beta-induced b-catenin translocation in a human fibroblast cell line and in mouse primary isolated lung fibroblasts. Conversely, TGF beta-induced a-smooth muscle actin expression did not seem to be inhibited in these fibroblasts. Our data suggest that exogenous administration of unphosphorylated PTEN might be a promising strategy to restore TGF beta-induced loss of PTEN activity and reduce aberrant TGF beta-induced ECM production from epithelial cells and fibroblasts in lung fibrosis as compared with wild-type PTEN induction.

    Scopus

    PubMed

  28. The new-defined mesenchymal stromal/stem cell marker has a protective role in the development of acute lung injury International conference

    Nakahara Yoshio, Hashimoto Naozumi, Sakamoto Koji, Ando Akira, Inoue Masahide, Suzuki Atsushi, Enomoto Atsushi, Hasegawa Yoshinori

    EUROPEAN RESPIRATORY JOURNAL  2019.9.28 

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  29. Late Breaking Abstract - Long-term Effect of Pulmonary Rehabilitation under Nintedanib treatment in Idiopathic Pulmonary Fibrosis (FITNESS study) International conference

    Ogura Takashi, Mori Yoshihiro, Kataoka Kensuke, Nishiyama Osamu, Ando Masahiko, Arizono Shinichi, Ogawa Tomoya, Shiraki Akira, Ichikado Kazuya, Ishimoto Hiroshi, Ito Hiroyuki, Sakamoto Koji, Tomii Keisuke, Tomioka Hiromi, Tsuda Toru, Kozu Ryo, Kondoh Yasuhiro

    EUROPEAN RESPIRATORY JOURNAL  2021.9.5 

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    Presentation type:Oral presentation (general)  

    DOI: 10.1183/13993003.congress-2021.RCT2905

  30. Immune checkpoint inhibitor for advanced or recurrent non-small cell lung cancer patients with poor performance status International conference

    Koyama Junji, Kimura Tomoki, Oi Hajime, Yamano Yasuhiko, Yokoyama Toshiki, Matsuda Toshiaki, Kataoka Kensuke, Matsuzawa Reiko, Fukihara Jun, Sakamoto Koji, Morise Masahiro, Hashimoto Naozumi, Kondoh Yasuhiro, Hasegawa Yoshinori

    ANNALS OF ONCOLOGY  2019.10 

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    Language:English   Presentation type:Poster presentation  

    DOI: 10.1093/annonc/mdz343.108

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Research Project for Joint Research, Competitive Funding, etc. 1

  1. 異常上皮細胞から再考した肺線維症の病態形成と二次発癌の機序の解明

    2021.12

    GSK ジャパン  2021年度 GSK ジャパン研究助成 

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    Authorship:Principal investigator  Grant type:Other

    Grant amount:\2000000

KAKENHI (Grants-in-Aid for Scientific Research) 5

  1. 間質性肺炎急性増悪病態における新規病的微小環境因子・ミトコンドリアDNAの役割

    Grant number:21K08202  2021.4 - 2024.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    阪本 考司, 芳川 豊史, 若原 恵子, 橋本 直純, 猪股 弥生

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    特発性肺線維症(IPF)は中高年に発症する進行性難治性の肺疾患である。急性増悪はIPF患者の約4割に突然発症する死亡率の高い合併症であるが、原因が分かっておらず発症の予測や治療法の開発が進んでいない。我々は最近、IPF患者さんの体液中のミトコンドリアDNAの増加が急性増悪の発症を予測しうることを発見した。これにヒントを得た本研究は、急性増悪発症のメカニズムとして肺に存在するマクロファージの異常活性化とミトコンドリアの代謝異常が関与していると仮定して、新たに急性増悪の動物モデルを作成し治療標的と診断法の開発を目指します。

  2. 好塩基球を介した2型炎症調節機構の解明ーアレルギー性・好酸球性肺疾患と肺恒常性

    Grant number:21K08456  2021.4 - 2024.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    若原 恵子, 阪本 考司, 橋本 直純

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    Authorship:Coinvestigator(s) 

    本研究では、2型炎症が創傷治癒と恒常性維持、アレルギー・好酸球性疾患の正・負の両面に関わっていることに注目し、そのコントロールを行っている細胞が好塩基球であるという仮説のもと、好塩基球のフェノタイプ(病原性・非病原性)を探索すること、フェノタイプを調節する因子を探ることを目的としている。特に呼吸器疾患に注目し、肺・気道における好塩基球の役割について検討を行う。

  3. Immune-pathological diagnostic artificial intelligence development research for pulmonary fibrosis using fibrotic foci-specific enhanced micro-CT

    Grant number:20K21599  2020.7 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

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    Authorship:Coinvestigator(s)  Grant type:Competitive

  4. 呼吸器疾患患者に対するリハビリテーション方策(振動刺激療法)の新規開拓

    Grant number:20K10709  2020.4 - 2024.3

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    井上 貴行

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    従来のリハビリテーション(リハ)の主要な方策は運動療法であるが、呼吸器疾患患者には軽労作でも重度の低酸素症状を来す患者や循環動態の不安定な患者など積極的な運動療法が行えない症例が数多く存在するため、運動療法の代替手段の開発が必要となっている。一方、振動刺激(VS)には筋萎縮の抑制や筋力の増大などの効果があることが報告されており、運動療法の代替手段となり得ることが実証されつつある。そこで本研究は、呼吸器疾患患者に対してVSを用いたリハを行うことで、筋萎縮や筋力、体力、日常生活動作、生活の質の低下を予防および抑制、さらには改善する効果が得られるかを網羅的に無作為化比較対照試験により検証する。

  5. 老化関連長鎖ノンコーディングRNAの制御による肺線維症難治性の克服

    Grant number:18K15948  2018.4 - 2022.3

    日本学術振興会  科学研究費助成事業  若手研究

    阪本 考司

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    加齢関連難治肺疾患である肺線維症において、線維化誘導性の細胞老化に陥った線維芽細胞が難治性の病態形成に寄与するとの仮説から、新規の細胞運命決定である長鎖ノンコーディングRNA(lncRNA)に注目し、同病態の線維芽細胞の細胞老化を制御するlncRNA群を同定することで疾患の新たな治療介入標的や疾患のバイオマーカーにすることを目指している。R2年度は以下の研究を進めた。
    lncRNAの発現調節による細胞表現型制御:昨年度に同定したIPF関連lncRNAの一つXを線維芽細胞に形質導入し、向線維化性や細胞老化の表現型を評価したところ、lncRNA-Xの発現回復はIPF由来の老化線維芽細胞においてp16/p21などの老化関連制御因子の発現抑制を誘導することが分かった。さらに、lncRNA-Xの遺伝子欠損マウスを作成し、その肺の表現型を評価した。lncRNA-X欠失細胞の肺組織では老化関連βガラクトシダーゼ染色陽性の老化細胞の増多が認められた。さらにlncRNA-X欠失マウスにブレオマイシンを用いて肺線維症を誘導し、線維化の程度を検討している。
    さらにIPFの病態形成に関わる新たな機能性lncRNA候補を同定したため、予備的な機能解析を開始した。
    また細胞老化により病態形成を媒介するミトコンドリアDNAの肺線維症へ寄与を解析した。ミトコンドリア代謝異常を反映して、IPFの患者由来の血清ではミトコンドリアDNAの濃度が上昇しており、その増多がIPF患者の不良な予後、および急性増悪の発症と相関することを発見した。
    バイオマーカーの検索のための臨床検体収集は、コロナウイルスの蔓延による受診抑制、臨床検体への取り扱いの制限などで遅れている。
    研究計画を一年延長して最終年度は血清からのlncRNA定量検出を進める。マウスモデルについては新たに細胞老化に関わる経路を制御する因子の欠損マウスでの解析を進める。

 

Teaching Experience (On-campus) 6

  1. 臓器別臨床講義 呼吸器

    2021

  2. 生涯健康と医学「大気環境と呼吸器疾患」

    2020

  3. 臓器別臨床講義 呼吸器

    2020

  4. 臓器別臨床講義 呼吸器

    2019

  5. 臓器別臨床講義 呼吸器

    2018

  6. 臓器別臨床講義 呼吸器

    2017

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Social Contribution 1

  1. 特発性間質性肺炎~最新の治療と日常生活の注意点について~

    Role(s):Lecturer

    名古屋市瑞穗保健センター  難病講演会  2018.7

Media Coverage 4

  1. The cells combating a deadly lung disease Internet

    American Association for the Advancement of Science (AAAS)  EurekAlert  https://www.eurekalert.org/news-releases/773991  2021.7

  2. ナノ素材による健康被害のメカニズムが明らかに Internet

    名古屋大学 学術研究・産学官連携推進本部  名大研究フロントライン  https://www.youtube.com/watch?v=QKIcuDphFQc&t=1s  2021.7

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    Author:Other 

  3. 人工微粒子、細胞に有害活性酸素 肺の炎症原因に、名古屋大 Internet

    共同通信  地方紙と共同通信のよんななニュース  https://nordot.app/778048216281759744?c=39546741839462401  2021.6

  4. 名古屋大、指定難病「特発性肺線維症」の疾患進行の運命を握る線維芽細胞を世界で初めて同定~特発性肺線維症克服へ向けての新展開~ Internet

    日経バイオテク  https://bio.nikkeibp.co.jp/atcl/release/21/05/31/10796/  2021.5

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    Author:Other