Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Naoki Hamada Last modified date:2021.09.14

Assistant Professor / Research Institute for Diseases of the Chest Graduate School of Medical Sciences Kyushu University / Respiratory Medicine / Kyushu University Hospital


Papers
1. Noriyuki Enomoto, Sakae Homma, Naohiko Inase, Yasuhiro Kondoh, Takeshi Saraya, Hajime Takizawa, Yoshikazu Inoue, Hiroshi Ishii, Yoshio Taguchi, Shinyu Izumi, Yasuhiko Yamano, Yoshinori Tanino, Yasuhiko Nishioka, Mikio Toyoshima, Koshi Yokomura, Shiro Imokawa, Naoki Koshimizu, Takehisa Sano, Taisuke Akamatsu, Hiroshi Mukae, Motoyasu Kato, Naoki Hamada, Hirofumi Chiba, Shinobu Akagawa, Shigeo Muro, Hironori Uruga, Hiroyuki Matsuda, Yusuke Kaida, Miho Kanai, Kazutaka Mori, Masafumi Masuda, Hironao Hozumi, Tomoyuki Fujisawa, Yutaro Nakamura, Noriyoshi Ogawa, Takafumi Suda, Prospective nationwide multicentre cohort study of the clinical significance of autoimmune features in idiopathic interstitial pneumonias, Thorax, 10.1136/thoraxjnl-2020-216263., 2021.07.
2. Furuie H, Arimura-Omori M, Hamada N, Yanagihara T, Kiyohara C., The Association of Aging-Related Polymorphisms with Susceptibility to Lung Cancer: A Case-Control Study in a Japanese Population., Asian Pacific Journal of Cancer Prevention, DOI:10.31557/APJCP.2021.22.4.1279, 22, 4, 1279-1285, 2021.04.
3. Ogata H, Harada E, Takao T, Ijichi K, Hamada N, Matsumoto K., Mycobacterium avium pleuritis with multiple nodules in the pleura., Respirology Case Report, doi: 10.1002/rcr2.608., 8, 6, e00608, 2020.06.
4. Ogata H, Harada E, Moriya S, Fukuyama S, Suzuki K, Shiraishi Y, Ando H, Uryu K, Shinozaki S, Ide M, Sakamoto A, Nakanishi T, Hamada N, Yoneshima Y, Ota K, Kohashi K, Tateishi Y, Miyashita Y, Oda Y, Matsumoto K., Pleuropulmonary paragonimiasis with multiple nodules in the pleura., Internal Medicine, doi: 10.2169/internalmedicine.4457-20, 59, 15, 1879-1881, 2020.08.
5. Suzuki, Kunihiro; Yanagihara, Toyoshi; Matsumoto, Koichiro; Chong, Sy Giin; Ando, Hiroyuki; Ide, Maako; Arimura-Omori, Masako; Hata, Kentaro; Hamada, Naoki, Immune-checkpoint kinetics for T cells in anti-MDA5 positive interstitial lung disease, RHEUMATOLOGY, 10.1093/rheumatology/keaa412, 60, 1, E14-E16, 2021.01.
6. Yanagihara T, Suzuki K, Egashira A, Ogo N, Asoh T, Nara T, Takatsuki K, Yoshizawa S, Chong SG, Hamada N, Maeyama T., Nintedanib and intensive immunosuppressive therapy to treat rapidly progressive interstitial lung disease presenting anti-ARS antibodies., Respiratory Medicine Case Reports, doi: 10.1016/j.rmcr.2020.101272., 31, 101272, 2020.10.
7. Minegishi Y, Gemma A, Homma S, Kishi K, Azuma A, Ogura T, Hamada N, Taniguchi H, Hattori N, Nishioka Y, Tanizawa K, Johkoh T, Yokoyama T, Mori K, Taguchi Y, Ebina M, Inase N, Hagiwara K, Ohnishi H, Mukae H, Inoue Y, Kuwano K, Chiba H, Ohta K, Tanino Y, Sakai F, Sugiyama U., Acute exacerbation of idiopathic interstitial pneumonias related to chemotherapy for lung cancer: nationwide surveillance in Japan., ERJ Open Res, doi: 10.1183/23120541.00184-2019., 6, 2020.06.
8. Masako Arimura-Omori, Chikako Kiyohara, Toyoshi Yanagihara, Yuzo Yamamoto, Saiko Ogata-Suetsugu, Eiji Harada, Naoki Hamada, Toru Tsuda, Shohei Takata, Ikuko Shimabukuro, Nobuhiko Nagata, Kazuhiro Yatera, Ryo Torii, Masaki Okamoto, Masaki Fujita, Yoichi Nakanishi, Association between telomere-related polymorphisms and the risk of ipf and copd as a precursor lesion of lung cancer
Findings from the fukuoka tobacco-related lung disease (fold) registry, Asian Pacific Journal of Cancer Prevention, 10.31557/APJCP.2020.21.3.667, 21, 3, 667-673, 2020.03, Background: Lung cancer coexisting with idiopathic pulmonary fibrosis (IPF) or chronic obstructive pulmonary disease (COPD) can lead to poor prognosis. Telomere-related polymorphisms may be implicated in the pathogenesis of these three lung diseases. As to elucidate the mechanism of lung cancer via IPF or COPD may enable early detection and early treatment of the disease, we firstly examined the association between telomere-related polymorphisms and the risk of IPF and COPD in a case-control study. Materials and Methods: A total of 572 patients with IPF (n = 155) or COPD (n = 417), who were derived from our on-going cohort study, and controls (n = 379), who were derived from our previous case-control study, were included in this study. Telomerase reverse transcriptase (TERT) rs2736100, telomere RNA component (TERC) rs1881984, and oligonucleotide/oligosaccharide-binding fold containing1 (OBFC1) rs11191865 were genotyped with real-time PCR using TaqMan fluorescent probes. Unconditional logistic regression was used to assess the adjusted odds ratios and 95% confidence intervals. Results: TERT rs2736100 was significantly associated with the risk of IPF; increases in the number of this risk allele increased the risk of IPF (Ptrend = 0.008). Similarly, TERT rs2736100 was associated with the risk of COPD. In regard to the combined action of the three loci, increasing numbers of "at-risk" genotypes increased the risk of IPF in a dose-dependent manner (P trend=0.003). Conclusions: TERT rs2736100 was associated with the risks of both IPF and COPD in a Japanese population. A combination of the "at-risk" genotypes might be important to identify the population at risk for IPF more clearly..
9. Suzuki K, Yanagihara T, Matsumoto K, Kusaba H, Yamauchi T, Ikematsu Y, Tanaka K, Otsubo K, Inoue H, Yoneshima Y, Iwama E, Arimura-Omori M, Harada E, Hamada N, Okamoto I, Nakanishi Y., Immune-checkpoint profiles for T cells in bronchoalveolar lavage fluid of patients with immune-checkpoint inhibitor-related interstitial lung disease., International Immunology, doi: 10.1093/intimm/dxaa022. , 2020.04.
10. Saiko Ogata-Suetsugu, Naoki Hamada, Toru Tsuda, Shohei Takata, Yasuhiko Kitasato, Naoyuki Inoue, Nobuhiko Nagata, Kazuhiro Yatera, Hiroshi Mukae, Chiharu Yoshii, Tomoaki Hoshino, Masaki Fujita, Kentaro Watanabe, Shoji Tokunaga, Yoichi Nakanishi, Characteristics of tobacco-related lung diseases in Fukuoka Prefecture, Japan
A prospective, multi-institutional, observational study, Respiratory Investigation, 10.1016/j.resinv.2019.10.002, 58, 1, 74-80, 2020.01, Background: Tobacco smoking causes a variety of smoking-related diseases, death, and economic damage. Despite targeted anti-smoking campaigns, tobacco-related deaths are expected to increase in Japan. We investigated the current state of non-cancerous lung diseases such as idiopathic interstitial pneumonias (IIPs), chronic obstructive pulmonary disease (COPD), and combined pulmonary fibrosis and emphysema (CPFE), which are known to be highly related to tobacco smoking. Methods: This prospective multi-institutional observational study involved 29 major hospitals within the Fukuoka Prefecture area (Fukuoka tobacco-related lung disease registry study group). Patients diagnosed with IIPs, including CPFE and COPD, registered from September 1, 2013 to April 30, 2016 were included. Clinical background information, laboratory and pulmonary function test results, findings of imaging tests, including chest radiography and chest computed tomography, and DNA isolated from peripheral blood were collected from each patient. Follow-up surveillance involved collection of data regarding the exacerbation of disease and death until 5 years of registration. In the present study, we report the baseline characteristics of the patients registered in this surveillance study. Results: Overall, 1016 patients (524 with IIPs, including 145 CPFE and 492 with COPD) were enrolled. Among the patients with COPD, 96.8% were current or former smokers. Among the patients with IIPs, 69.9% were current or former smokers. Conclusion: This study revealed the current status of lung diseases potentially related to tobacco smoking in Fukuoka Prefecture. Both COPD and CPFE were highly related to tobacco smoking, whereas 30% of patients with IIPs had never smoked..
11. Yuri Tachibana, Hiroyuki Taniguchi, Yasuhiro Kondoh, Kensuke Kataoka, Naoki Hamada, Toshihiro Hashiguchi, Kazuya Ichikado, Tomoo Kishaba, Shuntaro Sato, Emiko Udo, Mikiko Hashisako, Junya Fukuoka, Pulmonary interstitial emphysema is a risk factor for poor prognosis and a cause of air leaks, Respiratory Investigation, 10.1016/j.resinv.2019.03.008, 2019.01, Background: Pulmonary interstitial emphysema is a rare, abnormal condition in which air pressure from the alveolar airspace tears the adjacent interstitial tissues of the lung and causes the formation of cystic spaces. Pulmonary interstitial emphysema is a known indication for mechanical ventilation in premature infants with neonatal respiratory distress syndrome, and it can be observed in various types of interstitial lung disease. Nevertheless, its pathogenesis and clinical impact remain unknown. Methods: We reviewed data from 433 cases of interstitial lung disease from an external consultation archive. Multidisciplinary diagnosis along with clinical and follow-up data, including events of air leaks such as pneumothorax and mediastinal emphysema, were obtained and compared to those of 150 control cases of interstitial lung disease without pulmonary interstitial emphysema. Results: We found 22 (5.1%)cases of interstitial lung disease with pulmonary interstitial emphysema. The diagnoses included idiopathic pulmonary fibrosis (5/22 [22.7%]), pleuroparenchymal fibroelastosis (4/22 [18.2%]), chronic hypersensitivity pneumonia (4/22 [18.2%]), and others (9/22 [40.9%]). Cases involving pulmonary interstitial emphysema demonstrated a significantly higher frequency of air leaks than did those without pulmonary interstitial emphysema (12/22 [54.5%]versus 23/150 [15.3%]; P < 0.001; odds ratio, 6.63)and were associated with worse prognosis (P = 0.009 [log-rank])and a lower median percent forced vital capacity (73.2% versus 84.0%; P < 0.001). Conclusions: We found that pulmonary interstitial emphysema is an independent factor for poor prognosis, which also shows a trend to cause air leaks, including pneumothorax and mediastinal emphysema..
12. Kentaro Tanaka, Toyoshi Yanagihara, Yuki Ikematsu, Hiroyuki Inoue, Keiichi Ota, Eiji Kashiwagi, Kunihiro Suzuki, Naoki Hamada, ario takeuchi, Katsunori Tatsugami, Masatoshi Eto, Kayo Ijichi, Yoshinao Oda, Kohei Otsubo, Yasuto Yoneshima, Eiji Iwama, Yoichi Nakanishi, Isamu Okamoto, Detection of identical T cell clones in peritumoral pleural effusion and pneumonitis lesions in a cancer patient during immune-checkpoint blockade, Oncotarget, 10.18632/oncotarget.25743, 9, 55, 30587-30593, 2018.07, Although immune-related adverse events (irAEs) of treatment with immunecheckpoint inhibitors may be due to cellular immunity mediated by T lymphocytes, their pathogenesis has remained unknown. Here we collected bronchoalveolar lavage fluid (BALF) from a cancer patient with nivolumab-induced pneumonitis and isolated mononuclear cells for next-generation sequencing of the complementarity-determining region of the T cell receptor (TCR) β chain. Mononuclear cells in peritumoral pleural effusion isolated from the patient were similarly analyzed, and the results obtained for the two specimens were compared. A substantial number of TCRβ clones in BALF were also identified among lymphocytes in the peritumoral pleural effusion. Such a correlation was not apparent between TCRβ clones in BALF and those in peripheral blood. Moreover, many tumor-associated clones with a read frequency of =0.10% were also present in BALF. Our data suggest that irAEs might be induced by drugactivated lymphocytes originating from tumor tissue. Deep sequencing will thus be indispensable for investigations of the immune-based pathogenesis of, and the development of optimal treatments for, irAEs..
13. Toyoshi Yanagihara, Yuki Ikematsu, Koji Kato, Akiko Yonekawa, Satoko Ideishi, Taro Tochigi, Takeshi Sugio, Kohta Miyawaki, Kentaro Tanaka, Eiji Harada, Naoki Hamada, Yoichi Nakanishi, Expression of PD-1 and PD-L1 on cytotoxic T lymphocytes and immune deficiency in a patient with adult T cell leukemia/lymphoma, Annals of Hematology, 10.1007/s00277-017-3146-z, 97, 2, 359-360, 2018.02.
14. Kohei Otsubo, Isamu Okamoto, Naoki Hamada, Yoichi Nakanishi, Anticancer drug treatment for advanced lung cancer with interstitial lung disease, Respiratory Investigation, 10.1016/j.resinv.2018.03.002, 2018.01, Interstitial lung disease (ILD) is a risk factor for lung cancer development and is frequently observed in patients with lung cancer. Individuals with ILD have been excluded from most prospective clinical trials of lung cancer therapies because of the risk of ILD acute exacerbation. Thus, the optimal anticancer drug treatment for such patients has yet to be established. Tyrosine kinase inhibitors are avoided for the treatment of advanced non–small cell lung cancer (NSCLC) with ILD because of the concern of acute exacerbation, and information on the effects of immune-checkpoint inhibitors is limited in these patients. Only three prospective single-arm studies of cytotoxic chemotherapies for advanced lung cancer with ILD have been reported. Based on the results of these studies and those of retrospective analyses, carboplatin and either paclitaxel or nab-paclitaxel are often selected in daily clinical practice for patients with NSCLC and ILD, whereas platinum plus etoposide is selected for those with small cell lung cancer and ILD. Although the antitumor activity of first-line platinum-based chemotherapy appears similar in advanced lung cancer patients with and without ILD, its impact on overall survival of the former patients is limited. The risks and benefits of chemotherapy must therefore be carefully explained before treatment initiation, and careful follow-up is necessary for such patients, especially those with the usual interstitial pneumonia pattern, a risk factor for chemotherapy-related exacerbation. Prospective clinical studies with large patient populations are still required to establish the appropriate treatments for advanced lung cancer with ILD..
15. Toyoshi Yanagihara, Norio Yamamoto, Yasuaki Kotetsu, Naoki Hamada, Eiji Harada, Kunihiro Suzuki, Kayo Ijichi, Yoshinao Oda, Yoichi Nakanishi, Interstitial pneumonia caused by dabigatran, Respiratory Medicine Case Reports, 10.1016/j.rmcr.2017.10.009, 23, 10-12, 2018.01, We describe the case of a 73-year-old man who experienced dry cough and exertional dyspnea after dabigatran administration. Chest radiographs revealed the development of bilateral consolidative and ground glass opacity, and transbronchial lung biopsy showed organized materials in the alveolar spaces with moderate inflammatory infiltrate and focal fibrosis. Lung opacity gradually disappeared after discontinuing dabigatran. To date, there has been only one report regarding dabigatran-induced lung injury, except for alveolar hemorrhage and eosinophilic pneumonia. Therefore, we should consider that any drug can cause various types of lung injuries..
16. Toyoshi Yanagihara, Yuzo Yamamoto, Naoki Hamada, Kunihiro Suzuki, Saiko Ogata-Suetsugu, Eiji Harada, Tetsuzo Tagawa, Minako Fujiwara, Mikiko Hashisako, Junya Fukuoka, Yoichi Nakanishi, Recurrent idiopathic pulmonary hemosiderosis after long-term remission presented with Sjogren's syndrome
Idiopathic no more?, Respiratory Medicine Case Reports, 10.1016/j.rmcr.2018.06.013, 25, 68-72, 2018.01, We report a case of recurrent idiopathic pulmonary hemosiderosis after a long-term remission presented with Sjögren's syndrome. The patient was diagnosed with IPH due to repeated pneumonia and blood sputum in his childhood. He was admitted to our hospital due to exertional dyspnea and dry cough with bilateral ground-glass opacity in chest computed tomography at the age of 32. Video-assisted thoracoscopic surgery was performed and the specimens showed nonspecific interstitial pneumonia pattern with diffuse, chronic alveolar hemorrhage, suggesting recurrence of IPH. He was also diagnosed with Sjögren's syndrome. Further immunological studies will reveal the pathogenesis of IPH..
17. Kunihiro Suzuki, Toyoshi Yanagihara, Tetsuya Yokoyama, Takashige Maeyama, Saiko Ogata-Suetsugu, Masako Arimura-Omori, Hironori Mikumo, Naoki Hamada, Eiji Harada, Kazuyoshi Kuwano, Taishi Harada, Yoichi Nakanishi, Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice, Biology Open, 10.1242/bio.026005, 6, 12, 1869-1875, 2017.12, Bax is a pro-apoptotic member of the Bcl-2 family of proteins, and plays a central role in mitochondria-dependent apoptosis. Several lines of evidence have implied that Bax is involved in both epithelial apoptosis and fibroblast proliferation in idiopathic pulmonary fibrosis; however, the mechanisms remain unknown. Bax-inhibiting peptide V5 (BIP-V5) exhibits membrane permeability and inhibits the activation of Bax. The purpose of this study was to investigate whether the control of Bax activity by BIP-V5 reduces the degree of bleomycin-induced lung injury. C57BL/6J mice were administered bleomycin and BIP-V5 intratracheally on day 0. Bronchoalveolar lavage fluid and lung tissue were obtained on day 7. Human pulmonary alveolar epithelial cells (A549 cells) and mouse pulmonary alveolar epithelial cells (LA-4 cells) were stimulated with bleomycin to induce apoptosis. Administration of BIP-V5 improved the survival rate and degree of bleomycin-induced lung injury by suppressing Bax activation in mice. BIP-V5 treatment decreased bleomycin-induced apoptosis of alveolar epithelial cell lines (A549 cells and LA-4 cells) by suppressing Bax activation. These results indicate that administration of BIP-V5 may constitute a novel therapeutic strategy against lung injury..
18. Saiko Ogata-Suetsugu, Naoki Hamada, Koichi Takayama, Kazuya Tsubouchi, Masako Arimura, Nakanishi Y, The clinical Value of serum soluble interleukin-2 receptor in sarcoidosis


, Sarcoidosis Vasculitis and Diffuse Lung Diseases, 34, 41-47, 2017.10.
19. Tetsuya Yokoyama, Toyoshi Yanagihara, K Suzuki, Naoki Hamada, S Ogata-Suetsugu, K Tsubouchi, H Mikumo, C Ikeda-Harada, T Maeyama, Kazuyoshi Kuwano, Nakanishi Y, Depletion of club cells attenuates bleomycin-induced lung injury and fibrosis in mice., J Inflamm (Lond), 10.1186/s12950-017-0168-1, 2017.09.
20. Naoki Hamada, Toyoshi Yanagihara, Kunihiro Suzuki, Saiko Ogata-Suetsugu, Eiji Harada, Hironori Mikumo, M Arimura, Nakanishi Y, Treatment with a programmed cell death-1-specific antibody has little effect on afatinib- and naphthalene-induced acute pneumonitis in mice, Biochemical and Biophysical Research Communications, doi.org/10.1016/j.bbrc.2017.07.148, 491, 656-661, 2017.07.
21. Saiko Ogata-Suetsugu, Naoki Hamada, Koichi Takayama, Kazuya Tsubouchi, Masako Arimura, Nakanishi Y, The clinical value of serum soluble interleukin-2 receptor in pulmonary sarcoidosis., SARCOIDOSIS VASCULITIS AND DIFFUSE LUNG DISEASES, 34, 6, 41-47, 2017.05.
22. Hironori Mikumo, Toyoshi Yanagihara, Naoki Hamada, Eiji Harada, Saiko Ogata-Suetsugu, Chika Ikeda-Harada, Masako Arimura, Kunihiro Suzuki, Tetsuya Yokoyama, Nakanishi Y, Neutrophil elastase inhibitor sivelestat ameliorates gefitinib-naphthalene-induced acute pneumonitis in mice., Biochemical and Biophysical Research Communications , 10.1016/j.bbrc.2017.03.031, 486, 1, 205-209, 2017.04.
23. Tomonobu Kawaguchi, Toyoshi Yanagihara, Tetsuya Yokoyama, Saiko Ogata-Suetsugu, Naoki Hamada, Chika Ikeda-Harada, Kunihiro Suzuki, Takashige Maeyama, Kazuyoshi Kuwano, Nakanishi Y, Probucol attenuates hyperoxia-induced lung injury in mice., PLoS ONE, 10.1371/journal.pone.0175129., 12, 4, e0175129, 2017.04.
24. Hironori Mikumo, Naoki Hamada, Eiji Harada, Toyoshi Yanagihara, Saiko Ogata-Suetsugu, Hidetake Yabuuchi, Kayo Ijichi, Koichi Takayama, Nakanishi Y, A case of immunoglobulin G4-related respiratory disease with multiple lung cysts: A case report., Respiratory Medicine Case Reports, Respir Med Case Rep. 2017 Apr 8;21:89-92. doi: 10.1016/j.rmcr.2017.03.023., 21, 89-92, 2017.04.
25. Yuzo Yamamoto, Kiyohara C, Naoki Hamada, Saiko Ogata-Suetsugu, Nakanishi Y, Biological interaction of cigarette smoking on the association between genetic polymorphisms involved in inflammation and the risk of lung cancer: A case-control study in Japan., Oncology Letters, 10.3892/ol.2017.5867., 13, 5, 3873-3881, 2017.03.
26. Ogata-Suetsugu S, Toyoshi Yanagihara, Naoki Hamada, Ikeda-Harada C, Yokoyama T, Suzuki K, Kawaguchi T, Maeyama T, Kuwano K, Nakanishi Y, Amphiregulin suppresses epithelial cell apoptosis in lipopolysaccharide-induced lung injury in mice., Biochemical and Biophysical Research Communications, doi: 10.1016/j.bbrc.2017.01.142. , 2017.01.
27. Yuzo Yamamoto, Kiyohara C, Saiko Ogata-Suetsugu, Naoki Hamada, Nakanishi Y, Association between genetic polymorphisms involved in the hypoxia-inducible factor pathway and lung cancer risk: A case-control study in Japan., Asia-Pacific Journal of Clinical Oncology, doi: 10.1111/ajco.12640, 2016.10.
28. Yuji Yoshida, Nobuhiko Nagata, Nobuko Tsurua, Yasuhiko Kitasato, Kentaro Wakamatsu, Michihiro Yoshimi, Hiroshi Ishii, Takako Hirota, Naoki Hamada, Masaki Fujita, Kazuki Nabeshima, Fumiaki Kiyomi, Kentaro Watanabe, Heterogeneous clinical features in patients with pulmonary fibrosis showing histology of pleuroparenchymal fibroelastosis, Respiratory Investigation, 10.1016/j.resinv.2015.11.002., 54, 3, 162-169, 2016.05.
29. Yuzo Yamamoto, Okamoto I., Kohei Otsubo, Eiji Iwama, Naoki Hamada, Harada T, Koichi Takayama, Yoichi Nakanishi, Severe acute interstitial lung disease in a patient with anaplastic lymphoma kinase rearrangement-positive non small cell lung cancer treated with afatinib, Investigational New Drugs, 10.1007/s10637-015-0284-9., 33, 5, 1148-1150, 2015.10.
30. Kazuya Tsubouchi, Naoki Hamada, Kayo Ijichi, Toshiro Umezaki, Koichi Takayama, Yoichi Nakanishi, Spontaneous improvement of laryngeal sarcoidosis resistant to systemic corticosteroid administration, Respirology Case Report, 10.1002/rcr2.118., 3, 3, 112-114, 2015.09.
31. Hamada N, Maeyama T, Kawaguchi T, Yoshimi M, Fukumoto J, Yamada M, Yamada S, Kuwano K, Nakanishi Y:, The role of High mobility group box1in pulmonary fibrosis. , Am J Respir Cell Mol Biol. , 39(4): 440-7, 2008.10.
32. Yoshimi M, Maeyama T, Yamada M, Hamada N, Fukumoto J, Kawaguchi T, Kuwano K, Nakanishi Y, Recombinant human erythropoietin reduces epithelial cell apoptosis and attenuates bleomycin-induced pneumonitis in mice., Respirology, 13(5): 639-45, 2008.09.
33. Yamada M, Kuwano K, Maeyama T, Hamada N, Yoshimi M, Nakanishi Y, Kasper M. , Dual-imunohistochemistry provides little evidence for epithelial-mesenchymal tansition in pulmonary fibrosis. , Histochem Cell Biol, 129(4):453-62. , 2008.01.
34. Yamada M, Kuwano K, Maeyama T, Yoshimi M, Hamada N, Fukumoto J, Egashira K, Hiasa K, Takayama K, Nakanishi Y, Gene transfer of soluble transforming growth factor type II receptor by in vivo electroporation attenuates lung injury and fibrosis. , J Clin Pathol, 60(8):916-20, 2007, 2007.08.
35. Hamada N, Kuwano K, Yamada M, Hagimoto N, Hiasa K, Egashira K, Nakashima N, Maeyama T, Yoshimi M, Nakanishi Y., Anti-vascular endothelial growth factor gene therapy attenuates lung injury and fibrosis in mice. , J Immunol, 175, 2, 1224-1231, 175:1224-1231, 2005.07.
36. Nakashima N, Kuwano K, Maeyama T, Hagimoto N, Yoshimi M, Hamada N, Yamada M, Nakanishi Y., The p53-Mdm2 association in epithelial cells in idiopathic pulmonary fibrosis and non-specific interstitial pneumonia., J Clin Pathol, 10.1136/jcp.2004.022632, 58, 6, 583-589, 58(6):583-9., 2005.06.
37. Inoshima I, Kuwano K, Hamada N, Yoshimi M, Maeyama T, Hagimoto N, Nakanishi Y, Hara N, Induction of CDK inhibitor p21 gene as a new therapeutic strategy against pulmonary fibrosis. , Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00209.2003, 286, 4, L727-L733, 286(4):727-733, 2004.04.
38. Fujita M, Ye Q, Ouchi H, Nakashima N, Hamada N, Hagimoto N, Kuwano K, Mason RJ, Nakanishi Y, Retinoic acid fails to reverse emphysema in adult mouse models., Thorax, 10.1136/thx.2003.010785, 59, 3, 224-230, 59:224-230, 2004.03.
39. Kuwano K, Nakashima N, Inoshima I, Hagimoto N, Fujita M, Yoshimi M, Maeyama T, Hamada N, Watanabe K, Hara N., Oxidative stress in lung epithelial cells from patients with idiopathic interstitial pneumonias. , Eur Respir J , 10.1183/09031936.03.00063203, 21, 2, 232-240, 21: 232-240, 2003.02.
40. Kuwano K, Hagimoto N, Maeyama T, Fujita M, Yoshimi M, Inoshima I, Nakashima N, Hamada N, Watanabe K, Hara N, Mitochondria-mediated apoptosis of lung epithelial cells in idiopathic interstitial pneumonias., Lab Invest, 10.1097/01.LAB.0000045084.81853.76, 82, 12, 1695-1706, 82: 1695-1706, 2002.10.