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新實 彰男ニイミ アキオ

所属部署医学研究科呼吸器・免疫アレルギー内科学分野
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Last Updated :2020/06/02

研究者基本情報

学歴

  •  - 1985年, 京都大学, 医学部

学位

  • 京都大学医学部医学科/博士(医学)

所属学協会

  • American College of Chest Physicians
  • European Thoracic Society
  • 日本気管食道科学会
  • 日本職業・環境アレルギー学会
  • 日本化学療法学会
  • 日本癌学会
  • American Thoracic Society
  • 日本サルコイドーシス/肉芽腫性疾患学会
  • 国際喘息学会日本・北アジア部会
  • 日本肺癌学会
  • 日本感染症学会
  • 日本結核病学会
  • 日本呼吸器内視鏡学会
  • 日本アレルギー学会
  • 日本呼吸器学会
  • 日本内科学会

委員歴

  • Faculty of 2013 American Cough Conference
  • 国際学術雑誌“CHEST” Editorial Board member(2010年-)
  • 国際学術雑誌"Journal of Thoracic Disease"Editorial Board Member(2013-)
  • 国際学術雑誌"Pulmonary Medicine" Esitorial Board member(2009-)
  • 国際学術雑誌"Cough" Editorial Board member(2004-)
  • 日本結核病学会 編集委員会委員(2013-)
  • 日本結核病学会 倫理委員会委員(2012-)
  • 日本アレルギー学会 「診療行為に関連した死亡の調査分析モデル事業」中部地域評価委員(2013-)
  • 日本アレルギー学会 専門医制度委員会委員(2011-)
  • 日本アレルギー学会 「アレルギー」編集委員(2009-)
  • 日本アレルギー学会 学術大会委員(2008-2011、2009-2011同委員長)
  • 日本アレルギー学会 試験問題作成委員会委員長 (2011年-)
  • 日本アレルギー学会 「喘息予防・管理ガイドライン(2009, 2012)」作成委員
  • 日本呼吸器学会 平成26年度学会賞選考委員長(2014-)
  • 日本呼吸器学会 COI委員会副委員長(2014-)
  • 日本呼吸器学会 財務委員会副委員長(2014-)
  • 日本呼吸器学会 和文誌編集委員会査読責任者(2012-)
  • 日本呼吸器学会 専門医制度審議会委員(2004-2012)
  • 日本呼吸器学会 咳嗽に関するガイドライン作成委員会委員(2003-)
  • 日本内科学会 専門医試験委員会呼吸器分野試験問題作成委員(2005-2007)

経歴

  • 研究職歴(日)【日R】
  • 研究職歴(日)【日R】

研究活動情報

研究キーワード

    臨床的・形態学的研究, 慢性咳嗽, 喘息

論文

  • Genome-wide association study identifies three new susceptibility loci for adult asthma in the Japanese population, Tomomitsu Hirota, Atsushi Takahashi, Michiaki Kubo, Tatsuhiko Tsunoda, Kaori Tomita, Satoru Doi, Kimie Fujita, Akihiko Miyatake, Tadao Enomoto, Takehiko Miyagawa, Mitsuru Adachi, Hiroshi Tanaka, Akio Niimi, Hisako Matsumoto, Isao Ito, Hironori Masuko, Tohru Sakamoto, Nobuyuki Hizawa, Masami Taniguchi, John J. Lima, Charles G. Irvin, Stephen P. Peters, Blanca E. Himes, Augusto A. Litonjua, Kelan G. Tantisira, Scott T. Weiss, Naoyuki Kamatani, Yusuke Nakamura, Mayumi Tamari, NATURE GENETICS, 43, (9) 893 - U108,   2011年09月, Bronchial asthma is a common inflammatory disease caused by the interaction of genetic and environmental factors(1,2). Through a genome-wide association study and a replication study consisting of a total of 7,171 individuals with adult asthma (cases) and 27,912 controls in the Japanese population, we identified five loci associated with susceptibility to adult asthma. In addition to the major histocompatibility complex and TSLP-WDR36 loci previously reported, we identified three additional loci: a USP38-GAB1 locus on chromosome 4q31 (combined P = 1.87 x 10(-12)), a locus on chromosome 10p14 (P = 1.79 x 10(-15)) and a gene-rich region on chromosome 12q13 (P = 2.33 x 10(-13)). We observed the most significant association with adult asthma at rs404860 in the major histocompatiblity complex region (P = 4.07 x 10(-23)), which is close to rs2070600, a SNP previously reported for association with FEV(1)/FVC in genome-wide association studies for lung function. Our findings offer a better understanding of the genetic contribution to asthma susceptibility.
  • Inflammatory subtypes in cough variant asthma: Association with maintenance doses of inhaled corticosteroids., Matsuoka H, Niimi A, Matsumoto H, Takemura M, Ueda T, Yamaguchi M, Jinnai M, Inoue H, Ito I, Chin K, Mishima M, Chest., 138, 1418 - 25,   2010年
  • Specific IgE Response to Trichophyton and Asthma Severity, Hirofumi Matsuoka, Akio Niimi, Hisako Matsumoto, Tetsuya Ueda, Masaya Takemura, Masafumi Yamaguchi, Makiko Jinnai, Kojiro Otsuka, Tsuyoshi Oguma, Tomoshi Takeda, Isao Ito, Kazuo Chin, Ryoichi Amitani, Michiaki Mishima, CHEST, 135, (4) 898 - 903,   2009年04月, Background: Sensitization to Trichophyton, a major dermatophyte, has been associated with asthma. Whether such sensitization is generally associated with the severity of asthma, like other molds such as Alternaria, is unknown. Methods: We compared 258 patients with asthma, which was classified by severity as mild (n = 123), moderate (101), or severe (34), and 114 healthy control subjects, with regard to specific IgE titers against Trichophyton rubrum and other common allergens such as mixed molds, house-dust mite, cat dander, dog dander, Japanese cedar pollen, mixed Graminea pollens and mixed weed pollens. Results: Positive rate of Trichophyton-specific IgE was higher in the patients with moderate asthma (15.8%) than in the-control subjects (7.0%, p = 0.04) and patients with mild asthma (4.9%, p < 0.006), and it was also higher in the patients with severe asthma (32.4%) than in control subjects (p = 0.0001), and patients with mild asthma (p < 0.0001) and moderate asthma (p = 0.04), but it did not differ between the control subjects and patients with mild asthma. The positive rates of mixed molds, cat dander, and dog dander were almost invariably higher in patients in all asthma subgroups than in the control subjects but did not differ among patients in the three asthma subgroups. The positive rates of other allergens were not different in all groups. Reanalysis of positive rate of Trichophyton-specific IgE after excluding 52 subjects with positive results for mixed molds showed a similar statistical trend to that of the original cohort. This may negate the potential effect of cross-reactivity to these molds. Multivariate analysis of asthma subgroups identified positive IgE results for Trichophyton as an independent determinant of asthma severity. Conclusions: Specific IgE response to Trichophyton may be associated with more severe asthma.
  • Patients' characteristics associated with unsuccessful sputum induction in asthma., Matsuoka H, Niimi A, Matsumoto H, Ueda T, Takemura M, Yamaguchi M, Jinnai M, Chang L, Otsuka K, Oguma T, Takeda T, Chin K, Mishima M, J Allergy Clin Immunol 2008, 121, 774 - 6,   2008年
  • TGFB1 promoter polymorphism C-509T and pathophysiology of asthma., Ueda T, Niimi A, Matsumoto H, Takemura M, Yamaguchi M, Matsuoka H, Jinnai M, Chin K, Minakuchi M, Cheng L, Shirakawa T, Mishima M, J Allergy Clin Immunol 2008, 121, 659 - 664,   2008年
  • TGFB1 promoter polymorphism C-509T and pathophysiology of asthma., Ueda T, Niimi A, Matsumoto H, Takemura M, Yamaguchi M, Matsuoka H, Jinnai M, Chin K, Minakuchi M, Cheng L, Shirakawa T, Mishima M, J Allergy Clin Immunol 2008, 121, 659 - 664,   2008年
  • Role of small airways in asthma: Investigation using high-resolution computed tomography, Tetsuya Ueda, Akio Niimi, Hisako Matsumoto, Masaya Takemura, Toyohiro Hirai, Masafumi Yamaguchi, Hirofumi Matsuoka, Makiko Jinnai, Shigeo Muro, Kazuo Chin, Michiaki Mishima, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 118, (5) 1019 - 1025,   2006年11月, Background: Small airways may have an important role in asthma but are more difficult to assess pathologically than central airways. Computed tomographic indices of lung density are assumed to reflect air trapping and may be a useful noninvasive measure of small airways disease, but their pathophysiological relevance remains undetermined. Objective: To evaluate lung density on high-resolution computed tomography and examine its correlations with clinical and physiologic variables in 29 patients with stable asthma. Methods: Both lungs were scanned at full-inspiratory and fullexpiratory phases to quantify percentage of lung field occupied by low attenuation area (LAA%; < -960 Hounsfield units) and mean lung density. Asthma severity, pulmonary function, methacholine airway sensitivity and reactivity, and sputum eosinophil counts were evaluated. Results: The mean lung density increased and LAA% decreased in all patients at expiratory phase compared with inspiratory phase. The inspiratory density indices and expiratory mean lung density correlated only with FEV1/forced vital capacity (FVC). Expiratory LAA% correlated more strongly than other variables with FEV1/FVC and with indices of peripheral airflow obstruction. Expiratory/inspiratory ratios of LAA% and mean lung density correlated, the former more strongly, with disease severity, residual volume/total lung capacity, and airway sensitivity, as well as with indices of global (FEV1 and FEV1/FVC) and peripheral airflow obstruction. Conclusion: Expiratory/inspiratory high-resolution computed tomography is useful for assessing small airways disease in asthma. Small airways involvement is associated with airflow obstruction, airway hypersensitivity, and more severe disease. Clinical implications: Small airways are an important therapeutic target in asthma.
  • Role of small airways in asthma: Investigation using high-resolution computed tomography, Tetsuya Ueda, Akio Niimi, Hisako Matsumoto, Masaya Takemura, Toyohiro Hirai, Masafumi Yamaguchi, Hirofumi Matsuoka, Makiko Jinnai, Shigeo Muro, Kazuo Chin, Michiaki Mishima, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 118, (5) 1019 - 1025,   2006年11月, Background: Small airways may have an important role in asthma but are more difficult to assess pathologically than central airways. Computed tomographic indices of lung density are assumed to reflect air trapping and may be a useful noninvasive measure of small airways disease, but their pathophysiological relevance remains undetermined. Objective: To evaluate lung density on high-resolution computed tomography and examine its correlations with clinical and physiologic variables in 29 patients with stable asthma. Methods: Both lungs were scanned at full-inspiratory and fullexpiratory phases to quantify percentage of lung field occupied by low attenuation area (LAA%; < -960 Hounsfield units) and mean lung density. Asthma severity, pulmonary function, methacholine airway sensitivity and reactivity, and sputum eosinophil counts were evaluated. Results: The mean lung density increased and LAA% decreased in all patients at expiratory phase compared with inspiratory phase. The inspiratory density indices and expiratory mean lung density correlated only with FEV1/forced vital capacity (FVC). Expiratory LAA% correlated more strongly than other variables with FEV1/FVC and with indices of peripheral airflow obstruction. Expiratory/inspiratory ratios of LAA% and mean lung density correlated, the former more strongly, with disease severity, residual volume/total lung capacity, and airway sensitivity, as well as with indices of global (FEV1 and FEV1/FVC) and peripheral airflow obstruction. Conclusion: Expiratory/inspiratory high-resolution computed tomography is useful for assessing small airways disease in asthma. Small airways involvement is associated with airflow obstruction, airway hypersensitivity, and more severe disease. Clinical implications: Small airways are an important therapeutic target in asthma.
  • Nature of airway inflammation and remodeling in chronic cough, A Niimi, A Torrego, AG Nicholson, BG Cosio, TB Oates, KF Chung, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 116, (3) 565 - 570,   2005年09月, Background: Chronic cough may be a result of asthma and nonasthma causes, but it is unclear whether there are specific inflammatory or remodeling changes. Objective: We determined airway mucosal changes in patients presenting with asthmatic cough and cough associated with nonasthmatic causes. Methods: Patients with chronic cough of nonasthmatic (n = 33; postnasal drip/rhinitis in 6, gastroesophageal reflux in 5, bronchiectasis in 3, and idiopathic in 19) and asthmatic (n = 14) causes and 15 healthy controls underwent fiberoptic bronchoscopy. Morphometry of bronchial biopsies and capsaicin cough sensitivity were assessed. Results: Compared with controls, submucosal eosinophils and neutrophils were increased in patients with asthmatic cough (P < .005) and submucosal mast cells in patients with nonasthmatic cough (P = .01). Subbasement membrane thickness, goblet cell area, vascularity, and vessel size were also increased in both groups. Smooth muscle area was higher only in patients with nonasthmatic cough (P = .0007 vs control and P = .019 vs asthmatic cough). None of the pathologic changes were related to the duration of coughing. Cough sensitivity was heightened in patients with nonasthmatic cough compared with controls and patients with asthmatic cough. The degree of goblet cell hyperplasia and epithelial shedding positively correlated with cough sensitivity in patients with nonasthmatic cough (r = 0.43; P = .01; and r = 0.40; P = .02, respectively). Conclusion: Features of airway wall remodeling are prominent in the airways with nonasthmatic as well as asthmatic cough. These are linked to chronic cough rather than to asthma. Mast cell hyperplasia rather than eosinophilia is distinctive for nonasthmatic cough.
  • Nature of airway inflammation and remodeling in chronic cough, A Niimi, A Torrego, AG Nicholson, BG Cosio, TB Oates, KF Chung, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 116, (3) 565 - 570,   2005年09月, Background: Chronic cough may be a result of asthma and nonasthma causes, but it is unclear whether there are specific inflammatory or remodeling changes. Objective: We determined airway mucosal changes in patients presenting with asthmatic cough and cough associated with nonasthmatic causes. Methods: Patients with chronic cough of nonasthmatic (n = 33; postnasal drip/rhinitis in 6, gastroesophageal reflux in 5, bronchiectasis in 3, and idiopathic in 19) and asthmatic (n = 14) causes and 15 healthy controls underwent fiberoptic bronchoscopy. Morphometry of bronchial biopsies and capsaicin cough sensitivity were assessed. Results: Compared with controls, submucosal eosinophils and neutrophils were increased in patients with asthmatic cough (P < .005) and submucosal mast cells in patients with nonasthmatic cough (P = .01). Subbasement membrane thickness, goblet cell area, vascularity, and vessel size were also increased in both groups. Smooth muscle area was higher only in patients with nonasthmatic cough (P = .0007 vs control and P = .019 vs asthmatic cough). None of the pathologic changes were related to the duration of coughing. Cough sensitivity was heightened in patients with nonasthmatic cough compared with controls and patients with asthmatic cough. The degree of goblet cell hyperplasia and epithelial shedding positively correlated with cough sensitivity in patients with nonasthmatic cough (r = 0.43; P = .01; and r = 0.40; P = .02, respectively). Conclusion: Features of airway wall remodeling are prominent in the airways with nonasthmatic as well as asthmatic cough. These are linked to chronic cough rather than to asthma. Mast cell hyperplasia rather than eosinophilia is distinctive for nonasthmatic cough.
  • Relationship of airway wall thickening to an imbalance between matrix metalloproteinase-9 and its inhibitor in asthma, H Matsumoto, A Niimi, M Takemura, T Ueda, M Minakuchi, R Tabuena, K Chin, T Mio, Y Ito, S Muro, T Hirai, S Morita, S Fukuhara, M Mishima, THORAX, 60, (4) 277 - 281,   2005年04月, Background: The balance between matrix metalloproteinase- 9 ( MMP- 9) and tissue inhibitor of metalloproteinase- 1 ( TIMP- 1) may be critical in extracellular matrix remodelling, a characteristic of asthmatic airways. An excess of TIMP- 1 over MMP- 9 has been associated with chronic airflow obstruction but the mechanisms underlying this association remain unknown. Recent computed tomographic ( CT) studies indicate that airway wall thickening is associated with chronic airflow obstruction. Methods: Sputum levels of MMP- 9, TIMP- 1, and their molar ratio were examined in 26 patients with stable asthma and their relationship with pulmonary function and airway wall thickness, assessed by a validated CT technique which measured wall area corrected by body surface area ( WA/ BSA), the ratio of WA to outer wall area ( WA%), and the absolute wall thickness corrected by root BSA of a segmental bronchus ( T/ ! BSA), was examined. Results: Sputum MMP- 9 levels were inversely correlated with WA% and TIMP- 1 levels were positively correlated with WA/ BSA and T/ root BSA. The MMP- 9/ TIMP- 1 molar ratio was inversely correlated with WA% and T/! BSA and positively correlated with post- bronchodilator values of mid- forced expiratory flow and maximum expiratory flow at the quartile of lung volume. Conclusion: Excess TIMP- 1 may have a pathogenetic role in airway wall thickening in asthmatic patients which may result in chronic airflow obstruction.
  • Increased expression of transient receptor potential vanilloid-1 in airway nerves of chronic cough., Groneberg DA, Niimi A, Dinh QT, Cosio B, Hew M, Fischer A, Chung KF, Am J Respir Crit Care Med 2004, 170, 1276 - 80,   2004年
  • Relationship of airway wall thickness to airway sensitivity and airway reactivity in asthma., Niimi A, Matsumoto H, Takemura M, Ueda T, Chin K, Mishima M, Am J Respir Crit Care Med 2003, 168, 983 - 8,   2003年
  • Airway wall thickness in asthma assessed by computed tomography - Relation to clinical indices, A Niimi, H Matsumoto, R Amitani, Y Nakano, M Mishima, M Minakuchi, K Nishimura, H Itoh, T Izumi, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 162, (4) 1518 - 1523,   2000年10月, Postmortem studies have shown that airway wall thickening is present in asthmatic patients and may play a pathophysiologic role. We investigated the presence and characteristics of airway wall thickening in patients with asthma, using helical computed tomography. Eighty-one asthmatic patients and 28 healthy control subjects were studied cross-sectionally. Airway wall thickness was assessed by a validated method on the basis of wall area (WA), WA corrected by body surface area (WA/BSA), and WA%, defined as (WA/total area) x 100 at the apical bronchus of the right upper lobe. Airway luminal area (Ai) and Ai/BSA were also examined. Asthma duration and severity, pulmonary function, and serum eosinophil cationic protein levels were evaluated. Intraobserver and interobserver reproducibility of WA, WA%, and Ai measurements were good. As compared with control, WA, WA/BSA, and WA% were significantly increased in patients with mild (n = 13), moderate (39), and severe persistent (22) asthma but not in patients with intermittent asthma (7). Comparison of the four asthmatic subgroups demonstrated thicker airways in more severe disease, but no difference in Ai or Ai/BSA. When all asthmatic patients were analyzed together, WA and WA/BSA correlated with the duration, although weakly, and severity of asthma. WA and WA/BSA negatively correlated with FEV1 (percentage of predicted), FEV1/FVC (%), and FEF25-75% (percentage of predicted), whereas WA% negatively correlated with only FEV1. We conclude that airway wall thickening occurs in patients with asthma and is not limited to those with severe disease. The degree of airway wall thickening may relate to the duration and severity of disease and the degree of airflow obstruction.
  • Airway remodelling in cough-variant asthma, A Niimi, H Matsumoto, M Minakuchi, M Kitaichi, R Amitani, LANCET, 356, (9229) 564 - 565,   2000年08月, Subepithelial-layer thickening, a pathological feature of airway remodelling, is present in cough-variant asthma. In bronchial biopsy samples we found mean subepithelial-layer thickness was 7.1 (SE 0.4) mu m in patients with cough-variant asthma, 8.6 (0.4) mu m in patients with classic asthma with wheezing, and 5.0 (0.2) mu m in healthy controls. Thickness was significantly higher in patients with asthma than in controls, and was significantly greater in those with classic asthma than in those with cough-variant asthma. Early anti-inflammatory treatment might, therefore, be beneficial in cough-variant asthma, as recommended in classic asthma.
  • Eosinophilic inflammation in cough variant asthma., Niimi A, Amitani R, Suzuki K, Tanaka E, Murayama T, Kuze F, Eur Respir J 1998, 11, (5) 1064 - 1069,   1998年
  • Late respiratory response and associated eosinophilic inflammation induced by repeated exposure to toluene diisocyanate in guinea pigs, A Niimi, R Amitani, K Yamada, KI Tanaka, F Kuze, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 97, (6) 1308 - 1319,   1996年06月, Objective: The study was designed to establish an animal model of toluene diisocyanate (TDI)-induced late respiratory response and to investigate airway inflammatory cell dynamics in this model. Methods: Guinea pigs were exposed to 2,4-TDI dissolved in ethyl acetate by nasal application according to three schedules. Schedule 1 consisted of sensitization and multiple challenge (n = 58): 10% TDI was applied once daily for 7 days (sensitization) followed by challenges with 5% TDI once weekly for 4 weeks. Schedule 2 consisted of sensitization only (n = 5). 10% TDI was applied once daily for 7 days. Schedule 3 consisted of single challenge only (n = 12): 5% TDI was applied only once. As controls, ethyl acetate was applied according to the three schedules described above. Each animal was premedicated with metyrapone before each challenge. Bronchoalveolar lavage and histologic examination were performed at various times after the last challenge. Results: Schedule 1 induced immediate and late respiratory responses at a prevalence of 63% and 56%, respectively. Schedules 2 and 3 induced an immediate response in some animals but no late response. Neither immediate nor late response was observed in control animals. All of the subgroups of schedule I that developed late responses (examined at 2, 3, 6, 24 and 168 hours) showed a significant increase of eosinophils in bronchoalveolar lavage fluid and tissue compared with the corresponding control of each (examined at the same time points). Two of the subgroups with late responses (examined at 3 and 6 hours) were compared with their corresponding subgroups, which were given the same treatment, failed to develop late response, and were examined at the same time points; they again proved to have a significant increase of eosinophils in both samples. Subgroups of schedule 1 without late response (30 minutes, 3 and 6 hours), schedule 2 (6 hours), or schedule 3 (2 and 6 hours) did not show significant changes in lavage or tissue cell composition, except for the schedule 1 subgroup examined at 6 hours, which showed a significant increase of eosinophils only in the tissue compared with its control. Conclusions: Sensitization and multiple challenge with TDI induced immediate and/or late respiratory responses at a high prevalence in guinea pigs. Eosinophilic but not neutrophilic inflammation was involved in the late response.

受賞

  •   2012年, Top 5% of reviewers for CHEST for 2012
  •   2012年, 日本アレルギー協会 第2回真鍋奨学助成(2012年度)
  •   2010年, 平成22年度日本呼吸器学会 熊谷賞
  •   2010年, Top reviewers for CHEST for 2010
  •   2010年, アストラゼネカ・リサーチ・グラント2010
  •   2009年, Top 75 reviewers for CHEST for 2009
  •   2005年, 第42回(2005年度)ベルツ賞1等賞(共著)
  •   2004年, 平成16年度American College of Chest Physician 日本部会賞
  •   2004年, アストラゼネカ・リサーチ・グラント2004
  •   2000年, 2000年度 アストラゼネカ喘息研究奨励助成
  •   1996年, 平成8年度日本アレルギー協会国際交流助成

競争的資金

  • ヒトiPS細胞を用いた肺組織幹細胞の探索とⅡ型肺胞上皮細胞誘導への挑戦(基盤C、2011-2013)
  • 咳喘息と典型的喘息の病態生理学的特徴と 予後決定因子に関する包括的研究(基盤C、2011-2015)
  • iPS細胞を用いた難治性呼吸器疾患の病態 解明と新規治療法の開発(基盤A、2010-2013)
  • 慢性閉塞性肺疾患における末梢気道上皮間葉移行の分子メカニズムの解明(基盤C、2008-2010)
  • COPDのphenotypingに関する包括的研究(基盤A、2006-2009)
  • 健常者における咳受容体感受性の規定因子:血清ACE活性、ACE遺伝子多型の関与についての研究(基盤C、2001-2002)
  • 気道および肺胞領域の炎症性肺疾患の病態抑制機序の検討(基盤C、2000-2001)
  • 気管支喘息におけるTrichophytonの関与についての研究?抗真菌薬治療の検討を含めて?(平成9・10年度奨励研究 A)
  • 慢性咳嗽の病態における下気道炎症の関与(平成7年度奨励研究 A)

社会貢献活動情報

社会貢献活動

  • 第4回小児免疫アレルギー実践セミナー愛知ランチョンセミナーにて講演, 大学,   2013年03月17日 - 2013年03月17日, 「成人喘息における最新の病態評価」をテーマに講演
  • 東京都医師会主催 日本医師会生涯教育講座にて講演, 地域団体・NPO,   2013年02月14日 - 2013年02月14日, 「長引く咳の治療戦略」をテーマに講演
  • 平成24年度がん・生活習慣病講演会にて講演, 地域団体・NPO,   2013年01月24日 - 2013年01月24日, 「タバコ成人病COPDは治療できる病気です~正しく理解して進行を防ぎましょう~」をテーマに講演
  • 朝日新聞「患者を生きる」の取材を受ける。, 民間企業,   2013年01月17日 - 2013年01月17日, 朝日新聞掲載の「患者を生きる」の中で慢性のせきをテーマに取材を受ける。
  • 朝日新聞 夕刊「体とこころの通信簿」の取材を受ける。, 民間企業,   2012年11月27日 - 2012年11月27日, 朝日新聞掲載予定の「体とこころの通信簿」のため、長引く咳の原因、治療法や注意すべき症状などについて取材を受ける。
  • 第599回大垣内科会講演会にて講演, 地域団体・NPO,   2012年11月21日 - 2012年11月21日, 「長引く咳の診断と治療」をテーマに講演
  • 平成24年度第3回練馬区医師会学術部呼吸器勉強会にて講演, 地域団体・NPO,   2012年11月20日 - 2012年11月20日, 「慢性咳嗽の診断と治療-咳嗽に関するガイドライン第2版の紹介を含めて-」をテーマに講演
  • 昭和区医師会学術講演会にて講演, 地域団体・NPO,   2012年11月17日 - 2012年11月17日, 「慢性咳嗽の診療-咳喘息を中心に-」をテーマに講演
  • 日本内科学会信越支部第47回生涯教育講演会にて講演, その他,   2012年10月28日 - 2012年10月28日, 「日本内科学会信越支部第47回生涯教育講演会」の中で講演
  • 名市大旧第2内科開業医会学術講演会にて講演, 地域団体・NPO,   2012年10月20日 - 2012年10月20日, 「慢性咳嗽の診断と治療」をテーマに講演
  • 市民医療講座にて講演, 行政,   2012年10月14日 - 2012年10月14日, 「どうして咳が長引くの?」をテーマにいなべ市を対象に市民医療講座を開催する。
  • 第162回飛騨臨床医会にて講演, 行政,   2012年10月12日 - 2012年10月12日, 「長引く咳の診断と治療」をテーマに講演
  • 沼津区内科医会学術講演会にて講演, その他,   2012年09月21日 - 2012年09月21日, 「長引く咳の診断と治療-咳喘息を中心に-」
  • 地域医療連携推進懇話会にて講演, 民間企業,   2012年09月08日 - 2012年09月08日, 「慢性咳嗽の診断と治療」をテーマに講演
  • 愛知県保険医協会内科臨床研究会にて講演, 民間企業,   2012年09月01日 - 2012年09月01日, 「慢性咳嗽の診断と治療」をテーマに講演
  • 第13回肺の日「市民公開講座」の講師, 大学,   2012年08月05日 - 2012年08月05日, タバコの健康被害、COPDについて市民に啓蒙し、タバコのない社会づくりを目指す。
  • 第6回相模原臨床アレルギーセミナーにて講演, 地域団体・NPO,   2012年08月03日 - 2012年08月03日, 「喘息病態の多様性を考慮した治療戦略」をテーマに講演
  • 春日井市民病院講演会にて講演, 行政,   2012年07月23日 - 2012年07月23日, 「長引く咳の診断と治療」をテーマに講演
  • 第55回岐阜県内科医会講演会にて講演, 地域団体・NPO,   2012年04月22日 - 2012年04月22日, 「慢性咳嗽の診断と治療」をテーマに講演


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