start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2024 dt-pub=20240925 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=放射線治療品質管理の重要性と標準化に向けた実践に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TANIMOTOYuki en-aut-sei=TANIMOTO en-aut-mei=Yuki kn-aut-name=谷本祐樹 kn-aut-sei=谷本 kn-aut-mei=祐樹 aut-affil-num=1 ORCID= affil-num=1 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil=岡山大学大学院ヘルスシステム統合科学研究科 END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue=12 article-no= start-page=e8364 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2023 dt-pub=20231221 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Nontuberculous mycobacterial abscess of lacrimal sac and eyelid debridement: Case report en-subtitle= kn-subtitle= en-abstract= kn-abstract=A 56-year-old otherwise healthy woman developed abscess from dacryocystitis in the right lower eyelid. The smear of puncture fluid showed acid-fast bacilli and Mycobacterium abscessus was identified after a month. The early start of clarithromycin/ethambutol was switched to clarithromycin/levofloxacin. Debridement specimen after 7-month treatment showed granulomatous tissue with no bacilli. en-copyright= kn-copyright= en-aut-name=MatsuoToshihiko en-aut-sei=Matsuo en-aut-mei=Toshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TanakaTakehiro en-aut-sei=Tanaka en-aut-mei=Takehiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamadaKiyoshi en-aut-sei=Yamada en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NoseMotoko en-aut-sei=Nose en-aut-mei=Motoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University kn-affil= affil-num=2 en-affil=Department of Pathology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Plastic and Reconstructive Surgery, Okayama University Hospital kn-affil= affil-num=4 en-affil=Department of Clinical Laboratory, Okayama University Hospital kn-affil= affil-num=5 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= en-keyword=debridement kn-keyword=debridement en-keyword=eyelid kn-keyword=eyelid en-keyword=lacrimal sac kn-keyword=lacrimal sac en-keyword=Mycobacterium abscessus kn-keyword=Mycobacterium abscessus en-keyword=nontuberculous mycobacteria kn-keyword=nontuberculous mycobacteria END start-ver=1.4 cd-journal=joma no-vol=77 cd-vols= no-issue=1 article-no= start-page=65 end-page=70 dt-received= dt-revised= dt-accepted= dt-pub-year=2023 dt-pub=202302 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effect of a Cyclooxygenase-2 Inhibitor in Combination with (?)-Epigallocatechin Gallate or Polyphenon E on Cisplatin-Induced Lung Tumorigenesis in A/J Mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=We investigated the effects of celecoxib combined with (?)-epigallocatechin-3-gallate (EGCG) or polyphenon E in a cisplatin-induced lung tumorigenesis model. Four-week-old female A/J mice were divided into seven groups: (i) Control, (ii) 150 mg/kg celecoxib (150Cel), (iii) 1,500 mg/kg celecoxib (1500Cel), (iv) EGCG+150 mg/kg celecoxib (EGCG+150Cel), (v) EGCG+1,500 mg/kg celecoxib (EGCG+1500Cel), (vi) polyphenon E+150 mg/kg celecoxib (PolyE+150Cel), and (vii) polyphenon E+1,500 mg/kg celecoxib (PolyE+1500Cel). All mice were administered cisplatin (1.62 mg/kg of body weight, i.p.) 1×/week for 10 weeks and sacrificed at week 30; the numbers of tumors on the lung surface were then determined. The tumor incidence and multiplicity (no. of tumors/mouse, mean±SD) were respectively 95% and 2.15±1.50 in Control, 95% and 2.10±1.29 in 150Cel, 86% and 1.67±1.20 in 1500Cel, 71% and 1.38±1.24 in EGCG+150Cel, 67% and 1.29±1.38 in EGCG+1500Cel, 80% and 1.95±1.36 in PolyE+150Cel, and 65% and 1.05±0.10 in PolyE+1500Cel. The combination of high-dose celecoxib with EGCG or polyphenon E significantly reduced multiplicity in cisplatin-induced lung tumors. en-copyright= kn-copyright= en-aut-name=SatoKen en-aut-sei=Sato en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KuboToshio en-aut-sei=Kubo en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KatayamaHideki en-aut-sei=Katayama en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KishinoDaizo en-aut-sei=Kishino en-aut-mei=Daizo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OkadaToshiaki en-aut-sei=Okada en-aut-mei=Toshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HisamotoAkiko en-aut-sei=Hisamoto en-aut-mei=Akiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MimotoJunko en-aut-sei=Mimoto en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=MaedaYoshionobu en-aut-sei=Maeda en-aut-mei=Yoshionobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= affil-num=1 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of General Internal Medicine 4, Kawasaki Medical School kn-affil= affil-num=3 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Medicine, Yamaguchi-Ube Medical Center kn-affil= affil-num=5 en-affil=Department of Medicine, Yamaguchi-Ube Medical Center kn-affil= affil-num=6 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of General Internal Medicine 4, Kawasaki Medical School kn-affil= affil-num=10 en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Medicine, Yamaguchi-Ube Medical Center kn-affil= affil-num=12 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=13 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=14 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=celecoxib kn-keyword=celecoxib en-keyword=cisplatin kn-keyword=cisplatin en-keyword=EGCG kn-keyword=EGCG en-keyword=lung tumor kn-keyword=lung tumor en-keyword=polyphenon E kn-keyword=polyphenon E END start-ver=1.4 cd-journal=joma no-vol=12 cd-vols= no-issue= article-no= start-page=301 end-page=315 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220330 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A study of teachers’ sensitizing reflection kn-title=教師の感性的な省察力に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=教師教育研究における近年の課題として，「教師の指導技術を担保している思考過程を解明する。」「理論と実践の課題を解消する。」という二つが挙げられる。本研究では，これらを解決する糸口として，「感性」と「行為の中の省察」に着目した。理論と実践の両面から，「教師の感性的な省察力」について，質的に考察することを目的とし，「感性」の論点を整理するための文献研究と教師の省察力を観る実験を行った。本研究で得られた知見として，以下の３点が示唆された。@教師に求められる「感性」の働きには，非言語情報の認識と，その認識を元にした想像（イメージ）力の二つが重要であり，この二つには関連がある。A教師の「感性的な省察力」は段階を追った構造として捉えるものではなく，なだらかなスペクトラム（連続体）上で捉えられるべきものである。B「感性」は理性と二項対立的な概念でなく，一体化したものとして捉えられるべきものである。 en-copyright= kn-copyright= en-aut-name=TanimotoRyuichi en-aut-sei=Tanimoto en-aut-mei=Ryuichi kn-aut-name=谷本竜一 kn-aut-sei=谷本 kn-aut-mei=竜一 aut-affil-num=1 ORCID= en-aut-name=SakoHaruko en-aut-sei=Sako en-aut-mei=Haruko kn-aut-name=酒向治子 kn-aut-sei=酒向 kn-aut-mei=治子 aut-affil-num=2 ORCID= affil-num=1 en-affil=Okayama Saidaiji Elementary School kn-affil=岡山市立西大寺小学校 affil-num=2 en-affil=Graduate School of Education, Okayama University kn-affil=岡山大学学術研究院教育学域 en-keyword=感性(sensitizing reflection) kn-keyword=感性(sensitizing reflection) en-keyword=省察(reflection) kn-keyword=省察(reflection) en-keyword=教師教育(teacher education) kn-keyword=教師教育(teacher education) en-keyword=体育科教育(physical education) kn-keyword=体育科教育(physical education) END start-ver=1.4 cd-journal=joma no-vol=21 cd-vols= no-issue=1 article-no= start-page=45 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Photodynamic diagnostic ureteroscopy using the VISERA ELITE video system for diagnosis of upper-urinary tract urothelial carcinoma: a prospective cohort pilot study en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background The advantages of photodynamic diagnostic technology using 5-aminolevulinic acid (ALA-PDD) have been established. The aim of this prospective cohort study was to evaluate the usefulness of ALA-PDD to diagnose upper tract urothelial carcinoma (UT-UC) using the Olympus VISERA ELITE video system. Methods We carried out a prospective, interventional, non-randomized, non-contrast and open label cohort pilot study that involved patients who underwent ureterorenoscopy (URS) to detect UT-UC. 5-aminolevulinic acid hydrochloride was orally administered before URS. The observational results and pathological diagnosis with ALA-PDD and traditional white light methods were compared, and the proportion of positive subjects and specimens were calculated. Results A total of 20 patients were enrolled and one patient who had multiple bladder tumors did not undergo URS. Fifteen of 19 patients were pathologically diagnosed with UT-UC and of these 11 (73.3%) were ALA-PDD positive. Fourteen of 19 patients were ALA-PDD positive and of these 11 were pathologically diagnosed with UC. For the 92 biopsy specimens that were malignant or benign, the sensitivity for both traditional white light observation and ALA-PDD was the same at 62.5%, whereas the specificities were 73.1% and 67.3%, respectively. Of the 38 specimens that were randomly biopsied without any abnormality under examination by both white light and ALA-PDD, 11 specimens (28.9%) from 5 patients were diagnosed with high grade UC. In contrast, four specimens from 4 patients, which were negative in traditional white light observation but positive in ALA-PDD, were diagnosed with carcinoma in situ (CIS). Conclusions Our results suggest that ALA-PDD using VISERA ELITE is not sufficiently applicable for UT-UC. Nevertheless, it might be better particularly for CIS than white light and superior results would be obtained using VISERA ELITE II video system. Trial registration: The present clinical study was approved by the Okayama University Institutional Review Board prior to study initiation (Application no.: RIN 1803-002) and was registered with the UMIN Clinical Trials Registry (UMIN-CTR), Japan (Accession no.: UMIN000031205). en-copyright= kn-copyright= en-aut-name=WadaKoichiro en-aut-sei=Wada en-aut-mei=Koichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ArakiMotoo en-aut-sei=Araki en-aut-mei=Motoo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TanimotoRyuta en-aut-sei=Tanimoto en-aut-mei=Ryuta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SadahiraTakuya en-aut-sei=Sadahira en-aut-mei=Takuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WatariShogo en-aut-sei=Watari en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MaruyamaYuki en-aut-sei=Maruyama en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MitsuiYosuke en-aut-sei=Mitsui en-aut-mei=Yosuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NakajimaHirochika en-aut-sei=Nakajima en-aut-mei=Hirochika kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=AcostaHerik en-aut-sei=Acosta en-aut-mei=Herik kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KatayamaSatoshi en-aut-sei=Katayama en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=IwataTakehiro en-aut-sei=Iwata en-aut-mei=Takehiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=NishimuraShingo en-aut-sei=Nishimura en-aut-mei=Shingo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=TakamotoAtsushi en-aut-sei=Takamoto en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=SakoTomoko en-aut-sei=Sako en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=EdamuraKohei en-aut-sei=Edamura en-aut-mei=Kohei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=KobayashiYasuyuki en-aut-sei=Kobayashi en-aut-mei=Yasuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=WatanabeMasami en-aut-sei=Watanabe en-aut-mei=Masami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=WatanabeToyohiko en-aut-sei=Watanabe en-aut-mei=Toyohiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=NasuYasutomo en-aut-sei=Nasu en-aut-mei=Yasutomo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= affil-num=1 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Urology, Kagawa Prefectural Central Hospital kn-affil= affil-num=4 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Urology, Fukuyama City Hospital kn-affil= affil-num=9 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=11 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=12 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=13 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=14 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=15 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=16 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=17 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=18 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=19 en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Photodynamic diagnosis kn-keyword=Photodynamic diagnosis en-keyword=5-Aminolevulinic acid kn-keyword=5-Aminolevulinic acid en-keyword=ALA-PDD kn-keyword=ALA-PDD en-keyword=Upper urinary tract urothelial carcinoma kn-keyword=Upper urinary tract urothelial carcinoma en-keyword=VISERA ELITE video system kn-keyword=VISERA ELITE video system END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20201227 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=MYCN-amplified neuroblastomaに対するMYCN抑制を介したテロメラーゼ標的腫瘍溶解ウイルス治療 kn-title=Elimination of MYCN-Amplified Neuroblastoma Cells by Telomerase-Targeted Oncolytic Virus via MYCN Suppression en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoTerutaka en-aut-sei=Tanimoto en-aut-mei=Terutaka kn-aut-name=谷本光 kn-aut-sei=谷本 kn-aut-mei=光 aut-affil-num=1 ORCID= affil-num=1 en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil=岡山大学大学院医歯薬学総合研究科 END start-ver=1.4 cd-journal=joma no-vol=15 cd-vols= no-issue=8 article-no= start-page=e0236935 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200827 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Nintedanib can be used safely and effectively for idiopathic pulmonary fibrosis with predicted forced vital capacity <= 50%: A multi-center retrospective analysis en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background
Nintedanib is a multi-kinase inhibitor approved for idiopathic pulmonary fibrosis (IPF); however, its efficacy and safety for patients with IPF and restricted pulmonary function remain unclear. Therefore, the objective of this study was to determine the efficacy and safety of nintedanib for patients with IPF and forced vital capacity (FVC) ? 50%.
Methods
This was a multi-center retrospective study performed by the Okayama Respiratory Disease Study Group. Patients were allocated into FVC ? 50% and FVC > 50% groups based on their predicted FVC. The primary endpoints were FVC changes from baseline after 6 and 12 months.
Results
45 patients were eligible for the study. 18 patients had FVC ? 50%, and 27 patients had FVC > 50%. Overall, 31 and 19 patients underwent pulmonary function tests at 6 and 12 months after initiating nintedanib, respectively. FVC changes from baseline at 6 and 12 months after initiating nintedanib were comparable between the two groups. Adverse events were seen in all patients, and the rates of patients who discontinued nintedanib were also comparable (38.9% vs. 37.0%, p = 1.000). Multiple regression analysis showed that age and forced expiratory volume in 1 second (FEV1)/FVC were negatively correlated with changes in FVC at 6 months after initiating nintedanib.
Conclusions
Our data suggest that nintedanib can be a useful agent for IPF patients, including those with a low FVC, and that age and FEV1/FVC are predictive markers for changes in FVC following nintedanib treatment. en-copyright= kn-copyright= en-aut-name=SenooSatoru en-aut-sei=Senoo en-aut-mei=Satoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TaniguchiAkihiko en-aut-sei=Taniguchi en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OdaNaohiro en-aut-sei=Oda en-aut-mei=Naohiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ItanoJunko en-aut-sei=Itano en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HigoHisao en-aut-sei=Higo en-aut-mei=Hisao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HaraNaofumi en-aut-sei=Hara en-aut-mei=Naofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=WatanabeHiromi en-aut-sei=Watanabe en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KanoHirohisa en-aut-sei=Kano en-aut-mei=Hirohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=SuwakiToshimitsu en-aut-sei=Suwaki en-aut-mei=Toshimitsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=FuchimotoYasuko en-aut-sei=Fuchimoto en-aut-mei=Yasuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KajimotoKazuhiro en-aut-sei=Kajimoto en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=IchikawaHirohisa en-aut-sei=Ichikawa en-aut-mei=Hirohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=KudoKenichiro en-aut-sei=Kudo en-aut-mei=Kenichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=ShibayamaTakuo en-aut-sei=Shibayama en-aut-mei=Takuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=KuyamaShoichi en-aut-sei=Kuyama en-aut-mei=Shoichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=20 ORCID= en-aut-name=Okayama Respiratory Disease Study Group (ORDSG) en-aut-sei=Okayama Respiratory Disease Study Group (ORDSG) en-aut-mei= kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=21 ORCID= affil-num=1 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences kn-affil= affil-num=3 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=10 en-affil=Department of Respiratory Medicine, Okayama City Hospital kn-affil= affil-num=11 en-affil=Department of Respiratory Medicine, Japan Organization of Occupational Health and Safety Okayama Rosai Hospita kn-affil= affil-num=12 en-affil=Department of Respiratory Medicine, Japanese Red Cross Kobe Hospita kn-affil= affil-num=13 en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital kn-affil= affil-num=14 en-affil=Department of Respiratory Medicine, National Hospital Organization Okayama Medical Center kn-affil= affil-num=15 en-affil=Department of Respiratory Medicine, National Hospital Organization Okayama Medical Center kn-affil= affil-num=16 en-affil=Department of Respiratory Medicine, National Hospital Organization Minami-Okayama Medical Center kn-affil= affil-num=17 en-affil=Department of Respiratory Medicine, National Hospital Organization Iwakuni Clinical Center kn-affil= affil-num=18 en-affil=Department of Respiratory Medicine, Japan Organization of Occupational Health and Safety Okayama Rosai Hospital kn-affil= affil-num=19 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=20 en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=21 en-affil= kn-affil= END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=3 article-no= start-page=185 end-page=189 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200223 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Deterioration of high-resolution computed tomography findings predicts disease progression after initial decline in forced vital capacity in idiopathic pulmonary fibrosis patients treated with pirfenidone en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background
Pirfenidone suppresses the decline of forced vital capacity (FVC) in patients with idiopathic pulmonary fibrosis (IPF). However, IPF progresses in some patients despite treatment. We analyzed patients with meaningful FVC declines during pirfenidone treatment and explored the factors predictive of disease progression after FVC decline.
Methods
This study was a retrospective, multicenter, observational study conducted by the Okayama Respiratory Disease Study Group. We defined initial decline in %FVC as 5% or greater per 6-month period during pirfenidone treatment. IPF patients who were treated with pirfenidone and experienced an initial decline from December 2008 to September 2017 were enrolled.
Results
We analyzed 21 patients with IPF. After the initial decline, 4 (19.0%) patients showed improvement in disease, 11 (52.4%) showed stable disease, and 6 (28.6%) showed progressive disease. There was no significant correlation between %FVC reduction on initial decline and subsequent %FVC change (p = 0.475). Deterioration of high-resolution computed tomography (HRCT) findings on initial decline was observed significantly more often in the progressive versus improved/stable disease groups (100% vs 20.0%, p = 0.009).
Conclusions
We revealed that deterioration of HRCT findings may predict disease progression after the initial decline in %FVC in IPF patients treated with pirfenidone. en-copyright= kn-copyright= en-aut-name=HigoHisao en-aut-sei=Higo en-aut-mei=Hisao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TaniguchiAkihiko en-aut-sei=Taniguchi en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SenooSatoru en-aut-sei=Senoo en-aut-mei=Satoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ItanoJunko en-aut-sei=Itano en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=WatanabeHiromi en-aut-sei=Watanabe en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OdaNaohiro en-aut-sei=Oda en-aut-mei=Naohiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KayataniHiroe en-aut-sei=Kayatani en-aut-mei=Hiroe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IchikawaHirohisa en-aut-sei=Ichikawa en-aut-mei=Hirohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=ShibayamaTakuo en-aut-sei=Shibayama en-aut-mei=Takuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KajimotoKazuhiro en-aut-sei=Kajimoto en-aut-mei=Kazuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name= OKAYAMA respiratory disease study group (ORDSG) en-aut-sei= OKAYAMA respiratory disease study group (ORDSG) en-aut-mei= kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= affil-num=1 en-affil=Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Okayama University Hospital kn-affil= affil-num=3 en-affil=Okayama University Hospital kn-affil= affil-num=4 en-affil=Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=8 en-affil=National Hospital Organization Okayama Medical Center kn-affil= affil-num=9 en-affil=KKR Takamatsu Hospita kn-affil= affil-num=10 en-affil=National Hospital Organization Okayama Medical Center kn-affil= affil-num=11 en-affil=Kobe Red Cross Hospital kn-affil= affil-num=12 en-affil=National Hospital Organization Minami-Okayama Medical Center kn-affil= affil-num=13 en-affil=Okayama Rosai Hospital kn-affil= affil-num=14 en-affil=Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=15 en-affil=Okayama University Hospital kn-affil= affil-num=16 en-affil= kn-affil= en-keyword=Idiopathic pulmonary fibrosis kn-keyword=Idiopathic pulmonary fibrosis en-keyword=High-resolution computed tomography kn-keyword=High-resolution computed tomography en-keyword=Pirfenidone kn-keyword=Pirfenidone en-keyword=Forced vital capacity kn-keyword=Forced vital capacity END start-ver=1.4 cd-journal=joma no-vol=117 cd-vols= no-issue=1 article-no= start-page=99 end-page=110 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20190709 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Alteration of Membrane Physicochemical Properties by Two Factors for Membrane Protein Integration en-subtitle= kn-subtitle= en-abstract= kn-abstract= After a nascent chain of a membrane protein emerges from the ribosomal tunnel, the protein is integrated into the cell membrane. This process is controlled by a series of proteinaceous molecular devices, such as signal recognition particles and Sec translocons. In addition to these proteins, we discovered two endogenous components regulating membrane protein integration in the inner membrane of Escherichia coli. The integration is blocked by diacylglycerol (DAG), whereas the blocking is relieved by a glycolipid named membrane protein integrase (MPIase). Here, we investigated the influence of these integration-blocking and integration-promoting factors on the physicochemical properties of membrane lipids via solid-state NMR and fluorescence measurements. These factors did not have destructive effects on membrane morphology because the membrane maintained its lamellar structure and did not fuse in the presence of DAG and/or MPIase at their effective concentrations. We next focused on membrane flexibility. DAG did not affect the mobility of the membrane surface, whereas the sugar chain in MPIase was highly mobile and enhanced the flexibility of membrane lipid headgroups. Comparison with a synthetic MPIase analog revealed the effects of the long sugar chain on membrane properties. The acyl chain order inside the membrane was increased by DAG, whereas the increase was cancelled by the addition of MPIase. MPIase also loosened the membrane lipid packing. Focusing on the transbilayer movement, MPIase reduced the rapid flip-flop motion of DAG. On the other hand, MPIase could not compensate for the diminished lateral diffusion by DAG. These results suggest that by manipulating the membrane lipids dynamics, DAG inhibits the protein from contacting the inner membrane, whereas the flexible long sugar chain of MPIase increases the opportunity for interaction between the membrane and the protein, leading to membrane integration of the newly formed protein. en-copyright= kn-copyright= en-aut-name=NomuraKaoru en-aut-sei=Nomura en-aut-mei=Kaoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YamaguchiToshiyuki en-aut-sei=Yamaguchi en-aut-mei=Toshiyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MoriShoko en-aut-sei=Mori en-aut-mei=Shoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FujikawaKohki en-aut-sei=Fujikawa en-aut-mei=Kohki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NishiyamaKen-ichi en-aut-sei=Nishiyama en-aut-mei=Ken-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ShimanouchiToshinori en-aut-sei=Shimanouchi en-aut-mei=Toshinori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MorigakiKenichi en-aut-sei=Morigaki en-aut-mei=Kenichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=ShimamotoKeiko en-aut-sei=Shimamoto en-aut-mei=Keiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences kn-affil= affil-num=2 en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences kn-affil= affil-num=3 en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences kn-affil= affil-num=4 en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences kn-affil= affil-num=5 en-affil=Department of Biological Chemistry and Food Sciences, Faculty of Agriculture, Iwate University kn-affil= affil-num=6 en-affil=Graduate School of Environmental Science, Okayama University kn-affil= affil-num=7 en-affil=Graduate School of Agricultural Science, Kobe University kn-affil= affil-num=8 en-affil=Biosignal Research Center, Kobe University kn-affil= affil-num=9 en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences kn-affil= END start-ver=1.4 cd-journal=joma no-vol=129 cd-vols= no-issue=3 article-no= start-page=207 end-page=209 dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=20171201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Report of the 15th Annual Meeting of the Japanese Society of Medical Oncology kn-title=第15回日本臨床腫瘍学会学術総会開催報告 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Hematology and Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=5 article-no= start-page=453 end-page=457 dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=201710 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Protective Effects of Bisoprolol against Acute Exacerbation in Moderate-to-Severe Chronic Obstructive Pulmonary Disease en-subtitle= kn-subtitle= en-abstract= kn-abstract= Although recent retrospective studies suggested that the use of β-blockers appears to help improve the mortality rate and decrease the rate of exacerbation in chronic obstructive pulmonary disease (COPD) patients with heart failure, the effects of β-blockers on COPD patients without heart failure have not been established. Based on previous reports, we have launched a multicenter, prospective, single-arm phase II study to evaluate the preventive effect of the cardioselective β-blocker bisoprolol in COPD exacerbation, in Japanese individuals with moderate-to-severe COPD who do not have heart failure but do have hypertension requiring the use of medication. The primary endpoint is the rate of mild-to-severe COPD exacerbation. The results of this study will clarify whether bisoprolol can prevent exacerbation in COPD patients without heart failure. en-copyright= kn-copyright= en-aut-name=TaniguchiAkihiko en-aut-sei=Taniguchi en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OdaNaohiro en-aut-sei=Oda en-aut-mei=Naohiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MorichikaDaisuke en-aut-sei=Morichika en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OzeIsao en-aut-sei=Oze en-aut-mei=Isao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IchikawaHirohisa en-aut-sei=Ichikawa en-aut-mei=Hirohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=FujiiUtako en-aut-sei=Fujii en-aut-mei=Utako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=2 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=4 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=5 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=6 en-affil=Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute kn-affil= affil-num=7 en-affil=National Hospital Organization Minami-Okayama Medical Center kn-affil= affil-num=8 en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital kn-affil= affil-num=9 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=10 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=11 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= affil-num=12 en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital kn-affil= en-keyword=chronic obstructive pulmonary disease kn-keyword=chronic obstructive pulmonary disease en-keyword=β-blocker kn-keyword=β-blocker en-keyword=bisoprolol kn-keyword=bisoprolol en-keyword=exacerbation kn-keyword=exacerbation en-keyword=heart failure kn-keyword=heart failure END start-ver=1.4 cd-journal=joma no-vol=128 cd-vols= no-issue=3 article-no= start-page=243 end-page=244 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=20161201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The 7th Japanese Society of Hematology, International Symposium kn-title=第7 回日本血液学会（IJH）国際シンポジウム報告 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=1 ORCID= affil-num=1 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 END start-ver=1.4 cd-journal=joma no-vol=128 cd-vols= no-issue=3 article-no= start-page=207 end-page=212 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=20161201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Long-term survival of two patients with esophageal neuroendocrine carcinoma who underwent multidisciplinary therapy kn-title=集学的治療により長期生存が得られた食道神経内分泌癌の2 例 en-subtitle= kn-subtitle= en-abstract= kn-abstract=　Esophageal neuroendocrine carcinoma （ECC） is rare and has a poor prognosis when presenting with vascular invasion and distant metastasis from an early stage. Multidisciplinary therapy with surgery, chemotherapy, and radiation therapy may prolong survival in patients with advanced ECC, but there is as yet no standard therapy for advanced ECC. We treated two patients who have achieved long-term survival （＞ 4 years） who underwent multidisciplinary therapy, including chemotherapy, for ECC. Our experience with these two cases suggests that multidisciplinary therapy, including chemotherapy, may be effective for treating ECC at an advanced stage. en-copyright= kn-copyright= en-aut-name=GotodaTatsuhiro en-aut-sei=Gotoda en-aut-mei=Tatsuhiro kn-aut-name=後藤田達洋 kn-aut-sei=後藤田 kn-aut-mei=達洋 aut-affil-num=1 ORCID= en-aut-name=KawanoSeiji en-aut-sei=Kawano en-aut-mei=Seiji kn-aut-name=川野誠司 kn-aut-sei=川野 kn-aut-mei=誠司 aut-affil-num=2 ORCID= en-aut-name=KonoYoshiyasu en-aut-sei=Kono en-aut-mei=Yoshiyasu kn-aut-name=河野吉泰 kn-aut-sei=河野 kn-aut-mei=吉泰 aut-affil-num=3 ORCID= en-aut-name=MiuraKou en-aut-sei=Miura en-aut-mei=Kou kn-aut-name=三浦公 kn-aut-sei=三浦 kn-aut-mei=公 aut-affil-num=4 ORCID= en-aut-name=KanzakiHiromitsu en-aut-sei=Kanzaki en-aut-mei=Hiromitsu kn-aut-name=神崎洋光 kn-aut-sei=神崎 kn-aut-mei=洋光 aut-affil-num=5 ORCID= en-aut-name=IwamuroMasaya en-aut-sei=Iwamuro en-aut-mei=Masaya kn-aut-name=岩室雅也 kn-aut-sei=岩室 kn-aut-mei=雅也 aut-affil-num=6 ORCID= en-aut-name=KawaharaYoshiro en-aut-sei=Kawahara en-aut-mei=Yoshiro kn-aut-name=河原祥朗 kn-aut-sei=河原 kn-aut-mei=祥朗 aut-affil-num=7 ORCID= en-aut-name=TanakaTakehiro en-aut-sei=Tanaka en-aut-mei=Takehiro kn-aut-name=田中健大 kn-aut-sei=田中 kn-aut-mei=健大 aut-affil-num=8 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name=吉野正 kn-aut-sei=吉野 kn-aut-mei=正 aut-affil-num=9 ORCID= en-aut-name=ShirakawadYasuhiro en-aut-sei=Shirakawad en-aut-mei=Yasuhiro kn-aut-name=白川靖博 kn-aut-sei=白川 kn-aut-mei=靖博 aut-affil-num=10 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name=田端雅弘 kn-aut-sei=田端 kn-aut-mei=雅弘 aut-affil-num=11 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=12 ORCID= en-aut-name=OkadaHiroyuki en-aut-sei=Okada en-aut-mei=Hiroyuki kn-aut-name=岡田裕之 kn-aut-sei=岡田 kn-aut-mei=裕之 aut-affil-num=13 ORCID= affil-num=1 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 affil-num=2 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 affil-num=3 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 affil-num=4 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 affil-num=5 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 affil-num=6 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 affil-num=7 en-affil=Department of Endoscopy, Okayama University Hospital kn-affil=岡山大学病院　光学医療診療部 affil-num=8 en-affil=Department of Pathology, , Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　病理学（腫瘍病理） affil-num=9 en-affil=Department of Pathology, , Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　病理学（腫瘍病理） affil-num=10 en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化管外科学 affil-num=11 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍内科学 affil-num=12 en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍内科学 affil-num=13 en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine， Dentistry and Pharmaceutical Sciences kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・肝臓内科学 en-keyword=食道神経内分泌腫瘍（esophageal neuroendocrine carcinoma） kn-keyword=食道神経内分泌腫瘍（esophageal neuroendocrine carcinoma） en-keyword=小細胞癌（small cell carcinoma） kn-keyword=小細胞癌（small cell carcinoma） en-keyword=集学的治療（multidisciplinary therapy） kn-keyword=集学的治療（multidisciplinary therapy） END start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=5 article-no= start-page=429 end-page=433 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201610 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Phase I/IIa Study of Low Dose Subcutaneous Interleukin-2 (IL-2) for Treatment of Refractory Chronic Graft Versus Host Disease en-subtitle= kn-subtitle= en-abstract= kn-abstract=Chronic graft versus host disease (cGVHD) remains a major problem for long survivors after allogeneic hematopoietic stem cell transplantation (HSCT). Currently, corticosteroid therapy is effective for cGVHD as the first line therapy. However, prolonged therapy with corticosteroids causes various severe adverse events. To develop the new therapeutic strategy of cGVHD, we have launched a multicenter phase I/IIa clinical trial of low dose subcutaneous interleukin-2 (IL-2) for treatment of steroid refractory cGVHD, which is constituted of 2 sequential phases (induction phase and maitanance phase). This study will provide the new therapeutic option for patients with refractory cGVHD after allogeneic HSCT. en-copyright= kn-copyright= en-aut-name=AsanoTakeru en-aut-sei=Asano en-aut-mei=Takeru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsuokaKen-ichi en-aut-sei=Matsuoka en-aut-mei=Ken-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IyamaSatoshi en-aut-sei=Iyama en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OhashiKazuteru en-aut-sei=Ohashi en-aut-mei=Kazuteru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=InamotoYoshihiro en-aut-sei=Inamoto en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OhwadaChikako en-aut-sei=Ohwada en-aut-mei=Chikako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MurataMakoto en-aut-sei=Murata en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SatakeAtsushi en-aut-sei=Satake en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=YoshidaChikamasa en-aut-sei=Yoshida en-aut-mei=Chikamasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=NakaseKoichi en-aut-sei=Nakase en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MoriYasuo en-aut-sei=Mori en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= affil-num=2 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Medical Oncology and Hematology, Sapporo Medical University Hospital kn-affil= affil-num=4 en-affil=Hematology division, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital kn-affil= affil-num=5 en-affil=Department of Hematopoietic Stem Cell Transplantation, National Cancer Center Hospital kn-affil= affil-num=6 en-affil=Department of Hematology, Chiba University Hospital kn-affil= affil-num=7 en-affil=Department of Hematology and Oncology, Nagoya University Graduate School of Medicine kn-affil= affil-num=8 en-affil=First Department of Internal Medicine, Kansai Medical University kn-affil= affil-num=9 en-affil=Division of Hematology, National Hospital Organization Minami-Okayama Medical Center kn-affil= affil-num=10 en-affil=Division of Hematology, Ehime Prefectural Central Hospital kn-affil= affil-num=11 en-affil=Department of Hematology and Oncology, Kyushu University Hospital kn-affil= affil-num=12 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= en-keyword=chronic GVHD kn-keyword=chronic GVHD en-keyword=allogeneic HSCT kn-keyword=allogeneic HSCT en-keyword=steroid refractory kn-keyword=steroid refractory en-keyword=IL-2 kn-keyword=IL-2 END start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=5 article-no= start-page=409 end-page=412 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201610 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=An Open-labeled, Multicenter Phase II Study of Tamibarotene in Patients with Steroid-refractory Chronic Graft-versus-Host Disease en-subtitle= kn-subtitle= en-abstract= kn-abstract=Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity following allogeneic hematopoietic cell transplantation (HSCT). Retinoic acid (tamibarotene) exerts multiple effects on cell differentiation and is clinically used for the treatment of acute promyelocytic leukemia. Tamibarotene down-regulates both Th1 and Th17 differentiation in donor T cells after allogeneic HSCT, resulting in attenuation of experimental chronic GVHD. Based on preclinical data, we have launched a phase II study of tamibarotene in patients with steroid-refractory chronic GVHD. This study will clarify whether tamibarotene can exert beneficial effects in patients with steroid-refractory chronic GVHD. en-copyright= kn-copyright= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=InamotoYoshihiro en-aut-sei=Inamoto en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NakamaeHirohisa en-aut-sei=Nakamae en-aut-mei=Hirohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SawaMasashi en-aut-sei=Sawa en-aut-mei=Masashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MoriYasuo en-aut-sei=Mori en-aut-mei=Yasuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OhashiKazuteru en-aut-sei=Ohashi en-aut-mei=Kazuteru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=FujiwaraShin-ichiro en-aut-sei=Fujiwara en-aut-mei=Shin-ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= affil-num=2 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Hematopoietic Stem Cell Transplantation, National Cancer Center Hospital kn-affil= affil-num=4 en-affil=Department of Hematology, Osaka City University Hospital kn-affil= affil-num=5 en-affil=Department of Hematology and Oncology, Anjo Kosei Hospital kn-affil= affil-num=6 en-affil=Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences kn-affil= affil-num=7 en-affil=Hematology Division, Tokyo Metropolitan Cancer and Infectious Diseases Center kn-affil= affil-num=8 en-affil=Division of Hematology, Department of Medicine, Jichi Medical University kn-affil= affil-num=9 en-affil=Department of Hematology and Oncology, Okayama University Hospital kn-affil= en-keyword=Am80 kn-keyword=Am80 en-keyword=tamibarotene kn-keyword=tamibarotene en-keyword=retinoid kn-keyword=retinoid en-keyword=chronic GVHD kn-keyword=chronic GVHD en-keyword=steroid-refractory GVHD kn-keyword=steroid-refractory GVHD END start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=4 article-no= start-page=273 end-page=277 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201608 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Heerfordt’s Syndrome Associated with a High Fever and Elevation of TNF-α en-subtitle= kn-subtitle= en-abstract= kn-abstract=Heerfordt?s syndrome is a rare manifestation of sarcoidosis and is defined as a combination of facial palsy, parotid swelling, and uveitis, associated with a low-grade fever. We report a case of Heerfordt?s syndrome presenting with a high fever and increased serum tumor necrosis factor alpha (TNF-α) levels. The patient had facial palsy, parotid swelling, uveitis, and swelling of the right supraclavicular and hilar lymph nodes. Corticosteroid therapy was initiated, and her symptoms soon resolved completely, in tandem with a decrease in TNF-α serum levels. en-copyright= kn-copyright= en-aut-name=MakimotoGo en-aut-sei=Makimoto en-aut-mei=Go kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YoshikawaMao en-aut-sei=Yoshikawa en-aut-mei=Mao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TaniguchiAkihiko en-aut-sei=Taniguchi en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= affil-num=2 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= affil-num=3 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= affil-num=4 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= affil-num=5 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= affil-num=6 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= affil-num=7 en-affil=Department of Respiratory and Allergy Medicine, Okayama University Hospital kn-affil= en-keyword=Heerfordt?s syndrome kn-keyword=Heerfordt?s syndrome en-keyword=sarcoidosis kn-keyword=sarcoidosis en-keyword=TNF-α kn-keyword=TNF-α END start-ver=1.4 cd-journal=joma no-vol=70 cd-vols= no-issue=4 article-no= start-page=243 end-page=253 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201608 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effect of Vandetanib on Lung Tumorigenesis in Transgenic Mice Carrying an Activating Egfr Gene Mutation en-subtitle= kn-subtitle= en-abstract= kn-abstract=Vandetanib (ZactimaTM) is a novel, orally available inhibitor of both vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR) tyrosine kinase. In the present study, a line of transgenic mice with a mouse Egfr gene mutation (delE748-A752) corresponding to a human EGFR mutation (delE746-A750) was established. The transgenic mice developed atypical adenomatous hyperplasia to adenocarcinoma of the lung at around 5 weeks of age and died of lung tumors at approximately 17 weeks of age. In the mice treated with vandetanib (6mg/kg/day), these lung tumors disappeared and the phosphorylations of EGFR and VEGFR-2 were reduced in lung tissues to levels comparable to those of non-transgenic control mice. The median overall survival time of the transgenic mice was 28 weeks in the vandetanib-treated group and 17 weeks in the vehicle-treated group. Vandetanib significantly prolonged the survival of the transgenic mice (log-rank test, p＜0.01); resistance to vandetanib occurred at 20 weeks of age and the animals died from their lung tumors at about 28 weeks of age. These data suggest that vandetanib could suppress the progression of tumors harboring an activating EGFR mutation. en-copyright= kn-copyright= en-aut-name=OsawaMasahiro en-aut-sei=Osawa en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OhashiKadoaki en-aut-sei=Ohashi en-aut-mei=Kadoaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KuboToshio en-aut-sei=Kubo en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakataSaburo en-aut-sei=Takata en-aut-mei=Saburo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=Takata Minoru en-aut-sei=Takata en-aut-mei=Minoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of General Internal Medicine 4, Kawasaki Medical School kn-affil= affil-num=7 en-affil=Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Kyoto University kn-affil= affil-num=8 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=9 en-affil=Department of Haematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=vandetanib kn-keyword=vandetanib en-keyword=VEGFR kn-keyword=VEGFR en-keyword=EGFR kn-keyword=EGFR en-keyword=nonsmall cell lung cancer kn-keyword=nonsmall cell lung cancer en-keyword=transgenic mouse kn-keyword=transgenic mouse END start-ver=1.4 cd-journal=joma no-vol=128 cd-vols= no-issue=2 article-no= start-page=125 end-page=128 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=20160801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The effectiveness of team-based learning (TBL) as a new teaching approach kn-title=新教育技法「チーム基盤型学習（TBL）」の有用性 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=SunoManabu en-aut-sei=Suno en-aut-mei=Manabu kn-aut-name=須野学 kn-aut-sei=須野 kn-aut-mei=学 aut-affil-num=1 ORCID= affil-num=1 en-affil=Center for the Development of Medical and Health Care Education, Okayama University kn-affil=岡山大学医療教育統合開発センター en-keyword=アクティブラーニング（active learning） kn-keyword=アクティブラーニング（active learning） en-keyword=チーム基盤型学習（team-based learning） kn-keyword=チーム基盤型学習（team-based learning） en-keyword=問題基盤型学習（problem-based learning） kn-keyword=問題基盤型学習（problem-based learning） END start-ver=1.4 cd-journal=joma no-vol=128 cd-vols= no-issue=1 article-no= start-page=67 end-page=68 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=20160401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The 55th Annual Meeting of the Japanese Society for Lymphoreticular Tissue Research kn-title=第55回日本リンパ網内系学会総会報告 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 END start-ver=1.4 cd-journal=joma no-vol=127 cd-vols= no-issue=3 article-no= start-page=213 end-page=218 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=20151201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A case report of giant ectopic pheochromocytoma conversion therapy with radioisotope therapy and chemotherapy followed by curative resection kn-title=術前内照射および化学療法が著効し,根治切除し得た巨大異所性褐色細胞腫の1例 en-subtitle= kn-subtitle= en-abstract= kn-abstract=A 46-year-old man was found to be positive for occult blood at a medical checkup and was revealed to have a 14-cm tumor on the right side of abdominal aorta by a subsequent abdominal CT scan. The endocrinology laboratory data showed elevations in the levels of serum noradrenaline, and ectopic pheochromocytoma was suspected. The tumor was compressing the inferior vena cava and portal vein, the superior mesenteric artery and the pancreas. Since it would be difficult to cure by operation, neoadjuvant therapy was started using radioisotope therapy by I-131 metaiodobenzylguanidine (131I-MIBG) and chemotherapy (CVD therapy ; cyclophosphamide, vincristine, dacarbazine). He was treated with three courses of radioisotope therapy and 16 courses of chemotherapy, which significantly reduced the tumor size. This made radical resection possible ; we were able to avoid the merger excision of great vessels and other organs. On pathological and immunopathological findings, the tumor was diagnosed as ectopic　pheochromocytoma. Regarding the safety and curability of the treatment, neoadjuvant therapy may be useful in treating very large tumors that show invasion of other organs. en-copyright= kn-copyright= en-aut-name=YasuiKazuya en-aut-sei=Yasui en-aut-mei=Kazuya kn-aut-name=安井和也 kn-aut-sei=安井 kn-aut-mei=和也 aut-affil-num=1 ORCID= en-aut-name=UmedaYuzo en-aut-sei=Umeda en-aut-mei=Yuzo kn-aut-name=楳田祐三 kn-aut-sei=楳田 kn-aut-mei=祐三 aut-affil-num=2 ORCID= en-aut-name=KumanoKenjiro en-aut-sei=Kumano en-aut-mei=Kenjiro kn-aut-name=熊野健二郎 kn-aut-sei=熊野 kn-aut-mei=健二郎 aut-affil-num=3 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name=田端雅弘 kn-aut-sei=田端 kn-aut-mei=雅弘 aut-affil-num=4 ORCID= en-aut-name=OtsukaFumio en-aut-sei=Otsuka en-aut-mei=Fumio kn-aut-name=大塚文男 kn-aut-sei=大塚 kn-aut-mei=文男 aut-affil-num=5 ORCID= en-aut-name=YagiTakahito en-aut-sei=Yagi en-aut-mei=Takahito kn-aut-name=八木孝仁 kn-aut-sei=八木 kn-aut-mei=孝仁 aut-affil-num=6 ORCID= en-aut-name=FujiwaraToshiyoshi en-aut-sei=Fujiwara en-aut-mei=Toshiyoshi kn-aut-name=藤原俊義 kn-aut-sei=藤原 kn-aut-mei=俊義 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 en-keyword=異所性褐色細胞腫（ectopic pheochromocytoma） kn-keyword=異所性褐色細胞腫（ectopic pheochromocytoma） en-keyword=化学療法（chemo therapy） kn-keyword=化学療法（chemo therapy） en-keyword=131I-MIBG kn-keyword=131I-MIBG END start-ver=1.4 cd-journal=joma no-vol=21 cd-vols= no-issue=2 article-no= start-page=367 end-page=368 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201302 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Antibiotic sensitivity of bacteria on the oral mucosa after hematopoietic cell transplantation en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name=曽我賢彦 kn-aut-sei=曽我 kn-aut-mei=賢彦 aut-affil-num=1 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=EbinumaTakayuki en-aut-sei=Ebinuma en-aut-mei=Takayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MaedaHiroshi en-aut-sei=Maeda en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Division of Hospital Dentistry, Central Clinical Department, Okayama University Hospital affil-num=2 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Pathophysiology?Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Pathophysiology?Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Pathophysiology?Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=5 article-no= start-page=261 end-page=266 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=201510 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Pilot Analysis of Asbestos-induced Diffuse Pleural Thickening with Respiratory Compromise en-subtitle= kn-subtitle= en-abstract= kn-abstract=We investigated the clinical features of asbestos-induced diffuse pleural thickening (DPT) with severe respiratory compromise. We conducted a retrospective study of consecutive subjects with asbestos-induced DPT. Medical data such as initial symptoms, radiological findings, respiratory function test results, and clinical course were collected and analyzed. There were 24 patients between 2003 and 2012. All were men, and the median age at the development of DPT was 74 years. The top occupational category associated with asbestos exposure was dockyard workers. The median duration of asbestos exposure was 35.0 years, and the median latency from first exposure to the onset of DPT was 49.0 years. There were no significant differences in respiratory function test results between the higher and lower Brinkman index groups or between unilateral and bilateral DPT. Thirteen patients had a history of benign asbestos pleural effusion (BAPE), and the median duration from pleural fluid accumulation to DPT with severe respiratory compromise was 28.4 months. DPT with severe respiratory compromise can develop after a long latency following occupational asbestos exposure and a history of BAPE. en-copyright= kn-copyright= en-aut-name=NojimaDaisuke en-aut-sei=Nojima en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=FujimotoNobukazu en-aut-sei=Fujimoto en-aut-mei=Nobukazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KatoKatsuya en-aut-sei=Kato en-aut-mei=Katsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FuchimotoYasuko en-aut-sei=Fuchimoto en-aut-mei=Yasuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KishimotoTakumi en-aut-sei=Kishimoto en-aut-mei=Takumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Medical Oncology, Okayama Rosai Hospital affil-num=3 en-affil= kn-affil=Department of Radiology, Okayama University Hospital affil-num=4 en-affil= kn-affil=Department of Respiratory Medicine Okayama Rosai Hospital affil-num=5 en-affil= kn-affil=Department of Allergy and Respiratory Medicine (Thoracic Oncology), Okayama University Hospital affil-num=6 en-affil= kn-affil=Department of Internal Medicine, Okayama Rosai Hospital affil-num=7 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=asbestos kn-keyword=asbestos en-keyword=pleural thickening kn-keyword=pleural thickening en-keyword=MRC dyspnea scale kn-keyword=MRC dyspnea scale en-keyword=respiratory function test kn-keyword=respiratory function test en-keyword=costophrenic angle kn-keyword=costophrenic angle END start-ver=1.4 cd-journal=joma no-vol=22 cd-vols= no-issue=6 article-no= start-page=1679 end-page=1683 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201406 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Distribution of oral mucosal bacteria with mecA in patients undergoing hematopoietic cell transplantation en-subtitle= kn-subtitle= en-abstract= kn-abstract=[Purpose] We recently reported frequent detection of antibiotic-resistant bacteria on the oral mucosa during the period of hematopoietic cell transplantation (HCT) and suggested an association between oral mucositis and antibiotic-resistant bacterial infection. Methicillin-resistant Staphylococcus spp. were frequently detected, and the oral cavity may be a reservoir of the gene mediating methicillin resistance, mecA. Here, we examined the frequency of mecA carriers in patients undergoing HCT. [Methods] Fifty-nine patients (male (M)?=?37, female (F)?=?22, 47.3?±?11.0 years) receiving HCT were enrolled in this study. Buccal swab samples were obtained four times from day ?7 to day +20 (once/week), and mecA was detected by PCR. Fifty-two subjects without systemic disease, who completed dental treatment, especially periodontal treatment (M?=?21, F?=?31, 55.4?±?14.2 years), were also enrolled as controls and checked for mecA on the oral mucosa. [Results] Seventy-six percent (45/59) of the HCT patients carried mecA at least once in the study period (days ?7 to +20), while no control subjects had mecA. The frequency of mecA carriers was 19.2 % from days ?7 to ?1, while it was significantly increased on days +7 to +13 and +14 to +20, with frequencies of 60.9 and 63.2 %, respectively (P?5/μL. Gastroenteroscopy revealed an acute gastric and duodenal mucosal lesion that was treated successfully via endoscopic hemoclipping. Bone marrow aspiration revealed marked megakaryocyte proliferation with atypia of naked nuclei and marrow hypercellularity (90% cellularity). A fluorescence in situ hybridization test could not detect the BCR-ABL fusion gene. Bone marrow aspiration later revealed further abnormalities of megakaryocytes. The patient died from cerebral bleeding. The present case fulfilled 2 of the 3 major criteria of primary myelofibrosis according to the World Health Organization 2008 classification:namely, megakaryocytic hyperplasia with hypercellular marrow and granulocytic hyperplasia. However, the megakaryocytic abnormality was not strictly compatible with the criteria. Instead, we considered prefibrotic primary myelofibrosis as a possibility, although myelodysplastic syndrome/myeloproliferative neoplasm, unclassifiable (MDS/MPN-U) was technically the correct diagnosis. The present case shows that MPN diagnosis remains difficult and suggests that other cases of peripheral leukocytosis with diagnosed MDS/MPN-U might include similar findings. en-copyright= kn-copyright= en-aut-name=OtaSeisuke en-aut-sei=Ota en-aut-mei=Seisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HiramatsuYasushi en-aut-sei=Hiramatsu en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KondoEisei en-aut-sei=Kondo en-aut-mei=Eisei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KasaharaAkinori en-aut-sei=Kasahara en-aut-mei=Akinori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakadaSaimon en-aut-sei=Takada en-aut-mei=Saimon kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=UmenaSachio en-aut-sei=Umena en-aut-mei=Sachio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NoguchiToshio en-aut-sei=Noguchi en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MatsumuraTadashi en-aut-sei=Matsumura en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Internal Medicine, Himeji St. Mary?s Hospital affil-num=2 en-affil= kn-affil=Department of Hematologic Internal Medicine, Himeji Red Cross Hospital affil-num=3 en-affil= kn-affil=Department of Hematology and Oncology, Okayama University Hospital affil-num=4 en-affil= kn-affil=Department of Internal Medicine, Himeji St. Mary?s Hospital affil-num=5 en-affil= kn-affil=Department of Internal Medicine, Himeji St. Mary?s Hospital affil-num=6 en-affil= kn-affil=Department of Internal Medicine, Himeji St. Mary?s Hospital affil-num=7 en-affil= kn-affil=Department of Internal Medicine, Himeji St. Mary?s Hospital affil-num=8 en-affil= kn-affil=Department of Hematology and Oncology, Okayama University Hospital affil-num=9 en-affil= kn-affil=Department of Internal Medicine, Himeji St. Mary?s Hospital en-keyword=prefibrotic primary myelofibrosis kn-keyword=prefibrotic primary myelofibrosis en-keyword=leukocytosis kn-keyword=leukocytosis en-keyword=anemia kn-keyword=anemia en-keyword=acute gastric mucosal lesion kn-keyword=acute gastric mucosal lesion en-keyword=multiple cerebral hemorrhages kn-keyword=multiple cerebral hemorrhages END start-ver=1.4 cd-journal=joma no-vol=326 cd-vols= no-issue=2 article-no= start-page=201 end-page=209 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140815 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Everolimus prolonged survival in transgenic mice with EGFR-driven lung tumors en-subtitle= kn-subtitle= en-abstract= kn-abstract=Everolimus is an orally administered mTOR inhibitor. The effect, and mechanism of action, of everolimus on lung cancers with an epidermal growth factor receptor (EGFR) mutation remain unclear. Four gefitinib-sensitive and -resistant cell lines were used in the present work. Growth inhibition was determined using the MTT assay. Transgenic mice carrying the EGFR L858R mutation were treated with everolimus (10 mg/kg/day), or vehicle alone, from 5 to 20 weeks of age, and were then sacrificed. To evaluate the efficacy of everolimus in prolonging survival, everolimus (10 mg/kg/day) or vehicle was administered from 5 weeks of age. The four cell lines were similarly sensitive to everolimus. Expression of phosphorylated (p) mTOR and pS6 were suppressed upon treatment with everolimus in vitro, whereas the pAKT level increased. The numbers of lung tumors with a long axis exceeding 1 mm in the everolimus-treated and control groups were 1.9 +/- 0.9 and 9.4 +/- 3.2 (t-test, p<0.001), respectively. pS6 was suppressed during everolimus treatment. Although apoptosis and autophagy were not induced in everolimus-treated EGFR transgenic mice, angiogenesis was suppressed. The median survival time in the everolimus-treated group (58.0 weeks) was significantly longer than that in the control group (31.2 weeks) (logrank test, p<0.001). These findings suggest that everolimus had an indirect effect on tumor formation by inhibiting angiogenesis and might be effective to treat lung tumors induced by an activating EGFR gene mutation. en-copyright= kn-copyright= en-aut-name=YasugiMasayuki en-aut-sei=Yasugi en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OhashiKadoaki en-aut-sei=Ohashi en-aut-mei=Kadoaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HaradaDaijiro en-aut-sei=Harada en-aut-mei=Daijiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NinomiyaTakashi en-aut-sei=Ninomiya en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MurakamiToshi en-aut-sei=Murakami en-aut-mei=Toshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HondaYoshihiro en-aut-sei=Honda en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Kawasaki Hosp, Kawasaki Med Sch, Dept Gen Internal Med 4 affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=11 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med en-keyword=Non-small cell lung cancer kn-keyword=Non-small cell lung cancer en-keyword=Adenocarcinoma kn-keyword=Adenocarcinoma en-keyword=Everolimus kn-keyword=Everolimus en-keyword=mTOR kn-keyword=mTOR en-keyword=EGFR kn-keyword=EGFR END start-ver=1.4 cd-journal=joma no-vol=322 cd-vols= no-issue=1 article-no= start-page=168 end-page=177 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140310 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Src mediates ERK reactivation in gefitinib resistance in non-small cell lung cancer en-subtitle= kn-subtitle= en-abstract= kn-abstract=To study epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance mechanisms, we established a novel gefitinib-resistant lung cancer cell line derived from an EGFR-mutant non-small cell lung cancer cell line (PC-9) pretreated with 4-(methylnitrosamino)1-(3-pyridy1)-1-butanone (designated PC9-GR). We found that gefitinib substantially suppressed the EGFR signaling pathway, whereas ERK was reactivated after several hours in PC9-GR but not in PC-9. The combination of gefitinib with ERK inhibition (by U0126) restored gefitinib susceptibility in PC9-GR, but PI3K-Akt inhibition with LY294002 did not. Although the levels of phosphorylated Src were up-regulated simultaneously with ERK reactivation, neither ERK suppression using U0126 nor an ERK-specific siRNA induced Src phosphorylation. Furthermore, dual inhibition of EGFR and Src restored gefitinib sensitivity in PC9-GR in vitro and in vivo. In conclusion, our results indicate that Src-mediated ERK reactivation may play a role in a novel gefitinib resistance mechanism, and that the combined use of gefitinib with a Src inhibitor may be a potent strategy to overcome this resistance. en-copyright= kn-copyright= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HaradaDaijiro en-aut-sei=Harada en-aut-mei=Daijiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YasugiMasayuki en-aut-sei=Yasugi en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HottaKatsuyuki en-aut-sei=Hotta en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Kawasaki Hosp, Kawasaki Med Sch, Dept Gen Internal Med 4 affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ Hosp, Dept Resp Med en-keyword=EGFR kn-keyword=EGFR en-keyword=Src kn-keyword=Src en-keyword=ERK kn-keyword=ERK en-keyword=Lung cancer kn-keyword=Lung cancer en-keyword=Gefitinib kn-keyword=Gefitinib en-keyword=Resistance kn-keyword=Resistance END start-ver=1.4 cd-journal=joma no-vol=45 cd-vols= no-issue=7 article-no= start-page=1379 end-page=1387 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201407 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Low-grade B-cell lymphoma presenting primarily in the bone marrow en-subtitle= kn-subtitle= en-abstract= kn-abstract=Cases of low-grade B-cell lymphoma presenting primarily in the bone marrow are rare, and its clinicopathology remains unclear. We retrospectively examined patients with low-grade B-cell lymphoma presenting primarily in the bone marrow. Fourteen patients met the inclusion criteria, including 5 with lymphoplasmacytic lymphoma (LPL), 3 with chronic lymphocytic leukemia/small lymphocytic lymphoma, 2 with follicular lymphoma (FL), and 4 with low-grade B-cell lymphoma not otherwise specified (LGBCL-NOS). The median age was 69.5 years (range, 42-89 years), and a slight male predominance was noted (9 men and 5 women, 1.8: 1). Immunohistochemically, all cases were positive for CD20. One case was positive for CD138. Both cases of FL were positive for CD10 and B-cell lymphoma 2 (BCL-2), and immunoglobulin heavy locus (IgH)/B-cell lymphoma 2 rearrangement was observed by fluorescence in situ hybridization. The myeloid differentiation primary response gene (88) leucine to proline mutation was observed in 3 of 5 LPL, 1 of 2 FL, and 2 of 4 LGBCL-NOS patients. Paraproteinemia was observed in 10 patients; IgM and IgG paraproteinemia were observed in 6 and 3 patients, respectively. In this patient series, 3 patients had died at a median follow-up of 36.5 months; the cause of death of 1 LPL patient was malignant lymphoma itself. Thus, low-grade B-cell lymphoma presenting primarily in the bone marrow has various subtypes, and approximately one-third of the patients had LGBCL-NOS. The immunophenotypic features and myeloid differentiation primary response gene (88) leucine to proline mutation data of LGBCL-NOS suggested that some cases present with characteristics similar to those of LPL or marginal zone lymphoma. en-copyright= kn-copyright= en-aut-name=IwataniKayoko en-aut-sei=Iwatani en-aut-mei=Kayoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakataKatsuyoshi en-aut-sei=Takata en-aut-mei=Katsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SatoYasuharu en-aut-sei=Sato en-aut-mei=Yasuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Miyata-TakataTomoko en-aut-sei=Miyata-Takata en-aut-mei=Tomoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IwakiNoriko en-aut-sei=Iwaki en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=CuiWei en-aut-sei=Cui en-aut-mei=Wei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=Sawada-KitamuraSeiko en-aut-sei=Sawada-Kitamura en-aut-mei=Seiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SonobeHiroshi en-aut-sei=Sonobe en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TamuraMaiko en-aut-sei=Tamura en-aut-mei=Maiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=SaitoKatsuhiko en-aut-sei=Saito en-aut-mei=Katsuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=MiyataniKatsuya en-aut-sei=Miyatani en-aut-mei=Katsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=YamasakiRie en-aut-sei=Yamasaki en-aut-mei=Rie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=YamadoriIchiro en-aut-sei=Yamadori en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=TerasakiYasushi en-aut-sei=Terasaki en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=NakamuraNaoya en-aut-sei=Nakamura en-aut-mei=Naoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=7 en-affil= kn-affil=Kanazawa Univ Hosp, Div Pathol affil-num=8 en-affil= kn-affil=Chugoku Cent Hosp, Div Pathol affil-num=9 en-affil= kn-affil=Hiroshima City Hosp, Div Pathol affil-num=10 en-affil= kn-affil=Toyama City Hosp, Dept Pathol affil-num=11 en-affil= kn-affil=Mitoyo Gen Hosp, Div Pathol affil-num=12 en-affil= kn-affil=Natl Hosp Org Iwakuni, Ctr Clin, Div Pathol affil-num=13 en-affil= kn-affil=Natl Hosp Org Okayama, Med Ctr, Div Pathol affil-num=14 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=15 en-affil= kn-affil=Toyama City Hosp, Div Hematol affil-num=16 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=17 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=18 en-affil= kn-affil=Tokai Univ, Inst Med Sci, Dept Pathol affil-num=19 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol en-keyword=Low-grade B cell lymphoma kn-keyword=Low-grade B cell lymphoma en-keyword=Bone marrow kn-keyword=Bone marrow en-keyword=LGBCL-NOS kn-keyword=LGBCL-NOS en-keyword=MYD88 kn-keyword=MYD88 END start-ver=1.4 cd-journal=joma no-vol=83 cd-vols= no-issue=1 article-no= start-page=30 end-page=36 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effect of AZD1480 in an epidermal growth factor receptor-driven lung cancer model en-subtitle= kn-subtitle= en-abstract= kn-abstract=Objective: STAT3 plays a vital role in inducing and maintaining a pro-carcinogenic inflammatory microenvironment and is reported to be a critical mediator of the oncogenic effects of EGFR mutations. STAT3 activation is mediated through JAK family kinases. We investigated the effect of the JAK1/2 inhibitor AZD1480 on lung tumors induced by an activating EGFR mutation. Materials and methods: Three EGFR tyrosine kinase inhibitor-resistant cell lines (RPC-9, PC-9/Van-R and PC-9/ER3) established from PC-9 harboring an EGFR exon19 deletion mutation were used. Growth inhibition was measured using an MIT assay. Effects of AZD1480 were also evaluated in the xenograft model and in the EGFR transgenic mice model. Protein expressions were assessed by immunoblotting and immunohistochemistry. Group differences were compared using Student's t-test. To evaluate the efficacy of AZD1480 on survival, AZD1480 or vehicle was administered orally from 7 weeks of age of the transgenic mice. Overall survival curves were calculated using the Kaplan-Meier method. Results: The sensitivities of resistant and parent cells to AZD1480 were similar in vitro. AZD1480 (30 or 50 mg/kg/day, per os) reduced angiogenesis and revealed significant tumor regression in a mouse xenograft model: Subsequently, the transgenic mice were treated with AZD1480 (30 mg/kg/day) or vehicle alone. The numbers of lung tumors (long axis exceeding 1 mm) in the AZD1480-treated group and control group were 0.37 +/- 0.18 and 2.25 +/- 0.53 (p <0.001), respectively. AZD1480 treatment suppressed pSTAT3, pJAK1, pJAK2 and angiogenesis. The median survival time in the AZD1480-treated group (217 days) was significantly greater than that in the control group (106 days) (log-rank test, p <0.0001). Conclusion: AZD1480 may be effective against lung tumors driven by an activating EGER mutation. en-copyright= kn-copyright= en-aut-name=MurakamiToshi en-aut-sei=Murakami en-aut-mei=Toshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NinomiyaTakashi en-aut-sei=Ninomiya en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YasugiMasaaki en-aut-sei=Yasugi en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HondaYoshihiro en-aut-sei=Honda en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KuboToshio en-aut-sei=Kubo en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HottaKatsuyuki en-aut-sei=Hotta en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Internal Med 4 affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=4 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Internal Med 4 affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=11 en-affil= kn-affil=Okayama Univ Hosp, Dept Allergy & Resp Med en-keyword=Lung cancer kn-keyword=Lung cancer en-keyword=Oncogene addiction kn-keyword=Oncogene addiction en-keyword=EGFR kn-keyword=EGFR en-keyword=JAK2 kn-keyword=JAK2 en-keyword=STAT3 kn-keyword=STAT3 en-keyword=Transgenic mice kn-keyword=Transgenic mice END start-ver=1.4 cd-journal=joma no-vol=20 cd-vols= no-issue=2 article-no= start-page=183 end-page=191 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201402 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Mammalian Target of Rapamycin Inhibitors Permit Regulatory T Cell Reconstitution and Inhibit Experimental Chronic Graft-versus-Host Disease en-subtitle= kn-subtitle= en-abstract= kn-abstract=Chronic graft-versus-host disease (GVHD) remains a major late complication of allogeneic bone marrow transplantation (BMT). In a previous study, impaired thymic negative selection of the recipients permitted the emergence of pathogenic T cells that cause chronic GVHD using MHC class II-deficient (H2-Ab1 KO) B6 into OH model and CD4(+) T cells isolated from chronic GVHD mice caused chronic GVHD when administered into the secondary recipients. In this study, we evaluated the kinetics of regulatory T cell (Treg) reconstitution in wild type B6 into C3H model. After myeloablative conditioning, host Tregs disappeared rapidly, followed by expansion of Tregs derived from the donor splenic T cell inoculum. However, the donor splenic T cell derived Treg pool contracted gradually and was almost completely replaced by newly generated donor bone marrow (BM)-derived Tregs in the late post-transplantation period. Next, we compared the effects of cyclosporine (CSA) and mammalian target of rapamycin (mTOR) inhibitors on Treg reconstitution. Administration of CSA significantly impaired Treg reconstitution in the spleen and thymus. In contrast, BM-derived Treg reconstitution was not impaired in mTOR inhibitor-treated mice. Histopathological examination indicated that mice treated with GSA, but not mTOR inhibitors, showed pathogenic features of chronic GVHD on day 120. Mice treated with CSA until day 60, but not mTOR inhibitors, developed severe chronic GVHD followed by adoptive transfer of the pathogenic CD4(+) T cells isolated from H2-Ab1 KO into C3H model. These findings indicated that long-term use of CSA impairs reconstitution of BM-derived Tregs and increases the liability to chronic GVHD. The choice of immunosuppression, such as calcineurin inhibitor-free GVHD prophylaxis with mTOR inhibitor, may have important implications for the control of chronic GVHD after BMT. en-copyright= kn-copyright= en-aut-name=SugiyamaHaruko en-aut-sei=Sugiyama en-aut-mei=Haruko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamasujiYoshiko en-aut-sei=Yamasuji en-aut-mei=Yoshiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MatsuokaKen-ichi en-aut-sei=Matsuoka en-aut-mei=Ken-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KondoEisei en-aut-sei=Kondo en-aut-mei=Eisei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=ShinagawaKatsuji en-aut-sei=Shinagawa en-aut-mei=Katsuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanakaTakehiro en-aut-sei=Tanaka en-aut-mei=Takehiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TakeuchiKengo en-aut-sei=Takeuchi en-aut-mei=Kengo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TeshimaTakanori en-aut-sei=Teshima en-aut-mei=Takanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=2 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=3 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=4 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=5 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=6 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=7 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=8 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=10 en-affil= kn-affil=Japanese Fdn Canc Res, Inst Canc, Pathol Project Mol Target affil-num=11 en-affil= kn-affil=Hokkaido Univ, Dept Hematol affil-num=12 en-affil= kn-affil=Okayama Univ, Gradu Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol en-keyword=Chronic graft-versus-host disease (GVHD) kn-keyword=Chronic graft-versus-host disease (GVHD) en-keyword=Cyclosporine kn-keyword=Cyclosporine en-keyword=Mammalian target of rapamycin (mTOR) inhibitor kn-keyword=Mammalian target of rapamycin (mTOR) inhibitor en-keyword=Regulatory T cell kn-keyword=Regulatory T cell END start-ver=1.4 cd-journal=joma no-vol=100 cd-vols= no-issue=2 article-no= start-page=254 end-page=257 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201207 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Histological and immunohistochemical features of gingival enlargement in a patient with AML en-subtitle= kn-subtitle= en-abstract= kn-abstract=Here, we discuss the pathophysiology of leukemia-associated gingival enlargement based on a case of acute myelomonocytic leukemia (AML-M4) with typical gingival enlargement. Uniquely, this patient was well enough to allow full periodontal examination and incisional gingival biopsy to be performed both before and after chemotherapy. The patient was a 39-year-old Japanese woman with AML-M4 showing gingival enlargement. Histological and immunohistochemical features of gingiva and bacterial counts in the periodontal pockets were examined before and after chemotherapy. The results were as follows: (1) infiltration of myelomonocytic blasts in enlarged gingiva; (2) resolution of gingival enlargement with complete remission of AML by anticancer chemotherapy; and (3) the numbers of bacteria in the periodontal pockets were not high and were not altered before or after chemotherapy. In patients with AML-M4, remarkable mucosal enlargement is not generally observed in the body except in the gingiva. We hypothesized that antigens derived from periodontal bacteria, even if they are not present in large numbers, could act as chemoattractants for myelomonocytic leukemic cells. en-copyright= kn-copyright= en-aut-name=SonoiNorihiro en-aut-sei=Sonoi en-aut-mei=Norihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MaedaHiroshi en-aut-sei=Maeda en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IchimuraKoichi en-aut-sei=Ichimura en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AoyamaKazutoshi en-aut-sei=Aoyama en-aut-mei=Kazutoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=LoganRichard en-aut-sei=Logan en-aut-mei=Richard kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=Raber-DurlacherJudith en-aut-sei=Raber-Durlacher en-aut-mei=Judith kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Pathophysiol Periodontal Sci, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ Hosp, Cent Clin Dept, Div Hosp Dent affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Pathophysiol Periodontal Sci, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=10 en-affil= kn-affil=Univ Adelaide, Fac Hlth Sci, Sch Dent affil-num=11 en-affil= kn-affil=Acad Ctr Dent Amsterdam, Dept Periodontol affil-num=12 en-affil= kn-affil=Okayama Univ, Dept Pathophysiol Periodontal Sci, Grad Sch Med Dent & Pharmaceut Sci en-keyword=Gingival enlargement kn-keyword=Gingival enlargement en-keyword=Acute myelomonocytic leukemia kn-keyword=Acute myelomonocytic leukemia en-keyword=Pathogenesis kn-keyword=Pathogenesis en-keyword=Histology kn-keyword=Histology en-keyword=Immunohistochemistry kn-keyword=Immunohistochemistry END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=11 article-no= start-page=1440 end-page=1446 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201311 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Lower gefitinib dose led to earlier resistance acquisition before emergence of T790M mutation in epidermal growth factor receptor-mutated lung cancer model en-subtitle= kn-subtitle= en-abstract= kn-abstract=Non-small-cell lung cancers with epidermal growth factor receptor (EGFR) mutations are sensitive to EGFR tyrosine kinase inhibitors (TKIs); however, unlike cytotoxic agents, it is generally accepted that minimal doses of drugs inhibiting target molecules are sufficient when molecular-targeted agents, including EGFR-TKIs, are used. Thus, any utility of higher doses remains unclear. We compared low-dose (15mg/kg) gefitinib therapy with high-dose (50mg/kg) therapy using an EGFR-mutated lung cancer xenograft model. Both gefitinib doses induced tumor shrinkage, but tumors regrew in the low-dose group within 1month, whereas tumors in the high-dose group did not. Neither the T790M mutation nor MET amplification was apparent in regrown tumors. We also compared outcomes after two doses of gefitinib (5 and 25mg/kg) in a transgenic EGFR-mutated lung cancer mouse model. In line with the results obtained using the xenograft model, both gefitinib doses completely inhibited tumor growth, but tumors treated with the lower dose of gefitinib developed earlier drug resistance. In conclusion, a low gefitinib dose caused tumors to become drug-resistant prior to acquisition of the T790M mutation or MET amplification in EGFR-mutated models of lung cancer. This suggests that it is important to optimize the EGFR-TKI dose for treatment of EGFR mutation-associated lung cancer. Gefitinib may need to be given at a dose greater than the minimum required for inhibition of target molecules. en-copyright= kn-copyright= en-aut-name=HayakawaHiromi en-aut-sei=Hayakawa en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OhashiKadoaki en-aut-sei=Ohashi en-aut-mei=Kadoaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NinomiyaTakashi en-aut-sei=Ninomiya en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YasugiMasayuki en-aut-sei=Yasugi en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakataSaburo en-aut-sei=Takata en-aut-mei=Saburo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SakaiKatsuya en-aut-sei=Sakai en-aut-mei=Katsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MatsumotoKunio en-aut-sei=Matsumoto en-aut-mei=Kunio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Natl Hosp Org, Shikoku Canc Ctr, Dept Thorac Oncol affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Kanazawa Univ, Canc Res Inst, Div Tumor Dynam & Regulat affil-num=8 en-affil= kn-affil=Kanazawa Univ, Canc Res Inst, Div Tumor Dynam & Regulat affil-num=9 en-affil= kn-affil=Kawasaki Med Univ affil-num=10 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=11 en-affil= kn-affil=Okayama Univ Hosp, Dept Resp Med END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=2 article-no= start-page=151 end-page=153 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Guideline for the treatment of acute exacerbations of COPD and chronic bronchitis kn-title=慢性呼吸器疾患（COPD，気管支拡張症，陳旧性肺結核等）の気道感染症治療ガイドライン en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=国立病院機構南岡山医療センター　呼吸器・アレルギー内科 END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=2 article-no= start-page=143 end-page=150 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Molecular targeted therapy in myeloma and lymphoma kn-title=リンパ腫・骨髄腫 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=SaekiKyosuke en-aut-sei=Saeki en-aut-mei=Kyosuke kn-aut-name=佐伯恭昌 kn-aut-sei=佐伯 kn-aut-mei=恭昌 aut-affil-num=1 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name=前田嘉信 kn-aut-sei=前田 kn-aut-mei=嘉信 aut-affil-num=2 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=2 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=3 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 en-keyword=骨髄腫 kn-keyword=骨髄腫 en-keyword=リンパ腫 kn-keyword=リンパ腫 en-keyword=分子標的治療薬 kn-keyword=分子標的治療薬 END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=2 article-no= start-page=133 end-page=135 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Treatment for a non-compliant patient with cancer and epilepsy kn-title=癌告知後の精神症状の治療に難渋したてんかん既往のある癌患者の１例 en-subtitle= kn-subtitle= en-abstract= kn-abstract=　A 58-year-old man with cervical esophageal cancer and a history of epilepsy was treated with chemoradiotherapy from May of 2013. When tube feeding was initiated due to aspiration pneumonitis, the patient showed a degree of irritability that affected routine staff work and treatment compliance. We attempted to perform supportive care for maladjustment by the notice, the fast, and the tube feeding, but there was no improvement. After we added carbamazepine, primidone, and propericiazine (which had been canceled at the initiation of the tube feeding) to the patient's intravenous phenytoin, the symptoms and treatment compliance improved significantly. We concluded that the causes of the patient's irritability were maladjustment and his epilepsy. en-copyright= kn-copyright= en-aut-name=MinamiDaisuke en-aut-sei=Minami en-aut-mei=Daisuke kn-aut-name=南大輔 kn-aut-sei=南 kn-aut-mei=大輔 aut-affil-num=1 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name=市原英基 kn-aut-sei=市原 kn-aut-mei=英基 aut-affil-num=2 ORCID= en-aut-name=OkabeNobuyuki en-aut-sei=Okabe en-aut-mei=Nobuyuki kn-aut-name=岡部伸幸 kn-aut-sei=岡部 kn-aut-mei=伸幸 aut-affil-num=3 ORCID= en-aut-name=YokomichiNaosuke en-aut-sei=Yokomichi en-aut-mei=Naosuke kn-aut-name=横道直佑 kn-aut-sei=横道 kn-aut-mei=直佑 aut-affil-num=4 ORCID= en-aut-name=KougeNoriko en-aut-sei=Kouge en-aut-mei=Noriko kn-aut-name=高下典子 kn-aut-sei=高下 kn-aut-mei=典子 aut-affil-num=5 ORCID= en-aut-name=KajizonoMakoto en-aut-sei=Kajizono en-aut-mei=Makoto kn-aut-name=鍛治園誠 kn-aut-sei=鍛治園 kn-aut-mei=誠 aut-affil-num=6 ORCID= en-aut-name=AkimotoYutaka en-aut-sei=Akimoto en-aut-mei=Yutaka kn-aut-name=秋元悠 kn-aut-sei=秋元 kn-aut-mei=悠 aut-affil-num=7 ORCID= en-aut-name=HoriKeisuke en-aut-sei=Hori en-aut-mei=Keisuke kn-aut-name=堀圭介 kn-aut-sei=堀 kn-aut-mei=圭介 aut-affil-num=8 ORCID= en-aut-name=MatsubaraMinoru en-aut-sei=Matsubara en-aut-mei=Minoru kn-aut-name=松原稔 kn-aut-sei=松原 kn-aut-mei=稔 aut-affil-num=9 ORCID= en-aut-name=NasuJunichiro en-aut-sei=Nasu en-aut-mei=Junichiro kn-aut-name=那須淳一郎 kn-aut-sei=那須 kn-aut-mei=淳一郎 aut-affil-num=10 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=11 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=12 ORCID= en-aut-name=MatsuokaJunzi en-aut-sei=Matsuoka en-aut-mei=Junzi kn-aut-name=松岡順治 kn-aut-sei=松岡 kn-aut-mei=順治 aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　緩和支持医療科 affil-num=2 en-affil= kn-affil=岡山大学病院　血液・腫瘍・呼吸器内科 affil-num=3 en-affil= kn-affil=岡山大学病院　精神科神経科 affil-num=4 en-affil= kn-affil=岡山大学病院　緩和支持医療科 affil-num=5 en-affil= kn-affil=岡山大学病院　看護部 affil-num=6 en-affil= kn-affil=岡山大学病院　薬剤部 affil-num=7 en-affil= kn-affil=岡山大学病院　消化器内科 affil-num=8 en-affil= kn-affil=岡山大学病院　消化器内科 affil-num=9 en-affil= kn-affil=岡山大学病院　消化器内科 affil-num=10 en-affil= kn-affil=岡山大学病院　消化器内科 affil-num=11 en-affil= kn-affil=岡山大学病院　血液・腫瘍・呼吸器内科 affil-num=12 en-affil= kn-affil=岡山大学病院　血液・腫瘍・呼吸器内科 affil-num=13 en-affil= kn-affil=岡山大学病院　緩和支持医療科 en-keyword=てんかん（epilepsy） kn-keyword=てんかん（epilepsy） en-keyword=易怒性（irritability） kn-keyword=易怒性（irritability） en-keyword=適応障害（maladjustment） kn-keyword=適応障害（maladjustment） END start-ver=1.4 cd-journal=joma no-vol=14 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130120 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background: Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it's role in the inflammatory response of elastase-induced emphysema remains unclear. Methods: In a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL) fluid. Results: Wild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment. Conclusions: These data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression. en-copyright= kn-copyright= en-aut-name=KurimotoEtsuko en-aut-sei=Kurimoto en-aut-mei=Etsuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=WasedaKoichi en-aut-sei=Waseda en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TaniguchiAkihiko en-aut-sei=Taniguchi en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IkedaGenyo en-aut-sei=Ikeda en-aut-mei=Genyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KogaHikari en-aut-sei=Koga en-aut-mei=Hikari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KataokaMikio en-aut-sei=Kataoka en-aut-mei=Mikio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=IwakuraYoichiro en-aut-sei=Iwakura en-aut-mei=Yoichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=GelfandErwin W. en-aut-sei=Gelfand en-aut-mei=Erwin W. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med affil-num=11 en-affil= kn-affil=Univ Tokyo, Inst Med Sci, Ctr Expt Med & Syst Biol affil-num=12 en-affil= kn-affil=Natl Jewish Hlth, Dept Pediat, Div Cell Biol affil-num=13 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med en-keyword=IL-17 kn-keyword=IL-17 en-keyword=Elastase kn-keyword=Elastase en-keyword=Emphysema kn-keyword=Emphysema en-keyword=Chronic obstructive pulmonary disease kn-keyword=Chronic obstructive pulmonary disease END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=1 article-no= start-page=49 end-page=54 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Molecular targeted therapies in leukemia kn-title=白血病および白血病類縁疾患における分子標的治療 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name=前田嘉信 kn-aut-sei=前田 kn-aut-mei=嘉信 aut-affil-num=1 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=2 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 en-keyword=白血病 kn-keyword=白血病 en-keyword=分子標的薬 kn-keyword=分子標的薬 en-keyword=チロシンキナーゼ阻害薬 kn-keyword=チロシンキナーゼ阻害薬 END start-ver=1.4 cd-journal=joma no-vol=12 cd-vols= no-issue=5 article-no= start-page=589 end-page=597 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201305 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Afatinib Prolongs Survival Compared with Gefitinib in an Epidermal Growth Factor Receptor-Driven Lung Cancer Model en-subtitle= kn-subtitle= en-abstract= kn-abstract=An irreversible ErbB family blocker is expected to inhibit tumors with activating epidermal growth factor receptor (EGFR) mutations more strongly than reversible EGFR tyrosine kinase inhibitors and to overcome acquired resistance to the T790M secondary mutation. Eleven-week-old transgenic mice with Egfr exon 19 deletion mutation were treated with afatinib, gefitinib, or vehicle for 4 weeks. All mice were sacrificed at 15 weeks of age, and the number of superficial left lung tumors with a long axis exceeding 1 mm was counted. The afatinib-treated group had significantly fewer tumors than the vehicle group (P < 0.01) and tended to have fewer tumors than the gefitinib-treated group (P = 0.06). Pathologically, gefitinib-treated mice had clearer, more nodular tumors than afatinib-treated mice. Immunoblotting showed that afatinib suppressed not only pEGFR but also pHER2, and induced apoptosis for longer periods than gefitinib. Subsequently, when each drug was administered 5 days per week until death, afatinib significantly enhanced mouse survival compared with gefitinib (median survival time: 456 days vs. 376.5 days; log-rank test, P < 0.01). Finally, the combination of afatinib with bevacizumab was found to be superior to either drug alone in exon 19 deletion/T790M and L858R/T790M xenograft tumors. Overall, afatinib was more potent than gefitinib in tumors harboring an exon 19 deletion mutation, and the combination of afatinib with bevacizumab efficiently suppressed tumors harboring the T790M secondary mutation. en-copyright= kn-copyright= en-aut-name=NinomiyaTakashi en-aut-sei=Ninomiya en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MurakamiToshi en-aut-sei=Murakami en-aut-mei=Toshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=HondaYoshihiro en-aut-sei=Honda en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KuboToshio en-aut-sei=Kubo en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MinamiDaisuke en-aut-sei=Minami en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KudoKenichiro en-aut-sei=Kudo en-aut-mei=Kenichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Kawasaki Hosp, Dept Gen Internal Med 4, Kawasaki Med Sch affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=11 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med END start-ver=1.4 cd-journal=joma no-vol=44 cd-vols= no-issue=9 article-no= start-page=1927 end-page=1936 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201309 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Distinct morphologic, phenotypic, and clinical-course characteristics of indolent peripheral T-cell lymphoma en-subtitle= kn-subtitle= en-abstract= kn-abstract=Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) consists of a heterogeneous group of lymphomas. Patients. generally show an aggressive clinical course and very poor outcome. Although the 2008 World Health Organization classification of PTCL-NOS includes 3 variants, low-grade lymphoma is not Included. Of 277 PTCL-NOS cases recorded in our consultation files, we examined the clinicopathologic characteristics of 10 patients with T-cell lymphomas composed of small-sized cells with slight nuclear atypia. Eight patients showed extranodal involvement (5 patients, spleen; 3 patients, thyroid), and 5 patients were at clinical stage I or II. Histologically, all samples presented diffuse infiltrate of small lymphoid cells, with few mitotic figures. Immunohistologically, all samples were positive for CD3, and CD:20 Was detected in 5 samples. All samples showed a low Ki-67 labeling index (mean, 1.05%), and 7 samples were positive for central memory T-cell markers. Clonal T-cell receptor gamma chain and/or alpha-beta chain gene rearrangements were detected in all 10 patients. Five patients received chemotherapy, whereas for 3 patients, treatment consisted only of observation following surgical resection of the spleen or thyroid. Nine patients were alive at a median follow-up time of 19.5 months, whereas 1 patient died of an unrelated disease. The present study strongly indicates that T-cell lymphoma with small-sized lymphoma cells and a low Ki-67 labeling index is a distinct variant. Recognition of this novel lymphoma subtype, which should not be defined merely as PTCL-NOS, should be seriously considered. en-copyright= kn-copyright= en-aut-name=HayashiEiko en-aut-sei=Hayashi en-aut-mei=Eiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakataKatsuyoshi en-aut-sei=Takata en-aut-mei=Katsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SatoYasuharu en-aut-sei=Sato en-aut-mei=Yasuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TashiroYukie en-aut-sei=Tashiro en-aut-mei=Yukie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TachiyamaYoshiro en-aut-sei=Tachiyama en-aut-mei=Yoshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=Sawada-KitamuraSeiko en-aut-sei=Sawada-Kitamura en-aut-mei=Seiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HiramatsuYasushi en-aut-sei=Hiramatsu en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SugiguchiShun en-aut-sei=Sugiguchi en-aut-mei=Shun kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NoseSoichiro en-aut-sei=Nose en-aut-mei=Soichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=HirokawaMitsuyoshi en-aut-sei=Hirokawa en-aut-mei=Mitsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=AndoMidori en-aut-sei=Ando en-aut-mei=Midori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=Abd MaderLamia en-aut-sei=Abd Mader en-aut-mei=Lamia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=4 en-affil= kn-affil=Imakiire Gen Hosp, Dept Pathol affil-num=5 en-affil= kn-affil=Hiroshima Nishi Med Ctr, Div Pathol affil-num=6 en-affil= kn-affil=Kanazawa Univ Hosp, Div Pathol affil-num=7 en-affil= kn-affil=Himeji Red Cross Hosp, Dept Hematol & Oncol affil-num=8 en-affil= kn-affil=Tonami Gen Hosp, Dept Pathol affil-num=9 en-affil= kn-affil=Okayama Saiseikai Gen Hosp, Dept Pathol affil-num=10 en-affil= kn-affil=Kuma Hosp, Dept Diagnost Pathol affil-num=11 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=12 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol affil-num=13 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=14 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol & Oncol affil-num=15 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pathol en-keyword=Indolent PTCL kn-keyword=Indolent PTCL en-keyword=CD20 kn-keyword=CD20 en-keyword=Ki-67 kn-keyword=Ki-67 en-keyword=Memory T cell kn-keyword=Memory T cell en-keyword=Good prognosis kn-keyword=Good prognosis END start-ver=1.4 cd-journal=joma no-vol=12 cd-vols= no-issue=6 article-no= start-page=737 end-page=747 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130606 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Matrix-Embedded Osteocytes Regulate Mobilization of Hematopoietic Stem/Progenitor Cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=The bone marrow (BM) niche comprises multiple cell types that regulate hematopoietic stem/progenitor cell (HSPC) migration out of the niche and into the circulation. Here, we demonstrate that osteocytes, the major cellular component of mature bone, are regulators of HSPC egress. Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts. This rapid response is likely under control of the sympathetic nervous system, since osteocytes express the β2-adrenergic receptor and surgical sympathectomy prevents it. Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF. Taken together, these results indicate that the BM/bone niche interface is critically controlled from inside of the bone matrix and establish an important physiological role for skeletal tissues in hematopoietic function. en-copyright= kn-copyright= en-aut-name=AsadaNoboru en-aut-sei=Asada en-aut-mei=Noboru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KatayamaYoshio en-aut-sei=Katayama en-aut-mei=Yoshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=SatoMari en-aut-sei=Sato en-aut-mei=Mari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MinagawaKentaro en-aut-sei=Minagawa en-aut-mei=Kentaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WakahashiKanako en-aut-sei=Wakahashi en-aut-mei=Kanako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KawanoHiroki en-aut-sei=Kawano en-aut-mei=Hiroki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KawanoYuko en-aut-sei=Kawano en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=SadaAkiko en-aut-sei=Sada en-aut-mei=Akiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IkedaKyoji en-aut-sei=Ikeda en-aut-mei=Kyoji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MatsuiToshimitsu en-aut-sei=Matsui en-aut-mei=Toshimitsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=3 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=4 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=5 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=6 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=7 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=8 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=9 en-affil= kn-affil=Department of Bone and Joint Disease, National Center for Geriatrics and Gerontology (NCGG) affil-num=10 en-affil= kn-affil=Hematology, Department of Medicine, Kobe University Graduate School of Medicine affil-num=11 en-affil= kn-affil=Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=319 cd-vols= no-issue=4 article-no= start-page=417 end-page=423 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130215 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Vandetanib is effective in EGFR-mutant lung cancer cells with PTEN deficiency en-subtitle= kn-subtitle= en-abstract= kn-abstract=The effectiveness of vandetanib, an agent that targets RET, VEGFR and EGFR signaling, against EGFR-mutant lung cancer cells with PTEN loss was investigated. Two EGFR mutant non-small cell lung cancer (NSCLC) cell lines, PC-9 (PTEN wild type) and NCI-H1650 (PTEN null), were used. We transfected an intact FTEN gene into H1650 cells and knocked down PTEN expression in PC-9 cells using shRNA. The effectiveness of gefitinib and vandetanib was assessed using a xenograft model. While PC-9 cells were more resistant to vandetanib than gefitinib, H1650 cells were more sensitive to vandetanib than gefitinib. Both gefitinib and vandetanib suppressed the activation of EGFR and MAPK in H1650 cells, although phosphorylated AKT levels were not affected. In an H1650 cell xenograft model, vandetanib was also more effective than gefitinib. Although PTEN-transfected H1650 cells did not show restoration of sensitivity to gefitinib in vitro, the xenograft tumors responded to gefitinib and vandetanib. Knockdown of PTEN in PC-9 cells caused resistance to gefitinib. In conclusion, vandetanib might be effective in NSCLC with EGFR mutations that lack FTEN expression. The contribution of PTEN absence to vandetanib activity in NSCLC cells harboring EGFR mutations should be further examined. en-copyright= kn-copyright= en-aut-name=TakedaHiromasa en-aut-sei=Takeda en-aut-mei=Hiromasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OhashiKadoaki en-aut-sei=Ohashi en-aut-mei=Kadoaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MinamiDaisuke en-aut-sei=Minami en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KataokaItaru en-aut-sei=Kataoka en-aut-mei=Itaru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Internal Med 4 affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ Hosp, Dept Resp Med en-keyword=Lung cancer kn-keyword=Lung cancer en-keyword=Vandetanib kn-keyword=Vandetanib en-keyword=Gefitinib kn-keyword=Gefitinib en-keyword=EGFR kn-keyword=EGFR en-keyword=VEGFR kn-keyword=VEGFR en-keyword=PTEN kn-keyword=PTEN END start-ver=1.4 cd-journal=joma no-vol=67 cd-vols= no-issue=5 article-no= start-page=319 end-page=324 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201310 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Preparation of Enteric-coated Capsules of Beclomethasone Dipropionate for Patients with Intestinal Graft-versus-Host Disease and a Case Study en-subtitle= kn-subtitle= en-abstract= kn-abstract=Graft-versus-host disease (GVHD) is a major concern in transplantation patients. Gut GVHD is accompanied by diarrhea, abdominal pain, and/or melena. Although oral treatment with corticosteroids (CSs) is effective in treating gut GVHD, it can cause adverse reactions that affect the entire body. Topical administration of CSs can be effective in treating diseases in which lesions are limited locally, because adverse reactions can then be alleviated. In this study, we examine and discuss an enteric-coated beclomethasone dipropionate (BDP) capsule (BDP-EC) formulated at Okayama University Hospital. The BDP-EC did not dissolve in solution 1 (pH1.2), and began disintegrating in solution 2 (pH6.8) after 5min, with a mean dissolution rate at 15min of 85%. We then used the capsule to treat a patient who developed gut GVHD after allogeneic hematopoietic stem cell transplantation. Clinically, the frequency of diarrhea decreased after BDP-EC administration. In addition, we were able to decrease the prednisolone equivalent dose. Symptoms associated with adverse reactions to BDP were not observed during the hospitalization period. These findings suggest that the administration of BDP-EC in the early stages of gut GVHD may allow a reduction in the initial doses of systemic CSs. en-copyright= kn-copyright= en-aut-name=MurakawaKiminaka en-aut-sei=Murakawa en-aut-mei=Kiminaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SatoTomoaki en-aut-sei=Sato en-aut-mei=Tomoaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KitamuraYoshihisa en-aut-sei=Kitamura en-aut-mei=Yoshihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SendoToshiaki en-aut-sei=Sendo en-aut-mei=Toshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Pharmacy, Okayama University Hospital affil-num=2 en-affil= kn-affil=Department of Pharmacy, Okayama University Hospital affil-num=3 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Pharmacy, Okayama University Hospital affil-num=5 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Pharmacy, Okayama University Hospital en-keyword=beclomethasone kn-keyword=beclomethasone en-keyword=intestinal graft-versus-host disease kn-keyword=intestinal graft-versus-host disease en-keyword=enteric-coated capsule kn-keyword=enteric-coated capsule en-keyword=in-hospital formulation kn-keyword=in-hospital formulation END start-ver=1.4 cd-journal=joma no-vol=14 cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130124 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Inhibition of neutrophil elastase attenuates airway hyperresponsiveness and inflammation in a mouse model of secondary allergen challenge: neutrophil elastase inhibition attenuates allergic airway responses en-subtitle= kn-subtitle= en-abstract= kn-abstract=Background: Chronic asthma is often associated with neutrophilic infiltration in the airways. Neutrophils contain elastase, a potent secretagogue in the airways, nonetheless the role for neutrophil elastase as well as neutrophilic inflammation in allergen-induced airway responses is not well defined. In this study, we have investigated the impact of neutrophil elastase inhibition on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in previously sensitized and challenged mice. Methods: BALB/c mice were sensitized and challenged (primary) with ovalbumin (OVA). Six weeks later, a single OVA aerosol (secondary challenge) was delivered and airway inflammation and airway responses were monitored 6 and 48 hrs later. An inhibitor of neutrophil elastase was administered prior to secondary challenge. Results: Mice developed a two-phase airway inflammatory response after secondary allergen challenge, one neutrophilic at 6 hr and the other eosinophilic, at 48 hr. PAR-2 expression in the lung tissues was enhanced following secondary challenge, and that PAR-2 intracellular expression on peribronchial lymph node (PBLN) T cells was also increased following allergen challenge of sensitized mice. Inhibition of neutrophil elastase significantly attenuated AHR, goblet cell metaplasia, and inflammatory cell accumulation in the airways following secondary OVA challenge. Levels of IL-4, IL-5 and IL-13, and eotaxin in BAL fluid 6 hr after secondary allergen challenge were significantly suppressed by the treatment. At 48 hr, treatment with the neutrophil elastase inhibitor significantly reduced the levels of IL-13 and TGF-beta 1 in the BAL fluid. In parallel, in vitro IL-13 production was significantly inhibited in spleen cells from sensitized mice. Conclusion: These data indicate that neutrophil elastase plays an important role in the development of allergic airway inflammation and hyperresponsiveness, and would suggest that the neutrophil elastase inhibitor reduced AHR to inhaled methacholine indicating the potential for its use as a modulator of the immune/inflammatory response in both the neutrophil-and eosinophil-dominant phases of the response to secondary allergen challenge. en-copyright= kn-copyright= en-aut-name=KogaHikari en-aut-sei=Koga en-aut-mei=Hikari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FuchimotoYasuko en-aut-sei=Fuchimoto en-aut-mei=Yasuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IkedaGenyo en-aut-sei=Ikeda en-aut-mei=Genyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WasedaKoichi en-aut-sei=Waseda en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OnoKatsuichiro en-aut-sei=Ono en-aut-mei=Katsuichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KataokaMikio en-aut-sei=Kataoka en-aut-mei=Mikio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=GelfandErwin W. en-aut-sei=Gelfand en-aut-mei=Erwin W. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=9 en-affil= kn-affil=Natl Jewish Hlth, Dept Pediat, Div Cell Biol affil-num=10 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci affil-num=11 en-affil= kn-affil=Okayama Univ, Dept Hematol Oncol Allergy & Resp Med, Grad Sch Med Dent & Pharmaceut Sci en-keyword=Neutrophil kn-keyword=Neutrophil en-keyword=Elastase kn-keyword=Elastase en-keyword=Airway kn-keyword=Airway en-keyword=Hyperresponsiveness kn-keyword=Hyperresponsiveness en-keyword=Asthma kn-keyword=Asthma END start-ver=1.4 cd-journal=joma no-vol=125 cd-vols= no-issue=2 article-no= start-page=119 end-page=127 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The treatment strategy for clinical stage III non-small cell lung cancer kn-title=臨床病期V期肺非小細胞癌に対する治療戦略 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院 呼吸器・アレルギー内科 en-keyword=concomitant chemoradiotherapy kn-keyword=concomitant chemoradiotherapy en-keyword=third generation kn-keyword=third generation en-keyword=surgery kn-keyword=surgery END start-ver=1.4 cd-journal=joma no-vol=125 cd-vols= no-issue=2 article-no= start-page=103 end-page=107 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Duodenal follicular lymphoma lacks AID but expresses BACH2 and has memory B cell characteristics kn-title=十二指腸濾胞性リンパ腫はAIDの発現を欠くがBACH2の発現を有しmemoryB細胞としての性質を有する en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakataKatsuyoshi en-aut-sei=Takata en-aut-mei=Katsuyoshi kn-aut-name=高田尚良 kn-aut-sei=高田 kn-aut-mei=尚良 aut-affil-num=1 ORCID= en-aut-name=SatoYasuharu en-aut-sei=Sato en-aut-mei=Yasuharu kn-aut-name=佐藤康晴 kn-aut-sei=佐藤 kn-aut-mei=康晴 aut-affil-num=2 ORCID= en-aut-name=NakamuraNaoya en-aut-sei=Nakamura en-aut-mei=Naoya kn-aut-name=中村直哉 kn-aut-sei=中村 kn-aut-mei=直哉 aut-affil-num=3 ORCID= en-aut-name=TokunakaMami en-aut-sei=Tokunaka en-aut-mei=Mami kn-aut-name=徳中摩美 kn-aut-sei=徳中 kn-aut-mei=摩美 aut-affil-num=4 ORCID= en-aut-name=MikiYukari en-aut-sei=Miki en-aut-mei=Yukari kn-aut-name=三木由香里 kn-aut-sei=三木 kn-aut-mei=由香里 aut-affil-num=5 ORCID= en-aut-name=KikutiYara Yukie en-aut-sei=Kikuti en-aut-mei=Yara Yukie kn-aut-name=菊池イアーラ幸江 kn-aut-sei=菊池 kn-aut-mei=イアーラ幸江 aut-affil-num=6 ORCID= en-aut-name=IgarashiKazuhiko en-aut-sei=Igarashi en-aut-mei=Kazuhiko kn-aut-name=五十嵐和彦 kn-aut-sei=五十嵐 kn-aut-mei=和彦 aut-affil-num=7 ORCID= en-aut-name=ItoEtsuro en-aut-sei=Ito en-aut-mei=Etsuro kn-aut-name=伊藤悦郎 kn-aut-sei=伊藤 kn-aut-mei=悦郎 aut-affil-num=8 ORCID= en-aut-name=HarigaeHideo en-aut-sei=Harigae en-aut-mei=Hideo kn-aut-name=張替秀雄 kn-aut-sei=張替 kn-aut-mei=秀雄 aut-affil-num=9 ORCID= en-aut-name=KatoSeiichi en-aut-sei=Kato en-aut-mei=Seiichi kn-aut-name=加藤省一 kn-aut-sei=加藤 kn-aut-mei=省一 aut-affil-num=10 ORCID= en-aut-name=HayashiEiko en-aut-sei=Hayashi en-aut-mei=Eiko kn-aut-name=林詠子 kn-aut-sei=林 kn-aut-mei=詠子 aut-affil-num=11 ORCID= en-aut-name=OkaTakashi en-aut-sei=Oka en-aut-mei=Takashi kn-aut-name=岡剛史 kn-aut-sei=岡 kn-aut-mei=剛史 aut-affil-num=12 ORCID= en-aut-name=HoshiiYoshinobu en-aut-sei=Hoshii en-aut-mei=Yoshinobu kn-aut-name=星井嘉信 kn-aut-sei=星井 kn-aut-mei=嘉信 aut-affil-num=13 ORCID= en-aut-name=TariAkira en-aut-sei=Tari en-aut-mei=Akira kn-aut-name=田利晶 kn-aut-sei=田利 kn-aut-mei=晶 aut-affil-num=14 ORCID= en-aut-name=OkadaHiroyuki en-aut-sei=Okada en-aut-mei=Hiroyuki kn-aut-name=岡田裕之 kn-aut-sei=岡田 kn-aut-mei=裕之 aut-affil-num=15 ORCID= en-aut-name=MohamadoABD Alkader Lamia en-aut-sei=Mohamado en-aut-mei=ABD Alkader Lamia kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name=前田嘉信 kn-aut-sei=前田 kn-aut-mei=嘉信 aut-affil-num=17 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=18 ORCID= en-aut-name=KinoshitaTomohiro en-aut-sei=Kinoshita en-aut-mei=Tomohiro kn-aut-name=木下朝博 kn-aut-sei=木下 kn-aut-mei=朝博 aut-affil-num=19 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name=吉野正 kn-aut-sei=吉野 kn-aut-mei=正 aut-affil-num=20 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科病理学（腫瘍病理） affil-num=3 en-affil= kn-affil=東海大学医学部　病理診断学講座 affil-num=4 en-affil= kn-affil=東海大学医学部　病理診断学講座 affil-num=5 en-affil= kn-affil=香川保健医療短期大学 affil-num=6 en-affil= kn-affil=東海大学医学部　病理診断学講座 affil-num=7 en-affil= kn-affil=東北大学大学院医学系研究科 生物化学分野 affil-num=8 en-affil= kn-affil=弘前大学医学部　小児科学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・免疫病学分野 affil-num=10 en-affil= kn-affil=名古屋大学病院　病理部 affil-num=11 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=12 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=13 en-affil= kn-affil=山口大学医学部　病理学 affil-num=14 en-affil= kn-affil=広島赤十字・原爆病院　消化器内科 affil-num=15 en-affil= kn-affil=岡山大学病院　光学診療部 affil-num=16 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） affil-num=17 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科血液・腫瘍・呼吸器内科学 affil-num=18 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科血液・腫瘍・呼吸器内科学 affil-num=19 en-affil= kn-affil=愛知がんセンター　血液細胞療法部 affil-num=20 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 病理学（腫瘍病理） en-keyword=follicular lymphoma kn-keyword=follicular lymphoma en-keyword=gastrointestinal tract kn-keyword=gastrointestinal tract en-keyword=BACH2 kn-keyword=BACH2 en-keyword=memory B cell kn-keyword=memory B cell END start-ver=1.4 cd-journal=joma no-vol=103 cd-vols= no-issue=10 article-no= start-page=1795 end-page=1802 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201210 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=JAK2-related pathway induces acquired erlotinib resistance in lung cancer cells harboring an epidermal growth factor receptor-activating mutation en-subtitle= kn-subtitle= en-abstract= kn-abstract=Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, such as gefitinib and erlotinib, are effective for non-small cell lung cancer with activating EGFR mutations. However, even in patients with an initial dramatic response to such a drug, acquired resistance develops after 612 similar to months. A secondary mutation of T790M in EGFR and amplification of the MET gene account for this resistance; however, the mechanism(s) of approximately 30% of acquired resistance cases remain unknown. We established an erlotinib-resistant lung cancer cell line named PC-9/ER3 that harbors an EGFR mutation after continuously exposing PC-9 cells to erlotinib. PC-9/ER3 cells were 136-fold more resistant to erlotinib than the parental cells. Although the PC-9/ER3 cells did not carry the T790M mutation or MET amplification and had similar levels of phosphorylated (p) STAT3, pJAK2 increased in the resistant cells. It was found in the present study that 312 similar to h of exposure to erlotinib in both cell lines did not affect pJAK2 expression, but did result in increased pSTAT3 expression. pAkt in PC-9/ER3 cells was less suppressed than in PC-9 cells, although pEGFR and pMAPK were markedly suppressed in both cell lines. The combined treatment of erlotinib plus a JAK2 inhibitor (JSI-124) suppressed pAkt in PC-9/ER3 cells. Similarly, the combination of erlotinib plus JSI-124 or siRNA against JAK2 restored sensitivity to erlotinib in PC-9/ER3 cells. The combination of erlotinib plus JSI-124 was also effective for reducing PC-9/ER3 tumors in a murine xenograft model. Our results suggest that the activation of JAK2 partially accounts for acquired erlotinib resistance.(Cancer Sci, doi: 10.1111/j.1349-7006.2012.02363.x, 2012) en-copyright= kn-copyright= en-aut-name=HaradaDaijiro en-aut-sei=Harada en-aut-mei=Daijiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NinomiyaTakashi en-aut-sei=Ninomiya en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YasugiMasayuki en-aut-sei=Yasugi en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KuboToshio en-aut-sei=Kubo en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakedaHiromasa en-aut-sei=Takeda en-aut-mei=Hiromasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OhashiKadoaki en-aut-sei=Ohashi en-aut-mei=Kadoaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TakataSaburo en-aut-sei=Takata en-aut-mei=Saburo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Internal Med 4 affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=8 en-affil= kn-affil=Okayama Univ Hosp, Dept Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=11 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=12 en-affil= kn-affil=Okayama Univ Hosp, Dept Resp Med END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=1 article-no= start-page=78 end-page=84 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201301 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Subpopulation of small-cell lung cancer cells expressing CD133 and CD87 show resistance to chemotherapy en-subtitle= kn-subtitle= en-abstract= kn-abstract=Tumors are presumed to contain a small population of cancer stem cells (CSCs) that initiate tumor growth and promote tumor spreading. Multidrug resistance in CSCs is thought to allow the tumor to evade conventional therapy. This study focused on expression of CD133 and CD87 because CD133 is a putative marker of CSCs in some cancers including lung, and CD87 is associated with a stem-cell-like property in small-cell lung cancer (SCLC). Six SCLC cell lines were used. The expression levels of CD133 and CD87 were analyzed by real-time quantitative reverse transcription-polymerase chain reaction and flow cytometry. CD133+/- and CD87+/- cells were isolated by flow cytometry. The drug sensitivities were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Non-obese diabetic/severe combined immunodeficiency mice were used for the tumor formation assay. SBC-7 cells showed the highest expression levels of both CD133 and CD87 among the cell lines. CD133-/CD87-, CD133+/CD87-, and CD133-/CD87+ cells were isolated from SBC-7 cells; however, CD133+/CD87+ cells could not be obtained. Both CD133+/CD87- and CD133-/CD87+ subpopulations showed a higher resistance to etoposide and paclitaxel and greater re-populating ability than the CD133-/CD87- subpopulation. CD133+/CD87- cells contained more G0 quiescent cells than CD133-/CD87- cells. By contrast, CD133-/CD87- cells showed the highest tumorigenic potential. In conclusion, both CD133 and CD87 proved to be inadequate markers for CSCs; however, they might be beneficial for predicting resistance to chemotherapy. (Cancer Sci 2013; 104: 7884) en-copyright= kn-copyright= en-aut-name=KuboToshio en-aut-sei=Kubo en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OsawaMasahiro en-aut-sei=Osawa en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HaradaDaijiro en-aut-sei=Harada en-aut-mei=Daijiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NinomiyaTakashi en-aut-sei=Ninomiya en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YamaneHiromichi en-aut-sei=Yamane en-aut-mei=Hiromichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=2 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Internal Med 4 affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=8 en-affil= kn-affil=Kawasaki Med Univ, Dept Gen Internal Med 4 affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol affil-num=10 en-affil= kn-affil=Okayama Univ Hosp, Dept Resp Med END start-ver=1.4 cd-journal=joma no-vol=10 cd-vols= no-issue=9 article-no= start-page=1720 end-page=1727 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201109 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Liposomal Delivery of MicroRNA-7-Expressing Plasmid Overcomes Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor-Resistance in Lung Cancer Cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) have been strikingly effective in lung cancers harboring activating EGFR mutations. Unfortunately, the cancer cells eventually acquire resistance to EGFR-TKI. Approximately 50% of the acquired resistance involves a secondary T790M mutation. To overcome the resistance, we focused on EGFR suppression using microRNA-7 (miR-7), targeting multiple sites in the 30-untranslated region of EGFR mRNA. Two EGFR-TKI-sensitive cell lines (PC-9 and H3255) and two EGFR-TKI-resistant cell lines harboring T790M (RPC-9 and H1975) were used. We constructed miR-7-2 containing miR-7-expressing plasmid. After transfection of the miR-7-expressing plasmid, using cationic liposomes, a quantitative PCR and dual luciferase assay were conducted to examine the efficacy. The antiproliferative effect was evaluated using a cell count assay and xenograft model. Protein expression was examined by Western blotting. The miR-7 expression level of the transfectants was approximately 30-fold higher, and the luciferase activity was ablated by 92%. miR-7 significantly inhibited cell growth not only in PC-9 and H3255 but also in RPC-9 and H1975. Expression of insulin receptor substrate-1 (IRS-1), RAF-1, and EGFR was suppressed in the four cell lines. Injection of the miR-7-expressing plasmid revealed marked tumor regression in a mouse xenograft model using RPC-9 and H1975. EGFR, RAF-1, and IRS-1 were suppressed in the residual tumors. These findings indicate promising therapeutic applications of miR-7-expressing plasmids against EGFR oncogene-addicted lung cancers including T790M resistance by liposomal delivery. Mol Cancer Ther; 10(9); 1720-7. en-copyright= kn-copyright= en-aut-name=RaiKammei en-aut-sei=Rai en-aut-mei=Kammei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ItoSachio en-aut-sei=Ito en-aut-mei=Sachio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KashiharaHiromi en-aut-sei=Kashihara en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=YasudaTatsuji en-aut-sei=Yasuda en-aut-mei=Tatsuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShimizuKenji en-aut-sei=Shimizu en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Genet affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Chem affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Genet affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol & Resp Med END start-ver=1.4 cd-journal=joma no-vol=125 cd-vols= no-issue=1 article-no= start-page=57 end-page=66 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=20130401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Lung cancer and molecular targeted drugs kn-title=肺癌と分子標的薬 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=1 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 en-keyword=肺癌 kn-keyword=肺癌 en-keyword=分子プロファイリング kn-keyword=分子プロファイリング en-keyword=分子標的薬 kn-keyword=分子標的薬 en-keyword=EGFR遺伝子変異 kn-keyword=EGFR遺伝子変異 en-keyword=ALK融合遺伝子 kn-keyword=ALK融合遺伝子 END start-ver=1.4 cd-journal=joma no-vol=67 cd-vols= no-issue=1 article-no= start-page=1 end-page=8 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201302 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Chronic Graft-versus-Host Disease: Disease Biology and Novel Therapeutic Strategies en-subtitle= kn-subtitle= en-abstract= kn-abstract=Graft-versus-host disease (GVHD) is a major complication after allogeneic hematopoietic stem cell transplantation. Chronic GVHD often presents with clinical manifestations that resemble those observed in autoimmune diseases. Standard treatment is 1-2mg/kg/day of prednisone or an equivalent dose of methylprednisolone, with continued administration of a calcineurin inhibitor for steroid sparing. However, the prognosis of steroid-refractory chronic GVHD remains poor. Classically, chronic GVHD was said to involve predominantly Th2 responses. We are now faced with a more complex picture, involving possible roles for thymic dysfunction, transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF), B cells and autoantibodies, and Th1/Th2/Th17 cytokines, as well as regulatory T cells (Tregs), in chronic GVHD. More detailed research on the pathophysiology of chronic GVHD may facilitate the establishment of novel strategies for its prevention and treatment. en-copyright= kn-copyright= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=chronic GVHD kn-keyword=chronic GVHD en-keyword=Th17 kn-keyword=Th17 en-keyword=Am80 kn-keyword=Am80 en-keyword=regulatory T cell (Treg) kn-keyword=regulatory T cell (Treg) en-keyword=steroid-refractory kn-keyword=steroid-refractory END start-ver=1.4 cd-journal=joma no-vol=19 cd-vols= no-issue=7 article-no= start-page=995 end-page=1000 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201107 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Bacterial substitution of coagulase-negative staphylococci for streptococci on the oral mucosa after hematopoietic cell transplantation en-subtitle= kn-subtitle= en-abstract= kn-abstract=Coagulase-negative staphylococci (CoNS) are frequently isolated from blood cultures of hematopoietic cell transplantation (HCT) patients. Generally, the use of central venous catheters is recognized as a significant risk factor for CoNS infection, while the impact of CoNS infection from oral ulcerative mucositis, which occurs frequently in HCT, may be underestimated. Here, we examined the bacteria on the buccal mucosa after HCT. Sixty-one patients were examined for bacteria on the buccal mucosa routinely once a week from 1 week before to 3 weeks after allogeneic HCT. Subjects were divided into groups with short and long periods of antibiotic use, and differences in bacterial substitution were evaluated. The relationships between type of HCT (conventional HCT or RIST) and bacterial substitution were also evaluated. The changes in detection frequencies of CoNS and alpha-streptococci from before to 3 weeks after HCT were significant (P < 0.05, chi (2) test): 14.5-53.3% and 92.7-53.1%, respectively. Significant bacterial substitution of CoNS for streptococci was observed in the long-term antibiotic use group (P < 0.05, chi (2) test), but also occurred in cases with short-term or no antibiotic use. No relationships between type of HCT (conventional HCT or RIST) were observed. Bacterial substitution of CoNS for streptococci occurred frequently on the buccal mucosa after HCT. In addition to antibiotic use, environmental factors may be involved in bacterial substitution. It is important to consider the presence of oral mucositis in CoNS infection after HCT. en-copyright= kn-copyright= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IshimaruFumihiko en-aut-sei=Ishimaru en-aut-mei=Fumihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MaedaHiroshi en-aut-sei=Maeda en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NishimuraFusanori en-aut-sei=Nishimura en-aut-mei=Fusanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ affil-num=2 en-affil= kn-affil=Okayama Univ affil-num=3 en-affil= kn-affil=Okayama Univ affil-num=4 en-affil= kn-affil=Okayama Univ affil-num=5 en-affil= kn-affil=Okayama Univ affil-num=6 en-affil= kn-affil=Okayama Univ affil-num=7 en-affil= kn-affil=Okayama Univ en-keyword=Bacterial substitution kn-keyword=Bacterial substitution en-keyword=Oral mucosa kn-keyword=Oral mucosa en-keyword=Hematopoietic cell transplantation kn-keyword=Hematopoietic cell transplantation en-keyword=Coagulase-negative Staphylococcus kn-keyword=Coagulase-negative Staphylococcus en-keyword=Bacteremia kn-keyword=Bacteremia END start-ver=1.4 cd-journal=joma no-vol=18 cd-vols= no-issue=3 article-no= start-page=395 end-page=398 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201003 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Total bacterial counts on oral mucosa after using a commercial saliva substitute in patients undergoing hematopoietic cell transplantation en-subtitle= kn-subtitle= en-abstract= kn-abstract=The commercial saliva substitute OralbalanceA (R) has been reported to alleviate symptoms of postradiotherapy xerostomia in head and neck cancer patients. OralbalanceA (R) may also be effective for xerostomia in patients undergoing hematopoietic cell transplantation (HCT) with high-dose chemotherapy and total-body irradiation. However, HCT patients are in a severely compromised condition, and saliva substitute must not promote infection. We reported previously that OralbalanceA (R) has antimicrobial effects against microbial species detected during HCT in vitro. This study was performed to determine the in vivo effects of OralbalanceA (R) on oral mucosal total bacterial counts in patients undergoing HCT. A total of 18 neutropenic patients undergoing HCT were enrolled in this study. Before and after 1 week of OralbalanceA (R) use, bacterial samples were obtained from patients by wiping an area of I center dot 1 cm on the buccal mucosa with sterilized cotton swabs. Total bacterial counts of the obtained samples were examined by quantitative polymerase chain reaction amplification of the bacterial 16S ribosomal RNA gene. As controls, bacterial samples were also obtained from ten healthy subjects, and total bacterial counts were examined. No significant increase in bacterial count was observed with use of OralbalanceA (R). None of the patients showed bacterial counts above the range found in healthy controls after using OralbalanceA (R). In neutropenic patients undergoing HCT, OralbalanceA (R) did not increase the total counts of oral mucosal bacteria beyond the range found in healthy controls. Oral care using OralbalanceA (R) may alleviate the symptoms induced by hyposalivation without promoting infection. en-copyright= kn-copyright= en-aut-name=SugiuraYuko en-aut-sei=Sugiura en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamabeKokoro en-aut-sei=Yamabe en-aut-mei=Kokoro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsutaniSoichiro en-aut-sei=Tsutani en-aut-mei=Soichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoIchiro en-aut-sei=Tanimoto en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MaedaHiroshi en-aut-sei=Maeda en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KokeguchiSusumu en-aut-sei=Kokeguchi en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IshimaruFumihiko en-aut-sei=Ishimaru en-aut-mei=Fumihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=NishimuraFusanori en-aut-sei=Nishimura en-aut-mei=Fusanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ affil-num=2 en-affil= kn-affil=Okayama Univ affil-num=3 en-affil= kn-affil=Okayama Univ affil-num=4 en-affil= kn-affil=Okayama Univ affil-num=5 en-affil= kn-affil=Okayama Univ affil-num=6 en-affil= kn-affil=Okayama Univ affil-num=7 en-affil= kn-affil=Okayama Univ affil-num=8 en-affil= kn-affil=Okayama Univ affil-num=9 en-affil= kn-affil=Okayama Univ affil-num=10 en-affil= kn-affil=Okayama Univ affil-num=11 en-affil= kn-affil=Okayama Univ affil-num=12 en-affil= kn-affil=Okayama Univ en-keyword=Hematopoietic cell transplantation kn-keyword=Hematopoietic cell transplantation en-keyword=Xerostomia kn-keyword=Xerostomia en-keyword=Saliva substitute kn-keyword=Saliva substitute END start-ver=1.4 cd-journal=joma no-vol=18 cd-vols= no-issue=1 article-no= start-page=115 end-page=119 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201001 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Oral mucositis in patients receiving reduced-intensity regimens for allogeneic hematopoietic cell transplantation: comparison with conventional regimen en-subtitle= kn-subtitle= en-abstract= kn-abstract=Severe oral mucositis induced by allogeneic hematopoietic cell transplantation (HCT) is associated with intolerable pain and risk of systemic bacteremia infection. Differences between conventional HCT and reduced-intensity regimens for allogeneic HCT (RIST) may influence the occurrence and severity of oral mucositis. Here, we evaluated oral mucositis in patients undergoing RIST and compared the results with those in conventional allogeneic HCT patients to facilitate predictive measures for mucositis. A total of 127 consecutive patients undergoing HCT (conventional, 63; RIST, 64) were included in this study. Severity of oral mucositis during HCT period was evaluated daily. Differences in severity of mucositis among HCT types were analyzed. Use of morphine to control pain due to oral mucositis was evaluated in each HCT method. The severity of oral mucositis was reduced in patients undergoing RIST. Worsening of oral mucositis was delayed in patients receiving RIST. Use of morphine to control pain due to oral mucositis was significantly decreased in patients undergoing RIST compared with those receiving conventional allogeneic HCT. The severity of oral mucositis was reduced and the peak day of oral mucositis was delayed in RIST patients compared with those receiving conventional HCT. en-copyright= kn-copyright= en-aut-name=TakahashiKanayo en-aut-sei=Takahashi en-aut-mei=Kanayo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MurayamaYumeno en-aut-sei=Murayama en-aut-mei=Yumeno kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=UdagawaMika en-aut-sei=Udagawa en-aut-mei=Mika kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NishimotoHitomi en-aut-sei=Nishimoto en-aut-mei=Hitomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SugiuraYuko en-aut-sei=Sugiura en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ Hosp affil-num=2 en-affil= kn-affil=Okayama Univ Hosp affil-num=3 en-affil= kn-affil=Okayama Univ Hosp affil-num=4 en-affil= kn-affil=Okayama Univ Hosp affil-num=5 en-affil= kn-affil=Okayama Univ Hosp affil-num=6 en-affil= kn-affil=Okayama Univ Hosp affil-num=7 en-affil= kn-affil=Okayama Univ Hosp affil-num=8 en-affil= kn-affil=Okayama Univ Hosp affil-num=9 en-affil= kn-affil=Okayama Univ en-keyword=Hematopoietic cell transplantation kn-keyword=Hematopoietic cell transplantation en-keyword=Oral mucositis kn-keyword=Oral mucositis en-keyword=Reduced-intensity regimens kn-keyword=Reduced-intensity regimens END start-ver=1.4 cd-journal=joma no-vol=17 cd-vols= no-issue=5 article-no= start-page=581 end-page=587 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200905 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Febrile neutropenia and periodontitis: lessons from a case periodontal treatment in the intervals between chemotherapy cycles for leukemia reduced febrile neutropenia en-subtitle= kn-subtitle= en-abstract= kn-abstract=Oral and systemic infections arising from the oral cavity are significant problems in clinical management of patients undergoing leukemia treatment. However, there is significant disparity in the reported incidences of development of periodontal infections. Evidence is limited to those showing the systemic influence of periodontal infection in neutropenic patients. This study indicated an association between febrile neutropenia (FN) and periodontitis in a case in which periodontal treatment in the intervals between chemotherapy cycles reduced FN in subsequent courses of chemotherapy and hematopoietic transplantation (HCT). Periodontal treatment was performed in a 61-year-old man with advanced periodontitis, who received HCT following three cycles of chemotherapy. After recovery from neutropenia induced by initial chemotherapy, periodontal treatment was performed in each chemotherapy interval period. Following extraction of teeth with severe advanced periodontitis, all teeth were subjected to periodontal pocket curettage and root planning, which are common periodontal treatments to reduce periodontal pockets harboring anaerobic periodontal bacteria, before HCT. Periodontal treatment successfully reduced periodontal pockets from 4.1 +/- 1.5 mm to 3.0 +/- 0.6 mm, which was almost within the healthy range (< 3.0 mm), before HCT. The frequency of FN decreased significantly with increasing cycles of chemotherapy, and decreases in FN corresponded to progress of periodontal treatment. Blood cultures obtained a total of 12 times throughout leukemia treatment were all negative. The observations reported here indicate the importance of periodontal treatment in clinical management of patients undergoing leukemia treatment to prevent FN, although all blood cultures were negative. en-copyright= kn-copyright= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YamasujiYoshiko en-aut-sei=Yamasuji en-aut-mei=Yoshiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KudoChieko en-aut-sei=Kudo en-aut-mei=Chieko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=Matsuura-YoshimotoKaori en-aut-sei=Matsuura-Yoshimoto en-aut-mei=Kaori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamabeKokoro en-aut-sei=Yamabe en-aut-mei=Kokoro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SugiuraYuko en-aut-sei=Sugiura en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IshimaruFumihiko en-aut-sei=Ishimaru en-aut-mei=Fumihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=NishimuraFusanori en-aut-sei=Nishimura en-aut-mei=Fusanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ affil-num=2 en-affil= kn-affil=Okayama Univ affil-num=3 en-affil= kn-affil=Okayama Univ affil-num=4 en-affil= kn-affil=Okayama Univ affil-num=5 en-affil= kn-affil=Okayama Univ affil-num=6 en-affil= kn-affil=Okayama Univ affil-num=7 en-affil= kn-affil=Okayama Univ affil-num=8 en-affil= kn-affil=Okayama Univ affil-num=9 en-affil= kn-affil=Okayama Univ affil-num=10 en-affil= kn-affil=Okayama Univ affil-num=11 en-affil= kn-affil=Okayama Univ en-keyword=Febrile neutropenia kn-keyword=Febrile neutropenia en-keyword=Periodontitis kn-keyword=Periodontitis en-keyword=Chemotherapy kn-keyword=Chemotherapy en-keyword=Leukemia kn-keyword=Leukemia END start-ver=1.4 cd-journal=joma no-vol=16 cd-vols= no-issue=10 article-no= start-page=1197 end-page=1200 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=200810 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Evaluation of xerostomia in hematopoietic cell transplantation by a simple capacitance method device en-subtitle= kn-subtitle= en-abstract= kn-abstract=Goals Hematopoietic cell transplantation (HCT) may lead to the development of xerostomia. However, there have been few reports of xerostomia in HCT patients based on objective data. We investigated moisture in the oral mucosa in patients undergoing HCT by the capacitance method using a convenient device, Moisture Checker for Mucus (R) (MCM; Life Co., Ltd., Saitama, Japan). Subjects and methods Thirty-six patients undergoing HCT at Okayama University Hospital of Medicine and Dentistry (Male=22, Female=14; age=41.6 +/- 16.2 years old) were enrolled in this study. Moisture in the oral mucosa was measured by MCM in accordance with the manufacturer's instructions. The results were obtained as MCM values (%), which are the weight percentage of water content in the oral mucosal epithelium. As controls, moisture of the oral mucosa was also examined in healthy volunteers (Male=27, Female=35; age=43.0 +/- 14.6 years old). Main results Throughout the examination period, MCM values were significantly lower in patients who underwent HCT than in controls. The degree of mucosal moisture in HCT patients showed wide interindividual differences. Conclusion The degree of mucosal moisture in HCT patients was low and showed wide interindividual differences. Evaluation of xerostomia using such a device may contribute to appropriate oral care with saliva substitute. en-copyright= kn-copyright= en-aut-name=SugiuraYuko en-aut-sei=Sugiura en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NishideSachiko en-aut-sei=Nishide en-aut-mei=Sachiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KonoKotoe en-aut-sei=Kono en-aut-mei=Kotoe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakahashiKanayo en-aut-sei=Takahashi en-aut-mei=Kanayo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IshimaruFumihiko en-aut-sei=Ishimaru en-aut-mei=Fumihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NishimuraFusanori en-aut-sei=Nishimura en-aut-mei=Fusanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ affil-num=2 en-affil= kn-affil=Okayama Univ affil-num=3 en-affil= kn-affil=Okayama Univ Hosp Med & Dent affil-num=4 en-affil= kn-affil=Okayama Univ Hosp Med & Dent affil-num=5 en-affil= kn-affil=Okayama Univ Hosp Med & Dent affil-num=6 en-affil= kn-affil=Okayama Univ affil-num=7 en-affil= kn-affil=Okayama Univ affil-num=8 en-affil= kn-affil=Okayama Univ affil-num=9 en-affil= kn-affil=Okayama Univ affil-num=10 en-affil= kn-affil=Okayama Univ en-keyword=xerostomia kn-keyword=xerostomia en-keyword=hematopoietic cell transplantation kn-keyword=hematopoietic cell transplantation en-keyword=hyposalivation kn-keyword=hyposalivation END start-ver=1.4 cd-journal=joma no-vol=19 cd-vols= no-issue=2 article-no= start-page=303 end-page=307 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201102 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Progress of oral care and reduction of oral mucositis-a pilot study in a hematopoietic stem cell transplantation ward en-subtitle= kn-subtitle= en-abstract= kn-abstract=Oral mucositis is a common symptomatic complication associated with hematopoietic stem cell transplantation (HCT). We use simple strategies aimed to reduce oral mucositis by keeping the oral cavity clean and moist. Here, we report on the progress of oral care and the changes in the degree of oral mucositis. The purpose of this pilot study is to evaluate the effects of our strategies on the prevalence and the severity of oral mucositis. Fifty-three consecutive patients from 2003 to 2006 administered with conventional allogeneic HCT were enrolled in this study. The degree of oral mucositis was evaluated daily in all patients. Our oral care program was divided into two periods: "examination and trial period (2003 and 2004)" and "intensive oral care period (2005 and 2006)." In the latter, an oral care regimen was carried out systematically by a multidisciplinary team. Using our oral care strategies, the prevalence of ulcerative oral mucositis was decreased significantly. The rate was reduced from 76% (10 of 13) of patients with ulcerative oral mucositis in 2003 to only 20% (3 of 15) in 2006. Our pilot study suggests that oral mucositis in HCT patients can be alleviated by simple strategies aimed at keeping the oral cavity clean and moist. en-copyright= kn-copyright= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SugiuraYuko en-aut-sei=Sugiura en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahashiKanayo en-aut-sei=Takahashi en-aut-mei=Kanayo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NishimotoHitomi en-aut-sei=Nishimoto en-aut-mei=Hitomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ affil-num=2 en-affil= kn-affil=Okayama Univ affil-num=3 en-affil= kn-affil=Okayama Univ Hosp Med & Dent affil-num=4 en-affil= kn-affil=Okayama Univ Hosp Med & Dent affil-num=5 en-affil= kn-affil=Okayama Univ affil-num=6 en-affil= kn-affil=Okayama Univ affil-num=7 en-affil= kn-affil=Okayama Univ en-keyword=Oral care kn-keyword=Oral care en-keyword=Supportive care kn-keyword=Supportive care en-keyword=Oral mucositis kn-keyword=Oral mucositis en-keyword=Hematopoietic stem cell transplantation kn-keyword=Hematopoietic stem cell transplantation END start-ver=1.4 cd-journal=joma no-vol=16 cd-vols= no-issue=4 article-no= start-page=421 end-page=424 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=200804 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Antimicrobial effects of the saliva substitute, Oralbalance (R), against microorganisms from oral mucosa in the hematopoietic cell transplantation period en-subtitle= kn-subtitle= en-abstract= kn-abstract=Goals The commercially available saliva substitute Oralbalance (R) has been reported to alleviate symptoms of post-radiotherapy xerostomia in head and neck cancer patients. Oralbalance (R) may also be effective for xerostomia in patients undergoing hematopoietic cell transplantation (HCT) with high-dose chemotherapy and total-body irradiation. However, HCT patients are severely compromised, and saliva substitute must therefore not promote infection. This study was performed to determine the effects of Oralbalance (R) on microbial species identified during HCT. Patients and methods Microbial identification of oral mucosa was performed in 28 patients undergoing HCT. The antimicrobial effects of Oralbalance (R) against bacteria and fungi detected in the HCT period were examined in vitro. Briefly, bacteria and fungi were spread on agar plates, and 0.1g of Oralbalance (R) gel was applied (about phi 1cm). After incubation at 37 degrees C for 24h, the presence of a transparent zone of inhibition around Oralbalance (R) was observed. Main results Not only bacterial species constituting normal flora of the oral mucosa but also those not usually constituting normal flora, e.g., coagulase-negative Staphylococcus, were detected. A transparent zone was observed around Oralbalance (R) in all bacterial species examined. No transparent zone was observed for Candida albicans, but growth was inhibited in the area where Oralbalance (R) was applied. Conclusions Oralbalance (R) does not facilitate increases in microorganisms in the HCT period. Oral care with Oralbalance (R) does not promote infection in patients undergoing HCT. en-copyright= kn-copyright= en-aut-name=SugiuraYuko en-aut-sei=Sugiura en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SogaYoshihiko en-aut-sei=Soga en-aut-mei=Yoshihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TanimotoIchiro en-aut-sei=Tanimoto en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KokeguchiSusumu en-aut-sei=Kokeguchi en-aut-mei=Susumu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NishideSachiko en-aut-sei=Nishide en-aut-mei=Sachiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KonoKotoe en-aut-sei=Kono en-aut-mei=Kotoe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakahashiKanayo en-aut-sei=Takahashi en-aut-mei=Kanayo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=FujiiNobuharu en-aut-sei=Fujii en-aut-mei=Nobuharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=IshimaruFumihiko en-aut-sei=Ishimaru en-aut-mei=Fumihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=YamabeKokoro en-aut-sei=Yamabe en-aut-mei=Kokoro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TsutaniSoichiro en-aut-sei=Tsutani en-aut-mei=Soichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=NishimuraFusanori en-aut-sei=Nishimura en-aut-mei=Fusanori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=TakashibaShogo en-aut-sei=Takashiba en-aut-mei=Shogo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ affil-num=2 en-affil= kn-affil=Okayama Univ affil-num=3 en-affil= kn-affil=Okayama Univ affil-num=4 en-affil= kn-affil=Okayama Univ affil-num=5 en-affil= kn-affil=Okayama Univ Hosp affil-num=6 en-affil= kn-affil=Okayama Univ Hosp affil-num=7 en-affil= kn-affil=Okayama Univ Hosp affil-num=8 en-affil= kn-affil=Okayama Univ affil-num=9 en-affil= kn-affil=Okayama Univ affil-num=10 en-affil= kn-affil=Okayama Univ affil-num=11 en-affil= kn-affil=Okayama Univ affil-num=12 en-affil= kn-affil=Okayama Univ affil-num=13 en-affil= kn-affil=Okayama Univ affil-num=14 en-affil= kn-affil=Okayama Univ en-keyword=Hematopoietic cell transplantation kn-keyword=Hematopoietic cell transplantation en-keyword=Xerostomia kn-keyword=Xerostomia en-keyword=Saliva substitute kn-keyword=Saliva substitute en-keyword=Antimicrobial activity kn-keyword=Antimicrobial activity END start-ver=1.4 cd-journal=joma no-vol=124 cd-vols= no-issue=3 article-no= start-page=207 end-page=210 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20121203 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Liposomal delivery of microRNA-7-expressing plasmid overcomes epidermal growth factor receptor tyrosine kinase inhibitor resistance in lung cancer cells kn-title=EGFRチロシンキナーゼ阻害薬耐性肺癌細胞に対するmicroRNA-7発現プラスミドのリポソームを用いた導入による克服の検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=RaiKammei en-aut-sei=Rai en-aut-mei=Kammei kn-aut-name=頼冠名 kn-aut-sei=頼 kn-aut-mei=冠名 aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name=瀧川奈義夫 kn-aut-sei=瀧川 kn-aut-mei=奈義夫 aut-affil-num=2 ORCID= en-aut-name=ItoSachio en-aut-sei=Ito en-aut-mei=Sachio kn-aut-name=伊藤佐智夫 kn-aut-sei=伊藤 kn-aut-mei=佐智夫 aut-affil-num=3 ORCID= en-aut-name=KashiharaHiromi en-aut-sei=Kashihara en-aut-mei=Hiromi kn-aut-name=柏原宏美 kn-aut-sei=柏原 kn-aut-mei=宏美 aut-affil-num=4 ORCID= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name=市原英基 kn-aut-sei=市原 kn-aut-mei=英基 aut-affil-num=5 ORCID= en-aut-name=YasudaTatsuji en-aut-sei=Yasuda en-aut-mei=Tatsuji kn-aut-name=保田立二 kn-aut-sei=保田 kn-aut-mei=立二 aut-affil-num=6 ORCID= en-aut-name=ShimizuKenji en-aut-sei=Shimizu en-aut-mei=Kenji kn-aut-name=清水憲二 kn-aut-sei=清水 kn-aut-mei=憲二 aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　分子遺伝学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞化学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　分子遺伝学 affil-num=8 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 en-keyword=microRNA7 kn-keyword=microRNA7 en-keyword=EGFR kn-keyword=EGFR en-keyword=oncogene addiction kn-keyword=oncogene addiction en-keyword=lung cancer kn-keyword=lung cancer en-keyword=liposome kn-keyword=liposome END start-ver=1.4 cd-journal=joma no-vol=124 cd-vols= no-issue=3 article-no= start-page=197 end-page=201 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20121203 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Synthetic retinoid Am80 ameliorates chronic graft-versus-host disease by downregulating Th1 and Th17 kn-title=合成レチノイドAm80はTh1とTh17を抑制することにより慢性移植片対宿主病を改善する en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name=西森久和 kn-aut-sei=西森 kn-aut-mei=久和 aut-affil-num=1 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name=前田嘉信 kn-aut-sei=前田 kn-aut-mei=嘉信 aut-affil-num=2 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 en-keyword=慢性移植片対宿主病 kn-keyword=慢性移植片対宿主病 en-keyword=同種造血幹細胞移植 kn-keyword=同種造血幹細胞移植 en-keyword=Th17細胞 kn-keyword=Th17細胞 en-keyword=Th1細胞 kn-keyword=Th1細胞 en-keyword=Am80 kn-keyword=Am80 END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=7 article-no= start-page=1562 end-page=1569 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20100401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Down-regulation of BiP/GRP78 sensitizes resistant prostate cancer cells to gene-therapeutic overexpression of REIC/Dkk-3 en-subtitle= kn-subtitle= en-abstract= kn-abstract=We have recently shown that an adenovirus carrying REIC/Dkk-3 (Ad-REIC) exhibits a potent tumor-specific cell-killing function for various human cancers. It has also become evident that some human cancers are resistant to Ad-REIC-induced apoptosis. The aim of the present study was to determine the molecular mechanisms of resistance to Ad-REIC. First, we isolated resistant clones from a human prostate cancer cell line, PC3, after repeated exposure to Ad-REIC. Infection efficiency of the adenovirus vector and expression level of REIC/Dkk-3 in the resistant clones were similar to those in the parental PC3 cells. By screening for alteration in levels and functional status of proteins involved in Ad-REIC-induced apoptosis, we found that BiP/GRP78, an ER-residing chaperone protein, was expressed at higher levels consistently among resistant cells. Expression levels of BiP and rates of apoptosis induced by Ad-REIC were inversely correlated. Down-regulation of BiP with siRNA sensitized the resistant cells to Ad-REIC in vivo as well as in culture. These results indicate that BiP is a major determinant of resistance to Ad-REIC-induced apoptosis. Thus BiP is useful for diagnosis of inherent and acquired resistance of cancers and also as a target molecule to overcome resistance to the gene therapeutic Ad-REIC. en-copyright= kn-copyright= en-aut-name=TanimotoRyuta en-aut-sei=Tanimoto en-aut-mei=Ryuta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SakaguchiMasakiyo en-aut-sei=Sakaguchi en-aut-mei=Masakiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AbarzuaFernando en-aut-sei=Abarzua en-aut-mei=Fernando kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KataokaKen en-aut-sei=Kataoka en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KuroseKaoru en-aut-sei=Kurose en-aut-mei=Kaoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MurataHitoshi en-aut-sei=Murata en-aut-mei=Hitoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NasuYasutomo en-aut-sei=Nasu en-aut-mei=Yasutomo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KumonHiromi en-aut-sei=Kumon en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HuhNam-Ho en-aut-sei=Huh en-aut-mei=Nam-Ho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=REIC kn-keyword=REIC en-keyword=Dkk kn-keyword=Dkk en-keyword=apoptosis kn-keyword=apoptosis en-keyword=GRP78 kn-keyword=GRP78 en-keyword=ER stress kn-keyword=ER stress END start-ver=1.4 cd-journal=joma no-vol=284 cd-vols= no-issue=21 article-no= start-page=14236 end-page=14244 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20090522 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Overexpression of REIC/Dkk-3 in Normal Fibroblasts Suppresses Tumor Growth via Induction of Interleukin-7 en-subtitle= kn-subtitle= en-abstract= kn-abstract=We previously showed that the tumor suppressor gene REIC/Dkk-3, when overexpressed by an adenovirus (Ad-REIC), exhibited a dramatic therapeutic effect on human cancers through a mechanism triggered by endoplasmic reticulum stress. Adenovirus vectors show no target cell specificity and thus may elicit unfavorable side effects through infection of normal cells even upon intra-tumoral injection. In this study, we examined possible effects of Ad-REIC on normal cells. We found that infection of normal human fibroblasts (NHF) did not cause apoptosis but induced production of interleukin (IL)-7. The induction was triggered by endoplasmic reticulum stress and mediated through IRE1 alpha, ASK1, p38, and IRF-1. When Ad-REIC-infected NHF were transplanted in a mixture with untreated human prostate cancer cells, the growth of the cancer cells was significantly suppressed. Injection of an IL-7 antibody partially abrogated the suppressive effect of Ad-REIC-infected NHF. These results indicate that Ad-REIC has another arm against human cancer, an indirect host-mediated effect because of overproduction of IL-7 by mis-targeted NHF, in addition to its direct effect on cancer cells. en-copyright= kn-copyright= en-aut-name=SakaguchiMasakiyo en-aut-sei=Sakaguchi en-aut-mei=Masakiyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KataokaKen en-aut-sei=Kataoka en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=AbarzuaFernando en-aut-sei=Abarzua en-aut-mei=Fernando kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TanimotoRyuta en-aut-sei=Tanimoto en-aut-mei=Ryuta kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WatanabeMasami en-aut-sei=Watanabe en-aut-mei=Masami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MurataHitoshi en-aut-sei=Murata en-aut-mei=Hitoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ThanSwe Swe en-aut-sei=Than en-aut-mei=Swe Swe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KuroseKaoru en-aut-sei=Kurose en-aut-mei=Kaoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KashiwakuraYuji en-aut-sei=Kashiwakura en-aut-mei=Yuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=OchiaiKazuhiko en-aut-sei=Ochiai en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=NasuYasutomo en-aut-sei=Nasu en-aut-mei=Yasutomo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=KumonHiromi en-aut-sei=Kumon en-aut-mei=Hiromi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=HuhNam-ho en-aut-sei=Huh en-aut-mei=Nam-ho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=11 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=12 en-affil= kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences affil-num=13 en-affil= kn-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences END start-ver=1.4 cd-journal=joma no-vol=66 cd-vols= no-issue=4 article-no= start-page=329 end-page=334 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201208 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Effect of Taurine on Acinar Cell Apoptosis and Pancreatic Fibrosis in Dibutyltin Dichloride-induced Chronic Pancreatitis en-subtitle= kn-subtitle= en-abstract= kn-abstract=The relationship between pancreatic fibrosis and apoptosis of pancreatic acinar cells has not been fully elucidated. We reported that taurine had an anti-fibrotic effect in a dibutyltin dichloride (DBTC)-chronic pancreatitis model. However, the effect of taurine on apoptosis of pancreatic acinar cells is still unclear. Therefore, we examined apoptosis in DBTC-chronic pancreatitis and in the AR42J pancreatic acinar cell line with/without taurine. Pancreatic fibrosis was induced by a single administration of DBTC. Rats were fed a taurine-containing diet or a normal diet and were sacrificed at day 5. The AR42J pancreatic acinar cell line was incubated with/without DBTC with taurine chloramines. Apoptosis was determined by using terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. The expression of Bad and Bcl-2 proteins in the AR42J cells lysates was detected by Western blot analysis. The apoptotic index of pancreatic acinar cells in DBTC-administered rats was significantly increased. Taurine treatment inhibited pancreatic fibrosis and apoptosis of acinar cells induced by DBTC. The number of TUNEL-positive cells in the AR42J pancreatic acinar cell lines was significantly increased by the addition of DBTC. Incubation with taurine chloramines ameliorated these changes. In conclusion, taurine inhibits apoptosis of pancreatic acinar cells and pancreatitis in experimental chronic pancreatitis. en-copyright= kn-copyright= en-aut-name=MatsushitaKoki en-aut-sei=Matsushita en-aut-mei=Koki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MizushimaTakaaki en-aut-sei=Mizushima en-aut-mei=Takaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ShirahigeAkinori en-aut-sei=Shirahige en-aut-mei=Akinori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TaniokaHiroaki en-aut-sei=Tanioka en-aut-mei=Hiroaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SawaKiminari en-aut-sei=Sawa en-aut-mei=Kiminari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OchiKoji en-aut-sei=Ochi en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KoideNorio en-aut-sei=Koide en-aut-mei=Norio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=apoptosis kn-keyword=apoptosis en-keyword=chronic pancreatitis kn-keyword=chronic pancreatitis en-keyword=pancreatic acinar cells kn-keyword=pancreatic acinar cells en-keyword=taurine kn-keyword=taurine END start-ver=1.4 cd-journal=joma no-vol=66 cd-vols= no-issue=3 article-no= start-page=245 end-page=251 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201206 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Selective Cyclooxygenase-2 Inhibitor Prevents Cisplatin-induced Tumorigenesis in A/J Mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=Cisplatin is used to treat lung cancer;however, it is also a known carcinogen. Cyclooxygenase-2 (COX-2) inhibitors have been shown to prevent carcinogen-induced experimental tumors. We investigated the effect of a COX-2 inhibitor, celecoxib, on cisplatin-induced lung tumors. One hundred twenty 4-week-old A/J mice were divided into 6 groups:group 1, no treatment;group 2, low-dose celecoxib (150mg/kg);group 3, high-dose celecoxib (1,500mg/kg);group 4, cisplatin alone;group 5, cisplatin plus low-dose celecoxib;and group 6, cisplatin plus high-dose celecoxib. Mice in groups 4-6 were administered cisplatin (1.62mg/kg, i.p.) once a week for 10 weeks between 7 and 16 weeks of age. All mice were sacrificed at week 30. Tumor incidence was 15.8% in group 1, 25% in group 2, 26.3% in group 3, 60% in group 4, 50% in group 5, and 50% in group 6. Tumor multiplicity was 0.2, 0.3, 0.3, 1.3, 1.0, and 0.6 in groups 1-6, respectively. Tumor multiplicity in the cisplatin-treated mice was reduced by celecoxib treatment in a dose-dependent manner (p＜0.05, group 4 vs. group 6). Celecoxib significantly reduced COX-2 expression in cisplatin-induced tumors (p＜0.01, group 4 vs. group 6). en-copyright= kn-copyright= en-aut-name=OkadaToshiaki en-aut-sei=Okada en-aut-mei=Toshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KishinoDaizo en-aut-sei=Kishino en-aut-mei=Daizo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KatayamaHideki en-aut-sei=Katayama en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KuyamaShouichi en-aut-sei=Kuyama en-aut-mei=Shouichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SatoKen en-aut-sei=Sato en-aut-mei=Ken kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MimotoJunko en-aut-sei=Mimoto en-aut-mei=Junko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine affil-num=2 en-affil= kn-affil=Department of General Internal Medicine 4, Kawasaki Hospital, Kawasaki Medical School affil-num=3 en-affil= kn-affil=Department of Medicine, Yamaguchi-Ube Medical Center affil-num=4 en-affil= kn-affil=Department of Medicine, Yamaguchi-Ube Medical Center affil-num=5 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine affil-num=6 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine affil-num=7 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine affil-num=8 en-affil= kn-affil=Department of Medicine, Yamaguchi-Ube Medical Center affil-num=9 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine affil-num=10 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital en-keyword=cisplatin kn-keyword=cisplatin en-keyword=non-small cell lung cancer kn-keyword=non-small cell lung cancer en-keyword=celecoxib kn-keyword=celecoxib en-keyword=cyclooxygenase-2 kn-keyword=cyclooxygenase-2 en-keyword=chemoprevention kn-keyword=chemoprevention END start-ver=1.4 cd-journal=joma no-vol=124 cd-vols= no-issue=1 article-no= start-page=75 end-page=77 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20120401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Japanese guidelines for the management of community-acquired pneumonia kn-title=市中肺炎の診療ガイドライン en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 END start-ver=1.4 cd-journal=joma no-vol=124 cd-vols= no-issue=1 article-no= start-page=5 end-page=8 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20120401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Alloantigen expression on non-hematopoietic cells reduces graft-versus-leukemia effects in mice kn-title=同種抗原による移植片対白血病効果減弱のメカニズム en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=AsakuraShoji en-aut-sei=Asakura en-aut-mei=Shoji kn-aut-name=朝倉昇司 kn-aut-sei=朝倉 kn-aut-mei=昇司 aut-affil-num=1 ORCID= en-aut-name=HashimotoDaigo en-aut-sei=Hashimoto en-aut-mei=Daigo kn-aut-name=橋本大吾 kn-aut-sei=橋本 kn-aut-mei=大吾 aut-affil-num=2 ORCID= en-aut-name=TakashimaShuichiro en-aut-sei=Takashima en-aut-mei=Shuichiro kn-aut-name=高嶋秀一郎 kn-aut-sei=高嶋 kn-aut-mei=秀一郎 aut-affil-num=3 ORCID= en-aut-name=SugiyamaHaruko en-aut-sei=Sugiyama en-aut-mei=Haruko kn-aut-name=杉山暖子 kn-aut-sei=杉山 kn-aut-mei=暖子 aut-affil-num=4 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name=前田嘉信 kn-aut-sei=前田 kn-aut-mei=嘉信 aut-affil-num=5 ORCID= en-aut-name=AkashiKoichi en-aut-sei=Akashi en-aut-mei=Koichi kn-aut-name=赤司浩一 kn-aut-sei=赤司 kn-aut-mei=浩一 aut-affil-num=6 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=7 ORCID= en-aut-name=TeshimaTakanori en-aut-sei=Teshima en-aut-mei=Takanori kn-aut-name=豊嶋崇徳 kn-aut-sei=豊嶋 kn-aut-mei=崇徳 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=国立病院機構岡山医療センター　血液内科 affil-num=2 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=3 en-affil= kn-affil=九州大学大学院　病態修復内科学 affil-num=4 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=5 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=6 en-affil= kn-affil=九州大学病院　遺伝子細胞療法部 affil-num=7 en-affil= kn-affil=岡山大学病院　血液・腫瘍内科 affil-num=8 en-affil= kn-affil=九州大学病院　遺伝子細胞療法部 en-keyword=同種造血幹細胞移植 kn-keyword=同種造血幹細胞移植 en-keyword=移植片対白血病効果 kn-keyword=移植片対白血病効果 en-keyword=programmed death-1 (PD-1) kn-keyword=programmed death-1 (PD-1) en-keyword=programmed death ligand-1 (PD-L1) kn-keyword=programmed death ligand-1 (PD-L1) END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=6 article-no= start-page=403 end-page=406 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201112 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Successful Extracorporeal Life Support for Life-threatening Hypercapnia with Bronchiolitis Obliterans after Allogeneic Hematopoietic Stem Cell Transplantation en-subtitle= kn-subtitle= en-abstract= kn-abstract=Bronchiolitis obliterans (BO) is a disease with a poor prognosis, and a key factor that limits long-term survival after allogeneic hematopoietic stem cell transplantation (HSCT). We here report a case of a 31-year woman with acute lymphatic leukemia, which was treated by chemotherapy and HSCT, and consequently developed BO 2 years after HSCT. A non-tuberculous mycobacterial infection occurred and showed gradual exacerbation. She started taking anti-mycobacterial drugs, but lost appetite, felt tired and finally lost consciousness one month after beginning medication. Arterial blood gas revealed marked hypercapnia. Using extracorporeal life support (ECLS), the carbon dioxide concentration was reduced and her consciousness recovered. To our knowledge, this is the first case in which ECLS was successfully used for hypercapnia in a patient with BO. en-copyright= kn-copyright= en-aut-name=WasedaKoichi en-aut-sei=Waseda en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IchibaShingo en-aut-sei=Ichiba en-aut-mei=Shingo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MurakamiToshi en-aut-sei=Murakami en-aut-mei=Toshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TeradoMichihisa en-aut-sei=Terado en-aut-mei=Michihisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NaganoOsamu en-aut-sei=Nagano en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MaedaYoshinobu en-aut-sei=Maeda en-aut-mei=Yoshinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=UjikeYoshihito en-aut-sei=Ujike en-aut-mei=Yoshihito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=11 en-affil= kn-affil=Department of Emergency and Critical Care Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=12 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=extracorporeal life support kn-keyword=extracorporeal life support en-keyword=hypercapnia kn-keyword=hypercapnia en-keyword=bronchiolitis obliterans kn-keyword=bronchiolitis obliterans en-keyword=noninvasive positive pressure ventilation kn-keyword=noninvasive positive pressure ventilation END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=6 article-no= start-page=353 end-page=362 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201112 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Targeting Angiogenesis in Cancer Therapy en-subtitle= kn-subtitle= en-abstract= kn-abstract=Angiogenesis is an essential process in tumor growth. The concept of angiogenesis, when proposed by Folksman in 1971, had a great impact on cancer research and therapy, as the survival and proliferation of cancer depend on angiogenesis, which could be a target of cancer therapy. In subsequent decades, numerous antiangiogenic agents were developed, and some of them have been applied clinically. However, angiogenesis includes a complex and multistep process that has not been sufficiently elucidated. In this review, we focus on signaling pathways related with tumor angiogenesis and several antiangiogenic agents approved by the United States Food and Drug Administration or under investigation. en-copyright= kn-copyright= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=angiogenesis kn-keyword=angiogenesis en-keyword=cancer kn-keyword=cancer END start-ver=1.4 cd-journal=joma no-vol=123 cd-vols= no-issue=3 article-no= start-page=221 end-page=225 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20111201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Acute respiratory distress syndrome following infection of influenza A (H1N1) virus kn-title=新型インフルエンザウイルス（A/H1N1）感染後にARDSを来たした1例 en-subtitle= kn-subtitle= en-abstract= kn-abstract=A 28-year-old man with a history of mental retardation was admitted to our hospital because of dyspnea, cough and high fever. His SpO(2) level at room-environmental conditions was in the eighties, and his chest radiograph showed diffuse infiltrates in both lungs. He was diagnosed as suffering from influenza A by a rapid influenza virus antigen test. The echocardiogram showed no evidence of left cardiac failure; therefore, his symptoms were consistent with acute respiratory distress syndrome (ARDS). Oseltamivir was started, and antibiotics were also given because of the possibility of secondary bacterial infection. Due to respiratory failure and low blood pressure, which suggested septic shock, intensive treatments including mechanical ventilation were performed. Corticosteroid therapy was started for ARDS and sepsis, and these therapies improved his respiratory condition. Polymerase chain reaction of his pharyngeal swab revealed that he had influenza A (H1N1). This is the first case of ARDS following infection by influenza A (H1N1) virus in Japan. en-copyright= kn-copyright= en-aut-name=TaniguchiAkihiko en-aut-sei=Taniguchi en-aut-mei=Akihiko kn-aut-name=谷口暁 kn-aut-sei=谷口 kn-aut-mei=暁 aut-affil-num=1 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name=宮原信明 kn-aut-sei=宮原 kn-aut-mei=信明 aut-affil-num=2 ORCID= en-aut-name=NakaharaAtsushi en-aut-sei=Nakahara en-aut-mei=Atsushi kn-aut-name=中原淳 kn-aut-sei=中原 kn-aut-mei=淳 aut-affil-num=3 ORCID= en-aut-name=TakataSaburo en-aut-sei=Takata en-aut-mei=Saburo kn-aut-name=高田三郎 kn-aut-sei=高田 kn-aut-mei=三郎 aut-affil-num=4 ORCID= en-aut-name=SakugawaRyo en-aut-sei=Sakugawa en-aut-mei=Ryo kn-aut-name=佐久川亮 kn-aut-sei=佐久川 kn-aut-mei=亮 aut-affil-num=5 ORCID= en-aut-name=NaganoOsamu en-aut-sei=Nagano en-aut-mei=Osamu kn-aut-name=長野修 kn-aut-sei=長野 kn-aut-mei=修 aut-affil-num=6 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=7 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name=金廣有彦 kn-aut-sei=金廣 kn-aut-mei=有彦 aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=9 ORCID= en-aut-name=UjikeYoshito en-aut-sei=Ujike en-aut-mei=Yoshito kn-aut-name=氏家良人 kn-aut-sei=氏家 kn-aut-mei=良人 aut-affil-num=10 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=2 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=3 en-affil= kn-affil=岡山大学病院　救急科 affil-num=4 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=5 en-affil= kn-affil=岡山赤十字病院　呼吸器内科 affil-num=6 en-affil= kn-affil=岡山大学病院　救急科 affil-num=7 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=8 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=9 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=10 en-affil= kn-affil=岡山大学病院　救急科 affil-num=11 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 en-keyword=インフルエンザ Ａ (influenza A) kn-keyword=インフルエンザ Ａ (influenza A) en-keyword=H1N1 kn-keyword=H1N1 en-keyword=急性呼吸促迫症候群 (acute respiratory distress syndrome) kn-keyword=急性呼吸促迫症候群 (acute respiratory distress syndrome) END start-ver=1.4 cd-journal=joma no-vol=74 cd-vols= no-issue=1 article-no= start-page=80 end-page=84 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201110 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A phase II study of amrubicin and topotecan combination therapy in patients with relapsed or extensive-disease small-cell lung cancer: Okayama Lung Cancer Study Group Trial 0401 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Backgrounds: Chemotherapy is a mainstay in the treatment of extensive-disease small-cell lung cancer (ED-SCLC), although the survival benefit remains modest. We conducted a phase II trial of amrubicin (a topoisomerase II inhibitor) and topotecan (a topoisomerase I inhibitor) in chemotherapy-na?ve and relapsed SCLC patients. Methods: Amrubicin (35 mg/m(2)) and topotecan (0.75 mg/m(2)) were administered on days 3-5 and 1-5, respectively. The objective response rate (ORR) was set as the primary endpoint, which was assessed separately in chemotherapy-na?ve and relapsed cases. Results: Fifty-nine patients were enrolled (chemotherapy-na?ve 31, relapsed 28). The ORRs were 74% and 43% in the chemotherapy-na?ve and relapsed cases, respectively. Survival data were also promising, with a median progression-free survival time and median survival time of 5.3 and 14.9 months and 4.7 and 10.2 months in the chemotherapy-na?ve and relapsed cases, respectively. Even refractory-relapsed cases responded to the treatment favorably (27% ORR). The primary toxicity was myelosuppression with grades 3 or 4 neutropenia in 97% of the patients, which led to grades 3 or 4 febrile neutropenia in 41% of the patients and two toxic deaths. Conclusion: This phase II study showed the favorable efficacy and moderate safety profiles of a topotecan and amrubicin two-drug combination especially in relapsed patients with ED-SCLC. en-copyright= kn-copyright= en-aut-name=NogamiNaoyuki en-aut-sei=Nogami en-aut-mei=Naoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HottaKatsuyuki en-aut-sei=Hotta en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KuyamaShoichi en-aut-sei=Kuyama en-aut-mei=Shoichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChikamoriKenichi en-aut-sei=Chikamori en-aut-mei=Kenichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShibayamaTakuo en-aut-sei=Shibayama en-aut-mei=Takuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KishinoDaizo en-aut-sei=Kishino en-aut-mei=Daizo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HosokawaShinobu en-aut-sei=Hosokawa en-aut-mei=Shinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TamaokiAkihiko en-aut-sei=Tamaoki en-aut-mei=Akihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=HaritaShingo en-aut-sei=Harita en-aut-mei=Shingo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=ShinkaiTetsu en-aut-sei=Shinkai en-aut-mei=Tetsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= affil-num=1 en-affil= kn-affil=Department of Respiratory Medicine, NHO Shikoku Cancer Center affil-num=2 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital affil-num=3 en-affil= kn-affil=Department of Medicine, Chugoku Central Hospital affil-num=4 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital affil-num=5 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital affil-num=6 en-affil= kn-affil=Department of Respiratory Medicine, NHO Yamaguchi-Ube Medical Center affil-num=7 en-affil= kn-affil=Department of Medicine, NHO Minami-Okayama Medical Center affil-num=8 en-affil= kn-affil=Department of Respiratory Medicine, NHO Yamaguchi-Ube Medical Center affil-num=9 en-affil= kn-affil=Department of Respiratory Medicine, Okayama Red Cross Hospital affil-num=10 en-affil= kn-affil=Department of Respiratory Medicine, Okayama Institute of Health and Prevention affil-num=11 en-affil= kn-affil=Department of Medicine, Chugoku Central Hospital affil-num=12 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital affil-num=13 en-affil= kn-affil=Department of Respiratory Medicine, NHO Yamaguchi-Ube Medical Center affil-num=14 en-affil= kn-affil=Department of Respiratory Medicine, NHO Shikoku Cancer Center affil-num=15 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital en-keyword=Lung cancer kn-keyword=Lung cancer en-keyword=Topotecan kn-keyword=Topotecan en-keyword=Amrubicin kn-keyword=Amrubicin en-keyword=Chemo-naive kn-keyword=Chemo-naive en-keyword=Sensitive relapse kn-keyword=Sensitive relapse en-keyword=Refractory relapse kn-keyword=Refractory relapse END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=4 article-no= start-page=259 end-page=263 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201108 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Is Adenosine Deaminase in Pleural Fluid a Useful Marker for Differentiating Tuberculosis from Lung Cancer or Mesothelioma in Japan, a Country with Intermediate Incidence of Tuberculosis? en-subtitle= kn-subtitle= en-abstract= kn-abstract=The objective of this study was to evaluate the utility of the determination of adenosine deaminase (ADA) level in pleural fluid for the differential diagnosis between tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE) in Japan, a country with intermediate incidence of tuberculosis (TB). We retrospectively reviewed the clinical records of 435 patients with pleural effusion and investigated their pleural ADA levels as determined by an auto analyzer. ROC analysis was also performed. The study included patients with MPE (n＝188), TPE (n＝124), benign nontuberculous pleural effusion (n＝94), and pleural effusion of unknown etiology (n＝29). The median ADA level in the TPE group was 70.8U/L, which was significantly higher than that in any other groups (p＜0.05). The area under the curve (AUC) in ROC analysis was 0.895. With a cut-off level for ADA of 36U/L, the sensitivity, specificity, positive predictive value, and negative predictive value were 85.5%, 86.5%, 69.7%, and 93.6%, respectively. As many as 9% of patients with lung cancer and 15% of those with mesothelioma were false-positive with this ADA cutoff setting. Although the ADA activity in pleural fluid can help in the diagnosis of TPE, it should be noted that some cases of lung cancer or mesothelioma show high ADA activity in geographical regions with intermediate incidence of TB, in contrast to high prevalence areas. en-copyright= kn-copyright= en-aut-name=OgataYoshiko en-aut-sei=Ogata en-aut-mei=Yoshiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AoeKeisuke en-aut-sei=Aoe en-aut-mei=Keisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HirakiAkio en-aut-sei=Hiraki en-aut-mei=Akio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MurakamiKazuo en-aut-sei=Murakami en-aut-mei=Kazuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KishinoDaizo en-aut-sei=Kishino en-aut-mei=Daizo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ChikamoriKenichi en-aut-sei=Chikamori en-aut-mei=Kenichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MaedaTadashi en-aut-sei=Maeda en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduated School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Medical Oncology, NHO Yamaguchi-Ube Medical Center affil-num=3 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduated School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Respiratory Medicine, NHO Yamaguchi-Ube Medical Center affil-num=5 en-affil= kn-affil=Department of Medical Oncology, NHO Yamaguchi-Ube Medical Center affil-num=6 en-affil= kn-affil=Department of Medical Oncology, NHO Yamaguchi-Ube Medical Center affil-num=7 en-affil= kn-affil=Department of Medical Oncology, NHO Yamaguchi-Ube Medical Center affil-num=8 en-affil= kn-affil=Department of Medical Oncology, NHO Yamaguchi-Ube Medical Center affil-num=9 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduated School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduated School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=pleural effusion kn-keyword=pleural effusion en-keyword=adenosine deaminase kn-keyword=adenosine deaminase en-keyword=tuberculosis kn-keyword=tuberculosis en-keyword=lung cancer kn-keyword=lung cancer en-keyword=mesothelioma kn-keyword=mesothelioma END start-ver=1.4 cd-journal=joma no-vol=123 cd-vols= no-issue=2 article-no= start-page=85 end-page=89 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Hepatic toxicity and prognosis in HCV-infected patients with diffuse large B-cell lymphoma in the rituximab era kn-title=HCV感染がRCHOP療法下でのDLBCLにおける 肝障害と予後に与える影響 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=EnnishiDaisuke en-aut-sei=Ennishi en-aut-mei=Daisuke kn-aut-name=遠西大輔 kn-aut-sei=遠西 kn-aut-mei=大輔 aut-affil-num=1 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 en-keyword=HCV kn-keyword=HCV en-keyword=diffuse large B-cell lymphoma kn-keyword=diffuse large B-cell lymphoma en-keyword=rituximab kn-keyword=rituximab en-keyword=hepatic toxicity kn-keyword=hepatic toxicity END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=3 article-no= start-page=215 end-page=218 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201106 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Churg-Strauss Syndrome with Necrosis of Toe Tips en-subtitle= kn-subtitle= en-abstract= kn-abstract=Churg-Strauss syndrome (CSS) is a granulomatous necrotizing vasculitis of unknown etiology associated with bronchial asthma. Despite affecting small to medium-sized vessels, necrosis of the digits due to vasculitis is extremely rare. We report a case of CSS with necrosis of the toe tips. A 37-year-old woman with asthma, who had been diagnosed with CSS 2 years ago, was admitted to our hospital with an exacerbation of CSS. The patient had a high grade fever and complained of abdominal pain and numbness of the lower extremities. Blood examination revealed marked eosinophilia. The fever pattern, abdominal pain and blood eosinophilia showed improvement by combination treatment with prednisolone and cyclophosphamide. However, the color of her right toe tips changed, and necrosis finally resulted despite antithrombotic therapy. Arteriography showed narrowing of the dorsalis pedis artery and of the more peripheral arteries of her right leg. Stump plasty with negative pressure dressing therapy for the toe tips, but not amputation, was done to preserve the leg function. While numbness of the extremities remained, no recurrence of necrosis was seen. Clinicians need to be aware that rare complications of CSS, including necrosis of the digits, can occur. en-copyright= kn-copyright= en-aut-name=WasedaKoichi en-aut-sei=Waseda en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=HasegawaKenjiro en-aut-sei=Hasegawa en-aut-mei=Kenjiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NojimaDaisuke en-aut-sei=Nojima en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IkedaGenyo en-aut-sei=Ikeda en-aut-mei=Genyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OkadaChiharu en-aut-sei=Okada en-aut-mei=Chiharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KimataYoshihiro en-aut-sei=Kimata en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Plastic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Allergy, National Hospital Organization Minami-Okayama Medical Center affil-num=9 en-affil= kn-affil=Department of Plastic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=bronchial asthma kn-keyword=bronchial asthma en-keyword=Churg-Strauss syndrome kn-keyword=Churg-Strauss syndrome en-keyword=eosinophilia kn-keyword=eosinophilia en-keyword=necrosis of toe tips kn-keyword=necrosis of toe tips en-keyword=stump plasty kn-keyword=stump plasty END start-ver=1.4 cd-journal=joma no-vol=123 cd-vols= no-issue=1 article-no= start-page=49 end-page=52 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The care of rare respiratory diseases in Japan kn-title=希少呼吸器疾患の治療・管理 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=1 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 affil-num=2 en-affil= kn-affil=岡山大学病院　呼吸器・アレルギー内科 en-keyword=希少疾病用医薬品 kn-keyword=希少疾病用医薬品 en-keyword=特発性間質性肺炎 kn-keyword=特発性間質性肺炎 en-keyword=特発性肺線維症 kn-keyword=特発性肺線維症 en-keyword=ピルフェニドン kn-keyword=ピルフェニドン END start-ver=1.4 cd-journal=joma no-vol=123 cd-vols= no-issue=1 article-no= start-page=13 end-page=18 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Effects of vandetanib on lung adenocarcinoma cells harboring epidermal growth factor receptor T790M mutation in vivo kn-title=生体内におけるEGFR T790M遺伝子変異を持つ肺腺癌細胞に対するバンデタニブの効果 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name=市原英基 kn-aut-sei=市原 kn-aut-mei=英基 aut-affil-num=1 ORCID= en-aut-name=OhashiKadoaki en-aut-sei=Ohashi en-aut-mei=Kadoaki kn-aut-name=大橋圭明 kn-aut-sei=大橋 kn-aut-mei=圭明 aut-affil-num=2 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name=瀧川奈義夫 kn-aut-sei=瀧川 kn-aut-mei=奈義夫 aut-affil-num=3 ORCID= en-aut-name=OsawaMasahiro en-aut-sei=Osawa en-aut-mei=Masahiro kn-aut-name=大澤昌宏 kn-aut-sei=大澤 kn-aut-mei=昌宏 aut-affil-num=4 ORCID= en-aut-name=OginoAtsuko en-aut-sei=Ogino en-aut-mei=Atsuko kn-aut-name=荻野敦子 kn-aut-sei=荻野 kn-aut-mei=敦子 aut-affil-num=5 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=6 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 en-keyword=バンデタニブ kn-keyword=バンデタニブ en-keyword=VEGFR kn-keyword=VEGFR en-keyword=EGFR kn-keyword=EGFR en-keyword=T790M遺伝子変異 kn-keyword=T790M遺伝子変異 en-keyword=肺腺癌 kn-keyword=肺腺癌 END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=7 article-no= start-page=1925 end-page=1932 dt-received= dt-revised= dt-accepted= dt-pub-year=1957 dt-pub=19570731 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on Parathion Poisoning Part 4. The Function of the Reticulo-endotherial System in Parathion Poisonig kn-title=パラチオン中毒に関する研究 第4編 パラチオン中毒の網内系機能に及ぼす影響 en-subtitle= kn-subtitle= en-abstract= kn-abstract=In the rabbits, dogs and patients with parathion poisoning, the function of the reticulo-endotherial system was examined by means of carbon black phagocytosis (Sugiyama) and congo-red test (Adler & Reimann). Results are as follows: 1) In the acute parathion poisoning, the function of the reticulo-endotherial sytem presented itself the disturbances such as the decrease of phagocytosis and the increase of congo-red index at the early stage of the poisoning. 2) With daily injection of small doses of parathion, similar disturbances ever noted, and lasted longer. 3) The recovery of the function of the reticulo-endotherial system was similar to that of blood cholinesterase activity. en-copyright= kn-copyright= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=7 article-no= start-page=1915 end-page=1924 dt-received= dt-revised= dt-accepted= dt-pub-year=1957 dt-pub=19570731 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on Parathion Poisoning Part 3. Parathion poisonig in Experimental Anemias kn-title=パラチオン中毒に関する研究 第3編 貧血家兎に於けるパラチオン中毒 en-subtitle= kn-subtitle= en-abstract= kn-abstract=In the rabbits with bleeding anemia, the red cell cholinesterase was inhibited following subcutaneous injection of 10 mg/kg parathion as in the cases of normal rabbits, while the recovery of red cell cholinesterase was faster and greater than that of the normal, and moreover, it was estimated to be above the normal value. Changes of serum cholinesterase activity was the same as those of red cell cholinesterase. On the contrary, in the rabbits with anemia induced by repeated injections of bezol, slower recovery of red cell cholinesterase was observed, but the serum cholinesterase activity was similar to that of the control. In both these anemic cases, almost no difference in LD(50) of parathion could be detected. en-copyright= kn-copyright= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=7 article-no= start-page=1909 end-page=1914 dt-received= dt-revised= dt-accepted= dt-pub-year=1957 dt-pub=19570731 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on Parathion Poisoning Part 2. Parathion Poisoning in Experimental Liver Injury kn-title=パラチオン中毒に関する研究 第2編 肝障碍家兎に於けるパラチオン中毒 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Using the rabbits whose liver had been been injured with injection of 20% CCl(4) in oliveoil (1 cc/kg) every two days and administering parathion 24 hours after the third CCl(4) injection, the following results were obtained: 1) In rabbitts with injured liver serum cholinesterase activity reached its maximum 24 hours after the 3rd CCl(4) injection and returned to the original level, showing the improvement in the function of bromsulfalein excretion. 2) In the group with parathion injection 3 mg/kg each, serum cholinesterase activity was inhibited to the highest degree 3-6 hours after the parathion injection as in the healthy rabbits, but the slackening of cholinesterase activity in the injured was less marked than in the healthy, and lasted longer. 3) The LD(50) in the rabbits with injured liver was 3.88 (2.645.70) mg/kg, while the LD(50) in the healthy rabbits is 10 mg/kg. 4) In the injured rabbits parathion had no influence upon the recovery of the function of bromsulfalein excretion. en-copyright= kn-copyright= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=7 article-no= start-page=1899 end-page=1908 dt-received= dt-revised= dt-accepted= dt-pub-year=1957 dt-pub=19570731 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on Parathion Poisoning Part 1. Histological Changes in Various Organs of Labaratory Rabbits with Parathion Poisonig kn-title=パラチオン中毒に関する研究 第1編 パラチオン中毒家兎諸臓器の組織像 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Histolgical changes in rabbits with acute and chronic parathion intoxication have been examined, and the results are as follows: 1) In the rabbit with chronic parathion poisoning induced by repeated parathion injections, histological changes were the most remarkable in the central nervous system, and in lethal cases were of circulatory disturbances such edema, hyperemia and bleeding. 2) On the contrary, in the moderate cases with acute poisonig, the changes were not so remarkable, and a month later almost no change was observed. 3) Such changes above menthioned might be caused by circulatory disturbances due to the anticholinergic action of parathion, and again the direct action of parathion for such changes should perhaps not be neglected. en-copyright= kn-copyright= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=71 cd-vols= no-issue=6-2 article-no= start-page=3193 end-page=3196 dt-received= dt-revised= dt-accepted= dt-pub-year=1959 dt-pub=19590515 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Experimental Studies on the Nature of Radiation Disturbances Part 2 A anemize substance which is produced in the peripheral blood with X-ray or Co(60)irradiation kn-title=放射線障害の本態に関する実験的研究 第2編 催貧血に就いて en-subtitle= kn-subtitle= en-abstract= kn-abstract=We attempted to reserch that a poison are produced in blood when the blood are irradiated, and whether such poison causes tissue injuries secondarily or not. Experimental Method: After the rabbits blood of removing serum in test tube are irradiated with great doses of X-rays or Co(60) at a time, such blood injected to other healthy rabbits, and then we research to what change are brought in such case, and we find out following matter. Experimental Results: The peripheral blood cell count reduced after transfusions, the function of the reticuloendotherial system falled and the apperance of Heinz's body erythrocytes were remarkable. In view of these facts, it seems to be produced a toxic substance in the peripheral blood of the rabbit irradiated with X-ray or Co(60), and the the toxic substance causes radiation injuries secondarily. en-copyright= kn-copyright= en-aut-name=YamamotoM. en-aut-sei=Yamamoto en-aut-mei=M. kn-aut-name=山本道夫 kn-aut-sei=山本 kn-aut-mei=道夫 aut-affil-num=1 ORCID= en-aut-name=NishishitaS. en-aut-sei=Nishishita en-aut-mei=S. kn-aut-name=西下創一 kn-aut-sei=西下 kn-aut-mei=創一 aut-affil-num=2 ORCID= en-aut-name=AndoR. en-aut-sei=Ando en-aut-mei=R. kn-aut-name=安東龍 kn-aut-sei=安東 kn-aut-mei=龍 aut-affil-num=3 ORCID= en-aut-name=NobukiS. en-aut-sei=Nobuki en-aut-mei=S. kn-aut-name=信木茂生 kn-aut-sei=信木 kn-aut-mei=茂生 aut-affil-num=4 ORCID= en-aut-name=KojimaS. en-aut-sei=Kojima en-aut-mei=S. kn-aut-name=小島澄一 kn-aut-sei=小島 kn-aut-mei=澄一 aut-affil-num=5 ORCID= en-aut-name=TanimotoJ. en-aut-sei=Tanimoto en-aut-mei=J. kn-aut-name=谷本潤一 kn-aut-sei=谷本 kn-aut-mei=潤一 aut-affil-num=6 ORCID= en-aut-name=AkagiK. en-aut-sei=Akagi en-aut-mei=K. kn-aut-name=赤木瑩子 kn-aut-sei=赤木 kn-aut-mei=瑩子 aut-affil-num=7 ORCID= en-aut-name=ShiakuT. en-aut-sei=Shiaku en-aut-mei=T. kn-aut-name=塩飽健 kn-aut-sei=塩飽 kn-aut-mei=健 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=2 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=3 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=4 en-affil= kn-affil= affil-num=5 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=6 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=7 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=8 en-affil= kn-affil=岡山大学医学部放射線医学教室 END start-ver=1.4 cd-journal=joma no-vol=122 cd-vols= no-issue=3 article-no= start-page=237 end-page=242 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=20101201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The present status of rare diseases in Japan kn-title=希少疾患とそれらへの対応 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器・アレルギー内科学 en-keyword=希少疾患 kn-keyword=希少疾患 en-keyword=orphan drug kn-keyword=orphan drug en-keyword=難治性疾患 kn-keyword=難治性疾患 en-keyword=医薬品開発 kn-keyword=医薬品開発 en-keyword=新薬承認 kn-keyword=新薬承認 END start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=5 article-no= start-page=285 end-page=291 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201010 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Cancer of Unknown Primary Site:A Review of 28 Cases and the Efficacy of Cisplatin/Docetaxel Therapy at a Single Institute in Japan en-subtitle= kn-subtitle= en-abstract= kn-abstract=We evaluated the efficacy and toxicity of cisplatin/docetaxel (CDDP/TXT) chemotherapy and identified prognostic factors in Japanese patients with cancer of unknown primary site (CUP). Twenty-eight consecutive patients seen at a single institute were reviewed retrospectively. Sixteen patients were treated with TXT 80mg/m2, followed by CDDP 75mg/m2. The overall response rate to CDDP/TXT treatment was 62.5%, with a median survival time (MST) of 22.7 months. Common adverse reactions were myelosuppression and hyponatremia. The MST of all 28 patients with CUP was 8.3 months, and the 1-year overall survival rate was 45.6%. Univariate analysis identified 5 prognostic factors:performance status, liver involvement, bone involvement, pleural involvement, and lymph node involvement. In conclusion, CDDP/TXT chemotherapy is effective with tolerable toxicity in patients with CUP. Japanese patients with CUP might be chemosensitive and may survive longer. en-copyright= kn-copyright= en-aut-name=NishimoriHisakazu en-aut-sei=Nishimori en-aut-mei=Hisakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakahashiShunji en-aut-sei=Takahashi en-aut-mei=Shunji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=EnnishiDaisuke en-aut-sei=Ennishi en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KobayashiTakayuki en-aut-sei=Kobayashi en-aut-mei=Takayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SanoKoji en-aut-sei=Sano en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShinozakiEiji en-aut-sei=Shinozaki en-aut-mei=Eiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=YokoyamaMasahiro en-aut-sei=Yokoyama en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MishimaYuko en-aut-sei=Mishima en-aut-mei=Yuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TeruiYasuhito en-aut-sei=Terui en-aut-mei=Yasuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=ChinKeisho en-aut-sei=Chin en-aut-mei=Keisho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=MizunumaNobuyuki en-aut-sei=Mizunuma en-aut-mei=Nobuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=ItoYoshinori en-aut-sei=Ito en-aut-mei=Yoshinori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= en-aut-name=NishimuraSeiichiro en-aut-sei=Nishimura en-aut-mei=Seiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=14 ORCID= en-aut-name=TakeuchiKengo en-aut-sei=Takeuchi en-aut-mei=Kengo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=15 ORCID= en-aut-name=IshikawaYuichi en-aut-sei=Ishikawa en-aut-mei=Yuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=16 ORCID= en-aut-name=OguchiMasahiko en-aut-sei=Oguchi en-aut-mei=Masahiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=17 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=18 ORCID= en-aut-name=HatakeKiyohiko en-aut-sei=Hatake en-aut-mei=Kiyohiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=19 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology, Allergy, and Respiratory Medicine, Okayama University Hospital affil-num=2 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=3 en-affil= kn-affil=Department of Hematology, Oncology, Allergy, and Respiratory Medicine, Okayama University Hospital affil-num=4 en-affil= kn-affil=Department of Hematology, Oncology, Allergy, and Respiratory Medicine, Okayama University Hospital affil-num=5 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=6 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=7 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=8 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=9 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=10 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=11 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=12 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=13 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital affil-num=14 en-affil= kn-affil=Division of Breast Surgery, Cancer Institute Hospital affil-num=15 en-affil= kn-affil=Division of Pathology, Cancer Institute of the Japanese Foundation for Cancer Research affil-num=16 en-affil= kn-affil=Division of Pathology, Cancer Institute of the Japanese Foundation for Cancer Research affil-num=17 en-affil= kn-affil=Division of Radiology, Cancer Institute Hospital affil-num=18 en-affil= kn-affil=Department of Hematology, Oncology, Allergy, and Respiratory Medicine, Okayama University Hospital affil-num=19 en-affil= kn-affil=Division of Medical Oncology and Hematology, Cancer Institute Hospital en-keyword=cancer of unknown primary site (CUP) kn-keyword=cancer of unknown primary site (CUP) en-keyword=cisplatin kn-keyword=cisplatin en-keyword=docetaxel kn-keyword=docetaxel en-keyword=prognosis kn-keyword=prognosis END start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=3 article-no= start-page=181 end-page=187 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201006 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Interstitial Lung Disease during Trimethoprim/Sulfamethoxazole Administration en-subtitle= kn-subtitle= en-abstract= kn-abstract=We studied clinical and radiographic features of interstitial lung disease (ILD) during trimethoprim/sulfamethoxazole (TMP/SMX) administration. Ten patients who had received prednisolone treatment for underlying diffuse pulmonary disease showed various ILDs after introduction of TMP/SMX. The radiographic features of the ILDs were not consistent with infectious disease or exacerbation of the underlying disease, and these diagnoses were excluded radiographically and on clinical grounds during the differential diagnosis of the ILDs. These ILDs emerged relatively early after introduction of TMP/SMX, which is consistent with the former case report of drug-induced ILD (DI-ILD) caused by TMP/SMX. Therefore DI-ILDs caused by TMP/SMX were suspected in these cases. In most of these cases, the ILDs were clinically mild and disappeared immediately although administration of TMP/SMX was continued. en-copyright= kn-copyright= en-aut-name=YuzurioSyota en-aut-sei=Yuzurio en-aut-mei=Syota kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HoritaNaokatsu en-aut-sei=Horita en-aut-mei=Naokatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ShiotaYutaro en-aut-sei=Shiota en-aut-mei=Yutaro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Department of Respiratory Medicine, Kure-Kyosai Hospital affil-num=2 en-affil= kn-affil=Department of Respiratory Medicine, Kure-Kyosai Hospital affil-num=3 en-affil= kn-affil=Department of Respiratory Medicine, Kure-Kyosai Hospital affil-num=4 en-affil= kn-affil=Department of Hematology, Oncology, Respiratory Medicine, and Allergology, Okayama University Medical School and Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Hematology, Oncology, Respiratory Medicine, and Allergology, Okayama University Medical School and Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=drug-induced interstitial lung disease kn-keyword=drug-induced interstitial lung disease en-keyword=trimethoprim/sulfamethoxazole kn-keyword=trimethoprim/sulfamethoxazole en-keyword=clinical characteristic kn-keyword=clinical characteristic en-keyword=radiographic findings kn-keyword=radiographic findings END start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=1 article-no= start-page=33 end-page=37 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201002 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Triplet Chemotherapy with Cisplatin, Docetaxel, and Irinotecan for Patients with Recurrent or Refractory Non-small Cell Lung Cancer en-subtitle= kn-subtitle= en-abstract= kn-abstract=

We examined the feasibility of triplet chemotherapy using cisplatin, docetaxel, and irinotecan for patients with recurrent or refractory non-small cell lung cancer (NSCLC), retrospectively. Twenty-five patients (21 men and 4 women) with NSCLC and good performance status who were <70 years old were analyzed. The median age was 58 years. Most patients had performance status 1 (16/25), stage IV disease (18/25) and adenocarcinoma-histology (16/25). Cisplatin and docetaxel were given on day 1 and irinotecan on day 2;the cycle was repeated every 3 weeks. The objective response rate was 39.1% (95% confidence interval:18.7-59.5%). The median survival time and actual 2-, 3-, and 5-year survival rates were 14.3 months, 32%, 20%, and 8%, respectively. Of note, only 6 patients were treated with gefitinib at the recurrence after triplet chemotherapy;of these, 4 (67%) achieved a partial response, which might result in favorable survival. Grade 3/4 toxicities consisted of neutropenia (100%), neutropenic fever (56%), nausea/vomiting (40%), and diarrhea (16%);no cases of treatment-related death occurred. Triplet chemotherapy showed impressive survival data in our clinical trial, but proved too toxic for use in treating patients with NSCLC in the clinical practice.

en-copyright= kn-copyright= en-aut-name=FujimotoNobukazu en-aut-sei=Fujimoto en-aut-mei=Nobukazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=FujiwaraYoshiro en-aut-sei=Fujiwara en-aut-mei=Yoshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ToyookaShinichi en-aut-sei=Toyooka en-aut-mei=Shinichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=UmemuraShigeki en-aut-sei=Umemura en-aut-mei=Shigeki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital affil-num=4 en-affil= kn-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Cancer and Thoracic Surgery, Okayama University Hospital affil-num=6 en-affil= kn-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Respiratory Medicine, Okayama University Hospital affil-num=8 en-affil= kn-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=cisplatin kn-keyword=cisplatin en-keyword=docetaxel kn-keyword=docetaxel en-keyword=irinotecan kn-keyword=irinotecan en-keyword=triplet chemotherapy kn-keyword=triplet chemotherapy en-keyword=gefitinib kn-keyword=gefitinib END start-ver=1.4 cd-journal=joma no-vol=64 cd-vols= no-issue=2 article-no= start-page=75 end-page=83 dt-received= dt-revised= dt-accepted= dt-pub-year=2010 dt-pub=201004 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Experimental Pulmonary Granuloma Mimicking Sarcoidosis Induced by Propionibacterium acnes in Mice en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Propionibacterium acnes has been implicated as an etiologic agent of sarcoidosis since the isolation of this bacterium from sarcoid lesions. We experimentally produced a murine pulmonary granuloma model using P. acnes with several features that simulate sarcoidosis. Mice were sensitized with heat-killed P. acnes and complete Freund's adjuvant and were subsequently challenged with heat-killed P. acnes at 2-week intervals. P. acnes-challenged mice developed epitheloid cell granulomas in the lungs. These mice showed a pulmonary immune response characterized by an increased number of T-lymphocytes, especially CD4 cells, and the ratio of CD4/CD8 in bronchoalveolar lavage (BAL) fluid also increased. Furthermore, significant elevations in both angiotensin-converting enzyme (ACE) serum levels and antibody titers against P. acnes were observed. Mice sensitized with P. acnes without complete Freund's adjuvant were capable of forming pulmonary granulomas, which appeared to be caused by indigenous P. acnes. The genome of P. acnes was found in the lungs, BAL cells, hilar lymph nodes, liver, and spleen in non-sensitized mice, which were thought to be germ-free. These results suggest that the immune response against indigenous P. acnes may play an important role in the pathogenesis of granuloma formation in a murine model.

en-copyright= kn-copyright= en-aut-name=IioKouji en-aut-sei=Iio en-aut-mei=Kouji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=IioTomoe Ueno en-aut-sei=Iio en-aut-mei=Tomoe Ueno kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OkuiYuhei en-aut-sei=Okui en-aut-mei=Yuhei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IchikawaHirohisa en-aut-sei=Ichikawa en-aut-mei=Hirohisa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=NakataYasunari en-aut-sei=Nakata en-aut-mei=Yasunari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KataokaMikio en-aut-sei=Kataoka en-aut-mei=Mikio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Field of Medical Technology, Graduate School of Health Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Field of Medical Technology, Graduate School of Health Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Field of Medical Technology, Graduate School of Health Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Field of Medical Technology, Graduate School of Health Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Field of Medical Technology, Graduate School of Health Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=Propionibacterium acnes kn-keyword=Propionibacterium acnes en-keyword=experimental granuloma kn-keyword=experimental granuloma en-keyword=sarcoidosis kn-keyword=sarcoidosis END start-ver=1.4 cd-journal=joma no-vol=63 cd-vols= no-issue=2 article-no= start-page=71 end-page=78 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200904 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Expression of thyroglobulin on follicular dendritic cells of thyroid mucosa-associated lymphoid tissue (MALT) lymphoma en-subtitle= kn-subtitle= en-abstract= kn-abstract=

Reportedly, thyroid mucosa-associated lymphoid tissue (MALT) lymphoma is closely associated with Hashimoto's thyroiditis. However, it remains unknown which antigen is closely associated with thyroid MALT lymphoma. We examined whether B cell response to thyroglobulin (Tg), which is a common thyroid-specific autoantigen, is related etiologically to the pathogenesis of thyroid MALT lymphoma. Expression of human Tg antigens and Cluster of differentiation (CD) 35 was examined immunohistochemically in 15 cases of thyroid MALT lymphoma using paraffin-embedded, formalin-fixed tissue specimens. In all cases of thyroid MALT lymphoma, human Tg was detected immunohistochemically in the follicular epithelial cells and follicular dendritic cells (FDCs). These FDCs were positive by double immunostaining for anti-human Tg rabbit polyclonal antibody (Ab) and for CD35. Results showed that the Tg, a thyroid autoantigen, had immunostained the germinal center of the thyroid MALT lymphoma. The Tg was present in the FDCs, as revealed by the staining pattern of the germinal center;this fact was confirmed by double immunostaining of anti-human Tg mouse monoclonal Ab and anti-CD35 mouse monoclonal Ab. The results of our study suggest that Tg is an autoantigen that is recognized by thyroid MALT lymphoma cells.

en-copyright= kn-copyright= en-aut-name=MunemasaMitsuru en-aut-sei=Munemasa en-aut-mei=Mitsuru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YoshinoTadashi en-aut-sei=Yoshino en-aut-mei=Tadashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KobayashiKeita en-aut-sei=Kobayashi en-aut-mei=Keita kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MiyakeTakayoshi en-aut-sei=Miyake en-aut-mei=Takayoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=SakugawaSumie Takase en-aut-sei=Sakugawa en-aut-mei=Sumie Takase kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MannamiTomohiko en-aut-sei=Mannami en-aut-mei=Tomohiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=ShinagawaKatsuji en-aut-sei=Shinagawa en-aut-mei=Katsuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=AkagiTadaatsu en-aut-sei=Akagi en-aut-mei=Tadaatsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Pathology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=thyroglobulin kn-keyword=thyroglobulin en-keyword=follicular dendritic cells kn-keyword=follicular dendritic cells en-keyword=mucosa-associated lymphoid tissue lymphoma kn-keyword=mucosa-associated lymphoid tissue lymphoma END start-ver=1.4 cd-journal=joma no-vol=63 cd-vols= no-issue=4 article-no= start-page=213 end-page=216 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200908 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Successful voriconazole treatment of invasive pulmonary aspergillosis in a patient with acute biphenotypic leukemia en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A 23-year old woman with acute biphenotypic leukemia (ABL) complained of chest pain with cough, high fever and hemoptysis during induction chemotherapy, although she had been treated with anti-biotics and micafungin. We made a clinical diagnosis of invasive pulmonary aspergillosis (IPA) based on a consolidation in the right upper lung field on a chest radiograph as well as a high level of serum beta-D-glucan (with no evidence of tuberculosis and candidiasis). We changed her treatment from micafungin to voriconazole. Later, we discovered an air-crescent sign by CT scan that supported the diagnosis of IPA. Following voriconazole treatment, clinical symptoms ceased and abnormal chest shadows improved gradually and concurrently with a recovery of neutrophils. IPA must be considered in immunocompromised patients with pulmonary infiltrates who do not respond to broad-spectrum antibiotics. Serological tests and CT findings can aid in early diagnosis of IPA, which, along with treatment for IPA, will improve clinical outcomes.

en-copyright= kn-copyright= en-aut-name=KobayashiKoichiro en-aut-sei=Kobayashi en-aut-mei=Koichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OgasawaraMasahiro en-aut-sei=Ogasawara en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KiyamaYoshio en-aut-sei=Kiyama en-aut-mei=Yoshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MiyazonoTakayoshi en-aut-sei=Miyazono en-aut-mei=Takayoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KagawaKumiko en-aut-sei=Kagawa en-aut-mei=Kumiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ImaiKiyotoshi en-aut-sei=Imai en-aut-mei=Kiyotoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HiranoTeiichi en-aut-sei=Hirano en-aut-mei=Teiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KobayashiNaoki en-aut-sei=Kobayashi en-aut-mei=Naoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=KasaiMasaharu en-aut-sei=Kasai en-aut-mei=Masaharu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=3 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=4 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=5 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=6 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=7 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=8 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital affil-num=9 en-affil= kn-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Hematology, Sapporo Hokuyu Hospital en-keyword=invasive pulmonary aspergillosis kn-keyword=invasive pulmonary aspergillosis en-keyword=voriconazole kn-keyword=voriconazole en-keyword=acute biphenotypic leukemia kn-keyword=acute biphenotypic leukemia en-keyword=febrile neutropenia kn-keyword=febrile neutropenia en-keyword=?-D-glucan kn-keyword=?-D-glucan END start-ver=1.4 cd-journal=joma no-vol=56 cd-vols= no-issue=3 article-no= start-page=129 end-page=134 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=200206 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Comparison of chemosensitivity tests: clonogenic assay versus MTT assay. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

When the development of chemotherapeutic agents reaches the clinical trial stage, it is necessary to perform drug sensitivity tests quickly in order to select the most promising agents for the treatment of cancer. In order to assess the possibility of using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay as a substitute for the human tumor clonogenic assay (HTCA), we evaluated the correlation between the results obtained by these 2 assays in 5 human lung cancer cell lines. The correlation coefficient between the results of the HTCA and the MTT assay was 0.673, indicating a relatively good correlation. The correlation was most prominent in platinum analogues (r = 0.939) and good in anthracyclines/anthracenedione (r = 0.611). However, no significant correlation was observed in vinca alkaloids, etoposide, irinotecan, SN-38 (an active metabolite of irinotecan), and rhizoxin. The results of the MTT assay showed a high degree of correlation with those of the HTCA in predicting the sensitivity of cancer cell lines to platinum analogues, and anthracyclines/anthracenedione. These results suggest that the MTT assay may be more convenient and quickly performed than the HTCA and can replace HTCA in evaluating the effects of anticancer agents, especially the platinum analogues and anthracyclines/anthracenedione.

en-copyright= kn-copyright= en-aut-name=KawadaKazuhiko en-aut-sei=Kawada en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YoneiToshiro en-aut-sei=Yonei en-aut-mei=Toshiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HaradaMine en-aut-sei=Harada en-aut-mei=Mine kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=National Okayama Medical Center affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Kyushu University, Fukuoka affil-num=8 en-affil= kn-affil=Okayama University en-keyword=chemosensitivity test kn-keyword=chemosensitivity test en-keyword=3-(4 kn-keyword=3-(4 en-keyword=5-dimethylthiazol-2-yl)-2 kn-keyword=5-dimethylthiazol-2-yl)-2 en-keyword=5-diphenyltertrazolium bromide (MTT) assay kn-keyword=5-diphenyltertrazolium bromide (MTT) assay en-keyword=clonogenic assay kn-keyword=clonogenic assay END start-ver=1.4 cd-journal=joma no-vol=56 cd-vols= no-issue=5 article-no= start-page=223 end-page=227 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=200210 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Camptothecin induces urokinase-type plasminogen activator gene-expression in human RC-K8 malignant lymphoma and H69 small cell lung cancer cells. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

We previously reported that anthracyclines, which could generate reactive oxygen species (ROS), could induce the urokinase-type plasminogen activator (uPA) gene expression in human RC-K8 malignant lymphoma cells and in H69 small cell lung cancer (SCLC) cells. In screening other uPA-inducible anti-cancer agents, we found that camptothecin (CPT) and its derivative, SN38, could induce uPA in RC-K8 and H69 cells. CPT and SN38, which are also used for the treatment of lymphoma and SCLC, significantly increased the uPA accumulation in the conditioned media of both cells in a dose-dependent manner. The maximum induction of uPA mRNA levels was observed 24 h after stimulation. Pretreatment with pyrrolidine dithiocarbamate (PDTC), an anti-oxidant, inhibited the CPT-induced uPA mRNA expression. Thus, CPT induces uPA through gene expression, and, therefore, CPT may influence the tumor-cell biology by up-regulating the uPA/plasmin system.

en-copyright= kn-copyright= en-aut-name=ShibakuraMisako en-aut-sei=Shibakura en-aut-mei=Misako kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NiiyaKenji en-aut-sei=Niiya en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KiguchiToru en-aut-sei=Kiguchi en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=NakataYasunari en-aut-sei=Nakata en-aut-mei=Yasunari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=CPT kn-keyword=CPT en-keyword=SN38 kn-keyword=SN38 en-keyword=uPA kn-keyword=uPA en-keyword=RC-K8 kn-keyword=RC-K8 en-keyword=H69 kn-keyword=H69 END start-ver=1.4 cd-journal=joma no-vol=56 cd-vols= no-issue=5 article-no= start-page=261 end-page=266 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=200210 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Daily low-dose cisplatin and concurrent thoracic irradiation for poor-risk patients with unresectable non-small-cell lung cancer. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

A pilot study was conducted to assess the efficacy and feasibility of daily low-dose cisplatin with concurrent thoracic irradiation for clinically unresectable non-small-cell lung cancer (NSCLC). Patients with inoperable NSCLC who had poor risk factors such as advanced age, poor performance status, poor lung function, or concomitant active malignancy were entered into the study. Low-dose cisplatin (6 mg/m2) was administered daily before concurrent thoracic irradiation (2 Gy/day; total dose of 60 Gy) was given. Twenty-five patients were registered. The majority of the patients had either stage IIIA (24.0%) or stage IIIB (60.0%) disease. Fifteen patients (60.0%) completed the planned treatment. Both chemotherapy and radiotherapy were stopped in 3 patients (12.0%) due to poor response, and 7 patients (28.0%) partly received radiotherapy alone as a result of their toxicity response. The proportion of total administered dose to planned dose was 90.9% for chemotherapy and 99.3% for radiotherapy, which were comparable to those in previous studies for LA-NSCLC patients without poor risk factors. Grade 3 leukopenia and neutropenia developed in 14 patients (56.0%) and 10 patients (40.0%), respectively, but grade 4 toxicity was not encountered. Grade 3 pneumonitis and esophagitis were observed in 4 patients (16.0%) and 2 patients (8.0%), respectively. The overall response rate was 60.0%. The median survival time was 22 months, and the 2-year survival rate was 50.3%. Daily low-dose cisplatin and concurrent thoracic irradiation were well tolerated even by poor-risk patients with NSCLC, and showed a therapeutic efficacy similar to that for good-risk patients.

en-copyright= kn-copyright= en-aut-name=TakataIchiro en-aut-sei=Takata en-aut-mei=Ichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KatayamaHideki en-aut-sei=Katayama en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakemotoMitsuhiro en-aut-sei=Takemoto en-aut-mei=Mitsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HirakiYoshio en-aut-sei=Hiraki en-aut-mei=Yoshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HaradaMine en-aut-sei=Harada en-aut-mei=Mine kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Kyushu University, Fukuoka affil-num=10 en-affil= kn-affil=Okayama University en-keyword=non-small-cell lung cancer kn-keyword=non-small-cell lung cancer en-keyword=concurrent chemoradiotherapy kn-keyword=concurrent chemoradiotherapy en-keyword=low-dose cisplatin kn-keyword=low-dose cisplatin en-keyword=poor-risk factor kn-keyword=poor-risk factor END start-ver=1.4 cd-journal=joma no-vol=60 cd-vols= no-issue=3 article-no= start-page=173 end-page=179 dt-received= dt-revised= dt-accepted= dt-pub-year=2006 dt-pub=200606 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Recent improvement in lung cancer screening: a comparison of the results carried out in two different time periods. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

To evaluate recent improvements in lung cancer screening, we compared the results of recently conducted lung cancer screening with those of a previous screening. This study compared the survival of lung cancer patients detected by lung cancer screening conducted between 1976 and 1984 (early period) with that conducted between 1989 and 1997 (late period). Two hundred seventy-six patients with lung cancer were detected in the early period and 541 patients with lung cancer were detected in the late period. The median survival time (late : 49.8 vs. early : 27.8 months) and the 5-year survival rate (late : 47.8 vs. early : 34.8%) of the patients with lung cancer detected in the late period were significantly better than those in the early period (p = 0.0054). Among patients undergoing resection, the proportion of pathological stage I patients in the late period was significantly higher than that in the early period (late : 60.8 vs. early : 54.9%, p = 0.005). Multivariate analysis showed that the screening time period was a significant prognostic factor (hazard ratio = 0.685, 95% confidence interval : 0.563-0.832, p = 0.0002). These results were consistent with the findings of case-control studies of lung cancer screening programs in the late period recently conducted in Japan, which also showed a greater efficacy for screening than for previous case-control studies in the early period.

en-copyright= kn-copyright= en-aut-name=KitajimaTakuji en-aut-sei=Kitajima en-aut-mei=Takuji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=NishiiKenji en-aut-sei=Nishii en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ShibayamaTakuo en-aut-sei=Shibayama en-aut-mei=Takuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=GembaKenichi en-aut-sei=Gemba en-aut-mei=Kenichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KodaniTsuyoshi en-aut-sei=Kodani en-aut-mei=Tsuyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=HottaKatsuyuki en-aut-sei=Hotta en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=SobueTomotaka en-aut-sei=Sobue en-aut-mei=Tomotaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama Institute of Health and Prevention affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=National Sanatorium Minami-Okayama Hospital affil-num=5 en-affil= kn-affil=Okayama Rousai Hospital affil-num=6 en-affil= kn-affil=Okayama Institute of Health and Prevention affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University affil-num=11 en-affil= kn-affil=National Cancer Center Research Institute en-keyword=lung cancer kn-keyword=lung cancer en-keyword=screening kn-keyword=screening en-keyword=survival kn-keyword=survival en-keyword=lung cancer mortality kn-keyword=lung cancer mortality END start-ver=1.4 cd-journal=joma no-vol=60 cd-vols= no-issue=5 article-no= start-page=295 end-page=298 dt-received= dt-revised= dt-accepted= dt-pub-year=2006 dt-pub=200610 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Severe Interstitial Pneumonia Induced by Paclitaxel in a Patient with Adenocarcinoma of the Lung en-subtitle= kn-subtitle= en-abstract= kn-abstract=A 71-year-old Japanese man with adenocarcinoma of the lung developed interstitial pneumonia after treatment with paclitaxel. The patient had acute chills and fever on the fourth day after the second exposure to paclitaxel, rapidly got worse despite empiric therapies, and developed prolonged respiratory failure requiring mechanical ventilation. Four months later, he died of respiratory failure due to progression of both interstitial pneumonia and lung cancer. This is the first case developing fatal paclitaxel-induced pulmonary toxicity to date. Interstitial pneumonia should be considered one of the possible life-threatening complications during treatment with paclitaxel. en-copyright= kn-copyright= en-aut-name=SuzakiNoriyuki en-aut-sei=Suzaki en-aut-mei=Noriyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HirakiAkio en-aut-sei=Hiraki en-aut-mei=Akio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=UeokaHiroshi en-aut-sei=Ueoka en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=KozukiToshiyuki en-aut-sei=Kozuki en-aut-mei=Toshiyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KanehiroArihiko en-aut-sei=Kanehiro en-aut-mei=Arihiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University affil-num=9 en-affil= kn-affil=Okayama University affil-num=10 en-affil= kn-affil=Okayama University en-keyword=paclitaxel kn-keyword=paclitaxel en-keyword=adverse effect kn-keyword=adverse effect en-keyword=lung cancer kn-keyword=lung cancer en-keyword=interstitial pneumonia kn-keyword=interstitial pneumonia END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20091231 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=BiP/GRP78の抑制によるREIC/Dkk3遺伝子治療抵抗性前立腺がんの感受性化 kn-title=Down-regulation of BiP/GRP78 sensitizes resistant prostate cancer cells to gene-therapeutic overexpression of REIC/Dkk3 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoRyuta en-aut-sei=Tanimoto en-aut-mei=Ryuta kn-aut-name=谷本竜太 kn-aut-sei=谷本 kn-aut-mei=竜太 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol=68 cd-vols= no-issue=9 article-no= start-page=1557 end-page=1559 dt-received= dt-revised= dt-accepted= dt-pub-year=1956 dt-pub=19560930 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Influence of Parathion-poisoing on the Function of Reticulo-endotherial System kn-title=パラチオン中毒の網内系機能に及ぼす影響 en-subtitle= kn-subtitle= en-abstract= kn-abstract=The function of reticulo-endotherial system was examined by means of the carbon black phagocytosis (Sugiyama) and the congo-red test (Adler and Reimann). 1. The decrease of phagocytosis and the increase of congo-red index take place 2-3 days after subcutaneous injection of parathion (8 mg/kg for rabbits, 1-3 mg/kg for dogs). 2. Daily injecting the small dose of parathion (1 mg/kg for rabbits, 1-2 mg/kg for dogs), the disturbance above mentioned is also proved, and it goes on longer. 3. At the onset of parathion-poisoning in man, the congo-red index shows very high and returns to normal after 10-20 days. It is concluded that the function of reticulo-endotherial system is out of order by the parathion-poisoning, and it remains after 10-20 days. en-copyright= kn-copyright= en-aut-name=NambaTatsuji en-aut-sei=Namba en-aut-mei=Tatsuji kn-aut-name=難波達治 kn-aut-sei=難波 kn-aut-mei=達治 aut-affil-num=1 ORCID= en-aut-name=KimuraKiichiro en-aut-sei=Kimura en-aut-mei=Kiichiro kn-aut-name=木村基一郎 kn-aut-sei=木村 kn-aut-mei=基一郎 aut-affil-num=2 ORCID= en-aut-name=NakayamaAkitoshi en-aut-sei=Nakayama en-aut-mei=Akitoshi kn-aut-name=中山章壮 kn-aut-sei=中山 kn-aut-mei=章壮 aut-affil-num=3 ORCID= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=4 ORCID= en-aut-name=MaedaAkira en-aut-sei=Maeda en-aut-mei=Akira kn-aut-name=前田昭 kn-aut-sei=前田 kn-aut-mei=昭 aut-affil-num=5 ORCID= en-aut-name=TambaraShigeo en-aut-sei=Tambara en-aut-mei=Shigeo kn-aut-name=丹原茂雄 kn-aut-sei=丹原 kn-aut-mei=茂雄 aut-affil-num=6 ORCID= en-aut-name=KimuraTakashi en-aut-sei=Kimura en-aut-mei=Takashi kn-aut-name=木村峻士 kn-aut-sei=木村 kn-aut-mei=峻士 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=2 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=3 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=4 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=5 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=6 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=7 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=68 cd-vols= no-issue=9 article-no= start-page=1551 end-page=1556 dt-received= dt-revised= dt-accepted= dt-pub-year=1956 dt-pub=19560930 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Influence of Parathion-poisoning on Respiratory and Circulatory Function and the Effects of some Therapeutics kn-title=パラチオン中毒に於ける呼吸及び循環機能並びに之に及ぼす治療剤の影響 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Respiratory movement and blood pressure were recorded on the dog with parathion-poisoning. 1. After a few minutes of increasing of rate and amplitude, the respiratory movement go down weaker and irregular. Thus the movement ceases by a single intravenous injection of 10 mg/kg parathion. Blood pressure shows transitory rise, then it falls gradually and is attended by a marked slowing of the heart beats after respiratory failure. 2. The changes caused by parathion injection are protected by 5 mg/kg atropine i. v. 3. The atropine- like effects are displayed, too, by 1 mg/kg Tropin, 4 mg/kg Finalin and 3 mg/kg Pro-banthin i. v. 4. Intravenous injection of 100 mg/kg Theraptique, 20 mg/kg Guronsan and 300 mg/kg Sod. thiosulf. are of no use, besides the former display a brief period of strong respiratory stimulation. en-copyright= kn-copyright= en-aut-name=NambaTatsuji en-aut-sei=Namba en-aut-mei=Tatsuji kn-aut-name=難波達治 kn-aut-sei=難波 kn-aut-mei=達治 aut-affil-num=1 ORCID= en-aut-name=HachiyaRyoma en-aut-sei=Hachiya en-aut-mei=Ryoma kn-aut-name=蜂谷良馬 kn-aut-sei=蜂谷 kn-aut-mei=良馬 aut-affil-num=2 ORCID= en-aut-name=KimuraKiichiro en-aut-sei=Kimura en-aut-mei=Kiichiro kn-aut-name=木村基一郎 kn-aut-sei=木村 kn-aut-mei=基一郎 aut-affil-num=3 ORCID= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=4 ORCID= en-aut-name=NakayamaAkitoshi en-aut-sei=Nakayama en-aut-mei=Akitoshi kn-aut-name=中山章壮 kn-aut-sei=中山 kn-aut-mei=章壮 aut-affil-num=5 ORCID= en-aut-name=NakazawaTakeshi en-aut-sei=Nakazawa en-aut-mei=Takeshi kn-aut-name=中沢峻士 kn-aut-sei=中沢 kn-aut-mei=峻士 aut-affil-num=6 ORCID= en-aut-name=TambaraShigeo en-aut-sei=Tambara en-aut-mei=Shigeo kn-aut-name=丹原茂雄 kn-aut-sei=丹原 kn-aut-mei=茂雄 aut-affil-num=7 ORCID= en-aut-name=MaedaAkira en-aut-sei=Maeda en-aut-mei=Akira kn-aut-name=前田昭 kn-aut-sei=前田 kn-aut-mei=昭 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=2 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=3 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=4 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=5 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=6 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=7 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=8 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=68 cd-vols= no-issue=8 article-no= start-page=1207 end-page=1209 dt-received= dt-revised= dt-accepted= dt-pub-year=1956 dt-pub=19560831 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The Fate of Parathion in vivo kn-title=生体におけるパラチオンの運命 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Parathion is distributed equally in the poisoned human bodies, as it has been in the case of experimental animals, and disappeared after 24-48 hours. This may be attributed to the splitting of parathion both p-nitrophenol and diethyl (thio) phosphate. The most part of p-nitrophenol is excreted in the urin within 1-2 days and only a part of it prolonged into a week accompaniing no sign of poisoning. It is said that diethyl (thio) phosphate is excreted similary, but poisonus (1/4-1/5 of parathion) for the human bodies and animals. The splitting above mentioned is based on the enzym action, including cholinesterase which is found in the animal sera and organ extracts. The parathion splitting action of serum is inhibited in the case of various kinds of disease. en-copyright= kn-copyright= en-aut-name=NambaTatsuji en-aut-sei=Namba en-aut-mei=Tatsuji kn-aut-name=難波達治 kn-aut-sei=難波 kn-aut-mei=達治 aut-affil-num=1 ORCID= en-aut-name=TanimotoHajime en-aut-sei=Tanimoto en-aut-mei=Hajime kn-aut-name=谷本一 kn-aut-sei=谷本 kn-aut-mei=一 aut-affil-num=2 ORCID= en-aut-name=KimuraKiichiro en-aut-sei=Kimura en-aut-mei=Kiichiro kn-aut-name=木村基一郎 kn-aut-sei=木村 kn-aut-mei=基一郎 aut-affil-num=3 ORCID= en-aut-name=FukuharaArimitsu en-aut-sei=Fukuhara en-aut-mei=Arimitsu kn-aut-name=福原有光 kn-aut-sei=福原 kn-aut-mei=有光 aut-affil-num=4 ORCID= en-aut-name=YamadaMinoru en-aut-sei=Yamada en-aut-mei=Minoru kn-aut-name=山田稔 kn-aut-sei=山田 kn-aut-mei=稔 aut-affil-num=5 ORCID= en-aut-name=NakazawaTakeshi en-aut-sei=Nakazawa en-aut-mei=Takeshi kn-aut-name=中沢彪 kn-aut-sei=中沢 kn-aut-mei=彪 aut-affil-num=6 ORCID= en-aut-name=ShiromotoTetsuzo en-aut-sei=Shiromoto en-aut-mei=Tetsuzo kn-aut-name=城本鉄蔵 kn-aut-sei=城本 kn-aut-mei=鉄蔵 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=2 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=3 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=4 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=5 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=6 en-affil= kn-affil=岡山大学医学部平木内科教室 affil-num=7 en-affil= kn-affil=岡山大学医学部平木内科教室 END start-ver=1.4 cd-journal=joma no-vol=57 cd-vols= no-issue= article-no= start-page=113 end-page=114 dt-received= dt-revised= dt-accepted= dt-pub-year=1986 dt-pub=198607 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=1600Kcalの食事を試食して en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=中村寿美江 kn-aut-sei=中村 kn-aut-mei=寿美江 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=石湯和子 kn-aut-sei=石湯 kn-aut-mei=和子 aut-affil-num=2 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本悦子 kn-aut-sei=谷本 kn-aut-mei=悦子 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部附属病院三朝分院看護部 affil-num=2 en-affil= kn-affil=岡山大学医学部附属病院三朝分院看護部 affil-num=3 en-affil= kn-affil=岡山大学医学部附属病院三朝分院看護部 END start-ver=1.4 cd-journal=joma no-vol=72 cd-vols= no-issue=3 article-no= start-page=995 end-page=998 dt-received= dt-revised= dt-accepted= dt-pub-year=1960 dt-pub=19600228 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Hemolytic, Anemia-Inducing Substance in Cancer Tissue kn-title=癌組織中の溶血性細胞毒に就いて en-subtitle= kn-subtitle= en-abstract= kn-abstract=In 1959 we discovered that a hemolytic, anemia-inducing substance is produced in the animals exposed to X-rays. Since then we have found that when this substnce is injeted intravenously into animals, there occur disturbances in the blood, spleen and bone marrow. And also it has become clear that this substance brings about Heinz's body appearance in erythrocytes. As Heinz's body also appears in cancer anemia and it is transformed into hemolysin, it may be assumed that the hemolytic, anemia-inducing substance is contained also in cancer tissue. Upon such assumption we have compared the hemolytic capacity of the extract obtained from the fresh gastric cancer tissue resscted at operation with that of the extract from normal gastric tissue. As the result, we have recognized that this hemolytic, anemia-inducing substance is contained considerably in cancer tissue. en-copyright= kn-copyright= en-aut-name=YamamotoMichio en-aut-sei=Yamamoto en-aut-mei=Michio kn-aut-name=山本道夫 kn-aut-sei=山本 kn-aut-mei=道夫 aut-affil-num=1 ORCID= en-aut-name=NobukiSigeo en-aut-sei=Nobuki en-aut-mei=Sigeo kn-aut-name=信木茂生 kn-aut-sei=信木 kn-aut-mei=茂生 aut-affil-num=2 ORCID= en-aut-name=SiakuTakeru en-aut-sei=Siaku en-aut-mei=Takeru kn-aut-name=塩飽健 kn-aut-sei=塩飽 kn-aut-mei=健 aut-affil-num=3 ORCID= en-aut-name=AkagiKeiko en-aut-sei=Akagi en-aut-mei=Keiko kn-aut-name=赤木瑩子 kn-aut-sei=赤木 kn-aut-mei=瑩子 aut-affil-num=4 ORCID= en-aut-name=SiakuMidori en-aut-sei=Siaku en-aut-mei=Midori kn-aut-name=塩飽緑 kn-aut-sei=塩飽 kn-aut-mei=緑 aut-affil-num=5 ORCID= en-aut-name=IgutiYosiko en-aut-sei=Iguti en-aut-mei=Yosiko kn-aut-name=井口与志子 kn-aut-sei=井口 kn-aut-mei=与志子 aut-affil-num=6 ORCID= en-aut-name=TanimotoJunichi en-aut-sei=Tanimoto en-aut-mei=Junichi kn-aut-name=谷本潤一 kn-aut-sei=谷本 kn-aut-mei=潤一 aut-affil-num=7 ORCID= en-aut-name=KojimaSumikazu en-aut-sei=Kojima en-aut-mei=Sumikazu kn-aut-name=小島澄一 kn-aut-sei=小島 kn-aut-mei=澄一 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=2 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=3 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=4 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=5 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=6 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=7 en-affil= kn-affil=岡山大学医学部放射線医学教室 affil-num=8 en-affil= kn-affil=岡山大学医学部放射線医学教室 END start-ver=1.4 cd-journal=joma no-vol=121 cd-vols= no-issue=3 article-no= start-page=173 end-page=175 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20091201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Relief of cancer pain in a non small cell lung cancer patient by a polyhedral approach kn-title=多角的アプローチにより癌性疼痛のコントロールを得ることができた非小細胞肺癌の一例 en-subtitle= kn-subtitle= en-abstract= kn-abstract=We report a case of cancer-related pain relieved by a polyhedral approach. A woman in her late 30s with advanced non small cell lung cancer suffered from back pain caused by the cancer invasion to a thoracic vertebra. She could not take a sufficient dose of opioid due to its adverse effects. A supplementary analgesic was not found to be effective. Palliative radiation was considered desirable, but she could not maintain a dorsal position for irradiation due to back pain. Continuous epidural anesthesia was then introduced. Epidural anesthesia allowed her to lie in a spine position for radiation therapy. After completion of radiation therapy, her back pain was relieved with a low dose of transdermal fentanyl without epidural anesthesia. en-copyright= kn-copyright= en-aut-name=IchiharaEiki en-aut-sei=Ichihara en-aut-mei=Eiki kn-aut-name=市原英基 kn-aut-sei=市原 kn-aut-mei=英基 aut-affil-num=1 ORCID= en-aut-name=MatsuokaJunji en-aut-sei=Matsuoka en-aut-mei=Junji kn-aut-name=松岡順治 kn-aut-sei=松岡 kn-aut-mei=順治 aut-affil-num=2 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name=瀧川奈義夫 kn-aut-sei=瀧川 kn-aut-mei=奈義夫 aut-affil-num=3 ORCID= en-aut-name=MatsuzakiTakashi en-aut-sei=Matsuzaki en-aut-mei=Takashi kn-aut-name=松崎孝 kn-aut-sei=松崎 kn-aut-mei=孝 aut-affil-num=4 ORCID= en-aut-name=KatsuiKuniaki en-aut-sei=Katsui en-aut-mei=Kuniaki kn-aut-name=勝井邦彰 kn-aut-sei=勝井 kn-aut-mei=邦彰 aut-affil-num=5 ORCID= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=6 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　緩和医療学講座 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　緩和医療学講座 affil-num=3 en-affil= kn-affil=岡山大学病院　血液・腫瘍・呼吸器・アレルギー内科 affil-num=4 en-affil= kn-affil=岡山大学病院　麻酔科蘇生科 affil-num=5 en-affil= kn-affil=岡山大学病院　放射線科 affil-num=6 en-affil= kn-affil=岡山大学病院　血液・腫瘍・呼吸器・アレルギー内科 affil-num=7 en-affil= kn-affil=岡山大学病院　血液・腫瘍・呼吸器・アレルギー内科 en-keyword=癌性疼痛 (cancer-related pain) kn-keyword=癌性疼痛 (cancer-related pain) en-keyword=硬膜外ブロック　(epidural anesthesia) kn-keyword=硬膜外ブロック　(epidural anesthesia) en-keyword=放射線療法 (radiation therapy) kn-keyword=放射線療法 (radiation therapy) END start-ver=1.4 cd-journal=joma no-vol=97 cd-vols= no-issue=11-12 article-no= start-page=1001 end-page=1007 dt-received= dt-revised= dt-accepted= dt-pub-year=1985 dt-pub=19851230 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the fecal E. coli-form in the environmental waters III. Evaluation as an indicator of water pollution using the fecal E. coli-form kn-title=環境水域における糞便性大腸菌群に関する研究 第III報 糞便性大腸菌群を用いた汚染指標とその評価 en-subtitle= kn-subtitle= en-abstract= kn-abstract=There was no distinct differnce between the two regression lines of total E. coli-form and fecal E. coli-form investigated from 1978 to 1980 and in 1985. Target value of fecal E. coli-form decided in the investigation from 1978 to 1980 was applied to the investigation in 1985, which was recognized to be appropriate. Sampling stations where the ratio (%) of fecal E. coli-form against total E. coli-form is high are located in the suburbs of small and middle cities without river basin sewerage system. At present, even in a case having attained the quality standard value of total E. coli-form, the same disposition as that for the unattained should be done if the case has not attained the quality value of fecal E. coli-form. en-copyright= kn-copyright= en-aut-name=TanimotoHirokazu en-aut-sei=Tanimoto en-aut-mei=Hirokazu kn-aut-name=谷本浩一 kn-aut-sei=谷本 kn-aut-mei=浩一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部公衆衛生学教室 en-keyword=Fecal E. coli-form kn-keyword=Fecal E. coli-form en-keyword=water pollution kn-keyword=water pollution en-keyword=Biological indicator kn-keyword=Biological indicator en-keyword=Evaluation kn-keyword=Evaluation END start-ver=1.4 cd-journal=joma no-vol=121 cd-vols= no-issue=1 article-no= start-page=53 end-page=55 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20090401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Infection control in Japan kn-title=感染症法 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部・歯学部附属病院　呼吸器・アレルギー内科 END start-ver=1.4 cd-journal=joma no-vol=121 cd-vols= no-issue=1 article-no= start-page=29 end-page=33 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20090401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Mid-West Japan Cancer Professional Education Consortium kn-title=中国四国広域プロ養成プログラム ―チーム医療を担うがん専門医療人の育成―www.chushiganpro.jp en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MatsuokaJunji en-aut-sei=Matsuoka en-aut-mei=Junji kn-aut-name=松岡順治 kn-aut-sei=松岡 kn-aut-mei=順治 aut-affil-num=1 ORCID= en-aut-name=NaomotoYoshio en-aut-sei=Naomoto en-aut-mei=Yoshio kn-aut-name=猶本良夫 kn-aut-sei=猶本 kn-aut-mei=良夫 aut-affil-num=2 ORCID= en-aut-name=TabataMasahiro en-aut-sei=Tabata en-aut-mei=Masahiro kn-aut-name=田端雅弘 kn-aut-sei=田端 kn-aut-mei=雅弘 aut-affil-num=3 ORCID= en-aut-name=ShirakawaYasuhiro en-aut-sei=Shirakawa en-aut-mei=Yasuhiro kn-aut-name=白川靖博 kn-aut-sei=白川 kn-aut-mei=靖博 aut-affil-num=4 ORCID= en-aut-name=HottaKatsuyuki en-aut-sei=Hotta en-aut-mei=Katsuyuki kn-aut-name=堀田勝幸 kn-aut-sei=堀田 kn-aut-mei=勝幸 aut-affil-num=5 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=6 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name=田中紀章 kn-aut-sei=田中 kn-aut-mei=紀章 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・腫瘍外科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・腫瘍外科学 affil-num=3 en-affil= kn-affil=岡山大学医学部・歯学部附属病院　腫瘍センター affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・腫瘍外科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　消化器・腫瘍外科学 en-keyword=がんプロ kn-keyword=がんプロ en-keyword=チーム医療 kn-keyword=チーム医療 en-keyword=大学院 kn-keyword=大学院 END start-ver=1.4 cd-journal=joma no-vol=72 cd-vols= no-issue= article-no= start-page=66 end-page=70 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=20020201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The relationship between the magnetic resonance imaging of the lumbar spine and lowback pain kn-title=腰痛症患者における腰椎MRI画像所見の検討 en-subtitle= kn-subtitle= en-abstract=(Purpose) Magnetic resonance imaging (MRI) is essential to diagnosis of diseases which happen low back pain. The purpose of this study was to investigate the relationship between low back pain and the characteristics on MRI scans of the lumbar spine. (Materials and Methods) We performed MRI examinations of lumbar spine in 30 patients with low back pain and examined the prevalence of abnormal findings on MRI scans of the lumbar spine in 30 patients with low back pain. (Results) Overall in present study, all patients with low back pain had abnormalities around the lumbar spines on MRI. Disc degeneration was present in one or more lumbar levels in 27 (90% ) of all the subjects. The disc degeneration was most commonly observed at U/LS, where 18 (60% ) of all the subjects displayed evidence of disc degeneration. Disc herniation was found in 10 (33.3% ) of all the subjects. Nerve root compression at one level or more was observed in 8 (26.7% ) of the subjects. Compression fracture at one level or more was observed in 6 (20% ) of all the subjects. Spa therapy improved low back pain in 17 (56. 7% ) of the subjects. (Conclusion) All patients with low back pain had abnormalities around the lumbar spines on MRI. Because spa therapy improved low back pain, morphological abnormalities on MRI scans don't always connect with functional abnormalities and symptoms. kn-abstract=(目的) MRlは腰痛をきたす疾患の診断に必須な検査法である｡腰痛と腰椎MRl所見との関係を明らかにすることを目的として検討した｡(対象と方法)腰痛を訴えた30例を対象とし､腰椎MRl所見の頻度を調査した｡全例に温泉療法を施行した｡　 (結果)全症例において腰椎MRl上異常所見を認めた｡少なくとも1つ以上の椎間板の変性病変をもつ症例は30例中27例(90% )で､椎間板変性はL4/5levelで最も多く認められた(30例中18例)｡椎間板ヘルニア を示す症例は30例中10例(33.3% )であった｡神経根圧迫を持つ症例は30例中8例(26.7% )であった｡腰椎圧迫骨折を持つ症例は30例中6例(20% )であった｡温泉療法により腰痛が改善した症例は30例中17例(56.7% )であった｡　 (結論)腰痛症患者は腰椎MR止異常所見を有した｡温泉療法により腰痛の改善を認めたので､MRL上で認めた形態学的異常は必ずしも機能的異常や症状に直結しないと思われた｡ en-copyright= kn-copyright= en-aut-name=TakataShingo en-aut-sei=Takata en-aut-mei=Shingo kn-aut-name=高田真吾 kn-aut-sei=高田 kn-aut-mei=真吾 aut-affil-num=1 ORCID= en-aut-name=YokoiTadashi en-aut-sei=Yokoi en-aut-mei=Tadashi kn-aut-name=横井正 kn-aut-sei=横井 kn-aut-mei=正 aut-affil-num=2 ORCID= en-aut-name=NishidaNorikazu en-aut-sei=Nishida en-aut-mei=Norikazu kn-aut-name=西田典数 kn-aut-sei=西田 kn-aut-mei=典数 aut-affil-num=3 ORCID= en-aut-name=OkamotoMakoto en-aut-sei=Okamoto en-aut-mei=Makoto kn-aut-name=岡本誠 kn-aut-sei=岡本 kn-aut-mei=誠 aut-affil-num=4 ORCID= en-aut-name=TsugenoHirofumi en-aut-sei=Tsugeno en-aut-mei=Hirofumi kn-aut-name=柘野浩史 kn-aut-sei=柘野 kn-aut-mei=浩史 aut-affil-num=5 ORCID= en-aut-name=AshidaKozo en-aut-sei=Ashida en-aut-mei=Kozo kn-aut-name=芦田耕三 kn-aut-sei=芦田 kn-aut-mei=耕三 aut-affil-num=6 ORCID= en-aut-name=HosakiYasuhiro en-aut-sei=Hosaki en-aut-mei=Yasuhiro kn-aut-name=保ｱ泰弘 kn-aut-sei=保ｱ kn-aut-mei=泰弘 aut-affil-num=7 ORCID= en-aut-name=MifuneTakashi en-aut-sei=Mifune en-aut-mei=Takashi kn-aut-name=御舩尚志 kn-aut-sei=御舩 kn-aut-mei=尚志 aut-affil-num=8 ORCID= en-aut-name=MitsunobuFumihiro en-aut-sei=Mitsunobu en-aut-mei=Fumihiro kn-aut-name=光延文裕 kn-aut-sei=光延 kn-aut-mei=文裕 aut-affil-num=9 ORCID= en-aut-name=TanizakiYoshiro en-aut-sei=Tanizaki en-aut-mei=Yoshiro kn-aut-name=谷崎勝朗 kn-aut-sei=谷崎 kn-aut-mei=勝朗 aut-affil-num=10 ORCID= en-aut-name=NiiyaKenji en-aut-sei=Niiya en-aut-mei=Kenji kn-aut-name=新谷憲治 kn-aut-sei=新谷 kn-aut-mei=憲治 aut-affil-num=11 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=12 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=2 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=3 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=4 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=5 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=6 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=7 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=8 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=9 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=10 en-affil= kn-affil=岡山大学医学部附属病院三朝分院内科 affil-num=11 en-affil= kn-affil=岡山大学医学部第二内科 affil-num=12 en-affil= kn-affil=岡山大学医学部第二内科 en-keyword=腰痛症 (Disc disease) kn-keyword=腰痛症 (Disc disease) en-keyword=MRl (Magnetic resonance imaglng) kn-keyword=MRl (Magnetic resonance imaglng) en-keyword=椎間板変性 (Lumbar spine) kn-keyword=椎間板変性 (Lumbar spine) END start-ver=1.4 cd-journal=joma no-vol=72 cd-vols= no-issue= article-no= start-page=45 end-page=54 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=20020201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=脂質代謝に関連した気管支喘息患者における白血球ロイコトリエン産生能に対するα-リノレン酸食の効果 kn-title=Effects of alpha -linolenic acid-rich supplementationon leukotriene generation by leucocytes in patientswith asthma associated with lipometabolism en-subtitle= kn-subtitle= en-abstract=エゴマ油のようなα-リノレン酸食が他のn-3系不飽和脂肪酸食において報告されてきた様に喘息患者の白血球ロイコトリエン(LTs)産生能を抑制すると考えられる｡そこでエゴマ油(n-3系脂肪酸)を摂取した気管支喘息患者の臨床所見を比較することによって白血球ロイコトリエン(LT)C4の抑制に影響する因子を検討した。A群はエゴマ油摂取により白血球LTC4の産生能が抑制された群であり､B群は白血球LTC4の産生能が抑制されなかった群である｡A群では食事摂取2週後(P<0.05),4週後(P<0.05)に白血球LTC4産生能が低下した｡逆にB群では摂取4週後有意に増加した(P<0.05)0 2群間で食事摂取4遡後に白血球LTC4産生能に有意差がみられた(P<0.05)｡ピークフロー値(PEF)､努力性肺活量(FVC)､1秒量(FEV(1))といった呼吸機能はA群において食事摂取4週後に有意に上昇した(P<0.05)｡食事摂取前のPEF､FVC､FEV(1)､V(25)はA群,B群の2群間で有意差がみられた｡A群において血清総コレステロール､低比重リポ蛋白(LDL)コレステロール､リン脂質は食事摂取4週後に有意に低下した｡食事摂取前の血清総コレステロール､中性脂肪､高比重リポ蛋白コレステロール､LDLコレステロール､リン脂質において2群間に有意差がみられた｡血清中性脂肪､LDLコレステロールは食事摂取4週後2群間に有意差がみられた｡気管支喘息患者のある群へのエゴマ油食はLTC4産生能を抑制し､それには呼吸機能や脂質代謝といった臨床因子が関連していると考えられた｡ kn-abstract=Dietary sources of a -linolenic acid, such as perilla seed oil, may have the capacity to inhibit the generation of leukotrienes (LTs) by leucocytes in patients with asthma, as has been reported with the consumption of other long - chain n- 3 fatty a-cids. The factors affecting the suppression of leukotriene (LT) C4 generation by leucocytes were examined by comparing the clinical features of patients with asthma who had been given dietary perilla seed oil (n - 3 fatty acids). Group A consisted of patients in whom the leucocyte generation of dietary perilla seed oil LTC4 was suppressed by this procedure. Group B consisted of those in whom LTC4 generation was not suppressed. LTC4 generation by leucocytes significantly decreased in group A for two (P<0.05) and four weeks (P40y.o.), or intractable and non-in-tractable asthma. Clinical and allergic examinations were evaluated in each asthma group. Sixty nine percent of the late onset asthmatics had perennial type attacks. IgG-as well as IgE-mediated allergic reactions were suggested by the findings of immediate skin reaction, IgE RIST and RAST score to Candida allergen and reactivity of basophils to anti-immunoglobulin antisera in LOIA. Neutrophils in bronchoalveolar lavage fluid increased significantly in LOIA as compared with the early onset intractable asthma (EOIA) groups (p<0.05). In the pulmonary function test, a striking fall of % V25 was observed in both EOIA ans LOIA. The chest X-ray film frequently revealed microndular shadows in LOIA. Marked morphological changes in the transbronchial lung biopsied specimens were observed in the late onset asthmatics. These findings suggest that a non-IgE reaction, neutrophil infiltration in the local allergic site and histolpgical changes of lung tissue lead to LOIA. en-copyright= kn-copyright= en-aut-name=NakayamaKengo en-aut-sei=Nakayama en-aut-mei=Kengo kn-aut-name=中山堅吾 kn-aut-sei=中山 kn-aut-mei=堅吾 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=late onset kn-keyword=late onset en-keyword=intractable asthma kn-keyword=intractable asthma en-keyword=IgG kn-keyword=IgG en-keyword=neutrophil kn-keyword=neutrophil en-keyword=transbronchoscopic lung biopsy kn-keyword=transbronchoscopic lung biopsy END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=5-6 article-no= start-page=433 end-page=443 dt-received= dt-revised= dt-accepted= dt-pub-year=1992 dt-pub=1992 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on pathogenesis of intractable asthma Part 1. Characteristices of clinical and immuno-pathological findings in intractable asthma kn-title=難治性喘息の発症病態に関する研究　第1編　難治性喘息の臨床的検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the pathogenesis of intractable asthma, clinical features, allergic examinations, pulmonary functions and histological finding were evaluated in 27 intractable asthmatics compared with 33 non-intractable asthmatics. Almost all of the intractable asthmatics had chronic and perennial asthma attacks and also had highly frequent episodes of respiratory infection. IgG-as well as IgE-mediated allergic reactions were proved by the findings of skin reaction, IgE RAST score, precipitating antibody and reactivity of basophils to anti-immunoglobulin antisera in the intractable asthmatics but not in the non-intactable asthmatics. Neutrophils of BALF and peripheral blood increased markedly in the intractable asthmatics as compared with the non-intractable asthmatics. The fall of % V(25) on flow volume curve in the intractable asthmatics, indicated small air way obstruction. Micronodular shadows on the chest X-ray film were frequently seen in the intractable asthmatics. Many histological findings were shown on lung specimens obtained by TBLB in the intrac-table asthmatics. These findings indicate that multiple factors of allergic reaction mediated by IgG, migrated neutrophils and organic changes of lung tissue lead to severe and intractable asthma attack. en-copyright= kn-copyright= en-aut-name=NakayamaKengo en-aut-sei=Nakayama en-aut-mei=Kengo kn-aut-name=中山堅吾 kn-aut-sei=中山 kn-aut-mei=堅吾 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=intractable asthma kn-keyword=intractable asthma en-keyword=Candida kn-keyword=Candida en-keyword=IgG kn-keyword=IgG en-keyword=neutrophil kn-keyword=neutrophil en-keyword=transbronchoscopic lung biopsy kn-keyword=transbronchoscopic lung biopsy END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=11-12 article-no= start-page=1117 end-page=1125 dt-received= dt-revised= dt-accepted= dt-pub-year=1992 dt-pub=199212 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the role of interferon gamma (IFN-γ) in the pathogenesis of bronchial asthma : Evaluation of IFN-γ production induced by Candida or mite antigen in comparison with other factors of lymphocytic function kn-title=気管支喘息における interferon-γ (IFN-γ) 産生能に関する研究 第2編 気管支喘息における IFN-γ 産生能と各種リンパ球機能との比較検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=It is known that IFN-γ, T-cell lymphokine, has potent effects on immunoglobulin synthesis, leukotrienes synthesis and delayed-type hypersensitivity. These factors are thought to be closely related to allergic reactions in bronchial asthma. Therefore, IFN-γ production from peripheral blood mononuclear cells induced by Candida or mite antigen was examined in asthmatics, and relations with other lymphocytic functions were studied to eluciate the role of IFN-γ. The results were as follows : (1) There was a significant correlation between IFN-γ production and Candida specific serum IgG1 antibody. (2) There was a significant correlation between IFN-γ production and lymphocyte blastgenesis induced by Candida antigen. (3) High levels of IFN-γ production were observed in asthmatics with positive late phase or delayed phase skin reaction to Candida antigen compared to asthmatics with negative late phase or delayed phase skin reaction. (4) Asthmatics with positive Candida or mite specific IgE radioallergosorbent test(RAST) showed a low level of IFN-γ production compared to asthmatics with negative IgE RAST. These results indicate that asthmatics with low IgE antibody and activated lymphocytes show high levels of IFN-γ production, and in these low IgE asthmatics, IFN-γ may play an important role in the allergic reactions of bronchial asthma. en-copyright= kn-copyright= en-aut-name=KimuraGoro en-aut-sei=Kimura en-aut-mei=Goro kn-aut-name=木村五郎 kn-aut-sei=木村 kn-aut-mei=五郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=bronchial asthma kn-keyword=bronchial asthma en-keyword=delayed-type hypersensitivity kn-keyword=delayed-type hypersensitivity en-keyword=IFN-γ kn-keyword=IFN-γ en-keyword=IgE antibody kn-keyword=IgE antibody en-keyword=IgG1 antibody kn-keyword=IgG1 antibody END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=7-8 article-no= start-page=853 end-page=861 dt-received= dt-revised= dt-accepted= dt-pub-year=1992 dt-pub=199208 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the mechanism of initial attack in intractable asthma Part 1. The possible role of various respiratory viruses in bronchial asthma kn-title=難治性喘息の発症に関する研究 第1編 気管支喘息の発症における各種気道感染ウイルスの役割に関する検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Allergen exposure leads to production of the specific IgE antibody and bronchospasm in atopic asthmatics. However, in adult cases with non-atopic asthma, the mechanism of asthma attack is still unknown. We observed that many adult asthmatics had fever and cold symptoms immediately before developing their first attack. Therefore, we measured the serum antibody titers against nine viruses (Influenza A and B, Adenovirus, RSV, Coxsackie B type 3, CMV, Parainfluenza type 1, 2, and 3), and analyzed their relationship with other clinical paremeters to elucidate the possible role of virus infection in inducing asthma attack. (1) No difference in antibody titers was observed between atopic and non-atopic asthmatics. (2) Steroid-dependent asthmatics had a higher antibody against CMV, and lower antibody against Coxsackie virus as compared with non-steroid dependent patients. (3) The anti-CMV antibody showed a significant correlation with the specific IgG antibody and lymphocyte blastogenesis to Candida antigen. (4) To examine the cross reactivity between Candida antigen and CMV, Candida antigen-specific-human monoclonal antibody was used but the result was negative. These findings suggest that the relationship between CMV and Candida is important in the pathogenesis of non-atopic adult asthmatics, although the mechanism is still unknown. en-copyright= kn-copyright= en-aut-name=TakataMinoru en-aut-sei=Takata en-aut-mei=Minoru kn-aut-name=高田穣 kn-aut-sei=高田 kn-aut-mei=穣 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=intractable asthma kn-keyword=intractable asthma en-keyword=viral infection kn-keyword=viral infection en-keyword=Candida antigen kn-keyword=Candida antigen END start-ver=1.4 cd-journal=joma no-vol=104 cd-vols= no-issue=7-8 article-no= start-page=833 end-page=842 dt-received= dt-revised= dt-accepted= dt-pub-year=1992 dt-pub=199208 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the allergic features of severe bronchial asthma kn-title=気管支喘息の重症化要因に関する検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=The allergic responses to mite and Candida antigen were analyzed in atopic and non-atopic asthmatics to clarify the mechanisms of severe bronchial asthma. Skin responses and serum level of antigen specific IgE to mite antigen were lower in severe atopic asthmatics, especially in intractable atopic asthmatics. The serum level of antigen specific IgG1 and responses of peripheral blood lymphocytes to mite antigen showed no difference with severity in either type of asthma. Atopic severe asthmatics had higher serum levels of antigen specific IgE antibodies to Candida antigen and higher serum levels of antigen specific IgG1 antibodies to Candida antigen than atopic mild and moderate asthmatics. Non-atopic severe asthmatics had higher serum levels of antigen specific IgG1 antibodies to Candida antigen and higher responses of peripheral blood lymphocyte to Candida antigen than non-atopic mild and moderate asthmatics. In atopic and non-atopic severe asthmatics, bronchial provocation tests by Candida antigen showed higher positive responses than mild and moderate asthmatics. These findings suggest that a common mechanism makes asthma severe in atopic and non-atopic asthma and that Candida antigen plays an important role in both types of asthma. en-copyright= kn-copyright= en-aut-name=NambaYasuo en-aut-sei=Namba en-aut-mei=Yasuo kn-aut-name=難波康夫 kn-aut-sei=難波 kn-aut-mei=康夫 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=気管支喘息 kn-keyword=気管支喘息 en-keyword=重症化 kn-keyword=重症化 en-keyword=病型 kn-keyword=病型 en-keyword=カンジダ kn-keyword=カンジダ END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=5-6 article-no= start-page=619 end-page=628 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=1993 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Stusies on the pathogenesis in diffuse panbronchiolitis Part 2. Immune responses in diffuse panbronchiolitis kn-title=びまん性汎細気管支炎の病態に関する研究　第2編　びまん性汎細気管支炎患者の免疫能 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Various immunological processes are suspected of having some relationship with the onset of diffuse panbronchiolitis (DPB). Therefore, the cellular and humoral immunity of patients with DPB were studied. Sera of patients with DPB showed a high frequency of positive RA factor and high titer of cold agglutinin. Delayed skin tests with phytohemagglutinin (PHA) and purified protein derivative (PPD) in patients with DPB revealed normal responses to PHA as nonspecific mitogen and suppressed responses to PPD as specific antigen, although lymphocyte blastogenesis in vitro showed suppressed responses to PHA. The proportion of lymphocytes in bronchoalveolar lavage (BAL) fluid of DPB patients equaled that of normal controls. Furthermore, the CD4/CD8 ratio of T-cell subsets in BAL fluid of DPB patients were significantly lower than that of normal controls, although the CD4/CD8 ratio in peripheral blood of DPB were significantly higher than that in normal controls. The percentage of B-cells in the peripheral blood of DPB patients was hihger than that in normal controls. These data suggest that the activation of cellular and humoral immune mechanisms could play an important role in the pathogenesis of DPB. en-copyright= kn-copyright= en-aut-name=ShiraishiTakamasa en-aut-sei=Shiraishi en-aut-mei=Takamasa kn-aut-name=白石高昌 kn-aut-sei=白石 kn-aut-mei=高昌 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=びまん性汎細気管支炎 kn-keyword=びまん性汎細気管支炎 en-keyword=気管支肺胞洗浄 kn-keyword=気管支肺胞洗浄 en-keyword=リンパ球サブセット kn-keyword=リンパ球サブセット en-keyword=皮内反応 kn-keyword=皮内反応 en-keyword=リンパ球幼若化反応 kn-keyword=リンパ球幼若化反応 END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=5-6 article-no= start-page=611 end-page=618 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=1993 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Stusies on the pathogenesis in diffuse panbronchiolitis Part 1. Cellular components in bronchoalveolar lavage fluid of diffuse panbronchiolitis kn-title=びまん性汎細気管支炎の病態に関する研究　第1編　びまん性汎細気管支炎患者の気道細胞反応 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Diffuse panbronchiolitis (DPB) is known as a chronic progressive inflammation of the peripheral airway followed by lethal respiratory failure. Bronchoalveolar lavage (BAL) was performed to clarify the pathogenesis of DPB compared to chronic bronchitis. The recovery rate of BAL fluid in DPB decreased, but total cell count increased enormously. Furthermore, increased proportions of neutrophils in BAL fluid from DPB patients was characteristic and included a relative decrease in alveolar macrophages. Patients with DPB were classified based on the presence or absence chronic airway infection with Pseudomonas aeruginosa. There was no significant difference in cellular components of BAL fluid among the patients with or without Pseudomonas infection. Patients with DPB showed both obstructive and restrictive ventilatory disturbances. There was no correlation between parameters of these respiratory functions and total cell counts or various cellular proportions in BAL fluid. Infiltrating cell density around bronchioles of patients with DBP was measured. Significantly higher cell density was shown in patinets with DPB compared to other disease controls. There were also significant negative correlations between cell density and respiratory parameters such as % vital capacity, % V50 and % V25. These results indicate that remarkable increase in neutrophils in BAL fluid and the marked cell infiltration around bronchioles in DPB patients could play a crucial role in the pathogenesis of DPB. en-copyright= kn-copyright= en-aut-name=ShiraishiTakamasa en-aut-sei=Shiraishi en-aut-mei=Takamasa kn-aut-name=白石高昌 kn-aut-sei=白石 kn-aut-mei=高昌 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=びまん性汎細気管支炎 kn-keyword=びまん性汎細気管支炎 en-keyword=慢性気管支炎 kn-keyword=慢性気管支炎 en-keyword=気管支肺胞洗浄 kn-keyword=気管支肺胞洗浄 en-keyword=緑膿菌 kn-keyword=緑膿菌 en-keyword=細気管支領域細胞密度 kn-keyword=細気管支領域細胞密度 END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=5-6 article-no= start-page=561 end-page=571 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=1994 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Clinical studies on inhalation provocatopn test of Candida antigen in bronchial asthma kn-title=気管支喘息におけるカンジダ抗原吸入誘発試験の臨床的検討―遅延型気道反応を中心に― en-subtitle= kn-subtitle= en-abstract= kn-abstract=Various allergic mechanisma participate in the reversible bronchospasms of an asthma attack. Candida albicans was suspected as the causative antigen in late-onset and severe intractable asthma. In this study, inhalation provocation test was performed with Candida antigen to evaluate the asthmatic responses of asthmatic patients with positive skin reaction to Candida antigen. More than 20% decrease in park flow after antigen inhalation was considered an asthmatic response and such responses were classified as immediate (IAR), late (LAR) or delayed (DeAR) depending on the time course after antigen inhalation. Provocation tests induced asthmatic responses in 26(42.6%) patients and 11(42.3%) showed DeAR. Eight of the 11 patients with DeARs had late onst asthma and 7 patients had intractable asthma. Furthermore, patients with DeARs showed higher lymphocyte responses to Candida antigen than those with IAR or LAR. These date indicate that EeAR to Canidia antigen plays an important role in the pathogenesis of severe intractable asthma. en-copyright= kn-copyright= en-aut-name=InokiAtsuhiro en-aut-sei=Inoki en-aut-mei=Atsuhiro kn-aut-name=猪木篤弘 kn-aut-sei=猪木 kn-aut-mei=篤弘 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=難治性喘息 kn-keyword=難治性喘息 en-keyword=カンジダ抗原 kn-keyword=カンジダ抗原 en-keyword=吸入誘発試験 kn-keyword=吸入誘発試験 en-keyword=遅延型気道反応 kn-keyword=遅延型気道反応 en-keyword=リンパ球幼若化反応 kn-keyword=リンパ球幼若化反応 END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=5-6 article-no= start-page=539 end-page=547 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=1994 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Mechanism of immunotherapy related to the production of antigen specific IgG subclass antibodies and leukotrienes in bronchial asthmatics kn-title=気管支喘息患者における減感作療法に作用機序に関する研究―抗原特異的IgGサブクラス抗体とロイコトリエン産生能に及ぼす影響について― en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the mechanism of immunotherapy in bronchial asthma, the level of mite specific IgG subclass asntibodies (total IgG, IgG(1), IgG(4)) and the production of leukotrienes (LTB(4), LTC(4)) released from leukocytes were examined. Eighteen mite-sensitive asthmatic patiens who received immunotherapy with house dust extract for 1 year were dividel into two groups, the responsive patients and non-responsive patients. Before treatment and 1 year after treatment, the levels of mite specific serum IgG subclass antibodies were measured by enzyme-linked immunosorbent assay (ELISA) and the levels of LTs were measured by high performance liquid chromatography (HPLC). In the responsive group, the level of mite specific serum IgG(4) antibody was significantly increased (p<0.05), and the level of mite specific serum total IgG and IgG(1) antibody was decreased. The release of LTB(4) and LTC(4) from leukocytes stimulated by mite antigen was significantly decreased (p<0.05,p<0.05). These results indicate that increases in the antigen specific IgG(4) and the inhibiton of chemical madiators play important roles in the mechanism of immunotherapy. en-copyright= kn-copyright= en-aut-name=KatagiSachie en-aut-sei=Katagi en-aut-mei=Sachie kn-aut-name=片木幸恵 kn-aut-sei=片木 kn-aut-mei=幸恵 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=bronchial asthma kn-keyword=bronchial asthma en-keyword=immunotherapy kn-keyword=immunotherapy en-keyword=IgG subclass antibodies kn-keyword=IgG subclass antibodies en-keyword=leukotrienes kn-keyword=leukotrienes END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=5-6 article-no= start-page=527 end-page=537 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=1994 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the cause of intractable asthma using animal model Part 2. Immunoglobulin G, chemical mediators and cell reactions in BALF and peripheral blood of chronic asthma model kn-title=慢性喘息モデルによる喘息の難治化要因に関する研究　第2編　肺局所や血液中における出現細胞及び液性反応に関する検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the mechanism of intractable asthma, we examined the cellular content and chemical mediators in BALF and peripheral blood of a chronic asthma model which we had already established by inhalation of ascaris suum antigen. The serum levels of antigen specific IgG antibody on the eighth day were signicantly higher than those before inhalation. The serum levels of antigen specific IgG(1) antibody increased on the eighth day compared with levels before inhalation. The serum levels of antigen specific IgG(2) antibody as a blocking antibody increased and immediat asthmatic response (IAR) gradually improved until the fourth day. The number of eosinophils after eight days of inhalation was decrease in peripheral blood but was significantly increased in BAL and lung tissue. The serum levels of LTC(4) after eight days of inhalation decreased significanlty compared to those after one day of inhalation. LTB4 concentration in BAL after eight days of inhalation were significanlty lower than those after one day of inhalation. Histamine concentrations were increased in BAL in both the IAR and dual asthmatic response (DAR) animal model. These data suggest that intractable asthma was induced by many kinds of chemical mediators produced by inflammatory cells including eosinophils, mast cell-basophils, neutrophils and lymphocytes. en-copyright= kn-copyright= en-aut-name=SuganoHisashi en-aut-sei=Sugano en-aut-mei=Hisashi kn-aut-name=菅野尚 kn-aut-sei=菅野 kn-aut-mei=尚 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=chronic asthma kn-keyword=chronic asthma en-keyword=guinea pig kn-keyword=guinea pig en-keyword=IgG subclass antibodies kn-keyword=IgG subclass antibodies en-keyword=leukotrienes kn-keyword=leukotrienes en-keyword=histamine kn-keyword=histamine END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=5-6 article-no= start-page=517 end-page=525 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=1994 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the cause of intractable asthma using animal model Part 1. Establishment of a chronic asthma model by repeated antigen inhalation kn-title=慢性喘息モデルによる喘息の難治化要因に関する研究　第1編　抗原の繰り返し吸入による慢性喘息モデルの作製 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To elucidate the cause of intractable asthma, guinea pigs were actively sensitized by intraperitoneal injection of ascaris suum as an antigen. We repeated the inhalation of aerosolized ascaris antigen eight times in the animal models which consisted of a non-treated group, a metopirone-treated group and a steroid-treated group. We investigated the course of asthmatic response by evaluating the ratio of expirations to inspirations after the inhalation challenge. The frequency of late asthmatic response (LAR) was increased by repeated inhalation of the antigen. There was no significant differnce in the frequency between non-treated group and steroid-treated group, but the metopirone-treated group showed strong LAR compared with the other two groups. The intensity of LAR was gradually increased and that of immediate asthmatic response (LAR) was decreased in the metopirone-treated group. Finally, we established a chronic asthma model in which LAR was strong and the asthma attack was prolonged over twenty-four hours. These results suggest that the model will be useful in clarifying the causes of intractable asthma in humans. en-copyright= kn-copyright= en-aut-name=SuganoHisashi en-aut-sei=Sugano en-aut-mei=Hisashi kn-aut-name=菅野尚 kn-aut-sei=菅野 kn-aut-mei=尚 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=chronic asthma kn-keyword=chronic asthma en-keyword=animal model kn-keyword=animal model en-keyword=guinea pig kn-keyword=guinea pig en-keyword=re-inhalation kn-keyword=re-inhalation en-keyword=late asthmatic response kn-keyword=late asthmatic response END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=5-6 article-no= start-page=455 end-page=464 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=1993 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=On localization of inhaled antigens in late asthmatic response in an animal model kn-title=遅発型気道反応の発現機序に関する基礎的研究―吸入抗原の局在について― en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the initiation of late asthmatic response (LAR), the localization and fate of inhaled antigens were studied using an animal model of LAR. Guinea pigs were sensitized by ascaris suum and aluminum gel. Radioiodinated ascaris suum and ovalbumin as control were subsequently injected into the trachea of the guinea pig to determine the radioactivity of bronchoalveolar lavege (BAL) cells and fluid (BALF) components before and after LAR. The localization of antigens was also examined by autoradiography of BAL cells and lung tissue sections. The radioactivity of radioiodinated ascaris in BAL cells and lung tissue increased during LAR with increases in macrophages and neutrophils, although in non-responding animals inhaled antigens gradualy disappeared from the airway. The radioactivity of radioiodinated ovalbumin gradually decreased regardless of LAR. Autoradiographic study showed that the inhaled antigens were located in the cytoplasm of alveolar macrophages in BALF and lung tissue. These data indicate that inhaled antigens may accumulate and migrate with numerous inflammatory cells such as macrophages and neutrophils in late phase bronchial response. en-copyright= kn-copyright= en-aut-name=TakedaKatsuyuki en-aut-sei=Takeda en-aut-mei=Katsuyuki kn-aut-name=武田勝行 kn-aut-sei=武田 kn-aut-mei=勝行 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=alveolar macrophage kn-keyword=alveolar macrophage en-keyword=guinea pig kn-keyword=guinea pig en-keyword=(125)I-ascaris kn-keyword=(125)I-ascaris en-keyword=late asthmatic response (LAR) kn-keyword=late asthmatic response (LAR) en-keyword=localization of inhaled antigen kn-keyword=localization of inhaled antigen END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=3-4 article-no= start-page=341 end-page=351 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=1993 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the pathogenesis of lung cancer with interstitial pneumonia Part 1. Analysis of the clinical features of intersitial pneumonia in lung cancer kn-title=肺癌のびまん性肺線維化病態に関する研究　第1編　肺癌に随伴するびまん性間質性陰影の臨床的検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Clinical features and findings on chest x-ray were analyzed to clarify the relationship between lung cancer and interstitial pneumonia. Of 262 patients with lung cancer, 69 patients (26.3%) had interstitial pneumonia. Patients with interstitial pneumonia (LC with IP) were older than those without interstitial pneumonia (LC without IP). The incidence of LC with IP cases among males and smokers were 29.2% and 29.3%, respectively. There were no significant differences among histlogic types and clinical stages of lung cancer. More cases of LC with IP had cancer in the lower (42.0%) and peripheral (76.8%) areas on chest x-ray films. Cancer was frequently located within the interstitial shadow on chest x-ray film. Among 40 patients with idiopathic interstitial pneumonia associated lung cancer (IIP with LC), there were 38 males and 32 smokers. No dominant histlogic subtype of lung cancer was noted in IIP with LC, though the most frequent was adenocarcinoma (16 cases, 40%). In IIP with LC, the site of cancer was associated with active fibrotic changes in interstitial pneumonia. These data strongly suggest that carcinogenic factors were related to the fibrotic changes in interstitial pneumonia. en-copyright= kn-copyright= en-aut-name=ShibayamaTakuo en-aut-sei=Shibayama en-aut-mei=Takuo kn-aut-name=柴山卓夫 kn-aut-sei=柴山 kn-aut-mei=卓夫 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=Lung cancer kn-keyword=Lung cancer en-keyword=Idiopathic interstitial pneumonia kn-keyword=Idiopathic interstitial pneumonia en-keyword=Chest X-ray finding kn-keyword=Chest X-ray finding END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=3-4 article-no= start-page=305 end-page=314 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=1994 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the treatment of intractable asthman Part 1. Effect of Saiboku-to on cell-mediated allergy in the experimental asthma using guinea pigs kn-title=難治性喘息の治療に関する研究　第1編　モルモット喘息モデルにおける細胞反応型アルルギーに対する柴朴湯の効果 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Saiboku-to seems to be a useful drug in the teatment of intractable asthmatics. The pharmacological effect of Saiboku-to was examined in an experimental model of bronchial asthma with cell-mediated allergy in guinea pigs. The fundings revealed that Saiboku-to inhibited the late asthmatic response. It suppressed the lymphocyte blastogensis by ascaris antigen and eosinophil infiltration into BALF and peribronchial tissue. Moreover, Saiboku-to lowered the levls of LTB4 and LTC4 in the cardiac blood, but not the antigen-specific IgG subclass. These findings suggest that the inhibitory effect of Saiboku-to on the late asthmatic response is caused by the suppression of cell-mediated allergy. en-copyright= kn-copyright= en-aut-name=OkamotoShoichi en-aut-sei=Okamoto en-aut-mei=Shoichi kn-aut-name=岡本章一 kn-aut-sei=岡本 kn-aut-mei=章一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=Saiboku-to kn-keyword=Saiboku-to en-keyword=cell-mediated allergy kn-keyword=cell-mediated allergy en-keyword=actively sensitized model kn-keyword=actively sensitized model en-keyword=lymphocyte kn-keyword=lymphocyte en-keyword=leukotrienes kn-keyword=leukotrienes END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=1-2 article-no= start-page=195 end-page=204 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=19930227 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the mechanism of late asthmatic response using a technique of bronchoalveolar lavage Part 2. Bronchial reaction after inhalation of Candida allergen in bronchial asthmatics kn-title=気管支喘息における遅発型気道反応の機序に関する研究　第2編　Candida 抗原による遅発型気道反応局所の細胞反応及びロイコトリエンの変動 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the mechanism of late asthmatic response (LAR) which is related to intractable asthmatic attacks, cellular and humoral components at the sites of LAR were examined by bronchoalveolar lavage fluid (BALF) obtained after bronchial inhalation of Candida allergen. BAL examination was performed 2 hours after the LAR attack. The differential cell count was obtained and the level of leukotrienes (LTs) in the BALF and peripheral blood determined by high performance liquid chromatography. The percentages of eosinophils and basophil・mast cells and neutrophils were statistically high in the BALF after LAR compared with the level in the non-attack state (p<0.05 p<0.01). The level of LTC(4) was significantly higher in the BALF after LAR (p<0.01), and LTB(4) also showed a similar tendency at LAR. However, LTD(4) could not be detected in the BALF after LAR or in the non-attack stage. On the other hands, the percentage of neutorphils and LTB4 level in circulating blood showed a peak before LAR, and then decreased markedly during LAR. Eosinophils also decreased significantly during LAR, but the plasma LTC(4) level increased significantly during LAR. These findings suggest that neutrophils, eosinophils and basophil・mast cells play an important role in the pathogensis of intractable asthma attack and LAR following release of leukotrienes. en-copyright= kn-copyright= en-aut-name=NambaKunihiro en-aut-sei=Namba en-aut-mei=Kunihiro kn-aut-name=難波一弘 kn-aut-sei=難波 kn-aut-mei=一弘 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=Candida antigen kn-keyword=Candida antigen en-keyword=bronchoalveolar lavage kn-keyword=bronchoalveolar lavage en-keyword=inflammatory cell kn-keyword=inflammatory cell en-keyword=late asthmatic response kn-keyword=late asthmatic response en-keyword=leukotrienes kn-keyword=leukotrienes END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=1-2 article-no= start-page=119 end-page=126 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=19930227 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on anti-HTLV-T antibody in interstitial lung diseases Part 1. Western blot analysis for anti-HTLV-T antibody and HTLV-T related reaction in DBP and IIP kn-title=間質性肺疾患における抗 HTLV-T抗体に関する研究　第1編 DPB, IIPにおける抗 HTLV-T抗体並びに HTLV-T関連反応の Western blot 法による検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=By the immunofluorescent assay for the anti-HTLV-T antibody, the serum of many patients with diffuse panbronchiolitis (DBP) and idiopathic interstitial pneumonia (IIP) show two types of cytoplasmic fluorescence. One is a granular pattern in the MT-1 cell and diffuse pattern in the MT-2 cell. This is the typical pattern for the anti-HTLV-T antibody. The other is a diffuse pattern in the MT-1 and/or MT-2 cells. This pattern has been designated as HTLV-T related reaction. These serum reactions were investigated by Western blot analysis with an MT-2 cell lysate as antigen. Although about 20% of the patients with DBP and IIP were considered to be suffering from HTLV-T associated bronchiolo-alveolar disorder (HABA) because they showed the typical pattern of anti-HTLV-T antibody, only those patients with HABA were shown to have the antibodies against HTLV-T specific proteins (p19, p24, p28, pr53 and gp68). On the other hand, the patients with HTLV-T related reaction had neither the antibodies against any HTLV-T proteins nor the other protein components of MT-2. Thus, Western blot analysis revealed that antibodies against HTLV-T specific proteins were present only in the patients with HABA. en-copyright= kn-copyright= en-aut-name=UenoKatsumi en-aut-sei=Ueno en-aut-mei=Katsumi kn-aut-name=植野克巳 kn-aut-sei=植野 kn-aut-mei=克巳 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=びまん性汎細気管支炎 kn-keyword=びまん性汎細気管支炎 en-keyword=特発性間質性肺炎 kn-keyword=特発性間質性肺炎 en-keyword=HTLV-T抗体 kn-keyword=HTLV-T抗体 en-keyword=HTLV-T関連反応 kn-keyword=HTLV-T関連反応 en-keyword=Western blot 法 kn-keyword=Western blot 法 END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=9-10 article-no= start-page=859 end-page=869 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=199310 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=ADF in the lung tissues of HTLV-I associated bronchiolo-alveolar disorder : HABA kn-title=HTLV-I 関連細気管支・肺胞異常症 (HABA) における肺組織中 ADF の検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=ATL-derived factor (ADF) is an acid protein, molecular weight about 13KD, which is related to cell classification, activation, and various viral infections. The localization of ADF was studied in the lung tissues of HTLV-I associated bronchiolo-alveolar disorder : HABA, diffuse panbronchiolitis : DPB, and idiopathic interstitial pneumonia : IIP. The localization of ADF in the lung tissues was demonstrated by immunohistochemical staining with anti-ADF antibody as the first antibody, which was made by affinity purification. In all 4 cases of HABA, one of 6 cases of DPB, and two of 5 cases of IIP, staining of the lung tissue was positive. ADF was demonstrated in the bronchial epithelia, alveolar epithelia, vascular endothelia, and desquamative cells in HABA cases as the result of the study. ADF was also restrictively demonstrated in bronchial epithelia in DPB and IIP cases. The case of DPB in which ADF was demonstrated also showed positive HTLV-I related reaction. In conclusion, the localization of ADF in the lung tissues was demonstrated in HABA, DPB and IIP, suggesting immunological abnormalities based upon infections from HTLV-I or a related retrovirus. en-copyright= kn-copyright= en-aut-name=KitamuraTomoki en-aut-sei=Kitamura en-aut-mei=Tomoki kn-aut-name=北村智樹 kn-aut-sei=北村 kn-aut-mei=智樹 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=HTLV-I Associated Bronchiolo-alveolar Disorder : HABA kn-keyword=HTLV-I Associated Bronchiolo-alveolar Disorder : HABA en-keyword=ATL-derived factor : ADF kn-keyword=ATL-derived factor : ADF en-keyword=Diffuse panbronchiolitis kn-keyword=Diffuse panbronchiolitis en-keyword=Idiopathic interstitial pneumonia kn-keyword=Idiopathic interstitial pneumonia en-keyword=Anti HTLV-I antibody kn-keyword=Anti HTLV-I antibody END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=7-8 article-no= start-page=759 end-page=770 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=199308 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the pathogenesis of anti-IgE autoantibody in bronchial asthma kn-title=気管支喘息における血清抗 IgE 自己抗体の基礎的並びに臨床的研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the pathogenesis of asthma especially intractable asthma, we measured the serum levels of anti-IgE autoantibody in 46 asthmatics and 39 healthy subjects, using solid-phase enzyme immunoassay. The serum levels of anti-IgE autoantibody in bronchial asthmatics were significantly higher than those in healthy subjects (p<0.01). The levels of anti-IgE autoantibody in 25 atopic asthmatics were also significantly higher than those in 19 non-atopic asthmatics (p<0.01). Futhermore, significant correlation was observed between the levels of anti-IgE autoantibody and serum IgE (r=0.576, p<0.01). House dust and Candida (p<0.01) specific IgE (RAST) positive asthmatics also tended to have higher serum levels of anti-IgE autoantibody. However, no significant relation was observed between the serum levels of anti-IgE autoantibody and the severity of asthma. Moreover, anti-IgE autoantibody was not significantly related to specific IgG subclass antibody or lymphocyte blastogenesis to mite and Candida, or with the numbers of eosinophils and basophils in peripheral blood. These findings suggest that anti-IgE autoantibody play an important role in the pathogenesis of bronchial asthma, especially atopic asthma associated with IgE-dependent mechanisms. en-copyright= kn-copyright= en-aut-name=YamagataKoichi en-aut-sei=Yamagata en-aut-mei=Koichi kn-aut-name=山縣浩一 kn-aut-sei=山縣 kn-aut-mei=浩一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=抗 IgE 自己抗体 kn-keyword=抗 IgE 自己抗体 en-keyword=アトピー型喘息 kn-keyword=アトピー型喘息 en-keyword=IgE 抗体 kn-keyword=IgE 抗体 en-keyword=IgG アイソタイプ抗体 kn-keyword=IgG アイソタイプ抗体 en-keyword=酵素抗体法 kn-keyword=酵素抗体法 END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=11-12 article-no= start-page=1143 end-page=1157 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=199412 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the pathogenesis of diffuse panbronchiolitis (DPB) in regard of the effects of erythromycin therapy kn-title=びまん性汎細気管支炎の病態に関する研究―エリスロマイシンの作用機序を中心に― en-subtitle= kn-subtitle= en-abstract= kn-abstract=DPB has been known as a chronic respiratory infection with poor prognosis until introduction of erythromycin (EM) therapy with low-dose and long-term administration. As symptoms and prognosis of DPB were improved enormously under EM therapy, EM therapy on DPB was analyzed to clarify the action and mechanisms. EM in a daily dese of 600 mg was administered to 9 patients with DPB for about 38 months and 7 normal volunteers for 2 months. Most patients with DPB showed the relief of symptoms within 2 months, although the EM concentrations in the blood and sputa were lower than the antibacterial therapeutic level. Immunological examination revealed the decrease in cold agglutinin titer and CD4/CD8 ratio after EM therapy. The neutrophil chemotactic factor (NCF) derived from the mononuclear cell culture of DPB patients was higher than that in the normal control. EM therapy decreased the level of NCF not only in patients with DPB but also in normal volunteers. These findings indicate that the immunological effects of EM play an important role in the treatment of DPB. en-copyright= kn-copyright= en-aut-name=IrieShoichiro en-aut-sei=Irie en-aut-mei=Shoichiro kn-aut-name=入江正一郎 kn-aut-sei=入江 kn-aut-mei=正一郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=diffuse panbronchiolitis kn-keyword=diffuse panbronchiolitis en-keyword=erythromycin kn-keyword=erythromycin en-keyword=リンパ球 kn-keyword=リンパ球 en-keyword=neutrophil chemotatic factor kn-keyword=neutrophil chemotatic factor END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=9-10 article-no= start-page=1025 end-page=1033 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=199410 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A new asthma classification based on its pathophysiology using IgE antibody (RAST) and lymphocyte activation as parameters kn-title=気管支喘息における病態に基づく新しい病型分類に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To establish a new classification in bronchial asthma, antigen-induced immediate asthmatic response (IAR) and late asthmatic response (LAR) to mite and Candida were compared with antigen specific IgE antibody (IgE RAST) and lymphocyte blastogenesis (Ly-BL) in asthmatics. Half of asthmatics with a high score on mite IgE RAST could not be provoked to IAR, although almost all of patients with house dust-induced IAR showed a high score on mite IgE RAST. However, asthmatics with enhanced Ly-BL following exposure to mite and Candida showed highly provoked LAR by antigen inhalation, and LAR patients showed significantly enhanced Ly-BL by both antigens (p<0.01). Bronchial asthmatics were classified into the following 4 groups using those parameters ; A group (IgE RAST+, Ly-BL-), B group (IgE RAST+, Ly-BL+), C group (IgE RAST-, Ly-BL+), D group (IgE RAST-,Ly-BL-). Half of the patients with IAR belonged to the A and B groups, and almost all of the LAR patients were in the B or C group. Patients in the A group predominantly showed early onset, however patients in the B and C groups showed late onset. A and B group patients were mild or moderate asthmatics, but severe asthmatics belonged to the C and D groups. These data suggest that the C group showed only Ly-BL led LAR by "cell-mediated allergy" in late onset severe asthma. en-copyright= kn-copyright= en-aut-name=KimuraKazuhi en-aut-sei=Kimura en-aut-mei=Kazuhi kn-aut-name=木村和陽 kn-aut-sei=木村 kn-aut-mei=和陽 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=asthma classification kn-keyword=asthma classification en-keyword=lymphocyte blastogenesis kn-keyword=lymphocyte blastogenesis en-keyword=Candida kn-keyword=Candida en-keyword=house dust・mite kn-keyword=house dust・mite en-keyword=IgE RAST kn-keyword=IgE RAST END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7-8 article-no= start-page=907 end-page=915 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=199408 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Establishment of antigen specific T cell clones from asthmatic patients including evaluation of cytokine production kn-title=気管支喘息における抗原特異的 T cell clone の樹立とサイトカイン産生能に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the pathogenesis of bronchial asthma, we establishied T cell clones specific for Candida antigen and for mite antigen from the peripheral blood of three asthmatic patients. Flow cytometric analysis was performed on these clones. The surface phenotype of all clones was helper/inducer type. These clones were analyzed for the ability to produce interferon gammma (IFN-γ) and interleukin 4 (IL-4). The T cell clone established from tne patient who showed late asthmatic response (LAR) after bronchial inhalation of Candida, as well as the clones from the patient who showed IAR and LAR after inhalation of housedust mite, produced a higher amount of IFN-γ and lower amount of IL-4. The T cell clone established from the patient who were under corticosteroid therapy and showed IAR after inhalation of Candida produced lower amounts of IFN-γ and IL-4, which seemed to be inhibition of cytokine production from antigen specific T cell clone by corticosteroids. These findings indicate that T cell clones established from the patients who showed LAR produced a large amount of IFN-γ, suggesting that IFN-γ plays an important role in allergic reactions of LAR. en-copyright= kn-copyright= en-aut-name=MiyaharaNobuaki en-aut-sei=Miyahara en-aut-mei=Nobuaki kn-aut-name=宮原信明 kn-aut-sei=宮原 kn-aut-mei=信明 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=antigen specific T cell clone kn-keyword=antigen specific T cell clone en-keyword=IFN-γ kn-keyword=IFN-γ en-keyword=bronchial asthma kn-keyword=bronchial asthma en-keyword=late asthmatic response (LAR) kn-keyword=late asthmatic response (LAR) END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7-8 article-no= start-page=883 end-page=892 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=199408 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Xanthoma cells in sputa of patients with chronic obstructive lung diseases kn-title=慢性閉塞性肺疾患における喀痰中 Xanthoma cell に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Alveolar macrophages attack various foreign bodies inspired through the airway and destroy cell debris. Furthermore, a part of the surfactant produced by alveolar epithelium would be phagocytized by alveolar macrophages forming foamy cells in lung tissue. These formy cells could be detected by oil red O staining as xanthoma cells in sputa of patients with airway diseases. Therefore, xanthoma cells in sputa of patients with DPB, chronic bronchitis and bronchial asthma were evaluated to clarify the role in the pathogenesis of these respiratory diseases. All patients with DBP expectorated enormous amounts of xanthoma cells in sputa while 88% of the patients with chronic bronchitis and 41% of those with bronchial asthma had sputa containing xanthoma cells in a smaller number than DBP. Increased xanthoma cells were shown in DPB with longer disease duration, lower vital capacity, lower atrerial blood oxygen pressure, and pseudomonas infection. However, extreme obstruction of small airway diminished xanthoma cells in sputa. Xanthoma cells were shown in bronchial asthma especially in late onset and intractable asthmatics. These findings indicate that xanthoma cells in sputa reflect the existence of organic changes in the small airway which disturb the drainage of surfactant from alveolar area to bronchial trees. en-copyright= kn-copyright= en-aut-name=KawauchiKazuhisa en-aut-sei=Kawauchi en-aut-mei=Kazuhisa kn-aut-name=河内和久 kn-aut-sei=河内 kn-aut-mei=和久 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=びまん性汎細気管支炎 kn-keyword=びまん性汎細気管支炎 en-keyword=気管支喘息 kn-keyword=気管支喘息 en-keyword=喀痰 kn-keyword=喀痰 en-keyword=oil red O 染色 kn-keyword=oil red O 染色 en-keyword=xanthoma cell kn-keyword=xanthoma cell END start-ver=1.4 cd-journal=joma no-vol=106 cd-vols= no-issue=7-8 article-no= start-page=743 end-page=750 dt-received= dt-revised= dt-accepted= dt-pub-year=1994 dt-pub=199408 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Studies on the occurrence of bronchial asthma Part 2. Lymphocytes activated by Cytomegalovirus kn-title=気管支喘息の発症に関する研究　第2編　喘息患者におけるサイトメガロウイルス抗原によるリンパ球幼若化反応の検討 en-subtitle= kn-subtitle= en-abstract= kn-abstract=The possible role of virus infection in the occurrence and attack of asthma was examined by measuring the lymphocyte transformation test to CMV in 44 asthmatic and 14 healthy subjects and analyzed their relation to the clinical parameters. CMV-induced lymphocyte reactivity (CMV-LR) in adult asthmatics was significantly higher than that in the healthy controls. A positive correlation was observed between CMV-LR titer and CMV-complement fixation (CMV-CF) antibody titers (r=0.35). In adult asthmatics, the CMV-LR in the high IgE titer (100U/ml≦) group was significantly higher than that in the low IgE titer (<100U/ml) group. These findings suggest that CMV is an important factor in the pathogenesis of adult asthma mediated by lymphocytes and probably IgE, although the precise mechanism in still unknown. en-copyright= kn-copyright= en-aut-name=OkamotoMakoto en-aut-sei=Okamoto en-aut-mei=Makoto kn-aut-name=岡本誠 kn-aut-sei=岡本 kn-aut-mei=誠 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=bronchial asthma kn-keyword=bronchial asthma en-keyword=viral infection kn-keyword=viral infection en-keyword=Cytomegalovirus kn-keyword=Cytomegalovirus en-keyword=IgE kn-keyword=IgE en-keyword=CMV-LTT kn-keyword=CMV-LTT END start-ver=1.4 cd-journal=joma no-vol=108 cd-vols= no-issue=3-6 article-no= start-page=117 end-page=127 dt-received= dt-revised= dt-accepted= dt-pub-year=1996 dt-pub=19960629 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Erythromycin therapy in patients with diffuse panbronchiolitis kn-title=びまん性汎細気管支炎の病態に関する研究―エリスロマイシン少量長期投与を中心に― en-subtitle= kn-subtitle= en-abstract= kn-abstract=Low dose and long-term erythromycin (EM) therapy showed obvious improvement of symptoms and prognosis in patients with DPB. However, mechanisms involved in these clinical effects of EM therapy remain controversial. In this study, the clinical effects of EM therapy on respiratory function, bacterial flora in the lower airway and serum levels of soluble IL-2 receptor (sIL-2R) as an indicator of T-cell activation were examined. All parameters of respiratory functions in patients with DPB including % VC, % FEV 1.0, % V50, % V25 and V50/V25 showed marked improvements within 6 months of EM therapy. Continuous administration of EM for 6 to 24 months produced minimal changes in these respiratory functions though decreases in some parameters were observed in patients with advanced clinical stage and in eldely patients. The increase of % FEV 1.0 exceeded those of % V50 and % V25 after EM therapy. This indicates severe pathological changes in small airways or variable effects of EM therapy. Bacterial species and sensitivities to antibiotics showed no apparent changes after long-term EM therapy. The serum levels of sIL-2R in patients with DPB were higher than those in normal controls. With EM therapy, serum levels of sIL-2R decreased rapidly within 6 months, but these levels remained higher than those in normal controls, even after long-term EM therapy. en-copyright= kn-copyright= en-aut-name=FukudaTomoko en-aut-sei=Fukuda en-aut-mei=Tomoko kn-aut-name=福田智子 kn-aut-sei=福田 kn-aut-mei=智子 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第二内科学教室 en-keyword=diffuse panbronchiolitis kn-keyword=diffuse panbronchiolitis en-keyword=erythromycin kn-keyword=erythromycin en-keyword=呼吸機能 kn-keyword=呼吸機能 en-keyword=soluble IL-2 reseptor kn-keyword=soluble IL-2 reseptor en-keyword=喀痰中細菌叢 kn-keyword=喀痰中細菌叢 END start-ver=1.4 cd-journal=joma no-vol=113 cd-vols= no-issue=3 article-no= start-page=235 end-page=239 dt-received= dt-revised= dt-accepted= dt-pub-year=2001 dt-pub=20011231 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=抗体による血液腫瘍の治療 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯学総合研究科　病態制御科学専攻（第二内科） en-keyword=モノクローナル抗体 kn-keyword=モノクローナル抗体 en-keyword=血液腫瘍 kn-keyword=血液腫瘍 en-keyword=CD 20 kn-keyword=CD 20 en-keyword=CD 33 kn-keyword=CD 33 en-keyword=キメラ抗体 kn-keyword=キメラ抗体 END start-ver=1.4 cd-journal=joma no-vol=115 cd-vols= no-issue=1 article-no= start-page=63 end-page=68 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050530 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=重度急性呼吸器症候群SARS en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=2 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=田端雅弘 kn-aut-sei=田端 kn-aut-mei=雅弘 aut-affil-num=3 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=金廣有彦 kn-aut-sei=金廣 kn-aut-mei=有彦 aut-affil-num=4 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=上岡博 kn-aut-sei=上岡 kn-aut-mei=博 aut-affil-num=5 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=6 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=渡邊都貴子 kn-aut-sei=渡邊 kn-aut-mei=都貴子 aut-affil-num=7 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=草野展周 kn-aut-sei=草野 kn-aut-mei=展周 aut-affil-num=8 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=小出典男 kn-aut-sei=小出 kn-aut-mei=典男 aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部附属病院　第二内科 affil-num=2 en-affil= kn-affil=岡山大学医学部附属病院　第二内科 affil-num=3 en-affil= kn-affil=岡山大学医学部附属病院　第二内科 affil-num=4 en-affil= kn-affil=岡山大学医学部附属病院　第二内科 affil-num=5 en-affil= kn-affil=岡山大学医学部附属病院　第二内科 affil-num=6 en-affil= kn-affil=岡山大学医学部附属病院　第二内科 affil-num=7 en-affil= kn-affil=岡山大学医学部附属病院 affil-num=8 en-affil= kn-affil=岡山大学医学部附属病院　中央検査部 affil-num=9 en-affil= kn-affil=岡山大学医学部附属病院　中央検査部 en-keyword=SARS kn-keyword=SARS en-keyword=伝幡経路 kn-keyword=伝幡経路 en-keyword=対策 kn-keyword=対策 en-keyword=緊急報告 kn-keyword=緊急報告 END start-ver=1.4 cd-journal=joma no-vol=116 cd-vols= no-issue=3 article-no= start-page=287 end-page=292 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050131 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=多剤耐性結核と肺非結核性抗酸菌症 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=佐久川亮 kn-aut-sei=佐久川 kn-aut-mei=亮 aut-affil-num=2 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=3 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯学総合研究所　血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯学総合研究所　血液・腫瘍・呼吸器内科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯学総合研究所　血液・腫瘍・呼吸器内科学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯学総合研究所　血液・腫瘍・呼吸器内科学 en-keyword=多剤耐性結核菌 kn-keyword=多剤耐性結核菌 en-keyword=DOTS kn-keyword=DOTS en-keyword=非結核性抗酸菌 kn-keyword=非結核性抗酸菌 en-keyword=MAC 症 kn-keyword=MAC 症 en-keyword=M. kansasii 症 kn-keyword=M. kansasii 症 END start-ver=1.4 cd-journal=joma no-vol=119 cd-vols= no-issue=3 article-no= start-page=285 end-page=292 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080104 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=II Standard treatment for advanced lung cancer kn-title=II 肺癌の内科的治療 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KiuraKatsuyuki en-aut-sei=Kiura en-aut-mei=Katsuyuki kn-aut-name=木浦勝行 kn-aut-sei=木浦 kn-aut-mei=勝行 aut-affil-num=1 ORCID= en-aut-name=TakigawaNagio en-aut-sei=Takigawa en-aut-mei=Nagio kn-aut-name=瀧川奈義夫 kn-aut-sei=瀧川 kn-aut-mei=奈義夫 aut-affil-num=2 ORCID= en-aut-name=OzeIsao en-aut-sei=Oze en-aut-mei=Isao kn-aut-name=尾瀬功 kn-aut-sei=尾瀬 kn-aut-mei=功 aut-affil-num=3 ORCID= en-aut-name=YasugiMasayuki en-aut-sei=Yasugi en-aut-mei=Masayuki kn-aut-name=八杉昌幸 kn-aut-sei=八杉 kn-aut-mei=昌幸 aut-affil-num=4 ORCID= en-aut-name=OchiNobuaki en-aut-sei=Ochi en-aut-mei=Nobuaki kn-aut-name=越智宣昭 kn-aut-sei=越智 kn-aut-mei=宣昭 aut-affil-num=5 ORCID= en-aut-name=HaradaDaijiro en-aut-sei=Harada en-aut-mei=Daijiro kn-aut-name=原田大二郎 kn-aut-sei=原田 kn-aut-mei=大二郎 aut-affil-num=6 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科 血液・腫瘍・呼吸器内科学 en-keyword=放射線化学療法 kn-keyword=放射線化学療法 en-keyword=分子標的治療 kn-keyword=分子標的治療 en-keyword=血管新生阻害薬 kn-keyword=血管新生阻害薬 en-keyword=受容体チロシンキナーゼ阻害薬 kn-keyword=受容体チロシンキナーゼ阻害薬 END start-ver=1.4 cd-journal=joma no-vol=120 cd-vols= no-issue=1 article-no= start-page=95 end-page=96 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080501 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=MicroRNAs kn-title=マイクロ RNA en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 END start-ver=1.4 cd-journal=joma no-vol=120 cd-vols= no-issue=1 article-no= start-page=23 end-page=28 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080501 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Allogeneic hematopoietic stem cell transplantation from anHLA-haploidentical related donor based on feto-maternal tolerance kn-title=母子間免疫寛容理論に基づく同種造血幹細胞移植 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MatsuokaKen-ichi en-aut-sei=Matsuoka en-aut-mei=Ken-ichi kn-aut-name=松岡賢市 kn-aut-sei=松岡 kn-aut-mei=賢市 aut-affil-num=1 ORCID= en-aut-name=AoyamaKazutoshi en-aut-sei=Aoyama en-aut-mei=Kazutoshi kn-aut-name=青山一利 kn-aut-sei=青山 kn-aut-mei=一利 aut-affil-num=2 ORCID= en-aut-name=KoyamaMotoko en-aut-sei=Koyama en-aut-mei=Motoko kn-aut-name=小山幹子 kn-aut-sei=小山 kn-aut-mei=幹子 aut-affil-num=3 ORCID= en-aut-name=HashimotoDaigo en-aut-sei=Hashimoto en-aut-mei=Daigo kn-aut-name=橋本大吾 kn-aut-sei=橋本 kn-aut-mei=大吾 aut-affil-num=4 ORCID= en-aut-name=AsakuraShoji en-aut-sei=Asakura en-aut-mei=Shoji kn-aut-name=朝倉昇司 kn-aut-sei=朝倉 kn-aut-mei=昇司 aut-affil-num=5 ORCID= en-aut-name=IchinoheTatsuo en-aut-sei=Ichinohe en-aut-mei=Tatsuo kn-aut-name=一戸辰夫 kn-aut-sei=一戸 kn-aut-mei=辰夫 aut-affil-num=6 ORCID= en-aut-name=TanimotoMitsune en-aut-sei=Tanimoto en-aut-mei=Mitsune kn-aut-name=谷本光音 kn-aut-sei=谷本 kn-aut-mei=光音 aut-affil-num=7 ORCID= en-aut-name=TeshimaTakanori en-aut-sei=Teshima en-aut-mei=Takanori kn-aut-name=豊嶋崇徳 kn-aut-sei=豊嶋 kn-aut-mei=崇徳 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=4 en-affil= kn-affil=九州大学病院　遺伝子細胞療法部 affil-num=5 en-affil= kn-affil=国立病院機構岡山医療センター　血液内科 affil-num=6 en-affil= kn-affil=京都大学大学院医学研究科　血液腫瘍内科学 affil-num=7 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学 affil-num=8 en-affil= kn-affil=九州大学病院　遺伝子細胞療法部 en-keyword=同種造血幹細胞移植 kn-keyword=同種造血幹細胞移植 en-keyword=移植片対宿主病 kn-keyword=移植片対宿主病 en-keyword=HLA 不適合移植 kn-keyword=HLA 不適合移植 en-keyword=非遺伝母 HLA 抗原 kn-keyword=非遺伝母 HLA 抗原 en-keyword=母子間免疫寛容 kn-keyword=母子間免疫寛容 END start-ver=1.4 cd-journal=joma no-vol=6 cd-vols= no-issue= article-no= start-page=35 end-page=40 dt-received= dt-revised= dt-accepted= dt-pub-year=1996 dt-pub=19960229 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A subjective well-being of the aged - psychological characteristics of elderly people of 90 or older - kn-title=高齢者の主観的幸福感に関する研究 ―90歳以上の特徴― en-subtitle= kn-subtitle= en-abstract=The population of the aged is currently increasing with advanced medical science and technology. The aged have become to keep their lives long. In this paper, We especially focused on their psychological characteristics of elderly people of 90 and older to offer high quality of nursing care for them. We interviewed 50 patients of 80 years and older about a subjective well-being, using a questionaire based on Philadelphia Geriatric Center Morale Scale. And also we asked 50 nurses, who took care of them exclusively, a questinaire about their images of the aged. We report as follows : 1. The nurses estimated that their images of the second group (range : 90 years old ~) were better than the first group (range : 80~89 years old). 2. In subjective well-being which Philadelphia Geriatric Center Morale Scale showed, above-mentioned both groups were similar in total scores. However, each item was marked differently by them. 3. In both groups, their subjective well-being correlated with good images for them. kn-abstract=高齢化社会の到来に伴い一言で老人といっても幅広い年代が対象となり、一律に老人では説明できない。実際看護をしていると90歳をすぎた老人はその年代迄にはない、穏やかさ、焦りのなさ、人生を達観しているような感じを受けることが多い。そこで90歳以上の老人にみられるイメージや心理面の特徴を明らかにし看護実践の一助としたいと考えた。方法は80歳以上の入院患者50名に身体、生活、家族面からみた現状、他者から見たイメージ、主観的幸福感を調査した。その結果、90歳以上は80歳代にくらべ看護者に肯定的イメージに受け取られる傾向にあった。主観的幸福感を示すモラール得点の総合点では差はなかったが得点する内容に差が見られ、80歳は積極的な生き方で得点しているものが多く90歳代は現状に満足している点で得点している者が多かった。看護者からみたイメージと本人の主観的幸福感は両年代とも肯定的イメージで相関した。 en-copyright= kn-copyright= en-aut-name=IkedaToshiko en-aut-sei=Ikeda en-aut-mei=Toshiko kn-aut-name=池田敏子 kn-aut-sei=池田 kn-aut-mei=敏子 aut-affil-num=1 ORCID= en-aut-name=KondoMasuko en-aut-sei=Kondo en-aut-mei=Masuko kn-aut-name=近藤益子 kn-aut-sei=近藤 kn-aut-mei=益子 aut-affil-num=2 ORCID= en-aut-name=SakuraiKeiko en-aut-sei=Sakurai en-aut-mei=Keiko kn-aut-name=桜井桂子 kn-aut-sei=桜井 kn-aut-mei=桂子 aut-affil-num=3 ORCID= en-aut-name=FutoyuYoshiko en-aut-sei=Futoyu en-aut-mei=Yoshiko kn-aut-name=太湯好子 kn-aut-sei=太湯 kn-aut-mei=好子 aut-affil-num=4 ORCID= en-aut-name=AshikiAkemi en-aut-sei=Ashiki en-aut-mei=Akemi kn-aut-name=阿式明美 kn-aut-sei=阿式 kn-aut-mei=明美 aut-affil-num=5 ORCID= en-aut-name=SeitaReiko en-aut-sei=Seita en-aut-mei=Reiko kn-aut-name=清田玲子 kn-aut-sei=清田 kn-aut-mei=玲子 aut-affil-num=6 ORCID= en-aut-name=TanimotoNobuko en-aut-sei=Tanimoto en-aut-mei=Nobuko kn-aut-name=谷本伸子 kn-aut-sei=谷本 kn-aut-mei=伸子 aut-affil-num=7 ORCID= en-aut-name=AndoSakiko en-aut-sei=Ando en-aut-mei=Sakiko kn-aut-name=安藤佐記子 kn-aut-sei=安藤 kn-aut-mei=佐記子 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医療技術短期大学部看護学科 affil-num=2 en-affil= kn-affil=岡山大学医療技術短期大学部看護学科 affil-num=3 en-affil= kn-affil=岡山県看護教育研究会(老人看護分科会) affil-num=4 en-affil= kn-affil=岡山県看護教育研究会(老人看護分科会) affil-num=5 en-affil= kn-affil=岡山県看護教育研究会(老人看護分科会) affil-num=6 en-affil= kn-affil=岡山県看護教育研究会(老人看護分科会) affil-num=7 en-affil= kn-affil=岡山県看護教育研究会(老人看護分科会) affil-num=8 en-affil= kn-affil=岡山県看護教育研究会(老人看護分科会) en-keyword=高齢者 (the aged people) kn-keyword=高齢者 (the aged people) en-keyword=イメージ (image of the aged) kn-keyword=イメージ (image of the aged) en-keyword=幸福感 (well-being) kn-keyword=幸福感 (well-being) END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue=2 article-no= start-page=59 end-page=64 dt-received= dt-revised= dt-accepted= dt-pub-year=2001 dt-pub=20010324 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A study of x-rays protection in a hip-joint radiography examination kn-title=股関節X線撮影時の女性生殖腺防護についての検討 en-subtitle= kn-subtitle= en-abstract=Usually in a hip-joint radiographic examination for the youth including children, the gonads should be well protected with an appropriate lead shield etc. Since the male gonads are in the outside of the body, if covered with a lead shield, the shield can protect them. However, in the case of the female, since the gonads of exist in a pelvic cavity, the lead shield is cut to a specific pattern so that it can protect the ovaries and the womb, and it is set on the abdomen during the radiographic exposure. Since the scattered radiation on an X-ray film can be removed with the grid, the image of a lead shield is obtained clearly, and the gonads seem to be protected completely. The shield can not protect the gonads of the female from the scattered radiation, though it protects them almost completely from the primary X-rays beam. Therefore, the gonads have radioactive contamination from scattered radiation. Then, in order to estimate the amount of scattered radiation under the lead shield, the dose under the shield was measured by using a phantom in this research, changing lead shield width, the tube-voltage, and the monitoring depth of a phantom. As a results, the dose under the lead shield was observed considerably and showed the peak at the depth of 3 or 4cm. Therefore, it was thought that a careful caution was required for obviating lead shield in clinical. kn-abstract=幼小児を含めた若年者の股関節X線撮影検査においては鉛板などで生殖腺を防護して行うのが通常である。男性の場合は生殖腺は体外に露出しているので，それを鉛板で包むようにすればある程度目的は達成される。しかし，女性の場合，生殖腺は骨盤腔内に存在するため，卵巣及び子宮を防護でき診断目的領域にかからないように鉛板を成形し，腹壁上に置いて撮影する。X斬写真上ではグリッドで散乱線を除去しているため，鉛板の陰影がくっきりと撮影され，生殖腺は完全に防護されているように見える。しかし，体内では散乱線によるかなりの被曝があるものと考えられる。そこで今回，鉛板下の散乱線量を鉛板幅及び電圧を変化させ，ファントム内各深さの散乱線量を測定した。その結果，鉛板下の散乱線量が相当量認められ，その量は深さ3〜4cmでピークを形成した。鉛板幅による変化は幅が狭いほど線量は大きくなり，電圧による変化は60kVと80kVを比べると80kVの方が多くなった。これを鉛板なしの場合と比較すると，ファントム内意さが増すにしたがい増大した。したがって，臨床において鉛板がずれて再撮影をすることのないよう細心の注意が必要であると考えられた。 en-copyright= kn-copyright= en-aut-name=NakagiriYoshitada en-aut-sei=Nakagiri en-aut-mei=Yoshitada kn-aut-name=中桐義忠 kn-aut-sei=中桐 kn-aut-mei=義忠 aut-affil-num=1 ORCID= en-aut-name=MaruyamaToshinori en-aut-sei=Maruyama en-aut-mei=Toshinori kn-aut-name=丸山敏則 kn-aut-sei=丸山 kn-aut-mei=敏則 aut-affil-num=2 ORCID= en-aut-name=GotoSachiko en-aut-sei=Goto en-aut-mei=Sachiko kn-aut-name=後藤佐知子 kn-aut-sei=後藤 kn-aut-mei=佐知子 aut-affil-num=3 ORCID= en-aut-name=AzumaYoshiharu en-aut-sei=Azuma en-aut-mei=Yoshiharu kn-aut-name=東義晴 kn-aut-sei=東 kn-aut-mei=義晴 aut-affil-num=4 ORCID= en-aut-name=ShibuyaKoichi en-aut-sei=Shibuya en-aut-mei=Koichi kn-aut-name=澁谷光一 kn-aut-sei=澁谷 kn-aut-mei=光一 aut-affil-num=5 ORCID= en-aut-name=TamuraEri en-aut-sei=Tamura en-aut-mei=Eri kn-aut-name=田村恵里 kn-aut-sei=田村 kn-aut-mei=恵里 aut-affil-num=6 ORCID= en-aut-name=TanimotoEriko en-aut-sei=Tanimoto en-aut-mei=Eriko kn-aut-name=谷本江利子 kn-aut-sei=谷本 kn-aut-mei=江利子 aut-affil-num=7 ORCID= en-aut-name=ToriiFumiko en-aut-sei=Torii en-aut-mei=Fumiko kn-aut-name=鳥居史子 kn-aut-sei=鳥居 kn-aut-mei=史子 aut-affil-num=8 ORCID= en-aut-name=TakedaYoshihiro en-aut-sei=Takeda en-aut-mei=Yoshihiro kn-aut-name=竹田芳弘 kn-aut-sei=竹田 kn-aut-mei=芳弘 aut-affil-num=9 ORCID= en-aut-name=SugitaKatsuhiko en-aut-sei=Sugita en-aut-mei=Katsuhiko kn-aut-name=杉田勝彦 kn-aut-sei=杉田 kn-aut-mei=勝彦 aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 affil-num=2 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 affil-num=3 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 affil-num=4 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 affil-num=5 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 affil-num=6 en-affil= kn-affil=岡山大学医療技術短期大学部診療放射線技術学科　学生 affil-num=7 en-affil= kn-affil=岡山大学医療技術短期大学部診療放射線技術学科　学生 affil-num=8 en-affil= kn-affil=岡山大学医療技術短期大学部診療放射線技術学科　学生 affil-num=9 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 affil-num=10 en-affil= kn-affil=岡山大学医学部保健学科放射線技術科学専攻 en-keyword=股関節X線撮影 (Radiography Examination of Hip-joint) kn-keyword=股関節X線撮影 (Radiography Examination of Hip-joint) en-keyword=医療被爆 (Patient Dose) kn-keyword=医療被爆 (Patient Dose) en-keyword=X線測定 (Dosimetry) kn-keyword=X線測定 (Dosimetry) en-keyword=生殖腺防護 (X-rays Protection of the Gonads) kn-keyword=生殖腺防護 (X-rays Protection of the Gonads) END start-ver=1.4 cd-journal=joma no-vol=85 cd-vols= no-issue=1 article-no= start-page=15 end-page=21 dt-received= dt-revised= dt-accepted= dt-pub-year=1996 dt-pub=19960201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Screening Isolation and Characterization of Thermophilic and Acidophilic Bacteria kn-title=好熱性好酸性細菌の検索，単離および諸性質の検討 en-subtitle= kn-subtitle= en-abstract=我々、人間を含め生物が最も広く、かつ最も多く分布している所は、中性付近のpH,20℃~37℃の温度、1気圧、そして適当な栄養素と塩分を含んでいる場所である。その一方、地球上には我々の目から見て生命の存在が許されないような環境、すなわち極限(特殊)環境が多数ある。高温地帯、高塩濃度の塩湖、強酸あるいは強アルカリ性の場所、そして光も届かない海底等がそれに該当する。近年では、生物によって非常に過酷と思われる極限環境に好んで棲息する微生物が数多く単離されている。これらの微生物群は極限環境微生物と総称されている。極限環境微生物は、自分のおかれた環境に適応するために種々の特殊な能力を獲得してきた。特殊な能力ゆえに、最近では利用の幅も広がってきている。1970年代以降、好アルカリ性細菌由来のプロテアーゼ及びセルラーゼが衣料用洗剤に配合されるようになった。海底から石油分解細菌が単離されており、応用研究に期待がもたれている。人間が発見してきた極限環境微生物はほんの氷山の一角にしか過ぎず、今後、人類にとってさらに有益な微生物が単離されるかもしれない。以上のようなことから、この分野の研究は大きな可能性を秘めたものであると思われる。我々の研究室では、極限環境微生物の中でも特に好酸性細菌に焦点を当てて研究を行ってきた。Acidiphilium属細菌は、1981年にアメリカのハリソンにより初めて単離された一群の好酸性従属栄養細菌(1属6種)である1)。我々は、これまでにAcidiphilium属細菌より、各種制限酵素2)~7)、グリセロール3-リン酸デヒドゲナーゼ8)などの有用酵素の検索、単離、精製を行ってきた。また、同じく好酸性の従属栄養細菌である。Acidobacterium属細菌より、β-グルコシダーゼなどの糖質関連酵素の精製も行ってきた9)。それらと並行してAcidiphilium属細菌の分子育種の系の確立を目指して、宿主ベクター系の開発も進めてきた10),11)。一方、高温環境の好んで棲息する好熱性細菌はタンパク質の大部分が変性する60℃以上の世界でも生育できることから、産生する酵素の耐熱性について詳細に研究されてきた。その結果、高熱性細菌の酵素より得られた知見を基に、部位特異的変異の手法を用いて常温菌の酵素の熱安定性を人為的に向上できるまでに至った。その他にも、好熱性細菌の研究は遺伝子工学や進化生物の発展上、大きな役割を担ってきた。高度好熱性細菌Thermusaquaticus由来のDNAポリメラーゼが12)、PCR技術の発達に寄与し、分子生物学分野のみならず犯罪捜査の際のDNA鑑定等に応用されているのは、その代表例の一例である。これらのことから好熱性と好酸性の両方性質を併せ持つ好熱性好酸性細菌に注目し検索、単離及び諸性質の検討を試みた。全国各地の泉質が酸性である温泉でサンプルを採取して、それから53株の好熱性好酸性細菌を単離することがでた。以下に単離菌株の諸性質に関する研究を報告する。 kn-abstract=We have isolated 53 thermophilic and acidophilic bacteria from about 150 samples from acidic hot springs. All the strains isolated exhibited growth only at high temperatures and low pH ranges. We extensively characterized the strain UZ-1 which was isolated from Unzen spa. This strain was found to be a gram-negative, aerobic and heterotrophic bacterium. The DNA base composition was 63 mol% GC. Growth occurs over a range of 37℃ to 65℃ with an optimum temperature of 60℃, and between pH 2.0 and pH 6.0 with an optimum pH of 3.0. On the other hand, the optimum temperature of the other 6 isolated strains was 70℃. We report, in this paper, the characteristics of the isolated strains. en-copyright= kn-copyright= en-aut-name=TanimotoYasuhide en-aut-sei=Tanimoto en-aut-mei=Yasuhide kn-aut-name=谷本保英 kn-aut-sei=谷本 kn-aut-mei=保英 aut-affil-num=1 ORCID= en-aut-name=InagakiKenji en-aut-sei=Inagaki en-aut-mei=Kenji kn-aut-name=稲垣賢二 kn-aut-sei=稲垣 kn-aut-mei=賢二 aut-affil-num=2 ORCID= en-aut-name=TanakaHidehiko en-aut-sei=Tanaka en-aut-mei=Hidehiko kn-aut-name=田中英彦 kn-aut-sei=田中 kn-aut-mei=英彦 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 affil-num=2 en-affil= kn-affil=岡山大学 affil-num=3 en-affil= kn-affil=岡山大学 en-keyword=screening and isolation of bacteria kn-keyword=screening and isolation of bacteria en-keyword=acidophiles kn-keyword=acidophiles en-keyword=thermophiles kn-keyword=thermophiles END start-ver=1.4 cd-journal=joma no-vol=88 cd-vols= no-issue=1 article-no= start-page=39 end-page=45 dt-received= dt-revised= dt-accepted= dt-pub-year=1999 dt-pub=199902 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Changes in Pollen Fertility of 'Nyoho' Strawberry in Relation to Light Intensity, Temperature and Leaf Carbohydrate and Mineral Concentration kn-title=イチゴ’女峰’花粉稔性の変化と日射量、気温並びに体内炭水化物、無機養分濃度との関係 en-subtitle= kn-subtitle= en-abstract=促成栽培したイチゴ’女峰’の’成り疲れ’と同時に発生する受精不良による奇形果発生要因を明らかにするため、イチゴ生産者の15棟のビニルハウスの花粉稔性の変化を調査し、気象要因、葉中無機養分および炭水化物濃度との関係について解析した。花粉稔性は、気温、日射量が低下し、着果負担が増大する1,2月に急激に低下したことから、奇形果発生の原因が花粉稔性の低下にあることが示された。花粉稔性と開花前1〜3日の日射量、当日の戸外の最低気温、葉中炭水化物濃度との間に高い相関が認められなかった。CO2施肥によって腋果房収穫開始期（1月）の花粉稔性が高まったことから、低日射と過重な着果負担による光合成産物不足が花粉稔性低下の大きな原因であると考えられた。 kn-abstract=Changes in pollen fertility in forcing strawberry cv. Nyoho(Fragaria×ananassa Duch.)were investigated to clarify the factors affecting fruit malformation caused by poor fertilization which occurs with plant dwarfing and yeild decreace in February to March .Pollen were sampled from 15 greenhouses of strawberry growers,and relationships between pollen germination and climatic factors,mineral and carbohydrate concentration in leaves were analyzed.Pollen fertility decreased in January and February with decrease in light intensity and outside air temprerature,and increace in fruit load.It was suggested that the occurrence of fruit malfomation may be mainly caused by the decrease in pollen fetillity. There were highly significant relationships between the pollen fertility and light intensity in 1 to 3 days before anthesis,minimum outside air temperature on the day of anthesis,and carbohyrates,P,K and Ca concentration in the leaves.No constant relationship could be found between polln fertility and leaf N concentration.Pollen fertility at the beginning of harvest for second inflorescence(January)was improved with CO2 enrichment.These results indicate that the poor pollen development may result from the shortage of photosynthate caused by low light and fruit load. en-copyright= kn-copyright= en-aut-name=YoshidaYuichi en-aut-sei=Yoshida en-aut-mei=Yuichi kn-aut-name=吉田裕一 kn-aut-sei=吉田 kn-aut-mei=裕一 aut-affil-num=1 ORCID= en-aut-name=TanimotoKeiichiro en-aut-sei=Tanimoto en-aut-mei=Keiichiro kn-aut-name=谷本圭一郎 kn-aut-sei=谷本 kn-aut-mei=圭一郎 aut-affil-num=2 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 affil-num=2 en-affil= kn-affil=香川大学農学部 en-keyword=Fragaria×ananassa Duch. kn-keyword=Fragaria×ananassa Duch. en-keyword=pollen kn-keyword=pollen en-keyword=light energy kn-keyword=light energy en-keyword=nitorogen nutrition kn-keyword=nitorogen nutrition en-keyword=CO2 enrichment kn-keyword=CO2 enrichment END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=重心系エネルギー1.96TeVでの陽子-反陽子衝突におけるWのμ論崩壊過程を用いたW+γ生成の測定 kn-title=Measurement of the W+γ Production in W to Muon Decay Channel in Proton-Antiproton Collisions at √s=1.96 TeV en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoNaho en-aut-sei=Tanimoto en-aut-mei=Naho kn-aut-name=谷本奈穂 kn-aut-sei=谷本 kn-aut-mei=奈穂 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=20040325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=睡眠時における口腔顔面運動,身体運動ならびに食道内pHの関連性 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoYuko en-aut-sei=Tanimoto en-aut-mei=Yuko kn-aut-name=谷本裕子 kn-aut-sei=谷本 kn-aut-mei=裕子 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=自由曲面を目標形状とする溶接ビード自動仕上げシステムの研究開発とその応用 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TanimotoKeiji en-aut-sei=Tanimoto en-aut-mei=Keiji kn-aut-name=谷本圭司 kn-aut-sei=谷本 kn-aut-mei=圭司 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=20020325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=歯周病原性細菌Actinobacillus actinomycetemcomitans の線毛発現に関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本一郎 kn-aut-sei=谷本 kn-aut-mei=一郎 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1996 dt-pub=19960325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=甲状腺疾患におけるアポトーシスの関与:組織化学的検討 kn-title=Apoptosis in Thyroid Diseases:A Histochemical Study en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本千佳子 kn-aut-sei=谷本 kn-aut-mei=千佳子 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=19970325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=小児気管支喘息における血清および喀痰中 Eosinophil cationic proteinの臨床的意義 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本清隆 kn-aut-sei=谷本 kn-aut-mei=清隆 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1962 dt-pub=19620606 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=放射線大量照射時に発生する細胞毒に就いて en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本潤一 kn-aut-sei=谷本 kn-aut-mei=潤一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1985 dt-pub=19851231 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=環境水域における糞便性大腸菌群に関する研究 第T編 BGLB培地高温法による糞便性大腸菌群の選択性について 第U編 河川水汚染の生物指標として糞便性大腸菌群の検討 第V編 糞便性大腸菌群を用いた汚染指標とその評価 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本浩一 kn-aut-sei=谷本 kn-aut-mei=浩一 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1968 dt-pub=19680930 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=家兎唾液腺の水分,塩分ならびに蛋白質分泌の相関性について en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=谷本義文 kn-aut-sei=谷本 kn-aut-mei=義文 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=19930328 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=気管支喘息における好塩基球の動態に関する研究 第1編フローサイトメトリーを用いたヒト末梢血好塩基球の高純度分離法について) 第2編各種サイトカインによるヒト好塩基球の遊走活性に関する検討) kn-title=1. Purification of human blood basophils using negative selection by flow cytometry ; 2. Effects of cytokines on human basophil chemotaxis en-subtitle= kn-subtitle= en-abstract= kn-abstract=1.Basophils were purified from peripheral blood of normal donors using Percoll discontinuous gradients and negative selection by flow cytometry. The mean purity of basophils obtained was 84.7 +/- 4.1 (s.d.)% (range 77.3-90.0%, n = 13). The overall yield of these procedures was 16.0 +/- 2.6% (range 11.0-19.9%, n = 13), and cell viability of purified basophils exceeded 90%. Properties of highly purified basophils obtained by flow cytometry did not differ from those of partially enriched basophil preparations from Percoll discontinuous gradients in respect of: (i) intracellular histamine content; (ii) percentage of spontaneous histamine release in buffer; and (iii) percentage of histamine release triggered by ionophore A 23187 or anti-IgE. Moreover, purified basophils responded chemotactically to complement C5a in a dose-dependent manner. These findings suggest that our procedure for purification of human basophils does not affect the functions of basophils and may be useful for in vitro studies on the role of basophils in hypersensitivity reactions such as bronchial asthma. ; 2.Basophil chemotactic activity (BCA) of eight recombinant human (rh) cytokines was examined. Highly purified basophils were obtained by Percoll discontinuous gradients, followed by negative selection using flow cytometry. Then BCA was measured by means of modified Boyden chamber method. Both interleukin (IL)-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) had much more potent BCA than complement C5a, leukotriene B4 and platelet activating factor, well known as granulocyte chemotactic factors. Chemotaxis rather than chemokinesis was shown in chequerboard analysis of basophil migration induced by IL-3 and GM-CSF. Relatively high concentrations of IL-5 also induced basophil migration, although predominantly chemokinetic. IL-8 had apparent BCA, which was not so high as that of C5a. In contrast, IL-2, IL-4, interferon(IFN)-gamma and granulocyte colony-stimulating factor (G-CSF) had no significant BCA. These findings suggest that IL-3, IL-5, GM-CSF and, perhaps, IL-8 have an effect on basophil migration as well as modulation of basophil mediator release and may provide some insight into the basophil accumulation observed in late-phase allergic responses. en-copyright= kn-copyright= en-aut-name=TanimotoYasushi en-aut-sei=Tanimoto en-aut-mei=Yasushi kn-aut-name=谷本安 kn-aut-sei=谷本 kn-aut-mei=安 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END