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4 results on '"Koji, Unoura"'

1. Erlotinib for elderly patients with non-small-cell lung cancer: Subset analysis from a population-based observational study by the Ibaraki Thoracic Integrative (POSITIVE) Research Group

Author

Takeo Endo, Mitsuaki Sakai, Keiko Uchiumi, Takayuki Kaburagi, Masaharu Inagaki, Takeshi Nawa, Koichi Kamiyama, Yoshihiro Nishimura, Kenji Hayashihara, Toshihiko Fukuoka, Katsunori Kagohashi, Koji Kishi, Koichi Kurishima, Nobuyuki Hizawa, Takefumi Saito, Kinya Furukawa, Yoko Shinohara, Koji Unoura, Yukio Sato, Akihiro Nomura, Hiroichi Ishikawa, Hiroaki Satoh, Hideo Ichimura, Toshio Hashimoto, Takeshi Matsumura, and Hiroyuki Nakamura

Subjects
Subset Analysis, erlotinib, Cancer Research, medicine.medical_specialty, Pathology, Population, Subgroup analysis, elderly, Internal medicine, medicine, Lung cancer, education, education.field_of_study, business.industry, Incidence (epidemiology), Cancer, Articles, medicine.disease, Confidence interval, population-based, respiratory tract diseases, non-small-cell lung cancer, Oncology, observational study, Erlotinib, business, medicine.drug
Abstract

The incidence and mortality of lung cancer have increased worldwide over the last decades, with an observed increased incidence particularly among elderly populations. It has not yet been determined whether erlotinib therapy exhibits the same efficacy and safety in elderly and younger patients with non-small-cell lung cancer (NSCLC). The aim of this retrospective subgroup analysis of data from a population-based observational study was to assess the efficacy and safety of erlotinib in an elderly (≥75 years, n=74) and a younger group of patients (

Published
2013
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2. Epithelial-mesenchymal transition in chronic hypersensitivity pneumonitis

Author

Makito, Yasui, Yasunari, Miyazaki, Keiko, Mitaka, Masahiro, Ishizuka, Koji, Unoura, Meiyo, Tamaoka, Yuki, Sumi, and Naohiko, Inase

Subjects
Epithelial-Mesenchymal Transition, Interleukin-13, Macrophages, Pulmonary Fibrosis, Epithelial Cells, Mice, Inbred Strains, Fibroblasts, Th1 Cells, Cadherins, Actins, DNA-Binding Proteins, Mice, Inbred C57BL, Pulmonary Alveoli, Transforming Growth Factor beta1, Disease Models, Animal, Mice, Th2 Cells, Animals, Humans, Collagen, Interleukin-4, Lung Diseases, Interstitial, Myofibroblasts, Bronchioles, Transcription Factors
Abstract

Chronic hypersensitivity pneumonitis (HP) causes progressive and irreversible pulmonary fibrosis, a disease also observed in conjunction with idiopathic pulmonary fibrosis (IPF). Previous studies have demonstrated that the myofibroblast, a cell type whose origins involve the epithelial-mesenchymal transition (EMT), may play a role in the pathogenesis of IPF. The goal of this study was to determine whether EMT has a role in the pathogenesis of chronic HP. Lung specimens from a chronic HP model and from patients with chronic HP were analyzed. Cellular co-localization of epithelial and mesenchymal markers on the same alveolar epithelial cells (AECs) were examined using immunohistochemistry and cadherin switching by western blotting as indicators of EMT. EMT cells in the AECs were significantly more prevalent in lung specimens from Th2-prone A/J mice than in specimens from Th1-prone C57BL/6 mice. The percentage of EMT cells was correlated with the mRNA expressions of IL-13 and TGF-β1, the fibrosis score, and the collagen content in the A/J mice. In human, EMT cells in the AECs were significantly more prevalent in lungs specimens from patients with usual interstitial pneumonia pattern than in specimens from patients with nonspecific interstitial pneumonia pattern at the moderate stage of fibrosis. In conclusion, EMT may play an important role in the fibrotic process of chronic HP under the Th2-biased environment.

Published
2011

3. Higher serum CCL17 may be a promising predictor of acute exacerbations in chronic hypersensitivity pneumonitis.

Author

Yasunari Miyazaki, Koji Unoura, Tomoya Tateishi, Takumi Akashi, Tamiko Takemura, Makoto Tomita, Naohiko Inase, and Yasuyuki Yoshizawa

Subjects
*SERUM, *HYPERSENSITIVITY pneumonitis, *DISEASE exacerbation, *CHEMOKINE receptors, *INTERLEUKIN-4, *LYMPHOCYTES, *BIOMARKERS
Abstract

Background: Recent research has suggested that the Th1 and Th2 chemokine/cytokine axis contributes to the development of chronic hypersensitivity pneumonitis (HP). Acute exacerbations (AE) are significant factors in the prognosis of chronic HP. Little is known, however, about these biomarkers in association with AE in chronic HP patients. Methods: Fifty-six patients with chronic HP were evaluated, including 14 patients during episodes of AE. Th1 mediators (C-X-C chemokine ligand [CXCL]10 and interferon [IFN]-γ), Th2 mediators (C-C chemokine ligand [CCL]17, interleukin-4, and interleukin-13), and pro-fibrotic mediator (transforming growth factor [TGF]-β) were measured to evaluate the mediators as predictors of AE. C-C chemokine receptor (CCR)4 (receptor for CCL17)-positive lymphocytes were quantified in lung specimens. Results: Serum CCL17 levels at baseline independently predicted the first episode of AE (HR, 72.0; 95% CI, 5.03- 1030.23; p = 0.002). AE was significantly more frequent in the higher-CCL17 group (⩾285 pg/ml) than in the lower- CCL17 group (<285 pg/ml) (log-rank test, p = 0.0006; 1-year incidence: higher CCL17 vs. lower CCL17, 14.3% vs. 0.0%). Serum CCL17 levels and CCR4-positive cells during episodes of AE were increased from the baseline (p = 0.01 and 0.031). Conclusions: Higher serum concentrations of CCL17 at baseline may be predictive of AE in patients with chronic HP, and CCL17 may contribute to the pathology of AE by inducing the accumulation of CCR4-positive lymphocytes in the lungs. [ABSTRACT FROM AUTHOR]

Published
2013
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4. Identification of fungal DNA in BALF from patients with home-related hypersensitivity pneumonitis

Author

Yasunari Miyazaki, Takashi Sugita, Meiyo Tamaoka, Koji Unoura, Naohiko Inase, and Yuki Sumi

Subjects
Pulmonary and Respiratory Medicine, Adult, Male, Trichosporon asahii, Social Environment, Polymerase Chain Reaction, Aspergillus fumigatus, law.invention, Microbiology, Young Adult, Japan, Trichosporon, Fusarium, law, medicine, Humans, Trichosporon mucoides, DNA, Fungal, Polymerase chain reaction, Antibodies, Fungal, Aged, Aged, 80 and over, biology, Base Sequence, Bronchoalveolar lavage fluid, Fungal genetics, Gene Amplification, Amplicon, Middle Aged, biology.organism_classification, medicine.disease, Fungal DNA, Mycoses, Female, Hypersensitivity pneumonitis, Polymorphism, Restriction Fragment Length, Alveolitis, Extrinsic Allergic
Abstract

Summary Background In Japan, a major type of home-related hypersensitivity pneumonitis (HP) is summer-type HP, which is caused by Trichosporon asahii ( T. asahii ) or Trichosporon mucoides . Some patients with home-related HP test negative for antibodies against Trichosporon ; yet, a causative mold antigen cannot be identified. Methods We analyzed 19 patients with home-related HP, 8 healthy volunteers, and 35 patients with other diseases. We extracted DNA from cell pellets of bronchoalveolar lavage fluid (BALF), amplified the DNA by PCR using Trichosporon -specific primers or other fungus-specific primers, and cloned as well as sequenced the PCR amplicon. Other primers used were specific for Acremonium chrysogenum , Aspergillus fumigatus , Aspergillus niger , Fusarium napiforme , Humicola fuscoatra , Penicillium corylophilum , and Pezizia domiciliana . Results We detected Trichosporon DNA ( n = 17) and F. napiforme DNA ( n = 2) by PCR in 19 patients with home-related HP; however, these species were not identified in healthy volunteers. After sequencing of the PCR amplicon for Trichosporon species, we identified T. asahii ( n = 11), Trichosporon japonicum ( n = 1), and Cryptococcus uzbekistanesis ( n = 4). Conclusion We could detect fungal DNA in BALF cell pellets from patients with home-related HP. These data suggest that this method might be useful to detect antigens responsible for home-related HP.

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