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Dive into the research topics where Hiroto Matsuoka is active.

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Featured researches published by Hiroto Matsuoka.


The Journal of Pathology | 2003

Sustained interleukin-6 signalling leads to the development of lymphoid organ-like structures in the lung

Sho Goya; Hiroto Matsuoka; Masahide Mori; Hiroshi Morishita; Hiroshi Kida; Yoichiro Kobashi; Terufumi Kato; Yoshio Taguchi; Tadashi Osaki; Isao Tachibana; Kazuyuki Yoshizaki; Ichiro Kawase; Seiji Hayashi

A variety of pathological changes are seen in lymphoproliferative disorders of the lung but the histogenesis of these abnormalities is not yet fully understood. We previously showed that adenovirus vector‐mediated transient expression of both the human interleukin‐6 (IL‐6) and IL‐6 receptor (IL‐6R) genes, but not the IL‐6 gene alone, in the rat lung induced lymphocytic alveolitis. In the present study, we explored the lung pathology of human IL‐6 and IL‐6R double transgenic mice to elucidate the effects of prolonged IL‐6 signalling on the lung. The transgenic animals developed mononuclear cell accumulation in peribronchovascular regions, but little infiltration into alveolar spaces. Immunohistochemical analysis revealed that the cellular accumulations contained not only mixtures of inflammatory cells but also lymphoid tissue‐like structures. As the expression of CXCL13/BLC, the indispensable chemokine for lymphoid organogenesis, was recognized in the B cell follicles of the pulmonary lesions, we speculate that this chemokine plays an inductive role in the development of the lymphoid tissue‐like structures. These structures were distinguished from bronchus‐associated lymphoid tissues (BALTs) by their location and by the lack of lymphoepithelium, which is a characteristic of BALT. These findings imply that IL‐6 signalling may play a role in the pathogenesis of lymphoproliferative disorders of the lung. Copyright


Biochemical and Biophysical Research Communications | 1986

Determination of the molecular size of the hepatic H1-receptor by target size analysis.

Nai Ping Wang; Hiroyuki Fukui; Hiroto Matsuoka; Hiroshi Wada

The molecular sizes of histamine H1-receptors of rat, rabbit, human, pig, guinea-pig, chicken, dog, and bovine liver were investigated by radiation inactivation and determined to be 100,000 to 160,000 daltons in all the animals examined. Statistical analysis showed that the hepatic H1-receptors have a common size of 128,000 +/- 63,000 daltons. Saturation analysis showed that the [3H]mepyramine binding constant was not changed by irradiation, while the binding capacity decreased with increase in the radiation dose.


Inflammation | 2004

Increased Level of Soluble E-Selectin in the Serum from Patients with Idiopathic Pulmonary Fibrosis

Seiji Hayashi; Kin′ya Abe; Hiroto Matsuoka; Sho Goya; Hiroshi Morishita; Masahide Mori; Toru Arai; Hiroshi Kida; Kazumi Nishino; Yoshito Takeda; Tadashi Osaki; Isao Tachibana; Kentaro Kimura; Soichiro Yokota; Yoshikazu Inoue; Mitsunori Sakatani

To elucidate the biological significance of selectin for idiopathic pulmonary fibrosis, we titrated the serum soluble E-selectin. From 31 cases of idiopathic pulmonary fibrosis patients without signs or symptoms of infection, the serum was obtained and the concentration was titrated by enzyme-linked immunosorbent assay. The serum soluble E-selectin titer was significantly higher than that of healthy controls. However, significant elevation was not observed in the sera from the patients with other pulmonary diseases, such as pulmonary emphysema, sarcoidosis, or bronchiectasis. In the patients with idiopathic pulmonary fibrosis, the number of white blood cells, C-reactive protein or lactate dehydrogenase activity did not show a significant relationship with the soluble E-selectin titer. About 16 out of the 31 idiopathic fibrosis patients, the serum surfactant apoprotein-A titer, which is a parameter of the disease activity of idiopathic pulmonary fibrosis, was also tested. The surfactant apoprotein-A titer was loosely correlated with the soluble E-selectin titer. These observations suggest that E-selectin may be relevant to the pathogenesis of idiopathic pulmonary fibrosis, and it may be a novel clinical parameter for idiopathic pulmonary fibrosis.


Inflammation | 1999

Effects of in vivo Soluble Selectin Gene Introduction on LPS-Induced Leukocyte Accumulation in the Murine Lung

Kin'ya Abe; Toru Arai; Masahide Mori; Hiroshi Kida; Sho Goya; Hiroto Matsuoka; Tadashi Osaki; Isao Tachibana; Seiji Hayashi

The selectin family adhesion molecules exert a crucial role in accumulation of leukocytes at the site of inflammation. To test the biological effects of soluble selectin on lung inflammation, we introduced an expression plasmid vector of soluble selectin gene via HVJ-liposome into a murine model of LPS-induced lung injury. The myeloperoxidase activity in LPS-injected mice was suppressed by the in vivo injection of soluble P-selectin gene relative to control mice. On the contrary, soluble E- or L-selectin genes did not exert suppressive effects. Our observations suggest that P-selectin plays a crucial role in the initial steps of lung inflammation, and exogenous introduction of soluble P-selectin by in vivo gene transfer method may be a useful strategy for regulating inflammation of the lung.


Oncology Research | 2007

Short-term gefitinib treatment brought about a long-term regression of bronchioloalveolar carcinoma without EGFR gene alterations: a case report.

Takashi Kijima; Mayumi Suzuki; Kayo Ueda; Seigo Minami; Yoshito Takeda; Sho Goya; Hiroto Matsuoka; Toru Kumagai; Mitsuhiro Yoshida; Tadashi Osaki; Isao Tachibana; Soichiro Yokota; Ichiro Kawase

The tyrosine kinase inhibitor (TKI) of the epidermal growth factor receptor (EGFR) gefitinib has beneficial effect in some patients with refractory advanced non-small cell lung cancer (NSCLC). However, the majority of responders eventually develop acquired resistance during the course of prolonged continuous treatment. Here we present a case of 76-year-old Japanese female, who had never smoked, with poor performance status from bronchioloalveolar carcinoma (BAC), in whom a brief initial 5-week administration of gefitinib resulted in dramatic antitumor effects that lasted approximately 8.5 months after cessation of the treatment. Furthermore, the relapsed tumor later regressed again by re-treatment with the TKI. She survived 26 months since she first took gefitinib. Unexpectedly, neither sensitizing mutations for EGFR-TKIs nor increased copy numbers were detected in EGFR gene of her BAC cells. This case suggests that, in some patients with NSCLC, even short-term administration of gefitinib may bring about clinical benefits and disease response comparable to the standard long-term daily dosing schedule. Short-term use of gefitinib will also be able to minimize the expensive medical cost of the TKI. The potential role of short-term or pulse-dose therapy with EGFR-TKIs should be clarified in further prospective studies. Moreover, it is urgent to develop better strategies by which we could distinguish responders to the TKIs from nonresponders among patients who do not have any EGFR gene alterations.


Internal Medicine | 2018

Spontaneous Regression of Allergic Bronchopulmonary Mycosis Due to Curvularia lunata

Shingo Nasu; Shingo Satoh; Kazunori Shimizu; Osamu Matsuno; Hiroshi Morishita; Takashi Yaguchi; Kunimitsu Kawahara; Hiroto Matsuoka

Allergic bronchopulmonary mycosis (ABPM) is a pulmonary hypersensitivity disease mainly caused by Aspergillus fumigatus. The mainstay treatment for ABPM is systemic corticosteroid therapy. A 25-year-old man presented with pulmonary infiltrates. His peripheral eosinophil, total serum IgE, and serum Aspergillus-specific IgE levels were elevated. The patient tested positive in a skin test for Aspergillus. However, sputum cultures revealed a Curvularia lunata infection. We therefore diagnosed ABPM possibly caused by C. lunata, which is rare in Japan. The clinical state of the patient improved under observation. Identification of the causative fungus is an important aspect of the ABPM diagnosis.


Lung | 2006

A case of alpha-thalassemia-2 associated with pulmonary infarction.

Seiji Hayashi; Hiroto Matsuoka; Teruo Harano; K. Harano; Hiroshi Nakahara; Isao Tachibana; Hiroshi Kida; Tomio Kawasaki; Shingo Kyotani; Yoshihiro Oka; Mitsunori Sakatani; Ichiro Kawase

Pulmonary infarction is an entity of medical significance that develops concurrently in beta-thalassemia but not in alpha-thalassemia. The reason for this difference is yet to be elucidated. We have evaluated a 21-year-old male alpha-thalassemia-2 patient who had profound microcytic anemia and pulmonary infarction. Analysis of the alpha-globin gene revealed -alpha3.7/alpha alpha genotype. His mother also had the same heterozygous gene deletion, though she had neither anemia nor pulmonary infarction. Since the patient had no other predisposition to pulmonary infarction, it is suggested that there is a close etiologic relationship between morphologic abnormality of the erythrocytes caused by alpha-thalassemia-2 and development of pulmonary infarction.


Somatic Cell and Molecular Genetics | 1999

Introduction of plasmid DNA and oligonucleotides into lung epithelial cells by the hemagglutinating virus of Japan (HVJ)-liposome method.

Mitsuhiro Yoshida; Seiji Hayashi; Junko Sakuma-Mochizuki; Kin'nya Abe; Toru Arai; Masahide Mori; Sho Goya; Hiroto Matsuoka; Yasufumi Kaneda; Tadamitsu Kishimoto

The hemagglutinating virus of Japan (HVJ) fused with liposomes provides a unique transfection vehicle with characteristics of both virus vector and liposome. Here we investigate the efficiency and safety of the HVJ-liposome technique in delivering foreign genes and oligonucleotides into the lung of the Wistar rat. A plasmid vector containing the Escherichia coli β-galactosidase (β-gal) gene and the chicken β-actin promoter was transfected via the trachea using the HVJ-liposome method. Cytochemical staining showed expression of exogenous β-gal activity in airway epithelial cells, alveolar macrophages, and alveolar type II cells. This activity persisted at least 28 days after administration of the genes. FITC-labeled oligonucleotides also were introduced into the same types of lung cells as those expressing β-gal. After instillation of HVJ-liposome, anti-HVJ antibodies were detected in the sera of the rats, but even after repeated administration of HVJ-liposome, no marked histopathologic change was observed while exogenous β-gal expression was detected in pulmonary cells.


American Journal of Physiology-lung Cellular and Molecular Physiology | 2000

Introduction of the interleukin-10 gene into mice inhibited bleomycin-induced lung injury in vivo

Toru Arai; Kin′ya Abe; Hiroto Matsuoka; Mitsuhiro Yoshida; Masahide Mori; Sho Goya; Hiroshi Kida; Kazumi Nishino; Tadashi Osaki; Isao Tachibana; Yasufumi Kaneda; Seiji Hayashi


American Journal of Physiology-lung Cellular and Molecular Physiology | 2002

A p38 MAPK inhibitor, FR-167653, ameliorates murine bleomycin-induced pulmonary fibrosis

Hiroto Matsuoka; Toru Arai; Masahide Mori; Sho Goya; Hiroshi Kida; Hiroshi Morishita; Hiroshi Fujiwara; Isao Tachibana; Tadashi Osaki; Seiji Hayashi

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