5 results on '"Takeyuki Kurosawa"'
Search Results
2. Primary malignant pericardial mesothelioma with increased serum mesothelin diagnosed by surgical pericardial resection: A case report
- Author
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Keishi Sugino, Sakae Homma, Kazutoshi Isobe, Takeyuki Kurosawa, Yuri Fukasawa, and Yoshinobu Hata
- Subjects
Cancer Research ,medicine.medical_specialty ,Pathology ,Pleural effusion ,Pericardial Mesothelioma ,030204 cardiovascular system & hematology ,Pericardial effusion ,03 medical and health sciences ,0302 clinical medicine ,Cardiac tamponade ,medicine ,Pericardium ,Mesothelin ,Mesothelioma ,Fluorodeoxyglucose ,biology ,business.industry ,Articles ,medicine.disease ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,biology.protein ,Radiology ,business ,medicine.drug - Abstract
A 37-year-old female smoker without a history of exposure to asbestos was referred to our hospital with persistent pericardial effusion. Chest computed tomography imaging examination revealed an irregular thickened pericardium with large amounts of pericardial effusion and a small pleural effusion. Fluorodeoxyglucose (FDG) positron emission tomography imaging demonstrated intrapericardial FDG accumulation. Blood tests revealed an increase in serum mesothelin levels. Examination of a surgically resected specimen revealed a grayish-white thickening of the pericardium, with a straw-colored mucinous pericardial effusion. Histopathological examination confirmed the diagnosis of epithelioid malignant mesothelioma. Although the patient's condition temporarily improved, with decreased levels of serum mesothelin during chemotherapy with carboplatin and pemetrexed, she succumbed to cardiac tamponade 18 months after the initial onset of the symptoms. Primary malignant pericardial mesothelioma (PMPM) is an extremely rare and refractory disorder. Thus, an early definitive diagnosis and timely treatment are crucial for the management of PMPM. more...
- Published
- 2016
- Full Text
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3. Lack of whey acidic protein four disulphide core (WFDC) 2 protease inhibitor causes neonatal death from respiratory failure in mice
- Author
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Yutaka Suzuki, Shin-ichi Tomizawa, Kazuyuki Ohbo, Selma Dizdarević, Masahide Seki, Kuniko Nakajima, Takayuki Shirakawa, Kazushige Kuroha, Risa Matsunaga, Haruhiko Koseki, Yasunari Miyazaki, Uroš Radović, Michio Ono, Takeyuki Kurosawa, Ikue Hoshi, Masataka Nakamura, Toshio Suda, and Go Nagamatsu more...
- Subjects
0301 basic medicine ,Lung ,Respiratory disease ,Neuroscience (miscellaneous) ,Medicine (miscellaneous) ,respiratory system ,Biology ,Lamellar granule ,medicine.disease ,Peripheral blood mononuclear cell ,General Biochemistry, Genetics and Molecular Biology ,Protease inhibitor (biology) ,Microbiology ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Immunology and Microbiology (miscellaneous) ,WFDC2 ,Respiratory failure ,medicine ,biology.protein ,Whey Acidic Protein ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Respiratory failure is a life-threatening problem for pre-term and term infants, yet many causes remain unknown. Here, we present evidence that whey acidic protein (WAP) four-disulfide core domain protease inhibitor 2 (Wfdc2), a protease inhibitor previously unrecognized in respiratory disease, may be a causal factor in infant respiratory failure. Wfdc2 transcripts are detected in the embryonic lung and analysis of a Wfdc2-GFP knock-in mouse line shows that both basal and club cells, and type II alveolar epithelial cells (AECIIs), express Wfdc2 neonatally. Wfdc2-null-mutant mice display progressive atelectasis after birth with a lethal phenotype. Mutant lungs have multiple defects, including impaired cilia and the absence of mature club cells from the tracheo-bronchial airways, and malformed lamellar bodies in AECIIs. RNA sequencing shows significant activation of a pro-inflammatory pathway, but with low-quantity infiltration of mononuclear cells in the lung. These data demonstrate that Wfdc2 function is vitally important for lung aeration at birth and that gene deficiency likely causes failure of the lung mucosal barrier. more...
- Published
- 2019
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- View/download PDF
4. A murine model of acute lung injury identifies growth factors to promote tissue repair and their biomarkers
- Author
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Shion Miyoshi, Soh Yamazaki, Sakae Homma, Akira Oikawa, Takashi Nishina, Tetuo Mikami, Takeyuki Kurosawa, and Hiroyasu Nakano
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Male ,Acute Lung Injury ,Mice, Transgenic ,Lung injury ,Biology ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,Genetics ,medicine ,Animals ,Humans ,Diphtheria Toxin ,Promoter Regions, Genetic ,030304 developmental biology ,Bone Marrow Transplantation ,0303 health sciences ,Wound Healing ,Lung ,Regeneration (biology) ,Gene Expression Profiling ,Cell Biology ,respiratory system ,Interleukin 11 ,Mice, Inbred C57BL ,Disease Models, Animal ,medicine.anatomical_structure ,chemistry ,Apoptosis ,Alveolar Epithelial Cells ,Cancer research ,Metabolome ,Biomarker (medicine) ,Intercellular Signaling Peptides and Proteins ,Female ,Muramidase ,Bone marrow ,Lysozyme ,Biomarkers ,Heparin-binding EGF-like Growth Factor - Abstract
Type II alveolar epithelial cells (AEC2s) play a crucial role in the regeneration of type I AECs after acute lung injury. The mechanisms underlying the regeneration of AEC2s are not fully understood. To address this issue, here, we investigated a murine model of acute lung injury using mice expressing human Diphtheria Toxin Receptor (DTR) under the control of Lysozyme M promoter (LysM-DTR). DT injection induced the depletion of AEC2s, alveolar macrophages, and bone marrow (BM)-derived myeloid cells in LysM-DTR mice, and the mice died within 6 days after DT injection. Apoptotic AEC2s and bronchiolar epithelial cells appeared at 24 hr, whereas Ki67-positive proliferating cells appeared in the alveoli and bronchioles in the lung of LysM-DTR mice at 72-96 hr after DT injection. Transfer of wild-type BM cells into LysM-DTR mice accelerated the regeneration of AEC2s along with the up-regulation of several growth factors. Moreover, several metabolites were significantly decreased in the sera of LysM-DTR mice compared with WT mice after DT injection, suggesting that these metabolites might be biomarkers to predict AEC2s injury. Together, LysM-DTR mice might be useful to identify growth factors to promote lung repair and the metabolites to predict the severity of lung injury. more...
- Published
- 2018
5. Depletion of myeloid cells exacerbates hepatitis and induces an aberrant increase in histone H3 in mouse serum
- Author
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Soichiro Kakuta, Osamu Nakabayashi, Nico van Rooijen, Masaki Ohmuraya, Masato Tanaka, Soh Yamazaki, Yasuo Uchiyama, Tetsuo Mikami, Sanae Miyake, Takeyuki Kurosawa, Hiroyasu Nakano, Xuehua Piao, Sachiko Komazawa-Sakon, Yuko Kojima, Minoru Tanaka, and Akira Oikawa more...
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0301 basic medicine ,Genetically modified mouse ,Kupffer Cells ,Apoptosis ,Mice, Transgenic ,Biology ,Hepatitis ,Histones ,03 medical and health sciences ,Histone H3 ,Mice ,0302 clinical medicine ,medicine ,Animals ,Myeloid Cells ,Tissue homeostasis ,Hepatology ,Tumor Necrosis Factor-alpha ,Interleukin ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,Immunology ,Cancer research ,Disease Progression ,Hepatocytes ,Tumor necrosis factor alpha ,Bone marrow ,030215 immunology - Abstract
Tissue-resident macrophages and bone marrow (BM)-derived monocytes play a crucial role in the maintenance of tissue homeostasis; however, their contribution to recovery from acute tissue injury is not fully understood. To address this issue, we generated an acute murine liver injury model using hepatocyte-specific Cflar-deficient (CflarHep-low) mice. Cellular FLICE-inhibitory protein (cFLIP) expression was downregulated in Cflar-deficient hepatocytes, which thereby increased susceptibility of hepatocytes to death receptor-induced apoptosis. CflarHep-low mice developed acute hepatitis and recovered with clearance of apoptotic hepatocytes at 24 hours after injection of low doses of tumor necrosis factor α (TNFα), which could not induce hepatitis in wild-type (WT) mice. Depletion of Kupffer cells (KCs) by clodronate liposomes did not impair clearance of dying hepatocytes or exacerbate hepatitis in CflarHep-low mice. To elucidate the roles of BM-derived monocytes and neutrophils in clearance of apoptotic hepatocytes, we examined the effect of depletion of these cells on TNFα-induced hepatitis in CflarHep-low mice. We reconstituted CflarHep-low mice with BM cells from transgenic mice in which human diphtheria toxin receptor (hDTR) was expressed under control of the Lysozyme M (LysM) promoter. TNFα-induced infiltration of myeloid cells, including monocytes and neutrophils, was completely ablated in DT-pretreated LysM-DTR BM-reconstituted CflarHep-low mice, whereas KCs remained present in the livers. Under these experimental conditions, LysM-DTR BM-reconstituted CflarHep-low mice rapidly developed severe hepatitis and succumbed within several hours after TNFα injection. We found that serum interleukin (IL)-6, TNFα, and histone H3 were aberrantly increased in LysM-DTR BM-reconstituted, but not in WT BM-reconstituted, CflarHep-low mice following TNFα injection. Conclusion: These findings indicate an unexpected role of myeloid cells in decreasing serum IL-6, TNFα, and histone H3 levels via the suppression of TNFα-induced hepatocyte apoptosis. This article is protected by copyright. All rights reserved. more...
- Published
- 2016
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