26 results on '"Takumi Kiwamoto"'
Search Results
2. Negative-pressure pulmonary Hemorrhaging Due to Severe Obstructive Sleep Apnea
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Toshihiro Shiozawa, Ryoko Ogawa, Norio Takayashiki, Yuko Morishima, Takahiro Takeishi, Takumi Kiwamoto, Nobuyuki Hizawa, Yuko Tsukahara, Kenya Kuramoto, Mizu Nonaka, Masayuki Noguchi, Hisayuki Oshima, Sosuke Matsumura, Chio Sakai, Masayuki Nakajima, and Masashi Matsuyama
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Adult ,Lung Diseases ,Male ,Polysomnography ,medicine.medical_treatment ,Case Report ,Hemorrhage ,Computed tomography ,030204 cardiovascular system & hematology ,Young Adult ,03 medical and health sciences ,0302 clinical medicine ,negative-pressure pulmonary edema (NPPE) ,Internal Medicine ,medicine ,Humans ,Continuous positive airway pressure ,Sleep Apnea, Obstructive ,Continuous Positive Airway Pressure ,medicine.diagnostic_test ,business.industry ,continuous positive airway pressure (CPAP) treatment ,Infant, Newborn ,obstructive sleep apnea (OSA) ,General Medicine ,respiratory system ,medicine.disease ,respiratory tract diseases ,Bloody ,Obstructive sleep apnea ,Bronchoalveolar lavage ,Anesthesia ,Sputum ,030211 gastroenterology & hepatology ,medicine.symptom ,business ,Vasculitis ,negative-pressure pulmonary hemorrhaging (NPPH) - Abstract
A 24-year-old man with a history of bloody sputum for 6 months was referred to our hospital with suspected alveolar hemorrhaging due to vasculitis. Chest computed tomography showed ground-glass opacities in both lungs, and an examination of his bronchoalveolar lavage fluid showed alveolar hemorrhaging. However, no evidence of vasculitis was found, and subsequent polysomnographic testing confirmed that he had severe obstructive sleep apnea (OSA). Since the alveolar hemorrhaging improved after the initiation of continuous positive airway pressure treatment, the diagnosis was negative-pressure alveolar hemorrhaging due to severe OSA.
- Published
- 2021
3. Therapie des kleinzelligen Lungenkarzinoms bei neu diagnostizierten Patienten mit schlechtem Performance-Status
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Takumi Kiwamoto, Toshihiro Shiozawa, Ikuo Sekine, Kensuke Nakazawa, Yuko Morishima, Nobuyuki Hizawa, Ryoko Ogawa, and Yuka Aida
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business.industry ,Medicine ,business - Abstract
Das kleinzellige Lungenkarzinom (small-cell lung cancer, SCLC) reagiert sehr empfindlich auf eine platinbasierte Chemotherapie. Bei Patienten, die bei der Erstdiagnose einen schlechten Performance-Status (PS) aufweisen, ist die Indikation jedoch umstritten. In der vorliegenden Arbeit überprüften wir retrospektiv alle klinischen Verläufe von Patienten mit histopathologisch gesichertem SCLC und schlechtem Performance-Status, das heißt PS 3 und 4 gemäß Eastern Cooperative Oncology Group. Von 18 Patienten erhielten 12 eine Chemotherapie und 6 lediglich eine supportive Therapie. Unter den Chemotherapie-Zyklen kam es bei 7 Patienten (58,3%, einschließlich der PS-4-Fälle) zu einer Verbesserung des Performance-Status, bei 2 Patienten (16,7%) blieb er stabil und bei 3 Patienten (25%) verschlechterte er sich. Darüber hinaus zeigten 5 Patienten ein partielles Ansprechen auf die Chemotherapie (Ansprechrate von 41,7%). Zehn (10) Patienten (83,3%) entwickelten eine Neutropenie Grad 3 bis 4 und bei 5 Patienten (41,7%) trat eine febrile Neutropenie Grad 3 auf; eine nicht-hämatologische Toxizität Grad 4 wurde nicht festgestellt. Ein 77-jähriger männlicher Patient mit PS 3 verstarb infolge einer behandlungsbedingten Lungentoxizität (Grad 5). Es zeigte sich kein wesentlicher Unterschied in der Überlebensdauer zwischen Patienten mit PS 3 und PS 4, selbst dann nicht, wenn Patienten, die lediglich eine supportive Therapie erhalten hatten, in die Analyse einbezogen wurden. Die Behandlung hatte einen positiven Effekt auf das Überleben: Nach der Chemotherapie lag die 6-Monats-Überlebensrate der Patienten mit PS 3 und 4 bei 66,7%. Demgegenüber starben alle Patienten, die nur eine supportive Therapie erhalten hatten, innerhalb von 5 Monaten. Diese Ergebnisse sprechen dafür, dass eine Chemotherapie nicht nur bei ausgewählten SCLC-Patienten mit PS 3, sondern auch solchen mit PS 4 indiziert ist.
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- 2020
4. Transcription Factor T-bet Attenuates the Development of Elastase-induced Emphysema in Mice
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Hirofumi Sakurai, Satoru Takahashi, Takumi Kiwamoto, Keigyou Yoh, Yukio Ishii, Yuko Morishima, Shigen Hayashi, Yosuke Matsuno, Yoshiya Tsunoda, and Nobuyuki Hizawa
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CD4-Positive T-Lymphocytes ,0301 basic medicine ,Neutrophils ,Clinical Biochemistry ,Adaptive Immunity ,Pathogenesis ,Mice ,0302 clinical medicine ,Medicine ,RNA, Small Interfering ,Lung ,Mice, Knockout ,Mice, Inbred BALB C ,Pancreatic Elastase ,biology ,Elastase ,Nuclear Receptor Subfamily 1, Group F, Member 1 ,hemic and immune systems ,respiratory system ,Chemotaxis, Leukocyte ,Phenotype ,medicine.anatomical_structure ,Pulmonary Emphysema ,Cytokines ,Female ,RNA Interference ,Interleukin 17 ,medicine.symptom ,Bronchoalveolar Lavage Fluid ,Pulmonary and Respiratory Medicine ,chemical and pharmacologic phenomena ,Inflammation ,Alveolar cells ,03 medical and health sciences ,Immune system ,Animals ,Interleukin 6 ,Molecular Biology ,business.industry ,Macrophages ,Editorials ,Cell Biology ,Immunity, Innate ,Lymphocyte Subsets ,respiratory tract diseases ,030104 developmental biology ,030228 respiratory system ,Immunology ,biology.protein ,T-Box Domain Proteins ,business - Abstract
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by peripheral airways inflammation and emphysema. Emerging evidence indicates a contribution of both innate and adaptive immune cells to the development of COPD. Transcription factor T-bet modulates the function of immune cells and therefore might be involved in the pathogenesis of COPD. To elucidate the role for T-bet in elastase-induced emphysema, pathological phenotypes were compared between wild-type and T-bet-/- mice. T-bet-/- mice demonstrated enhanced emphysema development on histological analyses, with higher values of mean linear intercept and dynamic compliance relative to wild-type mice. The number of neutrophils in BAL fluids, lung IL-6 and IL-17 expression, and the proportion of CD4+ T cells positive for IL-17 or retinoic acid receptor-related orphan receptor-γt were higher in T-bet-/- mice than in wild-type mice. Although T-bet downregulates cytokine expression in bone marrow-derived macrophages and MH-S cells, a murine alveolar cell line, depending on the surrounding environment, IL-6 expression in alveolar macrophages isolated from elastase-treated mice was not dependent on T-bet. Coculture of bone marrow-derived macrophages and CD4+ T cells revealed that T-bet regulation of IL-17 expression was dependent on CD4+ T cells. Neutralizing antibodies against IL-6R or IL-17 ameliorated the development of emphysema in T-bet-/- mice. In conclusion, we demonstrate that T-bet ameliorates elastase-induced emphysema formation by modulating the host immune response in the lungs.
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- 2019
5. Small-Cell Lung Cancer Treatment of Newly Diagnosed Patients with Poor Performance Status
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Tohru Sakamoto, Yuka Aida, Kensuke Nakazawa, Yuko Morishima, Nobuyuki Hizawa, Takumi Kiwamoto, Ikuo Sekine, Ryoko Ogawa, and Toshihiro Shiozawa
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0301 basic medicine ,medicine.medical_specialty ,medicine.medical_treatment ,Case Report ,Neutropenia ,Gastroenterology ,lcsh:RC254-282 ,Small-cell lung cancer ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Chemotherapy ,Poor performance status ,Lung cancer ,Survival rate ,Platinum ,Response rate (survey) ,business.industry ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,Toxicity ,business ,Febrile neutropenia ,Supportive care - Abstract
Small-cell lung cancer (SCLC) is highly sensitive to platinum-based chemotherapy. However, its indication in patients with a poor performance status (PS) at initial diagnosis is controversial. We retrospectively reviewed all clinical courses of pathologically diagnosed SCLC patients with poor PS, Eastern Cooperative Oncology Group PS 3 and 4. Among 18 patients, 12 were treated with chemotherapy and 6 with supportive care alone. During the chemotherapy courses, PS improved in 7 (58.3%, including the PS 4 cases), remained stable in 2 (16.7%), and deteriorated in 3 (25%) patients. Moreover, 5 patients showed partial responses to chemotherapy (response rate of 41.7%). Grade 3-4 neutropenia developed in 10 (83.3%) patients and grade 3 febrile neutropenia occurred in 5 (41.7%) patients, but no grade 4 non-hematological toxicity was noted. Mortality associated with lung toxicity (grade 5) due to treatment occurred in a 77-year-old-male patient with PS 3. No substantial difference in survival was observed between patients with PS 3 and 4, even when including those treated with supportive care alone. Treatment had a positive effect on survival: after chemotherapy, the 6-month survival rate of PS 3 and 4 patients was 66.7%. In contrast, all patients treated with supportive care alone died within 5 months. These findings suggest that chemotherapy is indicated in selected SCLC patients not only with PS 3, but also with PS 4. (C) 2019 The Author(s) Published by S. Karger AG, Basel
- Published
- 2019
6. Pasteurella multocida pneumonia with hemoptysis: A case report
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Hiroko Watanabe, Hiroaki Ishikawa, Yuka Aida, Kazutaka Fujita, Nobuyuki Hizawa, Takumi Kiwamoto, and Haruna Kitazawa
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Pulmonary and Respiratory Medicine ,Pathology ,medicine.medical_specialty ,Hemoptysis ,Pasteurella multocida ,animal diseases ,Case Report ,Antibiotic therapy ,medicine ,otorhinolaryngologic diseases ,Pasteurella ,Respiratory system ,lcsh:RC705-779 ,Bronchiectasis ,biology ,business.industry ,Pasteurella canis ,lcsh:Diseases of the respiratory system ,respiratory system ,biology.organism_classification ,medicine.disease ,Pasteurellosis ,Pneumonia ,business - Abstract
Pasteurella multocida, which colonizes upper respiratory and digestive tracts, is a leading cause of respiratory diseases in many host species. Here, we describe a case of P. multocida pneumonia with hemoptysis. A 72-year-old female diagnosed with bronchiectasis with a 36-year history presented with a worsened infiltrative and granular shadow in the lower right lobe and lingular segment. Bronchial lavage fluid culturing suggested Pasteurella pneumonia. P. multocida was confirmed by 16S rRNA sequencing. The patient was readmitted to our hospital because of hemoptysis, and she was treated successfully with antibiotic therapy. The possibility of P. multocida infection must be considered in patients who own pets. Keywords: Pasteurella multocida, Pasteurella canis, Hemoptysis, Pasteurellosis
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- 2019
7. Sulforaphane ameliorates steroid insensitivity through an Nrf2-dependent pathway in cigarette smoke-exposed asthmatic mice
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Yuko Morishima, Masayuki Nakajima, Yukio Ishii, Mio Kawaguchi, Shih Yuan Hayashi, Masayuki Yamamoto, Yosuke Matsuno, Nobuyuki Hizawa, Takumi Kiwamoto, Kazufumi Yoshida, Hirofumi Sakurai, and Yoshiya Tsunoda
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0301 basic medicine ,Antioxidant ,Ovalbumin ,medicine.medical_treatment ,Histone Deacetylase 2 ,Pharmacology ,medicine.disease_cause ,environment and public health ,Biochemistry ,Dexamethasone ,Steroid ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,Downregulation and upregulation ,Isothiocyanates ,Physiology (medical) ,Tobacco ,medicine ,Animals ,Anti-Asthmatic Agents ,RNA, Messenger ,Lung ,Asthma ,Mice, Knockout ,Mice, Inbred BALB C ,Nuclear Respiratory Factor 1 ,Histone deacetylase 2 ,business.industry ,respiratory system ,medicine.disease ,Disease Models, Animal ,Drug Combinations ,Oxidative Stress ,030104 developmental biology ,Gene Expression Regulation ,chemistry ,Sulfoxides ,Female ,Tobacco Smoke Pollution ,business ,Oxidative stress ,Signal Transduction ,medicine.drug ,Sulforaphane - Abstract
Oxidative stress induced by cigarette smoke and other environmental pollutants contributes to refractory asthma. To better understand the role of smoking in asthma, we investigated the effects of cigarette smoke on allergic airway responses in mice and examined expression of nuclear factor-E2-related factor-2 (Nrf2) and its downstream factors, because Nrf2 is known to play a pivotal role in antioxidant responses. OVA-sensitized and challenged BALB/c mice were exposed to cigarette smoke and then treated with dexamethasone, sulforaphane (an activator of Nrf2), or their combination. Upon exposure to cigarette smoke, Nrf2 and associated transcripts were upregulated in response to oxidative stress, and asthmatic responses were steroid resistant. In OVA-sensitized and challenged mice exposed to cigarette smoke and treated with sulforaphane, Nrf2-mediated antioxidant responses were upregulated to a greater extent, and steroid sensitivity of asthmatic responses was restored. Moreover, the expression and activity of histone deacetylase 2 (HDAC2), a key regulator of steroid responsiveness, was reduced in mice exposed to cigarette smoke, but restored by sulforaphane treatment. No effects of sulforaphane were observed in Nrf2-deficient mice. These findings indicate that cigarette smoke induces steroid unresponsiveness in asthmatic airways, and that sulforaphane restores steroid sensitivity via upregulation of Nrf2 and enhancement of HDAC2 expression and activity. Thus, Nrf2 may serve as a potential molecular target for cigarette smoke-related refractory asthma resistant to steroid therapy.
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- 2018
8. Mesalazine-induced lung injury in a child; the value of bronchoscopy
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Isho Izumi, Takuro Sato, Manabu Tagawa, Takumi Kiwamoto, and Ryo Sumazaki
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medicine.medical_specialty ,medicine.diagnostic_test ,business.industry ,Anti-Inflammatory Agents, Non-Steroidal ,Lung Injury ,Lung injury ,medicine.disease ,Gastroenterology ,Ulcerative colitis ,chemistry.chemical_compound ,Mesalazine ,chemistry ,Bronchoscopy ,Internal medicine ,Pediatrics, Perinatology and Child Health ,Medicine ,Humans ,Colitis, Ulcerative ,business ,Child ,Mesalamine ,Value (mathematics) - Published
- 2021
9. Has2 deficiency enhances OVA-induced airway inflammation and hyperresponsiveness in mice
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Masashi Matsuyama, Nobuyuki Hizawa, Hirofumi Sakurai, Yukio Ishii, Yuko Morishima, Takumi Kiwamoto, Hajime Osawa, Yosuke Matsuno, Yoshiya Tsunoda, Mingma Thsering Sherpa, and Shigen Hayashi
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Inflammation ,Mice, Inbred BALB C ,biology ,business.industry ,Ovalbumin ,Immunology ,Airway hyperresponsiveness ,CD44 ,Respiratory System ,Airway inflammation ,Disease Models, Animal ,Mice ,biology.protein ,Immunology and Allergy ,Medicine ,Animals ,Bronchial Hyperreactivity ,business ,Bronchoalveolar Lavage Fluid ,Lung - Published
- 2020
10. Clinical significance of invariant natural killer T cells and IL-5 in acute eosinophilic pneumonia
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Yukio Ishii, Yuko Morishima, Kazufumi Yoshida, Yosuke Matsuno, Masashi Matsuyama, Nobuyuki Hizawa, and Takumi Kiwamoto
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lcsh:Immunologic diseases. Allergy ,Adult ,Male ,Adolescent ,government.form_of_government ,Young Adult ,Text mining ,Immunology and Allergy ,Medicine ,Humans ,Clinical significance ,Pulmonary Eosinophilia ,Interleukin 5 ,Invariant natural killer T-cell ,Lung ,Aged ,Aged, 80 and over ,business.industry ,General Medicine ,Middle Aged ,Acute eosinophilic pneumonia ,Immunology ,Acute Disease ,government ,Natural Killer T-Cells ,Female ,Interleukin-5 ,lcsh:RC581-607 ,business ,Bronchoalveolar Lavage Fluid - Published
- 2020
11. Enhanced Type 2 and Non-Type 2 Allergic Airway Inflammation in Elovl6-Deficient Mice
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Kai Yazaki, Masashi Matsuyama, Yuko Morishima, Hajime Osawa, Yosuke Matsuno, Yukio Ishii, Hirofumi Sakurai, Mingma Thsering Sherpa, Nobuyuki Hizawa, Masayuki Nakajima, Takumi Kiwamoto, and Kazufumi Yoshida
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Allergic airway inflammation ,business.industry ,Immunology ,Deficient mouse ,Medicine ,business - Published
- 2020
12. Landiolol hydrochloride ameliorates acute lung injury in a rat model of early sepsis through the suppression of elevated levels of pulmonary endothelin-1
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Taro Mizutani, Yujiro Matsuishi, Sohel Zaedi, Shila Akhtar, Subrina Jesmin, Nobutake Shimojo, Takumi Kiwamoto, Chishimba Nathan Mowa, Nobuyuki Hizawa, Yoshiaki Inoue, Sakuramoto Hideaki, Satoru Kawano, Yoshiya Tsunoda, and Tanzila Khatun
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Male ,0301 basic medicine ,Morpholines ,Acute Lung Injury ,Adrenergic beta-Antagonists ,Down-Regulation ,030204 cardiovascular system & hematology ,Lung injury ,Pharmacology ,General Biochemistry, Genetics and Molecular Biology ,Sepsis ,03 medical and health sciences ,0302 clinical medicine ,Animals ,Urea ,Medicine ,RNA, Messenger ,Rats, Wistar ,General Pharmacology, Toxicology and Pharmaceutics ,Receptor ,Lung ,Endothelin-1 ,Tumor Necrosis Factor-alpha ,business.industry ,General Medicine ,Landiolol ,medicine.disease ,Endothelin 1 ,respiratory tract diseases ,030104 developmental biology ,medicine.anatomical_structure ,Anesthesia ,Circulatory system ,business ,Endothelin receptor ,medicine.drug - Abstract
Among the dysfunctions and pathologies associated with sepsis, the underlying molecular mechanisms of sepsis-induced acute lung injury (ALI) are poorly understood. Endothelin (ET)-1, a potent vasoconstrictor and pro-inflammatory peptide, is known to be involved in the pathogenesis of ALI in a rat model of sepsis. Here, we investigated whether landiolol hydrochloride, an ultra-short-acting β-blocker, plays a crucial role in ameliorating and attenuating LPS-induced ALI through modulation of the ET-1 system. Male Wistar rats at 8 weeks of age were administered with either saline or lipopolysaccharide (LPS) for three hours (3 h) and some of the LPS-administered rats were continuously treated with landiolol for 3 h. ALI was induced by LPS, including levels of both circulatory and pulmonary TNF-α and IL-6 but [PaO2] was significantly decreased. LPS also induced a significant increase in levels of pulmonary ET-1 and ET-A receptor, but levels of ET-B receptor, which has vasodilating effects, were remarkably diminished. Further, LPS administration upregulated the pulmonary expression of HIF-1α. Finally, the treatment of LPS-administered rats with landiolol for 3 h ameliorated and prevented ALI, normalized the altered levels of pulmonary ET-1 and ET-A receptors. Landiolol also induced significant down-regulation of ET-B receptor in lung tissues in the early hours (phase) of sepsis. However, Landiolol treatment had no effect on the up-regulated inflammatory mediators (TNF-α, IL-6) in both plasma and lung tissues during sepsis, and expression of pulmonary HIF-1α also remained unchanged after landiolol treatment. Collectively, these data led us to conclude that landiolol may ameliorate sepsis-induced ALI via the pulmonary ET system.
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- 2016
13. Deletion of Elovl6 Alters Fatty Acid Composition in Lung Tissue and Enhances Allergic Airway Inflammation
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Yuko Morishima, Mingma Thsering Sherpa, Masashi Matsuyama, Yukio Ishii, Yosuke Matsuno, Hideyuki Sakurai, Nobuyuki Hizawa, Masayuki Nakajima, Kazufumi Yoshida, Yoshiya Tsunoda, and Takumi Kiwamoto
- Subjects
Allergic airway inflammation ,business.industry ,Immunology ,Medicine ,Fatty acid composition ,business ,Lung tissue - Published
- 2019
14. Hyaluronan Synthase 2 (HAS2) Mediates Airway Inflammation and Remodeling in Chronic Ovalbumin Model of Asthma
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Yuko Morishima, Mingma Thsering Sherpa, Kazufumi Yoshida, Yoshiya Tsunoda, Yukio Ishii, Nobuyuki Hizawa, Masayuki Nakajima, Takumi Kiwamoto, Yosuke Matsuno, Hajime Osawa, and Masashi Matsuyama
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Ovalbumin ,biology ,business.industry ,Immunology ,Airway inflammation ,medicine ,biology.protein ,medicine.disease ,Hyaluronan Synthase 2 ,business ,Asthma - Published
- 2019
15. Serum Soluble Interleukin-2 Receptor as a Possible Biomarker for the Early Detection and Follow-up of Nivolumab-Induced Pneumonitis
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Yuko Morishima, Ikuo Sekine, Toshihiro Shiozawa, Masashi Matsuyama, Kazufumi Yoshida, Yosuke Matsuno, Kensuke Nakazawa, Takumi Kiwamoto, and Nobuyuki Hizawa
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Pulmonary and Respiratory Medicine ,Interleukin 2 ,Adult ,Male ,Lung Neoplasms ,Early detection ,Antineoplastic Agents, Immunological ,Carcinoma, Non-Small-Cell Lung ,Carcinoma ,Medicine ,Humans ,Receptor ,Pneumonitis ,business.industry ,Follow up studies ,Receptors, Interleukin-2 ,Pneumonia ,medicine.disease ,Early Diagnosis ,Nivolumab ,Oncology ,Cancer research ,Biomarker (medicine) ,business ,Biomarkers ,medicine.drug ,Follow-Up Studies - Published
- 2018
16. Paraneoplastic limbic encephalitis with late‑onset magnetic resonance imaging findings: A case report
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Toshihiro Shiozawa, Kazuhiro Ishii, Nobuyuki Hizawa, Takashi Hosaka, Yuuki Yabuuchi, Kensuke Nakazawa, Akira Tamaoka, Yoshiya Tsunoda, Takumi Kiwamoto, Haruna Kitazawa, Shinsuke Homma, and Akiko Ishii
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Nervous system ,Cancer Research ,Pathology ,medicine.medical_specialty ,medicine.diagnostic_test ,business.industry ,Cancer ,Magnetic resonance imaging ,Late onset ,Articles ,medicine.disease ,Temporal lobe ,03 medical and health sciences ,0302 clinical medicine ,Cerebrospinal fluid ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,medicine ,Differential diagnosis ,Lung cancer ,business ,030217 neurology & neurosurgery - Abstract
Paraneoplastic limbic encephalitis (PLE), a paraneoplastic neurological syndrome (PNS), is a rare nervous system disorder that results from the indirect effects of tumors and is commonly associated with small-cell lung cancer (SCLC). Previous studies have reported that magnetic resonance imaging (MRI) may be useful for diagnosing LE. Temporal lobe abnormalities are observed using T2-weighted and fluid-attenuated inversion recovery sequences; however, such abnormalities are detected in only 60% of patients with PLE. The present study describes a case of PLE associated with SCLC, in which LE was observed using MRI 26 days after the first convulsive seizure. Although the serum and cerebrospinal fluid analyses for onconeural antibodies were negative, the findings of this case indicate that PLE should be considered in the differential diagnosis, and that repeated brain MRI may be more helpful for diagnosis, as the brain MRI findings may be normal during the early stages of PLE.
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- 2017
17. Overexpression of GATA-3 Protects against the Development of Hypersensitivity Pneumonitis
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Keigyou Yoh, Satoru Takahashi, Shinsuke Homma, Tohru Sakamoto, Norihiro Kikuchi, Yosuke Matsuno, Akihiro Nomura, Yuko Morishima, Takumi Kiwamoto, Morio Ohtsuka, Nobuyuki Hizawa, Takashi Iizuka, Norihiro Haraguchi, and Yukio Ishii
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Pulmonary and Respiratory Medicine ,medicine.medical_treatment ,Mice, Transgenic ,Inflammation ,GATA3 Transcription Factor ,Critical Care and Intensive Care Medicine ,Pathogenesis ,Interferon-gamma ,Mice ,Antigen ,Interferon ,Intensive care ,Animals ,Medicine ,Saccharopolyspora rectivirgula ,RNA, Messenger ,biology ,Tumor Necrosis Factor-alpha ,business.industry ,Interleukins ,medicine.disease ,biology.organism_classification ,Mice, Inbred C57BL ,Disease Models, Animal ,Cytokine ,Immunology ,medicine.symptom ,T-Box Domain Proteins ,business ,Hypersensitivity pneumonitis ,Alveolitis, Extrinsic Allergic ,Saccharopolyspora ,medicine.drug - Abstract
Hypersensitivity pneumonitis (HP) is mediated by a Th1 immune response. Transcription factor GATA binding protein-3 (GATA-3) is believed to be a key regulator of Th2 differentiation and thus might play regulatory roles in the pathogenesis of hypersensitivity pneumonitis (HP).We examined the effect of GATA-3 overexpression on the development of HP in mice.Wild-type C57BL/6 mice and GATA-3-overexpressing mice of the same background were used in this study. HP was induced by repeated exposure to Saccharopolyspora rectivirgula, the causative antigen of farmer's lung.Antigen exposure resulted in a marked inflammatory response with enhanced pulmonary expression of T-bet and the Th1 cytokine interferon (IFN)-gamma in wild-type mice. The degree of pulmonary inflammation was much less severe in GATA-3-overexpressing mice. The induction of T-bet and IFN-gamma genes was suppressed, but a significant induction of Th2 cytokines, including IL-5 and IL-13, was observed in the lungs of GATA-3-overexpressing mice after antigen exposure. Supplementation with recombinant IFN-gamma enhanced lung inflammatory responses in GATA-3-overexpressing mice to the level of wild-type mice. Because antigen-induced IFN-gamma production predominantly occurred in CD4+ T cells, nude mice were transferred with CD4+ T cells from either wild-type or GATA-3-overexpressing mice and subsequently exposed to antigen. Lung inflammatory responses were significantly lower in nude mice transferred with CD4+ T cells from GATA-3-overexpressing mice than in those with wild-type CD4+ T cells, with a reduction of lung IFN-gamma level.These results indicate that overexpression of GATA-3 attenuates the development of HP by correcting the Th1-polarizing condition.
- Published
- 2007
18. Niflumic Acid and AG-1478 Reduce Cigarette Smoke-Induced Mucin Synthesis
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Yuko Morishima, Yukio Ishii, Akihiro Nomura, Kiyohisa Sekizawa, Yosuke Matsuno, Shinsuke Homma, Ahmed E. Hegab, Takashi Iizuka, Takumi Kiwamoto, and Tohru Sakamoto
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Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,biology ,business.industry ,Niflumic acid ,Mucin ,Bronchial mucus ,respiratory system ,Critical Care and Intensive Care Medicine ,Mucus ,Molecular biology ,Endocrinology ,In vivo ,Epidermal growth factor ,Internal medicine ,biology.protein ,Medicine ,Epidermal growth factor receptor ,Signal transduction ,Cardiology and Cardiovascular Medicine ,business ,medicine.drug - Abstract
Background Cigarette smoke induces bronchial mucus secretion. However, the mechanism of this induction is still unidentified. In this study, we investigated the role of the putative calcium-activated chloride channel 1 (CLCA1) and its blocker, niflumic acid, in cigarette smoke-induced mucin synthesis both in vivo and in vitro. Methods and results Sprague-Dawley rats were exposed to cigarette smoke for 4 weeks. The CLCA1, epidermal growth factor receptor (EGFR), and MUC5AC expressions were increased in the trachea and lung tissues. Goblet-cell hyperplasia with marked mucin staining was detected in the tracheal and bronchial epithelium. In the human bronchial epithelial cell line NCI-H292, cigarette smoke solution also induced mucin production as well as the RNA and protein expressions of CLCA1, EGFR, and MUC5AC. Both in vivo and in vitro, the induction of MUC5AC and mucin synthesis were inhibited by niflumic acid, and/or a selective EGFR tyrosine kinase inhibitor, AG-1478. Niflumic acid also blocked the epidermal growth factor-induced MUC5AC and mucin staining in the NCI-H292 cell line. Conclusion Both EGFR and niflumic acid-sensitive chloride channels (probably CLCA1) are dependently affecting the mucin production as a part of a single complex signaling pathway. CLCA1 may be a key signaling member that can be targeted with pharmacologic interventions to treat mucus hypersecretion.
- Published
- 2007
19. Suppression of eosinophilic airway inflammation by treatment with α-galactosylceramide
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Kazuko Shibuya, Kiyohisa Sekizawa, Masaru Taniguchi, Yuko Morishima, Yukio Ishii, Toru Kimura, Akira Shibuya, Tohru Sakamoto, Takumi Kiwamoto, Takashi Iizuka, Akihiro Nomura, Yosuke Matsuno, and Ahmed E. Hegab
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medicine.diagnostic_test ,biology ,business.industry ,Immunology ,chemical and pharmacologic phenomena ,Inflammation ,respiratory system ,Eosinophil ,Natural killer T cell ,Immunoglobulin E ,chemistry.chemical_compound ,Ovalbumin ,Bronchoalveolar lavage ,medicine.anatomical_structure ,chemistry ,Eosinophilic ,medicine ,biology.protein ,Immunology and Allergy ,lipids (amino acids, peptides, and proteins) ,VCAM-1 ,medicine.symptom ,business - Abstract
To clarify the essential role of NKT cells in allergy, we investigated the contribution of NKT cells to the pathogenesis of eosinophilic airway inflammation using α-galactosylceramide (α-GalCer), a selective ligand for NKT cells. Although continuous administration of α-GalCer during ovalbumin (OVA) sensitization increased OVA-specific IgE levels and worsened eosinophil inflammation, a single administration of α-GalCer at the time of OVA challenge completely prevented eosinophilic infiltration in wild-type mice. This inhibitory effect of α-GalCer was associated with a decrease in airway hyperresponsiveness, an increase in IFN-γ, and decreases in IL-4, IL-5 and IL-13 levels in the bronchoalveolar lavage fluids. Analysis of lung lymphocytes revealed that production of IFN-γ increased in NK cells, but not in T or NKT cells, following α-GalCer administration. Induction of vascular cell adhesion molecule-1 in the lungs of wild-type mice was also significantly attenuated by treatment with α-GalCer. These effects of α-GalCer were abrogated in Jα281–/– mice, which lack NKT cells, and in wild-type mice treated with anti-IFN-γ Ab. Hence, our data indicate that α-GalCer suppresses allergen-induced eosinophilic airway inflammation, possibly by inducing a Th1 bias that results in inhibition of eosinophil adhesion to the lung vessels. See accompanying commentary: http://dx.doi.org/10.1002/eji.200535425
- Published
- 2005
20. Reply
- Author
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Michael Tiemeyer, Takumi Kiwamoto, Zhou Zhu, Bruce S. Bochner, and Toshihiko Katoh
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Text mining ,Information retrieval ,business.industry ,Immunology ,Immunology and Allergy ,Medicine ,business - Published
- 2015
21. A case of familial pulmonary mycobacterium avium complex disease
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Shigeo Otsuka, Naoto Keicho, Takefumi Saito, Yukiko Miura, Ataru Moriya, Minako Hijikata, Nariaki Kokuho, Masashi Matsuyama, Kei Shimizu, Kenji Hayashihara, and Takumi Kiwamoto
- Subjects
Adult ,Male ,Cystic Fibrosis Transmembrane Conductance Regulator ,Human leukocyte antigen ,Disease ,Cftr gene ,Antigen ,Japan ,Risk Factors ,Diabetes mellitus ,Genotype ,Internal Medicine ,Medicine ,Humans ,Mycobacterium avium complex ,Genetic Predisposition to Disease ,Cation Transport Proteins ,Aged ,Mycobacterium avium-intracellulare Infection ,biology ,HLA-A Antigens ,business.industry ,General Medicine ,Middle Aged ,biology.organism_classification ,medicine.disease ,Pedigree ,Menopause ,Immunology ,Female ,business - Abstract
We report one Japanese familial line in which there were three pulmonary MAC patients and one suspected patient over two generations, most of whom were diagnosed with the nodular/bronchiectatic type. In all patients, life circumstances and bacterial strains differed at the time of diagnosis. This suggests that the genes thought to affect patient susceptibility to pulmonary MAC disease may be involved in this family line. Comprehensive genotypic analysis of the CFTR gene, HLA typing, and analysis of the NRAMP1 polymorphisms were performed in seven members of this family. The results suggest that female sex and menopause might be associated with onset of pulmonary MAC of the nodular/bronchiectatic type, and HLA-A26 antigen and diabetes mellitus might be involved in disease exacerbations.
- Published
- 2010
22. Transcription factors T-bet and GATA-3 regulate development of airway remodeling
- Author
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Yukio Ishii, Shinsuke Homma, Kiyohisa Sekizawa, Yuko Morishima, Satoru Takahashi, Keigyou Yoh, Ahmed E. Hegab, Takumi Kiwamoto, Akihiro Nomura, Kazusa Ishizaki, Atsuko Maeda, Takashi Iizuka, Yosuke Matsuno, and Tohru Sakamoto
- Subjects
Pulmonary and Respiratory Medicine ,Chemokine CCL11 ,medicine.medical_treatment ,Immunoglobulins ,Mice, Transgenic ,GATA3 Transcription Factor ,Critical Care and Intensive Care Medicine ,Pathogenesis ,Interferon-gamma ,Mice ,Th2 Cells ,Fibrosis ,Transforming Growth Factor beta ,Intensive care ,medicine ,Animals ,Transcription factor ,Lung ,Hyperplasia ,business.industry ,Mucins ,Muscle, Smooth ,Hypertrophy ,respiratory system ,Th1 Cells ,medicine.disease ,Mucus ,Asthma ,respiratory tract diseases ,Eosinophils ,Disease Models, Animal ,Cytokine ,Chemokines, CC ,Immunology ,Goblet Cells ,Interleukin-4 ,business ,Airway ,T-Box Domain Proteins ,Transcription Factors - Abstract
Airway remodeling is an important feature of chronic asthma that causes irreversible airflow obstruction. Although asthma is considered to be a Th2 disease, the role of T-bet and GATA-3, the key transcription factors for differentiation toward Th1 and Th2 cells, in the pathogenesis of airway remodeling is poorly understood.We therefore examined the effects of GATA-3 or T-bet induction of Th1/Th2 bias on the development of airway remodeling in mice.The development of airway remodeling after repeated allergen challenges was analyzed using transgenic mice overexpressing either GATA-3 or T-bet.The degrees of subepithelial fibrosis and airway smooth muscle hyperplasia after repeated allergen exposure were significantly enhanced in mice overexpressing GATA-3, compared with wild-type mice. Allergen-induced goblet cell hyperplasia and mucus hypersecretion were significantly lower in mice overexpressing T-bet than in wild-type mice. Eosinophilic airway inflammation increased in mice overexpressing GATA-3, but decreased in mice overexpressing T-bet after repeated allergen exposure. Cytokine analysis revealed that the Th1/Th2 cytokine balance shifted to Th2 in lung homogenates and lung T cells of mice overexpressing GATA-3, whereas this balance shifted to Th1 in those of mice overexpressing T-bet after allergen exposure. Lung transforming growth factor-beta and eotaxin levels were associated with the degree of subepithelial fibrosis and eosinophilic airway inflammation, respectively.Overall, the results indicate that development of airway remodeling is regulated by the lung Th1/Th2 bias induced by GATA-3 and T-bet.
- Published
- 2006
23. Effect of inhaled steroids on increased collagen synthesis in asthma
- Author
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Yuko Morishima, Akihiro Nomura, Takumi Kiwamoto, Tohru Sakamoto, Sachiko Kai, Takashi Iizuka, Kiyohisa Sekizawa, and Yukio Ishii
- Subjects
Pulmonary and Respiratory Medicine ,Adult ,Male ,medicine.medical_specialty ,medicine.drug_class ,Enzyme-Linked Immunosorbent Assay ,Gastroenterology ,Severity of Illness Index ,Fluticasone propionate ,Leukocyte Count ,Pulmonary Disease, Chronic Obstructive ,fluids and secretions ,Internal medicine ,Forced Expiratory Volume ,Administration, Inhalation ,Medicine ,Humans ,Glucocorticoids ,Asthma ,Aged ,Inhalation ,business.industry ,Respiratory disease ,Sputum ,Eosinophil ,Middle Aged ,Transforming Growth Factor alpha ,medicine.disease ,Prognosis ,Immunohistochemistry ,Peptide Fragments ,respiratory tract diseases ,Eosinophils ,Procollagen peptidase ,medicine.anatomical_structure ,Immunology ,Corticosteroid ,Female ,medicine.symptom ,business ,Biomarkers ,Procollagen ,medicine.drug - Abstract
Background: We previously reported that sputum levels of procollagen type I C-terminal peptide (PICP), a marker of ongoing collagen type I deposition, are increased in proportion to airway inflammation in asthma patients. Objectives: In this study, we examined the effect of inhaled corticosteroids on increased collagen synthesis in step 2–4 asthmatics. Methods: We compared the sputum PICP concentrations of 25 steroid-naive asthmatics, 25 normal volunteers, and 10 subjects with chronic obstructive pulmonary disease. Asthma subjects were also instructed to start fluticasone propionate treatment, and the percentage of forced expiratory volume in 1 s, sputum eosinophil counts, sputum PICP concentrations, and sputum transforming growth factor-β-positive cell counts before treatment were compared with those 1 month after treatment. Results: Sputum PICP concentrations were detected in the following order: asthma group ≧ chronic obstructive pulmonary disease group > control group. Asthma patients showing high sputum PICP belonged to step 4, although there was no correlation between sputum PICP and asthma severity. Treatment with fluticasone propionate not only significantly improved the mean percentage of forced expiratory volume in 1 s (from 66.7 to 87.2%), but also decreased the mean sputum eosinophil counts (from 13.4 to 5.8%), the mean sputum PICP concentrations (from 30.8 to 10.2 ng/ml), and the mean sputum tumor growth factor-β-positive cells (from 11.3 to 2.8%). Nevertheless, a significant difference in sputum PICP concentrations was still observed between the control group and the steroid-treated asthma group. Conclusions: The present results suggest that inhaled corticosteroid treatment might reduce sputum indexes of collagen metabolism and eosinophilic inflammation in asthma patients.
- Published
- 2005
24. Role of 15-deoxy delta(12,14) prostaglandin J2 and Nrf2 pathways in protection against acute lung injury
- Author
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Takumi Kiwamoto, Koji Uchida, Tohru Sakamoto, Mie Mochizuki, Akihiro Nomura, Toru Kimura, Yuko Morishima, Yukio Ishii, Ahamed E. Hegab, Masayuki Yamamoto, Yosuke Matsuno, Ken Itoh, Kiyohisa Sekizawa, and Takashi Iizuka
- Subjects
Pulmonary and Respiratory Medicine ,NF-E2-Related Factor 2 ,Prostaglandin ,Inflammation ,Lung injury ,Pharmacology ,Critical Care and Intensive Care Medicine ,Carrageenan ,chemistry.chemical_compound ,Mice ,Intensive care ,Parenchyma ,Medicine ,Animals ,Cyclooxygenase Inhibitors ,Nitrobenzenes ,Mice, Inbred BALB C ,Respiratory Distress Syndrome ,Sulfonamides ,medicine.diagnostic_test ,Cyclooxygenase 2 Inhibitors ,business.industry ,Prostaglandin D2 ,Macrophages ,Pneumonia ,respiratory system ,respiratory tract diseases ,DNA-Binding Proteins ,Disease Models, Animal ,Bronchoalveolar lavage ,Eicosanoid ,chemistry ,Cyclooxygenase 2 ,Prostaglandin-Endoperoxide Synthases ,Immunology ,Trans-Activators ,medicine.symptom ,business - Abstract
Acute lung injury (ALI) is a disease process that is characterized by diffuse inflammation in the lung parenchyma. Recent studies demonstrated that cyclooxygenase-2 (COX-2) induced at the late phase of inflammation aids in the resolution of inflammation by generating 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2). Transcription factor Nrf2 is activated by electrophiles and exerts antiinflammatory effects by inducing the gene expression of antioxidant and detoxification enzymes.Because 15d-PGJ2 is an endogenous electrophile, we hypothesized that it protects against ALI by activating Nrf2.To test this hypothesis, we generated a reversible ALI model by intratracheal injection of carrageenin, an inducer of acute inflammation, whose stimulation has been known to induce COX-2.We found that ALI induced by carrageenin was markedly exacerbated in Nrf2-knockout mice, compared with wild-type mice. Analysis of bronchoalveolar lavage fluids also revealed that the magnitude and the duration of acute inflammation, indicated by albumin concentration and the number of neutrophils, were significantly enhanced in Nrf2-knockout mice. Treatment of wild-type mice with NS-398, a selective COX-2 inhibitor, significantly exacerbated ALI to the level of Nrf2-knockout mice. In the lungs of NS-398-treated wild-type mice, both the accumulation of 15d-PGJ2 and the induction of Nrf2 target antioxidant genes were significantly attenuated. Exogenous administration of 15d-PGJ2 reversed the exacerbating effects of NS-398 with the induction of antioxidant genes.These results demonstrated in vivo that 15d-PGJ2 plays a protective role against ALI by exploiting the Nrf2-mediated transcriptional pathway.
- Published
- 2005
25. Association analysis of tissue inhibitor of metalloproteinase2 gene polymorphisms with COPD in Egyptians
- Author
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Yukio Ishii, Akihiro Nomura, Tohru Sakamoto, Toru Kimura, Yuko Morishima, Hosam H. Massoud, Wataru Saitoh, Hosny M. Massoud, Takumi Kiwamoto, Takashi Iizuka, Kiyohisa Sekizawa, Yoshiyuki Uchida, Ahmed E. Hegab, Mie Mochizuki, and Khalid M. Hassanein
- Subjects
Pulmonary and Respiratory Medicine ,Male ,TIMP2 ,Genotype ,Population ,Pathogenesis ,Pulmonary Disease, Chronic Obstructive ,Gene Frequency ,medicine ,COPD ,Humans ,Genetic Predisposition to Disease ,Polymorphism ,Egyptian ,education ,Gene ,Allele frequency ,Genetic association ,Genetics ,education.field_of_study ,Tissue Inhibitor of Metalloproteinase-2 ,Polymorphism, Genetic ,business.industry ,Middle Aged ,medicine.disease ,Genotype frequency ,Case-Control Studies ,Immunology ,business - Abstract
Proteinase/antiproteinase imbalance is recognized to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). A relative increase in the activities of matrix metalloproteinases might be caused by mutations of tissue inhibitor of metalloproteinase2 (TIMP2). Recently, two polymorphisms of the TIMP2 gene, +853 G/A and −418 G/C (+551 and −720 from the translation initiation site), have been shown to be associated with the development of COPD in the Japanese population. In this study, a case-control association analysis for these polymorphisms was conducted in the Egyptian population using 106 COPD patients and 72 healthy controls. The genotype frequency of +853 G/A was significantly different between the patient and the control groups ( P =0.029), although no significant difference was detected in the allele frequency between the two groups. These results suggest that the +853 G/A polymorphism of the TIMP2 gene might be associated with COPD across ethnicities. In contrast, neither the distributions of genotype nor allele frequencies of –418 G/C were significantly different between the two groups, raising the possibility that a combination of different genetic factors contributes to the development of COPD in different ethnic groups.
- Published
- 2005
26. Mice with Attenuated Expression of the α2,3 Sialyltransferase ST3gal-III (St3gal3) Display Enhanced Allergic Eosinophilic Airway Inflammation
- Author
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Ronald L. Schnaar, Mary Brummet, Mary G. Motari, Takumi Kiwamoto, Bruce S. Bochner, and Zhou Zhu
- Subjects
Pathology ,medicine.medical_specialty ,biology ,business.industry ,Sialyltransferase ,Immunology ,Airway inflammation ,ST3Gal III ,ST3GAL3 ,Eosinophilic ,biology.protein ,Immunology and Allergy ,Medicine ,business - Published
- 2013
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