Publications by authors named "Jinushi E"

We encountered a dairy farmer and his son with farmer's lung who had worked on the same farm for 25 years and 5 years, respectively. The son was admitted to our hospital because of cough, sputum, and shortness of breath. Chest computed tomography (CT) on admission revealed diffuse ground-glass opacities in both lung fields.

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A 75-year-old asymptomatic woman was admitted to our hospital after an abnormal shadow was found on a chest roentgenogram. Chest computed tomography showed a round mass in the right lower lobe. Magnetic resonance imaging showed the mass with high signal intensity on T2-weighted images and intermediate signal intensity on T1-weighted images.

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A 58-year-old man with von Recklinghausen's disease was admitted for further investigation of right chest pain. Chest X-ray revealed multiple emphysematous bullae in both lungs and a tumor shadow in the right upper lobe. Bronchofiberscopy was performed, but an adequate specimen was not obtained.

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A 51-year old woman was admitted to our hospital because of status asthmaticus. Electrocardiography (ECG) revealed ST-segment elevation in leads II.III.

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A 58-year-old asymptomatic man was referred for investigation of an abnormal shadow on chest X-ray films. Chest computed tomography (CT) revealed an infiltrative shadow containing an air-bronchogram. Video-assisted thoracic surgery was performed for a lung biopsy of an abnormal region in the right upper lobe of the lung.

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Rationale: The human cholinergic receptor muscarinic-1 (CHRM1) is widely distributed in the lungs. In patients with asthma, CHRM1 may be involved in airway constriction, airway epithelial cell proliferation, and airway inflammation. The CHRM1 gene is located on chromosome 11q13, which is one of the candidate loci for asthma and atopy.

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Background: Nonspecific airway hyperresponsiveness (AHR), a cardinal feature of asthma, is thought to result from several genetic and environmental factors. Asymptomatic AHR in nonasthmatic healthy subjects might be a risk factor for the development of asthma. Genetic variations in codons 16 and 27 of the human beta(2)-adrenergic receptor (beta(2)-AR) alter receptor function in vitro and are associated with various asthma-related phenotypes, including asthma severity and AHR.

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Article Synopsis
  • A 30-year-old woman developed high fever and difficulty breathing after 11 days of minocycline treatment for a skin burn, leading to a diagnosis of drug-induced pneumonia.
  • Discontinuing minocycline resulted in significant clinical and radiographic improvements, confirmed by analysis of bronchoalveolar lavage fluid showing increased white blood cells.
  • The study highlights the changes in inflammatory cell types and cytokine levels over time, indicating how certain cytokines like TNF-alpha, IL-8, and IL-5 may be involved in the pneumonia's inflammatory response.
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We investigated airway hyperresponsiveness (AHR) by the continuous inhalation method using an Astograph(R) in 105 asthmatics and 141 non-asthmatic asymptomatics. The range of Dmin (1 U=one minute inhalation of 1 mg/ml of methacholine) of asthmatics was 0.001 to 28.

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The CC chemokine regulated upon activation, normal T-cell expressed and secreted (RANTES) attracts eosinophils, basophils, and T cells during inflammation and immune response, indicating a possible role for this chemokine in asthma. Both the -403A and -28G alleles of the RANTES promoter region exhibit significantly enhanced promoter activity in reporter constructs in vitro. We therefore investigated the genetic influence of these alleles on the development of asthma using case-control analysis in a Japanese population (298 patients with asthma and 311 control subjects).

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Background: Several studies have shown that nitric oxide (NO) plays a role in the regulation of the T(H)1/T(H)2 balance, indicating the potential for NO to contribute to the development of atopy and several other allergic diseases, including bronchial asthma. NO synthase 2 (NOS2) is critically involved in the synthesis of NO during several inflammatory states, and the gene encoding NOS2 is located at chromosome 17q11.2-q12, where 2 genome scans have identified a candidate locus for atopy and asthma.

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Background: Increasing evidence indicates that total serum IgE levels are largely determined by genetic factors, and we recently established that the -109C/T promoter polymorphism at FCER1B is a genetic factor that affects total serum IgE levels. The gene encoding cytotoxic T lymphocyte antigen 4 (CTLA4) is another candidate factor in high IgE responsiveness, because B7-CD28/CTLA4 interaction can promote the differentiation and development of the T(H)2 lymphocyte subset.

Objective: We intended to determine whether CTLA4 is associated with increased levels of total serum IgE or with the development of asthma or atopy.

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Mediastinal lymphangioma is rare disease. Above all cavernous type of mediastinal lymphangioma is very rare. We report 5 cases of mediastinal lymphangioma including cavernous type.

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Genetic factors are important in defining total serum IgE levels. Linkage analyses have localized a gene or genes that influence atopic phenotype at chromosome 11q13. Variants of the FCER1B gene have been identified, which are associated with an increased risk of developing atopy and bronchial asthma.

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A number of chemokines are produced by alveolar cells in the course of inflammatory reactions of sarcoidosis. C-C chemokine receptor 2 (CCR2) is a prominent receptor for the monocyte chemoattractant protein (MCP) group of C-C chemokines. A transition causing a valine to isoleucine substitution in transmembrane domain I of the CCR2 gene (CCR2-64I) that has a protective effect against the progression of human immunodeficiency virus-1 (HIV-1) disease has been described.

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We encountered three adults with varicella and bronchial mucosal lesions. Respiratory symptoms were minimal in all three. Chest X-ray films showed bilateral, diffuse, small, nodular shadows.

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