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M Ueda

Publications and source records attributed to M Ueda.

At least 1,621 records · Page 90Linked to original sources
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Oxidized phosphatidylcholine in alveolar macrophages in idiopathic interstitial pneumonias.

It has been suggested that oxidative stress plays a pathogenic role in idiopathic interstitial pneumonias. Macrophage- or neutrophil-derived oxidants seem to be important sources of oxidative stress in this group of inflammatory disorders. Recent experimental studies have revealed that oxidative injury during inflammation or apoptosis can change phosphatidylcholine of cell membrane into its oxidized form, which serves as a ligand for macrophage scavenger receptor CD36. Recently, we developed a monoclonal antibody against oxidized phosphatidylcholine. Using this novel antibody, we performed an immunohistochemical investigation to clarify the localization of oxidized phosphatidylcholine in lung tissues of idiopathic interstitial pneumonias and a relationship between oxidized phosphatidylcholine localization and CD36 expression. Lung specimens obtained from patients with desquamative (n = 8) or usual interstitial pneumonia (n = 15) were studied. Thirteen normal lung tissues were also examined as controls. Antibodies against oxidized phosphatidylcholine, CD36, epithelial cells, macrophages, and neutrophils were used as primary antibodies. The positive cell number was counted by computer-aided morphometry. While there were no oxidized phosphatidylcholine-positive cells in normal lungs, lungs of desquamative or usual interstitial pneumonia contained large numbers of oxidized phosphatidylcholine-positive cells in the alveolar spaces. Double-staining analysis revealed that most oxidized phosphatidylcholine-positive cells were macrophages. The oxidized phosphatidylcholine-positive cells were increased in association with the increase in the densities of macrophages (Rs = 0.87, p < 0.0001) and neutrophils (Rs = 0.89, p < 0.0001). Accumulated macrophages also showed distinct CD36 expression. These findings suggest that oxidative stress and the related product, oxidized phosphatidylcholine, play an important role in the pathophysiology of idiopathic interstitial pneumonias.

Aged↗
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Nicorandil affords cardioprotection in patients with acute myocardial infarction treated with primary percutaneous transluminal coronary angioplasty: assessment with thallium-201/iodine-123 BMIPP dual SPECT.

BACKGROUND: It has been reported that nicorandil restores blood flow to reperfused myocardium in patients with acute myocardial infarction. However, whether nicorandil might decrease infarct size remains unclear. The aim of this study was to assess the effect of nicorandil on infarct size with thallium-201/beta-methyl-p-iodophenyl pentadecanoic acid (BMIPP) dual-isotope single photon emission computed tomography. METHODS: A total of 62 patients were randomly assigned to receive intravenous nicorandil (4 mg in 5 minutes at admission, immediately followed by 6 mg/hr over a 24-hour period) or placebo. All patients were divided into 4 groups: Group N-a, 16 patients with preexisting angina treated with nicorandil; N-b, 15 patients without preexisting angina treated with nicorandil; C-a, 14 patients with preexisting angina given placebo; C-b, 17 patients without preexisting angina given placebo. Tl-201/BMIPP imaging was performed in the 62 patients within 7 days after admission. Dual-isotope single photon emission computed tomographic images were quantified by severity index with a polar map. RESULTS: The BMIPP severity index was similar among the 4 groups. Only the thallium severity index in the N-a group was significantly less (P<.05). The ratio of the thallium severity index to that of BMIPP in the N-a group was significantly decreased compared with those of the other groups. CONCLUSION: Nicorandil has a protective effect in patients with acute myocardial infarction and preexisting angina treated with primary balloon angioplasty.

Angina, Unstable↗
PubMedDate not supplied

Role of intercellular adhesion molecule 1 in acute lung injury induced by candidemia.

Candidemia, a complication often affecting immunocompromised patients, is a common cause of acute lung injury. Yeast-phase Candida albicans has been shown to express a protein that is antigenically and structurally related to Mac-1. C. albicans is reported to stimulate intercellular adhesion molecule 1 (ICAM-1) expression on endothelial cells. In this study, the authors examined the role of ICAM-1 in acute lung injury induced by candidemia. The authors cultured rat pulmonary artery endothelial cells (RPAEC) and investigated the effect of anti-ICAM-1 antibodies on adhesion of C. albicans to RPAEC. In addition, the authors administered anti-ICAM-1 antibodies to rats to examine the effect of the antibodies on experimentally induced candidemia. Survival rates, lung wet-to-dry (W/D) weight ratios, bronchoalveolar lavage (BAL) fluid, histopathological findings, and colony-forming units (CFUs) of lung C. albicans were examined. The adherence of C. albicans to RPAEC was significantly decreased by anti-ICAM-1 antibodies. Anti-ICAM-1 antibodies significantly increased survival, decreased lung W/D weight ratios, decreased neutrophil counts in the BAL fluid, reduced microscopic lung injury, and decreased the quantity of lung C. albicans. These results indicate that ICAM-1 plays a role in adherence of C. albicans to pulmonary vascular endothelial cells, which likely leads to invasion of lung tissue by the organism.

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