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排序方式: 共有9117条查询结果,搜索用时 15 毫秒
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Role of macrophage migration inhibitory factor in otitis media with effusion in adults 总被引:4,自引:0,他引:4
Kariya S Okano M Aoji K Kosaka M Chikumoto E Hattori H Yuen K Nishioka S Nishioka K Nishizaki K 《Clinical and diagnostic laboratory immunology》2003,10(3):417-422
Otitis media with effusion (OME) is one of the most common ear diseases. Bacterial endotoxins and several inflammatory cytokines appear to be involved in the pathogenesis of OME in children; however, little is known of the immunological aspects of the onset of OME in adults. We sought to determine the presence of macrophage migration inhibitory factor (MIF) as well as interleukin 1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), RANTES (regulated upon activation, normal T-cell expressed and presumably secreted), and endotoxin in middle ear effusions (MEEs) from adult patients with OME. In addition, the levels of MIF in MEEs from adults and children were compared. MEE was obtained from 95 adults and 11 children. The levels of MIF, IL-1beta, TNF-alpha, and RANTES were determined by enzyme-linked immunosorbent assay, and the concentrations of endotoxin and total protein were determined by the Endospec assay and bicinchoninic acid assay, respectively. MIF was detected in 97.9% of the MEEs from adults, while endotoxin, IL-1beta, TNF-alpha, and RANTES were detected in 96.8, 12.6, 5.3, and 43.9%, respectively. In addition, the level of MIF was significantly higher than those of endotoxin, IL-1beta, and TNF-alpha. A positive correlation between the levels of MIF and endotoxin was observed. MIF and endotoxin were detected in 81.8 and 72.7%, respectively, of the MEEs from the children. The level of MIF was significantly higher in the children, and conversely that of endotoxin was significantly higher in the adults. These results suggest that the interaction between MIF and endotoxin may promote fluid collection in the middle ear, particularly in adults. 相似文献
44.
Yamamoto A Nakayama M Kurosawa Y Sugo K Karasawa H Ogawa T Takasaki T Tashiro M Kurane I 《Journal of virological methods》2002,104(2):195-201
Japanese encephalitis virus-specific IgM is a reliable indicator for serodiagnosis of Japanese encephalitis. A particle agglutination (PA) assay system was developed to detect anti-Japanese encephalitis virus IgM in human serum samples. The newly developed PA assay consisted of hydroxyapatite-coated nylon beads and V-bottom 96-well microplates. Hydroxyapatite-coated nylon beads were coated with Japanese encephalitis virus antigens. Japanese encephalitis virus antigen-coated, hydroxyapatite-coated nylon beads agglutinated in the IgM-captured wells when anti-Japanese encephalitis virus IgM-positive serum samples were used. A button pattern was formed at the bottom of the wells when anti-Japanese encephalitis virus IgM-negative serum samples were used. Thirty anti-Japanese encephalitis virus IgM-positive serum samples from Japanese encephalitis-confirmed cases were tested by the PA assay. All these serum samples were determined to be Japanese encephalitis virus IgM-positive. IgM titers determined by the PA assay corresponded to those determined by enzyme-linked immunosorbent assay. The titers were consistent in two independent PA assays. These results indicate that the newly developed PA assay is a reliable method for detecting anti-Japanese encephalitis virus IgM in human serum samples and that this assay will be a suitable diagnostic system especially in rural areas of Asia. 相似文献
45.
Keiko Wakui Toshiro Nishida Jun-ichiro Masuda Takeshi Itoh Daisuke Katsumata Tsutomu Ohno Yoshimitsu Fukushima 《Journal of human genetics》1991,36(2):149-153
We report a malformed female infant withde novo interstitial deletion of 4q[46,XX,del(4)(q27q28.2)]. The MN blood type analysis of the family members showed that the patient had an intact blood group-MN locus. The locus of the gene responsible for the MN antigen activity is confined to a 4q28.2–4q31.1 segment on the basis of the result of this patient and the previous mapping data. 相似文献
46.
47.
Kurosawa H 《Rinsho byori. The Japanese journal of clinical pathology》2000,48(12):1118-1124
The natural history of COPD such as pulmonary emphysema demonstrates that FEV1 rapidly declines in smokers who are susceptible to cigarette smoke. The susceptible smokers who quit smoking do not regain only a little, but the rate of the FEV1 decline is no longer steep. These have been interpreted that early detection of this obstructive impairment is the most important issue to prevent the progression to severe emphysema. Pulmonary function tests, at least a measure of FEV1, in the all middle-aged smokers have been particularly recommended. The smokers with abnormal FEV1 defect should be advised to quit smoking. In moderate and severe cases, after staging of the disease by pulmonary function and exercise tests, assessments of complicated factors such as eosinophilic bronchitis are clinically important for constructing therapeutic strategies. Asthmatic component can be assessed by eosinophil count in the sputum and/or reversibility of the pulmonary function after challenging of bronchodilater inhalations. In the severe stage of the disease, examinations such as arterial blood gas analysis and pulse oxymetric measure are critical because oxygen therapy for the patients with respiratory failure has been known to improve survival prognosis. Portable devices which can assess arterial oxygen saturation during daily activity will be useful to decide its indication or to titrate oxygen. In conclusion, clinical examination in COPD, particularly in pulmonary emphysema in this paper, should appropriately be planned in each stage of the disease, or in each clinical purpose. 相似文献
48.
M Kurosawa Y Okayama S Kobayashi K Obata 《International archives of allergy and applied immunology》1990,92(4):349-355
Rat mast cell granules and plasma membrane fractions were obtained by homogenization of highly purified rat mast cells and isolation in a Percoll gradient and a sucrose gradient, respectively. Immunostaining of rat mast cells, granules and plasma membrane fractions was performed with mouse monoclonal antibody M6764 which was produced against the crude membrane fractions of the neural tubes. Rat mast cells and granules were immunostained with the monoclonal antibody, but not the plasma membrane fractions. The granules fixed with glutaraldehyde-paraformaldehyde showed ring-like forms. Chloroform-methanol treatment did not effect the staining of rat mast cells and granules with the monoclonal antibody. Western blotting analysis of rat mast cells and granules with the monoclonal antibody showed broad protein bands ranging from 100 to 250 kD. 相似文献
49.
Rat mast cell granules were obtained by homogenization of highly purified rat mast cells and isolated in a Percoll gradient. DPI synthesis in rat mast cell granules was assayed by measuring the incorporation of 32P from [gamma 32P] ATP into DPI in the absence of exogenous phosphatidylinositol (PI). Lipids were isolated with methanol/chloroform/HC1 and were separated by thin-layer chromatography on oxalic acid impregnated silica gel plates. DPI areas were identified by staining with iodine, scraped and measured for 32P radioactivity. The addition of PMA to the granules caused an increase of DPI synthesis, which can be catalysed by PI kinase. Neither an inactive phorbol ester, 4-alpha-phorbol-12, 13-didecanoate, nor dimethyl sulfoxide (DMSO) used as a solvent for PMA had any effect. The effect of PMA in the DPI synthesis was dose-dependent and maximal effects were observed at 10-100 ng/ml. Dose-response curves of the effects of PMA in DPI synthesis in the granules corresponded to those of other biochemical effects of PMA in rat mast cells, such as mediator release mediated through the activation of protein kinase C. These results suggest that PMA may directly affect PI kinase or indirectly regulate its activity in rat mast cell granules. 相似文献
50.
Matsuo T Wanaka K Asada R 《Rinsho byori. The Japanese journal of clinical pathology》2005,53(7):622-629
Heparin-induced thrombocytopenia(HIT) due to immunological mechanisms is known as an important adverse reaction to heparin treatment, and heparin treatment should be applied while keeping in mind the risk of onset of HIT 5-14 days after the initiation of heparin. The presence of HIT had not been fully recognized in clinical practice in Japan despite the management of HIT being well confirmed in Western countries. Recognition of HIT has increased since argatroban, a direct thrombin inhibitor, obtained the approval of the FDA for prevention and treatment of HIT. Although the incidence of HIT in Japan has not yet been clarified, there is some evidence that HIT is encountered in critically ill patients undergoing heparin anticoagulation. Clinical diagnosis of HIT is performed by means of thrombocytopenia of a drop of 50% or 100 x 10(30/microl for 5 -14 days after starting heparin treatment. Confirmatory laboratory tests examine whether the patients have antibodies against heparin/PF4 complexes or not. Two assay tests for detecting heparin/PF4 complex antibodies are available in Japan. As a functional test, the heparin-induced platelet aggregation method is easily performed and the result is obtained in a short time. The result of the test has, however, been misleading due to the selection of donors. Low platelet activity of the donors on the addition of heparin induces a negative response in spite of positive antibodies in the sample. Before testing samples, it is important to check heparin reactivity of the donor's platelets. Enzyme immunoassay detecting the antibodies is available as a commercial kit. Sensitivity obtained by enzyme immunoassay is very high and often introduces false-positives. Careful attention to interpretation of the result is required. Treatment of HIT should be started at the time of recognition of thrombocytopenia while antibody testing for HIT is performed. As an alternative anticoagulant to heparin, argatroban should immediately be applied to avoid complication of thrombosis. Thrombocytopenia and hypercoagulability quickly recover to the preheparin level by the appropriate use of argatroban. 相似文献