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排序方式: 共有219条查询结果,搜索用时 15 毫秒
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Yoshinori Seko Shigeru Ishiyama Toshiro Nishikawa Takeshi Kasajima Michiaki Hiroe Shin Suzuki Sugao Ishiwata Sachio Kawai Yuetsu Tanaka Miyuki Azuma Tetsuji Kobata Hideo Yagita Ko Okumura Ryozo Nagai 《Cardiovascular pathology》2002,11(3):166-170
BACKGROUND: T-cell-mediated myocardial damage is known to be involved in acute myocarditis and dilated cardiomyopathy. Recently, we found that tumor necrosis factor (TNF) ligand superfamily costimulatory molecules, especially 4-1BBL, played an important role in the myocardial damage of murine acute viral myocarditis. METHODS AND RESULTS: To investigate the roles for CD27L, CD30L, OX40L and 4-1BBL, which belong to TNF ligand superfamily, in the development of acute myocarditis and dilated cardiomyopathy, we analyzed the expression of these antigens in the myocardial tissues of patients with acute myocarditis and dilated cardiomyopathy. We also examined expression of the receptors for these molecules, CD27, CD30, OX40 and 4-1BB, which belong to TNF receptor superfamily, on the infiltrating cells. Strong expression of CD27L, CD30L and 4-1BBL and weak to moderate expression of OX40L was found in the cardiac myocytes of patients with acute myocarditis. Moderate expression of CD27L, CD30L and 4-1BBL and weak expression of OX40L was found on the cardiac myocytes of patients with dilated cardiomyopathy. Most of the infiltrating cells expressed CD27, CD30 and 4-1BB and a part of the infiltrating cells expressed OX40. CONCLUSIONS: Our findings suggest that expression of TNF ligand superfamily costimulatory molecules on cardiac myocytes may play a role in the cell-mediated myocardial damage in patients with acute myocarditis and dilated cardiomyopathy as in murine viral myocarditis. 相似文献
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Sakamoto Kazumasa Ito Kiyoaki Yotsuyanagi Hiroshi Yatsuhashi Hiroshi Tanaka Yasuhito Hige Shuhei Takikawa Yasuhiro Ueno Yoshiyuki Yamamoto Kazuhide Imazeki Fumio Inoue Jun Kurosaki Masayuki Umemura Takeji Toyoda Hidenori Mita Eiji Michitaka Kojiro Maeshiro Tatsuji Yamada Norie Suetsugu Atsushi Kawanaka Miwa Seko Yuya Matsuura Kentaro Okumura Akinori Fukuzawa Yoshitaka Sugiyama Masaya Mizokami Masashi Yoneda Masashi 《Journal of gastroenterology》2022,57(12):971-980
Journal of Gastroenterology - Hepatitis B virus (HBV) is one of the most prevalent chronic viral infections that causes chronic hepatitis B (CHB). In Japan, genotypes B and C account for most of... 相似文献
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Design and creation of a Ca2+ binding site in human lysozyme to enhance structural stability. 总被引:7,自引:2,他引:7 下载免费PDF全文
R Kuroki Y Taniyama C Seko H Nakamura M Kikuchi M Ikehara 《Proceedings of the National Academy of Sciences of the United States of America》1989,86(18):6903-6907
A Ca2+ binding site like an EF-hand motif was designed and created in human lysozyme by replacing both Gln-86 and Ala-92 with aspartic acids by site-directed mutagenesis. The mutant human lysozyme (D86/92-lysozyme) was expressed and secreted by yeast. One Ca2+ was found to bind one molecule of the purified protein with the binding constant 5.0 x 10(6) M-1. The enzymatic activity of holo-D86/92-lysozyme against glycol chitin at 40 degrees C was 2-fold higher than that of the native lysozyme. Maximal activity of the holo-D86/92-lysozyme was observed at 80 degrees C, where its relative activity normalized to the value at 40 degrees C was 6-fold and 17-fold higher than those of the native and apoenzymes, respectively. The activities of the native lysozyme and apo-D86/92-lysozyme were maximum at 65 degrees C-70 degrees C. Moreover, D86/92-lysozyme was more stable against protease digestion than the native lysozyme. These results indicate that the creation of the calcium binding site like an EF-hand motif in the human lysozyme enhances its structural stability. 相似文献
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Taniguchi T Ko M Seko S Nishida O Inoue F Kobayashi H Saiga T Okamoto M Fukuse T 《Gut》2004,53(5):770-771
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Expression of intercellular adhesion molecule-1 in rat heart with ischemia/reperfusion and limitation of infarct size by treatment with antibodies against cell adhesion molecules. 总被引:6,自引:0,他引:6 下载免费PDF全文
T. Yamazaki Y. Seko T. Tamatani M. Miyasaka H. Yagita K. Okumura R. Nagai Y. Yazaki 《The American journal of pathology》1993,143(2):410-418
To elucidate the mechanism(s) of myocardial reperfusion injury, we investigated the roles of cell adhesion molecules on both leukocytes and vascular endothelial cells in the reperfused myocardia. We found that within 2 hours after reperfusion leukocytes began to infiltrate into the rat myocardia subjected to 30 minutes of ischemia and clarified, for the first time, that the expression of intercellular adhesion molecule-1 was enhanced on the capillary and venous endothelial cells from 8 to 96 hours after the start of reperfusion. Furthermore, pretreatment with individual monoclonal antibodies against cell adhesion molecules (CD11a, CD11bc, CD18, and intercellular adhesion molecule-1) reduced not only the infiltration of leukocytes but also the area of infarction in the reperfused hearts. These observations suggest that cell adhesion molecules play a critical role in the pathogenesis of myocardial reperfusion injury. 相似文献
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Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide. Nonalcoholic steatohepatitis (NASH), a severe form of NAFLD, can lead to hepatocellular carcinoma (HCC) and hepatic failure. The development and progression of NAFLD are determined by environmental and genetic factors. The effect of genetic factors has been demonstrated by familial studies, twin studies and several cross-sectional studies. In the past 10 years, genome-wide association studies have revealed several single nucleotide polymorphisms (SNPs) associated with the pathology of NAFLD. Among them, the Patatin-like phospholipase domain-containing 3 (PNPLA3) gene variant I148M showed a strong relationship with the development and progression of NAFLD, NASH, and NAFLD-related HCC. The transmembrane 6 superfamily member 2 (TM6SF2) gene variant E167 K was also associated with NAFLD, and it has a relationship with cardiovascular disease. Furthermore, several genes have been proposed as candidate genes to be associated with NAFLD based on case–control studies. We conducted a comprehensive literature search and review on the genetic background of NAFLD. 相似文献