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請使用永久網址來引用或連結此文件:
http://ir.cmu.edu.tw/ir/handle/310903500/29061
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| 題名: | Pleural effusions in febrile medical ICU patients - Chest ultrasound study |
| 作者: | Tu, CY;Hsu, WH;Hsia, TC;Chen, HJ;Tsai, KD;Hung, CW;Shih, CM |
| 貢獻者: | 附設醫院內科部呼吸治療科;China Med Univ Hosp, Dept Internal Med, Div Pulm & Crit Care Med, Taichung, Taiwan |
| 日期: | 2004 |
| 上傳時間: | 2010-09-24 14:20:14 (UTC+8) |
| 出版者: | AMER COLL CHEST PHYSICIANS |
| 摘要: | In the presence of external Ca2+, pretreatment of neutrophils with 3-(5'-hydroxymethyl-2-furyl)-1-benzyl indazole (YC-1) inhibited the cyclopiazonic acid (CPA)-induced [Ca2+](i) elevation in a concentration- but not a time-dependent manner, while YC-1 had no effect on the Ca2+ signals in a Ca2+-free medium. YC-1 failed to inhibit ATP- and interleukin-8 (IL-8)-induced [Ca2+](i) changes. Addition of YC-1 after cell activation strongly inhibited the CPA-induced [Ca2+](i) changes. In a classical Ca2+ readdition protocol, a similar extent inhibition of Ca2+ spike by YC-1 introduced either prior to or after CPA stimulation was obtained. In rat neutrophils, mRNA for endothelial differentiation gene (edg)1, edg5, edg6 and edg8, the putative targets for sphingosine 1-phosphate (S1P), could be detected. However, S1P was found to have little effect on Ca2+ signals. YC-1 did not inhibit but enhanced the sphingosine-induced [Ca2+](i) changes. Inhibition by YC-1 of CPA-induced [Ca2+](i) changes was not prevented by 7-nitroindazole and N-(3-aminomethyl)benzylacetamidine (1400W), two nitric oxide synthase (NOS) inhibitors, by aristolochic acid, a phospholipase A(2) inhibitor, or by suspension in a Na+-deprived medium. YC-1 did not affect the mitochondrial membrane potential. Moreover, YC-1 did not alter [Ca2+](i) changes in response to ionomycin after CPA and formyl-Met-Leu-Phe (fMLP) stimulation in a Ca2+-free medium. YC-1 had no effect on the basal [Ca2+](i) level, the pharmacologically isolated plasma membrane Ca2+-ATPase activity, and Ba2+ entry into CPA-activated cells. YC-1 alone resulted in the accumulation of actin filaments in neutrophils, while significantly reduced the intensity of actin filament staining in the subsequent activation with CPA. These results indicate that YC-1 inhibited CPA-activated store-operated Ca2+ entry (SOCE) probably through the direct blockade of channel activation and/or the disruption of the integrity of the actin cytoskeleton necessary for supporting Ca2+ entry pathway in neutrophils. (C) 2004 Elsevier Inc. All rights reserved. |
| 關聯: | CHEST 126(4):1274-1280 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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