Prediction of stone disease by discriminant analysis and artificial neural networks in genetic polymorphisms: a new method

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 台中附設醫院 > 期刊論文 > Item 310903500/29317

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/29317

题名:	Prediction of stone disease by discriminant analysis and artificial neural networks in genetic polymorphisms: a new method
作者:	Chiang, D;Chiang, HC;Chen, WC;Tsai, FJ
贡献者:	附設醫院泌尿部;China Med Coll Hosp, Dept Urol, Taichung 404, Taiwan;China Med Coll Hosp, Dept Med Genet, Taichung, Taiwan;China Med Coll Hosp, Dept Paediat, Taichung, Taiwan;Natl Taiwan Univ, Dept Management, Taipei 10764, Taiwan;Ching Yun Inst Technol, Chungli, Taiwan
日期:	2003
上传时间:	2010-09-24 14:31:51 (UTC+8)
出版者:	BLACKWELL PUBLISHING LTD
摘要:	The inhibition of formyl-methionyl-leucyl-phenylalanine (fMLP)-induced superoxide anion (O-2(.-)) generation by 2-benzyloxybenzaldehyde (CCY1a) was investigated in rat neutrophils, and the underlying mechanism of this inhibition was assessed. CCY1a concentration-dependently inhibited O-2(.-) generation (IC50 = 18.5 +/- 4.3 muM). In cell-free systems, CCY1a failed to alter O-2(.-) generation during dihydroxyfumaric acid autoxidation, in phorbol 12-myristate 13-acetate (PMA)-activated neutrophil particulate NADPH oxidase preparations, or during arachidonic acid-induced NADPH oxidase activation. CCY1a increased cellular cyclic AMP (cAMP) levels in a time- and concentration-dependent manner, and this cAMP-elevating effect was inhibited by the adenylyl cyclase inhibitor 9-(tetrahydro-2'-furyl)adenine (SQ22536), adenosine deaminase (ADA), and the adenosine receptor antagonist 8-(p-sulfophenyl)theophylline. In neutrophils, inhibition of O-2(.-) generation by CCY1a was partially reversed by the protein kinase A inhibitor (9R,10S,12S)2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-1][1,6]benzodiazocine-10- carboxylic acid, hexyl ester (KT5720). CCY1a did not affect fMLP-induced p38 mitogen-activated protein kinase phosphorylation, but concentration-dependently attenuated the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt (IC50 about 31.3 and 19.4 muM, respectively). The plateau phase, but not the initial spike, of fMLP-induced [Ca2+](i) changes was inhibited by CCY1a in a concentration-dependent manner. CCY1a inhibition of Ca2+ entry, ERK, and Akt phosphorylation was not prevented by SQ22536 or ADA. fMLP-induced phospholipase D (PLD) activation was inhibited by CCY1a (IC50 = 13.9 +/- 2.0 muM). ADA and KT5720 did not prevent the inhibition of PLD activation by CCY1a. Collectively, these results indicate that the inhibition by CCY1a of fMLP-induced O-2(.-) generation in rat neutrophils can probably be attributed to the increase in cAMP levels, and to the blockade of Ca2+ entry, suppression of Akt, and PLD activation via cAMP-independent mechanisms. (C) 2003 Elsevier Science Inc. All rights reserved.
關聯:	BJU INTERNATIONAL 91(7):661-666
显示于类别:	[台中附設醫院] 期刊論文

文件中的档案:

没有与此文件相关的档案.

在CMUR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....