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RISS 인기검색어
- 검색키워드
- 저자 : Xianwu Cheng (검색결과 3 건)
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Kim, Hyun Soo,Woo, Jong Shin,Kim, Bu Yong,Jang, Hyun Hee,Hwang, Seung Joon,Kwon, Sung Jin,Choi, Eun Young,Kim, Jin Bae,Cheng, Xianwu,Jin, Enze,Kim, Woo Shik,Kim, Kwon Sam,Kim, Weon Elsevier 2014 Atherosclerosis Vol.233 No.2
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>Several biomarkers reflecting inflammatory or proteolytic activity have been known to represent plaque vulnerability. Moreover, a recent study confirmed that contrast-enhanced ultrasound (CEUS) can visualize intraplaque neovascularization (IPN) and demonstrate plaque vulnerability. In this study, we tried to demonstrate that IPN detected by CEUS was correlated with several well-known biomarkers and clinical outcome in patients with coronary artery disease (CAD).</P> <P><B>Methods</B></P> <P>Patients with stable CAD were screened by conventional carotid ultrasound and patients with carotid plaque thickness more than 2 mm were performed by CEUS for the presence of IPN. Plasma levels of biomarkers and clinical outcomes were evaluated.</P> <P><B>Results</B></P> <P>Among consecutive 89 patients fulfilled the inclusion criteria, 30 patients without IPN (group 1) and 59 patients with IPN (group 2) were analyzed. There were no significant difference in baseline characteristics except for mean age (62.9 ± 10.1 yrs versus 68.4 ± 9.6 yrs, <I>p</I> = 0.015). On multivariate analysis, only MMP-9 (<I>p</I> = 0.021, 95% CI 1.002–1.027) showed a significant association with IPN. But patients with IPN showed only trend for a history of cardiovascular disease (CVD) (44% versus 30%, <I>p</I> = 0.19) and one-year cardiovascular events (CVE) (6.8% versus 3.3%, <I>p</I> = 0.50) compared to group 1. Maximum plaque thickness (<I>p</I> = 0.04, 95% CI 1.230–6.322) showed a significant correlation with the clinical outcome including CVD or CVE.</P> <P><B>Conclusion</B></P> <P>MMP-9 correlated with IPN on CEUS. For clinical implication, however, large prospective studies are needed.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We examine intraplaque neovascularization using contrast enhanced ultrasound. </LI> <LI> We model correlation between intraplaque neovascularization with biomarkers. </LI> <LI> The factors to affect clinical outcomes would be examined including intraplaque neovascularization. </LI> <LI> Only MMP-9 showed a significant association with intraplaque neovascularization. </LI> <LI> Maximum plaque thickness showed a significant correlation with the clinical outcome. </LI> </UL> </P>
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Hong, Seong Hun,Jang, Hyun Hee,Lee, So Ra,Lee, Kyung Hye,Woo, Jong Shin,Kim, Jin Bae,Kim, Woo-Shik,Min, Byung Il,Cho, Ki Ho,Kim, Kwon Sam,Cheng, Xianwu,Kim, Weon Springer International 2015 Heart and vessels Vol.30 No.1
<P>Lysophosphatidylcholine (LPC) generated from oxidized low-density lipoprotein by lipoprotein-associated phospholipase A2 plays a key role in plaque inflammation and vulnerability. Endothelial progenitor cells (EPCs) can repair injured endothelium and exert anti-inflammatory effects of vulnerable plaque. We study the impact and mechanisms of LPC on UEA-1 and acLDL binding EPCs (UEA-1(+)acLDL(+) EPCs). UEA-1(+)acLDL(+) EPCs from coronary artery disease (CAD) patients were cultured and exposed to LPC at different concentrations and different timepoints. We determined the significant concentration (40 관M). UEA-1(+)acLDL(+) EPCs were preincubated for 30 min with pravastatin (20 관M) with LY249002, a specific inhibitor of the Akt signaling pathway, and exposed for 24 h to LPC 40 관M. The survival, migration, adhesion, and proliferation of UEA-1(+)acLDL(+) EPCs were assessed. To examine the mechanisms of LPC toxicity and pravastatin effects, phosphorylated Akt and endothelial nitric oxide synthase (eNOS) levels and the ratio of Bcl-2/Bax protein expression were assessed. LPC induced apoptosis and impaired migration and adhesion of UEA-1(+)acLDL(+) EPCs significantly. The detrimental effects of LPC were attenuated by pravastatin. However, when UEA-1(+)acLDL(+) EPCs were pretreated with pravastatin and LY249002, a specific inhibitor of the Akt signaling pathway, simultaneously, the beneficial effects of pravastatin were abolished. Furthermore, LPC suppressed Akt and eNOS phosphorylation and increased Bcl-2/Bax expression. The effects of LPC on Akt/eNOS and Bcl-2/Bax activity were reversed by pravastatin. In conclusion, LPC inhibited UEA-1(+)acLDL(+) EPCs survival and impaired its functions, and these were attributable to inhibition of the Akt/eNOS and Bcl-2/Bax pathway. Pravastatin reversed the detrimental action of LPC. These findings suggest that LPC inhibition can be a possible strategy for CAD through EPC revitalization.</P>
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Increased Serum Cathepsin K in Patients with Coronary Artery Disease
Xiang Li,Lan Cui,Yuzi Li,Jiyong Jin,Dehao Jin,Xiangshan Li,Yanna Rei,Haiying Jiang,Guangxian Zhao,Guang Yang,Enbo Zhu,Yongshan Nan,Xianwu Cheng 연세대학교의과대학 2014 Yonsei medical journal Vol.55 No.4
Purpose: Cathepsin K is a potent collagenase implicated in human and animal atherosclerosis-based vascular remodeling. This study examined the hypothesis that serum CatK is associated with the prevalence of coronary artery disease (CAD). Materials and Methods: Between January 2011 and December 2012, 256 consecutive subjects were enrolled from among patients who underwent coronary angiography and percutaneous coronary intervention treatment. A total of 129 age-matched subjects served as controls. Results: The subjects’ serum cathepsin K and high sensitive C-reactive protein (hs-CRP) and high-density lipoprotein cholesterolwere measured. The patients with CAD had significantly higher serum cathepsinK levels compared to the controls (130.8±25.5 ng/mL vs. 86.9±25.5 ng/mL, p<0.001), and the patients with acute coronary syndrome had significantly higher serum cathepsin K levels compared to those with stable angina pectoris (137.1± 26.9 ng/mL vs. 102.6±12.9 ng/mL, p<0.001). A linear regression analysis showed that overall, the cathepsin K levels were inversely correlated with the high-density lipoprotein levels (r=-0.29, p<0.01) and positively with hs-CRP levels (r=0.32, p<0.01). Multiple logistic regression analyses shows that cathepsin K levels were independent predictors of CAD (odds ratio, 1.76; 95% confidence interval, 1.12 to 1.56; p<0.01). Conclusion: These data indicated that elevated levels of cathepsin K are closely associated with the presence of CAD and that circulating cathepsin K serves a useful biomarker for CAD.
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