http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Park, Jonghanne,Hwang, Injoo,Kim, Sung-Jean,Youn, Seock-Won,Hur, Jin,Kim, Hyo-Soo Elsevier 2018 Biochemical and biophysical research communication Vol.495 No.2
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor atorvastatin has been reported to exert vasculo-protective action in diabetes. We investigated the vasculo-protective mechanism of atorvastatin by evaluating its effect on two major pathogenic molecules, FOXO1 and ICAM1, mediated by S-phase kinase-associated protein 2 (Skp2) in diabetic endothelial dysfunction.</P> <P><B>Approach and results</B></P> <P>[1] FOXO1: Hyperglycemic condition increased FOXO1 protein level in endothelial cells, which was reversed by atorvastatin. This atorvastatin effect was obliterated by treatment of protease inhibitor, suggesting that atorvastatin induces degradation of FOXO1. Immunoprecipitation showed that atorvastatin facilitated the binding of Skp2 to FOXO1, leading to ubiquitination and degradation of FOXO1.</P> <P>[2] ICAM-1: Increased ICAM1 in high glucose condition was reduced by atorvastatin. But this effect of atorvastatin was obliterated when Skp2 was inhibited, suggesting that atorvastatin enhances binding of Skp2 to ICAM1 leading to degradation. Actually, ubiquitination and degradation of ICAM-1 were reduced when Skp2 was inhibited. In vitro monocyte adhesion assay revealed that atorvastatin reduced monocyte adhesion on endothelial cells in high glucose condition, which was reversed by Skp2 knock-down.</P> <P><B>Conclusion</B></P> <P>Atorvastatin strengthens Skp2 binding to FOXO1 or ICAM1, leading to ubiquitination and degradation. Skp2-dependent ubiquitination of major pathogenic molecules is the key mechanism for statin's protective effect on endothelial function in diabetes.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The molecular mechanism of statin in diabetes to reduce the endothelial cell (EC) dysfunction and inflammation is proposed. </LI> <LI> In high-glucose exposure, increased FOXO1 and ICAM1 leads to EC dysfunction and increased monocyte adhesion. </LI> <LI> Atorvastatin facilitates ubiquitin-mediated degradation of FOXO1 and ICAM1 through Skp2 in EC exposed to high-glucose. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Lee, Joo Myung,Hwang, Doyeon,Park, Jonghanne,Kim, Kyung-Jin,Ahn, Chul,Koo, Bon-Kwon American Heart Association 2015 Circulation Vol.132 No.5
<P><B>Background—</B></P><P>Emergency coronary artery bypass grafting for unsuccessful percutaneous coronary intervention (PCI) is now rare. We aimed to evaluate the current safety and outcomes of primary PCI and nonprimary PCI at centers with and without on-site surgical backup.</P><P><B>Methods and Results—</B></P><P>We performed an updated systematic review and meta-analysis by using mixed-effects models. We included 23 high-quality studies that compared clinical outcomes and complication rates of 1 101 123 patients after PCI at centers with or without on-site surgery. For primary PCI for ST-segment–elevation myocardial infarction (133 574 patients), all-cause mortality (without on-site surgery versus with on-site surgery: observed rates, 4.8% versus 7.2%; pooled odds ratio [OR], 0.99; 95% confidence interval, 0.91–1.07; <I>P</I>=0.729; <I>I</I><SUP>2</SUP>=3.4%) or emergency coronary artery bypass grafting rates (observed rates, 1.5% versus 2.4%; pooled OR, 0.76; 95% confidence interval, 0.56–1.01; <I>P</I>=0.062; <I>I</I><SUP>2</SUP>=42.5%) did not differ by presence of on-site surgery. For nonprimary PCI (967 549 patients), all-cause mortality (observed rates, 1.6% versus 2.1%; pooled OR, 1.15; 95% confidence interval, 0.94–1.41; <I>P</I>=0.172; <I>I</I><SUP>2</SUP>=67.5%) and emergency coronary artery bypass grafting rates (observed rates, 0.5% versus 0.8%; pooled OR, 1.14; 95% confidence interval, 0.62–2.13; <I>P</I>=0.669; <I>I</I><SUP>2</SUP>=81.7%) were not significantly different. PCI complication rates (cardiogenic shock, stroke, aortic dissection, tamponade, recurrent infarction) also did not differ by on-site surgical capability. Cumulative meta-analysis of nonprimary PCI showed a temporal decrease of the effect size (OR) for all-cause mortality after 2007.</P><P><B>Conclusions—</B></P><P>Clinical outcomes and complication rates of PCI at centers without on-site surgery did not differ from those with on-site surgery, for both primary and nonprimary PCI. Temporal trends indicated improving clinical outcomes in nonprimary PCI at centers without on-site surgery.</P>
Jo, Sang-Ho,Lee, Joo Myung,Park, Jonghanne,Kim, Hyo-Soo S. Karger AG 2015 Cardiology Vol.130 No.1
<P>Abstract</P><P><B><I>Objectives:</I></B> This meta-analysis investigated the impact of renin-angiotensin-aldosterone system (RAAS) blockade on the occurrence of contrast-induced nephropathy (CIN). <B><I>Methods:</I></B> Twelve studies comparing the use of RAAS blockade in a total of 4,493 patients undergoing a contrast-using procedure were included. The primary endpoint was the overall postprocedural incidence of CIN. <B><I>Results:</I></B> In the overall pooled analysis, there was no significant difference between the two groups, RAAS blockade ‘used' versus ‘not-used', in the incidence of postprocedural CIN in the random-effects model (OR 1.27, 95% CI 1.77-2.11, p = 0.351, I<SUP>2</SUP> = 61.9%). In the stratified analysis, however, for chronic RAAS blockade users, the continuation of the drug was significantly associated with a higher incidence of CIN compared with discontinuation (OR 2.06, 95% CI 1.62-2.61, p < 0.001, I<SUP>2</SUP> = 0.0%). A hazard of continuation was marked in a subgroup of older patients or in patients with chronic kidney disease. For drug-naïve patients, however, administration of RAAS blockade before contrast procedures did not reduce the development of CIN significantly (OR 0.52, 95% CI 0.23-1.16, p = 0.108, I<SUP>2</SUP> = 34.2%). <B><I>Conclusion:</I></B> Discontinuation of RAAS blockade in chronic users is associated with a significantly lower incidence of CIN, whereas administration of RAAS blockade as a preventive measure for naïve patients did not show a significant effect on the incidence of CIN.</P><P>© 2014 S. Karger AG, Basel</P>
Lee, Joo Myung,Kim, Hyun Kuk,Lim, Kyung Seob,Park, Jun-Kyu,Choi, Ki Hong,Park, Jonghanne,Hwang, Doyeon,Rhee, Tae-Min,Yang, Jeong Hoon,Shin, Eun-Seok,Nam, Chang-Wook,Doh, Joon-Hyung,Hahn, Joo-Yong,Koo, Elsevier 2018 JACC. Cardiovascular interventions Vol.11 No.8
<P><B>Abstract</B></P> <P><B>Objectives</B></P> <P>The aim of this study was to investigate the influence of microvascular damage in one vessel territory on invasively measured physiological parameters in the other vessel, using a porcine microvascular damage model.</P> <P><B>Background</B></P> <P>Although fractional flow reserve (FFR)-guided decision-making for the nonculprit stenosis in patients with acute myocardial infarction has been reported to be better than angiography-guided revascularization, there have been debates regarding the influence of microvascular dysfunction on measured FFR in nonculprit vessels.</P> <P><B>Methods</B></P> <P>In Yorkshire swine, microvascular damage was induced with selective intracoronary injection of microspheres (100 μm × 10<SUP>5</SUP> each) into the left anterior descending artery (LAD). Coronary stenosis was created in both the LAD and the left circumflex artery (LCx) using balloon catheters. Coronary physiological changes were assessed with index of microcirculatory resistance (IMR) and FFR at baseline and at each subsequent injection of microsphere up to a fifth dose in both the LAD and LCx. Measurements were repeated 5 times at each stage, and a total of 424 measurements were made in 12 Yorkshire swine models.</P> <P><B>Results</B></P> <P>The median area stenosis in LAD and LCx was 48.1% (interquartile range: 40.8% to 50.4%) and 47.9% (interquartile range: 31.1% to 62.9%), respectively. At baseline, FFR in the LAD was lower than that in the LCx (0.89 ± 0.01 and 0.94 ± 0.01; p < 0.001). There was no difference in the IMR (18.4 ± 5.8 U and 17.9 ± 1.2 U; p = 0.847). With repeated injections of microspheres, IMR in LAD was significantly increased, up to 77.7 ± 15.7 U (p < 0.001). Given the same stenosis, FFR in the LAD was also significantly increased, up to 0.98 ± 0.01 along with IMR increase (p < 0.001). Conversely, IMR and FFR were not changed in the LCx throughout repeated injury to the LAD territory (p = 0.105 and p = 0.286 for IMR and FFR, respectively). The increase in LAD IMR was mainly driven by the increase in hyperemic mean transit time (p < 0.001).</P> <P><B>Conclusions</B></P> <P>In Yorkshire swine models, local microvascular damage increased both FFR and IMR in a vessel supplying target myocardial territory. However, IMR and FFR were maintained in the other vessel. These physiological results in swine support the concept that FFR measurement might provide useful information for evaluating nonculprit lesions in clinical settings involving significant acute myocardial injury.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Lim, Woo-Hyun,Seo, Won-Woo,Choe, Wonseok,Kang, Chan-Koo,Park, Jonghanne,Cho, Hyun-Ju,Kyeong, San,Hur, Jin,Yang, Han-Mo,Cho, Hyun-Jai,Lee, Yoon-Sik,Kim, Hyo-Soo The Association 2011 Arteriosclerosis, thrombosis, and vascular biology Vol.31 No.12
<P>In contrast to CD34, vascular endothelial-cadherin (VE-cadherin) is exclusively expressed on the late endothelial progenitor cells (EPC) whereas not on the early or myeloid EPC. Thus, VE-cadherin could be an ideal target surface molecule to capture circulating late EPC. In the present study, we evaluated whether anti-VE-cadherin antibody-coated stents (VE-cad stents) might accelerate endothelial recovery and reduce neointimal formation through the ability of capturing EPC.</P>
Lee, Joo Myung,Bang, Ji-In,Koo, Bon-Kwon,Hwang, Doyeon,Park, Jonghanne,Zhang, Jinlong,Yaliang, Tong,Suh, Minseok,Paeng, Jin Chul,Shiono, Yasutsugu,Kubo, Takashi,Akasaka, Takashi American Heart Association, Inc. 2017 Circulation. Cardiovascular imaging Vol.10 No.11
<P>Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02388412.</P>
The Effects of Preoperative Aspirin on Coronary Artery Bypass Surgery: a Systematic Meta-Analysis
Doyeon Hwang,Joo Myung Lee,Tae-Min Rhee,Young-Chan Kim,Jiesuck Park,Jonghanne Park,Chul Ahn,Young Bin Song,Joo-Yong Hahn,Ki-Bong Kim,Young-Tak Lee,Bon-Kwon Koo 대한심장학회 2019 Korean Circulation Journal Vol.49 No.6
Background and ObjectivesAspirin plays an important role in the maintenance of graft patency and the prevention of thrombotic event after coronary artery bypass graft surgery (CABG). However, the use of preoperative aspirin is still under debate due to the risk of bleeding. MethodsFrom PubMed, EMBASE, and Cochrane Central Register of Controlled Trials, data were extracted by 2 independent reviewers. Meta-analysis using random effect model was performed. ResultsWe performed a systemic meta-analysis of 17 studies (12 randomized controlled studies and 5 non-randomized registries) which compared clinical outcomes of 9,101 patients who underwent CABG with or without preoperative aspirin administration. Preoperative aspirin increased chest tube drainage (weighted mean difference 177.4 mL, 95% confidence interval [CI], 41.3–313.4; p=0.011). However, the risk of re-operation for bleeding was not different between the preoperative aspirin group and the control group (3.2% vs. 2.4%; odds ratio [OR], 1.23; 95% CI, 0.94–1.60; p=0.102). There was no difference in the rates of all-cause mortality (1.6% vs. 1.5%; OR, 0.98; 95% CI, 0.64–1.49; p=0.920) and myocardial infarction (MI) (8.7% vs. 10.4%; OR, 0.83; 95% CI, 0.66–1.04; p=0.102) between patients with and without preoperative aspirin administration. ConclusionsAlthough aspirin increased the amount of chest tube drainage, it was not associated with increased risk of re-operation for bleeding. In addition, the risks of early postoperative all-cause mortality and MI were not reduced by using preoperative aspirin.
Prognostic Impact of β-Blocker Dose After Acute Myocardial Infarction
Hwang, Doyeon,Lee, Joo Myung,Kim, Hyun Kuk,Choi, Ki Hong,Rhee, Tae-Min,Park, Jonghanne,Park, Taek Kyu,Yang, Jeong Hoon,Song, Young Bin,Choi, Jin-Ho,Hahn, Joo-Yong,Choi, Seung-Hyuk,Koo, Bon-Kwon,Kim, Y UNKNOWN 2019 CIRCULATION JOURNAL Vol.83 No.2
Hwang, In-Chang,Kim, Ju-Young,Kim, Ji-Hyun,Lee, Joo-Eun,Seo, Ji-Yun,Lee, Jae-Won,Park, Jonghanne,Yang, Han-Mo,Kim, Soon-Ha,Cho, Hyun-Jai,Kim, Hyo-Soo Lippincott, WilliamsWilkins 2018 Hypertension Vol.71 No.6
<▼1><P>Supplemental Digital Content is available in the text.</P></▼1><▼2><P>Opening of mitochondrial permeability transition pore and Ca<SUP>2+</SUP> overload are main contributors to myocardial ischemia–reperfusion injury, which paradoxically causes a wide variety of myocardial damage. We investigated the protective role of a novel necrosis inhibitor (NecroX-7; NecX) against myocardial ischemia–reperfusion injury using in vitro and in vivo models. H9C2 rat cardiomyoblasts and neonatal cardiomyocytes were exposed to hypoxia–reoxygenation stress after pre-treatment with NecX, vitamin C, a combination of vitamin C and E, N-acetylcysteine, an apoptosis inhibitor (Z-VAD-fmk), or cyclosporine A. The main mechanism of cell death after hypoxia–reoxygenation stress was not apoptosis but necrosis, which was prevented by NecX. Protective effect of NecX was based on its potent reactive oxygen species scavenging activity, especially on mitochondrial reactive oxygen species. NecX preserved mitochondrial membrane potential through prevention of Ca<SUP>2+</SUP> influx and inhibition of mitochondrial permeability transition pore opening, which was more potent than that by cyclosporine A. Using Sprague-Dawley rats exposed to myocardial ischemia for 45 minutes followed by reperfusion, we compared therapeutic efficacies of NecX with cyclosporine A, vitamin C, a combination of vitamin C and E, and 5% dextrose, each administered 5 minutes before reperfusion. NecX markedly inhibited myocardial necrosis and reduced fibrotic area to a greater extent than did cyclosporine A and other treated groups. In addition, NecX preserved systolic function and prevented pathological dilatory remodeling of left ventricle. The novel necrosis inhibitor has a significant protective effect against myocardial ischemia–reperfusion injury through inhibition of mitochondrial permeability transition pore opening, indicating that it is a promising candidate for cardioprotective adjunctive measure on top of reperfusion therapy.</P></▼2>