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Search Results: 1 - 10 of 21638 matches for " Hyo-Soo Kim "
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Integrin-linked Kinase: It's Role in the Vascular System
Seung-Pyo Lee,Seock-Won Youn,Hyo-Soo Kim
International Journal of Biomedical Science , 2007,
Abstract: Integrin-linked kinase (ILK) is an intracellular molecule that binds to the cytoplasmic domain of β1 and β3-integrin. It has been previously demonstrated in various epithelial cell lines to mediate the ‘outside-in’ signals into the cells and to control the survival of these cells by controlling the phosphorylation of various downstream proteins, such as protein kinase B/Akt (PKB/Akt). We now present in this review the important role of ILK in the vascular system with particular emphasis on its role in endothelial cells (ECs). The results presented here demonstrate that ILK is essential for the proper function, structure and survival of ECs and finally, for the process of neovascularization.
A multicenter, prospective, randomized, controlled trial evaluating the safety and efficacy of intracoronary cell infusion mobilized with granulocyte colony-stimulating factor and darbepoetin after acute myocardial infarction: study design and rationale of the 'MAGIC cell-5-combination cytokine trial'
Hyun-Jae Kang, Min-Kyung Kim, Myung-Gon Kim, Dong-Ju Choi, Jung-Han Yoon, Young-Bae Park, Hyo-Soo Kim
Trials , 2011, DOI: 10.1186/1745-6215-12-33
Abstract: The 'MAGIC Cell-5-Combination Cytokine Trial' is a multicenter, prospective, randomized, 3-arm, controlled trial with blind evaluation of the endpoints. A total of 116 patients will randomly receive one of the following three treatments: an intravenous darbepoetin infusion and intracoronary infusion of peripheral blood stem cells mobilized with G-CSF (n = 58), an intracoronary infusion of peripheral blood stem cells mobilized with G-CSF alone (n = 29), or conventional therapy (n = 29) at phase I. Patients with left ventricular ejection fraction < 45% at 6 months, in the patients who received stem cell therapy at phase I, will receive repeated cell therapy at phase II. The objectives of this study are to evaluate the safety and efficacy of combination cytokine therapy with erythropoietin and G-CSF (phase I) and repeated progenitor/stem cell treatment (phase II).This is the first study to evaluate the safety and efficacy of combination cytokine based progenitor/stem cell treatment.http://www.ClinicalTrials.gov webcite identifier: NCT00501917.Recent clinical trials reported favorable effects of stem/progenitor cell transplantation in patients with acute myocardial infarction (AMI), suggesting that stem cell transplantation is feasible, safe, and effective for improvement of left ventricular (LV) systolic function and myocardial perfusion [1-3]. Granulocyte colony-stimulating factor (G-CSF) alone is mostly ineffective for improvement of LV systolic function [4]. But G-CSF is effective for stem/progenitor cell mobilization and local delivery of mobilized stem/progenitor cell by G-CSF improved cardiac function in patients with myocardial infarction [2,3,5-8]. However, degree of improvement by G-CSF based stem/progenitor cell therapy is modest and similar to that of bone marrow stem cell therapy. There are reasonable explanations of limited efficacy of current stem/progenitor cell therapy using G-CSF, such as, low homing-efficiency, poor long-term survival of infused stem/
Comparative Study of Efficacy of Dopaminergic Neuron Differentiation between Embryonic Stem Cell and Protein-Based Induced Pluripotent Stem Cell
Yoo-Wook Kwon, Yeon-Ju Chung, Joonoh Kim, Ho-Jae Lee, Jihwan Park, Tae-Young Roh, Hyun-Jai Cho, Chang-Hwan Yoon, Bon-Kwon Koo, Hyo-Soo Kim
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0085736
Abstract: In patients with Parkinson's disease (PD), stem cells can serve as therapeutic agents to restore or regenerate injured nervous system. Here, we differentiated two types of stem cells; mouse embryonic stem cells (mESCs) and protein-based iPS cells (P-iPSCs) generated by non-viral methods, into midbrain dopaminergic (mDA) neurons, and then compared the efficiency of DA neuron differentiation from these two cell types. In the undifferentiated stage, P-iPSCs expressed pluripotency markers as ES cells did, indicating that protein-based reprogramming was stable and authentic. While both stem cell types were differentiated to the terminally-matured mDA neurons, P-iPSCs showed higher DA neuron-specific markers' expression than ES cells. To investigate the mechanism of the superior induction capacity of DA neurons observed in P-iPSCs compared to ES cells, we analyzed histone modifications by genome-wide ChIP sequencing analysis and their corresponding microarray results between two cell types. We found that Wnt signaling was up-regulated, while SFRP1, a counter-acting molecule of Wnt, was more suppressed in P-iPSCs than in mESCs. In PD rat model, transplantation of neural precursor cells derived from both cell types showed improved function. The present study demonstrates that P-iPSCs could be a suitable cell source to provide patient-specific therapy for PD without ethical problems or rejection issues.
Additive Value of B-Type Natriuretic Peptide on Rest -Dipyridamole Stress -Sestamibi Gated Myocardial SPECT in Patients with Normal Left Ventricular Systolic Function
Jung-Ju Sir,Young-Seok Cho,Woo-Young Chung,Bon-Kwon Koo,In-Ho Chae,Dong-Ju Choi,Hyo-Soo Kim,Byung-Hee Oh,Young-Bae Park
Cardiology Research and Practice , 2010, DOI: 10.4061/2010/642045
Abstract: We evaluated whether BNP has additive value to SPECT in patients with normal left ventricular (LV) systolic function. Data from 224 consecutive patients who underwent rest -dipyridamole stress -sestamibi gated SPECT and coronary angiography due to chest pain were analyzed. Patients with true positive SPECT showed significant higher BNP level than those with false positive defect (38.5 (19.0–79.8) versus 19.0 (9.3–35.8), ). Patients with true negative SPECT also showed significantly lower BNP level than those with false negative SPECT (39.0 (23.0–77.0) versus 22.0 (15.0–43.0), ). In multivariate analyses, elevated BNP level (using a cut-off value of 23.0?pg/mL) was the strongest and independent predictor of CAD in overall patients (OR 2.75, 95% CI: 1.50–5.023, ) and patients with positive SPECT (OR 3.34, 95% CI: 1.51–7.37, ). The area under the receiver-operating characteristic curve for CAD in overall patients and patients with positive SPECT was 0.673 (95% CI: 0.603–0.743, ) and 0.694 (95% CI: 0.602–0.786, ), respectively. This study suggests that BNP level has additive diagnostic value to SPECT findings in predicting CAD in patients with normal LV systolic function. 1. Introduction Previous studies have reported that B-type natriuretic peptide (BNP), synthesized as pre-proBNP mainly in the ventricular myocardium and secreted in response to ventricular volume and pressure overload, has close relation with angiographic severity and could be a potential biomarker for myocardial ischemia even in patients with preserved LV systolic function [1–4]. In patients with coronary artery disease, myocardial ischemia may cause transient left ventricular (LV) systolic and diastolic dysfunction and consequently increase LV wall stress, leading to elevated plasma natriuretic peptide level or directly promotes the release of natriuretic peptide independent from left ventricular wall stress [5, 6]. Recently, it was discovered that natriuretic peptides are associated with exercise-induced myocardial ischemia in patients with coronary artery disease and BNP level at rest can significantly improve diagnostic power of treadmill test in patients with suspected coronary artery disease and normal left ventricular ejection fraction [7–11]. Stress myocardial perfusion imaging is also widely used noninvasive modality for the diagnosis and risk stratification of patients with suspected myocardial ischemia [12, 13]. The incidence of myocardial perfusion abnormalities at rest or during stress is a hallmark of coronary artery disease [14]. The sensitivity of stress technetium-99m
Peroxisome Proliferator-Activated Receptor-Gamma Agonists Suppress Tissue Factor Overexpression in Rat Balloon Injury Model with Paclitaxel Infusion
Jun-Bean Park, Baek-Kyung Kim, Yoo-Wook Kwon, Dominik N. Muller, Hyun-Chae Lee, Seock-Won Youn, Young-Eun Choi, Sae-Won Lee, Han-Mo Yang, Hyun-Jai Cho, Kyung Woo Park, Hyo-Soo Kim
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0028327
Abstract: The role and underlying mechanisms of rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist, on myocardial infarction are poorly understood. We investigated the effects of this PPAR-γ agonist on the expression of tissue factor (TF), a primary molecule for thrombosis, and elucidated its underlying mechanisms. The PPAR-γ agonist inhibited TF expression in response to TNF-α in human umbilical vein endothelial cells, human monocytic leukemia cell line, and human umbilical arterial smooth muscle cells. The overexpression of TF was mediated by increased phosphorylation of mitogen-activated protein kinase (MAPK), which was blocked by the PPAR-γ agonist. The effective MAPK differed depending on each cell type. Luciferase and ChIP assays showed that transcription factor, activator protein-1 (AP-1), was a pivotal target of the PPAR-γ agonist to lower TF transcription. Intriguingly, two main drugs for drug-eluting stent, paclitaxel or rapamycin, significantly exaggerated thrombin-induced TF expression, which was also effectively blocked by the PPAR-γ agonist in all cell types. This PPAR-γ agonist did not impair TF pathway inhibitor (TFPI) in three cell types. In rat balloon injury model (Sprague-Dawley rats, n = 10/group) with continuous paclitaxel infusion, the PPAR-γ agonist attenuated TF expression by 70±5% (n = 4; P<0.0001) in injured vasculature. Taken together, rosiglitazone reduced TF expression in three critical cell types involved in vascular thrombus formation via MAPK and AP-1 inhibitions. Also, this PPAR-γ agonist reversed the paclitaxel-induced aggravation of TF expression, which suggests a possibility that the benefits might outweigh its risks in a group of patients with paclitaxel-eluting stent implanted.
Vascular Calcifying Progenitor Cells Possess Bidirectional Differentiation Potentials
Hyun-Ju Cho equal contributor,Hyun-Jai Cho equal contributor,Ho-Jae Lee,Myung-Kang Song,Ji-Yun Seo,Yeon-Hee Bae,Ju-Young Kim,Hae-Young Lee,Whal Lee,Bon-Kwon Koo,Byung-Hee Oh,Young-Bae Park,Hyo-Soo Kim
PLOS Biology , 2013, DOI: 10.1371/journal.pbio.1001534
Abstract: Vascular calcification is an advanced feature of atherosclerosis for which no effective therapy is available. To investigate the modulation or reversal of calcification, we identified calcifying progenitor cells and investigated their calcifying/decalcifying potentials. Cells from the aortas of mice were sorted into four groups using Sca-1 and PDGFRα markers. Sca-1+ (Sca-1+/PDGFRα+ and Sca-1+/PDGFRα?) progenitor cells exhibited greater osteoblastic differentiation potentials than Sca-1? (Sca-1?/PDGFRα+ and Sca-1?/PDGFRα?) progenitor cells. Among Sca-1+ progenitor populations, Sca-1+/PDGFRα? cells possessed bidirectional differentiation potentials towards both osteoblastic and osteoclastic lineages, whereas Sca-1+/PDGFRα+ cells differentiated into an osteoblastic lineage unidirectionally. When treated with a peroxisome proliferator activated receptor γ (PPARγ) agonist, Sca-1+/PDGFRα? cells preferentially differentiated into osteoclast-like cells. Sca-1+ progenitor cells in the artery originated from the bone marrow (BM) and could be clonally expanded. Vessel-resident BM-derived Sca-1+ calcifying progenitor cells displayed nonhematopoietic, mesenchymal characteristics. To evaluate the modulation of in vivo calcification, we established models of ectopic and atherosclerotic calcification. Computed tomography indicated that Sca-1+ progenitor cells increased the volume and calcium scores of ectopic calcification. However, Sca-1+/PDGFRα? cells treated with a PPARγ agonist decreased bone formation 2-fold compared with untreated cells. Systemic infusion of Sca-1+/PDGFRα? cells into Apoe?/? mice increased the severity of calcified atherosclerotic plaques. However, Sca-1+/PDGFRα? cells in which PPARγ was activated displayed markedly decreased plaque severity. Immunofluorescent staining indicated that Sca-1+/PDGFRα? cells mainly expressed osteocalcin; however, activation of PPARγ triggered receptor activator for nuclear factor-κB (RANK) expression, indicating their bidirectional fate in vivo. These findings suggest that a subtype of BM-derived and vessel-resident progenitor cells offer a therapeutic target for the prevention of vascular calcification and that PPARγ activation may be an option to reverse calcification.
Study design and rationale of 'Influence of Cilostazol-based triple anti-platelet therapy on ischemic complication after drug-eluting stent implantation (CILON-T)' study: A multicenter randomized trial evaluating the efficacy of Cilostazol on ischemic vascular complications after drug-eluting stent implantation for coronary heart disease
Seung-Pyo Lee, Jung-Won Suh, Kyung Woo Park, Hae-Young Lee, Hyun-Jae Kang, Bon-Kwon Koo, In-Ho Chae, Dong-Ju Choi, Seung-Woon Rha, Jang-Whan Bae, Myeong-Chan Cho, Taek-Geun Kwon, Jang-Ho Bae, Hyo-Soo Kim, CILON-T investigators
Trials , 2010, DOI: 10.1186/1745-6215-11-87
Abstract: CILON-T trial was a prospective, randomized, open-label, multi-center, near-all-comer trial to demonstrate the superiority of triple anti-platelet therapy to dual anti-platelet therapy in reducing 6 months' major adverse cardiovascular/cerebrovascular events, composite of cardiac death, nonfatal myocardial infarction, target lesion revascularization and ischemic stroke. It also tested whether triple anti-platelet therapy is superior to dual anti-platelet therapy in inhibiting platelet reactivity in patients receiving percutaneous coronary intervention with drug-eluting stent. Total 960 patients were randomized to receive either dual anti-platelet therapy or triple anti-platelet therapy for 6 months and also, randomly stratified to either lipophilic statin (atorvastatin) or non-lipophilic statin (rosuvastatin) indefinitely. Secondary endpoints included all components of major adverse cardiovascular/cerebrovascular events, platelet reactivity as assessed by VerifyNow P2Y12 assay, effect of statin on major adverse cardiovascular/cerebrovascular events, bleeding complications, and albumin-to-creatinine ratio to test the nephroprotective effect of cilostazol. Major adverse cardiovascular/cerebrovascular events will also be checked at 1, 2, and 3 years to test the 'legacy' effect of triple anti-platelet therapy that was prescribed for only 6 months after percutaneous coronary intervention.CILON-T trial will give powerful insight into whether triple anti-platelet therapy is superior to dual anti-platelet therapy in reducing ischemic events and platelet reactivity in the real-world unselected patients treated with drug-eluting stent for coronary heart disease. Also, it will verify the laboratory and clinical significance of drug interaction between lipophilic statin and clopidogrel.National Institutes of Health Clinical Trials Registry (ClinicalTrials.gov identifier# NCT00776828).Current guidelines recommend at least 6 months of dual anti-platelet agents, consisting of aspi
Paraoxonase 1 Gene Polymorphism Does Not Affect Clopidogrel Response Variability but Is Associated with Clinical Outcome after PCI
Kyung Woo Park, Jin Joo Park, Jeehoon Kang, Ki-Hyun Jeon, Si-Hyuck Kang, Jung-Kyu Han, Sang Eun Lee, Han-Mo Yang, Hae-Young Lee, Hyun-Jae Kang, Bon-Kwon Koo, Byung-Hee Oh, Young-Bae Park, Hyo-Soo Kim
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0052779
Abstract: Background Paraoxonase (PON) is a high-density-lipoprotein (HDL) associated enzyme with antioxidative and anti-atherogenic property. Its function is associated with coronary artery disease and its activity genetically controlled. We evaluated whether genetic variation of PON-1 is associated with clinical outcome in a large cohort of Korean patients with drug-eluting stents implantation. Methods A total of 1676 patients with drug-eluting stent implantation were enrolled in the prospective CROSS-VERIFY cohort from June 2006 to June 2010. We genotyped the PON1-Q192R gene, measured clopidogrel on-treatment platelet reactivity (OPR), and analyzed lipid profiles. The primary endpoint was the composite of cardiac death, myocardial infarction, and stent thrombosis at 12 months. Results PON-1 genotyping data were available in 1336 patients. Since the Q-allele is associated with decreased PON-activity, we analyzed the outcome between patients with QQ/QR (815 patients, 61%) and those with RR-genotype (521 patients, 39%). After adjustment for common cardiac risk factors, the QQ/QR-genotype was an independent predictor of the primary thrombotic endpoint with an 11-fold increased risk (HR 11.6, 95% CI: 1.55–87.0), but not repeat revascularization (HR 1.12, 95% CI: 0.78–1.61). The QQ/QR-genotype was not associated with OPR (QQ/QR: 231±86 PRU vs. RR 236±82 PRU, p = 0.342) but higher small-dense LDL levels (1.20±0.12 mg/dL vs. 0.76±0.15 mg/dL, p = 0.027). The increased risk of thrombotic outcomes was more profound in acute coronary syndrome (ACS) patients compared with non-ACS patients. Conclusion PON1 Q-allele is an independent predictor of worse cardiovascular outcome independent of platelet function and is associated with significantly higher levels of small dense LDL-C.
Efficacies of the new Paclitaxel-eluting Coroflex Please? Stent in percutaneous coronary intervention; comparison of efficacy between Coroflex Please? and Taxus? (ECO-PLEASANT) trial: study rationale and design
Jae-Bin Seo, Hui-Kyung Jeon, Kyung-Woo Park, Jong-Seon Park, Jang-Ho Bae, Sang-Wook Kim, Keon-Woong Moon, Jae-Woong Choi, Sang-Gon Lee, Woo-Young Chung, Tae-Jin Youn, Soo-Joong Kim, Doo-Il Kim, Byung-Ok Kim, Min-Su Hyon, Keum-Soo Park, Tae-Joon Cha, Hweung-Kon Hwang, Seung-Ho Hur, Hyo-Soo Kim
Trials , 2009, DOI: 10.1186/1745-6215-10-98
Abstract: In the comparison of Efficacy between COroflex PLEASe? ANd Taxus? stent(ECO-PLEASANT) trial, approximately 900 patients are being prospectively and randomly assigned to the either type of Coroflex Please? stent and Taxus Liberte? stent via web-based randomization. The primary endpoint is clinically driven target vessel revascularization at 9 months. The secondary endpoints include major cardiac adverse events, target vessel failure, stent thrombosis and angiographic efficacy endpoints.The ECO-PLEASANT trial is the study not yet performed to directly compare the efficacy and safety of the Coroflex Please? versus Taxus Liberte? stent. On the basis of this trial, we will be able to find out whether the Coroflex Please? stent is non-inferior to Taxus Liberte? stent or not.ClinicalTrials.gov number, NCT00699543.Previous randomized trials have shown the efficacy of a slow-release polymeric sirolimus-eluting stent (Cypher?, Cordis, Warren, NJ, USA), paclitaxel-eluting stent (Taxus?, Boston Scientific, Natick, MA, USA), and zotarolimus-eluting stent (Endeavor?, Medtronic, Minneapolis, MN, USA) over bare metal stents in reducing neointimal hyperplasia, late luminal loss, and angiographic restenosis leading to decreased target lesion revascularization [1-11] The Paclitaxel-eluting Coroflex Please? stent is a newly developed drug eluting stent using the Coroflex? stent platform combined with the drug paclitaxel contained in a polymer coating[12]In the PECOPS I, which was one-arm observational study, the results of Coroflex Please? stent were within the range of other Paclitaxel-eluting coronary stents [12,13] Compared with binary restenosis rate of 7.9% in Taxus IV trial, Coroflex? Please stent showed 7.8% of restenosis rate[7] The 3.1% of 30 day MACE rate is within the range of other trials with stents eluting Paclitaxel or Sirolimus. The 6 month MACE rates in PECOPS I were 8.0%, which was similar to 7.8%, and 8.5% in Taxus II MR and SR, respectively[6] In Taxus IV, 9 month f
Carriage of the V279F Null Allele within the Gene Encoding Lp-PLA2 Is Protective from Coronary Artery Disease in South Korean Males
Yangsoo Jang,Dawn Waterworth,Jong-Eun Lee,Kijoung Song,Sujin Kim,Hyo-Soo Kim,Kyung Woo Park,Hyun-Jai Cho,Il-Young Oh,Jeong Euy Park,Bok-Soo Lee,Hyo Jeong Ku,Dong-Jik Shin,Jong Ho Lee,Sun Ha Jee,Bok-Ghee Han,Hye-Yoon Jang,Eun-Young Cho,Patrick Vallance,John Whittaker,Lon Cardon,Vincent Mooser
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018208
Abstract: The Asia-specific PLA2G7 994G-T transversion leads to V279F substitution within the lipoprotein-associated phospholipase-A2 (Lp-PLA2) and to absence of enzyme activity in plasma. This variant offers a unique natural experiment to assess the role of Lp-PLA2 in the pathogenesis of coronary artery disease (CAD) in humans. Given conflicting results from mostly small studies, a large two-stage case-control study was warranted.
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