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Lee, J.M.,Park, J.,Kang, J.,Jeon, K.H.,Jung, J.h.,Lee, S.E.,Han, J.K.,Kim, H.L.,Yang, H.M.,Park, K.W.,Kang, H.J.,Koo, B.K.,Kim, S.H.,Kim, H.S. Elsevier/North-Holland Biomedical Press 2015 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.184 No.-
Background: Studies have reported conflicting results regarding efficacy of mechanical hemodynamic support using intra-aortic balloon pump (IABP) or percutaneous ventricular assisted device (pVAD) in patients undergoing high-risk PCI. We performed a Bayesian network meta-analysis comparing the safety and efficacy of mechanical hemodynamic support devices and medical therapy (MT). Methods and results: RCTs comparing overall mortality of IABP versus MT or IABP versus pVAD in high-risk PCI populations were included. The primary endpoint was overall mortality, using the longest available follow-up in each study. This analysis included 2843 patients from 13 trials. In network meta-analysis, overall survival benefit was not significant with IABP (RR 0.84, 95% CrI 0.56-1.24) or pVAD (RR 0.95, 95% CrI 0.42-2.06), compared with MT. IABP or pVAD also did not show early survival benefit compared with MT. In terms of bleeding, pVAD was the worst (versus IABP: RR 29.4, 95% CrI 5.99-221.0; versus MT: RR 41.7, 95% CrI 8.19-330.0), which was mainly driven by the higher incidence of bleeding in the ECMO and TandemHeart, while IABP was worse than MT (RR 1.41, 95% CrI 1.01-2.08). The incidence of acute limb ischemia or vascular complication was not different between treatment groups. Conclusions: In this meta-analysis, routine elective use of IABP or pVAD did not reduce mortality, while it increased bleeding, compared with MT in high-risk PCI population or even in the patients with cardiogenic shock. Thoughtful selection of appropriate patients and balancing the risk and benefit should be the prerequisites to the use of mechanical hemodynamic support devices.
Lee, S.H.,Moon, S.J.,Park, M.J.,Kim, E.K.,Moon, Y.M.,Cho, M.L. Elsevier/North-Holland Biomedical Press 2014 IMMUNOLOGY LETTERS Vol.160 No.1
Graft-versus-host disease (GVHD) caused by transplanted donor T cells remains the major obstacle of allogeneic bone marrow transplantation (BMT). Previous reports have suggested that IL-17-producing helper T (Th17) cells mediate the development of acute GVHD (aGVHD). Protein inhibitor of activated STAT3 (PIAS) inhibits the activity of the transcription factor STAT3, which is a pivotal transcription factor for Th17 differentiation. To elucidate whether PIAS3 could inhibit the development of aGVHD, pcDNA-PIAS3 or mock vector was administered in a murine model of aGVHD by intramuscular injection and subsequent electroporation. The results demonstrated that PIAS3 overexpression by pcDNA-vector administration significantly attenuated the clinical severity and histopathological severities of aGHVD involving the skin, liver, intestine, and lung. Additionally, the STAT3 activities in aGVHD target organs were suppressed by PIAS3 overexpression. Furthermore, phosphorylated (p) STAT3 activity in the spleen was profoundly attenuated in PIAS3-overexpressing GVHD mice. Interestingly, flow cytometric analysis demonstrated that the populations of CD21<SUP>high</SUP>CD23<SUP>low</SUP> marginal zone B cells were dramatically expanded in PIAS3-overexpressing mice. PIAS3-induced inhibition of aGVHD was largely related to the downregulation of Th1 and Th17 and the upregulation of Th2 and Treg populations. Both populations of pSTAT3<SUP>Tyr705</SUP>-expressing Th17 cells and B cells were significantly reduced in the spleens of PIAS3-overexpressing mice, whereas pSTAT5 activity was increased. In addition to CD4<SUP>+</SUP>CD25<SUP>+</SUP>Foxp3<SUP>+</SUP> Treg cells, the populations of CD8<SUP>+</SUP>CD25<SUP>+</SUP>Foxp3<SUP>+</SUP> Treg cells were also expanded by treatment with PIAS3. These data suggest the therapeutic potential of PIAS3 in the development of aGVHD through reciprocal regulation of Th17/Treg lineages.
Predictors of recurrent sudden cardiac death in patients associated with coronary vasospasm
Lee, K.H.,Park, H.W.,Cho, J.G.,Yoon, N.S.,Kim, S.S.,Rhew, S.H.,Jeong, Y.W.,Jang, S.Y.,Cho, J.Y.,Jeong, H.C.,Park, K.H.,Sim, D.S.,Yoon, H.J.,Kim, K.H.,Hong, Y.J.,Kim, J.H.,Ahn, Y.,Jeong, M.H.,Park, J.C Elsevier/North-Holland Biomedical Press 2014 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.172 No.2
Novel self-expandable, stent-based transcatheter pulmonic valve: A preclinical animal study
Kim, G.B.,Lim, H.G.,Kim, Y.J.,Choi, E.Y.,Kwon, B.S.,Jeong, S. Elsevier/North-Holland Biomedical Press 2014 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.173 No.1
Background: Because transcatheter implantation of pulmonary valve is indicated for limited-size dysfunctional right ventricular outflow tract only as a balloon-expandable stent, we investigated the feasibility of a large-diameter self-expandable valved stent and the durability of the valve after >6months. Methods: We made a nitinol-wire-based, self-expandable valved stent with leaflets made from porcine pericardium. The porcine pericardium was treated with α-galactosidase, glutaraldehyde, and glycine after decellularization. After cutting the inguinal or cervical area, we implanted a valved stent in 12 sheep through the femoral or jugular vein by using an 18-Fr delivery catheter, controlling the catheter handles and hook block under fluoroscopic and echocardiographic guidance. Results: The mean body weight of sheep was 43.9kg. We successfully implanted valved stents (diameter: 24mm in 7 sheep, 26mm in 5 sheep) in good position in 8 sheep, in the main pulmonary artery (PA) in 2 sheep, and in the right ventricular outlet tract (RVOT) in 2 sheep. We sacrificed 8 sheep (6 sheep in good position, 1 sheep in the main PA, and 1 sheep in the RVOT) after >6months. Five of the 6 sheep implanted in good position showed well-preserved valve morphology at the time of sacrifice. Histologic findings after routine sacrifice showed well-maintained collagen wave structure and no visible calcification in all explanted valve leaflets. Conclusions: Transcatheter implantation of a nitinol-wire-based, self-expandable valved stent in the pulmonic valve was feasible, and stents implanted in good position showed well-preserved valve leaflets with functional competence in the mid-term results.
Ha, C.H.,Kim, S.,Chung, J.,An, S.H.,Kwon, K. Elsevier/North-Holland Biomedical Press 2013 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.168 No.4
Background: Extracorporeal shock wave has been used in the noninvasive treatment of various diseases including musculoskeletal disorders. In particular, shock wave with low energy level showed anti-inflammatory effect and increased angiogenesis in ischemic tissues. However, the detailed cellular pathway in endothelial signaling is not fully understood. We investigate the role of shock wave with low energy level in angiogenic gene expression and underlying molecular mechanism by comparing the laminar and oscillatory fluid shear stresses in endothelial cells. Methods and results: We show that shock wave with low energy level (0.012-0.045mJ/mm<SUP>2</SUP>) stimulated phosphorylation of Akt, eNOS and Erk ½ in a time-dependent manner which is similar to the effect of laminar fluid shear stress. The transfection of endothelial cells with siRNA encoding VEGFR2, VE-cadherin and PECAM-1 inhibited shock wave-induced phosphorylation of Akt, eNOS and Erk ½ and angiogenic gene expressions, including Akt, eNOS, KLF2/4, and Nur77. Moreover, mechanical stimulation through extracorporeal shock wave induced endothelial cell migration and tube formation. Conclusions: Our results demonstrate that shock wave-induced Akt/eNOS phosphorylation and angiogenic gene expression were mediated through the mechanosensory complex formation involving VEGFR-2, VE-cadherin and PECAM-1 which was similar to the effect of laminar shear stress.
Son, J.N.,Lho, Y.,Shin, S.,Kwon, S.H.,Moon, K.C.,Ha, E. Elsevier/North-Holland Biomedical Press 2011 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.146 No.3
Carbamylation is a post-translational modification, pathophysiological consequences of which remain poorly understood. Very recently, an alternative and dominant mechanism for cyanate formation and protein carbamylation at sites of atherosclerotic plaque was reported. Thus, we investigated the effect and signaling pathway of carbamylated low-density lipoprotein (cLDL) on apoptosis and reactive oxygen species (ROS) generation in human umbilical vein endothelial cells (HUVECs). Human LDL was carbamylated, copper-oxidized, and characterized. Immunoblot, real-time PCR, and flow cytometric analyses were performed. Intracellular ROS generation was determined. Transfection with small interfering RNA (siRNA) was also performed. Treatment of cLDL (20 and 100μg/ml) for 24h upregulated lectin-like oxidized LDL receptor (LOX-1) in HUVECs. cLDL also increased ROS generation and induced apoptosis. Exposure of HUVECs with cLDL (100μg/ml) attenuated phosphorylation of endothelial nitric oxide synthase (eNOS) and increased phosphorylation of ERK½ MAPK. Poly ADP-ribose polymerase (PARP) cleavage and expression of p53 were also increased by cLDL treatment. Treatment of ROS scavenger attenuated PARP cleavage and p53 expression. Inhibition of LOX-1 by siRNA against LOX-1 reversed both cLDL stimulated ROS generations and apoptosis. These results together suggest that cLDL induces ROS generations as well as apoptosis via LOX-1 mediated pathway in HUVECs and may play a critical role in atherogenesis.