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Habib O.,Konkuk University | Habib O.,CHA Medical University | Habib G.,Konkuk University | Moon S.-H.,Konkuk University | And 6 more authors.
Molecules and Cells | Year: 2014

Induced pluripotent stem cells (iPSCs) are capable of unlimited self-renewal and can give rise to all three germ layers, thereby providing a new platform with which to study mammalian development and epigenetic reprogramming. However, iPSC generation may result in subtle epigenetic variations, such as the aberrant methylation of the Dlk1-Dio3 locus, among the clones, and this heterogeneity constitutes a major drawback to harnessing the full potential of iPSCs. Vitamin C has recently emerged as a safeguard to ensure the normal imprinting of the Dlk1-Dio3 locus during reprogramming. Here, we show that vitamin C exerts its effect in a manner that is independent of the reprogramming kinetics. Moreover, we demonstrate that reprogramming cells under 2i conditions leads to the early upregulation of Prdm14, which in turn results in a highly homogeneous population of authentic pluripotent colonies and prevents the abnormal silencing of the Dlk1-Dio3 locus. © The Korean Society for Molecular and Cellular Biology. All rights reserved. Source


Kim Y.S.,Chonnam National University | Kim J.S.,Bundang CHA General Hospital | Kwon J.S.,Chonnam National University | Jeong M.H.,Chonnam National University | And 4 more authors.
International Heart Journal | Year: 2010

Despite development of therapeutic modalities, myocardial ischemia-reperfusion (I/R) injury remains an important cause of cardiac dysfunction. Multiple strategies exist experimentally, but few are clinically available. Nuclear factor kappa-B (NF-κB) is a key transcription factor in the inflammatory response and is implicated in I/R injury. We hypothesized that the NFκB inhibitor BAY 11-7082 (BAY) would decrease the extent of injury after myocardial I/R. Hypoxiareoxygenation (H/R) was induced in rat neonatal cardiomyocytes with or without BAY pretreatment. NF-κB activation, vascular cell adhesion molecule (VCAM)-1, and monocyte chemoattractant protein (MCP)-1 were assayed by immunocytochemistry, Western blot or reverse transcriptase-polymerase chain reaction (RT-PCR). Sprague-Dawley rats (n = 7) were administered BAY (130 μg/kg) and I/R was induced by ligation of the left anterior descending artery (LAD) for 30 minutes followed by reperfusion. Infarct size was analyzed after 24 hours. At 2 weeks, echocardiography was performed to evaluate ventricular function and hearts were analyzed for fibrosis and apoptosis. BAY treatment inhibited NF-κB p65 activation, as well as VCAM-1 and MCP-1 expression induced by H/R in cardiomyocytes. Compared with control rats, BAY pretreated rats showed reduced infarct size. Echocardiograms demonstrated preserved systolic function as a fractional shortening in the BAY+I/R group (P < 0.05). Fibrosis was reduced in the BAY+I/R group (P < 0.05) and apoptosis was also reduced in the BAY+I/R group (P < 0.05). In the rat myocardial I/R injury model, BAY significantly reduced the infarct size, and preserved myocardial function. These data demonstrate that a currently available and well-tolerated inhibitor of NF-κB can decrease the risk of myocardial injury associated with I/R. Source


Ree P.H.,Bundang CHA General Hospital | Hahn W.B.,Bundang CHA General Hospital | Chang S.W.,Bundang CHA General Hospital | Jung S.H.,Bundang CHA General Hospital | And 3 more authors.
Fetal Diagnosis and Therapy | Year: 2011

Objective: The purpose of this study was to determine whether second-trimester maternal serum markers including inhibin A are useful for the detection of preeclampsia. Methods: Between January 2005 and March 2009, we analyzed the data of 4,764 subjects who underwent second-trimester multiple-marker screening for Down syndrome. Serum samples were assayed at 15+0 to 20+6 weeks for maternal serum alpha-fetoprotein (MSAFP), human chorionic gonadotrophin (hCG), unconjugated estriol (uE3) and inhibin A. We reviewed all medical records retrospectively, and assessed the relationships of several markers with preeclampsia using logistic regression analysis. Results: The study sample included 41 patients who developed preeclampsia and a control group consisting of the other 4,723 healthy subjects treated between January 2005 and March 2009. There were no significant differences in gestational ages at blood sampling, maternal weights, gravidity and parity between the two groups. However, the mean ages, Apgar scores, gestational age at delivery and neonatal weights were significantly different between the study group and the control group. The levels of markers in the study group were significantly increased compared to the control group, 1.76 ± 2.68 for inhibin A, 1.18 ± 0.69 for MSAFP, and 1.62 ± 1.18 for hCG, but uE3 did not differ significantly between the two groups. The AUC of inhibin A was 0.715, but the AUC of a three-marker combination model (0.800) was even better. A mid-trimester inhibin A concentration of 1.5 MoM or greater had a sensitivity of 60% and a false-positive rate of 16% for the prediction of preeclampsia. Inhibin A was the best predictor of preeclampsia. Three other markers were reliable predictive markers of preeclampsia. Conclusions: Inhibin A and other second-trimester serum markers may be useful for early detection of preeclampsia. Inhibin A was in fact the most important predictable marker among the markers we surveyed. The results of this study support those of previous studies, and provide quantified data elucidating the occurrence of preeclampsia. Copyright © 2011 S. Karger AG. Source

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