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Search Results: 1 - 10 of 7370 matches for " Jae-Woong Choi "
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Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke: implications in comorbidities of COPD
Gnanapragasam Arunachalam, Isaac K Sundar, Jae-woong Hwang, Hongwei Yao, Irfan Rahman
Journal of Inflammation , 2010, DOI: 10.1186/1476-9255-7-34
Abstract: Adult male and female wild-type (WT) mice of genetic background C57BL/6J and ApoE-/- mice were exposed to CS, and lung inflammatory responses, oxidative stress (lipid peroxidation products), mechanical properties as well as airspace enlargement were assessed.The lungs of ApoE-/- mice showed augmented inflammatory response and increased oxidative stress with development of distal airspace enlargement which was accompanied with decline in lung function. Interestingly, the levels and activities of matrix metalloproteinases (MMP-9 and MMP-12) were increased, whereas the level of eNOS was decreased in lungs of CS-exposed ApoE-/- mice as compared to air-exposed ApoE-/- mice or CS-exposed WT mice.These findings suggest that CS causes premature emphysema and a decline of lung function in mice susceptible to cardiovascular abnormalities via abnormal lung inflammation, increased oxidative stress and alterations in levels of MMPs and eNOS.Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation resulting from excessive airway inflammatory response mediated by cigarette smoke (CS). Comorbidities such as cardiovascular disease, diabetes, lung cancer, and osteoporosis are more prevalent in smokers and patients with COPD [1-3]. Recent studies have shown that smokers with altered forced expiratory volume in one second (FEV1) and airflow limitation are associated with arterial stiffness, exaggerated atherosclerosis and vice-versa [2,4,5]. Growing evidence also indicates that inflammation, endothelial dysfunction and oxidative modification of lipids play an important role in the pathogenesis of atherosclerosis and COPD [3,6,7]. In addition to CS, alcohol consumption is also one among the important contributing factors involved in the pathogenesis of COPD and atherosclerosis and their co-morbidities [8,9].Apolipoprotein E-deficient (ApoE-/-) mice develop atherosclerosis due to an accumulation of cholesterol ester-enriched particles in the blood resul
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
Network-based Isoform Quantification with RNA-Seq Data for Cancer Transcriptome Analysis
Wei Zhang,Jae-Woong Chang,Lilong Lin,Kay Minn,Baolin Wu,Jeremy Chien,Jeongsik Yong,Hui Zheng,Rui Kuang
Computer Science , 2014,
Abstract: High-throughput mRNA sequencing (RNA-Seq) is widely used for transcript quantification of gene isoforms. Since RNA-Seq data alone is often not sufficient to accurately identify the read origins from the isoforms for quantification, we propose to explore protein domain-domain interactions as prior knowledge for integrative analysis with RNA-seq data. We introduce a Network-based method for RNA-Seq-based Transcript Quantification (Net-RSTQ) to integrate protein domain-domain interaction network with short read alignments for transcript abundance estimation. Based on our observation that the abundances of the neighboring isoforms by domain-domain interactions in the network are positively correlated, Net-RSTQ models the expression of the neighboring transcripts as Dirichlet priors on the likelihood of the observed read alignments against the transcripts in one gene. The transcript abundances of all the genes are then jointly estimated with alternating optimization of multiple EM problems. In simulation Net-RSTQ effectively improved isoform transcript quantifications when isoform co-expressions correlate with their interactions. qRT-PCR results on 25 multi-isoform genes in a stem cell line, an ovarian cancer cell line, and a breast cancer cell line also showed that Net-RSTQ estimated more consistent isoform proportions with RNA-Seq data. In the experiments on the RNA-Seq data in The Cancer Genome Atlas (TCGA), the transcript abundances estimated by Net-RSTQ are more informative for patient sample classification of ovarian cancer, breast cancer and lung cancer. All experimental results collectively support that Net-RSTQ is a promising approach for isoform quantification.
Network-Based Isoform Quantification with RNA-Seq Data for Cancer Transcriptome Analysis
Wei Zhang?,Jae-Woong Chang?,Lilong Lin?,Kay Minn?,Baolin Wu?,Jeremy Chien?,Jeongsik Yong?,Hui Zheng?,Rui Kuang
PLOS Computational Biology , 2015, DOI: 10.1371/journal.pcbi.1004465
Abstract: High-throughput mRNA sequencing (RNA-Seq) is widely used for transcript quantification of gene isoforms. Since RNA-Seq data alone is often not sufficient to accurately identify the read origins from the isoforms for quantification, we propose to explore protein domain-domain interactions as prior knowledge for integrative analysis with RNA-Seq data. We introduce a Network-based method for RNA-Seq-based Transcript Quantification (Net-RSTQ) to integrate protein domain-domain interaction network with short read alignments for transcript abundance estimation. Based on our observation that the abundances of the neighboring isoforms by domain-domain interactions in the network are positively correlated, Net-RSTQ models the expression of the neighboring transcripts as Dirichlet priors on the likelihood of the observed read alignments against the transcripts in one gene. The transcript abundances of all the genes are then jointly estimated with alternating optimization of multiple EM problems. In simulation Net-RSTQ effectively improved isoform transcript quantifications when isoform co-expressions correlate with their interactions. qRT-PCR results on 25 multi-isoform genes in a stem cell line, an ovarian cancer cell line, and a breast cancer cell line also showed that Net-RSTQ estimated more consistent isoform proportions with RNA-Seq data. In the experiments on the RNA-Seq data in The Cancer Genome Atlas (TCGA), the transcript abundances estimated by Net-RSTQ are more informative for patient sample classification of ovarian cancer, breast cancer and lung cancer. All experimental results collectively support that Net-RSTQ is a promising approach for isoform quantification. Net-RSTQ toolbox is available at http://compbio.cs.umn.edu/Net-RSTQ/.
NF-κB Inducing Kinase, NIK Mediates Cigarette Smoke/TNFα-Induced Histone Acetylation and Inflammation through Differential Activation of IKKs
Sangwoon Chung, Isaac K. Sundar, Jae-Woong Hwang, Fiona E. Yull, Timothy S. Blackwell, Vuokko L. Kinnula, Michael Bulger, Hongwei Yao, Irfan Rahman
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023488
Abstract: Background Nuclear factor (NF)-κB inducing kinase (NIK) is a central player in the non-canonical NF κB pathway, which phosphorylates IκB kinase α (IKKα) resulting in enhancement of target gene expression. We have recently shown that IKKα responds to a variety of stimuli including oxidants and cigarette smoke (CS) regulating the histone modification in addition to its role in NF-κB activation. However, the primary signaling mechanism linking CS-mediated oxidative stress and TNFα with histone acetylation and pro-inflammatory gene transcription is not well understood. We hypothesized that CS and TNFα increase NIK levels causing phosphorylation of IKKα, which leads to histone acetylation. Methodology To test this hypothesis, we investigated whether NIK mediates effects of CS and TNFα on histone acetylation in human lung epithelial cells in vitro and in lungs of mouse exposed to CS in vivo. CS increased the phosphorylation levels of IKKα/NIK in lung epithelial cells and mouse lungs. NIK is accumulated in the nuclear compartment, and is recruited to the promoters of pro-inflammatory genes, to induce posttranslational acetylation of histones in response to CS and TNFα. Cells in which NIK is knocked down using siRNA showed partial attenuation of CSE- and TNFα-induced acetylation of histone H3 on pro-inflammatory gene promoters. Additional study to determine the role of IKKβ/NF-κB pathway in CS-induced histone acetylation suggests that the canonical pathway does not play a role in histone acetylation particularly in response to CS in mouse lungs. Conclusions Overall, our findings provide a novel role for NIK in CS- and TNFα-induced histone acetylation, especially on histone H3K9.
Mitogen- and Stress-Activated Kinase 1 (MSK1) Regulates Cigarette Smoke-Induced Histone Modifications on NF-κB-dependent Genes
Isaac K. Sundar, Sangwoon Chung, Jae-woong Hwang, John D. Lapek, Michael Bulger, Alan E. Friedman, Hongwei Yao, James R. Davie, Irfan Rahman
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031378
Abstract: Cigarette smoke (CS) causes sustained lung inflammation, which is an important event in the pathogenesis of chronic obstructive pulmonary disease (COPD). We have previously reported that IKKα (I kappaB kinase alpha) plays a key role in CS-induced pro-inflammatory gene transcription by chromatin modifications; however, the underlying role of downstream signaling kinase is not known. Mitogen- and stress-activated kinase 1 (MSK1) serves as a specific downstream NF-κB RelA/p65 kinase, mediating transcriptional activation of NF-κB-dependent pro-inflammatory genes. The role of MSK1 in nuclear signaling and chromatin modifications is not known, particularly in response to environmental stimuli. We hypothesized that MSK1 regulates chromatin modifications of pro-inflammatory gene promoters in response to CS. Here, we report that CS extract activates MSK1 in human lung epithelial (H292 and BEAS-2B) cell lines, human primary small airway epithelial cells (SAEC), and in mouse lung, resulting in phosphorylation of nuclear MSK1 (Thr581), phospho-acetylation of RelA/p65 at Ser276 and Lys310 respectively. This event was associated with phospho-acetylation of histone H3 (Ser10/Lys9) and acetylation of histone H4 (Lys12). MSK1 N- and C-terminal kinase-dead mutants, MSK1 siRNA-mediated knock-down in transiently transfected H292 cells, and MSK1 stable knock-down mouse embryonic fibroblasts significantly reduced CS extract-induced MSK1, NF-κB RelA/p65 activation, and posttranslational modifications of histones. CS extract/CS promotes the direct interaction of MSK1 with RelA/p65 and p300 in epithelial cells and in mouse lung. Furthermore, CS-mediated recruitment of MSK1 and its substrates to the promoters of NF-κB-dependent pro-inflammatory genes leads to transcriptional activation, as determined by chromatin immunoprecipitation. Thus, MSK1 is an important downstream kinase involved in CS-induced NF-κB activation and chromatin modifications, which have implications in pathogenesis of COPD.
Alpha 1,3-Galactosyltransferase Deficiency in Pigs Increases Sialyltransferase Activities That Potentially Raise Non-Gal Xenoantigenicity
Jong-Yi Park,Mi-Ryung Park,Deug-Nam Kwon,Min-Hui Kang,Mihye Oh,Jae-Woong Han,Ssang-Goo Cho,Chankyu Park,Dong-Ku Kim,Hyuk Song,Jae-Wook Oh,Jin-Hoi Kim
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/560850
Abstract: We examined whether deficiency of the GGTA1 gene in pigs altered the expression of several glycosyltransferase genes. Real-time RT-PCR and glycosyltransferase activity showed that 2 sialyltransferases [α2,3-sialyltransferase (α2,3ST) and α2,6-sialyltransferase (α2,6ST)] in the heterozygote GalT KO liver have higher expression levels and activities compared to controls. Enzyme-linked lectin assays indicated that there were also more sialic acid-containing glycoconjugate epitopes in GalT KO livers than in controls. The elevated level of sialic-acid-containing glycoconjugate epitopes was due to the low level of α-Gal in heterozygote GalT KO livers. Furthermore, proteomics analysis showed that heterozygote GalT KO pigs had a higher expression of NAD
Comparison of Measured Rain Attenuation in the 12.25?GHz Band with Predictions by the ITU-R Model
Dong You Choi,Jae Young Pyun,Sun Kuh Noh,Sang Woong Lee
International Journal of Antennas and Propagation , 2012, DOI: 10.1155/2012/415398
Abstract: Quantitative analysis and prediction of radio attenuation is necessary in order to improve the reliability of satellite-earth communication links and for economically efficient design. For this reason, many countries have made efforts to develop their own rain attenuation prediction models that are suited to their rain environment. In this paper, we present the results of measurements of rain-induced attenuation in vertically polarized signals propagating at 12.25 GHz during certain rain events, which occurred in the rainy wet season of 2001 and 2007 at Yong-in, Korea. The rain attenuation over the link path was measured experimentally and compared with the attenuation obtained using the ITU-R model.
Effects of prostaglandin F on small intestinal interstitial cells of Cajal
Chan Guk Park, Young Dae Kim, Man Yoo Kim, Jae Woong Koh, Jae Yeoul Jun, Cheol Ho Yeum, Insuk So, Seok Choi
World Journal of Gastroenterology , 2011,
Abstract: AIM: To explore the role of prostaglandin F2α (PGF2α)) on pacemaker activity in interstitial cells of Cajal (ICC) from mouse small intestine.METHODS: In this study, effects of PGF2α in the cultured ICC cells were investigated with patch clamp technology combined with Ca2+ image analysis.RESULTS: Externally applied PGF2α (10 μmol/L) produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The application of flufenamic acid (a non-selective cation channel inhibitor) or niflumic acid (a Cl- channel inhibitor) abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF2α-induced tonic inward currents. In addition, the tonic inward currents induced by PGF2α were not inhibited by intracellular application of 5’-[-thio]diphosphate trilithium salt. Pretreatment with Ca2+ free solution, U-73122, an active phospholipase C inhibitor, and thapsigargin, a Ca2+-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the PGF2α-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the PGF2α-induced effects on pacemaker currents. When recording intracellular Ca2+ ([Ca2+]i) concentration using fluo-3/AM, PGF2α broadly increased the spontaneous [Ca2+]i oscillations.CONCLUSION: These results suggest that PGF2α can modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via [Ca2+]i regulation
On Certain Subclasses of Multivalent Functions Associated with a Family of Linear Operators  [PDF]
Jae Ho Choi
Advances in Pure Mathematics (APM) , 2011, DOI: 10.4236/apm.2011.14040
Abstract: Making use of a linear operator Iλp(a,c), which is defined here by means of the Hadamard product (or convolution), we introduce some new subclasses of multivalent functions and investigate various inclusion properties of these subclasses. Some radius problems are also discussed.
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