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Search Results: 1 - 10 of 27581 matches for " Jae-Won Lee "
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The dialectics of media’s role in the public sphere
Jae-won Lee,Leo W Jeffres
Bodhi: An Interdisciplinary Journal , 2009, DOI: 10.3126/bodhi.v3i1.2807
Abstract: DOI: 10.3126/bodhi.v3i1.2807 Bodhi Vol.3(1) 2009 p.1-9
The Disciplinary Direction and Structure of Journalism and Media Education
Jae-won Lee,Won-yong Kim
Bodhi: An Interdisciplinary Journal , 2008, DOI: 10.3126/bodhi.v2i1.2861
Abstract: Reviewing the communication industry, the cybernetics pioneer Norbert Wiener (1950) once offered a very disturbing observation: "The people who have elected communication as a career so often have nothing more to communicate." It's more than half a century from the days of his comment on us, but are we in any better shape now?
Throughput and Energy Efficiency of a Cooperative Hybrid ARQ Protocol for Underwater Acoustic Sensor Networks
Arindam Ghosh,Jae-Won Lee,Ho-Shin Cho
Sensors , 2013, DOI: 10.3390/s131115385
Abstract: Due to its efficiency, reliability and better channel and resource utilization, cooperative transmission technologies have been attractive options in underwater as well as terrestrial sensor networks. Their performance can be further improved if merged with forward error correction (FEC) techniques. In this paper, we propose and analyze a retransmission protocol named Cooperative-Hybrid Automatic Repeat reQuest (C-HARQ) for underwater acoustic sensor networks, which exploits both the reliability of cooperative ARQ (CARQ) and the efficiency of incremental redundancy-hybrid ARQ (IR-HARQ) using rate-compatible punctured convolution (RCPC) codes. Extensive Monte Carlo simulations are performed to investigate the performance of the protocol, in terms of both throughput and energy efficiency. The results clearly reveal the enhancement in performance achieved by the C-HARQ protocol, which outperforms both CARQ and conventional stop and wait ARQ (S&W ARQ). Further, using computer simulations, optimum values of various network parameters are estimated so as to extract the best performance out of the C-HARQ protocol.
Normalized Contact Force to Minimize "Electrode-Lead" Resistance in a Nanodevice
Seung-Hoon Lee,Jun Bae,Seung Woo Lee,Jae-Won Jang
Physics , 2014,
Abstract: In this report, the contact resistance between "electrode" and "lead" is investigated for reasonable measurements of samples' resistance in a polypyrrole (PPy) nanowire device. The sample's resistance, including "electrode-lead" contact resistance, shows a decrease as force applied to the interface increases. Moreover, the sample's resistance becomes reasonably similar to, or lower than, values calculated by resistivity of PPy reported in previous studies. The decrease of electrode-lead contact resistance by increasing the applying force was analyzed by using Holm theory: the general equation of relation between contact resistance ($R_H$) of two-metal thin films and contact force ($R_H$ $\propto$ $1/\sqrt{F}$). The present investigation can guide a reliable way to minimize electrode-lead contact resistance for reasonable characterization of nanomaterials in a microelectrode device.
Leptin Increases TNF-α Expression and Production through Phospholipase D1 in Raw 264.7 Cells
Se-Min Lee, Hye-Jin Choi, Cheong-Hae Oh, Jae-Won Oh, Joong-Soo Han
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0102373
Abstract: Epidemiological evidence suggests that obesity is associated with inflammation of the respiratory tract and the pathogenesis of asthma. The purpose of this study was to examine the role of phospholipase D1 (PLD1) in leptin-induced expression of the proinflammatory cytokine, tumor necrosis factor (TNF)-α, and to suggest a molecular link between obesity and respiratory tract inflammation. We investigated whether leptin, a typical adipocytokine, plays a role in the expression of TNF-α through increased PLD1 activity in Raw 264.7. Leptin enhanced the activity of PLD1 through activation of PLCγ and Src, while PLD1 siRNA decreased the leptin-induced expression and production of TNF-α. Leptin-induced PLD activation was also inhibited by a PLCγ inhibitor (PAO) and Src kinase inhibitor (PP2), indicating that PLCγ and Src kinase are upstream activators of PLD1. Down-regulation of PLD1 also completely blocked activation of p70S6K, an activator of JNK. Leptin-induced expression of TNF-α was also prevented by inhibition of p70S6K and JNK. Taken together, these results indicate that PLD1 acts as an important regulator of leptin-induced expression of TNF-α by participating in the PLCγ/Src/PLD1/PA/p70S6K/JNK pathway.
Phloroglucinol Inhibits the Bioactivities of Endothelial Progenitor Cells and Suppresses Tumor Angiogenesis in LLC-Tumor-Bearing Mice
Yi-Hong Kwon, Seok-Yun Jung, Jae-Won Kim, Sang-Hun Lee, Jun-Hee Lee, Boo-Yong Lee, Sang-Mo Kwon
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0033618
Abstract: Background There is increasing evidence that phloroglucinol, a compound from Ecklonia cava, induces the apoptosis of cancer cells, eventually suppressing tumor angiogenesis. Methodology/Principal Findings This is the first report on phloroglucinol's ability to potentially inhibit the functional bioactivities of endothelial progenitor cells (EPCs) and thereby attenuate tumor growth and angiogenesis in the Lewis lung carcinoma (LLC)-tumor-bearing mouse model. Although Phloroglucinol did not affect their cell toxicity, it specifically inhibited vascular endothelial growth factor (VEGF) dependent migration and capillary-like tube formation of EPCs. Our matrigel plug assay clearly indicated that orally injected phloroglucinol effectively disrupts VEGF-induced neovessel formation. Moreover, we demonstrated that when phloroglucinol is orally administered, it significantly inhibits tumor growth and angiogenesis as well as CD45?/CD34+ progenitor mobilization into peripheral blood in vivo in the LLC-tumor-bearing mouse model. Conclusions/Significance These results suggest a novel role for phloroglucinol: Phloroglucinol might be a modulator of circulating EPC bioactivities, eventually suppressing tumorigenesis. Therefore, phloroglucinol might be a candidate compound for biosafe drugs that target tumor angiogenesis.
Intratumoral delivery of IL-18 naked DNA induces T-cell activation and Th1 response in a mouse hepatic cancer model
Chi-Young Chang, Jienny Lee, Eun-Young Kim, Hae-Jung Park, Choon-Hyuck Kwon, Jae-Won Joh, Sung-Joo Kim
BMC Cancer , 2007, DOI: 10.1186/1471-2407-7-87
Abstract: Plasmid vectors encoding IL-18 were transferred directly into the liver 7 days after tumor injection to restrict IL-18 expression within the tumor site. The IL-18 protein level was increased in the liver 4 days after plasmid injection, and a marked antitumoral effect was observed at day 7. Antitumor effects were evaluated by measuring tumor regression, immune cell population, and IFN-γ production.The IL-18 plasmid controlled the growth of hepatic tumors and proliferation of splenic immune cells. Moreover, treatment of CT26 tumors with the IL-18 plasmid significantly enhanced the population of the effector T and NK cells in the spleen and peripheral blood. In spleen, the population of CD4+CD62Low cells was augmented in response to IL-18 on day 7. These results are consistent with the increase in CD4+ T cells secreting IFN-γ, but not CD8+ T cells. The marked reduction of tumor growth in tumor-bearing mice was associated with the maintenance of IFN-γ production in spleen in response to IL-18. These antitumoral effects were maintained until 14 days after plasmid injection.Our results suggest that direct plasmid DNA transfer of IL-18 with no accompanying reagents to augment transfection efficiency may be useful in tumor immunotherapy.Effective eradication of established tumors and generation of a lasting systemic immune response with a simple gene delivery system are important goals for cancer gene immunotherapy [1]. Cytokines are the most extensively studied immunostimulatory agents in cancer gene therapy [2]. Interferon-γ-inducing factor (IL-18) is a recently characterized murine and human cytokine. The murine IL-18 gene encodes a precursor protein of 192 amino acids, which is processed to a mature protein containing 157 residues [3]. This cytokine, produced by Kupffer cells, is a potent inducer of IFN-γ production by T cells and a costimulatory factor for T cell activation [4,5]. Accumulating evidence that IL-18 is a multifunctional cytokine that shares several biolog
Full-length cDNA sequences from Rhesus monkey placenta tissue: analysis and utility for comparative mapping
Dae-Soo Kim, Jae-Won Huh, Young-Hyun Kim, Sang-Je Park, Sang-Rae Lee, Kyu-Tae Chang
BMC Genomics , 2010, DOI: 10.1186/1471-2164-11-427
Abstract: From rhesus monkey placenta full-length cDNA libraries, 2000 full-length cDNA sequences were determined and 1835 rhesus placenta cDNA sequences longer than 100 bp were collected. These sequences were annotated based on homology to human genes. Homology search against human RefSeq mRNAs revealed that our collection included the sequences of 1462 putative rhesus monkey genes. Moreover, we identified 207 genes containing exon alterations in the coding region and the untranslated region of rhesus monkey transcripts, despite the highly conserved structure of the coding regions. Approximately 10% (187) of all full-length cDNA sequences did not represent any public human RefSeq mRNAs. Intriguingly, two rhesus monkey specific exons derived from the transposable elements of AluYRa2 (SINE family) and MER11B (LTR family) were also identified.The 1835 rhesus monkey placenta full-length cDNA sequences described here could expand genomic resources and information of rhesus monkeys. This increased genomic information will greatly contribute to the development of evolutionary biology and biomedical research.The rhesus monkey (Macaca mulatta) is one of the species of Macaca, an Old World monkey. On the basis of DNA sequence comparison complemented by fossil evidence, the divergence of humans and Old World monkeys is estimated at about 25 million years ago [1]. The relationship between humans and rhesus monkeys is even more important because biomedical research has come to depend on these primates as experimental animal models [2]. Due to their genetic, physiologic, and metabolic similarity to humans, this species serves as an essential research tool in neuroscience, behavioral biology, reproductive physiology, neuroendocrinology, endocrinology, cardiovascular studies, pharmacology and many other areas [3-5].The draft sequence of the rhesus monkey genome, which has an important evolutionary position, was published in 2007 [2]. The final challenge comes in the understanding of basic r
Removal of arsenate and arsenite from aqueous solution by waste cast iron

Nag-Choul Choi,Song-Bae Kim,Soon-Oh Kim,Jae-Won Lee,Jun-Boum Park,

环境科学学报(英文版) , 2012,
Abstract: The removal of As(III) and As(V) from aqueous solution was investigated using waste cast iron, which is a byproduct of the iron casting process in foundries. Two types of waste cast iron were used in the experiment: grind precipitate dust (GPD) and cast iron shot (CIS). The X-ray diffraction analysis indicated the presence of Fe0 on GPD and CIS. Batch experiments were performed under different concentrations of As(III) and As(V) and at various initial pH levels. Results showed that waste cast iron was effective in the removal of arsenic. The adsorption isotherm study indicated that the Langmuir isotherm was better than the Freundlich isotherm at describing the experimental result. In the adsorption of both As(III) and As(V), the adsorption capacity of GPD was greater than CIS, mainly due to the fact that GPD had higher surface area and weight percent of Fe than CIS. Results also indicated the removal of As(III) and As(V) by GPD and CIS was influenced by the initial solution pH, generally decreasing with increasing pH from 3.0 to 10.5. In addition, both GPD and CIS were more effective at the removal of As(III) than As(V) under given experimental conditions. This study demonstrates that waste cast iron has potential as a reactive material to treat wastewater and groundwater containing arsenic.
Soluble CD93 Levels in Patients with Acute Myocardial Infarction and Its Implication on Clinical Outcome
Jong-Chan Youn, Hee Tae Yu, Jae-Won Jeon, Hye Sun Lee, Yangsoo Jang, Young Woo Park, Yong-Beom Park, Eui-Cheol Shin, Jong-Won Ha
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0096538
Abstract: Background Inflammation plays a key role in the pathogenesis of acute myocardial infarction (MI). However, it is unclear whether marker of immune activation will provide prognostic information in these patients. We hypothesized that circulating levels of soluble CD93 (sCD93), a soluble form of transmembrane glycoprotein CD93, is increased in acute MI patients and its level would be associated with clinical outcomes in patients with acute MI. Methods We measured circulating levels of sCD93 in 120 patients with acute MI (63±13 yrs, M:F = 85:35) and in 120 age, sex-matched control subjects. In patients with acute MI, clinical characteristics, echocardiographic and laboratory findings were assessed at the time of initial enrollment. The primary outcome was defined as all-cause and cardiovascular death. Results Circulating sCD93 levels were significantly higher in patients with acute MI than in control subjects (552.1±293.7 vs. 429.8±114.2 ng/mL, p<0.0001). Upon in vitro inflammatory stimulation, increased CD93 shedding was demonstrated in acute MI patients but not in control subjects. During follow up period (median 208 days, 3-1058 days), the primary outcome occurred in 18 (15%) patients (9 cardiovascular deaths). Circulating levels of sCD93 were associated with all cause (p<0.0001) and cardiovascular (p<0.0001) mortality in patients with acute MI. Multivariate Cox regression analysis revealed that initial sCD93 level was found to be an independent predictor of all cause (p = 0.002) and cardiovascular mortality (p = 0.033) when controlled for age and left ventricular ejection fraction. Conclusions Circulating levels of sCD93 are elevated in patients with acute MI and their levels were associated with adverse clinical outcomes.
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