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김대곤,엄윤성,홍지형,이석조,석광설,이대균,이은정,방선애 한국대기환경학회 2004 한국대기환경학회지 Vol.20 No.3
The main purpose of this study was to characterize the air pollutants emission factors in electric power plant (EPP) using fossil fuels. The electric power plant is a major air pollution source, thus knowing the emission characteristics of electric power plant is very important to develop a control strategy. The major air pollutants of concern from EPP stacks are particulate matter (PM), sulfur oxides (SOx), nitrogen oxides (NOx), carbon monoxide (CO) and heavy metals. Throughout the study. the following results arc estimated: - PM : 8.671E-05∼8.724E+01 PM emission (kg) per fuel burned (ton) - SOx: 4.749E-04∼7.877E+01 SOx emission (kg) per fuel burned (ton) - NOx : 1.578E-02∼9.857E+00 NOx emission (kg) per fuel burned (ton) - CO : 3.800E-04∼1.291E+00 CO emission (kg) per fuel burned (ton) - Hg : 1.220E+01∼3.108E+02 Hg emission (mg) per fuel burned (ton) From the statistical analysis by Wilcoxon signed ranks test between the emission factors of ours and U.S. EPA's. we can yielded that: p > 0.05.
p34 is a novel regulator of the oncogenic behavior of NEDD4-1 and PTEN
Hong, S-W,Moon, J-H,Kim, J-S,Shin, J-S,Jung, K-A,Lee, W-K,Jeong, S-Y,Hwang, J J,Lee, S-J,Suh, Y-A,Kim, I,Nam, K-Y,Han, S,Kim, J E,Kim, K-p,Hong, Y S,Lee, J-L,Lee, W-J,Choi, E K,Lee, J S,Jin, D-H,Kim, Macmillan Publishers Limited 2014 CELL DEATH AND DIFFERENTIATION Vol.21 No.1
PTEN is one of the most frequently mutated or deleted tumor suppressors in human cancers. NEDD4-1 was recently identified as the E3 ubiquitin ligase for PTEN; however, a number of important questions remain regarding the role of ubiquitination in regulating PTEN function and the mechanisms by which PTEN ubiquitination is regulated. In the present study, we demonstrated that p34, which was identified as a binding partner of NEDD4-1, controls PTEN ubiquitination by regulating NEDD4-1 protein stability. p34 interacts with the WW1 domain of NEDD4-1, an interaction that enhances NEDD4-1 stability. Expression of p34 promotes PTEN poly-ubiquitination, leading to PTEN protein degradation, whereas p34 knockdown results in PTEN mono-ubiquitination. Notably, an inverse correlation between PTEN and p34/NEDD4-1 levels was confirmed in tumor samples from colon cancer patients. Thus, p34 acts as a key regulator of the oncogenic behavior of NEDD4-1 and PTEN.
Kim, S Y,S Hong, Y,K Shim, E,Kong, S-Y,Shin, A,Baek, J Y,Jung, K H Nature Publishing Group 2013 The British journal of cancer Vol.109 No.6
<P><B>Background:</B></P><P>S-1 is an oral fluoropyrimidine that mimics infusional 5-fluorouracil. The aim of this phase II trial was to explore the clinical efficacy of the triplet regimen TIROX, which consists of S-1, irinotecan and oxaliplatin.</P><P><B>Methods:</B></P><P>Forty-two chemo-naive patients with metastatic colorectal cancer (mCRC) were planned to be enrolled and be treated with irinotecan 150 mg m<SUP>−2</SUP> followed by oxaliplatin 85 mg m<SUP>−2</SUP> on day 1 and S-1 80 mg m<SUP>−2</SUP> per day from day 1 to 14 every 3 weeks. Polymorphisms in the <I>UGT1A1</I>, <I>UGT1A6</I>, <I>UGT1A7</I> and <I>CYP2A6</I> genes were analysed.</P><P><B>Results:</B></P><P>Between July 2007 and February 2008, 43 patients were enrolled. An objective response was noted in 29 patients (67.4%, 95% confidence interval: 53.4–81.4), of which 2 achieved durable complete responses. The median progression-free survival was 10.0 months and the median overall survival was 19.2 months. Significant grade 3 or 4 adverse events were neutropenia (45.2%), febrile neutropenia (9.5%), diarrhoea (7.1%) and vomiting (9.5%). Increased gastrointestinal toxicities were associated with the presence of <I>UGT1A6*2</I> or <I>UGT1A7*3</I> and an improved tumour response was noted in those without variant alleles of <I>CYP2A6</I> or <I>UGT1A1*60</I>.</P><P><B>Conclusion:</B></P><P>The combination of S-1, irinotecan and oxaliplatin showed favourable efficacy and tolerability in untreated patients with mCRC.</P>
Hong, S.J.,Kim, S.K.,Ko, E.B.,Yun, C.H.,Han, S.H. Pergamon Press 2017 Molecular immunology Vol.81 No.-
<P>Staphylococcus aureus is a Gram-positive pathogen that can cause chronic skin inflammation, pneumonia, and septic shock. The immunomodulatory functions of wall teichoic acid (WTA), a glycopolymer abundantly expressed on the Gram-positive bacterial cell wall, are poorly understood. Here, we investigated the role of WTA in the phenotypic and functional activation of human monocyte-derived dendritic cells (DCs) treated with ethanol-killed S. aureus. WTA-deficient S. aureus mutant (Delta tagO) exhibited attenuated binding and internalization to DCs compared to the wild-type. Delta tagO induced lower expression of maturation markers on and cytokines in DCs than the wild-type S. aureus. Furthermore, autologous human peripheral blood mononuclear cells cocultured with Delta tagO-treated DCs exhibited a marked reduction in T cell proliferative activity, the expression of activation markers, and the production of cytokines compared to the wild-type S. aureus-stimulated DCs. Collectively, these results suggest that WTA is an important cell wall component of S. aureus for the induction of DC maturation and activation. (C) 2016 Elsevier Ltd. All rights reserved.</P>
Park, S. J.,Kim, S. M.,Moon, J. H.,Kim, J. H.,Shin, J. S.,Hong, S. W.,Shin, Y. J.,Lee, D. H.,Lee, E. Y.,Hwang, I. Y. Springer Science + Business Media 2016 Tumour biology Vol.37 No.4
<P>Pancreatic cancer is one of the most lethal cancers and remains a major unsolved health problem. Less than 20 % of patients are surgical candidates, and the median survival for non-resected patients is approximately 3 to 4 months. Despite the existence of many conventional cancer therapies, few targeted therapies have been developed for pancreatic cancer. Combination therapy using erlotinib and gemcitabine is an approved standard chemotherapy for advanced pancreatic cancer, but it has marginal therapeutic benefit. To try to improve the therapeutic outlook, we studied the efficacy of another combination treatment and the relevance to E-cadherin in human pancreatic cancer cells. We treated two human pancreatic cancer cell lines with the histone deacetylase inhibitor (HDACi) SAHA. Interestingly, in these Panc-1 and Capan1 cells, we observed that the expression levels of E-cadherin and phosphorylated EGFR were gradually upregulated after treatment with SAHA. Furthermore, these cells underwent induced cell death after exposure to the combination treatment of SAHA and erlotinib. In Panc-1 cells, overexpression of E-cadherin activated the phosphorylation of EGFR and increased the cell sensitivity to erlotinib. In Capan1 cells, knocking down E-cadherin decreased the expression of phosphorylated EGFR, and these cells did not respond to erlotinib. Therefore, we demonstrated the efficacy of the combined treatment with SAHA and erlotinib in human pancreatic cancer cells, and we determined that the increased efficacy was due, at least in part, to the effects of SAHA on the expression of E-cadherin. Our studies suggest that E-cadherin may be a potent biomarker for pancreatic cancer.</P>
석광설,방선애,홍지형,이석조,김대곤,이대균,허정숙,이은정 한국대기환경학회 2004 한국대기환경학회지 Vol.20 No.4
The purpose of this study is 10 estimate of emission factors of the air pollutants for the melting furnaces for the iron and steel industry. The result of this study is able to obtain the emission factor of particulate matters (PM), sulfur dioxide, nitrogen oxides for melting furnace. The emission factors of each pollutants were as follows: - the emission factor varied between 6.13E-03 ∼ 6.12E-01kg/ton for PM - 1.59E-01 ∼ 2.45E+00kg/ton for S0₂ - 6.82E-02 ∼ 6.88E-01kg/ton for NOx, respectively. Analysis of the differences in the emission factors of ours and U.S. EPA's yielded the following results for the Wilcoxon method: p>0.05. The statistical analysis showed no differences in the our emission factors and U.S. EPA's
An, B.S.,Ahn, H.J.,Kang, H.S.,Jung, E.M.,Yang, H.,Hong, E.J.,Jeung, E.B. North-Holland 2013 Molecular and cellular endocrinology Vol.375 No.1
We examined the effects of estradiol (E2), 4-tert-octylphenol (OP), and bisphenol A (BPA) on uterine contractions in immature rats. The expression and localization of contraction-associated proteins (CAPs), and contractility of rat uterus with a collagen gel contraction assay were analyzed. E2, OP, and BPA all increased oxytocin (OT)-related pathway, while the prostaglandin-related signaling was reduced. Interestingly, E2 and estrogenic compounds showed distinct effects on the contractile activity of uterine cells. E2 enhanced the contractility, while OP and BPA significantly decreased it. Immunohistochemical analysis of CAPs showed distinct regulation of prostaglandin F receptor localization by E2 and estrogenic compounds, which may explain the different contractile activities of those reagents. In summary, we demonstrate that E2, OP, and BPA regulate CAP expression in a similar manner in the immature rat uterus, however, the effects on contractile activity were modulated differently. These findings suggest that OP and BPA interfere with uterine contractility.
Hong, S.K.,Choo, E.H.,Ihm, S.H.,Chang, K.,Seung, K.B. W.B.Saunders [etc.] 2017 clinical and experimental Vol.76 No.-
<P>Obesity-induced myocardial fibrosis may lead to diastolic dysfunction and ultimately heart failure. Activation of the transforming growth factor (TGF)-beta 1 and its downstream Smad2/3 pathways may play a pivotal role in the pathogenesis of obesity-induced myocardial fibrosis, and the antidiabetic dipeptidyl peptidase 4 inhibitors (DPP4i) might affect these pathways. We investigated whether DPP4i reduces myocardial fibrosis by inhibiting the TGF-beta 1 and Smad2/3 pathways in the myocardium of a diet-induced obesity (DIO) rat model. Eight-week-old male spontaneously hypertensive rats (SHRs) were fed either a normal fat diet (chow) or a high-fat diet (HFD) and then the HFD-fed SHRs were randomized to either the DPP4i (MK-0626) or control (distilled water) groups for 12 weeks. At 20 weeks old, all the rats underwent hemodynamic and metabolic studies and Doppler echocardiography. Compared with the normal fat diet (chow)-fed SHRs, the HFD-fed SHRs developed a more intense degree of hyperglycemia and dyslipidemia and showed a constellation of left ventricular (LV) diastolic dysfunction, and exacerbated myocardial fibrosis, as well as activation of the TGF-beta 1 and Smad2/3 pathways. DPP4i significantly improved the metabolic and hemodynamic parameters. The echocardiogram showed that DPP4i improved the LV diastolic dysfunction (early to late ventricular filling velocity [E/A] ratio, 1.49 +/- 0.21 vs. 1.77 +/- 0.09, p < 0.05). Furthermore, DPP4i significantly reduced myocardial fibrosis and collagen production by the myocardium and suppressed TGF-beta 1 and phosphorylation of Smad2/3 in the heart. In addition, DPP4i decreased TGF-beta 1-induced collagen production and TGF-beta 1-mediated phosphorylation and nuclear translocation of Smad2/3 in rat cardiac fibroblasts. In conclusion, DPP4 inhibition attenuated myocardial fibrosis and improved LV diastolic dysfunction in a DIO rat model by modulating the TGF-beta 1 and Smad2/3 pathways. (C) 2017 Elsevier Inc. All rights reserved.</P>