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- 저자 : Yang J. E. (검색결과 848 건)
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Kim, Y.-K.,Park, H.-W.,Yang, J.-S.,Oh, S.-Y.,Chang, Y.-S.,Shin, E.-S.,Lee, J.-E.,Kim, S.,Gho, Y. S.,Cho, S.-H.,Min, K.-U.,Kim, Y.-Y. Blackwell Scientific Publications 2007 Clinical and experimental allergy Vol.37 No.4
<P>Summary</P><P>Background</P><P>The hyper-sensitivity reaction of IgE, with its high-affinity receptors (FcϵRI), is central to the phenomenon of atopic diseases.</P><P>Objective</P><P>To evaluate the genetic effects of non-synonymous single-nucleotide polymorphisms (SNPs) of FcϵRI on intermediate phenotypes of asthma, i.e. atopy and airway hyper-responsiveness (AHR), in the Korean general population.</P><P>Subjects and methods</P><P>Atopy and AHR were evaluated in a cohort of 2055 subjects, aged 10–18 years, using skin prick tests (SPTs) for common aeroallergens and total serum IgE and methacholine bronchial provocation tests. All FcϵRI-α, FcϵRI-β, and FcϵRI-γ gene exons of 24 healthy subjects were sequenced to locate informative non-synonymous SNPs (minor allele frequency >2%). Informative SNPs were then scored, using the high-throughput single base extension method. Relative risk (RR) was determined by multiple logistic regression analysis, after adjusting for confounding factors. The functional relevance of non-synonymous SNPs was analysed using the sorting intolerant from tolerant (SIFT) program.</P><P>Results</P><P>The SNP search found only one informative non-synonymous SNP in FcϵRI-β: E237G (minor allele frequency=0.21). The positive rate of AHR was lower among subjects with the 237<SUP>*</SUP>E allele than among those with 237<SUP>*</SUP>G [RR (95% confidence interval)=0.41 (0.19–0.89); <I>P</I>=0.01]. However, the E237G substitution was not associated with either a positive SPT response or total serum IgE levels. Sequence evolution analysis predicted that the E237G variation is an intolerant amino acid substitution, with functional importance.</P><P>Conclusion</P><P>In the Korean general population, AHR is significantly associated with the E237G polymorphism of FcϵRI-β, which results in an intolerant amino acid substitution.</P>
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Ko, A.R.,Yang, E.J.,Kim, M.S.,Ju, S.J. Pergamon Press 2016 Deep-sea research. Part II, Topical studies in oce Vol.123 No.-
The Amundsen Sea is characterized by a continental shelf, long-term sea ice, and many coastal polynyas with high biological productivity. Euphausia superba and Euphausia crystallorophias, which are dominant Antarctic krill, are major prey for most predators, such as fishes, birds, and marine mammals. An understanding of the feeding ecology of krill may provide the information for the structure and function of the Amundsen Sea ecosystem. Thus, we applied two biochemical approaches (fatty acids and stable isotopes) to determine the trophodynamics of adult krill in the Amundsen Sea. There were no significant differences in lipid contents between the two species, but the dominant storage lipids were different. Triacylglycerol (TAG) was dominant in E. superba, but wax esters (WE) were dominant in E. crystallorophias due to their different living strategies. Furthermore, the lipid content of E. crystallorophias displayed a spatial variation, being highest on the glacial edge. It was difficult to understand the feeding strategy and food source using only the fatty acid compositions of krill and in situ particulate organic matter. However, we found that specific FA ratios (18:1ω9/18:1ω7 and PUFA/SFA) and the nitrogen isotope ratio (δ<SUP>15</SUP>N) provide more insight into the feeding ecology of krill, such as feeding strategy and trophic position. These ratios suggest that E. crystallorophias consistently showed a higher degree of carnivorous feeding than E. superba in the Amundsen Sea during the austral summer. In conclusion, adult E. superba might more directly obtain their energy from in situ primary producers in the open sea, but, in the Amundsen Sea Polynya, adult E. crystallorophias seems to obtain their energy mainly through the microbial loop (microzooplankton). If so, E. crystallolophias would be a key player not only to transfer the energy from microbes to higher trophic levels but also to control the carbon and nitrogen cycle in the Amundsen Sea Polynya.
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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.
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Yang, Y M,Lee, W H,Lee, C G,An, J,Kim, E-S,Kim, S H,Lee, S-K,Lee, C H,Dhanasekaran, D N,Moon, A,Hwang, S,Lee, S J,Park, J-W,Kim, K M,Kim, S G Macmillan Publishers Limited 2015 Oncogene Vol.34 No.22
Hepatocellular carcinoma (HCC) has a poor prognosis owing to aggressive phenotype. Gα<SUB>12</SUB> gep oncogene product couples to G-protein-coupled receptors, whose ligand levels are frequently increased in tumor microenvironments. Here, we report Gα<SUB>12</SUB> overexpression in human HCC and the resultant induction of zinc-finger E-box-binding homeobox 1 (ZEB1) as mediated by microRNA deregulation. Gα<SUB>12</SUB> expression was higher in HCC than surrounding non-tumorous tissue. Transfection of Huh7 cell with an activated mutant of Gα<SUB>12</SUB> (Gα<SUB>12</SUB>QL) deregulated microRNA (miRNA or miR)-200b/a/429, -194-2/192 and -194-1/215 clusters in the miRNome. cDNA microarray analyses disclosed the targets affected by Gα<SUB>12</SUB> gene knockout. An integrative network of miRNAs and mRNA changes enabled us to predict ZEB1 as a key molecule governed by Gα<SUB>12</SUB>. Decreases of miR-200a/b, -192 and -215 by Gα<SUB>12</SUB> caused ZEB1 induction. The ability of Gα<SUB>12</SUB> to decrease p53 levels, as a result of activating protein-1 (AP-1)/c-Jun-mediated mouse double minute 2 homolog induction, contributed to transcriptional deregulation of the miRNAs. Gα<SUB>12</SUB>QL induced ZEB1 and other epithelial–mesenchymal transition markers with fibroblastoid phenotype change. Consistently, transfection with miR-200b, -192 or -215 mimic prevented the ability of Gα<SUB>12</SUB>QL to increase tumor cell migration/invasion. In xenograft studies, sustained knockdown of Gα<SUB>12</SUB> decreased the overall growth rate and average volume of tumors derived from SK-Hep1 cell (mesenchymal-typed). In HCC patients, miR-192, -215 and/or -200a were deregulated with microvascular invasion or growth advantage. In the HCC samples with higher Gα<SUB>12</SUB> level, a correlation existed in the comparison of relative changes of Gα<SUB>12</SUB> and ZEB1. In conclusion, Gα<SUB>12</SUB> overexpressed in HCC causes ZEB1 induction by deregulating p53-responsive miRNAs, which may facilitate epithelial–mesenchymal transition and growth of liver tumor. These findings highlight the significance of Gα<SUB>12</SUB> upregulation in liver tumor progression, implicating Gα<SUB>12</SUB> as an attractive therapeutic target.
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Leakage Currents of a Fast Switching Thyristor Made by Proton Irradiation Method
E.D. Kim,C.L. Zhang,S.C. Kim,N.K. Kim,J.Z. Zhu,B.F. Yang 전력전자학회 2004 ICPE(ISPE)논문집 Vol.- No.-
A thyristor with a VRRM of 1,600V was made with 200μm of N-base width from 60Ω·cm NTD-Si wafer and the proton irradiation was employed for improving its switching performance. This study showed that 4.7MeV-proton irradiation gives a narrow distribution of induced defects in the middle of N-drift region with its width of 10μm, which resulted in a superior trade-off relation between its static and dynamic characteristics. It was found that 3.7MeV and 5.9MeV protons remarkably increased the forward leakage current IDRM and the reverse leakage current IRRM, respectively. The increased IDRM and IRRM are attributed to the induced defects in the depletion layers of thyristor junctions J2 and J1, respectively.
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J. E. Lee,Y. S. Lee,H. J. Yoo,K. J. Lee,J. J. Park,B. K. Yang,H. T. Cheong,C. K. Park 한국동물번식학회 2012 Reproductive & Developmental Biology(Supplement) Vol.36 No.2s
In ruminants, Interferon-τ (IFN-τ) has the role of recognizing pregnancy signals produced by the embryo and it may have an important role during the luteolysis. Therefore, the purpose of the present study was to investigate the effect of IFN-τ on prostaglandin synthesis, cyclooxygenase-2 (COX-2) gene expression in vitro and secretion of progesterone (P4) in vivo. The epithelial and stromal cells isolated from bovine endometrium were cultured with different doses of IFN-τ (0, 0.02, 0.2 and 2 μg/ml). Human chorionic gonadotropin (hCG, 1.5 IU/ml) was used as a positive control. Prostaglandin E2 and F2α levels in the culture media were analyzed by enzyme immunoassays, and total RNA was extracted from the cells for RT-PCR. P4 concentrations in blood samples were assayed by chemiluminescent immunoassay system. In epithelial cells, COX-2 gene expression was increased in the presence of IFN-τ (p<0.05), but it was not significantly different in all groups of stromal cells except 2 μg/ml IFN-τ group (p<0.05). Although IFN-τ did not affect PGE2 and PGF2α production in epithelial cells, it decreased PGE2 and PGF2α production significantly in stromal cells (p<0.05). In vivo experiment, the P4 concentrations in blood sample was significantly increased after injection of 1 μg/ml IFN-τ. These results indicate that PG production was mediated by COX-2 expression in the stromal cells but it did not affect in the epithelial cells, and suggest that treatment of IFN-τ was to improve the implantation environment of uterine by maintenance of high P4 concentration. * This work was carried out with the support of “Cooperative Research Program for Agriculture Science & Technology Development (Project No. PJ907008)” Rural Development Administration, Republic of Korea.
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Yang, S.J.,Je Lee, W.,Kim, E.A.,Dal Nam, K.,Hahn, H.G.,Young Choi, S.,Cho, S.W. North-Holland ; Elsevier Science Ltd 2014 european journal of pharmacology Vol.736 No.-
Thiazole derivatives are attractive candidates for drug development because they can be efficiently synthesized and are active against a number of diseases and conditions, including diabetes. In our present study, we investigated the anti-inflammatory and antioxidant properties of N-adamantyl-4-methylthiazol-2-amine (KHG26693), a new thiazole derivative, in a streptozotocin (STZ)-induced model of diabetes mellitus. STZ-induced diabetic rats were intraperitoneally administered KHG26693 (3mg/kg-body weight/day) for 4 weeks. KHG26693 administration significantly decreased blood glucose, triglycerides, and cholesterol and increased insulin. KHG26693 also suppressed several inflammatory responses in STZ-induced diabetic rats, as evidenced by decreased levels of serum tumor necrosis factor-α, interleukin-1β, and nitric oxide. Additionally, KHG26693 significantly modulated hepatic lipid peroxidation, catalase and superoxide dismutase activity, and the nonenzymatic antioxidant status (e.g., vitamins C and E), and reduced the glutathione content. These anti-inflammatory/antioxidative actions occurred as a result of the downregulation of inducible nitric oxide synthase and nuclear factor-kappa B. Taken together, our results suggest that KHG26693 successfully reduces the production of oxidative stress in STZ-induced diabetic rats by regulating the oxidation-reduction system, specifically increasing antioxidant capacity. Furthermore, KHG26693 treatment significantly reverted the key enzymes of glucose metabolism, such as glucokinase, glucose-6-phosphatase, glycogen synthase, glycogen phosphorylase, and fructose-1,6-bisphosphatase, to near-normal levels in liver tissues. These results indicate that KHG26693 normalizes disturbed glucose metabolism by enhancing glucose utilization and decreasing liver glucose production via insulin release, suggesting the possibility of future diabetes treatments.
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