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박욱열(Uk-Yeol Park),이종호(Jong-Ho Lee) 한국경영학회 2018 한국경영학회 통합학술발표논문집 Vol.2018 No.8
창업은 세계적으로 新성장동력과 생존전략의 하나로 비중 있게 논의되고 있다. 창업에 대한 관심과 지원은 지속적으로 이루어지고 있다. 이러한 배경 하에 지식기반 창업기업은 여러 산업 분야에서 혁신의 견인차 역할을 수행할 뿐만 아니라 국가 경제발전의 일익을 담당하고 있다. 지식기반창업은 창업의 측면에서 경제적 파급효과가 높기 때문에 기술기반 창업기업의 고용 증가율이 다른 타 산업의 창업기업보다 높은 것으로 나타나고 있다. 본 연구에서는 지식기반산업과 업종을 정의하고 산업연관표와 매칭할 수 있는 산업부문별 세부산업을 재분류하였다. 이를 바탕으로 산업연관분석을 이용하여 지식기반 산업의 최종수요 발생 시에 경제적 파급효과를 분석하였다. 연구의 결과를 바탕으로 볼 때 지식기반창업 업종은 타 산업에 부가가치 유발효과, 고용유발효과의 파급력이 높은 것으로 나타났다. 따라서 지식기반창업의 육성을 통해 경제성장의 새로운 新성장동력으로써 역할은 물론, 파급효과를 이용하여 전체 산업의 성장을 견인하는 기회로 활용할 수 있을 것으로 판단된다.
AP2α is essential for MUC8 gene expression in human airway epithelial cells
Moon, Uk Yeol,Kim, Chang-Hoon,Choi, Jae Young,Kim, Yoon-Ju,Choi, Yeon Ho,Yoon, Ho-Geun,Kim, Hyeyoung,Yoon, Joo-Heon Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.110 No.6
<P>Mucins are high molecular weight proteins that make up the major components of mucus. Hypersecretion of mucus is a feature of several chronic inflammatory airway diseases. MUC8 is an important component of airway mucus, and its gene expression is upregulated in nasal polyp epithelium. Little is known about the molecular mechanisms of MUC8 gene expression. We first observed overexpression of activator protein-2alpha (AP2α) in human nasal polyp epithelium. We hypothesized that AP2α overexpression in nasal polyp epithelium correlates closely with MUC8 gene expression. We demonstrated that phorbol 12-myristate 13-acetate (PMA) treatment of the airway epithelial cell line NCI-H292 increases MUC8 gene and AP2α expression. In this study, we sought to determine which signal pathway is involved in PMA-induced MUC8 gene expression. The results show that the protein kinase C and mitogen-activating protein/ERK kinase (MAPK) pathways modulate MUC8 gene expression. PD98059 or ERK1/2 siRNA and RO-31-8220 or PKC siRNA significantly suppress AP2α as well as MUC8 gene expression in PMA-treated cells. To verify the role of AP2α, we specifically knocked down AP2α expression with siRNA. A significant AP2α knock-down inhibited PMA-induced MUC8 gene expression. While dominant negative AP2α decreased PMA-induced MUC8 gene expression, overexpressing wildtype AP2α increased MUC8 gene expression. Furthermore, using lentiviral vectors for RNA interference in human nasal polyp epithelial cells, we confirmed an essential role for AP2α in MUC8 gene expression. From these results, we concluded that PMA induces MUC8 gene expression through a mechanism involving PKC, ERK1/2, and AP2α activation in human airway epithelial cells. J. Cell. Biochem. 110: 1386–1398, 2010. © 2010 Wiley-Liss, Inc.</P>
Patients with systemic lupus erythematosus have abnormally elevated Epstein–Barr virus load in blood
Moon, Uk Yeol,Park, Su Jin,Oh, Sang Taek,Kim, Wan-Uk,Park, Sung-Hwan,Lee, Sang-Heon,Cho, Chul-Soo,Kim, Ho-Youn,Lee, Won-Keun,Lee, Suk Kyeong BioMed Central 2004 Arthritis research & therapy Vol.6 No.4
<P>Various genetic and environmental factors appear to be involved in systemic lupus erythematosus (SLE). Epstein–Barr virus (EBV) is among the environmental factors that are suspected of predisposing to SLE, based on the characteristics of EBV itself and on sequence homologies between autoantigens and EBV antigens. In addition, higher titers of anti-EBV antibodies and increased EBV seroconversion rates have been observed in SLE patients as compared with healthy control individuals. Serologic responses do not directly reflect EBV status within the body. Clarification of the precise status of EBV infection in SLE patients would help to improve our understanding of the role played by EBV in this disease. In the present study we determined EBV types in SLE patients (<I>n </I>= 66) and normal control individual (<I>n </I>= 63) by direct PCR analysis of mouthwash samples. We also compared EBV load in blood between SLE patients (<I>n </I>= 24) and healthy control individuals (<I>n </I>= 29) using semiquantitative PCR assay. The number of infections and EBV type distribution were similar between adult SLE patients and healthy control individuals (98.5% versus 94%). Interestingly, the EBV burden in peripheral blood mononuclear cells (PBMCs) was over 15-fold greater in SLE patients than in healthy control individuals (mean ± standard deviation: 463 ± 570 EBV genome copies/3 μg PBMC DNA versus 30 ± 29 EBV genome copies/3 μg PBMC DNA; <I>P </I>= 0.001), suggesting that EBV infection is abnormally regulated in SLE. The abnormally increased proportion of EBV-infected B cells in the SLE patients may contribute to enhanced autoantibody production in this disease.</P>