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Association of chronic viral hepatitis B with insulin resistance.
Lee, Jeong Gyu,Lee, Sangyeoup,Kim, Yun Jin,Cho, Byung Mann,Park, Joo Sung,Kim, Hyung Hoi,Cheong, Jaehun,Jeong, Dong Wook,Lee, Yu Hyun,Cho, Young Hye,Bae, Mi Jin,Choi, Eun Jung WJG Press 2012 WORLD JOURNAL OF GASTROENTEROLOGY Vol.18 No.42
<P>To investigate the relationship between chronic viral hepatitis B (CVHB) and insulin resistance (IR) in Korean adults.</P>
Hepatocyte-specific Prominin-1 protects against liver injury-induced fibrosis by stabilizing SMAD7
Lee Hyun,Yu Dong-Min,Bahn Myeong-Suk,Kwon Young-Jae,Um Min Jee,Yoon Seo Yeon,Kim Ki-Tae,Lee Myoung-Woo,Jo Sung-Je,Lee Sungsoo,Koo Seung-Hoi,Jung Ki Hoon,Lee Jae-Seon,Ko Young-Gyu 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Prominin-1 (PROM1), also known as CD133, is expressed in hepatic progenitor cells (HPCs) and cholangiocytes of the fibrotic liver. In this study, we show that PROM1 is upregulated in the plasma membrane of fibrotic hepatocytes. Hepatocellular expression of PROM1 was also demonstrated in mice (Prom1CreER; R26TdTom) in which cells expressed TdTom under control of the Prom1 promoter. To understand the role of hepatocellular PROM1 in liver fibrosis, global and liver-specific Prom1-deficient mice were analyzed after bile duct ligation (BDL). BDL-induced liver fibrosis was aggravated with increased phosphorylation of SMAD2/3 and decreased levels of SMAD7 by global or liver-specific Prom1 deficiency but not by cholangiocyte-specific Prom1 deficiency. Indeed, PROM1 prevented SMURF2-induced SMAD7 ubiquitination and degradation by interfering with the molecular association of SMAD7 with SMURF2. We also demonstrated that hepatocyte-specific overexpression of SMAD7 ameliorated BDL-induced liver fibrosis in liver-specific Prom1-deficient mice. Thus, we conclude that PROM1 is necessary for the negative regulation of TGFβ signaling during liver fibrosis.
Hydrogen Peroxide Activates p70^S6k Signaling Pathway
Bae, Gyu-Un,Seo, Dong-Wan,Kwon, Hyoung-Keun,Lee, Hoi Young,Hong, Sungyoul,Lee, Zee-Won,Ha, Kwon-Soo,Lee, Hyang-Woo,Han. Jeung-Whan 성균관대학교 약학연구소 1999 成均藥硏論文集 Vol.11 No.-
We investigated a possible role of reactive oxygen species (ROS) in p70^S6k activation, which plays an important role in the progression of cells from G_0/G_1 to S phase of the cell cycle by translational up-regulation of a family of mRNA transcripts that encode for components of the protein synthetic machinery. Treatment of mouse epidermal cell JB6 with H_2O_2 generated extracellularly by glucose/glucose oxidase led to the activation of p70^S6k and p90^Rsk and to phosphorylation of p42^MAPK/p44^MAPK. The activation of p70^S6k and p90^Rsk was dose-dependent and transient, maximal activities being in extracts treated for 15 and 30 min, respectively. Further characterization of ROS-induced activation of p70^S6k using specific inhibitors for p70^S6k signaling pathway, rapamycin, and wortmannin revealed that ROS acted up-stream of the rapamycin-sensitive component FRAP/RAFT and wortmannin-sensitive component phosphatidylinositol 3-kinase, because both inhibitors caused the inhibition of ROS-induced p70^S6k activity. In addition, Ca^2+ chelation also inhibited ROS-induced activation of p70^S6k, indicating that Ca^2+ is a mediator of p70^S6k activation by ROS. However, down-regulation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive protein kinase C (PKC) by chronic pretreatment with TPA or a specific PKC inhibitor Ro-31-8220 did not block the activation of p70^S6k by ROS, indicating that the activation of TPA-responsive PKC was not required for stimulation of p70^S6k activity by H_2O_2 in JB6 cells. Exposure of JB6 cells to platelet-derived growth factor or epidermal growth factor led to a rapid increase in H_2O_2, phosphorylation, and activation of p70^S6k, which were antagonized by the pretreatment of catalase. Taken together, the results suggest that ROS act as a messenger in growth factor-induced p70^S6k signaling pathway.
강신몽,이원태,고영창,최상규,김윤희,이홍석,서재관,윤중진,이혜경,최득린,김종열,윤창육,변명식,이장홍 大韓法醫學會 1991 대한법의학회지 Vol.15 No.2
Individual identification is an important part in medicolegal field especially in mass disaster. At July, 27, 1989, KAL KE-803 was crashed on landing at Tripoli International Airport, Liba. The plane was caught in fire and sixty eight Koreans were sacrified. The majority of victims were severely charred and injured. The authors examed all dead bodies and successfully identified all the cases through visual, anthropological, odontological, radiological and pathological methods including fingerprint and blood typing.
Quasi-surface emission in vertical organic light-emitting transistors with network electrode.
Keum, Chang-Min,Lee, In-Ho,Lee, Sin-Hyung,Lee, Gyu Jeong,Kim, Min-Hoi,Lee, Sin-Doo Optical Society of America 2014 Optics express Vol.22 No.12
<P>We demonstrate a vertical-type organic light-emitting transistor (VOLET) with a network electrode of closed topology for quasi-surface emission. In our VOLET, the spatial distribution of the surface emission depends primarily on the relative scale of the aperture in the network electrode to the characteristic length for the charge carrier recombination. Due to the closed topology in the network of the source electrode, the charge transport and the resultant carrier recombination are substantially extended from individual network boundaries toward the corresponding aperture centers in the source electrode. The luminance was found to be well-controlled by the gate voltage through an organic semiconducting layer over the network source electrode.</P>
Recombinant human erythropoietin produced in milk of transgenic pigs
Park, Jin-Ki,Lee, Yun-Keun,Lee, Poongyeon,Chung, Hak-Jae,Kim, Sungwoo,Lee, Hyun-Gi,Seo, Myung-Kyu,Han, Joo-Hee,Park, Chun-Gyu,Kim, Hun-Taek,Kim, Yong-Kook,Min, Kwan-Sik,Kim, Jin-Hoi,Lee, Hoon-Taek,Cha Elsevier 2006 Journal of biotechnology Vol.122 No.3
<P><B>Abstract</B></P><P>We have developed a line of transgenic swine harboring recombinant human erythropoietin through microinjection into fertilized one cell pig zygotes. Milk from generations F<SUB>1</SUB> and F<SUB>2</SUB> transgenic females was analyzed, and hEPO was detected in milk from all lactating females at concentrations of approximately 877.9±92.8IU/1ml. The amino acid sequence of rhEPO protein in the transgenic pig milk matched that of commercial rhEPO produced from cultured animal cells. In addition, an F-36 cell line, which proliferates in the presence of hEPO or commercial EPO, was induced to synthesize erythroid by extracts from tg sow milk. This study provides evidence that production of purified rhEPO from transgenic pig milk is a potentially valuable technology, and can be used as a cost-effective alternative in clinical applications as well as providing other clinical advantages.</P>