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특별강연 및 일반연제 발표 : CMV 항체 양성 반응을 가진 신장 이식 환자에서 pp(65) 항원 혈증 감사에 의한 CMV 감염의 추적 관찰
이방훈 ( Lee Bang Hun ),오하영 ( O Ha Yeong ),허우성 ( Heo U Seong ),김춘관 ( Kim Chun Gwan ),김신우 ( Kim Sin U ),이혁 ( Lee Hyeog ),김성민 ( Kim Seong Min ),백경란 ( Baeg Gyeong Lan ),이남용 ( Lee Nam Yong ),김성주 ( Kim Seong 대한신장학회 1999 춘계학술대회 초록집 Vol.18 No.2
췌담도 ; 췌관 stent후 병발된 췌관석을 동반한 췌관 변화
윤재훈 ( Yun Jae Hun ),백상현 ( Baeg Sang Hyeon ),조경란 ( Jo Gyeong Lan ),최호순 ( Choe Ho Sun ),이오영 ( Lee O Yeong ),한동수 ( Han Dong Su ),손주현 ( Son Ju Hyeon ),함준수 ( Ham Jun Su ),이민호 ( Lee Min Ho ),이동후 ( Lee Dong 대한소화기학회 2003 대한소화기학회 추계학술대회 Vol.2003 No.-
<서론> 내시경적 췌관 배액관의 단기적인 효과는 인정받고 있으나 장기적인 췌관 배액술의 효과와 안정성에 있어 문제가 제기되고 있다. 췌관 배액술 후 만성 췌장염과 같은 췌관의 변화(이차분지의 확장, 췌관 벽의 불규칙한 변화, 협착, 주췌관의 섬유화)를 볼 수 있는데, 이런 변화가 일시적인지, 회복 가능한 변화인지에 대해 아직 논란이 있다. 이러한 췌관 변화의 기전으로 첫째, stent와 무관한 본래 췌장질환의 진행 과정일 수도 있고 둘째, stent의
폐암 수술 후 흉벽의 종양 재발 검출에 있어 TI-201 폐 SPECT의 유용성
유영훈 ( Yu Yeong Hun ),김형중 ( Kim Hyeong Jung ),안철민 ( An Cheol Min ),김세규 ( Kim Se Gyu ),백효채 ( Baeg Hyo Chae ),이두연 ( Lee Du Yeon ),정경영 ( Jeong Gyeong Yeong ),윤미진 ( Yun Mi Jin ),박상준 ( Park Sang Jun ),문성욱 ( 대한결핵 및 호흡기학회 2002 Tuberculosis and Respiratory Diseases Vol.53 No.5
백서 경동맥 손상 모델에서 신생내막형성에 미치는 Erythropoietin 효과
김기훈 ( Kim Gi Hun ),권경희 ( Kwon Gyeong Hui ),백승훈 ( Baeg Seung Hun ),박병현 ( Park Byeong Hyeon ),조정구 ( Jo Jeong Gu ) 대한내과학회 2003 대한내과학회지 Vol.65 No.5
목적 : 신생내막증식이 관상동맥의 풍선성형술 후의 재협착이나 혈액투석을 위해 만든 동정맥루의 협착의 중요한 기전 중의 하나로 알려져 있고 erythropoietin 투여가 이러한 신생내막증식을 유발하여 협착을 일으키는지에 대해서는 아직 논란이 많다. 이에 본 연구자는 in vivo 연구로 백서의 경동맥 혈관손상 모델을 만든 후 erythropoietin을 투여하여 신생내막증식에 erythropoietin 투여가 미치는 영향을 보고자 하였다. 방법 : 인 Background : Neointimal hyperplasia is major cause of instent restenosis in coronary artery and stenosis in arteriovenous fisula for hemodialysis. Erythropoietin is known to show proliferative effect on vascular smooth muscle cells in vitro study, but the
김병학,예상규,Yun Sook Min,Jung Sook Choi,Gyeong-Hun Baeg,Youngsoo Kim,신종욱,김태윤 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.5
Persistently activated JAK/STAT3 signaling pathway plays a pivotal role in various human cancers including major carcinomas and hematologic tumors, and is implicated in cancer cell survival and proliferation. Therefore, inhibition of JAK/STAT3 signaling may be a clinical application in cancer therapy. Here, we report that 2-cyclohexylimino-6-methyl-6,7-dihydro-5H-benzo [1,3]oxathiol-4-one (BOT-4-one), a small molecule inhibitor of JAK/STAT3 signaling, induces apoptosis through inhibition of STAT3 activation. BOT-4-one suppressed cytokine (upd)-induced tyrosine phosphorylation and transcriptional activity of STAT92E,the sole Drosophila STAT homolog. Consequently,BOT-4-one significantly inhibited STAT3 tyrosine phosphorylation and expression of STAT3 downstream target gene SOCS3 in various human cancer cell lines, and its effect was more potent in JAK3-activated Hodgkin’s lymphoma cell line than in JAK2-activated breast cancer and prostate cancer cell lines. In addition, BOT-4-one-treated Hodgkin’s lymphoma cells showed decreased cell survival and proliferation by inducing apoptosis through down-regulation of STAT3 downstream target anti-apoptotic gene expression. These results suggest that BOT-4-one is a novel small molecule inhibitor of JAK3/STAT3 signaling and may have therapeutic potential in the treatment of human cancers harboring aberrant JAK3/STAT3 signaling,specifically Hodgkin’s lymphoma.
Kim, Byung-Hak,Min, Yun-Sook,Choi, Jung-Sook,Baeg, Gyeong-Hun,Kim, Young-Soo,Shin, Jong-Wook,Kim, Tae-Yoon,Ye, Sang-Kyu Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.5
Persistently activated JAK/STAT3 signaling pathway plays a pivotal role in various human cancers including major carcinomas and hematologic tumors, and is implicated in cancer cell survival and proliferation. Therefore, inhibition of JAK/STAT3 signaling may be a clinical application in cancer therapy. Here, we report that 2-cyclohexylimino-6-methyl-6,7-dihydro-5H-benzo [1,3]oxathiol-4-one (BOT-4-one), a small molecule inhibitor of JAK/STAT3 signaling, induces apoptosis through inhibition of STAT3 activation. BOT-4-one suppressed cytokine (upd)-induced tyrosine phosphorylation and transcriptional activity of STAT92E, the sole $Drosophila$ STAT homolog. Consequently, BOT-4-one significantly inhibited STAT3 tyrosine phosphorylation and expression of STAT3 downstream target gene SOCS3 in various human cancer cell lines, and its effect was more potent in JAK3-activated Hodgkin's lymphoma cell line than in JAK2-activated breast cancer and prostate cancer cell lines. In addition, BOT-4-one-treated Hodgkin's lymphoma cells showed decreased cell survival and proliferation by inducing apoptosis through down-regulation of STAT3 downstream target anti-apoptotic gene expression. These results suggest that BOT-4-one is a novel small molecule inhibitor of JAK3/STAT3 signaling and may have therapeutic potential in the treatment of human cancers harboring aberrant JAK3/STAT3 signaling, specifically Hodgkin's lymphoma.
Evaluation of sewage sludge incineration ash as a potential land reclamation material
Lin, Wenlin Yvonne,Ng, Wei Cheng,Wong, Belinda Shu Ee,Teo, Serena Lay-Ming,Sivananthan, Gayathiri d/o,Baeg, Gyeong Hun,Ok, Yong Sik,Wang, Chi-Hwa Elsevier 2018 Journal of hazardous materials Vol.357 No.-
<P><B>Abstract</B></P> <P>This study evaluated the potential of utilising sewage sludge incineration ash as a land reclamation material. Toxicity assessment of the leachate of the ash was carried out for both terrestrial and marine organisms. Both the fruit fly <I>Drosophila melanogaster</I> and barnacle <I>Amphibalanus amphitrite</I> showed that both bottom and fly ash leached at liquid-to-solid (L/S) ratio 5 did not substantially affect viabilities. The leachate carried out at L/S 10 was compared to the European Waste Acceptance Criteria and the sewage sludge ashes could be classified as non-hazardous waste. The geotechnical properties of the sewage sludge ash were studied and compared to sand, a conventional land reclamation material, for further evaluation of its potential as a land reclamation material. It was found from direct shear test that both bottom and fly ashes displayed similar and comparable shear strength to that of typical compacted sandy soil based on the range of internal friction angle obtained. However, the consolidation profile of bottom ash was significantly different from sand, while that of fly ash was more similar to sand. Our study showed that the sewage sludge ash has the potential to be used as a land reclamation material.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Toxicity of fresh & aged sewage sludge incineration fly & bottom ash was evaluated. </LI> <LI> Terrestrial (fruit fly) & marine organisms (barnacle) were used for toxicity study. </LI> <LI> Leachates of ashes had no adverse toxicity on both fruit fly and barnacle tested. </LI> <LI> Fly ash (compared to bottom ash) had more similar geotechnical properties to sand. </LI> <LI> This study showed the potential in using sewage sludge ashes as fill material. </LI> </UL> </P>
MS-1020 is a novel small molecule that selectively inhibits JAK3 activity
Kim, Byung-Hak,Oh, Sei-Ryang,Yin, Chang-Hong,Lee, Sangku,Kim, Eun-Ah,Kim, Min-Seok,Sandoval, Claudio,Jayabose, Somasundaram,Bach, Erika A.,Lee, Hyeong-Kyu,Baeg, Gyeong-Hun Blackwell Publishing Ltd 2010 British journal of haematology Vol.148 No.1
<P>Summary</P><P>In order to identify Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling inhibitors, a cell-based high throughput screening was performed using a plant extract library that identified <I>N</I>b-(&agr;-hydroxynaphthoyl)serotonin called MS-1020 as a novel JAK3 inhibitor. MS-1020 potently inhibited persistently-active STAT3 in a cell type-specific manner. Further examination showed that MS-1020 selectively blocked constitutively-active JAK3 and consistently suppressed interleukin-2-induced JAK3/STAT5 signalling but not prolactin-induced JAK2/STAT5 signalling. Furthermore, MS-1020 affected cell viability only in cancer cells harbouring persistently-active JAK3/STATs, and <I>in vitro</I> kinase assays showed MS-1020 binds directly with JAK3, blocking its catalytic activity. Therefore, the present study suggested that this reagent selectively inhibits JAK3 and subsequently leads to a block in STAT signalling. Finally, MS-1020 decreased cell survival by inducing apoptosis via down-regulation of anti-apoptotic gene expression. These results suggest that MS-1020 may have therapeutic potential in the treatment of cancers harbouring aberrant JAK3 signalling.</P>