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당뇨병 및 내당능장애가 없는 정상 성인에서 인슐린 저항성과 혈중 Apolipoprotein B 및 대사증후군 인자와의 연관성
황상태 ( Hwang Sang Tae ),성기철 ( Seong Gi Cheol ),김병진 ( Kim Byeong Jin ),김범수 ( Kim Beom Su ),강진호 ( Kang Jin Ho ),이만호 ( Lee Man Ho ),박정로 ( Park Jeong Lo ),이은정 ( Lee Eun Jeong ),이원영 ( Lee Won Yeong ),김선우 ( 대한내과학회 2004 대한내과학회지 Vol.66 No.2
Background : Insulin resistance is associated with greatly increased risk of coronary artery disease. Serum apolipoprotein B and the ratio of apo A-1/Apo B are important markers of the coronary artery disease. The aim of this study was to assess the assoc
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Ahn, Bum Ju,Le, Hoang,Shin, Min Wook,Bae, Sung-Jin,Lee, Eun Ji,Lee, Sung Yi,Yang, Ju Hee,Wee, Hee-Jun,Cha, Jong-Ho,Seo, Ji Hae,Lee, Hye Shin,Lee, Hyo-Jong,Arai, Ken,Lo, Eng H.,Jeon, Sejin,Oh, Goo Taeg American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.32
<P>Ninjurin1 is involved in the pathogenesis of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, by mediating leukocyte extravasation, a process that depends on homotypic binding. However, the precise regulatory mechanisms of Ninjurin1 during inflammation are largely undefined. We therefore examined the pro-migratory function of Ninjurin1 and its regulatory mechanisms in macrophages. Interestingly, Ninjurin1-deficient bone marrow-derived macrophages exhibited reduced membrane protrusion formation and dynamics, resulting in the impairment of cell motility. Furthermore, exogenous Ninjurin1 was distributed at the membrane of filopodial structures in Raw264.7 macrophage cells. In Raw264.7 cells, RNA interference of Ninjurin1 reduced the number of filopodial projections, whereas overexpression of Ninjurin1 facilitated their formation and thus promoted cell motility. Ninjurin1-induced filopodial protrusion formation required the activation of Rac1. In Raw264.7 cells penetrating an MBEC4 endothelial cell monolayer, Ninjurin1 was localized to the membrane of protrusions and promoted their formation, suggesting that Ninjurin1-induced protrusive activity contributed to transendothelial migration. Taking these data together, we conclude that Ninjurin1 enhances macrophage motility and consequent extravasation of immune cells through the regulation of protrusive membrane dynamics. We expect these findings to provide insight into the understanding of immune responses mediated by Ninjurin1.</P>
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Lee, Jae Young,Park, Younggeun,Pun, San,Lee, Sung Sik,Lo, Joe F.,Lee, Luke P. The Royal Society of Chemistry 2015 Nanoscale Vol.7 No.23
<P>Intracellular Cyt c release profiles in living human neuroblastoma undergoing amyloid β oligomer (AβO)-induced apoptosis, as a model Alzheimer's disease-associated pathogenic molecule, were analysed in a real-time manner using plasmon resonance energy transfer (PRET)-based spectroscopy.</P>
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Lee, Sae-lo-oom,Ryu, Hwani,Son, A-rang,Seo, Bitna,Kim, Jooyoung,Jung, Seung-Youn,Song, Jie-Young,Hwang, Sang-Gu,Ahn, Jiyeon Hindawi Publishing Corporation 2016 Oxidative medicine and cellular longevity Vol.2016 No.-
<P>Although many studies have examined the roles of hypoxia and transforming growth factor- (TGF-) <I>β</I> separately in the tumor microenvironment, the effects of simultaneous treatment with hypoxia/reoxygenation and TGF-<I>β</I> on tumor malignancy are unclear. Here, we investigated the effects of redox signaling and oncogenes on cell proliferation and radioresistance in A549 human lung cancer cells in the presence of TGF-<I>β</I> under hypoxia/reoxygenation conditions. Combined treatment with TGF-<I>β</I> and hypoxia activated epidermal growth factor receptor (EGFR) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a redox-sensitive transcription factor. Interestingly, Nrf2 knockdown suppressed the effects of combined treatment on EGFR phosphorylation. In addition, blockade of EGFR signaling also suppressed induction of Nrf2 following combined treatment with hypoxia and TGF-<I>β</I>, indicating that the combined treatment induced positive crosstalk between Nrf2 and EGFR. TGF-<I>β</I> and hypoxia/reoxygenation increased the accumulation of reactive oxygen species (ROS), while treatment with N-acetyl-<SMALL>L</SMALL>-cysteine abolished the activation of Nrf2 and EGFR. Treatment with TGF-<I>β</I> under hypoxic conditions increased the proliferation of A549 cells compared with that after vehicle treatment. Moreover, cells treated with the combined treatment exhibited resistance to ionizing radiation (IR), and knockdown of Nrf2 increased IR-induced cell death under these conditions. Thus, taken together, our findings suggested that TGF-<I>β</I> and hypoxia/reoxygenation promoted tumor progression and radioresistance of A549 cells through ROS-mediated activation of Nrf2 and EGFR.</P>
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삽사리의 가계 분석에 사용할수 있는 DNA probe의 선정
이상로,이호섭,정운복,탁연빈,박희천,김종봉,하지홍 대구효성가톨릭대학교 자연과학연구소 1991 基礎科學硏究論集 Vol.1991 No.1
DNA지문법은 범죄감식, 친자감별, 가계분석, twin zygosity의 결정, 집단 유전학, 행동 생태학 등의 분야(jeffreys et al., 1985:Gill et al., 1985, 1987 : Lander, 1989:Neufeld and Colman, 1990)에서 널리 활용될 뿐만 아니라 멸종위기에 처한 동식물의 육종과 보존을 위해서도 없어서는 안되는 중요한 연구방법이 되었다.(Georges et al., 1988:Burke et al., 1989). 최근 미국에서는 멸종위기에 처한 퓨마와 매의 보존을 위해 이들 동물들에 대한 RFLP연구를 행했는데 현존집단내 혈통관계에 대한 중요한 정보를 얻을 수 있었다
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Lee Wan-Hsuan,Lin Chien-Chin,Tsai Xavier Cheng-Hong,Hsu Chia-Lang,Yao Chi-Yuan,Tien Feng-Ming,Lo Min-Yen,Chang Yu-Sung,Kuo Yuan-Yeh,Yu Shan-Chi,Liu Ming-Chih,Yuan Chang-Tsu,Tseng Mei-Hsuan,Peng Yen-Li 대한혈액학회 2026 Blood Research Vol.61 No.1
Purpose Myelodysplastic syndromes/neoplasms (MDS) represent a heterogeneous group of clonal hematopoietic disorders with variable prognosis. While several risk models exist, the prognostic role of immune-related biomarkers remains unclear. This study aimed to determine whether the lymphocyte-to-monocyte (L/M) ratio at diagnosis serves as an independent prognostic factor in MDS and to explore its biological correlates. Methods A retrospective analysis of 554 patients with primary MDS diagnosed at the National Taiwan University Hospital was conducted. Patients were stratified by an L/M ratio cutoff of 1.5, determined by maximally selected rank statistics. Clinical, cytogenetic, and mutational profiles were assessed. Survival outcomes were analyzed using Kaplan–Meier methods and multivariable Cox regression incorporating IPSS-R, IPSS-M, and WHO-2022/ICC classifications. RNA sequencing was performed on diagnostic bone marrow samples to evaluate transcriptomic differences between groups. Results Patients with L/M ratio > 1.5 were younger, had lower platelet counts, more advanced subtypes, and higher frequencies of STAG2 and U2AF1 mutations. Elevated L/M ratio was significantly associated with inferior leukemiafree and overall survival, independent of established prognostic models. Adverse prognostic effects were mitigated by allogeneic hematopoietic stem cell transplantation but not by hypomethylating agents. Transcriptomic analysis revealed downregulation of inflammatory pathways (IL-2–STAT5, IL6–JAK–STAT3, interferon responses) and the p53 pathway, along with enrichment of MYC targets in the high L/M group. Conclusion An elevated L/M ratio is an independent and readily available biomarker that predicts poor outcomes in MDS. Integration of this parameter into existing risk models may refine prognostication and guide treatment intensity. Transcriptomic findings suggest immune suppression and p53 deregulation underlie its adverse impact, highlighting potential therapeutic avenues.
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