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사람 혈청 Vitronectin의 정제 및 항 Vitronectin 다클론 항체의 생산
장윤혜,김백남,이성순,문경,김승후,이재담 大韓免疫學會 1996 大韓免疫學會誌 Vol.18 No.2
Background: Vitronectin is one of major cell- adhesive glycoprotein in mammalian serum and plasma ; the other is fibronectin. It is a mixture of 65 and 75kDa protein in plasma which promotes spreading of a variety of cultured cells ,inhibits the cytotoxicity of membrane attacks complex C5b-7 and modulates thrombin-antithrombin III activity. Human plasma and serum contain 10-40mg of vitronectin per 100ml,but only a few mg or less of vitronectin can be isolated with a 0.5-20% recovery efficiency through very long processes or with expensive,commercially available monoclonal antibody. In this study, we purified the vitronectin from human plasma and produced anti-vitronectin polyclonal antibody using purified vitronectin. Methods: Vitronectin was purified from the human plasma by heparin-sepharose column and its efficacy was measured by cell spreading assay. Anti-vitronectin polyclonal antibody produced and confirmed by ELISA and immunoblotting. Results: This procedures produced about 0.8mg vitronectin from 100ml human plasma within 2 days. 1) Purified vitronectin promoted spreading of HepG2 hepatoma cells on substrates with a half maximal activity at 0.lug/ml. 2) In SDS-PAGE analysis of purified protein, 2 bands were found and their molecular weights were 75kDa and 65kDa,respectively. 3) The immunoblotting assay showed that the bands of molecular were same site as SDSPAGE analysis. Conclusion: Simple,rapid purified vitronectin by heparin-sepharose column and anti-vitronectin antibody may facilitate the elucidation of vitronectin function and action mechanism in human body.
종설논문 : 의사-제약회사 상호관계가 연구에 미치는 영향
김승후 ( Seong Who Kim ),홍정화 ( Jeong Hwa Hong ),김옥주 ( Ock Joo Kim ) 한국의료윤리학회 2011 한국의료윤리학회지 Vol.14 No.3
This article examines the influence of physician-pharmaceutical industry interaction upon medical research. We analyze some of the problems arising from pharmaceutical companies` sponsorship of clinical trials, such as biased results caused by multiple trials with predictable outcomes and publication biases. Furthermore, we propose specific measures to address and overcome these problems.
( Sang-min Kim ),( Jae-wan Huh ),( Eun-young Kim ),( Min-kyung Shin ),( Ji-eun Park ),( Seong Who Kim ),( Wooseong Lee ),( Bongkun Choi ),( Eun-ju Chang ) 생화학분자생물학회 2019 BMB Reports Vol.52 No.2
Endothelial dysfunction-induced lipid retention is an early feature of atherosclerotic lesion formation. Apoptosis of vascular smooth muscle cells (VSMCs) is one of the major modulating factors of atherogenesis, which accelerates atherosclerosis progression by causing plaque destabilization and rupture. However, the mechanism underlying VSMC apoptosis mediated by endothelial dysfunction in relation to atherosclerosis remains elusive. In this study, we reveal differential expression of several genes related to lipid retention and apoptosis, in conjunction with atherosclerosis, by utilizing a genetic mouse model of endothelial nitric oxide synthase (eNOS) deficiency manifesting endothelial dysfunction. Moreover, eNOS deficiency led to the enhanced susceptibility against pro-apoptotic insult in VSMCs. In particular, the expression of aggrecan, a major proteoglycan, was elevated in aortic tissue of eNOS deficient mice compared to wild type mice, and administration of aggrecan induced apoptosis in VSMCs. This suggests that eNOS deficiency may elevate aggrecan expression, which promotes apoptosis in VSMC, thereby contributing to atherosclerosis progression. These results may facilitate the development of novel approaches for improving the diagnosis or treatment of atherosclerosis. [BMB Reports 2019; 52(2): 145-150]
Han, Myung Woul,Lee, Jong Cheol,Kim, Young Min,Cha, Hee Jeong,Roh, Jong-Lyel,Choi, Seung-Ho,Nam, Soon Yuhl,Cho, Kyung-Ja,Kim, Seong Who,Kim, Sang Yoon SAGE Publications 2015 Otolaryngology-head and neck surgery Vol.152 No.1
<P><B>Objective</B></P><P>The development of biomarkers for the prediction of lymph node metastasis and prognosis is critical for deciding the treatment modality of tongue cancer. The purpose of our study is to investigate the clinical implications of epithelial-mesenchymal transition (EMT) expression in tongue cancer.</P><P><B>Study Design</B></P><P>Historical cohort study</P><P><B>Setting</B></P><P>Tertiary-care hospital.</P><P><B>Subjects and Methods</B></P><P>The study included 95 subjects with tongue cancer who underwent wide excision and neck dissection. According to characteristics of immunohistochemical staining for E-cadherin and vimentin, we classified the tumors as complete EMT phenotype, incomplete EMT phenotype, or epithelial phenotype. The correlation between risk factors and nodal metastasis was assessed, and disease-free survival (DFS) was analyzed.</P><P><B>Results</B></P><P>Positive lymph nodes were detected in 46 (48.4%) patients and was found to correlate significantly with depth of invasion ≥4 mm and EMT expression on multivariate analysis (<I>P</I> = .030, <I>P</I> = .022, respectively). The mean follow-up period of all patients was 96.3 months (range, 6-149 months). Overall 5-year DFS was 61.7%. On multivariate analysis, the only factors affecting DFS were nodal stage and EMT expression (<I>P</I> = .033, <I>P</I> = .021, respectively).</P><P><B>Conclusions</B></P><P>Our study reveals that EMT expression is a significant biomarker for predicting lymph node metastasis and tumor recurrence in tongue cancer. Evaluation of EMT expression in tongue cancer can allow therapy to be offered accordingly.</P>
Seung Eun Lee,Jung Eun Jang,Hyun Sik Kim,Min Kyo Jung,Myoung Seok Ko,Mi-Ok Kim,Hye Sun Park,Wonil Oh,Soo Jin Choi,Hye Jin Jin,Sang-Yeob Kim,Yun Jae Kim,Seong Who Kim,Min Kyung Kim,Chang Ohk Sung,Chan- 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
The administration of mesenchymal stem cells (MSCs) was shown to attenuate overt as well as early diabetic nephropathy in rodents, but the underlying mechanism of this beneficial effect is largely unknown. Inflammation and mitochondrial dysfunction are major pathogenic factors in diabetic nephropathy. In this study, we found that the repeated administration of MSCs prevents albuminuria and injury to tubular epithelial cells (TECs), an important element in the progression of diabetic nephropathy, by improving mitochondrial function. The expression of M1 macrophage markers was significantly increased in diabetic kidneys compared with that in control kidneys. Interestingly, the expression of arginase-1 (Arg1), an important M2 macrophage marker, was reduced in diabetic kidneys and increased by MSC treatment. In cultured TECs, conditioned media from lipopolysaccharide-activated macrophages reduced peroxisomal proliferator-activated receptor gamma coactivator 1α (Pgc1a) expression and impaired mitochondrial function. The coculture of macrophages with MSCs increased and decreased the expression of Arg1 and M1 markers, respectively. Treatment with conditioned media from cocultured macrophages prevented activated macrophage-induced mitochondrial dysfunction in TECs. In the absence of MSC coculture, Arg1 overexpression in macrophages reversed Pgc1a suppression in TECs. These observations suggest that MSCs prevent the progression of diabetic nephropathy by reversing mitochondrial dysfunction in TECs via the induction of Arg1 in macrophages.
Homotypic Interaction of Stabilin-2 Plays a Critical Role in Lymph Node Metastasis of Tongue Cancer
HAN, MYUNG WOUL,LEE, JONG CHEOL,PARK, SEUNG-YOON,KIM, YOUNG MIN,CHO, KYUNG-JA,KIM, SEONG WHO,LEE, MYUNGJIN,NAM, SOON YUHL,KIM, IN-SAN,KIM, SANG YOON Potamitis Press 2016 Anticancer research Vol. No.
<P>Background/Aim: Lymph node (LN) metastasis of solid types of tumors has important clinical significance and it is therefore critical to identify molecular biomarkers that would enable the selection of patients with LN metastases. Patients and Methods: We evaluated the expression of stabilin-2 in primary oral tongue tumors and metastatic LNs using immunohistochemical staining. The correlation between risk factors and nodal metastasis was assessed and disease-free survival was analyzed. Results: Stabilin-2 expression remained a significant predictor of LN metastasis and the factor affecting recurrence in tongue cancer. Most importantly, all metastatic tumors of tongue, lung, stomach and colon cancers stained positive for stabilin-2 and stabilin-2 was expressed strongly in the sinusoidal endothelial cell of metastatic LNs. Conclusion: Stabilin-2 can play a critical role in the first entrapping step of LN metastasis through homotypic interaction with the lymphatic endothelium and appears to be a tumor biomarker predicting for LN metastasis in patients with solid tumors.</P>
Kim, Sun A,Kwak, Jihye,Nam, Hae Yun,Chun, Sung Min,Lee, Byoung Wook,Lee, Hyang Ju,Khang, Shin Kwang,Kim, Seong Who Springer Science and Business Media LLC 2013 Modern pathology Vol.26 No.5
<P>WNT inhibitory factor-1 (WIF1) is an antagonist of the WNT signaling pathway. We investigated the relationship between WIF1 promoter methylation and regulation of the WNT/β-catenin signaling pathway, tumor grade, and survival in patients with astrocytoma. This study included 86 cases of astrocytoma, comprising 20 diffuse astrocytomas and 66 glioblastomas. In addition, 17 temporal lobectomy specimens from patients with epilepsy were included as controls. The ratio of methylated DNA to total methylated and unmethylated DNA (% methylation) was measured by methylation- and unmethylation-specific PCR. Representative tumor tissue was immunostained for WIF1, β-catenin, cyclin D1, c-myc, and isocitrate dehydrogenase 1. Levels of WIF1 promoter methylation, mRNA expression, and protein expression in a glioblastoma cell line were compared before and after demethylation treatment. The mean percent methylation of the WIF1 promoter in astrocytomas was higher than that in control brain tissue. WIF1 protein expression was lower in the tumor group with >5% methylation than in the group with <5% methylation. Cytoplasmic β-catenin staining was more frequently observed in tumors with a low WIF1 protein expression level. Demethylation treatment of a glioblastoma cell line increased WIF1 mRNA and protein expression. Increased WIF1 promoter methylation and decreased WIF1 protein expression were not related to patient survival. In conclusion, WIF1 expression is downregulated by promoter methylation and is an important mechanism of aberrant WNT/β-catenin pathway activation in astrocytoma pathogenesis.</P>