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김현정,백주은,하혜정,양중일,함종렬,장세호,전은실 대한내과학회 2003 대한내과학회지 Vol.64 No.1
저자들은 28세의 그레이브스 병으로 진단 받은 환자에서 그레이브스 병의 악화에 동반되어막성 신병증이 발생함을 경험하여 보고하조가 한다. 자가면역 갑상선 질환과 이에 동반되는 막성 신병증간의 연관관계는 아직 명확하지 않으나, 질환의 발병기전을 고려할 때 두 질환간의 관련성이 제시되고 있으므로 자가면역 갑상선 질환 환자에서 진단 혹은 치료를 하는 과정에서 요검사를 시행하여 혈뇨와 단백뇨의 유무를 관찰하는 것은 필요하다고 생각한다. Membranous nephropathy is one of the most common causes of the nephrotic syndrome in adults. Membranous nephropathy is known as a disease associated with many other disorders and the presumed etiology of the disease is a deposition of circulating immune complexes. But, it has rarely been reported in association with autoimmune thyroiditis. We report a case of membranous nephropathy associated with Graves' disease and review the literature regarding this disease entity. (Korean J Med 64:130-136, 2003)
Resistance to Cytotoxic Chemotherapy Is Induced by NK Cells in Non-Hodgkin`s Lymphoma Cells
( Dae Ho Cho ),( Young In Kim ),( Jae Seung Kang ),( Eun Sil Hahm ),( Yool Hee Yang ),( Dae Jin Kim ),( Seong Han Kim ),( Yeong Seok Kim ),( Dae Young Hur ),( Hyun Jeong Park ),( Young Il Hwang ),( Ta 전남대학교 약품개발연구소 2004 약품개발연구지 Vol.13 No.-
Lee, Young-Sun,Kim, Yeong-Seok,Kim, Dae-Jin,Hur, Dae-Young,Kang, Jae-Seung,Kim, Young-In,Hahm, Eun-Sil,Cho, Dae-Ho,Hwang, Young-Il,Lee, Wang-Jae The Korean Association of Immunobiologists 2006 Immune Network Vol.6 No.2
Background: CM1 (Centrocyte/-blast Marker I) defined by a mAb developed against concanavalin-A activated PBMC, is expressed specifically on a subpopulation of centroblasts and centrocytes of human germinal center (GC) B cells. Burkitt lymphoma (BL) is a tumor consisting of tumor cells with the characteristics of GC B cell. Previously we reported that CM1 ligation with anti-CM1 mAb induced apoptosis in Ramos $(IgM^{high})$ and Raji $(IgM^{low})$ cells. Methods & Results: In the present study, we observed that CM1 ligation with anti-CM1 mAb induced Fas ligand and Fas expression in Ramos cells, but not in Raji cells. Furthermore, anti-Fas blocking antibody, ZB4, blocked CM1-mediated apoptosis effectively in Ramos cells, but not in Raji cells. Increased mitochondrial membrane permeabilization, which was measured by $DiOC_6$, was observed only in Raji cells. In contrast to no significant change of Bax known as pro-apoptotic protein, anti-apoptotic protein Bcl-2 was significantly decreased in Raji cells. In addition, we observed that CM1 ligation increased release of mitochondrial cytochrome c and upregulated caspase-9 activity in Raji cells. Conclusion: These results suggest that apoptosis induced by CM1-ligation is mediated by Fas-Fas ligand interaction in Ramos cells, whereas apoptosis is mediated by down-regulation of Bcl-2 and subsequent decrease of mitochondrial membrane potential in Raji cells.