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라미부딘 장기투여 중 발생한 B 형 간염 바이러스 YMDD 영역의 유전자변이
이종훈(Jong Hun Lee),신우원(Woo Won Shin),안현숙(Hyun Sook Ahn),성명식(Myung Sik Seong),조정환(Jeong Hwan Cho),정동엽(Dong Yup Jung),강기태(Ki Tae Kang),김병희(Byung Hee Kim),노명환(Myung Hwan Roh),한상영(Sang Young Han),최석렬(Seok 대한내과학회 2001 대한내과학회지 Vol.61 No.4
N/A Background: The emergence of YIDD or YVDD mutant hepatitis B virus (HBV), with point mutation in the YMDD motif of DNA polymerase gene, has been reported in patient s with lamivudine treatment group. The aims of this study was to investigate the emergence of mutant HBV during long-term lamivudine therapy using nested polymerase chain reaction (PCR) method and direct DNA sequencing. Methods: Twenty-one chronic hepatitis B patients with HBeAg and HBV DNA positive were evaluated. During lamivudine therapy, there were reported breakthroughs of HBV DNA (over 50pg/mL) when investigated the emergence of YMDD mutants by nested PCR method using restriction fragment length polymorphism (RFLP) in all patients. Direct DNA sequencing of HBV DNA polymerase gene including YMDD motif was also performed. Results: There were 13 patients (61.9%) with YIDD mutant and 8 patients (38.1%) with YVDD mutant. The result s of direct DNA sequencing were consistent with those of nested PCR data based on RFLP. The breakthrough was occurred at 15 to 106 weeks (57.9±23.6). At the point of breakthrough, the level of ALT was 74.8±117.7 (14-546) IU/L, and it was lower than the level of ALT before the therapy. Conclusion: In the long-term therapy of lamivudine, the emergence of YMDD motif mutant HBV was related to the breakthrough of HBV DNA and YIDD mutant was frequent. The nested PCR method using RFLP may be simple and sensitive to detect the YMDD motif mutant HBV. (Korean J Med 61:374-383, 2001)
사람 암세포주 K562 , U937 및 쥐 암세포주 P388 , FM3A 에서의 항암제 다제내성 기전 및 내성극복
도현국(Hyun Kuk Doh),김재석(Jae Seok Kim),손지원(Ji Weon Son),성명식(Myung Sik Sung),김종성(Jong Seong Kim),김선희(Sun Hee Kim),정병선(Byung Sun Jung) 대한내과학회 1992 대한내과학회지 Vol.43 No.3
N/A Background: To study the mechanism of multidrug resistnce (MDR) and overcome MDR in cancer cells, we investigated the combination effects of anticancer agents with calmodulin inhibitors (e,g trifluoroperazine (TFP) and W-7), calcium function modifiers (e.g., quinidine and verapamil) and a protein kinase-C activator (e.g., phorbol ester) in chronic myelogenous leukemic cells, histiocytic lymphoma cells and breast cancer cells. Methods: Some MDR mutant sublines which had cross-resistance to colchicine, actinomycm D, adriamycin and vinblastine were isolated from K562, U937 and FM3A cell lines. MTT analysis was used to measure the level of the cytotoxicity, The cytotoxicity and the combination effects were compared by IC50 (1nhibition concentration50) to control group. Results: In case of U937/MDR, TFP increased the combination effect to tenfold in colchicine (COL), eightfold in vinblastine (VLB) and thirteenfold in actinomycin D (ACT-D). Quinidine increased the effect to threefold in COL, fourfold in VLB and sevenfold in ACT-D. Verapamil also increased the effect to sevenfold in COL, sixfold in VLB fivefold in ACT-D. In case of K562/MDR, TFP, quinidine and verapamil each increased the combination effect to sixfold, twelvefold and thirteenfold in COL and sixfold, fivefold and fivefold in adriamycin (ADM). W-7 in concentration of 20uM increased the combination effect to six point sevenfold in ACT-D, twofold in COL and two point threefold in ADM. In the combination of COL with 0.48uM TPA, the cytotoxicity was reduced to two point eightfold in case of FM3A/MDR. TPA (12-0-tetradecanoyl phorbol 13-acetate), in concentration of 0.48uM, a phorbol ester, reduced the cytotoxicity to two point eightfold in case of FM3A/ MDR. Conclusion: When the combination effects of anticancer agents with calmodulin inhibitors (e.g TFP and W -7) and calcium function modifiers (e.g., quinidine and verapamil) were examined, the cytotoxicity changes of anticancer agents were small in drug sensitive cells. But in MDR cells, the combination effects were prominent. The reduced cytotoxicity of anticancer agents by TPA suggested that protein kinase-C might be related with the mechanism of acquiring drug resistance on cancer cells.
김종성,김재석,손지원,최석렬,신우원,성명식 대한소화기내시경학회 1992 Clinical Endoscopy Vol.12 No.1
The majority of the cysts developed in pancreas are inflammatory pseudocyst but neoplastic cysts are rarely encountered Especially, mucinous cystadenoma which was begun and originated from epithelial cell of pancreatic duct is difficult to differentiate from pseudocysts by preoperative clinical, laboratory and radiologic findings. Mucinous cystadenoma has a malignant potentiality, so complete excision of cystadenoma is the treatment of choice. Recently, we experienced one case of mucionus cystadenoma in 37 year-old female, we report it with a review of the literature.