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2001년 경기도와 강원도에서 채집한 Apodemus Mice 유래 한타바이러스의 혈청학적 및 유전학적 특성
남재환(Jae-Hwan Nam),유정희(Cheong-Hee Yu),황경아(Kyung-A Hwang),천정은(Jung-Eun Chun),최택균(Teak-Kyun Choi),최우영(Woo-Young Choi),김인범(In-Bum Kim),이찬희(Chan-Hee Lee),주영란(Young-Ran Ju),박근용(Keun-Yong Park) 대한미생물학회 2002 Journal of Bacteriology and Virology Vol.32 No.1
배양포유동물세포에서 환경돌연변이원에 의해 유발된 자매염색분체교환의 분석에 관한 연구
이석우,남정구,남재환,이병광,김은영,이승길 ( Sok Woo Lee,Joung Koo Nam,Jae Hwan Nam,Byoung Kwang Lee,Eun Young Kim,Seung Gil Lee ) 한국환경생물학회 1991 환경생물 : 환경생물학회지 Vol.9 No.2
The assay of SCEs has been used to measure mutagenicity induced several mutagens to high vertebrates. In this study, we used BHK-21, CHO-K1 and human peripheral lymphocyte as culture cell, and calcium chloride dihydrate(CaCl_2·2H_2O), sodium hypochloride(NaOCl), phenol(C_6H_5OH), benzo(a)pyrene(C_20H_12), carbon tetrachloride(CCl_4) and chloroform(CHCl_3) as mutagens. We examined and compared frequency between spontaneous and induced SCEs by mutagens. The mean spontaneous SCEs of human lymphocyte from 4 donors is scored 6.92±1.54(SCEs/cell) and BHK-21 is scored 0.18±0.03(SCEs/chromosome) and CHO-K1 is scored 0.61±0.08(SCEs/chromosome). In order to decided concentration of mutagens which is enough to induce SCEs and to effect SCEs score, we observed cell cytotoxicity and cell metaphase dependent on several concentration of mutagens. And then, using that concentration as control, we examined SCEs frequency induced three different concentration of mutagen. The increase of SCEs frequency induced by calcium chloride dihydrate is very little, but benzo(a)pyrene and phenol are great increase. Especially, we cannot find metaphase over 0.006mM benzo(a)pyrene and 1mM phenol. Although the increase of SCEs frequency induced by CHCl_3 is little, we observed many acentromeric chromosome in cell culture over 25mM CHCl_3. And we detected that SCEs frequency related with chromosome length of test cell.
강태훈(Tae-Hoon Kang),채수림(Soo-Lim Chae),최우영(Woo-Young Choi) , 박찬(Chan Park),남재환(Jae-Hwan Nam),주영란(Young-Ran Joo),박근영(Keun-Yong Park),조해월(Hae-Wol Cho),김인범(In-Beom Kim) 대한해부학회 2005 Anatomy & Cell Biology Vol.38 No.3
일본뇌염바이러스 (JEV)는 사람에 있어서는 급성뇌염을 유발하고, 다양한 배양세포에 있어서는 해로운 영향을 줄 것이라고 알려져 있다. 본 연구는 일본뇌염바이러스 (JEV)에 감염된 생쥐의 뇌에서 세포자멸사가 발생하는지를 알아보고자 하였다. JEV에 감염된 생쥐 뇌의 특정부위에서의 DNA파쇄는 DNA oligonucleosomal laddering을 관찰함으로써 확인하였고, 진행중인 세포자멸사는 in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) 기법으로 관찰하였다. TUNEL 염색과 JEV 항원에 대한 염색법을 이용하여 이중면역염색법을 시행한 결과, 감염된 많은 신경세포들이 TUNEL 면역염색성을 나타내었다. 이와 같은 결과는 생쥐 뇌에서 JEV 감염에 의해 유도된 세포사멸은 세포자멸사성 기작과 연관이 있으며, 따라서 이러한 세포자멸사는 일본뇌염에 따른 병 발생에 중요한 역할을 하는 것으로 보인다. Japanese encephalitis virus (JEV) may cause acute encephalitis in humans and induce severe cytopathic effects in various types of cultured cells. To investigate whether JEV infection induces apoptosis, we examined DNA fragmentation and apoptosis in the specific region of the JEV infected mouse brain by DNA oligonucleosomal laddering and in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) technique and immunohistochemical study. JEV infections in the mouse brain were detected in the telencephalon, the diencephalons, and the brain stem, but not in the cerebellum and the hippocampus. Fragmentation of cellular DNA into oligonucleosome-length ladders was only observed in tissue samples prepared from the cerebral cortex. In addition, the large number of TUNEL-positive cells was observed in the cerebral cortex. Double-labeling experiment with TUNEL staining and immunostaining for the JEV showed that TUNEL-positive neurons containing JEV immunoreactivity. These results suggest that JEV infection may evoke apoptotic neuronal death in the mouse brain, which plays an important role in the pathogenesis of Japanese encephalitis.
1996년부터 2005년까지 혈청검사로 진단된 신증후출혈열의 역학적 특성 분석
노윤태(Yoon-Tae Noh),조정은(Jung-Eun Cho),한명국(Myung Guk Han),이나연(Na-Yeon Lee),김수연(Su-Yeon Kim),주재신(Chaeshin Chu),이호동(Ho-Dong Lee),남재환(Jae-Hwan Nam),박근용(Keun-Yong Park),신영학(Young-Hack Shin),조해월(Hae Wol Cho) 대한미생물학회 2006 Journal of Bacteriology and Virology Vol.36 No.4