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Degradation of Phenanthrene by Sphingomonas sp. 1-21 Isolated from Oil Contaminated Soil
RYEOM, TAI-KYUNG,LEE, IL-GYU,SON, SEUNG-YEOL,AHN, TAE-YOUNG 한국미생물 · 생명공학회 2000 Journal of microbiology and biotechnology Vol.10 No.5
A phenanthrene-degrading bacterium, Strain 1-21, was isolated from oil-contaminated soil. This strain was a Gramnegative, aerobic, and rod-shaped bacterium, and exhibited a 99% sequence similarity of 16S rDNA to that of Sphingomonas subarctica. The major cellular fatty acid was a summed feature 7 (18:1 w7c, 18:1 w9t, 18:1 w12t), which is a characteristic of the Sphingomonas species. When 200 and 1,000ppm of phenanthrene was added as the sole carbon source, Strain 1-21 degraded 98% and 67% after 10 days of incubation, respectively. Futhermore, this strain was also able to utilize naphthalene and fluorene as sole carbon and energy sources.
마우스 피부암 발생과정에 있어서 2,3,7,8-Tetrachlorodibenzo-pDioxin (TCDD) 처리에 의한 유전자발현 변화 연구
Ryeom Tai Kyung,Kim Ok Hee,Kong Mi Kyung,Park Mi Sun,Jee Seung Wan,Eom Mi Ok,Kang Ho Il 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.1
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanism of carcinogenesis by TCDD is unclear, it is considered to be a non-genotoxic compound and tumor promoter. In our experiment, we investigated the effects of TCDD on gene expression in mouse skin carcinogenesis. We used cDNA microarray to detect the differential gene expression in tumors induced in hairless mouse skin by MNNG plus TCDD protocol. We found that erb-2, c-ets2 and p27$^{kip1}$ were significantly up-regulated, but TNFR2, AKT-l, integrin $\beta$l, maspin, IGF-l, c-raf-l, Rb were significantly down-regulated, in tumor region, respectively. We also found that the expression of 53 genes involved in cen cycle, signal transduction, apoptosis, adhesion molecule, angiogenesis, and invasion, were changed two fold more, in tumor surrounding region. These data suggest that TCDD alters the expression of a large array of genes involved in apoptosis, cytokine production and angiogenesis in mouse skin carcinogenesis.
마우스 피부암 발생과정에 있어서 2,3,7,8-Tetrachlorodibenzo-p-Dioxin(TCDD)처리에 의한 유전자발현 변화 연구
염태경(Tai Kyung Ryeom),김옥희(Ok Hee Kim),강미경(Mi Kyung Kang),박미선(Misun Park),지승완(Seung Wan Jee),엄미옥(Mi Ok Eom),강호일(Hoil Kang) 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.1
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanism of carcinogenesis by TCDD is unclear, it is considered to be a non-genotoxic compound and tumor promoter. In our experiment, we investigated the effects of TCDD on gene expression in mouse skin carcinogenesis. We used cDNA microarray to detect the differential gene expression in tumors induced in hairless mouse skin by MNNG plus TCDD protocol. We found that erb-2, c-ets2 and p27^(kip1) were significantly up-regulated, but TNFR2, AKT-1, integrin β1, maspin, IGF-1, c-raf-1, Rb were significantly down-regulated, in tumor region, respectively. We also found that the expression of 53 genes involved in cell cycle, signal transduction, apoptosis, adhesion molecule, angiogenesis, and invasion, were changed two fold more, in tumor surrounding region, These data suggest that TCDD alters the expression of a large array of genes involved in apoptosis, cytokine production and angiogenesis in mouse skin carcinogenesis.
2,3,7,8-TCDD의 세포형질전환 및 내성획득에 관여하는 세포내 인자에 관한 연구
염태경(Tai Kyung Ryeom),최영실(Young Sill Choi),김옥희(Ok Hee Kim),강호일(Hoil Kang) 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.1
To enhance our understanding of toxicity mediated through the pathway by which TCDD stimulates gene expression, we have investigated genes whose expressions are changed after treatment with TCDD and/or MNNG in human Chang liver cell. First, we treated with MNNG and TCDD for two weeks to transform human Chang liver cell. We obtained cell looks like to be transformed and compared the differential gene expression by using cDNA chip (Macrogen) which carrys genes related with signal transduction pathways, oncogenes and tumor suppressor genes, etc. We found that TCDD up- or down-regulated 203 and 111 genes including oncogenes and tumor suppressor genes in human Chang liver cell two fold or more, respectively. Second, we compared the differential gene expression after treatment with TCDD only by using cDNA chip (Superarray) which carrys genes related with cell cycle regulations, and found that TCDD up regulated genes related with cell proliferation as well as cell growth inhibition in human Chang liver cell two fold or more, respectively. These results suggest that toxicity induced by TCDD may reflect sustained alterations in the expression of many genes and that the changes reflect both direct and indirect effects of TCDD.
Chemical Transformation of Human Keratinocytes by 2,3,7,8-Tetrachlorodibenxo-ρ-dioxin
Mi-Kyung Kang,Young-Sill Choi,Tai-Kyung Ryeom,Mi-Ok Eom,Mi-Sun Park,Seung-Wan Jee,Kang-Ryune Kim,Ok-Hee Kim,Hoil Kang 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.3
2,3,7,8-Tetrachlorodibenzo-ρ-dioxin (TCDD) is a ubiquitous, persistent environmental contaminant and the most powerful carcinogen categorized by IARC. Although the mechanism of carcinogenesis by TCDD is poorly understood, several studies have shown that the skin is one of target organs for TCDD. In this study, we investigated the neoplastic transformation of human keratinocyte-derived cell line, HaCaT, by chemical transformation method using N-methyl-N'-nitro-N-nitorsoguanidine (MNNG) and TCDD. We found that subsequent exposure to TCDD for 3 weeks after initial exposure to MNNG markedly induced transformed cells. It was suggested that TCDD can act as a potent promoter in HaCaT cells. Furthermore, these transformed cells showed morphological alternations in soft agar and increased telomerase activity. Therefore, the TCDD treatment of HaCaT cells by initiated with MNNG could promote neoplastic transformation without stimulation by exogenous growth factors. As a result, TCDD had a strong potency as a promoter in nontumorigenic immortalized human epidermal keratinocytes.
Chemical Transformation of Human Keratinocytes by 2,3,7,8-Tetrachlorodibenxo-$\rho$-dioxin
Kang, Mi-Kyung,Choi, Young-Sill,Ryeom, Tai-Kyung,Eom, Mi-Ok,Park, Mi-Sun,Jee, Seung-Won,Kim, Kang-Ryune,Kim, Ok-Hee,Kang, Ho-Il Korean Environmental Mutagen Society 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.3
2,3,7,8-Tetrachlorodibenzo-$\rho$-dioxin(TCDD) is a ubiquitous, persistent environmental contaminant and the most powerful carcinogen categorized by IARC. Although the mechanism of carcinogenesis by TCDD is poorly understood, several studies have shown that the skin is one of target organs far TCDD. In this study, we investigated the neoplastic transformation of human keratinocyte-derived cell line, HaCaT, by chemical transformation method using N-methyl-N'-nitro-N-nitrorsoguanidine(MNNG) and TCDD. We found that subsequent exposure to TCDD for 3 weeks after initial exposure to MNNG markedly induced transformed cells. It was suggested that TCDD can act as a potent promoter in HaCaT cells. Furthermore, these transformed cells showed morphological alternations in soft agar and increased telomerase activity. Therefore, the TCDD treatment of HaCaT cells by initiated with MNNG could promote neoplastic transformation without stimulation by exogenous growth factors. As a result, TCDD had a strong potency as a promoter in nontumorigenic immortalized human epidermal keratinocytes.
사람의 정상 피부세포 및 폐세포의 발암에 미치는 2,3,7,8-tetrachlorodibenzo-ρ -dioxin의 영향
강미경(Mi Kyung Kang),염태경(Tai Kyung Ryeom),김강련(Kang Ryune Kim),김옥희(Ok Hee Kim),강호일(Hoil Kang) 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.3
2,3,7,8-Tetrachlorodibenzo-ρ-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although TCDD is recognized as potent carcinogens, relatively little is known about their role in the tumor promotion and carcinogenesis. It is known that TCDD can increase of cancer risk from various types of tissue by a mechanism possibly involving the aryl hydrocarbon receptor (AhR) activation. In this study, effects of TCDD on cellular proliferation of normal human skin and lung fibroblasts, Detroit551 and WI38 cells were investigated. In addition, to enhance our understanding of TCDD-mediated carcinogenesis, we have investigated process in which expression of Erk1/2, cyclinD1, oncogene such as Ha-ras and c-myc, and their cognate signaling pathway. TCDD that are potent activators of AhR-mediated activity was found to induce significant increase of cytochrome P4501A1 mRNA expression, suggesting a presence of functional AhR. These results support that CYP1A1 enzyme may be involved in the generation of TCDD-induced toxicity. Moreover mitogen-activated protein kinases (MAPKs) phosphorylation and cyclin D1 overexpression are induced by TCDD, which corresponded with the progression of cellular proliferation. However, TCDD did not affected Haras and c-myc mRNA expression. Taken together, it seems that TCDD are could be a part of cellular proliferation in non-tumorigenic normal human cells such as Detroit551 and WI38 cells through the upregulation of MAPKs signaling pathway regulating growth of cell population. Therefore, AhR-activating TCDD could potentially contribute to tumor promotion and Detroit551 and WI38 cells have been used as a detection system of tumorigenic effects of TCDD.
사람 백혈구 및 위 조직중의 8-Hydroxy-2'-Deoxyguanosine 측정에 관한 연구
강호일(Hoil Kang),엄미옥(Mi Ok Eom),박미선(Misun Park),염태경(Tai Kyung Ryeom),지승완(Seung Wan Jee),전해명(Hea Myung Jeon),김옥희(Ok Hee Kim) 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.1
In the present study, we have measured 8-hydroxy-2'-deoxyguanosine in DNA of stomach cancers, adjacent stomach cancer tissues, normal stomach tissues and peripheral blood leukocytes of the same stomach cancer patients (n=48) to investigate their etiological association with gastric cancer and possibility whether peripheral blood leukocytes can use surrogate marker for early stomach cancer diagnosis by HPLC/ECD system. In normal stomach tissues, we found that 8-hydroxy-2'-deoxyguanosine levels in tissues infected with Helicobacter pylori were 1.4 fold higher than those in tissues without infected with Helicobacter pylori. However, in adjacent stomach cancer tissues, we found that 8-hydroxy-2'-deoxyguanosine levels in tissues infected with Helicobacter pylori were 1.5 fold lower than those in tissues without infected with Helicobacter pylori. In stomach cancer tissues, 8-hydroxy-2'-deoxyguanosine levels in tissues infected with Helicobacter pylori were not significantly different from those in tissues without infected with Helicobacter pylori. In Helicobacter pylori-negative specimens, 8-hydroxy-2'-deoxyguanosine levels of adjacent stomach cancer tissues were found to be significantly higher than those of normal stomach and cancer tissues. The 8-hydroxy-2'-deoxygnanosine levels of female were 1.7 fold higher than those of male in peripheral blood leukocytes of the same stomach cancer patients. The 8-hydroxy-2'-deoxyguanosine levels in Helicobacter pylori-negative specimens among adjacent stomach cancer tissues were found to be reversely correlated with those in peripheral blood leukocytes, suggesting that 8-hydroxy-2'-deoxyguanosine in peripheral blood leukocytes may not use as surrogate marker for the early diagnosis of human stomach cancer.