• Proceedings of the Korea Crystallographic Association Conference
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• 2003.11a
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• pp.11-11
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• 2003

• Proceedings of the Korean Nuclear Society Conference
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• 2001.05a
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• pp.399.2-399
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• 2001

• Proceedings of the Korean Nuclear Society Conference
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• 1999.05a
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• pp.388-388
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• 1999

• Proceedings of the Zoological Society Korea Conference
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• 1995.10b
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• pp.325.2-325
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• 1995

No Abstract, See Full Text

• Preventive Nutrition and Food Science
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• v.4 no.2
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• pp.107-112
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• 1999

Effect of solvent extracts and juice supernatants from kimchis on the growth of various human cancer cells was studied, comparing with the actions on the normal cells. Inhibitory effect of kimchi extracts on[3H] thymidine incorporation n cancer cells was also investigated. The methanol extract, hexane extract and methanol soluble fraction (MSF) of 3-week fermented kimchi did not have growth inhibitory effect on Ac2F rat normal liver cells at the concentrations of 0.5~2%. However, marked decrease in the growth of AGS human gastric cancer cells was shown by the treatment of those extacts. The juice from the kimchi samples also suppressed the growth of K-562 human leukemia cells and MG-63 human osteosarcoma cells. Especially, the juice of 3-week fermented kimchi exhibited the strong growth inhibitory effect in MG-63 human osteosarcoma cells. At the photomicrographs, growth inhibition and morphological change of the cells treated with kimchi juice were observed. And the solvent extracts of 3-week fermented kimchi suppressed the growth of cancer morethan the extracts or juices from fresh and 6-week fermented kimchi. When AGS human gastric cancer cels were treated with the extracts of 3-week fermented kimchi, [3H] thymidine incorporation in the cells also decreased. These results showed that kimchi extracts and juices had growth inhibitory effects on human osteosarcoma, leukemia and gastric cancer cells, but had no toxicity to the normal cells. We suggest that kimchi might have anticancer effect in part due to inhibition of the growth and DNA synthesis of cancer cells.

• Journal of Photoscience
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• v.9 no.2
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• pp.451-453
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• 2002

A new concept of "photo" -antisense method has been evaluated, where the inhibition of gene expression by the conventional antisense method is enhanced by photochemical binding between antisense oligonucleotides conjugated with photo-reactive compound and target mRNA or DNA. Fluorescein labeled oligodeoxyribonucleotides (F-DNA) was delivered to cell nuclei in the encapsulated form in multilamellar lecithin liposomes with neutral charge. F-DNA was previously shown to photo-bind to the complementary stranded DNA, and the delivery system using neutral liposome to be effective in normal human keratinocytes. In the present study, we used human kidney cancer G401.2/6TG.1 cell line to be advantageous in reproducible experiments. p53 was adopted as a target gene since antisense sequence information has been accumulated. The nuclear localization ofF-DNA was identified by comparing the fluorescence ofF-DNA with that of Hoechst 33258 under fluorescence microscope. After 7hr incubation to accumulate p53 protein induced by UV -B, p53 protein was quantified by Western blot. After 2hrs from F-DNA application, about 30% of cell population incorporated F-DNA in their nuclei with some morphological change possibly due to liposomal toxicity. Irradiation of visible light longer than 400nm from solar simulator at this time enhanced the inhibitory action of antisense F-DNA. The present results suggest that photo-antisense method is promising to control gene expression in time and space dependent manner. Further improvement of F-DNA delivery to cancer cells in the stability and toxicity is in progress. progress.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.6
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• pp.671-676
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• 1998

In the present study, we first examined whether the changes in the DNA binding activities of the transcription factors, cAMP response element binding protein (CREB) and activator protein-1 (AP-1) mediate the long-term effects of morphine in differentiated SH-SY5Y human neuroblastoma cells. The increases in CREB and AP-1 DNA binding activities were time-dependent up to 6 days of morphine treatment (1, 4, and 6 days). However, the significant reduction in the DNA binding activities of CREB and AP-1 was observed after 10 days of chronic morphine $(10\;{\mu}M)$ administration. Secondly, we examined whether the changes of CREB and AP-1 DNA binding activities could be modulated by dopamine and haloperidol. Dopamine cotreatment moderately increased the levels of the CREB and AP-1 DNA binding activities induced by 10 days of chronic morphine treatment, and haloperidol cotreatment also resulted in a moderate increase of the CREB and AP-1 DNA binding activities. However, dopamine or haloperidol only treatment showed a significant increase or decrease of the CREB and AP-1 DNA binding activities, respectively. In the case of acute morphine treatment, the CREB and AP-1 DNA binding activities were shown to decrease in a time-dependent manner (30, 60, 90, and 120 min). Taken these together, in differentiated SH-SY5Y cells, morphine tolerance seems to involve simultaneous changes of the CREB and AP-1 DNA binding activities. Our data also suggest the possible involvement of haloperidol in prevention or reversal of morphine tolerance at the transcriptional level.

• Korean Journal of Microbiology
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• v.40 no.2
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• pp.65-72
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• 2004

Instability of some eukaryotic sequence propagated in prokaryotic hosts is a frequently observed phenomenon. It is well documented that long inverted repeats, AT-rich sequences with structures like Z-DNA are extremely unstable in E. coli. These sequences may either be under-represented or even lost when cloned in E. coli. When we analyzed the polymorphic pattern for several tandom repeat (TR) in human SCKI gene, we found some TR regions were frequently deleted from plasmids and had difficult problem for their sequencing. These regions may result in non-clonability of the DNA sequence. Here we have cloned two difficult TR regions under low temperature and made two library for DNA sequencing using a nebulizer or sonicator. This study will help to determine the unstable genomic elements in complex mammalian genome.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.12
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• pp.4915-4918
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• 2014

Background and Aims: Advances in the treatment of cervical cancer over the last decade have predominantly involved the development of genes directed at molecular targets. Gene therapy is recognized to be a novel method for the treatment of cervical cancer. Genes can be administered into target cells via nanocarriers. This study aimed to develop systemically administrable nano-vectors. Floate (Fa) containing gene loaded nanoparticles (NPs) could target HeLa human cervical cancer cells through combination with receptors on the cells to increase the nuclear uptake of genetic materials. Methods: Fa was linked onto Poly (ethylene glycol)-b-poly (D, L-lactide) (PEG-PLA) to form Fa-PEG-PLA, and the resulting material was used to load plasmids of enhanced green fluorescence protein (pEGFP) to obtain gene loaded nanoparticles (Fa-NPs/DNA). Physical-chemical characteristics, in vitro release and cytotoxicity of Fa-NPs/DNA were evaluated. The in vitro transfection efficiency of Fa-NPs/DNA was evaluated in HeLa cells and human umbilical vein endothelial cells (HUVEC). PEG-PLA without Fa was used to load pEGFP from NPs/DNA as a control. Results: Fa-NPs/DNA has a particle size of 183 nm and a gene loading quantity of 92%. After 72h of transfection, Fa-NPs/DNA displayed over 20% higher transfection efficiency than NPs/DNA and 40% higher than naked DNA in HeLa cells. However, in HUVECs, no significant difference appeared between Fa-NPs/DNA and NPs/DNA. Conclusions: Fa-PEG-PLA NPs could function as excellent materials for gene loading. This nano-approach could be used as tumor cell targeted medicine for the treatment of cervical cancer.

• Journal of Preventive Medicine and Public Health
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• v.37 no.4
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• pp.373-380
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• 2004

Objectives : There has been gradually increasing concern about the adverse health effects of electromagnetic radiation originating from cell phones which are widely used in modern life. Cell phone radiation may affect human health by increasing free radicals of human blood cells. This study has been designed to identify DNA damage of blood cells by electromagnetic radiation caused by cell phone use. Methods : This study investigated the health effect of acute exposure to commercially available cell phones on certain parameters such as an indicator of DNA damage for 14 healthy adult volunteers. Each volunteer during the experiment talked over the cell phone with the keypad facing the right side of the face for 4 hours. The single cell gel electrophoresis assay (Comet assay), which is very sensitive in detecting the presence of DNA strand-breaks and alkali-labile damage in individual cells, was used to assess peripheral blood cells (T-cells, B-cells, granulocytes) from volunteers before and after exposure to cell phone radiation. The parameters of Comet assay measured were Olive Tail Moment and Tail DNA %. Results : The Olive Tail Moment of B-cells and granulocytes and Tail DNA % of B-cells and granulocytes were increased by a statistically significant extent after 4-hour use of a cell phone compared with controls. Conclusion : It is concluded that cell phone radiation caused the DNA damage during the 4 hours of experimental condition. Nonetheless, this study suggested that cell phone use may increase DNA damage by electromagnetic radiation and other contributing factors.