• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.70.2-70.2
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• 2007

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• Proceedings of the PSK Conference
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• 2002.10a
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• pp.368.2-368.2
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• 2002

Fruits of Hovenia dulcis T. (Rhamnaceae) was called ′jiguja ′ in oriental medicine which has been used for diuresis, remove of hangover and leaves has been used for detoxified the alcohol. From the MeOH Extraction. five compounds were isolated by column chromatography and elucidated as quercetin quercetin-3-O-rhamnose. quercetin-3-O-gal(6"1") rha, quercetin-3-O-glc(6"${\rightarrow}$1")glc, and kaemferol through specroscopic methods. (omitted)

• Food Science and Preservation
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• v.12 no.2
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• pp.184-189
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• 2005

In order to select probiotics having both a high survival rate and an ability to inhibit virulent pathogens, we have screened lactic acid bacteria and yeasts from Jeot-gal to examine their resistance to artificial gastric and bile juice. After being introduced in the artificial gastric acid for 2 hr, the isolated lactic acid bacteria and yeast were incubated for 24 hrs in the artificial bile juice. In particular, the strain ML 36, ML 128, and ML 178 survived the longest during 2 hr incubation period in the artificial gastric acid. All 3 strains of lactic acid bacteria, and 2 strains of yeast demonstrated higher growth rates than control in the artificial bile. In addition, the antimicrobial activity of lactic acid bacteria and yeasts was investigated to determine their efficiency as probiotic organisms. The lactic acid bacteria inhibited Gram positive and negative bacteria, while the yeast was marginally inhibited.

• Korean Journal of Microbiology
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• v.36 no.3
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• pp.236-241
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• 2000

A defensin is an inducible antibacterial peptide from a fleshfly and contains 40 residues basic peptide with six cysteines. For the consiruction of recombinant S cerevisiae expressing defensin, the structural gene coding for active defensin was chemically synthesized and fused in fiam to GAP promoter, MFul preprosequence and the GAL7 transcription terminator, generating a recombinant plasnlid pGMD18. S. ce~evisine 2805 Gells were transror~ned to uracil prototroph by the pGMDl8 arid the transformed cells showing antibacterial activity against 111. luteus TAM1056 were selected by growth inhibition zone assay. The optimal culture conditions for the unprovement of the defensin production of a selected tmdonnant were investigated. The optirmzed medium containing 0.4% yeast extract, 2% corn steep liquor, 2.5% glucose and 0.05% $C_2CO_3$, could be determined and the optimum lemperature. and initial pH could be detennnied as $28^{\circ}C$ and pH 3, ~mpectively. The optimized conditioiis revealed the trvofold Increase in the cell growth and the fourfold in the antibaclerial activity. coinpar-ed with tllc Yl'D medium.

• Tuberculosis and Respiratory Diseases
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• v.48 no.5
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• pp.682-698
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• 2000

Glucocorticoid receptor (GR) functions as a suppressor of inflammation by inhibiting the expression of many cytokine genes activated by NF-${\kappa}B$. The goal of this study is to investigate the mechanism by which GR repress NF-${\kappa}B$ activation in lung epithelial cells. We used A549 and BEAS-2B lung epithelia! cell lines. Using Ig$G{\kappa}$-NF-${\kappa}B$ luciferase reporter gene construct, we found that dexamethasone significantly suppressed TNF-$\alpha$-induced NF-${\kappa}B$ activation and the overexpression of GR showed dose-dependent reduction of TNF-$\alpha$-induced NF-${\kappa}B$ activity in both cell lines. However, DNA binding of NF-${\kappa}B$ induced by TNF-$\alpha$ in electromobility shift assay was not inhibited by dexamethasone. Super shift assay with anti-p65 antibody demonstrated the existence of p65 in NF-${\kappa}B$ complex induced by $\alpha$ Western blot showed that $I{\kappa}B{\alpha}$ degradation induced by TNF-$\alpha$ was not affected by dexamethasone and $I{\kappa}B{\kappa}$ was not induced by dexamethasone, neither. To evaluate p65 specific transactivation, we adopted co-transfection study of Gal4-p65TA1 or TA2 fusion protein expression system together with 5xGal4-luciferase vector. Co-transfection of GR with Gal4-p65TA1 or TA2 repressed luciferase activity profoundly to the level of 10-20% of p65TA1- or TA2-induced transcriptional activity. And this transrepressional effect was abolished by co-transfection of CBP of SRC-1 expression vectors. These results suggest that GR-mediated transrepression of NF-${\kappa}B$ in lung epithelial cells is through competing for binding to limiting amounts of transcriptional coactivators, CBP or SRC-1.

• The Korean Journal of Food And Nutrition
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• v.10 no.3
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• pp.407-413
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• 1997

The antimutagenic mechanism of cinnamaldeyde on mutagenesis induced by 4-nitroquinoline-1-oxide(4-NQO) and N-metyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in various DNA repair-deficient strains, E. coli B/r and K-12 series. Cinnamaldehyde did not show any effects not only on the $\beta$-galactosidase activities of GW1060 and GW1103(recA441) which synthesizes $\beta$-galactosidase consitutively at 41$^{\circ}C$ but also on that of GW1107[lexA51 (Def)] in which the SOS response always occur. These results suggest that cinnamaldehyde dose not change the function of RecA which positively controls the SOS response as well as not acting as the repressor like LexA. In addition, no inhibitory effect of cinnamaldehyde was observed on the growth of Trp+ revertant and the delay of viable cell growth was also not found by adding cinnamaldehyde. Despite the decrease in the number of revertants, a significant increase in survival of 4-NQO treated cells was observed in E. coli WP2s(uvrA), ZA159($\Delta$uvrB) and TK603(uvrA). But these effects disappeared in excision-proficient strain WP2(uvrA+) and lexA-deficient strains(CM561 and CM611). The enhancement of survival was not found in WP67(uvrA polA) deficient in polymerase I which ligates the gap between complementary DNA. From the above results, we assume that cinnamaldehyde might show antimutagenic effect by enhancing an error-free recombinational repair system.

• KSBB Journal
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• v.9 no.3
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• pp.339-345
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• 1994

Deletions between UASG and the GALI TATA box reduced glucose repression and allowed constitutive expression of the gene product in the absence of galactose. The relative inducer level (ratio of galactose/glucose concentrations) affected the extent of gene expression and glucose repression. Glucose repression was reduced by a factor of 2 to 5 as the relative inducer level increased. In the medium containing galactose only, induction of ${\beta}$-galactosidase synthesis by galactose increased with plasmid copy number. On the contrary, plasmid copy number did not affect significantly ${\beta}$-galactosidase synthesis in the medium containing both glucose and galactose (2% glucose＋2% galactose), which might be due to glucose repression caused by high glucose concentration. However, when the medium contained the relatively high inducer level (0.4% glucose＋0.8% galactose), ${\beta}$-galactosidase synthesis increased with plasmid copy number, indicating that the beneficial effect of higher galactose concentration was weaker than the repressive effect of higher glucose concentration.

• Journal of Radiation Protection and Research
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• v.36 no.3
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• pp.119-126
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• 2011

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging, and contributes to harmful effects in cultured cells and animal tissues. mtDNA biogenesis genes (NRF-1, TFAM) are essential for the maintenance of mtDNA, as well as the transcription and replication of mitochondrial genomes. Considering that oxidative stress is known to affect mitochondrial biogenesis, we hypothesized that ionizing radiation (IR)-induced reactive oxygen species (ROS) causes mtDNA deletion by modulating the mitochondrial biogenesis, thereby leading to cellular senescence. Therefore, we examined the effects of IR on ROS levels, cellular senescence, mitochondrial biogenesis, and mtDNA deletion in IMR-90 human lung fibroblast cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated at 4 or 8 Gy. Old cells at PD55, and H2O2-treated young cells at PD 39, were compared as a positive control. The IR increased the intracellular ROS level, senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity, and mtDNA common deletion (4977 bp), and it decreased the mRNA expression of NRF-1 and TFAM in IMR-90 cells. Similar results were also observed in old cells (PD 55) and $H_2O_2$-treated young cells. To confirm that a increase in ROS level is essential for mtDNA deletion and changes of mitochondrial biogenesis in irradiated cells, the effects of N-acetylcysteine (NAC) were examined. In irradiated and $H_2O_2$-treated cells, 5 mM NAC significantly attenuated the increases of ROS, mtDNA deletion, and SA-${\beta}$-gal activity, and recovered from decreased expressions of NRF-1 and TFAM mRNA. These results suggest that ROS is a key cause of IR-induced mtDNA deletion, and the suppression of the mitochondrial biogenesis gene may mediate this process.

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.2
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• pp.248-253
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• 1997

The paper describes the activation mode and the glycosic linkage of anti-complementary polysaccharide isolated from Cinnamomum cassia. The polysaccharide fractions, CC-IIIa, CC-IIIb, and CC-IIIc, activated C3 component existed in normal human serum and produced C3 cleavage segments, C3a and C3b. The polysaccharide, CC-2-IIIa-3 activated the complement system both in the presence and absence of $Ca^{++}$, suggesting that it involved in both classical and alternative complement pathways. Methylation of CC-2-IIIa-3 was performed with methylsulphinyl carbanion and methyl iodide in DMSO. The methylated products was hydrolyzed, then converted into the partially methylated alditol acetates. Gas chromatography-mass spectrometry(GC-MS) revealed derivatives of terminal $Glc{\rho}$ and $Gal{\rho}$, 1,2-linked $Rha{\rho}$, 1,6-linked $Man{\rho}$, 1,3-linked $Glc{\rho}$, 1,6-linked $Gal{\rho}$ etc.

• Biomolecules & Therapeutics
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• v.27 no.3
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• pp.283-289
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• 2019

Brain aging induces neuropsychological changes, such as decreased memory capacity, language ability, and attention; and is also associated with neurodegenerative diseases. However, most of the studies on brain aging are focused on neurons, while senescence in astrocytes has received less attention. Astrocytes constitute the majority of cell types in the brain and perform various functions in the brain such as supporting brain structures, regulating blood-brain barrier permeability, transmitter uptake and regulation, and immunity modulation. Recent studies have shown that SIRT1 and SIRT2 play certain roles in cellular senescence in peripheral systems. Both SIRT1 and SIRT2 inhibitors delay tumor growth in vivo without significant general toxicity. In this study, we investigated the role of tenovin-1, an inhibitor of SIRT1 and SIRT2, on rat primary astrocytes where we observed senescence and other functional changes. Cellular senescence usually is characterized by irreversible cell cycle arrest and induces senescence- associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity. Tenovin-1-treated astrocytes showed increased SA-${\beta}$-gal-positive cell number, senescence-associated secretory phenotypes, including IL-6 and IL-$1{\beta}$, and cell cycle-related proteins like phospho-histone H3 and CDK2. Along with the molecular changes, tenovin-1 impaired the wound-healing activity of cultured primary astrocytes. These data suggest that tenovin-1 can induce cellular senescence in astrocytes possibly by inhibiting SIRT1 and SIRT2, which may play particular roles in brain aging and neurodegenerative conditions.