• Journal of the Korean Society of Safety
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• v.14 no.2
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• pp.109-115
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• 1999

The release of gas from the LPG storage tank by the rupture or leakage can occure explosion and this causes serious damage to people and structures. In this study, the explosion effect and damaging distance were measured for the LPG cloud explosion to perform the quantitative risk assessment for the PSM, and the effective parameters on the explosion were found. The gas dispersion and mass contaminant in the explosion limits were calculated by using DEGADIS, and it was converted to TNT equivalency and damaging distance. As a result, the wind speed was the most effective parameter on the diffusion rate and TNT equivalency, and the damaging distance were increased with decrease of wind speed and surface roughness.

• Environmental Mutagens and Carcinogens
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• v.19 no.2
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• pp.112-115
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• 1999

The action mechanism of the inhibitory effect of some natural products on the DNA strand break and DNA damage was investigated in vitro and in vivo. In the E. coli chromosomal DNA strand break experiment in vitro, three mushroom water extracts were effective on the DNA strand breaking by daunorubicin. Phellinus linteus water extract inactivated daunorubicin, a DNA strand breaking agent, but did not protect DNA from daunorubicin-induced DNA strand breaking. Agaricus blazei water extract inhibited DNA strand breaking action of daunorubicin not only by daunorubicin inactivation, but also by DNA protection from daunorubicin. An inhibitory effect of Ganoderma lucidum water extract on the DNA strand break was based on the DNA protection rather than daunorubicin inactivation. In vivo mutagen assay system (SOS-chromotest), among three mushroom water extracts Phellinus linteus water extract was the most effective one on the inhibition of DNA damage by 4-NQO. The results suggest that all three mushroom water extracts inhibit daunorubicin-induced DNA damage and in vivo DNA damaging action of 4-NQO by the reaction of mutagen inactivation or DNA protection from the mutagen.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.631-640
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• 1999

The present study investigated the stimulatory effects of iron (or ascorbate) on cyclosporine-induced kidney mitochondrial damage. Damaging effect of $50\;{\mu}M$ cyclosporine plus $20\;{\mu}M\;Fe^{2+}$ on mitochondrial lipids and proteins of rat kidney and hyaluronic acid was greater than the summation of oxidizing action of each compound alone, except sulfhydryl oxidation. Cyclosporine and $100\;{\mu}M$ ascorbate showed an enhanced damaging effect on lipids but not on proteins. The peroxidative action of cyclosporine on lipids was enhanced with increasing concentrations of $Fe^{2+}.$ Ferric ion $(20\;{\mu}M)$ also interacted with cyclosporine to stimulate lipid peroxidation. Damaging action of cyclosporine on mitochondrial lipids was enhanced by ascorbate $(100\;{\mu}M\;and\;1\;mM)$. Iron chelators, DTPA and EDTA, attenuated carbonyl formation induced by cyclosporine plus ascorbate. Cyclosporine $(100\;{\mu}M)$ and $50\;{\mu}M\;Fe^{2+}$ $(or\;100\;{\mu}M\;ascorbate)$ synergistically stimulated degradation of $2-{\alpha}$ deoxyribose. Cyclosporine $(1\;to\;100\;{\mu}M)$ reduced ferric ion in a dose dependent manner, which is much less than ascorbate action. Addition of $Fe^{2+}$ caused a change in absorbance spectrum of cyclosporine in $230{\sim}350$ nm of wavelengths. The results show that cyclosporine plus iron (or ascorbate) exerts an enhanced damaging effect on kidney mitochondria. Iron and ascorbate appear to promote the nephrotoxicity induced by cyclosporine.

• Advances in nano research
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• v.4 no.1
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• pp.45-50
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• 2016

Data of Raman spectroscopy from graphene and few-layer graphene (FLG) irradiated by SEM electron beam in the range of energies 0.2 -30 keV are presented. The obvious effect of damaging the nanostructures by all used beam energies for specimens placed on insulator substrates ($SiO_2$) was revealed. At the same time, no signs of structural defects were observed in the cases when FLG have been arranged on metallic substrate. A new physical mechanism of under threshold energy defect production supposing possible formation of intensive electrical charged puddles on insulator substrate surface is suggested.

• Toxicological Research
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• v.7 no.2
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• pp.157-163
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• 1991

The effect of patulin, a mycotoxin, on the growth of Escherichia coli cell was investigated. E. coli cell elongation usually shown in SOS-response for DNA repair was induced by 20 mg of patulin per ml. After staining the E. coli chromosome with fluorescence dye(DAPI, 4', 6-diamino-2-phenyl-indole), chromosomal DNA partitioning was not affected by patulin. The observation indicateds that patulin acts as a DNA damaging agent which is effective for E. coli cell elongation introduced by the inhibition of septum formation.

• Korean Journal of Food Science and Technology
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• v.22 no.5
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• pp.590-595
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• 1990

The destructive effect of peroxidized lipid on the amino acid in protein isolate and the proteolytic activity of protease were studied in the model system of rice bran. The content of amino acids in the protein isolate decreased significantly when they reacted with peroxidized lipid (pov. 1200 meq/kg). Most of amino acids were lost by more than 90% in salt soluble protein isolates when analyzed by the method of enzyme hydrolysis. Formaldehyde reduced the activity most severely among peroxidized products. Formic acid, peroxidized lipid and hydroperoxide were also found to reduce the protease activity. The damaging effect of the secondary products on the protease activity was more serious than that of the primary products of lipid peroxidation. The destruction of amino acids in the total protein and Inhibition of protease activity by the peroxidized lipid were apparent.

• Molecular & Cellular Toxicology
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• v.1 no.1
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• pp.26-31
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• 2005

The detection and the regulation of man-made synthetic chemicals and the establishment of toxicity that may pose a genetic hazard in our environment are subjects of great concern because of its close correlation between environmental contamination and human health. Since the tens of thousands of man-made chemicals that have been introduced into the environment in the last few decades must also be tested for their damaging effect on DNA, the agents that cause this damage must be identified.

• Journal of Life Science
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• v.26 no.3
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• pp.376-386
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• 2016

Apoptosis induction has been proposed as an efficient mechanism by which malignant tumor cells can be removed following chemotherapy. The intrinsic mitochondria-dependent apoptotic pathway is frequently implicated in chemotherapy-induced tumor cell apoptosis. Since DNA-damaging agent (DDA)-induced apoptosis is mainly regulated by the tumor suppressor protein p53, and since more than half of clinical cancers possess inactive p53 mutants, microtubule-damaging agents (MDAs), of which apoptotic effect is mainly exerted via p53-independent routes, can be promising choice for cancer chemotherapy. Recently, we found that the apoptotic signaling pathway induced by MDAs (nocodazole, 17α-estradiol, or 2-methoxyestradiol) commonly proceeded through mitotic spindle defect-mediated prometaphase arrest, prolonged Cdk1 activation, and subsequent phosphorylation of Bcl-2, Mcl-1, and Bim in human acute leukemia Jurkat T cells. These microtubule damage-mediated alterations could render the cellular context susceptible to the onset of mitochondria-dependent apoptosis by triggering Bak activation, Δψm loss, and resultant caspase cascade activation. In contrast, when the MDA-induced Bak activation was inhibited by overexpression of anti-apoptotic Bcl-2 family proteins (Bcl-2 or Bcl-xL), the cells in prometaphase arrest failed to induce apoptosis, and instead underwent mitotic slippage and endoreduplication cycle, leading to formation of populations with 8N and 16N DNA content. These data indicate that cellular apoptogenic mechanism is critical for preventing polyploid formation following MDA treatment. Since the formation of polyploid cells, which are genetically unstable, may cause acquisition of therapy resistance and disease relapse, there is a growing interest in developing new combination chemotherapies to prevent polyploidization in tumors after MDA treatment.

• The Journal of Korean Medicine
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• v.20 no.1 s.37
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• pp.91-105
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• 1999

The effects of Yinjin and Yinjinsaryongsangagambang on a DNA damaging agent, etoposide-induced apoptosis, cell viability, cell cycle progression, and mRNA expression of apoptosis-related genes of human hepatocyte cell line HepG2 were investigated using tryphan blue exclusion assay, MTT assay, flow cytometry, immunocytometric analysis of PCNA, and quantitative RT-PCR analysis. MTT assay showed that Yinjin and Yinjinsaryongsangagambang increases cellular viability of HepG2 cells in a dosage-dependent manner. Stimulation of cell cycle progression by Yinjin or Yinjinsaryongsangagambang was detected by flow cytometric analysis of the DNA content and immunocytometric analysis of PCNA expression. A significant reduction of a DNA-damaging agent, etoposide-induced apoptosis were found in both Yinjin and Yinjinsaryongsangagambang-treated cells in dosage-dependent manner. In overall, 3-fold reduction of apoptosis was recognized in $10.0\;{\mu}g/ml$ of Yinjin or Yinjinsaryongsangagambang-treated cells compared to untreated cells. Although the difference is not significant, Yinjinsaryongsangagambang showed slightly higher effect on the inhibition of apoptosis than Yinjin. From flow cytometric analysis of apoptosis, while 39.9% of untreated cells showed etoposide-induced apoptotic cell death, only 19.6% or 17.4% of Yinjin or Yinjinsaryongsangagambang-treated cells were fond at apoptotic sub G1 phase, respectively. Interestingly, strong induction of Gadd45-mRNA was observed from Yinjin or Yinjinsaryongsangagambang-treated cells. However, no changes in expression levels of p53 and Waf1 were detected, demonstrating that induction of Gadd45 mRNA expression by Yinjin or Yinjinsaryongsangagambang occurs by p53-independent mechanism. Marked mRNA inductions of two apoptosis-inhibiting genes, Bcl-2 and Bcl- XL, were found in both Yinjin or Yinjinsaryongsangagambang-treated HepG2 cells while no changes was detected in expression levels of an apoptosis-promoting gene, Bax.

• 보존과학연구
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• s.17
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• pp.123-160
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• 1996

There have been many studies and experiments regarding exhibition lighting. Many experiments on photochemical damaging effect and visibility resulted in a practice limited to assigning light levels and adjusting annual exposure time. The three damaging factors to the artifacts are intrinsicsusceptibility to absorb radiant energy, spectral distribution of light source and intensity of illumination and time of exposure. Dividing all the artfacts into three categories to suggest a recommended illuminance level causes some problems. Blue wool, for example, used as the reference material for susceptibility, is not a standard material representing museum artifacts. In the most light sensitive category, ISO class I or anything below have been excluded. The exposure time of one soure can be three times more than another sourece. The spectral distribution of the light source and the relative spectral responsibility of the artifact are not considered in the practice. So in case of very light sensitive material, the recommended illuminance is only the referring value and it is indispensable to check the characteristic of susceptibility of each artifacts. Daylighting is prevailing method to solve the psychological need of the visitors. However, it sould transparent, and should not diffused, and the green-house effect must be considered. llluminance uniformity should based on the maximum illuminance to handle the limitation of exposure for the conservation of a large sensitive object such as a painting. Damage index is not absolute reference for selecting the lighting source because it is experimented from the paper of low grade then calculated. Visibility should be increased by reducing the visual noiseand by planning of appropriate luminance contrast. This paper reviews the problems with the previous studies and experiment sand the current exhibition lighting design practice. The plan for museum showcase lighting is to check the susceptibility and to raise the visibility simultaneously.