• Advanced Industrial SCIence
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• v.2 no.3
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• pp.1-7
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• 2023

Recently, it is increasing that a issue of concern about radiation exposure. It affects soil, water, air, crops, etc., and in the long term, environmental pollution and food pollution occur, and it is considered to cause social problems and economic damage. Radiation exposure causes diseases and health problems, but as a method for diagnosing diseases, nuclear medicine tests such as X-ray imaging, CT, and PET-CT are conducted, and radiation isotopes are exposed for the purpose of cancer treatment. A Hungarian case study on radiation in water, particularly drinking water, following the release of radioactive waste from Fukushima, and an examination of the Larsemann Hills area in Antarctica, found that it was within the prescribed radioactivity limits of drinking water recommended by the World Health Organization. We looked at radioprotective agents, focusing on DNA damage, cell and organ damage, and cancer, and also investigated various literatures on ACE inhibitors, antioxidants, and natural substances among restoration materials. Although exposed to radiation in everyday life, the reason why it can be safe is probably because there is a radiation protection material and a recovery material for radiation exposure, so we are trying to find possible materials.

• Journal of Applied Biological Chemistry
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• v.54 no.4
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• pp.258-264
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• 2011

The Korean edible mountainous vegetable, byeongpungssam, Cacalia firma Komar. (CFK) is a wild plant found in the intermountain areas in Korea. The aim of this study was to investigate its free radical scavenging activity using 1,1-diphenyl-2-picryl-hydrazyl, 2,2-azinobis(3-ethylbenozothiazoline- 6-sulfonic acid) diammonium salt, ferric reducing/antioxidant power assays, an electron spin resonance spectroscopy. We also examined its protective effect against oxidative DNA damage using agarose electrophoresis of ethanol extract of CFK. The protective activity of the extract against the DNA damage induced by HO${\cdot}$ radicals was compared to epicatechin, ascorbic acid and trolox as reference antioxidant compounds. Total phenolic content in the extract was determined spectrometrically according to the Folin-Ciocalteu procedure and calculated as gallic acid equivalents. Total polyphenolic content of the extract was measured in the leaves ($161.53{\pm}1.07{\mu}g/g$) and shoot ($142.45{\pm}0.56{\mu}g/g$). The antioxidant potential of the extracts against some radicals and DNA damage by HO${\cdot}$ radicals showed over 60%, respectively.

• Korean Journal of Microbiology
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• v.45 no.2
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• pp.91-98
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• 2009

Infectious bursal disease (IBD) caused by the infectious bursal disease virus (IBDV) has an important economic impact on the poultry industry worldwide. This study examined the adjuvant effects of a plasmid encoding chicken interleukin-6 (pcDNA-ChIL-6) and levamisole (LMS) on in ovo prime-boost vaccination using a genetic vaccine (pcDNA-VP243) to prime in chicken followed by a killed-vaccine boost. A pcDNA-VP243 was injected into the amniotic sac alone or in combination with a pcDNA-ChIL-6 or LMS at embryonation day 18, followed by an intramuscular injection of killed IBD vaccine at 1 week of age. The chicken were orally challenged with very virulent IBDV (vvIBDV) strain at 3 weeks of age and observed for 10 days. No mortality was observed in the groups that received the pcDNA-VP243 alone and pcDNA-VP243 plus pcDNA-ChIL-6 or LMS compared to 100% mortality in unvaccinated challenge control group. However, as determined by bursal damage (the presence of IBDV RNA, B/B ratio, and lesion score), a pcDNA-VP243 alone group was superior to pcDNA-VP243 plus pcDNA-ChIL-6 or LMS groups in the protection against post-challenge. These findings suggest that in ovo priming with genetic vaccine and boosting with killed vaccine is an effective strategy for protecting chicken against vvIBDV and the addition of pcDNA-ChIL-6 or LMS did not enhance protective immunity.

• Tuberculosis and Respiratory Diseases
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• v.61 no.4
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• pp.366-373
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• 2006

Background: Paraquat is extremely toxic chemical material, which generates reactive oxygen species (ROS), causing multiple organ failure. In particular, paraquat leads to irreversible progressive pulmonary fibrosis. Exaggerated cell deaths exceeding the normal repair of type II pneumocytes leads to mesenchymal cells proliferation and fibrosis. This study examined the followings; i) whether or not paraquat induces cell death in lung epithelial cells; ii) whether or not paraquat-induced cell deaths are apoptosis or necrosis; and iii) the effects of N-acetylcysteine, dexamethasone, and bcl-2 on paraquat-induced cell deaths. Methods: A549 and BEAS-2B lung epithelial cell lines were used. The cell viability and apoptosis were evalluated using a MTT assay, Annexin V staining was monitored by fluorescence microscopy, The level of bcl-2 inhibition was examined by establishing stable A549 pcDNA3-bcl-2 cell lines throung the transfection of pcDNA3-bcl-2 with the mock. Results: Paraquat decreased the cell viability in A549 and BEAS-2B cells in a dose and time dependent manner. The Annexin V assay showed that apoptosis was the type of paraquat-induced cell death. Paraquat-induced cell deaths was significantly inhibited by N-acetylcysteine, dexamethasone, and bcl-2 overexpression. The cell viability of A549 cells treated with N-acetylcysteine, and dexamethasone on the paraquat-induced cell deaths were increased significantly by 10 ~ 20%, particularly at high doses. In addition, the cell viability of A549 pcDNA3-bcl-2 cells overexpressing bcl-2 was significantly higher than the untransfected A549 cells. Conclusion: Paraquat induces apoptotic cell deaths in lung epithelial cells in a dose and time dependent manner. The paraquat-induced apoptosis of lung epithelial cells might occur through the mitochondrial pathway.

• 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.

• Korean Journal of Ecology and Environment
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• v.54 no.4
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• pp.272-279
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• 2021

A pump-type eDNA filtering system that can control voltage and hydraulic pressure respectively has been developed, and applied a filter case that can filter out without damaging the filter. The filtering performance of the developed system was evaluated by comparing the eDNA concentration with the conventional vacuum-pressured filtering method at the catchment conduit intake reservoir. The developed system was divided into a voltage control (manual pump system) method and a pressure control (automatic pump system) method, and the pressure was measured during filtering and the pressure change of each system was compared. The voltage control method started with 65 [KPa] at the beginning of the filtering, and as the filtering time elapsed, the amount of filtrate accumulated in the filter increased, so the pressure gradually increased. As a result of controlling the pressure control method to maintain a constant pressure according to the designed algorithm, there was a difference in the width of the hydraulic pressure fluctuation during the filtering process according to the feedback time of the hydraulic pressure sensor, and it was confirmed that the pressure was converged to the target pressure. The filtering performance of the developed system was confirmed by measuring the eDNA concentration and comparing the voltage control method and the hydraulic control method with the control group. The voltage control method obtained similar results to the control group, but the hydraulic control method showed lower results than the control group. It is considered that the low eDNA concentration in the hydraulic control method is due to the large pressure deviation during filtering and maintaining a constant pressure during the filtering process. Therefore, rather than maintaining a constant pressure during filtering, it was confirmed that a voltage control method in which the pressure is gradually increased as the filtrate increases with the lapse of filtering time is suitable for collecting eDNA. As a result of comparing the average concentration of eDNA in lentic zone and lotic zone as a control group, it was found to be 96.2 [ng µL^-1] and 88.4 [ng µL^-1l], respectively. The result of comparing the average concentration of eDNA by the pump method was also high in the lentic zone sample as 90.7 [ng µL^-1] and 74.8 [ng µL^-1] in the lentic zone and the lotic zone, respectively. The high eDNA concentration in the lentic zone is thought to be due to the influence of microorganisms including the remaining eDNA.

• Environmental Mutagens and Carcinogens
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• v.18 no.2
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• pp.71-76
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• 1998

Exposure to environmental toxicants can cause cellular problems including the interference of DNA repair processes which may lead to the development of cancer. The existence of toxicant-induced DNA repair abnormality was investigated using mice exposed in vivo to genotoxic chemicals and then challenging their exposed lymphocytes in vitro with bleomycin. The repair of bleomycin-induced DNA damage as estimated by the frequency of chromosome aberrations was determined. Our data indicates that the observed aberration frequencies after in vivo exposure to N-methyl-N'-nitro-N-nitnsoguanidine (MNNG) and in vitro challenge with bleomycin are consistently higher than expected. The enhanced response is not due to the induction of chromosome damage by 25 or 50 mg/kg MNNG since the chemical did not cause chromosome aberrations in lymphocytes of these mice. The observed response after the combined exposure to benzo[a]pyrene (BP) and bleomycin was significantly lower than expected with low in vivo doses of BP (50 mg/kg) and then significantly higher than expected with the high doses (200 mg/kg). We interpret our data to indicate that in vivo exposure to genotoxic agents can cause abnormal DNA repair activities. The response is, however, independent of the clastogenic activities of the inducing chemicals, but dependent upon the inducing agents and on the exposure doses.

• Toxicological Research
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• v.22 no.2
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• pp.75-85
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• 2006

This study was designed to evaluate the possible DNA damaging effects of T-2 toxin using an alkaline single cell gel electrophoresis (SCGE) comet assay and also to investigate toxic effects in chickens. A total of 20 chickens were used in these experiments. Graded concentrations of dietary T-2 toxin (0, 4, 8, and $16{\mu}g/g$ of diet) were given to groups of 5 broiler chickens. In comet assay, The DNA damage was analysed by the tail extent moment (TEM) and tail length (TL), which were used as markers of DNA strand breaks in SCGE. A significant dose-dependent increase in the extent of DNA migration as well as in the percentage of cells with tails was observed after treatment with T-2 toxin (P<0.05). Treatment with the low T-2 toxin ($4{\mu}/g$ of diet) induced a relatively low level of DNA damage in comparison with the high T-2 toxin ($16{\mu}/g$ of diet) group. The growth rate was significantly reduced by concentrations of 8, and $16{\mu}/g$ of diet (P < 0.05). The feed conversion ratio were significantly affected by any concentrations (P < 0.05). The relative weight of the spleen, and lung was decreased by the growth inhibitory concentrations. The bursa of Fabricius, thymus, and kid- ney were decreased in relative weight by concentrations of $16{\mu}/g$ of diet. The relative weight of the liver and heart were unaffected. The hemoglobin (Hb), hematocrit (HCT), and mean corpuscular hemoglobin (MCH) were decreased at concentration of $16{\mu}/g$ of diet. As compared with control chickens, there was no marked change in serum components except uric acid in T-2 treated chickens. All lymphoid tissues retained atrophic and lymphoid cell depletion throughout the three weeks trial.

• The Korean Journal of Mycology
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• v.23 no.2 s.73
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• pp.129-138
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• 1995

DNA fragment being able to restore in vitro activity of ${\beta}-1,3-glucan$ synthase was cloned by transformation of the Saccharomyces cerevisiae LP353 mutant strain with genomic library constructed in the YCp50. For the selection of transformants which showed no detectable phenotype linked to recovery of the defect in ${\beta}-1,3-glucan$ synthase activity, the colony autoradiography was succesfully applied. The restriction map of the cloned DNA fragment, which is 8.5-kb in length, was constructed. Both the YEplac195 and the YCp50 carrying the 8.5-kb fragment increased ${\beta}-1,3-glucan$ synthase activity of LP353 by two fold. Neither the YEplac195 nor the YCp50 carrying the 8.5-kb DNA fragment, however, complemented the temperature-dependent osmotic sensitivity which is another distinctive phenotype of LP353. Subcloning experiments indicated that a functional region was located in 4.8-kb BglII-KpnI fragment. The 4.8-kb fragment was also able to increase the level of ${\beta}-1,3-glucan$ content in cell wall as well as the resistance of cells to cell wall lytic enzyme, ${\beta}-1,3-glucanase$. The growth rate of the LP353 with 4.8-kb fragment was almost same as that of wild type strain in liquid medium with 1.2 M sorbitol at nonpermissive temperature. Taken these results together, the 4.8-kb fragment seemed to contain the BGS2 gene for ${\beta}-1,3-glucan$ synthase activity in yeast S. cerevisiae.

• Journal of KIISE:Databases
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• v.34 no.2
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• pp.119-132
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• 2007

In molecular biology, approximate subsequence search is one of the most important operations. In this paper, we propose an accurate and efficient method for approximate subsequence search in large DNA databases. The proposed method basically adopts a binary trie as its primary structure and stores all the window subsequences extracted from a DNA sequence. For approximate subsequence search, it traverses the binary trie in a breadth-first fashion and retrieves all the matched subsequences from the traversed path within the trie by a dynamic programming technique. However, the proposed method stores only window subsequences of the pre-determined length, and thus suffers from large post-processing time in case of long query sequences. To overcome this problem, we divide a query sequence into shorter pieces, perform searching for those subsequences, and then merge their results. To verify the superiority of the proposed method, we conducted performance evaluation via a series of experiments. The results reveal that the proposed method, which requires smaller storage space, achieves 4 to 17 times improvement in performance over the suffix tree based method. Even when the length of a query sequence is large, our method is more than an order of magnitude faster than the suffix tree based method and the Smith-Waterman algorithm.