• KSBB Journal
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• v.26 no.4
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• pp.305-310
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• 2011

This study was carried out to establish the optimum condition of cell disruption with a sonicator for the detection of the spore, Bacillus anthracis ${\Delta}$-sterne for the purpose of developing automatic fluorometer. The efficiency of sonication on the ${\Delta}$-sterne spore disruption was very weak. The ${\Delta}$-sterne spore with zirconia bead showed greater disruption than the ${\Delta}$-sterne spore alone when sonificated. The volumn of the zirconia bead added in the spore solution has little effect on the disruption efficiency. The detection limit of the ${\Delta}$-sterne spore with zirconia bead and the ${\Delta}$-sterne spore alone was $10^6$ CFU/mL and $5{\times}10^7$ CFU/mL respectively, when sample was sonicated for 20 seconds with a sonicator probe of 13 mm diameter.

• Molecules and Cells
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• v.28 no.4
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• pp.403-406
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• 2009

Rev is an essential regulatory protein for HIV-1 replication. Rev (11-20) is known as the significant region regarding the function of a nuclear entry inhibitory signal (NIS) of Rev. In this study, anticandidal effects and mechanism of action of Rev (11-20) were investigated. The result exhibited that Rev (11-20) contained candidacidal activities. To understand target site(s) of Rev (11-20), the intracellular localization of the peptide was investigated. The result showed that Rev (11-20) rapidly accumulated in the fungal cell surface. The cell wall regeneration test also indicated that Rev (11-20) exerted its anticandidal activity to fungal plasma membrane rather than cell wall. The fluorescent study using 1,6-diphenyl-1,3,5-hexatriene (DPH) further confirmed the membrane-disruption mechanism(s) of Rev (11-20). The present study suggests that Rev (11-20) possesses significant potential regarding therapeutic agents for treating fungal diseases caused by Candida species in humans.

• Journal of Life Science
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• v.8 no.2
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• pp.197-202
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• 1998

The cell of Kluyveromyces fragilis yeast, which is worthy of an algal substitute, was disrupted by a chemical treatment to increase the digestion of filter-feeders that yeasts are fed to. The optimum conditions of the chemical treatment were obtained by incubating yeasts at 3$0^{\circ}C$ for one hour after treated by 1 M of Na$_{2}$-EDTA that was dissolved in 0.2 M of Tris-buffer and by 0.3 m of 2-mercaptoethanol. The percentage of protop[last production was about 30%. The percentage could be doubled by the pretreatment of three times of 30 seconds sonication.

• Molecules and Cells
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• v.42 no.3
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• pp.218-227
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• 2019

This study was designed to determine the effects of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on vascular smooth muscle cell (VSMC) apoptosis and extracellular matrix (ECM) disruption in a murine abdominal aortic aneurysm (AAA) model. After injection of PVT1-silencing lentiviruses, AAA was induced in Apolipoprotein E-deficient ($ApoE^{-/-}$) male mice by angiotensin II (Ang II) infusion for four weeks. After Ang II infusion, mouse serum levels of pro-inflammatory cytokines were analysed, and aortic tissues were isolated for histological, RNA, and protein analysis. Our results also showed that PVT1 expression was significantly upregulated in abdominal aortic tissues from AAA patients compared with that in controls. Additionally, Ang II treatment significantly increased PVT1 expression, both in cultured mouse VSMCs and in AAA murine abdominal aortic tissues. Of note, the effects of Ang II in facilitating cell apoptosis, increasing matrix metalloproteinase (MMP)-2 and MMP-9, reducing tissue inhibitor of MMP (TIMP)-1, and promoting switching from the contractile to synthetic phenotype in cultured VSMCs were enhanced by overexpression of PVT1 but attenuated by knockdown of PVT1. Furthermore, knockdown of PVT1 reversed Ang II-induced AAA-associated alterations in mice, as evidenced by attenuation of aortic diameter dilation, marked adventitial thickening, loss of elastin in the aorta, enhanced aortic cell apoptosis, elevated MMP-2 and MMP-9, reduced TIMP-1, and increased pro-inflammatory cytokines. In conclusion, our findings demonstrate that knockdown of lncRNA PVT1 suppresses VSMC apoptosis, ECM disruption, and serum pro-inflammatory cytokines in a murine Ang II-induced AAA model.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 2000.10a
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• pp.176-177
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• 2000

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.4
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• pp.888-894
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• 2009

It has been reported that silibinin, a natural polyphenolic flavonoid, induces cell death in various cancer cell types. However, the underlying mechanisms by which silibinin induces apoptosis in human glioma cells are poorly understood. The present study was therefore undertaken to examine the effect of silibinin on glioma cell apoptosis and to determine its underlying mechanism in human glioma cells. Apoptosis was estimated by FACS analysis. Reactive oxygen species (ROS) generation and mitochondrial membrane potential (${\Psi}m$) were measured using fluorescence dyes DCFH-DA and $DiOC_6$(3), respectively. Cytochrome c release from mitochondria and caspase-3 activation were estimated by Western blot analysis using specific antibodies. Exposure of cells to 30 mM silibinin induced apoptosis starting at 6 h, with increasing effects after 12-48h in a time-dependent manner. Silibinin caused ROS generation and disruption of ym, which were associated with the silibinin-induced apoptosis. The silibinin-induced ROS generation and disruption in ym were prevented by inhibitors of mitochondrial electron transport chain. The hydrogen peroxide scavenger catalase blocked ROS generation and apoptosis induced by silibinin. Silibinin induced cytochrome c release into cytosolic fraction and its effect was prevented by catalase and cyclosporine A. Silibinin treatment caused caspase-3 activation, which was inhibited by DVED-CHO and cyclosporine A. Pretreatment of caspase inhibitors also protected against the silibinin-induced apoptosis. These findings indicate that ROS generation plays a critical role in the initiation of the silibinin-induced apoptotic cascade by mediation of the mitochondrial apoptotic pathway including the disruption of ${\Psi}m$, cytochrome c release, and caspase-3 activation.

• Environmental Engineering Research
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• v.11 no.3
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• pp.143-148
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• 2006

The ultrasonics is a new technology in waste activated sludge(WAS) treatment. Ultrasonic treatment is well known method for the break up of microbial cells to extract out a variety of intercellular materials inside microorganism cell. This study was done to investigate the effects of the ultrasonic frequency and power on disruption of biosolids in WAS and to examine the effect on methane production of WAS treated by ultrasonics. Biosolids disruption with ultrasound is more effective at ultrasonic frequency of 40 kHz and power of 0.3 watt/mL. In the digestion with WAS pretreated by sonication time for 10 minute at 40 kHz and 0.3 watt/mL, the total quantity of generated methane increased by 75%, as compared with experimental control(non-treatment).

• Transactions of the Korean Society of Mechanical Engineers A
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• v.32 no.10
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• pp.831-835
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• 2008

We present a continuous electrical cell lysis chip, using a DC bias voltage to generate the focused high electric field for cell lysis as well as the electroosmotic flow for cell transport. The previous cell lysis chips apply an AC voltage between micro-gap electrodes for cell lysis and use pumps or valves for cell transport. The present DC chip generates high electrical field by reducing the width of the channel between a DC electrode pair, while the previous AC chips reducing the gap between an AC electrode pair. The present chip performs continuous cell pumping without using additional flow source, while the previous chips need additional pumps or valves for the discontinuous cell loading and unloading in the lysis chambers. The experimental study features an orifice whose width and length is 20 times narrower and 175 times shorter than the width and length of a microchannel. With an operational voltage of 50 V, the present chip generates high electric field strength of 1.2 kV/cm at the orifice to disrupt cells with 100% lysis rate of Red Blood Cells and low electric field strength of 60 V/cm at the microchannel to generate an electroosmotic flow of $30{\mu}m/s{\pm}9{\mu}m/s$. In conclusion, the present chip is capable of continuous self-pumping cell lysis at a low voltage; thus, it is suitable for a sample pretreatment component of a micro total analysis system or lab-on-a-chip.

• KSBB Journal
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• v.21 no.5
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• pp.341-346
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• 2006

This study was carried out to establish the optimum condition for cell disruption with a sonificator in the detection of the gram negative bacteria, E. coli for the purpose of developing automatic fluorometer. The efficiency of sonification on the E. coli disruption was greatly dependent on the diameter of sonificator probe tip. The larger sonificator probe diameter showed greater disruption effect. Sonificator probe of 13 mm diameter was the most efficient one for E. coli when sonificated for 20 seconds. The efficiency of the E. coli disruption differed greatly according to the depth of sonificator probe tip sank in the sample solution. The shorter the distance between probe tip end and the bottom of the container, the higher the disruption efficiency. The detection limit of E. coli was $5{\times}10^5CFU/m{\ell}$ when sample was sonificated for 20 seconds with a sonificator probe of 13 mm diameter.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.213-217
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• 2013

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the ${\beta}$-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (${\beta}$-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the ${\beta}$-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.