• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2010.05a
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• pp.503-506
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• 2010

In this paper, we apply the system in VMEbus to increase the stability and viability to implement a redundant network protocol. Typically, methods for increasing the viability of the system applied by the redundancy scheme between the two processes by configuring the network in between the two is to implement redundancy. However, the physical network in the process of the failure or when the loss function may not perform properly. These issues are complementary processes as a way to ensure stability between the VMEbus communication protocol is presented through a redundant network. In this paper, a direct implementation of the protocol and experimental results confirm the validity of these measures is to.

• Biomolecules & Therapeutics
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• v.19 no.4
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• pp.451-459
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• 2011

Peroxiredoxins (Prxs) have a critical role in protecting cells against oxidative damage generated by reactive oxygen species (ROS). PrxI and PrxII are more than 90% homologous in their amino acid sequences, and both proteins reduce $H_2O_2$. In this study, an over-expression plasmid carrying PrxI was transfected into $PrxII^{-/-}$ mouse embryonic fibroblasts (MEFs) to investigate potential compensatory relationships between PrxI and PrxII. ROS levels induced by oxidative stress were increased in $PrxII^{-/-}$ MEFs as compared to wild-type MEFs. Moreover, exposure of $PrxII^{-/-}$ MEFs to $H_2O_2$ caused a reduction in cell viability of about 10%, and the proportion of cell death was increased compared to mock-treated $PrxII^{-/-}$ MEFs. However, transient over-expression of PrxI in $PrxII^{-/-}$ MEFs conferred increased resistance against the oxidative damage, as evidenced by increased cell viability and reduced intracellular ROS levels under $H_2O_2$ stress conditions. The findings suggest that over-expressed PrxI can partly compensate for the loss of PrxII function in PrxII-deficient MEFs.

• Advances in nano research
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• v.11 no.6
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• pp.657-665
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• 2021

The present work aimed to explore green approach via aqueous leaves extract of Murraya koenigii (ALEMk) for the synthesis of silver nanoparticles (AgNPsMk) in single step. The synthesis process was visualized with a color change and monitored by employing UV/Visible spectroscopy and a clear peak attained at 420 nm confirming the synthesis of AgNPsMk. The possible functional groups present in the extract which participated in the synthesis of AgNPsMk were identified with the help of FTIR spectroscopy. Further characterization using TEM images revealed the spherical shape of AgNPsMk with average particle size of 20 nm displaying well dispersion throughout the solution. Pronounced antioxidant activities of AgNPsMk at increased concentrations observed which evidencing strong radical scavenging ability. Moreover, AgNPsMk exhibited strong antibacterial behavior when tested against bacterial strains of Escherichia coli and Bacillus subtilis. Moving ahead, in vitro cytotoxicity work revealed potent cell viability loss appearing in AU565 and HeLa cancer cell lines on exposure to AgNPsMk at increased concentration. Finally, in vivo assessment carried out inside male Wistar rats indicated non toxic effect on examined liver tissues besides biochemical analysis including bilirubin, alkaline phosphtase (ALP) and serum glutamate pyruvate transaminase (SGPT) which found within the normal range when compared with control. The prior research work profoundly apprises the potential of green synthesized AgNPsMk to play a significant role in biomedical applications and formulations.

• Korean Journal of Agricultural Science
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• v.49 no.2
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• pp.259-267
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• 2022

Although pesticides are recognized as necessary substances to improve agricultural production, exposure to pesticides is known to have a direct or indirect adverse effect on the reproductive function of mammals. The present study examines the effects of mancozeb, a well-known fungicide, on the fertility capacity of spermatozoa. Boar spermatozoa exposed to varying concentrations of mancozeb (0.01 - 0.5 µM) were evaluated for motility, motion kinetic parameters, viability, acrosome integrity and the generation of intracellular reactive oxygen species (ROS) after 30 min or 2 hrs of incubation. A significant reduction in the motility of spermatozoa was observed upon exposure to mancozeb. Similarly, there was a significant reduction of the motion kinematics of sperm treated with mancozeb as compared to untreated controls (p < 0.05). The sperm viability percentage and acrosome integrity also showed dose-dependent decreases upon exposure to mancozeb. High concentrations of mancozeb (0.2 - 0.5 µM) induced higher levels of intracellular ROS production, which resulted in the loss of the sperm membrane and decreased sperm motility due to oxidative stress. Taken together, the results here indicate that direct exposure to mancozeb affects the sperm fertility capacity. Hence, careful research that examines the interaction between reproduction and environmental toxins is crucial to prevent fertility disorders in animals.

• Molecules and Cells
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• v.26 no.2
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• pp.158-164
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• 2008

Arsenic trioxide (ATO) affects many biological processes such as cell proliferation, apoptosis, differentiation and angiogenesis. L-buthionine sulfoximine (BSO) is an inhibitor of GSH synthesis. We tested whether ATO reduced the viability of lung cancer A549 cells in vitro, and investigated the in vitro effect of the combination of ATO and BSO on cell viability in relation to apoptosis and the cell cycle. ATO caused a dose-dependant decrease of viability of A549 cells with an $IC_{50}$ of more than $50{\mu}m$. Low doses of ATO or BSO ($1{\sim}10{\mu}m$) alone did not induce cell death. However, combined treatment depleted GSH content and induced apoptosis, loss of mitochondrial transmembrane potential (${\Delta}{\Psi}_m$) and cell cycle arrest in G2. Reactive oxygen species (ROS) increased or decreased depending on the concentration of ATO. In addition, BSO generally increased ROS in ATO-treated A549 cells. ROS levels were at least in part related to apoptosis in cells treated with ATO and/or BSO. In conclusion, we have demonstrated that A549 lung cells are very resistant to ATO, and that BSO synergizes with clinically achievable concentration of ATO. Our results suggest that combination treatment with ATO and BSO may be useful for treating lung cancer.

• Animal cells and systems
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• v.9 no.4
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• pp.191-198
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• 2005

The effects of 6-aminonicotinamide (6-AN) on viability of IMR32 neuroblastoma cells in the presence of ATP or $NAD^+$ have been investigated. 6-AN caused marked reduction in cell viability and similar observations were also made with cells treated with 6-AN+ATP. However, cells treated with $6-AN+NAD^+$ showed cell viability similar to untreated cells. Morphologically, 6-AN and 6-AN+ATP treated cells showed loss of neurites, polyhedric shapes, shrinkage of cell bodies and formation of lysed cells, while $6-AN+NAD^+$ cells did not show any such changes. The flow cytometry analysis demonstrated that 6-AN increased cell population in $G_0/G_1$ phase and decreased cell population in Sand $G_2/M$ phase following a 72 h exposure. Western blot analysis showed that 6-AN stimulated a substantial increase in the level of the cdk inhibitor $p27^{kip1}$, but lowered the levels of cdk2, cyclin E and p-Rb. However, cdc25A and p53R2 were not significantly affected. Immunofluorscence staining of $p27^{kip1}$, cdk2, cyclin E and p-Rb revealed close correlation between the signal observed in the Western blot analysis. 6AN+ATP treated cells showed similar results obtained with 6-AN treated cells in expression of cdk2, cyclin E, p-Rb proteins and $p27^{kip1}$, $6-AN+NAD^+$ cells showed greater expression of cdk2, cyclin E and p-Rb than those in 6-AN and 6-AN+ATP treated cells. The results suggest that 6-AN induced the $G_0/G_1$ phase arrest in IMR32 neuroblastoma cell lines through the increase of $p27^{kip1}$ and the decrease of cdk2, cyclin E and p-Rb.

• Journal of the Korean Institute of Landscape Architecture International Edition
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• no.1
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• pp.43-52
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• 2001

One of the major environmental issues Japanese cities is now facing with is the conservation of seminatural landscapes for the restoration of ecological integrity of urban areas. The satoyama landscape, which includes coppice woodlands, agricultural areas and rural settlements, is seen as an indispensable semi-natural landscape, formed as a result of man-nature interaction. However, because of the loss of the economic viability they are now abandoned and in the process of losing their ecological values. Today a number of local municipalities as well as NPO groups are involved in the conservation projects of these landscapes. Although satoyama landscapes are commonly believed to have maintained their character over the years, historical studies have revealed that these landscapes have experienced constant and dynamic changes due to a variation in human impacts. It is therefore understood that the conservation projects on satoyama landscapes should not intend to restore their past condition, but should wet the goal of maintaining their dynamic character by promoting ecological roles which the landscapes may play in the contemporary world. EXPO2005 project in Aichi Prefecture is a good example of a development project underway on satoyama landscapes which intend to conserve the landscapes by stimulating contemporary ecological for them. In EXPO2005 project the key issue was the conservation of semi-natural landscapes formed by constant and intensive human impacts over the centuries and thus allowing endemic and endangered species to be accommodated. The planning team proposed a scheme to restore economic viability of satoyama landscapes. The scheme involves re-introducing intensive human impacts through a new management system with an innovative technology. This may restore the economic viability of lumbers provided form satoyama woodlands. EXPO2005 is understood as a model case which stimulates contemporary ecological functions of satoyama landscapes by applying innovative planning concepts.

• The Journal of Korean Obstetrics and Gynecology
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• v.18 no.1
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• pp.29-44
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• 2005

To address the ability of Herba Portulacae(HP) to induce cell death, we investigated the effect of HP on cell viability. Twenty-four hours later, loss of viability occurred following HP exposure in a dose-dependent manner. The treatment of HP, a commonly used herb formulation in Korea, Japan and China, caused a decrease in cell viability. HP also resulted in apoptotic morphology a brightly blue-fluorescent condensed nuclei by Hoechst 33258-staining, and reduction of cell volume. Our results show that 2mg/ml HP induces mitochondria membrane potential collapse. Immunoblotting data also shows that the expression of Bcl-2, antiaoptotic protein, decrease by the addition of HP. This GFP-Bax overexpression system shows that an important pro-apoptotic Bcl-2-family protein, Bax is translocated to mitochondria by the addition of 2mg/ml HP. Inerestingly, MAPK inhibitor study shows that p38 MAPK inhibitor, SB203580 inhibits HP-induced cell death and caspase-3 activation in HP-treated HeLa cells. Furthermore, HP transiently but significantly induces p38 activation. But P38 MAPK inhibitor does not have any effect on the translocation of Bax. Considering these results, HP induces apoptosis via p38 MAPK activation. But the pathway does not involve the translocation of Bax.

• Journal of Acupuncture Research
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• v.36 no.1
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• pp.33-37
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• 2019

Background: This study was designed to investigate the potential effects of Galgeungyulpitang for whitening and elasticity treatment by examining its effect on melanoma cells. Methods: The effects of Galgeungyulpitang on B16/F10 melanoma cell viability, production of melanin, tyrosinase and elastase, were investigated. Cell viability was measured by colorimetric assay that assesses cell metabolic activity (MTT assay). Melanin was measured by Hosei's method, tyrosinase was measured by Yogi's method and elastase was measured by James's method. Results: At concentrations higher than $500{\mu}g/mL$ Galgeungyulpitang, cell viability was significantly reduced ($p{\leq}0.05$). At concentrations of $500{\mu}g/mL$ and lower, morphological changes were not observed. The rate of melanin synthesis was significantly reduced to $73.49%{\pm}2.92%$ at a concentration of $500{\mu}g/mL$ Galgeungyulpitang compared with untreated cells (p < 0.05). Extracellular tyrosinase production was not significantly decreased in vitro, however, intracellular tyrosinase production was significantly reduced to $76.06%{\pm}2.17%$ when treated with Galgeungyulpitang at a concentration of $500{\mu}g/mL$ compared with the control (p < 0.05). Elastase Type 1 production was significantly reduced to $74.98%{\pm}3.24%$ and $69.62%{\pm}4.66%$ at concentrations of 250 and $500{\mu}g/mL$ Galgeungyulpitang, respectively (p < 0.05). Elastase Type 4 production was significantly reduced to $72.77%{\pm}3.52%$ at concentrations of 250 and $500{\mu}g/mL$ (p < 0.05). Conclusion: The results in this study showed that Galgeungyulpitang may inhibit melanin and tyrosinase synthesis, and inhibit elastase production, suggesting that Galgeungyulpitang may be potentially beneficial for skin whitening and loss of skin elasticity treatments.

• Molecules and Cells
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• v.45 no.6
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• pp.365-375
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• 2022

Long non-coding RNAs (lncRNAs) may be important regulators in the progression of ankylosing spondylitis (AS). The competing endogenous RNA (ceRNA) activity of lncRNAs plays crucial roles in osteogenesis. We identified the mechanism of the differentially expressed lncRNA MALAT1 in AS using bioinformatic analysis and its ceRNA mechanism. The interaction of MALAT1, microRNA-558, and GSDMD was identified using integrated bioinformatics analysis and validated. Loss- and gain-of-function assays evaluated their effects on the viability, apoptosis, pyroptosis and inflammation of chondrocytes in AS. We found elevated MALAT1 and GSDMD but reduced miR-558 in AS cartilage tissues and chondrocytes. MALAT1 contributed to the suppression of cell viability and facilitated apoptosis and pyroptosis in AS chondrocytes. GSDMD was a potential target gene of miR-558. Depletion of MALAT1 expression elevated miR-558 by inhibiting GSDMD to enhance cell viability and inhibit inflammation, apoptosis and pyroptosis of chondrocytes in AS. In summary, our key findings demonstrated that knockdown of MALAT1 served as a potential suppressor of AS by upregulating miR-558 via the downregulation of GSDMD expression.