• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.12
• /
• pp.7265-7270
• /
• 2013

Objective: The present study was designed to investigate the probable mechanisms of synthetic retinoid 4-amino-2-tri-fluoromethyl-phenyl ester (ATPR) inhibition of the proliferation and migration of A549 human lung carcinoma cells. Materials and Methods: After the A549 cells were treated with different concentrations of ATPR or all-trans retinoic acid (ATRA) for 72 h, scratch-wound assays were performed to assess migration. Immunofluorescence was used to determine the distribution of CAV1 and $RXR{\alpha}$, while expression of CAV1, MLCK, MLC, P38, and phosphorylation of MLC and P38 were detected by Western blotting. Results: ATPR could block the migration of A549 cells. The relative migration rate of ML-7 group had significantly decreased compared with control group. In addition, ATPR decreased the expression of a migration related proteins, MLCK, and phosphorylation of MLC and P38. ATPR could also influence the expression of RARs or RXRs. At the same time, CAV1 accumulated at cell membranes, and $RXR{\alpha}$ relocated to the nucleus after ATPR treatment. Conclusions: Caveolae may be implicate in the transport of ATPR to the nucleus. Change in the expression and distribution of $RXR{\alpha}$ may be implicated in ATPR inhibition of A549 cell proliferation. The mechanisms of ATPR reduction in A549 cell migration may be associated with expression of MLCK and phosphorylation of MLC and P38.

• Journal of Nutrition and Health
• /
• v.21 no.3
• /
• pp.173-181
• /
• 1988

Various types of evidence suggest that some changes in cellular in cellular calcium may well signal the initiation of a chain of events leading to the physiological effects of the bone resorbing agents. The effects of 1,25-dihydorxycholecalciferol, $1.25\textrm{(OH)}_2\textrm{D}_3$, Ca ionophore A23187 and calcium antagonist, diltiazem on bone resprption and the cellular transport of Ca were investigated. Bone $^{45}\textrm{Ca}$ desaturation experiment was realized in isolated heterogenous rat bone cells after equilibrating the cells with $^{45}\textrm{Ca}$. Results of $^{45}\textrm{Ca}$ desaturation experiments were analysed by fitting the $^{45}\textrm{Ca}$ desaturation curve to a model of 2 exponential terms which indicated the presence of 2 exchangeable cellular calcium pools. $1.25\textrm{(OH)}_2\textrm{D}_3$ (0.5ng/$m\ell$) induced significantly bone resorption which was decreased by the physiological dose of diltiazeme(above 5nmol/$m\ell$) although it was ineffective alone. Ionophore A23187 (0.2$\mu\textrm{g}$/$m\ell$) decreased Ca release from bone but no additivity of effect with diltiazem(20nmol/$m\ell$) was observed. $1.25\textrm{(OH)}_2\textrm{D}_3$ (0.5ng/$10^{6}$ cells) had a moderate effect on the two kinetic phases of $^{45}\textrm{Ca}$ desaturation curve and these values were normalized when diltiazeme (20nmol/$10^{6}$ cells) was added along with $1.25\textrm{(OH)}_2\textrm{D}_3$. Ionophore($0.05\mu\textrm{g}$/$10^{6}$ cells) alone increased specifically the value of the slow turnover rate which was not affected by addition of diltiazem. The hypothesis concerning the involvement of calcium in bone resorption seems in fact to be verified in case of $1.25\textrm{(OH)}_2\textrm{D}_3$ but more unsettled for Ca inophore A23187.

• Journal of the Korean Chemical Society
• /
• v.41 no.3
• /
• pp.144-149
• /
• 1997

Organic electroluminescence devices(ELD) were fabricated using by molecularly doped method with N,N'-diphenyl-N,N'-bis(3-methylphenyl)-1,1'-biphenyl-4,4'-diamine(TPD) as a hole transport agent, squarylium dye as an emitting agent, and side chain liquid crystalline polymer(MCH) as matrix for TPD. An indium-tin-oxide(ITO) coated glass and an Mg electrode were used as the hole and the electron injecting electrode, respectively. The highest stability of ELD was obtained by spin coating method using dichloroethane as a solvent at a polymer/TPD concentration of 0.005 wt%. For the EL cell with ITO/polymer-TPD/SQ dye/Mg structure, we achieved light red luminescence at a current of 102 mA/$cm^2$ with an applied voltage of 23 V.

• Korean Journal of Oriental Medicine
• /
• v.8 no.2 s.9
• /
• pp.95-107
• /
• 2002

Yukmijihwang-tang(YM) is a noted herbal prescription in Chinese and Korean traditional medicines, and it has been known to reinforce the vital essence and has been widely used for a variety of disease such as stroke, osteoporosis, anti-tumor, and hypothyrodism. Regarding its traditional use, YM has been known to reinforce the Yin (vital essence) of liver and kidney. Also it has been known to reinforce nutrition and biological function in brain. Recently, studies suggested that YM increase antioxidant activities and exert the protective effect against oxidant-induced liver cell injury. We investigated the high-throughput gene expression analysis on the Yukmijihwang-tang administrated in SD rats. Microarray data were validated on a limited number of genes by semiquantitative RT-PCR and Western blot analyses. The recent availability of microarrays provides an attractive strategy for elaborating an unbiased molecular profile of large number of genes in drug discovery This experimental approach offers the potential to identify molecules or cellular pathways not previously associated with herbal medicine. Total RNA from normal control brain and Yukmijihwang-tang administrated brain were hybridized to microarrays containing 10,000 rat genes. The 52 genes were found to be up-regulated(twice or more) excluding EST gene. The nine genes were found to be down-regulated(twice or more) excluding EST gene. Gene array technology was used to identify for the first time many genes expression pathway analysis that arecell cycle pathway, apoptosis pathway, electron transport chain pathway, cytoplasmic ribosomal protein pathway, fatty acid degradation pathway, and TGF-beta signaling pathway. These differentially expressed genes pathway analysis have not previously been iavestigated in the context of herbal medicine efficacy and represent novel factors for further study of the mechanism of herbal medicine efficacy.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
• /
• 2000.05b
• /
• pp.316-319
• /
• 2000

In the case of immobilizing of glucose oxidase into polypyrrole (PPy) using electrosynthesis, the glucose oxidase (GOx) forms a coordinate bond with the polymer's backbone. However, because of intrinsic insulation and net-chain of the enzyme, the charge transfer and mass transport are obstructed during the film growth. Therefore, the film growth is dull. We synthesized the enzyme electrode by electropolymerization added some organic solvent, A formative seeds of film growth is delayed by adding the solvent. The delay is induced by radical transfer between the solvent and pyrrole monomer. In the case of adding ethanol, the radical transfer shares the contribution of dopant between electrolyte anion and GOx polyanion. This may lead to increase amount of immobilized the enzyme in ppy. However, adding tetrahydrofuran (THF), the radical transfer is more brisk, resulting in short chained polymer. Therefore, the doping level is lowered and then amount of immobilized of enzyme is decreased. For the UV absorption spectra of synthetic solution before synthesis and after, in the case of ethanol added, the optical density was slightly decreased for the GOx peaks. It suggests amount of GOx in the solution was decreased and amount of GOx in the film was increased. We established qualitatively that amount of immobilization can be improved by adding a little ethanol in the synthetic solution. It is due to radical transfer reaction. The radical transfer shares the contribution of dopant between small and fast electrolyte anion and big and slow GOx polyanion.

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

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.17
• /
• pp.7223-7228
• /
• 2014

The MYH11 gene may be related to cell migration and adhesion, intracellular transport, and signal transduction. However, its relationship with prognosis is still uncertain. The aim of this study was to investigate correlations between MYH11 gene expression and prognosis in 58 patients with stage II and III colorectal cancer. Quantitative real-time polymerase chain reaction was performed in fresh CRC tissues to examine mRNA expression, and immunohistochemistry was performed with paraffin-embedded specimens for protein expression. On univariate analysis, MYH11 expression at both mRNA and protein levels, perineural invasion and lymphovascular invasion were related to disease-free survival (p<0.05; log-rank test). Cancers with lower MYH11 expression were more likely to have a poor prognosis. Otherwise, MYH11 expression was unrelated to patient clinicopathological features. On multivariate analysis, low MYH11 expression proved to be an independent adverse prognosticator (p<0.05). These findings show that MYH11 can contribute to predicting prognosis in stage II and III colorectal cancers.

• KSII Transactions on Internet and Information Systems (TIIS)
• /
• v.11 no.7
• /
• pp.3465-3479
• /
• 2017

Information-Centric Vehicular Ad Hoc Network (IC-VANET) is a promising network architecture for the future intelligent transport system. Video streaming applications over IC-VANET not only enrich infotainment services, but also provide the drivers and pedestrians real-time visual information to make proper decisions. However, due to the characteristics of wireless link and frequent change of the network topology, the packet loss seriously affects the quality of video streaming applications. In this paper, we propose a REceiver-Driven loss reCOvery Mechanism (REDCOM) to enhance video dissemination over IC-VANET. A Markov chain based estimation model is introduced to capture the real-time network condition. Based on the estimation result, the proposed REDCOM recovers the lost packets by requesting additional forward error correction packets. The REDCOM follows the receiver-driven model of IC-VANET and does not require the infrastructure support to efficiently overcome packet losses. Experimental results demonstrate that the proposed REDCOM improves video quality under various network conditions.

• Journal of Advanced Marine Engineering and Technology
• /
• v.38 no.5
• /
• pp.589-601
• /
• 2014

Natural gas hydrate (NGH) is emerging as a new eco-friendly source of energy to replace fossil fuels in the 21st century. It is well known that the Natural Gas Hydrate contains large amount of natural gas about 170 times as much as its volume and it is easy to be stored and transported safely at about $-20^{\circ}C$ under atmospheric pressure due to so called "self-preservation effect". The option of gas transport by gas hydrate pellets carrier has been investigated and developed in various industry and academy. The natural gas hydrate pellet carrier is on major link in a potential gas hydrate process chain, starting with the extraction of natural gas from the reservoir, followed by the production of hydrate pellets and the transportation to an onshore terminal for further processing or marketing. In recent years, Korean project team supported by Korean Government has been working on the development of NGH total systems including novel NGH carrier since 2011. In order to increase the knowledge on the NGH pellet carrier developed and to understand the major hazards that could have significant impact on the safety of the vessel, this paper presents and evaluates the pros and cons of cargo holds, loading and unloading systems through the analysis of current patent technology. Based on the proven and well-known technologies as well as potential measures to mitigate sintering and minimize mechanical stress on the hydrate pellet in the self-preservation state, this study presents the conceptual and basic design for NGH carrier.

• Molecules and Cells
• /
• v.37 no.9
• /
• pp.672-684
• /
• 2014

The exact causes of cell death in Parkinson's disease (PD) remain unknown despite extensive studies on PD.The identification of signaling and metabolic pathways involved in PD might provide insight into the molecular mechanisms underlying PD. The neurotoxin 1-methyl-4-phenylpyridinium ($MPP^+$) induces cellular changes characteristic of PD, and $MPP^+$-based models have been extensively used for PD studies. In this study, pathways that were significantly perturbed in $MPP^+$-treated human neuroblastoma SH-EP cells were identified from genome-wide gene expression data for five time points (1.5, 3, 9, 12, and 24 h) after treatment. The mitogen-activated protein kinase (MAPK) signaling pathway and endoplasmic reticulum (ER) protein processing pathway showed significant perturbation at all time points. Perturbation of each of these pathways resulted in the common outcome of upregulation of DNA-damage-inducible transcript 3 (DDIT3). Genes involved in ER protein processing pathway included ubiquitin ligase complex genes and ER-associated degradation (ERAD)-related genes. Additionally, overexpression of DDIT3 might induce oxidative stress via glutathione depletion as a result of overexpression of CHAC1. This study suggests that upregulation of DDIT3 caused by perturbation of the MAPK signaling pathway and ER protein processing pathway might play a key role in $MPP^+$-induced neuronal cell death. Moreover, the toxicity signal of $MPP^+$ resulting from mitochondrial dysfunction through inhibition of complex I of the electron transport chain might feed back to the mitochondria via ER stress. This positive feedback could contribute to amplification of the death signal induced by $MPP^+$.