• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.9 no.5
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• pp.155-161
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• 2009

This paper proposes a high capacity data hiding method using modulus function of pixel-value differencing (PVD) and least significant bit (LSB) replacement method. Many novel data hiding methods based on LSB and PVD methods were presented to enlarge hiding capacity and provide an imperceptible quality. A small difference value for two consecutive pixels is belonged to a smooth area and a large difference one is located on an edge area. In our proposed method, the secret data are hidden on the smooth area by the LSB substitution method and PVD method on the edge area. From the experimental results, the proposed method sustains a higher capacity and still a good quality compared with other LSB and modified PVD methods.

• BMB Reports
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• v.48 no.6
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• pp.354-359
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• 2015

Vascular smooth muscle cells (VSMCs) undergo death during atherosclerosis, a widespread cardiovascular disease. Recent studies suggest that oxidative damage occurs in VSMCs and induces atherosclerosis. Here, we analyzed oxidative damage repair in VSMCs and found that VSMCs are hypersensitive to oxidative damage. Further analysis showed that oxidative damage repair in VSMCs is suppressed by a low level of poly (ADP-ribosyl)ation (PARylation), a key post-translational modification in oxidative damage repair. The low level of PARylation is not caused by the lack of PARP-1, the major poly(ADP-ribose) polymerase activated by oxidative damage. Instead, the expression of poly(ADP-ribose) glycohydrolase, PARG, the enzyme hydrolyzing poly(ADP-ribose), is significantly higher in VSMCs than that in the control cells. Using PARG inhibitor to suppress PARG activity facilitates oxidative damage-induced PARylation as well as DNA damage repair. Thus, our study demonstrates a novel molecular mechanism for oxidative damage-induced VSMCs death. This study also identifies the use of PARG inhibitors as a potential treatment for atherosclerosis. [BMB Reports 2015; 48(6): 354-359]

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.1
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• pp.69-79
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• 2020

Aging is one of the risk factors for the development of cardiovascular diseases. During the progression of cellular senescence, cells enter a state of irreversible growth arrest and display resistance to apoptosis. As a flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated the relationship between quercetin-induced apoptosis and the inhibition of cellular senescence, and determined the mechanism of oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H₂O₂) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated β-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Along with senescence, expression of the anti-apoptotic protein Bcl-2 was observed to increase and the levels of proteins related to the apoptosis pathway were observed to decrease. Quercetin induced apoptosis through the activation of AMP-activated protein kinase. This action led to the alleviation of oxidative stress-induced VSMC senescence. Furthermore, the inhibition of AMPK activation with compound C and siRNA inhibited apoptosis and aggravated VSMC senescence by reversing p53-p21 and p16 pathways. These results suggest that senescent VSMCs are resistant to apoptosis and quercetin-induced apoptosis attenuated the oxidative stress-induced senescence through activation of AMPK. Therefore, induction of apoptosis by polyphenols such as quercetin may be worthy of attention for its anti-aging effects.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.4
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• pp.415-421
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• 2017

We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent $K^+$ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The $IC_{50}$ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were $9.54{\pm}1.33{\mu}M$ and $0.75{\pm}0.10$, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.

• BMB Reports
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• v.50 no.12
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• pp.628-633
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• 2017

Gastrin-releasing peptide (GRP) has been reported to be implicated in the pathogenesis of inflammatory disorders. The migration and proliferation of vascular smooth muscle cells (VSMCs) are key components of vascular inflammation that leads to the development of atherosclerosis. The present study aimed to investigate the molecular effect of GRP on VSMC proliferation and migration. We report that GRP significantly enhanced the proliferation and migration of rat VSMCs. GRP increased mRNA and protein expression of matrix metalloproteinase-2 and -9 (MMP-2/9) in VSMCs. The induction of MMP-2/9 by GRP was regulated by the activation of the signal transducer and activator of transcription-3 (STAT3). In addition, STAT3-knockdown of VSMCs by siRNA or blockade of the GRP receptor inhibited GRP-induced migration of VSMCs. Taken together, our findings indicate that GRP promotes the migration of VSMCs through upregulation of MMP-2/9 via STAT3 activation.

• Journal of Electrical Engineering and Technology
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• v.12 no.2
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• pp.890-903
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• 2017

The problem of determining a smooth and collision-free path with maximum possible speed for a Mobile Robot (MR) which is chasing a moving target in a dynamic environment is addressed in this paper. Genetic Network Programming with Reinforcement Learning (GNP-RL) has several important features over other evolutionary algorithms such as it combines offline and online learning on the one hand, and it combines diversified and intensified search on the other hand, but it was used in solving the problem of MR navigation in static environment only. This paper presents GNP-RL based on predicting collision positions as a first attempt to apply it for MR navigation in dynamic environment. The combination between features of the proposed collision prediction and that of GNP-RL provides safe navigation (effective obstacle avoidance) in dynamic environment, smooth movement, and reducing the obstacle avoidance latency time. Simulation in dynamic environment is used to evaluate the performance of collision prediction based GNP-RL compared with that of two state-of-the art navigation approaches, namely, Q-Learning (QL) and Artificial Potential Field (APF). The simulation results show that the proposed GNP-RL outperforms both QL and APF in terms of smooth movement and safer navigation. In addition, it outperforms APF in terms of preserving maximum possible speed during obstacle avoidance.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.27 no.8
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• pp.1174-1181
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• 2003

The flow around a circular cylinder was controlled by attaching O-rings to reduce drag force acting on the cylinder. Four experimental models were tested in this study; one smooth cylinder of diameter D (D=60mm) and three cylinders fitted with O-rings of diameters d=0.0167 D, 0.05D and 0.067 D with pitches of PPD=2D, 1D, 0.5D and 0.25D. The drag force, mean velocity and turbulence Intensity profiles in the near wake behind the cylinders were measured for Reynolds numbers based on the cylinder diameter in the range of Re$_{D}$=7.8$\times$10$^3$~1.2$\times$10$^{5}$ . At Re$_{D}$=1.2$\times$10$^{5}$ , the cylinder fitted with O-rings of d=0.0167D in a pitch interval of 0.25D shows the maximum drag reduction of about 5.4%, compared that with the smooth cylinder. The drag reduction effect of O-rings of d=0.067D is not so high. For O-ring circulars, as the Reynolds number increases, the peak location of turbulence intensity shifts downstream and the peak magnitude is decreased. Flow field around the cylinders was visualized using a smoke-wire technique to see the flow structure qualitatively. The size of vortices and vortex formation region formed behind the O-ring cylinders are smaller, compared with the smooth cylinder.der.

• Journal of the Korean Chemical Society
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• v.46 no.3
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• pp.205-212
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• 2002

Bioactive compounds of Chung-pi methoxy flavonoids were isolated by column chromatography and preparative chromatography, and investigated on the smoothing effect for the tracheal smooth muscle of rats. The tracheal smooth muscles of rats were treated with acetylcholine ($ED_{50}:3${\times}$10^{-6}M$) and with chromatographic fractions. We found that six-methoxylated flavonoid (nobiletin) was the most active compound fro the smoothing effect of which the contracted tracheal smooth muscle was screened with further separated ethyl acetate fraction. This result shows how nobiletin and its analogues could be using as a promising drug of bronchial asthma.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.215-221
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• 2005

We investigated the effects of testosterone and dihydrotestosterone on inflammatory response of iNOS and COX-2 expression in rat vascular smooth muscle cells. Rat vascular smooth muscle cells (VSMC) stimulated with bacterial lipopolysaccharide $(LPS;\;10{\mu}g/ml)$ for 24 hours were incubated with increasing amounts of testosterone and dihydrotestosterone (1 and 100 nM). LPS was found to induce inflammatory response of iNOS and COX-2 mRNA and protein in VSMC. These processes were affected by male sex steroid hormones. For 3 hours, however, pretreatment of the cells with 100 nM each of testosterone and dihydrotestosterone suppressed LPS induced iNOS and COX-2 protein expression. RT-PCR analysis revealed that testosterone and dihydrotestosterone did not inhibit mRNA expression of iNOS and COX-2 stimulated by 24 hours of LPS incubation. Proliferation rate was slower in VSMC treated with testosterone and dihydrotestosterone. Testosterone enhanced androgen receptor expression, and LPS significantly reduced androgen receptor protein expression in VSMC. These results indicate that the expression of both iNOS and COX-2 proteins was suppressed by testosterone and dihydrotestosterone in LPS stimulated VSMC and leading to reduction of vascular inflammation.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.797-808
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• 1997

Nitric oxide (NO) has been 3mown as a mediator of nonadrenergic, noncholinergic inhibitory neurotransmitter in intestinal smooth muscles. It has been suggested that NO donor such as sodium nitroprusside (SNP) produces relaxation of smooth muscle via activation of guanylate cyclase and elevation of cGMP levels. We have therefore investigated the effects of NO, using SNP, on muscle tension in the longitudinal smooth muscle of guinea-pig ileum. The possible role of cGMP was also investigated as well as the involvement of $K^+$ channel on SNP-induced inhibitory effect. The results are summarized as follows; high KCI-or CCh-activated contractions were inhibited by SNP in a concentration-dependent manner. 8-Br-cGMP also showed a similar effect in that of SNP TEA (1 mM) significantly reduced the SNP-induced inhibitory effect. SNP-induced effect was forther reduced by the presence of 10 mM TEA. On the other hand, 4-AP (0.1 mM), glibenclamide $(10\;{\mu}M)$ and apinain $(0.1\;{\mu}M)$ showed little effects on SNP-induced relaxation. Zaprinast significantly potentiated the SNP-induced inhibitory effect in all ranges. ODQ also significantly decreased the SNP-induced inhibitory effect. Pretreatment with CPA $(10\;{\mu}M)$ slightly reduced the SNP-induced inhibitory effect. From the above results, both effect mediated by NO and cGMP might be responsible for the activation of $Ca^{2+}$-activated $K^+$ channel by SNP in guinea-rig ileum. And this $K^+$ channel activation by SNP also contributes to the SNP-induced membrane hyperpolarization and relaxation.