• The Korean Journal of Physiology
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• v.30 no.2
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• pp.269-278
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• 1996

The mechanism of impaired endothelium-dependent relaxation in the aorta of one-kidney, one clip Goldblatt hypertensive (1K,1C-GBH) rats was investigated. 8 week-old Wistar-Kyoto (WKY) rats were made hypertensive by left renal artery stenosis with contralateral nephrectomy. Endothelium-dependent relaxation was significantly reduced in 1K,1C-GBH rats as compared with WKY rats. However, the relaxation by sodium nitroprusside in 1K,1C-GBH rats was not reduced as compared with WKY rats. The impairment of endothelium-dependent relaxation in 1K,1C-GBH rats was partially restored by the pretreatment of indomethacin or SQ29548. When the nitric oxide production was inhibited by L-nitroarginine methyl ester, acetylcholine (ACh) induced a endothelium-dependent contraction that was greater in 1K,1C-GBH rats than in WKY rats. Endothelium-dependent contraction by ACh was completely abolished by indomethacin or SQ29548. However, imidazole, tranylcypromine and superoxide dismutase did not affect the endothelium-dependent contraction in 1K,1C-GBH rats. These results suggest that impaired endothelium-dependent relaxation in the 1K,1C-GBH rats might be due to the simultaneous release of EDCF, and that prostaglandin B2 may be involved as a mediator of endothelium-dependent contraction.

• BMB Reports
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• v.45 no.3
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• pp.177-182
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• 2012

Camellia japonica oil (CJ oil) has been used traditionally in East Asia to nourish and soothe the skin as well as help restore the elasticity of skin. CJ oil has also been used on all types of bleeding instances. However, little is known about its anti-inflammatory effects. Therefore, the anti-inflammatory effects of CJ oil and its mechanisms of action were investigated. CJ oil inhibited LPS-induced production of NO, $PGE_2$, and TNF-${\alpha}$ in RAW264.7 cells. In addition, expression of COX-2 and iNOS genes was reduced. To evaluate the mechanism of the anti-inflammatory activity of CJ oil, LPS-induced activation of AP-1 and NF-${\kappa}B$ promoters was found to be significantly reduced by CJ oil. LPS-induced phosphorylation of $I{\kappa}B{\alpha}$, ERK, p38, and JNK was also attenuated. Our results indicate that CJ oil exerts anti-inflammatory effects by downregulating the expression of iNOS and COX-2 genes through inhibition of NF-${\kappa}B$ and AP-1 signaling.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.27 no.10
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• pp.1393-1400
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• 2003

Ignition of hydrogen and oxygen in the "third limit" is theoretically investigated in the stagnation point flow with activation energy asymptotics. With the steady-state approximations of H, OH, O and HO$_2$, a two-step reduced kinetic mechanism is derived for the regime lower than the crossover temperature T$_{c}$ at which the rates of production and consumption of all radicals are equal. Appropriate scaling of Damkohler number successfully provides the explicit relationship between pressure, temperature and strain rate at ignition. It is shown that, compared with those for the counterflow, ignition temperatures for the stagnation point flow are considerably increased with increasing the system pressure. This is because ignition in the "third limit" is characterized by the production of reduction of $H_2O$$_2$, which is reduced by wall effect. Strain rate substantially affects ignition temperature because key reaction rates of $H_2O$$_2$ are comparably with its transport rate, while the mixture temperature and the hydrogen composition do not significantly affect ignition temperature.e.

• The Journal of Advanced Prosthodontics
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• v.9 no.3
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• pp.217-223
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• 2017

PURPOSE. This study investigated the effects of silver nanoparticle (SN) loading into hydraulic calcium silicate-based Portland cement on its mechanical, antibacterial behavior and biocompatibility as a novel dental bone substitute. MATERIALS AND METHODS. Chemically reduced colloidal SN were combined with Portland cement (PC) by the concentrations of 0 (control), 1.0, 3.0, and 5.0 wt%. The physico-mechanical properties of silver-Portland cement nanocomposites (SPNC) were investigated through X-ray diffraction (XRD), setting time, compressive strength, solubility, and silver ion elution. Antimicrobial properties of SPNC were tested by agar diffusion against Streptococcus mutans and Streptococcus sobrinus. Cytotoxic evaluation for human gingival fibroblast (HGF) was performed by MTS assay. RESULTS. XRD certified that SN was successfully impregnated in PC. SPNC at above 3.0 wt% significantly reduced both initial and final setting times compared to control PC. No statistical differences of the compressive strength values were detected after SN loadings, and solubility rates of SPNC were below 3.0%, which are acceptable by ADA guidelines. Ag ion elutions from SPNC were confirmed with dose-dependence on the concentrations of SN added. SPNC of 5.0 wt% inhibited the growth of Streptococci, whereas no antimicrobial activity was shown in control PC. SPNC revealed no cytotoxic effects to HGF following ISO 10993 (cell viability > 70%). CONCLUSION. Addition of SN promoted the antibacterial activity and favored the bio-mechanical properties of PC; thus, SPNC could be a candidate for the futuristic dental biomaterial. For clinical warrant, further studies including the inhibitory mechanism, in vivo and long-term researches are still required.

• Journal of Applied Biological Chemistry
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• v.44 no.3
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• pp.105-112
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• 2001

Insect pests can be controlled through direct application of insecticides. Insect control by residual protectants is relatively inexpensive and has an advantage of destroying all stages of infestations. The efficacy of control is largely determined by the concentration of insecticides to which the pest species is exposed. A reduction in the period of control in the field afforded by a specific level of a protectant indicates that resistance has developed. An increase in the level of protectant is required to maintain control, and the efficacy of currently used insecticides has been severely reduced by insecticide resistance in pest species. Development of resistance to particular insecticide varies with species because insecticide resistance is often correlated with increased levels of certain enzymes, which are cytochrome P450-dependent monooxygenases, glutathione S-transferases and esterases. Some sections of insecticide molecules can be modified by one or more of these primary enzymes. A reduction in the sensitivity of the action site of a xenobiotic also constitutes a mechanism of resistance. Acetylcholinesterase is a major target site for insecticide action, as are axonal sodium ion channels and ${\gamma}$-aminobutyric acid receptors. Development of reduced sensitivity of these target sites to insecticides usually occurs. This review not only may contribute to a better understanding of insecticide resistance, but also illustrates the gaps still present for a full biochemical understanding of the resistance.

• Transactions of the Korean Society of Mechanical Engineers B
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• v.28 no.6
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• pp.646-651
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• 2004

When the water flowing inside of the heat transfer equipments such as heat exchangers, condensers, and boilers is heated, calcium, magnesium sulfate, and other minerals in the water are deposited and built up for scales on the heat transfer surfaces. When those scales accumulate on the heat transfer surfaces, their performance of the heat transfer become progressively reduced due to the increase of the heat transfer resistance. The mechanism of this reduced heat transfer is called fouling. This study investigated the formation of the fouling in a heat exchanger with river and tap water flowed inside of it as a coolant. In order to visualize the formation of the fouling and to measure the fouling coefficients, a lab-scale heat exchanging system was used. Based on the experimental results, it was found that the formation of fouling for river water was quite different with the formation for tap water.

• YAKHAK HOEJI
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• v.46 no.6
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• pp.466-471
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• 2002

Oxidative stress is considered to be associated with many diseases, such as inflammatory and cardiovascular diseases, aging and cancer. An important etiological mechanism of these diseases may be a causal relationship between the presence of oxidants and the generation of lipid hydroperoxides derived from enzymatic reactions or xenobiotic metabolism. The hydroperoxides can be decomposed to alkoxy- (ROㆍ) and peroxy- (ROOㆍ) free radicals that can oxidize other cell components, resulting in changes in enzyme activity or the generation of mediators, which can cause further cell damage. The aim of this study was to evaluate the ability of aqueous extract from the roots of Platycodon grandiflorum A. DC (Campanulaceae), Changkil (CK), to affect cellular response in primary cultures of rat hepatocytes to t-butyl hydroperoxide (t-BHP) induced oxidative stress and hepatotoxicity. CK-treated cells showed an increased resistance to oxidative challenge, as revealed by a higher percent of survival capacity in respect to control cells. CK reduced t-BHP-enhanced lipid peroxidation measured as production of malondialdehyde and enhanced intracellular reduced glutathione depletion by t-BHP. Furthermore, CK protected from the t-BHP-induced intracellular generation of reactive oxygen species assessed by monitoring dichlorodihydrofluorescein fluorescence. It can be concluded that CK exerts an antioxidant action inside the cell, responsible for the observed modulation of the cellular response to oxidative challenge, and CK have a marked antioxidative and hepatoprotective potency.

• ETRI Journal
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• v.36 no.2
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• pp.293-300
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• 2014

As the system-on-chip (SoC) design becomes more complex, the test costs are increasing. One of the main obstacles of a test cost reduction is the limited number of test channels of the ATE while the number of pins in the design increases. To overcome this problem, a new test architecture using a channel sharing compliant with IEEE Standard 1149.1 and 1500 is proposed. It can significantly reduce the pin count for testing a SoC design. The test input data is transmitted using a test access mechanism composed of only input pins. A single test data output pin is used to measure the sink values. The experimental results show that the proposed architecture not only increases the number of sites to be tested simultaneously, but also reduces the test time. In addition, the yield loss owing to the proven contact problems can be reduced. Using the new architecture, it is possible to achieve a large test time and cost reduction for complex SoC designs with negligible design and test overheads.

• BMB Reports
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• v.45 no.8
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• pp.458-463
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• 2012

We investigated the mechanisms involved in KHG26377 regulation of glutamate dehydrogenase (GDH) activity, focusing on the roles of SIRT4 and SIRT3. Intraperitoneal injection of mice with KHG26377 reduced GDH activity with concomitant repression of glucose-induced insulin secretion. Consistent with their known functions, SIRT4 ribosylated GDH and reduced its activity, and SIRT3 deacetylated GDH, increasing its activity. However, KHG26377 did not affect SIRT4-mediated ADP-ribosylation/inhibition or SIRT3-mediated deacetylation/activation of GDH. KHG26377 had no effect on SIRT4 protein levels, and did not alter total GDH, acetylated GDH, or SIRT3 protein levels in pancreatic mitochondrial lysates. These results suggest that the mechanism by which KHG26377 inhibits GDH activity and insulin secretion does not involve ADP-ribosylation of GDH by SIRT4 or deacetylation of GDH by SIRT3.

• BMB Reports
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• v.50 no.8
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• pp.411-416
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• 2017

The endoplasmic reticulum (ER) membrane protein complex subunit 6 (EMC6) is a novel human autophagy-related molecule. Here, using tissue microarray and immunohistochemistry, we report that EMC6 protein is lost or reduced in glandular cells of patients with gastric adenocarcinoma, compared to normal stomach mucosa. Overexpression of EMC6 in gastric cancer cells inhibited cell growth, migration, invasion, and induced apoptosis and cell cycle arrest at S-phase. Further investigation suggested that EMC6 overexpression in BGC823 human adenocarcinoma gastric cancer cells reduced tumorigenicity in a xenograft model, demonstrating that EMC6 has the characteristics of a tumor suppressor. This is the first study to show that EMC6 induces cell death in gastric cancer cells. The molecular mechanism of how EMC6 functions as a tumor suppressor needs to be further explored.