• Elastomers and Composites
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• 제49권1호
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• pp.1-12
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• 2014

전투기 연료필터의 막힘은 조종사 생명과 전투기의 손실에 큰 영향을 줄 수 있다. 따라서 결함 연구는 사고를 미연에 방지하는데 매우 중요하다. 전투기 연료필터는 제트 연료에 포함된 다양한 불순물을 여과하는 중요한 기능을 수행한다. 연료 필터는 시간당 1,330 파운드의 유속으로 공급되는 제트 연료에 함유된 10 ${\mu}m$ 크기 이하의 불순물을 여과한다. 필터는 운영시간 기준 500 시간마다 교체되어야 한다. 그러나 500 시간이 도달하기 훨씬 전에 연료 필터의 막힘 현상으로 경고등이 켜지고 있다. 이와 같은 유사한 결함이 최근에 반복적으로 발생하고 있다. 그러므로, 이 연구에서는 전투기의 연료 필터 막힘에 대한 원인을 FT-IR microcopy, FE-SEM/EDS, 총 황함량 분석기와 같은 다양한 분석기술을 이용하여 조사하였다. 결론적으로, 연료 필터를 막히게 한 물질은 내부 연료 탱크용 실란트에서 기인한 가류 촉진제로 확인되었다. 그리고 연료 탱크내에서 가류 촉진제 블루밍 현상에 의해 연료필터를 막히게 하는 물질의 형성에 대한 메커니즘을 제시하였다.

• 약학회지
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• 제40권6호
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• pp.727-733
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• 1996

2-(Allylthio)pyrazine is effective in selectively suppressing constitutive and inducible expression of cytochrome P450 2E1. The effect of 2-(allylthio)pyrazine against potentiat ed chemical injury was studied in rats. Vitamin-A pretreatment of rats substantially increased carbon tetrachloride hepatotoxicity, as supported by an ~4-fold increase in serum alanine aminotransferase (ALT) activity. Concomitant pretreatment of rats with 2-(allylthio)pyrazine at the daily dose of 200mg/kg resulted in a 76% decrease in vitamin-A-potentiated hepatotoxicity, which supported the possibility that 2-(allylthio)pyrazine protects the liver against chemical-induced hepatic injury by the mechanism associated with Kupffer cell inactivation. Pyridine pretreatment caused substantial enhancement in carbon tetrachloride hepatotoxicity. 2-(Allylthio)pyrazine treatment of rats reduced the pyridine-potentiated toxicity in a dose-dependent manner. Animals treated with both pyridine and 2-(allylthio)pyrazine prior to intoxicating dose of CCl$_4$ resulted in 85% and 47% decreases in pyridine-increased triglycerides and cholesterol levels in the liver. The protective effect of 2-(allylthio)pyrazine on the DNA strand breakage induced by benzenetriol was assessed by measuring the conversion of supercoiled ${\Phi}x$-174 DNA to the open relaxed form. 2-(Allylthio)pyrazine blocked the benzenetriol-induced conversion of supercoiled DNA to open circular form in a dose-dependent manner. The presence of 2-(allylthio)pyrazine at the doses from I to 10mM in the incubation mixture containing 5 ${\mu}$M benzenetriol completely protected benzenetriol-induced DNA strand breakage with the EC50 for the 2-(allylthio)pyrazine blocking being noted as ~220 ${\mu}$M, whereas allyl disulfide exerted protecting effect at relatively high concentrations (i.e. ~850 ${\mu}$M), suggesting that 2-(allylthio)pyrazine effectively scavenges the reactive oxygen species. These results provide evidence that 2-(allylthio)pyrazine blocks vitamin A- or pyridine-potentiated CCl$_4$ hepatotoxicity and that the agent is active in protecting DNA by scavenging the reactive oxygen species.

• BMB Reports
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• 제35권3호
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• pp.313-319
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• 2002

N-Acetyl-$\beta$-D-hexosaminidase ($\beta$-HexNAc'ase) (EC 3.2.1.52) was purified from rice seeds (Oryza sative L. var. Dongjin) using ammonium sulfate (80%) precipitation, Sephadex G-150, CM-Sephadex, and DEAE-Sephadex chromatography, sequentially. The activities were separated into 7 fractions($F_1-F_7$) by CM-Sephadex chromatography. Among them, F6 was further purified to homogeneity with a 13.0% yield and 123.3 purification-fold. The molecular mass was estimated to be about 52 kDa on SDS-PAGE and 37.4 kDa on Sephacryl S-300 gel filtration. The enzyme catalyzed the hydrolysis of both p-nitrophenyl-N-acetyl-$\beta$-D-hexosaminide (pNP-GlcNAc) and p-nitrophenyl-N-acetyl-$\beta$-D-hexosaminide (pNP-GalNAc) as substrates, which are typical properties of $\beta$-HexNAc'ase. The ratio of the pNP-GlcNAc'ase activity to the pNP-GalNAc'ase activity was 4.0. However, it could not hydrolyze chitin, chitosan, pNP-$\beta$-glucopyranoside, or pNP-$\beta$-glucopyranoside. The enzyme showed $K_m$, $V_{max}$ and $K_{cat}$ for pNP-GlcNAc of 1.65 mM, $79.49\;mM\;min^{-1}$, and $4.79{\times}10^6\;min^{-1}$, respectively. The comparison of kinetic values for pNP-GlcNAc and pNP-GalNAc revealed that the two enzyme activities are associated with a single binding site. The purified enzyme exhibited optimum pH and temperature for pNP-GlcNAc of 5.0 and $50^{\circ}C$, respectively. The enzyme activity for pNP-GlcNAc was stable at pH 5.0-5.5 and $20-40^{\circ}C$. The enzyme activity was completely inhibited at a concentration of 0.1 mM $HgCl_$ and $AgNO_3$, suggesting that the intact thiol group is essential for activity. Chloramine T completely inhibited the activity, indicating the possible involvement of methionines in the mechanism of the enzyme.

• 대한수의학회지
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• 제36권1호
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• pp.83-91
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• 1996

Activation of $K^+$ channels induces relaxation of smooth muscles by reducing electrical excitability and cytosolic free $Ca^{2+}$ level. ${\beta}$-adrenergic agonist isoproterenol is known to induce relaxation of the uterine smooth muscle by membrane hyperpolarization and $K^+$ efflux. Recently it is suggested that the activity of $Ca^{2+}$-activated $K^+$ channel was increased by isoproterenol in the uterine myocytes isolated from myometrium of the pregnant rat. However, the type of $K^+$ channel mediating the relaxant effect of isopreterenol in the tissue level has not yet studied. In this work, we investigated the type of $K^+$ channels involved in the isoproterenol-induced relaxation of uterine smooth muscle by measuring the integrated insometric tension of the estrogen-treated isolated nonpregnant rat uterus. Contraction of uterine tissue was induced by oxytocin (0.2nM, 2~3 contractions/min) or high KCl(20~80mM). The result are as follows : 1. Isoproterenol($10^{-10}{\sim}10^{-4}M$) inhibited oxytocin-induced contraction of isolated rat uterus($EC_{50}=1.17{\times}10^{-10}M$). 2. Isoproterenol($10^{-10}{\sim}10^{-4}M$) effectively inhibited uterine contraction induced by low KCl(20~40mM) but little those induced by high KCl(60~80mM). 3. Relaxant effect of isoproterenol($10^{-10}{\sim}10^{-4}M$) on 0.2nM oxytocin-induced contraction was effectively reduced by 4-aminopyridine(3, 10mM) but little by TEA(10~30mM), $Ba^{2+}$($1{\sim}30{\mu}M$) and glibenclamide($100{\mu}M$). Our data suggest that the relaxant effect of isoproterenol is mediated by the $K^+$ channel(s) which can be blocked by 4-aminopyridine.

• 한국환경농학회지
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• 제21권2호
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• pp.102-108
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• 2002

염류장애에 의한 작물의 생육저해 원인을 밝혀내기 위하여 상추를 대조양액과 대조양액에 30 mM 및 50 mM $KNO_3$를 첨가하여 염류농도를 높인 양액 등 3가지 조건에서 재배하였으며, 이때 이들 양액의 EC는 각각 1.0, 4.5, 6.5 dS/m 이었다. 뿌리세포의 원형질막 및 액포막에 위치한 $H^+$-ATPase 활성은 각각에 특이적 저해제인 vanadate와 $NO_3^-$를 이용하여 측정하였다. 대조양액에서 재배한 상추 뿌리의 ATPase 활성은 $356\pm1.5$ nmol/min/mg protein이었으며, 30 mM과 50 mM $KNO_3$를 첨가한 양액에서는 활성이 대조활성에 비하여 각각 1.6배, 1.9배 증가하였다. 이것은 상추가 염류장애시 뿌리조직의 ATPase 활성증가를 통하여 적응함을 보여주는 것이며, 활성증가는 주로 액포막 $H^+$-ATPase 활성증가에 의해 이루어짐을 확인하였다. 마이크로솜 ATPase 활성에 미치는 여러 가지 중금속 이온들의 효과를 측정하였으며, 중금속 이온은 100 ${\mu}M$ 농도에서 콩류에 따라 활성을 10$\sim$25% 저해하였다. 특히, $Cu^{2+}$는 주로 액포막 $H^+$-ATPase 활성을 저해함을 확인하였다. 본 연구의 결과로부터 상추는 염류집적 환경에서 뿌리의 ATPase 활성, 특히 액포막에 위치한 $H^+$-ATPase 활성을 증가시켜 적응하며, $Cu^{2+}$는 주로 액포막 $H^+$-ATPase 활성을 저해하는 성분으로 뿌리의 ATPase 활성변화 연구에 유용하게 이용될 수 있음을 확인하였다.

• Elastomers and Composites
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• 제48권2호
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• pp.172-179
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• 2013

고분자 소재의 충격강도 증대를 위해 충격보강제를 이용하는 경우가 많다. 본 연구에서는 충격보강제가 함유된 나일론6에 대해서 충격보강 원리를 분석하고자 충격시험을 모사하였다. 이를 위해 나일론6에 포함된 충격보강제인 고무 첨가제의 모델링을 시도하였다. 모델링을 토대로 충격시험을 모사하고 충격시편 단면에서의 응력 분포 및 방향을 통해 충격강도 증대 원리를 관찰하였다. 시편 단면에서 충격보강제 유무에 따른 해석을 하여 비교하였고, 충격보강을 위해 사용되는 고무첨가제의 표면처리 여부에 따른 해석도 수행하여 응력을 비교하였다. 해석결과 노치에서 발생한 응력이 내부로 전파되면서 충격보강제 주변으로 경로가 바뀌면서 응력이 감소되는 현상이 나타났다. 특히 충격보강제를 함유한 시편에서 노치부 표면의 응력이 낮았다. 또한, 크랙이 발생하는 방향과 직각인 방향의 주 응력 크기도 충격보강제를 포함한 시편에서 낮게 나타났다. 이로 인해 크랙의 전파가 감소되고 충격강도가 증대되었다고 분석된다. 이러한 컴퓨터모사 방법은 복합재료의 물성 증대 원인을 파악하는데 활용할 수 있다고 판단된다.

• Archives of Pharmacal Research
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• 제22권5호
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• pp.485-490
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• 1999

The mechanism of action of fish oil (FO), currently used in different chronic inflammatory conditions such as rheumatoid arthritis (RA), is not completely understood, although it is thought that it could alter the metabolism of endogenous autacoids. In addition, we hypothesized that the known capability of fatty acids (FA) of stabilizing serum albumin and perhaps other proteins, may be of pharmacological relevance considering that it is shared by other anti-rheumatic agents (e.g. nonsteroidal antiinflammatory drugs). Thus, we studied the effect of oral administration of FO and corn oil (CO), a vegetable oil with a different composition, on the stability of rat serum proteins, evaluated buy a classical in vitro method based on heat-induced protein denaturation. FO, and, to a lower extent, CO inhibited heat-induced denaturation of rat serum (RS): based on the inhibitory activity (EC50) of the major fatty acids against heat-induced denaturation of RS in vitro, it was possible to speculate the in vivo effects of palmitic acid (C16:0) and eicosapentaenoic acid (EPA, C20:5, n-3) may be more relevant than that of linolenic acid (C18:2). To better investigate this phenomenon, we extracted albumin from the serum of animals treated or not with FO with a one-step affinity chromatography technique, obtaining high purity rat serum albumin preparations (RSA-CTRL and RSA-FO), as judged by SDS-PAGE with Coomassie blue staining. When these RSA preparations were heated at $70^{\circ}C$ for 30 min, it was noted that RSA-FO was much more stable than RSA-CTRL, presumably due to higher number of long chain fatty acids (FA) such as palmitic acid or EPA. In conclusion, we provided evidences that oral administration of FO in the rat stabilizes serum albumin, due to an increase in the number of protein bound long chain fatty acids (e.g. palitic acid and EPA). We speculate that the stabilization of serum albumin and perhaps other proteins could prevent changes of antigenicity due to protein denaturation and glycosylation, which may trigger pathological autoimmune responses, suggesting that this action may be involved in the mode of action of FO in RA and other chronic inflammatory diseases.

• Tuberculosis and Respiratory Diseases
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• 제38권1호
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• pp.8-15
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• 1991

It has been well known that the integrity of airway epithelium is important in development of bronchial hyperreactivity and bronchial asthma. But the mechanisms involved are still unclear. To evaluate that airway epithelium is able to modulate the contraction of guinea pig tracheal smooth muscle, we investigated the responsiveness of intact and epithelium-denuded tracheal strips to histamine and acetylcholine. And to evaluate whether cyclooxgenase products play a role in this modulatory mechanism, we also investigated the effect of indomethacin pretreatment on the tracheal responsiveness to histamine. Results were as follows: 1) In guinea pig tracheal smooth muscle the presence of airway epithelium significantly reduced the response to histamine. 2) In the presence of indomethacin dose-response curves and $EC_{50}$ values were similar between intact and epithelium-denuded tracheal strips, that is, indomethacin abolished the influence of epithelium on the contracion of tracheal smooth muscle. 3) The response of tracheal smooth muscle to acetylcholine was similar both in the presence and absence of epithelium. These results suggest that airway epithelium of guinea pig may generate an inhibitory signal to decrease the response of tracheal smooth muscle to histamine and cyclooxygenase products may contrbute to the modulation of airway epithelium on the contracion of tracheal smooth muscle.

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 2002년도 학술대회지
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• pp.66-83
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• 2002

Recently, we have provided evidence that ginsenosides, the active components of Panax ginseng, utilize pertussis toxin (PTX)-insensitive $G{\alpha}_{q/11}-phospholipase\;C-{\beta}3(PLC-{\beta}3)$ signal transduction pathway for the enhancement of $Ca^{2+}-activated\;Cl^{-}$ current in the Xenopus oocyte (British J. Pharmacol. 132, 641-647, 2001; JBC 276, 48797-48802, 2001). Other investigators have shown that stimulation of receptors linked to $G{\alpha}-PLC$ pathway inhibits the activity of G proteincoupled inwardly rectifying $K^+$ (GIRK) channel. In the present study, we sought to determine whether ginsenosides influenced the activity of GIRK 1 and GIRK 4 (GIRK 1/4) channels expressed in the Xenopus oocyte, and if so, the underlying signal transduction mechanism. In oocyte injected with GIRK 1/4 channel cRNAs, bath-applied ginsenosides inhibited high potassium (HK) solution-elicited GIRK current $(EC_{50}:4.9{\pm}4.3\;{\mu}g/ml).$ Pretreatment of the oocyte with PTX reduced the HK solution-elicited GIRK current by $49\%,$ but it did not alter the inhibitory ginsenoside effect on GIRK current. Prior intraoocyte injection of cRNA(s) coding $G{\alpha}_q,\;G{\alpha}_{11}\;or\;G{\alpha}_q/G{\alpha}_{11},\;but\;not\;G{\alpha}_{i2}\;or\;G{\alpha}_{oA}$ attenuated the inhibitory ginsenoside effect. Injection of cRNAs coding $G{\beta}_{1{\gamma}2}$ also attenuated the ginsenoside effect. Similarly, injection of the cRNAs coding regulators of G protein signaling 1, 2 and 4 (RGS1, RGS2 and RGS4), which interact with $G{\alpha}_i\;and/or\;G{\alpha}_{q/11}$ and stimulates the hydrolysis of GTP to GDP in active GTP-bound $G{\alpha}$ subunit, resulted in a significant reduction of ginsenoside effect on GIRK current. Preincubation of GIRK channel-expressing oocyte in PLC inhibitor (U73122) or protein kinase C (PKC) inhibitor (staurosporine or chelerythrine) blocked the inhibitory ginsenoside effect on GIRK current. On the other hand, intraoocyte injection of BAPTA, a free $Ca^{2+}$ chelator, had no significant effect on the ginsenoside action. Taken together, these results suggest that ginsenosides inhibit the activity of GIRK 1/4 channel expressed in the Xenopus oocyte through a PTX-insensitive and $G{\alpha}_{q/11}$-,PLC-and PKC-mediated signal transduction pathway.

• 대한본초학회지
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• 제37권4호
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• pp.31-38
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• 2022

Objectives : In this study, we investigated the synergistic protective effects of medicinal herbal mixture (HME) including Mori Ramulus (MR), Acanthopanacis Cortex (AC), Eucommiae Cortex (EC), and Black soybean (BS) in C2C12 cells, mouse myoblasts. Methods : Effects of HME on cell viability of C2C12 myoblasts were monitored by MTT assay. Anti-atrophic activity of HME was determined in myoblasts and myotubes under oxidative stress by H₂O₂. C2C12 myoblasts were differentiated into myotubes in a medium containing 2% horse serum for 6 days. After that, we measured that expression of MyoD and myogenine, the myogenic regulatory factors, to identify the mechanism of inhibiting muscle atophy after HME treatment. In addition, suppression of phosphorylation of Akt, FoxO3a and MARF-1, transcription factors of degradation proteins were analyzed via western blotting. Results : As a result of MTT, HME there was no show cytotoxicity up to a concentration of 1 mg/ml. The cytoprotective effects on oxidative stressed myoblast and myotube was better in HME extract than those of MR, AC, EU, and BS, respectively. HME treatment in Myotube induced by oxidative stress after H₂O₂ treatment increased Myo D, Myogenine activation, and Akt, FoxO3a phosphorylation and decreased expression of MuRF-1. As the results, HME has synergistic effects on protection against proteolysis of C2C12 myotubes through activation of the Akt signaling pathway under oxidative stress. Conclusions : These results suggest that HME may also be useful as a preventing and treating material for skeletal muscle atrophy caused by age-related diseases.