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Comparison of Outcomes Between STEMI and NSTEMI patients with Totally Occluded IRA
( Sang Woong Choi ),( Yun Kyeong Cho ),( Jae Pil Lee ),( Jihyun Sohn ),( Hyun Ok Cho ),( Hyoung Seob Park ),( Hyuck Jun Yoon ),( Hyungseop Kim ),( Chang Wook Nam ),( Seung Ho Hur ),( Yoon Nyun Kim ),( 대한내과학회 2012 대한내과학회 추계학술발표논문집 Vol.2012 No.1
Sung, Hui-Jin,Choi, Mun-Jeoung,Ok, Seong-Ho,Lee, Soo Hee,Hwang, Il Jeong,Kim, Hee Sook,Chang, Ki Churl,Shin, Il-Woo,Lee, Heon-Keun,Park, Kyeong-Eon,Chung, Young-Kyun,Sohn, Ju-Tae Canadian Science Publishing 2012 Canadian journal of physiology and pharmacology Vol.90 No.7
<P> Mepivacaine is an aminoamide-linked local anesthetic with an intermediate duration that intrinsically produces vasoconstriction both in vivo and in vitro. The aims of this in-vitro study were to examine the direct effect of mepivacaine in isolated rat aortic rings and to determine the associated cellular mechanism with a particular focus on endothelium-derived vasodilators, which modulate vascular tone. In the aortic rings with or without endothelium, cumulative mepivacaine concentration-response curves were generated in the presence or absence of the following antagonists: N<SUP>ω</SUP>-nitro-l-arginine methyl ester [l-NAME], indomethacin, fluconazole, methylene blue, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one [ODQ], verapamil, and calcium-free Krebs solution. Mepivacaine produced vasoconstriction at low concentrations (1 × 10<SUP>−3</SUP> and 3 × 10<SUP>−3</SUP> mol/L) followed by vasodilation at a high concentration (1 × 10<SUP>−2</SUP> mol/L). The mepivacaine-induced contraction was higher in endothelium-denuded aortae than in endothelium-intact aortae. Pretreatment with l-NAME, ODQ, and methylene blue enhanced mepivacaine-induced contraction in the endothelium-intact rings, whereas fluconazole had no effect. Indomethacin slightly attenuated mepivacaine-induced contraction, whereas verapamil and calcium-free Krebs solution more strongly attenuated this contraction. The vasoconstriction induced by mepivacaine is attenuated mainly by the endothelial nitric oxide - cyclic guanosine monophosphate pathway. In addition, mepivacaine-induced contraction involves cyclooxygenase pathway activation and extracellular calcium influx via voltage-operated calcium channels. </P>
Ok, Seong Ho,Bae, Sung Il,Kwon, Seong Chun,Park, Jung Chul,Kim, Woo Chan,Park, Kyeong Eon,Shin, Il Woo,Lee, Heon Keun,Chung, Young Kyun,Choi, Mun Jeoung,Sohn, Ju Tae The Korean Pain Society 2014 The Korean Journal of Pain Vol.27 No.3
Background: A toxic dose of bupivacaine produces vasodilation in isolated aortas. The goal of this in vitro study was to investigate the cellular mechanism associated with bupivacaine-induced vasodilation in isolated endothelium-denuded rat aortas precontracted with phenylephrine. Methods: Isolated endothelium-denuded rat aortas were suspended for isometric tension recordings. The effects of nifedipine, verapamil, iberiotoxin, 4-aminopyridine, barium chloride, and glibenclamide on bupivacaine concentration-response curves were assessed in endothelium-denuded aortas precontracted with phenylephrine. The effect of phenylephrine and KCl used for precontraction on bupivacaine-induced concentration-response curves was assessed. The effects of verapamil on phenylephrine concentration-response curves were assessed. The effects of bupivacaine on the intracellular calcium concentration ($[Ca^{2+}]_i$) and tension in aortas precontracted with phenylephrine were measured simultaneously with the acetoxymethyl ester of a fura-2-loaded aortic strip. Results: Pretreatment with potassium channel inhibitors had no effect on bupivacaine-induced relaxation in the endothelium-denuded aortas precontracted with phenylephrine, whereas verapamil or nifedipine attenuated bupivacaine-induced relaxation. The magnitude of the bupivacaine-induced relaxation was enhanced in the 100mM KCl-induced precontracted aortas compared with the phenylephrine-induced precontracted aortas. Verapamil attenuated the phenylephrine-induced contraction. The magnitude of the bupivacaine-induced relaxation was higher than that of the bupivacaine-induced $[Ca^{2+}]_i$ decrease in the aortas precontracted with phenylephrine. Conclusions: Taken together, these results suggest that toxic-dose bupivacaine-induced vasodilation appears to be mediated by decreased calcium sensitization in endothelium-denuded aortas precontracted with phenylephrine. In addition, potassium channel inhibitors had no effect on bupivacaine-induced relaxation. Toxic-dose bupivacaine-induced vasodilation may be partially associated with the inhibitory effect of voltage-operated calcium channels.
Sohn, Sang-Hyun,Kim, Si-Kwan,Kim, Young-Ock,Kim, Hyung-Don,Shin, Yu-Su,Yang, Seung-Ok,Kim, Seung-Yu,Lee, Sang-Won The Korean Society of Ginseng 2013 Journal of Ginseng Research Vol.37 No.4
The aim of this study was to determine and compare the preventive effect of Korean White Ginseng and Red Ginseng on oxidative stress in $H_2O_2$-treated HepG2 cells. The roots of ginseng were extracted with 70% methanol and partitioned with butanol to obtain saponin fractions, which have been known as bioactive constituents of ginseng. 2',7'-Dichlorofluorescein diacetate (DCF-DA) assay and malondialdehyde (MDA) content were measured for evaluating intracellular reactive oxygen species (ROS) generation. Also, mRNA expressions and activities of antioxidant enzymes were analyzed to determine the antioxidant activity of saponin or non-saponin fractions of ginsengs. According to DCF-DA assay, $H_2O_2$-induced MDA release and ROS generation were significantly reduced by treatment with saponin fractions of white and red ginseng roots. Also, saponin fractions increased effectively intracellular antioxidant enzyme activities including catalase, glutathione peroxidase and superoxide dismutase in $H_2O_2$-treated HepG2 hepatoma cells. In general, red ginseng was more effective than white ginseng for reducing oxidative stress. These results indicate that administration of red ginseng may certainly contribute relatively stronger than white ginseng to prevent from damaging liver function by oxidative stress.
Ok-Sang Jung,Young-A Lee,Younkyoo Kim,Youn Soo Sohn Korean Chemical Society 1994 Bulletin of the Korean Chemical Society Vol.15 No.8
Studies of Co(N-N)(3,6-DBSQ)(3,6-DBCat)(N-N=4,7-dimethyl-1 ,10-phenanthroline, 5-chloro-1,10-phenanthroline; DBSQ=di-tert-butylsemiquinonato; DBCat=di-tert-butylcatecholato) have been carried out on the bistability by intramolecular cobalt-quinone electron transfer in solid state. The title complexes dominantly exist as $Co^{III}$(N-N)(3,6-DBSQ)(3,6-DBCat) at room temperature and display a significant bistability on temperature variation. Subtle change in optical spectra and magnetic properties is observed when diimine ligands are changed.