• Proceedings of the Botanical Society of Korea Conference
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• 2001.04a
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• pp.12-12
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• 2001

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.95-100
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• 2004

Ischemic preconditioning (IPC) has been accepted as a heart protection phenomenon against ischemia and reperfusion (I/R) injury. The activation of ATP-sensitive potassium $(K_{ATP})$ channels and the release of myocardial nitric oxide (NO) induced by IPC were demonstrated as the triggers or mediators of IPC. A common action mechanism of NO is a direct or indirect increase in tissue cGMP content. Furthermore, cGMP has also been shown to contribute cardiac protective effect to reduce heart I/R-induced infarction. The present investigation tested the hypothesis that $K_{ATP}$ channels attenuate DNA strand breaks and oxidative damage in an in vitro model of I/R utilizing rat ventricular myocytes. We estimated DNA strand breaks and oxidative damage by mean of single cell gel electrophoresis with endonuclease III cutting sites (comet assay). In the I/R model, the level of DNA damage increased massively. Preconditioning with a single 5-min anoxia, diazoxide $(100\;{\mu}M)$, SNAP $(300\;{\mu}M)$ and 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate (8-pCPT-cGMP) $(100\;{\mu}M)$ followed by 15 min reoxygenation reduced DNA damage level against subsequent 30 min anoxia and 60 min reoxygenation. These protective effects were blocked by the concomitant presence of glibenclamide $(50\;{\mu}M)$, 5-hydroxydecanoate (5-HD) $(100\;{\mu}M)$ and 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate, Rp-isomer (Rp-8-pCPT-cGMP) $(100\;{\mu}M)$. These results suggest that NO-cGMP-protein kinase G (PKG) pathway contributes to cardioprotective effect of $K_{ATP}$ channels in rat ventricular myocytes.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.3
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• pp.305-313
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• 1999

To explore whether $Cl^-$ channel blockers interact with the ATP-sensitive $K^+\;(K_{ATP})$ channel, I have examined the effect of two common $Cl^-$ channel blockers on the $K_{ATP}$ channel activity in isolated rat ventricular myocytes using patch clamp techniques. In inside-out patches, 4,4'-diisothio-cyanatostilbene- 2,2'-disulfonic acid (DIDS) and niflumic acid applied to bath solution inhibited the $K_{ATP}$ channel activity in a concentration-dependent manner with $IC_{50}$ of 0.24 and 927 ${\mu}M,$ respectively. The inhibitory action of DIDS was irreversible whereas that of niflumic acid was reversible. Furthermore, DIDS-induced block was not recovered despite exposure to ATP (1 mM). In cell-attached and inside-out patches, DIDS blocked the pinacidil- or 2,4-dinitrophenol (DNP)-induced $K_{ATP}$ channel openings. In contrast, niflumic acid did not block the pinacidil-induced $K_{ATP}$ channel openings in inside-out patches, but inhibited it in cell-attached patches. DIDS and niflumic acid produced additional block in the presence of ATP and did not affect current-voltage relationship and channel kinetics. All these results indicate that DIDS among $Cl^-$ channel blockers specifically blocks the cardiac $K_{ATP}$ channel.

• Korean Journal of Plant Resources
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• v.28 no.6
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• pp.743-751
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• 2015

Reynoutria japonica and R. sachalinensis have been used as medicinal resources in Korea. However, it is difficult to identify and determine these medicinal herbs correctly because they are usually customized and purchased as the fragmented rhizomes types. To develop molecular markers for distinguishing two species, we analyzed and compared the chloroplast DNA sequences of seven loci (atpB, matK, ccD-psaI, atpF-H, trnL-trnF, psbK-I and rpl32-trnL). Among them, we found two effective SNPs in psbK-I region for R. japonica and atpF-H region for R. sachalinensis. Based on these SNP sites, we designed the new R. japonica- specific primer which is able to amplify 300 bp fragment in psbK-I region. A similar strategy was applied for the atpF-H region of R. sachalinensis. These molecular markers would be successfully applied to recognize R. japonica and R. sachalinensis.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.59-68
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• 1999

Chemically induced hypoxia has been shown to induce a depletion of ATP. Since intracellular free $Mg^{2+}\;([Mg^{2+}]_i)$ appears to be tightly regulated following cellular energy depletion, we hypothesized that the increase in $[Mg^{2+}]_i$ would result in $Mg^{2+}$ extrusion following hormonal stimulation. To determine the relation between $Mg^{2+}$ efflux and cellular energy state in a hypoxic rat heart and isolated myocytes, $[Mg^{2+}]_i,$ ATP and $Mg^{2+}$ content were measured by using mag-fura-2, luciferin-luciferase and atomic absorbance spectrophotometry. $Mg^{2+}$ effluxes were stimulated by norepinephrine (NE) or cAMP analogues, respectively. $Mg^{2+}$ effluxes induced by NE or cAMP were more stimulated in the presence of metabolic inhibitors (MI). Chemical hypoxia with NaCN (2 mM) caused a rapid decrease of cellular ATP within 1 min. Measurement of $[Mg^{2+}]_i$ confirmed that ATP depletion was accompanied by an increase in $[Mg^{2+}]_i.$ No change in $Mg^{2+}$ efflux was observed when cells were incubated with MI. In the presence of MI, the cAMP-induced $Mg^{2+}$ effluxes were inhibited by quinidine, imipramine, and removal of extracellular $Na^+.$ In addition, after several min of perfusion with $Na^+-free$ buffer, a large increase in $Mg^{2+}$ efflux occurred when $Na^+-free$ buffer was switched to 120 mM $Na^+$ containing buffer. A similar $Mg^{2+}$ efflux was observed in myocytes. These effluxes were inhibited by quinidine and imipramine. These results indicate that the activation of $Mg^{2+}$ effluxes by hormonal stimulation is directly dependent on intracellular $Mg^{2+}$ contents and that these $Mg^{2+}$ effluxes appear to occur through the $Na^+-dependent\;Na^+/Mg^{2+}$ exchange system during chemical hypoxia.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.581-589
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• 1998

A regulating mechanism of the ATP-sensitive potassium channels $(K_{ATP}\;channels)$ is yet to fully explained. This study was carried out to investigate the effects of intracellular application of monocarboxylates (acetate, formate, lactate, and pyruvate) on $K_{ATP}$ channels in isolated rabbit ventricular myocytes. Single channel currents of $K_{ATP}$ channels were recorded using the excised inside-out or permeabilized attached (open-cell) patch-clamp technique at room temperature. Intracellular application of acetate, formate and pyruvate led to an inhibition of channel activity, whereas intracellular application of lactate increased channel activity. These effects were reversible upon washout. Analysis of single channel kinetics showed that monocarboxylates did not affect open-time constant and close-time constant. These results suggest that monocarboxylates participate in modulating $K_{ATP}$ channels activity in cardiac cells and that modulation of $K_{ATP}$ channels activity may resolve the discrepancy between the low $K_i$ in excised membrane patches and high levels of intracellular ATP concentration during myocardial ischemia or hypoxia.

• The Journal of Korean Academic Society of Nursing Education
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• v.24 no.4
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• pp.463-477
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• 2018

Purpose: This study identifies correlations among information needs and knowledge about prenatal genetic screening and diagnosis (I-PGSD & K-PGSD), and attitude toward terminating pregnancy (ATP) among pregnant women in South Korea. Methods: A descriptive survey was conducted from January 2013 to April 2014 in South Korea. 222 pregnant women responded to three questionnaires developed by the authors. The questionnaire for I-PGSD consisted of 19 questions; 18 questions for K-PGSD; and 10 questions for ATP. Results: Mean scores were $80.46{\pm}11.73$ for I-PGSD; $14.86{\pm}3.74$ for K-PGSD; and $33.71{\pm}6.13$ for ATP. The ATP score was positively correlated with the I-PGSD and K-PGSD scores, but statistically significant with only I-PGSD (p=.006). I-PGSD scores were higher than average on three genetic syndromes (Down, Patau, and Edwards syndrome), on management after the diagnosis of positive fetal aneuploidy, and on test result interpretation after the amniocentesis and level II fetal ultrasonogram. Conclusions: In light of current legal and moral controversy regarding terminating pregnancy and rapidly advancing prenatal genetic testing technology, more prenatal genetic education for nurses and nursing students who teach pregnant women is needed. In addition, more professional counseling services provided by trained nurses are also required.

• The Journal of Natural Sciences
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• v.5 no.2
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• pp.3-11
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• 1992

As concentration of ADP was increased, the rate of phosphocreatine formation by respiring heart mitochondria was increased. The value of apparent Km of the phosphocreatine-forming mitochondria for ADP was estimated to be 0.0185 mM. This value was much lower than that of Km for ATP (0.31 mM) which was determined from the reaction of the soluble form of mitochondrial creatine kinase. The concentration of ATP remained constant during the respiring in the presence of ADP. The rate of accumulation of oxidative-phosphorylated ATP in the mitochondrial respiration medium was continuously monitored as a function of ADP concentration with the firefly luciferase-coupled assay. In that case, exogenous creatine did not affect the rate of accumulation of ATP, indicating that phosphocreatine-forming (i.e.,respiring) mitochondria in the presence of ADP did not use the ATP in the medium as a substrate.These results suggest that the heart mitochondrial creatine kinase bound to the inner membrane functionally tight-coupled to the oxidative phosphorylating system with respect to the respired ATP.

• Biomolecules & Therapeutics
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• v.12 no.1
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• pp.25-33
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• 2004

In this study we investigated whether ATP loss was involved in the potentiated death of immunostimulated rat primary astrocytes in glucose-deprived condition. Rat primary astrocytes immunostimulated with LPS plus IFN-${\gamma}$ for 48 h underwent death upon glucose deprivation, which dependent on the production of peroxynitrite. Intracellular ATP level synergistically decreased by glucose deprivation in immunostimulated astrocytes but not in control cells, and the loss of ATP occurred well ahead of the LDH release. The synergistic cell death and ATP loss by immunostimulation and glucose deprivation were inhibited by iNOS inhibitor (L-NAME and L-NNA) or peroxynitrite decomposition catalyst (also a superoxide anion scavenger), Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP). Exogenous addition of peroxynitrite generator, SIN-l timedependently induced ATP loss and cell death in the glucose-deprived astrocytes. Depletion of intracellular glutathione (GSH) and dis겨ption of mitochondrial transmembrane potential (MTP) were also observed under same conditions. Supply cellular ATP by the addition of exogenous adenosine or ATP during glucose deprivation inhibited ATP depletion, GSH depletion, MTP disruption and cell death in SIN-l treated or immunostimulated astrocytes. This study showed that perturbation in the regulation of intracellular ATP level in immunostimulated astrocytes might make them more vulnerable to energy challenging stimuli.

• Journal of Preventive Medicine and Public Health
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• v.35 no.4
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• pp.269-274
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• 2002

Objectives : To evaluate the elect of glutathione(GSH) on lead induced modulation of nitric oxide(NO) synthesis, and to examine how lead modulates NO production in macrophages. Methods : This study was observed in a culture of RAW 264.7 cells, which originated from a tumor in a Balb/c mouse that was induced by the Abelson murine leukemia virus. The compounds investigated were lead chloride, N-acetyl-cystein(NAC), and Buthionine Sulfoximine( BSO). Results : ATP synthesis in RAW 264.7 cells was unchanged by each lead concentration exposure in a dose dependent manner. The NO synthesis was decreased when exposed to lead($PbCl_2$) concentration $0.5{\mu}M$. The presence of $300{\mu}M$ NAC, used as a pretreatment in the culture medium, caused the recovery of the lead induced decrease in NO synthesis, but in the presence of $300{\mu}M$ BSO as a pretreatment, there was no recoverey. Pretreatment with NAC and BSO had no affect on ATP synthesis at any of the lead concentrations used. Conclusions : These results indicated that GSH has a protective effect toward lead toxicity, and suggested that the inhibition of NO production in macrophage due to lead toxicity may be related to cofactors of iNOS (inducible nitric oxide synthase)