• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.61-61
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• 2003

We have cloned the CGR1 gene encoding glutathione reductase (GR) which catalyzes the reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH) from Candida albicans. The cgr1/cgr1 mutants were not viable when CaMAL2 promoter repressed the CGR1 expression. The growth of the mutants could be partially overcome by thiol compounds such as GSH, dithiothreitol, cysteine, N-acetylcysteine and GSSG. Interestingly, C. albicans with CGR1 overexpressed showed defective hyphal growth on solid medium and attenuated virulence. We have also cloned the GCS1 gene encoding ${\gamma}$-glutamylcysteine synthetase which catalyzes the first step of glutathione biosynthesis. The gcs1/gcs1 mutants were nonviable in minimal defined medium. The growth of the mutants could be resumed by supplementing with GSH, GSSG and ${\gamma}$-glutamylcysteine in the medium. The mutants had increased intracellular D-erythroascorbic acid level up to 2.25-fold when transferred to GSH-free medium. When the mutants were depleted of GSH, they showed typical markers of apoptosis. In conclusion, these results suggest that glutathione is an essential metabolite, and involved in hyphal growth, virulence and apoptosis in C. albicans.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.1
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• pp.33-40
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• 2001

The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier $K^+\;(K_{DR})$ channel function in isoproterenol-induced hypertrophy. It has been proposed that $K_{DR}$ channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary $K_{DR}$ channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary $K_{DR}$ channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the $K_{DR}$ current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary $K_{DR}$ channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of $K_{DR}$ channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.

• Korean Journal of Chemical Engineering
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• v.35 no.12
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• pp.2452-2463
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• 2018

Surface treatment of sol-gel bioglass is required to increase its biomedical applications. In this study, a dielectric barrier discharge (DBD) plasma treatment in atmospheric pressure was performed on the surface of [$SiO_2-CaO-P_2O_5-B_2O_3$] sol-gel derived glass. The obtained bioglass was treated by plasma using discharge current 12 mA with an exposure period for 30 min. The type of discharge can be characterized by measuring the discharge current and applied potential waveform and the power dissipation. Apatite formation on the surface of the DBD-treated and untreated samples after soaking in simulated body fluid (SBF) at $37^{\circ}C$ is characterized by Fourier transform infrared spectroscopy (FTIR), X-Ray diffraction (XRD), inductively coupled plasma (ICP-OES) and scanning electron microscopy coupled with energy dispersive spectroscopy (SEM/EDS). We observed a marked increase in the amount of apatite deposited on the surface of the treated plasma samples than those of the untreated ones, indicating that DBD plasma treatment is an efficient method and capable of modifying the surface of glass beside effectively transforming it into highly bioactive materials.

• Journal of Powder Materials
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• v.25 no.6
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• pp.459-465
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• 2018

Most commercially available detonation nanodiamonds (DNDs) require further processing to qualify for use in biomedical applications, as they often contain many impurities and exhibit poor dispersibility in aqueous media. In this work, DNDs are modified to improve purity and impart a high colloidal stability to the particles. The dispersive and adsorption properties of modified DNDs are evaluated in terms of the suitability of DNDs as carriers for non-steroidal anti-inflammatory drugs (NSAIDs) in transdermal delivery. The study of adsorption on strongly positively and strongly negatively charged DNDs showed their high loading capacity for NSAIDs, and a pronounced relationship between the drugs and the particles' charges. Experiments on long-term desorption carried out with DND/NSAID complexes indicate that the nanoparticles exert a sustained effect on the drug release process.

• Journal of Powder Materials
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• v.27 no.6
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• pp.458-463
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• 2020

Hispidin is a secondary metabolite found in numerous medicinal mushrooms that has attracted significant attention, owing to its distinct biological effects, including antioxidant, anti-inflammatory, antitumor, and cytoprotective properties. Experiments are being carried out to study the interaction of detonation nanodiamonds (DNDs) with synthetic and natural hispidin sourced from extracts of Pholiota sp. fungus. The bioluminescence method is used to determine the adsorption/desorption properties of DNDs toward hispidin. It is found that hispidin forms strong conjugates with DNDs, and the use of various eluents does not result in a significant release of the adsorbed hispidin molecules. DND-bovine serum albumin (BSA) complex, where DNDs serve as a carrier for the protein and the latter acts as a hispidin sorbent, has been developed and applied in hispidin adsorption/desorption tests. The results support the use of the DNDs as a carrier for hispidin in medical applications. They also advocate the application of the DND-BSA complex for isolating the substance from fungal extracts.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.6
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• pp.733-742
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• 1998

Background: We have previously reported that not only cGMP but also 8-Br-cGMP or 8-pCPT-cGMP, specific and potent stimulators of cGMP-dependent protein kinase (cGMP-PK), increased basal L-type calcium current $(I_{Ca})$ in rabbit ventricular myocytes. Our findings in rabbit ventricular myocytes were entirely different from the earlier findings in different species, suggesting that the activation of cGMP-PK is involved in the facilitation of $I_{Ca}}$ by cGMP. However, there is no direct evidence that cGMP-PK can stimulate $I_{Ca}}$ in rabbit ventricular myocytes. In this report, we focused on the direct effect of cGMP-PK on $I_{Ca}}$ in rabbit ventricular myocytes. Methods and Results: We isolated single ventricular myocytes of rabbit hearts by using enzymatic dissociation. Regulation of $I_{Ca}}$ by cGMP-PK was investigated in rabbit ventricular myocytes using whole-cell voltage clamp method. $I_{Ca}}$ was elicited by a depolarizing pulse to +10 mV from a holding potential of -40 mV. Extracellular 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate (8-pCPT-cGMP), potent stimulator of cGMP-dependent protein kinase (cGMP-PK), increased basal $I_{Ca}}$. cGMP-PK also increased basal $I_{Ca}}$. The stimulation of basal $I_{Ca}}$ by cGMP-PK required both 8-Br-cGMP in low concentration and intracellular ATP to be present. The stimulation of basal $I_{Ca}}$ by cGMP-PK was blocked by heat inactivation of the cGMP-PK and by bath application of 8-(4-chlorophenylthio)-guanosine-3',5'-cyclic monophosphate, Rp-isomer (Rp-pCPT-cGMP), a phosphodiesterase-resistant cGMP-PK inhibitor. When $I_{Ca}}$ was increased by internal application of cGMP-PK, IBMX resulted in an additional stimulation of $I_{Ca}}$. In the presence of cGMP-PK, already increased $I_{Ca}}$ was potentiated by bath application of isoprenaline or forskolin or intracellular application of cAMP. Conclusions: We present evidence that cGMP-PK stimulated basal $I_{Ca}}$ by a direct phosphorylation of L-type calcium channel or associated regulatory protein in rabbit ventricular myocytes.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.133-141
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• 1994

The discharge patterns and peripheral nerve inputs to cardiovascular neurons were investigated in rostral ventrolateral medulla (RVLM) and raphe nucleus of cats. The data from the two were compared to determine their roles in cardiovascular regulation and the endogenous analgesic system. Animals were anesthetized with ${\alpha}-chloralose$ and single cell activities were recorded by carbon-filament microelectrode and their relationships with cardiovascular activity were analyzed. In RVLM area, a total of thirty-three cells were identified as cardiovascular neurons. During one cardiac cycle, the mean discharge rate of the neurons was $1.96{\pm}0.29$ and the peak activity was observed 45 ms after the systolic peak of arterial blood pressure. Thirteen cells could be activated antidromically by stimulation of the the $T_2$ intermediolateral nucleus. Forty-three raphe neurons were identified as cardiovascular neurons whose mean discharge rate during one cardiac cycle was $1.02{\pm}0.12$. None of these cells could be activated antidromically. Study of the interval time histogram of RVLM neurons revealed that the time to the first peak was $128{\pm}20.0\;ms$, being shorter than the period of a cardiac cycle. The same parameter found from the raphe neurons was $481{\pm}67.2\;ms$, which was much longer than the cardiac cycle length. Of seventeen RVLM neurons examined ten received only the peripheral $A{\delta}-afferent$ inputs, whereas six RVLM neurons received both $A{\delta}-$ and C-inputs; the remaining one cell received an inhibitory peripheral C-input. In contrast, nine of eleven raphe neurons were found to receive $A{\delta}-inputs$ only. We conclude that the main output of cardiovascular regulatory influences are mediated through the RVLM neurons. The cardiovascular neurons in the raphe nucleus appear to serve as interneurons transferring cardiovascular afferent information to the raphespinal neurons mediating the endogenous analgesic mechanisms.

• Nutrition Research and Practice
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• v.5 no.3
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• pp.246-252
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• 2011

Bioelectrical impedance analysis (BIA) models must be validated against a reference method in a representative population sample before they can be accepted as accurate and applicable. The purpose of this study was to compare the eight-electrode BIA method with DEXA as a reference method in the assessment of body composition in Korean adults and to investigate the predictive accuracy and applicability of the eight-electrode BIA model. A total of 174 apparently healthy adults participated. The study was designed as a cross-sectional study. FM, %fat, and FFM were estimated by an eight-electrode BIA model and were measured by DEXA. Correlations between BIA_%fat and DEXA_%fat were 0.956 for men and 0.960 for women with a total error of 2.1%fat in men and 2.3%fat in women. The mean difference between BIA_%fat and DEXA_%fat was small but significant (P < 0.05), which resulted in an overestimation of $1.2{\pm}2.2$%fat (95% CI: -3.2-6.2%fat) in men and an underestimation of $-2.0{\pm}2.4$%fat (95% CI: -2.3-7.1%fat) in women. In the Bland-Altman analysis, the %fat of 86.3% of men was accurately estimated and the %fat of 66.0% of women was accurately estimated to within 3.5%fat. The BIA had good agreement for prediction of %fat in Korean adults. However, the eight-electrode BIA had small, but systemic, errors of %fat in the predictive accuracy for individual estimation. The total errors led to an overestimation of %fat in lean men and an underestimation of %fat in obese women.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.415-425
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• 1999

$[K^+]_o$ can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of $[K^+]_o$ in the range of $5{\sim}15$ mM may affect tensions of blood vessels and cause relaxation of agonist-induced precontracted vascular smooth muscle $(K^+-induced$ relaxation). In this study, effect of the increase in extracellular $K^+$ concentration on the agonist-induced contractions of various arteries including resistant arteries of rabbit was examined, using home-made Mulvany-type myograph. Extracellular $K^+$ was increased in three different ways; from initial 1 to 3 mM, from initial 3 to 6 mM, or from initial 6 to 12 mM. In superior mesenteric arteries, the relaxation induced by extracellular $K^+$ elevation from initial 6 to 12 mM was the most prominent among the relaxations induced by the elevations in three different ways. In cerebral arteries, the most prominent relaxation was produced by the elevation of extracellular $K^+$ from initial 1 to 3 mM and a slight relaxation was provoked by the elevation from initial 6 to 12 mM. In superior mesenteric arteries, $K^+-induced$ relaxation by the elevation from initial 6 to 12 mM was blocked by $Ba^{2+}\;(30\;{\mu}M)$ and the relaxation by the elevation from 1 to 3 mM or from 3 to 6 mM was not blocked by $Ba^{2+}.$ In cerebral arteries, however, $K^+-induced$ relaxation by the elevation from initial 3 to 6 mM was blocked by $Ba^{2+},$ whereas the relaxation by the elevation from 1 to 3 mM was not blocked by $Ba^{2+}.$ Ouabain inhibited all of the relaxations induced by the extracellular $K^+$ elevations in three different ways. In cerebral arteries, when extracellular $K^+$ was increased to 14 mM with 2 or 3 mM increments, almost complete relaxation was induced at 1 or 3 mM of initial $K^+$ concentration and slight relaxation occurred at 6 mM. TEA did not inhibit $Ba^{2+}-sensitive$ relaxation at all and NMMA or endothelial removal did not inhibit $K^+-induced$ relaxation. Most conduit arteries such as aorta, carotid artery, and renal artery were not relaxed by the elevation of extracellular $K^+.$ Among conduit arteries, trunk of superior mesenteric artery and basilar artery were relaxed by the elevations of $[K^+]_o.$ These data suggest that $K^+-induced$ relaxation has two independent components, $Ba^{2+}-sensitive$ and $Ba^{2+}-insensitive$ one and there are different mechanisms for $K^+-induced$ relaxation in various arteries.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.393-404
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• 1999

We have reported that hypoxia stimulates EDRF(s) release from endothelial cells and the release may be augmented by previous hypoxia. As a mechanism, it was hypothesized that reoxygenation can stimulate EDRF(s) release from endothelial cells and we tested the hypothesis via bioassay experiment. In the bioassay experiment, rabbit aorta with endothelium was used as EDRF donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2a}\;(3{\times}10^{-6}\;M)$ which was added to the solution perfusing through the aorta. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $O_2/5%\;CO_2$ mixed gas. Hypoxia/reoxygenation were interexchanged at intervals of 2 minutes (intermittent hypoxia). In some experiments, endothelial cells were exposed to 10-minute hypoxia (continuous hypoxia) and then exposed to reoxygenation and intermittent hypoxia. In other experiments, the duration of reoxygenation was extended from 2 minutes to 5 minutes. When the donor aorta was exposed to intermittent hypoxia, hypoxia stimulated EDRF(s) release from endothelial cells and the hypoxia-induced EDRF(s) release was augmented by previous hypoxia/reoxygenation. When the donor aorta was exposed to continuous hypoxia, there was no increase of hypoxia-induced EDRF(s) release during hypoxia. But, after the donor aorta was exposed to reoxygenation, hypoxia-induced EDRF(s) release was markedly increased. When the donor aorta was pretreated with nitro-L-arginine $(10^{-5}$ M for 30 minutes), the initial hypoxia-induced EDRF(s) release was almost completely abolished, but the mechanism for EDRF(s) release by the reoxygenation and subsequent hypoxia still remained to be clarified. TEA also blocked incompletely hypoxia-induced and hypoxia/reoxygenation-induced EDRF(s) release. EDRF(s) release by repetitive hypoxia and reoxygenation was completely blocked by the combined treatment with nitro-L-arginine and TEA. Cytochrome P450 blocker, SKF-525A, inhibited the EDRF(s) release reversibly and endothelin antgonists, BQ 123 and BQ 788, had no effect on the release of endothelium-derived vasoactive factors. Superoxide dismutase (SOD) and catalase inhibited the EDRF(s) release from endothelial cells. From these data, it could be concluded that reoxygenation stimulates EDRF(s) release and hypoxia/reoxygenation can release not only NO but also another EDRF from endothelial cells by the production of oxygen free radicals.