• Journal of Embryo Transfer
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• v.20 no.3
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• pp.191-200
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• 2005

Many studies have shown that the development of mouse early 2-cell embryos in vitro is related with the intracellular $Ca^{2+}$ changes. In ICR strain mouse, the development of embryos arrests at early 2-cell stage, but the arrested early 2-cell embryos can be rescued by the addition of $Ca^{2+}$-related materials. Acetylcholine (ACh) increases intracellular $Ca^{2+}$ concentration ([$Ca^{2+}$]i) via the mAChR-PLC-IP3 pathway in mouse oocytes. We examined whether ACh rescues 2-cell block in mouse. In early 2-cell embryos, ACh increased [$Ca^{2+}$]i in a dose-dependent manner (p<0.001), and had an effect on rescue of 2-cell block and embryonic development. To identify the signal pathway involved in ACh-induced rescue of 2-cell block, we first applied an agonist of ACh receptor (AChR). Like ACh, carbachol increased intracellular $Ca^{2+}$ concentration ([$Ca^{2+}$]i) and atropine, an antagonist of ACh receptor, blocked the ACh-induced $Ca^{2+}$ increase. In $Ca^{2+}$-free medium, ACh also increased [$Ca^{2+}$]i, indicating that $Ca^{2+}$ increased by ACh is mainly released from the intracellular $Ca^{2+}$ store. The ACh-induced $Ca^{2+}$ increase was blocked by PLC inhibitor (U73122), ryanodine receptor (RyR) antagonist (dantrolene), and CaM KII inhibitor (KN-93), but not by IP3R antagonists (xestospongin C). These results show that ACh increases intracellular $Ca^{2+}$ concentration via mAChR/PLC/RyR, and this contributes to the rescue of 2-cell block.

• Analytical Science and Technology
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• v.11 no.6
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• pp.495-498
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• 1998

The effect of high concentration ion matrix on the analysis of low anion concentration in the suppressed ion chromatography was studied. The anions studied were $Br^-$, $NO_3{^-}$, $HPO_4^{2-}$, $SO_4^{2-}$, and $C_2O_4^{2-}$ in the presence of excess NaCl and $CaCl_2$. In this study we suggested that the erroneous results in the suppressed ion chromatographic determination of small concentration of anions were not caused by the interaction of large amount of cation in the suppressor, but by the interaction of cation with concerned anion in the original solution. The error in the analysis of such anion can not be eliminated just by dilution. Therefore, we suggested that standard addition method might be adequate for analyses of those samples.

• Korean Journal of Materials Research
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• v.22 no.12
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• pp.664-668
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• 2012

ZnO nanorods were successfully fabricated on Zn foil by chemical bath deposition (CBD) method. The ZnO precursor concentration and immersion time affected the surface morphologies, structure, and electrical properties of the ZnO nanorods. As the precursor concentration increased, the diameter of the ZnO nanorods increased from ca. 50 nm to ca. 150 nm. The thicknesses of the ZnO nanorods were from ca. $1.98{\mu}m$ to ca. $2.08{\mu}m$. ZnO crystalline phases of (100), (002), and (101) planes of hexagonal wurtzite structure were confirmed by XRD measurement. The fabricated ZnO nanorods showed a photoluminescene property at 380 nm. Especially, the ZnO nanorods deposited for 6 h in solution with a concentration of 0.005M showed a stronger (101) peak than they did (100) or (002) peaks. In addition, these ZnO nanorods showed a good electrical property, with the lowest resistance among the four samples, because the nanorods were densely in contact and relatively without pores. Therefore, a ZnO nanorod substrate is useful as a highly sensitive biochip substrate to detect biomolecules using an electrochemical method.

• Fashion & Textile Research Journal
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• v.21 no.3
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• pp.356-362
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• 2019

This study investigated the substantivity of anionic dyes for cationic-modified new rayon (cocell) fabric treated with cationic agent (CA), 3-(Chloro-2-hydroxypropyl)-trimethylammonium chloride (CA). We also investigate the dyeability of cationic-modified new rayon fabric after dyeing with gallut. CA was converted in an aqueous solution of sodium hydroxide into epoxypropyl trimethylammonium chloride. Treating with this epoxy reagent modified the hydroxyl groups of the new rayon fabric into the trimethylammonium group through ether linkage. The introduction of new cationic sites into new rayon fabric by pretreating with cationic agent improved the substantivity of the Gallnut dye with the new rayon dyebath. The degree of the cationization of cationic-modified new rayon and cotton fabric was evaluated by nitrogen (N) content. This study extracted the colorant of gallnut with hot water at $90^{\circ}C$ and 120 min. Cationic-modified new rayon fabric dyed with extracted solution from gallnut according to concentration of gallnut, dyeing temperature, dyeing time and concentration of cationic agent. Dyeability (K/S) was obtained by CCM observation after dyeing with gallut solution. In addition, fastness to washing and light were also investigated. The degree of crystallinity of new rayon and cotton fabric were 42.15% and 54.94%, respectively. N (%) content of cationic-modified new rayon was higher than the cationic-modified cotton. Dyeability (K/S) increased significantly with the increasing concentration of CA and gallut.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.143-150
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• 1994

The whole-cell mode of the patch clamp technique was used to study $Ca^{2+}-activated\;Cl^-\;current$ $(I_{Cl_{Ca}})$ in gastric antral myocytes. Extracellular application of caffeine evoked $Ca^{2+}-activated\;current$. In order to isolate the chloride current from background current, all known systems were blocked with specific blockers. The current-voltage relationship of caffeine-induced current showed outward rectification and it reversed at around $E_{Cl^-}$. The shift of reversal potential upon the alteration of external and internal chloride concentrations was well fitted with results which were calculated by the Nernst equation. Extracellular addition of N-phenylanthranilic acid and niflumic acid which are known anion channel blockers abolished the caffeine induced current. Intracellular application of a high concentration of EGTA also abolished this current. Application of c-AMP, c-GMP, heparin, or $AIF^-_4$ made no remarkable changes to this current. Sodium replacement with the impermeable cation N-methylglucamine or with $Cd^{2+}$ rarely affected this current. From the above results it is suggested that the caffeine induced current was a $Cl^-$ current and it was activated by intracellular $Ca^{2+}$.

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.225-232
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• 1995

The present study was conducted to evaluate the effect of phorbol 12,13-dibutyrate (PDBu) on the contraction of rabbit jugular vein in vitro. PDBu concentrations of greater than 10 nM induced a periodic contraction which was composed of rapid contraction, plateau and slow relaxation. The frequency of periodic contraction increased as PDBu concentration increased. The PDBu-induced contraction was inhibited by staurosporine (100 nM), it was not changed by tetrodotoxin $(1\;{\mu}M).$ In $Ca^{2+}$-free medium, PDBu induced a sustaining contraction, but not periodic contraction. Addition of $Ca^{2+}$ to medium evoked periodic contraction which was inhibited by nifedipine, PDBu concentrations of greater than $0.1\;{\mu}M$ increased ^{45}Ca^{2+}$ uptake without changing $^{45}Ca^{2+}$ efflux. Charybdotoxin and apamin, $Ca^{2+}$-activated K^{+}$ channel blockers, did not affect the PDBu-induced periodic contraction, whereas tetraethylammonium (TEA) abolished the periodicity. Pinacidil $(10\;{\mu}M).$, a potassium channel activator, blocked PDBu induced periodic contraction, which was recovered by glybenclamide $(10\;{\mu}M).$. In high potassium solution, PDBu did not produce the periodic contraction. These results suggest that the PDBu-induced periodicity of contraction is modulated by voltage dependent $Ca^{2+}$ channel and ATP-sensitive $K^{+}$ channel.

• Journal of Microbiology
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• v.35 no.2
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• pp.152-157
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• 1997

Infection of human fibroblast (HF) cells with human cytomegalovirus (HCMV) result in changes in the intracellular level of second messengers. Since nitric oxide (NO) production has been known to be related with other second messengers, it is probable that HCMV infection of HF cells may involve NO. To test this possibility, the amount of NO was measured following ogenous addition of NO generators such as sodium nitroprusside (SNP) or S-nitroso-N-a-cetylpenicillamine (SNAP) immediately after HCMV infection, however, inhibited virus multiplication. Furthermore, immunoblot experiment using monoclonal antibody to HCMV major immediate early (MIE) proteins or CAT assay using pCMVIE/CAT (plasmid containing CAT gene driven by HCMV MIE promoter) revealed that SNP or SNAP blocked the MIE gene expression. SNP was more effective than SNAP in hibiting HCMV multiplication or MIE gene expression. SNP produced more NO than SNAP in inhibiting HCMV multiplication or MIE gene expression. SNP produced more NO than SNAP. Although the mechanism for the inhibition of HCMV multiplication and MIE gene expression by NO is still elusive some correlation with NO-mediated inhibition of HCMV-induced increase in cytosolic free Ca$\^$2+/ concentration ([Ca$\^$2+/]) was observed. The increase of [Ca$\^$2+/] following HCMV infection was inhibited by SNP, and less effectively by SNAP. Raising [Ca$\^$2+/ with bromo-A23187 partially reversed the SNP block of MIE gene expression. Thus, there appear to e some relationships among NO. [Ca$\^$2+/], and HCMV MIE gene expression.

• Korean Journal of Materials Research
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• v.24 no.12
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• pp.671-676
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• 2014

It is known that bones get damaged by accidents and aging. Since the discovery of Bioglass, various kinds of ceramics have been also found to bond to living bone; some of these ceramics are already being clinically used as bone-repairing materials. In the present study, antibacterial calcium silicate gel ($Ag-30CaO{\cdot}70SiO_2$ gel) was prepared by sol-gel method in order to control the microstructure, which is related to the dissolution rate and induction period of apatite formation in body environment. In addition, biological $Ag-30CaO{\cdot}70SiO_2$ is tested. This was done to impart antimicrobial activity to the $30CaO{\cdot}70SiO_2$. Ag ion was added during sol-gel synthesis to replace the $H_2O$ added during the making of the $30CaO{\cdot}70SiO_2$ gel, which has silver solutions of various concentration. After the sol-gel process, 1N-$HNO_3$ solution was used to wash the gel when synthesizing the gel, in order to maintain the porous structure and remove PEG, water soluble polymers. Then, the apatite forming ability of the sol-gel derived CaO-$SiO_2$ gels was investigated using simulated body fluid (SBF), which had almost the same ion concentration as that of human blood plasma. The gels were analyzed by FT-IR spectroscopy, SEM observation, XRD, and fluorescent microscopy. The apatite was successfully created even after washing the gel; apatite is present in an amorphous state, and was found to affect the concentration of the Ag ion in cells in MC3T3 live & dead assay results. From these results, it is suggested that a good material that can be used to repair defects of nature bone is $Ag-30CaO{\cdot}70SiO_2$ gel.

• International Journal of Oral Biology
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• v.31 no.4
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• pp.127-133
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• 2006

[ $H_2O_2$ ], a member of reactive oxygen species (ROS), is known to be involved in the mediation of physiological functions in a variety of cell types. However, little has been known about the physiological role of $H_2O_2$ in exocrine cells. Therefore, in the present study, the effect of $H_2O_2$ on cholecystokinin (CCK)-evoked $Ca^{2+}$ mobilization and amylase release was investigated in rat pancreatic acinar cells. Stimulation of the acinar cells with sulfated octapeptide form of CCK (CCK-8S) induced biphasic increase in amylase release. Addition of $30\;{\mu}M\;H_2O_2$ enhanced amylase release caused by 10 pM CCK-8S, but inhibited the amylase release induced by CCK-8S at concentrations higher than 100 pM. An ROS scavenger, $10\;{\mu}M$ Mn(III)tetrakis(4-benzoic acid)porphyrin chloride, increased amylase release caused by CCK-8S at concentrations higher than 100 pM, although lower concentrations of CCK-8S-induced amylase release was not affected. To examine whether the effect of $H_2O_2$ on CCK-8S-induced amylase release was exerted via modulation of intracellular $Ca^{2+}$ signaling, we measured the changes in intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in fura-2 loaded acinar cells. Although $30\;{\mu}M\;H_2O_2$ did not induce any increase in $[Ca^{2+}]_i$ by itself, it increased the frequency and amplitude of $[Ca^{2+}]_i$ oscillations caused by 10 pM CCK-8S. However, $30\;{\mu}M\;H_2O_2$ had little effect on 1 nM CCK-8S-induced increase in $[Ca^{2+}]_i$. ROS scavenger, 1 mM N-acetylcysteine, did not affect $[Ca^{2+}]_i$ changes induced by 10 pM or 1 nM CCK-8S. Therefore, it was concluded that $30\;{\mu}M\;H_2O_2$ enhanced low concentration of CCK-8S-induced amylase release probably by increasing $[Ca^{2+}]_i$ oscillations while it inhibited high concentration of CCK-8S-induced amylase release.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.1
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• pp.29-35
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• 2005

To prove the buffering contribution of mitochondria to the increase of intracellular $Ca^{2+}$ level ($[Ca^{2+}]_i$) via background nonselective cation channel (background NSCC), we examined whether inhibition of mitochondria by protonophore carbonylcyanide m-chlorophenylhydrazone (CCCP) affects endothelial $Ca^{2+}$ entry and $Ca^{2+}$ buffering in freshly isolated rabbit aortic endothelial cells (RAECs). The ratio of fluorescence by fura-2 AM ($R_{340/380}$) was measured in RAECs. Biological state was checked by application of acetylcholine (ACh) and ACh ($10{\mu}M$) increased $R_{340/380}$ by $1.1{\pm}0.15$ ($mean{\pm}S.E.$, n=6). When the external $Na^+$ was totally replaced by $NMDG^+$, $R_{340/380}$ was increased by $1.19{\pm}0.17$ in a reversible manner (n=27). $NMDG^+$-induced $[Ca^{2+}]_i$ increase was followed by oscillatory decay after $[Ca^{2+}]_i$ reached the peak level. The increase of $[Ca^{2+}]_i$ by $NMDG^+$ was completely suppressed by replacement with $Cs^+$. When $1{\mu}M$ CCCP was applied to bath solution, the ratio of $[Ca^{2+}]_i$ was increased by $0.4{\pm}0.06$ (n=31). When $1{\mu}M$ CCCP was used for pretreatment before application of $NMDG^+$, oscillatory decay of $[Ca^{2+}]_i$ by $NMDG^+$ was significantly inhibited compared to the control (p＜0.05). In addition, $NMDG^+-induced$ increase of $[Ca^{2+}]_i$ was highly enhanced by pretreatment with $2{\mu}M$ CCCP by $320{\pm}93.7$%, compared to the control ($mean{\pm}S.E.$, n=12). From these results, it is concluded that mitochondria might have buffering contribution to the $[Ca^{2+}]_i$ increase through regulation of the background NSCC in RAECs.