• Journal of the Korean Ceramic Society
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• v.28 no.5
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• pp.373-382
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• 1991

The effect of Ca/P mole ratio (Ca/P=1.60, 1.67, 1.75) in the initial solution on the mechanical properties of alumina added hydroxyapatite was investigated. Hydroxyapatite was synthesized by precipitation method using Ca(NO3)2$.$4H2O and (NH4)2HPO4 as starting materials and 5 wt% of ${\alpha}$-Al2O3 was added to precipitation solution. The powder was calcined at 800$^{\circ}C$ and sintered at 1,150∼1,400$^{\circ}C$ under water vapor atmosphere. With the increasing of Ca/P mole ration in the initial solution, the amount of tricalcium phosphate formed from the decomposition of hydroxyapatite reduced and the sinterability and mechanical properties were increased. The bending strength and Vickers hardness of the specimen sintered at 1,300$^{\circ}C$ with the Ca/P mole ratio of 1.75 in the initial solution were 230 MPa and 650 kg/$\textrm{mm}^2$, respectively. The improvement of mechanical properties was attributed to not only the effect of Ca/P mole ratio but also the strengthening of sintered body by Al substitution for P ions.

• Journal of the Korean Ceramic Society
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• v.53 no.6
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• pp.670-675
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• 2016

Calcium phosphate crystallites were prepared by wet chemical method for use in artificial bone. In order to obtain ${\beta}$-tricalcium phosphate (TCP), nano-crystalline calcium phosphate (CaP) was precipitated at $37^{\circ}C$ and at $pH5.0{\pm}0.1$ under stirring using highly active $Ca(OH)_2$ in DI water and an aqueous solution of $H_3PO_4$. The precipitated nano-crystalline CaP solution was kept at $90^{\circ}C$ for the growth of CaP crystallites. Through the growing process of CaP crystallites, we were able to obtain various sizes of rectangular CaP crystallites according to the crystal growing times. Dry nano-crystalline CaP powders at $37^{\circ}C$ were mixed with dry macro-crystalline CaP crystallites and the shaped mixture sample was fired at $1150^{\circ}C$ to make a ${\beta}-TCP$ block. Several tens of nm powders were uniformly coated on the surface, which was comprised of powders of several tens of ${\mu}m$, using a vibrator. The mixing ratio between the nanometer powders and the micrometer powders greatly affected the mechanical strength of the mixture block; the most appropriate ratio of these two materials was 50 wt% to 50 wt%. The sintered block showed improved mechanical strength, which was caused by the solid state interaction between the nano-crystalline ${\beta}-TCP$ and the macro-crystalline ${\beta}-TCP$.

• Molecules and Cells
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• v.39 no.4
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• pp.322-329
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• 2016

Voltage-gated $Ca^{2+}$ ($Ca_V$) channels are dynamically modulated by Gprotein-coupled receptors (GPCR). The $M_1$ muscarinic receptor stimulation is known to enhance $Ca_V2.3$ channel gating through the activation of protein kinase C (PKC). Here, we found that $M_1$ receptors also inhibit $Ca_V2.3$ currents when the channels are fully activated by PKC. In whole-cell configuration, the application of phorbol 12-myristate 13-acetate (PMA), a PKC activator, potentiated $Ca_V2.3$ currents by ~two-fold. After the PMA-induced potentiation, stimulation of $M_1$ receptors decreased the $Ca_V2.3$ currents by $52{\pm}8%$. We examined whether the depletion of phosphatidylinositol 4,5-bisphosphate ($PI(4,5)P_2$) is responsible for the muscarinic suppression of $Ca_V2.3$ currents by using two methods: the Danio rerio voltage-sensing phosphatase (Dr-VSP) system and the rapamycin-induced translocatable pseudojanin (PJ) system. First, dephosphorylation of $PI(4,5)P_2$ to phosphatidylinositol 4-phosphate (PI(4)P) by Dr-VSP significantly suppressed $Ca_V2.3$ currents, by $53{\pm}3%$. Next, dephosphorylation of both PI(4)P and $PI(4,5)P_2$ to PI by PJ translocation further decreased the current by up to $66{\pm}3%$. The results suggest that $Ca_V2.3$ currents are modulated by the $M_1$ receptor in a dual mode-that is, potentiation through the activation of PKC and suppression by the depletion of membrane $PI(4,5)P_2$. Our results also suggest that there is rapid turnover between PI(4)P and $PI(4,5)P_2$ in the plasma membrane.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.2
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• pp.105-111
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• 2010

Inositol 1,4,5-trisphosphate receptors ($InsP_3Rs$) modulate $Ca^{2+}$ release from intracellular $Ca^{2+}$ store and are extensively expressed in the membrane of endoplasmic/sarcoplasmic reticulum and Golgi. Although caffeine and 2-aminoethoxydiphenyl borate (2-APB) have been widely used to block $InsP_3Rs$, the use of these is limited due to their multiple actions. In the present study, we examined and compared the ability of caffeine and 2-APB as a blocker of $Ca^{2+}$ release from intracellular $Ca^{2+}$ stores and $Ca^{2+}$ entry through store-operated $Ca^{2+}$ (SOC) channel in the mouse pancreatic acinar cell. Caffeine did not block the $Ca^{2+}$ entry, but significantly inhibited carbamylcholine (CCh)-induced $Ca^{2+}$ release. In contrast, 2-APB did not block CCh-induced $Ca^{2+}$ release, but remarkably blocked SOC-mediated $Ca^{2+}$ entry at lower concentrations. In permeabilized acinar cell, caffeine had an inhibitory effect on InsP3-induced $Ca^{2+}$ release, but 2-APB at lower concentration, which effectively blocked $Ca^{2+}$ entry, had no inhibitory action. At higher concentrations, 2-APB has multiple paradoxical effects including inhibition of Ins$P_3$-induced $Ca^{2+}$ release and direct stimulation of $Ca^{2+}$ release. Based on the results, we concluded that caffeine is useful as an inhibitor of $InsP_3R$, and 2-APB at lower concentration is considered a blocker of $Ca^{2+}$ entry through SOC channels in the pancreatic acinar cell.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.3
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• pp.1803-1806
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• 2013

Purpose: Carbohydrate antigen (CA) 242 is inversely related to prognosis in many cancers. However, few data regarding CA 242 in esophageal cancer (EC) are available. The aim of this study was to determine the prognostic value of CA 242 and propose an optimum cut-off point in predicting survival difference in patients with esophageal squamous cell carcinoma (ESCC). Methods: A retrospective analysis was conducted of 192 cases. A receiver operating characteristic (ROC) curve for survival prediction was plotted to verify the optimum cuf-off point. Univariate and multivariate analyses were performed to evaluate prognostic parameters for survival. Results: The positive rate for CA 242 was 7.3% (14/192). The ROC curve for survival prediction gave an optimum cut-off of 2.15 (U/ml). Patients with CA 242 ${\leq}$ 2.15 U/ml had significantly better 5-year survival than patients with CA 242 >2.15 U/ml (45.4% versus 22.6%; P=0.003). Multivariate analysis showed that differentiation (P=0.033), CA 242 (P=0.017), T grade (P=0.004) and N staging (P<0.001) were independent prognostic factors. Conclusions: Preoperative CA 242 is a predictive factor for long-term survival in ESCC, especially in nodal-negative patients. We conclude that 2.15 U/ml may be the optimum cuf-off point for CA 242 in predicting survival in ESCC.

• Asian-Australasian Journal of Animal Sciences
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• v.9 no.6
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• pp.715-722
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• 1996

To determine relationships of biochemical parameters involved in Ca metabolism with eggshell quality, serum Ca level, duodenal and uterine calcium binding protein (CaBP) and uterine carbonic anhydrase (CA) activities were measured using 102-week old hens. Three groups of chickens were selected, those showing high quality (HQ) and low quality (LQ) eggshells and non-laying activity (NE). NE hens exhibited significantly (p < 0.05) lower serum Ca levels than laying hens. HQ and LQ hens were not different in the Ca level, indicating that serum Ca level was not good indicator of hen's ability to produce different quality eggshells. Duodenal CaBPs was highest in HQ and lowest in NE (p < 0.10). Uterine CaBPs of LQ and NE were not different and lower significantly (p<0.10) than that of HQ, suggesting that CaBP played an important role in determining eggshell quality. Uterine CA activities of the three groups were significantly different (p < 0.01) ; highest in HQ and lowest in NE, suggesting intimate relationship between CA and Eggshell quality.

• Journal of Chest Surgery
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• v.43 no.4
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• pp.345-355
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• 2010

Background: Extracellular and intracellular pH ($pH_o$ and $pH_i$), which can be changed in various pathological conditions such as hypoxia, affects vascular contractility. To elucidate the mechanism to alter vascular contractility by pH, the effects of pH on reactivity to vasocontracting agents, intracellular $Ca^{2+}$ influx, and $Ca^{2+}$ sensitivity in vascular smooth muscle were examined. Material and Method: Isometric contractions in rat superior mesenteric arteries (SMA) were observed. Intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) was recorded by microfluorometer using Fura-2/acetoxylmethyl ester in muscle cells. $pH_o$ was increased from 7.4 to 7.8 or decreased to 6.9 or 6.4. $pH_i$ was decreased by applying $NH_4^+$ or propionic acid or modulated by changing $pH_o$ after increasing membrane permeability using $\beta$-escin. Result: Decreases in $pH_o$ from 7.4 to 6.9 or 6.4 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the right and significantly increased half maximal effective concentration (EC50) to NE or SE. Increase in $pH_o$ from 7.4 to 7.8 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the left and significantly reduced EC50 to NE or SE. NE increased $[Ca^{2+}]_i$ in cultured smooth muscle cells from SMA and the increased $[Ca^{2+}]_i$ was reduced by decreases in $pH_o$. NE-induced contraction was inhibited by $NH_4^+$, whereas the resting tension was increased by $NH_4^+$ or propionic acid. When the cell membrane of SMA was permeabilized using ${\beta}$-escin, SMA was contracted by increasing extracellular $Ca^{2+}$ concentration from 0 to $10{\mu}M$ and the magnitude of contraction was decreased by a decrease in $pH_o$ and vice versa. Conclusion: From these results, it can be concluded that a decrease in $pH_o$ might inhibit vascular contraction by reducing the reactivity of vascular smooth muscle to vasoactive agents, $Ca^{2+}$ influx and the sensitivity of vascular smooth muscle to $Ca^{2+}$.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.177-183
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• 2008

The layers of keratinocytes form an acid mantle on the surface of the skin. Herein, we investigated the effects of acidic pH on the membrane current and $[Ca^{2+}]_c$ of human primary keratinocytes from foreskins and human keratinocyte cell line (HaCaT). Acidic extracellular pH ($pH_e{\leq}5.5$) activated outwardly rectifying $Cl^-$ current ($I_{Cl,pH}$) with slow kinetics of voltage-dependent activation. $I_{Cl,pH}$ was potently inhibited by an anion channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS, 73.5% inhibition at 1${\mu}$M). $I_{Cl,pH}$ became more sensitive to $pH_e$ by raising temperature from $24^{circ}C$ to $37^{circ}C$. HaCaT cells also expressed $Ca^{2+}$-activated $Cl^-$ current ($I_{Cl,Ca}$), and the amplitude of $I_{Cl,Ca}$ was increased by relatively weak acidic $pH_e$ (7.0 and 6.8). Interestingly, the acidic $pH_e$ (5.0) also induced a sharp increase in the intracellular [$Ca^{2+}$] (${\triangle}[Ca^{2+}]_{acid}$) of HaCaT cells. The ${\triangle}[Ca^{2+}]_{acid}$ was independent of extracellular $Ca^{2+}$, and was abolished by the pretreatment with PLC inhibitor, U73122. In primary human keratinocytes, 5 out of 28 tested cells showed ${\triangle}[Ca^{2+}]_{acid}$. In summary, we found $I_{Cl,pH}$ and ${\triangle}[Ca^{2+}]_{acid}$ in human keratinocytes, and these ionic signals might have implication in pathophysiological responses and differentiation of epidermal keratinocytes.

• BMB Reports
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• v.42 no.9
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• pp.561-567
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• 2009

Although many plant-derived phenolic compounds display antioxidant effects in biological systems, their mechanism of action remains controversial. In this study, the mechanism by which p-coumaric acid (p-CA) performs its antioxidant action was investigated in bovine aortic endothelial cells under oxidative stress due to high levels of glucose (HG) and arachidonic acid (AA), a free fatty acid. p-CA prevented lipid peroxidation and cell death due to HG+AA without affecting the production of reactive oxygen species. The antioxidant effect of p-CA was not decreased by buthionine-(S,R)-sulfoximine, an inhibitor of cellular GSH synthesis. In contrast, pretreatment with p-CA caused the induction of peroxidases that decomposed t-butyl hydroperoxide in a p-CA-dependent manner. Furthermore, the antioxidant effect of p-CA was significantly mitigated by methimazole, which was shown to inhibit the catalytic activity of 'p-CA peroxidases' in vitro. Therefore, it is suggested that the induction of these previously unidentified 'p-CA peroxidases' is responsible for the antioxidant effect of p-CA.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.1
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• pp.41-48
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• 1998

The present study was undertaken to characterize homocysteic acid (HCA)-and cysteic acid (CA)-mediated formation of inositol phosphates (InsP) in primary culture of rat cerebellar granule cells. HCA and CA stimulated InsP formation in a dose-dependent manner, which was prevented by the N-methyl-D-aspartate (NMDA) receptor antagonist D,L-2-amino-5-phosphopentanoic acid (APV). CA-, but not HCA-, mediated InsP formation was in part prevented by the metabotropic glutamate receptor antagonist ?${\alpha}$-methyl-4-carboxyphenylglycine ($({\pm})$-MCPG). Both HCA- and CA-mediated increases in intracellular calcium concentration were completely blocked by APV, but were not altered by $({\pm})$-MCPG. CA-mediated InsP formation was in part prevented by removal of endogenous glutamate. In contrast, the glutamate transport blocker L-aspartic acid-${\beta}$-hydroxamate synergistically increased CA responses. These data indicate that in cerebellar granule cells HCA mediates InsP formation wholly by activating NMDA receptor. In contrast, CA stimulates InsP formation by activating both NMDA receptor and metabotropic glutamate receptor, and in part by releasing endogenous glutamate into extracellular milieu.