• Journal of Nutrition and Health
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• v.26 no.2
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• pp.145-155
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• 1993

A factorial experiment was conducted to determine the influence of phytate(0 or 10g/kg diet) and calcium (Ca)(3 or 10g/kg diet) intakes on Ca, P and Zn metabolism by growing female rats. Food intake and weight were similar for the all groups, however, phytate ingestion for six weeks depressed femur growth. The low Ca plus phytate group showed the lowest Ca content of total femur and this was related to a significant decrease of Ca retention. Phytate intake depressed zinc(Zn) absorption in the first metabolic collection. This inhibitory effect of phytate on Zn absorption was improved in the low Ca plus phytate group after several weeks. Impared Zn absorption however remained in the high Ca plus phytate group which was reflected in the lowest Zn content of femur, phytate intake with high Ca also depressed phosphorous(P) absorption and serum and urinary P. These adverse effects of phytate on Zn and P absorption when the dietary Ca was high could explain reduced femur weight despite the highest concentration of femur Ca(mg/g ash) in this group. Results suggest that phytate can adversely affect not only Ca metabolism but Zn and P utilization. Thus, for the normal bone growth when phytate intake is high, the ingesion of Ca, P, Zn and other minerals should be enhanced.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.241-247
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• 2014

To investigate the underlying mechanisms of C18 fatty acids (stearic acid, oleic acid, linoleic acid and ${\alpha}$-linolenic acid) on mast cells, we measured the effect of C18 fatty acids on intracellular $Ca^{2+}$ mobilization and histamine release in RBL-2H3 mast cells. Stearic acid rapidly increased initial peak of intracellular $Ca^{2+}$ mobilization, whereas linoleic acid and ${\alpha}$-linolenic acid gradually increased this mobilization. In the absence of extracellular $Ca^{2+}$, stearic acid ($100{\mu}M$) did not cause any increase of intracellular $Ca^{2+}$ mobilization. Both linoleic acid and ${\alpha}$-linolenic acid increased intracellular $Ca^{2+}$ mobilization, but the increase was smaller than that in the presence of extracellular $Ca^{2+}$. These results suggest that C18 fatty acid-induced intracellular $Ca^{2+}$ mobilization is mainly dependent on extracellular $Ca^{2+}$ influx. Verapamil dose-dependently inhibited stearic acid-induced intracellular $Ca^{2+}$ mobilization, but did not affect both linoleic acid- and ${\alpha}$-linolenic acid-induced intracellular $Ca^{2+}$ mobilization. These data suggest that the underlying mechanism of stearic acid, linoleic acid and ${\alpha}$-linolenic acid on intracellular $Ca^{2+}$ mobilization may differ. Linoleic acid and ${\alpha}$-linolenic acid significantly increased histamine release. Linoleic acid (C18:2: ${\omega}$-6)-induced intracellular $Ca^{2+}$ mobilization and histamine release were more prominent than ${\alpha}$-linolenic acid (C18:3: ${\omega}$-3). These data support the view that the intake of more ${\alpha}$-linolenic acid than linoleic acid is useful in preventing inflammation.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.101-107
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• 2002

In the present study, the postnatal developmental changes in the expressional levels of cardiac sarcoplasmic reticulum (SR) $Ca^{2+}$ regulatory proteins, i.e. $Ca^{2+}-ATPase,$ phospholamban, and $Ca^{2+}$ release channel, were investigated. Both SR $Ca^{2+}-ATPase$ and phospholamban mRNA levels were about 35% of adult levels at birth and gradually increased to adult levels. Protein levels of both SR $Ca^{2+}-ATPase$ and phospholamban, which were measured by quantitative immunoblotting, were closely correlated with the mRNA levels. The initial rates of $Ca^{2+}$ uptake at birth were about 40% of adult rates and also increased gradually during the myocardial development. Consequently, the relative phospholamban/$Ca^{2+}-ATPase$ ratio was 1 in developmental hearts. $Ca^{2+}$ release channel (ryanodine receptor) mRNA was about $50{\sim}60%$ at birth and increased gradually to adult level throughout the postnatal rat heart development. $^3[H]ryanodine$ binding increased gradually during postnatal myocardial development, which was closely correlated with ryanodine mRNA expression levels during the development except the ryanodine mRNA level at birth. These findings indicate that cardiac SR $Ca^{2+}-ATPase,$ phospholamban, and $Ca^{2+}$ release channel are expressed coordinately, which may be necessary for intracellular $Ca^{2+}$ regulation during the rat heart development.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.2
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• pp.53-57
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• 2003

The glutamate receptors (GluRs) are key receptors for modulatory synaptic events in the central nervous system. It has been reported that glutamate increases the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) and induces cytotoxicity. In the present study, we investigated whether the glutamate-induced $[Ca^{2+}]_i$ increase was associated with the activation of ionotropic (iGluR) and metabotropic GluRs (mGluR) in substantia gelatinosa neurons, using spinal cord slice of juvenile rats (10${\sim}21 day). $[Ca^{2+}]_i$ was measured using conventional imaging techniques, which was combined with whole-cell patch clamp recording by incorporating fura-2 in the patch pipette. At physiological concentration of extracellular $Ca^{2+}$, the inward current and $[Ca^{2+}]_i$ increase were induced by membrane depolarization and application of glutamate. Dose-response relationship with glutamate was observed in both $Ca^{2+}$ signal and inward current. The glutamate-induced $[Ca^{2+}]_i$ increase at holding potential of -70 mV was blocked by CNQX, an AMPA receptor blocker, but not by AP-5, a NMDA receptor blocker. The glutamate-induced $[Ca^{2+}]_i$ increase in $Ca^{2+}$ free condition was not affected by iGluR blockers. A selective mGluR (group I) agonist, RS-3,5-dihydroxyphenylglycine (DHPG), induced $[Ca^{2+}]_i$ increase at holding potential of -70 mV in SG neurons. These findings suggest that the glutamate-induced $[Ca^{2+}]_i$ increase is associated with AMPA-sensitive iGluR and group I mGluR in SG neurons of rats.

• The Korean Journal of Physiology
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• v.28 no.1
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• pp.27-35
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• 1994

We investigated the alterations in basal tone of aortic strips by changing the Ca concentration, basal $^{45}Ca$ uptake and $^3H-nitrendipine$ binding of the single cells of aortic smooth muscles in the spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. While the basal tone of the aortic strips in WKY rats was not affected by alteration of Ca concentration, that in SHR was decreased by the removal of Ca from the bath solution and was recovered by the restoration of Ca to normal levels. This contraction increased in a Ca concentration-dependent manner and reached a maximum at 2 mM Ca. The basal tone of aorta in SHR was suppressed by verapamil $(10^{-6}M)$. The basal tone of aorta in SHR increased about 50% in the strips of endothelial rubbing, compared with that of intact endothelium. Basal $^{45}Ca$ uptake in the aortic single smooth muscle cells of SHR was greater than that of WKY (p<0.01), Specific bindings of $[^3H]nitrendipine$ in the aortic single smooth muscles of SHR and WKY were saturable. The dissociation constant $(K_d)\;was\;0.71{\pm}0.15\;and\;1.18{\pm}0.08nM$ SHR, respectively, and the difference in $K_d$ between two strains was statistically significant (p<0.03). The maximal binding capacity $(B_{max})\;was\;34.6{\pm}3.2\;and\;47.4{\pm}4.3\;fmol/10^6$ SHR respectively, and the difference of $(B_{max})$ between two strains was statistically significant (p<0.05). from the above results, it is suggested that the increase of Ca influx via potential-operated Ca channels and the increase of the number of dihydropyridine-sensitive Ca channels contribute to high basal tone of the aortic strips in SHR.

• Journal of Chest Surgery
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• v.24 no.3
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• pp.229-244
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• 1991

A bioassay technique and organ bath study were performed to analyze the effects of extracellular $Ca^{2+}$ and $Ca^{2+}$-antagonists on endothelium-derived relaxing factor[s][EDRF] released from the endothelial cells of rabbit aorta. Transverse strips with intact endothelium or damaged endothelium were used for the mechanical contraction experiment using organ bath. Long segment including thoracic and abdominal aorta with endothelium [EDRF donor aorta] was perfused with Tyrode solution which was aerated with 95% $O_2-5%$ $CO_2$ mixed gas and kept at 35oC. The perfusate was bioassayed with a transverse strip of thoracic aorta with damaged endothelium. The test strip was contracted with nor-epinephrine and acetylcholine was used to stimulate the release of EDRF from endothelial cells. The results obtained were as follows; 1] The endothelium-dependent relaxation[EDR] induced by acetylcholine was biphasic; an initial rapid relaxation followed by a slow relaxation. 2] EDR induced by acetylcholine was reduced gradually with the decrease in the concentration of extracellular $Ca^{2+}$. The effect of extracellular $Ca^{2+}$ on EDR was more prominent in the late slow relaxation phase. 3] EDR to acetylcholine was not altered by acute exposure to organic $Ca^{2+}$-antagonists. Pretreatment with verapamil to the EDRF donor aortic segment did not alter the magnitude of EDR. 4] Among the inorganic $Ca^{2+}$-antagonists $Mn^{2+}$ and $Cd^{2+}$ did not inhibit EDR, whereas $Co^{2+}$ and $La^{3+}$ inhibited EDR. 5] The inhibitory response of $Co^{2+}$ to EDR developed when infused directly on the test strip. That of $La^{3+}$, however, was evoked when added to solution perfusing the donor aortic segment. The above results suggest that $Ca^{2+}$-antagonists do not affect EDR and the inhibitory effect of $Ca^{2+}$ results from influencing the action of EDRF on vascular smooth muscle, whereas that of $La^{3+}$ results from its action on the release of EDRF from endothelial cells.

• Journal of the Korean Institute of Telematics and Electronics D
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• v.36D no.10
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• pp.31-36
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• 1999

The $CaSiN_2:Eu$ and $CaSiN_2:Tb$ phosphors were synthesized and analyzed to develop new nitride compound phosphors. $Ca_3N_2$, $Si_3N_4$ and $EuF_3$(or $TbF_3$) powders were mixed, cold-pressed, and sintered to synthesize $CaSiN_2:Eu$ and $CaSiN_2:Tb$ phosphors. Photoluminescence(PL) and electroluminescence(EL) characteristics of the synthesized phosphors were measured and found to be similar to general emission spectra of 뗘 and Tb ion, respecticely. Threshold voltage($V_{th)$) and luminance of the $CaSiN_2:Eu$ TFEL device fabricated by sputtering were 90 V and 1.62 $cd/m^2$ at 280 V, respectively. The charge-voltage(Q-V) and transferred charge-phosphor field($Q_t-F_p$) characteristics of the TFEL devices were also measured.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2004.11a
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• pp.371-374
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• 2004

저온동시 소성용(low temperature co-fired ceramics, LTCC) 마이크로파 유전체을 만들기 위해 $Ca(Li_{1/4}Nb_{3/4})O_3$ 마이크로파 유전체 세라믹스에 zinc-borosililcate glass를 첨가하여 소결 특성과 마이크로파 유전 특성을 조사하였다. $Ca(Li_{1/4}Nb_{3/4})O_3$과 $0.7Ca(Li_{1/4}Nb_{3/4})O_3-0.3CaTiO_3$에 zinc-borosilicate를 $5{\sim}30wt%$ 첨가하여 소결한 결과 $875{\sim}925^{\circ}C$에서 동시 소성이 가능한 것으로 확인되었으며 zinc-borosilicate glass의 함량이 증가할수록 저온에서 소성이 가능하였지만 과량의 액상과 2차상이 형성되면서 유전율과 품질계수가 저하되는 경향을 나타내었다. $Ca(Li_{1/4}Nb_{3/4})O_3$에 5wt%의 zinc-borosilicate를 첨가하여 $900^{\circ}C$에서 소성한 결과 가장 우수한 유전 특성$(\epsilon_r=17.45,\;Q{\times}f_0=5487)$을 나타내었고, 유전율을 높이기 위해 $CaTiO_3$를 0.3mol% 첨가한 $0.7Ca(Li_{1/4}Nb_{3/4})O_3-0.3CaTiO_3$에 10wt%의 zinc-borosilicate를 첨가하여 $925^{\circ}C$에서 소성한 결과 가장 우수한 유전특성$(\epsilon_r=44.92,\;Q{\times}f_0=5567)$을 나타내었다.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2008.11a
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• pp.195-195
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• 2008

CAS계 유리에 $CaCO_3-Al_2O_3$ 혼합물 및 화합물을 10, 30 wt% 첨가하여 저온 소걸 및 마이크로파 유전 특성을 고찰하였다. CAS계 유리의 연화온도는 $841^{\circ}C$ 이며, CAS계 유리에 $CaCO_3$ 와 30 wt%의 $CaCO_3-Al_2O_3$ 혼합물을 melting되며, 10 wt%의 $CaCO_3$, $Al_2O_3$, $1CaCO_3-1Al_2O_3$ 혼합물 및 $CaAl_2O_4$ 화합물를 10 wt% 첨가하였을 때 $900^{\circ}C$ 이하에서 소걸이 가능하였다. 복합체의 XRD 상 분석 결과, CaCO3를 첨가하였을 때에는 모든 조성이 비정질을 나타내었고, $Al_2O_3$와 $1CaCO_3-1Al_2O_3$ 혼합물은 $Al_2O_3$ 결정상이 생성되었고, $CaAl_2O_4$ 화합물은 $CaAl_2Si_2O_8$의 hexagonal와 anorthite 결정상이 생성되었다. 따라서 CAS-10 (A, C-A, CA) 복합체는 $900^{\circ}C$에서 각각 유전율 ($\varepsilon_r$) 6.4, 6.9, 5.15 와 품질계수 ($Q^*f$) 2,400, 1,500, 3,000의 마이크로파 유전 특성을 나타내어 LTCC 기판 재료로 사용이 가능하며, 특히 $CaAl_2O_4$ 화합물을 사용하였을 때 가장 우수한 유전 특성을 나타내는 것을 확인하였다.