• The Korean Journal of Physiology and Pharmacology
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• v.12 no.1
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• pp.31-35
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• 2008

Lysophosphatidylcholine (LPC), a metabolite of membrane phospholipids by phospholipase $A_2$, has been considered responsible for the development of abnormal vascular reactivity during atherosclerosis. $Ca^{2+}$ influx was shown to be augmented in atherosclerotic artery which might be responsible for abnormal vascular reactivity. However, the mechanism underlying $Ca^{2+}$ influx change in atherosclerotic artery remains undetermined. The purpose of the present study was to examine the effects of LPC on L-type $Ca^{2+}$ current $(I_{Ca(L)})$ activity and to elucidate the mechanism of LPC-induced change of $I_{Ca(L)}$ in rabbit portal vein smooth muscle cells using whole cell patch clamp. Extracellular application of LPC increased $I_{Ca(L)}$ through whole test potentials, and this effect was readily reversed by washout. Steady state voltage dependency of activation or inactivation properties of $I_{Ca(L)}$ was not significantly changed by LPC. Staurosporine (100 nM) or chelerythrine $(3{\mu}M)$, which is a potent inhibitor of PKC, significantly decreased basal $I_{Ca(L)}$, and LPC-induced increase of $I_{Ca(L)}$ was significantly suppressed in the presence of PKC inhibitors. On the other hand, application of PMA, an activator of PKC, increased basal $I_{Ca(L)}$ significantly, and LPC-induced enhancement of $I_{Ca(L)}$ was abolished by pretreatment of the cells with PMA. These findings suggest that LPC increased $I_{Ca(L)}$ in vascular smooth muscle cells by a pathway that involves PKC, and that LPC-induced increase of $I_{Ca(L)}$ might be, at least in part, responsible for increased $Ca^{2+}$ influx in atherosclerotic artery.

• Korean Journal of Veterinary Research
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• v.41 no.4
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• pp.467-475
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• 2001

Cardiac arrest, hypoxia, shock or seizure has been known to induce cerebral ischemia. This study was designed to investigate the effect of ischemia on hippocampal pyramidal layer induced by transient bilateral occlusion of the common carotid arteries. Mature Mongolian gerbils were sacrificed at days 2, 4, and 7 after carotid occlusion for 10 minutes. Sham-operated gerbils of control group were subjected to the same protocol except for carotid occlusion. During operation for ischemia, body temperature was maintained $37{\pm}0.5^{\circ}C$ in all gerbils. Paraffin-embedded brain tissue blocks were cut into coronal slices and stained with H-E stain or immunostain by TUNEL method. Neurons with the oval and prominent nucleus and without the eosinophilic cytoplasm in the subfield of hippocamapal pyramidal layer were calculated as to be viable neurons. Their chromatins were condensed or clumped. Their nuclei appeared multiangular or irregularly shrinked. The width of the pyramidal layer was reduced due to the loss of nuclei. At day 2 after reperfusion, some neurons in the CA1 subfield were slightly eosinophilic. But most neurons in the CA2 subfield were strongly eosinophilic. At day 4 day, most neurons in the CA1 subfield were severely damaged and at day 7 day, only a few survived neurons were observed. Survived neurons per longitudinal 1mm sector in the CA1, CA2, CA3, and CA4 subfields of pyramidal layer were investigated. At day 2, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 104.5/mm (54.3%), 51.0/mm (33.8%), 105.5/mm (85.6%), and 124.3/mm (93.5%) compared to the nonischemic control group, respectively. At day 4, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfields were 3.2/mm (1.7%), 51.5/mm(34.2%), 95.3/mm (77.4%), and 112.5/mm (84.6%), respectively. At day 7, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 0.8/mm (0.4%), 5.7/mm(3.8%), 9.8/mm (8.0%), and 5.0/mm (3.7%), respectively. The mean numbers of apoptotic positive neurons in the CA1 subfield at day 2, 4, and 7 after reperfusion were 67.8/mm, 153.2/mm and 123.7/mm, respectively. These results suggest that the transient cerebral ischemia cause severe damages in most neurons at day 7 and that the prosminent apoptotic positive neurons in hippocampal pyramidal layer are the delayed neuronal death induced by ischemia.

• Journal of the Korean Crystal Growth and Crystal Technology
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• v.5 no.3
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• pp.291-298
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• 1995

Abstract The growth and dissolution behaviour of reaction phase was studied during dissolution reaction between sintered alumina and $CaMgSiO_4$ at $1600^{\circ}C$ for various times. The formation of $CaO{\cdot}6Al_2O_3$ an intermediate reaction phase, and $CaMgSiO_4$ spinel, the final reaction product were observed during dissolution reaction of alumina into $CaMgSiO_4$ liquid phase. The growth and dissolution shape of $CaO{\cdot}6Al_2O_3$, an intermediate phase, was quite different.

• Journal of the Mineralogical Society of Korea
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• v.15 no.1
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• pp.78-84
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• 2002

New pyrochlore-type phases($A_2$$B_2$$O_{7}$) were synthesized in the systems: CaO-C$eO_2$-T$iO_2$, CaO-$UO_2$(T$hO_2$)-Z$rO_2$, CaO-$UO_2$(T$hO_2$)-$Gd_2$$O_3$-T$iO_2$-Z$rO_2$, 및 CaO-T$hO_2$-S$nO_2$. The starting materials were pressed with the pressure of 200~400 MPa and sintered at 1500~ 155$0^{\circ}C$ for 4~8 hours in air and at 1300~ 135$0^{\circ}C$ for 5 ~50 hours under oxygen atmosphere. The products were characterized using XRD, SEM/EDS and TEM. In the bulk compositions of CaCe$Ti_2$$O_{7}$, CaTh$Zr_2$$O_{7}$,($Ca_{0.5}$ Gd$Th_{0.5}$)(ZrTi)$O_{7}$) ($Ca_{0.5}$Gd$Th_{0.5}$)(ZrTi)$O_{7}$, ($Ca_{0.5}$G$dU_{0.5}$)(ZrTi)$O_{7}$ and CaTh$Sn_2$$O_{7}$ , pyrochlore was the major phase, together with other oxide phase $of_2$$O_{7}$ fluorite structure. In the samples with target compositions CaU$Zr_2$$O_2$및 $Ca_{0.5}$ G$dU_{0.5}$)$Zr_2$T$iO_{7}$ pyrochlore was not identified, but a fluorite-structured phase was detected. The formation factor as the stable phase depended on crystal chemical characteristics of the actinide and lanthanide elements of the system concerned.

• Resources Recycling
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• v.5 no.3
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• pp.50-55
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• 1996

The synthesis of Ca,,(PO,),(OH), by adding (NFIa)J),HPO, to lhe solution of Ca(NO,), dlssolvad CaO in HNO, and contmlled pH with NH,OH was carried out for certain time at room temperahire and atmosphere. Ca,,(PO,),(OH), was rorrned at the range from pN 10 to pH 13. The particle s~zeof Ca,,(PO,),(OH)i was 0.1-0.5 &In. Thc optimum reaction lime was 30 min, and the temperature was 40-70$^{\circ}$C. the shape also was not changed in spite of heating to iDVC hr 1 hour the c~ystalliratian temperature was 90$^{\circ}$C Ca,,(PO,),(OH), was calcinatcd and the shape also was not changzd, in spile of hcaling to 500$^{\circ}$C for 1 hour. But Ca,,(PO,),(OH), calcinated for lhour al 800$^{\circ}$C was changed to the spheric particle of Ca,,,(PO,),(OH),, CaO and Ca,(PO,),.

• Resources Recycling
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• v.4 no.1
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• pp.38-45
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• 1995

The objective of this study was to investigate the effect of temperature on the formation of CaCO, polymorphs(i.e.,calcite, aragonite, vaterite) and on the crystal shape of CaCO,.The reaction systems were rnvestigated at the temperature range of 2.0%-85.3r, at the fixed cmditions ofconcentration and pressure, 2X10-' M, atomospheric pressure, respectively.The reaction systems studied include a Ca(HCO.,),-Air bubble, O Ca(OH)s-CO,, @ Ca(OH),-H,CO, ,Ca(OH1,-Na>CO,, O Ca(OH),-K,CO,, @ Ca(OH),-(NH,),CO,, D CaC1,-Na,CO,, CaC1,-K3C03, 8 CaC1,-(NH,,),CO,, 0 Ca(N0,X-Na,CO,, 03 Ca(N0,X-QCO,. 0 Ca(NO,),-(NH,XCO,. The results obtained are summarizedas follows:Calcite is formed at the temperature range of 2t-80"C and the highest calcite yield was obtained at 30%.Aragonite begins to be formed at the temperature range of 41.0%-53.0%. and the higher temperature is thehigher yield is obtained. pH of the reaction system affect the yield of aragonite, and the yield reaches the highestpercentage at the pH range of 10.0-11.0, and at the conditions of pH 12.3 or over, aragonite is scarcely formed.Vaterlle is fnrmed at the temperature range of 40.0% or less, and transites utterly to calcite within 10-60mmutes in the case of bemg residenced in mother liqmd which C1 is not contained, and within 140hours inthe case of containing CI-.s in the case of containing CI-.

• The Journal of Korean Institute of Electromagnetic Engineering and Science
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• v.15 no.5
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• pp.486-492
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• 2004

In this paper, we newly propose the binary CA-CDMA(constant amplitude CDMA) system using pre-coding method to solve the high PAPR problem caused by multi-user signal transmission in the CDMA system. 4-user CA-CDMA, the basis of proposed binary CA-CDMA system, makes binary output signal for 4 input users. It produces the output of binary(${\pm}$2) amplitude by using a parity signal resulting from the XOR operation of 4 users data. Another sub-channel or more bandwidth is not necessary because it is transmitted together with user data and can be easily recovered in the receiver. The extension of the number of users can be possible by the simple repetition of the basic binary 4-user CA-CDMA. For example, binary 16-user CA-CDMA is made easily by allocating the four 4-user CA-CDMA systems in parallel and leading the four outputs to the fifth 4-user CA-CDMA system as input, because the output signal of each 4-user CA-CDMA is also binary. By the same extension procedure, binary 64 and 256-user CA-CDMA systems can be made with the constant amplitude. As a result, the code rate of this proposed CA-CDMA system is just 1 and binary CA-CDMA does not change the transmission rate with the constant output signal(PAPR = 0 ㏈). Therefore, the power efficiency of the HPA can be maximized without the nonlinear distortion. From the simulation results, it is verified that the conventional CDMA system has multi-level output signal, but the proposed binary CA-CDMA system always produces binary output. And it is also found that the BER of conventional CDMA system is increased by nonlinear HPA, but the BER of proposed binary CA-CDMA system is not changed.

• Journal of Microbiology and Biotechnology
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• v.18 no.2
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• pp.365-368
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• 2008

Calcium entry through $Ca_v3.2Ca^{2+}$ channels plays essential roles for various physiological events including thalamic oscillation, muscle contraction, hormone secretion, and sperm acrosomal reaction. In this study, we examined how protein tyrosine phosphatases or protein tyrosine kinases affect $Ca_v3.2Ca^{2+}$ channels reconstituted in Xenopus oocytes. We found that $Ca_v3.2$ channel activity was reduced by 25% in response to phenylarsine oxide (tyrosine phosphatase inhibitor), whereas it was augmented by 19% in response to Tyr A47 or herbimycin A (tyrosine kinase inhibitors). However, other biophysical properties of $Ca_v3.2$ currents were not significantly changed by the drugs. These results imply that $Ca_v3.2$ channel activity is capable of being increased by activation of tyrosine phosphatases, but is decreased by activation of tyrosine kinases.

• Solar Energy
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• v.15 no.1
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• pp.73-84
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• 1995

The present paper is on the utilization of a thermal decomposition reaction $Ca(OH)_2=CaO+H_2O$, for thermal energy storage. One of the important problems in this case is how to heat up and decompose the particle of $Ca(OH)_2$ effectively where the thermal conduction is poor. In this study, the effects of Cu-plates which are placed in the $Ca(OH)_2$ packed bed as heat transfer fins are investigated experimentally. The results show that the Cu-plates are very effective for heat transfer and the thermal decomposition in the $Ca(OH)_2$ packed bed. The amount of time to dehydrate took less than a half than that without fins under the conditions of this study.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.2
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• pp.199-205
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• 1999

Vibrio vulnificus cytolysin caused platelet cytolysis and increased intracellular calcium concentration $([Ca^{2+}]_i)$ of rat platelets in a concentration-dependent manner. In the presence of V. vulnificus cytolysin (3 HU/ml), lactate dehydrogenase (LDH) activity was increased from $1.3{\pm}0.4%$ of control to $64.3{\pm}3.4%$ in platelet suspension buffer. In $Ca^{2+}-free$ platelet suspension buffer, however, V. vulnificus cytolysin did not induce $[Ca^{2+}]_i$ increase and LDH release. Addition of EGTA (2 mM) to suspension buffer after the initial $Ca^{2+}$ influx reversed $[Ca^{2+}]_i$ to the control level. However, a $Ca^{2+}$ channel blocker verapamil $(20\;{\mu}M)$ or mefenamic acid $(20\;{\mu}M)$ did not inhibit V. vulnificus cytolysin-induced $[Ca^{2+}]_i$ increase and LDH release. Divalent cations such as $Co^{2+},\;Cd^{2+}\;or\;Mn^{2+}$ (2 mM each) also did not alter V. vulnificus cytolysin-induced $[Ca^{2+}]_i$ increase and LDH release. V. vulnificus cytolysin (3 HU/ml)-induced calcium influx was completely blocked by lanthanum (2 mM). Lanthanum (2 mM) also completely blocked V. vulnificus cytolysin (3 HU/ml)-induced LDH release. Osmotic protectants such as, raffinose, sucrose or PEG600 (50 mM each) did not inhibit the lytic activity of V. vulnificus cytolysin. In conclusion, lanthanum sensitive $Ca^{2+}$ influx plays a significant role in Vibrio vulnificus cytolysin-induced platelet cytolysis and thrombocytopenia in V. vulnificus infection.