• Clinical and Experimental Pediatrics
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• 제49권12호
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• pp.1340-1347
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• 2006

목 적 : IGF-I 프로모터 CA repeat 유전자 다형성이 혈청 IGF-I농도에 미치는 영향에 대해서는 일치되지 않은 결과들이 보고되어 있다. 저자들은 한국인 소아 및 청소년을 대상으로 IGF-I 유전자형의 분석을 실시하였고, CA repeat 유전자 다형성이 혈청 IGF-I 농도에 미치는 영향을 조사하였다. 방 법 : 신장 계측에 의해 1998년에 제작된 한국소아 표준 신장표에 의거하여 나이에 따른 평균 신장 2표준편차 안에 속하는 소아 및 청소년 243명을 대상으로 하였다. 유전자형의 분석은 유전자 염기서열분석을 실시하였다. CA repeat 회수에 따른 대립유전자의 분포를 조사하였고, 이를 바탕으로 유전자형을 분류하였다. 결 과 : 한국인 소아 및 청소년에서는 IGF-I 프로모터 CA repeat 3' end 부위에 2 bp 크기의 결손이 있었다. CA repeat의 분포는 17부터 23까지였으며, 19 repeat가 39.3%의 빈도로 가장 높았다. 유전자형을 살펴보면 한국인 소아의 63.8%가 19 CA repeat를 하나 이상 가지고 있어서, 이 유전자형이 야생형으로 생각된다. 유전자형은 36명(14.8%)은 19 CA repeat(192 bp allele) homozygous, 119명(49.0%)은 heterozygous, 88명은 (36.2%) 19 CA repeat noncarrier 였다. 유전자형에 따른 키, 체중, BMI는 세군 모두에서 유의한 차이가 없었다. 유전자형에 따른 혈청 IGF-I 농도도 19 CA noncarrier군에서 $526.70{\pm}177.67ng/mL$로, 19 CA homozygous군 $570.06{\pm}207.91ng/mL$에 비해 낮았으나 세군 사이에 유의한 차이가 없었다. 유전자형과 나이에 따른 혈청 IGF-I 농도와의 상관관계를 분석하였을때 19 CA homozygote 군(r=0.7181; P<0.0001), heterozygote 군(r=0.5506; P<0.0001) 그리고 19 CA noncarrier군 모두에서 유의한 양의 상관관계를 보였다(r=0.5155; P<0.0001). 결 론 : 한국인 소아 및 청소년에서 19 CA repeat 3' end 부위에 2 bp 크기의 G, A 뉴클레오타이드의 결손이 관찰되었다. IGF-I 유전자의 CA repeat 분포는 17부터 23까지였으며, 19 repeat의 빈도가 39.3%로 가장 높았다. 키, 체중, BMI 그리고 혈청 IGF-I 농도는 유전자형에 따라 유의한 차이가 없었다. 그리고 IGF-I 유전자형과 나이에 따른 혈청 IGF-I 농도 사이에는 유전자형에 관계없이 모든 군에서 유의한 양의 상관관계를 나타내었다. 그러므로 건강한 소아 및 청소년에서는 IGF-I 유전자 다형성이 혈청 IGF-I 농도에 영향을 미치지 않는다.

• Asian-Australasian Journal of Animal Sciences
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• 제27권1호
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• pp.1-9
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• 2014

Calcium (Ca) and phosphorus (P) are minerals that have important physiological functions in the body. For formulation of diets for pigs, it is necessary to consider an appropriate Ca:P ratio for an adequate absorption and utilization of both minerals. Although both minerals are important, much more research has been conducted on P digestibility than on Ca digestibility. Therefore, this review focuses on aspects that are important for the digestibility of Ca. Only values for apparent total tract digestibility (ATTD) of Ca have been reported in pigs, whereas values for both ATTD and standardized total tract digestibility (STTD) of P in feed ingredients have been reported. To be able to determine STTD values for Ca it is necessary to determine basal endogenous losses of Ca. Although most Ca is absorbed in the small intestine, there are indications that Ca may also be absorbed in the colon under some circumstances, but more research to verify the extent of Ca absorption in different parts of the intestinal tract is needed. Most P in plant ingredients is usually bound to phytate. Therefore, plant ingredients have low digestibility of P due to a lack of phytase secretion by pigs. During the last 2 decades, inclusion of microbial phytase in swine diets has improved P digestibility. However, it has been reported that a high inclusion of Ca reduces the efficacy of microbial phytase. It is possible that formation of insoluble calcium-phytate complexes, or Ca-P complexes, not only may affect the efficacy of phytase, but also the digestibility of P and Ca. Therefore, Ca, P, phytate, and phytase interactions are aspects that need to be considered in Ca digestibility studies.

• 한국수소및신에너지학회논문집
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• 제26권6호
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• pp.600-608
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• 2015

As a candidate for cheap oxygen carrier, $CaSO_4$ based oxygen carriers have been developing. However, research on reaction characteristics and side reaction of $CaSO_4$ based oxygen carrier is very limited. There are many possible reactions for main components of syngas from coal. In this study, we prepared three $CaSO_4$ based oxygen carriers ($CaSO_4$-$Fe_2O_3$/bentonite, $CaSO_4$-$K_2CO_3$/bentonite, $CaSO_4$-CaO/bentonite) and performed reduction tests by hydrogen. Cyclic reduction-oxidation tests up to $5^{th}$ cycle are also conducted using hydrogen as fuel. Reduction reactivity of those $CaSO_4$ based oxygen carriers were compared with that of NiO based oxygen carrier (OCN703-1100). Real weight change fractions of $CaSO_4$ based oxygen carriers were higher than theoretical oxyen transfer capacity and reactivity of these particles decreased with the number of cycle increased. To check possible side reaction of $CaSO_4$ based oxygen carriers, $CaSO_4$ decomposition tests were carried out and $SO_2$ was detected even at $700^{\circ}C$. Consequently, we could conclude that $CaSO_4$ based oxygen carriers decompose and release $SO_2$ and this reaction lead reactivity decay of $CaSO_4$ based oxygen carries.

• The Korean Journal of Physiology and Pharmacology
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• 제14권2호
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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.

• The Korean Journal of Physiology and Pharmacology
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• 제2권2호
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• pp.133-145
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• 1998

$Ca^{2+}-signals$ in endothelial cells are determined by release from intracellular stores and entry through the plasma membrane. In this review, the nature of $Ca^{2+}$ entry and mechanisms of its control are reviewed. The following ion channels play a pivotal role in regulation of the driving force for $Ca^{2+}$ entry: an inwardly rectifying $K^+$ channel, identified as Kir2.1, a big-conductance, $Ca^{2+}-activated$ $K^+$ channel (hslo) and at least two $Cl^-$ channels (a volume regulated $Cl^-$ channel, VRAC, and a $Ca^{2+}$ activated $Cl^-$ channel, CaCC). At least two different types of $Ca^{2+}$-entry channels exist: 1. A typical CRAC-like, highly selective $Ca^{2+}$ channel is described. Current density for this $Ca^{2+}$ entry is approximately 0.1pA/pF at 0 mV and thus 10 times smaller than in Jurkat or mast cells. 2. Another entry pathway for $Ca^{2+}$ entry is a more non-selective channel, which might be regulated by intracellular $Ca^{2+}$. Although detected in endothelial cells, the functional role of trp1,3,4 as possible channel proteins is unclear. Expression of trp3 in macrovascular endothelial cells from bovine pulmonary artery induced non-selective cation channels which are probably not store operated or failed to induce any current. Several features as well as a characterisation of $Ca^{2+}$-oscillations in endothelial cells is also presented.

• 한국재료학회지
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• 제3권4호
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• pp.410-421
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• 1993

Bi-Sr-Ca-O 초전도성계에서 $Bi_2O_3-(Sr_2CaCu_2O_x$)의 pseude binary계를 선택하여 $Sr_2CaCu_2O_x$에 $Bi_2O_3$를 5%단위로 40 cation mole% Bi까지 첨가하면서 $850^{\circ}C$ 초전도상 및 공존하는 상들의 평형 및 반응 경로들을 XRD, SEM, EDS, DTA를 이용하여 분석하였다. Bi의 함량이 35 mole% Bi보다 클 때에는 $Bi_2Sr_2CaCu_2O_8$상과 공존하는 액상이 형성되며 2212상의 액상으로 존재하며 액상의 냉각시 제일 먼저 $Bi_2Sr_2CaCu_2O_8$상 주의에 석출된 것이 관찰되었다.

• The Korean Journal of Physiology and Pharmacology
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• 제24권3호
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• pp.277-286
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• 2020

Polycystic kidney disease 2-like-1 (PKD2L1), also known as polycystin-L or TRPP3, is a non-selective cation channel that regulates intracellular calcium concentration. Calmodulin (CaM) is a calcium binding protein, consisting of N-lobe and C-lobe with two calcium binding EF-hands in each lobe. In previous study, we confirmed that CaM is associated with desensitization of PKD2L1 and that CaM N-lobe and PKD2L1 EF-hand specifically are involved. However, the CaM-binding domain (CaMBD) and its inhibitory mechanism of PKD2L1 have not been identified. In order to identify CaM-binding anchor residue of PKD2L1, single mutants of putative CaMBD and EF-hand deletion mutants were generated. The current changes of the mutants were recorded with whole-cell patch clamp. The calmidazolium (CMZ), a calmodulin inhibitor, was used under different concentrations of intracellular. Among the mutants that showed similar or higher basal currents with that of the PKD2L1 wild type, L593A showed little change in current induced by CMZ. Co-expression of L593A with CaM attenuated the inhibitory effect of PKD2L1 by CaM. In the previous study it was inferred that CaM C-lobe inhibits channels by binding to PKD2L1 at 16 nM calcium concentration and CaM N-lobe at 100 nM. Based on the results at 16 nM calcium concentration condition, this study suggests that CaM C-lobe binds to Leu-593, which can be a CaM C-lobe anchor residue, to regulate channel activity. Taken together, our results provide a model for the regulation of PKD2L1 channel activity by CaM.

• The Korean Journal of Physiology and Pharmacology
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• 제2권5호
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• pp.611-616
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• 1998

Although the $Ca^{2+}-activated\;K^+\;(I_{K,Ca})$ channel is known to play an important role in the maintenance of resting membrane potential, the regulation of the channel in physiological condition is not completely understood in vascular myocytes. In this study, we investigated the role of cytoplasmic $Mg^{2+}$ on the regulation of $I_{K,Ca}$ channel in pulmonary arterial myocytes of the rabbit using the inside-out patch clamp technique. $Mg^{2+}$ increased open probability (Po), but decreased the magnitude of single channel current. $Mg^{2+}-induced$ block of unitary current showed strong voltage dependence but increase of Po by $Mg^{2+}$ was not dependent on the membrane potential. The apparent effect of $Mg^{2+}$ might, thus, depend on the proportion between opposite effects on the Po and on the conductance of $I_{K,Ca}$ channel. In low concentration of cytoplasmic $Ca^{2+},\;Mg^{2+}$ increased $I_{K,Ca}$ by mainly enhancement of Po. However, at very high concentration of cytoplasmic $Ca^{2+},$ such as pCa 5.5, $Mg^{2+}$ decreased $I_{K,Ca}$ through the inhibition of unitary current. Moreover, $Mg^{2+}$ could activate the channel even in the absence of $Ca^{2+}.\;Mg^{2+}$ might, therefore, partly contribute to the opening of $I_{K,Ca}$ channel in resting membrane potential. This phenomenon might explain why $I_{K,Ca}$ contributes to the resting membrane potential where membrane potential and concentration of free $Ca^{2+}$ are very low.

• The Korean Journal of Physiology and Pharmacology
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• 제6권2호
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• pp.93-99
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• 2002

Effects of oxidized low-density lipoprotein (ox-LDL), $1-{\alpha}-stearoyl-lysophosphatidylcholine$ (LPC), on intracellular $Ca^{2+}$ concentration were examined in mouse endothelial cells by measuring intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ with fura 2-AM and reverse transcription-polymerase chain reaction (RT-PCR). LPC increased $[Ca^{2+}]_i$ under the condition of 1.5 mM $[Ca^{2+}]_o$ but did not show any effect under the nominally $Ca^{2+}-free$ condition. Even after the store depletion with $30{\mu}M$ 2,5-di-tert- butylhydroquinone (BHQ) or $30{\mu}M$ ATP, LPC could still increase the $[Ca^{2+}]_i$ under the condition of 1.5 mM $[Ca^{2+}]_o.$ The time required to increase [$Ca{2+}$]i (about 1 minute) was longer than that for ATP-induced $[Ca^{2+}]_i$ increase $(10{\sim}30\;seconds).$ LPC-induced $[Ca^{2+}]_i$ increase was completely blocked by $1{\mu}M\;La^{3+}.$ Transient receptor potential channel(trpc) 4 mRNA was detected with RT-PCR. From these results, we suggest that LPC increased $[Ca^{2+}]_i$ via the increase of $Ca^{2+}$ influx through the $Ca^{2+}$ routes which exist in the plasma membrane.

• The Korean Journal of Physiology and Pharmacology
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• 제15권6호
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• pp.431-436
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• 2011

Vascular smooth muscle cells can obtain a proliferative function in environments such as atherosclerosis in vivo or primary culture in vitro. Proliferation of vascular smooth muscle cells is accompanied by changes in ryanodine receptors (RyRs). In several studies, the cytosolic $Ca^{2+}$ response to caffeine is decreased during smooth muscle cell culture. Although caffeine is commonly used to investigate RyR function because it is difficult to measure $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) directly, caffeine has additional off-target effects, including blocking inositol trisphosphate receptors and store-operated $Ca^{2+}$ entry. Using freshly dissociated rat aortic smooth muscle cells (RASMCs) and cultured RASMCs, we sought to provide direct evidence for the operation of RyRs through the $Ca^{2+}$- induced $Ca^{2+}$ -release pathway by directly measuring $Ca^{2+}$ release from SR in permeabilized cells. An additional goal was to elucidate alterations of RyRs that occurred during culture. Perfusion of permeabilized, freshly dissociated RASMCs with $Ca^{2+}$ stimulated $Ca^{2+}$ release from the SR. Caffeine and ryanodine also induced $Ca^{2+}$ release from the SR in dissociated RASMCs. In contrast, ryanodine, caffeine and $Ca^{2+}$ failed to trigger $Ca^{2+}$ release in cultured RASMCs. These results are consistent with results obtained by immunocytochemistry, which showed that RyRs were expressed in dissociated RASMCs, but not in cultured RASMCs. This study is the first to demonstrate $Ca^{2+}$ release from the SR by cytosolic $Ca^{2+}$ elevation in vascular smooth muscle cells, and also supports previous studies on the alterations of RyRs in vascular smooth muscle cells associated with culture.