• Communications of Mathematical Education
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• v.3
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• pp.229-249
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• 1997

폴리아가 그의 저서 ‘How to Solve It.'에서 주창한 문제 해결의 모형은 이렇게 해석될 수 있다. 곧, 절대 다수의 수학 문제는 조건문 (p${\rightarrow}$q)의 명제 형식으로 분해된다는 것이다. 그리하여 순조롭게 발생되는 문제 해법의 전과정은 아래와 같이 마치 징검다리를 놓듯 추이율(transitivity)을 연거퍼 적용하는(이른바 연추적이라 함) 절차이다. (p: 주어진 정보) ${\rightarrow}$ ${\cdots}$ ${\rightarrow}$ ${\cdots}$ ${\rightarrow}$ (구하는 정보: q) 이것은, 일반적으로, 추이율이 성립하는 모든 관계(relation)의 연추적 확인 과정으로 확장될 수 있다. 요컨대 항진식 (p${\rightarrow}$r) ${\wedge}$ (r${\rightarrow}$q) ${\rightarrow}$ (p${\rightarrow}$q)의 보장 아래 관계의 추이율 xRz ${\wedge}$ zRy ${\rightarrow}$ xRy 로 연결되는 온갖 경로를 포괄한다. 이상과 같이 정식화되는 이 도식의 한계와 효용은 (1) 모든 문제가 조건문의 형태를 갖추고 있는 것은 아니며, (2) 조건문 형식의 문제라도 해법이 반드시 연추적으로 발생되는 법도 아니고, (3) 더구나 이것이 해법 발생의 만능 열쇠는 아닐뿐더러, (4) 발상을 촉진하는 데는 교육공학적으로 더 정교한 배려가 필요하므로, (5) 초보 단계에서 행동 수정을 위한 치유 목적으로 사용됨이 바람직하다.

• 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.

• The Korean Journal of Pharmacology
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• v.31 no.2
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• pp.207-217
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• 1995

To investigate the functional and immunological properties of the Ca-release channel in the sarcoplasmic reticulum(SR) of the eel skeletal muscle, $[^3H]ryanodine$ binding, SDS gel electrophoresis, $^{45}Ca\;release$ studies, and immunoblot assay were carried out in the SR of the eel skeletal muscle. Maximal binding sites(Bmax) and $K_D$ values of $[^3H]ryanodine$ for Ca-release channel of the SR of the eel skeletal muscle were $19.44{\pm}1.40\;pmole/mg$ protein and $15.55{\pm}1.69\;nM$, respectively. $[^3H]Ryanodine$ binding to RyR was increased by calcium and AMP. The SR of the eel skeletal muscle has two high molecular weight bands on the SDS PAGE. The mobility of upper band was more slower than the single band of the rabbit skeletal muscle, and that of the lower band was similar with the single band of canine cardiac muscle. Vesicular $^{45}Ca-release$ was activated by calcium. Ca-induced $^{45}Ca-release$ was significantly inhibited by $MgCl_2(2\;mM)$, ruthenium red$(10\;{/mu}M)$ or tetracaine(1 mM), but not by high concentration of calcium itself. AMP-induced $^{45}Ca-release$ was slightly occurred only in the absence of calcium, it was not inhibited by $MgCl_2$ or ruthenium red. Caffeine also increased $^{45}Ca-release$ from the SR vesicles, but it was not affected by $MgCl_2$ or ruthenium red. Polyclonal Ab against rat skeletal muscle RyR is reacted with that of rabbit, but not reacted with that of the eel skeletal muscle. These results suggested that ryanodine receptor of the SR of the eel skeletal muscle is showing some similar properties with that of mammalian skeletal muscle, but might be an another isotype channel having two bands which is less sensitive to AMP, not cross-reacted with antisera against rat RyR, and not inhibited by high concentration of calcium.

• Proceedings of the Korean Biophysical Society Conference
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• 2001.06a
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• pp.46-46
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• 2001

Evidence has suggested that an anion channel blocker, 4, 4'-diisothiocyanatostilbene-2, 2' disulfonic acid (DIDS) could trigger Ca release from skeletal sarcoplasmic reticulum (SR) by binding to a 30 kDa SR protein. Since the high molecular weight $Ca^{2＋}$ release channel (CRC)/ryanodine receptor (RyR) is the main SR protein that conducts $Ca^{2＋}$ efflux in skeletal muscles, the relationship between CRC and the 30kDa protein remains to be elucidated.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.1
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• pp.53-59
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• 2011

The secretion of insulin from pancreatic ${\beta}$-cells is triggered by the influx of $Ca^{2+}$ through voltage-dependent $Ca^{2+}$ channels. The resulting elevation of intracellular calcium ($[Ca^{2+}]_i$) triggers additional $Ca^{2+}$ release from internal stores. Less well understood are the mechanisms involved in $Ca^{2+}$ mobilization from internal stores after activation of $Ca^{2+}$ influx. The mobilization process is known as calcium-induced calcium release (CICR). In this study, our goal was to investigate the existence of and the role of caffeine-sensitive ryanodine receptors (RyRs) in a rat pancreatic ${\beta}$-cell line, INS-1 cells. To measure cytosolic and stored $Ca^{2+}$, respectively, cultured INS-1 cells were loaded with fura-2/AM or furaptra/AM. $[Ca^{2+}]_i$ was repetitively increased by caffeine stimulation in normal $Ca^{2+}$ buffer. However, peak $[Ca^{2+}]_i$ was only observed after the first caffeine stimulation in $Ca^{2+}$ free buffer and this increase was markedly blocked by ruthenium red, a RyR blocker. KCl-induced elevations in $[Ca^{2+}]_i$ were reduced by pretreatment with ruthenium red, as well as by depletion of internal $Ca^{2+}$ stores using cyclopiazonic acid (CPA) or caffeine. Caffeine-induced $Ca^{2+}$ mobilization ceased after the internal stores were depleted by carbamylcholine (CCh) or CPA. In permeabilized INS-1 cells,$Ca^{2+}$ release from internal stores was activated by caffeine, $Ca^{2+}$, or ryanodine. Furthermore, ruthenium red completely blocked the CICR response in perrneabilized cells. RyRs were widely distributed throughout the intracellular compartment of INS-1 cells. These results suggest that caffeine-sensitive RyRs exist and modulate the CICR response from internal stores in INS-1 pancreatic ${\beta}$-cells.

• Advances in Energy Research
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• v.1 no.1
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• pp.13-33
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• 2013

The present work is an attempt to provide an overview, about the status of R&D and current trends in Hydrogen Production using High Temperature Reactors. Bibliographic references from the INIS database, the Science Direct database and the NTIS database were downloaded and analyzed. Ten year data on the subject, published between 2001 and 2010, was selected for the study. Appropriate qued ry formulations on these databases, resulted in the retrieval of 621 unique bibliographic records. Using the content analysis method, all the records were analyzed. Part One of the analysis details Scientometric R&D indicators, Part Two is a subject-based analysis, grouped under: A. International Initiatives and Programmes for Hydrogen Production; B. European R&D initiatives for Hydrogen production; C. National Initiatives and Programmes for Nuclear Hydrogen Production; D. Reactor Technologies for Nuclear Hydrogen production; E. Fuel Developments; F. Hydrogen Production Processes using HTRs and G. Materials Consideration for Nuclear Hydrogen Production. The results of this analysis are summarized in the study.

• Molecules and Cells
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• v.20 no.1
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• pp.51-56
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• 2005

Excitation-contraction coupling (ECC) proteins in the human heart were characterized using human atrial tissues from different age groups. The samples were classified into one infant group (Group A: 0.2-7 years old) and three adult groups (Group B: 21-30; Group C: 41-49; Group D: 60-66). Whole homogenates (WH) of atrial tissues were assayed for ligand binding, $^{45}Ca^{2+}$ uptake and content of ECC proteins by Western blotting. Equilibrium [$^3H$]ryanodine binding to characterize the ryanodine receptor (RyR) of the sarcoplasmic reticulum (SR) showed that the maximal [$^3H$]ryanodine binding ($B_{max}$) to RyR was similar in all the age groups, but the dissociation constant ($k_d$) of ryanodine was higher in the infant group than the adult groups. Oxalate-supported $^{45}Ca^{2+}$ uptake into the SR, a function of the SR SERCA2a activity, was lower in the infant group than in the adult groups. Similarly, [$^3H$]PN200-110 binding, an index of dihydropyridine receptor (DHPR) density, was lower in the infant group. Expression of calsequestrin and triadin assessed by Western blotting was similar in the infant and adult groups, but junctin expression was considerably higher in the adult groups. These differences in key ECC proteins could underlie the different $Ca^{2+}$ handling properties and contractility of infant hearts.

• International Journal of Highway Engineering
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• v.4 no.4 s.14
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• pp.23-39
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• 2002

This study dealt with developing a new approach for finding properties which might represent rut resistance characteristics of asphalt mixture under static loading. Two aggregates, a normal asphalt (pen 60-80) and 5 polymer-modified asphalts were used in preparation of 12 dense-graded mixtures. Marshall mix design was used in determination of OAC and each mixture at the OAC was prepared for a newly-developed Kim test on Marshall specimen (S=10cm) and gyratory specimen (S=15cm), and for wheel tracking test. Kim test used Marshall loading frame and specimens were conditioned for 30min at $60^{\circ}C$ before loading through Kim tester an apparatus consisting of a loading column and a specimen and column holder Diameter (D) of column was 3cm and 4cm with each column having different radius (r) of round cut at the bottom. The static load was applied at 50mm/min in axial direction of the specimen, not in diametral direction. The maximum load ($P_{max}$) and vertical deformation (y) at $P_{max}$ point were obtained from the test. A strength value was calculated based on the $P_{max}$ r, D and y by using the equation $K_D = 4P_{max}/{\pi}(D-2(r-\sqrt{2ry-y^2}))^2$ and is defined as the deformation strength ($kgf/cm^2$). The values of $P_{max}$/y and $K_I=K_D/y$ were also calculated. In general the leading column diameter and radius of round cut were significant factors affecting $K_D$ and $P_{max}$ values while specimen diameter was not. The statistical analyses showed the $K_D$ had the best correlation with rut depth and dynamic stability. The next best correlation was found from $P_{max}$ which was followed by $P_{max}$/y and $K_I$ in order.

• Natural Product Sciences
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• v.25 no.2
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• pp.136-142
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• 2019

Ischemia/reperfusion-induced myocardial injury is the main cause of acute myocardial infarction. Dendropanax morbifera $L{\acute{e}}veille$ has been used in traditional medicines for the treatment of various diseases such as headache, infectious diseases, and general debility. However, the effect of extract from D. morbifera (EDM) on myocardial ischemic injury is still unknown. In this study, the effects of EDM on neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury were investigated. The viability of cardiomyocytes with H (30 min)/R (1 h) decreased; however, treatment with EDM significantly inhibited H/R injury-induced cardiomyocyte death. Further, we observed that reactive oxygen species (ROS) generation and intracellular calcium concentration ($Ca^{2+}{_i}$) were significantly reduced in EDM-treated cardiomyocytes compared with that in H/R-injured positive control. In addition, western blotting results showed that EDM attenuated abnormal changes of RyR2 and SERCA2a genes in hypoxic cardiomyocytes. These results suggest that EDM ameliorates ROS generation and $Ca^{2+}{_i}$ homeostasis to prevent dysregulation of calcium regulatory proteins in the heart, thereby exerting cardioprotective effects and reducing hypoxia-induced cardiomyocyte damage, which verifies the potential use of EDM as a new therapeutic agent for the treatment of myocardial ischemic injury.

• YAKHAK HOEJI
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• v.59 no.4
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• pp.158-163
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• 2015

Cardiac myocytes are subjected to fluid shear stress during each contraction and relaxation. Under pathological conditions, such as valve disease, heart failure or hypertension, shear stress in cardiac chamber increases due to high blood volume and pressure. The shear stress induces proarrhythmic longitudinal global $Ca^{2+}$ waves in atrial myocytes. In the present study, we further explored underlying cellular mechanism for the shear stress-induced longitudinal global $Ca^{2+}$ wave in isolated rat atrial myocytes. A shear stress of ${\sim}16dyn/cm^2$ was applied onto entire single myocyte using pressurized fluid puffing. Confocal $Ca^{2+}$ imaging was performed to measure local and global $Ca^{2+}$ signals. Shear stress elicited longitudinally propagating global $Ca^{2+}$ wave (${\sim}80{\mu}m/s$). The occurrence of shear stress-induced atrial $Ca^{2+}$ wave was eliminated by the inhibition of ryanodine receptors (RyRs) or inositol 1,4,5-trisphosphate receptors ($IP_3Rs$). In addition, pretreatment of phospholipase C (PLC) inhibitor U73122, but not its inactive analogue U73343, abolished the generation of longitudinal $Ca^{2+}$ wave under shear stress. Our data suggest that shear-induced longitudinal $Ca^{2+}$ wave may be induced by $Ca^{2+}$-induced $Ca^{2+}$ release through the RyRs which is triggered by $PLC-IP_3R$ signaling in atrial myocytes.