• Proceedings of the Korea Water Resources Association Conference
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• 2009.05a
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• pp.734-739
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• 2009

낙동강하구둑은 바다로부터의 염수칩입을 방지하고 하구둑 상류의 지속적인 용수 공급을 위해 1987년에 건설되었으며 이로 인해 낙동강 상류로부터 유입되는 유사가 낙동강하구둑 근처에서의 유속 감소로 인해 상류 접근수로에 퇴적되는 문제가 발생하고 있다. 이러한 낙동강하구둑 상류의 퇴적되는 유사로 인해 낙동강하류의 하상이 상승되고 통수단면이 축소되는 현상이 발생할 수 있으며 이는 홍수범람의 위험성을 가중 시키는 원인이 될 수 있다. 따라서 매년 하구둑 상류 접근수로에서는 퇴적되는 유사를 제거하기 위해 하구둑 건설 이후에 매년 준설 작업이 수행되고 있으며 최근에 이를 대체할 수 있는 여러 방법들이 여러 연구를 통해 검토되고 있는 실정이다. 특히 하폭이 급격하게 증가하는 하구둑 상류 2 km 지점은 매년 준설 작업 전에 시행되는 측량 자료에 의하면 이 지점에 많은 양의 유사가 퇴적되는 것으로 나타났다. 따라서 낙동강하구둑 접근수로에서 매년 준설되는 퇴사를 하구둑 상류 2 km 지점 우안 쪽을 매립함으로써 하도를 인위적으로 축소시켜 유속을 증가시키고 결과적으로 퇴사량을 경감 시킬 수 있을 것으로 예측된다. 이러한 하도 축소를 이용한 퇴사 저감 방법의 적용성 검토를 위해 2차원 수치모형인 RMA2 모형과 SED2D 모형을 이용하여 흐름 및 하상변동 분석하였다.

• Biomedical Science Letters
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• v.16 no.4
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• pp.299-305
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• 2010

KCNE1 is the causal gene of long QT syndrome. KCNE1 gene is located in chromosome 21. In compliance with this KCNE1 gene the proteins come out. KCNE1 is responsible for $K^+$ channel which maintains the normal function of the heart muscle for contraction. Affected individuals manifest prolongation of the QT interval on electrocardiongrams, a sign of abnormal cardiac repolarization. The clinical features of LQT result from episodic cardiac arrhythmias, such as torsade de pointes and ventricular fibrllation. Blood DNA was isolated and kept in $4^{\circ}C$ refrigerator. The KCNE1 gene was amplified by PCR method and about 414 bp band was identified by agarose gel electrophoresis. PCR products were inserted into pGEX-4T-1 vector in order to express KCNE1 protein after treatment with IPTG SDS-PAGE was carried out and the protein band which was about 47 kDa was clearly odserved. Results of this study would contribute to the detailed understanding of KCNE1 protein function and to designing better treatment of Long QT symdrome.

• BMB Reports
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• v.47 no.2
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• pp.69-79
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• 2014

$Ca^{2+}$ release from intracellular stores and influx from extracellular reservoir regulate a wide range of physiological functions including muscle contraction and rhythmic heartbeat. One of the most ubiquitous pathways involved in controlled $Ca^{2+}$ influx into cells is store-operated $Ca^{2+}$ entry (SOCE), which is activated by the reduction of $Ca^{2+}$ concentration in the lumen of endoplasmic or sarcoplasmic reticulum (ER/SR). Although SOCE is pronounced in non-excitable cells, accumulating evidences highlight its presence and important roles in skeletal muscle and heart. Recent discovery of STIM proteins as ER/SR $Ca^{2+}$ sensors and Orai proteins as $Ca^{2+}$ channel pore forming unit expedited the mechanistic understanding of this pathway. This review focuses on current advances of SOCE components, regulation and physiologic and pathophysiologic roles in muscles. The specific property and the dysfunction of this pathway in muscle diseases, and new directions for future research in this rapidly growing field are discussed.

• Journal of the Korean Society of Combustion
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• v.8 no.3
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• pp.15-23
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• 2003

Partial quenching structure of turbulent diffusion flames in a turbulent mixing layer is investigated by the method of flame hole dynamics in order to develop a prediction model for turbulent flame lift off. The essence of flame hole dynamics is derivation of the random walk mapping, from the flame-edge theory, which governs expansion or contraction of flame holes initially created by local quenching events. The numerical simulation for flame hole dynamics is carried out in two stages. First, a direct numerical simulation is performed for constant-density fuel-air channel mixing layer to obtain the turbulent flow and mixing fields, from which a time series of two dimensional scalar dissipation rate array is extracted at a fixed virtual flame surface horizontally extending from the end of split plate to the downstream. Then, the Lagrangian simulation of the flame hole random walk mapping projected to the scalar dissipation rate array yields temporally evolving turbulent extinction process and its statistics on partial quenching characteristics. The statistical results exhibit that the chance of partial quenching is strongly influenced by the crossover scalar dissipation rate while almost unaffected by the iteration number of the mapping that can be regarded as a flame-edge speed.

• Korean Journal of Pharmacognosy
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• v.36 no.1 s.140
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• pp.17-20
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• 2005

We previously reported that the exogenous administration of cumambrin A, a sesquiterpene lactone from the dried flowers of Chrysanthemum boreale Makino has a pharmacological effect on normalization of blood pressure in the spontaneously hypertensive rats (SHR). In the present study, we further investigated the effect of cumambrin A on the relaxation of phenylephrine-induced precontracted rat aortic artery rings. The potency of cumambrin A was than compared to verapamil, a well known $Ca^{2+}-channel$ blocker. The results demonstrate that the isolated rat aortic arteries are relaxed to basal tension at a concentration of $5{\times}10^{-5}\;M$ cumambrin A treatment. The results also show that the phenylephrine-induced contraction is inhibited by a pretreatment of cumambrin A. Co-treatment of cumambrin A and verapamil showed a strong synergetic effect on the relaxation of rat aortic artery rings. Thus, these data demonstrate that cumambrin A is a potent relaxant of rat aortic smooth muscle and suggest that cumambrin A modulates intracellular or extracellular $Ca^{2+}$ mobilization.

• Korean Journal of Veterinary Service
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• v.19 no.2
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• pp.154-162
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• 1996

The effcets of adenosine 5'-triphosphate(ATP) were investigated on the uterine smooth muscle motility in the pig. The results were summarized as follows: 1. The effects of the porcine uterine smooth muscle and the contractile responses increased between the concentration of ATP $10^{-5}$ and $10^{-3}$ M with a dose-dependent manner. 2. The contractile response induced by ATP($10^{-4}$ M) was not blocked by pretreatment with cholinergic receptor blocker, atropine ($10^{-6}$ M) 3. The contractile response induced by ATP ($10^{-4}$ M) was not blocked by pretreatment with $\alpha$ -adrenergic receptor blocker, phentolamine(10$^{-6}$ M) and ${\beta}$-adrenergic blocker, propranolol ($10^{-6}$ M). 4. The contractile response induced by ATP($10^{-4}$ M) was not appeared in 4Ca^{++}$ -free medium. As the concentration of $Ca^{++}$ in $Ca^{++}$ -free medium was increased, the contractile response induced by ATP ($10^{-4}$ M) was enhenced but was completely inhibited by pretreatment with $Ca^{++}$ -channel blocker, papaverine($10^{-6}$ M) or verapamil($10^{-6}$ M). From these results, it was conclued that the effects of ATP were the contraction mediated by purinergic receptor in uterine smooth muscle of pig.

• Journal of the Korean Society of Physical Medicine
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• v.10 no.2
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• pp.95-98
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• 2015

PURPOSE: This study was conducted to devise a method of preventing water infiltration into the surface electrodes during EMG measurements underwater and on the ground and to check the reliability of Electromyography (EMG) measurements when underwater. METHODS: Six healthy adults were selected as subjects in this study. The measurements in this study were conducted in pool dedicated to underwater exercise and physical therapy room in the hospital building. An MP150 (Biopac Systems, US, 2010) and a BioNomadix 2-channel wireless EMG transmitter (Biopac Systems, US, 2012) was used to examine the muscle activity of rectus femoris, biceps femoris, tibialis anterior, gastrocnemius of dominant side. The subjects repeated circulation tasks on the ground for more than 10 min for enough surface electrode attachment movement. After a 15-min break, subjects performed the circulation task underwater(water depth 1.1m, water temperature $33.5^{\circ}C$, air temperature $27^{\circ}C$), as on the ground, for more than 10 min, and the MVIC of each muscle was measured again. SPSS v20.0 was used for all statistical computations. RESULTS: The maximum voluntary isometric contraction (MVIC) values between the underwater and on the ground measurements showed no significant differences in all four muscles and showed a high intraclass correlation coefficient (ICC) of >0.80. CONCLUSION: We determined that EMG measurements obtained underwater could be used with high reliability, comparable to ground measurements.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.103-109
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• 1988

Cyclobuxine D, extracted from Buxus microphylla var. koreana Nakai, is a steroidal alkaloid. Many pharmacological effects of cyclobuxine D were examined in our Lab. Cyclobuxine D showed a significant bradycardic effect in the rat heart and an inhibitory action on acetylcholine and $Ba^{++}-induced$ contraction of the longitudinal muscle isolated from the rabbit jejunum. In this study, we investigated the effect of cyclobuxine D on the contractile response-elicited by acetylcholine, oxytocin and $Ba^{++}$ in rat uterine. In order to analyse the inhibitory action of cyclobuxine D on the smooth muscle, we examined the inhibitory action of cyclobuxine D against the contractile response of the high potassium-depolarized rat ileum to calcium. Concentration-dependent decrease in the peak tension and duration of the acetylcholine, oxytocin and $Ba^{++}-induced$ contraction in the isolated rat uterus was observed when cyclobuxine D was added to the organ bath. The isolated longitudinal muscle from the rat ileum was immersed calcium-depleted potassium-depolarizing solution. Ten minutes after, 1.8 mM $CaCl_2$ was added to muscle bath and elicited a biphasic increase in muscle tension. Cyclobuxine D $(6.2{\times}10^{-5}\;M)$ produced an appreciable inhibition of both components of the mechanical response. In addition, $3.1{\times}10^{-4}\;M$ cyclobuxine D, introduced at a point when the tonic response had reached its maximum level, caused the muscle to exhibit a rapid lose of tension. Based on these experimental results, we propose the possibility that the inhibitory action of cyclobuxine D on the acetylcholine, oxytocin and $Ba^{++}-induced$ contraction in the isolated rat uterus may be due to blocking potassium-activated calcium channels, voltage-sensitive calcium channels.

• Korean Journal of Veterinary Research
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• v.43 no.3
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• pp.361-371
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• 2003

The vasorelaxant actions and blood pressure lowering of the ${\alpha}_2$-adrenoceptor agonists (${\alpha}_2$-AAs) clonidine and xylazine were investigated in rat isolated aortic rings and anesthesized rats. Both clonidine and xylazine produced a concentration-dependent inhibition of the sustained contraction induced by norepinephrine (NE), but not by KCl. NE-induced contractions were attenuated partly by nifedipine or verapamil, voltage dependent $Ca^{2+}$ channel blockers. These $Ca^{2+}$ channel blockers-resistant contractions were abolished by clonidine or xylazine. Inhibitory effects of a ${\alpha}_2$-AAs on contractions could be reversed by ryanodine, an intracellular $Ca^{2+}$, transport blocker, and tetrabutylammonium (TBA), a $Ca^{2+}$ activated $K^+$ channel blocker, but not by nifedipine, glibenclamide or removal of extracellular $Ca^{2+}$ and endothelium. Moreover, ${\alpha}_2$-AAs produced relaxation in NE-precontracted isolated intact aortic rings in a concentration-dependent manner, but not in KCl-precontracted rings. The relaxant effects of ${\alpha}_2$-AAs were inhibited by ryanodine and TBA, but not by nifedipine, glibenclamide, N (G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG), 2-nitro-4-carboxyphenyl N,N-diphenylcarhurnte (NCDC), lithium sulfate, staurosporine or removal of extracellular $Ca^{2+}$ and endothelium. In vivo, infusion of xylazine elicited significant decrease in anerial blood pressure. This xylazinelowered blood pressure was completely inhibited by the intravenous injection of TBA, but not by the intravenous injection of glibenclamide, L-NNA, L-NAME, AG, nifedipine, lithium sulfate or saponin.. These findings showed that the receptor-mediated and ${\alpha}_2$-adrenoceptor A-stimulated endothelium-independent vasorelaxant effect may be explained by decreasing intracellular $Ca^{2+}$ release and activation of $Ca^{2+}$-activated $K^+$ channels, which may contribute to the hypotensive effects of ${\alpha}_2$-AAs in rats.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.5
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• pp.297-303
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• 2012

This study was designed to elucidate high $K^+$-induced relaxation in the human gastric fundus. Circular smooth muscle from the human gastric fundus greater curvature showed stretch-dependent high $K^+$ (50 mM)-induced contractions. However, longitudinal smooth muscle produced stretch-dependent high $K^+$-induced relaxation. We investigated several relaxation mechanisms to understand the reason for the discrepancy. Protein kinase inhibitors such as KT 5823 (1 ${\mu}M$) and KT 5720 (1 ${\mu}M$) which block protein kinases (PKG and PKA) had no effect on high $K^+$-induced relaxation. $K^+$ channel blockers except 4-aminopyridine (4-AP), a voltage-dependent $K^+$ channel ($K_V$) blocker, did not affect high $K^+$ -induced relaxation. However, N(G)-nitro-L-arginine and 1H-(1,2,4)oxadiazolo (4,3-A)quinoxalin-1-one, an inhibitors of soluble guanylate cyclase (sGC) and 4-AP inhibited relaxation and reversed relaxation to contraction. High $K^+$-induced relaxation of the human gastric fundus was observed only in the longitudinal muscles from the greater curvature. These data suggest that the longitudinal muscle of the human gastric fundus greater curvature produced high $K^+$-induced relaxation that was activated by the nitric oxide/sGC pathway through a $K_V$ channel-dependent mechanism.