• Journal of KIISE:Computer Systems and Theory
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• v.30 no.1
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• pp.33-49
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• 2003

Recently, there have been large storage demands for manipulating multimedia data. To solve the tremendous storage demands, one of the major researches is the SAN(Storage Area Network) that provides the local file requests directly from shared-disk storage and also eliminates the server bottlenecks to performance and availability. SAN also improve the network latency and bandwidth through new channel interface like FC(Fibre Channel). But to manipulate the efficient storage network like SAN, traditional local file system and distributed file system are not adaptable and also are lack of researches in terms of a metadata structure for large-scale inode object such as file and directory. In this paper, we describe the architecture and design issues of our shared-disk file system and provide the efficient bitmap for providing the well-formed block allocation in each host, extent-based semi flat structure for storing large-scale file data, and two-phase directory structure of using Extendible Hashing. Also we describe a detailed algorithm for implementing the file system's device driver in Linux Kernel and compare our file system with the general file system like EXT2 and shard disk file system like GFS in terms of file creation, directory creation and I/O rate.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.19-29
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• 1996

The neurological manifestations of AIDS include dementia, encountered even in the absence of opportunistic superinfection or malignancy. The AIDS Dementia Complex appears to be associated with several neuropathological abnormalities, including astrogliosis and neuronal injury or loss. How can HIV-1 result in neuronal damage if neurons themselves are only rarely, if ever, infected by the vitus\ulcorner In vitro experiments from several different laboratiories have lent support to the existence of HIV- and immune-related toxins. In one recently defined pathway to neuronal injury, HIV-infected macrophages/microglia as well as macrophages activated by HIV-1 envelope protein gp120 appear to secrete excitants/neurotoxins. These substances may include arachidonic acid, platelet-activating factor, free radicals (NO - and O$_2$), glutamate, quinolinate, cysteine, cytokines (TNF-${\alpha}$, IL1-B, IL-6), and as yet unidentified factors emanating from stimulated macrophages and possibly reactive astrocytes. A final common pathway for newonal suscepubility appears to be operative, similar to that observed in stroke, trauma, epilepsy, and several neurodegenerative diseases, including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves excessive activation of N-methyl-D-aspartate (NMDA) receptor-operated channels, with resultant excessive influx of Ca$\^$2+/ leading to neuronal damage, and thus offers hope for future pharmacological intervention. This chapter reviews two clinically-tolerated NMDA antagonists, memantine and nitroglycerin; (ⅰ) Memantine is an open-channel blocker of the NMDA-associated ion channel and a close congener of the anti-viral and anti-parkinsonian drug amantadine. Memantine blocks the effects of escalating levels of excitotoxins to a greater degree than lower (piysiological) levels of these excitatory amino acids, thus sparing to some extent normal neuronal function. (ⅱ) Niuoglycerin acts at a redox modulatory site of the NMDA receptor/complex to downregulate its activity. The neuroprotective action of nitroglycerin at this site is mediated by n chemical species related to nitric oxide, but in a higher oxidation state, resulting in transfer of an NO group to a critical cysteine on the NMDA receptor. Because of the clinical safety of these drugs, they have the potential for trials in humans. As the structural basis for redox modulation is further elucidated, it may become possible to design even better redox reactive reagents of chinical value. To this end, redox modulatory sites of NMDA receptors have begun to be characterized at a molecular level using site-directed mutagenesis of recombinant subunits (NMDAR1, NMDAR2A-D). Two types of redox modulation can be distinguished. The first type gives rise to a persistent change in the functional activity of the receptor, and we have identified two cysteine residues on the NMDARI subunit (#744 and #798) that are responsible for this action. A second site, presumably also a cysteine(s) because <1 mM N-ethylmaleimide can block its effect in native neurons, underlies the other, more transient redox action. It appears to be at this, as yet unidentified, site on the NMDA receptor that the NO group acts, at least in recombinant receptors.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.4
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• pp.217-239
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• 2011

We carried out a series of experiment demonstrating the role of mitochondria in the cytosolic and mitochondrial $Ca^{2+}$ transients and compared the results with those from computer simulation. In rat ventricular myocytes, increasing the rate of stimulation (1~3 Hz) made both the diastolic and systolic [$Ca^{2+}]$ bigger in mitochondria as well as in cytosol. As L-type $Ca^{2+}$ channel has key influence on the amplitude of $Ca^{2+}$ -induced $Ca^{2+}$ release, the relation between stimulus frequency and the amplitude of $Ca^{2+}$ transients was examined under the low density (1/10 of control) of L-type $Ca^{2+}$ channel in model simulation, where the relation was reversed. In experiment, block of $Ca^{2+}$ uniporter on mitochondrial inner membrane significantly reduced the amplitude of mitochondrial $Ca^{2+}$ transients, while it failed to affect the cytosolic $Ca^{2+}$ transients. In computer simulation, the amplitude of cytosolic $Ca^{2+}$ transients was not affected by removal of $Ca^{2+}$ uniporter. The application of carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP) known as a protonophore on mitochondrial membrane to rat ventricular myocytes gradually increased the diastolic [$Ca^{2+}$] in cytosol and eventually abolished the $Ca^{2+}$ transients, which was similarly reproduced in computer simulation. The model study suggests that the relative contribution of L-type $Ca^{2+}$ channel to total transsarcolemmal $Ca^{2+}$ flux could determine whether the cytosolic $Ca^{2+}$ transients become bigger or smaller with higher stimulus frequency. The present study also suggests that cytosolic $Ca^{2+}$ affects mitochondrial $Ca^{2+}$ in a beat-to-beat manner, however, removal of $Ca^{2+}$ influx mechanism into mitochondria does not affect the amplitude of cytosolic $Ca^{2+}$ transients.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.5
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• pp.207-213
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• 2007

This study was designed to characterize ureteral smooth muscle motility and also to study the effect of forskolin(FSK) and isoproterenol(ISO) on smooth muscle contractility in murine ureter. High $K^+$(50 mM) produced tonic contraction by $0.17{\pm}0.06mN$(n=19). Neuropeptide and neurotransmitters such as serotonin($5{\mu}M$), histamine($20{\mu}M$), and carbarchol(CCh, $10{\sim}50{\mu}M$) did not produce significant contraction. However, CCh($50{\mu}M$) produced slow phasic contraction in the presence of 25 mM $K^+$. Cyclopiazonic acid(CPA, $10{\mu}M$), SR $Ca^{2+}$-ATPase blocker, produced tonic contraction(0.07 mN). Meanwhile, inhibition of mitochondria by protonophore carbnylcyanide m-chlorophenylhydrazone(CCCP) also produced weak tonic contraction(0.01 mN). The possible involvement of $K^+$ channels was also pursued. Tetraethyl ammonium chloride(TEA, 10 mM), glibenclamide($10{\mu}M$) and quinidine($20{\mu}M$) which are known to block $Ca^{2+}$-activated $K^+$ channels($K_{Ca}$ channel), ATP-sensitive $K^+$ channels($K_{ATP}$) and nonselective $K^+$ channel, respectively, did not elicit any significant effect. However, $Ba^{2+}$($1{\sim}2mM$), blocker of inward rectifier $K^+$ channels($K_{IR}$ channel), produced phasic contraction in a reversible manner, which was blocked by $1{\mu}M$ nicardipine, a blocker of dehydropyridine-sensitive voltage-dependent L-type $Ca^{2+}$ channels($VDCC_L$) in smooth muscle membrane. This $Ba^{2+}$-induced phasic contraction was significantly enhanced by $10{\mu}M$ cyclopiazonic acid(CPA) in the frequency and amplitude. Finally, regulation of $Ba^{2+}$-induced contraction was studied by FSK and ISO which are known as adenylyl cyclase activator and $\beta$-adrenergic receptor agonist, respectively. These drugs significantly suppressed the frequency and amplitude of $Ba^{2+}$-induced contraction(p<0.05). These results suggest that $Ba^{2+}$ produces phasic contraction in murine ureteral smooth muscle which can be regulated by FSK and $\beta$-adrenergic stimulation.

• Nuclear Engineering and Technology
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• v.53 no.1
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• pp.61-68
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• 2021

Experiments of vertically upward steam-water two-phase flow have been carried out in single-side heated narrow rectangular channel with a gap of 3 mm. Flow patterns were identified and classified through visualization directly. Slug flow was only observed at 0.2 MPa but replaced by block-bubble flow at 1.0 MPa. Flow pattern maps at the pressure of 0.2 MPa and 1.0 MPa were plotted and the difference was analyzed. The experimental data has been compared with other flow pattern maps and transition criteria. The results show reasonable agreement with Hosler's, while a wide discrepancy is observed when compared with air-water two-phase experimental data. Current criteria developed based on air-water experiments poorly predict bubble-slug flow transition due to the different formation and growth of bubbles. This work is significant for researches on heat transfer, bubble dynamics and flow instability.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.39-49
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• 1996

In the present study, we observed change in intracellular $Ca^{2+}$$([Ca^{2+}]_i)$ as measured with the fluorescent $Ca^{2+}-indicator$ fura-2 in association with force development of the rat basilar arteries during activation by$K^+$ depolarizing solution and U46619, a thromboxane analogue, in the absence and the presence of calcitonin-gent related peptide (CGRP). CGRP (30 and 100 nM) caused a concentration-dependent inhibition of U46619-induced contraction with decrease in $[Ca^{2+}]_i$, whereas it did not exert any effect on the $K^+$ (90 mM)-induced contraction and increase in $[Ca^{2+}]_i$, Further, $[Ca^{2+}]_i-force$ relationships were determined by plotting the ratio of $F_{340}/F_{380}$ $([Ca^{2+}]_i)$ as a function of the force induced by U46619, and the results were compared with those obtained in the presence of CGRP. The curves obtained in the presence of CGRP (30 and 100 nM) were significantly moved to downward without right shift of the curves suggesting that CGRP inhibited the U46619-induced contraction only by mediation of reduction in $[Ca^{2+}]_i$ with out any change in the sensitivity of contractile apparatus to $Ca^{2+}$. The CGRP-induced attenuation of $[Ca^{2+}]_i$ and force development was significantly inhibited under pretreatment with CGRP $(8{\sim}37)$ fragment (100 nM), a CGRP1 receptor antagonist. Both the reduced contraction and reduction in $[Ca^{2+}]_i$ caused by CGRP were fully reversed by pretreatment with charybdotoxin (100 nM) and iberiotoxin (100 nM), large conductance $Ca^{2+}-activated$ $K^+$ channel blockers, but not by apamin (300 nM), a small conductance $Ca^{2+}-activated$ $K^+$ channel blocker, and glibenclamide ( 1 ${\mu}M$), an ATP-sensitive $K^+$ channel blocker. In conclusion, it is suggested that the CGRP1 receptor, upon activation by CGRP, are coupled to opening of $Ca^{2+}-activated$ $K^+$ channel and cause to decrease in $[Ca^{2+}]_i$, thereby leading to vasodilation of the rat basilar artery. However, it is not defined that the mechanism underlying vasodilation whether the $K^+$ channel blockers, charybdotoxin and iberiotoxin directly block the CGRP receptors and that CGRP-evoked relaxation is dependent on the cyclic AMP or $K^+$ channel opening or both actions.

• Magazine of the Korean Society of Agricultural Engineers
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• v.13 no.1
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• pp.2206-2217
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• 1971

Spillway and discharge channel of reservoirs require the Control of Large volume of water under high pressure. The energies at the downstream end of spillway or discharge channel are tremendous. Therefore, Some means of expending the energy of the high-velocity flow is required to prevent scour of the riverbed, minimize erosion, and prevent undermining structures or dam it self. This may be accomplished by Constructing an energy dissipator at the downstream end of spillway or discharge channel disigned to dissipated the excessive energy and establish safe flow Condition in the outlet channel. There are many types of energy dissipators, stilling basins are the most familar energy dissipator. In the stilling basin, most energies are dissipated by hydraulic jump. stilling basins have some length to cover hydraulic jump length. So stilling basins require much concrete works and high construction cost. Flip bucket type energy dissipators require less construction cost. If the streambed is composed of firm rock and it is certain that the scour will not progress upstream to the extent that the safety of the structure might be endangered, flip backet type energy dissipators are the most recommendable one. Following items are tested and studied with bucket radius, $R=7h_2$,(medium of $4h_2{\geqq}R{\geqq}10h_2$). 1. Allowable upstream channel slop of bucket. 2. Adequate bucket lip angle for good performance of flip bucket. Also followings are reviwed. 1. Scour by jet flow. 2. Negative pressure distribution and air movement below nappe flow. From the test and study, following results were obtained. 1. Upstream channel slope of bucket (S=H/L) should be 0.25<H/L<0.75 for good performance of flip bucket. 2. Adequated lip angle $30^{\circ}{\sim}40^{\circ}$ are more reliable than $20^{\circ}{\sim}30^{\circ}$ for the safety of structures.

• Journal of the Institute of Electronics Engineers of Korea TC
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• v.48 no.8
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• pp.15-26
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• 2011

In this paper, we present a new beamforming scheme for a downlink of multiuser multiple-input multipleoutput (MIMO) communication systems. Recently, a block-diagonalization (BD) algorithm has been proposed for the multiuser MIMO downlink where both a base station and each user have multiple antennas. However, the BD algorithm is not efficient when the number of supported streams per user is smaller than that of receive antennas. Since the BD method utilizes the space based on the channel matrix without considering the receive combining, the degree of freedom for beamforming cannot be fully exploited at the transmitter. In this paper, we optimize the receive beamforming vector under a zero forcing (ZF) constraint, where all inter-user interference is driven to zero. We propose an efficient algorithm to find the optimum receive vector by an iterative procedure. The proposed algorithm requires two phase values feedforward information for the receive combining vector. Also, we present another algorithm which needs only one phase value by using a decomposition of the complex general unitary matrix. Simulation results show that the proposed beamforming scheme outperforms the conventional BD algorithm in terms of error probability and obtains the diversity enhancement by utilizing the degree of freedom at the base station.

• Journal of the Korean Institute of Gas
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• v.21 no.4
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• pp.92-102
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• 2017

Fischer-Tropsch synthesis reaction converts syngas (mixture of CO and H2) to valuable hydrocarbon products. Simulation of low temperature Fischer -Tropsch Synthesis reaction and heat transfer at intensified process condition using catalyst filled single and multichannel microchannel reactor is considered. Single channel model simulation indicated potential for process intensification (higher GHSV of $30000hr^{-1}$ in presence of theoretical Cobalt based super-active catalyst) while still achieving CO conversion greater than ~65% and $C_{5+}$ selectivity greater than ~74%. Conjugate heat transfer simulation with multichannel reactor block models considering three different combinations of reactor configuration and coolant type predicted ${\Delta}T_{max}$ equal to 23 K for cross-flow configuration with wall boiling coolant, 15 K for co-current flow configuration with subcooled coolant, and 13 K for co-current flow configuration with wall boiling coolant. In the range of temperature maintained (498 - 521 K), chain growth probability calculated is desirable for low-temperature Fisher-Tropsch Synthesis.