• The Korean Journal of Petroleum Geology
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• v.5 no.1_2 s.6
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• pp.36-47
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• 1997

This study presents multi-variable sequence model for a broader application of sequence concept proposed by Exxon group. The concept of the multi-variable model is based on the fact that internal organization and boundary type of the sequences are determined by three varying factors including 3rd-order cycles of eustasy, and tectonic movement and sediment influx with 2nd-order changes. Instead of Exxon group's systems tracts, this model adopts parasequence sets as the fundamental building blocks of the sequence, because they are descriptive stratigraphic units simply defined by internal stacking pattern, reflecting interactions of accommodation and sediment influx. Seven sequence types which vary in number and type of internal parasequence sets are formulated as associations of four types of accommodation development and three grades of sediment influx. In the southwestern margin of Ulleung Basin, the multi-variable sequence analysis of shelf-slope sequence shows systematic changes in stratal patterns and the numbs, of constituent parasequence sets (i.e. sequence type). These changes are interpreted to reflect temporal and spatial changes in type and rate of tectonic movement and sediment influx, as a result of back-arc opening and closing. During the back-arc opening, rapid subsidence, continuous rise of relative sea level, and high sediment influx gave rise to sequences dominantly of single progradational parasequence set. In the early stage of back-arc closing accompanied by local contractional deformation, different types of sequences contemporaneously formed depending on the spatial changes in tectonically-controlled accommodation and influx rates. During the subsequent slow back-arc subsidence, rise-dominated relative sea-level cycle was coupled with moderate to high sedimentation rate to have resulted in sequences consisting of $2~3$ parasequence sets.

• The Korean Journal of Physiology
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• v.23 no.2
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• pp.329-337
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• 1989

Cardiac muscles show stimulation frequency-dependent tension changes i.e. Bowditch phenomenon and Woodworth phenomenon, the former is an increase of tension with the increase of stimulation frequency, whereas the latter is an increase of tension with a decrease of stimulation frequency. Bowditch phenomenon is seen in the range of frequency 1.0 cps and above, and Woodworth phenomenon below the frequency 1.0 cps in the most of mammalian cardiac atrium. To throw some light on the possible mechanism of both phenomena in rat atrium, influences of drugs affecting $Ca^{2+}$ influx through the plasma membrane $(verapamil,\;La^{3+},\;norepinephrine)$ and $Ca^{2+}$ release from sarcoplasmic reticulum (SR) on frequency-tension curve were studied. The results obtained are summarized as follows: 1) At low temperature $(27.5^{\circ}C)$, both Bowditch and Woodworth phenomenon were demonstrated. But Bowditch phenomenon disappeared at the temperature above $(32.5^{\circ}C)$. 2) At $(27.5^{\circ}C)$, in the presence of verapamil, a $Ca^{2+}$ channel blocker, a time course of change in the frequency-tension was studied. It was found that Bowditch phenomenon was affected before the Woodworth phenomenon, then the former was completely disappeared. At $(32.5^{\circ}C)$, where no Bow-ditch is seen in normal atrial muscle, Bowditch phenomenon was reappeared by an administration of norepinephrine suggesting again that slow inward current of such as $Ca^{2+}$ channel is closely related to Bowditch phenomenon. 3) At $27.5^{\circ}C$, in the presence of $La^{3+}$, although tensions were decreased at all stimulation frequencies, Bowditch and Woodworth phenomenon were still demonstrated. However in the presence of both $La^{3+}$ and verapamil, Bowditch phenomena was disappeared suggesting that $La^{3+}$ is less effective in blocking $Ca^{2+}$ channel than verapamil. 4) At $27.5^{\circ}C$, in the presence of ryanodine, an inhibitor of calcium release from SR, Woodworth phenomenon was disappeared, which was consistent with previous reports of others, suggesting that $Ca^{2+}$ release from SR is closely related to Woodworth phenomenon. From the above findings, it may be concluded that Bowditch phenomenon is dependent on the magnitude of $Ca^{2+}$ influx through slow channel and Woodworth phenomenon is dependent on the amount of $Ca^{2+}$ stored in SR.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.259-265
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• 2017

Excessive influx and the subsequent rapid cytosolic elevation of $Ca^{2+}$ in neurons is the major cause to induce hyperexcitability and irreversible cell damage although it is an essential ion for cellular signalings. Therefore, most neurons exhibit several cellular mechanisms to homeostatically regulate cytosolic $Ca^{2+}$ level in normal as well as pathological conditions. Delayed rectifier $K^+$ channels ($I_{DR}$ channels) play a role to suppress membrane excitability by inducing $K^+$ outflow in various conditions, indicating their potential role in preventing pathogenic conditions and cell damage under $Ca^{2+}$-mediated excitotoxic conditions. In the present study, we electrophysiologically evaluated the response of $I_{DR}$ channels to hyperexcitable conditions induced by high $Ca^{2+}$ pretreatment (3.6 mM, for 24 hours) in cultured hippocampal neurons. In results, high $Ca^{2+}$-treatment significantly increased the amplitude of $I_{DR}$ without changes of gating kinetics. Nimodipine but not APV blocked $Ca^{2+}$-induced $I_{DR}$ enhancement, confirming that the change of $I_{DR}$ might be targeted by $Ca^{2+}$ influx through voltage-dependent $Ca^{2+}$ channels (VDCCs) rather than NMDA receptors (NMDARs). The VDCC-mediated $I_{DR}$ enhancement was not affected by either $Ca^{2+}$-induced $Ca^{2+}$ release (CICR) or small conductance $Ca^{2+}$-activated $K^+$ channels (SK channels). Furthermore, PP2 but not H89 completely abolished $I_{DR}$ enhancement under high $Ca^{2+}$ condition, indicating that the activation of Src family tyrosine kinases (SFKs) is required for $Ca^{2+}$-mediated $I_{DR}$ enhancement. Thus, SFKs may be sensitive to excessive $Ca^{2+}$ influx through VDCCs and enhance $I_{DR}$ to activate a neuroprotective mechanism against $Ca^{2+}$-mediated hyperexcitability in neurons.

• The Korean Journal of Pharmacology
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• v.17 no.1 s.28
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• pp.1-8
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• 1981

The $Na^+$-induced calcium release and the effect of sodium on the transmitochondrial calcium flux were observed in mitochondria isolated from pig ventricular myocardium by Milipore filtration technique using radioisotope $^{45}Ca$. The release of calcium from cardiac mitochondria was induced by small amount of sodium, and was promoted by increasing sodium concentration in the incubation medium. The extent of the $Na^+$-induced calcium release was much greater in the absence of extramitochondrial calcium than in the presence of calcium. At steady state of calcium binding on the mitochondrial membrane unidirectional calcium influx was inhibited by sodium and unidirectional calcium efflux was increased., From the above results, it was suggested that calcium might be released from cardiac mitochondria in exchange with sodium through the mediation of the postulated '$Na^+/Ca^{++}$ exchange' mechanism.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.417-424
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• 1996

The present study was done to examine the involvement of protein kinase C and protein tyrosine kinase in intracellular $Ca^{2+}$ mobilization in C5a-stimulated neutrophils. Although protein kinase C inhibitors, staurosporine and H-7 inhibited intracellular $Ca^{2+}$ release in C5a-stimulated neutrophils, they did not affect $Ca^{2+}$ influx across the plasma membrane and elevation of $[Ca^{2+}]_i$ C5a-induced intracellular $Ca^{2+}$ release and $Ca^{2+}$ influx were inhibited by protein tyrosine kinase inhibitors, genistein and methyl-2,5-dihydroxycinnamate. ADP-evoked elevation of $[Ca^{2+}]_i$ was inhibited by genistein and methyl-2,5-dihydroxycinnamate but was not affectd by staurosporine and H-7. Genistein and methyl-2,5-dihydroxycinnamate reduced the store-regulated $Ca^{2+}$ influx in thapsigargin-treated neutrophils, while the effect of staurosporine and H-7 was not detected. When neutrophils were preincubated wih phorbol 12-myristate 13-acetate, the stimulatory effect of C5a on the elevation of $[Ca^{2+}]_i$ was reduced. These results suggest that protein tyrosine kinase may be involved in control of intracellular $Ca^{2+}$ release and $Ca^{2+}$ influx across the plasma membrane in C5a-activated neutrophils.

• Journal of the Economic Geographical Society of Korea
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• v.16 no.2
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• pp.218-232
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• 2013

One of the most interesting points in the era of globalization and transnationalism is the movement of people, namely migration. This research aims to explain the discourse of marginalization on Korean-Chinese by Korean merchants as the migrants expand their shops in the Chinese Food Culture Street. The Chinese Food Culture Street has been formed by Korean-Chinese restaurants and shops for the process of differentiation from the Garibong-Daelim area. Korean merchants in the street are not opposed to the influx of Korean-Chinese into Korea, however they do not want to the influx of them into the Jayang area. As the influx of Korean-Chinese into this street has increased, so the Korean merchants in the street have marginalized them as dangerous element for local security, as immoral beings cling to their business, and as the main reason for the regional underdevelopment. However, this marginalization of Korean-Chinese makes difficult to understand the real change of local area, because there has been some positive effects by the influx of them such as the improvement of surrounding environment and the elevation of local imagination. This research clearly suggest that the marginalization of migrants by major society is from the fixed idea and prejudice, and this research suggest the need to further study on the occupation and change of local by migrants.

• Journal of Korean Biological Nursing Science
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• v.1 no.1
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• pp.25-41
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• 1999

Physiological activity of osteoblast including bone formation is known to be closely related to the increase of intracellular $Ca^{2+}$ activity($[Ca^{2+}]_i$) in osteoblast. $Ca^{2+}$ is an important intracellular messenger in diverse cellular functions, and regulation of its level is mediated by the transmembrane $Ca^{2+}$ movement via $Ca^{2+}$ channels, $Na^+-Ca^{2+}$ exchange, and by intracellular $Ca^{2+}$ movement through the intracellular stores. The purpose of this study is to investigate how the intracellular $Ca^{2+}$ is regulated in osteoblast-like cells(OLCs) by measuring $Ca^{2+}$ activity with cell imaging technique. OLCs were isolated from femur and tibia of neonatal rats, and cultured for 7 days. Cultured OLCs were loaded with a $Ca^{2+}$-sensitive fluorescent dye, Fura-2, and fluorescence images were monitored with a cooled CCD camera. The images were processed and analyzed with an image analyzing software. The results were as follows. (1) $[Ca^{2+}]_i$ of OLC decreased as the $Ca^{2+}$ concentration in the superfusing Tyrode solution was lowered. When $Na^+$ concentration in the superfusing solution was decreased, $[Ca^{2+}]_i$ increased.. These suggest that $Ca^{2+}$ flux occurs via the $Na^+-Ca^{2+}$ exchange mechanism. (2) When $Na^+$ in the superfusing solution was removed. a transient $Ca^{2+}$, increase($Ca^{2+}$ spike) was occasionally observed. However, $Ca^{2+}$ spike was not observed after adding 1 ${\mu}M$ thapsigargin. This implies that the generation of $Ca^{2+}$ spike is mediated by the release of $Ca^{2+}$ from endoplasmic reticulum(ER). (3) As the $Ca^{2+}$ concentration in the superfusing solution was raised, the frequency of 0mM $Na^+$-induced $Ca^{2+}$ spike increased, suggesting that $Ca^{2+}$-induced $Ca^{2+}$ release(CICR) mechanism exists. (4) After $[Ca^{2+}]_i$ was decreased with the superfusion of $Ca^{2+}$-free solution containing thapsigargin, the recovery of $[Ca^{2+}]_i$ with reperfusion of 2.5mM $Ca^{2+}$ solution transiently exceeded the control level, suggesting that the depletion of $Ca^{2+}$ in ER induces $Ca^{2+}$ influx from extracellular medium via store-operated $Ca^{2+}$ influx(SOCI) mechanism. (5) $[Ca^{2+}]_i$ was not affected by the superfusion of 25mM $K^+$ Tyrode solution. These results suggest that intracellular $Ca^{2+}$ activity in osteoblast is regulated by transmembrane $Ca^{2+}$ flux via $Na^+-Ca^{2+}$ exchange, $Ca^{2+}$ release from the internal store (ER) via $Ca^{2+}$-induced $Ca^{2+}$ release, and store-operated $Ca^{2+}$ influx across the cell membrane.

• Journal of the Korean Society for Marine Environment & Energy
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• v.10 no.1
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• pp.1-12
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• 2007

Mooring survey for measurement of tidal current and suspended sediments was carried out at 4 inlets of Yeoja Bay in April, 2000 in order to understand the source of sediment supply. Net suspended sediment transport load during 2 tidal cycles through the M-1(West Inlet) was $133.88\;kg{\cdot}m^{-1}$ toward the Yeoja Bay, whereas the flux through the M-2(Jabal Inlet) was outward the Bay with the amount of $146.43\;kg{\cdot}m^{-1}$. The influx through the M-3 and 4(Bulgyo and Dong Isa Stream) was $23.25\;kg{\cdot}m^{-1}$ and $4,312.31\;kg{\cdot}m^{-1}$ toward the Yeoja Bay, respectively. Influx of suspended sediment on Yeoja Bay mainly occurred in the Dong Isa Stream. In the wet season the composition of surface was coarser-grained than dry season, possibly due to the influx of silty sediment from Dong Isa Stream In the wet season.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.3
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• pp.311-319
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• 2018

Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (${\Delta}{\psi}_m$). Therefore, pharmacological manipulation of ${\Delta}{\psi}_m$ can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ${\Delta}{\psi}_m$ against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices. Results demonstrated that nobiletin treatment significantly increased cell viability against glutamate toxicity ($100{\mu}M$, 20 min) in primary cortical neurons. Real-time imaging-based fluorometry data reveal that nobiletin evokes partial mitochondrial depolarization in these neurons. Nobiletin markedly attenuated mitochondrial calcium overload and reactive oxygen species (ROS) generation in glutamate ($100{\mu}M$)-stimulated cortical neurons and isolated pure mitochondria exposed to high concentration of $Ca^{2+}$ ($5{\mu}M$). Nobiletin-induced partial mitochondrial depolarization in intact neurons was confirmed in isolated brain mitochondria using a fluorescence microplate reader. Nobiletin effects on basal ${\Delta}{\psi}_m$ were completely abolished in $K^+-free$ medium on pure isolated mitochondria. Taken together, results demonstrate that $K^+$ influx into mitochondria is critically involved in partial mitochondrial depolarization-related neuroprotective effect of nobiletin. Nobiletin-induced mitochondrial $K^+$ influx is probably mediated, at least in part, by activation of mitochondrial $K^+$ channels. However, further detailed studies should be conducted to determine exact molecular targets of nobiletin in mitochondria.

• Proceedings of the Zoological Society Korea Conference
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• 2001.10a
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• pp.201.2-201
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• 2001

No Abstract, See Full Text