• The Korean Journal of Physiology and Pharmacology
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• v.5 no.5
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• pp.413-421
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• 2001

An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of $K^+$ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured $Ca^{2+}-activated\;K\;(K_{Ca})$ currents and delayed rectifier K $(K_{dr})$ currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of $K_{Ca}$ channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of $K_{Ca}$ channel to $Ca^{2+}$ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of $K_{Ca}$ channel by TEA were more sensitive in hypertrophy. $K_{dr}$ current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of $K_{dr}$ current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of $K_{Ca}$ channels and $K_{dr}$ channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2002.11a
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• pp.276-279
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• 2002

$Bi_{2}Sr_{2}CaCu_{2}O_{x}$ was prepared by the conventional method of solid state reaction and SHS method. The samples were annealed in different atmosphere in order to examine the influence of atmospheres on the carbon contents in the $Bi_{2}Sr_{2}CaCu_{2}O_{x}$ compound. The lowest carbon content in $Bi_{2}Sr_{2}CaCu_{2}O_{x}$ could be attended when the sample was annealed in $O_{2}$ at $800^{\circ}C$ for 100 hours. The $CO_{2}$ in air pollute the samples and increase the carbon content in the sintering process. The critical current density of the $Bi_{2}Sr_{2}CaCu_{2}O_{x}$ samples will decrease with the increasing carbon contents in the samples. The impurity carbon will deposit in the grain boundary, which makes critical current density lower.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.95-101
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• 2005

In the heart, $Na^{+}-Ca^{2+}$ exchange (NCX) is the major $Ca^{2+}$ extrusion mechanism. NCX has been considered as a relaxation mechanism, as it reduces global $[Ca^{2+}]_i$ raised during activation. However, if NCX locates in the close proximity to the ryanodine receptor, then NCX would curtail $Ca^{2+}$ before its diffusion to global $Ca^{2+}_i$ This will result in a global $[Ca^{2+}]_i$ decrease especially during its ascending phase rather than descending phase. Therefore, NCX would decrease the myocardial contractility rather than inducing relaxation in the heart. This possibility was examined in this study by comparing NCX-induced extrusion of $Ca^{2+}$ after its release from SR in the presence and absence of global $Ca^{2+}_i$ transient in the isolated single rat ventricular myocytes by using patch-clamp technique in a whole-cell configuration. Global $Ca^{2+}_i$ transient was controlled by an internal dialysis with different concentrations of BAPTA added in the pipette. During stimulation with a ramp pulse from +100 mV to -100 mV for 200 ms, global $Ca^{2+}_i$ transient was suppressed only mildly, and completely at 1 mmol/L, and 10 mmol/L BAPTA, respectively. In these situations, ryanodine-sensitive inward NCX current was compared using $100{\mu}mol/L$ ryanodine, $Na^+$ depletion, 5 mmol/L $NaCl_2$ and $1{\mu}mol/L$ nifedipine. Surprisingly, the result showed that the ryanodine-sensitive inward NCX current was well preserved after 10 mmol/L BAPTA to 91 % of that obtained after 1 mmol/L BAPTA. From this result, it is concluded that most of the NCX-induced $Ca^{2+}$ extrusion occurs before the $Ca^{2+}$ diffuses to global $Ca^{2+})i$ in the rat ventricular myocyte.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.8
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• pp.3663-3673
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• 2016

Cervical cancer (CaCx) is the second most fatal cancer contributing to 14% of cancers in Indian females, which account for 25.4% and 26.5% of the global burden of CaCx prevalence and mortality, respectively. Persistent infection with high-risk human papilloma virus (HPV- strains 16 and 18) is the most important risk factor for precursors of invasive CaCx. Comprehensive prevention strategies for CaCx should include screening and HPV vaccination. Three screening modalities for CaCx are cytology, visual inspection with acetic acid, and HPV testing. There is no Indian national policy on CaCx prevention, and screening of asymptomatic females against CaCx is practically non-existent. HPV vaccines can make a major breakthrough in the control of CaCx in India which has high disease load and no organized screening program. Despite the Indian Government's effort to introduce HPV vaccination in the National Immunization Program and bring down vaccine cost, challenges to implementing vaccination in India are strong such as: inadequate epidemiological evidence for disease prioritization, duration of vaccine use, parental attitudes, and vaccine acceptance. This paper reviews the current epidemiology of CaCx and HPV in India, and the current status of HPV vaccination in the country. This article stresses the need for more research in the Indian context, to evaluate interventions for CaCx and assess their applicability, success, scalability and sustainability within the constraints of the Indian health care system.

• Journal of the Korean Ceramic Society
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• v.32 no.9
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• pp.1033-1039
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• 1995

The current experiment has quantitatively investigated the effect of the content of CaO and SiO2 on the microstructure, density, electrical resistivity, power loss and initial permeability of manganese zinc ferrites. The density increased initially with CaO and SiO2 content and the further addition showed an adverse effect. The excess addition of CaO and SiO2 developed a discontinuous grain growth with numerous pores inside grains and lowered the electrical resistivity. The initial permeability decreased with increasing the content of SiO2. The samples with relatively low power loss showed that half of the total loss at 10$0^{\circ}C$, 100 kHz and 2000 Gauss was due to the eddy current loss.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.2
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• pp.177-181
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• 2015

The subfornical organ (SFO) is one of circumventricular organs characterized by the lack of a normal blood brain barrier. The SFO neurons are exposed to circulating glutamate ($60{\sim}100{\mu}M$), which may cause excitotoxicity in the central nervous system. However, it remains unclear how SFO neurons are protected from excitotoxicity caused by circulating glutamate. In this study, we compared the glutamate-induced whole cell currents in SFO neurons to those in hippocampal CA1 neurons using the patch clamp technique in brain slice. Glutamate ($100{\mu}M$) induced an inward current in both SFO and hippocampal CA1 neurons. The density of glutamate-induced current in SFO neurons was significantly smaller than that in hippocampal CA1 neurons (0.55 vs. 2.07 pA/pF, p<0.05). To further identify the subtype of the glutamate receptors involved, the whole cell currents induced by selective agonists were then compared. The current densities induced by AMPA (0.45 pA/pF) and kainate (0.83 pA/pF), non-NMDA glutamate receptor agonists in SFO neurons were also smaller than those in hippocampal CA1 neurons (2.44 pA/pF for AMPA, p<0.05; 2.34 pA/pF for kainate, p< 0.05). However, the current density by NMDA in SFO neurons was not significantly different from that of hippocampal CA1 neurons (1.58 vs. 1.47 pA/pF, p>0.05). These results demonstrate that glutamate-mediated action through non-NMDA glutamate receptors in SFO neurons is smaller than that of hippocampal CA1 neurons, suggesting a possible protection mechanism from excitotoxicity by circulating glutamate in SFO neurons.

• The Korean Journal of Physiology
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• v.27 no.2
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• pp.139-150
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• 1993

We have reported that dopamine potentiates spontaneous contractions dose-dependently in guinea-pig antral circular muscle strips (Hwang et al, 1991). To clarify the underlying excitatory mechanism of dopamine on the gastric smooth muscle, the effects of dopamine on voltage-dependent $Ca^{2+}\;currents\;and\;Ca^{2+}\;-dependent\;K^+\;currents$ were observed in enzymatically dispersed guinea-pig gastric myocytes using the whole-cell voltage-clamp technique. Experiments were also done using isometric tension recording and conventional intracellular microelectrode techniques. 1) The effect of dopamine on the spontaneous contraction of antral circular muscle strips of the guinea-pig was excitatory in a dose-dependent manner, and was blocked by phentolamine, an ${\alpha}-adrenoceptor$ blocker. 2) The slow waves were not changed by dopamine. 3) The voltage-operated inward $Ca^{2+}$ current was not influenced by dopamine. 4) The $Ca^{2+}\;-dependent\;K^+$ outward current, which might reflect the changes of intracellular calcium concentration, was enhanced by dopamine. This effect was abolished by phentolamine. 5) The enhancing effect of dopamine on the $Ca^{2+}\;-dependent\;K^+$ current disappeared with heparin which is known to block the action of $InsP_3$. From these results, it is suggested that dopamine acts via $InsP_3-mediated\;Ca^{2+}$ mobilization from intracellular stores and such action potentiates the spontaneous contraction of guinea-pig gastric smooth muscle.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.81-81
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• 2003

Glibenclamide, a sulfonylurea derivative, has been used in tile treatment of type II diabetes mellitus. Recent studies provided evidence that glibenclamide, in addition to blocking ATP-sensitive $K^{+}$ channels, also affected Na$^{+}$-K$^{+}$ pumps and L-type $Ca^{2+}$ channels in noncardiac cells. The effect of glibenclamide on the cardiac muscle is not clearly known. In the present study, the effects of glibenclamide on intracellular Na$^{+}$ concentration ([Na$^{+}$]$_{i}$ ), twitch tension, $Ca^{2+}$ transient, and membrane potential were investigated in isolated guinea-pig ventricular myocytes. Glibenclamide at concentration of 200 $\mu$M increased [Na$^{+}$]$_{i}$ by 3.9$\pm$0.4 mM (mean $\pm$ SE, n=12), decreased twitch tension by 36.1 $\pm$ 4.0％ (mean $\pm$ SE, n=8), reduced $Ca^{2+}$ transient by 24.4$\pm$5.1％ (mean $\pm$ SE, n=3), slightly depolarized diastolic membrane potential, and did not change action potential duration. To determine whether inhibitions of Na$^{+}$-K$^{+}$ pumps and L-type $Ca^{2+}$ channels are responsible for the increase of [Na$^{+}$]$_{i}$ and the decrease of twitch tension, we tested effects of glibenclamide on Na$^{+}$-K$^{+}$ pump current and L-type $Ca^{2+}$ current. Glibenclamide decreased Na$^{+}$-K$^{+}$ pump current and L-type $Ca^{2+}$ current in a concentration-dependent manner.t in a concentration-dependent manner.

• Journal of Chest Surgery
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• v.22 no.4
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• pp.548-561
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• 1989

In single atrial cells isolated from the rabbit the properties of inward current of Na-Ca exchange were investigated using the whole cell voltage clamp technique. The current was recorded during repolarization following brief 2 ms depolarizing pulse to +40 mV from a holding potential of * 70 mV. Followings are the results obtained: 1. When stimulated every 30 seconds, the inward currents were activated and reached peak values 6-12 ms after the beginning of depolarizing pulse. The mean current amplitude was 342 pA/cell. 2. The current decayed spontaneously from the peak activation and the time course of the relaxation showed two different phases fast and slow phase. The time constants were 10-18 ms and 60-140 ms, respectively. 3. The recovery of inward current was tested by paired pulse of various intervals. The peak current recovered exponentially with time constant of 140 ms and 1 p M isoprenaline accelerated the recovery process. 4. Relaxation time course was also affected by pulse interval and time constant of the fast phase was reduced almost linearly according to the decrease of pulse interval between 30 sec and 1 sec. 5. The peak activation was increased in magnitude by long prepulse stimulation, 5 p M Bay K, 1 p M isoprenaline or internal and external application of c-AMP. 6. The relaxation time constant of the fast phase was prolonged by 5 p M Bay K or c-AMP, and shortened by isoprenaline. However the time course of the slow relaxation phase was not so much changed. From the above results, it could be concluded that increase of the calcium current by Bay K or c-AMP results in the potentiation and prolongation of intracellular calcium transient, and the facilitation of Ca uptake by SR might be a mechanism of shortening the time constant of current relaxation by short interval stimulation or isoprenaline.

• Proceedings of the Korean Biophysical Society Conference
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• 2001.06a
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• pp.26-26
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• 2001

Inactivation of N-type calcium current has been reported to be both voltage dependent and Ca$\^$2＋/ dependent. We have investigated the effects of Ba$\^$2＋/ and Ca$\^$2＋/ on N-channel inactivation in rat superior cervical ganglion neurons using the whole cell configuration of patch clamp technique. Inactivation was larger in Ca$\^$2＋/ than in Ba$\^$2＋/ even with 20 mM BAPTA.(omitted)