• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.93.1-93.1
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• 2006

• Journal of Life Science
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• v.14 no.5
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• pp.882-890
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• 2004

Gap junction is a membrane structure facilitating the direct transmission of several ions and small molecules between two cells. It is also called an 'intercellular channel' to distinguish it from other well-known cellular channels (e.g. sodium and potassium channels). Gap junction channels are not passive conduits, rather the ion channels modulated by several stimuli including pH, calcium ion, voltage, and a chemical modification (mainly known as phosphorylation). Among them, the effects of voltage on the gating of gap junction channels have been well studied. Gap junction channels are more sensitive to the transjunctional potential ($V_j$) between two cells rather than the membrane potential($V_m$) between inside and outside the cell. In this review, I will summarize the general properties of gap junction channel and discuss the gating mechanism for the gap channels.

• Molecules and Cells
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• v.20 no.3
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• pp.315-324
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• 2005

Pain is an unpleasant sensation experienced when tissues are damaged. Thus, pain sensation in some way protects body from imminent threat or injury. Peripheral sensory nerves innervated to peripheral tissues initially respond to multiple forms of noxious or strong stimuli, such as heat, mechanical and chemical stimuli. In response to these stimuli, electrical signals for conducting the nociceptive neural signals through axons are generated. These action potentials are then conveyed to specific areas in the spinal cord and in the brain. Sensory afferent fibers are heterogeneous in many aspects. For example, sensory nerves are classified as $A{\alpha}$, $-{\beta}$, $-{\delta}$ and C-fibers according to their diameter and degree of myelination. It is widely accepted that small sensory fibers tend to respond to vigorous or noxious stimuli and related to nociception. Thus these fibers are specifically called nociceptors. Most of nociceptors respond to noxious mechanical stimuli and heat. In addition, these sensory fibers also respond to chemical stimuli [Davis et al. (1993)] such as capsaicin. Thus, nociceptors are considered polymodal. Recent advance in research on ion channels in sensory neurons reveals molecular mechanisms underlying how various types of stimuli can be transduced to neural signals transmitted to the brain for pain perception. In particular, electrophysiological studies on ion channels characterize biophysical properties of ion channels in sensory neurons. Furthermore, molecular biology leads to identification of genetic structures as well as molecular properties of ion channels in sensory neurons. These ion channels are expressed in axon terminals as well as in cell soma. When these channels are activated, inward currents or outward currents are generated, which will lead to depolarization or hyperpolarization of the membrane causing increased or decreased excitability of sensory neurons. In order to depolarize the membrane of nerve terminals, either inward currents should be generated or outward currents should be inhibited. So far, many cationic channels that are responsible for the excitation of sensory neurons are introduced recently. Activation of these channels in sensory neurons is evidently critical to the generation of nociceptive signals. The main channels responsible for inward membrane currents in nociceptors are voltage-activated sodium and calcium channels, while outward current is carried mainly by potassium ions. In addition, activation of non-selective cation channels is also responsible for the excitation of sensory neurons. Thus, excitability of neurons can be controlled by regulating expression or by modulating activity of these channels.

• Journal of The Korean Society of Clinical Toxicology
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• v.14 no.1
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• pp.60-65
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• 2016

Aconitum is a genus of various species of flowering plants that belongs to the Family Ranunculaceae. Most Aconitum sp. have extremely toxic alkaloid substances such as aconitine, mesaconitine and hypaconitine. Among these substances, aconitine can cause fatal cardiotoxicity by activating sodium channels followed by calcium channels in myocardial cells. Even though there have been various therapeutic plans suggested comprising antidotes based on diverse case reports and studies, there is no confirmatory treatment protocol for aconite poisoning. Here, we report an aconite poisoning patient who had refractory ventricular tachyarrhythmia that did not respond to intravenous amiodarone therapies even though they were sustained for over 2 hours, but showed successful recovery following intravenous fat emulsions (IFE) therapy.

• Korea-Australia Rheology Journal
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• v.15 no.1
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• pp.1-7
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• 2003

A new method is introduced to build up organic/organic multilayer films composed of cationic poly(allylamine hydrochloride) (PAH) and negatively charged poly (sodium 4-styrenesulfonate) (PSS) using the spinning process. The adsorption process is governed by both the viscous force induced by fast solvent elimination and the electrostatic interaction between oppositely charged species. On the other hand, the centrifugal and air shear forces applied by the spinning process significantly enhances desorption of weakly bound polyelectrolyte chains and also induce the planarization of the adsorbed polyelectrolyte layer. The film thickness per bilayer adsorbed by the conventional dipping process and the spinning process was found to be about 4 ${\AA}$ and 24 ${\AA}$, respectively. The surface of the multilayer films prepared with the spinning process is quite homogeneous and smooth. Also, a new approach to create multilayer ultrathin films with well-defined micropatterns in a short process time is Introduced. To achieve such micropatterns with high line resolution in organic multilayer films, microfluidic channels were combined with the convective self-assembly process employing both hydrogen bonding and electrostatic intermolecular interactions. The channels were initially filled with polymer solution by capillary pressure and the residual solution was then removed by the .spinning process.

• 한국신재생에너지학회:학술대회논문집
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• 2008.05a
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• pp.165-168
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• 2008

A numerical analysis was conducted to predict the heat transfer characteristics of a solar receiver which is subject to very high heat fluxes and temperatures for solar thermal applications. The concentration ratio of the solar receiver ranges 1000 and the concentrated heat is required to be transported to a certain distance for specific applications. This study deals with a solar receiver according to internal geometry variation incorporating high-temperature heat pipe. The isothermal characteristics in the receiver section is of major concern. The diameter of the solar thermal receiver was 120 mm and the length was 400 mm and the angle of receiver end wall set $90^{\circ},\;60^{\circ},\;45^{\circ},\;30^{\circ}$. And the diameter of the heat pipe was 12.7 mm, 48 axial channels of the same dimensions were attached to the outer wall of the receiver with even spacing in the circumferential direction. The channels are changed to high-temperature sodium heat pipes. Commercial softwares were employed to deal with the radiative heat transfer inside the receiver cavity and the convection heat transfer along the channels. The numerical results are compared and analyzed from the view point of high-temperature solar receiver.

• The Korean Journal of Emergency Medical Services
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• v.24 no.3
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• pp.155-160
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• 2020

Torsades de pointes refers to polymorphic ventricular tachycardia (PMVT), which is caused by the suppression of potassium channels owing to genetic and electrolytic abnormalities, resulting in the extension of the QT interval. Symptoms range from spontaneous circulation recovery to fainting and sudden death. Defibrillation, magnesium correction, and the use of lidocaine as an antiarrhythmic agent are recommended as treatments for persistent torsades de pointes. Currently, only amiodarone is available in the ambulance; however, torsades de pointes does not respond efficiently to amiodarone because it suppresses potassium channels and increases the refractory period of the myocardium. Lidocaine, in contrast, reduces the relative refractory period of the myocardium caused by suppressing sodium channels; thus, it inhibits the occurrence of and treats arrhythmia. In cases where PMVT did not respond to defibrillation, the administration of lidocaine showed no difference in survival and discharge rates compared to amiodarone. Thus, ambulances must be equipped with provisions to administer lidocaine.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.649-660
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• 2018

Migraine is a neurological disorder characterized by recurrent and disabling severe headaches. Although several anticonvulsant drugs that block voltagedependent $Na^+$ channels are widely used for migraine, far less is known about the therapeutic actions of carbamazepine on migraine. In the present study, therefore, we characterized the effects of carbamazepine on tetrodotoxin-resistant (TTX-R) $Na^+$ channels in acutely isolated rat dural afferent neurons, which were identified by the fluorescent dye DiI. The TTX-R $Na^+$ currents were measured in medium-sized DiIpositive neurons using the whole-cell patch clamp technique in the voltage-clamp mode. While carbamazepine had little effect on the peak amplitude of transient $Na^+$ currents, it strongly inhibited steady-state currents of transient as well as persistent $Na^+$ currents in a concentration-dependent manner. Carbamazepine had only minor effects on the voltage-activation relationship, the voltage-inactivation relationship, and the use-dependent inhibition of TTX-R $Na^+$ channels. However, carbamazepine changed the inactivation kinetics of TTX-R $Na^+$ channels, significantly accelerating the development of inactivation and delaying the recovery from inactivation. In the current-clamp mode, carbamazepine decreased the number of action potentials without changing the action potential threshold. Given that the sensitization of dural afferent neurons by inflammatory mediators triggers acute migraine headaches and that inflammatory mediators potentiate TTX-R $Na^+$ currents, the present results suggest that carbamazepine may be useful for the treatment of migraine headaches.

• Journal of The Korean Society of Clinical Toxicology
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• v.4 no.2
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• pp.166-169
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• 2006

Poisonings caused by 'mad honey' are known to occur in response to grayanotoxins, which bind to sodium channels in the cell membrane, increasing membrane sodium permeability and preventing inactivation. Mild symptoms of mad honey intoxication are dizziness, weakness, hypersalivation, nausea, vomiting, and paresthesia. Severe intoxication, however, leads to serious cardiac manifestations such as atrioventricular block, dose-dependent hypotension, bradycardia, and respiratory depression. Atropine and vasoactive drugs improve symptoms of both bradycardia and respiratory rate depression. We report an unusual case of saliva-type hyperamylasemia in a mad honey poisoning patient who developed clinically significant bradycardia. She recovered fully within 3 days following atropine administration and medical treatment.

• International Journal of Oral Biology
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• v.40 no.4
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• pp.211-216
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• 2015

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium ($BK_{ca}$) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of $Ca^{2+}$ that induces $Ca^{2+}$-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective $BK_{Ca}$ channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove $Ca^{2+}$ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through $BK_{ca}$ channels, which are activated by intracellular $Ca^{2+}$ increase via activation of RyR of $Ca^{2+}$ stores.