Cho, Susie;Kim, Heung-Chul;Chong, Sung-Tae;Klein, Terry A.;Kwon, Deok Ho;Lee, Si Hyeock;Kim, Ju Hyeon
Parasites, Hosts and Diseases
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v.58
no.1
/
pp.99-102
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2020
Two-point mutations (V419L and L925I) on the voltage-sensitive sodium channel of bed bugs (Cimex lectularius) are known to confer pyrethroid resistance. To determine the status of pyrethroid resistance in bed bugs in Korea, resistance allele frequencies of bed bug strains collected from several US military installations in Korea and Mokpo, Jeollanamdo, from 2009-2019 were monitored using a quantitative sequencing. Most bed bugs were determined to have both of the point mutations except a few specimens, collected in 2009, 2012 and 2014, having only a single point mutation (L925I). No susceptible allele was observed in any of the bed bugs examined, suggesting that pyrethroid resistance in bed bug populations in Korea has reached a serious level. Large scale monitoring is required to increase our knowledge on the distribution and prevalence of pyrethroid resistance in bed bug populations in Korea. Based on present study, it is urgent to restrict the use of pyrethroids and to introduce effective alternative insecticides. A nation-wide monitoring program to determine the pyrethroid resistance level in bed bugs and to select alternative insecticides should be implemented.
Cells can resist and even recover from stress induced by acute hypoxia, whereas chronic hypoxia often leads to irreversible damage and eventually death. Although little is known about the response(s) to acute hypoxia in neuronal cells, alterations in ion channel activity could be preferential. This study aimed to elucidate which channel type is involved in the response to acute hypoxia in rat pheochromocytomal (PC12) cells as a neuronal cell model. Using perfusing solution saturated with 95% $N_2$ and 5% $CO_2$, induction of cell hypoxia was confirmed based on increased intracellular $Ca^{2+}$ with diminished oxygen content in the perfusate. During acute hypoxia, one channel type with a conductance of about 30 pS (2.5 pA at -80 mV) was activated within the first 2~3 min following onset of hypoxia and was long-lived for more than 300 ms with high open probability ($P_o$, up to 0.8). This channel was permeable to $Na^+$ ions, but not to $K^+$, $Ca^+$, and $Cl^-$ ions, and was sensitively blocked by amiloride (200 nM). These characteristics and behaviors were quite similar to those of epithelial sodium channel (ENaC). RT-PCR and Western blot analyses confirmed that ENaC channel was endogenously expressed in PC12 cells. Taken together, a 30-pS ENaC-like channel was activated in response to acute hypoxia in PC12 cells. This is the first evidence of an acute hypoxia-activated $Na^+$ channel that can contribute to depolarization of the cell.
Methoxyverapamil, $Ca^{2+}$ channel blocker, when given intravenously by means of bolus, produced the transient increase of urine flow, and then methoxyverapamil was infused in this experiments. Methoxyverapamil, when infused into vein, elicited the increase of urine flow ancampanied with the increased glomeralar filtration rate(GFR), renal plasma flow(RPF), excretion amounts of sodium and potassium in urine($E_{Na},\;E_k$) and osmolar clearance(Cosm), wherease produced the no change of free water clearance($C_{H2O}$) and the reduction of reabsorption rates of sodium and potassium in reral tubules($R_{Na},\;R_k$). Methoxyverapamil, when infused into a renal artery, exhibited the diuretic action in only infused Kidney, at this time changes of renal function were the same aspect to that of intravenously infused methoxyverapamil. Methoxyverapamil, when infused into a carotid artery, exhibited the decreased urine flow along with the reduction of Cosm, $C_{H2O}\;and\;E_{Na}$. Above results suggest that methoxyverapamil possess both the diuretic action by direct action in kidney and antidiuretic action through the central function.
Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
/
1999.05a
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pp.434-437
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1999
An EM pump is used for the purpose of transporting the electrically conducting liquid sodium of the high temperature that is used as a coolant in the liquid metal reactor. In the present study, the pilot pump has been designed and manufactured for the high temperature of $600^{\circ}C$ by the equivalent circuit materials and the consideration of the materials and functions. The length and diameter of the pump are given as 84 cm and 10 cm each due to the fixed geometry of the circulation system to be installed. The characteristic of the developing pressure and efficiency is found out by using Laithewaite\`s standard design formula. It is shown that the developing pressure and efficiency are maximized at the frequency of 15 Hz from the curve. The annular channel gap of 3.95 mm is selected in the range of the reasonable hydraulic frictional loss. The components of the pump consist of the material for the high temperature. And then, the pump is manufactured to have the nominal flowrate of 40 1/min and developing Pressure of 1.3 bar.
The caudal subnucleus of the spinal trigeminal nucleus (medullary dorsal horn; MDH) receives direct inputs from small diameter primary afferent fibers that predominantly transmit nociceptive information in the orofacial region. Recent studies indicate that reactive oxygen species (ROS) is involved in persistent pain, primarily through spinal mechanisms. In this study, we aimed to investigate the role of xanthine/xanthine oxidase (X/XO) system, a known generator of superoxide anion ($O_2{^-}$), on membrane excitability in the rat MDH neurons. For this, we used patch clamp recording and confocal imaging. An application of X/XO ($300{\mu}M/30mU$) induced membrane depolarization and inward currents. When slices were pretreated with ROS scavengers, such as phenyl N-tert-butylnitrone (PBN), superoxide dismutase (SOD), and catalase, X/XO-induced responses decreased. Fluorescence intensity in the DCF-DA and DHE-loaded MDH cells increased on the application of X/XO. An anion channel blocker, 4,4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS), significantly decreased X/XO-induced depolarization. X/XO elicited an inward current associated with a linear current-voltage relationship that reversed near -40 mV. X/XO-induced depolarization reduced in the presence of $La^{3+}$, a nonselective cation channel (NSCC) blocker, and by lowering the external sodium concentration, indicating that membrane depolarization and inward current are induced by influx of $Na^+$ ions. In conclusion, X/XO-induced ROS modulate the membrane excitability of MDH neurons, which was related to the activation of NSCC.
SPLITT fractionation (SF) allows continuous (and thus a preparative scale) separation of micronsized particles into two size fractions ('fraction-a' and 'fraction-b'). SF is usually carried out in a thin rectangular channel with two inlets and two outlets, which is equipped with flow stream splitters at the inlet and the outlet of the channel, respectively. A new large scale splitter-less gravitational SF (GSF) system had been assembled, which was designed to eliminate the flow stream splitters and thus is operated by the full feed depletion (FFD) mode (FFD-GSF). In the FFD mode, there is only one inlet through which the sample is fed. There is no carrier liquid fed into the channel, and thus prevents the sample dilution. The effects of the sample-feeding flow rate, the channel thickness on the fractionation efficiency (FE, number % of particles that have the size predicted by theory) of FFD-GSF was investigated using industrial polyurethane (PU) latex beads. The carrier liquid was water containing 0.1% FL-70 (particle dispersing agent) and 0.02% sodium azide (used as bactericide). The sample loading rate was varied from about 4 to 7 L/hr with the sample concentration fixed at 0.01%. The GSF channel thickness was varied from 900 to $1300{\mu}m$. Particles exiting the GSF channel were collected and monitored by optical microscopy (OM). Sample recovery was monitored by collecting the fractionated particles on a $0.45{\mu}m$ membrane filter. It was found that FE of fraction-a was increased as the channel thickness increases, and FE of fraction-b was increased as the flow rate was increased. In all cases, the sample recovery has higher than 95%. It seems the new splitter-less FFD GSF system could become a useful tool for large scale separations of various types of micron-sized particles.
Park, Choon-ok;Kim, Yang-mi;Haan, Jae-hee;Hong, Seong-geun
Korean Journal of Veterinary Research
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v.34
no.1
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pp.25-36
/
1994
The inward tail current after a short depolarizing pulse has been known as Na-Ca exchange current activated by intracellular calcium which forms late plateau of the action potential in rabbit atrial myocytes. Chloride conductance which is also dependent upon calcium concentration has been reported as a possible tail current in many other excitable tissues. Thus, in order to investigate the exsitance of the calcium activated chloride current and its contribution to tail current, whole cell voltage clamp measurement has been made in single atrial cells of the rabbit. The current was recorded during repolarization following a brief 2 ms depolarizing pulse to +40mV from a holding potential of -70mV. When voltage-sensitive transient outward current was blocked by 2 mM 4-aminopyridine or replacement potassium with cesium, the tail current were abolished by ryanodine$(1{\mu}M)$ or diltiazem$(10{\mu}M)$ and turned out to be calcium dependent. The magnitudes of the tail currents were increased when intracellular chloride concentration was increased to 131 mM from 21 mM. The current was decreased by extracellular sodium reduction when intracellular chloride concentration was low(21 mM), but it was little affected by extracellular sodium reduction when intracellual chloride concentration was high(131 mM). The current-voltage relationship of the difference current before and after extracellular sodium reduction, shows an exponential voltage dependence with the largest magnitude of the current occurring at negative potentials, with is similar to current-voltage relationship at negative potentials, which is similar to current-voltage relationship of Na-Ca exchange current. The current was also decreased by $10{\mu}M$ niflumic acid and 1 mM bumetanide, which is well known anion channel blockers. The reversal potentials shifted according to changes in chloride concentration. The current-voltage relationships of the niflumic acid-sensitive currents in high and low concentration of chloride were well fitted to those predicted as chloride current. From the above results, it is concluded that calcium activated chloride component exists in the tail current with Na-Ca exchange current and it shows the reversal of tail current. Therefore it is thought that in the physiologic condition it leads to rapid end of action potential which inhibits calcium influx and it contributes to maintain the low intracellular calcium concentration with Na-Ca exchange mechanism.
Objectives: The pulp is the center of the tooth containing nerves and blood vessels. The condition in which the pulp becomes inflamed due to caries or periodontitis is called pulpitis. Pulpitis is a difficult-to-treat disease and causes peripheral nerve tissue changes and severe pain; however, the relationship between neuronal activity and voltage-gated sodium channel 1.7 (Nav1.7) expression in the trigeminal ganglion (TG) during pulpitis has not been well studied. In this study, we found that experimentally induced pulpitis activates Nav1.7 expression in the periphery, leading to neuronal overexpression in the TG. Thus, we sought to identify ways to regulate this process. Methods: Acute pulpitis was induced in rat maxillary molars by treating the pulp with allyl isothiocyanate (AITC). Three days later, in vivo optical imaging was used to record and compare neural activities in the TG. Western blotting was used to identify molecular changes in terms of the expression of extracellular signal-regulated kinase (ERK), c-Fos, transient receptor potential ankyrin 1 (TRPA1), and collapsin response mediator protein-2 (CRMP2) in the brain stem. Results: The results confirmed the neurological changes in the TGs of the pulpitis model, and histological and molecular biological evidence confirmed that increased Nav1.7 expression induced by pulpitis leads to pain. Furthermore, selective inhibition of Nav1.7 resulted in changes in neural activity, suggesting that pulpitis induces increased Nav1.7 expression, and that effective control of Nav1.7 could potentially reduce pain. Conclusions: The inhibition of overexpressed Nav1.7 channels may modulate nociceptive signal processing in the brain and effectively control pain associated with pulpitis.
This study was carried out to investigate the physiological changes induced acutely with the low doses of lead acetate in the synaptosomes from the cerebrum and brain stem of the rat. The general uptake patterns of [$^3$H]-serotonin were observed in synaptosomes, as a model of presynaptic nerve terminal, from the cerebrum and brain stem. And the effects of the low doses of lead acetate on the uptake process were investigated id vitro and in vivo. The Km value of the uptake of the [$^3$H]-serotonin by the synaptosomes was 0.5 $\mu$M in the cerebrum and 0.1 $\mu$M in the brain stem. These low values reveal that the synaptosomes from the cerebrum and the brain stem have a high affinity to [$^3$H]-serotonin, especially in brain stem. The uptake of $\mu$M-serotonin was dependant on the sodium and potassium ions. When being treated with ouabain, the $Na^+$$-K^+$ ATPase inhibitor, the uptake of [$^3$H]-serotonin was reduced. This supports strongly that the uptake of [$^3$H]-serotonin was sensitive to the changes of the concentrations of the sodium and potassium ions. When the calcium channel blocker, verapamil, was treated, the uptake of [$^3$H]-serotonin was changed only in synaptosomes from the brain stem. The uptake of [$^3$H]-serotonin was reduced by the lead treatment in the synaptosomes from the cerebrum and brain stem in vitro and in vivo. [lead acetate, synaptosomes, $^3$H-serotonin, rat]
Na Kyeong Park;Seong Woo Choi;Soon-Jung Park;JooHan Woo;Hyun Jong Kim;Woo Kyung Kim;Sung-Hwan Moon;Hun-Jun Park;Sung Joon Kim
The Korean Journal of Physiology and Pharmacology
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v.28
no.4
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pp.313-322
/
2024
Mutations within the SCN5A gene, which encodes the α-subunit 5 (NaV1.5) of the voltage-gated Na+ channel, have been linked to three distinct cardiac arrhythmia disorders: long QT syndrome type 3, Brugada syndrome (BrS), and cardiac conduction disorder. In this study, we have identified novel missense mutations (p.A385T/R504T) within SCN5A in a patient exhibiting overlap arrhythmia phenotypes. This study aims to elucidate the functional consequences of SCN5A mutants (p.A385T/R504T) to understand the clinical phenotypes. Whole-cell patch-clamp technique was used to analyze the NaV1.5 current (INa) in HEK293 cells transfected with the wild-type and mutant SCN5A with or without SCN1B co-expression. The amplitude of INa was not altered in mutant SCN5A (p.A385T/R504T) alone. Furthermore, a rightward shift of the voltage-dependent inactivation and faster recovery from inactivation was observed, suggesting a gain-of-function state. Intriguingly, the co-expression of SCN1B with p.A385T/R504T revealed significant reduction of INa and slower recovery from inactivation, consistent with the loss-of-function in Na+ channels. The SCN1B dependent reduction of INa was also observed in a single mutation p.R504T, but p.A385T co-expressed with SCN1B showed no reduction. In contrast, the slower recovery from inactivation with SCN1B was observed in A385T while not in R504T. The expression of SCN1B is indispensable for the electrophysiological phenotype of BrS with the novel double mutations; p.A385T and p.R504T contributed to the slower recovery from inactivation and reduced current density of NaV1.5, respectively.
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