• The Korean Journal of Physiology and Pharmacology
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• v.17 no.6
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• pp.553-558
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• 2013

Spinal dorsal horn nociceptive neurons have been shown to undergo long-term synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD). Here, we focused on the spinothalamic tract (STT) neurons that are the main nociceptive neurons projecting from the spinal cord to the thalamus. Optical technique using fluorescent dye has made it possible to identify the STT neurons in the spinal cord. Evoked fast mono-synaptic, excitatory postsynaptic currents (eEPSCs) were measured in the STT neurons. Time-based tetanic stimulation (TBS) was employed to induce long-term potentiation (LTP) in the STT neurons. Coincident stimulation of both pre- and postsynaptic neurons using TBS showed immediate and persistent increase in AMPA receptor-mediated EPSCs. LTP can also be induced by postsynaptic spiking together with pharmacological stimulation using chemical NMDA. TBS-induced LTP observed in STT neurons was blocked by internal BAPTA, or $Ni^{2+}$, a T-type VOCC blocker. However, LTP was intact in the presence of L-type VOCC blocker. These results suggest that long-term plastic change of STT neurons requires NMDA receptor activation and postsynaptic calcium but is differentially sensitive to T-type VOCCs.

• Design & Manufacturing
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• v.6 no.2
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• pp.24-30
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• 2012

In this study, the hot forging technology for precision forming of spline teeth of the inner race in the auto-transmission was developed in order to minimize its finishing allowance. Several blocker and finisher shapes for the precision hot forging process of the inner race were proposed and the forging processes were analyzed using the three-dimensional finite element method. The optimum hot forging process was obtained considering some parameters such as metal flow patterns, forging defects and forming load. Blocker and finisher dies for the hot forging process were designed by selecting the most suitable shapes obtained from the finite element analysis. Experimental works were also performed in order to verify the optimum design of hot forging process.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.1
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• pp.112-117
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• 2013

We studied the modulation of pacemaker activities by Samchulkunbi-tang (SCKB) in cultured interstitial cells of Cajal (ICC) from murine small intestine with the whole-cell patch-clamp technique. Externally applied SCKB produced membrane depolarization in the current-clamp mode. The pretreatment with $Ca^{2+}$-free solution and thapsigargin, a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker potentials and suppressed the SCKB-induced action. The application of flufenamic acid (a nonselective cation channel blocker) abolished the generation of pacemaker potentials by SCKB. However, the application of niflumic acid (a chloride channel blocker) did not inhibit the generation of pacemaker potentials by SCKB. In addition, the membrane depolarizations were inhibited by not only GDP-${\beta}$-S, which permanently binds G-binding proteins, but also U-73122, an active phospholipase C inhibitor. These results suggest that SCKB modulates the pacemaker activities by nonselective cation channels and external $Ca^{2+}$ influx and internal $Ca^{2+}$ release via G-protein and phospholipase C-dependent mechanism. Therefore, the ICC are targets for SCKB and their interaction can affect intestinal motility.

• Korean Journal of Veterinary Service
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• v.31 no.4
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• pp.457-463
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• 2008

The sex steroid hormone estradiol-$17{\beta}(E_2)$ mediate their biological effects on development, differentiation and maintenance of reproductive tract and other target tissue through gene regulation by nuclear steroid receptors. Although the importance of $E_2$ in many physiological process has been reported, but little is known about the effects of $E_2$ on primary cultured chicken hepatocyte. therefore, in the present study, we have examined the effect of $E_2$ on cell proliferation and it's related signal cascades. $E_2$ increase $[^3H]$-thymidine incorporation in time-(${\leq}8hr$) and dose-($10^{-10}M$)dependent manner and treatment of $E_2$ increased the phosphorylation of p44/43 MAPKs(p44/42 mitogen-activated protein kinase) and JNK(c-Jun N-terminal kinase) in a time dependent manner. In addition, PD98059(p44/42 blocker, $10^{-5}M$), SP600125(JNK blocker, $10^{-6}M$) blocked the estrogen-induced increase in $[^3H]$-thymidine incorporation. In conclusion, $E_2$ stimulates the proliferation of primary cultured chicken hepatocytes and this action is mediated by p44/42 MAPKs and JNK signal transduction pathway.

• Journal of the Korean Applied Science and Technology
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• v.23 no.4
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• pp.355-361
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• 2006

[1,2,4]-Triazole derivatives were synthesized by 5 steps. Benzimidazole was refluxed with ethyl chloroacetate to give 1H-benzimidazole-acetic acid ethyl ester (1) over 52% yield. Ester (1) was refluxed with hydrazine hydrate in the presence of ethanol to afford 1H-benzimidazole-1-acetic acid, hydrazide (2). 5-Benzoimidazol-1-ylmethyl-4H-[1,2,4]triazole-3-thiol (4) was made via coupling of compound (2) with methyl isothiocyanate, followed by cyclization of 1H-benzimidazole-1-acetic acid, 2-[(methylamino) thioxomethyl]hydrazide (3) on reflux, and finally the target compounds (6a-6v) were synthesized by general substitution reaction. Compounds (6a-6v) were screened for T-type calcium channel blocker using the fluorescence assay by FDSS6000. All compounds (6a-6v) did not show better activities than control compound, mibefradil.

• Clinical and Experimental Reproductive Medicine
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• v.21 no.1
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• pp.111-119
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• 1994

"Spontaneous" hardening of the zona pellucida of mouse oocytes during in vitro culture is most likely due to cortical granules exocytosis. Thus the purpose of the present study was to determine whether the exocytosis factor is involved in spontaneous zona pellucida hardening during in vitro culture of the mouse. The results obtained form these experiments were summarized as follows; 1. When a protein synthesis inhibitor(100${\mu}g$/ml puromycin) was added to the culture medium, it did not prevent spontaneous ZPH of mouse oocyte during in vitro culture. 2. Calmodulin antagonists (trifluoperazine and chlorpromazine) and calcium channel blocker (verapamil) had no inhibitory effect in spontaneous ZPH. 3. A microtubule assembly inhibitor, colcemid had some inhibitory effect on spontaneous ZPH. 4. Treatment with a microfillament formation blocker(cytochalasin-B) at 1${\mu}g$/ml concentration, resulted in the excellent inhibitory effect on spontaneous ZPH. However cytochalasin-B did not inhibit ethanol-induced ZPH.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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• pp.461-467
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• 2009

The auditory cortex (A1) encodes the acquired significance of sound for the perception and interpretation of sound. Nitric oxide (NO) is a gas molecule with free radical properties that functions as a transmitter molecule and can alter neural activity without direct synaptic connections. We used whole-cell recordings under voltage clamp to investigate the effect of NO on spontaneous GABAergic synaptic transmission in mechanically isolated rat auditory cortical neurons preserving functional presynaptic nerve terminals. GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) in the A1 were completely blocked by bicuculline. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), reduced the GABAergic sIPSC frequency without affecting the mean current amplitude. The SNAP-induced inhibition of sIPSC frequency was mimicked by 8-bromoguanosine cyclic 3',5'-monophosphate, a membrane permeable cyclic-GMP analogue, and blocked by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger. Blockade of presynaptic $K^+$ channels by 4-aminopyridine, a $K^+$ channel blocker, increased the frequencies of GABAergic sIPSCs, but did not affect the inhibitory effects of SNAP. However, blocking of presynaptic $Ca^{2+}$ channels by $Cd^{2+}$, a general voltage-dependent $Ca^{2+}$ channel blocker, decreased the frequencies of GABAergic sIPSCs, and blocked SNAP-induced reduction of sIPSC frequency. These findings suggest that NO inhibits spontaneous GABA release by activation of cGMP-dependent signaling and inhibition of presynaptic $Ca^{2+}$ channels in the presynaptic nerve terminals of A1 neurons.

• KSBB Journal
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• v.13 no.1
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• pp.71-76
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• 1998

Tissue biosensor for mearsuring sodium channel blockers, such tetrodotoxin(TTX), saxitoxin (STX) and paralytic shellfish poisoning(PSP) consisted of frog bladder membrane, and $Na^{+}$ electrode. The proposed biosensor was applied to determine Chinese drug and dry or wet Porphyra yezonesis $Na^{+}$ channel blockers below the detection limit of the standard mouse bio-assay while the observed detection limit didn't cause human poisoning. The proposed biosensor system may be used for future $Na^{+}$ channel blockers monitoring within the marine environment.

• Journal of The Korean Society of Clinical Toxicology
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• v.18 no.1
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• pp.1-10
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• 2020

Pharmaceutical agents are the most common causes of poisoning in Korea. Calcium channel blockers (CCBs) are commonly used in Korea for the management of hypertension and other cardiovascular diseases, but are associated with a risk of mortality due to overdose. Due to the frequent fatalities associated with CCB overdose, it is essential that the emergency physician is capable of identifying CCB intoxication, and has the knowledge to manage CCB overdose. This article reviews the existing clinical guidelines, retrospective studies, and systematic reviews on the emergency management of CCB overdose. The following are the varied treatments of CCB overdose currently administered. 1) For asymptomatic patients: observation with enough time and decontamination, if indicated. 2) For symptomatic patients: infusion of calcium salt, high dose insulin therapy, and vasopressor (norepinephrine) or atropine for bradycardia. 3) For patients refractory to the first line therapy or with refractory shock or impending arrest: lipid emulsion therapy and extracorporeal membrane oxygenation. 4) As adjunct therapy: phosphodiesterase inhibitors, glucagon, methylene blue, pacemaker for AV block. Small CCB ingestion is known to be fatal for pediatric patients. Hence, close observation for sufficient time is required.

• 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.