• Title/Summary/Keyword: Transient recovery voltage

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Open channel block of Kv1.4 potassium channels by aripiprazole

  • Park, Jeaneun;Cho, Kwang-Hyun;Lee, Hong Joon;Choi, Jin-Sung;Rhie, Duck-Joo
    • The Korean Journal of Physiology and Pharmacology
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    • v.24 no.6
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    • pp.545-553
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    • 2020
  • Aripiprazole is a quinolinone derivative approved as an atypical antipsychotic drug for the treatment of schizophrenia and bipolar disorder. It acts as with partial agonist activities at the dopamine D2 receptors. Although it is known to be relatively safe for patients with cardiac ailments, less is known about the effect of aripiprazole on voltage-gated ion channels such as transient A-type K+ channels, which are important for the repolarization of cardiac and neuronal action potentials. Here, we investigated the effects of aripiprazole on Kv1.4 currents expressed in HEK293 cells using a whole-cell patch-clamp technique. Aripiprazole blocked Kv1.4 channels in a concentration-dependent manner with an IC50 value of 4.4 μM and a Hill coefficient of 2.5. Aripiprazole also accelerated the activation (time-to-peak) and inactivation kinetics. Aripiprazole induced a voltage-dependent (δ = 0.17) inhibition, which was use-dependent with successive pulses on Kv1.4 currents without altering the time course of recovery from inactivation. Dehydroaripiprazole, an active metabolite of aripiprazole, inhibited Kv1.4 with an IC50 value of 6.3 μM (p < 0.05 compared with aripiprazole) with a Hill coefficient of 2.0. Furthermore, aripiprazole inhibited Kv4.3 currents to a similar extent in a concentration-dependent manner with an IC50 value of 4.9 μM and a Hill coefficient of 2.3. Thus, our results indicate that aripiprazole blocked Kv1.4 by preferentially binding to the open state of the channels.

A Capacitorless Low-Dropout Regulator With Enhanced Response Time (응답 시간을 향상 시킨 외부 커패시터가 없는 Low-Dropout 레귤레이터 회로)

  • Yeo, Jae-Jin;Roh, Jeong-Jin
    • Journal of IKEEE
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    • v.19 no.4
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    • pp.506-513
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    • 2015
  • In this paper, an output-capacitorless, low-dropout (LDO) regulator is designed, which consumes $4.5{\mu}A$ quiescent current. Proposed LDO regulator is realized using two amplifier for good load regulation and fast response time, which provide high gain, high bandwidth, and high slew rate. In addition, a one-shot current boosting circuit is added for current control to charge and discharge the parasitic capacitance at the pass transistor gate. As a result, response time is improved during load-current transition. The designed circuit is implemented through a $0.11-{\mu}m$ CMOS process. We experimentally verify output voltage fluctuation of 260mV and recovery time of $0.8{\mu}s$ at maximum load current 200mA.

Design of AC/DC Combined V2X System for Small Electric Vehicle (소형 전기차 적용을 위한 AC/DC 복합 V2X 시스템 설계)

  • Kim, Yeong-Jung;Chang, Young-Hag;Moon, Chae-Joo
    • The Journal of the Korea institute of electronic communication sciences
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    • v.17 no.4
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    • pp.617-624
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    • 2022
  • The small electric vehicles equipped with V2X(vehicle to everything) systems may provide more information and function to the existing navigation system of the vehicle. The key components of V2X technology include V2V (vehicle to vehicle), V2N(vehicle to network) and V2I (vehicle to infrastructure). This study is to design and implementation of VI type E-PTO which is interfaced with external equipments, the work designs the components of E-PTO such as DC/DC converter, DC/AC converter, battery bidirectional charging system etc. Also, it implements the devices and control systems for driving. The test results of VI type E-PTO components showed allowable 10% requirements of transient voltage variation rate and recovery time within 100ms for start/stop and normal operation.

Effect of Reperfusion after 20 min Ligation of the Left Coronary Artery in Open-chest Bovine Heart: An Ultrastructural Study (재관류가 허혈 심근세포의 미세구조에 미치는 영향 : 재관류 손상에 관한 연구)

  • 이종욱;조대윤;손동섭;양기민;라봉진;김호덕
    • Journal of Chest Surgery
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    • v.31 no.8
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    • pp.739-748
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    • 1998
  • Background: It has been well documented that transient occlusion of the coronary artery causes myocardial ischemia and finally cell death when ischemia is sustained for more than 20 minutes. Extensive studies have revealed that ischemic myocardium cannot recover without reperfusion by adequate restoration of blood flow, however, reperfusion can cause long-lasting cardiac dysfunction and aggravation of structural damage. The author therefore attempted to examine the effect of postischemic reperfusion on myocardial ultrastructure and to determine the rationales for recanalization therapy to salvage ischemic myocardium. Materials and methods: Young Holstein-Friesian cows(130∼140 Kg body weight; n=40) of both sexes, maintained with nutritionally balanced diet and under constant conditions, were used. The left anterior descending coronary artery(LAD) was occluded by ligation with 4-0 silk snare for 20 minutes and recanalized by release of the ligation under continuous intravenous drip anesthesia with sodium pentobarbital(0.15 mg/Kg/min). Drill biopsies of the risk area (antero-lateral wall) were performed at just on reperfusion(5 minutes), 1-, 2-, 3-, 6-, 12-hours after recanalization, and at 1-hour assist(only with mechanical respiration and fluid replacement) after 12-hour recanalization. The materials were subdivided into subepicardial and subendocardial tissues. Tissue samples were examined with a transmission electron microscope (Philips EM 300) at the accelerating voltage of 60 KeV. Results: After a 20-minute ligation of the LAD, myocytes showed slight to moderate degree of ultrastructural changes including subsarcolemmal bleb formation, loss of nuclear matrix, clumping of chromatin and margination, mitochondrial destruction, and contracture of sarcomeres. However, microvascular structures were relatively well preserved. After 1-hour reperfusion, nuclear and mitochondrial matrices reappeared and intravascular plugging by polymorphonuclear leukocytes or platelets was observed. However, nucleoli and intramitochondrial granules reappeared within 3 hours of reperfusion and a large number of myocytes were recovered progressively within 6 hours of reperfusion. Recovery was apparent in the subepicardial myocytes and there were no distinct changes in the ultrastructure except narrowed lumen of the microvessels in the later period of reperfusion. Conclusions: It is likely that the ischemic myocardium could not be salvaged without adequate restoration of coronary flow and that the microvasculature is more resistant to reversible period of ischemia than subendocardium and subepicardium. Therefore, thrombolysis and/or angioplasty may be a rational method of therapy for coronarogenic myocardial ischemia. However, it may take a relatively longer period of time to recover from ischemic insult and reperfusion injury should be considered.

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