• Journal of Photoscience
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• 제1권1호
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• pp.75-82
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• 1994

General features of the fluorescence depolarization are briefly reviewed. Molecular rotations and electronic excitation transports are considered to account for the fluorescence depolarization. Various molecular systems studied by the fluorescence depolarization are described. The FiSrster theory which forms a basis for the energy transfer is revisited. Several theoretical treatments for the fluorescence depolarization in liquid and solid phases such as classical hydrodynamics, probability distribution function, Green's function formalism, molecular dynamics simulation and Monte Carlo methods are introduced.

• BMB Reports
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• 제31권5호
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• pp.468-474
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• 1998

Membrane depolarization in PC12 cells induces calcium influx via an L-type voltage-sensitive calcium channel (L-VSCC) and increases intracellular free calcium, which leads to tyrosine phosphorylation of epidermal growth factor (EGF) receptor and the associated adaptor protein, She. This activated EGF receptor complex then can activate mitogen-activated protein (MAP) kinase, as in nerve growth factor (NGF) receptor activation. In the present study, we investigated the role of EGF receptor in the signaling pathway initiated by membrane depolarization of PC12 cells. Prolonged membrane depolarization induced phosphorylation of extracellular signal-regulated kinase (ERK) within 1 min in undifferentiated PC12 cells. Pretreatment of PC12 cells with the calcium chelator EGTA abolished depolarization-stimulated ERK phosphorylation, but NGF-induced phosphorylation of ERK was not affected. The chronic treatment of phorbol ester, which down-regulated the activity of protein kinase C (PKC), did not affect the phosphorylation of ERK upon depolarization. In the presence of an inhibitor of EGF receptor, neither depolarization nor calcium ionophore increased the level of ERK phosphorylation. These data imply that the EGF receptor is functionally necessary to activate ERK and neurite outgrowth in response to the prolonged depolarization in PC12 cells, and also that PKC is apparently not involved in this signaling pathway.

• International Journal of Oral Biology
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• 제33권3호
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• pp.117-123
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• 2008

Reactive oxygen species (ROS) are toxic agents that may be involved in various neurodegenerative diseases. Recent studies indicate that ROS can act as modulators of neuronal activity, and are critically involved in persistent pain primarily through spinal mechanisms. In the present study, whole cell patch clamp recordings were carried out to investigate the effects of tert-buthyl hydroperoxide (t-BuOOH), an ROS, on neuronal excitability and the mechanisms underlying changes of membrane excitability. In current clamp condition, application of t-BuOOH caused a reversible membrane depolarization and firing activity in substantia gelatinosa (SG) neurons. When slices were pretreated with phenyl-N-tert-buthylnitrone (PBN) and ascorbate, ROS scavengers, t-BuOOH failed to induce membrane depolarization. However, isoascorbate did not prevent t-BuOOH-induced depolarization, suggesting that the site of ROS action is intracellular. The t-BuOOH-induced depolarization was not blocked by pretreatment with dithiothreitol (DTT), a sulfhydryl-reducing agent. The membrane-impermeant thiol oxidant 5,5-dithiobis 2-nitrobenzoic acid (DTNB) failed to induce membrane depolarization, suggesting that the changes of neuronal excitability by t-BuOOH are not caused by the modification of extrathiol group. The t-BuOOH-induced depolarization was suppressed by the phospholipase C (PLC) blocker U-73122 and inositol triphosphate ($IP_3$) receptor antagonist 2-aminoethoxydiphenylbolate (APB), and after depletion of intracellular $Ca^{2+}$ pool by thapsigargin. These data suggest that ROS generated by peripheral nerve injury can induce central sensitization in spinal cord, and t-BuOOH-induced depolarization may be regulated by intracellular $Ca^{2+}$ store mainly via $PLC-IP_3$ pathway.

• 대한원격탐사학회지
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• 제32권2호
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• pp.97-104
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• 2016

본 연구에서는 일본 오사카에서 AERONET 선포토미터로 관측된 데이터를 분석하여 440, 675, 870, 1020 nm 파장에서의 입자 편광소멸도를 산출하였다. 산출된 결과는 같은 지역에서 측정된 라이다 자료로부터 얻어진 532 nm에서의 입자 편광소멸도와 비교하였다. 두 값은 440 nm를 제외하고는 잘 일치되는 결과를 보였고, 상관계수($R^2$)는 440, 675, 870, 1020 nm에서 각각 0.28, 0.81, 0.88 0.89의 값을 보였다. 가장 높은 상관계수를 보인 1020 nm에서의 입자 편광소멸도를 기준으로 값의 변화에 따른 입자의 혼합정도를 확인하였을 때, 순수 황사의 경우 높은 편광소멸도를 보이고 오염입자가 혼합될수록 값이 낮아짐을 보였다. 이는 단산란 알베도와 입자 크기 분포를 통하여 확인하였다.

• 대한원격탐사학회지
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• 제32권3호
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• pp.245-251
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• 2016

황사의 주요 발원지인 중국 북부 둔황지역에 선포토미터를 설치하여 440, 675, 870 그리고 1020 nm 채널에서 황사의 파장별 입자편광소멸도를 산출하였다. 이와 함께 발원한 황사가 장거리 수송과정에 위치한 제주 고산과 일본 오사카에 설치된 선포토미터를 함께 분석하였다. 황사 발원지에서 1020 nm 파장에서 입자편광소멸도가 0.34로 가장 높은 수치를 보였다. 또한, 초미세먼지농도가 증가하는 경우 입자편광소멸도는 감소하는 경향을 보였다. 우리는 본 연구에서 선포토미터의 입자편광소멸도 산출을 통해 에어로졸에서 황사의 구성 비율이 변화함을 확인하였다.

• 대한의용생체공학회:의공학회지
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• 제15권4호
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• pp.407-412
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• 1994

This paper describes the construction of an anisotropic three dimensional ventricular model based on the bidomain model. The cardiac activation process in the normal cardiac cell and the myocardial ischemic cell are simulated by the Huygen's principle. The depolarization process in the myocardial ischemia displays the delayed activation compared to the normal state. The repolarization process is simulated by the myocardial potential at the arbitrary ellapsed time after activation process. Using the potential data, the equivalent cardiac source at the arbitrary time can be computed. In conclusion, this simulation suggests the possibilities of the depolarization and the repolarization process in the normal and abnormal myocardiac cells.

• 한국대기환경학회지
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• 제11권4호
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• pp.315-321
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• 1995

The purpose of this report is to describe the lidar measurement of depolarization ratios of particulate matter (Depolarization Ratio of Yellow Sand) and to discuss the transformation of aerosols due to Yellow Sand event. The scattering profile shows high level during Yellow Sand event and scattering layers are thicker as compared to other seasons in about 3 .sim. 8km, and the values and mode height of scattering ratio corresponed with depolarization ratio. A distribution of total depolarization ratio during the observation period was 44.7 percent among total cases of 0.03 < Dt < 0.5 with scattering ratio > 30 and relative humidity < 30 was satisfied (popular Yellow Sand type).

• 한국세라믹학회지
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• 제40권3호
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• pp.225-228
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• 2003

A Bender typed Multilayer Actuator(BMA) for decreasing the depolarization effect was designed and fabricated. Unlike bimorph and multimorph actuators in which depolarization occurred, the BMA did not generate depolarization because the polarization and the electric field directions are the same. The simulated results indicate that higher displacement of the BMA can be achieved by increasing input voltage. Compared with the multimorph actuator, the proposed actuator is expected to extend a life time as well as acceptable voltage range.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.167.1-167.1
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• 2003

Here we show that panaxadiol, a ginseng saponin with a dammarane skeleton, induces acute apoptotic cell death in human hepatoma SK-HEP-1 cells as evidenced by analysis of DNA fragmentation, caspase activation, and changes in cell morphology. The kinetic study showed that panaxadiol-induced apoptosis is associated with depolarization of mitochondrial membrane potential and cytochrome c release. Sequential activations of caspases-depolarization of mitochondrial membrane potential and cytochrome c release. Sequential activations of caspases-9, and -3, or -7, but not of caspase 8 coincide well in a time dependent manner with mitochondrial membrane depolarization and cytochrome c release from mitochondria during apoptosis of SK-HEP-1 cells induced by treatment with panaxadiol. (omitted)

• International Journal of Oral Biology
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• 제33권4호
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• pp.217-221
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• 2008

Bicuculline is one of the most commonly used $GABA_A$ receptor antagonists in electrophysiological research. Because of its poor water solubility, bicuculline quaternary ammonium salts such as bicuculline methiodide (BMI) and bicuculline methbromide are preferred. However, a number of studies have shown that BMI has non-$GABA_A$ receptor-mediated effects. The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) is implicated in the processing of nociceptive signaling. In this study, we investigated whether BMI has non-GABA receptor-mediated activity in Vc SG neurons using a whole cell patch clamp technique. SG neurons were depolarized by application of BMI ($20{\mu}M$) using a high $Cl^-$ pipette solution. GABA ($30-100{\mu}M$) also induced membrane depolarization of SG neuron. Although BMI is known to be a $GABA_A$ receptor antagonist, GABA-induced membrane depolarization was enhanced by co-application with BMI. However, free base bicuculline (fBIC) and picrotoxin (PTX), a $GABA_A$ and $GABA_C$ receptor antagonist, blocked the GABA-induced response. Furthermore, BMI-induced membrane depolarization persisted in the presence of PTX or an antagonist cocktail consisting of tetrodotoxin ($Na^+$ channel blocker), AP-5 (NMDA receptor antagonist), CNQX (non-NMDA receptor antagonist), and strychnine (glycine receptor antagonist). Thus BMI induces membrane depolarization by directly acting on postsynaptic Vc SG neurons in a manner which is independent of $GABA_A$ receptors. These results suggest that other unknown mechanisms may be involved in BMI-induced membrane depolarization.