• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.297-297
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• 1994

It has been known that adrenal corticosteroids influence the expression of adrenomedullary catecholamine-synthetizing enzymes and also suppress the emission of axonal-like processes in cultured chromaffin cells. In the present study, it was attempted ta investigate the effect of 17${\alpha}$-estradiol on catecholamine(CA) secretion evoked by acetylcholine(ACh), DMPP, McN-A-343, excess K$\^$+/ and Bay-K-8644 from the isolated perfused rat adrenal gland. The perfusion of 17${\alpha}$-estradiol (10$\^$-6/ 10$\^$-4/M) me an adrenal vein for 20min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.5 ${\times}$ 10$\^$-3/M), DMPP (10$\^$-4/M for 2min), McN-A-343 (10$\^$-4/M for 4min) and Bay-K-8644 (10$\^$-5/M for 4min), while did not affect the CA secretory effect of high K$\^$+/(5.6 x 10$\^$-2/M). Also, in the presence of 17${\beta}$-estradiol, CA secretion of ACh, DMPP and McN-A-343 without any effect on excess K$\^$+/-evoked CA secretion. However, in adrenal glands preloaded with 17${\alpha}$-estradiol (10$\^$-5/M) plus tamoxifen (10$\^$-5/M), which is known to be a selective antagonist of estrogen receptors (for 20min), CA secretory responses evoked by ACh, DMPP and McN-A-343 were considerably recovered as compared to that of 17${\alpha}$-estradiol only, but excess K$\^$+/-induced CA secretion was not affected.

• Archives of Pharmacal Research
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• v.15 no.2
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• pp.115-125
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• 1992

An attempt was made to investigate the effect of TMB-8[3, 4, 5-trimethoxybenzoate-8 (N, N-diethylamino) octyl ester], which is known to be an inhibitor of intracellular $Ca^{2+}$ release, on catecholamines (CA) secretion evoked by Ach, excess $K^+$, DMPP, McN-A-343 and caffeine from the isolated perfused rat adrenal glands and to cleaify its mechanism of action. The pretreatment with a low dose of TMB-8 $(10 \mu{M)}$ for 20 min led to marked inhibition in CA secretion evoked by Ach (5.32 mM), excess K^+$ (56 mM), DMPP $(100\;\mu{M)}$, McN-A-343 $(100 \mu{M)}$ and BAY-K 8644 $(10^{-5}M)$. Caffeine-induced CA secretion was simimlar to that of control only during the first periods (0-3 min) but thereafter maked inhibition in CA secretion evoked by caffeine was observed during the rest periods up to 30 min. The increased moderate concentration of TMB-8 $(30 \;\mu{M)}$ caused the result similar to that of $10 \;\mu{M}$ TMB-8. However, in adrenal glands preloaded with a high dose of TMB-8 $(100\;\mu{M)}$, CA releases evoked by Ach, excess $K^+$, DMPP, McN-A-343 and caffeine were almost completely blocked by the drug. These experimental data demonstrate that TMB-8 may inhibit cholinergic receptor-mediated and also depolarization-dependent Ca secretion, suggenesting that these TMB-8 effects seem to be mediated through inhibiting influx of extracellular calcium into the rat adrenal medullary chromaffin cells as well as reducing the release of calcium from intracellular sources.

• 한국전기화학회:학술대회논문집
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• 1998.10a
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• pp.24-24
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• 1998

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.242-242
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• 1996

The influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K$\^$+/ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100 uM) into an adrenal vein for 20min produced relatively a dose-dependent inhibition in CA secretion evoked by ACh (5.32mM), excess K$\^$+/ (56mM), DMPP (a selective nicotinic receptor agonist, 100uM for 2min), McN-A-343 (a muscarinic receptor agonist, 100uM for 4min), Bay-K-8644 (a calcium channel activator, 10 uM for 4min) and cyclopiazonic acid (a releaser of intracellular Ca$\^$2+/, 10uM for 4min).

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.20 no.2 s.33
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• pp.171-178
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• 2007

Objective : The aim of this study was to evaluate Yangdorak and D.I.T.I. for analysis of Symptom-complexes. Method : This study was selected 26 acne patients in Dongshin University Oriental Medical Hospital. We used Yangdorak (SME5800N, Sord Medicom Co., Korea) and D.I.T.I. (Digital Infrared Thermal Imaging 256, Dorex Inc, Orange CA, USA) and investigated the results of Yangdorak and D.I.T.I.. We made a comparison according to Deficiency or Excess(虛實) of acne patients. Result : In comparing Yangdorak results according to Deficiency or Excess(虛實) of acne patients, Triple-energizer(三焦), Intestine(大腸), Liver(肝), Stomach(胃) meridian in Excess group are higher than Deficiency group, and Kidney(腎) meridian in Deficiency group are lower than Excess group. D.I.T.I. reveald hyperthemia of face and chest on acne patients. The temperature of face and chest on Excess group is higher than Deficiency group. There is no statistically significant value compared with data of other group.

• The Korean Journal of Physiology
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• v.21 no.1
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• pp.1-12
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• 1987

There is evidence that the effect of extracellular $Ca^{2+}$ on heart rate is temperature-dependent: at $38^{\circ}C$ excess $Ca^{2+}$ induces positive chronotropic response, whereas at $30^{\circ}C$ there is no significant chronotropic effect of $Ca^{2+}$. The cause of this temperature-dependency, however, remains still unclear. Therefore, this study was undertaken to investigate the chronotropic effect of external $Ca^{2+}$ at different temperature in the isolated rabbit atria and in the small strips of SA node cut perpendicularly to crista terminalis. In the isolated atria, the $Ca^{2+}$ effect was temperature-dependent: at $35^{\circ}C$ excess $Ca^{2+}$ evoked positive chronotropic response, while at $30^{\circ}C$ there was no significant changes in sinus rate. On the contrary, in the small SA strips external $Ca^{2+}$ induced negative chronotropic effect. At $35^{\circ}C$ changes in $Ca^{2+}$ concentration from 2 to 4, 6, and 10 mM decreased the sinus rate by $2.7{\pm}1.6%$, $11.2{\pm}3.7%$ and $23.2{\pm}8.1%$ respectively. Lowering the temperature to $30^{\circ}C$, the negative chronotropic effect of $Ca^{2+}$ became greater. With intracellular microelectrodes transmembrane potential was recorded in the small SA strips at $30^{\circ}C$, $35^{\circ}C$ and $38^{\circ}C$. As temperature increased from 30 to $38^{\circ}C$, sinus rate was accelerated by $13/min/^{\circ}C$, $APD_{50}$(action ptential duration from peak to 50% repolarization) decreased by $5\;msec/^{\circ}C$, and amplitude of action potential was slightly decreased. With an increase in $Ca^{2+}$ concentrations from 0.5 to 6 mM, overshoot increased and MDP decreased. These $Ca^{2+}$ effects on the overshoot and MDP of action potentials were not altered by temperature. But the $Ca^{2+}$ effects on the rates of diastolic depolarization, systolic depolarization and repolarization were modified by temperature. Discrpancy of the chronotropic effects of $Ca^{2+}$ between isolated atria and small SA strips was discussed.

• Journal of the Korean Ceramic Society
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• v.32 no.9
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• pp.1033-1039
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• 1995

The current experiment has quantitatively investigated the effect of the content of CaO and SiO2 on the microstructure, density, electrical resistivity, power loss and initial permeability of manganese zinc ferrites. The density increased initially with CaO and SiO2 content and the further addition showed an adverse effect. The excess addition of CaO and SiO2 developed a discontinuous grain growth with numerous pores inside grains and lowered the electrical resistivity. The initial permeability decreased with increasing the content of SiO2. The samples with relatively low power loss showed that half of the total loss at 10$0^{\circ}C$, 100 kHz and 2000 Gauss was due to the eddy current loss.

• Journal of Plant Biology
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• v.39 no.3
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• pp.173-177
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• 1996

A novel calcium binding protein (CaBP) was purified to electrophoretic homogeneity from Dunaliella salina. In the course of purification experiment, this CaBP was identified as a monomer and its molecular weight was about 21 kDand isoelectric point (pI) value was about 4.1 using isoelectrofocusing. This CaBP was able to bind Ca2+ even in the pressence of an excess MgCl2 and KCI both in solution. In the SDS-PAGE, the Ca2+-bound form was slower than the Ca2+-free form in the nondenaturing PAGE. This means that the CaBP undergoes conformational change in the Ca2+-bound condition. Furthermore, UV absorption spectrum and fluorescence intensity of this CaBP was investigated. UV absorption peak was appeared at about 258 nm and decreased somewhat in Ca2+-bound condition. In the measurement of fluorescence, maximum intensity was appeared at 303 nm and decreased in Ca2+-bound state, similarly as UV absorption spectrum. These show distinct changes upon Ca2+-binding, which indicate of structural and/or dynamic changes largely reminiscent of other members of the EF-hand Ca2+-binding protein family.

• Korea-Australia Rheology Journal
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• v.21 no.1
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• pp.59-69
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• 2009

The prediction of pressure drop for a droplet flow in a confined micro channel is presented using FE-FTM (Finite Element - Front Tracking Method). A single droplet is passing through 5:1:5 contraction - straight narrow channel - expansion flow domain. The pressure drop is investigated especially when the droplet flows in the straight narrow channel. We explore the effects of droplet size, capillary number (Ca), viscosity ratio ($\chi$) between droplet and medium, and fluid elasticity represented by the Oldroyd-B constitutive model on the excess pressure drop (${\Delta}p^+$) against single phase flow. The tightly fitted droplets in the narrow channel are mainly considered in the range of $0.001{\leq}Ca{\leq}1$ and $0.01{\leq}{\chi}{\leq}100$. In Newtonian droplet/Newtonian medium, two characteristic features are observed. First, an approximate relation ${\Delta}p^+{\sim}{\chi}$ observed for ${\chi}{\geq}1$. The excess pressure drop necessary for droplet flow is roughly proportional to $\chi$. Second, ${\Delta}p^+$ seems inversely proportional to Ca, which is represented as ${\Delta}p^+{\sim}Ca^m$ with negative m irrespective of $\chi$. In addition, we observe that the film thickness (${\delta}_f$) between droplet interface and channel wall decreases with decreasing Ca, showing ${\delta}_f{\sim}Ca^n$ Can with positive n independent of $\chi$. Consequently, the excess pressure drop (${\Delta}p^+$) is strongly dependent on the film thickness (${\delta}_f$). The droplets larger than the channel width show enhancement of ${\Delta}p^+$, whereas the smaller droplets show no significant change in ${\Delta}p^+$. Also, the droplet deformation in the narrow channel is affected by the flow history of the contraction flow at the entrance region, but rather surprisingly ${\Delta}p^+$ is not affected by this flow history. Instead, ${\Delta}p^+$ is more dependent on ${\delta}_f$ irrespective of the droplet shape. As for the effect of fluid elasticity, an increase in ${\delta}_f$ induced by the normal stress difference in viscoelastic medium results in a drastic reduction of ${\Delta}p^+$.

• YAKHAK HOEJI
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• v.45 no.4
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• pp.419-425
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• 2001

The neuronal cell death induced by excess glutamate (Glu) has been implicated in many acute and chronic neurodegenerative diseases including cerebral ischemia. Glu-induced elevation of intra-cellular $Ca^{2+}$ plays a critical role in the excitotoxicity, partly through the activation of a variety of $Ca^{2+}$ dependent enzymes. In the present study, we investigated the Glu-induced modulation of $Ca^{2+}$/calmodulin-dependent protein kinase IV (CaMK IV), a multifunctional enzyme abundantly present in the nuclei of neurons. The exposure of cultured rat cortical neurons to $100{\mu}$M Glu for 3 min dramatically increased CaMK IV activity up to 4.5-fold of the control-treated enzyme activity. The activation was very rapid, reaching peak at 3 min and then declined gradually. Under the same experimental conditions, time-dependent acute and delayed neuronal cell death was observed. Immunoblot analyses using specific antibodies showed that the expressions of CaMK IV and $CaMKK_{\alpha}$ were time-dependently modulated by Glu. Taken together, these results imply that the modulation of CaMK IV activity by Glu may be involved in the cascade of events resulting in neuronal cell death in cortical cultures.