• The Korean Journal of Physiology and Pharmacology
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• v.1 no.3
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• pp.225-231
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• 1997

As it has been reported that the depolarization-induced norepinephrine (NE) release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor and various lines of evidence indicate the involvement of adenylate cyclase system in $A_1-adenosine$ post-receptor mechanism in hippocampus, it was attempted to delineate the role of adenylate cyclase system in the $A_1-receptor-mediated$ control of NE release in this study. Slices from rat hippocampus were equilibrated with $[^3H]-NE$ and the release of the labelled products was evoked by electrical stimulation.(3 Hz, $5Vcm^{-1}$, 2 ms, rectangular pulses). The influence of various agents on the evoked tritium-outflow was investigated. $N^6-Cyclopentyladenosine$ (CPA), a specific $A_1-adenosine$ receptor agonist, in concentrations Tanging from 0.1 to $10{\mu}M$ decreased the $[^3H]-NE$ release in a dose-dependent mauler without any change of basal rate of release. 8-Cyclopentyl-1,3-dipropylxanthine (DPCPX, $2{\mu}M$), a selective $A_1-receptor$ antagonist, inhibited the CPA effect. The responses to N-ethylmaleimide $(3&10{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked NE-release and the CPA effects were completely abolished by NEM pretreatment. Forskolin, a specific adenylate cyclase activator, in concentrations ranging from 0.1 to $30{\mu}M$ increased the evoked and basal rate of NE release in a dose-dependent manner and the CPA effects were inhibited by forskolin pretreatment. Rolipram $(1&10{\mu}M)$, a phosphodiesterase inhibitor, did not affect the evoked NE release but reduced the CPA effect. And 8-bromo-cAMP $(100&300{\mu}M)$, a membrane permeable cAMP analogue inhibited the CPA effect significantly. These results suggest that the $A_1-adenosine$ heteroreceptor plays an important role in NE-release via nucleotide-binding protein $G_i$ in the rat hippocampus and that the adenylate cyclase system might be participated in this process.

• Toxicological Research
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• v.14 no.3
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• pp.333-339
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• 1998

Sambutoxin, a newly purified mycotoxin in Koea, caused hemorrhage in the stomach and intestine of rats. To elucidate the mechanism of hemorrhage, effects of sambutoxin on rabbit platelet aggregation were investigated. First of all, the effects of sambutoxin on the platelet aggregation response and ATP release from platelet by various appregating factors were investigated. And then the role of $Ca^{2+}$ on the platelet aggregation was investigated by flow cytometer. Finally, morphological effect of sambutoxin on platelet ultrastructure was examined by transmission electron microscope. Sambutoxin inhibited aggregation induced by ADP, collagen, thrombin, and arachidonic acid and decreased platelet activating factor-induced disaggregation time in a dose dependent manner. Sambutoxin also decreased thrombin and arachidonic acid-induced ATP release, but increased all factors induced $Ca^{2+}$ release. Sambutoxin showed severe ultrastructural changes of platelet such as appearance of disorganization debri of cellular organelle in intercellular space. Our results indicate that sambutoxin inhibitis rabbit platelet aggregation, and it may be party due to the decrease of ATP release. However, it is not clear whether the antiaggregating effect of sambutoxin is related to $Ca^{2+}$ increase.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.11 no.10
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• pp.4047-4054
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• 2010

We studied the release characteristics of the marine sediment which could facilitate sea eutrophication through some lab-scale simulation experiments. Environmental indicators such as pH, ORP(oxidation reduction potential), nitrogens, and phosphates were measured in order to calculate the corresponding release rates. $CaO_2$, an oxygen releasing compound was used to determine how it would effect on the natural process of sedimental release. COD, ammonia nitrogen, phosphorous compounds were less released under the oxic environment caused by $CaO_2$. This basic data will help developing methodology for reducing marine eutrophication which may be initiated by the sedimental release.

• Journal of the Korean Society of Clothing and Textiles
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• v.3 no.2
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• pp.29-36
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• 1979

In order to control free formaldehyde release from fabric finished with urea-formaldehyde precondensate, the resin finished fabric was padded in urea or acylamide solution, dried and cured at $140^{\circ}C$. The effect of aftertreatment with urea or acrylamide on free formaldehyde release and on characteristics of resin finished fabric were examined. It was shown that aftertreatment with urea was effective to control free formaldehyde release, the free formaldelyde content in aftertreated fabric could be reduced from 900 ppm to 200 ppm and formaldehyde release under accelerated storage condition was also reduced from 8000 ppm to 1000 ppm. Polyacrylamide formed in the fiber during aftertreatment appeared to be a formaldehyde capture. Especially by washing the aftertreated fabric, the ability to control formaldehyde release under accelerated condition was not dimimished in contrast with aftertreated with unea. It suggests that polyacrylamide can be used as a formaldehyde capture which withstand diminution from washing.

• The Journal of Churna Manual Medicine for Spine and Nerves
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• v.4 no.1
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• pp.19-29
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• 2009

Objectives: The purpose of this study is to evaluate the therapeutic effect of acupuncture treatment of acute ankle sprain combined with positional release therapy. Methods: A prospective randomized single blind study between positional release group and knee flexed supine position group was conducted. Patients with ankle sprain within 48 hours were evaluated by Ankle injury grade chart(AIGC). In group A, positional release therapy was combined with acupuncture, whereas in group B, acupuncture was conducted in knee flexed supine position. The treatment was planned for a duration of 1 week, 3times a week. In AIGC scores, VAS, weight bearing time and weight bearing time in blind were followed up and compared. Results and Conclusion: The VAS score decreased in both group. Weight bearing time increased in group B, weight bearing time in blind increased in group A. Comparing the therapeutic effect of each group, group A had significant effectiveness in weight bearing time in blind. So we may conclude that Acupuncture treatment combined with positional release therapy is effective and recommandable at early stage of ankle sprain.

• Journal of Pharmaceutical Investigation
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• v.41 no.2
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• pp.67-73
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• 2011

Ion exchange resins can be one of the good carriers for sustained drug release. However, the sustained release may not be enough only with themselves and hence film coating with rate controlling polymers can be applied to have a further effect on the drug release. Due to the environmental and economic issues of organic solvent for the polymer coating, aqueous polymeric systems were selected to develop dosage forms. Among the many aqueous polymeric dispersions for the film coating, EC (ethylcellulose) based polymers such as Aquacoat$^{(R)}$ ECD and Surelease$^{(R)}$ were evaluated.A fluid-bed coating was applied as a processing method. The drug release rate was quite dependent on the coating level so the release rate could be modified easily by changing different levels of the coating. The drug release rate in the Aquacoat$^{(R)}$ coated resin particles was strongly dependent on curing, which is a thermal treatment to make homogeneous films and circumvent drug release changes during storage. After dissolution test using the compressed tablets in which the coated resin particles are contained, inhomogeneous coating and even pores could be observed showing that the mechanical properties of EC were not resistant to granulation and compaction process. However, when tablets were prepared in different batches, the release profiles were almost identical showing the feasibility of the coated resin particle as incorporated into the tablet formulation.

• Korean Journal of Veterinary Research
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• v.38 no.3
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• pp.508-517
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• 1998

There is evidence that the sympathetic nervous system exerts a control on thyroid function via an adrenergic innervation of thyroid cells. Although it is clear that the inhibitory effects of catecholamines result from an activation of ${\alpha}_1$-adrenoceptors, the mechanisms involved in ${\alpha}_1$-stimulation are not fully understood. The effects of methoxamine and protein kinase C (PKC) activator on the release of thyroxine ($T_4$) from mouse thyroid were studied to clarify the role of PKC in the regulation of $T_4$ release in vitro. The glands were incubated in the medium, samples of the medium were assayed for $T_4$ by EIA kits. Methoxamine inhibited the TSH-stimulated $T_4$ release. This inhibition was reversed by prazosin, an ${\alpha}_1$-adrenergic antagonist. Futhermore, the inhibitory effect of methoxamine on the $T_4$ release stimulated by TSH was prevented by chloroethylclonidine, an ${\alpha}_{1b}$-adrenoceptor antagonist, but not by WB4101, an ${\alpha}_{1a}$-adrenoceptor antagonist. Also methoxamine inhibited the forskolin-, cAMP- or IBMX-stimulated $T_4$ release. These inhibition were reversed by PKC inhibitors, such as staurosporine and $H_7$. PMA, a PKC activator, completely inhibited the TSH-stimulated $T_4$ release, and its inhibition was reversed by staurosporine and $H_7$, but not by chelerythrine. R59022 (a diacylglycerol kinase inhibitor), like methoxamine, also inhibited the TSH-stimulated $T_4$ release, and its inhibition was also reversed by staurosporine. The present study suggests that methoxamine inhibition of $T_4$ release from mouse thyroid can be induced by activation of the ${\alpha}_{1b}$-adrenoceptors and that it is mediated through the ${\alpha}_1$-adrenoceptor-stimulated PKC formation.

• Toxicological Research
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• v.13 no.4
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• pp.359-365
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• 1997

Many factors are known to be responsible for cerebral ischemic injury, such as excitatory neurotransmitters, increased intraneuronal calcium, or disturbance of cellular energy metabolism. Recently, oxygen free radicals, formed during ischemia/reperfusion, have been proposed as one of the main causes of ischemia/reperfusion injury. Therefore, to investigate the role of oxygen free radical during ischemia/reperfusion, in the present study the effect of endogenous oxygen free radical scavenger, superoxide dismutase / catalase(SOD / catalase) on the release of [$^3$H]-5-hydroxytryptamine([$^3$H]-5-HT) during hypoxia/reoxygenation in rat hippocampal slices was measured. The hippocampus was obtained from the rat brain and sliced 400 gm thickness with manual chopper. After 30 min's preincubation in the normal buffer, the slices were incubated for 20 min in a buffer containing [$^3$H]-5-HT(0.1 $\mu$M, 74 $\mu$Ci) for uptake, and washed. To measure the release of [$^3$H]-5-HT into the buffer, the incubation medium was drained off and refilled every ten minutes through a sequence of 14 tubes. Induction of hypoxia for 20 min (gassing it with 95% N$_2$/5% CO$_2$) was done in the 6th and 7th tube, and oxygen free radical scavenger, SOD / catalase was added 10 minutes prior to induction of hypoxia. The radioactivity in each buffer and the tissue were counted using liquid scintillation counter and the results were expressed as a percentage of the total activity. When slices were exposed to hypoxia for 20 min, [$^3$H]-5-HT release was markedly decreased and a rebound release of [$^3$H]-5-HT was observed on the post-hypoxic reoxygenation period. SOD / catalase did not changed the release of [$^3$H]-5-HT in control group, but inhibited the decrease of [$^3$H]-5-HT release in hypoxic period and rebound increase of [$^3$H]-5-HT in reoxygenation period. This result suggest that superoxide anion may play a role in the hypoxic-, and reoxygenation-induced change of [$^3$H]-5-HT release in rat hippocampal slices.

• Toxicological Research
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• v.14 no.4
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• pp.483-488
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• 1998

During cerebral ischemia two important factors such as hypoxia and reduction of glucose can act as modulating stressor affecting the release of amine neurotransmitters including 5-hydroxytryptamine (5-HT). This study was performed to investigate the effect of glucose deprivation on the oxygen deprivation-induced changes of [3H]-5-HT release in the rat hippocampal slices. Experimental groups were divided into 4 groups for this study: normoxic/normoglycemic group, oxygen-deprived group, glucose-deprived group, and oxygen/glucose-deprived group. The hippocampus of rat brain was sliced by 400 $\mu\textrm{m}$ thickness with manual chopper. After 30 minutes preincubation in the normal buffer, the slices were incubated for 20 min in buffer containing [3H]-5-HT (0.1 M, 74 $\mu\textrm$Ci) for uptake. To measure the release of [3H]-5-HT into the buffer, the incubation medium was drained of and refilled with fresh buffer every ten minutes through a sequence of 14 tubes. Oxygen deprivation by gassing with 95% $N_2$/5% $CO_2$ and/or glucose deprivation was done in the 6th and 7th tube. The radioactivities in each buffer and the tissue were counted using scintillation counter. The results were expressed as fractional release. When slices were exposed to oxygen-deprived media for 20 min, the diminution followed by the rebound release of [3H]-5-HT was observed during the post-oxygen deprived period. However, glucose deprivation or oxygen/glucose deprivation markedly increased the release of [3H]-5-HT. which was opposite to the pattern observed in oxygen-deprived group. These results suggested that oxygen deprivation itself inhibits [3H]-5-HT release in rat hippocampal slices during oxygen-deprived period, but additional glucose deprivation convert the inhibitory response to increase of [3H]-5-HT release.

• YAKHAK HOEJI
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• v.29 no.2
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• pp.70-75
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• 1985

The influence of polyethylene glycol derivatives on heparin release from cylindrical monolithic type silicone segment devices was examined in physical saline solution. This water-soluble carrier caused the devices to absorb the water in aqueous media. The release rate of heparin from the devices was increased as molecular weight of polyethylene glycol was increased. Water soluble carrier incorporated into silitone segment devices permits controlled release of heparin that otherwise would be released extremly slowly from the polymer. Heparin released from the silicone segment containing polyethylene glycol showed the first-order kinetics. Without changing the release-pattern, the release rate of heparin could be controlled by varing molecular weight of polyethylene glycol, the water-soluble carrier and depleting polyethylene glycol on the outlayer of devices. The mechanism of release probably showed the creation of pore or microdomine through the devices secondary to the swelling.