• The Journal of Korea Robotics Society
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• v.11 no.1
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• pp.26-32
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• 2016

A variable release torque-based compliance spring-clutch (VCSC) is presented. VCSC is a safe joint to reduce the impact of collisions between humans and robots. It is composed of four functional plates, balls, springs to make some functions in compliant movement, release mechanism, gravity compensation during its work. Also, it can estimate torque applied to a joint by using distance sensor and parameters of cam profile. The measured variable torque of prototype is 4.3~7.6 Nm and release torque is 4.3 Nm. In our future studies, a calibration for torque estimation will be conducted.

• YAKHAK HOEJI
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• v.39 no.6
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• pp.616-621
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• 1995

The effect of WK101 on compound 48/80-induced anaphylaxis was studied in rat. WK101 was found to exhibit a inhibitory activity on the compound 48/80-induced anaphylaxis. WK101 also inhibited the serum histamine release induced in anaphylaxis by compound 48/80. The effect of WK101 on the histamine release from rat peritoneal mast cells was studied. WK101 ($10^{3}-1mg/ml$) inhibited the histamine release induced by compound 48/80($5{\;}\mu\textrm{g}/ml$) in rat peritoneal mast cells. To clarify the mechanism of these inhibitons, we investigated the effects of WK101 on cAMP and intracellular calcium content of rat peritoneal mast cell. The content of cAMP in mast cells, when WK101 was added, was increased transiently, and was significantly increased more 53 fold at 10 sec than that of basal cells. Moreover, WK101 inhibited intracellular calcium release induced by compoound 48/80. This results suggest that WK101 may be useful for the prevention and treatment of allergy-related disease.

• Journal of ILASS-Korea
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• v.8 no.4
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• pp.9-16
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• 2003

The Purpose of this study is to investigate the relationships between the local heat release rate and CH concentration have been investigated by numerical simulations of methane-air premixed flames. And simultaneous CH and OH PLIF(Planar Laser Induced Fluorescence) measurement has been also conducted for lean premixed flame as well as for laminar flames. Numerical simulations are conducted for laminar premixed flames and turbulent ones by using PREMIX in CHEMKIN and two dimensional DNS code with GRI mechanism version 2.11, respectively. In the case of laminar premixed flame, the distance between the peak of heat release rate and that of CH concentration is under $91{\mu}m$ for all equivalence ratio calculated in present work. Even for the premixed flame in high intensity turbulence, the distribution of the heat release rate coincides with that of CH mole fraction. For CH PLIF measurements in the laminar premixed flame burner, CH fluorescence intensity as a function of equivalence ratio shows a similar trend with CH mole fraction computed by GRI mechanism. Simultaneous CH and OH PLIF measurement gave us useful information of instantaneous reaction zone. In addition, CH fluorescence can be measured even for lean conditions where CH mole fraction significantly decreases compared with that of stoichiometric condition. It was found that CH PLIF measurements can be applicable to the estimation of the spatial fluctuations of heat release rate in the engine combustion.

• The Korean Journal of Physiology
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• v.20 no.2
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• pp.236-248
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• 1986

Alterations of renin-angiotensin system have been suggested as one of the mechanisms increasing arterial blood pressure in experimental and clinical hypertension. But the exact nature of high blood pressure in the early and late phase of renal hypertension is still controversial. To clarify the nature of renin release in both unclipped and clipped kidney of two kidney one clip Goldblatt lypertensive rat, experiments have been done in kidney slices, which were obtained from the rats of 3 and 7 days of operation. Basal rate of renin release was suppressed in unclipped kidney slices compared to clipped kidney Norepinephrine increased renin release from unclipped kidney slices, but not from clipped kidney slices. Suppressions by angiotensin Il and arginine vasopressin of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. Increases by verapamil and trifluoperazine of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. These results suggest that the negative feedback control mechanism of the renin-angiotensin system by angiotensin Il and arginine vasopressin is attenuated in the clipped kidney of two kidney one clip Goldblatt hypertensive rat, and that one of the altered mechanisms may be caused by certain regulatory changes of intracellular calcium and/or calcium-calmodulin complex in the juxtaglomerular cells.

• Biomolecules & Therapeutics
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• v.5 no.1
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• pp.94-99
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• 1997

Capsaicin is known to be an analgesic agent, affecting the synthesis, storage, , transport and release of substance p, the principal neurotransmitter of pain from periphery to the central nervous system(CNS). DA-5018, a newly synthesized capsaicin derivative has shown potent analgesic effect comparable to that of morphine in various rat models of experimentally inducted acute pairs. In this study the mechanism of analgesic actlvity of DA-5018 was examined. First, the electrically-evoked contraction of guinea pig trachea was inhibited by DA-5018 and these inhibition was recovered by incubation with capsafepine(3$\muM$), capsaicin receptor antagonist and this result suggested that DA-5018 has affinity on capsaicin receptor. The correlation between the norciceptive threshold and the release of substance P was evaluated. In vivo perfusion of slices of the rat spinal cord with DA-5018(10, 100$\muM$) produced a significant increase of the release of substance P and this increase was less than that of capsaicin(10$\muM$). The norciceptive threshold of rat treated with DA-5018(1 mg/kg, p.o) in tall pinch test increased from 2.9$\pm$0.3 to 23.5 $\pm$6.61. Tail pinch latency increased to a maximun at 15 min after DA-5018 treatment and then declined to control values by 120 min. The capsaicin-evoked release ot substance P from the spinal cord slices of rat treated with DA-5018 reduced from 2.38$\pm$ 0.79 to 0.69$\pm$ 0.26 pg/mg wet weight. This reduction reached to a minium at 15 min after DA-5018 treatment and then recovered to control value by 120 min. These results mean that analgesic activity of DA-5018 is due to release of substance P The effect of DA-5018 cream on electrically-evoked neurogenic inflammation of rat saphenous nerve was compared with capsaicin (zostrix-HP). DA-5018 showed 34% inhibition of the neurogenic extravasation while capsaicin showed significant 67% inhibition. This result indicates that the potency of DA-5018 in the release of substance P is less than that of capsaicin. These results suggest that the release of substance P is partially involved in the mechanism of analgesic action of DA-50l8.

• Archives of Pharmacal Research
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• v.9 no.4
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• pp.193-199
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• 1986

The release of heparin from monolithic devices composed of different ratios of polythylene oxide (PEO MW 20,000) and hydrophobic polydimethylsiloxane or polyurethane was investigated. Water soluble PEO blended into the polymers provided a controlled release of heparin. The release rate of heparin could be controlled by varying the content of PEO. The heparin release rate from the devices increased as the content of PEO in the devices increased. The release mechanism may be associated with the creation of pore of domain through the devices following the swelling and the change in the physical structure of the polymer network. Hydrophobic polydimethylsiloxanes and polyurethanes containing PEO can provide an antith rombogenic material for prologed release of heparin from blended system.

• YAKHAK HOEJI
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• v.45 no.6
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• pp.677-682
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• 2001

investigate action of ethanol on histamine release from rat peritoneal mast cells, we compared the inhibitory effect of ethanol with those of calcium antagonists in mechanism of between ATP and compound 48/80-induced histamine release. Ethanol dose-dependently inhibited 100 ${\mu}{\textrm}{m}$ ATP-induced histamine release, whereas did not inhibit 1 $\mu\textrm{g}$/ml compound 48/80-induced histamine release. Verapamil, TMB-8 and EGTA dose-dependently inhibited ATP-induced histamine release, but did not inhibit compound 48/80-induced histamine release. Such an inhibitory effect of calcium antagonist was similar to that of ethanol. These results suggest that the inhibitory effect of ethanol on histamine release from rat peritoneal mast cells is mediated via disturbance of calcium mobilization..

• YAKHAK HOEJI
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• v.45 no.3
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• pp.282-286
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• 2001

To investigate the different mechanism between ATP and compound 48/80 (C$_{48}$80/)-induced histamine release, we observed effects of calcium antagonists in histamine release of rat peritoneal mast cells. Verapamil and diltiazem (voltage-dependent calcium channel blocker) and TMB-8 (a blocker of intracellular calcium release) significantly inhibited ATP-induced histamine release, but did not inhibit $C_{48}$80/-induced histamine release. Econazole (a blocker of receptor-operated calcium channel) dose-dependently inhibited both ATP and $C_{48}$80/-induced histamine release, but inhibitory effect of econazole in ATP-induced histamine release was more potent than that in $C_{48}$80/-induced histamine. EGTA dose-dependently inhibited ATP and $C_{48}$80/-induced histamine release, but $C_{48}$80/-induced histamine release was slightly inhibited by high concentrations (>2 mM) of EGTA. These results suggest that ATP-induced histamine release is related to broth intracellular calcium release and extracellular calcium influx via voltage-dependent calcium channel and receptor-operated calcium channel. $C_{48}$80/-induced histamine release is related to extracellular calcium influx, especially by receptor-operated calcium channel rather than voltage-dependent calcium channel.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.393-404
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• 1999

We have reported that hypoxia stimulates EDRF(s) release from endothelial cells and the release may be augmented by previous hypoxia. As a mechanism, it was hypothesized that reoxygenation can stimulate EDRF(s) release from endothelial cells and we tested the hypothesis via bioassay experiment. In the bioassay experiment, rabbit aorta with endothelium was used as EDRF donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2a}\;(3{\times}10^{-6}\;M)$ which was added to the solution perfusing through the aorta. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $O_2/5%\;CO_2$ mixed gas. Hypoxia/reoxygenation were interexchanged at intervals of 2 minutes (intermittent hypoxia). In some experiments, endothelial cells were exposed to 10-minute hypoxia (continuous hypoxia) and then exposed to reoxygenation and intermittent hypoxia. In other experiments, the duration of reoxygenation was extended from 2 minutes to 5 minutes. When the donor aorta was exposed to intermittent hypoxia, hypoxia stimulated EDRF(s) release from endothelial cells and the hypoxia-induced EDRF(s) release was augmented by previous hypoxia/reoxygenation. When the donor aorta was exposed to continuous hypoxia, there was no increase of hypoxia-induced EDRF(s) release during hypoxia. But, after the donor aorta was exposed to reoxygenation, hypoxia-induced EDRF(s) release was markedly increased. When the donor aorta was pretreated with nitro-L-arginine $(10^{-5}$ M for 30 minutes), the initial hypoxia-induced EDRF(s) release was almost completely abolished, but the mechanism for EDRF(s) release by the reoxygenation and subsequent hypoxia still remained to be clarified. TEA also blocked incompletely hypoxia-induced and hypoxia/reoxygenation-induced EDRF(s) release. EDRF(s) release by repetitive hypoxia and reoxygenation was completely blocked by the combined treatment with nitro-L-arginine and TEA. Cytochrome P450 blocker, SKF-525A, inhibited the EDRF(s) release reversibly and endothelin antgonists, BQ 123 and BQ 788, had no effect on the release of endothelium-derived vasoactive factors. Superoxide dismutase (SOD) and catalase inhibited the EDRF(s) release from endothelial cells. From these data, it could be concluded that reoxygenation stimulates EDRF(s) release and hypoxia/reoxygenation can release not only NO but also another EDRF from endothelial cells by the production of oxygen free radicals.

• Journal of Pharmaceutical Investigation
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• v.19 no.4
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• pp.185-190
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• 1989

The release of angiotensin and ${\alpha}-amylase$ from monolithic devices of different molecular weight of polyethylene glycol (PEC) grafted polyurethane copolymer was investigated. Water-soluble PEG grafted polymer provided a controlled release of angiotensin and ${\alpha}-amylase$. The release rate of angiotensin and ${\alpha}-amylase$ could be controlled by varying the molecular weight of PEC grafted. The release mechanism may be associated with the creation of pore or domain through the devices following the gel swelling and self-aggregation by PEC grafted polymer. Hydrophobic polyurethane grafted with PEG can provide a biomaterial for prolonged release of angiotensin and ${\alpha}-amylase$ from angiotensin and ${\alpha}-amylase$ blended system.