• Journal of the Korean GEO-environmental Society
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• v.14 no.10
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• pp.17-27
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• 2013

This paper explores stress release induced by unloading in dry sand. A series of model tests were carried out to measure stresses developed in testing sand during loading and those released during unloading for different boundary conditions. It was found that stress in the sand increased linearly with applied load. At the onset of unloading, almost no stress release was observed. Significant stress release took place when the shear stress in the sand induced by unloading exceeded the frictional resistance and caused movement of sand particles. The initiation and the magnitude of stress release depend on the stress condition prior to unloading, the decrease of external load, and also the frictional resistance in sand. A new conceptual stress-release model was next developed based on the model test results by considering the fundamental frictional behavior of granular materials.

• Journal of Pharmaceutical Investigation
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• v.18 no.4
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• pp.169-174
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• 1988

The release of heparin from monolithic devices composed of different ratios of polyethylene oxide-polypropylene oxide (PEO-PPO) and hydrophobic polyurethane was investigated. The release rate of heparin could be controlled by varying the PEO-PPO content. The heparin release rate from the devices increased as the content of PEO-PPO in the devices increased. The release mechanism may be associated with creation of micro-channels and pores through the devices following the change in the physical structure of the polymer network. Hydrophobic polyurethane containing PEO-PPO can provide an antithrombogenic material for prolonged release of heparin from a heparin blended system.

• 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.

• Toxicological Research
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• v.12 no.2
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• pp.195-201
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• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.

• Proceedings of the KSME Conference
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• 2001.11b
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• pp.853-858
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• 2001

The knowledge of flame structure is essential for control of combustion instability phenomena. Some results of an experimental study on mechanism of naturally occurring combustion oscillations with a single dominant frequency are presented. Tests were conducted in a laboratory-scale dump combustor at atmospheric pressure. Sound level meter was used to track the pressure wave inside the combustor. The observed instability was a longitudinal mode with a frequency of $\sim341.8Hz$. Instability map was obtained at the condition of inlet temperature of $360^{\circ}C$, mean velocities of $8.5\sim10.8m/s$ and well premixed mixture. It showed that combustion instability was susceptible to occur in the lean conditions. In this study, unstable flame was observed from stoichiometric to 0.7 in overall equivalence ratio. At selected unstable conditions, phase-resolved OH chemiluminescence images were captured to investigate flame structure with various mean velocities. As mean velocity is increased, the flame grows and global heat release was changed. Due to these effects, combustion instability can be maintained at more lean air-fuel ratio. Also, these results give an insight to the controlling mechanism for an increasing heat release at maximum pressure.

• Archives of Pharmacal Research
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• v.27 no.12
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• pp.1245-1252
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• 2004

Although ascorbate (vitamin C) has been shown to have anti-cancer actions, its effect on human hepatoma cells has not yet been investigated, and thus, the exact mechanism of this action is not fully understood. In this study, the mechanism by which ascorbate induces apoptosis using HepG2 human hepatoblastoma cells is investigated. Ascorbate induced apoptotic cell death in a dose-dependent manner in the cells, was assessed through flow cytometric analysis. Contrary to expectation, ascorbate did not alter the cellular redox status, and treatment with antioxidants (N-acetyl cysteine and N,N-diphenyl-p-phenylenediamine) had no influence on the ascorbate-induced apoptosis. However, ascorbate induced a rapid and sustained increase in intracellular $Ca^{2+}$ concentration. EGTA, an extracellular $Ca^{2+}$ chelator did not significantly alter the ascorbate-induced intracellular $Ca^{2+}$ increase and apoptosis, whereas dantrolene, an intracellular $Ca^{2+}$ release blocker, completely blocked these actions of ascorbate. In addition, phospholipase C (PLC) inhibitors (U-73122 and manoalide) significantly suppressed the intracellular $Ca^{2+}$ release and apoptosis induced by ascorbate. Collectively, these results suggest that ascorbate induced apoptosis without changes in the cellular redox status in HepG2 cells, and that the PLC-coupled intracellular $Ca^{2+}$ release mechanism may mediate ascorbate-induced apoptosis.

• Journal of Pharmaceutical Investigation
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• v.17 no.2
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• pp.75-78
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• 1987

The release rate of heparin from monolithic devices composed of raffinose, ${\beta}-cyclodextrin$, polyethylene oxide (Mw 20,000, PEO), and hydrophobic polyether urethane (biomer) was investigated. Water soluble raffinose, ${\beta}-cyclodextrin$, and PEO blended into the biomer provided a controlled release of heparin. The release rate of heparin could be controlled by the content of raffinose, ${\beta}-cyclodextrin$, and PEO in the devices. The mechanism of release rate increased by the raffinose, ${\beta}-cyclodextrin$, and PEO may result from the formation of channels and pores in the biomer matrices following the swelling and the change in the physical structure of polymer net work. Hydrophobic polyurethane containing raffinose, ${\beta}-cyclodextrin$, and PEO can provide a hydrophilic antithrombogenic material for prolonged release of heparin.

• YAKHAK HOEJI
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• v.43 no.1
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• pp.55-60
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• 1999

To investigate analgesic mechanism of capsaicin and its analogues (capaicinoids) adenosine release was measured by high performance liquid chromatography from rat spinal cord synaptosomes. Exposure of synaptosomes to $K^+$ and morphine produced a dose dependent release of adenosine in the presence of $Ca^{++}$. Capsaicin (0.1, 1, $10{\;}{\mu}M$), and its analogues: NE-19550 (1, 10, $100{\;}{\mu}M$), DMNE (1, 10, $100{\;}{\mu}M$) and KR 25018 (0.1, 1, $10{\;}{\mu}M$) produced a concentration dependent release of adenosine in the presence of $Ca^{++}$. Nifedifine, L-type voltage sensitive calcium channel blocker, inhibited $K^+$ (6, 12 mM)-and morphine ($10{\;}{\mu}M$)-evoked release of adenosine partially. Capsazepine, a novel capsaicin selective antagonist, blocked only capsaicin and capsaicinoids induced release of adenoside. Therefore, it is suggested that the adenosine release by capsaicin and capsaicinoids having antinociceptive effects involves actvation of capsaicin specific receptor and capsaicin sensitive $Ca^{++}$. channel.

• Journal of Pharmaceutical Investigation
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• v.23 no.4
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• pp.207-211
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• 1993

Reservoir type devices were designed for long-term implantable drug delivery system. The reservoir type device was prepared with the polymethacrylic acid gel coated with polyurethane membrane. Release controlling agent (RCA) were employed to control drug release from devices via generation of micropores in the membranes. The polyurethane membrane functioned as a rate controlling barrier. The drug release pattern of hydrogel demonstrated zero order kinetics. The release rate of drugs could be regulated by varying hydrophobicity/hydrophilicity and content of the RCA, as well as the thickness of the polyurethane membrane. The release of drugs from this system was governed by pore mechanism via simple diffusion and osmotic pressure.

• YAKHAK HOEJI
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• v.35 no.1
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• pp.11-14
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• 1991

Ro09-0198, a cyclic peptide isolated from culture filtrates of Streptoverticillium griseove-rticillatum, induced platelet aggregation and serotonin release simultaneously. LDH release was not observed. Addition of peptide to rat platelet, loaded with $Ca^{2+}$ chelator quin-2, caused immediate rise in cytosolic free $Ca^{2+}$. Liposomal membrane containing phosphatidylethanolamine was damaged by peptide and released $^{45}Ca$ dose dependently.