• Journal of Pharmaceutical Investigation
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• v.30 no.1
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• pp.27-32
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• 2000

Various release test methods have been applied for the evaluation of nicotine release in vitro from commercial patches. However, whether and how the release data reflect the permeation of nicotine across the skin, is not fully elucidated. To predict in vivo bioavailability from in vitro release tests, correlation between in vitro release and in vitro skin permeation was assessed in the present study. Release of nicotine from three commercial patches was measured for 24 hours under nine experimental conditions which were classified depending on the apparatus (i.e., paddle over disk, cylinder and reciprocating holder) and dissolution media (i.e., phosphate buffer pH 7.4, water and the 1 % phosphoric acid pH 1.5). In vitro permeation of nicotine from the patches across the human cadaver skin was also measured using a diffusion cell. The release of nicotine was better explained by the Higuchi's equation rather than by the first order rate equation. Correlation between the release rate and the in vitro skin permeation differed among the patches. However, in general, the cylinder method, in which water is used as a dissolution medium, showed the highest correlation among the nine release test conditions.

• IE interfaces
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• v.22 no.1
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• pp.1-9
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• 2009

As the LCD fabrication factories (Fab) are highly capital-intensive and the markets are very competitive, it is an essential requirement of operational management to achieve full-capacity production while meeting customer demands on time. In a typical LCD Fab, medium-term schedules such as release plans and production plans are critical to achieve the goal of full-capacity production and on-time delivery. Presented in this paper is a framework for weekly planning system generating medium-term schedules using a finite-capacity planning method. Also this paper presents a release planning method applying capacityfiltering algorithm, especially backward capacity-filtering procedure, which is one of the finite-capacity planning methods. In addition, performance analyses using actual data of a TFT-LCD Fab show that the proposed method is superior to existing methods or commercial S/W products generating release plans.

• Environmental Engineering Research
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• v.10 no.4
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• pp.199-204
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• 2005

Experiments were performed to estimate the organic release from the aquifer soil in riverbank and/or riverbed filtration via a kinetic approach. Organic release was assumed as a reaction of first order regarding concentrations in both soil and water phases. The reaction rate constants were obtained by comparing the model predictions with the experimental data of organic release reaction and the equilibrium distribution of organic matter between water and soil phases. Results show that the organic release from the aquifer soil was not negligible under normal conditions in Korea reaching 4.7mg-COD/L-day. This indicates that manganese and iron start to be released from aquifer soil in the riverbank filtration in the middle reach of the Nakdong river if the travel time of the filtrate exceeds about 5 days. It was also seen that the COD of the soil organic matter was 0.89mg-COD/mg-OM and that 65% of the COD was BOD5.

• Proceedings of the Korean Society of Propulsion Engineers Conference
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• 2001.04a
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• pp.1-6
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• 2001

In this paper, edge delaminations in cracked composite plates are analytically investigated. A theoretical model based upon a sub-laminate approach is used to determine the strain energy release rate, $G^{ed}$, in [$\pm$$\theta_m$/$90_n$]$_s$ carbon/epoxy laminates loaded in tension. The analysis provides closed-form expressions for the reduced stiffness due to edge delamination and matrix cracking and the total energy release rate. The parameters controlling the laminate behaviour are identified. It is shown that the available energy for edge delamination is increased notably due to transverse ply cracking. Also thermal stresses increase substantially the strain energy release rate and this effect is magnified by the presence of matrix cracking. Prediction for the edge delamination onset strain is presented and compared with experimental data. The analysis could be applied to ceramic matrix composite laminates where similar mechanisms develop, but further experimental evidence is required.

• Food Science and Biotechnology
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• v.16 no.1
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• pp.8-17
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• 2007

The main purpose of flavor research using conventional extraction methods, such as solvent extraction, distillation, and dynamic headspace, is to effectively extract, identify, and quantify flavor volatiles present in food matrices. In recent flavor research, the importance of understanding flavor release during mastication is increasing, because only volatiles available in the headspace contribute to the perception of food 'flavors'. Odor potency differs among flavor volatiles, and the physicochemical characteristics of flavor volatiles affect their release behavior and interaction with various food matrices. In this review, a general overview of flavor release and flavor-food interactions within frozen dessert systems is given with emphasis on chemical, physiological, and perceptual aspects. Chemical and sensory analysis methods competent for investigating such flavor-food interactions are illustrated. Statistical analysis techniques recommended for data acquired from such experiments are also discussed.

• The Journal of Fisheries Business Administration
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• v.36 no.1 s.67
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• pp.121-138
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• 2005

This study was conducted to investigate the economic effect of the release of seed flounder to the central area of the West Sea, which was analyzed into both direct and indirect effects. The results showed that based on the data collected from partial area, the economic effect of flounder seed release reached 6.97 times, average catch proportion was 32.27$\%$, and recapture rate was 11.26$\%$, suggesting that economic effect was very high. In addition, it was observed that the recapture rate was greatly higher than 2.05$\%$, that of Break-Even-Point. It was noted that the increased catch by the release of seed flounder resulted in the increase in commission of sales and the increase in sports fishing. Another economic effect observed were diverse including the increase in income of fishing village, elevated spirit to proper management of fisheries resources, maintaining of willingness to live in fishing village through activation of local fishing village, prevention of illegal fishing including capture of juvenile fish, and the increase in the supply of sea food of high quality. It is emphasized that although the investigation was conducted in the same area, the results will vary by size at release, time at release and other factors. Finally, there is a need to expand species and area of study for more active economic analysis incorporating natural sciences.

• The Korean Journal of Physiology
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• v.25 no.1
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• pp.61-67
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• 1991

In order to determine possible relationships between the renin-angiotensin system and nephron heterogeneity, we compared the response of renin release and the angiotensin-converting enzyme (ACE) activity from different areas of the rat kidney. We used the renal cortical slices from the capsular surface to the juxtamedullary junction. Slices from outer one-third of the cortex were designated as outer cortical slices (OC), middle one-third as midcortical slices (MC), and inner one-third as inner cortical slices (IC). The renal renin content markedly decreased from OC and MC to IC. The basal lenin release was higher in OC than in MC or IC. On the contrary the percent change of renin release in response to L-isoproterenol was significantly higher in MC than in OC or IC. By TMB-8, the renin release in MC by $231{\pm}21%$ was higher than OC by $171{\pm}19%$ or IC by $$162{\pm}19. Angiotensin II suppressed renin release in OC and MC by $68{\pm}2,\;71{\pm}4%$ respectively, but only $40{\pm}7%$ in IC. The ACE activity was higher in IC than in OC, MC, medulla and papilla. The present data indicate that renin content and basal lenin release gradulally decreased from outer (OC) to inner (IC) cortex. The renin release in response to beta-adrenergic agonist, L-isoproterenol and intracellular calcium antagonist, TMB-8 were higher in MC than in OC and IC, but angiotensin II suppressed renin release less in IC than in OC and MC. It is suggested that juxtaglomerular cells of outer, mid-and inner cortices show a difference in renin release response to the stimuli.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.630-636
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• 2021

Eupafolin, a constituent of the aerial parts of Phyla nodiflora, has neuroprotective property. Because reducing the synaptic release of glutamate is crucial to achieving pharmacotherapeutic effects of neuroprotectants, we investigated the effect of eupafolin on glutamate release in rat cerebrocortical synaptosomes and explored the possible mechanism. We discovered that eupafolin depressed 4-aminopyridine (4-AP)-induced glutamate release, and this phenomenon was prevented in the absence of extracellular calcium. Eupafolin inhibition of glutamate release from synaptic vesicles was confirmed through measurement of the release of the fluorescent dye FM 1-43. Eupafolin decreased 4-AP-induced [Ca²⁺]_i elevation and had no effect on synaptosomal membrane potential. The inhibition of P/Q-type Ca²⁺ channels reduced the decrease in glutamate release that was caused by eupafolin, and docking data revealed that eupafolin interacted with P/Q-type Ca²⁺ channels. Additionally, the inhibition of calcium/calmodulin-dependent protein kinase II (CaMKII) prevented the effect of eupafolin on evoked glutamate release. Eupafolin also reduced the 4-AP-induced activation of CaMK II and the subsequent phosphorylation of synapsin I, which is the main presynaptic target of CaMKII. Therefore, eupafolin suppresses P/Q-type Ca²⁺ channels and thereby inhibits CaMKII/synapsin I pathways and the release of glutamate from rat cerebrocortical synaptosomes.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.87-94
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• 2005

It is not clear whether $Ca^{2+}-induced$ $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that $Ca^{2+}$ entry via voltage-gated L-type $Ca^{2+}$ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR $Ca^{2+}$ release in the regulation of ANP release and whether $Ca^{2+}$ entry via L-type $Ca^{2+}$ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR $Ca^{2+}$ release, increased atrial myocytic ANP release ($8.69{\pm}3.05$, $19.55{\pm}1.09$, $27.31{\pm}3.51$, and $18.91{\pm}4.76$% for 1, 2, 3, and $6{\mu}M$ ryanodine, respectively; all P<0.01) with concomitant decrease in atrial stroke volume and pulse pressure in a dose-dependent manner. In the presence of thapsigargin, an inhibitor of SR $Ca^{2+}$ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type $Ca^{2+}$ channel with nifedipine abolished ryanodine-induced increase in ANP release ($0.69{\pm}5.58$% vs. $27.31{\pm}3.51$%; P＜0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that $Ca^{2+}$-induced $Ca^{2+}$ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.