• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.243-254
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• 1994

Inflammatory diseases, allergic and asthmatic disorders are caused by the mediator release from the activation of the phospholipase C (PLC), phospholipase D (PLD), methyltransferase or adenylate cyclase etc. during IgG or IgE cross-linking of high affinity receptors on mast cells or basophil surface. One important enzyme activated after IgG or IgE receptor cross-linking is PLD, the enzyme which converts phosphatidylcholine (PC) to phosphatidic acid (PA). Under the hypothesis that these may be some differences in mediator release according to the difference in PLD activity, we attempted to confirm the ginseng saponin effects on the PLD activity. We examined the PLD activity during the passively sensitized mast cell activation in the presence of single component of ginsenosides $(Rc,\;Rg_1,\;Rg_2,\;Rg_3)$. We also measured the amount of mediators (histamine and leukotrienes) released by stimulating with ovalbumin (OA) or calcium ionophore (CaI), Guinea Pig lung mast cells were purified using enzyme digestion, count current elutriation, and discontinuous Percoll density gradient. In purified mast cells prelabeled with $[^3H]$ arachidonic acid or $[^3H]$ palmitic acid, PLD activity was assessed more directly by the production of labeled PEt by PLD-mediated transphosphatidylation in the presence of ethanol. Histanine release was determined by Spectrophotofluorometry, and leukotrienes by radioimmunoassay. The PLD activity during the passively sensitized mast cell activation is increased up to $3{\sim}5times$. The PLD activity during the passively sensitized mast cell activation in the presence of all ginsenosides is decreased up to $4{\sim}11$ times. $Rg_l\;and\;Rg_2$ ginsenoside pretreatment decreased histamine and leukotrienes by 50% in the OA-induced or by 40% in the Cal-induced mast cell after passively sensitization. Rc pretreatment poorly decreased histamine but leukotrienes decreased by 70% in the OA-induced or by 35% in the Cal-induced mast cell. $Rg_3$ ginsenoside pretreatment increased histamine release without challenging OA or Cal but leukotrienes decreased. These observations indicate that single unit of ginsenosldes may be an important contributor to inhibit the release of histamine and leukotrienes in the guinea pig lung mast cells, that inhibits the PLD-mediated formation of DAG evoked by mast cell activation.

• Korean Journal of Food Science and Technology
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• v.32 no.5
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• pp.1198-1205
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• 2000

Effect of inhibitions of three kinds of Ginkgo biloba extracts(Ginkgo biloba extract, Ginkgolide A, and Ginkgolide B) on induction of reactive oxygen species and release of inflammation mediator arachidonic acid were tested. Three kinds of Ginkgo biloba extracts could not inhibit the pyrogallol auto-oxidation, but they showed the hydrogen atom donating activity in DPPH assay. When 10 ${\mu}M$ hydrogen peroxide and 400 ${\mu}g/mL$ of three kinds of Ginkgo biloba extracts were added to U937 monocytic macrophage, the induction of lipid peroxidation was not observed. The Ginkgo biloba extract showed the most powerful inhibition among the extracts. And only Ginkgolide A was good for the inhibition of the protein degradation. The release of inflammation mediator arachidonic acid was induced by adding TPA and calcimycin to U937. In this assay, even 10 ${\mu}g/mL$ of three different Ginkgo biloba extracts excellently blocked the release of arachidonic acid. Particularly, the inhibition efficiency of Ginkgolide B was about 11 times higher than that of induction, and was about 4 times higher than that of the control of noninduction. This result suggests that the release of arachidonic acid is not inhibited by the antioxidant activity of Ginkgo biloba extracts, but a pre-step of the release of arachidoinc acid is inhibited by Ginkgo biloba extracts.

• The Korean Journal of Nuclear Medicine
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• v.39 no.6
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• pp.421-429
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• 2005

Purpose: It has been postulated that dopamine release in the striatum underlies the reinforcing properties of nicotine. Substantial evidence in the animal studies demonstrates that nicotine interacts with dopaminergic neuron and regulates the activation of the dopaminergic system. The aim of this study was to visualize the dopamine release by smoking in human brain using PET scan with $[^{11}C]raclopride$. Materials and Methods: Five male non-smokers or ex-smokers with an abstinence period longer than 1 year (mean age of $24.4{\pm}1.7$ years) were enrolled in this study $[^{11}C]raclopride$, a dopamine D2 receptor radioligand, was administrated with bolus-plus-constant infusion. Dynamic PET was performed during 120 minutes ($3{\times}20s,\;2{\times}60s,\;2{\times}120s,\;1{\times}180s\;and\;22{\times}300s$). following the 50 minute-scanning, subjects smoked a cigarette containing 1 mg of nicotine while in the scanner. Blood samples for the measurement of plasma nicotine level were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minute after smoking. Regions for striatal structures were drawn on the coronal summed PET images guided with co-registered MRI. Binding potential, calculated as (striatal-cerebellar)/cerebellar activity, was measured under equilibrium condition at baseline and smoking session. Results: The mean decrease in binding potential of $[^{11}C]raclopride$ between the baseline and smoking in caudate head, anterior putamen and ventral striatum was 4.7%, 4.0% and 7.8%, respectively. This indicated the striatal dopamine release by smoking. Of these, the reduction in binding potential in the ventral striatum was significantly correlated with the cumulated plasma level of the nicotine (Spearman's rho=0.9, p=0.04). Conclusion: These data demonstrate that in vivo imaging with $[^{11}C]raclopride$ PET could measure nicotine-induced dopamine release in the human brain, which has a significant positive correlation with the amount or nicotine administered bt smoking.

• Applied Chemistry for Engineering
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• v.8 no.4
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• pp.560-567
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• 1997

A new approach to obtain stable $W_1/O/W_2$ multiple emulsions has been studied ; The basis of the interfacial interaction between a PCL-PEO-PCL triblock copolymer and a lipophilic emulsifier in the dispersed oil phase was examined. $W_1/O/W_2$ multiple emulsions were prepared by the two-step method. Arlacel P-l35 was used as a liphophilic emulsifier and Synperonic PE/F 127 as a hydrophilic one. Eutanol-G was used as an oil phase. NaCl was encapsulated within the multiple emulsion droplets as the internal marker and its release rate studies were carried out. The suability of the multiple emulsions have been assessed by measuring Separation Ratios(%) and microscopic observations. The release of NaCl was significantly reduced in $W_1/O/W_2$ multiple emulsions containing PCL-PEO-PCL triblock copolymer(2k-4k-2k or 6k-4k-6k) in the oil phase. It may be concluded that the copolymer and the emulsifier form effective interfacial complex to enhance stability and to control the release rate. The effective diffusion coefficients of the NaCl were estimated as $2.64{\times}10^{-15}s$and $3.23{\times}10^{-16}gcm^2/s$ for the $W_1/O/W_2$ multiple emulsion containing 1.2 wt % of PCL-PEO-PCL triblock copolymers with compositions of 2k-4k-2k and 6k-4k-2k, respectively. The rate of release decreased with the increase of the initial concentration of NaCl. The results were examined in view of Higuchi mechanism. A kinetic model which is similar to the model for release of dispersed drugs from a polymeric matrix was found to be suitable for the release of NaCl from $W_1/O/W_2$ multiple emulsions.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.475-483
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• 1994

Background: N-acetylcysteine(ACE) is used both orally and intravenously in a variety of experimental pathologies resembling human disease states which exhibit endothelial toxicity as a result of oxidative stress, including acute pulmonary oxygen toxicity, septicemia and endotoxin shock. Despite these observations in vivo, it is not certain how this thiol drug produces its protective effects. ACE is a cysteine derivative which is able to direct1y react with oxygen radicals and may also act as a cysteine and glutathione(GSH) precursor following deacetylation. In this paper, we tried to know whether the therapeutic doses of ACE can modify the inflammatory function of the neutrophils and can increase the glutathione level of plasma in chronic obstructive pulmonary disease(COPD) patients. In addition, the effect of ACE to the purified neutrophil in terms of superoxide release and glutathione synthesis were observed. Method: Firstly, we gave 600mg of ACE for seven days and compare the release of superoxide, luminol-enhanced chemiluminescence from the neutrophils, neutrophil chemotaxis, and plasma GSH levels before and after ACE treatment in COPD patients. Secondly, we observed the dose dependent effect of ACE to the purified neutrophil's superoxide release and GSH levels in vitro. Results: 1) Usual oral therapeutic doses(600mg per day) of ACE for seven days did affect neither on the neutrophil's superoxide release, chemiluminescence, chemotaxis, nor on the plasma GSH concentration in the COPD patients. 2) ACE decreases the purified neutrophil's superoxide release and increase the GSH production in dose dependent fashion in vitro. Conclusion: Despite the fact that oral ACE treatment did not affect on the neutrophil's inflammatory function and plasma GSH concentration in COPD patients in usual therapeutic doses, it decreases the superoxide release and increases the GSH production from the isolated neutrophils in high molar concentrations. These findings suggest that to obtain an antioxidative effects of ACE, it might be needed to increase the daily dosage of ACE or therapeutic duration or change the route of adminisration in COPD patients.

• Journal of Environmental Science International
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• v.7 no.1
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• pp.46-51
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• 1998

The effects of aloe on the MDA(malondialdehyde) and the blood biochemical components of heavy metal poisoning in SD rat were examined and the following results were obtained. In rat liver homogenate intoxicated with $CdCl_2$, lipidperoxide was increased each 2.37times(24h), 3.31times(72h) but lipidperoxide In aloe administration groups was lower each 47% , 64% than in heavy metal group. In rat kidney homo- genate intoxicated with $CdCl_2$, lipidperoxide was increased 1.85times(24h), 1.33times(72h) but lipidperoxide in groups was almost the same as that of normal group. Lipidperoxide of kidney homogenate was slightly decreased as time passed. Also heavy metal poisoning rats showed high levels(1.38-2.50times) of serum AST, ALT and BUN. However. the administration of aloe significantly inhibited the reduction of them. These results suggest that Cd-induced hepatic and renal injury, via increase llpidpero)Ode and release of AST, ALT and BUN. Aloe may be used to inhibit or prevent the hepatic and renal toxicity which results from the heavy metal.

• Journal of Radiation Protection and Research
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• v.13 no.1
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• pp.8-20
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• 1988

The annual individual and collective doses to the thyroids of four age-dependent groups due to the in-take of I-131 released from the Younggwang nuclear power plant NU-1 & 2, Korea, are estimated using the model presented in ICRP 29. Sensitivity and robustness of the model are analyzed. In case of 0.12% fuel defect during normal operation, the collective dose is founded to be 3.05${\times}10^{-3}$man-thyroid-Sv, which is higher than the value calculated by the GASPAR code, 2.3${\times}10^{-3}$man-thyroid-Sv. The maximal individual annual doses resulting from an acute release are higher than those calculated under the assumption of continuous release by $1.4{\sim}1.7$ times. The most important pathway to the infant is milk and, in contrast, that to child, teen and adult is ingestion of crops. The model used is the calculation appears to be influenced by the variables such as roubstness-index. The weighted committed dose equivalent obtained by the ICRP 29 model is slightly higher than that calculated by the three-compartment model.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.2
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• pp.149-158
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• 2000

The present study was attempted to examine the effect of staurosporine (STS) on secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused rat adrenal gland and to establish its mechanism of action. The perfusion of STS $(3{\times}10^{-7}{\sim}3{\times}10^{-8}\;M)$ into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh $(5.32{\times}10^{-3}\;M),$ high $K^+\;(5.6{\times}10^{-2}\;M),$ DMPP $(10^{-4}\;M\;for\;2\;min),$ McN-A-343 $(10^{-4}\;M\;for\;2\;min),$ cyclopiazonic acid $(10^{-5}\;M\;for\;4\;min)$ and Bay-K-8644 $(10^{-5}\;M\;for\;4\;min).$ Also, in the presence of tamoxifen $(2{\times}10^{-6}\;M),$ which is known to be a protein kinase inhibitor, CA secretory responses evoked by ACh, high $K^+,$ DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with STS $(10^{-7}\;M)$ under the presence of phorbol-12, 13-dibutyrate $(10^{-7}\;M),$ a specific activator of protein kinases (for 20 min), the inhibitory effect of STS on CA secretory responses evoked by ACh, high $K^+,$ DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid was greatly recovered to the extent of the control release as compared to those in the presence of STS only. These results demonstrate that STS causes the marked inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization, indicating strongly that this effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells through preventing activation of protein kinases. Furthermore, these findings also suggest that these STS-sensitive protein kinases play a modulatory role partly in regulating the rat adrenomedullary CA secretion.

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.1
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• pp.34-41
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• 2017

Objective: Two experiments were performed to evaluate the effects of coated slow-release urea on nutrient digestion, ruminal fermentation, nitrogen utilization, blood glucose and urea concentration (Exp 1), and average daily gain (ADG; Exp 2) of steers. Methods: Exp 1: Eight ruminally fistulated steers [$503{\pm}28.5kg$ body weight (BW)] were distributed into a d $4{\times}4$ Latin square design and assigned to treatments: control (CON), feed grade urea (U2), polymer-coated slow-release urea A (SRA2), and polymer-coated slow-release urea B (SRB2). Dietary urea sources were set at 20 g/kg DM. Exp 2: 84 steers ($350.5{\pm}26.5kg$ initial BW) were distributed to treatments: CON, FGU at 10 or 20 g/kg diet DM (U1 and U2, respectively), coated SRA2 at 10 or 20 g/kg diet DM (SRA1 and SRA2, respectively), and coated SRB at 10 or 20 g/kg diet DM (SRB1 and SRB2, respectively). Results: Exp 1: Urea treatments (U2+SRA2+SRB2) decreased (7.4%, p = 0.03) the DM intake and increased (11.4%, p<0.01) crude protein digestibility. Coated slow-release urea (SRA2+-SRB2) showed similar nutrient digestibility compwared to feed grade urea (FGU). However, steers fed SRB2 had higher (p = 0.02) DM digestibility compared to those fed SRA2. Urea sources did not affect ruminal fermentation when compared to CON. Although, coated slow-release urea showed lower (p = 0.01) concentration of $NH_3-N$ (-10.4%) and acetate to propionate ratio than U2. Coated slow-release urea showed lower (p = 0.02) urinary N and blood urea concentration compared to FGU. Exp 2: Urea sources decreased (p = 0.01) the ADG in relation to CON. Animals fed urea sources at 10 g/kg DM showed higher (12.33%, p = 0.01) ADG compared to those fed urea at 20 g/kg DM. Conclusion: Feeding urea decreased the nutrient intake without largely affected the nutrient digestibility. In addition, polymer-coated slow-release urea sources decreased ruminal ammonia concentration and increased ruminal propionate production. Urea at 20 g/kg DM, regardless of source, decreased ADG compared both to CON and diets with urea at 10 g/kg DM.

• Journal of Korean Society of Environmental Engineers
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• v.22 no.1
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• pp.141-148
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• 2000

In this study, effects of substrates and nitrate on biological phosphorus release in EBPR(enhanced biological phosphorus removal) process were examined using batch test apparatus at anaerobic conditions. The sludge used in this experiments was taken from SBR(sequencing batch reactor) treating swine wastewater at aeration period. Phosphorus release rates obtained with substrates of FSW(fermented swine wastewater), acetate, propionate, domestic wastewater and methanol were 6.19, 5.99, 1.52, 1.2 and $1.03mgP/gVSS{\cdot}hr$, respectively. Those observed with acetate and FSW were 4~5 times greater than those with propionate, methanol and domestic wastewater. Therefore phosphorus release rates were significantly affected by type of substrate added at anaerobic condition. Phosphorus release was greatly affected by concentration of nitrate in anoxic condition. Comparing to acetate, propionate and FSW, phosphorus release was observed after almost completely depletion of nitrate concentration with methanol and domestic wastewater added as substrate. In the cases supplied with acetate, propionate and FSW, phosphorus release rates were less influenced by a nitrate concentration than those with methanol and domestic wastewater.