• Journal of the Korean GEO-environmental Society
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• v.11 no.11
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• pp.63-75
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• 2010

There are several remediation technologies for heavy metal contaminated soils but increasing cost limits the application of the technology if the contaminated area is large. Therefore, stabilization, which blocks the release of heavy metals or makes slow the release, is one of the applicable technology for the heavy metal contaminated soil. Current study is an applicability test for a smelter area with various stabilizer such as magnetite, hematite, zeolite-A, zeolite-X, zeolite-Y, zinc oxide, calcium oxide, carbon trioxide, manganese oxide, manganese dioxide, fish bone, sodium phosphate. The soil contaminated with arsenic, lead, copper, nickel, and zinc could not be stabilized only one stabilizer which is known to have stability for certain metal. Many of the stabilizer works for a few metal but not all of the heavy metal. In several cases, stabilizers increase the release of the other metals while they stabilize some metals. In general, the stabilizing efficiency was increased with time. For Ni, Pb, calcium oxide, carbon trioxide, manganese oxide had good stabilizing effect in water extractable portion. For Cu, manganese oxide, zeolite showed good results especially in the exchangeable portion of the sequential extraction. For As, magnetite had good ability but most of the metal oxide which showed good result for other heavy metals increased with the release of As. Current study suggest that multiple stabilizers are needed for the contaminated soil and dose of the stabilizer and stabilizing time should be carefully considered for the soil contaminated with various metals.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.11-15
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• 1995

Serotonergic neurons in medulla oblongata play an important role in the endogenous descending pain inhibitory system. To illucidate the factors involved in the regulation of medullary serotonergic neurons, we studied the effects of cholecystokinin (CCK) and agents acting on various second messenger systems on 5-hydroxytryptamine (5-HT) release from cultured neurons of rat fetal (gestational age 14th day) medulla oblongata. Cultured cells maintained for 10 days in vitro were stimulated for 48 hours with CCK or other neuropeptides at 10 micromolar concentration. CCK ($10{\mu}M$) and substance P ($10{\mu}M$) significantly increased. 5-HT release. However, somatostatin, proctolin, thyrotropin releasing hormone, and interleukin-6 did not have any effects on 5-HT release. Nimodipine ($1{\mu}M$), a calcium channel blocker, almost completely, and calmidazolium ($1{\mu}M$), a calmodulin antagonist, significantly inhibited the CCK-induced 5-HT release. The total 5-HT content (intracellular 5-HT plus released 5-HT) was significantly increased by CCK. However, the intracellular 5-HT content was not significantly changed by CCK. Forskolin ($5{\mu}M$), an adenylate cyclase activiator, but not $2{\mu}M$ phorbol myristate acetate (PMA), a protein kinase C activator, significantly enhanced 5-HT release. The total 5-HT content (intracellular 5-HT plus released 5-HT) was significantly increased by forskolin. However, the intracellular 5-HT content was not significantly changed by forskolin. PMA had no effect on intracellular 5-HT levels. These results suggest that CCK regulates serotonergic neurons in the medulla oblongata by enhancing 5-HT secretion through calcium influx and caimodulin, and that cyclic AMP system but not protein kinase C system is involved in 5-HT release.

• The Korean Journal of Physiology
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• v.26 no.2
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• pp.123-128
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• 1992

The present study was undertaken to examine if endogenous nitric oxide is partly responsible for the high calcium induced vasorelaxation in vitro. Isolated porcine coronary arterial rings were suspended in the tissue chamber and their changes in isometric tension were recorded. KCI little affected the vascular tension in the calcium free media, but subsequent addition of cumulative doses of $CaCl_3$ from 1 to 40 mM caused a contraction followed by complete relaxation. The maximum tension was noted at the calcium concentration in the media of 5 mM, and then the tension progressively declined at 10-40 mM. The relaxation was slightly attenuated in the endothelium-denuded preparation. The relaxation was converted into a contraction by the addition of methylene blue. The relaxation response was not affected in the presence of indomethacin, but was significantly attenuated by $N^w-nitro-L-arginine$ methyl ester pretreatment. These results suggest that the calcium induced vasorelaxation is in part attributable to the release of endogenous nitric oxide.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.1
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• pp.51-57
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• 2015

The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of grampositive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (U73122), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by U73122 and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.57-66
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• 1996

To investigate properties of Ca-release channel in the reptile skeletal muscle, electrophoretical analysis, purification of RyR, $[^3H]ryanodine$binding study, and $^{45}Ca-release$ were carried out in the SR vesicles prepared from the snake skeletal muscle. The snake SR vesicle has the single high molecular weight protein band on SDS-PAGE, and its mobility was similar with that of rat skeletal SR vesicles. The high molecular weight band on SDS-PACE was found in the $[^3H]ryanodine$ peak fractions $(Fr_{5-7})$ obtained from the purification step of the RyR. Maximal binding site and Kd of the snake SR RyR were 6.36 pmole/mg protein and 17.62 nM, respectively. Specific binding of $[^3H]ryanodine$ was significantly increased by calcium and AMP (P<0.05), but not or slightly inhibited by tetracaine, ruthenium red (5.4%), or $MgCl_2$ (21%). $^{45}Ca-release$ from the SR vesicles loaded passively was significantly increased by the low concentration of calcium $(1{\sim}10{\mu}M)$ and AMP (5 mM)(P<0.05), but significantly decreased by the high concentration $(300{\mu}M)$ of calcium, tetracaine (1 mM), ruthenium red $(10{\mu}M)$, and $MgCl_2$ (2 mM)(P <0.05). From the above results, it is suggested that snake SR vesicles also have the RyR showing the similar properties to those of mammalian skeletal RyR with the exceptions of no or slight inhibition of $[^3H]ryanodine-binding$ by tetracaine, ruthenium red, or $MgCl_2$.

• Journal of Pharmaceutical Investigation
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• v.25 no.2
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• pp.153-161
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• 1995

Alginic acid is a hydrophilic , colloidal polysaccharide obtained from cell wall of seaweed or brown algae and has a broad range of applications. Alginlc acid becomes alginate gel bead due to its cation-induced gelation. Dried alginate beads can be reswollen according to environmental pH. The purpose of this paper is to explore the possible applicability of alginate beads as an oral controlled release system of ibuprofen. In this experiment ibuprofen was incorporated in alginate beads and alginate beads were treated with various methods. Ibuprofen release from alginate beads in phosphate buffer (pH 7.4) was laster than in distilled water and dilute HCl. The release of ibuprofen was more sustained in bead than simple mixture and coprecipitate of ibuprofen and sodium alginate. The dissolution rate of ibuprofen was decreased in using of bead that hardened with formaldehyde. The dissolution rate of the drug from the bead was the fastest in 12 hour dried beads, 1.5%-sodium alginate concentration and 1%-calcium chloride concentration. Sodium alginate bead can be used as a sustaind release drug delivery system of water-insoluble drugs.

• Biotechnology and Bioprocess Engineering:BBE
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• v.9 no.3
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• pp.191-195
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• 2004

Drug delivery systems that are based on pectin have been studied for colon specific delivery using the specific activity of colon microflora. The aim of this study was to design a novel method of manufacturing pectin microspheres without oils and surfactants and to investigate the potential use of the pectin microspheres as an oral colon-specific drug carrier. The pectin microspheres were successfully formed using the spray drying method and crosslinking with calcium chloride. From the crosslinked pectin microspheres, indomethacin (IND) release was more suppressed than its release from non-crosslinked microspheres. In a low pH (pH 1.4) environment, the pectin microspheres released IND at an amount of about 18${\pm}$2% of the total loaded weight for 24 h while the release rate of IND was stimulated at neutral pH (pH 7.4). IND release from the pectin microspheres was increased by the addition of pectinase. The results clearly demonstrate that the pectin microspheres that were prepared by the spray drying and crosslinking methods are potential carriers for colon-specific drug deliveries.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.2
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• pp.59-64
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• 2008

In our previous study, we found that spermine and putrescine inhibited spontaneous and acetylcholine (ACh)-induced contractions of guinea-pig stomach via inhibition of L-type voltage- dependent calcium current ($VDCC_L$). In this study, we also studied the effect of spermidine on mechanical contractions and calcium channel current ($I_{Ba}$), and then compared its effects to those by spermine and putrescine. Spermidine inhibited spontaneous contraction of the gastric smooth muscle in a concentration-dependent manner ($IC_{50}=1.1{\pm}0.11mM$). Relationship between inhibition of contraction and calcium current by spermidine was studied using 50 mM high $K^+$-induced contraction: Spermidine (5 mM) significantly reduced high $K^+$ (50 mM)-induced contraction to 37${\pm}$4.7% of the control (p<0.05), and inhibitory effect of spermidine on $I_{Ba}$ was also observed at a wide range of test potential in current/voltage (I/V) relationship. Pre- and post-application of spermidine (5 mM) also significantly inhibited carbachol (CCh) and ACh-induced initial and phasic contractions. Finally, caffeine (10 mM)-induced contraction which is activated by $Ca^{2+}$-induced $Ca^{2+}$ release (CICR), was also inhibited by pretreatment of spermidine (5 mM). These findings suggest that spermidine inhibits spontaneous and CCh-induced contraction via inhibition of $VDCC_L$ and $Ca^{2+}$ releasing mechanism in guinea-pig stomach.

• Asian Journal of Turfgrass Science
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• v.10 no.2
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• pp.105-115
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• 1996

To find out the mineral cycles of calcium, magnesium and sodium in dynamic grassland cosystems in a steady state condition, this investigation was conducted along the northwest side on Mt. Kwanak. The experimental results may he suromarized on the communities of a Zoysia japonica and a Miscanthus sinesis as follows. As compared with some properties of the surface soils among two semi-natural grasslands, cal- cium (Ca) was greater quantity in a Zoysia japonica, whereas, in a Miscanthus sicensis, sodium (Na)and magnesium (Mg) were greater in Mt. Kwanak. For the case of steady production and release, the ratio of annual mineral production to the amount accumulated on the top of mineral soil in a steady state provides the estimates of release constant k. The release constants of Ca, Mg and Na of the litter were 0.42, 0.25 and 0.29 in the Zoysia japonica grassland, and were 0.41, 0.54 arid 0.62 in the Miscanthus sinensis grassland, respect- ively. The half times of Ca, Mg and Na required for the release or accumulation of the litter on the grassland were 1.65, 2.77 and 2.39 in the Zoysia japonica, and were 1.69, 1.28 and 1.12 in the Miscauthus sinensis, respectively. The increasing order of the turnover parameters of the elements was Ca, Na and Mg in the Zoysia japonica grassland, and was Na, Mg and Ca in the Miscanthus Si nens is grassland. The amounts of annual cycles for Ca, Mg, Na in the grassland ecosystem under the steady-state conditions were 1.29, 0.20 and 0.12 g /m$^2$ in the Zoysia japonica grassland and 3.91, 1.04 and 0.61 g /m$^2$ in the Miscanthus sinensis grassland.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.2
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• pp.199-205
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• 1999

Vibrio vulnificus cytolysin caused platelet cytolysis and increased intracellular calcium concentration $([Ca^{2+}]_i)$ of rat platelets in a concentration-dependent manner. In the presence of V. vulnificus cytolysin (3 HU/ml), lactate dehydrogenase (LDH) activity was increased from $1.3{\pm}0.4%$ of control to $64.3{\pm}3.4%$ in platelet suspension buffer. In $Ca^{2+}-free$ platelet suspension buffer, however, V. vulnificus cytolysin did not induce $[Ca^{2+}]_i$ increase and LDH release. Addition of EGTA (2 mM) to suspension buffer after the initial $Ca^{2+}$ influx reversed $[Ca^{2+}]_i$ to the control level. However, a $Ca^{2+}$ channel blocker verapamil $(20\;{\mu}M)$ or mefenamic acid $(20\;{\mu}M)$ did not inhibit V. vulnificus cytolysin-induced $[Ca^{2+}]_i$ increase and LDH release. Divalent cations such as $Co^{2+},\;Cd^{2+}\;or\;Mn^{2+}$ (2 mM each) also did not alter V. vulnificus cytolysin-induced $[Ca^{2+}]_i$ increase and LDH release. V. vulnificus cytolysin (3 HU/ml)-induced calcium influx was completely blocked by lanthanum (2 mM). Lanthanum (2 mM) also completely blocked V. vulnificus cytolysin (3 HU/ml)-induced LDH release. Osmotic protectants such as, raffinose, sucrose or PEG600 (50 mM each) did not inhibit the lytic activity of V. vulnificus cytolysin. In conclusion, lanthanum sensitive $Ca^{2+}$ influx plays a significant role in Vibrio vulnificus cytolysin-induced platelet cytolysis and thrombocytopenia in V. vulnificus infection.