• Macromolecular Research
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• v.13 no.6
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• pp.499-505
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• 2005

Ordered mesoporous materials with a hydrothermally-stable, protozeolitic framework were prepared by exploring the direct conversion of inorganic species based on co-surfactant templating systems. To confer hydrothermal stability on the mesoporous aterials, the organic-inorganic hybrids were heat-treated in strongly basic media. Co-surfactant templating systems of cetyltrimethylammonium bromide [$C_{16}H_{13}(CH_{3})_{3}$NBr, CTAB] with 1,3,5-trim­ethylbenzene (TMB) or a nonionic block copolymer of poly(ethylene oxide )-b-poly(propylene oxide )-b-poly(ethyl­ene oxide) ($EO_{20}PO_{70}EO_{20}$) were employed to improve the hydrothermal stability of the organic-inorganic self-assembly during the solid rearrangement process of the inorganic species. The mesoscopic ordering of the pore structure and geometry was identified by X-ray diffraction, small angle neutron scattering and electron microscopy.

• 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.43 no.5
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• pp.659-664
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• 1999

To investigate the difference of contractile mechanism between KCI and phenylephrine-induced contraction, we observed effects of $Ca^{2+}$ antagonists and protein kinase inhibitors on aorta contraction of rats. Verapamil dose-dependently inhibited the contraction induced by KCI and phenylephrine, the inhibitory effect of verapamil was more potent in KCI-induced contraction than phenylephrine-induced contraction. Econazole and TMB-8 significantly inhibited CKI-induced contraction but did not inhibit phenylephrine-induced contraction. Staurosporine dose-dependently inhibited both KCI and phenylephrine-induced contraction. Genistein and calmodulin antagonists (W-7 and trifluoperazine) also inhibited both contraction in a dose dependent manner. However, the inhibitory effects of genistein and calmodulin antagonists were more potent in phenylephrine-induced contraction than KCI-induced contraction. These results suggest that involvements of $Ca^{2+}$ channel and protein kinase in rat aorta contraction were dependent on agonist causing aorta smooth muscle contraction.

• Journal of the Korean Chemical Society
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• v.67 no.6
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• pp.415-419
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• 2023

In this study, we report the one-pot synthesis of reduced graphene oxide (rGO) containing platinum nanoparticles with catalytic activity to break down hydrogen peroxide as a peroxidase-mimicking catalyst. A single reducing agent was used to reduce graphene oxide and a platinum precursor at a moderately low temperature of 70℃. The rGO was homogeneously decorated with platinum nanoparticles. The catalytic activity of Pt-rGO was investigated for the oxidation of 3,3',5,5'- tetramethylbenzidine (TMB), a peroxidase substrate, in the presence of hydrogen peroxide. The Pt-rGO coupled with glucose oxidase was also able to detect glucose at millimolar concentrations (up to 1 mM). Our results show that the Pt-rGO composite is a promising catalyst for the detection of hydrogen peroxide. This method was also applied for the detection of glucose.

• Korean Journal of Food Science and Technology
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• v.36 no.6
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• pp.959-967
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• 2004

To screen probiotic lactic acid bacteria with potent adhesive property on human colonic mucosa, colonic mucin-binding assay was introduced. This colonic mucin-binding assay actually measures the binding activity of surface lectin-like protein (SLP) on colonic mucin, and the optimal conditions were examined. The optimal pH for colonic mucin coating on plate wells was 4.8, and ${\times}24,000$ diluted solution of commercially available horseradish peroxidase (HRP) conjugated streptoavidin yielded good results, for rapid screening, $5.0\;{\mu}g/mL$ of biotinylated SLP from lactic acid bacteria was optimal, and optimal scintillation time of 3,3',5,5'-tetramethyl benzidine (TMB) was 10 min. These conditions were useful for both rapid selection and quantitative analysis of lactic acid bacteria that have high adhesion property to human intestinal tract. Among 50 strains of lactic acid bacteria, including 32 type culture strains and 18 isolated strains from infant feces, Lactobacillus species FSB-1 isolated from kimchi showed the highest binding activity to colonic mucin. From taxonomical viewpoints based on morphological study, physico-biochemical study, partial 16S rDNA seguencing, and phylogenetic analysis, L. species FSB-1 was identified as Lactobacillus brevis.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.83-91
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• 1999

Angiotensin II (ANG II) has a biphasic effect on $Na^+$ transport in proximal tubule: low doses of ANG II increase the $Na^+$ transport, whereas high doses of ANG II inhibit it. However, the mechanisms of high dose ANG II-induced inhibition on $Na^+$ uptake are poorly understood. Thus the aim of the present study was to investigate signal transduction pathways involved in the ANG II-induced inhibition of $Na^+$ uptake in the primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. ANG II $(10^{-9}\;M)-induced$ inhibition of $Na^+$ uptake was blocked by losartan $(10^{-8}\;M,\;AT_1\;antagonist),$ but not by PD123319 $(10^{-8}\;M,\;AT_2\;antagonist)$ (P<0.05). ANG II-induced inhibition of $Na^+$ uptake was also completely abolished by neomycin $(10^{-4}\;M,$ PLC inhibitor), W-7 $(10^{-4}\;M,$ calmodulin antagonist), and $AACOCF_3\;(10^{-6}\;M,\;PLA_2\;inhibitor)$ (P<0.05). ANG II significantly increased $[^3H]arachidonic$ acid (AA) release compared to control. The ANG II-induced $[^3H]AA$ release was blocked by losartan, $AACOCF_3,$ neomycin, and W-7, but not by PD123319. ANG II-induced $[^3H]AA$ release in the presence of extracellular $Ca^{2+}$ was greater than in $Ca^{2+}-free$ medium, and it was partially blocked by TMB-8 $(10^{-4}\;M,$ intracelluar $Ca^{2+}$ mobilization blocker). However, in the absence of extracellular $Ca^{2+},$ it was completely blocked by TMB-8. In addition, econazole $(10^{-6}\;M,$ cytochrome P-450 monooxygenase inhibitor) and indomethacin $(10^{-6}\;M,$ cyclooxygenase inhibitor) blocked ANG II-induced inhibition of $Na^+$ uptake, but NGDA $(10^{-6}\;M,$ lipoxygenase inhibitor) did not affect it. In conclusion, $PLA_2-mediated$ AA release is involved in ANG II-induced inhibition of $Na^+$ uptake and is modulated by $[Ca^{2+}]_i$ in the PTCs.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.43-55
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• 1993

The present study was conducted to examine the characteristics of histamine on catecholamine secretion in the isolated perfused rat adrenal gland and to clarify the mechanism of its secretory action. Histamine (37.5 to 150 ug) injected into an adrenal vein evoked a dose-dependent significant secretory response of catecholamines (CA) from the rat adrenal gland. However, upon the repeated injection of histamine (150 ug) at 120 min intervals, CA secretion was rapidly decreased after third injection of histamine. Tachyphylaxis to releasing effects of CA evoked by histamine was observed by the repeated administration. The histamine-induced CA secretion was markedly inhibited by the pretreatment with chlorisondamine, diphenhydramine, ranitidine, $Ca^{++}-free$ Krebs solution, nicardipine and TMB-8 while was not affected by pirenzepine. Moreover, the CA secretion evoked by ACh was considerably reduced by the prior perfusion of histamine $(6.8{\times}10^{-5} M)$ for 30 min. These experimental data suggest that histamine causes secretion of CA in a calcium dependent manner from the perfused rat adrenal gland and that its secretory effect is mediated through activation of both $H_1-$ and $H_2-histaminergic$ receptors located in adrenal medulla, which may be associated with stimulation of cholinergic nicotinic receptors.

• Journal of the korean academy of Pediatric Dentistry
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• v.30 no.4
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• pp.626-636
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• 2003

Pediococcus pentosaceus K1270 was isolated from naturally fermented kimchi and identified based on the 16S rDNA sequence as well as cultural and biochemical characteristics. This strain strongly inhibited the formation of biofilm by Streptococcus mutans Ingbritt. K1270 also showed antibacterial activity against S. mutans Ingbritt. It was observed that K1270 strain produced hydrogen peroxide on MRS agar supplemented with 3, 3, 5, 5-tetramethylbenzidine (TMB) and peroxidase and the inhibitory effect of K1270 strain on the biofilm formation was reversed by the addition of catalase in part. Culture supernatant of K1270 inhibited the biofilm formation and the multiplication of S. mutans Ingbritt. This inhibitory effect of culture supernatant was decreased slightly by the addition of catalase and abolished by heat or trypsin treatment. Thus, this study suggests that P. pentosaceus K1270 inhibit the biofilm formation through the inhibition of the replication of S. mutans Ingbritt by producing hydrogen peroxide and bacteriocin.

• Journal of the Korean Chemical Society
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• v.53 no.6
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• pp.683-692
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• 2009

The synthesis of a novel series of nickel(II) complexes with new ligands derived from hydrazones of isoniazid have been reported in present work. The complexes have general compositions [$Ni(L)_2X_2$] or $[Ni(L)_3](ClO_4)_2$ {L = N-isonicotinamido-furfuraldimine (INH-FFL), N-isonicotinamido-3',4',5'-trimethoxybenzaldimine (INH-TMB) or N-isonicotinamido-cinnamalidene (INH-CIN) and X = $Cl^-$, ${NO_3}^-$, $ NCS^-$ or $CH_3COO^-$}. The ligands hydrazones behave as neutral bidentates (N and O donor) through the carbonyl oxygen and azomethine nitrogen. The new complexes with octahedral geometry have been characterized by elemental analysis, molecular weight determinations, magnetic susceptibility/moment, thermogravimetric, electrochemical and spectroscopic studies viz. infrared and electronic spectra. On the basis of conductivity measurements in nitrobenzene ($PhNO_2$) solution the [$Ni(L)_2X_2$] and $[Ni(L)_3](ClO_4)_2$ complexes have been found to be non-electrolytes and 1:2 electrolytes, respectively. Thermal properties have also been investigated, which support the geometry of the complexes. Antibacterial and antifungal properties of nickel(II) complexes and few standard drugs have also been examined and it has been observed that the complexes have moderate antibacterial activities.

• Archives of Pharmacal Research
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• v.21 no.6
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• pp.664-670
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• 1998

The role of intracellular $Ca^{2+}$, in the regulation of tumor cell proliferation by products of arachidonic acid (AA) metabolism was investigated using U-373 MG human as trocytoma cells. Treatment with nordihydroguaiaretic acid (NDGA), a lipoxygenase (LOX) inhibitor, or caffeic acid (CA), a specific 5-LOX inhibitor, suppressed proliferation of the tumor cells in a dose-dependent manner. However, indomethacin (indo), a cyclooxygenase (COX) inhibitor, did not significantly alter proliferation of the tumor cells. At anti-proliferative concentrations, NDGA and CA significantly inhibited intracellular $Ca^{2+}$ release induced by carbachol, a known intracelluar $Ca^{2+}$ agonist in the tumor cells. Exogenous administration of leukotriene $B_4(LTB_4)$, an AA metabolite of LOX pathway, enhanced proliferation of the tumor cells in a concentration-dependent fashion. In addition, $LTB_4$, induced intracelluar $Ca^{2+}$ release. Intracellular $Ca^{2+}$-inhibitors, such as an intracellular $Ca^{2+}$ chelator (BAPTA) and intracellular $Ca^{2+}$-release inhibitors (dantrolene and TMB-8), significantly blocked the LTB4-induced enhancement of cell proliferation and intracellular $Ca^{2+}$ release. These results suggest that LOX activity may be critical for cell proliferation of the human astrocytoma cells and that intracelluar $Ca^{2+}$ may play a major role in the mechanism of action of LOX.