• Analytical Science and Technology
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• v.8 no.3
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• pp.299-304
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• 1995

The adsorption behaviors of Ba(II), Cr(II), Fe(II) and Cu(II) on the N, N'-bispalmtoyl 1, 12-diaza-3, 4:9, 10-dibenzo-5, 8-cyclopentadecane (hexadecyl $NtnOenH_4$)-octadecylsilanized silicas(ODS) were investigated with water as the mobile phase. Binding constants for metal ions were measured in aqueous solution. The order of binding constants(K) and the degree of sorption(E) were Ba(II)$NtnOenH_4$-octadecyisiianized silicas(ODS) increased with concentration of metal ions, and the degree of adsorption was found to be affected by the cation-chelation mechanism. The experimental results showed good efficiency for separation of Cu(II) from mixtures of Ba(II), Cr(II), Fe(II) and Cu(II) in aqueous solution.

• Journal of the Korean Crystal Growth and Crystal Technology
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• v.8 no.2
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• pp.350-355
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• 1998

Dysprosium monotitanate $(Dy_2TiO_5)$ powder was synthesized by a simple mixed-oxide ceramics process using ethylene glycol (EG). Ethylene glycol, as the organic carrier for the metal cations, was used for polymerization mechanism. The successful used of a non-chelating polymer for the mixed-oxide ceramic process indicated that cation chelation is not the only route for creating stable ceramic precursors. Characterization of the powders by various thermal analysis, microscopy, and diffraction methods has been carried out.

• Bulletin of the Korean Chemical Society
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• v.20 no.7
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• pp.796-800
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• 1999

Three anthrylazacrown ethers in which the anthracene fluorophore π system is separated from the electron donor atoms by one methylene group were synthesized, and their photophysical study was accomplished. These fluorescent compounds showed a maximum fluorescence intensity at pH=5 in aqueous solutions and a decrease in fluorescence intensity upon binding of paramagnetic metal cations (Mn 2+ (d 5 ), Co 2+ (d 7 ), Cu 2+ (d 9 )). The decrease in fluorescence intensity may be attributed to the paramagnetic effect of metal cations to deactivate the excited state by the nonradiative quenching process. The benzylic nitrogen was found to play an important role in changing fluorescence intensity. From the observed linear Stern-Volmer plot and the fluorescence lifetime independence of the presence of metal ions, it was inferred that the chelation enhanced fluorescence quenching (CHEQ) mechanism in the system is a ground state static quenching process. Enhanced fluorescence was also observed when an excess Na + ion was added to the quenched aqueous solution, and it was attributed to cation displacement of a complexed fluorescence quencher.

• Archives of Pharmacal Research
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• v.27 no.3
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• pp.305-313
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• 2004

The effect of diazoxide, a $K^{+}$channel opener, on apoptotic cell death was investigated in HepG2 human hepatoblastoma cells. Diazoxide induced apoptosis in a dose-dependent manner and this was evaluated by flow cytometric assays of annexin-V binding and hypodiploid nuclei stained with propidium iodide. Diazoxide did not alter intracellular $K^{+}$concentration, and various inhibitors of $K^{+}$channels had no influence on the diazoxide-induced apoptosis; this implies that $K^{+}$channels activated by diazoxide may be absent in the HepG2 cells. However, diazoxide induced a rapid and sustained increase in intracellular $Ca^{2+}$ concentration, and this was completely inhibited by the extracellular $Ca^{2+}$ chelation with EGTA, but not by blockers of intracellular $Ca^{2+}$ release (dantrolene and TMB-8). This result indicated that the diazoxide-induced increase of intracellular $Ca^{2+}$ might be due to the activation of a Ca2+ influx pathway. Diazoxide-induced $Ca^{2+}$ influx was not significantly inhibited by either voltage-operative $Ca^{2+}$ channel blockers (nifedipinen or verapamil), or by inhibitors of $Na^{+}$, $Ca^{2+}$-exchanger (bepridil and benzamil), but it was inhibited by flufenamic acid (FA), a $Ca^{2+}$-permeable nonselective cation channel blocker. A quantitative analysis of apoptosis by flow cytometry revealed that a treatment with either FA or BAPTA, an intracellular $Ca^{2+}$ chelator, significantly inhibited the diazoxide-induced apoptosis. Taken together, these results suggest that the observed diazoxide-induced apoptosis in the HepG2 cells may result from a $Ca^{2+}$ influx through the activation of $Ca^{2+}$-permeable non-selective cation channels. These results are very significant, and they lead us to further suggest that diazoxide may be valuable for the therapeutic intervention of human hepatomas.