• 분석과학
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• 제8권3호
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• pp.299-304
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• 1995

정지상으로서 N, N'-bispalmtoyl 1, 12-diaza-3, 4:9,10-dibenzo-5, 8-cyclopentadecane (hexadecyl $NtnOenH_4$)-octadecylsilanized silicas(ODS)와 이동상으로 물을 사용하여 Ba(II), Cr(II), Fe(II) 및 Cu(II)의 흡착특성을 조사하였다. 수용액상 Ba(II), Cr(II), Fe(II) 및 Cu(II)의 결합상수와 흡착도를 조사한 결과 그 순위는 Ba(II)$NtnOenH_4$-octadecylsilanized silicas(ODS)에 흡측되는 금속이온의 농도 증가는 cation chelation mechanism에 의해 설명할 수 있었다. 또한 수용액상에서 Ba(II), Cr(II), Fe(II) 및 Cu(II)이 혼합된 용액에서 Cu(II)의 분리효율이 다른 이온들에 비해서 좋게 나타남을 알 수 있었다.

• 한국결정성장학회지
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• 제8권2호
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• pp.350-355
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• 1998

Ethylene glycol을 polymeric carrier로 사용한 새로운 화학적 세라믹 분말 제조 공정에 의하여 $(Dy_2TiO_5)$ 분말을 제조하였다. Chelation 공정의 생략에도 불구하고, 고순도의 미세한 입자를 갖는 세라믹 분말 제조가 가능함을 확인하였다. 열분석, 미세구조분석, 회절분석 등으로 분말특성을 평가하였다.

• Bulletin of the Korean Chemical Society
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• 제20권7호
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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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• 제27권3호
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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.