Complexation of actinides and lanthanides with carboxylic organic ligands is known to facilitate migration of radionuclides from deep geological disposal systems of spent nuclear fuel. In order to examine the ligand-dependent structures of trivalent actinides and lanthanides, a series of Eu(III)-aliphatic dicarboxylate compounds, Eu2(oxalate)3(H2O)6, Eu2(malonate)3(H2O)6, and Eu2(succinate)3(H2O)2, were synthesized and characterized by using X-ray crystallography and time-resolved laser fluorescence spectroscopy. Powder X-ray diffraction results captured the transition of the coordination modes of aliphatic dicarboxylate ligands from side-on to end-on binding as the carbon chain length increases. This transition is illustrated in malonate bindings involving a combination of side-on and end-on modes. Strongly enhanced luminescence of these solid compounds, especially on the hypersensitive peak, indicates a low site symmetry of these solid compounds. Luminescence lifetimes of the compounds were measured to be increased, which is ascribed to the displacement of water molecules in the innersphere of Eu center upon bindings of the organic ligands. The numbers of remaining bound water molecules estimated from the increased luminescence lifetimes were in good agreement with crystal structures. The excitation-emission matrix spectra of these crystalline polymers suggest that oxalate ligands promote the sensitized luminescence of Eu(III), especially in the UV region. In the case of malonate and succinate ligands, charge transfer occurs in the opposite direction from Eu(III) to the ligands under UV excitation, resulting in weaker luminescence.

본 연구에서는 PEN 수지 안전관리를 위하여 HPLC-UV검출기를 이용한 2,6-NDC 및 2,6-NDA 분석법을 확립하였다. 분석법 검증 결과, 2,6-NDC 및 2,6-NDA 모두 0.002μg/mL 검출한계, 0.005 μg/mL 정량한계 및 0.05~1 μg/mL의 농도 범위에서 r2= 0.999 이상의 직선성을 확인할 수있었다. 또한 회수율도 90~110%임을 확인할 수 있었다.

In this study DMT(Dimethylterephthalate), NDC(Dimethyl-2, 6-Naphthalene Dicarboxylate) were used to synthesize polyester polyol which shows enhanced storage stability, improved flame retardancy, and good compressive strength. If DMT and NDC react respectively with DEG(Diethylene Glycol) which is kind of linear diol, the obtained polyester polyols tend to crystallize easily after the reaction. In case of DMT, PA(Phthalic Anhydride) which has asymmetric structure was introduced to retard the crystallization. In case of NDC, DPG(Dipropylene Glycol) which has an methyl side chain was introduced to prevent the crystallization. It was found that to introduce DPG was much more effective method to prevent the crystallization than PA. NDC and DMT were reacted together with DPG for various compositions of NDC:DMT(8:2, 6:4, 4:6 mol ratio). The obtained NDC-DMT-DPG based polyester polyol showed improved flame retardancy, and good compressive strength with increasing the content of NDC.

L-trans-pyrrolidine-2,4-dicarboxylate (PDC) is a potent inhibitor of glutamate transporters. In our current study, we investigated whether the neuronal death induced by PDC involves mechanisms other than excitotoxicity in mixed mouse cortical cultures. Cortical cultures at 13-14 days in vitro were used and cell death was assessed by measuring the lactate dehydrogenase efflux into bathing media. Glutamate and PDC both induced neuronal death in a concentration-dependent manner but the neurotoxic effects of glutamate were found to be more potent than those of PDC. Treatment with 10, 100 and 200 M PDC equally potentiated 50 M glutamate-induced neuronal death. The neuronal death induced by 75 M glutamate was almost abolished by treatment with the NMDA antagonists, MK-801 and AP-5, but was unaffected by NBQX (an AMPA antagonist), trolox (antioxidant), BDNF or ZVAD-FMK (a pan-caspase inhibitor). However, the neuronal death induced by 200 M PDC was partially but significantly attenuated by single treatments with MK-801, AP-5, trolox, BDNF or ZVAD-FMK but not NBQX. Combined treatments with MK-801 plus trolox, MK-801 plus ZVAD-FMK or MK-801 plus BDNF almost abolished neuronal death, whereas combined treatments with trolox plus ZVADFMK, trolox plus BDNF or ZVAD-FMK plus BDNF did not enhance the inhibitory action of any single treatment with these drugs. These results demonstrate that the neuronal death induced by PDC involves not only in the excitotoxicity induced by the accumulation of glutamate but also the oxidative stress induced by free radical generation. This suggests that apoptotic neuronal death plays a role in PDCinduced oxidative neuronal injury.