Ruthenium Carbonyl Clusters in Faujasite Cages: Synthesis and Characterization.

The synthesis of the intrafaujasite anchoring of ruthenium carbonyl clusters involves the adsorption of metal carbonyl species or metal ion exchange into faujasite cages followed by reductive carbonylation under an atmosphere of CO and H(2). The characterization of the structure and properties of these samples was based on a multianalytical approach, including FT-IR, UV-vis, PXRD, and EXAFS spectroscopies, CO/H(2) gas chemisorption, and (13)CO isotopic exchange. From this study, several key points emerge. (a) [Ru(3)(CO)(12)] clusters thermally diffused into dehydrated faujasite cages. (b) [Ru(3)(CO)(12)] guests in Na(56)Y were thermally activated, in a hydrogen atmosphere, generating intrafaujasite [H(4)Ru(4)(CO)(12)]. (c) Hexammineruthenium(III) complexes in Na(56)X and Na(56)Y underwent progressive thermal activation, in a CO and H(2) atmosphere. The generation process was considered to occur through conversion of the intermediates [Ru(NH(3))(5)(CO)](2+) and Ru(I)(CO)(3) to [Ru(6)(CO)(18)](2)(-). (d) A rapid (13)CO/(12)CO isotopic exchange was found to reversibly occur for [Ru(6)(CO)(18)](2)(-)/Na(56)X under H(2) coexistence. (e) Internal and external confinement of ruthenium carbonyl clusters were compared. (f) Oxidation fragmentation under an O(2) atmosphere and reductive regeneration under a CO and H(2) atmosphere were found to reversibly occur for [Ru(6)(CO)(18)](2)(-) guests. (g) Intrafaujasite anchoring of ruthenium carbonyl clusters showed a strong interaction with the extraframework Na(+) alpha-cage cations, through involvement of the oxygen end of the bridging or equatorial terminal carbonyl ligands.

Basic fibroblast growth factor protects C17.2 cells from radiation-induced injury through ERK1/2.

AIMS: To establish a radiation-induced neural injury model using C17.2 neural stem cells (NSCs) and to investigate whether basic fibroblast growth factor (bFGF) can protect the radiation-induced injury of C17.2 NSCs. Furthermore, we aim to identify the possible mechanisms involved in this model. METHODS: C17.2 NSCs received a single exposure (3, 6, and 9 Gy, respectively) at a dose rate of 300 cGy/min with a control group receiving 0 Gy. Different concentrations of bFGF were added for 24 h, 5 min postirradiation. The MTS assay and flow cytometry were used to detect cytotoxicity and apoptosis. Expression of FGFR1, ERK1/2, and p-ERK1/2 proteins was detected with or without U0126 was pretreated prior to C17.2 NSCs receiving irradiation. RESULTS: C17.2 NSCs showed a dose-dependent cell death as the dose of radiation was increased. Additionally, the rate of apoptosis in the C17.2 NSCs reached 31.2 ± 1.23% in the 6 Gy irradiation group, which was the most significant when compared to the other irradiation treated groups. bFGF showed protective effect on cell apoptosis in a dose-dependent manner. The mean percentage of apoptotic cells decreased to 7.83 ± 1.75% when 100 ng/mL bFGF was given. Furthermore, U0126 could block the protective effect of bFGF by inhibiting the phosphorylation of ERK1/2. CONCLUSIONS: An in vitro cellular model of radiation-induced apoptosis of NSCs, in C17.2 NSCs, was developed successfully. Additionally, bFGF can protect neurons from radiation injury in vitro via the ERK1/2 signal transduction pathway.

[Correlations between PBDEs and thyroid hormone concentrations in adults from production source area].

Polybrominated diphenyl ethers (PBDEs) concentrations in 36 resident serum samples from PBDEs production source area were analyzed by gas chromatography/negative chemical ionization/mass spectrometry(GC-NCI-MS) method, and the concentrations of thyroid hormones were determined as well. The sigma5PBDEs (BDE-28, -47, -153, -183, -209) concentrations(lipid weight) in serum ranged from 130.3 to 4 478.4 ng x g(-1), with an average value of 529.9 ng x g(-1). BDE-209 was a dominant PBDE congener, on average accounting for 69.8% of the total PBDEs concentrations. Spearman rank correlation coefficient was calculated between PBDEs and thyroid hormone, it showed that there were high significant negative correlation between BDE-28, -47, -153, -183 and thyroid-stimulating hormone (TSH), and significant negative correlation was also found between BDE-183 and free thyroxine (fT4). Additionally, there were significant positive correlation between BDE-28, -47 and triiodothyronine (T3), as well as between BDE-28, -153, -183 and free triiodothyronine(fT3). In summary, the concentrations of PBDEs in serum in this study were at a high level, and BDE-209 was the predominant congener. The exposure to the PBDEs may affect thyroid hormone levels, and the further research should focus on the relationship between PBDEs and thyroid hormone concentrations.