No abstract

A series of unsymmetrical 2,6-bis(imino)pyridylcobalt(II) complexes, {2-[2,6-(CH(C(6)H(5))(2))(2)-4-Me-C(6)H(2)N==C(CH(3))]-6-(2,6-R(1)(2)-4-R(2)-C(6)H(2)N==CCH(3))-C(5)H(3)NCoCl(2)} where R(1) = Me, Et or (i)Pr, R(2) = H or Me, together with the new symmetrical complex 2,6-[2,6-(CH(C(6)H(5))(2))(2)-4-Me-C(6)H(2)N==C(CH(3))](2)-C(5)H(3)NCoCl(2), were synthesized. All of the compounds were fully characterized by (1)H NMR and IR spectroscopy, as well as by elemental analysis. The molecular structures of Co1 (R(1) = Me, R(2) = H) and Co5 (R(1) = Et, R(2) = Me) were further confirmed by single crystal X-ray diffraction, which indicated that the cobalt centres were penta-coordinate with a pseudo square-pyramidal geometry. Upon treatment with MAO or MMAO, these cobalt pre-catalysts exhibited higher activities than any previously reported cobalt pre-catalysts, with values as high as 4.64 × 10(6) g PE mol(-1)(Co) h(-1) for ethylene polymerization at atmospheric pressure. The polyethylenes obtained were of high molecular weight and narrow molecular weight distribution.

Cadmium (Cd) is a known nephrotoxic element. In this study, the primary cultures of rat proximal tubular (rPT) cells were treated with low doses of cadmium acetate (2.5 and 5 microM) to investigate its cytotoxic mechanism. A progressive loss in cell viability, together with a significant increase in the number of apoptotic and necrotic cells, were seen in the experiment. Simultaneously, elevation of intracellular [Ca(2+)]i and reactive oxygen species (ROS) levels, significant depletion of mitochondrial membrane potential(Delta Psi) and cellular glutathione (GSH), intracellular acidification, and inhibition of Na(+), K(+)-ATPase and Ca(2+)-ATPase activities were revealed in a dose-dependent manner during the exposure, while the cellular death and the apoptosis could be markedly reversed by N-acetyl-L-cysteine (NAC). Also, the calcium overload and GSH depletion were significantly affected by NAC. In conclusion, exposure of rPT cells to low-dose cadmium led to cellular death, mediated by an apoptotic and a necrotic mechanism. The apoptotic death might be the chief mechanism, which may be mediated by oxidative stress. Also, a disorder of intracellular homeostasis induced by oxidative stress and mitochondrial dysfunction is a trigger of apoptosis in rPT cells.

Co3O4 nanosheets are straightforwardly fabricated through an in situ dealloying and oxidation process of etching CoAl alloy in alkaline solutions. X‐ray diffraction and electron spectroscopy characterizations demonstrate the formation of a Co3O4 nanostructure with an intricate hierarchical nanosheet morphology comprising interconnected nanoslices with the diameter as small as 6 nm. Upon calcination in O2 atmosphere, these novel Co3O4 nanosheets exhibit excellent catalytic activity toward CO oxidation in normal feed gas at ambient temperature. Catalytic tests reveal the strong influence of calcination temperature on the resultant catalytic activities, whereby 300 °C is found to be preferable possibly due to an optimum balance between the surface area and the amount of active species as compared with 200 and 450 °C. Moreover, Co3O4 nanosheets showed good time‐on‐stream catalytic stability; CO conversion at T50 (the temperature for 50 % CO conversion) reduced to 37 % after 20 h, and at T100 (the temperature for full CO conversion) the conversion only decreased to about 90 % after 15 h.

A new PC(sp(3))P ligand N,N'-bis(diphenylphosphino)dipyrromethane [PCH2P] (1) was prepared and its iron, cobalt and nickel chemistry was explored. Two pincer-type complexes [PCHP]Fe(H)(PMe3)2 (2) and [PCHP]Co(PMe3)2 (4) were synthesized in the reaction of with Fe(PMe3)4 and Co(Me)(PMe3)4. 1 reacted with Co(PMe3)4 and Ni(PMe3)4 to afford Co(0) and Ni(0) complexes [PCH2P]Co(PMe3)2 (3) and [PCH2P]Ni(PMe3)2 (5). The structures of complexes 2-5 were determined by X-ray diffraction.

No abstract

Designing MoS2 nanocatalysts rich with active edge sites by engineering of the nanostructures is an effective strategy to enhance their catalytic activity.

No abstract