Residual fraction of REEs accounted for the majority of their total concentrations. Middle REEs were more easily leached than other REEs, especially in clayey silt sediment REEs contents in the surface sediment from the intertidal Bohai Sea were consistent with data from the upper continental crust and China shallow sea sediments, indicating that they were generally unaffected by heavily anthropogenic effects from adjacent areas. (C) 2014 SN-38 mw Elsevier Inc. All rights reserved.”
“Alpinetin,

a novel plant flavonoid derived from Alpinia katsumadai Huyata, has been reported to have anti-inflammatory properties. However, the anti-inflammatory mechanism of alpinetin has not been Fully elucidated. The purpose of this study was to investigate the anti-inflammatory mechanism of alpinetin in modifying lipopolysaccharide (LPS)-induced signaling pathways in human THP-1 macrophages. The cells were stimulated with [PS in the presence or absence of alpinetin. The pro-inflammatory cytokines were evaluated by ELISA and qRT-PCR. Toll-like receptor 4 (TLR4),

nuclear factor-kappa B (NF-kappa B), inhibitory kappa B (I kappa B alpha) protein, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and PPAR-gamma were determined by Western blotting. The results showed that alpinetin inhibited TNF-alpha, IL-6 and IL-1 beta expression in LPS-stimulated human THP-1 macrophages in a dose-dependent manner. Western blot analysis showed that alpinetin suppressed LPS-induced NF-kappa B activation, Elafibranor order I kappa B alpha degradation, phosphorylation of ERK, JNK and P38. Furthermore, alpinetin could significantly down-regulated the expression of TLR4 stimulating by [PS. We also found that alpinetin could activate PPAR-gamma and the anti-inflammatory

effects of alpinetin can be reversed by GW9662, a specific antagonist for PPAR-gamma. These results suggest that alpinetin activates PPAR-gamma, thereby attenuating TLR4 expression and TLR4 mediated NF-kappa B and MAPK activation and the release of proinflammatory HDAC inhibitor cytokines. These findings suggest that alpinetin may be a therapeutic agent against inflammatory diseases. (C) 2013 Published by Elsevier B.V,”
“To investigate azithromycin susceptibility in Shigella sonnei in the United States, we examined the azithromycin minimum inhibitory concentrations (MICs) of outbreak and routine human S. sonnei isolates. Isolate susceptibility clustered at 8 mg/L, but three isolates displayed higher MICs (>64 mg/L) to azithromycin. All three isolates contained a plasmid-encoded mphA gene, known to encode a macrolide-2′-phosphotransferase enzyme. Transformation of the mphA gene into Escherichia coli DH10B allowed the transfer of decreased susceptibility to azithromycin.