Removal of heavy metal chromium using cross-linked chitosan composite nanofiber mats.

Uniform chitosan composite nanofiber mats (CS/PAAS) containing 4.0 wt% polyacrylic acid sodium loading have been prepared by electrospinning, followed by annealing at elevated temperature to improve solvent resistance and mechanical strength. The CS/PAAS nanofiber mats have been characterized by scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FT-IR) and tensile strength analysis. The prepared nanofiber mats have been shown to be much better than the pristine chitosan powder to adsorb the chromium (VI) ion. SEM-Energy dispersive X-ray spectroscopic (SEM-EDS) and positron annihilation lifetime spectroscopic (PALS) analysis show that Cr(VI) ion can freely permeate into the composite nanofiber and coordinate with the internal chitosan chain molecules. The adsorption abilities of these cross-linked CS/PAAS nanofiber mats are dependent on the chitosan contents as well as N-atom basicity of the chitosan chain. The adsorption capacity toward Cr(VI) ion was improved to 78.92 mg/g after modification of the chelating ligands for the cross-linked CS/PAAS composite nanofibers.

Co-biodegradation of anthracene and naphthalene by the bacterium Acinetobacter johnsonii.

NAP (Naphthalene) and ANT (anthracene) usually co-exist in environment and possessed interactional effects on their biodegradation in environment. Presently, a strain of Acinetobacter johnsonii was employed to degrade NAP and ANT in single- and dual-substrate systems. NAP was utilized as prefer substrate by cells to accelerate ANT biodegradation. As much as 200 mg L-1 ANT could be entirely degraded with 1,500 mg L-1 NAP, which was beyond bacterial potential in single substrate system. Especially, the shortest biodegradation period (103 h) for ANT was observed with the presence of 50 mg L-1 NAP. By contrast, ANT showed strong inhibition on NAP degradation, while the peak biodegradation of 1,950 mg L-1 NAP with 50 mg L-1 ANT could still proceed. By introducing an inhibition constant parameter to fit the inhibition on cells, modeling indicated the substrate inhibition for NAP and ANT over the concentrations of 174 and 49 mg L-1, respectively. Furthermore, enzyme assay revealed the pathway of meta fission in NAP biodegradation due to the appearance of catechol 2,3-dioxygenase activity, and low-level lipase excretion was also found in both NAP and ANT biodegradation, but hardly affect NAP and ANT biodegradation in the present study. To research the interplay of NAP and ANT is conducive to targeted decontamination.

Ceramide-activated phosphatase mediates fatty acid-induced endothelial VEGF resistance and impaired angiogenesis.

Endothelial dysfunction, including endothelial hyporesponsiveness to prototypical angiogenic growth factors and eNOS agonists, underlies vascular pathology in many dysmetabolic states. We investigated effects of a saturated free fatty acid, palmitic acid (PA), on endothelial cell responses to VEGF. PA-pretreated endothelial cells had markedly diminished Akt, eNOS, and ERK activation responses to VEGF, despite normal VEGFR2 phosphorylation. PA inhibited VEGF-induced angiogenic cord formation in Matrigel, and PA-treated endothelial cells accumulated early species (C16) ceramide. The serine palmitoyltransferase inhibitor myriocin reversed these defects. Protein phosphatase 2A (PP2A) became more eNOS-associated in PA-treated cells; the PP2A inhibitor okadaic acid reversed PA-induced signaling defects. Mice fed a diet high in saturated fat for 2 to 3 weeks had impaired i) aortic Akt and eNOS phosphorylation to infused VEGF, ii) ear angiogenic responses to intradermal adenoviral-VEGF injection, and iii) vascular flow recovery to hindlimb ischemia as indicated by laser Doppler and αVß3 SPECT imaging. High-fat feeding did not impair VEGF-induced signaling or angiogenic responses in mice with reduced serine palmitoyltransferase expression. Thus, de novo ceramide synthesis is required for these detrimental PA effects. The findings demonstrate an endothelial VEGF resistance mechanism conferred by PA, which comprises ceramide-induced, PP2A-mediated dephosphorylation of critical activation sites on enzymes central to vascular homeostasis and angiogenesis. This study defines potential molecular targets for preservation of endothelial function in metabolic syndrome.