Nanoporous NiO thin film electrodes were obtained via plasma-assisted microwave sintering and characterized by means of a combination of electrochemical techniques and X-ray photoelectron spectroscopy (XPS). The aim of this study is the elucidation of the nature of the surface changes introduced by the redox processes of this nanostructured material. NiO undergoes two distinct electrochemical processes of oxidation in aqueous electrolyte with the progress of NiO anodic polarization. These findings are consistent with the sequential formation of oxyhydroxide species at the surface, the chemical nature of which was assessed by XPS. Electronic relaxation effects in the Ni 2p spectra clearly indicated that the superficial oxyhydroxide species resulted to be β-NiOOH and γ-NiOOH. We also show for the first time spectral evidence of an electrochemically generated Ni(IV) species. This study has direct relevance for those applications in which NiO electrodes are utilized in aqueous electrolyte, namely catalytic water splitting or electrochromism, and may constitute a starting point for the comprehension of electronic phenomena at the NiO/organic electrolyte interface of cathodic dye-sensitized solar cells (p-DSCs).

There are strong associations between plaque vascularity, quantity of intraplaque haemorrhage and presence of symptomatic carotid occlusive disease.

No abstract

Increasing evidence points to the fact that defects in the resolution of inflammatory pathways predisposes individuals to the development of chronic inflammatory diseases, including diabetic complications such as accelerated atherosclerosis. The resolution of inflammation is dynamically regulated by the production of endogenous modulators of inflammation, including lipoxin A4 (LXA). Here, we explored the therapeutic potential of LXA and a synthetic LX analog (Benzo-LXA) to modulate diabetic complications in the streptozotocin-induced diabetic ApoE mouse and in human carotid plaque tissue ex vivo. The development of diabetes-induced aortic plaques and inflammatory responses of aortic tissue, including the expression of ,, , and, was significantly attenuated by both LXA and Benzo-LXA in diabetic ApoE mice. Importantly, in mice with established atherosclerosis, treatment with LXs for a 6-week period, initiated 10 weeks after diabetes onset, led to a significant reduction in aortic arch plaque development (19.22 ± 2.01% [diabetic]; 12.67 ± 1.68% [diabetic + LXA]; 13.19 ± 1.97% [diabetic + Benzo-LXA]). Secretome profiling of human carotid plaque explants treated with LXs indicated changes to proinflammatory cytokine release, including tumor necrosis factor-α and interleukin-1β. LXs also inhibited platelet-derived growth factor-stimulated vascular smooth muscle cell proliferation and transmigration and endothelial cell inflammation. These data suggest that LXs may have therapeutic potential in the context of diabetes-associated vascular complications.

This study confirms the central role played by activated neutrophils in the early stages of reperfusion injury and also suggests a role for plasma mediators in mediating cardiopulmonary dysfunction during major vascular surgery.

In a randomized comparison of nevirapine or abacavir with zidovudine plus lamivudine, routine viral load monitoring was not performed, yet 27% of individuals with viral failure at week 48 experienced resuppression by week 96 without switching. This supports World Health Organization recommendations that suspected viral failure should trigger adherence counseling and repeat measurement before a treatment switch is considered.

No abstract

Lung injury following reperfusion results from endothelial damage caused by release of cytotoxic products by activated neutrophils (PMN) in the pulmonary microvasculature. This process is facilitated by the release of pro-inflammatory cytokines and arachidonic metabolites following the outset of reperfusion. This study aimed to evaluate the effect of plasma obtained before and after revascularisation on neutrophil and endothelial cell activation. Plasma (IR-plasma) was obtained from venous blood samples taken before and during aortic cross-clamping, and 5, 40 and 60 min following clamp removal in seven patients undergoing elective infrarenal aortic aneurysm resection. PMN from healthy volunteers (n = 5) were incubated with these plasma samples or with fMLP (N-formylmethionyl-leucyl-phenylalanine) as positive control for 30 min and assessed flow-cytometrically for CD11b expression. Human endothelial cells (ECV-304) were incubated with IR plasma for 2, 4 and 6 h or with tumour necrosis factor (TNF) (20 ng/ml) as positive control and assessed for ICAM-1 expression. Incubation with IR plasma resulted in a significant increase from pre-clamp in PMN CD11b expression. A similar trend was seen in endothelial cell ICAM-1 expression following 2 h incubation. These results indicate that reperfusion-induced endothelial dysfunction may be mediated by plasma factors released upon revascularisation which facilitate neutrophil-endothelial interaction through up-regulation of adhesion receptor expression.