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Abstract\ud \ud In this paper, we present the design of nanostructured multilayer absorbers, carried out with the aid of a genetic algorithm (GA). Waveguide measurements are performed to recover the dielectric properties of micrographite single-walled carbon nanotube, micrographite walled carbon nanotube, carbon nanofiber, and fullerene-based composite materials. Conductive fillers are uniformly dispersed in an epoxy resin at different weight percentages (1, 3, 5 wt.%). The electromagnetic (EM) analysis is performed embedding the forward/backward propagation matrix formalism in an in-house GA, thus able to carry out optimization upon oblique incidence over a finite angular range. Developed code minimizes both the reflection and the transmission coefficients under the thickness minimization constraint. Comparison between micrographite and nanopowders absorbers is presented and discussed, when a broadband quasi-perfect absorber is achieved among the X-band combining the two filler families, i.e., exhibiting a loss factor greater than 90% in most of the band, for a thickness of about 1 cm. It is demonstrated that the nanofillers with higher aspect ratio mainly contribute to the EM absorption. Findings are of interest in both radar-absorbing material and shielding structures

Apoptosis and aging share common mechanisms in oxidative stress and mitochondrial involvement. Treatment of cultured neuroblastoma cells with a radical initiator induced apoptosis; raise in hydrogen peroxide and release of cytochrome c from mitochondria preceded collapse of mitochondrial potential and cell death. In rat hepatocytes treated with adriamycin incubation with exogenous Coenzyme Q10 counteracted the drug-induced increase of hydrogen peroxide and the fall of the mitochondrial potential, thus demonstrating the quinone antioxidant effect. Complex I activity and its rotenone sensitivity decreased in brain cortex non-synaptic mitochondria from old rats; a 5 kb mitochondrial DNA deletion was found only in the old rats. A similar behavior was found in human platelets from old individuals. The postulated energy decline was confirmed by the inhibitor sensitivities of platelet aggregation and lactate production. The lack of the 5 kb deletion in platelets throws doubts on mitochondrial DNA lesions as the only causes of mitochondrial dysfunction in aging.

We have evalued the effects of a diet containing normal amounts of lipids and a marginal content of vitamin B6 on lipid peroxidation. Pyridoxal phosphate concentrations of plasma and liver indicated that an initial deficiency state was reached. Vitamin B6 deficiency led to peroxidative stress: TBARS production was higher in the liver (+18·6%) and even more in the heart (+61%) of deficient rats as compared with controls. Furthermore, significant stimulation of glutathione‐dependent enzymes occurred in both heart and liver of deficient rats: glutathione peroxidase activity increased in heart (+144%) and liver (+505%); glutathione reductase increased in heart (+54·9%) and liver (+15·5%). No difference in the total glutathione content of the organs of the two groups was observed. The reduced glutathione/oxidized glutathione ratio was significantly lower in deficient rats. Although the activity of glutathione‐dependent enzymes was significantly greater in deficient rats than in controls, this stimulation was only partially able to counteract the peroxidative damage due to vitamin B6 deficiency.

International audienc

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