RESUMEN
Spin-dependent transport in ferromagnet/organic-ferromagnet/ferromagnet junctions is investigated theoretically under different alignment of magnetization orientations. The results demonstrate a significant current rectification at low bias voltages, and the rectifying direction relies on the relative magnetization orientation in each component. The orbital analysis demonstrates two underlying mechanisms for the rectification, the slight structural asymmetry of the molecule from spin radicals and distinct spin match between conducting electrons and the magnetic molecule upon the reversal of bias. The latter is responsible for the strong low-bias rectification and relies on the magnetization alignment. The effects of parameter strength, temperature and size on the rectification are discussed. This work explores a new route to achieve high-performance molecular rectifiers operating at low bias with controlled rectifying direction.
RESUMEN
The aim of this study was to investigate the effect of propofol pretreatment on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the role of the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathway in this procedure. Survival was determined 48 h after LPS injection. At 1 h after LPS challenge, the lung wet- to dry-weight ratio was examined, and concentrations of protein, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) were determined using the bicinchoninic acid method or ELISA. Lung injury was assayed via lung histological examination. PI3K and p-Akt expression levels in the lung tissue were determined by Western blotting. Propofol pretreatment prolonged survival, decreased the concentrations of protein, TNF-α, and IL-6 in BALF, attenuated ALI, and increased PI3K and p-Akt expression in the lung tissue of LPS-challenged rats, whereas treatment with wortmannin, a PI3K/Akt pathway specific inhibitor, blunted this effect. Our study indicates that propofol pretreatment attenuated LPS-induced ALI, partly by activation of the PI3K/Akt pathway.