The

origins of discrepancies in the interface trap densities determined from the different methods are discussed. Commonly observed features in the CV characteristics of high-k/In(0.53)Ga(0.47)As interfaces are interpreted and guidelines are developed to obtain reliable estimates for interface trap densities and the degree of Fermi level (un) pinning for high-k/In(0.53)Ga(0.47)As interfaces. (C) 2010 American Institute of Physics. [doi:10.1063/1.3520431]“
“Evaluation of: Lunde CS, Hartouni SR, Janc JW, Mammen M, Humphrey PP, Benton BM: Telavancin disrupts the functional integrity of the bacterial membrane through targeted interaction with the cell wall precursor lipid II. Antimicrob. Agents Chemother. 53, 3375-3383 (2009). It has been selleck chemical previously demonstrated that telavancin has a dual mechanism of action: inhibition of the transglycosylation process of peptidoglycan cell wall synthesis by the formation of a complex with the D-alanyl-D-alanine precursors; and depolarization of the bacterial membrane. In this article

the mechanism by which telavancin disrupts the bacterial cell membrane was studied by Lunde and colleagues using a variety of Staphylococcus aureus Galardin Proteases inhibitor strains. The authors demonstrated that telavancin-induced depolarization requires both the AZD2014 concentration presence of lipid II as well as an interaction between telavancin and D-alanyl-D-alanine residues. The authors were also able to show that telavancin’s depolarization effect on membrane potential occurs in diverse S. aureus strains including those with decreased susceptibility to vancomycin and daptomycin. This study takes a significant step forward in our understanding of the concentration-dependent bactericidal activity of telavancin, a drug recently approved for use in skin and skin structure infections caused

by Gram-positive cocci.”
“Background and aims: Hyperglycemia and diabetes are associated with increased formation of advanced glycation end products and enhanced oxidative stress, leading to the progression of diabetic vascular disease. We have investigated the mechanisms by which AGE-modified bovine albumin (AGE-BSA) induces reactive oxygen species (ROS) generation, leading to nuclear factor-erythroid 2-related factor (Nrf2) dependent induction of the antioxidant genes heme oxygenase-1 (HO-1) and NADPH: quinone oxidoreductase 1 (NQO1) in bovine aortic endothelial cells.

Methods and results: AGE-BSA (100 mu g ml (1), 0-24 h), but not native BSA, elicited time-dependent increases in ROS generation, Nrf2 nuclear translocation and enhanced mRNA and protein expression of HO-1 and NQO1, but not glutathione peroxidase-1.