We tested the effects of coupling strength between SAN cells in the models, as well as the effects of fibroblasts and interspersed atrial cells. Although we could simulate single cell experimental data supporting Saracatinib mouse the “”multiple cell type”" hypothesis, 2D “”non-uniform”" models did not simulate expected tissue behavior, such as central pacemaking. When we considered the atrial effects alone in a simple homogeneous “”uniform”"

model, central pacemaking initiation and impulse propagation in simulations were consistent with experiments. Introduction of fibroblasts in our simulated tissue resulted in various effects depending on the density, distribution, and fibroblast-myocyte coupling strength. Incorporation of atrial cells in our simulated SAN tissue had little effect on SAN electrophysiology. Our tissue model simulations suggest atrial electrotonic effects as plausible to account for SAN heterogeneity, sequence, and rate of propagation. Fibroblasts can act as obstacles, current sinks or shunts to conduction in the SAN depending find more on their orientation, density, and coupling.”
“We consider the problem of electron states related to the strongly localized potential of a single impurity in graphene. Our model simulates the effect of

a neutral impurity atom (substituting for the carbon atom) on the energy spectrum of electrons near the Dirac points. The model also can describe the effect of an adatom on the surface of graphene. We take into account the internal spin-orbit interaction, which essentially modifies the structure of electron bands near the Dirac points, leading effectively to an energy gap. This might result in the occurrence of additional impurity states in the vicinity of the energy gap. As a result, the spin-orbit gap in graphene can be experimentally unobservable due to a large number of adsorbed light atoms

at the graphene surface, which create the impurity states in the gap. (C) 2011 American Institute Selleckchem AZD4547 of Physics. [doi: 10.1063/1.3598130]“
“Binding of specific ligands to the receptor for advanced glycation end-products (RAGE) can trigger a series of signal transductions, which leads to pathogenesis in many chronic degenerative diseases, including cancer. Alternative splicing of RAGE mRNA has resulted in many variants, including RAGE variant 1 (RAGEv1). This particular splice variant of RAGE can provide a major soluble form of RAGE in blood circulation, which can neutralize deleterious ligands, thus diminishing signaling that can lead to inflammation and pathogenesis in cancer cells. However, the molecular mechanisms involved in suppressing signaling cascades in the cells are unknown. We investigated the molecular role of the RAGEv1 isoform in modulating NF-kappa B and TNF-alpha gene expression in human hepatocellular carcinoma HepG2 cells.