We identified this temperature as corresponding to a crossover transition to an order-disorder regime. Above similar to 700 K strong band overlapping, merging, and smearing of modes are consequence of thermal fluctuations and chemical disorder. Vibrational modes show band Angiogenesis inhibitor splits

in the ferroelectric phase as emerging from triple degenerated species as from a paraelectric cubic phase above T-C similar to 1090 K. Temperature dependent x-ray absorption near edge structure (XANES) at the Fe K edge shows that lower temperature Fe3+ turns into Fe2+. While this matches the FeO wustite XANES profile, the Bi L-III-edge downshift suggests a high temperature very complex bond configuration at the distorted A perovskite site. Overall, our local structural measurements reveal high temperature defect-induced irreversible lattice changes, below, and above the ferroelectric transition, in an environment lacking of long-range coherence. We did not find an insulator to metal transition prior to melting. (C) 2010 American Institute of Physics. [doi:10.1063/1.3486515]“
“Signaling pathways mediate the effect of

external stimuli on gene expression in cells. The signaling proteins in these pathways interact with each other and their HIF-1 cancer phosphorylation levels often serve as indicators for the activity of signaling pathways. Several signaling pathways have been identified in mammalian cells but the crosstalk between them is not well understood. Alliance for Cellular Signaling (AfCS) has measured time-course data in RAW 264.7 macrophage cells on important SB525334 concentration phosphoproteins, such as the mitogen-activated protein kinases (MAPKs) and signal transducer and

activator of transcription (STATs), in single-and double-ligand stimulation experiments for 22 ligands. In the present work, we have used a data-driven approach to analyze the AfCS data to decipher the interactions and crosstalk between signaling pathways in stimulated macrophage cells. We have used dynamic mapping to develop a predictive model using a partial least squares approach. Significant interactions were selected through statistical hypothesis testing and were used to reconstruct the phosphoprotein signaling network. The proposed data-driven approach is able to identify most of the known signaling interactions such as protein kinase B (Akt) -> glycogen synthase kinase 3 alpha/beta (GSK alpha/beta) etc., and predicts potential novel interactions such as P38 -> RSK and GSK -> ezrin/radixin/moesin. We have also shown that the model has good predictive power for extrapolation. Our novel approach captures the temporal causality and directionality in intracellular signaling pathways. Further, case specific analysis of the phosphoproteins in the network has led us to propose hypothesis about inhibition (phosphorylation) of GSK alpha/beta via P38.