An analysis is developed to predict the Raman shift in deformed silicon that takes

into account all the components of the stress or strain tensor; the results selleck of the model are then used as inputs to the analysis for direct comparison with measured peak shifts as a function of distance from the TSV. Good agreement between the measured and predicted peak shifts is obtained for the case of the intact oxide stack. A discrepancy between the measured and predicted shifts was observed adjacent to the TSV with the oxide stack removed; further modeling suggests the discrepancy is explained by the formation of a small void at the TSV-silicon interface during etching. The combined measurement-modeling approach serves to both validate the model, in this case for TSV design, and to extend the measurement capability https://www.selleckchem.com/products/ipi-145-ink1197.html of confocal Raman microscopy to complex stress fields. (C) 2011 American Institute of Physics. [doi:10.1063/1.3644971]“
“The ligand activated transcription factor aryl hydrocarbon receptor (AhR) has been studied for many decades in toxicology as the ligand for the environmental contaminant dioxin. However,

AhR has recently emerged as a critical physiological regulator of immune responses affecting both innate and adaptive systems, and several AhR ligands with different pharmacological profiles have recently been studied. The current review discusses new insights into the role of AhR signalling and AhR ligands on the regulation of the immune system, with a focus on regulatory T cells which maintain immune tolerance. Notably, AhR is expressed and modulates the development of two induced regulatory CD4(+) T cell subsets, the forkhead box P3-positive (Foxp3(+)) regulatory T cells (iTreg) and the IL-10-secreting type

1 regulatory T (T(R)1) cells, through different signalling pathways. We will finally discuss www.selleckchem.com/products/BKM-120.html how AhR ligands could be exploited to alleviate human autoimmune diseases. Clearly, drugs targeted against AhR should promote the development of new strategies to fight against autoimmune diseases.”
“Global ischemia selectively induces CA1 neuronal death in the hippocampus. Pretreatment with non-lethal ischemia (i.e. ischemic preconditioning) prevents CA1 neuronal death induced by lethal ischemia. While ischemic tolerance is a well-known phenomenon, the underlying molecular mechanisms are not fully understood. Cytoskeletal proteins including alpha-spectrin, tau, and microtubule-associated protein 2 (MAP-2) are indispensable for the maintenance of neuronal homeostasis. Here, we report the effects of ischemic preconditioning on the ischemia-induced degradation of cytoskeletal proteins alpha-spectrin, tau, and MAP-2 in the rat CA1 region. We found that most neurons of the CA1 region had died after 5 min of ischemia. However, exposing the brain to 3 min of ischemic preconditioning 3 days earlier significantly reduced the number of neuronal death.