“Numerical methods based on the Reynolds Averaged Navier-Stokes (RANS) and Large Eddy Simulation (LES) equations are applied to the thermal selleck prediction of flows representative of those found in and around electronics systems and components. Low Reynolds number flows through a heated ribbed channel, around a heated cube and within a complex electronics system case are investigated using linear
and nonlinear LES models, hybrid RANS-LES and RANS-Numerical-LES (RANS-NLES) methods. Flow and heat transfer predictions using these techniques are in good agreement with each other and experimental data for a range of grid resolutions. Using second order central differences, the RANS-NLES method performs well for all simulations. (C) 2011 Elsevier Inc. All rights reserved.”
“In GDC-0994 in vitro current cancer treatment protocols, such as radiation and chemotherapy, side effects on normal cells
are major obstacles to radical therapy. To avoid these side effects, a cancer cell-specific approach is needed. One way to specifically target cancer cells is to utilize a cancer specific promoter to express a cytotoxic gene (suicide gene therapy) or a viral gene required for viral replication (oncolytic virotherapy). For this purpose, the selected promoter should have minimal activity in normal cells to avoid side effects, and high activity in a wide variety of cancers to obtain optimal therapeutic Staurosporine cell line efficacy. In contrast to the AFP, CEA and PSA promoters, which have high activity only in a limited spectrum of tumors, the E2F1 promoter exhibits high activity in wide variety of cancers. This is based on the mechanism of carcinogenesis. Defects in
the RB pathway and activation of the transcription factor E2F, the main target of the RB pathway, are observed in almost all cancers. Consequently, the E2F1 promoter, which is mainly regulated by E2F, has high activity in wide variety of cancers. However, E2F is also activated by growth stimulation in normal growing cells, suggesting that the E2F1 promoter may also be highly active in normal growing cells. In contrast, we found that the tumor suppressor ARF promoter is activated by deregulated E2F activity, induced by forced inactivation of pRB, but does not respond to physiological E2F activity induced by growth stimulation. We also found that the deregulated E2F activity, which activates the ARF promoter, is detected only in cancer cell lines. These observations suggest that ARF promoter is activated by E2F only in cancer cells and therefore may be more cancer cell-specific than E2F1 promoter to drive gene expression. We show here that the ARF promoter has lower activity in normal growing fibroblasts and shows higher cancer cell-specificity compared to the E2F1 promoter.