Influence of a classical homogeneous gravitational field on dissipative dynamics of the Jaynes-Cummings model with phase damping

In this paper, we study the dissipative dynamics of the Jaynes-Cummings model with phase damping in the presence of a classical homogeneous gravitational field. The model consists of a moving two-level atom simultaneously exposed to the gravitational field and a single-mode traveling radiation field in the presence of the phase damping. We present a quantum treatment of the internal and external dynamics of the atom based on an alternative su(2) dynamical algebraic structure. By making use of the super-operator technique, we obtain the solution of the master equation for the density operator of the quantum system, under the Markovian approximation. Assuming that initially the radiation field is prepared in a Glauber coherent state and the two-level atom is in the excited state, we investigate the influence of gravity on the temporal evolution of collapses and revivals of the atomic population inversion, atomic dipole squeezing, atomic momentum diffusion, photon counting statistics and quadrature squeezing of the radiation field in the presence of phase damping.Comment: 25 pages, 15 figure

Ligation of lymphocyte function-associated antigen-1 on monocytes decreases very late antigen-4-mediated adhesion through a reactive oxygen species-dependent pathway

Monocyte-endothelial adhesion plays an important role in monocyte trafficking and hence is important for immune responses and pathogenesis of inflammatory diseases including atherosclerosis. The cross-talk between different integrins on monocytes may be crucial for a coordinated regulation of the cellular adhesion during the complex process of transendothelial migration. By using monoclonal antibodies and recombinant intercellular adhesion molecule 1 (ICAM-1) to engage lymphocyte function-associated antigen 1 (LFA-1) on monocytic cells, we found that the cellular adhesion to vascular cell adhesion molecule 1 (VCAM-1) mediated by very late antigen 4 (VLA-4) was suppressed after this treatment and the suppression depended on the presence of reactive oxygen species (ROSs). Inhibition of production of RoSs through the use of inhibitor of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, but not inhibitors of mitochondrial electron transport chain or xanthine oxidase, revealed that this suppression on VLA-4-mediated cellular binding was mediated by Ross produced by phagocyte NADPH oxidase. Activation of phosphoinositol-3 kinase and Akt appears to mediate this NADPH oxidase activation through p47 phox phosphorylation and Rac-1 activation. Our results provide a novel pathway in which Ross play a critical role in integrin cross-talk in monocytes. This signaling pathway may be important for cellular transition from firm arrest to diapedesis during monocyte trafficking. (C) 2004 by The American Society of Hematology

A Study of Two Approximate Methods of Analyzing Cylindrical Shell Roofs

Office of Naval Research. Department of the Navy.Contract Nonr 1834(03)Project NR 064-18

Advanced Glycation End Products Down-regulate Gap Junctions in Human Hepatoma SKHep 1 Cells via the Activation of Src-Dependent ERK1/2 and JNK/SAPK/AP1 Signaling Pathways

Hyperglycemia and advanced glycation end products (AGEs) are associated with an elevated risk of developing several cancers in diabetic patients. However, the detailed mechanisms remain to be elucidated. The mechanism of AGE-bovine serum albumin (BSA) on gap junction intercellular communication in human hepatoma cell line, SKHep 1, was investigated. Both Cx32 and Cx43 are major gap junction forming proteins in the liver, the loss of which has been shown to facilitate tumorigenesis. Although the MTT assay results showed that AGE-BSA significantly increased cell growth by 31%, AGE-BSA down-regulated Cx32 and Cx43 expression in a dose- and time-dependent manner. The present study also demonstrated that ERK1/2 and JNK/SAPK were significantly activated by AGE BSA and that Src, ERK1/2, and JNK/SAPK inhibitors significantly reversed the reduction of Cx32 and Cx43 proteins by AGE-BSA. Taken together, these results strongly support the hypothesis that Src-dependent ERK1/2 and JNK/SAPK/AP1 signaling pathways play a key role in AGE BSA-mediated down-regulation of Cx32 and Cx43 protein expression in SKHep 1 cells