Quantum Computing of Quantum Chaos in the Kicked Rotator Model

We investigate a quantum algorithm which simulates efficiently the quantum kicked rotator model, a system which displays rich physical properties, and enables to study problems of quantum chaos, atomic physics and localization of electrons in solids. The effects of errors in gate operations are tested on this algorithm in numerical simulations with up to 20 qubits. In this way various physical quantities are investigated. Some of them, such as second moment of probability distribution and tunneling transitions through invariant curves are shown to be particularly sensitive to errors. However, investigations of the fidelity and Wigner and Husimi distributions show that these physical quantities are robust in presence of imperfections. This implies that the algorithm can simulate the dynamics of quantum chaos in presence of a moderate amount of noise.Comment: research at Quantware MIPS Center http://www.quantware.ups-tlse.fr, revtex 11 pages, 13 figs, 2 figs and discussion adde

Atherogenic effects of Chlamydia pneumoniae: refuting the innocent bystander hypothesis.

Item does not contain fulltextOBJECTIVE: Serologic evidence of Chlamydia pneumoniae infection and atherosclerosis was first demonstrated in patients with ischemic heart disease in 1988. Subsequently, the organism has been detected in several cardiovascular lesions. Outside of observational reports, few studies mechanistically link vascular infection with C. pneumoniae and atherogenesis. To better define its pathophysiologic role, we examined the influence of C. pneumoniae infection of human vascular smooth muscle cells on vascular smooth muscle cell proliferation, cell-cycle protein expression, and inflammatory cytokine release. METHODS: Human aortic vascular smooth muscle cells were inoculated with C. pneumoniae in culture. Proliferation was assessed by mitochondrial activity, direct cell counting, and immunohistochemical staining for proliferating cell nuclear antigen. Electromobility gel shift assays probed for the antiproliferative cell-cycle protein p53. Supernatants were assayed for the mitogens interleukin-6 and interleukin-8 by enzyme-linked immunosorbent assay. RESULTS: After C. pneumoniae inoculation, vascular smooth muscle cell proliferation increased 2-fold by mitochondrial activity and more than 3-fold by cell numbers. C. pneumoniae infection promoted a 3-fold increase in proliferating cell nuclear antigen expression, which was associated with decreased nuclear binding of p53. Compared with control, C. pneumoniae inoculation resulted in a 2.5-fold increase in released interleukin-6 and interleukin-8. In each experiment, the influence of C. pneumoniae was abrogated by concomitant treatment with the macrolide antibiotic azithromycin. CONCLUSIONS: C. pneumoniae induced human vascular smooth muscle cell proliferation and proliferating cell nuclear antigen expression, down-regulated p53, and promoted release of prototypical atherogenic cytokines. These in vitro findings indicate that C. pneumoniae is more than an innocent bystander, rather it is a pathophysiologic participant in atherogenesis warranting elimination

Atherogenic effects of Chlamydia pneumoniae: refuting the innocent bystander hypothesis.

Item does not contain fulltextOBJECTIVE: Serologic evidence of Chlamydia pneumoniae infection and atherosclerosis was first demonstrated in patients with ischemic heart disease in 1988. Subsequently, the organism has been detected in several cardiovascular lesions. Outside of observational reports, few studies mechanistically link vascular infection with C. pneumoniae and atherogenesis. To better define its pathophysiologic role, we examined the influence of C. pneumoniae infection of human vascular smooth muscle cells on vascular smooth muscle cell proliferation, cell-cycle protein expression, and inflammatory cytokine release. METHODS: Human aortic vascular smooth muscle cells were inoculated with C. pneumoniae in culture. Proliferation was assessed by mitochondrial activity, direct cell counting, and immunohistochemical staining for proliferating cell nuclear antigen. Electromobility gel shift assays probed for the antiproliferative cell-cycle protein p53. Supernatants were assayed for the mitogens interleukin-6 and interleukin-8 by enzyme-linked immunosorbent assay. RESULTS: After C. pneumoniae inoculation, vascular smooth muscle cell proliferation increased 2-fold by mitochondrial activity and more than 3-fold by cell numbers. C. pneumoniae infection promoted a 3-fold increase in proliferating cell nuclear antigen expression, which was associated with decreased nuclear binding of p53. Compared with control, C. pneumoniae inoculation resulted in a 2.5-fold increase in released interleukin-6 and interleukin-8. In each experiment, the influence of C. pneumoniae was abrogated by concomitant treatment with the macrolide antibiotic azithromycin. CONCLUSIONS: C. pneumoniae induced human vascular smooth muscle cell proliferation and proliferating cell nuclear antigen expression, down-regulated p53, and promoted release of prototypical atherogenic cytokines. These in vitro findings indicate that C. pneumoniae is more than an innocent bystander, rather it is a pathophysiologic participant in atherogenesis warranting elimination