136 resultados para 2005-02-BS


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We study a protocol for two-qubit-state guidance that does not rely on feedback mechanisms. In our scheme, entanglement can be concentrated by arranging the interactions of the qubits with a continuous variable ancilla. By properly post-selecting the outcomes of repeated measurements performed on the state of the ancilla, the qubit state is driven to have a desired amount of purity and entanglement. We stress the primary role played by the first iterations of the protocol. Inefficiencies in the detection operations can be fully taken into account. We also discuss the robustness of the guidance protocol to the effects of an experimentally motivated model for mixedness of the ancillary states.

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A long-lived coherent state and nonlinear interaction have been experimentally demonstrated for the vibrational mode of a trapped ion. We propose an implementation of quantum computation using coherent states of the vibrational modes of trapped ions. Differently from earlier experiments, we consider a far-off resonance for the interaction between external fields and the ion in a bidimensional trap. By appropriate choices of the detunings between the external fields, the adiabatic elimination of the ionic excited level from the Hamiltonian of the system allows for beam splitting between orthogonal vibrational modes, production of coherent states, and nonlinear interactions of various kinds. In particular, this model enables the generation of the four coherent Bell states. Furthermore, all the necessary operations for quantum computation, such as preparation of qubits and one-qubit and controlled two-qubit operations, are possible. The detection of the state of a vibrational mode in a Bell state is made possible by the combination of resonant and off-resonant interactions between the ion and some external fields. We show that our read-out scheme provides highly efficient discrimination between all the four Bell states. We extend this to a quantum register composed of many individually trapped ions. In this case, operations on two remote qubits are possible through a cavity mode. We emphasize that our remote-qubit operation scheme does not require a high-quality factor resonator: the cavity field acts as a catalyst for the gate operation.

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A new spectrometer, electron radical interaction chamber, has been developed to study dissociative electron attachment to unstable molecules such as free radicals. It includes a trochoidal electron monochromator and a time-of-flight mass spectrometer. Radicals are generated with a microwave discharge at 2.45 GHz. Preliminary data are presented for radicals formed when a mixture of helium and sulphur dioxide was passed through the microwave discharge. Several new resonances are observed with the discharge on. Resonances at 0 eV (S-), 0.8, 1.2, 3.0 eV (SO-) and 3.7 eV (SO- and S2O-) are assigned to the radical S2O2 and a resonance at 1.6 eV (S-) is assigned to S2O. No new resonances have been assigned to SO, which was also generated in the microwave discharge.

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Experimental and theoretical studies of one-electron capture in collisions of He2+ ions with H2O molecules have been carried out in the range 0.025-12 keV amu(-1) corresponding to typical solar wind velocities of 70-1523 km s(-1). Translational energy spectroscopy (TES), photon emission spectroscopy (PES), and fragment ion spectroscopy were employed to identify and quantify the collision mechanisms involved. Cross sections for selective single electron capture into n=1, 2, and 3 states of the He+ ion were obtained using TES while PES provided cross sections for capture into the He+(2p) and He+(3p) states. Our model calculations show that He+(n=2) and He+(n=3) formation proceeds via a single-electron process governed by the nucleus-electron interaction. In contrast, the He+(1s) formation mechanism involves an exothermic two-electron process driven by the electron-electron interaction, where the potential energy released by the electron capture is used to remove a second electron thereby resulting in fragmentation of the H2O molecule. This process is found to become increasingly important as the collision energy decreases. The experimental cross sections are found to be in reasonable agreement with cross sections calculated using the Demkov and Landau-Zener models.

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The present study was undertaken to test whether inhibition of the proangiogenic inflammatory cytokine tumor necrosis factor (TNF)-alpha can modulate retinal hypoxia and preretinal neovascularization in a murine model of oxygen-induced retinopathy (OIR). OIR was produced in TNF-alpha-/- and wild-type (WT) control C57B6 neonatal mice by exposure to 75% oxygen between postnatal days 7 and 12 (P7 to P12). Half of each WT litter was treated with the cytokine inhibitor semapimod (formerly known as CNI-1493) (5 mg/kg) by daily intraperitoneal injection from the time of reintroduction to room air at P12 until P17. The extent of preretinal neovascularization and intraretinal revascularization was quantified by image analysis of retinal flat-mounts and retinal hypoxia correlated with vascularization by immunofluorescent localization of the hypoxia-sensitive drug pimonidazole (hypoxyprobe, HP). HP adducts were also characterized by Western analysis and quantified by competitive enzyme-linked immunosorbent assay. TNF-alpha-/- and WT mice showed a similar sensitivity to hyperoxia-induced retinal ischemia at P12. At P13 some delay in early reperfusion was evident in TNFalpha-/- and WT mice treated with semapimod. However, at P17 both these groups had significantly better vascular recovery with less ischemic/hypoxic retina and preretinal neovascularization compared to untreated retinopathy in WT mice. Immunohistochemistry showed deposition of HP in the avascular inner retina but not in areas underlying preretinal neovascularization, indicating that such aberrant vasculature can reduce retinal hypoxia. Inhibition of TNF-alpha significantly, improves vascular recovery within ischemic tissue and reduces pathological neovascularization in OIR. HP provides a useful tool for mapping and quantifying tissue hypoxia in experimental ischemic retinopathy.