967 resultados para driving while impaired


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Pyramidal neurons (PyNs) in ‘higher’ brain are highly susceptible to acute stroke injury yet ‘lower’ brain regions better survive global ischemia, presumably because of better residual blood flow. Here we show that projection neurons in ‘lower’ brain regions of hypothalamus and brainstem intrinsically resist acute stroke-like injury independent of blood flow in the brain slice. In contrast `higher` projection neurons in neocortex, hippocampus, striatum and thalamus are highly susceptible. In live brain slices from rat deprived of oxygen and glucose (OGD), we imaged anoxic depolarization (AD) as it propagates through these regions. AD, the initial electrophysiological event of stroke, is a depolarizing front that drains residual energy in compromised gray matter. The extent of AD reliably determines ensuing damage in higher brain, but using whole-cell recordings we found that all CNS neurons do not generate a robust AD. Higher neurons generate strong AD and show no functional recovery in contrast to neurons in hypothalamus and brainstem that generate a weak and gradual AD. Most dramatically, lower neurons recover their membrane potential, input resistance and spike amplitude when oxygen and glucose is restored, while higher neurons do not. Following OGD, new recordings could be acquired in all lower (but not higher) brain regions, with some neurons even withstanding multiple OGD exposure. Two-photon laser scanning microscopy confirmed neuroprotection in lower, but not higher gray matter. Specifically pyramidal neurons swell and lose their dendritic spines post-OGD, whereas neurons in hypothalamus and brainstem display no such injury. Exposure to the Na+/K+ ATPase inhibitor ouabain (100 μM), induces depolarization similar to OGD in all cell types tested. Moreover, elevated [K+]o evokes spreading depression (SD), a milder version of AD, in higher brain but not hypothalamus or brainstem so weak AD correlates with the inability to generate SD. In summary, overriding the Na+/K+ pump using OGD, ouabain or elevated [K+]o evokes steep and robust depolarization of higher gray matter. We show that this important regional difference can be largely accounted for by the intrinsic properties of the resident neurons and that Na+/K+ ATPase pump efficiency is a major determining factor generating strong or weak spreading depolarizations.

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Entanglement transfer processes from a continuous-variable (CV) to a qubit system have primary importance in quantum information processing due to some practical implications in the realization of a quantum network. A CV system can propagate entanglement while a qubit system is easy to manipulate. We study conditions to entangle two atomic qubits with a two-mode squeezed field driving two cavities containing the atoms.

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The acceleration of multi-MeV protons from the rear surface of thin solid foils irradiated by an intense (similar to 10(18) W/cm(2)) and short (similar to 1.5 ps) laser pulse has been investigated using transverse proton probing. The structure of the electric field driving the expansion of the proton beam has been resolved with high spatial and temporal resolution. The main features of the experimental observations, namely, an initial intense sheath field and a late time field peaking at the beam front, are consistent with the results from particle-in-cell and fluid simulations of thin plasma expansion into a vacuum.

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In electromigration (EM) experiments on metallic wires, a flux of atoms can lead to motion of the centre of mass (COM) of the wire. Hence, it may be tempting to assume that the flow of current produces a net force on the wire as a whole. We point out, on the basis of known momentum-balance arguments, that the net force on a metallic wire due to a passing steady-state current is zero. This is possible, because in addition to EM driving forces, acting on scattering centres, there are counterbalancing forces, acting on the rest of the system. Drift of the COM in EM experiments occurs inevitably because the substrate keeps the crystal lattice of the wire fixed, while allowing diffusion of defects in the bulk of the wire. This drift is not evidence for a net force on the wire.

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We report on our findings of the bright, pulsating, helium atmosphere white dwarf GD 358, based on time-resolved optical spectrophotometry. We identify 5 real pulsation modes and at least 6 combination modes at frequencies consistent with those found in previous observations. The measured Doppler shifts from our spectra show variations with amplitudes of up to 5.5 km s-1 at the frequencies inferred from the flux variations. We conclude that these are variations in the line-of-sight velocities associated with the pulsational motion. We use the observed flux and velocity amplitudes and phases to test theoretical predictions within the convective driving framework, and compare these with similar observations of the hydrogen atmosphere white dwarf pulsators (DAVs). The wavelength dependence of the fractional pulsation amplitudes (chromatic amplitudes) allows us to conclude that all five real modes share the same spherical degree, most likely, l=1. This is consistent with previous identifications based solely on photometry. We find that a high signal-to-noise mean spectrum on its own is not enough to determine the atmospheric parameters and that there are small but significant discrepancies between the observations and model atmospheres. The source of these remains to be identified. While we infer Teff =24 kK and log g ~ 8.0 from the mean spectrum, the chromatic amplitudes, which are a measure of the derivative of the flux with respect to the temperature, unambiguously favour a higher effective temperature, 27 kK, which is more in line with independent determinations from ultra-violet spectra.

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This paper introduces a novel interface designed to help blind and visually impaired people to explore and navigate on the Web. In contrast to traditionally used assistive tools, such as screen readers and magnifiers, the new interface employs a combination of both audio and haptic features to provide spatial and navigational information to users. The haptic features are presented via a low-cost force feedback mouse allowing blind people to interact with the Web, in a similar fashion to their sighted counterparts. The audio provides navigational and textual information through the use of non-speech sounds and synthesised speech. Interacting with the multimodal interface offers a novel experience to target users, especially to those with total blindness. A series of experiments have been conducted to ascertain the usability of the interface and compare its performance to that of a traditional screen reader. Results have shown the advantages that the new multimodal interface offers blind and visually impaired people. This includes the enhanced perception of the spatial layout of Web pages, and navigation towards elements on a page. Certain issues regarding the design of the haptic and audio features raised in the evaluation are discussed and presented in terms of recommendations for future work.

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Suppression of angiogenesis during diabetes is a recognized phenomenon but is less appreciated within the context of diabetic retinopathy. The current study has investigated regulation of retinal angiogenesis by diabetic serum and determined if advanced glycation end products (AGEs) could modulate this response, possibly via AGE-receptor interactions. A novel in vitro model of retinal angiogenesis was developed and the ability of diabetic sera to regulate this process was quantified. AGE-modified serum albumin was prepared according to a range of protocols, and these were also analyzed along with neutralization of the AGE receptors galectin-3 and RAGE. Retinal ischemia and neovascularization were also studied in a murine model of oxygen-induced proliferative retinopathy (OIR) in wild-type and galectin-3 knockout mice (gal3(-/-)) after perfusion of preformed AGEs. Serum from nondiabetic patients showed significantly more angiogenic potential than diabetic serum (P <0.0001) and within the diabetic group, poor glycemic control resulted in more AGEs but less angiogenic potential than tight control (P <0.01). AGE-modified albumin caused a dose-dependent inhibition of angiogenesis (P <0.001), and AGE receptor neutralization significantly reversed the AGE-mediated suppression of angiogenesis (P <0.01). AGE-treated wild-type mice showed a significant increase in inner retinal ischemia and a reduction in neovascularization compared with non-AGE controls (P <0.001). However, ablation of galectin-3 abolished the AGE-mediated increase in retinal ischemia and restored the neovascular response to that seen in controls. The data suggest a significant suppression of angiogenesis by the retinal microvasculature during diabetes and implicate AGEs and AGE-receptor interactions in its causation.