Maximal entanglement versus entropy for mixed quantum states

Maximally entangled mixed states are those states that, for a given mixedness, achieve the greatest possible entanglement. For two-qubit systems and for various combinations of entanglement and mixedness measures, the form of the corresponding maximally entangled mixed states is determined primarily analytically. As measures of entanglement, we consider entanglement of formation, relative entropy of entanglement, and negativity; as measures of mixedness, we consider linear and von Neumann entropies. We show that the forms of the maximally entangled mixed states can vary with the combination of (entanglement and mixedness) measures chosen. Moreover, for certain combinations, the forms of the maximally entangled mixed states can change discontinuously at a specific value of the entropy. Along the way, we determine the states that, for a given value of entropy, achieve maximal violation of Bell's inequality

Approaching Zero-Temperature Metallic States in Mesoscopic Superconductor-Normal-Superconductor Arrays

Systems of superconducting islands placed on normal metal films offer tunable realizations of two-dimensional (2D) superconductivity; they can thus elucidate open questions regarding the nature of 2D superconductors and competing states. In particular, island systems have been predicted to exhibit zero-temperature metallic states. Although evidence exists for such metallic states in some 2D systems, their character is not well understood: the conventional theory of metals cannot explain them, and their properties are difficult to tune. Here, we characterize the superconducting transitions in mesoscopic island-array systems as a function of island thickness and spacing. We observe two transitions in the progression to superconductivity; both transition temperatures exhibit unexpectedly strong depression for widely spaced islands. These depressions are consistent with the system approaching zero-temperature metallic states. The nature of the transitions and the state between them is explained using a phenomenological model involving the stabilization of superconductivity on each island via a weak coupling to and feedback from its neighbors.Comment: 15 pages, 5 figure

Intermittent Hypoxia-Induced Cognitive Deficits Are Mediated by NADPH Oxidase Activity in a Murine Model of Sleep Apnea

Background: In rodents, exposure to intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), is associated with neurobehavioral impairments, increased apoptosis in the hippocampus and cortex, as well as increased oxidant stress and inflammation. Excessive NADPH oxidase activity may play a role in IH-induced CNS dysfunction. Methods and Findings: The effect of IH during light period on two forms of spatial learning in the water maze and well as markers of oxidative stress was assessed in mice lacking NADPH oxidase activity (gp91phox _/Y) and wild-type littermates. On a standard place training task, gp91phox _/Y displayed normal learning, and were protected from the spatial learning deficits observed in wild-type littermates exposed to IH. Moreover, anxiety levels were increased in wild-type mice exposed to IH as compared to room air (RA) controls, while no changes emerged in gp91phox _/Y mice. Additionally, wild-type mice, but not gp91phox _/Y mice had significantly elevated levels of NADPH oxidase expression and activity, as well as MDA and 8-OHDG in cortical and hippocampal lysates following IH exposures. Conclusions: The oxidative stress responses and neurobehavioral impairments induced by IH during sleep are mediated, at least in part, by excessive NADPH oxidase activity, and thus pharmacological agents targeting NADPH oxidase may provid

Hippocampal hypertrophy and sleep apnea: A role for the ischemic preconditioning?

The full impact of multisystem disease such as obstructive sleep apnoea (OSA) on regions of the central nervous system is debated, as the subsequent neurocognitive sequelae are unclear. Several preclinical studies suggest that its purported major culprits, intermittent hypoxia and sleep fragmentation, can differentially affect adult hippocampal neurogenesis. Although the prospective biphasic nature of chronic intermittent hypoxia in animal models of OSA has been acknowledged, so far the evidence for increased 'compensatory' neurogenesis in humans is uncertain. In a cross-sectional study of 32 patients with mixed severity OSA and 32 non-apnoeic matched controls inferential analysis showed bilateral enlargement of hippocampi in the OSA group. Conversely, a trend for smaller thalami in the OSA group was noted. Furthermore, aberrant connectivity between the hippocampus and the cerebellum in the OSA group was also suggested by the correlation analysis. The role for the ischemia/hypoxia preconditioning in the neuropathology of OSA is herein indicated, with possible further reaching clinical implications. © 2013 Rosenzweig et al