40 research outputs found

    Analytical results on quantum interference and magnetoconductance for strongly localized electrons in a magnetic field: Exact summation of forward-scattering paths

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    We study quantum interference effects on the transition strength for strongly localized electrons hopping on 2D square and 3D cubic lattices in the presence of a magnetic field B. These effects arise from the interference between phase factors associated with different electron paths connecting two distinct sites. For electrons confined on a square lattice, with and without disorder, we obtain closed-form expressions for the tunneling probability, which determines the conductivity, between two arbitrary sites by exactly summing the corresponding phase factors of all forward-scattering paths connecting them. An analytic field-dependent expression, valid in any dimension, for the magnetoconductance (MC) is derived. A positive MC is clearly observed when turning on the magnetic field. In 2D, when the strength of B reaches a certain value, which is inversely proportional to twice the hopping length, the MC is increased by a factor of two compared to that at zero field. We also investigate transport on the much less-studied and experimentally important 3D cubic lattice case, where it is shown how the interference patterns and the small-field behavior of the MC vary according to the orientation of B. The effect on the low-flux MC due to the randomness of the angles between the hopping direction and the orientation of B is also examined analytically.Comment: 24 pages, RevTeX, 8 figures include

    Manifestation of triplet superconductivity in superconductor-ferromagnet structures

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    We study proximity effects in a multilayered superconductor/ferromagnet (S/F) structure with arbitrary relative directions of the magnetization M{\bf M}. If the magnetizations of different layers are collinear the superconducting condensate function induced in the F layers has only a singlet component and a triplet one with a zero projection of the total magnetic moment of the Cooper pairs on the M{\bf M} direction. In this case the condensate penetrates the F layers over a short length ξJ\xi_J determined by the exchange energy JJ. If the magnetizations M{\bf M} are not collinear the triplet component has, in addition to the zero projection, the projections ±1\pm1. The latter component is even in the momentum, odd in the Matsubara frequency and penetrates the F layers over a long distance that increases with decreasing temperature and does not depend on JJ (spin-orbit interaction limits this length). If the thickness of the F layers is much larger than ξJ\xi_J, the Josephson coupling between neighboring S layers is provided only by the triplet component, so that a new type of superconductivity arises in the transverse direction of the structure. The Josephson critical current is positive (negative) for the case of a positive (negative) chirality of the vector M{\bf M}. We demonstrate that this type of the triplet condensate can be detected also by measuring the density of states in F/S/F structures.Comment: 14 pages; 9 figures. Final version, to be published in Phys. Rev.

    Age-related shift in LTD is dependent on neuronal adenosine A(2A) receptors interplay with mGluR5 and NMDA receptors

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    Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline. An association between a polymorphism of the adenosine A2A receptor (A2AR) encoding gene-ADORA2A, and hippocampal volume in AD patients was recently described. In this study, we explore the synaptic function of A2AR in age-related conditions. We report, for the first time, a significant overexpression of A2AR in hippocampal neurons of aged humans, which is aggravated in AD patients. A similar profile of A2AR overexpression in rats was sufficient to drive age-like memory impairments in young animals and to uncover a hippocampal LTD-to-LTP shift. This was accompanied by increased NMDA receptor gating, dependent on mGluR5 and linked to enhanced Ca(2+) influx. We confirmed the same plasticity shift in memory-impaired aged rats and APP/PS1 mice modeling AD, which was rescued upon A2AR blockade. This A2AR/mGluR5/NMDAR interaction might prove a suitable alternative for regulating aberrant mGluR5/NMDAR signaling in AD without disrupting their constitutive activity

    A synthetic epoxyeicosatrienoic acid analogue prevents the initiation of ischemic acute kidney injury

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    AIM: Imbalances in cytochrome P450 (CYP)‐dependent eicosanoid formation may play a central role in ischemic acute kidney injury (AKI). We reported previously that inhibition of 20-hydroxyeicosatetraenoic acid (20-HETE) action ameliorated ischemia/reperfusion (I/R)-induced AKI in rats. Now we tested the hypothesis that enhancement of epoxyeicosatrienoic acid (EET) actions may counteract the detrimental effects of 20-HETE and prevent the initiation of AKI. METHODS: Male Lewis rats underwent right nephrectomy and ischemia was induced by 45 min clamping of the left renal pedicle followed by up to 48 h of reperfusion. Circulating CYP-eicosanoid profiles were compared in patients who underwent cardiac surgery with (n = 21) and without (n = 38) developing postoperative AKI. RESULTS: Ischemia induced an about eightfold increase of renal 20-HETE levels, whereas free EETs were not accumulated. To compensate for this imbalance, a synthetic 14,15-EET analogue was administered by intrarenal infusion before ischemia. The EET analogue improved renal reoxygenation as monitored by in vivo parametric MRI during the initial 2 h reperfusion phase. The EET analogue improved PI3K- as well as mTORC2-dependent rephosphorylation of Akt, induced inactivation of GSK-3β, reduced the development of tubular apoptosis and attenuated inflammatory cell infiltration. The EET analogue also significantly alleviated the I/R-induced drop in creatinine clearance. Patients developing postoperative AKI featured increased preoperative 20-HETE and 8,9-EET levels. CONCLUSIONS: Pharmacological interventions targeting the CYP-eicosanoid pathway could offer promising new options for AKI prevention. Individual differences in CYP-eicosanoid formation may contribute to the risk of developing AKI in clinical settings
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