66 research outputs found

    Quantum interference and the formation of the proximity effect in chaotic normal-metal/superconducting structures

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    We discuss a number of basic physical mechanisms relevant to the formation of the proximity effect in superconductor/normal metal (SN) systems. Specifically, we review why the proximity effect sharply discriminates between systems with integrable and chaotic dynamics, respectively, and how this feature can be incorporated into theories of SN systems. Turning to less well investigated terrain, we discuss the impact of quantum diffractive scattering on the structure of the density of states in the normal region. We consider ballistic systems weakly disordered by pointlike impurities as a test case and demonstrate that diffractive processes akin to normal metal weak localization lead to the formation of a hard spectral gap -- a hallmark of SN systems with chaotic dynamics. Turning to the more difficult case of clean systems with chaotic boundary scattering, we argue that semiclassical approaches, based on classifications in terms of classical trajectories, cannot explain the gap phenomenon. Employing an alternative formalism based on elements of quasiclassics and the ballistic σ\sigma-model, we demonstrate that the inverse of the so-called Ehrenfest time is the relevant energy scale in this context. We discuss some fundamental difficulties related to the formulation of low energy theories of mesoscopic chaotic systems in general and how they prevent us from analysing the gap structure in a rigorous manner. Given these difficulties, we argue that the proximity effect represents a basic and challenging test phenomenon for theories of quantum chaotic systems.Comment: 21 pages (two-column), 6 figures; references adde

    Quantum nondemolition measurement of mechanical motion quanta

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    The fields of opto- and electromechanics have facilitated numerous advances in the areas of precision measurement and sensing, ultimately driving the studies of mechanical systems into the quantum regime. To date, however, the quantization of the mechanical motion and the associated quantum jumps between phonon states remains elusive. For optomechanical systems, the coupling to the environment was shown to preclude the detection of the mechanical mode occupation, unless strong single photon optomechanical coupling is achieved. Here, we propose and analyse an electromechanical setup, which allows to overcome this limitation and resolve the energy levels of a mechanical oscillator. We find that the heating of the membrane, caused by the interaction with the environment and unwanted couplings, can be suppressed for carefully designed electromechanical systems. The results suggest that phonon number measurement is within reach for modern electromechanical setups.Comment: 8 pages, 5 figures plus 24 pages, 11 figures supplemental materia

    Quantum Disorder and Quantum Chaos in Andreev Billiards

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    We investigate the crossover from the semiclassical to the quantum description of electron energy states in a chaotic metal grain connected to a superconductor. We consider the influence of scattering off point impurities (quantum disorder) and of quantum diffraction (quantum chaos) on the electron density of states. We show that both the quantum disorder and the quantum chaos open a gap near the Fermi energy. The size of the gap is determined by the mean free time in disordered systems and by the Ehrenfest time in clean chaotic systems. Particularly, if both times become infinitely large, the density of states is gapless, and if either of these times becomes shorter than the electron escape time, the density of states is described by random matrix theory. Using the Usadel equation, we also study the density of states in a grain connected to a superconductor by a diffusive contact.Comment: 20 pages, 10 figure

    Endothelial dysfunction and diabetes: roles of hyperglycemia, impaired insulin signaling and obesity

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    Cholinergic receptor pathways involved in apoptosis, cell proliferation and neuronal differentiation

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    Acetylcholine (ACh) has been shown to modulate neuronal differentiation during early development. Both muscarinic and nicotinic acetylcholine receptors (AChRs) regulate a wide variety of physiological responses, including apoptosis, cellular proliferation and neuronal differentiation. However, the intracellular mechanisms underlying these effects of AChR signaling are not fully understood. It is known that activation of AChRs increase cellular proliferation and neurogenesis and that regulation of intracellular calcium through AChRs may underlie the many functions of ACh. Intriguingly, activation of diverse signaling molecules such as Ras-mitogen-activated protein kinase, phosphatidylinositol 3-kinase-Akt, protein kinase C and c-Src is modulated by AChRs. Here we discuss the roles of ACh in neuronal differentiation, cell proliferation and apoptosis. We also discuss the pathways involved in these processes, as well as the effects of novel endogenous AChRs agonists and strategies to enhance neuronal-differentiation of stem and neural progenitor cells. Further understanding of the intracellular mechanisms underlying AChR signaling may provide insights for novel therapeutic strategies, as abnormal AChR activity is present in many diseases

    Calcium in the heart: when it's good, it's very very good, but when it's bad, it's horrid

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    Ca(2+) increases in the heart control both contraction and transcription. To accommodate a short-term increased cardiovascular demand, neurohormonal modulators acting on the cardiac pacemaker and individual myocytes induce an increase in frequency and magnitude of myocyte contraction respectively. Prolonged, enhanced function results in hypertrophic growth of the heart, which is initially also associated with greater Ca(2+) signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca(2+) signalling capacity and cardiac output are reduced. Here, the role that Ca(2+) plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca(2+) fluxes will be discussed
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