144 research outputs found

    Scanning Quantum Decoherence Microscopy

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    The use of qubits as sensitive magnetometers has been studied theoretically and recent demonstrated experimentally. In this paper we propose a generalisation of this concept, where a scanning two-state quantum system is used to probe the subtle effects of decoherence (as well as its surrounding electromagnetic environment). Mapping both the Hamiltonian and decoherence properties of a qubit simultaneously, provides a unique image of the magnetic (or electric) field properties at the nanoscale. The resulting images are sensitive to the temporal as well as spatial variation in the fields created by the sample. As an example we theoretically study two applications of this technology; one from condensed matter physics, the other biophysics. The individual components required to realise the simplest version of this device (characterisation and measurement of qubits, nanoscale positioning) have already been demonstrated experimentally.Comment: 11 pages, 5 low quality (but arXiv friendly) image

    Resource Utilization Due to Breakthrough Pain in Patients With Chronic Painful Conditions

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    Objectives Primary: To capture healthcare resource consumption and work loss in a population of patients with chronic pain who have pain flares from one or more non-cancer conditions. Secondary: To explore the relationship between anxiety, depression, and pain in this population

    Perception of Breakthrough Pain in Patients with Chronic Painful Conditions

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    Objective: To understand how patients with chronic non-cancer pain define and describe pain flares

    Renormalized Path Integral for the Two-Dimensional Delta-Function Interaction

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    A path-integral approach for delta-function potentials is presented. Particular attention is paid to the two-dimensional case, which illustrates the realization of a quantum anomaly for a scale invariant problem in quantum mechanics. Our treatment is based on an infinite summation of perturbation theory that captures the nonperturbative nature of the delta-function bound state. The well-known singular character of the two-dimensional delta-function potential is dealt with by considering the renormalized path integral resulting from a variety of schemes: dimensional, momentum-cutoff, and real-space regularization. Moreover, compatibility of the bound-state and scattering sectors is shown.Comment: 26 pages. The paper was significantly expanded and numerous equations were added for the sake of clarity; the main results and conclusions are unchange

    Hypoxia Reduces Arylsulfatase B Activity and Silencing Arylsulfatase B Replicates and Mediates the Effects of Hypoxia

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    This report presents evidence of 1) a role for arylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase) in mediating intracellular oxygen signaling; 2) replication between the effects of ARSB silencing and hypoxia on sulfated glycosaminoglycan content, cellular redox status, and expression of hypoxia-associated genes; and 3) a mechanism whereby changes in chondroitin-4-sulfation that follow either hypoxia or ARSB silencing can induce transcriptional changes through galectin-3. ARSB removes 4-sulfate groups from the non-reducing end of chondroitin-4-sulfate and dermatan sulfate and is required for their degradation. For activity, ARSB requires modification of a critical cysteine residue by the formylglycine generating enzyme and by molecular oxygen. When primary human bronchial and human colonic epithelial cells were exposed to 10% O2×1 h, ARSB activity declined by ∼41% and ∼30% from baseline, as nuclear hypoxia inducible factor (HIF)-1α increased by ∼53% and ∼37%. When ARSB was silenced, nuclear HIF-1α increased by ∼81% and ∼61% from baseline, and mRNA expression increased to 3.73 (±0.34) times baseline. Inversely, ARSB overexpression reduced nuclear HIF-1α by ∼37% and ∼54% from baseline in the epithelial cells. Hypoxia, like ARSB silencing, significantly increased the total cellular sulfated glycosaminoglycans and chondroitin-4-sulfate (C4S) content. Both hypoxia and ARSB silencing had similar effects on the cellular redox status and on mRNA expression of hypoxia-associated genes. Transcriptional effects of both ARSB silencing and hypoxia may be mediated by reduction in galectin-3 binding to more highly sulfated C4S, since the galectin-3 that co-immunoprecipitated with C4S declined and the nuclear galectin-3 increased following ARSB knockdown and hypoxia
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