127 research outputs found

    Full Counting Statistics of Non-Commuting Variables: the Case of Spin Counts

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    We discuss the Full Counting Statistics of non-commuting variables with the measurement of successive spin counts in non-collinear directions taken as an example. We show that owing to an irreducible detector back-action, the FCS in this case may be sensitive to the dynamics of the detectors, and may differ from the predictions obtained with using a naive version of the Projection Postulate. We present here a general model of detector dynamics and path-integral approach to the evaluation of FCS. We concentrate further on a simple "diffusive" model of the detector dynamics where the FCS can be evaluated with transfer-matrix method. The resulting probability distribution of spin counts is characterized by anomalously large higher cumulants and substantially deviates from Gaussian Statistics.Comment: 11 pages, 3 figure

    The lesson of causal discovery algorithms for quantum correlations: Causal explanations of Bell-inequality violations require fine-tuning

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    An active area of research in the fields of machine learning and statistics is the development of causal discovery algorithms, the purpose of which is to infer the causal relations that hold among a set of variables from the correlations that these exhibit. We apply some of these algorithms to the correlations that arise for entangled quantum systems. We show that they cannot distinguish correlations that satisfy Bell inequalities from correlations that violate Bell inequalities, and consequently that they cannot do justice to the challenges of explaining certain quantum correlations causally. Nonetheless, by adapting the conceptual tools of causal inference, we can show that any attempt to provide a causal explanation of nonsignalling correlations that violate a Bell inequality must contradict a core principle of these algorithms, namely, that an observed statistical independence between variables should not be explained by fine-tuning of the causal parameters. In particular, we demonstrate the need for such fine-tuning for most of the causal mechanisms that have been proposed to underlie Bell correlations, including superluminal causal influences, superdeterminism (that is, a denial of freedom of choice of settings), and retrocausal influences which do not introduce causal cycles.Comment: 29 pages, 28 figs. New in v2: a section presenting in detail our characterization of Bell's theorem as a contradiction arising from (i) the framework of causal models, (ii) the principle of no fine-tuning, and (iii) certain operational features of quantum theory; a section explaining why a denial of hidden variables affords even fewer opportunities for causal explanations of quantum correlation

    Cartan's spiral staircase in physics and, in particular, in the gauge theory of dislocations

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    In 1922, Cartan introduced in differential geometry, besides the Riemannian curvature, the new concept of torsion. He visualized a homogeneous and isotropic distribution of torsion in three dimensions (3d) by the "helical staircase", which he constructed by starting from a 3d Euclidean space and by defining a new connection via helical motions. We describe this geometric procedure in detail and define the corresponding connection and the torsion. The interdisciplinary nature of this subject is already evident from Cartan's discussion, since he argued - but never proved - that the helical staircase should correspond to a continuum with constant pressure and constant internal torque. We discuss where in physics the helical staircase is realized: (i) In the continuum mechanics of Cosserat media, (ii) in (fairly speculative) 3d theories of gravity, namely a) in 3d Einstein-Cartan gravity - this is Cartan's case of constant pressure and constant intrinsic torque - and b) in 3d Poincare gauge theory with the Mielke-Baekler Lagrangian, and, eventually, (iii) in the gauge field theory of dislocations of Lazar et al., as we prove for the first time by arranging a suitable distribution of screw dislocations. Our main emphasis is on the discussion of dislocation field theory.Comment: 31 pages, 8 figure

    Persistent currents, flux quantization, and magnetomotive forces in normal metals and superconductors (Review Article)

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    The notion of persistent current comes back to orbital currents in normal metals, semiconductors and even insulators displaying diamagnetic behavior in weak magnetic fields, but came to focus at the discovery of current persistence and magnetic flux quantization at large fields in atomically big but macroscopically small (mesoscopic) objects. The phenomenon bears much similarity with supercurrents in superconductive metals. We will review progress in developing of our understanding of the physical and technological aspects of this phenomenon. The exact solution for currents, magnetic moments and magnetomotive forces (torques) in crossed magnetic fields are presented. Time-dependent phenomena in crossed magnetic and electric fields, and in possibility of spontaneous persistent currents and of work extraction from static and dynamic quantum states are discussed

    Early inhaled budesonide for the prevention of bronchopulmonary dysplasia

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    BACKGROUND Systemic glucocorticoids reduce the incidence of bronchopulmonary dysplasia among extremely preterm infants, but they may compromise brain development. The effects of inhaled glucocorticoids on outcomes in these infants are unclear. METHODS We randomly assigned 863 infants (gestational age, 23 weeks 0 days to 27 weeks 6 days) to early (within 24 hours after birth) inhaled budesonide or placebo until they no longer required oxygen and positive-pressure support or until they reached a postmenstrual age of 32 weeks 0 days. The primary outcome was death or bronchopulmonary dysplasia, confirmed by means of standardized oxygen-saturation monitoring, at a postmenstrual age of 36 weeks. RESULTS A total of 175 of 437 infants assigned to budesonide for whom adequate data were available (40.0%), as compared with 194 of 419 infants assigned to placebo for whom adequate data were available (46.3%), died or had bronchopulmonary dysplasia (relative risk, stratified according to gestational age, 0.86; 95% confidence interval [CI], 0.75 to 1.00; P = 0.05). The incidence of bronchopulmonary dysplasia was 27.8% in the budesonide group versus 38.0% in the placebo group (relative risk, stratified according to gestational age, 0.74; 95% CI, 0.60 to 0.91; P = 0.004); death occurred in 16.9% and 13.6% of the patients, respectively (relative risk, stratified according to gestational age, 1.24; 95% CI, 0.91 to 1.69; P = 0.17). The proportion of infants who required surgical closure of a patent ductus arteriosus was lower in the budesonide group than in the placebo group (relative risk, stratified according to gestational age, 0.55; 95% CI, 0.36 to 0.83; P = 0.004), as was the proportion of infants who required reintubation (relative risk, stratified according to gestational age, 0.58; 95% CI, 0.35 to 0.96; P = 0.03). Rates of other neonatal illnesses and adverse events were similar in the two groups. CONCLUSIONS Among extremely preterm infants, the incidence of bronchopulmonary dysplasia was lower among those who received early inhaled budesonide than among those who received placebo, but the advantage may have been gained at the expense of increased mortality

    Learning to live together: mutualism between self-splicing introns and their hosts

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    Group I and II introns can be considered as molecular parasites that interrupt protein-coding and structural RNA genes in all domains of life. They function as self-splicing ribozymes and thereby limit the phenotypic costs associated with disruption of a host gene while they act as mobile DNA elements to promote their spread within and between genomes. Once considered purely selfish DNA elements, they now seem, in the light of recent work on the molecular mechanisms regulating bacterial and phage group I and II intron dynamics, to show evidence of co-evolution with their hosts. These previously underappreciated relationships serve the co-evolving entities particularly well in times of environmental stress

    Neuroimaging in anxiety disorders

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    Neuroimaging studies have gained increasing importance in validating neurobiological network hypotheses for anxiety disorders. Functional imaging procedures and radioligand binding studies in healthy subjects and in patients with anxiety disorders provide growing evidence of the existence of a complex anxiety network, including limbic, brainstem, temporal, and prefrontal cortical regions. Obviously, “normal anxiety” does not equal “pathological anxiety” although many phenomena are evident in healthy subjects, however to a lower extent. Differential effects of distinct brain regions and lateralization phenomena in different anxiety disorders are mentioned. An overview of neuroimaging investigations in anxiety disorders is given after a brief summary of results from healthy volunteers. Concluding implications for future research are made by the authors

    What scans we will read: imaging instrumentation trends in clinical oncology

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    Oncological diseases account for a significant portion of the burden on public healthcare systems with associated costs driven primarily by complex and long-lasting therapies. Through the visualization of patient-specific morphology and functional-molecular pathways, cancerous tissue can be detected and characterized non- invasively, so as to provide referring oncologists with essential information to support therapy management decisions. Following the onset of stand-alone anatomical and functional imaging, we witness a push towards integrating molecular image information through various methods, including anato-metabolic imaging (e.g., PET/ CT), advanced MRI, optical or ultrasound imaging. This perspective paper highlights a number of key technological and methodological advances in imaging instrumentation related to anatomical, functional, molecular medicine and hybrid imaging, that is understood as the hardware-based combination of complementary anatomical and molecular imaging. These include novel detector technologies for ionizing radiation used in CT and nuclear medicine imaging, and novel system developments in MRI and optical as well as opto-acoustic imaging. We will also highlight new data processing methods for improved non-invasive tissue characterization. Following a general introduction to the role of imaging in oncology patient management we introduce imaging methods with well-defined clinical applications and potential for clinical translation. For each modality, we report first on the status quo and point to perceived technological and methodological advances in a subsequent status go section. Considering the breadth and dynamics of these developments, this perspective ends with a critical reflection on where the authors, with the majority of them being imaging experts with a background in physics and engineering, believe imaging methods will be in a few years from now. Overall, methodological and technological medical imaging advances are geared towards increased image contrast, the derivation of reproducible quantitative parameters, an increase in volume sensitivity and a reduction in overall examination time. To ensure full translation to the clinic, this progress in technologies and instrumentation is complemented by progress in relevant acquisition and image-processing protocols and improved data analysis. To this end, we should accept diagnostic images as “data”, and – through the wider adoption of advanced analysis, including machine learning approaches and a “big data” concept – move to the next stage of non-invasive tumor phenotyping. The scans we will be reading in 10 years from now will likely be composed of highly diverse multi- dimensional data from multiple sources, which mandate the use of advanced and interactive visualization and analysis platforms powered by Artificial Intelligence (AI) for real-time data handling by cross-specialty clinical experts with a domain knowledge that will need to go beyond that of plain imaging

    Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

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    Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
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