1,959 research outputs found

    Finite-time quantum-to-classical transition for a Schroedinger-cat state

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    The transition from quantum to classical, in the case of a quantum harmonic oscillator, is typically identified with the transition from a quantum superposition of macroscopically distinguishable states, such as the Schr\"odinger cat state, into the corresponding statistical mixture. This transition is commonly characterized by the asymptotic loss of the interference term in the Wigner representation of the cat state. In this paper we show that the quantum to classical transition has different dynamical features depending on the measure for nonclassicality used. Measures based on an operatorial definition have well defined physical meaning and allow a deeper understanding of the quantum to classical transition. Our analysis shows that, for most nonclassicality measures, the Schr\"odinger cat dies after a finite time. Moreover, our results challenge the prevailing idea that more macroscopic states are more susceptible to decoherence in the sense that the transition from quantum to classical occurs faster. Since nonclassicality is prerequisite for entanglement generation our results also bridge the gap between decoherence, which appears to be only asymptotic, and entanglement, which may show a sudden death. In fact, whereas the loss of coherences still remains asymptotic, we have shown that the transition from quantum to classical can indeed occur at a finite time.Comment: 9+epsilon pages, 4 figures, published version. Originally submitted as "Sudden death of the Schroedinger cat", a bit too cool for APS policy :-

    In search of clarity about parity

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    First paragraph: Andy Clark's Supersizing the Mind: Embodiment, Action, and Cognitive Extension (Clark 2008) is, among other things, a characteristically bold and timely defence of the extended mind hypothesis (Clark and Chalmers 1998). According to this hypothesis, which Clark here calls EXTENDED, the physical mechanisms of mind (the material vehicles that realize cognition) sometimes extend beyond the traditional boundaries of skull and skin, such that "actions and loops through nonbiological structure [sometimes count] as genuine aspects of extended cognitive processes" (p. 85). In the brief treatment that follows I cannot hope to engage with everything that is worthy of discussion in Clark's rich and exciting text, so I shall content myself with exploring and assessing a central thread in his argument for EXTENDED. That thread revolves around what is called the parity principle. Here is how that principle is formulated in Supersizing the Mind (p. 77, drawing on Clark and Chalmers 1998, p. 8): If, as we confront some task, a part of the world functions as a process which, were it to go on in the head, we would have no hesitation in accepting as part of the cognitive process, then that part of the world is (for that time) part of the cognitive process. The general idea is this: if there is functional equality with respect to governing intelligent behaviour (for example, in the way stored information is poised to guide such behaviour), between the causal contribution of certain internal elements and the causal contribution of certain external elements, and if the internal elements concerned already qualify as the proper parts of a cognitive trait (system, state, process, mechanism, architecture...), then there is no good reason to deny equivalent status to the relevant external elements. Parity of causal contribution mandates parity of status with respect to the cognitive

    Genetic contribution to radiographic severity in osteoarthritis of the knee

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    Objective Knee osteoarthritis (OA) has a significant genetic component. The authors have assessed the role of three variants reported to influence risk of knee OA with p<5×10–8 in determining patellofemoral and tibiofemoral Kellgren Lawrence (K/L) grade in knee OA cases. Methods 3474 knee OA cases with sky-line and weight-bearing antero-posterior x-rays of the knee were selected based on the presentation of K/L grade ≥2 at either the tibiofemoral or patellofemoral compartments for one or both knees. Patients belonging to three UK cohorts, were genotyped for rs143383, rs4730250 and rs11842874 mapping to the GDF5, COG5 and MCF2L genes, respectively. The association between tibiofemoral K/L grade and patellofemoral K/L grade was assessed after adjusting for age, gender and body mass index. Results No significant association was found between the rs4730250 and radiographic severity. The rs11842874 mapping to MCF2L was found to be nominally significantly associated with patellofemoral K/L grade as a quantitative trait (p=0.027) but not as a binary trait. The GDF5 single nucleotide polymorphism rs143383 was associated with tibiofemoral K/L grade (β=0.05 (95% CI 0.02 to 0.08) p=0.0011). Conclusions Our data indicate that within individuals affected by radiographic knee OA, OAGDF5 has a modest but significant effect on radiographic severity after adjustment for the major risk factors

    Normalization and centering of array-based heterologous genome hybridization based on divergent control probes

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    <p>Abstract</p> <p>Background</p> <p>Hybridization of heterologous (non-specific) nucleic acids onto arrays designed for model-organisms has been proposed as a viable genomic resource for estimating sequence variation and gene expression in non-model organisms. However, conventional methods of normalization that assume equivalent distributions (such as quantile normalization) are inappropriate when applied to non-specific (heterologous) hybridization. We propose an algorithm for normalizing and centering intensity data from heterologous hybridization that makes no prior assumptions of distribution, reduces the false appearance of homology, and provides a way for researchers to confirm whether heterologous hybridization is suitable.</p> <p>Results</p> <p>Data are normalized by adjusting for Gibbs free energy binding, and centered by adjusting for the median of a common set of control probes assumed to be equivalently dissimilar for all species. This procedure was compared to existing approaches and found to be as successful as Loess normalization at detecting sequence variations (deletions) and even more successful than quantile normalization at reducing the accumulation of false positive probe matches between two related nematode species, <it>Caenorhabditis elegans </it>and <it>C. briggsae</it>. Despite the improvements, we still found that probe fluorescence intensity was too poorly correlated with sequence similarity to result in reliable detection of matching probe sequence.</p> <p>Conclusions</p> <p>Cross-species hybridizations can be a way to adapt genome-enabled tools for closely related non-model organisms, but data must be appropriately normalized and centered in a way that accommodates hybridization of nucleic acids with diverged sequence. For short, 25-mer probes, hybridization intensity alone may be insufficiently correlated with sequence similarity to allow reliable inference of homology at the probe level.</p

    The genetic contribution to severe post-traumatic osteoarthritis

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    Objective: to compare the combined role of genetic variants loci associated with risk of knee or hip osteoarthritis (OA) in post-traumatic (PT) and non-traumatic (NT) cases of clinically severe OA leading to total joint replacement. Methods: A total of 1590 controls, 2168 total knee replacement (TKR) cases (33.2% PT) and 1567 total hip replacement (THR) cases (8.7% PT) from 2 UK cohorts were genotyped for 12 variants previously reported to be reproducibly associated with risk of knee or hip OA. A genetic risk score was generated and the association with PT and NT TKR and THR was assessed adjusting for covariates. Results: For THR, each additional genetic risk variant conferred lower risk among PT cases (OR=1.07, 95% CI 0.96 to 1.19; p=0.24) than NT cases (OR 1.11, 95% CI 1.06 to 1.17; p=1.55×10−5). In contrast, for TKR, each risk variant conferred slightly higher risk among PT cases (OR 1.12, 95% CI 1.07 to 1.19; p=1.82×10−5) than among NT cases (OR 1.08, 95% CI 1.03 to 1.1; p=0.00063). Conclusions: Based on the variants reported to date PT TKR cases have at least as high a genetic contribution as NT cases

    The effect of FTO variation on increased osteoarthritis risk is mediated through body mass index : a mendelian randomisation study

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    Objective: Variation in the fat mass and obesity-associated (FTO) gene influences susceptibility to obesity. A variant in the FTO gene has been implicated in genetic risk to osteoarthritis (OA). We examined the role of the FTO polymorphism rs8044769 in risk of knee and hip OA in cases and controls incorporating body mass index (BMI) information. Methods: 5409 knee OA patients, 4355 hip OA patients and up to 5362 healthy controls from 7 independent cohorts from the UK and Australia were genotyped for rs8044769. The association of the FTO variant with OA was investigated in case/control analyses with and without BMI adjustment and in analyses matched for BMI category. A mendelian randomisation approach was employed using the FTO variant as the instrumental variable to evaluate the role of overweight on OA. Results: In the meta-analysis of all overweight (BMI≥25) samples versus normal-weight controls irrespective of OA status the association of rs8044769 with overweight is highly significant (OR[CIs] for allele G=1.14 [01.08 to 1.19], p=7.5×10−7). A significant association with knee OA is present in the analysis without BMI adjustment (OR[CIs]=1.08[1.02 to 1.14], p=0.009) but the signal fully attenuates after BMI adjustment (OR[CIs]=0.99[0.93 to 1.05], p=0.666). We observe no evidence for association in the BMI-matched meta-analyses. Using mendelian randomisation approaches we confirm the causal role of overweight on OA. Conclusions: Our data highlight the contribution of genetic risk to overweight in defining risk to OA but the association is exclusively mediated by the effect on BMI. This is consistent with what is known of the biology of the FTO gene and supports the causative role of high BMI in OA

    Cognition in Context: Phenomenology, Situated Robotics and the Frame Problem

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    The frame problem is the difficulty of explaining how non-magical systems think and act in ways that are adaptively sensitive to context-dependent relevance. Influenced centrally by Heideggerian phenomenology, Hubert Dreyfus has argued that the frame problem is, in part, a consequence of the assumption (made by mainstream cognitive science and artificial intelligence) that intelligent behaviour is representation-guided behaviour. Dreyfus’ Heideggerian analysis suggests that the frame problem dissolves if we reject representationalism about intelligence and recognize that human agents realize the property of thrownness (the property of being always already embedded in a context). I argue that this positive proposal is incomplete until we understand exactly how the properties in question may be instantiated in machines like us. So, working within a broadly Heideggerian conceptual framework, I pursue the character of a representationshunning thrown machine. As part of this analysis, I suggest that the frame problem is, in truth, a two-headed beast. The intra-context frame problem challenges us to say how a purely mechanistic system may achieve appropriate, flexible and fluid action within a context. The inter-context frame problem challenges us to say how a purely mechanistic system may achieve appropriate, flexible and fluid action in worlds in which adaptation to new contexts is open-ended and in which the number of potential contexts is indeterminate. Drawing on the field of situated robotics, I suggest that the intra-context frame problem may be neutralized by systems of special purpose adaptive couplings, while the inter-context frame problem may be neutralized by systems that exhibit the phenomenon of continuous reciprocal causation. I also defend the view that while continuous reciprocal causation is in conflict with representational explanation, special-purpose adaptive coupling, as well as its associated agential phenomenology, may feature representations. My proposal has been criticized recently by Dreyfus, who accuses me of propagating a cognitivist misreading of Heidegger, one that, because it maintains a role for representation, leads me seriously astray in my handling of the frame problem. I close by responding to Dreyfus’ concerns
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