Zero-point quantum fluctuations in cosmology

We re-examine the classic problem of the renormalization of zero-point quantum fluctuations in a Friedmann-Robertson-Walker background. We discuss a number of issues that arise when regularizing the theory with a momentum-space cutoff, and show explicitly how introducing non-covariant counter-terms allows to obtain covariant results for the renormalized vacuum energy-momentum tensor. We clarify some confusion in the literature concerning the equation of state of vacuum fluctuations. Further, we point out that the general structure of the effective action becomes richer if the theory contains a scalar field phi with mass m smaller than the Hubble parameter H(t). Such an ultra-light particle cannot be integrated out completely to get the effective action. Apart from the volume term and the Einstein-Hilbert term, that are reabsorbed into renormalizations of the cosmological constant and Newton's constant, the effective action in general also has a term proportional to F(phi)R, for some function F(phi). As a result, vacuum fluctuations of ultra-light scalar fields naturally lead to models where the dark energy density has the form rho_{DE}(t)=rho_X(t)+rho_Z(t), where rho_X is the component that accelerates the Hubble expansion at late times and rho_Z(t) is an extra contribution proportional to H^2(t). We perform a detailed comparison of such models with CMB, SNIa and BAO data.Comment: 23 pages, 9 figures. v3: refs added. To appear in Phys. Rev.

Actinomycosis of the parotid masquerading as malignant neoplasm.

BACKGROUND: Primary actinomycosis of the parotid gland is of rare occurrence and can mimic a malignant neoplasm both clinically as well as radiologically. CASE PRESENTATION: We present here a case of primary actinomycosis of the parotid gland presenting with a parotid mass lesion with erosion of skull bones. CONCLUSIONS: Clinical presentation of cervico-facial actinomycosis is characterized by the presence of a suppurative or indurative mass with discharging sinuses. The lesion demonstrates characteristic features on fine needle aspiration cytology and histology, however at times the findings are equivocal

Machine learning-derived phenotypic trajectories of asthma and allergy in children and adolescents : protocol for a systematic review

INTRODUCTION: Development of asthma and allergies in childhood/adolescence commonly follows a sequential progression termed the 'atopic march'. Recent reports indicate, however, that these diseases are composed of multiple distinct phenotypes, with possibly differential trajectories. We aim to synthesise the current literature in the field of machine learning-based trajectory studies of asthma/allergies in children and adolescents, summarising the frequency, characteristics and associated risk factors and outcomes of identified trajectories and indicating potential directions for subsequent research in replicability, pathophysiology, risk stratification and personalised management. Furthermore, methodological approaches and quality will be critically appraised, highlighting trends, limitations and future perspectives. METHODS AND ANALYSES: 10 databases (CAB Direct, CINAHL, Embase, Google Scholar, PsycInfo, PubMed, Scopus, Web of Science, WHO Global Index Medicus and WorldCat Dissertations and Theses) will be searched for observational studies (including conference abstracts and grey literature) from the last 10 years (2013-2023) without restriction by language. Screening, data extraction and assessment of quality and risk of bias (using a custom-developed tool) will be performed independently in pairs. The characteristics of the derived trajectories will be narratively synthesised, tabulated and visualised in figures. Risk factors and outcomes associated with the trajectories will be summarised and pooled estimates from comparable numerical data produced through random-effects meta-analysis. Methodological approaches will be narratively synthesised and presented in tabulated form and figure to visualise trends. ETHICS AND DISSEMINATION: Ethical approval is not warranted as no patient-level data will be used. The findings will be published in an international peer-reviewed journal. PROSPERO REGISTRATION NUMBER: CRD42023441691.Peer reviewe

LNCS

Static program analyzers are increasingly effective in checking correctness properties of programs and reporting any errors found, often in the form of error traces. However, developers still spend a significant amount of time on debugging. This involves processing long error traces in an effort to localize a bug to a relatively small part of the program and to identify its cause. In this paper, we present a technique for automated fault localization that, given a program and an error trace, efficiently narrows down the cause of the error to a few statements. These statements are then ranked in terms of their suspiciousness. Our technique relies only on the semantics of the given program and does not require any test cases or user guidance. In experiments on a set of C benchmarks, we show that our technique is effective in quickly isolating the cause of error while out-performing other state-of-the-art fault-localization techniques

Sensitization to molecular dog allergens in an adult population : Results from the West Sweden Asthma Study

Background: As the prevalence of dog allergy rises, component resolved diagnosis might improve the diagnosis, understanding of the clinical outcomes and the effectiveness of immunotherapy. Considering the paucity of data in adults, the current study characterized the patterns of sensitization to dog molecular allergens in an adult population. Methods: Data were derived from the West Sweden Asthma Study, a population-based and representative sample of adults from western Sweden. Of the 2006 subjects clinically examined, 313 participants sensitized to whole dog allergen extract were measured for specific immunoglobulin E (sIgE) levels to Can f 1, Can f 2, Can f 3, Can f 4, Can f 5 and Can f 6 using ImmunoCAP™. Polysensitization was defined as sensitization to ≥3 components. Overlapping sensitization was defined as having concomitant sensitization to at least two dog molecular allergen families (lipocalin, albumin or prostatic kallikrein). Results: Of 313, 218 (70%) subjects tested positive to at least one dog allergen component. Sensitization to Can f 1 (43%) was the most common, followed by Can f 5 (33%) among molecular allergens, while sensitization to lipocalins (56%) was the most common among component families. Polysensitization was found in 22% of all participants and was more common in participants with than in those without asthma. Subjects with asthma were less likely to be monosensitized to Can f 5 than those without asthma. Subjects with asthma had higher IgE levels of Can f 3, Can f 4 and Can f 6 than those without asthma. Overlapping sensitizations also differed between those with asthma and allergic rhinitis and those without. Conclusion: Increased knowledge about the sensitization patterns of dog allergen components can aid in defining their role in asthma and rhinitis. In complex clinical cases of dog allergy, a detailed analysis of dog allergen components can provide additional information on the nature of sensitization.publishedVersionPeer reviewe

A Configurable CEGAR Framework with Interpolation-Based Refinements

International audienceCorrectness of software components in a distributed system is a key issue to ensure overall reliability. Formal verification techniques such as model checking can show design flaws at early stages of development. Abstraction is a key technique for reducing complexity by hiding information, which is not relevant for verification. Counterexample-Guided Abstraction Refinement (CEGAR) is a verification algorithm that starts from a coarse abstraction and refines it iteratively until the proper precision is obtained. Many abstraction types and refinement strategies exist for systems with different characteristics. In this paper we show how these algorithms can be combined into a configurable CEGAR framework. In our framework we also present a new CEGAR configuration based on a combination of abstractions, being able to perform better for certain models. We demonstrate the use of the framework by comparing several configurations of the algorithms on various problems, identifying their advantages and shortcomings

The M235T Polymorphism in the AGT Gene and CHD Risk: Evidence of a Hardy-Weinberg Equilibrium Violation and Publication Bias in a Meta-Analysis

BACKGROUND: The M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD). METHODOLOGY/PRINCIPAL FINDINGS: A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias. CONCLUSIONS/SIGNIFICANCE: The pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases

Cell-based screen for altered nuclear phenotypes reveals senescence progression in polyploid cells after Aurora kinase B inhibition.

Cellular senescence is a widespread stress response and is widely considered to be an alternative cancer therapeutic goal. Unlike apoptosis, senescence is composed of a diverse set of subphenotypes, depending on which of its associated effector programs are engaged. Here we establish a simple and sensitive cell-based prosenescence screen with detailed validation assays. We characterize the screen using a focused tool compound kinase inhibitor library. We identify a series of compounds that induce different types of senescence, including a unique phenotype associated with irregularly shaped nuclei and the progressive accumulation of G1 tetraploidy in human diploid fibroblasts. Downstream analyses show that all of the compounds that induce tetraploid senescence inhibit Aurora kinase B (AURKB). AURKB is the catalytic component of the chromosome passenger complex, which is involved in correct chromosome alignment and segregation, the spindle assembly checkpoint, and cytokinesis. Although aberrant mitosis and senescence have been linked, a specific characterization of AURKB in the context of senescence is still required. This proof-of-principle study suggests that our protocol is capable of amplifying tetraploid senescence, which can be observed in only a small population of oncogenic RAS-induced senescence, and provides additional justification for AURKB as a cancer therapeutic target.This work was supported by the University of Cambridge, Cancer Research UK, Hutchison Whampoa; Cancer Research UK grants A6691 and A9892 (M.N., N.K., C.J.T., D.C.B., C.J.C., L.S.G, and M.S.); a fellowship from the Uehara Memorial Foundation (M.S.).This is the author accepted manuscript. The final version is available from the American Society for Cell Biology via http://dx.doi.org/10.1091/mbc.E15-01-000