On the frequency of N2H+ and N2D+

Context : Dynamical studies of prestellar cores search for small velocity differences between different tracers. The highest radiation frequency precision is therefore required for each of these species. Aims : We want to adjust the frequency of the first three rotational transitions of N2H+ and N2D+ and extrapolate to the next three transitions. Methods : N2H+ and N2D+ are compared to NH3 the frequency of which is more accurately known and which has the advantage to be spatially coexistent with N2H+ and N2D+ in dark cloud cores. With lines among the narrowests, and N2H+ and NH3 emitting region among the largests, L183 is a good candidate to compare these species. Results : A correction of ~10 kHz for the N2H+ (J:1-0) transition has been found (~0.03 km/s) and similar corrections, from a few m/s up to ~0.05 km/s are reported for the other transitions (N2H+ J:3-2 and N2D+ J:1-0, J:2-1, and J:3-2) compared to previous astronomical determinations. Einstein spontaneous decay coefficients (Aul) are included

On cascade decays of squarks at the LHC in NLO QCD

In this paper we present an analysis at NLO of the contribution from squark-squark production to the experimental signature 2j + 2l + missing E_T (+X) with opposite-sign same flavor leptons, taking into account decays and experimental cuts. We consider the case in which one squark decays directly into the lightest neutralino chi^0_1 and the other one into the second lightest neutralino and subsequently into l^+l^-chi^0_1 via an intermediate slepton. On one hand we study effects of the NLO corrections on invariant mass distributions which can be used for future parameter determination. On the other hand we analyze the impact on predictions for cut-and-count searches using this experimental signature.Comment: 21 pages, 10 figure

Electroweak corrections to squark-antisquark production at the LHC

We present the calculation of the electroweak corrections for squark-antisquark pair production at the LHC within the Minimal Supersymmetric Standard Model. Taking into account all possible chirality and light-flavor configurations, we evaluate the NLO EW corrections, which are of O(a_s^2 a), as well as the subleading tree-level contributions of O(a_s a) and O(a^2). Numerical results are presented for several scans in the SUSY parameter space and relevant differential distributions are investigated. The impact of the electroweak corrections is nonnegligible and strongly depends on the chirality configuration of the produced squarks. Our analysis includes a discussion of photon-gluon initiated processes with a focus on the impact of the corresponding large PDF uncertainties.Comment: 33 pages, 12 figures; V2: Original results unchanged. Various minor modifications. Matches version published in JHE

Electroweak and QCD corrections to top-pair hadroproduction in association with heavy bosons

We compute the contribution of order $\alpha_S^2\alpha^2$ to the cross section of a top-antitop pair in association with at least one heavy Standard Model boson -- $Z$, $W^\pm$, and Higgs -- by including all effects of QCD, QED, and weak origin and by working in the automated MadGraph5_aMC@NLO framework. This next-to-leading order contribution is then combined with that of order $\alpha_S^3\alpha$, and with the two dominant lowest-order ones, $\alpha_S^2\alpha$ and $\alpha_S\alpha^2$, to obtain phenomenological results relevant to a 8, 13, and 100~TeV $pp$ collider.Comment: 27 pages, 8 figure

Weak corrections to Higgs hadroproduction in association with a top-quark pair

We present the calculation of the next-to-leading contribution of order $\alpha_S^2\alpha^2$ to the production of a Standard Model Higgs boson in association with a top-quark pair at hadron colliders. All effects of weak and QCD origin are included, whereas those of QED origin are ignored. We work in the MadGraph5_aMC@NLO framework, and discuss sample phenomenological applications at a 8, 13, and 100 TeV $pp$ collider, including the effects of the dominant next-to-leading QCD corrections of order $\alpha_S^3\alpha$.Comment: 29 pages, 38 figure

Explicit dynamics simulation of blade cutting of thin elastoplastic shells using "directional" cohesive elements in solid-shell finite element models

The intentional or accidental cutting of thin shell structures by means of a sharp object is of interest in many engineering applications. The process of cutting involves several types of nonlinearities, such as large deformations, contact, crack propagation and, in the case of laminated shells, delamination. In addition to these, a special difficulty is represented by the blade sharpness, whose accurate geometric resolution would require meshes with characteristic size of the order of the blade curvature radius. A computational finite element approach for the simulation of blade cutting of thin shells is proposed and discussed. The approach is developed in an explicit dynamics framework. Solid-shell elements are used for the discretization, in view of possible future inclusion in the model of delamination processes. Since a sharp blade can interfere with the transmission of cohesive forces between the crack flanks in the cohesive process zone, standard cohesive interface elements are not suited for the simulation of this type of problems unless extremely fine meshes, with characteristic size comparable to the blade curvature radius, are used. To circumvent the problem, the use of a new type of directional cohesive interface element, previously proposed for the simulation of crack propagation in elastic shells, is further developed and reformulated for application to the cutting of elastoplastic thin structures, discretized by solid-shell elements. The proposed approach is validated by means of application to several cutting problems of engineering interest

The n-acetyl phenylalanine glucosamine derivative attenuates the inflammatory/catabolic environment in a chondrocyte-synoviocyte co-culture system

Osteoarthritis (OA), the most prevalent degenerative joint disease, still lacks a true disease-modifying therapy. The involvement of the NF-κB pathway and its upstream activating kinases in OA pathogenesis has been recognized for many years. The ability of the N-acetyl phenylalanine glucosamine derivative (NAPA) to increase anabolism and reduce catabolism via inhibition of IKKα kinase has been previously observed in vitro and in vivo. The present study aims to confirm the chondroprotective effects of NAPA in an in vitro model of joint OA established with primary cells, respecting both the crosstalk between chondrocytes and synoviocytes and their phenotypes. This model satisfactorily reproduces some features of the previously investigated DMM model, such as the prominent induction of ADAMTS-5 upon inflammatory stimulation. Both gene and protein expression analysis indicated the ability of NAPA to counteract key cartilage catabolic enzymes (ADAMTS-5) and effectors (MCP-1). Molecular analysis showed the ability of NAPA to reduce IKKα nuclear translocation and H3Ser10 phosphorylation, thus inhibiting IKKα transactivation of NF-κB signalling, a pivotal step in the NF-κB-dependent gene expression of some of its targets. In conclusion, our data confirm that NAPA could truly act as a disease-modifying drug in OA

Chronic fatigue syndrome: A hypothesis focusing on the autonomic nervous system

Chronic fatigue syndrome is a debilitating illness of unknown aetiology, with estimated levels of prevalence of up to about 8.7/100,000 in the U.S.A. Like pain fatigue it is a personal, emotionally rich experience, which may originate from peripheral or central sites (or both). The nature of the symptoms is complex and reflects the interaction of the patient with the environment and cultural milieu. Accordingly the common use of the same terminology for different types of fatigue may be misleading. Autonomic activation is a key component of both real and simulated physical exercise. Alterations in autonomic nervous system activity are a key component of several physiopathological conditions. In chronic fatigue syndrome disturbances in autonomic activity, and in other homoeostatic mechanisms, such as the hormonal and immune systems, have been reported recently. In this review we followed the hypothesis that in chronic fatigue syndrome the paradoxical condition of disturbing somatic symptoms in the absence of organic evidence of disease might be addressed by focusing on attending functional correlates. In particular we addressed possible alterations in cardiovascular autonomic control, as can be assessed by spectral analysis of R-R interval and systolic arterial pressure variability. With this approach, in subjects complaining of unexplained fatigue, we obtained data suggesting a condition of prevailing sympathetic modulation of the sino-atrial node at rest, and reduced responsiveness to excitatory stimuli. Far from considering the issue resolved, we propose that in the context of the multiple physiological and psychological interactions involved in the perception and self-reporting of symptoms, attendant changes in physiological equivalents might furnish a convenient assessment independent from subjective components. Indices of sympathetic modulation could, accordingly, provide quantifiable signs of the interaction between subject's efforts and environmental demands, independently of self descriptions, which could provide convenient measurable outcomes, both for diagnosis and treatment titration in chronic fatigue syndrome