Distances to Galactic X-ray binaries with Gaia DR2

Precise and accurate measurements of distances to Galactic X-ray binaries (XRBs) reduce uncertainties in the determination of XRB physical parameters. We have cross-matched the XRB catalogues of Liu, van Paradijs & van den Heuvel to the results of Gaia Data Release 2. We identify 86 XRBs with a Gaia candidate counterpart, of which 32 are low-mass X-ray binaries (LMXBs) and 54 are high-mass X-ray binaries (HMXBs). Distances to Gaia candidate counterparts are, on average, consistent with those measured by Hipparcos and radio parallaxes. When compared to distances measured by Gaia candidate counterparts, distances measured using Type I X-ray bursts are systematically larger, suggesting that these bursts reach only 50 per cent of the Eddington limit. However, these results are strongly dependent on the prior assumptions used for estimating distance from the Gaia parallax measurements. Comparing positions of Gaia candidate counterparts for XRBs in our sample to positions of spiral arms in the Milky Way, we find that HMXBs exhibit mild preference for being closer to spiral arms; LMXBs exhibit mild preference for being closer to interarm regions. LMXBs do not exhibit any preference for leading or trailing their closest spiral arm. HMXBs exhibit a mild preference for trailing their closest spiral arm. The lack of a strong correlation between HMXBs and spiral arms may be explained by star formation occurring closer to the mid-point of the arms, or a time delay between star formation and HMXB formation manifesting as a spatial separation between HMXBs and the spiral arm where they formed

Large-Scale Structure in Brane-Induced Gravity II. Numerical Simulations

We use N-body simulations to study the nonlinear structure formation in brane-induced gravity, developing a new method that requires alternate use of Fast Fourier Transforms and relaxation. This enables us to compute the nonlinear matter power spectrum and bispectrum, the halo mass function, and the halo bias. From the simulation results, we confirm the expectations based on analytic arguments that the Vainshtein mechanism does operate as anticipated, with the density power spectrum approaching that of standard gravity within a modified background evolution in the nonlinear regime. The transition is very broad and there is no well defined Vainshtein scale, but roughly this corresponds to k_*~ 2 at redshift z=1 and k_*~ 1 at z=0. We checked that while extrinsic curvature fluctuations go nonlinear, and the dynamics of the brane-bending mode C receives important nonlinear corrections, this mode does get suppressed compared to density perturbations, effectively decoupling from the standard gravity sector. At the same time, there is no violation of the weak field limit for metric perturbations associated with C. We find good agreement between our measurements and the predictions for the nonlinear power spectrum presented in paper I, that rely on a renormalization of the linear spectrum due to nonlinearities in the modified gravity sector. A similar prediction for the mass function shows the right trends. Our simulations also confirm the induced change in the bispectrum configuration dependence predicted in paper I.Comment: 19 pages, 13 figures. v2: corrected typos, added more simulations, better test of predictions in large mass regime. v3: minor changes, published versio

A prospective analysis of the injury incidence of young male professional football players on artificial turf

Background: The effects of synthetic surfaces on the risk of injuries is still debated in literature and the majority of published data seems to be contradictory. For such reasons the understanding of injury incidence on such surfaces, especially in youth sport, is fundamental for injury prevention. Objectives: The aim of this study was to prospectively report the epidemiology of injuries in young football players, playing on artificial turfs, during a one sports season. Patients and Methods: 80 young male football players (age 16.1 ± 3.7 years; height 174 ± 6.6 cm; weight 64.2 ± 6.3 kg) were enrolled in a prospective cohort study. The participants were then divided in two groups; the first included players age ranging from 17 to 19 (OP) whereas the second included players age ranging from 13 to 16 (YP). Injury incidence was recorded prospectively, according to the consensus statement for soccer. Results: A total of 107 injuries (35 from the OP and 72 from the YP) were recorded during an exposure time of 83.760 hours (incidence 1.28/1000 per player hours); 22 during matches (incidence 2.84/1000 per player hours, 20.5%) and 85 during training (incidence 1.15/1000 per player hours, 79.5%). Thigh and groin were the most common injury locations (33.6% and 21.5%, respectively) while muscle injuries such as contractures and strains were the most common injury typologies (68.23%). No statistical differences between groups were displayed, except for the rate of severe injuries during matches, with the OP displaying slightly higher rates compared to the YP. Severe injuries accounted for 10.28% of the total injuries reported. The average time lost due to injuries was 14 days. Re-injuries accounted for 4.67% of all injuries sustained during the season. Conclusions: In professional youth soccer injury rates are reasonably low. Muscle injuries are the most common type of injuries while groin and thigh the most common locations. Artificial turf pitches don’t seem to contribute to injury incidence in young football players

A study of the association of HLA DR, DQ, and complement C4 alleles with systemic lupus erythematosus in Iceland

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldOBJECTIVE: To perform an exploratory analysis of the relative contribution of single MHC genes to the pathogenesis of systemic lupus erythematosus (SLE) in a homogenous white population. METHODS: MHC class II alleles and C4 allotypes were determined in 64 SLE patients and in ethnically matched controls. HLA-DR and DQ typing was performed by polymerase chain reaction amplification with sequence specific primers. C4 allotypes were determined by agarose gel electrophoresis. RESULTS: The frequency of C4A*Q0 was significantly higher in patients than in controls (46.9% v 25.3%, p = 0.002). HLA-DRB1, DQA1, and DQB1 alleles in the whole group of SLE patients were not significantly different from those of controls. On the other hand increase in DRB1*03 was observed in the group of patients with C4A*Q0, as compared with patients with other C4A allotypes (p = 0.047). There was no significant correlation between severe and mild disease, as judged by the SLEDAI, and HLADR, DQ alleles and comparing the patients with C4A*Q0 with those with other C4A allotypes there was no significant difference regarding clinical manifestations. CONCLUSION: The results are consistent with the argument that C4A deficiency contributes independently to susceptibility and the pathogenesis of SLE. C4A*Q0 in SLE patients in Iceland shows weaker linkage disequilibrium with DR3 genes than reported in most other white populations and emphasises the role of ethnicity

APC loss in breast cancer leads to doxorubicin resistance via STAT3 activation

Resistance to chemotherapy is one of the leading causes of death from breast cancer. We recently established that loss of Adenomatous Polyposis Coli (APC) in the Mouse Mammary Tumor Virus – Polyoma middle T (MMTV-PyMT) transgenic mouse model results in resistance to cisplatin or doxorubicin-induced apoptosis. Herein, we aim to establish the mechanism that is responsible for APC-mediated chemotherapeutic resistance. Our data demonstrate that MMTV-PyMT;ApcMin/+ cells have increased signal transducer and activator of transcription 3 (STAT3) activation. STAT3 can be constitutively activated in breast cancer, maintains the tumor initiating cell (TIC) population, and upregulates multidrug resistance protein 1 (MDR1). The activation of STAT3 in the MMTV-PyMT;ApcMin/+ model is independent of interleukin 6 (IL-6); however, enhanced EGFR expression in the MMTV-PyMT;ApcMin/+ cells may be responsible for the increased STAT3 activation. Inhibiting STAT3 with a small molecule inhibitor A69 in combination with doxorubicin, but not cisplatin, restores drug sensitivity. A69 also decreases doxorubicin enhanced MDR1 gene expression and the TIC population enhanced by loss of APC. In summary, these results have revealed the molecular mechanisms of APC loss in breast cancer that can guide future treatment plans to counteract chemotherapeutic resistance