Measurements of the χ\chic_c and χ\chib_b quarkonium states in ρ\rhoρ\rho collisions with the ATLAS experiment

The chi_b bottomonium states are observed through the reconstruction of the radiative decays chi_b(nP)→Upsilon(1S) gamma using 4.4/fb of pp collision data collected at sqrt(s) = 7 TeV with the ATLAS experiment. The production of the chi_b(1P) and chi_b(2P) bottomonium states is observed in addition to a candidate for a new bottomonium state, consistent with theoretical expectations for the chi_b(3P) states. The production-averaged mass barycentre for the chi_b(3P) candidate is measured to be 10541$\pm$11 (stat.) $\pm$ 30 (syst.) MeV. The consequences of this discovery for our understanding of bottomonium production phenomenology in hadronic collisions is reviewed. The production of the chi_c1 and chi_c2 charmonium states has been measured in sqrt(s) = 7 TeV pp collisions with the ATLAS experiment using a data sample representing an integrated luminosity of 4.5/fb. The prompt and non-prompt production cross sections for the chi_c1 and chi_c2 states are measured within the region | y(J/psi)| < 0.75. These measurements suggest that 24-28% of prompt J/psi are produced in feed-down from radiative chi_c1 and chi_c2 decays. The production of the chi_c2 state, relative to the chi_c1 state, is measured for both prompt and non-prompt production processes. This collection of measurements is compared to a number of theoretical predictions for chi_cJ production at the LHC. The branching fraction B(B$\pm$→chi_c1 K$\pm$) = (4.9$_pm$$\pm$ (stat.) $\pm$0.6 (syst.))x 10^-4 is also measured with the same dataset and chi_c event selection

Evidence of continued injecting drug use after attaining sustained treatment-induced clearance of the hepatitis C virus: implications for reinfection

Background: People who inject drugs (PWID) are at the greatest risk of hepatitis C virus (HCV) infection, yet are often denied immediate treatment due to fears of on-going risk behaviour. Our principal objective was to examine evidence of continued injecting drug use among PWID following successful treatment for HCV and attainment of a sustained viral response (SVR). Methods: PWID who attained SVR between 1992 and June 2012 were selected from the National Scottish Hepatitis C Clinical Database. Hospitalisation and mortality records were sourced for these patients using record linkage techniques. Our primary outcome variable was any hospitalisation or death, which was indicative of injecting drugs post-SVR. Results: The cohort comprised 1170 PWID (mean age at SVR 39.6y; 76% male). The Kaplan Meier estimate of incurring the primary outcome after three years of SVR was 10.59% (95% CI, 8.75–12.79) After adjusting for confounding, the risk of an injection related hospital episode or death post-SVR was significantly increased with advancing year of SVR: AHR:1.07 per year (95% CI, 1.01–1.14), having a pre-SVR acute alcohol intoxication-related hospital episode: AHR:1.83 (95% CI, 1.29–2.60), and having a pre-SVR opiate or injection-related hospital episode: AHR:2.59 (95% CI, 1.84–3.64). Conclusion: Despite attaining the optimal treatment outcome, these data indicate that an increasing significant minority of PWID continue to inject post-SVR at an intensity which leads to either hospitalisation or death and increased risk of reinfection

Immune or genetic-mediated disruption of CASPR2 causes pain hypersensitivity due to enhanced primary afferent excitability

Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized. Human CASPR2 autoantibodies, when injected into mice, were peripherally restricted and resulted in mechanical pain-related hypersensitivity in the absence of neural injury. We therefore investigated the mechanism by which CASPR2 modulates nociceptive function. Mice lacking CASPR2 (Cntnap2 ) demonstrated enhanced pain-related hypersensitivity to noxious mechanical stimuli, heat, and algogens. Both primary afferent excitability and subsequent nociceptive transmission within the dorsal horn were increased in Cntnap2 mice. Either immune or genetic-mediated ablation of CASPR2 enhanced the excitability of DRG neurons in a cell-autonomous fashion through regulation of Kv1 channel expression at the soma membrane. This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability

A search for R-parity-violating supersymmetry in final states containing many jets in pp collisions at √s=13TeV with the ATLAS detector

A search for R-parity-violating supersymmetry in final states with high jet multiplicity is presented. The search uses 140fb−1 of proton-proton collision data at √s=13TeV collected by the ATLAS experiment during Run 2 of the Large Hadron Collider. The results are interpreted in the context of R-parity-violating supersymmetry models that feature prompt gluino-pair production decaying directly to three jets each or decaying to two jets and a neutralino which subsequently decays promptly to three jets. No significant excess over the Standard Model expectation is observed and exclusion limits at the 95% confidence level are extracted. Gluinos with masses up to 1800 GeV are excluded when decaying directly to three jets. In the cascade scenario, gluinos with masses up to 2340 GeV are excluded for a neutralino with mass up to 1250 GeV

Dissociation of brain activation in autism and schizotypal personality disorder during social judgements

Background There are overlaps between autism and schizophrenia but these are particularly pronounced, especially in social domains, for higher functioning individuals with autism spectrum disorders (ASD) or schizotypal personality disorder (SPD). It is not known whether these overlapping social deficits result from shared or distinct brain mechanisms. We therefore compared social cognition in ASD and SPD using functional magnetic resonance imaging (fMRI). Methods Twenty-one individuals with SPD, 28 with ASD and 33 controls were compared with respect to clinical symptoms using the Positive and Negative Syndrome Scale; social cognition, using a social judgment task and Ekman 60 faces task; and brain activation using an fMRI task of social judgment. Results The ASD and SPD groups showed few differences in symptoms or social cognition. However, fMRI showed that, compared to ASD, the SPD group showed significantly greater activation during social compared to gender judgments in the amygdala and 3 clusters: right posterior cerebellum, extending into fusiform and inferior temporal gyri; left posterior cerebellum; and left intraparietal sulcus extending through medial portions of the temporal gyri into the fusiform gyrus (all P < .05 family-wise error corrected). Control activations lay between the ASD and SPD groups. Conclusions Although social cognitive deficits in ASD and SPD appear superficially similar they are the result of different brain mechanisms. These findings have implications for therapeutic interventions targeted at social dysfunction in these conditions