Brueckner Rearrangement Effects in Λ5^5_\LambdaHe and ΛΛ6^6_{\Lambda\Lambda}He

Rearrangement effects in light hypernuclei are investigated in the framework of the Brueckner theory. We can estimate without detailed numerical calculations that the energy of the $\alpha$-core is reduced by more than 2.5 MeV when the $\Lambda$ adheres to $^4$He to form $^5_\Lambda$He. Similar assessment of rearrangement contributions is essential to deduce the strength of $\Lambda\Lambda$ interaction from experimentally observed $\Delta B_{\Lambda\Lambda}$. The recently observed experimental value of $\sim$ 1 MeV for the $\Delta B_{\Lambda\Lambda}$ of \hll suggests that the matrix element of $$ in \hll is around -2 MeV.Comment: 7 pages, to appear in Phys. Rev.

Four-body cluster structure of A=7−10A=7-10 double-Λ\Lambda hypernuclei

Energy levels of the double-$\Lambda$ hypernuclei $_\Lambda^{}$$_\Lambda^7$He, $_\Lambda^{}$$_\Lambda^7$Li, $_\Lambda^{}$$_\Lambda^8$Li, $_\Lambda^{}$$_\Lambda^9$Li, $_\Lambda^{}$$_\Lambda^9$Be and $_\Lambda^{}$$_\Lambda^{10}$Be are predicted on the basis of the $\alpha+x+\Lambda +\Lambda$ four-body model with $x=n, p, d, t, ^3$He and $\alpha$, respectively.Comment: 27 pages (preprint style), 12figures submitted to Phys. Rev.

Measurements of differential production cross sections for a Z boson in association with jets in pp collisions at root s=8 TeV

Peer reviewe

Charged-particle nuclear modification factors in PbPb and pPb collisions at √=sNN=5.02 TeV

The spectra of charged particles produced within the pseudorapidity window |η| < 1 at √ sNN = 5.02 TeV are measured using 404 µb −1 of PbPb and 27.4 pb−1 of pp data collected by the CMS detector at the LHC in 2015. The spectra are presented over the transverse momentum ranges spanning 0.5 < pT < 400 GeV in pp and 0.7 < pT < 400 GeV in PbPb collisions. The corresponding nuclear modification factor, RAA, is measured in bins of collision centrality. The RAA in the 5% most central collisions shows a maximal suppression by a factor of 7–8 in the pT region of 6–9 GeV. This dip is followed by an increase, which continues up to the highest pT measured, and approaches unity in the vicinity of pT = 200 GeV. The RAA is compared to theoretical predictions and earlier experimental results at lower collision energies. The newly measured pp spectrum is combined with the pPb spectrum previously published by the CMS collaboration to construct the pPb nuclear modification factor, RpA, up to 120 GeV. For pT > 20 GeV, RpA exhibits weak momentum dependence and shows a moderate enhancement above unity

Performance Of The Alice Experiment At The Cern Lhc

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Measurement of single-diffractive dijet production in proton–proton collisions at √s=8Te with the CMS and TOTEM experiments

Measurements are presented of the single-diffractive dijet cross section and the diffractive cross section as a function of the proton fractional momentum loss ξ and the four-momentum transfer squared t. Both processes pp→pX and pp→Xp, i.e. with the proton scattering to either side of the interaction point, are measured, where X includes at least two jets; the results of the two processes are averaged. The analyses are based on data collected simultaneously with the CMS and TOTEM detectors at the LHC in proton–proton collisions at s=8Te during a dedicated run with β∗=90m at low instantaneous luminosity and correspond to an integrated luminosity of 37.5nb-1. The single-diffractive dijet cross section σjjpX, in the kinematic region ξ&amp;lt; 0.1 , 0.03&amp;lt;|t|&amp;lt;1Ge2, with at least two jets with transverse momentum pT&amp;gt;40Ge, and pseudorapidity | η| &amp;lt; 4.4 , is 21.7±0.9(stat)-3.3+3.0(syst)±0.9(lumi)nb. The ratio of the single-diffractive to inclusive dijet yields, normalised per unit of ξ, is presented as a function of x, the longitudinal momentum fraction of the proton carried by the struck parton. The ratio in the kinematic region defined above, for x values in the range - 2.9 ≤ log 10x≤ - 1.6 , is R=(σjjpX/Δξ)/σjj=0.025±0.001(stat)±0.003(syst), where σjjpX and σjj are the single-diffractive and inclusive dijet cross sections, respectively. The results are compared with predictions from models of diffractive and nondiffractive interactions. Monte Carlo predictions based on the HERA diffractive parton distribution functions agree well with the data when corrected for the effect of soft rescattering between the spectator partons. © 2020, CERN for the benefit of the CMS and TOTEM collaborations

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)