The flux of ultra-high-energy cosmic rays along the supergalactic plane measured at the Pierre Auger Observatory

International audienceUltra-high-energy cosmic rays are known to be mainly of extragalactic origin, and their propagation is limited by energy losses, so their arrival directions are expected to correlate with the large-scale structure of the local Universe. In this work, we investigate the possible presence of intermediate-scale excesses in the flux of the most energetic cosmic rays from the direction of the supergalactic plane region using events with energies above 20 EeV recorded with the surface detector array of the Pierre Auger Observatory up to 31 December 2022, with a total exposure of 135,000 km^2 sr yr. The strongest indication for an excess that we find, with a post-trial significance of 3.1σ, is in the Centaurus region, as in our previous reports, and it extends down to lower energies than previously studied. We do not find any strong hints of excesses from any other region of the supergalactic plane at the same angular scale. In particular, our results do not confirm the reports by the Telescope Array collaboration of excesses from two regions in the Northern Hemisphere at the edge of the field of view of the Pierre Auger Observatory. With a comparable exposure, our results in those regions are in good agreement with the expectations from an isotropic distribution

Large-scale cosmic ray anisotropies with 19 years of data from the Pierre Auger Observatory

International audienceResults are presented for the measurement of large-scale anisotropies in the arrival directions of ultra-high-energy cosmic rays detected at the Pierre Auger Observatory during 19 years of operation, prior to AugerPrime, the upgrade of the Observatory. The 3D dipole amplitude and direction are reconstructed above $4\,$EeV in four energy bins. Besides the established dipolar anisotropy in right ascension above $8\,$EeV, the Fourier amplitude of the $8$ to $16\,$EeV energy bin is now also above the $5\sigma$ discovery level. No time variation of the dipole moment above $8\,$EeV is found, setting an upper limit to the rate of change of such variations of $0.3\%$ per year at the $95\%$ confidence level. Additionally, the results for the angular power spectrum are shown, demonstrating no other statistically significant multipoles. The results for the equatorial dipole component down to $0.03\,$EeV are presented, using for the first time a data set obtained with a trigger that has been optimized for lower energies. Finally, model predictions are discussed and compared with observations, based on two source emission scenarios obtained in the combined fit of spectrum and composition above $0.6\,$EeV

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo