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The inclusive J/ψ production has been studied in Pn-Pb and pp collisions at the centre-of-mass energy per nucleon pair sNN−−−√=5.02 TeV, using the ALICE detector at the CERN LHC. The J/ψ meson is reconstructed, in the centre-of-mass rapidity interval 2.5<y<4 and in the transverse-momentum range pT<12 GeV/c, via its decay to a muon pair. In this Letter, we present results on the inclusive J/ψ cross section in pp collisions at s√=5.02 TeV and on the nuclear modification factor RAA. The latter is presented as a function of the centrality of the collision and, for central collisions, as a function of the transverse momentum pT of the J/ψ. The measured RAA values indicate a suppression of the J/ψ in nuclear collisions and are then compared to our previous results obtained in Pb-Pb collisions at sNN−−−√=2.76 TeV. The ratio of the RAA values at the two energies is also computed and compared to calculations of statistical and dynamical models. The numerical value of the ratio for central events (0-10\% centrality) is 1.17±0.04(stat)±0.20(syst). In central events, as a function of pT, a slight increase of RAA with collision energy is visible in the region 2<pT<6 GeV/c. Theoretical calculations provide a good description of the measurements, within uncertainties.
The inclusive J/ψ production has been studied in Pb–Pb and pp collisions at the centre-of-mass energy per nucleon pair √sNN=5.02 TeV, using the ALICE detector at the CERN LHC. The J/ψ meson is reconstructed, in the centre-of-mass rapidity interval 2.5<y<4 and in the transverse-momentum range pT<12 GeV/c, via its decay to a muon pair. In this Letter, we present results on the inclusive J/ψ cross section in pp collisions at √s=5.02 TeV and on the nuclear modification factor RAA. The latter is presented as a function of the centrality of the collision and, for central collisions, as a function of the transverse momentum pT of the J/ψ. The measured RAA values indicate a suppression of the J/ψ in nuclear collisions and are then compared to our previous results obtained in Pb–Pb collisions at √sNN=2.76 TeV. The ratio of the RAA values at the two energies is also computed and compared to calculations of statistical and dynamical models. The numerical value of the ratio for central events (0–10% centrality) is 1.17±0.04(stat)±0.20(syst). In central events, as a function of pT, a slight increase of RAA with collision energy is visible in the region 2<pT<6 GeV/c. Theoretical calculations qualitatively describe the measurements, within uncertainties.
Pathogenic variants in PRRT2, encoding the proline-rich transmembrane protein 2, have been associated with an evolving spectrum of paroxysmal neurologic disorders. Based on a cohort of children with PRRT2-related infantile epilepsy, this study aimed at delineating the broad clinical spectrum of PRRT2-associated phenotypes in these children and their relatives. Only a few recent larger cohort studies are on record and findings from single reports were not confirmed so far. We collected detailed genetic and phenotypic data of 40 previously unreported patients from 36 families. All patients had benign infantile epilepsy and harbored pathogenic variants in PRRT2 (core cohort). Clinical data of 62 family members were included, comprising a cohort of 102 individuals (extended cohort) with PRRT2-associated neurological disease. Additional phenotypes in the cohort of patients with benign sporadic and familial infantile epilepsy consist of movement disorders with paroxysmal kinesigenic dyskinesia in six patients, infantile-onset movement disorders in 2 of 40 individuals, and episodic ataxia after mild head trauma in one girl with bi-allelic variants in PRRT2. The same girl displayed a focal cortical dysplasia upon brain imaging. Familial hemiplegic migraine and migraine with aura were reported in nine families. A single individual developed epilepsy with continuous spikes and waves during sleep. In addition to known variants, we report the novel variant c.843G>T, p.(Trp281Cys) that co-segregated with benign infantile epilepsy and migraine in one family. Our study highlights the variability of clinical presentations of patients harboring pathogenic PRRT2 variants and expands the associated phenotypic spectrum.