Refine
Year of publication
- 2020 (3) (remove)
Document Type
- Article (3)
Language
- English (3)
Has Fulltext
- yes (3)
Is part of the Bibliography
- no (3)
Keywords
- GWAS (1)
- antiepileptic drugs (1)
- genetic generalized epilepsy (1)
- lamotrigine (1)
- levetiracetam (1)
- pharmacoresistance (1)
- valproic acid (1)
Institute
The production of Ξ(1321)− and Ξ¯¯¯¯(1321)+ hyperons in inelastic p+p interactions is studied in a fixed target experiment at a beam momentum of 158 GeV/c. Double differential distributions in rapidity y and transverse momentum pT are obtained from a sample of 33M inelastic events. They allow to extrapolate the spectra to full phase space and to determine the mean multiplicity of both Ξ− and Ξ¯¯¯¯+. The rapidity and transverse momentum spectra are compared to transport model predictions. The Ξ− mean multiplicity in inelastic p+p interactions at 158 GeV/c is used to quantify the strangeness enhancement in A+A collisions at the same centre-of-mass energy per nucleon pair.
A measurement of charged hadron pair correlations in two-dimensional ηφ space is presented. The analysis is based on total 30 million central Be + Be collisions observed in the NA61/SHINE detector at the CERN SPS for incident beam momenta of 19A, 30A, 40A, 75A, and 150A GeV/c. Measurements were carried out for unlike-sign and like-sign charge hadron pairs independently. The C(η, φ) correlation functions were compared with results from a similar analysis on p + p interactions at similar beam momenta per nucleon. General trends of the backto-back correlations are similar in central Be + Be collisions and p + p interactions, but are suppressed in magnitude due to the increased combinatorial background. Predictions from the Epos and UrQMD models are compared to the measurements. Evolution of an enhancement around (η, φ) = (0, 0) with incident energy is observed in central Be + Be collisions. It is not predicted by both models and almost non-existing in proton–proton collisions at the same momentum per nucleon.
Aim: Pharmacoresistance is a major burden in epilepsy treatment. We aimed to identify genetic biomarkers in response to specific antiepileptic drugs (AEDs) in genetic generalized epilepsies (GGE). Materials & methods: We conducted a genome-wide association study (GWAS) of 3.3 million autosomal SNPs in 893 European subjects with GGE – responsive or nonresponsive to lamotrigine, levetiracetam and valproic acid. Results: Our GWAS of AED response revealed suggestive evidence for association at 29 genomic loci (p <10-5) but no significant association reflecting its limited power. The suggestive associations highlight candidate genes that are implicated in epileptogenesis and neurodevelopment. Conclusion: This first GWAS of AED response in GGE provides a comprehensive reference of SNP associations for hypothesis-driven candidate gene analyses in upcoming pharmacogenetic studies.