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Background: Misconceptions about ADHD stigmatize affected people, reduce credibility of providers, and prevent/delay treatment. To challenge misconceptions, we curated findings with strong evidence base. Methods: We reviewed studies with more than 2000 participants or meta-analyses from five or more studies or 2000 or more participants. We excluded meta-analyses that did not assess publication bias, except for meta-analyses of prevalence. For network meta-analyses we required comparison adjusted funnel plots. We excluded treatment studies with waiting-list or treatment as usual controls. From this literature, we extracted evidence-based assertions about the disorder. Results: We generated 208 empirically supported statements about ADHD. The status of the included statements as empirically supported is approved by 80 authors from 27 countries and 6 continents. The contents of the manuscript are endorsed by 366 people who have read this document and agree with its contents. Conclusions: Many findings in ADHD are supported by meta-analysis. These allow for firm statements about the nature, course, outcome causes, and treatments for disorders that are useful for reducing misconceptions and stigma.
We report measurements of the production of prompt D0, D+, D*+ and D+s mesons in Pb–Pb collisions at the centre-of-mass energy per nucleon-nucleon pair sNN−−−√=5.02 TeV, in the centrality classes 0–10%, 30–50% and 60–80%. The D-meson production yields are measured at mid-rapidity (|y| < 0.5) as a function of transverse momentum (pT). The pT intervals covered in central collisions are: 1 < pT< 50 GeV/c for D0, 2 < pT< 50GeV/c for D+, 3 < pT< 50GeV/c for D*+, and 4 < pT< 16GeV/c for D +s mesons. The nuclear modification factors (RAA) for non-strange D mesons (D0, D+, D*+) show minimum values of about 0.2 for pT = 6–10 GeV/c in the most central collisions and are compatible within uncertainties with those measured at s√NN=2.76 TeV. For D +s mesons, the values of RAA are larger than those of non-strange D mesons, but compatible within uncertainties. In central collisions the average RAA of non-strange D mesons is compatible with that of charged particles for pT> 8 GeV/c, while it is larger at lower pT. The nuclear modification factors for strange and non-strange D mesons are also compared to theoretical models with different implementations of in-medium energy loss.
We report the measured transverse momentum (pT) spectra of primary charged particles from pp, p-Pb and Pb-Pb collisions at a center-of-mass energy sNN−−−√=5.02 TeV in the kinematic range of 0.15 < pT< 50 GeV/c and |η| < 0.8. A significant improvement of systematic uncertainties motivated the reanalysis of data in pp and Pb-Pb collisions at sNN−−−√=2.76 TeV, as well as in p-Pb collisions at sNN−−−√=5.02 TeV, which is also presented. Spectra from Pb-Pb collisions are presented in nine centrality intervals and are compared to a reference spectrum from pp collisions scaled by the number of binary nucleon-nucleon collisions. For central collisions, the pT spectra are suppressed by more than a factor of 7 around 6–7 GeV/c with a significant reduction in suppression towards higher momenta up to 30 GeV/c. The nuclear modification factor RpPb, constructed from the pp and p-Pb spectra measured at the same collision energy, is consistent with unity above 8 GeV/c. While the spectra in both pp and Pb-Pb collisions are substantially harder at sNN−−−√=5.02 TeV compared to 2.76 TeV, the nuclear modification factors show no significant collision energy dependence. The obtained results should provide further constraints on the parton energy loss calculations to determine the transport properties of the hot and dense QCD matter.
Bipolar disorder (BD) is a heritable mental illness with complex etiology. While the largest published genome-wide association study identified 64 BD risk loci, the causal SNPs and genes within these loci remain unknown. We applied a suite of statistical and functional fine-mapping methods to these loci, and prioritized 22 likely causal SNPs for BD. We mapped these SNPs to genes, and investigated their likely functional consequences by integrating variant annotations, brain cell-type epigenomic annotations, brain quantitative trait loci, and results from rare variant exome sequencing in BD. Convergent lines of evidence supported the roles of SCN2A, TRANK1, DCLK3, INSYN2B, SYNE1, THSD7A, CACNA1B, TUBBP5, PLCB3, PRDX5, KCNK4, AP001453.3, TRPT1, FKBP2, DNAJC4, RASGRP1, FURIN, FES, YWHAE, DPH1, GSDMB, MED24, THRA, EEF1A2, and KCNQ2 in BD. These represent promising candidates for functional experiments to understand biological mechanisms and therapeutic potential. Additionally, we demonstrated that fine-mapping effect sizes can improve performance and transferability of BD polygenic risk scores across ancestrally diverse populations, and present a high-throughput fine-mapping pipeline (https://github.com/mkoromina/SAFFARI).