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The e+e−→D+sDs1(2536)− and e+e−→D+sD∗s2(2573)− processes are studied using data samples collected with the BESIII detector at center-of-mass energies from 4.530 to 4.946~GeV. The absolute branching fractions of Ds1(2536)−→D¯∗0K− and D∗s2(2573)−→D¯0K− are measured for the first time to be (35.9±4.8±3.5)% and (37.4±3.1±4.6)%, respectively. The measurements are in tension with predictions based on the assumption that the Ds1(2536) and D∗s2(2573) are dominated by a bare cs¯ component. The e+e−→D+sDs1(2536)− and e+e−→D+sD∗s2(2573)− cross sections are measured, and a resonant structure at around 4.6~GeV with a width of 50~MeV is observed for the first time with a statistical significance of 15σ in the e+e−→D+sD∗s2(2573)− process. It could be the Y(4626) found by the Belle collaboration in the D+sDs1(2536)− final state, since they have similar masses and widths. There is also evidence for a structure at around 4.75~GeV in both processes.
Autism spectrum disorder (ASD) is a highly heritable disorder of complex and heterogeneous aetiology. It is primarily characterized by altered cognitive ability including impaired language and communication skills and fundamental deficits in social reciprocity. Despite some notable successes in neuropsychiatric genetics, overall, the high heritability of ASD (~90%) remains poorly explained by common genetic risk variants. However, recent studies suggest that rare genomic variation, in particular copy number variation, may account for a significant proportion of the genetic basis of ASD. We present a large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD. Our strategy, homozygous haplotype (HH) mapping, aims to detect homozygous segments of identical haplotype structure that are shared at a higher frequency amongst ASD patients compared to parental controls. The analysis was performed on 1,402 Autism Genome Project trios genotyped for 1 million single nucleotide polymorphisms (SNPs). We identified 25 known and 1,218 novel ASD candidate genes in the discovery analysis including CADM2, ABHD14A, CHRFAM7A, GRIK2, GRM3, EPHA3, FGF10, KCND2, PDZK1, IMMP2L and FOXP2. Furthermore, 10 of the previously reported ASD genes and 300 of the novel candidates identified in the discovery analysis were replicated in an independent sample of 1,182 trios. Our results demonstrate that regions of HH are significantly enriched for previously reported ASD candidate genes and the observed association is independent of gene size (odds ratio 2.10). Our findings highlight the applicability of HH mapping in complex disorders such as ASD and offer an alternative approach to the analysis of genome-wide association data.
While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
Although autism spectrum disorders (ASDs) have a substantial genetic basis, most of the known genetic risk has been traced to rare variants, principally copy number variants (CNVs). To identify common risk variation, the Autism Genome Project (AGP) Consortium genotyped 1558 rigorously defined ASD families for 1 million single-nucleotide polymorphisms (SNPs) and analyzed these SNP genotypes for association with ASD. In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10−8. When a smaller replication sample was analyzed, the risk allele at rs4141463 was again over-transmitted; yet, consistent with the winner's curse, its effect size in the replication sample was much smaller; and, for the combined samples, the association signal barely fell below the P < 5 × 10−8 threshold. Exploratory analyses of phenotypic subtypes yielded no significant associations after correction for multiple testing. They did, however, yield strong signals within several genes, KIAA0564, PLD5, POU6F2, ST8SIA2 and TAF1C.
We measure the Born cross section for the reaction e+e−→ηhc from s√=4.129 to 4.600~GeV using data sets collected by the BESIII detector running at the BEPCII collider. A resonant structure in the cross section line shape near 4.200~GeV is observed with a statistical significance of 7σ. The parameters of this resonance are measured to be \MeasMass\ and \MeasWidth, where the first uncertainties are statistical and the second systematic.
Observation of η_(c)(1S, 2S) and χ_(cJ) decays to 2(π⁺π^(−))η via ψ(3686) radiative transitions
(2024)
Based on 2.7×109 ψ(3686) decays collected with the BESIII detector, the radiative decay ψ(3686)→γ2(π+π−)η is investigated to measure properties of S- and P-wave charmonium states. The branching fraction of the decay ηc(1S)→2(π+π−)η, which is found to have a strong dependence on the interference pattern between ηc(1S) and non-ηc(1S) processes, is measured in both destructive and constructive interference scenarios for the first time. The mass and width of the ηc(1S) are measured to be M=(2984.14±0.13±0.38) MeV/c2 and Γ=(28.82±0.11±0.82) MeV, respectively. Clear signals for the decays of the χcJ(J=0,1,2) and the ηc(2S) to 2(π+π−)η are also observed for the first time, and the corresponding branching fractions are measured. The ratio of the branching fractions between the ηc(2S) and ηc(1S) decays is significantly lower than the theoretical prediction, which might suggest different dynamics in their decays.
Based on (2712.4±14.3)×106 ψ(3686) events, we investigate four hadronic decay modes of the P-wave charmonium spin-singlet state hc(1P1)→h+h−π0/η (h=π or K) via the process ψ(3686)→π0hc at BESIII. The hc→π+π−π0 decay is observed with a significance of 9.6σ after taking into account systematic uncertainties. Evidences for hc→K+K−π0 and hc→K+K−η are found with significances of 3.5σ and 3.3σ, respectively, after considering the systematic uncertainties. The branching fractions of these decays are measured to be B(hc→π+π−π0)=(1.36±0.16±0.14)×10−3, B(hc→K+K−π0)=(3.26±0.84±0.36)×10−4, and B(hc→K+K−η)=(3.13±1.08±0.38)×10−4, where the first uncertainties are statistical and the second are systematic. No significant signal of hc→π+π−η is found, and the upper limit of its decay branching fraction is determined to be B(hc→π+π−η)<4.0×10−4 at 90% confidence level.
Using 9.0 fb−1 of e+e− collision data collected at center-of-mass energies from 4.178 to 4.278 GeV with the BESIII detector at the BEPCII collider, we perform the first search for the radiative transition χc1(3872)→γψ2(3823). No χc1(3872)→γψ2(3823) signal is observed. The upper limit on the ratio of branching fractions B(χc1(3872)→γψ2(3823),ψ2(3823)→γχc1)/B(χc1(3872)→π+π−J/ψ) is set as 0.075 at the 90\% confidence level. Our result contradicts theoretical predictions under the assumption that the χc1(3872) is the pure charmonium state χc1(2P).
We report the first amplitude analysis of the decays D0→π+π−η and D+→π+π0η using a data sample taken with the BESIII detector at the center-of-mass energy of 3.773 GeV, corresponding to an integrated luminosity of 7.9 fb−1. The contribution from the process D0(+)→a0(980)+π−(0) is significantly larger than the D0(+)→a0(980)−(0)π+ contribution. The ratios B(D0→a0(980)+π−)/B(D0→a0(980)−π+) and B(D+→a0(980)+π0)/B(D+→a0(980)0π+) are measured to be 7.5+2.5−0.8stat.±1.7syst. and 2.6±0.6stat.±0.3syst., respectively. The measured D0 ratio disagrees with the theoretical predictions by orders of magnitudes, thus implying a substantial contribution from final-state interactions.
The process e+e−→pp¯π0 is studied at 20 center-of-mass energies ranging from 2.1000 to 3.0800 GeV using 636.8 pb−1 of data collected with the BESIII detector operating at the BEPCII collider. The Born cross sections for e+e−→pp¯π0 are measured with high precision. Since the lowest center-of-mass energy, 2.1000 GeV, is less than 90 MeV above the pp¯π0 energy threshold, we can probe the threshold behavior for this reaction. However, no anomalous threshold enhancement is found in the cross sections for e+e−→pp¯π0.