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Using e+e− collision data at ten center-of-mass energies between 2.644 and 3.080 GeV collected with the BESIII detector at BEPCII and corresponding to an integrated luminosity of about 500 pb−1, we measure the cross sections and effective form factors for the process e+e−→Ξ0Ξ¯0 utilizing a single-tag method. A fit to the cross section of e+e−→Ξ0Ξ¯0 with a pQCD-driven power function is performed, from which no significant resonance or threshold enhancement is observed. In addition, the ratio of cross sections for the processes e+e−→Ξ−Ξ¯+ and Ξ0Ξ¯0 is calculated using recent BESIII measurement and is found to be compatible with expectation from isospin symmetry.
Based on 586 pb−1 of e+e− annihilation data collected at a center-of-mass energy of s√=4.6 GeV with the BESIII detector at the BEPCII collider, the absolute branching fraction of Λ+c→pK0Sη decays is measured for the first time to be B(Λ+c→pK0Sη)=(0.414±0.084±0.028)%, where the first uncertainty is statistical and the second is systematic. The result is compatible with a previous CLEO result on the relative branching fraction B(Λ+c→pK0Sη)B(Λ+c→pK−π+), and consistent with theoretical predictions of SU(3) flavor symmetry.
The Born cross sections of the e+e− → +¯ − and e+e− → −¯ + processes are determined for centerof-mass energy from 2.3864 to 3.0200 GeV with the BESIII detector. The cross section lineshapes can be described properly by a pQCD function and the resulting ratio of effective form factors for the + and − is consistent with 3. In addition, ratios of the + electric and magnetic form factors, |GE /GM |, are obtained at three center-of-mass energies through an analysis of the angular distributions. These measurements, which are studied for the first time in the off-resonance region, provide precision experimental input for understanding baryonic structure. The observed new features of the ± form factors require more theoretical discussions for the hyperons.
Born cross sections for the processes e+e− → ωη and e+e− → ωπ0 have been determined for centerof-mass energies between 2.00 and 3.08 GeV with the BESIII detector at the BEPCII collider. The results obtained in this work are consistent with previous measurements but with improved precision. Two resonant structures are observed. In the e+e− → ωη cross sections, a resonance with a mass of (2176 ± 24 ± 3) MeV/c2 and a width of (89 ± 50 ± 5) MeV is observed with a significance of 6.2σ. Its properties are consistent with the φ(2170). In the e+e− → ωπ0 cross sections, a resonance denoted Y (2040) is observed with a significance of more than 10σ. Its mass and width are determined to be (2034 ± 13 ± 9) MeV/c2 and (234 ± 30 ± 25) MeV, respectively, where the first uncertainties are statistical and the second ones are systematic.
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.