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By analyzing e+e− annihilation data corresponding to an integrated luminosity of 2.93fb−1 collected at the center-of-mass energy of 3.773\,GeV with the BESIII detector, we report the first observations of the doubly Cabibbo-suppressed decays D+→K+π0π0 and D+→K+π0η. The branching fractions of D+→K+π0π0 and D+→K+π0η are measured to be (2.1±0.4stat±0.1syst)×10−4 and (2.1±0.5stat±0.1syst)×10−4 with statistical significances of 8.8σ and 5.5σ, respectively. In addition, we search for the subprocesses D+→K∗(892)+π0 and D+→K∗(892)+η with K∗(892)+→K+π0. The branching fraction of D+→K∗(892)+η is determined to be (4.4+1.8−1.5stat±0.2syst)×10−4, with a statistical significance of 3.2σ. No significant signal for D+→K∗(892)+π0 is found and we set an upper limit on the branching fraction of this decay at the 90\% confidence level to be 5.4×10−4.
Using e+e− annihilation data corresponding to a total integrated luminosity of 6.32 fb−1 collected at center-of-mass energies between 4.178 and 4.226 GeV with the BESIII detector, we perform an amplitude analysis of the decay D+s→K0SK0Sπ+ for the first time. An enhancement is observed in the K0SK0S mass spectrum near 1.7 GeV/c2, which was not seen in D+s→K+K−π+ in an earlier work, implying the existence of an isospin one partner of the f0(1710). The branching fraction of the decay D+s→K0SK0Sπ+ is determined to be B(D+s→K0SK0Sπ+)=(0.68±0.04stat±0.01syst)%.
A search for invisible decays of the Λ baryon is carried out in the process 𝐽/𝜓→Λ¯Λ based on (1.0087±0.0044)×1010 𝐽/𝜓 events collected with the BESIII detector located at the BEPCII storage ring. No signals are found for the invisible decays of Λ baryon, and the upper limit of the branching fraction is determined to be 7.4×10−5 at the 90% confidence level. This is the first search for invisible decays of baryons; such searches will play an important role in constraining dark sector models related to the baryon asymmetry.
Using J/ψ radiative decays from 9.0 billion J/ψ events collected by the BESIII detector, we search for di-muon decays of a CP-odd light Higgs boson (A0), predicted by many new physics models beyond the Standard Model, including the Next-to-Minimal Supersymmetric Standard Model. No evidence for the CP-odd light Higgs production is found, and we set 90% confidence level upper limits on the product branching fraction B(J/ψ→γA0)×B(A0→μ+μ−) in the range of (1.2−778.0)×10−9 for 0.212≤mA0≤3.0 GeV/c2. The new measurement is a 6-7 times improvement over our previous measurement, and is also slightly better than the BaBar measurement in the low-mass region for tanβ=1.
Using J/ψ radiative decays from 9.0 billion J/ψ events collected by the BESIII detector, we search for di-muon decays of a CP-odd light Higgs boson (A0), predicted by many new physics models beyond the Standard Model, including the Next-to-Minimal Supersymmetric Standard Model. No evidence for the CP-odd light Higgs production is found, and we set 90% confidence level upper limits on the product branching fraction B(J/ψ→γA0)×B(A0→μ+μ−) in the range of (1.2−778.0)×10−9 for 0.212≤mA0≤3.0 GeV/c2. The new measurement is a 6-7 times improvement over our previous measurement, and is also slightly better than the BaBar measurement in the low-mass region for tanβ=1.
Using J/ψ radiative decays from 9.0 billion J/ψ events collected by the BESIII detector, we search for di-muon decays of a CP-odd light Higgs boson (A0), predicted by many new physics models beyond the Standard Model, including the Next-to-Minimal Supersymmetric Standard Model. No evidence for the CP-odd light Higgs production is found, and we set 90% confidence level upper limits on the product branching fraction B(J/ψ→γA0)×B(A0→μ+μ−) in the range of (1.2−778.0)×10−9 for 0.212≤mA0≤3.0 GeV/c2. The new measurement is a 6-7 times improvement over our previous measurement, and is also slightly better than the BaBar measurement in the low-mass region for tanβ=1.
Using (10.087±0.044)×109 𝐽/𝜓 events collected by the Beijing Spectrum III (BESIII) detector at the Beijing Electron Positron Collider II (BEPCII) collider, we search for the hyperon semileptonic decay Ξ−→Ξ0𝑒−¯𝜈𝑒. No significant signal is observed and the upper limit on the branching fraction ℬ(Ξ−→Ξ0𝑒−¯𝜈𝑒) is set to be 2.59×10−4 at 90% confidence level. This result is one order of magnitude more strict than the previous best limit.
Using a data set corresponding to an integrated luminosity of 6.32 fb−1 recorded by the BESIII detector at center-of-mass energies between 4.178 and 4.226 GeV, an amplitude analysis of the decay D+s → π+π0π0 is performed, and the relative fractions and phases of different intermediate processes are determined. The absolute branching fraction of the decay D+s → π+π0π0 is measured to be (0.50 ± 0.04stat ± 0.02syst)%. Theabsolute branching fraction of the intermediate process D+s → f0(980)π+, f0(980) → π0π0 is determined to be (0.28 ± 0.04stat ± 0.04syst)%.
Using a data sample of e+e− collision data corresponding to an integrated luminosity of 2.93 fb−1 collected with the BESIII detector at a center-of-mass energy of s=3.773GeV, we search for the singly Cabibbo-suppressed decays D0→π0π0π0, π0π0η, π0ηη and ηηη using the double tag method. The absolute branching fractions are measured to be B(D0→π0π0π0)=(2.0±0.4±0.3)×10−4, B(D0→π0π0η)=(3.8±1.1±0.7)×10−4 and B(D0→π0ηη)=(7.3±1.6±1.5)×10−4 with the statistical significances of 4.8σ, 3.8σ and 5.5σ, respectively, where the first uncertainties are statistical and the second ones systematic. No significant signal of D0→ηηη is found, and the upper limit on its decay branching fraction is set to be B(D0→ηηη)<1.3×10−4 at the 90% confidence level.
Using a data sample of 448.1 × 106 ψ(3686) events collected with the BESIII detector at the BEPCII collider, we report the first observation of the electromagnetic Dalitz decay ψ(3686) → η e+e−, with significances of 7.0σ and 6.3σ when reconstructing the η meson via its decay modes η → γπ+π− and η → π+π−η (η → γγ ), respectively. The weighted average branching fraction is determined to be B(ψ(3686) → η e+e−) = (1.90 ± 0.25 ± 0.11) × 10−6, where the first uncertainty is statistical and the second systematic.
We report a search for a dark photon using 14.9~fb−1 of e+e− annihilation data taken at center-of-mass energies from 4.13 to 4.60~GeV with the BESIII detector operated at the BEPCII storage ring. The dark photon is assumed to be produced in the radiative annihilation process of e+e− and to predominantly decay into light dark matter particles, which escape from the detector undetected. The mass range from 1.5 to 2.9~GeV is scanned for the dark photon candidate, and no significant signal is observed. The mass dependent upper limits at the 90% confidence level on the coupling strength parameter ϵ for a dark photon coupling with an ordinary photon vary between 1.6×10−3 and 5.7×10−3.
In Ref. [1] the BESIII collaboration published a cross section measurement of the process e+e− → π+π− in the energy range between 600 and 900 MeV. In this corrigendum, we report a corrected evaluation of the statistical errors in terms of a fully propagated covariance matrix. The correction also yields a reduced statistical uncertainty for the hadronic vacuum polarization contribution to the anomalous magnetic moment of the muon, which now reads as aππ,LO μ (600 − 900 MeV) = (368.2 ± 1.5stat ± 3.3syst) × 10−10. The central values of the cross section measurement and of aππ,LO μ , as well as the systematic uncertainties remain unchanged.
Using 5.9 pb−1 of e+e− annihilation data collected at center-of-mass energies from 3.640 to 3.701 GeV with the BESIII detector at the BEPCII Collider, we measure the observed cross sections of e+e−→K0SX (where X=anything). From a fit to these observed cross sections with the sum of continuum and ψ(3686) and J/ψ Breit-Wigner functions and considering initial state radiation and the BEPCII beam energy spread, we obtain for the first time the inclusive decay branching fraction B(ψ(3686)→K0SX)=(16.04±0.29±0.90)%, where the first uncertainty is statistical and the second is systematic.
Using 448.1 × 106 ψ(3686) decays collected with the BESIII detector at the BEPCII e+e− storage rings, the branching fractions and angular distributions of the decays χcJ → Ξ−Ξ¯¯¯¯+ and Ξ0Ξ¯¯¯¯0 (J = 0, 1, 2) are measured based on a partial-reconstruction technique. The decays χc1 → Ξ0Ξ¯¯¯¯0 and χc2 → Ξ0Ξ¯¯¯¯0 are observed for the first time with statistical significances of 7σ and 15σ, respectively. The results of this analysis are in good agreement with previous measurements and have significantly improved precision.
Relative fractions and phases of the intermediate decays are determined. With the detection efficiency estimated by the results of the amplitude analysis, the branching fraction of Dþ s → K−Kþπþπ0 decay is measured to be ð5.42 0.10stat 0.17systÞ%.
Inhibition of fatty acid synthesis (FAS) stimulates tumor cell death and reduces angiogenesis. When SH-SY5Y cells or primary neurons are exposed to hypoxia only, inhibition of FAS yields significantly enhanced cell injury. The pathophysiology of stroke, however, is not only restricted to hypoxia but also includes reoxygenation injury. Hence, an oxygen-glucose-deprivation (OGD) model with subsequent reoxygenation in both SH-SY5Y cells and primary neurons as well as a murine stroke model were used herein in order to study the role of FAS inhibition and its underlying mechanisms. SH-SY5Y cells and cortical neurons exposed to 10 h of OGD and 24 h of reoxygenation displayed prominent cell death when treated with the Acetyl-CoA carboxylase inhibitor TOFA or the fatty acid synthase inhibitor cerulenin. Such FAS inhibition reduced the reduction potential of these cells, as indicated by increased NADH2+/NAD+ ratios under both in vitro and in vivo stroke conditions. As observed in the OGD model, FAS inhibition also resulted in increased cell death in the stroke model. Stroke mice treated with cerulenin did not only display increased brain injury but also showed reduced neurological recovery during the observation period of 4 weeks. Interestingly, cerulenin treatment enhanced endothelial cell leakage, reduced transcellular electrical resistance (TER) of the endothelium and contributed to poststroke blood-brain barrier (BBB) breakdown. The latter was a consequence of the activated NF-κB pathway, stimulating MMP-9 and ABCB1 transporter activity on the luminal side of the endothelium. In conclusion, FAS inhibition aggravated poststroke brain injury as consequence of BBB breakdown and NF-κB-dependent inflammation.
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.
Ependymomas encompass a heterogeneous group of central nervous system (CNS) neoplasms that occur along the entire neuroaxis. In recent years, extensive (epi-)genomic profiling efforts have identified several molecular groups of ependymoma that are characterized by distinct molecular alterations and/or patterns. Based on unsupervised visualization of a large cohort of genome-wide DNA methylation data, we identified a highly distinct group of pediatric-type tumors (n = 40) forming a cluster separate from all established CNS tumor types, of which a high proportion were histopathologically diagnosed as ependymoma. RNA sequencing revealed recurrent fusions involving the pleomorphic adenoma gene-like 1 (PLAGL1) gene in 19 of 20 of the samples analyzed, with the most common fusion being EWSR1:PLAGL1 (n = 13). Five tumors showed a PLAGL1:FOXO1 fusion and one a PLAGL1:EP300 fusion. High transcript levels of PLAGL1 were noted in these tumors, with concurrent overexpression of the imprinted genes H19 and IGF2, which are regulated by PLAGL1. Histopathological review of cases with sufficient material (n = 16) demonstrated a broad morphological spectrum of tumors with predominant ependymoma-like features. Immunohistochemically, tumors were GFAP positive and OLIG2- and SOX10 negative. In 3/16 of the cases, a dot-like positivity for EMA was detected. All tumors in our series were located in the supratentorial compartment. Median age of the patients at the time of diagnosis was 6.2 years. Median progression-free survival was 35 months (for 11 patients with data available). In summary, our findings suggest the existence of a novel group of supratentorial neuroepithelial tumors that are characterized by recurrent PLAGL1 fusions and enriched for pediatric patients.