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he Born cross sections for the process 𝑒+𝑒−→𝜂′𝜋+𝜋− at different center-of-mass energies between 2.00 and 3.08 GeV are reported with improved precision from an analysis of data samples collected with the BESIII detector operating at the BEPCII storage ring. An obvious structure is observed in the Born cross section line shape. Fit as a Breit-Wigner resonance, it has a statistical significance of 6.3𝜎 and a mass and width of 𝑀=(2111±43±25) MeV/𝑐2 and Γ=(135±34±30) MeV, where the uncertainties are statistical and systematic, respectively. These measured resonance parameters agree with the measurements of BABAR in 𝑒+𝑒−→𝜂′𝜋+𝜋− and BESIII in 𝑒+𝑒−→𝜔𝜋0 within two standard deviations.
Observation of a near-threshold structure in the K⁺ recoil-mass spectra in e⁺e⁻ → K⁺(Dₛ⁻D*⁰+Dₛ*⁻D⁰)
(2021)
We report a study of the processes of 𝑒+𝑒−→𝐾+𝐷−𝑠𝐷*0 and 𝐾+𝐷*−𝑠𝐷0 based on 𝑒+𝑒− annihilation samples collected with the BESIII detector operating at BEPCII at five center-of-mass energies ranging from 4.628 to 4.698 GeV with a total integrated luminosity of 3.7 fb−1. An excess of events over the known contributions of the conventional charmed mesons is observed near the 𝐷−𝑠𝐷*0 and 𝐷*−𝑠𝐷0 mass thresholds in the 𝐾+ recoil-mass spectrum for events collected at √𝑠=4.681 GeV. The structure matches a mass-dependent-width Breit-Wigner line shape, whose pole mass and width are determined as (3982.5+1.8
−2.6±2.1) MeV/𝑐2 and (12.8+5.3−4.4±3.0) MeV, respectively. The first uncertainties are statistical and the second are systematic. The significance of the resonance hypothesis is estimated to be 5.3 𝜎 over the contributions only from the conventional charmed mesons. This is the first candidate for a charged hidden-charm tetraquark with strangeness, decaying into 𝐷−𝑠𝐷*0 and 𝐷*−𝑠𝐷0. However, the properties of the excess need further exploration with more statistics.
We report a study of the processes of e+e−→K+(D−sD∗0+D∗−sD0) based on e+e− annihilation samples collected with the BESIII detector operating at BEPCII at five center-of-mass energies ranging from 4.628 to 4.698 GeV with a total integrated luminosity of 3.7 fb−1. An excess over the known contributions of the conventional charmed mesons is observed near the D−sD∗0 and D∗−sD0 mass thresholds in the K+ recoil-mass spectrum for events collected at s√=4.681 GeV. The structure matches a mass-dependent-width Breit-Wigner line shape, whose pole mass and width are determined as (3982.5+1.8−2.6±2.1) MeV/c2 and (12.8+5.3−4.4±3.0) MeV, respectively. The first uncertainties are statistical and the second are systematic. The significance of the resonance hypothesis is estimated to be 5.3 σ over the contributions only from the conventional charmed mesons. This is the first candidate of the charged hidden-charm tetraquark with strangeness, decaying into D−sD∗0 and D∗−sD0. However, the properties of the excess need further exploration with more statistics.
Hypoxia-induced long non-coding RNA Malat1 is dispensable for renal ischemia/reperfusion-injury
(2018)
Renal ischemia-reperfusion (I/R) injury is a major cause of acute kidney injury (AKI). Non-coding RNAs are crucially involved in its pathophysiology. We identified hypoxia-induced long non-coding RNA Malat1 (Metastasis Associated Lung Adenocarcinoma Transcript 1) to be upregulated in renal I/R injury. We here elucidated the functional role of Malat1 in vitro and its potential contribution to kidney injury in vivo. Malat1 was upregulated in kidney biopsies and plasma of patients with AKI, in murine hypoxic kidney tissue as well as in cultured and ex vivo sorted hypoxic endothelial cells and tubular epithelial cells. Malat1 was transcriptionally activated by hypoxia-inducible factor 1-α. In vitro, Malat1 inhibition reduced proliferation and the number of endothelial cells in the S-phase of the cell cycle. In vivo, Malat1 knockout and wildtype mice showed similar degrees of outer medullary tubular epithelial injury, proliferation, capillary rarefaction, inflammation and fibrosis, survival and kidney function. Small-RNA sequencing and whole genome expression analysis revealed only minor changes between ischemic Malat1 knockout and wildtype mice. Contrary to previous studies, which suggested a prominent role of Malat1 in the induction of disease, we did not confirm an in vivo role of Malat1 concerning renal I/R-injury.