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Based on 4.5 fb−1 of e+e− collision data accumulated at center-of-mass energies between 4599.53 MeV and 4698.82 MeV with the BESIII detector, the decay Λ+c→nK0Sπ+π0 is observed for the first time with a significance of 9.2σ. The branching fraction is measured to be (0.85±0.13±0.03)%, where the first uncertainty is statistical and the second systematic, which differs from the theoretical prediction based on isospin by 4.4σ. This indicates that there may be resonant contributions or some unknown dynamics in this decay.
The absolute branching fraction of the decay Λc(2625)+→Λ+cπ+π− is measured for the first time to be (50.7±5.0stat.±4.9syst.)% with 368.48 pb−1 of e+e− collision data collected by the BESIII detector at the center-of-mass energies of s√=4.918 and 4.950 GeV. This result is lower than the naive prediction of 67\%, obtained from isospin symmetry, by more than 2σ, thereby indicating that the novel mechanism referred to as the \textit{threshold effect}, proposed for the strong decays of Λc(2595)+, also applies to Λc(2625)+. This measurement is necessary to obtain the coupling constants for the transitions between s-wave and p-wave charmed baryons in heavy hadron chiral perturbation theory. In addition, we search for the decay Λc(2595)+→Λ+cπ+π−. No significant signal is observed, and the upper limit on its branching fraction is determined to be 80.8\% at the 90\% confidence level.
Using data samples with an integrated luminosity of 4.67 fb−1 collected by the BESIII detector operating at the BEPCII collider, we search for the process e+e−→η′ψ(2S) at center-of-mass energies from 4.66 to 4.95 GeV. No significant signal is observed, and upper limits for the Born cross sections σB(e+e−→η′ψ(2S)) at the 90\% confidence level are determined.
The Cabbibo-favored decay Λ+c→Ξ0K+π0 is studied for the first time using 6.1 fb−1 of e+e− collision data at center-of-mass energies between 4.600 and 4.840 GeV, collected with the BESIII detector at the BEPCII collider. With a double-tag method, the branching fraction of the three-body decay Λ+c→Ξ0K+π0 is measured to be (7.79±1.46±0.71)×10−3, where the first and second uncertainties are statistical and systematic, respectively. The branching fraction of the two-body decay Λ+c→Ξ(1530)0K+ is (5.99±1.04±0.29)×10−3, which is consistent with the previous result of (5.02±0.99±0.31)×10−3. In addition, the upper limit on the branching fraction of the doubly Cabbibo-suppressed decay Λ+c→nK+π0 is 7.1×10−4 at the 90% confidence level. The upper limits on the branching fractions of Λ+c→Σ0K+π0 and ΛK+π0 are also determined to be 1.8×10−3 and 2.0×10−3, respectively.
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.
Systemic treatment is necessary for one third of patients with renal cell carcinoma. No valid biomarker is currently available to tailor personalized therapy. In this study we established a representative panel of patient derived xenograft (PDX) mouse models from patients with renal cell carcinomas and determined serum levels of high mobility group B1 (HMGB1) protein under treatment with sunitinib, pazopanib, sorafenib, axitinib, temsirolimus and bevacizumab. Serum HMGB1 levels were significantly higher in a subset of the PDX collection, which exhibited slower tumor growth during subsequent passages than tumors with low HMGB1 serum levels. Pre-treatment PDX serum HMGB1 levels also correlated with response to systemic treatment: PDX models with high HMGB1 levels predicted response to bevacizumab. Taken together, we provide for the first time evidence that the damage associated molecular pattern biomarker HMGB1 can predict response to systemic treatment with bevacizumab. Our data support the future evaluation of HMGB1 as a predictive biomarker for bevacizumab sensitivity in patients with renal cell carcinoma.