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Based on 368.5 pb−1 of 𝑒+𝑒− collision data collected at center-of-mass energies 4.914 and 4.946 GeV by the BESIII detector, the 𝑒+𝑒−→𝜙𝜒𝑐1(3872) process is searched for the first time. No significant signal is observed and the upper limits at the 90% confidence level on the product of the Born cross section 𝜎(𝑒+𝑒−→𝜙𝜒𝑐1(3872)) and the branching fraction ℬ[𝜒𝑐1(3872)→𝜋+𝜋−𝐽/𝜓] at 4.914 and 4.946 GeV are set to be 0.85 and 0.96 pb, respectively. These measurements provide useful information for the production of the 𝜒𝑐1(3872) at 𝑒+𝑒− colliders and deepen our understanding about the nature of this particle.
The processes hc→γP(P=η′, η, π0)) are studied with a sample of (27.12±0.14)×108 ψ(3686) events collected by the BESIII detector at the BEPCII collider. The branching fractions of hc→γη′ and hc→γη are measured to be (1.40±0.11±0.04±0.10)×10−3 and (3.77±0.55±0.13±0.26)×10−4, respectively, where the first uncertainties are statistical, the second systematic, and the third from the branching fraction of ψ(3686)→π0hc. The ratio Rhc=B(hc→γη)B(hc→γη′) is calculated to be (27.0±4.4±1.0)%. The measurements are consistent with the previous results with improved precision by a factor of 2. The results are valuable for gaining a deeper understanding of η−η′ mixing, and its manifestation within quantum chromodynamics. No significant signal is found for the decay hc→γπ0, and an upper limit is placed on its branching fraction of B(hc→γπ0)<5.0×10−5, at the 90\% confidence level.
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.