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Using (448.1±2.9)×106 ψ(3686) events collected with the BESIII detector, we perform the first search for the weak baryonic decay ψ(3686)→Λ+cΣ¯−+c.c.. The analysis procedure is optimized using a blinded method. No significant signal is observed, and the upper limit on the branching fraction (B) of ψ(3686)→Λ+cΣ¯−+c.c. is set to be 1.4×10−5 at the 90\% confidence level.
Using (448.1±2.9)×106 ψ(3686) events collected with the BESIII detector, we perform the first search for the weak baryonic decay ψ(3686)→Λ+cΣ¯−+c.c.. The analysis procedure is optimized using a blinded method. No significant signal is observed, and the upper limit on the branching fraction (B) of ψ(3686)→Λ+cΣ¯−+c.c. is set to be 1.4×10−5 at the 90\% confidence level.
Based on 7.33 fb−1 of e+e− collision data taken at center-of-mass energies between 4.128 and 4.226 GeV with the BESIII detector, we measure the branching fraction of D∗+s→D+sπ0 relative to that of D∗+s→D+sγ to be (6.16±0.43±0.19)%. The first uncertainty is statistical and the second one is systematic. By using the world average value of the branching fraction of D∗+s→D+se+e−, we determine the branching fractions of D∗+s→D+sγ and D∗+s→D+sπ0 to be (93.57±0.44±0.19)% and (5.76±0.44±0.19)%, respectively.
Study of ψ(3686) → ΛΛ¯ω
(2022)
Based on a data sample of (448.1±2.9)×106 ψ(3686) events collected with the BESIII detector at the BEPCII collider, the branching fraction of ψ(3686)→ΛΛ¯ω is measured to be (3.30±0.34(stat.)±0.29(syst.))×10−5 for the first time. In addition, the Λω (or Λ¯ω) invariant mass spectra is studied and the potential presence of excited Λ states has been investigated.
Based on a sample of (10.09±0.04)×109 J/ψ events collected with the BESIII detector operating at the BEPCII storage ring, a partial wave analysis of the decay J/ψ→γηη′ is performed. An isoscalar state with exotic quantum numbers JPC=1−+, denoted as η1(1855), has been observed for the first time with statistical significance larger than 19σ. Its mass and width are measured to be (1855±9+6−1)~MeV/c2 and (188±18+3−8)~MeV, respectively. The product branching fraction B(J/ψ→γη1(1855)→γηη′) is measured to be (2.70±0.41+0.16−0.35)×10−6. The first uncertainties are statistical and the second are systematic. In addition, an upper limit on the branching ratio B(f0(1710)→ηη′)/B(f0(1710)→ππ) is determined to be 1.61×10−3 at 90\% confidence level, which lends support to the hypothesis that the f0(1710) has a large glueball component.
Based on (10087±44)×106 J/ψ events collected with the BESIII detector, the process J/ψ→γπ+π−η′ is studied using two dominant decay channels of the η′ meson, η′→γπ+π− and η′→ηπ+π−,η→γγ. The X(2600) is observed with a statistical significance larger than 20σ in the π+π−η′ invariant mass spectrum, and it has a strong correlation to a structure around 1.5 GeV/{\it c}2 in the π+π− invariant mass spectrum. A simultaneous fit on the π+π−η′ and π+π− invariant mass spectra with the two η′ decay modes indicates that the mass and width of the X(2600) state are 2617.8±2.1+18.2−1.9 MeV/{\it c}2 and 200±8+20−17 MeV, respectively. The corresponding branching fractions are measured to be B(J/ψ→γX(2600))⋅B(X(2600)→f0(1500)η′)⋅B(f0(1500)→π+π−) = (3.39±0.18+0.91−0.66)×10−5 and B(J/ψ→γX(2600))⋅B(X(2600)→f′2(1525)η′)⋅B(f′2(1525)→π+π−) = (2.43±0.13+0.31−1.11)×10−5, where the first uncertainties are statistical, and the second systematic.
We recently reported that expression levels of tumor necrosis factor (TNF) receptors, TNFR1 and TNFR2, are significantly changed in the brains and cerebral spinal cerebral fluid (CSF) with Alzheimer's disease (AD). Moreover, we also found that, in an Alzheimer's mouse model, genetic deletion of TNF receptor (TNFR1) reduces amyloid plaques and amyloid beta peptides (Abeta) production through beta-secretase (BACE1) regulation. TNF-alpha converting enzyme (TACE/ADAM-17) does not only cleave pro- TNF-alpha but also TNF receptors, however, whether the TACE activity was changed in the CSF was not clear. In this study, we examined TACE in the CSF in 32 AD patients and 27 age-matched healthy controls (HCs). Interestingly, we found that TACE activity was significantly elevated in the CSF from AD patients compared with HCs. Furthermore, we also assayed the CSF levels of TACE cleaved soluble forms of TNFR1 and TNFR2 in the same patients. We found that AD patients had higher levels of both TACE cleaved soluble TNFR1 (sTNFR1) and TNFR2 (sTNFR2) in the CSF compared with aged- and gender-matched healthy controls. Levels of sTNFR1 correlated strongly with the levels of sTNFR2 (rs = 0.567-0.663, p < 0.01). The levels of both sTNFR1 and sTNFR2 significantly correlated with the TACE activity (rs = 0.491-0.557, p < 0.05). To examine if changes in TACE activity and in levels of cleaved soluble TNFRs are an early event in the course of Alzheimer's disease, we measured these molecules in the CSF from 47 patients with mild cognitive impairment (MCI) which is considered as a preclinical stage of AD. Unexpectedly, we found significantly higher levels of TACE activity and soluble TNFR in the MCI group. These results suggest that TACE activity and soluble TNF receptors may be potential diagnostic candidate biomarkers in AD and MCI.