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The decays of χc2→K+K−π0, KSK±π∓ and π+π−π0 are studied with the ψ(3686) data samples collected with the Beijing Spectrometer (BESIII). For the first time, the branching fractions of χc2→K∗K¯¯¯¯¯, χc2→a±2(1320)π∓/a02(1320)π0 and χc2→ρ(770)±π∓ are measured. Here K∗K¯¯¯¯¯ denotes both K∗±K∓ and K∗0K¯¯¯¯¯0+c.c., and K∗ denotes the resonances K∗(892), K∗2(1430) and K∗3(1780). The observations indicate a strong violation of the helicity selection rule in χc2 decays into vector and pseudoscalar meson pairs. The measured branching fractions of χc2→K∗(892)K¯¯¯¯¯ are more than 20 times larger than that of χc2→ρ(770)±π∓, which implies the effects are largely due to U-spin symmetry breaking, rather than just isospin symmetry breaking in charmonium decays.
The process 𝑒+𝑒−→𝜙𝜂′ has been studied for the first time in detail using data sample collected with the BESIII detector at the BEPCII collider at center of mass energies from 2.05 to 3.08 GeV. A resonance with quantum numbers 𝐽𝑃𝐶=1−− is observed with mass 𝑀=(2177.5±4.8(stat)±19.5(syst))MeV/𝑐2 and width Γ=(149.0±15.6(stat)±8.9(syst)) MeV with a statistical significance larger than 10𝜎, including systematic uncertainties. If the observed structure is identified with the 𝜙(2170), then the ratio of partial width between the 𝜙𝜂′ by BESIII and 𝜙𝜂 by BABAR is (ℬ𝑅𝜙𝜂Γ𝑅𝑒𝑒)/(ℬ𝑅𝜙𝜂′Γ𝑅𝑒𝑒)=0.23±0.10(stat)±0.18(syst), which is smaller than the prediction of the 𝑠¯𝑠𝑔 hybrid models by several orders of magnitude.
We report the first observation of the semimuonic decay 𝐷+→𝜔𝜇+𝜈𝜇 using an 𝑒+𝑒− collision data sample corresponding to an integrated luminosity of 2.93 fb−1 collected with the BESIII detector at a center-of-mass energy of 3.773 GeV. The absolute branching fraction of the 𝐷+→𝜔𝜇+𝜈𝜇 decay is measured to be ℬ𝐷+→𝜔𝜇+𝜈𝜇=(17.7±1.8stat±1.1syst)×10−4. Its ratio with the world average value of the branching fraction of the 𝐷+→𝜔𝑒+𝜈𝑒 decay probes lepton flavor universality and it is determined to be ℬ𝐷+→𝜔𝜇+𝜈𝜇/ℬPDG 𝐷+→𝜔𝑒+𝜈𝑒=1.05±0.14, in agreement with the standard model expectation within one standard deviation.
We measure the Born cross sections of the process 𝑒+𝑒−→𝐾+𝐾−𝐾+𝐾− at center-of-mass (c.m.) energies, √𝑠, between 2.100 and 3.080 GeV. The data were collected using the BESIII detector at the BEPCII collider. An enhancement at √𝑠=2.232 GeV is observed, very close to the 𝑒+𝑒−→Λ¯Λ production threshold. A similar enhancement at the same c.m. energy is observed in the 𝑒+𝑒−→𝜙𝐾+𝐾− cross section. The energy dependence of the 𝐾+𝐾−𝐾+𝐾− and 𝜙𝐾+𝐾− cross sections differs significantly from that of 𝑒+𝑒−→𝜙𝜋+𝜋−.
Using 𝑒+𝑒−→Λ+𝑐¯Λ−𝑐 production from a 567 pb−1 data sample collected by BESIII at 4.6 GeV, a full angular analysis is carried out simultaneously on the four decay modes of Λ+𝑐→𝑝𝐾0𝑆, Λ𝜋+, Σ+𝜋0, and Σ0𝜋+. For the first time, the Λ+𝑐 transverse polarization is studied in unpolarized 𝑒+𝑒− collisions, where a nonzero effect is observed with a statistical significance of 2.1𝜎. The decay asymmetry parameters of the Λ+𝑐 weak hadronic decays into 𝑝𝐾0𝑆, Λ𝜋+, Σ+𝜋0 and Σ0𝜋+ are measured to be 0.18±0.43(stat)±0.14(syst), −0.80±0.11(stat)±0.02(syst), −0.57±0.10(stat)±0.07(syst), and −0.73±0.17(stat)±0.07(syst), respectively. In comparison with previous results, the measurements for the Λ𝜋+ and Σ+𝜋0 modes are consistent but with improved precision, while the parameters for the 𝑝𝐾0𝑆 and Σ0𝜋+ modes are measured for the first time.
A partial-wave analysis of the decay 𝐽/𝜓→𝐾+𝐾−𝜋0 has been made using (223.7±1.4)×106 𝐽/𝜓 events collected with the BESIII detector in 2009. The analysis, which is performed within the isobar-model approach, reveals contributions from 𝐾*2(1430)±, 𝐾*2(1980)± and 𝐾*4(2045)± decaying to 𝐾±𝜋0. The two latter states are observed in 𝐽/𝜓 decays for the first time. Two resonance signals decaying to 𝐾+𝐾− are also observed. These contributions cannot be reliably identified and their possible interpretations are discussed. The measured branching fraction 𝐵(𝐽/𝜓→𝐾+𝐾−𝜋0) of (2.88±0.01±0.12)×10−3 is more precise than previous results. Branching fractions for the reported contributions are presented as well. The results of the partial-wave analysis differ significantly from those previously obtained by BESII and BABAR.
Using a data sample of 448.1×106 𝜓(3686) events collected at √𝑠=3.686 GeV with the BESIII detector at the Beijing Electron-Positron Collider II, we search for the rare decay 𝐽/𝜓→𝜙𝑒+𝑒− via 𝜓(3686)→𝜋+𝜋−𝐽/𝜓. No signal events are observed and the upper limit on the branching fraction is set to be ℬ(𝐽/𝜓→𝜙𝑒+𝑒−)<1.2×10−7 at the 90% confidence level, which is still about one order of magnitude higher than the Standard Model prediction.
Using a data sample of 448.1×106 ψ(3686) events collected at s√= 3.686 GeV with the BESIII detector at the BEPCII, we search for the rare decay J/ψ→ϕe+e− via ψ(3686)→π+π−J/ψ. No signal events are observed and the upper limit on the branching fraction is set to be B(J/ψ→ϕe+e−)<1.2×10−7 at the 90\% confidence level, which is still about one order of magnitude higher than the Standard Model prediction.
The decays of χc2→K+K−π0, KSK±π∓ and π+π−π0 are studied with the ψ(3686) data samples collected with the Beijing Spectrometer (BESIII). For the first time, the branching fractions of χc2→K∗K¯¯¯¯¯, χc2→a±2(1320)π∓/a02(1320)π0 and χc2→ρ(770)±π∓ are measured. Here K∗K¯¯¯¯¯ denotes both K∗±K∓ and K∗0K¯¯¯¯¯0+c.c., and K∗ denotes the resonances K∗(892), K∗2(1430) and K∗3(1780). The observations indicate a strong violation of the helicity selection rule in χc2 decays into vector and pseudoscalar meson pairs. The measured branching fractions of χc2→K∗(892)K¯¯¯¯¯ are more than 20 times larger than that of χc2→ρ(770)±π∓, which implies the effects are largely due to U-spin symmetry breaking, rather than just isospin symmetry breaking in charmonium decays.
We study the hadronic decays of Λ+c to the final states Σ+η and Σ+η′, using an e+e− annihilation data sample of 567 pb−1 taken at a center-of-mass energy of 4.6 GeV with the BESIII detector at the BEPCII collider. We find evidence for the decays Λ+c→Σ+η and Σ+η′ with statistical significance of 2.5σ and 3.2σ, respectively. Normalizing to the reference decays Λ+c→Σ+π0 and Σ+ω, we obtain the ratios of the branching fractions B(Λ+c→Σ+η)B(Λ+c→Σ+π0) and B(Λ+c→Σ+η′)B(Λ+c→Σ+ω) to be 0.35±0.16±0.03 and 0.86±0.34±0.07, respectively. The upper limits at the 90\% confidence level are set to be B(Λ+c→Σ+η)B(Λ+c→Σ+π0)<0.58 and B(Λ+c→Σ+η′)B(Λ+c→Σ+ω)<1.2. Using BESIII measurements of the branching fractions of the reference decays, we determine B(Λ+c→Σ+η)=(0.41±0.19±0.05)% (<0.68%) and B(Λ+c→Σ+η′)=(1.34±0.53±0.21)% (<1.9%). Here, the first uncertainties are statistical and the second systematic. The obtained branching fraction of Λ+c→Σ+η is consistent with the previous measurement, and the branching fraction of Λ+c→Σ+η′ is measured for the first time.
The decays of χc2→K+K−π0, KSK±π∓ and π+π−π0 are studied with the ψ(3686) data samples collected with the Beijing Spectrometer (BESIII). For the first time, the branching fractions of χc2→K∗K¯¯¯¯¯, χc2→a±2(1320)π∓/a02(1320)π0 and χc2→ρ(770)±π∓ are measured. Here K∗K¯¯¯¯¯ denotes both K∗±K∓ and K∗0K¯¯¯¯¯0+c.c., and K∗ denotes the resonances K∗(892), K∗2(1430) and K∗3(1780). The observations indicate a strong violation of the helicity selection rule in χc2 decays into vector and pseudoscalar meson pairs. The measured branching fractions of χc2→K∗(892)K¯¯¯¯¯ are more than 10 times larger than the upper limit of χc2→ρ(770)±π∓, which is so far the first direct observation of a significant U-spin symmetry breaking effect in charmonium decays.
Background: Gan–Dou–Fu–Mu decoction (GDFMD) improves liver fibrosis in experimental and clinical studies including those on toxic mouse model of Wilson disease (Model). However, the mechanisms underlying the effect of GDFMD have not been characterized. Herein, we deciphered the potential therapeutic targets of GDFMD using transcriptome analysis.
Methods: We constructed a tx-j Wilson disease (WD) mouse model, and assessed the effect of GDFMD on the liver of model mice by hematoxylin and eosin, Masson, and immunohistochemical staining. Subsequently, we identified differentially expressed genes (DEGs) that were upregulated in the Model (Model vs. control) and those that were downregulated upon GDFMD treatment (compared to the Model) using RNA-sequencing (RNA-Seq). Biological functions and signaling pathways in which the DEGs were involved were determined by gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses. A protein–protein interaction (PPI) network was constructed using the STRING database, and the modules were identified using MCODE plugin with the Cytoscape software. Several genes identified in the RNA-Seq analysis were validated by real-time quantitative PCR. Results: Total of 2124 DEGs were screened through the Model vs. control and Model vs. GDFMD comparisons, and dozens of GO and KEGG pathway terms modulated by GDFMD were identified. Dozens of pathways involved in metabolism (including metabolic processes for organic acids, carboxylic acids, monocarboxylic acids, lipids, fatty acids, cellular lipids, steroids, alcohols, eicosanoids, long-chain fatty acids), immune and inflammatory response (such as complement and coagulation cascades, cytokine–cytokine receptor interaction, inflammatory mediator regulation of TRP channels, antigen processing and presentation, T-cell receptor signaling pathway), liver fibrosis (such as ECM-receptor interactions), and cell death (PI3K-Akt signaling pathway, apoptosis, TGF-beta signaling pathway, etc.) were identified as potential targets of GDFMD in the Model. Some hub genes and four modules were identified in the PPI network. The results of real-time quantitative PCR analysis were consistent with those of RNA-Seq analysis. Conclusions: We performed gene expression profiling of GDFMD-treated WD model mice using RNA-Seq analysis and found the genes, pathways, and processes effected by the treatment. Our study provides a theoretical basis to prevent liver fibrosis resulting from WD using GDFMD.
AIM: To evaluate and compare the effect of combined transarterial chemoembolization (TACE) and arterial administration of Bletilla striata (a Chinese traditional medicine against liver tumor) versus TACE alone for the treatment of hepatocellular carcinoma (HCC) in ACI rats.
METHODS: Subcapsular implantation of a solid Morris hepatoma 3 924A (2 mm3) in the liver was carried out in 30 male ACI rats. Tumor volume (V1) was measured by magnetic resonance imaging (MRI) on day 13 after implantation. The following different agents of interventional treatment were injected after retrograde catheterization via gastroduodenal artery (on day 14), namely, (A) TACE (0.1 mg mitomycin + 0.1 ml Lipiodol) + Bletilla striata (1.0 mg) (n=10); (B) TACE + Bletilla striata (1.0 mg) + ligation of hepatic artery (n=10), (C) TACE alone (control group, n=10). Tumor volume (V2) was assessed by MRI (on day 13 after treatment) and the tumor growth ratio (V2/V1) was calculated.
RESULTS: The mean tumor volume before (V1) and after (V2) treatment was 0.0355 cm3 and 0.2248 cm3 in group A, 0.0374 cm3 and 0.0573 cm3 in group B, 0.0380 cm3 and 0.3674 cm3 in group C, respectively. The mean ratio (V2/V1) was 6.2791 in group A, 1.5324 in group B and 9.1382 in group C. Compared with the control group (group C), group B showed significant inhibition of tumor growth (P<0.01), while group A did not (P>0.05). None of the animals died during implantation or in the postoperative period.
CONCLUSION: Combination of TACE and arterial administration of Bletilla striata plus ligation of hepatic artery is more effective than TACE alone in the treatment of HCC in rats.
After five years of running at RHIC, and on the eve of the LHC heavy-ion program, we highlight the status of femtoscopic measurements. We emphasize the role interferometry plays in addressing fundamental questions about the state of matter created in such collisions, and present an enumerated list of measurements, analyses and calculations that are needed to advance the field in the coming years.
The adaptor molecule stimulator of IFN genes (STING) is central to production of type I IFNs in response to infection with DNA viruses and to presence of host DNA in the cytosol. Excessive release of type I IFNs through STING-dependent mechanisms has emerged as a central driver of several interferonopathies, including systemic lupus erythematosus (SLE), Aicardi–Goutières syndrome (AGS), and stimulator of IFN genes-associated vasculopathy with onset in infancy (SAVI). The involvement of STING in these diseases points to an unmet need for the development of agents that inhibit STING signaling. Here, we report that endogenously formed nitro-fatty acids can covalently modify STING by nitro-alkylation. These nitro-alkylations inhibit STING palmitoylation, STING signaling, and subsequently, the release of type I IFN in both human and murine cells. Furthermore, treatment with nitro-fatty acids was sufficient to inhibit production of type I IFN in fibroblasts derived from SAVI patients with a gain-of-function mutation in STING. In conclusion, we have identified nitro-fatty acids as endogenously formed inhibitors of STING signaling and propose for these lipids to be considered in the treatment of STING-dependent inflammatory diseases.
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.