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We report on new measurements of Cabibbo-suppressed semileptonic D+s decays using 3.19 fb−1 of e+e− annihilation data sample collected at a center-of-mass energy of 4.178~GeV with the BESIII detector at the BEPCII collider. Our results include branching fractions B(D+s→K0e+νe)=(3.25±0.38(stat.)±0.16(syst.))×10−3 and B(D+s→K∗0e+νe)=(2.37±0.26(stat.)±0.20(syst.))×10−3 which are much improved relative to previous measurements, and the first measurements of the hadronic form-factor parameters for these decays. For D+s→K0e+νe, we obtain f+(0)=0.720±0.084(stat.)±0.013(syst.), and for D+s→K∗0e+νe, we find form-factor ratios rV=V(0)/A1(0)=1.67±0.34(stat.)±0.16(syst.) and r2=A2(0)/A1(0)=0.77±0.28(stat.)±0.07(syst.).
Using a data sample with an integrated luminosity of 2.93 fb−1 taken at the center-of-mass energy of 3.773 GeV, we search for the Majorana neutrino (𝜈𝑚) in the lepton number violating decays 𝐷→𝐾𝜋𝑒+𝑒+. No significant signal is observed, and the upper limits on the branching fraction at the 90% confidence level are set to be ℬ(𝐷0→𝐾−𝜋−𝑒+𝑒+)<2.8×10−6, ℬ(𝐷+→𝐾0𝑆𝜋−𝑒+𝑒+)<3.3×10−6 and ℬ(𝐷+→𝐾−𝜋0𝑒+𝑒+)<8.5×10−6. The Majorana neutrino is searched for with different mass assumptions ranging from 0.25 to 1.0 GeV/𝑐2 in the decays 𝐷0→𝐾−𝑒+𝜈𝑚,𝜈𝑚→𝜋−𝑒+ and 𝐷+→𝐾0𝑆𝑒+𝜈𝑚,𝜈𝑚→𝜋−𝑒+, and the upper limits on the branching fraction at the 90% confidence level are at the level of 10−7∼10−6, depending on the mass of the Majorana neutrino. The constraints on the mixing matrix element |𝑉𝑒𝜈𝑚|2 are also evaluated.
Using a low background data sample of 9.7×105 𝐽/𝜓→𝛾𝜂′, 𝜂′→𝛾𝜋+𝜋− events, which are 2 orders of magnitude larger than those from the previous experiments, recorded with the BESIII detector at BEPCII, the decay dynamics of 𝜂′→𝛾𝜋+𝜋− are studied with both model-dependent and model-independent approaches. The contributions of 𝜔 and the 𝜌(770)−𝜔 interference are observed for the first time in the decays 𝜂′→𝛾𝜋+𝜋− in both approaches. Additionally, a contribution from the box anomaly or the 𝜌(1450) resonance is required in the model-dependent approach, while the process specific part of the decay amplitude is determined in the model-independent approach.
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.
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.
Based on an 𝑒+𝑒− collision data sample corresponding to an integrated luminosity of 567 pb−1 taken at the center-of-mass energy of √𝑠=4.6 GeV with the BESIII detector, we measure the absolute branching fraction of the inclusive decay Λ+𝑐→Λ+𝑋 to be ℬ(Λ+𝑐→Λ+𝑋)=(38.2+2.8−2.2±0.9)% using the double-tag method, where 𝑋 refers to any possible final state particles. In addition, we search for direct 𝐶𝑃 violation in the charge asymmetry of this inclusive decay for the first time, and obtain 𝒜𝐶𝑃≡[ℬ(Λ+𝑐→Λ+𝑋)−ℬ(¯Λ−𝑐 → ¯Λ+𝑋)]/[ℬ(Λ+𝑐→Λ+𝑋)+ℬ(¯Λ−𝑐 → ¯Λ+𝑋)]=(2.1+7.0−6.6±1.6)%, a statistically limited result with no evidence of 𝐶𝑃 violation.
The decay 𝐽/𝜓→𝛾𝛾𝜙 is studied using a sample of 1.31×109 𝐽/𝜓 events collected with the BESIII detector. Two structures around 1475 MeV/𝑐2 and 1835 MeV/𝑐2 are observed in the 𝛾𝜙 invariant mass spectrum for the first time. With a fit on the 𝛾𝜙 invariant mass, which takes into account the interference between the two structures, and a simple analysis of the angular distribution, the structure around 1475 MeV/𝑐2 is found to favor an assignment as the 𝜂(1475) and the mass and width for the structure around 1835 MeV/𝑐2 are consistent with the 𝑋(1835). The statistical significances of the two structures are 13.5𝜎 and 6.3𝜎, respectively. The results indicate that both 𝜂(1475) and 𝑋(1835) contain a sizeable 𝑠¯𝑠 component.
Using a data sample of 𝑒+𝑒− collisions corresponding to an integrated luminosity of 567 pb−1 collected at a center-of-mass energy of √𝑠=4.6 GeV with the BESIII detector, we measure the absolute branching fraction of the inclusive semileptonic Λ+𝑐 decay with a double-tag method. We obtain ℬ(Λ+𝑐→𝑋𝑒+𝜈𝑒)=(3.95±0.34±0.09)%, where the first uncertainty is statistical and the second systematic. Using the known Λ+𝑐 lifetime and the charge-averaged semileptonic decay width of nonstrange charmed mesons (𝐷0 and 𝐷+), we obtain the ratio of the inclusive semileptonic decay widths Γ(Λ+𝑐→𝑋𝑒+𝜈𝑒)/¯Γ(𝐷→𝑋𝑒+𝜈𝑒)=1.26±0.12.
Using a data sample of 448.1×106 𝜓(3686) events collected with the BESIII detector operating at the BEPCII, we perform search for the hadronic transition ℎ𝑐→𝜋+𝜋−𝐽/𝜓 via 𝜓(3686)→𝜋0ℎ𝑐. No signals of the transition are observed, and the upper limit on the product branching fraction ℬ(𝜓(3686)→𝜋0ℎ𝑐)ℬ(ℎ𝑐→𝜋+𝜋−𝐽/𝜓) at the 90% confidence level (C.L.) is determined to be 2.0×10−6. This is the most stringent upper limit to date.
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.
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.