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With the data samples taken at center-of-mass energies from 2.00 to 3.08 GeV with the BESIII detector at the BEPCII collider, a partial wave analysis on the e+e−→π+π−π0 process is performed. The Born cross sections for e+e−→π+π−π0 and its intermediate processes e+e−→ρπ and ρ(1450)π are measured as functions of s√. The results for e+e−→π+π−π0 are consistent with previous results measured with the initial state radiation method within one standard deviation, and improve the uncertainty by a factor of ten. By fitting the line shapes of the Born cross sections for the e+e−→ρπ and ρ(1450)π, a structure with mass M=2119±11±15 MeV/c2 and width Γ=69±30±5MeV is observed with a significance of 5.9σ, where the first uncertainties are statistical and the second ones are systematic. This structure can be intepreteted as an excited ω state.
In the effective field theory, the massless dark photon γ′ can only couple with the Standard Model particle through operators of dimension higher than four, thereby offering a high sensitivity to the new physics energy scale. Using 7.9 fb−1 of e+e− collision data collected at s√=3.773 GeV with the BESIII detector at the BEPCII collider, we measure the effective flavor-changing neutral current coupling of cuγ′ in D0→ωγ′ and D0→γγ′ processes to search for the massless dark photon. No significant signals are observed, and the upper limits at the 90% confidence level on the massless dark photon branching fraction are set to be 1.1×10−5 and 2.0×10−6 for D0→ωγ′ and D0→γγ′, respectively. These results provide the most stringent constraint on the new physics energy scale associated with cuγ′ coupling in the world, with the new physics energy scale related parameter |C|2+|C5|2<8.2×10−17 GeV−2 at the 90% confidence level, playing a unique role in the dark sector search with the charm sector.
A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets
(2018)
NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCRB6C14R strain. Ly5.1C14R NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46C14R in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1C14R mice had normal number of NK cells, they showed an increased number of early maturation stage NK cells. CD49a+ILC1s were also increased but these cells lacked the expression of TRAIL. ILC3s that expressed NKp46 were not detectable and were not apparent when examined by T-bet expression. Thus, the C14R mutation reveals that NKp46 is important for NK cell and ILC differentiation, maturation and function.