A search for a massless dark photon gamma' is conducted using 4.5 fb(-1) of e(+)e(-) collision data collected at center-of-mass energies between 4.600 and 4.699 GeV with the BESIII detector at ...BEPCII. No significant signal is observed, and the upper limit on the branching fraction B(Lambda(+)(c) -> p gamma') is determined to be 8.0 x 10(-5) at 90% confidence level.
Using (10.087±0.044)×10^{9} J/ψ events collected with the BESIII detector at the BEPCII storage ring, the processes Λp→Λp and Λover ¯p→Λover ¯p are studied, where the Λ/Λover ¯ baryons are produced ...in the process J/ψ→ΛΛover ¯ and the protons are the hydrogen nuclei in the cooling oil of the beam pipe. Clear signals are observed for the two reactions. The cross sections in -0.9≤cosθ_{Λ/Λover ¯}≤0.9 are measured to be σ(Λp→Λp)=(12.2±1.6_{stat}±1.1_{syst}) and σ(Λover ¯p→Λover ¯p)=(17.5±2.1_{stat}±1.6_{syst}) mb at the Λ/Λover ¯ momentum of 1.074 GeV/c within a range of ±0.017 GeV/c, where the θ_{Λ/Λover ¯} are the scattering angles of the Λ/Λover ¯ in the Λp/Λover ¯p rest frames. Furthermore, the differential cross sections of the two reactions are also measured, where there is a slight tendency of forward scattering for Λp→Λp, and a strong forward peak for Λover ¯p→Λover ¯p. We present an approach to extract the total elastic cross sections by extrapolation. The study of Λover ¯p→Λover ¯p represents the first study of antihyperon-nucleon scattering, and these new measurements will serve as important inputs for the theoretical understanding of the (anti)hyperon-nucleon interaction.Using (10.087±0.044)×10^{9} J/ψ events collected with the BESIII detector at the BEPCII storage ring, the processes Λp→Λp and Λover ¯p→Λover ¯p are studied, where the Λ/Λover ¯ baryons are produced in the process J/ψ→ΛΛover ¯ and the protons are the hydrogen nuclei in the cooling oil of the beam pipe. Clear signals are observed for the two reactions. The cross sections in -0.9≤cosθ_{Λ/Λover ¯}≤0.9 are measured to be σ(Λp→Λp)=(12.2±1.6_{stat}±1.1_{syst}) and σ(Λover ¯p→Λover ¯p)=(17.5±2.1_{stat}±1.6_{syst}) mb at the Λ/Λover ¯ momentum of 1.074 GeV/c within a range of ±0.017 GeV/c, where the θ_{Λ/Λover ¯} are the scattering angles of the Λ/Λover ¯ in the Λp/Λover ¯p rest frames. Furthermore, the differential cross sections of the two reactions are also measured, where there is a slight tendency of forward scattering for Λp→Λp, and a strong forward peak for Λover ¯p→Λover ¯p. We present an approach to extract the total elastic cross sections by extrapolation. The study of Λover ¯p→Λover ¯p represents the first study of antihyperon-nucleon scattering, and these new measurements will serve as important inputs for the theoretical understanding of the (anti)hyperon-nucleon interaction.
The singly Cabibbo suppressed decay Λ + c → pη′ is measured using 4.5 fb −1 of e + e − collision data collected at center-of-mass energies between 4.600 and 4.699 GeV with the BESIII detector at ...BEPCII. Evidence for Λ + c → pη′ with a statistical significance of 3.6σ is reported with a double-tag approach. The Λ + c → pη′ absolute branching fraction is determined to be (5.62 +2.46 −2.04 ±0.26)×10 −4 , where the first and second uncertainties are statistical and systematic, respectively. Our result is consistent with the branching fraction obtained by the Belle collaboration within the uncertainty of 1σ.
Quantum-correlated ψ(3770)→DD‾ decays collected by the CLEO-c experiment are used to perform a first measurement of F+4π, the fractional CP-even content of the self-conjugate decay D→π+π−π+π−, ...obtaining a value of 0.737±0.028. An important input to the measurement comes from the use of D→KS0π+π− and D→KL0π+π− decays to tag the signal mode. This same technique is applied to the channels D→π+π−π0 and D→K+K−π0, yielding F+πππ0=1.014±0.045±0.022 and F+KKπ0=0.734±0.106±0.054, where the first uncertainty is statistical and the second systematic. These measurements are consistent with those of an earlier analysis, based on CP-eigenstate tags, and can be combined to give values of F+πππ0=0.973±0.017 and F+KKπ0=0.732±0.055. The results will enable the three modes to be included in a model-independent manner in measurements of the unitarity triangle angle γ using B∓→DK∓ decays, and in time-dependent studies of CP violation and mixing in the D0D‾0 system.
SPONASTRIME dysplasia is an autosomal-recessive spondyloepimetaphyseal dysplasia characterized by spine (spondylar) abnormalities, midface hypoplasia with a depressed nasal bridge, metaphyseal ...striations, and disproportionate short stature. Scoliosis, coxa vara, childhood cataracts, short dental roots, and hypogammaglobulinemia have also been reported in this disorder. Although an autosomal-recessive inheritance pattern has been hypothesized, pathogenic variants in a specific gene have not been discovered in individuals with SPONASTRIME dysplasia. Here, we identified bi-allelic variants in TONSL, which encodes the Tonsoku-like DNA repair protein, in nine subjects (from eight families) with SPONASTRIME dysplasia, and four subjects (from three families) with short stature of varied severity and spondylometaphyseal dysplasia with or without immunologic and hematologic abnormalities, but no definitive metaphyseal striations at diagnosis. The finding of early embryonic lethality in a Tonsl−/− murine model and the discovery of reduced length, spinal abnormalities, reduced numbers of neutrophils, and early lethality in a tonsl−/− zebrafish model both support the hypomorphic nature of the identified TONSL variants. Moreover, functional studies revealed increased amounts of spontaneous replication fork stalling and chromosomal aberrations, as well as fewer camptothecin (CPT)-induced RAD51 foci in subject-derived cell lines. Importantly, these cellular defects were rescued upon re-expression of wild-type (WT) TONSL; this rescue is consistent with the hypothesis that hypomorphic TONSL variants are pathogenic. Overall, our studies in humans, mice, zebrafish, and subject-derived cell lines confirm that pathogenic variants in TONSL impair DNA replication and homologous recombination-dependent repair processes, and they lead to a spectrum of skeletal dysplasia phenotypes with numerous extra-skeletal manifestations.
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