30 research outputs found

    Study of CP violation in Dalitz-plot analyses of B0 --> K+K-KS, B+ --> K+K-K+, and B+ --> KSKSK+

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    We perform amplitude analyses of the decays B0K+KKS0B^0 \to K^+K^-K^0_S, B+K+KK+B^+ \rightarrow K^+K^-K^+, and B+KS0KS0K+B^+ \to K^0_S K^0_S K^+, and measure CP-violating parameters and partial branching fractions. The results are based on a data sample of approximately 470×106470\times 10^6 BBˉB\bar{B} decays, collected with the BABAR detector at the PEP-II asymmetric-energy BB factory at the SLAC National Accelerator Laboratory. For B+K+KK+B^+ \to K^+K^-K^+, we find a direct CP asymmetry in B+ϕ(1020)K+B^+ \to \phi(1020)K^+ of ACP=(12.8±4.4±1.3)A_{CP}= (12.8\pm 4.4 \pm 1.3)%, which differs from zero by 2.8σ2.8 \sigma. For B0K+KKS0B^0 \to K^+K^-K^0_S, we measure the CP-violating phase βeff(ϕ(1020)KS0)=(21±6±2)\beta_{\rm eff} (\phi(1020)K^0_S) = (21\pm 6 \pm 2)^\circ. For B+KS0KS0K+B^+ \to K^0_S K^0_S K^+, we measure an overall direct CP asymmetry of ACP=(45+4±2)A_{CP} = (4 ^{+4}_{-5} \pm 2)%. We also perform an angular-moment analysis of the three channels, and determine that the fX(1500)f_X(1500) state can be described well by the sum of the resonances f0(1500)f_0(1500), f2(1525)f_2^{\prime}(1525), and f0(1710)f_0(1710).Comment: 35 pages, 68 postscript figures. v3 - minor modifications to agree with published versio

    XLF deficiency results in reduced N-nucleotide addition during V(D)J recombination

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    Repair of DNA double-strand breaks (DSBs) by the nonhomologous end-joining pathway (NHEJ) is important not only for repair of spontaneous breaks but also for breaks induced in developing lymphocytes during V(D)J (variable [V], diversity [D], and joining [J] genes) recombination of their antigen receptor loci to create a diverse repertoire. Mutations in the NHEJ factor XLF result in extreme sensitivity for ionizing radiation, microcephaly, and growth retardation comparable to mutations in LIG4 and XRCC4, which together form the NHEJ ligation complex. However, the effect on the immune system is variable (mild to severe immunodeficiency) and less prominent than that seen in deficiencies of NHEJ factors ARTEMIS and DNA-dependent protein kinase catalytic subunit, with defects in the hairpin opening step, which is crucial and unique for V(D)J recombination. Therefore, we aimed to study the role of XLF during V(D)J recombination. We obtained clinical data from 9 XLF-deficient patients and performed immune phenotyping and antigen receptor repertoire analysis of immunoglobulin (Ig) and T-cell receptor (TR) rearrangements, using next-generation sequencing in 6 patients. The results were compared with XRCC4 and LIG4 deficiency. Both Ig and TR rearrangements showed a significant decrease in the number of nontemplated (N) nucleotides inserted by terminal deoxynucleotidyl transferase, which resulted in a decrease of 2 to 3 amino acids in the CDR3. Such a reduction in the number of N-nucleotides has a great effect on the junctional diversity, and thereby on the total diversity of the Ig and TR repertoire. This shows that XLF has an important role during V(D)J recombination in creating diversity of the repertoire by stimulating N-nucleotide insertion
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