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Measurements of cross section of e⁺e⁻ → pp¯π⁰ at center-of-mass energies between 4.008 and 4.600 GeV
(2017)
Based on e+e− annihilation data samples collected with the BESIII detector at the BEPCII collider at 13 center-of-mass energies from 4.008 to 4.600 GeV, measurements of the Born cross section of e+e− → pp¯π0 are performed. No significant resonant structure is observed in the measured energy dependence of the cross section. The upper limit on the Born cross section of e+e− → Y (4260) → pp¯π0 at the 90% C.L. is determined to be 0.01 pb. The upper limit on the ratio of the branching fractions B(Y (4260)→pp¯π0) B(Y (4260)→π+π− J/ψ) at the 90% C.L. is determined to be 0.02%.
We report the first measurements of absolute branching fractions for the W -exchange-only processes + c → 0K + and + c → (1530)0K + with the double-tag technique, by analyzing an e+e− collision data sample, that corresponds to an integrated luminosity of 567 pb−1 collected at a center-of-mass energy of 4.6 GeV by the BESIII detector. The branching fractions are measured to be B(+c → 0K +) = (5.90 ± 0.86 ± 0.39) × 10−3 and B(+c → (1530)0K +) = (5.02 ± 0.99 ± 0.31) × 10−3, where the first uncertainties are statistical and the second systematic. Our results are more precise than the previous relative measurements.
Using a data sample of 448.1 × 106 ψ(3686) events collected with the BESIII detector at the BEPCII collider, we report the first observation of the electromagnetic Dalitz decay ψ(3686) → η e+e−, with significances of 7.0σ and 6.3σ when reconstructing the η meson via its decay modes η → γπ+π− and η → π+π−η (η → γγ ), respectively. The weighted average branching fraction is determined to be B(ψ(3686) → η e+e−) = (1.90 ± 0.25 ± 0.11) × 10−6, where the first uncertainty is statistical and the second systematic.
By analyzing 2.93 fb−1 of data taken at the ψ(3770) resonance peak with the BESIII detector, we measure the branching fractions for the hadronic decays D+ → K0S K0S K +, D+ → K0S K0Sπ+, D0 → K0S K0S and D0 → K0S K0S K0S . They are determined to be B(D+ → K0S K0S K +) = (2.54 ± 0.05stat. ± 0.12sys.) × 10−3, B(D+ → K0S K0Sπ+) = (2.70 ± 0.05stat. ± 0.12sys.) × 10−3, B(D0 → K0S K0S ) = (1.67 ± 0.11stat. ± 0.11sys.) × 10−4 and B(D0 → K0S K0S K0S ) = (7.21 ± 0.33stat. ± 0.44sys.) × 10−4, where the second one is measured for the first time and the others are measured with significantly improved precision over the previous measurements.
We report the first measurement of the absolute branching fraction for Λ+c→Λμ+νμ. This measurement is based on a sample of e+e− annihilation data at a center-of-mass energy of s√=4.6 GeV collected with the BESIII detector at the BEPCII storage rings. The sample corresponds to an integrated luminosity of 567 pb−1. The branching fraction is determined to be B(Λ+c→Λμ+νμ)=(3.49±0.46(stat)±0.27(syst))%. In addition, we calculate the ratio B(Λ+c→Λμ+νμ)/B(Λ+c→Λe+νe) to be 0.96±0.16(stat)±0.04(syst).
Previous studies in developing Xenopus and zebrafish reported that the phosphate transporter slc20a1a is expressed in pronephric kidneys. The recent identification of SLC20A1 as a monoallelic candidate gene for cloacal exstrophy further suggests its involvement in the urinary tract and urorectal development. However, little is known of the functional role of SLC20A1 in urinary tract development. Here, we investigated this using morpholino oligonucleotide knockdown of the zebrafish ortholog slc20a1a. This caused kidney cysts and malformations of the cloaca. Moreover, in morphants we demonstrated dysfunctional voiding and hindgut opening defects mimicking imperforate anus in human cloacal exstrophy. Furthermore, we performed immunohistochemistry of an unaffected 6-week-old human embryo and detected SLC20A1 in the urinary tract and the abdominal midline, structures implicated in the pathogenesis of cloacal exstrophy. Additionally, we resequenced SLC20A1 in 690 individuals with bladder exstrophy-epispadias complex (BEEC) including 84 individuals with cloacal exstrophy. We identified two additional monoallelic de novo variants. One was identified in a case-parent trio with classic bladder exstrophy, and one additional novel de novo variant was detected in an affected mother who transmitted this variant to her affected son. To study the potential cellular impact of SLC20A1 variants, we expressed them in HEK293 cells. Here, phosphate transport was not compromised, suggesting that it is not a disease mechanism. However, there was a tendency for lower levels of cleaved caspase-3, perhaps implicating apoptosis pathways in the disease. Our results suggest SLC20A1 is involved in urinary tract and urorectal development and implicate SLC20A1 as a disease-gene for BEEC.
Immunotherapy with oncolytic herpes simplex virus-1 therapy offers an innovative, targeted, less-toxic approach for treating brain tumors. However, a major obstacle in maximizing oncolytic virotherapy is a lack of comprehensive understanding of the underlying mechanisms that unfold in CNS tumors/associated microenvironments after infusion of virus. We demonstrate that our multiplex biomarker screening platform comprehensively informs changes in both topographical location and functional states of resident/infiltrating immune cells that play a role in neuropathology after treatment with HSV G207 in a pediatric Phase 1 patient. Using this approach, we identified robust infiltration of CD8+ T cells suggesting activation of the immune response following virotherapy; however there was a corresponding upregulation of checkpoint proteins PD-1, PD-L1, CTLA-4, and IDO revealing a potential role for checkpoint inhibitors. Such work may ultimately lead to an understanding of the governing pathobiology of tumors, thereby fostering development of novel therapeutics tailored to produce optimal responses.