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By analyzing an e+e− annihilation data sample corresponding to an integrated luminosity of 2.93 fb−1 collected at a center-of-mass energy of 3.773 GeV with the BESIII detector, we measure the branching fraction of the D0→ρ−μ+νμ decay for the first time. We obtain BD0→ρ−μ+νμ=(1.35±0.09stat±0.09syst)×10−3. Using the world average of BD0→ρ−e+νe, we find a branching fraction ratio of BD0→ρ−μ+νμ/BD0→ρ−e+νe=0.90±0.11, which agrees with the theoretical expectation of lepton flavor universality within the uncertainty. Combining the world average of BD+→ρ0μ+νμ and the lifetimes of D0(+), we obtain a partial decay width ratio of ΓD0→ρ−μ+νμ/(2ΓD+→ρ0μ+νμ)=0.71±0.14, which is consistent with the isospin symmetry expectation of one within 2.1σ. For the reported values of BD0→ρ−μ+νμ/BD0→ρ−e+νe and ΓD0→ρ−μ+νμ/2ΓD+→ρ0μ+νμ, the uncertainty is the quadratic sum of the statistical and systematic uncertainties.
By analyzing an e+e− annihilation data sample corresponding to an integrated luminosity of 2.93 fb−1 collected at a center-of-mass energy of 3.773 GeV with the BESIII detector, we measure the branching fraction of the D0→ρ−μ+νμ decay for the first time. We obtain BD0→ρ−μ+νμ=(1.35±0.09stat±0.09syst)×10−3. Combining with theoretical predictions, we extract the CKM matrix element |Vcd|=0.204±0.007stat±0.007syst±0.014theory. Using the world average of BD0→ρ−e+νe, we find a branching fraction ratio of BD0→ρ−μ+νμ/BD0→ρ−e+νe=0.90±0.11, which agrees with the theoretical expectation of lepton flavor universality within the uncertainty. Combining the world average of BD+→ρ0μ+νμ and the lifetimes of D0(+), we obtain a partial decay width ratio of ΓD0→ρ−μ+νμ/(2ΓD+→ρ0μ+νμ)=0.71±0.14, which is consistent with the isospin symmetry expectation of one within 2.1σ. For the reported values of BD0→ρ−μ+νμ/BD0→ρ−e+νe and ΓD0→ρ−μ+νμ/2ΓD+→ρ0μ+νμ, the uncertainty is the quadratic sum of the statistical and systematic uncertainties.
By analyzing an e+e− annihilation data sample corresponding to an integrated luminosity of 2.93 fb−1 collected at a center-of-mass energy of 3.773 GeV with the BESIII detector, we measure the branching fraction of the D0→ρ−μ+νμ decay for the first time. We obtain BD0→ρ−μ+νμ=(1.35±0.09stat±0.09syst)×10−3. Using the world average of BD0→ρ−e+νe, we find a branching fraction ratio of BD0→ρ−μ+νμ/BD0→ρ−e+νe=0.90±0.11, which agrees with the theoretical expectation of lepton flavor universality within the uncertainty. Combining the world average of BD+→ρ0μ+νμ and the lifetimes of D0(+), we obtain a partial decay width ratio of ΓD0→ρ−μ+νμ/(2ΓD+→ρ0μ+νμ)=0.71±0.14, which is consistent with the isospin symmetry expectation of one within 2.1σ. For the reported values of BD0→ρ−μ+νμ/BD0→ρ−e+νe and ΓD0→ρ−μ+νμ/2ΓD+→ρ0μ+νμ, the uncertainty is the quadratic sum of the statistical and systematic uncertainties.
Cross sections of the process 𝑒+𝑒−→𝜋0𝜋0𝐽/𝜓 at center-of-mass energies between 3.808 and 4.600 GeV are measured with high precision by using 12.4 fb−1 of data samples collected with the BESIII detector operating at the BEPCII collider facility. A fit to the measured energy-dependent cross sections confirms the existence of the charmoniumlike state 𝑌(4220). The mass and width of the 𝑌(4220) are determined to be (4220.4±2.4±2.3) MeV/𝑐2 and (46.2±4.7±2.1) MeV, respectively, where the first uncertainties are statistical and the second systematic. The mass and width are consistent with those measured in the process 𝑒+𝑒−→𝜋+𝜋−𝐽/𝜓. The neutral charmonium-like state 𝑍𝑐(3900)0 is observed prominently in the 𝜋0𝐽/𝜓 invariant-mass spectrum, and, for the first time, an amplitude analysis is performed to study its properties. The spin-parity of 𝑍𝑐(3900)0 is determined to be 𝐽𝑃=1+, and the pole position is (3893.1±2.2±3.0)−𝑖(22.2±2.6±7.0) MeV/𝑐2, which is consistent with previous studies of electrically charged 𝑍𝑐(3900)±. In addition, cross sections of 𝑒+𝑒− → 𝜋0𝑍𝑐(3900)0 → 𝜋0𝜋0𝐽/𝜓 are extracted, and the corresponding line shape is found to agree with that of the 𝑌(4220).
The Born cross sections of the process e+e−→D∗0D∗−π+ at center-of-mass energies from 4.189 to 4.951 GeV are measured for the first time. The data samples used correspond to an integrated luminosity of 17.9fb−1 and were collected by the BESIII detector operating at the BEPCII storage ring. Three enhancements around 4.20, 4.47 and 4.67 GeV are visible. The resonances have masses of 4209.6±4.7±5.9MeV/c2, 4469.1±26.2±3.6MeV/c2 and 4675.3±29.5±3.5MeV/c2 and widths of 81.6±17.8±9.0MeV, 246.3±36.7±9.4MeV, and 218.3±72.9±9.3MeV, respectively, where the first uncertainties are statistical and the second systematic. The first and third resonances are consistent with the ψ(4230) and ψ(4660) states, respectively, while the second one is compatible with the ψ(4500) observed in the e+e−→K+K−J/ψ process. These three charmoniumlike ψ states are observed in e+e−→D∗0D∗−π+ process for the first time.
A precision measurement of the matrix elements for η→π+π−π0 and η→π0π0π0 decays is performed using a sample of (10087±44)×106 J/ψ decays collected with the BESIII detector. The decay J/ψ→γη is used to select clean samples of 631,686 η→π+π−π0 decays and 272,322 η→π0π0π0 decays. The matrix elements for both channels are in reasonable agreement with previous measurements. The non-zero gX2Y term for the decay mode η→π+π−π0 is confirmed, as reported by the KLOE Collaboration, while the other higher-order terms are found to be insignificant. Dalitz plot asymmetries in the η→π+π−π0 decay are also explored and are found to be consistent with charge conjugation invariance. In addition, a cusp effect is investigated in the η→π0π0π0 decay, and no obvious structure around the π+π− mass threshold is observed.
The Born cross section of the process e+e−→ηJ/ψ at a center-of-mass energy s√=3.773 GeV is measured to be (8.89±0.88±0.42) pb, using a data sample collected with the BESIII detector operating at the BEPCII storage ring. The decay ψ(3770)→ηJ/ψ is observed for the first time with a statistical significance of 7.4σ. From a fit to the dressed cross-section line-shape of e+e−→ηJ/ψ from s√=3.773 to 4.600 GeV we obtain the branching fraction of the decay ψ(3770)→ηJ/ψ to be (11.6±6.1±1.0)×10−4 when the ψ(3770) decay amplitude is added coherently to the other contributions, and (7.9±1.0±0.7)×10−4 when it is added incoherently. Here the first uncertainties are statistical and the second are systematic.
Cross sections for the process e+e−→K0SK0SJ/ψ at center-of-mass energies from 4.128 to 4.950 GeV are measured using data samples with a total integrated luminosity of 21.2 fb−1 collected by the BESIII detector operating at the BEPCII storage ring. The Y(4230) state is observed in the energy dependence of the e+e−→K0SK0SJ/ψ cross section for the first time with a statistical significance of 26.0σ. In addition, an enhancement around 4.710 GeV, called the Y(4710), is seen with a statistical significance of 4.2σ. There is no clear structure around 4.484 GeV. Using a fit with a coherent sum of three Breit-Wigner functions, we determine the mass and width of the Y(4230) state to be 4226.9±6.6±21.9 MeV/c2 and 71.7±16.2±31.4 MeV, respectively, and the mass and width of the Y(4710) state to be 4704.0±52.3±69.5 MeV/c2 and 183.2±114.0±90.8 MeV, respectively, where the first uncertainties are statistical and the second are systematic. In addition, the average Born cross section ratio of e+e−→K0SK0SJ/ψ to e+e−→K+K−J/ψ is measured to be 0.388+0.035−0.028±0.016, or 0.426+0.038−0.031±0.018 if three-body phase space is considered.
The Cabibbo-allowed weak radiative decay Λ+c→Σ+γ has been searched for in a sample of Λ+cΛ¯−c pairs produced in e+e− annihilations, corresponding to an integrated luminosity of 4.5fb−1 collected with the BESIII detector at center-of-mass energies between 4.60 and 4.70 GeV. No excess of signal above background is observed, and we set an upper limit on the branching fraction of this decay to be B(Λ+c→Σ+γ)<4.4×10−4 at a confidence level of 90\%, which is in agreement with Standard Model expectations.
Using a data sample collected with the BESIII detector operating at the BEPCII storage ring, the Born cross section of the process 𝑒+𝑒−→𝜂𝐽/𝜓 at a center-of-mass energy √𝑠=3.773 GeV is measured to be (8.88±0.87±0.42) pb. We fit the cross section line shape before correcting for the initial state radiation from √𝑠=3.773 to 4.600 GeV to obtain the branching fraction ℬ(𝜓(3770)→𝜂𝐽/𝜓). We obtain ℬ(𝜓(3770)→𝜂𝐽/𝜓)=(11.3±5.9±1.1)×10−4 when the 𝜓(3770) decay amplitude is added coherently to the other contributions, and (8.7±1.0±0.8)×10−4 when it is added incoherently. Here the quoted uncertainties are statistical and systematic, respectively. In both cases, the statistical significance of 𝜓(3770) resonance is above 7𝜎. This is the first time the decay 𝜓(3770)→𝜂𝐽/𝜓 is observed with a statistical significance greater than 5𝜎.
Based on 7.33 fb−1 of e+e− collision data taken at center-of-mass energies between 4.128 and 4.226 GeV with the BESIII detector, we measure the branching fraction of D∗+s→D+sπ0 relative to that of D∗+s→D+sγ to be (6.16±0.43±0.19)%. The first uncertainty is statistical and the second one is systematic. By using the world average value of the branching fraction of D∗+s→D+se+e−, we determine the branching fractions of D∗+s→D+sγ and D∗+s→D+sπ0 to be (93.57±0.44±0.19)% and (5.76±0.44±0.19)%, respectively.
Based on 7.33 fb−1 of e+e− collision data taken at center-of-mass energies between 4.128 and 4.226 GeV with the BESIII detector, we measure the branching fraction of D∗+s→D+sπ0 relative to that of D∗+s→D+sγ to be (6.16±0.43±0.19)%. The first uncertainty is statistical and the second one is systematic. By using the world average value of the branching fraction of D∗+s→D+se+e−, we determine the branching fractions of D∗+s→D+sγ and D∗+s→D+sπ0 to be (93.57±0.44±0.19)% and (5.76±0.44±0.19)%, respectively.
A search for the charged lepton flavor violating decay 𝐽/𝜓→𝑒±𝜏∓ with 𝜏∓→𝜋∓𝜋0𝜈𝜏 is performed with about 10×109 𝐽/𝜓 events collected with the BESIII detector at the BEPCII. No significant signal is observed, and an upper limit is set on the branching fraction ℬ(𝐽/𝜓→𝑒±𝜏∓)<7.5×10−8 at the 90% confidence level. This improves the previously published limit by two orders of magnitude.
Alterations in dendritic spine numbers are linked to deficits in learning and memory. While we previously revealed that postsynaptic plasticity-related gene 1 (PRG-1) controls lysophosphatidic acid (LPA) signaling at glutamatergic synapses via presynaptic LPA receptors, we now show that PRG-1 also affects spine density and synaptic plasticity in a cell-autonomous fashion via protein phosphatase 2A (PP2A)/β1-integrin activation. PRG-1 deficiency reduces spine numbers and β1-integrin activation, alters long-term potentiation (LTP), and impairs spatial memory. The intracellular PRG-1 C terminus interacts in an LPA-dependent fashion with PP2A, thus modulating its phosphatase activity at the postsynaptic density. This results in recruitment of adhesome components src, paxillin, and talin to lipid rafts and ultimately in activation of β1-integrins. Consistent with these findings, activation of PP2A with FTY720 rescues defects in spine density and LTP of PRG-1-deficient animals. These results disclose a mechanism by which bioactive lipid signaling via PRG-1 could affect synaptic plasticity and memory formation.
Background/Objectives: Sharing the bed with a partner is common among adults and impacts sleep quality with potential implications for mental health. However, hitherto findings are contradictory and particularly polysomnographic data on co-sleeping couples are extremely rare. The present study aimed to investigate the effects of a bed partner's presence on individual and dyadic sleep neurophysiology.
Methods: Young healthy heterosexual couples underwent sleep-lab-based polysomnography of two sleeping arrangements: individual sleep and co-sleep. Individual and dyadic sleep parameters (i.e., synchronization of sleep stages) were collected. The latter were assessed using cross-recurrence quantification analysis. Additionally, subjective sleep quality, relationship characteristics, and chronotype were monitored. Data were analyzed comparing co-sleep vs. individual sleep. Interaction effects of the sleeping arrangement with gender, chronotype, or relationship characteristics were moreover tested.
Results: As compared to sleeping individually, co-sleeping was associated with about 10% more REM sleep, less fragmented REM sleep (p = 0.008), longer undisturbed REM fragments (p = 0.0006), and more limb movements (p = 0.007). None of the other sleep stages was significantly altered. Social support interacted with sleeping arrangement in a way that individuals with suboptimal social support showed the biggest impact of the sleeping arrangement on REM sleep. Sleep architectures were more synchronized between partners during co-sleep (p = 0.005) even if wake phases were excluded (p = 0.022). Moreover, sleep architectures are significantly coupled across a lag of ± 5min. Depth of relationship represented an additional significant main effect regarding synchronization, reflecting a positive association between the two. Neither REM sleep nor synchronization was influenced by gender, chronotype, or other relationship characteristics.
Conclusion: Depending on the sleeping arrangement, couple's sleep architecture and synchronization show alterations that are modified by relationship characteristics. We discuss that these alterations could be part of a self-enhancing feedback loop of REM sleep and sociality and a mechanism through which sociality prevents mental illness.
Background: Patients with chronic hepatitis C virus (HCV) infection and active or previous hepatitis B virus (HBV) are at risk of HBV reactivation (HBV-R) during direct-acting antiviral (DAA) therapy. Recent reports suggest that HBV-R may even occur several months after completion of DAA therapy. The aim of this study was to assess the risk of HBV-R in patients with resolved HBV after successful DAA therapy during long-term follow-up (FU).
Methods: Among 848 patients treated for chronic HCV, all patients with resolved HBV and long-term FU data were eligible for inclusion. Patients were HBV DNA/hepatitis B surface antigen (HBsAg)–negative at the end of therapy (EOT) and were followed for up to 52 weeks thereafter. Patients underwent regular alanine transaminase (ALT) testing, and additional HBV DNA/HBsAg testing was performed at FU week 12, end of FU, and in case of an ALT increase above the upper limit of normal (>ULN).
Results: A total of 108 patients were followed up for a mean (range) of 41.5 (24–52) weeks after EOT. None of the patients experienced reverse HBsAg seroconversion or reappearance of HBV DNA. One patient received a liver transplantation; 1 patient was diagnosed with de novo hepatocellular carcinoma, and 2 patients died. Eighteen patients (16.7%) had increased ALT levels (grade 0/1). Of those, the majority were male (72.2%) and significantly more patients had cirrhosis (66.7% vs 36.2%, P = .015) or received ribavirin as part of their treatment regimen (86.7% vs 46.8%, P = .041). None of these were associated with HBV-R.
Conclusions: Our results indicate that the risk of HBV-R in patients with resolved HBV treated with DAAs for HCV is low during long-term follow-up.
Despite multidisciplinary local and systemic therapeutic approaches, the prognosis for most patients with brain metastases is still dismal. The role of adaptive and innate anti-tumor response including the Human Leukocyte Antigen (HLA) machinery of antigen presentation is still unclear. We present data on the HLA class II-chaperone molecule CD74 in brain metastases and its impact on the HLA peptidome complexity.
We analyzed CD74 and HLA class II expression on tumor cells in a subset of 236 human brain metastases, primary tumors and peripheral metastases of different entities in association with clinical data including overall survival. Additionally, we assessed whole DNA methylome profiles including CD74 promoter methylation and differential methylation in 21 brain metastases. We analyzed the effects of a siRNA mediated CD74 knockdown on HLA-expression and HLA peptidome composition in a brain metastatic melanoma cell line.
We observed that CD74 expression on tumor cells is a strong positive prognostic marker in brain metastasis patients and positively associated with tumor-infiltrating T-lymphocytes (TILs). Whole DNA methylome analysis suggested that CD74 tumor cell expression might be regulated epigenetically via CD74 promoter methylation. CD74high and TILhigh tumors displayed a differential DNA methylation pattern with highest enrichment scores for antigen processing and presentation. Furthermore, CD74 knockdown in vitro lead to a reduction of HLA class II peptidome complexity, while HLA class I peptidome remained unaffected.
In summary, our results demonstrate that a functional HLA class II processing machinery in brain metastatic tumor cells, reflected by a high expression of CD74 and a complex tumor cell HLA peptidome, seems to be crucial for better patient prognosis.
Ecological speciation assumes reproductive isolation to be the product of ecologically based divergent selection. Beside natural selection, sexual selection via phenotype-assortative mating is thought to promote reproductive isolation. Using the neotropical fish Poecilia mexicana from a system that has been described to undergo incipient ecological speciation in adjacent, but ecologically divergent habitats characterized by the presence or absence of toxic H2S and darkness in cave habitats, we demonstrate a gradual change in male body colouration along the gradient of light/darkness, including a reduction of ornaments that are under both inter- and intrasexual selection in surface populations. In dichotomous choice tests using video-animated stimuli, we found surface females to prefer males from their own population over the cave phenotype. However, female cave fish, observed on site via infrared techniques, preferred to associate with surface males rather than size-matched cave males, likely reflecting the female preference for better-nourished (in this case: surface) males. Hence, divergent selection on body colouration indeed translates into phenotype-assortative mating in the surface ecotype, by selecting against potential migrant males. Female cave fish, by contrast, do not have a preference for the resident male phenotype, identifying natural selection against migrants imposed by the cave environment as the major driver of the observed reproductive isolation.
Background: Atypical EGFR mutations occur in 10%-30% of non-small-cell lung cancer (NSCLC) patients with EGFR mutations and their sensitivity to classical epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKI) is highly heterogeneous. Patients harboring one group of uncommon, recurrent EGFR mutations (G719X, S768I, L861Q) respond to EGFR-TKI. Exon 20 insertions are mostly insensitive to EGFR-TKI but display sensitivity to exon 20 inhibitors. Clinical outcome data of patients with very rare point and compound mutations upon systemic treatments are still sparse to date.
Patients and methods: In this retrospective, multicenter study of the national Network Genomic Medicine (nNGM) in Germany, 856 NSCLC cases with atypical EGFR mutations including co-occurring mutations were reported from 12 centers. Clinical follow-up data after treatment with different EGFR-TKIs, chemotherapy and immune checkpoint inhibitors were available from 260 patients. Response to treatment was analyzed in three major groups: (i) uncommon mutations (G719X, S7681, L861Q and combinations), (ii) exon 20 insertions and (iii) very rare EGFR mutations (very rare single point mutations, compound mutations, exon 18 deletions, exon 19 insertions).
Results: Our study comprises the largest thus far reported real-world cohort of very rare EGFR single point and compound mutations treated with different systemic treatments. We validated higher efficacy of EGFR-TKI in comparison to chemotherapy in group 1 (uncommon), while most exon 20 insertions (group 2) were not EGFR-TKI responsive. In addition, we found TKI sensitivity of very rare point mutations (group 3) and of complex EGFR mutations containing exon 19 deletions or L858R mutations independent of the combination partner. Notably, treatment responses in group 3 (very rare) were highly heterogeneous. Co-occurring TP53 mutations exerted a non-significant trend for a detrimental effect on outcome in EGFR-TKI-treated patients in groups 2 and 3 but not in group 1.
Conclusions: Based on our findings, we propose a novel nNGM classification of atypical EGFR mutations.
Background and Aims: Chronic infection with the hepatitis B virus (HBV) is a major health issue worldwide. Recently, single nucleotide polymorphisms (SNPs) within the human leukocyte antigen (HLA)-DP locus were identified to be associated with HBV infection in Asian populations. Most significant associations were observed for the A alleles of HLA-DPA1 rs3077 and HLA-DPB1 rs9277535, which conferred a decreased risk for HBV infection. We assessed the implications of these variants for HBV infection in Caucasians.
Methods: Two HLA-DP gene variants (rs3077 and rs9277535) were analyzed for associations with persistent HBV infection and with different clinical outcomes, i.e., inactive HBsAg carrier status versus progressive chronic HBV (CHB) infection in Caucasian patients (n = 201) and HBsAg negative controls (n = 235).
Results: The HLA-DPA1 rs3077 C allele was significantly associated with HBV infection (odds ratio, OR = 5.1, 95% confidence interval, CI: 1.9–13.7; p = 0.00093). However, no significant association was seen for rs3077 with progressive CHB infection versus inactive HBsAg carrier status (OR = 2.7, 95% CI: 0.6–11.1; p = 0.31). In contrast, HLA-DPB1 rs9277535 was not associated with HBV infection in Caucasians (OR = 0.8, 95% CI: 0.4–1.9; p = 1).
Conclusions: A highly significant association of HLA-DPA1 rs3077 with HBV infection was observed in Caucasians. However, as a differentiation between different clinical courses of HBV infection was not possible, knowledge of the HLA-DPA1 genotype cannot be translated into personalized anti-HBV therapy approaches.