Refine
Has Fulltext
- yes (120)
Is part of the Bibliography
- no (120)
Keywords
- e +-e − Experiments (9)
- Particle and Resonance Production (4)
- Spectroscopy (4)
- BESIII (3)
- Charm Physics (3)
- Exotics (3)
- Quarkonium (3)
- Electroweak Interaction (2)
- Born cross section measurement (1)
- Branching fraction (1)
- Branching fractions (1)
- CP violation (1)
- Cancer genomics (1)
- Charmed mesons (1)
- Charmonium (-like) (1)
- Chemorefractory advanced gastric cancer (1)
- Dark photon (1)
- Dark sector (1)
- Electroweak interaction (1)
- FOLFIRI (1)
- FOS: Physical sciences (1)
- Flavor symmetries (1)
- Flavour Physics (1)
- Hadronic decays (1)
- High Energy Physics - Experiment (hep-ex) (1)
- Invisible decays (1)
- Lepton colliders (1)
- Long non-coding RNAs (1)
- Polarization (1)
- Proteomics (1)
- QCD (1)
- Semi-leptonic decays (1)
- Sunitinib (1)
- Transcriptomics (1)
- Tyrosine kinase inhibitor (1)
- VEGF (1)
- Y states (1)
- charmonium-like states (1)
- electron-positron collision (1)
- hadron spectroscopy (1)
- helicity amplitude analysis (1)
- photochemistry (1)
- photoisomerization (1)
- phytochromes (1)
- tetrapyrrole-binding photoreceptors (1)
- tetraquark (1)
- time-resolved spectroscopy (1)
- Λ+c baryon (1)
Institute
- Physik (113)
- Medizin (4)
- Biochemie, Chemie und Pharmazie (1)
- Geschichtswissenschaften (1)
Background: As a multi-targeted anti-angiogenic receptor tyrosine kinase (RTK) inhibitor sunitinib (SUN) has been established for renal cancer and gastrointestinal stromal tumors. In advanced refractory esophagogastric cancer patients, monotherapy with SUN was associated with good tolerability but limited tumor response.
Methods: This double-blind, placebo-controlled, multicenter, phase II clinical trial was conducted to evaluate the efficacy, safety and tolerability of SUN as an adjunct to second and third-line FOLFIRI (NCT01020630). Patients were randomized to receive 6-week cycles including FOLFIRI plus sodium folinate (Na-FOLFIRI) once every two weeks and SUN or placebo (PL) continuously for four weeks followed by a 2-week rest period. The primary study endpoint was progression-free survival (PFS). Preplanned serum analyses of VEGF-A, VEGF-D, VEGFR2 and SDF-1α were performed retrospectively.
Results: Overall, 91 patients were randomized, 45 in each group (one patient withdrew). The main grade ≥3 AEs were neutropenia and leucopenia, observed in 56 %/20 % and 27 %/16 % for FOLFIRI + SUN/FOLFIRI + PL, respectively. Median PFS was similar, 3.5 vs. 3.3 months (hazard ratio (HR) 1.11, 95 % CI 0.70–1.74, P = 0.66) for FOLFIRI + SUN vs. FOLFIRI + PL, respectively. For FOLFIRI + SUN, a trend towards longer median overall survival (OS) compared with placebo was observed (10.4 vs. 8.9 months, HR 0.82, 95 % CI 0.50–1.34, one-sided P = 0.21). In subgroup serum analyses, significant changes in VEGF-A (P = 0.017), VEGFR2 (P = 0.012) and VEGF-D (P < 0.001) serum levels were observed.
Conclusions: Although sunitinib combined with FOLFIRI did not improve PFS and response in chemotherapy-resistant gastric cancer, a trend towards better OS was observed. Further biomarker-driven studies with other anti-angiogenic RTK inhibitors are warranted.
Trial registration: This study was registered prospectively in the NCT Clinical Trials Registry (ClinicalTrials.gov) under NCT01020630 on November 23, 2009 after approval by the leading ethics committee of the Medical Association of Rhineland-Palatinate, Mainz, in coordination with the participating ethics committees (see Additional file 2) on September 16, 2009.
The family of phytochrome photoreceptors contains proteins with different domain architectures and spectral properties. Knotless phytochromes are one of the three main subgroups classified by their distinct lack of the PAS domain in their photosensory core module, which is in contrast to the canonical PAS-GAF-PHY array. Despite intensive research on the ultrafast photodynamics of phytochromes, little is known about the primary kinetics in knotless phytochromes. Here, we present the ultrafast Pr ⇆ Pfr photodynamics of SynCph2, the best-known knotless phytochrome. Our results show that the excited state lifetime of Pr* (~200 ps) is similar to bacteriophytochromes, but much longer than in most canonical phytochromes. We assign the slow Pr* kinetics to relaxation processes of the chromophore-binding pocket that controls the bilin chromophore’s isomerization step. The Pfr photoconversion dynamics starts with a faster excited state relaxation than in canonical phytochromes, but, despite the differences in the respective domain architectures, proceeds via similar ground state intermediate steps up to Meta-F. Based on our observations, we propose that the kinetic features and overall dynamics of the ultrafast photoreaction are determined to a great extent by the geometrical context (i.e., available space and flexibility) within the binding pocket, while the general reaction steps following the photoexcitation are most likely conserved among the red/far-red phytochromes.
Introduction: Evidence from a number of open-label, uncontrolled studies has suggested that rituximab may benefit patients with autoimmune diseases who are refractory to standard-of-care. The objective of this study was to evaluate the safety and clinical outcomes of rituximab in several standard-of-care-refractory autoimmune diseases (within rheumatology, nephrology, dermatology and neurology) other than rheumatoid arthritis or non-Hodgkin's lymphoma in a real-life clinical setting.
Methods: Patients who received rituximab having shown an inadequate response to standard-of-care had their safety and clinical outcomes data retrospectively analysed as part of the German Registry of Autoimmune Diseases. The main outcome measures were safety and clinical response, as judged at the discretion of the investigators.
Results: A total of 370 patients (299 patient-years) with various autoimmune diseases (23.0% with systemic lupus erythematosus, 15.7% antineutrophil cytoplasmic antibody-associated granulomatous vasculitides, 15.1% multiple sclerosis and 10.0% pemphigus) from 42 centres received a mean dose of 2,440 mg of rituximab over a median (range) of 194 (180 to 1,407) days. The overall rate of serious infections was 5.3 per 100 patient-years during rituximab therapy. Opportunistic infections were infrequent across the whole study population, and mostly occurred in patients with systemic lupus erythematosus. There were 11 deaths (3.0% of patients) after rituximab treatment (mean 11.6 months after first infusion, range 0.8 to 31.3 months), with most of the deaths caused by infections. Overall (n = 293), 13.3% of patients showed no response, 45.1% showed a partial response and 41.6% showed a complete response. Responses were also reflected by reduced use of glucocorticoids and various immunosuppressives during rituximab therapy and follow-up compared with before rituximab. Rituximab generally had a positive effect on patient well-being (physician's visual analogue scale; mean improvement from baseline of 12.1 mm).
Conclusions: Data from this registry indicate that rituximab is a commonly employed, well-tolerated therapy with potential beneficial effects in standard of care-refractory autoimmune diseases, and support the results from other open-label, uncontrolled studies.
Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders.
The Born cross sections of the e+e− → D*+D*− and e+e− → D*+D− processes are measured using e+e− collision data collected with the BESIII experiment at center-of-mass energies from 4.085 to 4.600 GeV, corresponding to an integrated luminosity of 15.7 fb−1. The results are consistent with and more precise than the previous measurements by the Belle, Babar and CLEO collaborations. The measurements are essential for understanding the nature of vector charmonium and charmonium-like states.
We report the first measurements of the absolute branching fractions of D0 → K0 Lϕ, D0 → K0Lη, D0 → K0Lω, and D0 → K0Lη0, by analyzing 2.93 fb−1 of eþe− collision data taken at a center-of-mass energy of 3.773 GeV with the BESIII detector. Taking the world averages of the branching fractions of D0 → K0Sϕ, D0 → K0Sη, D0 → K0Sω, and D0 → K0Sη0, the K0S − K0L asymmetries RðD0; XÞ in these decay modes are obtained. The CP asymmetries in these decays are also determined. No significant CP violation is observed
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.
Improved measurement of the branching fractions of the inclusive decays D⁺ → Kₛ⁰X and D⁰ → Kₛ⁰X
(2023)
By analyzing 2.93 fb−1 of 𝑒+𝑒− collision data taken at the center-of-mass energy of 3.773 GeV with the BESIII detector, the branching fractions of the inclusive decays 𝐷+→𝐾0 𝑆𝑋 and 𝐷0→𝐾0 𝑆𝑋 are measured to be (33.11±0.13±0.36)% and (20.75±0.12±0.20)%, respectively, where the first uncertainties are statistical and the second are systematic. These results are consistent with the world averages of previous measurements, but with much improved precision.
Glioblastoma is the most common malignant primary brain tumor. To date, clinically relevant biomarkers are restricted to isocitrate dehydrogenase (IDH) gene 1 or 2 mutations and O6-methylguanine DNA methyltransferase (MGMT) promoter methylation. Long non-coding RNAs (lncRNAs) have been shown to contribute to glioblastoma pathogenesis and could potentially serve as novel biomarkers. The clinical significance of HOXA Transcript Antisense RNA, Myeloid-Specific 1 (HOTAIRM1) was determined by analyzing HOTAIRM1 in multiple glioblastoma gene expression data sets for associations with prognosis, as well as, IDH mutation and MGMT promoter methylation status. Finally, the role of HOTAIRM1 in glioblastoma biology and radiotherapy resistance was characterized in vitro and in vivo. We identified HOTAIRM1 as a candidate lncRNA whose up-regulation is significantly associated with shorter survival of glioblastoma patients, independent from IDH mutation and MGMT promoter methylation. Glioblastoma cell line models uniformly showed reduced cell viability, decreased invasive growth and diminished colony formation capacity upon HOTAIRM1 down-regulation. Integrated proteogenomic analyses revealed impaired mitochondrial function and determination of reactive oxygen species (ROS) levels confirmed increased ROS levels upon HOTAIRM1 knock-down. HOTAIRM1 knock-down decreased expression of transglutaminase 2 (TGM2), a candidate protein implicated in mitochondrial function, and knock-down of TGM2 mimicked the phenotype of HOTAIRM1 down-regulation in glioblastoma cells. Moreover, HOTAIRM1 modulates radiosensitivity of glioblastoma cells both in vitro and in vivo. Our data support a role for HOTAIRM1 as a driver of biological aggressiveness, radioresistance and poor outcome in glioblastoma. Targeting HOTAIRM1 may be a promising new therapeutic approach.
Using 7.33 fb−1 of e+e− collision data collected by the BESIII detector at center-of-mass energies between 4.128 and 4.226~GeV, we observe for the first time the decay D±s→ωπ±η with a statistical significance of 7.6σ. The measured branching fraction of this decay is (0.54±0.12±0.04)%, where the first uncertainty is statistical and the second is systematic.
Observation of resonance structures in e⁺e⁻ → π⁺π⁻ψ₂(3823) and mass measurement of ψ₂(3823)
(2022)
Using a data sample corresponding to an integrated luminosity of 11.3 fb−1 collected at center-of-mass energies from 4.23 to 4.70 GeV with the BESIII detector, we measure the product of the 𝑒+𝑒−→𝜋+𝜋−𝜓2(3823) cross section and the branching fraction ℬ[𝜓2(3823)→𝛾𝜒𝑐1]. For the first time, resonance structure is observed in the cross section line shape of 𝑒+𝑒−→𝜋+𝜋−𝜓2(3823) with significances exceeding 5𝜎. A fit to data with two coherent Breit-Wigner resonances modeling the √𝑠-dependent cross section yields 𝑀(𝑅1)=4406.9±17.2±4.5 MeV/𝑐2, Γ(𝑅1)=128.1±37.2±2.3 MeV, and 𝑀(𝑅2)=4647.9±8.6±0.8 MeV/𝑐2, Γ(𝑅2)=33.1±18.6±4.1 MeV. Though weakly disfavored by the data, a single resonance with 𝑀(𝑅)=4417.5±26.2±3.5 MeV/𝑐2, Γ(𝑅)=245±48±13 MeV is also possible to interpret data. This observation deepens our understanding of the nature of the vector charmoniumlike states. The mass of the 𝜓2(3823) state is measured as (3823.12±0.43±0.13) MeV/𝑐2, which is the most precise measurement to date.
Using data samples collected with the BESIII detector operating at the BEPCII storage ring, the cross section of the inclusive process e+e−→η+X, normalized by the total cross section of e+e−→hadrons, is measured at eight center-of-mass energy points from 2.0000 GeV to 3.6710 GeV. These are the first measurements with momentum dependence in this energy region. Our measurement shows a significant discrepancy from calculations with the existing fragmentation functions. To address this discrepancy, a new QCD analysis is performed at the next-to-next-to-leading order with hadron mass corrections and higher twist effects, which can explain both the established high-energy data and our measurements reasonably well.
Based on electron positron collision data collected with the BESIII detector operating at the BEPCII storage rings, the differential cross sections of inclusive π0 and K0S production as a function of hadron momentum, normalized by the total cross section of the e+e−→ hadrons process, are measured at six center-of-mass energies from 2.2324 to 3.6710 GeV. Our results with a relative hadron energy coverage from 0.1 to 0.9 significantly deviate from several theoretical calculations based on existing fragmentation functions, especially at lower energies.
Based on electron positron collision data collected with the BESIII detector operating at the BEPCII storage rings, the differential cross sections of inclusive π0 and K0S production as a function of hadron momentum, normalized by the total cross section of the e+e−→ hadrons process, are measured at six center-of-mass energies from 2.2324 to 3.6710 GeV. Our results with a relative hadron energy coverage from 0.1 to 0.9 significantly deviate from several theoretical calculations based on existing fragmentation functions, especially at lower energies.
The decay 𝜂𝑐(2𝑆)→𝜋+𝜋−𝜂 is searched for through the radiative transition 𝜓(3686)→𝛾𝜂𝑐(2𝑆) using 448 million 𝜓(3686) events accumulated at the BESIII detector. The first evidence of 𝜂𝑐(2𝑆)→𝜋+𝜋−𝜂 is found with a statistical significance of 3.5𝜎. The product of the branching fractions of 𝜓(3686)→𝛾𝜂𝑐(2𝑆) and 𝜂𝑐(2𝑆)→𝜋+𝜋−𝜂 is measured to be Br(𝜓(3686)→𝛾𝜂𝑐(2𝑆))×Br(𝜂𝑐(2𝑆)→𝜋+𝜋−𝜂)=(2.97±0.81±0.26)×10−6, where the first uncertainty is statistical and the second one is systematic. The branching fraction of the decay 𝜂𝑐(2𝑆)→𝜋+𝜋−𝜂 is determined to be Br(𝜂𝑐(2𝑆)→𝜋+𝜋−𝜂)=(42.4±11.6±3.8±30.3)×10−4, where the third uncertainty is transferred from the uncertainty of the branching fraction of 𝜓(3686)→𝛾𝜂𝑐(2𝑆).
The decay $\eta_c(2S)\to\pipieta$ is searched for through the radiative transition ψ(3686)→γηc(2S) using 448 million ψ(3686) events accumulated at the BESIII detector. The first evidence of ηc(2S)→π+π−η is found with a statistical significance of 3.5σ. The product of the branching fractions of ψ(3686)→γηc(2S) and $\eta_c(2S)\to\pipieta$ is measured to be $Br(\psi(3686)\to\gamma\eta_c(2S))\times Br(\eta_c(2S)\to\pipieta)=(2.97\pm0.81\pm0.26)\times10^{-6}$, where the first uncertainty is statistical and the second one is systematic. The branching fraction of the decay $\eta_c(2S)\to\pipieta$ is determined to be $Br(\eta_c(2S)\to\pipieta)=(42.4\pm11.6\pm3.8\pm30.3)\times10^{-4}$, where the third uncertainty is transferred from the uncertainty of the branching fraction of ψ(3686)→γηc(2S).
The decay $\eta_c(2S)\to\pipieta$ is searched for through the radiative transition ψ(3686)→γηc(2S) using 448 million ψ(3686) events accumulated at the BESIII detector. The first evidence of ηc(2S)→π+π−η is found with a statistical significance of 3.5σ. The product of the branching fractions of ψ(3686)→γηc(2S) and $\eta_c(2S)\to\pipieta$ is measured to be $Br(\psi(3686)\to\gamma\eta_c(2S))\times Br(\eta_c(2S)\to\pipieta)=(2.97\pm0.81\pm0.26)\times10^{-6}$, where the first uncertainty is statistical and the second one is systematic. The branching fraction of the decay $\eta_c(2S)\to\pipieta$ is determined to be $Br(\eta_c(2S)\to\pipieta)=(42.4\pm11.6\pm3.8\pm30.3)\times10^{-4}$, where the third uncertainty is transferred from the uncertainty of the branching fraction of ψ(3686)→γηc(2S).
We report a search for a heavier partner of the recently observed Zcs(3985)− state, denoted as Z′−cs, in the process e+e−→K+D∗−sD∗0+c.c., based on e+e− collision data collected at the center-of-mass energies of s√=4.661, 4.682 and 4.699 GeV with the BESIII detector. The Z′−cs is of interest as it is expected to be a candidate for a hidden-charm and open-strange tetraquark. A partial-reconstruction technique is used to isolate K+ recoil-mass spectra, which are probed for a potential contribution from Z′−cs→D∗−sD∗0 (c.c.). We find an excess of Z′−cs→D∗−sD∗0 (c.c.) candidates with a significance of 2.9σ, after considering systematic uncertainties, at a mass of (4123.5±0.7stat.±1.1syst.)MeV/c2. As the data set is limited in size, the upper limits are evaluated at the 90% confidence level on the product of the Born cross section and the branching fraction of Z′−cs→D∗−sD∗0, σBorn⋅B at the three energy points, under different assumptions of the Z′−cs mass from 4.120 to 4.140 MeV and of the width from 10 to 50 MeV. Under various mass and width assumptions, the upper limits of σBorn⋅B are found to lie in the range of 2∼6, 3∼7 and 3∼6 pb at s√=4.661, 4.682 and 4.699 GeV, respectively. The larger data samples that will be collected in the coming years will allow a clearer picture to emerge concerning the existence and nature of the Z′−cs state.
The Ξ0 asymmetry parameters are measured using entangled quantum Ξ0 − Ξ¯ 0 pairs from a sample of ð448.1 2.9Þ × 106 ψð3686Þ events collected with the BESIII detector at BEPCII. The relative phase between the transition amplitudes of the Ξ0Ξ¯ 0 helicity states is measured to be ΔΦ ¼ −0.050 0.150 0.020 rad, which implies that there is no obvious polarization at the current level of statistics. The decay parameters of the Ξ0 hyperon ðαΞ0 ; αΞ¯ 0 ; ϕΞ0 ; ϕΞ¯ 0 Þ and the angular distribution parameter ½αψð3686Þ and ΔΦ are measured simultaneously for the first time. In addition, the CP asymmetry observables are determined to be AΞ0 CP ¼ ðαΞ0 þ αΞ¯ 0 Þ=ðαΞ0 − αΞ¯ 0 Þ ¼ −0.007 0.082 0.025 and ΔϕΞ0 CP ¼ ðϕΞ0 þ ϕΞ¯ 0 Þ=2 ¼ −0.079 0.082 0.010 rad, which are consistent with CP conservation.