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The processes hc→γP(P=η′, η, π0)) are studied with a sample of (27.12±0.14)×108 ψ(3686) events collected by the BESIII detector at the BEPCII collider. The branching fractions of hc→γη′ and hc→γη are measured to be (1.40±0.11±0.04±0.10)×10−3 and (3.77±0.55±0.13±0.26)×10−4, respectively, where the first uncertainties are statistical, the second systematic, and the third from the branching fraction of ψ(3686)→π0hc. The ratio Rhc=B(hc→γη)B(hc→γη′) is calculated to be (27.0±4.4±1.0)%. The measurements are consistent with the previous results with improved precision by a factor of 2. The results are valuable for gaining a deeper understanding of η−η′ mixing, and its manifestation within quantum chromodynamics. No significant signal is found for the decay hc→γπ0, and an upper limit is placed on its branching fraction of B(hc→γπ0)<5.0×10−5, at the 90\% confidence level.
Based on (2.712±0.014)×109 ψ(3686) events collected by the BESIII collaboration, evidence of the hadronic decay hc→K0SK+π−+c.c. is found with a significance of 4.3σ in the ψ(3686)→π0hc process. The branching fraction of hc→K0SK+π−+c.c. is measured to be (7.3±0.8±1.8)×10−4, where the first and second uncertainties are statistical and systematic, respectively. Combining with the exclusive decay width of ηc→KK¯π, our result indicates inconsistencies with both pQCD and NRQCD predictions.
Using 2.93 fb−1 of e+e− collision data collected with the BESIII detector at the center-of-mass energy of 3.773 GeV, we investigate the semileptonic decays D+→π+π−ℓ+νℓ (ℓ=e and μ). The D+→f0(500)μ+νμ decay is observed for the first time. By analyzing simultaneously the differential decay rates of D+→f0(500)μ+νμ and D+→f0(500)e+νe in different ℓ+νℓ four-momentum transfer intervals, the product of the relevant hadronic form factor ff0+(0) and the magnitude of the c→d Cabibbo-Kobayashi-Maskawa matrix element |Vcd| is determined to be ff0+(0)|Vcd|=0.0787±0.0060stat±0.0033syst for the first time. With the input of |Vcd| from the global fit in the standard model, we determine ff0+(0)=0.350±0.027stat±0.015syst. The absolute branching fractions of D+→f0(500)(π+π−)μ+νμ and D+→ρ0(π+π−)μ+νμ are determined as (0.72±0.13stat±0.10syst)×10−3 and (1.64±0.13stat±0.11syst)×10−3. Combining these results with those of previous BESIII measurements on their semielectronic counterparts from the same data sample, we test lepton flavor universality by measuring the branching fraction ratios BD+→ρ0μ+νμ/BD+→ρ0e+νe=0.88±0.10 and BD+→f0(500)μ+νμ/BD+→f0(500)e+νe = 1.14±0.28, which are compatible with the standard model expectation.
Using 2.93 fb−1 of e+e− collision data collected with the BESIII detector at the center-of-mass energy of 3.773 GeV, we investigate the semileptonic decays D+→π+π−ℓ+νℓ (ℓ=e and μ). The D+→f0(500)μ+νμ decay is observed for the first time. By analyzing simultaneously the differential decay rates of D+→f0(500)μ+νμ and D+→f0(500)e+νe in different ℓ+νℓ four-momentum transfer intervals, the product of the relevant hadronic form factor ff0+(0) and the magnitude of the c→d Cabibbo-Kobayashi-Maskawa matrix element |Vcd| is determined to be ff0+(0)|Vcd|=0.0787±0.0060stat±0.0033syst for the first time. With the input of |Vcd| from the global fit in the standard model, we determine ff0+(0)=0.350±0.027stat±0.015syst. The absolute branching fractions of D+→f0(500)(π+π−)μ+νμ and D+→ρ0(π+π−)μ+νμ are determined as (0.72±0.13stat±0.10syst)×10−3 and (1.64±0.13stat±0.11syst)×10−3. Combining these results with those of previous BESIII measurements on their semielectronic counterparts from the same data sample, we test lepton flavor universality by measuring the branching fraction ratios BD+→ρ0μ+νμ/BD+→ρ0e+νe = 0.88±0.10 and BD+→f0(500)μ+νμ/BD+→f0(500)e+νe = 1.14±0.28, which are compatible with the standard model expectation.
We present cross sections for the reaction e+e−→K0SK0L at center-of-mass energies ranging from 3.51 GeV to 4.95 GeV using data samples collected in the BESIII experiment, corresponding to a total integrated luminosity of 26.5 fb−1. The ratio of neutral-to-charged kaon form factors at large momentum transfers (12 GeV2<Q2<25 GeV2) is determined to be 0.21±0.01, which indicates a small but significant effect of flavor-SU(3) breaking in the kaon wave function, and consequently excludes the possibility that flavor-SU(3) breaking is the primary reason for the strong experimental violation of the pQCD prediction |F(π±)|/|F(K±)|=f2π/f2K, where F(π±) and F(K±) are the form factors, and fπ and fK are the decay constants of charged pions and kaons, respectively. We also observe a significant signal for the charmless decay ψ(3770)→K0SK0L for the first time. Within a 1σ contour of the likelihood value, the the branching fraction for ψ(3770)→K0SK0L is determined to be B=(2.63+1.40−1.59)×10−5, and the relative phase between the continuum and ψ(3770) amplitudes is ϕ=(−0.39+0.05−0.10)π. The branching fraction is in good agreement with the S- and D-wave charmonia mixing scheme proposed in the interpretation of the "ρπ puzzle" between J/ψ and ψ(3686) decays.
A search has been performed for the semileptonic decays D0→K0SK−e+νe, D+→K0SK0Se+νe and D+→K+K−e+νe, using 7.9 fb−1 of e+e− annihilation data collected at the center-of-mass energy s√=3.773 GeV by the BESIII detector operating at the BEPCII collider. No significant signals are observed, and upper limits are set at the 90\% confidence level of 2.13×10−5, 1.54×10−5 and 2.10×10−5 for the branching fractions of D0→K0SK−e+νe, D+→K0SK0Se+νe and D+→K+K−e+νe, respectively.
Dynamic imaging of landmark organelles, such as nuclei, cell membrane, nuclear envelope, and lipid droplets enables image-based phenotyping of functional states of cells. Multispectral fluorescent imaging of landmark organelles requires labor-intensive labeling, limits throughput, and compromises cell health. Virtual staining of label-free images with deep neural networks is an emerging solution for this problem. Multiplexed imaging of cellular landmarks from scattered light and subsequent demultiplexing with virtual staining saves the light spectrum for imaging additional molecular reporters, photomanipulation, or other tasks. Published approaches for virtual staining of landmark organelles are fragile in the presence of nuisance variations in imaging, culture conditions, and cell types. This paper reports model training protocols for virtual staining of nuclei and membranes robust to cell types, cell states, and imaging parameters. We developed a flexible and scalable convolutional architecture, named UNeXt2, for supervised training and self-supervised pre-training. The strategies we report here enable robust virtual staining of nuclei and cell membranes in multiple cell types, including neuromasts of zebrafish, across a range of imaging conditions. We assess the models by comparing the intensity, segmentations, and application-specific measurements obtained from virtually stained and experimentally stained nuclei and membranes. The models rescue the missing label, non-uniform expression of labels, and photobleaching. We share three pre-trained models, named VSCyto3D, VSCyto2D, and VSNeuromast, as well as VisCy, a PyTorch-based pipeline for training, inference, and deployment that leverages the modern OME-Zarr format.
The free energy of TAP-solutions for the SK-model of mean field spin glasses can be expressed as a nonlinear functional of local terms: we exploit this feature in order to contrive abstract REM-like models which we then solve by a classical large deviations treatment. This allows to identify the origin of the physically unsettling quadratic (in the inverse of temperature) correction to the Parisi free energy for the SK-model, and formalizes the true cavity dynamics which acts on TAP-space, i.e. on the space of TAP-solutions. From a non-spin glass point of view, this work is the first in a series of refinements which addresses the stability of hierarchical structures in models of evolving populations.
Oncogenic transformation of lung epithelial cells is a multi-step process, frequently starting with the inactivation of tumor suppressors and subsequent activating mutations in proto-oncogenes, such as members of the PI3K or MAPK family. Cells undergoing transformation have to adjust to changes, such as metabolic requirements. This is achieved, in part, by modulating the protein abundance of transcription factors, which manifest these adjustments. Here, we report that the deubiquitylase USP28 enables oncogenic reprogramming by regulating the protein abundance of proto-oncogenes, such as c-JUN, c-MYC, NOTCH and ΔNP63, at early stages of malignant transformation. USP28 is increased in cancer compared to normal cells due to a feed-forward loop, driven by increased amounts of oncogenic transcription factors, such as c-MYC and c-JUN. Irrespective of oncogenic driver, interference with USP28 abundance or activity suppresses growth and survival of transformed lung cells. Furthermore, inhibition of USP28 via a small molecule inhibitor reset the proteome of transformed cells towards a ‘pre-malignant’ state, and its inhibition cooperated with clinically established compounds used to target EGFRL858R, BRAFV600E or PI3KH1047R driven tumor cells. Targeting USP28 protein abundance already at an early stage via inhibition of its activity therefore is a feasible strategy for the treatment of early stage lung tumours and the observed synergism with current standard of care inhibitors holds the potential for improved targeting of established tumors.