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We report on the charged particle identification (PID) systems for the upcoming Belle II experiment. The time of propagation counter in the central region and the proximity focusing ring imaging Cherenkov counters with aerogel radiator in the forward region will be used as the PID devices. They are expected to provide a kaon identification efficiency of more than 94% at a low pion misidentification probability of 4%. The motivation for the upgrade, method and status of both systems are discussed.

The Time-Of-Propagation (TOP) counter is a novel ring-imaging Cherenkov detector that primarily consists of a quartz bar radiator, micro-channel plate photomultipliers and front-end readout electronics. These TOP counters are installed in the central region of the Belle II detector to provide the crucial information on the charged particle identification (PID). Here, we present an overview of PID studies in Belle II, with a focus on the performance of the TOP detector. The results presented are from the recently recorded data which show reasonable agreement with the expectations from the simulation studies.

We report on new flavor tagging algorithms developed to determine the quark-flavor content of bottom ( ) mesons at Belle II. The algorithms provide essential inputs for measurements of quark-flavor mixing and charge-parity violation. We validate and evaluate the performance of the algorithms using hadronic decays with flavor-specific final states reconstructed in a data set corresponding to an integrated luminosity of 62.8 fb-1, collected at the resonance with the Belle II detector at the SuperKEKB collider. We measure the total effective tagging efficiency to be εeff=(30.0±1.2(stat)±0.4(syst))%for a category-based algorithm and εeff=(28.8±1.2(stat)±0.4(syst))%for a deep-learning-based algorithm.

A bstract We report a search for the lepton-flavor-violating decays τ ± → ℓ ± α ( ℓ = e , μ ), where α is an undetected spin-0 particle, such as an axion-like particle using 736 × 10 6 tau lepton pairs collected by the Belle detector at the KEKB asymmetric-energy e + e − collider. We find no evidence of signal and obtain the most stringent upper limits on the branching fractions at 95% confidence level: ( τ ± → e ± α ) < (0.4–6.4) × 10 − 4 and ( τ ± → μ ± α ) < (0.2–3.5) × 10 − 4 at 95% confidence level for an α mass in the range 0.0 ≤ m α ≤ 1.6 GeV/ c 2 .

A bstract We present measurements of the branching fractions for the decays B → Kμ + μ − and B → Ke + e − , and their ratio ( R K ), using a data sample of 711 fb − 1 that contains 772 × 10 6 B B ¯ events. The data were collected at the ϒ(4 S ) resonance with the Belle detector at the KEKB asymmetric-energy e + e − collider. The ratio R K is measured in five bins of dilepton invariant-mass-squared ( q 2 ): q 2 ∈ (0 . 1 , 4 . 0) , (4 . 00 , 8 . 12) , (1 . 0 , 6 . 0), (10 . 2 , 12 . 8) and ( > 14 . 18) GeV 2 /c 4 , along with the whole q 2 region. The R K value for q 2 ∈ (1 . 0 , 6 . 0) GeV 2 /c 4 is 1.03 − 0.24 + 0.28 ± 0 . 01. The first and second uncertainties listed are statistical and systematic, respectively. All results for R K are consistent with Standard Model predictions. We also measure CP -averaged isospin asymmetries in the same q 2 bins. The results are consistent with a null asymmetry, with the largest difference of 2.6 standard deviations occurring for the q 2 ∈ (1 . 0 , 6 . 0) GeV 2 /c 4 bin in the mode with muon final states. The measured differential branching fractions, d ℬ /dq 2 , are consistent with theoretical predictions for charged B decays, while the corresponding values are below the expectations for neutral B decays. We have also searched for lepton-flavor-violating B → Kμ ± e ∓ decays and set 90% confidence-level upper limits on the branching fraction in the range of 10 − 8 for B + → K + μ ± e ∓ , and B 0 → K 0 μ ± e ∓ modes.

A bstract Charged lepton flavor violation is forbidden in the Standard Model but possible in several new physics scenarios. In many of these models, the radiative decays τ ± → ℓ ± γ ( ℓ = e, μ ) are predicted to have a sizeable probability, making them particularly interesting channels to search at various experiments. An updated search via τ ± → ℓ ± γ using full data of the Belle experiment, corresponding to an integrated luminosity of 988 fb − 1 , is reported for charged lepton flavor violation. No significant excess over background predictions from the Standard Model is observed, and the upper limits on the branching fractions, B ( τ ± → μ ± γ ) ≤ 4 . 2 × 10 − 8 and B ( τ ± → e ± γ ) ≤ 5 . 6 × 10 − 8 , are set at 90% confidence level.

A bstract We report a new measurement of the e + e − → ϒ( nS ) π + π − ( n = 1 , 2 , 3) cross sections at energies from 10 . 52 to 11 . 02 GeV using data collected with the Belle detector at the KEKB asymmetric-energy e + e − collider. We observe a new structure in the energy dependence of the cross sections; if described by a Breit-Wigner function its mass and width are found to be M = 10752.7 ± 5.9 − 1.1 + 0.7 MeV / c 2 and Γ = 35.5 − 11.3 − 3.3 + 17.6 + 3.9 MeV, where the first error is statistical and the second is systematic. The global significance of the new structure including systematic uncertainty is 5.2 standard deviations. We also find evidence for the e + e − → ϒ (1 S ) π + π − process at the energy 10 . 52 GeV, which is below the B B ¯ threshold.

A bstract We report a measurement of the electric dipole moment of the τ lepton ( dτ ) using an 833 fb − 1 data sample collected near the Υ(4 S ) resonance, with the Belle detector at the KEKB asymmetric-energy e + e − collider. Using an optimal observable method, we obtain the real and imaginary parts of d τ as Re( d τ ) = ( − 0 . 62 ± 0 . 63) × 10 − 17 e cm and Im( d τ ) = ( − 0 . 40 ± 0 . 32) × 10 − 17 e cm, respectively. These results are consistent with null electric dipole moment at the present level of experimental sensitivity and improve the sensitivity by about a factor of three.

Abstract Background An in vitro damage model has been established in our lab using human colonoids grown as 2D monolayers. Upon being subjected to repeated rounds of air-liquid interface (ALI) growth and injury by submergence, these colonoid monolayers lost their barrier integrity and regrowth potential. Changes in mRNA expression and DNA methylation in genes from this human model of injury were similar to those that occur in Inflammatory Bowel Disease (IBD) and colon cancer. Significant morphological changes were observed in these monolayers after they were subjected to subsequent rounds of submergence injury, compared to when they were differentiated in ALI. Purpose Submergence injury is predicted to be involved in unfolded protein response (UPR) activation which can specifically alter translation. Hence proteomics studies will help undertand these changes. Method To determine if these changes are mirrored in the proteomes of damaged colonoids, we employed a Single-Plot, Solid-Phase-enhanced Sample Preparation (SP3) technology for Mass Spectrometry (MS) based proteomics analysis to characterize these monolayers at baseline, once they were differentiated in ALI, after one and five rounds of injury after differentiation in ALI, and after stimulation with the Toll-like receptor 5 (TLR5) agonist FliC. Hierarchical clustering, enrichment analysis, volcano plot analysis after pre-processing and normalization of the proteomics data set revealed differentially expressed proteins across various groups of monolayers. Result(s) Preliminary proteomic data analysis revealed changes in the profile of proteins involved in cellular differentiation, mitochondrial proteins, hypoxia upregulated proteins, those responsible for the maintenance and reorganization of the cytoskeletal structure and Golgi structure. These changes in protein profile may account for the significant morphological changes observed in these monolayers when subjected to submergence injury. Some outliers in monolayers subjected to microbial stimulation included proteins involved in regulation of extracellular matrix dependent motility and components of Adaptor Protein Complexes. Further studies are needed to ascertain if these account for the protective effect of FliC on these monolayers. Conclusion(s) This study suggests that the submergence injury to these healthy human derived colonoid monolayers leads to changes in their protein profile which mirror those seen in case of acute and chronic inflammation like IBD and colon cancer. It corroborates with the findings of gene expression and epigenetic analyses using the in vitro model established in our lab. Please acknowledge all funding agencies by checking the applicable boxes below CCC Disclosure of Interest None Declared