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Based on a data sample of (448.1±2.9)×106 ψ(3686) decays collected with the BESIII experiment, a search for the flavor changing neutral current transition ψ(3686) → Λ+cp¯¯¯e+e−+c.c. is performed for the first time. No signal candidates are observed and the upper limit on the branching fraction of ψ(3686) → Λ+cp¯¯¯e+e− is determined to be 1.7×10−6 at the 90\% confidence level. The result is consistent with expectations from the Standard Model, and no evidence for new physics is found.
Using a data sample of (448.1±2.9)×106 ψ(3686) events collected with the BESIII detector at the BEPCII collider, we present measurements of branching fractions for the decays χcJ→Σ+Σ¯− and Σ0Σ¯0. The decays χc1,2→Σ+Σ¯− and Σ0Σ¯0 are observed for the first time, and the branching fractions for χc0→Σ+Σ¯− and Σ0Σ¯0 decays are measured with improved precision. The branching fraction ratios between the charged and neutral modes are consistent with the prediction of isospin symmetry.
Measurement of e⁺e⁻ → KK̄J/ψ cross sections at center-of-mass energies from 4.189 to 4.600 GeV
(2018)
We investigate the process e+e−→KK¯J/ψ at center-of-mass energies from 4.189 to 4.600 GeV using 4.7 fb−1 of data collected by the BESIII detector at the BEPCII collider. The Born cross sections for the reactions e+e−→K+K−J/ψ and K0SK0SJ/ψ are measured as a function of center-of-mass energy. The energy dependence of the cross section for e+e−→K+K−J/ψ is shown to differ from that for π+π−J/ψ in the region around the Y(4260). In addition, there is evidence for a structure around 4.5 GeV in the e+e−→K+K−J/ψ cross section that is not present in π+π−J/ψ.
We search for rare decays of D mesons to hadrons accompany with an electron-positron pair (h(h')e+e−), using an e+e− collision sample corresponding to an integrated luminosity of 2.93 fb−1 collected with the BESIII detector at s√ = 3.773 GeV. No significant signals are observed, and the corresponding upper limits on the branching fractions at the 90% confidence level are determined. The sensitivities of the results are at the level of 10−5∼10−6, providing a large improvement over previous searches.
In integrative structural biology/hybrid modeling approaches, we integrate structural models of macromolecules and experimental data to obtain faithful representations of the structures underlying the data. For example, in ensemble refinement by reweighting we first generate structural ensembles of flexible and dynamic biological macromolecules in molecular simulations. In a subsequent reweighting step, we refine the statistical weights of the structures to strike a balance between the information provided by simulations and by experimental data. For the "Bayesian inference of ensembles" approach (BioEn), we present two complementary methods to solve the underlying challenging high-dimensional optimization problem. We systematically investigate reliability, accuracy, and efficiency of these methods and integrate molecular dynamics simulations of the disordered peptide Ala-5 and NMR J-couplings. We provide an open-source library free of charge at https://github.com/bio-phys/BioEn.
Tubulogenesis is essential for the formation and function of internal organs. One such organ is the trachea, which allows gas exchange between the external environment and the lungs. However, the cellular and molecular mechanisms underlying tracheal tube development remain poorly understood. Here, we show that the potassium channel KCNJ13 is a critical modulator of tracheal tubulogenesis. We identify Kcnj13 in an ethylnitrosourea forward genetic screen for regulators of mouse respiratory organ development. Kcnj13 mutants exhibit a shorter trachea as well as defective smooth muscle (SM) cell alignment and polarity. KCNJ13 is essential to maintain ion homeostasis in tracheal SM cells, which is required for actin polymerization. This process appears to be mediated, at least in part, through activation of the actin regulator AKT, as pharmacological increase of AKT phosphorylation ameliorates the Kcnj13 mutant trachea phenotypes. These results provide insights into the role of ion homeostasis in cytoskeletal organization during tubulogenesis.
Abstract
Inhibition of midbrain dopamine neurons is thought to underlie the signaling of events that are less rewarding than expected and drive learning based on these negative prediction errors. It has recently been shown that Kv4.3 channels influence the integration of inhibitory inputs in specific subpopulations of dopamine neurons. The functional properties of Kv4.3 channels are themselves strongly determined by the binding of auxiliary β-subunits; among them KChIP4a stands-out for its unique combination of modulatory effects. These include decreasing surface membrane trafficking and slowing inactivation kinetics. Therefore, we hypothesized that KChIP4a expression in dopamine neurons could play a crucial role in behavior, in particular by affecting the computation of negative prediction errors. We developed a mouse line where the alternative exon that codes for the KChIP4a splice variant was selectively deleted in midbrain dopamine neurons. In a reward-based reinforcement learning task, we observed that dopamine neuron-specific KChIP4a deletion selectively accelerated the rate of extinction learning, without impacting the acquisition of conditioned responses. We further found that this effect was due to a faster decrease in the initiation rate of goal-directed behaviors, and not faster increases in action disengagement. Furthermore, computational fitting of the behavioral data with a Rescorla-Wagner model confirmed that the observed phenotype was attributable to a selective increase in the learning rate from negative prediction errors. Finally, KChIP4a deletion did not affect performance in other dopamine-sensitive behavioral tasks that did not involve learning from disappointing events, including an absence of effects on working memory, locomotion and novelty preference. Taken together, our results demonstrate that an exon- and midbrain dopamine neuron-specific deletion of an A-type K+ channel β-subunit leads to a selective gain of function in extinction learning.
One Sentence Summary
Exon- and midbrain dopamine neuron-specific deletion of the Kv4 channel β-subunit KChIP4a selectively accelerates extinction learning
We examine the fine structure of clausal right-node raising constructions in Japanese, and argue that there are sentences in which a tensed verb is right-node-raised out of coordinated tensed clauses as well as sentences in which a verb stem is right-node-raised out of coordinated tenseless phrases. In the latter case, the tense morpheme has to be assumed to take a tenseless complement clause, and we note that the existence of such a structure contradicts the so-called lexicalist hypothesis, according to which a verb stem and the tense morpheme immediately following it always form a morphosyntactic constituent.