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Institute
Using 𝑒+𝑒−→Λ+𝑐¯Λ−𝑐 production from a 567 pb−1 data sample collected by BESIII at 4.6 GeV, a full angular analysis is carried out simultaneously on the four decay modes of Λ+𝑐→𝑝𝐾0𝑆, Λ𝜋+, Σ+𝜋0, and Σ0𝜋+. For the first time, the Λ+𝑐 transverse polarization is studied in unpolarized 𝑒+𝑒− collisions, where a nonzero effect is observed with a statistical significance of 2.1𝜎. The decay asymmetry parameters of the Λ+𝑐 weak hadronic decays into 𝑝𝐾0𝑆, Λ𝜋+, Σ+𝜋0 and Σ0𝜋+ are measured to be 0.18±0.43(stat)±0.14(syst), −0.80±0.11(stat)±0.02(syst), −0.57±0.10(stat)±0.07(syst), and −0.73±0.17(stat)±0.07(syst), respectively. In comparison with previous results, the measurements for the Λ𝜋+ and Σ+𝜋0 modes are consistent but with improved precision, while the parameters for the 𝑝𝐾0𝑆 and Σ0𝜋+ modes are measured for the first time.
Utilizing the data set corresponding to an integrated luminosity of 3.19 fb−1 collected by the BESIII detector at a center-of-mass energy of 4.178 GeV, we perform an amplitude analysis of the D+s→π+π−π+ decay. The sample contains 13,797 candidates with a signal purity of ∼80%. The amplitude and phase of the contributing ππ S wave are measured based on a quasi-model-independent approach, along with the amplitudes and phases of the P and D waves parametrized by Breit-Wigner models. The fit fractions of different intermediate decay channels are also reported.
Using a data sample of (1.0087±0.0044)×1010 J/ψ decay events collected with the BESIII detector at the center-of-mass energy of s√=3.097 GeV, we present a search for the hyperon semileptonic decay Ξ0→Σ−e+νe which violates the ΔS=ΔQ rule. No significant signal is observed, and the upper limit on the branching fraction B(Ξ0→Σ−e+νe) is determined to be 1.6×10−4 at the 90% confidence level. This result improves the previous upper limit result by about one order of magnitude.
Using a data sample of (1.0087±0.0044)×1010 J/ψ decay events collected with the BESIII detector at the center-of-mass energy of s√=3.097 GeV, we present a search for the hyperon semileptonic decay Ξ0→Σ−e+νe which violates the ΔS=ΔQ rule. No significant signal is observed, and the upper limit on the branching fraction B(Ξ0→Σ−e+νe) is determined to be 1.6×10−4 at the 90% confidence level. This result improves the previous upper limit result by about one order of magnitude.
Using 2.93 fb−1 of 𝑒+𝑒− annihilation data collected at a center-of-mass energy √𝑠=3.773 GeV with the BESIII detector operating at the BEPCII collider, we search for the semileptonic 𝐷0(+) decays into a 𝑏1(1235)−(0) axial-vector meson for the first time. No significant signal is observed for either charge combination. The upper limits on the product branching fractions are ℬ𝐷0→𝑏1(1235)−𝑒+𝜈𝑒·ℬ𝑏1(1235) −→ 𝜔𝜋−<1.12×10−4 and ℬ𝐷+→𝑏1(1235)0𝑒+𝜈𝑒·ℬ𝑏1(1235)0→𝜔𝜋0<1.75×10−4 at the 90% confidence level.
Relative fractions and phases of the intermediate decays are determined. With the detection efficiency estimated by the results of the amplitude analysis, the branching fraction of Dþ s → K−Kþπþπ0 decay is measured to be ð5.42 0.10stat 0.17systÞ%.
Major mood disorders, which primarily include bipolar disorder and major depressive disorder, are the leading cause of disability worldwide and pose a major challenge in identifying robust risk genes. Here, we present data from independent large-scale clinical data sets (including 29 557 cases and 32 056 controls) revealing brain expressed protocadherin 17 (PCDH17) as a susceptibility gene for major mood disorders. Single-nucleotide polymorphisms (SNPs) spanning the PCDH17 region are significantly associated with major mood disorders; subjects carrying the risk allele showed impaired cognitive abilities, increased vulnerable personality features, decreased amygdala volume and altered amygdala function as compared with non-carriers. The risk allele predicted higher transcriptional levels of PCDH17 mRNA in postmortem brain samples, which is consistent with increased gene expression in patients with bipolar disorder compared with healthy subjects. Further, overexpression of PCDH17 in primary cortical neurons revealed significantly decreased spine density and abnormal dendritic morphology compared with control groups, which again is consistent with the clinical observations of reduced numbers of dendritic spines in the brains of patients with major mood disorders. Given that synaptic spines are dynamic structures which regulate neuronal plasticity and have crucial roles in myriad brain functions, this study reveals a potential underlying biological mechanism of a novel risk gene for major mood disorders involved in synaptic function and related intermediate phenotypes.
Insurance guarantee schemes aim to protect policyholders from the costs of insurer insolvencies. However, guarantee schemes can also reduce insurers’ incentives to conduct appropriate risk management. We investigate stock insurers’ risk-shifting behavior for insurance guarantee schemes under the two different financing alternatives: a flat-rate premium assessment versus a risk-based premium assessment. We identify which guarantee scheme maximizes policyholders’ welfare, measured by their expected utility. We find that the risk-based insurance guarantee scheme can only mitigate the insurer’s risk-shifting behavior if a substantial premium loading is present. Furthermore, the risk-based guarantee scheme is superior for improving policyholders’ welfare compared to the flat-rate scheme when the mitigating effect occurs.
This article explores life insurance consumption in 31 European countries from 2003 to 2012 and aims to investigate the extent to which market transparency can affect life insurance demand. The cross-country evidence for the entire sample period shows that greater market transparency, which resolves asymmetric information, can generate a higher demand for life insurance. However, when considering the financial crisis period (2008-2012) separately, the results suggest a negative impact of enhanced market transparency on life insurance consumption. The mixed findings imply a trade-off between the reduction in adverse selection under greater market transparency and the possible negative effects on life insurance consumption during the crisis period due to more effective market discipline. Furthermore, this article studies the extent to which transparency can influence the reaction of life insurance demand to bad market outcomes: i.e., low solvency ratios or low profitability. The results indicate that the markets with bad outcomes generate higher life insurance demand under greater transparency compared to the markets that also experience bad outcomes but are less transparent.
A greater firm-level transparency through enhanced disclosure provides more information regarding the risk situation of an insurer to its outside stakeholders such as stock investors and policyholders. The disclosure of the insurer's risktaking can result in negative influences on, for example, its stock performance and insurance demand when stock investors and policyholders are risk-averse. Insurers, which are concerned about the potential ex post adverse effects of risk-taking under greater transparency, are thus inclined to limit their risks ex ante. In other words, improved firm-level transparency can induce less risktaking incentive of insurers. This article investigates empirically the relationship between firm-level transparency and insurers' strategies on capitalization and risky investments. By exploring the disclosure levels and the risk behavior of 52 European stock insurance companies from 2005 to 2012, the results show that insurers tend to hold more equity capital under the anticipation of greater transparency, and this strategy on capital-holding is consistent for different types of insurance businesses. When considering the influence of improved transparency on the investment policy of insurers, the results are mixed for different types of insurers.