Test of shell-model interactions for nuclear structure calculations

The binding energy and excitation spectra of 6Li are calculated in a no-core shell-model space giving encouraging results. The results of this calculation are then treated as a theoretical experiment, against which different effective-interaction approximations are compared. In this way insight into the perturbation expansion for the effective interaction is obtained

How to regulate bank dividends? Is capital regulation an answer?

This paper is a contribution to the debate on “how to regulate banks' dividend payout behaviour”, a question that has attracted special attention of academicians as well as policy makers since the onset of 2007–08 financial crisis. In this paper, we examine whether common equity based capital regulation and more stringent risk based capital requirements force banks to restrict dividend payments. Common equity based capital regulation is likely to restrict bank dividends by limiting the sources of new capital for banks. Similarly more stringent risk based capital requirements are likely to force banks to retain profits to meet regulatory capital requirements. We use an international sample of 8689 banks from 58 countries over the pre-crisis period 1998–2007 for empirical analysis. Results show that banks paid lower dividends, were less likely to pay dividends and were less likely to pay excessive dividends in countries where regulators imposed common equity based capital regulation and more stringent risk based capital requirements for the banking industry during the pre-crisis period. We also extend our sample period from 1998 to 2012 and observe that regulatory capital requirements are less effective in restricting bank dividend payments during crisis period. From a policy perspective, we suggest that regulators can limit banks' options to raise new capital from non-common equity based sources and can impose more stringent risk based capital requirements to restrict banks from dividend over-payments in good times. While regulators can use blanket restrictions on sector wise dividend payments in bad times

Thermodynamic evidence for pressure-induced bulk superconductivity in the Fe-As pnictide superconductor CaFe2As2

We report specific-heat and resistivity experiments performed in parallel in a Bridgman-type of pressure cell in order to investigate the nature of pressure-induced superconductivity in the iron pnictide compound CaFe2As2. The presence of a pronounced specific-heat anomaly at Tc reveals a bulk nature of the superconducting state. The thermodynamic transition temperature differs dramatically from the onset of the resistive transition. Our data indicates that superconductivity occurs in the vicinity of a crystallographic phase transition. We discuss the discrepancy between the two methods as caused by strain-induced superconducting precursors formed above the bulk thermodynamic transition due to the vicinity of the structural instability

Effects of national culture on bank risk-taking behavior

Theory suggests that national culture influences bank risk-taking behavior directly by conditioning the decision-making of human participants. This study uses an international sample of banks from 75 countries and examines the direct effects of national culture on bank risk-taking behavior. We measure national culture with four dimensions – uncertainty avoidance, individualism vs. collectivism, masculinity vs. femininity and power distance – from Hofstede's framework of national culture. We find strong evidence that bank risk-taking is significantly higher in countries which have high individualism, low uncertainty avoidance, and low power distance cultural values. We confirm main results using alternate cultural dimensions from House et al. (2004. Culture, Leadership, and Organizations. Sage)’s framework of national culture, using alternative bank risk-taking proxies, and using instrumental variables analysis for endogeneity issues. This paper adds to our understanding by finding that cultural values lead to bank risk-taking decisions that may deviate in systematic and geographically predictable ways

Bank Size, Risk-taking and Capital Regulation in Bangladesh

This study examines the impact of bank size on bank regulatory capital ratios and risk-taking behavior using a panel dataset of 30 Bangladeshi commercial banks over the period 2008-2012. The relationship between bank regulatory capital ratios and bank risk-taking is also examined. For empirical analysis, generalized methods of moments (GMM) panel method are used to explore the relationships among bank size, regulatory capital ratios and risk-taking behavior. Empirical results show that large banks hold lower amount of capital and take higher level of risk. Findings also show a reverse relationship between bank capital levels and bank risk-taking; that is, banks holding higher levels of regulatory capital are significantly less risky. Findings of this study has important implications for the Bangladeshi government, policy makers, banking regulators and bank stakeholders regarding bank size, regulatory capital requirements and overall banking sector risk-taking behavior

A switch element in the autophagy E2 Atg3 mediates allosteric regulation across the lipidation cascade

Autophagy depends on the E2 enzyme, Atg3, functioning in a conserved E1-E2-E3 trienzyme cascade that catalyzes lipidation of Atg8-family ubiquitin-like proteins (UBLs). Molecular mechanisms underlying Atg8 lipidation remain poorly understood despite association of Atg3, the E1 Atg7, and the composite E3 Atg12-Atg5-Atg16 with pathologies including cancers, infections and neurodegeneration. Here, studying yeast enzymes, we report that an Atg3 element we term E123IR (E1, E2, and E3-interacting region) is an allosteric switch. NMR, biochemical, crystallographic and genetic data collectively indicate that in the absence of the enzymatic cascade, the Atg3(E123IR) makes intramolecular interactions restraining Atg3's catalytic loop, while E1 and E3 enzymes directly remove this brace to conformationally activate Atg3 and elicit Atg8 lipidation in vitro and in vivo. We propose that Atg3's E123IR protects the E2 similar to UBL thioester bond from wayward reactivity toward errant nucleophiles, while Atg8 lipidation cascade enzymes induce E2 active site remodeling through an unprecedented mechanism to drive autophagy

SUMO Modification Stabilizes Enterovirus 71 Polymerase 3D To Facilitate Viral Replication.

Accumulating evidence suggests that viruses hijack cellular proteins to circumvent the host immune system. Ubiquitination and SUMOylation are extensively studied posttranslational modifications (PTMs) that play critical roles in diverse biological processes. Cross talk between ubiquitination and SUMOylation of both host and viral proteins has been reported to result in distinct functional consequences. Enterovirus 71 (EV71), an RNA virus belonging to the family Picornaviridae, is a common cause of hand, foot, and mouth disease. Little is known concerning how host PTM systems interact with enteroviruses. Here, we demonstrate that the 3D protein, an RNA-dependent RNA polymerase (RdRp) of EV71, is modified by small ubiquitin-like modifier 1 (SUMO-1) both during infection and in vitro Residues K159 and L150/D151/L152 were responsible for 3D SUMOylation as determined by bioinformatics prediction combined with site-directed mutagenesis. Also, primer-dependent polymerase assays indicated that mutation of SUMOylation sites impaired 3D polymerase activity and virus replication. Moreover, 3D is ubiquitinated in a SUMO-dependent manner, and SUMOylation is crucial for 3D stability, which may be due to the interplay between the two PTMs. Importantly, increasing the level of SUMO-1 in EV71-infected cells augmented the SUMOylation and ubiquitination levels of 3D, leading to enhanced replication of EV71. These results together suggested that SUMO and ubiquitin cooperatively regulated EV71 infection, either by SUMO-ubiquitin hybrid chains or by ubiquitin conjugating to the exposed lysine residue through SUMOylation. Our study provides new insight into how a virus utilizes cellular pathways to facilitate its replication. IMPORTANCE: Infection with enterovirus 71 (EV71) often causes neurological diseases in children, and EV71 is responsible for the majority of fatalities. Based on a better understanding of interplay between virus and host cell, antiviral drugs against enteroviruses may be developed. As a dynamic cellular process of posttranslational modification, SUMOylation regulates global cellular protein localization, interaction, stability, and enzymatic activity. However, little is known concerning how SUMOylation directly influences virus replication by targeting viral polymerase. Here, we found that EV71 polymerase 3D was SUMOylated during EV71 infection and in vitro Moreover, the SUMOylation sites were determined, and in vitro polymerase assays indicated that mutations at SUMOylation sites could impair polymerase synthesis. Importantly, 3D is ubiquitinated in a SUMOylation-dependent manner that enhances the stability of the viral polymerase. Our findings indicate that the two modifications likely cooperatively enhance virus replication. Our study may offer a new therapeutic strategy against virus replication