The magnetic, electronic, and light-induced topological properties in two-dimensional hexagonal FeX2 (X = Cl, Br, I) monolayers

Topological materials are fertile ground for investigating topological phases of matter and topological phase transitions. In particular, the quest for novel topological phases in 2D materials is attracting fast growing attention. Here, using Floquet-Bloch theory, we propose to realize chiral topological phases in 2D hexagonal FeX2 (X=Cl, Br, I) monolayers under irradiation of circularly polarized light. Such 2D FeX2 monolayers are predicted to be dynamical stable, and exhibit both ferromagnetic and semiconducting properties. To capture the full topological physics of the magnetic semiconductor under periodic driving, we adopt ab initio Wannier-based tight-binding methods for the Floquet-Bloch bands, with the light-induced band gap closings and openings being obtained as the light field strength increases. The calculations of slab with open boundaries show the existence of chiral edge states. Interestingly, the topological transitions with branches of chiral edge states changing from zero to one and from one to two by tuning the light amplitude are obtained, showing that the topological floquet phase of high Chern number can be induced in the present Floquet-Bloch systems

Inhibition of Rac1 reduces store overload-induced calcium release and protects against ventricular arrhythmia

Rac1 is a small GTPase and plays key roles in multiple cellular processes including the production of reactive oxygen species (ROS). However, whether Rac1 activation during myocardial ischaemia and reperfusion (I/R) contributes to arrhythmogenesis is not fully understood. We aimed to study the effects of Rac1 inhibition on store overload-induced Ca2+ release (SOICR) and ventricular arrhythmia during myocardial I/R. Adult Rac1f/f and cardiac-specific Rac1 knockdown (Rac1ckd) mice were subjected to myocardial I/R and their electrocardiograms (ECGs) were monitored for ventricular arrhythmia. Myocardial Rac1 activity was increased and ventricular arrhythmia was induced during I/R in Rac1f/f mice. Remarkably, I/R-induced ventricular arrhythmia was significantly decreased in Rac1ckd compared to Rac1f/f mice. Furthermore, treatment with Rac1 inhibitor NSC23766 decreased I/R-induced ventricular arrhythmia. Ca2+ imaging analysis showed that in response to a 6 mM external Ca2+ concentration challenge, SOICR was induced with characteristic spontaneous intracellular Ca2+ waves in Rac1f/f cardiomyocytes. Notably, SOICR was diminished by pharmacological and genetic inhibition of Rac1 in adult cardiomyocytes. Moreover, I/R-induced ROS production and ryanodine receptor 2 (RyR2) oxidation were significantly inhibited in the myocardium of Rac1ckd mice. We conclude that Rac1 activation induces ventricular arrhythmia during myocardial I/R. Inhibition of Rac1 suppresses SOICR and protects against ventricular arrhythmia. Blockade of Rac1 activation may represent a new paradigm for the treatment of cardiac arrhythmia in ischaemic heart disease

S-Nitrosylation of STIM1 by Neuronal Nitric Oxide Synthase Inhibits Store-Operated Ca\u3csup\u3e2 +\u3c/sup\u3e Entry

Store-operated Ca2 + entry (SOCE) mediated by stromal interacting molecule-1 (STIM1) and Orai1 represents a major route of Ca2 + entry in mammalian cells and is initiated by STIM1 oligomerization in the endoplasmic or sarcoplasmic reticulum. However, the effects of nitric oxide (NO) on STIM1 function are unknown. Neuronal NO synthase is located in the sarcoplasmic reticulum of cardiomyocytes. Here, we show that STIM1 is susceptible to S-nitrosylation. Neuronal NO synthase deficiency or inhibition enhanced Ca2 + release-activated Ca2 + channel current (ICRAC) and SOCE in cardiomyocytes. Consistently, NO donor S-nitrosoglutathione inhibited STIM1 puncta formation and ICRAC in HEK293 cells, but this effect was absent in cells expressing the Cys49Ser/Cys56Ser STIM1 double mutant. Furthermore, NO donors caused Cys49- and Cys56-specific structural changes associated with reduced protein backbone mobility, increased thermal stability and suppressed Ca2+ depletion-dependent oligomerization of the luminal Ca2 +-sensing region of STIM1. Collectively, our data show that S-nitrosylation of STIM1 suppresses oligomerization via enhanced luminal domain stability and rigidity and inhibits SOCE in cardiomyocytes

Effect of realistic out-of-plane dopant potentials on the superfluid density of overdoped cuprates

Recent experimental papers on hole-doped overdoped cuprates have argued that a series of observations showing unexpected behavior in the superconducting state imply the breakdown of the quasiparticle-based Landau-BCS paradigm in that doping range. In contrast, some of the present authors have argued that a phenomenological "dirty $d$-wave" theoretical analysis explains essentially all aspects of thermodynamic and transport properties in the superconducting state, provided the unusual effects of weak, out-of-plane dopant impurities are properly accounted for. Here we attempt to place this theory on a more quantitative basis by performing $\textit{ab-initio}$ calculations of dopant impurity potentials for LSCO and Tl-2201. These potentials are more complex than the pointlike impurity models considered previously, and require calculation of forward scattering corrections to transport properties. Including realistic, ARPES-derived bandstructures, Fermi liquid renormalizations, and vertex corrections, we show that the theory can explain semiquantitatively the unusual superfluid density measurements of the two most studied overdoped materials.Comment: 19 page, 13 figure