Single nonmagnetic impurity resonance in FeSe-based 122-type superconductors as a probe for pairing symmetry

We study the effect of a single non-magnetic impurity in A$_{y}$Fe$_{2-x}$Se$_{2}$ (A=K, Rb, or Cs) superconductors by considering various pairing states based on a three-orbital model consistent with the photoemission experiments. The local density of states on and near the impurity site has been calculated by solving the Bogoliubov-de Gennes equations self-consistently. The impurity-induced in-gap bound states are found only for attractive impurity scattering potential, as in the cases of doping of Co or Ni, which is characterized by the strong particle-hole asymmetry, in the nodeless $d_{x^2-y^2}$ wave pairing state. This property may be used to probe the pairing symmetry of FeSe-based 122-type superconductors.Comment: 7 pages, 7 figure

Thorium-doping induced superconductivity up to 56 K in Gd1-xThxFeAsO

Following the discovery of superconductivity in an iron-based arsenide LaO1-xFxFeAs with a superconducting transition temperature (Tc) of 26 K[1], Tc was pushed up surprisingly to above 40 K by either applying pressure[2] or replacing La with Sm[3], Ce[4], Nd[5] and Pr[6]. The maximum Tc has climbed to 55 K, observed in SmO1-xFxFeAs[7, 8] and SmFeAsO1-x[9]. The value of Tc was found to increase with decreasing lattice parameters in LnFeAsO1-xFx (Ln stands for the lanthanide elements) at an apparently optimal doping level. However, the F- doping in GdFeAsO is particularly difficult[10,11] due to the lattice mismatch between the Gd2O2 layers and Fe2As2 layers. Here we report observation of superconductivity with Tc as high as 56 K by the Th4+ substitution for Gd3+ in GdFeAsO. The incorporation of relatively large Th4+ ions relaxes the lattice mismatch, hence induces the high temperature superconductivity.Comment: 4 pages, 3 figure

Superconductivity in LaFeAs1−x_{1-x}Px_{x}O: effect of chemical pressures and bond covalency

We report the realization of superconductivity by an isovalent doping with phosphorus in LaFeAsO. X-ray diffraction shows that, with the partial substitution of P for As, the Fe$_2$As$_2$ layers are squeezed while the La$_2$O$_2$ layers are stretched along the c-axis. Electrical resistance and magnetization measurements show emergence of bulk superconductivity at $\sim$10 K for the optimally-doped LaFeAs$_{1-x}$P$_{x}$O ($x=0.25\sim0.3$). The upper critical fields at zero temperature is estimated to be 27 T, much higher than that of the LaFePO superconductor. The occurrence of superconductivity is discussed in terms of chemical pressures and bond covalency.Comment: 5 pages, 6 figures, more data presente

Structural and superconducting properties in LaFeAs1-xSbxO1-yFy

We report the antimony (Sb) doping effect in a prototype system of iron-based supercon-ductors LaFeAsO1-yFy (y=0, 0.1, 0.15). X-ray powder diffraction indicates that the lattice pa-rameters increase with Sb content within the doping limit. Rietveld structural refinements show that, with the partial substitution of Sb for As, while the thickness of the Fe2As2 layers increases significantly, that of the La2O2 layers shrinks simultaneously. So a negative chemical pressure is indeed "applied" to the superconducting-active Fe2As2 layers, in con-trast to the effect of positive chemical pressure by the phosphorus doping. Electrical resis-tance and magnetic susceptibility measurements indicate that, while the Sb doping hardly influences the SDW anomaly in LaFeAsO, it recovers SDW order for the optimally-doped sample of y=0.1. In the meantime, the superconducting transition temperature can be raised up to 30 K in LaFeAs1-xSbxO1-yFy with x=0.1 and y=0.15. The Sb doping effects are discussed in term of both J1-J2 model and Fermi Surface (FS) nesting scenario.Comment: 7 pages, 4 figures, 1 table. to be published in Science in China Series

Within-Compound Versus Public Latrine Access and Child Feces Disposal Practices in Low-Income Neighborhoods of Accra, Ghana.

In crowded urban settlements in low-income countries, many households rely on shared sanitation facilities. Shared facilities are not currently considered "improved sanitation" because of concerns about whether hygiene conditions sufficiently protect users from the feces of others. Prevention of fecal exposure at a latrine is only one aspect of sanitary safety. Ensuring consistent use of latrines for feces disposal, especially child feces, is required to reduce fecal contamination in households and communities. Household crowding and shared latrine access are correlated in these settings, rendering latrine use by neighbors sharing communal living areas as critically important for protecting one's own household. This study in Accra, Ghana, found that household access to a within-compound basic latrine was associated with higher latrine use by children of ages 5-12 years and for disposal of feces of children < 5 years, compared with households using public latrines. However, within-compound access was not associated with improved child feces disposal by other caregivers in the compound. Feces was rarely observed in household compounds but was observed more often in compounds with latrines versus compounds relying on public latrines. Escherichia coli and human adenovirus were detected frequently on household surfaces, but concentrations did not differ when compared by latrine access or usage practices. The differences in latrine use for households sharing within-compound versus public latrines in Accra suggest that disaggregated shared sanitation categories may be useful in monitoring global progress in sanitation coverage. However, compound access did not completely ensure that households were protected from feces and microbial contamination

TLR7 gain-of-function genetic variation causes human lupus

Although circumstantial evidence supports enhanced Toll-like receptor 7 (TLR7) signalling as a mechanism of human systemic autoimmune disease evidence of lupus-causing TLR7 gene variants is lacking. Here we describe human systemic lupus erythematosus caused by a TLR7 gain-of-function variant. TLR7 is a sensor of viral RNA and binds to guanosine. We identified a de novo, previously undescribed missense TLR7Y264H variant in a child with severe lupus and additional variants in other patients with lupus. The TLR7Y264H variant selectively increased sensing of guanosine and 2',3'-cGMP1 and was sufficient to cause lupus when introduced into mice. We show that enhanced TLR7 signalling drives aberrant survival of B cell receptor (BCR)-activated B cells, and in a cell-intrinsic manner, accumulation of CD11c+ age-associated B cells and germinal centre B cells. Follicular and extrafollicular helper T cells were also increased but these phenotypes were cell-extrinsic. Deficiency of MyD88 (an adaptor protein downstream of TLR7) rescued autoimmunity, aberrant B cell survival, and all cellular and serological phenotypes. Despite prominent spontaneous germinal-centre formation in Tlr7Y264H mice, autoimmunity was not ameliorated by germinal-centre deficiency, suggesting an extrafollicular origin of pathogenic B cells. We establish the importance of TLR7 and guanosine-containing self-ligands for human lupus pathogenesis, which paves the way for therapeutic TLR7 or MyD88 inhibition