Fully gapped superconductivity in Ni-pnictide superconductors BaNi2As2 and SrNi2P2

We have performed low-temperature specific heat $C$ and thermal conductivity $\kappa$ measurements on the Ni-pnictide superconductors BaNi$_2$As$_2$ ($T_\mathrm{c}$=0.7 K and SrNi$_2$P$_2$ ($T_\mathrm{c}$=1.4 K). The temperature dependences $C(T)$ and $\kappa(T)$ of the two compounds are similar to the results of a number of s-wave superconductors. Furthermore, the concave field responses of the residual $\kappa$ for BaNi$_2$As$_2$ rules out the presence of nodes on the Fermi surfaces. We postulate that fully gapped superconductivity could be universal for Ni-pnictide superconductors. Specific heat data on Ba$_{0.6}$La$_{0.4}$Ni$_2$As$_2$ shows a mild suppression of $T_\mathrm{c}$ and $H_\mathrm{c2}$ relative to BaNi$_2$As$_2$.Comment: 5 pages, 3 figures, to be published in J. Phys.: Conf. Se

Thermal Conductivity of Pr_{1.3-x}La_{0.7}Ce_xCuO_4 Single Crystals and Signatures of Stripes in an Electron-Doped Cuprate

It was recently demonstrated that the anisotropic phonon heat transport behavior is a good probe of the stripe formation in La_{2-x}Sr_xCuO_4 (LSCO) [X. F. Sun {\it et al.}, Phys. Rev. B {\bf 67}, 104503 (2003)]. Using this probe, we examined an electron-doped cuprate Pr_{1.3-x}La_{0.7}Ce_xCuO_4 (PLCCO) and found that essentially the same features as those in LSCO are observed. Moreover, the in-plane resistivity \rho_{ab} of lightly-doped PLCCO shows metallic behavior (d\rho_{ab}/dT > 0) in the N\'eel ordered state with a mobility comparable to that in LSCO. It is discussed that these peculiar properties in common with LSCO signify the existence of stripes in electron-doped cuprates.Comment: 4 pages, 4 figures, revised version accepted for publication in Phys. Rev. Let

Low-temperature magneto-thermal transport investigation of a Ni-based superconductor BaNi2As2: Evidence for fully gapped superconductivity

We have performed low-temperature specific heat and thermal conductivity measurements of the Ni-based superconductor BaNi$_2$As$_2$ ($T_\mathrm{c}$ = 0.7 K) in magnetic field. In zero field, thermal conductivity shows $T$-linear behavior in the normal state and exhibits a BCS-like exponential decrease below $T_\mathrm{c}$. The field dependence of the residual thermal conductivity extrapolated to zero temperature is indicative of a fully gapped superconductor. This conclusion is supported by the analysis of the specific heat data, which are well fit by the BCS temperature dependence from $T_\mathrm{c}$ down to the lowest temperature of 0.1 K.Comment: Physical Review Letters, to be publishe

The secondary KIT mutation p.Ala510Val in a cutaneous mast cell tumour carrying the activating mutation p.Asn508Ile confers resistance to masitinib in dogs

Background: Gain-of-function mutations in KIT are driver events of oncogenesis in mast cell tumours (MCTs) affecting companion animals. Somatic mutations of KIT determine the constitutive activation of the tyrosine kinase receptor leading to a worse prognosis and a shorter survival time than MCTs harbouring wild-type KIT. However, canine MCTs carrying KIT somatic mutations generally respond well to tyrosine kinase inhibitors; hence their presence represents a predictor of treatment effectiveness, and its detection allows implementing a stratified medical approach. Despite this, veterinary oncologists experience treatment failures, even with targeted therapies whose cause cannot be elucidated. The first case of an MCT-affected dog caused by a secondary mutation in the tyrosine kinase domain responsible for resistance has recently been reported. The knowledge of this and all the other mutations responsible for resistance would allow the effective bedside implementation of a deeply stratified and more effective medical approach. Case presentation: The second case of a canine MCT carrying a different resistance mutation is herein described. The case was characterised by aggressive behaviour and early metastasis unresponsive to both vinblastine- and masitinib-based treatments. Molecular profiling of the tumoural masses revealed two different mutations; other than the already known activating mutation p.Asn508Ile in KIT exon 9, which is tyrosine kinase inhibitor-sensitive, a nearly adjacent secondary missense mutation, p.Ala510Val, which had never before been described, was detected. In vitro transfection experiments showed that the secondary mutation did not cause the constitutive activation by itself but played a role in conferring resistance to masitinib. Conclusions: This study highlighted the importance of the accurate molecular profiling of an MCT in order to improve understanding of the molecular mechanism underlying tumourigenesis and reveal chemoresistance in MCTs for more effective therapies. The detection of the somatic mutations responsible for resistance should be included in the molecular screening of MCTs, and a systematic analysis of all the cases characterised by unexpected refractoriness to therapies should be investigated in depth at both the genetic and the phenotypic level

Crystal fields, disorder, and antiferromagnetic short-range order in Yb0.24Sn0.76Ru

We report extensive measurements on a new compound (Yb0.24Sn0.76)Ru that crystallizes in the cubic CsCl structure. Valence band photoemission and L3 x-ray absorption show no divalent component in the 4f configuration of Yb. Inelastic neutron scattering (INS) indicates that the eight-fold degenerate J-multiplet of Yb3+ is split by the crystalline electric field (CEF) into a {\Gamma}7 doublet ground state and a {\Gamma}8 quartet at an excitation energy 20 meV. The magnetic susceptibility can be fit very well by this CEF scheme under the assumption that a {\Gamma}6 excited state resides at 32 meV; however, the {\Gamma}8/{\Gamma}6 transition expected at 12 meV was not observed in the INS. The resistivity follows a Bloch- Gr\"uneisen law shunted by a parallel resistor, as is typical of systems subject to phonon scattering with no apparent magnetic scattering. All of these properties can be understood as representing simple local moment behavior of the trivalent Yb ion. At 1 K, there is a peak in specific heat that is too broad to represent a magnetic phase transition, consistent with absence of magnetic reflections in neutron diffraction. On the other hand, this peak also is too narrow to represent the Kondo effect in the {\Gamma}7 ground state doublet. On the basis of the field-dependence of the specific heat, we argue that antiferromagnetic shortrange order (possibly co-existing with Kondo physics) occurs at low temperatures. The long-range magnetic order is suppressed because the Yb site occupancy is below the percolation threshold for this disordered compound

Thermal and magnetic properties of a low-temperature antiferromagnet Ce4_4Pt12_{12}Sn25_{25}

We report specific heat ($C$) and magnetization ($M$) of single crystalline Ce$_4$Pt$_{12}$Sn$_{25}$ at temperature down to $\sim$50mK and in fields up to 3T. $C/T$ exhibits a sharp anomaly at 180mK, with a large $\Delta C/T\sim$30J/molK$^2$-Ce, which, together with the corresponding cusp-like magnetization anomaly, indicates an antiferromagnetic (AFM) ground state with a N\'eel temperature $T_N$=180mK. Numerical calculations based on a Heisenberg model reproduce both zero-field $C$ and $M$ data, thus placing Ce$_4$Pt$_{12}$Sn$_{25}$ in the weak exchange coupling $J<J_c$ limit of the Doniach diagram, with a very small Kondo scale $T_K\ll T_N$. Magnetic field suppresses the AFM state at $H^*\approx$0.7T, much more effectively than expected from the Heisenberg model, indicating additional effects possibly due to frustration or residual Kondo screening.Comment: 8 pages, 7 figures, accepted for publication in Phys. Rev.

Cellular inhibitor of apoptosis 1 (cIAP-1) degradation by caspase 8 during TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.

TNF-related apoptosis-inducing ligand (TRAIL) is a potential chemotherapeutic agent with high selectivity for malignant cells. Many tumors, however, are resistant to TRAIL cytotoxicity. Although cellular inhibitors of apoptosis 1 and 2 (cIAP-1 and -2) are often over-expressed in cancers, their role in mediating TRAIL resistance remains unclear. Here, we demonstrate that TRAIL-induced apoptosis of liver cancer cells is associated with degradation of cIAP-1 and X-linked IAP (XIAP), whereas cIAP-2 remains unchanged. Lower concentrations of TRAIL causing minimal or no apoptosis do not alter cIAP-1 or XIAP protein levels. Silencing of cIAP-1 expression, but not XIAP or cIAP-2, as well as co-treatment with a second mitochondrial activator of caspases (SMAC) mimetic (which results in rapid depletion of cIAP-1), sensitizes the cells to TRAIL. TRAIL-induced loss of cIAP-1 and XIAP requires caspase activity. In particular, caspase 8 knockdown stabilizes both cIAP-1 and XIAP, while caspase 9 knockdown prevents XIAP, but not cIAP-1 degradation. Cell-free experiments confirmed cIAP-1 is a substrate for caspase 8, with likely multiple cleavage sites. These results suggest that TRAIL-mediated apoptosis proceeds through caspase 8-dependent degradation of cIAP-1. Targeted depletion of cIAP-1 by SMAC mimetics in conjunction with TRAIL may be beneficial for the treatment of human hepatobiliary malignancies