New Phase Induced by Pressure in the Iron-Arsenide Superconductor K-Ba122

The electrical resistivity rho of the iron-arsenide superconductor Ba1-xKxFe2As2 was measured in applied pressures up to 2.6 GPa for four underdoped samples, with x = 0.16, 0.18, 0.19 and 0.21. The antiferromagnetic ordering temperature T_N, detected as a sharp anomaly in rho(T), decreases linearly with pressure. At pressures above around 1.0 GPa, a second sharp anomaly is detected at a lower temperature T_0, which rises with pressure. We attribute this second anomaly to the onset of a phase that causes a reconstruction of the Fermi surface. This new phase expands with increasing x and it competes with superconductivity. We discuss the possibility that a second spin-density wave orders at T_0, with a Q vector distinct from that of the spin-density wave that sets in at T_N.Comment: Two higher K concentrations were added, revealing a steady expansion of the new phase in the T-P phase diagra

Universal heat conduction in the iron-arsenide superconductor KFe2As2 : Evidence of a d-wave state

The thermal conductivity of the iron-arsenide superconductor KFe2As2 was measured down to 50 mK for a heat current parallel and perpendicular to the tetragonal c-axis. A residual linear term (RLT) at T=0 is observed for both current directions, confirming the presence of nodes in the superconducting gap. Our value of the RLT in the plane is equal to that reported by Dong et al. [Phys. Rev. Lett. 104, 087005 (2010)] for a sample whose residual resistivity was ten times larger. This independence of the RLT on impurity scattering is the signature of universal heat transport, a property of superconducting states with symmetry-imposed line nodes. This argues against an s-wave state with accidental nodes. It favors instead a d-wave state, an assignment consistent with five additional properties: the magnitude of the critical scattering rate for suppressing Tc to zero; the magnitude of the RLT, and its dependence on current direction and on magnetic field; the temperature dependence of the thermal conductivity.Comment: To appear in Physical Review Letter

Doping evolution of the superconducting gap structure in the underdoped iron arsenide Ba1-xKxFe2As2 revealed by thermal conductivity

The thermal conductivity kappa of the iron-arsenide superconductor Ba1-xKxFe2As2 was measured for heat currents parallel and perpendicular to the tetragonal c axis at temperatures down to 50 mK and in magnetic fields up to 15 T. Measurements were performed on samples with compositions ranging from optimal doping (x = 0.34; Tc = 39 K) down to dopings deep into the region where antiferromagnetic order coexists with superconductivity (x = 0.16; Tc = 7 K). In zero field, there is no residual linear term in kappa(T) as T goes to 0 at any doping, whether for in-plane or inter-plane transport. This shows that there are no nodes in the superconducting gap. However, as x decreases into the range of coexistence with antiferromagnetism, the residual linear term grows more and more rapidly with applied magnetic field. This shows that the superconducting energy gap develops minima at certain locations on the Fermi surface and these minima deepen with decreasing x. We propose that the minima in the gap structure arise when the Fermi surface of Ba1-xKxFe2As2 is reconstructed by the antiferromagnetic order

Insulin Resistance and Metabolic Hepatocarcinogenesis with Parent-of-Origin Effects in A×B Mice

Insulin resistance is a defining feature of metabolic syndrome and type 2 diabetes mellitus but also may occur independently of these conditions. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of these disorders, increases the risk of hepatocellular carcinoma (HCC). However, mechanisms linking hyperinsulinemia to NAFLD and HCC require clarification. We describe a novel model of primary insulin resistance and HCC with strong parent-of-origin effects. Male AB6F1 (A/JCr dam × C57BL/6 sire) but not B6AF1 (B6 dam × A/J sire) mice developed spontaneous insulin resistance, NAFLD, and HCC without obesity or diabetes. A survey of mitochondrial, imprinted, and sex-linked traits revealed modest associations with X-linked genes. However, a diet-induced obesity study, including B6.A chromosome substitution–strain (consomic) mice, showed no segregation by sex chromosome. Thus, parent-of-origin effects were specified within the autosomal genome. Next, we interrogated mechanisms of insulin-associated hepatocarcinogenesis. Steatotic hepatocytes exhibited adipogenic transition characterized by vacuolar metaplasia and up-regulation of vimentin, adipsin, fatty acid translocase (CD36), peroxisome proliferator–activated receptor-γ, and related products. This profile was largely recapitulated in insulin-supplemented primary mouse hepatocyte cultures. Importantly, pyruvate kinase M2, a fetal anabolic enzyme implicated in the Warburg effect, was activated by insulin in vivo and in vitro. Thus, our study reveals parent-of-origin effects in heritable insulin resistance, implicating adipogenic transition with acquired anabolic metabolism in the progression from NAFLD to HCC.National Institutes of Health (U.S.) (NIH grant AA016563)National Institutes of Health (U.S.) (NIH grant CA067529)National Institutes of Health (U.S.) (NIH grant P01CA0267)National Institutes of Health (U.S.) (NIH grant P30ES02109)National Institutes of Health (U.S.) (NIH grant RR007036)National Institutes of Health (U.S.) (NIH grant CA158661)National Institutes of Health (U.S.) (NIH grant CA016086

From d-wave to s-wave pairing in the iron-pnictide superconductor (Ba,K)Fe2As2

The nature of the pairing state in iron-based superconductors is the subject of much debate. Here we argue that in one material, the stoichiometric iron pnictide KFe2As2, there is overwhelming evidence for a d-wave pairing state, characterized by symmetry-imposed vertical line nodes in the superconducting gap. This evidence is reviewed, with a focus on thermal conductivity and the strong impact of impurity scattering on the critical temperature Tc. We then compare KFe2As2 to Ba0.6K0.4Fe2As2, obtained by Ba substitution, where the pairing symmetry is s-wave and the Tc is ten times higher. The transition from d-wave to s-wave within the same crystal structure provides a rare opportunity to investigate the connection between band structure and pairing mechanism. We also compare KFe2As2 to the nodal iron-based superconductor LaFePO, for which the pairing symmetry is probably not d-wave, but more likely s-wave with accidental line nodes

HDAC-mediated control of ERK- and PI3K-dependent TGF-β-induced extracellular matrix-regulating genes

Histone deacetylases (HDACs) regulate the acetylation of histones in the control of gene expression. Many non-histone proteins are also targeted for acetylation, including TGF-ß signalling pathway components such as Smad2, Smad3 and Smad7. Our studies in mouse C3H10T1/2 fibroblasts suggested that a number of TGF-ß-induced genes that regulate matrix turnover are selectively regulated by HDACs. Blockade of HDAC activity with trichostatin A (TSA) abrogated the induction of a disintegrin and metalloproteinase 12 (Adam12) and tissue inhibitor of metalloproteinases-1 (Timp-1) genes by TGF-ß, whereas plasminogen activator inhibitor-1 (Pai-1) expression was unaffected. Analysis of the activation of cell signalling pathways demonstrated that TGF-ß induced robust ERK and PI3K activation with delayed kinetics compared to the phosphorylation of Smads. The TGF-ß induction of Adam12 and Timp-1 was dependent on such non-Smad signalling pathways and, importantly, HDAC inhibitors completely blocked their activation without affecting Smad signalling. Analysis of TGF-ß-induced Adam12 and Timp-1 expression and ERK/PI3K signalling in the presence of semi-selective HDAC inhibitors valproic acid, MS-275 and apicidin implicated a role for class I HDACs. Furthermore, depletion of HDAC3 by RNA interference significantly down-regulated TGF-ß-induced Adam12 and Timp-1 expression without modulating Pai-1 expression. Correlating with the effect of HDAC inhibitors, depletion of HDAC3 also blocked the activation of ERK and PI3K by TGF-ß. Collectively, these data confirm that HDACs, and in particular HDAC3, are required for activation of the ERK and PI3K signalling pathways by TGF-ß and for the subsequent gene induction dependent on these signalling pathways

The programming of sequences of saccades

Saccadic eye movements move the high-resolution fovea to point at regions of interest. Saccades can only be generated serially (i.e., one at a time). However, what remains unclear is the extent to which saccades are programmed in parallel (i.e., a series of such moments can be planned together) and how far ahead such planning occurs. In the current experiment, we investigate this issue with a saccade contingent preview paradigm. Participants were asked to execute saccadic eye movements in response to seven small circles presented on a screen. The extent to which participants were given prior information about target locations was varied on a trial-by-trial basis: participants were aware of the location of the next target only, the next three, five, or all seven targets. The addition of new targets to the display was made during the saccade to the next target in the sequence. The overall time taken to complete the sequence was decreased as more targets were available up to all seven targets. This was a result of a reduction in the number of saccades being executed and a reduction in their saccade latencies. Surprisingly, these results suggest that, when faced with a demand to saccade to a large number of target locations, saccade preparation about all target locations is carried out in paralle

Parallel Mechanisms for Visual Search in Zebrafish

This research was funded by project grant G1000053 from the National Centre for the Replacement, Reduction and Refinement of animals in research (NC3Rs; UK) and by the Medical Research Council (MRC; UK). CHB is a Royal Society (UK) Research Fellow