ABSTRACT
Microwave measurements of the London penetration depth and critical temperature T_{c} were used to show evidence of a disordered-driven transition from s_{±} to s_{++} order parameter symmetry in optimally doped Ba(Fe_{1-x}Rh_{x})_{2}As_{2} single crystals, where disorder was induced by means of 3.5 MeV proton irradiation. Signatures of such a transition, as theoretically predicted [V. D. Efremov et al., Phys. Rev. B 84, 180512(R) (2011)PRBMDO1098-012110.1103/PhysRevB.84.180512], are found as a drop in the low-temperature values of the London penetration depth and a virtually disorder-independent superconducting T_{c}. We show how these experimental observations can be described by multiband Eliashberg calculations in which the effect of disorder is accounted for in a suitable way. To this aim, an effective two-band approach is adopted, allowing us to treat disorder in a range between the Born approximation and the unitary limit.
ABSTRACT
One of the open issues concerning iron-based superconductors is whether the s± wave model is able to account for the overall effects of impurity scattering, including the low rate of decrease of the critical temperature with the impurity concentration. Here we investigate Ba1-x K x Fe2As2 crystals where disorder is introduced by Au-ion irradiation. Critical temperature, T c , and London penetration depth, λ L , were measured by a microwave resonator technique, for different values of the irradiation fluence. We compared experimental data with calculations made on the basis of the three-band Eliashberg equations, suitably accounting for the impurity scattering. We show that this approach is able to explain in a consistent way the effects of disorder both on T c and on λ L (T), within the s± wave model. In particular, a change of curvature in the low-temperature λ L (T) curves for the most irradiated crystals is fairly well reproduced.
ABSTRACT
The tau gene has been found to be the locus of dementia with rigidity linked to chromosome 17. Exonic and intronic mutations have been described in a number of families. Here we describe a P301S mutation in exon 10 of the tau gene in a new family. Two members of this family were affected. One individual presented with frontotemporal dementia, whereas his son has corticobasal degeneration, demonstrating that the same primary gene defect in tau can lead to 2 distinct clinical phenotypes. Both individuals developed rapidly progressive disease in the third decade. Neuropathologically, the father presented with an extensive filamentous pathology made of hyperphosphorylated tau protein. Biochemically, recombinant tau protein with the P301S mutation showed a greatly reduced ability to promote microtubule assembly.
