Ultralow-dissipative conductivity by Dirac fermions in BaFe2_2As2_2

We report on the anomalous behavior of the complex conductivity of BaFe$_{2}$As$_{2}$, which is related to the Dirac cone, in the terahertz (THz)-frequency region. Above the spin-density-wave (SDW) transition temperature, the conductivity spectra follow the Drude model. In the SDW state, the imaginary part of the complex conductivity, $\sigma_2$, is suppressed in comparison to that expected according to the Drude model. The real part, $\sigma_1$, exhibits nearly Drude-like behavior. This behavior (i.e., almost no changes in $\sigma_1$ and the depression of $\sigma_2$) can be regarded as the addition of extra conductivity without any dissipations in the Drude-type conductivity. The origin of this ultralow-dissipative conductivity is found to be due to conductivity contribution from quasiparticles within the Dirac cone. In other words, we are able to observe the dynamics of Dirac fermions through the conductivity spectra of BaFe$_2$As$_2$, clearly and directly.Comment: 5pages, 3 figure

Polygenic burden in focal and generalized epilepsies

© The Author(s) (2019).Rare genetic variants can cause epilepsy, and genetic testing has been widely adopted for severe, paediatric-onset epilepsies. The phenotypic consequences of common genetic risk burden for epilepsies and their potential future clinical applications have not yet been determined. Using polygenic risk scores (PRS) from a European-ancestry genome-wide association study in generalized and focal epilepsy, we quantified common genetic burden in patients with generalized epilepsy (GE-PRS) or focal epilepsy (FE-PRS) from two independent non-Finnish European cohorts (Epi25 Consortium, n = 5705; Cleveland Clinic Epilepsy Center, n = 620; both compared to 20 435 controls). One Finnish-ancestry population isolate (Finnish-ancestry Epi25, n = 449; compared to 1559 controls), two European-ancestry biobanks (UK Biobank, n = 383 656; Vanderbilt biorepository, n = 49 494), and one Japaneseancestry biobank (BioBank Japan, n = 168 680) were used for additional replications. Across 8386 patients with epilepsy and 622 212 population controls, we found and replicated significantly higher GE-PRS in patients with generalized epilepsy of European-ancestry compared to patients with focal epilepsy (Epi25: P = 1.64×10-15; Cleveland: P = 2.85×10-4; Finnish-ancestry Epi25: P = 1.80×10-4) or population controls (Epi25: P = 2.35×10-70; Cleveland: P = 1.43×10-7; Finnish-ancestry Epi25: P = 3.11×10-4; UK Biobank and Vanderbilt biorepository meta-analysis: P = 7.99×10-4). FE-PRS were significantly higher in patients with focal epilepsy compared to controls in the non-Finnish, non-biobank cohorts (Epi25: P = 5.74×10-19; Cleveland: P = 1.69×10-6). European ancestry-derived PRS did not predict generalized epilepsy or focal epilepsy in Japanese-ancestry individuals. Finally, we observed a significant 4.6-fold and a 4.5-fold enrichment of patients with generalized epilepsy compared to controls in the top 0.5% highest GE-PRS of the two non-Finnish European cohorts (Epi25: P = 2.60×10-15; Cleveland: P = 1.39×10-2). We conclude that common variant risk associated with epilepsy is significantly enriched in multiple cohorts of patients with epilepsy compared to controls-in particular for generalized epilepsy. As sample sizes and PRS accuracy continue to increase with further common variant discovery, PRS could complement established clinical biomarkers and augment genetic testing for patient classification, comorbidity research, and potentially targeted treatment