Current-induced effective magnetic field in La0.67Sr0.33MnO3/LaAlO3/SrTiO3 structures

We investigate the current-induced effective magnetic field H-eff in La0.67Sr0.33MnO3 (18)/LaAlO3(0,2,6)/SrTiO3 (LSMO/LAO/STO) structures by using the planar Hall effect (PHE), where numbers in parentheses give the nominal thickness of the given layer in unit cells. In all the structures, applying an in-plane current creates an in-plane H-eff orthogonal to the current direction, and the direction of H-eff for the LSMO/LAO(6)/STO structure is opposite to that for the LSMO/LAO(0,2)/STO structures. At low temperature, the sign of the PHE coefficient originating from the spin-orbit interaction (SOI) for the LSMO/LAO(6)/STO structure is also opposite to that for the LSMO/LAO(0,2)/STO structures, which suggests that the SOI in the LSMO layer is modified by the LAO(6)/STO structure. The direction of H-eff is consistent with that induced by the SOI at the interface of the LSMO layer, and thus the opposite-polarity H-eff detected in the LSMO/LAO(6)/STO structure can be related to the SOI variation induced by the LAO(6)/STO structure

Peculiar magnetotransport properties in La0.67Sr0.33MnO3/LaAlO3/SrTiO3

We have investigated the planar Hall effect (PHE) and the anisotropic magnetoresistance (AMR) in La0.67Sr0.33MnO3/LaAlO3/SrTiO3 (LSMO/LAO/STO) and LSMO/STO structures, where the LSMO (LAO) thickness was 13 unit cells (u.c.) and 18 u.c. (8 u.c. and 6 u.c.). The LAO/STO structures under the LSMO layers are conductive, which is consistent with the formation of a two-dimensional electron system (2DES) at the LAO/STO interface. The magnetotransport measurements show that the sign of the PHE coefficient for the LSMO/LAO/STO structures is opposite to that for the LSMO/STO structures, whereas the AMR coefficient, which is generally correlated with the PHE coefficient, is negative for both structures at temperatures below ∼175 K. The LAO/STO structures show no apparent PHE or AMR, and the coefficients obtained thus originate from the LSMO. These results suggest that the 2DES and/or the LSMO/LAO interface affect the PHE in the LSMO layer

Targeted next-generation sequencing for detection of PIK3CA mutations in archival tissues from patients with Klippel–Trenaunay syndrome in an Asian population

Abstract Background Klippel–Trenaunay syndrome (KTS) is a rare slow-flow combined vascular malformation with limb hypertrophy. KTS is thought to lie on the PIK3CA-related overgrowth spectrum, but reports are limited. PIK3CA encodes p110α, a catalytic subunit of phosphatidylinositol 3-kinase (PI3K) that plays an essential role in the PI3K/AKT/mammalian target of rapamycin (mTOR) signaling pathway. We aimed to demonstrate the clinical utility of targeted next-generation sequencing (NGS) in identifying PIK3CA mosaicism in archival formalin-fixed paraffin-embedded (FFPE) tissues from patients with KTS. Results Participants were 9 female and 5 male patients with KTS diagnosed as capillaro-venous malformation (CVM) or capillaro-lymphatico-venous malformation (CLVM). Median age at resection was 14 years (range, 5–57 years). Median archival period before DNA extraction from FFPE tissues was 5.4 years (range, 3–7 years). NGS-based sequencing of PIK3CA achieved an amplicon mean coverage of 119,000x. PIK3CA missense mutations were found in 12 of 14 patients (85.7%; 6/8 CVM and 6/6 CLVM), with 8 patients showing the hotspot variants E542K, E545K, H1047R, and H1047L. The non-hotspot PIK3CA variants C420R, Q546K, and Q546R were identified in 4 patients. Overall, the mean variant allele frequency for identified PIK3CA variants was 6.9% (range, 1.6–17.4%). All patients with geographic capillary malformation, histopathological lymphatic malformation or macrodactyly of the foot had PIK3CA variants. No genotype–phenotype association between hotspot and non-hotspot PIK3CA variants was found. Histologically, the vessels and adipose tissues of the lesions showed phosphorylation of the proteins in the PI3K/AKT/mTOR signaling pathway, including p-AKT, p-mTOR, and p-4EBP1. Conclusions The PI3K/AKT/mTOR pathway in mesenchymal tissues was activated in patients with KTS. Amplicon-based targeted NGS could identify low-level mosaicism from low-input DNA extracted from FFPE tissues, potentially providing a diagnostic option for personalized medicine with inhibitors of the PI3K/AKT/mTOR signaling pathway