Temperature dependence of spin diffusion length and spin Hall angle in Au and Pt

We have studied the spin transport and the spin Hall effect as a function of temperature for platinum (Pt) and gold (Au) in lateral spin valve structures. First, by using the spin absorption technique, we extract the spin diffusion length of Pt and Au. Secondly, using the same devices, we have measured the spin Hall conductivity and analyzed its evolution with temperature to identify the dominant scattering mechanisms behind the spin Hall effect. This analysis confirms that the intrinsic mechanism dominates in Pt whereas extrinsic effects are more relevant in Au. Moreover, we identify and quantify the phonon-induced skew scattering. We show that this contribution to skew scattering becomes relevant in metals such as Au, with a low residual resistivity.Comment: 13 pages, 5 figure

Seebeck Effect in Nanoscale Ferromagnets

We present a theory of the Seebeck effect in nanoscale ferromagnets with dimensions smaller than the spin diffusion length. The spin accumulation generated by a temperature gradient strongly affects the thermopower. We also identify a correction arising from the transverse temperature gradient induced by the anomalous Ettingshausen effect. The effect of an induced spin-heat accu- mulation gradient is considered as well. The importance of these effects for nanoscale ferromagnets is illustrated by ab initio calculations for dilute ferromagnetic alloys.Comment: 5 pages, 2 figure

Interfacial mechanism in the anomalous Hall effect of Co/Bi2_2O3_3 bilayers

Oxide interfaces are a source of spin-orbit coupling which can lead to novel spin-to-charge conversion effects. In this work the contribution of the Bi$_2$O$_3$ interface to the anomalous Hall effect of Co is experimentally studied in Co/Bi$_2$O$_3$ bilayers. We evidence a variation of 40% in the AHE of Co when a Bi$_2$O$_3$ capping layer is added to the ferromagnet. This strong variation is attributed to an additional source of asymmetric transport in Co/Bi$_2$O$_3$ bilayers that originates from the Co/Bi$_2$O$_3$ interface and contributes to the skew scattering.Comment: 7 pages, 4 figure

Tuning the spin Hall effect of Pt from the moderately dirty to the superclean regime

We systematically measure and analyze the spin diffusion length and the spin Hall effect in Pt with a wide range of conductivities using the spin absorption method in lateral spin valve devices. We observe a linear relation between the spin diffusion length and the conductivity, evidencing that the spin relaxation in Pt is governed by the Elliott-Yafet mechanism. We find a single intrinsic spin Hall conductivity ($\sigma_{SH}^{int}=1600\pm150\: \Omega^{-1}cm^{-1}$) for Pt in the full range studied which is in good agreement with theory. For the first time we have obtained the crossover between the moderately dirty and the superclean scaling regimes of the spin Hall effect by tuning the conductivity. This is equivalent to that obtained for the anomalous Hall effect. Our results explain the spread of the spin Hall angle values in the literature and find a route to maximize this important parameter.Comment: 11 pages, 4 figure

Unveiling the mechanisms of the spin Hall effect in Ta

Spin-to-charge current interconversions are widely exploited for the generation and detection of pure spin currents and are key ingredients for future spintronic devices including spin-orbit torques and spin-orbit logic circuits. In case of the spin Hall effect, different mechanisms contribute to the phenomenon and determining the leading contribution is peremptory for achieving the largest conversion efficiencies. Here, we experimentally demonstrate the dominance of the intrinsic mechanism of the spin Hall effect in highly-resistive Ta. We obtain an intrinsic spin Hall conductivity for $\beta$-Ta of -820$\pm$120 ($\hbar$/e) $\Omega^{-1}cm^{-1}$ from spin absorption experiments in a large set of lateral spin valve devices. The predominance of the intrinsic mechanism in Ta allows us to linearly enhance the spin Hall angle by tuning the resistivity of Ta, reaching up to -35$\pm$3%, the largest reported value for a pure metal.Comment: 9 pages and 4 figures + Supplemental Material (2 pages, 3 figures

Computer Aided Classification of Neuroblastoma Histological Images Using Scale Invariant Feature Transform with Feature Encoding

Neuroblastoma is the most common extracranial solid malignancy in early childhood. Optimal management of neuroblastoma depends on many factors, including histopathological classification. Although histopathology study is considered the gold standard for classification of neuroblastoma histological images, computers can help to extract many more features some of which may not be recognizable by human eyes. This paper, proposes a combination of Scale Invariant Feature Transform with feature encoding algorithm to extract highly discriminative features. Then, distinctive image features are classified by Support Vector Machine classifier into five clinically relevant classes. The advantage of our model is extracting features which are more robust to scale variation compared to the Patched Completed Local Binary Pattern and Completed Local Binary Pattern methods. We gathered a database of 1043 histologic images of neuroblastic tumours classified into five subtypes. Our approach identified features that outperformed the state-of-the-art on both our neuroblastoma dataset and a benchmark breast cancer dataset. Our method shows promise for classification of neuroblastoma histological images

Mutations That Affect the Surface Expression of TRPV6 Are Associated with the Upregulation of Serine Proteases in the Placenta of an Infant

Recently, we reported a case of an infant with neonatal severe under-mineralizing skeletal dysplasia caused by mutations within both alleles of the TRPV6 gene. One mutation results in an in frame stop codon (R510stop) that leads to a truncated, nonfunctional TRPV6 channel, and the second in a point mutation (G660R) that, surprisingly, does not affect the Ca2+ permeability of TRPV6. We mimicked the subunit composition of the unaffected heterozygous parent and child by coexpressing the TRPV6 G660R and R510stop mutants and combinations with wild type TRPV6. We show that both the G660R and R510stop mutant subunits are expressed and result in decreased calcium uptake, which is the result of the reduced abundancy of functional TRPV6 channels within the plasma membrane. We compared the proteomic profiles of a healthy placenta with that of the diseased infant and detected, exclusively in the latter two proteases, HTRA1 and cathepsin G. Our results implicate that the combination of the two mutant TRPV6 subunits, which are expressed in the placenta of the diseased child, is responsible for the decreased calcium uptake, which could explain the skeletal dysplasia. In addition, placental calcium deficiency also appears to be associated with an increase in the expression of proteases

Mutations that affect the surface expression of TRPV6 are associated with the upregulation of serine proteases in the placenta of an infant

Recently, we reported a case of an infant with neonatal severe under-mineralizing skeletal dysplasia caused by mutations within both alleles of the TRPV6 gene. One mutation results in an in frame stop codon (R(510)stop) that leads to a truncated, nonfunctional TRPV6 channel, and the second in a point mutation (G(660)R) that, surprisingly, does not affect the Ca(2+) permeability of TRPV6. We mimicked the subunit composition of the unaffected heterozygous parent and child by coexpressing the TRPV6 G(660)R and R(510)stop mutants and combinations with wild type TRPV6. We show that both the G(660)R and R(510)stop mutant subunits are expressed and result in decreased calcium uptake, which is the result of the reduced abundancy of functional TRPV6 channels within the plasma membrane. We compared the proteomic profiles of a healthy placenta with that of the diseased infant and detected, exclusively in the latter two proteases, HTRA1 and cathepsin G. Our results implicate that the combination of the two mutant TRPV6 subunits, which are expressed in the placenta of the diseased child, is responsible for the decreased calcium uptake, which could explain the skeletal dysplasia. In addition, placental calcium deficiency also appears to be associated with an increase in the expression of proteases