Impact of inherent energy barrier on spin-orbit torques in magnetic-metal/semimetal heterojunctions.

Spintronic devices are based on heterojunctions of two materials with different magnetic and electronic properties. Although an energy barrier is naturally formed even at the interface of metallic heterojunctions, its impact on spin transport has been overlooked. Here, using diffusive spin Hall currents, we provide evidence that the inherent energy barrier governs the spin transport even in metallic systems. We find a sizable field-like torque, much larger than the damping-like counterpart, in Ni81Fe19/Bi0.1Sb0.9 bilayers. This is a distinct signature of barrier-mediated spin-orbit torques, which is consistent with our theory that predicts a strong modification of the spin mixing conductance induced by the energy barrier. Our results suggest that the spin mixing conductance and the corresponding spin-orbit torques are strongly altered by minimizing the work function difference in the heterostructure. These findings provide a new mechanism to control spin transport and spin torque phenomena by interfacial engineering of metallic heterostructures.

Spin-orbit torque manipulated by fine-tuning of oxygen-induced orbital hybridization.

Current-induced spin-orbit torques provide an effective way to manipulate magnetization in spintronic devices, promising for fast switching applications in nonvolatile memory and logic units. Recent studies have revealed that the spin-orbit torque is strongly altered by the oxidation of heterostructures with broken inversion symmetry. Although this finding opens a new field of metal-oxide spin-orbitronics, the role of the oxidation in the spin-orbit physics is still unclear. Here, we demonstrate a marked enhancement of the spin-orbit torque induced by a fine-tuning of oxygen-induced modification of orbital hybridization. This is evidenced by a concomitant enhancement of the interface spin-orbit torque, interface spin loss, and interface perpendicular magnetic anisotropy within a narrow range of the oxidation level of metallic heterostructures. This result reveals the crucial role of the atomic-scale effects in the generation of the spin-orbit torques, opening the door to atomic-level engineering of the spin-orbit physics.

RANKL, Ephrin-Eph and Wnt10b are key intercellular communication molecules regulating bone remodeling in autologous transplanted goldfish scales.

This study aimed to investigate the precise data of gene expression, functions, and chronological relationships amongst communication molecules involved in the bone remodeling process with an in vivo model using autologous transplanted scales of goldfish. Autotransplantation of methanol-fixed cell-free scales triggers scale resorption and regeneration, as well as helps elucidate the process of bone remodeling. We investigated osteoclastic markers, osteoblastic markers, and gene expressions of communicating molecules (RANKL, ephrinB2, EphB4, EphA4, Wnt10b) by qPCR, in situ hybridization for Wnt10b, and immunohistochemistry for EphrinB2 and EphA4 proteins to elucidate the bone remodeling process. Furthermore, functional inhibition experiments for the signaling of ephrinB2/Eph, ephrin/EphA4, and Wnt10b using specific antibodies, revealed that these proteins are involved in key signaling pathways promoting normal bone remodeling. Our data suggests that the remodeling process comprises of two successive phases. In the first absorption phase, differentiation of osteoclast progenitors by RANKL is followed by the bone absorption by mature, active osteoclasts, with the simultaneous induction of osteoblast progenitors by multinucleated osteoclast-derived Wnt10b, and proliferation of osteoblast precursors by ehprinB2/EphB4 signaling. Subsequently, during the second formation phase, termination of bone resorption by synergistic cooperation occurs, with downregulation of RANKL expression in activated osteoblasts and Ephrin/EphA4-mediated mutual inhibition between neighboring multinucleated osteoclasts, along with simultaneous activation of osteoblasts via forward and reverse EphrinB2/EphB4 signaling between neighboring osteoblasts. In addition, the present study shows that autologous transplantation of methanol-fixed cell-free scale is an ideal in vivo model to study bone remodeling.

Effects of hyperglycemia on bone metabolism and bone matrix in goldfish scales.

Increased risk of fracture associated with type 2 diabetes has been a topic of recent concern. Fracture risk is related to a decrease in bone strength, which can be affected by bone metabolism and the quality of the bone. To investigate the cause of the increased fracture rate in patients with diabetes through analyses of bone metabolism and bone matrix protein properties, we used goldfish scales as a bone model for hyperglycemia. Using the scales of seven alloxan-treated and seven vehicle-treated control goldfish, we assessed bone metabolism by analyzing the activity of marker enzymes and mRNA expression of marker genes, and we measured the change in molecular weight of scale matrix proteins with SDS-PAGE. After only a 2-week exposure to hyperglycemia, the molecular weight of α- and ß-fractions of bone matrix collagen proteins changed incrementally in the regenerating scales of hyperglycemic goldfish compared with those of euglycemic goldfish. In addition, the relative ratio of the γ-fraction significantly increased, and a δ-fraction appeared after adding glyceraldehyde-a candidate for the formation of advanced glycation end products in diabetes-to isolated type 1 collagen in vitro. The enzymatic activity and mRNA expression of osteoblast and osteoclast markers were not significantly different between hyperglycemic and euglycemic goldfish scales. These results indicate that hyperglycemia is likely to affect bone quality through glycation of matrix collagen from an early stage of hyperglycemia. Therefore, non-enzymatic glycation of collagen fibers in bone matrix may lead to the deterioration of bone quality from the onset of diabetes.