Although both theoretical predictions and experimental observations have demonstrated that the Gilbert damping is anisotropic at ferromagnet/semiconductor interface possessing robust interfacial spin-orbit coupling, it is not well understood whether non-local Gilbert damping driven by spin pumping in heavy metal/ferromagnetic metallic bilayers is anisotropic or not. Here, we investigated the angular and frequency dependence of magnetic relaxation in epitaxial Pd/Fe films on MgO(001) substrates. After disentangling parasitic contributions, we unambiguously observe that the non-local Gilbert damping is isotropic in the Fe(001) plane, suggesting that the spin transport across the Pd/Fe interface is independent of the Fe magnetization orientation. First principles calculations reveal that the effective spin mixing conductance of the Pd/Fe interface is nearly invariant for different magnetization directions, in good agreement with the experimental observations. These results offer valuable insight into spin transport in metallic bilayers, and facilitate the development of nextgeneration spintronic devices.
ABSTRACT.We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferatoractivated receptor gamma (PPARg)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARg activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARg and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARg mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARg mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARg mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARg/AKT signaling pathway.
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