Modulating Exchange Bias, Anisotropic Magnetoresistance, and Planar Hall Resistance of Flexible Co/MnN Epitaxial Bilayers on Mica by Bending Strain.

The integration of ferromagnetic/antiferromagnetic bilayers with exchange bias effect on flexible substrates is crucial for flexible spintronics. Here, the epitaxial Co/MnN bilayers are deposited on mica by facing-target sputtering. A large in-plane exchange bias field (HEB) of 1800 Oe with a coercive field (HC) of 2750 Oe appears in the Co (3.8 nm)/MnN (15.0 nm) bilayer at 5 K after field cooling from 300 to 5 K. Effective interfacial exchange energy Jeff of the Co/MnN bilayer is 0.83 erg/cm2. The strain-induced maximum increase of HEB and HC reaches 18% and 21%, respectively, in the Co(3.8 nm)/MnN(15.0 nm) bilayer. Strain-modulated HEB is attributed to the change of interfacial exchange coupling between Co and MnN layers. HEB is inversely proportional to Co thickness but independent of MnN thickness. The change of HEB is less than 5% after 100 bending cycles, indicating mechanical durability. The out-of-plane exchange bias also appears since Co spins are not fully reversed due to the strong pinning effect. Anisotropic magnetoresistance (AMR) and planar Hall resistance (Rxy) show obvious hysteresis due to HEB. Exchange bias-induced phase difference of AMR and Rxy almost remains unchanged at different bending strains. The results provide the basis for understanding the bending strain tailored exchange bias.

Partial loss of psychiatric risk gene Mir137 in mice causes repetitive behavior and impairs sociability and learning via increased Pde10a.

Genetic analyses have linked microRNA-137 (MIR137) to neuropsychiatric disorders, including schizophrenia and autism spectrum disorder. miR-137 plays important roles in neurogenesis and neuronal maturation, but the impact of miR-137 loss-of-function in vivo remains unclear. Here we show the complete loss of miR-137 in the mouse germline knockout or nervous system knockout (cKO) leads to postnatal lethality, while heterozygous germline knockout and cKO mice remain viable. Partial loss of miR-137 in heterozygous cKO mice results in dysregulated synaptic plasticity, repetitive behavior, and impaired learning and social behavior. Transcriptomic and proteomic analyses revealed that the miR-137 mRNA target, phosphodiesterase 10a (Pde10a), is elevated in heterozygous knockout mice. Treatment with the Pde10a inhibitor papaverine or knockdown of Pde10a ameliorates the deficits observed in the heterozygous cKO mice. Collectively, our results suggest that MIR137 plays essential roles in postnatal neurodevelopment and that dysregulation of miR-137 potentially contributes to neuropsychiatric disorders in humans.