Mesoscovic magnetic/semiconductor heterostructures

We report the experimental results of Fe and Fe3O4 nanostructures on GaAs(100) surfaces and hybrid Ferromagnetic/Semiconductor/Ferromagnetic (FM/SC/FM) spintronic devices. Element specific x-ray magnetic circular dichroism (XMCD) measurements have shown directly that Fe atoms on the GaAs(100)-4 x 6 surface are ferromagnetic. Within coverages of 2.5 to 4.8 ML superparamagnetic nanoclusters are formed and exhibiting strong uniaxial anisotropy, of the order of 6.0 x 10(5) erg/cm(3). The coercivities of epitaxial Fe dot arrays films grown on GaAs(100) were observed to be dependent on the separation and size of the dots indicating that interdot dipolar coupling affects the magnetization processes in these dots. In addition Fe3O4 films grown on deformed GaAs(100) substrates have been observed to form nanostripes following the topography of the substrate and magneto-optical Kerr effect (MOKE) measurements showed that these nanostripes have uniaxial magnetic anisotropy with easy axis perpendicular to the length of the nanostripes. Meanwhile the FM/SC/FM vertical device has exhibited a biasing current dependent on MR characteristics, with a maximum change of 12% in the MR observed, indicating for the first time a large room temperature spin injection and detection

Loss-of-Function and Gain-of-Function Mutations in KCNQ5 Cause Intellectual Disability or Epileptic Encephalopathy

KCNQ5 is a highly conserved gene encoding an important channel for neuronal function; it is widely expressed in the brain and generates M-type current. Exome sequencing identified de novo heterozygous missense mutations in four probands with intellectual disability, abnormal neurological findings, and treatment-resistant epilepsy (in two of four). Comprehensive analysis of this potassium channel for the four variants expressed in frog oocytes revealed shifts in the voltage dependence of activation, including altered activation and deactivation kinetics. Specifically, both loss-of-function and gain-of-function KCNQ5 mutations, associated with increased excitability and decreased repolarization reserve, lead to pathophysiology

Loss-of-Function and Gain-of-Function Mutations in KCNQ5 Cause Intellectual Disability or Epileptic Encephalopathy

KCNQ5 is a highly conserved gene encoding an important channel for neuronal function; it is widely expressed in the brain and generates M-type current. Exome sequencing identified de novo heterozygous missense mutations in four probands with intellectual disability, abnormal neurological findings, and treatment-resistant epilepsy (in two of four). Comprehensive analysis of this potassium channel for the four variants expressed in frog oocytes revealed shifts in the voltage dependence of activation, including altered activation and deactivation kinetics. Specifically, both loss-of-function and gain-of-function KCNQ5 mutations, associated with increased excitability and decreased repolarization reserve, lead to pathophysiology