Modulation of domain wall dynamics in TbFeCo single layer nanowire

We demonstrate the possibility to write and modulate the magnetic domain walls in a TbFeCo single layer nanowire (300 nm width, 150 $\mu$m length). To realize this, a tiny magnetic domain was nucleated by an Oersted field produced by a 1.6 MHz pulse current (35 mA in amplitude, 5-40 ns in length) crossed the wire. To write the wall to the wire, a DC current was used to drive the nucleated domain (with two walls in two sides) to the wire in accordance with spin-transfer torque mechanism. A critical current density of $J_c = 3.5\times10^{10} Am^{-2}$ was required to control the motion of the walls in the wire. It was found that the size of the domain moving in the wire could be adjusted by either external field or the length of the nucleated pulse current. This could be considered as an important note for writing process in domain wall spin-torque devices, especially, memory elements.Comment: 14 pages, 5 figure

Categorization of 77 dystrophin exons into 5 groups by a decision tree using indexes of splicing regulatory factors as decision markers

<p>Abstract</p> <p>Background</p> <p>Duchenne muscular dystrophy, a fatal muscle-wasting disease, is characterized by dystrophin deficiency caused by mutations in the <it>dystrophin </it>gene. Skipping of a target <it>dystrophin </it>exon during splicing with antisense oligonucleotides is attracting much attention as the most plausible way to express dystrophin in DMD. Antisense oligonucleotides have been designed against splicing regulatory sequences such as splicing enhancer sequences of target exons. Recently, we reported that a chemical kinase inhibitor specifically enhances the skipping of mutated <it>dystrophin </it>exon 31, indicating the existence of exon-specific splicing regulatory systems. However, the basis for such individual regulatory systems is largely unknown. Here, we categorized the <it>dystrophin </it>exons in terms of their splicing regulatory factors.</p> <p>Results</p> <p>Using a computer-based machine learning system, we first constructed a decision tree separating 77 authentic from 14 known cryptic exons using 25 indexes of splicing regulatory factors as decision markers. We evaluated the classification accuracy of a novel cryptic exon (exon 11a) identified in this study. However, the tree mislabeled exon 11a as a true exon. Therefore, we re-constructed the decision tree to separate all 15 cryptic exons. The revised decision tree categorized the 77 authentic exons into five groups. Furthermore, all nine disease-associated novel exons were successfully categorized as exons, validating the decision tree. One group, consisting of 30 exons, was characterized by a high density of exonic splicing enhancer sequences. This suggests that AOs targeting splicing enhancer sequences would efficiently induce skipping of exons belonging to this group.</p> <p>Conclusions</p> <p>The decision tree categorized the 77 authentic exons into five groups. Our classification may help to establish the strategy for exon skipping therapy for Duchenne muscular dystrophy.</p

Mirror-symmetric Magneto-optical Kerr Rotation using Visible Light in [(GeTe)2(Sb2Te3)1]n Topological Superlattices

Interfacial phase change memory (iPCM), that has a structure of a superlattice made of alternating atomically thin GeTe and Sb2Te3 layers, has recently attracted attention not only due to its superior performance compared to the alloy of the same average composition in terms of energy consumption but also due to its strong response to an external magnetic field (giant magnetoresistance) that has been speculated to arise from switching between topological insulator (RESET) and normal insulator (SET) phases. Here we report magneto-optical Kerr rotation loops in the visible range, that have mirror symmetric resonances with respect to the magnetic field polarity at temperatures above 380 K when the material is in the SET phase that has Kramers-pairs in spin-split bands. We further found that this threshold temperature may be controlled if the sample was cooled in a magnetic field. The observed results open new possibilities for use of iPCM beyond phase-change memory applications

Muscle and Heart Function Restoration in a Limb Girdle Muscular Dystrophy 2I (LGMD2I) Mouse Model by Systemic FKRP Gene Delivery

Mutations in fukutin-related protein (FKRP) gene cause a wide spectrum of disease phenotypes including the mild limb-girdle muscular dystrophy 2I (LGMD2I), the severe Walker-Warburg syndrome, and muscle-eye-brain disease. FKRP deficiency results in α-dystroglycan (α-DG) hypoglycosylation in the muscle and heart, which is a biochemical hallmark of dystroglycanopathies. To study gene replacement therapy, we generated and characterized a new mouse model of LGMD2I harboring the human mutation leucine 276 to isoleucine (L276I) in the mouse alleles. The homozygous knock-in mice (L276IKI) mimic the classic late onset phenotype of LGMD2I in both skeletal and cardiac muscles. Systemic delivery of human FKRP gene by AAV9 vector in the L276IKI mice, at either neonatal age or at the age of 9 months, rendered body wide FKRP expression and restored glycosylation of α-DG in both skeletal and cardiac muscles. FKRP gene therapy ameliorated dystrophic pathology and cardiomyopathy such as muscle degeneration, fibrosis, and myofiber membrane leakage, resulting in restoration of muscle and heart contractile functions. Thus, these results demonstrated that the treatment based on FKRP gene replacement was effective