Magnetic skyrmion moved by the spin-Hall effect is promising for the application of the generation racetrack memories. However, the Magnus force causes a deflected motion of skyrmion, which limits its application. Here, we create an antiferromagnetic skyrmion by injecting a spin-polarized pulse in the nanostripe and investigate the spin Hall effect-induced motion of antiferromagnetic skyrmion by micromagnetic simulations. In contrast to ferromagnetic skyrmion, we find that the antiferromagnetic skyrmion has three evident advantages: (i) the minimum driving current density of antiferromagnetic skyrmion is about two orders smaller than the ferromagnetic skyrmion; (ii) the velocity of the antiferromagnetic skyrmion is about 57 times larger than the ferromagnetic skyrmion driven by the same value of current density; (iii) antiferromagnetic skyrmion can be driven by the spin Hall effect without the influence of Magnus force. In addition, antiferromagnetic skyrmion can move around the pinning sites due to its property of topological protection. Our results present the understanding of antiferromagnetic skyrmion motion driven by the spin Hall effect and may also contribute to the development of antiferromagnetic skyrmion-based racetrack memories.
Abstract-Cytochrome P450 1B1, expressed in vascular smooth muscle cells, can metabolize arachidonic acid in vitro into several products including 12-and 20-hydroxyeicosatetraenoic acids that stimulate vascular smooth muscle cell growth. This study was conducted to determine whether cytochrome P450 1B1 contributes to angiotensin II-induced rat aortic smooth muscle cell migration, proliferation, and protein synthesis. Angiotensin II stimulated migration of these cells, measured by the wound healing approach, by 1. Metabolism of arachidonic acid to 5-, 12-, 15-, and 20-hydoxyeicosatetraenoic acids in these cells was not altered, but angiotensin II-and arachidonic acid-induced reactive oxygen species production and extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase activity were inhibited by 2,4,3Ј,5Ј-tetramethoxystilbene and cytochrome P450 1B1 small hairpin RNA (shRNA) and by Tempol, which inactivates reactive oxygen species. Tempol did not alter cytochrome P450 1B1 activity. These data suggest that angiotensin II-induced vascular smooth muscle cell migration and growth are mediated by reactive oxygen species generated from arachidonic acid by cytochrome P450 1B1 and activation of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase. (Hypertension. 2010;55:1461-1467.) Key Words: angiotensin II Ⅲ CYP1B1 Ⅲ vascular smooth muscle cell growth Ⅲ ROS T he renin-angiotensin system is one of the major components of the mechanisms that contribute to the regulation of blood volume and vascular resistance. 1 Angiotensin II (Ang II), the main biologically active agent of this system, also stimulates vascular smooth muscle cell (VSMC) hypertrophy and/or hyperplasia and inflammation and contributes to the development of hypertension, atherosclerosis, heart failure, and restenosis after vascular injury. [1][2][3][4][5][6] The pathophysiological actions of Ang II are mediated by activation of Ն1 serine-threonine and tyrosine kinase, generation of oxygen radicals, 7-9 and/or release of arachidonic acid (AA) by cytosolic phospholipase A 2 (cPLA 2 ) and production of its metabolites, 12-hydroxyeicosatetraenoic acid (12-HETE) and 20-HETE, generated via lipoxygenase and/or cytochrome P450 (CYP) 4A, respectively. 10 -18 Both 12-and 20-HETE promote VSMC migration, hyperplasia, and/or hypertrophy. 11,19 -22 CYP enzymes that metabolize xenobiotics, including polycyclic aromatic hydrocarbons and endobiotics, such as fatty acids and retinoids, are also expressed in extrahepatic tissues, including the cardiovascular system. 23-27 CYP1A1-encoded enzymes are expressed in vascular endothelium and smooth muscle cells, with much higher levels of activity in endothelial cells, whereas CYP1B1 is highly expressed in VSMCs and, to a lesser degree, in endothelial cells, 28,29 but shear stress upregulates mRNA and protein levels of CYP1A1 and CYP1B1 in endothelial cells. 30 Whether CYP1A1 and CYP1B1 contribute to the vascular function is not known. Recombinant CYP1B1 has been shown to me...
Chiral magnets endowed with topological spin textures are expected to have promising applications in next‐generation magnetic memories. In contrast to the well‐studied 2D or 3D magnetic skyrmions, the authors report the discovery of 1D nontrivial magnetic solitons in a transition metal dichalcogenide 2H‐TaS2 via precise intercalation of Cr elements. In the synthetic Cr1/3TaS2 (CTS) single crystal, the coupling of the strong spin–orbit interaction from TaS2 and the chiral arrangement of the magnetic Cr ions evoke a robust Dzyaloshinskii–Moriya interaction. A magnetic helix having a short spatial period of ≈25 nm is observed in CTS via Lorentz transmission electron microscopy. In a magnetic field perpendicular to the helical axis, the helical spin structure transforms into a chiral soliton lattice (CSL) with the spin structure evolution being consistent with the chiral sine‐Gordon theory, which opens promising perspectives for the application of CSL to fast‐speed nonvolatile magnetic memories. This work introduces a new paradigm to soliton physics and provides an effective strategy for seeking novel 2D magnets.
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