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1.
Nat Nanotechnol ; 14(7): 691-697, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31011219

RESUMO

Spin waves may constitute key components of low-power spintronic devices. Antiferromagnetic-type spin waves are innately high-speed, stable and dual-polarized. So far, it has remained challenging to excite and manipulate antiferromagnetic-type propagating spin waves. Here, we investigate spin waves in periodic 100-nm-wide stripe domains with alternating upward and downward magnetization in La0.67Sr0.33MnO3 thin films. In addition to ordinary low-frequency modes, a high-frequency mode around 10 GHz is observed and propagates along the stripe domains with a spin-wave dispersion different from the low-frequency mode. Based on a theoretical model that considers two oppositely oriented coupled domains, this high-frequency mode is accounted for as an effective antiferromagnetic spin-wave mode. The spin waves exhibit group velocities of 2.6 km s-1 and propagate even at zero magnetic bias field. An electric current pulse with a density of only 105 A cm-2 can controllably modify the orientation of the stripe domains, which opens up perspectives for reconfigurable magnonic devices.

2.
Oncol Rep ; 34(2): 755-62, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-26062728

RESUMO

Multidrug resistance (MDR) remains a formidable challenge in the use of chemotherapy and represents a powerful obstacle to the treatment of leukemia. ATP-binding cassette subfamily B member 1 (ABCB1) is a recognized factor which causes MDR and is closely related to poor outcome and relapse in leukemia. Ongoing research concerning the strategy for inhibiting the abnormally high activity of the ABCB1 transporter is critically needed. In the present study, we sought to elucidate the interaction between ABCB1 transporter and butorphanol. Our results showed that butorphanol significantly antagonized ABCB1-mediated drug efflux and increased the intracellular drug concentration by inhibiting the transport activity of ABCB1 in leukemia cells. Mechanistic investigations demonstrated that butorphanol did not alter the protein expression or localization of ABCB1 in HL60/VCR and K562/ADR cells. Furthermore, homology modeling indicated that butorphanol could fit into the large drug-binding cavity of ABCB1 and form a binding conformation. In conclusion, butorphanol reversed the ABCB1-mediated MDR in leukemia cells by directly suppressing the efflux activity of ABCB1.


Assuntos
Butorfanol/administração & dosagem , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Leucemia/tratamento farmacológico , Subfamília B de Transportador de Cassetes de Ligação de ATP/antagonistas & inibidores , Subfamília B de Transportador de Cassetes de Ligação de ATP/genética , Antineoplásicos/administração & dosagem , Linhagem Celular Tumoral , Doxorrubicina/administração & dosagem , Resistência a Múltiplos Medicamentos/genética , Humanos , Leucemia/genética , Leucemia/patologia , Proteínas de Neoplasias/biossíntese , Paclitaxel/administração & dosagem
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