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Spin dephasing via the spin-orbit interaction (SOI) is a major mechanism limiting the electron spin lifetime in III-V zincblende quantum wells. The dephasing can be suppressed in GaAs(111) quantum wells by applying an electric field. The suppression has been attributed to the compensation of the intrinsic SOI associated by the bulk inversion asymmetry (BIA) of the GaAs lattice by a structural induced asymmetry (SIA) SOI term induced by an electric field. We provide direct experimental evidence for this mechanism by demonstrating the transition between the BIA-dominated to a SIA-dominated regime via photoluminescence measurements carried out over a wide range of applied fields. Spin lifetimes exceeding 100~ns are obtained near the compensating electric field, thus making GaAs (111) QWs excellent candidates for the electrical storage and manipulation of spins.
We present a microscopic theory for transport of the spin polarized charge density wave with both electrons and holes in the $(111)$ GaAs quantum wells. We analytically show that, contradicting to the commonly accepted belief, the spin and charge mot
We show by spatially and time-resolved photoluminescence that the application of an electric field transverse to the plane of an intrinsic GaAs (111) quantum well (QW) allows the transport of photogenerated electron spins polarized along the directio
Photoluminescence (PL) and reflectivity spectra of a high-quality InGaAs/GaAs quantum well structure reveal a series of ultra-narrow peaks attributed to the quantum confined exciton states. The intensity of these peaks decreases as a function of temp
The electron spin dynamics in (111)-oriented GaAs/AlGaAs quantum wells is studied by timeresolved photoluminescence spectroscopy. By applying an external field of 50 kV/cm a two-order of magnitude increase of the spin relaxation time can be observed
(111) Silicon quantum wells have been studied extensively, yet no convincing explanation exists for the experimentally observed breaking of 6 fold valley degeneracy into 2 and 4 fold degeneracies. Here, systematic sp3d5s* tight-binding and effective