We theoretically investigate the dephasing of a central spin-1 model. An interesting mechanism of spin decoherence is found with this model, namely, hyperfine mediated spectral diffusion. This mechanism contains the features of both the dipolar-interactions-induced spectral diffusion and the hyperfine mediated interactions. We also find an anomalous magnetic field dependence of decoherence, which is caused by the competition between crystal field splitting and Zeeman splitting of the central spin. As the external magnetic field increases, in the V type level structure regime, the decoherence rate becomes much stronger; while in the cascade type level structure regime, just like localized electron spin in quantum dots, the decoherence rate becomes much weaker.
We theoretically study the interplay of spin-orbit and hyperfine interactions in dynamical nuclear polarization in two-electron semiconductor double quantum dots near the singlet-triplet ($S\ensuremath{-}{T}_{+}$) anticrossing. The goal of the scheme under study is to extend the singlet-triplet ($S\ensuremath{-}{T}_{0}$) qubit decoherence time
T2∗ by dynamically transferring the polarization from the electron spins to the nuclear spins. This polarization transfer is achieved by cycling the electron spins over the $S\ensuremath{-}{T}_{+}$ anticrossing. Here, we investigate, both quantitatively and qualitatively, how this hyperfine-mediated dynamical polarization transfer is influenced by the Rashba and Dresselhaus spin-orbit interaction. In addition to
T2∗, we determine the singlet return probability
Ps, a quantity that can be measured in experiments. Our results suggest that the spin-orbit interaction establishes a mechanism that can polarize the nuclear spins in the direction opposite to that of hyperfine-mediated nuclear spin polarization. In materials with relatively strong spin-orbit coupling, this interplay of spin-orbit and hyperfine-mediated nuclear spin polarizations prevents any notable increase in the $S\ensuremath{-}{T}_{0}$ qubit decoherence time
T2∗.