Spin-Hall effect in semiconductor heterostructures with cubic Rashba spin-orbit interaction

We study the spin-Hall effect in systems with weak cubic Rashba spin-orbit interaction. To this end we derive particle and spin diffusion equations and explicit expressions for the spin-current tensor in the diffusive regime. We discuss the impact of electric fields on the Green's functions and the diffusion equations and establish a relationship between the spin-current tensor and the spin diffusion equations for the model under scrutiny. We use our results to calculate the edge spin-accumulation in a spin-Hall experiment and show that there is also a new Hall-like contribution to the electric current in such systems.Comment: 14 page

On boundary conditions for spin diffusion equations with Rashba spin-orbit interaction

We reexamine the boundary conditions of spin diffusion equations for dirty semiconductor heterostructures with weak linear Rashba spin-orbit interaction. Doing so, we focus on the influence of tangent derivatives of the particle density at the boundary on the magnetization. Such derivatives are associated with a spin accumulation in the presence of a density gradient. We show that the tangent derivatives enter the boundary conditions and argue that the spin-Hall effect is absent in such systems because of this fact.Comment: 7 page

On the relevance of PS exposure as a regulatory event forADAM10-mediated substrate release

The “a disintegrin and metalloproteinase 10” (ADAM10) shedding activity is vital for several physiological and pathophysiological processes. Although ADAM10 activity in these processes is comprehensively described, little is known about the mechanism controlling the protease shedding activity. As a transmembrane protease, the plasma membrane itself may play an essential role in the regulation of ADAM10 shedding activity. Phosphatidylserine (PS) exposure was shown before to be the major regulatory mechanism of ADAM17 shedding activity, the structural and functional closest relative to ADAM10. In a series of experiments with different cell types, the headgroup of phosphatidylserine (OPS) showed a competitive inhibitory effect on ADAM10-mediated substrate release, presumably by abolishing ADAM10 interaction with PS. This inhibitory effect of OPS on ADAM10-mediated substrate release was shown for multiple ADAM10 substrates and stimuli, indicating that PS exposure is in general essential for ADAM10-mediated substrate release. Overexpression of phospholipid scramblase TMEM16F/ANO6 contributed to PS exposure and led to enhanced ADAM10-mediated substrate release. Hyperactive TMEM16F/ANO6 mutant (human ANO6 D408G) showed enhanced PS exposure in conjunction with increased ADAM10-mediated substrate release, without any stimulation. B-cells from a patient with the Scott syndrome showed TMEM16F/ANO6-related impaired PS scrambling, resulting in the absence of ADAM10 shedding activity. Furthermore, biophysical experiments with a peptide version of the ADAM10 stalk domain indicated a direct interaction of ADAM10 with PS. The mutation of the positively charged amino acids in the stalk domain of ADAM10 significantly reduced the ability of the proteases to release its substrate betacellulin. These results highlight the importance of the positively charged amino acids in the ADAM10 stalk domain for the interaction with PS and substrate shedding

Theory of spin-Hall transport of heavy holes in semiconductor quantum wells

Based on a proper definition of the spin current, we investigate the spin-Hall effect of heavy holes in narrow quantum wells in the presence of Rashba spin-orbit coupling by using a spin-density matrix approach. In contrast to previous results obtained on the basis of the conventional definition of the spin current, we arrive at the conclusion that an electric-field-induced steady-state spin-Hall current does not exist in both, pure and disordered infinite samples. Only an ac field can induce a spin-Hall effect in such systems.Comment: 6 pages, submitted to J. Phys.: Condens. Matte

Current-induced spin polarization and the spin Hall effect: a quasiclassical approach

The quasiclassical Green function formalism is used to describe charge and spin dynamics in the presence of spin-orbit coupling. We review the results obtained for the spin Hall effect on restricted geometries. The role of boundaries is discussed in the framework of spin diffusion equations.Comment: 10 pages, 5 figures, Submitted to Solid State Communications Special Issue on "Fundamental Phenomena in Low Dimensional Electron Systems". Special Issue Editors: Marco Polini, Michele Governale, Hermann Grabert, Vittorio Pellegrini, and Mario Tos

On dispersive energy transport and relaxation in the hopping regime

A new method for investigating relaxation phenomena for charge carriers hopping between localized tail states has been developed. It allows us to consider both charge and energy {\it dispersive} transport. The method is based on the idea of quasi-elasticity: the typical energy loss during a hop is much less than all other characteristic energies. We have investigated two models with different density of states energy dependencies with our method. In general, we have found that the motion of a packet in energy space is affected by two competing tendencies. First, there is a packet broadening, i.e. the dispersive energy transport. Second, there is a narrowing of the packet, if the density of states is depleting with decreasing energy. It is the interplay of these two tendencies that determines the overall evolution. If the density of states is constant, only broadening exists. In this case a packet in energy space evolves into Gaussian one, moving with constant drift velocity and mean square deviation increasing linearly in time. If the density of states depletes exponentially with decreasing energy, the motion of the packet tremendously slows down with time. For large times the mean square deviation of the packet becomes constant, so that the motion of the packet is ``soliton-like''.Comment: 26 pages, RevTeX, 10 EPS figures, submitted to Phys. Rev.

On the structure of the energy distribution function in the hopping regime

The impact of the dispersion of the transport coefficients on the structure of the energy distribution function for charge carriers far from equilibrium has been investigated in effective-medium approximation for model densities of states. The investigations show that two regimes can be observed in energy relaxation processes. Below a characteristic temperature the structure of the energy distribution function is determined by the dispersion of the transport coefficients. Thermal energy diffusion is irrelevant in this regime. Above the characteristic temperature the structure of the energy distribution function is determined by energy diffusion. The characteristic temperature depends on the degree of disorder and increases with increasing disorder. Explicit expressions for the energy distribution function in both regimes are derived for a constant and an exponential density of states.Comment: 16 page

Combined Knockout of RIPK3 and MLKL Reveals Unexpected Outcome in Tissue Injury and Inflammation

Necroptosis, initially identified as a backup cell death program when apoptosis is hindered, is a prominent feature in the etiology and progression of many human diseases, such as ischemic injury and sepsis. Receptor-interacting protein kinase 3 (RIPK3) is the cardinal regulator of this cell death modality, recruiting and phosphorylating the executioner mixed lineage kinase domain-like protein (MLKL) to signal necroptosis, which is terminated by a cellular plasma membrane rupture and the leakage of intracellular contents from dying cells. Experimental data to date indicate that RIPK3 and MLKL is the core machinery essential for all necroptotic cell death responses. By using CRISPR/Cas9 (clustered regularly interspaced short palindromic repeat/CRISPR-associated protein 9) technology, we showed that Ripk3 and Mlkl knockout and Ripk3/Mlkl double-knockout in necroptosis-sensitive cell lines extensively block susceptibility to necroptosis, in each case to an indistinguishable degree. In vivo studies using Ripk3- or Mlkl-deficient mice validated kidney ischemia reperfusion injury and high-dose tumor necrosis factor (TNF) availability, as druggable targets in necroptotic-mediated pathologies. Here, we demonstrated that Ripk3 or Mlkl-deficient mice are protected to a similar extent from kidney ischemia reperfusion injury and TNF-induced toxicity. Remarkably, in contrast to each single knockout, Ripk3/Mlkl double-deficient mice did not have appreciable protection from either of the above necroptotic-mediated pathologies. Paradoxically, the double-knockout mice resembled, in each case, the vulnerable wild-type mice, revealing novel complexities in the mechanisms of inflammation-driven diseases, due to aberrant cell death