Intrinsic electric polarization in spin-orbit coupled semiconductor heterostructures

We present Maxwell equations with source terms for the electromagnetic field interacting with a moving electron in a spin-orbit coupled semiconductor heterostructure. We start with the eight--band ${\bm k}{\bm p}$ model and derive the electric and magnetic polarization vectors using the Gordon--like decomposition method. Next, we present the ${\bm k}{\bm p}$ effective Lagrangian for the nonparabolic conduction band electrons interacting with electromagnetic field in semiconductor heterostructures with abrupt interfaces. This Lagrangian gives rise to the Maxwell equations with source terms and boundary conditions at heterointerfaces as well as equations for the electron envelope wave function in the external electromagnetic field together with appropriate boundary conditions. As an example, we consider spin--orbit effects caused by the structure inversion asymmetry for the conduction electron states. We compute the intrinsic contribution to the electric polarization of the steady state electron gas in asymmetric quantum well in equilibrium and in the spin Hall regime. We argue that this contribution, as well as the intrinsic spin Hall current, are not cancelled by the elastic scattering processes.Comment: 12 pages, 3 figure

Magneto-gyrotropic effects in semiconductor quantum wells (review)

Magneto-gyrotropic photogalvanic effects in quantum wells are reviewed. We discuss experimental data, results of phenomenological analysis and microscopic models of these effects. The current flow is driven by spin-dependent scattering in low-dimensional structures gyrotropic media resulted in asymmetry of photoexcitation and relaxation processes. Several applications of the effects are also considered.Comment: 28 pages, 13 figure

Depairing currents in the superconductor/ferromagnet proximity system Nb/Fe

We have investigated the behaviour of the depairing current J_{dp} in ferromagnet/superconductor/ferromagnet (F/S/F) trilayers as function of the thickness d_s of the superconducting layers. Theoretically, J_{dp} depends on the superconducting order parameter or the pair density function, which is not homogeneous across the film due to the proximity effect. We use a proximity effect model with two parameters (proximity strength and interface transparency), which can also describe the dependence of the superconducting transition temperature T_c on d_s. We compare the computations with the experimentally determined zero-field critical current J_{c0} of small strips (typically 5~ \mu m wide) of Fe/Nb/Fe trilayers with varying thickness d_{Nb} of the Nb layer. Near T_c the temperature dependence J_{c0}(T) is in good agreement with the expected behaviour, which allows extrapolation to T = 0. Both the absolute values of J_{c0}(0) and the dependence on d_{Nb} agree with the expectations for the depairing current. We conclude that J_{dp} is correctly determined, notwithstanding the fact that the strip width is larger than both the superconducting penetration depth and the superconducting coherence length, and that J_{dp}(d_s) is correctly described by the model.Comment: 10 pages, 5 figures, submitted to PR

Effect of the Surface on the Electron Quantum Size Levels and Electron g-Factor in Spherical Semiconductor Nanocrystals

The structure of the electron quantum size levels in spherical nanocrystals is studied in the framework of an eight--band effective mass model at zero and weak magnetic fields. The effect of the nanocrystal surface is modeled through the boundary condition imposed on the envelope wave function at the surface. We show that the spin--orbit splitting of the valence band leads to the surface--induced spin--orbit splitting of the excited conduction band states and to the additional surface--induced magnetic moment for electrons in bare nanocrystals. This additional magnetic moment manifests itself in a nonzero surface contribution to the linear Zeeman splitting of all quantum size energy levels including the ground 1S electron state. The fitting of the size dependence of the ground state electron g factor in CdSe nanocrystals has allowed us to determine the appropriate surface parameter of the boundary conditions. The structure of the excited electron states is considered in the limits of weak and strong magnetic fields.Comment: 11 pages, 4 figures, submitted to Phys. Rev.

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease

BACKGROUND: Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization. RESULTS: During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events. CONCLUSIONS: Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)