Effect of strain on surface diffusion in semiconductor heteroepitaxy

We present a first-principles analysis of the strain renormalization of the cation diffusivity on the GaAs(001) surface. For the example of In/GaAs(001)-c(4x4) it is shown that the binding of In is increased when the substrate lattice is expanded. The diffusion barrier \Delta E(e) has a non-monotonic strain dependence with a maximum at compressive strain values (e 0) studied. We discuss the consequences of spatial variations of both the binding energy and the diffusion barrier of an adatom caused by the strain field around a heteroepitaxial island. For a simplified geometry, we evaluate the speed of growth of two coherently strained islands on the GaAs(001) surface and identify a growth regime where island sizes tend to equalize during growth due to the strain dependence of surface diffusion.Comment: 10 pages, 8 figures, LaTeX2e, to appear in Phys. Rev. B (2001). Other related publications can be found at http://www.rz-berlin.mpg.de/th/paper.htm

Three-dimensional quantization of the electromagnetic field in dispersive and absorbing inhomogeneous dielectrics

A quantization scheme for the phenomenological Maxwell theory of the full electromagnetic field in an inhomogeneous three-dimensional, dispersive and absorbing dielectric medium is developed. The classical Maxwell equations with spatially varying and Kramers-Kronig consistent permittivity are regarded as operator-valued field equations, introducing additional current- and charge-density operator fields in order to take into account the noise associated with the dissipation in the medium. It is shown that the equal-time commutation relations between the fundamental electromagnetic fields $\hat E$ and $\hat B$ and the potentials $\hat A$ and $\hat \phi$ in the Coulomb gauge can be expressed in terms of the Green tensor of the classical problem. From the Green tensors for bulk material and an inhomogeneous medium consisting of two bulk dielectrics with a common planar interface it is explicitly proven that the well-known equal-time commutation relations of QED are preserved

Spontaneous emission in a planar Fabry-Perot microcavity

Published versio

Sleep and immune function

Sleep and the circadian system exert a strong regulatory influence on immune functions. Investigations of the normal sleep–wake cycle showed that immune parameters like numbers of undifferentiated naïve T cells and the production of pro-inflammatory cytokines exhibit peaks during early nocturnal sleep whereas circulating numbers of immune cells with immediate effector functions, like cytotoxic natural killer cells, as well as anti-inflammatory cytokine activity peak during daytime wakefulness. Although it is difficult to entirely dissect the influence of sleep from that of the circadian rhythm, comparisons of the effects of nocturnal sleep with those of 24-h periods of wakefulness suggest that sleep facilitates the extravasation of T cells and their possible redistribution to lymph nodes. Moreover, such studies revealed a selectively enhancing influence of sleep on cytokines promoting the interaction between antigen presenting cells and T helper cells, like interleukin-12. Sleep on the night after experimental vaccinations against hepatitis A produced a strong and persistent increase in the number of antigen-specific Th cells and antibody titres. Together these findings indicate a specific role of sleep in the formation of immunological memory. This role appears to be associated in particular with the stage of slow wave sleep and the accompanying pro-inflammatory endocrine milieu that is hallmarked by high growth hormone and prolactin levels and low cortisol and catecholamine concentrations

Artificial antigen presenting cells for detection and desensitisation of auto-reactive T cells associated with type 1 diabetes

Autoimmune diseases and in particular type 1 diabetes rely heavily on treatments that target the symptoms rather than prevent the underlying disease. One of the barriers to better therapeutic strategies is the inability to detect and efficiently target rare autoreactive T-cell populations that are major drivers of these conditions. Here, we develop a unique artificial antigen presenting cell (aAPC) system from biocompatible polymer particles that allows specific encapsulation of bioactive ingredients. Using our aAPC we demonstrate that we are able to detect rare autoreactive CD4 populations in human patients and using mouse models we demonstrate that our particles are able to induce desensitization in the autoreactive population. This system provides a promising tool that can be used in the prevention of autoimmunity before disease onset

Artificial antigen presenting cells for detection and desensitisation of auto-reactive T cells associated with Type 1 diabetes

Autoimmune diseases and in particular type 1 diabetes rely heavily on treatments that target the symptoms rather than prevent the underlying disease. One of the barriers to better therapeutic strategies is the inability to detect and efficiently target rare autoreactive T-cell populations that are major drivers of these conditions. Here, we develop a unique artificial antigen-presenting cell (aAPC) system from biocompatible polymer particles that allows specific encapsulation of bioactive ingredients. Using our aAPC, we demonstrate that we are able to detect rare autoreactive CD4 populations in human patients, and using mouse models, we demonstrate that our particles are able to induce desensitization in the autoreactive population. This system provides a promising tool that can be used in the prevention of autoimmunity before disease onset