Entanglement witnesses and geometry of entanglement of two--qutrit states

We construct entanglement witnesses with regard to the geometric structure of the Hilbert--Schmidt space and investigate the geometry of entanglement. In particular, for a two--parameter family of two--qutrit states that are part of the magic simplex we calculate the Hilbert--Schmidt measure of entanglement. We present a method to detect bound entanglement which is illustrated for a three--parameter family of states. In this way we discover new regions of bound entangled states. Furthermore we outline how to use our method to distinguish entangled from separable states.Comment: 23 pages, 8 figure

Evaluation of Measurement Performance in Averaging Quantization System with Noise

Statistical description of quantization process is common in the theory of quantization. For the case of nonsubtractive dither theoretical analyses of the dithered quantizer have been confronted with experimental results. As a quantization system one-chip microcomputer with the analog-to-digital converter on a chip has been used. Generally valid criteria for dithered system performance have been practically applied for Gaussian dither. Interaction of natural noise present in the signal with an added Gaussian noise of several different disperses and influence of differential nonlinearity of the converter has been observed

Bowen-York Tensors

There is derived, for a conformally flat three-space, a family of linear second-order partial differential operators which send vectors into tracefree, symmetric two-tensors. These maps, which are parametrized by conformal Killing vectors on the three-space, are such that the divergence of the resulting tensor field depends only on the divergence of the original vector field. In particular these maps send source-free electric fields into TT-tensors. Moreover, if the original vector field is the Coulomb field on $\mathbb{R}^3\backslash \lbrace0\rbrace$, the resulting tensor fields on $\mathbb{R}^3\backslash \lbrace0\rbrace$ are nothing but the family of TT-tensors originally written down by Bowen and York.Comment: 12 pages, Contribution to CQG Special Issue "A Spacetime Safari: Essays in Honour of Vincent Moncrief

Interferon γ and lymphotoxin or tumor necrosis factor act synergistically to induce macrophage killing of tumor cells and schistosomula of schistosoma mansoni

Macrophages play a crucial role in the defense against tumors and parasites. Activation of tumoricidal and microbicidal effector mechanisms requires stimulation of macrophages with macrophage-activating factors (MAF). One such MAF is interferon γ (IFN-γ). In some assays, substantial activity of IFN-γ on murine macrophages, however, is only observed in synergy with lipopolysaccharide (LPS) or other cytokines (1). In addition, certain cytokines have been shown to induce monocyte or macrophage activation in the absence of IFN-γ (2-5). We previously described lymphokines in the supernatant of a murine T cell clone that synergized with IFN-γ in the induction of tumoricidal and schistosomulicidal murine macrophages (1). We called this lymphokine(s) macrophage cytotoxicityinducing factor 2 (MCIF2)(1). A candidate for MCIF2 was lymphotoxin (LT), because the T cell clone supernatant contained high amounts of LT. LT is functionally homologous and structurally related to the macrophage product tumor necrosis factor (TNF). Therefore, we tested whether recombinant (r) LT or rTNF can function as MAF. We report here that rLT or rTNF synergize with rIFN-γ in the induction of tumoricidal and schistosomulicidal murine macrophages

Evaluation of Muscat types and clones for the local market

Ten European clones and selections of 'Muscat blanc' were investigated about their variability in genetic and enological behavior. The SSR profile of about 120 loci allowed to differentiate most of them. Nevertheless the differences within the variety are rare and do not reflect the heterogeneity of  observed variability. One of the clones (B41/5) represents an earlier ripening type where the overall quality was independent from sugar content. A 27-1 clone was one of the clones with steady high rating concerning wine quality. An interesting alternative for early ripening areas could be the late ripening 'Goldmuskateller' due to the higher stability against Botrytis. One of the samples was not true to type and represented this cultivar

Influenza virus differentially activates mTORC1 and mTORC2 signaling to maximize late stage replication

<div><p>Influenza A virus usurps host signaling factors to regulate its replication. One example is mTOR, a cellular regulator of protein synthesis, growth and motility. While the role of mTORC1 in viral infection has been studied, the mechanisms that induce mTORC1 activation and the substrates regulated by mTORC1 during influenza virus infection have not been established. In addition, the role of mTORC2 during influenza virus infection remains unknown. Here we show that mTORC2 and PDPK1 differentially phosphorylate AKT upon influenza virus infection. PDPK1-mediated phoshorylation of AKT at a distinct site is required for mTORC1 activation by influenza virus. On the other hand, the viral NS1 protein promotes phosphorylation of AKT at a different site via mTORC2, which is an activity dispensable for mTORC1 stimulation but known to regulate apoptosis. Influenza virus HA protein and down-regulation of the mTORC1 inhibitor REDD1 by the virus M2 protein promote mTORC1 activity. Systematic phosphoproteomics analysis performed in cells lacking the mTORC2 component Rictor in the absence or presence of Torin, an inhibitor of both mTORC1 and mTORC2, revealed mTORC1-dependent substrates regulated during infection. Members of pathways that regulate mTORC1 or are regulated by mTORC1 were identified, including constituents of the translation machinery that once activated can promote translation. mTORC1 activation supports viral protein expression and replication. As mTORC1 activation is optimal midway through the virus life cycle, the observed effects on viral protein expression likely support the late stages of influenza virus replication when infected cells undergo significant stress.</p></div