Let $\def \xmlpi #1{}\def \mathsfbi #1{\boldsymbol {\mathsf {#1}}}\let \le =\leqslant \let \leq =\leqslant \let \ge =\geqslant \let \geq =\geqslant \def \Pr {\mathit {Pr}}\def \Fr {\mathit {Fr}}\def \Rey {\mathit {Re}}R$ be a semiprime ring with extended centroid $C$ and with maximal right ring of quotients $Q_{mr}(R)$. Let $d{:}\ R\to Q_{mr}(R)$ be an additive map and $b\in Q_{mr}(R)$. An additive map $\delta {:}\ R\to Q_{mr}(R)$ is called a (left) $b$-generalized derivation with associated map $d$ if $\delta (xy)=\delta (x)y+bxd(y)$ for all $x, y\in R$. This gives a unified viewpoint of derivations, generalized derivations and generalized $\sigma $-derivations with an X-inner automorphism $\sigma $. We give a complete characterization of $b$-generalized derivations of $R$ having nilpotent values of bounded index. This extends several known results in the literature.

The Gemini Planet Image (GPI) is a new, high-contrast, exoplanet-imaging, facility instrument for the Gemini South observatory, scheduled to begin science observations in 2014. The GPI Exoplanet Survey (GPIES) has been awarded 890 hours to image and spectrally and polarimetrically characterize young, giant planets within 100 parsecs of the solar system. In preparation for the survey, we have developed a framework for simulating GPI observations and generating end-to-end survey simulations. We present new extensions to this modeling effort and our latest results. We discuss systematic methods for scheduling the survey to ensure that the population of discovered planets is useful in constraining formation models and possibly distinguishing between gravitational collapse and core accretion as the primary formation mechanism.

The experimental studies of Brucei group trypanosomes presented here demonstrate that the balance of host and parasite factors, especially IFN-γ GPI-sVSG respectively, and the timing of cellular exposure to them, dictate the predominant MP and DC activation profiles present at any given time during infection and within specific tissues. The timing of changes in innate immune cell functions following infection consistently support the conclusion that the key events controlling host resistance occur within a short time following initial exposure to the parasite GPI substituents. Once the changes in MP and DC activities are initiated, there appears little that the host can do to reverse these changes and alter the final outcome of these regulatory events. Instead, despite the availability of multiple innate and adaptive immune mechanisms that can control parasites, there is an inability to control trypanosome numbers sufficiently to prevent the emergence and establishment of virulent trypanosomes that eventually kill the host. Overall it appears that trypanosomes have carefully orchestrated the host innate and adaptive immune response so that parasite survival and transmission, and alterations of host immunity, are to its ultimate benefit.

The glycosylphosphatidylinositol (GPI) anchor of Plasmodium falciparum is thought to function as a critical toxin that contributes to severe malarial pathogenesis by eliciting the production of proinflammatory responses by the innate immune system of mammalian hosts. Analysis of the fine structure of P. falciparum GPI suggests a requirement for the presence of both core glycan and lipid moieties in the recognition and signalling of parasite glycolipids by host immune cells. It has been demonstrated that GPI anchors of various parasitic protozoa can mediate cellular immune responses via members of the Toll-like family of pattern recognition receptors (TLRs). Recent studies indicate that GPI anchors of P. falciparum and other protozoa are preferentially recognized by TLR-2, involving the MyD88-dependent activation of specific signalling pathways that mediate the production of proinflammatory cytokines and nitric oxide from host macrophages in vitro. However, the contribution of malaria GPI toxin to severe disease syndromes and the role of specific TLRs or other pattern recognition receptors in innate immunity in vivo is only just beginning to be characterized. A better understanding of the molecular mechanisms underlying severe malarial pathogenesis may yet lead to substantial new insights with important implications for the development of novel therapeutics for malaria treatment.

Let K be a commutative ring with unity, R a prime K-algebra of characteristic different from 2, d and δ non-zero derivations of R, f (x1,…, xn) a multilinear polynomial over K.If

then f(x1,…,xnis central-valued on R.