Two \u3ci\u3eEntomophthora\u3c/i\u3e Species Associated with Disease Epizootics of the Alfalfa Weevil, \u3ci\u3eHypera Postica\u3c/i\u3e (Coleoptera: Curculionidae), in Ontario

Recent studies have shown that disease epizootics in Ontario populations of the alfalfa weevil, Hypera postica (Gyllenhal), are caused by a complex of two fungi

A Cellular Automata Model with Probability Infection and Spatial Dispersion

In this article, we have proposed an epidemic model by using probability cellular automata theory. The essential mathematical features are analyzed with the help of stability theory. We have given an alternative modelling approach for the spatiotemporal system which is more realistic and satisfactory from the practical point of view. A discrete and spatiotemporal approach are shown by using cellular automata theory. It is interesting to note that both size of the endemic equilibrium and density of the individual increase with the increasing of the neighborhood size and infection rate, but the infections decrease with the increasing of the recovery rate. The stability of the system around the positive interior equilibrium have been shown by using suitable Lyapunov function. Finally experimental data simulation for SARS disease in China and a brief discussion conclude the paper

Syndromic surveillance to assess the potential public health impact of the Icelandic volcanic ash plume across the United Kingdom, April 2010

The Eyjafjallajökull volcano in Iceland erupted on 14 April 2010 emitting a volcanic ash plume that spread across the United Kingdom and mainland Europe. The Health Protection Agency and Health Protection Scotland used existing syndromic surveillance systems to monitor community health during the incident: there were no particularly unusual increases in any of the monitored conditions. This incident has again demonstrated the use of syndromic surveillance systems for monitoring community health in real time

The Leishmania donovani Ortholog of the Glycosylphosphatidylinositol Anchor Biosynthesis Cofactor PBN1 Is Essential for Host Infection

Visceral leishmaniasis is a deadly infectious disease caused by Leishmania donovani, a kinetoplastid parasite for which no licensed vaccine is available. To identify potential vaccine candidates, we systematically identified genes encoding putative cell surface and secreted proteins essential for parasite viability and host infection. We identified a protein encoded by LdBPK_061160 which, when ablated, resulted in a remarkable increase in parasite adhesion to tissue culture flasks. Here, we show that this phenotype is caused by the loss of glycosylphosphatidylinositol (GPI)-anchored surface molecules and that LdBPK_061160 encodes a noncatalytic component of the L. donovani GPI-mannosyltransferase I (GPI-MT I) complex. GPI-anchored surface molecules were rescued in the LdBPK_061160 mutant by the ectopic expression of both human genes PIG-X and PIG-M, but neither gene could complement the phenotype alone. From further sequence comparisons, we conclude that LdBPK_061160 is the functional orthologue of yeast PBN1 and mammalian PIG-X, which encode the noncatalytic subunits of their respective GPI-MT I complexes, and we assign LdBPK_061160 as LdPBN1. The LdPBN1 mutants could not establish a visceral infection in mice, a phenotype that was rescued by constitutive expression of LdPBN1. Although mice infected with the null mutant did not develop an infection, exposure to these parasites provided significant protection against subsequent infection with a virulent strain. In summary, we have identified the orthologue of the PBN1/PIG-X noncatalytic subunit of GPI-MT I in trypanosomatids, shown that it is essential for infection in a murine model of visceral leishmaniasis, and demonstrated that the LdPBN1 mutant shows promise for the development of an attenuated live vaccine

Software performance estimation strategies in a system-level design tool

High-level cost and performance estimation, coupled with a fast hardware/software co-simulation framework, is a key enabler to a fast embedded system design cycle. Unfortunately, the problem of deriving such estimates without a detailed implementation available is difficult.In this paper we describe two approaches to solve software cost and performance estimation problem, and how they are used in an embedded system design environment. A source-based approach uses compilation onto a virtual instruction set, and allows one to quickly obtain estimates without the need for a compiler for the target processor. An object-based approach translates the assembler generated by the target compiler to “assembler-level,” functionally equivalent t C. In both cases the code is annotated with timing and other execution related information (e.g., estimated memory accesses) and is used as a precise, yet fast, software simulation model. We contrast the precision and speed of these two techniques comparing them with those obtainable by a state-of-the-art cycle-based processor model

The central conserved region (CCR) of respiratory syncytial virus (RSV) G protein modulates host miRNA expression and alters the cellular response to infection

Respiratory Syncytial Virus (RSV) infects respiratory epithelial cells and deregulates host gene expression by many mechanisms including expression of RSV G protein (RSV G). RSV G protein encodes a central conserved region (CCR) containing a CX3C motif that functions as a fractalkine mimic. Disruption of the CX3C motif (a.a. 182–186) located in the CCR of the G protein has been shown to affect G protein function in vitro and the severity of RSV disease pathogenesis in vivo. We show that infection of polarized Calu3 respiratory cells with recombinant RSV having point mutations in Cys173 and 176 (C173/176S) (rA2-GC12), or Cys186 (C186S) (rA2-GC4) is associated with a decline in the integrity of polarized Calu-3 cultures and decreased virus production. This is accompanied with downregulation of miRNAs let-7f and miR-24 and upregulation of interferon lambda (IFNλ), a primary antiviral cytokine for RSV in rA2-GC12/rA2-GC4 infected cells. These results suggest that residues in the cysteine noose region of RSV G protein can modulate IFN λ expression accompanied by downregulation of miRNAs, and are important for RSV G protein function and targeting