Modelling tidal energy extraction in a depth-averaged coastal domain

An extension of actuator disc theory is used to describe the properties of a tidal energy device, or row of tidal energy devices, within a depth-averaged numerical model. This approach allows a direct link to be made between an actual tidal device and its equivalent momentum sink in a depth-averaged domain. Extended actuator disc theory also leads to a measure of efficiency for an energy device in a tidal stream of finite Froude number, where efficiency is defined as the ratio of power extracted by one or more tidal devices to the total power removed from the tidal stream. To demonstrate the use of actuator disc theory in a depth-averaged model, tidal flow in a simple channel is approximated using the shallow water equations and the results are compared with the published analytical solutions. © 2010 © The Institution of Engineering and Technology

Phosphorylation of elongation factor-2 from the lepidopteran insect, spodoptera frugiperda

AbstractIn mammalian cells, protein synthesis can be regulated at the level of elongation by the phosphorylation of elongation factor 2 (eEF-2) by a highly specific Ca2+/calmodulin-dependent kinase. In this report, we show that eEF-2 from a cell line derived from the insect, Spodoptera frugiperda, is a substrate for mammalian eEF-2 kinase and that phosphorylation is Ca2+-dependent. Furthermore, two-dimensional peptide mapping shows that the kinase phosphorylates the same sites in Spodoptera eEF-2 as those phosphorylated in the rabbit protein. However, we were unable to detect an eEF-2 kinase in Spodoptera cells

Summary of experiments.

(I) General comments and highlights. (II) Scald: Fungicidal control. 82BA21, 82E18, 82MT19, 82WH23, 82WH23. (III) Scald: Opportunity trial on fungicidal control. 82AL85, 82BA22, 82MT20. (IV) Scald: Epidemic in segregating populations. (V) Scald: Host reaction in hill plots and single plants. 82MT21, 82BA23, (VI) Scald: Seeding rate in evaluating cultivars for resistance. 82MT22, (VII) Net-type net blotch: Screening fungicides. 82BA25, 82KA25. (VIII) Net-type net blotch: Reactions in single plants and hill plots. 82A3, 82BA26. (IX) Spot-type net blotch: Screening fungicides. 82C16. (X) Spot-type net blotch: Potential yield losses. 82C14, 82C15. (XI) Effect of simulated stubble mulching on disease and yield. 82BA36, 82BA35, 82C32, 82MT43,82N27. (XII) Maximising barley yield: Fungicide x growth regulator x cultivar. 82E19,. (XIII) Maximising barley yield: Fungicide x cultivar x nitrogen. (XIV) Variation in pathogenicity of scald, net blotch and powdery mildew. (XV) Unidentified leaf spot on forrest barley. (XVI) Opportunity trial on powdery mildew

Integrating Resource Defence Theory with a Neural Nonapeptide Pathway to Explain Territory-Based Mating Systems

1 Texas Research Institute for Environmental Studies, Sam Houston State University, Huntsville, TX 77341 USA; Department of Biology, Case Western Reserve University, Cleveland, OH 44106 USA. 2 Department of Integrative Biology, The University of Texas at Austin, Austin, TX 78712 USA. 3 Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712 USA. 4 Institute for Neuroscience, The University of Texas at Austin, Austin, TX 78712 USA.The ultimate-level factors that drive the evolution of mating systems have been well studied, but an evolutionarily conserved neural mechanism involved in shaping behaviour and social organization across species has remained elusive. Here, we review studies that have investigated the role of neural arginine vasopressin (AVP), vasotocin (AVT), and their receptor V1a in mediating variation in territorial behaviour. First, we discuss how aggression and territoriality are a function of population density in an inverted-U relationship according to resource defence theory, and how territoriality influences some mating systems. Next, we find that neural AVP, AVT, and V1a expression, especially in one particular neural circuit involving the lateral septum of the forebrain, are associated with territorial behaviour in males of diverse species, most likely due to their role in enhancing social cognition. Then we review studies that examined multiple species and find that neural AVP, AVT, and V1a expression is associated with territory size in mammals and fishes. Because territoriality plays an important role in shaping mating systems in many species, we present the idea that neural AVP, AVT, and V1a expression that is selected to mediate territory size may also influence the evolution of different mating systems. Future research that interprets proximate-level neuro-molecular mechanisms in the context of ultimate-level ecological theory may provide deep insight into the brain-behaviour relationships that underlie the diversity of social organization and mating systems seen across the animal kingdom.This work was supported by an Engineering Plus NSF-ADVANCE Opportunity grant to R.G. O., and NSF Grants IOS-0843712 and IOS-1354942, an Alfred P. Sloan Foundation Fellowship, the Dwight W. and Blanche Faye Reeder Centennial Fellowship in Systematic and Evolutionary Biology, and an Institute for Cellular and Molecular Biology Fellowship to H.A.H.Integrative Biolog

Jobseekers Regime and Flexible New Deal, the Six Month Offer and Support for the Newly Unemployed evaluations: An early process study

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Mutational analysis of fructose-1,6-bisphosphate aldolase of Neisseria meningitidis serogroup B

Fructose-1,6-bisphosphate aldolase (FBA) is a classical cytoplasmic glycolytic enzyme which, despite lacking a predicted signal peptide, has been demonstrated to be expressed and transported to the surface of numerous Gram-positive bacteria and shown to interact with host molecules and perform non-glycolytic biological functions. Genome-based studies have also demonstrated that the glycolytic pathway appears to be non-functional in the meningococcus due to absence of phosphofructokinase, one of the important enzymes in this pathway. This study aimed to investigate whether the FBA, a so-called housekeeping enzyme, is required for maximal in vitro growth of N. meningitidis. An FBA knock-out mutant was created in N. meningitidis using an inverse polymerase chain reaction (PCR) and allelic exchange methodology. Phenotypic analysis of FBA-deficient mutant strains such as growth profiling experiments showed that the FBA-deficient mutant grew at the same rate (in broth culture and on solid media) as the wild-type strain, suggesting that FBA is not required for optimal growth of N. meningitidis under the in vitro conditions tested. No differences in either colony or bacterial cell morphology (using light microscopy) were observed. In summary, despite being a central enzyme in the glycolytic cycle, FBA is not required for in vitro growth of N. meningitidis.Key words: Neisseria meningitidis, aldolase, mutagenesis, growth kinetics, glycolytic cycle

Minnowbrook V: 2006 Workshop on Unsteady Flows in Turbomachinery

This volume contains materials presented at the Minnowbrook V 2006 Workshop on Unsteady Flows in Turbomachinery, held at the Syracuse University Minnowbrook Conference Center, New York, on August 20-23, 2006. The workshop organizers were John E. LaGraff (Syracuse University), Martin L.G. Oldfield (Oxford University), and J. Paul Gostelow (University of Leicester). The workshop followed the theme, venue, and informal format of four earlier workshops: Minnowbrook I (1993), Minnowbrook II (1997), Minnowbrook III (2000), and Minnowbrook IV (2003). The workshop was focused on physical understanding of unsteady flows in turbomachinery, with the specific goal of contributing to engineering application of improving design codes for turbomachinery. The workshop participants included academic researchers from the United States and abroad and representatives from the gas-turbine industry and U.S. Government laboratories. The physical mechanisms discussed were related to unsteady wakes, active flow control, turbulence, bypass and natural transition, separation bubbles and turbulent spots, modeling of turbulence and transition, heat transfer and cooling, surface roughness, unsteady CFD, and DNS. The workshop summary and the plenary discussion transcripts clearly highlight the need for continued vigorous research in the technologically important area of unsteady flows in turbomachines. This volume contains abstracts and copies of select viewgraphs organized according to the workshop sessions. Full-color viewgraphs and animations are included in the CD-ROM version only (Doc.ID 20070024781)

Uptake of Neisserial autotransporter lipoprotein (NalP) promotes an increase in human brain microvascular endothelial cell metabolic activity

Neisseria meningitidis is normally a human nasopharyngeal commensal but is also capable of causing lifethreatening sepsis and meningitis. N. meningitidis secretes several virulence-associated proteins including Neisserial autotransporter lipoprotein (NalP), an immunogenic, type Va autotransporter harboring an S8-family serine endopeptidase domain. NalP has been previously characterized as a cell-surface maturation protease which processes other virulence-associated meningococcal surface proteins, and as a factor contributing to the survival of meningococci in human serum due to its ability to cleave complement factor C3. Here, recombinant NalP (rNalP) fragments were purified and used to investigate the interaction of NalP with host cells. Flow cytometry and confocal microscopy demonstrated binding and uptake of rNalP into different human cell types. High-resolution microscopy confirmed that internalized rNalP predominantly localized to the perinuclear region of cells. Abolition of rNalP protease activity using site-directed mutagenesis did not influence uptake or subcellular localization, but inactive rNalP (rNalPS426A) was unable to induce an increase in human brain microvascular endothelial cell metabolic activity provoked by proteolytically-active rNalP. Our data suggests a more complex and multifaceted role for NalP in meningococcal pathogenesis than was previously understood which includes novel intra-host cell functions

The role of glyceraldehyde 3-phosphate dehydrogenase (GapA-1) in Neisseria meningitidis adherence to human cells

BackgroundGlyceraldehyde 3-phosphate dehydrogenases (GAPDHs) are cytoplasmic glycolytic enzymes, which although lacking identifiable secretion signals, have also been found localized to the surface of several bacteria (and some eukaryotic organisms); where in some cases they have been shown to contribute to the colonization and invasion of host tissues. Neisseria meningitidis is an obligate human nasopharyngeal commensal which can cause life-threatening infections including septicaemia and meningitis. N. meningitidis has two genes, gapA-1 and gapA-2, encoding GAPDH enzymes. GapA-1 has previously been shown to be up-regulated on bacterial contact with host epithelial cells and is accessible to antibodies on the surface of capsule-permeabilized meningococcal cells. The aims of this study were: 1) to determine whether GapA-1 was expressed across different strains of N. meningitidis; 2) to determine whether GapA-1 surface accessibility to antibodies was dependant on the presence of capsule; 3) to determine whether GapA-1 can influence the interaction of meningococci and host cells, particularly in the key stages of adhesion and invasion.ResultsIn this study, expression of GapA-1 was shown to be well conserved across diverse isolates of Neisseria species. Flow cytometry confirmed that GapA-1 could be detected on the cell surface, but only in a siaD-knockout (capsule-deficient) background, suggesting that GapA-1 is inaccessible to antibody in in vitro-grown encapsulated meningococci. The role of GapA-1 in meningococcal pathogenesis was addressed by mutational analysis and functional complementation. Loss of GapA-1 did not affect the growth of the bacterium in vitro. However, a GapA-1 deficient mutant showed a significant reduction in adhesion to human epithelial and endothelial cells compared to the wild-type and complemented mutant. A similar reduction in adhesion levels was also apparent between a siaD-deficient meningococcal strain and an isogenic siaD gapA-1 double mutant.ConclusionsOur data demonstrates that meningococcal GapA-1 is a constitutively-expressed, highly-conserved surface-exposed protein which is antibody-accessible only in the absence of capsule. Mutation of GapA-1 does not affect the in vitro growth rate of N. meningitidis, but significantly affects the ability of the organism to adhere to human epithelial and endothelial cells in a capsule-independent process suggesting a role in the pathogenesis of meningococcal infection