A multigrid accelerated hybrid unstructured mesh method for 3D compressible turbulent flow

 A cell vertex finite volume method for the solution of steady compressible turbulent flow problems on unstructured hybrid meshes of tetrahedra, prisms, pyramids and hexahedra is described. These hybrid meshes are constructed by firstly discretising the computational domain using tetrahedral elements and then by merging certain tetrahedra. A one equation turbulence model is employed and the solution of the steady flow equations is obtained by explicit relaxation. The solution process is accelerated by the addition of a multigrid method, in which the coarse meshes are generated by agglomeration, and by parallelisation. The approach is shown to be effective for the simulation of a number of 3D flows of current practical interest. Sponsored by The Research Council of Norway, project number 125676/410 Dedicated to the memory of Prof. Mike Crisfield, a respected colleague     

Experimental evidence of a relationship between monomer plasma residence time and carboxyl group retention in acrylic acid plasma polymers

Decreasing carboxyl retention in deposits from the glow region of an acrylic acid plasma was measured by X-ray photoelectron spectroscopy and chemical derivatisation as the collection distance from the monomer vapour inlet was increased. Volatilisation of plasma polymerised acrylic acid was detected after trifluoroethanol derivatisation; this is correlated with evaporation of low molecular weight components observed previously.     

A noncompetitive peptide inhibitor of the nicotinic acetylcholine receptor from Conus purpurascens venom

A paralytic peptide, psi-conotoxin Piiie has been purified and characterized from Conus purpurascens venom. Electrophysiological studies indicate that the peptide inhibits the nicotinic acetylcholine receptor (nAChR). However, the peptide does not block the binding of alpha-bungarotoxin, a competitive nAChR antagonist. Thus, psi-conotoxin Piiie appears to inhibit the receptor at a site other than the acetylcholine-binding site. As ascertained by sequence analysis, mass spectrometry, and chemical synthesis, the peptide has the following covalent structure: HOOCCLYGKCRRYOGCSSASCCQR* (O = 4-trans hydroxyproline; * indicates an amidated C-terminus). The disulfide connectivity of the toxin is unrelated to the alpha- or the alphaA-conotoxins, the Conus peptide families that are competitive inhibitors of the nAChR, but shows homology to the mu-conotoxins (which are Na+ channel blockers).     

A magnetic resonance imaging study of planum temporale asymmetry in men with developmental dyslexia

The influence of ionic strength and composition on the binding and inhibition of human leukocyte elastase by glycosaminoglycans with variable degree and position of sulfation was investigated. The kinetic mechanism of inhibition had a hyperbolic, mixed-type character with a competitive component that was promoted by low ionic strength, reduced by phosphate ions, and which also depended on the substrate and glycosaminoglycan structure. Enzyme binding was a cooperative phenomenon that varied with ionic strength and composition. The inhibition patterns correlated with the cationic character of elastase and with the distribution of arginines on its molecular surface, most notably with residues located in the vicinity of the substrate binding region. The order of affinity for elastase binding was chondroitin 4-sulfate < chondroitin 6-sulfate < dermatan sulfate, iduronate-containing derivatives being superior with respect to the glucuronate-containing counterparts. Additional sulfation at both the 4- and 6- positions or at the N- and 4-positions of the N-acetylgalactosamine moiety decidedly improved the inhibitory efficiency. The results highlight a fundamental physiological role of enzyme-glycosaminoglycan interactions. In the azurophil granule of the human polymorphonuclear neutrophil, elastase and other enzymes are bound to a matrix of chondroitin 4-sulfate because this is the only glycosaminoglycan that simultaneously offers good binding for enzyme compartmentalization together with prompt release from the bound state at the onset of phagocytosis.     

Solving ML equations for 2-parameter Poisson-process models forungrouped software-failure data

Existence conditions are given for maximum likelihood (ML) parameter estimates for several families of 2-parameter software-reliability Poisson-process models. For each such model, the ML equations can be expressed in terms of one equation in one unknown. Bounds are given on solutions to these one equation problems to serve as initial intervals for search algorithms like bisection. Uniqueness of the solutions is established in some cases. Solutions are also tabulated for certain simple cases. Results are given for ungrouped failure data (exact times are available for all failures). ML estimation problems for such a situation are treated as limiting cases of problems based on failure times grouped into intervals of decreasing mesh