957 resultados para Moldenke, Harold N. (Harold Norman), 1909-


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In shallow waters, such as those found close to berth structures, the wash from a manoeuvring ship’s propeller can cause erosion of the seabed. This erosion can be increased if the wash intersects a berth structure. A number of researchers have undertaken model studies and used regression analysis to develop predictive relationships for the scouring action. This paper presents an experimental investigation with Artificial Neural Networks (ANN’s), used to analyse the results. The purpose of using ANN’s was to examine the prediction accuracy of the Networks in comparison with previous regression analysis methods. ANN’s were found to provide a more accurate method of predicting propeller wash scour than the equations presented by previous investigators.

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The mean velocity and turbulence intensity are the two main inputs to investigate the ship propeller induced seabed scouring resulting from a vessel is manoeuvring within a port where the underkeel clearances are low. More accurate data including the turbulence intensity is now available by using the laser doppler anemometry (LDA) measurement system and computational fluid dynamics (CFD) approach. Turbulence intensity has a loose definition, which is the velocity fluctuation as the root mean square (RMS) referenced to a mean flow velocity. However, the velocity fluctuation and mean velocity can be the overall value includingxy and z directions or the value of a single component. LDA and CFD results were obtained from two different acquisition systems (Dantec LDA system and Fluent CFD package) and therefore the outputs cannot be compared directly. An effective method is proposed for comparing the turbulence intensity between the experimental measurements and the computational predictions within a ship propeller jet. The flow patterns of turbulence intensity within a ship propeller jet are presented by using the LDA measurements and CFD results from turbulence models of standard k-e, RNG k-e, realizable ke, standard k?, SST k?and Reynolds stresses.

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We have demonstrated a self-aligned process to fabricate organized iron nanowires on a planarized surface with wire dimensions down to 50 nm. Polishing was used to expose an alternating silicon silicon dioxide edge and a dual selective metal deposition process produced the nanowires. The initial selective deposition produced a tungsten layer on the exposed polysilicon regions. The discovery that selective chemical vapor deposition of iron from Fe(CO)(5) precursor on dielectric surfaces over tungsten surfaces is the key factor that enables the self-alignment of the iron nanowires. Dimensions of the wires are determined by the thickness of the thermal oxide. (c) 2007 The Electrochemical Society.

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Alzheimer's disease (AD) and age-related macular degeneration (AMD) are both neurodegenerative disorders which share common pathological and biochemical features of the complement pathway. The aim of this study was to investigate whether there is an association between well replicated AMD genetic risk factors and AD. A large cohort of AD (n = 3898) patients and controls were genotyped for single nucleotide polymorphisms (SNPs) in the complement factor H (CFH), the Age-related maculopathy susceptibility protein 2 (ARMS2) the complement component 2 (C2), the complement factor B (CFB), and the complement component 3 (C3) genes. While significant but modest associations were identified between the complement factor H, the age-related maculopathy susceptibility protein 2, and the complement component 3 single nucleotide polymorphisms and AD, these were different in direction or genetic model to that observed in AMD. In addition the multilocus genetic model that predicts around a half of the sibling risk for AMD does not predict risk for AD. Our study provides further support to the hypothesis that while activation of the alternative complement pathway is central to AMD pathogenesis, it is less involved in AD.

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Although several studies have described an association between Alzheimer disease (AD) and genetic variation of mitochondrial DNA (mtDNA), each has implicated different mtDNA variants, so the role of mtDNA in the etiology of AD remains uncertain.

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Psychotic symptoms occur in ~40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional deficits. They show heritability up to 61% and have been proposed as a marker for a disease subtype suitable for gene mapping efforts. We undertook a combined analysis of three genome-wide association studies (GWASs) to identify loci that (1) increase susceptibility to an AD and subsequent psychotic symptoms; or (2) modify risk of psychotic symptoms in the presence of neurodegeneration caused by AD. In all, 1299 AD cases with psychosis (AD+P), 735 AD cases without psychosis (AD-P) and 5659 controls were drawn from Genetic and Environmental Risk in AD Consortium 1 (GERAD1), the National Institute on Aging Late-Onset Alzheimer's Disease (NIA-LOAD) family study and the University of Pittsburgh Alzheimer Disease Research Center (ADRC) GWASs. Unobserved genotypes were imputed to provide data on >1.8 million single-nucleotide polymorphisms (SNPs). Analyses in each data set were completed comparing (1) AD+P to AD-P cases, and (2) AD+P cases with controls (GERAD1, ADRC only). Aside from the apolipoprotein E (APOE) locus, the strongest evidence for association was observed in an intergenic region on chromosome 4 (rs753129; 'AD+PvAD-P' P=2.85 × 10(-7); 'AD+PvControls' P=1.11 × 10(-4)). SNPs upstream of SLC2A9 (rs6834555, P=3.0 × 10(-7)) and within VSNL1 (rs4038131, P=5.9 × 10(-7)) showed strongest evidence for association with AD+P when compared with controls. These findings warrant further investigation in larger, appropriately powered samples in which the presence of psychotic symptoms in AD has been well characterized.Molecular Psychiatry advance online publication, 18 October 2011; doi:10.1038/mp.2011.125.