Design and analysis issues of integrated control systems for high-speed civil transports

A study was conducted to identify, rank, and define development plans for the critical guidance and control design and analysis issues as related to economically viable and environmentally acceptable high-speed civil transport. The issues were identified in a multistep process. First, pertinent literature on supersonic cruise aircraft was reviewed, and experts were consulted to establish the fundamental characteristics and problems inherent to supersonic cruise aircraft. Next, the advanced technologies and strategies being pursued for the high-speed civil transport were considered to determine any additional unique control problems the transport may have. Finally, existing technologies and methods were examined to determine their capabilities for the design and analysis of high-speed civil transport control systems and to identify the shortcomings and issues. Three priority levels - mandatory, highly beneficial, and desirable - were established. Within each of these levels, the issues were further ranked. Technology development plans for each issue were defined. Each plan contains a task breakdown and schedule

Effect of noise on coupled chaotic systems

Effect of noise in inducing order on various chaotically evolving systems is reviewed, with special emphasis on systems consisting of coupled chaotic elements. In many situations it is observed that the uncoupled elements when driven by identical noise, show synchronization phenomena where chaotic trajectories exponentially converge towards a single noisy trajectory, independent of the initial conditions. In a random neural network, with infinite range coupling, chaos is suppressed due to noise and the system evolves towards a fixed point. Spatiotemporal stochastic resonance phenomenon has been observed in a square array of coupled threshold devices where a temporal characteristic of the system resonates at a given noise strength. In a chaotically evolving coupled map lattice with logistic map as local dynamics and driven by identical noise at each site, we report that the number of structures (a structure is a group of neighbouring lattice sites for whom values of the variable follow certain predefined pattern) follow a power-law decay with the length of the structure. An interesting phenomenon, which we call stochastic coherence, is also reported in which the abundance and lifetimes of these structures show characteristic peaks at some intermediate noise strength.Comment: 21 page LaTeX file for text, 5 Postscript files for figure

Analysis of the putative role of CR1 in Alzheimer’s disease: Genetic association, expression and function

Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b/C4b receptor (CR1 or CD35) that are associated with late onset AD. Here, anti-CR1 antibodies (Abs) directed against different epitopes of the receptor, were used to localize CR1 in brain, and relative binding affinities of the CR1 ligands, C1q and C3b, were assessed by ELISA. Most Abs tested stained red blood cells in blood vessels but showed no staining in brain parenchyma. However, two monoclonal anti-CR1 Abs labeled astrocytes in all of the cases tested, and this reactivity was preabsorbed by purified recombinant human CR1. Human brain-derived astrocyte cultures were also reactive with both mAbs. The amount of astrocyte staining varied among the samples, but no consistent difference was conferred by diagnosis or the GWAS-identified SNPs rs4844609 or rs6656401. Plasma levels of soluble CR1 did not correlate with diagnosis but a slight increase was observed with rs4844609 and rs6656401 SNP. There was also a modest but statistically significant increase in relative binding activity of C1q to CR1 with the rs4844609 SNP compared to CR1 without the SNP, and of C3b to CR1 in the CR1 genotypes containing the rs6656401 SNP (also associated with the larger isoform of CR1) regardless of clinical diagnosis. These results suggest that it is unlikely that astrocyte CR1 expression levels or C1q or C3b binding activity are the cause of the GWAS identified association of CR1 variants with AD. Further careful functional studies are needed to determine if the variant-dictated number of CR1 expressed on red blood cells contributes to the role of this receptor in the progression of AD, or if another mechanism is involved