223 research outputs found

    Characteristics of the transmission loss apparatus at NASA Langley Research Center

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    A description of the Transmission Loss Apparatus at NASA Langley Research Center, which is specifically designed to accommodate general aviation type aircraft structures, is presented. The measurement methodology, referred to as the Plate Reference Method, is discussed and compared with the classical method as described in the Standard of the American Society for Testing and Materials. This measurement procedure enables reliable and accurate noise transmission loss measurements down to the 50 Hz one-third octave band. The transmission loss characteristics of add-on acoustical treatments, applied to the basic structure, can be established by inclusion of appropriate absorption corrections for the treatment

    Broad band sound from wind turbine generators

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    Brief descriptions are given of the various types of large wind turbines and their sound characteristics. Candidate sources of broadband sound are identified and are rank ordered for a large upwind configuration wind turbine generator for which data are available. The rotor is noted to be the main source of broadband sound which arises from inflow turbulence and from the interactions of the turbulent boundary layer on the blade with its trailing edge. Sound is radiated about equally in all directions but the refraction effects of the wind produce an elongated contour pattern in the downwind direction

    Investigation of fuselage acoustic treatment for a twin-engine turboprop aircraft in flight and laboratory tests

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    A flight and laboratory study of sidewall acoustic treatment for cabin noise control is described. In flight, cabin noise levels were measured at six locations with three treatment configurations. Noise levels from narrow-band analysis are reduced to one-third octave format and used to calculate insertion loss, IL, defined as the reduction of interior noise associated with the addition of a treatment. Laboratory tests used a specially constructed structural panel modeled after the propeller plane section of the aircraft sidewall, and acoustic treatments representing those used in flight. Lab measured transmission loss and absorption values were combined using classical acoustic procedures to obtain a prediction of IL. Comparison with IL values measured in flight for the boundary layer component of the noise indicated general agreement

    Measurement and prediction of broadband noise from large horizontal axis wind turbine generators

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    A method is presented for predicting the broadband noise spectra of large wind turbine generators. It includes contributions from such noise sources as the inflow turbulence to the rotor, the interactions between the turbulent boundary layers on the blade surfaces with their trailing edges and the wake due to a blunt trailing edge. The method is partly empirical and is based on acoustic measurements of large wind turbines and airfoil models. Spectra are predicted for several large machines including the proposed MOD-5B. Measured data are presented for the MOD-2, the WTS-4, the MOD-OA, and the U.S. Windpower Inc. machines. Good agreement is shown between the predicted and measured far field noise spectra

    Sequence and structure of the mouse gene coding for the largest neurofilament subunit.

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    We have determined the complete nucleotide sequence of the mouse gene encoding the neurofilament NF-H protein. The C-terminal domain of NF-H is very rich in charged amino acids (aa) and contains a 3-aa sequence, Lys-Ser-Pro, that is repeated 51 times within a stretch of 368 aa. The location of this serine-rich repeat in the phosphorylated domain of NF-H indicates that it represents the major protein kinase recognition site. The nfh gene shares two common intron positions with the nfl and nfm genes, but has an additional intron that occurs at a location equivalent to one of the introns in non-neuronal intermediate filament-coding genes. This additional nfh intron may have been acquired via duplication of a primordial intermediate filament gene

    The probability to initiate X chromosome inactivation is determined by the X to autosomal ratio and x chromosome specific allelic properties.

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    Background: In female mammalian cells, random X chromosome inactivation (XCI) equalizes the dosage of X-encoded gene products to that in male cells. XCI is a stochastic process, in which each X chromosome has a probability to be inactivated. To obtain more insight in the factors setting up this probability, we studied the role of the X to autosome (X:A) ratio in initiation of XCI, and have used the experimental data in a computer simulation model to study the cellular population dynamics of XCI. Methodology/Principal Findings: To obtain more insight in the role of the X:A ratio in initiation of XCI, we generated triploid mouse ES cells by fusion of haploid round spermatids with diploid female and male ES cells. These fusion experiments resulted in only XXY triploid ES cells. XYY and XXX ES lines were absent, suggesting cell death related either to insufficient X-chromosomal gene dosage (XYY) or to inheritance of an epigenetically modified X chromosome (XXX). Analysis of active (Xa) and inactive (Xi) X chromosomes in the obtained triploid XXY lines indicated that the initiation frequency of XCI is low, resulting in a mixed population of XaXiY and XaXaY cells, in which the XaXiY cells have a small proliferative advantage. This result, and findings on XCI in diploid and tetraploid ES cell lines with different X:A ratios, provides evidence that the X:A ratio determines the probability for a given X chromosome to be inactivated. Furthermore, we found that the kinetics of the XCI process can be simulated using a probability for an X chromosome to be inactivated that is proportional to the X:A ratio. These simulation studies re-emphasize our hypothesis that the probability is a function of the concentration of an X-encoded activator of XCI, and of X chromosome specific allelic properties determining the threshold for this activator. Conclusions: The present findings reveal that the probability for an X chromosome to be inactivated is proportional to the X:A ratio. This finding supports the presence of an X-encoded activator of the XCI process. © 2009 Monkhorst et al

    Control of developmentally primed erythroid genes by combinatorial co-repressor actions

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    How transcription factors (TFs) cooperate within large protein complexes to allow rapid modulation of gene expression during development is still largely unknown. Here we show that the key haematopoietic LIM-domain-binding protein-1 (LDB1) TF complex contains several activator and repressor components that together maintain an erythroid-specific gene expression programme primed for rapid activation until differentiation is induced. A combination of proteomics, functional genomics and in vivo studies presented here identifies known and novel co-repressors, most notably the ETO2 and IRF2BP2 proteins, involved in maintaining this primed state. The ETO2-IRF2BP2 axis, interacting with the NCOR1/SMRT co-repressor complex, suppresses the expression of the vast majority of archetypical erythroid genes and pathways until its decommissioning at the onset of terminal erythroid differentiation. Our experiments demonstrate that multimeric regulatory complexes feature a dynamic interplay between activating and repressing components that determines lineage-specific gene expression and cellular differentiation

    Fine-structured multi-scaling long-range correlations in completely sequenced genomes—features, origin, and classification

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    The sequential organization of genomes, i.e. the relations between distant base pairs and regions within sequences, and its connection to the three-dimensional organization of genomes is still a largely unresolved problem. Long-range power-law correlations were found using correlation analysis on almost the entire observable scale of 132 completely sequenced chromosomes of 0.5 × 106 to 3.0 × 107 bp from Archaea, Bacteria, Arabidopsis thaliana, Saccharomyces cerevisiae, Schizosaccharomyces pombe, Drosophila melanogaster, and Homo sapiens. The local correlation coefficients show a species-specific multi-scaling behaviour: close to random correlations on the scale of a few base pairs, a first maximum from 40 to 3,400 bp (for Arabidopsis thaliana and Drosophila melanogaster divided in two submaxima), and often a region of one or more second maxima from 105 to 3 × 105 bp. Within this multi-scaling behaviour, an additional fine-structure is present and attributable to codon usage in all except the human sequences, where it is related to nucleosomal binding. Computer-generated random sequences assuming a block organization of genomes, the codon usage, and nucleosomal binding explain these results. Mutation by sequence reshuffling destroyed all correlations. Thus, the stability of correlations seems to be evolutionarily tightly controlled and connected to the spatial genome organization, especially on large scales. In summary, genomes show a complex sequential organization related closely to their three-dimensional organization

    The detailed 3D multi-loop aggregate/rosette chromatin architecture and functional dynamic organization of the human and mouse genomes

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    Background: The dynamic three-dimensional chromatin architecture of genomes and its co-evolutionary connection to its function—the storage, expression, and replication of genetic information—is still one of the central issues in biology. Here, we describe the much debated 3D architecture of the human and mouse genomes from the nucleosomal to the megabase pair level by a novel approach combining selective high-throughput high-resolution chromosomal interaction capture (T2C), polymer simulations, and scaling analysis of the 3D architecture and the DNA sequence. Results: The genome is compacted into a chromatin quasi-fibre with ~5 ± 1 nucleosomes/11 nm, folded into stable ~30–100 kbp loops forming stable loop aggregates/rosettes connected by similar sized linkers. Minor but significant variations in the architecture are seen between cell types and functional states. The architecture and the DNA sequence show very similar fine-structured multi-scaling behaviour confirming their co-evolution and the above. Conclusions: This architecture, its dynamics, and accessibility, balance stability and flexibility ensuring genome integrity and variation enabling gene expression/regulation by self-organization of (in)active units already in proximity. Our results agree with the heuristics of the field and allow “architectural sequencing” at a genome mechanics level to understand the inseparable systems genomic properties

    The Hydrophobic Core of Twin-Arginine Signal Sequences Orchestrates Specific Binding to Tat-Pathway Related Chaperones

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    Redox enzyme maturation proteins (REMPs) bind pre-proteins destined for translocation across the bacterial cytoplasmic membrane via the twin-arginine translocation system and enable the enzymatic incorporation of complex cofactors. Most REMPs recognize one specific pre-protein. The recognition site usually resides in the N-terminal signal sequence. REMP binding protects signal peptides against degradation by proteases. REMPs are also believed to prevent binding of immature pre-proteins to the translocon. The main aim of this work was to better understand the interaction between REMPs and substrate signal sequences. Two REMPs were investigated: DmsD (specific for dimethylsulfoxide reductase, DmsA) and TorD (specific for trimethylamine N-oxide reductase, TorA). Green fluorescent protein (GFP) was genetically fused behind the signal sequences of TorA and DmsA. This ensures native behavior of the respective signal sequence and excludes any effects mediated by the mature domain of the pre-protein. Surface plasmon resonance analysis revealed that these chimeric pre-proteins specifically bind to the cognate REMP. Furthermore, the region of the signal sequence that is responsible for specific binding to the corresponding REMP was identified by creating region-swapped chimeric signal sequences, containing parts of both the TorA and DmsA signal sequences. Surprisingly, specificity is not encoded in the highly variable positively charged N-terminal region of the signal sequence, but in the more similar hydrophobic C-terminal parts. Interestingly, binding of DmsD to its model substrate reduced membrane binding of the pre-protein. This property could link REMP-signal peptide binding to its reported proofreading function
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