231 research outputs found

    Ultrasonic Attenuation Measurement Using Backscattering Technique

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    Ultrasonic backscattering measurements by means of spatial averaging technique were carried out in steel to determine the ultrasonic attenuation coefficient. The attenuation coefficients were evaluated from the exponential decay of the backscattering signal. The results were compared with those obtained by evaluating the amplitude decay of the main pulse. Good agreement is observed provided the condition α s · λ \u3c\u3c 1 is valid, i.e. Rayleigh scattering with d/λ ≤ 0.2 and/or weak elastic anisotropy of the single crystal. Otherwise multiple scattering becomes dominant and the amplitude decay of the backscattering curve is no longer related to the attenuation coefficient

    Characterization of Defects and Heterogeneities in Silicon Nitride and Silicon Carbide by Different NDE Methods

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    The brittleness of ceramic materials like silicon nitride and silicon carbide makes it necessary to fabricate homogeneous structures and to detect small defects in the region of 10 to 100 microns diameter. In the German program on NDE for the gas turbine therefore a study was made to compare different NDE methods and to develop new techniques. Tests were made with ultrasonics, microradiography, vibration analysis, acoustic emission and optical-holographical interferometry on test samples and real components of the gas turbine (rotor, stator, combustor). The results show that especially microradiography with projection technique and X-ray focus of ≈ 10 µm diameter, ultrasonics with different kind of transducers, equipment and wave modes in the frequency range until about 150 MHz are well suited to detect the small defects and to characterize structure heterogeneities. Vibration analysis seems to be a good method to compare many samples of the same kind and to detect matter of the fabrication process data. The comparison between UT, vibration analysis, acoustic emission and destructive tests (fracture strength) indicates that there are more or less correlations between NDE and the destructive analysis

    Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction

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    Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confocal microscopy and immunogold-electron microscopy, these filaments are localized to the non-compacted adaxonal myelin compartment. Genetic disruption of these filaments in Sept8-mutant mice causes myelin outfoldings as a very specific neuropathology. Septin filaments thus serve an important function in scaffolding the axon/myelin-unit, evidently a late stage of myelin maturation. We propose that pathological or aging-associated diminishment of the septin/anillin-scaffold causes myelin outfoldings that impair the normal nerve conduction velocity

    Conservation and divergence of myelin proteome and oligodendrocyte transcriptome profiles between humans and mice

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    Human myelin disorders are commonly studied in mouse models. Since both clades evolutionarily diverged approximately 85 million years ago, it is critical to know to what extent the myelin protein composition has remained similar. Here, we use quantitative proteomics to analyze myelin purified from human white matter and find that the relative abundance of the structural myelin proteins PLP, MBP, CNP, and SEPTIN8 correlates well with that in C57Bl/6N mice. Conversely, multiple other proteins were identified exclusively or predominantly in human or mouse myelin. This is exemplified by peripheral myelin protein 2 (PMP2), which was specific to human central nervous system myelin, while tetraspanin-2 (TSPAN2) and connexin-29 (CX29/GJC3) were confined to mouse myelin. Assessing published scRNA-seq-datasets, human and mouse oligodendrocytes display well-correlating transcriptome profiles but divergent expression of distinct genes, including Pmp2, Tspan2, and Gjc3. A searchable web interface is accessible via www.mpinat.mpg.de/myelin. Species-dependent diversity of oligodendroglial mRNA expression and myelin protein composition can be informative when translating from mouse models to humans

    Theatre and time ecology: deceleration in Stifters Dinge

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    This article explores the production of ‘time ecology’ in two works of postdramatic theatre: Heiner Goebbels’ Stifters Dinge (2007) and Philippe Quesne’s L’Effet de Serge (2007). By focusing on the practice of deceleration, it argues that theatre’s ecological potential resides not so much in its ability to represent the world, but rather in its capacity for producing new types of temporal experience that purposefully seek to break with modernity’s regime of historicity and the accelerated rhythms that it has given rise to. Importantly, my concern with deceleration is not an argument for slowness per se; on the contrary, I am interested in highlighting the presence of multiple and interpenetrating timescales and rhythms. As well as exposing the full extent of theatre’s temporal potential, such a concern with postdramatic ‘chronographies’ offers an implicit critique of dramatic theatre’s extant practices of eco-dramaturgy that, all too often, attempt to construct a linear narrative which is invested in conventional sequential models of temporality (beginning, middle, end)

    Split-Cre Complementation Indicates Coincident Activity of Different Genes In Vivo

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    Cre/LoxP recombination is the gold standard for conditional gene regulation in mice in vivo. However, promoters driving the expression of Cre recombinase are often active in a wide range of cell types and therefore unsuited to target more specific subsets of cells. To overcome this limitation, we designed inactive “split-Cre” fragments that regain Cre activity when overlapping co-expression is controlled by two different promoters. Using transgenic mice and virus-mediated expression of split-Cre, we show that efficient reporter gene activation is achieved in vivo. In the brain of transgenic mice, we genetically defined a subgroup of glial progenitor cells in which the Plp1- and the Gfap-promoter are simultaneously active, giving rise to both astrocytes and NG2-positive glia. Similarly, a subset of interneurons was labelled after viral transfection using Gad67- and Cck1 promoters to express split-Cre. Thus, split-Cre mediated genomic recombination constitutes a powerful spatial and temporal coincidence detector for in vivo targeting
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