Residual strain monitoring during composite manufacturing

This work explores a new possibility in accurate measurement of multi-axial residual strains during the production of composite structures. It investigates the usability of the polarization dependent loss (PDL) of an optical fibre Bragg grating as a sensitive indicator of multi-axial residual strains. The experimental work presented is done on a cross-ply carbon fibre reinforced polymer fabricated using an autoclave cycle

Correcting cold wire measurements in isotropic turbulence with a DNS database

We estimate the effect of the finite spatial resolution of a cold wire for scalar measurements, using a database from direct numerical simulations (DNS). These are for homogeneous isotropic turbulence at low Taylor-microscale Reynolds number (≃ 42) and Schmidt number unity. Correction factors for the scalar variance, scalar mean dissipation rate, and mixed velocity-scalar derivative skewness are evaluated, for a sensor length of up to 15 times the Batchelor length scale. The largest attenuation effect is found on the dissipation rate, followed by the scalar variance. The mixed skewness,which is affected the least, is overestimated

Evidence that Orai1 does not contribute to store-operated TRPC1 channels in vascular smooth muscle cells.

Ca(2+)-permeable store-operated channels (SOCs) mediate Ca(2+) entry pathways which are involved in many cellular functions such as contraction, growth, and proliferation. Prototypical SOCs are formed of Orai1 proteins and are activated by the endo/sarcoplasmic reticulum Ca(2+) sensor stromal interaction molecule 1 (STIM1). There is considerable debate about whether canonical transient receptor potential 1 (TRPC1) proteins also form store-operated channels (SOCs), and if they do, is Orai1 involved. We recently showed that stimulation of TRPC1-based SOCs involves store depletion inducing STIM1-evoked Gαq/PLCβ1 activity in contractile vascular smooth muscle cells (VSMCs). Therefore the present work investigates the role of Orai1 in activation of TRPC1-based SOCs in freshly isolated mesenteric artery VSMCs from wild-type (WT) and Orai1(-/-) mice. Store-operated whole-cell and single channel currents recorded from WT and Orai1(-/-) VSMCs had similar properties, with relatively linear current-voltage relationships, reversal potentials of about +20mV, unitary conductances of about 2pS, and inhibition by anti-TRPC1 and anti-STIM1 antibodies. In Orai1(-/-) VSMCs, store depletion induced PLCβ1 activity measured with the fluorescent phosphatidylinositol 4,5-bisphosphate/inositol 1,4,5-trisphosphate biosensor GFP-PLCδ1-PH, which was prevented by knockdown of STIM1. In addition, in Orai1(-/-) VSMCs, store depletion induced translocation of STIM1 from within the cell to the plasma membrane where it formed STIM1-TRPC1 interactions at discrete puncta-like sites. These findings indicate that activation of TRPC1-based SOCs through a STIM1-activated PLCβ1 pathway are likely to occur independently of Orai1 proteins, providing evidence that TRPC1 channels form genuine SOCs in VSMCs with a contractile phenotype

Temperature insensitive cure cycle monitoring of cross-ply composite laminates using the polarization dependent loss property of FBG

very important aspect of the composite manufacturing process is the appearance of residual strains and stresses during the curing cycle. Composites exhibit large residual strains after curing. Therefore, in this paper, we propose to follow the evolution of the polarization depend loss peaks (amplitude and wavelength) of fibre Bragg gratings during the manufacturing of the composite material to highlight the residual strains appearanc

Regulatory Architecture of Non-Apoptotic Cell Death Program in C. Elegans

Cell death is prevalent in animal development, homeostasis, and disease. While apoptotic cell death has been extensively studied, many dying cells in development do not exhibit apoptotic morphology, and mice lacking core apoptotic regulators have mostly normal rates of developmental programmed cell death. However, little is known about how alternative death programs are set in motion. In the nematode Caenorhabditis elegans, most cells fated to die by apoptosis are eliminated as young, undifferentiated cells, for no obvious functional reasons. The male nematode’s linker cell, in contrast, dies as an older, differentiated cell, whose life and death subserve precise and important functions. The linker cell first undertakes a long migration along a characteristic path, elongating the male gonad into its proper, mature shape. Once the gonad has attained its final shape and the linker cell has completed its migration, the linker cell then dies to connect the gonad to the environment and allow male fertility. Linker cell death is genetically and morphologically non-apoptotic. Instead, this death program requires the temporal regulator LIN-29, the SARM-like protein TIR-1, the mitogen-activated protein kinase kinase (MAPKK) SEK-1, and the glutamine-rich protein PQN-41. SARM and MAPKKs have been implicated in non-apoptotic degeneration of axon distal segments following axotomy, and some developmental and pathological cell death events in vertebrates resemble the morphology of the dying linker cell. Thus, the molecular mechanism governing linker cell death may be conserved; however, neither the initiating death signals nor the target/s of linker cell death regulators are known. Using classical genetics, I have investigated the initiating mechanisms of linker cell death. I have characterized the cell-autonomous involvement of a histone 3, lysine 4 methyltransferase complex centered on the Trithorax/MLL-like catalytic subunit SET-16. I then demonstrated that two opposing spatial cues, the Wnt ligands EGL-20 and LIN-44, cooperate with LIN-29 to control linker cell death initiation. I showed that the Abdominal- B-like Hox transcription factor NOB-1 likely acts upstream of these two Wnt pathways, and that the Tailless/Tlx nuclear hormone receptor NHR-67 acts in parallel to these regulators to promote linker cell death in addition to linker cell migration. Finally, I show that the Wnt pathways and all known linker cell death mediators require the heat shock factor HSF-1 for cell death. Importantly, HSF-1 function in linker cell death is distinct from, and competes with, its role in stress responses. My studies demonstrate that HSF-1, previously thought to be primarily protective, is a key downstream regulator of a nonapoptotic cell death program. I have also developed a method to isolate large numbers of linker cells from staged worms populations, to enable a comprehensive characterization of the transcriptional program driving linker cell death

Expanding distribution of lethal amphibian fungus Batrachochytrium salamandrivorans in Europe

Emerging fungal diseases can drive amphibian species to local extinction. During 2010-2016, we examined 1,921 urodeles in 3 European countries. Presence of the chytrid fungus Batrachochytrium salamandrivorans at new locations and in urodeles of different species expands the known geographic and host range of the fungus and underpins its imminent threat to biodiversity