Recovery of electronic wastes as fillers for electromagnetic shielding in building components: an LCA study

The present study reports the development of sandwich panels for building walls having electromagnetic interference (EMI) shielding abilities. Conductive polymer composites (CPCs) have started being employed as EMI shielding materials. In this paper we propose the use of a conductive polymer composite flat sheet made of high-density polyethylene (HDPE) recovered from municipal solid wastes (MSW) used as polymeric matrix, “doped” with dispersed metal fillers recycled from e-wastes. Test results proved that the recycled metal fillers enhance the electrical conductivity and enable EMI shielding. Different sandwich panels were discussed in the context of building applications, using identical HDPE/metal-filler EMI sheets, but different thermal insulation material (polystyrene and glass wool). The life cycle assessment (LCA) methodology was applied to evaluate the environmental impact generated during the following steps: a) recycling of thermoplastic materials from MSW; b) recovering of metallic components from waste PCB; c) re-use of the recovered components into sandwich panels with electromagnetic shielding properties for buildings. The goal of the LCA was to perform a comparative analysis of the composite sandwich structures manufactured to be used as EMI shielding in buildings applications in order to assist the materials selection and eco-design. By means of the LCA results it was possible to manufacture a building component with good EMI shielding properties and reduced environmental impact

Multi-scale computational homogenisation to predict the long-term durability of composite structures

A coupled hygro-thermo-mechanical computational model is proposed for fibre reinforced polymers, formulated within the framework of Computational Homogenisation (CH). At each macrostructure Gauss point, constitutive matrices for thermal, moisture transport and mechanical responses are calculated from CH of the underlying representative volume element (RVE). A degradation model, developed from experimental data relating evolution of mechanical properties over time for a given exposure temperature and moisture concentration is also developed and incorporated in the proposed computational model. A unified approach is used to impose the RVE boundary conditions, which allows convenient switching between linear Dirichlet, uniform Neumann and periodic boundary conditions. A plain weave textile composite RVE consisting of yarns embedded in a matrix is considered in this case. Matrix and yarns are considered as isotropic and transversely isotropic materials respectively. Furthermore, the computational framework utilises hierarchic basis functions and designed to take advantage of distributed memory high performance computing

On the fatigue response of a bonded repaired aerospace composite using thermography

Lock-in thermography was employed to investigate the repair efficiency of a bonded repaired aerospace composite subjected to step-wise cycling mechanical loading. The studied component (substrate) was artificially damaged with a 5 mm circular notch and subsequently repaired with a tapered bonded patch. Critical and sub-critical damage of the repaired component was monitored via thermography during 5 Hz tension–tension fatigue. The examination of the acquired thermographs enabled the identification of the patch debonding propagation as well as the quantification of the stress magnification at the patch ends and the locus of the circular notch. It was found that fatigue mechanical loading yields both thermoelastic and hysterestic phenomena with the latter being more prominent prior to the failure of the studied repaired component

Spleen Tyrosine Kinase (Syk) Regulates Systemic Lupus Erythematosus (SLE) T Cell Signaling

Engagement of the CD3/T cell receptor complex in systemic lupus erythematosus (SLE) T cells involves Syk rather than the zeta-associated protein. Because Syk is being considered as a therapeutic target we asked whether Syk is central to the multiple aberrantly modulated molecules in SLE T cells. Using a gene expression array, we demonstrate that forced expression of Syk in normal T cells reproduces most of the aberrantly expressed molecules whereas silencing of Syk in SLE T cells normalizes the expression of most abnormally expressed molecules. Protein along with gene expression modulation for select molecules was confirmed. Specifically, levels of cytokine IL-21, cell surface receptor CD44, and intracellular molecules PP2A and OAS2 increased following Syk overexpression in normal T cells and decreased after Syk silencing in SLE T cells. Our results demonstrate that levels of Syk affect the expression of a number of enzymes, cytokines and receptors that play a key role in the development of disease pathogenesis in SLE and provide support for therapeutic targeting in SLE patients

FADS2 Function Loss at the Cancer Hotspot 11q13 Locus Diverts Lipid Signaling Precursor Synthesis to Unusual Eicosanoid Fatty Acids

Background: Genes coding for the fatty acid desaturases (FADS1, 2, 3) localized at the cancer genomic hotspot 11q13 locus are required for the biosynthesis of 20 carbon polyunsaturated fatty acids (PUFA) that are direct eicosanoid precursors. In several cancer cell lines, FADS2 encoded D6 and D8 desaturation is not functional. Methodology/Principal Findings: Analyzing MCF7 cell fatty acids with detailed structural mass spectrometry, we show that in the absence of FADS2 activity, the FADS1 product D5-desaturase operates to produce 5,11,14–20:3 and 5,11,14,17–20:4. These PUFA are missing the 8–9 double bond of the eicosanoid signaling precursors arachidonic acid (5,8,11,14–20:4) and eicosapentaenoic acid (5,8,11,14,17–20:5). Heterologous expression of FADS2 restores D6 and D8-desaturase activity and normal eicosanoid precursor synthesis. Conclusions/Significance: The loss of FADS2-encoded activities in cancer cells shuts down normal PUFA biosynthesis, deleting the endogenous supply of eicosanoid and downstream docosanoid precursors, and replacing them with unusual butylene-interrupted fatty acids. If recapitulated in vivo, the normal eicosanoid and docosanoid cell signaling milieu would be depleted and altered due to reduction and substitution of normal substrates with unusual substrates, with unpredictable consequences for cellular communication