Fundamental analysis of the failure of polymer-based fiber reinforced composites

A mathematical model is described which will permit predictions of the strength of fiber reinforced composites containing known flaws to be made from the basic properties of their constituents. The approach was to embed a local heterogeneous region (LHR) surrounding the crack tip into an anisotropic elastic continuum. The model should (1) permit an explicit analysis of the micromechanical processes involved in the fracture process, and (2) remain simple enough to be useful in practical computations. Computations for arbitrary flaw size and orientation under arbitrary applied load combinations were performed from unidirectional composites with linear elastic-brittle constituent behavior. The mechanical properties were nominally those of graphite epoxy. With the rupture properties arbitrarily varied to test the capability of the model to reflect real fracture modes in fiber composites, it was shown that fiber breakage, matrix crazing, crack bridging, matrix-fiber debonding, and axial splitting can all occur during a period of (gradually) increasing load prior to catastrophic fracture. The computations reveal qualitatively the sequential nature of the stable crack process that precedes fracture

Fracturing highly disordered materials

We investigate the role of disorder on the fracturing process of heterogeneous materials by means of a two-dimensional fuse network model. Our results in the extreme disorder limit reveal that the backbone of the fracture at collapse, namely the subset of the largest fracture that effectively halts the global current, has a fractal dimension of $1.22 \pm 0.01$. This exponent value is compatible with the universality class of several other physical models, including optimal paths under strong disorder, disordered polymers, watersheds and optimal path cracks on uncorrelated substrates, hulls of explosive percolation clusters, and strands of invasion percolation fronts. Moreover, we find that the fractal dimension of the largest fracture under extreme disorder, $d_f=1.86 \pm 0.01$, is outside the statistical error bar of standard percolation. This discrepancy is due to the appearance of trapped regions or cavities of all sizes that remain intact till the entire collapse of the fuse network, but are always accessible in the case of standard percolation. Finally, we quantify the role of disorder on the structure of the largest cluster, as well as on the backbone of the fracture, in terms of a distinctive transition from weak to strong disorder characterized by a new crossover exponent.Comment: 5 pages, 4 figure

Sustainable development, poverty eradication and reducing inequalities

This chapter takes sustainable development as the starting point and focus for analysis. It considers the broad and multifaceted bi-directional interplay between sustainable development, including its focus on eradicating poverty and reducing inequality in their multidimensional aspects, and climate actions in a 1.5°C warmer world. These fundamental connections are embedded in the Sustainable Development Goals (SDGs). The chapter also examines synergies and trade-offs of adaptation and mitigation options with sustainable development and the SDGs and offers insights into possible pathways, especially climate-resilient development pathways towards a 1.5°C warmer world

Microglial amyloid beta clearance is driven by PIEZO1 channels

Background Microglia are the endogenous immune cells of the brain and act as sensors of pathology to maintain brain homeostasis and eliminate potential threats. In Alzheimer's disease (AD), toxic amyloid beta (A beta) accumulates in the brain and forms stiff plaques. In late-onset AD accounting for 95% of all cases, this is thought to be due to reduced clearance of A beta. Human genome-wide association studies and animal models suggest that reduced clearance results from aberrant function of microglia. While the impact of neurochemical pathways on microglia had been broadly studied, mechanical receptors regulating microglial functions remain largely unexplored. Methods Here we showed that a mechanotransduction ion channel, PIEZO1, is expressed and functional in human and mouse microglia. We used a small molecule agonist, Yoda1, to study how activation of PIEZO1 affects AD-related functions in human induced pluripotent stem cell (iPSC)-derived microglia-like cells (iMGL) under controlled laboratory experiments. Cell survival, metabolism, phagocytosis and lysosomal activity were assessed using real-time functional assays. To evaluate the effect of activation of PIEZO1 in vivo, 5-month-old 5xFAD male mice were infused daily with Yoda1 for two weeks through intracranial cannulas. Microglial Iba1 expression and A beta pathology were quantified with immunohistochemistry and confocal microscopy. Published human and mouse AD datasets were used for in-depth analysis of PIEZO1 gene expression and related pathways in microglial subpopulations. Results We show that PIEZO1 orchestrates A beta clearance by enhancing microglial survival, phagocytosis, and lysosomal activity. A beta inhibited PIEZO1-mediated calcium transients, whereas activation of PIEZO1 with a selective agonist, Yoda1, improved microglial phagocytosis resulting in A beta clearance both in human and mouse models of AD. Moreover, PIEZO1 expression was associated with a unique microglial transcriptional phenotype in AD as indicated by assessment of cellular metabolism, and human and mouse single-cell datasets. Conclusion These results indicate that the compromised function of microglia in AD could be improved by controlled activation of PIEZO1 channels resulting in alleviated A beta burden. Pharmacological regulation of these mechanoreceptors in microglia could represent a novel therapeutic paradigm for AD.Peer reviewe

Nonmonotonic fracture behavior of polymer nanocomposites

Polymer composite materials are widely used for their exceptional mechanical properties, notably their ability to resist large deformations. Here, we examine the failure stress and strain of rubbers reinforced by varying amounts of nano-sized silica particles. We find that small amounts of silica increase the fracture stress and strain, but too much filler makes the material become brittle and consequently fracture happens at small deformations. We thus find that as a function of the amount of filler there is an optimum in the breaking resistance at intermediate filler concentrations. We use a modified Griffith theory to establish a direct relation between the material properties and the fracture behavior that agrees with the experiment

Antimalarial drug artemether inhibits neuroinflammation in BV2 microglia through Nrf2-dependent mechanisms

Artemether, a lipid-soluble derivative of artemisinin has been reported to possess anti-inflammatory properties. In this study, we have investigated the molecular mechanisms involved in the inhibition of neuroinflammation by the drug. The effects of artemether on neuroinflammation-mediated HT22 neuronal toxicity were also investigated in a BV2 microglia/HT22 neuron co-culture. To investigate effects on neuroinflammation, we used LPS-stimulated BV2 microglia treated with artemether (5-40µM) for 24 hours. ELISAs and western blotting were used to detect pro inflammatory cytokines, nitric oxide, PGE2, iNOS, COX-2 and mPGES-1. BACE-1 activity and Aβ levels were measured with ELISA kits. Protein levels of targets in NF-kappaB and p38 MAPK signalling, as well as HO-1, NQO1 and Nrf2 were also measured with western blot. NF-kappaB binding to the DNA was investigated using EMSA. MTT, DNA fragmentation and ROS assays in BV2-HT22 neuronal co-culture were used to evaluate the effects of artemether on neuroinflammation-induced neuronal death. The role of Nrf2 in the anti-inflammatory activity of artemether was investigated in BV2 cells transfected with Nrf2 siRNA. Artemether significantly suppressed pro-inflammatory mediators (NO/iNOS, PGE2/COX-2/mPGES-1, TNFα, and IL-6), Aβ and BACE-1 in BV2 cells following LPS stimulation. These effects of artemether were shown to be mediated through inhibition of NF-kappaB and p38MAPK signalling. Artemether produced increased levels of HO-1, NQO1 and GSH in BV2 microglia. The drug activated Nrf2 activity by increasing nuclear translocation of Nrf2 and its binding to antioxidant response elements in BV2 cells. Transfection of BV2 microglia with Nrf2 siRNA resulted in the loss of both anti-inflammatory and neuroprotective activities of artemether. We conclude that artemether induces Nrf2 expression and suggest that Nrf2 mediates the anti-inflammatory effect of artemether in BV2 microglia. Our results suggest that this drug has a therapeutic potential in neurodegenerative disorders

Bonding to aged surfaces: A thermally-aged epoxy

It is common experience that aged surfaces are often difficult to bond to. We report an examination of bonding to thermally-aged epoxy surfaces, using as the adhesive the same epoxy as that of the aged surface. The cured and postcured epoxy was aged at 200 ° C, with the ageing time varying from 2 to 8 h. The fracture energy of the bond line was measured by mode I cleavage under conditions of relatively slow crack growth. The bondline fracture energy was found to decrease logarithmically with ageing time. The fracture energies for bonds to surfaces aged for 2, 4, and 8 h at 200 ° C were 0.077, 0.059, and 0.050 kJ M −2 , respectively. These compare to 0.13 kJ M −2 for a bond to an unaged surface and 0.21 kJ m −2 for bulk fracture. Fracture surfaces resulting from both slow and rapid fracture were examined by optical and scanning electron microscopy. Fracture features different from those arising from bulk fracture were found. Areas with ‘good’ adhesion occurred amidst fields of featureless fracture surface; the frequency and size of these areas decreased with increased ageing time. Evidence of plastic deformation was found, always occurring on the new side of the bond: ridges parallel with crack propagation at high crack speeds and subsurface undulations perpendicular to crack propagation at low speeds. The bond has the effect of channelling the crack along the bondline, but fracture does not always remain exactly at the interface. Fracture often occurred a relatively constant distance away from the interface, suggesting that the presence of the interface was felt for some distance.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44698/1/10853_2004_Article_BF00584867.pd