Study of localized damage in composite laminates using micro-macro approach

A robust multiscale scheme referred to as micro–macro method has been developed for the prediction of localized damage in fiber reinforced composites and implemented in a finite element framework. The micro–macro method is based on the idea of partial homogenization of a structure. In this method, the microstructural details are included in a small region of interest in the structure and the rest is modeled as a homogeneous continuum. The solution to the microstructural fields is then obtained on solving the two different domains, simultaneously. This method accurately predicts local stress fields in stress concentration regions and is computationally efficient as compared with the solution of a full scale microstructural model. This scheme has been applied to obtain localized damage at high and low stress zones of a V-notched rail shear specimen. The prominent damage mechanisms under shear loading, namely, matrix cracking and interfacial debonding, have been modeled using Mohr–Coulomb plasticity and traction separation law, respectively. The average stress at the notch has been found to be 44% higher than the average stresses away from the notch for a 90 N shear load. This stress rise is a direct outcome of the geometry of the notch.

Verification of a novel material model to predict damage in composite structures

An intralaminar damage model (IDM), based on continuum damage mechanics, was developed for the simulation of composite structures subjected to damaging loads. This model can capture the complex intralaminar damage mechanisms, accounting for mode interactions, and delaminations. Its development is driven by a requirement for reliable crush simulations to design composite structures with a high specific energy absorption. This IDM was implemented as a user subroutine within the commercial finite element package, Abaqus/Explicit[1]. In this paper, the validation of the IDM is presented using two test cases. Firstly, the IDM is benchmarked against published data for a blunt notched specimen under uniaxial tensile loading, comparing the failure strength as well as showing the damage. Secondly, the crush response of a set of tulip-triggered composite cylinders was obtained experimentally. The crush loading and the associated energy of the specimen is compared with the FE model prediction. These test cases show that the developed IDM is able to capture the structural response with satisfactory accuracy

Experimental Autoimmune Uveoretinitis (EAU)-Related Tissue Damage and Angiogenesis Is Reduced in CCL2−/−CX3CR1gfp/gfp Mice

Purpose: To investigate the roles of the CCL2-CCR2 and CX3CL1-CX3CR1 pathways in experimental autoimmune uveoretinitis (EAU)-mediated retinal tissue damage and angiogenesis.

Methods: The C57BL/6J wild-type (WT) and CCL2−/−CX3CR1gfp/gfp (double knockout [DKO]) mice were immunized with IRBP1-20. Retinal inflammation and tissue damage were evaluated clinically and histologically at different days postimmunization (p.i.). Retinal neovascular membranes were evaluated by confocal microscopy of retinal flat mounts, and immune cell infiltration by flow cytometry.

Results: At day 25 p.i., DKO mice had lower clinical and histological scores and fewer CD45highCD11b+ infiltrating cells compared with WT mice. The F4/80+macrophages constitute 40% and 21% and CD11b+Gr-1+Ly6G+ neutrophils constitute 10% and 22% of retinal infiltrating cells in WT and DKO mice, respectively. At the late stages of EAU (day 60–90 p.i.), DKO and WT mice had similar levels of inflammatory score. However, less structural damage and reduced angiogenesis were detected in DKO mice. Neutrophils were rarely detected in the inflamed retina in both WT and DKO mice. Macrophages and myeloid-derived suppressor cells (MDSCs) accounted for 8% and 3% in DKO EAU retina, and 19% and 10% in WT EAU retina; 71% of infiltrating cells were T/B-lymphocytes in DKO EAU retina and 50% in WT EAU retina.

Conclusions: Experimental autoimmune uveoretinitis–mediated retinal tissue damage and angiogenesis is reduced in CCL2−/−CX3CR1gfp/gfp mice. Retinal inflammation is dominated by neutrophils at the acute stage and lymphocytes at the chronic stage in these mice. Our results suggest that CCR2+ and CX3CR1+monocytes are both involved in tissue damage and angiogenesis in EAU.

Influence of Boundary Conditions on the Low Velocity Impact Damage Carbon Fibre Reinforced Plastic Plates (ICTWS2014-0501)

No abstract available

In Vitro and In Vivo Anti-Schistosomal Activity of the Alkylphospholipid Analog Edelfosine

Background: Schistosomiasis is a parasitic disease caused by trematodes of the genus Schistosoma. Five species of Schistosoma are known to infect humans, out of which S. haematobium is the most prevalent, causing the chronic parasitic disease schistosomiasis that still represents a major problem of public health in many regions of the world and especially in tropical areas, leading to serious manifestations and mortality in developing countries. Since the 1970s, praziquantel (PZQ) is the drug of choice for the treatment of schistosomiasis, but concerns about relying on a single drug to treat millions of people, and the potential appearance of drug resistance, make identification of alternative schistosomiasis chemotherapies a high priority. Alkylphospholipid analogs (APLs), together with their prototypic molecule edelfosine (EDLF), are a family of synthetic antineoplastic compounds that show additional pharmacological actions, including antiparasitic activities against several protozoan parasites.

Methodology/Principal Findings: We found APLs ranked edelfosine> perifosine> erucylphosphocholine> miltefosine for their in vitro schistosomicidal activity against adult S. mansoni worms. Edelfosine accumulated mainly in the worm tegument, and led to tegumental alterations, membrane permeabilization, motility impairment, blockade of male-female pairing as well as induction of apoptosis-like processes in cells in the close vicinity to the tegument. Edelfosine oral treatment also showed in vivo schistosomicidal activity and decreased significantly the egg burden in the liver, a key event in schistosomiasis.

Conclusions/Significance: Our data show that edelfosine is the most potent APL in killing S. mansoni adult worms in vitro. Edelfosine schistosomicidal activity seems to depend on its action on the tegumental structure, leading to tegumental damage, membrane permeabilization and apoptosis-like cell death. Oral administration of edelfosine diminished worm and egg burdens in S. mansoni-infected CD1 mice. Here we report that edelfosine showed promising antischistosomal properties in vitro and in vivo.

Contrasting damage characteristics in direct incidence and surface plasmon mediated single-shot laser ablation of aluminium films

Thin, oxidised Al films grown an one face of fused silica prisms are exposed. tinder ambient conditions, to single shots from an excimer laser operating at wavelength 248 nm. Preliminary characterisation of the films using attenuated total reflection yields optical and thickness data for the Al and Al oxide layers; this step facilitates the subsequent, accurate tuning of the excimer laser pulse to the: surface plasmon resonance at the Al/(oxide)/air interface and the calculation of the fluence actually absorbed by the thin film system. Ablation damage is characterised using scanning electron, and atomic force microscopy. When the laser pulse is incident, through the prism on the sample at less than critical angle, the damage features are molten in nature with small islands of sub-micrometer dimension much in evidence, a mechanism of film melt-through and subsegment blow-off due to the build up of vapour pressure at the substrate/film interface is appropriate. By contrast, when the optical input is surface plasmon mediated, predominately mechanical damage results with the film fragmenting into large flakes of dimensions on the order of 10 mu m. It is suggested that the ability of surface plasmons to transport energy leads to enhanced, preferential absorption of energy at defect sites causing stress throughout the film which exceeds the ultimate tensile stress for the film: this in turn leads to film break-up before melting can onset. (C) 1998 Elsevier Science B.V.

Mechanisms of DNA Damage Response to Targeted Irradiation in Organotypic 3D Skin Cultures

DNA damage (caused by direct cellular exposure and bystander signaling) and the complex pathways involved in its repair are critical events underpinning cellular and tissue response following radiation exposures. There are limited data addressing the dynamics of DNA damage induction and repair in the skin particularly in areas not directly exposed. Here we investigate the mechanisms regulating DNA damage, repair, intracellular signalling and their impact on premature differentiation and development of inflammatory-like response in the irradiated and surrounding areas of a 3D organotypic skin model. Following localized low-LET irradiation (225 kVp X-rays), low levels of 53BP1 foci were observed in the 3D model (3.8±0.28 foci/Gy/cell) with foci persisting and increasing in size up to 48 h post irradiation. In contrast, in cell monolayers 14.2±0.6 foci/Gy/cell and biphasic repair kinetics with repair completed before 24 h was observed. These differences are linked to differences in cellular status with variable level of p21 driving apoptotic signalling in 2D and accelerated differentiation in both the directly irradiated and bystander areas of the 3D model. The signalling pathways utilized by irradiated keratinocytes to induce DNA damage in non-exposed areas of the skin involved the NF-κB transcription factor and its downstream target COX-2.

An indirect bridge inspection method incorporating a wavelet-based damage indicator and pattern recognition

In recent years, there has been a move towards the development of indirect structural health monitoring (SHM)techniques for bridges; the low-cost vibration-based method presented in this paper is such an approach. It consists of the use of a moving vehicle fitted with accelerometers on its axles and incorporates wavelet analysis and statistical pattern recognition. The aim of the approach is to both detect and locate damage in bridges while reducing the need for direct instrumentation of the bridge. In theoretical simulations, a simplified vehicle-bridge interaction model is used to investigate the effectiveness of the approach in detecting damage in a bridge from vehicle accelerations. For this purpose, the accelerations are processed using a continuous wavelet transform as when the axle passes over a damaged section, any discontinuity in the signal would affect the wavelet coefficients. Based on these coefficients, a damage indicator is formulated which can distinguish between different damage levels. However, it is found to be difficult to quantify damage of varying levels when the vehicle’s transverse position is varied between bridge crossings. In a real bridge field experiment, damage was applied artificially to a steel truss bridge to test the effectiveness of the indirect approach in practice; for this purpose a two-axle van was driven across the bridge at constant speed. Both bridge and vehicle acceleration measurements were recorded. The dynamic properties of the test vehicle were identified initially via free vibration tests. It was found that the resulting damage indicators for the bridge and vehicle showed similar patterns, however, it was difficult to distinguish between different artificial damage scenarios.

BRCA1, FANCD2 and Chk1 are potential molecular targets for the modulation of a radiation-induced DNA damage response in bystander cells

Radiotherapy is an important treatment option for many human cancers. Current research is investigating the use of molecular targeted drugs in order to improve responses to radiotherapy in various cancers. The cellular response to irradiation is driven by both direct DNA damage in the targeted cell and intercellular signalling leading to a broad range of bystander effects. This study aims to elucidate radiation-induced DNA damage response signalling in bystander cells and to identify potential molecular targets to modulate the radiation induced bystander response in a therapeutic setting. Stalled replication forks in T98G bystander cells were visualised via bromodeoxyuridine (BrdU) nuclear foci detection at sites of single stranded DNA. γH2AX co-localised with these BrdU foci. BRCA1 and FANCD2 foci formed in T98G bystander cells. Using ATR mutant F02-98 hTERT and ATM deficient GM05849 fibroblasts it could be shown that ATR but not ATM was required for the recruitment of FANCD2 to sites of replication associated DNA damage in bystander cells whereas BRCA1 bystander foci were ATM-dependent. Phospho-Chk1 foci formation was observed in T98G bystander cells. Clonogenic survival assays showed moderate radiosensitisation of directly irradiated cells by the Chk1 inhibitor UCN-01 but increased radioresistance of bystander cells. This study identifies BRCA1, FANCD2 and Chk1 as potential targets for the modulation of radiation response in bystander cells. It adds to our understanding of the key molecular events propagating out-of-field effects of radiation and provides a rationale for the development of novel molecular targeted drugs for radiotherapy optimisation.

Modelling Static and Dynamic FRP-Concrete Bond Behaviour Using a Local Concrete Damage Model

This paper presents a study on the bond behaviour of FRP-concrete bonded joints under static and dynamic loadings, by developing a meso-scale finite element model using the K&C concrete damage model in LS-DYNA. A significant number of single shear experiments under static pull-off loading were modelled with an extensive parametric study covering key factors in the K&C model, including the crack band width, the compressive fracture energy and the shear dilatation factor. It is demonstrated that the developed model can satisfactorily simulate the static debonding behaviour, in terms of mesh objectivity, the load-carrying capacity and the local bond-slip behaviour, provided that proper consideration is given to the selection of crack band width and shear dilatation factor. A preliminary study of the effect of the dynamic loading rate on the debonding behaviour was also conducted by considering a dynamic increase factor (DIF) for the concrete strength as a function of strain rate. It is shown that a higher loading rate leads to a higher load-carrying capacity, a longer effective bond length, and a larger damaged area of concrete in the single shear loading scenario.

Attenuation of urokinase activity during experimental ischaemia protects the cerebral barrier from damage through regulation of matrix metalloproteinase-2 and NAD(P)H oxidase

Ischaemic injury impairs the integrity of the blood-brain barrier (BBB). In this study, we investigated the molecular causes of this defect with regard to the putative correlations among NAD(P)H oxidase, plasminogen-plasmin system components, and matrix metalloproteinases. Hence, the activities of NAD(P)H oxidase, matrix metalloproteinase-2, urokinase-type plasminogen activator (uPA), and tissue-type plasminogen activator (tPA), and superoxide anion levels, were assessed in human brain microvascular endothelial cells (HBMECs) exposed to oxygen-glucose deprivation (OGD) alone or OGD followed by reperfusion (OGD + R). The integrity of an in vitro model of BBB comprising HBMECs and astrocytes was studied by measuring transendothelial electrical resistance and the paracellular flux of albumin. OGD with or without reperfusion (OGD ± R) radically perturbed barrier function while concurrently enhancing uPA, tPA and NAD(P)H oxidase activities and superoxide anion release in HBMECs. Pharmacological inactivation of NAD(P)H oxidase attenuated OGD ± R-mediated BBB damage through modulation of matrix metalloproteinase-2 and tPA, but not uPA activity. Overactivation of NAD(P)H oxidase in HBMECs via cDNA electroporation of its p22-phox subunit confirmed the involvement of tPA in oxidase-mediated BBB disruption. Interestingly, blockade of uPA or uPA receptor preserved normal BBB function by neutralizing both NAD(P)H oxidase and matrix metalloproteinase-2 activities. Hence, selective targeting of uPA after ischaemic strokes may protect cerebral barrier integrity and function by concomitantly attenuating basement membrane degradation and oxidative stress.

PKC-β exacerbates in vitro brain barrier damage in hyperglycemic settings via regulation of RhoA/Rho-kinase/MLC2 pathway

Stroke patients with hyperglycemia (HG) develop higher volumes of brain edema emerging from disruption of blood-brain barrier (BBB). This study explored whether inductions of protein kinase C-β (PKC-β) and RhoA/Rho-kinase/myosin-regulatory light chain-2 (MLC2) pathway may account for HG-induced barrier damage using an in vitro model of human BBB comprising human brain microvascular endothelial cells (HBMEC) and astrocytes. Hyperglycemia (25 mmol/L D-glucose) markedly increased RhoA/Rho-kinase protein expressions (in-cell westerns), MLC2 phosphorylation (immunoblotting), and PKC-β (PepTag assay) and RhoA (Rhotekin-binding assay) activities in HBMEC while concurrently reducing the expression of tight junction protein occludin. Hyperglycemia-evoked in vitro barrier dysfunction, confirmed by decreases in transendothelial electrical resistance and concomitant increases in paracellular flux of Evan's blue-labeled albumin, was accompanied by malformations of actin cytoskeleton and tight junctions. Suppression of RhoA and Rho-kinase activities by anti-RhoA immunoglobulin G (IgG) electroporation and Y-27632, respectively prevented morphologic changes and restored plasma membrane localization of occludin. Normalization of glucose levels and silencing PKC-β activity neutralized the effects of HG on occludin and RhoA/Rho-kinase/MLC2 expression, localization, and activity and consequently improved in vitro barrier integrity and function. These results suggest that HG-induced exacerbation of the BBB breakdown after an ischemic stroke is mediated in large part by activation of PKC-β.

Numerical prediction of the low-velocity impact damage and compression after impact strength of composite laminates

Low-velocity impact damage can drastically reduce the residual mechanical properties of the composite structure even when there is barely visible impact damage. The ability to computationally predict the extent of damage and compression after impact (CAI) strength of a composite structure can potentially lead to the exploration of a larger design space without incurring significant development time and cost penalties. A three-dimensional damage model, to predict both low-velocity impact damage and compression after impact CAI strength of composite laminates, has been developed and implemented as a user material subroutine in the commercial finite element package, ABAQUS/Explicit. The virtual tests were executed in two steps, one to capture the impact damage and the other to predict the CAI strength. The observed intra-laminar damage features, delamination damage area as well as residual strength are discussed. It is shown that the predicted results for impact damage and CAI strength correlated well with experimental testing.

Investigations into the Control of Biofilm Damage with Relevance to Built Heritage (BIODAM)

This publication describes the results of a 3 year EC-funded R&D project (BIODAM) which investigated the effects of biological colonisation on heritage surfaces and evaluated of novel, low toxicity treatments for their ability to control of biofilms and for their compatibility with conservation products.