Predicting low-velocity impact damage on a stiffened composite panel

An intralaminar damage model, based on a continuum damage mechanics approach, is presented to model the damage mechanisms occurring in carbon fibre composite structures incorporating fibre tensile and compressive breakage, matrix tensile and compressive fracture, and shear failure. The damage model, together with interface elements for capturing interlaminar failure, is implemented in a finite element package and used in a detailed finite element model to simulate the response of a stiffened composite panel to low-velocity impact. Contact algorithms and friction between delaminated plies were included, to better simulate the impact event. Analyses were executed on a high performance computer (HPC) cluster to reduce the actual time required for this detailed numerical analysis. Numerical results relating to the various observed interlaminar damage mechanisms, delamination initiation and propagation, as well as the model’s ability to capture post-impact permanent indentation in the panel are discussed. Very good agreement was achieved with experimentally obtained data of energy absorbed and impactor force versus time. The extent of damage predicted around the impact site also corresponded well with the damage detected by non destructive evaluation of the tested panel.

Element-Free Galerkin modelling of composite damage

Delamination and matrix cracking are routine damage mechanisms, observed by post-mortem analysis of laminated structures containing geometrical features such as notches or bolts. Current finite element tools cannot explicitly model an intralaminar matrix microcrack, except if the location of the damage is specified a priori. In this work, a meshless technique, the Element-Free Galerkin (EFG) method, is utilized for the first time to simulate delamination (interlaminar) and intralaminar matrix microcracking in composite laminates.

Optimization strategy for minimizing damage in postbuckling stiffened panels

Composite materials are finding increasing use on primary aerostructures to meet demanding performance targets while reducing environmental impact. This paper presents a finite-element-based preliminary optimization methodology for postbuckling stiffened panels, which takes into account damage mechanisms that lead to delamination and subsequent failure by stiffener debonding. A global-local modeling approach is adopted in which the boundary conditions on the local model are extracted directly from the global model. The optimization procedure is based on a genetic algorithm that maximizes damage resistance within the postbuckling regime. This routine is linked to a finite element package and the iterative procedure automated. For a given loading condition, the procedure optimized the stacking sequence of several areas of the panel, leading to an evolved panel that displayed superior damage resistance in comparison with nonoptimized designs.

Stiffener debonding mechanisms in post-buckled CFRP aerospace panels

This paper describes the fractographic analysis of five CFRP post-buckled skin/stringer panels that were tested to failure in compression. The detailed damage mechanisms for skin/stiffener detachment in an undamaged panel were characterised and related to the stress conditions during post-buckling; in particular the sites of peak twist (at buckling nodes) and peak bending moments (at buckling anti-nodes). The initial event was intralaminar splitting of the +45 degrees plies adjacent to the skin/stiffener interface, induced by high twist at a nodeline. This was followed by mode II delamination, parallel to +/- 45 degrees plies and then lengthwise (0 degrees) shear along the stiffener centreline. The presence of defects or damage was found to influence this failure process, leading to a reduction in strength. This research provides an insight into the processes that control post-buckled performance of stiffened panels and suggests that 2D models and element tests do not capture the true physics of skin/stiffener detachment: a full 3D approach is required.

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

Optimising postbuckling composite panels for damage resistance

The design of current composite primary aerostructures, such as fuselage or wing stiffened panels, tends to be conservative due to the susceptibility of the relatively weak skin-stiffener interface. This weakness is due to through-thickness stresses which are exacerbated by deformations due to buckling. This paper presents a finite-elementbased optimization strategy, utilizing a global-local modelling approach, for postbuckling stiffened panels which takes into account damage mechanisms which may lead to delamination and subsequent failure of the panel due to stiffener debonding. A genetic algorithm was linked to a finite element package to automate the iterative procedure and maximize the damage resistance of the panel in postbuckling. For a given loading condition, the procedure optimized the panel’s skin layup leading to a design displaying superior damage resistance compared to non-optimized designs

Understanding the Interaction between Low-Energy Electrons and DNA Nucleotides in Aqueous Solution

Reactions that can damage DNA have been simulated using a combination of molecular dynamics and density functional theory. In particular, the damage caused by the attachment of a low energy electron to the nucleobase. Simulations of anionic single nucleotides of DNA in an aqueous environment that was modeled explicitly have been performed. This has allowed us to examine the role played by the water molecules that surround the DNA in radiation damage mechanisms. Our simulations show that hydrogen bonding and protonation of the nucleotide by the water can have a significant effect on the barriers to strand breaking reactions. Furthermore, these effects are not the same for all four of the bases.

Modelling the crush behaviour of thermoplastic composites

Thermoplastic composites are likely to emerge as the preferred solution for meeting the high-volume production demands of passenger road vehicles. Substantial effort is currently being directed towards the development of new modelling techniques to reduce the extent of costly and time consuming physical testing. Developing a high-fidelity numerical model to predict the crush behaviour of composite laminates is dependent on the accurate measurement of material properties as well as a thorough understanding of damage mechanisms associated with crush events. This paper details the manufacture, testing and modelling of self-supporting corrugated-shaped thermoplastic composite specimens for crashworthiness assessment. These specimens demonstrated a 57.3% higher specific energy absorption compared to identical specimen made from thermoset composites. The corresponding damage mechanisms were investigated in-situ using digital microscopy and post analysed using Scanning Electron Microscopy (SEM). Splaying and fragmentation modes were the 2 primary failure modes involving fibre breakage, matrix cracking and delamination. A mesoscale composite damage model, with new non-linear shear constitutive laws, which combines a range of novel techniques to accurately capture the material response under crushing, is presented. The force-displacement curves, damage parameter maps and dissipated energy, obtained from the numerical analysis, are shown to be in a good qualitative and quantitative agreement with experimental results. The proposed approach could significantly reduce the extent of physical testing required in the development of crashworthy structures.  

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.

Creation of damage-free ferroelectric nanocapacitors via focused ion beam milling

We present a novel method for creating damage-free ferroelectric nanostructures with a focused ion beam milling machine. Using a standard e-beam photoresist followed by a dilute acid wash, nanostructures ranging in size from 1 mu m down to 250 nm were created in a 90 nm thick lead zirconate titanate ( PZT) wafer. Transmission electron microscopy and piezoresponse force microscopy ( PFM) confirmed that the surfaces of the nanostructures remained damage free during fabrication, and showed no gallium implantation, and that there was no degradation of ferroelectric properties. In fact DC strain loops, obtained using PFM, demonstrated that the nanostructures have a higher piezoresponse than unmilled films. As the samples did not have any top hard mask, the method presented is unique as it allows for imaging of the top surface to understand edge effects in well-defined nanostructures. In addition, as no post-mill annealing was necessary, it facilitates investigation of nanoscale domain mechanisms without process-induced artefacts.

Resistance mechanisms to cancer chemotherapy

Resistance to chemotherapy ('drug resistance') is a fundamental problem that limits the effectiveness of many chemotherapies currently used to treat cancer. Drug resistance can occur due to a variety of mechanisms, such as increased drug inactivation, drug efflux from cancer cells, enhanced repair of chemotherapy-induced damage, activation of pro-survival pathways and inactivation of cell death pathways. In this article, we review some of the major mechanisms of drug resistance and discuss how new molecularly-targeted therapies are being increasingly used to overcome these resistance mechanisms.

What role for DNA damage and repair in the bystander response?

The radiation-induced bystander effect challenges the accepted paradigm of direct DNA damage in response to energy deposition driving the biological consequences of radiation exposure. With the bystander response, cells which have not been directly exposed to radiation respond to their neighbours being targeted. In our own studies we have used novel targeted microbeam approaches to specifically irradiate parts of individual cells within a population to quantify the bystander response and obtain mechanistic information. Using this approach it has become clear that energy deposited by radiation in nuclear DNA is not required to trigger the effect, with cytoplasmic irradiation required. Irradiated cells also trigger a bystander response regardless of whether they themselves live or die, suggesting that the phenotype of the targeted cell is not a determining factor. Despite this however, a range of evidence has shown that repair status is important for dealing with the consequences of a bystander signal. Importantly, repair processes involved in the processing of dsb appear to be involved suggesting that the bystander response involves the delayed or indirect production of dsb-type lesions in bystander cells. Whether these are infact true dsb or complexes of oxidised bases in combination with strand breaks and the mechanisms for their formation, remains to be elucidated.