Anisotropic damage mechanics as a novel approach to improve pre-and post-failure borehole stability analysis

Anisotropic damage distribution and evolution have a profound effect on borehole stress concentrations. Damage evolution is an irreversible process that is not adequately described within classical equilibrium thermodynamics. Therefore, we propose a constitutive model, based on non-equilibrium thermodynamics, that accounts for anisotropic damage distribution, anisotropic damage threshold and anisotropic damage evolution. We implemented this constitutive model numerically, using the finite element method, to calculate stress–strain curves and borehole stresses. The resulting stress–strain curves are distinctively different from linear elastic-brittle and linear elastic-ideal plastic constitutive models and realistically model experimental responses of brittle rocks. We show that the onset of damage evolution leads to an inhomogeneous redistribution of material properties and stresses along the borehole wall. The classical linear elastic-brittle approach to borehole stability analysis systematically overestimates the stress concentrations on the borehole wall, because dissipative strain-softening is underestimated. The proposed damage mechanics approach explicitly models dissipative behaviour and leads to non-conservative mud window estimations. Furthermore, anisotropic rocks with preferential planes of failure, like shales, can be addressed with our model.

Chromatin modifications involved in the DNA damage response to double strand breaks

In eukaryotes, genomic DNA is tightly compacted into a protein-DNA complex known as chromatin. This dense structure presents a barrier to DNA-dependent processes including transcription, replication and DNA repair. The repressive structure of chromatin is overcome by ATP-dependent chromatin remodelling complexes and chromatin-modifying enzymes. There is now ample evidence that DNA double-strand breaks (DSBs) elicit various histone modifications (such as acetylation, deacetylation, and phosphorylation) that function combinatorially to control the dynamic structure of the chromatin microenvironment. The role of these mechanisms during transcription and replication has been well studied, while the research into their impact on regulation of DNA damage response is rapidly gaining momentum. How chromatin structure is remodeled in response to DNA damage and how such alterations influence DSB repair are currently significant questions. This review will summarise the major chromatin modifications and chromatin remodelling complexes implicated in the DNA damage response to DSBs.

Damage diagnosis for complex steel truss bridges using multi-layer genetic algorithm

Considerate amount of research has proposed optimization-based approaches employing various vibration parameters for structural damage diagnosis. The damage detection by these methods is in fact a result of updating the analytical structural model in line with the current physical model. The feasibility of these approaches has been proven. But most of the verification has been done on simple structures, such as beams or plates. In the application on a complex structure, like steel truss bridges, a traditional optimization process will cost massive computational resources and lengthy convergence. This study presents a multi-layer genetic algorithm (ML-GA) to overcome the problem. Unlike the tedious convergence process in a conventional damage optimization process, in each layer, the proposed algorithm divides the GA’s population into groups with a less number of damage candidates; then, the converged population in each group evolves as an initial population of the next layer, where the groups merge to larger groups. In a damage detection process featuring ML-GA, as parallel computation can be implemented, the optimization performance and computational efficiency can be enhanced. In order to assess the proposed algorithm, the modal strain energy correlation (MSEC) has been considered as the objective function. Several damage scenarios of a complex steel truss bridge’s finite element model have been employed to evaluate the effectiveness and performance of ML-GA, against a conventional GA. In both single- and multiple damage scenarios, the analytical and experimental study shows that the MSEC index has achieved excellent damage indication and efficiency using the proposed ML-GA, whereas the conventional GA only converges at a local solution.

Damage identification and condition assessment of building structures using frequency response functions and neural networks

This thesis investigated the viability of using Frequency Response Functions in combination with Artificial Neural Network technique in damage assessment of building structures. The proposed approach can help overcome some of limitations associated with previously developed vibration based methods and assist in delivering more accurate and robust damage identification results. Excellent results are obtained for damage identification of the case studies proving that the proposed approach has been developed successfully.

Cutaneous markers of photo-damage and risk of basal cell carcinoma of the skin : a meta-analysis

BACKGROUND: Epidemiologic research has demonstrated that cutaneous markers of photo-damage are associated with risk of basal cell carcinoma (BCC). However there has been no previous attempt to calculate pooled risk estimates. METHODS: We conducted a systematic review and meta-analysis after extracting relevant studies published up to January 2013 from five electronic databases. Eligible studies were those that permitted quantitative assessment of the association between histologically-confirmed BCC and actinic keratoses, solar elastosis, solar lentigines, or telangiectasia. RESULTS: Seven eligible studies were identified and summary odds ratios (OR) were calculated using both random and quality effects models. Having more than ten actinic keratoses was most strongly associated with BCC, conferring up to a 5-fold increase in risk (OR: 4.97; 95% CI: 3.26, 7.58). Other factors, including solar elastosis, solar lentigines, and telangiectasia had weaker but positive associations with BCC with ORs around 1.5. CONCLUSIONS: Markers of chronic photo-damage are positively associated with BCC. The presence of actinic keratoses was the most strongly associated with BCC of the markers examined. IMPACT: This work highlights the relatively modest association between markers of chronic ultraviolet exposure and BCC.

The suitability of using accumulated plastic strain to assess the damage at the rail-wheel interfaces

Numerous Abaqus [1] finite element analyses have been carried out using various plasticity models to investigate the effect of friction force on the rail head in relation to both the development of the accumulated plastic strain (PEEQ) and the changes in the depth of PEEQ distribution in the wheel-rail contact. The normal force distribution on the rail head was assumed to be Hertzian. The tangential force was implemented as a fraction of the normal force in the subroutine. Each analysis was carried out for a single pass and the effect of various friction coefficient values has been observed.

Damage assessment in beams and plates using variations in modal properties

Damage detection using modal properties is a widely accepted method. However, quantifying such damage using modal properties is still not well established. With this in mind, a research project is presently underway towards the development of a procedure to detect, locate and quantify damage in structural components using the variations in modal properties. A novel vibration based parameter called Vibration based Damage Index is introduced into the damage assessment procedure. This paper presents the early part of the research project which treats flexural members. The proposed procedure is validated using experimental data and/or theoretical techniques and illustrated through application. Outcomes of this research highlight the ability of the proposed procedure to successfully detect, locate and quantify damage in flexural structural components using the modal properties of the first few modes.

Controlling whole blood activation and resultant clot properties on various material surfaces : a possible therapeutic approach for enhancing bone healing

Injured bone initiates the healing process by forming a blood clot at the damaged site. However, in severe damage, synthetic bone implants are used to provide structural integrity and restore the healing process. The implant unavoidably comes into direct contact with whole blood, leading to a blood clot formation on its surface. Despite this, most research in bone tissue engineering virtually ignores the important role of a blood clot in supporting healing. Surface chemistry of a biomaterial is a crucial property in mediating blood-biomaterials interactions, and hence the formation of the resultant blood clot. Surfaces presenting mixtures of functional groups carboxyl (–COOH) and methyl (–CH3) have been shown to enhance platelet response and coagulation activation, leading to the formation of fibrin fibres. In addition, it has been shown that varying the compositions of these functional groups and the length of alkyl groups further modulate the immune complement response. In this study, we hypothesised that a biomaterial surface with mixture of –COOH/–CH3(methyl), –CH2CH3 (ethyl) or –(CH2)3CH3 (butyl) groups at different ratios would modulate blood coagulation and complement activation, and eventually tailor the structural and functional properties of the blood clot formed on the surface, which subsequently impacts new bone formation. Firstly, we synthesised a series of materials composed of acrylic acid (AA), and methyl (MMA), ethyl (EMA) or butyl methacrylates (BMA) at different ratios and coated on the inner surfaces of incubation vials. Our surface analysis showed that the amount of –COOH groups on the surface coatings was lower than the ratios of AA prepared in the materials even though the surface content of –COOH groups increased with increasing in AA ratios. It was indicated that the surface hydrophobicity increased with increasing alkyl chain length: –CH 3 > –CH2CH3 > –(CH2)3CH3, and decreased with increasing –COOH groups. No significant differences in surface hydrophobicity was found on surfaces with –CH3 and –CH2CH3 groups in the presence of –COOH groups. The material coating was as smooth as uncoated glass and without any major flaws. The average roughness of material-coated surface (3.99 ± 0.54 nm) was slightly higher than that of uncoated glass surface (2.22 ± 0.29 nm). However, no significant differences in surface average roughness was found among surfaces with the same functionalities at different –COOH ratios nor among surfaces with different alkyl groups but the same –COOH ratios. These suggested that the surface functional groups and their compositions had a combined effect on modulating surface hydrophobicity but not surface roughness. The second part of our study was to investigate the effect of surface functional groups and their compositions on blood cascade activation and structural properties of the formed clots. It was found that surfaces with –COOH/–(CH2)3CH3 induced a faster coagulation activation than those with –COOH/–CH3 and –CH2CH3, regardless of the –COOH ratios. An increase in –COOH ratios on –COOH/–CH3 and –CH2CH3 surfaces decreased the rate of activation. Moreover, all material-coated surfaces markedly reduced the complement activation compared to uncoated glass surfaces, and the pattern of complement activation was entirely similar to that of surface-induced coagulation, suggesting there is an interaction between two cascades. The clots formed on material-coated surfaces had thicker fibrin with a tighter network at the exterior when compared to uncoated glass surfaces. Compared to the clot exteriors, thicker fibrins with a loose network were found in clot interiors. Coated surfaces resulted in more rigid clots with a significantly slower fibrinolysis after 1 h of lysis when compared to uncoated glass surfaces. Significant differences in fibrinolysis after 1 h of lysis among clots on material-coated surfaces correlated well with the differences in fibrin thickness and density at clot exterior. In addition, more growth factors were released during clot formation than during clot lysis. From an intact clot, there was a correlation between the amount of PDGF-AB release and fibrin density. Highest amount of PDGF-AB was released from clots formed on surfaces with 40% –COOH/60% –CH 3 (i.e. 65MMA). During clot lysis, the release of PDGF-AB also correlated with the fibrinolytic rate while the release of TGF-â1 was influenced by the fibrin thickness. This suggested that different clot structures led to different release profiles of growth factors in clot intact and degrading stages. We further validated whether the clots formed on material-coatings provide the microenvironment for improved bone healing by using a rabbit femoral defect model. In this pilot study, the implantation of clots formed on 65MMA coatings significantly increased new bone formation with enhanced chondrogenesis, osteoblasts activity and vascularisation, but decreased inflammatory macrophage number at the defects after 4 weeks when compared to commercial bone grafts ChronOSTM â-TCP granules. Empty defects were observed when blood clot formation was inhibited. In summary, our study demonstrated that surface functional groups and their relative ratios on material coatings synergistically modulate activation of blood cascades, resultant fibrin architecture, rigidity, susceptibility to fibrinolysis as well as growth factor release of the formed clots, which ultimately alter the healing microenvironment of injured bones.

Assessment of damages for wrongful birth and consolidation in advance care directives

The recent decision of Waller v James involved a claim by the plaintiff parents for damages for wrongful birth against the defendant doctor, Dr James, a gynaecologist with a practice in infertility and IVF procedures, who had been consulted by the plaintiffs. The second plaintiff, Mr Waller suffered an inherited anti-thrombin deficiency (ATD), a condition which results in a propensity for the blood to clot, at least in adults. Dr James subsequently recommended IVF treatment. The first plaintiff, Mrs Waller became pregnant after the first cycle of IVF treatment. Her son Keeden was born on 10 August 2000 with a genetic anti-thrombin deficiency. Keeden was released from hospital on 14 August 2000. However, he was brought back to the hospital the next day with cerebral thrombosis (CSVT). As a result of the thrombosis, he suffered permanent brain damage, cerebral palsy and related disabilities. The plaintiffs alleged that the defendant was in breach of contract and his common law duty of care to the plaintiffs in failing to inform them, or cause them to be informed, of the hereditary aspects of ATD. They further alleged that, had they been properly informed, they would not have proceeded to conceive a child using the male plaintiff’s sperm and therefore avoided the harm that had befallen them. The plaintiffs claimed damages to compensate them for their losses, including psychiatric and physical injuries and the costs of having, raising and caring for Keeden. The defendant was held to be not liable in negligence by Justice Hislop of the Supreme Court of New South Wales because a finding was made on medical causation which was adverse to the plaintiffs claim.

Evaluation of the alkaline comet assay and urinary 3-methyladenine excretion for monitoring DNA damage in melanoma patients treated with dacarbazine and tamoxifen

Purpose: To develop, using dacarbazine as a model, reliable techniques for measuring DNA damage and repair as pharmacodynamic endpoints for patients receiving chemotherapy. Methods: A group of 39 patients with malignant melanoma were treated with dacarbazine 1 g/m2 i.v. every 21 days. Tamoxifen 20 mg daily was commenced 24 h after the first infusion and continued until 3 weeks after the last cycle of chemotherapy. DNA strand breaks formed during dacarbazine-induced DNA damage and repair were measured in individual cells by the alkaline comet assay. DNA methyl adducts were quantified by measuring urinary 3-methyladenine (3-MeA) excretion using immunoaffinity ELISA. Venous blood was taken on cycles 1 and 2 for separation of peripheral blood lymphocytes (PBLs) for measurement of DNA strand breaks. Results: Wide interpatient variation in PBL DNA strand breaks occurred following chemotherapy, with a peak at 4 h (median 26.6 h, interquartile range 14.75- 40.5 h) and incomplete repair by 24 h. Similarly, there was a range of 3-MeA excretion with peak levels 4-10 h after chemotherapy (median 33 nmol/h, interquartile range 20.448.65 nmol/h). Peak 3-MeA excretion was positively correlated with DNA strand breaks at 4 h (Spearman's correlation coefficient, r = 0.39, P = 0.036) and 24 h (r = 0.46, P = 0.01). Drug-induced emesis correlated with PBL DNA strand breaks (Mann Whitney U-test, P = 0.03) but not with peak 3-MeA excretion. Conclusions: DNA damage and repair following cytotoxic chemotherapy can be measured in vivo by the alkaline comet assay and by urinary 3-MeA excretion in patients receiving chemotherapy.

Fatigue damage initiation life prediction for heterogeneous metals

In particle-strengthened metallic alloys, fatigue damage incubates at inclusion particles near the surface or at the change of geometries. Micromechanical simulation of inclusions such that the fatigue damage incubation mechanisms can be categorized. As micro-plasticity gradient field around different inclusions is different, a novel concept for nonlocal evaluation of micro-plasticity intensity is introduced. The effects of void aspects ration and spatial distributions are quantified for fatigue incubation life in the high-cycle fatigue regime. At last, these effects are integrated based on the statistical facts of inclusions to predict the fatigue life of structural components.

Modal flexibility method for structural damage detection in suspension bridges

Suspension bridges meet the steadily growing demand for lighter and longer bridges in today’s infrastructure systems. These bridges are designed to have long life spans, but with age, their main cables and hangers could suffer from corrosion and fatigue. There is a need for a simple and reliable procedure to detect and locate such damage, so that appropriate retrofitting can be carried out to prevent bridge failure. Damage in a structure causes changes in its properties (mass, damping and stiffness) which in turn will cause changes in its vibration characteristics (natural frequencies, modal damping and mode shapes). Methods based on modal flexibility, which depends on both the natural frequencies and mode shapes, have the potential for damage detection. They have been applied successfully to beam and plate elements, trusses and simple structures in reinforced concrete and steel. However very limited applications for damage detection in suspension bridges have been identified to date. This paper examines the potential of modal flexibility methods for damage detection and localization of a suspension bridge under different damage scenarios in the main cables and hangers using numerical simulation techniques. Validated finite element model (FEM) of a suspension bridge is used to acquire mass normalized mode shape vectors and natural frequencies at intact and damaged states. Damage scenarios will be simulated in the validated FE models by varying stiffness of the damaged structural members. The capability of damage index based on modal flexibility to detect and locate damage is evaluated. Results confirm that modal flexibility based methods have the ability to successfully identify damage in suspension bridge main cables and hangers.

Damage detection in cable structures using vibration characteristics

Cable structures find many applications such as in power transmission, in anchors and especially in bridges. They serve as major load bearing elements in suspension bridges, which are capable of spanning long distances. All bridges, including suspension bridges, are designed to have long service lives. However, during this long life, they become vulnerable to damage due to changes in loadings, deterioration with age and random action such as impacts. The main cables are more vulnerable to corrosion and fatigue, compared to the other bridge components, and consequently reduces the serviceability and ultimate capacity of the bridge. Detecting and locating such damage at the earliest stage is challenging in the current structural health monitoring (SHM) systems of long span suspension bridges. Damage or deterioration of a structure alters its stiffness, mass and damping properties which in turn modify its vibration characteristics. This phenomenon can therefore be used to detect damage in a structure. The modal flexibility, which depends on the vibration characteristics of a structure, has been identified as a successful damage indicator in beam and plate elements, trusses and simple structures in reinforced concrete and steel. Successful application of the modal flexibility phenomenon to detect and locate the damage in suspension bridge main cables has received limited attention in recent research work. This paper, therefore examines the potential of the modal flexibility based Damage Index (DI) for detecting and locating damage in the main cable of a suspension bridge under four different damage scenarios. Towards this end, a numerical model of a suspension bridge cable was developed to extract the modal parameters at both damaged and undamaged states. Damage scenarios considered in this study with varied location and severity were simulated by changing stiffness at particular locations of the cable model. Results confirm that the DI has the potential to successfully detect and locate damage in suspension bridge main cables. This simple method can therefore enable bridge engineers and managers to detect and locate damage in suspension bridges at an early stage, minimize expensive retrofitting and prevent bridge collapse.

Effects of wireless sensor network uncertainties on output-only modal-based damage identification

The use of Wireless Sensor Networks (WSNs) for Structural Health Monitoring (SHM) has become a promising approach due to many advantages such as low cost, fast and flexible deployment. However, inherent technical issues such as data synchronization error and data loss have prevented these distinct systems from being extensively used. Recently, several SHM-oriented WSNs have been proposed and believed to be able to overcome a large number of technical uncertainties. Nevertheless, there is limited research examining effects of uncertainties of generic WSN platform and verifying the capability of SHM-oriented WSNs, particularly on demanding SHM applications like modal analysis and damage identification of real civil structures. This article first reviews the major technical uncertainties of both generic and SHM-oriented WSN platforms and efforts of SHM research community to cope with them. Then, effects of the most inherent WSN uncertainty on the first level of a common Output-only Modal-based Damage Identification (OMDI) approach are intensively investigated. Experimental accelerations collected by a wired sensory system on a benchmark civil structure are initially used as clean data before being contaminated with different levels of data pollutants to simulate practical uncertainties in both WSN platforms. Statistical analyses are comprehensively employed in order to uncover the distribution pattern of the uncertainty influence on the OMDI approach. The result of this research shows that uncertainties of generic WSNs can cause serious impact for level 1 OMDI methods utilizing mode shapes. It also proves that SHM-WSN can substantially lessen the impact and obtain truly structural information without having used costly computation solutions.