Final report : a software diagnostic tool for evaluating distress mechanisms in bridges exposed to aggressive environments

Durability issues of reinforced concrete construction cost millions of dollars in repair or demolition. Identification of the causes of degradation and a prediction of service life based on experience, judgement and local knowledge has limitations in addressing all the associated issues. The objective of this CRC CI research project is to develop a tool that will assist in the interpretation of the symptoms of degradation of concrete structures, estimate residual capacity and recommend cost effective solutions. This report is a documentation of the research undertaken in connection with this project. The primary focus of this research is centred on the case studies provided by Queensland Department of Main Roads (QDMR) and Brisbane City Council (BCC). These organisations are endowed with the responsibility of managing a huge volume of bridge infrastructure in the state of Queensland, Australia. The main issue to be addressed in managing these structures is the deterioration of bridge stock leading to a reduction in service life. Other issues such as political backlash, public inconvenience, approach land acquisitions are crucial but are not within the scope of this project. It is to be noted that deterioration is accentuated by aggressive environments such as salt water, acidic or sodic soils. Carse, 2005, has noted that the road authorities need to invest their first dollars in understanding their local concretes and optimising the durability performance of structures and then look at potential remedial strategies.

Damage propagation in reinforced concrete frames under external blast loading

Iconic and significant buildings are the common target of bombings by terrorists causing large numbers of casualties and extensive property damage. Recent incidents were external bomb attacks on multi-storey buildings with reinforced concrete frames. Under a blast load circumstance, crucial damage initiates at low level storeys in a building and may then lead to a progressive collapse of whole or part of the structure. It is therefore important to identify the critical initial influence regions along the height, width and depth of the building exposed to blast effects and the structure response in order to assess the vulnerability of the structure to disproportionate and progressive collapse. This paper discusses the blast response and the propagation of its effects on a two dimensional reinforced concrete (RC) frame, designed to withstand normal gravity loads. The explicit finite element code, LS DYNA is used for the analysis. A complete RC portal frame seven storeys by six bays is modelled with reinforcement details and appropriate materials to simulate strain rate effects. Explosion loads derived from standard manuals are applied as idealized triangular pressures on the column faces of the numerical models. The analysis reports the influence of blast propagation as displacements and material yielding of the structural elements in the RC frame. The effected regions are identified and classified according to the load cases. This information can be used to determine the vulnerability of multi-storey RC buildings to various external explosion scenarios and designing buildings to resist blast loads.

Towards a rule-based matrix for evaluating distress mechanisms in bridges

The effective management of bridge stock involves making decisions as to when to repair, remedy, or do nothing, taking into account the financial and service life implications. Such decisions require a reliable diagnosis as to the cause of distress and an understanding of the likely future degradation. Such diagnoses are based on a combination of visual inspections, laboratory tests on samples and expert opinions. In addition, the choice of appropriate laboratory tests requires an understanding of the degradation mechanisms involved. Under these circumstances, the use of expert systems or evaluation tools developed from “realtime” case studies provides a promising solution in the absence of expert knowledge. This paper addresses the issues in bridge infrastructure management in Queensland, Australia. Bridges affected by alkali silica reaction and chloride induced corrosion have been investigated and the results presented using a mind mapping tool. The analysis highights that several levels of rules are required to assess the mechanism causing distress. The systematic development of a rule based approach is presented. An example of this application to a case study bridge has been used to demonstrate that preliminary results are satisfactory.

Evaluation of distress mechanisms in bridges exposed to aggressive environments.

There are about 2500 bridges in Queensland, Australia. Majority of these structures require significant repairs around the halfway mark of their design life with probably 1% or less reaching a 100 year design life. (Carse, 2005). This is due to the fact that bridges constructed in aggressive environments such as the coastal regions experience accelerated deterioration. As a result, maintaining the service delivery of these assets has become one of the important issues for the Queensland Department of Main Roads (QDMR).

Towards a Rule-based matrix for evaluating distress mechanisms in bridges

One of the key issues facing public asset owners is the decision of refurbishing aged built assets. This decision requires an assessment of the “remaining service life” of the key components in a building. The remaining service life is significantly dependent upon the existing condition of the asset and future degradation patterns considering durability and functional obsolescence. Recently developed methods on Residual Service Life modelling, require sophisticated data that are not readily available. Most of the data available are in the form of reports prior to undertaking major repairs or in the form of sessional audit reports. Valuable information from these available sources can serve as bench marks for estimating the reference service life. The authors have acquired similar informations from a public asset building in Melbourne. Using these informations, the residual service life of a case study building façade has been estimated in this paper based on state-of-the-art approaches. These estimations have been evaluated against expert opinion. Though the results are encouraging it is clear that the state-of-the-art methodologies can only provide meaningful estimates provided the level and quality of data are available. This investigation resulted in the development of a new framework for maintenance that integrates the condition assessment procedures and factors influencing residual service life

The distribution and spread of citrus canker in Emerald, Australia

Citrus canker is a disease of citrus and closely related species, caused by the bacterium Xanthomonas citri subsp. citri. This disease, previously exotic to Australia, was detected on a single farm [infested premise-1, (IP1). IP is the terminology used in official biosecurity protocols to describe a locality at which an exotic plant pest has been confirmed or is presumed to exist. IP are numbered sequentially as they are detected] in Emerald, Queensland in July 2004. During the following 10 months the disease was subsequently detected on two other farms (IP2 and IP3) within the same area and studies indicated the disease first occurred on IP1 and spread to IP2 and IP3. The oldest, naturally infected plant tissue observed on any of these farms indicated the disease was present on IP1 for several months before detection and established on IP2 and IP3 during the second quarter (i.e. autumn) 2004. Transect studies on some IP1 blocks showed disease incidences ranged between 52 and 100% (trees infected). This contrasted to very low disease incidence, less than 4% of trees within a block, on IP2 and IP3. The mechanisms proposed for disease spread within blocks include weather-assisted dispersal of the bacterium (e.g. wind-driven rain) and movement of contaminated farm equipment, in particular by pivot irrigator towers via mechanical damage in combination with abundant water. Spread between blocks on IP2 was attributed to movement of contaminated farm equipment and/or people. Epidemiology results suggest: (i) successive surveillance rounds increase the likelihood of disease detection; (ii) surveillance sensitivity is affected by tree size; and (iii) individual destruction zones (for the purpose of eradication) could be determined using disease incidence and severity data rather than a predefined set area.

Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1

Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.

Mechanisms of improvement in treatment for depression : test of a self-efficacy and performance model

Tested D. J. Kavanagh's (1983) depression model's explanation of response to cognitive-behavioral treatment among 19 20–60 yr old Ss who received treatment and 24 age-matched Ss who were assigned to a waiting list. Measures included the Beck Depression Inventory and self-efficacy (SE) and self-monitoring scales. Rises in SE and self-monitored performance of targeted skills were closely associated with the improved depression scores of treated Ss. Improvements in the depression of waiting list Ss occurred through random, uncontrolled events rather than via a systematic increase in specific skills targeted in treatment. SE regarding assertion also predicted depression scores over a 12-wk follow-up.

Investigation of molecular mechanisms regulating biomineralization of pearl oyster Pinctada maxima

Biomineralization is a process encompassing all mineral containing tissues produced within an organism. The most dynamic example of this process is the formation of the mollusk shell, comprising a variety of crystal phases and microstructures. The organic component incorporated within the shell is said to dictate this remarkable architecture. Subsequently, for the past decade considerable research have been undertaken to identify and characterize the protein components involved in biomineralization. Despite these efforts the general understanding of the process remains ambiguous. This study employs a novel molecular approach to further the elucidation of the shell biomineralization. A microarray platform has been custom generated (PmaxArray 1.0) from the pearl oyster Pinctada maxima. PmaxArray 1.0 consists of 4992 expressed sequence tags (ESTs) originating from the mantle, an organ involved in shell formation. This microarray has been used as the primary tool for three separate investigations in an effort to associate transcriptional gene expression from P. maxima to the process of shell biomineralization. The first investigation analyzes the spatial expression of ESTs throughout the mantle organ. The mantle was dissected into five discrete regions and each analyzed for gene expression with PmaxArray 1.0. Over 2000 ESTs were differentially expressed among the tissue sections, identifying five major expression regions. Three of these regions have been proposed to have shell formation functions belonging to nacre, prismatic calcite and periostracum. The spatial gene expression map was confirmed by in situ hybridization, localizing a subset of ESTs from each expression region to the same mantle area. Comparative sequence analysis of ESTs expressed in the proposed shell formation regions with the BLAST tool, revealed a number of the transcripts were novel while others showed significant sequence similarities to previously characterized shell formation genes. The second investigation correlates temporal EST expression during P. maxima larval ontogeny with transitions in shell mineralization during the same period. A timeline documenting the morphologicat microstructural and mineralogical shell characteristics of P. maxima throughout larval ontogeny has been established. Three different shell types were noted based on the physical characters and termed, prodissoconch I, prodissoconch 11 and dissoconch. PmaxArray 1.0 analyzed ESTs expression of animals throughout the larval development of P. maxima, noting up-regulation of 359 ESTs in association with the shell transitions from prodissoconch 1 to prodissoconch 11 to dissoconch. Comparative sequence analysis of these ESTs indicates a number of the transcripts are novel as well as showing significant sequence similarities between ESTs and known shell matrix associated genes and proteins. These ESTs are discussed in relation to the shell characters associated with their temporal expression. The third investigation uses PmaxArray 1.0 to analyze gene expression in the mantle tissue of P. maxima specimens exposed to sub-lethal concentrations of a shell-deforming toxin, tributyltin (TBT). The shell specific effects of TBT are used in this investigation to interpret differential expression of ESTs with respect to shell formation functions. A lethal and sublethal TBT concentration range was established for P. maxima, noting a concentration of 50 ng L- 1 TBT as sub-lethal over a 21 day period. Mantle tissue from P. maxima animals treated with 50 ng L- 1 TBT was assessed for differential EST expression with untreated control animals. A total of 102 ESTs were identified as differentially expressed in association with TBT exposure, comparative sequence identities included an up-regulation of immunity and detoxification related genes and down-regulation of several shell matrix genes. A number of transcripts encoding novel peptides were additionally identified. The potential actions of these genes are discussed with reference to TBT toxicity and shell biomineralization. This thesis has used a microarray platform to analyze gene expression in spatial, temporal and toxicity investigations, revealing the involvement of numerous gene transcripts in specific shell formation functions. Investigation of thousands of transcripts simultaneously has provided a holistic interpretation of the organic components regulating shell biomineralization.

Wear mechanisms and scale effects in two-body abrasion

The ‘particle size effect’ and its manifestation in abrasion still attracts considerable debate as to its origins and the ranking of its likely causes. Experiments have been conducted to study the important contribution that the formation of wear debris can have on the progression of wear. The experiments consist of unlubricated (dry) pin-on-disk tests with silicon carbide coated paper of varying particle size, with different pin material, diameter and loads. It has been observed that the influence of debris formation on wear rate is more pronounced for fine abrasives and soft-wearing materials. Consequently, it is proposed that the particle size effect can be explained in terms of geometrical scaling and the evolution of third-body effects with diminishing particle diameter.

Enhancement of DNA repair using topical T4 endonuclease V does not inhibit melanoma formation in Cdk4R24C/R24C/Tyr-NrasQ61K mice following neonatal UVR

To further investigate the use of DNA repair-enhancing agents for skin cancer prevention, we treated Cdk4R24C/R24C/NrasQ61K mice topically with the T4 endonuclease V DNA repair enzyme (known as Dimericine) immediately prior to neonatal ultraviolet radiation (UVR) exposure, which has a powerful effect in exacerbating melanoma development in the mouse model. Dimericine has been shown to reduce the incidence of basal-cell and squamous cell carcinoma. Unexpectedly, we saw no difference in penetrance or age of onset of melanoma after neonatal UVR between Dimericine-treated and control animals, although the drug reduced DNA damage and cellular proliferation in the skin. Interestingly, epidermal melanocytes removed cyclobutane pyrimidine dimers (CPDs) more efficiently than surrounding keratinocytes. Our study indicates that neonatal UVR-initiated melanomas may be driven by mechanisms other than solely that of a large CPD load and/or their inefficient repair. This is further suggestive of different mechanisms by which UVR may enhance the transformation of keratinocytes and melanocytes.

Damage assessment of 3D reinforced concrete frame under external explosion loading

Multi-storey buildings are highly vulnerable to terrorist bombing attacks in various parts of the world. Large numbers of casualties and extensive property damage result not only from blast overpressure, but also from the failing of structural components. Understanding the blast response and damage consequences of reinforced concrete (RC) building frames is therefore important when assessing multi-storey buildings designed to resist normal gravity loads. However, limited research has been conducted to identify the blast response and damage of RC frames in order to assess the vulnerability of entire buildings. This paper discusses the blast response and evaluation of damage of three-dimension (3D) RC rigid frame under potential blast loads scenarios. The explicit finite element modelling and analysis under time history blast pressure loads were carried out by LS DYNA code. Complete 3D RC frame was developed with relevant reinforcement details and material models with strain rate effect. Idealised triangular blast pressures calculated from standard manuals are applied on the front face of the model in the present investigation. The analysis results show the blast response, as displacements and material yielding of the structural elements in the RC frame. The level of damage is evaluated and classified according to the selected load case scenarios. Residual load carrying capacities are evaluated and level of damage was presented by the defined damage indices. This information is necessary to determine the vulnerability of existing multi-storey buildings with RC frames and to identify the level of damage under typical external explosion environments. It also provides basic guidance to the design of new buildings to resist blast loads.

Damage assessment in structures using vibration characteristics

Changes in load characteristics, deterioration with age, environmental influences and random actions may cause local or global damage in structures, especially in bridges, which are designed for long life spans. Continuous health monitoring of structures will enable the early identification of distress and allow appropriate retrofitting in order to avoid failure or collapse of the structures. In recent times, structural health monitoring (SHM) has attracted much attention in both research and development. Local and global methods of damage assessment using the monitored information are an integral part of SHM techniques. In the local case, the assessment of the state of a structure is done either by direct visual inspection or using experimental techniques such as acoustic emission, ultrasonic, magnetic particle inspection, radiography and eddy current. A characteristic of all these techniques is that their application requires a prior localization of the damaged zones. The limitations of the local methodologies can be overcome by using vibration-based methods, which give a global damage assessment. The vibration-based damage detection methods use measured changes in dynamic characteristics to evaluate changes in physical properties that may indicate structural damage or degradation. The basic idea is that modal parameters (notably frequencies, mode shapes, and modal damping) are functions of the physical properties of the structure (mass, damping, and stiffness). Changes in the physical properties will therefore cause changes in the modal properties. Any reduction in structural stiffness and increase in damping in the structure may indicate structural damage. This research uses the variations in vibration parameters to develop a multi-criteria method for damage assessment. It incorporates the changes in natural frequencies, modal flexibility and modal strain energy to locate damage in the main load bearing elements in bridge structures such as beams, slabs and trusses and simple bridges involving these elements. Dynamic computer simulation techniques are used to develop and apply the multi-criteria procedure under different damage scenarios. The effectiveness of the procedure is demonstrated through numerical examples. Results show that the proposed method incorporating modal flexibility and modal strain energy changes is competent in damage assessment in the structures treated herein.