Novel approaches for monitoring effects of steel corrosion in reinforced concrete

Corrosion of steel reinforcement is a common deterioration mechanism in reinforced concrete structures. This deterioration impacts the safety of the structure and may require extensive repair and maintenance work.There is currently no method available for accurately measuring internal corrosion damage non-destructively.Therefore, establishing correlations between outer signs of corrosion, such as crack pattern and width, and the corresponding internal corrosion morphology and level is of significant interest.However, prior research has shown that relying solely on crack width as a performance indicator for corrosion damage is inadequate. Hence, further research is needed to study the corrosion and cracking processes in reinforced concrete to be able to identify and quantify underlying physical processes and factors.To contribute to knowledge in the field, this thesis focuses on novel approaches for non-destructive monitoring of the effects of steel corrosion in small-scale reinforced concrete samples.In this work, time-resolved neutron and X-ray Computed Tomography were applied to link the evolution of material phases to kinematics.Further, two independent studies, one using neutron and the other using X-ray Computed Tomography, were used to quantify corrosion-induced deformations within concrete. These deformations were successfully quantified, and the identified locations of concrete cracking correlated well with the observed strain localisation.Interestingly, the kinematics quantified allowed for the detection of strain localisation in areas where concrete cracks were too small to be visually identified from the image data, indicating the potential for early-stage concrete crack detection.Additionally, an expression for the average volumetric strain in the compressed corrosion layer was derived based on the evolution of material phases within the sample.Further, an experimental setup was designed to monitor corrosion-induced deformations adjacent to the steel-concrete interface using an open-ended steel tube instrumented with an optical fibre for distributed strain sensing.X-ray Computed Tomography allowed for quantitative and qualitative assessment of corrosion level and concrete cracking. The corrosion-induced deformations in the steel tube were found to be non-uniform, indicating a non-uniform distribution of radial stress around the steel. This non-uniformity correlated well with the location of the corrosion-induced cracks, with extension hoop strains observed in the steel tube at the location of these cracks, and contraction hoop strains observed in between them.Corrosion was more severe in bands along the steel, coinciding with the position of the longitudinal cracks.The research conducted in this work demonstrated the potential of non-destructive monitoring of steel corrosion in reinforced concrete.For future research aiming at increasing the fundamental understanding of corrosion-induced concrete cracking, it is essential to integrate advanced experimental techniques with numerical modelling

A two-stage study of steel corrosion and internal cracking revealed by multimodal tomography

Modeling of corrosion-induced cracking is limited by lacking knowledge on the behavior of corrosion products. In this work, the corrosion and cracking processes were experimentally investigated in 3D at two different stages. The processes were measured at micro-structural scale, applying nondestructive neutron and X-ray computed tomography in two scans at different stages in the corrosion process. A method to evaluate the average volumetric strain of the compressed corrosion layer was proposed and displacements in the concrete matrix were measured. Strain localization revealed cracks not directly visible in the images. Multimodal tomography demonstrated to be an effective method for investigating steel corrosion in reinforced concrete

Physiological levels of nitrate support anoxic growth by denitrification of Pseudomonas aeruginosa at growth rates reported in cystic fibrosis lungs and sputum

© 2014 Line, Alhede, Kolpen, Kuhl, Ciofu, Bjarnsholt, Moser, Toyofuku, Nomura, H0i'by and Jensen. Chronic Pseudomonas aeruginosa lung infection is the most severe complication in patients with cystic fibrosis (CF). The infection is characterised by the formation of biofilm surrounded by numerous polymorphonuclear leukocytes (PMNs) and strong O2 depletion in the endobronchial mucus. We have reported that O2 is mainly consumed by the activated PMNs, while O2 consumption by aerobic respiration is diminutive and nitrous oxide (N2O) is produced in infected CF sputum. This suggests that the reported growth rates ofP. aeruginosa in lungs and sputum may result from anaerobic respiration using denitrification. The growth rate of P. aeruginosa achieved by denitrification at physiological levels (~400 μM) of nitrate (NO3-) is however, not known. Therefore, we have measured growth rates of anoxic cultures of PAO1 and clinical isolates (n = 12) in LB media supplemented with NO3- and found a significant increase of growth when supplementing PAO1 and clinical isolates with > 150 μM NO3- and 100 μM NO3-, respectively. An essential contribution to growth by denitrification was demonstrated by the inability to establish a significantly increased growth rate by a denitrification deficient ΔnirS-N mutant at <1 mM of NO3-. Activation of denitrification could be achieved by supplementation with as little as 62.5 μM of NO3- according to the significant production of N2O by the nitrous oxide reductase deficient ΔnosZ mutant. Studies of the promoter activity, gene transcripts and enzyme activity of the four N-oxide reductases in PAO1 (Nar, Nir, Nor, Nos) further verified the engagement of denitrification, showing a transient increase in activation and expression and rapid consumption of NO3- followed by a transient increase of NO2-. Growth rates obtained by denitrification in this study were comparable to our reported growth rates in the majority of P. aeruginosa cells in CF lungs and sputum. Thus, we have demonstrated that denitrification is required for P. aeruginosa growth in infected endobronchial CF mucus

In silico analyses of metagenomes from human atherosclerotic plaque samples

Background Through several observational and mechanistic studies, microbial infection is known to promote cardiovascular disease. Direct infection of the vessel wall, along with the cardiovascular risk factors, is hypothesized to play a key role in the atherogenesis by promoting an inflammatory response leading to endothelial dysfunction and generating a proatherogenic and prothrombotic environment ultimately leading to clinical manifestations of cardiovascular disease, e.g., acute myocardial infarction or stroke. There are many reports of microbial DNA isolation and even a few studies of viable microbes isolated from human atherosclerotic vessels. However, high-resolution investigation of microbial infectious agents from human vessels that may contribute to atherosclerosis is very limited. In spite of the progress in recent sequencing technologies, analyzing host-associated metagenomes remain a challenge. Results To investigate microbiome diversity within human atherosclerotic tissue samples, we employed high-throughput metagenomic analysis on: (1) atherosclerotic plaques obtained from a group of patients who underwent endarterectomy due to recent transient cerebral ischemia or stroke. (2) Presumed stabile atherosclerotic plaques obtained from autopsy from a control group of patients who all died from causes not related to cardiovascular disease. Our data provides evidence that suggest a wide range of microbial agents in atherosclerotic plaques, and an intriguing new observation that shows these microbiota displayed differences between symptomatic and asymptomatic plaques as judged from the taxonomic profiles in these two groups of patients. Additionally, functional annotations reveal significant differences in basic metabolic and disease pathway signatures between these groups. Conclusions We demonstrate the feasibility of novel high-resolution techniques aimed at identification and characterization of microbial genomes in human atherosclerotic tissue samples. Our analysis suggests that distinct groups of microbial agents might play different roles during the development of atherosclerotic plaques. These findings may serve as a reference point for future studies in this area of research

Complete Genome Sequence of the Cystic Fibrosis Pathogen Achromobacter xylosoxidans NH44784-1996 Complies with Important Pathogenic Phenotypes

Achromobacter xylosoxidans is an environmental opportunistic pathogen, which infects an increasing number of immunocompromised patients. In this study we combined genomic analysis of a clinical isolated A. xylosoxidans strain with phenotypic investigations of its important pathogenic features. We present a complete assembly of the genome of A. xylosoxidans NH44784-1996, an isolate from a cystic fibrosis patient obtained in 1996. The genome of A. xylosoxidans NH44784-1996 contains approximately 7 million base pairs with 6390 potential protein-coding sequences. We identified several features that render it an opportunistic human pathogen, We found genes involved in anaerobic growth and the pgaABCD operon encoding the biofilm adhesin poly-?-1,6-N-acetyl-D-glucosamin. Furthermore, the genome contains a range of antibiotic resistance genes coding efflux pump systems and antibiotic modifying enzymes. In vitro studies of A. xylosoxidans NH44784-1996 confirmed the genomic evidence for its ability to form biofilms, anaerobic growth via denitrification, and resistance to a broad range of antibiotics. Our investigation enables further studies of the functionality of important identified genes contributing to the pathogenicity of A. xylosoxidans and thereby improves our understanding and ability to treat this emerging pathogen