Elastic and statistically brittle (ESB) model, damage localization and catastrophic rupture

In this paper, an elastic and statistically brittle (ESB) model is applied to the process of damage evolution induced catastrophic rupture and the influence of localization and softening on catastrophic rupture is discussed. According to the analysis, the uncertainty of catastrophic rupture should be attributed to the unknown scale of localized zone. Based on the elastic and statistically brittle model but local mean field approximation, the relation between the scale of localized zone and catastrophic rupture is obtained and then justified with experiments. These results can not only give a deeper understanding of the mechanism governing catastrophic rupture, but also provide a possible tool to foresee the occurrence of catastrophic rupture.

The elasto-damage theory of the components assembling model

The potential energy in materials is well approximated by pair functional which is composed of pair potentials and embedding energy. During calculating material potential energy, the orientational component and the volumetric component are derived respectively from pair potentials and embedding energy. The sum of energy of all these two kinds of components is the material potential. No matter how microstructures change, damage or fracture, at the most level, they are all the changing and breaking atomic bonds. As an abstract of atomic bonds, these components change their stiffness during damaging. Material constitutive equations have been formulated by means of assembling all components' response functions. This material model is called the component assembling model. Theoretical analysis and numerical computing indicate that the proposed model has the capacity of reproducing some results satisfactorily, with the advantages of great conceptual simplicity, physical explicitness, and intrinsic induced anisotropy, etc.

Effect of Neonatal Asphyxia on the Impairment of the Auditory Pathway by Recording Auditory Brainstem Responses in Newborn Piglets: A New Experimentation Model to Study the Perinatal Hypoxic-Ischemic Damage on the Auditory Syste

Introduction Hypoxia-ischemia (HI) is a major perinatal problem that results in severe damage to the brain impairing the normal development of the auditory system. The purpose of the present study is to study the effect of perinatal asphyxia on the auditory pathway by recording auditory brain responses in a novel animal experimentation model in newborn piglets. Method Hypoxia-ischemia was induced to 1.3 day-old piglets by clamping 30 minutes both carotid arteries by vascular occluders and lowering the fraction of inspired oxygen. We compared the Auditory Brain Responses (ABRs) of newborn piglets exposed to acute hypoxia/ischemia (n = 6) and a control group with no such exposure (n = 10). ABRs were recorded for both ears before the start of the experiment (baseline), after 30 minutes of HI injury, and every 30 minutes during 6 h after the HI injury. Results Auditory brain responses were altered during the hypoxic-ischemic insult but recovered 30-60 minutes later. Hypoxia/ischemia seemed to induce auditory functional damage by increasing I-V latencies and decreasing wave I, III and V amplitudes, although differences were not significant. Conclusion The described experimental model of hypoxia-ischemia in newborn piglets may be useful for studying the effect of perinatal asphyxia on the impairment of the auditory pathway.

A bone remodelling model coupling micro-damage growth and repair by 3D BMU-activity.

Bone as most of living tissues is able, during its entire lifetime, to adapt its internal microstructure and subsequently its associated mechanical properties to its specific mechanical and physiological environment in a process commonly known as bone remodelling. Bone is therefore continuously renewed and micro-damage, accumulated by fatigue or creep, is removed minimizing the risk of fracture. Nevertheless, bone is not always able to repair itself completely. Actually, if bone repairing function is slower than micro-damage accumulation, a type of bone fracture, usually known as "stress fracture", can finally evolve. In this paper, we propose a bone remodelling continuous model able to simulate micro-damage growth and repair in a coupled way and able therefore to predict the occurrence of "stress fractures". The biological bone remodelling process is modelled in terms of equations that describe the activity of basic multicellular units. The predicted results show a good correspondence with experimental and clinical data. For example, in disuse, bone porosity increases until an equilibrium situation is achieved. In overloading, bone porosity decreases unless the damage rate is so high that causes resorption or "stress fracture".

A flexural crack model for damage detection in reinforced concrete structures

The use of changes in vibration data for damage detection of reinforced concrete structures faces many challenges that obstruct its transition from a research topic to field applications. Among these is the lack of appropriate damage models that can be deployed in the damage detection methods. In this paper, a model of a simply supported reinforced concrete beam with multiple cracks is developed to examine its use for damage detection and structural health monitoring. The cracks are simulated by a model that accounts for crack formation, propagation and closure. The beam model is studied under different dynamic excitations, including sine sweep and single excitation frequency, for various damage levels. The changes in resonant frequency with increasing loads are examined along with the nonlinear vibration characteristics. The model demonstrates that the resonant frequency reduces by about 10% at the application of 30% of the ultimate load and then drops gradually by about 25% at 70% of the ultimate load. The model also illustrates some nonlinearity in the dynamic response of damaged beams. The appearance of super-harmonics shows that the nonlinearity is higher when the damage level is about 35% and then decreases with increasing damage. The restoring force-displacement relationship predicted the reduction in the overall stiffness of the damaged beam. The model quantitatively predicts the experimental vibration behaviour of damaged RC beams and also shows the damage dependency of nonlinear vibration behaviour. © 2011 Published under licence by IOP Publishing Ltd.

Altered gene expression and DNA damage in peripheral blood cells from Friedreich's ataxia patients: cellular model of pathology.

The neurodegenerative disease Friedreich's ataxia (FRDA) is the most common autosomal-recessively inherited ataxia and is caused by a GAA triplet repeat expansion in the first intron of the frataxin gene. In this disease, transcription of frataxin, a mitochondrial protein involved in iron homeostasis, is impaired, resulting in a significant reduction in mRNA and protein levels. Global gene expression analysis was performed in peripheral blood samples from FRDA patients as compared to controls, which suggested altered expression patterns pertaining to genotoxic stress. We then confirmed the presence of genotoxic DNA damage by using a gene-specific quantitative PCR assay and discovered an increase in both mitochondrial and nuclear DNA damage in the blood of these patients (p<0.0001, respectively). Additionally, frataxin mRNA levels correlated with age of onset of disease and displayed unique sets of gene alterations involved in immune response, oxidative phosphorylation, and protein synthesis. Many of the key pathways observed by transcription profiling were downregulated, and we believe these data suggest that patients with prolonged frataxin deficiency undergo a systemic survival response to chronic genotoxic stress and consequent DNA damage detectable in blood. In conclusion, our results yield insight into the nature and progression of FRDA, as well as possible therapeutic approaches. Furthermore, the identification of potential biomarkers, including the DNA damage found in peripheral blood, may have predictive value in future clinical trials.