Safety assessment of masonry arch bridges considering the fracturing benefit

The evolutionary analysis of the fracturing process is an effective tool to assess of the structural bearing capacity of masonry arch bridges. Despite their plain basic assumptions, it must be remarked that elastic analysis and plastic or limit analysis can hardly be used to describe the response and predict damage for moderate or service load levels in masonry arch bridges. Therefore, a fracture mechanics-based analytical method with elastic-softening regime for masonry is suitable in order to study the global structural behaviour of arch bridges, highlighting how the arch thrust line is affected by crack formation, and the maximum admissible load evaluated by means of linear elastic fracture mechanics is larger than the load predicted by elasticity theory. Such an increment in terms of bearing capacity of the arch bridge can be defined "fracturing benefit", and it is analogous to the "plastic benefit" of the plastic limit analysis. The fracturing process, which takes into account the fracture initiation and propagation in the masonry arch bulk, occurs before the set-in of the conditions established by means of the plastic limit analysis. In the present paper, the study of the elastic-fracture-plastic transitions is performed for three monumental masonry arch bridges with different shallowness and slenderness ratios. This application returns an accurate and effective whole service life assessment of masonry arch bridges, and more in general it can be suitable for a great number of historical masonry structures still having strategic or heritage importance in the infrastructure systems

Funicularity in elastic domes: Coupled effects of shape and thickness

An historical overview is presented concerning the theory of shell structures and thin domes. Early conjectures proposed, among others, by French, German, and Russian Authors are discussed. Static and kinematic matrix operator equations are formulated explicitly in the case of shells of revolution and thin domes. It is realized how the static and kinematic matrix operators are one the adjoint of the other, and, on the other hand, it can be rigorously demonstrated through the definition of stiffness matrix and the application of virtual work principle. In this context, any possible omission present in the previous approaches becomes evident. As regards thin shells of revolution (thin domes), the elastic problem results to be internally statically-determinate, in analogy to the case of curved beams, being characterized by a system of two equilibrium equations in two unknowns. Thus, the elastic solution can be obtained just based on the equilibrium equations and independently of the shape of the membrane itself. The same cannot be affirmed for the unidimensional elements without flexural stiffness (ropes). Generally speaking, the static problem of elastic domes is governed by two parameters, the constraint reactions being assumed to be tangential to meridians at the dome edges: the shallowness ratio and the thickness of the dome. On the other hand, when the dome thickness tends to zero, the funicularity emerges and prevails, independently of the shallowness ratio or the shape of the dome. When the thickness is finite, an optimal shape is demonstrated to exist, which minimizes the flexural regime if compared to the membrane one

Scale-dependent maximum reinforcement percentage in reinforced concrete beams

The Cohesive/Overlapping Crack Model is able to describe the transition between cracking and crushing failures occurring in reinforced concrete beams by increasing beam depth and/or steel percentage. Within this Nonlinear Fracture Mechanics model, the tensile and compressive ultimate behaviors of the concrete matrix are modeled through two different process zones that advance independently one of another. Moreover, this model is able to investigate local mechanical instabilities occurring in the structural behavior of reinforced concrete structures: tensile snap-back and snap-through, which are due to concrete cracking or steel fracture, and the compressive snap-back occurring at the end of the plastic plateau, which is generated by the unstable growth of the crushing zone. In this context, the application of the Cohesive/Overlapping Crack Model highlights that the ductility, which is represented by the plastic rotation capacity of a reinforced concrete element subjected to bending, decreases as reinforcement percentage and/or beam depth increase. Thus, a scale-dependent maximum reinforcement percentage beyond which concrete crushing occurs prior to steel yielding is demonstrated to exist. In particular, the maximum steel percentage results to be inversely proportional to h0.25, h being the beam depth. In this way, a rational and quantitative definition of over-reinforcement is provided as a steel percentage depending on the beam depth

Scale effects in the post-cracking behaviour of fibre-reinforced concrete beams

The scale effects on the global structural response of fibre-reinforced concrete (FRC) beams subjected to bending are discussed in the framework of Fracture Mechanics by means of the Updated Bridged Crack Model (UBCM). This model predicts different post-cracking regimes depending on two dimensionless numbers: the reinforcement brittleness number, NP, which is related to the fibre volume fraction, Vf; and the pull-out brittleness number, Nw, which is related to the fibre embedment length, wc. Both these dimensionless numbers depend on the beam depth, h, which, keeping the other variables to be constant, drives a ductile-to-brittle transition in the post-cracking regime of the composite. The critical value of the reinforcement brittleness number, NPC, allows for prediction of the minimum (critical) specimen size, hmin, which, analogously to the minimum fibre volume fraction, Vf,min, is required to achieve a stable post-cracking response. Numerical simulations are compared to experimental results reported in the scientific literature, in which FRC specimens, characterized by the same fibre volume fraction but different sizes, are tested in bending

A review on acoustic emission monitoring for damage detection in masonry structures

Acoustic emission monitoring is widely used for damage detection in materials research and for site monitoring. Its use for masonry structures is however challenging due to the highly heterogenic nature of masonry and rapid signal attenuation. However, the non-invasive nature and high sensitivity of the technique also provide interesting opportunities, especially for historical masonry structures, to locate damage, identify severity of damage and rate of deterioration. Aim of this paper is to provide an extensive literature review on the application of the acoustic emission technique for masonry structures, addressing specific challenges and recent findings. AE-based methods for damage assessment in masonry are discussed in view of monitoring approaches, wave propagation, source location and crack development under static, fatigue and creep loading. Site applications are discussed for identifying crack location and crack propagation in historical masonry towers, buildings and masonry arch bridges. The paper concludes with future challenges identified in this research field

‘Stay Home Without a Home’: Report from a webinar on the right to housing in Covid-19 lockdown times

This Update reports from a webinar on the impacts of lockdown measures put in place globally amid the Covid-19 pandemic on the right to housing and linked political struggles. Three main threads emerged from the conversation: the impacts of the pandemic are deepening pre-existing housing inequalities, while governments’ responses are largely insufficient; activists and contentious actors worldwide are changing their framings and repertoires to adapt to lockdown measures and attempt to radicalize their action; possibilities, albeit limited, are opening for the construction of global networks of struggle.info:eu-repo/semantics/publishedVersio

Cardiac overexpression of melusin protects from dilated cardiomyopathy due to long-standing pressure overload.

We have previously shown that genetic ablation of melusin, a muscle specific beta 1 integrin interacting protein, accelerates left ventricle (LV) dilation and heart failure in response to pressure overload. Here we show that melusin expression was increased during compensated cardiac hypertrophy in mice subjected to 1 week pressure overload, but returned to basal levels in LV that have undergone dilation after 12 weeks of pressure overload. To better understand the role of melusin in cardiac remodeling, we overexpressed melusin in heart of transgenic mice. Echocardiography analysis indicated that melusin over-expression induced a mild cardiac hypertrophy in basal conditions (30% increase in interventricular septum thickness) with no obvious structural and functional alterations. After prolonged pressure overload (12 weeks), melusin overexpressing hearts underwent further hypertrophy retaining concentric LV remodeling and full contractile function, whereas wild-type LV showed pronounced chamber dilation with an impaired contractility. Analysis of signaling pathways indicated that melusin overexpression induced increased basal phosphorylation of GSK3beta and ERK1/2. Moreover, AKT, GSK3beta and ERK1/2 were hyper-phosphorylated on pressure overload in melusin overexpressing compared with wild-type mice. In addition, after 12 weeks of pressure overload LV of melusin overexpressing mice showed a very low level of cardiomyocyte apoptosis and stromal tissue deposition, as well as increased capillary density compared with wild-type. These results demonstrate that melusin overexpression allows prolonged concentric compensatory hypertrophy and protects against the transition toward cardiac dilation and failure in response to long-standing pressure overload

Recessive mutations in muscle-specific isoforms of FXR1 cause congenital multi-minicore myopathy

FXR1 is an alternatively spliced gene that encodes RNA binding proteins (FXR1P) involved in muscle development. In contrast to other tissues, cardiac and skeletal muscle express two FXR1P isoforms that incorporate an additional exon-15. We report that recessive mutations in this particular exon of FXR1 cause congenital multi-minicore myopathy in humans and mice. Additionally, we show that while Myf5-dependent depletion of all FXR1P isoforms is neonatal lethal, mice carrying mutations in exon-15 display non-lethal myopathies which vary in severity depending on the specific effect of each mutation on the protein