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Abstract This paper reports results of laboratory and 3D numerical modeled pull-out tests with steel ladders and polymeric strip reinforcements. These types of reinforcement are commonly used in reinforced soil walls constructed with concrete facing elements. Laboratory pull-out tests are required to determine accurate and realistic pull-out strength values considering the interaction of specific reinforcement and backfill materials under different confining pressures (i.e., trying to simulate the different reinforcement layer arrangements and load conditions in actual reinforced soil walls). International design Codes for reinforced soil walls provide default values for pull-out strength. However, in many cases, default values are too conservative and/or are not strictly specified for particular reinforcement types. Pull-out tests can be difficult and expensive to perform, thus not being common nor worth for the vast majority of reinforced soil wall projects. Consequently, calibrated numerical models can be useful to predict pull-out response under site-specific conditions, and provide further understanding of the mechanisms involved in the soil-reinforcement interaction. Details of the numerical approach, including relevant aspects of the soil-reinforcement interfaces, are described. Examples of calibrated numerical predictions for pull-out loads, displacements, and soil-dilatancy effects are presented. The influence of reinforcement, soil and interface stiffnesses is shown. Numerical results provide useful insight for future modelling works of the complex interaction between type-specific backfill materials and reinforcement element, relevant for investigation and/or practical design of reinforced soil walls.

Macrophages show remarkable phenotypic plasticity in response to environmental signals. Although it is generally less considered, cytoskeletal changes in macrophages influence their phenotype, including phagocytosis and secretion of soluble cytokines. Influenza virus NS1A-binding protein (Ivns1abp) belongs to the Kelch family of proteins that play a central role in actin cytoskeleton dynamics by directly associating with F-actin and by protecting against actin derangement. Due to its role in cytoskeleton preservation, the Ivns1abp gene might be a critical regulator of the macrophage phenotype and function under inflammatory conditions. In this study, we determine that the modulation of the Ivns1abp gene in macrophages could modify resistance to macrophages against inflammation and maintain functional phagocytosis. Our results indicate that inflammatory insults inhibit the Ivns1abp gene, whereby phagocytosis is inhibited and the ability of macrophages to induce proliferation and repair of damaged cells is compromised. Furthermore, our results show that inflammatory insults alter the activity of the transcription factor c-myc, a factor which directly modulates the expression of the Ivns1abp gene. In conclusion, this study demonstrates a central role of lvns1abp in promoting and preserving a reparative macrophage phenotype and resistance to this inflammatory environment. [ABSTRACT FROM AUTHOR]