The problem of a crack impinging on an interface has been thoroughly investigated in the last three decades due to its important role in the mechanics and physics of solids. In the current investigation, this problem is revisited in view of the recent progresses on the phase field approach of brittle fracture. In this concern, a novel formulation combining the phase field approach for modeling\ud brittle fracture in the bulk and a cohesive zone model for pre-existing adhesive interfaces is herein proposed to investigate the competition between crack penetration and deflection at an interface. The model, implemented within the finite element method framework using a monolithic fully implicit solution strategy, is applied to provide a further insight into the understanding of the role of model parameters on the above competition. In particular, in this study, the role of the fracture toughness ratio between the interface and the adjoining bulks and of the characteristic fracture-length scales of the dissipative models is analyzed. In the case of a brittle interface, the asymptotic predictions based on linear elastic fracture mechanics criteria for crack penetration, single\ud deflection or double deflection are fully captured by the present method. Moreover, by increasing the size of the process zone along the interface, or by varying the internal length scale of the phase field model, new complex phenomena are emerging, such as simultaneous crack penetration and deflection and the transition from single crack penetration to deflection and penetration with\ud subsequent branching into the bulk. The obtained computational trends are in very good agreement with previous experimental observations and the theoretical considerations on the competition and interplay between both fracture mechanics models open new research perspectives for the simulation and understanding of complex fracture patterns

We investigated several phenotypic and functional parameters of T cell-mediated immunity in a large series of common variable immunodeficiency (CVID) patients. We demonstrated that the vast majority of CVID patients presented multiple T cell abnormalities intimately related among them, the severity of which was reflected in a parallel loss of CD4⁺ naive T cells. A strong correlation between the number of CD4⁺ naive T cells and clinical features was observed, supporting the subgrouping of patients according to their number of naive CD4⁺ T lymphocytes. A reduced thymic output and disrupted CD4⁺ and CD8⁺ TCR repertoires paralleled the contraction of CD4⁺ naive T cell pools. The evaluation of activation markers and cytokine production indicated a strong T cell activation that was significantly related to the increased levels of T cell turnover and apoptosis. Finally, discrete genetic profiles could be demonstrated in groups of patients showing extremely diverse T cell subset composition and function. Naive CD4⁺ T cell levels were significantly associated with the switched memory B cell-based classification, although the concordance between the respective subgroups did not exceed 58.8%. In conclusion, our data highlight the key role played by the T cell compartment in the pathogenesis of CVID, pointing to the need to consider this aspect for classification of this disease.