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In this work, the phase-field approach to fracture is extended to model fatigue failure in high- and low-cycle regime. The fracture energy degradation due to the repeated externally applied loads is introduced as a function of a local energy accumulation variable, which takes the structural loading history into account. To this end, a novel definition of the energy accumulation variable is proposed, allowing the fracture analysis at monotonic loading without the interference of the fatigue extension, thus making the framework generalised. Moreover, this definition includes the mean load influence of implicitly. The elastoplastic material model with the combined nonlinear isotropic and nonlinear kinematic hardening is introduced to account for cyclic plasticity. The ability of the proposed phenomenological approach to naturally recover main features of fatigue, including Paris law and Wöhler curve under different load ratios is presented through numerical examples and compared with experimental data from the author’s previous work. Physical interpretation of additional fatigue material parameter is explored through the parametric study.

We present a three-dimensional mathematical framework for modeling the evolving geometry, structure, and mechanical properties of a representative straight cylindrical artery subjected to changes in mean blood pressure and flow. We show that numerical predictions recover prior findings from a validated two-dimensional framework, but extend those findings by allowing effects of transmural gradients in wall constituents and vasoactive molecules to be simulated directly. Of particular note, we show that the predicted evolution of the residual stress related opening angle in response to an abrupt, sustained increase in blood pressure is qualitatively similar to measured changes when one accounts for a nonlinear transmural distribution of pre-stretched elastin. We submit that continuum-based constrained mixture models of arterial adaptation hold significant promise for deepening our basic understanding of arterial mechanobiology and thus for designing improved clinical interventions to treat many different types of arterial disease and injury.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation and oxidant/antioxidant imbalance. Glutathione is the most abundant cellular low-molecular weight thiol and the glutathione redox cycle is the fundamental component of the cellular antioxidant defence system. Concentration of total glutathione and catalytic activities of glutathione peroxidase and glutathione reductase were determined in peripheral blood of patients (n = 109) and healthy subjects (n = 51). Concentration of total glutathione in patients was not changed in comparison to healthy controls. However, we found statistically significant difference between patients with moderate and severe disease stages. Glutathione reductase activity was increased, while glutathione proxidase activity was decreased in the patients with COPD, when compared to healthy controls. We found no significant difference in glutathione peroxidase and glutathione reductase activities between stages. Patients who smoked had lower concentration of total glutathione compared with former smokers and never-smoking patients. Lung function parameters were inversely associated with glutathione level. Evidence is presented for differential modulation of glutathione peroxidase and glutathione reductase activities in peripheral blood of patients with stable COPD. We suppose that in addition to glutathione biosynthesis, glutathione reductase-dependent regulation of the glutathione redox state is vital for protection against oxidative stress.

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