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In applications involving fretting wear damage, surfaces with high yield strength and wear resistance are required. In this study, the mechanical responses of materials with graded nanostructured surfaces during fretting sliding are investigated and compared to homogeneous materials through a systematic computational study. A three-dimensional finite element model is developed to characterize the fretting sliding characteristics and shakedown behavior with varying degrees of contact friction and gradient layer thicknesses. Results obtained using a representative model material (i.e., 304 stainless steel) demonstrate that metallic materials with a graded nanostructured surface could exhibit a more than 80% reduction in plastically deformed surface areas and volumes, resulting in superior fretting damage resistance in comparison to homogeneous coarse-grained metals. In particular, a graded nanostructured material can exhibit elastic or plastic shakedown, depending on the contact friction coefficient. Optimal fretting resistance can be achieved for the graded nanostructured material by decreasing the friction coefficient (e.g., from 0.6 to 0.4 in 304 stainless steel), resulting in an elastic shakedown behavior, where the plastically deformed volume and area exhibit zero increment in the accumulated plastic strain during further sliding. These findings in the graded nanostructured materials using 304 stainless steel as a model system can be further tailored for engineering optimal fretting damage resistance. 

The nanoscopic deformation of ⟨111⟩ nanotwinned copper nanopillars under strain rates between 10^−5/s and 5×10^−4/s was studied by using in situ transmission electron microscopy. The correlation among dislocation activity, twin boundary instability due to incoherent twin boundary migration and corresponding mechanical responses was investigated. Dislocations piled up in the nanotwinned copper, giving rise to significant hardening at relatively high strain rates of 3–5×10^−4/s. Lower strain rates resulted in detwinning and reduced hardening, while corresponding deformation mechanisms are proposed based on experimental results. At low/ultralow strain rates below 6×10^−5/s, dislocation activity almost ceased operating, but the migration of twin boundaries via the 1/4 ⟨10-1⟩ kink-like motion of atoms is suggested as the detwinning mechanism. At medium strain rates of 1–2×10^−4/s, detwinning was decelerated likely due to the interfered kink-like motion of atoms by activated partial dislocations, while dislocation climb may alternatively dominate detwinning. These results indicate that, even for the same nanoscale twin boundary spacing, different nanomechanical deformation mechanisms can operate at different strain rates. 

Physics-informed deep learning helps detect unknown internal structures and defects with limited nondestructive measurements. 

Red blood cells (RBCs) are subjected to recurrent changes in shear stress and oxygen tension during blood circulation. The cyclic shear stress has been identified as an important factor that alone can weaken cell mechanical deformability. The effects of cyclic hypoxia on cellular biomechanics have yet to be fully investigated. As the oxygen affinity of hemoglobin plays a key role in the biological function and mechanical performance of RBCs, the repeated transitions of hemoglobin between its R (high oxygen tension) and T (low oxygen tension) states may impact their mechanical behavior. The present study focuses on developing a novel microfluidics-based assay for characterization of the effect of cyclic hypoxia on cell biomechanics. The capability of this assay is demonstrated by a longitudinal study of individual RBCs in health and sickle cell disease subjected to cyclic hypoxia conditions of various durations and levels of low oxygen tension. Viscoelastic properties of cell membranes are extracted from tensile stretching and relaxation processes of RBCs induced by the electrodeformation technique. Results demonstrate that cyclic hypoxia alone can significantly reduce cell deformability, similar to the fatigue damage accumulated through cyclic mechanical loading. RBCs affected by sickle cell disease are less deformable (significantly higher membrane shear modulus and viscosity) than normal RBCs. The fatigue resistance of sickle RBCs to the cyclic hypoxia challenge is significantly inferior to normal RBCs, and this trend is more significant in mature erythrocytes of sickle cells. When oxygen affinity of sickle hemoglobin is enhanced by anti-sickling drug treatment of 5-hydroxymethyl-2-furfural (5-HMF), sickle RBCs show ameliorated resistance to fatigue damage induced by cyclic hypoxia. These results illustrate that an important biophysical mechanism underlying RBC senescence in which cyclic hypoxia challenge alone can lead to mechanical degradation of the RBC membrane. We envision the application of this assay can be further extended to RBCs in other blood diseases and other types of cells. 

Fatigue arising from cyclic straining is a key factor in the degradation of properties of engineered materials and structures. Fatigue can also induce damage and fracture in natural biomaterials, such as bone, and in synthetic biomaterials used in implant devices. However, the mechanisms by which mechanical fatigue leads to deterioration of physical properties and contributes to the onset and progression of pathological states in biological cells have hitherto not been systematically explored. Here we present a general method that employs amplitude-modulated electrodeformation and microfluidics for characterizing mechanical fatigue in single biological cells. This method is capable of subjecting cells to static loads for prolonged periods of time or to large numbers of controlled mechanical fatigue cycles. We apply the method to measure the systematic changes in morphological and biomechanical characteristics of healthy human red blood cells (RBCs) and their membrane mechanical properties. Under constant amplitude cyclic tensile deformation, RBCs progressively lose their ability to stretch with increasing fatigue cycles. Our results further indicate that loss of deformability of RBCs during cyclic deformation is much faster than that under static deformation at the same maximum load over the same accumulated loading time. Such fatigue-induced deformability loss is more pronounced at higher amplitudes of cyclic deformation. These results uniquely establish the important role of mechanical fatigue in influencing physical properties of biological cells. They further provide insights into the accumulated membrane damage during blood circulation, paving the way for further investigations of the eventual failure of RBCs causing hemolysis in various hemolytic pathologies. 

Cell–cell adhesions are often subjected to mechanical strains of different rates and magnitudes in normal tissue function. However, the rate-dependent mechanical behavior of individual cell–cell adhesions has not been fully characterized due to the lack of proper experimental techniques and therefore remains elusive. This is particularly true under large strain conditions, which may potentially lead to cell–cell adhesion dissociation and ultimately tissue fracture. In this study, we designed and fabricated a single-cell adhesion micro tensile tester (SCAµTT) using two-photon polymerization and performed displacement-controlled tensile tests of individual pairs of adherent epithelial cells with a mature cell–cell adhesion. Straining the cytoskeleton–cell adhesion complex system reveals a passive shear-thinning viscoelastic behavior and a rate-dependent active stress-relaxation mechanism mediated by cytoskeleton growth. Under low strain rates, stress relaxation mediated by the cytoskeleton can effectively relax junctional stress buildup and prevent adhesion bond rupture. Cadherin bond dissociation also exhibits rate-dependent strengthening, in which increased strain rate results in elevated stress levels at which cadherin bonds fail. This bond dissociation becomes a synchronized catastrophic event that leads to junction fracture at high strain rates. Even at high strain rates, a single cell–cell junction displays a remarkable tensile strength to sustain a strain as much as 200% before complete junction rupture. Collectively, the platform and the biophysical understandings in this study are expected to build a foundation for the mechanistic investigation of the adaptive viscoelasticity of the cell–cell junction.