Search

Porous media that display a gradient in the structure of their networks are common in nature, but the understanding of the drainage patterns in such media is still limited. We propose a theoretical framework that allows to better quantify these patterns, and we validate it both with experiments in 3D printed models and with numerical simulations.

Abstract We present a subcritical fracture growth model, coupled with the elastic redistribution of the acting mechanical stress along rugous rupture fronts. We show the ability of this model to quantitatively reproduce the intermittent dynamics of cracks propagating along weak disordered interfaces. To this end, we assume that the fracture energy of such interfaces (in the sense of a critical energy release rate) follows a spatially correlated normal distribution. We compare various statistical features from the obtained fracture dynamics to that from cracks propagating in sintered polymethylmethacrylate (PMMA) interfaces. In previous works, it has been demonstrated that such an approach could reproduce the mean advance of fractures and their local front velocity distribution. Here, we go further by showing that the proposed model also quantitatively accounts for the complex self-affine scaling morphology of crack fronts and their temporal evolution, for the spatial and temporal correlations of the local velocity fields and for the avalanches size distribution of the intermittent growth dynamics. We thus provide new evidence that an Arrhenius-like subcritical growth is particularly suitable for the description of creeping cracks.

Mechanical pain (or mechanical algesia) can both be a vital mechanism warning us for dangers or an undesired medical symptom important to mitigate. Thus, a comprehensive understanding of the different mechanisms responsible for this type of pain is paramount. In this work, we study the tearing of porcine skin in front of an infrared camera, and show that mechanical injuries in biological tissues can generate enough heat to stimulate the neural network. In particular, we report local temperature elevations of up to 24°C around fast cutaneous ruptures, which shall exceed the threshold of the neural nociceptors usually involved in thermal pain. Slower fractures exhibit lower temperature elevations, and we characterise such dependency to the damaging rate. Overall, we bring experimental evidence of a novel—thermal—pathway for direct mechanical algesia. In addition, the implications of this pathway are discussed for mechanical hyperalgesia, in which a role of the cutaneous thermal sensors has priorly been suspected. We also show that thermal dissipation shall actually account for a significant portion of the total skin's fracture energy, making temperature monitoring an efficient way to detect biological damages.

The surface morphology of faults controls the spatial anisotropy of their frictional properties and hence their mechanical stability. Such anisotropy is only rarely studied in seismology models of fault slip, although it might be paramount to understand the seismic rupture in particular areas, notably where slip occurs in a direction different from that of the main striations of the fault. To quantify how the anisotropy of fault surfaces affects the friction coefficient during sliding, we sheared synthetic fault planes made of plaster of Paris. These fault planes were produced by 3D-printing real striated fault surfaces whose 3D roughness was measured in the field at spatial scales from millimeters to meters. Here, we show how the 3D-printing technology can help for the study of frictional slip. The results show that fault anisotropy controls the coefficient of static friction, with μS//, the friction coefficient along the striations being three to four times smaller than μS⊥, the friction coefficient along the orientation perpendicular to the striations. This is true both at the meter and the millimeter scales. The anisotropy in friction and the average coefficient of static friction are also shown to decrease with the normal stress applied to the faults, as a result of the increased surface wear under increased loading.

Mechanical algesia is an important process for the preservation of living organisms, allowing potentially life-saving reflexes or decisions when given body parts are stressed. Yet, its various underlying mechanisms remain to be fully unraveled. Here, we quantitatively discuss how the detection of painful mechanical stimuli by the human central nervous system may, partly, rely on thermal measurements. Indeed, most fractures in a body, including microscopic ones, release some heat, which diffuses in the surrounding tissues. Through this physical process, the thermo-sensitive TRP proteins, that translate abnormal temperatures into action potentials, shall be sensitive to damaging mechanical inputs. The implication of these polymodal receptors in mechanical algesia has been regularly reported, and we here provide a physical explanation for the coupling between thermal and mechanical pain. In particular, in the human skin, we show how the neighboring neurites of a broken collagen fiber can undergo a sudden thermal elevation that ranges from a fraction to tens of degrees. As this theoretical temperature anomaly lies in the sensibility range of the TRPV3 and TRPV1 cation channels, known to trigger action potentials in the neural system, a degree of mechanical pain can hence be generated.