Studying the mechanical properties of aortic tissue is important for determining future medical intervention for both healthy and diseased conditions. While previous uniaxial, biaxial, and inflation experiments have provided valuable insights, the effects of shear and combined loading modes remain less explored. In this study, we examine the response of porcine descending thoracic aorta under large-amplitude oscillatory shear and normal compression. Circular samples (0.5 in diameter) were tested using an Anton Paar MCR302 rheometer in a parallel plate configuration. The top plate applied a compressive strain of 5 × 10 ^-4 N · m for torque), demonstrating that goodness of fit alone is insufficient for model selection. Across all three models, increasing compressive strain produced a consistent monotonic increase in the isotropic matrix stiffness parameter, indicating progressive recruitment of the collagen fiber network under through-thickness compression. The HGO and vanGOH models recovered stable fiber orientation angles near 45 ^∘ across all compression levels. The Fung-type model exhibited parameter identifiability problems and produced degenerate fiber orientations, suggesting that its single-exponential coupling structure is poorly suited to this loading regime. These results highlight how pre-compression modulates the mechanical response of arterial tissue under shear, providing new insight into the multiaxial mechanics of the aortic wall.
In the recent paper (Melly and Czekanski 2026), a viscoelasticity theory was formulated in terms of “viscous potentials.” Such formulation started proliferating in scientific literature (e.g. Pioletti et al. 1998, Ghahfarokhi et al. 2020, Upadhyay et al. 2020). Seemingly simple, it has an intrinsic flaw – the inability to accommodate strain jumps. The jumps lead to unphysical infinities in stresses, which is unacceptable. We emphasize this issue in the present note.
Continuum mechanical models of growth in solid biological tissues and multicellular aggregates (such as spheroids and organoids) have traditionally treated growth as a simple increase in the natural (stress-free) volume of the body. At the cellular level, this corresponds to stress-free expansion of individual cells driven by mass accumulation. In reality, however, multicellular growth is primarily governed by proliferation, which involves not only active cell enlargement but also changes in cell number. The latter arises from topological transition events such as division and apoptosis, both of which play central roles in maintaining cell size homeostasis in growing populations. Furthermore, cells can reorganize spatially through simple neighbor exchange via intercalation, a topological transition that provides a mechanism for stress relaxation. Despite their biological significance, the mechanical implications and the active versus passive nature of these cellular processes during growth remain poorly explored. In this study, we address this gap by examining the interplay between growth mechanics, the underlying cellular processes, and cellular activity. To this end, we employ morpho-viscoelasticity, a continuum theory for growth in viscoplastic confluent cell aggregates, and implement it within a finite element framework. Through numerical simulations, we investigate the mechano-biochemical feedback in spheroid growth. The results highlight the nontrivial roles of cell size homeostasis and cellular reorganization in regulating cell stresses and morphologies within growing aggregates, offering mechanistic insights relevant for spheroid and organoid engineering applications.
Recent numerical simulations of 3-D pipe flows using the modified Navier–Stokes formulation, enhanced with a finite viscous strength, have highlighted the crucial role of material instabilities in the onset of turbulence. In the present work, we use the viscous strength model to capture material instabilities that can affect aortic blood flow in the presence of local dilation. We perform 3-D numerical simulations of the pulsatile flow through a pipe with an axisymmetric bulge, which imitates the aneurysm dilation. The pulsatile flow conforms to the cardiac cycle. The simulation results show that the local dilation can significantly enhance wall shear stress, especially during the systolic phase. The material instabilities originated during the dilated region possibly lead to the formation of localized perturbations, which evolve into global turbulence.
In this contribution, we propose a hyperelastic isotropic material model whose stress–strain response is non-linear even at infinitesimal deformations and cannot thus be linearized. As a result, the superposition principle does not apply and the generalized Hooke law is not valid even at small strains. A further unusual feature of this material model is that Poisson’s ratio can be greater than 0.5 in full agreement with the laws of thermodynamics. In particular, for the proposed strain energy function, a value of ν =0.644 is reached. The model response appears to be plausible in various deformation states such as uniaxial tension/compression, simple shear, and pure dilation.
