A continuum model for tissues with moderate cell density.

Cells sense mechanical stimuli to guide tissue growth and remodeling, a process called mechanotransduction, but it has still been challenging to model how forces affect cells in tissues with medium cell density. Common models like rule of mixtures (ROM) work well for cell dense tissues, and Eshelby's inclusion model fits cell sparse ones, but neither handles the in-between densities accurately. This study looks at how cell density, shape, and material properties affect stress in these tissues and suggests a better way to model them.

Biology and Hemodynamics of Aneurysm Rupture.

Predicting rupture risk in intracranial aneurysms is among one of the most critical questions in vascular surgery. The processes that govern an aneurysm growth are multifaceted and complex, but may be summarized into three components: hemodynamics, biology, and mechanics. We review and connect the literature in the three disciplines, identifying considerable strides in recent history and current gaps in research.

Characterizing Tissue Remodeling and Mechanical Heterogeneity in Cerebral Aneurysms.

Accurately assessing the complex tissue mechanics of cerebral aneurysms (CAs) is critical for elucidating how CAs grow and whether that growth will lead to rupture. The factors that have been implicated in CA progression - blood flow dynamics, immune infiltration, and extracellular matrix remodeling - all occur heterogeneously throughout the CA. Thus, it stands to reason that the mechanical properties of CAs are also spatially heterogeneous.

Multiscale model of fatigue of collagen gels.

Fatigue as a mode of failure becomes increasingly relevant with age in tissues that experience repeated fluctuations in loading. While there has been a growing focus on the mechanics of networks of collagen fibers, which are recognized as the predominant mechanical components of soft tissues, the network's fatigue behavior has received less attention. Specifically, it must be asked (1) how the fatigue of networks differs from that of its component fibers, and (2) whether this difference in fatigue behaviors is affected by changes in the network's architecture.