Continuum modeling of a neuronal cell under blast loading

Abstract

Traumatic brain injuries have recently been put under the spotlight as one of the most important causes of accidental brain dysfunctions. Significant experimental and modeling efforts are thus ongoing to study the associated biological, mechanical and physical mechanisms. In the field of cell mechanics, progresses are also being made at the experimental and modeling levels to better characterize many of the cell functions such as differentiation, growth, migration and death, among others. The work presented here aims at bridging both efforts by proposing a continuum model of neuronal cell submitted to blast loading. In this approach, cytoplasm, nucleus and membrane (plus cortex) are differentiated in a representative cell geometry, and different material constitutive models are adequately chosen for each one. The material parameters are calibrated against published experimental work of cell nanoindentation at multiple rates. The final cell model is ultimately subjected to blast loading within a complete fluid-structure interaction computational framework. The results are compared to the nanoindentation simulation and the specific effects of the blast wave on the pressure and shear levels at the interfaces are identified. As a conclusion, the presented model successfully captures some of the intrinsic intracellular phenomena occurring during its deformation under blast loading and potentially leading to cell damage. It suggests more particularly the localization of damage at the nucleus membrane similarly to what has already been observed at the overall cell membrane. This degree of damage is additionally predicted to be worsened by a longer blast positive phase duration. As a conclusion, the proposed model ultimately provides a new three dimensional computational tool to evaluate intracellular damage during blast loading.

Mechanical properties of gray and white matter brain tissue by indentation

“…This rheological difference is closely related to the microstructural architecture of gray and white matter tissue and reflects the network properties of white matter, similar to filled elastomers [14]. This is in agreement with recent studies, which have explained macroscopic viscoelasticity with the intracellular interaction between cytoplasm, nucleus, and membrane during cellular deformation [27]. Our long-time relaxation curves in Figure 8, right, with white matter plateau stresses of σ ∞ / σ 0 < 0.30 and relaxation times larger than 600s, agree both qualitatively and quantitatively with the white matter relaxation curves reported in the literature, for which the stresses decayed to σ ∞ / σ 0 < 0.30 and had still not fully converged after 500s [8].…”

“…The prototype example is traumatic brain injury [36], where extreme loading rates cause intracranial damage associated with a temporary or permanent loss of function [27]. On these scales, time dependency plays a critical role [40].…”

A computational model coupling mechanics and electrophysiology in spinal cord injury

“…Computational biomechanics simulations making use of finite element schemes have recently allowed for the identification of stress extrema and/or patterns at the tissue (Moore et al 2009;Nyein et al 2010;Cloots 2011;Cloots et al 2013;Gupta and Przekwas 2013) and cell scales (Jerusalem and Dao 2012) during TBI events (see these references for a complete literature review). Conversely, recent work building on the observation of "leaky" voltage-gated sodium ion channel after trauma (Wang et al 2009) has proposed a model of the resulting hyperpolarization-(left-)shifts of the ion channel current (Boucher et al 2012).…”

Computational investigation of in situ chondrocyte deformation and actin cytoskeleton remodelling under physiological loading

“…Debonding of chondrocytes from the ECM/PCM during extreme loading could be investigated [88]. Furthermore, the current modelling framework could be used to investigate the response of chondrocytes to high strain rate shock loading [89].…”