Biomechanics and modeling in mechanobiology
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Biomech Model Mechanobiol · Oct 2015
Predicting changes in cortical electrophysiological function after in vitro traumatic brain injury.
Finite element (FE) models of traumatic brain injury (TBI) are capable of predicting injury-induced brain tissue deformation. However, current FE models are not equipped to predict the biological consequences of tissue deformation, which requires the determination of tolerance criteria relating the effects of mechanical stimuli to biologically relevant functional responses. To address this deficiency, we present functional tolerance criteria for the cortex for alterations in neuronal network electrophysiological function in response to controlled mechanical stimuli. ⋯ Changes in electrophysiological parameters were dependent on strain and strain rate in a complex manner. Compared to the hippocampus, the cortex was less spontaneously active, less excitable, and less prone to significant changes in electrophysiological function in response to controlled deformation (strain or strain rate). Our study provides functional data that can be incorporated into FE models to improve their predictive capabilities of the in vivo consequences of TBI.
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Biomech Model Mechanobiol · Aug 2015
White matter tract-oriented deformation predicts traumatic axonal brain injury and reveals rotational direction-specific vulnerabilities.
A systematic correlation between finite element models (FEMs) and histopathology is needed to define deformation thresholds associated with traumatic brain injury (TBI). In this study, a FEM of a transected piglet brain was used to reverse engineer the range of optimal shear moduli for infant (5 days old, 553-658 Pa) and 4-week-old toddler piglet brain (692-811 Pa) from comparisons with measured in situ tissue strains. The more mature brain modulus was found to have significant strain and strain rate dependencies not observed with the infant brain. ⋯ The best predictors of TAI were the tract-oriented strain (6-7%), strain rate (38-40 s(-1), and strain times strain rate (1.3-1.8 s(-1) values exceeded by 90% of the brain. These tract-oriented strain and strain rate thresholds for TAI were comparable to those found in isolated axonal stretch studies. Furthermore, we proposed that the higher degree of agreement between tissue distortion aligned with white matter tracts and TAI may be the underlying mechanism responsible for more severe TAI after horizontal and sagittal head rotations in our porcine model of nonimpact TAI than coronal plane rotations.
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Biomech Model Mechanobiol · Jun 2015
Functional tolerance to mechanical deformation developed from organotypic hippocampal slice cultures.
In this study, we measured changes in electrophysiological activity after mechanical deformation of living organotypic hippocampal brain slice cultures at tissue strains and strain rates relevant to traumatic brain injury (TBI). Electrophysiological activity was measured throughout the hippocampus with a 60-electrode microelectrode array. Electrophysiological parameters associated with unstimulated spontaneous activity (neural event firing rate, duration, and magnitude), stimulated evoked responses (the maximum response [Formula: see text], the stimulus current necessary for a half-maximal response [Formula: see text], and the electrophysiological parameter m that is representative of firing uniformity), and paired-pulse responses (paired-pulse ratio at varying interstimulus intervals) were quantified for each hippocampal region (CA1, CA3, and DG). ⋯ Most changes in electrophysiology were dependent on strain and strain rate in a complex fashion, independent of hippocampal anatomy, with the notable exception of [Formula: see text]. Until it becomes possible to directly measure brain tissue deformation in vivo, finite element (FE) models will be necessary to simulate and predict the in vivo consequences of TBI. One application of our study is to provide functional relationships that can be incorporated into these FE models to enhance their biofidelity of accident and collision reconstructions by predicting biological outcomes in addition to mechanical responses.
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Biomech Model Mechanobiol · Jun 2013
Mechanics of blast loading on the head models in the study of traumatic brain injury using experimental and computational approaches.
Blast waves generated by improvised explosive devices can cause mild, moderate to severe traumatic brain injury in soldiers and civilians. To understand the interactions of blast waves on the head and brain and to identify the mechanisms of injury, compression-driven air shock tubes are extensively used in laboratory settings to simulate the field conditions. ⋯ The validated numerical models are then used to investigate the spatiotemporal distribution of stresses and pressure in the human skull and brain. By detailing the results from a series of careful experiments and numerical simulations, this paper demonstrates that: (1) Geometry of the head governs the flow dynamics around the head which in turn determines the net mechanical load on the head. (2) Biomechanical loading of the brain is governed by direct wave transmission, structural deformations, and wave reflections from tissue-material interfaces. (3) Deformation and stress analysis of the skull and brain show that skull flexure and tissue cavitation are possible mechanisms of blast-induced traumatic brain injury.
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Biomech Model Mechanobiol · Sep 2012
Computational assessment of bicuspid aortic valve wall-shear stress: implications for calcific aortic valve disease.
The bicuspid aortic valve (BAV) is associated with a high prevalence of calcific aortic valve disease (CAVD). Although abnormal hemodynamics has been proposed as a potential pathogenic contributor, the native BAV hemodynamic stresses remain largely unknown. Fluid-structure interaction models were designed to quantify the regional BAV leaflet wall-shear stress over the course of CAVD. ⋯ While the TAV and non-coronary BAV leaflets shared similar shear stress characteristics, the base of the fused BAV leaflet fibrosa exhibited strong abnormalities, which were modulated by the degree of calcification (6-fold, 10-fold and 16-fold TSM increase in the normal, mildly and severely calcified BAV, respectively, relative to the normal TAV). This study reveals the existence of major differences in wall-shear stress pulsatility and magnitude on TAV and BAV leaflets. Given the ability of abnormal fluid shear stress to trigger valvular inflammation, the results support the existence of a mechano-etiology of CAVD in the BAV.