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Damage biomechanics for neuronal membrane mechanoporation

机译:神经元膜力学造成的损伤生物力学

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In this paper, mechano-physiological damage evolution equations are developed to capture the disruption of neuronal membrane integrity and quantify neuronal cell death in the brain during mechanical insult. Traumatic brain injury involves multiscale structure-property relations where the mechanical behavior of the brain is phenomenologically characterized at the macroscale. However, damage largely occurs at the cellular level (microscale and nanoscale) due to the loss of ion homeostasis. To measure this neuronal death mechanism, molecular dynamics simulations were performed on a representative neuronal membrane, a 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC) bilayer structures. Pore density and pore growth due to membrane deformation were then quantified. The results showed that the pore growth and pore density rates were a function of stress state, but only the pore growth rate was a function of the strain rate. Mechano-physiological damage evolution equations were developed to capture the damage biomechanics of the POPC bilayer based on the pore density and growth rate responses. The proposed damage evolution equations were combined with the Nernst-Planck diffusion equation to produce a criterion based on the change of intracellular calcium ion concentration.
机译:本文在机械损伤期间开发了机械生理损伤演化方程以捕获神经元膜完整性的破坏,并在大脑中量化脑中的神经元细胞死亡。创伤性脑损伤涉及多尺度结构性质关系,其中大脑的机械行为在宏观上表现出特征。然而,由于离子稳定性的损失,损伤很大程度上发生在细胞水平(微尺寸和纳米级)。为了测量这种神经元死亡机制,在代表性神经元膜上进行分子动力学模拟,1-palmItoyl-2-Oxyoyl-磷脂酰胆碱(POPC)双层结构进行。然后量化由于膜变形引起的孔密度和孔生长。结果表明,孔生长和孔密度率是应力状态的函数,但只有孔生长速率是应变率的函数。开发了机械生理损伤演化方程以基于孔密度和生长速率反应来捕获POPC双层的损伤生物力学。所提出的损伤演化方程与NERNST-PLANCK扩散方程组合以产生基于细胞内钙离子浓度的变化的标准。

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