Abstract The turtle carapace is a biological composite shield consisting of a hard boney layer covered with a soft keratin-collagen bi-layer. The unique microstructure enables the turtle carapace to protect the underlying soft tissues from predator assaults. Recent experiments have shown that when the turtle carapace is subjected to dynamic loading, brittle fracture of the boney layer occurs, which is accompanied by delamination at the keratin-collagen and collagen-bone interfaces. To unveil the role of interfacial delamination, we propose a model of fracture in the multilayered microstructure of turtle carapace, in which brittle cracking in the boney layer, delamination of the soft bi-layer and plastic deformation in the bi-layer are taken into account. Calculations are carried out for crack propagation in the turtle carapace under dynamic loading; it is found that low strength of the keratin-collagen interface can activate large plastic deformation in the collagen layer and promote spreading of damage region in the keratin-collagen interface, which delays fracture of the boney layer. High toughness of the keratin-collagen interface increases plastic deformation in the soft bi-layer and suppresses crack propagation in the boney layer. We further reveal the role of mechanical properties of the collagen-bone interface. It is identified that high strength of the collagen-bone interface enables enhanced plastic dissipation in the soft bi-layer, retarding crack growth in the boney layer. The collagen-bone interface with high toughness plays a role in enhancing plastic deformation in the soft bi-layer, which potentially increases the resistance to crack growth in the boney layer. In addition, we explore the effect of strain rate sensitivity of the soft bi-layer. We show that decreasing the degree of strain rate sensitivity of the keratin layer can mitigate fracture of the boney layer. The findings of this study shed new light on the protection mechanisms of turtle carapace.

中文翻译：

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龟甲壳中的动态裂纹扩展

摘要 龟甲壳是一种生物复合盾牌，由坚硬的骨层和柔软的角蛋白-胶原双层组成。独特的微观结构使海龟的甲壳能够保护下面的软组织免受捕食者的袭击。最近的实验表明，当龟甲壳受到动态载荷时，骨层发生脆性断裂，并伴有角蛋白-胶原蛋白和胶原-骨界面的分层。为了揭示界面分层的作用，我们提出了龟甲壳多层微观结构中的断裂模型，其中考虑了骨层中的脆性开裂、软双层的分层和双层中的塑性变形. 计算了龟壳在动态载荷下的裂纹扩展；研究发现，角蛋白-胶原界面的低强度可以激活胶原层中较大的塑性变形，促进角蛋白-胶原界面损伤区域的扩散，从而延缓骨层的断裂。角蛋白-胶原蛋白界面的高韧性增加了软双层中的塑性变形并抑制了骨层中的裂纹扩展。我们进一步揭示了胶原-骨界面机械性能的作用。已经确定，胶原-骨界面的高强度能够增强软双层中的塑性耗散，从而延缓骨层中的裂纹扩展。具有高韧性的胶原-骨界面在软双层中起到增强塑性变形的作用，这可能会增加骨层对裂纹扩展的抵抗力。此外，我们探索了软双层的应变率敏感性的影响。我们表明，降低角蛋白层的应变率敏感性程度可以减轻骨层的骨折。这项研究的结果为乌龟甲壳的保护机制提供了新的线索。