Keckes Jozef, Burgert Ingo, Frühmann Klaus, Müller Martin, Kölln Klaas, Hamilton Myles, Burghammer Manfred, Roth Stephan V, Stanzl-Tschegg Stefanie, Fratzl Peter
Erich Schmid Institute for Materials Science, Austrian Academy of Sciences and Institute of Metal Physics, University of Leoben, Austria.
Nat Mater. 2003 Dec;2(12):810-4. doi: 10.1038/nmat1019. Epub 2003 Nov 16.
The remarkable mechanical properties of biological materials reside in their complex hierarchical architecture and in specific molecular mechanistic phenomena. The fundamental importance of molecular interactions and bond recovery has been suggested by studies on deformation and fracture of bone and nacre. Like these mineral-based materials, wood also represents a complex nanocomposite with excellent mechanical performance, despite the fact that it is mainly based on polymers. In wood, however, the mechanistic contribution of processes in the cell wall is not fully understood. Here we have combined tensile tests on individual wood cells and on wood foils with simultaneous synchrotron X-ray diffraction analysis in order to separate deformation mechanisms inside the cell wall from those mediated by cell-cell interactions. We show that tensile deformation beyond the yield point does not deteriorate the stiffness of either individual cells or foils. This indicates that there is a dominant recovery mechanism that re-forms the amorphous matrix between the cellulose microfibrils within the cell wall, maintaining its mechanical properties. This stick-slip mechanism, rather like Velcro operating at the nanometre level, provides a 'plastic response' similar to that effected by moving dislocations in metals. We suggest that the molecular recovery mechanism in the cell matrix is a universal phenomenon dominating the tensile deformation of different wood tissue types.
生物材料卓越的力学性能源于其复杂的层次结构以及特定的分子力学现象。对骨骼和珍珠母的变形与断裂研究表明了分子相互作用和键恢复的根本重要性。与这些基于矿物质的材料一样，木材也是一种具有优异力学性能的复杂纳米复合材料，尽管它主要基于聚合物。然而，在木材中，细胞壁内各过程的力学贡献尚未完全被理解。在此，我们将对单个木材细胞和木片进行的拉伸试验与同步加速器X射线衍射分析相结合，以便将细胞壁内部的变形机制与细胞间相互作用介导的机制区分开来。我们发现，超过屈服点的拉伸变形并不会降低单个细胞或木片的刚度。这表明存在一种主要的恢复机制，该机制会重新形成细胞壁内纤维素微纤丝之间的无定形基质，从而保持其力学性能。这种类似纳米级维可牢尼龙搭扣运作的粘滑机制，提供了一种类似于金属中移动位错所产生的“塑性响应”。我们认为，细胞基质中的分子恢复机制是一种普遍现象，主导着不同木材组织类型的拉伸变形。
