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纳米级机制解释了韧带组织在应变率增加时的变硬和强化。

Nano-scale mechanisms explain the stiffening and strengthening of ligament tissue with increasing strain rate.

机构信息

Department of Bioengineering, Imperial College London, London, SW7 2AZ, UK.

Department of Mechanical Engineering, University of Moratuwa, Moratuwa, Sri Lanka.

出版信息

Sci Rep. 2018 Feb 27;8(1):3707. doi: 10.1038/s41598-018-21786-z.

DOI:10.1038/s41598-018-21786-z
PMID:29487334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5829138/
Abstract

Ligament failure is a major societal burden causing disability and pain. Failure is caused by trauma at high loading rates. At the macroscopic level increasing strain rates cause an increase in failure stress and modulus, but the mechanism for this strain rate dependency is not known. Here we investigate the nano scale mechanical property changes of human ligament using mechanical testing combined with synchrotron X-ray diffraction. With increasing strain rate, we observe a significant increase in fibril modulus and a reduction of fibril to tissue strain ratio, revealing that tissue-level stiffening is mainly due to the stiffening of collagen fibrils. Further, we show that the reduction in fibril deformation at higher strain rates is due to reduced molecular strain and fibrillar gaps, and is associated with rapid disruption of matrix-fibril bonding. This reduction in number of interfibrillar cross-links explains the changes in fibril strain; this is verified through computational modelling.

摘要

韧带失效是造成残疾和疼痛的主要社会负担。失效是由高加载率的创伤引起的。在宏观层面上,增加应变速率会导致失效应力和模量的增加,但这种应变速率依赖性的机制尚不清楚。在这里,我们使用机械测试结合同步加速器 X 射线衍射来研究人韧带的纳米级机械性能变化。随着应变速率的增加,我们观察到原纤维模量显著增加,原纤维与组织应变比降低,这表明组织水平的增硬是主要由于胶原原纤维的增硬。此外,我们还表明,较高应变速率下原纤维变形的减少是由于分子应变和原纤维间隙的减少,并且与基质-原纤维结合的快速破坏有关。这种原纤维间交联数量的减少解释了原纤维应变的变化;这通过计算建模得到了验证。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/1516a6229ee7/41598_2018_21786_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/27d1d905f5f5/41598_2018_21786_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/c3318a68ebea/41598_2018_21786_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/16bd196da417/41598_2018_21786_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/1419c875e1e2/41598_2018_21786_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/1516a6229ee7/41598_2018_21786_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/27d1d905f5f5/41598_2018_21786_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/c3318a68ebea/41598_2018_21786_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/16bd196da417/41598_2018_21786_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/1419c875e1e2/41598_2018_21786_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d869/5829138/1516a6229ee7/41598_2018_21786_Fig5_HTML.jpg

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