Depth-dependent strain fields of articular cartilage under rolling load by the optimized digital image correlation technique.

It is significant to investigate the depth-dependent mechanical behaviors of articular cartilage under rolling load since considerable rolling occurs for cartilage joint in activities of daily living. In this study, the rolling experiments of articular cartilage were conducted by applying an optimized digital image correlation (DIC) technique for the first time and the depth-dependent normal strain and shear strain of cartilage were analyzed. It is found that the normal strain and shear strain values of different layers increase firstly and then decrease with rolling time, and they increase with increasing compressive strains. The normal strain and shear strain values decrease along cartilage depth with constant compressive strain. The normal strain values of different normalized depth decrease with increasing rolling rates. The shear strain values of superficial layer and middle layer decrease; however there are no major changes for the shear strain values of deep layer with increasing rolling rates. The normal strain values with different rolling time increase with increasing rolling numbers and the 30.6% increase in initial normal strain is observed from 1st to 99th cycle. The fitting relationship of the normal strain and normalized depth was obtained considering the effects of compressive strain and rolling rate and the fitting curves agree with the experimental results for cartilage very well.

[Development and application of the physical hypoxic models of C. elegans].

OBJECTIVE: To develop a suitable hypoxic injury model, which is important for revealing pathological molecular mechanism of hypoxia. METHODS: We focused on C. elegans by treatment with different hypoxic times and systematically observed mortality, movement, Cellular morphology and the related-protein expression of the animals. RESULTS: We demonstrated that hypoxia (0.2% partial pressure of oxygen) induced morphological cell defects, and then leading to death of C. elegans. The mortality of C. elegans increased along with hypoxic time, while hypoxia-inducible factor (HIF-1) was significantly up-regulated. In addition, by using neuron-specific transgenic wonns with green fluorescent protein--we observed the neuron-specffic injury caused by hypoxic stress. CONCLUSION: We successfully established an effective, convenient physical hypoxic model of C. elegans, which will facilitate the studies of hypoxic pathology and molecular mechanisms of hypoxic response in the future.