ABSTRACT
This study probed the protective effect of recombinant
ABSTRACT
Objective To study the damage propagation and evolution mechanism of cartilage under compressive loads.Methods The fiber-reinforced porous elastic model of cartilage with micro-defect was established by using finite element method,and the process of damage evolution under compressive loads was simulated and analyzed with parameters.The patterns of stress and strain distributions on cartilage matrix and collagen fiber at different damage extension stages were obtained.Results The strain in the surface and forefront of cartilage damage increased significantly with the increase of compression displacement,and they were obviously in positive correlation;in the process of damage evolution,there was a trend that cartilage extended to the deep and both sides simultaneously;cracks and damage in cartilage extended preferentially along the fiber tangent direction.With the aggravation of cartilage damage,the lateral extension speed was significantly faster than the longitudinal extension speed.Conclusions The process of cartilage damage extension has a close relationship with the distribution of fibers.The damages in matrix and fiber promote each other.The evolution speed and degree of cartilage vary constantly in different layers and at different stages.These results can provide the qualitative reference for prediction and repair of cartilage damage,as well as the theoretical basis for explaining pathological phenomena of damage degeneration and its clinic treatment.
ABSTRACT
Mycobacterium (M.) vaccae is a fast-growing species of saprophytic bacteria that is widely distributed. To understand the host immune responses induced by M. vaccae isolated from bovine submaxillary lymph nodes, C57BL/6 mice were infected with reference strain M. vaccae Bacillus Calmette-Guérin (BCG) and isolated M. vaccae using intraperitoneal injections. Comparison of the bacterial replication and organ pathology between M. vaccae and M. vaccae BCG revealed that M. vaccae was more malignant than M. vaccae in mice. We also demonstrated that serum from the M. vaccae-infected mice contained a higher expression level of gamma-interferon (IFN-γ), tumor necrosis factor alpha, monocyte chemoattractant protein-1, interleukin (IL)-4, IL-12, IL-10 and transforming growth factor beta than did the other groups, especially after week 4. Furthermore, when the numbers of CD3⁺CD4⁺IFN-γ⁺ and CD3⁺CD4⁺IL4⁺ cells in the infected mice were observed by flow cytometry, we found that a powerful T helper 1 (Th1) response was induced by M. vaccae infection, which was associated with the emergence of CD3⁺CD4⁺IFN-γ⁺ cells. However, the Th1 response declined over time, which was associated with appearance of the CD4⁺CD25⁺FoxP3⁺ and CD4⁺CD25⁺CD152⁺Treg cell reaction. In addition, a strong Th2 response was found. Finally, we found that M. vaccae infection increased the production of type I IFNs, which was associated with a reduced Th1 response.