On the yield criterion of porous materials by the homogenization approach and Steigmann-Ogden surface model.

In this work, we investigate the yield criterion of nanoporous materials by using homogenization approach and Steigmann-Ogden surface model. The representative volume element is proposed as an infinite matrix containing a tiny nanovoid. The matrix is incompressible, rigid-perfectly plastic, von Mises materials and nanovoids are dilute and equal in size. First, the constitutive of microscopic stress and microscopic strain rate is established based on the flow criterion. Secondly, according to the Hill's lemma, the relationship between the macroscopic equivalent modulus and the microscopic equivalent modulus is established by homogenization approach. Thirdly, the macroscopic equivalent modulus containing the Steigmann-Ogden surface model including surface parameters, porosity and nanovoid radius is derived from the trial microscopic velocity field. Finally, an implicit macroscopic yield criterion for nanoporous materials is developed. For surface modulus, nanovoids radius and porosity studies are developed through extensive numerical experiments. The research results in this paper have reference significance for the design and manufacture of nanoporous materials.

Inhibition of Sirt2 Alleviates Fibroblasts Activation and Pulmonary Fibrosis via Smad2/3 Pathway.

Idiopathic pulmonary fibrosis (IPF) is a fatal disease with unknown cause and limited treatment options. Its mechanism needs to be further explored. Sirtuin2 (Sirt2), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to be involved in the fibrosis and inflammation in the liver, kidney and heart. In this study, we aimed to evaluate the role of Sirt2 in pulmonary fibrosis. We found that Sirt2 expression was upregulated in transforming growth factor-ß1 (TGF-ß1) treated human embryonic lung fibroblasts. Sirt2 inhibitor AGK2 or the knockdown of Sirt2 expression by targeting small interfering RNA (siRNA) suppressed the fibrogenic gene α-SMA and Fibronectin expression in TGF-ß1 treated fibroblasts and primary lung fibroblasts derived from patients with IPF. In addition, Sirt2 inhibition suppresses the phosphorylation of Smad2/3. Co-immunoprecipitation (Co-IP) showed that there is interaction between Sirt2 and Smad3 in the TGF-ß1 treated lung fibroblasts. In bleomycin-induced pulmonary fibrosis in mice, AGK2 treatment significantly mitigated the degree of fibrosis and decreased the phosphorylation of Smad2/3. These data suggest that Sirt2 may participate in the development of IPF via regulating the Smad2/3 pathway. Inhibition of Sirt2 would provide a novel therapeutic strategy for this disease.