A Novel Equivalent Method for Computing Mechanical Properties of Random and Ordered Hyperelastic Cellular Materials.

Simulating the mechanical behavior of cellular materials stands as a pivotal step in their practical application. Nonetheless, the substantial multitude of unit cells within these materials necessitates a considerable finite element mesh, thereby leading to elevated computational expenses and requisites for formidable computer configurations. In order to surmount this predicament, a novel and straightforward equivalent calculation method is proposed for the computation of mechanical properties concerning both random and ordered hyper-elastic cellular materials. By amalgamating the classical finite element approach with the distribution attributes of cells, the proposed equivalent calculation method adeptly captures the deformation modes and force-displacement responses exhibited by cell materials under tensile and shear loads, as predicted through direct numerical simulation. This approach reflects the deformation characteristics induced by micro-unit cells, elucidates an equivalent principle bridging cellular materials and equivalent materials, and substantially curtails exhaustive computational burdens. Ultimately, this method furnishes an equivalent computational strategy tailored for the engineering applications of cellular materials.

PTPN18 promotes colorectal cancer progression by regulating the c-MYC-CDK4 axis.

Protein tyrosine phosphatase non-receptor type 18 (PTPN18) is often highly expressed in colorectal cancer (CRC), but its role in this disease remains unclear. We demonstrated that PTPN18 overexpression promotes growth and tumorigenesis in CRC cells and that PTPN18 deficiency yields the opposite results in vitro. Moreover, a xenograft assay showed that PTPN18 deficiency significantly inhibited tumorigenesis in vivo. PTPN18 activated the MYC signaling pathway and enhanced CDK4 expression, which is tightly associated with the cell cycle and proliferation in cancer cells. Finally, we found that MYC interacted with PTPN18 and increased the protein level of MYC. In conclusion, our results suggest that PTPN18 promotes CRC development by stabilizing the MYC protein level, which in turn activates the MYC-CDK4 axis. Thus, PTPN18 could be a novel therapeutic target in the future.