RESUMEN
Titanium alloy Ti6Al4V is a commonly used bone implant material, primarily prepared as a porous material to better match the elastic modulus of human bone. However, titanium alloy is biologically inert and does not have antibacterial properties. At the same time, the porous structure with a large specific surface area also increases the risk of infection, leading to surgical failure. In this paper, we prepared three porous samples with different porosities of 60%, 75%, and 85%, respectively (for short, 3D-60, 3D-75, and 3D-85) using 3D printing technology and clarified the mechanical properties. Through tensile experiments, when the porosity was 60%, the compressive modulus was within the elastic modulus of human bone. Anodic oxidation technology carried out the surface modification of a 3D-printed porous titanium alloy with 60% porosity. Through change, the different voltages and times on the TiO2 oxide layer on the 3D-printed porous titanium alloy are different, and it reveals the growth mechanism of the TiO2 oxide layer on a 3D-printed unique titanium alloy. The surface hydrophilic and antibacterial properties of 3D-printed porous titanium alloy were significantly improved after modification by anodic oxidation.
RESUMEN
PURPOSE: The objective of this study was to identify the potential regulatory mechanisms, diagnostic biomarkers, and therapeutic drugs for heart failure (HF). METHODS: Differentially expressed genes (DEGs) between HF and non-failing donors were screened from the GSE57345, GSE5406, and GSE3586 datasets. Database for Annotation Visualization and Integrated Discovery and Metascape were used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses respectively. The GSE57345 dataset was used for weighted gene co-expression network analysis (WGCNA). The intersecting hub genes from the DEGs and WGCNA were identified and verified with the GSE5406 and GSE3586 datasets. The diagnostic value of the hub genes was calculated through receiver operating characteristic analysis and net reclassification index (NRI). Gene set enrichment analysis (GSEA) was used to filter out the signaling pathways associated with the hub genes. SYBYL 2.1 was used for molecular docking of hub targets and potential HF drugs obtained from the connection map. RESULTS: Functional annotation of the DEGs showed enrichment of negative regulation of angiogenesis, endoplasmic reticulum stress response, and heart development. PTN, LUM, ISLR, and ASPN were identified as the hub genes of HF. GSEA showed that the key genes were related to the transforming growth factor-ß (TGF-ß) and Wnt signaling pathways. Sirolimus, LY-294002, and wortmannin have been confirmed as potential drugs for HF. CONCLUSION: We identified new hub genes and candidate therapeutic drugs for HF, which are potential diagnostic, therapeutic and prognostic targets and warrant further investigation.