Differential gene expression patterns in ST-elevation Myocardial Infarction and Non-ST-elevation Myocardial Infarction.

The ST-elevation Myocardial Infarction (STEMI) and Non-ST-elevation Myocardial Infarction (NSTEMI) might occur because of coronary artery stenosis. The gene biomarkers apply to the clinical diagnosis and therapeutic decisions in Myocardial Infarction. The aim of this study was to introduce, enrich and estimate timely the blood gene profiles based on the high-throughput data for the molecular distinction of STEMI and NSTEMI. The text mining data (50 genes) annotated with DisGeNET data (144 genes) were merged with the GEO gene expression data (5 datasets) using R software. Then, the STEMI and NSTEMI networks were primarily created using the STRING server, and improved using the Cytoscape software. The high-score genes were enriched using the KEGG signaling pathways and Gene Ontology (GO). Furthermore, the genes were categorized to determine the NSTEMI and STEMI gene profiles. The time cut-off points were identified statistically by monitoring the gene profiles up to 30 days after Myocardial Infarction (MI). The gene heatmaps were clearly created for the STEMI (high-fold genes 69, low-fold genes 45) and NSTEMI (high-fold genes 68, low-fold genes 36). The STEMI and NSTEMI networks suggested the high-score gene profiles. Furthermore, the gene enrichment suggested the different biological conditions for STEMI and NSTEMI. The time cut-off points for the NSTEMI (4 genes) and STEMI (13 genes) gene profiles were established up to three days after Myocardial Infarction. The study showed the different pathophysiologic conditions for STEMI and NSTEMI. Furthermore, the high-score gene profiles are suggested to measure up to 3 days after MI to distinguish the STEMI and NSTEMI.

The expression changes of PD-L1 and immune response mediators are related to the severity of primary bone tumors.

The expression pattern, diagnostic value, and association of PD-L1, IFN-γ and TGF-ß with bone tumor type, severity, and relapse are determined in this study. 300 human samples from patients with osteosarcoma, Ewing sarcoma, and GCT were enrolled. The PD-L1 gene and protein expression were assessed by qRT-PCR and immunohistochemistry, respectively. ELISA and flow cytometry was used to detect cytokines and CD4/CD8 T cell percentages, respectively. A considerable increase in PD-L1 level was detected in bone tumor tissues at both gene and protein levels that was considerable in osteosarcoma and Ewing sarcoma. A positive correlation was detected regarding the PD-L1 and tumor metastasis and recurrence in osteosarcoma and Ewing sarcoma. The increased IFN-γ level was detected in patients with metastatic, and recurrent osteosarcoma tumors that were in accordance with the level of TGF-ß in these samples. The simultaneous elevation of IFN-γ and TGF-ß was detected in Ewing sarcoma and GCT, also the CD4 + /CD8 + ratio was decreased significantly in patients with osteosarcoma compared to GCT tumors. The elevated levels of PD-L1, TGF- ß, and IFN-γ were associated with bone tumor severity that can provide insights into the possible role of this axis in promoting immune system escape, suppression, and tumor invasion.

Cellular crosstalk in atherosclerotic plaque microenvironment.

Atherosclerosis is an underlying pathology of many vascular diseases as a result of cellular, structural and molecular dysfunctions within the sub-endothelial space. This review deals with the events involved in the formation, growth and remodeling of plaque, including the cell recruitment, cell polarization, and cell fat droplets. It also describes cross talking between endothelial cells, macrophages, and vascular smooth muscle cells, as well as the cellular pathways involved in plaque development in the plaque microenvironment. Finally, it describes the plaque structural components and the role of factors involved in the rupture and erosion of plaques in the vessel. Video Abstract.