Int J Med Sci
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Antibodies targeting the immune checkpoint inhibitor, programmed cell death 1 (PD-1), have provided a breakthrough in the treatment of lung cancer. However, the function of PD-1 in natural killer (NK) cells of cancer patients remains unclear. Herein, we analyzed the expression of PD-1 on the NK cells in the peripheral blood of patients with lung cancer and found that the level of PD-1+ NK cells in patients was significantly higher than that in healthy individuals. ⋯ In addition, IL-2 could increase the expression of PD-1 on NK cells in vitro, indicating that high IL-2 level in the plasma is largely responsible for the abundance of PD-1+ NK cells in patients with lung cancer. These findings demonstrate intriguing mechanisms for understanding the expression of PD-1 on NK cells and the function of PD-1+ NK cells in lung cancer. This study confirms and extends previous studies demonstrating that PD-1 can negatively regulate the antitumor function of NK cells.
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Skin, as the major organ of a human body, is constantly exposed to PM2.5 stimulation, which may exert specific toxic influences on the physiology of skin. This study aims to investigate the effect of PM2.5 on the formation of inflammasomes in skin cells and to explore the potential mechanism linking PM2.5 and skin inflammation. ⋯ In addition, the upregulation of NLRP1 and IL-1β could be reversed by NF-κB inhibitor indicating that PM2.5 may promote NLRP1 expression through activating NF-κB pathway. Furthermore, high ROS level was also found in cells treated with PM2.5 and inhibition of ROS could also reverse NK-κB production stimulated by PM2.5 that means ROS is involved in this skin inflammation process.
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Background: Data on acute kidney injury (AKI) in patients with myocardial infarction (MI) who underwent percutaneous coronary intervention (PCI) after cardiac arrest are scarce. The prevalence of AKI, as classified by the Kidney Disease: Improving Global Outcomes (KDIGO) criteria; and its possible association with 30-day mortality were assessed. Methods: Data on 6387 patients with MI, 342 (5.3%) with out-of-hospital cardiac arrest or arrest immediately after admission before PCI, were retrospectively analyzed. ⋯ The adjusted OR for AKI KDIGO stages 1/2 and stage 3 were 3.68; 95% CI 1.53 to 8.32; p=0.002 and 29.10; 95% CI 8.31 to 101.88; p<0.0001, respectively. Conclusion: In patients resuscitated after MI undergoing PCI, AKI had a deleterious impact on the prognosis. A graded increase in the severity of AKI according to the KDIGO definition was associated with a progressively increased risk of 30-day mortality.
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Gastric cancer is a heterogeneous tumor that underlying molecular mechanisms are largely unclear. This study aimed to elucidate the expression level of HGF-c-MET in gastric cancer patients and to investigate the prognostic and diagnostic value of HGF-c-MET. In silico analysis of the TCGA and GEO database found that HGF and c-MET mRNA expression are significantly higher in gastric cancer tissues than those in peritumor tissues. ⋯ HGF was positively correlated with CD8+ T cell, CD4+ T cell, macrophage, neutrophil and dendritic cell. Furthermore, functional enrichment analysis and protein-protein interaction networks further shown that HGF-c-MET and related proteins mainly participated in growth factor receptor binding, protein tyrosine kinase activity and signaling receptor binding. Finally, outcome of GSEA analysis showed 13 shared KEGG pathways enriched in high expressed group of HGF and c-MET.
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Family with sequence similarity 83A (FAM83A) is a newly-found over-expressed oncogene in several types of cancers and associates with poor prognosis. However, the role that FAM83A may play in the carcinogenesis of non-small cell lung cancer (NSCLC) still needs to be defined. The present study aimed to investigate the function of FAM83A in NSCLC progression and to investigate the possible mechanism. ⋯ Western blotting showed that silencing FAM83A decreased the phosphorylation of ERK and PI3K/Akt/mTOR. On the other hand, overexpressing FAM83A in vitro enhanced cell proliferation and invasiveness, which was repressed by PI3K inhibitor and ERK inhibitor separately. Taken together, our study suggests that FAM83A promotes tumorigenesis of NSCLC at least partly via ERK and PI3K/Akt/mTOR pathways, making it a promising therapeutic target.