The aim of the study was to conduct a meta-analysis to evaluate the accuracy of neutrophil CD64, procalcitonin (PCT), and interleukin-6 (IL-6) for the diagnosis of sepsis. The sample articles were searched in various databases to collect published studies on the diagnosis of sepsis by neutrophil CD64, PCT, and IL-6. By using the Stata SE 15.0 software, forest plots and the area under the summary receiver operating characteristic curves were drawn. The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and area under the curve (AUC) were calculated. 54 articles were included in the study. The number of studies that evaluated the diagnostic value of neutrophil CD64, PCT, and interleukin-6 were 20, 39, and 15, respectively. The pooled sensitivity, specificity, and AUC of neutrophil CD64 for the diagnosis of sepsis were 0.88 [95% confidence interval (CI), 0.81–0.92], 0.88 (95% CI, 0.83–0.91), and 0.94 (95% CI, 0.91–0.96), respectively. The pooled sensitivity, specificity, and AUC of PCT for the diagnosis of sepsis were 0.82 (95% CI, 0.78–0.85), 0.78 (95% CI, 0.74–0.82), and 0.87 (95% CI, 0.83–0.89), respectively. Subgroup analysis showed that the AUC for PCT diagnosis of intensive care unit (ICU) sepsis was 0.86 (95% CI, 0.83–0.89) and the AUC for PCT diagnosis of non-ICU sepsis was 0.82 (95% CI, 0.78–0.85). The pooled sensitivity, specificity, and AUC of IL-6 for the diagnosis of sepsis were 0.72 (95% CI, 0.65–0.78), 0.70 (95% CI, 0.62–0.76), and 0.77 (95% CI, 0.73–0.80), respectively. Of the three biomarkers studied, neutrophil CD64 showed the highest diagnostic value for sepsis, followed by PCT, and IL-6. On the other hand, PCT showed a better diagnostic value for the diagnosis of sepsis in patients with severe conditions compared with that in patients with non-severe conditions.

Background: Previous studies have shown that RBM10 is a potential tumor suppressor protein that can inhibit proliferation and promote apoptosis of NSCLC. RBM10 can bind and modify RNA at the post transcriptional level.Method and results: Transwell and cell wound healing assay showed that RBM10 significantly inhibited the invasion and migration of NSCLC. CLIP-seq showed that among all RBM10 binding RNAs, lncRNA MALAT1 with high m6A methylation in lung cancer had the highest binding peak among all non-coding RNAs. RNA Immunoprecipitation has verified the direct combination of RBM10 and MALAT1. The rescue experiment confirmed that RBM10 affected the phosphorylation of PI3K/AKT/mTOR passway protein, the invasion and migration ability by regulating MALAT1. MeRIP-qPCR confirmed that RBM10 could inhibit MALAT1 m6A methylation levels by recruiting METTL3.Conclusion: These results suggest that RBM10, as an RNA-binding protein, may inhibit m6A methylation of MALAT1 by recruiting METTL3, and affect phosphorylation of the downstream PI3K/AKT/mTOR pathway by binding and regulating MALAT1, ultimately affecting the invasion and migration of NSCLC.