Purpose: To evaluate the diagnostic effect of umbilical cord blood procalcitonin (PCT) on fetal inflammatory response syndrome (FIRS). Methods: This prospective study assessed preterm infants (100 with FIRS and 124 controls) with gestational age <32 weeks. The groups were compared in terms of the incidence of complications associated with preterm birth. To identify whether FIRS was an independent risk factor for complications of preterm birth, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multivariable logistic regression models. Finally, we clarified the diagnostic efficiency by receiver operating characteristic curves. Results: Univariate analysis showed that the incidence of natural delivery, premature rupture of membranes (PROM) > 18h, antenatal antibiotic usage, chorioamnionitis, umbilical cord blood PCT, gestational age (GA), small for gestational age (SGA), bronchopulmonary dysplasia (BPD), early-onset sepsis (EOS), necrotizing enterocolitis (NEC), white matter injury (WMI), retinopathy of prematurity (ROP), and mortality were higher in the case group than the control group (p < 0.05). Multivariable analysis confirmed a significant association between FIRS and complications of preterm birth. The level of umbilical cord blood PCT of preterm infants could be used as a noninvasive diagnostic index for FIRS (cut-off value: 0.276 ng/ml). Conclusions: Umbilical cord blood PCT may be a reliable noninvasive diagnostic biomarker for FIRS. Chorioamnionitis, natural delivery, and the level of umbilical cord blood PCT are independent risk factors for FIRS in preterm infants, while GA was a protective factor for FIRS. FIRS is an independent risk factor for BPD, EOS, NEC, WMI and ROP.
Background: Bronchopulmonary dysplasia (BPD) remains a severe respiratory complication of preterm infants in neonatal intensive care units (NICUs). However, its pathogenesis has been unclear. Bioinformatics analysis, which can help us explore genetic alternations and recognize latent diagnostic biomarkers, has recently promoted the comprehension of the molecular mechanisms underlying disease occurrence and development. Methods: In this study, we identified key genes and miRNA-mRNA regulatory networks in BPD in preterm infants to elucidate the pathogenesis of BPD. We downloaded and analyzed miRNA and gene expression microarray datasets from the Gene Expression Omnibus database (GEO). Differentially expressed miRNA (DEMs) and differentially expressed genes (DEGs) were obtained through NetworkAnalyst. We performed pathway enrichment analysis using the Database for Annotation, Visualization and Integrated Discovery program (DAVID), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG). Then we used the STRING to establish protein–protein interactions and the Cytoscape tool to establish miRNA–mRNA regulatory networks. Results: We identified 19 significant DEMs and 140 and 33 significantly upregulated and downregulated DEGs, respectively. Functional enrichment analysis indicated that significant DEGs were associated with the antigen processing and presentation, and B-cell receptor signaling pathways in BPD. Key DEGs, such as CD19, CD79B, MS4A1, and FCGR2B were selected as hub genes in PPI networks. Conclusions: In this study, we screened out 19 DEMs that might play important roles in the regulatory networks of BPD. Higher expression of miRNAs such as miR-15b-5p, hsa-miR-32-5p, miR-3613-3p, and miR-33a-5p and lower expression of miRNAs such as miR-3960, miR-425-5p, and miR-3202 might be correlated with the process of BPD.
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