The association between maternal diabetes and neonatal seizures: a nested case-Control study.

Aim: We aimed to evaluate the association of pregestational diabetes mellitus (PGDM) and gestational diabetes mellitus (GDM) with neonatal seizures during neonatal hospitalization. Methods: In this nested case-control study, all data were collected from the data files of the National Vital Statistics System (NVSS) 2016-2021. Considering the effect of confounders, we used the propensity-score matching (PSM; case:control = 1:4) method to select the study population. The outcome was considered the occurrence of neonatal seizures. Univariate and multivariate logistic regression analyses were adopted to assess the association of PGDM and GDM with neonatal seizures. We also conducted stratified analyses according to gestational age, birthweight, 5 min Apgar score, and maternal age to explore the potential disparities. Results: After using the PSM method, a total of 6,674 cases of neonatal seizures and 26,696 controls were included. After adjusting for covariates, PGDM was associated with an increased risk of neonatal seizures [odds ratio (OR) = 1.51, 95% confidence interval (CI): 1.15-1.98], whereas the association between GDM and neonatal seizures is not statistically significant. In addition, the correlation between PGDM and increased risk of neonatal seizures was observed in neonates with a gestational age of 37-42 weeks and ≥42 weeks, with a 5 min Apgar score of ≥7, and with a maternal age of ≤40 years. Conclusion: PGDM was found to be closely associated with an increased risk of neonatal seizures. The findings of our study indicated that neonatologists should consider monitoring the incidence of neonatal seizures in neonates born to mothers with PGDM.

Divergent Roles of miR-3162-3p in Pulmonary Inflammation in Normal and Asthmatic Mice as well as Antagonism of miR-3162-3p in Asthma Treatment.

MicroRNA (miRNA) mimics or antagomirs hold great promise for asthma treatment compared with glucocorticoids as mainstay therapy for asthma. But the role of miRNA in regulating asthmatic inflammation is largely unclear. We previously reported that miR-3162-3p in the peripheral blood of children with asthma was obviously upregulated compared to that in healthy children. This study aimed to elucidate the role of miR-3162-3p in pulmonary inflammation in normal and asthmatic mice as well as preliminarily explore the potential of miR-3162-3p antagomir in asthma treatment. A noninvasive whole-body plethysmograph measured airway responsiveness. Both qRT-PCR and Western blot were used to detect the expression of miRNA, mRNA, or protein. Cells in bronchoalveolar lavage fluid were counted by platelet counting and Wright's staining. Inflammatory infiltration and mucus secretion were identified by hematoxylin and eosin and periodic acid-Schiff  staining, respectively. Cytokines in the lungs were detected by ELISA. The miR-3162-3p mimic intraperitoneally administered to normal mice decreased ß-catenin levels in the lungs without obviously altering the lung histology and cytokine levels. Antagonizing miR-3162-3p in ovalbumin-induced asthmatic mice effectively alleviated the typical features of asthma, such as airway hyper-responsiveness, airway inflammation, and Th1/Th2 cytokine imbalance, and concomitantly rescued the total and active ß-catenin expression. Collectively, we discovered divergent roles of miR-3162-3p in lung inflammation between normal and asthmatic mice. The anti-inflammatory effects of the miR-3162-3p antagomir were comparable to those of glucocorticoid treatment. Our study helped in understanding the contribution of miRNAs to the pathogenesis of asthma.

Adverse impact of ambient PM2.5 on expression and trafficking of surfactant protein A through reactive oxygen species damage to lamellar bodies.

Particulate matter with a diameter of less than 2.5 µm (PM2.5) easily deposits on lung alveoli and degrades human health. Surfactant protein A (SP-A) is the most abundant pulmonary surfactant protein stored in lamellar bodies (LBs) of alveolar epithelial type II cells. The impacts of PM2.5 on SP-A are multifaceted and intractable, and the underlying mechanism remains unclear. In this study, the expression and distribution of SP-A in Balb/c mice and A549 cells under PM2.5 exposure were investigated. The results showed that the low and medium concentration of PM2.5 gradually enhanced SP-A protein and mRNA expression, whereas the high concentration of PM2.5 conspicuously decreased SP-A protein but not its mRNA compared with the control. The trafficking of SP-A to LBs was gradually disturbed, and concomitantly, the lesions of LBs responsible for the transport and storage of SP-A protein were exacerbated with increased PM2.5 concentration. Reactive oxygen species production abundantly increased upon PM2.5 exposure, and it was antagonized by the oxidant inhibitor N-acetylcysteine. Subsequently, the injured LBs and the decrease in SP-A expression under exposure to the high concentration of PM2.5 were well rescued. The present study provides a new perspective to investigate the adverse effects of PM2.5 or diesel exhaust particles on other proteins transported to and stored in LBs.