Objective: To investigate the predictive value of lung ultrasound score (LUS) in the extubation failure from mechanical ventilation (MV) among premature infants with neonatal respiratory distress syndrome (RDS).Methods: The retrospective cohort study was conducted with a total of 314 RDS newborns who received MV support for over 24 h. After extubation from MV, infants were divided into extubation success and extubation failure groups. Extubation failure was defined as re-intubation within 48 h after extubation. Univariate and multivariate logistic regression analyses were used to identify the predictors of the extubation failure. The predictive effectiveness of the combined model and LUS in the extubation failure was assessed by receiver operating characteristic curve, area under curve (AUC), and internal validation.Results: 106 infants failed extubation from MV. The combined model for predicting the extubation failure was performed according to the predictors of gestational age, body length, birth weight, and LUS. The AUC of this combined model was 0.871 (sensitivity: 86.67%, specificity: 74.31%). The AUC of LUS was 0.858 (sensitivity: 84.00%, specificity: 80.69%), and the cutoff value was 18. There was no statistical difference in the predictive power between the combined model and LUS (Z = 0.880, P = 0.379). The internal validation result showed that the AUC of LUS was 0.855.Conclusions: LUS presented a good ability in predicting the extubation failure among RDS newborns after MV.

Background Hyperoxia induces lung injury through lung inflammation in premature infants, leading to bronchopulmonary dysplasia (BPD). Semaphorin 3A (SEMA3A) participates in diverse biological processes, including cell migration, angiogenesis, and inflammation. The effect of SEMA3A on hyperoxic lung injury of neonatal rats with BPD was investigated in this study. Methods Neonatal rats with BPD were established through hyperoxia treatment. Hematoxylin-eosin staining was used to evaluate histopathological analysis in lung tissues. SEMA3A expression was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot assay. Adeno-associated virus (AAV)-mediated over-expression of SEMA3A (AAV-SEMA3A) was administrated into hyperoxia-induced rats, and apoptosis was evaluated by TUNEL staining. Levels of inflammatory cytokines were investigated by enzyme-linked-immunosorbent serologic assay (ELISA). Results Hyperoxia-induced histopathological changes in lung tissue reduced alveolar number and enhanced alveolar interval and alveolar volume. SEMA3A was downregulated in lung tissue of hyperoxia-induced rats. AAV-SEMA3A injection attenuated hyperoxia-induced cell apoptosis in lung tissues by increasing Bcl-2 and decreasing Bax and cleaved caspase-3. Moreover, the enhanced levels of Interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, and tumor necrosis factor-α (TNF-α) in hyperoxia-induced rats were restored by AAV-SEMA3A injection by the downregulation of nuclear factor kappa B (NF-κB) phosphorylation. AAV-SEMA3A injection also ameliorated histopathological changes in lung tissues of hyperoxia-induced rats by increasing the number of radial alveolar count and decreasing the volume of mean linear intercept. Besides, the protein expression levels of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) phosphorylation were reduced in hyperoxia-induced rats post-AAV-SEMA3A injection. Conclusion Ectopical expression of SEMA3A suppressed hyperoxia-induced apoptosis and inflammation in neonatal rats, and ameliorated the histopathological changes through inactivation of ERK/JNK pathway.

IntroductionThe aim of this study was to investigate the proliferation and apoptosis of T24 after treatment with isoliquiritigenin (ISL) and to explore the underlying mechanism.Material and methodsT24 cells were divided into 6 groups and cultured. The five experimental groups were seeded into medium with 10, 20, 40, 80, and 160 µM ISL and the control group was administered with 0.01% DMSO. The cell morphology was observed using an optical microscope. The proliferation of cells and half maximal inhibitory concentration (IC50) were determined and calculated by MTS. Cell cycle and apoptosis were evaluated by flow cytometry. The migration ability of cells was detected by wound healing assay. The expression of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and proliferating cell nuclear antigen (PCNA) was determined by RT-qPCR and western blot.ResultsAt 24 h after treatment with ISL, morphology revealed that cell number diminished and the cell volume shrank with increasing concentration. According to the results of MTS, ISL significantly inhibited the T24 cell proliferation in a dose- and time-dependent manner. Flow cytometry showed that ISL could block the replication of T24 cell DNA from S phase to G2, therefore promoting cell apoptosis. Wound healing assay showed that at 48 h after treatment with ISL, the migration of T24 cells was remarkably inhibited. The results of RT-qPCR and Western blot revealed that after 24 h of treatment, the expression levels of Bcl-2 and PCNA were down-regulated, and the expression level of Bax was increased in the different dose of the ISL treated group.ConclusionsISL possesses detrimental effects on the viability of BC cell T24 in a dose-dependent manner via blocking the cell cycle and inducing apoptosis by down-regulation of PCNA and Bcl-2 expression and up-regulation of Bax expression.