Bilateral Vocal Fold Abduction Dysfunction: A Report of Two Neonatal Cases.

Stridor is caused by oscillation of the narrowed upper airway. The most common cause of neonatal stridor is laryngomalacia, followed by vocal fold abduction dysfunction. Herein, we present two neonatal cases of idiopathic dysfunction of vocal fold abduction. A neonate was admitted to the neonatal intensive care unit (NICU) on day 4 of life for inspiratory stridor, intermittent subcostal retraction, and cyanosis. A second neonate was admitted to the NICU on day 7 of life for inspiratory stridor and cyanosis when crying. Neither patient had dysmorphic features or unusual cardiac ultrasonography findings. The diagnosis was confirmed by laryngo-bronchoscopy. Conservative treatment with biphasic positive airway pressure was effective in both cases and symptoms resolved within a few months. Resolution of vocal fold abduction dysfunction was confirmed by repeat endoscopy. Clinical manifestations of vocal fold abduction dysfunction vary widely. Although most cases resolve spontaneously, prolonged tube feeding, or even tracheostomy, is needed in some severe cases. Diagnosis of vocal fold abduction dysfunction requires a laryngo-bronchoscopy study; thus, there may be a large number of undiagnosed patients. Vocal fold abduction dysfunction should be considered in the differential diagnosis for neonatal inspiratory stridor.

Transcriptome analysis of umbilical cord mesenchymal stem cells revealed fetal programming due to chorioamnionitis.

Although chorioamnionitis (CAM) has been demonstrated to be associated with numerous short- and long-term morbidities, the precise mechanisms remain unclear. One of the reasons for this is the lack of appropriate models for analyzing the relationship between the fetal environment and chorioamnionitis and fetal programming in humans. In this study, we aimed to clarify the fetal programming caused by CAM using the gene expression profiles of UCMSCs. From nine preterm neonates with CAM (n = 4) or without CAM (n = 5), we established UCMSCs. The gene expression profiles obtained by RNA-seq analysis revealed distinctive changes in the CAM group USMSCs. The UCMSCs in the CAM group had a myofibroblast-like phenotype with significantly increased expression levels of myofibroblast-related genes, including α-smooth muscle actin (p < 0.05). In the pathway analysis, the genes involved in DNA replication and G1 to S cell cycle control were remarkably decreased, suggesting that cellular proliferation was impaired, as confirmed by the cellular proliferation assay (p < 0.01-0.05). Pathway analysis revealed that genes related to white fat cell differentiation were significantly increased. Our results could explain the long-term outcomes of patients who were exposed to CAM and revealed that UCMSCs could be an in vitro model of fetal programming affected by CAM.