Exogenous NADPH could mitigate pyroptosis-induced brain injury in fetal mice exposed to gestational intermittent hypoxia.

OBJECTIVE: Obstructive Sleep Apnea (OSA) during pregnancy is characterized by intermittent hypoxia (IH) during sleep and will lead to the rise of oxidative stress in the fetal body. Pyroptosis, a type of inflammatory and programmable cell death mediated by Gasdermin D (GSDMD), plays a substantial role in oxygen deprivation's contribution to neural system damage. Existing research shows that Nicotinamide Adenine Dinucleotide Phosphate (NADPH) plays a protective role in alleviating brain tissue pyroptosis. We speculate that exogenous NADPH may play a protective role in OSA during pregnancy. METHODS: A model of GIH group was established to simulate the pathophysiological mechanisms of OSA during pregnant and AIR group was established by giving the same frequency. Sham group was established by injecting NS and the NADPH group was established and given exogenous NADPH. We utilized the Morris Water Maze to assess cognitive function impairment, Luxol Fast Blue (LBF) staining to confirm myelin sheath formation, TUNEL staining to examine cell death in fetal mice brain tissue, and Western blotting to detect pertinent protein expressions. RESULTS: The GIH group offspring exhibited decreases in spatial learning and memory abilities, reduced numbers of oligodendrocytes and formed myelin, as well as increased expression of pyroptosis-related proteins. The NADPH group offspring showed restoration in spatial learning and memory abilities increased counts of oligodendrocytes and formed myelin sheaths, in addition to decreased expression of pyroptosis-related. CONCLUSIONS: This study demonstrates that early injection of exogenous NADPH can alleviate the damage to fetal brain development caused by gestational intermittent hypoxia (GIH).

The prevalence of occult HBV infection in immunized children with HBsAg-positive parents: a hospital-based analysis.

BACKGROUND AND OBJECT: The risk of occult HBV infection (OBI) in children whose mothers are HBV carriers has received more widespread attention, but there were few reports to focus on the children with HBsAg-positive parents. In this study, we aimed to investigate the prevalence of OBI in immunized children with HBsAg-positive parents. METHODS: HBV-vaccinated Chinese hospitalized children with HBsAg-positive parents were analyzed in our investigation. Eligible subjects were tested using a standard nested PCR for all HBV genes, and analyzed by direct sequencing. RESULTS: There were 327 HBsAg-negative children included in the study out of about 9800 involved HBV-vaccinated hospitalized children. The positive rate of OBI was 3.1% (10/327) in the eligible children and 14.1% (46/327) with HBV DNA detectable. No significant differences were found between one and at least two regions positive groups (p > 0.05). The proportions of HBV DNA detectable in children with HBV father-carriers and mother-carriers were similar. The risk factors for HBV DNA-positive children could be male, anti-HBs levels, and anti-HBc positive. CONCLUSION: There are 3.1% of OBIs and 14.1% of suspected OBI in vaccinated children with HBsAg-positive parents. The potential risk of suspected OBI in children with HBsAg-positive father should not be ignored. Anti-HBc positivity may be a useful seromarker for suspected OBI screening in vaccinated children. To prevent HBV breakthrough infection, accurate and convenient method is needed to detect OBI timely and exhaustively.