In the present study, we aimed to explore gender differences in infant mortality and neonatal morbidity in mixed-gender twin pairs. Data were obtained from the US National Center for Health Statistics Linked Birth-Infant Death Cohort. A total of 108,038 pairs of mixed-gender twins were included in this analysis. Among the mixed-gender twins, no significant difference in the odds of fetal mortality between male twins (1.05%) and female co-twins (1.04%). However, male twins were at increased odds of neonatal mortality (adjusted OR 1.59; 95% CI 1.37, 1.85) and overall infant mortality (adjusted OR 1.43; 95% CI 1.27, 1.61) relative to their female co-twins. Congenital abnormalities (adjusted OR 1.38; 95% CI 1.27, 1.50) were identified significantly more frequently in male than female twins. Moreover, increased odds of having low 5-minute Apgar score (30 minutes (adjusted OR 1.31; 95% CI 1.17, 1.47), and respiratory distress syndrome (adjusted OR 1.45; 95% CI 1.26, 1.66) were identified in male twins relative to their female counterparts. The results of our study indicated that in mixed-gender twin pairs, the odds of infant mortality and neonatal morbidity were higher in male twins than their female co-twins.

Neonates are at high risk of meningitis and of resulting neurologic complications. Early recognition of neonates at risk of poor prognosis would be helpful in providing timely management. From January 2008 to June 2014, we enrolled 232 term neonates with bacterial meningitis admitted to 3 neonatology departments in Shanghai, China. The clinical status on the day of discharge from these hospitals or at a postnatal age of 2.5 to 3 months was evaluated using the Glasgow Outcome Scale (GOS). Patients were classified into two outcome groups: good (167 cases, 72.0%, GOS = 5) or poor (65 cases, 28.0%, GOS = 1–4). Neonates with good outcome had less frequent apnea, drowsiness, poor feeding, bulging fontanelle, irritability and more severe jaundice compared to neonates with poor outcome. The good outcome group also had less pneumonia than the poor outcome group. Besides, there were statistically significant differences in hemoglobin, mean platelet volume, platelet distribution width, C-reaction protein, procalcitonin, cerebrospinal fluid (CSF) glucose and CSF protein. Multivariate logistic regression analyses suggested that poor feeding, pneumonia and CSF protein were the predictors of poor outcome. CSF protein content was significantly higher in patients with poor outcome. The best cut-offs for predicting poor outcome were 1,880 mg/L in CSF protein concentration (sensitivity 70.8%, specificity 86.2%). After 2 weeks of treatment, CSF protein remained higher in the poor outcome group. High CSF protein concentration may prognosticate poor outcome in neonates with bacterial meningitis.

Large-for-gestational-age (LGA) babies have a higher risk of metabolic disease later in life, and their postnatal growth in early childhood may be associated with long-term adverse outcomes. This study aimed to determine childhood health outcomes of term LGA babies with different growth patterns. Data were obtained from the US Collaborative Perinatal Project for the years between 1959 and 1976. The growth trajectories of 3,316 term LGA babies were identified and odds ratios of obesity, growth restriction, low intelligence quotient (IQ), and high blood pressure (HBP) were calculated by logistic regression. Compared with term appropriate-for-gestational-age infants, term LGA babies without catch-down growth had increased risks of obesity (adjusted odds ratio (aOR) = 6.37, 95% confidence interval (CI): 5.24, 7.73) and HBP (aOR = 1.67, 95% CI: 1.37, 2.03). Those with high catch-down growth had higher risks of growth restriction (aOR = 2.21, 95% CI: 1.66, 2.95) and low IQ (aOR = 1.61, 95% CI: 1.04, 2.49). Nevertheless, infants with small catch-down growth had lower risks of obesity (aOR = 0.78, 95% CI: 0.63, 0.95), growth restriction (aOR = 0.28, 95% CI: 0.17, 0.46), low IQ (aOR = 0.66, 95% CI: 0.41, 1.06), and HBP (aOR = 0.89, 95% CI: 0.77, 1.04). According to our data, term LGA infants with small catch-down growth had no increased risks of adverse outcomes.

Premature infants often require oxygen supplementation, which can elicit bronchopulmonary dysplasia (BPD) and lead to mitochondrial dysfunction. Mitochondria play important roles in lung development, in both normal metabolism and apoptosis. Enhancing our comprehension of the underlying mechanisms in BPD development can facilitate the effective treatments. Plasma samples from BPD and non-BPD infants were collected at 36 weeks post-menstrual age and used for metabolomic analysis. Based on hyperoxia-induced animal and cell models, changes in mitophagy and apoptosis were evaluated following treatment with itaconic acid (ITA). Finally, the mechanism of action of ITA in lung development was comprehensively demonstrated through rescue strategies and administration of corresponding inhibitors. An imbalance in the tricarboxylic acid (TCA) cycle significantly affected lung development, with ITA serving as a significant metabolic marker for the outcomes of lung development. ITA improved the morphological changes in BPD rats, promoted SP-C expression, and inhibited the degree of alveolar type II epithelial cells (AEC II) apoptosis. Mechanistically, ITA mainly promotes the nuclear translocation of transcription factor EB (TFEB) to facilitate dysfunctional mitochondrial clearance and reduces apoptosis in AEC II cells by regulating autophagic flux. The metabolic imbalance in the TCA cycle is closely related to lung development. ITA can improve lung development by regulating autophagic flux and promote the nuclear translocation of TFEB, implying its potential therapeutic utility in the treatment of BPD.