Association of infant feeding patterns with body fat mass and obesity in the first 2 years of life: a longitudinal twin birth cohort study.

Childhood obesity is a major public health problem with no effective intervention. We explored the influence of feeding patterns on infants' growth indices within the first 2 years in a twin birth cohort. Dietary intake at 12 months was recorded with a food frequency questionnaire, and dietary patterns were identified by principal component analysis. Milk feeding methods in first 6 months were categorised as breastfeeding or exclusive formula feeding. Correlations between feeding patterns and infants' growth indices were examined via generalised estimating equations. Two dietary patterns were identified and neither of which was related to growth indices. Breastfed infants had a higher body fat mass (BFM) percentage at 12 months, a higher body mass index (BMI) increment from birth to 6 months and a lower BMI increment from 6 to 12 months. Breastfed infants were likely positively correlated with BFM at 12 months; as complementary food was added, the effect of breastfeeding on growth gradually decreased.

Interleukin-33 (IL-33) Increases Hyperoxia-Induced Bronchopulmonary Dysplasia in Newborn Mice by Regulation of Inflammatory Mediators.

BACKGROUND Interleukin-33 (IL-33) has been reported to affect chronic inflammation of the lungs, but its impact on hyperoxia-injured lungs in newborns remains obscure. This study aimed to investigate the role of IL-33 in the lungs of neonatal mice with hyperoxia-induced bronchopulmonary dysplasia (BPD). MATERIAL AND METHODS Twenty-four C57BL/6 baby mice were randomly separated into three groups: the on-air group (N=16); the O2 group (N=8); and the O2 + anti-IL-33 group (N=8). Forced mechanical ventilation with oxygen-rich air (MV-O2) was used in 16 mouse pups. The mouse pups were incubated in containers with either air or 85% O2 for 1, 3, 7, 14, 21, and 28 days after birth. At the end of the treatment period, the mouse lungs were studied by histology, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) to examine the expression of the pro-inflammatory mediators, including interleukin (IL)-1ß, chemokine (CC motif) ligand 1 (CXCL-1), and monocyte chemoattractant protein-1 (MCP-1). RESULTS Following forced MV-O2, increased levels of IL-33 in whole mouse lungs were associated with impaired alveolar growth and with changes consistent with BPD, including reduced numbers of enlarged alveoli, increased apoptosis, and increased expression of IL-1ß, CXCL-1, and MCP-1. IL-33 inhibition improved alveolar development in hyperoxia-impaired lungs and suppressed IL-1ß and MCP-1 expression and was associated with increased transforming growth factor-ß (TGF-ß) signaling, reduced pulmonary NF-κB activity and decreased expression of the TGF-ß inhibitor SMAD-7 in forced MV-O2 exposed mouse pups. CONCLUSIONS IL-33 increased hyperoxia-induced BPD in newborn mice by regulation of the expression of inflammatory mediators.

Analysis of perinatal risk factors for small-for-gestational-age and appropriate-for-gestational-age late-term infants.

To investigate the potential risk factors for small-for-gestational-age (SGA) and appropriate-for-gestational-age (AGA) late-term infants, 100 cases of single full-term SGA infants delivered in the Department of Obstetrics, The First Affiliated Hospital of Chongqing Medical University in 2017 were enrolled as the SGA group. A total of 100 healthy AGA who were born at the same time with the same gestational age were randomly included as the control group. The perinatal and postpartum adverse conditions of the two groups were recorded, and Apgar tests were performed on all newborns at 1 min (T1), 5 min (T2) and 10 min (T3) after birth. A follow-up survey was conducted in all patients at 6 and 12 months of age. At the second follow-up, the development quotient of the children was measured using the Gesell Developmental Schedule, and the perinatal risk factors of SGA were analyzed. The incidence of intrauterine distress, respiratory distress syndrome and infectious disease in the SGA group was significantly higher compared with that in the AGA group (P<0.05). The Apgar scores at T1, T2 and T3 were significantly lower in the SGA group compared with the AGA group (P<0.05). The Apgar score at T1 was lower compared with that at T2 in the SGA group (P<0.05), and the Apgar score at T2 was lower compared with that at T3 (P<0.05). The length of hospital stay in the SGA group was significantly longer compared with that in the AGA group (P<0.05). The development quotient at the 6 and 12th month in the SGA group was significantly lower compared with that in the AGA group (P<0.05). Logistic regression analysis showed that there was no correlation between SGA and maternal age, regardless of firstborn status, neonatal sex, mode of delivery and living environment. SGA was significantly associated with umbilical cord abnormalities, maternal pregnancy-induced hypertension, gestational diabetes, pregnancy infection and intrauterine distress (P<0.05). An abnormal umbilical cord, maternal pregnancy-induced hypertension, gestational diabetes, infection during pregnancy and intrauterine distress are all perinatal risk factors for SGA. Effective interventions are needed in clinical assessment to prevent the occurrence of SGA.