Objective:To investigate the difference of physical growth and neurodevelopmen between small for gestational age (SGA) preterm infants and appropriate for gestational age (AGA) preterm infants, and to promote follow-up management and early intervention in SGA preterm infants after discharge.Methods:Preterm infants, who were born at Guangzhou Women and Children′s Medical Center and received regular follow-up management after discharge in high-risk infants outpatient, were enrolled in this study from January 2015 to December 2018.According to gestational age and birth weight, the participants were divided into SGA group and AGA group.Height, weight, head circumference and Gesell outcomes of infants were observed at 6 months and 12 months of corrected age.Results:A total of 144 preterm infants were included in the study, including 63 cases in SGA group and 81 cases in AGA group. Height, weight and head circumference of the SGA group at 6 months and 12 months of corrected age were all lower than the AGA group ( P<0.05). In addition, adaptability, great movement, language, personal social interaction and development quotient in the SGA group were all lower than those in the AGA group at 6 months of corrected age ( P<0.05), while fine movement was not statistically significant ( P>0.05). At 12 months of corrected age, there were no statistically significant differences in adaptability, macro motor, fine motor, language, social interaction and development quotient between the two groups ( P>0.05). Conclusion:The physical growth of SGA preterm infants falls for behind that of AGA preterm infants.It is still unable for SGA preterm infants to achieve catch-up growth at 12 months of corrected age, their catch-up period may take longer, but the neurodevelopment can reach the same level of preterm AGA.The clinician should pay more attention to the follow-up management and early intervention after discharge.

Objective:To study the neurodevelopmental status of very/extremely low birth weight preterm infants with gestational age less than 32 weeks at the corrected age of 1 year.Methods:Preterm infants admitted to the Neonatology Department after birth at Guangzhou Women and Children′s Medical Center from January 2015 to December 2018 and followed up regularly to the high-risk infants clinic for at least 1 year after discharge were selected as the research subjects.According to the birth weight(BW), preterm infants were divided into very/extremely low birth weight group(BW<1 500 g), low birth weight group(1 500 g

BACKGROUND/OBJECTIVES: Previous research has shown maternal betaine supplementation alleviates fetal-derived hepatic steatosis. Therefore, this study examined the anti-inflammatory effect of maternal betaine intake in offspring mice and its mechanism.MATERIALS/METHODS: Female C57BL/6J mice and their offspring were randomly divided into 3 groups according to the treatment received during gestation and lactation: control diet (CD), fatty liver disease (FLD), and fatty liver disease + 1% betaine (FLD-BET). The FLD group was given a high-fat diet and streptozotocin (HFD + STZ), and the FLD-BET group was treated with HFD + STZ + 1% betaine. After weaning, the offspring mice were given a normal diet for 5 weeks and then dissected to measure the relevant indexes. RESULTS: Compared to the CD group, the offspring mice in the FLD group revealed obvious hepatic steatosis and increased serum levels of alanine aminotransferase, interleukin (IL)-6, and tumor necrosis factor (TNF)-α; maternal betaine supplementation reversed these changes. The hepatic mRNA expression levels of IL-6, IL-18, and Caspase-1 were significantly higher in the FLD group than in the CD group. Maternal betaine supplementation reduced the expression of IL-1β, IL-6, IL-18, and apoptosis-associated speck-like protein containing C-terminal caspase recruitment domain (ASC). Maternal betaine supplementation also reversed the increasing protein expressions of nitric oxide dioxygenase-like receptor family pyrin domain containing 3 (NLRP3), ASC, Caspase-1, IL-1β, and IL-18 in offspring mice exposed to HFD + STZ. Maternal betaine supplementation decreased the homocysteine (Hcy) and s-adenosine homocysteine (SAH) levels significantly in the livers. Furthermore, the hepatic Hcy concentrations showed significant inverse relationships with the mRNA expression of TNF-α, NLRP3, ASC, and IL-18. The hepatic SAH concentration was inversely associated with the IL-1β mRNA expression. CONCLUSIONS The lipotropic and anti-inflammatory effect of maternal betaine supplementation may be associated with the inhibition of NLRP3 inflammasome in the livers of the offspring mice.