It has been reported that folic acid supplementation before and/or during pregnancy could reduce the risk of congenital heart defects (CHDs). However, the results from limited epidemiologic studies have been inconclusive. We investigated the associations between maternal folic acid supplementation, dietary folate intake, and the risk of CHDs. A birth cohort study was conducted in 2010–2012 at the Gansu Provincial Maternity & Child Care Hospital in Lanzhou, China. After exclusion of stillbirths and multiple births, a total of 94 births were identified with congenital heart defects, and 9,993 births without any birth defects. Unconditional logistic regression was used to estimate the associations. Compared to non-users, folic acid supplement users before pregnancy had a reduced risk of overall CHDs (OR: 0.42, 95% CI: 0.21–0.86, P_trend = 0.025) after adjusted for potential confounders. A protective effect was observed for certain subtypes of CHDs (OR: 0.37, 95% CI: 0.16–0.85 for malformation of great arteries; 0.26, 0.10–0.68 for malformation of cardiac septa; 0.34, 0.13–0.93 for Atrial septal defect). A similar protective effect was also seen for multiple CHDs (OR: 0.49, 95% CI: 0.26–0.93, P_trend = 0.004). Compared with the middle quartiles of dietary folate intake, lower dietary folate intake (<149.88 μg/day) during pregnancy were associated with increased risk of overall CHDs (OR: 1.63, 95% CI: 1.01–2.62) and patent ductus arteriosus (OR: 1.85, 95% CI: 1.03–3.32). Women who were non-user folic acid supplement and lower dietary folate intake have almost 2-fold increased CHDs risk in their offspring. Our study suggested that folic acid supplementation before pregnancy was associated with a reduced risk of CHDs, lower dietary folate intake during pregnancy was associated with increased risk. The observed associations varied by CHD subtypes. A synergistic effect of dietary folate intake and folic acid supplementation was also observed.

This study aimed to identify the most useful ultrasound (US) features associated with definite neonatal necrotizing enterocolitis (NEC) and their prognostic values, particularly the calculated markers combined with important features.A total of 213 suspected ...

Background: To evaluate the independent and collective effects of maternal iron supplementation and dietary iron intake upon the risk of moderate preterm birth and its subtypes. Methods: In this birth cohort study, 1019 pregnant women with moderate preterm birth and 9160 women with term birth were recruited at Gansu Provincial Maternity and Child Care Hospital from 2010-2012 in China. Unconditional logistic regression models were utilized to evaluate the association between maternal iron supplementation, dietary iron intake, and the risk of moderate preterm birth and its subtypes. Results: Compared with non-users, iron supplement users exerted a protective effect upon the overall (OR=0.54, 95%CI=0.40-0.72) and spontaneous moderate preterm birth (OR=0.39, 95%CI=0.33-0.83). Compared with the 25th quartiles of dietary iron intake, either before or during pregnancy, it exerted a significantly protective effect upon those who had the highest quartiles of dietary iron intake (OR=0.87, 95%CI=0.82-0.95 for the highest quartiles of dietary iron intake before pregnancy OR=0.85, 95%CI=0.79-0.91). Positive association was observed between the additive scale and multiplicative scale for preterm birth, spontaneous preterm rather than medically indicated preterm. Conclusion: Iron supplements (60 mg/day) and high-iron intake (>25.86 mg/day before pregnancy, >30.46 mg/day during pregnancy) reduced the risk of moderate preterm birth. Positive correlation is found between the additive scale and multiplicative scale for preterm birth, spontaneous preterm birth.

Pregnancy complications are associated with abnormal cytotrophoblast differentiation and invasion. Hydrogen peroxide (H2O2) is an important mediator of oxidative ischemia/reperfusion stress in the placenta. Lycium barbarum polysaccharides (LBP) have been demonstrated to counteract oxidative free radicals. The effects of LBP in trophoblast HTR8/SVneo cells injured with H2O2 were examined. A cell counting kit‑8 assay was performed to detect the effect of LBP at different concentrations on the proliferative ability of H2O2 injured trophoblast cells. Flow cytometry was used to determine the levels of reactive oxygen species (ROS), mitochondria membrane potential (MMP) disruption and apoptosis. Superoxide dismutase (SOD) activity and lactate dehydrogenase (LDH) leakage into the supernatant was detected by ultraviolet spectrophotometry. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were performed to detect the expression of apoptosis‑associated factors, including survivin, hypoxia inducible factor 1‑α (HIF1‑α), Bcl‑2 apoptosis regulator (Bcl‑2), Bcl‑2 associated X apoptosis regulator (Bax). The results revealed that LBP protected the proliferative ability of trophoblast cells injured with H2O2 in a dose‑dependent manner. LBP inhibited the oxidative stress induced by H2O2, by reducing ROS and LDH levels and increasing SOD activity. Additionally, LBP decreased MMP disruption and cell apoptosis induced by H2O2, by increasing the mRNA and protein expression of survivin, HIF1‑α and Bcl‑2 and decreasing Bax expression. Therefore, it was concluded that LBP protected human trophoblast cells from H2O2‑induced oxidative stress and cell apoptosis via regulation of apoptosis‑associated factor expression. It will provide a novel strategy for the treatment of pregnancy complications.

We aimed to identify whether IL-1β (rs1143627, rs1143634 and rs16944), IL-6 (rs1800796), IL-10(rs1800872 and rs1800896), and vascular endothelial growth factor (VEGF) (rs1570360) gene polymorphisms were risk factors for recurrent pregnancy loss (RPL) in a population of women in northwestern China. A total of 150 women with a history of two or more unexplained and consecutive spontaneous abortions before their 24th gestational week and 150 age-matched women with at least two normal pregnancies and no history of pregnancy loss were included in the present study as cases and controls, respectively. We extracted genomic DNA from peripheral blood, and executed genotyping with the SNaPshot technique. Logistic regression analysis was conducted to determine the odds ratios (ORs) of the associations between the polymorphisms and RPL. Of the seven polymorphisms we studied, only IL-6 rs1800796 showed a statistically significant association with RPL, as we noted an elevated risk of RPL with the G allele (OR = 1.57; 95% CI, 1.10–2.24; p = .01). The risk of RPL in women with the GG + CG genotype (OR = 1.96; 95% CI, 1.19–3.21; p = .01) was also higher than that in women with the CC genotype. The present study thus indicated that the IL-6 gene rs1800796 polymorphism may serve as an important risk factor for RPL in this group of women from northwestern China.

Background: The association between maternal iron/zinc intake and the risk of low birth weight (LBW) in infants is still unclear. This study aimed to investigate the effects of iron and zinc daily intake preconception and during pregnancy on the risk of delivering LBW babies and to assess whether there is an interaction between iron and zinc intake on the risk of LBW. Methods: A nested case–control study was performed, including 565 cases and 7,510 controls in Lanzhou City, China. Eligible participants were interviewed about their diets and characteristics during pregnancy. Unconditional logistic regression was used to determine the association between dietary iron/zinc intake and the risk of LBW and its clinical subtypes. Multivariate-adjusted restricted cubic spline (RCS) models were applied to explore the nonlinear association between dietary iron/zinc intake levels and the risk of LBW. Results: Lower intake of iron/zinc preconception and during pregnancy was associated with a higher risk of LBW and some subtypes, and there was a nonlinear trend between iron/zinc intake and the occurrence risk of LBW (P_Nonlinear < 0.05). Moreover, the synergistic effects of low iron and low zinc intake on the risk of LBW were found. Conclusion: Efforts to promote iron and zinc intake preconception and during pregnancy need to be strengthened to reduce the local incidence of LBW.