中晚期早产儿不良神经发育结局的研究进展

近年来,随着医疗水平的不断提高,早产儿存活率得以大幅提升,但由于胎龄不足,早产儿相比足月儿不良神经发育结局发生的风险比例增高,神经发育问题逐渐成为早产儿早期发展面临的突出问题。中晚期早产儿约占早产儿总人数的80％,但目前极早产和超早产与神经发育障碍相关性的研究较多,中晚期早产与神经发育障碍相关性的研究较少。本文对中晚期早产儿神经发育结局进行综述,为临床早期评估中晚期早产儿神经发育状态提供依据。通过胎盘-脑轴生物标志物预测中晚期早产儿神经发育结局,对开展早期干预具有重要意义。     

妊娠相关焦虑对学龄前儿童执行功能的影响及性别差异

  目的  探讨母体妊娠相关焦虑对子代学龄前执行功能(EFs)的影响及性别差异,以期针对性优化子代生命早期发育环境。  方法  选取中国安徽出生队列2008年10月—2010年10月在安徽省马鞍山市妇幼保健院孕早期建卡的孕妇,收集孕妇一般情况和妊娠相关焦虑情况。对队列内的3 556名3~5岁儿童进行随访,收集儿童相关特征,采用《学龄前儿童执行功能评定量表》(父母版)评价其执行功能。  结果  与对照组相比,仅孕早期存在妊娠相关焦虑与学龄前男童工作记忆、计划/组织功能和总执行功能(GEC)异常风险有关[OR 值(95%CI)分别为 1.40(1.06~1.85),1.64(1.06~2.54),1.89(1.27~2.82)];孕早、晚期同时存在妊娠相关焦虑与学龄前男童抑制、工作记忆、计划/组织功能和 GEC 异常风险有关[ OR值(95%CI)分别为 2.60(1.45~4.67),2.45(1.69~3.57),2.23(1.28~3.88),3.27(2.03~5.28)]。 仅孕早期存在妊娠相关焦虑与学龄前女童抑制和工作记忆异常有关[OR 值(95%CI)分别为 1.79(1.13~2.83),1.45(1.07~1.98)];仅孕晚期存在妊娠相关焦虑与学龄前女童抑制功能异常有关[OR 值(95%CI)= 2.26(1.17~4.38)];孕早、晚期同时存在妊娠相关焦虑与学龄前女童抑制和工作记忆功能异常风险有关[OR 值(95%CI)分别为 2.45(1.40~4.28),2.02(1.35~3.01)]。  结论  妊娠相关焦虑显著影响子代学龄前儿童执行功能,并存在剂量反应关系。妊娠相关焦虑在男童中主要影响工作记忆、计划/组织功能和总执行功能,在女童主要影响其工作记忆和抑制功能。     

Maternal obesity induced by a ‘cafeteria’ diet in the rat does not increase inflammation in maternal,placental or fetal tissues in late gestation

IntroductionObesity during pregnancy can cause serious complications for maternal and infant health. While this has often been attributed to increased inflammation during obese pregnancy, human and animal studies exhibit variable results with respect to the inflammatory status of the mother, placenta and fetus. Cafeteria (CAF) feeding induces more inflammation than standard high-fat feeding in non-pregnant animal models. This study investigated whether maternal obesity induced by a CAF diet increases maternal, fetal or placental inflammation.MethodsMaternal obesity was established in rats by 8 weeks of pre-pregnancy CAF feeding. Maternal plasma inflammatory markers (IL-1β, IL-6, IL-10, IL-12p40, MCP1, GRO/KC, MIP-2 and TNFα) and expression of inflammatory genes (Tnfα, Il-6, Il-1β, Tlr2, Tlr4, Cox2 and Emr1) in maternal, placental and fetal tissues were measured at day 21 of gestation.ResultsDespite CAF animals having 63% more central body fat than controls at day 21 of gestation, plasma inflammatory markers were not increased; indeed, levels of IL-6, IL-12p40 and MIP2 were reduced slightly. Similarly, inflammatory gene expression remained largely unaffected by CAF feeding, except for slight reductions to Tlr4 and Emr1 expression in CAF maternal adipose tissue, and reduced Tlr4 expression in male labyrinth zone (LZ). The junctional zone (JZ) displayed increased Il-6 expression in CAF animals when fetal sexes were combined, but no inflammatory genes were affected by the CAF diet in fetal liver.ConclusionsMaternal obesity induced by a CAF diet before and during pregnancy does not increase the inflammatory status of the mother, placenta or fetus in late gestation.     

Association of maternal arsenic exposure with birth size: A systematic review and meta-analysis

ObjectivesChronic exposure to arsenic during pregnancy or early life continues to be a major global health problem worldwide, affecting hundreds of millions of people. However, its effects on birth size are uncertain. The aim of this study is to summarized the association between maternal arsenic exposure and birth size.MethodsA comprehensive literature search was conducted on the maternal arsenic exposure and birth size (birth weight, birth length, head circumference and chest circumference) through databases (PubMed, Qvid Medline, Web of Science, Cochrane and EMBASE), the last search was in March 2019. Heterogeneity was testes by using the Q statistic and stratifying for epidemiological factors. The possibility of publication bias was assessed through Begg’s test.ResultsA total of 12 studies provided sufficient data were included. Meta-analysis revealed that maternal arsenic exposure was associated with the decrease of birth weight (β = −25.0 g; 95% CI: −41.0, −9.0) and head circumference (β = −0.12 cm; 95% CI: −0.24, −0.01) in random-effect model, birth length (β = −0.12 cm; 95% CI: −0.17, −0.07) in fixed-effect model, no significant reduction was suggested in chest circumference (β = −0.74 cm; 95% CI: −1.78, 0.3). In addition, we found that the birth weight decreased stronger in women living in the Americas, or appling the exposure marker of urine.ConclusionsMaternal arsenic exposure is associated with the decrease of the birth weight, length and head circumference. Millions of people are still exposured to high-level arsenic, therefore, high quality epidemiologic studies that involve large samples are necessary to determine the precise relationships between maternal arsenic exposure with birth size. And that effective mitigation measures are also need to prevent arsenic exposure in women of reproductive age.     

Chicoric acid alleviates lipopolysaccharide-induced acute lung injury in mice through anti-inflammatory and anti-oxidant activities

Acute lung injury (ALI) is a severe clinical disease with high mortality rates. Chicoric acid (CA), an active component extracted from traditional Chinese medicine, was suggested to have anti-inflammatory and anti-oxidant activities. Inflammation and oxidative damage are implicated in the pathogenesis of ALI. In this study, we explored the protection effect of CA on LPS-induced ALI, and further discussed the possible molecular mechanisms. The results showed that CA could significantly improve the histological changes of LPS-induced acute lung injury. In addition, CA not only decreased LPS-stimulated protein leakage and lung wet/dry ratio but also reduced inflammatory cell infiltration, myeloperoxidase (MPO) activity and the generation of pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF). Meanwhile, CA lessened the reactive oxygen species (ROS) generation, and malondialdehyde (MDA) formation, and decreased glutathione (GSH) and superoxide dismutase (SOD) depletion, which were caused by LPS challenge. Furthermore, CA dramatically inhibited LPS-stimulated MAPK and NLRP3 activation and increased the expression of NAD (P) H: quinone oxidoreductase (NQO1), and dismutase (SOD), glutamate-cysteine ligase catalytic/modifier (GCLC/GCLM) subunit and heme oxygenase-1 (HO-1), as well as its upstream genes nuclear factor-erythroid 2-related factor 2 (Nrf2), which might be central to the protective effects of CA. In conclusion, these data indicated that the protective effects and mechanisms of CA on LPS-induced ALI and provided new insights for its application.