Background: Coronavirus disease 2019 (COVID-19) is a public health emergency of international concern and poses a threat to the mental health of pregnant women. Aim: The purpose of this study was to investigate the relationship between social support and anxiety, and the mediating effect of risk perception during the COVID-19 epidemic in the third trimester pregnant women in Qingdao, China. Methods: From 16 to 21 February 2020, an online survey was conducted, which collected the information on demographic data, anxiety, social support and risk perception to COVID-19 of women with established medical records in the ambulatory of the Department of Obstetrics at the Affiliated Hospital of Qingdao University. Anxiety was assessed by the Self-Rating Anxiety Scale (SAS), social support was assessed by the Social Support Rating Scale (SSRS) and risk perception was assessed by a self-designed questionnaire. Results: This study had 308 participants with an average of 31.02 ± 3.91 years. During the period of prevention and control of the epidemic, most pregnant women adopted protective measures, such as wearing masks (97.4%), washing hands frequently (88.3%) and staying at home (76.3%). The average SAS, SSRS and risk perception scores of the participants were 42.45 ± 6.98, 44.60 ± 7.00 and 21.60 ± 5.74, respectively. The total effect of maternal social support on anxiety was −2.63 (95% confidence interval (CI): −4.40 ~ −1.44, p < .001), the direct effect was −1.44 (95% CI: −2.74 ~ −0.35, p < .05) and the indirect effect was −1.19 (95% CI: −2.49 ~ −0.51, p < .001). Conclusion: The third trimester pregnant women had a high level of social support, a medium level of risk perception to COVID-19 and were susceptible to anxiety. Risk perception played a mediating role between social support and anxiety.

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Objective: To investigate the expression of advanced glycation end products (AGEs) and the receptor for AGE (RAGEs) in maternal blood, umbilical blood and placental tissues in women with severe preeclampsia (sPE) as well as any association with inflammatory processes. Methods: The expressions of AGEs, RAGE, tumor necrosis factor-alpha (TNF)-α and vascular cell adhesion molecule-1 (VCAM)-1 in placental tissues were measured using immunohistochemistry. The levels of AGEs, RAGE, TNF-α and VCAM-1 in maternal blood, umbilical blood and placental extracts were assessed using enzyme-linked immunosorbent assays. Placental RAGE, TNF-α and VCAM-1 mRNA expression levels were determined by PCR. Placental AGEs, RAGE, TNF-α and VCAM-1 protein levels were determined by western blotting. Results: The levels of AGEs, TNF-α and VCAM-1 in the maternal tissues and umbilical blood were significantly higher in the sPE group than in the normal pregnancy (NP) controls (p < 0.05). The serum level of sRAGE in the umbilical blood was lower in the sPE group than in the NP controls (p < 0.05), while sRAGE was higher in the maternal blood of sPE than in the NP (p < 0.05). The maternal serum levels of AGEs were positively correlated with that of TNF-α and VCAM-1 in the maternal blood. There were no correlations between the levels of RAGE, TNF-α or VCAM-1 in maternal blood or umbilical serum. There were no correlations between the levels of sRAGE and TNF-α or VCAM-1 in maternal blood or umbilical serum. The levels of AGEs were positively correlated with those of TNF-α and VCAM-1 in placental lysates. Conclusion: AGEs and RAGE appear to act as important mediators in regulating the inflammatory pathways of preeclampsia.

Placenta previa is a common complication in the third trimester of pregnancy and one of the main causes of postpartum haemorrhage and perinatal death. Pernicious placenta previa (PPP) means placenta previa occurs and placenta previa is attached to the scar from the previous caesarean section during the second pregnancy for a pregnant woman with a history of caesarean section (Yu, Hu et al., 2016). PPP leads to insufficient blood supply to the placenta, inducing placental adhesion or implantation, making it difficult for the placenta to be separated from the mother during delivery. It increases the risk of postpartum bleeding and endangering the life of the mother and child (Chitkara

Background Trophoblast dysfunction during pregnancy is fundamentally involved in preeclampsia. Several studies have revealed that human chorionic villous mesenchymal stem cells (CV-MSCs) could regulate trophoblasts function. Results To understand how human chorionic villous mesenchymal stem cells (CV-MSCs) regulate trophoblast function, we treated trophoblasts with CV-MSC supernatant under hypoxic conditions. Treatment markedly enhanced proliferation and invasion and augmented autophagy. Transcriptome and pathway analyses of trophoblasts before and after treatment revealed JAK2/STAT3 signalling as an upstream regulator. In addition, STAT3 mRNA and protein levels increased during CV-MSC treatment. Consistent with these findings, JAK2/STAT3 signalling inhibition reduced the autophagy, survival and invasion of trophoblasts, even in the presence of CV-MSCs, and blocking autophagy did not affect STAT3 activation in trophoblasts treated with CV-MSCs. Importantly, STAT3 overexpression increased autophagy levels in trophoblasts; thus, it positively regulated autophagy in hypoxic trophoblasts. Human placental explants also proved our findings by showing that STAT3 was activated and that LC3B-II levels were increased by CV-MSC treatment. Conclusion In summary, our data suggest that CV-MSC-dependent JAK2/STAT3 signalling activation is a prerequisite for autophagy upregulation in trophoblasts. Graphic abstract