Mediating role of perceived social support in the relationship between perceived stress and job burnout among midwives in the post-COVID-19 era.

AIM: The aim of this study was to explore the mediating role of perceived social support in the association between perceived stress and job burnout in midwives. DESIGN: A descriptive, cross-sectional online survey. METHODS: Using the stratified cluster sampling method, 329 midwives in 20 hospitals in China were selected as the participants. They completed self-report assessment measures of job burnout, perceived stress and perceived social support. RESULTS: 63.5% of the participants had job burnout. Perceived stress was negatively associated with social support (r = -.350, p < .01), while it was positively associated with job burnout (r = -.382, p < .01). Social support was negatively correlated with job burnout (r = -.569, p < .01). The total effect of perceived stress on job burnout was 0.474 (95% CI: 0.367 ~ 0.596, p < .01), the direct effect was 0.242 (95% CI: 0.142 ~ 0.355, p < .01), and the indirect effect was 0.232 (95% CI: 0.160 ~ 0.316, p < .01). Social support programmes for midwives should be implemented to control the impact of perceived stress on job burnout.

Chorionic villus-derived mesenchymal stem cell-mediated autophagy promotes the proliferation and invasiveness of trophoblasts under hypoxia by activating the JAK2/STAT3 signalling pathway.

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.

Nursing-sensitive quality indicators for pernicious placenta previa in obstetrics: A Delphi study based across Chinese institutions.

AIM: To identify a set of scientific, systematic and clinically applicable nursing-sensitive quality indicators for pernicious placenta previa (PPP). DESIGN: A modified Delphi-Consensus Technique. METHODS: According to literature retrieval published between 2009-2019, 38 nursing-sensitive quality indicators were chosen and a questionnaire was designed. An online survey was conducted in 20 hospitals in China, and data of experts' opinions were collected and analysed by improved Delphi method. RESULTS: 38 nursing-sensitive quality indicators were identified. The response rates in the two rounds of expert consultation were 97.4% and 100%, and the authoritative coefficients were 0.89 and 0.92. The coefficients of variation ranged from 0.04-0.28. The nursing-sensitive quality indicators were successfully constructed based on the modified Delphi technique.

Association between social support and anxiety among pregnant women in the third trimester during the coronavirus disease 2019 (COVID-19) epidemic in Qingdao, China: The mediating effect of risk perception.

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.

Downregulation of receptor tyrosine kinase-like orphan receptor 1 in preeclampsia placenta inhibits human trophoblast cell proliferation, migration, and invasion by PI3K/AKT/mTOR pathway accommodation.

INTRODUCTION: Invasive deficiency of the trophoblast and poor remodeling of the uterine spiral arteries were probably the primary pathogenesis causes of preeclampsia (PE). The expression of receptor tyrosine kinase-like orphan receptor 1 (ROR1) during embryogenesis had been previously confirmed and was closely related to the function of tumor cells, which was similar to the characteristics of trophoblasts. In this work, we investigated the expression profile of ROR1 in preeclampsia placentas and the functional role of ROR1 in trophoblast cells, as well as the associated molecular mechanisms. METHODS: The localization expression of ROR1 in the placenta was detected by immunohistochemistry in 20 cases of normal term pregnancy, preterm delivery, late-onset severe PE, and early-onset severe PE, respectively. The expression levels were determined by fluorescence quantitative PCR and Western blot. The influence of ROR1 on trophoblast proliferation, migration, invasion, and potential regulatory pathways was evaluated in HTR-8/SVneo cell lines by transient transfection methods. RESULTS: The levels of ROR1 in the placental tissues in PE were significantly lower than those in normal term pregnancy and preterm delivery. Moreover, the expression levels of ROR1 in early-onset severe PE were significantly lower than those in its late counterparts. ROR1 overexpression increased cell proliferation, migration, and invasion of HTR-8/SVneo cells, whereas its silencing had the opposite effect. Meanwhile, the phosphorylation levels of critical kinases in the PI3K/AKT/mTOR pathways were increased by ROR1 overexpression, whereas they were decreased by the silencing of ROR1. CONCLUSION: ROR1 might be involved in the development of PE through regulating trophoblast viability, migration, and invasion by PI3K/AKT/mTOR signaling pathway.

Accumulation of Advanced Glycation End Products Involved in Inflammation and Contributing to Severe Preeclampsia, in Maternal Blood, Umbilical Blood and Placental Tissues.

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.