This study aimed to explore the existing knowledge about midwives' views and experiences of providing care for women in the context of task shifting. We conducted a qualitative systematic review using meta-ethnography to describe the views and experiences of midwives on providing care in the context of task shifting. Comparative textual analysis of published qualitative studies involved translation of first-order key concepts and meanings from included studies to generate second-and third-order concepts. A grid was made to identify core findings and compare them reciprocally. Thirty-six qualitative studies met the inclusion criteria. The literature comprised of 32 first key concepts. Eight second-order constructs emerged, and three third-order interpretations were generated. The three overarching themes were: (1) midwives perceived themselves as providing culturally competent and high quality women-centered care; (2) they valued their profession but saw it as complex and challenging; (3) as health professionals, they reported a variety of organizational, cultural, and professional barriers to providing women-centered care. While performing a specific task in the task shifting context, midwives perceived their crucial roles and responsibilities, along with achieved value and reward. However, due to a range of existing barriers, the caring task posed great challenges in completely implementing women-centered care. It is essential for systems to identify and eliminate these barriers early, to consider midwives' emotional well-being, and to develop overall strategies to better support the midwifery workforce. Policy makers and administrators should establish a supportive environment to facilitate midwives to perform women-centered caring tasks in more effective and efficient ways.
Summary Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint tissue inflammation. Cyanidin‐3‐glucoside (C3G) is a major component in the flavonoid family and has shown anti‐inflammatory, anti‐oxidant and anti‐tumour activity. In this study, we investigated the effects of C3G on lipopolysaccharides (LPS)‐induced inflammation on human rheumatoid fibroblast‐like synoviocytes (FLS) and on collagen‐induced arthritis (CIA) mice model. We treated FLS with C3G followed by LPS induction, the expressions of tumour necrosis factor alpha (TNF‐α), interleukin 1 beta (IL‐1β) and IL‐6 and the activation of nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) and mitogen‐activated protein kinase (MAPK) signalling pathway were analyzed. CIA was induced in mice and the arthritic mice were treated with C3G for 3 weeks. The disease severity was compared between control and C3G treated mice. The serum levels of TNF‐α, IL‐1β and IL‐6 were analyzed by ELISA. C3G inhibited LPS‐induced TNF‐α, IL‐1β and IL‐6 expression in FLS. Moreover, C3G inhibited LPS‐induced p65 production and IκBa, p38, ERK and JNK phosphorylation. Administration of C3G significantly attenuated disease in mice with CIA and decreased the serum level of TNF‐α, IL‐1β and IL‐6. C3G inhibited LPS‐induced inflammation in human FLS by inhibiting activation of NF‐κB and MAPK signalling pathway. C3G exhibited therapeutic effects in mice with CIA.
Background and Objective: The establishment of maternal-fetal interface immune tolerance is essential for successful pregnancy.Studies have shown that spontaneous abortion, recurrent abortion, and fetal growth restriction are related to maternal-fetal interface immune dysfunction.Preeclampsia is an idiopathic condition related to pregnancy which manifests as hypertension, proteinuria, and other target organ damage after 20 weeks of gestation.Although the etiology of preeclampsia is still unknown, its pathogenesis is thought to be related to genetics, environment, and metabolism.In recent years, more and more studies have been conducted on the mechanism of immune tolerance at the maternal-fetal interface and the relationship between immune dysregulation and the pathogenesis of preeclampsia.This paper summarizes the latest studies on this topic in order to find new insights into the pathogenesis of preeclampsia and make a reflection on clinical diagnosis and treatment in different phenotype of preeclampsia. Methods:The research and latest progress published from 2000 to December 2021 on the relationship between maternal-fetal interface immune tolerance and preeclampsia were broadly retrieved and researched using PubMed and Web of Science databases. Key Content and Findings:The mechanism of natural killer cells (NK cells) and macrophages at the maternal-fetal interface in immune tolerance, as well as their cytotoxicity and cytokine secretion dysfunction, may be related to the pathogenesis of preeclampsia.The expression of nonclassical type I human leukocyte antigen (HLA) on extravillous trophoblast (EVT) cell were down-regulated in decidua of preeclampsia, which may induce increase EVT death caused by activating of cytotoxic NK cell.In addition, genetic polymorphism of nonclassical type I HLA on the EVT cell membrane may be related to the pathogenesis of preeclampsia, although this is likely to be a combination of 3 nonclassical type I HLA genotypes and requires sequencing to verify. Conclusions:We demonstrated how the maternal-fetal interface immune dysfunction contribute to the pathogenesis of preeclampsia, further study and clinical trial based on this theory of pathogenesis may reveal new immune treatment method of preeclampsia.
Neuromyelitis optica spectrum disorder (NMOSD) is a kind of immune mediated inflammatory demyelinating disease of the central nervous system manifesting with optic neuritis and acute transverse myelitis, which takes a relapsing or progression course. The exact etiology and pathogenesis are not clear. There are a lot of researches on immune pathogenesis; in addition, the pathogenesis also involves genetic, environmental, oxidative stress and other factors.
Key words:
Neuromyelitis optica spectrum disorder; Pathogenesis; Gene; Environment; Oxidative stress
This study aims to observe the changes of the umbilical venous-arterial index (VAI) and investigate its predictive power for fetal outcome during the second half of pregnancy.Fetuses with gestational age (GA) at 24-39 weeks were collected. According to the outcome score, neonates with outcome scores of 0, 1, or 2 were assigned to the control group, whereas those with scores of 3-12 were assigned to the compromised group. VAI was calculated as the ratio of normalized umbilical vein blood flow volume and umbilical artery pulsatility index. Regression analysis was performed to obtain the best-fitting curves between VAI and GA in the controls. Doppler parameters and perinatal outcomes were compared in both groups. Receiver operating characteristic analysis was used to assess the diagnostic performance of the VAI.A total of 833 (95%) fetuses had Doppler parameters and pregnancy outcomes documented. Compared with the controls, the VAI was significantly lower in the compromised group (83.2 vs. 184.8 ml/min/kg, p < 0.001). The sensitivity and specificity of VAI to predict compromised neonates were 95.15% (95% Cl, 89.14 to 97.91%) and 99.04% (95% CI: 98.03 to 99.53%), respectively at a cutoff value of 120 ml/min/kg.VAI presents better diagnostic performance than umbilical vein blood flow volume and umbilical artery pulsatility index. A cutoff value of 120 ml/min/kg might be used as the warning value for predicting the fetal outcome.
Numerous studies have confirmed the correlation of microRNAs (miRNAs) with human disease, yet few have explored the role of miR-135 in preeclampsia (PE). This study intends to discuss miR-135's function in inflammatory response in PE by modulating proprotein convertase subtilisin/kexin-6 (PCSK6) and NLR pyrin domain containing 3 (NLRP3).The venous blood and placental tissues were collected from PE pregnant women and 25 normal ones. The levels of miR-135, PCSK6 and NLRP3 in placenta tissues of patients were detected. Hypoxia/reoxygenation HTR-8/SVneo and HPT-8 models were established to mimic PE in vitro, and cell proliferation, colony formation, apoptosis rate, invasion, migration and inflammation were detected through gain-of and loss-of-function assays.MiR-135 was down-regulated, and PCSK6 and NLRP3 were up-regulated in PE patients. Up-regulating miR-135 or silencing PCSK6 strengthened colony formation ability, viability, invasion and migration ability, and weakened apoptosis and inflammation of H/R-treated HTR-8/SVneo and HPT-8 cells. Inhibition of NLRP3 negated the effects of silenced PCSK6 in H/R-treated HTR-8/SVneo and HPT-8 cells.Altogether, we demonstrate that up-regulated miR-135 or reduced PCSK6 attenuates inflammatory response in PE by restricting NLRP3 inflammasome, which provides novel therapy for PE treatment.
This study explores the epigenetic mechanism of MLL1 regulating trophoblast ferroptosis in preeclampsia (PE). A murine model of PE was established, and HTR-8/SVneo cells were induced by Erastin to establish an in vitro cell model. GSH, MDA, Fe2+, and ROS levels were measured to assess ferroptosis. MLL1, RBM15, TRIM72, ADMAM9, ASCL4, GPX4, and FTH1 expressions were detected by qRT-PCR or Western blot. ChIP analyzed H3K4me3 enrichment and MLL1 enrichment on RBM15 promoter. The binding of YTHDF2 or m6A to TRIM72 mRNA was determined by RIP. TRIM72 mRNA stability was detected after actinomycin D treatment. The binding of TRIM72 to ADAM9 and the ADAM9 ubiquitination level were detected by Co-IP. MLL1 was highly expressed in placental tissues of PE mice. Inhibition of MLL1 improved PE symptoms in mice, repressed ferroptosis in placental tissues, and inhibited Erastin-induced ferroptosis in vitro. MLL1 elevated RBM15 expression by increasing H3K4me3 on RBM15 promoter. RBM15 promoted the binding of TRIM72 to YTHDF2 by enhancing m6A modification on TRIM72 mRNA, thereby repressing TRIM72 expression. TRIM72 bound to ADAM9 and ubiquitinated it for degradation. In conclusion, MLL1 promotes placental trophoblast ferroptosis and aggravates PE symptoms via epigenetic regulation of RBM15/TRIM72/ADAM9 axis.
To investigate the status of the midwifery workforce and childbirth services in China and to identify the association between midwife staffing and childbirth outcomes.
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