Identification of syncytiotrophoblast-derived cf-RNA OPA1 to predict the occurrence of preeclampsia.

Background: Pre-eclampsia (PE) poses a significant threat to mothers and infants worldwide. Studies indicate that taking low-dose aspirin before the 16th week of pregnancy may prevent approximately 70 % of PE cases, highlighting the importance of predicting PE. Cell-free RNA (cf-RNA) exhibits significant changes in the maternal peripheral blood during early pregnancy, making cf-RNA analysis a promising and less invasive method for predicting PE.

Targeting CD301 macrophages inhibits endometrial fibrosis and improves pregnancy outcome.

Macrophages are a key and heterogeneous cell population involved in endometrial repair and regeneration during the menstrual cycle, but their role in the development of intrauterine adhesion (IUA) and sequential endometrial fibrosis remains unclear. Here, we reported that CD301 macrophages were significantly increased and showed their most active interaction with profibrotic cells in the endometria of IUA patients compared with the normal endometria by single-cell RNA sequencing, bulk RNA sequencing, and experimental verification. Increasing CD301 macrophages promoted the differentiation of endometrial stromal cells into myofibroblasts and resulted in extracellular matrix accumulation, which destroyed the physiological architecture of endometrial tissue, drove endometrial fibrosis, and ultimately led to female infertility or adverse pregnancy outcomes.

Ferroptosis contributes to endometrial fibrosis in intrauterine adhesions.

Intrauterine adhesions (IUA), characterized by endometrial fibrosis, is a challenging clinical issue in reproductive medicine. We previously demonstrated that epithelial-mesenchymal transition (EMT) and fibrosis of endometrial stromal cells (HESCs) played a vital role in the development of IUA, but the precise pathogenesis remains elucidated. Ferroptosis has now been recognized as a unique form of oxidative cell death, but whether it is involved in endometrial fibrosis remains unknown.

Elevated Placental microRNA-155 Is a Biomarker of a Preeclamptic Subtype.

Background: Preeclampsia is a complicated syndrome with marked heterogeneity. The biomarker-based classification for this syndrome is more constructive to the targeted prevention and treatment of preeclampsia. It has been reported that preeclamptic patients had elevated microRNA-155 (miR-155) in placentas or circulation.

The UCMSC-bFGF/Scaffold System Accelerates the Healing of the Uterine Full-Thickness Injury.

Severe uterine injury is a major cause of endometrial scar formation and female infertility. At present, the methods for accelerating injured uterine healing are still lacking. Genetic engineering modification of mesenchymal stem cells (MSCs) has been shown great promise in preclinical studies on regeneration.

Down-regulation of PBK inhibits proliferation of human endometrial stromal cells in thin endometrium.

Background: Thin endometrium (TE) is a challenging clinical issue in the reproductive medicine characterized by inadequate endometrial thickness, poor response to estrogen and no effective treatments currently. At present, the precise pathogenesis of thin endometria remains to be elucidated. We aimed to explore the related molecular mechanism of TE by comparing the transcriptome profiles of late-proliferative phase endometria between TE and matched controls.

The role of junctional adhesion molecule-C in trophoblast differentiation and function during normal pregnancy and preeclampsia.

Introduction: Junctional adhesion molecule-C (JAM-C) is an important regulator of many physiological processes, ranging from maintenance of tight junction integrity of epithelia to regulation of cell migration, homing and proliferation. Preeclampsia (PE) is a trophoblast-related syndrome with abnormal placentation and insufficient trophoblast invasion. However, the role of JAM-C in normal pregnancy and PE pathogenesis is unknown.

Placenta-derived IL-32β activates neutrophils to promote preeclampsia development.

Immune activation at the maternal-fetal interface is a main pathogenic factor of preeclampsia (PE). Neutrophils (PMNs) are activated in PE patients, but the mechanism and consequences of PMN activation need to be further explored. Here, we demonstrated that interleukin-32 (IL-32) expression was significantly upregulated in syncytiotrophoblasts (STBs) and that IL-32β was the major isoform with increased expression in the placenta of severe PE (sPE) patients.

Downregulation of CD151 induces oxidative stress and apoptosis in trophoblast cells via inhibiting ERK/Nrf2 signaling pathway in preeclampsia.

Preeclampsia (PE) is a pregnancy-related syndrome characterized by new-onset hypertension and proteinuria after gestational 20 weeks. Oxidative stress, resulting from the imbalance between the production of oxidants and antioxidants in placentas, is recognized as a key pathology of PE. To date, the molecules that regulate antioxidants production remain unclear.

HMGA2-induced epithelial-mesenchymal transition is reversed by let-7d in intrauterine adhesions.

Intrauterine adhesions (IUAs), the leading cause of uterine infertility, are characterized by endometrial fibrosis. The management of IUA is challenging because the pathogenesis of the disease largely unknown. In this study, we demonstrate that the mRNA and protein levels of high mobility group AT-hook 2 (HMGA2) were increased by nearly 3-fold (P < 0.

Experimental and numerical simulation study of the thermal hazards of four azo compounds.

Azo compounds (azos) possess diverse exothermic properties that enable their application in numerous industrial processes, but these properties also engender a corresponding diversity of thermal hazard profiles. This study employed an innovative approach to determine the specific thermal reactions and decomposition hazard profiles of azos. Four typical azos (AIBN, AMBN, ABVN, and AIBME) were assessed using three thermal calorimetry techniques, and results were subsequently analyzed using a nonlinear optimization model.