Tao Meng

The occurrence of ovarian vein thrombosis(OVT) prior to delivery and during cesarean section is exceedingly rare. Presently, the literature contains minima

Preeclampsia (PE) is a severe pregnancy‐specific disorder that poses significant risks to maternal and perinatal health. The pathophysiological mechanisms underlying PE are complex and not yet fully elucidated. This study focuses on the role of ferroptosis in PE and identifies a significant downregulation of the transcription factor hepatic leukemia factor (HLF) in PE placental tissues. Further investigations reveal that HLF transcriptionally activates solute carrier family 7 member 11 (SLC7A11) to inhibit trophoblast ferroptosis, thereby maintaining their proliferation, migration, and invasion functions. Additionally, Wilms' tumor 1–associating protein (WTAP), a key factor in N6‐methyladenosine (m6A) methylation, regulates HLF mRNA stability in an m6A‐dependent manner, influencing the expression of its downstream target SLC7A11. This study, for the first time, systematically clarifies the critical role of the WTAP/HLF/SLC7A11 signaling axis in the pathogenesis of PE from the perspective of ferroptosis. The findings offer a novel theoretical basis for further exploration of the molecular mechanisms of PE and potential intervention targets for precision therapy.

BACKGROUND Pulmonary arterial hypertension (PAH) in pregnancy is one of the major obstetric complications and is considered a contraindication to pregnancy as it is classified as a class IV risk in the revised risk classification of pregnancy by the World Health Organisation. Pregnancy, with its adaptive and expectant mechanical and hormonal changes, negatively affects the cardiopulmonary circulation in pregnant women. Do patients with repaired simple congenital heart disease (CHD) develop other pulmonary and cardiac complications during pregnancy? Can pregnant women with sudden pulmonary hypertension be treated and managed in time? In this paper, we present a case of a 39-year-old woman who underwent cesarean section at 33 wk' gestation and developed PAH secondary to repaired simple CHD. Our research began by a PubMed search for "pulmonary hypertension" and "pregnancy" and "CHD" case reports. Three cases were selected to review PAH in pregnancy after correction of CHD defects. These studies were reviewed, coupled with our own clinical experience. CASE SUMMARY Herein, a case involving a woman who underwent atrial septal defect repair at the age of 34, became pregnant five years later, and had a sudden onset of PAH and right heart failure secondary to symptoms of acute peripheral edema in the third trimester of her pregnancy. As a result, the patient underwent a cesarean section and gave birth to healthy twins. Within three days after cesarean delivery, her cardiac function deteriorated as the pulmonary artery pressure increased. Effective postpartum management, including diuresis, significant oxygen uptake, vasodilators, capacity and anticoagulants management, led to improvements in cardiac function and oxygenation. The patient was discharged from hospital with a stable recovery and transferred to local hospitals for further PAH treatment. CONCLUSION This case served as a reminder to obstetricians of the importance of pregnancy after repair of CHD. It is crucial for patients with CHD to receive early correction. It suggests doctors should not ignore edema of twin pregnancy. Also, it provides a reference for the further standardization of antenatal, intrapartum and postpartum management for patients with CHD worldwide.

It has been reported that LXR agonist can inhibit Aβ generation and alleviate Aβ-induced various adverse reactions in vivo and in vitro experiments, but the mechanisms have not been clarified. The ...

Alzheimer’s disease (AD) is a progressive neurodegenerative disease, characterized by Amyloid-β accumulation-induced neuronal injury. Emerging evidence shows that circular RNA (circRNA) is involved in AD development. The aim of this study was to illustrate the role of circ-HUWE1 in Amyloid-β accumulation-induced neuronal injury. Quantitative real-time PCR (qPCR) or western blot was conducted for the expression analysis of circ-HUWE1, miR-433-3p, and fibroblast growth factor 7 (FGF7). In functional assays, cell viability was determined by CCK-8 assay, and cell apoptosis was examined by flow cytometry assay, the protein levels of apoptosis-related markers, and caspase1 or caspase3 activity. The release of pro-inflammatory factors was monitored by ELISA. The predicted binding relationship between miR-433-3p and circ-HUWE1 or FGF7 was validated by dual-luciferase reporter assay. We discovered that circ-HUWE1 absence alleviated Amyloid-β-induced cell viability degradation, cell apoptosis, and inflammatory responses in SK-N-SH cells. MiR-433-3p was a target of circ-HUWE1, and miR-433-3p inhibition reversed the effects of circ-HUWE1 knockdown. In addition, FGF7 was a downstream target of miR-433-3p whose function could be abolished by FGF7 reintroduction. Circ-HUWE1 positively regulated FGF7 expression via competitively targeting miR-433-3p. Moreover, circ-HUWE1 knockdown activated the WNT signaling pathway in Amyloid-β-treated SK-N-SH cells by targeting the miR-433-3p/FGF7 axis. In conclusion, circ-HUWE1 knockdown alleviates Amyloid-β-induced neuronal injury in SK-N-SH cells via miR-433-3p release-mediated FGF7 depletion.

Recurrent pregnancy loss (RPL), pre‑eclampsia (PE), fetal growth restriction (FGR), and preterm delivery are examples of ‘great obstetrical syndromes’ (GOS). Placental dysfunction is the most common pathogenesis of GOS. In human pregnancies, the effects of uterine natural killer cells involve angiogenesis, promoting the remodeling of uterine spiral artery, and improving the invasion of trophoblast cells. The uNK cells supply killer immunoglobulin‑like receptors (KIRs), which come into contact with human leukocyte antigen‑C (HLA‑C) ligands expressed by extravillous trophoblast cells (EVTs). Numerous studies have investigated the association between GOS and KIR/HLA‑C combination. However, the outcomes have not been conclusive. The present review aimed to reveal the association between GOS and KIR/HLA‑C combination to screen out high‑risk pregnancies, strengthen the treatment of pregnancy complications, and reduce the frequency of adverse maternal and fetal outcomes. It has been reported that a female with a KIR AA genotype and a neonate with a paternal HLA‑C2 molecule is more prone to develop GOS and have a small fetus since less cytokines were secreted by uNK cells. Conversely, the combination of KIR BB haplotype (including the activating KIR2DS1) and HLA‑C2 can induce the production of cytokines and increase trophoblast invasion, leading to the birth of a large fetus. KIR/HLA‑C combinations may be applicable in selecting third‑party gametes or surrogates. Detection of maternal KIR genes and HLA‑C molecules from the couple could serve as useful markers for predicting and diagnosing GOS.

Pre‐eclampsia (PE) is a worldwide pregnancy‐related disorder. It is mainly characterized by defect migration and invasion of trophoblast cells. Recently, circular RNAs (circRNAs) have been believed to play a vital role in PE. The expression patterns and the biological functions of circRNAs in PE remain elusive. Here, we performed a circRNA microarray to identify putative PE‐related circRNAs. Bioinformatics analyses were used to screen the circRNAs which have potential relationships with pre‐eclampsia, and we identified a novel circRNA (circVRK1) that was up‐regulated in PE placenta tissues. By using HTR‐8/SVneo cells, circVRK1 knockdown significantly enhanced cell migration and invasion abilities, as well as epithelial‐mesenchymal transition (EMT). Mechanistically, we found that circVRK1 and PTEN could function as the ceRNAs to miR‐221‐3p. Overexpression of miR‐221‐3p promoted cell migration, invasion and EMT via regulating PTEN. The cotransfection of miR‐221‐3p inhibitor or PTEN reversed the effect from circVRK1 knockdown. Moreover, the circVRK1/miR‐221‐3p/PTEN axis greatly regulated Akt phosphorylation. In general, circVRK1 suppresses trophoblast cell migration, invasion and EMT, by acting as a ceRNA to miR‐221‐3p to regulate PTEN, and further inhibit PI3K/Akt activation. The purpose of this paper is to open wide insights to investigate the onset of PE and provide new potential therapeutic targets in PE.

Preeclampsia (PE) is a serious disease that occurs after 20 weeks during pregnancy. There are some aberrant microRNAs (miRNAs) that are associated with the etiology of PE. As discovered by scholars, there was an increased level of miR‐215‐5p in plasma of PE patients compared with the control group; nonetheless, there is still no knowledge of the mechanism of miR‐215‐5p in PE. We carried out the comparison of the expression levels of miR‐215‐5p, and the supposed target gene cell division cycle 6 (CDC6) in 30 placentas from PE patients as well as 30 placentas from normal pregnant women. The verification of the impacts of miR‐215‐5p and CDC6 was carried out by functional assays in HTR‐8/SVneo cells transfected with the miR‐215‐5p mimic or siR‐CDC6. As indicated by findings, miR‐215‐5p showed an apparent increase; conversely, CDC6 was inhibited in the experiment group. The upregulation of miR‐215‐5p inhibited both the migration and invasive potential of trophoblasts, besides decreasing the G1‐S transition and downregulating CDC6 in HTR‐8/SVneo cells; nonetheless, it did not significantly impact the cell proliferation. Furthermore, siR‐CDC6 replicated the functions of the miR‐215‐5p mimic. Also, the miR‐215‐5p mimic and siR‐CDC6 both decreased the epithelial‐mesenchymal transition (EMT) with additional E‐cadherin level and decreased the expressions of N‐cadherin as well as vimentin in trophoblast cells. To conclude, miR‐215‐5p decreased not only the migration but also the invasion of trophoblasts through regulating CDC6, which indicated that miR‐215‐5p might be associated with the etiology of PE.Significance of the study: More and more attention has been paid on the roles of miRNAs in the pathogenesis of PE. However, there is no study of miR‐215‐5p in the etiology of PE. We first investigated the mechanism of miR‐215‐5p in placental tissues and HTR‐8/SVneo cells. It was suggested that miR‐215‐5p decreased the abilities of migration and invasion of trophoblasts through regulating CDC6 in PE. miR‐215‐5p might be used as an target for the early diagnosis and treatment of PE in the future.

Recurrent pregnancy loss (RPL) commonly refers to three or more miscarriages that occur before 20 weeks of pregnancy. The immunological cause of RPL could be either an auto‐ or alloimmune‐related event or both. Because of the discovery of immunological abnormalities in RPL patients in clinical practice, several immunomodulatory therapies were introduced to maintain the immune balance at the maternal‐fetal interface. Intravenous immunoglobulin (IVIg) is one of the immunomodulators. In recent years, several studies have analyzed the therapeutic effect of IVIg on RPL patients with antiphospholipid syndrome (APS) or unexplained RPL. However, their results are controversial. IVIg can be used in RPL patients with APS who have previously failed in other treatments. It is recommended that IVIg infusion could be considered used before conception in RPL patients who have cellular immune abnormalities such as increased natural killer (NK) cell counts, NK cell cytotoxicity, or increased T helper (Th)1/Th2 ratio, depending on the cut‐off values of each hospital. The aim of this review was to summarize the mechanisms, efficacy, pharmacokinetics, and side effects associated with passive immunization using IVIg in immunologic RPL, according to the literature published in recent years. We hope that more obstetricians will be able to understand the timing and indication of IVIg properly in immunologic RPL patients and effectively enhance pregnancy outcomes for mothers and neonates.

Abiotic stresses limit the plant growth and productivity. Plants have developed various responsive mechanisms to survive these adverse environmental conditions. To better understand plants how to adapt environmental stress, we retrieved the Arabidopsis root responsive genes related to eight abiotic stresses (salt, cold, drought, osmotic, UV, wounding, heat, and heavy metal stresses) from the Gene Expression Omnibus (GEO) database. After quantile normalization of microarray data, a robust rank aggregation (RRA) algorithm was applied to determine the differentially expressed genes (DEGs). The resultant 213 DEGs, including 139 up-regulated and 74 down-regulated genes out of more than 20,000 genes, were further analyzed by the integrated bioinformatics approaches of PUBMED, PANTHER, DAVID, and STRING. The results indicated that the up-regulated DEGs were more positively involved in response to oxidative stress, regulation of transcription, and structure organization than the down-regulated DEGs. The former also had more complicated PPI interactions than the latter. Furthermore, qRT-PCR and enzyme activity have been done to validate the outcome of integrated bioinformatics analysis. Our work will facilitate to demonstrate the common molecular mechanisms responsive to differential abiotic stresses and these DEGs might be potential biomarkers for future abiotic stress-resistance studies.