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Objective To retrospectively analyze of factors influencing early preterm birth (EPB) and late preterm birth (LPB ) in pregnancy women with placenta previa complicated by placenta accreta spectrum disorders ( PAS ), and assess maternal and infant outcomes. Methods We included 590 cases of pregnancy women with placenta previa complicated by PAS who underwent cesarean sections at five hospitals in Wuhan and Xianning cities between January 2018 and June 2021. These patients were divided into three groups based on delivery gestational age : EPB, LPB, and term birth (TB). A multiple logistic regression model was employed to analyze the risk factors associated with EPB and LPB. Additionally, differences in early maternal and infant outcomes among these groups were examined. Results Among 590 pregnancy women with placenta previa complicated by PAS, the proportions of EPB and LPB were 9.7% and 54.4%. The use of uterine contraction inhibitors prior to cesarean section, vaginal bleeding, and previous cesarean sections history were identified as risk factors for both EPB and LPB. The proportion of severe postpartum hemorrhage was comparable between the EPB group and the LPB group ; however, the incidence of neonatal asphyxia, low birth weight infants, and the rate of newborns transferred to the Neonatal Intensive Care Unit (NICU) within 24 hours after cesarean delivery were significantly higher in the EPB group compared to the LPB group. Conclusions Placenta previa complicated by PAS predominantly leads to LPB. The history of prior cesarean sections, uterine contractions, and vaginal bleeding prior to cesarean section, are significantly associated with both EPB and LPB. During the perinatal period, efforts should be made to extend gestational weeks under close monitoring to minimize the incidence of premature births and thereby improve early maternal and infant outcomes. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the mechanism by which MALAT1 regulates CRY2 expression and participates in trophoblast migration and invasion. Three patients with unexplained recurrent spontaneous abortion, four patients with missed abortion, and four women who underwent artificial miscarriages were enrolled in this study. Quantitative reverse‐transcription polymerase chain reaction and western blot analysis were used to detect RNA and protein expression, respectively. Trophoblast migration and invasion were detected by wound‐healing and transwell invasion assays. RNA pull‐down and Co‐IP assays were used to indicate the interaction between MALAT1 and FBXW7 or the interaction between FBXW7 and CRY2. The results showed significantly decreased MALAT1 expression in the villous specimens from the RSA patients relative to that in the villous specimens from the missed abortion patients and the normal villous specimens. MALAT1 promoted trophoblast cell migration and invasion by negatively regulating CRY2 protein expression. MALAT1 recruited FBXW7 to impair CRY2 protein stability. In conclusion, MALAT1 downregulation in trophoblasts might be related to miscarriage. MALAT1 may recruit the E3 ubiquitin ligase FBXW7 to induce CRY2 ubiquitin‐mediated degradation and participate in trophoblast migration and invasion. [ABSTRACT FROM AUTHOR]

Introduction: Trophoblast plays a vital role in the embryonic implantation and function of the placenta. Exposure to a hyperglycemic environment results in the abnormal function of trophoblasts during fetoplacental development, which leads to maternal complications and poor fetal outcomes. However, the precise mechanisms of placental pathology during hyperglycemia remain elusive. We investigated the role of CYP1B1 in the functional behavior of the extravillous trophoblast (EVT) cell line HTR-8/SVneo under hyperglycemic condition.Methods: We determined the expression of CYP1B1 via real-time polymerase chain reaction and Western blot. Specific CYP1B1 inhibitors and small interfering RNA were used to knockdown CYP1B1, whereas an agonist and an adenovirus were used to overexpress CYP1B1. The proliferation, migration, and invasion of the EVT cell line (i.e. HTR-8/SVneo) were assessed via colony formation, 5-ethynyl-2-deoxyuridine, wound healing, and transwell assay.Results: CYP1B1 is highly expressed in placentas from women with gestational diabetes mellitus. The blockage of CYP1B1 inhibits EVT activities induced by hyperglycemia in vitro, including proliferation, migration, and invasion, whereas the exogenous expression of CYP1B1 exhibits the opposite effects.Discussion: Our study may offer a new method for regulating EVT motility under hyperglycemic condition via CYP1B1. [ABSTRACT FROM AUTHOR]

Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs) expressing microRNAs have been highlighted in human diseases. However, the detailed molecular mechanism of hucMSCs-derived exosomal miR-18b-3p on preeclampsia (PE) remains further investigation. We aimed to investigate the effect of exosomes and miR-18b-3p/leptin (LEP) on occurrence of PE. The morphology of the hucMSC and hucMSC-exosomes (Exos) was identified. The exosomes were infected with different lentivirus expressing miR-18b-3p to explore the role of miR-18b-3p in PE. The PE rat model was established by intraperitoneal injection of N-nitro-l-arginine methyl ester. The expression of LEP and miR-18b-3p was tested in PE rat placenta tissues. Also, the effect of exosomes on LEP and miR-18b-3p expression was detected. The systolic blood pressure (SBP), proteinuria, inflammatory factors, the weight of fetal rat and placenta and cell apoptosis in PE rats were detected. Finally, the relationship between miR-18b-3p and LEP was verified using dual-luciferase reporter gene assay and RNA pull-down assay. Exosomes, restoring miR-18b-3p or inhibiting LEP reduced SBP and proteinuria of PE rats as well as increased the weight of fetal rat and placenta, decreased serum levels of inflammatory factors as well as suppressed apoptotic cells of PE rats, exerting a suppressive effect on PE progression. miR-18b-3p was decreased and LEP was increased in placenta tissues of PE rats. LEP was the direct target gene of miR-18b-3p. Upregulation of miR-18b-3p or treatment of the exosomes suppressed LEP expression and reduced PE occurrence, while downregulation of miR-18b-3p had contrary effects. Downregulated LEP reversed the effect of miR-18b-3p reduction on PE rats. HucMSCs-derived exosomal miR-18b-3p targets LEP to participate in the occurrence and development of PE. This study may provide a novel theoretical basis for the mechanism and investigation of PE. [ABSTRACT FROM AUTHOR]

We present 2 cases of coronavirus disease 2019 (COVID-19)–associated severe respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during the third trimester of pregnancy. Both mothers and newborns had excellent outcomes. We failed to identify SARS-CoV-2 in all of the products of conception and the newborns. This report provided evidence of low risk of intrauterine infection by vertical transmission of SARS-CoV-2. [ABSTRACT FROM AUTHOR]

Objective The objective of the study was to investigate the association between peripheral levels of C-reactive protein (CRP) and cognitive decline that is defined by 2-5 years of cognitive change in general cognitive function or specific cognitive domain. Methods We searched PubMed and Google for prospective/longitudinal studies that report the association between peripheral levels of CRP and risk of cognitive decline in the nondementia population. Results Out of 479 related articles from PubMed and Google, four studies with a total of 5255 non-demented subjects that report odds ratio (OR)/relative risk/hazard ratio of CRP levels and decline in general cognition met our criteria for meta-analysis. The association between higher levels of CRP and risk of global cognitive decline was weak but significant (OR, 1.27 [95% CI, 1.02 to 1.58]). However, the systematic review from six other articles that were not suitable for meta-analysis revealed a marginal association between CRP and cognitive decline in certain domains. Conclusion Our analysis demonstrated a weak association between peripheral CRP level and global cognitive decline. Because of the small number of included studies and varied methodologies that they applied, caution should be taken when generalizing our finding to the full range of cognitive changes in different cognitive domains observed in non-demented people. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

A case report describing severe COVID‐19 and treatment strategy in a pregnant patient who delivered vaginally at 34 weeks. [ABSTRACT FROM AUTHOR]

Problem: Human pregnancy is a complex biological process, and spontaneous abortion is the most common complication of pregnancy. LncRNAs have been identified that play key roles in a variety of human diseases. Recently, lncRNAPVT1 was reported to relate to the pathogenesis and progression of pregnancy. However, the role and underlying mechanism of PVT1 in trophoblast cell dysfunction in spontaneous abortion remain largely unknown. Method of study: The effects of PVT1, miR‐424, and eIF5A on HTR8 cells and human villi tissues from spontaneous or induced abortions were investigated using CCK‐8 assay, EdU assay, real‐time polymerase chain reaction, Western blotting, cell transfection assays, cell migration assays, and luciferase reporter gene assays. Results: Overexpression of PVT1 promoted HTR8 cell viability, proliferation, and migration. Suppression of PVT1 promoted miR‐424 expression, and miR‐424 could modulate the effects of PVT1 in HTR8 cells. MiR‐424 exerted its function via regulation of eIF5A expression in HTR8 cells. PVT1 and eIF5A expression were decreased and miR‐424 was increased in clinical samples from spontaneous abortion, compared to samples from elective induced abortion. Conclusion: PVT1 regulates trophoblast cell function via modulation of a PVT1/miR‐424/eIF5A pathway. [ABSTRACT FROM AUTHOR]