Publications by authors named "Jinlai Meng"

Preeclampsia is one of the most severe obstetric complications, yet its pathogenesis remains unclear. Decidual natural killer (dNK) cells, the most abundant immune cells at the maternal-fetal interface, are closely associated with preeclampsia due to abnormalities in their quantity, phenotype, and function. This review summarizes the molecular mechanisms by which dNK cells regulate extravillous trophoblast (EVT) invasion, promote uterine spiral artery remodeling, and maintain immune tolerance.

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Article Synopsis
  • The study investigates the role of the chemokine fractalkine (CX3CL1) and its receptor CX3CR1 in the immune response during preeclampsia, focusing on macrophage function and trophoblast invasion.
  • Researchers analyzed placental and decidual tissues from 60 women, finding higher levels of CX3CL1 and CX3CR1 in severe preeclampsia cases compared to normotensive pregnancies.
  • The results suggest that the CX3CL1/CX3CR1 signaling pathway negatively impacts vascular endothelial growth factor (VEGF) expression and inhibits the invasion and migration abilities of trophoblast cells, which may contribute to complications in preeclamps
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The pathogenesis of preeclampsia (PE) has not been elucidated, but immune imbalance is known to be one of the main pathogeneses. Dysfunction of decidual macrophages can lead to PE, and the PD-1/PD-L1 signaling pathway is associated with macrophage polarization. However, the relationship between the influence of the PD-1/PD-L1 signaling pathway on macrophage polarization and the onset of PE has not been fully elucidated.

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Background: Preeclampsia (PE) is a common hypertensive pregnancy disorder associated with shallow trophoblast invasion. Although bone morphogenetic protein 2 (BMP2) has been shown to promote trophoblast invasion in vitro, its cellular origin and molecular regulation in placenta, as well as its potential role in PE, has yet to be established. Additionally, whether BMP2 and/or its downstream molecules could serve as potential diagnostic or therapeutic targets for PE has not been explored.

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Objective: Preeclampsia (PE) is a common but serious pregnancy complication that adversely affects both maternal and fetal health. However, the mechanisms of its pathogenesis remain unclear, and effective biomarkers for early diagnosis are still lacking.

Methods: In this retrospective study, comprehensive bioinformatic analysis and logistic regression analysis were used to compare profiles of 48 serum cytokines in 27 PE patients with those in 41 normotensive pregnant subjects.

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Inadequate trophoblastic infiltration and resulting placental hypoxia and inflammation comprise the core pathological basis of preeclampsia (PE). Maternally expressed gene 3 () is known to be involved in the pathogenesis of preeclampsia by inhibiting the migration and invasion of trophoblasts and promoting their apoptosis. Nevertheless, the specific underlying downstream molecular mechanism of is less well characterized.

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BACKGROUND Preeclampsia (PE) is a serious pregnancy disorder associated with immune tolerance imbalance. The etiology of preeclampsia has not been fully elucidated. The aim of this study was to clarify the possible role of the lymphocyte activation gene 3 (LAG-3)/fibrinogen-like protein 1 (FGL-1) signaling pathway in the immune imbalance of early-onset PE.

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The etiology of preeclampsia (PE) is still unknown, and excessive immune activation is an important component of its pathogenesis. Programmed cell death protein 1 (PD-1) is one of immune checkpoints which may prevent overactivated immune attack and lead to a tolerant immune microenvironment. Little is known about the involvement of PD-1-mediated immunoregulation at the maternal-fetal interface in PE.

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Background: Low-grade endometrial stromal sarcoma (LGESS) is a rare indolent tumor with a favorable prognosis. With the importance of improving quality of life recognized, fertility-sparing surgery may be an option for those young women. However, most of the reports suggested that stage IA patients might be candidates for fertility-sparing surgery, and adjuvant hormonal treatment was considered a feasible adjuvant therapy for reducing the recurrence risk of patients with LGESS and hysterectomy was recommended after the completion of pregnancy and delivery.

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MiR-125b regulates the kinds of cells that undergo apoptosis physiologically and pathologically. However, whether miR-125b affects the apoptotic behavior of trophoblasts and the underlying molecular regulatory mechanisms remains unclear. This study investigated the effect of miR-125b on apoptosis of HTR-8/SVneo cells in vitro.

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The typical hallmark of placenta accreta spectrum (PAS) disorders is increased implantation site intermediate trophoblast (ISIT) cell numbers. However, the extent of trophoblast proliferation and apoptosis have not been found to differ from those of normal placentation. MicroRNA-125a (miR-125a) induces apoptosis in colon cancer cell by targeting myeloid cell leukemia-1 gene ().

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Background: Polycystic ovary syndrome (PCOS) is a common endocrine disease characterized by hyperandrogenism, irregular menses, and polycystic ovaries. Several long non-coding RNAs (lncRNAs) are aberrantly expressed in PCOS patients; however, little is known about the effects of the lncRNA-low expression in tumor (lncRNA-LET) on PCOS. We aimed to explore the effects of lncRNA-LET on human granulosa-like tumor cell line, KGN.

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Objective: To assess the value of combined fetal karyotyping and chromosomal microarray analysis (CMA) for the verification of high-risk pregnancy signaled by noninvasive prenatal screening (NIPS) based on high-throughput sequencing.

Methods: One hundred and fifty-one pregnant women with high risks for aneuploidies of chromosomes 13, 18, 21, X and Y or pathological copy number variations (CNVs) by NIPS were subjected to amniocytic karyotyping and CMA analysis.

Results: One hundred and forty-two women were found to have a high risk for fetal chromosomal aneuploidies, which included 83 cases of trisomy 21, 17 cases of trisomy 18, 2 cases of trisomy 13, and 40 cases of sex chromosome aneuploidies.

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Background: This study aims to assess the diagnostic and prognostic value of Swansea criteria in diagnosing acute fatty liver of pregnancy (AFLP) in a Chinese population.

Methods: A retrospective study was conducted on 52 Chinese women diagnosed with AFLP. All selected cases were reassessed using the Swansea criteria with special focus on the noninvasive criteria, since performing a liver biopsy for this indication is rare in a Chinese population.

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Objective: Placenta accreta is defined as abnormal adhesion of placental villi to the uterine myometrium. Although this condition has become more common as a result of the increasing rate of cesarean sections, the underlying causative mechanism(s) remain elusive. Because microRNA-29a/b/c (miR-29a/b/c) have been shown to play important roles in placental development, this study evaluated the roles of these microRNAs in placenta accreta.

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Purpose: The purpose of this study was to describe some prenatal characteristics and laboratory findings of acute fatty liver of pregnancy (AFLP) and provide the clinicians with reasonable predictors and expectation in postpartum recovery.

Methods: At a tertiary referral center 43 patients with AFLP were entered into this retrospective study in 5 years based on the Swansea criteria. Emergent cesarean sections were performed within 24 h, and the criteria of recovery after operation was based on a uniform standard.

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Background: Because the future application of cell-free fetal DNA screening is expected to dramatically improve the diagnostic yield and reduce unnecessary invasive procedures, it is time to summarize the indications of invasive prenatal diagnosis. This retrospective study was performed to evaluate the changes and efficacies of indications of invasive procedures for detecting cytogenomic abnormalities from 2000 to 2012.

Material And Methods: From our regional obstetric unit, 7818 invasive procedures were referred by indications of advance maternal age (AMA), abnormal ultrasound findings (aUS), abnormal maternal serum screening (aMSS), and family history (FH).

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Objective: To investigate significance and correlation of free fetal DNA (fDNA) and beta-human chorionic gonadotropin (beta-hCG) in circulation in pregnant women with high-risk of Down's syndrome (DS).

Methods: Pregnant women with a male fetus at second trimester screening for Down's syndrome were chosen, including 5 women with a trisomy 21 fetus (DS group), 21 women with DS high-risk pregnant women (DS high-risk group) matched with 22 normal pregnant women as control group. Free fDNA in maternal plasma were extracted.

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Background: Measurement of free fetal DNA in maternal plasma opened a door for non-invasive prenatal diagnosis. Prenatal diagnosis of fetal ABO genotypes can provide a basis for the prevention and therapy of maternal-fetal incompatibility. We identified fetal ABO genotypes using fetal DNA in plasma from pregnant women with blood group O.

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Aim: The purpose of the study was to evaluate the feasibility and reliability of comparative genomic hybridization (CGH) in the detection of genomic imbalances in Chinese malformed fetuses.

Methods: Genomic DNA was extracted from umbilical cord blood or fresh amniotic fluid of 9 malformed fetuses and labeled with SpectrumGreen dUTP or SpectrumRed dUTP. A pair of CGH analyses in which the fluorochromes were exchanged was carried out for each sample.

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Objective: To study the effect and mechanism of the peripheral blood mononuclear cell (PBMC) invasion by HBV on artificial immunization in newborns.

Methods: Fifty-two newborns of HBsAg positive mothers were immunized with HBIG (hepatitis B immunoglobulin) and HBVac (hepatitis B vaccine) and were followed up for 7 months. The newborns' HBV-DNA in serum and in the PBMCs was detected with nested-PCR; anti-HBs was tested with solid phase radioimmunoassay (SP-RIA).

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Objectives: To study the effect and the mechanism of peripheral blood nuclear cells (PBMC) invaded by hepatitis B virus (HBV) on the artificial immunization in newborns.

Methods: Fifty-two newborns, whose mothers were hepatitis B surface antigen (HBsAg) positive, were immunized with hepatitis B immunoglobulin and hepatitis B vaccine (HBVac), and then followed for 7 months. The newborns' serum and PBMC HBV DNA was detected by nested-PCR, hepatitis B surface antibody (HBsAb) was tested with solid phase radioimmunoassay.

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