Project description:Objective: Mechanisms of preterm labour (PTL) are not fully elucidated. Cervical ripening plays an important role. We aimed to investigate possible differences in gene expression in human cervix between PTL and term labour (TL) and between PTL and preterm premature rupture of membranes (PPROM).
Project description:We compared fetal membrane tissue from preterm labor deliveries to fetal tissue from preterm labor with preterm prelabor rupture of membranes (PPROM) deliveries to further explore the concept that spontaneous preterm birth can result from the initializing of two separate but overlapping pathological events. Chorioamnion, separated into amnion and chorion, was collected from gestationally age-matched cases and controls within 15 minutes of birth, and analyzed using RNA sequencing. In our study, transcriptome analysis of preterm fetal membranes revealed distinct differentially expressed genes for PPROM, separate from preterm labor. This study is the first to report transcriptome data that reflects the individual pathophysiology of amnion and chorion tissue from PPROM deliveries.
Project description:Preterm premature rupture of membranes (PPROM), which precedes approximately 30–40% of preterm births, is the main cause of neonatal morbidity, mortality, and long-term sequelae. In particular, almost half of all PPRPM cases are frequently complicated by subclinical acute inflammation in the placenta and fetal tissue, commonly named as acute histologic chorioamnionitis [HCA]. Increasing evidences suggest that HCA carries additional risks to both the pregnant women and their fetuses, including greater risk of imminent preterm birth, as well as sepsis, neurologic morbidity, and mortality in neonates. More accurate and early prenatal predictive markers (especially noninvasive ones) are urgently needed for identifying subclinical HCA in the context of PPROM.To identify potential biomarkers in the plasma that could predict histologic chorioamnionitis (HCA) in women with preterm premature rupture of membranes (PPROM), using shotgun and targeted proteomic analyses.
Project description:Preterm birth (PTB) is a live birth delivered before 37 weeks of gestation (GW). About one-third of PTBs result from the preterm premature rupture of membranes (PPROM). Up to the present, the pathogenic mechanisms underlying PPROM are not clearly understood. Here, we investigated the differential expression of long chain non-coding RNAs (lncRNAs) in placentas of PTBs with PPROM, and their possible involvement in the pathogenic pathways leading to PPROM. A total number of 1954, 776, and 1050 lncRNAs were identified with a microarray from placentas of PPROM (group A), which were compared to full-term birth (FTB) (group B), PTB (group C), and premature rupture of membrane (PROM) (group D) at full-term, respectively. Instead of investigating the individual pathogenic role of each lncRNA involved in the molecular mechanism underlying PPROM, we have focused on investigating the metabolic pathways and their functions to explore what is the likely association and how they are possibly involved in the development of PPROM. Six groups, including up-regulation and down-regulation in the comparisons of A vs. B, A vs. C, and A vs. D, of pathways were analyzed. Our results showed that 22 pathways were characterized as up-regulated 7 down-regulated in A vs. C, 18 up-regulated and 15 down-regulated in A vs. D, and 33 up-regulated and 7 down-regulated in A vs. B. Functional analysis showed pathways of infection and inflammatory response, ECM-receptor interactions, apoptosis, actin cytoskeleton, and smooth muscle contraction are the major pathogenic mechanisms involved in the development of PPROM. Characterization of these pathways through identification of lncRNAs opened new avenues for further investigating the epigenomic mechanisms of lncRNAs in PPROM as well as PTB.
Project description:Preterm prelabour rupture of membranes beyond the 34th week of gestation (late PPROM) is frequently associated with the risk of the microbial invasion of the amniotic fluid (MIAC) and histological chorioamnionitis (HCA). Hence, we employed a Tandem Mass Tag-based approach to uncover amniotic fluid proteome response to the presence of MIAC and HCA in late PPROM. Protein dysregulation was associated with only five cases in the group of 15 women with confirmed MIAC and HCA. Altogether, 138 amniotic fluid proteins were changed in these five cases exclusively. These proteins were particularly associated with excessive neutrophil responses to infection, such as neutrophil degranulation and extracellular trap formation. We believe that the quantification of these proteins in amniotic fluid may assist in revealing women with the highest risk of excessive inflammatory response in late PPROM.
Project description:Investigation of lncRNA expression profile of gastric cancer A six chip study using total RNA extracted from three gastric cancer tissues and three paracancerous tissues
Project description:Polypectomy using an Endoloop PDS II (™) during pregnancy can be responsible for miscarriage and preterm delivery. Cervical polyps should not be removed in pregnant women except in cases where a malignancy is suspected.
Project description:Objective: We investigated whether birth in patients whose pregnancies are complicated by pre-labor premature rupture of the membranes (PPROM) is associated with translocation of microbes in maternal circulation and a systemic inflammatory process. Research Design and Methods: 66 pregnant patients admitted for PPROM [gestational age (GA) median [IQR]: 32±1 weeks] had maternal blood (MB) retrieved prior to birth and within 1-hour post-partum. Immediately after birth, fetal membranes (FM) and placental tissue were frozen in sterile fashion. Bacterial load was assessed by 16S rDNA gene amplification by qPCR. Multiplexed 16S amplicon libraries were sequenced on the Illumina platform and enrichment analysis performed using LfSe and EdgeR. Pro- and anti-inflammatory cytokines were measured in MB using multiplex immunoassay. Histological chorioamnionitis (HCA) and cord blood haptoglobin and IL-6 indicated fetal exposure to antenatal inflammation (Triple I). Results: Bacterial DNA was identified in MB both before and after birth. A significant decrease in MB bacterial DNA was observed within 1-hour post-delivery (p=0.004). Conversely, MB cytokines IL-6 and Il-10 increased significantly (p<0.05 for all) especially in pregnancies exposed to Triple I. Compared to placenta, FM carried a higher bacterial load (p<0.001) regardless of presence or absence of antenatal inflammation. FM had higher bacterial biodiversity with top representation from Mycoplasma spp although Mycoplasma was not found in MB either pre- or post-delivery. While no taxa were systematically enriched in MB post-delivery, sample-by-sample analysis identified three cases where a MB OTU had a match in FM and four cases with a match in placenta. Yet, the most abundant MB OTUs had no match in either tissues. Conclusion: In patients with PPROM, bacterial DNA is present in MB prior to birth but is rapidly removed after delivery in association with a robust immediate postpartum cytokine surge.