The aim of this study was to assess whether higher plasma formaldehyde concentration existed in women diagnosed with miscarriage and whether it contributed to higher risk of miscarriage in Chinese women.A case-control study was conducted in 118 women with a diagnosed miscarriage at the first trimester and 191 healthy women who delivered at term. Plasma levels of formaldehyde were measured by gas chromatography in conjunction with mass spectrometry after derivatization of the formaldehyde to the pentafluorophenylhydrazone and characteristics of the subjects including age, education level, occupation, family income, home decoration status, and exposure to second-hand smoke were recorded. Logistic regression analyses were performed to investigate the relationship between miscarriage and levels of formaldehyde.Women with miscarriage were comparable to controls in terms of age, education level, occupation, family income, and home decoration status. They were, however, more likely to be exposed to second-hand smoke. Plasma levels of formaldehyde were significantly higher in women with miscarriage (0.0944 ± 0.0105 vs. 0.0239 ± 0.0032 μg/mL, P < .001). Multivariate logistic regression showed that higher level of formaldehyde (odds ratio [OR]: 8.06, 95% confidence interval [CI]: 4.96–13.09) and exposure to second-hand smoke (OR: 3.60, 95% CI: 1.58–8.20) were independently and significantly associated with higher risk of miscarriage.Plasma levels of formaldehyde were significantly higher in women who were diagnosed with miscarriage than those who delivered at term and higher levels of formaldehyde was an independent risk factor for miscarriage, with higher levels being associated with higher risk of miscarriage.
The disruption of the inflammatory microenvironment in the uterus affects pregnancy outcome. However, the exact quantification and distribution of leukocyte subpopulations in the uterus in preeclampsia (PE) have not been clearly characterized. Inflammasomes promote the release of proinflammatory cytokines interleukin (IL)‐β and IL‐18. A higher expression of NLRP3 inflammasome in placentas contributes to excessive inflammation in PE. However, related studies on the uterus are scarce. We aimed to investigate changes in the infiltration of leukocyte subpopulations in decidual and uterine tissues, and explore the role of activation of uterine NLRP3 inflammasomes in PE. Decidual tissues were collected from normotensive pregnant women and preeclamptic women. A PE‐like model was established via administration of lipopolysaccharide to normal pregnant rats. Uterine and decidual tissues were collected from all experimental groups. It was found that the number of leukocytes was significantly elevated in decidual and uterine tissues in PE patients compared to normal controls. The leukocytes (predominantly macrophages and NK cells) particularly infiltrated into the decidua and uterine decidua in PE‐like rats, and these were sparse in the myometrium. The NLRP3 immunoreactivity in the uterus was extremely little in control rats, its immunoreactivity and caspase‐1 immunoreactivity were significantly elevated in the PE‐like rats; the mRNA expression results also indicated an upward trend in the activation of NLRP3 inflammasomes. These results support that leucocyte infiltration in the decidua and uterine deciduas, and the activation of NLRP3 inflammasome in the uterus, which participate in the pathogenesis, are responsible for the excessive inflammation at the maternal‐fetal interface during PE.
<b><i>Objectives:</i></b> The pathogenesis of preeclampsia (PE) is associated with impaired trophoblast invasion, which results in placental insufficiency. Our earlier studies demonstrated that tissue transglutaminase (tTG) is highly expressed in human PE serum. However, whether tTG participates in trophoblast invasion remains unclear. The aim of the present study was to determine the role and mechanism of tTG in regulating matrix metalloproteinase (MMP)-2/MMP-9 expression to reduce trophoblast invasiveness in PE. <b><i>Methods:</i></b> HTR-8/SVneo cells were transfected with a lentivirus vector and small interfering RNA targeting tTG. The protein level was detected by Western blotting. Cell proliferation and apoptosis were assessed by MTS and flow cytometry assays, respectively. Cell invasion was investigated by Transwell assay. In addition, the influence of tTG on PI3K and AKT mRNA levels in HTR-8/SVneo cells was evaluated using reverse transcription-quantitative PCR. <b><i>Results:</i></b> tTG-overexpression inhibited HTR-8/SVneo cell proliferation and invasion and promoted apoptosis. In addition, upregulation of tTG induced an increase of PI3K and phosphorylated AKT and a decrease of MMP-2 and MMP-9 expression. tTG-knockdown significantly promoted the proliferation and invasion of HTR-8/SVneo cells and inhibited the apoptosis. Furthermore, the PI3K expression level was reduced, and the MMP-2/MMP-9 protein levels were increased. <b><i>Conclusion:</i></b> Taken together, the present study demonstrated that tTG-overexpression inhibited HTR-8/SVneo cell invasion via reducing the expression of MMP-2 and MMP-9 by activating PI3K/AKT signaling pathway, which may lead to the occurrence or development of PE. The present data provide new insights into modulation of tTG expression as a potential therapeutic target for PE.
BackgroundThe effects of intrapartum fever associated with epidural analgesia in nulliparous women on the short-term maternal and neonatal outcomes are not well understood.Methods We included 2076 nulliparous women who received regular obstetric examination and gave birth at Guangzhou Women and Children’s Medical Center from January 1, 2020 to June 30, 2020. All cases were singleton full-term pregnancies, and all foetuses were in cephalic presentation. We allocated 817 women with temperature >38℃ during labour into the fever group and 1259 women with temperature ≤38℃ during labour to the non-fever group. The short-term maternal and neonatal outcomes in the two groups were compared. Results in the fever group, 8.3% of pregnant women converted to caesarean delivery. The conversion rate in the non-fever group was 5.2% (p = 0.004). The rates of mild neonatal asphyxia, severe neonatal asphyxia, and neonatal hospitalisation in the fever group were higher than those in the non-fever group (χ2 = 12.070, 6.325, and 6.821, respectively, all P<0.05). The 1194 pregnant women in the fever group who had vaginal deliveries spent 756.46 ± 256.43 minutes in the first stage of labour and 65.74 ± 47.63 minutes in the second stage, significantly longer than the 749 women who had vaginal deliveries in the non-fever group (P<0.001, P=0.001). The assisted delivery rate for vaginal delivery in the fever group was 49.0%, significantly higher than that in the non-fever group (2=49.738, P<0.001). The rates of mild neonatal asphyxia, severe neonatal asphyxia, neonatal acidosis, and neonatal hospitalisation with vaginal delivery in the fever group were higher than those in the non-fever group (2=15.375, 6.597, 22.265, and 7.322, respectively, and p<0.001, 0.010, <0.001, and 0.007, respectively).Conclusions Epidural analgesia-associated intrapartum fever in nulliparous women increased the rates of short-term adverse maternal and neonatal outcomes, indicating that efforts are needed to prevent incidence of intrapartum fever due to administration of epidural analgesia.
Low molecular weight heparin (LMWH) has been successfully applied in the treatment of pregnancy complications associated with pro-thrombotic and antiphospholipid syndrome (APS). The underlying mechanism remains enigmatic. The purpose of this study was to explore the effects of time and dosage of LMWH on the proliferation and apoptosis of human trophoblast. The biological function of LMWH on primary trophoblast was evaluated by quantitative real-time PCR (qRT-PCR), by detecting the expression of proliferation genes SDS22, APPL1, CyclinB1, as well as the expression of apoptosis-related gene Survivin. Our results showed that the treatment time and dosage of LMWH have critical effects on trophoblast proliferation and apoptosis. LMWH had the most obvious effect on promoting trophoblast proliferation and could suppress apoptosis at the concentration of 0.1 IU/ml at 72 h. This study thus provides detailed mechanism of the biological effects of LMWH on trophoblast, and sheds light on the effective clinical application of LMWH in pregnancy complications.
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