The Influence of CD40/CD40L, MMP2/MMP9 on Uterine Artery Blood Flow and Their Expression in Recurrent Miscarriage.

Objective: This study aims to investigate the expression levels of soluble CD40L (sCD40L), matrix metalloproteinase 2 (MMP2), and matrix metalloproteinase 9 (MMP9) in the serum of patients experiencing recurrent abortion and their impact on uterine artery blood flow. Methods: A cohort of 200 patients with recurrent abortion was selected for this investigation. The levels of sCD40L, MMP2, and MMP9 in serum were assessed using ELISA, while ultrasound was employed to measure the pulsatility index (PI) and resistance index (RI) in uterine artery blood flow. Pregnancy outcomes were observed, and the expression of CD40/CD40L and MMP2/MMP9 in villi tissues was compared between patients experiencing recurrent abortion failure and those with normal pregnancies. Results: In the successful pregnancy group of patients with recurrent spontaneous abortion (RSA), serum levels of sCD40L, MMP2, and MMP9 were significantly lower than those in the failed pregnancy group. Additionally, both RI and PI were notably reduced. The expression of each gene showed a correlation with RI and PI. Furthermore, the expression levels of CD40, CD40L, MMP2, and MMP9 in the pregnancy failure group were significantly higher than in the normal voluntary termination group. Conclusion: Serum levels of sCD40L, MMP2, and MMP9, along with non-invasive and easily accessible indicators such as PI and RI in uterine artery blood flow measured by ultrasound, emerge as potential predictive markers for the outcome of recurrent miscarriage pregnancies. Moreover, these indicators can serve as valuable evaluation markers in clinical practice, facilitating the monitoring of treatment effectiveness for recurrent miscarriage.

Fetal Meconium Peritonitis: A Clinical Study of Nine Cases.

Objective: To explore the prenatal ultrasonographic characteristics and pregnancy outcomes of fetal meconium peritonitis (FMP). Methods: Nine patients diagnosed with FMP by routine prenatal examination between January 2015 and December 2020 were identified. Both prenatal ultrasonographic characteristics and pregnancy outcomes associated with these patients were retrospectively analyzed. Results: The mean gestational age at the time of FMP diagnosis was 31.3 ± 4.8 weeks, and the mean gestational age of delivery was 35.1 ± 5.1 weeks. Prenatal ultrasonographic findings at the time of diagnosis in these patients included intestinal dilatation (9/9, 100%), intraperitoneal calcification (8/9, 88.9%), fetal ascites (5/9, 55.6%), intraperitoneal pseudocyst (5/9, 55.6%), and polyhydramnios (6/9, 66.7%). Analyses of the etiological basis for meconium peritonitis in 5 of the 8 live births that underwent surgical treatment revealed 4 cases of congenital volvulus and 1 case of jejunal atresia. Conclusion: The prenatal ultrasound manifestations of fetal meconium peritonitis are diverse, and the different grades of prenatal ultrasound manifestations can provide important information for the treatment of perinatal infants.

Preeclampsia serum upregulates CD40/CD40L expression and induces apoptosis in human umbilical cord endothelial cells.

BACKGROUND: The endothelial cell dysfunction observed in preeclampsia (PE) may be induced by CD40/CD40L signaling. This study investigated the role of CD40/CD40L in the pathogenesis of PE by comparing the effect of maternal serum obtained from healthy pregnant women and PE patients on HUVEC cell growth, apoptosis and CD40/CD40L expression. METHODS: Maternal serum was obtained from 20 patients with PE (PE group) as well as 20 healthy pregnant women (control group). The human umbilical endothelial cell line, CRL1730, was cultured in the presence of maternal serum for 24, 48, and 72 h after which cell growth and apoptosis were assessed by MTT and flow cytometry analysis, respectively. CD40/CD40L expression was determined using flow cytometry and RT-PCR analyses. RESULTS: As compared to CRL1730 cells treated with control sera, those treated with PE sera had altered morphology, decreased cell growth, increased apoptosis and greater CD40/CD40L protein and mRNA expression. Stimulation of CD40/CD40L protein and mRNA expression by PE sera was greatest at 24 h. CONCLUSIONS: PE sera may induce endothelial cell damage possibly through increased CD40/CD40L expression in early-onset PE. Further studies are necessary to determine the factor(s) in PE sera responsible for the observed changes in endothelial cell viability.