Fatal amniotic fluid embolism: incidence, risk factors and influence on perinatal outcome.

PURPOSE: This study aimed to estimate the incidence of fatal amniotic fluid embolism, describe its risk factors, and analyze perinatal outcomes. METHODS: Maternity cases and newborn records of amniotic fluid embolism were collected from the Zhejiang Maternal Surveillance System from October 2006 to October 2019. This study strictly limited the diagnostic criteria for AFE and excluded suspicious cases in order to minimize false-positive AFE cases. The risk factors of fatal amniotic fluid embolism and the relationship between perinatal prognosis and AFE were investigated using logistic regression analysis, estimating the adjusted odds ratios (aORs) and 95% confidence intervals (CIs). RESULTS: 149 cases of amniotic fluid embolism were registered, of which 80 cases were fatal. The estimated fatal AFE incidence was 0.99 per 100,000. The occurrence of fatal AFE was significantly correlated with spontaneous vaginal delivery (aOR 12.3, 95% CI 3.3-39.2) and cardiac arrest (aOR 64.8, 95% CI 14.6-287.8). The average diagnosis time of fatal AFE is 85.51 min, and the peak period of female death is 1-12 h after the onset of the disease, accounting for 60% (48/80) of cases. Fatal amniotic embolism is a cause of intrauterine fetal death and fetal death during delivery (aOR 11.957, 95% CI 1.457-96.919; aOR 13.152, 95% CI 1.636-105.723). Of the 149 confirmed AFE cases, 11 cases of stillbirth occurred, 12 cases were stillborn, and 7 cases of neonatal death were reported. The perinatal mortality rate was 202 per 1000. CONCLUSIONS: Early detection, diagnosis, and treatment of amniotic fluid embolism are essential to avoiding fatal AFE. Clinicians should fully evaluate the pros and cons of choosing the delivery method for pregnant women. When cardiac arrest occurs in women with amniotic fluid embolism, obstetricians should be particularly careful and provide timely and effective treatment to minimize the fatality rate. The outcome of AFE is not only related to maternal survival but also plays a decisive role in the prognosis of the infant over the perinatal period.

MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells.

Cervical cancer (CC) ranks as the second most frequent tumor in women, and CC stem cells have been vital in the tumorigenesis of CC. Recently, the metastasis- associated in colon cancer 1 (MACC1) gene was proven to be a promising biomarker of CC. However, the role and mechanism of MACC1 in CC remain undetermined. Expressions of MACC1 were estimated by qRT-PCR, immunohistochemistry, and Western blot assays in cervical cancer tissues and cells. Three siRNAs were generated to knockdown expressions of MACC1 in CC cells. After knockdown of MACC1 or/and Colivelin treatment, cell migration, invasion, apoptosis, and stemness were evaluated through a series of functional experiments including Transwell, flow cytometry, Hoechst staining, and sphere-formation assays. MACC1 was found to express more highly in CC tissues in comparison with corresponding non-tumor tissues at both mRNA and protein levels. Functionally, the knocking- down of MACC1 significantly repressed migration and invasion, and induced apoptosis of CC cells. Also, knockdown of MACC1 was discovered to suppress sphere-formation of CC cells and downregulate OCT4 and Nanog. It was proved that knockdown of MACC1 had a significant blocking effect on the AKT/STAT3 pathway. In addition, we verified that treatment with the STAT3 activator (Colivelin) had significant reversal effects on the malignant behaviors of CC cells and CC stemness. Our study concluded that MACC1 might be a novel regulator of CC by regulating the AKT/STAT3 pathway to change the migration, invasion, apoptosis, and cancer stemness of CC cells.