Serum PLGF level was lower in women who subsequently developed severe PE early in the second trimester, suggesting its role in prediction of PE.

Preterm birth (PTB) is defined as a birth that occurs before 37 weeks of gestation, which is the leading cause of perinatal morbidity and mortality. 1 The inherent cervical length and strength are two main features of the cervix that determine whether a pregnant woman is at risk for spontaneous PTB. 2 A short cervix identified by transvaginal ultrasound in the second trimester of pregnancy is associated with a significant risk of spontaneous PTB. It is recognized that the measurement of cervical length in the second trimester can identify high-risk women that may benefit from progesterone prophylaxis. 3,4 However, the low sensitivity and positive predictive value have limited the clinical utility of cervical length assessment as a universal screening tool. 5-7 In the first trimester of pregnancy, the presence of the undeveloped lower uterine segment and the variable degree of the curvature of the endocervical canal have generated significant technical challenges for the cervical length to be measured, which

No abstract

Immune activation at the maternal-fetal interface is a main pathogenic factor of preeclampsia (PE). Neutrophils (PMNs) are activated in PE patients, but the mechanism and consequences of PMN activation need to be further explored. Here, we demonstrated that interleukin-32 (IL-32) expression was significantly upregulated in syncytiotrophoblasts (STBs) and that IL-32β was the major isoform with increased expression in the placenta of severe PE (sPE) patients. Furthermore, the level of IL-32 expression in the placenta was correlated with its level in the serum of sPE patients, indicating that IL-32 in the serum is derived mainly from the placenta. Then, in vitro experiments showed that IL-32β could highly activate PMNs and that these IL-32β-activated PMNs were better able to adhere to endothelial cells (HUVECs) and enhance the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) in HUVECs, which could be reversed by preincubation with the NADPH oxidase inhibitor VAS 2870. In addition, we showed that IL-32β mainly activated PMNs by binding to proteinase 3. Finally, IL-32β administration induced a PE-like phenotype in a pregnant mouse model. This study provides evidence of the involvement of IL-32β in the pathogenesis of PE.

This is the first report of prenatal diagnosis performed in families with oculocutaneous albinism type II (OCA2). Also, this report reveals three novel mutations of the P gene.