[Impact and potential mechanism of human α-defensin 1 on low-density lipoprotein oxidation ability of ECV304 cells].

OBJECTIVE: To explore the role and potential mechanism of human α-defensin 1 (HNP-1) on low-density lipoprotein (LDL) oxidation ability of human endothelial cells (EVC304). METHODS: Post incubation with LDL for 3 h, the malondialdehyde (MDA) and protein carbonyl (PCO) were detected in untreated ECV304 (control) and in HNP-1 transfected ECV304 in the presence and absence of siRNA against HNP-1. Flow cytometry and fluorescence microscopy were used to detect the generation of oxygen free radical in the ECV304 which have been pretreated by LDL, LPS and HNP-1, respectively. RESULT: Compared with control group, MDA level was significantly increased in HNP-1 transfected [(4.21 ± 0.03) vs. (3.15 ± 0.02) nmol/mg · pro] or in HNP-1 stimulated ECV304 cells [(14.49 ± 1.10) vs. (9.47 ± 1.18) nmol/mg · pro], which could be significantly downregulated by siRNA [(3.76 ± 0.48) vs. (4.54 ± 0.28) nmol/mg·pro, all P < 0.05]. PCO was also significantly increased in HNP-1 transfected ECV304 cells. The levels of free radical were significantly increased in HNP-1 transfected or HNP-1 stimulated ECV304 cells. CONCLUSION: HNP-1 can enhance the LDL oxidation ability of human endothelial cells via promoting the generation of free radicals.

Comparison of the left and right ventricular size and systolic function of low-risk fetuses in the third trimester: Which is more dominant?

Objective: To quantify fetal cardiovascular parameters utilizing fetal-specific 2D speckle tracking technique and to explore the differences in size and systolic function of the left and right ventricles in low-risk pregnancy. Methods: A prospective cohort study was performed in 453 low-risk single fetuses (28+0-39+6 weeks) to evaluate ventricular size [i.e., end-diastolic length (EDL), end-systolic length (ESL), end-diastolic diameter (ED), end-systolic diameter (ES), end-diastolic area, end-systolic area, end-diastolic volume (EDV), and end-systolic volume (ESV)] and systolic function [i.e., ejection fraction (EF), stroke volume (SV), cardiac output (CO), cardiac output per kilogram (CO/KG), and stroke volume per kilogram (SV/KG)]. Results: This study showed that (1) the reproducibility of the interobserver and intraobserver measurements was good to excellent (ICC 0.626-0.936); (2) with advancing gestation, fetal ventricular size and systolic function increased, whereas right ventricular (RV) EF decreased and left ventricular (LV) EF was not significantly changed; (3) LV length was longer than RV length in diastole (2.24 vs. 1.96 cm, P < 0.001) and systole (1.72 vs. 1.52 cm, P < 0.001); (4) LV ED-S1 and ES-S1 were shorter than the RV ED-S1 and ES-S1 (12.87 vs. 13.43 mm, P < 0.001; 5.09 vs. 5.61 mm, P < 0.001); (5) there were no differences between the LV and RV in EDA or EDV; (6) the mean EDV ratio of right-to-left ventricle was 1.076 (95% CI, 1.038-1.114), and the mean ESV ratio was 1.628 (95% CI, 1.555-1.701); (7) the EF, CO and SV of the LV were greater than the RV (EF: 62.69% vs. 46.09%, P < 0.001; CO: 167.85 vs. 128.69 ml, P < 0.001; SV: 1.18 vs. 0.88 ml, P < 0.001); (8) SV and CO increased with ED-S1 and EDL, but EF was not significantly changed. Conclusion: Low-risk fetal cardiovascular physiology is characterized by a larger RV volume (especially after 32 weeks) and greater LV outputs (EF, CO, SV, SV/KG and CO/KG).

Association between abnormal uterine artery pulsatility index and the risk of fetal congenital heart defects: a hospital-based cohort study.

To explore the associations between high uterine artery pulsatility index (UtA-PI) values and congenital heart disease (CHD) risk and whether they differed between singleton and multiple pregnancies. This hospital-based cohort study involving 52,047 pregnant women who underwent prenatal examinations from 2012 to 2016. Infants born to the included pregnant women were followed until 42 days after birth to identify those with CHDs. Generalized estimating equations were used to estimate the associations of high right UtA-PI (> 95th percentile) values with maternal preeclampsia and fetal CHDs. Logistic regression analyses were conducted using path analysis models to quantify the effect of high right UtA-PI values on fetal CHD risk. A total of 42,552 women and 43,470 infants (147 with CHDs) were included. Preeclampsia risk was associated with a high right UtA-PI in singleton-pregnant women (adjusted PR, 3.01; 95% CI 2.57-3.52). CHD risk was marginally associated with a high right UtA-PI in singleton-pregnant women (adjusted PR, 2.26, 95% CI 1.03-4.95). Considering only two factors, 96.0% of the fetal CHD risk was mediated by preeclampsia in singleton-pregnant women, while 93.8% of the risk was related to a high right UtA-PI in multiple-pregnant women. A high right UtA-PI was marginally associated with an increased fetal CHD risk in singleton-pregnant women and might play an important role in multiple-pregnant women. Further studies are warranted to confirm these findings given the high loss to follow-up rate.