Objective::To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model.Methods::Pregnant rats ( n=60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups),and were studied on the 17 th, 19 th, and 21 st gestational days (GD) ( n=5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons. Results::A significant difference was found in placenta weight ( F=8.10, P<0.05), fetal rat weight ( F=40.86, P<0.05), fetal rat length ( F=61.61, P<0.05), and fetal rat tail length ( F=55.63, P<0.05) among four groups on the 17 th ,19 th , and 21 st GD.What’s more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant ( F=2.48, P<0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46±0.15 vs. 0.24±0.09, P<0.05), EE (0.46±0.15 vs. 0.17±0.04, P>0.05), and IR (0.46±0.15 vs. 0.22±0.15, P>0.05) groups at 19 th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42±0.05 vs. 0.58±0.12, P<0.05), UCN (0.43±0.01 vs. 0.47±0.16, P>0.05), and WFS1 (0.57±0.07 vs. 0.74±0.12, P>0.05) protein in the EE-IR group was subsided compared to the IR group at 17 th GD. Conclusion::Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.

Objective::To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model.Methods::Pregnant rats ( n=60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups),and were studied on the 17 th, 19 th, and 21 st gestational days (GD) ( n=5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons. Results::A significant difference was found in placenta weight ( F=8.10, P<0.05), fetal rat weight ( F=40.86, P<0.05), fetal rat length ( F=61.61, P<0.05), and fetal rat tail length ( F=55.63, P<0.05) among four groups on the 17 th ,19 th , and 21 st GD.What’s more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant ( F=2.48, P<0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46±0.15 vs. 0.24±0.09, P<0.05), EE (0.46±0.15 vs. 0.17±0.04, P>0.05), and IR (0.46±0.15 vs. 0.22±0.15, P>0.05) groups at 19 th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42±0.05 vs. 0.58±0.12, P<0.05), UCN (0.43±0.01 vs. 0.47±0.16, P>0.05), and WFS1 (0.57±0.07 vs. 0.74±0.12, P>0.05) protein in the EE-IR group was subsided compared to the IR group at 17 th GD. Conclusion::Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.

Objective:To investigate the safety, efficacy and application indication of intra-operative cell salvage (IOCS) in cesarean section.Methods:A total of 1 265 pregnant women who received IOCS blood transfusion during cesarean section in 11 tertiary A hospitals from August 2016 to January 2019 were collected and divided into <1 500 ml group (796 cases) and ≥1 500 ml group (469 cases) according to the amount of blood loss during cesarean section. The general clinical data, ultrasonic imaging data, perinatal and puerperium indicators were analyzed retrospectively. The risk factors of intraoperative blood loss ≥1 500 mL using IOCS transfusion were analyzed by logistic multivariate regression.Results:(1) A total of 848 001 ml of blood was recovered and a total of 418 649 ml of blood was transfused in 1 265 pregnant women who received IOCS transfusions, which was equivalent to 23 258 U red blood cell suspension, greatly saving medical resources. The intraoperative blood loss in <1 500 ml group and ≥1 500 ml group was 800 ml (300-1 453 ml) and 2 335 ml (1 500-20 000 ml), respectively. No amniotic fluid embolism, severe adverse reactions, shock and death occurred in the two groups. (3) Multivariate regression analysis showed that age ≥35 years ( OR=1.5, 95% CI: 1.1-1.9), prenatal hemoglobin level <110 g/L ( OR=1.7, 95% CI: 1.3-2.2), history of uterine surgery ( OR=1.8, 95% CI: 1.3-2.6), placenta previa ( OR=1.9, 95% CI: 1.1-3.1), placenta accreta ( OR=2.6, 95% CI: 1.8-3.9), blood pool in the placenta ( OR=1.6, 95% CI: 1.1-2.3), abnormal posterior placenta muscle wall ( OR=1.8, 95% CI: 1.2-2.6), placenta projecting to the anterior uterine wall ( OR=3.0, 95% CI: 1.3-7.0) were risk factors for blood loss ≥1 500 ml in obstetric transfusion using IOCS technique, with statistical significance (all P<0.05). Conclusion:IOCS is safe and effective in cesarean section, which could save the medical resources and reduces medical expenses, however, it is necessary to strictly master the application indication.

Objective To investigate the effect of A53T α-synuclein on the expression of type 2 vesicular monoamine transporter (VMAT2) in neuronblastoma SH-SY5Y cells stably expressing A53T α-synuclein.Methods A53T α-synuclein eukaryotic plasmid was constructed by transfection of the SH-SY5Y cells using LipofectamineTM 2000, and a stable transfected monoclonal cell line was selected by G418.Western blotting and DCFH-DA staining were used to detect the effect of A53T α-synuclein overexpression on the expression of VMAT2 protein and level of reactive oxygen species (ROS).Results Western blotting showed that compared with the control group, the expression of VMAT2 protein was significantly decreased, and DCFH-DA staining showed that DCF signal was significantly increased (507.3 ±7.1) than that in the cell line stably expressing A53T α-synuclein (410.7 ±10.5) (P <0.05).Conclusions A53T α-synuclein can increase the intracellular ROS level by inhibiting the expression of VMAT2, thereby playing an important role in the pathogenesis of Parkinson′s disease.