Trophoblastic mitochondrial DNA induces endothelial dysfunction and NLRP3 inflammasome activation: Implications for preeclampsia.

Aims: Preeclampsia (PE) is characterised by systemic vascular endothelium dysfunction. Circulating trophoblastic secretions contribute to endothelial dysfunction, resulting in PE; however, the underlying mechanisms remain unclear. Herein, we aimed to determine the potential correlation between the release of trophoblastic mitochondrial deoxyribonucleic acid (DNA) (mtDNA) and endothelium damage in PE.

Low-dose aspirin inhibits trophoblast cell apoptosis by activating the CREB/Bcl-2 pathway in pre-eclampsia.

Excessive apoptosis of placental trophoblast cells is considered a major cause of pre-eclampsia (PE) pathogenesis. Phosphorylation of the widely expressed cAMP response element binding protein (CREB) regulates apoptosis and may be involved in PE incidence. Low-dose aspirin (LDA) is an effective approach for preventing PE with unclear mechanisms.

Surface electromyography of the pelvic floor at 6-8 weeks following delivery: a comparison of different modes of delivery.

Introduction And Hypothesis: The objective of this study was to compare the impact of different modes of delivery, especially forceps delivery (FD), on pelvic floor muscles (PFMs) through vaginal surface electromyography (sEMG) in primiparous women at early (6-8 weeks) postpartum.

Methods: A total of 1259 primiparous women with full-term singleton births were included in this cross-sectional study. Of these, 98 were delivered by forceps, 865 underwent spontaneous vaginal delivery (SD) and 296 underwent elective cesarean delivery (CD).

Osmotic water permeability diversification in primary trophoblast cultures from aquaporin 1-deficient pregnant mice.

Aim: Aquaporins (AQP) are water channel proteins, and some play an important role in maternal-fetal fluid exchange. The present study aimed to measure the osmotic water permeability in primary cultures of trophoblast cells from AQP1-deficient (AQP1(-/-) ) pregnant mice and to define the quantitative role of AQP1 in water transport across the trophoblast plasma membrane.

Material And Methods: Trophoblast cells were obtained from placental tissue cell culture of AQP1(-/-) pregnant mice and were characterized by cytokeratin 7 immunostaining.

Pregnant phenotype in aquaporin 8-deficient mice.

Aim: Aquaporin 8 (AQP8) is expressed within the female reproductive system but its physiological function reminds to be elucidated. This study investigates the role of AQP8 during pregnancy using AQP8-knockout (AQP8-KO) mice.

Methods: Homozygous AQP8-KO mice were mated, and the conception rate was recorded.

Maternal-fetal fluid balance and aquaporins: from molecule to physiology.

Maternal-fetal fluid balance is critical during pregnancy, and amniotic fluid is essential for fetal growth and development. The placenta plays a key role in a successful pregnancy as the interface between the mother and her fetus. Aquaporins (AQPs) form specific water channels that allow the rapid transcellular movement of water in response to osmotic/hydrostatic pressure gradients.

[Clinical outcomes and characteristics of concurrent eclampsia and hemolysis, elevated liver enzymes, and low platelets syndrome].

Objective: the purpose was to describe the outcomes and characteristics of the obstetric patients with concurrent eclampsia and hemolysis, elevated liver enzymes, and low platelets syndrome (HELLP) syndrome.

Methods: we retrospectively collected the materials between December 1999 and December 2008 in Obstetric Critical Care Center of Guangzhou. There were 76 patients in rolled then they were divided into two groups according to with or without HELLP syndrome.

[Correlation between sleep apnea hypopnea syndrome and preeclampsia and the possible pathogenesis of preeclampsia].

Objective: To investigate the relationship between sleep apnea-hypopnea syndrome (SAHS) and preeclampsia and the possible pathogenesis of the latter.

Methods: Twenty-five healthy pregnant women, 43 pregnant women with preeclampsia, and 27 with preeclampsia complicated by SAHS were enrolled in this study. Apnea-hypopnea index (AHI) and the lowest arterial oxygen saturation (LSaO2) were measured through a 7-hour polysomnography (PSG), and the maternal age, gestational age, body mass index and 24-hour urine protein were recorded.

[Clinical application of the Epworth sleepiness score in pregnant women with obstructive sleep apnea-hypopnea syndrome].

Objective: To provide a convenient method for screening obstructive sleep apnea-hypopnea syndrome (OSAHS) in pregnant women.

Methods: Seventy-eight pregnant women with suspected OSAHS were calculated for the EP index using Epworth sleepiness score (ESS) with also measurement of the neck circumference (NC) and body mass index (BMI). The apnea/hypopnea index (AHI) was calculated and the lowest SaO(2) (LSaO(2)) measured through a 7-h polysomnography (PSG).

[Expression of aquaporin-1 in human oligohydramnios placenta and fetal membranes].

Objective: To detect aquaporin-1 mRNA (AQP1) expression in human oligohydramnios placenta and fetal membranes.

Methods: Placenta and fetal membranes samples were obtained from 5 women with oligohydramnios and 5 with normal amniotic fluid volume. AQP-1 mRNA expression in the tissue samples was detected by semi-quantitative RT-PCR.

[Relationship between changes of endogenous nitric oxide synthase inhibitor and hydrolase and initiation of pre-eclampsia].

Objective: To investigate the role of dimethylarginine dimethylaminohydrolase-2 (DDAH-2)/asymmetric dimethylarginine (ADMA) in pathophiology of preeclampsia by detecting expression of DDAH-2 in placenta and serum plasma ADMA.

Methods: From Jan. 2004 to Jan.

[Expression of aquaporin 1 in human placenta and fetal membranes].

Objective: To detect aquaporin1 (AQP1) expression in normal human placenta and fetal membranes.

Methods: Human placenta and fetal membrane specimens were collected from 5 pregnant women with intact membranes undergoing elective cesarean sections at term. Expression and localization of AQP1 was detected by RT-PCR, Western blotting and immunohistochemistry.