An Evaluation of the Effects of Gestational Weight Gain on the Early Postpartum Pelvic Floor Using Transperineal Ultrasound.

OBJECTIVES: We herein evaluated the effects of gestational weight gain (GWG) on postpartum pelvic floor function using transperineal ultrasound (TPUS). METHODS: We analyzed retrospectively the data from 228 primiparous women with singleton pregnancies who were evaluated for postpartum pelvic floor function between February 2022 and October 2022. According to the 2009 Institute of Medicine guidelines regarding GWG, subjects were separated into three groups: inadequate GWG, recommended GWG, and excessive GWG. All underwent TPUS 6-10 weeks postpartum to assess bladder neck descent between rest and Valsalva (BND), retrovesical angle at Valsalva (RVA), urethral rotation angle between rest and Valsalva (URA), the area of levator hiatus at Valsalva (LHA), and abnormal pelvic floor function. Univariate and multivariate regression analyses were applied to explore the association measures between GWG and the pelvic floor. A P-value <.05 was considered statistically significant. RESULTS: Of the 228 primiparous women, 113 (49.6%) showed excessive GWG. Univariate analysis revealed that there were no statistical differences in ultrasonic parameters of the pelvic floor among the three groups (P > .05). After adjusting for potential confounders and using the recommended GWG group as a reference group, inadequate GWG was significantly associated with BND ≥25 mm (OR = 0.36, 95% CI = 0.14-0.93), and excessive GWG was significantly associated with uterine prolapse (OR = 2.79, 95% CI = 1.13-6.92). CONCLUSIONS: GWG was associated with the ultrasonic parameters of the female pelvic floor in the early postpartum period.

Endosulfan induces endothelial inflammation and dysfunction via IRE1α/NF-κB signaling pathway.

Cardiovascular diseases are related to vascular endothelial cell injury; our previous studies showed that endosulfan could cause hypercoagulation of blood by inducing endothelial cell injury. To clarify the mechanism of it, we treated human umbilical vein endothelial cells (HUVECs) with 0, 1, 5, and 10 µg/mL endosulfan, while in the inhibition groups, reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC, 3 mmol) and endoplasmic reticulum (ER) stress inhibitor (STF-083010, 10 µmol) were incubated prior to endosulfan. The results showed that endosulfan could induce inflammatory response and dysfunction by increasing the release of inflammatory cytokines such as interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) and endothelin-1 (ET-1), and inducing ROS production in HUVECs. We also found that endosulfan could cause ER damage, remarkably increase the expressions of inositol-requiring enzyme 1α (IRE1α), phosphorylated IRE1α (p-IRE1α), GRP78, XBP1, nuclear factor-kappa B (NF-κB), and phosphorylated NF-κB (p-NF-κB) in HUVECs. The presence of NAC antagonized the ROS production, expressions of IRE1α and p-IRE1α; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-κB, and p-NF-κB and attenuate IL-1ß, IL-6, TNF-α, VCAM-1, and ET-1 release induced by endosulfan. These results demonstrated that endosulfan-induced endothelial inflammation and dysfunction through the IRE1α/NF-κB signaling pathway may be triggered by oxidative stress. The study provided experimental basis for the correlation between environmental pollutants (endosulfan) and cardiovascular diseases.

BDE-209 induces autophagy and apoptosis via IRE1α/Akt/mTOR signaling pathway in human umbilical vein endothelial cells.

Recently, the essentiality and fatalness of cardiovascular diseases is attracting much attention. Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants, which could induce the toxic effect and have been implicated in the occurrence and development of cardiovascular diseases. However, it is unclear how autophagy and apoptosis induced by BDE-209 in endothelial cells are regulated. The aim of the present study was to investigate the effects of BDE-209 on human umbilical vein endothelial cells (HUVECs) and elucidate the mechanisms involved. HUVECs were treated with a wide range concentration of BDE-209 for 24 h. The appearance of autophagy was tested by the testing index such as outcomes of monodansylcadaverine (MDC) staining and lysotracker staining, observation of autophagosomes and conversion between autophagy marker light chain 3 (LC3)-I and LC3-II. Besides, the apoptotic cell rate was detected with flow cytometry. In addition, BDE-209 induced endoplasmic reticulum (ER) stress was detected by transmission electron microscopy (TEM). Our data suggest that the exposure of BDE-209 could induce autophagy, which was confirmed by MDC staining, transmission electron microscopy observation, lysotracker staining and LC3-I/LC3-II conversion. Besides, the ER stress-related inositol-requiring enzyme 1α (IRE1α)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway could be activated by reactive oxygen species (ROS) to regulate autophagy. Moreover, the apoptosis of endothelial cells was alleviated when autophagy was blocked by 3-Methyladenine (3-MA). The results demonstrated that BDE-209 could induce the production of ROS and ER stress, activate autophagy through IRE1α/AKT/mTOR signaling pathway and ultimately induce apoptosis of vascular endothelial cells. These findings indicate that exposure to PBDE is possible to be a potential risk factor for cardiovascular diseases.