Evaluation of the use versus nonuse of urinary catheterization during laparoscopic adnexal surgery: A randomized controlled trial.

We conducted a randomized controlled trial to assess the feasibility and safety of performing gynecological single-port transumbilical laparoscopic-assisted adnexal surgery without urethral catheterization in a day surgery setting. A total of 153 patients with adnexal disease were enrolled in this prospective randomized controlled trial (RCT). All subjects performed single-port transumbilical laparoscopic-assisted adnexal surgery between March 2021 and July 2022 in a day surgery center. After completion of the baseline survey, participants were randomized into one of three groups. Participants were randomized into one of three groups: uncatheterized (n = 51), intermittent catheterized (n = 51), or indwelling catheterized (n = 51). The primary outcomes were the incidence of lower urinary tract symptoms (LUTS) and microscopic hematuria, and the secondary outcomes included the incidence of urinary tract infection (UTI), the incidence of urinary retention, the incidence of bladder injury, the time till first urination, the time till first ambulation, the time till first exhaust, the time till first feeding and Kolcaba comfort score. The incidence of postoperative LUTS in the uncatheterized group (17.65%) was lower than that in the intermittent catheterized group (52.94%) and the indwelling catheterized group (84.31%), and there was significant difference between the two catheterized groups (P < 0.001). In the patients without vaginal manipulation, the incidence of microscopic hematuria in the uncatheterized group (0%) was lower than that in the intermittent catheterized group (37.50%) and the indwelling catheterized group (38.89%) (P < 0.05). There were no significant differences in the first urination time, first ambulation time, first exhaust time, first feeding time, and comfort score among the three groups (P > 0.05). Moreover, no urinary retention, UTI and bladder injury were recorded in the three groups. Gynecological single-port laparoscopic adnexal surgery without urinary catheter is safe and feasible in a day surgery ward, which can reduce the incidence of postoperative LUTS and microscopic hematuria.

A case control study of vNOTES hysterectomy with the da Vinci surgical system and conventional vNOTES hysterectomy.

The aim of the case control study was to compare surgical outcomes of transvaginal natural orifice transluminal endoscopic surgery (vNOTES) hysterectomy with the da Vinci surgical system (dVSS) and conventional vNOTES. A case control study was performed on 25 cases in our hospital. Patients (n = 8) who underwent vNOTES hysterectomy with dVSS were selected to compare with the control group (n = 17) consisted of patients who underwent conventional vNOTES. Patients in the 2 groups underwent different operations respectively, and no case was transferred to transabdominal laparoscopy. In the conventional vNOTES group, 1 patient happened intraoperative hemorrhage of about 1000 mL, and was treated with blood transfusion, and the other one of vNOTES hysterectomy with dVSS had poor incision healing within 1 month after surgery. The other patients had no intraoperative and postoperative complications. The difference of pain scores on the first day (P = .006) and the third day (P = .045) after the 2 surgical methods differed significantly. No statistical differences were observed in operation time, median hospital stay, blood loss, decreased hemoglobin 3 days after surgery, and postoperative white blood cell count. vNOTES hysterectomy with dVSS is safe and feasible, and can achieve the same effect as the conventional vNOTES hysterectomy. And this method may alleviate the pain of patients.

The maternal hair metabolome is capable of discriminating intrahepatic cholestasis of pregnancy from uncomplicated pregnancy.

Introduction: Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific liver disease associated with elevated bile acids in the blood. Diagnosis typically only occurs after the manifestation of clinical symptoms and the metabolic mechanisms underlying its development remain unclear. The aim of this study was to investigate potential specific metabolites and the underlying metabolic changes occurring during the development of ICP in the maternal plasma and hair metabolomes of women diagnosed with either ICP or having a healthy pregnancy. Methods: A total of 35 Chinese women with ICP and 42 healthy pregnancies were enrolled in our study. Plasma and hair samples, total bile acid levels (TBA), alanine transaminase levels (ALT), aspartate aminotransferase levels (AST), and additional clinical information were collected during the third trimester. Metabolites from maternal plasma and hair segments collected pre-conception and analyzed using gas chromatography-mass spectrometry (GC-MS). Results: Three plasma metabolites (p < 0.05, q < 0.38) and 21 hair metabolites (p < 0.05, q < 0.05) were significantly different between ICP and healthy pregnancies. A combination of the eight most significant hair metabolites in a multivariate receiver operating characteristic curve model showed the best area under the curve (AUC) was 0.885, whereas the highest AUC using metabolites from plasma samples was only 0.74. Metabolic pathway analysis revealed 32 pathways were significantly (p and q values < 0.05) affected in the hair samples of patients with ICP. Pathways associated with glutathione metabolism and ABC transporters were affected. No metabolic pathways were significantly affected in plasma. Discussion: Overall, this study showed that the hair metabolome could be more useful than the plasma metabolome for distinguishing ICP from normal pregnancy.

Exposure to higher concentrations of exogenous ELABELA causes HTR-8/SVneo trophoblast cell dysfunction: A possible pathogenesis of pre-eclampsia.

Pre-eclampsia (PE) is a multi-system disorder of pregnancy which constitute one of the leading causes of maternal and perinatal mortality worldwide. Dysfunction of trophoblast cells have been play an a significant role in the development and progression of PE. ELABELA (ELA), an endogenous apelin receptor (APJ) ligand, is a hormone secreted by the placenta into circulation, we previously identified ELA and its cognate apelin receptor (APJ) as proteins that are differentially expressed in the placentas of humans with PE. However, a fact known to few about the potential regulatory effects of ELA on the functions of trophoblast cells. In this study, our experiments showed that exogenous ELA did not effectively affect the proliferation and apoptosis of HTR-8/SVneo cells in higher concentrations but inhibited the invasion and migration capabilities. Studies have shown that the epithelial-mesenchymal transition (EMT) event of trophoblast cells is abnormal through regulate the P13K/AKT pathway in PE. First we confirmed APJ expression in HTR-8/SVneo cells and ELA suppressed P13K/AKT signalling pathway-related factors (AKT, phospho (p)-AKT) phosphorylation in HTR-8/SVneo cells in a concentration-dependent manner. Next, we found that treatment with higher concentrations of ELA or the P13K inhibitor LY294002 significantly increased the expression of ß-catenin which is the classical epithelial marker relative to the control group. Moreover, treatment with both LY294002 and ELA more strongly affected the ß-catenin expression and the HTR8/SVneo cells invasion and migration. These results demonstrate that ELA inhibits trophoblast cell functions by altering the ß-catenin expression get though the PI3K/AKT signalling pathway in PE. Thus, this result might provide a new therapeutic target for the treatment of PE.

How many missed abortions are caused by embryonic chromosomal abnormalities and what are their risk factors?

Introduction: Though embryonic chromosome abnormalities have been reported to be the most common cause of missed abortions, previous studies have mainly focused on embryonic chromosome abnormalities of missed abortions, with very few studies reporting that of non-missed abortion. Without chromosome studies of normal abortion samples, it is impossible to determine the risk factors of embryo chromosome abnormalities and missed abortion. This study aimed to investigate the maternal and embryonic chromosome characteristics of missed and non-missed abortion, to clarify the questions that how many missed abortions are caused by embryonic chromosomal abnormalities and what are their risk factors. Material and methods: This study was conducted on 131 women with missed or non-missed abortion from the Longitudinal Missed Abortion Study (LoMAS). Logistic regression analysis was used to identify the association between maternal covariates and embryonic chromosomal abnormalities and missed abortions. Data on the characteristics of women with abortions were collected. Results: The embryonic chromosome abnormality rate was only 3.9% in non-missed abortion embryos, while it was 64.8% in missed-abortion embryos. Assisted reproductive technology and prior missed abortions increased the risk of embryonic chromosome abnormalities by 1.637 (95% CI: 1.573, 4.346. p = 0.010) and 3.111 (95% CI: 1.809, 7.439. (p < 0.001) times, respectively. In addition, as the age increased by 1 year, the risk of embryonic chromosome abnormality increased by 14.4% (OR: 1.144, 95% CI: 1.030, 1.272. p = 0.012). Moreover, advanced age may lead to different distributions of chromosomal abnormality types. Conclusion: Nearly two-thirds of missed abortions are caused by embryonic chromosomal abnormalities. Moreover, advanced age, assisted reproductive technology, and prior missed abortions increase the risk of embryonic chromosomal abnormalities.

The prevalence and associated factors of metabolic syndrome in Chinese aging population.

Metabolic syndrome (MetS) is hitting high notes in the aging society in China. However, the prevalence and associated factors in Chinese aging population lack clarity to some extent. In the present study, we projected to inquire into the prevalence of MetS and its associated factors by analyzing datasets downloaded from the China Health and Retirement Longitudinal Study (CHARLS). Data comprising age, gender, socioeconomic status, lifestyle and health behaviors as well as blood biomarkers were subjected to descriptive statistics followed by univariate logistic regression and multivariate logistic regression. The overall prevalence of MetS was 33.38% (95% CI 32.42-34.34%). With age augments, prevalence increased during 40-70 years, while declined in participants aged 70 years above. Females had 2.94 times of risks (95% CI 2.55-3.39, P < 0.001). Marital status and alcohol consumption contributed nothing to the suffering of MetS. Participants with GDP per capita > 10,000 RMB and a non-agricultural hukou sustained higher risks than other participants (P < 0.05). Participants under education of middle school suffered 1.16 times of risks than other level of education (95% CI 1.01-1.34, P < 0.05). Smokers, participants with high low-density lipoprotein (LDL) or hyperuricemia or high glycosylated hemoglobin HbA1c sustained increased risks (P < 0.05). In Chinese aging population, with the augment of age, the prevalence ascended in men, while descended in women and was interfered by socioeconomic status, lifestyle and health behaviors as well as blood biomarkers, but not marital status and alcohol consumption.

Maternal dietary patterns and risk of gestational diabetes mellitus in twin pregnancies: a longitudinal twin pregnancies birth cohort study.

BACKGROUND: Gestational diabetes mellitus (GDM) is correlated with an increased risk of adverse perinatal outcomes for both the mother and offspring. Previous research has reported correlations between maternal dietary patterns and GDM, but such evidence for twin pregnancies is lacking. This study aimed to identify maternal dietary patterns in the second trimester and investigate their relationships with the risk of GDM among women who were pregnant with twins in China. METHODS: A longitudinal twin pregnancies birth cohort study of women who were pregnant with twins in China was conducted. Maternal dietary intake in the second trimester was recorded by using a food frequency questionnaire prior to the diagnosis of GDM among participants from the prospective twin pregnancies birth cohort in Chongqing City. GDM was diagnosed with a 75 g 2-h oral glucose tolerance test at 23-26 weeks of gestation. Dietary patterns were identified by principal components analysis, and the correlations between dietary pattern and GDM were examined using multivariable logistic regression analyses. RESULTS: Of the 324 participants, 101 (31.2%) were diagnosed with GDM. Four dietary patterns were identified: a vegetable-based pattern, a poultry-and-fruit-based pattern, a sweet-based pattern and a plant-protein-based pattern. Multivariate analysis showed that none of the dietary patterns were correlated with the risk of GDM among women who were pregnant with twins, but the sweet-based dietary pattern, which was associated with a higher GDM risk for quartile 4 versus quartile 1 (OR 2.69; 95% CI: 1.09, 6.66) among non-overweight women (prepregnancy BMI < 24.0). CONCLUSION: Dietary patterns were not correlated with later GDM risk among women who were pregnant with twins in western China, whereas a high intake of sweets was associated with a higher risk for GDM among women who were not overweight prior to pregnancy. TRIAL REGISTRATION: ChiCTR-OOC-16008203. Retrospectively registered on 1 April 2016.

Dysregulated expression of ACTN4 contributes to endothelial cell injury via the activation of the p38-MAPK/p53 apoptosis pathway in preeclampsia.

Preeclampsia (PE) is a hypertensive disease associated with increased endothelial cell dysfunction caused by systemic oxidative stress. Alpha-actinin-4 (ACTN4) is a member of the α-actinin family of actin crosslinking proteins that are upregulated in several types of cancer. However, its role in PE remains unclear. In this study, we found that ACTN4 was localized in placenta vascular endothelial cells (ECs), and its expression was downregulated in primary human umbilical vein endothelial cells (HUVECs) from severe preeclamptic patients compared to that in HUVECs from normotensive pregnant women. ACTN4 expression was also decreased in normotensive HUVECs treated with H2O2. Downregulation of ACTN4 by siRNA or H2O2 treatment promoted normotensive HUVEC apoptosis and increased p38-MAPK phosphorylation along with elevated levels of p53 phosphorylation, caspase cascade proteins, and bax and repressed expression of bcl-2. Conversely, upregulation of ACTN4 in PE HUVECs significantly inhibited apoptosis and decreased p38-MAPK phosphorylation compared to that of the PE HUVEC controls. In addition, overexpression of ACTN4 in normotensive HUVECs attenuated H2O2 treatment-induced apoptosis with decreased p53 phosphorylation, caspase cascade, and bax expression levels and increased expression of bcl-2 compared to that of only H2O2 treatment. Moreover, the suppression of ACTN4 induced apoptosis, which could be blocked by the p38-MAPK inhibitor SB202190. Collectively, these results demonstrate that dysregulated ACTN4 expression may be associated with PE due to its effects on endothelial cell apoptosis via the p38-MAPK/p53 apoptosis pathway.

Hypoxia-induced Downregulation of SRC-3 Suppresses Trophoblastic Invasion and Migration Through Inhibition of the AKT/mTOR Pathway: Implications for the Pathogenesis of Preeclampsia.

Preeclampsia (PE) is characterized by poor placentation, consequent on aberrant extravillous trophoblast (EVT) cell function during placental development. The SRC family of proteins is important during pregnancy, especially SRC-3, which regulates placental morphogenesis and embryo survival. Although SRC-3 expression in mouse trophoblast giant cells has been documented, its role in the functional regulation of extravillous trophoblasts and the development of PE remains unknown. This study found that SRC-3 expression was significantly lower in placentas from PE pregnancies as compared to uncomplicated pregnancies. Additionally, both CoCl2-mimicked hypoxia and suppression of endogenous SRC-3 expression by lentivirus short hairpin RNA attenuated the migration and invasion abilities of HTR-8/SVneo cells. Moreover, we demonstrated that SRC-3 physically interacts with AKT to regulate the migration and invasion of HTR-8 cells, via the AKT/mTOR pathway. We also found that the inhibition of HTR-8 cell migration and invasion by CoCl2-mimicked hypoxia was through the SRC-3/AKT/mTOR axis. Our findings indicate that, in early gestation, accumulation of HIF-1α inhibits the expression of SRC-3, which impairs extravillous trophoblastic invasion and migration by directly interacting with AKT. This potentially leads to insufficient uterine spiral artery remodeling and placental hypoperfusion, and thus the development of PE.

Interleukin-27 Inhibits Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition in Preeclampsia.

Preeclampsia (PE) is a pregnancy-specific disorder representing a major cause of maternal and perinatal morbidity and mortality. Invasive and migratory phenotypes are acquired by trophoblasts through the process of epithelial-mesenchymal transition (EMT). Studies have shown that trophoblast EMT events are dysregulated in PE and play an important role in its development. Dysregulation of interleukin (IL)-27 and IL-27R (T-cell cytokine receptor (TCCR)/WSX -1) is relevant to PE. In this study, our results demonstrated that IL-27 did not significantly affect the proliferation and apoptosis of HTR -8/SVneo trophoblast cells, while it did significantly inhibit trophoblast invasion and migration. The expression of EMT-related proteins in HTR-8/SVneo cells and extravillous explants was detected after treatment with IL-27. Expression of epithelial markers was increased, and mesenchymal marker expression was reduced. Furthermore, we found that IL-27 could induce significant phosphorylation of Signal Transducer and Activator of Transcription 1 (STAT1) and Signal Transducer and Activator of Transcription 3 (STAT3) in a time-dependent manner in HTR-8/SVneo cells. Selective inhibitors of STAT1 (STAT1 siRNA) and STAT3 (STAT3 siRNA) were used to determine whether both STAT1 and STAT3 are required for IL-27-mediated inhibition of EMT. STAT1 inhibition in IL-27-treated cells attenuated the IL-27 effect, while the inhibition of STAT3 activation had no effect on the development of the epithelial phenotype. These results demonstrate that IL-27 may inhibit trophoblast cell migration and invasion by affecting the EMT process through an STAT1-dominant pathway in PE.

Dysregulated Expression of RPS4Y1 (Ribosomal Protein S4, Y-Linked 1) Impairs STAT3 (Signal Transducer and Activator of Transcription 3) Signaling to Suppress Trophoblast Cell Migration and Invasion in Preeclampsia.

Normal placentation and a successful pregnancy depend on appropriate trophoblast cell migration and invasion. Inadequate trophoblast invasion and impaired spiral artery remodeling may lead to pregnancy-related disorders, such as preeclampsia. RPS4Y1 (ribosomal protein S4, Y-linked 1) is a member of the S4E family of ribosomal proteins. In this study, we found that RPS4Y1 levels were upregulated in placental samples collected from preeclamptic patients, when compared with the normotensive pregnant women. In vitro, inhibition of RPS4Y1 induced trophoblast cell invasion, promoted placental explant outgrowth, and increased STAT3 (signal transducer and activator of transcription 3) phosphorylation along with elevated expression of N-cadherin and vimentin. Conversely, overexpression of RPS4Y1 results in reduced trophoblast cell invasion and decreased STAT3 phosphorylation. In addition, the suppression of RPS4Y1 promotes trophoblast cell invasion, which could be abolished by the STAT3 knockdown. Meanwhile, we observed reductions of STAT3 phosphorylation expression in preeclampsia patients. Collectively, these results demonstrate that the level of RPS4Y1 expression may be associated with preeclampsia by affecting trophoblast cell migration and invasion via the STAT3/epithelial-mesenchymal transition pathway.

IL-27 induces a pro-inflammatory response in human fetal membranes mediating preterm birth.

Inflammation at the maternal-fetal interface has been shown to be involved in the pathogenesis of preterm birth. Interleukin 27 (IL-27), a heterodimeric cytokine, is known to mediate an inflammatory response in some pregnancy complications. In this study, we aimed to determine whether IL-27 could induce an inflammatory reaction at the maternal-fetal interface that would mediate the onset of preterm birth. We found elevated expression of IL-27 in human peripheral serum and elevated expression of its specific receptor (wsx-1) on fetal membranes in cases of preterm birth. Moreover, the release of inflammatory markers (CXCL10, IFN-γ, MCP-1, IL-6, IL-1ß and TNF-α), especially CXCL10, was markedly augmented upon stimulation of IL-27 in the fetal membranes. Additionally, IL-27 and IFN-γ cooperated to amplify the expression of CXCL10 in the fetal membranes. Moreover, the production of CXCL10 was increased in IL-27-treated fetal membrane through JNK, PI3K or Erk signaling pathways. Finally, MMP2 and MMP9 were activated by IL-27 in human fetal membranes, which may be related to the onset of preterm premature rupture of membranes (pPROM). In conclusion, for the first time, we reported that the aberrant expression of IL-27 could mediate an excessive inflammatory response in fetal membranes through the JNK, PI3K or Erk signaling pathways, which contributes to preterm birth.