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Background. Hysteroscopy is considered the gold standard for diagnosing intrauterine pathology. Traditional hysteroscopy requires the placement of a vaginal speculum and cervical forceps, which are large in diameter, causing discomfort and pain to the patient and even causing vagal reflexes. Aims. To investigate the impact and clinical value of vaginoscopy versus conventional hysteroscopy on pain, complications, and patient satisfaction in patients with endometrial polyps and to analyse the advantages of clinical application of vaginoscopy examination. Materials and Methods. One hundred and twenty-five patients with endometrial polyps treated in our hospital from May 2021 to December 2021 were selected for this study and divided into 52 cases in the hysteroscopy group and 73 cases in the vaginoscopy group according to the random remainder grouping method. Conventional hysteroscopy was used, and in the vaginoscopy group, vaginoscopy was performed. The impact of pain, complications, patient satisfaction, and clinical value of the two groups was observed and compared. Results. The time taken for the examination varied between the different hysteroscopic methods, with the hysteroscopy group taking the longest time compared to the vaginoscopy group (P < 0.01). The VAS scores immediately after the examination and 30 minutes after the examination were both significantly higher in the hysteroscopy group than in the vaginoscopy group (P < 0.01). The difference in NPY, PGE2, and 5-HT after the pain-causing mediator intervention was significantly better in the vaginoscopy group than in the hysteroscopy group. The difference in the incidence of complications such as abortion syndrome, cervical laceration, uterine perforation, and haemorrhage after treatment was significantly lower in the vaginoscopy group than in the hysteroscopy group. In the vaginoscopy group, the satisfaction rate was 91% significantly higher than that of the hysteroscopy group (P < 0.05). Conclusion. The vaginoscopy technique shortens the examination and treatment time, reduces patient pain, improves patient compliance, reduces the use of preintervention drugs and anaesthetics, and reduces complications. [ABSTRACT FROM AUTHOR]

Endometriosis is a benign, chronic inflammatory disease that commonly occurs in reproductive‐aged women. Epithelial‐mesenchymal transition (EMT) of endometrial epithelial cells plays an important role in the development of endometriosis. Recepteur d'origine nantais (RON), a receptor tyrosine kinase, has been reported to promote EMT and progression in tumours. However, whether and how RON mediates the EMT and endometriosis development is not known. Here, we found that RON activation could improve the migratory and invasive capabilities, change cellular morphologies, and decrease expression of E‐cadherin and increase expression of N‐cadherin in endometrial epithelial cells. Inhibition or knockdown of RON expression suppressed the migration and invasion of endometrial epithelial cells. Our studies also indicated that RON played its part in endometrial epithelial cells through protein kinase B (Akt) and mitogen‐activated protein kinase (MAPK) pathways. Treatment with a RON inhibitor could decrease the number of ectopic lesions in a mouse model of endometriosis and mediate expression of EMT markers in endometriotic lesions. These data suggest that RON contributed to endometriosis development by promoting EMT of endometrial epithelial cells. Therefore, RON may be a new therapeutic target for endometriosis. [ABSTRACT FROM AUTHOR]

Netrin-1 is an extracellular guidance cue of neuronal navigation, mediated through interaction with its main receptors, and is known to be crucial in the development of multiple chronic inflammatory diseases. However, the expression pattern and mechanism of netrin-1 in endometriosis are currently undefined. Here we report that netrin-1 expression peaked in peritoneal macrophages found in endometriosis. Netrin-1 induced angiogenesis in ovarian endometriomas through interaction with CD146 in vascular endothelial cells. Through another receptor, neogenin, netrin-1 promoted neurite growth and sensitization in endometriosis through the up-regulation of MAP4, TAU, and CGRP. Targeted knockdown of neogenin in dorsal root ganglion (DRG) nerve cells compromised its response to netrin-1 through inhibiting phosphorylation of ERK1/2. The inhibition of netrin-1 using a neutralizing antibody reduced vascular and nerve infiltration in rat endometriotic lesions. In summary, our results suggest that netrin-1 is an important factor that promotes neuroangiogenesis in endometriosis. • Netrin-1 is overexpressed in macrophages found in endometriosis. • Netrin-1 promotes neuroangiogenesis, thereby fostering the pathogenesis and development of endometriosis. • Netrin-1 facilitates sensory nerve infiltration and sensitization via its receptor neogenin through the MAPK pathway. [ABSTRACT FROM AUTHOR]

Endometriosis is an estrogen-dependent inflammatory gynecological disease whose pathogenesis is unclear. C-C motif chemokine ligand 18 (CCL18), a chemokine, is involved in several inflammatory diseases. In this study, we aimed to investigate the role of CCL18 in endometriosis and its underlying mechanisms. Human endometrium and peritoneal fluid were obtained from women with and without endometriosis for molecular studies. The expression level of CCL18 in each tissue sample was examined by RNA sequencing analysis, quantitative PCR analysis and immunohistochemistry staining. The effects of CCL18 on cell migration, tube formation and neurite growth were investigated in vitro using primary endometrial cells, human umbilical vein endothelial cells (HUVECs) and dorsal root ganglion (DRG) neurons, respectively. Moreover, the development of endometriosis in mice was studied in vivo by blocking CCL18. CCL18 was shown to be overexpressed in endometrial foci and peritoneal fluid in women with endometriosis and was positively correlated with endometriosis pain. In vitro, CCL18 promoted the migration of ectopic endometrial cells, tube formation of HUVECs, and nerve outgrowth of DRG neurons. More importantly, inhibition of CCL18 significantly suppressed lesion development, angiogenesis, and nerve infiltration in a mouse model of endometriosis. In conclusion, CCL18 may play a role in the progression of endometriosis by increasing endometrial cell migration and promoting neuroangiogenesis.

Rationale: This case report aims to describe the treatment of infected placenta accreta in the uterine horn by transabdominal temporary occlusion of internal iliac arteries., Patient Concerns: A 29-year-old female patient had a history of retained placenta for 28 days after labor induction in the second trimester of pregnancy because of fetal malformation., Diagnoses: Placenta accreta in the uterine horn was diagnosed by 3-dimensional ultrasound and magnetic resonance imaging, and the diagnosis was confirmed during the operation., Interventions: Laparotomy was performed to remove the placenta and repair the uterine defect after temporary occlusion of both internal iliac arteries., Outcomes: Body temperature and inflammatory markers were elevated at admission but returned to normal on the second day after surgery. Normal menstruation resumed approximately 1 month postoperatively. Ultrasound examination showed that the shape of the uterine cavity was normal. No postoperative complications were observed., Lessons: Temporary occlusion of the internal iliac artery can help effectively manage infected placenta accreta in the uterine horn., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

This study aimed to focus on the mechanism of circRNA polyribonucleotide nucleoside transferase 1 (circ-PNPT1)-mediated miR-889-3p/PAK1 on gestational diabetes mellitus (GDM). Placental tissues from normal pregnancy and GDM patients were collected to detect the levels of circ-PNPT1, miR-889-3p, and PAK1. The high glucose-induced human trophoblast cells HTR-8/SVneo were adopted to stimulate the GDM model in vitro (HG group) and were transfected with lentivirus to silence circ-PNPT1 (si-circ-PNPT1 group) and mimic to overexpress miR-889-3p (miR-889-3p group). Cell proliferation, apoptosis, migration, and invasion were detected by CKK-8, flow cytometry, Transwell, and scratch assay, respectively. The results showed that the expressions of circ-PNPT1 and PAK1 in the GDM patients were up-regulated, and miR-889-3p was down-regulated (P< 0.05). Compared with cells in the control group, the circ-PNPT1 and PAK1 in the HG group were up-regulated, and miR-889-3p was down-regulated (P< 0.05). The cell proliferation, migration, and invasion abilities were weakened, and the apoptosis rate increased (P< 0.05). E-cadherin protein was elevated, and the N-cadherin and Vimentin decreased (P< 0.05). Compared with the HG group, the expressions of circ-PNPT1 and PAK1 in the other two groups decreased, and miR-889-3p increased (P< 0.05). The cell proliferation, migration, and invasion were enhanced, and the apoptosis rate decreased (P< 0.05). E-cadherin, N-cadherin, and Vimentin decreased (P< 0.05). There were targeted binding sites for miR-889-3p with circ-PNPT1 and PAK1, indicating circ-PNPT1 promoted HG-induced trophoblast dysfunction through the miR-889-3p/PAK1 axis.

Indian hedgehog (Ihh) signaling regulates endometrial receptivity and is an indispensable mediator of embryonic implantation. Hedgehog signaling is known to regulate autophagy, and aberrant regulation of autophagy is critically implicated in the pathogenesis of endometriosis and adenomyosis. However, potential dysregulation of Ihh signaling and its role in autophagy modulation in these diseases remain obscure. In this study, we found that components of Ihh signaling were significantly decreased, whereas the autophagy marker protein, LC3BII, was significantly increased in endometrial tissues of women with endometriosis or adenomyosis. Inhibition of Ihh signaling with the small-molecule inhibitor GANT61 or Gli1 silencing in primary endometrial stromal cells increased autophagic activity, as measured by LC3 turnover assay and tandem mCherry-eGFP-LC3B fluorescence microscopy. Furthermore, we observed that GANT61 treatment significantly attenuated hydrogen peroxide-induced cell death, whereas disruption of autophagy with chloroquine diminished this effect. Collectively, these findings reveal that Ihh signaling is suppressed in endometrial tissues of patients with endometriosis or adenomyosis. This abnormal decrease may contribute to endometrial autophagy activation, which may promote aberrant survival of endometrial cells in ectopic sites in these two gynecological diseases.

Objective: To investigate the efficiency of uterine arterial embolization in induced labour among pregnant women with placenta previa., Methods: All pregnant women (20 cases) with placenta previa who received induced labour in Taizhou First People's Hospital between 2009 and 2014 were included in this retrospective study. All cases were given rivanol induction combined with uterine arterial embolization and mifepristone.The antepartum and postpartum history were reviewed., Results: 16 cases out of 20 delivered vaginally with small amount of bleeding. The other 4 cases got emergency cesarean delivery because of uncontrolled vaginal bleeding. No case needed hysterectomy.The average interval between the procedure and menstruation recover was 42 days., Conclusions: Uterine arterial embolization improves the efficiency of induced labour and shows advantages to postpartum haemorrhage and prevent infertility. Uterine arterial embolization is recommended as a effective management for pregnancies with placenta previa state.