Background This study aimed to evaluate the management of asymptomatic intrauterine lesions detected by ultrasonography. Methods Patients who underwent diagnostic hysteroscopy for asymptomatic lesions, including pre- and post-menopausal endometrial polyps, post-menopausal endometrial thickening (ET ≥5 mm) and reduplicative endometrial heterogeneity detected by transvaginal ultrasonography (TVUS), were recruited for this study. Results In the 792 recruited patients, the symptom-free focal masses within the uterine cavity detected by TVUS included 558 patients with pre- or post-menopausal endometrial polyps and 234 patients with postmenopausal endometrial thickening. No pre-menopausal patient presented with carcinoma. The polyp diameter (PD) was not identified as an independent risk factor for malignancy in this study. A significant difference ( P = 0.036, < 0.05) in both benign and malignant endometrial lesions was observed between two groups of post-menopausal women stratified using an endometrial thickness cut-off of ≥11 mm. The TVUS was highly sensitive (94%) for pre-menopausal polyps. This technique had a specificity and positive predictive value of 84.4 and 92.7%, respectively, for postmenopausal polyps. The TVUS was clearly valuable for ruling out polyps, as indicated by a negative likelihood ratio (LR-) of 0.087. Among postmenopausal women with endometrial thickening, the area under the receiver operating characteristic curve was 0.828 ( P < 0.001). An ET cut-off value of 12.5 mm yielded a sensitivity of 72.7% and specificity of 86%. Conclusion We recommend follow-up alone for women with asymptomatic uterine polyps, particularly those who are pre-menopausal. Additionally, gynaecologists should consider risk factors such as age, obesity, polycystic ovarian syndrome, and diabetes. Prospective long-term follow-up studies should be conducted after hysteroscopic polypectomy to evaluate the recurrence rate of endometrial lesions.

Background: Endometriosis is a benign gynecologic disease that causes chronic pelvic pain, dysmenorrhea and infertility and shares several characteristics with malignant tumors, afflicting women of reproductive age. Hexokinase 2 (HK2) plays an essential role as the first rate-limiting enzyme in the metabolic glycolysis pathway, and its abnormal elevation in tumors is associated with tumor genesis and metastasis. However, the expression and role of HK2 in endometriosis remain unclear. Methods: We sequenced the primary endometrial stromal cells from patients with endometrioma and utilized immunohistochemistry, quantitative real-time PCR and western blot to determine the expression of HK2. Then wound healing assays, cell invasion assays, cell proliferation assays were performed to explore the functions of HK2 in endometrial stromal cells. Furthermore, mice models of endometriosis were used to observe the effects of HK2 inhibitors in vivo. Lastly, glycolysis metabolism detection and transcriptome sequencing were carried out in HK2-knockdown endometrial stromal cells to analyze the mechanism of HK2 affecting cell function. Results: Endometrial stromal cells of endometrioma displayed active glycolysis metabolism and elevated expression of HK2. Downregulating HK2 reduced the migration, invasion and proliferation capacity of endometrial stromal cells. Knockdown of HK2 induced upregulation of signal transducer and activator of transcription 1 (STAT1) and their phosphorylation to attenuate the proliferation of endometrial stromal cells. Conclusions: HK2 is associated with the migration, invasion and proliferation of endometrial stromal cells, which might provide new insights into the pathogenesis and treatment of endometriosis.

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Background: This study aimed to establish a lipopolysaccharide (LPS)-induced primary ovarian insufficiency (POI) mouse model and to investigate the underlying mechanism.Methods: C57BL/6N female mice were intraperitoneally injected with low-dose LPS (0.5 mg/kg) once daily for 14 days, high-dose LPS (2.5 mg/kg) twice weekly for 2 weeks, and cyclophosphamide (CTX; 150 mg/kg) once weekly for 2 weeks. Ovarian function was assessed by measuring the length of the estrous cycle, the number of primordial follicles, and the levels of serum pituitary/ovarian hormones. Expression and production of interleukin 1β (IL-1β) were determined to evaluate ovarian inflammation. Histopathological examination was performed to examine ovarian fibrosis. TUNEL assay was carried out to evaluate granulosa cell apoptosis. Western blotting was performed to measure the levels of inflammation-, fibrosis-, and apoptosis-related proteins in mouse ovaries.Results: Like CTX, both low- and high-dose LPS administration significantly impaired ovarian functions in mice, as evidenced by extended lengths of estrous cycles, reduced counts of primordial follicles, and alterations in the levels of serum hormones. Also, LPS administration promoted granulosa cell apoptosis and ovarian fibrosis in mice. However, LPS but not CTX significantly promoted IL-1β expression and production in mice. Moreover, LPS treatment but not CTX significantly enhanced TLR, p-p65, p65, and MyD88 protein expression in mouse ovaries, suggesting that LPS differs from CTX in triggering ovarian inflammation. In general, continuous low-dose LPS stimulation was less potent than high-dose LPS stimulation in the above-mentioned effects.Conclusions: LPS induces ovarian inflammation, fibrosis, and granulosa cell apoptosis and can be used to establish a POI model in mice.

This study is aimed at establishing a lipopolysaccharide- (LPS-) induced primary ovarian insufficiency (POI) mouse model and investigating the underlying mechanism. C57BL/6N female mice were intraperitoneally injected with low-dose LPS (0.5 mg/kg) once daily for 14 days, high-dose LPS (2.5 mg/kg) twice weekly for 2 weeks, or cyclophosphamide (CTX; 150 mg/kg) once weekly for 2 weeks. Ovarian function was assessed by measuring the length of estrous cycle, the number of primordial follicles, and the levels of serum hormones. Expression and production of interleukin 1β (IL-1β) were determined to evaluate ovarian inflammation. Histopathological examination was performed to examine ovarian fibrosis. TUNEL assay was carried out to evaluate granulosa cell apoptosis. Western blotting was performed to measure the levels of inflammation-, fibrosis-, and apoptosis-related proteins in the mouse ovaries. Like CTX, both low- and high-dose LPS significantly impaired ovarian functions in mice, as evidenced by extended lengths of estrous cycles, reduced counts of primordial follicles, and alterations in the levels of serum hormones. Also, LPS promoted granulosa cell apoptosis and ovarian fibrosis in mice. However, LPS but not CTX promoted IL-1β expression and production in mice. Moreover, LPS but not CTX enhanced TLR, p-p65, p65, and MyD88 expression in mouse ovaries, suggesting that LPS differs from CTX in triggering ovarian inflammation. In general, continuous low-dose LPS stimulation was less potent than high-dose LPS to affect the ovarian functions. In conclusion, LPS may induce ovarian inflammation, fibrosis, and granulosa cell apoptosis and can be used to establish a POI model in mice.