Prediction of myofascial pelvic pain syndrome based on random forest model.

Objective: The objective is to construct a random forest model for predicting the occurrence of Myofascial pelvic pain syndrome (MPPS) and compare its performance with a logistic regression model to demonstrate the superiority of the random forest model. Methods: We retrospectively analyze the clinical data of female patients who underwent pelvic floor screening due to chronic pelvic pain at the Pelvic Floor Rehabilitation Center of the Third Affiliated Hospital of Zhengzhou University from January 2021 to December 2023. A total of 543 female patients meeting the study's inclusion and exclusion criteria are randomly selected from this dataset and allocated to the MPPS group. Furthermore, 702 healthy female patients who underwent pelvic floor screening during routine physical examinations within the same timeframe are randomly selected and assigned to the non-MPPS group. Chi-square test and rank-sum test are used to select demographic variables, pelvic floor pressure assessment data variables, and modified Oxford muscle strength grading data for logistic univariate analysis. The selected variables are further subjected to multivariate logistic regression analysis, and a random forest model is also established. The predictive performance of the two models is evaluated by comparing their accuracy, sensitivity, specificity, precision, receiver operating characteristic (ROC) curve, and area under the curve (AUC) area. Results: Based on a dataset of 1245 cases, we implement the random forest algorithm for the first time in the screening of MPPS. In this investigation, the Logistic regression model forecasts the accuracy, sensitivity, specificity, and precision of MPPS at 69.96 %, 57.46 %, 79.63 %, and 68.57 % respectively, with an AUC of the ROC curve at 0.755. Conversely, the random forest prediction model exhibits accuracy, sensitivity, specificity, and precision rates of 87.11 %, 90.66 %, 90.91 %, and 83.51 % respectively, with an AUC of the ROC curve at 0.942. The random forest model showcases exceptional predictive performance during the initial screening of MPPS. Conclusion: The random forest model has exhibited exceptional predictive performance in the initial screening evaluation of MPPS disease. The development of this predictive framework holds significant importance in refining the precision of MPPS prediction within clinical environments and elevating treatment outcomes. This research carries profound global implications, given the potentially elevated misdiagnosis rates and delayed diagnosis proportions of MPPS on a worldwide scale, coupled with a potential scarcity of seasoned healthcare providers. Moving forward, continual refinement and validation of the model will be imperative to further augment the precision of MPPS risk assessment, thereby furnishing clinicians with more dependable decision-making support in clinical practice.

Comparison of efficacy between laparoscopic pectopexy and laparoscopic high uterosacral ligament suspension in the treatment of apical prolapse-short term results.

To compare the clinical efficacy of laparoscopic pectopexy and laparoscopic high uterosacral ligament suspension in women suffering from apical prolapse. The clinical data of 170 patients with apical prolapse (POP-Q score ≥ II) treated in the Third Affiliated Hospital of Zhengzhou University from January 2018 to July 2020 were retrospectively analyzed to assess the clinical efficacy of three surgical methods [laparoscopic pectopexy with uterine preservation, laparoscopic pectopexy with hysterectomy, laparoscopic high uterosacral ligament suspension (LHUSLS) with hysterectomy]. Patients were divided into three groups depending on Surgical methods: laparoscopic uterine pectopexy group (n = 23), laparoscopic pectopexy with hysterectomy group (n = 78) and LHUSLS with hysterectomy group (n = 69). The POP-Q points before and after operation were analyzed. The operation-related indices, perioperative periods and post-operative complications were compared. 1. The operation time of laparoscopic uterine pectopexy group was the shortest (p < 0.05). There was no significant difference in the incidence of apical prolapse and new stress urinary incontinence among the three groups during the follow-up period (p > 0.05). 2. The POP-Q points (Aa, Ba, C) in the three groups were better than those before operation (p < 0.05). Laparoscopic pectopexy with hysterectomy group had better Ap, Bp and C points and a longer TVL than LHUSLS with hysterectomy group (p < 0.05). 3. The postoperative PFDI-20, PFIQ-7 and PISQ-12 scores of the three groups were significantly improved than those before operation (p < 0.05). The PISQ-12 scores in laparoscopic uterine pectopexy group were significantly higher than that in the other two groups one year after operation (p < 0.05). The study concludes that laparoscopic pectopexy and LHUSLS can significantly improve the quality of life and sexual function for patients with apical prolapse. One year after operation, laparoscopic pectopexy has a more satisfactory anatomical reduction than LHUSLS with hysterectomy. The laparoscopic uterine pectopexy group had lower postoperative complications and better sexual function than that with hysterectomy group. Laparoscopic pectopexy should be used for the treatment of apical prolapse (POP-Q score ≥ II) patients who aim to better clinical efficacy and sexual function improvement.

Subsequent ovarian yolk sac tumor after operation of ovarian mature teratoma: a case report and review of the literature.

Ovarian mature teratoma represents a benign ovarian tumor, while ovarian yolk sac tumor (YST, endodermal sinus tumor) is a rare malignant tumor predominantly affecting young women, often associated with a grim prognosis post-metastasis. Both ovarian mature teratoma and ovarian YST are germ cell tumors. There are few studies on the correlation between ovarian YST and mature teratoma. Recurrence or malignant transformation may occur following the surgical intervention for ovarian mature teratoma. However, the occurrence of YST subsequent to such procedures is notably rare. In this investigation, we reported a case involving a 24-year-old unmarried woman with both mature ovarian teratoma and YST within a brief 1-year interval. Regular reexamination protocols facilitated the early-stage detection of YST. The patient underwent surgical treatment, chemotherapy, and measures to preserve ovarian function, resulting in a favorable prognosis. Our primary purpose is to distill clinical insights from the diagnostic and therapeutic journey of this patient. Our purpose is to enhance medical professionals' awareness that YST may be secondary to mature teratoma. Additionally, we underscore the critical importance of routine postoperative surveillance for ovarian mature teratoma, emphasizing its pivotal role in early malignant tumor detection-a factor paramount to the prognosis of patients.

Effects of miR-363 on the Biological Activities of Eutopic Endometrial Stromal Cells in Endometriosis.

EMs is a kind of benign disease with certain malignant behaviors. The adhesion, invasive growth, and angiogenesis of ectopic endometrial cells are the pathological basis of EMs occurrence, but its etiology and pathogenesis have not been completely illustrated yet. In our research, we aim to investigate the role of miR-363 in the pathogenesis of endometriosis. Real-time quantitative PCR was used to detect the expression of miR-363 before and after ESC/NSC transfection. CCK-8, flow cytometry, and transwell assay were used to detect the effect of the miR-363 expression on cell proliferation, apoptosis, and invasion. The effects of the miR-363 expression on the contents of Fas/APO-1 and ICAM-1 in cell culture supernatant were detected by ELISA. qRT-PCR and WB assay were used to detect the effects of the miR-363 expression on the mRNA and protein expression levels of ICAM-1, MMP-7, and VEGF in ESC. The increased expression of miR-363 could inhibit the proliferation and invasion of ESC, promote apoptosis, and inhibit the secretion of FAS/APO-1 and ICAM-1. The knockdown expression of miR-363 promoted proliferation and invasion of NSC, inhibited apoptosis, and promoted secretion of FAS/APO-1 and ICAM-1. VCAM-1, VEGF, and MMP-7 were detected in ESCs before transfection. The protein expression level was higher than that of NSCs. Compared with pretransfection, the protein levels of VCAM-1, VEGF, and MMP-7 in the M-363 group were significantly downregulated. The downregulated expression of miR-363 was associated with a stronger cell proliferation ability, a lower cell apoptosis rate, and a stronger ESC. Migration is associated with invasiveness, proliferation, angiogenesis, and immune escape. The low expression of miR-363 promotes endogenesis through posttranscriptional regulation of target genes VCAM-1, MMP-7, and VEGF. The differential expression of miR-363 between ESC and NSC may be an important factor in the many biological differences between ESC and NSC.

MicroRNA let­7d­5p rescues ovarian cancer cell apoptosis and restores chemosensitivity by regulating the p53 signaling pathway via HMGA1.

Ovarian cancer (OC) is the gynecological malignancy type with the highest mortality rate in females. The regulatory effect of microRNAs (miRs) on their target genes serves a key role in tumor development. Therefore, in the present study, whether miR let­7d­5p targeting high mobility group A1 (HMGA1) regulated biological characteristics and chemosensitivity of OC cells by mediating the p53 signaling pathway was investigated. The let­7d­5p level was detected in OC tissues and adjacent normal tissues, followed by detection in OC cell lines SKOV3, A2780, OVCAR­3 and CaOV3, and human normal ovarian epithelial cell line (IOSE­80), in order to select the OC cell line for the following experiments. Subsequently, OC cells were treated with the let­7d­5p mimic, siHMGA1 and Tenovin­1. The targeting association between let­7d­5p and HMGA1 was then examined, and the OC cell viability, migration, cycle and apoptosis were evaluated. Subsequently, the chemosensitivity of OC cells to cisplatin was verified. Finally, expression levels of let­7d­5p, HMGA1, p21, B­cell lymphoma­2 (Bcl­2)­associated X (Bax), p27, p53 wild­type (p53wt), p53 mutated (p53mut), proliferating cell nuclear antigen (PCNA), cyclin­dependent kinase 2 (CDK2), matrix metallopeptidase (MMP)2, MMP9 and Bcl­2 were determined. As demonstrated in the results, let­7d­5p expression was low in OC tissues and had an increased reduction in the OVCAR­3 cell line. HMGA1 was confirmed as a target of let­7d­5p, and its expression was also silenced by let­7d­5p. let­7d­5p repressed OC cell viability, migration, cell cycle progression and apoptosis, while it promoted the chemosensitivity of OC cells to cisplatin by targeting HMGA1. The expression of let­7d­5p, p21, Bax, p27 and p53wt was increased, while that of HMGA1, p53mut, PCNA, CDK2, MMP2, MMP9 and Bcl­2 was reduced following cell transfection. The results in the present study provided evidence that let­7d­5p may suppress proliferation, and facilitate apoptosis and cisplatin chemosensitivity of OC cells by silencing HMGA1 via the p53 signaling pathway.

lncRNA WT1-AS inhibits the aggressiveness of cervical cancer cell via regulating p53 expression via sponging miR-330-5p.

BACKGROUND: Emerging evidences have demonstrated that lncRNAs play vital roles in various pathological processes, including cancer. The lncRNA WT1 antisense RNA (WT1-AS) serves as a tumor suppressor in various cancers. Nevertheless, the expression and precise function of WT1-AS in cervical carcinoma still remain not yet investigated. The objective of our study was to explore the expression of WT1-AS and its biological roles in cervical cancer. METHODS: Differences in the lncRNA expression profiles between cervical cancer and adjacent normal tissues were assessed by lncRNA expression microarray analysis. The expression of p53 in cervical cancer cell was assessed by qRT-PCR and immunofluorescence assay. Loss-of-function studies were used to explore the effect of lncRNA WT1-AS on the growth and metastasis of cervical cancer cell in vitro and in vivo. RESULTS: Our results demonstrated that WT1-AS was remarkably down-regulated in cervical carcinoma. Functional assays proved that up-regulation of WT1-AS significantly suppressed cervical cancer cell proliferation, migration and invasion. In addition, the luciferase reporter assay identified that miR-330-5p was the target of WT1-AS. Moreover, tumor suppressor p53 was identified as the direct target of miR-330-5p and alternation of miR-330-5p/p53 axis reversed the effects of WT1-AS in cervical cancer cell. CONCLUSION: Altogether, our findings suggested that WT1-AS was down-regulated in cervical carcinoma and WT1-AS suppressed cervical carcinoma cell- proliferation, migration and invasion through regulating the miR-330-5p/p53 axis.

Annexin A2 inhibition suppresses ovarian cancer progression via regulating ß-catenin/EMT.

Annexin A2 is a member of the Annexin family that acts as a Ca2+-dependent phospholipid and membrane binding protein, which is associated with the survival and spread of multiple neoplasms. However, the function of Annexin A2 in ovarian cancer progression remains unclear. In this study, we aimed to investigate the role and underlying molecular mechanism of Annexin A2 in cell proliferation and invasion in ovarian cancer. We found that the mRNA expression of Annexin A2 was upregulated in ovarian cancer tissues and cell lines. In the loss-of-function of Annexin A2, ß-catenin was indicated to be significantly suppressed and EMT constrained. Moreover, cell proliferation and invasion were both markedly inhibited by the downregulation of Annexin A2. Additionally, the overexpression of ß-catenin obviously reversed the effect of Annexin A2 on EMT, and cell proliferation and invasion, indicating that Annexin A2 suppression regulated EMT through controlling ß-catenin. Taken together, this study showed that Annexin A2 inhibition suppresses proliferation and invasion in ovarian cancer via ß-catenin/EMT, proposing the potential role of Annexin A2 in the prevention and treatment of ovarian cancer.

[Comparison among measures to prevent intrauterine adhesions after artificial abortion].

OBJECTIVE: To investigate the clinical efficacy of oral medicine and sodium hyaluronate in prevention of intrauterine adhesions after artificial abortion.
 METHODS: A total of 572 patients with early pregnancy termination through artificial abortion, who experienced two or more times of abortion, were retrospectively analyzed. Patients were randomly and voluntarily divided into 4 groups: an artificial cycle group, a drospirenone and ethinylestradiol tablets group, a sodium hyaluronate group, and a control group. The thickness of the endometrium, return time of menses, and the status of intrauterine adhesions were observed.
 RESULTS: The thickness of the endometrium in the artificial period group was greater than that in the control group (P<0.001). It was less in the drospirenone and ethinylestradiol tablets group comparing with that in the control group (P<0.001). There was no significant difference in the thickness of the endometrium between the sodium hyaluronate group and the control group (P=0.717). Return time of menses in the artificial menstrual cycle group and the drospirenone and ethinylestradiol tablets group was shorter than that in the control group (P<0.001). There was no significant difference in return time of menses between the sodium hyaluronate group and the control group (P=0.813). The incidence of intrauterine adhesions could be reduced by the 3 preventive measures (All P<0.01).
 CONCLUSION: Drugs for artificial cycle and drospirenone and ethinylestradiol tablets medication immediately after artificial abortion can effectively promote endometrial repair and reduce the incidence of intrauterine adhesions. However, for the patients with poor compliance, drospirenoneand ethinylestradiol tablets are the first choice for prevention of intrauterine adhesion.

[The expression of RhoC and Ki67 in cervical intraepithelial neoplasia and squamous carcinoma of cervix].

OBJECTIVE: To detect the expression of RhoC and Ki67 in squamous carcinoma of cervix and to reveal the correlation of RhoC and Ki67 with clinic pathological parameters of cervix carcinoma. METHODS: The expressions of RhoC and Ki67 were evaluated in 26 cases of cervical intraepithelial neoplasia (CIN) and 57 cases of squamous carcinoma of cervix(SCC) by immunohistochemistry, while 14 cases of normal cervical epithelium(NCE) were taken as control. RESULTS: Immunohistochemical staining demonstrated RhoC expression in 82.46% (47/57) of SCC, 15.38% (2/13) of CIN II/III, and negative expression in NCE and CIN I. The positive rate of RhoC expression in SCC was significantly higher than that in NCE and CIN (P < 0.05). The expression of RhoC in SCC was significantly correlated with pelvic lymph node metastasis and depth of stroma infiltration, but not correlated with age, FIGO staging,histologic grade and vascular space involvement. The positive rates of Ki67 expression in NCE, CIN I, CIN II/III and SCC were 28.57%, 38.46%, 100% and 96.49% respectively. The positive rates of Ki67 expression in SCC and CIN II/III were significantly higher than those in NCE and CIN I (P < 0.05). The expression of Ki67 in SCC was not correlated with the major clinic pathological parameters. There was no obvious relationship between the expression of RhoC gene and Ki67 antigen in SCC (P > 0. 05). CONCLUSIONS: The overexpression of RhoC may play an important role in the invasion and metastasis of SCC. RhoC may be a potential marker to identify SCC patients with high risk of invasion and metastasis.