Prolonged second stage of labor is associated with persistent urinary retention after forceps delivery: An observational study.

The occurrence of urinary retention is significantly higher in women undergoing forceps-assisted midwifery. However, the majority of these women typically regain the ability to urinate spontaneously within 72 hours after delivery. Instances of persistent urinary retention beyond this timeframe are relatively uncommon and have been rarely documented. This study aimed to investigate the risk factors associated with the persistence of urinary retention after forceps-assisted midwifery. A retrospective analysis was conducted on women who underwent forceps-assisted deliveries at the Obstetrics and Gynecology Hospital of Fudan University (China) between August 1, 2019 and December 1, 2019. The study involved collecting general clinical information of these women. Based on the duration of ureter retention, women who had a retention time >72 hours were categorized into group A, while those with a retention time <72 hours were allocated to group B. After performing analysis on the risk factors of persistent urinary retention following forceps delivery, the t test was utilized for analyzing single factors, while logistic regression analysis was employed for assessing multiple factors. Univariate analysis revealed a significant difference in the duration of the second stage of labor between group A and group B. However, logistic regression analysis did not indicate any significant difference between the 2 groups. Further research is still required to determine whether the association between persistent urinary retention following forceps delivery and prolonged second stage of labor is significant, considering the limited number of cases available for analysis.

A rare case of highly differentiated follicular carcinoma in ovary with FGFR4 Gly388Arg polymorphism: a case report and literature review.

BACKGROUND: Highly differentiated follicular carcinoma (HDFCO) is a rare form of struma-derived thyroid-type carcinoma in ovary, defined as ovarian struma spreading beyond ovary but consisting of benign thyroid tissues. No more than 30 cases of HDFCO have been reported since it was first recognized in 2008. The clinicopathologic and molecular features of HDFCO remain unclear up till now. CASE PRESENTATION: A 38-year-old, para 1 gravida 5 woman has a long history of recurrent right ovarian cysts. Histological evaluation showed the tumor progressed from ovarian mature cystic teratoma (OMCT) to highly differentiated follicular carcinoma (HDFCO) during three relapses. Whole-exome sequencing revealed the germline FGFR4 Gly388Arg polymorphism. Repeated operations were performed to remove lesions for the first two relapses. On the third recurrence, the patient received radical surgery with subsequent thyroidectomy and radioactive iodine ablation. No evidence of disease was observed by February 2022 (8 months). CONCLUSIONS: The germline FGFR4 Gly388Arg polymorphism may accelerate the malignant transformation of HDFCO, probably by working as a second hit in the developing spectrum.

[Comparison outcomes of three surgical procedures in treatment of severe pelvic organ prolapse and analysis of risk factors for genital prolapse recurrence].

OBJECTIVE: To investigate clinical significance and application of modified pelvic floor reconstruction developed by Peking Union Medical College Hospital (MPFR) in treatment of severe pelvic organ prolapse (POP) by comparing the effectiveness, quality of postoperative sexual life, life satisfaction and risk factors for POP recurrence with the following two surgical procedures: traditional total vaginal hysterectomy with anterior-posterior colporrhaphy (TVH-APC) and total vaginal hysterectomy with lateral colporrhaphy and sacrospinous ligament fixation and vaginal bridge repair and episiotomy (TVH-LC-SSLF-VBR-EP). METHODS: Totally 173 patients with severe POP and at least two compartments defects of pelvic floor underwent surgeries in the study, 86 patients (group A) were treated by MPFR with polypropylene mesh application, 58 (group B) were treated by TVH-APC, and 29 patients (group C) were treated by TVH-LC-SSLF-VBR-EP. Peri-operative data and outcomes of postoperative courses at 6, 12, 18 months were collected and analyzed, in the meantime, the risk factors of recurrence were studied. RESULTS: (1) No statistical difference was observed among the above 3 groups in terms of length of operation, amount of blood loss, length of hospital stay, and morbidity after surgery (P > 0.05). (2) Cost hospitalization was (11 448 ± 3049) Yuan in group A, which was significantly higher than (7262 ± 1607) Yuan in group B and (7140 ± 1817) Yuan in group C (P < 0.05). (3) The length of vaginal cuff of (7.5 ± 1.4) cm in group A and (5.6 ± 1.1) cm in group C were significantly longer than (7.1 ± 0.6) cm in group B (P < 0.05). The width of vaginal cuff of (4.3 ± 0.3) cm in group A was larger than (3.4 ± 0.3) cm in group B and (3.3 ± 0.4) cm in group C (P < 0.05). (4) The recurrence rate at 12 months after surgery was 12.8% (11/86) in group A, which was similar with 17.2% (5/29) in group C (P > 0.05) and significantly less than 36.2% (21/58) in group B (P < 0.05). The rate of active sexual life of 16.3% (14/86) in group A was significantly higher than 1.7% (1/58) in group B and 0 in group C (P < 0.05). The index of life quality improvement at 12 months after surgery was 48 ± 12 in group A, which was no less than 53 ± 16 in group C (P > 0.05) and higher than 27 ± 9 in group B (P < 0.05). (5) Mesh rejection was observed in 6 patients in group A within 3 months after surgery, while the posterior vaginal wall was exclusively involved. No difference was found in urinary retention or urinary incontinence among three groups (P > 0.05). (6) The severe degree of POP, type of surgical procedure (TVT-APC), anterior compartment defect of pelvic floor, and early days of performing pelvic floor reconstruction surgeries were high risk factors for POP recurrence (P < 0.05). CONCLUSIONS: MPFR has a better curative effect and lower recurrence rate on patients with POP. It can help patients regain integrity of anatomical structure and functions of pelvic floor. TVH-LC-SSLF-VBR-EP is also effective.

Angiogenesis, vasculogenesis, and vasculogenic mimicry in ovarian cancer.

Neovascularization is essential for tumor growth and metastasis. An adequate vasculature feeds tumor growth and enhances the potential of metastasis. For many years, tumor vessels were thought to be lined exclusively by endothelial cells (ECs). However, therapeutic benefits from the promising antiangiogenic strategy targeting genetically stable ECs are frequently limited by the development of resistance, implying an oversimplified view of tumor vasculature. In fact, latest studies have revealed that in addition to ECs, other cells including bone marrow-derived and plastic tumor cells do contribute to tumor vascularization, which is also indicated in ovarian cancer, the most lethal gynecologic malignancy characterized by widespread metastases within the peritoneal cavity upon diagnosis. Given the principle that tumor progression and metastasis are dependent on a persistent blood supply, it is logical that the capability of generating neovessels through diverse mechanisms of ovarian cancer is associated with its malignant potential. This review will discuss the diverse origins of ovarian cancer vascular cells and emphasize their clinical relevance (in the hope of providing insight into the prognostic assessment of women at risk for aggressive disease behavior) and alternative targets for therapeutic intervention.

Characteristics and differentiated mechanism of vascular endothelial cells-like derived from epithelial ovarian cancer cells induced by hypoxia.

A few highly aggressive and malignant tumor cells could acquire identities by turning on genes expressed by endothelial cells and recruit blood vessels to sustain tumor growth. Hypoxia was reported recently to play an essential role in these events. These 'plastic' tumor-cell phenotypes and the exact mechanism driving transendothelial differentiation by hypoxia-inducible factor (HIF)-1alpha is unclear. In this study, epithelial ovarian carcinoma cells were exposed to hypoxia and the tumor cells were transformed into endothelial cells-like (ECs-like). Typical endothelial features such as cell markers and uptaking of acetylated low density lipoprotein were identified constantly. Small interference RNA was used to block the expression of HIF-1alpha. Analysis revealed that hypoxia promotes transendothelial differentiation through stimulating HIF-1-dependent transcriptional expression of vascular endothelial growth factor (VEGF), VEGF receptor-2 (Flk-1) and P53, and through decreasing HIF-1-independent transcriptional expression of Cyclin D1. These results demonstrate that ECs-like derived from epithelial ovarian cancer cells are similar to endothelial progenitor cells rather than endothelial cells. HIF-1alpha is crucial but not unique in alternation of tumor cells towards ECs-like.

The reinforcement of invasion in epithelial ovarian cancer cells by 17 beta-Estradiol is associated with up-regulation of Snail.

OBJECTIVE: The transcription factor Snail, which is implicated in the triggering of epithelial-mesenchymal transitions (EMT), plays an important role in adhesion, invasion and metastasis of tumor cells. In the present study, we assessed 17beta-Estradiol (E2)'s effect on Snail, E-cadherin and MMP-2 expression of epithelial ovarian cancer cell line ES-2 and SKOV3. Then we induced Snail gene silencing by RNA interference to explore the effect of E2 on E-cadherin and MMP-2 expression when Snail gene expression was blocked. METHODS: Treated by 10(-8) M E2, Snail, E-cadherin and MMP-2 mRNA expression of the cells was measured by RT-PCR; Snail, MMP-2 protein expression was detected by IHC; and MMP-2 activity was determined by Zymography. E-cadherin protein level was measured by Western blot. We constructed the small interfering dsRNA expression vector (pRNAT-U6.1/Neo-Snail) targeting Snail gene, as well as a negative control vector (pRNAT-U6.1/Neo-Neg). Then the cells were transiently transfected with the vectors. Western blot and zymography were conducted to determine E-cadherin protein level and matrix metalloproteinase activity of the cells transfected with pRNAT-U6.1/Neo-Snail or pRNAT-U6.1/Neo-Neg after treated with E2 for 24 h. RESULTS: The expression of ER alpha mRNA and protein was negative in ES-2 cells and positive in SKOV3 cells, and ER beta expression was positive in both cell lines. 10(-8) mol/l E2 elevated expression of Snail and MMP-2 mRNA and protein in both ES-2 and SKOV3 cells, and reduced expression of E-cadherin mRNA and protein in SKOV3 cells. While in the RNAi group transfected with the small interfering dsRNA expression vector (pRNAT-U6.1/Neo-Snail) targeting Snail gene, E2 treatment did not have a significant effect on MMP-2 activity or E-cadherin protein in ES-2 and SKOV3 cells. CONCLUSIONS: 17beta-Estradiol increased Snail expression in both ER alpha-negative ES-2 cells and ER alpha-positive SKOV3 cells independent of the existence of ER alpha. The increase of MMP-2 expression in ES-2 and SKOV3 cells and decrease of E-cadherin expression in SKOV3 cells induced by E2 were associated with up-regulation of Snail.

Characterization of unilateral polycystic ovary compared with polycystic ovary syndrome.

Twelve patients with unilateral polycystic ovarian morphology demonstrated milder degrees of ovarian and other endocrine dysfunction than polycystic ovary syndrome patients and had fewer incidences of hyperprolactinemia and hyperandrogenism.

[Influence of estrogen and progestin on nm23-H1 expression in epithelial ovarian cancer cell lines via activation of phosphorylation signaling].

OBJECTIVE: To assess the estrogen and progestin's effect on protein expression of metastasis repression gene nm23-H1 via regulation of phosphorylation signaling in epithelial ovarian cancer cell line ES-2. METHODS: Ovarian clear cell adenocarcinom cell line ES-2 was treated by different doses of 17beta-estradiol (estrogen), medroxyprogestogen (progestin) and dimethyl sulfoxide (control group), and then the following experiments were conducted. (1) Change of the cell migration capacity after treatment with estrogen and progestin for 24 and 48 hours was measured by in vitro wound healing assay. (2) Transwell experiments were used to detect the ability of cell invasion, which was also used to inhibit the phosphorylation of protein kinase B (AKT) pathway with estrogen and progestin. (3) Change of nm23-H1, AKT and phosphorylated protein kinase B (pAKT) protein level of ES-2 cells after treated with estrogen and progestin was detected by western blot. (4) Cells were transfected with the small interfering RNA (siRNA) expression vector targeting AKT. The efficiency of cells transfected was calculated according to the number of cells with green fluorescent produced by cells transfected. Change of nm23-H1 expression was assessed. RESULTS: ES-2 cells treated with estrogen, progestin or vehicle all migrated into the wound surface after 24 and 48 hours. The migration of the cells treated with estrogen was (1.39 +/- 0.08) mm, significantly elevated (P = 0.029), and that of the cells treated with progestin was (1.96 +/- 0.07) mm, significantly decreased compared with cells treated with vehicle (P = 0.014). The cells were cultured in transwell after 24 hours. The invasion of the cells treated with estrogen was 119 +/- 13, significantly elevated (P = 0.015), and that of the cells treated with progestin was 78 +/- 8, significantly decreased compared with cells treated with vehicle (P = 0.006). Western blot results showed that 17beta-estradiol decreased nm23-H1 expression, and both effects were dose and time dependent (P = 0.020, P = 0.001). Progestin increased nm23-H1 expression in ES-2 cells, and both effects were dose and time dependent (P = 0.003, P = 0.002). 17beta-Estradiol elevated the expression of pAKT, which was also dose and time dependent (P = 0.001, P = 0.007), while progestin repressed pAKT expression which was also dose and time dependent (P = 0.012, P = 0.039). When cells were transfected with the siRNA expression vector targeting AKT, the effects of estrogen and progestin on nm23-H1 expression were both attenuated. CONCLUSIONS: Estrogen downregulates the expression of nm23-H1 via activation of the phosphorylation signaling, thus participated in the regulation of invasion and metastasis of epithelial ovarian cancer cells. Progestin upregulates the expression of nm23-H1, and might repress invasion and metastasis of tumor cells.

[Primary study of vasculogenic mimicry induced by hypoxia in epithelial ovarian carcinoma].

OBJECTIVE: To explore possibility of vasculogenic mimicry induced by hypoxia and the inhibitive effect by sirolimus in epithelial ovarian carcinoma in vitro. METHODS: Based on three-dimensional cell culture system developed by Matrigel, ovarian cell lines SKOV3 and ES2 were induced under conditions of hypoxia, hypoxia added with sirolimus and no-hypoxia, respectively. Potential formation of tumor channels and their characterization of network were observed by light microscopy and scanning electronic microscopy. Relative hypoxia-inducible factor (HIF) 1alpha mRNA expression was detected by RT-PCR simultaneously. RESULTS: The micrograph showed both SKOV3 and ES2 cells appeared expanded and re-shaped, then formed blood vessel-like structures such as cavity, channel, branch and network. These capabilities of cells were inhibited by sirolimus and no-hypoxia. The levels of HIF-1alpha mRNA expression of SKOV3 and ES2 were 0.801 +/- 0.034 and 0.736 +/- 0.059 under hypoxia, which were significantly higher than under hypoxia added with sirolimus (0.025 +/- 0.007, 0.231 +/- 0.035; P < 0.01, P < 0.05), and those under no-hypoxia (0.010 +/- 0.004, 0.011 +/- 0.002; both P < 0.01). CONCLUSIONS: Hypoxia plays a key role in development of vasculogenic mimicry in epithelial ovarian carcinoma. Sirolimus can inhibit vasculogenic mimicry effectively by blocking HIF-1alpha at transcription level.

[Correlation between local hormones and CD36 transcription level in women with polycystic ovary].

OBJECTIVE: To detect CD(36) expressions in polycystic ovary (PCO), and to explore its correlation with local androgen and insulin at transcription level. METHODS: From August 2002 to February 2003, 12 patients with asymmetric PCO, 15 primary or secondary infertile patients without endocrine disorders and 8 polycystic ovary syndrome (PCOS) with bilateral PCO were recruited. Extraction of follicular fluid and detection of testosterone (T), dehydroepiandrosterone sulfate (DHEAS), insulin (INS) and androstenedione (A(2)) were performed. Relative CD(36) mRNA expression level of human ovarian inner thecal cells was analyzed by auto image analysis system (IAS) after RT-PCR. RESULTS: The level of CD(36) mRNA expression in thecal cells was 0.24 +/- 0.07 in polycystic ovary of PCO group and 0.21 +/- 0.05 in bilateral ovaries of PCOS group, respectively, which were significantly lower than 0.83 +/- 0.13 in normal ovaries (P < 0.01). T and INS levels of follicle fluid in PCO were significantly higher than that in normal ovaries (P < 0.01). T and INS levels of follicle fluid were negatively related to CD(36) mRNA expression of follicular theca interna (r = -0.6810, r = -0.6708, P < 0.01). CONCLUSION: Decrease of scavenger receptor gene CD(36) mRNA may play a role in the pathogenesis of PCO by increasing the level of T and INS in follicular fluid.