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Placenta accreta spectrum (PAS) is an obstetric complication related to severe maternal morbidity and mortality, magnetic resonance imaging (MRI) can predict the bleeding risk and the adverse outcomes of the maternal caesarean section in PAS patients. The aim of the current study was to determine relationship of placenta area in sector 2 (S2) and cervical area measured by MRI with massive hemorrhage (MH) in complete placenta previa patients with PAS. One hundred and thirty-eight patients were diagnosed as PAS from January 2016 to December 2023 in the retrospective study. The patients were divided into two groups according to the estimated blood loss volume: MH group (estimated blood loss >2000 mL) and non-MH group (estimated blood loss ≤2000 mL). After adjusting for PAS grade and clinical variables, the correlation between placenta area in S2, cervical area and MH were evaluated with multivariate analysis. The evaluation capabilities of indicators were assessed using receiver operating characteristic (ROC) analysis. The placenta area in S2 of the MH group was significantly higher than that of the group without MH ( <0.001), on the contrary, cervical area was significantly lower in PAS patients with MH than that of the group without MH ( <0.001). After adjusting for the type of PAS, a placenta area in S2 ≥45 cm (OR, 4.805; 95% CI, 2.776-8.794; <0.05) and a cervical area <4.0 cm (OR, 4.015; 95% CI, 1.905-7.862; <0.05) were independently associated with an increased risk of MH. A positive association was found between the placental area and the amount of blood loss (r=0.748), and negative linear was found between the cervical area and the amount of blood loss (r=-0.682), between cervical area and placenta area (r=-0.575). Combined with placental area in S2 and cervical area, the sensitivity, specificity, and the area under the curve (AUC) for the predictive MH were 89.237%, 91.548%, and 0.910 (95% CI 0.858 ~ 0.963), respectively. The placenta area in S2 and cervical area measured by MRI show potential utility in identifying MH among patients with PAS, which may assist in preoperative risk stratification. These preliminary results require validation in future studies.

Background The surgical difficulty of cesarean delivery after a trial labor is often increased, leading to uterine lacerations, postpartum hemorrhage and other adverse outcomes. In the study, we aimed to identify and quantify risk factors that cause cesarean uterine lacerations during the first stage of labor. Methods This was a retrospective cohort review of all women with a singleton, cephalic fetus at term delivered by caesarean section at four large departments in China between January 2023 and December 2024. A least absolute shrinkage and selection operator (LASSO) and multivariate analysis were performed to identify labor related risk factors for cesarean uterine lacerations among patients that underwent cesarean delivery in the first stage of labor. The risk factors were used to construct a new score model to identify patients at risk for cesarean uterine lacerations. Results During the study period, there were 11,689 women delivered by caesarean section, 206 women had cesarean uterine lacerations and 824 pregnant women without cesarean uterine lacerations were included in the study. The following 6 high-risk factors were identified for cesarean uterine lacerations by LASSO regression and multiple regression: occiput transverse position, occiput posterior position, cervical dilatation (> 5 cm), station of the fetal head at the ischial spines ( > + 1), caput succedaneum (> 3 cm), and duration of labor (> 12 h). In clinical variables model, the ROC curve analysis showed that the sensitivity and specificity to predict cesarean uterine lacerations were 91.372% and 92.205% respectively, with AUC 0.892. Using our new score model, when the score point ≥ 6, the sensitivity and specificity in identifying cases at high risk for cesarean uterine lacerations were 92.168% and 91.605%, respectively, with AUC 0.902. Conclusions Increased risk of cesarean uterine lacerations in the first stage of labor is attributable mainly to fetal head position, larger cervical dilatation, lower fetal head, caput succedaneum, and duration of labor.

Background Ovarian cancer (OC) has the highest mortality rate among all gynecological malignancies. A hypoxic microenvironment is a common feature of solid tumors, including ovarian cancer, and an important driving factor of tumor cell survival and chemo- and radiotherapy resistance. Previous research identified the hypoxia-associated gene angiopoietin-like 4 (ANGPTL4) as both a pro-angiogenic and pro-metastatic factor in tumors. Hence, this work aimed to further elucidate the contribution of ANGPTL4 to OC progression. Methods The expression of hypoxia-associated ANGPTL4 in human ovarian cancer was examined by bioinformatics analysis of TCGA and GEO datasets. The CIBERSORT tool was used to analyze the distribution of tumor-infiltrating immune cells in ovarian cancer cases in TCGA. The effect of ANGPTL4 silencing and overexpression on the proliferation and migration of OVCAR3 and A2780 OC cells was studied in vitro, using CCK-8, colony formation, and Transwell assays, and in vivo, through subcutaneous tumorigenesis assays in nude mice. GO enrichment analysis and WGCNA were performed to explore biological processes and genetic networks associated with ANGPTL4. The results obtained were corroborated in OC cells in vitro by western blotting. Results Screening of hypoxia-associated genes in OC-related TCGA and GEO datasets revealed a significant negative association between ANGPTL4 expression and patient survival. Based on CIBERSORT analysis, differential representation of 14 distinct tumor-infiltrating immune cell types was detected between low- and high-risk patient groups. Silencing of ANGPTL4 inhibited OVCAR3 and A2780 cell proliferation and migration in vitro and reduced the growth rate of xenografted OVCAR3 cells in vivo. Based on results from WGCNA and previous studies, western blot assays in cultured OC cells demonstrated that ANGPTL4 activates the Extracellular signal-related kinases 1 and 2 (ERK1/2) pathway and this results in upregulation of c-Myc, Cyclin D1, and MMP2 expression. Suggesting that the above mechanism mediates the pro-oncogenic actions of ANGPTL4T in OC, the pro-survival effects of ANGPTL4 were largely abolished upon inhibition of ERK1/2 signaling with PD98059. Conclusions Our work suggests that the hypoxia-associated gene ANGPTL4 stimulates OC progression through activation of the ERK1/2 pathway. These findings may offer a new prospect for targeted therapies for the treatment of OC.

Background Abnormal protein localization due to disrupted nucleoplasmic transport is common in tumor cells, but its mechanisms are not well understood. Nuclear pore complexes and nuclear transporter proteins are crucial for protein transport between the nucleus and cytoplasm. Evidence increasingly shows that abnormal expression of karyopherin family proteins disrupts protein translocation, affecting processes like cell differentiation, proliferation, apoptosis, and transcriptional regulation. However, their functions and roles in ovarian cancer remain unclear. Methods The expression level of KPNA5 in ovarian cancer tissues and cells was detected by IHC, Western blot, and qPCR. CCK‐8 and colony formation assays were used to assess cell proliferation ability. Transwell assay was conducted to determine cell migration and invasion capacity. A xenograft model was used to assess the effect of KPNA5 on tumor growth in vivo. Results KPNA5 expression is downregulated in ovarian cancer (OC) tissues. Low KPNA5 levels were associated with poor survival in OC patients, validated by an OC tissue sample cohort. Overexpression of KPNA5 significantly suppressed OC cell proliferation, tumor growth, and invasion in both in vitro and in vivo studies. Mechanistically, KPNA5 recognizes nuclear localization signals (NLSs) in PTPN4, mediating its nuclear transport and inhibiting STAT3 phosphorylation and its downstream signaling pathway. Similarly, PTPN4 overexpression reduced OC cell viability and invasion, also suppressing STAT3 phosphorylation. Conclusions Our findings identify KPNA5 as a tumor suppressor in OC, presenting a potential therapeutic target for OC treatment.

Background Ovarian cancer is a common gynecological tumor with high malignant potential and poor prognosis. TRIM8, is involved in the development of various tumors, but its precise regulatory role in ovarian cancer is still unknown. Aims The aim of this study was to explore the specific mechanism by which TRIM8 regulates ovarian cancer. Materials and Methods We used bioinformatics analysis to screen for high expression of TRIM8 in ovarian cancer. The expression of TRIM8 in healthy and cancerous ovarian tissues was assessed by immunofluorescence. TRIM8 was silenced or overexpressed in ovarian cancer cell lines, with cell proliferation and migration evaluated by CCK8, transwell and clonal formation assays. The effect of TRIM8 on ovarian cancer cells in vivo was assessed by subcutaneous tumor formation experiments in nude mice. The potential interacting protein VDAC2 was identified by mass spectrometry. The mechanism underlying TRIM8 regulation of VDAC2 was evaluated by co‐immunoprecipitation and western blotting. Results TRIM8 was overexpressed in ovarian cancer. TRIM8 promoted the proliferation and migration of ovarian cancer cells in vitro and the growth of subcutaneous tumors in mice in vivo. TRIM8 interacted with VDAC2, weakened the stability of the protein, and promoted its polyubiquitination and subsequent degradation. Knockdown of VDAC2 increased the resistance of ovarian cancer cells to iron death, whereas overexpression of VDAC2 attenuated ovarian cancer progression induced by TRIM8 overexpression. Discussion TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation, these finding may provide new targets for the treatment of ovarian cancer. Conclusion TRIM8 degraded VDAC2 through the ubiquitination pathway, increased the resistance of ovarian cancer cells to iron death, and promoted the proliferation and migration of ovarian cancer. TRIM8 degraded VDAC2 through the ubiquitination pathway, increased the resistance of ovarian cancer cells to iron death, and promoted the proliferation and migration of ovarian cancer. This study is the initial demonstration of the cancer‐promoting effects of TRIM8 in ovarian cancer by means of a distinct mechanism that involves the regulation of VDAC2.

Purpose Depiction of pelvic lymph node metastasis (LNM) sites among patients with cervical cancer facilitates accurate determination of the extent of dissection and radiotherapy regimens. Methods A retrospective study of 1182 cervical cancer patients who underwent radical hysterectomy and pelvic lymph node dissection between 2008 and 2018 was performed. The number of removed pelvic lymph nodes and metastasis status in different anatomical regions was analyzed. The prognostic difference of patients with lymph node involvement stratified by various factors was analyzed by Kaplan–Meier method. Results The median number of pelvic lymph nodes detected was 22, mainly from obturator (29.54%) and inguinal (21.14%) sites. Metastatic pelvic lymph nodes were found in 192 patients, with obturator accounting for the highest percentage (42.86%). The patients with lymph node involvement in single site had better prognosis that those in multiple sites. The overall- ( P  = 0.021) (OS) and progression-free ( P  < 0.001) survival (PFS) curves of patients with inguinal lymph node metastases were worse compared to those with obturator site. There was no difference in the OS and PFS among patients with 2 and more than 2 lymph nodes involvement. Conclusion An explicit map of LNM in patients with cervical cancer was presented in this study. Obturator lymph nodes tended to be involved. The prognosis of patients with inguinal lymph node involvement was poor in contrast to that with obturator LNM. In patients with inguinal lymph node metastases, clinical staging needs to be reconsidered and extended radiotherapy to the inguinal region needs to be strengthened.

Purpose To elucidate the clinicopathological features and prognostic factors of minimal deviation adenocarcinoma (MDA) of the uterine cervix, a clinically rare but highly invasive disease. Methods This was a retrospective, observational, real-world study of 43 patients with pathologically confirmed MDA at the Obstetrics and Gynaecology Hospital of Fudan University between November 2010 and November 2021. Baseline clinicopathological data were collected and reviewed. Prognostic factors for progression-free survival (PFS) and overall survival (OS) were investigated by univariate and multivariate Cox proportional hazards analyses. Results Chief complaints included irregular vaginal discharge and/or bleeding (74.4%). Preoperative diagnosis was difficult, the detection rate was low (36.8%), all cases showed endophytic lesions, and 88.4% had deep stromal invasion, with biologically aggressive characteristics. The ovarian metastasis rate was high (16.3%, 7/43). The median maximum diameter of the tumour (MDOT) was 4.3 cm (range, 0.5–8.0 cm). MDOT was significantly associated with OS ( P  = 0.009), and the optimal cut-off value to define bulky MDA was 5.5 cm ( P  < 0.0001, χ= 21.161) using X-tile software. Independent prognostic factors included MDOT (HR = 10.095, P  = 0.001) and ovarian metastasis (HR = 5.888, P  = 0.008) for OS and MDOT (HR = 3.944, P  = 0.028), ovarian metastasis (HR = 9.285, P  = 0.001), and deep infiltration (HR = 3.627, P  = 0.048) for PFS. Conclusion Endophytic lesion development and ovarian metastasis are likely in MDA. A bulky tumour and ovarian metastasis indicate a worse prognosis. Given the special biological features of MDA, it is more appropriate to use 5.5 cm as the threshold for defining a bulky tumour than it is to use 4 cm. Ovary removal should be given higher priority to improve prognosis.

Globally, among gynecological malignancies, ovarian cancer (OC) stands as an important factor contributing to mortality. E3 ubiquitin ligase activity is a common characteristic found in the tripartite motif (TRIM) proteins, contributing significantly to post-translational modifications of various proteins. Among these TRIM proteins, TRIM15 has been linked to multiple cancer types. Nevertheless, the function of TRIM15 concerning OC has yet to be elucidated. We aimed to explore the role of TRIM15 in OC and shed light on the underlying mechanisms thereof. A bioinformatics analysis was conducted to investigate the variance in TRIM15 expression between normal ovarian tissues and OC tissues, and to explore the prognostic significance of TRIM15 in patients with OC. TRIM15 protein expression in OC tissues was detected using immunofluorescence. The impact of TRIM15 silencing and overexpression on the proliferation and migration of OC cells was assessed through various functional experiments, such as CCK-8, colony formation, and Transwell assays. Mass spectrometry analysis was performed to identify TRIM15-interacting substrates. The mechanism underlying substrate ubiquitination mediated by TRIM15 was further explored. Based on The Cancer Genome Atlas (TCGA) data and immunofluorescence analysis, OC tissues exhibited significant upregulation of TRIM15 expression. si-RNA-mediated silencing of TRIM15 suppressed the in vitro proliferation and migration of OVCAR3 and A2780 cells. Paxillin was selected as an interacting protein with TRIM15 by mass spectrometry. Mechanically, we discovered that TRIM15 mediated the ubiquitination of Paxillin via Lys11- and Lys29-linked polyubiquitin chains. Subsequent co-IP experiments revealed that TRIM15 could also enhance the interactions between Paxillin and its tyrosine kinase, FAK, thereby promoting the phosphorylation of Paxillin. We revealed a previously unknown mechanism by which TRIM15 ubiquitinates and phosphorylates Paxillin to promote OC progression. These findings suggest that targeting TRIM15 holds promise as a therapeutic approach to treat OC.

III-V Semiconductors containing a small amount of Bi, known as dilute bismides, have attracted great interest in recent years, due to the large band-gap reduction and other unique properties [1,2]. Previous studies have been pri- marily focused on the growth and optical properties of the GaAs-based bismuthides [3], while the properties of other dilute bismides are less well understood. Berding et al. [4] theoretically predicted that InPBi is expected to be an attractive candidate for narrow-gap applications. Experimentally, the InPBi alloy with good single crystal quality has been successfully synthesized recently and exhibits strong and broad photoluminescence at room temperature [5,6]. However, the electric transport characteristics of the InPBi alloy are poorly understood. In this work, we systematically investigate the effect of Bi incorporation on electric transport properties of the InP1-xBix alloys.

Development of hyperproducing strains is important for biomanufacturing of biochemicals and biofuels but requires extensive efforts to engineer cellular metabolism and discover functional components. Herein, we optimize and use the CRISPR-assisted editing and CRISPRi screening methods to convert a wild-type Corynebacterium glutamicum to a hyperproducer of l -proline, an amino acid with medicine, feed, and food applications. To facilitate l -proline production, feedback-deregulated variants of key biosynthetic enzyme γ-glutamyl kinase are screened using CRISPR-assisted single-stranded DNA recombineering. To increase the carbon flux towards l -proline biosynthesis, flux-control genes predicted by in silico analysis are fine-tuned using tailored promoter libraries. Finally, an arrayed CRISPRi library targeting all 397 transporters is constructed to discover an l -proline exporter Cgl2622. The final plasmid-, antibiotic-, and inducer-free strain produces l -proline at the level of 142.4 g/L, 2.90 g/L/h, and 0.31 g/g. The CRISPR-assisted strain development strategy can be used for engineering industrial-strength strains for efficient biomanufacturing. Corynebacterium glutamicum is a major workhorse in industrial biomanufacturing of amino acids. Here, the authors employ CRISPR-assisted rational flux-tuning and CRISPRi screening of a L-proline exporter to covert a wild-type C. glutamicum to a hyperproducer of L-proline.