Objectives. To investigate the predictors of telomerase reverse transcriptase (TERT) promoter mutations in adults suffered from high-grade glioma (HGG) through radiomics analysis, develop a noninvasive approach to evaluate TERT promoter mutations. Methods. 126 adult patients with HGG (88 in the training cohort and 38 in the validation cohort) were retrospectively enrolled. Totally 5064 radiomics features were, respectively, extracted from three VOIs (necrosis, enhanced, and edema) in MRI. Firstly, an optimal radiomics signature (Radscore) was established based on LASSO regression. Secondly, univariate and multivariate logistic regression analyses were performed to investigate important potential variables as predictors of TERT promoter mutations. Besides, multiparameter models were established and evaluated. Eventually, an optimal model was visualized as radiomics nomogram for clinical evaluations. Results. 6 radiomics features were selected to build Radscore signature through LASSO regression. Among them, 5 were from necrotic VOIs and 1 was from enhanced ones. With univariate and multivariate analysis, necrotic volume percentages of core (CNV), Age, Cho/Cr, Lac, and Radscore were significantly higher in TERTm than in TERTw (p<0.05). 4 models were built in our study. Compared with Model B (Age, Cho/Cr, Lac, and Radscore), Model A (Age, Cho/Cr, Lac, Radscore, and CNV) has a larger AUC in both training (0.955 vs. 0.917, p=0.049) and validation (0.889 vs. 0.868, p=0.039) cohorts. It also has higher performances in net reclassification improvement (NRI), integrated discrimination improvement (IDI), and decision curve analysis (DCA) evaluation. Conclusively, Model A was visualized as a radiomics nomogram. Calibration curve shows a good agreement between estimated and actual probabilities. Conclusions. Age, Cho/Cr, Lac, CNV, and Radscore are important indicators for TERT promoter mutation predictions in HGG. Tumor necrosis seems to be closely related to TERT promoter mutations. Radiomics nomogram based on multiparameter MRI and CNV has higher prediction accuracies.

Objective To observe the hemostatic effect of prophylactic uterine artery embolization (UAE) in patients with cesarean scar pregnancy (CSP) and to examine the risk factors for poor hemostasis. Methods Clinical data of 841 patients with CSP who underwent prophylactic UAE and curettage were retrospectively analyzed to evaluate the hemorrhage volume during curettage. A hemorrhage volume ≥200 mL was termed as poor hemostasis. The risk factors of poor hemostasis were analyzed and complications within 60 days postoperation were recorded. Results Among the 841 patients, 6.30% (53/841) had poor postoperative hemostasis. The independent risk factors of poor hemostasis were gestational sac size, parity, embolic agent diameter (>1000 μm), multivessel blood supply, and incomplete embolization. The main postoperative complications within 60 days after UAE were abdominal pain, low fever, nausea and vomiting, and buttock pain, with incidence rates of 71.22% (599/841), 47.44% (399/841), 39.12% (329/841), and 36.39% (306/841), respectively. Conclusions Prophylactic UAE before curettage in patients with CSP is safe and effective in reducing intraoperative hemorrhage. Gestational sac size, parity, embolic agent diameter, multivessel blood supply, and incomplete embolization of all arteries supplying blood to the uterus are risk factors of poor hemostasis.

Hyperglycemia mediated endothelial cells (ECs) injury is closely associated with diabetic vascular complications. It was revealed that DJ‑1 possesses cellular protective effects by suppressing oxidative stress. The present study aimed to investigate the beneficial effects of DJ‑1 on high glucose (HG)‑induced human umbilical vein endothelial cell (HUVEC) injury and to elucidate its underlying mechanisms. HUVECs were incubated under 5.5 mM (control group) or 25 mM D‑glucose (HG group) and then transfected with recombinant adenoviral vectors to overexpression of DJ‑1. Cell proliferation and apoptosis were measured using the EdU incorporation assay and flow cytometry with Annexin V-FITC/propidium iodide double staining, respectively. Apoptotic‑related proteins were determined using western blot analysis. Reactive oxygen species (ROS) production, lactate dehydrogenase (LDH) and nitric oxide (NO) levels, the content of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) were measured. Results demonstrated that overexpression of DJ‑1 promoted cell proliferation and inhibited HUVECs apoptosis stimulated by HG. DJ‑1 also suppressed the HG‑induced reduction in the Bcl‑2/Bax ratio and HG activated ROS generation in HUVECs. Furthermore, HG significantly increased the levels of LDH and MDA, and reduced the level of SOD; however, these effects were reversed by Ad‑DJ‑1 transfection. Furthermore, the cellular protective effect of overexpression of DJ‑1 enhanced p‑Akt/Akt ratio, eNOS activation and NO production, and these trends were partially reversed by a phosphatidylinositol‑4,5‑bisphosphate 3‑kinase (PI3K) inhibitor (LY294002). Taken together, the present study highlighted the involvement of DJ‑1 in HG‑related EC injury and identified that DJ‑1 exerts a cellular protective effect in HUVECs exposed to HG induced oxidative stress via activation of the PI3K/Akt‑eNOS signaling pathway.