Background: Predictors of outcomes following endovascular treatment (ET) for aneurysmal subarachnoid hemorrhage (aSAH) are not well-defined. Identifying them would be beneficial in determining which patients might benefit from ET. Objective: To identify the predictive factors for poor outcomes following ET for aSAH. Methods: 120 patients with ruptured cerebral aneurysms underwent endovascular embolization between January 2017 and December 2018. Blood pressure variability was examined using the standard deviation of the 24-hour systolic blood pressure (24hSSD) and 24-hour diastolic blood pressure (24hDSD). Predictors were identified through univariate and multivariate regression analysis. All patients were followed up for three months. Results: At follow-up, 86 patients (71.7%) had good outcomes and 34 (28.3%) had poor outcomes. Patients with poor outcomes had significantly higher 24hSSD than those with good outcomes (19.3 ± 5.5 vs 14.1 ± 4.8 mmHg; P < 0.001). The 24hDSD did not differ significantly between patients with good outcomes and those with poor outcomes (9.5 ± 2.3 vs 9.9 ± 3.5 mmHg; P = 0.464). The following were significant risk factors for poor outcomes after endovascular embolization: age ≥ 65 years (odds ratio [OR] = 23.0; 95% confidence interval [CI]: 3.0-175.9; P = 0.002); Hunt-Hess grade 3-4 (OR = 6.8; 95% CI: 1.1-33.7; P = 0.039); Fisher grade 3-4 (OR = 47.1; 95% CI: 3.8-586.5; P = 0.003); postoperative complications (OR = 6.1; 95% CI: 1.1-34.8; P = 0.042); and 24hSSD ≥ 15 mmHg (OR = 14.9; 95% CI: 4.0-55.2; P < 0.001). Conclusion: Elevated 24hSSD is a possibly treatable predictive factor for poor outcomes after ET for aSAH.

Glioma is one of the most commonly observed tumours, representing approximately 75% of brain tumours in the adult population. Generally, glioma therapy includes surgical resection followed by radiotherapy and chemotherapy. The transcription factor STAT3 (signal transducer and activator of transcription 3) is a promising target for the treatment of cancer and several other diseases. At nanomolar concentrations, SD‐36 induces rapid cellular degradation of STAT3 but cannot degrade other STAT proteins. The current study demonstrates the therapeutic efficacies of the STAT3 degraders SD‐36 against glioma, as well as understanding the elucidating mechanisms and identifying molecular markers that determine cell sensitivity to STAT3 degraders. Glioma cell lines possessed similar response patterns to SD‐36 but different responses to the STAT3 inhibitor Stattic. SD‐36 potently induced apoptosis in glioma cells along with a reduction in Mcl‐1 levels, which are critical for mediating the induction of apoptosis and enhancing TMZ‐induced apoptosis. Accordingly, SD‐36 sensitizes the antitumour effect of TMZ in patient‐derived xenograft. In addition, the downregulation of Mcl‐1 expression‐mediated antitumour effect of SD‐36 was analysed in cell‐derived xenograft. These observations need to be validated clinically to confirm the efficacy of STAT3 degraders in glioma.

BACKGROUND: The current understanding of untreated ruptured intracranial aneurysms has been limited by study design and inaccurate patient data. Multicenter clinical registry studies on untreated ruptured intracranial aneurysms in Chinese patients are scarce. We aimed to calculate the mortality of patients with untreated ruptured intracranial aneurysms in a current, clearly defined hospital cohort in China, with emphasis on mortality predictors over a 2-year period. METHODS: Patients with saccular untreated ruptured intracranial aneurysms were identified from the Chinese Multicenter Cerebral Aneurysm Database, a multicenter, prospective, observational database registered in China, which involved 32 tertiary medical centers covering 4 northern Chinese provincial regions. Patients with intracranial aneurysms, regardless of ruptured status, shape, age, or comorbidities, were consecutively included in 12 of 32 medical centers between 2017 and 2020. Survival probabilities were computed using the Kaplan-Meier method. Univariate and multivariate Cox regression analyses were conducted to determine the risk factors for the cumulative 2-year mortality. We analyzed the reasons for treatment decisions stratified by demographic characteristics and clinical features. RESULTS: For 941 enrolled patients, 58.6% of patients died within 1 month of symptom onset; and 68.1% within 2 years. 98 patients underwent surgical repair during follow-up. Multivariate Cox regression analysis identified Hunt and Hess grades 3 to 5 (hazard ratio, 1.54 [95% CI, 1.01–2.35]; P =0.047), loss of consciousness at symptom onset (hazard ratio, 1.56 [95% CI, 1.18–2.07]; P =0.002), and largest aneurysm size of ≥5 mm (hazard ratio, 1.29 [95% CI, 1.05–1.59]; P =0.014) as mortality predictors during the 2-year follow-up. Among patients who were successfully followed up, 42.6% (280) of them refused surgical treatment. CONCLUSIONS: Patients with poor Hunt and Hess grades, loss of consciousness at symptom onset, or largest aneurysms ≥5 mm in size showed a high mortality rate. A high number of treatment refusals was present in this study. These findings have implications for medical insurance policy, doctor-patient communication, and popular science education.