Objective: To study the factors affecting the survival and prognosis of patients with intracranial ependymoma. Methods:From January 2008 to January 2018, the prognoses of 276 patients with intracranial ependymoma were analyzed using Log-rank and Cox model analysis. The variables included sex, age, tumor location, tumor diameter, resection extent, pathological grade, Ki-67 index, postoperative radiotherapy, and postoperative chemotherapy. Results: Tumor location, resection extent, and postoperative radiothera-py could all affect the overall survival (OS) and progression-free survival (PFS) of patients with intracranial ependymoma (P<0.001) and independently affected the OS (P<0.001, P<0.001, and P=0.002, respectively) and PFS (P<0.001, P<0.001, and P=0.001, respectively). The Ki-67 index was an independent factor affecting PFS in patients with intracranial ependymoma (P<0.001). The supratentorial loca-tion and Ki-67 index≥10% were independent risk factors indicating poor prognosis (P<0.001). Total resection and postoperative radio-therapy were protective factors (P<0.001 and P=0.001, respectively). Conclusions: Tumor location, resection extent, Ki-67 index, and postoperative radiotherapy are independent factors affecting the prognosis of intracranial ependymoma. It is helpful to extend the PFS and OS of patients through complete tumor resection or postoperative radiotherapy.

Pulmonary hypertension (PH) is an extremely malignant pulmonary vascular disease of unknown etiology. ADAR1 is an RNA editing enzyme that converts adenosine in RNA to inosine, thereby affecting RNA expression. However, the role of ADAR1 in PH development remains unclear. In the present study, we investigated the biological role and molecular mechanism of ADAR1 in PH pulmonary vascular remodeling. Overexpression of ADAR1 aggravated PH progression and promoted the proliferation of pulmonary artery smooth muscle cells (PASMCs). Conversely, inhibition of ADAR1 produced opposite effects. High-throughput whole transcriptome sequencing showed that ADAR1 was an important regulator of circRNAs in PH. CircCDK17 level was significantly lowered in the serum of PH patients. The effects of ADAR1 on cell cycle progression and proliferation were mediated by circCDK17. ADAR1 affects the stability of circCDK17 by mediating A-to-I modification at the A5 and A293 sites of circCDK17 to prevent it from m1A modification. We demonstrate for the first time that ADAR1 contributes to the PH development, at least partially, through m1A modification of circCDK17 and the subsequent PASMCs proliferation. Our study provides a novel therapeutic strategy for treatment of PH and the evidence for circCDK17 as a potential novel marker for the diagnosis of this disease.