LncRNAs play critical roles in various pathophysiological and biological processes, such as protein translation, RNA splicing, and epigenetic modification. Indeed, abundant evidences demonstrated that lncRNA act as competing endogenous RNAs (ceRNAs) to participate in tumorigenesis. However, little is known about the underlying function of lncRNA in nonhomologous end joining (NHEJ) pathway 1 (LINP1) in pediatric and adolescent acute myeloid leukemia (AML). The expression of LINP1 was examined in AML patient samples by qRT‐PCR. Cell proliferation was examined by CCK‐8 and Edu assays. β‐Galactosidase senescence assay, mGlucose uptake assay, lactate production assay, and Gene Ontology (GO) analysis were performed for functional analysis. We found that LINP1 was significantly overexpressed in AML patients at diagnosis, whereas downregulated after complete remission (CR). Furthermore, knockdown of LINP1 expression remarkably suppressed glucose uptake and AML cell maintenance. Mechanistically, LINP1 was found to inhibit the glucose metabolism by suppressing the expression of HNF4a. Both LINP1 and HNF4a knockdown reduced the expression levels of AMPK phosphorylation and WNT5A, indicating for the first time that LINP1 strengthened the HNF4a‐AMPK/WNT5A signaling pathway involved in cell glucose metabolism modulation and AML cell survival. Taken together, our results indicated that LINP1 promotes the malignant phenotype of AML cells and stimulates glucose metabolism, which can be regarded as a potential prognostic marker and therapeutic target for AML.

Purpose To investigate the mid- and long-term effects of parent artery occlusion on the carotid cavernous fistula and on the quality of life of patients. Materials and methods One hundred and twenty-six patients with high-flow direct carotid cavernous fistulas were enrolled. The modified Rankin scale scores, the headache impact test and the short form health survey scores were used to evaluate the patients' clinical status. Results Fifty-two patients had parent artery occlusion, while the rest of the 74 patients had embolization of carotid cavernous fistulas with parent artery preservation. No periprocedural complications occurred. Eighteen patients in the parent artery occlusion group had low perfusion symptoms within two weeks following embolization, and three patients had Horner's syndrome on the ipsilateral side. At two months' follow-up, the patients with parent artery occlusion had a significantly ( P < 0.05) greater proportion of headache than patients with parent artery preservation. At 12 months, no significant ( P > 0.05) difference existed in the headache impact test scores in both groups. At 36 months' follow-up, the patients with parent artery occlusion had decreased SF-30 scores in all the eight health domains compared with patients treated with parent artery preservation, with a significant ( P < 0.05) lower score in general health, vitality and bodily pain in the parent artery occlusion compared with the parent artery preservation group. No recurrence was shown in patients with parent artery occlusion, but nine (12.2%) patients were recurrent in patients with parent artery preservation. Conclusion Parent artery occlusion may affect the quality of life of patients with carotid cavernous fistulas despite being an effective treatment option for high-flow direct fistulas.

Objectives: A growing number of studies demonstrate that long noncoding RNAs (lncRNAs) could act as biomarkers to determine the prognosis of acute myeloid leukemia (AML) patients. Nonetheless, the significance of lncRNAs in AML prognosis remains unclear. We conducted a meta-analysis to assess the prognostic indicators of abnormally expressed lncRNAs in AML. Methods: Literature was searched using PubMed, EMBASE, and Web of Science databases up to November 10, 2018. Results: Thirteen studies with 2755 individuals were included. The abnormal expression of lncRNAs was associated with worse overall survival (OS) in AML patients, especially in cytogenetically normal AML (CN-AML), and was associated with shorter disease-free survival and event-free survival. Subgroup analysis showed that high levels of HOTAIR and TUG1 were associated with poor OS. Discussion: Overexpression of lncRNA HOTAIR and TUG1 were reported in two separate studies, and correlated with worse AML prognoses. Conclusion: Abnormally expressed lncRNAs are significantly related to worse prognoses of AML patients and might serve as potential prognostic markers to predict the prognosis of AML patients.