Dysfunction of the glymphatic system in childhood absence epilepsy.

Objective: This study aimed to evaluate the glymphatic system in childhood absence epilepsy (CAE) using diffusion tensor image analysis along the paravascular space (DTI-ALPS) index. Methods: Forty-two CAE patients and 50 age- and gender-matched healthy controls (HC) were included in this study. All participants underwent scanning using a Siemens 3.0 T magnetic resonance scanner, and the DTI-ALPS index was calculated. The study compared the differences of DTI-ALPS index between CAE patients and the healthy controls. Additionally, this study also assessed the relationship between the DTI-ALPS index and clinical characteristics such as age, seizure frequency, and duration of epilepsy. Results: The DTI-ALPS index was lower in CAE patients compared to the healthy controls (1.45 ± 0.36 vs. 1.66 ± 0.30, p < 0.01). The DTI-ALPS index showed a negative correlation with the duration of epilepsy (r = -0.48, p < 0.01) and a positive correlation with age (r = 0.766, p < 0.01) in CAE patients. However, no significant correlation was observed between the DTI-ALPS index and seizure frequency. Conclusion: The results of this study indicate that children with CAE exhibit dysfunction in the glymphatic system of the brain, which might contribute to understanding the pathophysiological mechanism of CAE. The DTI-ALPS, as a non-invasive diagnostic marker, can be used to assess the function of the glymphatic system in CAE patients, providing promising applications in the diagnosis and research of CAE.

Down-regulation of MBNL1-AS1 contributes to tumorigenesis of NSCLC via sponging miR-135a-5p.

Lung cancer remains a big threat to human health. Growing evidence has reported the crucial regulatory effect of lncRNAs on NSCLC progression. Nevertheless, the detailed function of lncRNA MBNL1-AS1 involved in NSCLC development is poorly known. In our research, we confirmed that MBNL1-AS1 was significantly reduced in NSCLC patient tissues and NSCLC cells. Meanwhile, we reported that overexpression of MBNL1-AS1 obviously repressed A549 and H1975 cell proliferation, blocked cell cycle and inhibited the migration and invasion. Moreover, A549 and H1975 cell apoptosis was increased by the overexpression of MBNL1-AS1. Then, we predicted that miR-135a-5p was a potential target of MBNL1-AS1 and its level was correlated with MBNL1-AS1 in NSCLC negatively. Our previous study indicated miR-135a-5p could induce lung cancer progression through regulating LOXL4. Here, we found that MBNL1-AS1 was able to regulate miR-135a-5p expression negatively. The direct binding association between MBNL1-AS1 and miR-135a-5p was proved using dual-luciferase reporter assay and RIP experiment. Subcutaneous xenotransplanted tumor model was set up and it was confirmed increased MBNL1-AS1 remarkably restrained tumorigenic ability of NSCLC through sponging miR-135a-5p in vivo. To sum up, our data revealed the significance of the MBNL1-AS1 and miR-135a-5p in NSCLC. In conclusion, MBNL1-AS1 could be a new therapeutic target to treat NSCLC.