Objective: Internet gaming disorder (IGD) has been investigated by many behavioral and neuroimaging studies, for it has became one of the main behavior disorders among adolescents. However, few studies focused on the relationship between alteration of gray matter volume (GMV) and cognitive control feature in IGD adolescents.Methods: Twenty-eight participants with IAD and twenty-eight healthy age and gender matched controls participated in the study. Brain morphology of adolescents with IGD and healthy controls was investigated using an optimized voxel-based morphometry (VBM) technique. Cognitive control performances were measured by Stroop task, and correlation analysis was performed between brain structural change and behavioral performance in IGD group.Results: The results showed that GMV of the bilateral anterior cingulate cortex (ACC), precuneus, supplementary motor area (SMA), superior parietal cortex, left dorsal lateral prefrontal cortex (DLPFC), left insula, and bilateral cerebellum decreased in the IGD participants compared with healthy controls. Moreover, GMV of the ACC was negatively correlated with the incongruent response errors of Stroop task in IGD group.Conclusion: Our results suggest that the alteration of GMV is associated with the performance change of cognitive control in adolescents with IGD, which indicating substantial brain image effects induced by IGD.

Abstract. Recent studies suggest that long non-coding RNAs (lncRNAs) are more involved in human diseases than previously realized. A growing body of evidence links lncRNA mutation and dysregulation to diverse human diseases. However, the association of lncRNAs with the pathogenesis of lung fibrosis remains poorly understood. In this study, we detected changes in hydroxyproline and collagen levels, as well as the ultrastructure of lung tissue to develop a rat model of lung fibrosis. The differentially expressed lncRNAs and mRNA profiles between fibrotic lung and normal lung tissue were analyzed using microarrays. Gene Ontology analysis and pathway analysis were performed for further research. Two differentially expressed lncRNAs, namely, AJ005396 and S69206, were detected by in situ hybridization to validate the microarray data. The results revealed that the number of collagen fibers in the interstitial lung tissue significantly increased in the model group compared with the normal group. In total, 210 and 358 lncRNAs were upregulated and downregulated, respectively, along with 415 upregulated and 530 downregulated mRNAs in the rats with lung fibrosis. AJ005396 and S69206 were upregulated in the fibrotic lung tissue, consistent with the microarray data, and were located in the cytoplasm of the interstitial lung cells. In conclusion, the expression profile of the lncRNAs was significantly altered in the fibrotic lung tissue and these transcripts are potential molecular targets for inhibiting the development of lung fibrosis. IntroductionIdiopathic pulmonary fibrosis (IPF) is a common, chronic, progressive and usually lethal fibrotic lung disease with poor prognosis (1). This disease is characterized by focal areas of alveolar epithelial cell injury and the excessive proliferation of mesenchymal cells in the interstitium, which results in the excessive deposition of extracellular matrix (ECM) and distorted architecture leading to impaired gas exchange (2,3). Although many pathobiological concepts are emerging, including the role of aging and cellular senescence, oxidative stress, endoplasmic reticulum stress, cellular plasticity, microRNA (miRNA) and mechanotransduction, the molecular mechanisms behind IPF are not yet completely understood (4).The Encyclopedia of DNA Elements (ENCODE) project, which aimed to comprehensively characterize the human genome, has shown that >90% of the genome has been transcribed; however, only 1-2% of that is composed of genes (5). The majority of these transcripts are not translated into proteins and are, therefore, termed non-coding RNAs (ncRNAs).Long non-coding RNAs (lncRNAs), a type of ncRNA, vary in size from 200 bp to >100 kb, and are transcribed by RNA polymerase II (6). They play an important role in imprinting (7), enhancing various biological functions (8), X chromosome inactivation (9), chromatin structure (10) and genomic rearrangement during the generation of antibody diversity (11). Thus, lncRNAs are critical for normal development and, in many cases, are deregulated in d...

Oxidative stress is an important molecular mechanism underlying lung fibrosis. The mitochondrion is a major organelle for oxidative stress in cells. Therefore, blocking the mitochondrial signalling pathway may be the best therapeutic manoeuver to ameliorate lung fibrosis. Astaxanthin (AST) is an excellent antioxidant, but no study has addressed the pathway of AST against pulmonary oxidative stress and free radicals by the mitochondrion-mediated signalling pathway. In this study, we investigated the antioxidative effects of AST against H2O2- or bleomycin (BLM)-induced mitochondrial dysfunction and reactive oxygen species (ROS) production in alveolar epithelial cells type II (AECs-II) in vivo and in vitro. Our data show that AST blocks H2O2- or BLM-induced ROS generation and dose-dependent apoptosis in AECs-II, as characterized by changes in cell and mitochondria morphology, translocation of apoptotic proteins, inhibition of cytochrome c (Cyt c) release, and the activation of caspase-9, caspase-3, Nrf-2 and other cytoprotective genes. These data suggest that AST inhibits apoptosis in AECs-II cells through the ROS-dependent mitochondrial signalling pathway and may be of potential therapeutic value in lung fibrosis treatment.