Ying Hu

Short video addiction (SVA) has emerged as a growing behavioral and social issue, driven by the widespread use of digital platforms that provide highly engaging, personalized, and brief video content. We investigated the neuroanatomical and functional substrates of SVA symptoms, alongside brain transcriptomic and cellular characteristics, using Inter-Subject Representational Similarity Analysis (IS-RSA) and transcriptomic approaches. Behaviorally, we found that dispositional envy was associated with SVA. Structurally, SVA was positively correlated with increased morphological volumes in the orbitofrontal cortex (OFC) and bilateral cerebellum. Functionally, the dorsolateral prefrontal cortex (DLPFC), posterior cingulate cortex (PCC), cerebellum, and temporal pole (TP) exhibited heightened spontaneous activity, which was positively correlated with SVA severity. Transcriptomic and cellular analyses also showed specific genes linked to gray matter volume (GMV) associated with SVA, with predominant expression in excitatory and inhibitory neurons. These genes showed distinct spatiotemporal expression patterns in the cerebellum during adolescence. This study offers a comprehensive framework integrating structural, functional, and neurochemical evidence to highlight the neural-transcriptomic underpinnings of SVA symptoms in a non-clinical population.

Aneuploidy with chromosome instability is a cancer hallmark. We studied chromosome 7 copy number variation in gliomas and in primary cultures derived from them. We found tumor heterogeneity with cells having Chr7-CNV commonly occurs in gliomas, with a higher percentage of cells in high-grade gliomas carrying more than 2 copies of Chr7, as compared to low-grade gliomas. Interestingly, all Chr7-aneuploid cell types in the parental culture of established glioma cell lines reappeared in single-cell-derived subcultures. We then characterized the biology of three syngeneic glioma cultures dominated by different Chr7-aneuploid cell types. We found phenotypic divergence for cells following Chr7 missegregation, which benefited overall tumor growth in vitro and in vivo. Mathematical modeling suggested the involvement of chromosome instability and interactions among cell subpopulations in restoring the optimal equilibrium of tumor cell types. Both our experimental data and mathematical modeling demonstrated that the complexity of tumor heterogeneity could be enhanced by the existence of chromosomes with structural abnormality, in addition to their mis-segregations. Overall, our findings show, for the first time, the involvement of chromosome instability in maintaining tumor heterogeneity, which underlies the enhanced growth, persistence and treatment resistance of cancers. © 2013 Hu et al.