Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that affects approximately 8%–12% of children worldwide. Throughout an individual’s lifetime, ADHD can significantly increase risk for other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. The multifactorial causation of ADHD is reflected in the heterogeneity of this disorder, as indicated by its diversity of psychiatric comorbidities, varied clinical profiles, patterns of neurocognitive impairment and developmental trajectories, and the wide range of structural and functional brain anomalies. Although evidence-based treatments can reduce ADHD symptoms in a substantial portion of affected individuals, there is yet no curative treatment for ADHD. A number of theoretical models of the emergence and developmental trajectories of ADHD have been proposed, aimed at providing systematic guides for clinical research and practice. We conducted a comprehensive review of the current status of research in understanding the heterogeneity of ADHD in terms of etiology, clinical profiles and trajectories, and neurobiological mechanisms. We suggest that further research focus on investigating the impact of the etiological risk factors and their interactions with developmental neural mechanisms and clinical profiles in ADHD. Such research would have heuristic value for identifying biologically homogeneous subgroups and could facilitate the development of novel and more tailored interventions that target underlying neural anomalies characteristic of more homogeneous subgroups.
Background: Hepatocellular carcinoma (HCC) is one of the most prevalent tumors worldwide. However, the key roles of most molecules associated with tumor proliferation, invasion, and metastasis in HCC remain unclear. It is therefore important to explore potential mechanisms underlying tumorigenesis and to screen genes and pathways identified from such research for their role in pathogenesis. Materials and Methods: We selected microarray data GSE62043 consisting of paired tissue samples from 100 HCC patients, then these data were analyzed to identify differentially expressed genes (DEGs). Next, gene ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out to elucidate the biological processes, molecular function, cellular component (CC), and KEGG signaling pathways for the DEGs. We then constructed protein-protein interaction (PPI) networks, followed by a functional enrichment analysis, from which we obtained two significant gene modules. Finally, the gene expression data obtained from this test set were subjected to validation studies using an independent set of hepatocellular patient data archived in The Cancer Genome Atlas and Genotype-Tissue Expression (TCGA/GTEx) database. Results: A total of 425 DEGs were identified that met both of our criteria for significance: (1) a jlog2-fold change (FC)j ‡ 1.2 and (2) an adjusted p value <0.01. From these data, two significant gene modules, containing 28 pathway-related hub genes, were identified. Conclusion: Through application of a test/validation algorithm using HCC datasets from two independent databases, we identified a number of genes that could serve as potential biomarkers for the molecular diagnosis and therapeutic intervention of HCC, including the known genes, IGF1, IGF2, NDC80, CDK1, CENPF, CDCA8, CCNB1, BIRC5, NCAPG, and CDCA5, and the novel genes, CENPU and SPC25, which are associated with cell cycle, mitotic cell cycle, and organelle organization.
Both externalizing behavior and callous-unemotional (CU) traits in youth are precursors to later criminal offending in adulthood. It is posited that disruptions in reward and punishment processes may engender problematic behavior, such that CU traits and externalizing behavior may be linked to a dominant reward response style (e.g., heightened responsivity to rewards) and deficient punishment-processing. However, prior research has generated mixed findings and work examining both the sole and joint contribution of CU traits and externalizing problems related to functional brain alterations is lacking. In this pilot functional magnetic resonance imaging study, we measured externalizing behavior and CU traits in a community sample of adolescents (n = 29) and examined their impacts on brain activity associated with anticipation and receipt of reward and punishment using the Modified Monetary Incentive Delay task. We found that CU traits were associated with greater activation of the ventral striatum (VST) during reward anticipation. However, this effect became non-significant after controlling for externalizing behavior, indicating substantial overlap between the CU and externalizing measures in explaining VST activation when anticipating reward. In addition, externalizing behavior (but not CU) was significantly negatively associated with amygdala activation during punishment receipt, even after controlling for CU traits. The present findings extend previous evidence of hyper-responsivity to reward and hyporesponsivity to punishment in relation to psychopathic traits and antisocial behavior to non-clinical, non-incarcerated youths.
ABSTRACT. The aim of this study was to identify differentially expressed genes (DEGs) in renal medullary hypertension and reveal their pathogenic mechanisms. We downloaded the gene expression profile of GSE28360 from the Gene Expression Omnibus database. The profile included 14 samples (5 normal and 9 hypertension). The DEGs in normal and disease samples were distinguished with a false-discovery rate threshold of <0.05 and a fold-change value of >2 or <-2. We put the selected genes into the online program String 8.3 to obtain the protein-protein interaction network and selected the hub proteins. These hub proteins were then placed in the PANTHER database to determine hub protein-related pathways and explain their functions. Finally, we cleared up the singlenucleotide polymorphisms (SNPs) of the hub genes via combing with the National Center for Biotechnology SNP database. A total of 13 genes were identified as DEGs between normal and disease samples. Five selected hub proteins, B-cell translocation gene 2 (BTG2), FBJ murine osteosarcoma viral oncogene homolog (FOS), nuclear receptor subfamily 4, group A, member 1 (NR4A1), NR4A member 2 (NR4A2), and NR4A member 3 (NR4A3), were mainly related to angiogenesis and B-cell activation. After SNP analysis, 103, 103, 595, 150, and 493 SNPs were found to correspond to BTG2, FOS, NR4A1, NR4A2, and NR4A3, respectively. Our results suggest that pathways of angiogenesis and B-cell activation may involve in the progression of renal medulla hypertension.
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