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DEPTOR prevents lung tumorigenesis by inactivating the EGFR-mTOR indicators.
Chronic Infection of Hepatitis B virus (HBV) is one risk factor of hepatocellular carcinoma (HCC). Much effort has been made to research the process of HBV-associated HCC, but its molecular mechanisms of carcinogenesis remain vague. Here, weighted gene co-expression network analysis (WGCNA) was employed to explore the co-expressed modules and hub/key genes correlated to HBV-associated HCC. We found that genes of the most significant module related to HBV-associated HCC were enriched in DNA replication, p53 signaling pathway, cell cycle, and HTLV-1 infection associated pathway; these cellular pathways played critical roles in the initiation and development of HCC or viral infections. Furthermore, seven hub/key genes were identified based on the topological network analysis, and their roles in HCC were verified by expression and Kaplan-Meier survival analysis. Protein-protein interaction and KEGG pathway analysis suggested that these key genes may stimulate cellular proliferation to promote the HCC progression. This study provides new perspectives to the knowledge of the key pathways and genes in the carcinogenesis process of HBV-associated HCC, and our findings provided potential therapeutic targets and clues of the carcinogenesis of HBV-associated HCC.
It is widely acknowledged that recruitment to randomised controlled trials (RCTs) is challenging, particularly trials that operate across multiple sites. A research area in need of further high-quality evaluation, including RCTs, is school-based mental health interventions for refugee children and adolescents. However, engaging schools with interventions and associated evaluations can be challenging. click here This paper explores the application of behavioural insights, i.e. evidence-based understanding of how people behave and make decisions, to RCT recruitment at the school level via email communications. A pilot study of applying behavioural insights to mail outs attempting to recruit schools to a RCT of a trauma-focused group intervention for refugee children and adolescents experiencing symptoms of post-traumatic stress is reported. Rates of school involvement between the behavioural insights approach (n = 31) and a standard outreach approach (n = 65) are compared.

Schools were more likely to give a positive response to the mail out designed using the behavioural insights framework than standard outreach. Accounts of recruitment strategies such as this are valuable additions to the literature on RCT methodology given the potential for recruitment issues to affect trial operations.
Schools were more likely to give a positive response to the mail out designed using the behavioural insights framework than standard outreach. Accounts of recruitment strategies such as this are valuable additions to the literature on RCT methodology given the potential for recruitment issues to affect trial operations.In addition to providing structural support, caveolin-1 (Cav1), a component of lipid rafts, including caveolae, in the plasma membrane, is involved in various cellular mechanisms, including signal transduction. Although pre-synaptic membrane dynamics and trafficking are essential cellular processes during synaptic vesicle exocytosis/synaptic transmission and synaptic vesicle endocytosis/synaptic retrieval, little is known about the involvement of Cav1 in synaptic vesicle dynamics. Here we demonstrate that synaptic vesicle exocytosis is significantly impaired in Cav1-knockdown (Cav1-KD) neurons. Specifically, the size of the synaptic recycled vesicle pool is modestly decreased in Cav1-KD synapses and the kinetics of synaptic vesicle endocytosis are somewhat slowed. Notably, neurons rescued by triple mutants of Cav1 lacking palmitoylation sites mutants show impairments in both synaptic transmission and retrieval. Collectively, our findings implicate Cav1 in activity-driven synaptic vesicle dynamics-both exocytosis and endocytosis-and demonstrate that palmitoylation of Cav1 is important for this activity.
Given a collection of coexpression networks over a set of genes, identifying subnetworks that appear frequently is an important research problem known as mining frequent subgraphs. Maximal frequent subgraphs are a representative set of frequent subgraphs; A frequent subgraph is maximal if it does not have a super-graph that is frequent. In the bioinformatics discipline, methodologies for mining frequent and/or maximal frequent subgraphs can be used to discover interesting network motifs that elucidate complex interactions among genes, reflected through the edges of the frequent subnetworks. Further study of frequent coexpression subnetworks enhances the discovery of biological modules and biological signatures for gene expression and disease classification.

We propose a reverse search algorithm, called RASMA, for mining frequent and maximal frequent subgraphs in a given collection of graphs. A key innovation in RASMA is a connected subgraph enumerator that uses a reverse-search strategy to enumerate connen experiments enables the discovery of functional modules and subnetwork biomarkers. We have proposed a reverse search algorithm for mining maximal frequent subnetworks. Enrichment analysis of the extracted maximal frequent subnetworks reveals that subnetworks that are frequent are highly enriched with known biological ontologies.TMEM132D is a human gene identified with multiple risk alleles for panic disorders, anxiety and major depressive disorders. Defining a conserved family of transmembrane proteins, TMEM132D and its homologs are still of unknown molecular functions. By generating loss-of-function mutants of the sole TMEM132 ortholog in C. elegans, we identify abnormal morphologic phenotypes in the dopaminergic PDE neurons. Using a yeast two-hybrid screen, we find that NAP1 directly interacts with the cytoplasmic domain of human TMEM132D, and mutations in C. elegans tmem-132 that disrupt interaction with NAP1 cause similar morphologic defects in the PDE neurons. NAP1 is a component of the WAVE regulatory complex (WRC) that controls F-actin cytoskeletal dynamics. Decreasing activity of WRC rescues the PDE defects in tmem-132 mutants, whereas gain-of-function of TMEM132D in mammalian cells inhibits WRC, leading to decreased abundance of select WRC components, impaired actin nucleation and cell motility. We propose that metazoan TMEM132 family proteins play evolutionarily conserved roles in regulating NAP1 protein homologs to restrict inappropriate WRC activity, cytoskeletal and morphologic changes in the cell.
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