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Background Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) has been documented to implicate in diverse tumor progression. However, the mechanism of NEAT1 in glioma was rarely reported. Methods The levels of NEAT1, microRNA-152-3p (miR-152-3p) and chaperonin containing TCP1 subunit 6A (CCT6A) in glioma tissues and cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability, apoptotic rate, the migrated and invaded abilities of A172 and U251 cells were evaluated via cell counting kit-8 (CCK-8), flow cytometry and Transwell assay, respectively. The mice xenograft model was constructed to further verify the effect of NEAT1. The interactions between miR-152-3p and NEAT1 or CCT6A were predicted by starBase v2.0 or TargetScan, then luciferase reporter assay, RNA immunoprecipitation (RIP) and RNA pull-down assay were performed to validate the interaction. The protein level of CCT6A was detected by Western blot assay. Results The levels of NEAT1, CCT6A were highly expressed, but miR-152-3p was decreased in glioma tissues and cells. NEAT1 depletion or miR-152-3p mimics suppressed cell viability, migrated and invaded abilities but induced apoptotic rate in A172 and U251 cells, while the introduction of CCT6A partly counteracted these impacts. In addition, NEAT1 silencing impeded xenograft tumor growth in vivo. MiR-152-3p was verified as a direct target of NEAT1 and directly targeted CCT6A. CCT6A expression was upregulated by NEAT1 and reversed by miR-152-3p. Conclusion NEAT1 enhanced glioma progression, partially through miR-152-3p/CCT6A pathway. The novel regulatory network might contribute to the diagnosis and treatment of glioma.We aimed to evaluate lung cancer survival in never-smokers, both overall and specifically by sex, exposure to residential-radon, age, histological type, and diagnostic stage. We included lung cancer cases diagnosed in a multicentre, hospital-based, case-control-study of never-smoker patients, diagnosed from January-2011 to March-2015 (Lung Cancer Research In Never Smokers study). 369 never-smokers (79% women; median age 71 years; 80% adenocarcinoma; 66% stage IV) were included. Median overall survival, and at one, 3 and 5 years of diagnosis was 18.3 months, 61%, 32% and 22%, respectively. Higher median survival rates were obtained for younger age, adenocarcinoma, actionable mutations, and earlier-stage at diagnosis. Higher indoor radon showed a higher risk of death in multivariate analysis. learn more Median lung cancer survival in never-smokers seems higher than that in ever-smokers. Patients with actionable mutations have a significantly higher survival. Higher indoor-radon exposure has a negative effect on survival.Chimeric antigen receptor T (CAR-T) therapy faces at least two major obstacles in solid tumors, including to find specific antigen among the heterogeneous tumor mass and to overcome the inhibitory microenvironment. Developing novel strategies to overcome these difficulties has been the burning issue in immunotherapy. Here we came up with the concept of tagging cancer cells by tumor-targeting adenoviruses (Ad). We constructed recombinant Ads expressing CD19 tag driven by tumor-specific promoters, which could label antigenically different tumors for single anti-CD19 CAR-T recognition. One Ad, namely AdC68-TMC-tCD19 could mediate universal tag expression and functional immunological synapse formation between CAR-T and cancer cells. In premixed mice model, all tagged mice survived after CAR-T infusion and tumor volume were inhibited by 91.78%. Furthermore, we combined the tumor tagging ability with oncolysis and generated the replicative AdC68-Sur-E1A-TMC-tCD19. Oncolytic tagging system could diminish established tumors in vivo and prolong mice survival significantly. Therefore, we suggest the universal oncolytic Ad-tagging system in combination with single target CAR-T cells could be a powerful complement in immunotherapy against antigenically mismatched solid tumors.Reinforcement learning guides food decisions, yet how the brain learns from taste in humans is not fully understood. Existing research examines reinforcement learning from taste using passive condition paradigms, but response-dependent instrumental conditioning better reflects natural eating behavior. Here, we examined brain response during a taste-motivated reinforcement learning task and how measures of task-based network structure were related to behavioral outcomes. During a functional MRI scan, 85 participants completed a probabilistic selection task with feedback via sweet taste or bitter taste. Whole brain response and functional network topology measures, including identification of communities and community segregation, were examined during choice, sweet taste, and bitter taste conditions. Relative to the bitter taste, sweet taste was associated with increased whole brain response in the hippocampus, oral somatosensory cortex, and orbitofrontal cortex. Sweet taste was also related to differential community assignment of the ventromedial prefrontal cortex and ventrolateral prefrontal cortex compared to bitter taste. During choice, increasing segregation of a community containing the amygdala, hippocampus, and right fusiform gyrus was associated with increased sensitivity to punishment on the task's posttest. Further, normal BMI was associated with differential community structure compared to overweight and obese BMI, where high BMI reflected increased connectivity of visual regions. Together, results demonstrate that network topology of learning and memory regions during choice is related to avoiding a bitter taste, and that BMI is associated with increased connectivity of area involved in processing external stimuli. Network organization and topology provide unique insight into individual differences in brain response to instrumental conditioning via taste reinforcers.Antagonism of the functional ghrelin receptors impairs memory formation, but the underlying mechanisms are not well-known. We aimed to evaluate the effect of intracerebral injection of a ghrelin receptor antagonist (D-Lys-3-GHRP-6) on memory consolidation in the inhibitory avoidance task and on the gene expression levels of serotonin HT1A and HT7 receptors, glutamate GluN1 subunit of the NMDA and GluA1 subunit of the AMPA receptors and calcium/calmodulin kinase II-α in the hippocampus of rats. Thirty adult male rats were implanted with cannulas in their lateral ventricles. Three groups of animals (n=5) received D-Lys-3-GHRP-6 (0.5 and 5nM) or saline immediately post-training. Twenty-four hours later, memory retrieval was assessed. Three additional groups of animals (n=5) received D-Lys-3-GHRP-6 (0.5 and 5nM) or saline, but animals in these groups were decapitated, and their hippocampus was removed, 24 hours thereafter. The target gene expression levels were measured using a quantitative real-time PCR method. D-Lys-3-GHRP-6 impaired memory consolidation.
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