Rivasmcleod8803

MiR-1297 could be sponged by circ_PGPEP1, and its expression was downregulated in GC. MiR-1297 inhibitor could reverse the negatively regulation of circ_PGPEP1 knockdown on GC progression. Furthermore, we also found that E2F3 could be targeted by miR-1297, and its expression was positively regulated by circ_PGPEP1. Overexpression of E2F3 could invert the inhibitory effect of miR-1297 on GC progression. Animal experiments suggested that silenced circ_PGPEP1 could reduce GC tumor growth.

Our research showed that circ_PGPEP1 might serve as a potential biomarker for GC.

Our research showed that circ_PGPEP1 might serve as a potential biomarker for GC.

The consequence of treatment with antibiotics on the gut microbiota can be destructive. The antibiotics, however, can be utilized to understand the role of gut microbiota on the host physiology.

Earlier, we reported the efficacy of vancomycin in gut microbiota perturbation. We continued to understand the effect of restoration kinetics of perturbed gut microbiota on the immunity and behavior of Th1 (C57BL/6)- and Th2 (BALB/c)-biased mice.

We studied restoration kinetics of the gut microbiota for two months following the withdrawal of vancomycin treatment in both mice strains. We analyzed cecal microbiome composition, different behavioral assays, and expression of select genes associated with stress and barrier function in gut and brain.

Metagenomic analysis of gut microbiota revealed that the treatment with vancomycin caused a significant decrease in the relative abundance of Firmicutes and Bacteroidetes phyla with a time-dependent increase in Proteobacteria and Verrucomicrobia phyla. Maximum restoration (> 70%) of gut microbiota happened by the 15th day of withdrawal of vancomycin. BALB/c mice showed a more efficient restoration of gut microbiota compared to C57BL/6 mice. We established the correlation patterns of gut microbiota alteration and its effect on (a) the behavior of mice, (b) expression of key brain molecules, and (c) immunity-related genes.

The results revealed that the gut microbiome profiling, behavior, and immune responses varied significantly between Th1- and Th2-biased mice. By withdrawing the treatment with vancomycin of major gut microbes, important physiological and behavioral changes of both mice strains returned to the normal (untreated control) level.

The results revealed that the gut microbiome profiling, behavior, and immune responses varied significantly between Th1- and Th2-biased mice. By withdrawing the treatment with vancomycin of major gut microbes, important physiological and behavioral changes of both mice strains returned to the normal (untreated control) level.Gamblers are a heterogenous group in terms of the presence of comorbid psychopathology, maladaptive personality traits, and motivation to gamble. The Pathways Model, the most promising comprehensive framework to explain this heterogeneity, classifies gamblers into three subtypes. The aim of this review was to determine whether or not subtyping of gamblers based on the Pathways Model of problem and disordered gambling is valid. A literature review was conducted using the following online databases Academic Search Complete, PubMed, Web of Science, and PsychINFO. Studies were selected or excluded based on meeting predetermined criteria. Fourteen studies examining subtyping of gamblers based on the Pathways Model were reviewed and evaluated. Results suggest that in the adult population there are three subtypes of gamblers that largely coincide with the subtypes defined in the Pathways Model. Of these, the emotionally vulnerable subtype is the most problematic and inconsistent. In contrast, for adolescents, at least four gambler subtypes have been identified. ISX-9 The extant literature on subtyping of gamblers suffers from some severe limitations. Further research is required to fully validate the Pathways Model.Evidences show increase of positive attitudes of Nigerian adolescents towards gambling in the past decade. Nigerian adolescents have been shown to spend significant part of their academic time and resources on Soccer bets. This behaviour could act as a predisposing factor for poor academic performances and problem gambling at adulthood. The present study drew from the cognitive distortion model to examine the mediational role of near-miss in the erroneous cognition-betting intention association through a survey study design. Male adolescents (N = 237; Mean age = 17.37 years; SD = 4.13) of public schools in Nigeria who engage in Soccer betting took part in the study. They completed self-report measures of erroneous cognition, near-miss and betting intention. Results revealed that interpretative bias was not associated with near-miss while it was positively associated with betting intention. Illusion of control was positively associated with near-miss and betting intention. Near-miss was positively associated with betting intention and mediated the associations between interpretative bias and betting intention (negative mediation) and illusion of control, and betting intention (positive mediation). The theoretical and practical implications of the findings are discussed.

Reward-related processes may represent important transdiagnostic factors underlying eating pathology. Using the NIMH Research Domain Criteria as a guide, the current article reviews theories, behavioral and self-report assessments, and empirical findings related to reward learning in the eating disorders.

Data from behavioral tasks suggest deficits in reinforcement learning, which may become more pronounced with increasing disorder severity and duration. Self-report data strongly implicate positive eating and thinness/restriction expectancies (an element of reward prediction error) in the onset and maintenance of eating pathology. Finally, self-report measures of habit strength demonstrate relationships with eating pathology and illness duration; however, behavioral task data do not support relationships between eating pathology and a propensity towards general habit development. Existing studies are limited, but provide preliminary support for the presence of abnormal reward learning in eating disorders.