Positive digital communication among youth: The development and validation of the digital flourishing scale for adolescents.

Research has extensively studied the negative effects of digital communication on adolescents' well-being. However, positive digital experiences and behavior in adolescence are still poorly understood. The recently developed Digital Flourishing Scale addresses this gap and focuses on the positive perceptions of a user's experiences and behaviors in digital communication among adults. In this paper, we developed an adolescent version of this scale. Study 1 demonstrated the internal consistency of the scale and the same factor structure for adolescence as for adulthood: connectedness, civil participation, positive social comparison, authentic self-presentation, and self-control. Study 2 confirmed the identified factor structure with a second sample of adolescents and established measurement invariance across genders. The construct validity of the scale was confirmed by investigating associations with related constructs, including the basic psychological needs from self-determination theory (competence, autonomy, and relatedness), secure attachment to a close friend, Internet aggression, social media-induced inspiration, authenticity of posted positive content, and social media self-control failure. The results indicated that not all adolescents flourish equally online. Differences occurred depending on the adolescents' gender and socioeconomic status. The paper concludes that the newly developed scale is a valid and reliable measure for assessing adolescents' perceptions of digital thriving and digital empowerment.

Mir106b-25 and Mir17-92 Are Crucially Involved in the Development of Experimental Neuroinflammation.

MicroRNAs (miRNAs) are single-stranded RNA that have key roles in the development of the immune system and are involved in the pathogenesis of various autoimmune diseases. We previously demonstrated that two members of the miR106b-25 cluster and the miR17-92 paralog cluster were upregulated in T regulatory cells from multiple sclerosis (MS) patients. The aim of the present work was to clarify the impact of miR106b-25 and miR17-92 clusters in MS pathogenesis. Here, we show that the mice lacking miR17-92 specifically in CD4+ T cells or both total miR106b-25 and miR17-92 in CD4+ T cells (double knockout) are protected from Experimental Autoimmune Encephalomyelitis (EAE) development while depletion of miR106b-25 only does not influence EAE susceptibility. We suggest that the absence of miR106b does not protect mice because of a mechanism of compensation of miR17-92 clusters. Moreover, the decrease of neuroinflammation was found to be associated with a significant downregulation of pro-inflammatory cytokines (GM-CSF, IFNγ, and IL-17) in the spinal cord of double knockout EAE mice and a reduction of Th17 inflammatory cells. These results elucidate the effect of miR106b-25 and miR17-92 deletion in MS pathogenesis and suggest that their targeted inhibition may have therapeutic effect on disease course.