RESUMO
BACKGROUND: Social media can influence alcohol initiation behaviors such as sipping, which can lead to future adverse alcohol-related outcomes. Few studies have examined the role of problematic social media use, characterized by addiction, mood modification, tolerance, withdrawal, conflict, and relapse, especially in early adolescence. OBJECTIVE: To examine the prospective association between social media use and sipping alcohol in a nationwide sample of early adolescents, and the extent to which problematic social media use mediates the association. METHODS: We analyzed prospective data from the Adolescent Brain Cognitive Development Study (N = 7514; ages 9-10 years at baseline; 2016-2018) to estimate associations between social media time (Year 1) and alcohol sipping (Year 3) using modified Poisson regression, adjusting for confounders and testing problematic social media use (Year 2) as a mediator. RESULTS: Social media time (Year 1) was prospectively associated with 1.31 (95% confidence interval 1.20-1.43) times higher risk of new-onset sipping (Year 3). The association between social media time and new-onset alcohol sipping was partially mediated by problematic social media use at Year 2 (25.0% reduction in the association between the former two factors after adding problematic social media use, p = 0.002). CONCLUSIONS: Time spent on social media was associated with a higher risk of alcohol sipping in a diverse national sample of early adolescents, and the association was partially mediated by problematic social media use. Media literacy education and family media use plans could advise early adolescents about exposure to alcohol content on social media and warning signs for problematic use.
Assuntos
Comportamento do Adolescente , Mídias Sociais , Humanos , Adolescente , Consumo de Bebidas Alcoólicas/psicologia , Estudos Prospectivos , Comportamento do Adolescente/psicologia , PrevisõesRESUMO
Glutathione (GSH) is an important intracellular antioxidant responsible for neutralizing reactive oxygen species (ROS). Our laboratory previously demonstrated that the oral administration of liposomal GSH improves immune function against mycobacterium infections in healthy patients along with patients with HIV and Type 2 diabetes. We aim to determine if the topical application of a glutathione-cyclodextrin nanoparticle complex (GSH-CD) confers a therapeutic effect against mycobacterium infections. In our study, healthy participants received either topical GSH-CD (n = 15) or placebo (n = 15) treatment. Subjects were sprayed four times twice a day for three days topically on the abdomen. Blood draws were collected prior to application, and at 1, 4, and 72 h post-initial topical application. GSH, malondialdehyde (MDA), and cytokine levels were assessed in the processed blood samples of study participants. Additionally, whole blood cultures from study participants were challenged with Mycobacterium avium (M. avium) infection in vitro to assess mycobacterium survival post-treatment. Topical GSH-CD treatment was observed to elevate GSH levels in peripheral blood mononuclear cells (PBMCs) and red blood cells and decrease MDA levels in PBMCs 72 h post-treatment. An increase in plasma IL-2, IFN-γ, IL-12p70, and TNF-α was observed at 72 h post-topical GSH-CD treatment. Enhanced mycobacterium clearance was observed at 4 h and 72 h post-topical GSH-CD treatment. Overall, topical GSH-CD treatment was associated with improved immune function against M. avium infection. The findings of this pilot study suggest GSH-cyclodextrin complex formulation can be used topically as a safe alternative mode of GSH delivery in the peripheral blood.
RESUMO
Considerable measures have been implemented in healthcare institutions to screen for and treat tuberculosis (TB) in developed countries; however, in low- and middle-income countries, many individuals still suffer from TB's deleterious effects. TB is caused by an infection from the Mycobacterium tuberculosis (M. tb) bacteria. Symptoms of TB may range from an asymptomatic latent-phase affecting the pulmonary tract to a devastating active and disseminated stage that can cause central nervous system demise, musculoskeletal impairments, and genitourinary compromise. Following M. tb infection, cytokines such as interferons (IFNs) are released as part of the host immune response. Three main classes of IFNs prevalent during the immune defense include: type I IFN (α and ß), type II IFN (IFN-γ), and type III IFN (IFN-λ). The current literature reports that type I IFN plays a role in diminishing the host defense against M. tb by attenuating T-cell activation. In opposition, T-cell activation drives type II IFN release, which is the primary cytokine mediating protection from M. tb by stimulating macrophages and their oxidative defense mechanisms. Type III IFN has a subsidiary part in improving the Th1 response for host cell protection against M. tb. Based on the current evidence available, our group aims to summarize the role that each IFN serves in TB within this literature review.