The efficacy of smartphone-based mental health interventions for depressive symptoms:a meta-analysis of randomized controlled trials

The rapid advances and adoption of smartphone technology presents a novel opportunity for delivering mental health interventions on a population scale. Despite multi-sector investment along with wide-scale advertising and availability to the general population, the evidence supporting the use of smartphone apps in the treatment of depression has not been empirically evaluated. Thus, we conducted the first meta-analysis of smartphone apps for depressive symptoms. An electronic database search in May 2017 identified 18 eligible randomized controlled trials of 22 smartphone apps, with outcome data from 3,414 participants. Depressive symptoms were reduced significantly more from smartphone apps than control conditions (g=0.38, 95% CI: 0.24-0.52, p<0.001), with no evidence of publication bias. Smartphone interventions had a moderate positive effect in comparison to inactive controls (g=0.56, 95% CI: 0.38-0.74), but only a small effect in comparison to active control conditions (g=0.22, 95% CI: 0.10-0.33). Effects from smartphone-only interventions were greater than from interventions which incorporated other human/computerized aspects along the smartphone component, although the difference was not statistically significant. The studies of cognitive training apps had a significantly smaller effect size on depression outcomes (p=0.004) than those of apps focusing on mental health. The use of mood monitoring softwares, or interventions based on cognitive behavioral therapy, or apps incorporating aspects of mindfulness training, did not affect significantly study effect sizes. Overall, these results indicate that smartphone devices are a promising self-management tool for depression. Future research should aim to distil which aspects of these technologies produce beneficial effects, and for which populations

Viral infections in type 1 diabetes mellitus-why the beta cells?

Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic β-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against β cells. Epidemiological, clinical and pathology studies in humans support viral infection-particularly by enteroviruses (for example, coxsackievirus)-as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both β cells and the immune system. Cellular permissiveness to viral infection is modulated by innate antiviral responses that vary among different tissues or cell types. Some data indicate that pancreatic islet α cells trigger a more efficient antiviral response to infection with diabetogenic viruses than do β cells, and so are able to eradicate viral infections without undergoing apoptosis. This difference could account for the varying ability of islet-cell subtypes to clear viral infections and explain why chronically infected pancreatic β cells, but not α cells, are targeted by an autoimmune response and killed during the development of T1DM. These issues and attempts to target viral infection as a preventive therapy for T1DM are discussed in the present Review.SCOPUS: re.jinfo:eu-repo/semantics/publishe