Depression and exposure to violence among Venda and Northern Sotho adolescents in South Africa

Objective: Despite the high levels of violence in South Africa; a lacunae in research exists regarding the influence of violence exposure on children. This study investigated the correlation between children's exposure to violence and the development of psychological problems such as depression. Method: 186 Venda and 151 Northern Sotho adolescents were studied in a questionnaire survey to determine this relationship. Two measuring instruments were used: The Children's Depression Inventory and the Child Exposure to Violence Form. Results: When comparing gender; no significant differences were found in terms of overall exposure to violence between males and females. For depression; the total group of girls had a remarkably higher prevalence of depression. Regarding ethnic comparison; no significant differences were found in terms of overall exposure to violence or for witnessed events. However; the Venda adolescents had been victims significantly more often. Venda and Northern Sotho females had a similar prevalence of depression; but Northern Sotho boys had a higher depression rate than Venda boys. The correlation between victimisation and total group depression was relatively low for the Northern Sotho group; and non-existent for the Venda group. A significant correlation was found between total exposure to violence and depression for the overall group. Conclusion: This study indicates that adolescents' exposure to violence and subsequent mental health is an area of concern. However; adolescents could be taught effective coping and problem-solving techniques in schools to help empower them against stressors they might encounter

DNA vaccination encoding glutamic acid decarboxylase can enhance insulitis and diabetes in correlation with a specific Th2/3 CD4 T cell response in non-obese diabetic mice.

DNA vaccination encoding beta cell autoantigens has been shown very recently to prevent type I diabetes in non-obese diabetic (NOD) mice. However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. As this immune phenotype is associated strongly with beta cell destruction leading to diabetes, we have chosen to study the effects of plasmids encoding glutamic acid decarboxylase (GAD), a crucial beta cell autoantigen, in female NOD mice that developed a 'moderate' diabetes incidence. In the present study, 3-week-old female NOD mice were vaccinated twice in tibialis muscles with plasmid-DNA encoding 65-kDa GAD or betagalactosidase. In GAD-DNA immunized mice, diabetes cumulative incidence (P < 3.10(-3)) and insulitis (P < 7.10(-3)) increased significantly. Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). These cells were detected in spleen and in pancreatic lymph nodes. Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). Moreover, pancreatic lesions resembled Th2-related allergic inflammation. These results indicate, for the first time, that GAD-DNA vaccination could increase insulitis and diabetes in NOD mice. In addition, our study suggests that Th2/3 cells may have potentiated beta cell injury.