ABSTRACT
BACKGROUND: Social anxiety disorder (SAD) is a common mental health disorder affecting adolescents often associated with comorbidities like depression, suicide ideation and substance abuse. The objective of this study was to estimate the prevalence of social anxiety in adolescents and to explore its correlation with internet usage. METHODS: An exploratory cross-sectional study was conducted among 307 undergraduate students to screen for social anxiety and social phobia using a validated instrument, social interaction anxiety scale (SIAS). Young's internet addiction scale was used for measuring internet addiction. Respondents were categorised according to the scores obtained and later compared with their internet addiction behaviours. RESULTS: Internet addiction was seen in 93.8% of respondents. The prevalence of SAD was estimated to be 15.3%. Internet addiction was positively correlated with social anxiety score (Pearson correlation = 0.994, P < 0.001). CONCLUSION: More than 90% of participants had internet addiction, the majority had mild-moderate internet addiction. Social anxiety was present in more than one-third of the participants. SAD was found to be associated with internet addiction.
ABSTRACT
Earlier studies from our laboratory have shown myocardial dysfunction subsequent to chronic O(3) exposure in rats may be associated with a decrease in antioxidant reserve and increased activity of inflammatory mediators. The present study tested the hypothesis that O(3)-induced cardiac dysfunction in healthy adult rats may be due to changes in caveolin-1 and caveolin-3 levels. Sprague-Dawley rats were exposed 8 h/day for 28 and 56 days to filtered air or 0.8 ppm O(3). In order to assess the chronic effects to O(3), in vivo cardiac function was assessed by measuring LVDP, 24 h after termination of O(3) exposure. Compared to rats exposed to filtered air, LVDP values significantly decreased in all O(3)-exposed animals. This attenuation of cardiac function was associated with increased myocardial TNF-α levels and decreased myocardial activities of superoxidase dismutase. Progressive increases in the expression of myocardial TNF-α in 28 days and 56 days O(3)-exposed animals were followed by decreases in cardiac caveolin-1 levels. On the other hand, differential changes in the expression of caveolin-3 in hearts from 28 and 56 days O(3)-exposed animals were independent of intra-cardiac TNF-α levels. These novel findings suggest the interesting possibility that a balance between caveolin-1 and caveolin-3 may be involved in O(3)-mediated cardiac toxicity.
