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Is vigorous-intensity physical activity required for improving bone mass in adolescence? Findings from a Brazilian birth cohort.
UNLABELLED: The association between moderate and vigorous physical activity throughout adolescence and areal bone density (aBMD) at 18 years of age was evaluated. Vigorous-intensity physical activity at 11, 15, and 18 years was associated with aBMD in early adulthood, especially in boys. Cross-sectional analyses showed a positive association between moderate physical activity and aBMD. INTRODUCTION: To evaluate independent associations of moderate and vigorous physical activity (MPA, VPA) across adolescence with areal bone mineral density (aBMD). METHODS: Physical activity (PA) was assessed at 11, 15, and 18 years of age by self-report and at 18 years by accelerometry in the 1993 Pelotas Birth Cohort Study. Time spent in MPA and VPA was determined using metabolic equivalents and specific cutoffs based on raw acceleration. Lumbar spine and femoral neck aBMD were measured by DXA at 18 years. Statistical analyses evaluated the association of MPA and VPA with aBMD, after adjusting for skin color, asset index, current height and age at menarche, and peak strain score (based on ground reaction forces of PA). RESULTS: Lumbar spine and femoral neck aBMD were available for 3947 (49.9% of boys) and 3960 (49.6% of boys) individuals, respectively. Time spent in MPA at 11 and 15 years was not associated with aBMD. VPA at all time points was positively related to both lumbar spine and femoral neck aBMD in boys. Results were consistent for objectively measured VPA. Girls who achieved 75+ minutes/week of VPA in at least two follow-ups showed higher aBMD at 18 years of age. Boys who reached 75+ minutes/week of VPA at all follow-ups had on average 0.117 g/cm2 (95% CI: 0.090; 0.144) higher femoral neck aBMD than those who never achieved this threshold. CONCLUSIONS: Self-reported VPA but not MPA throughout adolescence was associated with aBMD. Recommendation for PA in young people should consider the importance of VPA.Authors also acknowledge the MRC Epidemiology PA Programme for
assisting with analyses and support of activity monitors funding bodies
Medical Research Council and Research Council of Norway
Dengue Virus Capsid Protein Usurps Lipid Droplets for Viral Particle Formation
Dengue virus is responsible for the highest rates of disease and mortality among the members of the Flavivirus genus. Dengue epidemics are still occurring around the world, indicating an urgent need of prophylactic vaccines and antivirals. In recent years, a great deal has been learned about the mechanisms of dengue virus genome amplification. However, little is known about the process by which the capsid protein recruits the viral genome during encapsidation. Here, we found that the mature capsid protein in the cytoplasm of dengue virus infected cells accumulates on the surface of ER-derived organelles named lipid droplets. Mutagenesis analysis using infectious dengue virus clones has identified specific hydrophobic amino acids, located in the center of the capsid protein, as key elements for lipid droplet association. Substitutions of amino acid L50 or L54 in the capsid protein disrupted lipid droplet targeting and impaired viral particle formation. We also report that dengue virus infection increases the number of lipid droplets per cell, suggesting a link between lipid droplet metabolism and viral replication. In this regard, we found that pharmacological manipulation of the amount of lipid droplets in the cell can be a means to control dengue virus replication. In addition, we developed a novel genetic system to dissociate cis-acting RNA replication elements from the capsid coding sequence. Using this system, we found that mislocalization of a mutated capsid protein decreased viral RNA amplification. We propose that lipid droplets play multiple roles during the viral life cycle; they could sequester the viral capsid protein early during infection and provide a scaffold for genome encapsidation
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