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The aim of this study was to cross-sectionally explore the association of obesity with spinal posture and mobility, commonly associated with musculoskeletal problems, by comparing the spinal parameters between 90 obese and 109 normal-weight children and adolescents. A non-invasive electromechanical device, the Idiag M360 (Idiag, Fehraltorf, Switzerland), was used to measure the spinal parameters. An age-and-sex-adjusted two-way analysis of variance (ANOVA) was used to determine postural and mobility differences between the two groups. Children and adolescents with obesity had significantly greater thoracic kyphosis [difference between groups (Δ) = 13.00, 95% CI 10.10–15.80, p < 0.0001] and thoracic extension (Δ = 6.5°, 95% CI 2.9°–11.6°, p = 0.005), as well as smaller mobility in thoracic flexion (Δ = 5.0°, 95% CI 1.2°–8.8°, p = 0.01), thoracic lateral flexion (Δ = 17.7°, 95% CI 11.6°–23.8°, p < 0.0001), lumbar flexion (Δ = 12.1°, 95% CI 8.7°–15.5°, p < 0.0001), lumbar extension (Δ = 7.1°, 95% CI 3.1°–12.2°, p = 0.003) and lumbar lateral flexion (Δ = 9.1°, 95% CI 5.5°–12.8°, p < 0.0001) compared to the normal-weight children and adolescents. These findings provide important information about the characteristics of the spine in children and adolescents with obesity and unique insights into obesity-related mechanical challenges that the spine has to withstand and strategies designed to improve spinal mobility in this young population.

Background Tumor necrosis factor super family (TNFSF) members regulate important processes involved in cell proliferation, survival and differentiation and are therefore crucial for the balance between homeostasis and inflammatory responses. Several members of the TNFSF are closely associated with inflammatory bowel disease (IBD). Thus, they represent interesting new targets for therapeutic treatment of IBD. Methodology/Principal Findings We have used mice deficient in TNFSF member HVEM in experimental models of IBD to investigate its role in the disease process. Two models of IBD were employed: i) chemical-induced colitis primarily mediated by innate immune cells; and ii) colitis initiated by CD4+CD45RBhigh T cells following their transfer into immuno-deficient RAG1-/- hosts. In both models of disease the absence of HVEM resulted in a significant reduction in colitis and inflammatory cytokine production. Conclusions These data show that HVEM stimulatory signals promote experimental colitis driven by innate or adaptive immune cells., PLoS ONE, 6 (4), ISSN:1932-6203