Association between regular participation in sports and leisure time behaviors in Brazilian adolescents: A cross-sectional study

<p>Abstract</p> <p>Background</p> <p>The belief that adolescents engaged in sports increase their overall physical activity level while simultaneously decreasing physical inactivity has been the foundation of many intervention programs in developing countries. The aim of this study was to analyze the association between regular participation in sports and both active behaviors and TV viewing during leisure time.</p> <p>Methods</p> <p>A total of 1752 Brazilian adolescents (812 = male and 940 = female) participated in this study. Regular participation in sports, as well as active behaviors (exemplified by walking or cycling) and TV viewing during leisure time were assessed by means of a questionnaire. The chi-square test analyzed the association between sports practice and leisure time behaviors, and the Poisson regression with robust variance indicated the magnitude of these associations.</p> <p>Results</p> <p>The prevalence of regular participation in sports was 14.8% (95% confidence interval 13.2% to 16.5%). After adjustment for all confounders, participation in sports was associated with, at the highest frequency, cycling (PR = 2.55 [1.80–3.60]) and walking (PR = 2.69 [1.98–3.64]) during leisure time. However, there was not an association between the participation in sports and frequency of TV viewing (PR = 1.28 [0.81–2.02]).</p> <p>Conclusion</p> <p>This study presented data indicating that the regular participation in sports is positively associated with a higher frequency of physically active behaviors during leisure time. However, the results did not support the hypothesis that the engagement in sports necessarily decreases leisure time spent in TV viewing.</p

Natural humoral immune response to ribosomal P0 protein in colorectal cancer patients

Tumor associated antigens are useful in colorectal cancer (CRC) management. The ribosomal P proteins (P0, P1, P2) play an important role in protein synthesis and tumor formation. The immunogenicity of the ribosomal P0 protein in head and neck, in breast and prostate cancer patients and the overexpression of the carboxyl-terminal P0 epitope (C-22 P0) in some tumors were reported

Molecular Mechanisms Generating and Stabilizing Terminal 22q13 Deletions in 44 Subjects with Phelan/McDermid Syndrome

In this study, we used deletions at 22q13, which represent a substantial source of human pathology (Phelan/McDermid syndrome), as a model for investigating the molecular mechanisms of terminal deletions that are currently poorly understood. We characterized at the molecular level the genomic rearrangement in 44 unrelated patients with 22q13 monosomy resulting from simple terminal deletions (72%), ring chromosomes (14%), and unbalanced translocations (7%). We also discovered interstitial deletions between 17–74 kb in 9% of the patients. Haploinsufficiency of the SHANK3 gene, confirmed in all rearrangements, is very likely the cause of the major neurological features associated with PMS. SHANK3 mutations can also result in language and/or social interaction disabilities. We determined the breakpoint junctions in 29 cases, providing a realistic snapshot of the variety of mechanisms driving non-recurrent deletion and repair at chromosome ends. De novo telomere synthesis and telomere capture are used to repair terminal deletions; non-homologous end-joining or microhomology-mediated break-induced replication is probably involved in ring 22 formation and translocations; non-homologous end-joining and fork stalling and template switching prevail in cases with interstitial 22q13.3. For the first time, we also demonstrated that distinct stabilizing events of the same terminal deletion can occur in different early embryonic cells, proving that terminal deletions can be repaired by multistep healing events and supporting the recent hypothesis that rare pathogenic germline rearrangements may have mitotic origin. Finally, the progressive clinical deterioration observed throughout the longitudinal medical history of three subjects over forty years supports the hypothesis of a role for SHANK3 haploinsufficiency in neurological deterioration, in addition to its involvement in the neurobehavioral phenotype of PMS