Morphofunctional features and physical fitness of boys 6 - 9 years old under the influence of various physical activity

The aim of this research was to investigate morphofunctional features and physical fitness of boys 6 - 9 years old under the influence of various physical activity. The research performed in 2020 comprised 246 boys of 6 - 9 years old with different physical activity (121 children who are not involved in sports; 79 martial artists and 46 gymnasts with experience of 8 months and 4 years old). It was found that systematic sports activities of 6 - 9 years old boys have a positive effect on physical fitness and optimize morphofunctional indicators of physical development. The effect of the sport on the physical development and fitness of the boys depends on the start date and time of training sessions: a higher level of young gymnasts physical fitness is accompanied by a more intense adaptation of the cardiovascular system relative to martial artists. Differences in morphofunctional state and physical fitness between boys who are not involved in sports and young athletes are least significant in 6 year old boys, intensifying as growing up and increasing sport experience. It is more typical for gymnasts

B-oligomer of pertussis toxin inhibits HIV-1 LTR-driven transcription through suppression of NF-kappaB p65 subunit activity.

The binding subunit of pertussis toxin (PTX-B) has been shown recently to inhibit the entry and postentry events in HIV-1 replication in primary T lymphocytes and monocyte-derived macrophages. While the effect of PTX-B on HIV-1 entry was shown to involve CCR5 desensitization, the mechanism of postentry inhibition remained unclear. In T lymphocytes, PTX-B affected transcription or stability of Tat-stimulated HIV-1 mRNAs. In this study, we sought to identify the mechanism of postentry inhibition of HIV-1 replication by PTX-B in U-937 promonocytic cells. We demonstrate that in these cells PTX-B inhibits expression of luciferase reporter gene controlled by the HIV-1 LTR promoter. This effect is Tat-independent and is not restricted to the HIV-1 LTR promoter. Instead, PTX-B activity is mediated through suppression of the cellular transcription factor, NF-kappaB. PTX-B inhibits phosphorylation and nuclear translocation of the p65 subunit of NF-kappaB. This effect is independent of the cytoplasmic NF-kappaB inhibitor, IkappaBalpha, as PTX-B stimulates phosphorylation and subsequent degradation of this protein. The suppressive activity of PTX-B on NF-kappaB p65 phosphorylation and nuclear translocation is delayed, suggesting that PTX-B signaling might initiate synthesis and cytoplasmic accumulation of a p65 phosphorylation inhibitor.Journal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe