99 research outputs found
Associations of physical activity and sedentary time with body composition in Brazilian young adults.
The findings of studies on the association between physical activity and adiposity are not consistent, and most are cross-sectional and used only self-reported measures. The aims of this study were to evaluate: 1) independent and combined cross-sectional associations of objectively-measured physical activity and sedentary time with body composition outcomes at 30 years, and 2) prospective associations of changes in self-reported physical activity from 23 to 30 years with the same outcomes in participants from the 1982 Pelotas (Brazil) Birth Cohort. Body mass index, waist circumference, visceral abdominal fat, fat mass index, and android/gynoid fat ratio were the outcomes. 3,206 participants were analysed. In cross-sectional analyses, higher objectively-measured moderate-to-vigorous physical activity was associated with lower body mass index (β = 0.017, 95%CI: -0.026; -0.009), waist circumference (β = -0.043, 95%CI: -0.061; -0.025), visceral abdominal fat (β = -0.006, 95%CI: -0.009; -0.003), and fat mass index (β = -0.015, 95%CI: -0.021; -0.009), independent of sedentary time. Sedentary time was independently associated only with higher fat mass index (β = 0.003, 95%CI: 0.001; 0.005). In longitudinal analyses, using self-reported measure, adiposity was lower among those who were consistently active or who became active. Adiposity was similar among the "became inactive" and "consistently inactive" subjects. Our findings suggest metabolic benefits from engagement in physical activity throughout young adulthood, with stronger associations on concurrent levels.SB, KKO and EDLR
are supported by the Medical Research Council (Unit Programme numbers: MC_UU_12015/2 and MC_
UU_12015/4)
Tecnologia alternativa para produção de túberas-semente de inhame e seus reflexos na produtividade
Effect of green banana pulp on physicochemical and sensory properties of probiotic yoghurt
Pervasive gaps in Amazonian ecological research
Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear un derstanding of how ecological communities respond to environmental change across time and space.3,4
While the increasing availability of global databases on ecological communities has advanced our knowledge
of biodiversity sensitivity to environmental changes,5–7 vast areas of the tropics remain understudied.8–11 In
the American tropics, Amazonia stands out as the world’s most diverse rainforest and the primary source of
Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepre sented in biodiversity databases.13–15 To worsen this situation, human-induced modifications16,17 may elim inate pieces of the Amazon’s biodiversity puzzle before we can use them to understand how ecological com munities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus
crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced
environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple or ganism groups in a machine learning model framework to map the research probability across the Brazilian
Amazonia, while identifying the region’s vulnerability to environmental change. 15%–18% of the most ne glected areas in ecological research are expected to experience severe climate or land use changes by
2050. This means that unless we take immediate action, we will not be able to establish their current status,
much less monitor how it is changing and what is being lostinfo:eu-repo/semantics/publishedVersio
Long-term effects of neonatal malnutrition on microbicide response, production of cytokines, and survival of macrophages infected by Staphylococcus aureus sensitive/resistant to methicillin
SARS-CoV-2 uses CD4 to infect T helper lymphocytes
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p
SARS-CoV-2 uses CD4 to infect T helper lymphocytes
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p
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