20 research outputs found

    Moderate exercise may attenuate some aspects of immunosenescence

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    BACKGROUND: Immunosenescence is related to the deterioration of many immune functions, which may be manifested in increased susceptibility to infection, cancer, and autoimmunity. Lifestyle factors, such as diet or physical activity, may influence the senescence of the immune system. It is widely accepted that moderate physical activity may cause beneficial effects for physical and psychological health as well as for the immune system activity in aged people. METHODS: Thirty elderly women aged 62 to 86 were subjected to a two-years authorized physical activity program. Peripheral blood lymphocytes distribution and the production of cytokines involved in the immune response development and regulation (IL-2, IL-4 and IFN-γ) were investigated. The same parameters were evaluated in two control groups of women: a sedentary group of 12 elderly women selected for the second round of the physical activity program and in a group of 20 sedentary young women. Flow cytometry methods were used for the examination of surface markers on peripheral blood lymphocytes and intracellular cytokines expression. RESULTS: The distribution of the main lymphocytes subpopulations in the peripheral blood of elderly women did not show changes after long-term moderate physical training. The percentage of lymphocytes expressing intracellular IL-2 was higher in the group of women attending 2-years physical activity program than in the control group of elderly sedentary women, and it was similar to the value estimated in the group of young sedentary women. There was no difference in the intracellular expression of IL-4 and IFN-γ between the active and elderly sedentary women. CONCLUSIONS: Our results suggest that moderate, long-term physical activity in elderly women may increase the production of IL-2, an important regulator of the immune response. This may help ameliorate immunosenescence in these women

    Knotted vs. Unknotted Proteins: Evidence of Knot-Promoting Loops

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    Knotted proteins, because of their ability to fold reversibly in the same topologically entangled conformation, are the object of an increasing number of experimental and theoretical studies. The aim of the present investigation is to assess, on the basis of presently available structural data, the extent to which knotted proteins are isolated instances in sequence or structure space, and to use comparative schemes to understand whether specific protein segments can be associated to the occurrence of a knot in the native state. A significant sequence homology is found among a sizeable group of knotted and unknotted proteins. In this family, knotted members occupy a primary sub-branch of the phylogenetic tree and differ from unknotted ones only by additional loop segments. These "knot-promoting" loops, whose virtual bridging eliminates the knot, are found in various types of knotted proteins. Valuable insight into how knots form, or are encoded, in proteins could be obtained by targeting these regions in future computational studies or excision experiments

    The use of comet assay in measuring DNA damage and repair efficiency in child, adult, and old age populations

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    In the present study, we used the Comet assay to estimate basal DNA damage in three distinct populations aged 5-10, 40-50, and 60-70 years old. The DNA damage induced by hydrogen peroxide and gamma-irradiation in the lymphocytes of these populations, as well as their repair activity, was also studied. Finally, we measured apoptosis and necrosis after the effect of these agents. Our results indicate that the older population (60-70 years old) showed higher basal levels of DNA damage and was more sensitive to the effects of the DNA-damaging agents than the adult one (40-50 years old), who, in turn, was more sensitive than the younger population (5-10 years old). A decline of the repair efficiency with age to the DNA damage induced by the two agents was also observed. Apoptosis and necrosis were also affected by age
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