Showing papers in "Experimental Gerontology in 1999"

TL;DR: A review of the current cellular and molecular bases underlying adverse glucocorticoid actions, and their relevance to brain aging is presented in this paper, with a focus on brain aging.

TL;DR: This review aims to recapitulate various studies on the role of free radicals in DNA damage-both nuclear as well as mitochondrial-the oxidative stress they impose on cells, the roles of antioxidants, the presence of autoantibodies, and their overall impact on the aging process.

TL;DR: The results suggest that human NK cells do not escape the aging process, although senescence have a differential effect on distinct NK cell biological functions, ranging from severe to negligible impairment, depending on the parameters considered.

TL;DR: The results suggest that the progressive accumulation of T cells showing many of the hallmarks of replicative senescence during aging, chronic infection, and autoimmune disease may, in part, reflect the diminished capacity of such cells to undergo normal programmed cell death.

TL;DR: Effects as summarized in this short review, are not always, at first sight, consistent and should be kept in mind, though, when considering the response of a cell to collagen.

TL;DR: It will evolve that the in vivo accumulation of oxidized calModulin cannot be the result of the reaction of an individual reactive oxygen species with calmodulin in homogenous solution alone, and complexation of calmodulins to cal modulin-binding proteins and protein turnover are additional parameters likely contributing to the accumulation of specifically modified calmod insulin.

TL;DR: Immunosenescence can be taken as a proof that the beneficial effects of the immune system, devoted to the neutralization of dangerous/harmful agents early in life and in adulthood, turn to be detrimental late in life, in a period largely not foreseen by evolution.

TL;DR: Monocytes of aged individuals, in contrast to a younger population, exhibit in vivo activation as well as imbalanced production of cytokines, which may contribute to impaired immune competence of aging.

TL;DR: In this article, age-related changes in the upper extremity performance of healthy community-dwelling elderly people, by using a longitudinal design, were found to be significantly different from those who participated in the longitudinal study.

TL;DR: P phenotypic and functional alterations can be shown in NK cells in healthy aging and these changes are compatible with the expansion of a mature NK subset.

TL;DR: The study confirms age-related upregulation of HLA-DR on CD3+ lymphocytes, shows some evidence for associated up regulation of CD25 onCD3+ cells in older subjects, and links serum TNF-alpha, IFN-gamma, and sIL2-R to T-lymphocyte activation.

TL;DR: It is hypothesized that large amounts of undegradable ceroid/lipofuscin within the acidic vacuolar compartment may interfere with lysosomal function, resulting in poor renewal of long-lived proteins and worn-out/damaged organelles, decreased adaptability, and cell death.

TL;DR: It is shown that carnosine does not affect cell attachment, but does increase longevity in PDs, and the plating efficiency of MRC-5 cells seeded at low density is strongly increased in young and senescent cells by carnosines, as shown by the growth of individual colonies.

TL;DR: Aging causes changes in the structure and function of the vessels that leads to an increase in the incidence of certain cardiovascular diseases, such as hypertension, coronary artery disease, heart failure, and postural hypotension with enhancement of both morbidity and mortality.

TL;DR: In this paper, the authors found that there was a significant age difference in the size of the infarct between the young adult and old mice, and that the old heart was more susceptible to injury after ischemia-reperfusion.

TL;DR: It is hypothesized that the enhanced sensitivity of ceroid/lipofuscin-loaded cells to oxidative stress may be caused by the increased amounts of lysosomal enzymes, known as mediators of oxidative damage, and/or by catalysis of intralysosomotropic oxidative reactions by lipofuscIn-associated iron.

TL;DR: Results reveal that histone variants of the H2A and H3 families are regulated during in vitro aging in the same manner as that during differentiation.

TL;DR: Characteristics of aging in long-term human T cell cultures will be summarized, and the parallels between the in vitro model and in vivo immunosenescence will be documented.

TL;DR: Many potential "new" risk factors may predispose to atherosclerotic diseases, but clinical trial proof of a causal role between several of these risk factors and CHD may be difficult to obtain unless selective interventions are developed to lower them.

TL;DR: Results show that a mild stress such as hypergravity, which has been previously shown to increase the longevity of males and resistance to heat shock in both sexes, is an environmental manipulation postponing aging in flies.

TL;DR: The red blood cell membrane showed a significantly increased cholesterol/phospholipid molar ratio and a concomitant increase in polyunsaturated fatty acids in phosphatidylcholine and in actin are likely to improve the membrane fluidity and to strengthen the membrane structure.

TL;DR: In this article, the authors identify age-related changes in the production of interleukin (IL)-10 and IL-12, and determine whether in vitro T cell proliferation can be enhanced in the elderly by modulation of these two key cytokines.

TL;DR: The data suggest that the expression of CD95 on the different subsets of lymphocytes can be considered a good marker for studies of immunosenescence, because it may be predictive of successful aging, and can partially explain the change in lymphocytes subsets in elderly.

TL;DR: A distinction is made between the steady-state hematopoiesis in aging and the developmental potential of stem cells, which offers a direct approach to further elucidate aging across the axis from primitive stem cells to the mature blood cells.

TL;DR: The results show that, in general, the above antioxidants cause an enhancement of the NK activity at all ages studied, this stimulation being higher with thioproline and N-acetylcysteine than with ascorbic acid and alpha-tocopherol.

TL;DR: The results suggest that the altered cellular immune responses observed in T lymphocytes with aging may be the result, at least in part, of an alteration in early events associated with signal transduction through the TcR/CD3 complex that translates into decreased activities of p56lck and ZAP-70.

TL;DR: Although hyperlipidemia appears to be involved both in plaque formation and wall thickness progression, the detailed mechanisms are not identical and in the oldest age group (above 80 years and in centenarians), high cholesterol values may not be a risk factor as in younger individuals.

TL;DR: In this article, the authors proposed a "immunological" hypothesis of atherogenesis based on the observation that nearly everybody shows protective cellular and humoral immune reactions against microbial heat shock protein 60 (HSP 60).

TL;DR: The advent of a new principle, amplification of the NO-signaling cascade by means of target organ selectiveosphodiesterase inhibition, has renewed interest in phosphodiesterases and cGMP.