Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress.

Telomerase is a ribonucleoprotein that counteracts telomere shortening and can immortalise human cells. There is also evidence for a telomere-independent survival function of telomerase. However, its mechanism is not understood.

Mitochondrial dysfunction is a possible cause of accelerated senescence of mesothelial cells exposed to high glucose.

High glucose has been found to accelerate cell senescence in vitro. The exact mechanism of this effect is, however, still poorly understood. In this paper we show that human peritoneal mesothelial cells (HPMCs) propagated under high (30mM) glucose were characterized by higher density of DNA double-strand breaks than cells exposed to standard (5mM) glucose concentration.

Downregulation of multiple stress defense mechanisms during differentiation of human embryonic stem cells.

Evolutionary theory predicts that cellular maintenance, stress defense, and DNA repair mechanisms should be most active in germ line cells, including embryonic stem cells that can differentiate into germ line cells, whereas it would be energetically unfavorable to keep these up in mortal somatic cells. We tested this hypothesis by examining telomere maintenance, oxidative stress generation, and genes involved in antioxidant defense and DNA repair during spontaneous differentiation of two human embryonic stem cell lines. Telomerase activity was quickly downregulated during differentiation, probably due to deacetylation of histones H3 and H4 at the hTERT promoter and deacetylation of histone H3 at hTR promoter.

DNA damage in telomeres and mitochondria during cellular senescence: is there a connection?

Cellular senescence is the ultimate and irreversible loss of replicative capacity occurring in primary somatic cell culture. It is triggered as a stereotypic response to unrepaired nuclear DNA damage or to uncapped telomeres. In addition to a direct role of nuclear DNA double-strand breaks as inducer of a DNA damage response, two more subtle types of DNA damage induced by physiological levels of reactive oxygen species (ROS) can have a significant impact on cellular senescence: Firstly, it has been established that telomere shortening, which is the major contributor to telomere uncapping, is stress dependent and largely caused by a telomere-specific DNA single-strand break repair inefficiency.

Role of respiration and glutathione in cadmium-induced oxidative stress in Escherichia coli K-12.

Cadmium is a widespread pollutant that has been associated with oxidative stress, but the mechanism behind this effect in prokaryotes is still unclear. In this work, we exposed two glutathione deficient mutants (DeltagshA and DeltagshB) and one respiration deficient mutant (DeltaubiE) to a sublethal concentration of cadmium. The glutathione mutants show a similar increase in reactive oxygen species as the wild type.

Exposure measurement in the association between periodontal disease and prematurity/low birth weight.

Aim: To compare the use of different definitions for exposure measurement in cases of association between periodontal disease (PD) and prematurity and/or low birth weight (PLBW).

Material And Methods: A database from a previous case-control study was used to compare four different definitions for periodontitis: at least one site with probing depth > or =4 mm (1); at least one site with clinical attachment loss (CAL)> or =3 mm (2); at least four teeth with one or more sites presenting probing depth > or =4 mm, with CAL> or =3 mm at the same site (3); and at least four teeth with one or more sites with probing depth > or =4 mm, with CAL> or =3 mm at the same site and presence of bleeding on probing (4). The PD frequency, diagnostic values and adjusted association measurements were calculated.

mtRF1a is a human mitochondrial translation release factor decoding the major termination codons UAA and UAG.

Human mitochondria contain their own genome, encoding 13 polypeptides that are synthesized within the organelle. The molecular processes that govern and facilitate this mitochondrial translation remain unclear. Many key factors have yet to be characterized-for example, those required for translation termination.

The association between postmenopausal osteoporosis and periodontal disease.

Background: The clinical importance of systemic bone loss as a contributory factor to alveolar bone loss and the subsequent loss of teeth merits further study, given that osteoporosis and periodontal disease lead to significantly increased morbidity and mortality and higher public expenditure of funds. This case-control study evaluated the association between osteoporosis and periodontal disease.

Methods: The sample consisted of 139 postmenopausal women: 48 in the case group (with periodontal disease) and 91 in the control group (without periodontal disease).

Premature senescence of mesothelial cells is associated with non-telomeric DNA damage.

Human peritoneal mesothelial cells (HPMCs) senesce in vitro after barely few population doublings. In this report, we show that senescence of HPMCs is associated with increased accumulation of gamma-H2A.X foci, which reveal DNA double-strand breaks.

Mitochondria and ageing: winning and losing in the numbers game.

Mitochondrial dysfunction has long been considered a key mechanism in the ageing process but surprisingly little attention has been paid to the impact of mitochondrial number or density within cells. Recent reports suggest a positive association between mitochondrial density, energy homeostasis and longevity. However, mitochondrial number also determines the number of sites generating reactive oxygen species (ROS) and we suggest that the links between mitochondrial density and ageing are more complex, potentially acting in both directions.

Methods for cell sorting of young and senescent cells.

Cellular senescence, the ultimate and irreversible loss of replicative capacity of cells in primary culture, has been a popular model for studying the aging process. However, the replicative life span of human fibroblasts is heterogeneous even in clonal populations, with the fraction of senescent cells increasing at each population doubling, rather than all cells entering senescence simultaneously. Thus, the study of individual cells in a mass culture is of extreme importance to the understanding of replicative senescence.

Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence.

Aging is an inherently stochastic process, and its hallmark is heterogeneity between organisms, cell types, and clonal populations, even in identical environments. The replicative lifespan of primary human cells is telomere dependent; however, its heterogeneity is not understood. We show that mitochondrial superoxide production increases with replicative age in human fibroblasts despite an adaptive UCP-2-dependent mitochondrial uncoupling.

[Nurse's concept in the managerial conception of a basic health unit].

This study is part of a larger survey called "Use of indicators in nurses' managerial practice in Basic Health Care Units in the city of Rio de Janeiro", which was carried out in the Basic Health Care Units of the Planning Area 5.3 and whose objectives were to identify nurses' conception regarding the tools required for management in those units and to discuss the role of management in organizing health services. The study is descriptive and data were collected in interviews with seven nurse managers.

Periodontal status as predictor of prematurity and low birth weight.

Objective: The objective was to verify the relation between periodontal status and prematurity/low birth weight.

Methods: a case control study of 211 women, 44 being mothers of children born with weight below 2.500g or gestational age of less than 37 weeks (case group) and 177 mothers of children born with weight of over 2.

Oxygen free radicals in cell senescence: are they signal transducers?

Oxygen free radicals have a major impact on senescence of primary human cells. In replicative senescence, which is induced by uncapping of telomeres, the rate of telomere shortening is largely determined by telomere-specific accumulation of DNA damage induced by reactive oxygen species (ROS). More intense ROS-generating stressors can induce premature senescence via generation of telomere-independent DNA damage.

Muscle delta13C change in Nile tilapia (Oreochromis niloticus) fingerlings fed on C3-or C4-cycle plants grain-based diets.

The effects of grain-based diets from C3 or C4-cycle plants on muscle delta(13)C change process in Nile tilapia (Oreochromis niloticus) fingerlings were investigated. Two groups of sex reversal males Nile tilapia fingerlings were fed with isoproteic (32.0% DP) and isocaloric (3200 kcal DE/kg) diets, differing from each other by their delta(13)C.

Muscle delta13C change in Nile tilapia (Oreochromis niloticus): effects of growth and carbon turnover.

The contribution of growth and turnover to the muscle delta(13)C change process was investigated using mathematical models which associate delta(13)C change to time of intake of a new diet or increase in body mass. Two groups of Nile tilapia (Oreochromis niloticus) were fed on diets based on C3 (delta(13)C=-25.64+/-0.

Mitochondrial dysfunction and cell senescence: cause or consequence?

The mitochondrial theory of aging remains to date one of the most popular theories of aging. One major model of aging is replicative senescence, where the irreversible loss of division potential of somatic cells occurs after a more or less constant number of cell divisions. Few data are available concerning the role of mitochondria in this model.

Extended lifespan and long telomeres in rectal fibroblasts from late-onset ulcerative colitis patients.

Objectives: Ulcerative colitis (UC) is characterized by damage to the intestinal epithelium and connective tissue. The causes of this damage could include changes in the ability of colonic fibroblasts to heal wounds and maintain epithelial cell proliferation. Telomeres shorten with each cell division and eventually signal senescence.

Mitochondria, telomeres and cell senescence.

The accumulation of oxidative damage is one of the most widely accepted causes of ageing. Mitochondrial dysfunction, in particular damage to the mitochondrial DNA has been hypothesised, more than thirty years ago, as responsible for increased production of reactive oxygen species (ROS) and, thus, as one possible causal factor for ageing. There is now a wealth of data that supports this hypothesis, which is mostly derived from models considering the ageing of post-mitotic or slowly dividing cells in vivo.

Genetic damage in exfoliated cells from oral mucosa of individuals exposed to X-rays during panoramic dental radiographies.

The genotoxic effects of X-ray emitted during dental panoramic radiography were evaluated in exfoliated cells from oral epithelium through a differentiated protocol of the micronucleus test. Thirty-one healthy individuals agreed to participate in this study and were submitted to this procedure for diagnosis purpose after being requested by the dentist. All of them answered a questionnaire before the examination.

HTLV-1 modifies the clinical and immunological response to schistosomiasis.

The immunological response in HTLV-1 infected individuals is characterized by a prominent Type-1 cytokine response with high production of IFN-gamma and TNF-alpha. In contrast, helminthic infections and in particular chronic schistosomiasis are associated with a predominant production of IL-4, IL-5, IL-10 and IL-13. Liver fibrosis is the main pathological finding in schistosomiasis that occurs after many years of infection.

Strain PM2, a novel methylotrophic fluorescent Pseudomonas sp.

A novel bacterial strain, PM2, capable of growing on methanol, was isolated in alkaline conditions from a soil inoculum. This bacterium was characterized at the physiological, biochemical and molecular level. Based on biochemical and molecular data strain PM2 was classified as a novel member of the group of fluorescent pseudomonads.