Happily (never after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

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Annika Höhn

2017-04-01

Full Text Available Aging is a complex phenomenon and its impact is becoming more relevant due to the rising life expectancy and because aging itself is the basis for the development of age-related diseases such as cancer, neurodegenerative diseases and type 2 diabetes. Recent years of scientific research have brought up different theories that attempt to explain the aging process. So far, there is no single theory that fully explains all facets of aging. The damage accumulation theory is one of the most accepted theories due to the large body of evidence found over the years. Damage accumulation is thought to be driven, among others, by oxidative stress. This condition results in an excess attack of oxidants on biomolecules, which lead to damage accumulation over time and contribute to the functional involution of cells, tissues and organisms. If oxidative stress persists, cellular senescence is a likely outcome and an important hallmark of aging. Therefore, it becomes crucial to understand how senescent cells function and how they contribute to the aging process. This review will cover cellular senescence features related to the protein pool such as morphological and molecular hallmarks, how oxidative stress promotes protein modifications, how senescent cells cope with them by proteostasis mechanisms, including antioxidant enzymes and proteolytic systems. We will also highlight the nutritional status of senescent cells and aged organisms (including human clinical studies by exploring trace elements and micronutrients and on their importance to develop strategies that might increase both, life and health span and postpone aging onset.

Best Practice Life Expectancy:An Extreme value Approach

OpenAIRE

Medford, Anthony

2017-01-01

Background: Whereas the rise in human life expectancy has been extensively studied, the evolution of maximum life expectancies, i.e., the rise in best-practice life expectancy in a group of populations, has not been examined to the same extent. The linear rise in best-practice life expectancy has been reported previously by various authors. Though remarkable, this is simply an empirical observation. Objective: We examine best-practice life expectancy more formally by using extreme value th...

Feeding blueberry diets in early life prevent senescence of osteoblasts and bone loss in ovariectomized adult female rats.

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Jian Zhang

Full Text Available Appropriate nutrition during early development is essential for maximal bone mass accretion; however, linkage between early nutrition, childhood bone mass, peak bone mass in adulthood, and prevention of bone loss later in life has not been studied.In this report, we show that feeding a high quality diet supplemented with blueberries (BB to pre-pubertal rats throughout development or only between postnatal day 20 (PND20 and PND34 prevented ovariectomy (OVX-induced bone loss in adult life. This protective effect of BB is due to suppression of osteoblastic cell senescence associated with acute loss of myosin expression after OVX. Early exposure of pre-osteoblasts to serum from BB-fed rats was found to consistently increase myosin expression. This led to maintenance osteoblastic cell development and differentiation and delay of cellular entrance into senescence through regulation of the Runx2 gene. High bone turnover after OVX results in insufficient collagenous matrix support for new osteoblasts and their precursors to express myosin and other cytoskeletal elements required for osteoblast activity and differentiation.These results indicate: 1 a significant prevention of OVX-induced bone loss from adult rats can occur with only 14 days consumption of a BB-containing diet immediately prior to puberty; and 2 the molecular mechanisms underlying these effects involves increased myosin production which stimulates osteoblast differentiation and reduces mesenchymal stromal cell senescence.

Gompertz-Makeham Life Expectancies: Expressions and Applications

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Missov, Trifon; Lenart, Adam

2013-01-01

In a population of individuals, whose mortality is governed by a Gompertz–Makeham hazard, we derive closed-form solutions to the life-expectancy integral, corresponding to the cases of homogeneous and gamma-heterogeneous populations, as well as in the presence/absence of the Makeham term. Derived...... expressions contain special functions that aid constructing high-accuracy approximations, which can be used to study the elasticity of life expectancy with respect to model parameters. Knowledge of Gompertz–Makeham life expectancies aids constructing life-table exposures....

Multiple chronic conditions and life expectancy

DEFF Research Database (Denmark)

DuGoff, Eva H; Canudas-Romo, Vladimir; Buttorff, Christine

2014-01-01

BACKGROUND: The number of people living with multiple chronic conditions is increasing, but we know little about the impact of multimorbidity on life expectancy. OBJECTIVE: We analyze life expectancy in Medicare beneficiaries by number of chronic conditions. RESEARCH DESIGN: A retrospective cohort...... study using single-decrement period life tables. SUBJECTS: Medicare fee-for-service beneficiaries (N=1,372,272) aged 67 and older as of January 1, 2008. MEASURES: Our primary outcome measure is life expectancy. We categorize study subjects by sex, race, selected chronic conditions (heart disease, cancer...... and increasing numbers of comorbid conditions. CONCLUSIONS: Social Security and Medicare actuaries should account for the growing number of beneficiaries with multiple chronic conditions when determining population projections and trust fund solvency....

Multiple chronic conditions and life expectancy: a life table analysis.

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DuGoff, Eva H; Canudas-Romo, Vladimir; Buttorff, Christine; Leff, Bruce; Anderson, Gerard F

2014-08-01

The number of people living with multiple chronic conditions is increasing, but we know little about the impact of multimorbidity on life expectancy. We analyze life expectancy in Medicare beneficiaries by number of chronic conditions. A retrospective cohort study using single-decrement period life tables. Medicare fee-for-service beneficiaries (N=1,372,272) aged 67 and older as of January 1, 2008. Our primary outcome measure is life expectancy. We categorize study subjects by sex, race, selected chronic conditions (heart disease, cancer, chronic obstructive pulmonary disease, stroke, and Alzheimer disease), and number of comorbid conditions. Comorbidity was measured as a count of conditions collected by Chronic Conditions Warehouse and the Charlson Comorbidity Index. Life expectancy decreases with each additional chronic condition. A 67-year-old individual with no chronic conditions will live on average 22.6 additional years. A 67-year-old individual with 5 chronic conditions and ≥10 chronic conditions will live 7.7 fewer years and 17.6 fewer years, respectively. The average marginal decline in life expectancy is 1.8 years with each additional chronic condition-ranging from 0.4 fewer years with the first condition to 2.6 fewer years with the sixth condition. These results are consistent by sex and race. We observe differences in life expectancy by selected conditions at 67, but these differences diminish with age and increasing numbers of comorbid conditions. Social Security and Medicare actuaries should account for the growing number of beneficiaries with multiple chronic conditions when determining population projections and trust fund solvency.

Changing mortality and average cohort life expectancy

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Robert Schoen

2005-10-01

Full Text Available Period life expectancy varies with changes in mortality, and should not be confused with the life expectancy of those alive during that period. Given past and likely future mortality changes, a recent debate has arisen on the usefulness of the period life expectancy as the leading measure of survivorship. An alternative aggregate measure of period mortality which has been seen as less sensitive to period changes, the cross-sectional average length of life (CAL has been proposed as an alternative, but has received only limited empirical or analytical examination. Here, we introduce a new measure, the average cohort life expectancy (ACLE, to provide a precise measure of the average length of life of cohorts alive at a given time. To compare the performance of ACLE with CAL and with period and cohort life expectancy, we first use population models with changing mortality. Then the four aggregate measures of mortality are calculated for England and Wales, Norway, and Switzerland for the years 1880 to 2000. CAL is found to be sensitive to past and present changes in death rates. ACLE requires the most data, but gives the best representation of the survivorship of cohorts present at a given time.

Forecasting Spanish natural life expectancy.

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Guillen, Montserrat; Vidiella-i-Anguera, Antoni

2005-10-01

Knowledge of trends in life expectancy is of major importance for policy planning. It is also a key indicator for assessing future development of life insurance products, substantiality of existing retirement schemes, and long-term care for the elderly. This article examines the feasibility of decomposing age-gender-specific accidental and natural mortality rates. We study this decomposition by using the Lee and Carter model. In particular, we fit the Poisson log-bilinear version of this model proposed by Wilmoth and Brouhns et al. to historical (1975-1998) Spanish mortality rates. In addition, by using the model introduced by Wilmoth and Valkonen we analyze mortality-gender differentials for accidental and natural rates. We present aggregated life expectancy forecasts compared with those constructed using nondecomposed mortality rates.

Molecular genetic approaches to the study of cellular senescence.

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Goletz, T J; Smith, J R; Pereira-Smith, O M

1994-01-01

Cellular senescence is an inability of cells to synthesize DNA and divide, which results in a terminal loss of proliferation despite the maintenance of basic metabolic processes. Senescence has been proposed as a model for the study of aging at the cellular level, and the basis for this model system and its features have been summarized. Although strong experimental evidence exists to support the hypothesis that cellular senescence is a dominant active process, the mechanisms responsible for this phenomenon remain a mystery. Investigators have taken several approaches to gain a better understanding of senescence. Several groups have documented the differences between young and senescent cells, and others have identified changes that occur during the course of a cell's in vitro life span. Using molecular and biochemical approaches, important changes in gene expression and function of cell-cycle-associated products have been identified. The active production of an inhibitor of DNA synthesis has been demonstrated. This may represent the final step in a cascade of events governing senescence. The study of immortal cells which have escaped senescence has also provided useful information, particularly with regard to the genes governing the senescence program. These studies have identified four complementation groups for indefinite division, which suggests that there are at least four genes or gene pathways in the senescence program. Through the use of microcell-mediated chromosome transfer, chromosomes encoding senescence genes have been identified; efforts to clone these genes are ongoing.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors Associated With Subjective Life Expectancy: Comparison With Actuarial Life Expectancy

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Jaekyoung Bae

2017-07-01

Full Text Available Objectives Subjective life expectancy (SLE has been found to show a significant association with mortality. In this study, we aimed to investigate the major factors affecting SLE. We also examined whether any differences existed between SLE and actuarial life expectancy (LE in Korea. Methods A cross-sectional survey of 1000 individuals in Korea aged 20-59 was conducted. Participants were asked about SLE via a self-reported questionnaire. LE from the National Health Insurance database in Korea was used to evaluate differences between SLE and actuarial LE. Age-adjusted least-squares means, correlations, and regression analyses were used to test the relationship of SLE with four categories of predictors: demographic factors, socioeconomic factors, health behaviors, and psychosocial factors. Results Among the 1000 participants, women (mean SLE, 83.43 years; 95% confidence interval, 82.41 to 84.46 years; 48% of the total sample had an expected LE 1.59 years longer than that of men. The socioeconomic factors of household income and housing arrangements were related to SLE. Among the health behaviors, smoking status, alcohol status, and physical activity were associated with SLE. Among the psychosocial factors, stress, self-rated health, and social connectedness were related to SLE. SLE had a positive correlation with actuarial estimates (r=0.61, p<0.001. Gender, household income, history of smoking, and distress were related to the presence of a gap between SLE and actuarial LE. Conclusions Demographic factors, socioeconomic factors, health behaviors, and psychosocial factors showed significant associations with SLE, in the expected directions. Further studies are needed to determine the reasons for these results.

FastStats: Life Expectancy

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... What's this? Submit What's this? Submit Button NCHS Home ... expectancy at birth, at 65, and 75 years of age by sex, race and Hispanic origin Health, United States 2016, table 15 [PDF – 9.8 MB] Life ...

In vitro senescence of immune cells.

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Effros, Rita B; Dagarag, Mirabelle; Valenzuela, Hector F

2003-01-01

Immune cells are eminently suitable model systems in which to address the possible role of replicative senescence during in vivo aging. Since there are more than 10(8) unique antigen specificities present within the total T lymphocyte population of each individual, the immune response to any single antigen requires massive clonal expansion of the small proportion of T cells whose receptors recognize that antigen. The Hayflick Limit may, therefore, constitute a barrier to effective immune function, at least for those T cells that encounter their specific antigen more than once over the life course. Application of the fibroblast replicative senescence model to the so-called cytotoxic or CD8 T cell, the class of T cells that controls viral infection and cancer, has revealed certain features in common with other cell types as well as several characteristics that are unique to T cells. One senescence-associated change that is T cell-specific is the complete loss of expression of the activation signaling surface molecule, CD28, an alteration that enabled the documentation of high proportions of senescent T cells in vivo. The T cell model has also provided the unique opportunity to analyze telomere dynamics in a cell type that has the ability to upregulate telomerase yet nevertheless undergoes senescence. The intimate involvement of the immune system in the control of pathogens and cancer as well as in modulation of bone homeostasis suggests that more extensive analysis of the full range of characteristics of senescent T cells may help elucidate a broad spectrum of age-associated physiological changes.

Density dependence triggers runaway selection of reduced senescence.

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Robert M Seymour

2007-12-01

Full Text Available In the presence of exogenous mortality risks, future reproduction by an individual is worth less than present reproduction to its fitness. Senescent aging thus results inevitably from transferring net fertility into younger ages. Some long-lived organisms appear to defy theory, however, presenting negligible senescence (e.g., hydra and extended lifespans (e.g., Bristlecone Pine. Here, we investigate the possibility that the onset of vitality loss can be delayed indefinitely, even accepting the abundant evidence that reproduction is intrinsically costly to survival. For an environment with constant hazard, we establish that natural selection itself contributes to increasing density-dependent recruitment losses. We then develop a generalized model of accelerating vitality loss for analyzing fitness optima as a tradeoff between compression and spread in the age profile of net fertility. Across a realistic spectrum of senescent age profiles, density regulation of recruitment can trigger runaway selection for ever-reducing senescence. This novel prediction applies without requirement for special life-history characteristics such as indeterminate somatic growth or increasing fecundity with age. The evolution of nonsenescence from senescence is robust to the presence of exogenous adult mortality, which tends instead to increase the age-independent component of vitality loss. We simulate examples of runaway selection leading to negligible senescence and even intrinsic immortality.

Political conditions and life expectancy in Europe, 1900-2008.

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Mackenbach, Johan P

2013-04-01

The rise of life expectancy in Europe has been a very uneven process, both in time and space. This paper aims to identify instances in which major political conditions are likely to have influenced the rise of life expectancy, focusing on formation and dissolution of states and supranational blocs and on differences between political regimes (democratic vs. authoritarian non-communist and communist rule). Data on life expectancy, cause-specific mortality and political conditions were compiled from existing data sources. Possible relations between political conditions and life expectancy were studied by direct comparisons of changes in life expectancy in countries with different political conditions but similar starting levels of life expectancy. We found that formation and dissolution of states often went together with convergence and divergence of life expectancy, respectively, and that otherwise similar countries that did or did not become part of the Soviet bloc had distinctly different life expectancy trajectories. Democratically governed states had higher life expectancies than authoritarian states throughout the 20th century. The gap narrowed between 1920 and 1960 due to rapid catching up of infectious disease control in both non-communist and communist authoritarian states. It widened again after 1960 due to earlier and more rapid progress in democratic states against cardiovascular disease, breast cancer, motor vehicle accidents and other causes of death that have become amenable to intervention. We conclude that the history of life expectancy in Europe contains many instances in which political conditions are likely to have had a temporary or more lasting impact on population health. This suggests that there is scope for further in-depth studies of the impact of specific political determinants on the development of population health in Europe. Copyright © 2012 Elsevier Ltd. All rights reserved.

Senescence Meets Dedifferentiation

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Givaty Rapp, Yemima; Ransbotyn, Vanessa; Grafi, Gideon

2015-01-01

Senescence represents the final stage of leaf development but is often induced prematurely following exposure to biotic and abiotic stresses. Leaf senescence is manifested by color change from green to yellow (due to chlorophyll degradation) or to red (due to de novo synthesis of anthocyanins coupled with chlorophyll degradation) and frequently culminates in programmed death of leaves. However, the breakdown of chlorophyll and macromolecules such as proteins and RNAs that occurs during leaf senescence does not necessarily represent a one-way road to death but rather a reversible process whereby senescing leaves can, under certain conditions, re-green and regain their photosynthetic capacity. This phenomenon essentially distinguishes senescence from programmed cell death, leading researchers to hypothesize that changes occurring during senescence might represent a process of trans-differentiation, that is the conversion of one cell type to another. In this review, we highlight attributes common to senescence and dedifferentiation including chromatin structure and activation of transposable elements and provide further support to the notion that senescence is not merely a deterioration process leading to death but rather a unique developmental state resembling dedifferentiation. PMID:27135333

Basal metabolic rate and the rate of senescence in the great tit

NARCIS (Netherlands)

Bouwhuis, Sandra; Sheldon, Ben C.; Verhulst, Simon; Koteja, Pawel

1. Between-individual variation in rates of senescence has recently been found to relate to natal and early-life conditions in several natural populations. Mechanistic theories of senescence have predicted between-individual variation in basal metabolic rate (BMR) to also underlie such variation in

Translational researches on leaf senescence for enhancing plant productivity and quality.

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Guo, Yongfeng; Gan, Su-Sheng

2014-07-01

Leaf senescence is a very important trait that limits yield and biomass accumulation of agronomic crops and reduces post-harvest performance and the nutritional value of horticultural crops. Significant advance in physiological and molecular understanding of leaf senescence has made it possible to devise ways of manipulating leaf senescence for agricultural improvement. There are three major strategies in this regard: (i) plant hormone biology-based leaf senescence manipulation technology, the senescence-specific gene promoter-directed IPT system in particular; (ii) leaf senescence-specific transcription factor biology-based technology; and (iii) translation initiation factor biology-based technology. Among the first strategy, the P SAG12 -IPT autoregulatory senescence inhibition system has been widely explored and successfully used in a variety of plant species for manipulating senescence. The vast majority of the related research articles (more than 2000) showed that crops harbouring the autoregulatory system displayed a significant delay in leaf senescence without any abnormalities in growth and development, a marked increase in grain yield and biomass, dramatic improvement in horticultural performance, and/or enhanced tolerance to drought stress. This technology is approaching commercialization. The transcription factor biology-based and translation initiation factor biology-based technologies have also been shown to be very promising and have great potentials for manipulating leaf senescence in crops. Finally, it is speculated that technologies based on the molecular understanding of nutrient recycling during leaf senescence are highly desirable and are expected to be developed in future translational leaf senescence research. © The Author 2014. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Life expectancies for individuals with psychiatric diagnoses.

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Hannerz, H; Borgå, P; Borritz, M

2001-09-01

The aim of the study was to estimate life expectancies in different diagnostic groups for individuals treated as inpatients at Swedish psychiatric clinics. All individuals, older than 18 y and alive on the first of January 1983, who had been registered in the National Hospital Discharge Registry by a psychiatric clinic in 1978-82, were monitored for mortality during 1983 by using the National Cause of Death Registry. The study group consisted of 91 385 men and 77 217 women. The patients were divided into nine diagnostic groups according to the principal diagnosis registered at the latest discharge. Actuarial mathematics was used to construct life expectancy tables, which present the number of years expected to live, by gender and diagnostic group. Expectancies of life were significantly shortened for both genders and in all nine diagnostic groups (with one exception). Mental disorders in general are life shortening. This fact should be recognised in community health when setting health priorities. It should also be addressed in curricula as well as in treatment and preventive programmes.

Life Expectancy in 2040

DEFF Research Database (Denmark)

Canudas-Romo, Vladimir; DuGoff, Eva H; Wu, Albert W.

2016-01-01

We use expert clinical and public health opinion to estimate likely changes in the prevention and treatment of important disease conditions and how they will affect future life expectancy. Focus groups were held including clinical and public health faculty with expertise in the six leading causes...

On the correspondence between CAL and lagged cohort life expectancy

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Michel Guillot

2011-04-01

Full Text Available It has been established that under certain mortality assumptions, the current value of the Cross-sectional Average length of Life (CAL is equal to the life expectancy for the cohort currently reaching its life expectancy. This correspondence is important, because the life expectancy for the cohort currently reaching its life expectancy, or lagged cohort life expectancy (LCLE, has been discussed in the tempo literature as a summary mortality measure of substantive interest. In this paper, we build on previous work by evaluating the extent to which the correspondence holds in actual populations. We also discuss the implications of the CAL-LCLE correspondence (or lack thereof for using CAL as a measure of cohort life expectancy, and for understanding the connection between CAL, LCLE, and underlying period mortality conditions.

Dental Status and Compression of Life Expectancy with Disability.

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Matsuyama, Y; Aida, J; Watt, R G; Tsuboya, T; Koyama, S; Sato, Y; Kondo, K; Osaka, K

2017-08-01

This study examined whether the number of teeth contributes to the compression of morbidity, measured as a shortening of life expectancy with disability, an extension of healthy life expectancy, and overall life expectancy. A prospective cohort study was conducted. A self-reported baseline survey was given to 126,438 community-dwelling older people aged ≥65 y in Japan in 2010, and 85,161 (67.4%) responded. The onset of functional disability and all-cause mortality were followed up for 1,374 d (follow-up rate = 96.1%). A sex-stratified illness-death model was applied to estimate the adjusted hazard ratios (HRs) for 3 health transitions (healthy to dead, healthy to disabled, and disabled to dead). Absolute differences in life expectancy, healthy life expectancy, and life expectancy with disability according to the number of teeth were also estimated. Age, denture use, socioeconomic status, health status, and health behavior were adjusted. Compared with the edentulous participants, participants with ≥20 teeth had lower risks of transitioning from healthy to dead (adjusted HR, 0.58 [95% confidence interval (CI), 0.50-0.68] for men and 0.70 [95% CI, 0.57-0.85] for women) and from healthy to disabled (adjusted HR, 0.52 [95% CI, 0.44-0.61] for men and 0.58 [95% CI, 0.49-0.68] for women). They also transitioned from disabled to dead earlier (adjusted HR, 1.26 [95% CI, 0.99-1.60] for men and 2.42 [95% CI, 1.72-3.38] for women). Among the participants aged ≥85 y, those with ≥20 teeth had a longer life expectancy (men: +57 d; women: +15 d) and healthy life expectancy (men: +92 d; women: +70 d) and a shorter life expectancy with disability (men: -35 d; women: -55 d) compared with the edentulous participants. Similar associations were observed among the younger participants and those with 1 to 9 or 10 to 19 teeth. The presence of remaining teeth was associated with a significant compression of morbidity: older Japanese adults' life expectancy with disability was

Identification of novel senescence-associated genes in ionizing radiation-induced senescent carcinoma cells

International Nuclear Information System (INIS)

Lee, Jae Seon; Kim, Bong Cho; Han, Na Kyung; Hong, Mi Na; Park, Su Min; Yoo, Hee Jung; Chu, In Sun; Lee, Sun Hee

2009-01-01

Cellular senescence is considered as a defense mechanism to prevent tumorigenesis. Ionizing radiation (IR) induces stress-induced premature senescence as well as apoptosis in various cancer cells. Senescent cells undergo functional and morphological changes including large and flattened cell shape, senescence-associated β-galactosidase (SA-βGal) activity, and altered gene expressions. Even with the recent findings of several gene expression profiles and supporting functional data, it is obscure that mechanism of IR-induced premature senescence in cancer cells. We performed microarray analysis to identify the common regulated genes in ionizing radiation-induced prematurely senescent human carcinoma cell lines

Physical activity extends life expectancy

Science.gov (United States)

Leisure-time physical activity is associated with longer life expectancy, even at relatively low levels of activity and regardless of body weight, according to a study by a team of researchers led by the NCI.

Dietary Animal Plasma Proteins Improve the Intestinal Immune Response in Senescent Mice.

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Miró, Lluïsa; Garcia-Just, Alba; Amat, Concepció; Polo, Javier; Moretó, Miquel; Pérez-Bosque, Anna

2017-12-11

Increased life expectancy has promoted research on healthy aging. Aging is accompanied by increased non-specific immune activation (inflammaging) which favors the appearance of several disorders. Here, we study whether dietary supplementation with spray-dried animal plasma (SDP), which has been shown to reduce the activation of gut-associated lymphoid tissue (GALT) in rodents challenged by S. aureus enterotoxin B (SEB), and can also prevent the effects of aging on immune system homeostasis. We first characterized GALT in a mouse model of accelerated senescence (SAMP8) at different ages (compared to mice resistant to accelerated senescence; SAMR1). Second, we analyzed the SDP effects on GALT response to an SEB challenge in SAMP8 mice. In GALT characterization, aging increased the cell number and the percentage of activated Th lymphocytes in mesenteric lymph nodes and Peyer's patches (all, p < 0.05), as well as the expression of IL-6 and TNF-α in intestinal mucosa (both, p < 0.05). With respect to GALT response to the SEB challenge, young mice showed increased expression of intestinal IL-6 and TNF-α, as well as lymphocyte recruitment and activation (all, p < 0.05). However, the immune response of senescent mice to the SEB challenge was weak, since SEB did not change cell recruitment or the percentage of activated Th lymphocytes. Mice supplemented with SDP showed improved capacity to respond to the SEB challenge, similar to the response of the young mice. These results indicate that senescent mice have an impaired mucosal immune response characterized by unspecific GALT activation and a weak specific immune response. SDP supplementation reduces non-specific basal immune activation, allowing for the generation of specific responses.

Cellular Senescence: A Translational Perspective

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James L. Kirkland

2017-07-01

Full Text Available Cellular senescence entails essentially irreversible replicative arrest, apoptosis resistance, and frequently acquisition of a pro-inflammatory, tissue-destructive senescence-associated secretory phenotype (SASP. Senescent cells accumulate in various tissues with aging and at sites of pathogenesis in many chronic diseases and conditions. The SASP can contribute to senescence-related inflammation, metabolic dysregulation, stem cell dysfunction, aging phenotypes, chronic diseases, geriatric syndromes, and loss of resilience. Delaying senescent cell accumulation or reducing senescent cell burden is associated with delay, prevention, or alleviation of multiple senescence-associated conditions. We used a hypothesis-driven approach to discover pro-survival Senescent Cell Anti-apoptotic Pathways (SCAPs and, based on these SCAPs, the first senolytic agents, drugs that cause senescent cells to become susceptible to their own pro-apoptotic microenvironment. Several senolytic agents, which appear to alleviate multiple senescence-related phenotypes in pre-clinical models, are beginning the process of being translated into clinical interventions that could be transformative.

[Expectation of life at birth: sex differentials, trends, limits].

Science.gov (United States)

Aubenque, M; Damiani, P

1981-01-01

Using information available at the end of 1979, the authors present and analyze data on expectation of life at birth in 119 countries. Differences between developing and developed countries, trends over time, sex differentials, and limits on life expectancy are examined. The analysis reveals limits of approximately 73 years for men and 80 for women in the most developed countries. In France, which displays excessive male mortality, expectation of life increases more slowly for men. The authors attribute these sex differentials both to biological factors and to behavioral factors and ways of life.

Natural Variation in the Sex Gap in Life Expectancy

DEFF Research Database (Denmark)

Lindahl-Jacobsen, Rune; Zarulli, Virginia; Christensen, Kaare

of these environmental factors whereas small differences would reflect a lower action of the factors and approach the ‘natural’ biological level. Here we examine variability in sex differences in life expectancy in 47 historical and contemporary human populations to address our hypothesis: large sex differences in life...... that females withstand harsh environments better then males in terms of survival, partly explaining their higher life expectancy. If this hypothesis is true and females survive environmental stressors better then males then large sex differences in life expectancies could reflect the action...

The Crossover between Life Expectancies at Birth and at Age One

DEFF Research Database (Denmark)

Canudas-Romo, Vladimir; Becker, S

2011-01-01

one are referred to here as imbalanced. This crossover occurs when infant mortality is equal to the inverse of life expectancy at age one. This simple relation between mortality at age zero and mortality after age one divides the world into countries that have achieved the crossover in life......The single most used demographic measure to describe population health is life expectancy at birth, but life expectancies at ages other than zero are also used in the study of human longevity. Our intuition tells us that the longest life expectancy is that of a newborn. However, historically......, the expectation of life at age one (e1) has exceeded the expectation of life at birth (e0). The crossover between e0 and e1 only occurred in the developed world in the second half of the twentieth century. Life tables for populations that have not achieved this crossing between life expectancy at birth and at age...

Identification of 30 protein species involved in replicative senescence and stress-induced premature senescence

DEFF Research Database (Denmark)

Dierick, Jean François; Kalume, Dário E; Wenders, Frédéric

2002-01-01

Exposure of human proliferative cells to subcytotoxic stress triggers stress-induced premature senescence (SIPS) which is characterized by many biomarkers of replicative senescence. Proteomic comparison of replicative senescence and stress-induced premature senescence indicates that, at the level...

Multilevel survival analysis of health inequalities in life expectancy

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Merlo Juan

2009-08-01

Full Text Available Abstract Background The health status of individuals is determined by multiple factors operating at both micro and macro levels and the interactive effects of them. Measures of health inequalities should reflect such determinants explicitly through sources of levels and combining mean differences at group levels and the variation of individuals, for the benefits of decision making and intervention planning. Measures derived recently from marginal models such as beta-binomial and frailty survival, address this issue to some extent, but are limited in handling data with complex structures. Beta-binomial models were also limited in relation to measuring inequalities of life expectancy (LE directly. Methods We propose a multilevel survival model analysis that estimates life expectancy based on survival time with censored data. The model explicitly disentangles total health inequalities in terms of variance components of life expectancy compared to the source of variation at the level of individuals in households and parishes and so on, and estimates group differences of inequalities at the same time. Adjusted distributions of life expectancy by gender and by household socioeconomic level are calculated. Relative and absolute health inequality indices are derived based on model estimates. The model based analysis is illustrated on a large Swedish cohort of 22,680 men and 26,474 women aged 65–69 in 1970 and followed up for 30 years. Model based inequality measures are compared to the conventional calculations. Results Much variation of life expectancy is observed at individual and household levels. Contextual effects at Parish and Municipality level are negligible. Women have longer life expectancy than men and lower inequality. There is marked inequality by the level of household socioeconomic status measured by the median life expectancy in each socio-economic group and the variation in life expectancy within each group. Conclusion Multilevel

PPARgamma Deficiency Counteracts Thymic Senescence

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David Ernszt

2017-11-01

Full Text Available Thymic senescence contributes to increased incidence of infection, cancer and autoimmunity at senior ages. This process manifests as adipose involution. As with other adipose tissues, thymic adipose involution is also controlled by PPARgamma. This is supported by observations reporting that systemic PPARgamma activation accelerates thymic adipose involution. Therefore, we hypothesized that decreased PPARgamma activity could prevent thymic adipose involution, although it may trigger metabolic adverse effects. We have confirmed that both human and murine thymic sections show marked staining for PPARgamma at senior ages. We have also tested the thymic lobes of PPARgamma haplo-insufficient and null mice. Supporting our working hypothesis both adult PPARgamma haplo-insufficient and null mice show delayed thymic senescence by thymus histology, thymocyte mouse T-cell recombination excision circle qPCR and peripheral blood naive T-cell ratio by flow-cytometry. Delayed senescence showed dose–response with respect to PPARgamma deficiency. Functional immune parameters were also evaluated at senior ages in PPARgamma haplo-insufficient mice (null mice do not reach senior ages due to metabolic adverse affects. As expected, sustained and elevated T-cell production conferred oral tolerance and enhanced vaccination efficiency in senior PPARgamma haplo-insufficient, but not in senior wild-type littermates according to ELISA IgG measurements. Of note, humans also show increased oral intolerance issues and decreased protection by vaccines at senior ages. Moreover, PPARgamma haplo-insufficiency also exists in human known as a rare disease (FPLD3 causing metabolic adverse effects, similar to the mouse. When compared to age- and metabolic disorder-matched other patient samples (FPLD2 not affecting PPARgamma activity, FPLD3 patients showed increased human Trec (hTrec values by qPCR (within healthy human range suggesting delayed thymic senescence, in accordance with

Does Physical Activity Increase Life Expectancy? A Review of the Literature

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C. D. Reimers

2012-01-01

Full Text Available Physical activity reduces many major mortality risk factors including arterial hypertension, diabetes mellitus type 2, dyslipidemia, coronary heart disease, stroke, and cancer. All-cause mortality is decreased by about 30% to 35% in physically active as compared to inactive subjects. The purpose of this paper was to synthesize the literature on life expectancy in relation to physical activity. A systematic PubMed search on life expectancy in physically active and inactive individuals was performed. In addition, articles comparing life expectancy of athletes compared to that of nonathletes were reviewed. Results of 13 studies describing eight different cohorts suggest that regular physical activity is associated with an increase of life expectancy by 0.4 to 6.9 years. Eleven studies included confounding risk factors for mortality and revealed an increase in life expectancy by 0.4 to 4.2 years with regular physical activity. Eleven case control studies on life expectancy in former athletes revealed consistently greater life expectancy in aerobic endurance athletes but inconsistent results for other athletes. None of these studies considered confounding risk factors for mortality. In conclusion, while regular physical activity increases life expectancy, it remains unclear if high-intensity sports activities further increase life expectancy.

Piper betle L. Modulates Senescence-Associated Genes Expression in Replicative Senescent Human Diploid Fibroblasts

Directory of Open Access Journals (Sweden)

Lina Wati Durani

2017-01-01

Full Text Available Piper betle (PB is a traditional medicine that is widely used to treat different diseases around Asian region. The leaf extracts contain various bioactive compounds, which were reported to have antidiabetic, antibacterial, anti-inflammatory, antioxidant, and anticancer effects. In this study, the effect of PB aqueous extracts on replicative senescent human diploid fibroblasts (HDFs was investigated by determining the expressions of senescence-associated genes using quantitative PCR. Our results showed that PB extracts at 0.4 mg/ml can improve cell proliferation of young (143%, presenescent (127.3%, and senescent (157.3% HDFs. Increased expressions of PRDX6, TP53, CDKN2A, PAK2, and MAPK14 were observed in senescent HDFs compared to young and/or presenescent HDFs. Treatment with PB extracts modulates the transcriptional profile changes in senescent HDFs. By contrast, expressions of SOD1 increased, whereas GPX1, PRDX6, TP53, CDKN2A, PAK2, and MAPK14 were decreased in PB-treated senescent HDFs compared to untreated senescent HDFs. In conclusion, this study indicates the modulation of PB extracts on senescence-associated genes expression of replicative senescent HDFs. Further studies warrant determining the mechanism of PB in modulating replicative senescence of HDFs through these signaling pathways.

Piper betle L. Modulates Senescence-Associated Genes Expression in Replicative Senescent Human Diploid Fibroblasts.

Science.gov (United States)

Durani, Lina Wati; Khor, Shy Cian; Tan, Jen Kit; Chua, Kien Hui; Mohd Yusof, Yasmin Anum; Makpol, Suzana

2017-01-01

Piper betle (PB) is a traditional medicine that is widely used to treat different diseases around Asian region. The leaf extracts contain various bioactive compounds, which were reported to have antidiabetic, antibacterial, anti-inflammatory, antioxidant, and anticancer effects. In this study, the effect of PB aqueous extracts on replicative senescent human diploid fibroblasts (HDFs) was investigated by determining the expressions of senescence-associated genes using quantitative PCR. Our results showed that PB extracts at 0.4 mg/ml can improve cell proliferation of young (143%), presenescent (127.3%), and senescent (157.3%) HDFs. Increased expressions of PRDX6 , TP53 , CDKN2A , PAK2 , and MAPK14 were observed in senescent HDFs compared to young and/or presenescent HDFs. Treatment with PB extracts modulates the transcriptional profile changes in senescent HDFs. By contrast, expressions of SOD1 increased, whereas GPX1 , PRDX6 , TP53 , CDKN2A , PAK2 , and MAPK14 were decreased in PB-treated senescent HDFs compared to untreated senescent HDFs. In conclusion, this study indicates the modulation of PB extracts on senescence-associated genes expression of replicative senescent HDFs. Further studies warrant determining the mechanism of PB in modulating replicative senescence of HDFs through these signaling pathways.

Obesity in adulthood and its consequences for life expectancy: a life-table analysis

NARCIS (Netherlands)

A. Peeters (Anna); J.J.M. Barendregt (Jan); F. Willekens; J.P. Mackenbach (Johan); A. Al Mamun; L.G.A. Bonneux (Luc)

2003-01-01

textabstractBACKGROUND: Overweight and obesity in adulthood are linked to an increased risk for death and disease. Their potential effect on life expectancy and premature death has not yet been described. OBJECTIVE: To analyze reductions in life expectancy and increases in

The Immortal Senescence.

Science.gov (United States)

Bianchi-Smiraglia, Anna; Lipchick, Brittany C; Nikiforov, Mikhail A

2017-01-01

Activation of oncogenic signaling paradoxically results in the permanent withdrawal from cell cycle and induction of senescence (oncogene-induced senescence (OIS)). OIS is a fail-safe mechanism used by the cells to prevent uncontrolled tumor growth, and, as such, it is considered as the first barrier against cancer. In order to progress, tumor cells thus need to first overcome the senescent phenotype. Despite the increasing attention gained by OIS in the past 20 years, this field is still rather young due to continuous emergence of novel pathways and processes involved in OIS. Among the many factors contributing to incomplete understanding of OIS are the lack of unequivocal markers for senescence and the complexity of the phenotypes revealed by senescent cells in vivo and in vitro. OIS has been shown to play major roles at both the cellular and organismal levels in biological processes ranging from embryonic development to barrier to cancer progression. Here we will briefly outline major advances in methodologies that are being utilized for induction, identification, and characterization of molecular processes in cells undergoing oncogene-induced senescence. The full description of such methodologies is provided in the corresponding chapters of the book.

Senescence is not inevitable

DEFF Research Database (Denmark)

Jones, Owen; Vaupel, James W.

2017-01-01

trajectories exists. These empirical observations support theoretical work indicating that a wide range of mortality and fertility trajectories is indeed possible, including senescence, negligible senescence and even negative senescence (improvement). Although many mysteries remain in the field...

Actuarial senescence in a long-lived orchid challenges our current understanding of ageing.

Science.gov (United States)

Dahlgren, Johan Petter; Colchero, Fernando; Jones, Owen R; Øien, Dag-Inge; Moen, Asbjørn; Sletvold, Nina

2016-11-16

The dominant evolutionary theory of actuarial senescence-an increase in death rate with advancing age-is based on the concept of a germ cell line that is separated from the somatic cells early in life. However, such a separation is not clear in all organisms. This has been suggested to explain the paucity of evidence for actuarial senescence in plants. We used a 32 year study of Dactylorhiza lapponica that replaces its organs each growing season, to test whether individuals of this tuberous orchid senesce. We performed a Bayesian survival trajectory analysis accounting for reproductive investment, for individuals under two types of land use, in two climatic regions. The mortality trajectory was best approximated by a Weibull model, showing clear actuarial senescence. Rates of senescence in this model declined with advancing age, but were slightly higher in mown plots and in the more benign climatic region. At older ages, senescence was evident only when accounting for a positive effect of reproductive investment on mortality. Our results demonstrate actuarial senescence as well as a survival-reproduction trade-off in plants, and indicate that environmental context may influence senescence rates. This knowledge is crucial for understanding the evolution of demographic senescence and for models of plant population dynamics. © 2016 The Author(s).

The effect of life expectancy on aggression and generativity: a life history perspective.

Science.gov (United States)

Dunkel, Curtis S; Mathes, Eugene; Papini, Dennis R

2010-09-23

Following a model that is inclusive of both dispositional and situational influences on life-history behaviors and attitudes, the effect of life expectancies on aggression and generativity was examined. Consistent with the hypotheses it was found that shorter life expectancies led to an increase in the desire to aggress and a decrease in the desire to engage in generative behaviors. The results are discussed in terms of how life history theory can be used to frame research on person-situation interactions.

Life expectancy living with HIV: recent estimates and future implications.

Science.gov (United States)

Nakagawa, Fumiyo; May, Margaret; Phillips, Andrew

2013-02-01

The life expectancy of people living with HIV has dramatically increased since effective antiretroviral therapy has been available, and still continues to improve. Here, we review the latest literature on estimates of life expectancy and consider the implications for future research. With timely diagnosis, access to a variety of current drugs and good lifelong adherence, people with recently acquired infections can expect to have a life expectancy which is nearly the same as that of HIV-negative individuals. Modelling studies suggest that life expectancy could improve further if there were increased uptake of HIV testing, better antiretroviral regimens and treatment strategies, and the adoption of healthier lifestyles by those living with HIV. In particular, earlier diagnosis is one of the most important factors associated with better life expectancy. A consequence of improved survival is the increasing number of people with HIV who are aged over 50 years old, and further research into the impact of ageing on HIV-positive people will therefore become crucial. The development of age-specific HIV treatment and management guidelines is now called for. Analyses on cohort studies and mathematical modelling studies have been used to estimate life expectancy of those with HIV, providing useful insights of importance to individuals and healthcare planning.

Inequalities in US Life Expectancy by Area Unemployment Level, 1990–2010

Science.gov (United States)

Singh, Gopal K.; Siahpush, Mohammad

2016-01-01

This study examined the association between unemployment and life expectancy in the United States during 1990–2010. Census-based unemployment rates were linked to US county-level mortality data. Life expectancies were calculated by age, sex, race, and unemployment level during 1990–2010. Differences in life expectancy were decomposed by age and cause of death. Life expectancy was consistently lower in areas with higher unemployment rates. In 2006–2010, those in areas with high unemployment rates (≥9%) had a life expectancy of 76.9 years, compared with 80.7 years for those in areas with low unemployment rates (unemployment and life expectancy was stronger for men than for women. Life expectancy ranged from 69.9 years among black men in high unemployment areas to 90.0 years among Asian/Pacific Islander women in low unemployment areas. Disparities persisted over time. In 1990–1992, life expectancy was 4.7 years shorter in high unemployment than in low unemployment areas. In 2006–2010, the life expectancy difference between the lowest and highest unemployment areas decreased to 3.8 years. Heart disease, cancer, homicide, unintentional injuries, diabetes, HIV/AIDS, and liver cirrhosis contributed most to the lower life expectancy in high unemployment areas. High unemployment areas recorded larger gains in life expectancy than low unemployment areas, contributing to the narrowing gap during 1990–2010. PMID:27073716

Dietary Animal Plasma Proteins Improve the Intestinal Immune Response in Senescent Mice

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Lluïsa Miró

2017-12-01

Full Text Available Increased life expectancy has promoted research on healthy aging. Aging is accompanied by increased non-specific immune activation (inflammaging which favors the appearance of several disorders. Here, we study whether dietary supplementation with spray-dried animal plasma (SDP, which has been shown to reduce the activation of gut-associated lymphoid tissue (GALT in rodents challenged by S. aureus enterotoxin B (SEB, and can also prevent the effects of aging on immune system homeostasis. We first characterized GALT in a mouse model of accelerated senescence (SAMP8 at different ages (compared to mice resistant to accelerated senescence; SAMR1. Second, we analyzed the SDP effects on GALT response to an SEB challenge in SAMP8 mice. In GALT characterization, aging increased the cell number and the percentage of activated Th lymphocytes in mesenteric lymph nodes and Peyer’s patches (all, p < 0.05, as well as the expression of IL-6 and TNF-α in intestinal mucosa (both, p < 0.05. With respect to GALT response to the SEB challenge, young mice showed increased expression of intestinal IL-6 and TNF-α, as well as lymphocyte recruitment and activation (all, p < 0.05. However, the immune response of senescent mice to the SEB challenge was weak, since SEB did not change cell recruitment or the percentage of activated Th lymphocytes. Mice supplemented with SDP showed improved capacity to respond to the SEB challenge, similar to the response of the young mice. These results indicate that senescent mice have an impaired mucosal immune response characterized by unspecific GALT activation and a weak specific immune response. SDP supplementation reduces non-specific basal immune activation, allowing for the generation of specific responses.

A comparison of oncogene-induced senescence and replicative senescence: implications for tumor suppression and aging.

Science.gov (United States)

Nelson, David M; McBryan, Tony; Jeyapalan, Jessie C; Sedivy, John M; Adams, Peter D

2014-06-01

Cellular senescence is a stable proliferation arrest associated with an altered secretory pathway, the senescence-associated secretory phenotype. However, cellular senescence is initiated by diverse molecular triggers, such as activated oncogenes and shortened telomeres, and is associated with varied and complex physiological endpoints, such as tumor suppression and tissue aging. The extent to which distinct triggers activate divergent modes of senescence that might be associated with different physiological endpoints is largely unknown. To begin to address this, we performed gene expression profiling to compare the senescence programs associated with two different modes of senescence, oncogene-induced senescence (OIS) and replicative senescence (RS [in part caused by shortened telomeres]). While both OIS and RS are associated with many common changes in gene expression compared to control proliferating cells, they also exhibit substantial differences. These results are discussed in light of potential physiological consequences, tumor suppression and aging.

Life History Patterns

DEFF Research Database (Denmark)

Jones, Owen

2016-01-01

of these patterns and highlights the need to consider senescence from a broad taxonomic scope to truly understand the evolution of aging. Keywords: Aging; Demography; Evolution; Fertility; Gompertz; Life span; Mortality; Ontogenescence; Reproduction; Reproductive senescence; Senescence; Survivorship...

Inequalities in US Life Expectancy by Area Unemployment Level, 1990–2010

Directory of Open Access Journals (Sweden)

Gopal K. Singh

2016-01-01

Full Text Available This study examined the association between unemployment and life expectancy in the United States during 1990–2010. Census-based unemployment rates were linked to US county-level mortality data. Life expectancies were calculated by age, sex, race, and unemployment level during 1990–2010. Differences in life expectancy were decomposed by age and cause of death. Life expectancy was consistently lower in areas with higher unemployment rates. In 2006–2010, those in areas with high unemployment rates (≥9% had a life expectancy of 76.9 years, compared with 80.7 years for those in areas with low unemployment rates (<3%. The association between unemployment and life expectancy was stronger for men than for women. Life expectancy ranged from 69.9 years among black men in high unemployment areas to 90.0 years among Asian/Pacific Islander women in low unemployment areas. Disparities persisted over time. In 1990–1992, life expectancy was 4.7 years shorter in high unemployment than in low unemployment areas. In 2006–2010, the life expectancy difference between the lowest and highest unemployment areas decreased to 3.8 years. Heart disease, cancer, homicide, unintentional injuries, diabetes, HIV/AIDS, and liver cirrhosis contributed most to the lower life expectancy in high unemployment areas. High unemployment areas recorded larger gains in life expectancy than low unemployment areas, contributing to the narrowing gap during 1990–2010.

Evaluating natural resource amenities in a human life expectancy production function

Science.gov (United States)

Neelam C. Poudyal; Donald G. Hodges; J.M. Bowker; H.K. Cordell

2009-01-01

This study examined the effect of natural resource amenities on human life expectancy. Extending theexisting model of the life expectancy production function, and correcting for spatial dependence, weevaluated the determinants of life expectancy using county level data. Results indicate that after controlling

Bayesian projection of life expectancy accounting for the HIV/AIDS epidemic

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Jessica Godwin

2017-11-01

Full Text Available Background: While probabilistic projection methods for projecting life expectancy exist, few account for covariates related to life expectancy. Generalized HIV/AIDS epidemics have a large, immediate negative impact on the life expectancy in a country, but this impact can be mitigated by widespread use of antiretroviral therapy (ART. Thus, projection methods for countries with generalized HIV/AIDS epidemics could be improved by accounting for HIV prevalence, the future course of the epidemic, and ART coverage. Methods: We extend the current Bayesian probabilistic life expectancy projection methods of Raftery et al. (2013 to account for HIV prevalence and adult ART coverage in countries with generalized HIV/AIDS epidemics. Results: We evaluate our method using out-of-sample validation. We find that the proposed method performs better than the method that does not account for HIV prevalence or ART coverage for projections of life expectancy in countries with a generalized epidemic, while projections for countries without an epidemic remain essentially unchanged. Conclusions: In general, our projections show rapid recovery to pre-epidemic life expectancy levels in the presence of widespread ART coverage. After the initial life expectancy recovery, we project a steady rise in life expectancy until the end of the century. Contribution: We develop a simple Bayesian hierarchical model for long-term projections of life expectancy while accounting for HIV/AIDS prevalence and coverage of ART. The method produces well-calibrated projections for countries with generalized HIV/AIDS epidemics up to 2100 while having limited data demands.

Gamma-Gompertz life expectancy at birth

OpenAIRE

Trifon I. Missov

2013-01-01

BACKGROUND The gamma-Gompertz multiplicative frailty model is the most common parametric modelapplied to human mortality data at adult and old ages. The resulting life expectancy hasbeen calculated so far only numerically. OBJECTIVE Properties of the gamma-Gompertz distribution have not been thoroughly studied. The focusof the paper is to shed light onto its first moment or, demographically speaking, characterizelife expectancy resulting from a gamma-Gompertz force of mortality. The paperprov...

Leaving Sweden behind: Gains in life expectancy in Canada.

Science.gov (United States)

Auger, Nathalie; Le Serbon, Emilie; Rostila, Mikael

2015-06-01

Sweden and Canada are known for quality of living and exceedingly high life expectancy, but recent data on how these countries compare are lacking. We measured life expectancy in Canada and Sweden during the past decade, and identified factors responsible for changes over time. We calculated life expectancy at birth for Canada and Sweden annually from 2000 to 2010, and determined the ages and causes of death responsible for the gap between the two countries using Arriaga's method. We determined how population growth, ageing, and mortality influenced the number of deaths over time. During 2000-2010, life expectancy in Canada caught up with Sweden for men, and surpassed Sweden by 0.4 years for women. Sweden lost ground owing to a slower reduction in circulatory and tumour mortality after age 65 years compared with Canada. Nonetheless, population ageing increased the number of deaths in Canada, especially for mental and nervous system disorders. In Sweden, the number of deaths decreased. In only one decade, life expectancy in Canada caught up and surpassed Sweden due to rapid improvements in circulatory and tumour mortality. Population ageing increased the number of deaths in Canada, potentially stressing the health care system more than in Sweden. © 2015 the Nordic Societies of Public Health.

Actuarial senescence in a long-lived orchid challenges our current understanding of ageing

Science.gov (United States)

Colchero, Fernando; Jones, Owen R.; Øien, Dag-Inge; Moen, Asbjørn; Sletvold, Nina

2016-01-01

The dominant evolutionary theory of actuarial senescence—an increase in death rate with advancing age—is based on the concept of a germ cell line that is separated from the somatic cells early in life. However, such a separation is not clear in all organisms. This has been suggested to explain the paucity of evidence for actuarial senescence in plants. We used a 32 year study of Dactylorhiza lapponica that replaces its organs each growing season, to test whether individuals of this tuberous orchid senesce. We performed a Bayesian survival trajectory analysis accounting for reproductive investment, for individuals under two types of land use, in two climatic regions. The mortality trajectory was best approximated by a Weibull model, showing clear actuarial senescence. Rates of senescence in this model declined with advancing age, but were slightly higher in mown plots and in the more benign climatic region. At older ages, senescence was evident only when accounting for a positive effect of reproductive investment on mortality. Our results demonstrate actuarial senescence as well as a survival–reproduction trade-off in plants, and indicate that environmental context may influence senescence rates. This knowledge is crucial for understanding the evolution of demographic senescence and for models of plant population dynamics. PMID:27852801

Gender gaps--Life expectancy and proportion of life in poor health.

Science.gov (United States)

Luy, Marc; Minagawa, Yuka

2014-12-01

The literature suggests that women report worse health but live longer than men--a phenomenon known as the gender paradox in health and mortality. Although studies examining the paradox abound, relatively little is known about mechanisms underlying the gap. With data on healthy life expectancy from the Global Burden of Disease Study 2010, this article analyses the relationship between length of life and health among men and women in 45 more-developed countries. The proportion of life spent in poor health is used as an indicator of health. This approach accounts for gender differences in longevity and illustrates the female health disadvantage pattern more clearly. Life expectancy at birth and the proportion of life in poor health are closely related for both genders. Furthermore, the larger the female excess in longevity, the larger the female excess in the proportion of life in poor health. By focusing on the proportion of life in poor health, this analysis suggests that women's longevity advantage translates into a health disadvantages relative to men. The results indicate that women suffer from poor health not in spite of living longer, but because they live longer.

Trends in healthy life expectancy in Japan: 1986 - 2004

Directory of Open Access Journals (Sweden)

Vanessa Yong

2009-04-01

Full Text Available This article examines the increasing life expectancy of Japanese men and women in relation to their health from 1986 to 2004. We computed healthy life expectancy for seven available time-points using the prevalence-based Sullivan method. The results showed that, for both sexes and at all ages, the gains in life expectancy prior to 1995 were mostly in years of good self-rated health, while the gains thereafter were in years of poor self-rated health. The exception was for women at age 85, among whom there was an almost continuous increase in the number of years in poor health. The proportion of life spent in different health states suggested evidence of morbidity compression until 1995, followed by an expansion of morbidity.

Years of potential life lost and life expectancy in schizophrenia

DEFF Research Database (Denmark)

Hjorthøj, Carsten; Stürup, Anne Emilie; McGrath, John J

2017-01-01

was least in the Asian study and greatest in Africa. The overall weighted average life expectancy was 64·7 years (95% CI 61·1-71·3), and was lower for men than women (59·9 years, 95% CI 55·5-64·3 vs 67·6 years, 63·1-72·1). Life expectancy was lowest in Asia and Africa. Timing of publication and risk of bias...... (Africa n=1, Asia n=1, Australia n=1, Europe n=7, and North America n=3) that involved up to 247 603 patients. Schizophrenia was associated with a weighted average of 14·5 years of potential life lost (95% CI 11·2-17·8), and was higher for men than women (15·9, 13·8-18·0 vs 13·6, 11·4-15·8). Loss...

Senescence in the wild: Insights from a long-term study on Seychelles warblers.

Science.gov (United States)

Hammers, Martijn; Kingma, Sjouke A; Bebbington, Kat; van de Crommenacker, Janske; Spurgin, Lewis G; Richardson, David S; Burke, Terry; Dugdale, Hannah L; Komdeur, Jan

2015-11-01

Senescence--the progressive age-dependent decline in performance--occurs in most organisms. There is considerable variation in the onset and rate of senescence between and within species. Yet the causes of this variation are still poorly understood, despite being central to understanding the evolution of senescence. Long-term longitudinal studies on wild animals are extremely well-suited to studying the impact of environmental and individual characteristics (and the interaction between the two) on senescence, and can help us to understand the mechanisms that shape the evolution of senescence. In this review, we summarize and discuss the insights gained from our comprehensive long-term individual-based study of the Seychelles warbler (Acrocephalus sechellensis). This species provides an excellent model system in which to investigate the evolution of senescence in the wild. We found that Seychelles warblers show senescent declines in survival and reproduction, and discuss how individual characteristics (body condition, body size) and environmental effects (low- versus high-quality environments) may affect the onset and rate of senescence. Further, we highlight the evidence for trade-offs between early-life investment and senescence. We describe how key cellular and physiological processes (oxidative stress and telomere shortening) underpinning senescence are affected by individual and environmental characteristics in the Seychelles warbler (e.g. food availability, reproductive investment, disease) and we discuss how such physiological variation may mediate the relationship between environmental characteristics and senescence. Based on our work using Seychelles warblers as a model system, we show how insights from long-term studies of wild animals may help unravel the causes of the remarkable variation in senescence observed in natural systems, and highlight areas for promising future research.

Actuarial senescence in a long-lived orchid challenges our current understanding of ageing

DEFF Research Database (Denmark)

Dahlgren, Johan; Colchero, Fernando; Jones, Owen

2016-01-01

The dominant evolutionary theory of actuarial senescence – an increase in death rate with advancing age – is based on the concept of a germ cell line that is separated from the somatic cells early in life. However, such a separation is not clear in all organisms. This has been suggested to explain...... the paucity of evidence for actuarial senescence in plants. We used a 32-year study of Dactylorhiza lapponica that replaces its organs each growing season, to test whether individuals of this tuberous orchid senesce. We performed a Bayesian survival trajectory analysis accounting for reproductive investment......, for individuals under two types of land-use, in two climatic regions. The mortality trajectory was best-approximated by a Weibull model, showing clear actuarial senescence. Rates of senescence in this model declined with advancing age, but were slightly higher in mown plots and in the more benign climatic region...

Dementia-free life expectancy (demFLE) in the Netherlands

NARCIS (Netherlands)

Perenboom, R.J.M.; Boshuizen, H.C.; Breteler, M.M.B.; Alewijn, O.; Water, H.P.A. van de

1996-01-01

To gain an insight into the burden of dementia in an aging society, life expectancy with dementia and its counterpart dementia-free life expectancy (DemFLE) in The Netherlands are presented. Sullivan's method was used to calculate DemFLE. For elderly living either independently or in homes for the

Life Expectancy of Brazilian Neurosurgeons.

Science.gov (United States)

Botelho, Ricardo Vieira; Jardim Miranda, Bárbara Cristina; Nishikuni, Koshiro; Waisberg, Jaques

2018-06-01

Life expectancy (LE) refers to the number of years that an individual is expected to survive. Emphasis is frequently placed on the relationship between LE and the conditions under which a population lives, but fewer studies have investigated the relationship between stress factors associated with specific professions and their effects on LE. The aim of this study is to evaluate Brazilian neurosurgeons' life expectancies (BNLEs) and compare them with those of physicians (both Brazilian and foreign) from other fields, as well as with Brazilian nondoctors. The Brazilian Society of Neurosurgery death registry was used to obtain data that compared LEs from non-neurosurgeon physicians, as described in the national and international literature. BNLEs were also compared with the LEs of Brazilian citizens. Fifty-one neurosurgeons died between 2009 and 2016. All were males. The mean age at death was 68.31 ± 17.71 years. Among all-cause mortality, the breakdown was 20% cardiovascular diseases, 39% malignancies, 10% external factors, 6% gastrointestinal disorders, 12% neurologic illnesses, and 14% unknown causes. BNLE was shorter than LE of male Brazilian citizens. LE was similar among neurosurgeons and other doctors but shorter compared with Brazilian citizens. Further research is needed to provide data that can add to and confirm these results. Copyright © 2018 Elsevier Inc. All rights reserved.

Understanding the contribution of suicide to life expectancy in South Korea

Directory of Open Access Journals (Sweden)

Aggie Noah

2016-09-01

Full Text Available Background: South Korea has the highest rate and highest rate of increase in suicide among developed countries. The suicide epidemic in Korea is an anomaly, and suicide rates are high for both men and women, with no signs of decreasing. Yet we do not know the extent to which suicide has reduced life expectancy in Korea. Objective: We investigated whether and to what extent the rapid increase in suicide has contributed to changes in Korean life expectancy, a key indicator of population health. Methods: We used a recently developed decomposition method that separates the contribution of suicide's effect on change in life expectancy into two parts: that due to change in the overall suicide incidence rate and that due to change in the mean age of suicide victims. Results: From 1995 to 2010, life expectancy increased by 6.5 years in Korea, with change in most causes of death contributing to its growth. We nonetheless find, as expected, that the rise in suicides reduced the increase in life expectancy from 1995 to 2010, so life expectancy in Korea is about 0.21 years lower than it would have been without the increase in suicides. Moreover, had the age of suicide victims remained stable, we project that Korea's life expectancy would be fully 0.70 years lower than it is. Conclusions: Although the growth in suicide was the largest single factor slowing the rise in Korean life expectancy, the effect would have been even larger had the age of suicide victims not increased.

Cellular senescence and organismal aging.

Science.gov (United States)

Jeyapalan, Jessie C; Sedivy, John M

2008-01-01

Cellular senescence, first observed and defined using in vitro cell culture studies, is an irreversible cell cycle arrest which can be triggered by a variety of factors. Emerging evidence suggests that cellular senescence acts as an in vivo tumor suppression mechanism by limiting aberrant proliferation. It has also been postulated that cellular senescence can occur independently of cancer and contribute to the physiological processes of normal organismal aging. Recent data have demonstrated the in vivo accumulation of senescent cells with advancing age. Some characteristics of senescent cells, such as the ability to modify their extracellular environment, could play a role in aging and age-related pathology. In this review, we examine current evidence that links cellular senescence and organismal aging.

Life expectancy in elderly patients following burns injury.

Science.gov (United States)

Sepehripour, Sarvnaz; Duggineni, Sirisha; Shahsavari, Somaya; Dheansa, Baljit

2018-05-18

Burn injuries commonly occur in vulnerable age and social groups. Previous research has shown that frailty may represent a more important marker of adverse outcome in healthcare rather than chronological age (Roberts et al., 2012). In this paper we determined the relationship between burn injury, frailty, co-morbidities and long-term survival. Retrospective data collection from patients aged 75 with burns injuries, treated and discharged at Queen Victoria Hospital. The Clinical Frailty Scale (Rockwood et al., 2005) was used to calculate frailty at the time of admission. The expected mortality age (life expectancy) of deceased patients was obtained from two survival predictors. The data shows a statistically significant correlation between frailty score and complications and a statistically significant correlation between total body surface area percentage and complications. No significant difference was found between expected and observed age of death or life expectancy amongst the deceased (p value of 0.109). Based on the data from our unit, sustaining a burn as an elderly person does not reduce life expectancy. Medical and surgical complications, immediate, early and late, although higher with greater frailty and TBSA of burn, but do not adversely affect survival in this population. Copyright © 2018 Elsevier Ltd. All rights reserved.

Selective insulin resistance in hepatocyte senescence

International Nuclear Information System (INIS)

Aravinthan, Aloysious; Challis, Benjamin; Shannon, Nicholas; Hoare, Matthew; Heaney, Judith; Alexander, Graeme J.M.

2015-01-01

Insulin resistance has been described in association with chronic liver disease for decades. Hepatocyte senescence has been demonstrated in chronic liver disease and as many as 80% of hepatocytes show a senescent phenotype in advanced liver disease. The aim of this study was to understand the role of hepatocyte senescence in the development of insulin resistance. Senescence was induced in HepG2 cells via oxidative stress. The insulin metabolic pathway was studied in control and senescent cells following insulin stimulation. GLUT2 and GLUT4 expressions were studied in HepG2 cells and human liver tissue. Further, GLUT2 and GLUT4 expressions were studied in three independent chronic liver disease cohorts. Signalling impairment distal to Akt in phosphorylation of AS160 and FoxO1 was evident in senescent HepG2 cells. Persistent nuclear localisation of FoxO1 was demonstrated in senescent cells despite insulin stimulation. Increased GLUT4 and decreased GLUT2 expressions were evident in senescent cells, human cirrhotic liver tissue and publically available liver disease datasets. Changes in GLUT expressions were associated with a poor clinical prognosis. In conclusion, selective insulin resistance is evident in senescent HepG2 cells and changes in GLUT expressions can be used as surrogate markers of hepatocyte senescence. - Highlights: • Senescent hepatocytes demonstrate selective insulin resistance. • GLUT changes act as markers of hepatocyte senescence and have prognostic value. • Study offers insight into long noticed intimacy of cirrhosis and insulin resistance

Selective insulin resistance in hepatocyte senescence

Energy Technology Data Exchange (ETDEWEB)

Aravinthan, Aloysious [Division of Gastroenterology and Hepatology, Department of Medicine, University of Cambridge, Cambridge (United Kingdom); Challis, Benjamin [Institute of Metabolic Sciences, University of Cambridge, Cambridge (United Kingdom); Shannon, Nicholas [Cancer Research UK Cambridge Institute, Cambridge (United Kingdom); Hoare, Matthew [Division of Gastroenterology and Hepatology, Department of Medicine, University of Cambridge, Cambridge (United Kingdom); Cancer Research UK Cambridge Institute, Cambridge (United Kingdom); Heaney, Judith [Division of Gastroenterology and Hepatology, Department of Medicine, University of Cambridge, Cambridge (United Kingdom); Foundation for Liver Research, Institute of Hepatology, London (United Kingdom); Alexander, Graeme J.M., E-mail: gja1000@doctors.org.uk [Division of Gastroenterology and Hepatology, Department of Medicine, University of Cambridge, Cambridge (United Kingdom)

2015-02-01

Insulin resistance has been described in association with chronic liver disease for decades. Hepatocyte senescence has been demonstrated in chronic liver disease and as many as 80% of hepatocytes show a senescent phenotype in advanced liver disease. The aim of this study was to understand the role of hepatocyte senescence in the development of insulin resistance. Senescence was induced in HepG2 cells via oxidative stress. The insulin metabolic pathway was studied in control and senescent cells following insulin stimulation. GLUT2 and GLUT4 expressions were studied in HepG2 cells and human liver tissue. Further, GLUT2 and GLUT4 expressions were studied in three independent chronic liver disease cohorts. Signalling impairment distal to Akt in phosphorylation of AS160 and FoxO1 was evident in senescent HepG2 cells. Persistent nuclear localisation of FoxO1 was demonstrated in senescent cells despite insulin stimulation. Increased GLUT4 and decreased GLUT2 expressions were evident in senescent cells, human cirrhotic liver tissue and publically available liver disease datasets. Changes in GLUT expressions were associated with a poor clinical prognosis. In conclusion, selective insulin resistance is evident in senescent HepG2 cells and changes in GLUT expressions can be used as surrogate markers of hepatocyte senescence. - Highlights: • Senescent hepatocytes demonstrate selective insulin resistance. • GLUT changes act as markers of hepatocyte senescence and have prognostic value. • Study offers insight into long noticed intimacy of cirrhosis and insulin resistance.

Blocking negative effects of senescence in human skin fibroblasts with a plant extract.

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Lämmermann, Ingo; Terlecki-Zaniewicz, Lucia; Weinmüllner, Regina; Schosserer, Markus; Dellago, Hanna; de Matos Branco, André Dargen; Autheried, Dominik; Sevcnikar, Benjamin; Kleissl, Lisa; Berlin, Irina; Morizot, Frédérique; Lejeune, Francois; Fuzzati, Nicola; Forestier, Sandra; Toribio, Alix; Tromeur, Anaïs; Weinberg, Lionel; Higareda Almaraz, Juan Carlos; Scheideler, Marcel; Rietveld, Marion; El Ghalbzouri, Abdoel; Tschachler, Erwin; Gruber, Florian; Grillari, Johannes

2018-01-01

There is increasing evidence that senescent cells are a driving force behind many age-related pathologies and that their selective elimination increases the life- and healthspan of mice. Senescent cells negatively affect their surrounding tissue by losing their cell specific functionality and by secreting a pro-tumorigenic and pro-inflammatory mixture of growth hormones, chemokines, cytokines and proteases, termed the senescence-associated secretory phenotype (SASP). Here we identified an extract from the plant Solidago virgaurea subsp. alpestris , which exhibited weak senolytic activity, delayed the acquisition of a senescent phenotype and induced a papillary phenotype with improved functionality in human dermal fibroblasts. When administered to stress-induced premature senescent fibroblasts, this extract changed their global mRNA expression profile and particularly reduced the expression of various SASP components, thereby ameliorating the negative influence on nearby cells. Thus, the investigated plant extract represents a promising possibility to block age-related loss of tissue functionality.

Losing ground--Swedish life expectancy in a comparative perspective.

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Sven Drefahl

Full Text Available BACKGROUND: In the beginning of the 1970s, Sweden was the country where both women and men enjoyed the world's longest life expectancy. While life expectancy continues to be high and increasing, Sweden has been losing ground in relation to other leading countries. METHODS: We look at life expectancy over the years 1970-2008 for men and women. To assess the relative contributions of age, causes of death, and smoking we decompose differences in life expectancy between Sweden and two leading countries, Japan and France. This study is the first to use this decomposition method to observe how smoking related deaths contribute to life expectancy differences between countries. RESULTS: Sweden has maintained very low mortality at young and working ages for both men and women compared to France and Japan. However, mortality at ages above 65 has become considerably higher in Sweden than in the other leading countries because the decrease has been faster in those countries. Different trends for circulatory diseases were the largest contributor to this development in both sexes but for women also cancer played a role. Mortality from neoplasms has been considerably low for Swedish men. Smoking attributable mortality plays a modest role for women, whereas it is substantially lower in Swedish men than in French and Japanese men. CONCLUSIONS: Sweden is losing ground in relation to other leading countries with respect to life expectancy because mortality at high ages improves more slowly than in the leading countries, especially due to trends in cardiovascular disease mortality. Trends in smoking rates may provide a partial explanation for the trends in women; however, it is not possible to isolate one single explanatory factor for why Sweden is losing ground.

Growing Disparities in Life Expectancy. Economic and Budget Issue Brief

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Manchester, Joyce; Topoleski, Julie

2008-01-01

In a continuation of long-term trends, life expectancy has been steadily increasing in the United States for the past several decades. Accompanying the recent increases, however, is a growing disparity in life expectancy between individuals with high and low income and between those with more and less education. The difference in life expectancy…

Identification of senescence-associated genes in human bone marrow mesenchymal stem cells

International Nuclear Information System (INIS)

Ryu, Eunsook; Hong, Su; Kang, Jaeku; Woo, Junghoon; Park, Jungjun; Lee, Jongho; Seo, Jeong-Sun

2008-01-01

Human bone marrow mesenchymal stem cells (hBMMSCs) are multipotent stem cells that can differentiate into several specialized cell types, including bone, cartilage, and fat cells. The proliferative capacity of hBMMSCs paves the way for the development of regenerative medicine and tissue engineering. However, long-term in vitro culture of hBMMSCs leads to a reduced life span of the cells due to senescence, which leads eventually to growth arrest. To investigate the molecular mechanism behind the cellular senescence of hBMMSCs, microarray analysis was used to compare the expression profiles of early passage hBMMSCs, late passage hBMMSCs and hBMMSCs ectopically expressing human telomerase reverse transcriptase (hTERT). Using an intersection analysis of 3892 differentially expressed genes (DEGs) out of 27,171 total genes analyzed, we identified 338 senescence-related DEGs. GO term categorization and pathway network analysis revealed that the identified genes are strongly related to known senescence pathways and mechanisms. The genes identified using this approach will facilitate future studies of the mechanisms underlying the cellular senescence of hBMMSCs

Senescence induction; a possible cancer therapy

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Kondoh Hiroshi

2009-01-01

Full Text Available Abstract Cellular immortalization is a crucial step during the development of human cancer. Primary mammalian cells reach replicative exhaustion after several passages in vitro, a process called replicative senescence. During such a state of permanent growth arrest, senescent cells are refractory to physiological proliferation stimuli: they have altered cell morphology and gene expression patterns, although they remain viable with preserved metabolic activity. Interestingly, senescent cells have also been detected in vivo in human tumors, particularly in benign lesions. Senescence is a mechanism that limits cellular lifespan and constitutes a barrier against cellular immortalization. During immortalization, cells acquire genetic alterations that override senescence. Tumor suppressor genes and oncogenes are closely involved in senescence, as their knockdown and ectopic expression confer immortality and senescence induction, respectively. By using high throughput genetic screening to search for genes involved in senescence, several candidate oncogenes and putative tumor suppressor genes have been recently isolated, including subtypes of micro-RNAs. These findings offer new perspectives in the modulation of senescence and open new approaches for cancer therapy.

Status of Women in Society and Life Expectancy at Birth

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Anica Novak

2015-03-01

Full Text Available The purpose of this paper is to investigate the influence of the status of women in society over life expectancy at birth. Based on the data of some of the socio-economic variables for 187 countries worldwide, collected by the United Nations within United Nations Development Programme – Human Development Report, we developed a regression model of life expectancy factors. Through empirical testing of the three hypotheses which refer to different aspects of the status of women in society, we found that the employment ratio between women and men has a statistically significant negative impact on life expectancy at birth, which is, at least at first glance, unexpected. At the same time, the number of teenage births per 100 women aged 15–19 as well as gender inequality has a statistically significant negative impact on life expectancy at birth.

Decennial trends and inequalities in healthy life expectancy: The HUNT Study, Norway.

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Storeng, Siri H; Krokstad, Steinar; Westin, Steinar; Sund, Erik R

2018-02-01

Norway is experiencing a rising life expectancy combined with an increasing dependency ratio - the ratio of those outside over those within the working force. To provide data relevant for future health policy we wanted to study trends in total and healthy life expectancy in a Norwegian population over three decades (1980s, 1990s and 2000s), both overall and across gender and educational groups. Data were obtained from the HUNT Study, and the Norwegian Educational Database. We calculated total life expectancy and used the Sullivan method to calculate healthy life expectancies based on self-rated health and self-reported longstanding limiting illness. The change in health expectancies was decomposed into mortality and disability effects. During three consecutive decades we found an increase in life expectancy for 30-year-olds (~7 years) and expected lifetime in self-rated good health (~6 years), but time without longstanding limiting illness increased less (1.5 years). Women could expect to live longer than men, but the extra life years for females were spent in poor self-rated health and with longstanding limiting illness. Differences in total life expectancy between educational groups decreased, whereas differences in expected lifetime in self-rated good health and lifetime without longstanding limiting illness increased. The increase in total life expectancy was accompanied by an increasing number of years spent in good self-rated health but more years with longstanding limiting illness. This suggests increasing health care needs for people with chronic diseases, given an increasing number of elderly. Socioeconomic health inequalities remain a challenge for increasing pensioning age.

Older adults' beliefs about physician-estimated life expectancy: a cross-sectional survey

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Bynum Debra L

2006-02-01

Full Text Available Abstract Background Estimates of life expectancy assist physicians and patients in medical decision-making. The time-delayed benefits for many medical treatments make an older adult's life expectancy estimate particularly important for physicians. The purpose of this study is to assess older adults' beliefs about physician-estimated life expectancy. Methods We performed a mixed qualitative-quantitative cross-sectional study in which 116 healthy adults aged 70+ were recruited from two local retirement communities. We interviewed them regarding their beliefs about physician-estimated life expectancy in the context of a larger study on cancer screening beliefs. Semi-structured interviews of 80 minutes average duration were performed in private locations convenient to participants. Demographic characteristics as well as cancer screening beliefs and beliefs about life expectancy were measured. Two independent researchers reviewed the open-ended responses and recorded the most common themes. The research team resolved disagreements by consensus. Results This article reports the life-expectancy results portion of the larger study. The study group (n = 116 was comprised of healthy, well-educated older adults, with almost a third over 85 years old, and none meeting criteria for dementia. Sixty-four percent (n = 73 felt that their physicians could not correctly estimate their life expectancy. Sixty-six percent (n = 75 wanted their physicians to talk with them about their life expectancy. The themes that emerged from our study indicate that discussions of life expectancy could help older adults plan for the future, maintain open communication with their physicians, and provide them knowledge about their medical conditions. Conclusion The majority of the healthy older adults in this study were open to discussions about life expectancy in the context of discussing cancer screening tests, despite awareness that their physicians' estimates could be inaccurate

Androgen receptor drives cellular senescence.

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Yelena Mirochnik

Full Text Available The accepted androgen receptor (AR role is to promote proliferation and survival of prostate epithelium and thus prostate cancer progression. While growth-inhibitory, tumor-suppressive AR effects have also been documented, the underlying mechanisms are poorly understood. Here, we for the first time link AR anti-cancer action with cell senescence in vitro and in vivo. First, AR-driven senescence was p53-independent. Instead, AR induced p21, which subsequently reduced ΔN isoform of p63. Second, AR activation increased reactive oxygen species (ROS and thereby suppressed Rb phosphorylation. Both pathways were critical for senescence as was proven by p21 and Rb knock-down and by quenching ROS with N-Acetyl cysteine and p63 silencing also mimicked AR-induced senescence. The two pathways engaged in a cross-talk, likely via PML tumor suppressor, whose localization to senescence-associated chromatin foci was increased by AR activation. All these pathways contributed to growth arrest, which resolved in senescence due to concomitant lack of p53 and high mTOR activity. This is the first demonstration of senescence response caused by a nuclear hormone receptor.

Trends Over 4 Decades in Disability-Free Life Expectancy in the United States.

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Crimmins, Eileen M; Zhang, Yuan; Saito, Yasuhiko

2016-07-01

To examine changes over 40 years (1970-2010) in life expectancy, life expectancy with disability, and disability-free life expectancy for American men and women of all ages. We used mortality rates from US Vital Statistics and data on disability prevalence in the community-dwelling population from the National Health Interview Survey; for the institutional population, we computed disability prevalence from the US Census. We used the Sullivan method to estimate disabled and disability-free life expectancy for 1970, 1980, 1990, 2000, and 2010. Over the 40 years, there was a steady increase in both disability-free life expectancy and disabled life expectancy. At birth, increases in disabled life and nondisabled life were equal for men (4.5 years); for women, at birth the increase in life with disability (3.6 years) exceeded the increase in life free of disability (2.7 years). At age 65 years, the increase in disability-free life was greater than the increase in disabled life. Across the life cycle, there was no compression of morbidity, but at age 65 years some compression occurred.

Effects of stress management training and problem solving on quality of life and life expectancy among infertile women

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Mohammad Reza Zarbakhsh Bahri

2013-08-01

Full Text Available Introduction: This study aims to evaluate the effectiveness of stress management training and problem-solving training on quality of life and life expectancy of infertile women was conducted.Material and Methods: The method of this study was experimental with pretest – posttest design with a control group. population of 400 infertile women who referred to infertility center in Rasht were randomized to 250 of them were selected and the quality of life and life expectancy of the study were the 45 members of the quality of life and life expectancy lower were more randomly in three groups of 15 people, including two experimental groups and one control group were replaced. Each experimental groups were trained for 10 sessions of 90 minutes, respectively, stress management and problem-solving. Upon completion of the training program, participants were assessed again.Results: The result of present study showed that there was a significant difference between the experimental groups and control group in the scores of quality of life and life expectancy (p0.05.Conclusion: Stress management and problem solving training were effective on life expectancy and quality of life of infertile women but there was no significant difference between the effectiveness of these two methods on life expectancy and quality of life of infertile women.

Socio-economic determinants of life expectancy in Nigeria (1980 - 2011).

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Sede, Peter I; Ohemeng, Williams

2015-01-01

Attainment of 70 years life expectancy by 2020 is one of the millennium development goals in Nigeria. This study examined the socio-economic determinants of life expectancy in Nigeria using data from 1980-2011. Judging from the endogeneity feature of the variables, A VAR and VECM frameworks were employed. Socio-economic features were proxy by secondary school enrolment, government expenditure on health, per capita income, unemployment rate and the Naira foreign exchange rate. It was found that, the conventional socio-economic variables such as per capita income, education and government expenditure on health considered to be highly effective in determining life expectancy of developing countries are not significant in the case of Nigeria. The study however suggests that, life expectancy in Nigeria could be improved if attention is given to quality of government health expenditure, unemployment and measures to halt the depreciation of the Nigerian Naira against major foreign currency.

[Life expectancy at birth in Colombia, 2000-2009: inequalities by region and gender].

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Eslava-Schmalbach, Javier H; Rincón, Carlos Javier; Guarnizo-Herreño, Carol Cristina

2013-01-01

Life expectancy is one of the measurements that have been used to monitor socioeconomic development within and among countries. During the last 30 years, life expectancy has increased worldwide mainly due to medical and technological developments. However, access to health care, new technologies and social determinants remain unevenly distributed among regions and countries in the world. To assess inequalities in life expectancy by gender and regions (departments) in Colombia between 2000 and 2009. Ecological study. Life expectancy was estimated for each Colombian department using yearly life tables from 2000 to 2009. We used data from the death registries and the estimated population series, provided by the Departamento Administrativo Nacional de Estadística (DANE). For the study period, estimates of life expectancy by departments were compared with those from Japan for the years 2000, 2006 and 2009, which is the country with the highest life expectancy in the world, and with the Colombian department with the highest life expectancy from 2000 to 2009. Compared with the highest life expectancy in the world, Colombian departments showed differences ranged between 5.7 and 21 years. We found significant differences between departments, with the largest difference being 15.3 years. Additionally, in some departments life expectancy decreased during the analyzed period. This study identified differences in life expectancy in Colombian departments suggesting inequalities in health and living conditions among them. These differences increased in some departments during the period 2000-2009.

The Relationship between Science Indicator and Life Expectancy in Pioneer Countries

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Maryam Moghadami

2016-01-01

Full Text Available ​Background and Objectives : The main objective of this study was to investigate the relationship between scientific productivity in the field of psychiatry and life expectancy in pioneer countries. Material and Methods : A rigorous search strategy was applied on Scopus database using psychiatry terms. The search results were narrowed to 2000-2012. No language limitation was applied. Life expectancy was extracted from World Bank database using Pearson correlation. Results : The search was led to 27516 articles. The US, England and Germany were identified as leading countries in producing the psychiatry articles, respectively. Pearson correlation test results indicated that there is a direct correlation between scientific products and life expectancy index. In other words, with the increase in producing scientific articles in psychiatry field, life expectancy rises as well. Conclusion : With increase in scientific productivity, life expectancy increases and mortality rate decreases. The results of this study can serve as a guiding document in the field of health and mental health. ​

Associations between Urban Sprawl and Life Expectancy in the United States

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Shima Hamidi

2018-04-01

Full Text Available In recent years, the United States has had a relatively poor performance with respect to life expectancy compared to the other developed nations. Urban sprawl is one of the potential causes of the high rate of mortality in the United States. This study investigated cross-sectional associations between sprawl and life expectancy for metropolitan counties in the United States in 2010. In this study, the measure of life expectancy in 2010 came from a recently released dataset of life expectancies by county. This study modeled average life expectancy with a structural equation model that included five mediators: annual vehicle miles traveled (VMT per household, average body mass index, crime rate, and air quality index as mediators of sprawl, as well as percentage of smokers as a mediator of socioeconomic status. After controlling for sociodemographic characteristics, this study found that life expectancy was significantly higher in compact counties than in sprawling counties. Compactness affects mortality directly, but the causal mechanism is unclear. For example, it may be that sprawling areas have higher traffic speeds and longer emergency response times, lower quality and less accessible health care facilities, or less availability of healthy foods. Compactness affects mortality indirectly through vehicle miles traveled, which is a contributor to traffic fatalities, and through body mass index, which is a contributor to many chronic diseases. This study identified significant direct and indirect associations between urban sprawl and life expectancy. These findings support further research and practice aimed at identifying and implementing changes to urban planning designed to support health and healthy behaviors.

Associations between urban sprawl and life expectancy in the United States

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Hamidi, Shima; Ewing, Reid; Tatalovich, Zaria; Grace, James B.; Berrigan, David

2018-01-01

In recent years, the United States has had a relatively poor performance with respect to life expectancy compared to the other developed nations. Urban sprawl is one of the potential causes of the high rate of mortality in the United States. This study investigated cross-sectional associations between sprawl and life expectancy for metropolitan counties in the United States in 2010. In this study, the measure of life expectancy in 2010 came from a recently released dataset of life expectancies by county. This study modeled average life expectancy with a structural equation model that included five mediators: annual vehicle miles traveled (VMT) per household, average body mass index, crime rate, and air quality index as mediators of sprawl, as well as percentage of smokers as a mediator of socioeconomic status. After controlling for sociodemographic characteristics, this study found that life expectancy was significantly higher in compact counties than in sprawling counties. Compactness affects mortality directly, but the causal mechanism is unclear. For example, it may be that sprawling areas have higher traffic speeds and longer emergency response times, lower quality and less accessible health care facilities, or less availability of healthy foods. Compactness affects mortality indirectly through vehicle miles traveled, which is a contributor to traffic fatalities, and through body mass index, which is a contributor to many chronic diseases. This study identified significant direct and indirect associations between urban sprawl and life expectancy. These findings support further research and practice aimed at identifying and implementing changes to urban planning designed to support health and healthy behaviors.

Associations between Urban Sprawl and Life Expectancy in the United States.

Science.gov (United States)

Hamidi, Shima; Ewing, Reid; Tatalovich, Zaria; Grace, James B; Berrigan, David

2018-04-26

In recent years, the United States has had a relatively poor performance with respect to life expectancy compared to the other developed nations. Urban sprawl is one of the potential causes of the high rate of mortality in the United States. This study investigated cross-sectional associations between sprawl and life expectancy for metropolitan counties in the United States in 2010. In this study, the measure of life expectancy in 2010 came from a recently released dataset of life expectancies by county. This study modeled average life expectancy with a structural equation model that included five mediators: annual vehicle miles traveled (VMT) per household, average body mass index, crime rate, and air quality index as mediators of sprawl, as well as percentage of smokers as a mediator of socioeconomic status. After controlling for sociodemographic characteristics, this study found that life expectancy was significantly higher in compact counties than in sprawling counties. Compactness affects mortality directly, but the causal mechanism is unclear. For example, it may be that sprawling areas have higher traffic speeds and longer emergency response times, lower quality and less accessible health care facilities, or less availability of healthy foods. Compactness affects mortality indirectly through vehicle miles traveled, which is a contributor to traffic fatalities, and through body mass index, which is a contributor to many chronic diseases. This study identified significant direct and indirect associations between urban sprawl and life expectancy. These findings support further research and practice aimed at identifying and implementing changes to urban planning designed to support health and healthy behaviors.

The Association Between Income and Life Expectancy in the United States, 2001-2014.

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Chetty, Raj; Stepner, Michael; Abraham, Sarah; Lin, Shelby; Scuderi, Benjamin; Turner, Nicholas; Bergeron, Augustin; Cutler, David

2016-04-26

The relationship between income and life expectancy is well established but remains poorly understood. To measure the level, time trend, and geographic variability in the association between income and life expectancy and to identify factors related to small area variation. Income data for the US population were obtained from 1.4 billion deidentified tax records between 1999 and 2014. Mortality data were obtained from Social Security Administration death records. These data were used to estimate race- and ethnicity-adjusted life expectancy at 40 years of age by household income percentile, sex, and geographic area, and to evaluate factors associated with differences in life expectancy. Pretax household earnings as a measure of income. Relationship between income and life expectancy; trends in life expectancy by income group; geographic variation in life expectancy levels and trends by income group; and factors associated with differences in life expectancy across areas. The sample consisted of 1,408,287,218 person-year observations for individuals aged 40 to 76 years (mean age, 53.0 years; median household earnings among working individuals, $61,175 per year). There were 4,114,380 deaths among men (mortality rate, 596.3 per 100,000) and 2,694,808 deaths among women (mortality rate, 375.1 per 100,000). The analysis yielded 4 results. First, higher income was associated with greater longevity throughout the income distribution. The gap in life expectancy between the richest 1% and poorest 1% of individuals was 14.6 years (95% CI, 14.4 to 14.8 years) for men and 10.1 years (95% CI, 9.9 to 10.3 years) for women. Second, inequality in life expectancy increased over time. Between 2001 and 2014, life expectancy increased by 2.34 years for men and 2.91 years for women in the top 5% of the income distribution, but by only 0.32 years for men and 0.04 years for women in the bottom 5% (P income individuals varied substantially across local areas. In the bottom income

Plant senescence and crop productivity

DEFF Research Database (Denmark)

Gregersen, Per L.; Culetic, Andrea; Boschian, Luca

2013-01-01

Senescence is a developmental process which in annual crop plants overlaps with the reproductive phase. Senescence might reduce crop yield when it is induced prematurely under adverse environmental conditions. This review covers the role of senescence for the productivity of crop plants....... With the aim to enhance productivity, a number of functional stay-green cultivars have been selected by conventional breeding, in particular of sorghum and maize. In many cases, a positive correlation between leaf area duration and yield has been observed, although in a number of other cases, stay...... plants, the expression of the IPT gene under control of senescence-associated promoters has been the most successful. The promoters employed for senescence-regulated expression contain cis-elements for binding of WRKY transcription factors and factors controlled by abscisic acid. In most crops...

Chemical Composition of Fine Particulate Matter and Life Expectancy

Science.gov (United States)

Dominici, Francesca; Wang, Yun; Correia, Andrew W.; Ezzati, Majid; Pope, C. Arden; Dockery, Douglas W.

2016-01-01

Background In a previous study, we provided evidence that a decline in fine particulate matter (PM2.5) air pollution during the period between 2000 and 2007 was associated with increased life expectancy in 545 counties in the United States. In this article, we investigated which chemical constituents of PM2.5 were the main drivers of the observed association. Methods We estimated associations between temporal changes in seven major components of PM2.5 (ammonium, sulfate, nitrate, elemental carbon matter, organic carbon matter, sodium, and silicon) and temporal changes in life expectancy in 95 counties between 2002 and 2007. We included US counties that had adequate chemical components of PM2.5 mass data across all seasons. We fitted single pollutant and multiple pollutant linear models, controlling for available socioeconomic, demographic, and smoking variables and stratifying by urban and nonurban counties. Results In multiple pollutant models, we found that: (1) a reduction in sulfate was associated with an increase in life expectancy; and (2) reductions in ammonium and sodium ion were associated with increases in life expectancy in nonurban counties only. Conclusions Our findings suggest that recent reductions in long-term exposure to sulfate, ammonium, and sodium ion between 2002 and 2007 are associated with improved public health. PMID:25906366

Rise, stagnation, and rise of Danish women's life expectancy

DEFF Research Database (Denmark)

Lindahl-Jacobsen, Rune; Rau, Roland; Jeune, Bernard

2016-01-01

Health conditions change from year to year, with a general tendency in many countries for improvement. These conditions also change from one birth cohort to another: some generations suffer more adverse events in childhood, smoke more heavily, eat poorer diets, etc., than generations born earlier...... favor forecasts that hinge on cohort differences. We use a combination of age decomposition and exchange of survival probabilities between countries to study the remarkable recent history of female life expectancy in Denmark, a saga of rising, stagnating, and now again rising lifespans. The gap between...... female life expectancy in Denmark vs. Sweden grew to 3.5 y in the period 1975-2000. When we assumed that Danish women born 1915-1945 had the same survival probabilities as Swedish women, the gap remained small and roughly constant. Hence, the lower Danish life expectancy is caused by these cohorts...

Causes of decreased life expectancy over the life span in bipolar disorder.

Science.gov (United States)

Kessing, Lars Vedel; Vradi, Eleni; McIntyre, Roger S; Andersen, Per Kragh

2015-07-15

Accelerated aging has been proposed as a mechanism explaining the increased prevalence of comorbid general medical illnesses in bipolar disorder. To test the hypothesis that lost life years due to natural causes starts in early and mid-adulthood, supporting the hypothesis of accelerated aging. Using individual data from nationwide registers of patient with a diagnosis of bipolar disorder we calculated remaining life expectancies before age 90 years for values of age 15, 25, 35…75 years among all individuals alive in year 2000. Further, we estimated the reduction in life expectancy due to natural causes (physical illnesses) and unnatural causes (suicide and accidents) in relation to age. A total of 22,635 patients with bipolar disorder were included in the study in addition to data from the entire Danish general population of 5.4 million people. At age 15 years, remaining life expectancy before age 90 years was decreased 12.7 and 8.9 life years, respectively, for men and women with bipolar disorder. For 15-year old boys with bipolar disorder, natural causes accounted for 58% of all lost life years and for 15-year old girls, natural causes accounted for 67% increasing to 74% and 80% for 45-year old men and women, respectively. Data concern patients who get contact to hospital psychiatry only. Natural causes of death is the most prevalent reason for lost life years already from adolescence and increases substantially during early and mid-adulthood, in this way supporting the hypothesis of accelerated aging. Early intervention in bipolar disorder should not only focus on improving outcome of the bipolar disorder but also on decreasing the risk of comorbid general medical illnesses. Copyright © 2015 Elsevier B.V. All rights reserved.

Trends in life expectancy by education in Norway 1961-2009.

Science.gov (United States)

Steingrímsdóttir, Olöf Anna; Næss, Øyvind; Moe, Joakim Oliu; Grøholt, Else-Karin; Thelle, Dag Steinar; Strand, Bjørn Heine; Bævre, Kåre

2012-03-01

Educational attainment and longevity are strongly related. Large population studies covering long periods to provide evidence of trends in educational inequalities regarding life expectancy are scarce though, especially prior to the 1980s. Our objective was to document changes in life expectancy by education in Norway in the period 1961-2009, and to determine whether the patterns differ between sexes. This is a register-based population study of all Norwegian residents over 34 years, with data from the National Central Population Registry and the National Education Database. For each calendar year during 1961-2009, death rates by 1 year age groups were calculated separately for each sex and three educational categories (primary, secondary and tertiary). Annual life tables were used to calculate life expectancy at age 35 (e ( 35 )) and survival probability for the three age-intervals 35-44, 45-64, and 65-90. All education groups increased their e ( 35 ) over time, but inequalities in e ( 35 ) between tertiary and primary educational categories widened 5.3 years for men and 3.2 years for women during the study period. The probability for women with primary education to survive to age 64 did not improve from 1961 to 2009. The gain in life expectancy lagged about 10 years in lower compared to higher education groups which might suggest that improvements in life sustaining factors reach different segments of the population at different times. The widening of the gap seems to have partly tapered off over the last two decades, and the changes in life expectancy should be followed carefully in the future to document the development.

Estimating increment-decrement life tables with multiple covariates from panel data: the case of active life expectancy.

Science.gov (United States)

Land, K C; Guralnik, J M; Blazer, D G

1994-05-01

A fundamental limitation of current multistate life table methodology-evident in recent estimates of active life expectancy for the elderly-is the inability to estimate tables from data on small longitudinal panels in the presence of multiple covariates (such as sex, race, and socioeconomic status). This paper presents an approach to such an estimation based on an isomorphism between the structure of the stochastic model underlying a conventional specification of the increment-decrement life table and that of Markov panel regression models for simple state spaces. We argue that Markov panel regression procedures can be used to provide smoothed or graduated group-specific estimates of transition probabilities that are more stable across short age intervals than those computed directly from sample data. We then join these estimates with increment-decrement life table methods to compute group-specific total, active, and dependent life expectancy estimates. To illustrate the methods, we describe an empirical application to the estimation of such life expectancies specific to sex, race, and education (years of school completed) for a longitudinal panel of elderly persons. We find that education extends both total life expectancy and active life expectancy. Education thus may serve as a powerful social protective mechanism delaying the onset of health problems at older ages.

Biomarkers of replicative senescence revisited

DEFF Research Database (Denmark)

Nehlin, Jan

2016-01-01

Biomarkers of replicative senescence can be defined as those ultrastructural and physiological variations as well as molecules whose changes in expression, activity or function correlate with aging, as a result of the gradual exhaustion of replicative potential and a state of permanent cell cycle...... arrest. The biomarkers that characterize the path to an irreversible state of cell cycle arrest due to proliferative exhaustion may also be shared by other forms of senescence-inducing mechanisms. Validation of senescence markers is crucial in circumstances where quiescence or temporary growth arrest may...... be triggered or is thought to be induced. Pre-senescence biomarkers are also important to consider as their presence indicate that induction of aging processes is taking place. The bona fide pathway leading to replicative senescence that has been extensively characterized is a consequence of gradual reduction...

Lipid profiling demonstrates that suppressing Arabidopsis phospholipase Dδ retards ABA-promoted leaf senescence by attenuating lipid degradation.

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Yanxia Jia

Full Text Available Senescence is the last phase of the plant life cycle and has an important role in plant development. Degradation of membrane lipids is an essential process during leaf senescence. Several studies have reported fundamental changes in membrane lipids and phospholipase D (PLD activity as leaves senesce. Suppression of phospholipase Dα1 (PLDα1 retards abscisic acid (ABA-promoted senescence. However, given the absence of studies that have profiled changes in the compositions of membrane lipid molecules during leaf senescence, there is no direct evidence that PLD affects lipid composition during the process. Here, we show that application of n-butanol, an inhibitor of PLD, and N-Acylethanolamine (NAE 12∶0, a specific inhibitor of PLDα1, retarded ABA-promoted senescence to different extents. Furthermore, phospholipase Dδ (PLDδ was induced in leaves treated with ABA, and suppression of PLDδ retarded ABA-promoted senescence in Arabidopsis. Lipid profiling revealed that detachment-induced senescence had different effects on plastidic and extraplastidic lipids. The accelerated degradation of plastidic lipids during ABA-induced senescence in wild-type plants was attenuated in PLDδ-knockout (PLDδ-KO plants. Dramatic increases in phosphatidic acid (PA and decreases in phosphatidylcholine (PC during ABA-induced senescence were also suppressed in PLDδ-KO plants. Our results suggest that PLDδ-mediated hydrolysis of PC to PA plays a positive role in ABA-promoted senescence. The attenuation of PA formation resulting from suppression of PLDδ blocks the degradation of membrane lipids, which retards ABA-promoted senescence.

Transcriptional analyses of natural leaf senescence in maize.

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Wei Yang Zhang

Full Text Available Leaf senescence is an important biological process that contributes to grain yield in crops. To study the molecular mechanisms underlying natural leaf senescence, we harvested three different developmental ear leaves of maize, mature leaves (ML, early senescent leaves (ESL, and later senescent leaves (LSL, and analyzed transcriptional changes using RNA-sequencing. Three sets of data, ESL vs. ML, LSL vs. ML, and LSL vs. ESL, were compared, respectively. In total, 4,552 genes were identified as differentially expressed. Functional classification placed these genes into 18 categories including protein metabolism, transporters, and signal transduction. At the early stage of leaf senescence, genes involved in aromatic amino acids (AAAs biosynthetic process and transport, cellular polysaccharide biosynthetic process, and the cell wall macromolecule catabolic process, were up-regulated. Whereas, genes involved in amino acid metabolism, transport, apoptosis, and response to stimulus were up-regulated at the late stage of leaf senescence. Further analyses reveals that the transport-related genes at the early stage of leaf senescence potentially take part in enzyme and amino acid transport and the genes upregulated at the late stage are involved in sugar transport, indicating nutrient recycling mainly takes place at the late stage of leaf senescence. Comparison between the data of natural leaf senescence in this study and previously reported data for Arabidopsis implies that the mechanisms of leaf senescence in maize are basically similar to those in Arabidopsis. A comparison of natural and induced leaf senescence in maize was performed. Athough many basic biological processes involved in senescence occur in both types of leaf senescence, 78.07% of differentially expressed genes in natural leaf senescence were not identifiable in induced leaf senescence, suggesting that differences in gene regulatory network may exist between these two leaf senescence

Arts and ageing; life expectancy of historical artists in the Low Countries.

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Fereshta Mirzada

Full Text Available Practising arts has been linked to lowering stress, anxiety and blood pressure. These mechanisms are all known to affect the ageing process. Therefore, we examine the relation between long-term involvement in arts and life expectancy at age 50 (LE50, in a cohort of 12,159 male acoustic, literary and visual artists, who were born between 1700 and 1899 in the Low Countries. We compared the life expectancy at age 50 of the various artists with the elite and middle class of that time. In the birth cohorts before 1850, acoustic (LE50:14.5-19.5 and literary artists (LE50:17.8-20.8 had a similar life expectancy at age 50 compared to the elite (LE50:18.0-19.0. Only visual artists (LE50:15.5-17.1 had a lower life expectancy at age 50 compared to the elite at that time. For the most recent birth cohorts from 1850 through 1899, the comparison between artists and the elite reversed and acoustic and literary artist had a lower life expectancy at age 50, while visual artists enjoyed a similar life expectancy at age 50. Although artists belonged to the middle socioeconomic class and lived predominantly in urban areas with poor living conditions, they had a life expectancy similar to the elite population. This is in line with observed favourable effects of practicing arts on health in the short-term. From our historical analysis, we hypothesize several mechanisms through which artistic creativity could influence the ageing process and life expectancy. These hypotheses, however, should be formally tested before any definite conclusions on effects of arts on ageing can be drawn.

Regional patterns of disability-free life expectancy and disability-adjusted life expectancy: global Burden of Disease Study.

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Murray, C J; Lopez, A D

1997-05-10

Information on non-fatal health outcomes of disease and injury has been largely neglected in health planning because of the conceptual and definitional complexity of measuring morbidity and disability in populations. One of our major objectives was to quantify disability for inclusion in health policy debates. We analysed these health outcomes in terms of disability-free life expectancy (DFLE) and disability-adjusted life expectancy (DALE). Published and unpublished data were systematically reviewed to estimate the incidence, prevalence, and duration of 483 disabling sequelae of 107 diseases and injuries. To ensure internal consistency of these estimates, a software programme (DISMOD) was applied many times until consistent parameters were identified. The severity of disability, on a scale of 0 (perfect health) to 1 (death), was measured in a deliberate manner by the person-trade-off method. Spearman's and Pearson's correlation coefficients were used to measure disability weights among groups. Prevalence of seven classes of disability was back-calculated from the distribution of each disabling sequela across disabilities. Prevalence for each class of disability for different age-sex groups was used to calculate seven forms of DFLE and DALE based on Sullivan's method. Prevalence of most disability classes is highest in sub-Saharan Africa and lowest in established market economies. Low-severity disabilities (class I and class II) are the most common. The expectation at birth of class I disability ranges from 6.5 years in established market economies to 14.7 years in sub-Saharan Africa, and for class II disabilities, from 8.5-18.4 years. DFLE varies significantly among regions: DFLE for class I disabilities at birth ranges from 9.9 years in sub-Saharan Africa to 47.7 years in established market economies for females and DFLE for class V disabilities ranges from 43.4 years for men in sub-Saharan Africa to 74.8 years for women in established market economies. The

Increasing life expectancy and the growing elderly population

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Helge Brunborg

2012-11-01

Full Text Available The life expectancy has increased rapidly in Norway in recent decades, with about ¼ year per year. The increase has been particularly fast for men, following a temporary decline in the 1950s and 1960s. Statistics Norway’s mortality projections using the Lee-Carter method indicate further improvements in this century – about 10 years higher life expectancy at birth. This implies significant mortality declines for older persons as the mortality is now small for young people. With no deaths below age 50 the life expectancy would be only 1-2 years higher.Population projections are for several reasons important for studying population ageing, including to have knowledge about the future age structure, and to estimate the effects of possible policy changes. In addition, the mortality projections are used for several other purposes than for projecting the population, such as calculating future pensions according to the new pension system, where life expectancy improvements reduce the annual pensions.The population projections show that the population will age regardless of plausible assumptions made about the demographic components births, deaths, immigration and emigration. Policies to affect these components may only marginally affect future ageing, and in some cases in the wrong direction. The only factor that may significantly affect the future ratio of the working to the non-working population, the potential support ratio, is that people work longer. This ratio will remain at the current level if the pension age is increased from the current 67 years to 78 years at the end of the century. This may be possible if the health of old persons continues to improve.

Trends in Disability-Free Life Expectancy in Japan, 1995–2004

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Hashimoto, Shuji; Kawado, Miyuki; Seko, Rumi; Murakami, Yoshitaka; Hayashi, Masayuki; Kato, Masahiro; Noda, Tatsuya; Ojima, Toshiyuki; Nagai, Masato; Tsuji, Ichiro

2010-01-01

Background In Japan, life expectancy at birth is currently the highest in the world. However, recent trends in disability-free life expectancy in Japan have not been examined. Methods We used data from Japanese national surveys for the period 1995–2004. These surveys included information on activity status measured by common self-reported instruments. The numbers of expected years with and without activity limitation were estimated by using the Sullivan method. Results The numbers of expected...

Potential Gains in Reproductive-Aged Life Expectancy by Eliminating Maternal Mortality

DEFF Research Database (Denmark)

Canudas-Romo, Vladimir; Liu, L; Zimmerman, L

2014-01-01

Objective: We assessed the change over time in the contribution of maternal mortality to a life expectancy calculated between ages 15 and 49, or Reproductive-Aged Life Expectancy (RALE). Our goal was to estimate the increase in RALE in developed countries over the twentieth century and the hypoth......Objective: We assessed the change over time in the contribution of maternal mortality to a life expectancy calculated between ages 15 and 49, or Reproductive-Aged Life Expectancy (RALE). Our goal was to estimate the increase in RALE in developed countries over the twentieth century....... Findings: In developed countries, five years in RALE were gained over the twentieth century, of which approximately 10%, or half a year, was attributable to reductions in maternal mortality. In sub-Saharan African countries, the possible achievable gains fluctuate between 0.24 and 1.47 years, or 6% and 44...

[The impact of hypertension on active life expectancy among senior citizens of Beijing].

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Zhang, Zhong-ying; Tang, Zhe; Feng, Ming

2010-07-01

The aim of the study is to explore the influence of hypertension on life expectancy (LE), active life expectancy (ALE) and active life expectancy/life expectancy (ALE/LE) among senior citizens in Beijin. The sample derived from Beijing multidimensional longitudinal study on aging, baseline survey consisted of 1847 elderly people aged 60 years and over dwelling in the communities from one urban district (Xuanwu), one suburban country (Daxing) and one mountainous country (Huairou) in Beijing, 2004. Cluster, stratified and randomly selected sampling technique was used and a follow-up program was carried out in 2007. The subjects were invited to fill in questionnaires at home through well-trained interviewers, together with medical history of hypertension and repeated blood pressure measurements adopted. The state of activity was defined according to whether they could perform activities of daily life (ADL). IMaCH software for multi-state life table method was used to calculate the life expectancy (LE), active life expectancy (ALE) and active life expectancy/life expectancy (ALE/LE) in people with hypertension and normal blood tension, as well as on those people with hypertension with or without cardio-cerebral disease. The study manifested that hypertensives were associated with the reduction of LE, ALE and ALE/LE compared to the normotensives. The ALE/LE was descending along with ageing, and the speed of reduction was much faster in the hypertensive group, especially within senile population. LE, ALE and LE/LE among the hypertensives with cardio-cerebral vascular diseases were shorter than the hypertensives without the disease. Difference in ALE/LE was striking in people with virile senility. Hypertension remarkably impacted the active life expectancy on senior citizens living in Beijing, especially for elderly. Hypertensives with cardio-cerebral vascular diseases exerted further influence on active life expectancy, particularly among population of virile senility

Transgenic plants with altered senescence characteristics

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Amasino, Richard M.; Gan, Susheng; Noh, Yoo-Sun

2002-03-19

The identification of senescence-specific promoters from plants is described. Using information from the first senescence-specific promoter, SAG12 from Arabidopsis, other homologous promoters from another plant have been identified. Such promoters may be used to delay senescence in commercially important plants.

A Petunia Homeodomain-Leucine Zipper Protein, PhHD-Zip, Plays an Important Role in Flower Senescence

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Chang, Xiaoxiao; Donnelly, Linda; Sun, Daoyang; Rao, Jingping; Reid, Michael S.; Jiang, Cai-Zhong

2014-01-01

Flower senescence is initiated by developmental and environmental signals, and regulated by gene transcription. A homeodomain-leucine zipper transcription factor, PhHD-Zip, is up-regulated during petunia flower senescence. Virus-induced gene silencing of PhHD-Zip extended flower life by 20% both in unpollinated and pollinated flowers. Silencing PhHD-Zip also dramatically reduced ethylene production and the abundance of transcripts of genes involved in ethylene (ACS, ACO), and ABA (NCED) biosynthesis. Abundance of transcripts of senescence-related genes (SAG12, SAG29) was also dramatically reduced in the silenced flowers. Over-expression of PhHD-Zip accelerated petunia flower senescence. Furthermore, PhHD-Zip transcript abundance in petunia flowers was increased by application of hormones (ethylene, ABA) and abiotic stresses (dehydration, NaCl and cold). Our results suggest that PhHD-Zip plays an important role in regulating petunia flower senescence. PMID:24551088

A Petunia homeodomain-leucine zipper protein, PhHD-Zip, plays an important role in flower senescence.

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Chang, Xiaoxiao; Donnelly, Linda; Sun, Daoyang; Rao, Jingping; Reid, Michael S; Jiang, Cai-Zhong

2014-01-01

Flower senescence is initiated by developmental and environmental signals, and regulated by gene transcription. A homeodomain-leucine zipper transcription factor, PhHD-Zip, is up-regulated during petunia flower senescence. Virus-induced gene silencing of PhHD-Zip extended flower life by 20% both in unpollinated and pollinated flowers. Silencing PhHD-Zip also dramatically reduced ethylene production and the abundance of transcripts of genes involved in ethylene (ACS, ACO), and ABA (NCED) biosynthesis. Abundance of transcripts of senescence-related genes (SAG12, SAG29) was also dramatically reduced in the silenced flowers. Over-expression of PhHD-Zip accelerated petunia flower senescence. Furthermore, PhHD-Zip transcript abundance in petunia flowers was increased by application of hormones (ethylene, ABA) and abiotic stresses (dehydration, NaCl and cold). Our results suggest that PhHD-Zip plays an important role in regulating petunia flower senescence.

A Petunia homeodomain-leucine zipper protein, PhHD-Zip, plays an important role in flower senescence.

Directory of Open Access Journals (Sweden)

Xiaoxiao Chang

Full Text Available Flower senescence is initiated by developmental and environmental signals, and regulated by gene transcription. A homeodomain-leucine zipper transcription factor, PhHD-Zip, is up-regulated during petunia flower senescence. Virus-induced gene silencing of PhHD-Zip extended flower life by 20% both in unpollinated and pollinated flowers. Silencing PhHD-Zip also dramatically reduced ethylene production and the abundance of transcripts of genes involved in ethylene (ACS, ACO, and ABA (NCED biosynthesis. Abundance of transcripts of senescence-related genes (SAG12, SAG29 was also dramatically reduced in the silenced flowers. Over-expression of PhHD-Zip accelerated petunia flower senescence. Furthermore, PhHD-Zip transcript abundance in petunia flowers was increased by application of hormones (ethylene, ABA and abiotic stresses (dehydration, NaCl and cold. Our results suggest that PhHD-Zip plays an important role in regulating petunia flower senescence.

Swedish medical students' expectations of their future life

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Andersson, Jenny; Johansson, Eva E.; Verdonk, Petra; Lagro-Janssen, Antoine; Hamberg, Katarina

2011-01-01

Objectives: To investigate future life expectations among male and female medical students in their first and final year. Methods The study was cross-sectional and conducted at a Swedish medical school. Out of 600 invited students, 507 (85%) answered an open-ended question about their future life, 298 (59%) first-year students and 209 (41%) last-year students. Women constituted 60% of the respondents. A mixed model design was applied; qualitative content analysis was utilized to create statistically comparable themes and categories. Results Students’ written answers were coded, categorized and clustered into four themes: “Work”, “Family”, “Leisure” and “Quality of personal life”. Almost all students included aspects of work in their answers. Female students were more detailed than male ones in their family concerns. Almost a third of all students reflected on a future work-life balance, but considerations regarding quality of personal life and leisure were more common among last-year students. Conclusions Today’s medical students expect more of life than work, especially those standing on the doorstep of working life. They intend to balance work not only with a family but also with leisure activities. Our results reflect work attitudes that challenge the health care system for more adaptive working conditions. We suggest that discussions about work-life balance should be included in medical curricula.

Treating Chronically Ill Diabetic Patients with Limited Life Expectancy: Implications for Performance Measurement

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Woodard, LeChauncy D.; Landrum, Cassie R.; Urech, Tracy H.; Profit, Jochen; Virani, Salim S.; Petersen, Laura A.

2012-01-01

Background/Objectives To validly assess quality-of-care differences among providers, performance measurement programs must reliably identify and exclude patients for whom the quality indicator may not be desirable, including those with limited life expectancy. We developed an algorithm to identify patients with limited life expectancy and examined the impact of limited life expectancy on glycemic control and treatment intensification among diabetic patients. Design We identified diabetic patients with coexisting congestive heart failure, chronic obstructive pulmonary disease, dementia, end-stage liver disease, and/or primary/metastatic cancers with limited life expectancy. To validate our algorithm, we assessed 5-year mortality among patients identified as having limited life expectancy. We compared rates of meeting performance measures for glycemic control between patients with and without limited life expectancy. Among uncontrolled patients, we examined the impact of limited life expectancy on treatment intensification within 90 days. Setting 110 Veterans Administration facilities; October 2006 – September 2007 Participants 888,628 diabetic patients Measurements Hemoglobin A1c (HbA1c) Quality measurement and performance-based reimbursement systems should acknowledge the different needs of this population. PMID:22260627

Causes of decreased life expectancy over the life span in bipolar disorder

DEFF Research Database (Denmark)

Kessing, Lars Vedel; Vradi, Eleni; McIntyre, Roger S

2015-01-01

BACKGROUND: Accelerated aging has been proposed as a mechanism explaining the increased prevalence of comorbid general medical illnesses in bipolar disorder. AIMS: To test the hypothesis that lost life years due to natural causes starts in early and mid-adulthood, supporting the hypothesis...... of accelerated aging. METHODS: Using individual data from nationwide registers of patient with a diagnosis of bipolar disorder we calculated remaining life expectancies before age 90 years for values of age 15, 25, 35…75 years among all individuals alive in year 2000. Further, we estimated the reduction in life...... expectancy due to natural causes (physical illnesses) and unnatural causes (suicide and accidents) in relation to age. RESULTS: A total of 22,635 patients with bipolar disorder were included in the study in addition to data from the entire Danish general population of 5.4 million people. At age 15 years...

Estimated life expectancy in a Scottish cohort with type 1 diabetes, 2008-2010.

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Livingstone, Shona J; Levin, Daniel; Looker, Helen C; Lindsay, Robert S; Wild, Sarah H; Joss, Nicola; Leese, Graham; Leslie, Peter; McCrimmon, Rory J; Metcalfe, Wendy; McKnight, John A; Morris, Andrew D; Pearson, Donald W M; Petrie, John R; Philip, Sam; Sattar, Naveed A; Traynor, Jamie P; Colhoun, Helen M

2015-01-06

Type 1 diabetes has historically been associated with a significant reduction in life expectancy. Major advances in treatment of type 1 diabetes have occurred in the past 3 decades. Contemporary estimates of the effect of type 1 diabetes on life expectancy are needed. To examine current life expectancy in people with and without type 1 diabetes in Scotland. We also examined whether any loss of life expectancy in patients with type 1 diabetes is confined to those who develop kidney disease. Prospective cohort of all individuals alive in Scotland with type 1 diabetes who were aged 20 years or older from 2008 through 2010 and were in a nationwide register (n=24,691 contributing 67,712 person-years and 1043 deaths). Differences in life expectancy between those with and those without type 1 diabetes and the percentage of the difference due to various causes. Life expectancy at an attained age of 20 years was an additional 46.2 years among men with type 1 diabetes and 57.3 years among men without it, an estimated loss in life expectancy with diabetes of 11.1 years (95% CI, 10.1-12.1). Life expectancy from age 20 years was an additional 48.1 years among women with type 1 diabetes and 61.0 years among women without it, an estimated loss with diabetes of 12.9 years (95% CI, 11.7-14.1). Even among those with type 1 diabetes with an estimated glomerular filtration rate of 90 mL/min/1.73 m2 or higher, life expectancy was reduced (49.0 years in men, 53.1 years in women) giving an estimated loss from age 20 years of 8.3 years (95% CI, 6.5-10.1) for men and 7.9 years (95% CI, 5.5-10.3) for women. Overall, the largest percentage of the estimated loss in life expectancy was related to ischemic heart disease (36% in men, 31% in women) but death from diabetic coma or ketoacidosis was associated with the largest percentage of the estimated loss occurring before age 50 years (29.4% in men, 21.7% in women). Estimated life expectancy for patients with type 1 diabetes in Scotland based on

Quantitative identification of senescent cells in aging and disease.

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Biran, Anat; Zada, Lior; Abou Karam, Paula; Vadai, Ezra; Roitman, Lior; Ovadya, Yossi; Porat, Ziv; Krizhanovsky, Valery

2017-08-01

Senescent cells are present in premalignant lesions and sites of tissue damage and accumulate in tissues with age. In vivo identification, quantification and characterization of senescent cells are challenging tasks that limit our understanding of the role of senescent cells in diseases and aging. Here, we present a new way to precisely quantify and identify senescent cells in tissues on a single-cell basis. The method combines a senescence-associated beta-galactosidase assay with staining of molecular markers for cellular senescence and of cellular identity. By utilizing technology that combines flow cytometry with high-content image analysis, we were able to quantify senescent cells in tumors, fibrotic tissues, and tissues of aged mice. Our approach also yielded the finding that senescent cells in tissues of aged mice are larger than nonsenescent cells. Thus, this method provides a basis for quantitative assessment of senescent cells and it offers proof of principle for combination of different markers of senescence. It paves the way for screening of senescent cells for identification of new senescence biomarkers, genes that bypass senescence or senolytic compounds that eliminate senescent cells, thus enabling a deeper understanding of the senescent state in vivo. © 2017 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Potential years lost and life expectancy in adults with newly diagnosed epilepsy.

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Granbichler, Claudia A; Zimmermann, Georg; Oberaigner, Willi; Kuchukhidze, Giorgi; Ndayisaba, Jean-Pierre; Taylor, Alexandra; Luef, Gerhard; Bathke, Arne C; Trinka, Eugen

2017-11-01

Studies using relative measures, such as standardized mortality ratios, have shown that patients with epilepsy have an increased mortality. Reports on more direct and absolute measure such as life expectancy are sparse. We report potential years lost and how life expectancy has changed over 40 years in a cohort of patients with newly diagnosed epilepsy. We analyzed life expectancy in a cohort of adult patients diagnosed with definite epilepsy between 1970 and 2010. Those with brain tumor as cause of epilepsy were excluded. By retrospective probabilistic record linkage, living or death status was derived from the national death registry. We estimated life expectancy by a Weibull regression model using gender, age at diagnosis, epilepsy etiology, and year of diagnosis as covariates at time of epilepsy diagnosis, and 5, 10, 15, and 20 years after diagnosis. Results were compared to the general population, and 95% confidence intervals are given. There were 249 deaths (105 women, age at death 19.0-104.0 years) in 1,112 patients (11,978.4 person-years, 474 women, 638 men). A substantial decrease in life expectancy was observed for only a few subgroups, strongly depending on epilepsy etiology and time of diagnosis: time of life lost was highest in patients with symptomatic epilepsy diagnosed between 1970 and 1980; the impact declined with increasing time from diagnosis. Over half of the analyzed subgroups did not differ significantly from the general population. This effect was reversed in the later decades, and life expectancy was prolonged in some subgroups, reaching a maximum in those with newly diagnosed idiopathic and cryptogenic epilepsy between 2001 and 2010. Life expectancy is reduced in symptomatic epilepsies. However, in other subgroups, a prolonged life expectancy was found, which has not been reported previously. Reasons may be manifold and call for further study. © 2017 The Authors. Epilepsia published by Wiley Periodicals, Inc. on behalf of International

Delayed animal aging through the recovery of stem cell senescence by platelet rich plasma.

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Liu, Hen-Yu; Huang, Chiung-Fang; Lin, Tzu-Chieh; Tsai, Ching-Yu; Tina Chen, Szu-Yu; Liu, Alice; Chen, Wei-Hong; Wei, Hong-Jian; Wang, Ming-Fu; Williams, David F; Deng, Win-Ping

2014-12-01

Aging is related to loss of functional stem cell accompanying loss of tissue and organ regeneration potentials. Previously, we demonstrated that the life span of ovariectomy-senescence accelerated mice (OVX-SAMP8) was significantly prolonged and similar to that of the congenic senescence-resistant strain of mice after platelet rich plasma (PRP)/embryonic fibroblast transplantation. The aim of this study is to investigate the potential of PRP for recovering cellular potential from senescence and then delaying animal aging. We first examined whether stem cells would be senescent in aged mice compared to young mice. Primary adipose derived stem cells (ADSCs) and bone marrow derived stem cells (BMSCs) were harvested from young and aged mice, and found that cell senescence was strongly correlated to animal aging. Subsequently, we demonstrated that PRP could recover cell potential from senescence, such as promote cell growth (cell proliferation and colony formation), increase osteogenesis, decrease adipogenesis, restore cell senescence related markers and resist the oxidative stress in stem cells from aged mice. The results also showed that PRP treatment in aged mice could delay mice aging as indicated by survival, body weight and aging phenotypes (behavior and gross morphology) in term of recovering the cellular potential of their stem cells compared to the results on aged control mice. In conclusion these findings showed that PRP has potential to delay aging through the recovery of stem cell senescence and could be used as an alternative medicine for tissue regeneration and future rejuvenation. Copyright © 2014 Elsevier Ltd. All rights reserved.

The Association Between Income and Life Expectancy in the United States, 2001–2014

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Chetty, Raj; Stepner, Michael; Abraham, Sarah; Lin, Shelby; Scuderi, Benjamin; Turner, Nicholas; Bergeron, Augustin; Cutler, David

2016-01-01

Importance The relationship between income and mortality is well established but remains poorly understood. Objectives To measure the level, temporal trend, and geographic variability in the association between income and life expectancy, and identify factors related to small area variation in this association. Design and Setting Income data for the US population were obtained from 1.4 billion de-identified tax records between 1999 and 2014. Mortality data were obtained from Social Security Administration death records. These data were used to estimate race- and ethnicity-adjusted life expectancy at 40 years of age by household income percentile, sex, and geographic area, and to evaluate factors associated with differences in life expectancy. Main Outcomes and Measures Relationship between income and life expectancy; trends in life expectancy by income group; geographic variation in life expectancy levels and trends by income group; and factors associated with differences in life expectancy across areas. Results The sample consisted of 1 408 287 218 person-year observations (mean age at which individuals were analyzed, 53.0 years; median household earnings among working individuals, $61 175 per year [mean, $97 725 per year]). Among those aged 40 to 76 years, there were 4 114 380 deaths among men (mortality rate, 596.3 per 100 000) and 2 694 808 deaths among women (mortality rate, 375.1 per 100 000). The analysis yielded four results. First, higher income was associated with greater longevity throughout the income distribution. The gap in life expectancy between the richest 1% and poorest 1% of individuals was 14.6 years (95% CI, 14.4 to 14.8 years) for men and 10.1 years (95% CI, 9.9 to 10.3 years) for women. Second, inequality in life expectancy increased over time. Between 2001 and 2014, life expectancy increased by 2.34 years for men and 2.91 years for women in the top 5% of the income distribution, but increased by only 0.32 years for men and 0.04 years for

Impact of selected risk factors on quality-adjusted life expectancy in Denmark

DEFF Research Database (Denmark)

Brønnum-Hansen, Henrik; Juel, Knud; Davidsen, Michael

2007-01-01

AIMS: The construct quality-adjusted life years (QALYs) combines mortality and overall health status and can be used to quantify the impact of risk factors on population health. The purpose of the study was to estimate the impact of tobacco smoking, high alcohol consumption, physical inactivity...... Health Survey 2000, and Danish EQ-5D values. RESULTS: The quality-adjusted life expectancy of 25-year-olds was 10-11 QALYs shorter for heavy smokers than for those who never smoke. The difference in life expectancy was 9-10 years. Men and women with high alcohol consumption could expect to lose about 5...... and 3 QALYs, respectively. Sedentary persons could expect to have about 7 fewer QALYs than physically active persons. Obesity shortened QALYs by almost 3 for men and 6 for women. CONCLUSIONS: Smoking, high alcohol consumption, physical inactivity, and obesity strongly reduce life expectancy and health...

Forecasting differences in life expectancy by education

NARCIS (Netherlands)

P.H.M. Van Baal (Pieter); F. Peters (Frederik); J.P. Mackenbach (Johan); W.J. Nusselder (Wilma)

2016-01-01

textabstractForecasts of life expectancy (LE) have fuelled debates about the sustainability and dependability of pension and healthcare systems. Of relevance to these debates are inequalities in LE by education. In this paper, we present a method of forecasting LE for different educational groups

Estimating life expectancies for US small areas: a regression framework

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Congdon, Peter

2014-01-01

Analysis of area mortality variations and estimation of area life tables raise methodological questions relevant to assessing spatial clustering, and socioeconomic inequalities in mortality. Existing small area analyses of US life expectancy variation generally adopt ad hoc amalgamations of counties to alleviate potential instability of mortality rates involved in deriving life tables, and use conventional life table analysis which takes no account of correlated mortality for adjacent areas or ages. The alternative strategy here uses structured random effects methods that recognize correlations between adjacent ages and areas, and allows retention of the original county boundaries. This strategy generalizes to include effects of area category (e.g. poverty status, ethnic mix), allowing estimation of life tables according to area category, and providing additional stabilization of estimated life table functions. This approach is used here to estimate stabilized mortality rates, derive life expectancies in US counties, and assess trends in clustering and in inequality according to county poverty category.

An Association of Total Health Expenditure with GDP and Life Expectancy

OpenAIRE

Zaman, Sojib Bin; Hossain, Naznin; Mehta, Varshil; Sharmin, Shuchita; Mahmood, Shakeel Ahmed Ibne

2017-01-01

Abstract Introduction: Gradual total health expenditure (THE) has become a major concern. It is not only the increased THE, but also its unequal growth in overall economy, found among the developing countries. If increased life expectancy is considered as a leverage for an individual’s investment in health services, it can be expected that as the life expectancy increases, tendency of health care investment will also experience a boost up. Objective: The aim of the present study wa...

Mortality and life expectancy in persons with severe unipolar depression

DEFF Research Database (Denmark)

Laursen, Thomas Munk; Musliner, Katherine L; Benros, Michael E

2016-01-01

BACKGROUND: Depression is a common psychiatric disorder, with a lifetime prevalence of 10-15% in the Danish population. Although depression is associated with excess mortality, it is not yet understood how this affects life expectancy. Our aim was to examine mortality rates and life expectancy...... in patients with unipolar depression compared to the general population, and to assess the impact of comorbid somatic illness and substance abuse. METHODS: We followed a Danish population-based cohort from 1995-2013 (N=5,103,699). The cohort included all residents in Denmark during the study period. Mortality...... rate ratios (MRRs) and life expectancy in persons with unipolar depression were calculated using survival analysis techniques. RESULTS: The overall MRR was 2.07 (95% Confidence Interval (CI): 2.05-2.09) in people with a previous unipolar depression diagnosis compared to the general Danish population...

Different transcriptional profiling between senescent and non-senescent human coronary artery endothelial cells (HCAECs) by Omeprazole and Lansoprazole treatment.

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Costarelli, Laura; Giacconi, Robertina; Malavolta, Marco; Basso, Andrea; Piacenza, Francesco; Provinciali, Mauro; Maggio, Marcello G; Corsonello, Andrea; Lattanzio, Fabrizia

2017-04-01

Recent evidence suggests that high dose and/or long term use of proton pump inhibitors (PPIs) may increase the risk of adverse cardiovascular events in older patients, but mechanisms underlying these detrimental effects are not known. Taking into account that the senescent endothelial cells have been implicated in the genesis or promotion of age-related cardiovascular disease, we hypothesized an active role of PPIs in senescent cells. The aim of this study is to investigate the changes in gene expression occurring in senescent and non-senescent human coronary artery endothelial cells (HCAECs) following Omeprazole (OPZ) or Lansoprazole (LPZ) treatment. Here, we show that atherogenic response is among the most regulated processes in PPI-treated HCAECs. PPIs induced down-regulation of anti-atherogenic chemokines (CXCL11, CXCL12 and CX3CL1) in senescent but not in non-senescent cells, while the same chemokines were up-regulated in untreated senescent cells. These findings support the hypothesis that up-regulated anti-atherogenic chemokines may represent a defensive mechanism against atherosclerosis during cellular senescence, and suggest that PPIs could activate pro-atherogenic pathways by changing the secretory phenotype of senescent HCAECs. Moreover, the genes coding for fatty acid binding protein 4 (FABP4) and piezo-type mechanosensitive ion channel component 2 (PIEZO2) were modulated by PPIs treatment with respect to untreated cells. In conclusions, our results show that long-term and high dose use of PPI could change the secretory phenotype of senescent cells, suggesting one of the potential mechanisms by which use of PPI can increase adverse outcomes in older subjects.

How much of the difference in life expectancy between Scottish cities does deprivation explain?

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Seaman, R; Mitchell, R; Dundas, R; Leyland, A H; Popham, F

2015-10-16

Glasgow's low life expectancy and high levels of deprivation are well documented. Studies comparing Glasgow to similarly deprived cities in England suggest an excess of deaths in Glasgow that cannot be accounted for by deprivation. Within Scotland comparisons are more equivocal suggesting deprivation could explain Glasgow's excess mortality. Few studies have used life expectancy, an intuitive measure that quantifies the between-city difference in years. This study aimed to use the most up-to-date data to compare Glasgow to other Scottish cities and to (i) evaluate whether deprivation could account for lower life expectancy in Glasgow and (ii) explore whether the age distribution of mortality in Glasgow could explain its lower life expectancy. Sex specific life expectancy was calculated for 2007-2011 for the population in Glasgow and the combined population of Aberdeen, Dundee and Edinburgh. Life expectancy was calculated for deciles of income deprivation, based on the national ranking of datazones, using the Scottish Index of Multiple Deprivation. Life expectancy in Glasgow overall, and by deprivation decile, was compared to that in Aberdeen, Dundee and Edinburgh combined, and the life expectancy difference decomposed by age using Arriaga's discrete method. Life expectancy for the whole Glasgow population was lower than the population of Aberdeen, Dundee and Edinburgh combined. When life expectancy was compared by national income deprivation decile, Glasgow's life expectancy was not systematically lower, and deprivation accounted for over 90 % of the difference. This was reduced to 70 % of the difference when carrying out sensitivity analysis using city-specific income deprivation deciles. In both analyses life expectancy was not systematically lower in Glasgow when stratified by deprivation. Decomposing the differences in life expectancy also showed that the age distribution of mortality was not systematically different in Glasgow after accounting for deprivation

Projected life expectancy of people with HIV according to timing of diagnosis

DEFF Research Database (Denmark)

Nakagawa, Fumiyo; Lodwick, Rebecca K; Smith, Colette J

2012-01-01

positive in 2010. The effect of altering the diagnosis rate was investigated. Results: Assuming a high rate of HIV diagnosis (median CD4 cell count at diagnosis, 432¿cells/µl), projected median age at death (life expectancy) was 75.0 years. This implies 7.0 years of life were lost on average due to HIV......Background and objectives: Effective antiretroviral therapy (ART) has contributed greatly toward survival for people with HIV, yet many remain undiagnosed until very late. Our aims were to estimate the life expectancy of an HIV-infected MSM living in a developed country with extensive access to ART...... and healthcare, and to assess the effect of late diagnosis on life expectancy. Methods: A stochastic computer simulation model of HIV infection and the effect of ART was used to estimate life expectancy and determine the distribution of potential lifetime outcomes of an MSM, aged 30 years, who becomes HIV...

The promise of prevention: the effects of four preventable risk factors on national life expectancy and life expectancy disparities by race and county in the United States.

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Goodarz Danaei

2010-03-01

Full Text Available There has been substantial research on psychosocial and health care determinants of health disparities in the United States (US but less on the role of modifiable risk factors. We estimated the effects of smoking, high blood pressure, elevated blood glucose, and adiposity on national life expectancy and on disparities in life expectancy and disease-specific mortality among eight subgroups of the US population (the "Eight Americas" defined on the basis of race and the location and socioeconomic characteristics of county of residence, in 2005.We combined data from the National Health and Nutrition Examination Survey and the Behavioral Risk Factor Surveillance System to estimate unbiased risk factor levels for the Eight Americas. We used data from the National Center for Health Statistics to estimate age-sex-disease-specific number of deaths in 2005. We used systematic reviews and meta-analyses of epidemiologic studies to obtain risk factor effect sizes for disease-specific mortality. We used epidemiologic methods for multiple risk factors to estimate the effects of current exposure to these risk factors on death rates, and life table methods to estimate effects on life expectancy. Asians had the lowest mean body mass index, fasting plasma glucose, and smoking; whites had the lowest systolic blood pressure (SBP. SBP was highest in blacks, especially in the rural South--5-7 mmHg higher than whites. The other three risk factors were highest in Western Native Americans, Southern low-income rural blacks, and/or low-income whites in Appalachia and the Mississippi Valley. Nationally, these four risk factors reduced life expectancy at birth in 2005 by an estimated 4.9 y in men and 4.1 y in women. Life expectancy effects were smallest in Asians (M, 4.1 y; F, 3.6 y and largest in Southern rural blacks (M, 6.7 y; F, 5.7 y. Standard deviation of life expectancies in the Eight Americas would decline by 0.50 y (18% in men and 0.45 y (21% in women if these risks

Educational differences in life expectancy over five decades among the oldest old in Norway.

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Kinge, Jonas Minet; Steingrímsdóttir, Ólöf Anna; Moe, Joakim Oliu; Skirbekk, Vegard; Næss, Øyvind; Strand, Bjørn Heine

2015-11-01

Socioeconomic inequalities in life expectancy have been shown among the middle aged and the youngest of the old individuals, but the situation in the oldest old is less clear. The aim of this study was to investigate trends in life expectancy at ages 85, 90 and 95 years by education in Norway in the period 1961-2009. This was a register-based population study including all residents in Norway aged 85 and over. Individual-level data were provided by the Central Population Register and the National Education Database. For each decade during 1961-2009, death rates by 1-year age groups were calculated separately for each sex and three educational categories. Annual life tables were used to calculate life expectancy at ages 85 (e85), 90 (e90) and 95 (e95). Educational differentials in life expectancy at each age were non-significant in the early decades, but became significant over time. For example, for the decade 2000-9, a man aged 90 years with primary education had a life expectancy of 3.4 years, while a man with tertiary education could expect to live for 3.8 years. Similar numbers in women were 4.1 and 4.5 years, respectively. Even among 95-year-old men, statistically significant differences in life expectancy were found by education in the two last decades. Education matters regarding remaining life expectancy also for the oldest old in Norway. Life expectancy at these ages is low, so a growth of 0.5 years in the life expectancy differential is sizeable. © The Author 2015. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Autocrine IL-6 mediates pituitary tumor senescence

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Fuertes, Mariana; Ajler, Pablo; Carrizo, Guillermo; Cervio, Andrés; Sevlever, Gustavo; Stalla, Günter K.; Arzt, Eduardo

2017-01-01

Cellular senescence is a stable proliferative arrest state. Pituitary adenomas are frequent and mostly benign, but the mechanism for this remains unknown. IL-6 is involved in pituitary tumor progression and is produced by the tumoral cells. In a cell autonomous fashion, IL-6 participates in oncogene-induced senescence in transduced human melanocytes. Here we prove that autocrine IL-6 participates in pituitary tumor senescence. Endogenous IL-6 inhibition in somatotroph MtT/S shRNA stable clones results in decreased SA-β-gal activity and p16INK4a but increased pRb, proliferation and invasion. Nude mice injected with IL-6 silenced clones develop tumors contrary to MtT/S wild type that do not, demonstrating that clones that escape senescence are capable of becoming tumorigenic. When endogenous IL-6 is silenced, cell cultures derived from positive SA-β-gal human tumor samples decrease the expression of the senescence marker. Our results establish that IL-6 contributes to maintain senescence by its autocrine action, providing a natural model of IL-6 mediated benign adenoma senescence. PMID:27902467

Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition.

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Blagosklonny, Mikhail V

2006-09-01

While ruling out programmed aging, evolutionary theory predicts a quasi-program for aging, a continuation of the developmental program that is not turned off, is constantly on, becoming hyper-functional and damaging, causing diseases of aging. Could it be switched off pharmacologically? This would require identification of a molecular target involved in cell senescence, organism aging and diseases of aging. Notably, cell senescence is associated with activation of the TOR (target of rapamycin) nutrient- and mitogen-sensing pathway, which promotes cell growth, even though cell cycle is blocked. Is TOR involved in organism aging? In fact, in yeast (where the cell is the organism), caloric restriction, rapamycin and mutations that inhibit TOR all slow down aging. In animals from worms to mammals caloric restrictions, life-extending agents, and numerous mutations that increase longevity all converge on the TOR pathway. And, in humans, cell hypertrophy, hyper-function and hyperplasia, typically associated with activation of TOR, contribute to diseases of aging. Theoretical and clinical considerations suggest that rapamycin may be effective against atherosclerosis, hypertension and hyper-coagulation (thus, preventing myocardial infarction and stroke), osteoporosis, cancer, autoimmune diseases and arthritis, obesity, diabetes, macula-degeneration, Alzheimer's and Parkinson's diseases. Finally, I discuss that extended life span will reveal new causes for aging (e.g., ROS, 'wear and tear', Hayflick limit, stem cell exhaustion) that play a limited role now, when quasi-programmed senescence kills us first.

Unemployment, disability and life expectancy in the United States: A life course study.

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Laditka, James N; Laditka, Sarah B

2016-01-01

Unemployment may be associated with health through factors including stress, depression, unhealthy behaviors, reduced health care, and loss of social networks. Little is known about associations of total lifetime unemployment with disability and life expectancy. People with high unemployment (≥the median) will live shorter lives with more disability than those with less unemployment. Data were nationally representative of African Americans and non-Hispanic whites, from the Panel Study of Income Dynamics (37 waves 1968-2011, n = 7,970, mean work years = 24.7). Seven waves (1999-2011, 58,268 person-years) measured disability in activities of daily living. We estimated monthly probabilities of disability and death associated with unemployment using multinomial logistic Markov models adjusted for age, sex, race/ethnicity, education, health status at baseline and throughout work life, and social support. We used the probabilities to create large populations with microsimulation, each individual having known monthly disability status, age 40 to death. We analyzed the populations to measure outcomes. Respectively for African American and white women and African American and white men, life expectancies (with 95% confidence intervals) from age 40 with low unemployment were ages: 77.1 (75.0-78.3), 80.6 (78.4-81.4), 71.4 (69.6-72.5), and 76.9 (74.9-77.9). Corresponding high unemployment results were: 73.7 (71.7-75.0), 77.5 (75.1-78.0), 68.4 (66.8-69.0), and 73.7 (71.5-74.3). The percentage of life disabled from age 40 was greater with high unemployment for the same groups, by 23.9%, 21.0%, 21.3%, and 21.1% (all p unemployment may be associated with a larger proportion of later life with disability and lower life expectancy. Copyright © 2016 Elsevier Inc. All rights reserved.

Phytohormones and microRNAs as sensors and regulators of leaf senescence: assigning macro roles to small molecules.

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Sarwat, Maryam; Naqvi, Afsar Raza; Ahmad, Parvaiz; Ashraf, Muhammad; Akram, Nudrat Aisha

2013-12-01

Ageing or senescence is an intricate and highly synchronized developmental phase in the life of plant parts including leaf. Senescence not only means death of a plant part, but during this process, different macromolecules undergo degradation and the resulting components are transported to other parts of the plant. During the period from when a leaf is young and green to the stage when it senesces, a multitude of factors such as hormones, environmental factors and senescence associated genes (SAGs) are involved. Plant hormones including salicylic acid, abscisic acid, jasmonic acid and ethylene advance leaf senescence, whereas others like cytokinins, gibberellins, and auxins delay this process. The environmental factors which generally affect plant development and growth, can hasten senescence, the examples being nutrient dearth, water stress, pathogen attack, radiations, high temperature and light intensity, waterlogging, and air, water or soil contamination. Other important influences include carbohydrate accumulation and high carbon/nitrogen level. To date, although several genes involved in this complex process have been identified, still not much information exists in the literature on the signalling mechanism of leaf senescence. Now, the Arabidopsis mutants have paved our way and opened new vistas to elucidate the signalling mechanism of leaf senescence for which various mutants are being utilized. Recent studies demonstrating the role of microRNAs in leaf senescence have reinforced our knowledge of this intricate process. This review provides a comprehensive and critical analysis of the information gained particularly on the roles of several plant growth regulators and microRNAs in regulation of leaf senescence. Copyright © 2013 Elsevier Inc. All rights reserved.

From the Hayflick mosaic to the mosaics of ageing. Role of stress-induced premature senescence in human ageing.

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Toussaint, Olivier; Remacle, Jose; Dierick, Jean-François; Pascal, Thierry; Frippiat, Christophe; Zdanov, Stéphanie; Magalhaes, Joao Pedro; Royer, Véronique; Chainiaux, Florence

2002-11-01

The Hayflick limit-senescence of proliferative cell types-is a fundamental feature of proliferative cells in vitro. Various human proliferative cell types exposed in vitro to many types of subcytotoxic stresses undergo stress-induced premature senescence (SIPS) (also called stress-induced premature senescence-like phenotype, according to the definition of senescence). The known mechanisms of appearance the main features of SIPS are reviewed: senescent-like morphology, growth arrest, senescence-related changes in gene expression, telomere shortening. Long before telomere-shortening induces senescence, other factors such as culture conditions or lack of 'feeder cells' can trigger either SIPS or prolonged reversible G(0) phase of the cell cycle. In vivo, 'proliferative' cell types of aged individuals are likely to compose a mosaic made of cells irreversibly growth arrested or not. The higher level of stress to which these cells have been exposed throughout their life span, the higher proportion of the cells of this mosaic will be in SIPS rather than in telomere-shortening dependent senescence. All cell types undergoing SIPS in vivo, most notably the ones in stressful conditions, are likely to participate in the tissular changes observed along ageing. For instance, human diploid fibroblasts (HDFs) exposed in vivo and in vitro to pro-inflammatory cytokines display biomarkers of senescence and might participate in the degradation of the extracellular matrix observed in ageing.

Gains in Life Expectancy Associated with Higher Education in Men.

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Bijwaard, Govert E; van Poppel, Frans; Ekamper, Peter; Lumey, L H

2015-01-01

Many studies show large differences in life expectancy across the range of education, intelligence, and socio-economic status. As educational attainment, intelligence, and socio-economic status are highly interrelated, appropriate methods are required to disentangle their separate effects. The aim of this paper is to present a novel method to estimate gains in life expectancy specifically associated with increased education. Our analysis is based on a structural model in which education level, IQ at age 18 and mortality all depend on (latent) intelligence. The model allows for (selective) educational choices based on observed factors and on an unobserved factor capturing intelligence. Our estimates are based on information from health examinations of military conscripts born in 1944-1947 in The Netherlands and their vital status through age 66 (n = 39,798). Our empirical results show that men with higher education have lower mortality. Using structural models to account for education choice, the estimated gain in life expectancy for men moving up one educational level ranges from 0.3 to 2 years. The estimated gain in months alive over the observational period ranges from -1.2 to 5.7 months. The selection effect is positive and amounts to a gain of one to two months. Decomposition of the selection effect shows that the gain from selection on (latent) intelligence is larger than the gain from selection on observed factors and amounts to 1.0 to 1.7 additional months alive. Our findings confirm the strong selection into education based on socio-economic status and intelligence. They also show significant higher life expectancy among individuals with higher education after the selectivity of education choice has been taken into account. Based on these estimates, it is plausible therefore that increases in education could lead to increases in life expectancy.

Senescent vs. non-senescent cells in the human annulus in vivo: Cell harvest with laser capture microdissection and gene expression studies with microarray analysis

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Ingram Jane A

2010-01-01

Full Text Available Abstract Background Senescent cells are well-recognized in the aging/degenerating human disc. Senescent cells are viable, cannot divide, remain metabolically active and accumulate within the disc over time. Molecular analysis of senescent cells in tissue offers a special challenge since there are no cell surface markers for senescence which would let one use fluorescence-activated cell sorting as a method for separating out senescent cells. Methods We employed a novel laser capture microdissection (LCM design to selectively harvest senescent and non-senescent annulus cells in paraffin-embedded tissue, and compared their gene expression with microarray analysis. LCM was used to separately harvest senescent and non-senescent cells from 11 human annulus specimens. Results Microarray analysis revealed significant differences in expression levels in senescent cells vs non-senescent cells: 292 genes were upregulated, and 321 downregulated. Genes with established relationships to senescence were found to be significantly upregulated in senescent cells vs. non-senescent cells: p38 (MPAK14, RB-Associated KRAB zinc finger, Discoidin, CUB and LCCL domain, growth arrest and DNA-damage inducible beta, p28ING5, sphingosine-1-phosphate receptor 2 and somatostatin receptor 3; cyclin-dependent kinase 8 showed significant downregulation in senescent cells. Nitric oxidase synthase 1, and heat shock 70 kDa protein 6, both of which were significantly down-regulated in senescent cells, also showed significant changes. Additional genes related to cytokines, cell proliferation, and other processes were also identified. Conclusions Our LCM-microarray analyses identified a set of genes associated with senescence which were significantly upregulated in senescent vs non-senescent cells in the human annulus. These genes include p38 MAP kinase, discoidin, inhibitor of growth family member 5, and growth arrest and DNA-damage-inducible beta. Other genes, including genes

Mitochondrial DNA Hypomethylation Is a Biomarker Associated with Induced Senescence in Human Fetal Heart Mesenchymal Stem Cells

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Dehai Yu

2017-01-01

Full Text Available Background. Fetal heart can regenerate to restore its normal anatomy and function in response to injury, but this regenerative capacity is lost within the first week of postnatal life. Although the specific molecular mechanisms remain to be defined, it is presumed that aging of cardiac stem or progenitor cells may contribute to the loss of regenerative potential. Methods. To study this aging-related dysfunction, we cultured mesenchymal stem cells (MSCs from human fetal heart tissues. Senescence was induced by exposing cells to chronic oxidative stress/low serum. Mitochondrial DNA methylation was examined during the period of senescence. Results. Senescent MSCs exhibited flattened and enlarged morphology and were positive for the senescence-associated beta-galactosidase (SA-β-Gal. By scanning the entire mitochondrial genome, we found that four CpG islands were hypomethylated in close association with senescence in MSCs. The mitochondrial COX1 gene, which encodes the main subunit of the cytochrome c oxidase complex and contains the differentially methylated CpG island 4, was upregulated in MSCs in parallel with the onset of senescence. Knockdown of DNA methyltransferases (DNMT1, DNMT3a, and DNMT3B also upregulated COX1 expression and induced cellular senescence in MSCs. Conclusions. This study demonstrates that mitochondrial CpG hypomethylation may serve as a critical biomarker associated with cellular senescence induced by chronic oxidative stress.

Possible Roles of Strigolactones during Leaf Senescence

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Yusuke Yamada

2015-09-01

Full Text Available Leaf senescence is a complicated developmental process that involves degenerative changes and nutrient recycling. The progress of leaf senescence is controlled by various environmental cues and plant hormones, including ethylene, jasmonic acid, salicylic acid, abscisic acid, cytokinins, and strigolactones. The production of strigolactones is induced in response to nitrogen and phosphorous deficiency. Strigolactones also accelerate leaf senescence and regulate shoot branching and root architecture. Leaf senescence is actively promoted in a nutrient-poor soil environment, and nutrients are transported from old leaves to young tissues and seeds. Strigolactones might act as important signals in response to nutrient levels in the rhizosphere. In this review, we discuss the possible roles of strigolactones during leaf senescence.

Senescence from glioma stem cell differentiation promotes tumor growth

International Nuclear Information System (INIS)

Ouchi, Rie; Okabe, Sachiko; Migita, Toshiro; Nakano, Ichiro; Seimiya, Hiroyuki

2016-01-01

Glioblastoma (GBM) is a lethal brain tumor composed of heterogeneous cellular populations including glioma stem cells (GSCs) and differentiated non-stem glioma cells (NSGCs). While GSCs are involved in tumor initiation and propagation, NSGCs' role remains elusive. Here, we demonstrate that NSGCs undergo senescence and secrete pro-angiogenic proteins, boosting the GSC-derived tumor formation in vivo. We used a GSC model that maintains stemness in neurospheres, but loses the stemness and differentiates into NSGCs upon serum stimulation. These NSGCs downregulated telomerase, shortened telomeres, and eventually became senescent. The senescent NSGCs released pro-angiogenic proteins, including vascular endothelial growth factors and senescence-associated interleukins, such as IL-6 and IL-8. Conditioned medium from senescent NSGCs promoted proliferation of brain microvascular endothelial cells, and mixed implantation of GSCs and senescent NSGCs into mice enhanced the tumorigenic potential of GSCs. The senescent NSGCs seem to be clinically relevant, because both clinical samples and xenografts of GBM contained tumor cells that expressed the senescence markers. Our data suggest that senescent NSGCs promote malignant progression of GBM in part via paracrine effects of the secreted proteins. - Highlights: • Non-stem glioma cells (NSGCs) lose telomerase and eventually become senescent. • Senescent NSGCs secrete pro-angiogenic proteins, such as VEGFs, IL-6, and IL-8. • Senescent NSGCs enhance the growth of brain microvascular endothelial cells. • Senescent NSGCs enhance the tumorigenic potential of glioma stem cells in vivo.

Senescence from glioma stem cell differentiation promotes tumor growth

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Ouchi, Rie [Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550 (Japan); Laboratory of Molecular Target Therapy of Cancer, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550 (Japan); Okabe, Sachiko; Migita, Toshiro [Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550 (Japan); Nakano, Ichiro [Department of Neurosurgery, Comprehensive Cancer Center, University of Alabama at Birmingham, 1824 6th Avenue South, Birmingham, AL 35233 (United States); Seimiya, Hiroyuki, E-mail: hseimiya@jfcr.or.jp [Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550 (Japan); Laboratory of Molecular Target Therapy of Cancer, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550 (Japan)

2016-02-05

Glioblastoma (GBM) is a lethal brain tumor composed of heterogeneous cellular populations including glioma stem cells (GSCs) and differentiated non-stem glioma cells (NSGCs). While GSCs are involved in tumor initiation and propagation, NSGCs' role remains elusive. Here, we demonstrate that NSGCs undergo senescence and secrete pro-angiogenic proteins, boosting the GSC-derived tumor formation in vivo. We used a GSC model that maintains stemness in neurospheres, but loses the stemness and differentiates into NSGCs upon serum stimulation. These NSGCs downregulated telomerase, shortened telomeres, and eventually became senescent. The senescent NSGCs released pro-angiogenic proteins, including vascular endothelial growth factors and senescence-associated interleukins, such as IL-6 and IL-8. Conditioned medium from senescent NSGCs promoted proliferation of brain microvascular endothelial cells, and mixed implantation of GSCs and senescent NSGCs into mice enhanced the tumorigenic potential of GSCs. The senescent NSGCs seem to be clinically relevant, because both clinical samples and xenografts of GBM contained tumor cells that expressed the senescence markers. Our data suggest that senescent NSGCs promote malignant progression of GBM in part via paracrine effects of the secreted proteins. - Highlights: • Non-stem glioma cells (NSGCs) lose telomerase and eventually become senescent. • Senescent NSGCs secrete pro-angiogenic proteins, such as VEGFs, IL-6, and IL-8. • Senescent NSGCs enhance the growth of brain microvascular endothelial cells. • Senescent NSGCs enhance the tumorigenic potential of glioma stem cells in vivo.

Emerging roles of lncRNAs in senescence

DEFF Research Database (Denmark)

Montes Resano, Marta; Lund, Anders H

2016-01-01

Cellular senescence is a complex stress response that leads to an irreversible state of cell growth arrest. Senescence may be induced by different stimuli such as telomere shortening, DNA damage or oncogenic insult among others. Senescent cells are metabolically highly active producing a wealth...

Persistent social inequality in life expectancy and disability-free life expectancy: Outlook for a differential pension age in Denmark?

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Brønnum-Hansen, Henrik; Eriksen, Mette Lindholm; Andersen-Ranberg, Karen; Jeune, Bernard

2017-06-01

The state old-age pension in Denmark increases to keep pace with the projected increase in average life expectancy (LE) without any regard to the social gap in LE and expected lifetime in good health. The purpose of this study was to compare changes in LE and disability-free life expectancy (DFLE) between groups of Danes with high, medium and low levels of education. Nationwide register data on education and mortality were combined with data from the Surveys of Health, Ageing and Retirement in Europe (SHARE) surveys in 2006-2007, 2010-2011 and 2013-2014 and the DFLE by educational level was estimated by Sullivan's method for each of these three time points. Between 2006-2007 and 2013-2014, LE among 65-year-old men and women with a low educational level increased by 1.3 and 1.0 years, respectively, and by 1.4 and 1.3 years for highly educated men and women. The gap in LE between people with high and low levels of education remained more than 2 years. In 2006-2007, 65-year-old men with a high level of education could expect 3.2 more years without disability than men of the same age with a low level of education. In 2013-2014, the difference was 2.9 years. For women, the results were 3.7 and 3.4 years, respectively. With the persistent social inequality in LE of more than 2 years and the continuous gap between high and low educational groups in DFLE of about 3 years, a differential pension age is recommended.

PML, SUMOylation and senescence

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Hugues eDe Thé

2013-07-01

Full Text Available Since its discovery, 25 years ago, PML has been an enigma. Implicated in the oncogenic PML/RARA fusion, forming elusive intranuclear domains, triggering cell death or senescence, controlled by and perhaps controlling SUMOylation... there are multiple PML-related issues. Here we review the reciprocal interactions between PML, senescence and SUMOylation, notably in the context of cellular transformation.

Are gaps in disability free life expectancies diminishing in Italy?

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Frova, Luisa; Burgio, Alessandra; Battisti, Alessandra

2010-01-01

This paper studies gender differences in disability free life expectancy (DFLE), taking into account mortality and disability contributions. After analysing the types of disability that account for such differences, it goes on to examine temporal variability and age contributions to mortality and disability variation. The method used is an extension of Arriaga’s model proposed by Nusselder. In 2005, disability free life expectancy at age 30 was 46.23 years for men and 48.74 years for women, w...

Effect of patient's life expectancy on the cost-effectiveness of treatment for ocular hypertension.

Science.gov (United States)

Kymes, Steven M; Plotzke, Michael R; Kass, Michael A; Boland, Michael V; Gordon, Mae O

2010-05-01

To assess the influence of expected life span on the cost-effectiveness of treating ocular hypertension to prevent primary open-angle glaucoma. We used a Markov simulation model to estimate the cost and benefit of ocular hypertension treatment over a person's remaining life. We examined the influence of age on the cost-effectiveness decision in 2 ways: (1) by evaluating specific age cohorts to assess the influence of age at the initiation of treatment; and (2) by evaluating the influence of a specific life span. At a willingness to pay $50,000/quality-adjusted life year to $100,000/quality-adjusted life year, treatment of people with a 2% or greater annual risk of developing glaucoma was cost-effective for people aged 45 years with a life expectancy of at least 18 remaining years. However, to be cost-effective, a person aged 55 years must have a life expectancy of 21 remaining years and someone aged 65 years must have a life expectancy of 23 remaining years. A person with ocular hypertension must have a life expectancy of at least 18 remaining years to justify treatment at a threshold of a 2% or greater annual risk of developing glaucoma. Persons at higher levels of risk require a life expectancy of 7 to 10 additional years to justify treatment.

Markers of T Cell Senescence in Humans

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Weili Xu

2017-08-01

Full Text Available Many countries are facing the aging of their population, and many more will face a similar obstacle in the near future, which could be a burden to many healthcare systems. Increased susceptibility to infections, cardiovascular and neurodegenerative disease, cancer as well as reduced efficacy of vaccination are important matters for researchers in the field of aging. As older adults show higher prevalence for a variety of diseases, this also implies higher risk of complications, including nosocomial infections, slower recovery and sequels that may reduce the autonomy and overall quality of life of older adults. The age-related effects on the immune system termed as “immunosenescence” can be exemplified by the reported hypo-responsiveness to influenza vaccination of the elderly. T cells, which belong to the adaptive arm of the immune system, have been extensively studied and the knowledge gathered enables a better understanding of how the immune system may be affected after acute/chronic infections and how this matters in the long run. In this review, we will focus on T cells and discuss the surface and molecular markers that are associated with T cell senescence. We will also look at the implications that senescent T cells could have on human health and diseases. Finally, we will discuss the benefits of having these markers for investigators and the future work that is needed to advance the field of T cell senescence markers.

Diverging Life Expectancies and Voting Patterns in the 2016 US Presidential Election

Science.gov (United States)

2017-01-01

Objectives. To assess whether voting patterns in the 2016 US presidential election were correlated with long-run trends in county life expectancy. Methods. I examined county-level voting data from the 2008 and 2016 presidential elections and assessed Donald Trump’s share of the 2016 vote, change in the Republican vote share between 2008 and 2016, and changes in absolute numbers of Democratic and Republican votes. County-level estimates of life expectancy at birth were obtained for 1980 and 2014 from the Institute for Health Metrics and Evaluation. Results. Changes in county life expectancy from 1980 to 2014 were strongly negatively associated with Trump’s vote share, with less support for Trump in counties experiencing greater survival gains. Counties in which life expectancy stagnated or declined saw a 10-percentage-point increase in the Republican vote share between 2008 and 2016. Conclusions. Residents of counties left out from broader life expectancy gains abandoned the Democratic Party in the 2016 presidential election. Since coming to power, the Trump administration has proposed cuts to health insurance for the poor, social programs, health research, and environmental and worker protections, which are key determinants of population health. Health gaps likely will continue to widen without significant public investment in population health. PMID:28817322

Diverging Life Expectancies and Voting Patterns in the 2016 US Presidential Election.

Science.gov (United States)

Bor, Jacob

2017-10-01

To assess whether voting patterns in the 2016 US presidential election were correlated with long-run trends in county life expectancy. I examined county-level voting data from the 2008 and 2016 presidential elections and assessed Donald Trump's share of the 2016 vote, change in the Republican vote share between 2008 and 2016, and changes in absolute numbers of Democratic and Republican votes. County-level estimates of life expectancy at birth were obtained for 1980 and 2014 from the Institute for Health Metrics and Evaluation. Changes in county life expectancy from 1980 to 2014 were strongly negatively associated with Trump's vote share, with less support for Trump in counties experiencing greater survival gains. Counties in which life expectancy stagnated or declined saw a 10-percentage-point increase in the Republican vote share between 2008 and 2016. Residents of counties left out from broader life expectancy gains abandoned the Democratic Party in the 2016 presidential election. Since coming to power, the Trump administration has proposed cuts to health insurance for the poor, social programs, health research, and environmental and worker protections, which are key determinants of population health. Health gaps likely will continue to widen without significant public investment in population health.

Effect of cytokinins on delaying petunia flower senescence: a transcriptome study approach.

Science.gov (United States)

Trivellini, Alice; Cocetta, Giacomo; Vernieri, Paolo; Mensuali-Sodi, Anna; Ferrante, Antonio

2015-01-01

Flower senescence is a fascinating natural process that represents the final developmental stage in the life of a flower. Plant hormones play an important role in regulating the timing of flower senescence. Ethylene is a trigger and usually accelerates the senescence rate, while cytokinins are known to delay it. The aim of this work was to study the effect of 6-benzylaminopurine (BA) on petal senescence by transcript profile comparison after 3 or 6 h using a cross-species method by hybridizing petunia samples to a 4 × 44 K Agilent tomato array. The relative content of ethylene, abscisic acid, anthocyanins, total carotenoids and total phenols that determine the physiological behaviours of the petal tissue were measured. BA treatment prolonged the flower life and increased the concentrations of phenols and anthocyanins, while total carotenoids did not increase and were lower than the control. The ethylene biosynthetic and perception gene expressions were studied immediately after treatment until 24 h and all genes were repressed, while ethylene production was strongly induced after 4 days. The microarray analyses highlighted that BA strongly affected gene regulation after 3 h, but only 14% of genes remained differentially expressed after 6 h. The most affected pathways and genes were those related to stress, such as heat shock proteins, abscisic acid (ABA) catabolism and its signalling pathway, lipid metabolism and antioxidant defence systems. A gene annotation enrichment analysis using DAVID showed that the most important gene clusters were involved in energy generation and conservation processes. In addition to the ethylene pathway, cytokinins seem to be strongly involved the regulation of the ABA response in flower tissues.

Animal-assisted interventions and quality of life: expectations among

Directory of Open Access Journals (Sweden)

Javier López-Cepero

2014-12-01

Full Text Available The present study assessed expectations among university students (N= 474, X= 22.7, SD=5.6 years towards the possible benefits of animal-assisted interventions on quality of life. Attitudes were measured with the Improving Quality of Life scale, which is an instrument created ad hoc that demonstrated adequate psychometric properties (four easily interpretable factors, with 49% of explained variance and alphas ranging from .76 to .89. The results showed that the participants (from the departments of Social, Health or Educational Sciences had very positive attitudes (high effect sizes, ES>.80 regardless of training. The experience of sharing households with pets was associated with better expectations. These findings emphasize the high expectations that future professionals in different fields hold regarding animal-assisted interventions, and highlight the current shortcomings in training curricula. The implications of these findings for the development of animal-assisted interventions are discussed.

The Lcn2-engineered HEK-293 cells show senescence under stressful condition

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Bahareh Bahmani

2015-05-01

Full Text Available Objective(s: Lipocalin2 (Lcn2 gene is highly expressed in response to various types of cellular stresses. The precise role of Lcn2 has not been fully understood yet. However, it plays a key role in controlling vital cellular processes such as proliferation, apoptosis and metabolism. Recently it was shown that Lcn2 decreases senescence and increases proliferation of mesenchymal stem cells (MSC with finite life span under either normal or oxidative stress conditions. However, Lcn2 effects on immortal cell line with infinite proliferation are not defined completely.  Materials and Material and Methods: HEK-293 cells were transfected with recombinant pcDNA3.1 containing Lcn2 fragment (pcDNA3.1-Lcn2. Expression of lipocalin2 in transfected cells was evaluated by RT-PCR, real time RT-PCR, and ELISA. Different cell groups were treated with H2O2 and WST-1 assay was performed to determine their proliferation rate. Senescence was studied by β-galactosidase and gimsa staining methods as well as evaluation of the expression of senescence-related genes by real time RT-PCR. Results: Lcn2 increased cell proliferation under normal culture condition, while the proliferation slightly decreased under oxidative stress.  This decrease was further found to be attributed to senescence. Conclusion: Our findings indicated that under harmful conditions, Lcn2 gene is responsible for the regulation of cell survival through senescence.

Stable knockdown of PASG enhances DNA demethylation but does not accelerate cellular senescence in TIG-7 human fibroblasts.

Science.gov (United States)

Suzuki, Toshikazu; Farrar, Jason E; Yegnasubramanian, Srinivasan; Zahed, Muhammed; Suzuki, Nobuo; Arceci, Robert J

2008-09-01

Demethylation of 5-methylcytosine in genomic DNA is believed to be one of the mechanisms underlying replicative life-span of mammalian cells. Both proliferation associated SNF2-like gene (PASG, also termed Lsh) and DNA methyltransferase 3B (Dnmt3b) knockout mice result in embryonic genomic hypomethylation and a replicative senescent phenotype. However, it is unclear whether gradual demethylation of DNA during somatic cell division is directly involved in senescence. In this study, we retrovirally transduced TIG-7 human fibroblasts with a shRNA against PASG and compared the rate of change in DNA methylation as well as the replicative life-span to control cells under low (3%) and ambient (20%) oxygen. Expression of PASG protein was decreased by approximately 80% compared to control cells following transduction of PASG shRNA gene. The rate of cell growth was the same in both control and PASG-suppressed cells. The rate of demethylation of DNA was significantly increased in PASG-suppressed cells as compared control cells. However, decreased PASG expression did not shorten the replicative life-span of TIG-7 cells. Culture under low oxygen extended the life-span of TIG-7 cells but did not alter the rate of DNA demethylation. While knockout of PASG during development results in genomic hypomethylation and premature senescence, our results show that while downregulation of PASG expression in a somatic cell also leads to DNA hypomethylation, there is no associated senescent phenotype. These results suggest differences in cellular consequences of hypomethylation mediated by PASG during development compared to that in somatic cells.

Whites but Not Blacks Gain Life Expectancy from Social Contacts

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Shervin Assari

2017-10-01

Full Text Available Background. Recent research suggests that the health gain from economic resources and psychological assets may be systematically larger for Whites than Blacks. Aim. This study aimed to assess whether the life expectancy gain associated with social contacts over a long follow up differs for Blacks and Whites. Methods. Data came from the Americans’ Changing Lives (ACL Study, 1986–2011. The sample was a nationally representative sample of American adults 25 and older, who were followed for up to 25 years (n = 3361. Outcome was all-cause mortality. The main predictor was social contacts defined as number of regular visits with friends, relatives, and neighbors. Baseline demographics (age and gender, socioeconomic status (education, income, and employment, health behaviors (smoking and drinking, and health (chronic medical conditions, obesity, and depressive symptoms were controlled. Race was the focal moderator. Cox proportional hazard models were used in the pooled sample and based on race. Results. More social contacts predicted higher life expectancy in the pooled sample. A significant interaction was found between race and social contacts, suggesting that the protective effect of more social contacts is smaller for Blacks than Whites. In stratified models, more social contacts predicted an increased life expectancy for Whites but not Blacks. Conclusion. Social contacts increase life expectancy for White but not Black Americans. This study introduces social contacts as another social resource that differentially affects health of Whites and Blacks.

Cellular and molecular aspects of quinoa leaf senescence.

Science.gov (United States)

López-Fernández, María Paula; Burrieza, Hernán Pablo; Rizzo, Axel Joel; Martínez-Tosar, Leandro Julián; Maldonado, Sara

2015-09-01

During leaf senescence, degradation of chloroplasts precede to changes in nuclei and other cytoplasmic organelles, RuBisCO stability is progressively lost, grana lose their structure, plastidial DNA becomes distorted and degraded, the number of plastoglobuli increases and abundant senescence-associated vesicles containing electronically dense particles emerge from chloroplasts pouring their content into the central vacuole. This study examines quinoa leaf tissues during development and senescence using a range of well-established markers of programmed cell death (PCD), including: morphological changes in nuclei and chloroplasts, degradation of RuBisCO, changes in chlorophyll content, DNA degradation, variations in ploidy levels, and changes in nuclease profiles. TUNEL reaction and DNA electrophoresis demonstrated that DNA fragmentation in nuclei occurs at early senescence, which correlates with induction of specific nucleases. During senescence, metabolic activity is high and nuclei endoreduplicate, peaking at 4C. At this time, TEM images showed some healthy nuclei with condensed chromatin and nucleoli. We have found that DNA fragmentation, induction of senescence-associated nucleases and endoreduplication take place during leaf senescence. This provides a starting point for further research aiming to identify key genes involved in the senescence of quinoa leaves. Published by Elsevier Ireland Ltd.

Why the racial gap in life expectancy is declining in the United States

Science.gov (United States)

Firebaugh, Glenn; Acciai, Francesco; Noah, Aggie J.; Prather, Christopher; Nau, Claudia

2014-01-01

BACKGROUND Blacks have lower life expectancy than whites in the United States. That disparity could be due to racial differences in the causes of death, with blacks being more likely to die of causes that affect the young, or it could be due to differences in the average ages of blacks and whites who die of the same cause. Prior studies fail to distinguish these two possibilities. OBJECTIVE In this study we determine how much of the 2000–10 reduction in the racial gap in life expectancy resulted from narrowing differences in the cause-specific mean age at death for blacks and whites, as opposed to changing cause-specific probabilities for blacks and whites. METHOD We introduce a method for separating the difference-in-probabilities and difference-inage components of group disparities in life expectancy. RESULTS Based on the new method, we find that 60% of the decline in the racial gap in life expectancy from 2000 to 2010 was attributable to reduction in the age component, largely because of declining differences in the age at which blacks and whites die of chronic diseases. CONCLUSION Our findings shed light on the sources of the declining racial gap in life expectancy in the United States, and help to identify where advances need to be made to achieve the goal of eliminating racial disparities in life expectancy. PMID:25580083

Why the racial gap in life expectancy is declining in the United States

Directory of Open Access Journals (Sweden)

Glenn Firebaugh

2014-10-01

Full Text Available Background: Blacks have lower life expectancy than whites in the United States. That disparity could be due to racial differences in the causes of death, with blacks being more likely to die of causes that affect the young, or it could be due to differences in the average ages of blacks and whites who die of the same cause. Prior studies fail to distinguish these two possibilities. Objective: In this study we determine how much of the 2000-10 reduction in the racial gap in life expectancy resulted from narrowing differences in the cause-specific mean age at death for blacks and whites, as opposed to changing cause-specific probabilities for blacks and whites. Methods: We introduce a method for separating the difference-in-probabilities and difference-in-age components of group disparities in life expectancy. Results: Based on the new method, we find that 60Š of the decline in the racial gap in life expectancy from 2000 to 2010 was attributable to reduction in the age component, largely because of declining differences in the age at which blacks and whites die of chronic diseases. Conclusions: Our findings shed light on the sources of the declining racial gap in life expectancy in the United States, and help to identify where advances need to be made to achieve the goal of eliminating racial disparities in life expectancy.

Swedish medical students' expectations of their future life.

OpenAIRE

Diderichsen, S.; Andersson, J.; Johansson, E.E.; Verdonk, P.; Lagro-Janssen, T.; Hamberg, K.

2011-01-01

Objectives: To investigate future life expectations among male and female medical students in their first and final year. Methods: The study was cross-sectional and conducted at a Swedish medical school. Out of 600 invited students, 507 (85%) answered an open-ended question about their future life, 298 (59%) first-year students and 209 (41%) last-year students. Women constituted 60% of the respondents. A mixed model design was applied; qualitative content analysis was utilized to create stati...

Strategy for determining life expectancy in mechanical components in an overall system

International Nuclear Information System (INIS)

Tenckhoff, E.; Erve, M.

1990-01-01

The safety standard at a nuclear power station achieved at the time of commissioning on the basis of the state of the art during the design and construction stage has to be maintained over the entire working life of the unit. Original design life expectancy is under review in the light of new safety experience and developments. The results of such analysis can serve not only preventive maintenance purposes but also as the basis for supporting and extending the planned or approved working life; they help increase availability. A comprehensive analysis strategy to establish the actual condition and residual life expectancy of components, systems and complete units has been developed by Siemens/KWU. The results of this analysis can lead to action to extend the life expectancy of components and systems and improvements in systems and subsystems. This report quotes a number of examples. 6 figs

Corroboration of the J-value model for life-expectancy growth in industrialised countries

OpenAIRE

Thomas, Philip

2017-01-01

After including an allowance for the gap between male and female life expectancies at birth diminishing over the past 50 years in industrialized countries, the J-value model incorporating “male catch-up” has been validated against actual UK data on life expectancy. A close correspondence has also been found between forecasts for life expectancy at birth in 35 countries made by the J-value model and those produced in a recent study that applied Bayesian model averaging to 21 demographic projec...

Faster Increases in Human Life Expectancy Could Lead to Slower Population Aging

Science.gov (United States)

2015-01-01

Counterintuitively, faster increases in human life expectancy could lead to slower population aging. The conventional view that faster increases in human life expectancy would lead to faster population aging is based on the assumption that people become old at a fixed chronological age. A preferable alternative is to base measures of aging on people’s time left to death, because this is more closely related to the characteristics that are associated with old age. Using this alternative interpretation, we show that faster increases in life expectancy would lead to slower population aging. Among other things, this finding affects the assessment of the speed at which countries will age. PMID:25876033

CIRCADIAN CLOCK-ASSOCIATED 1 Inhibits Leaf Senescence in Arabidopsis

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Yi Song

2018-03-01

Full Text Available Leaf senescence is an integral part of plant development, and the timing and progressing rate of senescence could substantially affect the yield and quality of crops. It has been known that a circadian rhythm synchronized with external environmental cues is critical for the optimal coordination of various physiological and metabolic processes. However, the reciprocal interactions between the circadian clock and leaf senescence in plants remain unknown. Here, through measuring the physiological and molecular senescence related markers of several circadian components mutants, we found that CIRCADIAN CLOCK-ASSOCIATED 1 inhibits leaf senescence. Further molecular and genetic studies revealed that CCA1 directly activates GLK2 and suppresses ORE1 expression to counteract leaf senescence. As plants age, the expression and periodic amplitude of CCA1 declines and thus weakens the inhibition of senescence. Our findings reveal an age-dependent circadian clock component of the process of leaf senescence.

Forecasting the Effects of Obesity and Smoking on U.S. Life Expectancy

OpenAIRE

Stewart, Susan T.; Cutler, David M.; Rosen, Allison B.

2009-01-01

Background: While increases in obesity over the past 30 years have adversely affected population health, there have been concomitant improvements due to reductions in smoking. Better understanding of the joint effects of these trends on longevity and quality of life will help policymakers target resources more efficiently. Methods: For each year from 2005 to 2020, we forecast life expectancy and qualityadjusted life expectancy for a representative 18 year old, assuming a continuation of past...

Decomposing changes in life expectancy: Compression versus shifting mortality

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Marie-Pier Bergeron-Boucher

2015-09-01

Full Text Available Background: In most developed countries, mortality reductions in the first half of the 20th century were highly associated with changes in lifespan disparities. In the second half of the 20th century, changes in mortality are best described by a shift in the mortality schedule, with lifespan variability remaining nearly constant. These successive mortality dynamics are known as compression and shifting mortality, respectively. Objective: To understand the effect of compression and shifting dynamics on mortality changes, we quantify the gains in life expectancy due to changes in lifespan variability and changes in the mortality schedule, respectively. Methods: We introduce a decomposition method using newly developed parametric expressions of the force of mortality that include the modal age at death as one of their parameters. Our approach allows us to differentiate between the two underlying processes in mortality and their dynamics. Results: An application of our methodology to the mortality of Swedish females shows that, since the mid-1960s, shifts in the mortality schedule were responsible for more than 70Š of the increase in life expectancy. Conclusions: The decomposition method allows differentiation between both underlying mortality processes and their respective impact on life expectancy, and also determines when and how one process has replaced the other.

Senescent mouse cells fail to overtly regulate the HIRA histone chaperone and do not form robust Senescence Associated Heterochromatin Foci

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Enders Greg H

2010-06-01

Full Text Available Abstract Background Cellular senescence is a permanent growth arrest that occurs in response to cellular stressors, such as telomere shortening or activation of oncogenes. Although the process of senescence growth arrest is somewhat conserved between mouse and human cells, there are some critical differences in the molecular pathways of senescence between these two species. Recent studies in human fibroblasts have defined a cell signaling pathway that is initiated by repression of a specific Wnt ligand, Wnt2. This, in turn, activates a histone chaperone HIRA, and culminates in formation of specialized punctate domains of facultative heterochromatin, called Senescence-Associated Heterochromatin Foci (SAHF, that are enriched in the histone variant, macroH2A. SAHF are thought to repress expression of proliferation-promoting genes, thereby contributing to senescence-associated proliferation arrest. We asked whether this Wnt2-HIRA-SAHF pathway is conserved in mouse fibroblasts. Results We show that mouse embryo fibroblasts (MEFs and mouse skin fibroblasts, do not form robust punctate SAHF in response to an activated Ras oncogene or shortened telomeres. However, senescent MEFs do exhibit elevated levels of macroH2A staining throughout the nucleus as a whole. Consistent with their failure to fully activate the SAHF assembly pathway, the Wnt2-HIRA signaling axis is not overtly regulated between proliferating and senescent mouse cells. Conclusions In addition to the previously defined differences between mouse and human cells in the mechanisms and phenotypes associated with senescence, we conclude that senescent mouse and human fibroblasts also differ at the level of chromatin and the signaling pathways used to regulate chromatin. These differences between human and mouse senescence may contribute to the increased propensity of mouse fibroblasts (and perhaps other mouse cell types to become immortalized and transformed, compared to human cells.

Evolution of senescence in nature: physiological evolution in populations of garter snake with divergent life histories.

Science.gov (United States)

Robert, Kylie A; Bronikowski, Anne M

2010-02-01

Evolutionary theories of aging are linked to life-history theory in that age-specific schedules of reproduction and survival determine the trajectory of age-specific mutation/selection balances across the life span and thus the rate of senescence. This is predicted to manifest at the organismal level in the evolution of energy allocation strategies of investing in somatic maintenance and robust stress responses in less hazardous environments in exchange for energy spent on growth and reproduction. Here we report experiments from long-studied populations of western terrestrial garter snakes (Thamnophis elegans) that reside in low and high extrinsic mortality environments, with evolved long and short life spans, respectively. Laboratory common-environment colonies of these two ecotypes were tested for a suite of physiological traits after control and stressed gestations. In offspring derived from control and corticosterone-treated dams, we measured resting metabolism; mitochondrial oxygen consumption, ATP and free radical production rates; and erythrocyte DNA damage and repair ability. We evaluated whether these aging biomarkers mirrored the evolution of life span and whether they were sensitive to stress. Neonates from the long-lived ecotype (1) were smaller, (2) consumed equal amounts of oxygen when corrected for body mass, (3) had DNA that damaged more readily but repaired more efficiently, and (4) had more efficient mitochondria and more efficient cellular antioxidant defenses than short-lived snakes. Many ecotype differences were enhanced in offspring derived from stress-treated dams, which supports the conclusion that nongenetic maternal effects may further impact the cellular stress defenses of offspring. Our findings reveal that physiological evolution underpins reptilian life histories and sheds light on the connectedness between stress response and aging pathways in wild-dwelling organisms.

Life Expectancy in Police Officers: A Comparison with the U.S. General Population

Science.gov (United States)

Violanti, John M.; Hartley, Tara A.; Gu, Ja K.; Fekedulegn, Desta; Andrew, Michael E.; Burchfiel, Cecil M.

2016-01-01

Previous epidemiological research indicates that police officers have an elevated risk of death relative to the general population overall and for several specific causes. Despite the increased risk for mortality found in previous research, controversy still exists over the life expectancy of police officers. The goal of the present study was to compare life expectancy of male police officers from Buffalo New York with the U.S. general male population utilizing an abridged life table method. On average, the life expectancy of Buffalo police officers in our sample was significantly lower than the U.S. population (mean difference in life expectancy =21.9 years; 95% CI: 14.5-29.3; ppolice officers was shorter and differences were more pronounced in younger age categories. Additionally, police officers had a significantly higher average probability of death than did males in the general population (mean difference= 0.40; 95% CI: 0.26,-0.54; ppolice officers was 21 times larger than that of the general population (Buffalo male officers vs. U.S. males = 21.7, 95% CI: 5.8-37.7). Possible reasons for shorter life expectancy among police are discussed, including stress, shift work, obesity, and hazardous environmental work exposures. PMID:24707585

Forging a signature of in vivo senescence.

Science.gov (United States)

Sharpless, Norman E; Sherr, Charles J

2015-07-01

'Cellular senescence', a term originally defining the characteristics of cultured cells that exceed their replicative limit, has been broadened to describe durable states of proliferative arrest induced by disparate stress factors. Proposed relationships between cellular senescence, tumour suppression, loss of tissue regenerative capacity and ageing suffer from lack of uniform definition and consistently applied criteria. Here, we highlight caveats in interpreting the importance of suboptimal senescence-associated biomarkers, expressed either alone or in combination. We advocate that more-specific descriptors be substituted for the now broadly applied umbrella term 'senescence' in defining the suite of diverse physiological responses to cellular stress.

Drying without senescence in resurrection plants

Science.gov (United States)

Griffiths, Cara A.; Gaff, Donald F.; Neale, Alan D.

2014-01-01

Research into extreme drought tolerance in resurrection plants using species such as Craterostigma plantagineum, C. wilmsii, Xerophyta humilis, Tortula ruralis, and Sporobolus stapfianus has provided some insight into the desiccation tolerance mechanisms utilized by these plants to allow them to persist under extremely adverse environmental conditions. Some of the mechanisms used to ensure cellular preservation during severe dehydration appear to be peculiar to resurrection plants. Apart from the ability to preserve vital cellular components during drying and rehydration, such mechanisms include the ability to down-regulate growth-related metabolism rapidly in response to changes in water availability, and the ability to inhibit dehydration-induced senescence programs enabling reconstitution of photosynthetic capacity quickly following a rainfall event. Extensive research on the molecular mechanism of leaf senescence in non-resurrection plants has revealed a multi-layered regulatory network operates to control programed cell death pathways. However, very little is known about the molecular mechanisms that resurrection plants employ to avoid undergoing drought-related senescence during the desiccation process. To survive desiccation, dehydration in the perennial resurrection grass S. stapfianus must proceed slowly over a period of 7 days or more. Leaves detached from the plant before 60% relative water content (RWC) is attained are desiccation-sensitive indicating that desiccation tolerance is conferred in vegetative tissue of S. stapfianus when the leaf RWC has declined to 60%. Whilst some older leaves remaining attached to the plant during dehydration will senesce, suggesting dehydration-induced senescence may be influenced by leaf age or the rate of dehydration in individual leaves, the majority of leaves do not senesce. Rather these leaves dehydrate to air-dryness and revive fully following rehydration. Hence it seems likely that there are genes expressed in

Life Expectancy and Economic Growth : The Role of the Demographic Transition

OpenAIRE

Cervellati, Matteo; Sunde, Uwe

2011-01-01

In this paper we investigate the causal effect of life expectancy on economic growth by explicitly accounting for the role of the demographic transition. In addition to focusing on issues of empirical identification, this paper emphasizes the role of the econometric specification. We present a simple theory of the economic and demographic transition where individuals' education and fertility decisions depend on their life expectancy. The theory predicts that before the demographic transition ...

Question order sensitivity of subjective well-being measures: focus on life satisfaction, self-rated health, and subjective life expectancy in survey instruments.

Science.gov (United States)

Lee, Sunghee; McClain, Colleen; Webster, Noah; Han, Saram

2016-10-01

This study examines the effect of question context created by order in questionnaires on three subjective well-being measures: life satisfaction, self-rated health, and subjective life expectancy. We conducted two Web survey experiments. The first experiment (n = 648) altered the order of life satisfaction and self-rated health: (1) life satisfaction asked immediately after self-rated health; (2) self-rated health immediately after life satisfaction; and (3) two items placed apart. We examined their correlation coefficient by experimental condition and further examined its interaction with objective health. The second experiment (n = 479) asked life expectancy before and after parental mortality questions. Responses to life expectancy were compared by order using ANOVA, and we examined interaction with parental mortality status using ANCOVA. Additionally, response time and probes were examined. Correlation coefficients between self-rated health and life satisfaction differed significantly by order: 0.313 (life satisfaction first), 0.508 (apart), and 0.643 (self-rated health first). Differences were larger among respondents with chronic conditions. Response times were the shortest when self-rated health was asked first. When life expectancy asked after parental mortality questions, respondents reported considering parents more for answering life expectancy; and respondents with deceased parents reported significantly lower expectancy, but not those whose parents were alive. Question context effects exist. Findings suggest placing life satisfaction and self-rated health apart to avoid artificial attenuation or inflation in their association. Asking about parental mortality prior to life expectancy appears advantageous as this leads respondents to consider parental longevity more, an important factor for true longevity.

A comparison of different methods for decomposition of changes in expectation of life at birth and differentials in life expectancy at birth

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P. K. Murthy

2005-04-01

Full Text Available Several methods were proposed to decompose the difference between two life expectancies at birth into the contribution by different age groups. In this study an attempt has been made to compare different methods with that of Chandra Sekar (1949 method. The methodologies suggested by Arriaga, Lopez and Ruzicka and Pollard have been extended. It is shown that all the three methods and also Chandra Sekar method in their modified (symmetrical form will be seen to produce the same result as that of United Nations, Pollard, Andreev and Pressat. Finally it is suggested to use symmetric formulae of the above methods because the percent contribution of total of the interaction terms to the difference in the life expectancy at birth is observed to be very negligible.

MicroRNA Regulation of Ionizing Radiation-Induced Premature Senescence

International Nuclear Information System (INIS)

Wang Yong; Scheiber, Melissa N.; Neumann, Carola; Calin, George A.; Zhou Daohong

2011-01-01

Purpose: MicroRNAs (miRNAs) have emerged as critical regulators of many cellular pathways. Ionizing radiation (IR) exposure causes DNA damage and induces premature senescence. However, the role of miRNAs in IR-induced senescence has not been well defined. Thus, the purpose of this study was to identify and characterize senescence-associated miRNAs (SA-miRNAs) and to investigate the role of SA-miRNAs in IR-induced senescence. Methods and Materials: In human lung (WI-38) fibroblasts, premature senescence was induced either by IR or busulfan (BU) treatment, and replicative senescence was accomplished by serial passaging. MiRNA microarray were used to identify SA-miRNAs, and real-time reverse transcription (RT)-PCR validated the expression profiles of SA-miRNAs in various senescent cells. The role of SA-miRNAs in IR-induced senescence was characterized by knockdown of miRNA expression, using anti-miRNA oligonucleotides or by miRNA overexpression through the transfection of pre-miRNA mimics. Results: We identified eight SA-miRNAs, four of which were up-regulated (miR-152, -410, -431, and -493) and four which were down-regulated (miR-155, -20a, -25, and -15a), that are differentially expressed in both prematurely senescent (induced by IR or BU) and replicatively senescent WI-38 cells. Validation of the expression of these SA-miRNAs indicated that down-regulation of miR-155, -20a, -25, and -15a is a characteristic miRNA expression signature of cellular senescence. Functional analyses revealed that knockdown of miR-155 or miR-20a, but not miR-25 or miR-15a, markedly enhanced IR-induced senescence, whereas ectopic overexpression of miR-155 or miR-20a significantly inhibited senescence induction. Furthermore, our studies indicate that miR-155 modulates IR-induced senescence by acting downstream of the p53 and p38 mitogen-activated protein kinase (MAPK) pathways and in part via regulating tumor protein 53-induced nuclear protein 1 (TP53INP1) expression. Conclusion: Our

Narrowing sex differences in life expectancy: regional variations, 1971-1991

Directory of Open Access Journals (Sweden)

Frank Trovato

2001-12-01

Full Text Available A number of industrialized nations have recently experienced some degrees of constriction in their long-standing sex differentials in life expectancy at birth. In this study we examine this phenomenon in the context of Canada’s regions between 1971 and 1991: Atlantic (Newfoundland, Nova Scotia, New Brunswick, Prince Edward Island; Quebec, Ontario, and the West (Manitoba, Saskatchewan, Alberta, British Columbia, Yukon and Northwest Territories. Decomposition analysis based on multiple decrement life tables is applied to address three questions: (1 Are there regional differentials in the degree of narrowing in the sex gap in life expectancy? (2 What is the relative contribution of major causes of death to observed sex differences in average length of life within and across regions? (3 How do the contributions of cause-of-death components vary across regions to either widen or narrow the sex gap in survival? It is shown that the magnitude of the sex gap is not uniform across the regions, though the differences are not large. The most important contributors to a narrowing of the sex gap in life expectancy are heart disease and external types of mortality (i.e., accidents, violence, and suicide, followed by lung cancer and other types of chronic conditions. In substantive terms these results indicate that over time men have been making sufficient gains in these causes of death as to narrow some of the gender gap in overall survival. Regions show similarity in these effects.

Senescence-associated β-galactosidase activity in the in vitro ovarian stromal fibroblasts

Directory of Open Access Journals (Sweden)

Lilian Chuaire-Noack

2011-04-01

Full Text Available A growing biological research field is the cellular senescence, a mechanism that has been associated, under certain circumstances, withmalignant transformation. Given the high incidence of ovarian cancerand its main origin from the ovarian surface epithelium, as well asthe possibility that an epithelial-mesenchymal transition occurs, weevaluated both the in vitro growth of stromal fibroblasts from the ovarian cortex and their β-galactosidase activity at pH 6,enzyme whose expression is considered as a marker of replicativesenescence. Methods: 48 samples of ovarian cortical fibroblasts fromdonors without a history of cancer were serially cultured untilthe end of their replicative life. β-galactosidase activity at pH 6was quantified in each passage by the chemiluminiscent method. Ascontrol, we used ovarian epithelial cell cultures from the samedonors. The enzyme activity was also evaluated in fibroblastspreviously induced to senescence by exposure to hydrogen peroxide.Results: The analysis of the enzyme activity and the replicativecapacity taken together showed that the fibroblast cultures reachedthe senescent state at passages 4-5, as what happened with the control epithelial cells. Fibroblasts induced to senescence showed high variability in the values of enzymatic activity. Conclusions:The similarity between both types of cells in reaching the senescent state deserves to be taken into account in relation to theepithelialmesenchymal transition that has been proposed to explaintheir behavior in the genesis of cancer arising from ovarian surfaceepithelium. Low β-galactosidase activity values at pH 6 would suggestpossible inactivation of the response pathways to oxidative stress.

Persistent Amplification of DNA Damage Signal Involved in Replicative Senescence of Normal Human Diploid Fibroblasts

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Masatoshi Suzuki

2012-01-01

Full Text Available Foci of phosphorylated histone H2AX and ATM are the surrogate markers of DNA double strand breaks. We previously reported that the residual foci increased their size after irradiation, which amplifies DNA damage signals. Here, we addressed whether amplification of DNA damage signal is involved in replicative senescence of normal human diploid fibroblasts. Large phosphorylated H2AX foci (>1.5 μm diameter were specifically detected in presenescent cells. The frequency of cells with large foci was well correlated with that of cells positive for senescence-associated β-galactosidase staining. Hypoxic cell culture condition extended replicative life span of normal human fibroblast, and we found that the formation of large foci delayed in those cells. Our immuno-FISH analysis revealed that large foci partially localized at telomeres in senescent cells. Importantly, large foci of phosphorylated H2AX were always colocalized with phosphorylated ATM foci. Furthermore, Ser15-phosphorylated p53 showed colocalization with the large foci. Since the treatment of senescent cells with phosphoinositide 3-kinase inhibitor, wortmannin, suppressed p53 phosphorylation, it is suggested that amplification of DNA damage signaling sustains persistent activation of ATM-p53 pathway, which is essential for replicative senescence.

Transcriptional profile of genes involved in ascorbate glutathione cycle in senescing leaves for an early senescence leaf (esl) rice mutant.

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Li, Zhaowei; Su, Da; Lei, Bingting; Wang, Fubiao; Geng, Wei; Pan, Gang; Cheng, Fangmin

2015-03-15

To clarify the complex relationship between ascorbate-glutathione (AsA-GSH) cycle and H2O2-induced leaf senescence, the genotype-dependent difference in some senescence-related physiological parameters and the transcript levels and the temporal patterns of genes involved in the AsA-GSH cycle during leaf senescence were investigated using two rice genotypes, namely, the early senescence leaf (esl) mutant and its wild type. Meanwhile, the triggering effect of exogenous H2O2 on the expression of OsAPX genes was examined using detached leaves. The results showed that the esl mutant had higher H2O2 level than its wild type at the initial stage of leaf senescence. At transcriptional level, the association of expression of various genes involved in the AsA-GSH cycle with leaf senescence was isoform dependent. For OsAPXs, the transcripts of two cytosolic OsAPX genes (OsAPX1 and OsAPX2), thylakoid-bound OsAPX8, chloroplastic OsAPX7 and peroxisomal OsAPX4 exhibited remarkable genotype-dependent variation in their expression levels and temporal patterns during leaf senescence, there were significantly increasing transcripts of OsAXP1 and OsAPX7, severely repressed transcripts of OsAPX4 and OsAPX8 for the esl rice at the initial leaf senescence. In contrast, the repressing transcript of OsAPX8 was highly sensitive to the increasing H2O2 level in the senescing rice leaves, while higher H2O2 concentration resulted in the enhancing transcripts of two cytosolic OsAPX genes, OsAPX7 transcript was greatly variable with different H2O2 concentrations and incubating duration, suggesting that the different OsAPXs isoforms played a complementary role in perceiving and scavenging H2O2 accumulation at various H2O2 concentrations during leaf senescence. Higher H2O2 level, increased AsA level, higher activities of APX and glutathione reductase (GR), and relatively stable GSH content during the entire sampling period in the leaves of esl mutant implied that a close interrelationship existed

The WRKY transcription factor family and senescence in switchgrass.

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Rinerson, Charles I; Scully, Erin D; Palmer, Nathan A; Donze-Reiner, Teresa; Rabara, Roel C; Tripathi, Prateek; Shen, Qingxi J; Sattler, Scott E; Rohila, Jai S; Sarath, Gautam; Rushton, Paul J

2015-11-09

Early aerial senescence in switchgrass (Panicum virgatum) can significantly limit biomass yields. WRKY transcription factors that can regulate senescence could be used to reprogram senescence and enhance biomass yields. All potential WRKY genes present in the version 1.0 of the switchgrass genome were identified and curated using manual and bioinformatic methods. Expression profiles of WRKY genes in switchgrass flag leaf RNA-Seq datasets were analyzed using clustering and network analyses tools to identify both WRKY and WRKY-associated gene co-expression networks during leaf development and senescence onset. We identified 240 switchgrass WRKY genes including members of the RW5 and RW6 families of resistance proteins. Weighted gene co-expression network analysis of the flag leaf transcriptomes across development readily separated clusters of co-expressed genes into thirteen modules. A visualization highlighted separation of modules associated with the early and senescence-onset phases of flag leaf growth. The senescence-associated module contained 3000 genes including 23 WRKYs. Putative promoter regions of senescence-associated WRKY genes contained several cis-element-like sequences suggestive of responsiveness to both senescence and stress signaling pathways. A phylogenetic comparison of senescence-associated WRKY genes from switchgrass flag leaf with senescence-associated WRKY genes from other plants revealed notable hotspots in Group I, IIb, and IIe of the phylogenetic tree. We have identified and named 240 WRKY genes in the switchgrass genome. Twenty three of these genes show elevated mRNA levels during the onset of flag leaf senescence. Eleven of the WRKY genes were found in hotspots of related senescence-associated genes from multiple species and thus represent promising targets for future switchgrass genetic improvement. Overall, individual WRKY gene expression profiles could be readily linked to developmental stages of flag leaves.

Life expectancy and life expectancy with disability of normal weight, overweight, and obese smokers and nonsmokers in Europe.

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Majer, Istvan M; Nusselder, Wilma J; Mackenbach, Johan P; Kunst, Anton E

2011-07-01

The goal of this study was to estimate life expectancy (LE) and LE with disability (LwD) among normal weight, overweight, and obese smokers and nonsmokers in Western Europe. Data from four waves (1998-2001) of the European Community Household Panel (ECHP) were used; a standardized multipurpose annual longitudinal survey. Self-reported health and socioeconomic information was collected repeatedly using uniform questionnaires for 66,331 individuals in nine countries. Health status was measured in terms of disability in daily activities. Multistate Markov (MSM) models were applied to obtain hazard ratios (HRs) and age-specific transition rates according to BMI and smoking status. Multistate life tables were computed using the predicted transition probabilities to estimate LE and LwD. Significant associations were observed between disability incidence and BMI (HR = 1.15 for overweight, HR = 1.64 for obese, compared to normal weight). The risk of mortality was negatively associated with overweight status among disabled (HR = 0.77). Overweight people had higher LE than people with normal-weight and obesity. Among women, overweight and obese nonsmokers expect 3.6 and 6.1 more years of LwD than normal weight persons, respectively. In contrast, daily smokers expect lower LE but a similar LwD. The same patterns were observed among people with high education and those with low education. To conclude, daily smoking is associated with mortality more than with disability, whereas obesity is associated with disability more than with mortality. The findings suggest that further tobacco control would contribute to increasing LE, while tackling the obesity epidemic is necessary to prevent an expansion of disability.

Life expectancy in individuals with type 2 diabetes: implications for annuities.

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Price, Hermione C; Clarke, Philip M; Gray, Alastair M; Holman, Rury R

2010-01-01

Insurance companies often offer people with diabetes ''enhanced impaired life annuity'' at preferential rates, in view of their reduced life expectancy. To assess the appropriateness of ''enhanced impaired life annuity'' rates for individuals with type 2 diabetes. Patients. There were 4026 subjects with established type 2 diabetes (but not known cardiovascular or other life-threatening diseases) enrolled into the UK Lipids in Diabetes Study. Measurements. Estimated individual life expectancy using the United Kingdom Prospective Diabetes Study (UKPDS) Outcomes Model. Subjects were a mean (SD) age of 60.7 (8.6) years, had a blood pressure of 141/83 (17/10) mm Hg, total cholesterol level of 4.5 (0.75) mmol/L, HDL cholesterol level of 1.2 (0.29) mmol/L, with median (interquartile range [IQR]) known diabetes duration of 6 (3-11) years, and HbA(1c) of 8.0% (7.2-9.0). Sixty-five percent were male, 91% white, 4% Afro-Caribbean, 5% Indian-Asian, and 15% current smokers. The UKPDS Outcomes Model median (IQR) estimated age at death was 76.6 (73.8-79.5) years compared with 81.6 (79.4-83.2) years, estimated using the UK Government Actuary's Department data for a general population of the same age and gender structure. The median (IQR) difference was 4.3 (2.8-6.1) years, a remaining life expectancy reduction of almost one quarter. The highest value annuity identified, which commences payments immediately for a 60-year-old man with insulin-treated type 2 diabetes investing 100,000, did not reflect this difference, offering 7.4K per year compared with 7.0K per year if not diabetic. The UK Government Actuary's Department data overestimate likely age at death in individuals with type 2 diabetes, and at present, ''enhanced impaired life annuity'' rates do not provide equity for people with type 2 diabetes. Using a diabetes-specific model to estimate life expectancy could provide valuable information to the annuity industry and permit more equitable annuity rates for those with type 2

Senescent intervertebral disc cells exhibit perturbed matrix homeostasis phenotype.

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Ngo, Kevin; Patil, Prashanti; McGowan, Sara J; Niedernhofer, Laura J; Robbins, Paul D; Kang, James; Sowa, Gwendolyn; Vo, Nam

2017-09-01

Aging greatly increases the risk for intervertebral disc degeneration (IDD) as a result of proteoglycan loss due to reduced synthesis and enhanced degradation of the disc matrix proteoglycan (PG). How disc matrix PG homeostasis becomes perturbed with age is not known. The goal of this study is to determine whether cellular senescence is a source of this perturbation. We demonstrated that disc cellular senescence is dramatically increased in the DNA repair-deficient Ercc1 -/Δ mouse model of human progeria. In these accelerated aging mice, increased disc cellular senescence is closely associated with the rapid loss of disc PG. We also directly examine PG homeostasis in oxidative damage-induced senescent human cells using an in vitro cell culture model system. Senescence of human disc cells treated with hydrogen peroxide was confirmed by growth arrest, senescence-associated β-galactosidase activity, γH2AX foci, and acquisition of senescence-associated secretory phenotype. Senescent human disc cells also exhibited perturbed matrix PG homeostasis as evidenced by their decreased capacity to synthesize new matrix PG and enhanced degradation of aggrecan, a major matrix PG. of the disc. Our in vivo and in vitro findings altogether suggest that disc cellular senescence is an important driver of PG matrix homeostatic perturbation and PG loss. Published by Elsevier B.V.

Oncogenic senescence: a multi-functional perspective

NARCIS (Netherlands)

Baker, D.J.; Alimirah, F.; Deursen, J.M.A. van; Campisi, J.; Hildesheim, J.

2017-01-01

Cellular senescence is defined as an irreversible growth arrest with the acquisition of a distinctive secretome. The growth arrest is a potent anticancer mechanism whereas the secretome facilitates wound healing, tissue repair, and development. The senescence response has also become increasingly

Cellular Senescence in Postmitotic Cells: Beyond Growth Arrest.

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Sapieha, Przemyslaw; Mallette, Frédérick A

2018-04-25

In mitotic cells, cellular senescence is a permanent state of G1 arrest, that may have evolved in parallel to apoptosis, to limit proliferation of damaged cells and oncogenesis. Recent studies have suggested that postmitotic cells are also capable of entering a state of senescence, although the repercussions of postmitotic cellular senescence (PoMiCS) on tissue health and function are currently ill-defined. In tissues made largely of post-mitotic cells, it is evolutionary advantageous to preserve cellular integrity and cellular senescence of post-mitotic cells may prevent stressor-induced tissue degeneration and promote tissue repair. Paradoxically, PoMiCS may also contribute to disease progression through the generation of inflammatory mediators, termed the senescence-associated secretory phenotype. Here, we discuss the potential roles of PoMiCS and propose to enlarge the current definition of cellular senescence to postmitotic terminally differentiated cells. Copyright © 2018 Elsevier Ltd. All rights reserved.

An economic analysis of life expectancy by gender with application to the United States.

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Leung, Michael C M; Zhang, Jie; Zhang, Junsen

2004-07-01

This paper presents an economic model to explain the behavior of life expectancy of both sexes. It explicitly examines the relationship between the gender gap in life expectancy and the gender gap in pay. It shows that as the latter narrows over the course of economic development, the former may initially expand but will eventually shrink. Simulation results from our model accord with the behavior of life expectancy for both sexes since the 1940s in the United States.

How long do centenarians survive? Life expectancy and maximum lifespan.

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Modig, K; Andersson, T; Vaupel, J; Rau, R; Ahlbom, A

2017-08-01

The purpose of this study was to explore the pattern of mortality above the age of 100 years. In particular, we aimed to examine whether Scandinavian data support the theory that mortality reaches a plateau at particularly old ages. Whether the maximum length of life increases with time was also investigated. The analyses were based on individual level data on all Swedish and Danish centenarians born from 1870 to 1901; in total 3006 men and 10 963 women were included. Birth cohort-specific probabilities of dying were calculated. Exact ages were used for calculations of maximum length of life. Whether maximum age changed over time was analysed taking into account increases in cohort size. The results confirm that there has not been any improvement in mortality amongst centenarians in the past 30 years and that the current rise in life expectancy is driven by reductions in mortality below the age of 100 years. The death risks seem to reach a plateau of around 50% at the age 103 years for men and 107 years for women. Despite the rising life expectancy, the maximum age does not appear to increase, in particular after accounting for the increasing number of individuals of advanced age. Mortality amongst centenarians is not changing despite improvements at younger ages. An extension of the maximum lifespan and a sizeable extension of life expectancy both require reductions in mortality above the age of 100 years. © 2017 The Association for the Publication of the Journal of Internal Medicine.

Accuracy of advanced cancer patients' life expectancy estimates: The role of race and source of life expectancy information.

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Trevino, Kelly M; Zhang, Baohui; Shen, Megan J; Prigerson, Holly G

2016-06-15

The objective of this study was to examine the source of advanced cancer patients' information about their prognosis and determine whether this source of information could explain racial disparities in the accuracy of patients' life expectancy estimates (LEEs). Coping With Cancer was a prospective, longitudinal, multisite study of terminally ill cancer patients followed until death. In structured interviews, patients reported their LEEs and the sources of these estimates (ie, medical providers, personal beliefs, religious beliefs, and other). The accuracy of LEEs was calculated through a comparison of patients' self-reported LEEs with their actual survival. The sample for this analysis included 229 patients: 31 black patients and 198 white patients. Only 39.30% of the patients estimated their life expectancy within 12 months of their actual survival. Black patients were more likely to have an inaccurate LEE than white patients. A minority of the sample (18.3%) reported that a medical provider was the source of their LEEs; none of the black patients (0%) based their LEEs on a medical provider. Black race remained a significant predictor of an inaccurate LEE, even after the analysis had been controlled for sociodemographic characteristics and the source of LEEs. The majority of advanced cancer patients have an inaccurate understanding of their life expectancy. Black patients with advanced cancer are more likely to have an inaccurate LEE than white patients. Medical providers are not the source of information for LEEs for most advanced cancer patients and especially for black patients. The source of LEEs does not explain racial differences in LEE accuracy. Additional research into the mechanisms underlying racial differences in prognostic understanding is needed. Cancer 2016;122:1905-12. © 2016 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons

Life expectancy and years of life lost in chronic obstructive pulmonary disease: Findings from the NHANES III Follow-up Study

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Robert M Shavelle

2009-03-01

Full Text Available Robert M Shavelle1, David R Paculdo1, Scott J Kush1, David M Mannino2, David J Strauss11Life Expectancy Project, San Francisco, CA, USA; 2Pulmonary Epidemiology Research Laboratory, University of Kentucky School of Medicine, Division of Pulmonary and Critical Care Medicine, Lexington, KY, USARationale: Previous studies have demonstrated that chronic obstructive pulmonary disease (COPD causes increased mortality in the general population. But life expectancy and the years of life lost have not been reported.Objectives: To quantify mortality, examine how it varies with age, sex, and other risk factors, and determine how life expectancy is affected.Methods: We constructed mortality models using the Third National Health and Nutrition Examination Survey, adjusting for age, sex, race, and major medical conditions. We used these to compute life expectancy and the years of life lost. Measurements and main results: Pulmonary function testing classifi ed patients as having Global Initiative on Obstructive Lung Disease (GOLD stage 0, 1, 2, 3 or 4 COPD or restriction. COPD is associated with only a modest reduction in life expectancy for never smokers, but with a very large reduction for current and former smokers. At age 65, the reductions in male life expectancy for stage 1, stage 2, and stages 3 or 4 disease in current smokers are 0.3 years, 2.2 years, and 5.8 years. These are in addition to the 3.5 years lost due to smoking. In former smokers the reductions are 1.4 years and 5.6 years for stage 2 and stages 3 or 4 disease, and in never smokers they are 0.7 and 1.3 years.Conclusions: Persons with COPD have an increased risk of mortality compared to those who do not, with consequent reduction in life expectancy. The effect is most marked in current smokers, and this is further reason for smokers to quit.Keywords: survival, mortality, longevity, COPD

CLCA2 as a p53-Inducible Senescence Mediator

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Chizu Tanikawa

2012-02-01

Full Text Available p53 is a tumor suppressor gene that is frequently mutated in multiple cancer tissues. Activated p53 protein regulates its downstream genes and subsequently inhibits malignant transformation by inducing cell cycle arrest, apoptosis, DNA repair, and senescence. However, genes involved in the p53-mediated senescence pathway are not yet fully elucidated. Through the screening of two genome-wide expression profile data sets, one for cells in which exogenous p53 was introduced and the other for senescent fibroblasts, we have identified chloride channel accessory 2 (CLCA2 as a p53-inducible senescence-associated gene. CLCA2 was remarkably induced by replicative senescence as well as oxidative stress in a p53-dependent manner. We also found that ectopically expressed CLCA2 induced cellular senescence, and the down-regulation of CLCA2 by small interfering RNA caused inhibition of oxidative stress-induced senescence. Interestingly, the reduced expression of CLCA2 was frequently observed in various kinds of cancers including prostate cancer, whereas its expression was not affected in precancerous prostatic intraepithelial neoplasia. Thus, our findings suggest a crucial role of p53/CLCA2-mediated senescence induction as a barrier for malignant transformation.

How many years of life did the fall of the Berlin Wall add? A projection of East German life expectancy.

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Vogt, Tobias C

2013-01-01

In the two decades since reunification, East Germans have experienced a large increase in life expectancy and a convergence with the West German mortality level. This gain in life expectancy appears even more impressive if we assume a different scenario in which the Berlin Wall did not fall, and the old East Germany still existed. This analysis takes into account that East German mortality would not have remained static without reunification. Thus, it shows how many years of life expectancy were actually added by the fall of the Berlin Wall. The analysis shows the improvements for single age groups by projecting life expectancy based on mortality levels during the 1970s and 1980s using the Lee-Carter method. I use national-level data for both sexes for East Germany before reunification. I find that, without reunification, current life expectancy at birth among East Germans would be 4.0 years lower for females and 5.7 years lower for males. I also show that older East Germans were the main demographic beneficiaries of reunification. Female and male mortality improvements in the age groups above 60 contributed up to 80% to the actual gains in life expectancy. Had the Berlin Wall not fallen, East German mortality would not have remained static but improved at a far slower rate. Thus, this counterfactual approach shows for the first time how many years of life were actually gained by reunification and how much of these gains were attributable to mortality improvements among the elderly. Copyright © 2013 S. Karger AG, Basel.

Political and social determinants of life expectancy in less developed countries: a longitudinal study

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Lin Ro-Ting

2012-01-01

Full Text Available Abstract Background This study aimed to examine the longitudinal contributions of four political and socioeconomic factors to the increase in life expectancy in less developed countries (LDCs between 1970 and 2004. Methods We collected 35 years of annual data for 119 LDCs on life expectancy at birth and on four key socioeconomic indicators: economy, measured by log10 gross domestic product per capita at purchasing power parity; educational environment, measured by the literacy rate of the adult population aged 15 years and over; nutritional status, measured by the proportion of undernourished people in the population; and political regime, measured by the regime score from the Polity IV database. Using linear mixed models, we analyzed the longitudinal effects of these multiple factors on life expectancy at birth with a lag of 0-10 years, adjusting for both time and regional correlations. Results The LDCs' increases in life expectancy over time were associated with all four factors. Political regime had the least influence on increased life expectancy to begin with, but became significant starting in the 3rd year and continued to increase, while the impact of the other socioeconomic factors began strong but continually decreased over time. The combined effects of these four socioeconomic and political determinants contributed 54.74% - 98.16% of the life expectancy gains throughout the lag periods of 0-10 years. Conclusions Though the effect of democratic politics on increasing life expectancy was relatively small in the short term when compared to the effects of the other socioeconomic factors, the long-term impact of democracy should not be underestimated.

PTTG1 attenuates drug-induced cellular senescence.

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Yunguang Tong

Full Text Available As PTTG1 (pituitary tumor transforming gene abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs. HCT116 cells devoid of PTTG1 (PTTG1(-/- exhibited enhanced drug sensitivity as assessed by measuring BrdU incorporation in vitro. Apoptosis, mitosis catastrophe or DNA damage were not detected, but features of senescence were observed using low doses of doxorubicin and TSA. The number of drug-induced PTTG1(-/- senescent cells increased ∼4 fold as compared to WT PTTG1-replete cells (p<0.001. p21, an important regulator of cell senescence, was induced ∼3 fold in HCT116 PTTG1(-/- cells upon doxorubicin or Trichostatin A treatment. Binding of Sp1, p53 and p300 to the p21 promoter was enhanced in PTTG1(-/- cells after treatment, suggesting transcriptional regulation of p21. p21 knock down abrogated the observed senescent effects of these drugs, indicating that PTTG1 likely suppresses p21 to regulate drug-induced senescence. PTTG1 also regulated SW620 colon cancer cells response to doxorubicin and TSA mediated by p21. Subcutaneously xenografted PTTG1(-/- HCT116 cells developed smaller tumors and exhibited enhanced responses to doxorubicin. PTTG1(-/- tumor tissue derived from excised tumors exhibited increased doxorubicin-induced senescence. As senescence is a determinant of cell responses to anti-neoplastic treatments, these findings suggest PTTG1 as a tumor cell marker to predict anti-neoplastic treatment outcomes.

Falling behind: life expectancy in US counties from 2000 to 2007 in an international context

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Ezzati Majid

2011-06-01

Full Text Available Abstract Background The United States health care debate has focused on the nation's uniquely high rates of lack of insurance and poor health outcomes relative to other high-income countries. Large disparities in health outcomes are well-documented in the US, but the most recent assessment of county disparities in mortality is from 1999. It is critical to tracking progress of health reform legislation to have an up-to-date assessment of disparities in life expectancy across counties. US disparities can be seen more clearly in the context of how progress in each county compares to international trends. Methods We use newly released mortality data by age, sex, and county for the US from 2000 to 2007 to compute life tables separately for each sex, for all races combined, for whites, and for blacks. We propose, validate, and apply novel methods to estimate recent life tables for small areas to generate up-to-date estimates. Life expectancy rates and changes in life expectancy for counties are compared to the life expectancies across nations in 2000 and 2007. We calculate the number of calendar years behind each county is in 2000 and 2007 compared to an international life expectancy time series. Results Across US counties, life expectancy in 2007 ranged from 65.9 to 81.1 years for men and 73.5 to 86.0 years for women. When compared against a time series of life expectancy in the 10 nations with the lowest mortality, US counties range from being 15 calendar years ahead to over 50 calendar years behind for men and 16 calendar years ahead to over 50 calendar years behind for women. County life expectancy for black men ranges from 59.4 to 77.2 years, with counties ranging from seven to over 50 calendar years behind the international frontier; for black women, the range is 69.6 to 82.6 years, with counties ranging from eight to over 50 calendar years behind. Between 2000 and 2007, 80% (men and 91% (women of American counties fell in standing against this

Leaf senescence and nutrient remobilisation in barley and wheat

DEFF Research Database (Denmark)

Gregersen, P L; Holm, P B; Krupinska, K

2008-01-01

Extensive studies have been undertaken on senescence processes in barley and wheat and their importance for the nitrogen use efficiency of these crop plants. During the senescence processes, proteins are degraded and nutrients are re-mobilised from senescing leaves to other organs, especially...... of chloroplasts is summarised. Rubisco is thought to be released from chloroplasts into vesicles containing stroma material (RCB = Rubisco-containing bodies). These vesicles may then take different routes for their degradation. Transcriptome analyses on barley and wheat senescence have identified genes involved...... in degradative, metabolic and regulatory processes that could be used in future strategies aimed at modifying the senescence process. The breeding of crops for characters related to senescence processes, e.g. higher yields and better nutrient use efficiency, is complex. Such breeding has to cope with the dilemma...

Evasion of Cell Senescence Leads to Medulloblastoma Progression

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Lukas Tamayo-Orrego

2016-03-01

Full Text Available How brain tumors progress from precancerous lesions to advanced cancers is not well understood. Using Ptch1+/− mice to study medulloblastoma progression, we found that Ptch1 loss of heterozygosity (LOH is an early event that is associated with high levels of cell senescence in preneoplasia. In contrast, advanced tumors have evaded senescence. Remarkably, we discovered that the majority of advanced medulloblastomas display either spontaneous, somatic p53 mutations or Cdkn2a locus inactivation. Consistent with senescence evasion, these p53 mutations are always subsequent to Ptch1 LOH. Introduction of a p53 mutation prevents senescence, accelerates tumor formation, and increases medulloblastoma incidence. Altogether, our results show that evasion of senescence associated with Ptch1 LOH allows progression to advanced tumors.

The impact of self-care education on life expectancy in acute coronary syndrome patients

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Mahshid Choobdari

2015-04-01

Conclusion: Hospitalized acute coronary syndrome patients have a lower levels of life expectancy. Their life expectancy can increase through providing them with self-care education, which will lead to their independence promotion and self-esteem.

Exercise Prevents Diet-Induced Cellular Senescence in Adipose Tissue.

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Schafer, Marissa J; White, Thomas A; Evans, Glenda; Tonne, Jason M; Verzosa, Grace C; Stout, Michael B; Mazula, Daniel L; Palmer, Allyson K; Baker, Darren J; Jensen, Michael D; Torbenson, Michael S; Miller, Jordan D; Ikeda, Yasuhiro; Tchkonia, Tamara; van Deursen, Jan M; Kirkland, James L; LeBrasseur, Nathan K

2016-06-01

Considerable evidence implicates cellular senescence in the biology of aging and chronic disease. Diet and exercise are determinants of healthy aging; however, the extent to which they affect the behavior and accretion of senescent cells within distinct tissues is not clear. Here we tested the hypothesis that exercise prevents premature senescent cell accumulation and systemic metabolic dysfunction induced by a fast-food diet (FFD). Using transgenic mice that express EGFP in response to activation of the senescence-associated p16(INK4a) promoter, we demonstrate that FFD consumption causes deleterious changes in body weight and composition as well as in measures of physical, cardiac, and metabolic health. The harmful effects of the FFD were associated with dramatic increases in several markers of senescence, including p16, EGFP, senescence-associated β-galactosidase, and the senescence-associated secretory phenotype (SASP) specifically in visceral adipose tissue. We show that exercise prevents the accumulation of senescent cells and the expression of the SASP while nullifying the damaging effects of the FFD on parameters of health. We also demonstrate that exercise initiated after long-term FFD feeding reduces senescent phenotype markers in visceral adipose tissue while attenuating physical impairments, suggesting that exercise may provide restorative benefit by mitigating accrued senescent burden. These findings highlight a novel mechanism by which exercise mediates its beneficial effects and reinforces the effect of modifiable lifestyle choices on health span. © 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

Global Trends in Life Expectancy: A Club Approach

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Ulla Lehmijoki

2009-01-01

Excluding the HIV prevalence rate from the threshold candidates re-allocates a considerable number of the members of the High AIDS club, indicating that incomes, literacy, and fertility are unable to predict AIDS completely. The similarity of economic and demographic conditions in the Low Literacy and High AIDS clubs, however, raises concerns about life expectancy convergence in the future.

Active life expectancy from annual follow-up data with missing responses.

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Izmirlian, G; Brock, D; Ferrucci, L; Phillips, C

2000-03-01

Active life expectancy (ALE) at a given age is defined as the expected remaining years free of disability. In this study, three categories of health status are defined according to the ability to perform activities of daily living independently. Several studies have used increment-decrement life tables to estimate ALE, without error analysis, from only a baseline and one follow-up interview. The present work conducts an individual-level covariate analysis using a three-state Markov chain model for multiple follow-up data. Using a logistic link, the model estimates single-year transition probabilities among states of health, accounting for missing interviews. This approach has the advantages of smoothing subsequent estimates and increased power by using all follow-ups. We compute ALE and total life expectancy from these estimated single-year transition probabilities. Variance estimates are computed using the delta method. Data from the Iowa Established Population for the Epidemiologic Study of the Elderly are used to test the effects of smoking on ALE on all 5-year age groups past 65 years, controlling for sex and education.

Location, vocation, procreation: how choice influences life expectancy in doctors.

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Holleyman, R; Vann Jones, S

2016-06-01

Stress and mortality are negatively correlated and it is generally accepted that certain professions are more stressful than others. Medical graduates begin as a relatively homogenous population who then choose vastly different career options making doctors an ideal population in which to try to assess whether job stress is likely to be causal to increased mortality. To establish the influence of various modifiable risk factors on the life expectancy of UK doctors. We analysed a decade of obituaries from the British Medical Journal published between January 2003 and December 2012. Data included age at death (AAD), specialty, region (deanery), marriage status and children. A total of 3068 obituaries were eligible for inclusion. Mean AAD was 78.5 years. Male sex was associated with a significantly increased AAD by an additional 3.8 years (95% CI 2.4-5.2 years, P affect life expectancy. While this does not necessarily reflect quality of life, the additional years of life gained from having extra children have a positive effect on your quantity of life. © The Author 2016. Published by Oxford University Press on behalf of the Society of Occupational Medicine. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Seasonal life history trade-offs in two leafwing butterflies: Delaying reproductive development increases life expectancy.

Science.gov (United States)

McElderry, Robert M

2016-04-01

Surviving inhospitable periods or seasons may greatly affect fitness. Evidence of this exists in the prevalence of dormant stages in the life cycles of most insects. Here I focused on butterflies with distinct seasonal morphological types (not a genetic polymorphism) in which one morphological type, or form, delays reproduction until favorable conditions return, while the other form develops in an environment that favors direct reproduction. For two butterflies, Anaea aidea and A. andria, I tested the hypothesis that the development of each seasonal form involves a differential allocation of resources to survival at eclosion. I assayed differences in adult longevity among summer and winter forms in either a warm, active environment or a cool, calm environment. Winter form adults lived 40 times longer than summer form but only in calm, cool conditions. The magnitude of this difference provided compelling evidence that the winter form body plan and metabolic strategy (i.e. resource conservatism) favor long term survival. This research suggests that winter form adults maintain lowered metabolic rate, a common feature of diapause, to conserve resources and delay senescence while overwintering. Copyright © 2016 Elsevier Ltd. All rights reserved.

Rough Set Theory based prognostication of life expectancy for terminally ill patients.

Science.gov (United States)

Gil-Herrera, Eleazar; Yalcin, Ali; Tsalatsanis, Athanasios; Barnes, Laura E; Djulbegovic, Benjamin

2011-01-01

We present a novel knowledge discovery methodology that relies on Rough Set Theory to predict the life expectancy of terminally ill patients in an effort to improve the hospice referral process. Life expectancy prognostication is particularly valuable for terminally ill patients since it enables them and their families to initiate end-of-life discussions and choose the most desired management strategy for the remainder of their lives. We utilize retrospective data from 9105 patients to demonstrate the design and implementation details of a series of classifiers developed to identify potential hospice candidates. Preliminary results confirm the efficacy of the proposed methodology. We envision our work as a part of a comprehensive decision support system designed to assist terminally ill patients in making end-of-life care decisions.

The emerging role of senescent cells in tissue homeostasis and pathophysiology

Directory of Open Access Journals (Sweden)

Kaoru Tominaga

2015-05-01

Full Text Available Cellular senescence is a state of permanent growth arrest and is thought to play a pivotal role in tumor suppression. Cellular senescence may play an important role in tumor suppression, wound healing, and protection against tissue fibrosis in physiological conditions in vivo. However, accumulating evidence that senescent cells may have harmful effects in vivo and may contribute to tissue remodeling, organismal aging, and many age-related diseases also exists. Cellular senescence can be induced by various intrinsic and extrinsic factors. Both p53/p21 and p16/RB pathways are important for irreversible growth arrest in senescent cells. Senescent cells secret numerous biologically active factors. This specific secretion phenotype by senescent cells may largely contribute to physiological and pathological consequences in organisms. Here I review the molecular basis of cell cycle arrest and the specific secretion phenotype in cellular senescence. I also summarize the current knowledge of the role of cellular senescence in vivo in physiological and pathological settings.

The Role of the S40 Gene Family in Leaf Senescence

Directory of Open Access Journals (Sweden)

Muhammad Jehanzeb

2017-10-01

Full Text Available Senescence affect different traits of plants, such as the ripening of fruit, number, quality and timing of seed maturation. While senescence is induced by age, growth hormones and different environmental stresses, a highly organized genetic mechanism related to substantial changes in gene expression regulates the process. Only a few genes associated to senescence have been identified in crop plants despite the vital significance of senescence for crop yield. The S40 gene family has been shown to play a role in leaf senescence. The barley HvS40 gene is one of the senescence marker genes which shows expression during age-dependent as well as dark-induced senescence. Like barley HvS40, the Arabidopsis AtS40-3 gene is also induced during natural senescence as well as in response to treatment with abscisic acid, salicylic acid, darkness and pathogen attack. It is speculated that rice OsS40 has a similar function in the leaf senescence of rice.

Life expectancies of South African adults starting antiretroviral treatment: collaborative analysis of cohort studies.

Science.gov (United States)

Johnson, Leigh F; Mossong, Joel; Dorrington, Rob E; Schomaker, Michael; Hoffmann, Christopher J; Keiser, Olivia; Fox, Matthew P; Wood, Robin; Prozesky, Hans; Giddy, Janet; Garone, Daniela Belen; Cornell, Morna; Egger, Matthias; Boulle, Andrew

2013-01-01

Few estimates exist of the life expectancy of HIV-positive adults receiving antiretroviral treatment (ART) in low- and middle-income countries. We aimed to estimate the life expectancy of patients starting ART in South Africa and compare it with that of HIV-negative adults. Data were collected from six South African ART cohorts. Analysis was restricted to 37,740 HIV-positive adults starting ART for the first time. Estimates of mortality were obtained by linking patient records to the national population register. Relative survival models were used to estimate the excess mortality attributable to HIV by age, for different baseline CD4 categories and different durations. Non-HIV mortality was estimated using a South African demographic model. The average life expectancy of men starting ART varied between 27.6 y (95% CI: 25.2-30.2) at age 20 y and 10.1 y (95% CI: 9.3-10.8) at age 60 y, while estimates for women at the same ages were substantially higher, at 36.8 y (95% CI: 34.0-39.7) and 14.4 y (95% CI: 13.3-15.3), respectively. The life expectancy of a 20-y-old woman was 43.1 y (95% CI: 40.1-46.0) if her baseline CD4 count was ≥ 200 cells/µl, compared to 29.5 y (95% CI: 26.2-33.0) if her baseline CD4 count was <50 cells/µl. Life expectancies of patients with baseline CD4 counts ≥ 200 cells/µl were between 70% and 86% of those in HIV-negative adults of the same age and sex, and life expectancies were increased by 15%-20% in patients who had survived 2 y after starting ART. However, the analysis was limited by a lack of mortality data at longer durations. South African HIV-positive adults can have a near-normal life expectancy, provided that they start ART before their CD4 count drops below 200 cells/µl. These findings demonstrate that the near-normal life expectancies of HIV-positive individuals receiving ART in high-income countries can apply to low- and middle-income countries as well. Please see later in the article for the Editors' Summary.

Life expectancies of South African adults starting antiretroviral treatment: collaborative analysis of cohort studies.

Directory of Open Access Journals (Sweden)

Leigh F Johnson

Full Text Available Few estimates exist of the life expectancy of HIV-positive adults receiving antiretroviral treatment (ART in low- and middle-income countries. We aimed to estimate the life expectancy of patients starting ART in South Africa and compare it with that of HIV-negative adults.Data were collected from six South African ART cohorts. Analysis was restricted to 37,740 HIV-positive adults starting ART for the first time. Estimates of mortality were obtained by linking patient records to the national population register. Relative survival models were used to estimate the excess mortality attributable to HIV by age, for different baseline CD4 categories and different durations. Non-HIV mortality was estimated using a South African demographic model. The average life expectancy of men starting ART varied between 27.6 y (95% CI: 25.2-30.2 at age 20 y and 10.1 y (95% CI: 9.3-10.8 at age 60 y, while estimates for women at the same ages were substantially higher, at 36.8 y (95% CI: 34.0-39.7 and 14.4 y (95% CI: 13.3-15.3, respectively. The life expectancy of a 20-y-old woman was 43.1 y (95% CI: 40.1-46.0 if her baseline CD4 count was ≥ 200 cells/µl, compared to 29.5 y (95% CI: 26.2-33.0 if her baseline CD4 count was <50 cells/µl. Life expectancies of patients with baseline CD4 counts ≥ 200 cells/µl were between 70% and 86% of those in HIV-negative adults of the same age and sex, and life expectancies were increased by 15%-20% in patients who had survived 2 y after starting ART. However, the analysis was limited by a lack of mortality data at longer durations.South African HIV-positive adults can have a near-normal life expectancy, provided that they start ART before their CD4 count drops below 200 cells/µl. These findings demonstrate that the near-normal life expectancies of HIV-positive individuals receiving ART in high-income countries can apply to low- and middle-income countries as well. Please see later in the article for the Editors' Summary.

Violence deaths and its impact on life expectancy: a comparison between Mexico and Brazil.

Science.gov (United States)

González-Pérez, Guillermo Julián; Vega-López, María Guadalupe; Souza, Edinilsa Ramos de; Pinto, Liana Wernersbach

2017-09-01

Using official data, this study analyzed violent deaths (homicide, suicide, events of undetermined intent and deaths due to legal intervention) in Brazil and Mexico in the three-year periods 2002-2004 and 2012-14, the impact of these causes of death on life expectancy in both countries and the role of the different age groups in years of life expectancy lost (YLEL). Abridged life tables were constructed for both countries for both periods. Temporary life expectancy and YLEL between zero and 80 years by selected causes and age groups were calculated for each triennium. The leading cause of YLEL among men was homicide in both periods in Brazil (1.5 years) and in the second period in Mexico (one year). Violent deaths (VD) accounted for around 16% of YLEL in Brazil and 13% in Mexico in 2012-2014. Among women, YLEL due to homicides and suicides showed the greatest relative increase in both countries, although VD accounted for barely 3% of total YLEL. The highest percentage of YLEL due to VDwas found among the 15 to 29 year age groups in both countries and for both sexes. The increase in rates of VD in Mexico, above all among young people, has curbed further increases in life expectancy in recent years, especially among men. Likewise, the high rates of VD in Brazil in both periods have hindered the growth of life expectancy.

Predatory senescence in ageing wolves.

Science.gov (United States)

MacNulty, Daniel R; Smith, Douglas W; Vucetich, John A; Mech, L David; Stahler, Daniel R; Packer, Craig

2009-12-01

It is well established that ageing handicaps the ability of prey to escape predators, yet surprisingly little is known about how ageing affects the ability of predators to catch prey. Research into long-lived predators has assumed that adults have uniform impacts on prey regardless of age. Here we use longitudinal data from repeated observations of individually-known wolves (Canis lupus) hunting elk (Cervus elaphus) in Yellowstone National Park to demonstrate that adult predatory performance declines with age and that an increasing ratio of senescent individuals in the wolf population depresses the rate of prey offtake. Because this ratio fluctuates independently of population size, predatory senescence may cause wolf populations of equal size but different age structure to have different impacts on prey populations. These findings suggest that predatory senescence is an important, though overlooked, factor affecting predator-prey dynamics.

Predatory senescence in aging wolves

Science.gov (United States)

MacNulty, Daniel R.; Smith, Douglas W.; Vucetich, John A.; Mech, L. David; Stahler, Daniel R.; Packer, Craig

2009-01-01

It is well established that ageing handicaps the ability of prey to escape predators, yet surprisingly little is known about how ageing affects the ability of predators to catch prey. Research into long-lived predators has assumed that adults have uniform impacts on prey regardless of age. Here we use longitudinal data from repeated observations of individually-known wolves (Canis lupus) hunting elk (Cervus elaphus) in Yellowstone National Park to demonstrate that adult predatory performance declines with age and that an increasing ratio of senescent individuals in the wolf population depresses the rate of prey offtake. Because this ratio fluctuates independently of population size, predatory senescence may cause wolf populations of equal size but different age structure to have different impacts on prey populations. These findings suggest that predatory senescence is an important, though overlooked, factor affecting predator-prey dynamics.

Protein oxidation and degradation during proliferative senescence of human MRC-5 fibroblasts.

Science.gov (United States)

Sitte, N; Merker, K; von Zglinicki, T; Grune, T

2000-03-01

One of the highlights of age-related changes of cellular metabolism is the accumulation of oxidized proteins. The aging process on a cellular level can be treated either as the ongoing proliferation until a certain number of cell divisions is reached (the Hayflick limit) or as the aging of nondividing cells, that is, the age-related changes in cells without proliferation. The present investigation was undertaken to reveal the changes in protein turnover, proteasome activity, and protein oxidation status during proliferative senescence. We were able to demonstrate that the activity of the cytosolic proteasomal system declines dramatically during the proliferative senescence of human MRC-5 fibroblasts. Regardless of the loss in activity, it could be demonstrated that there are no changes in the transcription and translation of proteasomal subunits. This decline in proteasome activity was accompanied by an increased concentration of oxidized proteins. Cells at higher proliferation stages were no longer able to respond with increased degradation of endogenous [(35)S]-Met-radiolabeled proteins after hydrogen peroxide- or quinone-induced oxidative stress. It could be demonstrated that oxidized proteins in senescent human MRC-5 fibroblasts are not as quickly removed as they are in young cells. Therefore, our study demonstrates that the accumulation of oxidized proteins and decline in protein turnover and activity of the proteasomal system are not only a process of postmitotic aging but also occur during proliferative senescence and result in an increased half-life of oxidized proteins.

Strigolactone Regulates Leaf Senescence in Concert with Ethylene in Arabidopsis.

Science.gov (United States)

Ueda, Hiroaki; Kusaba, Makoto

2015-09-01

Leaf senescence is not a passive degenerative process; it represents a process of nutrient relocation, in which materials are salvaged for growth at a later stage or to produce the next generation. Leaf senescence is regulated by various factors, such as darkness, stress, aging, and phytohormones. Strigolactone is a recently identified phytohormone, and it has multiple functions in plant development, including repression of branching. Although strigolactone is implicated in the regulation of leaf senescence, little is known about its molecular mechanism of action. In this study, strigolactone biosynthesis mutant strains of Arabidopsis (Arabidopsis thaliana) showed a delayed senescence phenotype during dark incubation. The strigolactone biosynthesis genes MORE AXIALLY GROWTH3 (MAX3) and MAX4 were drastically induced during dark incubation and treatment with the senescence-promoting phytohormone ethylene, suggesting that strigolactone is synthesized in the leaf during leaf senescence. This hypothesis was confirmed by a grafting experiment using max4 as the stock and Columbia-0 as the scion, in which the leaves from the Columbia-0 scion senesced earlier than max4 stock leaves. Dark incubation induced the synthesis of ethylene independent of strigolactone. Strigolactone biosynthesis mutants showed a delayed senescence phenotype during ethylene treatment in the light. Furthermore, leaf senescence was strongly accelerated by the application of strigolactone in the presence of ethylene and not by strigolactone alone. These observations suggest that strigolactone promotes leaf senescence by enhancing the action of ethylene. Thus, dark-induced senescence is regulated by a two-step mechanism: induction of ethylene synthesis and consequent induction of strigolactone synthesis in the leaf. © 2015 American Society of Plant Biologists. All Rights Reserved.

Moxie matters: associations of future orientation with active life expectancy.

Science.gov (United States)

Laditka, Sarah B; Laditka, James N

2017-10-01

Being oriented toward the future has been associated with better future health. We studied associations of future orientation with life expectancy and the percentage of life with disability. We used the Panel Study of Income Dynamics (n = 5249). Participants' average age in 1968 was 33.0. Six questions repeatedly measured future orientation, 1968-1976. Seven waves (1999-2011, 33,331 person-years) measured disability in activities of daily living for the same individuals, whose average age in 1999 was 64.0. We estimated monthly probabilities of disability and death with multinomial logistic Markov models adjusted for age, sex, race/ethnicity, childhood health, and education. Using the probabilities, we created large populations with microsimulation, measuring disability in each month for each individual, age 55 through death. Life expectancy from age 55 for white men with high future orientation was age 77.6 (95% confidence interval 75.5-79.0), 6.9% (4.9-7.2) of those years with disability; results with low future orientation were 73.6 (72.2-75.4) and 9.6% (7.7-10.7). Comparable results for African American men were 74.8 (72.9-75.3), 8.1 (5.6-9.3), 71.0 (69.6-72.8), and 11.3 (9.1-11.7). For women, there were no significant differences associated with levels of future orientation for life expectancy. For white women with high future orientation 9.1% of remaining life from age 55 was disabled (6.3-9.9), compared to 12.4% (10.2-13.2) with low future orientation. Disability results for African American women were similar but statistically significant only at age 80 and over. High future orientation during early to middle adult ages may be associated with better health in older age.

The effect of individual differences and manipulated life expectancies on the willingness to engage in sexual coercion.

Science.gov (United States)

Dunkel, Curtis S; Mathes, Eugene

2011-12-16

The role of the individual difference variables of mate value, short-term and long-term mating preferences, and life history strategy along with the manipulated variable of life expectancy were used to predict differences in the willingness to engage in sexually coercive behaviors. Short-term preferences and long-term preferences were correlated with the willingness to engage in sexual coercion at all life expectancies. Life history strategy was correlated with the willingness to engage in sexual coercion at only the shortest and longest life expectancies. Most importantly short-term and long-term mating preferences interacted with life expectancy to predict the willingness to engage in sexually coercive behaviors. Short life expectancies increased willingness in individuals with high short-term and low long-term preferences. The results are discussed in terms of the varying theories of sexual coercion with emphasis put on a life history approach.

Senescence and the pro-tumorigenic stroma.

Science.gov (United States)

Alspach, Elise; Fu, Yujie; Stewart, Sheila A

2013-01-01

Hayflick and Moorhead first described senescence in the late 1960's as a permanent growth arrest that primary cells underwent after a defined number of cellular divisions in culture. This observation gave rise to the hypothesis that cells contained an internal counting mechanism that limited cellular division and that this limit was an important barrier to cellular transformation. What began as an in vitro observation has led to an immense body of work that reaches into all fields of biology and is of particular interest in the areas of aging, tissue regeneration, and tumorigenesis. The initially simplistic view that senescence limits cellular division and contributes to aging while stymying tumorigenesis has now evolved into an important and complex biological process that has numerous caveats and often opposing effects on tumorigenesis. In this review, we limit our discussion to the complex role senescence plays in tumorigenesis. Throughout the review we attempt to draw many parallels to other systems including the role senescent cells play in the tumor microenvironment and their significant molecular and phenotypic similarities to cancer associated fibroblasts (CAFs).

The relationship between life expectancy and indexes of socioeconomy and nutrition at the prefectural level

OpenAIRE

Gao, Junke; Kakehashi, Masayuki

2006-01-01

It is well known that Japanese people have the longest life expectancy in the world at present. Variouspoints of view which focus on causal contexts are reported. The present study used a database at theprefectural level in Japan, which included Japanese life expectancy at birth, employment types of thehousehold, medical resources, medical expenses, and nutrition indexes in 2000. The purpose of the studywas to clarify the major related factors on Japanese life expectancy. The results suggest ...

Senescence rates in patients with end-stage renal disease

DEFF Research Database (Denmark)

Koopman, J J E; Rozing, M P; Kramer, Ada

2011-01-01

function of the Gompertz equation as a superior descriptor of senescence rate. Here, we tested both measures of the rate of senescence in a population of patients with end-stage renal disease. It is clinical dogma that patients on dialysis experience accelerated senescence, whereas those with a functional...

Molecular bases of cellular senescence: Hayflick phenomenon 50 years later

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Patrycja Sosińska

2016-03-01

Full Text Available Normal human somatic cells have strictly limited proliferative capacity and reach a state of senescence when it becomes exhausted. It is believed that senescence is a response to extensive and irreparable DNA injury, localized in telomeric and/or non-telomeric regions of the genome. Main cause of this damage is oxidative stress, increasing due to deteriorated function of mitochondria. Senescent cells accumulate in tissues during aging, which is causatively linked with the development of various pathologies in elderly individuals, including cancer. This paper, prepared exactly 50 years after Leonard Hayflick’s discovery of the relationship between cellular senescence and organismal aging is aimed at presenting the current knowledge about molecular determinants of senescence, with particular emphasis paid to the role of oxidative stress, effectors of senescence at the level of cell cycle, markers of this phenomenon, and the effect of senescent cells on the development of certain age-related diseases.

Use of NAP gene to manipulate leaf senescence in plants

Science.gov (United States)

Gan, Susheng; Guo, Yongfeng

2013-04-16

The present invention discloses transgenic plants having an altered level of NAP protein compared to that of a non-transgenic plant, where the transgenic plants display an altered leaf senescence phenotype relative to a non-transgenic plant, as well as mutant plants comprising an inactivated NAP gene, where mutant plants display a delayed leaf senescence phenotype compared to that of a non-mutant plant. The present invention also discloses methods for delaying leaf senescence in a plant, as well as methods of making a mutant plant having a decreased level of NAP protein compared to that of a non-mutant plant, where the mutant plant displays a delayed leaf senescence phenotype relative to a non-mutant plant. Methods for causing precocious leaf senescence or promoting leaf senescence in a plant are also disclosed. Also disclosed are methods of identifying a candidate plant suitable for breeding that displays a delayed leaf senescence and/or enhanced yield phenotype.

Factors affecting life expectancy: evidence from 1980-2009 data in Singapore, Malaysia, and Thailand.

Science.gov (United States)

Chan, Moon Fai; Devi, M Kamala

2015-03-01

The authors aim to examine the impact of demographic changes, socioeconomic inequality, and the availability of health care resources on life expectancy in Singapore, Malaysia, and Thailand. This is a cross-country study collecting annual data from 3 Southeast Asian countries from 1980 to 2008. Life expectancy is the dependent variable with demographics, socioeconomic status, and health care resources as the 3 main determinants. A structural equation model is used, and results show that the availability of more health care resources and higher levels of socioeconomic advantages are more likely to increase life expectancy. In contrast, demographic changes are more likely to increase life expectancy by way of health care resources. The authors suggest that more effort should be taken to expand and improve the coverage of health care programs to alleviate regional differences in health care use and improve the overall health status of people in these 3 Southeast Asian countries. © 2012 APJPH.

The Social Distribution of Health: Estimating Quality-Adjusted Life Expectancy in England.

Science.gov (United States)

Love-Koh, James; Asaria, Miqdad; Cookson, Richard; Griffin, Susan

2015-07-01

To model the social distribution of quality-adjusted life expectancy (QALE) in England by combining survey data on health-related quality of life with administrative data on mortality. Health Survey for England data sets for 2010, 2011, and 2012 were pooled (n = 35,062) and used to model health-related quality of life as a function of sex, age, and socioeconomic status (SES). Office for National Statistics mortality rates were used to construct life tables for age-sex-SES groups. These quality-of-life and length-of-life estimates were then combined to predict QALE as a function of these characteristics. Missing data were imputed, and Monte-Carlo simulation was used to estimate standard errors. Sensitivity analysis was conducted to explore alternative regression models and measures of SES. Socioeconomic inequality in QALE at birth was estimated at 11.87 quality-adjusted life-years (QALYs), with a sex difference of 1 QALY. When the socioeconomic-sex subgroups are ranked by QALE, a differential of 10.97 QALYs is found between the most and least healthy quintile groups. This differential can be broken down into a life expectancy difference of 7.28 years and a quality-of-life adjustment of 3.69 years. The methods proposed in this article refine simple binary quality-adjustment measures such as the widely used disability-free life expectancy, providing a more accurate picture of overall health inequality in society than has hitherto been available. The predictions also lend themselves well to the task of evaluating the health inequality impact of interventions in the context of cost-effectiveness analysis. Copyright © 2015 International Society for Pharmacoeconomics and Outcomes Research (ISPOR). Published by Elsevier Inc. All rights reserved.

The Contribution of Cytomegalovirus Infection to Immune Senescence Is Set by the Infectious Dose

Directory of Open Access Journals (Sweden)

Anke Redeker

2018-01-01

Full Text Available The relationship between human cytomegalovirus (HCMV infections and accelerated immune senescence is controversial. Whereas some studies reported a CMV-associated impaired capacity to control heterologous infections at old age, other studies could not confirm this. We hypothesized that these discrepancies might relate to the variability in the infectious dose of CMV occurring in real life. Here, we investigated the influence of persistent CMV infection on immune perturbations and specifically addressed the role of the infectious dose on the contribution of CMV to accelerated immune senescence. We show in experimental mouse models that the degree of mouse CMV (MCMV-specific memory CD8+ T cell accumulation and the phenotypic T cell profile are directly influenced by the infectious dose, and data on HCMV-specific T cells indicate a similar connection. Detailed cluster analysis of the memory CD8+ T cell development showed that high-dose infection causes a differentiation pathway that progresses faster throughout the life span of the host, suggesting a virus–host balance that is influenced by aging and infectious dose. Importantly, short-term MCMV infection in adult mice is not disadvantageous for heterologous superinfection with lymphocytic choriomeningitis virus (LCMV. However, following long-term CMV infection the strength of the CD8+ T cell immunity to LCMV superinfection was affected by the initial CMV infectious dose, wherein a high infectious dose was found to be a prerequisite for impaired heterologous immunity. Altogether our results underscore the importance of stratification based on the size and differentiation of the CMV-specific memory T cell pools for the impact on immune senescence, and indicate that reduction of the latent/lytic viral load can be beneficial to diminish CMV-associated immune senescence.

Innate immunity and cellular senescence: The good and the bad in the developmental and aged brain.

Science.gov (United States)

Santoro, Antonietta; Spinelli, Chiara Carmela; Martucciello, Stefania; Nori, Stefania Lucia; Capunzo, Mario; Puca, Annibale Alessandro; Ciaglia, Elena

2018-03-01

Ongoing studies evidence cellular senescence in undifferentiated and specialized cells from tissues of all ages. Although it is believed that senescence plays a wider role in several stress responses in the mature age, its participation in certain physiological and pathological processes throughout life is coming to light. The "senescence machinery" has been observed in all brain cell populations, including components of innate immunity (e.g., microglia and astrocytes). As the beneficial versus detrimental implications of senescence is an open question, we aimed to analyze the contribution of immune responses in regulatory mechanisms governing its distinct functions in healthy (development, organogenesis, danger patrolling events) and diseased brain (glioma, neuroinflammation, neurodeneration), and the putative connection between cellular and molecular events governing the 2 states. Particularly this review offers new insights into the complex roles of senescence both as a chronological event as age advances, and as a molecular mechanism of brain homeostasis through the important contribution of innate immune responses and their crosstalk with neighboring cells in brain parenchyma. We also highlight the impact of the recently described glymphatic system and brain lymphatic vasculature in the interplay between peripheral and central immune surveillance and its potential implication during aging. This will open new ways to understand brain development, its deterioration during aging, and the occurrence of several oncological and neurodegenerative diseases. ©2018 Society for Leukocyte Biology.

Predatory senescence in ageing wolves

Science.gov (United States)

MacNulty, D.R.; Smith, D.W.; Vucetich, J.A.; Mech, L.D.; Stahler, D.R.; Packer, C.

2009-01-01

It is well established that ageing handicaps the ability of prey to escape predators, yet surprisingly little is known about how ageing affects the ability of predators to catch prey. Research into long-lived predators has assumed that adults have uniform impacts on prey regardless of age. Here we use longitudinal data from repeated observations of individually-known wolves (Canis lupus) hunting elk (Cervus elaphus) in Yellowstone National Park to demonstrate that adult predatory performance declines with age and that an increasing ratio of senescent individuals in the wolf population depresses the rate of prey offtake. Because this ratio fluctuates independently of population size, predatory senescence may cause wolf populations of equal size but different age structure to have different impacts on prey populations. These findings suggest that predatory senescence is an important, though overlooked, factor affecting predator-prey dynamics. ?? 2009 Blackwell Publishing Ltd/CNRS.

Oxygen concentration modulates cellular senescence and autophagy in human trophoblast cells.

Science.gov (United States)

Seno, Kotomi; Tanikawa, Nao; Takahashi, Hironori; Ohkuchi, Akihide; Suzuki, Hirotada; Matsubara, Shigeki; Iwata, Hisataka; Kuwayama, Takehito; Shirasuna, Koumei

2018-02-15

We investigated the effect of oxygen concentrations on cellular senescence and autophagy and examined the role of autophagy in human trophoblast cells. Human first-trimester trophoblast cells (Sw.71) were incubated under 21%, 5%, or 1% O 2 concentrations for 24 hours. We examined the extent of senescence caused using senescence-associated β-galactosidase (SA-β-Gal) and senescence-associated secretory phenotype (SASP) as markers. Moreover, we examined the role of autophagy in causing cellular senescence using an autophagy inhibitor (3-methyladenine, 3MA). Physiological normoxia (5% O 2 ) decreased SA-β-Gal-positive cells and SASP including interleukin-6 (IL-6) and IL-8 compared with cultured cells in 21% O 2 . Pathophysiological hypoxia (1% O 2 ) caused cytotoxicity, including extracellular release of ATP and lactate dehydrogenase, and decreased senescence phenotypes. 3MA-treated trophoblast cells significantly suppressed senescence markers (SA-β-Gal-positive cells and SASP secretion) in O 2 -independent manner. We conclude that O 2 concentration modulates cellular senescence phenotypes regulating autophagy in the human trophoblast cells. Moreover, inhibiting autophagy suppresses cellular senescence, suggesting that autophagy contributes to oxygen stress-induced cellular senescence. © 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Is Post-Traumatic Stress Disorder Associated with Premature Senescence? A Review of the Literature

Science.gov (United States)

Lohr, James B.; Palmer, Barton W.; Eidt, Carolyn A.; Aailaboyina, Smitha; Mausbach, Brent T.; Wolkowitz, Owen M.; Thorp, Steven R.; Jeste, Dilip V.

2015-01-01

Post-Traumatic Stress Disorder (PTSD) has major public health significance. Evidence that PTSD may be associated with premature senescence (early or accelerated aging) would have major implications for quality of life and healthcare policy. We conducted a comprehensive review of published empirical studies relevant to early aging in PTSD. Our search included the PubMed, PsycINFO and PILOTS databases for empirical reports published since the year 2000 relevant to early senescence and PTSD, including: (1) biomarkers of senescence (leukocyte telomere length (LTL) and pro-inflammatory markers), (2) prevalence of senescence-associated medical conditions, and (3) mortality rates. All six studies examining LTL indicated reduced LTL in PTSD (pooled Cohen’s d = 0.76). We also found consistent evidence of increased pro-inflammatory markers in PTSD (mean Cohen’s ds), including C-reactive protein = 0.18, Interleukin-1 beta = 0.44, Interleukin-6 = 0.78, and tumor necrosis factor alpha = 0.81. The majority of reviewed studies also indicated increased medical comorbidity among several targeted conditions known to be associated with normal aging, including cardiovascular disease, type 2 diabetes mellitus, gastrointestinal ulcer disease, and dementia. We also found seven of 10 studies indicated PTSD to be associated with earlier mortality (average HR = 1.29). In short, evidence from multiple lines of investigation suggests that PTSD may be associated with a phenotype of accelerated senescence. Further research is critical to understand the nature of this association. There may be a need to re-conceptualize PTSD beyond the boundaries of mental illness, and instead as a full systemic disorder. PMID:25959921

Impact of HIV/AIDS mortality on South Africa's life expectancy and ...

African Journals Online (AJOL)

The study seeks to raise awareness and expand knowledge about the deleterious effect of HIV/AIDS mortality on South Africa's life expectancy, a country with a relatively high HIV/AIDS prevalence rate (19. percent). Using the multiple and associated single decrement life table techniques, the study estimates the total ...

Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse

NARCIS (Netherlands)

Demaria, Marco; O'Leary, Monique N.; Chang, Jianhui; Shao, Lijian; Liu, Su; Alimirah, Fatouma; Koenig, Kristin; Le, Catherine; Mitin, Natalia; Deal, Allison M.; Alston, Shani; Academia, Emmeline C.; Kilmarx, Sumner; Valdovinos, Alexis; Wang, Boshi; de Bruin, Alain; Kennedy, Brian K.; Melov, Simon; Zhou, Daohong; Sharpless, Norman E.; Muss, Hyman; Campisi, Judith

Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinfl ammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating cells nonspecifi cally, often with adverse reactions. In accord with prior

Healthy life expectancy and the correlates of self-rated health in Bangladesh in 1996 and 2002.

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Tareque, Md Ismail; Saito, Yasuhiko; Kawahara, Kazuo

2015-03-31

Life expectancy (LE) at birth has increased steadily in Bangladesh since its independence. When people live longer, quality of life becomes a central issue. This study examines whether healthy life expectancy (HLE) at ages 15, 25, 35, and 45 is keeping pace with LE at those ages between 1996 and 2002. It also seeks to investigate the correlates of self-rated health (SRH) in 1996 and 2002. We used data from the World Values Survey conducted in 1996 and 2002 among individuals 15 years and older. The Sullivan method was used to compute HLE. Socio-demographic differences and their association with different states of health were examined by chi-square and Pearson's correlation tests. Multiple linear regression models were fitted to examine the correlates of SRH. The results show that perceived health improved between 1996 and 2002. For males, statistically significant increases in the expected number of years lived in good SRH were found. Proportionally, in 2002, both males and females at ages 15, 25, 35 and 45 expected more life years in good health and fewer life years in fair and poor health than did their counterparts in 1996. Comparatively, males expected fewer life years spent in good health but a much larger proportion of expected life in good health than did females. Finally, in multivariate analyses, life satisfaction was the only factor found to be significantly and positively associated with SRH for males and females in both years, although in both years the association was much more pronounced for females than for males. This study documented changes in HLE during 1996-2002. Women outlive men, but they have a lower quality of life and are more likely to live a greater part of their remaining life in poor SRH. Life satisfaction as well as other significant factors associated with SRH should be promoted, with special attention given to women, to improve healthy life expectancy and the quality of life of the Bangladeshi people.

Age-related changes in somatic condition and reproduction in the Eurasian beaver: Resource history influences onset of reproductive senescence.

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Ruairidh D Campbell

Full Text Available Using 15 years of data from a stable population of wild Eurasian beavers (Castor fiber, we examine how annual and lifetime access to food resources affect individual age-related changes in reproduction and somatic condition. We found an age-related decline in annual maternal reproductive output, after a peak at age 5-6. Rainfall, an established negative proxy of annual resource availability for beavers, was consistently associated with lower reproductive output for females of all ages. In contrast, breeding territory quality, as a measure of local resource history over reproductive lifetimes, caused differences in individual patterns of reproductive senescence; animals from lower quality territories senesced when younger. Litter size was unrelated to maternal age, although adult body weight increased with age. In terms of resource effects, in poorer years but not in better years, older mothers produced larger offspring than did younger mothers, giving support to the constraint theory. Overall, our findings exemplify state-dependent life-history strategies, supporting an effect of resources on reproductive senescence, where cumulative differences in resource access, and not just reproductive strategy, mediate long-term reproductive trade-offs, consistent with the disposable soma and reproductive restraint theories. We propose that flexible life-history schedules could play a role in the dynamics of populations exhibiting reproductive skew, with earlier breeding opportunities leading to an earlier senescence schedule through resource dependent mechanisms.

Experience in determining the residual life expectancy of conventional thermal power stations

International Nuclear Information System (INIS)

Tolksdorf, E.

1990-01-01

A combination of computer analysis, degree of damage and approximate conversion to residual life expectancy gives acceptable results. There is considerable uncertainty in converting degree of damage to residual life expectancy, since structural component characteristics play a major role here. Structure damages play a major part in establishing the degree of damage. Damage categories are given, together with action if operations are to continue. Exhaustion calculations to TRD 508 are to be taken as conservative and as possible evidence of trends. 14 figs., 12 refs

Life expectancy gap between the Francophone majority and Anglophone minority of a Canadian population.

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Auger, Nathalie; Harper, Sam; Barry, Amadou D; Trempe, Normand; Daniel, Mark

2012-01-01

Language is an important determinant of health, but analyses of linguistic inequalities in mortality are scant, especially for Canadian linguistic groups with European roots. We evaluated the life expectancy gap between the Francophone majority and Anglophone minority of Québec, Canada, both over time and across major provincial areas. Arriaga's method was used to estimate the age and cause of death groups contributing to changes in the life expectancy gap at birth between 1989-1993 and 2002-2006, and to evaluate patterns across major provincial areas (metropolitan Montréal, other metropolitan centres, and small cities/rural areas). Life expectancy at birth was greater for Anglophones, but the gap decreased over time by 1.3 years (52% decline) in men and 0.9 years (47% decline) in women, due to relatively sharper reductions in Francophone mortality from several causes, except lung cancer which countered reductions in women. The life expectancy gap in 2002-2006 was widest in other metropolitan centres (men 5.1 years, women 3.2 years), narrowest in small cities/rural areas (men 0.8 years, women 0.7 years), and tobacco-related causes were the main contributors. Only young Anglophones time, but varied across areas of Québec. Tobacco-related causes accounted for the majority of the current life expectancy gap.

Forecasting the Effects of Obesity and Smoking on U.S. Life Expectancy

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Stewart, Susan T.; Cutler, David M.; Rosen, Allison B.

2015-01-01

Background Although increases in obesity over the past 30 years have adversely affected the health of the U.S. population, there have been concomitant improvements in health because of reductions in smoking. Having a better understanding of the joint effects of these trends on longevity and quality of life will facilitate more efficient targeting of health care resources. Methods For each year from 2005 through 2020, we forecasted life expectancy and quality-adjusted life expectancy for a representative 18-year-old, assuming a continuation of past trends in smoking (based on data from the National Health Interview Survey for 1978 through 1979, 1990 through 1991, 1999 through 2001, and 2004 through 2006) and past trends in body-mass index (BMI) (based on data from the National Health and Nutrition Examination Survey for 1971 through 1975, 1988 through 1994, 1999 through 2002, and 2003 through 2006). The 2003 Medical Expenditure Panel Survey was used to examine the effects of smoking and BMI on health-related quality of life. Results The negative effects of increasing BMI overwhelmed the positive effects of declines in smoking in multiple scenarios. In the base case, increases in the remaining life expectancy of a typical 18-year-old are held back by 0.71 years or 0.91 quality-adjusted years between 2005 and 2020. If all U.S. adults became nonsmokers of normal weight by 2020, we forecast that the life expectancy of an 18-year-old would increase by 3.76 life-years or 5.16 quality-adjusted years. Conclusions If past obesity trends continue unchecked, the negative effects on the health of the U.S. population will increasingly outweigh the positive effects gained from declining smoking rates. Failure to address continued increases in obesity could result in an erosion of the pattern of steady gains in health observed since early in the 20th century. PMID:19955525

Outcomes of Nordic mental health systems: life expectancy of patients with mental disorders

DEFF Research Database (Denmark)

Wahlbeck, Kristian; Westman, Jeanette; Nordentoft, Merete

2011-01-01

People with mental disorders evince excess mortality due to natural and unnatural deaths. The relative life expectancy of people with mental disorders is a proxy measure of effectiveness of social policy and health service provision.......People with mental disorders evince excess mortality due to natural and unnatural deaths. The relative life expectancy of people with mental disorders is a proxy measure of effectiveness of social policy and health service provision....

Members of the barley NAC transcription factor gene family show differential co-regulation with senescence-associated genes during senescence of flag leaves

DEFF Research Database (Denmark)

Christiansen, Michael W; Gregersen, Per L.

2014-01-01

-expressed with members of the NAC gene family. In conclusion, a list of up to 15 NAC genes from barley that are strong candidates for being regulatory factors of importance for senescence and biotic stress-related traits affecting the productivity of cereal crop plants has been generated. Furthermore, a list of 71...... in the NAC transcription factor family during senescence of barley flag leaves was studied. Several members of the NAC transcription factor gene family were up-regulated during senescence in a microarray experiment, together with a large range of senescence-associated genes, reflecting the coordinated...... activation of degradation processes in senescing barley leaf tissues. This picture was confirmed in a detailed quantitative reverse transcription–PCR (qRT–PCR) experiment, which also showed distinct gene expression patterns for different members of the NAC gene family, suggesting a group of ~15 out of the 47...

Senescence in the aging process [version 1; referees: 3 approved

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Richard GA Faragher

2017-07-01

Full Text Available The accumulation of ‘senescent’ cells has long been proposed to act as an ageing mechanism. These cells display a radically altered transcriptome and degenerative phenotype compared with their growing counterparts. Tremendous progress has been made in recent years both in understanding the molecular mechanisms controlling entry into the senescent state and in the direct demonstration that senescent cells act as causal agents of mammalian ageing. The challenges now are to gain a better understanding of how the senescent cell phenotype varies between different individuals and tissues, discover how senescence predisposes to organismal frailty, and develop mechanisms by which the deleterious effects of senescent cells can be ameliorated.

Physiology and molecular biology of petal senescence

NARCIS (Netherlands)

Doorn, van W.G.; Woltering, E.J.

2008-01-01

Petal senescence is reviewed, with the main emphasis on gene expression in relation to physiological functions. Autophagy seems to be the major mechanism for large-scale degradation of macromolecules, but it is still unclear if it contributes to cell death. Depending on the species, petal senescence

Comparative analyses of longevity and senescence reveal variable survival benefits of living in zoos across mammals.

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Tidière, Morgane; Gaillard, Jean-Michel; Berger, Vérane; Müller, Dennis W H; Bingaman Lackey, Laurie; Gimenez, Olivier; Clauss, Marcus; Lemaître, Jean-François

2016-11-07

While it is commonly believed that animals live longer in zoos than in the wild, this assumption has rarely been tested. We compared four survival metrics (longevity, baseline mortality, onset of senescence and rate of senescence) between both sexes of free-ranging and zoo populations of more than 50 mammal species. We found that mammals from zoo populations generally lived longer than their wild counterparts (84% of species). The effect was most notable in species with a faster pace of life (i.e. a short life span, high reproductive rate and high mortality in the wild) because zoos evidently offer protection against a number of relevant conditions like predation, intraspecific competition and diseases. Species with a slower pace of life (i.e. a long life span, low reproduction rate and low mortality in the wild) benefit less from captivity in terms of longevity; in such species, there is probably less potential for a reduction in mortality. These findings provide a first general explanation about the different magnitude of zoo environment benefits among mammalian species, and thereby highlight the effort that is needed to improve captive conditions for slow-living species that are particularly susceptible to extinction in the wild.

Senescence gives insights into the morphogenetic evolution of anamniotes

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Éric Villiard

2017-06-01

Full Text Available Senescence represents a mechanism to avoid undesired cell proliferation that plays a role in tumor suppression, wound healing and embryonic development. In order to gain insight on the evolution of senescence, we looked at its presence in developing axolotls (urodele amphibians and in zebrafish (teleost fish, which are both anamniotes. Our data indicate that cellular senescence is present in various developing structures in axolotls (pronephros, olfactory epithelium of nerve fascicles, lateral organs, gums and in zebrafish (epithelium of the yolk sac and in the lower part of the gut. Senescence was particularly associated with transient structures (pronephros in axolotls and yolk sac in zebrafish suggesting that it may play a role in the elimination of these tissues. Our data supports the notion that cellular senescence evolved early in vertebrate evolution to influence embryonic development.

Premature aging/senescence in cancer cells facing therapy: good or bad?

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Gonzalez, Llilians Calvo; Ghadaouia, Sabrina; Martinez, Aurélie; Rodier, Francis

2016-02-01

Normal and cancer cells facing their demise following exposure to radio-chemotherapy can actively participate in choosing their subsequent fate. These programmed cell fate decisions include true cell death (apoptosis-necroptosis) and therapy-induced cellular senescence (TIS), a permanent "proliferative arrest" commonly portrayed as premature cellular aging. Despite a permanent loss of proliferative potential, senescent cells remain viable and are highly bioactive at the microenvironment level, resulting in a prolonged impact on tissue architecture and functions. Cellular senescence is primarily documented as a tumor suppression mechanism that prevents cellular transformation. In the context of normal tissues, cellular senescence also plays important roles in tissue repair, but contributes to age-associated tissue dysfunction when senescent cells accumulate. Theoretically, in multi-step cancer progression models, cancer cells have already bypassed cellular senescence during their immortalization step (see hallmarks of cancer). It is then perhaps surprising to find that cancer cells often retain the ability to undergo TIS, or premature aging. This occurs because cellular senescence results from multiple signalling pathways, some retained in cancer cells, aiming to prevent cell cycle progression in damaged cells. Since senescent cancer cells persist after therapy and secrete an array of cytokines and growth factors that can modulate the tumor microenvironment, these cells may have beneficial and detrimental effects regarding immune modulation and survival of remaining proliferation-competent cancer cells. Similarly, while normal cells undergoing senescence are believed to remain indefinitely growth arrested, whether this is true for senescent cancer cells remains unclear, raising the possibility that these cells may represent a reservoir for cancer recurrence after treatment. This review discusses our current knowledge on cancer cell senescence and highlight questions

Gains in Life Expectancy Associated with Higher Education in Men

NARCIS (Netherlands)

Bijwaard, G.E.; van Poppel, F.W.A.; Ekamper, Peter; Lumey, L.H.

2015-01-01

Background Many studies show large differences in life expectancy across the range of education, intelligence, and socio-economic status. As educational attainment, intelligence, and socio-economic status are highly interrelated, appropriate methods are required to disentangle their separate

Targeting senescence cells in pancreatic cancer | IDRC ...

International Development Research Centre (IDRC) Digital Library (Canada)

Targeting senescence cells in pancreatic cancer. Cellular senescence is a programmed response to oncogenic (tumour-causing) stress that aims to halt the expansion of cells with malignant potential. It does this by stopping the proliferation of pre-cancerous lesions and recruitment of the immune system for their elimination.

Mortality and life expectancy of people with alcohol use disorder in Denmark, Finland and Sweden

DEFF Research Database (Denmark)

Westman, J; Wahlbeck, K; Laursen, T M

2014-01-01

OBJECTIVE: To analyse mortality and life expectancy in people with alcohol use disorder in Denmark, Finland and Sweden. METHOD: A population-based register study including all patients admitted to hospital diagnosed with alcohol use disorder (1 158 486 person-years) from 1987 to 2006 in Denmark......, Finland and Sweden. RESULTS: Life expectancy was 24-28 years shorter in people with alcohol use disorder than in the general population. From 1987 to 2006, the difference in life expectancy between patients with alcohol use disorder and the general population increased in men (Denmark, 1.8 years; Finland......, 2.6 years; Sweden, 1.0 years); in women, the difference in life expectancy increased in Denmark (0.3 years) but decreased in Finland (-0.8 years) and Sweden (-1.8 years). People with alcohol use disorder had higher mortality from all causes of death (mortality rate ratio, 3.0-5.2), all diseases...

Widening Life Expectancy Advantage of Hispanics in the United States: 1990-2010.

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Fenelon, Andrew; Blue, Laura

2015-08-01

We examine trends in the Hispanic longevity advantage between 1990 and 2010, focusing on the contribution of cigarette smoking. We calculate life expectancy at age 50 for Hispanics and non-Hispanic whites between 1990 and 2010. We use an indirect method to calculate the contribution of smoking to changes over time in life expectancy. Among women, the Hispanic advantage in life expectancy grows from 2.14 years in 1990 (95 % CI 1.99-2.30 years) to 3.53 years in 2010 (3.42-3.64 years). More than 40 % of this increase reflects widening differences in smoking-attributable mortality. The advantage for Hispanic men increases from 2.27 years (2.14-2.41 years) to 2.91 years (2.81-3.01 years), although smoking makes only a small contribution. Despite persistent disadvantage, US Hispanics have increased their longevity advantage over non-Hispanic whites since 1990, much of which reflects the continuing importance of cigarette smoking to the Hispanic advantage.

The search for evolutionary developmental origins of aging in zebrafish: a novel intersection of developmental and senescence biology in the zebrafish model system.

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Kishi, Shuji

2011-09-01

Senescence may be considered the antithesis of early development, but yet there may be factors and mechanisms in common between these two phenomena during the process of aging. We investigated whether any relationship exists between the regulatory mechanisms that function in early development and in senescence using the zebrafish (Danio rerio), a small freshwater fish and a useful model animal for genetic studies. We conducted experiments to isolate zebrafish mutants expressing an apparent senescence phenotype during embryogenesis (embryonic senescence). Some of the genes we thereby identified had already been associated with cellular senescence and chronological aging in other organisms, but many had not yet been linked to these processes. Complete loss-of-function of developmentally essential genes induce embryonic (or larval) lethality, whereas it seems like their partial loss-of-function (i.e., decrease-of-function by heterozygote or hypomorphic mutations) still remains sufficient to go through the early developmental process because of its adaptive plasticity or rather heterozygote advantage. However, in some cases, such partial loss-of-function of genes compromise normal homeostasis due to haploinsufficiency later in adult life having many environmental stress challenges. By contrast, any heterozygote-advantageous genes might gain a certain benefit(s) (much more fitness) by such partial loss-of-function later in life. Physiological senescence may evolutionarily arise from both genetic and epigenetic drifts as well as from losing adaptive developmental plasticity in face of stress signals from the external environment that interacts with functions of multiple genes rather than effects of only a single gene mutation or defect. Previously uncharacterized developmental genes may thus mediate the aging process and play a pivotal role in senescence. Moreover, unexpected senescence-related genes might also be involved in the early developmental process and

Arabidopsis CPR5 is a senescence-regulatory gene with pleiotropic functions as predicted by the evolutionary theory of senescence

NARCIS (Netherlands)

Jing, Hai-Chun; Anderson, Lisa; Sturre, Marcel J. G.; Hille, Jacques; Dijkwel, Paul P.

2007-01-01

Arabidopsis CPR5 is a senescence-regulatory gene with pleiotropic functions as predicted by the evolutionary theory of senescence Hai-Chun Jing1,2, Lisa Anderson3, Marcel J.G. Sturre1, Jacques Hille1 and Paul P. Dijkwel1,* 1Molecular Biology of Plants, Groningen Biomolecular Sciences and

Effects of physical activity on life expectancy with cardiovascular disease

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O.H. Franco (Oscar); C.E.D. de Laet (Chris); A. Peeters (Andrea); J. Jonker (Joost); J.P. Mackenbach (Johan); W.J. Nusselder (Wilma)

2005-01-01

textabstractBackground: Physical inactivity is a modifiable risk factor for cardiovascular disease. However, little is known about the effects of physical activity on life expectancy with and without cardiovascular disease. Our objective was to calculate the consequences of different physical

Importance of bio-medical and socio-economic factors for increase of life expectancy

Directory of Open Access Journals (Sweden)

Radivojević Biljana M.

2004-01-01

Full Text Available This paper analyzes the connection between life expectancy according to sex and numerous factors on which its level depends on. Statistical analysis understood application of correlation and regression analysis for determining the connection strength of life expectancy and researched factors separately and then all factors together, as well as separately groups of health-medical and socio-economic factors. The analysis was carried out for a group of developed countries, medium developed, mixed group and Yugoslavia (now SCG on available data for the second half of the 20th century. Analysis results for Yugoslavia showed that the greatest influence on life expectancy of all factors together were setting aside funds for social security (p<0.05. If only health-medical factors are observed, then child mortality up to 5 years and tumor mortality are in question. With women, the greatest influence is with child mortality up to five years old among all factors (life expectancy were the number of sick-beds with men (p<0.05, and with women the parameter of potentially lost years due to tumor (p<0.01. In medium developed countries the most influence on women's life expectancy was maternal mortality (p=0.014, and with men no researched factor was statistically significant. In the mixed sample, the strongest connection with men was with gross national income per capita (p<0.01, and with women with child mortality up to five years old (p=0.017. Therefore on the basis of the determined statistical importance of certain factors analysis showed that the influence of socio-economic factors on life expectancy was very strong in present conditions of mortality, not only in positive, but in negative direction as well, and that their influence in that second half of the 20th century was greater than the influence of health

Homicides In Mexico Reversed Life Expectancy Gains For Men And Slowed Them For Women, 2000-10.

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Aburto, José Manuel; Beltrán-Sánchez, Hiram; García-Guerrero, Victor Manuel; Canudas-Romo, Vladimir

2016-01-01

Life expectancy in Mexico increased for more than six decades but then stagnated in the period 2000-10. This decade was characterized by the enactment of a major health care reform-the implementation of the Seguro Popular de Salud (Popular Health Insurance), which was intended to provide coverage to the entire Mexican population-and by an unexpected increase in homicide mortality. We assessed the impact on life expectancy of conditions amenable to medical service-those sensitive to public health policies and changes in behaviors, homicide, and diabetes-by analyzing mortality trends at the state level. We found that life expectancy among males deteriorated from 2005 to 2010, compared to increases from 2000 to 2005. Females in most states experienced small gains in life expectancy between 2000 and 2010. The unprecedented rise in homicides after 2005 led to a reversal in life expectancy increases among males and a slowdown among females in most states in the first decade of the twenty-first century. Project HOPE—The People-to-People Health Foundation, Inc.

[Immunological theory of senescence].

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Drela, Nadzieja

2014-01-01

Senescence can result from decreased potential of the immune system to respond to foreign and self antigens. The most common effect is the inhibition to destroy dying and cancer cells and the decrease of the immune response to pathogens. Aging is closely related to inflammatory phenotype, which facilitate the development of age-related diseases. The mammal immune system is highly organized and adapted to react to a wide range of antigens. According to the immunological theory, the causative agents of senescence are multilevel changes of development and functions of immune cells. Some of changes can be beneficial for the maintenance of homeostasis and lifespan in continuously changing endogenous environment and immune history of the organism.

Assessment of the Effectiveness of Public Investment in the Increase in Life Expectancy

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Vadim Nikolaevich Kabanov

2015-11-01

Full Text Available The beginning of the 21st century was marked by the emergence of national projects in our country, which exactly correspond to the private integral indicators used by the UN in calculating the index of human capital development since 1996. The national project “Health care” is aimed at increasing life expectancy, “Education” – expanding the population’s access to knowledge, “Doubling GDP” – raising people’s income. Attaching equal importance to each indicator, the author of the article set a task to consider the economic efficiency of budgetary funds allocated to improve the nation’s health. The author assumed a proportion as the main hypotheses about the nature of correlation between life expectancy (H and expenditures on health care (G; the calculated coefficients of correlation (Pearson, r of dependence H = f(G for all RF subjects for 2003–2013 (0.49 < r < or = 0.97 confirmed the existence of correlation. The author proposed to use the slope of the straight H = f(G to x-axis as a quantitative value, indicating the economic efficiency of the transformation of budget expenditures to the increase in life expectancy. This indicator means that the achieved increase in life expectancy (Y axis motion depending on changes in budget expenditures on health (axis motion. The proposed indicator to estimate the socio-economic effectiveness of state investments in domestic health care guarantees the most objective and clear assessment, conducted on the basis of standard methods of mathematical statistics, ensuring a high accuracy of the calculations. The rate of rise in life expectancy, depending on the volume of public investment in health care, can be used for the scientific justification, for example, of the degree of Federal budget participation in the regional programs to promote national health

What has contributed to the change in life expectancy in Italy between 1980 and 1992?

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Ngongo, K N; Nante, N; Chenet, L; McKee, M

1999-07-01

Life expectancy at birth in southern Europe is known to be greater than expected in comparison with levels of economic development. This has been attributed to the 'Mediterranean diet'. There are, however, concerns that this comparative advantage is being lost. This paper examines the factors underlying changing life expectancy in Italy since 1980. The subjects of this analysis are obtained from data on all deaths in Italy between 1980 and 1992. Change in age specific death rates is calculated from selected causes and, using the method developed by Pollard, the contribution of deaths from different causes and at different ages to changing life expectancy at birth is estimated. Between 1980 and 1992, life expectancy at birth increased by 2.70 years for men and 2.75 years for women. Death rates have fallen among children and those over 40. In contrast, death rates have increased among men aged between 20 and 39 and have increased very slightly among women aged 25-29. Falling death rates from ischaemic heart disease are continuing to contribute to increasing life expectancy. Death rates from lung and breast cancer are rising among women but are compensated for by falling death rates from other cancers. Among men, falling death rates from cancer at younger ages are being offset by increases at older ages. The rising death rate among younger men is almost entirely due to AIDS, with accidents also making a small contribution. Life expectancy in Italy has improved throughout the 1980s, largely driven by falling death rates from cardiovascular diseases. Here are, however, some worrying trends, most notably the rising death rate among young men, due almost entirely to AIDS. The changing pattern of mortality has some similarities with Spain, another Mediterranean country, but there are also important differences.

Girassol ornamental: caracterização, pós-colheita e escala de senescência Ornamental sunflower: characterization, postharvest and senescence scale

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Gilberto Luiz Curti

2012-06-01

Full Text Available O girassol ornamental amplia o mercado de comercialização de plantas ornamentais no Brasil. Desta forma, este trabalho teve como objetivo apresentar uma caracterização do manejo pós-colheita e propor uma escala de senescência da cultura do girassol ornamental quanto à senescência, durabilidade das flores e referências de valores de comercialização. A produção de flores é uma atividade de alto risco pela fragilidade do produto, qualidades estéticas e as condições de produção, bem como a menor durabilidade pós-colheita do produto. Esse estudo propõe uma escala de senescência para cultivares de girassol ornamental quanto à senescência dos capítulos para atribuir diferentes remunerações e possibilidades de comercialização da cultura.The ornamental sunflower widen the market of ornamental plants in Brazil. Thus, this study aimed to present a characterization of post-harvest management and to propose a range of senescence stage of sunflower as an ornamental in relation to senescence, flower longevity and benchmark values of trade. The production of flowers is a high risk activity for the fragility of the product, aesthetic qualities and conditions of production as well as lower post-harvest durability of the product. This study proposes a range of senescence stages for ornamental sunflower cultivars as the aging of different chapters to assign salaries and marketability of the crop.

Stress-induced premature senescence (SIPS)--influence of SIPS on radiotherapy.

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Suzuki, Masatoshi; Boothman, David A

2008-03-01

Replicative senescence is a fundamental feature in normal human diploid cells and results from dysfunctional telomeres at the Hayflick cell division limit. Ionizing radiation (IR) prematurely induces the same phenotypes as replicative senescence prior to the Hayflick limit. This process is known as stress-induced premature senescence (SIPS). Since the cell cycle is irreversibly arrested in SIPS-induced cells, even if they are stimulated by various growth factors, it is thought that SIPS is a form of cell death, irreversibly eliminating replicating cells. IR-induced-focus formation of DNA repair proteins, a marker of DNA damage, is detected in SIPS as well as replicative senescent cells. Furthermore, both processes persistently induce cell cycle checkpoint mechanisms, indicating DNA damage created by ionizing radiation induces SIPS in normal cells, possibly by the same mechanisms as those occurring in replicative senescence. Interestingly, IR induces SIPS not only in normal cells, but also in tumor cells. Due to the expression of telomerase in tumor cells, telomere-dependent replicative senescence does not occur. However, SIPS is induced under certain conditions after IR exposure. Thus, cell death triggered by IR can be attributed to apoptosis or SIPS in tumor cells. However, metabolic function remains intact in SIPS-induced cancer cells, and recent studies show that senescence eliminate cells undergoing SIPS secrete various kinds of factors outside the cell, changing the microenvironment. Evidence using co-culture systems containing normal senescent stromal cells and epithelial tumor cells show that factors secreted from senescent stroma cells promote the growth of tumor epithelial cells both in vitro and in vivo. Thus, regulation of factors secreted from SIPS-induced stromal cells, as well as tumor cells, may affect radiotherapy.

Stress-induced premature senescence (SIPS). Influence of SIPS on radiotherapy

International Nuclear Information System (INIS)

Suzuki, Masatoshi; Boothman, D.A.

2008-01-01

Replicative senescence is a fundamental feature in normal human diploid cells and results from dysfunctional telomeres at the Hayflick cell division limit. Ionizing radiation (IR) prematurely induces the same phenotypes as replicative senescence prior to the Hayflick limit. This process is known as stress-induced premature senescence (SIPS). Since the cell cycle is irreversibly arrested in SIPS-induced cells, even if they are stimulated by various growth factors, it is thought that SIPS is a form of cell death, irreversibly eliminating replicating cells. IR-induced-focus formation of DNA repair proteins, a marker of DNA damage, is detected in SIPS as well as replicative senescent cells. Furthermore, both processes persistently induce cell cycle checkpoint mechanisms, indicating DNA damage created by ionizing radiation induces SIPS in normal cells, possibly by the same mechanisms as those occurring in replicative senescence. Interestingly, IR induces SIPS not only in normal cells, but also in tumor cells. Due to the expression of telomerase in tumor cells, telomere-dependent replicative senescence does not occur. However, SIPS is induced under certain conditions after IR exposure. Thus, cell death triggered by IR can be attributed to apoptosis or SIPS in tumor cells. However, metabolic function remains intact in SIPS-induced cancer cells, and recent studies show that senescence eliminate cells undergoing SIPS secrete various kinds of factors outside the cell, changing the microenvironment. Evidence using co-culture systems containing normal senescent stromal cells and epithelial tumor cells show that factors secreted from senescent stroma cells promote the growth of tumor epithelial cells both in vitro and in vivo. Thus, regulation of factors secreted from SIPS-induced stromal cells, as well as tumor cells, may affect radiotherapy. (author)

Sirtuins, Cell Senescence, and Vascular Aging.

Science.gov (United States)

Kida, Yujiro; Goligorsky, Michael S

2016-05-01

The sirtuins (SIRTs) constitute a class of proteins with nicotinamide adenine dinucleotide-dependent deacetylase or adenosine diphosphate-ribosyltransferase activity. Seven SIRT family members have been identified in mammals, from SIRT1, the best studied for its role in vascular aging, to SIRT7. SIRT1 and SIRT2 are localized in the nucleus and cytoplasm. SIRT3, SIRT4, and SIRT5 are mitochondrial, and SIRT6 and SIRT7 are nuclear. Extensive studies have clearly revealed that SIRT proteins regulate diverse cell functions and responses to stressors. Vascular aging involves the aging process (senescence) of endothelial and vascular smooth muscle cells. Two types of cell senescence have been identified: (1) replicative senescence with telomere attrition; and (2) stress-induced premature senescence without telomere involvement. Both types of senescence induce vascular cell growth arrest and loss of vascular homeostasis, and contribute to the initiation and progression of cardiovascular diseases. Previous mechanistic studies have revealed in detail that SIRT1, SIRT3, and SIRT6 show protective functions against vascular aging, and definite vascular function of other SIRTs is under investigation. Thus, direct SIRT modulation and nicotinamide adenine dinucleotide stimulation of SIRT are promising candidates for cardiovascular disease therapy. A small number of pilot studies have been conducted to assess SIRT modulation in humans. These clinical studies have not yet provided convincing evidence that SIRT proteins alleviate morbidity and mortality in patients with cardiovascular diseases. The outcomes of multiple ongoing clinical trials are awaited to define the efficacy of SIRT modulators and SIRT activators in cardiovascular diseases, along with the potential adverse effects of chronic SIRT modulation. Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

Stress-Induced Premature Senescence or Stress-Induced Senescence-Like Phenotype: One In Vivo Reality, Two Possible Definitions?

OpenAIRE

Toussaint, Olivier; Dumont, Patrick; Remacle, Jose; Dierick, Jean-Francois; Pascal, Thierry; Frippiat, Christophe; Magalhaes, Joao Pedro; Zdanov, Stephanie; Chainiaux, Florence

2002-01-01

No consensus exists so far on the definition of cellular senescence. The narrowest definition of senescence is irreversible growth arrest triggered by telomere shortening counting cell generations (definition 1). Other authors gave an enlarged functional definition encompassing any kind of irreversible arrest of proliferative cell types induced by damaging agents or cell cycle deregulations after overexpression of proto-oncogenes (definition 2). As stress increases, the proportion of cells in...

Inactivation of AKT Induces Cellular Senescence in Uterine Leiomyoma

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Xu, Xiaofei; Lu, Zhenxiao; Qiang, Wenan; Vidimar, Vania; Kong, Beihua

2014-01-01

Uterine leiomyomas (fibroids) are a major public health problem. Current medical treatments with GnRH analogs do not provide long-term benefit. Thus, permanent shrinkage or inhibition of fibroid growth via medical means remains a challenge. The AKT pathway is a major growth and survival pathway for fibroids. We propose that AKT inhibition results in a transient regulation of specific mechanisms that ultimately drive cells into cellular senescence or cell death. In this study, we investigated specific mechanisms of AKT inhibition that resulted in senescence. We observed that administration of MK-2206, an allosteric AKT inhibitor, increased levels of reactive oxygen species, up-regulated the microRNA miR-182 and several senescence-associated genes (including p16, p53, p21, and β-galactosidase), and drove leiomyoma cells into stress-induced premature senescence (SIPS). Moreover, induction of SIPS was mediated by HMGA2, which colocalized to senescence-associated heterochromatin foci. This study provides a conceivable molecular mechanism of SIPS by AKT inhibition in fibroids. PMID:24476133

Trends in healthy life expectancy among older Brazilian women between 1998 and 2008

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Marília Regina Nepomuceno

2015-01-01

Full Text Available OBJECTIVE To analyze conditional and unconditional healthy life expectancy among older Brazilian women. METHODS This cross-sectional study used the intercensal technique to estimate, in the absence of longitudinal data, healthy life expectancy that is conditional and unconditional on the individual’s current health status. The data used were obtained from the Pesquisa Nacional por Amostra de Domicílios (National Household Sample Survey of 1998, 2003, and 2008. This sample comprised 11,171; 13,694; and 16,259 women aged 65 years or more, respectively. Complete mortality tables from the Brazilian Institute of Geography and Statistics for the years 2001 and 2006 were also used. The definition of health status was based on the difficulty in performing activities of daily living. RESULTS The remaining lifetime was strongly dependent on the current health status of the older women. Between 1998 and 2003, the amount of time lived with disability for healthy women at age 65 was 9.8%. This percentage increased to 66.2% when the women already presented some disability at age 65. Temporal analysis showed that the active life expectancy of the women at age 65 increased between 1998-2003 (19.3 years and 2003-2008 (19.4 years. However, life years gained have been mainly focused on the unhealthy state. CONCLUSIONS Analysis of conditional and unconditional life expectancy indicated that live years gained are a result of the decline of mortality in unhealthy states. This pattern suggests that there has been no reduction in morbidity among older women in Brazil between 1998 and 2008.

[Deaths attributable to alcohol use and its impact on life expectancy in China, 2013].

Science.gov (United States)

Jiang, Y Y; Liu, S W; Ji, N; Zeng, X Y; Liu, Y N; Zhang, M; Wang, L M; Li, Y C; Zhou, M G

2018-01-10

Objective: To analyze the deaths attributable to alcohol use and its impact on people's life expectancy in China in 2013. Methods: The mortality data from the Disease Surveillance Points System and alcohol use data from China Chronic Disease Surveillance (2013) were used. The deaths attributed to alcohol use and its impact on the life expectancy of Chinese residents were estimated based on the principle of comparative risk assessment by calculating population attributable fraction. Results: In 2013, alcohol use resulted in 381 200 deaths, including 97 100 hemorrhagic stroke deaths, 88 200 liver cancer deaths, 61 400 liver cirrhosis deaths and 48 700 esophageal cancer deaths, and prevented 76 500 deaths, including 68 500, 4 900 and 3 100 deaths which might be caused by ischemic heart disease, hemorrhagic stroke and diabetes respectively. If risk factor of alcohol use is removed, the people's life expectancy would rise by an average of 0.43 years, especially in western China by 0.52 years, which was 0.12 years higher than that in eastern and central China, and the life expectancy of the population in rural and urban areas would rise by 0.48 years and 0.31 years respectively. Conclusions: Although alcohol has a protective effect on reducing ischemic heart disease, stroke and diabetes deaths, alcohol use is still a risk factor influencing the mortality and life expectancy of residents in China. It is necessary to take targeted measures to reduce the health problems caused by harmful use of alcohol.

Androgenetic, diffuse and senescent alopecia in men: practical evaluation and management.

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Torres, Fernanda

2015-01-01

Male baldness is the most common diagnosis in men that present with hair loss. It is a genetically determined condition that is clearly an androgen-dependent trait, mainly driven by dihydrotestosterone action on the hair follicles, leading to miniaturization. Although in general this condition is socially accepted as a natural process in a man's life, for some individuals it might significantly impact quality of life, reducing self-esteem and increasing stress. This chapter encompasses the most important aspects of the practical evaluation (clinical features, trichoscopy, trichogram, histopathology, relevant blood tests) and management of male baldness, diffuse baldness and senescent alopecia. © 2015 S. Karger AG, Basel.

The Splicing Factor SRSF1 as a Marker for Endothelial Senescence

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Blanco, Francisco Javier; Bernabéu, Carmelo

2012-01-01

Aging is the major risk factor per se for the development of cardiovascular diseases. The senescence of the endothelial cells (ECs) that line the lumen of blood vessels is the cellular basis for these age-dependent vascular pathologies, including atherosclerosis and hypertension. During their lifespan, ECs may reach a stage of senescence by two different pathways; a replicative one derived from their preprogrammed finite number of cell divisions; and one induced by stress stimuli. Also, certain physiological stimuli, such as transforming growth factor-β, are able to modulate cellular senescence. Currently, the cellular aging process is being widely studied to identify novel molecular markers whose changes correlate with senescence. This review focuses on the regulation of alternative splicing mediated by the serine–arginine splicing factor 1 (SRSF1, or ASF/SF2) during endothelial senescence, a process that is associated with a differential subcellular localization of SRSF1, which typically exhibits a scattered distribution throughout the cytoplasm. Based on its senescence-dependent involvement in alternative splicing, we postulate that SRSF1 is a key marker of EC senescence, regulating the expression of alternative isoforms of target genes such as endoglin (ENG), vascular endothelial growth factor A (VEGFA), tissue factor (T3), or lamin A (LMNA) that integrate in a common molecular senescence program. PMID:22470345

Accumulation of senescent cells in mitotic tissue of aging primates.

Science.gov (United States)

Jeyapalan, Jessie C; Ferreira, Mark; Sedivy, John M; Herbig, Utz

2007-01-01

Cellular senescence, a stress induced growth arrest of somatic cells, was first documented in cell cultures over 40 years ago, however its physiological significance has only recently been demonstrated. Using novel biomarkers of cellular senescence we examined whether senescent cells accumulate in tissues from baboons of ages encompassing the entire lifespan of this species. We show that dermal fibroblasts, displaying markers of senescence such as telomere damage, active checkpoint kinase ATM, high levels of heterochromatin proteins and elevated levels of p16, accumulate in skin biopsies from baboons with advancing age. The number of dermal fibroblasts containing damaged telomeres reaches a value of over 15% of total fibroblasts, whereas 80% of cells contain high levels of the heterochromatin protein HIRA. In skeletal muscle, a postmitotic tissue, only a small percentage of myonuclei containing damaged telomeres were detected regardless of animal age. The presence of senescent cells in mitotic tissues might therefore be a contributing factor to aging and age related pathology and provides further evidence that cellular senescence is a physiological event.

Ring-like distribution of constitutive heterochromatin in bovine senescent cells.

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Pichugin, Andrey; Beaujean, Nathalie; Vignon, Xavier; Vassetzky, Yegor

2011-01-01

Cells that reach "Hayflick limit" of proliferation, known as senescent cells, possess a particular type of nuclear architecture. Human senescent cells are characterized by the presence of highly condensed senescent associated heterochromatin foci (SAHF) that can be detected both by immunostaining for histone H3 three-methylated at lysine 9 (H3K9me3) and by DAPI counterstaining. We have studied nuclear architecture in bovine senescent cells using a combination of immunofluorescence and 3D fluorescent in-situ hybridization (FISH). Analysis of heterochromatin distribution in bovine senescent cells using fluorescent in situ hybridization for pericentric chromosomal regions, immunostaining of H3K9me3, centromeric proteins CENP A/B and DNA methylation showed a lower level of heterochromatin condensation as compared to young cells. No SAHF foci were observed. Instead, we observed fibrous ring-like or ribbon-like heterochromatin patterns that were undetectable with DAPI counterstaining. These heterochromatin fibers were associated with nucleoli. Constitutive heterochromatin in bovine senescent cells is organized in ring-like structures.

Ring-like distribution of constitutive heterochromatin in bovine senescent cells.

Directory of Open Access Journals (Sweden)

Andrey Pichugin

Full Text Available BACKGROUND: Cells that reach "Hayflick limit" of proliferation, known as senescent cells, possess a particular type of nuclear architecture. Human senescent cells are characterized by the presence of highly condensed senescent associated heterochromatin foci (SAHF that can be detected both by immunostaining for histone H3 three-methylated at lysine 9 (H3K9me3 and by DAPI counterstaining. METHODS: We have studied nuclear architecture in bovine senescent cells using a combination of immunofluorescence and 3D fluorescent in-situ hybridization (FISH. RESULTS: Analysis of heterochromatin distribution in bovine senescent cells using fluorescent in situ hybridization for pericentric chromosomal regions, immunostaining of H3K9me3, centromeric proteins CENP A/B and DNA methylation showed a lower level of heterochromatin condensation as compared to young cells. No SAHF foci were observed. Instead, we observed fibrous ring-like or ribbon-like heterochromatin patterns that were undetectable with DAPI counterstaining. These heterochromatin fibers were associated with nucleoli. CONCLUSIONS: Constitutive heterochromatin in bovine senescent cells is organized in ring-like structures.

Life expectancy inequalities in the elderly by socioeconomic status: evidence from Italy.

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Lallo, Carlo; Raitano, Michele

2018-04-12

Life expectancy considerably increased in most developed countries during the twentieth century. However, the increase in longevity is neither uniform nor random across individuals belonging to various socioeconomic groups. From an economic policy perspective, the difference in mortality by socioeconomic conditions challenges the fairness of the social security systems. We focus on the case of Italy and aim at measuring differences in longevity at older ages by individuals belonging to different socioeconomic groups, also in order to assess the effective fairness of the Italian public pension system, which is based on a notional defined contribution (NDC) benefit computation formula, whose rules do not take into account individual heterogeneity in expected longevity. We use a longitudinal dataset that matches survey data on individual features recorded in the Italian module of the EU-SILC, with information on the whole working life and until death collected in the administrative archives managed by the Italian National Social Security Institute. In more detail, we follow until 2009 a sample of 11,281 individuals aged at least 60 in 2005. We use survival analysis and measure the influence of a number of events experienced in the labor market and individual characteristics on mortality. Furthermore, through Kaplan-Meier simulations of hypothetical social groups, adjusted by a Brass relational model, we estimate and compare differences in life expectancy of individuals belonging to different socioeconomic groups. Our findings confirm that socioeconomic status strongly predicts life expectancy even in old age. All estimated models show that the prevalent type of working activity before retirement is significantly associated with the risk of death, even when controlling for dozens of variables as proxies of individual demographic and socioeconomic characteristics. The risk of death for self-employed individuals is 26% lower than that of employees, and life expectancy at

Homicides In Mexico Reversed Life Expectancy Gains For Men And Slowed Them For Women, 2000–10

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Aburto, José Manuel; Beltrán-Sánchez, Hiram; García-Guerrero, Victor Manuel; Canudas-Romo, Vladimir

2017-01-01

Life expectancy in Mexico increased for more than six decades but then stagnated in the period 2000–10. This decade was characterized by the enactment of a major health care reform—the implementation of the Seguro Popular de Salud (Popular Health Insurance), which was intended to provide coverage to the entire Mexican population—and by an unexpected increase in homicide mortality. We assessed the impact on life expectancy of conditions amenable to medical service—those sensitive to public health policies and changes in behaviors, homicide, and diabetes—by analyzing mortality trends at the state level. We found that life expectancy among males deteriorated from 2005 to 2010, compared to increases from 2000 to 2005. Females in most states experienced small gains in life expectancy between 2000 and 2010. The unprecedented rise in homicides after 2005 led to a reversal in life expectancy increases among males and a slowdown among females in most states in the first decade of the twenty-first century. PMID:26733705

Are global and regional improvements in life expectancy and in child, adult and senior survival slowing?

Directory of Open Access Journals (Sweden)

Ryan J Hum

Full Text Available Improvements in life expectancy have been considerable over the past hundred years. Forecasters have taken to applying historical trends under an assumption of continuing improvements in life expectancy in the future. A linear mixed effects model was used to estimate the trends in global and regional rates of improvements in life expectancy, child, adult, and senior survival, in 166 countries between 1950 and 2010. Global improvements in life expectancy, including both child and adult survival rates, decelerated significantly over the study period. Overall life expectancy gains were estimated to have declined from 5.9 to 4.0 months per year for a mean deceleration of -0.07 months/year2; annual child survival gains declined from 4.4 to 1.6 deaths averted per 1000 for a mean deceleration of -0.06 deaths/1000/year2; adult survival gains were estimated to decline from 4.8 to 3.7 deaths averted per 1000 per year for a mean deceleration of -0.08 deaths/1000/year2. Senior survival gains however increased from 2.4 to 4.2 deaths averted per 1000 per year for an acceleration of 0.03 deaths/1000/year2. Regional variation in the four measures was substantial. The rates of global improvements in life expectancy, child survival, and adult survival have declined since 1950 despite an increase in the rate of improvements among seniors. We postulate that low-cost innovation, related to the last half-century progress in health-primarily devoted to children and middle age, is reaping diminishing returns on its investments. Trends are uneven across regions and measures, which may be due in part to the state of epidemiological transition between countries and regions and disparities in the diffusion of innovation, accessible only in high-income countries where life expectancy is already highest.

Impact of particulate air pollution on quality-adjusted life expectancy in Canada.

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Coyle, Douglas; Stieb, Dave; Burnett, Richard T; DeCivita, Paul; Krewski, Daniel; Chen, Yue; Thun, Michael J

Air pollution and premature death are important public health concerns. Analyses have repeatedly demonstrated that airborne particles are associated with increased mortality and estimates have been used to forecast the impact on life expectancy. In this analysis, we draw upon data from the American Cancer Society (ACS) cohort and literature on utility-based measures of quality of life in relation to health status to more fully quantify the effects of air pollution on mortality in terms of quality-adjusted life expectancy. The analysis was conducted within a decision analytic model using Monte Carlo simulation techniques. Outcomes were estimated based on projections of the Canadian population. A one-unit reduction in sulfate air pollution would yield a mean annual increase in Quality-Adjusted Life Years (QALYs) of 20,960, with gains being greater for individuals with lower educational status and for males compared to females. This suggests that the impact of reductions in sulfate air pollution on quality-adjusted life expectancy is substantial. Interpretation of the results is unclear. However, the potential gains in QALYs from reduced air pollutants can be contrasted to the costs of policies to bring about such reductions. Based on a tentative threshold for the value of health benefits, analysis suggests that an investment in Canada of over 1 billion dollars per annum would be an efficient use of resources if it could be demonstrated that this would reduce sulfate concentrations in ambient air by 1 microg/m(3). Further analysis can assess the efficiency of targeting such initiatives to communities that are most likely to benefit.

Effect of gamma radiation and some growth regulators on ripening and senescence in mango fruits

International Nuclear Information System (INIS)

EL-Kady, S.M.A.

1982-01-01

The present investigation was undertaken during the seasons of 1979 and 1980 to study the effect of gamma irradiation, some growth regulators, benlate and 'vaporgard' on ripening and senescence of 'Hindi Be - Sinnara' mango fruits during storage under room conditions and also to determine the optimum treatment for maximum extension in shelf - life

Oxidative Stress Induces Senescence in Cultured RPE Cells.

Science.gov (United States)

Aryan, Nona; Betts-Obregon, Brandi S; Perry, George; Tsin, Andrew T

2016-01-01

The aim of this research is to determine whether oxidative stress induces cellular senescence in human retinal pigment epithelial cells. Cultured ARPE19 cells were subjected to different concentrations of hydrogen peroxide to induce oxidative stress. Cells were seeded into 24-well plates with hydrogen peroxide added to cell medium and incubated at 37°C + 5% CO2 for a 90-minute period [at 0, 300, 400 and 800 micromolar (MCM) hydrogen peroxide]. The number of viable ARPE19 cells were recorded using the Trypan Blue Dye Exclusion Method and cell senescence was measured by positive staining for senescence-associated beta-galactosidase (SA-beta-Gal) protein. Without hydrogen peroxide treatment, the number of viable ARPE19 cells increased significantly from 50,000 cells/well to 197,000 within 72 hours. Treatment with hydrogen peroxide reduced this level of cell proliferation significantly (to 52,167 cells at 400 MCM; to 49,263 cells at 800 MCM). Meanwhile, cells with a high level of positive senescence-indicator SA-Beta-Gal-positive staining was induced by hydrogen peroxide treatment (from a baseline level of 12% to 80% at 400 MCM and at 800 MCM). Our data suggests that oxidative stress from hydrogen peroxide treatment inhibited ARPE19 cell proliferation and induced cellular senescence.

Identification and characterization of secretory proteins during ionizing radiation-induced premature senescence

International Nuclear Information System (INIS)

Han, Na Kyung; Hong, Mi Na; Jung, Seung Hee; Kang, Kyoung Ah; Lee, Jae Seon; Chi, Seong Gil

2011-01-01

Cellular senescence was first described by Hayflick and Moorhead in 1961 who observed that cultures of normal human fibroblasts had a limited replicative potential and eventually became irreversibly arrest. The majority of senescent cells assume a characteristic flattened and enlarged morphological change, senescence associated β alactosidase positivity. Recently a large number of molecular phenotypes such as changes in gene expression, protein processing and chromatin organization have been also described. In contrast to apoptosis, senescence does not destroy the cells but leaves them metabolically and synthetically active and therefore able to affect their microenvironment. In particular, senescent fibroblasts and some cancer cells were found to secrete proteins with known or putative tumor-promoting functions such as growth factors or proteolytic enzymes. However, the knowledge about secreted proteins from senescent tumor cells and their functions to surrounding cells is still lacking. In this study, changes of senescence associated secretory protein expression profile were observed in MCF7 human breast cancer cells exposed to gamma-ray radiation using two dimensional electrophoresis. Also, we identified up-regulated secretory proteins during ionizing radiation-induced cellular senescence. Here, we show that senescent human breast cancer MCF7 cells promote the proliferation, invasion and migration of neighboring cells

Identification and characterization of secretory proteins during ionizing radiation-induced premature senescence

Energy Technology Data Exchange (ETDEWEB)

Han, Na Kyung; Hong, Mi Na; Jung, Seung Hee; Kang, Kyoung Ah; Lee, Jae Seon [Korea Institute of Radiological and Medical Sciences, Seoul (Korea, Republic of); Chi, Seong Gil [Korea University, Seoul (Korea, Republic of)

2011-05-15

Cellular senescence was first described by Hayflick and Moorhead in 1961 who observed that cultures of normal human fibroblasts had a limited replicative potential and eventually became irreversibly arrest. The majority of senescent cells assume a characteristic flattened and enlarged morphological change, senescence associated {beta} alactosidase positivity. Recently a large number of molecular phenotypes such as changes in gene expression, protein processing and chromatin organization have been also described. In contrast to apoptosis, senescence does not destroy the cells but leaves them metabolically and synthetically active and therefore able to affect their microenvironment. In particular, senescent fibroblasts and some cancer cells were found to secrete proteins with known or putative tumor-promoting functions such as growth factors or proteolytic enzymes. However, the knowledge about secreted proteins from senescent tumor cells and their functions to surrounding cells is still lacking. In this study, changes of senescence associated secretory protein expression profile were observed in MCF7 human breast cancer cells exposed to gamma-ray radiation using two dimensional electrophoresis. Also, we identified up-regulated secretory proteins during ionizing radiation-induced cellular senescence. Here, we show that senescent human breast cancer MCF7 cells promote the proliferation, invasion and migration of neighboring cells

Senescent phenotypes of skin fibroblasts from patients with Tangier disease

International Nuclear Information System (INIS)

Matsuura, Fumihiko; Hirano, Ken-ichi; Ikegami, Chiaki; Sandoval, Jose C.; Oku, Hiroyuki; Yuasa-Kawase, Miyako; Tsubakio-Yamamoto, Kazumi; Koseki, Masahiro; Masuda, Daisaku; Tsujii, Ken-ichi; Ishigami, Masato; Nishida, Makoto; Shimomura, Iichiro; Hori, Masatsugu; Yamashita, Shizuya

2007-01-01

Tangier disease (TD) is characterized by a deficiency of high density lipoprotein (HDL) in plasma and patients with TD have an increased risk for coronary artery disease (CAD). Recently, we reported that fibroblasts from TD exhibited large and flattened morphology, which is often observed in senescent cells. On the other hand, data have accumulated to show the relationship between cellular senescence and development of atherosclerotic CAD. The aim of the present study was to investigate whether TD fibroblasts exhibited cellular senescence. The proliferation of TD fibroblasts was gradually decreased at population doubling level (PDL) ∼10 compared with control cells. TD cells practically ceased proliferation at PDL ∼30. DNA synthesis was markedly decreased in TD fibroblasts. TD cells exhibited a higher positive rate for senescence-associated β-galactosidase (SA-β-gal), which is one of the biomarkers of cellular senescence in vitro. These data showed that TD cells reached cellular senescence at an earlier PDL compared with controls. Although, there was no difference in the telomere length of fibroblasts between TD and controls at the earlier passage (PDL 6), the telomere length of TD cells was shorter than that of controls at the late passage (PDL 25). Taken together, the current study demonstrates that the late-passaged TD fibroblasts showed senescent phenotype in vitro, which might be related to the increased cardiovascular manifestations in TD patients

Life expectancy of colon, breast, and testicular cancer patients: an analysis of US-SEER population-based data.

Science.gov (United States)

Capocaccia, R; Gatta, G; Dal Maso, L

2015-06-01

Cancer survivorship is an increasingly important issue in cancer control. Life expectancy of patients diagnosed with breast, colon, and testicular cancers, stratified by age at diagnosis and time since diagnosis, is provided as an indicator to evaluate future mortality risks and health care needs of cancer survivors. The standard period life table methodology was applied to estimate excess mortality risk for cancer patients diagnosed in 1985-2011 from SEER registries and mortality data of the general US population. The sensitivity of life expectancy estimates on different assumptions was evaluated. Younger patients with colon cancer showed wider differences in life expectancy compared with that of the general population (11.2 years in women and 10.7 in men at age 45-49 years) than older patients (6.3 and 5.8 at age 60-64 years, respectively). Life expectancy progressively increases in patients surviving the first years, up to 4 years from diagnosis, and then starts to decrease again, approaching that of the general population. For breast cancer, the initial drop in life expectancy is less marked, and again with wider differences in younger patients, varying from 8.7 at age 40-44 years to 2.4 at ages 70-74 years. After diagnosis, life expectancy still decreases with time, but less than that in the general population, slowly approaching that of cancer-free women. Life expectancy of men diagnosed with testicular cancer at age 30 years is estimated as 45.2 years, 2 years less than cancer-free men of the same age. The difference becomes 1.3 years for patients surviving the first year, and then slowly approaches zero with increasing survival time. Life expectancy provides meaningful information on cancer patients, and can help in assessing when a cancer survivor can be considered as cured. © The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Temporal polyethism, life expectancy, and entropy of workers of the ant Ectatomma vizottoi Almeida, 1987 (Formicidae: Ectatomminae).

Science.gov (United States)

Santana Vieira, Alexsandro; Desidério Fernandes, Wedson; Fernando Antonialli-Junior, William

2010-05-01

We investigated the changes in the behavioral repertoire over the course of life and determined the life expectancy and entropy of workers of the ant Ectatomma vizottoi. Newly emerged ants were individually marked with model airplane paint for observation of behaviors and determination of the age and life expectancy. Ants were divided into two groups: young and old workers. The 36 behaviors observed were divided into eight categories. Workers exhibit a clear division of tasks throughout their lives, with young workers performing more tasks inside the colony and old workers, outside, unlike species that have small colonies. This species also exhibits an intermediate life expectancy compared to workers of other species that are also intermediary in size. This supports the hypothesis of a relationship between size and maximum life expectancy, but it also suggests that other factors may also be acting in concert. Entropy value shows a high mortality rate during the first life intervals.

Delay of Iris flower senescence by protease inhibitors

NARCIS (Netherlands)

Pak, C.; Doorn, van W.G.

2005-01-01

asterisk inside a circle sign Visible senescence of the flag tepals in Iris x hollandica (cv. Blue Magic) was preceded by a large increase in endoprotease activity. Just before visible senescence about half of total endoprotease activity was apparently due to cysteine proteases, somewhat less than

Integration of multi-omics techniques and physiological phenotyping within a holistic phenomics approach to study senescence in model and crop plants.

Science.gov (United States)

Großkinsky, Dominik K; Syaifullah, Syahnada Jaya; Roitsch, Thomas

2018-02-12

The study of senescence in plants is complicated by diverse levels of temporal and spatial dynamics as well as the impact of external biotic and abiotic factors and crop plant management. Whereas the molecular mechanisms involved in developmentally regulated leaf senescence are very well understood, in particular in the annual model plant species Arabidopsis, senescence of other organs such as the flower, fruit, and root is much less studied as well as senescence in perennials such as trees. This review addresses the need for the integration of multi-omics techniques and physiological phenotyping into holistic phenomics approaches to dissect the complex phenomenon of senescence. That became feasible through major advances in the establishment of various, complementary 'omics' technologies. Such an interdisciplinary approach will also need to consider knowledge from the animal field, in particular in relation to novel regulators such as small, non-coding RNAs, epigenetic control and telomere length. Such a characterization of phenotypes via the acquisition of high-dimensional datasets within a systems biology approach will allow us to systematically characterize the various programmes governing senescence beyond leaf senescence in Arabidopsis and to elucidate the underlying molecular processes. Such a multi-omics approach is expected to also spur the application of results from model plants to agriculture and their verification for sustainable and environmentally friendly improvement of crop plant stress resilience and productivity and contribute to improvements based on postharvest physiology for the food industry and the benefit of its customers. © The Author(s) 2017. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Assessing senescence patterns in populations of large mammals

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Gaillard, J.-M.

2004-06-01

Full Text Available Theoretical models such as those of Gompertz and Weibull are commonly used to study senescence in survival for humans and laboratory or captive animals. For wild populations of vertebrates, senescence in survival has more commonly been assessed by fitting simple linear or quadratic relationships between survival and age. By using appropriate constraints on survival parameters in Capture-Mark-Recapture (CMR models, we propose a first analysis of the suitability of the Gompertz and the two-parameter Weibull models for describing aging-related mortality in free-ranging populations of ungulates. We first show how to handle the Gompertz and the two-parameter Weibull models in the context of CMR analyses. Then we perform a comparative analysis of senescence patterns in both sexes of two ungulate species highly contrasted according to the intensity of sexual selection. Our analyses provide support to the Gompertz model for describing senescence patterns in ungulates. Evolutionary implications of our results are discussed

In vivo inhibition of cysteine proteases provides evidence for the involvement of 'senescence-associated vacuoles' in chloroplast protein degradation during dark-induced senescence of tobacco leaves.

Science.gov (United States)

Carrión, Cristian A; Costa, María Lorenza; Martínez, Dana E; Mohr, Christina; Humbeck, Klaus; Guiamet, Juan J

2013-11-01

Breakdown of leaf proteins, particularly chloroplast proteins, is a massive process in senescing leaves. In spite of its importance in internal N recycling, the mechanism(s) and the enzymes involved are largely unknown. Senescence-associated vacuoles (SAVs) are small, acidic vacuoles with high cysteine peptidase activity. Chloroplast-targeted proteins re-localize to SAVs during senescence, suggesting that SAVs might be involved in chloroplast protein degradation. SAVs were undetectable in mature, non-senescent tobacco leaves. Their abundance, visualized either with the acidotropic marker Lysotracker Red or by green fluorescent protein (GFP) fluorescence in a line expressing the senescence-associated cysteine protease SAG12 fused to GFP, increased during senescence induction in darkness, and peaked after 2-4 d, when chloroplast dismantling was most intense. Increased abundance of SAVs correlated with higher levels of SAG12 mRNA. Activity labelling with a biotinylated derivative of the cysteine protease inhibitor E-64 was used to detect active cysteine proteases. The two apparently most abundant cysteine proteases of senescing leaves, of 40kDa and 33kDa were detected in isolated SAVs. Rubisco degradation in isolated SAVs was completely blocked by E-64. Treatment of leaf disks with E-64 in vivo substantially reduced degradation of Rubisco and leaf proteins. Overall, these results indicate that SAVs contain most of the cysteine protease activity of senescing cells, and that SAV cysteine proteases are at least partly responsible for the degradation of stromal proteins of the chloroplast.

Why is the gender gap in life expectancy decreasing? The impact of age- and cause-specific mortality in Sweden 1997-2014.

Science.gov (United States)

Sundberg, Louise; Agahi, Neda; Fritzell, Johan; Fors, Stefan

2018-04-13

To enhance the understanding of the current increase in life expectancy and decreasing gender gap in life expectancy. We obtained data on underlying cause of death from the National Board of Health and Welfare in Sweden for 1997 and 2014 and used Arriaga's method to decompose life expectancy by age group and 24 causes of death. Decreased mortality from ischemic heart disease had the largest impact on the increased life expectancy of both men and women and on the decreased gender gap in life expectancy. Increased mortality from Alzheimer's disease negatively influenced overall life expectancy, but because of higher female mortality, it also served to decrease the gender gap in life expectancy. The impact of other causes of death, particularly smoking-related causes, decreased in men but increased in women, also reducing the gap in life expectancy. This study shows that a focus on overall changes in life expectancies may hide important differences in age- and cause-specific mortality. It also emphasizes the importance of addressing modifiable lifestyle factors to reduce avoidable mortality.

End-of-life expectations and experiences among nursing home patients and their relatives

DEFF Research Database (Denmark)

Fosse, Anette; Schaufel, Margrethe Aase; Ruths, Sabine

2014-01-01

. CONCLUSION: Nursing home patients and their relatives wanted doctors more involved in end-of-life care. They expected doctors to acknowledge their preferences and provide guidance and symptom relief. PRACTICE IMPLICATIONS: High-quality end-of-life care in nursing homes relies on organization, funding......OBJECTIVE: Synthesize research about patients' and relatives' expectations and experiences on how doctors can improve end-of-life care in nursing homes. METHODS: We systematically searched qualitative studies in English in seven databases (Medline, Embase, PsycINFO, CINAHL, Ageline, Cochrane...... decision-makers reported uncertainty and distress when guidance from health personnel was lacking. They worried about staff shortage and emphasized doctor availability. Relatives and health personnel seldom recognized patients' ability to consent, and patients' preferences were not always recognized...

Active Life Expectancy and Functional Health Transition among Filipino Older People

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Grace T. Cruz

2007-12-01

Full Text Available The study provides a baseline information on the functional health transition patterns of older people and computes for the Active Life Expectancy (ALE using a multistate life table method. Findings on ALE demonstrate that females and urban residents live longer and have a greater proportion of their remaining life in active state compared to their counterparts. Health transition analysis indicates a significant proportion experiencing recovery. Age, sex, place of residence and health status/behavior indicators (self-assessed health, drinking and exercise display a significant influence on future health and mortality trajectories although surprisingly, education did not show any significant effect.

Stromal-epithelial interactions in aging and cancer: Senescent fibroblasts alter epithelial cell differentiation

Energy Technology Data Exchange (ETDEWEB)

Parrinello, Simona; Coppe, Jean-Philippe; Krtolica, Ana; Campisi, Judith

2004-07-14

Cellular senescence suppresses cancer by arresting cells at risk for malignant tumorigenesis. However, senescent cells also secrete molecules that can stimulate premalignant cells to proliferate and form tumors, suggesting the senescence response is antagonistically pleiotropic. We show that premalignant mammary epithelial cells exposed to senescent human fibroblasts in mice irreversibly lose differentiated properties, become invasive and undergo full malignant transformation. Moreover, using cultured mouse or human fibroblasts and non-malignant breast epithelial cells, we show that senescent fibroblasts disrupt epithelial alveolar morphogenesis, functional differentiation, and branching morphogenesis. Further, we identify MMP-3 as the major factor responsible for the effects of senescent fibroblasts on branching morphogenesis. Our findings support the idea that senescent cells contribute to age-related pathology, including cancer, and describe a new property of senescent fibroblasts--the ability to alter epithelial differentiation--that might also explain the loss of tissue function and organization that is a hallmark of aging.

Polyamines, peroxidase and proteins involved in the senescence ...

African Journals Online (AJOL)

Senescence is the natural aging process at the cellular level or range of phenomena associated with this process. The objective of this review was to show the involvement of substances that may be related to senescence in plants, such as polyamines, peroxidase and proteins. These substances were related with the ...

The effect of ethylene on sucrose-uptake by senescing petunia flowers.

OpenAIRE

2008-01-01

The influence of sucrose as an important factor in the vase-life of cut flowers has been dually noted. Sucrose is actively transported across the cell membrane via a symport system and the membrane-imbedded ATPase enzyme generates the required energy and proton gradient for the process. The activity of this enzyme decreases during the senescence of Petunia petals, concomitant with a decrease in sucrose-uptake in the post-climacteric phase. However, ATP does not appear to be limiting, indicati...

Determinants of life expectancy in eastern mediterranean region: a health production function.

Science.gov (United States)

Bayati, Mohsen; Akbarian, Reza; Kavosi, Zahra

2013-06-01

Determinants of health or health production function in health economics literature constitute noticeable issues in health promotion. This study aimed at estimating a health production function for East Mediterranean Region (EMR) based on the Grossman theoretical model. This ecological study was performed using the econometric methods. The panel data model was used in order to determine the relationship between life expectancy and socioeconomic factors. The data for 21 EMR countries between 1995 and 2007 were used. Fixed-effect-model was employed to estimate the parameters based on Hausman test. In estimating the health production function, factors such as income per capita (β=0.05, Pdeterminants of health status, proxied by life expectancy at birth. A notable result was the elasticity of life expectancy with respect to the employment rate and its significance level was different between males (β=0.13, P0.001). In order to improve the health status in EMR countries, health policymakers should focus on the factors which lie outside the healthcare system. These factors are mainly associated with economic growth and development level. Thus, the economic stabilisation policies with the aim of increasing the productivity, economic growth, and reducing unemployment play significant roles in the health status of the people of the region.

Mortality and life expectancy in homeless men and women in Rotterdam: 2001-2010.

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Wilma J Nusselder

Full Text Available BACKGROUND: Data on mortality among homeless people are limited. Therefore, this study aimed to describe mortality patterns within a cohort of homeless adults in Rotterdam (the Netherlands and to assess excess mortality as compared to the general population in that city. METHODS: Based on 10-year follow-up of homeless adults aged ≥ 20 years who visited services for homeless people in Rotterdam in 2001, and on vital statistics, we assessed the association of mortality with age, sex and type of service used (e.g. only day care, convalescence care, other within the homeless cohort, and also compared mortality between the homeless and general population using Poisson regression. Life tables and decomposition methods were used to examine differences in life expectancy. RESULTS: During follow-up, of the 2096 adult homeless 265 died. Among the homeless, at age 30 years no significant sex differences were found in overall mortality rates and life expectancy. Compared with the general Rotterdam population, mortality rates were 3.5 times higher in the homeless cohort. Excess mortality was larger in women (rate ratio [RR] RR 5.56, 95% CI 3.95-7.82 as compared to men (RR 3.31, 95% CI 2.91-3.77, and decreased with age (RR 7.67, 95% CI 6.87-8.56 for the age group 20-44 and RR 1.63, 95% CI 1.41-1.88 for the age group 60+ years. Life expectancy at age 30 years was 11.0 (95% CI 9.1-12.9 and 15.9 (95% CI 10.3-21.5 years lower for homeless men and women compared to men and women in the general population respectively. CONCLUSION: Homeless adults face excessive losses in life expectancy, with greatest disadvantages among homeless women and the younger age groups.

Mechanisms of Diabetes-Induced Endothelial Cell Senescence: Role of Arginase 1

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Esraa Shosha

2018-04-01

Full Text Available We have recently found that diabetes-induced premature senescence of retinal endothelial cells is accompanied by NOX2-NADPH oxidase-induced increases in the ureohydrolase enzyme arginase 1 (A1. Here, we used genetic strategies to determine the specific involvement of A1 in diabetes-induced endothelial cell senescence. We used A1 knockout mice and wild type mice that were rendered diabetic with streptozotocin and retinal endothelial cells (ECs exposed to high glucose or transduced with adenovirus to overexpress A1 for these experiments. ABH [2(S-Amino-6-boronohexanoic acid] was used to inhibit arginase activity. We used Western blotting, immunolabeling, quantitative PCR, and senescence associated β-galactosidase (SA β-Gal activity to evaluate senescence. Analyses of retinal tissue extracts from diabetic mice showed significant increases in mRNA expression of the senescence-related proteins p16INK4a, p21, and p53 when compared with non-diabetic mice. SA β-Gal activity and p16INK4a immunoreactivity were also increased in retinal vessels from diabetic mice. A1 gene deletion or pharmacological inhibition protected against the induction of premature senescence. A1 overexpression or high glucose treatment increased SA β-Gal activity in cultured ECs. These results demonstrate that A1 is critically involved in diabetes-induced senescence of retinal ECs. Inhibition of arginase activity may therefore be an effective therapeutic strategy to alleviate diabetic retinopathy by preventing premature senescence.

Increasing disability-free life expectancy among older adults in Palestine from 2006 to 2010.

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Brønnum-Hansen, Henrik; Duraidi, Mohammed; Qalalwa, Khaled; Jeune, Bernard

2015-04-01

The population of Palestine comprises almost 200 000 Palestinians aged 60 or older. The purpose of the study was to estimate disability-free life expectancy for Palestinians living in the West Bank and Gaza Strip and to evaluate changes from 2006 to 2010. The study combined mortality data and prevalence of activity limitation derived from the Palestinian Family Health Surveys carried out in 2006 and 2010. Based on questions about the ability to perform five basic daily activities, disability-free life expectancy was estimated. Changes between 2006 and 2010 were decomposed into contributions from changes in mortality and disability. Life expectancy at age 60 increased from 17.1 years in 2006 to 17.3 years in 2010 for men and from 18.7 years to 19.0 years for women. Disability-free life expectancy increased significantly, by 1.3 years for 60-year-old men (from 12.8 years to 14.1 years) and 1.8 years for 60-year-old women (from 12.6 years to 14.4 years). This increase was seen in the Gaza Strip as well as in the West Bank. While the modest contribution of the mortality effect did not differ between gender and regions, the strong contributions from the disability effects varied, being greatest for women in the Gaza Strip. The significant increase in disability-free life expectancy for both genders is remarkable and, to our knowledge, not seen in other low-income countries. This change may be due to decreasing incidence of disability and greater recovery from disability as a result of better prevention, care and rehabilitation of chronic diseases. © The Author 2014. Published by Oxford University Press on behalf of the European Public Health Association. All rights reserved.

Flavonoids and darkness lower PCD in senescing Vitis vinifera suspension cell cultures.

Science.gov (United States)

Bertolini, Alberto; Petrussa, Elisa; Patui, Sonia; Zancani, Marco; Peresson, Carlo; Casolo, Valentino; Vianello, Angelo; Braidot, Enrico

2016-10-26

Senescence is a key developmental process occurring during the life cycle of plants that can be induced also by environmental conditions, such as starvation and/or darkness. During senescence, strict control of genes regulates ordered degradation and dismantling events, the most remarkable of which are genetically programmed cell death (PCD) and, in most cases, an upregulation of flavonoid biosynthesis in the presence of light. Flavonoids are secondary metabolites that play multiple essential roles in development, reproduction and defence of plants, partly due to their well-known antioxidant properties, which could affect also the same cell death machinery. To understand further the effect of endogenously-produced flavonoids and their interplay with different environment (light or dark) conditions, two portions (red and green) of a senescing grapevine callus were used to obtain suspension cell cultures. Red Suspension cell Cultures (RSC) and Green Suspension cell Cultures (GSC) were finally grown under either dark or light conditions for 6 days. Darkness enhanced cell death (mainly necrosis) in suspension cell culture, when compared to those grown under light condition. Furthermore, RSC with high flavonoid content showed a higher viability compared to GSC and were more protected toward PCD, in accordance to their high content in flavonoids, which might quench ROS, thus limiting the relative signalling cascade. Conversely, PCD was mainly occurring in GSC and further increased by light, as it was shown by cytochrome c release and TUNEL assays. Endogenous flavonoids were shown to be good candidates for exploiting an efficient protection against oxidative stress and PCD induction. Light seemed to be an important environmental factor able to induce PCD, especially in GSC, which lacking of flavonoids were not capable of preventing oxidative damage and signalling leading to senescence.

Plant senescence and proteolysis: two processes with one destiny.

Science.gov (United States)

Diaz-Mendoza, Mercedes; Velasco-Arroyo, Blanca; Santamaria, M Estrella; González-Melendi, Pablo; Martinez, Manuel; Diaz, Isabel

2016-01-01

Senescence-associated proteolysis in plants is a complex and controlled process, essential for mobilization of nutrients from old or stressed tissues, mainly leaves, to growing or sink organs. Protein breakdown in senescing leaves involves many plastidial and nuclear proteases, regulators, different subcellular locations and dynamic protein traffic to ensure the complete transformation of proteins of high molecular weight into transportable and useful hydrolysed products. Protease activities are strictly regulated by specific inhibitors and through the activation of zymogens to develop their proteolytic activity at the right place and at the proper time. All these events associated with senescence have deep effects on the relocation of nutrients and as a consequence, on grain quality and crop yield. Thus, it can be considered that nutrient recycling is the common destiny of two processes, plant senescence and, proteolysis. This review article covers the most recent findings about leaf senescence features mediated by abiotic and biotic stresses as well as the participants and steps required in this physiological process, paying special attention to C1A cysteine proteases, their specific inhibitors, known as cystatins, and their potential targets, particularly the chloroplastic proteins as source for nitrogen recycling.

Increasing social inequality in life expectancy in Denmark

DEFF Research Database (Denmark)

Brønnum-Hansen, Henrik; Baadsgaard, Mikkel

2007-01-01

BACKGROUND: The purpose of the study was to determine trends in social inequality in mortality and life expectancy in Denmark. METHODS: The study was based on register data on educational level and mortality during the period 1981-2005 and comprised all deaths among Danes aged 30-60. Sex- and age...... with low and high educational level increased by 0.3 years. CONCLUSION: During the past 25 years, the social gap in mortality has widened in Denmark. In particular, women with a low educational level have been left behind....

Impact of bariatric surgery on life expectancy in severely obese patients with diabetes: A Decision analysis

Science.gov (United States)

Schauer, Daniel P.; Arterburn, David E.; Livingston, Edward H.; Coleman, Karen J.; Sidney, Steve; Fisher, David; O'Connor, Patrick; Fischer, David; Eckman, Mark H.

2014-01-01

Objective To create a decision analytic model to estimate the balance between treatment risks and benefits for severely obese patients with diabetes. Summary Background Data Bariatric surgery leads to many desirable metabolic changes, but long-term impact of bariatric surgery on life expectancy in patients with diabetes has not yet been quantified. Methods We developed a Markov state transition model with multiple Cox proportional hazards models and logistic regression models as inputs to compare bariatric surgery versus no surgical treatment for severely obese diabetic patients. The model is informed by data from three large cohorts: 1) 159,000 severely obese diabetic patients (4,185 had bariatric surgery) from 3 HMO Research Network sites, 2) 23,000 subjects from the Nationwide Inpatient Sample (NIS), and 3) 18,000 subjects from the National Health Interview Survey linked to the National Death Index. Results In our main analyses, we found that a 45 year-old female with diabetes and a BMI of 45 kg/m2 gained an additional 6.7 years of life expectancy with bariatric surgery (38.4 years with surgery vs. 31.7 without). Sensitivity analyses revealed that the gain in life expectancy decreased with increasing BMI, until a BMI of 62 kg/m2 is reached, at which point nonsurgical treatment was associated with greater life expectancy. Similar results were seen for both men and women in all age groups. Conclusions For most severely obese patients with diabetes, bariatric surgery appears to improve life expectancy; however, surgery may reduce life expectancy for the super obese with BMIs over 62 kg/m2. PMID:25844968

Enhanced molecular aging in late-life depression: the Senescent Associated Secretory Phenotype

Science.gov (United States)

Diniz, Breno Satler; Reynolds, Charles F.; Sibille, Etienne; Lin, Chien-Wei; Tseng, George; Lotrich, Francis; Aizenstein, Howard J.; Butters, Meryl A.

2016-01-01

Objective This study aims to investigate whether a systemic molecular pattern associated with aging (senescent-associated secretory phenotype – SASP) is elevated in adults with late-life depression (LLD), compared to never-depressed elderly comparison participants. Design Cross-sectional study. Participants We included 111 older adults (80 with LLD and 31 comparison participants) in this study. Measurement A panel of 22 SASP-related proteins was extracted from a previous multiplex protein panel performed in these participants. We conducted a principal component analysis to create the SASP index based on individual weights of each of protein. Results Participants with LLD showed a significantly increased SASP index compared to comparison participants, after controlling for age, depressive symptoms, medical comorbidity (CIRS-G) scores, gender, and cognitive performance (F(1,98)=7.3, p=0.008). Correlation analyses revealed that the SASP index was positively correlated with age (r=0.2, p = 0.03) and CIRS score (r=0.27, p=0.005), and negatively correlated with information processing speed (r=−0.34, p=0.001), executive function (r=−0.27, p=0.004) and global cognitive performance (r=−0.28, p=0.007). Conclusions To the best of our knowledge, this is the first study to show that a set of proteins (i.e., SASP index) primarily associated with cellular aging, is abnormally regulated and elevated in LLD. These results suggest that individuals with LLD display enhanced aging-related molecular patterns that are associated with higher medical comorbidity and worse cognitive function. Finally, we provide a set of proteins that can serve as potential therapeutic targets and biomarkers to monitor the effects of therapeutic or preventative interventions in LLD. PMID:27856124

Selective elimination of senescent cells by mitochondrial targeting is regulated by ANT2

DEFF Research Database (Denmark)

Hubackova, Sona; Davidova, Eliska; Rohlenova, Katerina

2018-01-01

and development of age-related diseases. We found that the anticancer agent mitochondria-targeted tamoxifen (MitoTam), unlike conventional anticancer agents, kills cancer cells without inducing senescence in vitro and in vivo. Surprisingly, it also selectively eliminates both malignant and non-cancerous senescent...... cells. In naturally aged mice treated with MitoTam for 4 weeks, we observed a significant decrease of senescence markers in all tested organs compared to non-treated animals. Mechanistically, we found that the susceptibility of senescent cells to MitoTam is linked to a very low expression level...... of adenine nucleotide translocase-2 (ANT2), inherent to the senescent phenotype. Restoration of ANT2 in senescent cells resulted in resistance to MitoTam, while its downregulation in non-senescent cells promoted their MitoTam-triggered elimination. Our study documents a novel, translationally intriguing role...

NAC Transcription Factors in Senescence: From Molecular Structure to Function in Crops

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Dagmara Podzimska-Sroka

2015-07-01

Full Text Available Within the last decade, NAC transcription factors have been shown to play essential roles in senescence, which is the focus of this review. Transcriptome analyses associate approximately one third of Arabidopsis NAC genes and many crop NAC genes with senescence, thereby implicating NAC genes as important regulators of the senescence process. The consensus DNA binding site of the NAC domain is used to predict NAC target genes, and protein interaction sites can be predicted for the intrinsically disordered transcription regulatory domains of NAC proteins. The molecular characteristics of these domains determine the interactions in gene regulatory networks. Emerging local NAC-centered gene regulatory networks reveal complex molecular mechanisms of stress- and hormone-regulated senescence and basic physiological steps of the senescence process. For example, through molecular interactions involving the hormone abscisic acid, Arabidopsis NAP promotes chlorophyll degradation, a hallmark of senescence. Furthermore, studies of the functional rice ortholog, OsNAP, suggest that NAC genes can be targeted to obtain specific changes in lifespan control and nutrient remobilization in crop plants. This is also exemplified by the wheat NAM1 genes which promote senescence and increase grain zinc, iron, and protein content. Thus, NAC genes are promising targets for fine-tuning senescence for increased yield and quality.

Integrin Beta 3 Regulates Cellular Senescence by Activating the TGF-β Pathway

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Valentina Rapisarda

2017-03-01

Full Text Available Cellular senescence is an important in vivo mechanism that prevents the propagation of damaged cells. However, the precise mechanisms regulating senescence are not well characterized. Here, we find that ITGB3 (integrin beta 3 or β3 is regulated by the Polycomb protein CBX7. β3 expression accelerates the onset of senescence in human primary fibroblasts by activating the transforming growth factor β (TGF-β pathway in a cell-autonomous and non-cell-autonomous manner. β3 levels are dynamically increased during oncogene-induced senescence (OIS through CBX7 Polycomb regulation, and downregulation of β3 levels overrides OIS and therapy-induced senescence (TIS, independently of its ligand-binding activity. Moreover, cilengitide, an αvβ3 antagonist, has the ability to block the senescence-associated secretory phenotype (SASP without affecting proliferation. Finally, we show an increase in β3 levels in a subset of tissues during aging. Altogether, our data show that integrin β3 subunit is a marker and regulator of senescence.

Educational differences in disability-free life expectancy: a comparative study of long-standing activity limitation in eight European countries.

Science.gov (United States)

Mäki, Netta; Martikainen, Pekka; Eikemo, Terje; Menvielle, Gwenn; Lundberg, Olle; Ostergren, Olof; Jasilionis, Domantas; Mackenbach, Johan P

2013-10-01

Healthy life expectancy is a composite measure of length and quality of life and an important indicator of health in aging populations. There are few cross-country comparisons of socioeconomic differences in healthy life expectancy. Most of the existing comparisons focus on Western Europe and the United States, often relying on older data. To address these deficiencies, we estimated educational differences in disability-free life expectancy for eight countries from all parts of Europe in the early 2000s. Long-standing severe disability was measured as a Global Activity Limitation Indicator (GALI) derived from the European Union Statistics on Income and Living Conditions (EU-SILC) survey. Census-linked mortality data were collected by a recent project comparing health inequalities between European countries (the EURO-GBD-SE project). We calculated sex-specific educational differences in disability-free life expectancy between the ages of 30 and 79 years using the Sullivan method. The lowest disability-free life expectancy was found among Lithuanian men and women (33.1 and 39.1 years, respectively) and the highest among Italian men and women (42.8 and 44.4 years, respectively). Life expectancy and disability-free life expectancy were directly related to the level of education, but the educational differences were much greater in the latter in all countries. The difference in the disability-free life expectancy between those with a primary or lower secondary education and those with a tertiary education was over 10 years for males in Lithuania and approximately 7 years for males in Austria, Finland and France, as well as for females in Lithuania. The difference was smallest in Italy (4 and 2 years among men and women, respectively). Highly educated Europeans can expect to live longer and spend more years in better health than those with lower education. The size of the educational difference in disability-free life expectancy varies significantly between countries

Closing the gap: increases in life expectancy among treated HIV-positive individuals in the United States and Canada.

Directory of Open Access Journals (Sweden)

Hasina Samji

Full Text Available Combination antiretroviral therapy (ART has significantly increased survival among HIV-positive adults in the United States (U.S. and Canada, but gains in life expectancy for this region have not been well characterized. We aim to estimate temporal changes in life expectancy among HIV-positive adults on ART from 2000-2007 in the U.S. and Canada.Participants were from the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD, aged ≥20 years and on ART. Mortality rates were calculated using participants' person-time from January 1, 2000 or ART initiation until death, loss to follow-up, or administrative censoring December 31, 2007. Life expectancy at age 20, defined as the average number of additional years that a person of a specific age will live, provided the current age-specific mortality rates remain constant, was estimated using abridged life tables.The crude mortality rate was 19.8/1,000 person-years, among 22,937 individuals contributing 82,022 person-years and 1,622 deaths. Life expectancy increased from 36.1 [standard error (SE 0.5] to 51.4 [SE 0.5] years from 2000-2002 to 2006-2007. Men and women had comparable life expectancies in all periods except the last (2006-2007. Life expectancy was lower for individuals with a history of injection drug use, non-whites, and in patients with baseline CD4 counts <350 cells/mm(3.A 20-year-old HIV-positive adult on ART in the U.S. or Canada is expected to live into their early 70 s, a life expectancy approaching that of the general population. Differences by sex, race, HIV transmission risk group, and CD4 count remain.

Analysis of individual cells identifies cell-to-cell variability following induction of cellular senescence.

Science.gov (United States)

Wiley, Christopher D; Flynn, James M; Morrissey, Christapher; Lebofsky, Ronald; Shuga, Joe; Dong, Xiao; Unger, Marc A; Vijg, Jan; Melov, Simon; Campisi, Judith

2017-10-01

Senescent cells play important roles in both physiological and pathological processes, including cancer and aging. In all cases, however, senescent cells comprise only a small fraction of tissues. Senescent phenotypes have been studied largely in relatively homogeneous populations of cultured cells. In vivo, senescent cells are generally identified by a small number of markers, but whether and how these markers vary among individual cells is unknown. We therefore utilized a combination of single-cell isolation and a nanofluidic PCR platform to determine the contributions of individual cells to the overall gene expression profile of senescent human fibroblast populations. Individual senescent cells were surprisingly heterogeneous in their gene expression signatures. This cell-to-cell variability resulted in a loss of correlation among the expression of several senescence-associated genes. Many genes encoding senescence-associated secretory phenotype (SASP) factors, a major contributor to the effects of senescent cells in vivo, showed marked variability with a subset of highly induced genes accounting for the increases observed at the population level. Inflammatory genes in clustered genomic loci showed a greater correlation with senescence compared to nonclustered loci, suggesting that these genes are coregulated by genomic location. Together, these data offer new insights into how genes are regulated in senescent cells and suggest that single markers are inadequate to identify senescent cells in vivo. © 2017 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Bring out your dead!: A study of income inequality and life expectancy in the United States, 2000-2010.

Science.gov (United States)

Hill, Terrence D; Jorgenson, Andrew

2018-01-01

We test whether income inequality undermines female and male life expectancy in the United States. We employ data for all 50 states and the District of Columbia and two-way fixed effects to model state-level average life expectancy as a function of multiple income inequality measures and time-varying characteristics. We find that state-level income inequality is inversely associated with female and male life expectancy. We observe this general pattern across four measures of income inequality and under the rigorous conditions of state-specific and year-specific fixed effects. If income inequality undermines life expectancy, redistribution policies could actually improve the health of states. Copyright © 2017 Elsevier Ltd. All rights reserved.

Targeting Senescent Cells : Possible Implications for Delaying Skin Aging: A Mini-Review

NARCIS (Netherlands)

Velarde, Michael C.; Demaria, Marco

2016-01-01

Senescent cells are induced by a wide variety of stimuli. They accumulate in several tissues during aging, including the skin. Senescent cells secrete proinflammatory cytokines, chemokines, growth factors, and proteases, a phenomenon called senescence-associated secretory phenotype (SASP), which are

Contrasting patterns of cytokinins between years in senescing aspen leaves

Czech Academy of Sciences Publication Activity Database

Edlund, E.; Novák, Ondřej; Karady, M.; Ljung, K.; Jansson, S.

2017-01-01

Roč. 40, č. 5 (2017), s. 622-634 ISSN 0140-7791 R&D Projects: GA ČR GA14-34792S; GA MŠk(CZ) LO1204 Institutional support: RVO:61389030 Keywords : leaf senescence * arabidopsis-thaliana * autumn senescence * gene-expression * populus-trichocarpa * mass-spectrometry * tobacco plants * translocation * biosynthesis * identification * autumn senescence * gene expression * metabolism * Populus tremula * profiling Subject RIV: CB - Analytical Chemistry, Separation OBOR OECD: Plant sciences, botany Impact factor: 6.173, year: 2016

Loss of life expectancy derived from a standardized mortality ratio in Denmark, Finland, Norway and Sweden.

Science.gov (United States)

Skriver, Mette Vinther; Væth, Michael; Støvring, Henrik

2018-01-01

The standardized mortality ratio (SMR) is a widely used measure. A recent methodological study provided an accurate approximate relationship between an SMR and difference in lifetime expectancies. This study examines the usefulness of the theoretical relationship, when comparing historic mortality data in four Scandinavian populations. For Denmark, Finland, Norway and Sweden, data on mortality every fifth year in the period 1950 to 2010 were obtained. Using 1980 as the reference year, SMRs and difference in life expectancy were calculated. The assumptions behind the theoretical relationship were examined graphically. The theoretical relationship predicts a linear association with a slope, [Formula: see text], between log(SMR) and difference in life expectancies, and the theoretical prediction and calculated differences in lifetime expectancies were compared. We examined the linear association both for life expectancy at birth and at age 30. All analyses were done for females, males and the total population. The approximate relationship provided accurate predictions of actual differences in lifetime expectancies. The accuracy of the predictions was better when age was restricted to above 30, and improved if the changes in mortality rate were close to a proportional change. Slopes of the linear relationship were generally around 9 for females and 10 for males. The theoretically derived relationship between SMR and difference in life expectancies provides an accurate prediction for comparing populations with approximately proportional differences in mortality, and was relatively robust. The relationship may provide a useful prediction of differences in lifetime expectancies, which can be more readily communicated and understood.

Increasing disability-free life expectancy among older adults in Palestine from 2006 to 2010

DEFF Research Database (Denmark)

Brønnum-Hansen, Henrik; Duraidi, Mohammed; Qalalwa, Khaled

2015-01-01

into contributions from changes in mortality and disability. RESULTS: Life expectancy at age 60 increased from 17.1 years in 2006 to 17.3 years in 2010 for men and from 18.7 years to 19.0 years for women. Disability-free life expectancy increased significantly, by 1.3 years for 60-year-old men (from 12.8 years to 14...... mortality data and prevalence of activity limitation derived from the Palestinian Family Health Surveys carried out in 2006 and 2010. Based on questions about the ability to perform five basic daily activities, disability-free life expectancy was estimated. Changes between 2006 and 2010 were decomposed.......1 years) and 1.8 years for 60-year-old women (from 12.6 years to 14.4 years). This increase was seen in the Gaza Strip as well as in the West Bank. While the modest contribution of the mortality effect did not differ between gender and regions, the strong contributions from the disability effects varied...

Development of a clinical prediction model to calculate patient life expectancy: the measure of actuarial life expectancy (MALE).

Science.gov (United States)

Clarke, M G; Kennedy, K P; MacDonagh, R P

2009-01-01

To develop a clinical prediction model enabling the calculation of an individual patient's life expectancy (LE) and survival probability based on age, sex, and comorbidity for use in the joint decision-making process regarding medical treatment. A computer software program was developed with a team of 3 clinicians, 2 professional actuaries, and 2 professional computer programmers. This incorporated statistical spreadsheet and database access design methods. Data sources included life insurance industry actuarial rating factor tables (public and private domain), Government Actuary Department UK life tables, professional actuarial sources, and evidence-based medical literature. The main outcome measures were numerical and graphical display of comorbidity-adjusted LE; 5-, 10-, and 15-year survival probability; in addition to generic UK population LE. Nineteen medical conditions, which impacted significantly on LE in actuarial terms and were commonly encountered in clinical practice, were incorporated in the final model. Numerical and graphical representations of statistical predictions of LE and survival probability were successfully generated for patients with either no comorbidity or a combination of the 19 medical conditions included. Validation and testing, including actuarial peer review, confirmed consistency with the data sources utilized. The evidence-based actuarial data utilized in this computer program design represent a valuable resource for use in the clinical decision-making process, where an accurate objective assessment of patient LE can so often make the difference between patients being offered or denied medical and surgical treatment. Ongoing development to incorporate additional comorbidities and enable Web-based access will enhance its use further.

Cytokine loops driving senescence

Czech Academy of Sciences Publication Activity Database

Bartek, Jiří; Hodný, Zdeněk; Lukáš, Jan

2008-01-01

Roč. 10, č. 8 (2008), s. 887-889 ISSN 1465-7392 Institutional research plan: CEZ:AV0Z50520514 Keywords : cellular senescence * cytokines * autocrine feedback loop Subject RIV: EB - Genetics ; Molecular Biology Impact factor: 17.774, year: 2008

Associations of Smoking, Physical Inactivity, Heavy Drinking, and Obesity with Quality-Adjusted Life Expectancy among US Adults with Depression.

Science.gov (United States)

Jia, Haomiao; Zack, Matthew M; Gottesman, Irving I; Thompson, William W

2018-03-01

To examine associations between four health behaviors (smoking, physical inactivity, heavy alcohol drinking, and obesity) and three health indices (health-related quality of life, life expectancy, and quality-adjusted life expectancy (QALE)) among US adults with depression. Data were obtained from the 2006, 2008, and 2010 Behavioral Risk Factor Surveillance System data. The EuroQol five-dimensional questionnaire (EQ-5D) health preference scores were estimated on the basis of extrapolations from the Centers for Disease Control and Prevention's healthy days measures. Depression scores were estimated using the eight-item Patient Health Questionnaire. Life expectancy estimates were obtained from US life tables, and QALE was estimated from a weighted combination of the EQ-5D scores and the life expectancy estimates. Outcomes were summarized by depression status for the four health behaviors (smoking, physical inactivity, heavy alcohol drinking, and obesity). For depressed adults, current smokers and the physically inactive had significantly lower EQ-5D scores (0.040 and 0.171, respectively), shorter life expectancy (12.9 and 10.8 years, respectively), and substantially less QALE (8.6 and 10.9 years, respectively). For nondepressed adults, estimated effects were similar but smaller. Heavy alcohol drinking among depressed adults, paradoxically, was associated with higher EQ-5D scores but shorter life expectancy. Obesity was strongly associated with lower EQ-5D scores but only weakly associated with shorter life expectancy. Among depressed adults, physical inactivity and smoking were strongly associated with lower EQ-5D scores, life expectancy, and QALE, whereas obesity and heavy drinking were only weakly associated with these indices. These results suggest that reducing physical inactivity and smoking would improve health more among depressed adults. Copyright © 2018. Published by Elsevier Inc.

RELATION BETWEEN QUALITY OF LIFE, CHOICE MAKING, AND FUTURE EXPECTATIONS IN ADULTS WITH INTELLECTUAL DISABILITY

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Vesna KOSTIKJ-IVANOVIKJ

2016-09-01

Full Text Available Introduction: Quality of life of individuals depends significantly on the ability to have control over everyday life, realized through the freedom to make choices from available options and self-determination. Objective: To determine the correlation between possibilities for making choices and expectations for the future with the quality of life in adults with intellectual disabilities according self-assessment and assessment by others. Methods: Descriptive, method of correlation and comparative analysis ware applied. From techniques, analysis of documents, surveys with the Quality of life questionnaire by Schalock and Keith and Questionnaire for expectations for the future by Speck, and scaling with the Scale for assessment of the opportunities for making choices by Kishi et al. Sample consisted of 130 intellectually disabled adults and 130 proxies. For establishing connection between the examined phenomena Pearson correlation coefficient (r was used, at p<0,01. Results: There is a strong correlation between the results obtained from the questionnaires about quality of life and opportunities for making choices, self-assessment r(130=0,497, p<0,01, assessment by others r(130=0,482, p<0,01. There is a correlation between the results obtained from the questionnaires about quality of life and expectations for the future, but not very strong, self-assessment r(130=0,233, p=0,008<0,01, assessment by others r(130=0,305, p<0,01. Conclusion: There is a correlation between opportunities for making choices and expectations for the future with the quality of life in adults with intellectual disabilities. To improve the quality of life in these individuals, it is necessary to design programs that will develop self-concept, abilities for self-determination and making personal choices.

Deacetylation of H4-K16Ac and heterochromatin assembly in senescence

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Contrepois Kévin

2012-08-01

Full Text Available Abstract Background Cellular senescence is a stress response of mammalian cells leading to a durable arrest of cell proliferation that has been implicated in tumor suppression, wound healing, and aging. The proliferative arrest is mediated by transcriptional repression of genes essential for cell division by the retinoblastoma protein family. This repression is accompanied by varying degrees of heterochromatin assembly, but little is known regarding the molecular mechanisms involved. Results We found that both deacetylation of H4-K16Ac and expression of HMGA1/2 can contribute to DNA compaction during senescence. SIRT2, an NAD-dependent class III histone deacetylase, contributes to H4-K16Ac deacetylation and DNA compaction in human fibroblast cell lines that assemble striking senescence-associated heterochromatin foci (SAHFs. Decreased H4-K16Ac was observed in both replicative and oncogene-induced senescence of these cells. In contrast, this mechanism was inoperative in a fibroblast cell line that did not assemble extensive heterochromatin during senescence. Treatment of senescent cells with trichostatin A, a class I/II histone deacetylase inhibitor, also induced rapid and reversible decondensation of SAHFs. Inhibition of DNA compaction did not significantly affect the stability of the senescent state. Conclusions Variable DNA compaction observed during senescence is explained in part by cell-type specific regulation of H4 deacetylation and HMGA1/2 expression. Deacetylation of H4-K16Ac during senescence may explain reported decreases in this mark during mammalian aging and in cancer cells.

Senescent T-Cells Promote Bone Loss in Rheumatoid Arthritis

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Johannes Fessler

2018-02-01

Full Text Available ObjectiveT-cells are critical players in the pathogenesis of osteoporosis in patients with rheumatoid arthritis (RA. Premature senescence of lymphocytes including the accumulation of senescent CD4+ T-cells is a hallmark feature of RA. Whether T-cell senescence is associated with bone loss in RA patients is elusive so far.MethodsThis includes a prospective study of consecutive patients with RA (n = 107, patients with primary osteopenia/-porosis (n = 75, and healthy individuals (n = 38. Bone mineral density (BMD was determined by dual-energy X-ray absorptiometry scan. Flow cytometry, magnetic-associated cell sorting, and cell culture experiments were performed to analyze the pro-osteoclastic phenotype and the function of senescent CD4+CD28− T-cells.ResultsPatients with osteopenia/-porosis yielded a higher prevalence of senescent CD4+CD28− T-cells than individuals with normal BMD, in the RA, as well as in the non-RA cohort. Receptor activator of nuclear factor kappa-B ligand (RANKL was expressed at higher levels on CD4+CD28− T-cells as compared to CD28+ T-cells. Stimulation with interleukin-15 led to an up-regulation of RANKL expression, particularly on CD28− T-cells. CD4+CD28− T-cells induced osteoclastogenesis more efficiently than CD28+ T-cells.ConclusionOur data indicate that senescent T-cells promote osteoclastogenesis more efficiently than conventional CD28+ T-cells, which might contribute to the pathogenesis of systemic bone loss in RA and primary osteoporosis.

Oxidative Stress Induces Endothelial Cell Senescence via Downregulation of Sirt6

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Rong Liu

2014-01-01

Full Text Available Accumulating evidence has shown that diabetes accelerates aging and endothelial cell senescence is involved in the pathogenesis of diabetic vascular complications, including diabetic retinopathy. Oxidative stress is recognized as a key factor in the induction of endothelial senescence and diabetic retinopathy. However, specific mechanisms involved in oxidative stress-induced endothelial senescence have not been elucidated. We hypothesized that Sirt6, which is a nuclear, chromatin-bound protein critically involved in many pathophysiologic processes such as aging and inflammation, may have a role in oxidative stress-induced vascular cell senescence. Measurement of Sirt6 expression in human endothelial cells revealed that H2O2 treatment significantly reduced Sirt6 protein. The loss of Sirt6 was associated with an induction of a senescence phenotype in endothelial cells, including decreased cell growth, proliferation and angiogenic ability, and increased expression of senescence-associated β-galactosidase activity. Additionally, H2O2 treatment reduced eNOS expression, enhanced p21 expression, and dephosphorylated (activated retinoblastoma (Rb protein. All of these alternations were attenuated by overexpression of Sirt6, while partial knockdown of Sirt6 expression by siRNA mimicked the effect of H2O2. In conclusion, these results suggest that Sirt6 is a critical regulator of endothelial senescence and oxidative stress-induced downregulation of Sirt6 is likely involved in the pathogenesis of diabetic retinopathy.

Exercise Prevents Diet-Induced Cellular Senescence in Adipose Tissue

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Schafer, M.J.; White, T.A.; Evans, G.; Tonne, J.M.; Verzosa, G.C.; Stout, M.B.; Mazula, D.L.; Palmer, A.K.; Baker, D.J.; Jensen, M.D.; Torbenson, M.S.; Miller, J.D.; Ikeda, Y.; Tchkonia, T.; Deursen, J.M.A. van; Kirkland, J.L.; LeBrasseur, N.K.

2016-01-01

Considerable evidence implicates cellular senescence in the biology of aging and chronic disease. Diet and exercise are determinants of healthy aging; however, the extent to which they affect the behavior and accretion of senescent cells within distinct tissues is not clear. Here we tested the

[Prediction of life expectancy for prostate cancer patients based on the kinetic theory of aging of living systems].

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Viktorov, A A; Zharinov, G M; Neklasova, N Ju; Morozova, E E

2017-01-01

The article presents a methodical approach for prediction of life expectancy for people diagnosed with prostate cancer based on the kinetic theory of aging of living systems. The life expectancy is calculated by solving the differential equation for the rate of aging for three different stage of life - «normal» life, life with prostate cancer and life after combination therapy for prostate cancer. The mathematical model of aging for each stage of life has its own parameters identified by the statistical analysis of healthcare data from the Zharinov's databank and Rosstat CDR NES databank. The core of the methodical approach is the statistical correlation between growth rate of the prostate specific antigen level (PSA-level) or the PSA doubling time (PSA DT) before therapy, and lifespan: the higher the PSA DT is, the greater lifespan. The patients were grouped under the «fast PSA DT» and «slow PSA DT» categories. The satisfactory matching between calculations and experiment is shown. The prediction error of group life expectancy is due to the completeness and reliability of the main data source. A detailed monitoring of the basic health indicators throughout the each person life in each analyzed group is required. The absence of this particular information makes it impossible to predict the individual life expectancy.

Modeling predicted that tobacco control policies targeted at lower educated will reduce the differences in life expectancy

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Bemelmans, W.J.E.; Lenthe, F. van; Hoogenveen, R.; Kunst, A.; Deeg, D.J.H.; Brandt, P.A. van den; Goldbohm, R.A.; Verschuren, W.M.M.

2006-01-01

Background and Objective: To estimate the effects of reducing the prevalence of smoking in lower educated groups on educational differences in life expectancy. Methods: A dynamic Markov-type multistate transition model estimated the effects on life expectancy of two scenarios. A "maximum scenario"

Gender inequality and the gender gap in life expectancy in the European Union.

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Kolip, Petra; Lange, Cornelia

2018-05-14

The gender gap in life expectancy (GGLE) varies substantially in EU 28 Member States. This paper addresses the question of whether gender inequality affects the GGLE as well as life expectancy (LE) in both genders. We conducted an ecological study and used the gender inequality index (GII) developed by the United Nations as well as the gender difference in LE in 2015. We found a correlation between GGLE and GII (r2=0.180) and between GII and LE of 0.418 (women) and 0.430 (men). Gender equality policies are still necessary and will have an effect on women's as well as men's health.

A competing risk model for reduction in life expectancy from radiogenic cancer

International Nuclear Information System (INIS)

Davis, H.T.

1978-01-01

Latent radiogenic cancer fatalities from reactor accidents are considered to be more important than early fatalities. However, early fatalities generally result in appreciable life shortening for the affected individual whereas latent cancer fatalities generally result in limited life shortening. In this report a mathematical model is developed to express the reduction in life expectancy from radiogenic cancer as a function of dose received. The model is then used to compare the linear model of latent radiogenic cancer incidence with several nonlinear models that have appeared in the literature. (author)

How do Major, Violent and Nonviolent Opposition Campaigns, Impact Predicted Life Expectancy at birth?

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Judith Stoddard

2013-08-01

Full Text Available This study compared the effects of major violent and nonviolent opposition campaigns for regime change, on predicted life expectancy at birth. The study measured life expectancy five and ten years after the campaign ended, so that deaths which occurred during the campaign would not be included in the metric, and thus enabling the study of changes made in the state on the social determinants affecting longevity, after the campaign was over. Life expectancy is one of the best reported World Development Indicators and is considered to be a good indication of the overall health and general living conditions of the state and therefore is an ideal indicator to reflect the changes made in the state following a major campaign. The results of this analysis showed that states have a hard time recovering from a major opposition campaign and initially drop behind the growth trend in the world average for predicted life expectancy at birth. But, the type of campaign that was waged and whether it was successful, greatly affects the state’s ability to recover. Encouragingly by a decade after the campaign ends, states that experienced a nonviolent campaign that was successful had caught up to the world average and inched ahead of it. This shows that on this important development indicator, new governments that were ushered into power by nonviolent social movements, had made positive changes in the state that enabled it to surpass world averages.

Relationships between the Active Aging Index and Disability-Free Life Expectancy: A Case Study in the Rajshahi District of Bangladesh.

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Tareque, Md Ismail; Hoque, Nazrul; Islam, Towfiqua Mahfuza; Kawahara, Kazuo; Sugawa, Makiko

2013-12-01

Life expectancy has increased considerably throughout the world. In Bangladesh, life expectancy has increased from about 53 years in 1975 to 69 years in 2010. However, it is unknown whether the increase in life expectancy is simultaneously accompanied by an increase in disability-free life expectancy (DFLE). The purpose of the study described in this article was to explore the relationship between life expectancy and DFLE in the Rajshahi District of Bangladesh by examining the relationships between the Active Aging Index (AAI) and DFLE. The study fi ndings suggest that urban, more-educated, elderly males are more active in all aspects of life and have longer DFLE. Females are found to outlive males but are more likely to live a greater part of their remaining life with disability. Positive correlations between the AAI and DFLE suggest that older adults could enjoy more DFLE by involving themselves in active aging activities.

Long-term cost and life-expectancy consequences of hypertension.

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Kiiskinen, U; Vartiainen, E; Puska, P; Aromaa, A

1998-08-01

To estimate hypertension's long-term cost and impact on life expectancy. A 19-year individual follow-up study. Subjects were categorized according to their baseline (1972) diastolic blood pressure (DBP) level into three groups: normotensive (DBP 104 mmHg). By using their social security identification numbers, we linked the subjects to a set of national registers covering hospital admissions, use of major drugs, absence due to sickness, disability pensions, and deaths. A random population sample of 10 284 men and women aged 25-59 years from the provinces of Kuopio and North Karelia in eastern Finland. The numbers of years of life and years of work lost, the cost of drugs and hospitalization, and the value of productivity lost due to disability and premature mortality. The difference in life expectancy between normotensive and severely hypertensive men was 2.7 years, of which 2.0 years was due to cardiovascular disease (CVD). Among women the corresponding differences were 2.0 and 1.5 years. Severely hypertensive men lost 2.6 years of work more than did normotensive men, of which 1.7 years was due to CVD. Among women the differences were 2.2 and 1.3 years. The mean undiscounted total costs (USA dollars at 1992 prices) were $132 500 among normotensive, $146 500 among mildly hypertensive, and $219 300 among severely hypertensive men, of which CVD accounted for 28, 39, and 43%, respectively. More than 90% of the total costs were indirect productivity losses. Among women the total costs were lower for all DBP categories, as were the shares of CVD-related costs. The proportional increase in costs on going from the lowest to the highest DBP category was, however, somewhat larger among women. On the population level, severe hypertension leads to considerable losses in terms of years of life lost, years of work lost, and costs. However, the overall impact of mild hypertension is much more limited.

New population and life expectancy estimates for the Indigenous population of Australia's Northern Territory, 1966-2011.

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Tom Wilson

Full Text Available The Indigenous population of Australia suffers considerable disadvantage across a wide range of socio-economic indicators, and is therefore the focus of many policy initiatives attempting to 'close the gap' between Indigenous and non-Indigenous Australians. Unfortunately, past population estimates have proved unreliable as denominators for these indicators. The aim of the paper is to contribute more robust estimates for the Northern Territory Indigenous population for the period 1966-2011, and hence estimate one of the most important of socio-economic indicators, life expectancy at birth.A consistent time series of population estimates from 1966 to 2011, based off the more reliable 2011 official population estimates, was created by a mix of reverse and forward cohort survival. Adjustments were made to ensure sensible sex ratios and consistency with recent birth registrations. Standard life table methods were employed to estimate life expectancy. Drawing on an approach from probabilistic forecasting, confidence intervals surrounding population numbers and life expectancies were estimated.The Northern Territory Indigenous population in 1966 numbered between 23,800 and 26,100, compared to between 66,100 and 73,200 in 2011. In 1966-71 Indigenous life expectancy at birth lay between 49.1 and 56.9 years for males and between 49.7 and 57.9 years for females, whilst by 2006-11 it had increased to between 60.5 and 66.2 years for males and between 65.4 and 70.8 for females. Over the last 40 years the gap with all-Australian life expectancy has not narrowed, fluctuating at about 17 years for both males and females. Whilst considerable progress has been made in closing the gap in under-five mortality, at most other ages the mortality rate differential has increased.A huge public health challenge remains. Efforts need to be redoubled to reduce the large gap in life expectancy between Indigenous and non-Indigenous Australians.

Physiological and biochemical aspects of flower development and senescence in Nicotiana plumbaginifolia Viv.

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Nisar Shaziya

2017-06-01

Full Text Available Healthy buds of Nicotiana plumbaginifolia growing in the Kashmir University Botanic Garden were selected for the present study. Flower development and senescence was divided into seven stages, viz., tight bud stage (I, mature bud stage (II, pencil stage (III, partially open stage (IV, open stage (V, partially senescent stage (VI and senescent stage (VII. Various physiological and biochemical changes were recorded at each stage of flower development and senescence. Floral diameter, fresh mass, dry mass and water content showed an increase up to flower opening (stage V and thereafter a significant decrease was recorded as the flower development progressed towards senescence through stages VI and VII. An increase in α-amino acids, total phenols and sugars was registered towards anthesis (stage V and a decrease in these parameters was recorded with senescence. Protease activity showed a significant increase towards senescence with a concomitant decrease in soluble proteins. Based on the quantitative analysis of various biochemical parameters, the flower opening in N. plumbaginifolia seems to be accompanied by an increase in the water content, soluble proteins, α‑amino acids and phenols. A decrease in these parameters, besides an increase in protease activity induces senescence in the beautiful flowers of N. plumbaginifolia. Understanding flower senescence may help in improving the postharvest performance of this beautiful ornamental flower to make it a potential material for the floriculture industry.

Long noncoding RNA PANDA and scaffold-attachment-factor SAFA control senescence entry and exit.

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Puvvula, Pavan Kumar; Desetty, Rohini Devi; Pineau, Pascal; Marchio, Agnés; Moon, Anne; Dejean, Anne; Bischof, Oliver

2014-11-19

Cellular senescence is a stable cell cycle arrest that limits the proliferation of pre-cancerous cells. Here we demonstrate that scaffold-attachment-factor A (SAFA) and the long noncoding RNA PANDA differentially interact with polycomb repressive complexes (PRC1 and PRC2) and the transcription factor NF-YA to either promote or suppress senescence. In proliferating cells, SAFA and PANDA recruit PRC complexes to repress the transcription of senescence-promoting genes. Conversely, the loss of SAFA-PANDA-PRC interactions allows expression of the senescence programme. Accordingly, we find that depleting either SAFA or PANDA in proliferating cells induces senescence. However, in senescent cells where PANDA sequesters transcription factor NF-YA and limits the expression of NF-YA-E2F-coregulated proliferation-promoting genes, PANDA depletion leads to an exit from senescence. Together, our results demonstrate that PANDA confines cells to their existing proliferative state and that modulating its level of expression can cause entry or exit from senescence.

Socioeconomic, remoteness and sex differences in life expectancy in New South Wales, Australia, 2001-2012: a population-based study.

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Stephens, Alexandre S; Gupta, Leena; Thackway, Sarah; Broome, Richard A

2017-01-10

Despite being one of the healthiest countries in the world, Australia displays substantial mortality differentials by socioeconomic disadvantage, remoteness and sex. In this study, we examined how these mortality differentials translated to differences in life expectancy between 2001 and 2012. Population-based study using mortality and estimated residential population data from Australia's largest state, New South Wales (NSW), between 2001 and 2012. Age-group-specific death rates by socioeconomic disadvantage quintile, remoteness (major cities vs regional and remote areas), sex and year were estimated via Poisson regression, and inputted into life table calculations to estimate life expectancy. Life expectancy decreased with increasing socioeconomic disadvantage in males and females. The disparity between the most and least socioeconomically deprived quintiles was 3.77 years in males and 2.39 years in females in 2012. Differences in life expectancy by socioeconomic disadvantage were mostly stable over time. Gender gaps in life expectancy ranged from 3.50 to 4.93 years (in 2012), increased with increasing socioeconomic disadvantage and decreased by ∼1 year for all quintiles between 2001 and 2012. Overall, life expectancy varied little by remoteness, but was 1.8 years higher in major cities compared to regional/remote areas in the most socioeconomically deprived regions in 2012. Socioeconomic disadvantage and sex were strongly associated with life expectancy. The disparity in life expectancy across the socioeconomic spectrum was larger in males and was stable over time. In contrast, gender gaps reduced for all quintiles between 2001 and 2012, and a remoteness effect was evident in 2012, but only for those living in the most deprived areas. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

The impact of smoking on gender differences in life expectancy: more heterogeneous than often stated

OpenAIRE

Luy, Marc; Wegner-Siegmundt, Christian

2014-01-01

Background: Throughout industrialized countries, tobacco consumption is seen as the predominant driver of both the trend and the extent of gender differences in life expectancy. However, several factors raise doubts to this generalization. We hypothesize that the impact of smoking on the gender gap is context-specific and differs between populations. Methods: We decompose the gender differences in life expectancy into fractions caused by smoking and other non-biological factors for 53 industr...

The Dual Role of Cellular Senescence in Developing Tumors and Their Response to Cancer Therapy

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Markus Schosserer

2017-11-01

Full Text Available Cellular senescence describes an irreversible growth arrest characterized by distinct morphology, gene expression pattern, and secretory phenotype. The final or intermediate stages of senescence can be reached by different genetic mechanisms and in answer to different external and internal stresses. It has been maintained in the literature but never proven by clearcut experiments that the induction of senescence serves the evolutionary purpose of protecting the individual from development and growth of cancers. This hypothesis was recently scrutinized by new experiments and found to be partly true, but part of the gene activities now known to happen in senescence are also needed for cancer growth, leading to the view that senescence is a double-edged sword in cancer development. In current cancer therapy, cellular senescence is, on the one hand, intended to occur in tumor cells, as thereby the therapeutic outcome is improved, but might, on the other hand, also be induced unintentionally in non-tumor cells, causing inflammation, secondary tumors, and cancer relapse. Importantly, organismic aging leads to accumulation of senescent cells in tissues and organs of aged individuals. Senescent cells can occur transiently, e.g., during embryogenesis or during wound healing, with beneficial effects on tissue homeostasis and regeneration or accumulate chronically in tissues, which detrimentally affects the microenvironment by de- or transdifferentiation of senescent cells and their neighboring stromal cells, loss of tissue specific functionality, and induction of the senescence-associated secretory phenotype, an increased secretory profile consisting of pro-inflammatory and tissue remodeling factors. These factors shape their surroundings toward a pro-carcinogenic microenvironment, which fuels the development of aging-associated cancers together with the accumulation of mutations over time. We are presenting an overview of well-documented stress

How Did Cause of Death Contribute to Racial Differences in Life Expectancy in the United States in 2010?

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... Technical Information Service NCHS How Did Cause of Death Contribute to Racial Differences in Life Expectancy in ... National Vital Statistics System, Mortality. What causes of death influenced the difference in life expectancy between the ...

Ages of origin and destination for a difference in life expectancy

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Elwood Carlson

2006-03-01

Full Text Available Decomposition of a difference in life expectancies may identify ages at which the difference originates in mortality differences, or may identify age at which the difference results in different values of person-years lived (life table population. This study shows that the two approaches are orthogonally related to each other, and derives an origin-destination decomposition matrix in which summing in one direction produces Andreev's origin-decomposition results, while summing in the other direction produces destination-decomposition corresponding to directly-observed differences in nLx values.

The male-female health-survival paradox and sex differences in cohort life expectancy in Utah, Denmark, and Sweden 1850-1910.

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Lindahl-Jacobsen, Rune; Hanson, Heidi A; Oksuzyan, Anna; Mineau, Geraldine P; Christensen, Kaare; Smith, Ken R

2013-04-01

In Utah, the prevalence of unhealthy male risk behaviors are lower than in most other male populations, whereas women experience higher mortality risk because of higher fertility rates. Therefore, we hypothesize that the Utah sex differential in mortality would be small and less than in Sweden and Denmark. Life tables from Utah, Denmark, and Sweden were used to calculate cohort life expectancies for men and women born in 1850-1910. The sex difference in cohort life expectancy was similar or larger in Utah when compared with Denmark and Sweden. The change over time in the sex differences in cohort life expectancy was approximately 2 years smaller for active Mormons in Utah than for other groups suggesting lifestyle as an important component for the overall change seen in cohort life expectancy. Sex differences in cohort life expectancy at the age of 50 years were similar for individuals actively affiliated with the Church of Jesus Christ of Latter-day Saints and for Denmark and Sweden. The hypothesis that a smaller sex difference in cohort life expectancies in Utah would be detected in relation to Denmark and Sweden was not supported. In Utah, the male-female differences in life expectancy remain substantial pointing toward biological mechanisms or other unmeasured risk factors. Copyright © 2013 Elsevier Inc. All rights reserved.

Senescence as biologic endpoint following pharmacological targeting of receptor tyrosine kinases in cancer.

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Francica, Paola; Aebersold, Daniel M; Medová, Michaela

2017-02-15

Cellular senescence was first described in 1961 in a seminal study by Hayflick and Moorhead as a limit to the replicative lifespan of somatic cells after serial cultivation. Since then, major advances in our understanding of senescence have been achieved suggesting that this mechanism is activated also by oncogenic stimuli, oxidative stress and DNA damage, giving rise to the concept of premature senescence. Regardless of the initial trigger, numerous experimental observations have been provided to support the notion that both replicative and premature senescence play pivotal roles in early stages of tumorigenesis and in response of tumor cells to anticancer treatments. Moreover, various studies have suggested that the induction of senescence by both chemo- and radiotherapy in a variety of cancer types correlates with treatment outcome. As it is widely accepted that cellular senescence may function as a fundamental barrier of tumor progression, the significance of senescence for clinical interventions that make use of novel molecular targeting-based modalities needs to be well defined. Interestingly, despite numerous studies evaluating efficacies of receptor tyrosine kinases (RTKs) targeting strategies in both preclinical and clinical settings, the relevance of RTKs inhibition-associated senescence in tumors remains less characterized. Here we review the available literature that describes premature senescence as a major mechanism following targeting of RTKs in preclinical as well as in clinical settings. Additionally, we discuss the possible role of diverse RTKs in regulating the induction of senescence following cellular stress and possible implications of this crosstalk in identification of biomarkers of inhibitor-mediated chemo- and radiosensitization approaches. Copyright © 2016 Elsevier Inc. All rights reserved.

Genome-wide evaluation of histone methylation changes associated with leaf senescence in Arabidopsis.

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Judy A Brusslan

Full Text Available Leaf senescence is the orderly dismantling of older tissue that allows recycling of nutrients to developing portions of the plant and is accompanied by major changes in gene expression. Histone modifications correlate to levels of gene expression, and this study utilizes ChIP-seq to classify activating H3K4me3 and silencing H3K27me3 marks on a genome-wide scale for soil-grown mature and naturally senescent Arabidopsis leaves. ChIPnorm was used to normalize data sets and identify genomic regions with significant differences in the two histone methylation patterns, and the differences were correlated to changes in gene expression. Genes that showed an increase in the H3K4me3 mark in older leaves were senescence up-regulated, while genes that showed a decrease in the H3K4me3 mark in the older leaves were senescence down-regulated. For the H3K27me3 modification, genes that lost the H3K27me3 mark in older tissue were senescence up-regulated. Only a small number of genes gained the H3K27me3 mark, and these were senescence down-regulated. Approximately 50% of senescence up-regulated genes lacked the H3K4me3 mark in both mature and senescent leaf tissue. Two of these genes, SAG12 and At1g73220, display strong senescence up-regulation without the activating H3K4me3 histone modification. This study provides an initial epigenetic framework for the developmental transition into senescence.

Escherichia coli producing colibactin triggers premature and transmissible senescence in mammalian cells.

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Thomas Secher

Full Text Available Cellular senescence is an irreversible state of proliferation arrest evoked by a myriad of stresses including oncogene activation, telomere shortening/dysfunction and genotoxic insults. It has been associated with tumor activation, immune suppression and aging, owing to the secretion of proinflammatory mediators. The bacterial genotoxin colibactin, encoded by the pks genomic island is frequently harboured by Escherichia coli strains of the B2 phylogenetic group. Mammalian cells exposed to live pks+ bacteria exhibit DNA-double strand breaks (DSB and undergo cell-cycle arrest and death. Here we show that cells that survive the acute bacterial infection with pks+ E. coli display hallmarks of cellular senescence: chronic DSB, prolonged cell-cycle arrest, enhanced senescence-associated β-galactosidase (SA-β-Gal activity, expansion of promyelocytic leukemia nuclear foci and senescence-associated heterochromatin foci. This was accompanied by reactive oxygen species production and pro-inflammatory cytokines, chemokines and proteases secretion. These mediators were able to trigger DSB and enhanced SA-β-Gal activity in bystander recipient cells treated with conditioned medium from senescent cells. Furthermore, these senescent cells promoted the growth of human tumor cells. In conclusion, the present data demonstrated that the E. coli genotoxin colibactin induces cellular senescence and subsequently propel bystander genotoxic and oncogenic effects.

Decomposing change in life expectancy : A bouquet of formulas in honor of Nathan Keyfitz's 90th birthday

NARCIS (Netherlands)

Vaupel, JW; Romo, VC

We extend Nathan Keyfitz research on continuous change in life expectancy over time by presenting and proving a new formula for decomposing such change. The formula separates change in life expectancy over time into two terms. The first term captures the general effect of reduction in death rates at

MicroRNA-33 promotes the replicative senescence of mouse embryonic fibroblasts by suppressing CDK6

Energy Technology Data Exchange (ETDEWEB)

Xu, Shun; Huang, Haijiao; Li, Nanhong; Zhang, Bing; Jia, Yubin; Yang, Yukun; Yuan, Yuan; Xiong, Xing-dong; Wang, Dengchuan; Zheng, Hui-ling [Institute of Aging Research, Guangdong Medical University, Dongguan (China); Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Dongguan (China); Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Zhanjiang (China); Liu, Xinguang, E-mail: xgliu64@126.com [Institute of Aging Research, Guangdong Medical University, Dongguan (China); Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Dongguan (China); Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Zhanjiang (China)

2016-05-13

MicroRNAs are a large class of tiny noncoding RNAs, which have emerged as critical regulators of gene expression, and thus are involved in multiple cellular processes, including cellular senescence. MicroRNA-33 has previously been established to exert crucial effect on cell proliferation, lipid metabolism and cholesterol metabolism. Nonetheless, the association between microRNA-33 and cellular senescence and its underlying molecular mechanism are far to be elucidated. The present study has attempted to probe into the effect of microRNA-33 on MEFs senescence. Our data unveiled that microRNA-33 was dramatically down-regulated in senescent MEFs compared to the young MEFs, and ectopic expression of microRNA-33 promoted MEFs senescence, while knock-down of microRNA-33 exhibited a protective effect against senescence phenotype. Moreover, we verified CDK6 as a direct target of microRNA-33 in mouse. Silencing of CDK6 induced the premature senescence phenotype of MEFs similarly as microRNA-33, while enforced expression of CDK6 significantly reverse the senescence-induction effect of microRNA-33. Taken together, our results suggested that microRNA-33 enhanced the replicative senescence of MEFs potentially by suppressing CDK6 expression. -- Highlights: •MicroRNA-33 was dramatically down-regulated in senescent MEF cells. •Altered expression of microRNA-33 exerted a critical role in MEFs senescence. •MicroRNA-33 promoted the replicative senescence of MEFs via targeting of CDK6.

MicroRNA-33 promotes the replicative senescence of mouse embryonic fibroblasts by suppressing CDK6

International Nuclear Information System (INIS)

Xu, Shun; Huang, Haijiao; Li, Nanhong; Zhang, Bing; Jia, Yubin; Yang, Yukun; Yuan, Yuan; Xiong, Xing-dong; Wang, Dengchuan; Zheng, Hui-ling; Liu, Xinguang

2016-01-01

MicroRNAs are a large class of tiny noncoding RNAs, which have emerged as critical regulators of gene expression, and thus are involved in multiple cellular processes, including cellular senescence. MicroRNA-33 has previously been established to exert crucial effect on cell proliferation, lipid metabolism and cholesterol metabolism. Nonetheless, the association between microRNA-33 and cellular senescence and its underlying molecular mechanism are far to be elucidated. The present study has attempted to probe into the effect of microRNA-33 on MEFs senescence. Our data unveiled that microRNA-33 was dramatically down-regulated in senescent MEFs compared to the young MEFs, and ectopic expression of microRNA-33 promoted MEFs senescence, while knock-down of microRNA-33 exhibited a protective effect against senescence phenotype. Moreover, we verified CDK6 as a direct target of microRNA-33 in mouse. Silencing of CDK6 induced the premature senescence phenotype of MEFs similarly as microRNA-33, while enforced expression of CDK6 significantly reverse the senescence-induction effect of microRNA-33. Taken together, our results suggested that microRNA-33 enhanced the replicative senescence of MEFs potentially by suppressing CDK6 expression. -- Highlights: •MicroRNA-33 was dramatically down-regulated in senescent MEF cells. •Altered expression of microRNA-33 exerted a critical role in MEFs senescence. •MicroRNA-33 promoted the replicative senescence of MEFs via targeting of CDK6.

The impact of cellular senescence in skin ageing: A notion of mosaic and therapeutic strategies.

Science.gov (United States)

Toutfaire, Marie; Bauwens, Emilie; Debacq-Chainiaux, Florence

2017-10-15

Cellular senescence is now recognized as one of the nine hallmarks of ageing. Recent data show the involvement of senescent cells in tissue ageing and some age-related diseases. Skin represents an ideal model for the study of ageing. Indeed, skin ageing varies between individuals depending on their chronological age but also on their exposure to various exogenous factors (mainly ultraviolet rays). If senescence traits can be detected with ageing in the skin, the senescent phenotype varies among the various skin cell types. Moreover, the origin of cellular senescence in the skin is still unknown, and multiple origins are possible. This reflects the mosaic of skin ageing. Senescent cells can interfere with their microenvironment, either via the direct secretion of factors (the senescence-associated secretory phenotype) or via other methods of communication, such as extracellular vesicles. Knowledge regarding the impact of cellular senescence on skin ageing could be integrated into dermatology research, especially to limit the appearance of senescent cells after photo(chemo)therapy or in age-related skin diseases. Therapeutic approaches include the clearance of senescent cells via the use of senolytics or via the cooperation with the immune system. Copyright © 2017 Elsevier Inc. All rights reserved.

The association between income and life expectancy revisited: deindustrialization, incarceration and the widening health gap.

Science.gov (United States)

Nosrati, Elias; Ash, Michael; Marmot, Michael; McKee, Martin; King, Lawrence P

2017-11-22

The health gap between the top and the bottom of the income distribution is widening rapidly in the USA, but the lifespan of America's poor depends substantially on where they live. We ask whether two major developments in American society, deindustrialization and incarceration, can explain variation among states in life expectancy of those in the lowest income quartile. Life expectancy estimates at age 40 of those in the bottom income quartile were used to fit panel data models examining the relationship with deindustrialization and incarceration between 2001 and 2014 for all US states. A one standard deviation (s.d.) increase in deindustrialization (mean = 11.2, s.d. = 3.5) reduces life expectancy for the poor by 0.255 years [95% confidence interval (CI): 0.090-0.419] and each additional prisoner per 1000 residents (mean = 4.0, s.d. = 1.5) is associated with a loss of 0.468 years (95% CI: 0.213-0.723). Our predictors explain over 20% of the state-level variation in life expectancy among the poor and virtually the entire increase in the life expectancy gap between the top and the bottom income quartiles since the turn of the century. In the USA between 2001 and 2014, deindustrialization and incarceration subtracted roughly 2.5 years from the lifespan of the poor, pointing to their role as major health determinants. Future research must remain conscious of the upstream determinants and the political economy of public health. If public policy responses to growing health inequalities are to be effective, they must consider strengthening industrial policy and ending hyper-incarceration. © The Author 2017; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association

The Pace and Shape of Senescence in Angiosperms

DEFF Research Database (Denmark)

Baudisch, Annette; Salguero-Gómez, Roberto; Jones, Owen

2013-01-01

1. Demographic senescence, the decay in fertility and increase in the risk of mortality with age, is one of the most striking phenomena in ecology and evolution. Comparative studies of senescence patterns of plants are scarce, and consequently, little is known about senescence and its determinants...... (‘senescence’), decreases (‘negative senescence’) or remains constant over age (‘negligible senescence’). 3. We extract mortality trajectories from ComPADRe III, a data base that contains demographic information for several hundred plant species. We apply age-from-stage matrix decomposition methods to obtain...... age-specific trajectories from 290 angiosperm species of various growth forms distributed globally. From these trajectories, we survey pace and shape values and investigate how growth form and ecoregion influence these two aspects of mortality using a Bayesian regression analysis that accounts...

Social gradient in life expectancy and health expectancy in Denmark

DEFF Research Database (Denmark)

Brønnum-Hansen, Henrik; Andersen, Otto; Kjøller, Mette

2004-01-01

Health status of a population can be evaluated by health expectancy expressed as average lifetime in various states of health. The purpose of the study was to compare health expectancy in population groups at high, medium and low educational levels.......Health status of a population can be evaluated by health expectancy expressed as average lifetime in various states of health. The purpose of the study was to compare health expectancy in population groups at high, medium and low educational levels....

Happier countries, longer lives: an ecological study on the relationship between subjective sense of well-being and life expectancy.

Science.gov (United States)

Evans, Grahame F; Soliman, Elsayed Z

2017-08-01

The relationship between sense of well-being and longevity is not well-established across populations of varying levels of socioeconomic status. We sought to examine the relationship between happiness, or subjective sense of well-being and life expectancy using data from 151 countries. This analysis is based on the 2012 Happy Planet Index project conducted by the Center of Well-Being of the New Economics Foundation, based in the United Kingdom. Well-being data for each country were taken from responses to the 'Ladder of Life' question in the 2012 Gallup World Poll in which participants were asked to rate their quality of life on a scale from 1 (worst possible life) to 10 (best possible life). Life expectancy and gross domestic product data were taken from the 2011 United Nations records. Ecological footprint data were taken from Global Footprint Network records. Subjective sense of well-being was highly correlated with life expectancy (Pearson correlation r = 0.71, p ecological footprint, and population, each 1 unit of the well-being scale was associated with an increase in life expectancy of 4.0 years (95% confidence interval = 2.7-5.3). In conclusion, better sense of well-being has a strong relationship with life expectancy regardless of economic status or population size, suggesting that governments should foster happiness in order to support long-living populations.

Interaction Mortality: Senescence May Have Evolved because It Increases Lifespan

DEFF Research Database (Denmark)

Wensink, M. J.; Wrycza, T. F.; Baudisch, A.

2014-01-01

Given an extrinsic challenge, an organism may die or not depending on how the threat interacts with the organism's physiological state. To date, such interaction mortality has been only a minor factor in theoretical modeling of senescence. We describe a model of interaction mortality that does...... not involve specific functions, making only modest assumptions. Our model distinguishes explicitly between the physiological state of an organism and potential extrinsic, age-independent threats. The resulting mortality may change with age, depending on whether the organism's state changes with age. We find...... that depending on the physiological constraints, any outcome, be it 'no senescence' or 'high rate of senescence', can be found in any environment; that the highest optimal rate of senescence emerges for an intermediate physiological constraint, i.e. intermediate strength of trade-off; and that the optimal rate...

Telomeres and replicative senescence: Is it only length that counts?

Science.gov (United States)

von Zglinicki, T

2001-07-26

Telomeres are well established as a major 'replicometer', counting the population doublings in primary human cell cultures and ultimately triggering replicative senescence. However, neither is the pace of this biological clock inert, nor is there a fixed threshold telomere length acting as the universal trigger of replicative senescence. The available data suggest that opening of the telomeric loop and unscheduled exposure of the single-stranded G-rich telomeric overhang might act like a semaphore to signal senescent cell cycle arrest. Short telomere length, telomeric single-strand breaks, low levels of loop-stabilizing proteins, or other factors may trigger this opening of the loop. Thus, both telomere shortening and the ultimate signalling into senescence are able to integrate different environmental and genetic factors, especially oxidative stress-mediated damage, which might otherwise become a thread to genomic stability.

How did national life expectation related to school years in developing countries - an approach using panel data mining.

Science.gov (United States)

Jian, Wen-Shan; Huang, Chen-Ling; Iqbal, Usman; Nguyen, Phung-Anh; Hsiao, George; Li, Hsien-Chang

2014-03-01

The purpose of the study was to probe into the changes in life expectancy associated with schooling years found by the Organization for Economic Co-operation and Development (OECD). The study was based on the OECD database from the period 2000 to 2006. The data of thirty countries were constructed to allow comparisons over time and across these countries. Panel data analysis was used to estimate the relationship of national education, as defined as school years, with life expectancy. The control factors considered were numbers of practicing physicians, practicing nurses, hospital beds, and GDP. We used fixed effects of both country and time through linear regression, the coefficient of school years in relation to life expectancy was statistically significant but negative. This finding is not in accord with the hypothesis that investing in human capital through education stimulates better health outcomes. Within developing countries, educational attainment is no longer keeping the same pace with life expectancy as before. Therefore, we suggest that an effective education policy should cover diverse topics, for example, balancing economic growth and mental hygiene, to improve national life expectancy. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

F4/80+ Macrophages Contribute to Clearance of Senescent Cells in the Mouse Postpartum Uterus.

Science.gov (United States)

Egashira, Mahiro; Hirota, Yasushi; Shimizu-Hirota, Ryoko; Saito-Fujita, Tomoko; Haraguchi, Hirofumi; Matsumoto, Leona; Matsuo, Mitsunori; Hiraoka, Takehiro; Tanaka, Tomoki; Akaeda, Shun; Takehisa, Chiaki; Saito-Kanatani, Mayuko; Maeda, Kei-Ichiro; Fujii, Tomoyuki; Osuga, Yutaka

2017-07-01

Cellular senescence, defined as an irreversible cell cycle arrest, exacerbates the tissue microenvironment. Our previous study demonstrated that mouse uterine senescent cells were physiologically increased according to gestational days and that their abnormal accumulation was linked to the onset of preterm delivery. We hypothesized that there is a mechanism for removal of senescent cells after parturition to maintain uterine function. In the current study, we noted abundant uterine senescent cells and their gradual disappearance in wild-type postpartum mice. F4/80+ macrophages were present specifically around the area rich in senescent cells. Depletion of macrophages in the postpartum mice using anti-F4/80 antibody enlarged the area of senescent cells in the uterus. We also found excessive uterine senescent cells and decreased second pregnancy success rate in a preterm birth model using uterine p53-deleted mice. Furthermore, a decrease in F4/80+ cells and an increase in CD11b+ cells with a senescence-associated inflammatory microenvironment were observed in the p53-deleted uterus, suggesting that uterine p53 deficiency affects distribution of the macrophage subpopulation, interferes with senescence clearance, and promotes senescence-induced inflammation. These findings indicate that the macrophage is a key player in the clearance of uterine senescent cells to maintain postpartum uterine function. Copyright © 2017 Endocrine Society.

The Effect of Economic Variables on Life Expectancy of Males and Females

Directory of Open Access Journals (Sweden)

Dilek TEKER

2012-09-01

Full Text Available In this study, the relationship between life expectancy of men and women in Turkey and socio-economic variables are examined. The effect of demographic and economic factors such as the ratio of health expenditures to GDP, the ratio of elderly to employable population, the number of hospital beds per thousand people, the number of doctors per thousand patients are analyzed for a period of 1975-2009. In this study, the unit root test is initialy applied to each data set and then the cointegration test results is interpreted to determine whether a meaningful relationship exists between indicators in the long-term. Finally, the effects of the underlying factors on men and women were examined by vector error correction model. These results support that each factor has a significant effect on the life expectancy of men and women in Turkey.

Trading Stages: Life Expectancies in Structured Populations

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Tuljapurkar, Shripad; Coulson, Tim; Horvitz, Carol

2012-01-01

Interest in stage-and age structured models has recently increased because they can describe quantitative traits such as size that are left out of age-only demography. Available methods for the analysis of effects of vital rates on lifespan in stage-structured models have not been widely applied because they are hard to use and interpret, and tools for age and stage structured populations are missing. We present easily interpretable expressions for the sensitivities and elasticities of life expectancy to vital rates in age-stage models, and illustrate their application with two biological examples. Much of our approach relies on trading of time and mortality risk in one stage for time and risk in others. Our approach contributes to the new framework of the study of age- and stage-structured biodemography. PMID:22664576

Influences of sex and activity level on physiological changes in individual adult sockeye salmon during rapid senescence.

Science.gov (United States)

Hruska, Kimberly A; Hinch, Scott G; Healey, Michael C; Patterson, David A; Larsson, Stefan; Farrell, Anthony P

2010-01-01

A noninvasive biopsy protocol was used to sample plasma and gill tissue in individual sockeye salmon (Oncorhynchus nerka) during the critical life stage associated with spawning-arrival at a spawning channel through senescence to death several days later. Our main objective was to characterize the physiological changes associated with rapid senescence in terms of the physiological stress/cortisol hypersecretion model and the energy exhaustion model. Salmon lived an average of 5 d in the spawning channel, during which time there were three major physiological trends that were independent of sexual status: a large increase in plasma indicators of stress and exercise (i.e., lactate and cortisol), a decrease in the major plasma ions (i.e., Cl(-) and Na(+)) and osmolality, and a decrease in gross somatic energy reserves. Contrary to a generalized stress response, plasma glucose decreased in approximately 2/3 of the fish after arrival, as opposed to increasing. Furthermore, plasma cortisol levels at spawning-ground arrival were not correlated with the degree of ionoregulatory changes during rapid senescence. One mechanism of mortality in some fish may involve the exhaustion of energy reserves, resulting in the inability to mobilize plasma glucose. Sex had a significant modulating effect on the degree of physiological change. Females exhibited a greater magnitude of change for gross somatic energy, osmolality, and plasma concentrations of Cl(-), Na(+), cortisol, testosterone, 11-ketotestosterone, 17,20beta-progesterone, and estradiol. The activity level of an individual on the spawning grounds appeared to influence the degree of some physiological changes during senescence. For example, males that received a greater frequency of attacks exhibited larger net decreases in plasma 11-ketotestosterone while on the spawning grounds. These results suggest that rapid senescence on spawning grounds is influenced by multiple physiological processes and perhaps behavior. This study

Stochastic variation in telomere shortening rate causes heterogeneity of human fibroblast replicative life span.

Science.gov (United States)

Martin-Ruiz, Carmen; Saretzki, Gabriele; Petrie, Joanne; Ladhoff, Juliane; Jeyapalan, Jessie; Wei, Wenyi; Sedivy, John; von Zglinicki, Thomas

2004-04-23

The replicative life span of human fibroblasts is heterogeneous, with a fraction of cells senescing at every population doubling. To find out whether this heterogeneity is due to premature senescence, i.e. driven by a nontelomeric mechanism, fibroblasts with a senescent phenotype were isolated from growing cultures and clones by flow cytometry. These senescent cells had shorter telomeres than their cycling counterparts at all population doubling levels and both in mass cultures and in individual subclones, indicating heterogeneity in the rate of telomere shortening. Ectopic expression of telomerase stabilized telomere length in the majority of cells and rescued them from early senescence, suggesting a causal role of telomere shortening. Under standard cell culture conditions, there was a minor fraction of cells that showed a senescent phenotype and short telomeres despite active telomerase. This fraction increased under chronic mild oxidative stress, which is known to accelerate telomere shortening. It is possible that even high telomerase activity cannot fully compensate for telomere shortening in all cells. The data show that heterogeneity of the human fibroblast replicative life span can be caused by significant stochastic cell-to-cell variation in telomere shortening.

Increased storage and secretion of phosphatidylcholines by senescent human peritoneal mesothelial cells.

Science.gov (United States)

Bartosova, Maria; Rudolf, Andras; Pichl, Sebastian; Schmidt, Kathrin; Okun, Jürgen G; Straub, Beate K; Rutkowski, Rafael; Witowski, Janusz; Schmitt, Claus P

2016-08-01

Human peritoneal mesothelial cells (HPMC) secrete phosphatidylcholines (PC) which form a lipid bilayer lining the peritoneum. They prevent frictions and adhesions and act as a barrier to the transport of water-soluble solutes while permitting water flux. PC may play an essential role in peritoneal integrity and function, the role of PD induced HPMC senescence on PC homeostasis, however, is unknown. HPMC cell lines were isolated from four non-uremic patients. Expression of the three PC synthesis genes (rt-PCR), and cellular storage and secretion of PC (ESI-mass-spectrometry) were analyzed in young and senescent HPMC (>Hayflick-limit). Senescent cells displayed significantly altered morphology; flow cytometry demonstrated extensive staining for senescence-associated beta galactosidase. Nine different PC were detected in HPMC with palmitoyl-myristoyl phosphatidylcholine (PMPC) being most abundant. In senescent HPMC mRNA expression of the three key PC synthesis genes was 1.5-, 2.4- and 6-fold increased as compared to young HPMC, with the latter, phosphatidylcholine cytidylyltransferase, being rate limiting. Intracellular storage of the nine PC was 75-450 % higher in senescent vs. young HPMC, PC secretion rates were 100-300 % higher. Intracellular PC concentrations were not correlated with the PC secretion rates. Electron microscopy demonstrated lamellar bodies, the primary storage site of PC, in senescent but not in young cells. Senescent HPMC store and secrete substantially more PC than young cells. Our findings indicate a novel protective mechanism, which should counteract peritoneal damage induced by chronic exposure to PD fluids.

Life Expectancies Applied to Specific Statuses: a History of the Indicators and the Methods of Calculation {Population, 3, 1998)

OpenAIRE

N. Brouard; J.-M. Robine; E. Cambois

1999-01-01

Cambois (Emmanuelle), Robin? (Jean-Marie), Brouard (Nicolas).- Life Expectancies Applied to Specific Statuses: A History of the Indicators and the Methods of Calculation Indicators of life expectancy applied to specific statuses, such as the state of health or professional status, were introduced at the end of the 1930s and are currently the object of renewed interest. Because they relate mortality to different domains (health, professional activity) applied life expectancies reflect simultan...

Chlorophyll loss associated with heat-induced senescence in bentgrass.

Science.gov (United States)

Jespersen, David; Zhang, Jing; Huang, Bingru

2016-08-01

Heat stress-induced leaf senescence is characterized by the loss of chlorophyll from leaf tissues. The objectives of this study were to examine genetic variations in the level of heat-induced leaf senescence in hybrids of colonial (Agrostis capillaris)×creeping bentgrass (Agrostis stolonifera) contrasting in heat tolerance, and determine whether loss of leaf chlorophyll during heat-induced leaf senescence was due to suppressed chlorophyll synthesis and/or accelerated chlorophyll degradation in the cool-season perennial grass species. Plants of two hybrid backcross genotypes ('ColxCB169' and 'ColxCB190') were exposed to heat stress (38/33°C, day/night) for 28 d in growth chambers. The analysis of turf quality, membrane stability, photochemical efficiency, and chlorophyll content demonstrated significant variations in the level of leaf senescence induced by heat stress between the two genotypes, with ColXCB169 exhibiting a lesser degree of decline in chlorophyll content, photochemical efficiency and membrane stability than ColXCB190. The assays of enzymatic activity or gene expression of several major chlorophyll-synthesizing (porphobilinogen deaminase, Mg-chelatase, protochlorophyllide-reductase) and chlorophyll-degrading enzymes (chlorophyllase, pheophytinase, and chlorophyll-degrading peroxidase) indicated heat-induced decline in leaf chlorophyll content was mainly due to accelerated chlorophyll degradation, as manifested by increased gene expression levels of chlorophyllase and pheophytinase, and the activity of pheophytinase (PPH), while chlorophyll-synthesizing genes and enzymatic activities were not differentially altered by heat stress in the two genotypes. The analysis of heat-induced leaf senescence of pph mutants of Arabidopsis further confirmed that PPH could be one enzymes that plays key roles in regulating heat-accelerated chlorophyll degradation. Further research on enzymes responsible in part for the loss of chlorophyll during heat

Decrease of old age population mortality in Yugoslavia: Chance to increase anticipated life expectancy

Directory of Open Access Journals (Sweden)

Radivojević Biljana M.

2002-01-01

Full Text Available This study analyzes the level and structure of old age population mortality in Yugoslavia with an aim to determine the intensity of realized changes and to provide an answer to how much they are significant and to approach the positive trends noted in developed countries in the latest period. Although it was insufficiently represented in the demographic analysis, the analysis of mortality in old people is gaining importance in the world. Apart from the reasons which result from the increase in the number of old people and thus their greater participation in the total number of deceased, enviable results have been achieved in decreasing old age mortality, which are more and more in focus of interest. While earlier research reported on the dominant influence of the decrease of younger age mortality to the increase of the expectation of life at birth, recent analysis precisely confirm the importance of decreasing mortality in old people. In mortality conditions from 1997/98, an additional 13.4 years of life in average is expected for men in Yugoslavia, and 15.2 for women. During more than five decades, the anticipated life expectancy for people over the age of 65 increased for only 1.2 years for men and 1.9 years for women. Out of that, the greatest increase was realized in the period 1950/51 - 1960/61 in both sexes. A small decrease in the average life expectancy was marked with men in the period 1960/61 - 1970/71, and with women in the latest period. Otherwise, all up to the eighties, the annual rate of increase was considerably lower than the rate of increase for zero year. It was only in the period 1980/81-1990/91 that faster growth had an anticipated life expectancy for the 65 years old. However, during the nineties unfavorable changes continued with the older, especially, female population. When comparing the values of the average life expectancy for people over 65 in Yugoslavia with corresponding values in developed countries, the lagging in

Senescence-related functional nuclear barrier by down-regulation of nucleo-cytoplasmic trafficking gene expression

International Nuclear Information System (INIS)

Kim, Sung Young; Ryu, Sung Jin; Ahn, Hong Ju; Choi, Hae Ri; Kang, Hyun Tae; Park, Sang Chul

2010-01-01

One of the characteristic natures of senescent cells is the hypo- or irresponsiveness not only to growth factors but also to apoptotic stress. In the present study, we confirmed the inhibition of nuclear translocation of activated p-ERK1/2 and NF-kB p50 in response to growth stimuli or LPS in the senescent human diploid fibroblasts. In order to elucidate the underlying mechanism for the senescence-associated hypo-responsiveness, we carried out the comparison study for gene expression profiles through microarray analysis. In consequence, we observed the vast reduction in expression of nucleo-cytoplasmic trafficking genes in senescent cells, when compared with those in young cells. Expression levels of several nucleoporins, karyopherin α, karyopherin β, Ran, and Ran-regulating factors were confirmed to be down-regulated in senescent HDFs by using RT-PCR and Western blot methods. Taken together, these data suggest the operation of certain senescence-associated functional nuclear barriers by down-regulation of the nucleo-cytoplasmic trafficking genes in the senescent cells.

Senescence-related functional nuclear barrier by down-regulation of nucleo-cytoplasmic trafficking gene expression

Energy Technology Data Exchange (ETDEWEB)

Kim, Sung Young; Ryu, Sung Jin; Ahn, Hong Ju; Choi, Hae Ri; Kang, Hyun Tae [Department of Biochemistry and Molecular Biology, Aging and Apoptosis Research Center, Institute on Aging, Seoul National University College of Medicine, Seoul 110-799 (Korea, Republic of); Park, Sang Chul, E-mail: scpark@snu.ac.kr [Department of Biochemistry and Molecular Biology, Aging and Apoptosis Research Center, Institute on Aging, Seoul National University College of Medicine, Seoul 110-799 (Korea, Republic of)

2010-01-01

One of the characteristic natures of senescent cells is the hypo- or irresponsiveness not only to growth factors but also to apoptotic stress. In the present study, we confirmed the inhibition of nuclear translocation of activated p-ERK1/2 and NF-kB p50 in response to growth stimuli or LPS in the senescent human diploid fibroblasts. In order to elucidate the underlying mechanism for the senescence-associated hypo-responsiveness, we carried out the comparison study for gene expression profiles through microarray analysis. In consequence, we observed the vast reduction in expression of nucleo-cytoplasmic trafficking genes in senescent cells, when compared with those in young cells. Expression levels of several nucleoporins, karyopherin {alpha}, karyopherin {beta}, Ran, and Ran-regulating factors were confirmed to be down-regulated in senescent HDFs by using RT-PCR and Western blot methods. Taken together, these data suggest the operation of certain senescence-associated functional nuclear barriers by down-regulation of the nucleo-cytoplasmic trafficking genes in the senescent cells.

Finding Shangri-La: Limiting the Impact of Senescence on Aging.

Science.gov (United States)

Trabucco, Sally E; Zhang, Hong

2016-03-03

Senescence plays an important role in the age-associated decline of tissue functions. Recent studies now show that targeting senescent cells can enhance the functions of stem/progenitor cells in aged mice and extend lifespan. Copyright © 2016 Elsevier Inc. All rights reserved.

Impact of income inequality on life expectancy in a highly unequal developing country: the case of Brazil.

Science.gov (United States)

Rasella, Davide; Aquino, Rosana; Barreto, Mauricio Lima

2013-08-01

Few studies have analysed the effects of income inequality on health in developing countries, particularly during economic growth, reduction of social disparities and reinforcement of the welfare and healthcare system. We evaluated the association between income inequality and life expectancy in Brazil, including the effect of social and health interventions, in the period 2000-2009. A panel dataset was created for the 27 Brazilian states over the referred time period. Multivariable linear regressions were performed using fixed-effects estimation with heteroscedasticity and serial correlation robust SEs. Models were fitted for life expectancy as a dependent variable, using the Gini index or a percentile income dispersion ratio as the main independent variable, and for demographic, socioeconomic and healthcare-related determinants as covariates. The Gini index, as the other measure of income inequality, was negatively associated with life expectancy (pincome inequality, contributing-together with PHC-to decreasing death rates in the population. Reducing income inequality may represent an important step towards improving health and increasing life expectancy, particularly in developing countries where inequalities are high.

Educational and sex differentials in life expectancies and disability-free life expectancies in São Paulo, Brazil, and urban areas in Mexico.

Science.gov (United States)

Beltrán-Sánchez, Hiram; Andrade, Flávia Cristina Drumond

2013-08-01

To estimate transition probabilities between disability states, total life expectancy, and the latter's decomposition into years spent disabled and disability-free by age, sex, and education among older adults in São Paulo, Brazil, and urban areas in Mexico. Applied a micro-simulation method (Interpolative Markov Chains) using longitudinal data. We found large between-country educational differences in incidence of and recovery from disability with higher rates in Mexico than in São Paulo, but no differences in mortality. Older adults in Mexico spent longer time being disability-free than in São Paulo for both levels of education. Males and females in São Paulo spent a larger fraction of their remaining life disabled at every age than their counterparts in urban areas in Mexico. There were educational differences in the prevalence of disability in São Paulo and urban areas in Mexico, and significant educational differences in disability incidence and recovery across sites.

The stagnation of the Mexican male life expectancy in the first decade of the 21st century

DEFF Research Database (Denmark)

Canudas-Romo, Vladimir; García-Guerrero, Víctor Manuel; Echarri-Cánovas, Carlos Javier

2015-01-01

OBJECTIVES: In the first decade of the 21st century, the Mexican life expectancy changed from a long trend of increase to stagnation. These changes concur with an increase in deaths by homicides that the country experienced in that decade, and an obesity epidemic that had developed over the last...... of life expectancy from 2000 to 2010. RESULTS: The apparent stagnation in life expectancy is the result of an increase in deaths by homicides and diabetes mellitus on the one hand, and the positive improvements observed in other causes of death on the other. The negative impact of homicides...... by 2 years if deaths by homicides and diabetes mellitus had been avoided....

Hunger influenced life expectancy in war-torn Sub-Saharan African countries.

Science.gov (United States)

Uchendu, Florence N

2018-04-27

Malnutrition is a global public health problem especially in developing countries experiencing war/conflicts. War might be one of the socio-political factors influencing malnutrition in Sub-Saharan African (SSA) countries. This study aims at determining the influence of war on corruption, population (POP), number of population malnourished (NPU), food security and life expectancy (LE) in war-torn SSA countries (WTSSA) by comparing their malnutrition indicators. Fourteen countries in WTSSA were stratified into zones according to war incidences. Countries' secondary data on population (POP), NPU, Food Security Index (FSI), corruption perceptions index (CPI), Global Hunger Index (GHI) and LE were obtained from global published data. T test, multivariate and Pearson correlation analyses were performed to determine the relationship between CPI, POP, GHI, FSI, NPU, male LE (MLE) and female LE (FLE) in WTSSA at p Malnutrition indicators were similarly affected in WTSSA. Hunger influenced life expectancy. Policies promoting good governance, equity, peaceful co-existence, respect for human right and adequate food supply will aid malnutrition eradication and prevent war occurrences in Sub-Saharan African countries.

Leading Causes of Death Contributing to Decrease in Life Expectancy Gap Between Black and White Populations: United States, 1999-2013.

Science.gov (United States)

Kochanek, Kenneth D; Anderson, Robert N; Arias, Elizabeth

2015-11-01

Life expectancy at birth has increased steadily since 1900 to a record 78.8 years in 2013. But differences in life expectancy between the white and black populations still exist, despite a decrease in the life expectancy gap from 5.9 years in 1999 to 3.6 years in 2013. Differences in the change over time in the leading causes of death for the black and white populations have contributed to this decrease in the gap in life expectancy. Between 1999 and 2013, the decrease in the life expectancy gap between the black and white populations was mostly due to greater decreases in mortality from heart disease, cancer, HIV disease, unintentional injuries, and perinatal conditions among the black population. Similarly, the decrease in the gap between black and white male life expectancy was due to greater decreases in death rates for HIV disease, cancer, unintentional injuries, heart disease, and perinatal conditions in black males. For black females, greater decreases in diabetes death rates, combined with decreased rates for heart disease and HIV disease, were the major causes contributing to the decrease in the life expectancy gap with white females. The decrease in the gap in life expectancy between the white and black populations would have been larger than 3.6 years if not for increases in death rates for the black population for aortic aneurysm, Alzheimer’s disease, and maternal conditions. For black males, the causes that showed increases in death rates over white males were hypertension, aortic aneurysm, diabetes, Alzheimer’s disease, and kidney disease, while the causes that showed increases in death rates for black females were Alzheimer’s disease, maternal conditions, and atherosclerosis. This NCHS Data Brief is the second in a series of data briefs that explore the causes of death contributing to differences in life expectancy between detailed ethnic and racial populations in the United States. The first data brief focused on the racial differences in life

Non-Cell Autonomous Effects of the Senescence-Associated Secretory Phenotype in Cancer Therapy

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Tareq Saleh

2018-05-01

Full Text Available In addition to promoting various forms of cell death, most conventional anti-tumor therapies also promote senescence. There is now extensive evidence that therapy-induced senescence (TIS might be transient, raising the concern that TIS could represent an undesirable outcome of therapy by providing a mechanism for tumor dormancy and eventual disease recurrence. The senescence-associated secretory phenotype (SASP is a hallmark of TIS and may contribute to aberrant effects of cancer therapy. Here, we propose that the SASP may also serve as a major driver of escape from senescence and the re-emergence of proliferating tumor cells, wherein factors secreted from the senescent cells contribute to the restoration of tumor growth in a non-cell autonomous fashion. Accordingly, anti-SASP therapies might serve to mitigate the deleterious outcomes of TIS. In addition to providing an overview of the putative actions of the SASP, we discuss recent efforts to identify and eliminate senescent tumor cells.

Calculating the Rate of Senescence From Mortality Data

DEFF Research Database (Denmark)

Koopman, Jacob J E; Rozing, Maarten P; Kramer, Anneke

2016-01-01

, they do not fit mortality rates at young and old ages. Therefore, we developed a method to calculate senescence rates from the acceleration of mortality directly without modeling the mortality rates. We applied the different methods to age group-specific mortality data from the European Renal Association......, the rate of senescence can be calculated directly from non-modeled mortality rates, overcoming the disadvantages of an indirect estimation based on modeled mortality rates....

Regulation of replicative senescence by NADP+ -dependent isocitrate dehydrogenase.

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Kil, In Sup; Huh, Tae Lin; Lee, Young Sup; Lee, You Mie; Park, Jeen-Woo

2006-01-01

The free radical hypothesis of aging postulates that senescence is due to an accumulation of cellular oxidative damage, caused largely by reactive oxygen species that are produced as by-products of normal metabolic processes. Recently, we demonstrated that the control of cytosolic and mitochondrial redox balance and the cellular defense against oxidative damage is one of the primary functions of cytosolic (IDPc) and mitochondrial NADP+ -dependent isocitrate dehydrogenase (IDPm) by supplying NADPH for antioxidant systems. In this paper, we demonstrate that modulation of IDPc or IDPm activity in IMR-90 cells regulates cellular redox status and replicative senescence. When we examined the regulatory role of IDPc and IDPm against the aging process with IMR-90 cells transfected with cDNA for IDPc or IDPm in sense and antisense orientations, a clear inverse relationship was observed between the amount of IDPc or IDPm expressed in target cells and their susceptibility to senescence, which was reflected by changes in replicative potential, cell cycle, senescence-associated beta-galactosidase activity, expression of p21 and p53, and morphology of cells. Furthermore, lipid peroxidation, oxidative DNA damage, and intracellular peroxide generation were higher and cellular redox status shifted to a prooxidant condition in the cell lines expressing the lower level of IDPc or IDPm. The results suggest that IDPc and IDPm play an important regulatory role in cellular defense against oxidative stress and in the senescence of IMR-90 cells.

Gender differences in life expectancy with and without disability among older adults in Ecuador.

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Egüez-Guevara, Pilar; Andrade, Flávia Cristina Drumond

2015-01-01

Knowledge on disability's impact among older women and men in Ecuador is limited. This paper provides gender-specific estimates of disability prevalence, life expectancy with and without disability, and the factors associated with gender differences in disability at older age in Ecuador (2009-2010). Data from the Health, Well-Being, and Aging Survey (SABE) Ecuador 2009 was used. Participants were 4480 men and women aged 60 and over. Life expectancy with and without disability was calculated using the Sullivan method. Logistic regression analyses were used to explore gender differences in disability prevalence. Two disability measures, indicating limitations in activities of daily living (ADL) and instrumental activities of daily living (IADL), were used. 60-year-old women in Ecuador can expect to live 16.3 years without ADL limitations compared to 16.9 years for men. Life expectancy without IADL limitations was 12.5 years for women and 15.5 years for men. At age 60, women's length of life with ADL and IADL disability was higher (7.9 years for women vs. 4.9 years for men with ADL, and 11.7 years for women vs. 6.3 years for men with IADL). After controlling for socioeconomic characteristics, chronic conditions and lifestyle factors, gender differences in ADL disability were not statistically significant. However, older women were 58% more likely (OR=1.58, 95% CI 1.27, 1.95) to report having IADL limitations than men, even after including control variables. Interventions should tackle chronic disease, physical inactivity, and socioeconomic differences to reduce women's vulnerability to disability in older age. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Insulin-like growth factor binding protein-6 delays replicative senescence of human fibroblasts

DEFF Research Database (Denmark)

Micutkova, Lucia; Diener, Thomas; Li, Chen

2011-01-01

Cellular senescence can be induced by a variety of mechanisms, and recent data suggest a key role for cytokine networks to maintain the senescent state. Here, we have used a proteomic LC-MS/MS approach to identify new extracellular regulators of senescence in human fibroblasts. We identified 26 e...

Muscarinic receptor plasticity in the brain of senescent rats: down-regulation after repeated administration of diisopropyl fluorophosphate

International Nuclear Information System (INIS)

Pintor, A.; Fortuna, S.; Volpe, M.T.; Michalek, H.

1988-01-01

Potential age-related differences in the response of Fischer 344 rats to subchronic treatment with diisopropylfluorophosphate (DFP) were evaluated in terms of brain cholinesterase (ChE) inhibition and muscarinic receptor sites. Male 3- and 24-month old rats were sc injected with sublethal doses of DFP for 2 weeks and killed 48 hrs after the last treatment. In the cerebral cortex, hippocampus and striatum of control rats a significant age-related reduction of ChE and of maximum number of 3 H-QNB binding sites (Bmax) was observed. The administration of DFP to senescent rats resulted in more pronounced and longer lasting syndrome of cholinergic stimulation, with marked body weight loss and 60% mortality. The percentage inhibition of brain ChE induced by DFP did not differ between young and senescent rats. As expected, in young rats DFP caused a significant decrease of Bmax, which in the cerebral cortex reached about 40%. In the surviving senescent rats, the percentage decrease of Bmax due to DFP with respect to age-matched controls was very similar to that of young animals, especially in the cerebral cortex. Thus there is great variability in the response of aged rats to DFP treatment, from total failure of adaptive mechanisms resulting in death to considerable muscarinic receptor plasticity

Muscarinic receptor plasticity in the brain of senescent rats: down-regulation after repeated administration of diisopropyl fluorophosphate

Energy Technology Data Exchange (ETDEWEB)

Pintor, A.; Fortuna, S.; Volpe, M.T.; Michalek, H.

1988-01-01

Potential age-related differences in the response of Fischer 344 rats to subchronic treatment with diisopropylfluorophosphate (DFP) were evaluated in terms of brain cholinesterase (ChE) inhibition and muscarinic receptor sites. Male 3- and 24-month old rats were sc injected with sublethal doses of DFP for 2 weeks and killed 48 hrs after the last treatment. In the cerebral cortex, hippocampus and striatum of control rats a significant age-related reduction of ChE and of maximum number of /sup 3/H-QNB binding sites (Bmax) was observed. The administration of DFP to senescent rats resulted in more pronounced and longer lasting syndrome of cholinergic stimulation, with marked body weight loss and 60% mortality. The percentage inhibition of brain ChE induced by DFP did not differ between young and senescent rats. As expected, in young rats DFP caused a significant decrease of Bmax, which in the cerebral cortex reached about 40%. In the surviving senescent rats, the percentage decrease of Bmax due to DFP with respect to age-matched controls was very similar to that of young animals, especially in the cerebral cortex. Thus there is great variability in the response of aged rats to DFP treatment, from total failure of adaptive mechanisms resulting in death to considerable muscarinic receptor plasticity.

Muscle Senescence in Short-Lived Wild Mammals, the Soricine Shrews Blarina brevicauda and Sorex palustris

Science.gov (United States)

HINDLE, ALLYSON G.; LAWLER, JOHN M.; CAMPBELL, KEVIN L.; HORNING, MARKUS

2015-01-01

Red-toothed (soricine) shrews are consummate predators exhibiting the highest energy turnovers and shortest life spans (ca. 18 months) of any mammal, yet virtually nothing is known regarding their physiological aging. We assessed the emerging pattern of skeletal muscle senescence (contractile/connective tissue components) in sympatric species, the semi-aquatic water shrew (WS), Sorex palustris, and the terrestrial short-tailed shrew (STS), Blarina brevicauda, to determine if muscle aging occurs in wild, short-lived mammals (H0: shrews do not survive to an age where senescence occurs), and if so, whether these alterations are species-specific. Gracilis muscles were collected from first-year (n = 17) and second-year (n = 17) field-caught shrews. Consistent with typical mammalian aging, collagen content (% area) increased with age in both species (S. palustris: ~50%; B. brevicauda: ~60%). Muscle was dominated by stiffer Type I collagen, and the ratio of collagen Type I:Type III more than doubled with age. The area ratio of muscle:collagen decreased with age in both species, but was considerably lower in adult STS, suggesting species-specificity of senescence. Extracellular space was age-elevated in B. brevicauda, but was preserved in S. palustris (~50 vs. 10% elevation). Though juvenile interspecific comparisons revealed no significance, adult WS myocytes had 68% larger cross-sectional area and occurred at 28% lower fibers/area than those of adult STS. We demonstrate that age-related muscle senescence does occur in wild-caught, short-lived mammals, and we therefore reject this classic aging theory tenet. Our findings moreover illustrate that differential age adjustments in contractile/connective tissue components of muscle occur in the two species of wild-caught shrews. PMID:19296507

The oxidative hypothesis of senescence

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Gilca M

2007-01-01

Full Text Available The oxidative hypothesis of senescence, since its origin in 1956, has garnered significant evidence and growing support among scientists for the notion that free radicals play an important role in ageing, either as "damaging" molecules or as signaling molecules. Age-increasing oxidative injuries induced by free radicals, higher susceptibility to oxidative stress in short-lived organisms, genetic manipulations that alter both oxidative resistance and longevity and the anti-ageing effect of caloric restriction and intermittent fasting are a few examples of accepted scientific facts that support the oxidative theory of senescence. Though not completely understood due to the complex "network" of redox regulatory systems, the implication of oxidative stress in the ageing process is now well documented. Moreover, it is compatible with other current ageing theories (e.g., those implicating the mitochondrial damage/mitochondrial-lysosomal axis, stress-induced premature senescence, biological "garbage" accumulation, etc. This review is intended to summarize and critically discuss the redox mechanisms involved during the ageing process: sources of oxidant agents in ageing (mitochondrial -electron transport chain, nitric oxide synthase reaction- and non-mitochondrial- Fenton reaction, microsomal cytochrome P450 enzymes, peroxisomal β -oxidation and respiratory burst of phagocytic cells, antioxidant changes in ageing (enzymatic- superoxide dismutase, glutathione-reductase, glutathion peroxidase, catalase- and non-enzymatic glutathione, ascorbate, urate, bilirubine, melatonin, tocopherols, carotenoids, ubiquinol, alteration of oxidative damage repairing mechanisms and the role of free radicals as signaling molecules in ageing.

The Relationship between Personality Traits and Life Expectancy in Patients with Multiple Sclerosis

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Leila Zaghari

2012-04-01

Full Text Available Objectives: Multiple Sclerosis is an incurable and chronic disease of the central nervous system. The main purpose of this survey is to compare the character types and life expectancy of patients suffering from M. S as compared with normal people. This survey was conducted using the Persian translation of NEO-FFI (NEO-Five Factor Inventory and Herth Life Expectancy. Methods:Thirty nine people suffering from multiple sclerosis, who were hospitalized in anursing home, were chosen. As a control group there were 39 healthy people who had no background of physical or mental diseases. These people were selected from educational centre scientific and the personnel of Islamic Azad University, Science and Research Campus. Healthy people were matched to control group according, to sex, gender, marital status and education. Results: To analyze the data, T tests were used. The results of the survey show that people suffering from multiple sclerosis were significantly different from healthy people in three factors, neuroticism, extraversion and openness. For life expectancy there was no significant difference between the two groups. Discussion: Peopleaffected by Multiple Sclerosis achieve higher marks levels of the function of neuroticism compared with the healthy people. They are also agreeableness in a lower state, due to the function of openness to experience compared with the safe ones and in a lower state compared with the healthy persons.

Age at migration and disability-free life expectancy among the elder Mexican-origin population

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Marc Garcia

2016-12-01

Full Text Available Background: Migration selectivity is thought to shape the health profiles of Mexican immigrants. Objective: This study examines how the experience of Mexican migration to the United States affects the health process and the quality of life in old age by age at migration, specific to sex. Methods: We use 20 years of data from the Hispanic Established Populations for the Epidemiologic Study of the Elderly to estimate the proportion of life spent disability-free prior to death across eight subgroups by sex, nativity, and age at migration among Mexican-origin elderly in the United States. Results: Female migrants are at a significant disadvantage in terms of IADL disability-free life expectancy relative to US-born women, particularly late-life migrants. Conversely, mid- and late-life male migrants exhibit an advantage in ADL disability-free life expectancy compared to their US-born counterparts. Conclusions: Foreign-born Mexican elders are not a homogeneous group. This issue merits special attention in the development of community-based long-term care programs in order to appropriately target the specific needs of different subgroups of older Mexican individuals entering their last decades of life. Contribution: This study contributes to immigrant health literature by providing a more comprehensive documentation of nativity differentials, by distinguishing subgroups of Mexican elderly by sex, nativity, and age at migration.

The effects of constant and alternating temperatures on the reproductive potential, life span, and life expectancy of Anastrepha fraterculus (Wiedemann (Dipteria: Tephritidae

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V. V. CARDOSO

Full Text Available Ovarian development, oviposition, larval eclosion, ornithine decarboxylase (ODC activity, ovarian, testis and ejaculatory apodeme measurements (length, width, and area, and the number of spermatozoa of Anastrepha fraterculus (Wiedemann were analyzed at alternating (20º/6ºC and 20º/13°C and constant (6°C; 25°C temperatures. Life span and life expectancy were also analyzed for both genders. All the results suggest that temperature, especially alternating temperatures, increase not only male and female reproductive potential but also their life span and life expectancy. These changes can be a powerful strategy triggered by A. fraterculus as a means to survive the stressful temperature conditions found in winter in the apple production region in Brazil, enabling this species to increase its population density and cause apple damage when spring begins.

The effects of constant and alternating temperatures on the reproductive potential, life span, and life expectancy of Anastrepha fraterculus (Wiedemann (Dipteria: Tephritidae

Directory of Open Access Journals (Sweden)

CARDOSO V. V.

2002-01-01

Full Text Available Ovarian development, oviposition, larval eclosion, ornithine decarboxylase (ODC activity, ovarian, testis and ejaculatory apodeme measurements (length, width, and area, and the number of spermatozoa of Anastrepha fraterculus (Wiedemann were analyzed at alternating (20masculine/6masculineC and 20masculine/13degreesC and constant (6degreesC; 25degreesC temperatures. Life span and life expectancy were also analyzed for both genders. All the results suggest that temperature, especially alternating temperatures, increase not only male and female reproductive potential but also their life span and life expectancy. These changes can be a powerful strategy triggered by A. fraterculus as a means to survive the stressful temperature conditions found in winter in the apple production region in Brazil, enabling this species to increase its population density and cause apple damage when spring begins.

Age distributions of Greenlandic dwarf shrubs support concept of negligible actuarial senescence

DEFF Research Database (Denmark)

Dahlgren, Johan; Rizzi, Silvia; Schweingruber, Fritz

2016-01-01

shrub species from 863 taproot samples collected in coastal east Greenland. Penalized composite link models (pclm) were used to fill gaps in the observed age ranges, caused by low species-specific sample sizes in relation to life span. Resulting distributions indicate that mortality patterns...... are independent of age. Actuarial senescence is thus negligible in these dwarf shrub populations. We suggest that smoothing techniques such as pclm enable consideration of noisy age data for determining age distributions. These distributions may, in turn, reveal age effects on demographic rates. Moreover, age...