Search

Purpose: Positing that successful aging has independent, yet related, dimensions that are both objective and subjective, we examine how early influences and contemporary characteristics define 4 groups of people. Design and Methods: Data were gathered from 5,688 persons aged 50-74 years living in New Jersey who participated in telephone interviews. Latent profile analysis defined people who age successfully according to both objective and subjective criteria, neither criteria, and one, but not the other, criteria. Multinomial logistic regression was used to examine the extent to which early influences and contemporary characteristics predict group membership. Results: Although characteristics observable early in life predict group membership, their influence is modified by current health behaviors and social support. The roles of education and incarceration feature prominently. Marital, work, and volunteer statuses, as well as moderate alcohol consumption, distinguish those aging successfully according to both criteria from the other 3 groups. Implications: Results help to define successful aging as a multidimensional construct having both objective and subjective dimensions, provide greater clarity regarding its correlates, and increase understanding of its modifiable aspects. Key Words: Successful aging, Latent profile analysis, Objective success, Subjective success, Multinomial logistic regression doi: 10.1093/geront/gnq041

Despite the vast amount of research on threatened and endangered green turtle populations, some uncertainty regarding stage durations, growth rates, and age at maturation remains. We used skeletochronology to address this gap in knowledge for green turtle populations in the North Atlantic Ocean that use coastal waters along the southeastern U.S. as developmental habitat. Oceanic stage duration was estimated at 1-7 years ( [Formula omitted] = 3 years). Several growth models, including von Bertalanffy, logistic, Gompertz, and power functions were evaluated for describing sex-specific length-at-age data. Ages at maturation estimated using mean size at nesting for females from each genetic sub-population contributing juveniles to this neritic foraging area were 44 years (Florida), 42.5 years (Costa Rica), and 42 years (Mexico), which were higher than previously reported ages. This implies that nesting populations comprising primarily individuals utilizing foraging grounds in the southeastern U.S. may take longer to recover than previously estimated., Author(s): Lisa R. Goshe [sup.1] , Larisa Avens [sup.1] , Frederick S. Scharf [sup.2] , Amanda L. Southwood [sup.2] Author Affiliations: (1) grid.422702.1, 0000 0001 1356 4495, NOAA Fisheries, Southeast [...]

In the past years, simple organisms such as yeasts and worms have contributed a great deal to aging research. Studies pioneered in Saccharomyces cerevisiae were useful to elucidate a significant number of molecular mechanisms underlying cellular aging and to discover novel longevity genes. Importantly, these genes proved many times to be conserved in multicellular eukaryotes. Consequently, such discovery approaches are being extended to other yeast models, such as Schizosaccharomyces pombe, Candida albicans, Kluyveromyces lactis, and Cryptococcus neoformans. In fission yeast, researchers have found links between asymmetrical cell division and nutrient signaling pathways with aging. In this review, we discuss the state of knowledge on the mechanisms controlling both replicative and chronological aging in S pombe and the other emergent yeast models. Key Words: Longevity--Yeast--Schizosaccharomyces pombe--Candida albicans--Replicative life span--Chronological life span. doi: 10.1093/gerona/glp152

The incidence of pulmonary fibrosis increases with age. Studies from our group have implicated circulating progenitor cells, termed fibrocytes, in lung fibrosis. In this study, we investigate whether the preceding determinants of inflammation and fibrosis were augmented with aging. We compared responses to intratracheal bleomycin in senescence-accelerated prone mice (SAMP), with responses in age-matched control senescence-accelerated resistant mice (SAMR). SAMP mice demonstrated an exaggerated inflammatory response as evidenced by lung histology. Bleomycin-induced fibrosis was significantly higher in SAMP mice compared with SAMR controls. Consistent with fibrotic changes in the lung, SAMP mice expressed higher levels of transforming growth factor-[beta]1 in the lung. Furthermore. SAMP mice showed higher numbers of fibrocytes and higher levels of stromal cell--derived factor-1 in the peripheral blood. This study provides the novel observation that apart from increases in inflammatory and fibrotic factors in response to injury, the increased mobilization of fibrocytes may be involved in age-related susceptibility to lung fibrosis. Key Words: Lung--Senescence--Bone marrow--Mice.

Dramatic advances in understanding mechanisms of aging have recently been made in model systems. Interventions have been devised that successfully enhance survival. Major issues still in need of resolution include whether these interventions not only increase survival but also enhance function, delay frailty, and can be translated into clinical application. It seems there are basic biologic findings close to being ready for translation. However, a number of barriers exist to translating these findings into realistic clinical interventions. Steps and resources needed include measuring not only survival but also impact of interventions on age-related disability, frailty, and onset of disease in model systems; development of clinically relevant measures of disability, frailty, and disease for each animal model and genetically tractable animal models of frailty; training and career-long funding mechanisms for geriatricians in basic science research and for basic scientists in geriatric issues; translationally capable review and funding mechanisms; emphasis on studies of interventions that can be initiated in later life for preventing or reversing disability; genetic association studies in humans to identify new candidate genes and pathways that correlate with disability, frailty, and age-related disease onset as well as longevity; study of exposure to environmental agents or toxins early in life on survival, disability, frailty, and disease in later life. Key Words: Healthspan--Translation--Animal studies of aging.

Background. This article examines how different parameterizations of age and time in modeling observational longitudinal data can affect results. Methods. When individuals of different ages at study entry are considered, it becomes necessary to distinguish between longitudinal and cross-sectional differences to overcome possible selection biases. Results. Various models were fitted using data from longitudinal studies with participants with different ages and different follow-up lengths. Decomposing age into two components--age at entry into the study (first age) and the longitudinal follow-up (time) compared with considering age alone--leads to different conclusions. Conclusions. In general, models using both first age and time terms performed better, and these terms are usually necessary to correctly analyze longitudinal data. Key Words: Mixed-effects models--Multilevel modeling--Observational study--Recruitment bias--Regression.

Biogerontologists and demographers have argued that the fastest, most cost-effective strategies for prevention of the medical problems that afflict those older than 60 years are likely to emerge from a deeper understanding of what factors time the aging process and how aging leads, in rough synchrony, to the many diseases and disabilities of aging. Biologists can support and refine this discussion by studies of slow-aging mice, of mice with disease-promoting mutations, of mice in which specific cellular responses have been abrogated by genetic or pharmaceutical interventions, of slow-aging dog and horse breeds, and of the factors, genetic and physiological, that coordinate lethal and nonlethal consequences of aging in people. More work is also needed to learn how timing of antiaging interventions can be used to optimize the balance between beneficial and undesirable effects. Key Words: Longevity--Health--Animal models--Interventions.

Aging is associated with a deterioration of the acute phase response to inflammatory challenges. However, the nature of these defects remains poorly defined. We analyzed the hepatic inflammatory response after intraperitoneal administration of lipopolysaccharide (LPS) given to Fisher 344 rats aged 6, 15, and 22-23 months. Induction of the acute phase proteins (APPs), haptoglobin, [alpha]-1-acid glycoprotein, and T-kininogen was reduced and/or retarded with aging. Initial induction of interleukin-6 in aged rats was normal, but the later response was increased relative to younger counterparts. An exacerbated hepatic injury was observed in aged rats receiving LPS, as evidenced by the presence of multiple microabscesses in portal tracts, confluent necrosis, higher neutrophil accumulation, and elevated serum levels of alanine aminotransferase, relative to younger animals. Our results suggest that aged rats displayed a reduced expression of APPs and increased hepatic injury in response to the inflammatory insult. Key Words: Liver--Inflammation--injury--Acute phase response--Aging.

The senescence-accelerated mouse (SAM) is an experimental model of aging, established through phenotypic selection from a common genetic pool of AKR/J mice. Here we use complementary DNA microarray, Western blot, and electrophoretic mobility shift assay to consider whether changes in fiver gene expression observed in 5-month-old SAM-prone 8 (P8) mice, compared to SAM-R1 controls, are similar to those reported in aged rodents. Livers from SAM-P8 mice presented 88 differentially expressed transcripts, 59% of which were upregulated and 41% were downregulated. Of these, 14% were related to inflammatory/immunity processes, 10% were related to the xenobiotic metabolism (XM) and 3% to nervous system pathophysiology (NSP). Depressed expression and activity of genes related to XM, and altered expression of genes related to NSP, are similar to changes observed in aged rodents. Increased expression of heat shock protein 1 and Jun-B, reduced activity of activator protein 1 and absence of nuclear factor-[kappa][BETA] activation indicate the lack of a strong liver inflammatory response in 5-month-old SAM-P8 mice. Key Words: SAM mice--Liver--Inflammation--Xenobiotic metabolism.

Laboratory experiments show us that the deleterious character of accumulated novel age-specific mutations is reduced and made less variable with increased age. While theories of aging predict that the frequency of deleterious mutations at mutation-selection equilibrium will increase with the mutation's age of effect, they do not account for these age-related changes in the distribution of de novomutational effects. Furthermore, no model predicts why this dependence of mutational effects upon age exists. Because the nature of mutational distributions plays a critical role in shaping patterns of senescence, we need to develop aging theory that explains and incorporates these effects. Here we propose a model that explains the age dependency of mutational effects by extending Fisher's geometrical model of adaptation to include a temporal dimension. Using a combination of simple analytical arguments and simulations, we show that our model predicts age-specific mutational distributions that are consistent with observations from mutationaccumulation experiments. Simulations show us that these age-specific mutational effects may generate patterns of senescence at mutation-selection equilibrium that are consistent with observed demographic patterns that are otherwise difficult to explain.

Abstract: Previous authors have shown analytically that the optimal equilibrium harvest rate ([U.sub.MSY]) for an iteroparous fish stock is a function of the slope of the stock-recruitment curve at low [...]

Elderly housing surveys consistently report that older Americans prefer to remain living in their homes for as long as they are physically able. This study uses hazard models to estimate the effects of family composition changes, health conditions, housing characteristics, and local policies and amenities on aging-in-place decisions by older homeowners in the 1972-1992 Panel Study of Income Dynamics. The empirical results show that increases in property taxes and utility costs, changes in family composition, and diminished physical well-being are negatively associated with aging in place. Increased home equity, greater financial resources, and stronger ties to the community are positively associated with aging in place. Taken together, these findings suggest that policies designed to reduce the user costs of homeownership or to enhance the functionality of elderly homeowners may facilitate aging in place. Keywords: elderly; housing; age in place

Recent studies have established that age is the major risk factor for vascular disease. Numerous aberrant changes occur in vascular structure and function during aging, and animal models are the primary means to determine the underlying mechanisms of age-mediated vascular pathology. The Fischer 344/Brown Norway F1 hybrid (F344xBN) rat thoracic aorta has been shown to display age-related pathology similar to what occurs in humans. This study utilized the F344xBN rat aorta and both morphometric and global gene expression analyses to identify appropriate time points to study vascular aging and to identify molecules associated with the development and progression of vascular pathology. In contrast to some previous studies that indicated age-related abrupt changes, a progressive increase in intimal and medial thickness, as well as smooth muscle cell-containing intimal protrusions, was observed in thoracic aorta. This structural vascular pathology was associated with a progressive, but nonlinear, increase in global differential gene expression. Gene products with altered mRNA and protein expression included inflammation-related molecules: specifically, the adhesion molecules ICAM-1 and VCAM-1 and the bone morphogenic proteins osteopontin and bone sialoprotein-1. Intimal-associated macrophages were found to increase significantly in number with age. Both systemic and tissue markers of oxidant stress, serum 8-isoprostane and 3-nitrotyrosine, respectively, were also found to increase during aging. The results demonstrate that major structural abnormalities and altered gene expression develop after 6 mo and that the progressive pathological development is associated with increased inflammation and oxidant stress. arterial remodeling; inflammation; microarray; oxidative stress

We investigated whether caloric restriction (CR) improves physical performance in a rodent model of aging, and whether this effect is accompanied with a decrease in visceral adipose tissue production of proinflammatory cytokines. Body composition, standardized physical performance measures, as well as in vitro visceral adipose tissue cytokine secretion and circulating levels of an inflammatory marker were cross-sectionally assessed in ad libitum (AL)-fed and lifelong CR Fischer 344 x Brown Norway male rats aged 18, 24, and 29 months. Fat to lean mass ratio increased and physical performance declined with age in the AL rats. Compared to AL rats, CR rats had lower fat mass, fat to lean ratio, adipose tissue secretion of interleukin-6, and circulating levels of C-reactive protein, and higher physical performance scores. Therefore, CR may be an effective intervention for improving functional status into advanced age and is perhaps mediated via a reduction in adipose tissue-generated proinflammatory cytokine production.

An optimal aging theory, in which there is an endogenous rise in mortality rates with age, is presented. The model expects maximum fertility to occur at an age when somatic growth ends. How biology can be integrated with economics is also explained.

Hutchinson-Gilford progeria syndrome (HGPS) is a rare, fatal genetic disorder that is characterized by segmental accelerated aging. The major causal mutation associated with HGPS triggers abnormal messenger RNA splicing of the lamin A gene leading to changes in the nuclear architecture. To date, two models have been proposed to explain how mutations in the lamin A gene could lead to HGPS, structural fragility and altered gene expression. We favor a compatible model that links HGPS to stem cell-driven tissue regeneration. In this model, nuclear fragility of lamin A-deficient cells increases apoptotic cell death to levels that exhaust tissues' ability for stem cell-driven regeneration. Tissue-specific differences in cell death or regenerative potential, or both, result in the tissue-specific segmental aging pattern seen in HGPS. We propose that the pattern of aging-related conditions present or absent in HGPS can provide insight into the genetic and environmental factors that contribute to normal aging.

We propose the LOU/c/jall rat as a possible model for research into aging. Physiological and behavioral data have been collected over the past 5 years, using lifelong and cross-sectional studies. The median life span of the rats was 29 months in males and 33-34 months in females. A low level of body fat throughout life was observed in both sexes. Basic phenomena of aging such as body weight loss, decrease in caloric intake, and dramatic drop in protein selection were noted from the age of 18 months in males and 28 months in females. A decline in muscle mass, depending on the sex and the type of muscle, was seen. These data allowed us to demonstrate physiological aging in male and female LOU/c/jall rats. The most interesting characteristics of this strain of rat for aging studies are longevity, and the absence of obesity and of severe pathologies. Further studies are required in order to confirm this last point.

The process of aging causes significant alterations in the facial appearance of individuals. When compared with other sources of variation in face images, appearance variation due to aging displays some unique characteristics. For example, aging variation is specific to a given individual; it occurs slowly and is affected significantly by other factors, such as health, gender, and lifestyle. Changes in facial appearance due to aging can even affect discriminatory facial features, resulting in deterioration of the ability of humans and machines to identify aged individuals. In this paper, we describe how the effects of aging on facial appearance can be explained using learned age transformations and present experimental results to show that reasonably accurate estimates of age can be made for unseen images. We also show that we can improve our results by taking into account the fact that different individuals age in different ways and by considering the effect of lifestyle. Our proposed framework can be used for simulating aging effects on new face images in order to predict how an individual might look like in the future or how he/she used to look in the past. The methodology presented has also been used for designing a face recognition system, robust to aging variation. In this context, the perceived age of the subjects in the training and test images is normalized before the training and classification procedure so that aging variation is eliminated. Experimental results demonstrate that, when age normalization is used, the performance of our face recognition system can be improved. Index Terms--Aging variation, statistical face models, face recognition.

Gompertz and Weibull functions imply contrasting biological causes of demographic aging. The terms describing increasing mortality with age are multiplicative and additive, respectively, which could result from an increase in the vulnerability of individuals to extrinsic causes in the Gompertz model and the predominance of intrinsic causes at older ages in the Weibull model. Experiments that manipulate extrinsic mortality can distinguish these biological models. To facilitate analyses of experimental data, we defined a single index for the rate of aging (omega) for the Weibull and Gompertz functions. Each function described the increase in aging-related mortality in simulated ages at death reasonably well. However, in contrast to the Weibull [omega.sub.W], the Gompertz [omega.sub.G] was sensitive to variation in the initial mortality rate independently of aging-related mortality. Comparisons between wild and captive populations appear to support the intrinsic-causes model for birds, but give mixed support for both models in mammals.

This essay presents some practical advice and suggestions for those who wish to use mice and rats in experiments on the biology of aging. Ten principles set forth guidance on choice of ages, choice of stocks, the importance of specific pathogen-free status, the uses of necropsy data, the dangers of pooling samples from different individuals, planning ahead for loss of aged mice to death and disease, the use of cost-adjusted power calculations, and the dangers of inferring causal associations from correlated age effects.

Research into the spiritual, friendship and intimacy experiences of a group of aged male Roman Catholic celibates supports the Psychosocial Withdrawal Models and Gero-transcendence Approach to theories of aging, under which the activities and relationships of the aged are believed to be affected by society's marginalization while simultaneously the elderly choose certain relationships over others. A change in connections often prompts increased autonomy, with connection and autonomy each threatened by inappropriate dependence and isolation. According to the Disengagement Theory, the elderly become less governed by rules, take on more individualized roles and expect their activity levels to change.

To lay the foundation for our model, we first describe existing conceptions of successful aging, underlying assumptions of development, and criteria for success. The model presented extends the discourse on this topic in three directions: (a) It frames the discussion of successful aging in the broader context of life course development; (b) it accounts for both normative and nonnormative (i.e., exceptional) success; and (c) it integrates motivational processes into a theory of successful aging. Successful aging is equated with the development and maintenance of primary control throughout the life course, which is achieved through control-related processes that optimize selection and failure compensation functions. Selection processes regulate the choice of action goals so that diversity is maintained and positive and negative trade-offs between performance domains and life stages are taken into account. Compensation mechanisms serve to maintain, enhance, and remediate competencies and motivational resources after failure experiences. Both compensation and selection processes are motivated by desires for primary control and can be characterized in terms of primary and secondary control processes.

The important factors which influence the accurate estimation of multiparametric survival model being fit are examined. The various types of data, fitting procedures, best fit definitions, smoothing and data reconstruction are investigated. The consequences which could result from methodological misuse are related to the values of final parameter estimates and their associated errors.

The analysis of Brinley plots reveals that, under certain conditions, the plot does not clearly reveal the correctness of an aging theory. The theory and performance models may be used to select and interpret graphed data. When performance identity assumptions are not obeyed, a full Brinley plot is insufficient to differentiate between various aging theories.

Based on the premise that scientists should periodically examine the history of their ideas and methodologies, this article focuses on the issue of continuity in the evolution of scientific knowledge about aging. Taking a twenty-five-year perspective, selected research questions and priorities in the biomedical, behavioral, and social domains of aging are used to exemplify the continuity of the gerontological knowledge base. This article concludes that there is considerable evidence of continuity, despite the strong influences of changing cohorts of people and external forces that have shaped new ideas and research questions in gerontology.

Understanding healthspan is arguably the most relevant clinical, social, and economic feature of aging research. The model systems of worm, fly, and mouse are potentially powerful tools to achieve this aim. These models provide two unique approaches. The first is based on genetic screening for gain or loss of function mutations that ameliorate senescence. Genetic factors discovered by this process permit us to recognize causal and regulatory mechanisms of aging. A related screen looks for compounds that slow aging or act upon proteins that were initially identified from genetic analysis. The second research strategy uses manipulations of targeted genetic factors to test causal explanations for aging. These studies include transgenic organisms and genetic epistasis analysis. Overall, genetically driven research with model organisms is largely responsible for the breakthrough of aging biology in the past 15 years. Aging in these contexts, however, has been measured almost exclusively from cohort survival statistics such as life expectancy and agespecific mortality. This is for a good reason. Manipulated factors that extend life span are thought to unambiguously slow senescence and thus to reflect underlying causes of the aging process. But this approach is also common for a practical reason--healthspan is a poorly defined commodity in humans, let alone for genetic animal model systems. It was the consensus of the working session that making healthspan an operational metric would be an innovation needed for the genetic power of model systems to address this aspect of human aging. Key Word: Functional senescence--Healthspan--Drosophila--C. elegans.

Health planning efforts for the population age 65 and over have been hampered continually by the lack of reliable estimates of the noninstitutionalized long-term care population. Until recently national estimates were virtually nonexistent, and reliable small area estimates remain unavailable. However, with the recent publication of several national surveys and the 1990 Census, synthetic estimates can be made for states and counties by using multivariate methods to model functional dependency at the national level, and then applying the predicted probabilities to corresponding state and county data. Using the 1984 National Health Interview Survey's Supplement on Aging and the 1986 Area Health Resources File System, we have produced log-linear regression models that include demographic and contextual variables as predictors of functional dependency among the noninstitutionalized population age 65 and over. Age, sex, race, and the percent of the 65 and over population who reside in poverty were found to be significant predictors of functional dependency. Applying these models to 1986 Medicare Enrollment Statistics, regression-adjusted synthetic estimates of two levels of functional dependency were produced for all states and--as examples of how the rates can be used to produce additional synthetic estimates--the largest County in each state. We also Produced point estimates and standard errors for the national prevalence of functional dependency among the noninstitutionalized population age 65 and over. (Am J Public Health 1990;81:335-343), Accurate estimation of the proportion of the population over age 65 that consists of functionally dependent people is necessary for health care planning, yet no clearly superior way of arriving at such an estimate has been developed. A method that uses log-linear regression models to estimate the numbers of noninstitutionalized dependent people over 65 is presented and applied to data drawn from several national and local surveys. This model allows for adjustments in the estimates due to several ''real-life'' factors, such as the effect of poverty on other factors that influence dependence (age, sex, race), and the fact that a small proportion (5 percent) of people older than 65 are not enrolled in Medicare. The results showed that age, sex, race, and poverty were the most important predictors of functional dependency. Using these variables, estimates of two levels of dependency were calculated for the individual states and selected counties. The two levels were ADL-dependent (people who have difficulty with the activities of daily life, such as dressing or eating), and those who could perform the activities of daily life but could not, for reasons of mobility, prepare meals, shop, or perform housework. The estimates are likely to prove useful for predicting the number of older people within a region who are likely to require long-term care. (Consumer Summary produced by Reliance Medical Information, Inc.)

The impairment of memory retention was assessed in old mice, aged 24 months, and young mice, aged 4 months. The mice were of the laboratory strain called C57BL/6Nnia. The relationship of memory impairment to changes in the function of neurotransmitters or hormones that affect memory processes was also examined. Neurotransmitters are naturally occurring substances that are involved in the movement of impulses along nerves. The 24-month-old mice were given drugs known to increase the retention of memory in younger mice. Eleven pharmacological agents enhanced memory retention in old mice at doses that were optimal in younger mice. Two agents, clonidine and ST 587, were ineffective at improving memory retention in 24-month-old mice at doses shown to be effective in younger mice. These two agents belong to a group of drugs known as alpha noradrenergic agonists, which bind and activate alpha receptors, specialized proteins on the cell membrane that trigger noradrenergic nervous system responses. These results show that old mice have a similar ability to retain memory as young mice, although older mice differ from younger mice with respect to alpha noradrenergic receptors. (Consumer Summary produced by Reliance Medical Information, Inc.)

'It's like trying to understand human psychology by interviewing two brothers,' says Harvard biologist Steven Austad. Austad is criticizing gerontology's traditional reliance on laboratory mice and rats to study the [...]

Allostatic load (AL) has been proposed as a new conceptualization of cumulative biological burden exacted on the body through attempts to adapt to life's demands. Using a multisystem summary measure of AL, we evaluated its capacity to predict four categories of health outcomes, 7 years after a baseline survey of 1,189 men and women age 70-79. Higher baseline AL scores were associated with significantly increased risk for 7-year mortality as well as declines in cognitive and physical functioning and were marginally associated with incident cardiovascular disease events, independent of standard socio-demographic characteristics and baseline health status. The summary AL measure was based on 10 parameters of biological functioning, four of which are primary mediators in the cascade from perceived challenges to downstream health outcomes. Six of the components are secondary mediators reflecting primarily components of the metabolic syndrome (syndrome X). AL was a better predictor of mortality and decline in physical functioning than either the syndrome X or primary mediator components alone. The findings support the concept of AL as a measure of cumulative biological burden.

Author(s): Susan E. Howlett [sup.1] [sup.2] , Kenneth Rockwood [sup.1] [sup.2] Author Affiliations: (1) Dalhousie University, Halifax, Canada (2) University of Manchester, UK Good preclinical models of ageing are needed [...]

David E. Harrison's objection to the use of animals with a short life span in the study of extending life span is justified, although the aim of experiments using Senescence-Accelerated Mouse strains is only to examine the method of accelerated aging at the level of cultured cells. If genes responsible for accelerated aging are discovered, they can help understand the true mechanism of aging and the concept of 'normal aging.'

We present a new evolutionary model of age at first birth in human females, a key component of each individual's life history and Darwinian fitness. The cornerstone of the model is a trade-off between maturing earlier at a shorter height, or later, at a taller height. The model's novelty is our focus on height rather than weight, and the benefit from height in terms of offspring survival rather than female fertility. Empirical analysis shows us that earlier maturers have a longer reproductive span and later maturers enjoy improved offspring survival. When fitted to parameters from a rural Gambian population, the model successfully predicts the median, 18 years, and the reaction norm for this population. Variation in model parameters, including growth rates, interbirth intervals, offspring mortality, or age at last birth, and their implications for optimal age at first birth are discussed. This model will be contrasted with previous models of optimal age at first birth in humans.

Human diploid fibroblast has a finite replicative life span in vitro and has been widely used as a model for the study of biological aging. In this study we examined the alterations in cellular signaling during aging by comparing the expression and activation of mitogen activated protein kinase (MAPK) in early passage (19 mean population doubling [MPD], young cells) and late passage (60 MPD, old cells) of human skin fibroblasts, Cells in log phase growth were incubated with 10ng/ml of themitogen IL-1B, for 10 to 30 minutes. Cells were lysed with ice cold lysis buffer containing inhibitors. As a measure of MAPK western blot analyses were performed for extracellular-regulated kinase (ERK1/2) and stress activated protein kinase, c-jun amino terminal kinase (JNK1/2). Old cells had a basal amount of ERK1/2 of 1.38 + 0.35 (mean +SEM, arbitrary units) which was significantly higher than the basal value of 0.46 +0.09 in young cells (p

This article examines several key features of the course of adult development in the cohort of women born during the baby boom. By focusing on the women in this group and comparing their experience with that of older cohorts and research on men, the authors demonstrate the need for models of aging that take account of the intersections of history, gender, and individual development. Concepts proposed as universal features of middle age (midlife crisis, generativity, aging), as well as those proposed as specific to women (empty nest, menopause) are examined. Perhaps most important, certain features not commonly viewed as particularly important in women's middle aging (midlife review, identity, confident power) are shown to be central. The need for further research examining these same processes among men and different groups of women is underscored.