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At least 1,027 records · Page 57Linked to original sources
PubMed1995

Longevity and migration of Wuchereria bancrofti infective larvae and their distribution pattern in relation to the resting and feeding behaviour of the vector mosquito, Culex quinquefasciatus.

The longevity, migration and distribution of infective larvae (L3) of Wuchereria bancrofti within the host mosquito were studied by feeding Culex quinquefasciatus on microfilaraemic human blood and allowing the microfilariae to develop to L3. The L3 were found to remain alive and active for 46-50 days, i.e. as long as the host mosquitoes survived. The larvae started their migration to the head of the mosquito soon after their development to L3, on day 13 after the initial, infective bloodmeal. Although more L3 were usually found in the head region of the mosquitoes than in the thorax or abdomen, the larvae showed an oscillatory pattern of movement between all three regions. This movement was significant in the mosquitoes fed only on microfilaraemic blood, but not in those that took a second bloodmeal on normal human blood on day 8 after the infective bloodmeal. The distribution of the L3 in the three regions of the mosquitoes was independent of parasite density. Observations on L3 movement over a 24-h period indicated that there were always more L3 in the head than in the thorax and abdomen and that the number of L3 in the head was maximal at 18.00 hours and minimal at 06.00 hours. When infective mosquitoes were fed on human blood through a Parafilm membrane, 45.2% of the L3 present in the mosquitoes were shed into the blood or on the membrane. All the L3 present in each mosquito migrated to its head during feeding.

Animals↗
PubMed2004

Association of late childbearing with healthy longevity among the oldest-old in China.

Statistical analysis of a large and unique longitudinal data-set demonstrates that childbearing after age 35 or 40 is associated with survival and healthy survival among very old Chinese women and men. The association is stronger for women than for men. The estimates are adjusted for a variety of confounding factors: demographic characteristics, family support, social connections, health practices, and health conditions. Further analysis based on an extension of the Fixed-Attributes Dynamics method shows that late childbearing is positively associated with long-term survival and healthy survival from ages 80-85 to 90-95 and 100-105. This association exists among oldest-old women and men, but, again, the effects are substantially stronger for women than for men. We discuss four possible factors that may explain why late childbearing affects healthy longevity at advanced ages: (1) social factors; (2) biological changes caused by late pregnancy and delivery; (3) genetic and other biological characteristics; and (4) selection.

Aged↗
PubMed2004

Popular perceptions of emerging influences on mortality and longevity in Bangladesh and West Bengal.

Relatively little is known about how environmental and pathological threats to human survival and longevity are perceived by the public. In this study in rural Bangladesh and West Bengal, India, which used individual interviews and focus-group discussions to investigate the changing costs of and motivations for reproduction, respondents were questioned about their perceptions of changes in mortality. The findings show that, while child mortality levels are perceived to have fallen dramatically in recent times, the health and survival prospects of the middle aged and the elderly are seen to have been better in the past. The perceived decline in adult health is attributed to environmental deterioration and lifestyle changes accompanying modernization. This paper explores people's reasons for this unexpected worldview. References to pesticides and chemical fertilizers as causes of death abound in their explanations and are seen to be associated with unhealthy agricultural practices and impiety.

Adult↗
PubMed1989

Why do women live longer than men? Biologic differences that influence longevity.

Women enjoy a natural relative immunity to coronary atherosclerosis compared with their male counterparts because of their sex hormone status, especially in the premenopausal years. This advantage is likely to be extended to the postmenopausal years by the current widespread prescription of estrogen (coupled with cyclic progestin) therapy. Currently available forms of exogenous estrogen preparations do not confer similar benefits on men, nor would their feminizing side effects be acceptable to men. Therefore, to narrow the sex differential in longevity, with its devastating burdens of loneliness and dependency on elderly women and monetary and time burdens on healthcare resources, men must adopt behaviors that reduce their risk of coronary artery disease. Such behaviors are cessation of cigarette smoking, early detection and long-term control of hypertension, and early detection and long-term control of dyslipoproteinemia (as best reflected in the ratio of low-density lipoprotein to high-density lipoprotein cholesterol). Fortunately, the recent advent of effective dietary and, especially, drug therapy for both hypertension and dyslipoproteinemia makes such approaches to reducing male cardiovascular mortality feasible, effective, and of acceptable cost in both economic and personal terms.

Adolescent↗
PubMed1985

Comparative studies on the effects of semipurified and commercial diet on longevity and spontaneous and induced lesions in the Syrian golden hamster.

Syrian golden hamsters were fed a semipurified or commercial diet from weaning throughout life. Bis(2-oxopropyl)nitrosamine (BOP) was administered at 8 weeks of age (10 mg/kg body wt, sc). Longevity was improved by 26% and 36% increases in the mean life-spans of male and female hamsters, respectively, fed the semipurified diets. Carcinogen treatment did not alter survival. The age-adjusted occurrence rates of pancreatic ductular proliferation, carcinomas, adenomas, and common duct polyps were higher in hamsters fed commercial diet; this indicates an earlier onset of these BOP-induced lesions in hamsters fed this diet. However, their overall incidences were generally similar when the two diet groups were compared. Acinar cell nodules were observed only in hamsters fed semipurified diets and were elevated in BOP-treated females. The onset of pancreatic ductular proliferation and adenomas, bile duct proliferation, parathyroid hyperplasia, and common duct papillary hyperplasia was earlier in females than in male hamsters, especially in groups fed commercial ration. Generalized vascular calcification was observed at an elevated rate and reached a higher overall incidence in hamsters fed commercial ration. The age-adjusted rate of amyloidosis was high in female hamsters and elevated in groups that consumed the commercial ration. In addition, colitis and islet cell hyperplasia occurred more often and earlier in hamsters fed commercial ration, but gallbladder stones occurred most in animals fed semipurified diet. This paper discusses the possible association between these and other observed lesions and survival.

Adenoma↗
PubMedDate not supplied

Decreased longevity and enhancement of age-dependent lesions in mice lacking the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha).

The nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha) is activated by peroxisome proliferators (PP), a large class of structurally diverse xenobiotic chemicals, hypolipidemic drugs, and endogenous lipids. PPARalpha alters the transcriptional programs of genes whose functions include lipid metabolism, inflammation, cell fate, and stress responses in liver, heart, kidney, and skin. Many of these genes are also under control of PPARalpha in the absence of exogenous peroxisome proliferator exposure. Mice that lack PPARalpha (PPARalpha-null mice) exhibit a number of defects in lipid metabolism and accumulate lipids in the liver. Here, we compared the age-dependent lesions in the liver, kidney, and heart in PPARalpha-null mice with those observed in wild-type SV129 mice, in the absence of exogenous chemical exposure. Groups of mice were sacrificed, at 6, 12, 18, 21, or 24 months of age, or allowed to age until moribund or found dead. PPARalpha-null mice had decreased longevity, due to a variety of causes. Statistically significant differences in the occurrence of a number of lesions between strains was observed. Hepatocellular carcinomas and multiple hepatocellular adenomas occurred in PPARa-null mice but not wild type mice. Various nonneoplastic spontaneous aging lesions occurred at higher incidence, shorter latency, or increased severity in PPARalpha-null mice compared with wild-type mice. In the liver, these included vacuolated hepatocytes and sinusoidal cells and mixed cell inflammation. The kidneys of PPARalpha-null mice exhibited higher incidences and severities of cortical mineralization. Minimal myocardial mineralization occurred at a higher incidence in PPARalpha-null mice. Our results imply that PPARalpha delays the development of some spontaneous lesions associated with aging in the liver, kidney, and heart of SV129 mice.

Adenoma, Liver Cell↗
PubMed2004

Parental longevity and prognosis in elderly patients with aggressive non-Hodgkin's lymphoma.

In general, elderly patients with aggressive non-Hodgkin's lymphoma (NHL) have a less favourable prognosis than younger patients. Established predictors of prognosis in NHL are less discriminatory in the elderly, which is why there is a need for additional markers giving guidance on treatment decisions and prediction of outcome. The expected length of life of an individual in the general population is intimately associated with that of his/her parents. The aim of this study was to test the hypothesis that parental longevity is associated with improved outcome also among elderly patients with aggressive NHL and thus serves as an easily accessible non-disease associated prognostic factor. A total of 220 patients ( > 60 years) with aggressive NHL with a median age of 71 years (range 60-86) were included. Patients were randomized to receive CHOP or CNOP (doxorubicin replaced with mitoxantrone) chemotherapy with or without the addition of granulocyte colony-stimulating factor. The median follow-up time was 56 (19-89) months. Parental data regarding age at death were available through parish offices for 425 (97%) parents. Relative risk (RR) of death (disease-specific and all-cause) associated with parental lifespan was assessed using Cox proportional hazards regression analyses, with adjustment for sex, age, prognostic index, symptoms, and calendar period of diagnosis. Maternal lifespan below (versus above) median was associated with a borderline significant reduced disease-specific (adjusted RR of death from NHL = 1.5; 95% confidence interval 1.0-2.1) and overall survival. The effect of maternal lifespan was somewhat more pronounced in patients receiving CHOP than CNOP treatment. Paternal lifespan below the median was associated with a borderline significant increased disease-specific (adjusted RR of death from NHL = 0.8 [0.5-1.0]) and overall survival. Combined, maternal, and paternal lifespan had little impact on survival. These effects were true also when CHOP and CNOP treated patients were analysed separately. Maternal and paternal lifespan may predict survival in NHL, but with opposing effects. At present parental age appears not to be a clinically useful predictor of prognosis in the elderly with aggressive NHL.

Aged↗
PubMedDate not supplied

Parental effects on offspring longevity--evidence from 17th to 19th century reproductive histories.

BACKGROUND: Family studies provide support for a modest genetic influence on offspring life span, although the magnitude of these correlations is small. AIM: The study aimed to clarify the relative contributions of parental age at birth and overall parental longevity on offspring lifespan, and to identify the biological and cultural mechanisms. SUBJECTS AND METHODS: Information was derived from two village genealogies (1650-1927) encompassing 9979 births (5315 males, 4664 females). Data selection was guided by the inclusion of information about parental age at birth and lifespan, offspring lifespan and cohort-specific life expectancy. RESULTS: Parental age at reproduction displayed a negative association with offspring survivability, which was caused by a host of biological as well as environmental factors. In contrast, parental lifespan was positively associated with offspring age at death. These effects differed by parent's and child's sex. CONCLUSION: The maternal age effect on female progeny is thought to be indicative of a preferential genetic load. From an evolutionary point of view, direct selection for maternal lifespan may be an adaptive strategy to enhance child survival prospects.

Cohort Studies↗
PubMedDate not supplied

Familial transmission of longevity.

The Tau model of phenotypic transmission has been used to analyze the familial correlations (nuclear families and extended families) of longevity at Arthez d'Asson (individuals born between 1686 and 1899). At birth, the transmissibility (t2) is very weak: 0.103; at 20 years old, t2 = 0.167; at 50 years old, t2 = 0.294. The effect of sibling environment on children's phenotype is s = 0.086 at birth, is thus null. A cohabitional effect between spouses: p = 0.167 appears after 50 years. There is no social homogamy effect via grandparents.

Adult↗
PubMed1984

Variation in longevity of rats: evidence for a systematic increase in lifespan over time.

Male-Sprague-Dawley rats (CrL:CD(SD)BR) were maintained under barrier conditions at Charles River Breeding Laboratories (Wilmington MA) from August, 1975, to July, 1983. Animals were provided food and water ad libitum. Survival data from 8 completed cohorts of 100 animals each and one continuing cohort reveal a highly significant linear increase in median lifespan, yielding a 26% increase in this parameter for cohorts born over a period of less than six years. The biological factors responsible for this increase are not clear at present. Nevertheless, these results in outbred rats, taken in conjunction with previous observations of a trend towards increased longevity in inbred mice, indicate that the assumption of cohort equivalence underlying many cross-sectional studies of biological aging may not be valid.

Aging↗
PubMed1997

Increased longevity of kinetin-fed Zaprionus fruitflies is accompanied by their reduced fecundity and enhanced catalase activity.

Kinetin, a cytokinin plant growth hormone, retards senescence in plants, delays aging in human cells in culture, slows down development of insects and prolongs their lifespan. We have now observed that the increased longevity of Kn-fed Zaprionus fruitflies was accompanied by an increase in the specific activity of catalase during developmental stages and in adult insects. In addition, the egg laying capacity of Kn-fed fruitflies was reduced drastically as compared with those kept on a normal diet. These results support the view that improved maintenance of the soma and prolongation of its life is achieved at the cost of decreased reproductive activity.

Aging↗
PubMed2004

Habitat size, recruitment, and longevity as factors limiting population size in stage-structured species.

Surprisingly little research has evaluated how habitat size may limit the population size of species that use different habitats at different stages of their lives. Here we develop simple discrete-time models to describe the population dynamics of species that use separate juvenile and adult habitats. Analytic solutions, model simulations, and elasticity and sensitivity analyses show that adult abundance is only limited by the size of the juvenile habitat when both adult habitat size and recruitment are much larger than juvenile habitat size. Juvenile habitat plays a marginally greater role in limiting population size for species with closed populations, where recruitment is proportional to adult abundance, versus open populations. Because adult populations often accumulate pulses of juveniles, adult habitat size can strongly limit population size over a broad range of parameter values, an effect that increases as the longevity of a species increases. Limited empirical research from a range of taxa supports these model predictions, although few studies were designed to actually test the limiting role of juvenile versus adult habitat. Future research must carefully evaluate whether and how processes at the juvenile stage affect adult abundance, and conservation efforts may be able to use this model to evaluate the cost-effectiveness, vis-a-vis increasing adult abundance, of time and money allocated to protecting juvenile habitats.

Animals↗
PubMed2004

Redox regulation in neurodegeneration and longevity: role of the heme oxygenase and HSP70 systems in brain stress tolerance.

Efficient functioning of maintenance and repair processes seems to be crucial for both survival and physical quality of life. This is accomplished by a complex network of the so-called longevity assurance processes, which are composed of several genes termed "vitagenes," among these, the heat shock system, a highly conserved mechanism responsible for the preservation and repair of cellular macromolecules, such as proteins, RNAs, and DNA. Recent studies have shown that the heat shock response contributes to establishing a cytoprotective state in a wide variety of human diseases, including ischemia and reperfusion damage, inflammation, cancer, as well as metabolic and neurodegenerative disorders. Recently, the involvement of the heme oxygenase (HO) pathway in antidegenerative mechanisms has received considerable attention, as it has been demonstrated that the expression of HO is closely related to that of amyloid precursor protein. HO induction occurs together with the induction of other heat shock proteins during various physiopathological conditions. The vasoactive molecule carbon monoxide and the potent antioxidant bilirubin, products of HO-catalyzed reaction, represent a protective system potentially active against brain oxidative injury. Given the broad cytoprotective properties of the heat shock response, molecules inducing this defense mechanism appear to be possible candidates for novel cytoprotective strategies. Particularly, manipulation of endogenous cellular defense mechanisms, via the heat shock response, through nutritional antioxidants or pharmacological compounds, may represent an innovative approach to therapeutic intervention in diseases causing tissue damage, such as neurodegeneration. Consistently, by maintaining or recovering the activity of vitagenes, it is feasible to delay the aging process and decrease the occurrence of age-related diseases with resulting prolongation of a healthy life span.

Aging↗
PubMed2005

Oxidative stress and aging: catalase is a longevity determinant enzyme.

Schriner and colleagues have reported an important advance in our understanding of the mechanisms controlling lifespan in mammalian species. A transgenic mouse strain was constructed (MCAT) with a C57BL/6J background that has about a 50-fold increase in expression in cardiac mitochondria and skeletal muscle of catalase enzyme activity. The MCAT strain was found to have reduced severity of age-dependent arteriosclerosis and increased genomic stability, as indicated by a decrease in oxidative stress and mitochondrial deletions in heart and muscle tissues. Most exciting, however, is that both median and maximum lifespan were increased about 17-21% compared to wild-type controls. It was disappointing that the Gompertz plot of the MCAT strain ran parallel to the wild-type control, indicating a delay in the onset of aging rather than a decrease in aging rate. Nevertheless, these results support the notion of a role for mitochondrial oxidative stress as a determinant of both healthspan and lifespan. In addition, the relatively large increase in lifespan resulting from upregulation of a single gene suggests the possibility that similar upregulation of relatively few key longevity determinant genes may result in dramatic increases in lifespan.

Aging↗
PubMed2000

Deficiency mapping of quantitative trait loci affecting longevity in Drosophila melanogaster.

In a previous study, sex-specific quantitative trait loci (QTL) affecting adult longevity were mapped by linkage to polymorphic roo transposable element markers, in a population of recombinant inbred lines derived from the Oregon and 2b strains of Drosophila melanogaster. Two life span QTL were each located on chromosomes 2 and 3, within sections 33E-46C and 65D-85F on the cytological map, respectively. We used quantitative deficiency complementation mapping to further resolve the locations of life span QTL within these regions. The Oregon and 2b strains were each crossed to 47 deficiencies spanning cytological regions 32F-44E and 64C-76B, and quantitative failure of the QTL alleles to complement the deficiencies was assessed. We initially detected a minimum of five and four QTL in the chromosome 2 and 3 regions, respectively, illustrating that multiple linked factors contribute to each QTL detected by recombination mapping. The QTL locations inferred from deficiency mapping did not generally correspond to those of candidate genes affecting oxidative and thermal stress or glucose metabolism. The chromosome 2 QTL in the 35B-E region was further resolved to a minimum of three tightly linked QTL, containing six genetically defined loci, 24 genes, and predicted genes that are positional candidates corresponding to life span QTL. This region was also associated with quantitative variation in life span in a sample of 10 genotypes collected from nature. Quantitative deficiency complementation is an efficient method for fine-scale QTL mapping in Drosophila and can be further improved by controlling the background genotype of the strains to be tested.

Animals↗
PubMed2003

Positive selection of Caenorhabditis elegans mutants with increased stress resistance and longevity.

We developed selective conditions for long-lived mutants of the nematode Caenorhabditis elegans by subjecting the first larval stage (L1) to thermal stress at 30 degrees for 7 days. The surviving larvae developed to fertile adults after the temperature was shifted to 15 degrees. A total of one million F(2) progeny and a half million F(3) progeny of ethyl-methanesulfonate-mutagenized animals were treated in three separate experiments. Among the 81 putative mutants that recovered and matured to the reproductive adult, 63 retested as thermotolerant and 49 (80%) exhibited a >15% increase in mean life span. All the known classes of dauer formation (Daf) mutant that affect longevity were found, including six new alleles of daf-2, and a unique temperature-sensitive, dauer-constitutive allele of age-1. Alleles of dyf-2 and unc-13 were isolated, and mutants of unc-18, a gene that interacts with unc-13, were also found to be long lived. Thirteen additional mutations define at least four new genes.

Animals↗
PubMed1996

Selection for longevity favors stringent metabolic control in Drosophila melanogaster.

Models of the evolution of life span predict, and gerontological studies show, a relation between nutrient use and life span. This study examines the role and comparative use of nutrients in long- and short-lived populations of D. melanogaster selectively bred for age-at-reproduction, without respect to metabolism or feeding rate. We test the hypotheses that selection for life span has favored the restriction of nutrient use and that the observed effect of low population density during development is a consequence of modifying nutrient use. The use of nutrients was measured here by the uptake of radiolabeled glucose, its incorporation into lipid and protein, and by the in vivo metabolic flux through the pentose shunt. Measurements show that uptake, incorporation, and flux are severely limited in long-lived stocks, compared to short-lived populations of the same stage and stage of development. Raising long-lived stocks at low population numbers relieves the restriction on metabolism in larvae, increasing incorporation and flux, and causes adult life span to decline. Larvae of long-lived populations appear to feed less actively, suggesting that the reduction in use of nutrients could simply be from reduced intake. Changes in total soluble protein correspond with measurements of uptake, incorporation, and flux. Soluble protein is substantially less in long-lived stocks, before pupation, but catches up in early adulthood to that in the short-lived populations. Despite different nutrient use by larval populations, only slight differences are found in development rate. They are insufficient to account for the differences observed in longevity.

Age Factors↗
PubMed1997

Heat-induced longevity extension in Drosophila. I. Heat treatment, mortality, and thermotolerance.

Survival data were collected on a total of 28,000 Drosophila melanogaster adults in order to investigate mortality patterns and induced physiological responses after a mild thermal stress. A brief, nonlethal heat treatment extends adult life span at normal temperatures by an average of 2 days (64), compared to nontreated controls of the same genotypes. Life expectancy is extended as a demographic consequence of reduced age-specific mortality over a period of up to several weeks after the heat treatment. Heat treatment also increases tolerance to subsequent, more severe thermal stress. Observations on single-sex populations suggest that heat-induced longevity extension is independent of the suppression of reproductive activity.

Acclimatization↗