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At least 865 records · Page 48Linked to original sources
PubMed1982

Granulopoiesis longevity in continuous bone marrow cultures and factor-dependent cell line generation: significant variation among 28 inbred mouse strains and outbred stocks.

Longevity of granulopoiesis in corticosteroid-supplemented continuous bone marrow cultures and generation of permanent WEHI-3 dialyzed conditioned medium (DCM)-dependent hematopoietic progenitor cell lines were evaluated for 28 inbred mouse strains and outbred stocks. Cultures from AKR/J, NZW, C58/J, DBA/2J, and C57BL/KsJ mice generated granulocytes for 45-58 weeks and released more than 10(5) murine sarcoma virus (MuSV) rescue units of endogenous retrovirus; nonadherent (NA) cells from 50% or more cultures produced permanent WEHI-3 DCM-dependent cell lines. Cultures from 129/J, BALB/cJ, SJL/J, RF/J, CD-1 Swiss, C57BR/cdJ, C57BL/Ka, CBA/J, RFM/Sn, NZB, C3H/HeJ, NIH Swiss [N:NIH(S)], C57BL/10J, C57L/J, SWR/J, HRS/J, and C57BL/6J mice generated granulocytes for 12-38 weeks; some released 10(1)-10(2) MuSV rescue units of retrovirus, and NA cells from less than 50% of cultures from all but SWR/J and C57L/J mice produced WEHI-3 DCM-dependent cell lines. Thus longevity of granulopoiesis in mouse continuous bone marrow cultures varies significantly among strains.

Animals↗
PubMed1994

Liposomal vincristine which exhibits increased drug retention and increased circulation longevity cures mice bearing P388 tumors.

Prolonged exposure to vincristine correlates with improved therapeutic activity. In this work, two methods are used to increase the circulation longevity of liposomal formulations of vincristine. The first involves incorporation of the ganglioside GM1, which acts to increase the circulation longevity of liposomal carriers, while the second approach relies on a modification of the vincristine encapsulation procedure which enhances drug retention. It is shown that these approaches are synergistic and increase the circulation half-life of vincristine from approximately 1 h to greater than 12 h. This results in a dramatic improvement in the therapeutic activity of liposomal vincristine as measured using a murine P388 lymphocytic leukemia model. At doses above 2 mg/kg, the optimized liposomal vincristine formulation cures greater than 50% of mice bearing the P388 tumor, whereas free vincristine results in no cures.

Animals↗
PubMed1993

[Studies on longevity tea].

This paper reports the preparation, physical and chemical identification and content determination of Longevity Tea. The preparation process is advanced, the content determination is simple and accurate and thus can be taken as standards for the quality control of Longevity Tea.

Drugs, Chinese Herbal↗
PubMed1993

Development and longevity of Nosopsyllus laeviceps kuzenkovi (Siphonaptera) from Inner Mongolia under laboratory conditions.

The development and longevity of Nosopsyllus laeviceps kuzenkovi (Yagubyants), a major plague vector among sylvan and campestral rodents in Inner Mongolia, China, was studied under controlled laboratory conditions of 11, 14, 17, 20, 23, 26, 29, and 35 C at 76% relative humidity (R.H.), and 32, 53, 76, 87, and 100% at 23 C. Development from egg to adult was shortest (21-23 days) under favorable conditions of 26 C at 76% R.H., but maximum survival to adulthood (84%) occurred at 23 C. Average longevity was 13.25 days (13.70 in females and 12.80 in males) at 17 C and 76% R.H.; it was longer at cooler and shorter at warmer temperatures. Findings provided experimental data that helped clarify seasonal fluctuations, summer mortality, generation cycles, and survival of compared flea species from Russia, Azerbaidzhan, and China.

Animals↗
PubMed2000

Estimation of apolipoprotein E genotype-specific relative mortality risks from the distribution of genotypes in centenarians and middle-aged men: apolipoprotein E gene is a "frailty gene," not a "longevity gene".

We developed a method to estimate genotype-specific average relative mortality risk, R, from genotype distributions in cross-sectional studies of people belonging to different age-groups, and applied the method to new data from a study of apolipoprotein E genotypes (apoE) in 177 Danish centenarians and data from a study of 40-year-old Danish men. Twenty-one percent of the centenarians were epsilon 2-carriers (genotypes epsilon 2 epsilon 2 and epsilon 3 epsilon 2) and 15% were epsilon 4-carriers (genotypes epsilon 4 epsilon 4 and epsilon 4 epsilon 3) compared to 13 and 29%, respectively, of the young men. The R-values were 0.95 (95% CI 0.88 to 1.02) for epsilon 2-carriers and 1.13 (95% CI 1.05 to 1.22) for epsilon 4-carriers, using epsilon 3 epsilon 3- and epsilon 4 epsilon 2 genotypes as reference. Corresponding values for epsilon 4-carriers were obtained by using published data from a French and a Finnish study of centenarians, whereas the values for epsilon 2-carriers were about 0.90 with these data. The method to estimate mortality risk and the results associate with the view that the apoE gene is a "frailty gene." On the other hand, if odds ratios are used to summarize data from studies of this kind, they are more impressive and may propagate the misconception that apoE is a "longevity gene".

Adult↗
PubMed2001

A gender--dependent genetic predisposition to produce high levels of IL-6 is detrimental for longevity.

Current literature indicates that elevated IL-6 serum levels are associated with diseases, disability and mortality in the elderly. In this paper, we studied the IL-6 promoter genetic variability at -174 C/G locus and its effect on IL-6 serum levels in a total of 700 people from 60 to 110 years of age, including 323 centenarians. We found that the proportion of homozygotes for the G allele at -174 locus decreases in centenarian males, but not in centenarian females. Moreover, we found that, only among males, homozygotes for the G allele at -174 locus have higher IL-6 serum levels in comparison with carriers of the C allele. On the whole, our data suggest that those individuals who are genetically predisposed to produce high levels of IL-6 during aging, i.e. -174 locus GG homozygous men, are disadvantaged for longevity.

Aged↗
PubMed1994

Changes in longevity and causes of death among persons with hemophilia A.

To examine recent changes in longevity and the causes of death among persons with hemophilia A, we evaluated death certificate data for persons who died in the United States from 1968 through 1989 and had hemophilia A or congenital Factor VIII disorder (ICD code 286.0) listed on the death certificate as one of the multiple causes of death. Multiple-cause-of-death mortality data for the United States from 1968 to 1989 were examined to compare death rates by year, focusing on death rates and causes of death for 1979-1981, 1983-1985, and 1987-1989. Gender, age group, race, geographic region, and median age at death of persons with hemophilia A and human immunodeficiency virus (HIV)-related disease listed as a cause of death were compared with those with hemophilia A without HIV-related disease. From 1968 through 1989, 2,792 hemophilia A deaths were reported. The death rate increased from 0.5 to 1.3 per 1,000,000 persons. From 1979-1981 through 1987-1989, mortality increased in all age groups above 9 years of age and age at death shifted markedly to lower ages. Median age at death decreased from 57 years in 1979-1981 to 40 years in 1987-1989. The percentage of deaths due to hemorrhage or diseases of the circulatory system decreased markedly as the result of the increase in deaths associated with HIV infection or infections other than HIV infection. Spread of HIV-1 infection in persons with hemophilia A has disrupted the reduction in mortality seen with factor replacement therapy, implementation of home care, and use of comprehensive hemophilia treatment centers. It is hoped that advances in the care of HIV-infected persons will improve survival in the hemophilia community.

Adolescent↗
PubMed1978

The familial component in longevity--a study of offspring of nonagenarians: III. Intrafamilial studies.

The effect of parental longevity on the length of survival of offspring has been examined according to selected demographic and environmental characteristics. The present study is based on 7,103 progeny, 20 years old or older. They were the sons and daughters of 1,766 men or women, 90 or more years old, who were alive in 1922-1930 at the time of ascertainment. The age at death of the other parent of the offspring is the basis of classification used in this analysis. A positive relationship was found between age at death of the non-proband parent and the age at death of the offspring. This relationship existed regardless of similarities or differences in the characteristics analyzed.

Adult↗
PubMed1990

Longevity factor in hominoid social organization.

In most primate groups emigration of the maturing young of one or the other sex tends to serve as an incest avoidance mechanism. Among most primate species it is the males who change groups. This supports the theory that, in terms of reproductive success, males should compete for mates and females should compete for resources. In hominoids the combination of increased longevity and greater female discrimination in mate selection seems responsible for female emigration. This may relate to the high frequency of patrilocality and male control of resources among human groups.

Animals↗
PubMed1997

Assessment of the longevity of the liver using a rat transplant model.

To assess the longevity of the liver, arterialized, orthotopic liver grafts were performed using syngeneic male BN/BiRij rats. Young (5-month-old) livers were transplanted into 5-month-old recipients (group I, n = 27), and old (28-month-old) livers were transplanted into 5-month-old rats (group II, n = 28). Recipient survival after transplantation was similar in both groups. The average age of the livers at the time of death was 16.7 months in group I and 39.1 months in group II. Four of the livers in group II survived for more than 4 years (48.1 to 52.4 months). Early deaths (less than 1 year) after transplantation were most commonly caused by biliary obstruction and cholangitis in both groups. Late deaths (more than 1 year) after grafting were mainly from heart failure or tumors. None of the animals died of liver failure or liver disease. Weight gain in the rats, total serum protein levels, and alanine transaminase levels after transplantation did not differ significantly between the two groups. There was a trend for the histological features of aging of the liver-fibrosis, bile duct proliferation, and pigment deposition-to become more prevalent as the livers became very old (mean age, 46 months). Nevertheless, typical aging changes, as individual findings, were absent in nearly half of the oldest organs. The alterations in morphology had no apparent effect on the ability of the livers to sustain the lives of the recipients. The liver of the BN/BiRij rat was capable of surviving far beyond the maximum life span of BN/BiRij rats, and rats in general. It did not become diseased in the process.

Age Factors↗
PubMed2001

Mouse coq7/clk-1 orthologue rescued slowed rhythmic behavior and extended life span of clk-1 longevity mutant in Caenorhabditis elegans.

The coq7/clk-1 gene was isolated from the long-lived mutant of Caenorhabditis elegans and was suggested to play a regulatory role in biological rhythm and longevity. The mouse COQ7 is homologous to Saccharomyces cerevisiae COQ7/CAT5 that is required for the biosynthesis of coenzyme Q (ubiquinone), an essential messenger in mitochondrial respiration. In the present study, we characterized the expression and processing of mouse COQ7. We found that COQ7 is highly expressed in tissues with high energy demand such as heart, muscle, liver, and kidney in mice. Biochemical analysis revealed that COQ7 is targeted to mitochondria where it is processed to mature form. Transgenic expression of mouse coq7 completely rescued the slowed rhythmic behaviors of clk-1 such as defecation. In life-span analysis, transgenic expression reverted the extended life span of clk-1 to the comparable level with wild-type control. These data strongly suggested that coq7 plays a pivotal role in the regulation of biological rhythms and the determination of life span in mammalian species.

Amino Acid Sequence↗
PubMed2000

Model assessments of the optimal design of nature reserves for maximizing species longevity.

Using a computational model for the population growth and dispersal of a model species in a fluctuating environment, we test three nature reserve geometries (one large, many small, and a self-similar distribution of reserve sizes) to determine which geometry maximizes species longevity. The self-similar distribution is a close approximation to the distribution of managed areas in the conterminous United States. We consider models with and without migration from or between reserve fragments and both short- and long-range dispersal mechanisms. The optimal geometry depends on the type of dispersal and on the relative probability of survival in protected and non-protected areas. When no migration is allowed from or between reserve fragments of the three geometries, many small equally sized reserves are the optimal geometry. When migration is allowed, the optimal geometry is a single large reserve when the survivability in non-protected areas is low and a self-similar distribution when the survivability is high.

Animal Population Groups↗
PubMed2001

The reliability theory of aging and longevity.

Reliability theory is a general theory about systems failure. It allows researchers to predict the age-related failure kinetics for a system of given architecture (reliability structure) and given reliability of its components. Reliability theory predicts that even those systems that are entirely composed of non-aging elements (with a constant failure rate) will nevertheless deteriorate (fail more often) with age, if these systems are redundant in irreplaceable elements. Aging, therefore, is a direct consequence of systems redundancy. Reliability theory also predicts the late-life mortality deceleration with subsequent leveling-off, as well as the late-life mortality plateaus, as an inevitable consequence of redundancy exhaustion at extreme old ages. The theory explains why mortality rates increase exponentially with age (the Gompertz law) in many species, by taking into account the initial flaws (defects) in newly formed systems. It also explains why organisms "prefer" to die according to the Gompertz law, while technical devices usually fail according to the Weibull (power) law. Theoretical conditions are specified when organisms die according to the Weibull law: organisms should be relatively free of initial flaws and defects. The theory makes it possible to find a general failure law applicable to all adult and extreme old ages, where the Gompertz and the Weibull laws are just special cases of this more general failure law. The theory explains why relative differences in mortality rates of compared populations (within a given species) vanish with age, and mortality convergence is observed due to the exhaustion of initial differences in redundancy levels. Overall, reliability theory has an amazing predictive and explanatory power with a few, very general and realistic assumptions. Therefore, reliability theory seems to be a promising approach for developing a comprehensive theory of aging and longevity integrating mathematical methods with specific biological knowledge.

Adult↗
PubMed1987

Longevity in the protozoa.

In ciliates there are examples of cells which have different proliferation potential in the macronucleus. Those species with limited macronuclear proliferation potential require sex to activate the reserve nucleus. In terms of the capital investment theory, some ciliates invested in their spare nucleus without loss of their original potential, while others accumulated debts and needed the reserve account to maintain life. Other cells neglected maintenance of their reserve account and failed unless their venture capital account was not a self-sustaining venture. Sex provided access to the reserve account and had to occur before deterioration of the reserve account. The question is not when cellular immortality was lost, but rather when immortality was partitioned from a mortal segment. The separation provided the option both for senescence and evolution in multicellular organisms. In colonial flagellates, separation of cells with infinite and finite cell lifespan potential occurred in some species, while in others the separation did not involve loss of immortality. In colonial flagellates, sex did not become an obligate stage. The immortal cells are haploid and could not accumulate damage and live (in contrast with the diploids in the ciliated protozoans). The present theory predicts that differences between species or cells with infinite versus finite lifespan potential may reveal differences in the critical determinants of longevity. Senescence could arise as an accident, as well as a design of nuclear differentiation. Cells therefore may have a much greater reserve for totipotency than would be predicted if they were assumed to lose immortality simply by the act of differentiation.

Aging↗
PubMed1994

Evidence for a life span-prolonging effect of a linear plasmid in a longevity mutant of Podospora anserina.

The linear mitochondrial plasmid pAL2-1 of the long-lived mutant AL2 of Podospora anserina was demonstrated to be able to integrate into the high molecular weight mitochondrial DNA (mtDNA). Hybridization analysis and densitometric evaluation of the mitochondrial genome isolated from cultures of different ages revealed that the mtDNA is highly stable during the whole life span of the mutant. In addition, and in sharp contrast to the situation in certain senescence-prone Neurospora strains, the mutated P. anserina mtDNA molecules containing integrated plasmid copies are not suppressive to wild-type genomes. As demonstrated by hybridization and polymerase chain reaction (PCR) analysis, the proportion of mtDNA molecules affected by the integration of pAL2-1 fluctuates between 10% and 50%. Comparative sequence analysis of free and integrated plasmid copies revealed four differences within the terminal inverted repeats (TIRs). These point mutations are not caused by the integration event since they occur subsequent to integration and at various ages. Interestingly, both repeats contain identical sequences indicating that the mechanism involved in the maintenance of perfect TIRs is active on both free and integrated plasmid copies. Finally, in reciprocal crosses between AL2 and the wild-type strain A, some abnormal progeny were obtained. One group of strains did not contain detectable amounts of plasmid pAL2-1, although the mtDNA was clearly of the type found in the long-lived mutant AL2. These strains exhibited a short-lived phenotype. In contrast, one strain was selected that was found to contain wild-type A-specific mitochondrial genomes and traces of pAL2-1. This strain was characterized by an increased life span. Altogether these data suggest that the linear plasmid pAL2-1 is involved in the expression of longevity in mutant AL2.

Base Sequence↗
PubMed1981

Evolution and longevity-assurance processes.

The role of the development of information fidelity systems in evolution is explored, with evidence that the loss in the ability to maintain the integrity of homeostasis in organisms over time, aging, is correlated with the loss in the ability to maintain integrity at the molecular biological level. Evolutionary-comparative analysis places an upper limit on the number of these systems important to the evolution of longevity in the primates, and suggests the importance of insuring the stability of information bearing macromolecules in evolution and the role of modulators of damage to these moieties in the expression of the senescent state.

Aging↗
PubMed1993

Genetic and environmental factors regulating the expression of an extended longevity phenotype in a long lived strain of Drosophila.

We have demonstrated that the expression of the ELP in our strains is the outcome of a genetically determined, environmentally modulated, event dependent, developmental process. Given the appropriate genetic and environmental conditions, we observe an early acting temporal progression of alterations in specific gene activity patterns which appear to give rise to functional phenotypic changes. The observed patterns are consistent with the interpretations drawn from our chromosome substitution and biomarker experiments. The interaction of specific environmental and genetic factors is sufficient to explain the observed plasticity of longevity in our L strain. Independently derived long lived strains may have altered different combinations of physiological mechanisms so as to give rise to a statistically equivalent ELP. Theoretically based conclusions obtained from only one set of sister strains may be difficult to extrapolate to other strains. Future work will involve the experimental verification of the genetic-environmental circuitry discussed here, using novel molecular genetic techniques to define, characterize, and isolate the genes involved in the expression of the ELP.

Animals↗
PubMed1991

Elevated high-density-lipoprotein cholesterol and normal triglycerides as markers of longevity.

Serum cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides of 85 year old home-living persons were compared to those of controls and of patients who had severe coronary artery disease (CAD) at an early age. Eighty-five-year-olds had higher serum HDL cholesterol than controls and patients with CAD. Patients with severe CAD had higher serum total cholesterol and serum triglycerides and lower HDL-cholesterol than other groups. When 85-year-old persons were divided into quintiles according to serum HDL cholesterol, women with highest HDL cholesterol had lowest mortality, men with lowest HDL cholesterol had highest mortality. We conclude that elevated HDL cholesterol is correlating with longevity and low HDL cholesterol with CAD at an early age.

Aged↗