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Results for “aging clock”

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At least 235 records · Page 13Linked to original sources
PubMed2003

The radiation of the Cape flora, southern Africa.

The flora of the south-western tip of southern Africa, the Cape flora, with some 9000 species in an area of 90,000 km2 is much more speciose than can be expected from its area or latitude, and is comparable to that expected from the most diverse equatorial areas. The endemism of almost 70%, on the other hand, is comparable to that found on islands. This high endemism is accounted for by the ecological and geographical isolation of the Cape Floristic Region, but explanations for the high species richness are not so easily found. The high species richness is accentuated when its taxonomic distribution is investigated: almost half of the total species richness of the area is accounted for by 33 'Cape floral clades'. These are clades which may have initially diversified in the region, and of which at least half the species are still found in the Cape Floristic Region. Such a high contribution by a very small number of clades is typical of island floras, not of mainland floras. The start of the radiation of these clades has been dated by molecular clock techniques to between 18 million years ago (Mya) (Pelargonium) and 8 Mya (Phylica), but only six radiations have been dated to date. The fossil evidence for the dating of the radiation is shown to be largely speculative. The Cenozoic environmental history of southern Africa is reviewed in search of possible triggers for the radiations, climatic changes emerge as the most likely candidate. Due to a very poor fossil record, the climatic history has to be inferred from larger scale patterns, these suggest large-scale fluctuations between summer wet (Palaeocene, Early Miocene) and summer dry climates (Oligocene, Middle Miocene to present). The massive speciation in the Cape flora might be accounted for by the diverse limitations to gene flow (dissected landscapes, pollinator specialisation, long flowering times allowing much phenological specialisation), as well as a richly complex environment providing a diversity of selective forces (geographically variable climate, much altitude variation, different soil types, rocky terrain providing many micro-niches, and regular fires providing both intermediate disturbances, as well as different ways of surviving the fires). However, much of this is based on correlation, and there is a great need for (a) experimental testing of the proposed speciation mechanisms, (b) more molecular clock estimates of the age and pattern of the radiations, and (c) more fossil evidence bearing on the past climates.

Africa, Southern↗
PubMed1994

Mitochondrial DNA sequence variation in human evolution and disease.

Germ-line and somatic mtDNA mutations are hypothesized to act together to shape our history and our health. Germ-line mtDNA mutations, both ancient and recent, have been associated with a variety of degenerative diseases. Mildly to moderately deleterious germ-line mutations, like neutral polymorphisms, have become established in the distant past through genetic drift but now may predispose certain individuals to late-onset degenerative diseases. As an example, a homoplasmic, Caucasian, tRNA(Gln) mutation at nucleotide pair (np) 4336 has been observed in 5% of Alzheimer disease and Parkinson disease patients and may contribute to the multifactorial etiology of these diseases. Moderately to severely deleterious germ-line mutations, on the other hand, appear repeatedly but are eliminated by selection. Hence, all extant mutations of this class are recent and associated with more devastating diseases of young adults and children. Representative of these mutations is a heteroplasmic mutation in MTND6 at np 14459 whose clinical presentations range from adult-onset blindness to pediatric dystonia and basal ganglial degeneration. To the inherited mutations are added somatic mtDNA mutations which accumulate in random arrays within stable tissues. These mutations provide a molecular clock that measures our age and may cause a progressive decline in tissue energy output that could precipitate the onset of degenerative diseases in individuals harboring inherited deleterious mutations.

Amino Acid Sequence↗
PubMed1972

Work and age.

Explore the source record for details and available documents.

Aged↗
PubMed2005

Proceedings of the SMBE Tri-National Young Investigators' Workshop 2005. Southern hemisphere springtails: could any have survived glaciation of Antarctica?

Throughout the Southern Hemisphere many terrestrial taxa have circum-Antarctic distributions. This pattern is generally attributed to ongoing dispersal (by wind, water, or migrating birds) or relict Gondwanan distributions. Few of these terrestrial taxa have extant representatives in Antarctica, but such taxa would contribute to our understanding of the evolutionary origins of the continental Antarctic fauna. Either these taxa have survived the harsh climate cooling in Antarctica over the last 23 Myr (Gondwanan/vicariance origin) or they have dispersed there more recently (<2 MYA). In this context, we examined mtDNA (COI) sequence variation in Cryptopygus and related extant Antarctic and subantarctic terrestrial springtails (Collembola). Sequence divergence was estimated under a maximum likelihood model (general time reversible+I+Gamma) between individuals from subantarctic islands, Australia, New Zealand, Patagonia, Antarctic Peninsula, and continental Antarctica. Recent dispersal/colonization (<2 MYA) of Cryptopygus species was inferred between some subantarctic islands, and there was a close association between estimated times of divergences based on a molecular clock and proposed geological ages of islands. Most lineages generally grouped according to geographic proximity or by inferred dispersal/colonization pathways. In contrast, the deep divergences found for the four endemic Antarctic species indicate that they represent a continuous chain of descent dating from the break up of Gondwana to the present. We suggest that the diversification of these springtail species (21-11 MYA) in ice-free glacial refugia throughout the Trans-Antarctic Mountains was caused by the glaciation of the Antarctic continent during the middle to late Miocene.

Animals↗
PubMed1998

Neuroimmunomodulation of aging. A program in the pineal gland.

We have investigated for 35 years the relationship between the neuroendocrine and the thymo-lymphatic, immune system. In the last decade we have shown that the pineal gland is a main adapter and fine synchronizer of environmental variables and endogenous messages into physiological modifications of basic functions. In particular the pineal gland itself seems to regulate, via circadian, night secretion of melatonin, all basic hormonal functions and also immunity. We have shown with several in vivo models that this fundamental role of the pineal gland decays during aging. Aging itself seems to be a strictly pineal-programmed event similar to growth and puberty. The continuation of our interventions with melatonin against the typical degenerative diseases of aging must be based on an accurate evaluation of its mechanisms of action. Melatonin being a ubiquitous molecule in nature, we suggest that it has acquired during evolution of the species numerous levels of activities. In fact, melatonin can be found in a large variety of cells and tissues, and bindings sites and "receptors" have been identified in many tissues and cells of the neuroendocrine and immune system. Therefore, the progressive understanding of the aging-programming role of the pineal gland also depends on studies of melatonin and its basic regulatory function. Our present studies will be described.

Aging↗
PubMed1996

Breathing, sleep state, and rectal temperature oscillations.

Overheating may cause terminal apnoea and cot death. Rectal temperature and breathing patterns were examined in normal infants at home during the first 6 months of life. Twenty one infants had continuous overnight rectal temperature and breathing recordings for 429 nights (mean 20.4 nights, range 7-30) spaced over the first six months of life. Periods when breathing was 'regular' were directly marked on single night records. Sleep state was determined from respiratory variables. 'Regular' breathing was a reliable marker of 'quiet' sleep (specificity 93%). The duration of 'quiet' sleep increased from 6 to 22 minutes from two weeks to three months of age and then remained static, as did the proportion of sleep spent in the quiet phase (9% to 34%). Rectal temperature fell during 66% of quiet sleep and usually rose during rapid eye movement (REM) sleep. The drop in rectal temperature was maximal at the start of quiet sleep, whereas the maximum rise during REM sleep was reached after 10 to 15 minutes. Oscillations in rectal temperature are associated with changes in sleep and breathing state. The maturation of rectal temperature patterns during the first six months of life are closely related to a maturation of sleep state and breathing patterns.

Aging↗
PubMed1986

The development of the small intestine.

The remarkable degree of coordination between the development of various aspects of gastrointestinal function suggests that the process may be triggered by a single or a few central mechanisms, such as weaning and (or) hormones. Precocious development of enzyme and transport function can be induced by exogenous thyroxine and corticosteroids, while thyroidectomy and adrenalectomy abolish the normal pattern of postnatal development. These hormones may have a primary or a permissive role. Activation of the dormant hormonal mechanism could be controlled by a genetically coded biologic clock, such as chronologic age, or by a biological signal such as body size and oral intake. Generally speaking, shortly after birth, there are increases in the intestinal mucosal surface area, brush border membrane enzymes, and carrier-mediated transport. These adaptive changes occur as a result of the genetic endowment of the animal, but may be modified by environmental factors, particularly nutrient intake.

Aging↗
PubMed2026

Sex-specific differences in liver DNA methylation patterns and epigenetic aging in mice.

Biological sex has been shown to influence aging outcomes, contributing to distinct trajectories in disease susceptibility and lifespan. DNA methylation patterns provide a quantitative measure of biological aging. This study investigated whether aged male and female mice display distinct liver DNA methylation patterns and differences in epigenetic aging. Liver samples were collected from 17 aged c57BL/6 mice (6 males, 11 females). Genomic DNA was extracted and bisulfite-converted before targeted enrichment of 2,045 murine age-associated CpG loci. Biological age (DNAge) was estimated using a previously developed DNA methylation-based predictor generated through elastic net regression. The difference (&#x394;DNAge) between DNAge and chronological age was computed. Sex-specific differences were assessed by comparing site-specific methylation ratios, &#x394;DNAge values, and through principal component analysis (PCA) and multiple linear regression. Twelve CpG sites across six genes (Fam84b, Zswim6, Hsf4, Mn1, Qprt, and Rapgefl1) showed significant sex-associated differences in methylation. Fam84b demonstrated the largest and most consistent sex-associated effect, with all three associated CpG sites showing higher methylation in males (regression coefficients: -0.204, -0.281, and -0.294). Zswim6 exhibited consistent lower methylation ratios in females, whereas the other genes showed higher methylation in females. There were no sex differences in biological age or &#x394;DNAge (P = 0.596). Although the epigenetic clock did not reveal differences between sexes in aging, aged mice did exhibit sex-specific liver methylation patterns different from those reported in younger mice, suggesting that sex-dependent epigenetic changes may emerge later in life and may reflect sexual dimorphism in liver function with age.NEW & NOTEWORTHY Males and females are known to age differently and develop certain diseases at different rates. Here, we examined the livers of aged male and female mice to see if they show different DNA methylation patterns. We found that aged male and female mice had distinct DNA methylation patterns at specific genes. Interestingly, most of these methylation differences were not present in younger mice, suggesting that sex differences in the genome may change with age.

Animals↗
PubMed2000

Telomere length inversely correlates with pulse pressure and is highly familial.

There is evidence that telomeres, the ends of chromosomes, serve as clocks that pace cellular aging in vitro and in vivo. In industrialized nations, pulse pressure rises with age, and it might serve as a phenotype of biological aging of the vasculature. We therefore conducted a twin study to investigate the relation between telomere length in white blood cells and pulse pressure while simultaneously assessing the role of genetic factors in determining telomere length. We measured by Southern blot analysis the mean length of the terminal restriction fragments (TRF) in white blood cells of 49 twin pairs from the Danish Twin Register and assessed the relations of blood pressure parameters with TRF. TRF length showed an inverse relation with pulse pressure. Both TRF length and pulse pressure were highly familial. We conclude that telomere length, which is under genetic control, might play a role in mechanisms that regulate pulse pressure, including vascular aging.

Adolescent↗
PubMed2003

Cerebral autoregulation in carotid artery occlusive disease assessed from spontaneous blood pressure fluctuations by the correlation coefficient index.

BACKGROUND AND PURPOSE: Estimation of dynamic cerebral autoregulation from spontaneous fluctuations of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) is an attractive monitoring option for cerebral hemodynamic impairment. We evaluated the correlation coefficient index method in patients with severe obstructive carotid disease and compared it with transfer function analysis (frequency domain approach to cerebral autoregulation) and CO2 vasomotor reactivity. METHODS: In 139 patients with severe unilateral carotid stenosis (>or=70%) or occlusion, CBFV (transcranial Doppler) and ABP (Finapres method) were recorded over 10 minutes. Correlations between systolic pressure, diastolic pressure, and mean ABP and CBFV oscillations over 1-minute epochs were averaged over 10 minutes to form the correlation coefficient indexes (Sx, Dx, Mx, respectively). Transfer function parameters (phase shift and gain between ABP and CBFV oscillations) were determined from the entire 10-minute period. CO2 reactivity was assessed by inhalation of 7% CO2. RESULTS: The correlation indexes Dx and Mx were significantly higher ipsilateral to stenosis and increased with degree of stenosis, indicating increasing dependence of CBFV on ABP and thus impairment of cerebral autoregulation. Dx and Mx correlated moderately but highly significantly with transfer function parameters and CO2 reactivity and showed a good level of agreement in detecting pathological values. Patients with a small variance of the 1-minute source correlations of Dx and Mx showed clearly better correlation values. Transfer function parameters and CO2 reactivity but not Dx and Mx were significantly poorer in patients with symptomatic stenosis or occlusion. CONCLUSIONS: The potential of the correlation coefficient indexes Dx and Mx in detecting hemodynamic impairment in patients with carotid stenosis is comparable to that of transfer function analysis and CO2 reactivity testing. In future, a combination of various hemodynamic tests might help to identify patients at risk for ischemic events.

Aged↗
PubMed2000

Telomerase and the cellular lifespan: implications of the aging process.

The aging process has multiple causes. However, there is now substantial evidence consistent with the hypothesis that (i) all normal mammalian somatic cells have a finite capacity to replicate and (ii) that gradual cell turnover throughout the lifespan of a mammal eventually exhausts this finite capacity. This results in a gradual accumulation of senescent (irreversibly post-mitotic) cells with increasing age. These cells display a radically different phenotype to their growing counterparts, which has the potential to compromise tissue function. Perhaps the best evidence for this is seen in Werner's syndrome, a rare genetic disease, in which patients display most of the features of accelerated aging, together with a profoundly compromised replicative lifespan in certain tissue lineages. Several classes of human cells are now known to count divisions by monitoring the progressive attrition of chromosomal ends (telomeres), leading to the activation of a p53-p21waf-dependent G1 checkpoint. Ectopic expression of telomerase has been shown to prevent senescence in several cell types and offers the potential for interventions in the aging process based on tissue engineering, gene therapy or homeografts. However, this telomere-driven senescence mechanism seems to be absent from rodents, which use telomere-independent means (perhaps based upon p14arf) to count divisions. Similar senescence pathways are now being reported in humans, and this, coupled with the demonstration of tissue-specific telomeric loss rates, has the potential to render strategies based on the use of telomerase dependent on the characteristics of the target tissue. Werner's syndrome may provide strong clues regarding the potential limitations and prospects of such future treatments.

Aging↗
PubMed2000

[Fundamental bases of biological rhythms].

The data and theoretical points given in the paper mould basically new views of molecular relationships underlying the function of living beings and biological rhythms. The authors' procedure for wedge biological fluid dehydration reveals a wide autowave spectrum that is clearly detectable when the fluid passes into the solid phase. A hypothesis of the autowave interaction of biologically active molecules is forwarded, which considers autowaves as a basis of organization of physiological and pathological processes occurring in the body.

Aging↗