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Human Ageing (human + ageing)
Selected AbstractsEQUALITY AND THE DUTY TO RETARD HUMAN AGEINGBIOETHICS, Issue 8 2010COLIN FARRELLY ABSTRACT Where does the aspiration to retard human ageing fit in the ,big picture' of medical necessities and the requirements of just healthcare? Is there a duty to retard human ageing? And if so, how much should we invest in the basic science that studies the biology of ageing and could lead to interventions that modify the biological processes of human ageing? I consider two prominent accounts of equality and just healthcare , Norman Daniels's application of the principle of fair equality of opportunity and Ronald Dworkin's account of equality of resources , and conclude that, once suitably amended and revised, both actually support the conclusion that anti-ageing research is important and could lead to interventions that ought to be considered ,medical necessities'. [source] In vitro response to Candida albicans in cultures of whole human blood from young and aged donorsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2007Celia Murciano Abstract Invasive infections with opportunistic fungi, such as Candida albicans, have become an increasing problem in aged adults in recent years. This work investigates the influence of human ageing on C. albicans recognition by toll-like receptors (TLRs), essential components of the innate immune system, using a cohort of 96 young (15,42 years) and aged (>70 years) human volunteers. No significant differences between aged and young donors were observed on (1) cell surface TLR2, TLR6 and TLR4 expression on lymphocytes, monocytes and granulocytes, (2) production of cytokines [IL-8, IL-1,, IL-6, IL-10, tumour necrosis factor (TNF)-, and IL-12p70] and prostaglandin E2 (PGE2) by whole human blood in response to C. albicans and (3) fungicidal activity of whole blood. A statistically significant higher titre of natural anti- C. albicans antibodies was found in plasma of volunteers between 80 and 95 years old when compared with other age groups, probably as a consequence of the increased levels of serum Ig that has been described in elderly subjects. Therefore, the results indicate that the increased susceptibility to C. albicans infections in the elderly is not a consequence of defects in TLRs expression or signalling, nor of an impaired fungicidal activity of blood. [source] The evolution of senescence from a comparative perspectiveFUNCTIONAL ECOLOGY, Issue 3 2008R. E. Ricklefs Summary 1Comparative studies of ageing address the evolutionary lability of the rate of ageing as an indication of potential for, and constraints on, the extension of life span. 2Experimental studies on ageing have focused on damage induced by reactive oxygen species (ROS) and other stresses, and on the mechanisms to prevent or repair this damage. Research on animal models has revealed genes with large effects on life span. However, the relevance of some animal models to human ageing is unclear and it is not known whether evolved differences in ageing involve such major gene effects. 3Studies on the demography of populations of vertebrates in the wild show that animals suffer from senescence in nature. Variation in the rate of ageing is consistent with evolutionary theory in that senescence is delayed in populations that suffer relatively low extrinsic mortality. 4Populations of longer-lived individuals suffer a higher proportion of ageing-related mortality, and thus stronger selection against early ageing. The presence of ageing-related deaths in these populations suggests a lack of suitable mechanisms that would further extend life span. 5Similar patterns of ageing-related mortality in wild and captive or domesticated populations indicate that most ageing-related death is caused by intrinsic factors, such as tumours and cardiovascular failure, rather than increasing vulnerability to extrinsic causes of mortality. 6Studies of several wild populations of long-lived birds suggest that ageing-related mortality is often catastrophic, with individuals maintaining high levels of condition until shortly before their demise. 7Comparative studies of many species suggest connections between early development and the pattern of ageing later in life, consistent with laboratory studies on variation within individual species. The physiological connections across the life span are not well understood. 8Comparative studies have provided important insights into the ageing process. However, we still lack information on important issues, including the causes of death in natural populations, the relationship of within- and between-population variation in the rate of ageing, the genetic basis of variation in rate of ageing in natural populations, and detailed longitudinal studies of individual health and reproductive success in relation to age at death. [source] Reductions in basal limb blood flow and vascular conductance with human ageing: role for augmented ,-adrenergic vasoconstrictionTHE JOURNAL OF PHYSIOLOGY, Issue 3 2001Frank A. Dinenno 1Basal whole-limb blood flow and vascular conductance decrease with age in men. We determined whether these age-associated changes in limb haemodynamics are mediated by tonically augmented sympathetic ,-adrenergic vasoconstriction. 2Seven young (28 ± 2 years; mean ±s.e.m.) and eight older (64 ± 2 years) healthy, normotensive adult men were studied. Baseline femoral artery blood flow (Doppler ultrasound) and calculated vascular conductance were 29 and 31 % lower, respectively, and vascular resistance was 53 % higher in the older men (all P < 0.001). 3Local (intra-femoral artery) ,-adrenergic receptor blockade with phentolamine evoked greater increases in femoral blood flow (105 ± 11 vs. 60 ± 6 %) and vascular conductance (125 ± 13 vs. 66 ± 7 %), and reductions in vascular resistance (55 ± 2 vs. 39 ± 3 %) in the experimental limb of the older compared with the young men (all P < 0.001). As a result, ,-adrenergic receptor blockade eliminated the significance of the age-associated differences in absolute levels of femoral blood flow (500 ± 51 vs. 551 ± 35 ml min,1), vascular conductance (6.02 ± 0.73 vs. 6.33 ± 0.26 U), and vascular resistance (0.17 ± 0.03 vs. 0.16 ± 0.01 U; P= 0.4,0.8, n.s.). Femoral haemodynamics in the control limb were unaffected by phentolamine administration in the contralateral (experimental) limb. Complete ,-adrenergic receptor blockade was demonstrated by the absence of vasoconstriction in the experimental limb in response to the cold pressor test. Local propranolol was administered to control for any ,-adrenergic effects of phentolamine. Propranolol did not affect haemodynamics in the experimental or control limbs. 4Our results indicate that the age-related reductions in basal limb blood flow and vascular conductance are mediated largely by chronically elevated sympathetic ,-adrenergic vasoconstriction. This may have important physiological and pathophysiological implications for the ageing human. [source] Strong and weak lifespan extension: what is most feasible and likely?AUSTRALASIAN JOURNAL ON AGEING, Issue 2 2006Jayne C Lucke Abstract Recent advances in biomedical science indicate that it may eventually be possible to intervene in the biological process of human ageing. This paper overviews the current state of the science of lifespan extension and promising future directions. It is uncertain whether ,strong' lifespan extension , the extension of human life beyond the maximum 122 years so far observed , will become a reality. It is more likely that cumulative effects of numerous scientific and biomedical advances in the treatment of common disease will produce ,weak' lifespan extension , the extension of average life expectancy. The practical application of molecular, genetic and nanomaterials research may also lead to advances in life expectancy. It is not too early to begin to consider the policy implications of either form of lifespan extension. [source] EQUALITY AND THE DUTY TO RETARD HUMAN AGEINGBIOETHICS, Issue 8 2010COLIN FARRELLY ABSTRACT Where does the aspiration to retard human ageing fit in the ,big picture' of medical necessities and the requirements of just healthcare? Is there a duty to retard human ageing? And if so, how much should we invest in the basic science that studies the biology of ageing and could lead to interventions that modify the biological processes of human ageing? I consider two prominent accounts of equality and just healthcare , Norman Daniels's application of the principle of fair equality of opportunity and Ronald Dworkin's account of equality of resources , and conclude that, once suitably amended and revised, both actually support the conclusion that anti-ageing research is important and could lead to interventions that ought to be considered ,medical necessities'. [source] The role of mitochondria in ageing and carcinogenesisCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2006M. A. Birch-Machin Summary Mitochondria can perform multiple cellular functions including energy production, cell proliferation and apoptosis. These organelles contain their own genetic material, mitochondrial DNA (mtDNA), which is maternally inherited. Although much smaller than the nuclear genome, mtDNA is equally important, as it has been hypothesized to play a crucial role in ageing and carcinogenesis. This is partly due to the fact that mitochondria represent the major site for the generation of cellular oxidative stress and play a key role in mediating programmed cell death (apoptosis). Damage to mtDNA is therefore an important contributor to human ageing, cancer and neurodegenerative diseases. The most relevant footprints of mtDNA damage are point mutations of single bases, or deletions of the 16.5-kb mitochondrial genome. This review will focus on the key roles of mitochondrial function and mtDNA in oxidative stress production and as a mediator of apoptosis, and on the use of mtDNA as a biomarker of sun exposure. This will be related to the contribution of mitochondria and mtDNA in the ageing process and cancer, with a specific focus on human skin. In conclusion, it is likely that the interplay between nuclear and mitochondrial genes may hold the final understanding of the mitochondrial role in these disease processes. [source] | |||||||||||||