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Aged Subjects (aged + subject)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Metabolic age modelling: the lesson from centenarians

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2000
G. Paolisso
Evolutionary theories of ageing, and data emerging from cellular and molecular biology of ageing, suggested that animals and humans capable of reaching an age close to the extreme limit of the life span should be equipped with a very efficient network of anti-ageing mechanisms. Indeed several evidences have demonstrated that starting from young to very old subjects, ageing is associated with a progressive remodelling. Thus, a new paradigm, the remodelling theory of age, was proposed. This theory, focusing on the human immune system, suggested that immunosenescence is the net result of the continuous adaptation of the body to the deteriorative changes occurring over time. According to this hypothesis, body resources are continuously optimized, and immunosenescence must be considered a very dynamic process including both loss and gain. Whether the metabolic pathways and the endocrine functions are also part of the age remodelling is not investigated. The aim of this review is to focus on the age-related changes in metabolic pathways and endocrine functions and to demonstrate that healthy centenarians (HC) represent the best living example of successful age-remodelling in whom the age remodelling has occurred without problems. In order to design the clinical picture of such successful ageing, anthropometric, endocrine and metabolic characteristics of healthy centenarians (HC), compared with aged subject, have been outlined. [source]

Effects of glucose ingestion on cardiac autonomic nervous system in healthy centenarians: differences with aged subjects

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2000
Paolisso
Background Spectral analysis of heart rate variability (HRV) investigates the cardiac autonomic nervous system (ANS) activity. In particular, low frequency/high frequency (LF/HF) is considered an index of cardiac sympatho-vagal balance and is stimulated by glucose ingestion in healthy subjects. No studies have evaluated the effect of glucose ingestion on cardiac ANS in centenarians. Materials and methods In 30 healthy centenarians (HC) and 25 aged subjects (AS) power spectral analysis of HRV was investigated during an oral glucose ingestion. Results Glucose ingestion rose LF/HF ratio in both groups studied. Such stimulatory effects were restrained to the first 60 min of the study. Independent of age, gender, body mass index (BMI) and fasting plasma norepinephrine and FT3 concentrations, HC had basal total power (1318 ± 546 vs. 1918 ± 818 msec2, P < 0.01), lower low frequency (LF) (33 ± 21 vs. 50 ± 11 n.u. , P < 0.03), and higher high frequency (HF) (74 ± 18 vs. 43 ± 15 n.u., P < 0.05) than AS. Consequently, LF/HF ratio (0.43 ± 0.07 vs. 0.91 ± 0.05, P < 0.02) was also lower in HC than in AS. In AS, but not in HC, the baseline LF/HF ratio correlated significantly with BMI (r = 0.48, P < 0.01), waist-hip-ratio (WHR) (r = 0.45, P < 0.02), fasting plasma insulin (r = 0.49, P < 0.01) and norepinephrine (r = 0.57, P < 0.02) concentration. Glucose ingestion was associated with a significant rise in LF/HF ratio in both groups studied but per cent changes in glucose mediated stimulation of LF/HF was lower in HC than in AS. In a control study, water administration did not affect power spectral parameters of HRV. Conclusion Our study demonstrates that basal- and glucose-stimulated LF/HF, an indirect index of cardiac sympatho-vagal balance, are lower in HC than in AS. [source]

Impaired efflux of cholesterol from aged cells and its molecular mechanism: A basis for age-related enhancement of atherosclerosis

GERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 3 2007
Shizuya Yamashita
Aging is one of the risk factors for atherosclerotic cardiovascular diseases, however, its molecular mechanism is currently unknown. Many types of cells in the atherosclerotic lesions are considered to have various biological abnormalities such as impaired lipid homeostasis and slow cell proliferation, which may be related to senescence at cellular levels. One of the common characteristics of senescent cells in vitro is the alteration of actin cytoskeletons, which were reported to be involved in the intracellular transport of lipids. Cholesterol efflux from the cells is the initial step of reverse cholesterol transport, a major protective system against atherosclerosis. Recently, we demonstrated that Cdc42, a member of the Rho -GTPase family, might be crucial for cellular lipid transport and cholesterol efflux based upon studies of Tangier cells that are deficient in ABCA1 gene. In the current review, we also indicate that the expression of Cdc42 is decreased in the cells from aged subjects in close association with the retarded intracellular lipid transport. Furthermore, the Cdc42 expression is reduced by culturing fibroblasts in vitro for a long duration. Werner syndrome (WS) is characterized by the early onset of senescent phenotypes including premature atherosclerotic cardiovascular diseases, although the underlying molecular mechanism for the enhanced atherosclerosis has not been fully understood yet. We examined the intracellular lipid transport and cholesterol efflux and the expression levels of cholesterol efflux-related molecules in skin fibroblasts obtained from patients with WS. Cholesterol efflux was markedly reduced in the WS fibroblasts in association with an increased cellular cholesterol content. Fluorescent recovery after photobleaching technique revealed that intracellular lipid transport around Golgi apparatus was markedly reduced when using a C6-NBD-ceramide as a tracer. Cdc42 protein and its guanosine 5,-triphosphate-bound active form were markedly reduced in the WS fibroblasts. The adenovirus-mediated complementation of wild-type Cdc42 corrected the impaired cholesterol efflux, intracellular lipid transport and cellular cholesterol levels in the WS fibroblasts. These data indicate that the reduced expression of Cdc42 might be responsible for the abnormal lipid transport, which in turn might be related to the accelerated cardiovascular manifestations in WS patients. The current review focuses on the impaired efflux of cholesterol from aged cells and its molecular mechanism as a basis for age-related enhancement of atherosclerosis. [source]

Yawning and subjective sleepiness in the elderly

JOURNAL OF SLEEP RESEARCH, Issue 3 2008
IOLE ZILLI
Summary Yawning is related to sleep/wake transitions and time of day, probably reflecting the time course of sleepiness. As aging modifies sleep,wake and sleepiness rhythms, we suppose that yawning frequency and its time course vary as a function of age. Thirteen aged healthy subjects (77.15 ± 4.09 years) and 12 young adults (24.41 ± 3.31 years) were instructed to keep their habitual sleep schedules for three consecutive work-days, during which they were required to signal every yawning occurrence and to evaluate hourly their sleepiness level. Results showed that aged subjects yawn less frequently than young adults, particularly during morning and mid-afternoon hours. The time course of yawning was different between the two age groups: aged subjects showed earlier morning peak and evening rise compared with young adults; in addition, aged subjects showed two minor peaks in-between. Differences as a function of age in the time course of yawning were associated with differences in the time course of sleepiness. The only exception pertained to the early morning yawning peak, which was close to the awakening but it was not associated with high sleepiness in aged subjects. Our study discloses that aging modifies yawning frequency and its time course. Furthermore, as in the elderly yawning after the awakening is not associated with high sleepiness level as in young adult, we put forward that sleepiness level and the proximity of sleep/wake transitions could separately affect yawning. [source]

Endothelium-dependent contractions in hypertension

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2005
Paul M Vanhoutte
1Endothelial cells, under given circumstances, can initiate contraction (constriction) of the vascular smooth muscle cells that surround them. Such endothelium-dependent, acute increases in contractile tone can be due to the withdrawal of the production of nitric oxide, to the production of vasoconstrictor peptides (angiotensin II, endothelin-1), to the formation of oxygen-derived free radicals (superoxide anions) and/or the release of vasoconstrictor metabolites of arachidonic acid. The latter have been termed endothelium-derived contracting factor (EDCF) as they can contribute to moment-to-moment changes in contractile activity of the underlying vascular smooth muscle cells. 2To judge from animal experiments, EDCF-mediated responses are exacerbated by aging, spontaneous hypertension and diabetes. 3To judge from human studies, they contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. 4Since EDCF causes vasoconstriction by activation of the TP-receptors on the vascular smooth muscle cells, selective antagonists at these receptors prevent endothelium-dependent contractions, and curtail the endothelial dysfunction in hypertension and diabetes. British Journal of Pharmacology (2005) 144, 449,458. doi:10.1038/sj.bjp.0706042 [source]