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Abraham Aviv

Publications and source records attributed to Abraham Aviv.

27 records · Page 2Linked to original sources
PubMed2004

Sodium glomerulopathy: tubuloglomerular feedback and renal injury in African Americans.

African Americans are prone to develop not only essential hypertension but also progressive renal injury. We present a simple model to explain salt-induced renal injury (sodium glomerulopathy) in African Americans, the central features of which are the tubuloglomerular feedback and the balance/imbalance between the vascular tones of the afferent and efferent glomerular arterioles. We propose that in African Americans, habitual consumption of high salt causes chronic intermittent tubular hyperperfusion of the macula densa, resulting in a rightward and upward resetting of the operating point for the tubuloglomerular feedback. The resetting of the operating point causes an imbalance between the vascular tones of the afferent/efferent arterioles, a rise in the glomerular capillary hydraulic pressure, and consequent hyperfiltration. Increased susceptibility to glomerular hyperfiltration of African Americans on a high salt intake may explain their proclivity to progressive renal injury associated with essential hypertension.

Black or African American↗
PubMed2003

Growth, telomere dynamics and successful and unsuccessful human aging.

This paper links mass trajectories with telomere dynamics to construct theoretical models of successful and unsuccessful aging in human beings. It couples parameters of telomere length in somatic cells, as expressed by the terminal restriction fragment (TRF), at birth and the rate of telomere attrition thereafter with nonlinear models of somatic growth to predict the probability of surviving disease free, based on the assumption that telomere length in replicating somatic cells is a surrogate indicator of aging determinants in humans. The models capture aspects of individual variation in successful and unsuccessful aging and the long-term consequences of rapid growth early in life.

Aging↗
PubMed2002

Telomeres, sex, reactive oxygen species, and human cardiovascular aging.

By undergoing erosion with each replicative cycle, telomeres chronicle the replicative history of human somatic cells in vitro and in vivo. In human beings the telomere is relatively short, inversely correlated with age, highly heritable, and longer in women than men. However, it is not established whether the dynamics of telomere attrition in vivo has a role in the biology of human aging. Telomere attrition may be modified by reactive oxygen species, the biology of which is governed by processes that are influenced by sex. Indices of cardiovascular aging in humans are correlated with telomere length and this relationship is characterized by sexual dimorphism. In the final analysis, the biology of reactive oxygen species may offer a common explanation for some interindividual variation in cardiovascular aging and age-dependent telomere attrition in humans.

Aging↗
PubMed2002

Salt consumption, reactive oxygen species and cardiovascular ageing: a hypothetical link.

Opinions about the impact of dietary salt on blood pressure have dominated the debate regarding 'salt sensitivity', which can be broadly defined as the blood pressure response to changes in sodium intake among individuals in a population. However, the larger question is whether salt consumption exerts significant biological effects independent of changes in blood pressure. Provisional answers to this question are reviewed based on newly discovered links between sodium metabolism and the generation of reactive oxygen species. These links suggest that, in a subset of the general population, salt consumption is a determinant in cardiovascular ageing.

Aging↗
PubMed2002

Chronology versus biology: telomeres, essential hypertension, and vascular aging.

There is considerable evidence that essential hypertension is closely linked to the growth, development, and aging of human beings. It is imperative, therefore, to introduce biological indicators of growth and aging into models developed to provide a better understanding of the etiology of essential hypertension. One of these indicators may well be the age-dependent telomere attrition rate in somatic cells. Telomere attrition registers the replicative history of somatic cells. As such, it chronicles not only the growth that results from the replication of somatic cells but also their turnover-a process that is strongly linked to inflammation and oxidative stress, which are key factors in the biology of human aging.

Aging↗
PubMed2002

Genomic association/linkage of sodium lithium countertransport in CEPH pedigrees.

Little is known about genetic determinants explaining variation in the erythrocyte sodium-lithium countertransport (SLC), an intermediate phenotype of essential hypertension. We characterized the SLC in immortalized lymphoblasts and showed that its behavior is similar to that of erythrocyte SLC. We then performed association and linkage analyses of the SLC in immortalized lymphoblasts from 5 large pedigrees from the Center d'Etude du Polymorphisme Humain (CEPH) genomics repository. The results of these analyses showed that a number of genomic regions harboring genes involved in glutathione metabolism might explain variations in SLC activity. These findings support evidence that thiol groups play a central role in SLC activity.

Alleles↗
PubMed2002

Loss of chromosome 16 from renal epithelial cells in humans.

This work explores the notion that low-frequency, acquired aneuploidy may play a role in complex genetic traits such as essential hypertension. To this end, renal epithelial cells in urinary sediments and in renal cysts were examined by fluorescent in situ hybridization with DNA probes specific for the heterochromatic and centromere regions of chromosomes 16 and 1. Chromosome 16 was probed because it harbors variant genes causing monogenic hypertension. These genes have also been investigated for their role in essential hypertension. Chromosome 1 was also probed as an internal control. Higher proportions of renal epithelial cells in the urinary sediments showed monosomy of chromosome 16 than monosomy of chromosome 1 (P<0.001). We also observed in epithelial cells of renal cysts a preponderance of monosomy for chromosome 16 over monosomy for chromosome 1 (P<0.024). Low-frequency loss of heterozygosity that results from acquired monosomy of chromosome 16 and perhaps other chromosomes may contribute to expression of complex genetic traits such as essential hypertension, in which the diverse phenotypic manifestations are poorly understood.

Adolescent↗
PubMed2002

Telomere length in the newborn.

Telomere length is similar in different organs of the human fetus but variable among fetuses. During extrauterine life telomere length is highly variable among individuals and longer in women than men. In the present work we addressed the following questions: 1) Are there sex-related differences in telomere length at birth? 2) Is there synchrony (i.e. correlation in length) of telomeres in tissues within the newborn? 3) Is the variability in telomere length among newborns as large as that in adults? We studied normal male and female newborns who donated DNA samples from three sources: white blood cells, umbilical artery, and foreskin. Telomere length was measured by the mean length of the terminal restriction fragments (TRF). TRF length was not different between male and female newborns. It was highly synchronized among the DNA samples from white blood cells, umbilical artery and skin within individual donors but exhibited a high variability among donors. We conclude that there is no evidence for the effect of sex on telomere length at birth, suggesting that longer telomeres in women than men arise from a slower rate of telomeric attrition in women. The variability in telomere length among newborns and synchrony in telomere length within organs of the newborn are consistent with the concept that variations in telomere length among adults are in large part attributed to determinants (genetic and environmental) that start exerting their effect in utero.

Adolescent↗