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Biomedical subjects

A Ruiz-Torres

Publications and source records attributed to A Ruiz-Torres.

At least 19 recordsLinked to original sources
PubMed2006

Relationship of serum leptin concentration with age, gender, and biomedical parameters in healthy, non-obese subjects.

It is known that the circulating levels of leptin, the adipocyte hormone implicated in the control of energy balance, are correlated with fat body mass (FBM), although the influences of other physiological conditions are not fully understood. We investigated the relationships of serum leptin concentration with age, gender, and 36 hormone-metabolic parameters in a sample of a well defined healthy population (n=246; age range 20-93 years), and in subgroups of lean individuals according to their body mass index (BMI), within similar age range and gender distribution. Only insulin secretion (positively) and testosteronemia (negatively, in males) show direct correlations. The other relationships are not significant but throughout collaborating variables, such as serum lipids, especially through FBM, lean body mass (LBM) through insulin secretion, and gender through FBM. In males, LBM correlates with insulin secretions, s-IGF-1 and with s-testosterone. The relationship between insulin secretion and LBM persists up to advanced age. From the present study it may be concluded that the positive relationship of leptin with insulin secretion and the negative one with testosterone, indicate direct implications of leptin in insulin signaling, as well as in male sexual development. Finally, the fact that the amount of secreted insulin depends on LBM and the latter on testosterone and IGF-1, indicates the importance of muscle mass in the control of insulin secretion.

Adipose Tissue↗
PubMed2005

On maximum human life span: interdisciplinary approach about its limits.

BACKGROUND: This is a theoretical approach on the question on how much maximally may extend the life of human individual. The starting point of this work was the biological consideration of two changes in human characteristics which took place during the last century up to now, namely human beings lived remarkably longer and are becoming taller. METHODS: Demography data and Gompertz deduced mathematics, either related to growth or survival, were the two columns on which the basis of this study has been supported. Respective equations were adapted to the purpose searched applying parameters of. normal body growth and cell growth in vitro. Having individual age on the abscisse, that of its crossing point with ordinate value indicates the age in which no more cell activity should exist, either of proliferation or migration. RESULTS: Despite rising life expectancy, whose extrapolation leads to remarkable enhance for future values, life span calculations with the help of our mathematic models do not indicate an extent beyond the limit of 120 years. Nevertheless hypothetically there is the exception of prolonging life out of the mentioned limit when growth and ageing would be proportional interrelated. Furthermore, when proliferation results of in vitro smooth muscle cell cultures were related to age of donor, its linear regression crosses the x-axis at an age of 110.16 years (mean value of different procedures of measurement) . This limit is not far from that using other cell activity parameters as migration (117.7 years when cessation) or such state of senescent (98 years when all cells involved). Nevertheless with the help of Gompertz equation putting growth in the ordinate (proliferation activity) instead mortality and donor age in the x-axis, the follow up of the curve is similar to that known of survival up to the age of 80. But this procedure does not seem adequate to obtain information on the limit of life potential because of later this curve becomes very flat reaching the end at age around 180; this seems not to be real but due to an artefact. Finally IGF-1 prolongs the cessation ( x-axis crossing point) of cell growing activity up to donor age of around 126.4 years. CONCLUSIONS: Human life span seems to be limited up to around 120 years, but growth process modulating factors could theoretically enhance it.

Biomarkers↗
PubMed2003

L-calcium channel blockade induced by diltiazem inhibits proliferation, migration and F-actin membrane rearrangements in human vascular smooth muscle cells stimulated with insulin and IGF-1.

During the atheroma plaque formation, smooth muscle cells (SMC) have to change their differentiated phenotype in order to proliferate, migrate and synthesize collagen. These phenotypic changes are stimulated by insulin and IGF-1, and we have studied the effect of L-type calcium channel blockade produced by diltiazem on such changes. Mitotic activity was measured using bromodeoxyuridine DNA incorporation, the migration capability as chemotaxis index in a Boyden chamber, and cytoskeleton changes related to SMC movement in immunofluorescence studies. Diltiazem (10(-7)-10(-6) M) reduced insulin-induced mitotic activity in cultured human vascular SMC more effectively than in IGF-1-induced mitotic activity, but at 10(-5) M, the inhibitory effects were similar. Diltiazem also showed a clear inhibition of migration ability, both under basal conditions (p < 0.05) and after addition of insulin (p = 0.0001) and IGF-1 (p < 0.0001). Finally, diltiazem inhibited membrane ruffling induced both by insulin and IGF-1 in a similar manner, and similar results were obtained with SMC from rat aorta. We conclude that substances blocking the L-type calcium channels such as diltiazem, could inhibit those processes which in vivo lead SMC to form the atheroma plaque.

Actins↗
PubMed1999

Age-related loss of proliferative activity of human vascular smooth muscle cells in culture.

This work studied the proliferation activity in cultures of vascular smooth muscle cells (SMC) from individuals of different ages. The cells derived from arteries of 12 donors of both sexes from 45 to 91 years of age. The main parameter considered was the 'proliferation rate' (cells grown per day in the different culture passages) taking into account the age of the donor. No significant relationship between age of the donor and the cell life in proliferation was found. On the contrary, the mean time of passage duration for reaching the maximum of proliferation as well as its 'efficiency' (maximum of proliferation rate registered/mean time of passage duration) show a statistically significant dependence on the age of the donor. Furthermore, the proliferation rate measured in each passage is statistically significant related to donor age. The regressions obtained show a similar negative slope (VC 4%). Considering the first five culture passages, the regression crosses the x-axis at the age of 105.6+/-11.7 years. This age in which no proliferative activity of human SMC would be expected lies near the limit of maximum life potential for human beings. Our results suggest that with advancing donor age there is an increasing number of senescent SMC either primarily transferred or appeared in the culture. Vascular SMC of individuals whose life is near the end would almost be all senescent and therefore show extremely low proliferation rates in the culture. If the proliferative activity of arterial SMC is a condition for atherogenesis, the proportion of senescent cells would be inversely related to the propensity of developing the atheroma because of the inability of these cells to divide.

Aged↗
PubMed1998

Insulin stimulates collagen synthesis in vascular smooth muscle cells from elderly patients.

The process of aging results in an increase in collagen in arterial walls, but the blood levels of insulin-like growth factor 1 (IGF-1) decrease remarkably as adults age. There is an almost simultaneous increase in insulin secretion, particularly in obese individuals. It is not known if, under these hormonal conditions, the enrichment of collagen in the arterial wall is due to insulin. We studied the effect of insulin on the production of collagen in vascular smooth muscle cells (VSMC) from elderly persons with high levels of insulin secretion after blocking the insulin receptors with a monoclonal antibody. Results were compared to those without insulin receptor blockage and to those with IGF-1. Despite the inhibition of 14C-glucose uptake, insulin clearly stimulated the release of procollagen III, and increased the collagen synthesis. The hydroxyproline labelling rate from 3H-proline increased to more than twice the control values. IGF-1 is a more potent effector than insulin, but the effect of insulin on the rate of collagen production became similar to IGF-1 when the specific receptors were blocked. The results indicate that under special conditions that occur with aging, insulin interacts with nonspecific receptors in VSMC, especially IGF-1, stimulating these cells to produce collagen.

Aged↗
PubMed1998

Phenotypic changes in vascular smooth muscle cells during aging: insulin effect on migration.

We examined the mechanisms by which insulin may be atherogenic during aging. We postulated that an increase in insulin secretion during aging produces growth factor effects on vascular smooth muscle cells (VSMCs), promoting these cells to synthesize collagen and to migrate. We have previously demonstrated that insulin stimulates collagen synthesis and release in senescent VSMCs that were obtained from a human organism with high levels of insulin secretion. Using the same experimental model, we now study the effects of insulin on VSMC migration. We demonstrate that insulin has a chemoattractant effect on VSMCs which occurs through insulin binding to its own specific receptors as opposed to its effect on collagen production. Blocking the insulin receptor significantly eliminates the insulin effect on cell migration. At the same molarity, the chemotactic effect of insulin is less pronounced than that of insulin-like growth factor-1. In spite of different mechanisms, there is a remarkable correlation between the insulin effects on collagen secretion and cell migration (r2 = 97%, p < 0.0005). Our results indicate that distinct but closely related mechanisms may exist by which insulin becomes atherogenic. Our results also suggest the importance of normal aging processes in the development of atherosclerosis.

Aged↗
PubMed1995

Ageing and prostate: age-related changes in androgen receptors of epithelial cells from benign hypertrophic glands compared with cancer.

Total and nuclear androgen receptors (AR) were studied from epithelial cells in internal and external prostatic zones in 51- to 86-year-old individuals with benign prostatic hyperplasia (BPH) (n = 68) and prostatic cancer (n = 9). We focussed on the role played by androgens on those processes, despite the fact that at these ages, its secretion has normally decreased. In BPH, the nuclear AR do not change, but total measured androgen receptors rise with age (r = 0.5, P < 0.01). Total or nuclear AR do not correlate with gland volume, despite its increase with age (r = 0.8, P < 0.05). In prostates less than 180 cc in volume, there is a significant correlation between size, serum total testosterone level (r = 0.53, P < 0.05) and prostatic specific antigen (PSA) (r = 0.63, P < 0.05). The amount of nuclear AR in cells from the external zone (infiltrated by cancer or healthy) is two times greater than in those from the internal region. Total receptor content of the external zone cells is also high, but the sample is too small to demonstrate an age dependence. The results suggest that ageing is accompanied by an accumulation of non-nuclear AR in the cytosol, that does not play a role in the development of BPH because the amount of nuclear receptors remains unaltered. The enrichment in nuclear receptors of the external zone cells, independently of the presence of cancer, points to a greater androgen dependence in these cells than in cells of the internal region.

Aged↗
PubMed1995

Are anthropometric changes in healthy adults caused by modifications in dietary habits or by aging?

The aim of this work was to investigate to what extent age-dependent anthropometric changes are causally related to changes in dietary habits. In a randomly obtained sample of 246 healthy adults in the age range of 20-90 years from a well-defined agrarian population, the intake of proteins, fat and carbohydrates in males decreases with age (r = -0.65, p < 0.001; r = -0.65, p < 0.001; r = -0.5, p < 0.01, respectively), but in females it remains unaltered (e.g. the mean +/- SD daily protein intake in young adult females is 74 +/- 31 vs. 71 +/- 11 g in individuals over 80); in males it decreases from 140 +/- 34 to 71 +/- 13 g. On the contrary, in both sexes the muscle-mass-related measurements decrease (r = -0.45, p < 0.001; vs. r = -0.41, p < 0.001; mean values of the quotient lean body mass with body length in young adult females and males were 41.9 +/- 4.4 and 52.7 +/- 5.9 vs. 35.0 +/- 3.1 and 43.2 +/- 5.0, respectively, in individuals over 80, p < 0.001 in both sexes). From 35 onwards, the daily urea excretion-as a marker of the protein degradation rate-declines significantly with age, but without a clear correlation to the protein intake (r = 0.38), as occurs during young adulthood (r = 0.63). Furthermore, body fat content tends to increase with age, but the differences are statistically significant only in males of very advanced age (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Homeostasis between lipid peroxidation and antioxidant enzyme activities in healthy human aging.

In healthy people the plasma malondialdehyde increases with age, however there is a simultaneous rise in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase in red blood cells, although both enzymes show a biphasic behaviour, that is, reaching the lowest values at 40-50 years of age to rise remarkably later on. No significant changes were found in the case of glutathione peroxidase but the age-dependent behaviour is similar to the other enzymes mentioned above. The activity of glutathione reductase shows a clear increase depending on age, up to middle age, with or without flavin adenine dinucleotide. We conclude that the increase in the activities of the anti-oxidant enzymes of the red blood cells during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation. Consequently, from the point of view of the parameters used the homeostasis between the production of free radicals and anti-oxidant systems seems to be maintained in the common, normal aging pattern.

Adolescent↗
PubMed1981

[Aging as inversion of growth: reaction of uric acid (author's transl)].

Independent from sex, the concentration of uric acid in serum decreases slowly in normal individuals from 55--58 years on. The older is an individual, the lower is the concentration of uric acid. This phenomenon is the consequence of a restriction of the synthesis of nucleic acids, parallel to ageing. Results suggests that the concentration of uric acids can be considered to be parameters of ageing.

Adult↗
PubMed1981

[Uricemia and uric acid quantities in urine under unbalanced diet (author's transl)].

Under exclusive intake of glucose or fat production of uric acid and growth is lowered in male rats. Just the same can be observed in adult animals. Loss in weight and impairment in production of uric acid seem to relate to each other. Growth-inhibition, i.e. weight reduction cannot be the reason for the obviously reduced synthesis of uric acid, because corresponding findings can not be ascertained in protein-fed animals in spite of weight-reduction. These findings suggest that synthesis of uric-acid depends on the intake of amino-acids. Thereby the pool of amino acids would be decisive for the synthesis-rate of nucleic acids. It might be conceivable, that the decrease of uric acid serum concentration during aging relates to the suggestion mentioned above.

Animals↗
PubMed1979

[The effect of thyroid hormone on the absorption of L-proline, chloramphenicol and digitoxin].

Using the method of the perfused small intestine preparation in situ, the influence of triiodothyronine on the absorption was investigated. The absorptions of L-proline and digitoxin were disturbed by the thyroid hormone in different ways, in contrast to chloramphenicol, where it is unaltered. The effects of triiodothyronine on the absorption of these substances are dose dependently different. Obviously the thyroid hormone can influence the absorption of proline and digitoxin in both ways, increase or decrease. The behaviour of digitoxin different from that of chloramphenicol points to this drug making use of active mechanisms concerned in the absorption.

Animals↗
PubMed1978

Collagen metabolism in granulating wounds of rat skin.

Collagen metabolism in granulating wounds of rat skin was studied with biochemical, isotopic and electron microscopical methods. Deposition of collagen in rat skin wounds was not only the result of an increase in collagen synthesis but it was also caused by a decrease in collagen degradation. Our investigations showed significant differences in the collagen turnover at different times of wound healing. Decreased collagen catabolism at the early stages of wound healing contributed decisively to collagen accumulation in the wound area. At later stages, during wound contraction and remodelling of the scar, the rate of collagen degradation rose. The above-mentioned results are discussed in the context of general criteria of scar formation.

Animals↗
PubMed1978

[Therapy of Marchiafava-Micheli's disease: Remission under therapy with Lynestrenol (author's transl)].

The remission of a case of Marchiafava-Micheli under therapy with Lynestrenol is represented. The observation period is 16 months. The therapeutical purpose--stabilizing the red cell membrane by increasing the serum cholesterol concentration--is discussed by laboratory findings. Moreover the clinical picture and other common treatments against this disease are demonstrated by the example of this case.

Adult↗