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Biomedical subjects

J Miquel

Publications and source records attributed to J Miquel.

At least 55 records · Page 3Linked to original sources

On Physaloptera sibirica Petrow et Gorbunow, 1931 (Nematoda: Physalopteridae) parasitizing Iberian mammals.

Faunistic and morphological study of Physaloptera sibirica PETROW et GORBUNOW, 1931 (Nematoda: Physalopteridae), a nematode isolated in Spain from three mammal species: red fox, Vulpes vulpes (LINNAEUS, 1758) (Carnivora: Canidae), eurasian badger, Meles meles (LINNAEUS, 1758) (Carnivora: Mustelidae), and garden dormouse, Eliomys quercinus (LINNAEUS, 1766) (Rodentia: Myoxidae) in the Iberian Peninsula. Morphological features of cephalic and caudal regions of males are presented for the first time by SEM (scanning electron microscopy).

Animals↗

Depletion of cytosolic GSH decreases the ATP levels and viability of synaptosomes from aged mice but not from young mice.

The effect of glutathione depletion on the viability of freshly isolated synaptosomes from whole brain was investigated in young and aged mice. Aging did not influence the GSH and ATP levels and the viability of these synaptosomes. However depletion of glutathione caused by the cytosolic glutathione inhibitor diethyl maleate (1 mM) resulted in a significant decline, after 60 min of incubation, in ATP levels and viability in the synaptosomes from aged mice but not in those from young mice. When synaptosomes were incubated in the presence of the mitochondrial glutathione inhibitor ethacrynic acid (0.2 mM) there was a similar decline in glutathione, ATP levels and synaptosomal viability, both in young and aged mice. These results emphasize the relative importance of the cytosolic glutathione pool for the maintenance of the plasma membrane integrity in synaptosomes from aged mice.

Adenosine Triphosphate↗

N-acetylcysteine protects against age-related decline of oxidative phosphorylation in liver mitochondria.

Since it has been proposed that oxygen radical inactivation of key enzymes plays a critical role in cell aging, we have investigated the effects of a thiolic free radical scavenger on the oxidative phosphorylation enzymes of liver mitochondria from female OF-1 mice. At 48 weeks of age a control group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of N-acetylcysteine. A 24-week treatment resulted in a significant increase in the specific activities of complex I, IV and V in the hepatic mitochondria of the N-acetylcysteine-treated animals as compared to aged controls.

Acetylcysteine↗

Glucose deprivation increases aspartic acid release from synaptosomes of aged mice.

To investigate the possible existence of age-related changes in excitatory amino acid release in brain, and the influence of glucose deprivation on this process, we have determined the release of endogenous aspartate and glutamate from synaptosomes freshly isolated from the cerebrum of young (12 months old) and aged (24 months old) mice. We found that there are no age-related changes in the synaptosomal release of aspartic and glutamic acids. However, in the absence of glucose in the medium of incubation aspartate and glutamate release was higher in old than in young animals (P < 0.05, and P = 0.09 respectively). Our results suggest that the ability of cerebral synaptosomes to release glutamate and aspartate remains functionally intact in old cerebrum, but there is an age-dependent dysfunction in this process linked to energy metabolism disturbances.

Age Factors↗

Epidemiologic aspects and results of applying the TRISS methodology in a Spanish trauma intensive care unit (TICU).

OBJECTIVE: Analysis of epidemiologic aspects in a trauma intensive care unit (TICU) and assessment of predicted outcomes. DESIGN: Prospective study. Samples collected over a 2-year period. SETTING: A Spanish TICU at a tertiary care centre. PATIENTS: A group of 404 trauma patients. INTERVENTIONS: TRISS methodology was applied. MAIN RESULTS: Mean age was 35.8 +/- 17 years. Mortality was 19.6% over a median ISS = 17. Blunt trauma was more frequent than penetrating trauma (90.1% versus 9.9%). Car accident was the major aetiological factor (32.4%) and the highest mortality was among struck pedestrians (26.4%). The cranial region showed the highest incidence of lesion (57.9%) and the neurological complications on stage were the commonest reported on the discharge forms (49.7%). Mechanical ventilatory support (MVS) was applied in 53.2% of patients, with a relative mortality of 35.8%. Survivors differed significantly from nonsurvivors in terms of age, Glasgow Coma Scale rating, RTS, ISS, TRISS, stage and number of complications reported. The risk factors found to be associated with mortality were injury to cranial and abdominal/pelvic regions and age over 65. The TRISS total accuracy was 0.88 (sensitivity = 0.67; specificity = 0.93; area under the ROC curve = 0.85 +/- 0.03). Forward stepwise logistic regression analysis selected age, ISS and RTS as the best predictors of survival. When our TRISS results were compared with those anticipated on the basis the MTOS, an injury severity mismatch appeared (z = 0.02; M = 0.78). CONCLUSIONS: We found a 19.6% mortality in the TICU. Cranial and abdominal/pelvic injury and age over 65 were the main risk factors on admittance. Clinically, we finally agreed with the majority of TRISS outcome predictions. However, we could not statistically validate the apparent clinical goodness of the TRISS methodology.

Adult↗

Impairment of mitochondrial oxidative phosphorylation in the brain of aged mice.

To elucidate the role of mitochondrial oxidative phosphorylation in neuronal aging, we have studied the activity of the respiratory complexes in the brain of young, adult and old mice. In synaptic mitochondria, we found a significant decrease in complexes IV (29%, P < 0.001) and V (21%, P < 0.01) in old as compared with adult mice. Nonsynaptic mitochondria also showed a senescent decrease in complexes I (15%, P < 0.01), II + III (34%, P < 0.01) and IV (17%, P < 0.01) activities. These findings suggest a dysfunction in mitochondrial oxidative phosphorylation in brain aging.

Aerobiosis↗

Age-related changes in glutathione and lipid peroxide content in mouse synaptic mitochondria: relationship to cytochrome c oxidase decline.

To elucidate the contribution of lipid peroxides and glutathione to brain aging, we have carried out a comparative study of their contents in synaptic mitochondria from young (10-week-old), adult (24-week-old), and senescent (72-week-old) mice. In synaptic mitochondria, there is a significant decline in lipid peroxide content (P < 0.01) and cytochrome c oxidase activity (P < 0.001) in senescent as compared to adult and young mice. By contrast, glutathione concentration showed an increase in senescent (P < 0.05) in comparison to the other age groups. Moreover, there was a significant inverse correlation between age and lipid peroxide content (r = -0.5, P < 0.001) or cytochrome c oxidase-specific activity (r = -0.58, P < 0.001). We suggest that this age-dependent decrease in lipid peroxide content in synaptic mitochondria may be the result of an age-related decline in the activity of the electron transport chain, with concomitant decrease in oxyradical production, in the senescent organelles.

Aging↗

Recent approaches in the analysis of weightlessness effects on arthropod development.

The concept of Biological Development refers to the extremely complex process by which every biological organism reproduces starting from a huge single cell, the fertilized egg. It includes all aspects of cellular and intercellular structure and function. In spite of many recent advances, especially at the molecular and genetical level, we are still far from fully understanding the details and mechanisms at work in developmental systems. It is even unclear what physical mechanisms are used by the different molecular components resulting in the emergence of these higher levels of organization. Newman and Comper, have extensively discussed the "generic" physical forces potentially involved in pattern formation, arguing that among others, gravitational effects could be involved in the production of cytoplasmic, tissue and extracellular matrix components rearrangements playing a role in morphogenesis. Although plagued with the problem of being a very weak force, specially at the tiny dimensions of cells, gravity is one of the "generic" physical forces that have been continuously operating on biological organisms during evolution. Few scientists would argue against the idea that at least in the early times of evolution, gravity could have been involved in shaping the spatial inhomogeneities behind the initial phases of development.

Animals↗

Stimulation by the antioxidant thioproline of the lymphocyte functions of old mice.

Diet supplementation with thioproline (thiazolidine-4-carboxylic acid), an intracellular sulfhydryl antioxidant and free radical scavenger, may slow the aging process of metazoans and prolongs their life span. In the present experiment Swiss mice fed thioproline (0.07%, w/w) from 13 to 22 months of age were used. Six- and 22-month-old mice fed standard diet were used as controls. Two important functions of lymphocytes, the proliferative response to the mitogen Concanavalin A (Con A) and the mobility, both spontaneous and directed to a chemoattractant gradient (chemotaxis), were analyzed in lymphocytes from axillary nodes, spleen and thymus. Mobility and chemotaxis were studied by Boyden's technique, using filters of 3 microns pore diameter, 3 h of incubation and fmet-leu-phe at 10(-8) M as chemoattractant. The proliferative response was estimated as 3H-thymidine incorporation in lymphocytes incubated for 72 h in the presence of Con A (1 and 5 micrograms/ml). The results show a decrease in mobility, chemotaxis and lymphoproliferative response in old mice in comparison to adults. However, a significant increase in these functions was observed in old mice fed thioproline. The advantage of using this antioxidant for immunostimulation during aging, a stage of life characterized by a decreased immune response, is discussed.

Aging↗

Oxygen-induced mitochondrial damage and aging.

Although the views of Harman and Gerschman provide a reasonable explanation for many of the effects of aging, they fail to explain why many cell types, from amoebae to mammalian spermatogonia, do not show a time-related involution, while other cells (especially the neurons) change with age. We feel that a better understanding of senescence (from the molecular to the organ and organismic levels) can be gained by integrating the free radical theory of aging with the classic concepts of Minot and Pearl on the role of cell differentiation and metabolic rate in, respectively, triggering and pacing senescence. In agreement with the above, we maintain that aging is the non-programmed but unavoidable "side effect" of oxy-radical damage to the membrane and genome of the mitochondria of irreversibly differentiated cells. If oxy-radical damage to mtDNA occurs, it will block the rejuvenation of the mitochondrial population by the process of organelle division, thus leading to bioenergetic decline and cellular death.

Aging↗

Changes with aging and physical exercise in ascorbic acid content and proliferative response of murine lymphocytes.

Ascorbic acid content and lymphoproliferative response to phytohemagglutinin were measured in lymphocytes from axillary nodes, spleen and thymus of young (15 +/- 2 weeks) and old (60 +/- 5 weeks) BALB/c mice. Ascorbic acid content in lymphocytes from spleen and thymus was found to be significantly higher and the lymphoproliferative response in the three immunocompetent organs significantly lower in old mice as compared to young mice. Moreover, young and old BALB/c mice were required to maintain a swimming activity until exhaustion (exhaustive exercise) or 90 min of swimming each day for a total of 20 days (continuous exercise). In both young and old mice the stress produced by exhaustive exercise and confirmed by the existence in serum of significantly increased levels of corticosterone compared to controls, caused a significant decrease in ascorbic acid content as well as in lymphoproliferative response. Continuous exercise, characterized by the presence in serum of significantly decreased levels of corticosterone compared to controls, produced the most significant decrease in ascorbic acid content from young and old murine lymphocytes. Moreover, this exercise resulted in a significant increase in lymphoproliferative response. Our results suggest that aging results in an increase in the ascorbic acid content of lymphocytes accompanied by a decline in the lymphoproliferative response in old BALB/c mice.

Aging↗

Effect of aging on metabolic zonation in rat liver: acinar distribution of GSH metabolism.

The effect of age on the glutathione antioxidant system and its acinar distribution in rat liver was studied. GSH/GSSG ratio in blood and liver was lower in old than in young rats. Hepatic glutathione peroxidase and glutathione S-transferase activities were higher in old than in young rats, whereas hepatic gamma-glutamyl transpeptidase activity was lower in old than in young rats. Glutathione reductase and glucose-6-phosphate dehydrogenase activities did not change with age in rat liver. Total glutathione levels and glutathione peroxidase activity were higher in periportal than in perivenous areas of young rats, but this heterogeneous distribution did not occur in old rats. No change with age was found in hepatic zonation of glutathione reductase and glucose-6-phosphate dehydrogenase.

Aging↗

Microgravity effects on Drosophila melanogaster development and aging: comparative analysis of the results of the Fly experiment in the Biokosmos 9 biosatellite flight.

The results are presented of the exposure of Drosophila melanogaster to microgravity conditions during a 15-day biosatellite flight, Biokosmos 9, in a joint ESA-URSS project. The experimental containers were loaded before launch with a set of Drosophila melanogaster Oregon R larvae so that imagoes were due to emerge half-way through the flight. A large number of normally developed larvae were recovered from the space-flown containers. These larvae were able to develop into normal adults confirming earlier results that Drosophila melanogaster of a wild-type constitution can develop normally in the absence of gravity. However, microgravity exposure clearly enhances the number of growing embryos laid by the flies and possibly slows down the developmental pace of the microgravity-exposed animals. Due to some problems in the experimental set-up, this slowing down needs to be verified in future experiments. No live adult that had been exposed to microgravity was recovered from the experiment, so that no life span studies could be carried out, but adult males emerged from the recovered embyros showed a slight shortening in life span and a lower performance in other experimental tests of aging. This agrees with the results of previous experiments performed by our groups.

Aging↗

An update on the mitochondrial-DNA mutation hypothesis of cell aging.

Our electron microscopic study of aging insects and mammals suggests that metazoan senescence is linked to a gradual process of mitochondrial breakdown (and lipofuscin accumulation) in fixed postmitotic cells. This led us to propose in the early 1980s an oxyradical-mitochondrial DNA damage hypothesis, according to which metazoan aging may be caused by mutation, inactivation or loss of the mitochondrial genome (mtDNA) in irreversibly differentiated cells. This extranuclear somatic gene mutation concept of aging is in agreement with the fact that mtDNA synthesis takes place at the inner mitochondrial membrane near the sites of formation of highly reactive oxygen species and their products. Mitochondrial DNA may be unable to counteract the damage inflicted by those by-products of respiration because, in contrast to the nuclear genome, it lacks excision and recombination repair. Since mtDNA contains the structural genes for 13 hydrophobic proteins of the respiratory chain and ATP synthase as well as mitochondrial rRNAs and tRNAs, damage to this organellar genome will decrease or prevent the 'rejuvenation' of the mitochondria through the process of macromolecular turnover and organelle fission. Thus deprived of the ability to regenerate their mitochondria, the fixed postmitotic cells will sustain a decrease in the number of functional organelles, with resulting decline in ATP production. At higher levels of biological organization, this will lead to a loss in the bioenergetic capacity of cells, with concomitant decreases in ATP dependent protein synthesis and specialized physiological function, thus paving the way for age related degenerative diseases. The above concept is supported by a wealth of recent observations confirming the genomic instability of mitochondria and suggesting that animal and human aging is accompanied by mtDNA deletions and other types of injury to the mitochondrial genome. Our hypothesis of mtDNA damage is integrated with the classic concepts of Weissman and Minot in order to provide a preliminary explanation of the evolutionary roots of aging and reconcile the programed and stochastic views of metazoan senescence.

Animals↗