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M Moreyra

Publications and source records attributed to M Moreyra.

5 recordsLinked to original sources

Computerized endoscopic surgical grasper.

We report a computerized endoscopic surgical grasper with computer control and a force feedback (haptic) user interface. The system uses standard unmodified grasper shafts and tips. The device can control grasping forces either by direct surgeon control, via teleoperation, or under software control. In this paper, we test an automated palpation function in which the grasper measures mechanical properties of the grasped tissue by applying a programmed series of squeezes. Experimental results show the ability to discriminate between the normal tissues of small bowel, lung, spleen, liver, colon, and stomach. We anticipate applications in telesurgery, clinical endoscopic surgery, surgical training, and research.

Endoscopes↗

Protein synthesis studies in skeletal muscle of aging rats. I. Alterations in nitrogen composition and protein synthesis using a crude polyribosome and pH 5 enzyme system.

The effect of aging on rat skeletal muscle protein synthesis was studied using a cell-free system. The activity of crude polyribosomes from hind-limb skeletal muscle was reduced by 40% in aged animals (22 to 24 months) and by 20% in the mature (12 months) animal compared with young (2 month) rats. In a poly Uridylic-acid-directed incorporation system the ribosomes from aged and mature animals showed a decrease in activity. Sucrose density gradient analysis also demonstrated a loss of heavy polyribosomes in aged and mature animals. The pH 5 enzyme fraction from aged and mature animals was less efficient than that from young rats in support of protein synthesis, suggesting a decreased activity of soluble factors. In conclusion, aging leads to a progressive decline in the efficiency of protein synthesis, associated with both the ribosome and soluble fractions of the cell.

Age Factors↗

Effect of testosterone on the rate of myofibrillar protein breakdown in castrated and adrenalectomized male rats measured by the urinary excretion of 3-methylhistidine.

Urinary output in N tau-methylhistidine (3-MeHis) was used to evaluate changes in myofibrillar protein breakdown rate in the skeletal muscles of castrated and adrenalectomized-castrated young male rats, and the response of breakdown to testosterone and corticosterone replacement. The castrated rats grew less well than intact control rats and excreted significantly less 3-MeHis. Administration of low and high doses of testosterone restored the weight of the levator ani of the castrated animals but failed to affect growth rate or 3-MeHis output. Although this might suggest that testosterone has an indirect effect on muscle turnover through changes in growth rate, this parallelism was not confirmed by studies on adrenalectomized-castrated rats. Adrenalectomy of castrated rats caused a further reduction in growth rate and in output of 3-MeHis, but administration of testosterone now reduced 3-MeHis output still further while stimulating growth. Treatment of the adrenalectomized-castrated rats with low doses of corticosterone increased growth modestly, while depressing 3-MeHis output, and again output of this metabolite was further reduced when testosterone was added to the treatment, although growth rate was unaffected. Finally, large doses of testosterone given to adrenalectomized-castrated rats receiving excessive amounts of corticosterone did not prevent the growth failure or the increased output of 3-MeHis due to the corticosteroid, though it appeared to reduce the magnitude of the response to corticosterone alone. It is concluded that the effects of testosterone on growth and on 3-MeHis output are not necessarily associated and that the functional status of the adrenal cortex modifies the response of myofibrillar breakdown rate to testosterone treatment.

Adrenalectomy↗

Interaction of thyroid status and diet on muscle protein breakdown in the rat, as measured by N tau-methylhistidine excretion.

The effects of thyroid status and of dietary protein and energy content on muscle protein breakdown have been compared in young rats, using urinary N tau-methylhistidine (3-methylhistidine; 3-Mehis) output as a measure of myofibrillar protein breakdown. Recently, thyroidectomized young rats receiving an adequate diet grew slowly and showed a reduction in 3-Mehis output, relative to the weight of their leg muscles. When the thyroidectomized rats were given 2-5 microgram thyroxine (T4) per 100 g body weight, output of 3-Mehis increased, even when growth was prevented by feeding a diet low in protein. This demonstrates that thyroid-status affects muscle protein breakdown through a mechanism other than via a change in growth rate. In confirmation of previous studies, administration of a diet low in protein to young rats prevented growth and reduced output of 3-Mehis relative to leg muscle weight. The reduction in protein breakdown is not likely to be due to reduced thyroid function, since the diet low in protein increased plasma total triiodothyronine (T3) levels. Furthermore, thyroidectomized rats fed the low-protein diet also underwent a decrease in output of 3-Mehis. In contrast to protein deficiency, a moderate dietary energy deficiency allowed some growth to occur, and output of 3-Mehis, relative to muscle mass, was not depressed. Nevertheless, total T3 concentration in the plasma of these animals was considerably reduced, indicating once more that total circulating thyroid hormone levels are not the only determinants of muscle protein breakdown. Finally, reduced plasma total T3 levels occurred in energy-deficient diets even in thyroidectomized rats receiving exogenous T4. This suggests that diet affects metabolism of the hormone independently of changes in secretory output from the thyroid gland.

Animals↗