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Biomedical subjects

P M Daniel

Publications and source records attributed to P M Daniel.

At least 19 recordsLinked to original sources
PubMed1987

Diabetes mellitus in the rat: diminution in the number of cells in the thymus and of lymphocytes in the blood.

In diabetic rats there is a rapid fall in the weight of the thymus with a great loss in the numbers of thymocytes. In this paper we show that there is also a marked diminution in the number of lymphocytes in the peripheral blood, although the numbers of neutrophils and monocytes are not affected. Since the thymus is thought to be the site in which T-lymphocytes develop, it is suggested that the paucity of lymphocytes in the peripheral circulation reflects the loss of cells from the thymus. The diminution in the number of circulating lymphocytes in diabetes may account for the liability of diabetics to suffer severely from infections.

Animals↗
PubMed1986

The influx of ascorbic acid into the rat's brain.

The influx of [14C]ascorbic acid into the rat's brain through the cerebral capillaries was measured by the steady-state initial-rate technique. Ascorbic acid was found to pass through the capillaries by a carrier-mediated process and by simple diffusion. The carrier system was found to have an apparent Vmax of 1.2 nmol . min-1 . g-1 of cerebral tissue and a Kt of 125 microM. The apparent constant of transfer, Kd, of the diffusional component was 0.98 microliter. min-1 . g-1. The contribution of the cerebral capillaries to the movement of ascorbic acid into the brain is discussed and was found to be the major route of entry into the brain for this vitamin.

Animals↗
PubMed1985

Atrophy of the thymus in rats rendered diabetic by streptozotocin.

The thymus atrophied rapidly in rats rendered diabetic by a single injection of streptozotocin. The weight of the gland was reduced to one-fifth of its original weight within three weeks. Histologically there was a great loss of cortical thymocytes and a marked increase in mast cells lying in the thickened fibrous tissue. These findings may have a bearing on the state of immune deficiency observed in animals with diabetes induced by streptozotocin.

Animals↗
PubMed1984

The effects of fasting on core temperature, blood glucose and body and organ weights in rats.

Male Wistar rats of about 300 g body weight were fasted from 1 to 7 d. They were weighed and had their temperature taken daily. At the end of the experimental period, they were anaesthetized and blood was taken for measurement of the glucose content. The animals were killed and various organs were taken and weighed. Over the first 24 h there were striking reductions in body weight, core temperature and level of blood glucose. Throughout the succeeding days of fasting, there was a gradual decrease in body weight and core temperature, while the level of the blood glucose was maintained at about 3 mmol X l-1. The decrease in body weight and core temperature was matched by the weight loss of the liver and skeletal muscles. The heart and the kidney and spleen were not affected over the first day, but thereafter their weight declined steadily. The brain, the testes and the lungs retained their mass throughout.

Animals↗
PubMed1982

The pathogenesis of transmissible spongiform encephalopathy: an ultrastructural study.

The brains of 9 spider monkeys, inoculated intracerebrally with brain suspension from kuru patients and of 3 normal control monkeys have been studied. All the animals were killed by perfusion with fixative, 8 during early incubation (ranging from 2 to 40 weeks) when healthy and free from neurological signs, one after 122 weeks when the disease was fully established. The most striking feature seen in every brain between the incubation times of 4 and 40 weeks was the formation of multilaminated membranes (ACPMs). These affected stretches of two apposed, mostly neuronal, plasma membranes over variable distances and created the impression of complex ribbon-or cord-like junctions. Their number varied with the length of incubation, reaching a peak at 13 weeks and declining thereafter. ACPMs were found throughout the grey matter, but they were most numerous in phylogenetically older regions of the brain, regions which also show the severest lesions in human kuru. It is suggested that ACPMs are initially due to an excessive synthesis of some membrane constituent by the perikaryon and various possibilities for their genesis are discussed. The hypothesis is advanced that they may be due to the reactivation of embryonic growth mechanisms and represent abortive junctions which, being formed in mature neurons, take a rather bizarre shape. Other changes such as the formation of somatic spines, an excessive number of dendritic spines including a high proportion with long tortuous necks, and the presence of binucleated neurons and numerous growth cones, point to the similarly immature pattern and would support this hypothesis. The material provided ample evidence that ACPMs, which can occupy as much as 26 per cent of a dendritic surface, give rise to intracytoplasmic vacuoles, which may therefore be regarded as secondary to a primary change in the permeability of the plasma membrane at the site of ACPMs. Individual single vacuoles could often build up into complex soap-bubble-like arrays, which were interpreted as the ultrastructural equivalent of histological status spongiosus. There is some evidence that the development of status spongiosus in other transmissible spongiform encephalopathies follows the same pattern.

Animals↗
PubMed1981

The effect of insulin upon the influx of tryptophan into the brain of the rabbit.

1. The effect of hyperinsulinaemia upon the influx of tryptophan into the brain was determined. A raised level of insulin was maintained in the circulation of rabbits for periods of up to 120 min by means of a continuous, programmed intravenous injection of the hormone, given by an electronically controlled variable-drive syringe. A similar, appropriately programmed, intravenous injection of glucose, given simultaneously with the insulin, maintained the concentration of the blood glucose within normal limits throughout each experiment, so that the results were not vitiated by the development of hypoglycaemia. 2. Raised levels of insulin in the blood affect the supply of tryptophan to the brain in two opposing ways: (a) by increasing the binding of tryptophan to the albumin in the blood, thereby reducing the level of the free tryptophan in the circulation by about a half, which would decrease the influx of tryptophan into the brain; (b) by simultaneously reducing the levels in the blood of six or more of the amino acids which compete with tryptophan for transport carriers into the brain, which would increase the influx of tryptophan. The net result of these two opposing effects is that insulin causes only a slight increase in the influx of tryptophan into the brain. 3. To account in quantitative terms for the effect of insulin upon the influx of tryptophan into the brain it proved necessary to make one assumption. This assumption was that a predictable proportion of the tryptophan which is loosely bound to blood albumin is being stripped off this protein by the transport carrier located on the luminal surface membranes of the endothelial cells during the passage of the blood through the cerebral capillaries. If this assumption is accepted the work reported here explains adequately the effect of insulin on the influx of tryptophan into the brain.

Amino Acids↗
PubMed1980

Factors affecting the supply of glucose to the heart of the rat, in vivo.

1. The influx of glucose into the heart of intact, living, anaesthetized rats was measured when the levels of insulin the blood were (a) low (as a result of fasting), (b) normal, and (c) high (as a result of injecting insulin). The findings showed that the transport of glucose into cardiac cells is carrier-mediated and is strongly insulin-independent. 2. The major barrier to the supply glucose to the heart from the circulating blood is at the surface membrane of the cardiac cells, rather than at the endothelium of the cardiac capillaries. 3. The extracellular space of the heart was measured and was found to be approximately 25% of the cardiac tissue. 4. During life, glucose, as well as its analogue, 3-O-methylglucose passes across the membranes of the cells of the heart by means of a transport system which is strongly dependent upon insulin and appears to be carried-mediated. A likely explanation for the effect of insulin is that it increases considerably the affinity of the transport carrier for glucose. Saturation of the carrier takes place when the levels of insulin and of glucose in the blood are high. However, when the concentration of insulin is low, e.g. during a fast, the affinity of the carrier for glucose is reduced so that saturation cannot be demonstrated. 5. It is suggested that the low level of insulin that is found in the blood in the early morning, which is due to the night fast, may lead to the cardiac dysfunction which often develops at that time.

Animals↗
PubMed1979

The effects of murine muscular dystrophy on the metabolic and homeostatic functions of the skeletal muscles.

The maintenance of blood glucose is largely dependent on the ability of the skeletal muscles to regulate the supply of amino acids for hepatic glucose production. This study shows that when muscles are damaged in muscular dystrophy the mechanisms by which this control is exerted are impaired. In normally fed congenitally dystrophic mice the blood glucose level was raised and there were significant reductions of the levels of the principal gluconeogenic amino acids in the circulation. This was a result of abnormal exchange of amino acids between the dystrophic muscles and the blood, apparently due to the use of amino acids to a considerable extent in place of glucose for energy metabolism within the diseased muscles. When dystrophic animals were fasted, further reductions in the levels of amino acids in the circulation, to abnormally low values, were caused by an increased use of these amino acids by the liver for gluconeogenesis. Although the reason for the excessive metabolism of amino acids in dystrophic muscle is not clear, such changes will favour muscle protein breakdown, and a stress such as fasting will further aggravate the process of muscle wasting by depleting still further the pool of amino acids in the body.

Amino Acids↗
PubMed1979

A comparative study of the portal vessels connecting the endocrine and exocrine pancreas, with a discussion of some functional implications.

We have examined the pattern of the capillaries of the pancreas in rabbits, rats, mice, guinea-pigs, cats and baboons, using arterial and venous injections of Berlin blue. In all these species we found extensive, direct connexions between the capillary beds of the islets and the exocrine tissue of the gland, forming a highly developed portal system. Some of the functional implications of these vascular connexions are discussed, particularly the influence of the islet hormones insulin, glucagon and somatostatin upon the exocrine cells.

Animals↗