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Biomedical subjects

M G Deo

Publications and source records attributed to M G Deo.

At least 73 records · Page 4Linked to original sources
PubMed1981

Implications of malnutrition in chemical carcinogenesis.

Epidemiological data indicate that life style, including dietary "imbalances", play a major role in etiology of human cancers. Although two thirds of the world population suffer from varying grades of protein-caloric malnutrition (PCM) today, no consistent pattern is found to be associated wih PCM both in man and laboratory animals. At the tissue level, depression of cellular proliferation by prolongation of DNA-synthetic phase is a characteristic lesion of PCM. Due to changes in liver mixed function oxidases, metabolism of drugs is affected. The cell-mediated immunity is depressed and there is a defective mobilisation of macrophages. These alterations would modulate carcinogenesis; some tend to enhance, while others inhibit tumorigenesis. The balance of evidence suggest that PCM is unlikely to have dominant modulating influence on carcinogenesis.

Adult↗
PubMed1981

Aflatoxin B1-induced injury in monkeys.

Short-term effects of small doses of aflatoxin (0.05 mg/kg of body weight twice a week) were studied in rhesus monkeys fed low-protein and high-protein diets. Animals on high- and low-protein diets without aflatoxin administration served as controls. There was no difference in weight gain, hemogram, serum protein levels, and liver function test results between aflatoxin-treated and control animals. However, morphological alterations in hepatocytes in the form of mild degenerative changes, focal areas of necrosis, and increased regenerative activity were seen in the aflatoxin-treated monkeys. Data on cell cycle analysis done by DNA content estimation through microfluorimetry on DNA-fluorescent, acriflavin-stained liver imprints revealed larger number of cells in the S and Gi2 phases in animals given aflatoxin. However, the changes in cell cycle, as well as in morphology, were more marked in the aflatoxin-treated, low-protein-diet group.

Aflatoxins↗
PubMed1980

Effects of undernutrition on the visually evoked responses in rats during development.

Effects of postnatal undernutrition on the maturation of the visually evoked responses (VERs) were investigated in rats. The VERs were recorded from the surface of the visual cortex in response to a flash of light. In the normal animals as age advanced, various components of the response appeared, their latencies shortened with an augmentation of their amplitude. The ability to follow repetitive stimulation at higher frequencies was also found to increase with age. In the undernourished rats, the appearance of the first positive wave (P1) was delayed, the latencies of P1, and the first negative wave (N1) were prolonged and the amplitudes were smaller as compared with their normal counterparts. These animals were unable to follow repetitive stimulation at higher frequencies. Though protein-calorie malnutrition retarded the ontogenetic maturation of the visual system, rehabilitation led to a significance "catch up".

Animals↗
PubMed1979

"Physiological" and cytotoxic cell death in protein deficiency. A study in developing cerebellum in rats.

Effects of undernutrition on natural ("physiological") and cytotoxic cell death due to X-irradiation was studied in developing cerebellum in rats. Undernutrition was induced right from birth by doubling the litter size. Animals reared in a litter of 8 served as controls. In order to get an idea of the relationship of cell death to phases of the cell cycle, the number of labelled dead cells, in the EGL of the fissure prima, was estimated, at time intervals following administration of 3HTdR in a group of 9-day-old rats. No differences were observed in the quantum of "physiological" cell death as well as in the rate of nuclear autolysis in the two groups. Undernutrition, however, prolonged the G2-M junction in animals X-irradiated with 200 rads. The kinetics of appearance of labelled dead cells suggested that irrespective of the diet the cells die immediately following mitosis, although the "decision to die" was taken at the end of S-phase. It is concluded that the reduction in cell number in the brain in undernutrition is not due to increased cell death.

Animals↗
PubMed1979

Adrenocortical function in experimental protein malnutrition.

Adrenocorticoid activity was investigated in experimentally induced protein malnutrition in Rhesus monkeys. Control studies were carried out in the same animals before inducing protein malnutrition. Plasma cortisol levels were elevated in the protein malnourished state. There was a total abolition of the diurnal rhythm of cortisol secretion. Fasting hypoglycemia was also observed in the protein malnourished state. It is concluded that increased adrenocorticoid activity and sustained steroidogenesis result from protein deficiency. Hypoglycemia may be an important stimulus, in addition to the metabolic stress imposed by the protein deprivation. The recognition of increased adrenocorticoid activity is important in a protein-deficient host, since the defense against infections might be impaired in such a situation.

Adrenal Cortex↗
PubMed1976

Undernutrition and the developing cerebellar cortex in the rat.

Undernutrition of the newborn rats, produced during the first 3 weeks by increasing the litter size and restricting the mother's diet, resulted in reduction of the body and brain weights of the experimental animals. One group of undernourished animals showed especially severe reduction of body and cerebellar weights. These animals, on the 10th postnatal day, had an immature cerebellar cortex corresponding to that of the 7th day postnatal control animals. The external granular layer persisted in the cerebellar cortex of the underweight animals until the 23rd day, while it disappeared by 20th day in the control animals. Mitotic activity was evident until the 21st postnatal day in these animals while it stopped in the normal animal by 16th postnatal day. There was no marked difference in the fine structure of the various cell types in the control and undernourished animals. Midsagittal tracings of the cerebellar cortex showed a reduced surface area in the undernourished animals, while the thickness of the external granular layer and molecular layer did not show any significant difference when compared to that of the control animals, thus showing a reduction in total cell number, but not per unit area. The normal morphological appearance of the cerebellar cortex in the underfed animals of higher weight probably indicates that these animals are adequately nourished in spite of the reduction in weight when compared to the control animals, which probably are overfed.

Animals↗
PubMed1976

Kinetics of mobilization of neutrophils and their marrow pool in protein-calorie deficiency.

Migration of marrow neutrophils under basal conditions and their mobilization, following subcutaneous implantation of cover slips, were investigated in groups of protein-deficient rats, using 3HTdR with sequential autoradiography of the peripheral blood smears. Animals fed a protein-rich diet served as controls. The pattern of appearance of labeled neutrophils in the blood was identical in the two groups under basal conditions. However, a higher percentag of labeled neutrophils appeared earlier in the blood following cover slip implantation in the deficient rats as compared to controls. The inflammatory exudate on the cover slips was low throughout the period of observation in deficient animals, with a delay in the appearance of monocytes. A pool of mature neutrophils resides in the bone marrow. It is proposed that in PCM there is atrophy of all neutrophil compartments, including that of the marrow pool, associated with a proportionate reduction in the efflux of cells from one compartment to another. This proportionate reduction in efflux would explain the normal kinetics of migration of neutrophils under basal conditions in the deficient rats in spite of a reduction in the marrow pool. On the other hand, in cover slip-implanted deficient rats, appearance of larger numbers of labeled neutrophils in the blood is attributed to a reduction in size of the marrow pool. This hypothesis is substantiated by the experiments in protein-deficient monkeys in which estimation of the marrow pool of neutrophils revealed a marked reduction in the deficient animals. It is further proposed that a diminuation of the marrow pool of neutrophils and retarded mobilization of cells at the site of inflammation are important mechanism responsible for the increased susceptibility of the malnourished host to infections.

Animals↗