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Biomedical subjects

V Ramalingaswami

Publications and source records attributed to V Ramalingaswami.

At least 37 records · Page 2Linked to original sources
PubMed1978

Epidemic of toxic hepatitis in India of possible mycotoxic origin.

An epidemic of liver disease, characterized by onset with high fever, rapidly progressive jaundice, and ascites occurred in a rural area of India. Several hundred people were affected and mortality was high. The epidemic was heralded by the appearance of similar features in the village dogs. Liver biopsy specimens from eight cases and autopsy material from one human case and two dogs were studied. Characteristic features were centrizonal scarring, hepatic venous occlusion, ductular proliferation and cholestasis, focal syncytial giant-cell tr-nsformation of hepatocytes, and pericellular fibrosis. Toxic quantities of aflatoxin B1 were found in samples of corn, the staple food grain of the people, that was obtained from the domestic food stores. The etiology of the disease could not be unequivocally established, but aflatoxins, perhaps in combination with other factors, may have been the cause.

Aflatoxins↗
PubMed1977

Study of an epidemic of jaundice, presumably due to toxic hepatitis, in Northwest India.

An epidemic of jaundice probably due to toxic hepatitis occurred in three adjoining districts of Northwest India during the period November and December, 1974. The dogs of the villages were affected first, then the human beings. Detailed clinical features, appropriate laboratory tests, and liver biopsies were studied. A retrospective epidemiological survey was carried out. The disease had a subacute onset starting with high fever, followed by rapidly progressive jaundice. Ascites appeared simultaneously and soon became quite massive. Hepatomegaly was recorded when ascites decreased. Liver function tests suggested cholestatic jaundice. The mortality rate in the hospital was 10%. Clinical features in dogs were similar, but mortality was almost 100%. Liver histology was characterized by (1) edema and collagenization of the central veins, never with thrombosis, (2) cholangiolar proliferation, (3) moderate to severe ballooning of the hepatocytes, (4) perisinusoidal fibrosis, (5) cholestasis, and finally, (6) cirrhosis with reverse lobulation. Etiology of this epidemic of hepatitis could not be unequivocally established. Critical analysis of the data suggests that some food toxin may have been a factor in the outbreak of this unusual epidemic of toxic hepatitis.

Adolescent↗
PubMed1976

Effect of vitamin A and undernutrition on the susceptibility of rodents to a malarial parasite Plasmodium berghei.

The ability of vitamin A deficient rats to resist infection with P. berghei was investigated. When 10 X 10(6) erythrocytes bearing the parasite/100 g body weight were given to the vitamin A protein energy undernourished rats, parasitemia developed in these animals at a faster pace than the controls. A high number (60% to 95%) of red blood cells (RBC) carrying the parasite were noticeable within 6 to 7 days after infection, at which time most animals in this group died. The pair-fed controls (protein-energy undernourished but supplemented with vitamin A) fared perceptibly better with an equivalent load of infection. Control ad libitum fed littermates were able to restrict the infection and neither high parasitemia nor death was noted in this group. Oral supplements of retinyl acetate to vitamin A deficient rats enabled the animals to recover from infection. A subclinical dose of 500 parasitized RBC given at an early stage of the vitamin A deficiency precipitated the deficiency symptoms at a faster rate and led to the development of higher order of parasitemia in these rats beginning from the 10th day after infection as compared to pair fed controls. The yield of glass adhering cells obtainable from peritoneal exudates was low in deficient rats. In vitro experiments further suggest a decrease in the capacity of the glass adhering peritoneal exudate cells in vitamin A deficient mice to clear the infection. This capacity was improved by addition of non glass adhering cells from sensitized control mice.

Animals↗
PubMed1975

Hepatitis-B virus and Indian childhood cirrhosis.

The surface and core componenets of hepatitis-B virus have not been detected in livers of patients suffering from Indian childhood cirrhosis using procedures such as immunoperoxidase, immunofluorescence, and orcein staining as well as electronmicroscopy. This finding, together with the other features of the disease, suggests that infection by this virus plays no significant role in the aetiology of Indian childhood cirrhosis.

Autopsy↗
PubMed1975

Protein deficiency in carbon tetrachloride-induced hepatic lesions.

The influence of protein deficiency on the hepatotoxicity of carbon tetrachloride (CCl4) was investigated in a group of rhesus monkeys. Animals fed a protein-rich diet served as controls. The results indicate that protein-deficiency protects the liver against acute hepatotoxicity of this drug. The protective effect is abolished if the animals are administered phenobarbital prior to the administration of CCl4. The protective action is due to a reduction, in protein deficiency, of the endoplasmic reticulum associated enzymes involved in hepatotoxicity of CCl4. Repeated administration of CCl4, which induces hepatic regeneration, resulted in disappearance of fat from periportal cells in protein-deficient animals. The regenerating cells (because of their better enzyme system) acquire "nutritional autonomy" and are thus able to synthesize adequate amounts of lipoproteins for mobilization of liver triglycerides.

Animals↗
PubMed1974

Lymphopoiesis in protein deficiency. Stathmokinetic and tritiated thymidine uptake studies of the mesenteric lymph node of the guinea pig.

In view of the depressed immunity in protein malnutrition, an assessment of the lymphoproliferative activity of the constantly stimulated mesenteric lymph node of the guinea pig was undertaken. A significant reduction of this activity was observed in protein deficiency. a) The germinal centers were reduced in number and size; new formation in the medulla was rarely seen. Lymphoid cells showed lowering of mitotic index and mitotic rate and prolongation of mitotic duration and turnover time. Nuclear labeling with (3)H-thymidine was focal and localized to the peripheral zone. b) Mitotic activity and nuclear labeling were less pronounced in the outer cortex and medulla and least in the paracortical area. Specific uptake of (3)H-thymidine paralleled the low labeling index. c) No appreciable reduction in the number of plasma cells in the medulla was observed. Serum gamma-globulin levels were not significantly altered, but albumin levels were consistently reduced. This was suggestive of preferential preservation of plasma cell activity in the malnourished host. d) There were significant lymphopenia and neutropenia with relative increase of neutrophils in the peripheral blood. This might indicate more severe involvement of lymphopoiesis than myelopoiesis in protein malnutrition.

Animals↗