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Biomedical subjects

R L Gross

Publications and source records attributed to R L Gross.

At least 55 records · Page 3Linked to original sources
PubMed1978

Inability of vitamin A deficiency to alter benzo(a)pyrene metabolism in Syrian hamsters.

Syrian golden hamsters were placed on a control or vitamin A-deficient diet. When their serum vitamin A content was significantly reduced, i.e., to less than 10% of controls, the hamsters were killed and lung aryl hydrocarbon hydroxylase activity and metabolism of benzo(a)pyrene were determined. The benzo(a)pyrene metabolite profile was similar with control and A-deficient systems, and only few quantitative differences were noted. Addition of beta-retinyl acetate to the in vitro incubations did not substantially affect benzo(a)pyrene metabolism.

Animals↗
PubMed1977

Naturally occurring toxic substances in foods.

Numerous chemical toxins, including normal components of natural foods, e.g., mycotoxins, and toxic chemicals as contaminants such as pesticides, fertilizers, food additives, and preservatives, which are potentially toxic to humans, are discussed. Potential toxicity, the hazard to man represented by most of these chemicals, may be low because the concentration in food may be low. The gap in our knowledge of long-term effects makes rational decisions as to allowable levels of these substances a major problem. On the other hand, nitrosamines and aflatoxins are toxins for which there exists a voluminous literature documentaing extreme biologic activity in experimental animals and indirect evidence for activity in man. Epidemiologic evidence has linked them to human cancers, and because of increasing evidence of long-term human exposure to these toxins either as inadvertent contaminants during food preparation or as the metabolites of mycotic infestation this possible hazard demands intensive investigation. An exhaustive review of data from epidemiologic surveys in various parts of the world, as well as from long-term laboratory studies, represents an impressive start in this direction.

Aflatoxins↗
PubMed1975

Abnormal spontaneous rosette formation and rosette inhibition in lung carcinoma.

Fifty-five children with CID and known ADA status were studies at a workshop held in Albany, New York. Erythrocyte ADA determinations were performed in 22 of the 55 patients, 13 of whom were ADA negative. The ADA defect appears to be transmitted as an autosomal recessive trait. Some patients with CID and ADA deficiency have characteristic radiologic abnormalities of the skeleton, which are not found in other illnesses. The thymus glands of all patients with CID and ADA deficiency who could be examined have evidence of thymic involution manifested by presence of Hassall's corpuscles and differentiated germinal epithelium; this is in contrast to "classic" thymus findings in CID with normal ADA. Adenosine deaminase probably plays an important, although as yet undefined, role in lymphocyte development and/or function. The deficiency of ADA in CID is the first enzyme defect observed in a deficiency disease of specific immunity.

Aged↗
PubMed1975

In vitro immunological studies on East African cancer patients. II. Increased sensitivity of blood lymphocytes from untreated Burkitt lymphoma patients to inhibition of spontaneous rosette formation.

Frozen aliquots of peripheral blood mononuclear cells from patients with Burkitt's lymphoma (BL) at various stages of the disease have been compared with samples from East African children who were healthy or who suffered from non-malinant disorders. Using the sheep-cell rosette test (which is believed to identify T-lymphocytes), we found a significant reduction in the proportion of rosette-forming cells (RFC) in the samples from untreated BL patients. After reduction of remission the difference between BL patients and controls was abolished. Rosette formation was more readily inhibited by anti-lymphocyte globulin (ALG) in samples from untreated BL patients than in controls. On induction of remission the rosette inhibition curve shifted towards the control values. The findings are compatible with the presence, in untreated BL, of a circulating factor which impairs the capacity of T-lymphocytes to form rosettes with sheep erythrocytes. It remains to be established whether the functional capacity of T-cells to protect the host against tumour proliferation is also impaired.

Africa, Eastern↗
PubMed1975

In vitro immunological studies on east african cancer patients. III. Spontaneous rosette formation by cells from Burkitt lymphoma biopsies.

Spontaneous rosette formation was observed in eight out of nine Burkitt lymphoma biopsies. These were examined fresh and/or after culture in vitro for up to 48 h. The percentage of rosettes varied from 3.7% to 38%. There was a tendency for the percentage of rosettes to increase with time in tissue culture. It is suggested that the rosette-forming cells are T-lymphocytes infiltrating the tumour and functioning as a host defence mechanism against the proliferating tumour cells.

Africa, Eastern↗
PubMed1975

Depressed cell-mediated immunity in megaloblastic anemia due to folic acid deficiency.

Cell-mediated immunity has been studied in patients with 1) megaloblastic anemia of folic acid deficiency, 2)megaloblastic anemia of pregnancy, or 3) iron-deficiency anemia. Using dinitrochlorobenzene skin tests, phytohemagglutinin-stimulated lymphocyte transformation, and rosette inhibition by antilymphocyte globulin, we have shown that cell-mediated immunity is depressed in megaloblastic anemia due to folate deficiency; this depression was reversed by folate treatment. Cell-mediated immunity was not impaired by iron-deficiency anemia. Suggested interactions between iron deficiency and folate metabolism were not clarified by these studies.

Adolescent↗