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Biomedical subjects

J J Vitale

Publications and source records attributed to J J Vitale.

At least 37 records · Page 2Linked to original sources
PubMed1976

Augmentation of ethanol absorption by mono- and disaccharides.

Assessment of the influence of nutritional substrates on the disposition of ingested ethanol from the blood requires, first, an understanding of the influence that these may exert upon ethanol absorption from the gastrointestinal tract. In this report, the effects of various carbohydrates on the intestinal absorption of ethanol were studied. When carbohydrates (50 mM) were perfused simultaneously with ethanol (50 mM) in vivo in the rat small bowel, ethanol absorption increased up to 34% (P less than 0.005) above controls receiving ethanol alone. Of the monosaccharides, fructose, 3-O-methylglucose, glucose, or galactose added to an ethanol perfusate, only glucose or galactose increased ethanol absorption over control animals receiving ethanol alone. Of the disaccharides tested, sucrose and maltose, but not lactose, enhanced ethanol absorption. Addition of varying concentrations of maltose to an ethanol perfusate augmented ethanol absorption in a direct proportion to the quantity of glucose absorbed, rather than to the quantity of maltose hydrolyzed. Augmentation of ethanol absorption by carbohydrates appears to be dependent upon sugar-active transport. Ethanol, dissolved in intraluminal water, may cross the mucosa in water absorbed during sugar-active transport. This quantity of ethanol is absorbed in addition to that which normally crosses the mucosa by diffusion down its concentration gradient.

Animals↗
PubMed1976

Delayed erythropoiesis in irradiated rats grafted with syngeneic marrow: effects of cytotoxic drugs and iron-deficiency anemia.

Erythropoiesis in spleens of lethally irradiated Lewis rats grafted with 4-35 X 10(6) syngeneic marrow cells was inhibited or delayed during the test period of 5 days; this was in marked contrast to observation in irradiated mice. The mechanism of this inhibition was the subject of this study. Pretreatment of recipients 9 days prior to irradiation with the cytotoxic drugs cyclophosphamide (CY), busulfan (BUS), or dimethylmyleran (DMM), or the induction of iron deficiency with anemia in recipients reversed this delayed erythropoiesis. However, neither iron-deficiency anemia nor pretreatment with BUS or DMM affected the ability of irradiated recipients to reject 20 to 50 X 10(6) allogeneic marrow cells. The administration of commercial preparations of erythropoietin to hosts stimulated erythropoiesis moderately. However, proliferation of syngeneic marrow cells was not enhanced when infused into lethally irradiated Spontaneous Hypertensive (SH) inbred-strain rats which have high levels of endogenous erythropoietin. Finally, plasma from irradiated rats treated with phenylhydrazine to produce severe anemia was rich in erythropoietin but failed to stimulate erythropoiesis in the cell transfer system. Two hypotheses are considered: (1) Irradiation inhibits the secretion of a factor (not erythropoietin) responsible for initiating early stages in differentiation of transplanted stem cells; iron-deficiency anemia and cytotoxic drugs stimulate the secretion of this factor. (2) Normal rats secrete a factor which suppresses erythropoiesis; iron-deficiency anemia and cytotoxic drugs inhibit the production or function of this factor. Cellular rather than humoral factors may by involved.

Anemia, Hypochromic↗
PubMed1975

Alcohol and alcohol-related deficiencies as carcinogens.

From the available evidence, alsohol ingestion per se does not appear to be carcinogenic. While alcoholism constitutes a major and serious social problem, it is not clear to what extent it constitutes a major health problem. We suggest that excessive alcohol ingestion coupled with a nutritional deficiency or some other insult (e.g., smoking) may be carcinogenic. Alcohol and/or several nutritional deficiencies usually associated with alcoholism have been shown to be immunosuppressive. The relationship between immunoincompetency and neoplasia has long been appreciated, and the exact role that alcohol and/or nutritional insults have in this relationship requires further investigation.

Alcoholism↗
PubMed1975

Possible role of nutrients in neoplasia.

The relationship between cancer and diet is supported by epidemiological evidence suggesting that diet is a factor in the development of cancer of various organs including the esophagus, stomach, liver, and large bowel. The role of depressed immunocompetency, especially during critical periods of growth and development, is stressed as a possible important consequence of nutritional insults leading to carcinoma. Study of the relationships among nutritional factors, host-defense mechanisms, and carcinogens to carcinogenesis is significant since, theoretically, manipulation of diet could suppress or prevent chemically induced cancers. The distinction should be emphasized, however, between "nutrients," those elements of one's intake that are essential because the body is unable to synthesize them de novo, and "diet," which refers to everything that is ingested. It is the components of diet, chemicals in particular, that are most convincingly implicated as carcinogens, while it is doubtful that nutrient deficiencies or excesses have a direct causal relationship with the onset or development of cancer. Rather, nutrition probably exerts its carcinogenic effects indirectly; nutrients possibly enhance chemical carcinogenesis multifactorially by mechanisms linked to their ability to: (a) act as carriers of carcinogens or their precursors; (b) alter intestinal flora so that carcinogenic reactions are facilitated; (c) enhance levels and reactivity of cocarcinogens; (d) influence absorptive properties or morphology of tissues so that carcinogenic activity is enhanced; and/or (e) modify host-defense mechanisms that normally protect the organism.

Africa↗