Taste loss associated with captopril treatment.
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Biomedical subjects
Publications and source records attributed to A Anderson.
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Methods are described for the analysis of the anti-coccidial drug, halofuginone, at concentrations of 3 ppm in chicken feed, using gas-liquid chromatography and high-performance liquid chromatography. Both methods are based on ethyl acetate extraction, partition into hydrochloric acid and purification and concentration using XAD-2 column chromatography. The precision and accuracy of both methods is given.
Melatonin was detected in the circulation of the near-term rhesus monkey (Macaca mulatta) and baboon (Papio papio) fetus. We determined whether the source could be the mother by studying placental transfer of melatonin in the rhesus monkey. When [3H]melatonin was administered i.v. to the mother it promptly appeared in the fetal circulation; the rates of disappearance of [3H]melatonin in the maternal and fetal circulations were parallel. The rapid decrease in circulating [3H]melatonin was associated with a rapid accumulation of [3H]melatonin-metabolites in the maternal and fetal circulations. Although the pattern of appearance of metabolites was similar in both circulations, relatively less [3H]melatonin-metabolites appeared in the fetal circulation. Acute changes in total maternal plasma melatonin, experimentally produced by giving a 20 min infusion of melatonin, were rapidly reflected in the fetus. This suggests that a daily rhythm in maternal melatonin would generate a similar rhythm in the fetus. The fetal monkey pineal was found to have the two enzymes necessary for the conversion of serotonin to melatonin. It is, however, not known whether fetal melatonin synthesis is rhythmic or the extent to which it could contribute to circulating melatonin levels at this or earlier stages of gestation.
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An immune binding technique was used for measuring the effects of certain amino acids on the rate of insulin biosynthesis. [13H]phenylalanine served as the radioactive precursor for insulin synthesized by isolated mouse pancreatic islets. L-Leucine was found to stimulate the insulin biosynthesis and this effect was observed already at a physiologic concentration in contrast to the much higher concentrations needed to stimulate insulin secretion in vitro. Furthermore, it was found that 2-aminonorbornane-2-carboxylic acid and alpha-ketoisocaproic acid shared with glucose and L-leucine the ability to stimulate insulin biosynthesis. In contrast, L-alanine, L-arginine adn D-leucine had no stimulatory effect in the absence of glucose, while in the presence of 5 mM glucose L-arginine decreased and L-alanine increased the incorporation rate of tritiated phenylalanine. The fact that many of those compounds which stimulated insulin biosynthesis have also been shown elsewhere to be metabolized by the B-cells supports the view that the rate of insulin biosynthesis may be substrate dependent.
The glucose-stimulated insulin release of pancreatic islets isolated either from normal mice or from mice with the obese-hyperglycemic syndrome (genotype ob/ob) was inhibited by somatostatin in the concentration range 10(-2) - 10(-4) mM. Islets prepared from the obese-hyperglycemic mice appeared most sensitive and there was a strong inhibitory action on the insulin release irrespective of whether the islets were exposed to somatostatin directly after isolation or after five days in tissue culture. There was, however, no effect of somatostatin on the glucose-stimulated insulin biosynthesis of the mouse islets. Neither was there an effect on the insulin biosynthesis of isolated islets from three days old rats, despite a previous report to the contrary. It is concluded that somatostatin does not affect the insulin biosynthesis of isolated islets at concentrations which inhibit insulin release.
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The protective effect of enternal and parenteral immunization with cholera toxin antigen against experimental cholera in rabbits was studied by using the small-bowel loop technique. Subcutaneous injection of crude toxin as well as purified toxin or toxoids gave rise to significant protection against toxin challenge. The enhanced resistance to toxin was found to correspond to a many-fold higher magnitude of protection against challenge with live vibrios. In the primary response the protection increased during the first month. Booster immunization gave rise to a further increased immunity which, however, declined rapidly. Multiple oral or repeated intraintestinal antigen administrations also induced protective antitoxic immunity although of less magnitude than that obtained by parenteral immunization. Enteral and, to a lesser extent, parenteral immunization gave rise to increased antitoxic antibody titers and immunoglobulin levels in intestinal washings and mucosa scraping. Immunoglobulin G (IgG) and IgG antitoxins predominated, but after enteral immunization total IgA and specific IgA antibodies occasionally reached levels similar to those for IgG. In serum, significantly increased antibody levels (IgG) were only recorded after parenteral immunization. Both the primary binding and the neutralizing antitoxin titers showed a stayistically significant correlation with the degree of protection against toxin challenge; however, for the neutralizing antibodies this correlation was not without exceptions. No relation to protection was found for intestinal antibodies. The results of the present study indicate that enternal as well as parenteral immunization with toxin antigen can give rise to effective cholera immunity. After enternal immunization, the protection appears to be medicated by locally synthesized antibodies. After parenteral vaccination both serum-derived and locally produced antibodies seem to be effective.