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Biomedical subjects

J Robbins

Publications and source records attributed to J Robbins.

At least 379 records · Page 21Linked to original sources
PubMed1972

Immunological studies of Y protein. A major cytoplasmic organic anion-binding protein in rat liver.

An antibody produced against rat Y protein, the major cytoplasmic organic anion-binding protein in liver, was characterized. The antibody precipitated Y protein from liver supernatant fractions and specifically removed the organic anion-binding capacity from this fraction.Y protein was detected by immunodiffusion with this antibody in the supernates of rat liver, kidney, and small intestinal mucosa and was not detected in supernates of 16 other tissues including bile and serum. Precipitation with anti-Y was not detected with supernates of liver from 20 other species, including man. Quantitative radial immunodiffusion revealed Y protein to constitute 4.5% of supernatant protein in rat liver and approximately 2% of supernatant protein in rat kidney and small intestinal mucosa. Phenobarbital administration increased the concentration of Y protein in rat liver by 280%, but not in kidney or small intestinal mucosa, and was associated with increased plasma disappearance of sulfobromphthalein sodium, indocyanine green, and bilirubin, and increased hepatic, but not kidney or small intestinal mucosal, content of these organic anions. These observations provide further evidence indicating that the concentration of Y protein is a major determinant of organic anion flux across the plasma membrane of the liver cell.Immunodiffusion and immunoelectrophoresis revealed serological identity between Y protein, cortisol metabolite-binding protein I. and the major azocarcinogen-binding protein.

Animals↗
PubMed1972

The use of lithium in the treatment of thyrotoxicosis.

Since lithium has been shown to inhibit release of iodine from the thyroid, we have investigated its therapeutic potential in thyrotoxicosis. Eight detailed (131)I kinetic studies were performed on seven thyrotoxic women and data was analyzed using a computer program. Lithium at serum levels of about 1 mEq liter decreased the loss of (131)I from the thyroid, led to a fall in serum (131)I levels and diminished urinary (131)I excretion. Computer simulation of the lithium effect required, in every case, that lithium inhibit hormonal and nonhormonal thyroid iodine release. In five cases a second lithium effect was required for a satisfactory fit of the model soluton with observed data: namely, an inhibition of hormone disappearance from serum. NEITHER INHIBITION OF RELEASE NOR OF HORMONE DISAPPEARANCE SEEMED TO BE AFFECTED BY METHIMAZOLE (RELEASE: 52% decrease without methimazole, 60% with methimazole; hormone disappearance: approximately 60% decrease in both). When Li(+) was discontinued, recovery of the iodine release rate and hormone disappearance rate over the observed time span was variable, ranging from no recovery to rates that exceeded pre-Li(+) values. When Li(+) is used alone its effect on serum hormone levels is diminished due to continued accumulation of iodide by the thyroid. Thus, serum thyroxine-iodine levels fell 21-30% in 6-8 days in patients who did not receive methimazole and 15-67% in the methimazole-treated subjects. For prolonged therapy, therefore, a thiocarbamide drug must be used in conjunction with Li(+). The similarity of inhibition of iodine release from the thyroid produced by Li(+) and iodides is discussed.

Adolescent↗
PubMed1970

Antithyroid effects of lithium.

Lithium has been reported to be goitrogenic when used for the treatment of manic-depressive psychosis. To investigate the effects of lithium on iodine metabolism, male Sprague-Dawley rats were placed on a low iodine (LID) or normal iodine diet (NID) containing enough Li(2)CO(3) to give serum lithium levels of 0.23-0.86 mEq/liter (human therapeutic range is 0.6-1.6 mEq/liter). The following effects were noted with lithium treatment: (a) thyroid weight increased concomitant with a slowing of thyroidal iodine release; (b) the ability to concentrate iodide was increased only after goiters were established; (c) on the LID, (131)I uptake was elevated throughout all phases of treatment, even when the release rate was normal; (d) iodine organification was unaffected but the proportion of (131)I present as iodothyronines was decreased; (e) the thyroidal (127)I content was increased; (f) despite these changes, the serum PBI remained normal as did the thyroxine turnover rate; and (g) thyrotropin (TSH) levels in serum were the same as controls except for a slight elevation early in the course of treatment; TSH levels did not correlate with goitrogenesis. When LiCl was injected in large doses into intact rats (giving serum lithium levels of 3.08-3.89 mEq/liter), the iodide concentrating mechanism, (131)I uptake, and (131)I release rates were depressed. Similar experiments in hypophysectomized rats receiving TSH demonstrated these to be local antithyroid effects not mediated through the pituitary. The discrepancy between acute and chronic responses to lithium, and the dissociation between the inhibition of iodine release and stimulatory effects is discussed.

Animals↗