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Biomedical subjects

K Banovac

Publications and source records attributed to K Banovac.

At least 55 records · Page 3Linked to original sources

Conversion of thyroxine to triiodothyronine and reverse triiodothyronine in human placenta and fetal membranes.

Conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and reverse 3,3',5'-triiodothyronine (rT3) was measured in vitro in human placenta and fetal membranes. T4 (5 micrograms/ml) was incubated in 0.15 mol/l phosphate buffer with tissue homogenates for 2 h at 37 degrees C, and the T3 and rT3 generated were determined in ethanol extract using RIA methods. The placenta and chorion homogenates converted more T4 to T3 than to rT3; the placenta was more active than the chorion. In both tissues the highest converting activity was found in microsomal fractions.

Chorion↗

Clinical significance of assay of thyroid-stimulating antibody in Graves' disease.

We correlated thyroid-stimulating antibody (direct thyroid stimulation method) with the clinical course of 187 patients with Graves' disease. Of 64 patients with newly diagnosed hyperthyroidism, 59 were positive; 36 of 38 patients tested early in therapy were positive. Twenty-eight patients received antithyroid drug therapy, and thyroid-stimulating antibody was measured at cessation of therapy; 13 patients, negative in the assay, remained in remission, and of 15 relapsed cases 12 were positive. Of 57 patients previously treated by various means for hyperthyroidism, 34 were positive, and they primarily had had relapse after initial treatment, then ablative therapy causing hypothyroidism. Six of 10 patients with euthyroid ophthalmopathy had a positive assay and an abnormal thyrotropin-releasing hormone (TRH) test or thyroid suppression test; the four negative patients had a normal TRH test. Thus measurement of thyroid-stimulating antibody appears effectively to reflect activity of the underlying disturbance in Graves' disease.

Antibodies↗

Episodic and TRH induced growth hormone release in primary hypothyroidism of man and rat.

In 27 hypothyroid subjects studied over 20 to 120 minutes, the concentration of serum growth hormone (GH) was variable with the amplitude and frequency of the secretory patterns similar to those reported by others for normal individuals. Serum GH, after the administration of thyrotropin releasing hormone (TRH) did not differ from values observed as spontaneous surges, in contrast to a consistent increase in thyrotropin and prolactin. Episodic secretion of GH persisted in thyroidectomized rats and did not differ significantly from that present in intact controls. It is concluded that episodic GH secretion is not abolished in primary hypothyroidism and that TRH is not a constant GH secretagogue in human subjects with hypothyroidism.

Adolescent↗

Competitive ligand - binding assay for thyroxine binding globulin. Comparison with TBG radioimmunoassay and T3 uptake test.

A simple and reproducible competitive ligand binding assay has been utilized to measure serum TBG concentration. In euthyroid subjects TBG concentration (mean +/- SD, mg/l) was 33.7 +/- 4; hyperthyroid 24 -/+ 6; T3-thyrotoxicosis 20 +/- 7; hypothyroid 37 -/+ 7; pregnant 67 -/+ 18; post-partum period 59.8 -/+ 17; oral contraceptives 45 -/+ 7. The correlation of CLBA with RIA measurement of TBG was significant (p less than 0.001). The estimations of serum TBG by CLBA correlated significantly with T3 uptake test (p less than 0.001), but at higher concentration of TBG correlation was non-linear. T4 : TBG ration according to serum T4 and TBG concentration provided a reliable index in the assessment of thyroid function.

Contraceptives, Oral↗

Similar serum concentrations of thyroid hormones in two geographically separate populations on disparate iodine intake.

Serum thyroid hormones were measured in Montreal, Canada (urinary iodine 446 +/- 164 micrograms/day) and Zagreb, Yugoslavia (urinary iodine 108 +/- 32 microgram/day). The serum concentrations of thyroxine and triiodothyronine in the two populations were almost identical. We conclude that dietary iodine, within accepted normal limits, is not a factor in determining serum thyroid hormone levels. The wide differences in reported serum triiodothyronine concentrations are related to methodological problems.

Adolescent↗

Hypothyroidism-induced changes in triiodothyronine binding to nuclei and cytosol-binding proteins in rat liver.

A tracer dose of [125I]T3 was given iv to normal, thyroidectomized, and propylthiouracil-fed rats and the distribution of radioactivity in serum and liver fractions was studied over 1 h. Total liver homogenate and serum 125I were higher at all times in hypothyroid rats and, in all groups, showed a continuous fall over the period studied. Hepatic nuclear 125I was maximal at 20 min in all and was greater in hypothyroid rats; there was more 125I in the hepatic cytosol of normal rats than in that from either thyroidectomized or propylthiouracil-fed animals. Binding studies with [125I]T3 and purified hepatic neclear preparations in vitro indicated that both the association constant, Ka (1.08-9.0 x 10(9) M-1) and the capacity (500-600 pg/mg DNA) in thyroidectomized and goitrogen-treated rats were similar to those obtained with normal animals. Cytosol, on the other hand, showed a decrease in binding capacity without change in affinity in livers of hypothyroid rats. Analysis of binding data by Hill plots indicated the presence of both positive and negative cooperativity in binding of T3 by rat liver cytosol proteins. In the in vitro experiments, higher serum radioactivity alone could not account for increases in the hepatic nuclear 125I in the hypothyroid rats because cytosol 125I (presumably in dynamic exchange with both blood and nuclei) was less. Consequently, cytosol T3-binding proteins may regulate the free T3 concentration in the cell and, thus influence the distribution of the hormone in other cellular compartments.

Animals↗

Decreased ratio of serum T3:rT3 in patients with hyperthyroidism.

In 14 hyperthyroid patient serum T4:rT3 ratio was significantly lower (399 +/- 20) than in the control subjects (572 +/- 20; p less than 0.001). A similar pattern was found for serum T3:rT3 ratio. In the hyperthyroid group the ratio was significantly lower (10.5 +/- 0.5) than in the control group (12.5 +/- 0.6; p less than 0.05). The data suggest that in hyperthyroidism the organism might shift conversion of T4 from biologically active T3 to poorly calorigenic rT3. It seems possible that the proportionately increased generation of rT3 than that of T3 may be a defence mechanism of the body, as it was found in systemic illnesses and starvation.

Adult↗

Relative increase of serum reverse T3 in patients with hypothyroidism.

In 17 hypothyroid patients serum T3: rT3 ratio was 7.5 /+- 1.1 which was significantly lower than in control subjects (12.2 /+- 0.6; p less than 0.001). The data suggest that in hypothyroidism the organism might shift conversion of T4 from biologically active T3 to biologically inactive rT3 which may not be a defense mechanism of the body, as it was found in chronic systemic illness.

Adult↗

Alterations in thyroxine metabolism produced by cutaneous application of microscope immersion oil: effects due to polychlorinated biphenyls.

A 30% solution of a polychlorinated biphenyl (PCB) mixture or a microscope immersion oil containing 34% PCB, when applied to the skin of rats, led to substantial increases in the biliary excretion of intravenously injected [125I]thyroxine (T4) in bile: plasma 125I ratios, in the biliary clearance rate of plasma [125I]T4, and in bile flow. Both PCB preparations also elevated liver weight, thyroid 125I uptake, and Sephadex uptake of [125I]triiodothyronine (T3), and depressed serum T4 concentrations; serum T3 levels were unaltered by the PCB solution or by the immersion oil containing PCB. PCB, either in mineral or immersion oil, reduced the free T4 index (serum T4 X fraction Sephadex T3 uptake), indicating a probable reduction in the concentration of free T4 in serum; the free T3 index, on the other hand, was elevated in PCB-treated rats. The same type of immersion oil, in which the PCB was replaced by a hydrogenated terphenyl, was without effect on any of the indices studied. Thus, the effects of microscope immersion oil on T4 metabolism were due to its PCB content. In thyroidectomized, T4-maintained rats, PCB in mineral oil again increased Sephadex uptake of [125I]T3, greatly reduced serum T4, and moderately reduced serum T3 levels; the free T4 index was substantially reduced and the free T3 index moderately lowered in treated animals. These data indicate that in PCB-treated rats both the peripheral conversion of T4 to T3 and thyroid T3 secretion were enhanced. The metabolic impact of thyroid hormone in PCB-treated animals was unchanged, as shown by normal activity of hepatic mitochondrial L-alpha-glycerophosphate dehydrogenase.

Administration, Topical↗