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Biomedical subjects

H Studer

Publications and source records attributed to H Studer.

At least 127 records · Page 7Linked to original sources
PubMed1977

Iodotyrosine deiodination in the normal and acutely TSH-stimulated thyroid.

The deiodination of L-MIT-125I was measured in rat thyroid homogenates and slices before and after acute TSH stimulation. Slices and homogenates were incubated with identical concentrations of tissue and substrate in the presence and absence of NADPH. 1 USP unit TSH added in vitro to thyroid slices failed to stimulate deiodination; a single in vivo ip injection of 3 USP units TSH was also unable to raise deiodinating activity. In contrast to TSH, NADPH added to homogenates and slices enhanced deiodination significantly. However, several arguments, including a review of the literature, strongly militate against the hypothesis of an increased intracellular concentration of the coenzyme NADPH being the prerequisite to enhanced deiodination. The results suggest that deiodinase activity in acutely stimulated thyroids is not limited by the intracellular concentration of the enzyme itself nor by the availability of co-enzyme. Therefore, the increased iodide release induced by acute TSH stimulation is a mere consequence of the enhanced thyroglobulin proteolysis and does not require higher enzyme concentration. It will be shown subsequently that a different conclusion must be drawn in experiments with chronic TSH stimulation.

Animals↗
PubMed1977

[Endocrinology of the chiasma syndromes (author's transl)].

A wealth of new knowledge about the function of the hypothalamo-hypophyseal system has been accumulated over the past ten years and progress keeps going at a fast pace. Several factors have contributed to this explosive growth: Pituitary hormones can now be measured by radio-immunoassay in body fluids, hypothalamic stimulating and inhibiting factors have been identified and are available for clinical studies and dynamic tests have been developed for detailed investigations of minor disturbances in the pituitary control system. A tremendous gain in accuracy of clinical diagnosis and endocrine follow-up is one of the consequences. Furthermore, new clinical pictures have emerged such as several variants of the hyperprolactinemia-hypogonadism syndrome or the concept of pituitary microadenoma. At the same time, neuropharmacology is also developing at a tremendous pace and exceedingly interesting perspectives linking neurotransmission with endocrinology and with various diseases of the brain are emerging. One highlight is the discovery of bromoergocryptine as a dopaminergic agonist, active in suppressing prolactin secretion as well as in treating Parkinsonism. In a second part of this presentation 5 cases with pituitary disease are presented. They were selected to cover part of the wide range of clinical signs and symptoms produced by tumours of the pituitary region. There is indeed no good relationship between ophthalmo-neurologic symptoms, destruction of the bony sella and endocrine disturbances.

Adenoma, Acidophil↗
PubMed1976

Inhibition of thyroglobulin biosynthesis and degradation by excess iodide. Synergism with lithium.

Lithium and excess iodide inhibit the release of thyroid hormone from preformed stores. We thus tested the hypothesis that this was due to an inhibition of thyroglobulin breakdown. Rats were pre-treated with propyl-thiouracil (PTU) for 3 weeks in order to deplete their thyroids of thyroglobulin. While the PTU was continued, lithium chloride (0.25 mEq./100 g weight) or potassium iodide (3 mg per rat) were injected every 12 h for d days. Thereafter the thyroglobulin content in thyroid gland homogenates was measured. PTU pre-treatment lowered the thyroglobulin content from 4.21 to 0.22 mg/100 mg gland. Lithium caused a marked re-accumulation of thyroglobulin to 0.60 mg/100 mg within 3 days. While iodide alone had only a borderline effect, it markedly potentiated the action of lithium and a combination of the two drugs increased the thyroglobulin content to 1.04 mg/100 mg. Thyroxine was injected into similarly pre-treated animals to suppress secretion of thyrotrophic hormone. This markedly inhibited the proteolysis of thyroglobulin and 1.3 mg/100 mg gland accumulated after 3 days. Excess iodide, given in addition to thyroxine, decreased the amount of thyroglobulin accumulated to 0.75 mg/100 mg gland. To study whether this could be explained by an inhibitory action of iodide on thyroglobulin biosynthesis, thyroid glands from animals treated with excess iodide were incubated in vitro in the presence of 0.2 mM iodide for 3 h. Iodide decreased the incorporation of radioactive leucine into total thyroidal protein and into thyroglobulin by 25 and 35% respectively. Iodide did not inhibit protein synthesis in the kidney, liver or muscle tissue. Thus, large doses of iodide selectively inhibit thyroglobulin biosynthesis.

Animals↗
PubMed1976

A transient rise of hormone secretion: a response of the stimulated rat thyroid gland to small increments of iodide supply.

Small doses of iodide (2 times 3.2 mug at 12 h interval), below those capable of inducing Wolff-Chaikoff effect, were injected into rats kept on a moderately low iodine diet. By means of a 125I equilibration technique as well as by direct measurement of cold T4, it was demonstrated that the level of circulating PB125I (representing iodothyronines as confirmed by column chromatography) increased by a mean of 40% within 24 h following the first iodide injection. The serum TSH concentration (measured by radioimmunoassay) was simultaneously depressed. Thus, in stimulated thyroid glands, a biologically significant fraction of an iodide load escapes autoregulatory control of iodothyronine synthesis. A small, transient increase of hormone release is likely to represent the physiological response of a normal gland to a sudden supplement of iodide supply. The ensuing depression of TSH secretion may be necessary for final adjustment of thyroid function. It is considered to be the last step in a cascade of mechanisms whose interaction keeps the thyroidal hormone output within narrow limits in the face of a fluctuating iodide supply. Failure of one or several of these mechanisms in the goitrous human gland could conceivable explain the phenomenon of "Jod Basedow".

Animals↗
PubMed1975

[Proceedings: Long-term therapy with steroids].

All glucocorticosteroids available at the present time exert a wide range of actions in every single cell of every organ. It is still not possible to dissociate the therapeutically desirable effects from the undesirable side effects, and whether this goal will ever be achieved is more than questionable. Thus, chronic treatment with steroids is invariably associated with side effects, but there are a number of therapeutic rules whose strict observance may prevent a patient in chronic need of steroid treatment from developing a second, iatrogenic disease. For example, there is strong evidence that spacing the administration or oral steroids, even without changing the 24 h dosage, may substantially decrease the steroid induced side effects without loss of therapeutic action. Another promising approach has been reported in the case of steroid dependent asthmatics, many of whom may be treated by inhalations of steroid esters with strong topical but low systemic effects.

Administration, Oral↗
PubMed1975

[When is a radioisotope diagnosis indicated in thyroid diseases and when is it superfluous?].

In response to the question when radioactive isotopes (radionuclides) are necessary or superfluous in the diagnostic workup of thyroid disease, the following observations can be made: 1. Radionuclides are almost ubiquitously used for the specific and relevant in-vitro tests for measuring the circulating thyroid hormones (T4 und T3, etc.) and necessitate a very small quantity of serum. They lead in approximately 90% of cases of the correct diagnosis, especially when supported by careful clinical workup. 2. The use of radionuclides is of unquestionable value for scanning the thyroid gland and thus permitting the localization of normal vs. ectopic thyroid tissue, and the recognition of active ("warm" or "hot") vs. inactive ("cold") areas, especially in nodular goiter. 3. As the best screening tests for hypo- or hyperthyroidism are those related to the level of circulating thyroid hormones (see above), thyroid radionuclide uptake tests have lost much of their diagnostic value. However, the measurement of thyroidal radionuclide uptake remains valuable whenever radioiodine treatment is considered and in detailed thyroid function studies, and its also useful in the follow-up of drug-treated hyperthyroid patients. Thyroid uptake measurements may be of particular interest in so-called dynamic tests (e.g. TSH-stimulation, T3-suppression). 4. Finally, attention is drawn to the fact that, according to AITCHISON et al. (1), our capacity to interpret multidimensional information properly is limited. Thus, experience and precise knowledge help to economize the use of radionuclides and permit minimal application with maximal output.

Binding Sites↗
PubMed1975

Autoradiographic localization of slow turnover iodocompounds within the follicular cells of the rat thyroid gland.

In addition to thyroglobulin, several low molecular wt iodinated glycopeptides are present in the thyroid gland. Some of these compounds are considered to be slowly metabolized remnants of intracellular lysis of engulfed colloid droplets. In this paper we present autoradiographic evidence obtained by light microscopy, suggesting that breakdown products of thyroglobulin digestion can indeed be located within the thyroid cells. The thyroid glands of rats were labeled with 125I to approach isotopic equilibrium. The tracer was then withdrawn from the otherwise unchanged high-iodine diet, and thyroidal radioactivity was washed out for 80 days. Autoradiographs of glands containing 10% or less of the tracer present at equilibrium showed the bulk of 125I within the follicular cells while the colloid was only slightly labeled. An additional finding was the presence of dense radioactive inclusions in the lumina of many follicles. They are assumed to represent clusters of thyroglobulin molecules not readily available to pinocytosis. In addition to autoradiographic evidence, the identity of intracellularly located radioactivity with slow-turnover enzyme-resistant iodocompounds is supported by double labeling experiments, using 125I as the "old" tracer, accumulating within the cells, and 131I as the "new" label representing intraluminal 19 S thyroglobulin. Experimental manipulations which tended to deplete the thyroid of thyroglobulin, increased the 125I/131I ratio in the gland as predicted by the working hypothesis. Thus, this paper describes a new kind of autoradiographic ring reaction due to a hitherto barely considered intracellular organic iodine pool.

Animals↗