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At least 505 records · Page 28Linked to original sources
PubMed1994

The expression of adhesion molecules in thyroid glands from patients with Graves' disease.

We studied the potential role of adhesion molecules in the pathogenesis of Graves' disease. Thyroid specimens of Graves' thyroid glands and control thyroid glands were stained with monoclonal antibodies against adhesion molecules by an immunohistologic method. Thyroid tissues obtained from patients with Graves' disease had an enhanced expression of intercellular adhesion molecule-1 (ICAM-1) on capillary endothelial cells around the thyroid follicles and on postcapillary endothelial cells in lesions with aggregates of mononuclear cells. Positive staining for ICAM-1, lymphocyte function-associated antigen-1 (LFA-1), and very late antigen-4 (VLA-4) was found on the infiltrating mononuclear cells. The postcapillary vascular endothelial cells expressed increased endothelial-leukocyte adhesion molecule-1 (ELAM-1), but not vascular cell adhesion molecule-1 (VCAM-1). VCAM-1 and ELAM-1 were detected on the dendritic-like cells in the germinal centers of lymphoid follicle-like areas. No significant expression of these adhesion molecules was detected on normal thyroid glands. These results suggest that the LFA-1/ICAM-1 and ELAM-1 pathways may be responsible for the migration of mononuclear cells into the thyroid glands of patients with Graves' disease, and that the VLA-4/VCAM-1 pathway plays a critical role in the cellular interactions that lead to the formation of B-memory cells and the excess production of antibodies.

Adult↗
PubMed1988

Effects of thyrotropin on the vascular conductance of the thyroid gland.

It is well established that TSH from the anterior pituitary is the principal stimulatory agent in the physiological regulation of the thyroid gland. Chronic elevations of plasma TSH induce hyperplasia and hypertrophy of thyroid follicular cells and enlargement of blood capillaries. At low plasma TSH levels the thyroid gland atrophies. We have examined the vascular conductance (C = blood flow/mean arterial pressure) of the thyroid gland and several other tissues over a wide range of endogenous plasma TSH concentrations and after treatment with bovine TSH (bTSH) in rats. Tissue blood flows were determined using 15 +/- 5-microns diameter 141Ce-labeled microspheres in a modification of the reference sample microsphere technique. The microspheres were injected directly into the left cardiac ventricle via a 23-gauge needle passed through the chest wall, while the reference blood sample was collected and systemic arterial blood pressure was monitored through femoral arterial catheters. After the animals were killed, tissues were cleaned and weighed, and the tissue radioactivity was determined. Blood samples for determination of plasma hormone levels were obtained from the jugular vein before the injection of microspheres. In the first series of experiments, the vascular C per mass of thyroid gland was significantly decreased 4 and 8 days after hypophysectomy. Treatment of hypophysectomized rats with bTSH (185 mU/100 g.day as a continuous iv infusion for 2 or 6 days) restored thyroid vascular C per mass of tissue to control levels. In the second series of experiments, we manipulated circulating plasma TSH levels in intact rats by 6 days of treatment with propylthiouracil (2.0 mg/day, ip), thyroid hormones (1.5 micrograms T4, 0.4 micrograms T3 or 3.0 micrograms T4, plus 0.8 micrograms T3/100 g.day, sc by continuous infusion), TRH (240 micrograms/day, iv, by continuous infusion), bTSH (800 mU/day, iv, by continuous infusion), or combinations of these treatments. The vascular C per mass of thyroid gland was significantly decreased at very low chronic plasma TSH levels and increased at very high chronic plasma TSH levels. Thyroid vascular C per mass was unchanged, however, over a broad intermediate range of plasma TSH concentrations encompassing normal values, despite alterations in the size and function of the thyroid gland. At these intermediate levels of TSH stimulation, the thyroid gland may respond by adding or subtracting functional units without changing the blood flow per unit. The amount of blood flow per functional unit may be altered only at very high or very low levels of TSH stimulation.

Adrenal Glands↗
PubMed1978

Association of serum antithyroid antibodies with lymphocytic infiltration of the thyroid gland: studies of seventy autopsied cases.

Postmortem histological examination of the thyroid gland and measurement of serum antithyroid antibodies were performed in 70 patients without overt thyroid disease. Lymphocytic infiltration, antithyroglobulin hemagglutination antibody (TGHA), and antithyroid microsomal hemagglutination antibody (MCHA) were found in 12, 2, and 9 cases, respectively. The incidence of lymphocytic infiltration in females was three times that in males. Ten of the 12 cases with lymphocytic infiltration had positive antibodies (either TGHA or MCHA), while 10 of 11 patients with positive antibodies showed lymphocytic infiltration. Thus, the correlation between morphological and serological findings was highly significant at P less than 0.001. The incidence of a small thyroid gland of less than 15 g in weight was higher in patients with lymphocytic infiltration and/or positive antibodies than in patients with a normal thyroid gland. These data suggest that positive serum antithyroid antibodies in subjects without overt thyroid disease may indicate the existence of lymphocytic infiltration in the thyroid gland, that is presumably subclinical autoimmune thyroiditis.

Adult↗
PubMed2006

Expression of sodium-iodide symporter mRNA in the thyroid gland of Xenopus laevis tadpoles: developmental expression, effects of antithyroidal compounds, and regulation by TSH.

The uptake of iodide represents the first step in thyroid hormone synthesis by thyroid follicular cells and is mediated by the sodium-iodide symporter (NIS). In mammals, expression of NIS is stimulated by TSH and transcription of the NIS gene involves regulation by the thyroid-specific transcription factors Pax8 and Nkx2.1. In this study, we examined the mRNA expression of NIS, Pax8 and Nkx2.1 in the thyroid gland of Xenopus laevis tadpoles by semi-quantitative reverse transcriptase (RT)-PCR. During spontaneous metamorphosis, NIS mRNA expression was low in premetamorphic tadpoles, increased throughout prometamorphosis, and peaked at climax stage 60. Analysis of TSH beta-subunit (TSHbeta) mRNA in the pituitary of the same tadpoles revealed a close temporal relationship in the expression of the two genes during metamorphosis, suggesting a regulatory role of TSH in the developmental expression of NIS. Treatment of tadpoles with goitrogenic compounds (sodium perchlorate and ethylenethiourea) increased TSHbeta mRNA expression (approximately twofold) and caused thyroid gland hyperplasia, confirming that feedback along the pituitary-thyroid axis was operative. Analysis of gene expression in the thyroid gland revealed that goitrogen treatment was correlated with increased expression of NIS mRNA (approximately 20-fold). In the thyroid gland organ culture experiments, bovine TSH (bTSH; 1 mU/ml) strongly induced NIS mRNA expression. This effect was mimicked by co-culture of thyroid glands with pituitaries from stage 58 tadpoles and by agents that increase intracellular cAMP (forskolin, dibutyryl-cAMP). In addition, it could be shown that thyroid glands of X. laevis tadpoles express Pax8 and Nkx2.1 mRNA in a developmentally regulated manner and that ex vivo treatment of thyroid glands with bTSH, forskolin, and cAMP analogs increased the expression of Pax8 and Nkx2.1 mRNA. This is the first report on developmental profiles and hormonal regulation of thyroid gland gene expression in amphibian tadpoles and, together, results reveal a critical role of TSH in the regulation of NIS mRNA expression in the thyroid gland of X. laevis tadpoles.

Animals↗
PubMedDate not supplied

[Mortality in carcinoma of the thyroid gland in Yugoslavia].

The article dealing with thyroid gland cancer in Yugoslavia is based on data on the mortality rate over the period from 1971 to 1985. During the observed period the average proportion of thyroid gland cancer was 0.51% (males-0.30%; females-0.81%) in the whole group of malignant tumours in Yugoslavia. In the same period the standardized mortality rate was 0.52 per 100,000 persons, with the following risk difference between sexes: males-0.40; females-0.63 per 100,000 persons. The mortality trend of thyroid gland cancer in Yugoslavia showed a slight increase from 1971 to 1985 (9y = 0.480 + 0.006x).

Adolescent↗
PubMed2001

[Thyroid tuberculosis associated with papillary microcarcinoma of the thyroid gland: a case report].

Tuberculosis of the thyroid gland is extremely uncommon. The infection may present first in the thyroid gland or appear secondary to a tuberculous process elsewhere in the body. The diagnosis is rarely made clinically because the different presentations of the disease often mimick malignancy or euthyroid nodular goitre. It is of interest to report a case of tuberculosis of the thyroid associated with papillary microcarcinoma of the gland. No tuberculous process elsewhere in the body has been found. The frequency of MCP on thyroidectomy specimens suggest that this association is incidental.

Adult↗
PubMed1976

Studies on proteolytic activity and function of the thyroid gland in rats administered excess iodide.

Thyroid auto-proteolytic activity in rats increased significantly only after several weeks of treatment with 1 mg iodide per day. Iodide added in vitro did not activate thyroid auto-proteolysis, nor was inhibition observed. Thyroid proteolytic activity was also tested using 131I-labelled heat-inactivated thyroid homogenate from control rats as substrate. Significantly increased proteolytic activity was again demonstrated in thyroid glands from rats on excess iodide for several weeks. The increased proteolytic activity is therefore probably not due to a decreased proteolytic resistance of thyroglobulin in the iodide-treated rats. Increased synthesis or decreased degradation of thyroid proteolytic enzymes is a more likely explanation for this phenomenon. These findings are at variance with those of some previous studies showing decreased proteolytic activity in thyroid glands from rats administered excess iodide. Since the rats remained euthyroid the increased auto-proteolysis, which occurred quite late, was considered an unexpected finding and it is at present not certain whether this is related to the successful adaptation. Treatment with iodide did not alter the thyroid and hypophyseal weight or histology. Serum free thyroxine level and thyrotropin concentration were also unaffected by excess iodide. The adaptation of the imtact rat thyroid to prolonged and excess iodide intake seems to occur without the assistance of an altered thyrotrophin secretion.

Animals↗
PubMed1976

Long-term effects on external radiation on the pituitary and thyroid glands.

Chronic damage following external irradiation of the normal pituitary and thyroid glands, delivered incidentally during radiotherapy of neoplasms of the head and neck may be more common than has been appreciated in the past. A case of a child who developed pituitary dwarfism 5 1/2 years after radiation therapy has been delivered for an embryonal rhabdomyosarcoma of the naso-pharynx is described. A review of similar cases from the literature is presented. Likewise, external irradiation of the normal thyroid gland produces a spectrum of radiation-induced syndromes. Clinical damage to the pituitary and thyroid glands is usually manifested months to years after treatment and is preceded by a long subclinical phase. A careful exclusion of these glands from radiation treatment fields is recommended whenever possible. An early detection of endocrine function abnormalities in patients receiving radiation to these glands is desirable, since appropriate treatment may prevent the deleterious effects of external irradiation of the pituitary and thyroid glands.

Adult↗
PubMed1995

Immunohistochemical demonstration of parathyroid hormone-related protein in thyroid gland of sheep.

Thyroid and parathyroid glands from normal adult sheep and sheep with vitamin D3-induced hypercalcemia were evaluated immunohistochemically for the presence of parathyroid hormone-related protein (PTHrP) and calcitonin (CT). Thyroid follicular cells, C-cells, and parathyroid chief cells stained moderately to strongly positive for PTHrP in both groups of sheep. C-cells were identified as cells positive for cytoplasmic staining of CT. Staining of C-cells for calcitonin in hypercalcemic sheep was diminished in intensity. The data demonstrated that PTHrP is present in the sheep thyroid and parathyroid glands. PTHrP may function as a local paracrine factor in these organs, but its staining intensity was not affected by the induction of hypercalcemia.

Animals↗
PubMed2003

[Pathomorphology of the thyroid gland after treatment of laryngeal cancer].

The aim of the report was the explanation of the pathogenesis of thyroid gland dysfunction after laryngeal cancer treatment. Assessment of histopathological specimens from thyroid gland was done. They were taken from the following patients: a) irradiated primary with the radical dose (n = 5), b) after combined therapy (n = 2) and c) at the autopsy from the persons aged between 30-80, without thyroid gland disease history (n = 30). It was found that the thyroid gland underwent degenerative changes after external irradiation or combined therapy, which became more intense with the passage of time. They consist among other things in diminishing of the follicle lining cells with the obliteration of the follicle structure of thyroid, damage to the blood vessel walls, fibrotic tissue proliferation with the following gland atrophy. In the histological specimens of the thyroid gland taken at the autopsy distinct obliteration of the follicle structure with the atrophy of follicle and intensified fibrotic process after 80 years of age was seen. Results of the investigations suggest that the main pathogenic factor in hypotyhyreosis after radiotherapy or combined therapy are the degenerative changes in the thyroid gland and their overlapping with circulatory disorders after surgery. Morphological changes in thyroid gland following aging increase the risk of hypotyhyreosis.

Adult↗
PubMed1990

[Structure of lymphatic vessels in the rat thyroid gland].

The lymphatic bed of the thyroid gland has been studied in 24 intact rats. Three techniques facilitating to reveal lymphatic vessels in the organ have been used: preparation of semithin sections, injection of the blood bed with methyl methacrylate with a successive chemical extraction of the preparations, injection of the blood bed with liquid solution of methyl methacrylate with a consecutive study of the preparations in the scanning electron microscope. Methods of electron histochemistry (revealing horseradish peroxidase) and kryofractography have been applied. Construction of the thyroid lymphatic bed, structure of the wall are described, fibroblastic membrane (F-membrane) is revealed and the signs are presented, that allow to differentiate F-membrane from endothelium of the lymphatic capillaries. The pathways of lymph outflow in the rat thyroid gland consist of the following links: interstitial space in the interlobular spaces of the gland, into them the tissue liquor (lymph) is filtered ; plates of the F-membrane regulating direction of excessive albumin-containing liquor in the lymphatic capillaries, surrounding groups of 5-11 follicles, embracing the microlobule of the gland and situating in the interlobular spaces, deferent lymphatic vessels.

Animals↗