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1
Veinot, John P., and Feroze N. Ghadially. "Melanosis Thyroidi." Ultrastructural Pathology 22, no. 5 (January 1998): 401–6. http://dx.doi.org/10.3109/01913129809103362.
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Kariyawasam, Dulanjalee, Latif Rachdi, Aurore Carré, Mercè Martin, Marine Houlier, Nathalie Janel, Jean-Maurice Delabar, Raphaël Scharfmann, and Michel Polak. "DYRK1A BAC Transgenic Mouse: A New Model of Thyroid Dysgenesis in Down Syndrome." Endocrinology 156, no. 3 (March 1, 2015): 1171–80. http://dx.doi.org/10.1210/en.2014-1329.
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Abstract The most common thyroid abnormality among Down syndrome (DS) children corresponds to a mildly elevated TSH, with T4 decreased or in the normal range and thyroid hypoplasia, from the neonatal period onward, which aggravate their mental impairment. Transgenic Dyrk1A mice, obtained by bacterial artificial chromosome engineering (mBACTgDyrk1A), have 3 copies of the Dyrk1A gene. The objective is to determine whether this transgenic Dyrk1A (Dyrk1A+/++) mouse is an adequate murine model for the study of thyroid dysgenesis in DS. Embryonic thyroid development from embryonic day 13.5 (E13.5) to E17.5 was analyzed in wild-type (WT) and Dyrk1A+/++ mice by immunofluorescence with anti-Nkx2–1, anti-thyroglobulin, and anti-T4 antibodies, markers of early thyroid development, hormonogenesis, and final differentiation, respectively. The expression of transcription factors Nkx2–1, Pax8, and Foxe1 involved in thyroidogenesis were studied by quantitative RT-PCR at the same embryonic stages. We then compared the adult phenotype at 8 to 12 weeks in Dyrk1A+/++ and WT mice for T4 and TSH levels, thyroidal weight, and histological analysis. Regarding thyroidal development, at E15.5, Dyrk1A+/++ thyroid lobes are double the size of WT thyroids (P = .01), but the thyroglobulin stained surface in Dyrk1A+/++ thyroids is less than a third as large at E17.5 (P = .04) and their differentiated follicular surface half the size (P = .004). We also observed a significant increase in Nkx2–1, Foxe1, and Pax8 RNA levels in E13.5 and E17.5 Dyrk1A+/++ embryonic thyroids. Dyrk1A+/++ young adult mice have significantly lower plasma T4 (2.4 ng/mL versus WT, 3.7 ng/mL; P = 0.019) and nonsignificantly higher plasma TSH (114 mUI/L versus WT, 73mUI/L; P = .09). In addition, their thyroids are significantly heavier (P = .04) and exhibit large disorganized regions. Dyrk1A overexpression directly leads to thyroidal embryogenetic, functional and morphological impairment. The young adult thyroid phenotype is probably a result of embryogenetic impairment. The Dyrk1A+/++ mouse can be considered a suitable study model for thyroid dysgenesis in DS.
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Diallo-Krou, Ericka, Jingcheng Yu, Lesley A. Colby, Ken Inoki, John E. Wilkinson, Dafydd G. Thomas, Thomas J. Giordano, and Ronald J. Koenig. "Paired Box Gene 8-Peroxisome Proliferator-Activated Receptor-γ Fusion Protein and Loss of Phosphatase and Tensin Homolog Synergistically Cause Thyroid Hyperplasia in Transgenic Mice." Endocrinology 150, no. 11 (September 24, 2009): 5181–90. http://dx.doi.org/10.1210/en.2009-0701.
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Approximately 35% of follicular thyroid carcinomas and a small fraction of follicular adenomas are associated with a t(2;3)(q13;p25) chromosomal translocation that fuses paired box gene 8 (PAX8) with the peroxisome proliferator-activated receptor-γ gene (PPARG), resulting in expression of a PAX8-PPARγ fusion protein, PPFP. The mechanism by which PPFP contributes to follicular thyroid neoplasia is poorly understood. Therefore, we have created mice with thyroid-specific expression of PPFP. At 1 yr of age, 25% of PPFP mice demonstrate mild thyroid hyperplasia. We bred these mice to mice with thyroid-specific single-allele deletion of the tumor suppressor Pten, denoted ThyPten+/−. In humans, PTEN deletion is associated with follicular adenomas and carcinomas, and in mice, deletion of one Pten allele causes mild thyroid hyperplasia. We found that PPFP synergizes with ThyPten+/− to cause marked thyroid hyperplasia, but carcinomas were not observed. AKT phosphorylation was increased as expected in the ThyPten+/− thyroids, and also was increased in the PPFP thyroids and in human PPFP follicular cancers. Staining for the cell cycle marker Ki-67 was increased in the PPFP, ThyPten+/−, and PPFP;ThyPten+/− thyroids compared with wild-type thyroids. Several genes with increased expression in PPFP cancers also were found to be increased in the thyroids of PPFP mice. This transgenic mouse model of thyroidal PPFP expression exhibits properties similar to those of PPFP thyroid cancers. However, the mice develop thyroid hyperplasia, not carcinoma, suggesting that additional events are required to cause follicular thyroid cancer.
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Lavado-Autric, Rosalia, Rosa Maria Calvo, Raquel Martinez de Mena, Gabriella Morreale de Escobar, and Maria-Jesus Obregon. "Deiodinase Activities in Thyroids and Tissues of Iodine-Deficient Female Rats." Endocrinology 154, no. 1 (January 1, 2013): 529–36. http://dx.doi.org/10.1210/en.2012-1727.
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Severe iodine deficiency is characterized by goiter, preferential synthesis, and secretion of T3 in thyroids, hypothyroxinemia in plasma and tissues, normal or low plasma T3, and slightly increased plasma TSH. We studied changes in deiodinase activities and mRNA in several tissues of rats maintained on low-iodine diets (LIDs) or LIDs supplemented with iodine (LID+I). T4 and T3 concentrations decreased in plasma, tissues, and thyroids of LID rats, and T4 decreased more than T3 (50%). The highest type 1 iodothyronine deiodinase (D1) activities were found in the thyroid, kidney, and the liver; pituitary, lung, and ovary had lower D1 activities; but the lowest levels were found in the heart and skeletal muscle. D1 activity decreased in all tissues of LID rats (10–40% of LID+I rats), except for ovary and thyroids, which D1 activity increased 2.5-fold. Maximal type 2 iodothyronine deiodinase (D2) activities were found in thyroid, brown adipose tissue, and pituitary, increasing 6.5-fold in thyroids of LID rats and about 20-fold in the whole gland. D2 always increased in response to LID, and maximal increases were found in the cerebral cortex (19-fold), thyroid, brown adipose tissue, and pituitary (6-fold). Lower D2 activities were found in the ovary, heart, and adrenal gland, which increased in LID. Type 3 iodothyronine deiodinase activity was undetectable. Thyroidal Dio1 and Dio2 mRNA increased in the LID rats, and Dio1 decreased in the lung, with no changes in mRNA expression in other tissues. Our data indicate that LID induces changes in deiodinase activities, especially in the thyroid, to counteract the low T4 synthesis and secretion, contributing to maintain the local T3 concentrations in the tissues with D2 activity.
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Wu, Sing-yung. "The effect of fasting on thyroidal T4-5'monodeiodinating activity in mice." Acta Endocrinologica 122, no. 2 (February 1990): 175–80. http://dx.doi.org/10.1530/acta.0.1220175.
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Abstract Complete fasting induces a significant decrease of serum T3 and a fall in TSH in rodents and man. To evaluate the effect of starvation on thyroidal T4 5'monodeiodinating activity, in vitro conversion of T4 to T3 by thyroid and liver homogenate from one to three days fasted mice was compared with homogenates from control mice on animal chow. 5'monodeiodinating activity was significantly lower in thyroid homogenates of fasted mice than in those of chow-fed control [100±5.0 and 92±5.0 pmol T3·(mg protein)−1·h−1 at 48 and 72 h fasting, respectively, vs 132±5.0 pmol T3·(mg protein)−1·h−1 of fed control, p<0.01]. A similar decrease in thyroidal 5'monodeiodinating activity was seen in the liver. The decrease in thyroidal 5'monodeiodinating activity induced by fasting was not reversed by the supplementation of homogenates with the thiol-protecting agent, dithiothreitol (0.2–4.0 mmol/l). Physiological replacement of T4, 0.58 nmol·(100 g)−1·day−1, did not alter the effect of starvation in either the thyroid or liver. TSH (0.02 IU/day) injection, on the other hand, stimulated 5'monodeiodinating activity in homogenates of thyroids from 3-days fasted mice which was no different from TSH-treated fed control. It is postulated that starvation-induced decrease in thyroidal T4 to T3 converting activity may play a role, together with decreased hepatic 5'monodeiodinating activity, in fasting-induced low serum T3 in mice.
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Yamashita, Shunichi, Motomori Izumi, and Shigenobu Nagataki. "Specific stimulatory effects of Graves' IgG on the release of triiodothyronine from the patients' own thyroids." Acta Endocrinologica 112, no. 2 (June 1986): 204–9. http://dx.doi.org/10.1530/acta.0.1120204.
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Abstract. The present study was undertaken to investigate the release of thyroid hormones from cultured thyroid slices of untreated patients with Graves' disease in response to autologous IgG and IgG from other untreated patients with Graves' disease. Thyroid tissue (8–10 mg) was obtained by needle biopsy from 11 untreated patients with Graves' disease, and each biopsy was divided into 5 slices. Slices were then cultured in Ham's F-12 synthetic media for 7 days with IgG (1.3 mg/ml) obtained from the same patients, IgG obtained from other untreated patients, normal IgG, or bovine TSH (1.3 mIU/ml). Media were changed every day, and the concentrations of triiodothyronine (T3) in the media were measured by radioimmunoassay (RIA), and the concentrations of thyroidal cAMP were measured by radioimmunoassay on the last day of culture after incubation with 10 mm theophylline at 37°C for 30 min. When thyroid slices were incubated with autologous IgG, the release of T3 increased from the 3rd day, and the increase was 3- to 10-fold above controls on the 5th day, and the production of thyroidal cAMP significantly increased 2- to 3-fold. However, when slices were incubated with IgG obtained from other untreated patients, the concentration of T3 in media and the production of thyroidal cAMP did not differ from that in controls. TSH increased the release of T3 from thyroid slices 2.5-to 10-fold above controls on the 5th day and the production of cAMP 4- to 5-fold. These results strongly suggest that thyroid hormone releasing IgG in patients with Graves' disease are highly specific for autologous thyroids. The mechanism of this specificity may involve the role of self-recognition, such as antiidiotype antibody or anti-major histocompatibility complex antibody.
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Krause, Kerstin, Stefan Karger, Oliver Gimm, Sien-Yi Sheu, Henning Dralle, Andrea Tannapfel, Kurt Werner Schmid, Corinne Dupuy, and Dagmar Fuhrer. "Characterisation of DEHAL1 expression in thyroid pathologies." European Journal of Endocrinology 156, no. 3 (March 2007): 295–301. http://dx.doi.org/10.1530/eje-06-0596.
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Iodotyrosine dehalogenase 1 (DEHAL1) is a transmembrane protein involved in the recycling of iodide in the human thyroid. The aim of the present study was (I) to investigate whether DEHAL1 expression is different in differentially functioning thyroid pathologies and (II) to evaluate DEHAL1 as a possible marker of thyroid cell differentiation. Design and methods: Real-time PCR for DEHAL1 and its isoform DEHAL1B was performed in a series of 105 thyroid specimens, including toxic thyroid nodules (TTN), Graves’ disease (GD) thyroids, benign cold thyroid nodules (CTN), normal thyroid tissues and thyroid cancers (follicular thyroid carcinomas (FTC), papillary thyroid carcinomas (PTC), partially differentiated thyroid cancers (PDTC) and anaplastic thyroid carcinomas (ATC)). In addition, DEHAL1 protein expression was studied by immunohistochemistry in 163 benign and malignant thyroid pathologies and normal thyroids. Results: (I) The highest DEHAL1 mRNA levels were found in GD thyroids, while downregulation of DEHAL1 and DEHAL1B mRNA occurred in PTC and ATC (P<0.001 and <0.05 respectively); (II) DEHAL1 protein was overexpressed in TTNs and GD thyroids with predominant apical staining in all samples; (III) a weaker and patchy staining pattern was found in CTNs and normal thyroids; (IV) in differentiated thyroid cancers (FTC and PTC), a diffuse cytoplasmic DEHAL1 expression was found; and (V) in PDTC and ATC, DEHAL1 expression was faint or absent. Conclusion: Upregulation of DEHAL1 protein expression and sublocalisation of DEHAL1 at the apical cell pole in TTNs and GD thyroids is consistent with increased thyroid hormone turnover during thyrotoxicosis. Diffuse cytoplasmatic localisation or downregulation of DEHAL1 expression in thyroid cancers suggests alteration or loss of DEHAL1 function during thyroid cell dedifferentiation.
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Adkison, L. R., S. Taylor, and W. G. Beamer. "Mutant gene-induced disorders of structure, function and thyroglobulin synthesis in congenital goitre (cog/cog) in mice." Journal of Endocrinology 126, no. 1 (July 1990): 51—NP. http://dx.doi.org/10.1677/joe.0.1260051.
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ABSTRACT We have investigated thyroid structure and function in mice homozygous for the chromosome 15 mutation, congenital goitre (cog). Abnormal thyroidal hypertrophy and reduced iodine uptake in cog/cog mice were observed as early as day 18 of gestation, corresponding to the onset of thyroid function. Growth continued unabated in mutants throughout the 10-month period of observation. By 2 months of age, thyroid cell hypertrophy obliterated nearly all follicular lumina in cog/cog glands and by 10 months mean mutant thyroid mass exceeded that of age-matched littermates. Twenty-fold serum concentrations of thyrotrophin were significantly increased at all ages examined. While wild type (+/+) and heterozygote (+/cog) mice are indistinguishable from each other, thyroids of homozygote mutants (cog/cog) and the +/cog type are easily discernible from thyroids of the +/+ type by microscopic and thyroglobulin (Tg) analyses. Thyrofollicular cells of both cog/cog and +/cog genotypes contain large vesicles of accumulated, non-glycosylated proteinaceous material not observed in cells from +/+ mice. Autoradiography showed 125I was incorporated only into Tg within recognizable follicular lumina of thyroids from +/cog mice. Serum concentrations of tri-iodothyronine are depressed during development in cog/cog mice. Serum concentrations of thyroxine are depressed during postnatal development but increase progressively to normal concentrations by 10 months of age. Our analyses indicate that full size Tg is produced in thyroid cells from cog/cog mice, though in a greatly reduced quantity, and that Tgs which are several sizes smaller than normal are also produced in both homozygote and heterozygote thyroids. In addition, we observed altered electrophoretic mobilities of 19S Tg and either the absence or greatly reduced quantities of one reduced 12S Tg form. Tg mRNA is apparently normal size in the mutant. However, there is a five- to tenfold reduction in the amount of polyadenylated Tg mRNA available that correlates with the decreased amounts of full size Tg seen in the mutant. Collectively, these findings suggest that the compensatory goitre of cog/cog mice results from disordered processing of Tg mRNA transcribed from the cog mutant gene. Journal of Endocrinology (1990) 126, 51–58
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Yu, Jing, Siyi Shen, Ying Yan, Lingxiao Liu, Rongkui Luo, Shengnan Liu, Yuting Wu, Yuying Li, Jingjing Jiang, and Hao Ying. "Iodide Excess Inhibits Thyroid Hormone Synthesis Pathway Involving XBP1-Mediated Regulation." Nutrients 15, no. 4 (February 9, 2023): 887. http://dx.doi.org/10.3390/nu15040887.
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Iodine is an essential micronutrient for producing thyroid hormone (TH); however, iodide excess can lead to adverse thyroidal effects. Unfortunately, the lack of a proper in vitro model system hampered the studies of the effect of iodide excess on thyroid physiology and pathology. Here, we demonstrated that excessive iodide intake downregulated the genes related to TH synthesis in the thyroids of mice. Since sodium iodide has no effect on these genes in cultured cell lines, we developed a three-dimensional (3D) culture system to enable the murine thyrocytes to form organoids in vitro with thyroid follicle-like structures and function and found that the in vivo effect of iodide excess could be mimicked in these thyroid organoids. Our data indicate that iodide excess mainly activated the XBP1-mediated unfolded protein response in both murine thyroid and thyroid organoids, while activation of XBP1 was able to mimic the sodium iodide effect on genes for the synthesis of TH in murine thyroid organoids. Lastly, our results suggest that XBP1 might transcriptionally repress the genes involved in the synthesis of TH. Based on these findings, we propose that iodide excess inhibits the transcription of genes related to TH synthesis through a mechanism involving XBP1-mediated action.
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Kusakabe, Takashi, Akio Kawaguchi, Nobuo Hoshi, Rumi Kawaguchi, Sayuri Hoshi, and Shioko Kimura. "Thyroid-Specific Enhancer-Binding Protein/NKX2.1 Is Required for the Maintenance of Ordered Architecture and Function of the Differentiated Thyroid." Molecular Endocrinology 20, no. 8 (August 1, 2006): 1796–809. http://dx.doi.org/10.1210/me.2005-0327.
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Abstract Thyroid-specific enhancer-binding protein (T/ebp)/Nkx2.1-null mouse thyroids degenerate by embryonic day (E) 12–13 through apoptosis whereas T/ebp/Nkx2.1-heterogyzgous mice exhibit hypothyroidism with elevated TSH levels. To understand the role of T/ebp/Nkx2.1 in the adult thyroid, a thyroid follicular cell-specific conditional knockout (KO) mouse line, T/ebp(fl/fl);TPO-Cre, was established that expresses Cre recombinase under the human thyroid peroxidase (TPO) gene promoter. These mice appeared to be healthy and exhibited loss of T/ebp/Nkx2.1 expression in many, but not all, thyroid follicular cells as determined by immunohistochemistry and real-time PCR, thus presenting a T/ebp-thyroid-conditional hypomorphic mice. Detailed analysis of the thyroids from T/ebp(fl/fl), T/ebp(fl/fl);TPO-Cre, and T/ebp(fl/ko) mice, where the latter mouse line is derived from crosses with the original T/ebp/Nkx2.1-heterozygous mice, revealed that T/ebp(fl/fl);TPO-Cre mice can be classified into two groups with different phenotypes: one having atrophic/degenerative thyroid follicles with frequent presence of adenomas and extremely high serum TSH levels, and the other having an altered thyroid structure with reduced numbers of extraordinary dilated follicles consisting of excessive numbers of follicular cells as compared with those usually found in the normal thyroid. The latter phenotype was also observed in aged T/ebp(fl/ko) mouse thyroids. In vitro three-dimensional thyroid primary cultures using thyroids from T/ebp(fl/fl);TPO-Cre, T/ebp(fl/ko), and T/ebp(fl/fl) mice, and the latter treated with recombinant adenovirus with and without Cre expression, demonstrated that only cells from T/ebp(fl/fl) mice without adeno-Cre treatment formed follicular structures. Taken together, these results suggest that T/ebp/Nkx2.1 is required for maintenance of the normal architecture and function of differentiated thyroids.
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Camargo, Rosalinda Yasato, Cristina Takami Kanamura, Celso Ubirajara Friguglietti, Célia Regina Nogueira, Sonia Iorcansky, Alfio José Tincani, Ana Karina Bezerra, et al. "Histopathological Characterization and Whole Exome Sequencing of Ectopic Thyroid: Fetal Architecture in a Functional Ectopic Gland from Adult Patient." International Journal of Endocrinology 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/4682876.
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Ectopic thyroid results from a migration defect of the developing gland during embryogenesis causing congenital hypothyroidism. But it has also been detected in asymptomatic individuals. This study aimed to investigate the histopathological, functional, and genetic features of human ectopic thyroids. Six samples were histologically examined, and the expression of the specific thyroid proteins was assessed by immunohistochemistry. Two samples were submitted to whole exome sequencing. An oropharynx sample showed immature fetal architecture tissue with clusters or cords of oval thyrocytes and small follicles; one sample exhibited a normal thyroid pattern while four showed colloid goiter. All ectopic thyroids expressed the specific thyroid genes and T4 at similar locations to those observed in normal thyroid. No somatic mutations associated with ectopic thyroid were found. This is the first immature thyroid fetal tissue observed in an ectopic thyroid due to the arrest of structural differentiation early in the colloid stage of development that proved able to synthesize thyroid hormone but not to respond to TSH. Despite the ability of all ectopic thyroids to synthetize specific thyroid proteins and T4, at some point in life, it may be insufficient to support body growth leading to hypothyroidism, as observed in some of the patients.
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Sugihara, Junichi, Aaron Wong, Hiroki Shimizu, Jinbo Zhao, Hae-Ra Cho, Yingchun Wang, Samuel Refetoff, Peter Arvan, and Mingyao Liu. "Thyroidal Transcriptomic Profiles of Pathoadaptive Responses to Congenital Hypothyroidism in XB130 Knockout Mice." Cells 11, no. 6 (March 12, 2022): 975. http://dx.doi.org/10.3390/cells11060975.
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Congenital hypothyroidism is a genetic condition in which the thyroid gland fails to produce sufficient thyroid hormone (TH), resulting in metabolic dysfunction and growth retardation. Xb130−/− mice exhibit perturbations of thyrocyte cytoskeleton and polarity, and develop postnatal transient growth retardation due to congenital hypothyroidism, leading ultimately to multinodular goiter. To determine the underlying mechanisms, we performed transcriptomic analyses on thyroid glands of mice at three age points: week 2 (W2, before visible growth retardation), W4 (at the nadir of growth); and W12 (immediately before full growth recovery). Using gene set enrichment analysis, we compared a defined set of thyroidal genes between Xb130+/+ and Xb130−/− mice to identify differentially enriched gene clusters. At the earliest postnatal stage (W2), the thyroid glands of Xb130−/− mice exhibited significantly downregulated gene clusters related to cellular metabolism, which continued to W4. Additionally, mutant thyroids at W4 and W12 showed upregulated gene clusters related to extracellular matrix, angiogenesis, and cell proliferation. At W12, despite nearly normal levels of serum TH and TSH and body size, a significantly large number of gene clusters related to inflammatory response were upregulated. Early postnatal TH deficiency may suppress cellular metabolism within the thyroid gland itself. Upregulation of genes related to extracellular matrix and angiogenesis may promote subsequent thyroid growth. Chronic inflammatory responses may contribute to the pathogenesis of multinodular goiter in later life. Some of the pathoadaptive responses of Xb130−/− mice may overlap with those from other mutations causing congenital hypothyroidism.
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Contempre, Bernard, Jacques E. Dumont, Jean-François Denel, and Marie-Christine Many. "Effects of selenium deficiency on thyroid necrosis, fibrosis and proliferation: a possible role in myxoedematous cretinism." European Journal of Endocrinology 133, no. 1 (July 1995): 99–109. http://dx.doi.org/10.1530/eje.0.1330099.
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Contempre B, Dumont JE, Denef J-F, Many M-C. Effects of selenium deficiency on thyroid necrosis, fibrosis and proliferation: a possible role in myxoedematous cretinism. Eur J Endocrinol 1995;133:99–109. ISSN 0804–4643 It has been suggested that selenium deficiency is a co-factor to iodine deficiency in the pathogenesis of myxoedematous cretinism. The mechanism proposed is that the generation of hydrogen peroxide is greatly increased in iodine-deficient thyroid glands, and that selenium is involved in the control of hydrogen peroxide and its derived free radicals. This study was carried out to investigate the effect of the possibly impaired cellular defence mechanism associated with selenium deficiency on thyroid necrosis and tissue repair. For this purpose, we studied thyroid tissue from selenium- (SE–) and/or iodine-deficient (I–) rats before and after an acute toxic iodine overload. In I– thyroids, necrotic cells were numerous. Acute iodine administration increased this effect. Necrosis was associated with transient infiltration of inflammatory cells. In 1–SE+ thyroids the tissue resumed its normal appearance. In 1–SE– thyroid glands, the iodide toxicity was stronger, with greater necrosis and inflammatory reaction. The inflammation resolved but was replaced by fibrotic tissue. Fifteen days after the toxic overload, the connective tissue volume was twice the control value. Before iodide overload, the proportion of dividing cells was equal in 1–SE+ and 1–SE– thyroids. Three days after the iodide overload, this proportion was increased in 1–SE+ thyroids but reduced in the 1–SE– thyroids. Overall, the 1–SE– thyroids had four times fewer dividing cells than the 1–SE+ thyroids. In summary, selenium deficiency coupled to iodine deficiency increased necrosis, induced fibrosis and impeded compensatory epithelial cell proliferation. These results are compatible with histological and functional descriptions of thyroid tissue from myxoedematous cretins. B Contempre, IRIBHN, C.P. 602, Free University of Brussels, Medicine Faculty, 808 route de Lennik, B-1070 Brussels, Belgium
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Banna, Fakhrul Amin Mohammad Hasanul, and Zakia Sultana. "Observation of Arteria Thyroidea Ima in Bangladeshi People: A Postmortem Study." Journal of Enam Medical College 8, no. 1 (February 7, 2018): 25–28. http://dx.doi.org/10.3329/jemc.v8i1.35432.
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Background: The thyroid is a brownish red, earliest endocrine gland in mammals. The blood flow to the thyroid gland is very high. The thyroid derives its arterial blood supply from three vessels; of these, the superior and inferior thyroid arteries are fairly constant. The third artery, the thyroidea ima, is an inconstant vessel. Diseases of thyroid may need surgical intervention.This study aims to find out the presence of the arteria thyroidea ima and its origin in Bangladeshi people.Objective: The present study was carried out on considering the day-to-day growing clinical importance, and insufficient morphological data and arterial supply by thyroidea ima artery of thyroid gland and possible geographical variations in Bangladeshi people. This study will also help in minimizing complications of thyroid surgery and tracheostomy.Materials and Methods: This descriptive crosssectional study was carried out on 54 postmortem human thyroid glands collected from individuals aged 5 to 65 years. Thyroid glands were collected from unclaimed dead bodies autopsied in the morgue of Sylhet M. A. G. Osmani Medical College, Sylhet. The collected specimens were examined by careful gross dissection method.Results: Thyroidea ima artery was present in 3.70% cases, which originated equally from brachiocephalic trunk and arch of aorta.Conclusion: Presence of this artery must be searched out during thyroid surgery and tracheostomy.J Enam Med Col 2018; 8(1): 25-28
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Becks, G. P., A. Logan, I. D. Phillips, J.-F. Wang, C. Smith, D. DeSousa, and D. J. Hill. "Increase of basic fibroblast growth factor (FGF) and FGF receptor messenger RNA during rat thyroid hyperplasia: temporal changes and cellular distribution." Journal of Endocrinology 142, no. 2 (August 1994): 325–38. http://dx.doi.org/10.1677/joe.0.1420325.
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Abstract Goitre was induced in adult rats by acute (1 or 2 weeks) or chronic (4 or 10 weeks) administration of methimazole together with a low iodine diet. Involution of thyroid growth was then observed at 16 weeks, 4 weeks after withdrawal of goitrogens and reversion to a normal diet. Experimental animals quickly became hypothyroid compared with controls and exhibited thyroid hyperplasia (control (n=10): total serum thyroxine (T4) 66 ±4 nmol/l, thyroid weight 5 ± 1 mg/100 g body weight, means± s.d.; experimental (n=10): T4 undetectable, thyroid weight 27 ±4 mg/100 g body weight after 2 weeks of treatment). Thyroid growth rate subsequently slowed between 2 and 10 weeks. Messenger RNA for basic fibroblast growth factor (basic FGF) and for the high-affinity FGF receptor, was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for basic FGF and its receptor were detectable in thyroids from control rats at all times, while none was detected in the livers from any animal. Basic FGF and receptor mRNAs increased, and were detected at greatest abundance in hyperplastic thyroids at 1 and 2 weeks respectively, during goitre formation, but subsequently declined in parallel with thyroid growth rate at 4 and 10 weeks. When quantified by radioimmunoassay, basic FGF extracted from thyroids was fivefold greater than in controls after 1 week of goitrogen treatment (control (n=4): 24±9 pmol/μg DNA; goitre (n=4): 100± 16 pmol/μg DNA; P<0·05). Basic FGF and FGF receptor mRNAs localized by in situ hybridization predominantly to the epithelial cell population within follicles. Localization by immunohistochemistry demonstrated that basic FGF was present in the thyroids of control rats, and was largely associated with the basement membrane of follicles. During thyroid hyperplasia, increased basic FGF immunoreactivity appeared over the cytoplasm of follicular epithelial cells and was lost from the extracellular matrix. Thyroid involution following removal of goitrogen/low iodine treatment was associated with a decrease in mRNA for basic FGF or its receptor, and a loss of immunoreactive basic FGF from the cytoplasm of follicular cells. These results suggest that autocrine expression of basic FGF and FGF receptor could contribute to thyroid hyperplasia in rats. Journal of Endocrinology (1994) 142, 325–338
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Rossi, R., P. Franceschetti, I. Maestri, E. Magri, L. Cavazzini, E. C. degli Uberti, and L. del Senno. "Evidence for androgen receptor gene expression in human thyroid cells and tumours." Journal of Endocrinology 148, no. 1 (January 1996): 77–85. http://dx.doi.org/10.1677/joe.0.1480077.
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Abstract Androgen-binding activity has been identified in normal and pathological thyroids, but evidence for the expression of the canonic androgen receptor (AR) in the thyroid has not been provided so far. In this study we have used reverse transcription (RT)-PCR to examine RNA expression of the canonic AR gene in human thyroid tissues, in primary cultures of human thyrocytes and in a variety of neoplastic thyroid cell lines (NPA, TPC and WRO). An AR cDNA fragment with the expected size of 262 bp was detected in normal tissues and cultured thyrocytes as well as in neoplastic cell lines, demonstrating that the gene for AR is indeed expressed in thyroid follicular cells. Immunocytochemical analysis revealed the presence of the AR protein in cancer cell lines and androgen treatment increased nuclear positivity to AR. In a survey of 35 thyroid tissues AR cDNA was detected in all the non-neoplastic samples (6 normal and 3 goitrous) and in 19 of 26 neoplastic samples. AR cDNA was not detected in 4 of the 9 follicular adenomas and in 3 of the 12 papillary carcinomas. AR was revealed by immunohistochemistry in 1 of 2 normal thyroids, in 1 goiter and in 1 of 2 neoplastic thyroids. These findings show the presence of the canonic AR in the human thyroid. Journal of Endocrinology (1996) 148, 77–85
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Kondo, Tetsuo, Nobuki Nakamura, Koichi Suzuki, Shin-ichi Murata, Akira Muramatsu, Akira Kawaoi, and Ryohei Katoh. "Expression of Human Pendrin in Diseased Thyroids." Journal of Histochemistry & Cytochemistry 51, no. 2 (February 2003): 167–73. http://dx.doi.org/10.1177/002215540305100205.
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We examined pendrin expression in various diseased thyroid tissues by immunohistochemistry (IHC) using antiserum raised against human pendrin and by real-time quantitative RT-PCR. In normal thyroids the antiserum reacted with the apical membrane of follicular cells and its immunoreactivity was faint. In Graves’ thyroids, the IHC expression of pendrin appeared in a pattern similar to that of normal thyroids but it was more extensive and stronger, especially in areas showing marked proliferation of follicular cells. The immunoreactivities of pendrin in nodular goiters varied from case to case. In follicular adenomas, pendrin was localized in the follicle-forming parts of the tumor but was negative in trabecular parts. Pendrin was negative in all follicular carcinomas, papillary carcinomas, and in one case of medullary carcinoma. In quantitive mRNA analysis, the relative values of pendrin mRNA were significantly low in papillary carcinoma ( p<0.01), whereas the values in other diseased thyroids were not significantly different from those in normal thyroids. These results suggest that pendrin may play a role in thyroid hormone production as the apical porter of chloride/iodide and investigation of pendrin leads to a better understanding of functional aspects of the iodine transportation system in thyroid diseases.
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Nikitski, Alyaksandr, Vladimir Saenko, Mika Shimamura, Masahiro Nakashima, Michiko Matsuse, Keiji Suzuki, Tatiana Rogounovitch, et al. "Targeted Foxe1 Overexpression in Mouse Thyroid Causes the Development of Multinodular Goiter But Does Not Promote Carcinogenesis." Endocrinology 157, no. 5 (March 16, 2016): 2182–95. http://dx.doi.org/10.1210/en.2015-2066.
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Abstract Recent genome-wide association studies have identified several single nucleotide polymorphisms in the forkhead box E1 gene (FOXE1) locus, which are strongly associated with the risk for thyroid cancer. In addition, our recent work has demonstrated FOXE1 overexpression in papillary thyroid carcinomas. To assess possible contribution of Foxe1 to thyroid carcinogenesis, transgenic mice overexpressing Foxe1 in their thyroids under thyroglobulin promoter (Tg-Foxe1) were generated. Additionally, Tg-Foxe1 mice were exposed to x-rays at the age of 5 weeks or crossed with Pten+/− mice to examine the combined effect of Foxe1 overexpression with radiation or activated phosphatidylinositol-3-kinase/Akt pathway, respectively. In 5- to 8-week-old Tg-Foxe1 mice, severe hypothyroidism was observed, and mouse thyroids exhibited hypoplasia of the parenchyma. Adult 48-week-old mice were almost recovered from hypothyroidism, their thyroids were enlarged, and featured colloid microcysts and multiple benign nodules of macrofollicular-papilloid growth pattern, but no malignancy was found. Exposure of transgenic mice to 1 or 8 Gy of x-rays and Pten haploinsufficiency promoted hyperplastic nodule formation also without carcinogenic effect. These results indicate that Foxe1 overexpression is not directly involved in the development of thyroid cancer and that proper Foxe1 dosage is essential for achieving normal structure and function of the thyroid.
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Saad, Ali G., Seena Kumar, Elaine Ron, Jay H. Lubin, Jerzy Stanek, Kevin E. Bove, and Yuri E. Nikiforov. "Proliferative Activity of Human Thyroid Cells in Various Age Groups and Its Correlation with the Risk of Thyroid Cancer after Radiation Exposure." Journal of Clinical Endocrinology & Metabolism 91, no. 7 (July 1, 2006): 2672–77. http://dx.doi.org/10.1210/jc.2006-0417.
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Abstract Context: The thyroid gland is vulnerable to the carcinogenic effects of ionizing radiation, and there is a well-documented inverse correlation between thyroid cancer and age at exposure, particularly for ages less than 20 yr. One of the factors responsible for this phenomenon may be more rapid cell proliferation in children. Objective: The objective of this study was to determine the proliferative rate of normal human thyroid cells in different age groups. Design: We used immunohistochemical analysis to determine the Ki-67 proliferative index in 117 thyroid glands obtained at autopsy, including 25 fetal thyroids (11–40 wk gestation), 55 childhood thyroids (0–19 yr), and 37 adult thyroids (20–60 yr). Results: The rate of Ki-67 labeling in the three groups was 7.4 ± 6.10, 0.23 ± 0.15, and 0.08 ± 0.04% respectively, demonstrating an overall trend for diminishing proliferative activity of thyroid cells with increasing age. However, a lack of correlation was noted between the slopes of cancer risk calculated from previous studies of irradiated populations and proliferative rate in the pediatric age intervals of 0–4 and 5–9 yr, suggesting that other factors are likely to be responsible for the particularly high sensitivity to radiation-induced thyroid cancer among the youngest children. Conclusions: Our findings of a general decrease in proliferative activity of thyroid cells with age may explain, at least in part, the higher risks of radiation-related thyroid cancer in children compared with adults. However, the variation in the rate of cell proliferation is unlikely to be responsible entirely for this phenomenon and other factors may also be involved.
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Robertson, S. M., M. A. Friend, and B. J. King. "Mild congenital goitre increases lamb mortality in southern New South Wales." Australian Journal of Experimental Agriculture 48, no. 7 (2008): 995. http://dx.doi.org/10.1071/ea08005.
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Congenital goitre, symptomatic of iodine deficiency, can be associated with elevated levels of lamb mortality. This study details an outbreak east of Wagga Wagga in southern NSW, where goitre has previously not been documented. Measurements were taken on flocks at two sites near Ladysmith. Up to 82% of dead lambs had thyroid : weight ratios of more than 0.4 g/kg bodyweight, potentially large enough to affect survival. Up to 16% of lambs surviving to marking had enlarged thyroids (i.e. estimated by palpation). Lambs with enlarged thyroids may be more prone to dystocia, with ewes requiring assistance at delivery. Sex and birthweight were not related to thyroid size, but of lambs surviving to marking, a greater proportion of Merino than crossbred lambs had enlarged thyroids. At the second site, growth rate from birth to marking but not to weaning was reduced in lambs with higher thyroid scores. The high incidence of goitre in these flocks suggests that iodine deficiency may be an important factor in lamb mortality in some years in this region, but is unlikely to be detected due to the relatively small degree of thyroid enlargement.
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Jayaraju, Rijo M., Azeem Mohiyuddin, Shuaib Merchant, Sagaya Raj, and Beauty Sasidharan. "Thyroidea Ima Artery: A Report of Two Cases." International Journal of Head and Neck Surgery 5, no. 2 (2014): 89–90. http://dx.doi.org/10.5005/jp-journals-10001-1188.
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ABSTRACT Thyroidea ima is a rare anomalous artery supplying the thyroid gland apart from the superior and inferior thyroid arteries. It is of surgical importance in thyroid, parathyroid and tracheal surgeries. Our study aims to highlight two cases of thyroidea ima artery found during thyroidectomy: • Case 1: Thyroidea ima artery was seen arising from the medial surface of the right common carotid artery in a female patient, who underwent total thyroidectomy. • Case 2: Thyroidea ima artery was seen arising from the anterior surface of the right innominate artery, in a female patient, who underwent right hemithyroidectomy. Conclusion Thyroidea ima artery, although a rare arterial variation, a thorough regional anatomic knowledge and meticulous dissection will not only help us in identifying such a vascular variation, also help us in preventing an accidental injury. How to cite this article Raj S, Mohiyuddin A, Merchant S, Jayaraju RM, Sasidharan B. Thyroidea Ima Artery: A Report of Two Cases. Int J Head Neck Surg 2014;5(2):89-90.
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Hassan, Bardes B., Lucas A. Altstadt, Wessel P. Dirksen, Said M. Elshafae, and Thomas J. Rosol. "Canine Thyroid Cancer: Molecular Characterization and Cell Line Growth in Nude Mice." Veterinary Pathology 57, no. 2 (February 21, 2020): 227–40. http://dx.doi.org/10.1177/0300985819901120.
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Thyroid cancer is the most common endocrine malignancy in dogs. Dogs and humans are similar in the spontaneous development of thyroid cancer and metastasis to lungs; however, thyroid cancer has a higher incidence of metastasis in dogs. This study developed a preclinical nude mouse model of canine thyroid cancer using a canine thyroid adenocarcinoma cell line (CTAC) and measured the expression of important invasion and metastasis genes in spontaneous canine thyroid carcinomas and CTAC cells. CTAC cells were examined by electron microscopy. Short tandem repeat analysis was performed for both the original neoplasm and CTAC cells. CTAC cells were transduced with luciferase and injected subcutaneously and into the tail vein. Tumors and metastases were monitored using bioluminescent imaging and confirmed with gross necropsy and histopathology. Invasion and metastasis genes were characterized in 8 follicular thyroid carcinomas (FTCs), 4 C-cell thyroid carcinomas, 3 normal thyroids, and CTAC cells. CTAC cells grew well as xenografts in the subcutis, and they resembled the primary neoplasm. Metastasis to the kidney and lung occurred infrequently following subcutaneous and tail vein injection of CTAC cells. STR analysis confirmed that CTAC cells were derived from the original neoplasm and were of canine origin. Finally, 24 genes were differentially expressed in spontaneous canine thyroid carcinomas, CTAC, and normal thyroids. This study demonstrated the usefulness of a nude mouse model of experimental canine thyroid carcinoma and identified potential molecular targets of canine follicular and C-cell thyroid carcinoma.
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Kabel, P. J., H. A. M. Voorbij, R. D. van der Gaag, W. M. Wiersinga, M. de Haan, and H. A. Drexhage. "Dendritic cells in autoimmune thyroid disease." Acta Endocrinologica 116, no. 1_Suppl (August 1987): S42—S48. http://dx.doi.org/10.1530/acta.0.114s042.
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Abstract. Dendritic cells form a morphologically distinct class of cells characterized by shape, reniform nucleus, absent to weak acid-phosphatase activity and strong Class II MHC determinant positivity. Functionally they are the most efficient cells in antigen presentation to T-lymphocytes which indicates their role in the initiation of an immune response. Using immunehistochemical techniques we studied the presence of dendritic cells in normal Wistar rat and human thyroids, in thyroids of BBW rats developing thyroid autoimmunity and in Graves' goitres. Dendritic cells could be identified in all thyroids studied and were positioned underneath the thyrocytes in between the follicles. Skin dendritic cells travel via lymphatics to draining lymph nodes, thus forming an antigen presenting cell system. It is likely that a similar cell system exists on the level of the thyroid for dendritic cells have also been detected in thyroid draining lymph nodes. In normal thyroid tissue of both human and rat dendritic cells were relatively scarce. During the initial phases of the thyroid autoimmune response in the BBW rat (before the appearance of Tg-antibodies in the circulation) numbers of thyroid dendritic cells increased. Intrathyroidal T-helper cells, B-cells or plasma cells could not be found. The thyroid draining lymph node contained large numbers of plasma cells. During the later stages of the thyroid autoimmune response in the BB/W rat (after the appearance of Tg-antibodies in the circulation) and in Graves' goitres dendritic cells were not only present in high number, but 20–30% were seen in contact with now-present intrathyroidal T-helper lymphocytes. The so-formed lymphoid cell aggregates were predominantly small (< 10 cells), but very large aggregates could also be detected. These large accumulations were highly organized and composed of T-cell zones, B-cell zones and numerous plasma cells. Such accumulations are reminiscent of secondary lymphoid organs. In view of these morphological data it is conceivable that thyroid dendritic cells are of prime importance in the presentation of autoantigen in thyroid autoimmune disease. Throughout the process of autosensitization in the BB/W rat thyroid epithelial cells stayed negative for Class II MHC determinants. This shows that Class II expression on thyrocytes is not prerequisite for thyroid autoimmunity to develop.
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da Costa, VM, DG Moreira, and D. Rosenthal. "Thyroid function and aging: gender-related differences." Journal of Endocrinology 171, no. 1 (October 1, 2001): 193–98. http://dx.doi.org/10.1677/joe.0.1710193.
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The effects of aging on human or animal thyroid function are still not well defined. We evaluated some aspects of thyroid function during aging using an animal model (young and old Dutch-Miranda rats). In old rats of both genders, serum thyroxine (T4) decreased but serum thyrotrophin (TSH) remained unaltered, suggesting a disturbance in the pituitary-thyroid feedback mechanism during aging. Serum tri-iodothyronine (T3) only decreased in old males, possibly because female rats are almost twice as efficient in hepatic T4 to T3 deiodination. Thyroidal T4-5'-deiodinase activity did not change much during aging, although it decreased slightly in males. Thyroidal iodothyronine-deiodinase type I mRNA expression but not total thyroidal enzymatic activity were higher in female than in male rats. Thus, ovarian/testicular hormones may modulate the expression and/or the activity of hepatic and thyroidal type I iodothyronine-deiodinase. Thyroperoxidase (TPO) and thyroglobulin (Tg) expression were higher in young male rats than in females. In males, TPO and Tg gene expression decreased with aging, suggesting that androgens might increase their expression. Our results showed that aging induces real changes in rat thyroid gland function and regulation, affecting at least pituitary, thyroid and liver functions. Furthermore, some of these changes were gender related, indicating that gonadal hormones may modulate thyroid gland function and regulation.
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Logan, A., C. Smith, G. P. Becks, A. M. Gonzalez, I. D. Phillips, and D. J. Hill. "Enhanced expression of transforming growth factor-β1 during thyroid hyperplasia in rats." Journal of Endocrinology 141, no. 1 (April 1994): 45–57. http://dx.doi.org/10.1677/joe.0.1410045.
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Abstract Transforming growth factor-β1 (TGF-β1) has been reported to influence the growth rate and iodine uptake and organification in vitro by isolated thyrocytes. We have determined changes in the expression and presence of TGF-β1 within the rat thyroid during goitre induction, and subsequent involution following goitrogen withdrawal. Hyperplastic goitres were induced in adult rats by administration of methimazole together with a low iodine diet for up to 12 weeks. Goitrogen-treated rats quickly became hypothyroid compared with controls, and exhibited thyroid hyperplasia and hypertrophy assessed by thyroid weight, and DNA and protein content (control: total serum thyroxine (T4) 66 ± 4 nmol/l, thyroid weight 5 ± 1 mg/100 g body weight, mean ± s.d., n = 10; 2 weeks goitrogen: T4 undetectable, thyroid weight 27 ± 4 mg/100 g, n = 10). Thyroid growth rate slowed subsequently between 2 and 10 weeks. Messenger RNA for TGF-β1 was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for TGF-β1 were detected in thyroids from control rats at all time-points, while TGF-β1 mRNA was barely detectable in liver. Thyroid TGF-β1 mRNA levels substantially and progressively increased at 1 and 2 weeks of goitrogen treatment respectively, and remained above control levels at 4 and 10 weeks. As thyroid involution occurred 4 weeks following goitrogen withdrawal, so thyroid TGF-β1 mRNA levels declined. In control animals, the cellular localization of TGF-β1 mRNA, determined by in situ hybridization, was found to be a subpopulation of follicular epithelial cells, and immunohistochemical co-localization of TGF-β1 and calcitonin identified these tentatively as parafollicular or C-cells. During goitre formation, abundant TGF-β1 mRNA and peptide were found to be widely distributed within the entire follicular epithelium. While this ubiquitous distribution had largely disappeared in the involuting gland, TGF-β1 peptide was retained within the parafollicular cells, which appeared more abundant than in thyroids from control animals. These results suggest that an increased local expression of TGF-β1, a putative growth inhibitor, during thyroid hyperplasia may contribute to the temporal stabilization of goitre size. Journal of Endocrinology (1994) 141, 45–57
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Pankiv, V. I. "Level of thyroid-stimulating hormone as basic diagnostic marker and criterion of treatment success of thyroid diseases." HEALTH OF WOMAN, no. 4(120) (May 30, 2017): 102–6. http://dx.doi.org/10.15574/hw.2017.120.102.
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In the article information is generalized on the aspects of early diagnostics of thyrois disorders. The value of thyroid-stimulating hormone is underlined as basic test for determination of the thyroid functional state and criterion of treatment success of thyroid diseases. Key words: thyroid, thyroid-stimulating hormone, diagnostics.
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Shimamura, Mika, Mami Nakahara, Florence Orim, Tomomi Kurashige, Norisato Mitsutake, Masahiro Nakashima, Shinji Kondo, et al. "Postnatal Expression of BRAFV600E Does Not Induce Thyroid Cancer in Mouse Models of Thyroid Papillary Carcinoma." Endocrinology 154, no. 11 (November 1, 2013): 4423–30. http://dx.doi.org/10.1210/en.2013-1174.
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The mutant BRAF (BRAFV600E) is the most common genetic alteration in papillary thyroid carcinomas (PTCs). The oncogenicity of this mutation has been shown by some genetically engineered mouse models. However, in these mice, BRAFV600E is expressed in all the thyroid cells from the fetal periods, and suppresses thyroid function, thereby leading to TSH elevation, which by itself promotes thyroid tumorigenesis. To overcome these problems, we exploited 2 different approaches, both of which allowed temporally and spatially restricted expression of BRAFV600E in the thyroid glands. First, we generated conditional transgenic mice harboring the loxP-neoR-loxP-BRAFV600E-internal ribosome entry site-green fluorescent protein sequence [Tg(LNL-BRAFV600E)]. The double transgenic mice (LNL-BRAFV600E;TPO-Cre) were derived from a high expressor line of Tg(LNL-BRAFV600E) mice and TPO-Cre mice; the latter expresses Cre DNA recombinase under the control of thyroid-specific thyroid peroxidase (TPO) promoter and developed PTC-like lesions in early life under normal serum TSH levels due to mosaic recombination. In contrast, injection of adenovirus expressing Cre under the control of another thyroid-specific thyroglobulin (Tg) promoter (Ad-TgP-Cre) into the thyroids of LNL-BRAFV600E mice did not induce tumor formation despite detection of BRAFV600E and pERK in a small fraction of thyroid cells. Second, postnatal expression of BRAFV600E in a small number of thyroid cells was also achieved by injecting the lentivirus expressing loxP-green fluorescent protein-loxP-BRAFV600E into the thyroids of TPO-Cre mice; however, no tumor development was again observed. These results suggest that BRAFV600E does not appear to induce PTC-like lesions when expressed in a fraction of thyroid cells postnatally under normal TSH concentrations.
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Ong, M., D. G. Malkin, and A. Malkin. "Activation of adrenal adenyl cyclase by anti-thyroid plasma membrane antibodies." Acta Endocrinologica 110, no. 2 (October 1985): 244–50. http://dx.doi.org/10.1530/acta.0.1100244.
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Abstract. We have previously shown that IgG isolated from rabbit anti-bovine thyroid plasma membrane (anti-BTPM) antiserum exhibits properties similar to thyroid stimulating antibodies (TSAb) in that it activates thyroid adenyl cyclase. In this study, the organ non-specificity of this reaction was investigated. It was observed that anti-BTPM IgG stimulated not only adenyl cyclase of bovine thyroid but also that of the adrenal. The stimulatory activities on the thyroid and adrenal adenyl cyclase were abolished by absorption of the IgG with bovine adrenal plasma membrane (BAPM). These results indicate that anti-BTPM antibodies, similar to TSAb, exert both thyroidal and extra-thyroidal effects. Thus anti-BTPM antibodies may be directed against antigenic determinants that are common to both thyroid and adrenal plasma membranes. Like the anti-BTPM IgG, anti-BAPM IgG also activated both thyroid and adrenal adenyl cyclase. However, when IgG of the anti-BAPM antiserum was absorbed with thyroid plasma membranes, only the thyroid, but not the adrenal stimulating activity was abolished. It was concluded that the anti-BAPM antiserum contained antibodies directed against membrane antigens specific for the adrenal as well as common antigens shared by the thyroid.
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Versloot, P. M., J. P. Schröder-Van Der Elst, D. Van Der Heide, and L. Boogerd. "Effects of marginal iodine deficiency during pregnancy: iodide uptake by the maternal and fetal thyroid." American Journal of Physiology-Endocrinology and Metabolism 273, no. 6 (December 1, 1997): E1121—E1126. http://dx.doi.org/10.1152/ajpendo.1997.273.6.e1121.
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Iodide uptake by the thyroid is an active process. Iodine deficiency and pregnancy are known to influence thyroid hormone metabolism. The aim of this study was to clarify the effects of iodine deficiency and pregnancy on iodide uptake by the thyroid. Radioiodide was injected intravenously into nonpregnant and 19-day pregnant rats receiving a normal or marginally iodine-deficient diet. The uptake of radioiodide by the thyroid was measured continuously for 4 h. The absolute iodide uptake by the maternal and fetal thyroid glands at 24 h was calculated by means of the urinary specific activity. Pregnancy resulted in a decrease in the absolute thyroidal iodide uptake. Marginal iodine deficiency had no effect on the absolute iodide uptake by the maternal thyroid. The decreased plasma inorganic iodide was compensated by an increase in thyroidal clearance. A similar compensation was not found for the fetus; the uptake of iodide by the fetal thyroid decreased by 50% during marginal iodine deficiency. This can lead to diminished thyroid hormone production, which will have a negative effect on fetal development, especially of the brain.
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Korsholm, Kirsten, Michala Reichkendler, Louise Alslev, Åse Krogh Rasmussen, and Peter Oturai. "Long-Term Follow-Up of Thyroid Incidentalomas Visualized with 18F-Fluorodeoxyglucose Positron Emission Tomography—Impact of Thyroid Scintigraphy in the Diagnostic Work-Up." Diagnostics 11, no. 3 (March 19, 2021): 557. http://dx.doi.org/10.3390/diagnostics11030557.
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Our objective was to evaluate the frequency of malignancy in incidental thyroidal uptake on 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) in a cohort of Danish patients, and furthermore to evaluate the impact of thyroid scinti-graphy in the diagnostic work-up. All whole-body PET/CT reports from 1 January 2010 to 31 December 2013 were retrospectively reviewed and further analyzed if visually increased thyroidal FDG uptake was reported. Patient electronic files were searched for further thyroid evaluation. Of 13,195 18F-FDG-PET/CT scans in 9114 patients, 312 PET/CT reports mentioned incidental thyroid FDG-uptake, and 279 patients were included in the study (3.1%). The thyroid was further investigated in 137 patients (49%), and 75 patients underwent thyroid scintigraphy. A total of 57 patients had a thyroid biopsy and 21 proceeded to surgery. Surgical specimens displayed malignancy in 10 cases, and one thyroid malignancy was found by autopsy. Hence, 11 patients were diagnosed with thyroid malignancies among 279 patients with incidental thyroid 18F-FDG uptake (3.9%). In 34 patients, a biopsy was avoided due to the results of the thyroid scintigraphy. We conclude that patients with thyroid incidentalomas can benefit from further diagnostic work-up including a thyroid scintigraphy.
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Knietsch, M., T. Spillmann, E. G. Grünbaum, R. Bauer, and M. Puille. "Radioiodine treatment of feline hyperthyroidism in Germany." Nuklearmedizin 41, no. 06 (2002): 245–51. http://dx.doi.org/10.1055/s-0038-1625296.
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SummaryAim: Establishment of radioiodine treatment of feline hyperthyroidism in veterinary routine in accordance with German radiation protection regulations. Patients and methods: 35 cats with proven hyperthyroidism were treated with 131I in a special ward. Thyroid uptake and effective halflife were determined using gammacamera dosimetry. Patients were released when measured whole body activity was below the limit defined in the German “Strahlenschutzverordnung”. Results: 17/20 cats treated with 150 MBq radioiodine and 15/15 cats treated with 250 MBq had normal thyroid function after therapy, normal values for FT3 and FT4 were reached after two and normal TSH levels after three weeks. In 14 cats normal thyroid function was confirmed by controls 3-6 months later. Thyroidal iodine uptake was 24 ± 10%, effective halflife 2.5 ± 0.7 days. Whole body activity <1 MBq was reached 13 ± 4 days after application of 131I. Radiation exposure of cat owners was estimated as 1.97 Sv/MBq for adults. Conclusion: Radioiodine therapy of feline hyper-thyroidism is highly effective and safe. It can easily be performed in accordance with German radiation protection regulations, although this requires hospitalisation for approximately two weeks. Practical considerations on radiation exposure of cat owners do not justify this long interval. Regulations for the veterinary use of radioactive substances similar to existing regulations for medical use in humans are higly desirable.
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Kandil, Emad, Mohamed Abdel Khalek, Wael G. Ibrahim, Haytham Alabbas, C. Lillian Yau, Paul Friedlander, Byron Crawford, and Bernard M. Jaffe. "Papillary thyroid carcinoma in black thyroids." Head & Neck 33, no. 12 (March 17, 2011): 1735–38. http://dx.doi.org/10.1002/hed.21656.
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Atiyeh, Bishara S., Amir Abdelnour, Fadi F. Haddad, and Hussein Ahmad. "Lingual thyroid: tongue-splitting incision for transoral excision." Journal of Laryngology & Otology 109, no. 6 (June 1995): 520–24. http://dx.doi.org/10.1017/s0022215100130609.
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AbstractTwo patients presenting to the Central Military Hospital of Beirut with symptomatic lingual thyroid are reported. I131 thyroid scanning revealed the lingual thyroid to be the only functional thyroid tissue present in each patient. Subsequent CT scanning demonstrated the large size of these ectopic thyroids causing significant mechanical obstruction. These were excised transorally using a posterior midline tonguesplitting incision and reimplanted in the rectus abdominis muscles.Details of this modified tongue-splitting surgical approach are described. A brief review of the literature concerning lingual thyroid and its surgical treatment is also presented as well as three patients operated on for lingual thyroid at the American University of Beirut Medical Centre between 1975 and 1994 using an external neck incision.
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Gambardella, Claudio, Ludovico Docimo, Giancarlo Candela, Giovanni Cozzolino, Federico Mongardini, Francesca Serilli, Giusiana Nesta, et al. "Thyroid-Bed Schwannoma Mimicking a Thyroid Neoplasm: A Challenging Diagnosis: Report of a Case and Literature Review." Medicina 58, no. 10 (September 24, 2022): 1345. http://dx.doi.org/10.3390/medicina58101345.
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Background: Schwannomas, also called neurinomas, are rare benign tumors of the neural cells that can develop from the sheaths of nervous structures of several districts, although the most frequent sites are the cranial nerves (25%–45%). Rarely, cases show neck schwannomas in the thyroid parenchyma, while the cases of thyroid-bed schwannomas mimicking a thyroid-gland lesions are anecdotal. Methods: We report the case of a 70-year-old man with a preoperative-imaging diagnosis of a thyroid neoplasm, confirmed as Thyr 4 by fine-needle cytology. Results: During surgery, an extra-thyroidal lesion was discovered, determined to be a neck schwannoma through definitive pathology. A literature review of cases of thyroid-bed-lesion schwannomas misinterpreted as thyroid neoplasms was carried out. Conclusions: In the case of suspicious extra-thyroidal lesions, we advocate for a close routine cooperation between the cytologist, the radiologist, and the surgeon in the attempt to reach an accurate preoperative diagnosis.
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Kazi, Amna, Sidra Hameed, Farheen Fatima, and Maham Waseem. "Pregnancy Related Thyroidal Dysfunction and its Feto-Maternal Outcomes." Pakistan Journal of Medical and Health Sciences 16, no. 11 (November 30, 2022): 180–81. http://dx.doi.org/10.53350/pjmhs20221611180.
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Aim: To detect the thyroidal dysfunction during pregnancy and the related outcomes. Study Design: Prospective study. Place and duration of study: Department of Obstetrics & Gynaecology, S. Z. Hospital Lahore from 01-01-2021 to 30-06-2022 Methodology: One thousand pregnant women in third trimester were enrolled for thyroid function test and screening, analysis of TSH, free T3 and T4 level. Results: Only 30 (3%) was having thyroid dysfunction while the dysfunction was reported highest in the women within 29-38 years of age. Most of the cases suffering from thyroid dysfunction are suffering from the subclinical hypothyroid condition (43%). The reduction in Apgar score was observed up to almost 3.59 times in newborns of thyroid dysfunction women. The risk of preeclampsia and cesarean section was also significantly raised in thyroidal dysfunction women. Odds ratio for low birth weight was observed as 6.32 with a significant association with thyroid dysfunction in pregnancy. Conclusion: There are poor feto-maternal outcomes of thyroid dysfunction during pregnancy with 43% of the cases as having subclinical hypothyroidism. Key words: Pregnancy, Thyroid dysfunction, Feto-maternal outcome
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Ramelli, Fabio, Ulrich Bürgi, Lotte Siebenhüner, Heinz Kohler, and Hugo Studer. "A disproportionate accumulation of fibrous tissue is not a causal factor in human goitre growth." Acta Endocrinologica 116, no. 4 (December 1987): 502–6. http://dx.doi.org/10.1530/acta.0.1160502.
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Abstract. Histological preparations from human nodular goitres reveal the presence of variable and sometimes considerable amounts of acellular material separating the individual follicles. Part of this interstitial tissue consists histologically of fibrous strands. However, quantitative data on the fibrous tissue content of goitres are scarce. In the present study the proportion of fibrous tissue in normal human thyroids and human goitres was determined biochemically by measuring their content of collagen, the predominant component of fibrous tissue. Total collagen content increased in parallel to thyroid weight. The relative collagen content, however, decreased slightly but significantly with increasing thyroid weight. The collagen/DNA ratio (= fibrous tissue/cell number ratio) was not higher in goitres than in normal human thyroids. These results indicate that in goitre growth, there is no disproportionate accumulation of fibrous tissue accompanying the multiplication of thyroid follicular cells. They are in line with the earlier findings that despite histological heterogeneity, the main component of nodular goitres is newly generated follicles.
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Yamashita, Kamejiro, Yuji Aiyoshi, Nobuaki Kuzuya, and Yoshinobu Koide. "Alterations of adrenergic systems in thyroid slices from patients with Graves' disease." Acta Endocrinologica 110, no. 3 (November 1985): 360–65. http://dx.doi.org/10.1530/acta.0.1100360.
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Abstract. The responses to TSH of tissue cAMP levels in thyroid slices from patients with Graves' disease were significantly lower than those in normal thyroid slices. Conversely, tissue cAMP levels in thyroid slices from these patients were greatly increased by β-adrenergic agonists, either isoproterenol or norepinephrine compared with those in normal thyroid slices. The elevation of cAMP levels induced by TSH in normal thyroid slices was significantly reduced by norepinephrine via α-adrenergic action as reported previously in canine thyroid slices, while such an elevation by TSH of cAMP levels in slices of Graves' disease thyroids was not inhibited, or rather increased by norepinephrine. These results indicate that, in addition to low responses to TSH, α- and β-adrenergic systems were functionally altered in thyroid tissues of patients with Graves' disease.
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Hichri, Maha, Georges Vassaux, Jean-Marie Guigonis, Thierry Juhel, Fanny Graslin, Julien Guglielmi, Thierry Pourcher, and Béatrice Cambien. "Proteomic Analysis of Iodinated Contrast Agent-Induced Perturbation of Thyroid Iodide Uptake." Journal of Clinical Medicine 9, no. 2 (January 23, 2020): 329. http://dx.doi.org/10.3390/jcm9020329.
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(1) Background: We recently showed that iodinated contrast media (ICM) reduced thyroid uptake of iodide independently of free iodide through a mechanism different from that of NaI and involving a dramatic and long-lasting decrease in Na/I symporter expression. The present study aimed at comparing the response of the thyroid to ICM and NaI using a quantitative proteomic approach. (2) Methods: Scintiscans were performed on ICM-treated patients. Micro Single-Photon Emission Computed Tomography (microSPECT/CT) imaging was used to assess thyroid uptakes in ICM- or NaI-treated mice and their response to recombinant human thyroid-stimulating hormone. Total thyroid iodide content and proteome was determined in control, NaI-, or ICM-treated animals. (3) Results: The inhibitory effect of ICM in patients was selectively observed on thyroids but not on salivary glands for up to two months after a systemic administration. An elevated level of iodide was observed in thyroids from NaI-treated mice but not in those from ICM animals. Exposure of the thyroid to NaI modulates 15 cellular pathways, most of which are also affected by ICM treatment (including the elF4 and P706SK cell signaling pathway and INSR identified as an upstream activator in both treatments). In addition, ICM modulates 16 distinct pathways and failed to affect thyroid iodide content. Finally, administration of ICM reduces thyroid-stimulating hormone (TSH) receptor expression which results in a loss of TSH-induced iodide uptake by the thyroid. (4) Conclusions: Common intracellular mechanisms are involved in the ICM- and NaI-induced reduction of iodide uptake. However, ICM fails to affect thyroid iodide content which suggests that the modulation of these common pathways is triggered by separate effectors. ICM also modulates numerous distinct pathways which may account for its long-lasting effect on thyroid uptake. These observations may have implications in the management of patients affected by differentiated thyroid carcinomas who have been exposed to ICM. They also provide the basis for the utilization of ICM-based compounds in radioprotection of the thyroid.
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Sawicka-Gutaj, Nadia, Mirosław Andrusiewicz, Agata Czarnywojtek, Joanna Waligórska-Stachura, Maciej Biczysko, Jerzy Skrobisz, Jerzy Sowiński, and Marek Ruchała. "Changes of Nicotinamide Phosphoribosyltransferase Expressions in Thyroid Glands of Patients with Different Thyroid Pathologies." BioMed Research International 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/1316390.
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Purpose. Our aim was to analyze NAMPT expression in thyroid tissue derived from patients with Graves’ disease with (GD) and without (GO) orbitopathy, patients with toxic nodular goiters (TNG) and thyroid cancers (TC), and healthy controls. Methods. 153 thyroid tissue samples of consecutive patients who underwent thyroidectomy were collected. Previous therapy with steroids was an exclusion criterion. We collected clinicopathological data of all subjects and we assessed NAMPT expression using qPCR. Results. We found the highest NAMPT expression in the thyroids of patients with GO (n = 20) and cancers (n = 40). Also, there was statistically significant NAMPT overexpression in patients with TNG (n = 30). Relatively low NAMPT expression was found in GD patients (n = 21) and in the control group (n = 39). In one-way ANCOVA, we confirmed that NAMPT expression differs between subgroups and that it is not influenced by age, BMI, or sex of patients. Conclusions. Reported alteration of NAMPT expression might suggest its involvement in thyroid pathologies. Observed NAMPT overexpression in patients with GO and its relatively low levels in thyroids of patients with GD without eye changes do not confirm causal relationship between NAMPT level and orbitopathy, but this needs further investigation.
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Corvilain, B., L. Collyn, J. van Sande, and J. E. Dumont. "Stimulation by iodide of H2O2generation in thyroid slices from several species." American Journal of Physiology-Endocrinology and Metabolism 278, no. 4 (April 1, 2000): E692—E699. http://dx.doi.org/10.1152/ajpendo.2000.278.4.e692.
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The regulation of thyroid metabolism by iodide involves numerous inhibitory effects. However, in unstimulated dog thyroid slices, a small inconstant stimulatory effect of iodide on H2O2 generation is observed. The only other stimulatory effect reported with iodide is on [1-14C]glucose oxidation, i.e., on the pentose phosphate pathway. Because we have recently demonstrated that the pentose phosphate pathway is controlled by H2O2generation, we study here the effect of iodide on basal H2O2 generation in thyroid slices from several species. Our data show that in sheep, pig, bovine, and to a lesser extent dog thyroid, iodide had a stimulatory effect on H2O2 generation. In horse and human thyroid, an inconstant effect was observed. We demonstrate in dogs that the stimulatory effect of iodide is greater in thyroids deprived of iodide, raising the possibility that differences in thyroid iodide pool may account, at least in part, for the differences between the different species studied. This represents the first demonstration of an activation by iodide of a specialized thyroid function. In comparison with conditions in which an inhibitory effect of iodide on H2O2 generation is observed, the stimulating effect was observed for lower concentrations and for a shorter incubation time with iodide. Such a dual control of H2O2 generation by iodide has the physiological interest of promoting an efficient oxidation of iodide when the substrate is provided to a deficient gland and of avoiding excessive oxidation of iodide and thus synthesis of thyroid hormones when it is in excess. The activation of H2O2 generation may also explain the well described toxic effect of acute administration of iodide on iodine-depleted thyroids.
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Noh, Jaeduk, Noboru Hamada, Hifumi Saito, Midori Yoshimoto, Hiroyuki Iwasaki, Osamu Ozaki, Yasuyuki Okamoto, Kunihiko Ito, and Hirotoshi Morii. "Inhibition by immunoglobulin G of synthesis of thyroid hormone in thyroid cultures from hypothyroid patients with goitrous Hashimoto's thyroiditis." Acta Endocrinologica 123, no. 5 (November 1990): 511–18. http://dx.doi.org/10.1530/acta.0.1230511.
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Abstract. Recently, thyroid microsomal antigen was identified as thyroid peroxidase, and thyroid microsomal antibody was found to inhibit thyroid peroxidase activity in vitro. We investigated the possibility that anti-microsomal antibody inhibits the iodination of tyrosine, in vivo. Immunoglobulin G with or without anti-microsomal antibody from hypothyroid patients with goitrous Hashimoto's thyroiditis inhibited thyroid hormone synthesis in cultured slices of normal human thyroid tissue. IgGs with anti-microsomal antibody inhibited 125I thyroidal uptake and thyroid hormone synthesis stimulated by TSH more than normal IgG did. However, the same results were obtained with IgGs without anti-microsomal antibody. This effect did not involve anti-microsomal antibody, anti-thyroglobulin antibody, TSH-binding inhibitor immunoglobulin, thyroid stimulation-blocking immunoglobulin, or the cAMP level of the thyroid tissue. The ratio of organic I to inorganic I with stimulation by TSH in slices incubated with IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis or normal IgG was not significantly different, but was significantly higher in slices incubated with methylmercaptoimidazole. Therefore, IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis mainly suppressed 125I thyroidal uptake, rather than inhibiting thyroid peroxidase activity. In addition, this IgG was present in the serum of 11 of the 12 hypothyroid patients with Hashimoto's thyroiditis studied. This IgG may be involved in the mechanism that causes hypothyroidism in some patients with goitrous Hashimoto's disease.
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Okamura, Ken, Kaori Sato, Mototaka Yoshinari, Hiroshi Ikenoue, Takeo Kuroda, Mizuho Nakagawa, Hiroshi Tsuji, Masakazu Washio, and Masatoshi Fujishima. "Recovery of the thyroid function in patients with atrophic hypothyroidism and blocking type TSH binding inhibitor immunoglobulin." Acta Endocrinologica 122, no. 1 (January 1990): 107–14. http://dx.doi.org/10.1530/acta.0.1220107.
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Abstract The prognosis of atrophic hypothyroidism with blocking type TSH-binding inhibitor immunoglobulin was studied. Among 45 patients (16 males and 29 females) with overt hypothyroidism (serum TSH >40 mU/l) without goitre, thyroid autoantibody to microsomal antigen was positive in 38 or 84.4%, and 4 or 8.9% had TSH-binding inhibitor immunoglobulin, which was shown to be a TSH-stimulation blocking antibody by cAMP production assay using cultured porcine thyroid cells. Thyroidal radioactive iodine uptake was low and thyroid hormone replacement therapy was required. Long-term follow up of 2 patients with strongly positive TSH-binding inhibitor immunoglobulin for 2 to 7 years, however, revealed recovery of the thyroid function after steroid therapy or spontaneously with iodide restriction, respectively, correlating with decrease in both TSH-binding inhibitor immunoglobulin and TSH-stimulation blocking antibody activities. Thyroidal radioactive iodine uptake became normal and histological examination of the thyroid in one patient revealed well-preserved thyroid follicles with lymphocytic infiltration. Recovery of thyroid function can be expected with a decrease in TSH-binding inhibitor immunoglobulin activity in atrophic hypothyroidism, which is not necessarily the end stage of chronic thyroiditis.
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Gurram, Deepthi, and M. R.Narasinga Rao. "A comparative study of support vector machine and logistic regression for the diagnosis of thyroid dysfunction." International Journal of Engineering & Technology 7, no. 1.1 (December 21, 2017): 326. http://dx.doi.org/10.14419/ijet.v7i1.1.9714.
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Thyroid is one of the vital diseases that influence individuals of any age group now a day. Infections of the thyroid, incorporate conditions related with extreme release of thyroid hormones (Hyper thyroidism) which is likewise called thyrotoxicosis and those related with thyroid hormone insufficiency (Hypothyroidism). Expectation of these two sorts of thyroid disease is critical for thyroid analysis. In this paper, support vector machines and logistic regression are proposed for predicting patients with thyrotoxicosis and without thyrotoxicosis. The outcomes demonstrate that, logistic regression perform well over support vector machine with 98.92% exactness.
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Lu, Changxue, Li Zhao, Hao Ying, Mark C. Willingham, and Sheue-yann Cheng. "Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma." Endocrinology 151, no. 4 (February 4, 2010): 1929–39. http://dx.doi.org/10.1210/en.2009-1017.
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TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRβPV/PV mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-β receptor (TRβ), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRβPV/PV mice were crossed with TSH receptor gene knockout (TSHR−/−) mice. Wild-type siblings of TRβPV/PV mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRβPV/PVTSHR−/− showed impaired growth with no occurrence of FTC. Both WT-PTU and TRβPV/PV mice displayed enlarged thyroids, but only TRβPV/PV mice developed metastatic FTC. Molecular analyses indicate that PV acted, via multiple mechanisms, to activate the integrins-Src-focal adhesion kinase-p38 MAPK pathway and affect cytoskeletal restructuring to increase tumor cell migration and invasion. Thus, growth stimulated by TSH is a prerequisite but not sufficient for metastatic cancer to occur. Additional genetic alterations (such as PV), destined to alter focal adhesion and migration capacities, are required to empower hyperplastic follicular cells to invade and metastasize. These in vivo findings provide new insights in understanding carcinogenesis of the human thyroid.
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IGBOKWE, Casmir O., and Daniel N. EZEASOR. "Age-related Microscopic Changes in the Thyroid Gland of West African Dwarf Goat During Foetal and Post-natal Periods of Development." Notulae Scientia Biologicae 9, no. 1 (March 30, 2017): 59–66. http://dx.doi.org/10.15835/nsb9110031.
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The histometric and histologic standard techniques were used to provide comprehensive information on the morphological changes in the thyroid gland of West African Dwarf goat during the foetal and postnatal development stages. The foetal age was determined using crown rump length and the pre-pubertal and pubertal age of animals was determined by dentition. The early foetal thyroid, surrounded by a thin capsule of dense irregular connective tissue, was continuous with well vascularised loose connective tissue septa. The parenchyma was composed of solid cell clusters of follicular epithelial cells surrounding small lumina. Follicular arrangement was indistinct in foetal thyroid by 50-70 days of gestational age and many follicles of different sizes were present by 95-125 days onwards. Significant variations in the mean follicular diameter, mean capsule thickness and mean epithelial cell height of the thyroids were observed in all stages of development. The mean large follicular diameter in the foetal, pre-pubertal and pubertal ages were 17.70 ± 0.09 µm, 54.41 ± 0.28 µm,142.77 ± 0.51 µm respectively. The follicular cells were of low cuboidal shape in foetuses, assumed high cuboidal or columnar form in pre-pubertal group and squamous in older pubertal age. Ultimobranchial follicles were encountered in early foetal goat thyroids, while focal areas of follicular cell hyperplasia were frequently seen in the older pubertal thyroids. The strong PAS-positive reaction increased strikingly from the 95-125 days foetal age, and by pubertal age all follicles were fully distended with colloid. Colloid vacuolation (colloid droplets) were encountered frequently by the age of 95-125 days, indicating the ability to synthesize hormones towards the last trimester of gestation. Parafollicular cells were distinguished by its pale cytoplasm and large nucleus at 75-90 days onwards. They were located basally and as clusters in the interfollicular tissue. This finding suggested possible high prenatal function for the thyroids of goats in the synthesis of thyroid hormones.
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Troshina, E. A., N. V. Mazurina, M. Iu Iukina, and N. A. Ogneva. "The influence of certain medicinal products on the function of the hypothalamo-pituitary-thyroid axis and the efficiency of substitution therapy with thyroid hormones." Problems of Endocrinology 56, no. 3 (June 15, 2010): 52–56. http://dx.doi.org/10.14341/probl201056352-56.
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The influence of various medicinal preparations on the function of the hypothalamo-pituitary-thyroid axis is discussed. Thyroidal status at different somatic diseases is considered alongside the efficiency of substitution therapy with thyroid hormones for the management of hypothyroidism.
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Müller, Kathrin, Dagmar Führer, Jens Mittag, Nora Klöting, Matthias Blüher, Roy E. Weiss, Marie-Christine Many, Kurt Werner Schmid, and Knut Krohn. "TSH Compensates Thyroid-Specific IGF-I Receptor Knockout and Causes Papillary Thyroid Hyperplasia." Molecular Endocrinology 25, no. 11 (November 1, 2011): 1867–79. http://dx.doi.org/10.1210/me.2011-0065.
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Abstract Although TSH stimulates all aspects of thyroid physiology IGF-I signaling through a tyrosine kinase-containing transmembrane receptor exhibits a permissive impact on TSH action. To better understand the importance of the IGF-I receptor in the thyroid in vivo, we inactivated the Igf1r with a Tg promoter-driven Cre-lox system in mice. We studied male and female mice with thyroidal wild-type, Igf1r+/−, and Igf1r−/− genotypes. Targeted Igf1r inactivation did transiently reduce thyroid hormone levels and significantly increased TSH levels in both heterozygous and homozygous mice without affecting thyroid weight. Histological analysis of thyroid tissue with Igf1r inactivation revealed hyperplasia and heterogeneous follicle structure. From 4 months of age, we detected papillary thyroid architecture in heterozygous and homozygous mice. We also noted increased body weight of male mice with a homozygous thyroidal null mutation in the Igf1r locus, compared with wild-type mice, respectively. A decrease of mRNA and protein for thyroid peroxidase and increased mRNA and protein for IGF-II receptor but no significant mRNA changes for the insulin receptor, the TSH receptor, and the sodium-iodide-symporter in both Igf1r+/− and Igf1r−/− mice were detected. Our results suggest that the strong increase of TSH benefits papillary thyroid hyperplasia and completely compensates the loss of IGF-I receptor signaling at the level of thyroid hormones without significant increase in thyroid weight. This could indicate that the IGF-I receptor signaling is less essential for thyroid hormone synthesis but maintains homeostasis and normal thyroid morphogenesis.
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Chowdhury, Md Sunny Anam, Mohshi Um Mokaddema, Tanzina Naushin, Simoon Salekin, Nabeel Fahmi Ali, Fatima Begum, and Sadia Sultana. "Ectopic thyroid gland- presentation at childhood, adolescent and adult life." Bangladesh Journal of Nuclear Medicine 17, no. 1 (March 10, 2015): 116–24. http://dx.doi.org/10.3329/bjnm.v17i1.22503.
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Ectopic thyroid is a rare entity that can appear at any age with different presentations. In this study we are reporting four cases of ectopic thyroid gland at different ages; two cases at childhood, one at adolescent and one at adult life. Among the two children, one having ectopic thyroid at the level of hyoid bone, presented with anterior neck swelling with no other symptom and another one having a lingual ectopic thyroid presented with features of hypothyroidism and obstructive features. The cases of adolescent and adult age are very rare cases of dual ectopic thyroid and ectopic thyroid tissue coexisting with normal thyroid gland respectively. Both of them presented with anterior neck swelling, with additional complaints of dysphagia and foreign body sensation by the adolescent patient. All the cases, ectopic thyroids were detected by Ultrasonogram and confirmed by radionuclide (99mTc) thyroid scan. DOI: http://dx.doi.org/10.3329/bjnm.v17i1.22503 Bangladesh J. Nuclear Med. 17(1): 116-124, January 2014
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Zantut-Wittmann, Denise Engelbrecht, Luís Henrique Barbosa Boechat, Glauce Aparecida Pinto, Miriam Aparecida da Silva Trevisan, and José Vassallo. "Autoimmune and non-autoimmune thyroid diseases have different patterns of cellular HLA class II expression." Sao Paulo Medical Journal 117, no. 4 (July 1999): 161–64. http://dx.doi.org/10.1590/s1516-31801999000400004.
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CONTEXT: Surface HLA-DR antigen is usually only expressed by antigen-presenting cells (APC). In autoimmune thyroid disease, follicle cells function as APC, thus expressing HLA-DR. However, non-autoimmune thyroid diseases may also express surface class II antigens. OBJECTIVE: To evaluate the presence and pattern of HLA class II expression in autoimmune and non-autoimmune thyroid disorders. DESIGN: Retrospective: histopathological and immunohistochemical analysis. LOCATION: Referral center, university hospital. SAMPLE: Ten histologically normal thyroids, 11 Graves’ disease, 7 Hashimoto’s thyroiditis, 10 atoxic multinodular goiter and 3 toxic adenomas were analyzed by immunohistochemistry, using a monoclonal antibody anti-HLA-DR. MAIN MEASUREMENTS: The presence of these antigens in thyroid follicular cells and their relation to inflammatory infiltrate was evaluated. The pattern of HLA-DR expression in thyroid follicular cells was analyzed: membrane, cytoplasmic or both. RESULTS: Although HLA-DR antigens were sparsely present in one of the 8 normal thyroids, in 6 of the 9 atoxic multinodular goiter and in 2 of the 3 toxic adenomas a net positivity could be seen in large areas. In all 5 Hashimoto’s thyroiditis and in 7 of the 10 Graves’ disease cases. This expression occurred in follicle cells either in contact with inflammatory cells or not. In non-autoimmune thyroid disease, HLA-DR positivity was essentially cytoplasmic, whereas in Graves’ disease and Hashimoto thyroiditis it was mainly in cell membranes. CONCLUSIONS: It is suggested that the HLA class II expression on the surface of follicle cells could be related to auto-antigen presentation to the immune system by these cells, leading to inflammation.
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Trajkovic-Arsic, Marija, Julia Müller, Veerle M. Darras, Claudia Groba, Sooyeon Lee, Debra Weih, Karl Bauer, Theo J. Visser, and Heike Heuer. "Impact of Monocarboxylate Transporter-8 Deficiency on the Hypothalamus-Pituitary-Thyroid Axis in Mice." Endocrinology 151, no. 10 (August 11, 2010): 5053–62. http://dx.doi.org/10.1210/en.2010-0593.
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In patients, inactivating mutations in the gene encoding the thyroid hormone-transporting monocarboxylate transporter 8 (Mct8) are associated with severe mental and neurological deficits and disturbed thyroid hormone levels. The latter phenotype characterized by high T3 and low T4 serum concentrations is replicated in Mct8 knockout (ko) mice, indicating that MCT8 deficiency interferes with thyroid hormone production and/or metabolism. Our studies of Mct8 ko mice indeed revealed increased thyroidal T3 and T4 concentrations without overt signs of a hyperactive thyroid gland. However, upon TSH stimulation Mct8 ko mice showed decreased T4 and increased T3 secretion compared with wild-type littermates. Moreover, similar changes in the thyroid hormone secretion pattern were observed in Mct8/Trhr1 double-ko mice, which are characterized by normal serum T3 levels and normal hepatic and renal D1 expression in the presence of very low T4 serum concentrations. These data strongly indicate that absence of Mct8 in the thyroid gland affects thyroid hormone efflux by shifting the ratio of the secreted hormones toward T3. To test this hypothesis, we generated Mct8/Pax8 double-mutant mice, which in addition to Mct8 lack a functional thyroid gland and are therefore completely athyroid. Following the injection of these animals with either T4 or T3, serum analysis revealed T3 concentrations similar to those observed in Pax8 ko mice under thyroid hormone replacement, indicating that indeed increased thyroidal T3 secretion in Mct8 ko mice represents an important pathogenic mechanism leading to the high serum T3 levels.