Relevant bibliographies by topics / Thyroidi

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Academic literature on the topic 'Thyroidi'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Thyroidi"

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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Dissertations / Theses on the topic "Thyroidi"

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Tcheandjieu, Gueliatcha Catherine Ines. "Etude des facteurs de risque génétiques et des interactions gène-environnement dans les cancers différenciés de la thyroïde." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS064.

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Contexte : L’incidence des cancers différenciés de la thyroïde (CDT) est caractérisée par de fortes variations géographiques et ethniques. L’un des plus forts taux d’incidence a été rapporté en Nouvelle-Calédonie et particulièrement dans la population mélanésienne. En dehors de l’exposition aux radiations ionisantes dans l’enfance et l’obésité, les facteurs de risque de CDT restent très mal connus. Bien qu’il ait été rapporté que ce cancer constitue une des localisations cancéreuses ayant la composante héréditaire la plus élevée, le rôle des facteurs génétiques a été jusqu’à présent peu étudié. Des études de cas familiaux et des études gène-candidat ont identifié des polymorphismes dans plusieurs gènes mais très peu de ces associations ont été répliquées. Des études d’association génomes entier (GWAS) ont également mis en évidence des régions de susceptibilité génétiques de CDT, les associations les plus robustes ont été rapportés sur les loci 9q22 et 14q13. Au final, l’ensemble des variants identifiés jusqu’à présent ne permettent d’expliquer qu’une faible part de l’héritabilité génétique dans l’étiologie des CDT, suggérant que d’autres facteurs de risque génétiques restent à découvrir.Objectifs : L’objectif général de ce travail était d’étudier les facteurs de risque génétique et leurs interactions avec les facteurs environnementaux. Plus spécifiquement, il s’agissait 1) d’étudier le rôle de gènes candidats ou de loci identifiés dans des études GWAS dans deux études cas-témoins menées en Nouvelle-Calédonie et en France métropolitaine 2) d’explorer plus en détail dans ces populations, les loci GWAS 9q22 et 14q13 pour l’identification des variants causaux ou d’autres variants candidats ; 3) d’identifier de nouveaux facteurs de risque génétiques dans les CDT chez les femmes en utilisant une approche dite par « pathway candidat » en combinant les données de deux études françaises et américaines.Matériels et méthodes : Les analyses portant sur les gènes candidats et les loci GWAS reposent sur deux populations d’études : une population européenne de 508 cas et 621 témoins issus des études cas-témoins conduites en France métropolitaine (étude CATHY) et en Nouvelle-Calédonie (NC) et une population mélanésienne de 156 cas et 114 témoins de l’étude de NC. Les approches pathway candidat ont porté dans un premier temps sur les femmes d’origine européenne de l’étude CATHY (365 cas/376 témoins) et d’une partie de l’étude cas-témoins Young-Thyr (83 cas/93 témoins) conduites en France métropolitaine. Dans un second temps, nous avons combiné ces sujets avec les femmes de l’étude cas-témoins USRT/UTMDACC (332 cas/443 témoins) conduite aux Etats-Unis.Résultats : Nous n’avons pas observé d’association entre les CDT et les polymorphismes des gènes identifiés précédemment par les études gène-candidat dans les populations européennes et mélanésiennes étudiées. Toutefois, nous avons montré que la délétion des gènes GSTM1 et GSTT1 pouvait moduler les associations rapportées entre l’obésité ou la consommation d’alcool et le risque de CDT. Nous avons répliqué chez les européens et chez les mélanésiens les associations avec des variants des loci GWAS 9q22, 14q13 et 2q35. Nous avons également mis en évidence, dans les régions GWAS 9q22 et 14q13 de nouveaux variants candidats à risque de CDT et rapporté des interactions entre ces variants et la parité ou la consommation de tabac. Les analyses par pathway portant sur une population de femmes d’origine européenne suggèrent des interactions entre la consommation d’alcool ou la consommation de tabac et les gènes impliqués dans le métabolisme de ces substances et des interactions entre l’âge aux premières règles, la prise de contraceptifs oraux et les gènes impliqués dans la biosynthèse et le métabolisme des hormones stéroïdiennes
Context : Differentiated thyroid cancer (DTC) incidence is characterized by considerable geographic and ethnic variations. Particularly high incidence rates were observed in Melanesian women of New Caledonia. Except for the exposure to ionizing radiation in childhood and obesity, the role of other DTC risk factors is not clearly established. Genetic factors have been suggested to play an important role in DTC risk since epidemiological studies have shown that DTC has a higher familial relative risk than any other cancers. Linkage studies in multiple-case DTC families and candidate gene studies have identified polymorphisms in several genes but very few have been replicated so far. Genome-wide association studies (GWAS) also identified several DTC susceptibility loci with the most robust associations reported on the loci 9q22 and 14q13. Only few susceptibility loci were highlighted by GWAS and the identified variants were shown to account less than 10% of the DTC familial risk, emphasizing that much remains to be discoveredObjectives: The main objective of this work was to study the role of genetic risk factors and their interaction with environmental factors in DTC risk. More specifically, we aimed to: 1) replicate the association between DTC risk and polymorphisms reported in candidate gene and GWAS studies in 2 case-control studies conducted in Metropolitan France and New Caledonia; 2) identify potential causal variants of DTC risk in GWAS loci 9q22 and 14q13 using fine-mapping approach; 3) identify new genetic risk factors for DTC in women using pathway approach by pooling data from 2 case-control studies conducted in France and USA..Materials and methods: The analysis of the candidate genes and of the GWAS loci were based on a European population of 508 cases and 621 controls from 2 case-control studies conducted in metropolitan France (CATHY study) and in New Caledonia (NC study) and, a Melanesian population of 156 cases and 114 controls from the NC study. The pathway analysis was conducted in a first step on European women from the CATHY study (365 cases/376 controls) and from the Young-Thyr study (83 cases /93 controls) both conducted in metropolitan France. In a second step, we pooled the data from CATHY/Young-Thyr study and USRT/UTMDACC study (332 cases/443 controls) conducted in the United States.Results: In Europeans and Melanesians, we found no association with polymorphisms reported previously by candidate genes studies. However, we observed that among these genes, GSTM1 and GSTT1 may modulate the associations between DTC risk and obesity or alcohol consumption. Some polymorphisms identified in GWAS studies at loci 9q22, 14q13 and 2q35 were replicated in Europeans and in Melanesians. In the GWAS loci 9q22 and 14q13, we identify new variants that can be functionally related to DTC pathogenesis in Europeans and Melanesians. We also reported interactions between some of these variants and parity or tobacco smoking. The analysis of candidate pathways in European women showed interactions between alcohol consumption or tobacco smoking and genes involved in the metabolism of these compounds and, between age at first menarche or oral contraception and genes involved in biosynthesis and metabolism of sex steroid hormones
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Guyétant, Serge. "Etudes morphologiques des cellules c humaines normales et pathologiques (doctorat : sciences morphologiques)." Angers, 1999. http://www.theses.fr/1999ANGE0510.

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Castanet, Mireille. "Mécanismes moléculaires impliqués dans les anomalies du développement de la glande thyroi͏̈de." Paris 5, 2002. http://www.theses.fr/2002PA05N124.

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Les dysgénésies thyroi͏̈diennes (DT), anomalies du développement de la thyroi͏̈de, regroupent principalement les ectopies, les athyréoses, et plus rarement, les hypoplasies et les lobes thyroi͏̈diens uniques. Si la physiopathologie est encore mal connue, 4 gènes ont été impliqués dans cette pathologie : TTF-1 (Thyroi͏̈d Transcription Factor 1), TTF-2, PAX8 et le gène du récepteur de la TSH (Thyroi͏̈d Stimulating Hormone). Dans ce travail, nous avons, tout d'abord démontré que les hypothiroi͏̈dies congénitales dues à une DT, présentaient un caractère familial indéniable. Nous avons ensuite réalisé une étude de liaison intra-familiale qui a permis de retrouver une co-ségrégation entre le phénotype pathologique et au moins.
Thyroi͏̈d dysgenesis (TD) are thyroid developmental abnomalities, including athyreosis, hemithyroi͏̈d, ectopic and hypoplasic thyroid gland. Up to now, four genes have been schown to be involved in this disorder : TTF-1 (Thyroi͏̈d Transcription Factor 1), TTF-2, PAX8 and the gene encoding for the receptor of the thyroi͏̈d stimulating hormone. In this study; we firstly demontrated that congenital hypothyroi͏̈dism due to TD had a familial character. We then performed linkage analysis that showed co-segregation between the disorder and at least one of the for candidate loci in the majority of the families studied. We then identified 7 mutations in 17 subjets affected by TD, thus confirming the role of these 4 genes
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Chapon, Christophe. "Les cancers différenciés de la thyroi͏̈de (médullaires exclus) : épidémiologie, diagnostic et traitement : à propos de 120 cas." Montpellier 1, 1993. http://www.theses.fr/1993MON11009.

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Allard, Saint-Albin Luc. "Les lymphomes malins primitifs de la thyroïde (revue de la littérature actuelle illustrée par une observation personnelle)." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25001.

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Cauquil-Gleizes, Sylvie. "Les cancers différenciés de la thyroi͏̈de : étude rétrospective de 88 cas." Montpellier 1, 1988. http://www.theses.fr/1988MON11253.

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Yee, Kin Tet Hoy Youn. "Analyse de 173 cancers thyroi͏̈diens : étude rétrospective." Bordeaux 2, 1992. http://www.theses.fr/1992BOR2M166.

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Thellier, Michel. "Maladie de von recklinghausen avec neurofibrome thyroidien et cancer medullaire de la thyroide." Lille 2, 1992. http://www.theses.fr/1992LIL2M088.

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Driessens, Natacha. "Contribution à l'étude du caractère mutagène de l'H2O2 dans la thyroide." Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209410.

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Les radiations ionisantes sont une cause établie de cancers de la thyroïde mais un nombre croissant de travaux évoque aussi le rôle potentiel du peroxyde d’hydrogène (H2O2) dans la pathogenèse des cancers thyroïdiens spontanés. Si les cassures double-brin de l’ADN (DSBs) sont considérées comme l’une des causes primaires de cancer, leur induction par l’H2O2 était plus controversée.

Lors de ce travail, nous avons voulu tester in vitro, dans différents modèles thyroïdiens, l’hypothèse selon laquelle l’H2O2 produit en grandes quantités in vivo pour oxyder l’iodure et synthétiser les hormones thyroïdiennes pouvait endommager l’ADN.

Les dégâts provoqués à l’ADN ont été évalués par le test des comètes (en milieu alcalin pour les cassures simple-brin (SSBs) et en milieu neutre pour les cassures double-brin de l’ADN) et quantitativement comparés à ceux produits par l’irradiation.

Nous avons montré dans une lignée cellulaire thyroïdienne de rat (PCCl3) que des concentrations non létales d’H2O2 (0.1 – 0.5 mM) tout comme l’irradiation (1 - 10 Gy) provoquaient une augmentation dépendante de la dose du nombre de SSBs et de DSBs.

L'induction de DSBs a été confirmée par la mesure du taux de phosphorylation de l’histone H2AX sur Sérine 139. L’induction de DSBs par l’H2O2 a également été observée dans des cultures primaires de thyroïdes humaines et dans des tranches de thyroïde de porcs.

L’utilisation de L-buthionine-sulfoximine (BSO), un agent qui empêche le renouvellement du glutathion cellulaire, a conduit à un abaissement du seuil d’observation des cassures de l’ADN induites par l’H2O2.

Nous avons également observé que les dommages de l’ADN étaient réparés plus lentement lorsqu’ils étaient provoqués par l’H2O2 plutôt que par l’irradiation.

Dans un second temps, nous avons exploré au niveau moléculaire les conséquences d’une exposition à 1 Gy d’irradiation γ ou à une concentration non létale d’H2O2 (0.05 – 0.2 mM) dans des cultures primaires de thyroïdes humaines et dans des lymphocytes T issus d’un même donneur. Nous avons étudié par micro-arrays les modifications du profil d’expression génétique de ces 2 types cellulaires afin de caractériser la spécificité de la réponse transcriptionnelle en fonction de la nature de l’agression, du type et de l’importance du dommage engendré ainsi que du type cellulaire.

Les 2 types cellulaires répondent de manière similaire à l’irradiation en termes de nombre de gènes régulés, avec un large recouvrement de réponses transcriptionnelles caractérisées par une forte sur-représentation de gènes impliqués dans l’apoptose et dans la réparation des dommages de l’ADN.

En revanche, la réponse transcriptionnelle à l’H2O2 est différente dans les 2 types cellulaires.

D’une part, les lymphocytes T qui montrent un dommage à l’ADN pour de plus faibles concentrations d’H2O2 que les thyrocytes présentent une réponse transcriptionnelle 1000 fois supérieure à celle observée dans les thyrocytes. D’autre part, les quelques gènes régulés dans les thyrocytes ne le sont pas dans les lymphocytes T. Il s’agit de gènes impliqués dans la défense contre les espèces réactives de l’oxygène (ROS). Ces résultats suggèrent l’existence de mécanismes de protection anti-oxydante spécifiquement développés dans les cellules thyroïdiennes.

En conclusion, ce travail a montré que l’H2O2, à des concentrations non létales, provoque des SSBs mais également des DSBs dans différents modèles thyroïdiens in vitro. La quantité de DSBs produite par l’H2O2 est comparable à celle observée après irradiation mais la vitesse de leur réparation est plus lente. D’autre part, en comparaison avec les lymphocytes T, les thyrocytes semblent particulièrement résistants aux effets de l’H2O2 et dotés de mécanismes de protection particulièrement performants et probablement partiellement inductibles contre les ROS.

Ces données soutiennent notre hypothèse de départ selon laquelle la production d’H2O2 dans la thyroïde pourrait jouer un rôle dans l’étiopathogénie des tumeurs thyroïdiennes, en particulier en cas de défenses anti-oxydantes altérées.


Doctorat en Sciences médicales
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Courbin, Véronique. "Le cancer médullaire de la thyroi͏̈de : expérience bordelaise à propos de 54 cas." Bordeaux 2, 1990. http://www.theses.fr/1990BOR25105.

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Books on the topic "Thyroidi"

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Reed, Larsen P., and Hennemann Georg, eds. The thyroid and its diseases. 6th ed. New York: Churchill Livingstone, 1996.

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J, Biersack H., and Grünwald F, eds. Thyroid cancer. Berlin: Springer, 2001.

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B, Bercu Barry, and Shulman Dorothy I, eds. Advances in perinatal thyroidology. New York: Plenum, 1991.

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Shepherd, Francis J. Le goitre: Origine, cours, cause, prophylaxie et traitement : quelques remarques sur l'anatomie et la physiologie de la glande thyroïde et sa tuméfaction ordinairement appelée goitre. Ottawa: [s.n.], 1997.

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Canada. Commission of Conservation. Committee on Public Health., ed. Goitre, its incidence, course, causation, prophylaxis and treatment: Some remarks on the anatomy and physiology of the thyroid gland and on the enlargement of the thyroid, usually called goitre. Ottawa: [s.n.], 1997.

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Doctor, es la tiroides?: Una glándula que regula nuestro cuerpo. Barcelona: Hispano Europea, 2011.

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A, Meier C., ed. Thyroid nodules and thyroid cancer. London: Baillière Tindall, 2000.

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Thyroid. 2nd ed. New York: Igaku-Shoin, 1996.

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Thyroid. New York: Igaku-Shoin, 1987.

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1930-, Cady Blake, and Rossi Ricardo L, eds. Surgery of the thyroid and parathyroid glands. 3rd ed. Philadelphia: Saunders, 1991.

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Book chapters on the topic "Thyroidi"

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Dohán, Orsolya, and Nancy Carrasco. "Thyroidal Iodide Transport and Thyroid Cancer." In Cancer Treatment and Research, 221–36. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/1-4020-8107-3_13.

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Bhansali, Anil, and Yashpal Gogate. "Extra-thyroidal Manifestations of Autoimmune Thyroid Disease." In Clinical Rounds in Endocrinology, 249–65. New Delhi: Springer India, 2015. http://dx.doi.org/10.1007/978-81-322-2398-6_11.

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McLeod, Donald S. A. "Papillary Thyroid Cancer with Microscopic Extra-thyroidal Extension." In Thyroid Cancer, 41–53. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-61919-0_6.

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Goretzki, P. E., A. Frilling, D. Simon, and H. D. Roeher. "Growth Regulation of Normal Thyroids and Thyroid Tumors in Man." In Hormone-Related Malignant Tumors, 48–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83816-3_6.

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McLeod, Donald S. A. "A Papillary Thyroid Cancer with Minimal Extra-thyroidal Extension." In Thyroid Cancer, 61–72. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22401-5_7.

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Wentworth, B. C., and R. K. Ringer. "Thyroids." In Avian Physiology, 452–65. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4862-0_20.

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Rijnberk, A. "Thyroids." In Clinical Endocrinology of Dogs and Cats, 35–59. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0105-6_3.

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Klam, Elie, and Dev Abraham. "Thyroid." In Metastatic Bone Disease, 85–88. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-5662-9_8.

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Grant, Frederick D., and S. Ted Treves. "Thyroid." In Pediatric Nuclear Medicine and Molecular Imaging, 99–129. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9551-2_5.

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Pickuth, Dirk. "Thyroid." In Essentials of Ultrasonography, 235–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79579-4_18.

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Conference papers on the topic "Thyroidi"

1

Gottlieb, O., S. R. Chipkin, L. Ioffe, and Y. Chait. "Self-Excited Oscillations in a System Model of the Human Thyroid." In ASME 2010 Dynamic Systems and Control Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/dscc2010-4287.

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The thyroid, the largest gland in the endocrine system, secretes hormones that regulate homeostatic functions within the body and promote normal growth and development. Recently, a detailed computational model of the thyroid gland has been derived and used to explain clinical observations regarding the thyroid gland’s ability to maintain its hormonal secretion target in the face of uncertain dietary iodine intake levels. In this paper we probe deeper into the thyroid’s nonlinear dynamics. We first reduce the original model to an eight-order dynamical system, analytically determine that a Hopf mechanism governs the loss of stability of thyroid equilibrium, culminating with numerically obtained periodic limit-cycle behavior beyond the critical threshold. We numerically investigate the orbital stability of periodic thyroid dynamics via its harmonic perturbation and construct a bifurcation structure that includes both periodic and subharmonic mode-locked solutions embedded within a set of quasiperiodic tori. An increase of the perturbation parameter reveals a similar and structurally stable bifurcation structure. Thus, the analysis of our nonlinear thyroid model shows that the gland can exhibit both a stable equilibrium and periodic limit-cycle behavior which can lose its orbital stability due to small harmonic perturbations.
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Pechuro, E. A., A. N. Batian, V. A. Kravchenko, and S. V. Petrenko. "ANALYSIS OF THE THYROID GLAND INCIDENCE RATE IN GORODNAYA RESIDENTS, STOLIN DISTRICT, BREST REGION, WHICH SUFFERED AS A RESULT OF THE ACCIDENT AT THE CHERNOBYL NUCLEAR POWER PLANT." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-114-117.

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At the beginning of 2020, 71 patients with thyroid diseases (nodular goiter, postoperative hypothyroidism, thyrotoxicosis, hypothyroidism, thyroid cancer) were identified, among which 14 % are men and 86 % are women. Thyroid cancer was diagnosed in 7 people, including 1 man and 6 women, which was 14.3 % and 85.7%, respectively. In the structure of morbidity, nodular goiter (26 cases) accounts for 37 %, postoperative hypothyroidism (17 cases) -24 %, primary hypothyroidism (15 cases) - 21 %, thyrotoxicosis (6 cases) - 8 %, cancer (7 cases) - 10%. The most common pathology of the thyroid gland in the study settlement is nodular goiter. The highest incidence rates were among men aged 51-60 years, and among women - in the age groups 51-60 years and 61-70 years. One of the possible reasons for nodular goiter incidence rate increasing is radioactive iodine incorporation at the stable iodine deficiency in this population.
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Yaglova, Nataliya, Sergey Obernikhin, and Ekaterina Timokhina. "CHANGES IN THYROID FUNCTION INDUCED BY SHIFTS OF HYDROGEN ISO-TOPES RATIO." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.16.

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Impact of short-term shift in deuterium body content on thyroid function was studied. In-creased functional activity of the thyroid gland, but without raise in rate of thyroxine to triiodothyronine conversion was found both after depletion and enrichment of deuterium body co
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Pechuro, E. A., A. N. Batian, V. А. Kravchenko, and S. V. Petrenko. "THYROID DISEASES IN THE RESIDENTS OF THE CITY LOCATION OF THE STOLINSKY DISTRICT OF THE BREST REGION FOR THE PERIOD FROM 2016 TO 2020." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute, 2021. http://dx.doi.org/10.46646/sakh-2021-1-314-317.

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In the settlement of Gorodnaya, at the beginning of 2020, 71 patients with thyroid diseases (nodular goiter, postoperative hypothyroidism, thyrotoxicosis, hypothyroidism) were registered, including 8 patients for the first time detected in 2019. According to the 2020 study, 7 people fell ill with thyroid cancer in the village - 1 man and 6 women, which amounted to 14.3% and 85.7%, respectively. The highest incidence rates were registered among men aged 51-60 years, and among women - in the age groups 51-60 years old and 61-70 years old. At the age of 21-30 years, thyroid gland pathology was registered in one person.
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Kurnikova, Irina, *. Ramchandra Sargar, Igor Tomashevsky, Natalia Zabrodina, and Tatiana Meleshkevich. "Novel Trends for the Use of X-ray ComputedTomography for the Etiological Diagnosis of Iodine Metabolism Disorders." In Human Systems Engineering and Design (IHSED 2021) Future Trends and Applications. AHFE International, 2021. http://dx.doi.org/10.54941/ahfe1001153.

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The authors have developed criteria for the quantitative assessmentof the concentration of intrathyroidal iodine by the density of the thyroid glandusing X-ray computed tomography (CT). The diagnostic capabilities of CT areshown in determining the genesis of thyroid dysfunction (etiological diagnosis)based on a retrospective analysis of 289 clinical observations.
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Timokhina, Ekaterina, Nataliya Yaglova, Sergey Obernikhin, and Valentin Yaglov. "DYNAMIC MORPHOLOGICAL CHANGES IN THE THYROID GLAND ASSOCIATED WITH DEPLETION OF DEUTERIUM BODY CONTENT." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.18.

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Dynamics of morphological changes in the thyroid gland of mice, consuming water with lower deuterium content, was studied. Primary changes in structure were indicative of more active hormone secretion. Later morphological signs of inhibited hormone secretion were found. The findings demonstrate sensitivity of thyroid cells to shifts in deuterium body con-tent.
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HUSSAIN, Zainab Khidhair, and Bushra Rashid Ibrahim. "COMPARISON BETWEEN CARDIAC ENZYMES IN PATIENTS WITH HYPOTHYROIDISM AND HYPERTHYROIDISM." In III.International Scientific Congress of Pure,Appliedand Technological Sciences. Rimar Academy, 2021. http://dx.doi.org/10.47832/minarcongress3-2.

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Thyroid hormones modify each cardiovascular system component, it's essential for the function and development off the cardiac system. Thyroid hormones and the cardiac enzyme were measured in (120) Iraqi women aged (20-65) years in three groups: patients with hypothyroidism, hyperthyroidism, and control. Thyroid hormones (TSH, T3, and T4) were measure by ELISA by using a procedure of TOSOH,CHINA, also, cardiac enzymes were determined by biochemical assay of Biosystem company, Barcelona. The results showed the level of CK enzyme increasing non significantly (53.61) between groups in hyperthyroidism (G1), hypothyroidism(G2) and was (151.40 ±8.86uk) and (127.80 ±21.82uk) respectively compared with control was (G3) (100.60 ±18.80 uk),also the level of Troponin- I enzyme increasing non significantly (213.42) between groups was in(G1) (430.20 ±53.38) (Pg/UL), (G2) was (369.20 ±75.75) (Pg/UL) and (G3) (275.60 ±76.18).In comparison the study showed decreasing non significantly in cardiac enzymes as AST and ALT. It concluded that non-significant effect of thyroid hormones on the level of cardiac enzyme in both patients with hypothyroidism and hyperthyroidism. Key words: Hyperthyroidism, Cardiac Enzyme, Hypothyroidism, Hormones, Troponin I.
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Zasimova, E. Z., and A. S. Golderova. "THE EFFECT OF A LONG VOYAGE CONDITIONS ON THE LEVEL OF STRESS-IMPLEMENTING HORMONES IN RIVER TRANSPORT WORKERS." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-222-225.

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Abstract: The stress-releasing hormones in river workers before and after a long voyage in Yakutia have been evaluated. We revealed a significant increase in the level of thyroid hormones (TSH, T3, T4) and testosterone, as well as a decrease in cortisol and integral thyroid index, that is indicating stress, as well as signs of depletion of adaptive mechanisms.
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Saji, Genn. "Estimation of Thyroid Doses From Land Contamination Maps for the Fukushima Disaster." In 2012 20th International Conference on Nuclear Engineering and the ASME 2012 Power Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icone20-power2012-55048.

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Starting with sketchy information acquired during the still on-going Fukushima Daiichi disaster, the thyroid doses were estimated, based on the detailed and precise Cs-137 land contamination density maps constructed through a joint effort of MEXT and US DOE/NNEA. The basic methodology has already been benchmarked in the assessment of the radiological consequences of the Chernobyl accident [1]. From the release fraction assessment based on the contamination maps as well as on-site meteorological data obtained and reported by TEPCO’s temporary monitoring cars, the heavy land contamination zone stretching to a NW direction was found induced with the hydrogen explosion which occurred in 1F1 at 15:36 of March 12, only one day after the tsunami. Due to this early iodine release, the shorter half-lived I-133 induced an additional 20% more thyroid doses from I-131 through inhalation. The results, as presented in Table 7 and Figure 3, predicted rather large thyroid doses, comparable but less than the author’ previous estimation of thyroid doses through inhalation pathway among the public living near the Chernobyl NPP during the disaster. However, age specific doses are more widely spreading among children aged less than 15 years old and not distinctively large among babies, thanks to early restriction of fresh milk. It should be noted that, above Zone V (300K-1000K/m2 in Cs-137), the estimated thyroid doses with a range of several tens of mGy are already of concern in a possible future outbreak of hypothyroidism. However, if the exposed individuals happened to be staying indoors at the time of plume passage, an order of magnitude of reduction is expected, although the alleviating effects depends on the airtightness of buildings. Even with these uncertainties, the estimated thyroid dose calls for continued health monitoring of those young residents who happened to be staying in these highly contaminated zones at the time of the plume passage.
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Koipish, A. E., and E. P. Zhyvitskaya. "MODELING OF DOSE LOADS ON THE THYROID GLAND IN THE EVENT OF AN ACCIDENT AT THE BELARUSIAN NUCLEAR POWER PLANT." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-1-331-334.

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The results of predictive assessment of dose loads on the thyroid gland in the event of an accident at the Belarusian NPP are presented. To simulate the transfer of radionuclides in the atmosphere and the forecast of radioactive fallout at the NPP, 4 scenarios of weather conditions were considered: 2 summer, 2 winter, with different categories of atmospheric stability. It has been established that in the area within a radius of 3 km around the Belarusian NPP in case of an out-of-design accident (scenarios 1-4), the total potential radiation dose of the thyroid gland will vary within 4,83E+03 -6,81E+03 mSv. The differences in the indicators of the total potential radiation dose of the thyroid gland are due to weather conditions. The highest predicted values are presented in winter scenario 3. The results show the need for iodine prophylaxis in the population at a distance of up to 3 km from the Belarusian NPP.
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Reports on the topic "Thyroidi"

1

Alessa, Mohammed, Tayba Wahedi, Jumanah Alsairafi, Nouf Almatrafi, Wisal Shuaib, Johara Alnafie, Fatimah Alzubaidi, and Soha Elmorsy. Prevalence of Thyroid cancer in Saudi Arabis: Systematic review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0088.

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Review question / Objective: What is the prevalence of Thyroid cancer among population in kingdom of Saudi Arabia?. The aim of this systematic review is to scrutinize the prevalence of thyroid cancer (TC) in Saudi Arabia and assess the relative frequency of subgroups related to types of thyroid cancer, age, and gender. Condition being studied: Thyroid cancer is an abnormal growth of cells that starts in the thyroid gland. There is four types of differentiated thyroid cancer, three of these cancer develop from the follicular cells, the papillary thyroid cancer, follicular thyroid cancer, Hürthle cell carcinoma, and one rare type develops from the thyroid’s C cells called medullary thyroid cancer. There is one undifferentiated thyroid cancer called anaplastic thyroid cancer.
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Pasqualoni, Sara Elizabeth. Thyroid for Life. Office of Scientific and Technical Information (OSTI), January 2016. http://dx.doi.org/10.2172/1237219.

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Rusanova, O. A., O. I. Emelyanova, and A. S. Trofimenko. PATTERNS OF PLASMA ANTI-THYROID HORMONE ANTIBODIES IN AUTOIMMUNE RHEUMATIC DISEASES WITH THYROID LESION. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-422.

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Stern, Paula H. Mechanism of Thyroid Hormone-Induced Osteoporosis. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada368354.

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Stern, Paula H. Mechanism of Thyroid Hormone-Induced Osteoporosis. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada340690.

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Stern, Paula H. Mechanism of Thyroid Hormone-Induced Osteoporosis. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391556.

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Zhao, Hao, Chunhao Liu, Yanlong Li, and Xiaoyi Li. Prognostic factors for survival in differentiated thyroid cancer with pulmonary metastases: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0026.

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Pulmonary metastasis (PM) is the most common form of distance metastasis in differentiated thyroid cancer (DTC), which has a poor prognosis. However, the prognostic risk factors are not yet well identified and analyzed. This systematic review and meta-analysis aims to fill this blank though identifying and discussing survival prognostic risk factors systematically for DTC patients with PM. Pulmonary metastasis (PM) is the most common form of distance metastasis in differentiated thyroid cancer (DTC), which has a poor prognosis. However, the prognostic risk factors are not yet well identified and analyzed. This systematic review and metastases aims to fill this blank though identifying and discussing survival prognostic risk factors systematically of DTC patients with PM. Condition being studied: differentiated thyroid cancer with pulmonary metastases.
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Clifton, K. H. Radiogenic neoplasia in thyroid and mammary clonogens. Office of Scientific and Technical Information (OSTI), May 1991. http://dx.doi.org/10.2172/6053460.

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Clifton, K. H. Radiogenic neoplasia in thyroid and mammary clonogens. Office of Scientific and Technical Information (OSTI), May 1992. http://dx.doi.org/10.2172/7279046.

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Vaughan, George M., Basil A. Pruitt, and Jr. Thyroid Function in Critical Illness and Burn Injury,. Fort Belvoir, VA: Defense Technical Information Center, July 1993. http://dx.doi.org/10.21236/ada277947.

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