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CELL. A small room in a prison. See Dungeon.

A Law Dictionary, Adapted to the Constitution and Laws of the United States. By John Bouvier. Published 1856.
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Iodide excess induces apoptosis in thyroid cells through a p53-independent mechanism involving oxidative stress.
Importantly, NIS gene expression levels were also detected to be very low in oncogene-transformed rat thyroid cell models, indicating an inverse correlation between oncogene activation and NIS expression in thyroid cancer models (82).
It seems that overexpression of AKT1 is capable of promoting cell proliferation, sensitization to TSH, and inhibiting apoptosis, but it is not sufficient to transform thyroid cells by itself (19,20).
Normal thyroid cells express phosphodiesterase subtypes PDE4, PDE5, PDE7, and PDE8 [43].
The thyroid nodule refers to the thyroid cells localized in the lesions caused by abnormal growth.
For example, in regions with severe selenium (Se) deficiency, a higher incidence of thyroiditis may be documented, due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells. Selenium-dependent enzymes are also key elements in the regulation of the immune system.
[22] showed autocrine IGF-1 production in papillary thyroid cancer cells and also demonstrated IGF-1 immunoreactivity in thyroid cell clone medium.
(b) MiR-195 expression in normal thyroid cell line Nthy-ori 3-1 and PTC cell lines K1 and BCPAP.
Furthermore, high BMI leads to hyperinsulinemia and IR that also contribute to increased thyroid cell proliferation and goiter formation.
Fusco, "Thyroid cell transformation requires the expression of the HMGA1 proteins," Oncogene, vol.
Papillary carcinoma forms 85-90% of thyroid cancers in iodide-sufficient countries, [17] while the remaining epithelial thyroid cell tumours are mainly follicular carcinomas.