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Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...

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Related Experiment Video

Updated: Jul 6, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Cyclooxygenase-2 expression in human thyroid disease.

K J Lee1, Y S Jung, W H Kim

  • 1Department of Surgery, School of Medicine, Ajou University, Suwon, South Korea.

Journal of Endocrinological Investigation
|March 26, 2008
PubMed
Summary
This summary is machine-generated.

Cyclooxygenase-2 (COX-2) is not significantly expressed in normal thyroid tissue. While present in thyroiditis and tumors, its expression levels do not correlate with clinical factors, suggesting it lacks clinical significance in thyroid disease.

Related Experiment Videos

Last Updated: Jul 6, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Area of Science:

  • Oncology
  • Molecular Biology
  • Pathology

Background:

  • Cyclooxygenase-2 (COX-2) is implicated in epithelial cell growth and is upregulated in gastrointestinal cancers.
  • Non-steroidal anti-inflammatory drugs (NSAIDs), which inhibit COX enzymes, are associated with reduced cancer incidence.
  • The role of COX-2 in human thyroid diseases remains largely undetermined.

Purpose of the Study:

  • To investigate the expression and potential involvement of COX-2 in various human thyroid diseases.
  • To determine if COX-2 expression correlates with clinical or pathological characteristics of thyroid tumors.

Main Methods:

  • Immunohistochemical staining and Western blot analysis were employed to detect COX-2 protein.
  • Thyroid tissue samples from 64 patients, including normal, thyroiditis, benign tumors, and malignant tumors (with or without metastasis), were analyzed.
  • Immunoreactivity scores were calculated to quantify COX-2 expression levels.

Main Results:

  • COX-2 protein was absent in normal thyroid tissues.
  • Significant COX-2 protein expression was detected in thyroiditis, benign tumors, and malignant tumors.
  • No significant differences in COX-2 expression levels were observed between different thyroid tissue types or with clinical/pathological characteristics.

Conclusions:

  • COX-2 protein expression is upregulated in thyroiditis and tumors but does not correlate with clinical or pathological features.
  • There is no significant difference in COX-2 expression between thyroiditis and thyroid tumors.
  • The upregulation of COX-2 in human thyroid diseases does not appear to hold clinical significance.