Effects of green tea polyphenols on iodide-induced autoimmune thyroiditis in nonobese diabetic mice.

Because green tea polyphenols (GTPs) possess anti-inflammatory properties and are effective in inhibiting autoimmune diseases in experimental settings, we examined whether GTPs prevented the development of autoimmune thyroiditis in iodide-treated nonobese diabetic (NOD) mice, an animal model of Hashimoto's thyroiditis (HT). Mice were given 0.05% iodide water or iodide water supplemented with 0.

Effects of synthetic retinoid Am80 on iodide-induced autoimmune thyroiditis in nonobese diabetic mice.

We examined whether a synthetic retinoid Am80 prevented the development of autoimmune thyroiditis in iodide-treated nonobese diabetic mice, an animal model of Hashimoto's thyroiditis (HT). Am80 (0, 0.1 or 1 mg/kg/day) was orally administered in feed during the 8-week iodide treatment.

The sphingosine 1-phosphate receptor modulator FTY720 prevents iodide-induced autoimmune thyroiditis in non-obese diabetic mice.

FTY720 is an immunomodulator that alters migration and homing of lymphocytes via sphingosine 1-phosphate receptors. This compound has been shown to be effective in suppressing autoimmune diseases in experimental and clinical settings. In the present study, we tested whether FTY720 prevented autoimmune thyroiditis in iodide-treated non-obese diabetic (NOD) mice, a model of Hashimoto's thyroiditis (HT) in humans.

Experimental autoimmune thyroiditis in human parvovirus B19 transgenic mice.

Viral infection is implicated as a cause of autoimmune diseases. Whereas its role in Hashimoto's thyroiditis (HT) remains undefined, recent studies suggested a link between human parvovirus B19 (B19) infection and HT. We tested such possibility by using B19 nonstructural protein 1 (NS1) transgenic C57BL/6 mice, which harbor nonpermissive genetic background (H-2(b)).

Erythrocyte zinc concentration as an indicator to distinguish painless thyroiditis-associated transient hypothyroidism from permanent hypothyroidism.

Red blood cell (RBC) zinc (Zn) concentration reflects a patient's mean thyroid hormone level over the preceding several months. The aim of this study was to examine whether RBC Zn level can be used as an indicator to distinguish painless thyroiditis-associated transient hypothyroidism (TH) from permanent hypothyroidism (PH). RBC Zn level was measured in 30 untreated PH patients with Hashimoto's thyroiditis and 7 untreated TH patients with painless thyroiditis in whom preceding transient thyrotoxicosis had been confirmed.

Effects of interleukin-6 blockade on the development of autoimmune thyroiditis in nonobese diabetic mice.

We explored the role of interleukin-6 (IL-6) in the development of autoimmune thyroiditis in nonobese diabetic (NOD) mice, an animal model of Hashimoto's thyroiditis, using anti-mouse IL-6 receptor antibody (MR16-1). Thyroiditis was induced by iodide ingestion or mouse thyroglobulin (Tg) immunization. Mice were injected intraperitoneally with saline, control rat IgG, or MR16-1 (2 or 8 mg).

Autonomously functioning thyroid nodule associated with thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis (TPP) is mainly associated with Graves' disease but rarely with autonomously functioning thyroid nodule (AFTN). We herein report a case of AFTN associated with TPP in which the latter resolved after (131) I therapy for the former. We analyzed the genes encoding thyrotropin receptor (TSHR), the alpha-subunit of the stimulatory G protein (Gsalpha), calcium channel CACNA1S and potassium channel KCNE3, and found that the patient does not carry the known mutations in these genes.

Effects of angiotensin II blockade on the development of autoimmune thyroiditis in nonobese diabetic mice.

We evaluated the effects of angiotensin II (Ang II) blockers, losartan, an Ang II receptor blocker, and enalapril, an angiotensin converting enzyme inhibitor, on the development of autoimmune thyroiditis in nonobese diabetic (NOD) mice, an animal model of Hashimoto's thyroiditis (HT). Mice were assigned into three groups, untreated, losartan-treated (30 mg/kg/day), and enalapril-treated (10 mg/kg/day) groups. Thyroiditis was induced by iodide ingestion (experiment 1) or mouse thyroglobulin (Tg) immunization (experiment 2).

Methylmercury inhibition of type II 5'-deiodinase activity resulting in a decrease in growth hormone production in GH3 cells.

We have recently reported that methylmercury (MeHg) inhibits type II iodothyronine 5'-deiodinase (D2) activity in mouse neuroblastoma NB41A3 cells. In the present study, we determined the biological significance of D2 inhibition by MeHg. GH3 rat pituitary tumor cells were treated with MeHg and D2 activity and production of a thyroid hormone-responsive gene product, growth hormone (GH) were analyzed.

Intrathyroidal persistence of human parvovirus B19 DNA in a patient with Hashimoto's thyroiditis.

Previous studies suggest a role of viral infection in the development of Hashimoto's thyroiditis (HT). Here we report a patient with HT in whom human parvovirus B19 (B19) DNA has been persistently detected in the thyroid regardless of the presence or absence of B19 DNA in peripheral blood mononuclear cells. In contrast to the DNA persistence, however, VP1 capsid protein was not detected in the thyroid by immunohistochemical studies.

Development of subclinical hyperthyroidism due to Graves' disease in a hypothyroid woman who had undergone hemithyroidectomy for adenomatous goiter and radiotherapy for nasopharyngeal cancer.

A variety of thyroid disorders develop following external radiation to head and neck cancers. Hypothyroidism is the most common clinical consequence of the radiotherapy and lifelong thyroid hormone replacement is required in many cases. Patients who received both hemithyroidectomy and the external radiation to the neck are at especially high risk for permanent hypothyroidism.

Effects of perinatal exposure to low doses of cadmium or methylmercury on thyroid hormone metabolism in metallothionein-deficient mouse neonates.

Perinatal exposure to cadmium (Cd) or methylmercury (MeHg) results in impaired neurodevelopment. Thyroid hormone is essential for normal brain development. However, the issue whether Cd or MeHg, especially at low doses, interrupts thyroid hormone action remains to be investigated.

Autoinduction of tumor necrosis factor-alpha in FRTL-5 rat thyroid cells.

Tumor necrosis factor-alpha (TNFalpha) may play a role in the development of autoimmune thyroiditis such as Hashimoto's thyroiditis. In the present study, we examined whether TNFalpha induced its own expression in FRTL-5 rat thyroid cells. Lipopolysaccharide (LPS) markedly increased TNFalpha mRNA levels in FRTL-5 cells as assessed by semiquantitative RT-PCR.

Methylmercury inhibits type II 5'-deiodinase activity in NB41A3 neuroblastoma cells.

Methylmercury (MeHg) is a well-known neurotoxicant and prenatal exposure to MeHg results in severe brain damage. Since MeHg has a high affinity for thiol groups, we sought to determine whether MeHg inhibited type II iodothyronine deiodinase (D2) activity, by which prohormone thyroxine (T4) is converted to active thyroid hormone, 3,5,3'-triiodothyronine (T3) in the brain, using NB41A3 mouse neuroblastoma cells. In MeHg-treated cells, D2 activity was inhibited in a dose- and time-dependent manner; relatively low concentrations of MeHg (30 nM) inhibited D2.

Experimental autoimmune thyroiditis in nonobese diabetic mice lacking interferon regulatory factor-1.

Interferon regulatory factor-1 (IRF-1) is pivotal in the regulation of interferon (IFN)-mediated immune reactions, and studies suggest that IRF-1 is involved in the development of autoimmune diseases. IRF-1+/+, +/-, and -/- nonobese diabetic (NOD) mice were immunized with mouse thyroglobulin (mTg) to determine whether IRF-1 is required in experimental autoimmune thyroiditis (EAT), a murine model for Hashimoto's thyroiditis (HT). IRF-1-deficient mice developed EAT and anti-mTg antibodies comparable to IRF-1+/+ and +/- mice.

Artifactually elevated serum-free thyroxine levels measured by equilibrium dialysis in a pregnant woman with familial dysalbuminemic hyperthyroxinemia.

Familial dysalbuminemic hyperthyroxinemia (FDH) is a familial autosomal dominant syndrome caused by abnormal albumin with an increased affinity for thyroxine (T4). Two types of mutations in the albumin gene, replacing the normal arginine 218 with a histidine (R218H) or a proline (R218P), have been reported to cause FDH. Here, we report a pregnant Japanese woman with FDH caused by the mutant albumin R218P.

Prevention of lymphocytic thyroiditis in iodide-treated non-obese diabetic mice lacking interferon regulatory factor-1.

Objective: Interferon regulatory factor-1 (IRF-1) is a critical regulator of interferon-gamma(IFNgamma)-mediated immune responses. To determine whether IRF-1 is involved in the pathogenesis of thyroiditis in animal models, we evaluated the incidence of iodide-induced lymphocytic thyroiditis (LT) in non-obese diabetic (NOD) mice lacking IRF-1 as well as IRF-1 +/+ and +/- mice.

Design: IRF-1 +/+, +/- and -/- NOD mice at 6 weeks of age were fed water (group 1) or iodide water (group 2) for 8 weeks.

Postpartum recurrence of Graves' hyperthyroidism can be prevented by the continuation of antithyroid drugs during pregnancy.

Objective: Previous studies recommend the discontinuation of antithyroid drug (ATD) therapy during pregnancy in women with well-controlled Graves' hyperthyroidism (GH). In this study, we investigated whether this termination of ATD therapy during pregnancy is beneficial in terms of postpartum GH recurrence.

Design: A nonrandomized, retrospective study.