Thyroid research: stepping forward.

It is eight years since Thyroid Research was launched with an aim to enhance opportunities for scientists and clinicians, working in the rapidly advancing field of thyroidology, to publish their research (Thyroid Res 1(1):1, 2008). Right from the outset, Thyroid Research aspired to become a prominent journal in thyroidology with high quality publications. Over the years, the journal has not only survived in the increasingly competitive field of open-access academic journal publication, it has also been making a steady progress towards achieving this ambitious goal. Now, Thyroid Research is ready to step forward to begin a new chapter in its publication.This article is freely available via Open Access. Click on the 'Additional Link' above to access the full-text from the publisher's site.Published

Dendritic cells in autoimmune disorders and cancer of the thyroid

Dendritic cells (DCs), considered as one of the crucial immune regulatory populations, are implicated in the immune pathology of various disorders. Also in the thyroid gland, DCs were shown to be involved in early and chronic phases of various types of autoimmunity — including Hashimoto’s thyroiditis and Graves’ disease. In thyroid malignant processes, DCs are suggested as an important element of both tumour defence and tumour immune evasion mechanisms. Recent findings emphasize a crucial role of interactions between particular DC subsets and other regulatory cell populations (e.g. FoxP3+ regulatory T cells) in thyroid pathology. Additionally, an increasing attention has been paid to the control of DC function by thyrometabolic conditions. (Folia Histochemica et Cytobiologica 2014, Vol. 52, No. 1, 18–28

Welcome to Thyroid Research

Welcome to the first issue of Thyroid Research, a new journal published by BioMed Central, which aims at providing a platform for both researchers and clinicians to discuss a broad spectrum of thyroidology and related issues. These include physiological mechanisms of thyroid hormone action, secretory regulations, immunological and genetic aspects and, finally, news and information on state-of-the-art diagnostic equipment and treatment protocols for more effective management of thyroid disorders

Thyroid function in children with growth hormone (GH) deficiency during the initial phase of GH replacement therapy - clinical implications

BACKGROUND: Normal thyroid hormone secretion or appropriate L-thyroxine (L-T(4)) substitution is necessary for the optimal effect of the growth hormone (GH) administration on growth rate. The decrease of free thyroxine (FT(4)) levels at recombinant human GH (rhGH) therapy onset has been reported in several studies. The aim of the present study was to evaluate the effect of rhGH administration on thyrotropin (TSH) and FT(4 )serum concentrations in children with GH deficiency (GHD) during the 1st year of therapy, as well as to assess potential indications to thyroid hormone supplementation in them. PATIENTS AND METHODS: The analysis involved data of 75 children (59 boys, 16 girls) with disorders of GH secretion (GHD, neurosecretory dysfunction - NSD) and partial GH inactivity (inactGH), who were treated with rhGH for - at least - one year. In all the children, body height and height velocity (HV) were assessed before and after 1 year of therapy, while TSH, FT(4), IGF-I and IGFBP-3 before treatment and after 3-6 months and 1 year of treatment. In the patients, who revealed hypothyroidism (HypoT), an appropriate L-T(4 )substitution was introduced immediately. The incidence of HypoT, occurring during the initial phase of rhGH therapy, was assessed, as well as its influence on the therapy effectiveness. RESULTS: Before rhGH substitution, there were no significant differences in either auxological indices or TSH and FT(4 )secretion, or IGF-I concentration and its bioavailability among the groups of patients. During the initial 3-6 months of rhGH administration, a significant decrease of FT(4 )serum concentration, together with a significant increase of IGF-I SDS and IGF-I/IGFBP-3 molar ratio was observed in all the studied groups. In 17 children, HypoT was diagnosed and L-T(4 )substitution was administered. Despite similar IGF-I secretion increase, the improvement of HV presented significantly lower in children with HypoT than in those who remained euthyroid all the time. CONCLUSIONS: The incidence of HypoT during the initial phase of GH treatment in children with GHD and the negative effect of even transient thyroid hormone deficiency on the growth rate should be taken into account

Effect of L-thyroxine treatment on peripheral blood dendritic cell subpopulations in patients with Hashimoto’s thyroiditis

Recent reports suggested dendritic cells (DCs) to be important players in the pathogenesis of autoimmune thyroid processes in humans. However, there are virtually no data addressing the influence of thyroid autoaggression-associated disturbances of thyrometabolic conditions on DCs biology. The aim of the study was to evaluate the influence of L-thyroxine supplementation on conventional and plasmacytoid peripheral blood DCs subtypes in patients with hypothyroidism due to Hashimoto’s thyroiditis (HT). Eighteen patients with newly diagnosed hypothyroidism due to HT were included into the study. All patients received L-thyroxine treatment with doses adjusted to reach euthyroidism. Peripheral blood DC subtypes structure and immunoregulatory phenotype were analyzed by flow cytometry in the same patient prospectively at two time points: (i) beforeand (ii) 3 months after beginning of L-thyroxine treatment (hypothyroidism vs. euthyroidism, respectively). Percentage of plasmacytoid DCs in peripheral blood mononuclear cells fraction was significantly decreased in the course of L-thyroxine treatment (0.27 ± 0.19 vs. 0.11 ± 0.08; p < 0.05), whereas we did not observe any changes in the number of conventional DCs. However, the phenotypic analysis showed a significant increase of conventional DCs expressing CD86 and CD91 (64.25 ± 21.6% vs. 86.3 ± 11%; p < 0.05 and 30.75 ± 11.66% vs. 44.5 ± 13.3%; p < 0.05; respectively) in euthyroid patients. Standard L-thyroxine supplementation in HT patients exerted significant immunoregulatory effects, associated with quantitative and phenotypic changes of peripheral blood DC subpopulations

Relation between functional polymorphism of catalase gene (- 262C>T) and recurrent depressive disorder

Abstract BACKGROUND: Numerous studies have provided information indicating the involvement of oxidative stress in the pathophysiology of depressive disorder (DD). The antioxidative system protects against the effects caused by reactive oxygen species (ROS). Catalase (CAT) is one of antioxidative enzymes observed to change their levels in the course of depression. The enzyme decomposes hydrogen peroxide (H 2 O 2 ), whose overproduction is a result of many processes taking place in depression. Therefore, functional polymorphism of the CAT gene can be a candidate marker of the risk of depression. DESIGN: The presented study assessed the correlation between -262C>T polymorphism of the CAT gene, which influences the increase of CAT expression and activity, and the risk of depression development. The study, carried out on a homogeneous group recruited from the Polish population, enrolled 149 healthy subjects and 149 depressive patients. The groups were age-matched. RESULTS: The obtained results indicate no correlation between -262C>T polymorphism of the CAT gene (both with respect to genotype distribution and allele frequency) and the risk of depression. Nevertheless, further studies assessing the correlations between depression and polymorphism of the genes encoding antioxidative enzymes on larger groups of subjects should be undertaken

Gene expression of key regulators of mitochondrial biogenesis is sex dependent in mice with growth hormone receptor deletion in liver

Mitochondrial biogenesis is an essential process for cell viability. Mice with disruption of the growth hormone receptor (GHR) gene (Ghr gene) in the liver (LiGHRKO), in contrast to long-lived mice with global deletion of the Ghr gene (GHRKO), are characterized by lack of improved insulin sensitivity and severe hepatic steatosis. Tissue-specific disruption of the GHR in liver results in a mouse model with dramatically altered GH/IGF1 axis. We have previously shown increased levels of key regulators of mitochondrial biogenesis in insulin-sensitive GHRKO mice. The aim of the present study is to assess, using real-time PCR, the gene expression of key regulators of mitochondrial biogenesis (Pgc1 alpha, Ampk, Sirt1, Nrf2 and Mfn2) and a marker of mitochondrial activity (CoxIV) in brains, kidneys and livers of male and female LiGHRKO and wild-type (WT) mice. There were significant differences between males and females. In the brain, expression of Pgc1 alpha, Ampk, Sirt1, Nrf2 and Mfn2 was lower in pooled females compared to pooled males. In the kidneys, expression of Ampk and Sirt1 was also lower in female mice. In the liver, no differences between males and females were observed. Sexual dimorphism may play an important role in regulating the biogenesis of mitochondria

Gene expression of key regulators of mitochondrial biogenesis is sex dependent in mice with growth hormone receptor deletion in liver

Abstract: Mitochondrial biogenesis is an essential process for cell viability. Mice with disruption of the growth hormone receptor (GHR) gene (Ghr gene) in the liver (LiGHRKO), in contrast to long-lived mice with global deletion of the Ghr gene (GHRKO), are characterized by lack of improved insulin sensitivity and severe hepatic steatosis. Tissue-specific disruption of the GHR in liver results in a mouse model with dramatically altered GH/IGF1 axis. We have previously shown increased levels of key regulators of mitochondrial biogenesis in insulin-sensitive GHRKO mice. The aim of the present study is to assess, using real-time PCR, the gene expression of key regulators of mitochondrial biogenesis (Pgc1α, Ampk, Sirt1, Nrf2 and Mfn2) and a marker of mitochondrial activity (CoxIV) in brains, kidneys and livers of male and female LiGHRKO and wild-type (WT) mice. There were significant differences between males and females. In the brain, expression of Pgc1α, Ampk, Sirt1, Nrf2 and Mfn2 was lower in pooled females compared to pooled males. In the kidneys, expression of Ampk and Sirt1 was also lower in female mice. In the liver, no differences between males and females were observed. Sexual dimorphism may play an important role in regulating the biogenesis of mitochondria

The Role of Snail-1 in Thyroid Cancer—What We Know So Far

Thyroid carcinomas, despite the usually indolent behaviour and relatively good overall prognosis, show a high tendency to gain invasive phenotype and metastasise in some cases. However, due to a relatively slow progression, the exact mechanisms governing the metastatic process of thyroid carcinomas, including the epithelial-to-mesenchymal transition (EMT), are poorly described. One of the best-known regulators of cancer invasiveness is Snail-1—a zinc-finger transcription factor that plays a key role as an EMT inducer. More and more attention is being paid to the role of Snail with regard to thyroid cancer development. Apart from the obvious implications in the EMT process, Snail-1 plays an important role in the regulation of chemoresistance of the thyroid cells and cancer stem cell (CSC) formation, and it also interacts with miRNA specific to the thyroid gland. The aim of this review was to summarise the knowledge on Snail-1, especially in the context of thyroid oncogenesis