Decrease in thyroid adenoma associated (THADA) expression is a marker of dedifferentiation of thyroid tissue

<p>Abstract</p> <p>Background</p> <p><it>Thyroid adenoma associated (THADA) </it>has been identified as the target gene affected by chromosome 2p21 translocations in thyroid adenomas, but the role of THADA in the thyroid is still elusive. The aim of this study was to quantify <it>THADA </it>gene expression in normal tissues and in thyroid hyper- and neoplasias, using real-time PCR.</p> <p>Methods</p> <p>For the analysis <it>THADA </it>and 18S rRNA gene expression assays were performed on 34 normal tissue samples, including thyroid, salivary gland, heart, endometrium, myometrium, lung, blood, and adipose tissue as well as on 85 thyroid hyper- and neoplasias, including three adenomas with a 2p21 translocation. In addition, <it>NIS </it>(<it>sodium-iodide symporter</it>) gene expression was measured on 34 of the pathological thyroid samples.</p> <p>Results</p> <p>Results illustrated that <it>THADA </it>expression in normal thyroid tissue was significantly higher (<it>p </it>< 0.0001, exact Wilcoxon test) than in the other tissues. Significant differences were also found between non-malignant pathological thyroid samples (goiters and adenomas) and malignant tumors (<it>p </it>< 0.001, Wilcoxon test, t approximation), anaplastic carcinomas (ATCs) and all other samples and also between ATCs and all other malignant tumors (<it>p </it>< 0.05, Wilcoxon test, t approximation). Furthermore, in thyroid tumors <it>THADA </it>mRNA expression was found to be inversely correlated with <it>HMGA2 </it>mRNA. <it>HMGA2 </it>expression was recently identified as a marker revealing malignant transformation of thyroid follicular tumors. A correlation between <it>THADA </it>and <it>NIS </it>has also been found in thyroid normal tissue and malignant tumors.</p> <p>Conclusions</p> <p>The results suggest <it>THADA </it>being a marker of dedifferentiation of thyroid tissue.</p

Differenzierung zwischen aktiver und passiver Komponente des D-Glucosetransports am proximalen Konvolut der Rattenniere / Differentiation of the active and passive components of d-glucose transport in the proximal tubule of rat kidney

Both, the net and unidirectional transport of d-glucose across the proximal tubule of rat kidney were studied by the technique of continuous microperfusion under the condition of zero netflux of water and sodium chlorid. When the active transport component was completely abolished by 10−4 M of phlorizin a small passive component could be demonstrated. The passive component was also observed in the non-phlorizin-poisoned stat to be additive to the active transport. Vmax of the actived-glucose transport was 6×10−10 mol×cm−2×sec−1. The passive glucose flux is proportional to the concentration difference between perfusate and serum. There is no difference between data of influx and efflux measurements. From this it is concluded that the passive d-glucose flux is a simple diffusion process. The permeability coefficient ford-glucose (PG) calculated from 3 different sets of experiments is 1.7×10−5 cm×sec−1. Active and passive glucose transport component can cancel out each other at a transtubular concentration difference of 33 mmol/l. Changes of the specific activity in the perfusate were measured under three different conditions (d-glucose concentration lumen: > plasma, lumen = plasma, lumen max and PG for the calculation (see appendix). The permeability of d-glucose across the proximal tubules is small. Therefore, under normal free flow condition the passive transport component plays no role in the d-glucose absorption. However, with greatly increasing transtubular concentration difference of d-glucose, e.q. due to a low glomerular filtration rate and a high serum d-glucose concentration, the passive transport component may be the rate limiting factor for the net transport of d-glucose