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The goal of this study was to investigate the influence of experimentally induced hypercalcaemia (after 100000 UI Vigantol and CaCl₂) on neuroendocrine cells (NECs) in the thyroid and airways in the rat. After 24 h, 7 days and 14 days the thyroid and lungs were collected. Paraffin sections were immunocytochemically stained with specific antibodies against CGRP, calcitonin (CT) and synaptophysin (SY) in the airway NECs and thyroid C cells. The largest hypercalcaemia were observed in experimental rats after 7 days. More significant changes in the number and size of neuroendocrine cells were observed in the thyroid gland as well as in the airways. In the airways only a slight increase in the number of neuroepithelial bodies (NEBs) was observed, some of which gave evidence of hypertrophy symptoms.
The enlargement of the thyroid is, in general, benign in origin and due to nodular goitre. Follicular cellular proliferation of thyroid nodules has been increasingly observed recently. With fine needle aspiration biopsy (FNAB) this is classified as a follicular tumour. These lesions present various patterns of vascularisation in ultrasound examination. The aim of the study was to establish the relation between follicular nodule vascularisation and the proliferative activity of various types of follicular cell. According to the manner of proliferation, patients were divided into groups as follows: (I) patients with hyperplastic nodules (46 cases), (II) patients with follicular adenoma (42 cases), and (III) patients with follicular cancer (9 cases). In each case B-mode sonography, Power Doppler, sonographically guided FNAB (S-FNAB), morphological examination and morphometry were performed. The proliferative activity was detected with immunohistochemical methods (PCNA, Ki 67 and MPM2) to determine the so-called “proliferative index”. The study revealed increased proliferative activity in tumours of malignant origin and increased vascularisation in coexistence with increased proliferation of the follicular cells. As assessed by Power Doppler, an increased flow pattern in the centre of the nodules correlates with increased proliferative activity. The results suggest that Power Doppler examination could be helpful in selecting nodules for FNAB, especially in multinodular goitre.
The effect of exposure to cadmium (Cd) on the function and structure of the thyroid with parathyroids and a relationship between Cd accumulation in these glands and their damage were studied on a male rat model corresponding to human exposure. For this purpose, male rats were treated with Cd in drinking water at concentration of 5 and 50 mg Cd/dm³ for 12 and 24 weeks. The function of the thyroid was evaluated based on the measurement of serum concentrations of triiodothyronine (T₃) and tetraiodothyronine (T₄), and immunohistochemical identification of hormones such as calcitonin (CT), calcitonin-gene related peptide (CGRP) and somatostatin (ST). To assess the parathyroid function immunohistochemical reaction for parathyroid hormone-related peptide (PTHrP) was performed. Histological structure of the thyroid and parathyroid glands was evaluated in a light microscope. Rats exposed to 5 and 50 mg Cd/dm³ showed changes in the epithelium of follicular cells, intensified remodeling of the glandular structure of the thyroid, mononuclear cell infiltrations in connective tissue and pale staining of colloid. Hypertrophy and hyperplasia of endocrine parathyroid cells were evident.The intensity of reactions for CT, ST, CGRP and PTHrP was weakened. Exposure to Cd had no effect on the T₃ and T₄ serum concentrations, except for a marked increase in the concentrations of both hormones after 24 weeks of exposure to 50 mg Cd/dm³ . All the Cd-induced changes were much more advanced at exposure to 50 mg Cd/dm³ than 5 mg Cd/dm³ . The seriously disturbed structure and function of the thyroid and parathyroids at a low Cd concentration (0.087 ± 0.005 µg/g) in these glands suggests that the damaging Cd influence may be due to its indirect rather than direct action. Based on the results it can be hypothesized that a human body chronically exposed to moderate and relatively high Cd levels may be at risk of damage to the thyroid and parathyroid glands.
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