Browsing by Author "Drndarević, Neda (6507610323)"

The purpose of this study was to investigate the possible mechanism of acute effect of ethanol on IgA expression in rat intestine. To this end, adult female Wistar rats showing diestrus day 1 were treated with (a) ethanol (2 or 4 g/kg, i.p.); (b) Nω-nitro-l-arginine-methyl ester (l-NAME), which inhibits the activity of all isoforms of nitric oxide synthase, (30 mg/kg, s.c.) followed by ethanol 3 h later; and (c) l-NAME (30 mg/kg, s.c.) followed by saline 3 h later. Saline-injected and untreated rats were used as controls. The animals were sacrificed 0.5 h after ethanol administration. Intestinal expression of IgA was evaluated by both immunohistochemistry and Western immunoblotting. Morphometric analysis showed that acute ethanol treatment increased the number of IgA-immunoreactive cells in a dose-dependent manner. Pretreatment with l-NAME abolished this action of alcohol. Injection of l-NAME followed by saline had no influence on the number of IgA + cells. The results, obtained by Western immunoblotting, paralleled our immunohistochemical findings. Taken together, these data suggest that acute effect of ethanol on intestinal IgA might be mediated by endogenous nitric oxide. © 2007 Elsevier B.V. All rights reserved.

The purpose of this study was to investigate the possible mechanism of acute effect of ethanol on IgA expression in rat intestine. To this end, adult female Wistar rats showing diestrus day 1 were treated with (a) ethanol (2 or 4 g/kg, i.p.); (b) Nω-nitro-l-arginine-methyl ester (l-NAME), which inhibits the activity of all isoforms of nitric oxide synthase, (30 mg/kg, s.c.) followed by ethanol 3 h later; and (c) l-NAME (30 mg/kg, s.c.) followed by saline 3 h later. Saline-injected and untreated rats were used as controls. The animals were sacrificed 0.5 h after ethanol administration. Intestinal expression of IgA was evaluated by both immunohistochemistry and Western immunoblotting. Morphometric analysis showed that acute ethanol treatment increased the number of IgA-immunoreactive cells in a dose-dependent manner. Pretreatment with l-NAME abolished this action of alcohol. Injection of l-NAME followed by saline had no influence on the number of IgA + cells. The results, obtained by Western immunoblotting, paralleled our immunohistochemical findings. Taken together, these data suggest that acute effect of ethanol on intestinal IgA might be mediated by endogenous nitric oxide. © 2007 Elsevier B.V. All rights reserved.

The pancreas appears to be a major source of ghrelin during fetal development, but the ontogeny of ghrelin cells in the human pancreas and their developmental relationship with α- and β-cells remain largely unknown. In the present study, we examined the dynamics of ghrelin cell growth, colocalization of ghrelin with major pancreatic hormones and defined the similarities and differences among developmental patterns of ghrelin-, glucagon- and insulin-expressing cells in the human pancreas. To this end, paraffin-embedded pancreatic tissue sections from human embryos and fetuses were assessed by immunohistochemistry. Ghrelin-positive cells were first detected in the pancreas of 11-week-old fetuses. With advancing gestational age, both ghrelin- and glucagon-expressing cells were increasingly observed at the periphery of the developing islets, whereas insulin-containing cells were typically found in the islet core. Double immunohistochemistry showed that ghrelin-expressing cells were clearly separate from insulin-, somatostatin- and pancreatic polypeptide-containing cells. In contrast, cells coexpressing ghrelin and glucagon were sporadically detected during both the early and late fetal periods. Furthermore, morphometric analysis revealed a similar trend in the volume density of ghrelin- and glucagon-positive cells, and a contrasting pattern in β-cell density at specific time points during the development of the human pancreas. This study demonstrates that the developmental pattern of ghrelin cells, although clearly distinct, is quite similar to that of glucagon-expressing cells. The obtained findings indicate a close lineage relationship between these cell populations, a functional relationship between their secretory products and an auto/paracrine mode of ghrelin-glucagon interaction in pancreatic development. © 2012 S. Karger AG, Basel.

BACKGROUND: Myoepitheliomas are tumors composed predominantly or exclusively of myoepithelial cells, usually arising in salivary glands. Cutaneous/soft tissue localization is very rare, especially for the malignant myoepitheliomas. CASE REPORT: We presented a case of myoepithelial carcinoma involving subcutaneous adipose tissue of the left forearm in a woman aged 62 years. The tumor was composed of epithelioid and hyaline cell types, arranged in diffuse sheets, nests and loose clusters within hyalinized and myxoid matrix. The neoplasm displayed high-grade cytologic atypia with some cells having pleomorphic, hyperchromatic nuclei, and others showing vesicular nuclei, large nucleoli with scattered bizarre giant cells. High mean mitotic count of 7 mitoses/10 high power filds and extensive necrosis favoured the diagnosis of malignancy. Immunohistochemical staining was positive for cytokeratin (AE1/AE3), epithelial membrane antigen, S-100 protein, glial fibrillary acidic protein, and vimentin. CONCLUSION: Considering the subcutaneous localization, myoepithelial immunophenotype and high-grade cytologic atypia the neoplasm was classified as a soft-tissue myoepithelial carcinoma.

Objective - To examine the possible pathological changes of the trigeminal vasculature in patients with neuralgia. Background - Such a study has never been performed before. The alterations of the trigeminal vessels could have important pathophysiological implications in the trigeminal neuralgia pathogenesis. Methods - The biopsy specimens for the electronmicroscopic (EM) and immunohistochemical examination were taken during a partial rhizotomy in 6 patients with trigeminal neuralgia and in 2 persons with trigeminal neuropathy. In addition, the 32 normal trigeminal nerves were used as the control specimens. Results - The vascular pathological alterations were noticed in 3 out of 6 neuralgia patients. The EM study revealed signs of apoptosis or degeneration, respectively, of some endothelial and smooth muscle cells in the wall of the trigeminal arterioles. The immune reactions against CD31, CD34, and α-smooth muscle actin in these cells were weaker than in the control specimens, but stronger against factor VIII. In addition, the arteriolar basement membranes, which were thickened, showed an intense laminin, fibronectin, and collagen IV immunoreactivity. Similarly, some endothelial cells and pericytes of the intratrigeminal capillaries also showed signs of apoptosis or degeneration, respectively. Their basement membrane was very thick and showed an intense immune reaction against laminin, fibronectin, and collagen IV. Conclusion - The observed pathological changes of the trigeminal vasculature could be the primary factor, while demyelination of the trigeminal nerve fibers could be the secondary process in some patients with neuralgia. © 2007 the Authors.

Objective - To examine the possible pathological changes of the trigeminal vasculature in patients with neuralgia. Background - Such a study has never been performed before. The alterations of the trigeminal vessels could have important pathophysiological implications in the trigeminal neuralgia pathogenesis. Methods - The biopsy specimens for the electronmicroscopic (EM) and immunohistochemical examination were taken during a partial rhizotomy in 6 patients with trigeminal neuralgia and in 2 persons with trigeminal neuropathy. In addition, the 32 normal trigeminal nerves were used as the control specimens. Results - The vascular pathological alterations were noticed in 3 out of 6 neuralgia patients. The EM study revealed signs of apoptosis or degeneration, respectively, of some endothelial and smooth muscle cells in the wall of the trigeminal arterioles. The immune reactions against CD31, CD34, and α-smooth muscle actin in these cells were weaker than in the control specimens, but stronger against factor VIII. In addition, the arteriolar basement membranes, which were thickened, showed an intense laminin, fibronectin, and collagen IV immunoreactivity. Similarly, some endothelial cells and pericytes of the intratrigeminal capillaries also showed signs of apoptosis or degeneration, respectively. Their basement membrane was very thick and showed an intense immune reaction against laminin, fibronectin, and collagen IV. Conclusion - The observed pathological changes of the trigeminal vasculature could be the primary factor, while demyelination of the trigeminal nerve fibers could be the secondary process in some patients with neuralgia. © 2007 the Authors.