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1

Alterations of cellular calcium depots in endocrine hypercalcemic syndromes

100%
Schafer H.
Folia Histochemica et Cytobiologica
|
1984
|
tom 22
|
nr 3-4
2
Content available remote

Dynamics of sodium retention in preascitic cirrhotic rats assessed through parathyroid hormone injection

86%
Sansoe G., Mastrocola R., Aragno M., Parola M.
Journal of Physiology and Pharmacology
|
2014
|
tom 65
|
nr 5
3
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Content available

Dissociation of parathyroid hormone and cyclic-3',5'AMP effects on Na-Pi uptake by cells isolated from proximal straight tubules of rat kidney

86%
Rybczynska A., Angielski S., Hoppe A.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 2
4

Parathyroid hormone level in blood of cows with different forms of clinical hypocalcaemia

86%
Kurek L., Stec A.
Bulletin of the Veterinary Institute in Puławy
|
2005
|
tom 49
|
nr 1
5

Immunocytochemical localization of PTHrP in human and rat salivary glands

86%
Seidel J., Zabel M., Surdyk-Zasada J., Kasprzak A., Radziemski A.
Folia Histochemica et Cytobiologica
|
2001
|
tom 39
|
nr 2
6

The profile of ErbB-Her family genes copy number assessed by real-time PCR in parathyroid adenoma and hyperplasia associated with sporadic primary hyperparathyroidism

72%
Bednarz N., Blaut K., Sworczak K., Oseka T., Bielawski K. P.
Acta Biochimica Polonica
|
2009
|
tom 56
|
nr 1
83-88
 Hyperparathyroidism (pHPT) is a relatively frequent endocrinopathy, however, the molecular mechanisms of its etiology remain poorly understood. This disorder is mainly associated with benign tumours (adenoma) and hyperplasia of the parathyroid, hence, the focus is directed also to genes that are likely to be involved in carcinogenesis. Among such genes are ErbB/Her family genes already used in diagnosis of other tumours (e.g., breast carcinoma) and reported also to play a role in development of endocrine lesions. So far, ErbB-1/Her-1/EGFR expression has been detected in pHPT-associated adenomas and hyperplasia as opposed to no expression in normal parathyroid tissue. Moreover, losses or gains of the fragments of chromosomes where ErbB/Her genes are located have been reported. In this study, the gene dosage of ErbB/Her family genes were determined for the first time in parathyroid adenomas, hyperplasia and morphologically unchanged tissue in order to establish their putative role in the development of the disease. Genomic DNA was isolated from 33 patients with sporadic hyperparathyroidism and the gene copy numbers were assessed using real-time PCR. The ErbB/Her genes' profile was unaltered in most of the examined samples. Two low-level amplifications of ErbB-1/Her-1/EGFR gene, two deletions of ErbB-2/Her-2, and six deletions of ErbB-4/Her-4 were found. The ErbB-3/Her-3 gene remained unaffected. No correlation with clinical parameters was found for any gene. Both the low number of alterations and a lack of their associations with clinical parameters exclude the prognostic value of the ErbB/Her genes family in parathyroid tumourigenesis. Nevertheless, the ErbB-4/Her-4 deletions seem to be interesting for further investigations, especially in the context of PTH secretion.
7

Immunohistochemistry in detection of paraneoplastic secretion of calcium regulating hormones

72%
Arps H., Dietel M., Otto U.
Folia Histochemica et Cytobiologica
|
1984
|
tom 22
|
nr 3-4
8

Coexpression of PTHrP and PTH-PTHrP receptor in a myoepithelial cell line derived from normal human breast

72%
Sopel M., Lis A.
Folia Histochemica et Cytobiologica
|
2000
|
tom 38
|
nr 2
9
Content available remote

Blockade of calcium channels and AT1 receptors prevents the hypertensive effect of calcilytic NPS 2143 in rats

58%
Rybczynska A., Jurska-Jasko A., Boblewski K., Lehmann A., Orlewska C.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 2
Calcilytics, antagonists of calcium receptor, decrease sensitivity of this receptor to plasma calcium concentration and increase parathyroid hormone (PTH) secretion. Moreover, it was recently indicated that calcilytic NPS 2143 induces hypertension in rats. This study tested whether the increase of mean arterial blood pressure (MAP) induced by NPS 2143 administration is mediated by calcium channel and angiotensin II type1 (AT1) receptor activity. Wistar rats were anaesthesized with Thiopental i.p. and infused i.v. with saline supplemented with the anaesthetic. Blood pressure was monitored continuously in the carotid artery. Effects of NPS 2143 administered i.v. as bolus on MAP in the presence and absence of felodypine and losartan were investigated. Both, felodipine and losartan pretreatment provoked a persistent MAP decrease by 18±3 and 14±3 mmHg, respectively. Infusion of NPS 2143 at 1 mg/kg b.w. confirmed hypertensive activity of calcilytic and increased blood pressure for 21±4 mmHg. In contrast, administration of NPS 2143 in felodipine as well as in losartan pretreated rats did not change MAP as compared to felodipine/control and losartan/control groups, respectively. Our study indicated that both the blockade of calcium channels and the AT1 receptor activity prevented the hypertensive effect of calcilytic NPS 2143. This finding might be particularly important in understanding the mechanisms that mediated blood pressure changes related to the activity of calcium receptor.
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