calcinosis/protease

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Fibroblast growth factor-23 mutants causing familial tumoral calcinosis are differentially processed.

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Prijava / prijava

Familial tumoral calcinosis (TC, OMIM 211900) is a heritable disorder characterized by hyperphosphatemia, normal or elevated serum 1,25-dihydroxyvitamin D, and often severe ectopic calcifications. Two recessive mutations in fibroblast growth factor-23 (FGF23), serine 71/glycine (S71G) and serine

Interaction of amorphous calcium phosphate with fibrin in vitro causes decreased fibrinolysis and altered protease profiles: implications for atherosclerotic disease.

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Prijava / prijava

Previously, we demonstrated that amorphous calcium phosphate (ACP), chemical precursor to apatite, strongly interacted with fibrin and facilitated binding of matrix metalloproteinase (MMP)-9, a type IV collagenase. Plasmin-dependent fibrinolysis resulted in coordinate MMP-9 activation. Here we

The Roles of Fibroblast Growth Factor (FGF)-23, α-Klotho and Furin Protease in Calcium and Phosphate Homeostasis : A Mini-Review.

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Prijava / prijava

The roles of calcitonin, parathormone and calcitriol in the regulation of plasma calcium and phosphate are well-established. However, in autosomal-dominant hypophosphatemic rickety patients, studies have revealed normal plasma levels of calcium, associated with normal thyroid and parathyroid

Molecular genetic and biochemical analyses of FGF23 mutations in familial tumoral calcinosis.

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Prijava / prijava

Fibroblast growth factor 23 (FGF23) is a hormone required for normal renal phosphate reabsorption. FGF23 gain-of-function mutations result in autosomal dominant hypophosphatemic rickets (ADHR), and FGF23 loss-of-function mutations cause familial hyperphosphatemic tumoral calcinosis (TC). In this

Polypeptide GalNAc-transferase T3 and familial tumoral calcinosis. Secretion of fibroblast growth factor 23 requires O-glycosylation.

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Prijava / prijava

Mutations in the gene encoding the glycosyltransferase polypeptide GalNAc-T3, which is involved in initiation of O-glycosylation, were recently identified as a cause of the rare autosomal recessive metabolic disorder familial tumoral calcinosis (OMIM 211900). Familial tumoral calcinosis is

The anticalcification effect of polyethylene glycol-immobilized on hexamethylene diisocyanate treated pericardium.

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Prijava / prijava

Pathologic calcification is thought to be the main cause of failure in the present generation tissue valves fabricated from glutaraldehyde pretreated bovine pericardium (BP). The present investigation describes the in vitro calcification and enzymatic degradation of bovine pericardia after

Calcium pyrophosphate crystal deposition disease and other crystal deposition diseases.

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Prijava / prijava

A number of cells, chemotactic factors, and inflammatory mediators are implicated in the complex mechanisms underlying crystal-mediated inflammation. Interleukin-8, released from mononuclear cells that have been exposed to urate and other crystals, is a potent chemotaxin and activator of

Molecular Imaging of Vulnerable Plaque.

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Prijava / prijava

Molecular imaging provides multiple imaging techniques to identify characteristics of vulnerable plaque including I) Inflammatory cells (the presence and metabolic activity of macrophages), II) synthesis of lipid and fatty acid in the plaque, III) the presence of hypoxia in severely inflamed

In vitro cytotoxicity of human endothelial cells in polymyalgia rheumatica and giant cell arteritis.

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Prijava / prijava

We studied sera from 20 patients with polymyalgia rheumatica (PMR)/giant cell arteritis (GCA), 15 patients with systemic lupus erythematosus (SLE), 15 patients with the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly, and telangietasia) and 33 age and sex

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