The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Calcium metabolism in Williams-Beuren syndrome.

Increased 1,25-dihydroxyvitamin D levels and decreased basal and calcium-stimulated calcitonin serum levels have been found in children with Williams-Beuren syndrome ( WBS). To determine whether isolated or combined disturbances of secretion or action of the calcium-regulating hormones may cause the tendency to hypercalcemia in WBS, we investigated several aspects of calcium metabolism in 27 normocalcemic children and adults, aged 2 to 47 years, with WBS. With the exception of slightly decreased 25-hydroxyvitamin D and slightly increased calcitonin in serum, all measured basal indexes of calcium and bone metabolism, including the serum levels of intact parathyroid hormone and 1,25-dihydroxyvitamin D, were comparable to control values. Total and extractable calcitonin, the latter representing the monomeric and biologically important form of the hormone, showed the same relative increase after a low-dose calcium infusion in patients and control subjects, indicating a normal capacity of the calcitonin-producing C cells of the thyroid gland in WBS. Furthermore, exogenous parathyroid hormone induced a normal response of 1,25-dihydroxyvitamin D, cyclic adenosine monophosphate, and phosphate excretion, indicating a normal response of the renal 25-hydroxyvitamin D-1 alpha-hydroxylase and the renal receptor-adenylate cyclase system to parathyroid hormone. These findings suggest that neither deficient calcitonin secretion nor increased renal sensitivity to parathyroid hormone is a feature of WBS in normocalcemic patients.[1]

References

  1. Calcium metabolism in Williams-Beuren syndrome. Kruse, K., Pankau, R., Gosch, A., Wohlfahrt, K. J. Pediatr. (1992) [Pubmed]
 
WikiGenes - Universities