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  • 1
    Electronic Resource
    Electronic Resource
    Plasma 1,25-dihydroxyvitamin D concentrations in cords, newborns, infants, and children (1980)
    Springer
    Calcified tissue international 30 (1980), S. 1-3 
    Details
    ISSN: 1432-0827
    Keywords: 1,25-(OH)2-D ; Children ; Newborns
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Plasma 1,25-dihydroxyvitamin D [1,25-(OH)2-D] was measured in cord serum, newborns, infants, and children. The mean for the values obtained from the six cords was significantly higher than the mean for the older children (6–15 years). The mean for the six newborns (0–1 week) was significantly higher than that for the older children. The mean for the nine infants (1 week-6 months) and the 14 younger children (6 months-6 years) was significantly higher than that for older children. The present study suggests that the perinatal period is associated with a marked increase in 1,25-(OH)2-D.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408599
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Activity of renal 25-hydroxyvitamin D3-1α-hydroxylase in a case of X-linked hypophosphataemic rickets (1984)
    Springer
    European journal of pediatrics 142 (1984), S. 219-222 
    Details
    ISSN: 1432-1076
    Keywords: Hypophosphataemic rickets ; 1,25(OH)2D ; 1α-hydroxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In 1974, a 2-year-old boy was diagnosed as having X-linked hypophosphataemic rickets (XLH) because of severe rickets and hypophosphataemia. The vitamin D metabolite concentrations, blood and urine chemistry and renal 25-hydroxyvitamin D3 (25 OHD3)-1α-hydroxlase were measured in 1982 (about 2 weeks after withdrawal of medication). 1α-hydroxylase was 392 pg/mg tissue/20 min in the patient, which was high compared with aged-matched controls (69.7±28.5 pg/mg tissue/20 min, mean ±SD, n=7). Our present studies showed that the 1α-hydroxylase activity in the patient with XLH was elevated. Therefore, the normal or low 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) concentrations in XLH patients could be due to accelerated catabolism of 1,25-(OH)2D3 or abnormally regulated 25OHD3-1α-hydroxylase in response to hypophosphataemia, although significantly elevated above that in normal controls.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442454
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Direct influence of antidepressants on GTP binding protein of adenylate cyclase in cell membranes of the cerebral cortex of rats (1988)
    Springer
    Journal of neural transmission 71 (1988), S. 165-175 
    Details
    ISSN: 1435-1463
    Keywords: Antidepressant ; adenylate cyclase ; GTP binding protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recently, it has been suggested that antidepressant drugs exert their pharmacological action through functional changes in the adrenergic-receptor coupled adenylate cyclase system. In the present research, we examined the direct effects of antidepressants on adenylate cyclase (A-cyclase) activity by in vitro incubation of cell membranes from the cerebral cortex of rats with these drugs. All antidepressants examined, such as imipramine, clomipramine, amitriptyline, desipramine, mianserin and zimelidine inhibited A-cyclase in a dose dependent manner. Antidepressants did not exert any influence on Mn2+-induced elevation of A-cyclase, but significantly suppressed F−-stimulated A-cyclase activity. GTP-induced elevation of A-cyclase was completely inhibited by prior incubation with antidepressants. Our conclusion, therefore, is that antidepressants may reduce A-cyclase activity not by inhibiting the function of the catalytic unit of A-cyclase, but by supressing the N-protein function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01245710
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    Paper (German National Licenses)
    Fulltext
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