In a case/control study, serum concentrations of vitamins A and E and major carotenoids were determined in patients with Alzheimer's disease, multi-infarct dementia and control subjects. The results showed that both Alzheimer's and multi-infarct dementia patients had significantly lower levels of vitamin E and beta-carotene than controls (vitamin E: 18.65 +/- 3.62 mumol/l in Alzheimer's disease and 15.80 +/- 6.93 mumol/l in multi-infarct dementia versus 30.03 +/- 12.03 mumol/l in controls; beta-carotene less than 0.13 to 0.42 mumol/l in Alzheimer's disease and less than 0.13 to 0.30 mumol/l in multi-infarct dementia versus 0.13 to 1.53 mumol/l in controls). Vitamin A was significantly reduced only in the Alzheimer's patients (1.56 +/- 0.78 mumol/l in Alzheimer's disease versus 2.13 +/- 0.86 mumol/l in controls).
The Schwartz formula (eGFR = kL/Scr, with k = 0.55) to determine the estimated glomerular filtration rate (eGFR) in children with chronic kidney disease (CKD), based on length (L) and serum creatinine (Scr) has recently been updated for enzymatic serum creatinine concentrations, resulting in k = 0.413. Based on a meta-analysis, we evaluated the validity of this updated equation and other published equations for healthy children. This is the first time that publicly available data for healthy children of uncorrected and body surface area (BSA)-corrected median GFR have been combined with median serum creatinine values and median lengths and weights from different sources in the literature to evaluate several statistical models to estimate GFR in children. For enzymatic serum creatinine, we show that the simple model for uncorrected GFR (uGFR = k'L(3)/Scr, with k' = 1.32 x 10(-5)) and the BSA-corrected GFR (cGFR = kL/Scr, analogous to the Schwartz formula), with an important age-dependent adaptation for k (k = 0.0414 x 1n (Age) + 0.3018), correlate extremely well with chromium-51-ethylenediamine tetra-acetic acid ((51)Cr-EDTA) data for children between 1 month and 14 years of age. With this age-dependent modification for k, presented here, the simple bedside calculation tool derived by Schwartz can be used for screening all children for CKD. When height information is not available, the Lund-Malmö equation is an excellent alternative.
The biliary excretion of the four isomers of bilirubin-IX was studied in Wistar rats (JJ) and homozygous Gunn rats (jj). Synthetic preparations of 14C-labelled pigments were used. 1. After intravenous administration, the alpha-isomer was rapidly excreted in conjugated form in bile of Wistar rats. In Gunn rats excretion was insignificant. In contrast, both rat species promptly excreted the non-alpha-isomers at rates that were comparable with that found for bilirubin-IXalpha in Wistar rats. 2. In normal rats about 16% of the beta- and delta-isomers and at least 50% of the gamma-isomer were excreted as ester conjugates of the injected parent bile pigments. Conjugation of the beta- and delta-isomers had occurred exclusively at the carboxyl groups of pyrrole ring D and C respectively. For bilirubin-IXgamma no preference for any carboxyl group could be established. 3. In homozygous Gunn rats the non-alpha-isomers were apparently excreted chemically unaltered. This suggests that, as for bilirubin-IXalpha, conjugation of the non-alpha-isomers is also deficient in Gunn rats.
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