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M Burk

Publications and source records attributed to M Burk.

25 records · Page 2Linked to original sources
PubMed1991

Crystal growth of calcium oxalate in urine of stone-formers and normal controls.

In this study, the relative crystal growth rate (Vcr) of calcium oxalate (Caox) and a number of other parameters were determined in 17-h daily (d) and 7-h nocturnal fractions (n) of whole urine from 20 recurrent Caox stone formers (SF) and 29 age-matched male normal controls (NC). Vcr, which was determined by the gel crystallization method (GCM), showed the largest difference between SF and NC among all parameters under investigation. Mean values (+/- SD) obtained for Vcr were: 0.73 +/- 0.58 (SF-d)/0.21 +/- 0.22 (NC-d; P less than 0.001) and 0.63+/- 0.58 (SF-n)/0.24 +/- 0.25 (NC-n; P less than 0.01). Significantly higher concentrations of Ca and lower concentrations of thermodynamic and kinetic effectors of Caox crystal growth were responsible for the higher crystal growth rates observed in SF as compared with NC, i.e., they should be partially causative in Caox urolithiasis. However, other properties of urine or the urinary tract (potentially, crystal agglomeration and adhesion) must be accounted for in the genesis of Caox stones.

Adult↗
PubMed1985

Synthesis and processing of human serum apolipoprotein AII in vitro and in Hep G2 cells.

The synthesis and structure of the primary translation product of apo AII in a human liver poly(A+) mRNA primed cell-free system and its cotranslational modification was studied parallel to studies in vivo with Hep G2 cells, a human hepatoma cell line. The primary translation product is a preproprotein containing 100 amino acid residues, which is cleaved by the signal peptidase of endoplasmic reticulum to pro-apo AII with the loss of the N-terminal pre-sequence consisting of 18 amino acid residues. Hep G2 cells contain about equal amounts of the proform of apolipoprotein AII and of mature apo AII. Approximately in the same ratio pro- and mature apo AII are secreted into the medium. Determination of the partial amino-acid sequence by automated Edman degradation of the labelled prepro- and proforms of apo AII led to the segmentation of the N-terminus of the primary translation product, consisting of 23 amino acid residues, into the pre-sequence (18 residues) and the pro-sequence (5 residues) with terminal Arg-Arg-residues at the cleavage site to apo AII. We must therefore correct our previously postulated 17 and 6 residues containing segmentation. So far no information has been obtained in which compartment and at what stage of posttranslational events the dimerization occurs by formation of the single disulfide bond at position Cys6 in the mature apo AII structure, leading to the symmetrical molecule.

Amino Acid Sequence↗
PubMed1983

On the interaction between digoxin and disopyramide.

Combined oral therapy with digoxin (0.375 mg/dl) and disopyramide (300 and 600 mg/dl) in nine subjects did not alter steady-state digoxin serum concentrations just before the daily single digoxin dose. Digoxin and creatinine clearances were not changed. After a bolus IV dose of 0.8 mg digoxin, volume of distribution (from 672 +/- 176 l to 407 +/- 153 l) and elimination t1/2 beta of digoxin were reduced significantly in five subjects after 600 mg oral disopyramide daily (from 40.2 +/- 11.7 hr to 22 +/- 7.3 hr). Total clearance and digoxin distribution t1/2 alpha did not change significantly. The clinical significance of this interaction is not clear.

Adult↗
PubMed1983

Disopyramide kinetics in renal impairment: determinants of interindividual variability.

Disopyramide kinetics were studied in 30 patients with normal to severely impaired renal function (endogenous creatinine clearance 7.6 to 116.9 ml/min/1.73 m2) after intravenous bolus injection. Serum concentration-time curves were fitted to an open two-compartment model. There was close correlation between renal disopyramide clearance and creatinine clearance (r = 0.922). Disopyramide body clearance or elimination rate constant (kel beta) and creatinine clearance did not correlate as closely (r = 0.756 and 0.644). Volume of distribution at steady state and extrarenal clearance of disopyramide both correlated slightly positively with renal function. Disopyramide body clearance and volume of distribution, but not kel beta, were found to be dose dependent. Disopyramide kinetics in renal impairment were not sufficiently predictable from clinical data of the patient because of great interindividual variation in drug disposition and renal and extrarenal elimination. Dosage regimen must therefore be based on individual response and controlled by the clinical effect and estimates of disopyramide serum concentration.

Adult↗