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J B Pedersen

Publications and source records attributed to J B Pedersen.

22 records · Page 2Linked to original sources
PubMed1985

A general method of deriving the best binding site model consistent with experimental binding data.

An analysis of binding data is presented which yields the best binding site model consistent with the experimental data. The analysis is applicable to homotropic binding and yields the number of independent sites, number of interacting sites (dimers and tetramers of sites), intrinsic association constants, and degree of interaction. The information is derived from the roots of a binding polynomial constructed by the fitted Adair constants.

Binding Sites↗
PubMed1984

Deep vein thrombosis detection by 99mTc-plasmin test and phlebography.

During a 2-year period the diagnostic value of 99mTc-labelled-plasmin test was evaluated in 63 patients admitted with clinical signs of deep vein thrombosis (DVT). In comparison with a conventional phlebography the diagnostic sensitivity and specificity of the plasmin test was 0.97 and 0.55, respectively. The predictive value in positive cases was 0.79 and in negative 0.92. The sensitivity was highest for thrombosis in the calf and popliteal regions, while the specificity was higher for thrombosis in the femoral veins. It is concluded that the 99mTc-labelled-plasmin test is suitable for DVT-screening in groups of high-risk patients and is simple and rapid. In positive cases the DVT diagnosis must be verified by phlebography.

Adolescent↗
PubMed1981

Urinary excretion of succinylacetone and delta-aminolevulinic acid in patients with hereditary tyrosinemia.

Succinylacetone was excreted in the urine from four patients, with hereditary tyrosinemia i.e., two patients with the severe infantile type with fatal outcome and two patients with less severe juvenile form. In the urine from two patients with neonatal transient tyrosinemia and from normal individuals succinylacetone was not detectable. The urinary excretion of delta-aminolevulinic acid was also increased in all patients with hereditary tyrosinemia compared to patients with neonatal transient tyrosinemia and to normal individuals. The results presented support the hypothesis of a deficiency of fumarylacetoacetase in hereditary tyrosinemia. Furthermore an analytical method for the quantitative determination of succinylacetone in urine using GC-MS is described.

Acetoacetates↗