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Biomedical subjects

E I Minder

Publications and source records attributed to E I Minder.

30 records · Page 2Linked to original sources
PubMed1992

Identification and quantification of ergotamine in human plasma by gas chromatography-mass spectrometry.

A highly sensitive and simple gas chromatographic-mass spectrometric method is described for the identification and quantification of ergotamine in plasma or serum. Ergotamine is extracted with chloroform from the alkalinized sample and detected by electron ionization mass spectrometry. This analytical method was selected for an intense high-mass ion ideal for the specific quantification. It shows good linearity in the range from 50 pg/ml to 50 ng/ml for ergotamine in plasma. The practicability of this method is demonstrated by determining the plasma concentration of ergotamine in a sample from a patient.

Chloroform↗
PubMed1992

Cytofluorometry as a diagnosis of protoporphyria.

Protoporphyria is a disorder that usually has cutaneous symptoms. Only in a few cases liver disease develops, invariably progressing to cirrhosis and liver failure. A case of a patient who suffered from photosensitivity as a result of protoporphyria since the age of 2 is described. At age 33, she first presented with cholestatic hepatitis. At age 40, liver failure developed requiring liver transplantation. Quantitative cytofluorometry proved to be a quick and simple method in the follow-up of her erythrocyte protoporphyrin levels before, during, and after transplantation. Fluorescence correlated well with the protoporphyrin levels obtained by high-performance liquid chromatography (r = 0.98), a comparably cumbersome and complicated method for the determination of protoporphyrin. In addition, single cell analysis enabled us to follow the effects of transfusion therapy on protoporphyrin levels of the patient's own erythrocytes, which has not been possible by previous methods. Thus, cytofluorometry might prove to be elegant and useful for screening and future studies on therapy and pathophysiology of protoporphyria.

Adult↗
PubMed1992

Prototype application of a robot in the clinical laboratory enabling fully automated quantification of fecal porphyrins.

Unpleasant specimens, sensitive analytes, and a lengthy chromatographic procedure were the main reasons we implemented fecal porphyrin analysis with a laboratory robot. We describe the system in detail and compare it with the same technique performed manually. The day-to-day variation of assays of standards was lower with the robot than with the manual operation: 8% (CV) for coproporphyrin I and 11% for protoporphyrin IX. We repeatedly analyzed a specimen from a healthy volunteer and determined that the specimen contained (in nmol/g dry wt) 7.1 (SD 0.7) for coproporphyrin I, 3.0 (SD 0.4) for coproporphyrin III, and 44.4 (SD 4.3) for protoporphyrin IX. Upper reference limits as measured in 20 healthy volunteers were 20 nmol/g dry wt for coproporphyrin I, 12 nmol/g for coproporphyrin III, and 80 nmol/g for protoporphyrin IX. We also present characteristic chromatograms for samples from various different porphyrias that exhibit abnormal fecal porphyrin excretion. Calculations of return on investment show that the robot, working at full capacity, is a profitable tool.

Autoanalysis↗
PubMed1989

Toxicity in a case of acute and massive overdose of chlordiazepoxide and its correlation to blood concentration.

In previous studies no correlation between blood concentration and toxicity was found in acute chlordiazepoxide overdose. We describe a case of acute overdosage with 5.2 g chlordiazepoxide, in which toxicity correlated to blood concentration of the second metabolite of chlordiazepoxide, to demoxepam. Therefore, it is recommended to determine not only chlordiazepoxide, but also its active metabolites in cases of overdose. This can easily been achieved using the described method, HPLC with photodiode array detection.

Anti-Anxiety Agents↗
PubMed1987

Identification of drugs in human serum by high-performance liquid chromatography with photodiode array detection and a search algorithm for ultraviolet spectra.

A system is described that identifies a number of unknown drugs (benzodiazepines, antidepressants and neuroleptics) in blood specimens for clinical-toxicological purposes. Reversed ion-pair high-performance liquid chromatography with a photodiode array detector saves the ultraviolet spectrum of every chromatographically significant peak. Post-run data-processing, provided by a microcomputer, retrieves candidate substances from a library of ultraviolet spectra. Selected standard ultraviolet spectra are compared with the unknown by five different similarity tests. The discriminatory efficiency of these algorithms has been determined. Multicomponent analysis, a built-in program of the spectrophotometer, provided the most reliable results.

Algorithms↗
PubMed1986

Measurement of 5-aminolaevulinic acid by reversed phase HPLC and fluorescence detection.

A new method for sensitive measurement of delta-aminolaevulinic acid (ALA) in biological material is described. ALA is derivatized with dansyl chloride, separated by HPLC and estimated using a fluorescence detector. The pretreatment of biological samples includes desamination of L-alpha-aminoacids with L-aminoacid-oxidase before dansylation. The sensitivity of the method is slightly below 1 pmol/injection for standards and the lower limit of quantification is 0.1 mumol/l for plasma and 10 nmol/l for cerebrospinal fluid. Reference values in plasma are 3.53 +/- 1.75 (SD) (n = 43) mumol/l and in packed erythrocytes they ranged from 6 to 26 mumol/l (mean: 14.0 +/- 5.5 mumol/l). In cerebrospinal fluid of non-porphyric individuals less than 2 nmol/l were recovered.

Aminolevulinic Acid↗
PubMed1984

Bufuralol metabolism in human liver: a sensitive probe for the debrisoquine-type polymorphism of drug oxidation.

The genetically controlled polymorphism causing decreased metabolism of debrisoquine is closely related to that of the metabolism of bufuralol and numerous other drugs and has important clinical consequences. A sensitive in vitro assay was developed which quantifies the production of 1'-hydroxy-bufuralol (carbinol) from bufuralol in human liver microsomes. Initial formation rates of carbinol suggested Michaelis-Menten kinetics with an apparent KM of 61 and 171 mumol l-1 and Vmax of 3.2 and 5.8 nmol mg-1 microsomal protein h-1 in two human liver samples. The Vmax in microsomes of thirty-two liver samples was 4.2 +/- 1.0 (SD) nmol carbinol mg-1 protein h-1. Metabolism of debrisoquine in vivo, as expressed by the 'metabolic ratio' of debrisoquine over 4-OH debrisoquine correlated (r = -0.65, P less than 0.01; n = 18) with carbinol production rate in microsomes in vitro. Microsomes of one individual identified as poor metabolizer of debrisoquine in vivo showed reduction of carbinol formation to 1.97 nmol mg-1 h-1. Mixing his microsomes with those of an extensive metabolizer resulted in additive formation of carbinol excluding mediation of the defect by a soluble inhibitor. These data support the concept of a primary defect in microsomal oxidation of bufuralol. The described assay offers a sensitive tool to investigate the molecular mechanism of the 'debrisoquine polymorphism'.

Adrenergic beta-Antagonists↗
PubMed1979

Radioimmunological determination of serum 3 beta-hydroxy-5-cholenoic acid in normal subjects and patients with liver disease.

A radioimmunoassay for the determination of 3 beta-hydroxy-5-cholenoic acid in human serum has been developed, using 3 beta-hydroxy-5-cholenoyl-thyroglobulin as immunogen and 3 beta-hydroxy-5-cholenoylglycyl-125I histamine as radioactive ligand. The association constant was 6.3 X 10(8) l/mol. Cross reactivity with other bile acids of human serum was not detectable, but was 5.6% with cholesterol. Serum sample preparation included extraction of 3 beta-hydroxy-5-cholenoic acid from serum, solvolysis of sulfates, hydrolysis of conjugates, and separation from cholesterol by thin-layer chromatography. Serum concentrations of 3 beta-hydroxy-5-cholenoic acid were 0.23 +/- SD 0.12 mumol/l and 0.21 +/- SD 0.09 mumol/l in healthy males and females, respectively. In patients with primary biliary cirrhosis the serum concentration of 3 beta-hydroxy-5-cholenoic acid and the quotient 3 beta-hydroxy-5-cholenoic acid over total 3 alpha-hydroxy-bile acids (measured enzymatically) were significantly higher (P less than 0.02) than in patients with chronic active hepatitis or alcoholic cirrhosis. Analysis of 17 sera with elevated concentration of 3 beta-hydroxy-5-cholenoic acid by radioimmunoassay and capillary gas-liquid chromatography showed a close correlation (r = 0.91, slope = 0.97) between the results of the two methods.

Adult↗
PubMedDate not supplied

Identification of a prevalent nonsense mutation (W283X) and two novel mutations in the porphobilinogen deaminase gene of Swiss patients with acute intermittent porphyria.

Acute intermittent porphyria (AIP) is an autosomal dominant disorder caused by decreased activity of porphobilinogen deaminase (PBGD), the third enzyme in the heme biosynthetic pathway. We report the first molecular analysis of PBGD gene mutations in AIP patients of Swiss origin. The PBGD gene of 18 Swiss AIP patients was analyzed by denaturing gradient gel electrophoresis screening of the genomic DNA and direct sequencing. Thirteen of the 18 patients (72%) carried a nonsense mutation G(849)-->A, W283X. In addition, 4 different mutations including 2 novel mutations (Q217L and Q292X), were identified in the 5 remaining AIP patients originating from both German- and Italian-speaking regions of Switzerland.

DNA Mutational Analysis↗