Biomedical subjects

D Smirnow

Publications and source records attributed to D Smirnow.

4 recordsLinked to original sources

PubMed2001

Prothrombin Scranton: substitution of an amino acid residue involved in the binding of Na+ (LYS-556 to THR) leads to dysprothrombinemia.

Several members of a family from Scranton, Pennsylvania were identified to have normal levels of prothrombin antigen while their prothrombin clotting activity was approximately 50% of normal. There has been no previous history of bleeding or other clinical manifestations in this family. The genomic DNA from the proband was amplified for all exons in the prothrombin gene and analyzed by single strand conformation polymorphism (SSCP)/heteroduplex analysis followed by DNA sequence analysis and restriction enzyme digestion. A mutation at nucleotide 20040 in exon 14 was identified and confirmed by restriction enzyme digestion. This mutation results in the substitution of Thr for Lys at amino acid 556. Amino acid 556 has been reported as one of the key residues for the binding of Na+ in the thrombin portion of the protein.

Adolescent↗

PubMed1996

Analysis of ecgonine and other cocaine biotransformation products in postmortem whole blood by protein precipitation-extractive alkylation and GC-MS.

Ecgonine is formed by the hydrolysis of both ester linkages in cocaine and is of interest as both a potential metabolite and a postmortem and postcollection artifact in biological specimens. Its extreme polarity and water solubility make its isolation very difficult, particularly from complex matrices such as postmortem whole blood. This procedure describes an initial protein precipitation followed by two derivatization steps, the first of which is to propylate organic acids and primary and secondary amines and the second of which is to form the p-nitrobenzoyl ester of organic alcohols. The resultant derivatized products are then subjected to cleanup using a standard extraction with n-butyl chloride as the solvent. Analysis of the extracts is performed by gas chromatography-mass spectrometry using deuterated internal standards, although the adducts would also be suitable for analysis by high-performance liquid chromatography. Significant quantities of ecgonine have been identified in postmortem whole blood samples using this method.

Alkylation↗

PubMed1996

Postmortem distribution and redistribution of morphine in man.

This study evaluated both site dependent differences and time dependent changes in postmortem morphine concentrations in man. In 32 deaths involving morphine, left ventricular blood, femoral blood, and cisternal cerebrospinal fluid, were collected as soon after death as possible (T1), and collected again together with iliac blood at the time of autopsy (T2). Samples were analyzed for morphine by radioimmunoassay. No evidence was found for changes in morphine concentration with respect to time at either central or peripheral sites, or in the cerebrospinal fluid. Ventricular blood morphine concentrations were however consistently higher than those in the peripheral compartment, represented by either femoral or iliac blood. This was particularly true when the ventricular morphine concentration exceeded 0.300 mg/L. At peripheral sites, femoral and iliac blood morphine concentrations were well correlated with each other, making either an appropriate site for collection of peripheral blood for toxicological testing.

Adult↗

PubMedDate not supplied

Lack of predictable site-dependent differences and time-dependent changes in postmortem concentrations of cocaine, benzoylecgonine, and cocaethylene in humans.

This study evaluated the stability of cocaine, benzoylecgonine, and cocaethylene in postmortem fluids in cases of cocaine-related death. Femoral and ventricular blood and cisternal cerebrospinal fluid were collected soon after death and again at the time of autopsy. In addition, iliac blood was collected at autopsy. There were no consistent patterns of site-specific differences for any of the analytes, and the central compartment showed both higher and lower concentrations than the peripheral. There was no consistent pattern of direction or magnitude of change in the concentrations with respect to time for any of the analytes. This is consistent with anecdotal reports from other workers and is believed to be a result of competing processes of tissue release and chemical and enzymatic degradation of the analytes. Postmortem cocaine and metabolite concentrations in blood are not necessarily reflective of the perimortem concentrations and should not be the primary consideration in determining the cause of death in suspected cocaine-related deaths.

Adult↗