Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0267964 (PAA)
 2,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ascitic fluid from patients with ovarian cancer contains high levels of fibrin(ogen) degradation products (FDP). Crosslinked fibrin derivatives were isolated by precipitation and separated by PAA-gel-electrophoresis. In order to evaluate the submolecular structure the total precipitate and single derivatives were investigated after cleavage of the disulfide bonds. The findings are related to the radioimmunological measurements of certain fibrinopeptides. Tumor ascites contains approximately ten times higher levels of crosslinked fibrin derivatives than cirrhosis ascites. The fibrinopeptide A content is similar, whereas the levels of plasmin-induced alpha-chain fragment are significantly higher in tumor ascites. The findings suggest a catabolism of fibrinogen in ascitic fluid via coagulation and fibrinolysis. In tumor ascites fibrinogen is catabolized to a significantly higher degree via the degradation of crosslinked fibrin. Crosslinked fibrin derivatives may therefore be usable as non-carcinoembryogenic tumor markers.
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PMID:[Markerfunction of crosslinked fibrin derivatives in ascitic fluid from patients with ovarian cancer: a comparison with ascitic fluid in liver cirrhosis]. 655 32

After reduction and splitting of disulfide linkages the fibrinmonomer and fibrin of 45 patients with histologically confirmed liver cirrhosis and 38 patients with chronic renal failure (serum creatinine greater than 5 mg%) were analysed by SDS-PAA electrophoresis. Furthermore the activity of factor XIII was measured immunologically. The results indicated no polymerization of alpha-chains of fibrin while gamma-dimers were formed regularly in 71% of patients with liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis the lack of alpha-polymerization correlated to the severity of the disease and to the decrease of factor XIII activity (no alpha-polymers formed when below 80% of normal). In renal failure this correlation was not demonstrable since in all cases the activity of factor XIII was within the normal range. After the addition of C14-labelled urea to normal plasma during clotting an incorporation of this tracer could be demonstrated by scintiscanner diamins like urea, forming in the course of renal failure, probably serve as the "wrong substrate" for the transaminidase factor XIII.
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PMID:Structure of fibrin and fibrinmonomer in renal and hepatic failure. 739 32