PubMed Health⌕ Search

Biomedical subjects

M M Jeleńska

Publications and source records attributed to M M Jeleńska.

12 recordsLinked to original sources

Coagulation parameters as predictors of DIC in patients with intact aortic aneurysm.

Clinically overt, preoperative, disseminated intravascular coagulation (DIC) is not common in patient with aortic aneurysm. However, cases with large and expanding aneurysm are especially prone for this coagulopathy. Contrary to the clinically overt form compensated DIC in patients with aortic aneurysm seems frequent and is probably underdiagnosed. The compensated DIC may be recognized, even without bleedings, by laboratory tests documenting the activated coagulation and fibrinolysis. We show that in about one third of patients with abdominal aorta aneurysm (AAA) compensated DIC can be identified. This enables the application of preoperative anticoagulation treatment to improve the intraoperative haemostasis.

Aortic Aneurysm↗

[Von Willebrand factor].

During the last decade a considerable amount of research has been dedicated to von Willebrand factor. In the first part of this article recent data on primary structure of von Willebrand factor and biosynthesis of von Willebrand factor multimers are presented. The second part focuses on the role of von Willebrand factor in hemostasis.

Amino Acid Sequence↗

Platelet-mediated collagen and fibrin retraction: effect of prostaglandins, cyclic AMP, calcium antagonists and N-ethylmaleimide.

Collagen gel retraction (CGR) and thrombin-induced fibrin clot retraction (FCR) could be abolished by EGTA and EDTA, trifluoperazine - a calmodulin inhibitor - and by NEM. Both processes appeared insensitive to hydrocortisone (up to 100 microM), indomethacin (up to 60 microM), PGI2 and its stable analogue 6-keto-PGE1 alpha (10 microM). A slight inhibitory effect on both CGR and FCR was provoked by dibutyryl-cAMP and PGD2. PGE1 1 microM strongly inhibited CGR and FCR. Possible interference of the inhibitors with anchorage of collagen and fibrin on platelet surface and with platelet contractile system is discussed.

Blood Platelets↗

The comparative ability of plasma and tissue transglutaminases to use collagen as a substrate.

Heat denatured type I and type III calf skin collagen were found to be substrates for guinea pig liver transglutaminase (R-glutaminyl-peptide:amine gamma-glutamyl-yltransferase, EC 2.3.2.13) but not for active plasma factor XIII (factor XIIIa). Liver transglutaminase was shown to catalyse incorporation of 14C-putrescine into subunits of denatured collagen of both types, cross-linking of the latter into high molecular weight polymers and their co-cross-linking to fibrin and fibrinogen. Factor XIIIa is inactive in these respects. None of these reactions was catalysed by liver transglutaminase and plasma factor XIIIa when nondenatured collagens both soluble or in the forms of reconstituted fibrils served as substrates. Some cross-linking of cleavage products of collagen type I (obtained by treatment with collagenase from human neutrophiles) was induced by liver transglutaminase and factor XIIIa. The results indicate that although appropriate glutamine and lysine residues for a epsilon-(gamma-glutamine) lysine cross-linked formation are present in collagen, the native conformation of collagen prevents the action of liver transglutaminase and factor XIIIa.

Animals↗

Radiation-induced aldehydes in collagen.

Aldehydes present in native and irradiated (30 krad) collagen were separated from its enzymic degradation products using molecular-sieve chromatography on Bio-Gel P-2 column. From the absorption spectra of N-methylbenzothiazolone hydrazone derivatives it was concluded that two out of five of the aldehydes separated from the irradiated collagen, were identical with those present in control collagen. The possible origin of three other aldehydes is discussed.

Aldehydes↗