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Biomedical subjects

J Aznar

Publications and source records attributed to J Aznar.

At least 253 records · Page 14Linked to original sources
PubMed1978

Isolation of fibrin(ogen) degradation products from normal plasma by affinity chromatographic study.

An attempt was made to develop a method to isolate directly the fibrinogenfibrin (FDP and/or fdp) degradation products from plasma by means of small chromatographic columns of activated Sepharose 4-B coupled with antifibrinogen serum. The study of the material adsorbed was performed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulphate (PAGE-SDS). Four electrophoretic bands with antigenic capacity against antifibrinogen serum were observed. The study of their molecular weights, of their polypeptide composition after reduction, and of their immunological response against antisera anti-D and anti-E allowed their identification as fibrinogen, D-dimer fragment, and fragment E, respectively. The possibility of using this technique for the differential diagnosis between a primary fibrinogenolysis and a secondary fibrinolysis in a thrombotic process is suggested, as well as its use in the control of thrombolytic therapy.

Chromatography, Affinity↗
PubMed1978

Hageman trait.

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Adult↗
PubMed1978

Fletcher factor deficiency: report of a new family.

3 cases of Fletcher factor deficiency in a family not related to the 6 families already published (Hathaway et al 1965, Hattersley & Hayse 1970, Abildgaard & Harrison 1974) are studied. In the family described here, 3 of 4 siblings have a Fletcher factor level of less than 1% and the fourth has a level of 46%; the Fletcher factor level in the father is 48% and in the mother 38%. This suggests an autosomal recessive transmission. Clinically they do not present spontaneous bleedings and only one of the siblings required a unit of blood after an amygdalectomy. It is also of interest to emphasize that 3 of the siblings suffered from congenital multiple arthrogryposis and that 2 of them presented the arthrogryposis together with the Fletcher factor deficiency, a circumstance which could have been favored by the consanguinity of the parents. The fact that the family described here is white and of Mediterranean origin contradicts the idea that there exists a special predisposition among members of the black race for this disease.

Adolescent↗
PubMed1978

Degradation of human fibrinogen by plasmin: isolation and partial characterization of an early degradation product.

The incubation of human fibrinogen with plasmin gives rise to an early degradation product with a molecular weight of 63,000, calculated by polyacrylamide-gel electrophoresis sodium dodecyl sulfate (PAGE-SDS); this product is resistant to the action of the plasmin for short incubation times and represents 1 +/- 0.2% of the original quantity of fibrinogen. The fragment was isolated from the incubated mixture by gel filtration and has a no-identity reaction with fibrinogen fragment D against fibrinogen fragments D antiserum. The reduction gives rise to three polypeptidic chains with molecular weights of 36,000, 17,000 and 10,000 (calculated by PAGE-SDS). Study of the carbohydrate content of these polypeptidic chains from the reduced 63,000 MW fragment indicates that there is only one electrophoretic region which contains periodic acid-Schiff (PAS) positive material. As the 63,000 MW fragment has a reaction against fibrinogen fragment D antiserum and also contains PAS positive material, according to Pepper and co-workers, it can be taken to arise from the HOOC-terminal region of fibrinogen.

Chromatography, Gel↗
PubMed1977

Study of the lipods in the skin lesions in Urbach-Wiethe disease.

A patient with Urbach-Wiethe disease was studied, with special attention given to the analysis of the skin and mucosal lesions. An eosinophilia in the peripheral blood and a diabetic tendency were found. The skin papules and mucosal plaques contain abundant lipids, especially cholesterol (66 percent) and phospholipids (27 percent).

Child, Preschool↗
PubMed1976

Effect of aspirin on platelet phospholipids.

It was observed that the acetylsalicylic acid "in vitro" (final concentration 10(-4) M) as well as "in vivo" (1 g of aspirin) caused a platelet phospholipids variation which basically consisted of: 1. A diminution of the phospholipids/proteins rate of 22%. 2. A reduction of sphingomyelin "in vivo" of 27.66% and "in vitro" of 16.82%. 3. An increase in phosphatidyl choline "in vivo" of 12.24% and "in vitro" 10.28%. The possible effects that these changes might have on the platelet function are evaluated.

Adult↗