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Biomedical subjects

G Sas

Publications and source records attributed to G Sas.

At least 55 records · Page 3Linked to original sources
PubMed1982

Distinction of two pathologic antithrombin III molecules: antithrombin III "Aalborg' and antithrombin III "Budapest'.

Plasma from two different thrombophilic families with functional inherited antithrombin III deficiency, i.e., with low antithrombin III activity but normal immunoreactive antithrombin III concentration, were investigated simultaneously in the same laboratory. The experiments (thrombin and Factor Xa inactivation, heparin affinity chromatography, modified two dimensional immunoelectrophoresis and gel filtration) showed a distinct difference between the two antithrombin III anomalies. The antithrombin III "Aalborg' had decreased thrombininactivating activity but normal Factor Xa-inactivating activity. The heparin affinity and the molecule weight are normal. The antithrombin III "Budapest' displays a more profound abnormality with pathologic thrombin and Factor Xa inactivation, decreased heparin affinity and abnormal molecular weight.

Antithrombin III↗
PubMed1980

[Cholesterol deficiency. A pathogenetic factor in chronic anemias? Preliminary report of a study in three states (author's transl)].

It has been shown in several studies that there is a statistically confirmed connection between cholesterol and Hb levels in the sense that hypocholesterolemia and anemia occur together particular frequently. This was demonstrated in an epidemiological cross-section study of 3958 patient data, and also that in a retrospective case control study of 159 anemias there was a concurrent hypocholesterolemia. It is postulated that a causal connection exists which is explained by the fact that cholesterol deficiency leads to rigidity of the erythrocytes.

Adult↗
PubMed1980

Heterogeneity of the "classical" antithrombin III deficiency.

We investigated two thrombophilic families with the "classical" type of antithrombin III deficiency, i.e., with a low antithrombin III level measured both by immunochemical and functional methods. We obtained different antithrombin III patterns in the plasma of the affected members of the two families with the modified two dimensional immunoelectrophoresis method (heparin in agarose). In one family, the electrophoretic mobility of the antithrombin III is identical with that of normal antithrombin III. In the other, the antithrombin III displayed a decreased electrophoretic mobility in the heparinized agarose gel. The relatively low affinity of this antithrombin III to heparin could be directly proved by the heparin-agarose affinity chromatography, too. These two different antithrombin III patterns were observed by other investigators at different families as well. On the basis of our simultaneous observations of these two families we propose a classification of the inherited congenital antithrombin III deficiencies.

Adolescent↗
PubMed1979

Specificity in the factor VIII response to vasopressin infusion in man.

Structural requirements of the systemic factor VIII response to intravenous vasopressin in man has been investigated using vasopressin analogues. With the analogues available the receptor specificity of this phenomenon could not be distinguished from those associated with the previously described plasminogen activator release or antidiuretic effects of this hormone. Further studies using 1-desamino-[8-D-arginine]vasopressin showed a dose-related release of both procoagulant and antigenic components of the factor VIII complex. The newly released factor VIII could not be distinguished from circulating factor VIII on the basis of molecular size, electrophoretic mobility or in vitro stability despite apparent differences in the duration of response of the procoagulant and antigenic components in vivo.

Adult↗
PubMed1978

[Cholesterol deficiency. A pathogenetic factor in chronic anemias? Preliminary report of a study in three states (author's transl)].

It has been shown in several studies that there is a statistically confirmed connection between cholesterol and Hb levels in the sense that hypocholesterolemia and anemia occur together particularly frequently. This was demonstrated in an epidemiological cross-section study of 3958 patient data, and also that in a retrospective case control study of 159 anemias there wasa concurrent hypocholesterolemia. It is explained by the fact that cholesterol deficiency leads to rigidity of the erythrocytes.

Aged↗