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Biomedical subjects

D L Heene

Publications and source records attributed to D L Heene.

At least 127 records · Page 7Linked to original sources
PubMed1979

Separation of fibrinogen degradation products (FDP) by means of adsorption to insolubilized fibrinmonomer (FM-ag).

The phenomenon of complex formation between fibrinmonomer and fibrinogen degradation products was investigated by means of adsorption of FDP to insolubilized thrombin-modified fibrinogen (FM-ag). Since it could be demonstrated that there are different adsorption characteristics for early FDP and late FDP, the possibility of separation of FDP by means of affinity chromatography on FM-ag columns was evaluated using plasmic digests of 3H-Ac-labelled fibrinogen. The identification of FDP was performed by disc-electrophoresis. The results indicate that the adsorption of early FDP is comparable to the behaviour of fibrinogen, whereas late FDP show essential difference in the affinity towards FM-ag, evident by the result that fragment E adsorbs only to a minimal extents. Fragments D and E derived from fibrinogen as well as from non-crosslinked fibrin, revealed identical adsorption characteristics. Under specified conditions the procedure is suitable as a preparative method for the separation of fragments D and E.

Adsorption↗
PubMed1977

Detection of thrombin-induced fibrinogen derivatives in thrombotic states.

Affinity chromatographic studies using insolubilized fibrinogen (fibrinogen-agarose) revealed that fibrin monomer present in plasma is selectively adsorbed to fibrinogen-agarose and may be quantitatively estimated following desorption. Analysis of plasma samples from patients with myocardial infarction, cirrhosis of the liver malignant diseases and DIC confirmed the presence of considerable amounts of fibrin monomer revealing concentrations between 3 and 15 mg/100 m1 plasma as compared to normal plasma (1.96 +/- 0.37 mg/100 m1, = 27). The method is suitable for the assessment of hypercoagulable states. Standard conditions for the procedure were evaluated using 3H-labelled fibrinogen and fibrin monomer.

Blood Coagulation↗
PubMed1976

Studies on chemically modified fibrinogen.

Treatment of fibrinogen with maleic acid anhydride renders fibrinogen unclottable depending on the degree of modification of the molecule. According to radioactive studies the release of fibrinopeptides by thrombin or reptilase is undisturbed. The incoagulability is due to inhibition of the polymerization process of fibrinmonomers derived from modified fibronogen, mainly caused by the increase of electronegative charges upon the fibrogen molecule. According to discelectrophoretic analysis modified fibrinogen fails to produce fragments D and E following plasmic digestion, however, may be degraded to high molecular weight products. Modified fibrinogen reveals some similarities to abnormal fibrinogens in congenital dysfibrinogenemia with regard to its functional properties.

Anhydrides↗
PubMed1975

[Hypodysfibrinogenemia: fibrinogen giessen II (author's transl)].

A new case of facultative hemorrhagic diathesis is described in a 19 year old female and the coagulatory anomaly examined. The experiments show that the coagulatory disturbance should be ascribed to a defective aggregation of fibrin monomers associated with hypofibrinogenemia. Some of its characteristics are the markedly prolonged thrombin-, reptilase-time as well prolonged prothrombin and partial thromboplastin time. The plasma fibrinogen concentration measured by the immunologic method is reduced. The streptokinase induced digestion of fibrinogen Giessen II plasma occurred at a slower rate than normal plasma with persistence of the large fibrinogen degradation products. Fibrinogen Giessen II appears to be a congenital hypodysfibrinogenemia with abnormality of fibrinogen resulting in delayed coagulation and a retarded fibrinogenolysis rate.

Adult↗
PubMed1975

[Coagulation tests in von Willebrand's disease(author's transl)].

The diagnosis of von Willebrand's disease can be made by a selected series of easily performed clotting tests. A STudy of 36 patients with the disease (all but one with a mild form) revealed a significantly increased reaction time in the thrombelastogram from 210 plus or minus 33 percent to 270 plus or minus 69 percent (P less than 0.001), and of the partial thromboplastin time from 43 plus or minus 3s to 54 plus or minus 9s (P less than 0.001 than 0.001). Factor VIII activity was corresponding significantly reduced from normal (127 plus or minus 51 percent) to 51 plus or minus 12 percent (P less than 0.001). Other plasma factors and platelet counts were within normal limits. A platelet defect was indicated by an abnormal change in the speed of clot formation (k-time) from 162 plus or minus 39 percent to 341 plus or minus 121 percent (P less than 0.001), maximal thrombelasticity from 121 plus or minus 16 percent to 75 plus or minus 22 percent (P less than 0.001), and marked reduction in platelet-factor 3 liberation from 122 plus or minus 59 percent to 23 plus or minus 16 percent (P less than 0.001). An increase in bleeding time, from 162 plus or minus 41s to 204 plus or minus 128s (P less than 0.05), was not always present. Recently introduced immunological methods for determining factor VIII and factor VIII-associated protein, as well as special platelet-function tests, give further information on the pathogenesis of the bleeding disease, but their complexity restricts them to special laboratories.

Blood Coagulation Factors↗