sodium-dodecyl-sulfate has been researched along with Blood-Coagulation-Disorders* in 4 studies
4 other study(ies) available for sodium-dodecyl-sulfate and Blood-Coagulation-Disorders
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Characterization of local hyperfibrinolysis in chronic subdural hematomas by SDS-PAGE and immunoblot.
Fibrinogen, fibrin monomer, and D dimer were analyzed in 41 cases of chronic subdural hematoma (SDH) to characterize local rebleeding, coagulation, and fibrinolysis using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Chronic SDH's were divided into five groups according to their appearance on computerized tomography: high-density, isodensity, low-density, mixed-density, and layering types. The concentration of fibrinogen, which indicates rebleeding, was higher in the mixed-density (15.7 +/- 3.4 mg/dl (mean +/- standard error of the mean)) and layering (15.7 +/- 2.6 mg/dl) types of hematoma, and lower in the low-density hematomas (1.4 +/- 0.6 mg/dl) compared with the isodense hematomas (6.9 +/- 1.1 mg/dl). Fibrin monomer, which indicates coagulative activity, had a distribution similar to that of fibrinogen: 87 +/- 22, 18 +/- 8, 175 +/- 40, and 177 +/- 23 micrograms/ml in isodense, low and mixed-density, and layering types of hematomas, respectively. The D dimer, which indicates fibrinolytic activity, was higher in the layering hematoma type (2032 +/- 384 micrograms/ml), and lower in low-density hematomas (301 +/- 164 micrograms/ml) compared to isodense (1310 +/- 256 micrograms/ml) and mixed-density (1039 +/- 207 micrograms/ml) types of hematomas. These observations suggest the following characterization of each type of chronic SDH. The layering type is active, with a high tendency to rebleed and for hyperfibrinolytic activity. The mixed-density type has a high tendency to rebleed with lower hyperfibrinolytic activity than the layering type. The low-density hematoma is stable with a low tendency to rebleed and to fibrinolytic activity. Topics: Adult; Aged; Aged, 80 and over; Blood Coagulation Disorders; Chronic Disease; Electrophoresis, Polyacrylamide Gel; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Hematoma, Subdural; Humans; Immunoblotting; Male; Middle Aged; Recurrence; Sodium Dodecyl Sulfate | 1994 |
Platelet glycoproteins of Bernard-Soulier syndrome: analysis by isoelectric focusing and sodium dodecyl sulfate polyacrylamide gel electrophoresis in a two-dimensional technique.
Topics: Blood Coagulation Disorders; Blood Platelets; Blood Protein Electrophoresis; Electrophoresis, Polyacrylamide Gel; Glycoproteins; Humans; Isoelectric Focusing; Periodic Acid-Schiff Reaction; Platelet Adhesiveness; Sodium Dodecyl Sulfate | 1982 |
[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)].
The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices. Topics: Blood Coagulation Disorders; Blood Platelets; Cell Count; Electrophoresis, Polyacrylamide Gel; Factor XIII; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Hemostasis; Humans; Liver Cirrhosis; Sodium Dodecyl Sulfate | 1978 |
Defect in the gamma polypeptide chain of a congenital abnormal fibrinogen (Paris I).
Topics: Blood Coagulation Disorders; Electrophoresis, Polyacrylamide Gel; Factor XIII; Fibrin; Fibrinogen; Humans; Molecular Weight; Peptides; Sodium Dodecyl Sulfate | 1974 |