Problems in the Coagulation of Plasma by Staphylocoagulase

Tager, Morris

doi:10.1111/j.1749-6632.1956.tb36629.x

Cited by 17 publications

(8 citation statements)

References 19 publications

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“…It has been stated that the plasma clot produced by coagulase is identical with a normal clot (Gerheim and Ferguson, 1949b;Tager, 1956b). Present findings do not agree with this statement.…”

Section: Morphology Of the Clot Produced By Coagulasecontrasting

confidence: 83%

Studies on the Mechanism of Action of Staphylocoagulase

Rubinstein

1958

Br J Haematol

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Section: Morphology Of the Clot Produced By Coagulasecontrasting

confidence: 83%

Studies on the Mechanism of Action of Staphylocoagulase

Rubinstein

1958

Br J Haematol

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“…Plasmin is known to inactivate coagulase (16). Staphylococcal Muller factor and staphylokinase are believed to activate plasminogen to plasmin (7,17).…”

Section: -mentioning

confidence: 99%

“…Plasmin is a blood serum protease which interferes with the coagulase reaction (16). Plasmin is inactivated by soybean trypsin inhibitor (13).…”

mentioning

confidence: 99%

Activation of Coagulase Clotting by Trypsin Inhibitor

Orth¹,

Anderson²,

Montgomery³

1969

Applied Microbiology

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Egg white trypsin inhibitor activated coagulase clotting when added to a final concentration between 2 and 60 mg/ml. The greatest increase in clotting rate was observed in reaction mixtures containing the lowest concentrations of serum and plasma. Maximal activation was reached with 40 mg of trypsin inhibitor per ml when either serum or plasma was used as the source of coagulase-reacting factor (CRF). The increased rate of clotting is partly due to inhibition of plasmin. Freezing and thawing reduced plasma clotting inhibition. Soybean trypsin inhibitor also activated the coagulase reaction. The increased rate of clotting was observed with a coagulase preparation from organisms which produced plasminogen activators and with the culture supernatant fraction from organisms which did not activate plasminogen to plasmin. The tube test for coagulase could be made more sensitive for some strains of staphylococci by increasing the concentration of CRF (added as plasma or serum) by adding trypsin inhibitor, or both.

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“…Other principal contenders, such as fibrinogen, have been essentially eliminated from consideration. The arguments for and against relating CRF to prothrombin have been recently summarized (1). The present study has sought to resolve an apparent inconsistency: the view that prothrombin and CRF are identical, and the separation of prothrombin and CRF activity by repeated Seitz filtration.…”

Section: Discussionmentioning

confidence: 97%

“…Although considerable progress has been achieved in the study of the coagulation of plasma by staphylocoagulase, the precise identity of the coagulase-reacting factor (CRF) has remained in doubt. The claims linking CRF with various factors involved in the dotting of blood have been recently summarized elsewhere (1). Questions pertaining to the possible relation of CRF to prothrombin have remained particularly challenging.…”

Section: (From the Department Of Bacteriology And Immunology Divisiomentioning

confidence: 99%

Studies on the Nature and the Purification of the Coagulase-Reacting Factor and Its Relation to Prothrombin

Tager

1956

The Journal of Experimental Medicine

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The coagulase-reacting factor (CRF) of human plasma has been purified, concentrated, and largely freed of prothrombin activity by Seitz filtration, absorbtion on hyflo-amphogel columns, controlled phosphate buffer elution, and fractional ammonium sulfate precipitation. The purified CRF preparations localized between the beta and the gamma globulin position on paper electrophoresis, and the principal of two components observed on analytical ultracentrifugation gave sedimentation rates between 2.75 and 3.07. Highly purified prothrombin preparations of Seegers effectively react with staphylocoagulase to lead to the coagulation of plasma. The electrophoretic and ultracentrifugal properties of the human prothrombin preparations examined differ significantly from those of the purified CRF. Derivatives of prothrombin, involving a loss of prothrombin activity, such as thrombin and "autoprothrombin," do not correspondingly lose in CRF function. The hypothesis is proposed that CRF activity is resident in some component or components of the prothrombin molecule not involved in prothrombin function per se, and that therefore prothrombin and CRF activity may either parallel each other when the molecule is intact or diverge when the smaller units only are involved.

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Problems in the Coagulation of Plasma by Staphylocoagulase

Cited by 17 publications

References 19 publications

Studies on the Mechanism of Action of Staphylocoagulase

Studies on the Mechanism of Action of Staphylocoagulase

Activation of Coagulase Clotting by Trypsin Inhibitor

Studies on the Nature and the Purification of the Coagulase-Reacting Factor and Its Relation to Prothrombin

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