Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

Hougie, Cecil; Barrow, Emily M.; Graham, John B.

doi:10.1172/jci103446

Cited by 256 publications

(90 citation statements)

References 28 publications

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“…and 720 volts. Under these conditions the thermocouple readings on the curtain during electrophoresis were 180 C. Before starting electrophoresis it was important to allow the instrument to stabilize for at least (11,12) and Stuart factor (13). D PAPER STRIP "Glass factor" is a term used to express the ability of certain fractions or of plasma treated with glass to shorten the recalcification time and improve prothrombin current applied.…”

Section: Methodsmentioning

confidence: 99%

Application of Continuous Flow Electrophoresis to the Study of the Blood Coagulation Proteins and the Fibrinolytic Enzyme System. I. Normal Human Materials1

Lewis¹,

Walters²,

Didisheim³

et al. 1958

J. Clin. Invest.

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Continuous flow filter paper electrophoresis, as developed by Svensson and Brattsen (1), Grassmann and Hannig (2-4) and Durrum (5), offers a method of plasma fractionation in which protein denaturation appears minimal. This study involves the testing of such fractions for biological activity in various coagulation systems. With the exception of fibrinogen, the coagulation proteins are present in plasma in minute amounts which, at the present time, can be assayed only by their activities in specific clotting systems. Many of these coagulation factors are readily denatured; thus, rigid control with particular attention to temperature is necessary to obtain good recovery of biological activity.Previous electrophoretic studies concerning distribution of plasma coagulation proteins have employed paper electrophoresis with elutions from cut strips. Owen and McKenzie (6) found prothrombin to coincide with a2 globulin, proconvertin (stable conversion factor) with ft globulin, proaccelerin (labile conversion factor) in a variable area between y and f8 peaks, antithrombin between /3 and a2, and fibrinogen remaining at the point of application. Using the same technique, Frick and Hagen (7) found Hageman factor activity in a fraction located between ft and -y globulin. On the other hand, the electrophoretic mobility of purified prothrombin was described by Seegers, McClaughry, and Fahey (8) as approximately equivalent to that of a, globulin. The

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Section: Methodsmentioning

confidence: 99%

Application of Continuous Flow Electrophoresis to the Study of the Blood Coagulation Proteins and the Fibrinolytic Enzyme System. I. Normal Human Materials1

Lewis¹,

Walters²,

Didisheim³

et al. 1958

J. Clin. Invest.

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“…Audrey Prower with a bleeding diathesis and in 1957 by Hougie et al 4 in a 36-year-old male patient, Mr Stuart (hence, Factor X is also known as StuartePrower Factor). Factor X is a vitamin K dependent, liver produced serine protease that serves as a pivotal role in coagulation as the first enzyme in the common pathways to thrombus formation.…”

Section: Introductionmentioning

confidence: 99%

Inherited Factor X (Stuart–Prower Factor) deficiency and its management

Chatterjee

Philip

Nair

et al. 2015

Medical Journal Armed Forces India

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“…This defect was also shown to be hereditary and became known as the Hageman factor, which was later called factor XII (fXII). Further milestones, including the discovery of the last remaining "major" procoagulant, namely fX ("Stuart Prower factor") in 1956, 5 laid the groundwork for the waterfall or cascade models of blood coagulation proposed by 2 groups on either side of the Atlantic. 6,7 In this paradigm, the causes of prolongation of the screening tests of coagulation, namely the PT and aPTT, could be fully explained.…”

Section: Introductionmentioning

confidence: 99%

Epidemiologic and clinical data linking factors XI and XII to thrombosis

Key

2014

Hematology

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Currently available evidence supports the contention that elevated levels of factor XI (fXI) are associated with a greater risk of venous thromboembolism and ischemic stroke, but, less convincingly, with myocardial infarction. Conversely, reduced plasma levels of fXI seem to offer some protection from venous thromboembolism and stroke, but not myocardial infarction. Factor XI-deficient patients are at risk for certain types of bleeding, particularly posttraumatic hemorrhage on mucosal surfaces where there is a high endogenous fibrinolytic activity. In contrast, the situation with fXII in human thrombosis remains enigmatic. Deficiency of fXII is clearly not associated with any bleeding risk, but neither does it seem to be protective against thrombosis. The longstanding debate as to whether partial fXII deficiency represents a risk factor for thrombosis remains unresolved, with seemingly conflicting results depending on study design, type of assay used, and analyte evaluated. The possibility that elevated fXII levels represent a risk factor for thrombosis is not borne out in the literature.

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Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

Cited by 256 publications

References 28 publications

Application of Continuous Flow Electrophoresis to the Study of the Blood Coagulation Proteins and the Fibrinolytic Enzyme System. I. Normal Human Materials1

Application of Continuous Flow Electrophoresis to the Study of the Blood Coagulation Proteins and the Fibrinolytic Enzyme System. I. Normal Human Materials1

Inherited Factor X (Stuart–Prower Factor) deficiency and its management

Epidemiologic and clinical data linking factors XI and XII to thrombosis

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