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Biomedical subjects

C Hougie

Publications and source records attributed to C Hougie.

15 recordsLinked to original sources
PubMed1978

"Passovoy defect".

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Blood Coagulation Tests↗
PubMed1978

The action of immobilized thrombin on factor VIII, fibrinogen and a synthetic tripeptide.

Bovine thrombin was insolubilized by attachment to cyanogen bromide-activated Sepharose (Sepharose-thrombin) or to activated (Affi-Gel 10) agarose containing a 10 A long arm (Affi-Gel-thrombin). Coupling in both instances approximated 7,000 units of thrombin per ml packed gel as determined by 125I-thrombin incorporation. The thrombin beads hydrolyzed the synthetic tripeptide Bz-Phe-Val-Arg-pNA (S-2160) at different rates, with the Sepharose-thrombin more active (220 esterase units per ml) than Affi-Gel thrombin (20.4 units per ml). The Km was significantly higher for the insolubilized thrombins (2 X 10(-3) M) than uncoupled thrombin (Km = 8 X 10(-5) M). The Sepharose-thrombin activated factor VIII significantly more rapidly than Affi-Gel-thrombin. Neither matrix-bound thrombin clotted a fibrinogen solution or liberated significant amounts of fibrinopeptides over 48 hr. This data indicates that a proteolysis of factor VIII, rather than a complex with thrombin, is the method of activation of factor VIII and that factor VIII is more accessible to the action of immobilized thrombin than is fibrinogen.

Animals↗
PubMed1978

The Passovoy defect: further characterization of a hereditary hemorrhagic diathesis.

We studied a coagulation abnormality present in 12 members of five kindreds who bruised easily and bled excessively after minor trauma. Their activated partial thromboplastin times were between 32 and 39 seconds (normal, 22.8 to 28.8 seconds). Prothrombin times, thrombin times, platelet-function tests and the levels of factors XII, XI, IX, VIII, prekallikrein and high-molecular-weight kininogen were normal. Within these kindreds inheritance of prolonged partial thromboplastin times followed an autosomal and probably dominant pattern. The prolonged thromboplastin times were corrected by normal plasma and by normal plasma adsorbed with celite, but there was no mutual correction between plasmas of the patients. These subjects shared a common defect in the intrinsic pathway of coagulation that we designate by the proband's surname, Passovoy.

Adolescent↗
PubMed1976

Number, location and severity of coronary arterial changes in steelhead trout (Salmo gairdnerii).

Steelhead trout (Salmo gairdnerii) were taken at three stages of sexual maturity to study their coronary arteries for arteriosclerotic lesions. At least 18 sections from the glutaraldehyde- and osmium-fixed arteries were obtained from each fish. Fish in the middle of the spawning migration and sexually mature fish at the spawning ground had lesions in about 20% of the arterial sections. These consisted of focal proliferations of smooth muscle cells projecting into the lumen through the broken elastic lamina with an intact endothelium around them. Sexually mature fish with patches of fungus on their head and back had twice as high a percentage of arterial sections with lesions as the first two groups of fish. Sexually immature fish were not studied. The lesions occurred approximately equally in all sizes of coronary arteries except for very small arteries. All lesions but one were focal; that lesion involved a third of the intima and the media. The lesions have no elastic lamina below the endothelium and seem to have no lipid.

Aging↗
PubMed1975

Passovoy factor.

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Blood Coagulation Factors↗
PubMed1975

Passovoy factor: A hitherto unrecognised factor necessary for haemostasis.

A moderate bleeding diathesis transmitted as an autosomal dominant was found in five members of four generations of the same family. The affected patients had prolonged partial thromboplastin-times and normal levels of all the known clotting-factors. The haemorrhagic diathesis was attributed to a deficiency of a hitherto unrecognised coagulation factor--i.e., the Passovoy facto.

Adult↗
PubMed1975

Plasma components which interfere with ristocetin-induced platelet aggregation.

Normal human plasma contains a component or components which interfere with ristocetin-induced platelet aggregation. Preliminary examination suggests a protein (or proteins) which binds ristocetin and competes more effectively for ristocetin than do the proteins involved in ristocetin-induced platelet aggregation. The presence of this protein in normal human plasma also prevents ristocetin-induced precipitation of plasma proteins at levels of ristocetin necessary to produce platelet aggregation (0.5-2.0 mg/ml). Serum contains an apparent two0fold increase of this component when compared with plasma. Heating serum at 56 degrees for one hour results in ad additional 2 to 4 forl increase. The presence of a ristocetin-binding protein in normal human plasma requires that this protein be saturated with ristocetin before ristocetin-induced platelet aggregation will occur. Variations in the ristocetin-binding protein(s) will cause apparent discrepancies in ristocetin-induced platelet aggregation in normal human plasmas.

Adsorption↗