Two years after the highly publicized NIH conference on the eradication of Helicobacter pylori, antimicrobial agents were not widely prescribed among the Pennsylvania Medicaid population. In treating this underserved population, physicians do not appear to be using recommendations developed by an NIH expert panel based on recent scientific advances.

SummaryWashed platelet suspensions contain active SF (surface factor or activation product), when prepared from normal (N) subjects or from patients deficient in factors Vili, IX or X, but not from a Hageman-deficient. Factor V-deficient plasmas were normalized by platelets from N, XII- and other subjects. Allowing for (a) the platelet prothromboplastic phospholipids, and (b) the above SF and AcG (V) effects, there was no evidence of any significant factors Vili, IX or X in the platelet plasmatic atmosphere. Since XII-platelets showed no true correction of plasmas deficient in Vili, IX or X, the minor “improvement” of test results in these (and N) plasmas on adding N, Vili-, IX- or X-platelets can be explained as a nonspecific surface factor effect. XII-platelets when incubated with normal plasma were normalized by adsorbing Hageman factor (XII) on their surface.

SummaryBlood platelet suspensions from normal (N) or hemophilia A (VIII-) subjects contain active SF (surface factor or activation product) in their plasmatic atmosphere. Since factor XII is an essential precursor, SF is not formed on platelets from a Hageman-deficient. Experimental evidence establishing these facts was obtained by means of clotting tests (PCa and PTT) and the thrombelastograph (TEG). The SF activity of normal platelets, like a plasma SF preparation, corrects the deficiencies in XII- plasmas, best tested in silicone or the stainless steel cuvette of the TEG. An anti-SF preparation inhibited the platelet SF activity. Allowing for the SF effect, there was no evidence for any significant factor VIII (AHF) in the platelet plasmatic atmospheres.How surface factor (SF) activation from precursors (XII, XI) in the plasma and plasmatic atmosphere of altering platelets may combine in a mutually reinforcing reaction to trigger intrinsic blood clotting is discussed. When stress, vascular injury, stasis, and other factors enter the picture, the stage may be set for the occurrence of thrombosis in vivo.

SummaryA basic biomathematical analysis of quantitative clotting test data becomes highly significant in the light of a complex logic which indicates a possible accord with certain postulated biophysical principles. Rectilinear plots are obtainable with one or other of two methods of analyzing the clotting-time data for an experimental system in which prothrombin is converted into thrombin by thrombokinase in the presence of specified cofactors.Determinants of enzymic activity fit the postulate of Michaelis-Menten kinetics and the Lineweaver-Burk double-reciprocal rectilinear plot. This holds when the ∼ substrate variable is (a) thrombokinase (as precursor of the true prothrombin-convertor enzyme), (b) specific cation (Ca++, Sr++, or Ba++), and (c) factor V (AcG). The validated assays are particularly meaningful in the case of factor V, and suggest a new system of unit age (AcGact)- Tentative Km values are given for these “substrate” functions.Determinants of effective thrombin (activated prothrombin) quasi-activity are studied by rectilinear log-log plots of endpoint clotting-times against the factor variable, when this is (a) prothrombin, (b) prothromboplastic phospholipid (cephalin), but (c) factor V (AcG) only to a limited extent. The discussion explains how these findings accord with certain colloidal principles that modify a basic enzyme formula based on “the inverse law.”Evidence of complexing of both substrate and enzyme with certain factors is provided, especially by exploring effects of successive suboptimal additions. The following mechanisms could explain the facts: (a) prothrombin + phospholipid form a colloidal (micellar) substrate complex ; (b) the true activating enzyme is thrombokinase after specific activation by cation (Ca++, normally) ; (c) factor V plays a dual role (in (a) and (b)), thus acting after the manner of an amboceptor. These key reactions should be added to the current “cascade” concept of blood clotting.

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