bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of Fibrinogen Split Products on Platelets
Authors: Barnhart M. I , Cress D. C , Henry R. L , Riddle J. M 
Published: June 2018

SummaryBreakdown products of fibrinogen and fibrin can play a role in hemostasis and also may be of consequence in thrombosis. β2 fibrinogen derivative D is an electropositive terminal proteolysis product of fibrinolysis which has the ability to aggregate platelets. The normal plasma concentration of such nonclottable fibrinogen relatives is 0.2 mg/ml. During fibrinolysis this concentration may reach 5 mg/ml plasma. Addition of β 2 fibrinogen D (raising the plasma concentration 0.1 to 5 mg/ml) either in vivo or in vitro induced platelet aggregations. Moreover, alterations in platelet morphology occurred which were obvious by electron microscopy.Platelet depletion was a consistent response to the infusion of purified β2 fibrinogen D (8 to 55 mg/kg body weight) into dogs. Circulating platelets decreased as much as 85% but were only temporarily aggregated and reappeared in the circulation within 1 to 5 hrs. Small platelet aggregates circulated while large aggregates were trapped in the microcirculation. Thrombin was not responsible for the platelet aggregations as neither prothrombin nor clottable fibrinogen were changed significantly. The transient nature and morphological features of the platelet response according to microscopic criteria were prominent during and after infusion of β2 fibrinogen D.In vitro studies included 3 systems; washed platelets, platelet rich plasma and whole blood. Positive results were obtained with all, but platelets in whole blood were most responsive. The magnitude of platelet aggregation and morphology correlated with the concentration of β2 fibrinogen D. Platelet aggregation induced by ADP (10~5 mg/ml) was compared with that induced by β2 fibrinogen D (0.09 to 0.72 mg/ml). With either reagent aggregates were of dendritic forms. Combination of the 2 reagents was additive but did not further change the morphology. Additional factors seem necessary for development of viscous metamorphosis.
Hypercoagulable State Induced in Humans by the Intravenous Administration of Purified Ellagic Acid
Authors: Girolami A , Cliffton E. E 
Published: June 2018

SummaryThe intravenous administration of ellagic acid induces a hypercoagulable state in humans. This is characterized by a striking shortening of the silicone clotting time and moderate shortening of the glass clotting time. No change in other coagulation parameter was noted. However, in one patient with a prolonged thromboplastin generation test, a correction of same was observed. The effect of ellagic acid is more prolonged in humans than in animals. There was no obvious toxic reaction to the administration of the drug.
The Prothrombin Time in the Newborn: Effect of Contact Activation
Authors: Shanberge J. N , Matsuoka T 
Published: June 2018

SummaryThe effect of foreign-surface contact on prothrombin conversion in adult plasma is compared to that of the newborn. The tests utilized in this comparison were the one-stage prothrombin time of Quick, the second stage of the thromboplastin generation test, and the prothrombin consumption test or the serum prothrombin time. In all of these there is much less acceleration produced by foreign-surface contact in the plasma of the newborn. Acceleration of the prothrombin conversion time is directly related to an increase in activity of factors VII and XL At no time could an increase in prothrombin activity be demonstrated. The decreased acceleration produced by foreign-surface contact in the plasma of the newborn is due primarily to a decreased level of factor VII as well as those factors necessary for its activation.
The Effect of Hirudin, a Potent Antithrombin, on the Thromboplastin Generation Test
Authors: Caldwell M. J 
Published: June 2018

SummaryThe presence of hirudin at the time adsorbed plasma and serum were combined in TGT inhibited the formation of the prothrombin converting activity. Hirudin, a potent antithrombin, probably exerted its inhibitory effect by neutralizing any thrombin which might form. If adsorbed plasma and serum were incubated together for a period as short as 1 to 3 min before the addition of hirudin, calcium and lipid, hirudin no longer exerted the same inhibitory effect, but, in order to exert the same inhibitory effect, had to be present in higher concentration. Preincubation of factor VIII deficient plasma with serum and calcium was not effective in overcoming hirudin inhibition, but preincubation with factor IX deficient serum with adsorbed plasma and calcium was able to overcome inhibition due to hirudin equally as well as normal serum.Once again the importance of traces of thrombin in the formation of activity capable of rapidly clotting substrate plasma in TGT has been shown by using a specific thrombin inhibitor. A thrombin dependent interaction appears to take place between adsorbed plasma and serum and also between product I and phospholipid.
Anticoagulant Properties of an Acid Mucopolysaccharide Preparation Isolated from Rat Kidney
Authors: Allalouf D , Ber A , Rechnic Jadwiga , Sharon N 
Published: June 2018

SummaryThe anticoagulant properties of an acid mucopolysaccharide preparation isolated from rat kidney were investigated. This preparation was characterized chemically in a previous work (1) and was found to contain heparin-like material.A qualitative similarity in the behaviour of our preparation to that of heparin becomes apparent from the results obtained in a number of tests in which heparin was also tested. Quantitatively, this preparation possessed in the recalcification test about 8% of the potency of the standard heparin preparation. Some of its subfractions obtained from a fractionation on an Ecteola-cellulose column exhibited a higher activity.This work supports previous findings on the chemical characterization of this preparation.
The Anticoagulant Activity of 3.3’-(p-Alkylthio-Benzylidene)-Bis-4-Hydroxycoumarins and Their Oxidation Products
Authors: Gumińska Maria , Eckstein M , Stachurska Barbara , Sulko J 
Published: June 2018

SummaryThe anticoagulant activity of 3.3’-(benzylidene)-bis-4-hydroxycoumarin derivatives has been estimated by one step Quick’s method. The derivatives contained the following groups in the para position of benzylidene residue: NCS- (I), CH3-S- (II), CH3-SO-(III), CH3-S02- (IV), C2H5-S- (V), C2H5-SO- (VI), C2H5-S02- (VII). All these compounds were much more active than 3.3’-(benzylidene)-bis-4-hydroxycoumarin itself.Compounds possessing the ethyl chain at the sulphur atom (V, VI, VII) were more active than methyl homologues (II, III, IV). Comparison of the activity of the series of thio-, sulphoxy-, and sulphonyl-derivatives showed that among methyl- and ethyl-derivatives those with the sulphoxy grouping (III, VI) displayed the greatest anticoagulant activity. The action of sulphonyl (IV, VII) and thio-derivatives (II, V) was weaker and shortest. The derivative with the NCS-group (I) possessed a relatively the lowest activity among the investigated compounds. 3.3’-(p-Ethylsulphoxybenzyl-idene)-bis-4-hydroxycoumarin (VI), with distinct biological activity reached about ½ of dicoumarol activity.
Study of Thrombin-Coagulase
Authors: Soulier J. P , Prou-Wartelle Odette , Hallé Liliane ,   with the technical assistance of
Published: June 2018

SummaryThe preparation of thrombin-coagulase is described. The properties of thrombin-coagulase are compared with those of biothrombin: kinetics, thermostability, adsorption, chromatography, esterase activity, clotting activity, action on platelets and on factors V and VIII, susceptibility to inhibitors.Biothrombin and thrombin-coagulase are closely related but distinct. Both apparently derive from prothrombin. Prothrombin and coagulase combine to form a complex: thrombin-coagulase wherein both factors are necessary for its activity. Possible explanations for the difference between thrombin-coagulase and biothrombin are proposed.
Determination of Fibrinogen (and Fibrinolysis) in Small Quantities of Plasma
Authors: Lázár G 
Published: June 2018

SummaryThe paper describes a simple method for the determination of fibrinogen and fibrinolysis especially suitable for serial examinations which may be performed with small amounts of plasma. In the procedures the amount of fibrin bound to the filter paper soaked in a thrombin solution is determined in the case of fibrinogen after washing, in that of fibrinolysis after incubation at 37° C and washing, by means of staining with fuchsine.
Studies on Aggregation and Adhesion of Platelets
Authors: Shively J. A , Gott C. L 
Published: June 2018

SummaryA modification of the Wright method for the evaluation of the aggregation and adhesive properties of platelets is described; the test is relatively simple and can be performed in a clinical laboratory.Using this procedure, the characteristics of platelets acidified to a pH of 6.5 from their normal pH by addition of small amounts of acid citrate dextrose (ACD) solution to platelet-rich plasma were evaluated. Aggregation and adhesive properties were decreased but returned to normal when the acidified platelets were resuspended in nonacidified platelet-poor plasma. These results confirm the transfusion and isotopie labeling survival studies using acidified platelets and indicate no significant injury of the platelets as exhibited by their aggregation and adhesive characteristics which are considered to be indicative of hemostatic function.
Platelet Numbers and Life Span in Acute and Chronic Renal Failure
Authors: Stewart J. H 
Published: June 2018

SummaryPlatelet numbers were estimated on all 225 patients admitted with severe renal failure to the Sydney Hospital Renal Unit in a 2 year period. Serial counts were per formed to determine the circumstances under which platelet numbers were restored to normal in patients with thrombocytopenia. Measurements of 51Cr-labelled autologous or homologous platelet life span were made in 37 patients with severe renal disease and in 8 control subjects.Thrombocytopenia occurred in one quarter of all patients with renal tubular necrosis, acute or subacute glomerulonephritis, or malignant hypertension, but only in one twelfth of those with severe uraemia due to chronic renal disease. Recovery of platelet numbers followed partial relief of uraemia by dialysis or return of renal function in 24 patients. In 2 patients the platelet count rose despite no relief of uraemia, and in 14, there was no recovery from thrombocytopenia before death. Severe infection, microangiopathy and malignant disease, although present in a number of patients, were not important causes of thrombocytopenia.The life span of autologous platelets, or of compatible, normal, homologous platelets given to subjects who had never received a previous blood transfusion, was normal in severe renal failure, and there was no significant difference between patients with various types or different severities of renal disease. The survival of homologous platelets was slightly or moderately reduced when given to patients who had received a previous blood transfusion.The mean recovery of autologous 51Cr-labelled platelets prepared in acid citrate was 58%, and of homologous platelets, 41 %.Thrombocytopenia in renal failure is presumed to be mainly due to impaired platelet production caused by the biochemical affects of azotaemia. The condition should be treated by peritoneal dialysis, and, when this is impossible or ineffective, by platelet transfusion.
Coagulation Factors in Pregnant Women and Premature Infants with and without the Respiratory Distress Syndrome
Authors: Markarian Marguerite , Lindley Annabelle , Jackson Jacqueline J. , Bannon Anne 
Published: June 2018

SummaryCoagulation factors (accelerator globulin, antihemophilic globulin, specific prothrombin, proconvertin complex and Stuart-Prower factor) in 82 low birth weight infants (750–1750 g), 22 normal adult controls and 38 pregnant women prior to delivery were studied at San Borja Hospital in Santiago, Chile.Pregnant women prior to delivery had significantly higher values of accelerator globulin, antihemophilic globulin, proconvertin complex and Stuart-Prower factor than adult controls, but there was no difference in specific prothrombin.The coagulation factors were similar in premature infants without RDS as compared to those with RDS (lived and died combined). However, premature infants with RDS who lived had higher values of prothrombin, proconvertin complex, Stuart-Prower factor at 25 hrs and accelerator globulin at 55 hrs of age than those with RDS who died. Most of these findings could be explained by impaired liver function in association with hypoxia.
Hemostasis as an Evolutionary Development
Authors: Quick A. J 
Published: June 2018

SummaryHemostasis is a complex physiological mechanism that has evolved as the organism increased in complexity and the need for safeguarding against loss of blood became progressively greater. The most primitive phase is vascular contraction which sufficed until the cardiovascular system made greater demands on the need for protection against hemorrhage. The developing of a coalescing blood cell constituted the second major advance in the mechanism of hemostasis, and it is very probable that the thrombocytes of avian and reptile blood and the platelets of mammalian blood represent the evolutionary end products of this phase. The clotting mechanism is the last step and is the third line defense against hemorrhage. Even in the higher forms of life including man, none of these steps in hemostasis have been supplanted, but rather have been supplemented. Therefore residua of the primary step are not only present but still functioning. To understand the problem of bleeding, it must be viewed from the global aspect of hemostasis.
A Distinction between the Role of Precursor and Activated Forms of Clotting Factors in the Genesis of Stasis Thrombi
Authors: Wessler S , Yin E. T , Gaston L. W , Nicol Iona 
Published: June 2018

Summary1. In vivo studies in rabbits have shown that the liver diminishes the thrombo-genicity of infused human serum.2. In vitro rabbit liver perfusions with human serum have demonstrated the loss of serum thrombogenicity within 5 min after the onset of the perfusion. Associated with this loss of thrombotic capacity is a marked decrease in the activation product (AP) and labile factor IX (PPA) activity in the infused serum.3. The liver appears to have the capacity to discriminate between circulating activated clotting activities such as AP and PPA and inactive procoagulants such as stable or genuine factor IX, factor VII and factor X. The latter are not cleared from the circulation by the liver.4. These studies provide some insight into the mechanism whereby circulating activated clotting activities and retarded blood flow predispose to thrombosis.
The Spectrum of von Willebrand’s Disease
Authors: Bowie E. J Walter , Didisheim P , Thompson J. H , Owen C. A 
Published: June 2018

SummaryPatients (from 5 kindreds) with variants of von Willebrand’s disease are described. In one kindred the depression of factor VIII was moderate (20 to 40% of normal) and transfusion of 500 ml of normal plasma led to an increase higher than anticipated and to an almost normal level of factor VIII 17 to 24 hrs later. This represents the usual type of von Willebrand’s disease.In the second kindred the concentration of factor VIII was less than 2 % of normal in the son and daughter, who had severe bleeding and hemarthroses.The third kindred was characterized by reduction of factor VIII and a long bleeding time as well as by a serum defect in the thromboplastin-generation test comparable to that seen in patients with hemophilia B, yet with normal levels of factors IX, X, and VII. The severity of the serum defect, the positive result with the Rumpel-Leede test, and the reduced platelet activity in the thromboplastin-generation test are all compatible with the diagnosis of thrombopathy or ‘‘thrombopathic hemophilia.” In two other kindreds, one patient had a long bleeding time and normal levels of factor VIII and another had a normal bleeding time and decrease of factor VIII. The last patient had the type of response to transfusion usually seen in von Willebrand’s disease.In four kindreds, platelet adhesiveness in vivo was found to be strikingly abnormal (virtually absent).It would appear, therefore, that von Willebrand’s disease forms a spectrum, and whether the kindreds reported simply reflect variations of a single genetic disease state or represent separate entities will be answered only by clarification of the underlying etiology of that disease.
Ultrastructural Observations on Platelet Adhesion Reactions
Authors: Erichson R. B , Cintron J. R 
Published: June 2018

SummaryThe interaction of platelets with collagen and with other platelets in collageninduced platelet aggregates has been studied with the electron microscope. The contours of aggregated platelets closely conformed to each other at a finite and regular distance, usually 200 to 300 Ångstroms. Structural conformity of platelets and collagen was less regular and occurred with a narrower separation. These findings are discussed in relation to observations of platelet interaction with fibrin and latex particles.
Some Aspects of Fibrin Clot Lysis and Its Inhibition by Human Serum
Authors: Gallimoke M. J , Shaw J. T. B 
Published: June 2018

SummaryThe lysis by plasmin of fibrin clots prepared from plasminogen-deficient fibrinogen, and by urokinase of similar clots prepared from plasminogen-rich fibrinogen has been studied. In a simple system containing no plasminogen the clot lysis time is inversely proportional to the concentration of added plasmin, and zero order kinetics are obeyed. The reciprocal of the lysis time is a measure of the fibrinolytic activity in the system, and may be used to study antiplasmins. When serum was included a reduction in reciprocal lysis time resulted, the extent of which varied linearly with the amount of serum added. These relationships persisted whether soluble or insoluble plasmin preparations were used and whether or not chloride ions were present. They indicate that serum antiplasmins behave as irreversible or pseudo-irreversible inhibitors. It was found that sodium chloride exerts a potentiating effect on fibrinolysis by plasmin, but does not influence the extent to which the enzyme is inhibited by serum antiplasmins.When fibrin clots were prepared from plasminogen-rich fibrinogen, and urokinase was included, a direct relationship was found to exist between the concentration of urokinase and the square of the reciprocal clot lysis time. When serum was added, vigorous inhibition of fibrinolysis resulted when sodium chloride was present; no inhibition was observed in its absence. It is proposed that sodium chloride weakens the interaction between plasminogen and fibrin in the clots, and renders the plasmin produced by the action of urokinase more susceptible to inhibition by antiplasmins. Evidence in support of this hypothesis is presented and the kinetics of fibrinolysis by plasmin, and its inhibition, are discussed.
The Nature of Heparin Antithrombin Action
Authors: Henstell H. H , Kligerman Miriam 
Published: June 2018

SummaryHeparin accelerated the activity of isolated or unopposed antithrombin. Neither calcium, platelets nor inhibitor were required. Optimal activity was at minimal concentrations.Heparin was not consumed or altered in the process of thrombin neutralization by heparinized plasma. The full heparin activity was manifest when additional plasma antithrombin was supplied.Thrombin neutralization was noted to be a function of the plasma antithrombin concentration. It was unrelated to the heparin concentration. Heparin did not increase the total antithrombic activity in samples with either very small or large quantities of thrombin and antithrombin.The heparin influenced thrombin neutralization only in the presence of antithrombin. It did not affect the thrombin-fibrinogen reaction. Polybrene blocked the heparin effect when added to the antithrombin, but did not affect heparin action when added subsequently to the fibrinogen substrate.
Two-Stage Procedure for the Quantitative Determination of Autoprothrombin III Concentration and Some Applications
Authors: Reno Ronald S , Seegers Walter H 
Published: June 2018

SummaryA two-stage assay procedure was developed for the determination of the autoprothrombin C titre which can be developed from prothrombin or autoprothrombin III containing solutions. The proenzyme is activated by Russell’s viper venom and the autoprothrombin C activity that appears is measured by its ability to shorten the partial thromboplastin time of bovine plasma.Using the assay, the autoprothrombin C titre was determined in the plasma of several species, as well as the percentage of it remaining in the serum from blood clotted in glass test tubes. Much autoprothrombin III remains in human serum. With sufficient thromboplastin it was completely utilized. Plasma from selected patients with coagulation disorders was assayed and only Stuart plasma was abnormal. In so-called factor VII, IX, and P.T.A. deficiency the autoprothrombin C titre and thrombin titre that could be developed was normal. In one case (prethrombin irregularity) practically no thrombin titre developed but the amount of autoprothrombin C which generated was in the normal range.Dogs were treated with Dicumarol and the autoprothrombin C titre that could be developed from their plasmas decreased until only traces could be detected. This coincided with a lowering of the thrombin titre that could be developed and a prolongation of the one-stage prothrombin time. While the Dicumarol was acting, the dogs were given an infusion of purified bovine prothrombin and the levels of autoprothrombin C, thrombin and one-stage prothrombin time were followed for several hours. The tests became normal immediately after the infusion and then went back to preinfusion levels over a period of 24 hrs.In other dogs the effect of Dicumarol was reversed by giving vitamin K1 intravenously. The effect of the vitamin was noticed as early as 20 min after administration.In response to vitamin K the most pronounced increase was with that portion of the prothrombin molecule which yields thrombin. The proportion of that protein with respect to the precursor of autoprothrombin C increased during the first hour and then started to go down and after 3 hrs was equal to the proportion normally found in plasma.
Measuring the Coagulability of Fibrinogen in Plasma by Isotopic Means
Authors: Regoeczi E. 
Published: June 2018

Summary1. A simple and reproducible technique for measuring the clottability of plasma fibrinogen using iodinated fibrinogen is described, the coefficient of variance being less than 1 %.2. In vivo experiments in rabbits and monkeys on one hand and in vitro studies with fibrinogens from various species on the other indicated that :a) Aliquots of a fibrinogen preparation iodinated at the same mean substitution level yield practically identical coagulabilities ;b) Aliquots of one labelled preparation when injected into several healthy animals or mixed with their plasmas give equal values for clottability;c) In normal animals, the clottable proportion of the circulating protein-bound radioactivity is at any time a function of the extra/intravascular distribution and of the catabolic rate of fibrinogen relative to the corresponding values of the contaminating labelled protein.3. The significance of the behaviour of the non-clottable protein-bound radioactivities during fibrinogen turnover experiments for the catabolic mechanism is discussed. It is suggested that fibrinogen catabolism is probably an intracellular process.