scholarly journals Purified Platelet Phospholipids and Blood Coagulation

Blood ◽  
1963 ◽  
Vol 22 (1) ◽  
pp. 19-34 ◽  
Author(s):  
JOHN H. FERGUSON ◽  
AARON J. MARCUS ◽  
A. JEAN ROBINSON
Keyword(s):  
Blood Coagulation ◽  
Partial Thromboplastin Time ◽  
Blood Clotting ◽  
Two Stage ◽  
End Points ◽  
End Point ◽  
Autoprothrombin C ◽  
Generation Test

Abstract Pure platelet phosphatidylserine (PS) and phosphatidylethanolamine (PE) are compared with brain cephalin (Ceph) in clotting-tests; (1) two-stage, using (a) stypven, (b) trypsin, (c) autoprothrombin-C; (2) PTT (partial thromboplastin time); (3) TGT (thromboplastin generation test); all showing "prothromboplastic" activity, except PE in the unmodified TGT. In validated bioassays (1a), log-log plots of end point clotting-times against phosphatide concentrations are rectilinear and parallel. End points related to equivalents of prothrombin-activated (EPA), or thrombin yield (ETY), make possible computation of reactivities in mixtures. Unlike brain PS ("antithromboplastic"), platelet P-lipids show no inhibitor but summate quantitatively with each other or with Ceph. Alterations in lipid reactivities include: (i) decrease during storage, (ii) increase in desoxycholate, (both assayable), (iii) anomalous ("oxidative") increase, in thromboplastic enzyme tests, invalidating bioassays. TGT’s (3) do not show (iii), but can quantitate certain reactivities. Besides suggesting the basis for a physiologic thromboplastic role of platelets, these methods offer means to explore biochemical bases of reactivities in identifiable lipids. These may be partly related to certain enzymes or intermediates in blood clotting reactions.

Rôle of Thrombin in Prothrombin Activation

1964 ◽  
Vol 12 (02) ◽  
pp. 484-488
Author(s):  
W. H Seegers ◽  
H Schröer ◽  
D Heene
Keyword(s):  
Partial Thromboplastin Time ◽  
Procoagulant Activity ◽  
Autoprothrombin C ◽  
Generation Test ◽  
Prothrombin Activation

SummaryThe partial thromboplastin time and purified thrombin were used to demonstrate the procoagulant power of thrombin. Only 0.007 μg of thrombin could be detected in prothrombin activation. Traces of thrombin and autoprothrombin C can fully account for the generation of procoagulant activity in the thromboplastin generation test. Inactivation of these two activities by antithrombin explains the disappearance of the procoagulant power in that test, so that there now remains no valid demonstration of the existence of plasma thromboplastin or of anti-plasma thromboplastin.

Blood Coagulation

1970 ◽  
Vol 24 (03/04) ◽  
pp. 345-351 ◽  
Author(s):  
Walter H. Seegers ◽  
Gary L. Grammens ◽  
Lowell E. McCoy
Keyword(s):  
Blood Coagulation ◽  
Two Stage ◽  
Platelet Factor ◽  
Hageman Factor ◽  
Basic Reaction ◽  
Analytical Reagents ◽  
Autoprothrombin C

SummaryPreparations of platelet factor 3 accelerated the conversion of purified autoprothrombin III (F-X) to autoprothrombin C (F-X?). The reaction was slow and the yields were low. Purified Hageman factor or purified autoprothrombin II (F-IX?) functioned as platelet cofactors. Each increased the yield of autoprothrombin C from purified autoprothrombin III above that obtained with platelet factor 3 alone. Hageman protein thus has a role in the direct acceleration of the first basic reaction in blood coagulation. Purified prothrombin was made refractory to the two-stage analytical reagents with Hageman factor.

Some Effects of Purified Autoprothrombin C in Blood Clotting

1966 ◽  
Vol 16 (03/04) ◽  
pp. 707-722 ◽  
Author(s):  
G Müller-Berghaus ◽  
W. H Seegers
Keyword(s):  
Prothrombin Time ◽  
Partial Thromboplastin Time ◽  
Blood Clotting ◽  
Blood Stream ◽  
Clotting Time ◽  
Glass Tubes ◽  
Low Levels ◽  
The Difference ◽  
Autoprothrombin C ◽  
Stage Analysis

SummaryPurified autoprothrombin C was added to rabbit blood or recalcified plasma in order to measure the exact influence on clotting time. At a concentration of 10 u of autoprothrombin C per ml blood there was clotting in 13 sec. At that concentration recalcified plasma clotted in 7 to 8 sec. In the acceleration of the whole blood clotting time with autoprothrombin C, the effect was greater in glass tubes than in silicone coated tubes. The difference was probably due to lipids from platelets. With autoprothrombin C at a concentration of 10 u/ml reaction mixture, the prothrombin time and partial thromboplastin time of plasma was brought down to 3 to 4 sec. The partial thromboplastin time supplied the most sensitive conditions for detecting autoprothrombin C activity. Less than 2 × 10−5 micrograms of autoprothrombin C were detected. Rabbits that were treated with Coumadin had their prothrombin concentration reduced to 9 u/ml plasma, as measured by two-stage analysis. Such plasma yielded twice as much thrombin when purified autoprothrombin C and purified Ac-globulin were used in the assay to determine the thrombin potential. Even when the prothrombin concentration was brought to low levels with Coumadin a partial thromboplastin time or prothrombin time of 7 sec was easily obtained by using autoprothrombin C as procoagulant. The important effect of Coumadin or related drugs is the reduction of prothrombin concentration. This involves a lowering of the autoprothrombin C potential as well as the thrombin potential of plasma, and also the amount of inhibitor that can be obtained from prothrombin.Normal blood was found to contain prethrombin in small amounts as well as prothrombin. The synthesis of prothrombin was stopped with Coumadin and it is likely that the residual prothrombin was in part utilized by degradation to prethrombin, inhibitor and autoprothrombin III. At the height of the anticoagulant effect the prethrombin concentration was higher than the prothrombin concentration. With the resumption of prothrombin synthesis, when vitamin K was given, it may be that prethrombin, inhibitor, and autoprothrombin III was first produced in the liver and some of the latter entered the blood stream to compensate for substrate deficiency. Free autoprothrombin III would account for the short prothrombin time observed before prothrombin concentration rose.

scholarly journals Blood coagulation in the 21st century: existing knowledge, current strategies for treatment and perspective

2020 ◽  
Vol 19 (1) ◽  
pp. 139-157
Author(s):  
N. A. Podoplelova ◽  
V. B. Sulimov ◽  
I. S. Ilin ◽  
A. S. Tashilova ◽  
M. A. Panteleev ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Blood Clotting ◽  
Coagulation Factors ◽  
New Drugs ◽  
Coagulation System ◽  
Modern World ◽  
Blood Coagulation Factors ◽  
Clotting System ◽  
Normal Hemostasis

Disorders in the blood coagulation system are the leading cause of death and disability in the modern world. So the search for new drugs that can prevent pathological thrombosis, while not affecting normal hemostasis, becomes more relevant than ever. Recent studies has been a revolution in the understanding of the principles of work and the regulation of blood coagulation. In addition, new, more effective approaches to drug development have now appeared. For example computer simulation methods that can significantly reduce the time and resources spent on the search for new candidate molecules. In the review, the blood clotting system, the molekular mechanisms of thrombosis, the role of blood coagulation factors Xa and XIa, and the urgency of developing new inhibitors of these targets are shown, and the most interesting inhibitors of factors Xa and XIa are presented.

The Effect of Trasylol on Blood Coagulation after Intravenous Injection

1967 ◽  
Vol 17 (01/02) ◽  
pp. 051-057
Author(s):  
J Gormsen ◽  
P Josephsen
Keyword(s):  
Blood Coagulation ◽  
Intravenous Injection ◽  
Significant Influence ◽  
Partial Thromboplastin Time ◽  
Thrombin Generation ◽  
Double Blind ◽  
Generation Test

SummaryThe in vivo effect of Trasylol® on the thromboplastin generation test, thrombin -generation test, the partial thromboplastin time and the thrombelastography has been examined in 50 patients. Furthermore 34 patients were given one of two preparations of “Trasylol”, distributed for a double-blind control. The dosis of Trasylol varied from 100,000 to 400,000 units. No significant influence on the various tests used was found.

Physics and clinical measurement

2014 ◽  
Author(s):  
Jeremy Prout ◽  
Tanya Jones ◽  
Daniel Martin
Keyword(s):  
Ionizing Radiation ◽  
Blood Coagulation ◽  
Radiation Protection ◽  
Blood Clotting ◽  
Point Of Care ◽  
Predictive Values ◽  
Clinical Measurement ◽  
Laboratory Results

This chapter includes general concepts of interpreting laboratory results such as specificity, sensitivity and predictive values. In the measurement of blood coagulation, the cell-based mechanism for blood clotting is explained and the role of point-of-care viscoelastic testing using thromboelastography is described. Effects of ionizing radiation, safe levels, and radiation protection are also included.

A Re-Appraisal of the Role of Blood Coagulation and Platelets in the Generalized Shwartzman Phenomenon

1966 ◽  
Vol 15 (03/04) ◽  
pp. 519-538 ◽  
Author(s):  
J Levin ◽  
E Beck
Keyword(s):  
Blood Coagulation ◽  
The State ◽  
Coagulation System ◽  
Renal Lesions ◽  
Intravascular Coagulation ◽  
Renal Glomeruli ◽  
Coagulation Mechanism ◽  
Shwartzman Phenomenon ◽  
Do So

SummaryThe role of intravascular coagulation in the production of the generalized Shwartzman phenomenon has been evaluated. The administration of endotoxin to animals prepared with Thorotrast results in activation of the coagulation mechanism with the resultant deposition of fibrinoid material in the renal glomeruli. Anticoagulation prevents alterations in the state of the coagulation system and inhibits development of the renal lesions. Platelets are not primarily involved. Platelet antiserum produces similar lesions in animals prepared with Thorotrast, but appears to do so in a manner which does not significantly involve intravascular coagulation.The production of adrenal cortical hemorrhage, comparable to that seen in the Waterhouse-Friderichsen syndrome, following the administration of endotoxin to animals that had previously received ACTH does not require intravascular coagulation and may not be a manifestation of the generalized Shwartzman phenomenon.

Blood Coagulation Studies and Extracorporeal Circulation in Man

1967 ◽  
Vol 18 (03/04) ◽  
pp. 634-646 ◽  
Author(s):  
N Thurnherr
Keyword(s):  
Blood Coagulation ◽  
Extracorporeal Circulation ◽  
Blood Clotting ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Fibrinolytic System ◽  
Open Heart ◽  
Clotting Factors ◽  
Blood Clotting Factors

SummaryBlood clotting investigations have been executed in 25 patients who have undergone open heart surgery with extracorporeal circulation. A description of alterations in the activity of blood clotting factors, the fibrinolytic system, prothrombin consumption and platelets during several phases of the operation is given.

Two-Stage Procedure for the Quantitative Determination of Autoprothrombin III Concentration and Some Applications

1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers
Keyword(s):  
Prothrombin Time ◽  
Factor Vii ◽  
Two Stage ◽  
Pronounced Increase ◽  
One Stage ◽  
Assay Procedure ◽  
Bovine Plasma ◽  
The One ◽  
Autoprothrombin C

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.

Impulsivity and Aggression: A Meta-analysis Using the UPPS Model of Impulsivity

2019 ◽  
Author(s):  
Konrad Bresin
Keyword(s):  
Structural Equation Modeling ◽  
Sensation Seeking ◽  
Structural Equation ◽  
Meta Analysis ◽  
The Other ◽  
Equation Modeling ◽  
Negative Urgency ◽  
Two Stage ◽  
Trait Impulsivity

Trait impulsivity has long been proposed to play a role in aggression, but the results across studies have been mixed. One possible explanation for the mixed results is that impulsivity is a multifaceted construct and some, but not all, facets are related to aggression. The goal of the current meta-analysis was to determine the relation between the different facets of impulsivity (i.e., negative urgency, positive urgency, lack of premeditation, lack of perseverance, and sensation seeking) and aggression. The results from 93 papers with 105 unique samples (N = 36, 215) showed significant and small-to-medium correlations between each facet of impulsivity and aggression across several different forms of aggression, with more impulsivity being associated with more aggression. Moreover, negative urgency (r = .24, 95% [.18, .29]), positive urgency (r = .34, 95% [.19, .44]), and lack of premeditation (r = .23, 95% [.20, .26]) had significantly stronger associations with aggression than the other scales (rs < .18). Two-stage meta-analytic structural equation modeling showed that these effects were not due to overlap among facets of impulsivity. These results help advance the field of aggression research by clarifying the role of impulsivity and may be of interest to researchers and practitioners in several disciplines.

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