bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect Of The Stable Prostacy Clin-nilic, 7-OXO-PGI2 On Some Haemostatic Parameters
Authors: Blaskó Gy , Körmöczy P , Stadler I , Simonidesz V , Tömösközy I 
Published: May 2019

7-oxo-PGI2 sodium salt produced by the Chinoin was investigated regarding some haemostatic and haemodynamic parameters. According to our results, 7-oxo-PGI2 is a powerful inhibitor of platelet aggregation induced by ADP and collagen (IC50: 10-15 ng/ml and 60-80 ng/ml respectively). It is stable in solution and the duration of its inhibitory effect on platelet aggregation in vitro is more than 3 hours (for PGI2 it is only 1,5 h ). Investigating the effect of this substance on the activities of the key-enzymes of blood coagulation (thrombin, Factor Xs and plasmin), we could neither demonstrate any effect on these enzyme activities nor on the inactivation of these enzymes by antithrombin-III and/or heparin at a concentration as high as 200 μg/ral.The relative potency of 7-oxo-PGI2 on isolated bovine coronary artery is one tenth, as compared to PGI2. It decreases the systolic and diastolic blood pressure with a relative potency of 1:20 to PGI2 without effecting the heart rate. Comparing its stimulatory effect on platelet adenylate cyclase to that of PGI2, we have found, that 1 μM of 7-o xo-PGI2 activates this enzyme to 246%, while 1 μM of PGI2 causes a 370% activation. The platelet disaggregating activity of this compound -tested on cat Achilles tendon - is comparable to the effect of the natural compound.The pharmacological profile of 7-oxo-PGI2 is similar to that of PGI , just even as another well known leading representativerGI -analogue - carboprostacyclin - , furthermore it is slightly preferred in certain conditions.
Platelet antibodies and circulating immune complexes in thrombocytopenic purpura
Authors: Wautier J , Kadeva H , Wautier M , Boizard B , Caen J 
Published: May 2019

Forty five patients with thrombocytopenia (Platelet count below 105/ul) have been studied. Platelet associated IgG (Plat IgG) was determined by the method of Dixon et al (Normal range 38 ± 16 x 10-16g). Circulating immune complexes were detected by the [3H] Clq precipitation and the PEG precipitation techniques.The sera were also tested for their thrombo-agglutinating activity (Aggl.). The results were:The [3H] Clq test and the PEG test were significantly more frequently positive in patients with high level of Plat IgG.The thromboagglutination seems to be independant of the level of Plat IgG. It could be correlated with the presence of circulating immune complexes in the serum.
A Chromogenic Factor X Assay With New Standardized Reagents
Authors: Friberger P , Lenne C 
Published: May 2019

A recently published method for Factor X (FX) assay (1) utilizing Russel's Viper Venom (RVV) and a chromogenic substrate has been further investigated by testing a large number of parameters. This method has been considered as a suitable method for monitoring coumarol treatment (Bergström et al).The conditions for the activation of FX by purified preparations of the RVV have been studied as well as the conditions for FXa determination with a new chromogenic substrate Bz-Ile-Glu(γ-piperidyl)-Gly-Arg-pNA (S-2337). Both purified factors and normal plasma have been used. The effect of plasma inhibitors as well as the selectivity of the method has been studied.The reproducibility and stability of the different reagents and standards have been studied and found to be good.The amount of FXa activity obtained from normal human plasma has been titrated with FXa inhibitors of known purity.1) Aurell L. et al, Thromb. Res., 11, 595 (1977)2) Bergström et al, Thromb. Res., 12, 531 (1978)
Abnormal Ristocetin-Aggregation of Platelets in Uraemia and on Haemodialysis Therapy
Authors: Woods H. F. , Turney J. , Weston M. J. 
Published: May 2019

Impaired platelet aggregation to ADP and collagen is recognised in uraemia and the loss of normal platelet function contributes to the prolonged capillary bleeding time observed in uraemia. in von Willebrand’s disease prolongation of capillary bleeding time is associated with impaired platelet aggregation to ristocetin because of a relative or absolute deficiency of the Factor VIII-Ristocetin Cofactor. We have studied platelet aggregation to ristocetin and Factor VIII coagulant activity (CA) and related antigen (RA) in 14 uraemic and 28 dialysed patients. Ristocetin aggregation (delta-0.D/min) was significantly less in uraemia (50 ± 21: m ± S.D) and in dialysis patients (38 ± 18) than in controls (78 ± 20). Factor VIII CA and RA were significantly higher in uraemic and dialysed patients than in controls.In crossover studies plasma from uraemic patients either enhanced or did not change ristocetin aggregation of normal platelets but plasma from dialysed patients impaired ristocetin aggregation of normal platelets. Plasma from dialysed patients was not contaminated by heparin. Thus in uraemia impaired platelet aggregation to ristocetin is unlikely to be due to a Factor VIII deficiency and may be due to a membrane defect as in Bernard-Soulier disease. in dialysed patients’ plasma there appears to be an additional circulating inhibitor of platelet-ristocetin interaction.
Molecular Properties of Bovine Hageman Factor
Authors: Claeys H. , Van Hoef B. , Collen D. 
Published: May 2019

Hageman factor was isolated from bovine plasma by CM-Sephadex, Ultrogel AcA-44 and DEAE-Sephadex chromatography, with a yield of 1.1 + 0.2 mg per liter plasma and a specific activity of 51 + 12 units per mg protein. The amino acid composition was similar to that reported for Human Hageman factor [Revak et al. 1974). The preparation previously characterized in our laboratory (Vth Cong. Paris 1975, Abstract n° 118) now appears to have been contraminated with a histidine rich protein. The present material could be adsorbed to and eluted from celite without loss of activity and without apparent generation of spontaneous activity.By SDS-polyacrylamide gel electrophoresis, two molecular forms of bovine Hageman factor could be distinguished : a single chain molecule with an estimated molecular weight of 80,000 and a two chain disulfide bonded molecule with mol. wts of 50,000 and 32,000. The amount of the two chain protein in different preparations varied between 0.25 and 1.00.Incubation with DF32P revealed that the two chain protein molecule was completely inhibited with the incorporation of 1.2 mol of DFP per mol of protein, whereas the single chain molecule did not incorporate DFP. These data suggest that the single chain molecule is a precursor form with inaccesible active site serine and the molecule in which the two chains are connected by disulfide bridge[s] is an activated or degraded form with accessible active serine. Similar structural properties have recently been described for human Hageman factor, in which the two chains of the activated form are however not disulfide linked (Griffin et al. 1976).
Arachidonic Acid Metabolites not Always Crucial for Thromboregulation?
Authors: Hornstra G. , Haddeman E. 
Published: May 2019

When blood platelets are triggered for aggregation, phospholipase A2 is activated resulting in the release of arachidonic acid (AA) from cell membrane phospholipids. AA is converted into prostaglandin endoperoxides (EP) by the cyclo-oxygenase enzyme system (CO). From EP’s, Thromboxane A2 (TxA2) is formed enzymatically. There is now considerable evidence that the AA-EP-TxA2 axis is of major importance for thromboregulation.However, recent findings indicate that under certain conditions an alternative regulatory mechanism may exist.In essential fatty acid (EFA-) deficient rats, platelets contain hardly any AA, the efficiency of which as a CO-substrate is severely depressed because of the competition of a fatty acid, specific of EFA-deficiency (C 20:3 n-9). The collagen- and thrombin-stimulated production of thrombogenic AA-metabolites (measured as malondialdehyde) is almost absent in EFA-deficient platelets. Nevertheless, platelet release is normal to increased.This finding points to a thromboregulatory mechanism different from the AA-EP-TxA2 axis. This, probably secondary, mechanism may be of significance for the prevention and therapy of thrombosis.
Oscillatory Response of Ristocetin Induced-Platelet Aggregation in Thrombasthenia
Authors: Chediak J. , Telfer M. , Vander Laan B. , Cohen I. 
Published: May 2019

Since the introduction of ristocetin as an aggregating agent for the diagnosis of von Willebrand’s disease, variable results have been reported on its effect on thrombasthenic platelets. The platelets from 10 thrombasthenic patients were subjected to aggregation with serially increasing concentrations of ristocetin. Unlike normal control platelets which showed normal irreversible aggregation using final concentrations of 1.25 mg/ml or higher, these platelets required increased concentrations of 1.8 and 2 mg/ml for maximal aggregation and intermediate concentrations (1.25 to 1.75 mg/ml) showed a cyclic oscillatory pattern of aggregation-disaggregation for 12–15 minutes, ending in partial disaggregation. If at this point creatine phosphate/creatine Phosphokinase (CP/CPK) or ATP were added the oscillatory pattern was reinstituted. Measurements of pH of the stirred platelet rich plasma (PRP) at the height and depth of oscillations changed only from 7.6 to 7.8 without correlation with the pattern. Incubation of the PRP with ADP prevented the ristocetin induced platelet aggregation; it was restored with the occurrence of oscillatory pattern upon addition of CP/CPK or ATP.The oscillatory phenomenon of thrombasthenic platelets in response to ristocetin is a unique finding. The constancy of the pH at different stages of the oscillatory waves ruled out the possibility of a gross electrostatic effect. The membrane defect reported in thrombasthenic platelets may play a role in these findings.
Platelet Aggregation in Patients with Ischemic Heart Disease, Transient Cerebral Ischemia and Peripheral Thrombo-Atherosclerosis
Authors: Gormsen J. , Nielsen J. D. , Andersen L. A. 
Published: May 2019

The threshold concentrations of ADP and adrenaline inducing platelet aggregation in vitro were determined in a Payton aggregometer in 90 normal controls, 30 patients with ischemic heart disease (IHS), in 34 with transient cerebral ischemia (TCI) and 22 with peripheral thrombo-atherosclerosis (PTA). The threshold concentrations were significantly lower in normal women ≥ 50 years old than in normal women < 50 years old.Compared with the corresponding control groups significantly lower threshold concentrations were found in following groups of patients: men and women ≥ 50 years with IHS (p < 0.005 and p < 0.001 respectively), men + women < 50 years with IHS (p < 0.05), men + women with TCI (p < 0.01), men + women ≥ 50 years with PTA (p < O.002 and p < 0.001 respectively), men + women < 50 years with PTA (p < 0.005).
Measurement of Nucleotide Pools in Platelets and Red Blood Cells Using High Pressure Liquid Chromatography
Authors: D’Souza L. , Glueck H. I. 
Published: May 2019

Release of adenine nucleotides during platelet aggregation is well established. The released adenosine diphosphate (ADP) is thought to cause secondary platelet aggregation. A high pressure liquid chromatographic technique has been used to measure accurately the various nucleotide pools in intact platelets, as well as their levels during various stages of aggregation. Accurate and highly reproducible measurements of 10-12 moles of all nucleotides are possible using the bonded microparticulate, Partisil −10 SAX column, a strong anion exchanger (Whatman Inc., Clifton, N. J.) and an electronic integrator. The method is a modification of an earlier method of P. Brown (1973), and G. Rao et al (1975). Using this technique we are able to obtain within 75 minutes a single step gradient separation of cyclic nucleotides (cAMP, cCMP, cGMP) as well as mono-, di-, and tri-phosphonucleosides. Sample sizes of 0.5 ml of platelet rich plasma are adequate for at least 3 estimations. Normal donor platelets show the following adenine nucleotide levels;* AMP 0.13 (0.14); ADP 1.64 (0.81); and ATP 4.90 (0.42) nanomoles per 1011 platelets. The method has certain advantages over the enzymatic or luciferase assays, since all the nucleotides can be simultaneously measured in a single step from a very small sample and there is no cross reactivity with any of the nucleotides. Similar studies of plasma and red blood cell nucleotides are possible with this technique.*Mean (standard deviation)
Kinetics of Thrombin Inhibition by Alpha2 Macroglobulin: Changes Induced by Prior Proteolysis of the Inhibitor by Trypsin
Authors: Tapon-Bretaudiere J. , Josso F. 
Published: May 2019

Plasma alpha2 macroglobulin (α2M) is able to inhibit serine esterases by a two-step reaction involving a first cleavage of the inhibitor molecule by the proteinase, followed by the formation of a molecular complex between the enzyme and the proteolyzed inhibitor. The rate of the inhibition reaction varies greatly from one proteinase to one another. Thus, α2M appears to be a ‘progressive” inhibitor of thrombin.Kinetics of thrombin inhibition by α2M was evaluated after prior treatment of the inhibitor by trypsin, either immobilized to avoid the secondary fixation of the enzyme to the proteolyzed inhibitor, or soluble, the enzyme excess being neutralized by soybean trypsin inhibitor (STI). In the second case, trypsin bound to α2M was assayed using a low molecular weight synthetic substrate (BApNA).When α2M was pretreated by immobilized trypsin, the reaction rate of the inhibition was increased without modification of the over-all neutralizing activity of α2M.Whenα2M was pretreated by soluble trypsin, it was found that STI in excess was able to displace trypsin bound to α2M. In these conditions, the treated α2M inhibited thrombin at a very rapid rate, the over-all neutralizing activity of α2M depending on the ratio STI/Trypsin.These findings demonstrate that (i) the binding of α2M to proteinases is reversible-(ii) the limiting factor of the inhibition rate of thrombin by «2M is the first proteolytic step of the inhibition reation.
Heparin and Venous Thrombo-Embolism
Authors: Kakkar V.V. 
Published: May 2019

Venous thromboembolism represents a serious hazard in patients confined to bed in hospital. Though the search for an effective method of prophylaxis has been going on for nearly the last 90 years, a method which is effective in the total elimination of this condition has yet to be developed. One promising approach is the use of low-dose heparin given subcutaneously.In this review: (a) the rationale for low-dose heparin will be considered in the context of present concepts of pathogenesis of venous thrombosis; (b) factors which govern the kinetics of clearance of heparin from the circulation will be compared following its intravenous and subcutaneous administration; (c) the recently published studies, where the efficacy of this form of prophylaxis against deep vein thrombosis and pulmonary embolism has been assessed, will be analysed, and (d) further possible developments in heparin prophylaxis includingthe use of semi-synthetic heparin analogue will be discussed.
Hypercoagulable State Expressed as the Molecular Increase in Theminute Population of Plasma Fibrinogen
Authors: Kazama M. , Maruyama Y. , Kinoshita T. , Matsuda J. , Nakamura I. , Abe T. 
Published: May 2019

It is expected that the hypercoagulable state would induce the qualitative alteration in the minute population of plasma fibrinogen.The plasmas of 120 cases were chromatographed on Biogel A-15m column and the elution profiles of fibrinogen complexes eluted at the initial part were analysed using staphylococcal clumping test on microtitration plate. The arbitrary scores for the hypercoagulability were given to each result according to the profile.

All of the normal plasma gave the profiles shown at the top of figures and the scores ranged 1-4. The plasmas of DIC used to give the profile shown at the middle with scores larger than 10, of which finding was highly coincident with the clinical diagnosis and sometimes more specific than any other test. The chromatography in cases of various thromboses including cerebral, myocardial and diabetes mellitus with vascular changes revealed the specific profile shown at the bottom with the scores 5-10. The thrombolytic therapy of these cases with urokinase resulted into the temporal disappearance of the specific profiles, but they re-appeared soon after the discontinuation of the therapy.
The Influence of Pivka II on Thrombin Generation in Liver Disease
Authors: Malia R.G. , Preton F.E. 
Published: May 2019

Thrombin generation and factor Xa activation have been studied in plasma samples from normal controls and from patients with various types of hepatic dysfunction. The patients were subdivided into groups according to the ratio procoagulant II/PIVKA II. PIVKA II was measured by Immunoelectrophoresis using a rabbit antibody raised against prothrombin. For those patients with a ratio greater than 0.70 the thrombin generation and Xa activation correlates well with the procoagulant factor II. Conversely patients with a ratio less than 0.5 exhibit inhibition within these same test systems. The administration of vitamin K abolishes this effect.It is concluded that PIVKA II plays an important role in the coagulation mechanism of patients with hepatic dysfunction associated with vitamin K deficiency.
Multiple Molecular forms of Factor VIII Antigen in Normal Individuals and von Willebrand’s Disease Patients
Authors: Zimmerman T. , Kimball J. , Edgington T. , Abildgaard C. 
Published: May 2019

Factor VIII antigen is present in normal individuals in multiple molecular forms which can be separated according to size. The smaller forms have little or no ristocetin co-factor activity. In order to evaluate the possibility that Factor VIII antigen forms of large size may be an artifact of in vitro aggregation, we have ultracentrifuged plasma on a 20% sucrose cushion at 37 C for 10 min at 254,000 xg (peak). The rate of clearing of Factor VIII antigen was compared to that of other plasma proteins. The results indicate that Factor VIII-related antigen forms of high S exist even when plasma is maintained at physiological temperature and analyzed with minimal delay, suggesting that these larger molecular forms also exist as such in vivo.In von Willebrand’s disease (vWd) all forms of Factor VIII antigen may be present but decreased in quantity (Type I) or large forms may be missing with smaller forms present in normal or increased quantities (Type II). Factor VIII antigen was isolated from plasma of three patients with Type I and three patients with Type II vWd by counter immunoelectrophoresis. The Factor VIII antigen was then reduced and electrophoresed on SDS-containing Polyacrylamide gels. The presence of carbohydrate was evaluated by staining with perchloric acid-Schiff’s reagent (PAS). The 210,000 MW Factor VIII antigen subunit from each patient was PAS-positive. Though subtle changes in carbohydrate content or composition could not be evaluated by this technique, a total defect of glycosylation is unlikely in this sample of vWd patients.
Case Histories
Authors: Evans Bruce E. , Cavalcanti Wellington 
Published: May 2019

Case 1. 71 year old Factor VIII 2.8%Diagnosis: five dental extractions, peripheral giant cell granulomaTreatment: local hemostatic agentsCase 2. 48 year old Factor VIII<1% (with inhibitor 100 B.U.)Diagnosis: four dental extractionsTreatment: local hemostatic agents; antifibrinolytic agentsCase 3. 36 year old Factor VIII 5.5%Diagnosis: 3 day old tongue lacerationTreatment: cryoprecipitate infusions; antifibrinolytic agentsCase 4. 26 year old Factor VIII<1%Diagnosis: 3 orthodontic extractions; 4 third molar extractionsTreatment: factor VIII concentrate infusions
Home Treatment for Children with Hemophilia
Authors: McWilliams N.B. , Ownby R. , Anderson L.C. 
Published: May 2019

Twenty-four hemophilic boys between the ages of 2 and 21, 4 with factor IX and 20 with factor VIII deficiency, have been on a home transfusion program for 2 to 22 months. Criteria for participation include: moderate or severe disease, family cooperation, accessible veins and attendance at Comprehensive Hemophilia Clinic. Strict guidelines are given to families for treating hemorrhages without physician consultation at home, versus those that must be seen by a physician.Only 1 child has required hospitalization for bleeding. One child has had clinical hepatitis on 2 occasions. No patient has developed an inhibitor. No complications related to nonprofessional I.V. administration have occurred. Of 18 boys tested for hepatitis B antibodies, 17 were positive. None has been positive for hepatitis B antigen. Of 12 boys with established severe arthropathy, 8 have had symptomatic improvement and 4 are stable. Of 12 boys with minimal or no arthropathy, all are stable except 1 who has developed chronic synovitis.Psycho-social benefits include a new found independence, improved living routine for family units and opportunities to participate in more activities. The mean cost/boy/month was $397.We conclude that home treatment for hemophilic children is both safe and effective and should be available to all children meeting the above criteria.
Are There any Differences in Thrombosis Prophylaxis and Side Effects Between Sodium and Calcium Heparin?
Authors: Bergqvist D. , Hallböök T. 
Published: May 2019

In clinical studies on low dose heparin both sodium and calcium heparin have been used but no comparative investigation has been made. The aim of this study therefore was to perform a double blind randomized comparison between sodium and calcium heparin on prophylaxis of postoperative thrombosis and possible side effects. 75 patients were included in the study, 39 receiving sodium heparin and 36 calcium heparin (Heparin Vitrum from the same heparin batch was used and the following dosis schedule was followed: 5000 IU s.c. 2 hours preoperatively and then every 12th hour for 5 days). The injection was given on the lateral aspect of the thigh. Deep vein thrombosis was diagnosed with 125I-fibrinogen test. The activity over the site for heparin injection was also measured. The patients were interviewed by a nurse for local reaction and she also judged haematoma formation from photographs. Bleeding tendency was measured as blood loss during operation and total transfusion need. The groups were comparable concerning age, sex and type of operation. The frequency of thrombosis was 40% in the sodium heparin group and 43% in the calcium heparin group, and the blood loss 318 and 454 ml respectively (p>0.05). There were no differences in the patients’ subjective local reaction to heparin injection or haematoma formation judged from the photographs. Nor did the 125I-fibrinogen activity over heparin injection sites differ between the two types of heparin.This study has thus shown that sodium and calcium heparin are identical from the point of view of prophylaxis of postoperative deep vein thrombosis and side effects, provided that the heparin batch is the same in both.