bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of Vitamin K on Pivka and its Associated Procoagulant Proteins in Liver Disease
Authors: Malia R.G. , Preston F.E. , Blackburn E.K. 
Published: May 2019

Vitamin K deficiency is associated with low procoagulant activity of the vitamin K-dependent clotting factors together with normal concentrations of an immunologically cross-reacting protein associated with the appropriate clotting factor.In this study we have examined the response of the clotting factors II, VII and X together with their appropriate related antigens to the intravenous administration of vitamin K1 in 14 patients with various forms of liver disease. We have also related the observed changes to alterations of the inhibitor activity of PIVKA as detected by the modified thrombotest.A relationship has been established between the rate of appearance of procoagulant activity and the rate of disappearance of PIVKA after the intravenous administration of vitamin K1 in those patients with thrombotest inhibitor activity. In this same group of patients it can also be shown that PIVKA is physico-chemically dissimilar to the related protein of normal individuals.Patients without thrombotest inhibitor activity appear to synthesise decreased amounts of a structurally normal protein which is not influenced by vitamin K.
In Vitro Spontaneous Platelet Aggregation in Cerebrovascular Disease
Authors: Cate J.W.ten 
Published: May 2019

Fifty patients from a group of 130 patients with transient ischemic attacks or cerebral infarction were found to demonstrate in vitro spontaneous platelet aggregation (SPA). This phenomenon occurred within 15 minutes when platelet-rich plasma samples (PRP) of these patients were stirred at 37°C in an aggregometer.In addition all patients showing SPA also demonstrated a lowthreshold concentration for the onset of ADP-induced second wave aggregation (ADP f.c. < 0.25 uM; normal range 0.75 + 0.2 uM). Of the remaining 80 patients 25 patients were found to be sensitive tolow concentrations of ADP.SPA remained present in samples of 8 patients studied when stored at room temperature for two hours. SPA was found to be dependant upon the presence of divalent cations and could be prevented by adenosine, phentolamine and aspirin. The following additional findings point towards a possible platelet defect:1. Platelets from 10 patients with SPA when isolated and resuspended in normal plasma still demonstrated SPA while isolated normal platelets in patients did not.2. Platelets demonstrating SPA showed an increased aggregation tendency upon incubation with ADP while normal platelets developed the expected refractory state for ADP.
Chronic Idiopathic Thrombocytopenic Purpura (ITP) 51-Cr-Platelet Kinetics and Splenectomy in 197 Patients
Authors: Gugliotta L. , Isacchi G. , Motta M. R. , Guarini A. , Bachetti G. , Mandelli F. , Tura S. 
Published: May 2019

51cr-Platelet Kinetics was studied in 197 patients with Chronic ITP of which 111 were submitted to splenectomy after the study.Platelet half life-span was always decreased (< 24 hours).Platelet, sequestration was splenic, spleno-hepatic, hepato-splenic, hepatic and diffuse in 56%, 18%, 1%, 6% and 19% of patients respectively. Platelet life-span and sequestration were not correlated with sex, age, platelet number, duration and severity of disease.101 patients with splenic and spleno-hepatic platelet sequestration underwent splenectomy. Their follow-up is 1-5 years. Complete (steady platelet level > 150,000μl) or partial (platelet level in between 80,000 and 15,000/μ1) remission was obtained in 83% and 6% of them respectively. In 10 patients with non-splenic platelet segue-stration complete and partial remission’after splenectomy were observed in 5 and 1 gases respectively.
51Cr-Platelet Kinetics is a reliable and useful predictor of the therapeutic value of splenectomy. However splenectomy should be considered also in selected case with non splenic platelet sequestration.
Hereditary Hypodysfibrinogenemia with Defective Release of Fibrinogenopeptide A (Fibrinogen Freiburg)
Authors: Böttcher D. , Hasler K. , Köttgen E. , Maurath J. 
Published: May 2019

A new autoaomally inherited hypodysfibrinogenemia was recognized in four members in three different generations of a family. Only one patient had a major bleeding episode after trauma, the other affected members had no history of excessive bleeding or thromboembolic disease.The thrombin time and Reptilase time of plasma were greatly prolonged and partially corrected by the addition of calcium. Patient plasma prolonged the thrombin time of normal plasma. Fibrinogen levels ranged between 10 to 20 mg/100ml when measured as thrombin-clottable protein, whereas immunologically the fibrinogen levels were only slightly reduced.Functionally the major defect was impaired release of fibrinogenopeptide A upon incubation of the purified abnormal fibrinogen (94% clottable protein) with thrombin and Reptilase. The abnormal fibrinogen showed a delayed polymerisation of its purified fibrin monomers. The described abnormal fibrinogen was indistinguishable from normal fibrinogen by polyacrylamide gel electrophoresis with and without sodium dodecyl sulfate.
Ultramicroscopio and Coagulation-Fibrinolytic Findings Induced by Tissue Thromboplastin
Authors: Nagata H. , Seya T. , Oguma Y. , Yamauchi M. , Murakoshi T. , Hasegawa H. 
Published: May 2019

We have studied the ulerastructures of t issue thromboplast in (T. Tbp) to demonst rate how It changes during coagulation.[Haterials and Methods]T. Tbp from lungs of rabbits was used for these studies. It was injected into ear veins of rabbits. Lungs were resected at several seconds, 10sec, 1 min, 5 min, 24 hrs or 48 hrs after the injection. Tljey were examined by transmission electron microscope.[Results] Concentrically arranged membrane structures of the injected T. Tbp disappeared in extremely short time after the injection.1 min after the injection, fibrin fibers were seen between single sheet of membrane and endothelial cells of capillaries. In the rabbit which had died suddenly after the injection of T. Tbp, multiple pulmonary thrombi made of fibrin and platelets were seen In capillaries. The endothelial cells of capillaries were destroyed and interstitial tissues were edematous.The hypercoagulable state was seen 10-30sec after the start of the Injection, indicating the shortening of r of TEG. Then, It gradually returned the level before injection. Moreover, changes of the measurements of fibrinogen, antiplasmin and prekallikrein were also seen after the injection.
Endotoxinaemia, Granulocytic Elastase Release (ELP), Coagulation Disorders and a ANtiprotease Behaviour in Cercopithecus Aethiops and Patients with Septicemia
Authors: Hofmann A. , Hofmann U. , Weinmann E. , Egbring R. , Havemann K. 
Published: May 2019

A.)As Aasen (1978) demonstrated, a rapid increase of granulocytic elastase in plasma occurs in dogs following the slow infusion of endotoxin. Working with green monkeys, we did not find severe thrombopenia, leucopenia, coagulation defects and ELP until after two high doses of E. coli endotoxines. Using two-dimensional-immunelectrophoresis ELP could be detected as a complex with α1AT. The coagulation defects occurring in both type’s of animals may be due to DIC and/or to direct proteolysis caused by released ELP, since i.v. administered ELP also leads to an increased consumption of coagulation factors.B.)Out of 80 patients with either proven or supposed septicemia, we found 40 with possitive endotoxine test results, half of whom had α1C -AT-ELP-complexes im plasma, as proven in one-dimensional-immunelectrophoresis. As expected, the coagulation defects were most distinctly reduced in these 20 patients, while α1AT arise α2M are found to be reduced.
Amino acid Sequence of a Peptide from Type III Collagen Involved in Platelet Adhesion
Authors: Fauvel F. , Legrand Y.J. , Bentz H. , Pignaud G. , Kühn K. , Caen J.P. 
Published: May 2019

The probable importance of the role of type III collagen in the initiation of thrombosis is due to its localization in the subendothelial layers of the vessel wall.The adhesion of platelets to type III has been therefore quantified by a method based on the filtration of non-adhesive 14C 5HT-labe11ed platelets through a Sepharose 2B column.Type III collagen was purified from calf skin by pepsin extraction and salt precipitation. Type III collagen was cleaved by cyanogen bromide and the adhesion induced by the resulting peptides was measured. The activity was attached to the central alpha l(III) CB4 peptide which was further cleaved by hydroxy lamine, chymotrypsin and trypsin. An adhesive potency was linked to three fragments (HA 1 obtained by hydroxylamine, C2 by chymotrypsin and T2 by trypsin) which possess a common portion of 9 amino-acids, localized in the central part of the alpha l(III) CB4 peptide and of the entire alpha 1(III) Chains, which probably represents the active part of type III collagen. Its activity could be due to a particular sterical conformation linked to the presence of 3 imino acid residues in the sequence Gly-Lys-Hyp-Gly-Glu-Hyp-Gly-Pro-Lys of this fragment.
Toxicity in Mice of Factor IX Concentrates
Authors: Magner A. , Aronson D.L. 
Published: May 2019

The use of Factor IX concentrates has been associated with thrombo-hemorrhagic problems presumed to be due to activated coagulants. High doses of Factor IX (2000 μ/kg) injected IP into mice result In death between 4 and 24 hours. Reduction with dithiothreitoi removes the toxic effect but no reduction IX toxicity is seen with enzyme inhibitors (DFP, soybean trvpsin inhibitor or heparin). Activation of the Factor IX concentrate by insoluhilized Kussells Viper Venom and Ca# yielded a decreased mortality despite a non-activated partial thromboplastln time of 20" at a 1/5000 dilution.These results implicate components other than activated components of the Vitamin K dependent enzymes In the toxicity of Factor IX concentrates.
Vital Microskopic Observation of Fluorescent Labelled Platelets
Authors: WeBelmarm G. , Kortenhaus H. , Schröer H. 
Published: May 2019

Platelets from platelet rich plasma (PRP) of Wistar rats were labelled by incubation with fluoroisothiocyanate (FITC) in Ringer-citrate-dextrose solution. Labelled platelets were reinjected into a tail vein of a rat previously prepared for vital-microscopic observation of the mesenteric vasculature. Using a low-level-light camera, labelled platelets could be observed by a fluorescence technique as distinct luminescent particles moving with the blood stream, and their rheological behaviour could be observed.
Results: Platelets moved with different velocities in the same vessel. Single platelets stuck temporarily to the vessel wall but no aggregation was observed. Extensive sticking has been observed in places of leukocyte-rolling. Using the described method it should be possible to alter platelets in vitro and to observe their behaviour in vivo after reinjection.
The Influence of Antiplatelet Drugs on Platelet Survival After Aortic Damage or Implantation of a Dacron Arterial Prosthesis
Authors: Wilkinson A.R. , Hawker R.J. , Hawker L.M. 
Published: May 2019

The effect of antiplatelet drugs on platelet survival, as measured by indium-III labelled platelets was studied in two groups of surgically treated animals. In the dog, platelet survival and loss were measured following surgery and implantation of a dacron arterial prosthesis. These same parameters were measured after aortic damage in the rat. Animals treated with the antiplatelet drugs, sulphinpyrazone and ticlopidine were compared with controls. In the dog, the sulphinpyrazone treated animals had a significantly increased platelet survival and decreased platelet loss following surgery (p<0.05). In the rat both ticlopidine and sulphinpyrazone showed significantly increased platelet survival and decreased loss of platelets following surgery when compared with controls (p< 0.001).We conclude that both ticlopidine and sulphinpyrazone merit evaluation as potential agents for reducing the risk of thrombotic occlusion in peripheral vascular disease and also in patients with arterial prostheses.
In Vitro Anticoagulant Activity of Esters of Heparin.
Authors: Mardiguian J. , Trillou M. , Marin J. 
Published: May 2019

Chemical modification of Heparin by esterification of its hydroxyl groups has been carried out in order to study its influence on the in vitro anticoagulant activity. Beef and pig mucosal Heparins have been fractionated by gel filtration and by ion-exchange chromatography to yield fractions which have been esterified.Two types of esters have been prepared : 4-chlorophenoxy-acetic and 4-chlorophenoxy-isobutyric.The anticoagulant activity of the these esters has been evaluated in vitro (using U.S.P. method, anti-Xa and anti-thrombin assays) and correlated with their chlorine content and U.V. absorption.This study shows that the in vitro anticoagulant activity of heparin is decreased by esterification of its OH groups, to an extent depending upon the type of ester, the molecular weight and the degree of substitution.The results of these experiments will be reported and discussed in detail.
Abnormal Factor VIII Molecule in Mild Von Willebrand’s Disease
Authors: Castillo R. , Maragall S. , Labal F. , Monteagudo J. , Ordinas A. 
Published: May 2019

In 22 cases with normal levels of the three entitles of factor VIII (VIII:C, VIIIR:AG and VIIIR:WF), FVIIIR:AG showed afaster anodal mobility and a lower concentration measured by immunoradiometric assay than that found with Laurell’s immunoelectrophoresis. Moreover, the factor VIII protein elution by agarose gel filtration of plasma and cryoprecipitate was delayed. Seven of those cases belong to a family in whom one of the member showed frequent bleeding episodes. In these individuals the FVIIIR;AG precipitation with Concanavalin A was determined and appeared decreased.On the other hand in 19 out of 20 subjects with classic moderate von willebrand’s disease (in whom the three entities of factor VIII were occasio nally reduced in parallele), FVIIIR:AG also showed a faster anodal uob{ 1-ty and the factor Vln protein elution by agarose gel filtration was delay ed.All these results suggest that patients with moderate von Willebrand’s disease show a qualitatively deficient factor VIII molecule synthesis, while the mildest cases may have normal levels of the three entities of the factor VIII.
Differential Reactivity of Three Specific Anti-VIII:C Antibodies in Haemophilia a Patients
Authors: Lavergne J.M. , Girma J.P. , Meyer D. 
Published: May 2019

Specific anti:VIII:C antibodies in three haemophilia A patients (high responders, cases 1-3) were purified by two proceduses. In a solid phase system, 125-1 IgG containing antiVIII:C antibodies was incubated with purified Factor VIII coupled to CNBr-activated Sepharase 2B. Specific antibodies were eluted using HCl-glycine buffer, pH 2.4 or 3.5.In a liquid phase system, 125-I IgG was incubated with Factor VIII; following precipitation with 3.5% PEG, the specific immune complexes were recovered by gel filtration.Anti-VIII : C antibodies were isolated by issociation at pH 2.4 or 3.5, followerd by Sephade x G 200 gel flltration. Using antibodies from case 1 (titre 1,000 Oxford IJ./ml), obtained by both procedures: a two-site IRMA demonstrated no VIII:C-Ag in twelve severe haemophllla A patlents and a normal amount in two haemophilia A+ patients. Cases 2 and 3 had a lower anti-VIII:C titre (100 anrl 150 U./ml) but their antibodies showed, in plasma, a hlgher affinlty for VIII:C-Ag than those of case 1. The affinity was estimated by displacement of the bound radioactivity in IRMA by competitive inhibition. Antibodies from case. 2 failed to dissociate from VIII :C-Ag at pH 3.5 or 2.4. Antihodies from case 3 did not dissoclate at pH 3.5 and only at pH 2.4 but were ineffective in the two-site IRMA. These results suggest that 1) there is no relationship between titre and affinity of anti-VIII:C antibodies; and 2) with the procedures of purification available only those antibodies with a high titre (≥1,000 U./ml) may be of use in IPMA.
Identification of Heterozygotes for Hemophilia B and VWD by Discriminant Analysis
Authors: Graham J.B. , Elston R.C. , Miller C.H. , Goldin L.R. , Kasper C.K. 
Published: May 2019

Published data from California (Blood 50:351, 1977) and unpublished data from N.C. on carriers of hemophilia B were examined statistically to determine the optimal methods of identifying the carriers. Factor IX:C assays were available on both groups, and IX:Ag assays were also available on the California women. Linear and quadratic discriminant analysis, univariate and bivariate, with and without the “jack-knife” procedure were utilized. The carriers from California were divided into 29 CRM- and 18 non-CRM-(CRM+) from the phenotypes of their male relatives. It was found that univariate linear discriminant analysis of IX:Ag assays was optimal for CRM- carriers, and l inear bi variate ana lysis of IX:C and IX:Ag assays for CRM+ carriers.Identifying heterozygotes for vWd was done most efficiently (81%) by trivariate linear I discriminant ana lysis utilizing assays for VIII:C, VIIIR:Ag, and VIIIR:WF. This was superior to: i) any single test alone (VIII:C; 15%, BT;17%, VIIIR:Ag;27%, VIIIR:W F;42%), ii) abnormal ratios (23%), and iii) one ab normal test of any type (58%). It was possible to identify asymtomatic “transmitters” as heterozygotes, even some who had all tests in the normal range.
Pathways of Blood Clotting Initiation by Cancer Cells
Authors: Semeraro N. 
Published: May 2019

Although available information indicates that cancer cells may activate blood coagulation, the precise mechanism remains still uncertain. A procoagulant with characteristics of tissue thromboplastin has been found in human benign and malignant tissues and in some experimental tumors. On the other hand it has been reported that extracts from malignant tissues directly activate coagulation factor X, due to the presence of a serine protease. We have investigated the procoagulscitic fluid. Cells from Lewis lung carcinoma (primary and metastasis), Ehrlich carcinoma ascites and JW sarcoma ascites were able to shorten markedly the recalcification time of normal, factor VIII and factor VII-deficient, not of factor X-deficient human plasma. The same cells did generate thrombin when mixed with a source of prothrombin and factor X, absorbed bovine serum (as a source of factor V), phospholipid and CaCl2.Cells from Sarcoma ISO ascites were completely inactive in both test systems. It was a included that cells from some experimental tumors, similarly to normal platelets, possess the capacity to directly activate coagulation factor X. This suggests the existence of an alternative “cellular” pathway in blood clotting initiation distinct from both the intrin sic and extrinsic mechanisms.(Supported by Italian CNR and NIH, NCI, USA).
Beta Thromboglobulin and Myocardial Infarction
Authors: Hughes A. , Daunt S. , Vass G. , Wickes J. 
Published: May 2019

Beta thromboglobulin. a platelet specific protein liberated during the release reaction, has been measured in normal individuals (n=285),and in patients presenting with acute chest pain. The latter group consisted of those with acute myocardial infarction (n=19),those with acute myocardial ischaemia (n=21),and those with chest pain of non cardiac origin (n-7). In the patient groups beta thromboglobulin was measured on admission to hospital, and thereafter daily until the patient was discharged. There was no significant difference between the normal population (mean 22.5 ng/ml),and the patients with with non cardiac chest pain (mean .24 ng/ml). There was a significant difference between the normal population and the patients with acute myocardial infarction (mean 34 ng/ml),and acute myocardial ischaemia (mean 33 ng/ml), p<0.001. There was also a significant difference between these two groups and the patients with non cardiac chest pain, p<0.01.We would conclude that platelet activation occurs in acute myocardial infarction and ischaemia, but it is not clear if this is a primary or a secondary phenomenon.
Hog and Beef Mucosal Heparin - In Vitro Study Using Different Assay Procedures
Authors: Aiach Martine , Kher A. , Mardiguian J. 
Published: May 2019

In a previous study, on healthy volunteers two purified heparin preparations, obtained from hog and beef mucosausing the same manufacturing procedure, were compared for anticoagulant activity. Heparin levels measured by anti Xa assays and AFTT were not statistically different following subcutaneous or intravenous heparin injection, (M. Aiach, A. Kher, A. Kichaud, J. Mardiguian, M. Trillou, M. Leclerc - Thrombosis Research, to be published). An in vitro study was undertaken to evaluate the biological activity of these two heparins : thrombin clotting time was performed in plasma. Anti Xa activities were compared in purified system using human antithrombin III, or in plasma, and bovine and human activated factor X were used. Residual F Xa was evaluated with chromogenic substrate and in a clotting assay. The results will be reported in detail.In conclusion, the biological activity in vitro is higher for hog mucosal than for beef mucosal heparin when evaluated with sensitive and accurate methods. The in vivo study does not confirm these data. This discrepancy between in vitro and in vivo studies could be explained by individual variation of in vivo response to heparin and by dissimilarities in the distribution of molecular weight between these two heparins.
Effect of Metabolic Control with Insulin on Plasma von Willebrand Factor Activity Growth Hormone, and Platelet Aggregation in Diabetes Mellitus
Authors: Colwell J.A. , Gonzalez J. , Sarji K.E. , Nair R.M.G. , Sagel J. 
Published: May 2019

Elevated plasma von Willebrand factor activity (ristocetin method:VIIIR:WFj and high plasma growth hormone (GH) levels occur in diabetes mellitus. Hypersensitivity of plate lets to aggregating agents is also seen. We have therefore studied the effect of short-term diabetic control with insulin on plasma VIIIR:WF, GH, and platelet aggregation.Tight metabolic control with insulin was instituted for two weeks in five insulin depend ent diabetic patients after a period of inadequate diabetic control. Overnight sleep studies were performed before and after the period of closely monitored insulin administration, and frequent determinations of plasma glucose, VIIIR:WF, and GH levels were done during sleep. Platelet aggregation thresholds to ADP, epinephrine, and arachid’lic acid were measured before and after tight control.We found that: (1) elevated plasma VIIIR:WF levels in diabetics persist during overnigh sleep, but were not altered by wide swings in GH levels; (2) short-term careful diabetic control with insulin lowered plasma VIIIR:WF levels towards normal in the majority of subjects tested; and (3) increased sensitivity of platelets to aggregating agents appeared during tight insulin therapy in those subjects studied.