bluuebunny/crossref_metadata_2025_split huggingface dataset:
Von Willebrand Factor And Platelet Deposition On Artificials Surfaces
Authors: Maisonneuve P , Pusineri C , Farges J P , Sultan Y 
Published: July 2018

Deposition of purified 125I. Von Willebrand factor (VWF) and 51Cr platelets on well characterized artificial surfaces (Rhone Poulenc Lab.) were studied in the in vitro circulcti.cn system of Baumgartner. Free silica silicone rubber, cationic and anionic polyelectrolyte complexe (PEC) were directly synthetised on the central rode of the perfusion chamber. Concentration of 125I VWF varying from 80 ug/ml to 1,5.103 ug/ml were circulated for 10 mn at a shear rate of 800 sec-1 On all surfaces VWF deposition is correlated with the VWF concentration in the circulating solution. With regard to the nature of the surfaces : whatever the concentration of VWF,silicones fixed hundred times less than PEC and among PEC the positively charged surfaces fixed 3 times more VWF than negatively charged PEC.Similarly 51Cr platelets resuspended in whole blood were studied in the same system at the same shear rate after 10 mn of circulation. It was found that platelet adherence on the various types of surfaces paralleled VWF deposition. In contrast no correlation between 125I Fibrinogen and platelet fixation on the surfaces was found.In another series of experiments the role of VWF on platelet adhesion to surfaces was tested. It was observed that fixa- tion of normal platelets resuspended in the blood of a severe VW patient was identical to the fixation of platelets resuspended in normal blood. And this was verified after 1,
3, 5 and 10 mn of circulation, assuming that platelet fixation, at least in these experimental conditions, is independent of the presence of VWF in the system and that the plateau is reached before the first minute of contact. It is more likely that the amount of VWF, fibrinogen and the number of platelets deposited on a surface are related to the intrinsic properties of this surface and characterize the surfaces. These results showed that, platelets and VW factor do not interact on artificial surfaces as it has been demonstrated for the subendothelium of the vessel wall.
Interaction Of Lectins With Human Platelet Membrane Glycoproteins In Crossed Immunoelectrophoresis
Authors: Zonneveld G T E , Roozeboom R , Sturk A , ten Cate J W 
Published: July 2018

Plasma membranes of human blood platelets contain a large number of glycoproteins (GP). It has been shown that these GPs play a major role in platelet function. Our aim is to isolate and characterize the GPs. Isolation can be achieved oy affinity chromatography. Crossed immunoelectro-phoresis CIE) was found to be an easy technique to test the usefullness of certain lectins. Rabbits were immunized with bound material of a Lens culinaris column. The antiserum obtained gave 2 precipitates in CIE against solubilised membranes. The slow moving precipitate consisted of GP IIb and IIIa. Several lectins were tested in the intermediate gel technique. Wheat Germ Agglutinin, soybean lectin and Riccinus communis 60 (group 1) interacted with the slow moving precipitate, while Pisum sativum, Ulex Europeus and leucoagglu- (group 2) only showed interaction with the fast precipitate. Riccinus communis 120 affected both precipitates. Helix pomatia and limulus lectin were without effect. A combination of affinity chromatography with a lectin of group 1 and a lectin of group 2 seems useful for isolation of GP IIb and IIIa.The interaction of lectins of different sugar specificity with the GPs in CIE are indicative for their lectin binding characteristics.
The Effect Of A Vasoactive Substance On The Fibrinolytic Activity Of Varicotic Veins And Experimental Thrombosis
Authors: Haas S , Von Eckstädt A Vitzthum , Wriedt-Lübbe A , Söhnchen R , Lill G , Blümel G 
Published: July 2018

Benzaron (2-Äthyl-3(4’-hydroxy-benzoyl)-Benzofuran)is used as a vasoactive substance in phlebology. In order to study its effect on the fibrinolytic activity of varicotic veins and thrombosis,two studies were performed.Study 1: 60 patients with stripping operations were randomly divided into two groups. One group was treated with benzaron 200 mg t.d.s.for two weeks,whereas the control group did not get any medication. Intraoperatively,a one cm segment was taken from the varicose vein and a one cm segment was excised from the vena saphena magna. The tissue specimens were shock frozen and later on,the fibrinolytic activity was determined by fibrinolysis autrography according to TODD.The intensity of lysis was estimated according to the classification of PANDOLFI.After treatment with benzaron,the fibrinolytic activity of the intima of the varicotic veins and the vena saphena magna was significantly increased in comparison with the control group.Study 2: An experimental thrombus formation was induced by endothelial lesion..This was performed by exposure of a one cm segment of the left jugular vein to hypothermia of-10°C for two minutes. The rats were pretreated with benzaron or placebo.24 hours later the thrombus size was determined by measurement of the weight using an analytical balance.In comparison with the control group the thrombus size was markedly reduced in the benzaron group.Conclusion:The reduction of venous thrombus formation after treatment with benzaron might be due to the enhancing effect of the substance on the fibrinolytic activity of the vessel wall. These findings should be considered in therapy of patients with reduced plasminogen activators in veins,e.g.in patients with varicosis.
Complex Formation Between Prothrombin And Staphylocoagulase
Authors: Lindhout M , Hendrix H , Hemker H 
Published: July 2018

Staphylocoagulase is a protein secreted by certain strains of Staphylococcus aureus. Addition of the extracellular protein to a human prothrombin preparation results in the generation of a thrombin-like activity.Our investigations on the prothrombin-staphylocoagulase interaction was undertaken in order to establish the kinetics of the complex formation, the mechanism of activation of prothrombin by staphylocoagulase and the enzymatic properties of the complex.Evidence for the formation of a equimolar complex between prothrombin and staphylocoagulase was obtained fromgelelec- trophoresis and titration experiments. The procedure,in order to study the kinetics of the complex formation, made use of a coupled assay in which D-Phe-Pip-L-Arg-p-nitroanilide hydrolysis by the complex was monitored. The second rate constant of the complex formation, as determined from pseudofirst order kinetics, is 4×l06sec-1M-1. The dissociationconstant of the complex was determined to be orders of magnitude less than 10-11M. Using 3H-DFP, no exchange was observed between prothrombin in the complex with free prothrombin. Analysis of the complex by gelelectrophoresisin the presence of Na-dodecyl sulfate and mercaptoethanol shows that proteolysis cannot account for the generation of thrombin-like activity. Small amounts of degradationproducts (prethrombin 1) were found.Thrombin-like activity was generated as a result of the interactions between staphylocoagulase and human prethrombin 1, human prethrombin 2 and bovine prethrombin 2. Indications for an interaction between staphylocoagulase and thrombin were obtained from experiments with anti-thrombin III and hirudin. Identical enzymatic properties of thrombin and the prothrombin-staphylocoagulase complex were observed towards small synthetic substrates and fibrinogen. No activity of the complex towards factor V, factor VIII and platelets was found.
Reduced Arteriosclerotic Plaque Thrombus Formation
Authors: Dujovny M , Kossovsky N , Loubeau J-M , Segal R , Nelson D 
Published: July 2018

Sixty surgical patients with cerebrovascular accidents and angiographically diagnosed carotid plaques were divided into two groups: .1) pre-treatment with aspirin (650mg/day) and dipyridamol (25mg/tid) (42 patients); 2) no treatments (18 patients). The control group consisted of 10 autopsy of patients dying for unrelated cause.SEM examination of the endarterectomy plaque revealed intact red blood cells in 12 of 42 pre-treated and 18 of 18 untreated specimens; degenerating red blood cells and cell fragments (24/42, 18/18); fibrin (24/42, 18/18) and white blood cells (15/42, 18/18). These were frequently enmeshed in large surface thrombi. Cholesterol crystals (6 μm) were matted on the plaque surface (12/42, 15/18), and spherical globules averaging 3 to 10 μm sporadically blanketed the surface (6/42, 6/18). Plaque from the asymptomatic controls was smaller and less thrombotic. Energy dispersive analysis x-rays (EDAX) of the inner surface of all 70 specimens (50 years old +) revealed surface calcium deposits and nodules in 18 of the surgical cases (12/42, 6/18), and diffuse calcium deposits in 6 controls.Treatment with aspirin and dipyridamol significantly reduces plaque thrombosis.
The Effect Of Dexamethasone On Basement Membrane Produced By Cultured Human Endo Thelial Cells
Authors: Piovella F , Ricetti M M , Almasio P , Ascari E 
Published: July 2018

Human endothelial cells from umbilical cord vein were grown to confluence on glass coverslips placed in Petri di= shes, in the presence or absence of dexamethasone. After ten days in culture, the cell monolayers were washed and treated with 0,5% Triton X lOO in Hank’s solution , The detergent-treated slides were then washed in Hank’s and examined by indirect immunofluorescence for fibronectin utilizing monospecific antibodies. Basement membranes produced by dexamethasone-treated cells showed a more intense fibrillar network of extensively overlapping fluorescent fibers if compared with controls.The effect of these pre-formed basement membranes on cellular spreading was subsequently studied. Human endothelial cells , previously grown in culture medium with out steroids, were detached by trypsin-EDTA solution,washed and cultured on the slides covered with the extracel lular matrix pre-formed in the presence or absence of dexamethasone. The higher fibronectin content of basement membranes pre-formed in the presence of dexamethasone allowed a more rapid attachement and a better spreading of endothelial cells if compared with control pre-formed basement membranes.
Intraplatelet And Plasma Serotonin Level In Normal Subjects And In Patients With Cerebrovascular Diseases
Authors: Kita E , Horiike N , Kyoi K , Utsumi S , Umegaki K 
Published: July 2018

Intraplatelet and plasma serotonin(5-hydroxytryptamine:5- HT) was assayed spectrophotometrically using O’phthaldialdehyde as the fluorescence inducer depend on the method of Durmmond and Golden, in 69 healthy volunteers and in 69 patients with various kinds of cerebrovascular diseases such as acute cerebral thrombosis within 72 hours from onset (13 cases), chronic cerebral thrombosis during 2 to 48 months from onset(27), and T I A(ll), RIND(2), S A H(5), intracerebral hematoma(7) and recurrent cerebral thrombosis under treatment.In normal controls, intraplatelet 5-HT level had the tendency of gradual decrease with the aging, on the other hand, plasma level of 5-HT in same subjects showed slight increse in elder groupe.In acute complete thrombosis, intraplatelet 5-HT level was significantly low compared with age matched controls with slightly elevated level in plasma. In the reversible stroke such as T I A and RIND, intraplatelet level was low as same as complete cases, but plasma level was within normal range. In other C V D, none of them showed significant change of 5-HT level either in platelet or plasma.Recurrent cerebral stroke patients under various periods of different treatment had enormous high level of intraplatelet 5-HT level with normal value of plasma.Above mentioned results suggest that in acute thrombusforming state, intraplatelet 5-HT level is reduced or we may say there circulate “exhausted” platelets in the plasma.
5'-N-Ethylcarboxamidoadenosine (NECA) Is A Potent, Stereospecific Inhibitor Of Human Platelet Aggregation
Authors: Cusack N J , Hourani S M O 
Published: July 2018

Adenosine is a vasodilator, and also inhibits platelet aggregation apparently by acting at an external membrane receptor to increase levels of platelet cyclic AMP. Certain analogues of adenosine retain activity as vasodilators, and also inhibit platelet aggregation by raising levels of platelet cyclic AMP. NECA is an extraordinarily potent vasodilator, so its effects on human platelet function were tested.NECA (1 μM) inhibited human platelet aggregation induced by ADP, 5-HT, thrombin and adrenaline mere powerfully than adenosine (1 μM). NECA, even at micrcmolar concentrations, was 5 to 10 times more potent than adenosine as an inhibitor of aggregation induced by ADP (5μM or 200μM) or adrenaline (200μM). NECA (Ka = 0.95μM) caused increases in levels of platelet cyclic AMP, which could be competitively inhibited by theophylline (Ki = 8μM), an adenosine receptor antagonist. However, here NECA was only about
1.3 times more potent than adenosine (Ka = 1.2μM). The effects of NECA, like those of adenosine, were completely stereospecific, the L enantiomer of NECA being inactive. NECA (10μM) did not prevent inhibition of PGE1-stimulated adenylate cyclase by ADP (5 μM).NECA is the most potent analogue of adenosine yet tested on human platelets, and is the first example of a 5' modification to retain significant inhibitory potency.
Human Fibrinogen Binds Edta And Citrate
Authors: Nieuwenhuizen W , Vermond A , Hermans J 
Published: July 2018

It was shown that EDTA and citrate make the carboxy-terminal parts of the γ-chains of fibrinogen more susceptible to plasmin degradation. This is an effect independent of the calcium-chelating properties of those compounds. Furthermore, EDTA prolongs the thrombin times decreases the heat stability and causes the formation of abnormal clots.This suggests a direct interaction of EDTA (and possibly also of citrate) with the fibrinogen molecule thereby causing a conformational change. The interaction of citrate and EDTA with fibrinogen was measured by direct binding studies (equilibrium dialysis).It was found that at pH 7.5 human fibrinogen binds 3.4 molecules of citrate with Kd = 1.4 x 10-4M or 0.4 molecules of EDTA with Kd = 2.2 x 10-5M. Citrate and EDTA compete for the same binding site(s). No binding of acetate could be demonstrated.The binding of EDTA and citrate shows a strong ^-dependence suggesting a (partly) ionogenic binding between charged areas on the fibrinogen molecule and charged groups on EDTA or citrateOur results support the idea that the binding of EDTA and citrate and the concomitant effect on the plasmin attack are independent of the effect of calcium ions
Prenatal Exclusion Of Haemophilia B By Assay Of Fetal Factor IXC and IXAg
Authors: Mibashan R S , Rodeck C H , Holmberg L , Thumpston J K , White J M , Gorer R , Nilsson I M , Campbell S 
Published: July 2018

Recognition of haemophilia B in utero has lagged behind that of classical haemophilia because of lower prevalence and wide emphasis on technical constraints. Pure fetal blood has been obtained at 18-20 weeks by fetoscopy (C.H.R) from 49 of 50 consecutive male fetuses at risk of haemophilia; 4 were pregnancies in obligate or strongly putative carriers of severe haemophilia B.Current immunoradiometric assays for VIII:CAg depend on both the availability of high titre human antibodies directed against VIII:C and the possibility of preparing highly specific 125I-IgG from human antiserumPlasma factor IXC in 40 control fetuses was 5.9-12.8 (mean 8.4) U/dl. A sensitive immunoradiometric assay (IRMA) for factor IXAg in 20 of these fetal plasmas gave values of 2.9-7.8 (mean 4.1) U/dl, and 1.8-10.0 U/dl in 9 other control fetuses.The 4 fetuses at risk of haemophilia B had plasma IXC levels of 7.9, 12.3, 9.4 ö 6.6 U/dl; they were regarded as unaffected, and the parents were counselled accordingly. To date, 3 of the 4 have been born and their clinical and laboratory normality confirmed. The corresponding IXAg levels (Malmö) were also normal — 3.6, 5.4, 4.8 ö 2.0 U/dl; but, despite absence of extraneous IXAg in these samples, exclusion of haemophilia B was not feasible in 2 of the 4 whose affected relatives were found to be CRMUsing pure cord blood obtained at fetoscopy, prenatal diagnosis by coagulant bioassay promises to be definitive and is not limited to CRM fetuses. The IRMA is valuable for diagnosis or confirmation in CRM cases, and in the rare instance (2%) of dilution by amniotic fluid.
Noninvasiv Screening For Acute Dvt By Means Of Leg Temperature Profiles And Venous Emptying Curves As Compared To Conventional Thermography And Phlebography
Authors: Nilsson E , Holmgren K , Jacobsson H , Johnsson H , Zetterquist S 
Published: July 2018

simplified thermographic technique has been developed to provide leg temperature profiles for diagnosis of acute DVT (DevethermR). The temperature profiles are obtained by manual scanning from the foot to the hip with an infrared radiation transducer attached to a position indicator. The diagnosis of DVT is based on side-differences in mean segmental leg temperature.In 200 patients admitted to hospital due to the clinical suspicion of acute DVT, the leg temperature profiles were pathological in 132 of those 140 patients who proved to have DVT at phlebography which means a sensitivity of 94%. False positive results were obtained in cases with e.g. varicose veins or regional infections but these errors could be reduced if the profiles were not only numerically evaluated but also subjected to pattern analyses. A combination with venous emptying curves as obtained from venous occlusion plethysmography further improved the specificity of the noninvasive diagnostic procedure. This combination also proved favourable for the differentiation between proximal and distal leg thromboses as well as acute and old DVT. Some of the patients were investigated with thermography by a scanning camera. The results correlated closely to those obtained with the simplified thermographic technique but without improving the diagnostic sensitivity.
Success Rate Of Fibrinolytic Therapy In Fresh And Old Deep Vein Thrombosis
Authors: Theiss W , Wirtzfeld A , Maubach P 
Published: July 2018

It is still a wide-held belief that fibrinolytic therapy can clear thrombi from deep veins only while they are fresh. We have therefore analysed retrospectively the phlebographic results obtained in 85 patients, all of whom had fibrinolytic therapy for thrombosis of the iliac and/or femoral veins with symptoms present for 1 day to 8 weeks prior to treatment. Streptokinase (n=46), urokinase (n=9), or both drugs successively (n=30) were administered according to our guidelines as recently outlined in detail (Klin. Wschr. 58:521, 1980; Med. Klin. 75:580, 1980) particular emphasis being placed on sufficient duration of thrombolytic therapy with no a priori time limit.Thus, S.C. administration of heparin seems to be as efficient and safe as administration of heparin I.V. in the treatment of patients with acute DVT.The number of cases grouped according to the lenghth of their history and their respective phlebographic outcome as well as the duration of thrombolytic therapy are listed in the table.It can be seen that the success rate was good, when the patient presented with a delay of up to 2 weeks; even during the third or fourth week of the thrombotic episode two thirds of the patients could still be improved. Thereafter the results were uniformly poor.Conclusion: Iliofemoral venous thrombosis can be treated successfully with fibrinolytic drugs for much longer after its onset than is generally accepted.
Hemorheological Effect Of Ticlopidine In Rats
Authors: Ono S , Ashida S , Abiko Y 
Published: July 2018

The hemorheological effect of ticlopidine was studied in rats ex vivo. Ticlopidine (30-300 mg/kg) was orally given to rats. Heparinized blood samples were taken from the carotid artery under pentobarbital anesthesia 3 hr after the drug administration for measurement of whole blood viscosity (ELD type cone-plate viscometer), micropore filtrability of red cells (Nuclepore membrane, 5 µm), erythrocyte sedimentation rate (ESR), hematocrit (Ht) and plasma fibrinogen. Red cell deformability was measured by counting the shear stressinduced cap-form cells under a scanning electronmicroscope. Mechanical flexibility of red cells was also studied by measuring hemolysis caused by turbulant flow.Ticlopidine treatment caused a significant decrease in whole blood viscosity (9.13 ± 0.15 and 6.17 ± 0.08 versus 9.80 ± 0.18 and 6.74 ± 0.09 Cp in control at 19.2 sec-1and 76.8 sec-1, respectively) and a significant increase in micropore filtrability of the red cells (0.54 ± 0.01 versus 0.40 ± 0.02 ml/min in control) without any changes in ESR, Ht and plasma fibrinogen. Ticlopidine also significantly stimulated the shear stress-induced shape change of the red cells to cap-form cells (12.08 ± 0.13 versus 8.66 ± 0.23 % in control) and prevented mechanical hemolysis caused by a turbulant flow (16.8 ± 1 . 6 versus 30.5 ± 2.5 % in control).In addition to the platelet aggregation inhibitory action the hemorheological action of this agent may be useful for improving microcirculation and protecting red cells from mechanical disruption by turbulant blood flow.Increase in the adenylate cyclase and Mg2+-activated adenosine triphosphatase activities in red cell membranes may be associated with the effect of ticlopidine to increase red cell deformability.
The Prothrombin Time: The Mechanism Of In Vitro Activation
Authors: Palmer R , Gralnick H 
Published: July 2018

We have described shortening of the prothrombin time (PT) when blood is collected in borosilicate or siliconized boro- silicate tubes. The shortening is time dependent and occurs more rapidly at 4° C than at room temperature. We have studied the mechanisms of in vitro activation of the PT utilizing normal blood and blood congenitally deficient in coagulation factors. We have found that the blood deficient in factor XI has the same rate of shortening of the PT as in normal blood, while blood deficient in factor IX has only 50/ that of normal and factor XII deficient blood does not have any in vitro activation. The blood deficient in Cl INH ihas the most severe shortening of the PT.Analysis of the coagulation factors affected during the in vitro activation of normal blood revealed that factor VII-X is increased and this is related primarily to factor VII activation. In borosilicate factor V did not change, factor IX decreased by 15-20% while factor XII showed no change in the assay system. The activation can be totally blocked by addition of Cl INH or corn trypsin inhibitor (specific inhibitor of XII activation) to whole blood. These studies indicate that the PT is shortened in vitro by at least two mechanisms of activation of whole blood: 1) factor XII is activated by surface contact with siliconized borosilicate or borosilicate and in turn, directly activates factor VII; 2) factor XIIa activates prekallikrein to kalli- krein which in turn activates factor IX. Factor IXa then activates factor VII and it would appear that approximately one-half of the activation of the PT is directly through this pathway. Inhibitors of factor XII activation, Cl INH and CFI can totally inhibit the activation in vitro. Thus, surface activation of factor XII is the pivotal reaction in the in vitro shortening of the PT in whole blood. These studies allow new strategies for the prevention of in vitro activation of the PT, and may allow for more precise measurement of the PT without concern for contact activation by the use of specific inhibitors.