bluuebunny/crossref_metadata_2025_split huggingface dataset:
A New Radioimmunoassay-Technique for Fibrinopeptide-a in Human Plasma
Authors: Harenberg J. , Zimmermann H. , Haas F. , Schmidt-Gayk H. 
Published: May 2019

Fibrinopeptide-A (FpA) is thought to be the most sensitive parameter to indicate hypercoagulability with increased fibrin formation in man. Previously described radioimmunoassays for FpA are very time consuming. We present therefore a modification of the assay, which is less time consuming, sensitive, reproducable and reliable. The following modifications were made on the original method: 1. plasma dialysis was omitted 2. performance on microtiter-plates 3. double antibody method.The sensitivity was improved to 0.16 ng FpA/ml plasma. The mean concentration of FpA in dialysed and undialysed plasma did not differ significantly (p<0,001). Effective separation of fibrinogen was achieved by aethanol extraction alone. The mean concentration of FpA correlate, highly, when the tracer was separated by charcoal or second antibody (r = 0.96). The recovery was improved to 85%.In healthy persons 0.16-2.5 ng FpA/ml plasma were measured. In patients with venous thrombosis or myocardial infarction in the history FpA was elevated significantly to 2.0 ng/ml-19.6 ng/ml, indicating that the FpA is a usefull tool in diagnosis of hypercoagulability.
A Hitherto Undescribed Naturally Occurring Plasma Antagonist of Activated Factor X Inhibitor (Antithrombin III)
Authors: Yin E.T. , Salsgiver W.J. , Tangen O. 
Published: May 2019

Circumstantial evidence suggested that normal human plasma contained a substance regulating the neutralization of F. Xa by F. Xa inhibitor (XaI), (Yin et.al., Adv. Exper. Med.& Biol., 52: 239, 1975, Plenum Press, N.Y.).This plasma component has now been isolated and partially purified in our laboratory, and tentatively designated as “Anti-Xal”.In experiments employing purified components, when Anti-Xal was incubated at 37°C with F. Xa. Xal and heparin for two minutes at pH7.5, the amount of F. Xa inhibited was inversely proportional to the Anti-XaI concentration. But, when the F. Xa was replaced by thrombin in the incubation mixture, the neutralization of thrombin clotting activity was undisturbed. Anti-Xa I was found to be neither PF3 nor PF6.These and other data strongly suggest that the “Antithrombin ill pathway” is more complex than currently believed to be. In circulating blood an equilibrium state must exist between Anti-Xal and Xal. Under certain conditions when the Anti-Xal activity is predominant the rate of F.Xa neutralization by Xal then becomes slower than the activation of prothrombin to thrombin by F.Xa.
Fibrinogen Logroño. A New Fibrinogen Molecular Variant
Authors: Fernandez J. , Lasierra J. , Narvaiza M.J. , Vilades E. , Palaciosy E. , Rocha E. 
Published: May 2019

We present a new molecular variant of fibrinogen. The majority of biological tests were normal except prolonged prothrombin and thrombin times, fibrinogen deficiency as quantified by a colourimetric method, and the polymerization of fibrin’s monomers. Normal thrombin times were obtained by addition of normal plasma, bovine thrombin, CaCl2, and by changes in pH and ionic strength.The study of the purified fibrinogen showed normal fibrinopeptides’ liberation and sialic acid and hexosamine levels. Fibrin stabilization, coagulability index = 64%, electrophoretic mobility, pI = 5.4 (N = 5.8), and S20,w = 10 (N = 8.2), were abnormal.
Influence of Platelet Inhibitory Drugs on the Thrombogenicity of Dacron Arterial Grafts Perfused in an Artificial Circulation
Authors: McCollum C.N. , Rajah S.M. , Crow M.J. , Kester R.C. 
Published: May 2019

The effect of Acetyl Salicylic Acid (ASA), Dipyridamole (DPM) and in combinations on the response of platelets to woven Dacron perfused in an artificial circulation was investigated. Circuits were perfused by heparinised blood donated by 6 volunteers after each had taken: -1) No drugs 2) ASA 300mg tds 3) DPM 100mg qds 4) ASA 300mg + DPM 75mg tds 5) ASA 80mg + DPM 75mg tds 6) ASA 80mg tds, for 1 week. Bleeding times were performed prior to each donation. Platelet functions were estimated during perfusion. Each grafts surface was examined by scanning electron microscopy (SEM) at the end of perfusion.Platelet inhibition by low dose ASA + DPM was accompanied by less extension of bleeding time, and we suggest that such combination may protect patency in Dacron grafts at risk.
Sulfinpyrazone in the Prevention of Cardiac Death: The Anturane Reinfarction Trial
Authors: Margulies E.H. 
Published: May 2019

The Anturane Reinfarction Trial is a randomized, double-blind, multicenter clinical trial comparing sulfinpyrazone (200 mg q.i.d.) and placebo in the prevention of cardiac mortality among patients with a recent documented myocardial infarction. Results represent data accumulated on 1475 eligible patients entered 25-35 days after myocardial Infarction and followed for an average of 8.4 months, and have been previously reported. The results indicated sulfinpyrazone was effective in reducing cardiac deaths with the most pronounced effect in reducing sudden cardiac death.The trial was completed in August, 1978. The final results represent data accumulated on 1528 eligible patients with an average follow-up of 16 months. All 106 deaths were of a cardiovascular nature (62 placebo, 43 sulfinpyrazone). Of the 105 cardiac deaths (62 placebo, 43 sulfinpyrazone), 59 were sudden cardiac deaths (37 placebo, 22 sulfinpyrazone), 35 were myocardial infarctions (18 placebo, 17 sulfinpyrazone) and 11 (7 placebo, 4 sulfinpyrazone) were of other cardiac causes. Various approaches of data analysis employed resulted in a statistically significant difference (p=0.047, Cox’s Method) attributable to sulfinpyrazone in reducing sudden cardiac death.Sulfinpyrazone was very well tolerated with the most frequently associated newly observed sign and symptom being minor gastrointestinal complaints.
Characteristics of the Major Platelet Membrane Site used in Binding to Collagen
Authors: Meyer F.A. , Frojmovic M.M. 
Published: May 2019

In binding to collagen surfaces, platelets seem to recognize the high content of proline and hydroxyproline.1 A site seems to be involved which can be blocked by preincubating platelets with soluble polymers rich in proline or hydroxyproline e.g. polyhydroxyproline (PHP). Binding to this site can also be blocked by interacting the platelets with low concentrations of ADP. Preincubation with 100 μg/ml PHP1 or 0.5 μM ADP produce 60±l0% reduction in adhesion.2 The action of PHP is immediate but that of ADP is delayed. The dose of ADP used produces shape change, PHP does not cause shape change. But shape change is irrelevant to the effect since also adhesion of fixed platelets is reduced by both treatments. Addition of ADP and PHP together does not produce greater inhibition of platelet adhesion than either agent alone showing that the same binding site must be influenced. However, ADP reduces adhesion also on albumin - and globulin-coated surfaces showing that the indirect effect of ADP influences other platelet binding sites as well. AMP (1 mM) blocks the effect of ADP but not of PHP. The receptor with which ADP interacts on the platelet surface is not directly involved in binding but can inactivate binding sites presumably through some local interaction mechanism.1. Meyer, F.A., Weisman, Z., Thromb. Res. 12, 431 (1978).2. Meyer, F.A., Weisman, Z. and Frojmovic, M.M. (this volume.
Kinetics of the Inhibitory Effect of Factor IXBm in the Activation of Factor X by Factor VII and Bovine Tissue Factor
Authors: Østerud B. , Kasper C.K. , Rapaport S.I. 
Published: May 2019

F.IXBm is giving a prolonged prothrombin time with bovine tissue factor (T.F.). In the present study the inhibitory effect of purified F.IXBm was tested in a F.VII assay that measures the ability of F.VII to activate F.X in the presence of bovine T.F. and Ca++, followed by the quantitation of formed F.Xa by the synthetic substrate benzoyl -L-Ile-Glu-Gly-L-Arg-p-nitroanilide. Experiments were carried out with different concentrations of F.IXBm and F.X, keeping the concentrations of F.VII and bovine T.F. constant. Lineweaver-Burk plot of the data showed that all the curves crossed the l/V axis in one point - no inhibition by F.IXBm at infinite concentratlons of F.X. Thus, F.IXBm acts as competitive in inhibitor to F.X in the activation of F.X by F.VII and bovine T.F. By plotting the 1/V against the inhibitor concentrations (F.IXBm conc), a Dixon plot, the Ki for F.IXBm was determined to be 0.017 μM.Normal F.IX was also found to be a competitive inhibitor to F.X but 4-5 times higher concentrations of F.IX were needed to give the same inhibition as F.IXBm. Utilizing human T.F. instead of bovine T.F. in this assay resulted in no significant inhibition by either F.IX of F.IXBm.
Studies of the Anti-Xa Activity of Human Plasma and Purified Antithrombin III
Authors: Barrowcliffe T.W. , Eggleton Anne C. 
Published: May 2019

When samples of purified antithrombin (At III) were compared to plasma at the same At III concentration, in the absence of heparin, the anti-Xa activity of plasma was considerably higher. In the presence of heparin the anti-Xa activity of purified At III was much greater than plasma. This was shown to be due to an inhibitory effect on the heparin. At III-Factor Xa interaction in plasma which could be removed by absorption with aluminium hydroxide [Al(OH)3]. This inhibition was dependent on the molecular weight of the heparin; low molecular weight heparin was inhibited less than high molecular weight heparin, and this probably accounts for the apparently high anti-Xa activity of low molecular weight heparin.A1(OH)3 absorption of plasma also increased its anti-Xa activity in the absence of heparin. Addition of Factor IX concentrate to the absorbed plasma reduced its anti-Xa activity to that of normal plasma, and studies with purified proteins showed that this effect was due to the prothrombin in the concentrate. The addition of Factor IX concentrate or prothrombin to purified At III did not affect its anti-Xa activity.These results suggest that, in addition to At III, there is another Xa-inhibitor in plasma which competes with prothrombin for binding of Factor Xa.
Fluid Dynamical Considerations of Platelet-Vessel Wall Interaction
Authors: Turitto V.T. 
Published: May 2019

Platelet adhesion to subendothelium is dependent on two distinct processes: (1) diffusive transport (T) of platelets to the surface and (2) platelet-subendothelial reactivity (R). The relative magnitude of T to R will determine which factors control the adhesion rate. Physical factors, specifically, wall shear rate (γ) and platelet diffusivity (D) influence T, whereas chemical alterations modify R. An increase in the magnitude of γ or D or a decrease in R tends toward R controlled adhesion. An increase in low rate or decrease in vessel dimensions increases γ, whereas D increases with both red cell concentration (up to 40 %) and γ.In flowing blood at shear rates comparable to those found in veins or large arteries (< 650 see-1), T determines platelet adhesion. Moderate alterations in R, such as produced by the addition to blood of 45 mM citrate, 10-100 nM prostacyclin or in von Willebrand factor depleted blood, have little effect on platelet adhesion values under these flow conditions. However, as shear rate is increased to values comparable to those in the microcirculation {1300-2600 sec-1), the same blood samples show values of platelet adhesion which are reduced compared to controls, and the reduction increases with shear rate Thus, measurements of R should be determined under controlled shear conditions which are high enough to be outside the range of predominantly transport controlled adhesion.
Inter-Relationships of dysfibrinogenaemia, Fetal Fibrinogen and Liver Cell Growth
Authors: Barr R.D. , Clause M.M. , Johnston M.A. 
Published: May 2019

When operationally defined as an excess of immunoassayable fibrinogen (IAF) over thrombin-clottable fibrinogen (TCF) of ≥ 1 g per L, dysfibrinogenaemia (DF) is demonstrable in more than 1/3 of patients with chronic liver diseases (CLD)1. Some features of this protein suggest a similarity to fetal fibrinogen.2
To further pursue these investigations, it was deemed necessary to identify a population of very young patients who were synthesizing fibrinogen rapidly. Twenty (2C Infected neonates, of gestational ages 24-41 weeks, were selected for study on the basic of TCF levels ≥5 g per L, Using antisera raised in sheep and rabbits, there was no demonstrable excess of IAF in the same plasma samples. Similar data were obtained fron assays in an unselected aeries of umbilical cord plasmas. These findings suggest either thet DF in CLD is not due to the renewed synthesis of fetal fibrinogen, or that fetal fibrinogen, like alpha-fetoprotein and fetal pre-albumin,3 is physiologically I evident only during early embryonic development.1. Barr, R.D. et al. J. Clin. Path. (1978) 31, 89.2. Barr, R.D. Blomedlcine (1979) in press.3. Tatarinov, Y, S. et al. Lancet (1978) 2, 1122.
A Non-Stasis Rabbit Model for the Detection of Factor IX Concentrate Thrombogenicity.
Authors: Prowse C.V. , Williams A.R. 
Published: May 2019

A method has been developed whereby aerial blood samples can be obtained from a rabbit over a period of four hours following infusion of potentially thrombogenic solutions. Infusion of 50 uAg thrombin over JO minutes produced intravascular coagulation for up to three hours after infusion as demonstrated by a decrease in factor VIII, increase in partial thromboplastin time and fibrin(ogen) degradation producta and a positive ethanol gelation teat. No change in fibrinogen, factor DC or platelet count was found. Saline infusion produced no change in any of these parameters.Infusion of a variety of factor IX concentrates at 100 u/kg shewed that those concentrates active in in vitro thrombogenicity teste produced a similar effect to thrombin in vivo and in addition may result in a drop in platelet count. Infesion of concentrates with low in vitro activity did not induce intravascular coagulation.
A Synthetic Thrombin Inhibitor Taking Extremely Active Stereo-Structure
Authors: Okamoto S. , Hijikata A. , Kikumoto R. , Tamao Y. 
Published: May 2019

The novel series of synthetic thrombin inhibitors reported by us in 1978 included the extremely potent, highly selective and less toxicinhibitors (No, 407 and No. 700). Extensive studies on the stereo-structure activity relationship around No. 700 were further made and No. 805 was found.Its I50 for fibrinogen-thrombin system was extremely small (0.03~0.04 μM), approximately 1/10 of that of No. 407. Selectivity to thrombin was satisfactorily high. From the characteristic stereo-structure of No, 805, stereo-geometry of the active site of thrombin, maybe assuming replica structure of No. 805, became more informative. LD50 was 140 mg/kg i. v. in rats and 210 mg/kg i. v. in mice. Per os administration of 20 mg/kg of No. 805 was able to prevent the decrease of platelet number due to thrombin infusion in rabbits. At 0.3 μM of No. 805 in plasma in rabbits, the carotid artery thrombi due to acetic acid application was also well prevented.
Similar Prolongation of Bleeding-Time After Low and High Doses of Acetylsalicylic Acid (ASA)
Authors: Dybdahl J.H. , Eika C. , Daae L. , Godal H.C. , Frislid K. , Wiik I. , Larsen S. 
Published: May 2019

In Lancet, 2, p,780, 1978, O’Grady and Moncada reported that high doses of aspirin did not lead to prolonged bleeding-time. Prompted by this observation, we examined 21 healthy male volunteers, aged 21-56 years. After an overnight fast, the bleeding-time was recorded in duplicate using Trombolette (Mannheim, Solingen, DBR). Thereafter, 0.425 or 3.825 g of ASA (GLOBOID, Nyco, Oslo, Norway) was given in a cross over study with a minimal interval of 14 days. Finally, the bleeding-time was repeated after two more hours of fasting.As is evident from the table, a significant increase in bleeding-time was observed after low as well as after high doses of ASA (p< 0.001). In addition, the bleeding-times obtained after ingestion of low and high doses of ASA were not significantly different (p = 0.22).
Phospholipase A2-Induced Platelet Aggregation, Release and Lysis.
Authors: Heinrich D. , Beckmann S. 
Published: May 2019

Activation of washed platelets by exogenous phospholipase A2 (PIA2) purified from crotalus terrificus terrificus venom was studied. Platelets were labeled with 14C-serotonin and 51chromium and resuspended in Tyrode/albumin (TA). With 1-5 μg/ml (final conc.) of crotalus PIA2 no direct platelet alterations were observed. These platelets, however, were refractory to collagen - but not to thrombin or HLA-specific antibodies.10-50 μg/ml crotalus PIA2 rapidly induced platelet aggregation and release 100 μg/ml crotalus PIA2 induced platelet lysis.PIA2-induced platelet alterations were inhibited by EDTA, PGE1, ASS and apyrase. Crotapotin, an acid peptid isolated from crotalus venom, forms complexes with crotalus PIA2 and specifically inhibits PIA2-induced platelet alterations.Conclusion: PIA2-induced platelet alterations are due to liberation of arachidonic acid from phospholipids of the platelet membrane inducing prostaglandin and thromboxane synthesis. With high concentrations of PIA2 breakdown of membrane phospholipids will lead to platelet lysis.
Heparin Prophylaxis Combined with DHE or Dextran in HIP Operations
Authors: Schöndorf T.H. , Weber U. 
Published: May 2019

162 elective hip operation patients were randomly allocated to: Group I: 5 000 U heparin injected s.c. 10 and 2 hours pre-operatively, then 8 hourly; Group II: heparin as above plus dextran 40 on three days; Group III: heparin as in group I combined with dihydroergotamine (DHE). The 125-I-fibrinogen test was routinely used for diagnosis of deep vein thrombosis (DVT), when positive, phlebography was performed.
DVT occurred in 8/55 patients in group I, in 9/54 in group II and in 2/53 in group III. (Chi-square test: I vs. III p = 0.054; II vs. III p = 0.028) .
Pulmonary embolism (confirmed at autopsy) occurred in one patient in both group I and II.In the three groups, the intra-operative transfusions, wound blood loss at the pre- and post-operative haematocrit did not differ.Platelet aggregation was only significantly lowered in group II.Heparin/DHE were most effective in preventing thromboemboli, dextran infusions did not improve heparin prophylaxis.Peridural anaesthesia performed in 83 - 87% of patients in all groups led to no complications following pre-operative heparin.
Experimental Arterial Thromboembolism in Baboons: Mechanism, Quantitation and Pharmacologic Prevention
Authors: Herker L.A. , Hanson S.R. 
Published: May 2019

A quantitative primate model of arterial thromboembolism has been developed that involves the kinetic measurements of 51Cr-platelets and 125I-fibrinogen by femoral arteriovenous cannulae in chaired baboons. Cannula platelet consumption (CPC) correlated directly with exposed cannular area for irradiated Silastic (IS) end polyurethane (correlation coefficients of 0.940 and 0.901 respectively; p < 0.001) and remained steady state for months. Fibrinogen was not measurably destroyed. CPC was independent of cannula flow rate, platelet count, heparin anticoagulation and ancrod defibrinogenationIn-platelet imaging of IS eannulae demonstrated luminal accumulation and subsequent embolization of irregular platelet masses that progressively occluded glomerular vessels with non-fibrin containing platelet thromboemboli.Oral administration of dipyridamole and sulfinpyrazone decreased cannula platelet consomption in a dose dependent manner with complete interruption at 20 and 250 u mol/kg body wt/day (in three divided doses) respectively, whereas oral acetylsalicylic acid (10-330 umol/kg/day) had no measurable effect on cannula platelet consumption. We conclude that this primate model simulates arterial thrombotic processes in man and that this model is suitable for the in vivo evaluation of biomaterials and of drugs that modify platelet behavior.
Replacement Therapy in Von Willebrand’s Disease
Authors: Sultan Y. 
Published: May 2019

Replacement therapy in patients with VWD for bleeding episodes or surgical procedures is not as well defined as treatment of patients with Hemophilia. In severe forms of the disease although it is aesy to obtain high levels of FVIII procoagulant activity after transfusion with FVIII concentrate it is more difficult to achieve a normal bleeding time (B.T.) and moreover to keep it normal throughout surgical procedures and healing.The normalization of B.T. is dependent on the kind of FVIII concentrates used. To demonstrate this, several commercial preparations of FVIII have been tested for their content in FVIII R Ag and FVIII RWF in comparison with the procoagulant activity ; they have also been tested in vivo for their ability to correct B.T.. shortening of B.T. is also dependent on the quantities injected ; it is more efficient to infuse large doses once a day or every other day, than fractionated doses F It is also dependent on the severity of the disease and the number of transfusions the patient previously received. Some problems remain unsolved, specially when all the parameters of the disease reach normal values in the circulating blood although B.T. is still prolonged.
A New Inhibitor of Factor XIII and Platelet Aggregation. Influence of Fibrin Stabilization on Thrombolysis
Authors: Ryckewaert J.J. , Soria J. , Soria C. , Samama M. , Maamer M. , Aurousseau M. , Otero A.M. 
Published: May 2019

Antifactor XIII and antiplatelet aggregation activities were discovered in vitro for a synthetic compound with a benzothiophen keton structure. It was found to inhibit the stabiliiation of fibrin as shown by S.D.S. Polyacrylamide gel electrophoresis of a clot previously dissociated by urea and mercaptoethanol, among other tests. The mechanism of action was studied using dansyl cadaverin incorporation into casein : the inhibitor effect was not competitive, related to the inactivation of factor XIIIa, and independant of calcium concentrations. It was much more pronounced in a purified system than in plasma, due to its binding to albumin. We therefore studied its possible displacement from albumin by various drugs.The thrombolytic activity of urokinase only slightly increased when clot stabilization was inhibited by the studied compound.
Effect of Sulfinpyrazone on Experimental Atherosclerosis in Rats
Authors: Horsch A.K. , Klaiber P. , Dennig K. , Hofmann W. 
Published: May 2019

Early atherosclerotic lesions in rat aortas were produced by synergy of cholesterol feeding (4 g cholesterol and 2 g cholate in Ioo g pellets) and immunological injury (5 repeated immunizations with 1 mg of horse-radishperoxidase). Cholesterol feeding and immunization was started the same day and resulted after 6 weeks in endothelial injury, intimal thickening and edema, in proliferation of intimal smooth muscle cells and in deposition of lipids and immune complexes in the arterial wall.100 rats were studied and no lesions were detected in the control group, minimal changes were seen in the animals receiving cholesterol or immunization alone, but lesions were constantly present in the group receiving both regimens. One group of cholesterol fed and immunized rats was given sulfinpyrazone from the beginning of the experiment (160 mg/kg/d) over the 6 weeks and a significant reduction in lesion formation was observed compared to the non treated animals. These results suggest a protection of the arterial wall by sulfinpyrazone in experimental atherosclerosis.