bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Comparison Between Low Molecular Weight Heparin (KABI 2165) and Standard Heparin in the Intravenous Treatment of Deep Venous Thrombosis
Authors: Bratt Göran , Törnebohm Eva , Granqvist Staffan , Åberg Wiveca , Lockner Dieter 
Published: July 2018

SummaryIn order to study whether a low molecular weight heparin (LMWH) of mw 4000 D is effective in the treatment of deep venous thrombosis (DVT), patients with DVT verified by phlebography were randomized to treatment by continuous intravenous infusion of either unfractionated heparin (UFH) or LMWH. The initial dose was 240 U (anti F Xa)/kg/12 h. TTiis study (study I) was stopped because of major bleeding in 2 newly operated patients in the LMWH group after 27 patients had been treated. The heparin activity measured as F Xa inhibition assayed in retrospect, was found to be much higher in the LMWH group (mean 1.6-2.0 anti F Xa U/ml) than in the UFH group (mean 0.5-0.8 anti F Xa U/ml).A second study was therefore initiated in which the DVT patients were randomly given UFH (240 U/kg/12 h) or LMWH only 120 U (anti F Xa)/kg/12 h, as initial doses (study II). In this study 27 patients could be evaluated, the mean heparin activity still being higher in the LMWH group (0.9-1.2 anti F Xa U/ml) than in the UFH group (0.5-0.7 anti F Xa U/ml).A second phlebographic investigation showed progression of thrombus size in 3 (11%) of the UFH patients of studies I and II (n = 29) and improvement in 14 (48%). There was no progression in any LMWH patient, 6 (50%) had improved in study I and 10 (77%) in study II. The mean decrease of thrombus size score (according to Marder) during treatment did not differ between the 3 groups.Antithrombin III decreased significantly in the UFH group but not in the LMWH groups. Aminotransferases increased in all 3 groups. There was no difference in mean capillary bleeding time between the 3 treatment groups.Although this material is relatively small, our findings suggest that LMWH seems to be of similar effectivity as UFH.
Platelet Sequestration During Hypothermia in Dogs Treated with Sulphinpyrazone and Ticlopidine - Reversibility Accelerated After Intra-Abdominal Rewarming
Authors: Pina-Cabral J M , Ribeiro-da-Silva A , Almeida-Dias A 
Published: July 2018

SummaryDuring body cooling, a progressive thrombocytopenia is observed, with platelet sequestration mainly in the liver. Platelets return progressively to the circulation during re warming. In this work the presence of platelet clumps is demonstrated by electron microscopy inside the hepatic sinusoids of dogs cooled to 20° C by immersion in iced water. Such clumps were not found either before cooling or after body rewarming. Similar platelet clumps in the hepatic microcirculation were found in two other groups of dogs cooled and rewarmed as before, but previously treated with the antiaggregants sulphinpyrazone or ticlopidine. Another group of dogs was cooled and rewarmed by intra-abdominal circulation of physiological saline respectively at 4° C and 40° C. In these animals a similar decrease of circulating platelets was observed. However, just after re warming was started, with the body temperature still at 22° C, sequestered platelets came back abruptly to circulation. We conclude that hepatic platelet sequestration induced by hypothermia appears mainly due to local haemodynamic conditions.
The Effects of Acute Smoking on Platelet Behaviour, Fibrinolysis and Haemorheology in Habitual Smokers
Authors: Belch J J F , McArdle B M , Burns P , Lowe G D O , Forbes C D 
Published: July 2018

SummaryThere is an increased frequency of arterial thrombosis in cigarette smokers. The changes in blood coagulation seen in these subjects have been studied by many workers but results have not always been in agreement. We wished to study the effects of acute .smoking on platelet behaviour, fibrinolysis and haemorheology in ten habitual smokers, and to compare these results with nonsmoking controls. Results show that the smoking group had higher plasma fibrinogen (p <0.04), lower plasminogen (p <0.02) and plasminogen activator (p <0.05), and higher plasma viscosity (p <0.003). The changes seen in cigarette smokers after smoking three cigarettes were an increase in the rate of platelet aggregation to ADP (p <0.02), an increase in α2M, (p <0.02), and factor VIII RAG (p <0.05). Plasma viscosity was decreased (p <0.02) as was red cell deformability (p >0.02).We confirm an increased tendency to hypercoagulability in smokers compared to controls which becomes more pronounced immediately after smoking three cigarettes.
On a Possible Interaction Between ADP and Mechanical Stimulation in Platelet Activation
Authors: Aursnes Ivar , Vikholm Vibeke 
Published: July 2018

SummaryFreshly drawn blood with inhibited plasma coagulation, but normal Ca++-concentration, was lightly centrifuged to produce platelet rich plasma (PRP). In order to minimize mixing of the various parts of the blood during the centrifugation, the red cells were centrifuged into a “cushion” of albumin in the bottom of the tube. Platelets harvested from the different parts of the centrifuge tube exhibited different degrees of activation, i. e. they possessed different abilities to aggregate when tested afterwards in an aggregometer. Complete ADP scavenging during the centrifugation inhibited the platelet activation, and it was therefore assumed that ADP released from red cells during the centrifugation was partly responsible for this. But as the ADP concentration at hand could be significantly reduced enzymatically without reducing the activation of the platelets by the centrifuge, mechanical stimulation during the centrifugation was postulated as a contributing factor. Prostaglandin synthesis inhibition during the centrifugation retarded the activation of the platelets in the tube.
Neutralization of the Local Negative Charge Carried by Glycoprotein (GP)-Ib in Ristocetin-Induced Platelet Agglutination
Authors: Tanoue K , Jung S M , Yamamoto N , Yamazaki H 
Published: July 2018

SummaryPretreatment of platelets with chymotrypsin dose-dependently decreased glycoprotein (GP)-Ib amounts as measured by SDS- PAGE, ristocetin-induced agglutination and platelet electrophoretic mobility (EPM). Decrease in platelet EPM in response to 0.75 mg/ml ristocetin alone were 7.0 ± 2.3 and 6.8 ± 4.3% (M ± S.E., n = 6) for control and chymotrypsin-treated platelets, respectively (p >0.2). Von Willebrand factor (vWF) alone had no effect on platelet EPM. However, in the presence of 0.75 mg/ml ristocetin, added vWF (2.9 μg/ml) caused a further 6.3 ± 3.8% decrease in control platelet EPM, but caused no significant decrease in the enzyme-treated platelets (p >0.05). In the presence of 0.3 mg/ml ristocetin, added vWF (2.9-14.5 μg/ml) caused a small but significant decrease in control platelet EPM, but caused no significant decrease in the enzyme-treated platelets.These findings suggested that the GP-Ib carrying negative charge decreased by binding of vWF might facilitate a mutual approach of the GP-Ib molecules and bridge formation by vWF between different platelets.
A Sequential Study of Plasma Histidine-Rich Glycoprotein and Plasminogen in Patients with Acute Myocardial Infarction and Deep Vein Thrombosis
Authors: Jespersen Jørgen , Gram Jørgen , Bach Elsa 
Published: July 2018

SummaryIn a prospective study of deep vein thrombosis (DVT), detected by the Tc-plasmin test, in 34 patients with acute myocardial infarction sequential determinations were made in plasma by immunologic methods of histidine-rich glycoprotein (HRG) and total plasminogen and the concentrations of free plasminogen calculated. Mean plasma HRG concentrations were consistently higher in the group of patients, in which Tc-plasmin scanning had revealed the existence of DVT. The effect of HRG caused the level of free plasminogen to be only 50–60% of the level of total plasminogen. Fluctuations of HRG caused only minor changes in free plasminogen concentrations. Our data suggest that HRG acts as a weak, negative acute phase reactant.
Platelet-Platelet Recognition During Aggregation: Distinct Mechanisms Determined by the Release Reaction
Authors: Agam Galila , Livne Avinoam 
Published: July 2018

SummaryFixed platelets, bearing covalently bound fibrinogen, were previously shown to participate passively in aggregation induced by thrombin or A23187. The bound fibrinogen was specifically required for the interaction. The present study examines the role of the release reaction in controlling the passive participation of the fixed platelets in aggregation. Aggregation of fresh platelets induced by low ADP concentration (≤2 μM) was not augmented by the fixed platelets, but was augmented when higher concentrations of ADP were employed. Fixed platelets failed to enhance aggregation of aspirin-treated fresh platelets induced by 10 μM ADP; the augmentation capability was reconstituted by a supernatant fraction from platelets activated by 10 μM ADP in the presence of EDTA. The binding of soluble fibrinogen to activated fresh platelets occurred regardless of the release reaction, but the interaction of fragmented fixed platelets bearing bound fibrinogen with aggregating fresh platelets was apparent only when release took place. It is concluded that fibrinogen covalently bound to fixed platelets is selectively recognized by released compound(s).
Influence of Yoga on Blood Coagulation
Authors: Chohan I S , Nayar H S , Thomas P , Geetha N S 
Published: July 2018

SummaryYoga is known to induce beneficial effects on physiological, biochemical and mental functions in man. Its effects on blood coagulation are not known. A study was conducted in seven previously untrained male adults who underwent a combination of yogic exercises, daily for one hour, over a period of four months. Parameters of blood coagulation were estimated before and after the end of yoga training. The following changes were observed: Fibrinolytic activity increased significantly with a concomitant fall in fibrinogen; activated partial thromboplastin time and platelet aggregation time were prolonged; blood and plasma platelets showed a rise; and both haemoglobin and heamatocrit were raised at the end of the training.These findings suggest that yoga induces a state of blood hypocoagulability. The impact of yoga on prevention of cardiovascular and thrombotic disorders is obvious.
Identification of Subpopulations of Human Urinary Plasminogen Activators
Authors: Hart David A , Kramer Robert , Cieplak Witold 
Published: July 2018

SummaryEnzymes functioning as plasminogen activators in commercial urokinase preparations and individual human urine concentrates were subjected to affinity chromatography on columns of lentil lectin-sepharose, ricin-sepharose, wheat germ agglutinin-sephar-ose, lotus lectin-sepharose and concanavalin A-sepharose.Chromatography of the enzymes from both sources yielded similar results for all lectins except lentil lectin. Urokinase from several commercial sources was approximately 50% adherent to lentil lectin-sepharose while only 5-10% of the urinary plasminogen activators from individuals was adherent to this lectin. SDS-PAGE followed by zymography indicated that the observed differences between commercial and individual samples could be due to the presence in urine concentrates of subpopulations of plasminogen activators which were absent from the commercial samples.
Outcome of Treatment of Deep-Vein Thrombosis with Urokinase: Relationship to Dosage, Duration of Therapy, Age of the Thrombus and Laboratory Changes
Authors: D’Angelo A , Mannucci P M 
Published: July 2018

SummaryForty-one patients with phlebographically proven DVT of the popliteal, femoral or iliac veins were treated with different regimens of urokinase (UK) given by continuous intravenous infusion. The four groups were comparable with respect to localization, extension and estimated age of the thrombi. Another phlebographic picture was taken within 48 hr after the end of UK infusion. Substantial lysis had occurred in 2 of 10 patients treated with 1500 U/kg/h for 2 days, in 4 of 11 treated with 2500/U/kg/h for 3 days, in 2 of 10 treated with 2500 U/kg/h for 7 days and in 4 of 10 treated with 4000 U/kg/h for 4 days. Only thrombi younger than 8 days could be lysed, with 61% (8/13) rate of lysis for thrombi less than 5 days old. Bleeding complications were observed more frequently with the higher doses and longer durations of therapy. The four treatment regimens all induced dose-dependent changes in fibrinogen, fibrin(ogen) degradation products, plasminogen and antiplasmin. Neither pre- nor postinfusion values of these parameters could differentiate patients with lysis from those without lysis. It is concluded that UK can provoke a high rate of thrombolysis of DVT treated early after the appearance of symptoms but that there is no relationship between UK-induced modifications of fibrinolysis and the outcome of therapy.
Effect of Venous Stasis on Vessel Wall Fibrinolysis
Authors: Stenberg Björn , Bylock Anders , Risberg Bo 
Published: July 2018

SummaryThe effects of prolonged venous stasis on release of plasminogen activators (PA) from the caval vein of rats were studied.PA activity was continuously reduced in the intimal layer and after 8 hr of stasis the reduction was statistically significant. After 2 and 3 days no intimal PA activity was found. The PA activity in the adventitial vasa vasorum was unchanged during the experimental period.
Human Leukocyte Elastase-Like Proteinase Purified by Affinity Chromatography with Suc-L-Tyr-D-Leu-D-Val-pNA, and Its Identification with Human Spleen Fibrinolytic Proteinase
Authors: Nagamatsu Y , Okamoto U , Tsuda Y , Okada Y 
Published: July 2018

SummaryElastase-like proteinase (ELP) extracted with 2 M NaClO4 from human leukocytes was purified by a new affinity chromatography technique with Suc-L-Tyr-D-Leu-D-Val-pNA, following delipidation, salting out and Sephadex gel chromatography. The purified preparation contained practically no chymotrypsin-like proteinase activity, and it was homogeneous on SDS polyacrylamide gel electrophoresis. The enzyme so purified readily degraded fibrin, fibrinogen, elastin and -Val type synthetic peptide substrates, such as Suc-L-Ala-L-Tyr-L-Leu-L-Val-pNA and Suc-L-Tyr-L-Leu-L-Val-pNA. A special increase in ELP activity by adding chaotropic ions was observed. The enzymatic properties of the ELP were very similar to those of spleen fibrinolytic proteinase (SFP). ELP and SFP were identified immunologically using mice antisera against purified ELP.
Acute Platelet Activation Induced by Smoking
Authors: Schmidt Kai Gjerløff , Rasmussen Jens Wæver 
Published: July 2018

SummaryIndices of acute in vivo platelet activation in response to cigarette smoking were sought in 10 healthy subjects. Judging by platelet aggregate ratio, platelet factor 4 and beta-thromboglobulin measurements, platelet activation took place from 10 to 30 min after smoking in most subjects. These signs correlated well with the results of scintigraphic studies showing signs of accumulation of 111-In-labelled platelets in the spleen in response to smoking.
Congenital Hemorrhagic Disorders in Jordan
Authors: Awidi Abdalla S 
Published: July 2018

SummaryThe results of a three year prospective study of inherited bleeding syndromes in Jordan is presented. There were 112 patients from 64 families. Of these there were 42 patients with hemophilia A, 23 with Glanzmann’s thrombasthenia, 22 with von Willebrand’s disease, 11 with Christmas disease, 6 with hypofibrinogenemia, 3 with afibrinogenemia, 2 with factor XIII deficiency, 2 with storage pool disease and 1 with factor XI deficiency. The pattern of inherited bleeding syndromes in Jordan is different from that seen in Europe and U.S.A. in that Glanzmann’s thrombasthenia is very common. High proportion of hemophiliacs were severe. Arthropathy was common. A significant number of bleeders had fatal hemorrhage. In a high proportion of patients, no family history of bleeding was found.
Evidence for Impaired Hepatic Vitamin K1 Metabolism in Patients Treated with N-Methyl-Thiotetrazole Cephalosporins
Authors: Bechtold H , Andrassy K , Jähnchen E , Koderisch J , Koderisch H , Weilemann L S , Sonntag H-G , Ritz E 
Published: July 2018

SummaryIn 8 patients on no oral intake and with parenteral alimentation, administration of cephalosporins with N-methyl-thiotetrazole side chain (moxalactam, cefamandole), was associated with prolongation of prothrombin time, appearance in the circulation of descarboxy-prothrombin (counter immunoelectrophoresis and echis carinatus assay) and diminution of protein C. Acute administration of 10 mg vitamin Ki was followed by the transient appearance of vitamin K1 2,3-epoxide, indicating an impaired hepatocellular regeneration of vitamin K1 from the epoxide. Impaired hepatic vitamin K1 metabolism, tentatively ascribed to the N-methyl-thiotetrazole group, is one (but possibly not the only) cause of bleeding complications and depression of vitamin K1dependent procoagulants in patients treated with the new class of cephalosporins.
Immunocytochemical Localization of Albumin and Factor XIII in Thin Cryo Sections of Human Blood Platelets
Authors: Sixma Jan J , van den Berg Agnes , Schiphorst Marion , Geuze Hans J , McDonagh Jan 
Published: July 2018

SummaryAlbumin and factor XIIIa2 were localized in human blood platelets by immunofluorescence and protein A-colloidal gold immuno-electron microscopy using thin and ultrathin cryosections of mildly fixed human blood platelets. Albumin was found in α-granules, co-distributing with β-thromboglobulin in double label experiments. In platelets directly fixed in plasma, without previous washing, albumin was also localized on the plasma membrane and in the surface connecting system. Factor XIIIa2 was localized diffusely through the entire cytoplasmic matrix.
Triglyceride-Rich Lipoproteins Are Responsible for Thrombin Generation Induced by Lipid Peroxides
Authors: Barrowcliffe T W , Gray E , Kerry P J , Gutteridge J M C 
Published: July 2018

SummaryPrevious studies have shown that lipid peroxides promote thrombin generation in platelet-poor plasma. In the present study, it has been shown that triglyceride-rich lipoproteins, especially chylomicra of dietary origin, are responsible for this procoagulant activity. The generation of thrombin by lipid peroxides is also enhanced by their inhibitory action on antithrombin III. These results suggest a possible new relationship between dietary fat, lipid peroxidation and thrombus formation.
Severe Inherited “Homozygous” Protein C Deficiency in a Newborn Infant
Authors: Estellés A , Garcia-Plaza I , Dasí A , Aznar J , Duart M , Sanz G , Pérez-Requejo J L , España F , Jimenez C , Abeledo G 
Published: July 2018

SummaryA relapsing clinical syndrome of skin lesions and disseminated intravascular coagulation (DIC) that showed remission with the infusion of fresh frozen plasma is described in a newborn infant with homozygous deficiency of protein C antigen.This patient presented since birth a recurrent clinical picture of DIC and ecchymotic skin lesions that resembled typical ecchymosis except for the fact that they showed immediate improvement with the administration of fresh frozen plasma. Using an enzyme linked immunosorbent assay method, the determination of protein C antigen levels in the patient, without ingestion of coumarin drugs, showed very low values (<1%).No other deficiencies in the vitamin-K-dependent factors or in anti thrombin III, antiplasmin, and plasminogen were found. Seven relatives of the infant had heterozygous deficiency in protein C antigen (values between 40-55%), without clinical history of venous thrombosis. The pedigree analysis of this family suggests an autosomal recessive pattern of inheritance for the clinical phenotype, although an autosomal dominant pattern has been postulated until now in other reported families.We conclude that our patient has a homozygous deficiency in protein C and this homozygous state may be compatible with survival beyond the neonatal period.
Heparin Cofactor II Determination - Levels in Normals and Patients with Hereditary Antithrombin III Deficiency and Disseminated Intravascular Coagulation
Authors: Tran Tri H , Duckert F 
Published: July 2018

SummaryA technique is described to completely remove antithrombin III (AT) from small amounts of human plasma by immunoaffinity chromatography on antibodies against human AT linked to Sepharose 4B. The level of heparin cofactor II (HCII) was not affected by the immunoadsorption. HCII activity was then determined by measuring the rate of human thrombin inhibition by 3 ways: a) activation with heparin in AT-free plasma, b) activation with dermatan sulfate in normal plasma and c) activation with dermatan sulfate in AT-free plasma. The normal range of HCII varied between 0.7-1.5 U/ml, as compared to a normal plasma pool containing by definition 1 U/ml. Highly significant correlations between assays as obtained from 40 normal plasmas proved the suitability of the 3 assays, although the progressive thrombin inhibition by AT, when not removed, contributed about one fifth to the thrombin inhibition by HCII in the presence of dermatan sulfate. There were also highly significant correlations between HCII activity and antigen, as determined by rocket immunoelectrophoresis using specific antibodies against HCII.Levels of HCII and AT were examined in 7 patients with hereditary AT deficiency and 7 patients with disseminated intravascular coagulation (DIC). In hereditary AT deficiency, whereas the AT activity was reduced by half, levels of HCII activity and antigen were in the normal range. In DIC, a parallel decrease of HCII and AT suggests that HCII may participate in the inhibition of thrombin released during DIC and thus provides an inhibitor reserve, once the AT level becomes subnormally low.
The Inhibitory Effect of Heparin and Related Glycosaminoglycans on Neutrophil Chemotaxis
Authors: Matzner Yaacov , Marx Gerard , Drexler Ruth , Eldor Amiram 
Published: July 2018

SummaryClinical observations have shown that heparin has antiinflammatory activities. The effect of heparin on neutrophil chemotaxis was evaluated in vitro in the Boyden Chamber. This method enabled differentiation between the direct effects of heparin on neutrophil migration and locomotion, and its effects on chemotactic factors. Heparin inhibited both the random migration and directed locomotion of human neutrophils toward zymosan-activated serum (ZAS) and F-met-leu-phe (FMLP). Inhibition was found to be dependent on the concentrations of the heparin and of the chemotactic factors. No specific binding of heparin to the neutrophils could be demonstrated, and heparin’s inhibitory effects were eliminated by simple washing of the cells. When added directly to the chamber containing chemotactic factor, heparin inhibited the chemotactic activity of ZAS but not that of FMLP, suggesting a direct inhibitory effect against C5a, the principal chemotactic factor in ZAS.Experiments performed with low-molecular-weight heparin, N-desulfated heparin, dextran sulfate, chondroitin sulfate and dextran indicated that the inhibitory effects of heparin on neutrophil chemotaxis are not related to its anticoagulant activity, but probably depend on the degree of sulfation of the heparin molecule.