bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Study of Human Platelet Esterases
Authors: Kilburn E. P , Firkin B. G 
Published: June 2018

Summary1. Platelet esterase activity has been estimated using a manometric technique. The most suitable substrate used was tributyrin. Tributyrinase activity corresponded with DFP32 uptake by the platelet and probably reflected overall esterase activity. Evidence has been presented that this enzyme is an integral part of the platelet.2. Platelet esterase activity rapidly diminished on storage at 4° C and was peculiarly susceptible to cell lysis. This activity may be an index of platelet viability.3. No direct correlation could be found between platelet esterase activity and platelet aggregation.
A Study of Factors Influencing the Enzymatic Elimination of Adenosine Diphosphate in Blood
Authors: Howe E. E , Bosshardt D. K 
Published: June 2018

SummaryThe red cells carry by far the greater part of the enzyme systems capable of eliminating adenosine diphosphate found in the blood but this activity is more concentrated in the platelets.These “ADPase” systems are strikingly stimulated by divalent cations with Mg++ being the most effective ion. Ca++, while possessing some effect, is antagonistic to Mg++ in the platelet system.A heat stable enhancing factor for the platelet “ADPase” system was shown to be present in platelet poor plasma. This factor was ineffective in preparations obtained from erythrocytes.
Comparison of In Vivo Effects on Components of the Canine Fibrinolytic Enzyme System of AMCHA Fed at Varying Dose Levels
Authors: Celander Evelyn , Celander D. R 
Published: June 2018

SummaryDogs were fed varying levels of trans-AMCHA (trans-4-aminomethyl-cyclohexane-1-carboxylic acid), a known inhibitor of the fibrinolytic enzyme system. Evidence that dialysis against citrate-veronal buffer in the cold for 24 hrs effectively removes AMCHA from plasma is presented. Determinations of antiactivator, antifibrinolysin, and proactivator were carried out on both dialyzed and undialyzed samples. At 55 mg/kg, a moderate immediate decrease in urokinase excretion occurred which was maintained throughout the time of drug administration. At higher levels, increases in antiactivator and decreases in proactivator and euglobulin lytic activity occurred, the extent of which could be roughly correlated with the amount of drug administered. No changes in either fibrinogen or antifibrinolysin were seen. An assay for the antiurokinase activity in canine plasma is described. The results are discussed in terms of the possible function of the fibrinolytic system as revealed by administration of inhibitors.
Thrombus Formation Time in Hemophilia An In Vitro Study
Authors: Giordano N. D , Radivoyevitch M , Goodsitt E 
Published: June 2018

SummaryAn in vitro study was performed with 14 hemophilia-A patients, using a simple wheel with an electrically driven motor to form thrombi.The findings are discussed in relationship to normal thrombi and a direct comparison was made in regard to rate of thrombus formation, thrombus length and morphological differences.A relationship between the above and clinical severity of the disease with some speculations on the possible role played by white and red cells on thrombus formation time, was also presented.
Activation of Hageman Factor by α-Adrenergic Stimulation
Authors: McKay D. G , Latour J.-G , Parrish Mary H. 
Published: June 2018

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.
Isolierung und Charakterisierung des fibrinstabilisierenden Faktors aus menschlichen Thrombozyten
Authors: Bohn H 
Published: June 2018

ZusammenfassungDer fibrinstabilisierende Faktor der menschlichen Thrombozyten wurde isoliert und rein in kristalliner Form erhalten. Seine Eigenschaften werden mit denen von Plasma-Faktor XIII verglichen. Physikalisch-chemisch unterscheidet sich der Thrombozyten-Faktor XIII wesentlich von dem aus Plasma isolierten Faktor XIII : die Molekulargewichte, die Untereinheiten sowie die Kohlenhydrat- und Aminosäurenzusammensetzung sind verschieden. Immunologisch zeigen die fibrinstabilisierenden Faktoren aus Plasma und Thrombozyten eine gewisse Übereinstimmung. Beide haben eine Antigendeterminante, die mit dem aktiven Zentrum in Zusammenhang stehen muß, gemeinsam; die gegen diesen Antigenbezirk gerichteten Antikörper hemmen die fibrinvernetzende Aktivität beider Faktoren. Eine zweite im Plasma-Faktor XIII vorkommende Antigendeterminante fehlt im Faktor XIII aus Thrombozyten.
The Appearance and Destruction of Platelet-Clumping Substance in Serum Added with Trypsin
Authors: Yamazaki H , Murase H , Ijiri H , Shimamoto Tatsuo 
Published: June 2018

SummaryNo platelet-clumping activity was detected in the serum collected from 10 rabbits. After incubation of the alkalinized serum for 2 to 4 min at 37° C with 1.6 or 3.2 mg/ml of trypsin, platelet-clumping activity was observed in all samples. The strongest response was observed in the serum incubated for 4 min with 3.2 mg/ml of trypsin. After incubation for over 8 min, the clumping activity decreased gradually. At any incubation time, the serum without trypsin or with 0.4 or 6.4 mg/ml of trypsin showed no clumping activity. After the above measurements of the activity, 100 u/ml of heparin was added to the serum and its pH value was adjusted to 5.6. In the serum without trypsin the clumping activity appeared. However, in the active serum with trypsin, the activity remained the same or decreased. The serum acidified to pH 5.6 with heparin, which showed platelet-clumping activity, was incubated at 37° C with 1.6, 3.2 or 6.4 mg/ml of trypsin. After incubation of the serum with 3.2 mg/ml of trypsin for 16 min, the activity was markedly reduced. After incubation with 6.4 mg/ml of trypsin for 2 min, the activity disappeared. After incubation with trypsin, the clumping activity was observed in BaSO4-adsorbed serum but was not observed in serum heated at 56° C for 1 min nor in serum to which EDTA was added in a final concentration of 0.1%. These results suggest that the precursor of the platelet-clumping substance was activated by trypsin, and the platelet-clumping substance and/or its precursor was destroyed by trypsin.
The Fibrinolytic System in Patients with Right Ventricular Failure Treated with Novurit
Authors: Worowski K , Gabryelewicz A , Prokopowicz J , Popławski A 
Published: June 2018

SummaryIt has been found that the activity of the fibrinolytic system is decreased in patients treated with Novurit. No changes were observed in patients treated with hydrochlorothiazide. Attention is drawn to the risk of administering organic mercurial diuretics to patients with a tendency toward hypercoagulability.
Structural Changes in Prothrombin during Activation: A Theory
Authors: Seegers Walter H. , Murano Genesio , McCoy Lowell 
Published: June 2018

SummaryProperties of the thrombin zymogen are quite different when in the form of prothrombin complex, DEAE-prothrombin (prothrombin) or prethrombin. When removed from the prothrombin complex, prothrombin spontaneously became refractory to the two-stage analytical reagents. No new N-terminal amino acids formed in association with this activation. A first step in prothrombin activation might be related to conformation. Repeatedly one mole of alanine was found as N-terminal amino acid for prothrombin and it is thus a single chain protein. Prethrombin did not have this alanine, but lysine and threonine, were found. Prethrombin, like thrombin, thus had two chains. After the conversion of prethrombin to thrombin with purified autoprothrombin C, a new N-terminal alanine amino acid was found attached to a peptide. Additionally peptides with N-terminal serine, lysine, and glycine were found. Threonine and isoleucine were again found as the N-terminal amino acids for 3.7 S thrombin and 3.2 S thrombin. As a working hypothesis, a perspective on the possible structure of prothrombin is outlined on the basis that it contains two moles of thrombin. Prethrombin probably forms when Ala1-peptide splits from a polypeptide chain which forms a loop held together by a disulfide bridge. Proteolysis probably also occurs in this loop. The postulated disulfide bridge would be the one which holds the A and B chains of thrombin together. In the conversion of prethrombin to thrombin, the first mole of thrombin would be set free. Then the Ala2-peptide released might correspond to the Ala1-peptide removed when prethrombin originally formed. Ala2-peptide thus would be related to the second mole of thrombin which could arise by further proteolysis including a split in the loop held together by a disulfide bridge. It is postulated that acidic peptides are attached to the main prothrombin polypeptide chain, to prethrombin, and to 3.7 S thrombin as satellite material.
Further Studies on Thrombin-Coagulase
Authors: Soulier J. P , Prou O , Hallé L 
Published: June 2018

SummaryA kinetic study of the interaction between prothrombin and staphylocoagulase shows that the thrombic activity which forms (thrombin-coagulase) is the result of a molecular complex in which the active site of prothrombin is exposed but other sites necessary for adsorption or inhibitors action are masked. The high speed of the activation, the independence from the temperature, and the fact that the yield of thrombin activity is directly related to the amount of each of the two reagents are the main arguments against an enzymatic splitting of prothrombin by staphylocoagulase. Some further properties of thrombin-coagulase complex are studied.
The Interaction of Platelets with Polymer Surfaces
Authors: Lyman D. J , Klein K. G , Brash J. L , Fritzinger B. K 
Published: June 2018

SummaryA direct relationship has been shown between platelet adhesion and critical surface tension of uncharged hydrophobic polymers when the air-blood interface is avoided. The similarity of this relationship to the previously observed relationship between critical surface tension and surface thrombogenicity suggests a possible major role for platelet activation as the initiating step in the surface-induced coagulation of blood on uncharged, hydrophobic polymers. The apparent damaging effects of a blood-air interface, as indicated by unusually heavy platelet adhesion suggests that such interfaces should be avoided in all blood/surface studies.
Studies of Platelet Aggregation, Plasma Adenosine Diphosphate Breakdown and Blood Coagulation in Magnesium Deficient Calves and Rats
Authors: Stevenson M. M , Yoder I. I 
Published: June 2018

SummaryADP-induced platelet aggregation and the breakdown of ADP in platelet-poor plasma of normal and magnesium deficient calves and rats have been studied. There was no statistically significant difference in ADP-induced platelet aggregation between the treated and untreated groups of animals. There was a significant difference in the ADP breakdown in platelet poor plasma of magnesium deficient rats as compared to the untreated animals. The platelet count of the magnesium deficient calves and in the citrated platelet-rich plasma of the magnesium deficient rats was not different from the normal. The thrombin clotting and partial thromboplastin times were significantly shortened in the magnesium deficient calves, but the prothrombin time was not affected. These findings suggest that pathological alterations in the serum magnesium levels that are still compatible with life do not influence adenosine diphosphate-induced platelet aggregation but do affect the breakdown of adenosine diphosphate in the plasma of rats. Just as magnesium administration may produce an anticoagulant effect, so may magnesium depletion produce a procoagulant effect in the blood of animals rendered magnesium deficient by diet. The clinical implications of this are discussed.
Blutgerinnung und Fibrinolyse im Nabelschnurblut
Authors: Gmür J. P , von Felten A , Straub P. W 
Published: June 2018

ZusammenfassungEs wurde die Blutgerinnung und Fibrinolyse in dem durch Punktion der Nabelschnurvene gewonnenen Blut von 140 Neugeborenen untersucht und die Resultate denjenigen zahlreicher früherer Arbeiten gegenübergestellt.1. Fibrinogen- und Faktor-V-Spiegel lagen praktisch immer im Erwachsenen-Normalbereich.2. Die Thrombinzeit war bei 85% der Neugeborenen verlängert. Eine Erhöhung des endogenen Heparins konnte als Ursache ausgeschlossen werden. Die Thrombinzeit-verlängerung der meisten Neugeborenen dürfte auf eine fibrinolytische Alteration des Fibrinogens zurückzuführen sein. Bei einigen Neugeborenen konnte aber die Existenz eines funktionell andersartigen, »fetalen« Fibrinogens nicht sicher ausgeschlossen werden.3. Die fibrinolytische Aktivität – bestimmt durch die Euglobulinlysezeit, die bovine, nicht erhitzte Fibrinplatte und die Immunelektrophorese auf Fibrinogenabbaupro-dukte – war bei rund 60% der Neugeborenen erhöht. Die Vollblutfibrinolyse und die Parakoagulation durch Protaminzugabe im Serum erwiesen sich hingegen als zu wenig empfindliche Methoden zur Erfassung der Fibrinolyse im Nabelschnurblut.
Beeinflussung der Wirkung einiger indirekter Antikoagulantien durch Monoaminoxydase-Hemmer
Authors: Reber K , Studer A 
Published: June 2018

ZusammenfassungDie Antikoagulantien Phenindione, Chiorphenadione, Diphenadione, Phen- procoumone, Chlorphenylpropyl-oxy-coumarin, Cumachlor und Acenocoumarol werden zusammen mit den Monoaminoxydase-Hemmern Phenylcy clopropyl- amin, Isocarboxazid, Iproniazid, Nialamid und l-p-Chlorbenzoyl-2-[oc-methyl- ß-(N-isopropyl-carbamyl)-aethyl-isopropyl]-hydrazin an der Patte untersucht im Hinblick darauf, ob die Kombinationen eine Modifikation der Gerinnungshemmung ergeben. Die gerinaungshemmende Wirkung einzelner Antikoagulantien wie Phenindione kann gesteigert werden, während sich die Wirkung anderer Antikoagulantien, wie z.B. Chlorphenadione und Phenprocoumone schlecht bzw. nicht beeinflussen läßt. Von den Monoaminoxydase-Hemmern zeigen Phenylcyclopropylamin und Nialamid in mehreren Fällen eine Steigerung der gerinnungshemmenden Wirkung, während Iproniazid in keinem Fall wirkam wird. Die übrigen Monoaminoxydase-Hemmer scheinen eine Mittelstellung einzunehmen.
Mechanism of Action and Some Properties of a Tissue Activator of Plasminogen
Authors: McCall Dolly Cannamela , Kline D. L 
Published: June 2018

Summary1.	Improvements in preparations of tissue activator and plasminogen and termination of activation by epsilon aminocaproic acid have permitted the use of a quantitative caseinolytic assay for the measurement of the plasmin formed. The following data indicate that the activation of plasminogen by tissue activator is catalytic :a)	Biphasic curve obtained when velocity was plotted against plasminogen concentration.b)	First order kinetics.c)	Dependence of the turnover number on tissue activator concentration.2.	The temperature and pH stability of tissue activator were similar to those reported for urokinase. Since both of these enzymes have now been shown to activate plasminogen by a catalytic mechanism, these data support the suggestion that urokinase may be an excretory form of tissue activator which has been released into the circulation.
Plasminogen Assay by Means of the Lysis Time Method
Authors: Berg W , Korsan-Bengtsen K , Ygge J 
Published: June 2018

SummaryThe lysis time method for the determination of plasminogen has been investigated using plasminogen-free thrombin and fibrinogen preparations.The experiments have shown that the lysis of a fibrin clot is the result of two consecutive reactions: the formation of fibrin which proceeds as a first order reaction and the degradation of fibrin which proceeds as a zero order reaction. Plasminogen is activated in a separate reaction. If the rate of the fibrin formation is much greater than the rate of degradation, the lysis of the fibrin clot is approximately of zero order in fibrin. The lysis time will then be inversely proportional to the plasmin concentration and proportional to the fibrinogen concentration. In a double logaritmic system the correlation between lysis time and plasmin activity is a straight line with a slope of 135°.Plasminogen is rapidly activated with streptokinase. Maximal activation is obtained only with a certain streptokinase concentration. Higher concentrations inactivate plasmin and with lower concentrations, the maximal activity is never reached. A spontaneous inactivation is seen after about 30 minutes. With urokinase, a higher maximal plasminogen activity is obtained than with streptokinase. Urokinase in higher concentrations does not inactivate plasmin.A standard assay for determination of plasminogen by the lysis time method has been worked out and is based on these results.
A Comparative Study of the Inhibitors of Fibrinolysis in Human, Dog and Rabbit Blood
Authors: Gallimore M. J , Nulkar M. V , Shaw JTB 
Published: June 2018

SummaryComparison of sera from dog, rabbit and man shows that dog serum contains most fibrinolytic inhibitor and human serum least. The inhibitors are potentiated by a variety of inorganic salts, of which sodium chloride is most effective. Euglobulin fractions precipitated from rabbit and human plasma at pH 5.3 contain small amounts of inhibitory material, whereas little remains in the corresponding dog euglobulin or in euglobulins from all three species when precipitated at pH 6.0. The potentiation of fibrinolytic inhibitors by sodium chloride differs between the three species, suggesting that their composition is not identical. Chloroform extraction removes a proportion of the inhibitory material from each serum.
Studies on the Adsorption and Activation of the Hageman Factor (Factor XII) by Collagen and Elastin
Authors: Niewiarowski St , Bańkowski E , Rogowicka Irena 
Published: June 2018

SummaryIt has been found that Hageman factor is adsorbed from normal human plasma by collagen and elastin. The adsorption is dependent upon the concentration of both substances and upon the adsorption time. The adsorption by collagen is almost selective. By the procedure of the repeated adsorption it is possible to obtain plasma containing 3-5% of Hageman factor normal value and normal amount of PTA (factor XI). At pH 9.5-10.0 the Hageman factor can be eluted in part from collagen shaken previously with human or pig plasma, its recovery in the eluates from elastin is poor.Experimental evidence is presented that the Hageman factor is activated following adsorption on collagen. The eluates from collagen have been compared with those prepared in a similar manner from kaolin and celite. All eluates possess clot promoting, TAMe arginine esterase and fibrinolytic activities. They shorten considerably the clotting time of the whole blood in siliconized tubes.It has been suggested that collagen may act as an intrinsic trigger of the blood coagulation in vivo by adsorbing and activating the Hageman factor.
Faktoren des fibrinoly tisch en Systems bei Leberkrankheiten
Authors: vandeLoo J , Schmiesing G 
Published: June 2018

ZusammenfassungBei 80 Leberkranken wurden Plasmin, Plasminogen und der sogenannte »Proaktivator« im Plasma bestimmt. Bei Kranken mit BLepatitis nnd Zirrhose ist gesteigerte spontane Plasminaktivität sowie deutliche Verminderung des »Proaktivators« nachweisbar, wogegen Plasminogen keine eindeutigen Veränderungen erkennen läßt. Bei akuter Hepatitis und akut-entzündlichen Stadien der Zirrhose ist der stärkste Abfall des »Proaktivators« zu messen, mit der Abheilung der Hepatitis geht ein langsamer Wiederanstieg parallel. Die normalen Proaktivatorwerte bei extrahepatischen Gallengangsverschlüssen sind möglicherweise als differentialdiagnostische Methoden zu verwerten.Die gesteigerte fibrinolytische Spontanaktivität bei Leberkrankheiten wird auf die kombinierte Wirkung einer vermehrten Freisetzung von Gewebsaktivatoren und Verminderung des Antiplasmins bezogen. Die Verminderung des sogenannten »Proaktivators« ist wahrscheinlich nicht durch erschöpfende Aktivierung des Systems, sondern durch ungenügende Nachlieferung aus der Leber als Bildungsstätte des »Proaktivators« bedingt.
Management of venous thromboembolism
Authors: Haas Sylvia 
Published: June 2018

SummaryThe therapy of deep venous thrombosis consists of several elements and depends on the localization, the age and the extent of the thrombus. In addition, the patient’s age and the life expectancy may influence the modality of treatment. The present overview discusses various types of initial therapy and long-term treatment of venous thromboembolism and also reviews future perspectives of pharmacological treatment. The initial treatment regimens comprise thrombolysis, thrombectomy, inferior vena cava filters and the anticoagulation with either unfractionated heparin or low molecular weight heparins. Thrombolysis is only effective in the initial phase of acute thromboembolic disorders, and the potential benefits must be balanced against the risk of hemorrhage. In the case of totally occlusive venous thrombosis, a successful outcome is more likely if the thrombolytic agent is infused into the thrombus via catheter directed thrombolysis. Thrombectomy should be considered in patients with acute iliofemoral venous thrombosis of less than seven days duration and a life expectancy of more than ten years. A filter device should be inserted in the inferior vena cava in patients with venous thrombosis above the knee when anticoagulation is contraindicated or when adequate anticoagulation fails to prevent recurrent embolism. The intravenous administration of unfractionated heparin has been the modality of choice for initial treatment of venous thromboembolism during several decades, however, this type of therapy requires an aPTT-adjusted dosing due to a broad interindividual variation of laboratory results. Numerous clinical trials have provided firm evidence that low molecular weight heparins given subcutaneously are significantly superior to intravenous, unfractionated heparin with regard to thrombus regression and reductions of severe hemorrhages, mortality and recurrent thromboembolism. Thus, these preparations may become the treatment of choice in the near future. Pulmonary embolism may be treated with low molecular weight heparins as well.Long-term treatment of venous thromboembolism is usually performed with oral anticoagulants. The recommended therapeutic range is an INR of 2.0 to 3.0, however the optimal duration of oral anticoagulant therapy for patients with acute proximal deep venous thrombosis is uncertain.Various thrômbin-inhibitors have been tested for initial treatment of thrombosis, however further investigations of their efficacy, safety and cost-effectiveness will have to provide firm evidence on their superiority when compared to unfractionated or low molecular weight heparins.
Das postthrombotische Syndrom
Authors: Wuppermann Th. 
Published: June 2018

ZusammenfassungDie häufige periphere Gefäßerkrankung postthrombotisches Syndrom leidet einerseits unter der verbreiteten Mißachtung seit langem bewährter Regeln, besonders bei der Kompressionsbehandlung. Andererseits sind die beträchtlichen Fortschritte der letzten 10 Jahre im Verständnis der Pathophysiologie, in der Diagnostik und der Therapie vielfach unbekannt geblieben.
Der Impact Factor
Authors: Finzen A. 
Published: June 2018

ZusammenfassungWissenschaftliche Leistungen leben von der Originalität ihrer Urheber. Der Versuch, sie zu quantifizieren, erscheint als Widerspruch in sich. Um so irritierender ist der Siegeszug des sogenannten Impact Factors, eines Konstrukts des amerikanischen Institute of Scientific Information (ISI), das den Anspruch stellt, über die Häufigkeit der Zitierung von - vom ISI erfaßten - Zeitschriften das Gewicht der in diesen publizierenden Wissenschaftler zu messen. Seit naturwissenschaftliche und medizinische Forschungseinrichtungen und Fakultäten dazu übergehen, den Impact Factor zur Grundlage für die Verteilung von Forschungsgeldern und zur Guillotine für wissenschaftliche Karrieren zu machen, schickt er sich an, die internationale Wissenschaftskultur zu verändern. Deshalb ist es an der Zeit, daß die Öffentlichkeit dieses Zeitgeistphänomen zur Kenntnis nimmt und sich mit seinen Folgen airseinandersetzt.