bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Autoprothrombin II-A on Epinephrine-Induced Platelet Aggregation of Normal- and Coumadin-Treated Dogs
Authors: Herman Gilbert E , Seegers Walter H , Henry Raymond L 
Published: July 2018

SummaryPlatelet-rich plasma from dogs and from coumadin-treated dogs aggregated at the same optimum concentration of epinephrine. Neither protein C nor its active form called autoprothrombin II-A was necessary for aggregation of dog platelets with epinephrine. For platelet aggregation, suboptimal concentrations of epinephrine were potentiated by addition of purified autoprothrombin II-A. The latter, by itself, induced platelet aggregation in high concentration.
Thromboxane Generation and Platelet Aggregation in Survivals of Myocardial Infarction
Authors: Szczeklik A , Gryglewski R J , Musiał J , Grodzińska L , Serwońska M , Marcinkiewicz E 
Published: July 2018

SummaryArachidonic acid (AA)-induced platelet aggregation was studied in platelet-rich plasma of 30 male patients who survived myocardial infarction and in 30 healthy men of similar age. Mean platelet aggregation thresholds to A A were 746 ± 62 μM, and 869 ± 57 μM, respectively. Only in 2 healthy subjects, but in 12 patients, irreversible platelet aggregation was induced consistently with low concentrations of AA, under 500 μM. The rate of conversion of AA to thromboxane A2 (TXA2) by platelets of these patients was augmented. Furthermore, less endogenous TXA2 was required to trigger aggregation of their platelets as compared to the controls. We have also shown that in platelet-poor plasma of these patients with “hyperreactive” platelets there exists a transferable factor which makes platelets of healthy subjects more prone to aggregatory action of AA.It is proposed that the assessment of platelet aggregability with AA provides a tool for identifying a subgroup of patients with coronary heart disease who might substantially benefit from the secondary preventive treatment with aspirin and with other antiplatelet drugs which inhibit the generation of TXA2 in platelets.
Smoking and Risk Factors in Deep Vein Thrombosis
Authors: Prescott R J , Jones D R B , Vasilescu C , Henderson J T , Ruckley C V 
Published: July 2018

SummaryThe incidence of deep vein thrombosis (DVT) as diagnosed by the 125I fibrinogen test (125IFT) was determined in a series of 300 newly admitted medical and 201 surgical patients. 6 medical patients died before 125IFT screening could be completed. The incidence of DVT was l4% in medical patients and 18% in surgical patients. Increasing age, a malignant condition and a past history of thromboembolism all increased the risk of DVT. Increasing levels of cigarette smoking were found to be associated with a reduced incidence of DVT. Although statistical significance was achieved at only the 10% level for this finding it is in agreement with the results from studies on patients with myocardial infarction. The protective effect of cigarette smoking was observed at all ages, and in both medical and surgical patients.
Cyclic Nucleotides in Platelet Function
Authors: Haslam R J , Davidson M M L , Fox J E B , Lynham J A 
Published: July 2018

SummaryInhibition of adenylate cyclase in intact platelets by addition of compounds such as 2’, 5’- dideoxyadenosine prevented the inhibition of platelet aggregation by PGE1 but did not affect the responses of platelets to aggregating agents in the absence of PGE1. This confirms that cyclic AMP mediates the effects of PGE1 but indicates that the level of cyclic AMP in unstimulated platelets is too low to affect the actions of aggregating agents. Studies on the phosphorylation of proteins in intact 32P-labelled platelets showed that PGE1 increased the phosphorylation of a membrane-bound polypeptide (P24) and prevented the increased phosphorylation of other polypeptides (P47 and P20) that occurred on addition of inducers of the release reaction. It is suggested that the cyclic AMP-dependent phosphorylation of P24 stimulates the active transport of Ca2+ out of the platelet cytosol, so preventing phosphorylation of P47 and P20, reactions which may be involved in the release mechanism. As increases in platelet cyclic GMP could be dissociated from both platelet aggregation and the release reaction, it is proposed that the bidirectional regulation of platelet function is achieved primarily by the opposing actions of increases in the concentrations of Ca2+ and cyclic AMP.
Characterization and Experimental Use of a Monospecific Antiserum to Factor IX
Authors: Pechet Liberto , Tiarks Cheryl Y , Chang Chin-Hai , Sudhindra Ramakrishna R , Lipworth Leslie 
Published: July 2018

SummaryPurified human factor IX was used to develop xenogeneic neutralizing and precipitating antibodies. The final antiserum (R2) neutralized only factor IX and was equivalent to 220 Bethesda-inhibitory units. It showed two precipitating lines, one of which disappeared after absorption with human albumin. On immunodiffusion and Laurell immunoelectrophoresis, the albumin-absorbed R2 antiserum showed one precipitin line of identity, or one rocket respectively, with normal plasma, a Red Cross factor IX preparation (rich in factors IX, II and X), the orginal antigen, and Hemophilia-B antigen-positive plasmas. No line or rocket developed with normal plasma absorbed with aluminum hydroxide or with antigen-negative Hemophilia B plasmas. We concluded that after absorption with albumin the antiserum R2 contained only factor IX neutralizing and precipitating antibodies.Experiments with various factor IX concentrates revealed that the majority contained excess factor IX antigen compared to their coagulant activity. In addition, crossed antigen-antibody electrophoresis uncovered differences in the migration of the factor IX of Konyne preparations, when done in the presence of EDTA or calcium.This monospecific antiserum to human factor IX was subsequently used to investigate a large population of hemophilia B patients and carriers.
Platelet Thrombospondin Interactions with Human High and Low Molecular Weight Kininogens
Authors: DeLa Cadena Raul A , Wyshock Edward G , Kunapuli Satya P , Schultze Robert L , Miller Michelle , Walz Daniel A , Colman Robert W 
Published: July 2018

SummaryMultifunctional proteins, e.g. high molecular weight kininogen (HK, 120 kDa) and the homotrimer, thrombospondin (TSP, 540 kDa), which have more than one domain on a single polypeptide chain, are particularly well-suited to be structural elements of extracellular matrices because of their ability to bind to several macromolecules. We now demonstrate that 125I-high molecular weight kininogen (HKa) cleaved by purified kallikrein forms a complex with purified intact platelet TSP (540 kDa). HK also complexed with a proteolytic fragment (450 kDa) of TSP, lacking its three identical heparin-binding domains (HBD, 30 kDa), but failed to bind to a more extensively proteolysed molecule (210 kDa) lacking the C-terminal globular domain indicating that the binding on TSP-450 kDa is confined to the C-terminus. The binding of HK to intact TSP and to its 450 kDa fragment was of high affinity (Kd = 17-52 nM), specific, concentration dependent and saturable. Furthermore, we found both forms of the light chain (LC) of HK (56 and 46 kDa) resulting from cleavage by plasma kallikrein bound to both intact TSP and HBD independent of the presence of calcium ions. However, neither the epitope recognized by monoclonal antibody (MAb) Cl 1C1 on domain 5 nor the prekallikrein binding site on domain 6 are involved, suggesting that the intervening proline-rich region may be the site of interaction. The heavy chain (HC) of HK required ionized calcium to bind to intact TSP or its 450 kDa homotrimer fragment. Purified immobilized low molecular weight kininogen (LK) which contains the identical HC as HK but a different LC was recognized by intact TSP but only in the presence of calcium ions. Since MAb 2B5 inhibited the interaction, domain 2 and/or domain 3 of the HC contains the binding site for TSP. The TSP-HK interaction may play a role in the platelet function since both glycoproteins are present within the a-granules of platelets.
A New, Automated and Accurate In Vitro Method to Quantify Endothelial Cells Attached to Vascular Prostheses
Authors: Visser Michel J T , van Lennep Alexander C D , Hajo van Bockel J , van Hinsbergh Victor W M , Slats Jan , Tanke Hans J 
Published: July 2018

SummaryOver a decade ago the idea of endothelial cell seeding was introduced in an attempt to improve the function of small caliber vascular prostheses. Although endothelial cell seeding is currently being applied clinically, several questions regarding the functional properties of the seeded endothelial cells remain. Evaluation of functional properties of endothelial cells on various types of vascular prostheses can be performed partly in vitro, but it is hampered by the fact that commonly used methods to quantify endothelial cells do not adequately apply to these cells on prosthetic materials.An accurate quantification method is described that is rapidly and easily applicable to endothelial cells attached to vascular prostheses. The method can also be used to quantify endothelial cells attached to culture dishes or microcarriers. Colorless, non-fluorescing, fluorescein-di-acetate was used, which was taken up by the attached endothelial cells, and which was then intracellularly converted to yellow fluorescein, emitting green fluorescence. Subsequently, triton-X-100 was appli-cated to release fluorescein and levels of fluorescence were measured with the automated aperture-defined microvolume (ADM) method, using an inverted fluorescence microscope to which a photometer was connected. The measured level of fluorescence is linearly related to endothelial cell numbers attached to prostheses. The accuracy and the reproducibility of cell countings are high.
Pulmonary Embolization in the Dog: Its Effects on Blood Coagulation and on Pulmonary Artery Pressures
Authors: Hampton James W. , Jaques William E. , Bird Robert M. , Selby David M. 
Published: July 2018

Summary1. Infusions containing particulate matter, viz. whole amniotic fluid, amniotic fluid sediment, and glass beads, produce in dogs changes in both early and late phases of the clotting reaction. These changes are associated with the development of pulmonary hypertension.2. When dogs were given an active fibrinolysin followed by an infusion of whole amniotic fluid, the alterations in the clotting mechanism were either delayed or did not appear. No pulmonary hypertension developed in these animals.3. We infer that infusions containing particulate matter will produce in dogs both pulmonary hypertension and changes in the clotting mechanism. Although these are independent changes, both are as closely related to the damage to the pulmonary vessels as they are to the biological nature of the infusions.
Über die Verwendung von Marcumar und Dicumarol bei der Langzeitbehandlung (Vergleichende Untersuchungen)
Authors: Clausen Johs , Andresen P , Gruelund Sv , Harsløf E , Holm Andersen U , Jørgensen J , Mose Chr 
Published: July 2018

ZusammenfassungEine alternierende Vergleichsprüfung bei Patienten, die einer Langdauerbehandlung mit Antikoagulantien unterzogen wurden, zeigte, daß sich die mit Marcumar behandelten Patienten leichter auf den optimalen Prothrombinwertbereich einstellen ließen als die mit Dicumarol behandelten Fälle. Bei den mit Dicumarol behandelten Kranken fanden sich in 13% Prothrombinwerte (bestimmt nach Owren) von > 30% oder <C 6%, während die entsprechende Vergleichszahl für Marcumar bei 7% lag. Im therapeutisch optimalen Bereich (8—16%) fanden sich 50% der mit Dicumarol behandelten Fälle und 63% der Kranken, denen Marcumar appliziert wurde. Unter den mit Marcumar behandelten Patienten fanden sich deutlich mehr gut eingestellte Fälle (62%) als unter den mit Dicumarol behandelten Kranken (46%). Auch die Zahl der ungenügend eingestellten Fälle war bei Marcumar mit 5% günstiger als bei Dicumarol mit 15%.
Glas Effect and Platelet Activity in Hageman Plasma
Authors: Ollendorff Preben 
Published: July 2018

SummaryAfter addition of a suspension of normal platelets the coagulation defect in Hageman plasma was corrected. The recalcification time became nearly normal and it was possible to activate the plasma by treatment with glass.Hageman serum was unable to accelerate thromboplastin activation in normal plasma. After addition of a platelet suspension and exposure to glass the Hageman serum became as active as normal serum treated in the same way.The results suggest that the Hageman trait might be caused by the presence of an excess of an inhibitor against glass activation and not by a deficiency in a clotting factor.A study of previously published data on the Hageman trait shows that it is possible to explain many observations by the presence of such an inhibitor.
The Role of Calcium and Divalent Metals in the Coagulation of Blood as Induced by Russell’s Viper Venom
Authors: Banerjee Renuka , Nath B. B , Devi Anima , Sakar N. K 
Published: July 2018

Summary1. The normal clotting time of plasma can be further reduced if Russell’s viper venom and calcium are preincubated and then added to the plasma instead of using them separately; the percentage of reduction in clotting time is dependent upon the time of incubation of RV venom and calcium.2. Incubation of the venom with the plasma on the contrary destroys the thromboplastic activity of the venom; here too, the percentage loss of RV venom thromboplastic activity depends upon the time of incubation.3. Among the many divalent metals tested such as Ba, Sr, Zn, Mg and Mn, only Ba and Sr were found to be capable of replacing Ca in the coagulation process (conversion of prothrombin to thrombin by RV venom), although they were less active than Ca when used at the same concentration range, furthermore Sr was more active than Ba.
Studies on Increased Heparin Resistance Measured by the Plasma Heparin Thrombin Time
Authors: Holger-Madsen T 
Published: July 2018

SummaryIncreased heparin resistance was found to remain unchanged in BaSO4-adsorbed plasma, but disappeared following adsorption with large quantities of Al(OH)3. The factor V content in the plasma could be considerably reduced without any alteration in the heparin resistance. Antihaemophilic globulin exerted no influence upon the heparin thrombin time. Tissue thromboplastin in quantities sufficient to accelerate the clotting of recalcified plasma considerably, did not affect the heparin thrombin time. Plasma thromboplastin had no antiheparin effect. Increased heparin resistance was — although usually less marked — still demonstrable in most cases in plasma defibrinated with thrombin from patients with a greatly shortened heparin thrombin time, but not in cases of less pronounced shortening. Fibrinogen prepared by the freeze-thaw technique from normal plasma and patient plasma showed no difference in reactivity to heparin and thrombin. In experiments on plasma mixtures, a shortening of the heparin thrombin time was still demonstrable at the ratio 9 parts of normal plasma to 1 part of plasma from patients with greatly increased heparin resistance. The antithrombin content of plasma was not reduced in increased heparin resistance.
Normal Fibrinolytic System in Blood in Congenital Afibrinogenemia and its Significance
Authors: Astrup Tage , van Creveld S 
Published: July 2018

Summary1. Detailed studies in a patient with afibrinogenemia disclosed a normal fibrinolytic system. Activation by the urine activator and with streptokinase was normal.2. The significance of this observation in relation to the role of fibrin formation in tissue repair and the specific problems of afibrinogenemic patients are discussed.
Die Beeinflussung des Gerinnungsfaktors IX durch Hydroxy-Cumarin- und Phenyl-Indandion-Derivate
Authors: Egli H , Schneider W 
Published: July 2018

ZusammenfassungEs wurde der Einfluß eines Hydroxy-Cumarin- (Marcumar) und eines Phenyl-Indandion-Präparates (Indaliton) auf die Aktivität des Faktors IX in Plasma und Serum mit modifizierter Methodik untersucht. Eine Wirkung der genannten Antikoagulantien ließ sich dabei nur im Serum, das entweder mit Glaswolle kontaktaktiviert oder nach erfolgter Kontaktaktivierung dekalzifizier. worden war, nachweisen. Sie wurde hingegen in dem verwendeten Zitratplasma und in Serumproben vermißt, die vor der Kontaktaktivierung dekalzifiziert worden waren. Daraus wird gefolgert, daß durch die genannten Antikoagulantien ein im Serum nachweisbarer Gerinnungsfaktor mit kalziumabhängiger Kontaktaktivierbarkeit vermindert wird. Die Frage nach entsprechender Beeinflussung des Plasmas muß offenbleiben, da die Bestimmung von Gerinnungsfaktoren mit kalziumabhängiger Kontaktaktivierbarkeit in dem von uns verwendeten dekalzifizierten Plasma nicht möglich ist. Unter Berücksichtigung anderer und eigener Befunde wird geschlossen, daß die im Serum unter der Wirkung der genannten Antikoagulantien nachweisbaren Aktivitätsveränderungen auf den Faktor IX oder den Präphasenakzelerator von Fisch zurückzuführen sind.
L’Accolement des Plaquettes aux Fibres Sous-endothéliales
Authors: Bounameaux Y 
Published: July 2018

Résumé1. L’auteur compare le comportement des plaquettes du lapin en présence de levures opsonisées, de particules de BaSO4 et de fragments d’aorte broyée.2. Il ne semble pas qu’on puisse envisager un mécanisme commun pour expliquer l’accolement des plaquettes à ces diverses surfaces. En effet, le NaCl hypertonique inhibe électivement la fixation aux levures opsonisées, le chauffage des plaquettes empêchant leur accolement aux fragments vasculaires. Le traitement des plaquettes par la papaïne détruit leur possibilité de se fixer à l’un quelconque des systèmes considérés. Cet enzyme supprime l’opsonisation des levur’es sans altérer la propriété adhésive des fragments vasculaires.3. Après 30 min à 60° C, les fragments aortiques ne permettent plus la fixation des plaquettes à leur niveau.4. Le complexe antigène-anticorps se comporte comme les levures opsonisées.5. Les plaquettes se fixent le mieux aux débris d’aorte à un pH de 6,5.6. La discussion met en évidence le parallélisme entre les faits observés vivo et in vitro.
Elektronenoptische Beobachtungen an menschlichen Blutplättchen während der viskosen Metamorphose
Authors: Parmeggiani A 
Published: July 2018

ZusammenfassungDer Ablauf der durch Thrombinzugabe ausgelösten viskösen Metamorphose (VM) menschlicher Blutplättchen in einem fibrinfreien System wurde an Hand von Ultradünnschnittpräparaten elektronenoptisch untersucht. Die Präpariertechnik wird beschrieben. Folgende Feststellungen wurden gemacht:1. Bei Präparaten, die 10 Sekunden nach Thrombinzugabe fixiert wurden, finden sich schon erste Veränderungen der Plättchen, insbesondere elektronenoptische Dichteunterschiede im Inneren und eine zunehmende Aggregationstendenz.2. Die rasch erfolgende Bildung großer Aggregate führt zu immer dichter gepackten Zellverbänden, in denen auch bei längerer Inkubationszeit die einzelnen Plättchen durch ihre intakten Membranen erkennbar bleiben.3. Im Innern großer Aggregate bildet sich, wahrscheinlich durch aktive Kontraktionsprozesse bewirkt, eine Mosaikstruktur dichtest gepackter Zellen aus, die im Extremfall zu völlig kompakten Massen zusammentreten.4. Innerhalb der 1. Minute nach Thrombinzugabe lösen sich die Granula im Innern der Plättchen auf. Es erklärt dies wahrscheinlich die Freisetzung von gerinnungs- und gefäßaktiven Substanzen im Laufe der VM.5. Eine kleine Anzahl Plättchen verhält sich inert. Solche Thrombozyten lagern sich höchstens an Aggregate an, treten aber nicht in sie ein; sie zeigen den typischen Granulazerfall nicht. Ihre Zahl scheint von der Thrombinkonzentration abzuhängen.6. Bei Anwesenheit von Fibrin wird die Plättchenmembran geschädigt.
Autoprothrombin C in Irregular Blood Clotting
Authors: Seegers Walter H. , Marciniak Eva 
Published: July 2018

SummaryIn this study autoprothrombin C was considered in relationship to the hemorrhagic diseases. Concentrates of autoprothrombin C were made from purified prothrombin known to be homogeneous by several criteria. These autoprothrombin C preparations were free of thrombin, and were almost a single component when analyzed by centrifugation. Autoprothrombin C corrected the partial thromboplastin time and produced prothrombin consumption in all the plasmas obtained from patients with hemorrhagic diseases except parahemophilia. In the case of hemophilia B prothrombin consumption was obtained with the addition of purified prothrombin or purified autoprothrombin II. In the case of Stuart plasma prothrombin consumption was rapid after the addition of purified prothrombin or purified prothrombin chromatographed on Amberlite ICR-50, but not after the addition of purified prothrombin that was chromatographed on DEAE cellulose. The latter prothrombin is an abnormal prothrombin molecule and does not readily yield autoprothrombin C. It is concluded that Stuart prothrombin is abnormal and that this is a molecular disease. There is no need to postulate the existence of factor X to account for the irregular prothrombin activation in Stuart plasma. The most important question considered was how can autoprothrombin C be generated from prothrombin to promote the autocatalytic activation of prothrombin. Certain prothrombin molecules do not yield this enzyme, but normal prothrombin does. However, it does so only under certain conditions of activation. By applying the new knowledge of prothrombin chemistry to blood clotting irregularities in hemorrhagic diseases the following main considerations highlight the common deviations: 1. Abnormal prothrombin molecule, 2. Changes related to the derivatives of prothrombin, 3. Accessories needed for the generation of autoprothrombin C so it can function in auto-catalysis are irregular, and 4. Accessories needed for the function of autoprothrombin C after it is out of the prothrombin molecule are irregular. In the first group is Stuart Plasma. In the second group falls hemophilia B (autoprothrombin II) and the so-called factor VII deficiency (autoprothrombin I). In the third group is hemophilia A. In the fourth group is parahemophilia, and the platelet abnormalities.
Methoden zur fluorimetrischen Bestimmung der fibrinolytischen Aktivität
Authors: Strässle R 
Published: July 2018

ZusammenfassungEs werden zwei Methoden vorgeschlagen, welche erlauben, unter Verwendung von Fluorescein-markiertem Rinderfibrin als Substrat die fibrinolytische Totalaktivität biologischer Flüssigkeiten in kurzer Zeit mit einem relativen Fehler von etwa ± 2% zu ermitteln. Die Methoden lassen sich, den Erfordernissen entsprechend, modifizieren.
Severe Isolated Prothrombin Deficiency : an Acquired State with Complete Recovery
Authors: Karpatkin Simon , Ingram G.I.C , B. Graham John 
Published: July 2018

SummaryA 62 year old man acquired a temporary, virtually complete, deficiency of prothrombin as measured by both the Iowa and Oxford 2-stage methods. The etiology agent (or agents) is not known, but one of the drugs listed in Table 1 or an interaction between several was probably responsible. There was no evidence of an inhibitor, and factors I (fibrinogen), V (AcG), VII (SPCA), VIII (AHF), IX (PTC), X (Stuart), and XII (Hageman) were demonstrated to be normal. There were other evidences of mild liver damage and the prothrombin deficiency did not respond immediately to injections of natural vitamin K. Greatly prolonged clotting times but only moderately prolonged prothrombin times and partial thromboplastin times were observed. Bleeding was very severe into many tissues. Thromboplastin generation proceeded normally in the patient’s pro-thrombin-deficient plasma, despite the appearance of only a trace of thrombin. This patient’s history and clotting profile argue against the concept that factor VII (SPCA) and IX (PTC) are derivatives of prothrombin.
Severe Congenital Hypoprothroinbinemia in a Negro Boy
Authors: Pool Judith G. , Desai Rajendra , Kropatkin Mona 
Published: July 2018

SummaryA case of severe congenital hypoprothrombinemia (level ca. 3%), complicated only by a moderate deficiency of factor VII (level ca. 45%) is reported in a 6 year old Negro boy.