bluuebunny/crossref_metadata_2025_split huggingface dataset:
Platelet-Collagen Interaction : Adhesion to Alpha 1 (I) CB6 and Alpha 1 (III) CB4 Peptides from Calf-Skin Collagen
Authors: Fauvel F. , Legrand Y. J. , Caen J. P. 
Published: May 2019

The interaction of blood platelets with collagen is the trigger of haemostasis and, at least partly, of thrombosis. Two types of fibrillar collagens (type I and type III), present in the vessel wall, can induce the adhesion of blood platelets. This study was designed to determine which part of their molecule is involved in that phenomenon. We then devised a quantitative test based upon differential filtration of non adhesive and adhesive 14c serotonin labeled platelets through a sepharose column for the evaluation of platelet adhesion to collagen or collagen derivatives. No differences were observed in the adhesive properties of calf-skin type I and type III collagens when the degree of multimerisation was identical. Isolated alpha 1 (I) and alpha 2 chains were not active ; but platelets adhered to reassociated (alpha .1 (I))3 trimers, not to (alpha 2)3 trimers ; in type I collagen, alpha 1 chains seems to have the most essential role for platelet adhesion. Various cyanogen bromide peptides were tested : only the 217 C-terminal amino acids alpha 1 CB6 from type I and the 149 central amino acids alpha 1 CB4 from type III were active.The adhesive properties of collagen seems then associated with chemical groupings localized in these peptides : a random folding of the entire isolated chains could make these “sites” unavailable to the platelets, whereas in the triple helix characteristic of fibrillar trimers, they would be more accessible. This could explain why fibrils and small peptides are active, while isolated chains are not.
Heparin Elimination in Patients with Various Diseases
Authors: Teien A. N. , Lie M. 
Published: May 2019

Heparin (100 U/kg bodyweight) has been administered as i. v. single injections and heparin concentration in plasma determined by polybrene titration (PT), previously shown to be an accurate assay for heparin concentration in plasma. Mean concentration half-life was 74.7 min. in normals (n=6),118.6 min. in a-nephric patients (n=5), 97.8 min. in uraemic patients with kidneys (n=6), 115.5 min. in patients with liver cirrhosis (n=6),79.6 min. in patients with disseminated cancer (n=5) and 59.3 min. in patients with hyper-lipaemia(n=6). The differences between mean values for the normals and the anephric patients or the patients with liver cirrhosis were highly significant (p<0.01). One patient with very high content of triglycerides in plasma (25.6 mmol/l) had an extremely short heparin half-life (33 min.). The plasma of this patient had a heparin neutralizing effect of 0.75 U/ml (measured by FT) . Short half-lives were also found in patients with thrombocytaemia or acute thrombo-embolic disorders.In normals and uraemic patients there was a significant fall in heparin co-factor activity from before heparin injection to 4 hours after injection (lO per cent and 20 per cent, p<0,05 and p<0,005»respectively),in contrast to no significant fall in patients with liver cirrhosis, A possible explanation may be that the normal liver removes heparin bound to At-III, and that this function is impaired in liver cirrhosis.
Inhibition of Platelet Aggregation by Brinolase Degradation Products of Fibrinogen and Serum Albumin
Authors: Roschlau W. H. E. 
Published: May 2019

Brinolase (fibrinolytic enzyme from Aspergillus oryzae) was observed to possess significant platelet aggregation inhibitory properties during and after thrombolytic therapeutic use. These platelet effects were found in vitro to be caused in part by intermediate products of fibrinogen digestion, namely low-molecular-weight peptides of approx. MW 2500. Human fibrinogen peptides were isolated, purified, and shown to have high inhibitory activity in platelet-rich plasma. Quantitative comparisons of attainable platelet inhibition in vitro and observed responses in vivo during administration of equivalent enzyme doses, however, suggested that total available fibrinogen, even if it were entirely converted to degradation products (which it is not), would be insufficient to account for observed platelet effects of brinolase therapy.Human serum albumin is also readily degraded by brinolase. Albumin degradation products were prepared in vitro by optimal incubation with the enzyme. Dose-response curves of inhibition of platelet aggregation were obtained with lyophilized peptides in platelet-rich plasma in vitro, and significant inhibition of platelet aggregation was observed in vivo following infusion of albumin degradation products into rabbits. The enzyme doses and amounts of substrates employed in all experiments were equivalent to the conditions of therapeutic fibrinolysis.Thus, albumin degradation products are considered to contribute a significant, if not the major, portion of platelet-active intermediates during clinical brinolase therapy. Albumin cleavage, which is unique to brinolase amongst clinical fibrinolytic enzymes, was shown to have biological effects of its own, but it may also serve to protect coagulation proteins from enzymatic destruction through competition for the enzyme during systemic brinolase therapy.
Blood Product Infusions to Maintain Normal Haemostasis Parameters in Low Birth Weight Neonates
Authors: Cash J. D. , Turner T. L. 
Published: May 2019

Haemostatic parameters were measured serially for 3 days in 58 infants, within 2 hours of birth. Twelve (21%) maintained normal coagulation profiles, whereas 46 (79%) had abnormal profiles. The abnormal group were randomly allocated to a control (23) and treatment subgroup (23).Treatment consisted of infusions of platelets, fibrinogen (cryoprecipitate) and/or factor II, VII, IX & X concentrate – whichever was appropriate, and repeated when necessary. Detailed post-mortem studies were performed on all infants who died.The results revealed a lower incidence of intraventricular haemorrhage in the treated subgroup, but this was not statistically significant. There was no difference in mortality between the two subgroups. No deleterious effects due to the administration of blood products;in particular, DIC or local thrombosis was not observed.It is concluded that although efforts to maintain normal haemostasis in these high risk neonates are possible and may be safe, they are without demonstrable benefit.
Methodological Problems Relating to the Eligibility of Clinical Outcomes in Cardiovascular Intervention Studies
Authors: Gent M. 
Published: May 2019

Many patients in long-term cardiovascular clinical trials fail to complete the study according to the original protocol and this raises questions of what should be done with the results from such patients. Examples of protocol failures would include (l) patients dropping out of the trial for reasons which may, or may not, be related to their treatment or clinical condition, (2) interruptions in treatment which may be patient- or physician-initiated, and (3) patients entered into the study who were subsequently found not to meet entry criteria. In practice, the decision to include an observed clinical outcome in the final analysis has usually depended on whether the outcome occurred before or subsequent to the patient leaving the study, and on whether or not the patient was on the allocated treatment at the time of the event.However, this approach is too simplistic and it can be shown that this will often lead to considerable bias in the evaluation of the treatment under study. The need for more specific decision procedures will be illustrated by examples in previously published trials of anticoagulants, platelet suppressive drugs, and thrombolytic agents.Recommendations for dealing with these problems will be made which would be pertinent to the several major intervention studies in myocardial infarction and stroke which are currently in progress.
The Role of Dihydroergotamine in the Prophylaxis of Postoperative Deep Vein Thrombosis
Authors: Kakkar V.V. , Stamatakis J.D. , Lawrence D. 
Published: May 2019

In randomly allocated trials, the prophylactic efficacy of DHE and a combination of DHE with heparin was investigated in 200 consecutive patients. Of 100 patients undergoing major surgery, 50 received 0.5 mgm. of DHE every 12 hours and 50 received 50000 units of heparin every 8 hours. The frequency of DVT, determined by the 125I-fibrinogen uptake test, was 20% in those receiving DHE compared with 4% in those receiving heparin, the difference being statistically significant (p 0.05).Of 100 patients undergoing total hip replacement arthroplasty, 50 received 5000 IU of heparin every 8 hours, and 50 received heparin according to the same regimen, together with 0.5 mgm. of DHE. DVT was detected by the 125I-fibrinogen test and venography. Twenty-six (52%) patients in the heparin group developed DVT, compared with 1– (20%) who received the combination; the difference in the incidence of thrombosis between the two groups was statistically highly significant (p 0.005).The effect of DHE on calf muscle blood flow was determined using Xenon133. There was significant increase in mean muscle blood flow 2 hours after the administration of 0.5 mgm. of DHE subcutaneously (p 0.05).It is concluded that a combination of DHE and heparin is more effectively than heparin alone in preventing postoperative DVT.
The Lipolytic Activity of Antithrombin III
Authors: Nakagawa M. , Okuda S. , Watada M. , Ijichi H. 
Published: May 2019

Antithrombin III in the circulating blood is known to play an important role on the coagulation mechanism of the blood and is reported to be decreased in its amount on the cases of myocardial infarction and arteriosclerosis, in the meanwhile the arteriosclerosis has been considered to be one of thrombogenic factors. This research was designed to investigate the effects of antithrombin III on the relationship between fibrin formation and atherosclerosis.Antithrombin III was purified from human defibrinated plasma by Heparin Sepharose Affinity Chromatography. Using this antithrombin III as an enzyme, its lipolytic activity was assayed spectrophotometrically detecting the produced free fatty acid from various substrates, Intralipid, Triolein, and Human Chylomicron respectively. Lipoprotein lipase activity was detected in the purified antithrombin III. Intralipid was hydrolyzed to a greater extent than triolein or chylomicron and it is concluded that antithrombin III in the circulating blood has not only the inhibitory activity of thrombin but also has the lipolytic activity. From these observations it is considered that this lipolytic activity is beneficial for preventing the developement of atherosclerosis and also of thrombosis.
In Vivo Assessment of Thromboresistant Materials by Determination of Platelet Survival
Authors: Coe N. , Collins R. , Jagoda A. , Brier D. , Lindon J. , Merrill E. , Cohen R. , Salzman E. 
Published: May 2019

The reactivity of potentially thromboresistant polymers was determined in sheep by measurement of the lifespan of Cr51-labelled platelets. Materials were tested as tubing (90-125 cm × 2.5-3 mm I.D.) interposed in a 7 cm silicone rubber carotid A.-ext. jugular V. shunt.Platelet lifespan decreased as the length of the basic silicone rubber shunt increased from 7 cm (“shunt control”, T½ 78.3 ± 11.6 S.D. hrs.; n = 18) to 50 cm (T½ 62.0 ± 7.5 hrs.; n=7; p< 0.001 vs. shunt control) but was longer than in sheep without a shunt (T½ 63.1 ± 11.2 hrs.; n=21; p<0.001 vs. shunt control), probably because of artifactual activation of platelets in blood sampling by needle puncture in the absence of a shunt. Of sixteen polymers studied in 42 sheep (n=117), all significantly shortened platelet lifespan except polyurethane (T½ 72.8 ± 12.1 hrs.; n=12) and non-cross-linked silica-free polydimethyl siloxane (T½ 69.8 ± 13.9 hrs.; n = 9). Polymethyl acrylate (PMA) (T½ 71.2 ± 5.4 hrs.; n=ll; p<0.04 vs. shunt control) was passivated by exposure to platelet free plasma before whole blood (T½ 90.3 ± 3.6 hrs.; n=5; ρ <0.05 vs. untreated PMA). Thus, the adsorbed film of plasma constituents has a lasting and decisive effect on thromboresistance of the surface. The long term behavior of an artificial surface may be dictated by the events of the first few seconds of blood-surface contact.
Studies on Anti-Platelet Antibodies. Its Correlation with ACID Phosphatases. Preliminary Results
Authors: Hendler H.N. , Sack E.S. 
Published: May 2019

The platelet factor 3 immuno-injury technic (Karpatkin and Siskind, Blood 33:795,1969) has been evaluated as a test for the detection of anti-platelet antibodies in 126 patients with quantitative and qualitative platelet disorders. Plasmatic acid phosphatases in platelet-poor plasma (PAP-PPP) were simultaneously determined in a selected group of patients. Also the effect of serum incubation (from patients and controls) on acid phosphatase availability of platelet-rich plasma (APA-PRP) was investigated.Anti-platelet antibodies were present in 52% of patients fulfilling the diagnostic criteria for idiopathic thrombocytopenic purpura and in 38% of patients with miscellaneous conditions. The following table express the results of acid phosphatase determina studied:Platelet destruction is the probable cause of the thrombocytopenia in the group with negative anti-platelet antibodies. Further, their serum lacks membrane-injury action. On the other hand the results in the group with positive antibodies suggest that heterogeneous immunologic mechanisms are operative
Circulating Crosslinked Fibrinoligomers. Clinical Observations and Turnover Studies in Rabbits
Authors: Graeff H. , von Hugo R. , Hafter R. 
Published: May 2019

Blood samples from patients with coagulation disorders in obstetrics and with advanced carcinoma of the kidney were examined for the presence of cross-linked fibrinoligomers. Quantitative gel filtration of ß-alanine precipitated plasma samples and chain characterization of isolated fibrin derivatives by SDS-PAA gel electrophoresis after reduction with mercaptoethanol were performed. Electrophoresis of immunoadsorbed material was additionally applied. In all cases of intravascular coagulation crosslinked fibrinoligomers in amounts of 8-25 per cent of the total fibrinogen content were observed. Severe cases revealed a molecular weight pattern of derivatives ranging from 5 million and more down to 45 000. X, Y, D, E and D-dimer were found in the ß-alanine supernatant. In 5 patients with advanced renal carcinoma a cross-linked dimeric derivative was observed predominantly.In vitro produced crosslinked 125 I-fibrinoligomers were injected into rabbits. Radioactivity was measured in gel filtrated fractions from ß-alanine precipitated samples, and a half-life time of approximately 7 hours of the high molecular weight fraction averaging 5 million daltons was found.It is concluded that circulating crosslinked fibrinoligomers which differ in regard to complex formation and half-life time to soluble fibrin monomer complexes may indicate intravascular coagulation.
Physiological and Clinical Significance of Disordered Cross-Linking of Fibrin
Authors: Lorand L. 
Published: May 2019

Disorders of fibrin stabilization are hemorrhagic conditions in which the patient’s plasma clot is lacking in inter-fibrin γ-glutamyl-ε-lysine isopeptide linkages. The primary defect occurs either because no fibrinoligase (FXIIIa) activity can be generated or because the enzyme cannot act on fibrin in the patient’s plasma. Distinction is made between hereditary disorders (Class I) and those appearing later in life because of an acquired inhibitor (Class II) directed against one of the steps on the pathway of fibrin stabilization:

Of the genetic deficiencies (Class I), Type I is characterized by a lack of zymogen activity in plasma and Type II by the unreactivity of the cross-linking sites of the patient’s fibrin [“dysfibrin(ogen)emias”] towards fibrinoligase.There are three varieties of Class II abnormalities. In Type I, the acquired inhibitor interferes with zymogen activation. Type II inhibitors affect transamidation by competing against fibrin for the enzyme. The Type III inhibitor combines with fibrin rendering it unreactive towards fibrinoligase. The Type I and III inhibitors appear to be autoimmune antibodies.(Ann. N. Y. Acad. Sei., 202, 6, 1972).Differential diagnostic criteria for this family of molecular disorders will be discussed.
Primary Shape Change of Thrombocytes and Platelet Aggregation after Administration of Acetyl Salicylic Acid (ASA)
Authors: Krzywanek H.J. , Breddin K. 
Published: May 2019

Studies using interference contrast microscopy (Nomarski optics) with immediate glutaraldehyde fixation of blood at venepuncture revealed the disc like shape of native thrombocytes. Soon after blood drawing platelets in citrate blood or PRP are swelling and the formation of pseudopodes can be observed. If citrate blood is incubated at 37°C, 38% of the thrombocytes have formed pseudopodes after 30 min. The form variation is inhibited in some platelet defects (storage pool disease, aspirin like defect) and is enhanced in certain malignancies (Hodgkin’s disease, bronchial carcinoma). After oral intake or intravenous administration of 1.0 g ASA the primary shape change is partly inhibited for a period of six hrs. with the greatest effect at two hrs. In contrast to this short lasting effect on primary shape change the inhibition of ADP or collagen-induced aggregation by a single dose of ASA can be demonstrated for at least four days.We suggest that the short lasting inhibition of the primary shape change of platelets may be responsible for the efficacy of ASA in postoperative thrombosis prophylaxis.Regular intake of ASA in doses of 0.5 g each at 6 - 8 hrs. intervals may be necessary to achieve a continuous antithrombotic effect. Our results may explain why studies on thrombosis prophylaxis with aspirin using 0.6 g (BMRC, 1973) or 0.3 g (Elwood, 1974) per day were inconclusive whereas 3 × 0.5 g reduced the thrombosis frequency significantly (Zekert, 1973, Loew, 1973).
Artificial Substrate Plasma for the Specific One-Stage Factor X Assay
Authors: Beeser H. , Kulzer R. 
Published: May 2019

As patients who are congenitally deficient in factor X are extremely rare natural substrate plasma for the specific one-stage factor X assay is only poorly available. Asbestos-filtered or charcoal-filtered ox plasma deficient both in factor X and VII is instead widely used as artificial factor X substrate plasma with Russel’s viper venom (BW) and cephalin or lecithin as the thromboplastic agent.We studied the practicability of removing separately factor X from the plasma of different species (man, horse, ox, sheep, swine) by several chromatographic procedures. Chromatography of swine plasma on DEAE-Sephadex A 25 yielded a substrate virtually free of factor X while containing adequate concentrations of fibrinogen and factor II, V and VII, Using different brands of commercial tissue thromboplastins the so prepared swine plasma has proved to be a specific artificial substrate plasma for the one-stage factor X assay. Calibration curves obtained by plotting the clotting times of various dilutions of pooled normal human plasma determined with this factor X assay system against the percentages showed a linear relationship from 100% to about 2% on log/log paper. Factor X determinations with our method on various patients’ plasmas (i.e. coumarin treatment, congenital factor X deficiency, liver disease) performed in parallel to the RVV-cephalin and the congenital factor X deficient plasma methods gave comparable results.As our specific artificial factor X deficient swine plasma is fairly simple prepared with a good yield, it has to be considered as an appropriate reagent to overcome the shortness of the rare congenital factor X deficient substrate plasma.
Fibrinogen-Fibrin Monomer Complexes in Cirrhosis of The Liver
Authors: Coccheri S. , Palareti G. , Poggi M. , Oca G. 
Published: May 2019

Positivity of paracoagulation tests in a previously studied group of 80 patients with chronic active liver disease did not exceed 5-10% of the cases. In the present study, plasma samples from 20 cases of decompensated liver cirrhosis, assessed by liver biopsy, were investigated by means of agarose cromatography. Fibrinogen related materials were measured immunologically and by Staphylococcal Clumping Test.First appearance of fibrinogen-like materials occurred at earlier fractions in cirrhotic patients in comparison with normal controls. The relative amount of soluble fibrin monomer complexes (SFMC) as referred to total fibrinogen was significantly increased. No correlation was found between the amount of SFMC and the severity of fibrinogen polymerisation defect.Circulating SFMC are therefore present in severe liver cirrhosis. However, DIC may not be the only proposed explanation for this finding.
Properties and Origin of C1-Inactivator Resistant Fibrinolytic Activity
Authors: Kluft C. 
Published: May 2019

Intrinsic and extrinsic activators contribute to the total fibrinolytic activity in plasma. It was found that a percentage of the activity in euglobulin fractions on fibrin plates is not inhibited by C1-inactivator. Studies were carried out to determine the origin and properties of this CI-inactivator resistant fibrinolytic activity (C1-RFA). The Cl-RFA is specifically increased in situations of stimulated fibrinolysis, e.g., in plasma after 15 min venous occlusion. Extrinsic activators (urokinase, human tissue activator and activator from perfused cadaver limbs) are resistant to C1-inactivator. This suggests that C1-RFA could be attributed to extrinsic activators.Study on the properties of C1-RFA in plasma after venous occlusion showed that the activity could be preserved in vitro by freezing the plasma. After coagulation in this plasma, C1-RFA was low suggesting strong adsorption to fibrin. The C1-RFA diminished gradually (50% in 90 min) at 37°C in vitro in plasma and blood, but was stable in euglobulin fractions. This indicates that its “lability” is due to inhibitors not found in euglobulin fractions but which are present in blood (also postmortem) and plasma after venous occlusion. In vivo disappearance of elevated activities is much more rapid than in vitro, which suggests a different clearing mechanism in vivo under conditions of stimulated fibrinolysis.
Heparin Neutralizing Activity (HNA) in Clinical Practice
Authors: Birk-Jensen A. Hurlet , Moriau M. , Beys C. Col-De , Vanderlinden M. , Masure R. 
Published: May 2019

HNA is measured in several pathological conditions by a biological assay.PFP, platelets and serun are compared.In PFP, HNA/ml is high in thrombocytosis, in acute DIC and in some thrombotic states; it is normal in most cases of thrombocytopenia. When expressed as units/109 platelets, PFP’s HNA is low in thrombocytopenia from hepatic origin.HNA/ml of PFP decreases during treatment with suloctidil; these last results are related to platelet survival time.Serum HNA, more than platelet HNA, reflects the antiheparin capacity of the blood and could be used to estimate the minimal amount of heparin required in therapy.