bluuebunny/crossref_metadata_2025_split huggingface dataset:
Collagens Of the Normal and Atherosclerotic Aortic Wall. Studies in authentict issue and In Organ And Cell Cultures
Authors: Aumailley M , Bricaud H 
Published: July 2018

In the vessel wall collagen is present as genetically different types. During atherogenesis intimal smooth muscle cell(SMC)proliferationand col lagen accumulation predispose to thrombosis. Therefore the aim of our study was first to characterize the authentic collagens in normal and atherosclerotic tissue, more specially type V col lagen, and second to find out whether there was a change in atherosclerosis in the newly synthesized collagens AH the investigations were carried out using normal and atherosclerotic tissue derived from animal and human aortas minus adventitia. From authentic tissue, pepsin solubi lized col lagens were submitted to ion-exchange chromatographies and identified using molecular sieve chromatographyandelectrophoresis(PAGE)astype I, III and V collagens. Using PAGE and studying SLS-crystal I ites type V col lagen was found to be present in intimaaswell asinmedia of normal and atherosclerotic aortas.After pulse-label experiments in organ culture of healthy and atherosclerotic specimens the newly synthesized col lagens were isolated using pepsin treatment and subsequent molecular sieve chromatography .Interstitial col lagens(type I and III)represented 80-85% of the total newly^yn- thesized col I age ns .Type III accounted for 16-31 % in explants from young specimens, for 30-36% when the explants were derived from older specimens and for 35-48%when the tissue were atherosclerotic. SMC were grown out from these tissue and investigated for their col lagen synthesis in primary and secondary cultures. With respect to relative distribution of the interstitial col lagens the data obtained were in the same range than in organ culture .Furthermore most of the interstitial col lagens were secreted into the incubation medium whereas type V collagen was found to be preferentially associated with the cell layer .These results showed that type I, III and V col lagen are present i n normal and atherosclerotic aortas from various sources. In atherosclerosis a slight change occurs in the newly synthesized col lagens. Furthermore with respect to these studies organ and cel I cu I ture systems I ead to simi lar resuIts.
New Morphological Findings On Platelets In Bernard-Soulier Syndrome
Authors: Mori K , Suzuki S , Sugai K , Hisa S , Hosoya A , Sakai H 
Published: July 2018

The mechnism of large platelet formation in Bernard- Soulier Syndrome has not yet been clarified. In this paper we present new morphological findings on large platelets in this disease.Case: A 30 year-old-male. He was admitted to our Department to evaluate hemorrhagic diathesis, because of his repeated nasal bleeding. Methods: l) Platelet retention was measured by the modified Salzman’s method and platelet aggregation test by various agents were performed using a Lumi -Aggregometer. 2) Glycoproteins in the platelet membrane were determined by polyacrylamide gel electrophoresis. 3) Light and electronmicroscopic examinations of the platelet and megakaryocyte were done.Results: Hematological examinations showed a prolonged bleeding time, mild thrombocytopenia, giant platelets in the peripheral blood and normal activities of all plasma clotting factors. The platelet function tests indicated normal platelet aggregation and release of ATP induced by ADP, collagen and thrombin by means of a Lumi-Aggregometer. However, they have markedly decreased by ristocetin and bovine fibrinogen. From these findings, the diagnosis of Bernard-Soulier Syndrome was made. Polyacrylamide gel electrophoresis of platelet membrane in this case showed decreased amount of fraction I in the glycoproteins, that is, a deficiency of negatively charged sialic acid. No abnormalities of megakaryocytes in the bone marrow were found by light microscopy, but electronmicroscopic examinations revealed that some platelets were clearly demarcated into two or three parts by circumferential microtubules.Conclusion: These evidences strongly suggest that giant platelets of Bernard-Soulier Syndrome are made from fusion of membrane of two or three platelets while they circulate in the peripheral blood stream.
Efficacy Of Different Heparin Regimens In Dialysis As Assessed By Radioimmunoassay For Fibrinogen/Fibrin Split Products
Authors: Kudryk B , Wilhelmsson S , Netré C , Robinson D , Blömback M 
Published: July 2018

Three different heparin regimens were employed to control clotting in uremic patients undergoing hemodialysis. The regimens differed with regard to dose prior to and/or during dialysis. The efficacy of heparin was checked with several parameters including blood levels of fibrinogen/fibrin split products. Blood was collected from each patient prior to and at three time points during dialysis. Samples were taken from both the blood inlet and outlet sides of the dialyser. Fibrinopeptide A (FPA) was determined by radioimmunoassay (RIA). Hi-2DSK (an Aα-chain derived split product) levels were measured by RIA using selected chromatography fractions of patient plasma and a new RIA method was used to measure plasma levels of split products which contain the Bβ 15-42 sequence.FPA levels were lower during heparin infusion but rose after it was terminated. Blood from the outlet efferent side of the dialyser usually showed higher FPA levels. Hi-2DSK and Bβ 15-42 concentrations were always high before and during dialysis, sometimes 10-20 times or more that found in normal subjects. However, they never showed the variation observed for FPA. Also, in most cases, the levels were similar regardless from which side of the dialyser the samples were obtained.All three regimens were equally as effective in preventing FPA generation in the dialyser. FPA estimation may be used to check adequacy of heparin dosage. Assays for the other two split products indicate no significant elevation of fibrino(geno)lysis during four hours of dialysis.
Platelet Aggregation In Relation To Cigarette Smoke, Carbon Monoxide (CO) And Nicotine
Authors: Mansouri A 
Published: July 2018

There is no doubt that the incidence of atherosclerosis is significantly increased in heavy smokers. Although this increase is most likely due to multiple factors, one factor which has been mostly incriminated is abnormal platelet function. In fact, it has been shown that the smokers have augmented platelet aggregability which might signify higher platelet turnover leading to athero- genesis. This work was undertaken to test directly the effect of smoke and its major constituents on platelet aggregation. Blood was obtained from healthy non-smokers without previous medication. Platelet rich plasma was prepared with standard methods. The aggregation was carried out with epinephrine, thrombin and arachidonic acid (AA) with and without smoke, CO and nicotine. It is shown that nicotine in concentrations up to 2 μg/ml (50 times higher than nicotine concentration in heavy smokers) has no effect on platelet aggregation regardless of the aggregating agent used. Carbon monoxide at high concentration inhibits tne secondary wave of aggregation when epinephrine is used (slope of secondary wave of aggregation 0.92 ± 0.25 for normal versus 0.53 ± 0.12 in the presence of CO) ano little or no aggregation takes place with thrombin ano AA. The smoke does not affect platelet aggregabi1ity when it is subjected to vacuum prior to use. These results indicate a) that the major effect of smoke on platelets is mediated by CO, b) carbon monoxide inhibits the secondary wave of aggregation (aspirin-like effect) contrary to what has been reported in vivo.These results suggest that smoke or its major components do not have any direct stimulatory effect on platelet aggregation.
Congenital Abnormal Antithrombin III
Authors: Sakuragawa N , Takahashi T , Horikoshi I 
Published: July 2018

We found a family which had congenitally abnormal antithrombin III (AT-III ) showing remarkable difference between biological and immunological activity. We studied genetic trait and effects of heparin and thrombin on AT-III.Case: A 23 years old female developed thrombophrebitis on her left leg in July, 1979. After a while she seemed to have developed thrombi on bilateral iliac vein. She had also abdominal tumor, and a cystic kidney was found to be by an exploratory laparatomy. Five days after the operation, she was hemiparalyzed on her left. Cranial angiography disclosed obstruction of right middle cerebral artery by thrombi. Laboratory findings were as follows: Fibrinogen 145 mg/dl, FDP 40 ug/ml, platelets 8.6xl04/cmm, a-PTT 30.6 sec and PT 100%. The biological activity of AT-III was 26%, which dissociated from immunological activity of 54 mg/dl. Two dimension immunoelectrophoretical analysis showed two or three peaks at the albumin area after the addition of heparin to normal AT-III. However her AT-III did not move from α2-macroglobulin area. Her parents were cousins each other, and her parents and her sister also had abnormal AT-III. This indicates congenitally abnormal AT-III is transmitted autosomally dominantly. The administration of concentrated AT-III preparation raised its concentrate to 70%, and coagulation disorders disappeared. Immunoelectrophoresis revealed that administered AT-III disappeared in five or seven days after infusion. Oral anticoagulant therapy could prevent thrombi formation.Conclusion: We found a patient who had abnormal AT-III which brought on intravascular coagulation. Biologically active AT-III was much less than immunologically active one. Immunoelectrophoresis disclosed this AT-III did not bind with heparin. We treated the patient with oral anticoagulant therapy. Abnormal AT-III is transmitted autosomally dominantly.
Disturbed Plasmatic Modulation Of Arachidonic Acid (AA) Metabolism In Platelets From Rats With Nephrotic Syndrome: An Early Parameter Of Thrombotic Risk?
Authors: Delaini F , Reyers L , Vitti G de Beilis , Poggi A , Donati M B 
Published: July 2018

The nephrotic syndrome in humans is associated with an increased risk for arterial and venous thrombosis, the pathogenesis of which appears to be very complex. We have developed an experimental model of nephrotic syndrome in rats which follows a single i.v. injection of adriamycin (AIM, 5-10 mg/kg b.w.). Starting from 2 weeks after ADM-injection, rats showed a remarkably increased susceptibility to thrombotic stimuli; indeed, the occlusion time of a polyethylene cannula inserted in the abdominal aorta was 22±15 hours in treated animals versus 62±5 in control animals (n=16, p< 0.001). Concomitantly the rats showed: increased plasma fibrinogen and factor VIII: C activity, shortened APTT, low antithrombin and markedly depressed fibrinolytic activity. Moreover, platelet-rich plasma (PRP) of treated rats produced significantly higher amounts of both malondialdehyde (MDA) (spectrophotometric assay) and thromboxane B2 (RIA) in response to AA. When MDA generation was studied with a kinetic approach, the PRP of nephrotic animals had significantly lower apparent Km for AA in respect to the controls (0.15 ± 0.07 mM AA versus 0.90 ± 0.25 mM AA, p<0.01). Washed platelets from both groups, in contrast, showed similar Km values for AA (0.10 mM ± 0.04 versus 0.12 ± 0.03).MDA generation by washed normal platelets resuspended in plasma was normal if plasma had been collected 1 or 3 days after ADM administration but was already significantly higher with plasma collected 5, 7 or 14 days after treatment. The concomitant mild hypoalbuminemia does not completely account for this plasma abnormality. Thus, in the model, an abnormal plasmatic modulation of platelet AA metabolism could be detected much earlier than the coagulation/fibrinolysis changes and the hypersensitivity to thrombotic stimuli.
Chromogenic Substrates And Activated Forms Of FXII: Comparison Between The α- And β-Forms And Selectivity With Regard To Plasma Kallikrein And FXIa
Authors: Aurell L , Gustavsson S , Friberger P 
Published: July 2018

Activated FXII of both the α-(MW 80000) and the β-(MW 28000) form was tested with a large number of chromogenic tri- and tetrapeptides. The activities of the two enzymes correlated well (r=0.84, n=30). The α-form appeared to have a somewhat higher specificity.The plasma kallikrein substrate S-2302 and the FXa substrate S-2222 have earlier been shown to be the commercially available substrates most sensitive to the β-form of activated FXII . The specific activities of both the α-and β-forms are the same with S-2302 in the system tris buffer pH 8.0 and I 0.05 at 37°C. At the enzyme concentration of 4 nmol/1, the change in absorbance per min was 0.02 which is in the suitable measuring range. This concentration is approximately equivalent to fully activated plasma diluted 1:100.From these findings, it could be confirmed that when plasma prekallikrein is assayed via contact activation with S-2302, there is a definite but small contribution to the hydrolysis of the substrate from activated FXII.A more selective substrate for activated FXII with regard to plasma kallikrein would be preferable in a plasma assay of FXII. S-2222 has these characteristics. At the substrate concentration of 0.33 mmol/1, the β-form of activated FXII splits S-2222 essentially as efficiently as S-2302 while plasma kallikrein is only 5% as efficient with S-2222 as with S-2302.Both types of substrates are insensitive to FXIa at concentrations obtainable in plasma samples suitably diluted for the assaying of FXII and plasma prekallikrein.
Application Of Enzymatic Methods On Chromogen Substrates In Animal’S Compared Coagulation
Authors: Potron G , LaFaurie M , Droulle C 
Published: July 2018

We have tried to realize a compared study of enzymes in coagulation and fibrinolysis in vertebrates; by using different synthetic chromogen substrates with kinetic measurements and determination of Michaelis constant according to Linewear and Burk (Km).Different species have been used in each class: two fishes,one amphibian, two birds, five mammals.“Thrombin-like” activity, released by Echis Carinatus venom, measured on Chromothrombin* Stago, is found constantly in mammals with a Km close to that of man, but weak in birds and not at all in fish.“Factor Xa-like” activity released by Russel viper’s venom, measured on S 2222 (Kabi) is found in all mammals and birds with a homogenous Km.“Kallikrein-like” activity determined on S 2302 (Kabi) after activation at 4°C by dextran, is weak in all animals.“Plasmin-like” activity measured on S 2251 (Kabi) after activation by Urokinase, is found again in all animals except frogs. All Km are homogenous except in dogs and birds.Two inhibitors have been studied in heterologous systems towards human thrombin and plasmin, and are found at a constant rate close to that of man, for antithrombin; and at more variable rates for total antiplasmin activity.
Partial Characterization Of An Igm Ciroiating Anticqagu- Lant In A Patient With Systemic Scleroderma
Authors: Hauert J , von Felten A 
Published: July 2018

All coagulation tests, utilizing phospholipids, were found to be prolonged in the plasma of a 71 year old wcman with systemic scleroderma. Hie patient had no spontaneous bleeding manifestations and underwent eye surgery for cataract without complications. Thrcmbin time and fibrinogen concentration were normal. Coagulation tests, performed with partial thromboplastin (APTT, factors VIII-XII), were more prolonged than those done with regular tissue thromboplastin (one-stage prothrombin time, factors II, V, VII, X). The addition of 1 part of the patient’s plasma (PP) to 99 parts of normal plasma (NP) resulted in a prolongation of the APTT from 34" to 49". No decrease of the anticoagulant activity (AA) was observed when freshly prepared intact platelets were incubated with the PP. However, incubation of PP with platelets, which had been 5 × frozen and thawed or incubated for 90 min in the presence of kaolin, partially neutralized AA.When the patient’s serum was fractionated on Bio-Gel A-5m, all the inhibitory activity was found in the IgM peak. The AA of the purified IgM fraction was quenched after incubation with an anti-IgM antiserum, but not with anti-IgA or anti-IgG. Incubation of the IgM fraction with stored washed human platelets also led to partial neutralization of the AA. The patient’s IgM adsorbed to lysophosphatidylserine, which had been coupled to octyl-Sepharose, but did not fix complement when incubated with phospholipid micelles consisting of phosphatidylserine-phosphatidylcholine (1:1) and cholesterol in excess.The absence of any bleeding manifestation in this patient; despite the presence of an extremely potent inhibitor against phospholipids, may be explained by the nonreactivity of the IgM inhibitor with fresh intact platelets.
The Effect Of Low Dose Intravenous Heparin On Anti-Factor Xa And Antithrombin III
Authors: Jennings S A , Heather B P , Greenhalgh R M 
Published: July 2018

Preoperative blood samples from 17 patients undergoing major abdominal surgery were examined by the thrombelasto-graph saline dilution test, which has previously been shown to be a predictor of the risk of early postoperative deep vein thrombosis (DVT)(Heather et al 1980). By this test 8 patients were predicted to be at low risk of developing a DVT and received no special prophylaxis. 9 patients were considered to be at risk and were treated with a subcutaneous dose of 1000 units of heparin with the premedication together with a low dose of intravenous heparin infusion from the induction of anaesthesia until 2 hours after operation. Plasma antithrombin III (ATIII) concentration and anti-factor Xa activity were measured preoperatively, on day 1 and on day 3. No early DVT occurred, as assessed by I125 fibrinogen scanning, in either the untreated low risk patients or in the high risk patients receiving heparin infusion. The high risk patients had lower levels of ATIII before operation than the low risk patients (75±9%; 98±39%) and significantly lower levels on day 3 (64±25%; 106±34% p<0.02). However, these lowered levels of ATIII appeared in the high risk group to be augmented by the significant increase in anti-factor Xa activity 127±64%. before operation, 217±89%, on day 1 (p<0.02). Furthermore, on day 3 the high risk patients had significantly greater activity than those patients in the low risk group (212±76%; 106±34% p<0.02).These results show that those patients at risk of developing a postoperative DVT had a significantly enhanced activation of anti-factor Xa, as a result of intravenous low dose heparin with the subsequent abolition of early venous thrombosis.
Low Molecular Weight Heparins: Anti-Xa/Aptt And Platelet Aggregation
Authors: Fussi F , Smith M R , Girolami A , Visentini L , Fabris F 
Published: July 2018

Porcine mucosal Heparin (mean molecular weight= 15.000 Dalton) has been chemically depolymerized in presence of peroxides and N-sulphate groups have been re-introduced by reaction with sulpho- trioxides of amines. The depolymerization has been stopped at different times and the products are essayed for Anti-Xa, APTT and their ratio. A rise in the ratio Anti-Xa/APTT has been observed.In order to check for an activity on the platelet aggregation, two sets of experiments have been carried out: in a first model, the 5-hydroxytrip- tamine (5-HT) release has been measured after addition of different quantities of products to washed platelets. One commercil Heparin gave a significant rise in 5-HT release whereas a normal porcine mucosal Heparin did not show any modification in basal values, nor significant modifications have been observed for low molecular weight heparins (10.000 to 7.000 D). Heparansulphate (HS) and Dermatansulphate (DS) show a slight anti-aggregating activity in this test.In a second model, the percentage inhibition in collagen induced platelet release has been measured in a platelet rich plasma (PRP). All the tested heparins show a very significant inhibition, whereas HS and DS have no inhibiting activity in this test.
Prevalence of Protein C Deficiency in the Healthy Population
Authors: Tait R C , Walker Isobel D , Reitsma P H , Islam S I A M , McCall Frances , Poort S R , Conkie J A , Bertina R M 
Published: July 2018

SummaryReported prevalence rates for protein C (PC) deficiency in the population at large have varied widely. The differences presumably reflect the existence of an apparently high number of clinically recessive forms of the deficiency. In an attempt to document more precisely the prevalence of PC deficiency in the healthy population we have measured PC activity in just under 10,000 blood donors in the West of Scotland. After repeat testing of donors with low results and then further observation and selection, 32 donors were identified who had individual mean PC activities below the age- and gender-specific study reference range. Assessment of available first degree relatives, and also PC gene analysis in 23 of these donors, allowed identification of at least 14 with an inheritable deficiency (8 by both family study and gene analysis, 3 by family study alone and 3 by gene analysis alone). Two recurring and seven unique point mutations, only one of which has been previously described, were identified. The observed prevalence of inherited PC deficiency was 1.45 per 1000 (95% Cl, 0.79/1000 to 2.43/1000). However after correcting for the possibility of missing some genuine inherited deficiencies we estimated the prevalence to be as high as 1 in 500. All cases of hereditary deficiency were asymptomatic with regard to thrombosis and none had a strong family history of thrombosis. These findings confirm the rather frequent occurrence of asymptomatic individuals with PC deficiency and support the hypothesis that additional defects in the anticoagulant pathways may be required to confer a high-thrombotic-risk phenotype.
Effect of an Impermeant Arginine-Modifying Reagent on the Responses of Rabbit Platelets to Agonists
Authors: Anderson Esther R , Au-Young Yum-Kin , Foulks James G 
Published: July 2018

SummaryThe importance of surface arginyl residues in platelet aggregation was investigated by studying the effects of an impermeant arginine-modifying reagent, p-sulfonylphenylglyoxal (PSPG), on platelet responses to various agonists. Pretreatment of resuspended rabbit platelets with 2-15 mM PSPG resulted in complete inhibition of aggregation responses to ADP and 5-HT, and a concentration-dependent inhibition of the preceding shape change. Aggregation responses to thrombin also were inhibited in a concentration-dependent manner. The protective effects of antagonists of these three agonists (P, y-methylene ATP forADP, hirudin for thrombin and phentolamine for 5-HT) during pretreatment of platelets with PSPG indicated that intact arginine residues form part of the receptor sites for ADP and for thrombin. Arginine residues are not part of the 5-HT receptor site itself, but seem to be important for the maintenance of the functional integrity of this site.
The Functional Defect of Factor VIII Leiden, a Genetic Variant of Coagulation Factor VIII
Authors: Mertens K , van Wijngaarden A , Bertina R M , Veltkamp J J 
Published: July 2018

SummaryFactor VIII Leiden is a genetic variant of coagulation factor VIII which has been detected in the plasma of a patient with mild haemophilia A. In this patient’s plasma factor VIII procoagulant antigen was in 5-fold excess over factor VIII procoagulant activity, indicating the presence of an abnormal factor VIII molecule. The variant factor VIII was isolated from the patient’s plasma, and its functional properties were studied in a factor X-activating system consisting of purified components. The isolated factor VIII Leiden was normally activated by factor Xa and by thrombin, but the activity of the factor Villa was about 3% of normal. The defect of factor Villa Leiden was studied by comparison with normal factor Villa in kinetic experiments of factor Xa formation. The results support the hypothesis that factor Villa Leiden has a reduced affinity for phospholipid-bound factor IXa in the intrinsic factor X-activating complex.