bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relation of Intraperitoneal and Intravascular Coagulation and Fibrinolysis Related Antigens in Peritoneal Dialysis
Authors: Gries E , Kopp J , Thomae U , Kuhlmann H 
Published: June 2018

SummaryPatients received 2,000 ml of dialysate intraperitoneally with five exchanges per day during continuous peritoneal dialysis (CAPD) for the treatment of terminal renal insufficiency. During a dwell time of 4 h the dialysate reached a total protein concentration up to 100 mg/dl by mass transfer of intravascular proteins. The composition is dependent on the molecular weight of the proteins. This results in an intraperitoneal hemostatic system of low concentration and different composition.We found an intraperitoneal fibrinogen cleavage and thrombin- antithrombin Ill-complex formation leading to increased levels of fibrinopeptide A (FPA: 33.3 ± 7.0 ng/ml) and thrombin-antithrombin Ill-complex (TAT: 4.7 ± 0.4 ng/ml) in plasma by mass transfer from dialysate to plasma. t-PA (tissue plasminogen activator) and PAI-1 (plasminogen activator inhibitor type 1) concentrations in plasma were within the normal range. The dialysate concentrations indicated a low local secretion. The fibrinolytic fibrin fragment D-dimer and the fibrinogen degradation product concentrations in plasma were greater than in dialysate. But the relations of the proteins between plasma and dialysate refer to a local intraperitoneal production as well.The results show that intraperitoneal coagulation predominates over fibrinolysis which is accompanied by an intravascular fibrinolysis in patients undergoing CAPD. Neoantigens produced in dialysate and diffused to plasma are comparable to changes seen in disseminated intravascular coagulation.
Contribution of Platelets to Increased Plasminogen Activator Inhibitor Type 1 in Severe Preeclampsia
Authors: Gilabert Juan , Estellés Amparo , Aznar Justo , España Francisco , Andrés Cristina , Santos Teresa , Vallés Juana 
Published: June 2018

SummaryPlasminogen activator inhibitor activity and antigen were evaluated in plasma, serum and platelet lysate in patients with severe preeclampsia (n = 12), and in normal pregnant women (n = 21). Other parameters, including β-thromboglobulin and platelet count, were also evaluated. A significant increase (p <0.05) in β-thromboglobulin was observed in platelet poor plasma of preeclamptic women when compared with that of normal pregnant women, and the platelet count was lower in the preeclamptic group than in the normal pregnant group. A significant increase in plasminogen activator inhibitor activity and antigen was observed in platelet poor plasma of the preeclamptic group as compared with normal pregnant women, whereas platelet lysate from preeclamptic women showed a significant decrease in both plasminogen activator inhibitor activity and antigen as compared with that of normal pregnant women. No correlation between β-thromboglobulin and plasminogen activator inhibitor type 1 antigen in platelet poor plasma was observed, but a significant inverse correlation (r = −0.78, p <0.05) between β-thromboglobulin in platelet poor plasma and plasminogen activator inhibitor-1 antigen in platelet lysate was obtained in preeclamptic patients. However, in platelet poor plasmas obtained from normal platelet rich plasmas activated with thrombin (0.1 IU/ml, 37° C, 1 min), an increase of about 300 ng/ ml in β-thromboglobulin was observed while the increase in plasminogen activator inhibitor was only 4 ng/ml. It is concluded that the contribution of platelet plasminogen activator inhibitor-1 to the increase in plasma plasminogen activator inhibitor-1 levels in preeclamptic patients is negligible but the possibility that intravascular platelet activation indirectly contributes “in vivo” to the increase in plasma plasminogen activator inhibitor-1 levels in severe preeclampsia patients cannot be ruled out.
Awareness of High Blood Pressure Stimulates Platelet Release Reaction
Authors: Rostrup Morten , Mundal Håvard Holth , Kjeldsen Sverre Erik , Gjesdal Knut , Eide Ivar 
Published: June 2018

SummaryThe present study aimed at testing the hypothesis of a link between mental stress and blood platelet function. Twenty-nine 19-year-old men were recruited from the 98th percentile of mean blood pressure (116 mmHg) at a routine medical screening. They were not informed about their elevated blood pressures at the time of the screening. One year later they were randomized into two groups. Group 1 (n = 16) was exposed to mental stress by a letter informing them about their high blood pressure, while group 2 (n = 13) was sent a neutral letter. At an examination 2 weeks later, heart rate (p <0.05) and plasma adrenaline (p <0.05) responses to a cold pressor test were exaggerated in the informed group. The plasma beta-thromoglobulin (pTG) concentration was elevated in the informed group (p <0.05) as was mean blood pressure (p <0.05). (3TG correlated positively with hematocrit (r = 0.59, p <0.005) and mean blood pressure (r = 0.43, p <0.05), and negatively with plasma HDL (r = −0.61, p = 0.001). The study shows that awareness of hypertension induces a hyperadrenergic state which is associated with the platelet release reaction. Under these circumstances platelet release seems to be correlated to established coronary heart disease risk factors.
β-TG and Plasma Catecholamines Levels after Sympathetic Stimuli in Hypertensives and Patients with Peripheral Vascular Disease
Authors: Catalano Maria , Russo Umberto , Belletti Sebastiano , Colombo Fabrizio , Belloni Armando , Rosso Gianfranco del , Lombardi Federico , Libretti Arnaldo 
Published: June 2018

SummaryThe influence of the sympathetic nervous system on platelet functions in vivo is still controversial. The aims of our study were to compare the response to various sympathetic stimuli in normal subjects and in patients with essential hypertension (HT) or peripheral vascular disease (PVD) and to evaluate any correlations among plasma levels of catecholamines, beta-thrombo-globulin (β-TG) and platelet factor 4 (PF4). In basal conditions β-TG and PF4 values in the HT patients were higher than those observed in the controls of the same age but lower than those of the PVD patients. Although the different sympathetic stimuli (90° tilting, handgrip, treadmill test, bicycle test) caused a significant increase of the plasma epinephrine (E) and norepinephrine (NE) levels, they did not modify the β-TG and PF4 levels in any of the groups studied. The platelet activation indices, therefore, regardless of the basal values, do not seem to be influenced by sympathetic stimulation.
Lack of Immune Response to Mouse IgG in Hemophilia A Patients Treated Chronically with Monoclate®, a Monoclonal Antibody Affinity Purified Factor VIII Preparation
Authors: Davis Hugh M , Brown Susan K , Nash David W , Pennetti Aniello M , Salzman Phyllis M , Schreiber Alian B , Haimovich Joseph 
Published: June 2018

SummaryHemophilia A is caused by factor VIII deficiency that historically has been treated with either a cryoprecipitate fraction of serum or factor VIII concentrate. Recently, the availability of affinity isolated factor VIII (Monoclate®) has allowed for a highly purified preparation for the chronic therapy of hemophilia A. This factor VIII preparation contains a trace quantity (<50 ng/ 100 I. U.) of mouse IgG. Immunoassays for the measurement of human IgG, IgJVl and IgE anti-mouse TgG antihody (HAMA) were developed and used to measure HAMA levels in hemophilia A patients undergoing chronic therapy with Monoclate® in three different clinical studies. Natural antibodies to mouse IgG were observed in patient sera prior to Monoclate® infusion. Data is presented demonstrating that induction of HAMA upon Monoclate® treatment does not occur. The low level of mouse IgG contained in Monoclate® appears to be below the threshold of immunogenicity. Most importantly, clinical symptoms related to hypersensitivity or anaphylaxis were never observed in any patient undergoing chronic therapy with Monoclate® in these clinical studies.
Blood Coagulation after Long Distance Running: Antithrombin III Prevents Fibrin Formation
Authors: Bärtsch Peter , Haeberli André , Werner Straub P 
Published: June 2018

SummaryPhysical exercise causes shortening of activated partial thromboplastin time (aPTT) and euglobulin clot lysis time. To investigate whether this activation of coagulation and fibrinolysis leads to in vivo thrombin or plasmin action after long distance running, 19 well trained male runners (36-65 years) were examined 5 to 53 min after termination of a 100 km race and 5 days later after at least 1 day without physical exercise. Compared to the control examination aPTT was decreased (30.2 ± 2.8 vs 35.3 ± 3.0 sec) and the following parameters were increased after the race: betathromboglobulin (40 ± 16 vs 23 ± 7 ng/ml), thrombin-antithrombin III (TAT) complexes (5.5 ± 3.4 vs 2.3 ± 0.7 pg/1), the fibrin(ogen) degradation products fragment E (57 ± 15 vs 35 ± 7 ng/ml) and B(3 15-42 (8.5 ± 2.5 vs 6.5 ± 2.5 ng/ml) (all p values <0.001). Platelet count, platelet factor 4, fibrinoepetide A (FPA) and haematocrit did not change significantly. Increased TAT complexes and unchanged FPA suggest that the generated thrombin was fully inactivated by antithrombin III (AT III) and did therefore not give rise to fibrin formation. The small increase of fibrin(ogen) degradation products indicates a minor in vivo activity of the fibrinolytic system. This investigation demonstrates the importance of AT III in the regulation of haemostasis in activated blood coagulation.
Characterization of a Monoclonal Antibody Specific to the Amino Terminus of the α-Chain of Human Fibrin
Authors: Mao Simon J T , Rechtin Ann E , Krstenansky John L , Jackson Richard L 
Published: June 2018

SummaryA peptide, Gly-Pro-Arg-Val-Val-Glu, corresponding to the first six residues of the amino terminus of the a-chain of human fibrin (desAA-fihrin) was prepared by solid-phase peptide synthesis. The peptide was covalently linked to keyhole-limpet hemocyanin (KLH) and used as an immunogen for preparing monoclonal antibodies. A monoclonal antibody specific to the hexapeptide, but not to KLH or fibrinogen, was produced. The antibody did not bind to thrombin-mediated clots prepared from either plasma or purified fibrinogen. However, immunoreactivity was detected when fibrin (prepared from fibrinogen) was solubilized with 8 M urea. In contrast, a monoclonal antibody specific to the amino terminus (Gly-His-Arg-Pro-Leu-Asp-Lys) of the (β-chain of fibrin recognized the epitope in clots. These results indicate that thrombin cleavage of fibrinogen produces a structural change in the amino terminal domain of the α-chain that makes it inaccessible to antibody interaction. In addition, our study suggests that the potential clinical application of monoclonal antibodies to localize fibrin-rich thrombi must take into account the final structure of clots.
Studies on Blood Coagulation and Fibrinolysis in Patients Bitten by Bothrops jararaca (jararaca)
Authors: Maruyama M , Kamiguti Aura S , Cardoso J L C , Sano-Martins Ida S , Chudzinski Ana M , Santoro M L , Morena P , Tomy Sandra C , Antonia Luci C , Mihara H , Kelen Eva M A 
Published: June 2018

SummaryThe blood coagulation and the fibrinolytic systems of nine patients envenomed by Bothrops jararaca in São Paulo (Brazil) were studied. Five of the accidents were caused by young snakes (<50 cm). On admission, four patients had non-clotting and three partially-clotting blood. Fibrinogen levels were decreased due to the thrombin-like activity of the venom as expected. Consequent secondary activation of the fibrinolytic system was evident from the low levels of alpha-2-antiplasmin and the high titres of fibrin(ogen) degradation products. High titres of cross-linked fibrin fragment D (D-dimer) in seven patients together with decreased platelet counts and/or factor V, and/or factor VIII in some, suggests intrinsic thrombin formation as these factors are not consumed in the defibrinogenation induced by venom thrombin-like fractions such as Ancrod and Batroxobin. However, normal or increased levels of antithrombin III in all and normal levels of factor II in eight patients do not support this interpretation. The existence of variable concentrations of other proteins in the venom of B. jararaca such as botrocetin and thrombocytin isolated from B. jararaca and B. atrox or crotalocytin from Crotaliis horridus venom should be considered. Such proteins are known to activate factors V, VIII, XIII, and platelets without affecting prothrombin (factor II) and antithrombin III. Slower recovery of the haemostatic disturbances after antivenom administration to patients bitten by young snakes suggests a more severe coagulopathy in such accidents. This is supported by clinical observations.
Impaired Fibrinolytic Capacity in Patients with Inflammatory Bowel Disease
Authors: Gris J C , Schved J F , Raffanel C , Dubois A , Aguilar-Martinez P , Arnaud A , Sanchez N , Sarlat C , Balmès J L 
Published: June 2018

SummaryThe venous occlusion test was applied to 17 patients with inflammatory bowel disease (IBD; 7 cases of Crohn’s disease, 10 cases of ulcerative colitis). Results were compared to those obtained in 20 healthy matched control subjects. Patients with IBD had significantly decreased t-PA Ag release (p <0.001) and had no significant vWF Ag release. Residual PAI activity was evidenced after venous stasis in the IBD group but not in the control group. Hypofibrinolysis was more important in patients with an evolutive IBD than in patients with IBD in remission. Impaired systemic fibrinolytic capacity might contribute to an increased risk for thromboembolic complications and to the pathogenesis of inflammatory bowel disease.
Low Anticoagulant Activity of High Sulphated Heparan Sulphates
Authors: Kovensky J , Sassetti B , Fernández Cirelli A , Kordich L 
Published: June 2018

SummaryTwo high sulphated heparin-like polysaccharides (LI, MW 16,000 and L2, MW 11,700) were isolated from rat liver tissues, after DEAE-cellulose chromatography. Heparan sulphates from heart and lung tissues were isolated for comparison and fractionated according to their molecular weight. The anticoagulant activities in vitro were studied using clotting antifactor Xa, antifactor IIa, and APTT assay methods, falling in a narrow range (5-44 IU/mg) although the wide variability m molecular weight and sulphate content. The heparan sulphate nature of fractions L1 and L2 (sulphate/disaccharide ratio 2.05 and 2.48, respectively) has been verified by: a) low iduronic/glucuronic acid ratio; b) nitrous acid degradation followed by gel chromatography; c) heparinase treatment followed by gel chromatography; d) electrophoretic behaviour. Native proteoglycans have been isolated and the glycosidic chains compared with L1 and L2. Their anticoagulant activities in vitro and the fact that antiXa clotting activity was not neutralized by protamine sulphate are in accordance with the results of structural studies.
In Vitro and In Vivo Antiaggregant Effects of Magnesium Halogenates
Authors: Cantón R , Manzanares J , Alvarez E , Zaragozá F 
Published: June 2018

SummaryThe in vitro antiplatelet aggregating activity of magnesium and magnesium associated with soluble citroflavomJids (hesperidin and eriodictin, 1:1) is well-established.The degree of inhibition of in vitro platelet aggregation activity produced by different concentrations of magnesium halogenates was determined. ADP (4 μM) was used to induce aggregation following Cardinal and Flowers’ (1) technique.Antithtombotic activity was studied in vivo. The differencein duration. of ADP-induced respiratory dysfunction was compared between animals fed 25 mg/kg magnesium halogenates for 10 days before testing and controls.An increase in circulating platelets was observed in rats treated with magnesium halogenates.
An Acquired Factor VIII Inhibitor Responsive to High-Dose Gamma Globulin
Authors: Green David , Kwaan Hau C 
Published: June 2018

SummaryA 55-year-old previously well woman noted easy bruising and developed a swollen, painful leg after minimal trauma. A compartment syndrome was diagnosed, and medial and lateral fasciotomies were performed with evacuation of a massive hematoma. However, blood rapidly reaccumulated in the wound. The VILI : C level was 2%, and 4 Bethesda units of factor VIII inhibitor were detected. After initial treatment with clotting factor concentrates and corticosteroids failed to control bleeding or reduce inhibitor titers, gamma globulin, 25 g daily for 5 days, was administered. The inhibitor became undetectable, VIII :C levels rose, and bleeding stopped. However, 5 days later VIII :C levels were again low and bleeding recurred. A second course of gamma globulin, 50 g daily for 2 days, was accompanied by a prompt increase in VIII :C, and uneventful recovery. In conclusion, in this patient with an autoantibody to Vili : C, a response to gamma globulin was observed on two occasions, and the second response came when steroids were being tapered and the patient was on no other medication.
Binding of Aggregated Immunoglobulins to the Human Platelet Fc Receptors: A Mechanism of Platelet to Platelet Bridging
Authors: Parbtani Anwar , Clark William F , Caveney Anita , Reid Bruce 
Published: June 2018

SummaryAggregated immunoglobulins react with human platelets by occupying the Fc receptors present on their surface, inducing aggregation and the release reaction. We studied the effect of heat aggregated gammaglobulins (HAGG) on ADP-induced aggregation of platelets. We used the minimum concentration of ADP required to induce a reversible aggregation of platelets without any substantial amount of serotonin (14C 5HT) release. EDTA (5 mM) added at the peak of platelet aggregation resulted in rapid deaggrcgation ot these platelets. However, incubation of platelets with HAGG at a dose that did not by itself induce any aggregation or release reaction, followed by ADP addition resulted in an irreversible platelet aggregation of greater magnitude accompanied by a substantial release of 14C-5HT. The addition of EDTA at the peak of platelet aggregation failed to deaggregate these platelets. To determine whether the augmented aggregation response and the inhibition of deaggiega-tion was due to HAGG or a consequence of platelet release products, we used thrombin-degranulated platelets. The augmented aggregation response and the inhibition of deaggregation due to HAGG and ADP could be demonstrated using these platelets. To confirm that the binding of HAGG to the platelet Pc receptors was responsible for these observations, we incubated platelets with an excess of Fc fragments of IgG prior to the addition of HAGG and ADP. This abolished the aggregation response observed previously. From this study we conclude that interplatelet bridging by HAGG renders the platelets hyperag-gregable and appears to be a mechanism involved in maintaining platelet aggregates.
Calibration of Lyophilized Standards for Ristocetin Cofactor Activity of von Willebrand Factor (vWF) Requires vWF-Deficient Plasma as Diluent for Dose-Response Curves
Authors: Rodeghiero Francesco , Castaman Giancarlo 
Published: June 2018

SummaryCalibration of local standards for ristocetin cofactor activity of von Willebrand’s factor (vWF : Rcof) against reference preparations is required to achieve a better standardization of this measurement. We have observed that in calibration assays (multiple line parallel bioassay) for vWF : Rcof, measured aggregometrically, the type of diluent used to obtain the dose-response curves exerted a critical influence on the final potency estimation when a fresh-frozen plasma against a lyophilized standard or two lyophilized preparations were to be compared. This pattern was observed with various commercial standards and also with the First International Reference Preparation for Factor VIII-Related Activités in Plasma. The choice of diluent was not relevant if two fresh-frozen plasma preparations were to be calibrated. Systematic experiments using as diluents Trissaline, Tris-buffered-albumin solution or vWF-deficient plasma (vW-plasma) showed that the ratio lyophilized/fresh-frozen preparations was invariably lower with albumin solution than with vW-plasma. Tris-saline partially corrected this discrepancy, but yielded less precise estimates. Preliminary results with cryosuper-natant-plasma seems to indicate that this material is a valid substitute for vW-plasma, but confirmatory experiments are required For the moment, plasma obtained from patients with severe type III vW-disease should be considered the “ideal” diluent for calibration assays involving lyophilized preparations.
Combined Use of DNA Probes in First-Trimester Prenatal Diagnosis of Hemophilia A
Authors: Sampietro M , Camerino G , Romano M , Cappellini M D , Fiorelli G , Brambati B , Guerneri S , Ferrari M , Travi M , Krachmalnicoff A , Mannucci P M 
Published: June 2018

SummaryFirst-trimester prenatal diagnoses of hemophilia A were heretofore obtained by using either intragenic factor VIII markers or linked cxtragcnic polymorphic markers. Postulating that the combined use of all the available intragenic and extragenic markers can render such diagnoses more frequently feasible and more reliable, we carried out ten first-trimester prenatal diagnoses in male fetuses at risk for hemophilia A by DNA analysis of chorionic villus employing in combination the intragenic Bcl I polymorphism and the St 14 (DXS 52) or DX 13 (DXS 15) extragenic probes. A diagnosis of hemophilia was obtained in three fetuses, with a diagnosis of normal fetus obtained in the remaining seven. Seven diagnoses are confirmed by factor VIII assays carried out at the time of abortion, in the mid-Trimester or at birth. A factor VIII probe recognizing Bcl I polymorphism was useful in 4 of 6 diagnoses; St 14, in 5 of 6; and DX 13 in 3 of 5. In two cases, St 14 was the only useful probe for diagnosis. Even though no recombination between extragenic probes and factor VIII gene was detected in this study, when only extragenic markers were informative we advised diagnostic confirmation on fetal plasma obtained by fetoscopy. Hence, first-trimester prenatal diagnosis of hemophilia A is feasible for the great majority of fetuses at risk through combined use of all the available intragenic and extragenic probes, providing key family members are available.
Factor XII, Plasma Prekallikrein, α2-Macroglobulin and C1-Inhibitor Levels in Renal Allograft Recipients During Immunosuppression with Cyclosporin A – Sequential Measurements over Four Months in 17 Patients
Authors: Lohri A , Huser B , Lämmle B , Oberholzer M , Thiel G , Duckert F 
Published: June 2018

SummaryFactor XII clotting activity (F XII), plasma prekallikrein amidolytic activity (PK), α2-Macroglobulin (α2-M) and C1-Inhibitor (C1-Inh) antigens have been measured in 17 patients immediately before and sequentially for up to four months after kidney transplantation. Before transplantation mean F XII and PK levels were normal (99 ± 27% and 102 ± 21%, respectively, mean ± S. D.) and α2-M and C1-Inh levels were slightly elevated (115 ± 55% and 129 ± 32%, respectively, mean ± S. D.). In the first two weeks after transplantation a significant decrease of F XII to 65 ± 27%, of PK to 67 ± 20% and of α2-M to 88 ± 42%, and a rise of C1-Inh to 201 ± 44% (mean ± S. D.) were observed (2 p <0.005). F XII levels four month after operation remained significantly (2 p <0.05) lower than preoperatively. PK and α2-M values, however, were significantly higher (2 p <0.05) at four months as compared to the pretransplant period. Mean F XII levels in the 17 patients at various time points after transplantation correlated positively with PK, α2-M and serum albumin and negatively with CyA level and dose and serum bilirubin. PK and α2-M correlated positively with each other and albumin and negatively with creatinine, bilirubin and CyA (2 p <0.01). Whether CyA has a direct influence on production or consumption of F XII, PK, α2-M and C1-Inh, or whether the changes merely reflect altered protein metabolism awaits further study.