bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immature Auditory Evoked Potentials in Children With Moderate–Severe Developmental Language Disorder
Authors: Kwok Elaine Y. L. , Joanisse Marc F. , Archibald Lisa M. D. , Cardy Janis Oram 
Published: July 2018

Purpose

Immature auditory processing has been proposed to underlie language impairments in children with developmental language disorder (DLD; also known as
specific language impairment
). Using newly available normative auditory evoked potential (AEP) waveforms, we estimated AEP maturity in individual children with DLD and explored whether this maturational index was related to their language abilities.

Method
AEPs were elicited by 225 trials of a 490-Hz pure tone. Using intraclass correlation and our previously established normative AEP waveforms of 7- to 10-year-old children with typical development, we estimated the age equivalent of the AEPs (AEP–age) from 21 children with DLD. The relation between AEP maturity and language was explored through regression analysis.

Results
AEP–age predicted 31% of the variance in the language abilities of children with DLD. The AEP–age of children with mild DLD was similar to their chronological age, whereas children with moderate–severe DLD showed, on average, a 1.3-year delay in their neural responses. AEP–age predicted receptive, but not expressive, language performance.

Conclusion
Maturation in auditory neural responses is a significant predictor of language ability, particularly in children with moderate–severe DLD.
Erfolgreich zurück in den Leistungssport nach Verletzung des oberen Sprunggelenks – Ein Fallbeispiel
Authors: Flore Zacharias , Keller Matthias , Welsch Götz , Kurz Eduard 
Published: July 2018

ZusammenfassungKriterienbasierte Rehabilitationsmodelle unter Berücksichtigung der Wundheilungsphasen rücken in der Nachbehandlung von Sportlern immer weiter in den
Vordergrund. Dabei orientiert sich die Rehabilitation einerseits an der verletzten Struktur, andererseits an den Anforderungen der entsprechenden Zielsportart.
Die Autoren stellen anhand eines Fallbeispiels aus dem Leistungsfußball einen möglichen Therapiealgorithmus nach Verletzungen des Sprunggelenks vor und zeigen,
wie funktionelle Tests ergänzt durch einen spezifischen Fragebogen in der Rehabilitation eingesetzt werden können.
Gleichgewichtstraining zur Verletzungsprävention und Leistungssteigerung
Authors: Keller Martin 
Published: July 2018

ZusammenfassungGleichgewicht ist eine essenzielle koordinative Fähigkeit. Es hilft, Verletzungen zu vermeiden, und sollte daher gezielt trainiert werden. Dabei stellt sich die
Frage, ob der Effekt bestimmter Übungen auf andere Situationen übertragbar ist und ob sich mit einer guten Übungsauswahl auch andere Leistungsparameter von
Athleten steigern lassen.
Concussion – Gehirnerschütterungen im Sport
Authors: Sutor Volker 
Published: July 2018

ZusammenfassungDie Gehirnerschütterung ist eine ernst zu nehmende Verletzung, die mit den unterschiedlichsten Symptomen auftritt. Besteht bei einem Sportler im Wettkampf der
Verdacht auf eine Gehirnerschütterung, sollte der Betroffene zu seiner eigenen Sicherheit sofort aus dem Spiel genommen werden. Bei adäquater Behandlung erholen
sich Verletzte vollständig und können schon bald wieder zum Sport zurückkehren.
Berufsbiografische Entwicklungen bei der Betreuung Sterbender
Authors: George Wolfgang M. 
Published: July 2018

ZusammenfassungEtwa die Hälfte aller Menschen beendet das Leben in einem Krankenhaus, ein Drittel davon auf einer Intensivstation. Welche Auswirkungen die Betreuung von Sterbenden außerhalb einer ausgewiesenen Palliativstation hat, untersucht eine Studie von Prof. Wolfgang George, der dazu die Daten von knapp 500 Teilnehmern auswerten konnte. Wir stellen die Ergebnisse vor.
Oral Anticoagulation Therapy in Pediatric Patients: a Prospective Study
Authors: Andrew Maureen , Marzinotto Velma , Brooker Lu Ann , Adams Margaret , Ginsberg Jeff , Freedom Robert , Williams William 
Published: July 2018

SummaryThere are no validated guidelines for administering or monitoring oral anticoagulant therapy in pediatric patients. A pediatric thromboembolism program at the Hospital for Sick Children, Toronto, prospectively monitored consecutive children requiring warfarin over an 18 month period. A uniform protocol was followed and dose adjustments based upon international normalized ratios (INRs). One hundred and fifteen consecutive children; 68 males and 47 females, received warfarin. The age distribution was: <ly (19); 1-5 ys (33); 6-10ys (20); 11-18 ys (43). Warfarin was used for secondary prevention of venous thromboembolism (n = 56) and primary prevention of thromboembolism (n = 59). Underlying disorders included: congenital heart disease (CHD) without mechanical valves (MV) (49); CHD with MV (18); cancer (8); longterm total parenteral nutrition (7); renal disorders (10); other (23). Treatment length was considered as short term (3-6 mths) n = 37 (32%); longterm (> 6 mths) n = 38 (33%); and lifelong n = 40 (35%) of children. While receiving warfarin, 95 children received concurrent longterm treatment with other drugs: 1 drug (28); 2 drugs (27); 3 drugs (21); 4 or more drugs (19).The amounts of warfarin/kg required to achieve INRs of 2 to 3 decreased with increasing age. Children <1 year of age required 0.32 ± 0.05 mg/kg whereas children 11-18 yrs required 0.09 ± 0.01 mg/kg; P <0.001. Monitoring warfarin required an average of 4.0 measurements per month and 1.5 dose changes per month. Changes in warfarin doses were primarily precipitated by drugs, intermittent illness, and changes in diet. A subgroup of children (n = 21) were treated with low dose warfarin either alone (n = 14) or following a course of full dose therapy (n = 7) to achieve an INR of 1.3 to 1.8. These children had persisting predisposing causes for new or recurrent thromboembolism. After the age of 1, the average dose required was 0.08 ± 0.01 mg/kg.Complications were rare. Two children had significant bleeding events that resolved without further morbidity. There were no recurrent thrombotic events while children were receiving warfarin. In summary, warfarin therapy is age and weight dependent in children; close monitoring is necessary because of changing requirements; and complications are infrequent when management is coordinated through one service.
Thrombin-Based Antithrombin Assays Show Overestimation of Antithrombin III Activity in Patients on Heparin Therapy due to Heparin Cofactor II Influence
Authors: Bohner Jürgen , von Pape Klaus-Werner , Blaurock Mathias 
Published: July 2018

SummaryAn extensive comparison has been performed on the clinical chemistry automate Hitachi 717 between thrombin-and Factor Xa-based methods for determination of antithrombin III activity. In 460 patients who did not receive any heparin therapy the agreement between assays was in general close although the thrombin-based methods resulted in slightly higher assignments of 0.3—2.6% antithrombin III activity. The discrepancy was, however, substantial in plasmas from patients receiving heparin of >20000 IU/day, resulting in plasma levels of heparin of 0.8-1.2 IU/ml. Thus, analysis of 102 patients showed that the thrombin-based methods resulted in, on average, 7-16% higher assignment of antithrombin III activity as compared to the Factor Xa-based method used.Addition of antibodies to antithrombin III and heparin cofactor II revealed that the discrepancy was primarily due to contribution of heparin cofactor II activity in the thrombin-based methods. The results thus suggest that the Factor Xa-based antithrombin III activity method provides more valid results in patients on heparin therapy.
Effects of Low Intensity Antithrombotic Regimes on the Haemoglobin Level
Authors: Meade T W , Howarth D J , Brennan P J 
Published: July 2018

SummaryThe effects on the haemoglobin level of low dose aspirin and of low intensity oral anticoagulation with warfarin separately and in combination have been established in men aged between 45 and 69 at high risk of ischaemic heart disease. The findings confirm that combined treatment with warfarin and aspirin (WA) leads to a clear excess of minor bleeding episodes over warfarin alone (W) or aspirin alone (A). Each separate treatment on its own (either W or A) leads to an increase in these episodes compared with those on placebo (P) treatment. However, neither combined treatment (WA) nor the separate treatments (W or A) cause a fall in haemoglobin levels over a period of up to two years.
Effect of Low Molecular Weight Heparin, Dextran and Their Combinations on Experimental Venous Thrombosis in Rabbits
Authors: Matthiasson Stefan E , Lindblad Bengt , Mätzsch Thomas , Holst Jan , Bergqvist David 
Published: July 2018

SummaryAn experimental model based on the combination of endothelial damage and flow reduction was used to induce jugular vein thrombosis in rabbits. The effect on thrombosis of a low molecular weight heparin (LMWH [Fragmin]), dextran 70, placebo and their combination was studied in a double-blind fashion with actual doses used in clinical thromboprophylaxis. Saline and polygeline were used as placebo in the control group. Four groups with 120 isolated vein segments in 60 animals were studied for presence of thrombus formation, occlusive thrombi and thrombus weights. Dextran reduced the thrombus weights (p = 0.048) and the formation of occlusive thrombi (p = 0.01), but not the formation of thrombi when compared with the placebo control group. Similarily, LMWH reduced the thrombus weights (p = 0.046), the formation of thrombi (p = 0.007) and occlusive thrombi (p = 0.0001). Compared with the LMWH group the group treated with the combination of LMWH and dextran was found to reduce the frequency of occlusive thrombi (p = 0.03) and numerically, but not significantly, further reduce the overall frequency of thrombosis (p = 0.18) and thrombus weights (p = 0.11). The results are consistent with an augmentation of the antithrombotic effect of LMWH by dextran 70. The need for further evaluation of the combined efficacy of LMWH and dextran is apparent from this study.
Demonstration of a Functionally Active tPA-Like Plasminogen Activator in Human Platelets
Authors: Wang D L , Pan Y T , Wang J J , Cheng C H , Liu C Y 
Published: July 2018

SummaryThe mechanism of platelet-enhanced fibrinolysis is unclear. We therefore investigated the fibrinolytic activity of human platelets and demonstrated that they contain a tissue plasminogen activator (tPA)- like plasminogen activator, abbreviated as tPA-like-PA. This activator was detected by ELISA in platelet incubation medium and in platelet Triton extracts. Plasminogen activation assays showed that this tPA- like-PA could induce plasminogen activation to form plasmin. Western blots of Triton extracts incubated with anti-tPA antibody demonstrated a major 64-kD protein band, compared to a 70-kD band for standard single chain tPA, plus a minor 118-kD band corresponding to a complex of tPA-like-PA and plasminogen activator inhibitor (PAI-1). Western blots of Triton extracts incubated with anti-PAI-1 antibody produced an approximately similar high-molecular-weight (118 kD) protein band. Fibrin zymographic analysis of affinity-purified tPA-like- PA demonstrated a major and a minor fibrin lysis zone, which approximately corresponded to the tPA-like-PA and its complex with PAI-1 observed by Western blots. Immunogold labelling and electron microscopy demonstrated that platelet activator, either as the free form or co-localized with PAI-1, was present in granules and in channels of the open canalicular system. We conclude that platelets contain a functionally active tPA-like-PA, whose low fibrinolytic activity might be due to its readily forming a complex with PAI-1. This functionally active tPA-like-PA might contribute to the enhanced fibrinolytic activity of platelets observed in platelet-rich thrombi.
Intramuscular Dermatan Sulfate MF701 in Patients with Hip Fracture: Relationship between Pharmacokinetics and Antithrombotic Efficacy
Authors: Imbimbo B P , Sié P , Agnelli G , Saivin S , Dupouy D , Damiani M , Houin G , Gianese F 
Published: July 2018

SummaryTwo groups of 23 and 84 patients with hip fracture received intramuscularly 100 and 300 mg dermatan sulfate (MF701) b. i. d., respectively, for the prophylaxis of deep vein thrombosis. Median duration of treatment was 17 and 16 days, respectively. Four blood samples were collected from each patient while under treatment. Plasma levels of dermatan sulfate were determined by a chromogenic substrate assay. A one-compartment model for multiple doses was employed to estimate the pharmacokinetic parameters. Fitting was applied to mean plasma concentrations calculated for each sampling time and weighted according to the number of samples available at each time. Thrombin clotting time was measured on the same plasma samples. Antithrombotic efficacy was assessed by bilateral venography.Plasma levels of dermatan sulfate increased gradually throughout the treatment, indicating a marked accumulation process. Time to reach steady-state was 14 or 9 days with 100 or 300 mg b. i. d., respectively. This was due to an apparent prolonged terminal half-life (68 or 43 h), which actually reflected slow absorption from the injection sites. The clinical efficacy of MF701 in preventing DVT was found to be dependent on the plasma concentration of the drug and also, but less significantly, on the prolongation of thrombin clotting time. Dermatan sulfate plasma levels greater than 9 μ/ml are advisable to optimize efficacy in hip fracture patients.
Anti-Glycoprotein Ib/IX and llb/llla Antibodies in Patients with Antiphospholipid Antibodies
Authors: Galli Monica , Daldossi Maria , Barbui Tiziano 
Published: July 2018

SummaryAntiphospholipid antibodies, namely lupus anticoagulant (LA), anticardiolipin (aCL) type A and type B antibodies, are frequently associated with immune-mediated thrombocytopenia. Antiphospholipid antibodies have been suggested to bind to the phospholipids of the platelet membrane, thus participating to the process of platelet destruction, which leads to thrombocytopenia. However, a clear antiphospholipid (aPL) demonstration of such a role has never been given for antibodies. Conversely, autoantibodies directed against membrane-associated glycoproteins (GP) have been shown to be pathogenet- ically linked to the development of thrombocytopenia in patients with idiopathic thrombocytopenic purpura. For this reason, we have measured anti-GPIb/IX and GPlIb/IIIa IgG in the plasma of 68 patients with aPL antibodies by ELISA. The monoclonal antibody-specific immobilization of platelet antigen (MAIPA) assay was used.Twenty-seven out of 68 patients with antiphospholipid antibodies (40%) had increased plasma levels of anti-GP antibodies. In particular, 7 of them had elevated anti-GPIIb/IIIa levels only, 6 had anti-GPIb/IX antibodies only, whereas in the remaining 14 cases both types of autoantibodies were found elevated. The level of anti-GP antibodies in plasma did not correlate with age, sex, clinical associated conditions, history of thrombosis, IgG aCL titer or the presence of a phospholipid- dependent inhibitor of coagulation. In contrast, a statistically significant association between thrombocytopenia and high anti-GP antibody titer was observed (p = 0.0458).To establish whether there was cross-reactivity between antiphospholipid and anti-GP antibodies, adsorption experiments were performed using eardiolipin-containing liposomes or washed, normal, resting platelets. When patients’ plasma was mixed with resting washed platelets, only anti-GP antibodies were adsorbed on platelet membrane and subsequently eluted from platelets. Conversely, binding to cardio- lipin-containing liposomes but not to platelet surface was demonstrated for antiphospholipid antibodies.In conclusion, our data indicate that high levels of anti-platelet glycoprotein antibodies are more frequently found in patients with antiphospholipid antibodies and thrombocytopenia and that they might be responsible, more than LA and/or aCL antibodies, for the development of thrombocytopenia.
Expression and Assembly of Procoagulant Complexes by Human Pleural Mesothelial Cells
Authors: Kumar Anuradha , Koenig Kathleen B , Johnson Alice R , Idell Steven 
Published: July 2018

SummaryMany pleural diseases involve fibrin deposition within the pleural cavity, an event that necessarily involves the mesothelium. This study of human pleural mesothelial cells (HPMC) was designed to determine how the mesothelium initiates and sustains the coagulation process. We used functional assays for activation of both factor X and prothrombin to examine expression and assembly of procoagulant activity by human pleural mesothelial cells in culture. The rates of factor Xa and thrombin formation were calcium-dependent. The rate of factor Xa formation in the presence of added factor VII increased in a concentration-dependent manner, suggesting that tissue factor is the primary procoagulant associated with HPMC. The fact that direct binding of radioiodinated factor Vila to HPMC was specific, concentration-dependent and saturable confirms that tissue factor is expressed on the cell surface. The rate of thrombin formation increased with factor Xa concentration, and the rate was 5-, 6-fold higher in presence of added factor Va indicating that HPMC support expression of prothrombinase activity. Further, direct binding of radioiodinated factor Xa to HPMC was specific, concentration-dependent and saturable, confirming that the cells support the assembly of the prothrombinase complex.
Platelet Shape Change in Whole Blood: Differential Effects of Endotoxin
Authors: Nystrom M L , Barradas M A , Jeremy J Y , Mikhailidis D P 
Published: July 2018

SummaryThe effect of endotoxic lipopolysaccharide (LPS) on platelet shape change (PSC; a preaggregation event) was investigated. PSC is accompanied by an increase in median platelet volume (MPV), which was measured using a channelyzer. In whole blood, but not in platelet rich plasma (PRP), LPS (final concentration 80 mg/1) caused an increase in MPV that could be detected for 2 h. When PRP (prepared from LPS- and saline-pretreated whole blood) was incubated for 40 min, the LPS-mediated increase in MPV could no longer be detected. Taken together, these data imply that PSC is both initiated and maintained by a labile factor(s) present in whole blood, but not in PRP.PRP was prepared from LPS-pretreated whole blood and incubated for 40 min to allow reversal of the LPS-induced PSC; further stimulation with LPS caused PSC. Platelets from LPS-pretreated whole blood also showed enhanced PSC with seioloum (J-HT), diminished PSC with platelet activating factor (PAF), and no change of response to ADP and collagen. Hence, LPS pretreatment of whole blood differentially alters responses of platelets to further stimulation with LPS and other agonists. A specific PAF antagonist completely abolished the effect of LPS on MPV. These data may contribute to an understanding of the cascading thrombotic events and thrombocylopeuia assoeialed wiib septicaemia.
Clopidogrel – a Platelet Inhibitor which Inhibits Thrombogenesis in Non-Anticoagulated Human Blood Independently of the Blood Flow Conditions
Authors: Roald Helge E , Marius Barstad R , Kierulf Peter , Skjørten Fredrik , Dickinson John P , Kieffer Gilles , Sakariassen Kjell S 
Published: July 2018

SummaryThe goal of the present study was to investigate the effect of 7 and 14 days of daily oral administration of 75 mg clopidogrel on collagen-induced thrombogenesis in flowing non-anticoagulated human blood. Blood was drawn directly from an antecubital vein over immobilised collagen type III fibrils positioned in a parallel-plate perfusion chamber. The wall shear rates at the collagen surface were those characteristic for veins (100 s−1), and for medium sized (650 s−1) and moderately stenosed (2600 s−1) arteries.Clopidogrel ingestion reduced the thrombus volume significantly (p <0.05) at 100 and 2600 s−1 (39 and 51% respectively). The β-thromboglobulin plasma levels were reduced concomitantly. However, it was not possible to measure accurately the thrombus volume at 650 s−1, due to loose packing of the platelet thrombi. Transmission electron micros-copy substantiated this observation and showed that clopidogrel profoundly reduced the platelet degranulation process (p <0.005). The inhibitory effect of clopidogrel on platelet consumption by the growing thrombi resulted apparently in higher platelet concentration at the collagen surface, which enhanced the platelet-collagen adhesion at all three shear rates (p <0.05). Despite the low deposition of fibrin on collagen, clopidogrel reduced significantly the fibrinopeptide A plasma levels and the fibrin deposition at shear rates below 650 s−1. This was apparently a consequence of the reduced platelet recruitment and the lower activation of platelets, since activated platelets in thrombi promote deposition of fibrin.Thus, it appears that clopidogrel inhibits thrombus formation in human blood primarily by interfering with platelet-platelet binding and the inhibition is effective independently of the wall shear rate.
Clinical Course of Factor VIII Inhibitors Developed after Exposure to a Pasteurised Dutch Concentrate Compared to Classic Inhibitors in Hemophilia A
Authors: Mauser-Bunschoten E P , Rosendaal F R , Nieuwenhuis H K , Roosendaal G , Briëf E , van den Berg H M 
Published: July 2018

SummaryAfter the introduction of a new pasteurised factor VIII concentrate (Factor VIII CPS-P) in The Netherlands in June 1990, an increase in the occurrence of inhibitors in hemophilia A patients was reported. The clinical course of this group of inhibitors (n = 12) was compared with hemophilia patients in whom an inhibitor developed before June 1990 (classic inhibitors) (n = 32). Striking differences were found between both groups not only in patient age (median 22 years versus 8 years) and number of exposure days (<50 − >1000 versus <50), as described in previous reports, but also in clinical course and response to treatment. In the recent group of inhibitors antibody titers showed a rapid decline when product was changed which was not the case in the group with classic inhibitors. In the group of classic inhibitors immune tolerance therapy with low dose factor VIII succeeded in 83%. Success was to a high degree dependent on the inhibitor level. In the group of recent inhibitors immune tolerance with the same concentrate was only successful in a single patient. However, once the patients were switched to another concentrate, antibody levels dropped to less than 2 BU/ml within 8 months in all patients.It seems likely that in this group of product associated inhibitors, treatment success was due to elimination of antigen stimulation rather than induction of immune tolerance.