Publications by authors named "Scharf R"

Background/aim: FK-506 (FK) and mycophenolic acid (MPA) are immunosuppressive agents used in kidney transplant recipients. Their effect on posttransplant thromboembolic complications is either controversial (FK) or has not been described (MPA). Thromboembolic events are among the consequences of platelet hyperaggregability which can be identified by measuring platelet aggregation.

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Recently, we have demonstrated that human platelet antigen 1b (HPA-1b or P1A2) is a hereditary risk factor for platelet thrombogenicity leading to premature myocardial infarction in preexisting coronary artery disease. However, HPA-lb does not represent a risk factor for coronary artery disease itself. The aim of our present study was to evaluate the role of HPA-lb on the outcome in patients after coronary-artery bypass surgery.

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Background: Venous thromboembolism is a leading cause of morbidity and mortality during pregnancy and the puerperium. However, the role of mutations in the prothrombin and factor V genes and other thrombophilic abnormalities as risk factors for thromboembolism in women during pregnancy and the pueperium is not known.

Methods: In a study of 119 women with a history of venous thromboembolism during pregnancy and the puerperium and 233 age-matched normal women, we measured the activity of antithrombin, protein C, protein S, and lupus anticoagulant.

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Complex interactions among constituents of blood, components of the subendothelial extracellular matrix, and artificial surfaces of cardiovascular devices are involved in the thrombogenesis following heart valve replacement. Recently, the molecular basis of some of these interactions has been studied in detail. These insights have extended our understanding of interactive processes between platelet receptors, adhesive macromolecules, and abnormal flow conditions during platelet adhesion and aggregation.

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Transfusion of whole blood is the most common and successful organ transplantation world wide. It is in use longer than any other transplantation procedure. With the exception of uses in situations of crisis, treatment with whole blood is nowadays obsolete.

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Factor VIII inhibitor is rare, but very serious postpartum complication. Bleeding diathesis caused by this inhibitor is called acquired haemophilia. Three women with postpartum inhibitor to factor VIII and life threatening bleeding were described.

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Conflicting results of an association between the human platelet antigen 1b (HPA-1b or PlA2) allele and the risk of myocardial infarction and coronary artery disease have been reported. To assess the reason for this discrepancy, we determined the HPA-1 genotype in 298 men who had undergone coronary angiography, including 124 individuals with myocardial infarction, 83 individuals with coronary artery disease but no history of myocardial infarction, and 91 control patients. Among patients with acute or recent onset myocardial infarction (< 1 year), the prevalence of HPA-1b was higher than among patients with coronary artery disease but without myocardial infarction (33 percent vs.

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Deep venous thromboses, in particular when recurrent, can be associated with chronic venous leg ulcers. Such complications are often seen in dermatology departments and frequently represent a therapeutic problem. Resistance to activated protein C (APCR) has recently been identified as the most frequent coagulation defect associated with an increased risk of venous thrombosis.

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Fetal alloimmune thrombocytopenia is caused by maternal immunization against a fetal platelet antigen and transplacental transfer of the antibody into the fetal circulation. Since 10-20% of the fetuses or newborns are threatened by intracranial hemorrhages, early management is required. Fetal blood sampling should be started between the 20th and 22nd week of gestation to assess fetal phenotype and platelet count.

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Genotyping of platelet alloantigens with the possibility of using any type of cellular material as a source of DNA has become a preferred procedure, particularly in thrombocytopenic patients when platelet counts are too low for phenotyping. Recently human platelet antigen 1 (HPA-1) has been identified as an inherited risk factor for coronary thrombosis. The different detection methods currently used have disadvantages for large-scale DNA diagnosis, including the need for electrophoresis (allele-specific restriction enzyme analysis, amplification with sequence-specific primers) or the potential risk of reduced specificity (allele-specific oligonucleotide hybridization).

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Patients with hemophilia A and circulating anticoagulant (factor VIII inhibitor) present a difficult, even unsolvable problem, particularly if they require surgical treatment and the inhibitor titer is high. During the 1986-1995 period 29 surgical procedures on inhibitor hemophilia A patients were performed in our center. Each of the cases had an individual character, and all demanded special clinical treatment.

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In 1993-94, 15 high responders were treated in our centre according to the Malmo protocol which was modified as follows: serial plasmapheresis was performed instead of extracorporeal adsorbtion to protein A for reducing inhibitor levels and, after the bolus dose to neutralize the inhibitor, factor VIII concentrate was administered by a continuous infusion. Thus, this regimen included continuous infusion of factor VIII(FVIII) for 1-4 weeks, iv cyclophosphamide for 2 days and orally for 8-10 days, and intravenous immunoglobulin (IVIG) from the fourth day for 5 days. All patients had been qualified for the treatment when the antibody level was < 15 BU mL(-1) .

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Activated protein C resistance is the most frequent cause of venous thrombosis. We describe a patient with extensive ulcerations and severe lymphedema of the legs after recurrent thrombosis. Laboratory tests revealed a pathologic activated protein C resistance and a reduced functional protein S.

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Resistance of coagulation factor Va to inactivation by activated protein C (APCR) is associated with a point mutation in which adenine is substituted for guanine at nucleotide 1691 in the gene coding for factor V (FV Leiden). To date, this mutation of factor V is the most frequent genetic risk factor for venous thrombophilia. In this report, we describe the adaptation of an automatable oligonucleotide ligation assay (OLA) to detect the mutation in polymerase chain reaction-amplified DNA samples from 40 normal, 20 affected heterozygous, and 3 affected homozygous individuals.

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We have evaluated the effect of maternal intravenous immunoglobulin G (ivIgG) treatment on platelet counts in fetal alloimmune thrombocytopenia. Seven patients were studied. All of them were multiparous women who had been immunized against the HPA-1a antigen during previous pregnancies and had given birth to at least one severely thrombocytopenic infant.

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Fetal alloimmune thrombocytopenia is caused by materno-fetal transfer of platelet antibodies. Since the thrombocytopenic fetus is threatened by intracranial hemorrhage, prenatal observation and, if necessary, treatment is required. However, the benefit of therapeutic options, including intravenous IgG (ivIgG), platelet transfusions or fetal IgG transfusions is still controversial.

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Dynamic light scattering measurements show that although Mg-actin polymerizes more rapidly than Ca-actin (actin at 0.04-0.4 mg/ml polymerized with 0.

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Counting statistics in the form of the variance-time curve provides an alternative to spectral analysis for point processes exhibiting 1/f beta-fluctuations, such as the heart beat. However, this is true only for beta < 1. Here, the case of general beta is considered.

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Unlabelled: Efficient on-line digitization is the prerequisite for computerized analysis of the electrical phenomena occurring during defibrillation. Conventional hardware presently provides only limited time resolution. The performance of various digitization rates for recording of voltage, current, and calculation of derived quantities like impedance, energy, and defibrillator capacitance was investigated.

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