Search results for "Blood coagulation"

showing 10 items of 154 documents

Activation of the contact-phase system on bacterial surfaces--a clue to serious complications in infectious diseases.

1998

Fever, hypotension and bleeding disorders are common symptoms of sepsis and septic shock. The activation of the contact-phase system is thought to contribute to the development of these severe disease states by triggering proinflammatory and procoagulatory cascades; however, the underlying molecular mechanisms are obscure. Here we report that the components of the contact-phase system are assembled on the surface of Escherichia coli and Salmonella through their specific interactions with fibrous bacterial surface proteins, curli and fimbriae. As a consequence, the proinflammatory pathway is activated through the release of bradykinin, a potent inducer of fever, pain and hypotension. Absorpt…

FeverFimbriaBradykininBiologyFibrinogenBradykininGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineMicrobiologySepsischemistry.chemical_compoundMiceBacterial ProteinsmedicineAnimalsEscherichia coli InfectionsInflammationSalmonella Infections AnimalSeptic shockEnterobacteriaceae InfectionsGeneral MedicineBlood Coagulation Disordersmedicine.diseaseShock SepticCoagulationchemistryShock (circulatory)ImmunologyFemalemedicine.symptomHypotensionmedicine.drugNature medicine
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Complete gangrene of penis in patient with arterial vascular disease.

2004

We present a clinical case of distal penile gangrene in a patient with peripheral vaso-occlusive disease that did not correlate with the extension of the intraoperative finding and required total penectomy. Surgical intervention at the onset of wet gangrene avoids the complication of sepsis.

GangreneMalePeripheral Vascular Diseasesmedicine.medical_specialtyArterial vascular diseasePenectomybusiness.industryUrologyBlood Coagulation DisordersMiddle Agedmedicine.diseaseWounds NonpenetratingSurgerySepsisGangrenemedicine.anatomical_structureMedicineHumansIn patientClinical casebusinessComplicationPenisPenisUrology
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Screening for multiple hereditary hypercoagulability factors using the amplification refractory mutation system

2003

Many hereditary factors have been implicated in the development of arterial and/or venous thromboembolic diseases. A number of these risk factors can be identified by the amplification refractory mutation system (ARMS). However, the underlying technical conditions for performing ARMS are highly variable, and depend on which risk factors are being analyzed. We have now developed a novel ARMS-based system to simultaneously screen for multiple hypercoagulability factors under identical PCR conditions. This can greatly simplify the process of screening for hereditary hypercoagulability.

GeneticsBase SequenceGenetic Carrier ScreeningHomozygoteGenetic Carrier ScreeningSingle-strand conformation polymorphismBlood ProteinsHematologyBlood Coagulation DisordersBiologymedicine.diseaseThrombophiliaBioinformaticsPolymerase Chain ReactionThrombosisBlood Coagulation FactorsRefractoryMutation (genetic algorithm)medicineCoagulopathyHumansMass ScreeningRisk factorDNA PrimersThrombosis Research
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Digestive vacuole of Plasmodium falciparum released during erythrocyte rupture dually activates complement and coagulation.

2012

Abstract Severe Plasmodium falciparum malaria evolves through the interplay among capillary sequestration of parasitized erythrocytes, deregulated inflammatory responses, and hemostasis dysfunction. After rupture, each parasitized erythrocyte releases not only infective merozoites, but also the digestive vacuole (DV), a membrane-bounded organelle containing the malaria pigment hemozoin. In the present study, we report that the intact organelle, but not isolated hemozoin, dually activates the alternative complement and the intrinsic clotting pathway. Procoagulant activity is destroyed by phospholipase C treatment, indicating a critical role of phospholipid head groups exposed at the DV surfa…

HemeproteinsMalePain ThresholdErythrocytesImmunologyComplement Pathway AlternativePlasmodium falciparumVacuoleBiochemistryHemolysisMonocytesMicrobiologyHypesthesiaRats Sprague-DawleyPhagocytosisparasitic diseasesAnimalsHumansMalaria FalciparumBlood CoagulationLungbiologyPhospholipase CHemozoinDextran SulfatePlasmodium falciparumCell BiologyHematologyIntracellular Membranesbiology.organism_classificationComplement systemRatsAntibody opsonizationImmunologyVacuolesAlternative complement pathwaySpleenWaste disposalBlood
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Reversal of rivaroxaban-induced alterations on hemostasis by different coagulation factor concentrates – in vitro studies with steady and circulating…

2015

BACKGROUND: Despite the good safety of rivaroxaban, there is limited information on strategies for urgent reversal of its antihemostatic effects.Methods and Results:Alterations of hemostasis induced by rivaroxaban (230 ng/ml) were assessed by using several tests applied to steady and circulating human blood. Effects on thrombin generation (TG) and thromboelastometry (TEM) parameters were measured. Modifications in platelet adhesive, aggregating and procoagulant activities were evaluated in studies with circulating blood. The potential reversal of prothrombin complex concentrates (PCCs; 50 IU/kg), activated PCCs (aPCCs; 75 IU/kg), or recombinant factor VIIa (rFVIIa; 270 μg/kg) was evaluated.…

HemostàsiaPharmacologyFibrinAssaigs clínics de medicamentsRivaroxabanMedicineHumansPlateletFactor VIIIaCoagulació sanguíniaRivaroxabanHemostasisFactor VIIIbiologybusiness.industryDrugsDrug testingGeneral MedicineBlood coagulationBlood Coagulation FactorsThromboelastometryCoagulationRecombinant factor VIIaHemostasisAnesthesiabiology.proteinCardiology and Cardiovascular MedicinebusinessPerfusionMedicamentsmedicine.drugCirculation journal : official journal of the Japanese Circulation Society
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Prothrombinase-Induced Clotting Time Assay for Determination of the Anticoagulant Effects of Unfractionated and Low-Molecular-Weight Heparins, Fondap…

2008

The prothrombinase-induced clotting time assay (PiCT, Pentapharm, Basel, Switzerland) is a clotting assay sensitive to factor Xa and factor IIa inhibitors. It is based on the addition of factor Xa and snake venom RVV-V (Russell viper venom factor V activator) specifically activating factor V and phospholipids to platelet-poor plasma. Following an incubation time, the mixture is recalcified and the clotting time is determined. An almost linear dose-response and high sensitivity of the assay for unfractionated heparin (UFH), low-molecular-weight heparins (LMWHs), r-hirudin, and argatroban was found. Fondaparinux showed a nonlinear dose-response. By using ex vivo samples, the following Pearson…

HeparinChemistryHirudinGeneral MedicineHeparin Low-Molecular-WeightPharmacologyFondaparinuxSensitivity and SpecificityFondaparinux SodiumArgatrobanThromboplastinThrombinFibrinolytic AgentsFondaparinuxBiochemistryClotting timePolysaccharidesProthrombinasemedicineHumansBlood Coagulation Testsmedicine.drugDiscovery and development of direct thrombin inhibitorsAmerican Journal of Clinical Pathology
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Pharmacokinetic properties of recombinant FVIIa in inherited FVII deficiency account for a large volume of distribution at steady state and a prolong…

2014

Pharmacokinetic properties of recombinant FVIIa in inherited FVII deficiency account for a large volume of distribution at steady state and a prolonged pharmacodynamic effect -

HeredityPharmacokinetic inherited Factor VII deficiencyFactor VII DeficiencySocio-culturaleFactor VIIaPharmacologySeverity of Illness IndexPharmacokineticsPredictive Value of Testshemic and lymphatic diseasesHumansMedicineGenetic Predisposition to DiseaseFVII deficiencyRegistriescardiovascular diseasesBlood CoagulationVolume of distributionbiologyCoagulantsbusiness.industryVascular biologyrFVIIaHematologyFactor VIIRecombinant ProteinsPhenotypeTreatment OutcomerFVIIa; FVII deficiency; pharmacokineticsRecombinant factor VIIaPharmacodynamicsbiology.proteinBlood Coagulation TestsSteady state (chemistry)Drug Monitoringbusinesspharmacokinetics
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Reversible graft versus host reaction as cause of erythrophagic splenomegaly in a child?

1977

The case history of a 9 months old infant with hepatosplenomegaly, pancytopnaenia and disturbances of clotting and cellular immune reactivity is reported. The spleen was removed and showed striking erythrophagocytosis by proliferating histiocytes, typical of "familial erythrophagocytic reticulosis" (Farquhar). A graft-versus-host reaction is discussed as a possible underlying cause. The favourable clinical course and full recovery point to an interrelation with primary hypersplenism.

Immunity CellularFamilial haemophagocytic reticulosisPathologymedicine.medical_specialtyPancytopeniabusiness.industryGraft versus host reactionHepatosplenomegalyInfantSpleenBlood Coagulation DisordersErythrophagocytosisGraft vs Host Reactionmedicine.anatomical_structureSplenomegalyPediatrics Perinatology and Child HealthImmunologymedicineHumansImmune reactivityFemalemedicine.symptombusinessHistiocyteHepatomegalyEuropean Journal of Pediatrics
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Crosstalk of the plasma contact system with bacteria.

2012

Activation of the plasma contact system triggers several cascade systems such as the kallikrein-kinin system, the intrinsic pathway of coagulation, the classical complement cascade and the fibrinolytic system. Recent studies have shown a critical role of the contact system for arterial and venous thrombus formation and thromboembolic disease. In contrast, the function of the contact system for host-defense reactions and its physiological functions have remained enigmatic. Experimental animal studies and clinical data have linked the contact system to bacterial infections with implications for sepsis disease. The present review summarizes the role of the contact system and its activation for…

Kallikrein-Kinin SystemVascular permeabilityBiologySepsisCapillary PermeabilitySepsismedicineAnimalsHumansComplement Pathway ClassicalThrombusBlood CoagulationFactor XIIFibrinInnate immune systemBacteriaFibrinolysisHematologyBacterial Infectionsmedicine.diseaseImmunity InnateComplement systemCrosstalk (biology)ImmunologySignal transductionSignal TransductionThrombosis research
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Biochemical biomarkers alterations in Coronavirus Disease 2019 (COVID-19)

2020

Abstract Coronavirus Disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a respiratory disease, which can evolve into multi-organ failure (MOF), leading to death. Several biochemical alterations have been described in COVID-19 patients. To date, many biomarkers reflecting the main pathophysiological characteristics of the disease have been identified and associated with the risk of developing severe disease. Lymphopenia represents the hallmark of the disease, and it can be detected since the early stage of infection. Increased levels of several inflammatory biomarkers, including c-reactive protein, have been found in COVID-19 patients and associ…

Kidney DiseaseClinical BiochemistryMyocardial InfarctionMedicine (miscellaneous)Disease030204 cardiovascular system & hematologySeverity of Illness Index0302 clinical medicineBiomarkers Coronavirus Infection030212 general & internal medicinebiochemical alterationAged 80 and overHealth PolicyLiver DiseasesMusclesLiver DiseaseRespiratory diseaseBlood Coagulation DisordersWater-Electrolyte BalancePathophysiologyC-Reactive ProteinDisease ProgressionCytokinesbiomarkerMuscleKidney DiseasesLiver dysfunctionCoronavirus InfectionsHumanCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Pneumonia Viralmacromolecular substances03 medical and health sciencesBetacoronavirusLymphopeniamedicineHumansCytokinePandemicsAgedInflammationBlood Coagulation DisorderBetacoronavirubusiness.industrySARS-CoV-2Biochemistry (medical)Public Health Environmental and Occupational HealthCOVID-19Biochemical biomarkersmedicine.diseaseImmunologyCytokine stormbusinesslaboratoryBiomarkers
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