Search results for "fibrinolysi"

showing 10 items of 97 documents

Hemostatic function in young subjects with central obesity: relationship with left ventricular function.

1995

This study was designed to evaluate coagulation and fibrinolysis activity and their relationship with left ventricular function in young obese subjects with central fat distribution. We assessed coagulation and fibrinolysis activity by evaluation of factor VII activity, fibrinogen and plasminogen, plasminogen activator inhibitor (PAI), and tissue plasminogen activator antigen basally (tPA1) and after venous occlusion (tPA2). These measures were evaluated in young (< 40 years) obese subjects with central fat distribution (n = 19) and in comparable lean subjects (n = 20). Blood glucose, triglycerides, total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A1 and apo B, fas…

AdultBlood GlucoseMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolismmedicine.medical_treatmentFibrinogenVentricular Function LeftSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundEndocrinologyWaist–hip ratioInternal medicineFibrinolysismedicineHumansInsulinObesityHemostatic functionBlood CoagulationApolipoproteins ATriglyceridesApolipoproteins BHemostasisbiologybusiness.industryCholesterolCholesterol HDLFibrinogenCentral obesity Hemostatic function left ventricular functionPlasminogenFactor VIISettore MED/11 - Malattie Dell'Apparato CardiovascolarePlasminogen InactivatorsEndocrinologychemistrybiology.proteinBody ConstitutionRegression AnalysisFemalebusinessPlasminogen activatormedicine.drugLipoproteinMetabolism: clinical and experimental
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ABNORMALLY HIGH THROMBOXANE BIOSYNTHESIS IN HOMOZYGOUS HOMOCYSTINURIA. EVIDENCE FOR PLATELET INVOLVEMENT AND PROBUCOL-SENSITIVE MECHANISM.

1993

Homocystinuria due to homozygous cystathionine beta-synthase deficiency is an inborn error of metabolism characterized by a high incidence of thrombosis and premature atherosclerosis. We evaluated TXA2 biosynthesis in vivo and several in vitro tests of platelet function in 11 homocystinuric patients and 12 healthy controls. In vitro, patients' platelet aggregation was within control values as were TXB2 formation, fibrinogen binding, and ATP secretion in response to thrombin. In contrast, the urinary excretion of 11-dehydro-TXB2, a major enzymatic derivative of TXA2, was > 2 SD of controls in all patients (1,724 +/- 828 pg/mg creatinine, mean +/- SD, in patients vs. 345 +/- 136 in controls, …

AdultBlood PlateletsMalemedicine.medical_specialtyAdolescentPlatelet AggregationThromboxaneProbucolHomocystinuriaInternal medicinemedicineHumansPlateletPlatelet activationChildBlood CoagulationbiologyAspirinChemistryFibrinolysisHomozygoteFibrinogen bindingThromboxanesGeneral Medicinemedicine.diseaseCystathionine beta synthaseEndocrinologyProbucolbiology.proteinlipids (amino acids peptides and proteins)FemaleHomocystinuriaCyclooxygenasemedicine.drugcirculatory and respiratory physiologyResearch Article
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Enzymatic modification of low-density lipoprotein in the arterial wall: a new role for plasmin and matrix metalloproteinases in atherogenesis.

2004

Objective— Functionally interactive proteases of the plasminogen/plasmin and the matrix metalloproteinase (MMP) system degrade and reorganize the extracellular matrix of the vessel wall in atherosclerosis. Here we investigated whether such proteases are able to confer atherogenic properties onto low density lipoprotein by nonoxidative modification. Methods and Results— Similar to the recently described enzymatically-modified low-density lipoprotein (E-LDL), native LDL exposed to plasmin or matrix MMP-2 or MMP-9 and cholesterylester-hydrolase (CEH) showed extensive deesterification, with ratios of free cholesterol to total cholesterol rising to 0.8 compared with 0.2 in native LDL. When the …

AdultLipoprotein modificationProteasesAdolescentPlasminArteriosclerosisBlotting WesternMatrix metalloproteinaseComplement Hemolytic Activity AssayMonocyteschemistry.chemical_compoundmedicineHumansTrypsinFibrinolysinComplement ActivationCells CulturedAgedbiologyMacrophagesAntibodies MonoclonalSodium Dodecyl SulfateLipoprotein(a)Middle AgedSterol EsteraseCell biologyLipoproteins LDLC-Reactive ProteinchemistryBiochemistryMatrix Metalloproteinase 9Low-density lipoproteinbiology.proteinMatrix Metalloproteinase 2lipids (amino acids peptides and proteins)Electrophoresis Polyacrylamide GelCardiology and Cardiovascular MedicinePlasminogen activatormedicine.drugLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Kallikrein–kinin system and fibrinolysis in hereditary angioedema due to factor XII gene mutation Thr309Lys

2009

In a subgroup of hereditary angioedema (HAE) patients with normal C1-esterase inhibitor levels, HAE is caused by a Thr309Lys mutation in the coagulation factor XII (F12) gene. The aim of this study was to examine elements of the kallikrein-kinin system ('contact system') and the downstream-linked coagulation, complement and fibrinolytic systems in the plasma of six patients with HAE caused by the Thr309Lys mutation and healthy probands. Blood samples were taken from participants during the symptom-free interval between attacks. Samples were analyzed for activity and concentrations of components of the kallikrein-kinin system and linked enzyme systems. The mean FXII clotting activity was 90%…

AdultMalemedicine.medical_specialtyAdolescentMutation MissenseKininsCoagulation Factor XIIFactor XIIaGene mutationYoung AdultInternal medicinemedicineHumansPoint MutationHereditary Angioedema Type IIIComplement Pathway ClassicalAgedAged 80 and overFactor XIIAngioedemaChemistryFibrinolysisDextran SulfateAngioedemas HereditaryPrekallikreinPrekallikreinBlood ProteinsHematologyGeneral MedicineMiddle AgedSilicon Dioxidemedicine.diseaseEnzyme ActivationEndocrinologyAmino Acid SubstitutionChromogenic CompoundsCoagulationTissue Plasminogen ActivatorHereditary angioedemaImmunologyFemaleKallikreinsmedicine.symptomcirculatory and respiratory physiologyBlood Coagulation &amp; Fibrinolysis
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Increased plasminogen activator inhibitor antigen levels in diabetic patients with stable angina

1991

PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. Ten healthy men of equivalent age served as controls. Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. TAT levels were increased in CAD, and sign…

AdultMalemedicine.medical_specialtyAntithrombin IIICoronary DiseaseStable anginaAngina PectorisFibrin Fibrinogen Degradation ProductsCoronary artery diseaseThrombinAntigenDiabetes mellitusInternal medicinemedicineHumanscardiovascular diseasesAgedbusiness.industryFibrinolysisPlasminogen activator inhibitor antigenAntithrombinFibrinogenHematologyGeneral MedicineMiddle Agedmedicine.diseaseObesityPlasminogen InactivatorsEndocrinologyDiabetes Mellitus Type 2Tissue Plasminogen ActivatorExercise TestbusinessPeptide Hydrolasesmedicine.drugBlood Coagulation &amp; Fibrinolysis
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Fibrinolysis in hypertriglyceridaemic subjects in response to venous occlusion.

1993

We have measured various fibrinolytic and coagulation parameters (t-PA antigen, PAI, fibrinogen, plasminogen and factor VII) before and after 10 min of venous occlusion in 20 hypertryglyceridaemic subjects (twelve males and eight females, age 38 +/- 4 years, body mass index 23 +/- 1.5) and 20 healthy normal subjects, matched for sex (twelve males and eight females), age (37 +/- 3.5 years) and body mass index (22.8 +/- 1.4). At rest, t-PA:Ag, PAI, fibrinogen, plasminogen and factor VII were significantly (P < 0.005) higher in hypertriglyceridaemic subjects than in normal controls. After venous occlusion, the increase in all parameters except t-PA:Ag was more marked in the patient group than …

AdultMalemedicine.medical_specialtyPathologymedicine.medical_treatmentFibrinogenHyperlipoproteinemia Type IVVeinschemistry.chemical_compoundAntigenInternal medicineOcclusionFibrinolysisPlasminogen Activator Inhibitor 1medicineHumansFactor VIIbusiness.industryFibrinolysisHypertriglyceridemiaFibrinogenPlasminogenHematologyGeneral MedicineFactor VIIMiddle Agedmedicine.diseaseConstrictionLipidsEndocrinologyApolipoproteinsCoagulationchemistryTissue Plasminogen ActivatorFemalebusinessBody mass indexmedicine.drugBlood coagulationfibrinolysis : an international journal in haemostasis and thrombosis
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Postoperative Reduction of Fibrinolysis as a Prognostic Factor of Fatal Outcome

2001

For the resection of an esophagus carcinoma a mortality rate of 2 to 30% was described, It is still unclear whether an abdominothoracic or transhiatal intervention is superior regarding the outcome. To investigate the prognostic value of fibrinolytic markers, plasmin-α2-antiplasmin (PAP) and D-dimer (DD) values were determined daily in the early postoperative period for 11days. In addition, the course of PAP and DD concentrations was compared with the method of esophagectomy. Of the 28 patients enclosed in the study, 5 died between day 10 and day 34 owing to adult respiratory distress syndrome and septicemia. The PAP and DD concentrations increased in survivors after surgery until day 5 an…

AdultMalemedicine.medical_specialtyTime FactorsFatal outcomeEsophageal Neoplasmsmedicine.medical_treatmentReference range030204 cardiovascular system & hematologySensitivity and SpecificityGastroenterologyFibrin Fibrinogen Degradation Products03 medical and health sciences0302 clinical medicineInternal medicineFibrinolysisD-dimermedicineHumansFibrinolysinPostoperative PeriodSurvival rateAgedalpha-2-AntiplasminRespiratory distressbusiness.industryFibrinolysisMortality rateHematologyGeneral MedicineMiddle AgedPrognosisAntifibrinolytic AgentsSurgeryEsophagectomySurvival RateROC CurveEsophagectomyFemalebusinessBiomarkers030215 immunologyClinical and Applied Thrombosis/Hemostasis
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The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events.

1999

Abstract OBJECTIVES The impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events. BACKGROUND An embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined. METHODS The relationship among the occurrence of major embolic events, echocardiographic vegetation size, endothelial cell activation, thrombin generation, fibrinolysis and APA was examined in 91 patie…

AdultMalemedicine.medical_specialtymedicine.medical_treatmentEnzyme-Linked Immunosorbent AssayGastroenterologyVon Willebrand factorRisk FactorsInternal medicinemental disordersFibrinolysisPlasminogen Activator Inhibitor 1medicineEndocarditisHumansRisk factorAgedRetrospective Studiesbiologybusiness.industryVascular diseaseFibrinolysisThrombinUltrasonography DopplerEndocarditis BacterialIntracranial Embolism and ThrombosisMiddle Agedmedicine.diseasePrognosisHeart ValvesCerebral AngiographyInfective endocarditisImmunologybiology.proteinAntibodies AntiphospholipidFemaleCardiology and Cardiovascular MedicineComplicationbusinessTomography X-Ray Computedpsychological phenomena and processesProtein CBiomarkersEchocardiography Transesophagealmedicine.drugFollow-Up StudiesProtein CJournal of the American College of Cardiology
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Pharmacological thrombolysis: one more weapon for free-flap salvage.

2005

Despite the high success rate of free-tissue transfer, thrombosis still complicates 5-30% of cases. Meticoulous technique, careful vessel selection, and pharmacological prophylaxis are not always enough to avoid thrombosis. Early diagnosis and reintervention provide the only way to salvage a thrombosed free flap, in case of either arterial or venous thrombosis. When kinking, torsion, or external compression of the pedicle are ruled out, and thrombectomy and redo of the anastomosis are unsuccessful, the last resort to save the flap is thrombolytic therapy. The authors present their experience with the salvage of two otherwise lost flaps by means of urokinase thrombolysis through direct intra…

AdultMalemedicine.medical_specialtymedicine.medical_treatmentFree flapAnastomosisTHERAPYSurgical FlapsMICROVASCULAR SURGERYFibrinolysismedicineMANAGEMENTHumansThrombolytic TherapyVeinUrokinaseAged 80 and overVenous Thrombosisbusiness.industrySTREPTOKINASE SALVAGEGraft SurvivalThrombolysisTHROMBECTOMYmedicine.diseaseThrombosisUrokinase-Type Plasminogen ActivatorSurgeryVenous thrombosismedicine.anatomical_structureSurgerybusinessmedicine.drugMicrosurgery
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In vitro Analysis of Synergistic Effects of Fibrinolytic Agents and Prostacyclin Analogues

1997

We investigated the in vitro thrombolytic effects of streptoki-nase, urokinase, alteplase and saruplase, alone or in combination, with the prostacyclin analogues, iloprost and taprostene. Human platelet-rich plasma was stimulated with collagen (1 μg/ml) to generate thrombi containing platelets and fibrin. Following treatment with fibrinolytic agents, lysis was allowed to proceed for 30 min and was then terminated with aprotinin (2,000 ClU/ml). To evaluate the combinatory effects of fibrinolytic agents and prostacyclin analogues, we used concentrations of fibrinolytic agents which reduced thrombi weight by less than 50%. Neither iloprost nor taprostene alone demonstrated any thrombolytic eff…

AdultMalemedicine.medical_treatmentProstacyclinPharmacologyFibrinolytic AgentsPhysiology (medical)Prostaglandins SyntheticFibrinolysismedicineHumansStreptokinaseIloprostUrokinaseChemistryFibrinolysisDrug SynergismHematologyDrug interactionEpoprostenolUrokinase-Type Plasminogen ActivatorIn vitroTissue Plasminogen Activatorcardiovascular systemFemaleSaruplaseFibrinolytic agentIloprostmedicine.drugPathophysiology of Haemostasis and Thrombosis
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