Search results for "Fibrin"

showing 10 items of 508 documents

Positive effect of platelet rich fibrin on osseointegration

2016

Background Leukocyte-platelet rich fibrin (L-PRF) is a second generation platelet concentrate clinically used to accelerate tissue healing and bone regeneration. Achieving reduced implant osseointegration time could provide immediate or early loading of implants. The aim of this study was to evaluate the L-PRF-induced osseointegration and bone-implant contact (BIC) in an experimental animal model. Material and Methods Twelve 4-month-old New Zealand white rabbits were used. Following general anesthesia, 3-5 mL of blood was obtained from the central artery in rabbit ear and L-PRF was prepared. Two implant cavities (5 mm long and 3 mm in diameter) were created in each tibia with a total of fou…

0106 biological sciencesBone RegenerationDentistry01 natural sciencesOsseointegrationFibrin03 medical and health sciences0302 clinical medicineOsseointegrationPlatelet-Rich Fibrin010608 biotechnologyEarly loadingAnimalsMedicinePlatelet concentrateBone regenerationMatrix for growth factorsGeneral DentistryDental ImplantsFibrinbiologybusiness.industryResearch030206 dentistry:CIENCIAS MÉDICAS [UNESCO]digestive system diseasesPlatelet-rich fibrinExperimental animalOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASbiology.proteinSurgeryRabbitsImplantOral SurgerybusinessPlatelet rich fibrinMedicina Oral Patología Oral y Cirugia Bucal
researchProduct

Incidence of Stent Thrombosis after Endovascular Treatment of Iliofemoral or Caval Veins in Patients with the Postthrombotic Syndrome.

2019

Abstract Background Patients with postthrombotic syndrome (PTS) treated with stents are at risk of stent thrombosis (ST). The incidence of ST in the presence and absence of anticoagulation therapy (AT) is unknown. Risk factors are not well understood. Patients and Methods From the prospective Swiss Venous Stent registry, we conducted a subgroup analysis of 136 consecutive patients with PTS. Incidence of ST was estimated from duplex ultrasound or venography, and reported for the time on and off AT. Baseline, procedural, and follow-up data were evaluated to identify factors associated with ST. Results Median follow-up was 20 (interquartile range [IQR] 9–40) months. AT was stopped in 43 (32%) …

0301 basic medicineAdultMalemedicine.medical_specialty2720 HematologyVenographySubgroup analysis610 Medicine & healthVena Cava Inferior030204 cardiovascular system & hematologyIliac VeinPostthrombotic Syndrome03 medical and health sciences0302 clinical medicineFibrinolytic AgentsInterquartile rangeRisk FactorsmedicineAlloysHumansCumulative incidenceRegistries610 Medicine & healthStrokemedicine.diagnostic_testbusiness.industryIncidence (epidemiology)10031 Clinic for AngiologyIncidenceHazard ratioEndovascular ProceduresAnticoagulantsThrombosisHematologyPhlebographyFemoral VeinMiddle Agedmedicine.diseaseConfidence intervalSurgery030104 developmental biologyTreatment OutcomeFemaleStentsbusinessSwitzerlandFollow-Up StudiesThrombosis and haemostasis
researchProduct

Numerous Fasciola plasminogen-binding proteins may underlie blood-brain barrier leakage and explain neurological disorder complexity and heterogeneit…

2019

15 páginas, 5 figuras y 1 tabla

0301 basic medicineAntifibrinolyticContact systemmedicine.drug_classmedicine.medical_treatment030231 tropical medicineBradykininInflammationNeurological disorderFibrinolysis systemProteomic and mass spectrometry analysesBlood–brain barrierFasciola excretome/secretomeProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlood-brain barrier leakageFibrinolysismedicineIndicators and preventionAcute and chronic phasesPlasminogen-binding proteinsFasciolabiologyHuman fascioliasis030108 mycology & parasitologymedicine.diseasebiology.organism_classificationInfectious Diseasesmedicine.anatomical_structurechemistryImmunologyAnimal Science and ZoologyParasitologymedicine.symptomNeurological disordersResearch Article
researchProduct

CD36-fibrin interaction propagates FXI-dependent thrombin generation of human platelets.

2019

Thrombin converts fibrinogen to fibrin and activates blood and vascular cells in thrombo-inflammatory diseases. Platelets are amplifiers of thrombin formation when activated by leukocyte- and vascular cell-derived thrombin. CD36 on platelets acts as sensitizer for molecules with damage-associated molecular patterns, thereby increasing platelet reactivity. Here, we investigated the role of CD36 in thrombin-generation on human platelets, including selected patients with advanced chronic kidney disease (CKD). Platelets deficient in CD36 or blocked by anti-CD36 antibody FA6.152 showed impaired thrombin generation triggered by thrombin in calibrated automated thrombography. Using platelets with …

0301 basic medicineBlood PlateletsCD36 AntigensCD36InflammationFibrinogenBiochemistryFibrin03 medical and health sciences0302 clinical medicineThrombinBlocking antibodyGeneticsmedicineHumansPlateletRenal Insufficiency ChronicMolecular BiologyFactor XIFibrinbiologyChemistryCell adhesion moleculeThrombinPlatelet ActivationBlood Coagulation FactorsCell biology030104 developmental biologybiology.proteinmedicine.symptom030217 neurology & neurosurgerycirculatory and respiratory physiologyBiotechnologymedicine.drugFASEB journal : official publication of the Federation of American Societies for Experimental BiologyREFERENCES
researchProduct

Impaired Platelet Function in Sept8-Deficient Mice In Vitro.

2020

AbstractSeptins (Septs) are a widely expressed protein family of 13 mammalian members, recognized as a unique component of the cytoskeleton. In human platelets, we previously described that SEPT4 and SEPT8 are localized surrounding α-granules and move to the platelet surface after activation, indicating a possible role in platelet physiology. In this study, we investigated the impact of Sept8 on platelet function in vitro using Sept8-deficient mouse platelets. Deletion of Sept8 in mouse platelets caused a pronounced defect in activation of the fibrinogen receptor integrin αIIbβ3, α-granule exocytosis, and aggregation, especially in response to the glycoprotein VI agonist convulxin. In contr…

0301 basic medicineBlood PlateletsGenotypePlatelet AggregationFibrinogen receptorIntegrinPlatelet Glycoprotein GPIIb-IIIa Complex030204 cardiovascular system & hematologyFibrinogenCytoplasmic GranulesExocytosisExocytosis03 medical and health sciences0302 clinical medicineLysosomeCrotalid VenomsmedicineAnimalsPlateletLectins C-TypeLactadherinMice KnockoutbiologyChemistryThrombinFibrinogenConvulxinHematologyPlatelet ActivationCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypebiology.proteinFemaleLysosomesSeptinsmedicine.drugThrombosis and haemostasis
researchProduct

Transcriptome-based repurposing of apigenin as a potential anti-fibrotic agent targeting hepatic stellate cells

2017

AbstractWe have used a computational approach to identify anti-fibrotic therapies by querying a transcriptome. A transcriptome signature of activated hepatic stellate cells (HSCs), the primary collagen-secreting cell in liver, and queried against a transcriptomic database that quantifies changes in gene expression in response to 1,309 FDA-approved drugs and bioactives (CMap). The flavonoid apigenin was among 9 top-ranked compounds predicted to have anti-fibrotic activity; indeed, apigenin dose-dependently reduced collagen I in the human HSC line, TWNT-4. To identify proteins mediating apigenin’s effect, we next overlapped a 122-gene signature unique to HSCs with a list of 160 genes encoding…

0301 basic medicineCirrhosisCellPharmacologyBiologyArticleCell LineTranscriptome03 medical and health scienceschemistry.chemical_compoundMiceDrug DiscoverymedicineHepatic Stellate CellsAnimalsHumansApigeninMultidisciplinaryDrug Repositioningmedicine.diseaseHepatic stellate cell activationAntifibrinolytic Agents3. Good health030104 developmental biologymedicine.anatomical_structurechemistryCell cultureApigeninHepatic stellate cellHepatic fibrosisTranscriptomeBiomarkersScientific Reports
researchProduct

Distinct contributions of complement factors to platelet activation and fibrin formation in venous thrombus development

2017

Expanding evidence indicates multiple interactions between the hemostatic system and innate immunity, and the coagulation and complement cascades. Here we show in a tissue factor (TF)-dependent model of flow restriction-induced venous thrombosis that complement factors make distinct contributions to platelet activation and fibrin deposition. Complement factor 3 (C3) deficiency causes prolonged bleeding, reduced thrombus incidence, thrombus size, fibrin and platelet deposition in the ligated inferior vena cava, and diminished platelet activation in vitro. Initial fibrin deposition at the vessel wall over 6 hours in this model was dependent on protein disulfide isomerase (PDI) and TF expressi…

0301 basic medicineComplement component 5biologyChemistryImmunologyCell BiologyHematologyComplement factor I030204 cardiovascular system & hematologymedicine.diseaseBiochemistryFibrinCell biologyComplement system03 medical and health sciences030104 developmental biology0302 clinical medicineCoagulationImmunologymedicinebiology.proteinPlateletPlatelet activationThrombusBlood
researchProduct

GAS6

2017

Venous thrombosis is determined by the recruitment of monocytes and neutrophils to the inflamed endothelium and is primarily influenced by the plasmatic coagulation system.1 Monocyte tissue factor (TF) was identified as the causative trigger for intraluminal fibrin formation and thrombus load in the inferior vena cava (IVC) stenosis model, resembling human deep vein thrombosis.1 Although monocyte TF is prothrombotic, the TF expressed by activated endothelial cells triggers proinflammatory protease-activated receptor signaling pathways.2,3 See accompanying article on page 1315 In the past years, GAS6 (growth arrest–specific gene-6) was described as a major regulatory protein of prothrombotic…

0301 basic medicineEndotheliumVena Cava Inferior030204 cardiovascular system & hematologyFibrinogenInferior vena cavaMonocytes03 medical and health sciencesTissue factor0302 clinical medicinemedicineHumansPlateletThrombusVenous ThrombosisGAS6business.industryImpaired platelet aggregationmedicine.disease030104 developmental biologymedicine.anatomical_structuremedicine.veinAnesthesiaCancer researchCardiology and Cardiovascular MedicinebusinessGasolinemedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct

Monitoring of rheologic variables during postoperative high-dose brachytherapy for uterine cancer.

2004

Oxygenation of tumor tissue has recently been assed an important prerequisite for the effectiveness of radiotherapy in cervical cancer. Hyperviscosity is a common phenomenon in malignancy and a cause of reduced oxygen transport capacity that would favour tissue hypoxia. Hemorheological variables were serially tested preoperatively, during four cycles of fractionated adjuvant IR192 HDR after loading radiation (HDR-AL) of the vaginal vault (weekly intervals), and 6 months postoperatively in patients with cervical (n=12) and endometrial cancer (n=26). Women who were scheduled for benign tumor surgery served as controls (n=29). Preoperatively, in cervical and endometrial cancer patients, mean …

0301 basic medicineErythrocyte Aggregationmedicine.medical_specialtymedicine.medical_treatmentBrachytherapyBrachytherapyUrologyUterine Cervical Neoplasms030204 cardiovascular system & hematologyHysterectomy03 medical and health sciencesLeukocyte Count0302 clinical medicineUterine cancermedicineHumansAgedCervical cancerbusiness.industryPlatelet CountEndometrial cancerOxygen transportFibrinogenHematologyGeneral MedicineMiddle Agedmedicine.diseaseBlood ViscosityCombined Modality TherapyCell HypoxiaSurgeryEndometrial NeoplasmsRadiation therapy030104 developmental biologyHemorheologyVaginal vaultFemaleRadiotherapy AdjuvantbusinessBiomarkersClinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
researchProduct

Annexin A2-Mediated Plasminogen Activation in Endothelial Cells Contributes to the Proangiogenic Effect of Adenosine A2A Receptors

2021

Adenosine A2A receptor mediates the promotion of wound healing and revascularization of injured tissue, in healthy and animals with impaired wound healing, through a mechanism depending upon tissue plasminogen activator (tPA), a component of the fibrinolytic system. In order to evaluate the contribution of plasmin generation in the proangiogenic effect of adenosine A2A receptor activation, we determined the expression and secretion of t-PA, urokinase plasminogen activator (uPA), plasminogen activator inhibitor-1 (PAI-1) and annexin A2 by human dermal microvascular endothelial cells stimulated by the selective agonist CGS-21680. The plasmin generation was assayed through an enzymatic assay a…

0301 basic medicineFarmacologiaAngiogenesisPlasminmedicine.medical_treatmentVasodilatadorsAdenosine A2A receptorRM1-950030204 cardiovascular system & hematologyTissue plasminogen activatormicrovascular endothelial cells03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFibrinolysismedicinePharmacology (medical)urokinase plasminogen activatorPharmacologytissue plasminogen activatorChemistryBrief Research Reportannexin A2adenosine receptorsCell biology030104 developmental biologyPlasminogen activator inhibitor-1plasminogen activator inhibitor-1Therapeutics. PharmacologyPlasminogen activatorProteïnesAnnexin A2medicine.drug
researchProduct