Search results for "Factor X"

showing 10 items of 80 documents

Is it necessary to alter anticoagulation therapy for tooth extraction in patients taking direct oral anticoagulants?

2017

Background The number of patients using direct oral anticoagulants (DOACs) instead of vitamin K antagonists (VKA) is increasing and there is limited data on the safety of tooth extractions in patients taking DOACs. The aim of this study was to compare the amount of bleeding (AOB) and postoperative complications after tooth extractions between patients taking VKAs and patients taking DOACs without altering the anticoaguation therapy. Material and Methods The study consisted of four groups: Direct thrombin inhibitor group, factor Xa inhibitor group, warfarin group and a control group. A single tooth was extracted in each patient and routine coagulation test values were recorded prior to extra…

AdultMalemedicine.medical_specialtyVitamin Kmedicine.drug_mechanism_of_actionFactor Xa InhibitorAdministration OralPostoperative Hemorrhage030204 cardiovascular system & hematologyDirect oral anticoagulants03 medical and health sciencesPostoperative Complications0302 clinical medicineRivaroxabanChi-square testmedicineHumansApixabanProspective StudiesProspective cohort studyGeneral DentistryAgedAged 80 and overbusiness.industryResearchWarfarinAnticoagulants030206 dentistryMiddle Aged:CIENCIAS MÉDICAS [UNESCO]DabigatranSurgeryRegimenOtorhinolaryngologyCoagulationDirect thrombin inhibitorUNESCO::CIENCIAS MÉDICASTooth ExtractionFemaleSurgeryAnalysis of varianceOral Surgerybusinessmedicine.drugMedicina Oral Patología Oral y Cirugia Bucal
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Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy.

2009

Background Hereditary angioedema caused by mutations in the factor XII gene is a recently described disease entity that occurs mainly in women. It differs from hereditary angioedema caused by C1 inhibitor deficiency. Objective To assess the clinical symptoms, factors triggering acute attacks, and treatments of this disease. Methods Thirty-five female patients with hereditary angioedema and the factor XII mutations p.Thr309Lys and p.Thr309Arg who came from 13 unrelated families were studied. The observation period was 8.4 years on average (range, 2-26 years). Results Patients had on average 12.7 ± 7.9 angioedema attacks per year. Recurrent facial swellings occurred in all patients; skin swel…

Adultmedicine.medical_specialtyAbdominal painAdolescentmedicine.medical_treatmentImmunologyMutation MissenseSeverity of Illness IndexC1-inhibitorYoung AdultRisk FactorsSurveys and QuestionnairesImmunology and AllergyMedicineHumansHereditary Angioedema Type IIIAge of OnsetChildProgesteroneDanazolPregnancyAngioedemabiologybusiness.industryDanazolAngioedemas HereditaryHormone replacement therapy (menopause)Middle Agedmedicine.diseaseDermatologySurgeryPedigreeTranexamic AcidHereditary angioedemaFactor XIIbiology.proteinFemalemedicine.symptombusinessmedicine.drugThe Journal of allergy and clinical immunology
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VITAMIN K-INDUCED MODIFICATION OF COAGULATION PHENOTYPE IN VKORC1 HOMOZYGOUS DEFICIENCY

2008

Summary.  Background: Combined vitamin K-dependent clotting factor (VKCF) deficiency type 2 (VKCFD2) is a rare bleeding disorder caused by mutated vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC1) gene. Methods and results: An Italian patient with moderate to severe bleeding tendency was genotyped, and found to be homozygous for the unique VKORC1 mutation (Arg98Trp) so far detected in VKCFD2. The activity levels of VKCFs were differentially reduced, and inversely related to the previously estimated affinity of procoagulant factor propeptides for the γ-carboxylase. The normal (factor IX) or reduced antigen levels (other VKCFs) produced a gradient in specific activities. Vitamin K su…

Adultmedicine.medical_specialtycoagulation factor levelsVitamin KProtein SMixed Function OxygenasesTissue factorchemistry.chemical_compoundInternal medicineVitamin K Epoxide ReductasesmedicineVKCFD2HumansFactor IXClotting factorCoagulation factor levels; Thrombin generation; Vitamin K supplementation; VKCFD2; VKORC1 mutation;biologyFactor VIIChemistryFactor XHomozygotevitamin K supplementationHematologyBlood Coagulation DisordersEndocrinologyTreatment OutcomeCoagulationthrombin generationImmunologyMutationbiology.proteinFemaleBlood Coagulation TestsVKCFD2 VKORC1 mutation coagulation factor levels thrombin generation vitamin K supplementationProtein Cmedicine.drugHalf-LifeVKORC1 mutation
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Coagulation signaling and cancer immunotherapy.

2019

The last decades have delineated many interactions of the hemostatic system with cancer cells that are pivotal for cancer-associated thrombosis, angiogenesis and metastasis. Expanding evidence shows that platelets, the tissue factor pathway, and proteolytic signaling involving protease-activated receptors (PARs) are also central players in innate and adaptive immunity. Recent studies in immune-competent mice have uncovered new immune-evasive roles of coagulation signaling networks in the development and growth of different preclinical tumor models. Tumor-type specific PAR1 signaling facilitates the escape from immune surveillance by cytotoxic T cells. In addition, tumor-associated macrophag…

Angiogenesismedicine.medical_treatmentReceptors Proteinase-ActivatedMacrophage polarization030204 cardiovascular system & hematology03 medical and health sciencesMice0302 clinical medicineCancer immunotherapyNeoplasmsmedicineAnimalsBlood CoagulationTumor microenvironmentInnate immune systembusiness.industryHematologyAcquired immune systemTumor antigen030220 oncology & carcinogenesisFactor XaCancer researchImmunotherapySignal transductionbusinessSignal TransductionThrombosis research
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Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial hypertension

2017

Multicellular interactions of platelets, leukocytes, and the blood vessel wall support coagulation and precipitate arterial and venous thrombosis. High levels of angiotensin II cause arterial hypertension by a complex vascular inflammatory pathway that requires leukocyte recruitment and reactive oxygen species production and is followed by vascular dysfunction. We delineate a previously undescribed, proinflammatory coagulation-vascular circuit that is a major regulator of vascular tone, blood pressure, and endothelial function. In mice with angiotensin II-induced hypertension, tissue factor was up-regulated, as was thrombin-dependent endothelial cell vascular cellular adhesion molecule 1 ex…

Blood PlateletsMale0301 basic medicinemedicine.medical_specialtyMacrophage-1 AntigenVascular Cell Adhesion Molecule-1Blood Pressure030204 cardiovascular system & hematologyThromboplastinMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinInternal medicinemedicineAnimalsHumansPlateletRats WistarEndothelial dysfunctionBlood CoagulationFactor XIAgedMice Knockoutbusiness.industryAngiotensin IIThrombinGeneral MedicineMiddle AgedOligonucleotides Antisensemedicine.diseaseAngiotensin IIMice Inbred C57BL030104 developmental biologyEndocrinologyBlood pressuremedicine.anatomical_structurePlatelet Glycoprotein GPIb-IX ComplexPathophysiology of hypertensionHypertensionFemalebusinessmedicine.drugBlood vesselScience Translational Medicine
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Targeting positive regulatory domain I-binding factor 1 and X box-binding protein 1 transcription factors by multiple myeloma-reactive CTL.

2005

Abstract Growing evidence indicates that multiple myeloma (MM) and other malignancies are susceptible to CTL-based immune interventions. We studied whether transcription factors inherently involved in the terminal differentiation of mature B lymphocytes into malignant and nonmalignant plasma cells provide MM-associated CTL epitopes. HLA-A*0201 (A2.1) transgenic mice were used to identify A2.1-presented peptide Ag derived from the plasma cell-associated transcriptional regulators, positive regulatory domain I-binding factor 1 (PRDI-BF1) and X box-binding protein 1 (XBP-1). A2.1-restricted CTL specific for PRDI-BF1 and XBP-1 epitopes efficiently killed a variety of MM targets. PRDI-BF1- and X…

Cytotoxicity ImmunologicX-Box Binding Protein 1Cellular differentiationImmunologyEpitopes T-LymphocyteMice TransgenicRegulatory Factor X Transcription FactorsBiologyEpitopeMiceImmune systemCell Line TumorHLA-A2 AntigenImmunology and AllergyAnimalsHumansTranscription factorAntigen PresentationB-LymphocytesCell DeathT-cell receptorCell DifferentiationCytotoxicity Tests ImmunologicX-Box Binding Protein 1Molecular biologyPeptide FragmentsCell biologyDNA-Binding ProteinsMice Inbred C57BLRepressor ProteinsCTL*Self ToleranceNIH 3T3 CellsPositive Regulatory Domain I-Binding Factor 1Multiple MyelomaCD8T-Lymphocytes CytotoxicTranscription FactorsJournal of immunology (Baltimore, Md. : 1950)
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Assembly of human contact phase proteins and release of bradykinin at the surface of curli-expressing Escherichia coli.

1996

Previous work has demonstrated that most strains of the human pathogen Streptococcus pyogenes bind kininogens through M protein, a fibrous surface protein and virulence determinant. Here we find that strains of several other pathogenic bacterial species, both Gram-positive and Gram-negative, isolated from patients with sepsis, also bind kininogens, especially kininogen (HK). The most pronounced interaction was seen between HK and Escherichia coli. Among clinical isolates of E. coli, the majority of the enterohaemorrhagic, enterotoxigenic, and sepsis strains, but none of the enteroinvasive and enteropathogenic strains, bound HK. Binding of HK to E. coli correlated with the expression of curl…

Factor XIIKininogenGram-Negative Facultatively Anaerobic RodsStaphylococcus aureusKininogensPrekallikreinVirulenceProteinsKallikreinBiologybiology.organism_classificationmedicine.disease_causeBradykininMicrobiologyMicrobiologyStreptococcus pneumoniaeStreptococcus pyogenesmedicineEscherichia coliHumansMolecular BiologyEscherichia coliBacteriacirculatory and respiratory physiologyMolecular microbiology
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Characterization of a partial exon 9/intron 9 deletion in the coagulation factor XII gene (F12) detected in two Turkish families with hereditary angi…

2014

Geneticsbiologybusiness.industrySequence analysisIntronHematologyGeneral MedicineCoagulation Factor XIImedicine.diseasePhenotypeMolecular biologyC1-inhibitorExonHereditary angioedemabiology.proteinMedicinebusinessGeneGenetics (clinical)Haemophilia
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CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models

2021

BACKGROUND: CD248 is a pro-inflammatory, transmembrane glycoprotein expressed by vascular smooth muscle cells (VSMC), monocytes/macrophages, and other cells of mesenchymal origin. Its distribution and properties are reminiscent of those of the initiator of coagulation, tissue factor (TF). OBJECTIVE: We examined whether CD248 also participates in thrombosis. METHODS: We evaluated the role of CD248 in coagulation using mouse models of vascular injury, and by assessing its functional interaction with the TF-factor VIIa (FVIIa)-factor X (FX) complex. RESULTS: The time to ferric chloride-induced occlusion of the carotid artery in CD248 knockout (KO) mice was significantly longer than in wild-typ…

InflammationFactor VIIa030204 cardiovascular system & hematologyInferior vena cavaArticleThromboplastin03 medical and health sciencesTissue factorchemistry.chemical_compoundMice0302 clinical medicineThrombinTissue factor pathway inhibitorAntigens CDAntigens NeoplasmmedicineAnimalsHumansMice KnockoutVenous Thrombosismedicine.diagnostic_testFactor XHematologyCoagulationchemistrymedicine.veinCancer researchProthrombin Timemedicine.symptommedicine.drugPartial thromboplastin time
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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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