Search results for "Kinin"

showing 10 items of 194 documents

Measurement of Bradykinin Formation and Degradation in Blood Plasma: Relevance for Acquired Angioedema Associated With Angiotensin Converting Enzyme …

2020

Bradykinin (BK)-mediated angioedema (AE) states are rare acquired or hereditary conditions involving localized edema of the subcutaneous and submucosal tissues. Citrated plasma from healthy volunteers or patients with hereditary angioedema (HAE) with normal level of C1-inhibitor (C1-INH) was used to investigate pathways of BK formation and breakdown relevant to AE physiopathology. The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements). The BK half-life was similarly increased ~5-fold following 2 daily oral doses of enalapril malea…

0301 basic medicinemedicine.medical_specialtykallikreinsPlasminBradykininTissue plasminogen activator03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineB2 receptorsOriginal ResearchplasminFactor XIIlcsh:R5-920tissue plasminogen activatorAngioedemabiologyhereditary angioedema with normal C1 inhibitor levelAngiotensin-converting enzymeGeneral MedicineKallikreinmedicine.disease030104 developmental biologyEndocrinology030228 respiratory systemchemistryHereditary angioedemabiology.proteinMedicinemedicine.symptombradykininlcsh:Medicine (General)medicine.drugFrontiers in Medicine
researchProduct

Deficiency of plasminogen activator inhibitor 2 in plasma of patients with hereditary angioedema with normal C1 inhibitor levels

2016

Background Hereditary angioedema with normal C1 inhibitor levels (HAE-N) is associated with a Factor XII mutation in 30% of subjects; however, the role of this mutation in the pathogenesis of angioedema is unclear. Objective We sought evidence of abnormalities in the pathways of bradykinin formation and bradykinin degradation in the plasma of patients with HAE-N both with and without the mutation. Methods Bradykinin was added to plasma, and its rate of degradation was measured by using ELISA. Plasma autoactivation was assessed by using a chromogenic assay of kallikrein formation. Plasminogen activator inhibitors (PAIs) 1 and 2 were also measured by means of ELISA. Results PAI-1 levels varie…

0301 basic medicinemedicine.medical_specialtymedicine.medical_treatmentImmunologyBradykinin030204 cardiovascular system & hematologyArticleC1-inhibitor03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineFibrinolysismedicineImmunology and AllergyFactor XIIAngioedemabiologybusiness.industryKallikreinmedicine.disease030104 developmental biologyEndocrinologychemistryPlasminogen activator inhibitor-1Hereditary angioedemabiology.proteinmedicine.symptombusinessJournal of Allergy and Clinical Immunology
researchProduct

Development of a Peptide-Based Sandwich Elisa for Human Tissue Prokallikrein with No Cross-Reactivity from Mature Kallikrein

2000

Human tissue prokallikrein is the enzymatically inactive zymogen of a serine proteinase involved in the liberation of vasoactive kinin peptides, and it is supposed that an impaired prokallikrein-to-kallikrein conversion is closely related to certain hypertensive and inflammatory disorders. Progress in understanding the biological role of the proenzyme has been limited by the absence of an accurate assay for the kallikrein precursor. We describe a sandwich enzyme-linked immunosorbent assay to measure human tissue prokallikrein using monospecific anti-peptide antibodies raised against propeptide derivatives. This method could detect a minimum concentration of 60 pg/ml prokallikrein and displa…

AdultImmunologyTissue kallikreinEnzyme-Linked Immunosorbent AssayPeptideCross Reactionsmedicine.disease_causeSensitivity and SpecificityCross-reactivityZymogenmedicineHumansProtein precursorPharmacologychemistry.chemical_classificationEnzyme Precursorsmedicine.diagnostic_testChemistryReproducibility of ResultsKallikreinKininMolecular biologyPeptide FragmentsBiochemistryImmunoassayKallikreinsJournal of Immunoassay
researchProduct

Parallel reduction of plasma levels of high and low molecular weight kininogen in patients with cirrhosis

1999

SummaryLittle is known about the regulation of high-molecular-weight-kininogen (HK) and low-molecular-weight-kininogen (LK) or the relationship of each to the degree of liver function impairment in patients with cirrhosis. In this study, we evaluated HK and LK quantitatively by a recently described particle concentration fluorescence immunoassay (PCFIA) and qualitatively by SDS PAGE and immunoblotting analyses in plasma from 33 patients with cirrhosis presenting various degrees of impairment of liver function. Thirty-three healthy subjects served as normal controls. Patients with cirrhosis had significantly lower plasma levels of HK (median 49 μg/ml [range 22-99 μg/ml]) and LK (58 μg/ml [15…

AdultLiver CirrhosisMalemedicine.medical_specialtyPathologyKininogen High-Molecular-WeightCirrhosisHigh-molecular-weight kininogenKininogen Low-Molecular-WeightSeverity of Illness IndexLiver diseaseLiver Function TestsInternal medicineBlood plasmaCholinesterasesHumansMedicineSerum AlbuminAgedKininogenbusiness.industryAlbuminHematologyBlood Coagulation DisordersMiddle Agedmedicine.diseaseLow-molecular-weight kininogenEndocrinologyProthrombin TimeFemaleLiver functionbusiness
researchProduct

Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

2016

Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells.…

AdultMale0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosisanimal structuresT-LymphocytesScienceMedizinGeneral Physics and AstronomyKininsCoagulation Factor XIIAdaptive ImmunityBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyReceptors Urokinase Plasminogen ActivatorAutoimmunityYoung Adult03 medical and health sciencesImmune systemddc:570medicineAnimalsHumansddc:610cardiovascular diseasesNeuroinflammationAgedFactor XIIMultidisciplinaryInterleukin-17QExperimental autoimmune encephalomyelitisCell DifferentiationDendritic CellsGeneral ChemistryMiddle Agedmedicine.diseaseAcquired immune systemMice Inbred C57BL030104 developmental biologyNeuroimmunologyFactor XIIImmunologyFemaleKallikreinscirculatory and respiratory physiologyNature Communications
researchProduct

Treatment of acute edema attacks in hereditary angioedema with a bradykinin receptor-2 antagonist (Icatibant)

2006

Background In hereditary angioedema, bradykinin is assumed to be the most important mediator of edema formation. Objective To assess whether the selective bradykinin receptor-2 antagonist Icatibant is effective in acute edema attacks of hereditary angioedema. Methods In this uncontrolled pilot study, 15 patients with 20 attacks were treated with Icatibant. The attacks were analyzed by using a standardized and validated visual analog scale measurement and compared with historical data of untreated attacks. Plasma bradykinin concentration was measured before and 4 hours after intravenous Icatibant treatment. Results Symptom intensity decreased within 4 hours after administration of Icatibant;…

AdultMaleImmunologyBradykininPilot ProjectsBradykininchemistry.chemical_compoundEcallantideIcatibantBradykinin B2 Receptor AntagonistsHumansImmunology and AllergyMedicineAngioedemaBradykinin receptorBradykinin B2 Receptor AntagonistsAngioedemabusiness.industryGenetic Diseases InbornMiddle Agedmedicine.diseasechemistryAnesthesiaAcute DiseaseHereditary angioedemaFemalemedicine.symptomB2 Bradykinin Receptorbusinessmedicine.drugJournal of Allergy and Clinical Immunology
researchProduct

Thoracoscopic sympathectomy at the T2 or T3 level facilitates bradykinin-induced protein extravasation in human forearm skin.

2010

Background.  The endogenous peptide bradykinin (BK) is an inflammatory mediator that induces nociceptor activation and sensitization as well as protein extravasation and vasodilation. Objective.  To test the hypothesis if sympathectomy affects BK-induced inflammation in humans. Methods.  Dermal microdialysis was employed on the volar forearm in 10 patients (21–41 years) with regional hyperhidrosis before and three months after preganglionic endoscopic transthoracic sympathetic clipping (ETSC) at the T2 or T3 level and in 10 healthy volunteers (22–36 years). After 60 minutes perfusion with Ringer's solution microdialysis fibers were perfused with BK 10−7 M and 10−5 M for 30 minutes followed …

AdultMaleMicrodialysismedicine.medical_treatmentMicrodialysisVasodilator AgentsBradykininVasodilationBradykininThoracic Vertebraechemistry.chemical_compoundYoung AdultForearmmedicineAnimalsHumansHyperhidrosisSympathectomySkinNeurogenic inflammationbusiness.industryThoracoscopyGeneral MedicineBlood ProteinsExtravasationRatsForearmAnesthesiology and Pain Medicinemedicine.anatomical_structurechemistrySympathectomyRegional Blood FlowAnesthesiaFemaleNeurology (clinical)businessPerfusionPain medicine (Malden, Mass.)
researchProduct

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 & Fibrinolysis
researchProduct

Hereditary Angioedema: Long-Term Treatment with One or More Injections of C1 Inhibitor Concentrate per Week

2009

<i>Background:</i> Hereditary angioedema due to C1 inhibitor deficiency (HAE-C1-INH) is characterized by recurrent edema attacks in various organs. The objective of the present study was to assess the efficacy and safety of weekly long-term replacement treatment with one or more injections of plasma-derived C1-INH concentrate per week (WLTC) in patients with HAE-C1-INH. <i>Methods:</i> Nineteen patients with HAE-C1-INH underwent WLTC for 9 years on average. The benefits and risks were determined based on regular recording by the patients of the severity and number of attacks at the beginning and the end of the study. <i>Results:</i> All patients reported …

AdultMalemedicine.medical_specialtyLong term treatmentC1 inhibitor deficiencyImmunologyBradykininGastroenterologyDrug Administration ScheduleC1-inhibitorEdemaInternal medicineHumansImmunology and AllergyMedicineProspective Studiesskin and connective tissue diseasesBradykinin Receptor AntagonistsC1 esterase inhibitor deficiencyAgedbiologyAngioedemabusiness.industryAngioedemas HereditaryGeneral MedicineMiddle Agedbacterial infections and mycosesmedicine.diseaseSurgeryHereditary angioedemaImmunologybiology.proteinmedicine.symptombusinessComplement C1 Inhibitor ProteinInternational Archives of Allergy and Immunology
researchProduct

A possible association between the CCK-AR gene and persistent auditory hallucinations in schizophrenia.

2004

AbstractRecent studies have suggested that DNA variations in the CCK-AR gene might predispose individuals to schizophrenia and particularly to auditory hallucinations (AH). The aim of this study is to assess the association between AH, using a specific scale for AH in schizophrenia (PSYRATS), and the CCK-AR polymorphism at 779 in a Spanish sample. A total of 105 DSM-IV schizophrenic patients with AH and 93 unrelated controls were studied. Twenty-two patients were considered as persistent auditory hallucinators, which showed similar clinical and demographic characteristic than patients with episodic AH, but with the exception of the PSYRATS values. The persistent AH group showed an excess of…

AdultMalemedicine.medical_specialtyPsychosisPeriodicityGenotypeHallucinationsSeverity of Illness IndexGenetic determinismLinkage Disequilibrium03 medical and health sciences0302 clinical medicineGene FrequencyInternal medicineSurveys and QuestionnairesSeverity of illnessmedicineHumansAlleleSex DistributionPsychiatryAllele frequencyGenetic associationDNA PrimersDemographyAuditory hallucinationPolymorphism Geneticmedicine.diseaseIntrons030227 psychiatryReceptor Cholecystokinin ADiagnostic and Statistical Manual of Mental DisordersPsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniaFemalemedicine.symptomPsychology030217 neurology & neurosurgeryEuropean psychiatry : the journal of the Association of European Psychiatrists
researchProduct