Search results for "Complement C1"

showing 10 items of 125 documents

Immunofluorescence studies on the subcomponents of the first component of complement (C1): detection of C1q and C1s in different cells of biopsy mate…

1981

The first component of complement (C1) is a macromolecule consisting of three distinct subcomponents, C1q, C1r, and C1s. In regard to its production site and its role in phagocytic processes it was of interest to find out whether these different subcomponents could be detected in human biopsy material only as a complex in individual cells or whether C1 subcomponents could be found on different cells. To study this question, monospecific fluorescein-labelled anti-human-C1q IgG and monospecific rhodamine-labelled anti-human C1q IgG were used. Biopsy material from human rectum was stained with fluoresceinated antisera, either by use of one antiserum or by double staining. Using this technique,…

Pathologymedicine.medical_specialtyImmunologyGuinea PigsFluorescent Antibody TechniqueImmunofluorescenceImmunoglobulin GAntibodiesGuinea pigCell membraneComplement C1medicineImmunology and AllergyMacrophageAnimalsHumansAntiserumbiologymedicine.diagnostic_testMacrophagesCell MembraneRectumHematologyStainingmedicine.anatomical_structureImmunoglobulin Gbiology.proteinRabbitsAntibodyImmunobiology
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C1q as a novel player in angiogenesis with therapeutic implication in wound healing

2014

We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa(-/-) mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and …

Pathologymedicine.medical_specialtycomplement C1qAngiogenesisImmunoblottingNeovascularization Physiologicchemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayIn situ hybridizationBiologyReal-Time Polymerase Chain ReactionangiogenesisMiceVasculogenesiscomplement; vasculogenesis; animal modelsimmune system diseasesmedicineangiogenesis; complement C1q; wound-healing; endothelial cellsHuman Umbilical Vein Endothelial CellsAnimalsHumanscomplementRats WistarIn Situ HybridizationCell ProliferationDNA PrimersTube formationMice KnockoutWound HealingMultidisciplinaryCell growthComplement C1qEndothelial CellsangiogenesivasculogenesiBiological Scienceswound-healingImmunohistochemistryanimal modelsendothelial cellsRatsMice Inbred C57BLReal-time polymerase chain reactionImmunohistochemistryWound healing
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Disease expression in women with hereditary angioedema

2008

Udgivelsesdato: 2008-Jun-11 OBJECTIVE: Fluctuations in sex hormones can trigger angioedema attacks in women with hereditary angioedema. Combined oral contraceptive therapies, as well as pregnancy, can induce severe attacks. The course of angioedema may be very variable in different women. STUDY DESIGN: Within the PREHAEAT project launched by the European Union, data on 150 postpubertal women with hereditary angioedema were collected in 8 countries, using a patient-based questionnaire. RESULTS: Puberty worsened the disease for 62%. Combined oral contraceptives worsened the disease for 79%, whereas progestogen-only pills improved it for 64%. During pregnancies, 38% of women had more attacks, …

PediatricsDiseaseMESH: HormonesMESH: Pregnancy0302 clinical medicinePregnancyMESH: ProgesteroneMESH: ChildImmunopathologyMESH: Contraceptives Oral CombinedMESH: Puberty030212 general & internal medicineskin and connective tissue diseasesProgesteronemedia_commonMESH: Middle AgedMESH: Complement Hemolytic Activity AssayMESH: Angioedema HereditaryVaginal deliveryfood and beveragesObstetrics and GynecologyMESH: Complement C4[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedMenstruation3. Good healthContraceptives Oral CombinedMESH: Pregnancy ComplicationsPillHereditary angioedemaFemalemedicine.symptomAdultmedicine.medical_specialtyMESH: PedigreeMESH: Complement C1 Inactivator ProteinsMESH: Menstruation[SDV.MHEP.GEO]Life Sciences [q-bio]/Human health and pathology/Gynecology and obstetrics03 medical and health sciencesmedicineMESH: AngioedemaHumansmedia_common.cataloged_instanceEuropean unionPregnancyMESH: HumansAngioedemabusiness.industryPubertyAngioedemas HereditaryMESH: AdultDelivery Obstetricmedicine.diseaseHormonesMESH: RecurrenceSurgeryMESH: Abdominal PainPregnancy Complications030228 respiratory systemMESH: Delivery ObstetricbusinessMESH: FemaleAmerican Journal of Obstetrics and Gynecology
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Expression of membrane C1q in human monocyte-derived macrophages is developmentally regulated and enhanced by interferon-γ

2001

The present study investigated when during "in vitro" maturation macrophages (MPhi) express membrane C1q (mC1q), and whether cell activation affects expression and function of mC1q. Although C1q mRNA was repeatedly detected in freshly isolated monocytes using reverse transcriptase-polymerase chain reaction, C1q protein was observed only in developing MPhi from day 1 to 4 on using immunodetection and flow cytometry. However, the quantity of mC1q and other MPhi membrane proteins differed strikingly in cells from different donors. We report here for the first time that CD14(+) and CD14(-) mC1q-bearing MPhi can develop, and that interferon-gamma increases mC1q display at the cell surface, and m…

PhagocytosisCD14CellLipopolysaccharide ReceptorsBiophysicsMonocyte/macrophageComplementEnzyme-Linked Immunosorbent AssayBiologyLymphocyte ActivationBiochemistryFlow cytometryInterferon-gammaPhagocytosisStructural BiologyGeneticsmedicineHumansMolecular BiologyCells CulturedC1qMessenger RNAmedicine.diagnostic_testComplement C1qMacrophagesCell DifferentiationCell BiologyFlow CytometryPrecipitin TestsMolecular biologyIn vitromedicine.anatomical_structureGene Expression RegulationMembrane proteinDifferentiationCell activationFEBS Letters
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Current drugs in early development for hereditary angioedema: potential for effective treatment

2014

Hereditary angioedema (HAE) through C1 inhibitor deficiency is a rare but important disease. It is characterized by recurrent episodes of angioedema, which commonly affects the skin (in the form of swelling in the extremities, face and genitals) as well as the gastrointestinal tract (abdominal pain attacks). In approximately 1% of cases of angiodema-related swelling, there is obstruction of the upper airway, which is potentially life-threatening. Therefore, HAE due to C1 inhibitor deficiency may be associated with significant morbidity and mortality. Recent research has added to our ever-increasing understanding of the pathogenesis of HAE, which has, in addition, new clinical trials with ne…

Pharmacologymedicine.medical_specialtyGastrointestinal tractAbdominal painAngioedemabusiness.industryAngioedemas HereditaryGeneral MedicineDiseasemedicine.diseaseDermatologySurgeryClinical trialPathogenesisTreatment OutcomeHereditary angioedemamedicineAnimalsHumansPharmacology (medical)medicine.symptomAirwaybusinessComplement C1 Inhibitor ProteinExpert Opinion on Investigational Drugs
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Activation of the first component of complement, C1: comparison of the effect of sixteen different enzymes on serum C1.

1983

In this study, the effect of sixteen different enzymes on serum C1 and its subcomponents was investigated. The sixteen enzymes could be divided into three groups. First, enzymes which activate native C1: trypsin (optimal concentration 2.4 x 10(-4) mM); alpha-chymotrypsin (2.3 x 10(3) mM); thrombin (1.0 x 10(-5) mM); plasmin (1.9 x 10(-5) mM); elastase (5.8 x 10(-5) mM); pronase (3.0 x 10(-6) mM). All these enzymes are serine esterase and activate native serum C1 bound to EAC4 at the given concentration within 10 min at 30 degrees C. Furthermore, native C1 inhibited by a pentosanpolysulfoester, Sp54, is unable to undergo the internal activation but can be externally activated by the serine e…

PlasminComplement Activating EnzymesImmunologyGuinea PigsDose-Response Relationship ImmunologicPronaseSerinechemistry.chemical_compoundComplement C1medicineImmunology and AllergyAnimalsHumansTrypsinFibrinolysinComplement Activationchemistry.chemical_classificationPentosan Sulfuric PolyesterbiologyHematologyTrypsinCarboxypeptidaseKineticsEnzymeBiochemistrychemistrybiology.proteinCollagenaseCattleRabbitsLysozymemedicine.drugPeptide HydrolasesImmunobiology
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Humoral autoreactivity directed against surfactant protein-A (SP-A) in rheumatoid arthritis synovial fluids.

2000

SUMMARY SP-A is found principally in the lung, and has been associated with lamellar bodies also found in the synovial joint. Both SP-A and C1q contain collagen-like regions, and SP-A and C1q have some structural similarities, both having a globular head region and a collagen-like tail. Here we are able to show that (i) autoreactivity to SP-A, as expressed by IgG and IgM autoantibodies, is present in synovial fluid (SF) isolated from patients with rheumatoid arthritis (RA); (ii) in absorption experiments only a limited degree of cross-reactivity between autoantibodies reactive with C1q and SP-A is observed; (iii) there is no cross-reactivity between autoantibodies reactive with type II coll…

Pulmonary Surfactant-Associated ProteinsKnee JointProteolipidsImmunologyType II collagenchemical and pharmacologic phenomenamedicine.disease_causeAutoantigensImmunoglobulin GAutoimmunityArthritis RheumatoidRheumatic DiseaseAntigenSynovial jointSynovial FluidmedicineImmunology and AllergySynovial fluidAnimalsHumansskin and connective tissue diseasesAutoantibodiesbiologyPulmonary Surfactant-Associated Protein AChemistryComplement C1qAutoantibodyPulmonary Surfactantsmedicine.anatomical_structureImmunoglobulin MImmunoglobulin MImmunoglobulin GImmunologybiology.proteinBinding Sites AntibodyCollagenPeptidesChickensDimerizationClinical and experimental immunology
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Treatment with C1-esterase inhibitor concentrate in type I or II hereditary angioedema: a systematic literature review.

2013

Hereditary angioedema (HAE) due to C1 esterase inhibitor (HAE-C1-INH) deficiency is a rare genetic disorder presenting with recurrent episodes of skin swellings, abdominal pain attacks, and potentially fatal laryngeal edema. This study was designed to review the efficacy and safety of pasteurized, human, plasma-derived C1-INH concentrate for the treatment of patients with HAE-C1-INH. A systematic search of electronic databases up to December 2011 was performed without language or date restrictions. Two reviewers completed the study selection using predefined inclusion criteria, tabulated, and analyzed the data. The data were inappropriate for meta-analysis; thus, a qualitative synthesis was…

Pulmonary and Respiratory MedicineAdultMaleAbdominal painmedicine.medical_specialtyAdolescentPlacebolaw.inventionYoung AdultQuality of lifeRandomized controlled triallawInternal medicineImmunology and AllergyMedicineHumansYoung adultChildRandomized Controlled Trials as TopicHereditary Angioedema Types I and IIbusiness.industryGeneral Medicinebacterial infections and mycosesmedicine.diseaseSystematic reviewTreatment OutcomeChild PreschoolHereditary angioedemaObservational studyFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinAllergy and asthma proceedings
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Efficacy of C1 esterase inhibitor concentrate in treatment of cutaneous attacks of hereditary angioedema.

2015

BACKGROUND Although treatment with C1 esterase inhibitor (C1-INH) concentrate is well established for hereditary angioedema (HAE) attacks in general, data that assess its efficacy for cutaneous attack treatment are sparse. OBJECTIVE To assess efficacy of plasma-derived, nanofiltered C1-INH concentrate for cutaneous attack treatment by comparing treated attacks from the uncontrolled I.M.P.A.C.T.2 study with historical data for untreated attacks. METHODS Cutaneous attack data from patients with HAE who were treated for cutaneous edema with 20 IU/kg body weight C1-INH concentrate in the uncontrolled I.M.P.A.C.T.2 study (38 patients) were compared with data from untreated patients from an histo…

Pulmonary and Respiratory MedicineAdultMalemedicine.medical_specialtyAdolescentUntreated groupPeripheral edemaGastroenterologySeverity of Illness IndexYoung AdultInternal medicineSeverity of illnessmedicineImmunology and AllergyHumansYoung adultChildAgedEnd pointbusiness.industryAngioedemas HereditaryGeneral MedicineArticlesMiddle Agedmedicine.diseasePeripheralC1 esteraseTreatment OutcomeHereditary angioedemaDisease ProgressionFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinAllergy and asthma proceedings
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Reversible inhibition of C1Q release from guinea pig macrophages by 2,2'-dipyridyl: Evidence for a posttranslational hydroxylation step in the biosyn…

1978

PyridinesMacrophagesGuinea PigsBiophysicsCell BiologyBiologyHydroxylationBiochemistryGuinea pigHydroxylationchemistry.chemical_compound22'-DipyridylBiochemistryBiosynthesischemistryStructural BiologyComplement C1GeneticsAnimalsReversible inhibitionMolecular BiologyCells CulturedFEBS letters
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