Search results for "Complement system"

showing 7 items of 157 documents

Studies on the mechanism of PMN activation II. by triggering the alternative pathway of complement activation

1982

By means of cobra venom factor (CVF) it is demonstrated that the stimulation of hexosemonophosphate shunt (HMPS) of human polymorphonuclear leukocytes (PMN) by zymosan (Z) and dextran sulfate (DS) is caused by at least two modes of activation: (a) via activation caused by phagocytosis, (b) via activated alternative pathway of complement activation (APC). Active factors of APC presented with phagocytizable objects strongly enhance activation of PMN. The effect of APC can be observed in serum-containing as well as in serum-free cultures. It can be demonstrated that in serum-free cultures the factors of APC participating in the activation of PMN are supplied by monocytes. By the use of synthet…

medicine.medical_specialtyNeutrophilsPhagocytosisComplement Pathway AlternativeDose-Response Relationship ImmunologicStimulationMonocyteschemistry.chemical_compoundPhagocytosisInternal medicinemedicineHumansComplement ActivationHematologyChemistryDextran SulfateZymosanZymosanDextransComplement C3HematologyGeneral MedicinePeptide FragmentsCell biologyComplement systemDextran sulfateBiochemistryComplement C3aAlternative complement pathwayCobra venom factorBlut
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Influence of the terminal complement-complex on reperfusion injury, no-reflow and arrhythmias: a comparison between C6-competent and C6-deficient rab…

1996

Objective: The complement system has been suggested to play a role in reperfusion injury which may result from an enhanced destruction of myocardial tissue or from an impairment of reflow. We investigated the influence of the C5b-9 complement complex on infarct size, reflow and arrhythmogenesis. Methods: Twenty-eight C6-competent rabbits and 18 rabbits with congenital C6 deficiency were subjected to either 30 min or 2 h of coronary artery occlusion followed by reperfusion. C6 deficiency was confirmed by the complement titration test and immunohistology. The triphenyl tetrazolium chloride method was used to delineate infarct size. Reflow into infarcted areas was evaluated histologically afte…

medicine.medical_specialtyTime FactorsPhysiologyMyocardial InfarctionIschemiaInfarctionMyocardial Reperfusion InjuryComplement Membrane Attack ComplexElectrocardiographyReperfusion therapyPhysiology (medical)Internal medicinemedicineAnimalscardiovascular diseasesComplement Activationbusiness.industryArrhythmias Cardiacmedicine.diseaseImmunohistochemistryComplement C6Complement systemRegional Blood FlowCoronary occlusionNo reflow phenomenoncardiovascular systemCardiologyRabbitsCardiology and Cardiovascular MedicineComplement membrane attack complexbusinessReperfusion injuryCardiovascular Research
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Influence of cold ischemia time on complement activation, neopterin, and cytokine release in liver transplantation.

2004

The aim of this study was to determine whether a cold ischemia time (CIT) of12 hours influences the activation of complement as well as the plasma concentrations of neopterin, interleukin (IL)-6, or IL-8 in orthotopic liver transplantation (OLT).Eighteen consecutive patients undergoing OLT using a veno-venous bypass technique were divided into 2 groups: duration of CIT12 hours (group 1; n = 11), and CIT12 hours (group 2; n = 7). Blood samples were drawn preoperatively, 1 minute before, and 120 minutes after reperfusion.Preoperatively, complement split products, neopterin, IL-6, and IL-8 levels did not differ between the groups. At 120 minutes after reperfusion, the concentrations of C3a, SC…

medicine.medical_specialtyTime Factorsmedicine.medical_treatmentIschemiaLiver transplantationGastroenterologyCold Ischemia TimeNeopterinchemistry.chemical_compoundIschemiaInternal medicinemedicineHumansComplement ActivationTransplantationbusiness.industryInterleukinsNeopterinInterleukinOrgan PreservationHypothermiamedicine.diseaseComplement systemLiver TransplantationTransplantationCold Temperaturesurgical procedures operativechemistryLiverImmunologyCytokinesSurgerymedicine.symptombusinessTransplantation proceedings
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Glucose-induced loss of glycosyl-phosphatidylinositol-anchored membrane regulators of complement activation (CD59, CD55) by in vitro cultured human u…

2000

Aims/hypothesis. This study examines whether increased glucose concentrations are responsible for a decreased expression of membrane regulators of complement activation molecules. The effect of high glucose in determining an increase in membrane attack complex deposition on endothelial cells was also investigated. Methods. Endothelial cells were isolated from umbilical cord tissue, cultured in the presence of increased concentrations of glucose, and the expression of CD46, CD55, and CD59 was detected by ELISA (enzyme-linked immunosorbent assay) and by flow cytometry. Glucose-treated endothelial cells were also incubated with antiendothelial cell antibodies and fresh complement to assess the…

medicine.medical_specialtyUmbilical VeinsEndotheliumGlycosylphosphatidylinositolsEndocrinology Diabetes and MetabolismCellCD59 AntigensCD59Complement Membrane Attack ComplexBiologyUmbilical veinMembrane Cofactor ProteinAntigens CDPregnancyInternal medicineInternal MedicinemedicineHumansComplement ActivationCells CulturedMembrane GlycoproteinsCD55 AntigensCD46Cell biologyComplement systemEndothelial stem cellEndocrinologymedicine.anatomical_structureGlucoseFemaleEndothelium VascularComplement membrane attack complexDiabetologia
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Neuronal immunoreactivity for mannose-binding lectin after venous occlusion-induced focal cerebral ischemia in rats

2012

Abstract A recent research reveals that complement activation exacerbates cerebral infarction. However, involvement of the lectin pathway, (the third complement activation pathway) in cerebral ischemia is not well studied. In this study, we investigated the appearance of mannose-binding lectin (MBL) in ischemic brain tissue. Male Wistar rats ( n  = 25) were divided into three groups: untreated control, sham, and vein occlusion (VO). Rats in the VO group had two adjacent photochemically occluded cortical veins. Regional cerebral blood flow (rCBF) was measured in the sham and VO groups. Rats were perfusion-fixed at 72 h in the sham group and at 3, 24, and 72 h after inducing ischemia in the V…

medicine.medical_specialtybusiness.industryCerebral infarctionGeneral NeuroscienceIschemiachemical and pharmacologic phenomenamedicine.diseaseVein occlusionComplement systemPsychiatry and Mental healthEndocrinologyCerebral blood flowInternal medicineLectin pathwayImmunologymedicineImmunohistochemistryNeurology (clinical)businessMannan-binding lectinNeurology, Psychiatry and Brain Research
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Mechanism of reperfusion damage after thrombolysis and ‘direct PTCA’

1997

Summary There is general agreement between cardiologists, that reperfusion of the infarct related coronary artery (PTCA) is the method of choice for the treatment of an acute myocardial infarction. However, the method utilized for inducing a rapid and complete reperfusion is still discussed. Even if thrombolysis will remain the method of choice for the major part of the population, part of the patient cohort with acute infarction will be treated by direct PTCA. Rapid reperfusion of ischemic myocardium reduces infarct size by limiting infarct extension into the entire area at risk, although a reperfusion damage is induced in the core ischemic area. This reperfusion damage has been convincing…

medicine.medical_specialtyeducation.field_of_studybusiness.industrymedicine.medical_treatmentPopulationInfarctionThrombolysismedicine.diseaseComplement systemClassical complement pathwayReperfusion therapymedicine.anatomical_structureInternal medicinemedicineCardiologycardiovascular diseasesMyocardial infarctioneducationbusinessArteryFibrinolysis and Proteolysis
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The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid…

2009

Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as…

musculoskeletal diseasesAdultMalemedicine.medical_specialtyComplement systemEndotheliumNeutrophilsArthritisInflammationComplement Membrane Attack ComplexArthritis RheumatoidEndothelium; Osteoprotegerin; Inflammation; Complement systemRheumatologyOsteoprotegerinInternal medicineCell AdhesionMedicineHumansPharmacology (medical)EndotheliumCells CulturedAgedInflammationEndothelial CellDose-Response Relationship Drugbusiness.industryNeutrophilSynovial MembraneOsteoprotegerinEndothelial CellsMiddle Agedmedicine.diseaseIn vitroComplement systemUp-RegulationEndothelial stem cellEndocrinologymedicine.anatomical_structureNeutrophil InfiltrationFemaleComplement system; Endothelium; Inflammation; Osteoprotegerin; Adult; Aged; Arthritis Rheumatoid; Cell Adhesion; Cells Cultured; Complement Membrane Attack Complex; Dose-Response Relationship Drug; Endothelial Cells; Endothelium Vascular; Female; Humans; Male; Middle Aged; Neutrophil Infiltration; Neutrophils; Osteoprotegerin; Synovial Membrane; Up-Regulation; Rheumatology; Pharmacology (medical)Endothelium Vascularmedicine.symptombusinessComplement membrane attack complexHuman
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