Search results for "MESH: Humans"

showing 10 items of 211 documents

Choice of second-line disease-modifying antirheumatic drugs after failure of methotrexate therapy for rheumatoid arthritis: A decision tree for clini…

2009

Objective To survey rheumatologists' preferences for the choice of a second-line disease-modifying antirheumatic drug (DMARD) after inadequate response with methotrexate (MTX) therapy in rheumatoid arthritis (RA). Methods Thirty-six rheumatologists stated their preferences for RA treatment after inadequate response with MTX therapy (optimal dose at least 6 months). From the initial scenario, we derived 54 vignettes varying by rheumatoid factor or anti–cyclic citrullinated peptide antibody presence, swollen joint count, Disease Activity Score in 28 joints, and structural damage. Respondents stated their preference among 5 therapeutic options: MTX continuation, switch to another conventional …

MESH: Antirheumatic AgentsMESH: Decision TreesMESH: Treatment FailureArthritisMESH: Antibodies Anti-IdiotypicMESH: Logistic ModelsLogistic regressionSeverity of Illness IndexArthritis Rheumatoid0302 clinical medicineimmune system diseasesImmunology and AllergyMESH: Data CollectionPharmacology (medical)Treatment Failure030212 general & internal medicinePractice Patterns Physicians'skin and connective tissue diseasesMESH: Arthritis RheumatoidData CollectionAntibodies Anti-Idiotypic3. Good healthMESH: Interleukin 1 Receptor Antagonist ProteinMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemAntirheumatic AgentsRheumatoid arthritismedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorImmunologyPeptides Cyclic03 medical and health sciencesRheumatologyRheumatoid FactorMESH: Severity of Illness IndexInternal medicineSeverity of illnessmedicineHumansRheumatoid factorMESH: Physician's Practice PatternsMESH: Peptides Cyclic030203 arthritis & rheumatologyAnakinraMESH: HumansTumor Necrosis Factor-alphabusiness.industryDecision Treesmedicine.diseaseRheumatologyInterleukin 1 Receptor Antagonist ProteinLogistic ModelsMethotrexateMESH: Tumor Necrosis Factor-alphaPhysical therapyMethotrexatebusinessArthritis & Rheumatism
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Clinical practice format for choosing a second-line disease modifying anti-rheumatic drug in early rheumatoid arthritis after failure of 6 months' fi…

2006

International audience; BACKGROUND: The objective was to develop a clinical practice format for choosing a second-line disease-modifying anti-rheumatic drug (DMARD) after a 6-month course of a first-line DMARD in patients with early RA. METHODS: A panel of 34 experts selected treatment option from various scenarios using the Thurstone pairwise method. The experts had to choose between two proposed DMARDs without proposing other options. The scenarios were obtained using the three items: DAS28, rheumatoid factor status and radiographic structural damage. A sample of 240 among 480 scenarios for each expert was taken at random. Responses given by at least 20% of the experts were considered per…

MESH: Antirheumatic AgentsMESH: Treatment FailureDiseaseReceptors Tumor Necrosis FactorEtanerceptArthritis Rheumatoid0302 clinical medicineMESH: Practice Guidelines as Topic030212 general & internal medicineTreatment Failureskin and connective tissue diseasesMESH: Immunoglobulin GMESH: Arthritis RheumatoidAnti rheumatic drugs3. Good healthClinical PracticeMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemRheumatoid arthritisAntirheumatic AgentsPractice Guidelines as TopicDrug Therapy CombinationLeflunomidemusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorFirst lineMESH: Drug Administration ScheduleDrug Administration ScheduleDecision Support Techniques03 medical and health sciencesRheumatologyRheumatoid FactorDmard therapymedicineRheumatoid factorHumansIntensive care medicine030203 arthritis & rheumatologyMESH: HumansMESH: Sulfasalazinebusiness.industryMESH: Biological MarkersMESH: Decision Support TechniquesEarly rheumatoid arthritisIsoxazolesmedicine.diseaseMESH: Receptors Tumor Necrosis FactorRadiographySulfasalazineMESH: Drug Therapy CombinationMethotrexateMESH: IsoxazolesImmunoglobulin GPhysical therapybusinessBiomarkersJoint bone spine
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Gallium modulates osteoclastic bone resorption in vitro without affecting osteoblasts.

2010

Gallium (Ga) has been shown to be effective in the treatment of disorders associated with accelerated bone loss, including cancer-related hypercalcemia and Paget's disease. These clinical applications suggest that Ga could reduce bone resorption. However, few studies have studied the effects of Ga on osteoclastic resorption. Here, we have explored the effects of Ga on bone cells in vitro.In different osteoclastic models [osteoclasts isolated from long bones of neonatal rabbits (RBC), murine RAW 264.7 cells and human CD14-positive cells], we have performed resorption activity tests, staining for tartrate resistant acid phosphatase (TRAP), real-time polymerase chain reaction analysis, viabili…

MESH: Bone ResorptionMESH: RabbitsGallium[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]MESH: Base Sequence[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMiceMESH: Alkaline PhosphataseMESH: Reverse Transcriptase Polymerase Chain Reaction[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]MESH: Animals[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemReverse Transcriptase Polymerase Chain ReactionCell DifferentiationMESH: GalliumResearch Papers[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Isoenzymes[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemMESH: Isoenzymes[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]RabbitsMESH: Cells Culturedmusculoskeletal diseasesMESH: Cell DifferentiationMESH: DNA PrimersAcid Phosphatase[SDV.CAN]Life Sciences [q-bio]/CancerIn Vitro TechniquesMESH: Acid Phosphatase[SDV.CAN] Life Sciences [q-bio]/Cancer[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansBone Resorption[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]MESH: Tartrate-Resistant Acid Phosphatase[SDV.IB.BIO]Life Sciences [q-bio]/Bioengineering/BiomaterialsMESH: MiceDNA PrimersMESH: In Vitro TechniquesMESH: OsteoblastsOsteoblastsMESH: HumansBase SequenceTartrate-Resistant Acid Phosphatase[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyAlkaline Phosphatase[SDV.IB.BIO] Life Sciences [q-bio]/Bioengineering/Biomaterials
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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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Cancer in Elderly Onset Inflammatory Bowel Disease: A Population-Based Study.

2016

IF 10.383; International audience; OBJECTIVES: Cancer may be a complication of inflammatory bowel disease (IBD) or its treatment. In elderly onset IBD patients the risk of malignancy is of particular concern. We studied this risk in a population-based cohort of elderly onset IBD patients.METHODS: In a French population-based cohort, we identified 844 patients aged >60 years at IBD diagnosis from 1988 to 2006, including 370 Crohn's disease (CD) and 474 ulcerative colitis (UC). We compared incidence of cancer among IBD patients with that observed in the French Network of population-based Cancer Registries (FRANCIM). Confidence interval (CI) was estimated assuming a Poisson-specific law for ra…

MESH: CarcinomaMaleNonmelanoma Skin-CancerInflammatory bowel disease0302 clinical medicineAdrenal Cortex HormonesAzathioprineMESH: IncidenceAge of OnsetAged 80 and overeducation.field_of_studyMESH: Middle AgedRheumatoid-ArthritisIncidenceGastroenterologyMESH: Follow-Up StudiesMESH: Anti-Inflammatory Agents Non-Steroidal3. Good health030220 oncology & carcinogenesisCohort030211 gastroenterology & hepatology[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: Immunosuppressive Agentsmedicine.medical_specialtyMESH: Age of OnsetMESH: Colitis Ulcerativedigestive systemMESH: Adrenal Cortex Hormones03 medical and health sciencesIntestinal NeoplasmsHumansCrohns-DiseaseeducationMESH: Intestinal NeoplasmsMESH: Protective FactorsMESH: AzathioprineAgedRetrospective StudiesMESH: HumansMESH: Crohn DiseaseTumor Necrosis Factor-alphaMESH: Retrospective Studiesmedicine.diseaseMESH: Inflammatory Bowel DiseasesInflammatory Bowel Diseasesdigestive system diseasesLymphoproliferative DisordersMethotrexateMESH: Tumor Necrosis Factor-alphaColitis UlcerativeComplicationMESH: FemaleProspective Observational CohortTime FactorsMESH: RegistriesMESH: Proportional Hazards ModelsMaintenance TherapyMESH: Aged 80 and overMESH: Lymphoproliferative DisordersCrohn DiseaseMESH: Risk FactorsRisk FactorsNeoplasmsMESH: NeoplasmsRegistriesUlcerative-ColitisMesalamineMESH: AgedIncidence (epidemiology)Anti-Inflammatory Agents Non-SteroidalMetaanalysisMiddle AgedhumanitiesMESH: MethotrexateFemaleFranceFrench PopulationColorectal NeoplasmsImmunosuppressive AgentsMESH: Myeloproliferative DisordersPopulationColorectal-CancerIncreased RiskInternal medicinemedicineProportional Hazards ModelsMyeloproliferative DisordersHepatologybusiness.industryMESH: Time FactorsCarcinomaCancerRetrospective cohort study[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: MesalamineProtective FactorsMESH: MaleMESH: FranceAge of onsetbusinessMESH: Colorectal NeoplasmsFollow-Up StudiesThe American journal of gastroenterology
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Early mitochondrial dysfunction, superoxide anion production, and DNA degradation are associated with non-apoptotic death of human airway epithelial …

2002

It has been shown that bacterial exoproducts may induce airway epithelium injury. During the epithelial repair process, the respiratory epithelial cells no more establish tight junctional intercellular complexes and may be particularly susceptible to bacterial virulence factors. In this study, we analyzed the effect of Pseudomonas aeruginosa exotoxin A (ETA) at different periods of time and concentrations on 16 HBE 14o(-) human bronchial epithelial cells in culture conditions inducing a phenotype of repairing cells. ETA treatment for 24 and 48 h led to the killing of 40.0 +/- 5.7% and 79.0 +/- 1.4% of the cells, respectively, as determined by the dimethylthiazole 2,5 diphenyl tetrazolium br…

MESH: Cell DeathMESH: ADP Ribose TransferasesMESH : DNAClinical BiochemistryCellApoptosisMESH : Dose-Response Relationship DrugMitochondrion[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMembrane PotentialsMESH: Dose-Response Relationship Drugchemistry.chemical_compoundSuperoxidesMESH: Intracellular MembraneMESH : DNA FragmentationRespiratory systemEnzyme InhibitorsCells CulturedADP Ribose TransferasesMESH : Cell SurvivalCell DeathSuperoxideMESH: DNAMESH: BronchiCaspase InhibitorsMESH : BronchiMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Cell SurvivalMESH: Enzyme InhibitorsMESH: Epithelial CellsMESH : ADP Ribose TransferasesIntracellularMESH: Cells CulturedPulmonary and Respiratory MedicineProgrammed cell deathCell SurvivalVirulence FactorsBacterial ToxinsExotoxinsBronchiDNA FragmentationRespiratory MucosaBiologyMicrobiologyNecrosisNasal PolypsMESH : Cells CulturedmedicineHumansMESH: DNA FragmentationMESH : Intracellular MembraneMolecular BiologyMESH : Enzyme InhibitorsMESH: HumansMESH: CaspasesDose-Response Relationship DrugMESH: ApoptosisMESH : HumansEpithelial CellsCell BiologyDNAIntracellular MembranesMESH: ExotoxinschemistryMESH: Bacterial ToxinsApoptosisMESH : ExotoxinsMESH : Cell DeathMESH : Bacterial ToxinsRespiratory epithelium[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMESH : CaspasesMESH : Apoptosis[ SDV.MHEP.PSR ] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract
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FRET multiphoton spectral imaging microscopy of 7-ketocholesterol and Nile Red in U937 monocytic cells loaded with 7-ketocholesterol.

2004

To show the effect of 7-ketocholesterol (7KC) on cellular lipid content by means of flow cytometry and the interaction of 7KC with Nile Red (NR) via ultraviolet fluorescence resonance energy transfer (FRET) excitation of NR on U937 monocytic cells by means of 2-photon excitation confocal laser scanning microscopy (CLSM).Untreated and 7KC-treated U937 cells were stained with NR and analyzed by flow cytometry and CLSM. 3D sequences of images were obtained by spectral analysis in a 2-photon excitation CLSM and analyzed by the factor analysis of medical image sequences (FAMIS) algorithm, which provides factor curves and images. Factor images are the result of the FAMIS image processing method, …

MESH: Cell DeathMESH: Fluorescence Resonance Energy TransferMESH: Mitochondria[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/ImagingMESH : Flow CytometryMESH: Flow CytometryMESH: U937 CellsMESH: MonocytesMonocytesMembrane PotentialsMESH : Staining and LabelingMESH : Microscopy Fluorescence MultiphotonOxazinesFluorescence Resonance Energy TransferImage Processing Computer-AssistedHumansMESH: Membrane PotentialsMESH: Microscopy ConfocalMESH : Membrane PotentialsMESH : Fluorescent DyesMESH : Microscopy ConfocalKetocholesterols[ SDV.IB.IMA ] Life Sciences [q-bio]/Bioengineering/ImagingFluorescent DyesMESH : KetocholesterolsMicroscopy ConfocalMESH: HumansMESH : OxazinesCell DeathStaining and LabelingMESH : HumansMESH: KetocholesterolsU937 CellsFlow CytometryMESH: Fluorescent DyesMESH: Image Processing Computer-AssistedMitochondriaMESH: Staining and Labeling[SDV.IB.IMA] Life Sciences [q-bio]/Bioengineering/ImagingMicroscopy Fluorescence MultiphotonMESH : MonocytesMESH : Fluorescence Resonance Energy TransferMESH : Cell DeathMESH : U937 CellsMESH: Microscopy Fluorescence MultiphotonMESH : MitochondriaMESH: OxazinesMESH : Image Processing Computer-Assisted
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Regulating TRAIL Receptor-Induced Cell Death at the Membrane: A Deadly Discussion

2011

Article Open access plus; International audience; The use of TRAIL/APO2L and monoclonal antibodies targeting TRAIL receptors for cancer therapy holds great promise, due to their ability to restore cancer cell sensitivity to apoptosis in association with conventional chemotherapeutic drugs in a large variety of tumors. TRAIL-induced cell death is tightly regulated right from the membrane and at the DISC (Death-Inducing Signaling Complex) level. The following patent and literature review aims to present and highlight recent findings of the deadly discussion that determines tumor cell fate upon TRAIL engagement.

MESH: Cell DeathMESH: Signal TransductionCancer ResearchApoptosisTRAILMESH : Models BiologicalscaffoldCell membrane0302 clinical medicineDrug DiscoveryMESH: AnimalsPharmacology (medical)Receptordeath effector domain0303 health sciencesCell DeathGeneral MedicineTRAIL-R4.3. Good healthCell biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSignal transductionMESH : Apoptosis Regulatory ProteinsSignal TransductionProgrammed cell deathc-FLIPdeath domainmedicine.drug_classMESH : Cell MembraneCancer therapyBiologyMonoclonal antibodyModels BiologicalArticle03 medical and health sciencesmedicineAnimalsHumansChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionMESH: HumansMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell MembraneMESH: Models BiologicalDISCReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMESH : Cell DeathFADDCancer cellMESH : AnimalsApoptosis Regulatory ProteinsMESH : ApoptosisMESH: Cell MembraneRecent Patents on Anti-Cancer Drug Discovery
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Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

2009

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guid…

MESH: Cell DeathcytofluorometryMESH : Microscopy Fluorescenceved/biology.organism_classification_rank.speciesCellMESH: Flow CytometryMESH: Microscopy FluorescenceApoptosisfluorescence microscopyMESH: Eukaryotic CellsAnnexin Vnecrosis0302 clinical medicineEukaryotic Cells/cytologyMitochondrial membrane permeabilizationScanningMESH : ImmunoblottingGeneticsApoptosis; Cell Death; Eukaryotic Cells/cytology; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence0303 health sciencesMicroscopyMESH : Spectrometry FluorescenceMESH: ImmunoblottingCell DeathMESH: Guidelines as Topic//purl.org/becyt/ford/3.1 [https]Bioquímica y Biología MolecularFlow Cytometry3. Good healthTunelMedicina Básicamedicine.anatomical_structureEukaryotic Cellscaspases030220 oncology & carcinogenesis//purl.org/becyt/ford/3 [https]MESH: Spectrometry FluorescenceMESH : Microscopy Electron ScanningProgrammed cell deathautophagyCIENCIAS MÉDICAS Y DE LA SALUDMESH: Microscopy Electron ScanningMESH : Flow CytometrycaspaseImmunoblottingGuidelines as TopicComputational biologyBiologyElectronFluorescenceArticle03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyModel organismddc:612mitotic catastropheMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Guidelines as Topic030304 developmental biologycell death; Apoptosis; caspase; autophagy; Oxidative stress; fluorescence microscopyMESH: Humansved/biologySpectrometryInterpretation (philosophy)MESH: ApoptosisMESH : Eukaryotic CellsMESH : HumansApoptosis; Eukaryotic Cells; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence; Cell Death; Molecular Biology; Cell Biologyimmunofluorescence microscopyCell BiologySpectrometry FluorescenceMicroscopy FluorescenceOxidative stressMESH : Cell DeathCancer cellMicroscopy Electron ScanningMESH : Apoptosis
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Involvement of complement pathways in patients with bacterial septicemia.

2007

The complement system is a major humoral portion of the innate immune system, playing a significant role in host defence against microorganisms. The biological importance of this system is underlined by the fact that at least three different pathways for its activation exist, the classical, the MBL and the alternative pathway. To elucidate the involvement of the classical and/or the MBL pathway during bacterial septicemia, 32 patients with gram-positive and 30 patients with gram-negative bacterial infections were investigated. In patients with gram-positive bacteria, a significant consumption of C1q (p=0.005) but not of mannose-binding lectin (MBL) (p=0.2) was found during the acute phase o…

MESH: Complement Pathway Mannose-Binding LectinLipopolysaccharidesSalmonellaMESH: Complement C1qLipopolysaccharideImmunologychemical and pharmacologic phenomenaBacteremiamedicine.disease_causeGram-Positive BacteriaMannose-Binding LectinMicrobiologyMESH: Gram-Positive Bacteria03 medical and health scienceschemistry.chemical_compoundClassical complement pathway0302 clinical medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyComplement Pathway ClassicalMESH: BacteremiaMolecular Biology030304 developmental biology0303 health sciencesInnate immune systemMESH: HumansbiologyComplement C1qLectinSalmonella entericaComplement Pathway Mannose-Binding LectinMESH: Complement Pathway Classicalbiology.organism_classificationbacterial infections and mycoses3. Good healthComplement systemMESH: Mannose-Binding LectinchemistryMESH: Salmonella entericaImmunologyAlternative complement pathwaybiology.proteinMESH: LipopolysaccharidesBacteria030215 immunologyMolecular immunology
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