Search results for "Mesh"

showing 10 items of 885 documents

Virulent synergistic effect between Enterococcus faecalis and Escherichia coli assayed by using the Caenorhabditis elegans model.

2008

5 pages; International audience; BACKGROUND: The role of enterococci in the pathogenesis of polymicrobial infections is still debated. The purpose of this study was to evaluate the effect of virulent enterococci in the presence or absence of Escherichia coli strains in the in vivo Caenorhabditis elegans model. PRINCIPAL FINDINGS: This study demonstrated that there was a synergistic effect on virulence when an association of enterococci and E. coli (LT50 = 1.6 days+/-0.1 according to the tested strains and death of nematodes in 4 days+/-0.5) was tested in comparison with enterococci alone (LT50 = 4.6 days+/-0.1 and death in 10.4 days+/-0.6) or E. coli alone (LT50 = 2.1+/-0.9 and deaths 6.6+/…

MESH : Virulence FactorsInfectious Diseases/Gastrointestinal InfectionsMESH : Escherichia colilcsh:MedicineMESH : Genotypemedicine.disease_causeMESH: Regression AnalysisPathogenesisMESH: GenotypeInfectious Diseases/Bacterial InfectionsMESH : Regression AnalysisGenotype[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisEnterococcus faecalis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH : Anti-Bacterial AgentsMESH : Enterococcus faecalislcsh:ScienceCaenorhabditis elegans0303 health sciencesMultidisciplinarybiologyMESH: Escherichia coliBacterial Infections3. Good healthAnti-Bacterial AgentsMicrobiology/Immunity to InfectionsMESH : Bacterial InfectionsGastroenterology and Hepatology/Gastrointestinal Infections[SDV.IMM]Life Sciences [q-bio]/ImmunologyRegression AnalysisMicrobiology/Cellular Microbiology and PathogenesisResearch ArticleMESH: Enterococcus faecalis[SDV.IMM] Life Sciences [q-bio]/ImmunologyGenotypeMESH: Bacterial InfectionsVirulence FactorsVirulenceEnterococcus faecalisMicrobiologyMESH : Caenorhabditis elegans03 medical and health sciencesIn vivoMESH: Anti-Bacterial AgentsMESH: Caenorhabditis elegansmedicineEscherichia coliAnimalsCaenorhabditis elegansEscherichia coli030304 developmental biologyMESH: Virulence Factors030306 microbiologylcsh:RMicrobiology/Medical Microbiology[SDV.EE.IEO] Life Sciences [q-bio]/Ecology environment/Symbiosisbiology.organism_classificationMESH : Disease Models AnimalDisease Models AnimalEnterococcuslcsh:QMESH : AnimalsMESH: Disease Models Animal[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/SymbiosisPloS one
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Mechanisms underlying the toxicity of lactone aroma compounds towards the producing yeast cells

2003

M. A G U E D O , L. B E N E Y , Y. W A C H EA N D J. - M. B E L I N. 2003. Aims: To study the fundamental mechanisms of toxicity of the fruity aroma compound c-decalactone, that lead to alterations in cell viability during its biotechnological production by yeast cells; Yarrowia lipolytica that is able to produce high amounts of this metabolite was used here as a model. Methods and Results: Lactone concentrations above 150 mg l )1 inhibited cell growth, depolarized the living cells and increased membrane fluidity. Infrared spectroscopic measurements revealed that the introduction of the lactone into model phospholipid bilayers, decreased the phase transition temperature. Moreover, the H + -…

MESH : YarrowiaMembrane FluidityMESH : Cell MembraneIntracellular pHMESH : Membrane FluidityYarrowiaFluorescence PolarizationApplied Microbiology and BiotechnologyMESH : PhospholipidsMembrane PotentialsCell membraneMESH : Spectroscopy Fourier Transform InfraredLactonesMESH : Hydrogen-Ion ConcentrationSpectroscopy Fourier Transform InfraredmedicineMembrane fluidityMESH : Membrane PotentialsViability assay[SDV.BC] Life Sciences [q-bio]/Cellular BiologySpectroscopyPhospholipidsAdenosine TriphosphatasesMESH : Adenosine Triphosphatasesbiology[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyCell growthCell MembraneYarrowiaGeneral MedicineHydrogen-Ion Concentrationbiology.organism_classificationBioproductionYeastMESH : Lactones[INFO.INFO-BT] Computer Science [cs]/Biotechnologymedicine.anatomical_structureBiochemistryFourier Transform InfraredMESH : Fluorescence Polarization[ INFO.INFO-BT ] Computer Science [cs]/BiotechnologyBiotechnologyJournal of Applied Microbiology
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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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Prises de décisions et dilemmes en situation d'interaction évaluative orale dans trois classes de CP

2021

International audience

MESH: CP ; Enseignement élémentaire ; Évaluation des élèves ; Interaction ; Oral ; Prise de décision[SHS.EDU]Humanities and Social Sciences/Education[SHS.EDU] Humanities and Social Sciences/EducationComputingMilieux_MISCELLANEOUS
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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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3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

2014

Objective Growing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas. Methods EZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879…

MESH: Cell DeathAdenosine[SDV]Life Sciences [q-bio]Cancer Treatmentlcsh:MedicineMESH: Flow CytometryApoptosischemistry.chemical_compoundSpectrum Analysis Techniques0302 clinical medicineCell MovementMolecular Cell BiologyMedicine and Health Sciences3-Deazaneplanocin AMESH: Epigenesis GeneticEnzyme Inhibitorslcsh:Science0303 health sciencesMultidisciplinaryCell DeathbiologyReverse Transcriptase Polymerase Chain ReactionEZH2Polycomb Repressive Complex 2DrugsCell migrationMESH: ChondrosarcomaFlow Cytometry3. Good healthHistone[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemOncologyConnective TissueCell ProcessesSpectrophotometry030220 oncology & carcinogenesisHistone methyltransferaseHistone MethyltransferasesMESH: 3-deazaneplanocinCytophotometryAnatomyMESH: Polycomb Repressive Complex 2Epigenetic therapyMESH: Histone methyltransferaseResearch ArticleProgrammed cell deathHistologyChondrosarcoma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular Biologymacromolecular substancesResearch and Analysis MethodsCell GrowthEpigenetic Therapy03 medical and health sciencesRheumatologyCell Line TumorMESH: Blotting WesternHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEZH2Tumors030304 developmental biologyMESH: Apoptosislcsh:RMESH: Histone-Lysine N-MethyltransferaseBiology and Life SciencesMESH: ImmunohistochemistryHistone-Lysine N-MethyltransferaseCell BiologyBiological TissueCartilageHistone methyltransferasechemistryApoptosisbiology.proteinCancer researchMESH: EZH2 protein humanlcsh:QCytometry
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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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