Search results for "MESH: Humans"

showing 10 items of 211 documents

Spike-in SILAC proteomic approach reveals the vitronectin as an early molecular signature of liver fibrosis in hepatitis C infections with hepatic ir…

2014

Hepatitis C virus (HCV)-induced iron overload has been shown to promote liver fibrosis, steatosis, and hepatocellular carcinoma. The zonal-restricted histological distribution of pathological iron deposits has hampered the attempt to perform large-scale in vivo molecular investigations on the comorbidity between iron and HCV. Diagnostic and prognostic markers are not yet available to assess iron overload-induced liver fibrogenesis and progression in HCV infections. Here, by means of Spike-in SILAC proteomic approach, we first unveiled a specific membrane protein expression signature of HCV cell cultures in the presence of iron overload. Computational analysis of proteomic dataset highlighte…

Liver CirrhosisProteomicshepatitis C virusMaleMESH: Isotope LabelingHSCmedicine.disease_causeBiochemistry0302 clinical medicineFibrosisMESH: Up-RegulationMembrane Proteinhepatic stellate cellliver fibrosishepatic iron overload0303 health sciencesbiologyMESH: ProteomicsMedicine (all)hepatocellular carcinomaBiomedicine; hepatitis c infection; liver fibrosis; hepatic iron overload; vitronectinHepatitis C[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM]Hepatitis CUp-Regulation3. Good healthcell culture-derived HCVIsotope Labeling030220 oncology & carcinogenesisHepatocellular carcinomaBiomedicine; Hepatic iron overload; Hepatitis C infection; Liver fibrosis; Vitronectin; Biomarkers; Cell Line; Hepatitis C; Humans; Iron Overload; Isotope Labeling; Liver Cirrhosis; Male; Membrane Proteins; Proteomics; Up-Regulation; Vitronectin; Molecular Biology; Biochemistry; Medicine (all)HCV[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyBiomarker (medicine)VitronectinMESH: Membrane ProteinsMESH: Liver CirrhosisHumanIron OverloadLiver CirrhosiHepatitis C virusvitronectinhepatitis c infectionCell LineMESH: Iron Overload03 medical and health sciencesmedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyMESH: Hepatitis CMESH: HumansMESH: Biological MarkersMembrane ProteinsLiver fibrosiProteomicBiomarkermedicine.diseaseMESH: VitronectinMESH: Maledigestive system diseasesMESH: Cell LineBiomedicineBiomedicine / Abbreviations: HCCHCVccImmunologyCancer researchHepatic stellate cellbiology.proteinSteatosisBiomarkersPROTEOMICS
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Dioxin emissions and soft-tissue sarcoma: results of a population-based case-control study.

2004

International audience; BACKGROUND: In 1998, the French Ministry of Environment revealed that of 71 French municipal solid waste incinerators processing more than 6 metric tons of material per hour, dioxin emission from 15 of them was above the 10 ng international toxic equivalency factor/m3 (including Besançon, emitting 16.3 ng international toxic equivalency factor/m3) which is substantially higher than the 0.1 international toxic equivalency factor/m3 prescribed by a European directive of 1994. In 2000, a macrospatial epidemiological study undertaken in the administrative district of Doubs, identified two significant clusters of soft-tissue sarcoma and non Hodgkin lymphoma in the vicinit…

MESH : Case-Control StudiesMESH : MaleMESH: Environmental ExposureMESH : AgedMESH : Child PreschoolMESH : Infant NewbornMESH : SarcomaMESH : DioxinsMESH : ChildMESH: Risk FactorsMESH: ChildMESH : AdolescentMESH: IncinerationMESH : Middle AgedMESH : FemaleMESH : Data Interpretation StatisticalMESH : FranceMESH : IncinerationMESH: AgedMESH: AdolescentMESH: HumansMESH: Middle AgedMESH: DioxinsMESH: Infant NewbornMESH: Child PreschoolMESH : HumansMESH: AdultMESH : Infant[ SDV.SPEE ] Life Sciences [q-bio]/Santé publique et épidémiologieMESH : AdultMESH: InfantMESH: Case-Control StudiesMESH : Risk FactorsMESH: MaleMESH: France[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologieMESH: Sarcoma[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieMESH: Data Interpretation StatisticalMESH: FemaleMESH : Soft Tissue NeoplasmsMESH : Environmental ExposureMESH: Soft Tissue Neoplasms
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Trefoil factor TFF1-induced protection of conjunctival cells from apoptosis at premitochondrial and postmitochondrial levels.

2008

PURPOSE. Goblet cells of the conjunctival epithelium synthesize and secrete TFF1 (Trefoil factor 1), a small protease-resistant peptide that, together with mucins, is responsible for the rheologic properties of the tear film. This study aimed to determine whether TFF1, whose synthesis increases in inflammatory conditions such as pterygium, could protect conjunctival cells from apoptosis. METHODS. Chang conjunctival cells, either wild-type or expressing TFF1 through stable transfection, were exposed to benzalkonium chloride (BAK) and ultraviolet (UV) irradiation to trigger apoptosis. The authors used cell fractionation to detect lipid raft‐associated proteins, coimmunoprecipitation to explor…

MESH : Cell LineMESH : Chromosomes Human Pair 21Chromosomes Human Pair 21CellApoptosisMESH: Flow CytometryMESH: Caspase 8Membrane Potentials0302 clinical medicineMESH: Mitochondrial MembranesMESH: Chromosomes Human Pair 21MESH : Membrane Potentials0303 health sciencesCaspase 8MESH : Caspase 8MESH : Benzalkonium CompoundsMESH : Tumor Suppressor ProteinsChromosome MappingFas receptorFlow CytometryXIAPMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Epithelial Cells030220 oncology & carcinogenesisMitochondrial MembranesTrefoil Factor-1MESH : MitochondriaMESH : TransfectionBenzalkonium CompoundsConjunctivaMESH: Benzalkonium CompoundsProgrammed cell deathMESH: Enzyme ActivationMESH : ConjunctivaUltraviolet RaysMESH : Flow CytometryMESH: MitochondriaMESH: ConjunctivaCaspase 3BiologyInhibitor of apoptosisCaspase 8TransfectionCell Line03 medical and health sciencesMESH : Mitochondrial Membranesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansMESH: Membrane PotentialsMESH: Tumor Suppressor Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH: HumansTumor Suppressor ProteinsMESH: ApoptosisMESH: TransfectionMESH : HumansEpithelial CellsMolecular biologyMESH: Cell LineEnzyme ActivationApoptosisMESH : Ultraviolet RaysMESH: Ultraviolet RaysMESH : Enzyme ActivationMESH: Chromosome MappingMESH : ApoptosisMESH : Chromosome Mapping
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Modulation of the hepatic fatty acid pool in peroxisomal 3-ketoacyl-CoA thiolase B-null mice exposed to the selective PPARalpha agonist Wy14,643

2009

10 pages; International audience; The peroxisomal 3-ketoacyl-CoA thiolase B (Thb) gene was previously identified as a direct target gene of PPARalpha, a nuclear hormone receptor activated by hypolipidemic fibrate drugs. To better understand the role of ThB in hepatic lipid metabolism in mice, Sv129 wild-type and Thb null mice were fed or not the selective PPARalpha agonist Wy14,643 (Wy). Here, it is shown that in contrast to some other mouse models deficient for peroxisomal enzymes, the hepatic PPARalpha signaling cascade in Thb null mice was normal under regular conditions. It is of interest that the hypotriglyceridemic action of Wy was reduced in Thb null mice underlining the conclusion t…

MESH : RNA MessengerMESH: Microsomes LiverMESH : PyrimidinesMono-unsaturated fatty acids n-7 and n-9MESH : Hepatocytes[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: Mice KnockoutPPARαBiochemistryMESH: Acetyl-CoA C-AcetyltransferaseStearoyl-CoA desaturase-1MESH: HepatocytesMicechemistry.chemical_compoundMESH : Lipid MetabolismWy14MESH: AnimalsPeroxisomal 3-ketoacyl-CoA thiolase BAcetyl-CoA C-AcetyltransferaseMESH: PPAR alphaMESH : Fatty AcidsMESH: Lipid MetabolismMice Knockoutchemistry.chemical_classificationThiolaseFatty Acids643General MedicinePeroxisomeMESH : Stearoyl-CoA DesaturaseMESH: Fatty AcidsMESH : Microsomes LiverMESH : Acetyl-CoA C-AcetyltransferaseMicrosomes LiverMono-unsaturated fatty acids n-7 and n-9; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα; Stearoyl-CoA desaturase-1; Wy14643lipids (amino acids peptides and proteins)Stearoyl-CoA DesaturasePolyunsaturated fatty acidmedicine.medical_specialtyMESH : PPAR alphaMESH : Mice Inbred C57BL[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiologyMESH: Mice Inbred C57BLInternal medicineMESH : MicePeroxisomesmedicineAnimalsHumansPPAR alphaRNA MessengerMESH: MiceMESH: RNA MessengerSCP2MESH: HumansMESH : HumansFatty acid[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyStearoyl-CoALipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinMice Inbred C57BLPyrimidinesEndocrinologychemistryMESH: PyrimidinesMESH: Stearoyl-CoA DesaturaseHepatocytesMESH : Mice KnockoutMESH : AnimalsStearoyl-CoA desaturase-1MESH : PeroxisomesBiochimie
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The human near-term myometrial beta 3-adrenoceptor but not the beta 2-adrenoceptor is resistant to desensitisation after sustained agonist stimulatio…

2004

International audience; 1. In order to compare the beta(2)- and beta(3)-adrenoceptor (beta-AR) desensitisation process in human near-term myometrium, we examined the influence of a pretreatment of myometrial strips with either a beta(2)- or a beta(3)-AR agonist (salbutamol or SR 59119A, respectively, both at 10 microm, for 5 and 15 h) on the relaxation and the cyclic adenosine monophosphate (cAMP) production induced by these agonists. 2. To assess some of the mechanisms potentially implicated in the beta-AR desensitisation process, we studied the influence of such treatment on the number of beta(2)- and beta(3)-AR binding sites, the beta(2)- and beta(3)-AR transcripts expression and the pho…

MESH : Receptors Adrenergic beta-3MESH : Adrenergic beta-AgonistsMESH : Receptors Adrenergic beta-2Adrenergic beta-3 Receptor AgonistsMESH : Analysis of VarianceMESH : Dose-Response Relationship DrugMESH: Adrenergic beta-Agonists[SDV.BC]Life Sciences [q-bio]/Cellular BiologyIn Vitro TechniquesMESH: Dose-Response Relationship DrugMESH: PregnancyPregnancyMESH: Analysis of VarianceHumansMESH: Protein BindingAlbuterolMESH : FemaleMESH : AlbuterolAdrenergic beta-2 Receptor Agonists[SDV.BC] Life Sciences [q-bio]/Cellular BiologyAnalysis of VarianceMESH: HumansDose-Response Relationship Drug[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : MyometriumMESH: AlbuterolMESH : HumansMESH : Protein BindingAdrenergic beta-AgonistsMESH : PregnancyReceptors Adrenergic beta-3PapersMyometriumMESH: MyometriumFemaleReceptors Adrenergic beta-2MESH: Receptors Adrenergic beta-3MESH: Receptors Adrenergic beta-2MESH: FemaleProtein Binding
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Sodium butyrate with UCN-01 has marked antitumour activity against cervical cancer cells.

2010

The effect of combining sodium butyrate (NaB), a histone deacetylase inhibitor, and 7-hydroxy-staurosporine (UCN-01) on cytotoxicity in human cervical carcinoma cells was evaluated.HeLa and CaSki cells were treated using NaB alone or in combination with staurosporine (STS) or its analog UCN-01. Cytotoxicity was determined by flow cytometry and morphological assays. Apoptotic pathways were characterized by Western blotting and immunostaining. CaSki cells were also xenografted into nude mice to assess the in vivo effects of NaB/UCN-01 combination.Treatment with NaB and STS or UCN-01 resulted in enhanced apoptosis of cancer cells. Apoptosis involved mitochondrial pathways and overexpression of…

MESH : StaurosporineMESH : Hela CellsMESH : Antineoplastic Combined Chemotherapy Protocolshealth care facilities manpower and servicesUterine Cervical NeoplasmsMESH: ButyratesMESH: Cell CycleApoptosisMESH: Papillomavirus Infections[ SDV.CAN ] Life Sciences [q-bio]/CancerMiceAntineoplastic Combined Chemotherapy ProtocolsMESH: AnimalsMESH: Human papillomavirus 18MESH : Human papillomavirus 18MESH : Femalehealth care economics and organizationsMESH: Human papillomavirus 16MESH : Papillomavirus InfectionsHuman papillomavirus 16Human papillomavirus 18Cell CycleMESH : Mice NudeMESH: Uterine Cervical NeoplasmsMESH: Antineoplastic Combined Chemotherapy ProtocolsButyratesMESH: Cell Growth ProcessesFemaleMESH: Xenograft Model Antitumor Assaysendocrine systemMESH: Cell Line TumoreducationMESH : Uterine Cervical NeoplasmsMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerCell Growth ProcessesMESH : Xenograft Model Antitumor Assays[SDV.CAN] Life Sciences [q-bio]/CancerCell Line TumorMESH : ButyratesMESH : MiceMESH : Cell CycleMESH: Mice Nudeotorhinolaryngologic diseasesAnimalsHumansMESH: MiceMESH: HumansMESH : Cell Line TumorMESH: ApoptosisPapillomavirus InfectionsMESH : HumansMESH : Human papillomavirus 16StaurosporineXenograft Model Antitumor AssaysMESH: Hela CellsMESH : Cell Growth ProcessesMESH: StaurosporineMESH : AnimalsMESH: FemaleMESH : ApoptosisHeLa Cells
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A follow-up study of a genome-wide association scan identifies a susceptibility locus for venous thrombosis on chromosome 6p24.1.

2010

International audience; To identify genetic susceptibility factors conferring increased risk of venous thrombosis (VT), we conducted a multistage study, following results of a previously published GWAS that failed to detect loci for developing VT. Using a collection of 5862 cases with VT and 7112 healthy controls, we identified the HIVEP1 locus on chromosome 6p24.1 as a susceptibility locus for VT. Indeed, the HIVEP1 rs169713C allele was associated with an increased risk for VT, with an odds ratio of 1.20 (95% confidence interval 1.13-1.27, p = 2.86 x 10(-9)). HIVEP1 codes for a protein that participates in the transcriptional regulation of inflammatory target genes by binding specific DNA …

MESH : Transcription Factors[SDV]Life Sciences [q-bio]Genome-wide association study030204 cardiovascular system & hematologyMESH : Chromosomes Human Pair 60302 clinical medicineGenetics(clinical)Genetics (clinical)GeneticsVenous Thrombosis0303 health sciencesMESH: Polymorphism Single NucleotideMESH : Polymorphism Single NucleotideMESH: Genetic Predisposition to DiseaseMESH: Follow-Up StudiesMESH: Transcription FactorsMESH : Venous ThrombosisMESH: Case-Control StudiesDNA-Binding ProteinsChromosomes Human Pair 6MESH : DNA-Binding ProteinsErratumMESH : Genome-Wide Association StudyMESH : Case-Control StudiesMESH: Chromosomes Human Pair 6Locus (genetics)BiologyPolymorphism Single NucleotideGenetic determinism03 medical and health sciencesReportGenetic predispositionGeneticsHumansGenetic Predisposition to DiseaseAlleleGene030304 developmental biologyMESH: Humans[ SDV ] Life Sciences [q-bio]MESH : Humanslinking inflammation protein atherothrombosis sequence riskCase-control studyChromosomeMESH : Follow-Up StudiesCase-Control StudiesMESH: Genome-Wide Association StudyMESH: Venous ThrombosisMESH : Genetic Predisposition to Disease030217 neurology & neurosurgeryMESH: DNA-Binding ProteinsFollow-Up StudiesGenome-Wide Association StudyTranscription Factors
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Comparison of different segmentation approaches without using gold standard. Application to the estimation of the left ventricle ejection fraction fr…

2011

International audience; A statistical method is proposed to compare several estimates of a relevant clinical parameter when no gold standard is available. The method is illustrated by considering the left ventricle ejection fraction derived from cardiac magnetic resonance images and computed using seven approaches with different degrees of automation. The proposed method did not use any a priori regarding with the reliability of each method and its degree of automation. The results showed that the most accurate estimates of the ejection fraction were obtained using manual segmentations, followed by the semiautomatic methods, while the methods with the least user input yielded the least accu…

MESH : Ventricular Function Left[ INFO.INFO-TS ] Computer Science [cs]/Signal and Image Processing[INFO.INFO-TS] Computer Science [cs]/Signal and Image Processing[ SPI.SIGNAL ] Engineering Sciences [physics]/Signal and Image processing02 engineering and technologyMESH: Regression AnalysisVentricular Function LeftArticleMESH: Ventricular Function Left030218 nuclear medicine & medical imagingMESH: Magnetic Resonance Imaging03 medical and health sciencesMESH : Heart0302 clinical medicine[INFO.INFO-TS]Computer Science [cs]/Signal and Image ProcessingMESH : Magnetic Resonance ImagingMESH : Regression Analysis0202 electrical engineering electronic engineering information engineeringHumansMedicineSegmentation[ SDV.IB ] Life Sciences [q-bio]/BioengineeringReliability (statistics)[SPI.SIGNAL] Engineering Sciences [physics]/Signal and Image processing[SDV.IB] Life Sciences [q-bio]/BioengineeringEjection fractionMESH: Humansbusiness.industryMESH : HumansHeartRegression analysisPattern recognitionImage segmentationGold standard (test)Magnetic Resonance ImagingMESH: Heartmedicine.anatomical_structureVentricleRegression AnalysisA priori and a posteriori020201 artificial intelligence & image processing[SDV.IB]Life Sciences [q-bio]/BioengineeringArtificial intelligencebusinessNuclear medicine[SPI.SIGNAL]Engineering Sciences [physics]/Signal and Image processing
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