Search results for "MESH : Humans"

showing 10 items of 113 documents

Very preterm birth: who has access to antenatal corticosteroid therapy?

2010

International audience; We describe the administration of antenatal corticosteroid therapy (ACT) for liveborn very preterm neonates in a population-based study. A total of 790 very preterm neonates (between 24 and 31 full weeks of gestation) were included in this regionally defined population of very preterm neonates in France. The main outcome measure was non-access to ACT. Data were analysed using logistic and polytomous models to control for neonatal and sociodemographic characteristics, mechanisms of very preterm birth and neonatal network organisation. As compared with level III, births in levels I-II maternity units were closely related to non-access to ACT (60.1% vs. 8.8%), but not t…

Gestational hypertensionPediatricsEpidemiologyMESH: Logistic ModelsHealth Services AccessibilityInfant Newborn Diseases[ SDV.CAN ] Life Sciences [q-bio]/CancerCohort Studies0302 clinical medicineMESH: PregnancyMESH : Health Services AccessibilityMESH: Risk FactorsAdrenal Cortex HormonesPregnancyRisk FactorsMESH: Maternal Health ServicesMESH : Socioeconomic FactorsMedicineChildbirthRupture of membranesMESH : FemaleMESH: Cohort StudiesMESH : Infant Newborn Diseaseseducation.field_of_studyMESH: Health Services Accessibility030219 obstetrics & reproductive medicineMESH: Middle AgedObstetricsMESH: Infant NewbornSmokingAge FactorsMiddle AgedMESH : AdultMESH : Risk Factors3. Good healthMESH : SmokingMESH : Infant PrematureMESH: Young AdultGestationFemaleFranceInfant PrematureMESH: Infant PrematureAdultmedicine.medical_specialtyMESH: SmokingMESH: Socioeconomic FactorsReferralAdolescentPopulationMESH : Young AdultMESH : Cohort StudiesMESH: Infant Newborn Diseases[SDV.CAN]Life Sciences [q-bio]/CancerMESH : Infant NewbornMESH: Adrenal Cortex HormonesMESH : Adrenal Cortex Hormones03 medical and health sciencesYoung Adult030225 pediatricsMESH : AdolescentVery Preterm BirthHumansMaternal Health ServicesMESH : Middle AgededucationMESH : FranceMESH: AdolescentMESH: Age FactorsPregnancyMESH: Humansbusiness.industryMESH : HumansInfant NewbornMESH: Adultmedicine.diseaseMESH: FranceMESH : PregnancyLogistic ModelsSocioeconomic FactorsPediatrics Perinatology and Child HealthMESH : Age FactorsbusinessMESH: FemaleMESH : Maternal Health ServicesMESH : Logistic Models
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Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

2014

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibros…

LipopolysaccharidesMESH: Signal TransductionMESH: InflammationMESH : Toll-Like Receptor 4Adipose tissueMESH : AdipocytesMESH : LipopolysaccharidesMicechemistry.chemical_compoundFibrosisAdipocyteAdipocytes[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: ObesityMESH: Animalslcsh:QH301-705.5Mice Inbred C3HToll-like receptorMESH : Diet High-FatMESH: Toll-Like Receptor 43. Good healthMESH: Insulin ResistanceAdipose TissueMESH: FibrosisMESH : Fibrosis[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : ObesityMESH : Insulin ResistanceMESH: Adipose TissueSignal Transductionmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyAdipose tissue macrophagesBiologyDiet High-FatMESH : Adipose TissueGeneral Biochemistry Genetics and Molecular BiologyImmune systemMESH : Mice Inbred C3HInternal medicineMESH : MicemedicineAnimalsHumansObesityMESH: Mice Inbred C3HMESH: MiceMESH: AdipocytesInflammationMESH : Signal TransductionMESH : InflammationMESH: HumansMESH : EndotoxemiaMESH : Humans3T3-L1medicine.diseaseFibrosisMESH : Disease Models AnimalEndotoxemiaToll-Like Receptor 4Disease Models AnimalMESH: Diet High-FatEndocrinologylcsh:Biology (General)chemistryMESH: EndotoxemiaMESH : AnimalsInsulin ResistanceMESH: Disease Models AnimalMESH: LipopolysaccharidesAdipocyte hypertrophyCell Reports
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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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[Postural balance following stroke: towards a disadvantage of the right brain-damaged hemisphere].

1999

International audience; In the light of studies published in the last ten years, we have suspected a differential influence of the sides of hemispheric cerebral lesions on posture and balance. A study was aimed at verifying this hypothesis, the method of which being original because many possible confounding factors such as age, sex as well as topography and size of the brain lesion have been taken into account in the statistical analysis. Inclusion criteria were: right-handed patients, first stroke, no previous disease which might have affected balance. Their postural abilities (ranging from 0 to 36) were assessed 90 +/- 3 days after stroke onset on a clinical scale. This clinical assessme…

MESH : MaleMESH : HumansMESH : AgedMESH : PostureMESH : Visual Fields[ SDV.NEU.SC ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive SciencesMESH : Vision DisordersMESH : BrainMESH : Postural BalanceMESH : Brain IschemiaMESH : Severity of Illness IndexMESH : FemaleMESH : Middle AgedMESH : Aged 80 and overMESH : Functional Laterality[SDV.NEU.SC] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences
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Resveratrol: preventing properties against vascular alterations and ageing.

2005

International audience; Cardiovascular diseases are the leading cause of death in developed countries where the common pathological substrate underlying this process is atherosclerosis. Several new concepts have emerged in relation to mechanisms that contribute to the regulation of the vascular diseases and associated inflammatory effects. Recently, potential antioxidants (vitamin E, polyphenols) have received much attention as potential anti-atherosclerotic agents. Among the polyphenols with health benefic properties, resveratrol, a phytoalexin of grape, seem to be a good candidate protecting the vascular walls from oxidation, inflammation, platelet aggregation, and thrombus formation. In …

MESH : Oxidative StressAgingAntioxidantPlatelet AggregationArteriosclerosismedicine.medical_treatmentResveratrolPharmacologymedicine.disease_causeMuscle Smooth Vascularchemistry.chemical_compoundMESH : VasodilationMESH : Foam CellsMESH : Platelet AggregationStilbenesMESH : Cardiovascular DiseasesMESH : Macrophageschemistry.chemical_classificationNeovascularization PathologicPhytoalexinfood and beveragesVasodilationBiochemistryCardiovascular Diseasesmedicine.symptomBiotechnologyLipoproteinsInflammationHealth PromotionMESH : LipoproteinsBiologyMESH : StilbenesMESH : ArteriosclerosismedicineHumans[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyReactive oxygen speciesMechanism (biology)MacrophagesMESH : HumansMESH : Neovascularization PathologicMESH : Muscle Smooth VascularMESH : AgingOxidative StresschemistryAgeingResveratrolMESH : Health PromotionOxidative stressFood ScienceFoam Cells
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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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