Search results for "Red"

showing 10 items of 23890 documents

Cardiac regenerative capacity is age- and disease-dependent in childhood heart disease

2018

Objective We sought to define the intrinsic stem cell capacity in pediatric heart lesions, and the effects of diagnosis and of age, in order to inform evidence-based use of potential autologous stem cell sources for regenerative medicine therapy. Methods Ventricular explants derived from patients with hypoplastic left heart syndrome (HLHS), tetralogy of Fallot (TF), dilated cardiomyopathy (DCM) and ventricular septal defect (VSD) were analyzed following standard in vitro culture conditions, which yielded cardiospheres (C-spheres), indicative of endogenous stem cell capacity. C-sphere counts generated per 5 mm3 tissue explant and the presence of cardiac progenitor cells were correlated to pa…

0301 basic medicineHeart Septal Defects VentricularAgingHeart diseaseCell TransplantationCardiovascular Proceduresmedicine.medical_treatmentCardiomyopathylcsh:Medicine030204 cardiovascular system & hematologyBiochemistryHypoplastic left heart syndromeTissue Culture TechniquesElectrocardiography0302 clinical medicineAnimal CellsHeart RegenerationHypoplastic Left Heart SyndromeNeurobiology of Disease and RegenerationMedicine and Health SciencesMorphogenesisBlood and Lymphatic System ProceduresMyocytes CardiacChildlcsh:ScienceCells CulturedTetralogy of FallotMultidisciplinaryStem CellsStem Cell TherapyDilated cardiomyopathyHeartStem-cell therapyCardiac Transplantationmedicine.anatomical_structureNeurologyChild PreschoolCardiologyTetralogy of Fallotcardiovascular systemStem cellCellular TypesAnatomyResearch ArticleCardiomyopathy Dilatedmedicine.medical_specialtyAdolescentHeart VentriclesSurgical and Invasive Medical Procedures03 medical and health sciencesInternal medicinemedicineHumansRegenerationVimentincardiovascular diseasesClinical GeneticsTransplantationbusiness.industrylcsh:RInfant NewbornCorrectionInfantBiology and Life SciencesProteinsMesenchymal Stem CellsCell BiologyOrgan Transplantationmedicine.diseaseCytoskeletal Proteins030104 developmental biologyVentricleCardiovascular Anatomylcsh:QbusinessOrganism DevelopmentDevelopmental BiologyStem Cell TransplantationPLoS ONE
researchProduct

Disentangling the effect of host genetics and gut microbiota on resistance to an intestinal parasite

2019

11 pages; International audience; Resistance to infection is a multifactorial trait, and recent work has suggested that the gut microbiota can also contribute to resistance. Here, we performed a fecal microbiota transplant to disentangle the contribution of the gut microbiota and host genetics as drivers of resistance to the intestinal nematode Heligmosomoides polygyrus. We transplanted the microbiota of a strain of mice (SJL), resistant to H. polygyrus, into a susceptible strain (CBA) and vice-versa. We predicted that if the microbiota shapes resistance to H. polygyrus, the FMT should reverse the pattern of resistance between the two host strains. The two host strains had different microbi…

0301 basic medicineHeligmosomoides polygyrusGut floramedicine.disease_causeFecal microbiota transplant0302 clinical medicinefluids and secretionsMESH: Fecal Microbiota TransplantationParasite hostingColonizationMESH: AnimalsMESH: Strongylida InfectionsDisease ResistanceGeneticsNematospiroides dubiusbiology[SDV.BA]Life Sciences [q-bio]/Animal biologyFecal Microbiota Transplantation3. Good healthInfectious DiseasesMESH: Nematospiroides dubiusGenetic Background030231 tropical medicineIntestinal parasiteHeterologousMice Inbred StrainsMESH: Disease ResistanceMESH: Host-Parasite InteractionsMESH: Mice Inbred Strainsdigestive systemMESH: Gastrointestinal MicrobiomeHost-Parasite Interactions03 medical and health sciencesImmunityparasitic diseasesmedicineAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyStrongylida InfectionsHost (biology)ImmunityLife history traitsMESH: Genetic Backgroundbiology.organism_classificationGastrointestinal MicrobiomeDisease Models Animalstomatognathic diseases030104 developmental biologyParasitologyHeligmosomoides polygyrusMESH: Disease Models Animal[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
researchProduct

Effects of Plant Sterols or β-Cryptoxanthin at Physiological Serum Concentrations on Suicidal Erythrocyte Death.

2018

The eryptotic and hemolytic effects of a phytosterol (PS) mixture (β-sitosterol, campesterol, stigmasterol) or β-cryptoxanthin (β-Cx) at physiological serum concentration and their effect against oxidative stress induced by tert-butylhydroperoxide (tBOOH) (75 and 300 μM) were evaluated. β-Cryptoxanthin produced an increase in eryptotic cells, cell volume, hemolysis, and glutathione depletion (GSH) without ROS overproduction and intracellular Ca2+influx. Co-incubation of both bioactive compounds protected against β-Cx-induced eryptosis. Under tBOOH stress, PS prevented eryptosis, reducing Ca2+influx, ROS overproduction and GSH depletion at 75 μM, and hemolysis at both tBOOH concentrations. β…

0301 basic medicineHemolysiErythrocytesCampesterolBeta-CryptoxanthinEryptosisStigmasterolPharmacologymedicine.disease_causeHemolysisβ-cryptoxanthin03 medical and health scienceschemistry.chemical_compound0302 clinical medicinetert-ButylhydroperoxidemedicineHumansCells Culturedphytosteroloxidative streStigmasterolChemistryCholesterolPhytosterolChemistry (all)PhytosterolsGeneral ChemistryGlutathionemedicine.diseaseSitosterolGlutathioneSitosterolsHemolysisErythrocyteOxidative Stress030104 developmental biologyCholesterolAgricultural and Biological Sciences (all)030220 oncology & carcinogenesiseryptosiGeneral Agricultural and Biological SciencesIntracellularOxidative stressHumanJournal of agricultural and food chemistry
researchProduct

The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans

2020

Hepatitis B virus (HBV) infection causes a self-limiting disease in most individuals. However, < 10% of infected subjects develop a chronic disease. Genetic host variability of polymorphic genes at the interface of innate and acquired immunity, such as killer immunoglobulin-like receptors (KIR), their human leucocyte antigen (HLA) and IgG allotypes (GM), could explain this different clinical picture. We previously showed a protective role of the KIR2DL3 gene for the development of chronic hepatitis B (CHB), and a detrimental role of the KIR ligand groups, HLA-A-Bw4 and HLA-C2. We have expanded the previous analysis genotyping patients for GM23 and GM3/17 allotypes. The comparison of the …

0301 basic medicineHepatitis B virusKIR LigandImmunologyhepatitis B viruHuman leukocyte antigenHLA-C Antigensmedicine.disease_causeRisk Assessment03 medical and health sciences0302 clinical medicineHepatitis B ChronicGene FrequencyImmunoglobulin Gm AllotypesRisk Factorskiller immunoglobulin-like receptorImmunology and AllergyMedicineHumansGenetic Predisposition to DiseaseGenotypingHepatitis B virusSettore MED/04 - Patologia Generalebiologybusiness.industryOriginal ArticlesProtective FactorsAcquired immune systemAllotypeγ marker030104 developmental biologyPhenotypeHLA-B AntigensReceptors KIR2DL3Case-Control StudiesImmunologyHost-Pathogen Interactionsbiology.proteinGene polymorphismAntibodyhepatitis B virus; human leucocyte antigen; killer immunoglobulin-like receptor; ? markerbusiness030215 immunologyhuman leucocyte antigen
researchProduct

Hepatitis B Virus Exploits ERGIC-53 in Conjunction with COPII to Exit Cells.

2020

Several decades after its discovery, the hepatitis B virus (HBV) still displays one of the most successful pathogens in human populations worldwide. The identification and characterization of interactions between cellular and pathogenic components are essential for the development of antiviral treatments. Due to its small-sized genome, HBV highly depends on cellular functions to produce and export progeny particles. Deploying biochemical-silencing methods and molecular interaction studies in HBV-expressing liver cells, we herein identified the cellular ERGIC-53, a high-mannose-specific lectin, and distinct components of the endoplasmic reticulum (ER) export machinery COPII as crucial factor…

0301 basic medicineHepatitis B virusSec24AEndosomeHBV assemblyVesicular Transport ProteinsN-glycosylationBiologymedicine.disease_causeEndoplasmic ReticulumTransfectionGenomeESCRTArticle03 medical and health sciencesN-linked glycosylationViral life cycleCell Line TumormedicineHBVHumansCOPIICOPIIlcsh:QH301-705.5Hepatitis B virus030102 biochemistry & molecular biologyEndosomal Sorting Complexes Required for TransportEndoplasmic reticulumVirionMembrane ProteinsGeneral MedicineHepatitis BHBV egressERGIC-53Cell biologyProtein Transport030104 developmental biologyMannose-Binding Lectinslcsh:Biology (General)HepatocytesLMAN-1COP-Coated VesiclesCells
researchProduct

Novel deletion in 11p15.5 imprinting center region 1 in a patient with Beckwith-Wiedemann syndrome provides insight into distal enhancer regulation a…

2016

Background Beckwith–Wiedemann syndrome (BWS) is an early-onset overgrowth disorder with a high risk for embryonal tumors. It is mainly caused by dysregulation of imprinted genes on chromosome 11p15.5; however, the driving forces in the development of tumors are not fully understood. Procedure We report on a female patient presenting with macrosomia, macroglossia, organomegaly and extensive bilateral nephroblastomatosis. Adjuvant chemotherapy was initiated; however, the patient developed hepatoblastoma and Wilms tumor at 5 and 12 months of age, respectively. Subsequent radiofrequency ablation of the liver tumor and partial nephrectomy followed by consolidation therapy achieved complete remis…

0301 basic medicineHepatoblastomaPathologymedicine.medical_specialtyBeckwith-Wiedemann SyndromeBeckwith–Wiedemann syndrome030105 genetics & hereditymedicine.disease_cause03 medical and health sciencesGenomic ImprintingInsulin-Like Growth Factor IIMacroglossiaMedicineHumansImprinting (psychology)NephroblastomatosisSequence Deletionbusiness.industryChromosomes Human Pair 11Infant NewbornWilms' tumorHematologyDNA Methylationmedicine.diseasePrognosis030104 developmental biologyCell Transformation NeoplasticPhenotypeOncologyPediatrics Perinatology and Child HealthCancer researchFemalemedicine.symptombusinessGenomic imprintingCarcinogenesisPediatric bloodcancer
researchProduct

Oxidative Stress-Induced Axon Fragmentation Is a Consequence of Reduced Axonal Transport in Hereditary Spastic Paraplegia SPAST Patient Neurons

2020

Hereditary spastic paraplegia (HSP) is a group of inherited disorders characterized by progressive spasticity and paralysis of the lower limbs. Autosomal dominant mutations in SPAST gene account for ∼40% of adult-onset patients. We have previously shown that SPAST patient cells have reduced organelle transport and are therefore more sensitive to oxidative stress. To test whether these effects are present in neuronal cells, we first generated 11 induced pluripotent stem (iPS) cell lines from fibroblasts of three healthy controls and three HSP patients with different SPAST mutations. These cells were differentiated into FOXG1-positive forebrain neurons and then evaluated for multiple aspects …

0301 basic medicineHereditary spastic paraplegiaOxidative phosphorylationSpastinmedicine.disease_causelcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASTAxonFragmentation (cell biology)hereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGeneral Neuroscienceperoxisomesaxon transportmedicine.diseaseepothilone Daxon degenerationCell biology030104 developmental biologymedicine.anatomical_structurenervous systemForebrainAxoplasmic transport030217 neurology & neurosurgeryOxidative stressFrontiers in Neuroscience
researchProduct

Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
researchProduct

DNA multigene characterization of Fasciola hepatica and Lymnaea neotropica and its fascioliasis transmission capacity in Uruguay, with historical cor…

2017

Background Fascioliasis is a pathogenic disease transmitted by lymnaeid snails and recently emerging in humans, in part due to effects of climate changes, anthropogenic environment modifications, import/export and movements of livestock. South America is the continent presenting more human fascioliasis hyperendemic areas and the highest prevalences and intensities known. These scenarios appear mainly linked to altitude areas in Andean countries, whereas lowland areas of non-Andean countries, such as Uruguay, only show sporadic human cases or outbreaks. A study including DNA marker sequencing of fasciolids and lymnaeids, an experimental study of the life cycle in Uruguay, and a review of hum…

0301 basic medicineHeredityPhysiologySnailsHelminth geneticsMoltingGeographical locationslaw.invention0302 clinical medicinelawRNA Ribosomal 16SMedicine and Health SciencesCluster AnalysisPhylogenyGalba truncatulaMammalsbiologyEcologylcsh:Public aspects of medicineAgricultureRuminants030108 mycology & parasitologyDNA HelminthGenetic MappingInfectious DiseasesTransmission (mechanics)Helminth InfectionsVertebratesResearch ArticleNeglected Tropical DiseasesMitochondrial DNAFascioliasisLivestocklcsh:Arctic medicine. Tropical medicineGenotypelcsh:RC955-962030231 tropical medicineDNA RibosomalRisk Assessment03 medical and health sciencesHepaticaBovinesAcanthaceaeDNA Ribosomal Spacerparasitic diseasesGeneticsParasitic DiseasesFasciola hepaticaAnimalsHumansHorsesSheepPublic Health Environmental and Occupational HealthOrganismsOutbreakGenetic VariationBiology and Life Scienceslcsh:RA1-1270Sequence Analysis DNAMolluscsParasitologia veterinàriaFasciola hepaticaSouth Americabiology.organism_classificationTropical DiseasesInvertebratesHaplotypesGastropodsVector (epidemiology)AmniotesUruguayCattlePeople and placesBestiarPhysiological ProcessesPLoS Neglected Tropical Diseases
researchProduct

Clinical and hormonal characteristics in heterozygote carriers of congenital adrenal hyperplasia

2020

Abstract Non-classical congenital adrenal hyperplasia (NC-CAH) includes a group of genetic disorders due to a broad class of CYP21A2 variants identifying a disease-causing ‘C’ genotype. The heterozygous carriers of CYP21 mutations are at increased risk of developing clinically evident hyperandrogenism, even though clinical and laboratory characteristics are still underestimated. With the aim of obtaining a more accurate delineation of the phenotype of heterozygous carrier of CAH, we analyzed clinical, biochemical and molecular characteristics in a cohort of Sicilian subjects. Fifty-seven females with biallelic and monoallelic CYP21A2 variants classifying NC-CAH (24) and heterozygous carrier…

0301 basic medicineHirsutismHydrocortisoneendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryPhysiologyOverweighturologic and male genital diseasesBiochemistrySettore MED/13 - Endocrinologia0302 clinical medicineEndocrinologySettore BIO/10 - BiochimicaGenotypeMedicineChildhirsutismPolycystic ovaryfemale genital diseases and pregnancy complications030220 oncology & carcinogenesisCohortMolecular MedicineFemalemedicine.symptomAdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAdolescentYoung Adult03 medical and health sciencesHumansCongenital adrenal hyperplasiaMolecular BiologyHeterozygous carrierAdrenal Hyperplasia Congenitalbusiness.industryHyperandrogenismCongenital adrenal hyperplasianutritional and metabolic diseasesHeterozygote advantageCell BiologyOverweightmedicine.diseaseOligomenorrhea17OHProgesterone deficiency030104 developmental biologyMutationSteroid 21-HydroxylaseHyperandrogenismbusinessThe Journal of Steroid Biochemistry and Molecular Biology
researchProduct