Search results for " anemia"

showing 10 items of 128 documents

Efficacy and Safety of Elbasvir/Grazoprevir in Patients with Chronic Hepatitis C Virus Infection and Inherited Blood Disorders: Final Data from the C…

2016

Abstract Background: Complications from chronic hepatitis C virus (HCV) infection are a major cause of morbidity and mortality among individuals with inherited blood disorders (IBLD). Inability to tolerate ribavirin and frequent comorbidities have limited HCV treatment options in these patients. The aim of the C-EDGE IBLD study was to evaluate the efficacy and safety of a once-daily, fixed-dose combination of elbasvir 50 mg (EBR, an NS5A inhibitor) and grazoprevir 100 mg (GZR, an NS3/4A protease inhibitor) in patients with HCV infection and IBLD, including those with hemoglobinopathies. Methods: C-EDGE-IBLD was a randomized, double-blind, placebo-controlled study of treatment-naïve and trea…

0301 basic medicineElbasvirbusiness.industryRibavirinImmunologyCell BiologyHematologyHepatitis Cmedicine.diseaseBiochemistryVirologySickle cell anemiaVirus03 medical and health scienceschemistry.chemical_compound030104 developmental biologyBlood DisorderchemistryGrazoprevirmedicineElbasvir GrazoprevirbusinessBlood
researchProduct

Visualising G-quadruplex DNA dynamics in live cells by fluorescence lifetime imaging microscopy

2020

Guanine rich regions of oligonucleotides fold into quadruple-stranded structures called G-quadruplexes (G4s). Increasing evidence suggests that these G4 structures form in vivo and play a crucial role in cellular processes. However, their direct observation in live cells remains a challenge. Here we demonstrate that a fluorescent probe (DAOTA-M2) in conjunction with fluorescence lifetime imaging microscopy (FLIM) can identify G4s within nuclei of live and fixed cells. We present a FLIM-based cellular assay to study the interaction of non-fluorescent small molecules with G4s and apply it to a wide range of drug candidates. We also demonstrate that DAOTA-M2 can be used to study G4 stability i…

0301 basic medicineFluorescence-lifetime imaging microscopyIndolesIntravital MicroscopyGuanineScienceGeneral Physics and Astronomy010402 general chemistryG-quadruplex01 natural sciencesGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health scienceschemistry.chemical_compoundMiceCell Line TumorAnimalsHumans030304 developmental biologyFluorescent Dyes0303 health sciencesMultidisciplinaryChemistryOligonucleotideCellular AssayQDNA HelicasesGeneral ChemistryDNAFibroblastsFluorescenceSmall moleculeChemical biologyFanconi Anemia Complementation Group Proteins0104 chemical sciencesMolecular ImagingG-QuadruplexesDNA helicase activity030104 developmental biologyMicroscopy FluorescenceGene Knockdown TechniquesBiophysicsFluorescent probesMolecular imagingRNA HelicasesNature Communications
researchProduct

FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
researchProduct

Paroxysmal nocturnal haemoglobinuria: When delay in diagnosis and long therapy occurs

2017

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare clonal disorder characterized by hemolytic anemia, bone marrow failure and thrombosis, caused by a somaticmutation in PIG-A gene that results in theabsence of CD55 and CD59, two important complement regulatory proteins. In thispaper, a case of PNH is retrospectively examined looking for clinical and laboratory features, and the entire course of the disease from the onset of the symptoms isdescribed, together with an adequate follow-up over a 7-years treatment period. Inthis case, the not specificity and the limited clinical relevance of the symptoms led to adelay in diagnosis. After thrombosis, Eculizumab therapy has been shown to be effec…

0301 basic medicineHemolytic anemiaPediatricsmedicine.medical_specialtyrenal failureParoxysmal nocturnal haemoglobinuriaparoxysmal nocturnal hemoglobinuriaCase ReportDiseaseCD5903 medical and health sciencesthrombotic eventshemic and lymphatic diseasesMedicineClinical significancebusiness.industrylcsh:RC633-647.5Bone marrow failureHematologylcsh:Diseases of the blood and blood-forming organsEculizumabEculizumabmedicine.diseaseThrombosisparoxysmal nocturnal hemoglo-binuria thrombotic events renal failure Eculizumab030104 developmental biologyParoxysmal nocturnal hemoglobinuriabusinessmedicine.drug
researchProduct

Responses of Saccharomyces cerevisiae Strains from Different Origins to Elevated Iron Concentrations

2015

ABSTRACT Iron is an essential micronutrient for all eukaryotic organisms. However, the low solubility of ferric iron has tremendously increased the prevalence of iron deficiency anemia, especially in women and children, with dramatic consequences. Baker's yeast Saccharomyces cerevisiae is used as a model eukaryotic organism, a fermentative microorganism, and a feed supplement. In this report, we explore the genetic diversity of 123 wild and domestic strains of S. cerevisiae isolated from different geographical origins and sources to characterize how yeast cells respond to elevated iron concentrations in the environment. By using two different forms of iron, we selected and characterized bot…

0301 basic medicineIronMicroorganismSaccharomyces cerevisiaeAnaemiaSaccharomyces cerevisiaeOxidative phosphorylationBiologymedicine.disease_causeApplied Microbiology and BiotechnologyEnvironmentalMicrobiology03 medical and health sciencesEnvironmental Microbiologymedicine030102 biochemistry & molecular biologyEcologyGene Expression ProfilingQR MicrobiologyIron deficiencymedicine.diseaseMicronutrientbiology.organism_classificationYeastOxidative Stress030104 developmental biologyBiochemistryIron-deficiency anemiaOxidative stressFood ScienceBiotechnologyApplied and Environmental Microbiology
researchProduct

Re-definition and supporting evidence toward Fanconi Anemia as a mitochondrial disease: Prospects for new design in clinical management

2021

Fanconi anemia (FA) has been investigated since early studies based on two definitions, namely defective DNA repair and proinflammatory condition. The former definition has built up the grounds for FA diagnosis as excess sensitivity of patients' cells to xenobiotics as diepoxybutane and mitomycin C, resulting in typical chromosomal abnormalities. Another line of studies has related FA phenotype to a prooxidant state, as detected by both in vitro and ex vivo studies. The discovery that the FA group G (FANCG) protein is found in mitochondria (Mukhopadhyay et al., 2006) has been followed by an extensive line of studies providing evidence for multiple links between other FA gene products and mi…

0301 basic medicineMitochondrial DNAMitochondrial DiseasesMitomycinMitochondrial diseaseClinical BiochemistryDiepoxybutaneReview ArticleMitochondrionBiologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaFANCGmedicineHumansClastogenCarnitinelcsh:QH301-705.5Coenzyme Q10lcsh:R5-920ProteinOrganic ChemistryMitochondrial nutrientProteinsmedicine.diseaseMitochondrial diseaseFanconi AnemiaPhenotypeClastogens030104 developmental biologylcsh:Biology (General)chemistryProoxidant stateCancer researchMitochondrial nutrientsMitochondrial dysfunctionlcsh:Medicine (General)030217 neurology & neurosurgeryHumanmedicine.drugRedox Biology
researchProduct

Mitoprotective Clinical Strategies in Type 2 Diabetes and Fanconi Anemia Patients: Suggestions for Clinical Management of Mitochondrial Dysfunction

2020

Oxidative stress (OS) and mitochondrial dysfunction (MDF) occur in a number of disorders, and several clinical studies have attempted to counteract OS and MDF by providing adjuvant treatments against disease progression. The present review is aimed at focusing on two apparently distant diseases, namely type 2 diabetes (T2D) and a rare genetic disease, Fanconi anemia (FA). The pathogenetic links between T2D and FA include the high T2D prevalence among FA patients and the recognized evidence for OS and MDF in both disorders. This latter phenotypic/pathogenetic feature—namely MDF—may be regarded as a mechanistic ground both accounting for the clinical outcomes in both diseases, and…

0301 basic medicinePhysiologymedicine.medical_treatmentClinical Biochemistrymitochondrial nutrientsDiseaseType 2 diabetesReviewBioinformaticsmedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoFanconi anemiamitochondrial dysfunctionmedicineoxidative stressMolecular Biologyfanconi anemiaCoenzyme Q10business.industrylcsh:RM1-950Mitochondrial nutrientCell Biologymedicine.diseasePhenotype030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisOxidative stretype 2 diabetesbusinessAdjuvantOxidative stressAntioxidants
researchProduct

Molecular strategies to increase yeast iron accumulation and resistance.

2018

All eukaryotic organisms rely on iron as an essential micronutrient for life because it participates as a redox-active cofactor in multiple biological processes. However, excess iron can generate reactive oxygen species that damage cellular macromolecules. The low solubility of ferric iron at physiological conditions increases the prevalence of iron deficiency anemia. A common strategy to treat iron deficiency consists of dietary iron supplementation. The baker’s yeast Saccharomyces cerevisiae is used as a model eukaryotic organism, but also as a feed supplement. In response to iron deficiency, the yeast Aft1 transcription factor activates cellular iron acquisition. However, when constituti…

0301 basic medicineSaccharomyces cerevisiae ProteinsTranscription GeneticIronSaccharomyces cerevisiaeBiophysicsSaccharomyces cerevisiaeBiochemistryCofactorBiomaterials03 medical and health sciencesFet3Gene Expression Regulation FungalCth2medicineBaker’s yeastYpk1Transcription factorAlleleschemistry.chemical_classificationReactive oxygen speciesbiologyKinaseIron deficiencyRespirationMetals and AlloysIron deficiencybiology.organism_classificationmedicine.diseaseYeastCell biologyIron toxicity030104 developmental biologychemistryIron-deficiency anemiaChemistry (miscellaneous)biology.proteinAft1Metallomics : integrated biometal science
researchProduct

The severe phenotype of Diamond-Blackfan anemia is modulated by heat shock protein 70.

2017

International audience; Diamond-Blackfan anemia (DBA) is a rare congenital bone marrow failure syndrome that exhibits an erythroid-specific phenotype. In at least 70% of cases, DBA is related to a haploinsufficient germ line mutation in a ribosomal protein (RP) gene. Additional cases have been associated with mutations in GATA1. We have previously established that the RPL11+/Mut phenotype is more severe than RPS19+/Mut phenotype because of delayed erythroid differentiation and increased apoptosis of RPL11+/Mut erythroid progenitors. The HSP70 protein is known to protect GATA1, the major erythroid transcription factor, from caspase-3 mediated cleavage during normal erythroid differentiation.…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesIdentificationApoptosis-Inducing FactorGata1 MutationsInhibits ApoptosisBiologyHsp7003 medical and health sciencesGermline mutationRed Cells Iron and Erythropoiesishemic and lymphatic diseasesmedicine[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyNuclear ImportErythropoiesisDiamond–Blackfan anemiaHuman ErythroblastsBone marrow failure[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyGATA1Hematologymedicine.diseasePhenotypeMolecular biology3. Good healthHsp70030104 developmental biologyRibosomal-ProteinsProtein Gene DeletionsErythropoiesisHaploinsufficiencyBlood advances
researchProduct

Type 1 diabetes associated autoimmunity.

2016

Diabetes mellitus is increasing in prevalence worldwide. The economic costs are considerable given the cardiovascular complications and co-morbidities that it may entail. Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the loss of insulin-producing pancreatic β-cells. The pathogenesis of T1D is complex and multifactorial and involves a genetic susceptibility that predisposes to abnormal immune responses in the presence of ill-defined environmental insults to the pancreatic islets. Genetic background may affect the risk for autoimmune disease and patients with T1D exhibit an increased risk of other autoimmune disorders such as autoimmune thyroid disease, Addison's dise…

0301 basic medicineendocrine systemendocrine system diseasesAutoimmune GastritisImmunology030209 endocrinology & metabolismAutoimmunityVitiligoDiseasemedicine.disease_causeCoeliac diseaseAutoimmunity03 medical and health sciencesIslets of LangerhansMice0302 clinical medicineImmunology and AllergyMedicineAnimalsHumansGenetic Predisposition to Diseasepernicious anemiaAutoimmune diseaseType 1 diabetesbusiness.industrymedicine.disease030104 developmental biologyDiabetes Mellitus Type 1Organ SpecificityImmunologybusinessAutoimmunity reviews
researchProduct