Search results for "Eos"

showing 10 items of 2714 documents

Differential staining of peripheral nuclear chromatin with Acridine orange implies an A-form epichromatin conformation of the DNA

2018

ABSTRACT The chromatin observed by conventional electron microscopy under the nuclear envelope constitutes a single layer of dense 30–35 nm granules, while ∼30 nm fibrils laterally attached to them, form large patches of lamin-associated domains (LADs). This particular surface “epichromatin” can be discerned by specific (H2A+H2B+DNA) conformational antibody at the inner nuclear envelope and around mitotic chromosomes. In order to differentiate the DNA conformation of the peripheral chromatin we applied an Acridine orange (AO) DNA structural test involving RNAse treatment and the addition of AO after acid pre-treatment. MCF-7 cells treated in this way revealed yellow/red patches of LADs atta…

0301 basic medicineDNA A-formRNase P03 medical and health scienceschemistry.chemical_compoundHumansLADsNADsMitosisOriginal ResearchStaining and LabelingDifferential stainingMetachromasiaAcridine orangeDNACell BiologyepichromatinAcridine OrangeChromatinnucleosome superbeadsChromatinStainingDNA structural test030104 developmental biologychemistryMCF-7 CellsBiophysicsNucleic Acid ConformationDNANucleus
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DNA Damage and Repair in Degenerative Diseases 2016

2016

Given the great importance of the integrity of DNA for the correct transmission of the genetic message, repairing the induced lesions to its molecular structure by different endogenous or exogenous origin is crucial for the maintenance of homeostasis and biological functions of living organisms.[...]

0301 basic medicineDNA RepairDNA damageEndogenyBiologyCatalysisEpigenesis GeneticInorganic Chemistrylcsh:Chemistry03 medical and health scienceschemistry.chemical_compoundAnimalsHumansDiseasePhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyOrganic ChemistryGeneral MedicineComputer Science ApplicationsCell biologyDietOxidative Stress030104 developmental biologyEditorialn/achemistrylcsh:Biology (General)lcsh:QD1-999DNAHomeostasisDNA DamageInternational Journal of Molecular Sciences
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Modification of DNA structure by reactive nitrogen species as a result of 2-methoxyestradiol–induced neuronal nitric oxide synthase uncoupling in met…

2020

Abstract 2-methoxyestradiol (2-ME) is a physiological anticancer compound, metabolite of 17β-estradiol. Previously, our group evidenced that from mechanistic point of view one of anticancer mechanisms of action of 2-ME is specific induction and nuclear hijacking of neuronal nitric oxide synthase (nNOS), resulting in local generation of nitro-oxidative stress and finally, cancer cell death. The current study aims to establish the substantial mechanism of generation of reactive nitrogen species by 2-ME. We further achieved to identify the specific reactive nitrogen species involved in DNA-damaging mechanism of 2-ME. The study was performed using metastatic osteosarcoma 143B cells. We detected…

0301 basic medicineDNA damageClinical BiochemistryBone NeoplasmsNitric Oxide Synthase Type INitric OxideBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePeroxynitrous AcidHumansMTT assayViability assaylcsh:QH301-705.5Reactive nitrogen speciesSettore CHIM/02 - Chimica FisicaOsteosarcomalcsh:R5-920Settore BIO/16 - Anatomia UmanaOrganic ChemistryDNAReactive Nitrogen Species2-MethoxyestradiolPeroxynitrous acid030104 developmental biologychemistrylcsh:Biology (General)Settore CHIM/03 - Chimica Generale E InorganicaCancer cellBiophysicslcsh:Medicine (General)030217 neurology & neurosurgeryPeroxynitrite2 methoxyestradiol nitric oxide chemotherapyResearch PaperRedox Biology
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Abacavir Induces Arterial Thrombosis in a Murine Model.

2018

Background The purinergic system is known to underlie prothrombotic and proinflammatory vascular programs, making the profile of experimental actions demonstrated by abacavir compatible with thrombogenesis. However, direct evidence of a prothrombotic effect by the drug has been lacking. Methods The present study appraised the effects of abacavir in a well-validated animal model of arterial thrombosis. The role of ATP-P2X7 receptors in the actions of the drug was also assessed, and the actions of recognized vascular-damaging agents and other nucleoside reverse-transcriptase inhibitors (NRTIs) were evaluated and compared to those of abacavir. Results Abacavir dose-dependently promoted thrombu…

0301 basic medicineDrugMaleAnti-HIV Agentsmedia_common.quotation_subject030204 cardiovascular system & hematologyPharmacologyProinflammatory cytokine03 medical and health sciences0302 clinical medicineimmune system diseasesAbacavirmedicineImmunology and AllergyAnimalsRofecoxibmedia_commonMice KnockoutDose-Response Relationship Drugbusiness.industryPurinergic receptorAntagonistvirus diseasesThrombosisPurinergic signallingmedicine.diseaseThrombosisDideoxynucleosidesDisease Models Animal030104 developmental biologyInfectious DiseasesReceptors Purinergic P2X7businessmedicine.drugThe Journal of infectious diseases
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Cardiovascular toxicity of abacavir: a clinical controversy in need of a pharmacological explanation.

2017

: There is a long-lasting controversy surrounding an association between abacavir (ABC) and an increased risk of cardiovascular disease in HIV-positive patients. Although differing in their specifics, a number of published cohort studies and clinical trials support such an association, usually relating it to recent exposure to the drug, independently of traditional predisposing factors. However, other clinical trials have failed to reveal such a relation and have pointed to methodological differences to explain discrepancies. Significantly, the controversy has been fueled by the lack of a credible mechanism of action to justify the putative detrimental actions of ABC. There is a myriad of c…

0301 basic medicineDrugVasculitisAnti-HIV Agentsmedia_common.quotation_subjectImmunologyHIV InfectionsDiseasePharmacologyBioinformaticsProinflammatory cytokine03 medical and health sciencesParacrine signallingchemistry.chemical_compound0302 clinical medicineAbacavirImmunology and AllergyMedicineHumans030212 general & internal medicineCyclic guanosine monophosphatemedia_commonbusiness.industryAtherosclerosis030112 virologyDideoxynucleosidesClinical trialInfectious DiseaseschemistryMechanism of actionCardiovascular Diseasesmedicine.symptombusinessmedicine.drugAIDS (London, England)
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The Transcription Factor MAZR/PATZ1 Regulates the Development of FOXP3+ Regulatory T Cells

2019

Summary: Forkhead box protein P3+ (FOXP3+) regulatory T cells (Treg cells) play a key role in maintaining tolerance and immune homeostasis. Here, we report that a T cell-specific deletion of the transcription factor MAZR (also known as PATZ1) leads to an increased frequency of Treg cells, while enforced MAZR expression impairs Treg cell differentiation. Further, MAZR expression levels are progressively downregulated during thymic Treg cell development and during in-vitro-induced human Treg cell differentiation, suggesting that MAZR protein levels are critical for controlling Treg cell development. However, MAZR-deficient Treg cells show only minor transcriptional changes ex vivo, indicating…

0301 basic medicineFOXP3PATZ1chemical and pharmacologic phenomenaBiologyTreg cellGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntestinal inflammationmedicineForkhead Box Protein P3Immune homeostasisColitisTranscription factorlcsh:QH301-705.5DSS-induced colitisMAZRT(reg)FOXP3hemic and immune systemsmedicine.diseaseCell biology030104 developmental biologyregulatory T cellslcsh:Biology (General)030217 neurology & neurosurgeryCell Reports
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Causes and consequences of DNA damage-induced autophagy.

2021

Abstract Autophagy is a quality control pathway that maintains cellular homeostasis by recycling surplus and dysregulated cell organelles. Identification of selective autophagy receptors demonstrated the existence of pathways that selectively degrade organelles, protein aggregates or pathogens. Interestingly, different types of DNA damage can induce autophagy and autophagy-deficiency leads to genomic instability. Recent studies provided first insights into the pathways that connect autophagy with the DNA damage response. However, the physiological role of autophagy and the identity of its targets after DNA damage remain enigmatic. In this review, we summarize recent literature on the target…

0301 basic medicineGenome instabilityDNA RepairDNA damageAutophagyCellular homeostasisProtein aggregationBiologyGenomic InstabilityCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinechemistry030220 oncology & carcinogenesisOrganelleAutophagyHumansReceptorMolecular BiologyDNADNA DamageMatrix biology : journal of the International Society for Matrix Biology
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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Identifying Biomarkers for Biological Age: Geroscience and the ICFSR Task Force

2021

The International Conference on Frailty and Sarcopenia Research Task Force met in March 2020, in the shadow of the COVID-19 pandemic, to discuss strategies for advancing the interdisciplinary field of geroscience. Geroscience explores biological mechanisms of aging as targets for intervention that may delay the physiological consequences of aging, maintain function, and prevent frailty and disability. Priorities for clinical practice and research include identifying and validating a range of biomarkers of the hallmarks of aging. Potential biomarkers discussed included markers of mitochondrial dysfunction, proteostasis, stem cell dysfunction, nutrient sensing, genomic instability, telomere d…

0301 basic medicineGerontologyAgingmedia_common.quotation_subjecthallmarks of agingTranslational researchfrailty03 medical and health sciencesSpecial Article030502 gerontologymedicineAnimalsHumansEpigeneticsFunction (engineering)Pandemicsresiliencemedia_commonGeroscienceSARS-CoV-2business.industryTask forceCOVID-19General Medicinemedicine.diseaseOmics030104 developmental biologyProteostasistranslational researchSarcopenia0305 other medical sciencebusinessBiomarkersThe Journal of Frailty & Aging
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Classic Models for New Perspectives: Delving into Helminth–Microbiota–Immune System Interactions

2018

Whilst a wealth of data indicate that infections by gastrointestinal helminths are accompanied by significant alterations in the composition of the vertebrate gut flora, little is known of the immune-molecular mechanisms that regulate host-parasite-microbiota interactions. 'Traditional' experimental models of gastrointestinal helminthiases, in which the role(s) of each of the components of this triad can be tested, provide an opportunity to advance research in this area. In this article, we propose the Echinostoma caproni-mouse system as a potentially useful tool for studies of the role of the host gut microbiota in preventing pathology and inducing parasite clearance via interleukin (IL)-2…

0301 basic medicineHelminthiasisHelminthiasisInterleukinBiologyGut floramedicine.diseasebiology.organism_classificationModels BiologicalHost-Parasite Interactions03 medical and health sciences030104 developmental biologyInfectious DiseasesImmune systemImmunological FactorsImmunityImmunologymedicineAnimalsHumansHelminthsParasitologyGut homeostasisTrends in Parasitology
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