Search results for "RAM"

showing 10 items of 35643 documents

Genome-wide association studies for milk production traits in Valle del Belice sheep using repeated measures

2019

Genome-wide association studies (GWASes) have become a powerful tool for identifying genomic regions associated with important traits in livestock. Milk production traits in dairy sheep are measured at different time points during their life span. Using phenotypic data generated from longitudinal traits could improve the power of association studies but until now have received less attention in GWASes as a methodology and has not been implemented. The aim of this study was to carry out a GWAS for milk production traits in Valle del Belice sheep using repeated measures. After quality control, 469 ewes and 37 228 SNPs were retained for the analysis, and phenotypic data included 5586 test-day …

0301 basic medicineCandidate genes longitudinal traits single nucleotide polymorphismsSingle-nucleotide polymorphismGenome-wide association studyBiologyPolymorphism Single NucleotideCandidate genes03 medical and health sciencessingle nucleotide polymorphismslongitudinal traitSettore AGR/17 - Zootecnica Generale E Miglioramento GeneticoAnimal sciencesingle nucleotide polymorphismGeneticsAnimalsGeneSheep DomesticGenetic associationbusiness.industry0402 animal and dairy scienceRepeated measures designcandidate gene04 agricultural and veterinary sciencesGeneral MedicineMilk production040201 dairy & animal sciencePhenotypeMilk030104 developmental biologyFemaleLivestockAnimal Science and Zoologybusinesslongitudinal traitsGenome-Wide Association Study
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Inflammatory Response Mechanisms of the Dentine–Pulp Complex and the Periapical Tissues

2021

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The fron…

0301 basic medicineCarcinogenesisRoot canalReviewimmune responselcsh:Chemistryodontoblast0302 clinical medicinePulpitislcsh:QH301-705.5SpectroscopyTissue homeostasisOdontoblastsPeriapical TissueIntracellular Signaling Peptides and ProteinsGeneral MedicineComputer Science ApplicationsCell biologyPeriradicularmedicine.anatomical_structureCarcinoma Squamous CellMouth NeoplasmsChemokinescarious lesionPeriapical GranulomaConnective tissueDental CariesBiologyNitric OxideCatalysisInorganic Chemistry03 medical and health sciencestertiary dentinestomatognathic systemAntigens NeoplasmmedicineAnimalsHumansddc:610Physical and Theoretical ChemistryApical foramenMolecular BiologyDental PulpRadicular CystNeuropeptidesOrganic ChemistryPulpitisMesenchymal Stem CellsComplement System Proteins030206 dentistryFibroblastsmedicine.diseasestomatognathic diseases030104 developmental biologyOdontoblastlcsh:Biology (General)lcsh:QD1-999DentinPulp (tooth)Nerve NetPeriapical PeriodontitisInternational Journal of Molecular Sciences
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MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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Induction of cancer cell stemness by depletion of macrohistone H2A1 in hepatocellular carcinoma.

2017

Hepatocellular carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell–like features and are responsible for tumor relapse, metastasis, and chemoresistance. The development of effective treatments for HCC will depend on a molecular-level understanding of the specific pathways driving CSC emergence and stemness. MacroH2A1 is a variant of the histone H2A and an epigenetic regulator of stem-cell function, where it promotes differentiation and, conversely, acts as a barrier to somatic-cell reprogramming. Here, we focused on the role played by the histone variant macroH2A1 as a potential epigenetic factor promoting CSC differentiation. In human HCC section…

0301 basic medicineCarcinoma HepatocellularBiologyMetastasisHistones03 medical and health sciencesCancer stem cellHistone H2AmedicineHumansEpigeneticsPhosphorylationCell ProliferationHepatologyCell growthGene Expression ProfilingLiver NeoplasmsTranscription Factor RelAHep G2 Cellsmedicine.disease030104 developmental biologyHistoneCancer cellCancer researchbiology.proteinNeoplastic Stem CellsReprogrammingHepatology (Baltimore, Md.)
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L-carnitine protects C2C12 cells against mitochondrial superoxide overproduction and cell death.

2017

International audience; AIMTo identify and characterize the protective effect that L-carnitine exerted against an oxidative stress in C2C12 cells.METHODSMyoblastic C2C12 cells were treated with menadione, a vitamin K analog that engenders oxidative stress, and the protective effect of L-carnitine (a nutrient involved in fatty acid metabolism and the control of the oxidative process), was assessed by monitoring various parameters related to the oxidative stress, autophagy and cell death.RESULTSAssociated with its physiological function, a muscle cell metabolism is highly dependent on oxygen and may produce reactive oxygen species (ROS), especially under pathological conditions. High levels o…

0301 basic medicineCell deathProgrammed cell deathMitochondrial superoxideMitochondrion03 medical and health sciences0302 clinical medicineSuperoxide anionsCarnitinemedicineCarnitineOverproductionOxygen specieschemistry.chemical_classificationReactive oxygen species[ SDV.IDA ] Life Sciences [q-bio]/Food engineeringBasic Studymusculoskeletal systemReactive AutophagyCell biologyMitochondria030104 developmental biologychemistryMuscletissuesC2C12030217 neurology & neurosurgerymedicine.drugWorld journal of biological chemistry
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Polyphenols from Pennisetum glaucum grains induce MAP kinase phosphorylation and cell cycle arrest in human osteosarcoma cells

2019

Abstract Osteosarcoma is the most common bone tumor with a high prevalence among children and adolescents. Polyphenols are widely investigated for their chemopreventive and chemotherapeutic proprieties. In the present study, we explored the pro-apoptotic effects of pearl millet, Pennisetum glaucum, phenolic compounds (PGPC) on osteosarcoma U-2OS cells. Our results show that PGPC induced U-2OS cells death, in a dose dependent manner, with an IC50 of 80 μg/mL. Annexin-V and 7-AAD staining show that PGPC induced cell death mainly through caspase-dependent apoptosis as shown by a decrease in cell death when co-treated with pan-caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketon…

0301 basic medicineCell signalingProgrammed cell deathCell cycle checkpointp38 mitogen-activated protein kinases[SDV]Life Sciences [q-bio]Medicine (miscellaneous)Pearl milletCell cycle arrest03 medical and health sciences0404 agricultural biotechnologyTX341-641Intracellular calciumProtein kinase BPI3K/AKT/mTOR pathwayCaspase030109 nutrition & dieteticsNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryCyclin-dependent kinase 2Polyphenols04 agricultural and veterinary sciencesU-2OS cells040401 food scienceMolecular biology3. Good healthApoptosisbiology.proteinFood Science
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General Aspects of Metal Ions as Signaling Agents in Health and Disease

2020

This review focuses on the current knowledge on the involvement of metal ions in signaling processes within the cell, in both physiological and pathological conditions. The first section is devoted to the recent discoveries on magnesium and calcium-dependent signal transduction—the most recognized signaling agents among metals. The following sections then describe signaling pathways where zinc, copper, and iron play a key role. There are many systems in which changes in intra- and extra-cellular zinc and copper concentrations have been linked to important downstream events, especially in nervous signal transduction. Iron signaling is mostly related with its homeostasis. However, it is also …

0301 basic medicineCell signalingProgrammed cell deathMetal ions in aqueous solutionCelllcsh:QR1-502DiseaseReviewBiochemistrySynaptic Transmissionlcsh:Microbiology03 medical and health sciences0302 clinical medicinemedicinecell signaling; metal homeostasis; ferroptosiscell signalingAnimalsFerroptosisHumansMolecular BiologyChemistryFerroptosisCell biology030104 developmental biologymedicine.anatomical_structureMetalsmetal homeostasisSignal transduction030217 neurology & neurosurgeryHomeostasisSignal TransductionBiomolecules
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Oxidative Stress and Vascular Dysfunction in the Retina: Therapeutic Strategies

2020

Many retinal diseases, such as diabetic retinopathy, glaucoma, and age-related macular (AMD) degeneration, are associated with elevated reactive oxygen species (ROS) levels. ROS are important intracellular signaling molecules that regulate numerous physiological actions, including vascular reactivity and neuron function. However, excessive ROS formation has been linked to vascular endothelial dysfunction, neuron degeneration, and inflammation in the retina. ROS can directly modify cellular molecules and impair their function. Moreover, ROS can stimulate the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) causing inflammation and cel…

0301 basic medicineCell signalingProgrammed cell deathPhysiologyClinical BiochemistryInflammationReviewmedicine.disease_causeBiochemistryProinflammatory cytokine03 medical and health sciences0302 clinical medicinemedicineoxidative stressEndothelial dysfunctionMolecular Biologyreactive oxygen speciesRetinabusiness.industrylcsh:RM1-950Cell Biologymedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacology030221 ophthalmology & optometryTumor necrosis factor alpharetinal diseasemedicine.symptombusinessvascular endotheliumOxidative stressAntioxidants
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MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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Cardiac Glycoside Glucoevatromonoside Induces Cancer Type-Specific Cell Death.

2018

Cardiac glycosides (CGs) are natural compounds used traditionally to treat congestive heart diseases. Recent investigations repositioned CGs as potential anticancer agents. To discover novel cytotoxic CG scaffolds, we selected the cardenolide glucoevatromonoside (GEV) out of 46 CGs for its low nanomolar anti-lung cancer activity. GEV presented reduced toxicity toward non-cancerous cell types (lung MRC-5 and PBMC) and high-affinity binding to the Na+/K+-ATPase α subunit, assessed by computational docking. GEV-induced cell death was caspase-independent, as investigated by a multiparametric approach, and culminates in severe morphological alterations in A549 cells, monitored by transmission el…

0301 basic medicineCell typeProgrammed cell deathNecroptosis03 medical and health sciences0302 clinical medicineglucoevatromonosideCytotoxic T cellPharmacology (medical)non-canonical cell deathOriginal ResearchA549 cellPharmacologyU937 cellbiologyChemistrylcsh:RM1-950apoptosisCalpaincardiac glycoside3. Good healthlung cancer030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinFrontiers in pharmacology
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