Search results for " Biologia"

showing 10 items of 700 documents

Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis …

2013

OBJECTIVES: Interleukin (IL)-23 has been implicated in the pathogenesis of ankylosing spondylitis (AS). The aim of the study was to clarify the mechanisms underlying the increased IL-23 expression in the gut of AS patients. METHODS: Consecutive gut biopsies from 30 HLA-B27(+) AS patients, 15 Crohn's disease (CD) patients and 10 normal subjects were obtained. Evidence for HLA-B27 misfolding was studied. Unfolded protein response (UPR) and autophagy were assessed by RT-PCR and immunohistochemistry. The contribution of UPR and autophagy in the regulation of IL-23 expression was evaluated in in vitro experiments on isolated lamina propria mononuclear cells (LPMCs). RESULTS: Intracellular coloca…

AdultMaleProtein FoldingBiopsyImmunologyATG5Gene ExpressionInflammationdigestive systemArticleGeneral Biochemistry Genetics and Molecular BiologyATG12Young AdultCrohn DiseaseRheumatologyDownregulation and upregulationSettore BIO/13 - Biologia Applicataankylosing spondylitisAutophagymedicineInterleukin 23HumansImmunology and AllergySpondylitis AnkylosingHLA-B27 AntigenAgedMucous Membranebusiness.industryAutophagyInterleukinIleitisMiddle AgedIntestinesInterleukin 23Settore MED/16 - ReumatologiaImmunologyInterleukin-23 Subunit p19Unfolded Protein ResponseUnfolded protein responseFemalemedicine.symptombusinessAnnals of the Rheumatic Diseases
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Identification of Biomarkers in Cerebrospinal Fluid and Serum of Multiple Sclerosis Patients by Immunoproteomics Approach

2014

Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the central nervous system. At present, the molecular mechanisms causing the initiation, development and progression of MS are poorly understood, and no reliable proteinaceous disease markers are available. In this study, we used an immunoproteomics approach to identify autoreactive antibodies in the cerebrospinal fluid of MS patients to use as candidate markers with potential diagnostic value. We identified an autoreactive anti-transferrin antibody that may have a potential link with the development and progression of MS. We found this antibody at high levels also in the serum of MS patients and created an immun…

AdultMaleProteomicsPathologymedicine.medical_specialtyImmunoproteinsimmunoproteomeCentral nervous systemDiseaseBiologymultiple sclerosisProteomicsArticlecerebrospinal fluidCatalysisImmunoproteomicslcsh:ChemistryInorganic ChemistryCerebrospinal fluidSettore BIO/13 - Biologia ApplicatamedicineHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyMultiple sclerosisOrganic ChemistryTransferrinCase-control studyGeneral MedicineMiddle Agedmedicine.diseaseComputer Science Applicationsmedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999Case-Control Studiesmultiple sclerosiserum biomarkerImmunologyanti-transferrin autoantibodiesbiology.proteinFemaleSettore MED/26 - Neurologiaanti-transferrin autoantibodieAntibodyBiomarkersInternational Journal of Molecular Sciences
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BRAF(V600E) mutation influences hypoxia-inducible factor-1alpha expression levels in papillary thyroid cancer

2010

Abstract Hypoxia-inducible factor-1alpha is found frequently overexpressed in solid tumors cells, exerting an important role in angiogenesis, glucose metabolism, cell proliferation, survival and invasion. In thyroid carcinomas, hypoxia-inducible factor-1alpha expression was found increased in differentiated, poorly differentiated, medullary and anaplastic variants. Hypoxia represents the principal stimulus responsible for hypoxia-inducible factor-1alpha induction. Other nonhypoxic stimuli increase hypoxia-inducible factor-1alpha synthesis through the activation of phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in a cell-type-specific manner. We have previously s…

AdultMaleProto-Oncogene Proteins B-rafAdolescentSettore BIO/11 - Biologia MolecolareSettore MED/08 - Anatomia PatologicaTransfectionhypoxia mutation carcinomaMixed Function OxygenasesSettore MED/13 - EndocrinologiaYoung AdultCell Line TumorBiomarkers TumorHumansGene SilencingThyroid NeoplasmsRNA Small InterferingAgedMiddle AgedGene Expression Regulation NeoplasticRepressor ProteinsAdenocarcinoma PapillaryGene Knockdown TechniquesMutationThyroidectomyFemale
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Rituximab modulates IL-17 expression in the salivary glands of patients with primary Sjögren's syndrome.

2014

OBJECTIVE: The aim of this study was to evaluate the role of rituximab (RTX) in modulating the expression of the IL-17/IL-23 pathway in the salivary glands (SGs) of patients with primary SS (pSS). METHODS: Consecutive SG biopsies were obtained from 15 patients with pSS before and after 1 year of RTX therapy. The SG expression of IL-17, IL-23p19 and p-STAT3 was evaluated by immunohistochemistry at baseline and after RTX therapy. The role of mast cells in pSS patients in modulating the Th17 response and the immunologic effect of RTX on mast cells were also studied in in vitro experiments. RESULTS: IL-17 was overexpressed in the SGs of patients with pSS mainly by infiltrating T cells and mast …

AdultMaleSTAT3 Transcription FactorSjogren SyndromeApoptosisIn Vitro TechniquesInterleukin-23Peripheral blood mononuclear cellSalivary GlandsAntibodies Monoclonal Murine-DerivedRheumatologystomatognathic systemSettore BIO/13 - Biologia ApplicataBiopsyHumansMedicinePharmacology (medical)Mast CellsAgedmedicine.diagnostic_testbusiness.industryInterleukinsInterleukin-17IL17Middle AgedMast cellIn vitroSettore MED/16 - ReumatologiaSjogren's SyndromeTreatment Outcomemedicine.anatomical_structureApoptosisAntirheumatic AgentsImmunologyTh17 CellsImmunohistochemistryFemaleRituximabInterferonsInterleukin 17businessRituximabSignal Transductionmedicine.drug
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Analysis of the gastrin-releasing peptide receptor gene in Italian patients with autism spectrum disorders

2008

The gastrin-releasing peptide receptor (GRPR) was implicated for the first time in the pathogenesis of Autism spectrum disorders (ASD) by Ishikawa-Brush et al. [Ishikawa-Brush et al. (1997): Hum Mol Genet 6: 1241-1250]. Since this original observation, only one association study [Marui et al. (2004): Brain Dev 26: 5-7] has further investigated, though unsuccessfully, the involvement of the GRPR gene in ASD. With the aim of contributing further information to this topic we have sequenced the entire coding region and the intron/exon junctions of the GRPR gene in 149 Italian autistic patients. The results of this study led to the identification of four novel point mutations, two of which, that…

AdultMalemedicine.medical_specialtyBALB 3T3 CellsAdolescentDNA Mutational AnalysisPopulationRett syndromeBiologyMiceCellular and Molecular NeuroscienceExonSettore BIO/13 - Biologia ApplicataInternal medicineGastrin-releasing peptideChlorocebus aethiopsmedicineGastrin-releasing peptide receptorAnimalsHumansPoint MutationAutistic DisorderChildautism gastrin-releasing peptide receptor signal transductionG-protein-coupled receptor association studyeducationGeneGenetics (clinical)AgedGeneticseducation.field_of_studyPoint mutationMiddle Agedmedicine.diseasePedigreeReceptors BombesinDevelopmental disorderPsychiatry and Mental healthEndocrinologyItalyCase-Control StudiesCOS CellsFemaleAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Aurora-A overexpression as an early marker of reflux-related columnar mucosa and Barrett's oesophagus.

2007

Abstract BACKGROUND: The development of oesophageal adenocarcinoma is generally closely associated with the presence of a specialised intestinal-type epithelium such as that found in Barrett's oesophagus (BO). A particular histological condition is when the distal oesophagus showing cardiac and/or fundic mucosa without intestinal metaplasia cannot be defined as 'Barrett's mucosa' [condition that we call 'columnar-lined oesophagus' (CLO)] and up till now, there has been no agreement in literature about the management of this condition. Aurora-A overexpression leads to centrosome amplification, chromosomal instability and aneuploidy in mammalian cells. PATIENTS AND METHODS: A prospective stud…

AdultMalemedicine.medical_specialtyPathologyEsophageal NeoplasmsSettore MED/06 - Oncologia MedicaAneuploidySettore BIO/11 - Biologia MolecolareAdenocarcinomaProtein Serine-Threonine KinasesSettore MED/08 - Anatomia PatologicaGastroenterologyBarrett EsophagusAurora KinasesInternal medicineBiopsymedicineHumansAurora-A overexpression Barrett’s oesophagus cell cycle columnar-lined oesophagus p53 proteinProspective StudiesEsophagusMucous Membranemedicine.diagnostic_testEsophageal diseasebusiness.industryIntestinal metaplasiaHematologyMiddle Agedmedicine.diseasemedicine.anatomical_structureOncologyDysplasiaBarrett's esophagusGastroesophageal RefluxFemalebusinessImmunostainingBiomarkers
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Calorie Restriction in Mammals and Simple Model Organisms

2014

Calorie restriction (CR), which usually refers to a 20–40% reduction in calorie intake, can effectively prolong lifespan preventing most age-associated diseases in several species. However, recent data from both human and nonhumans point to the ratio of macronutrients rather than the caloric intake as a major regulator of both lifespan and health-span. In addition, specific components of the diet have recently been identified as regulators of some age-associated intracellular signaling pathways in simple model systems. The comprehension of the mechanisms underpinning these findings is crucial since it may increase the beneficial effects of calorie restriction making it accessible to a broad…

AgingCalorie restrictionPopulationved/biology.organism_classification_rank.speciesRegulatorlcsh:MedicineReview ArticleBiologylongevity ageing calorie restriction dietBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyIntracellular signaling pathwaysSettore BIO/13 - Biologia ApplicataYeastsAnimalsHumansCaenorhabditis eleganseducationModel organismBeneficial effectsCaloric RestrictionMammalseducation.field_of_studyGeneral Immunology and Microbiologyved/biologylcsh:RGeneral MedicineCaloric intakeDietCalorie intakeDrosophila melanogasterBiochemistryEnergy IntakeSignal Transduction
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Progerin expression induces a significant downregulation of transcription from human repetitive sequences in iPSC-derived dopaminergic neurons.

2019

Repetitive DNA sequences represent about half of the human genome. They have a central role in human biology, especially neurobiology, but are notoriously difficult to study. The purpose of this study was to quantify the transcription from repetitive sequences in a progerin-expressing cellular model of neuronal aging. Progerin is a nuclear protein causative of the Hutchinson–Gilford progeria syndrome that is also incrementally expressed during the normal aging process. A dedicated pipeline of analysis allowed to quantify transcripts containing repetitive sequences from RNAseq datasets oblivious of their genomic localization, tolerating a sufficient degree of mutational noise, all with low c…

AgingRetroelementsTranscription GeneticAluInduced Pluripotent Stem CellsAlu elementDown-RegulationSettore BIO/11 - Biologia MolecolareRetrotransposonComputational biologyBiologySettore BIO/19 - Microbiologia GeneraleProgerinProgeriaSettore BIO/13 - Biologia ApplicataAlu ElementsRepetitive sequencemedicineRetrotransposonHumansDNA transposonRepeated sequenceGeneCellular SenescenceProgeriaintegumentary systemDopaminergic NeuronsFibroblastsmedicine.diseaseProgerinLamin Type ASettore BIO/18 - GeneticaSatelliteHuman genomeOriginal ArticleGeriatrics and GerontologyGeroScience
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Tor-Sch9 deficiency activates catabolism of the ketone body-like acetic acid to promote trehalose accumulation and longevity

2014

In mammals, extended periods of fasting leads to the accumulation of blood ketone bodies including acetoacetate. Here we show that similar to the conversion of leucine to acetoacetate in fasting mammals, starvation conditions induced ketone body-like acetic acid generation from leucine in S. cerevisiae. Whereas wild-type and ras2Δ cells accumulated acetic acid, long-lived tor1Δ and sch9Δ mutants rapidly depleted it through a mitochondrial acetate CoA transferase-dependent mechanism, which was essential for lifespan extension. The sch9Δ-dependent utilization of acetic acid also required coenzyme Q biosynthetic genes and promoted the accumulation of intracellular trehalose. These results indi…

AgingSaccharomyces cerevisiae ProteinsKetoneLongevitySaccharomyces cerevisiaeSaccharomyces cerevisiaePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAcetic acidSettore BIO/13 - Biologia ApplicataHumans2. Zero hungerchemistry.chemical_classificationbiologyCatabolismaging yeast nutrition acetic acid nutrientsTrehaloseOriginal ArticlesCell Biologybiology.organism_classificationchronological lifespanTrehaloseacetic acidSch9chemistryBiochemistryCoenzyme Q – cytochrome c reductaseKetone bodiesleucineLeucineProtein KinasesAging Cell
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Agonist-induced formation of FGFR1 homodimers and signaling differ among members of the FGF family

2011

Fibroblast growth factor receptor 1 (FGFR1) is known to be activated by homodimerization in the presence of both the FGF agonist ligand and heparan sulfate glycosaminoglycan. FGFR1 homodimers in turn trigger a variety of downstream signaling cascades via autophosphorylation of tyrosine residues in the cytoplasmic domain of FGFR1. By means of Bioluminescence Energy Resonance Transfer (BRET) as a sign of FGFR1 homodimerization, we evaluated in HEK293T cells the effects of all known FGF agonist ligands on homodimer formation. A significant correlation between BRET(2) signaling and ERK1/2 phosphorylation was observed, leading to a further characterization of the binding and signaling properties…

AgonistMAPK/ERK pathwaymedicine.drug_classBiophysicsSettore BIO/11 - Biologia MolecolareBiologyLigandsFibroblast growth factorSettore BIO/09 - FisiologiaBiochemistrychemistry.chemical_compoundFluorescence Resonance Energy TransfermedicineHumansReceptor Fibroblast Growth Factor Type 1Molecular BiologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Fibroblast growth factor receptor 1HEK 293 cellsAutophosphorylationCell BiologyHeparan sulfateFibroblast growth factors FGFR1 Homodimerization BRET MAPKCell biologyFibroblast Growth Factorsstomatognathic diseasesHEK293 CellschemistrySettore BIO/14 - FarmacologiaPhosphorylationHeparitin SulfateProtein MultimerizationBiochemical and Biophysical Research Communications
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