Search results for " Humans"

showing 10 items of 2466 documents

Subclinical gut inflammation in ankylosing spondylitis

2015

Purpose of review Subclinical gut inflammation has been described in a significant proportion of patients with ankylosing spondylitis (AS), up to 10% of them developing it during the time of clinically overt inflammatory bowel disease. Histologic, immunologic, and intestinal microbiota alterations characterize the AS gut. Recent findings Microbial dysbiosis as well as alterations of innate immune responses have been demonstrated in the gut of AS. Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic…

0301 basic medicineAnkylosing spondylitis; Gut inflammation; Innate lymphoid cells; Interleukin-17; Interleukin-23; Adaptive Immunity; Animals; Cytokines; Disease Models Animal; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity Innate; Inflammation; Inflammatory Bowel Diseases; Intestines; Macrophages; Mice; Spondylitis Ankylosing; Rheumatology; Medicine (all)MacrophageAdaptive ImmunityInterleukin-23Inflammatory bowel diseaseGastroenterologyMiceInterleukin 23InnateMedicineSubclinical infectionMedicine (all)Interleukin-17digestive oral and skin physiologyInnate lymphoid cellIntestineIntestinesCytokinesmedicine.symptomHumanAnkylosingmedicine.medical_specialtyDisease ModelInflammationdigestive system03 medical and health sciencesRheumatologyInternal medicineInnate lymphoid cellAnimalsHumansSpondylitis AnkylosingCytokineSpondylitisGut inflammationSpondylitiInflammationAnkylosing spondylitisAnimalbusiness.industryMacrophagesInflammatory Bowel DiseaseImmunityInflammatory Bowel Diseasesmedicine.diseaseImmunity InnateDysbiosiGastrointestinal MicrobiomeAnkylosing spondylitiDisease Models Animal030104 developmental biologyDysbiosisbusinessDysbiosisCurrent Opinion in Rheumatology
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Genotyping and Antifungal Susceptibility of Dipodascus capitatus Isolated in a Neonatal Intensive Care Unit of a Sicilian Hospital

2017

In August 2015, Dipodascus capitatus was isolated from two patients admitted to the neonatal intensive care unit. Nosocomial acquisition of the fungus was suspected and epidemiological studies were undertaken. The patients were simultaneously hospitalized, and the comparison of the two isolates by two independent molecular typing methods have confirmed clonal dissemination of a single strain of D. capitatus. Antimicrobial susceptibility testing was useful for identifying the appropriated antifungal therapy in micafungin. To our knowledge these are the first described cases of neonatal D. capitatus infection and also the first report of successful treatment by micafungin.

0301 basic medicineAntifungalGenotypingPediatricsmedicine.medical_specialtyClonal disseminationNeonatal intensive care unitmedicine.drug_class030106 microbiologyDipodascus03 medical and health sciencesEpidemiologymedicineDipodascus capitatuAntifungal SusceptibilityDipodascus capitatusGenotypingBiochemistry Genetics and Molecular Biology (all)biologyMedicine (all)MicafunginAntifungal Susceptibility; Dipodascus capitatus; Genotyping; Nosocomial Acquisition; Cross Infection; Dipodascus; Female; Genotype; Hospitals; Humans; Infant; Infant Newborn; Intensive Care Units Neonatal; Male; Mycoses; Sicily; Medicine (all); Biochemistry Genetics and Molecular Biology (all)biology.organism_classificationNosocomial AcquisitionAntifungal Susceptibility; Dipodascus capitatus; Genotyping; Nosocomial Acquisition; Medicine (all); Biochemistry Genetics and Molecular Biology (all)medicine.drug
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Spectrum of mutations in Italian patients with familial hypercholesterolemia: New results from the LIPIGEN study

2017

Abstract Background Familial hypercholesterolemia (FH) is an autosomal dominant disease characterized by elevated plasma levels of LDL-cholesterol that confers an increased risk of premature atherosclerotic cardiovascular disease. Early identification and treatment of FH patients can improve prognosis and reduce the burden of cardiovascular mortality. Aim of this study was to perform the mutational analysis of FH patients identified through a collaboration of 20 Lipid Clinics in Italy (LIPIGEN Study). Methods We recruited 1592 individuals with a clinical diagnosis of definite or probable FH according to the Dutch Lipid Clinic Network criteria. We performed a parallel sequencing of the major…

0301 basic medicineApolipoprotein ECandidate geneSettore MED/09 - Medicina InternaDatabases FactualApolipoprotein BDNA Mutational AnalysisFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosityPCSK90302 clinical medicineRisk FactorsReceptorsGeneticsHomozygoteAutosomal dominant traitPathogenic variantsGeneral MedicinePrognosisAPOB; Familial hypercholesterolemia; LDLR; PCSK9; Pathogenic variantsCholesterolPhenotypeItalyAutosomal Recessive HypercholesterolemiaApolipoprotein B-100lipids (amino acids peptides and proteins)Proprotein Convertase 9APOBCardiology and Cardiovascular MedicinePreliminary DataGenetic MarkersFamilial hypercholesterolemiaLDLRPCSK9APOBPathogenic variantsHeterozygoteFamilial hypercholesterolemiaBiologyPathogenic variantLDLHyperlipoproteinemia Type II03 medical and health sciencesDatabasesmedicineInternal MedicineHumansAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Internal Medicine; Cardiology and Cardiovascular MedicineGenetic Predisposition to DiseaseFactualPCSK9Settore MED/13 - ENDOCRINOLOGIAAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Cardiology and Cardiovascular Medicine; Internal Medicinemedicine.diseaseAtherosclerosis030104 developmental biologyLDLRReceptors LDLMutationbiology.proteinAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Apolipoprotein B-100; Atherosclerosis; Cholesterol; DNA Mutational Analysis; Databases Factual; Genetic Markers; Genetic Predisposition to Disease; Heterozygote; Homozygote; Humans; Hyperlipoproteinemia Type II; Italy; Phenotype; Preliminary Data; Prognosis; Proprotein Convertase 9; Receptors LDL; Risk Factors; Mutation; Internal Medicine; Cardiology and Cardiovascular Medicine
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CD36 gene polymorphism is associated with Alzheimer's disease.

2017

IF 3.112; International audience; CD36 gene encodes a membrane glycoprotein (type B scavenger receptor) present on the surface of many types of cells and having multiple cellular functions ranging from angiogenesis to gustatory perception of fatty acids. Using a case control genetic association approach we have analyzed selected single nucleotide polymorphisms (SNP's) in a total of 859 patients with Alzheimer's disease (AD) and controls and have identified the allele A in rs3211892 polymorphism of CD36 gene as significantly increasing the risk of AD. Additionally we have investigated, in the same sample of control subjects and patients, SNP's in ApoE gene and confirmed that the previously i…

0301 basic medicineApolipoprotein EMESH : Oxidative StressCD36 AntigensMaleMESH : Polymorphism GeneticCD36MESH : AgedMESH : Alzheimer DiseaseMESH : GenotypeBiochemistryGeneMESH: Genotype0302 clinical medicineMESH: CholesterolMESH : FemaleMESH : CholesterolGeneticsMESH: AgedMESH: Oxidative StressbiologyMESH: Polymorphism Single NucleotideMESH : Polymorphism Single NucleotideMESH: Genetic Predisposition to DiseaseGeneral Medicine3. Good healthMESH : Antigens CD36CholesterolInterleukin 18FemaleApoEGenotypeMESH : MaleSingle-nucleotide polymorphismPolymorphism Single NucleotideMMSEAssociation03 medical and health sciencesAlzheimer DiseaseMESH: Polymorphism GeneticSNPHumansGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAllelePolymorphism[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyGenetic associationAgedPolymorphism GeneticMESH: HumansMESH: Antigens CD36MESH : HumansMESH: MaleOxidative Stress030104 developmental biologybiology.proteinMESH : Genetic Predisposition to DiseaseGene polymorphismCD36MESH: Female030217 neurology & neurosurgeryMESH: Alzheimer Disease
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Novel iodoacetamido benzoheterocyclic derivatives with potent antileukemic activity are inhibitors of STAT5 phosphorylation

2016

Signal Transducer and Activator of Transcription 5 (STAT5) protein, a component of the STAT family of signaling proteins, is considered to be an attractive therapeutic target because of its involvement in the progression of acute myeloid leukemia. In an effort to discover potent molecules able to inhibit the phosphorylation-activation of STAT5, twenty-two compounds were synthesized and evaluated on the basis of our knowledge of the activity of 2-(3’,4’,5’-trimethoxybenzoyl)-3-iodoacetamido-6-methoxy benzo[b]furan derivative 1 as a potent STAT5 inhibitor. Most of these molecules, structurally related to compound 1, were characterized by the presence of a common 3’,4’,5’-trimethoxybenzoyl moi…

0301 basic medicineApoptosisAntineoplastic Agentchemistry.chemical_compoundBenzophenone0302 clinical medicinehemic and lymphatic diseasesFuranDrug DiscoverySTAT5 Transcription FactorTumor Cells CulturedThiopheneMoietyPhosphorylationSTAT5Molecular StructurebiologyChemistryBiological activityGeneral MedicineApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyLeukemia Myeloid Acute030220 oncology & carcinogenesisBCR/ABL expressing leukemiaApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Antineoplastic Agents; Apoptosis; Benzofurans; Benzophenones; Cell Proliferation; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; Humans; K562 Cells; Leukemia Myeloid Acute; Molecular Structure; Phosphorylation; STAT5 Transcription Factor; Structure-Activity Relationship; Tumor Cells Cultured; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyHumanStereochemistryAntineoplastic AgentsArticleNOBenzophenones03 medical and health sciencesK562 CellHumansStructure–activity relationshipBenzofuransCell ProliferationPharmacologyIndole testDose-Response Relationship DrugIn vitro antiproliferative activitySTAT5 inhibitorsDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryApoptosiSTAT5 inhibitorStructure-activity relationshipIn vitro030104 developmental biologybiology.proteinBenzofuranDrug Screening Assays AntitumorK562 Cells
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Virus-encoded microRNA contributes to the molecular profile of EBV-positive Burkitt lymphomas

2015

Burkitt lymphoma (BL) is an aggressive neoplasm characterized by consistent morphology and phenotype, typical clinical behavior and distinctive molecular profile. The latter is mostly driven by the MYC over-expression associated with the characteristic translocation (8;14) (q24; q32) or with variant lesions. Additional genetic events can contribute to Burkitt Lymphoma pathobiology and retain clinical significance. A pathogenetic role for Epstein-Barr virus infection in Burkitt lymphomagenesis has been suggested; however, the exact function of the virus is largely unknown. In this study, we investigated the molecular profiles (genes and microRNAs) of Epstein-Barr virus-positive and -negative…

0301 basic medicineBART6; Burkitt lymphoma; EBV; miRNA; pathogenesisEpstein-Barr Virus InfectionsHerpesvirus 4 HumanpathogenesiRNA-binding proteinRNA-Binding ProteinEpstein-Barr Virus Infectionhemic and lymphatic diseasesCluster AnalysisViralOligonucleotide Array Sequence AnalysisGeneticsBART6; Burkitt lymphoma; EBV; miRNA; pathogenesis; Burkitt Lymphoma; Cluster Analysis; Cytoskeletal Proteins; Epstein-Barr Virus Infections; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Gene Expression Regulation Viral; Herpesvirus 4 Human; Host-Pathogen Interactions; Humans; Immunohistochemistry; MicroRNAs; Neoplasm Proteins; Oligonucleotide Array Sequence Analysis; Phospholipase C delta; RNA Viral; RNA-Binding Proteins; Reverse Transcriptase Polymerase Chain Reaction; ras Proteins; OncologyReverse Transcriptase Polymerase Chain ReactionpathogenesisMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsBurkitt lymphomaRNA-Binding ProteinsMicroRNAPhenotypeImmunohistochemistryNeoplasm ProteinsHost-Pathogen InteractionGene Expression Regulation NeoplasticOncologyHost-Pathogen InteractionsRNA ViralHumanResearch PaperGene Expression Regulation ViralBART6BiologySettore MED/08 - Anatomia PatologicaVirusNeoplasm Protein03 medical and health sciencesEBVmicroRNACytoskeletal ProteinmedicineHumansEpstein–Barr virus infectionGenemiRNANeoplasticCluster AnalysiOligonucleotide Array Sequence AnalysiGene Expression ProfilingHerpesvirus 4ras Proteinmedicine.diseaseLymphomaGene expression profilingCytoskeletal ProteinsMicroRNAs030104 developmental biologyGene Expression Regulationras ProteinsRNABART6; EBV; burkitt lymphoma; miRNA; pathogenesisPhospholipase C deltaOncotarget
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Quantitative and qualitative profiles of circulating monocytes may help identifying tuberculosis infection and disease stages

2017

Tuberculosis (TB) is one of the most important cause of morbidity and death among infectious diseases, and continuous efforts are needed to improve diagnostic tools and therapy. Previous published studies showed that the absolute cells number of monocytes or lymphocytes in peripheral blood or yet the ratio of monocytes to lymphocytes displayed the ability to predict the risk of active TB. In the present study we evaluated the ratio of monocytes to lymphocytes variation and we also analyzed the ex-vivo expression of CD64 on monocytes as tools to identify biomarkers for discriminating TB stages. Significant differences were found when the average ratio of monocytes to lymphocytes of active TB…

0301 basic medicineBacterial DiseasesMalelcsh:MedicineMycobacterium tuberculosiMonocyteMonocytesWhite Blood Cells0302 clinical medicineAnimal CellsMedicine and Health SciencesLymphocyteslcsh:ScienceImmune ResponseAged 80 and overMultidisciplinarybiologyMiddle Aged3. Good healthActinobacteriamedicine.anatomical_structureInfectious DiseasesPhenotypeAdolescent; Adult; Aged; Aged 80 and over; Biomarkers; Case-Control Studies; Female; Humans; Male; Middle Aged; Monocytes; Mycobacterium tuberculosis; Phenotype; Tuberculosis; Young Adult; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Biomarker (medicine)Tuberculosis Diagnosis and ManagementFemaleCellular TypesCase-Control StudieResearch ArticleHumanAdultTuberculosisAdolescentTuberculosiImmune CellsImmunologyMycobacterium tuberculosis03 medical and health sciencesYoung AdultTuberculosis diagnosisDiagnostic MedicinemedicineHumansTuberculosisAgedBlood CellsBiochemistry Genetics and Molecular Biology (all)Receiver operating characteristicBacteriabusiness.industryMonocytelcsh:RCase-control studyOrganismsBiology and Life SciencesMycobacterium tuberculosisCell BiologyBiomarkerbiology.organism_classificationmedicine.diseaseTropical DiseasesConfidence interval030104 developmental biologyAgricultural and Biological Sciences (all)Case-Control StudiesImmunologylcsh:QbusinessBiomarkers030215 immunology
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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A clinical review on megalencephaly: A large brain as a possible sign of cerebral impairment

2017

Megalencephaly and macrocephaly present with a head circumference measurement 2 standard deviations above the age-related mean. However, even if pathologic events resulting in both megalencephaly and macrocephaly may coexist, a distinction between these two entities is appropriate, as they represent clinical expression of different disorders with a different approach in clinical work-up, overall prognosis, and treatment. Megalencephaly defines an increased growth of cerebral structures related to dysfunctional anomalies during the various steps of brain development in the neuronal proliferation and/or migration phases or as a consequence of postnatal abnormal events. The disorders associate…

0301 basic medicineBrain development030105 genetics & hereditymacrocephalybrain dysfunction large head macrocephaly megalencephaly metabolic disorders03 medical and health sciences0302 clinical medicinemedicinemegalencephalymetabolic disordersHumansMegalencephaly10. No inequalitybrain dysfunctionbusiness.industryMedicine (all)Macrocephalybrain dysfunction; large head; macrocephaly; megalencephaly; metabolic disorders; Humans; Observational Studies as Topic; Megalencephaly; Medicine (all)General Medicinemedicine.diseaseHead circumferenceObservational Studies as Topiclarge headMeasurement 2medicine.symptombusinessNeuroscience030217 neurology & neurosurgery
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Pathogenetic Mechanisms of Intratumoral Hemorrhage in Meningioma: The Role of Microvascular Differentiation

2016

The transformation of normal cells into neoplastic cells is based on a series of gradual and progressive processes . One of the most important aspects underlying the tumorigenesis ist hat neoplastic proliferation needs mechanisms to ensure cancer development, bypass the body's protective strategies, and survive the apoptotic mechanisms. Subsequently, measures to promote replicative immortality and vascular support will be required. If cancer develops in an area offering excellent vascularization, pre-existing vascular circuits can supporti ts growth .Otherwise,tumor angiogenetic mechanisms will trigger new vascular networks, which will be necessary for tumor survival and expansion. The latt…

0301 basic medicineCD31medicine.medical_specialtyPathologyH&E stainCD34cd31Computed tomographyHemorrhageMeningiomasMeningioma03 medical and health sciences0302 clinical medicinemedicineMeningeal NeoplasmsHumansCD34; Hemorrhage; Mechanism; Meningiomas; cd31Cerebral Hemorrhagecd31; CD34; Hemorrhage; Mechanism; Meningiomas; Cerebral Hemorrhage; Humans; Meningeal Neoplasms; Meningioma; Surgery; Neurology (clinical)medicine.diagnostic_testMechanism (biology)business.industrySettore MED/27 - NeurochirurgiaMagnetic resonance imagingSMA*medicine.disease030104 developmental biology030220 oncology & carcinogenesisSurgeryRadiologyCD34MechanismNeurology (clinical)businessMeningiomameningioma hemorrhage
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