Search results for "BIOMARKER"

showing 10 items of 3035 documents

ADAM10 in Alzheimer's disease: Pharmacological modulation by natural compounds and its role as a peripheral marker.

2019

Abstract Alzheimer’s disease (AD) represents a global burden in the economics of healthcare systems. Amyloid-β (Aβ) peptides are formed by amyloid-β precursor protein (AβPP) cleavage, which can be processed by two pathways. The cleavage by the α-secretase A Disintegrin And Metalloprotease 10 (ADAM10) releases the soluble portion (sAβPPα) and prevents senile plaques. This pathway remains largely unknown and ignored, mainly regarding pharmacological approaches that may act via different signaling cascades and thus stimulate non-amyloidogenic cleavage through ADAM10. This review emphasizes the effects of natural compounds on ADAM10 modulation, which eventuates in a neuroprotective mechanism. M…

0301 basic medicineFarmacologiaADAM10DiseaseRM1-950Natural compoundsCleavage (embryo)NeuroprotectionCatechin03 medical and health sciencesADAM10 ProteinAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseDisintegrinHumansSenile plaquesPharmacological modulationPharmacologyMetalloproteinaseAmyloid beta-PeptidesbiologyChemistryPlant ExtractsADAM10ProteinsGinkgo bilobaMembrane ProteinsGeneral Medicineα-SecretaseAlzheimer's disease030104 developmental biologyMalaltia d'AlzheimerNeuroprotective Agents030220 oncology & carcinogenesisPharmaceuticalbiology.proteinTherapeutics. PharmacologyAmyloid Precursor Protein SecretasesNeuroscienceAlzheimer’s diseaseProteïnesBiomarkersBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Higher physiopathogenicity byFasciola giganticathan by the genetically closeF. hepatica: experimental long-term follow-up of biochemical markers

2016

Background: Fascioliasis is caused by Fasciola hepatica and F. gigantica. The latter, always considered secondary in human infection, nowadays appears increasingly involved in Africa and Asia. Unfortunately, little is known about its pathogenicity, mainly due to difficulties in assessing the moment a patient first becomes infected and the differential diagnosis with F. hepatica. Methods: A long-term, 24-week, experimental study comparing F. hepatica and F. giganticawas made for the first time in the same animal model host, Guirra sheep. Serum biochemical parameters of liver damage, serum electrolytes, protein metabolism, plasma proteins, carbohydrate metabolism, hepatic lipid metabolism and…

0301 basic medicineFascioliasisMitochondrial DNAFasciola gigantica030231 tropical medicineAntibodies HelminthProtein metabolismSheep DiseasesPhysiologyCarbohydrate metabolismDiagnosis Differential03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSpecies SpecificityHepaticaparasitic diseasesAnimalsFasciola hepaticaBiochemical markersSheepbiologyPublic Health Environmental and Occupational HealthGeneral MedicineDNA Helminth030108 mycology & parasitologybiology.organism_classificationBlood proteinsFasciolaDisease Models AnimalInfectious DiseaseschemistryImmunoglobulin GParasitologyBiomarkersTransactions of The Royal Society of Tropical Medicine and Hygiene
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Bioactive potential of silica coatings and its effect on the adhesion of proteins to titanium implants

2018

There is an ever-increasing need to develop dental implants with ideal characteristics to achieve specific and desired biological response in the scope of improve the healing process post-implantation. Following that premise, enhancing and optimizing titanium implants through superficial treatments, like silica sol-gel hybrid coatings, are regarded as a route of future research in this area. These coatings change the physicochemical properties of the implant, ultimately affecting its biological characteristics. Sandblasted acid-etched titanium (SAE-Ti) and a silica hybrid sol-gel coating (35M35G30T) applied onto the Ti substrate were examined. The results of in vitro and in vivo tests and t…

0301 basic medicineGene Expression02 engineering and technologychemistry.chemical_compoundMiceColloid and Surface ChemistryCoatingCoated Materials Biocompatiblebone regenerationOsteogenesisTitaniumChemistrySurfaces and InterfacesGeneral MedicineAdhesion021001 nanoscience & nanotechnologySilicon DioxideRabbits0210 nano-technologyBiotechnologyTitaniumSilicon dioxideSurface Propertieschemistry.chemical_elementengineering.materialOsseointegrationPhase Transitionosteogenesis03 medical and health sciencesproteomicsIn vivoOsseointegrationCell Line Tumordental implantsAnimalsPhysical and Theoretical ChemistryBone regenerationDental ImplantsosteoimmunologyOsteoblastsTibiaInterleukin-6Complement System ProteinsAlkaline Phosphatase030104 developmental biologyengineeringBiophysicsImplantapolipoproteinsBiomarkers
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ESC-Derived BDNF-Overexpressing Neural Progenitors Differentially Promote Recovery in Huntington's Disease Models by Enhanced Striatal Differentiation

2016

Summary Huntington's disease (HD) is characterized by fatal motoric failures induced by loss of striatal medium spiny neurons. Neuronal cell death has been linked to impaired expression and axonal transport of the neurotrophin BDNF (brain-derived neurotrophic factor). By transplanting embryonic stem cell-derived neural progenitors overexpressing BDNF, we combined cell replacement and BDNF supply as a potential HD therapy approach. Transplantation of purified neural progenitors was analyzed in a quinolinic acid (QA) chemical and two genetic HD mouse models (R6/2 and N171-82Q) on the basis of distinct behavioral parameters, including CatWalk gait analysis. Explicit rescue of motor function by…

0301 basic medicineGene ExpressionBiochemistrychemistry.chemical_compoundMice0302 clinical medicineNeural Stem CellsNeurotrophic factorsGenes Reporterlcsh:QH301-705.5Neuronslcsh:R5-920NeurogenesisCell DifferentiationAnatomyembryonic stem cellsHuntington Diseaselcsh:Medicine (General)NeurogliaLocomotionNeurotrophinHuntington’s diseaseCell SurvivalBiologyMedium spiny neuronArticle03 medical and health sciencesHuntington's diseaseGeneticsmedicinestriatal differentiationAnimalsBrain-derived neurotrophic factorBrain-Derived Neurotrophic FactorCell Biologymedicine.diseaseCorpus StriatumTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)chemistrynervous systembiology.proteinNeuroscience030217 neurology & neurosurgeryBiomarkersDevelopmental BiologyQuinolinic acidStem Cell TransplantationStem Cell Reports
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Genetics and Gene Therapy of Anderson-Fabry Disease.

2018

Fabry's disease is a genetic disorder of X-linked inheritance caused by mutations in the alpha galactosidase A gene resulting in deficiency of this lysosomal enzyme. The progressive accumulation of glycosphingolipids, caused by the inadequate enzymatic activity, is responsible of organ dysfunction and thus of clinical manifestations. In the presence of a high clinical suspicion, a careful physical examination and specific laboratory tests are required, finally diagnosis of Fabry's disease is confirmed by the demonstration of absence or reduced alpha-galactosidase A enzyme activity in hemizygous men and gene typing in heterozygous females; in fact the performance of enzymatic activity assay …

0301 basic medicineGenetic enhancementChaperone therapyDisease030204 cardiovascular system & hematologyBioinformaticsMice0302 clinical medicineAlpha galactosidase ADrug DiscoveryGenetics (clinical)KidneybiologyTrihexosylceramidesGenetic disorderEnzyme replacement therapyDependovirusRecombinant ProteinsAlpha galactosidase A; Chaperone therapy; Enzyme replacement therapy; Fabry disease; Gene therapy; Viral vectors; Molecular Medicine; Molecular Biology; Genetics; Drug Discovery3003 Pharmaceutical Science; Genetics (clinical)Isoenzymesmedicine.anatomical_structureMolecular Medicinemedicine.symptomGenetic Vectors03 medical and health sciencesGene therapyViral vectorRare DiseasesGeneticGeneticsmedicineAnimalsHumansEnzyme Replacement TherapyMolecular BiologyAlpha-galactosidasebusiness.industryDrug Discovery3003 Pharmaceutical ScienceOrgan dysfunctionGenetic Therapymedicine.diseaseFabry diseaseDisease Models Animal030104 developmental biologyalpha-GalactosidaseMutationbiology.proteinFabry DiseasebusinessBiomarkersCurrent gene therapy
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miR-22 suppresses DNA ligase III addiction in multiple myeloma

2019

Multiple myeloma (MM) is a hematologic malignancy characterized by high genomic instability. Here we provide evidence that hyper-activation of DNA ligase III (LIG3) is crucial for genomic instability and survival of MM cells. LIG3 mRNA expression in MM patients correlates with shorter survival and even increases with more advanced stage of disease. Knockdown of LIG3 impairs MM cells viability in vitro and in vivo, suggesting that neoplastic plasmacells are dependent on LIG3-driven repair. To investigate the mechanisms involved in LIG3 expression, we investigated the post-transcriptional regulation. We identified miR-22-3p as effective negative regulator of LIG3 in MM. Enforced expression of…

0301 basic medicineGenome instabilityCancer ResearchmiR-22 LIG3DNA repairDNA damageDNA repairApoptosisLIG3ArticleDNA Ligase ATP03 medical and health sciences0302 clinical medicinemicroRNABiomarkers TumorTumor Cells CulturedHumansPoly-ADP-Ribose Binding ProteinsCell ProliferationmiRNAchemistry.chemical_classificationRegulation of gene expressionGene knockdownDNA ligaseLeukemiamicroRNAChemistryHematologyPrognosisXenograft Model Antitumor AssaysGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchpharmacologyDNA DamageLeukemia
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Exome-Wide Association Study on Alanine Aminotransferase Identifies Sequence Variants in the GPAM and APOE Associated With Fatty Liver Disease.

2021

BACKGROUND & AIMS: Fatty liver disease (FLD) is a growing epidemic that is expected to be the leading cause of end-stage liver disease within the next decade. Both environmental and genetic factors contribute to the susceptibility of FLD. Several genetic variants contributing to FLD have been identified in exome-wide association studies. However, there is still a missing hereditability indicating that other genetic variants are yet to be discovered. METHODS: To find genes involved in FLD, we first examined the association of missense and nonsense variants with alanine amino transferase at an exome-wide level in 425,671 participants from the UK Biobank. We then validated genetic variants wit…

0301 basic medicineGenome-wide association studyLiver disease0302 clinical medicineENRICHMENT ANALYSISNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseExomeCONFERS SUSCEPTIBILITYGeneticsINSULIN-RESISTANCEmedicine.diagnostic_testFatty liverGastroenterologyAlanine Transaminase1-Acylglycerol-3-Phosphate O-Acyltransferase3. Good healthGENOMEEuropePhenotypeLiver biopsy030211 gastroenterology & hepatologyNonalcoholic Fatty Liver DiseaseMAFLDSingle-nucleotide polymorphismBiologyTransaminaseRisk Assessment03 medical and health sciencesApolipoproteins ENAFLDmedicineGenetic predispositionHumansGenetic Predisposition to DiseaseHEPATIC STEATOSISGenetic associationMAFLD Phenotype Reproducibility of Results Risk Assessment Risk Factors Transcriptome Genetic Variation Metabolic Associated Fatty Liver Disease Nonalcoholic Fatty Liver Disease Transaminase 1-Acylglycerol-3-Phosphate O-Acyltransferase Alanine Transaminase Apolipoproteins E Biomarkers Europe Exome Gene Expression Profiling Genetic Predisposition to Disease Genome-Wide Association Study Humans Non-alcoholic Fatty Liver DiseaseHepatologyMUTATIONSGene Expression ProfilingGenetic VariationReproducibility of Resultsmedicine.diseaseX-RECEPTORGENE030104 developmental biology3121 General medicine internal medicine and other clinical medicineMetabolic Associated Fatty Liver DiseaseRNA-SEQ DATATranscriptomePATHOGENICITYBiomarkersGenome-Wide Association StudyGastroenterology
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Biology of frailty: Modulation of ageing genes and its importance to prevent age-associated loss of function

2016

Frailty is associated with loss of functional reserve as well as with the prediction of adverse events in the old population. The traditional criteria of frailty are based on five physical determinations described in the Cardiovascular Health Study. We propose that biological and genetic markers of frailty should be used to increase the predictive capacity of the established clinical indeces. In recent times, research for biological markers of frailty has gained impetus. Finding a biological markers with diagnostic and prognostic capacity would be a major milestone to identify frailty risk, and also pre-frailty status. In the first section of the manuscript, we review the available biomarke…

0301 basic medicineGerontologyAgingFrail ElderlyLongevityClinical BiochemistryPopulationPsychological interventionPhysical exercisePolymorphism Single NucleotideBiochemistryLongevity genes03 medical and health sciencesAnimalsHumansMedicineMuscle SkeletaleducationExerciseGeriatric AssessmentMolecular BiologyBeneficial effectsLoss functionAgedAged 80 and overInflammationeducation.field_of_studybusiness.industryEpistasis GeneticGeneral Medicine030104 developmental biologyPharmacological interventionsGene Expression RegulationAgeingMolecular MedicinebusinessBiomarkersSignal TransductionMolecular Aspects of Medicine
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Physical Activity and Nutrition INfluences In ageing (PANINI): consortium mission statement

2018

First paragraph: Current demographic trends indicate that by the year 2020, almost one in five of the European population will be aged 65 years or over. Although life expectancy is increasing by 2 years per decade, the period of life spent in good health is not keeping pace and most Europeans spend their last decade in poor health. Consequently, there is an urgent need to understand how lifestyle factors can influence age-related changes from gene to society level and how they may be integrated into a net effect of healthy ageing. It is also crucial to develop and validate interventions and health policies to ensure that more of our older adults have a healthy and active later life. This is…

0301 basic medicineGerontologyAgingPhysical activitybiomarkkeritravinto03 medical and health sciencesJournal ArticleMedicineMission statementPoint of ViewNutritionHigh prevalencemonitieteisyysMultidisciplinarybusiness.industryGeriatrics gerontologyPhysical activityBiomarkermedicine.disease3. Good healthAgeing030104 developmental biologyikääntyminenAgeing; Biomarkers; Multidisciplinary; Nutrition; Physical activity; Standardised measuresAgeingSarcopeniaStandardised measuresGeriatrics and Gerontologybusinessravitsemusfyysinen aktiivisuusBiomarkersAging Clinical and Experimental Research
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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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