Search results for "Cause"

showing 10 items of 6525 documents

Multicomponent Training Prevents Memory Deficit Related to Amyloid-β Protein-Induced Neurotoxicity.

2021

Background: Alzheimer’s disease (AD) is characterized by the accumulation of the amyloid-β peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. Objective: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aβ neurotoxicity. Methods: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-β peptide into their hippocampus. Results: We show that long-term multicomponent training prevents …

0301 basic medicineMaleHippocampusPhysical exercisePharmacologyHippocampal formationmedicine.disease_causeHippocampusLipid peroxidationStereotaxic Techniques03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysical Conditioning AnimalMedicineAnimalsRats WistarRecognition memoryMemory DisordersAmyloid beta-Peptidesbusiness.industryGeneral NeuroscienceNeurotoxicityBrainGeneral Medicinemedicine.diseaseRatsPsychiatry and Mental healthClinical PsychologyDisease Models AnimalOxidative Stress030104 developmental biologychemistryNeurotoxicity SyndromesLipid PeroxidationGeriatrics and GerontologybusinessAnaerobic exercise030217 neurology & neurosurgeryOxidative stressJournal of Alzheimer's disease : JAD
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Protective and causative killer Ig-like receptor (KIR) and metalloproteinase genetic patterns associated with Herpes simplex virus 1 (HSV-1) encephal…

2020

Abstract Background The cerebral innate immune system has a critical role in control processes of viral replication in the brain after primary infactivo and immunologic disregulation and inflammation has been reported as a primary determinant of pathogenesis and prognosis of subsequent HSV-1 related encephalitis (HSE). Interaction linking LTR3-activated DCs is also represented by the killer Ig-like receptor (KIR) + pathways on NK cells. Only a few studies analyzed the role of of MMP-9 activity regulating genetic polymorphism on clinical outcome of viral infections. Susceptibility to symptomatic encephalitis depends on SNC viral invasion and BBB disruption. We hypothesize that certain KIR ge…

0301 basic medicineMaleImmunologyHuman leukocyte antigenHerpesvirus 1 Humanmedicine.disease_causePathogenesisCohort StudiesMetalloprotease03 medical and health sciences0302 clinical medicineReceptors KIRHLA AntigensEncephalitiGenotypemedicineImmunology and AllergyHumansEncephalitis ViralHLA AntigenAllele frequencyAgedbusiness.industryHaplotypeHerpes SimplexMiddle Agedmedicine.diseaseHSV-1KIR030104 developmental biologyHerpes simplex virusNeurologyViral replicationMatrix Metalloproteinase 9ImmunologyMetalloproteasesFemaleNeurology (clinical)Cohort StudiebusinessInfectionMMP-9030217 neurology & neurosurgeryEncephalitis
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The significance of epidermal growth factor receptor uncommon mutations in non-small cell lung cancer: A systematic review and critical appraisal

2020

Uncommon epidermal growth factor receptor (EGFR) mutations collectively account for 10% of EGFR mutations, harboring heterogeneous molecular alterations within exons 18-21 with clinically variable responses to EGFR tyrosine kinase inhibitors (TKIs) in advanced Non-Small Cell Lung Cancer (NSCLC) patients. In addition, with the introduction of different NGS gene approach an improvement of EGFR mutations detection was reported. Today, no specific studies have prospectively evaluated uncommon sensitizing mutations in detail and no firm standard of care has been established in the first-line setting. The aim of this comprehensive review is to critically consider the clinical role of uncommon EGF…

0301 basic medicineMaleLung NeoplasmsPrognosiEGFRProtein Kinase Inhibitormedicine.disease_causeNSCLC03 medical and health sciencesExonErbB Receptors0302 clinical medicineCarcinoma Non-Small-Cell LungmedicineCarcinomaHumansRadiology Nuclear Medicine and imagingEpidermal growth factor receptorErbB ReceptorLung cancerGeneProtein Kinase InhibitorsRegulation of gene expressionMutationbiologybusiness.industryGeneral Medicinemedicine.diseasePrognosisTKIUncommon mutationErbB ReceptorsGene Expression Regulation NeoplasticLung Neoplasm030104 developmental biologyTreatment OutcomeOncology030220 oncology & carcinogenesisNGSMutationCancer researchbiology.proteinSystematic reviewFemalebusinessHuman
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Myeloid Cells Restrict MCMV and Drive Stress- Induced Extramedullary Hematopoiesis through STAT1

2019

Cytomegalovirus (CMV) has a high prevalence worldwide, is often fatal for immunocompromised patients, and causes bone marrow suppression. Deficiency of signal transducer and activator of transcription 1 (STAT1) results in severely impaired antiviral immunity. We have used cell- type restricted deletion of Stat1 to determine the importance of myeloid cell activity for the defense against murine CMV (MCMV). We show that myeloid STAT1 limits MCMV burden and infection- associated pathology in the spleen but does not affect ultimate clearance of infection. Unexpectedly, we found an essential role of myeloid STAT1 in the induction of extramedullary hematopoiesis (EMH). The EMH- promoting function…

0301 basic medicineMaleMuromegalovirusMyeloidIFN-II receptorReceptor Interferon alpha-betamonocytes signal transducer and activator of transcription Herpesviridae IFN-I receptor IFN-II receptor L-27 receptor TLR9 agonistmedicine.disease_causeVirus Replication0302 clinical medicineTLR9 agonistMyeloid CellsSTAT1Cells CulturedHerpesviridaeReceptors Interferonsignal transducer and activator of transcriptionvirus diseasesIL-27 receptorHerpesviridae InfectionsExtramedullary hematopoiesisKiller Cells NaturalHaematopoiesismedicine.anatomical_structureSTAT1 Transcription FactorBone marrow suppressionHematopoiesis ExtramedullaryFemalemonocytesBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.SpleenBiologyGeneral Biochemistry Genetics and Molecular BiologyHerpesviridaeArticle03 medical and health sciencesStress PhysiologicalmedicineAnimalsBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Receptors Interleukinmedicine.diseaseMice Inbred C57BL030104 developmental biologyImmunologySTAT proteinbiology.protein030217 neurology & neurosurgeryGene DeletionSpleenIFN-I receptor
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A possible role of FANCM mutations in male breast cancer susceptibility: Results from a multicenter study in Italy

2018

Abstract Introduction Breast cancer (BC) in men is a rare disease, whose etiology appears to be associated with genetic factors. Inherited mutations in BRCA1/2 genes account for about 10–15% of all cases. FANCM, functionally linked to BRCA1/2, has been suggested as a novel BC susceptibility gene. Our aim was to test if FANCM germline mutations could further explain male BC (MBC) susceptibility. Methods We screened the entire coding region of FANCM in 286 MBCs by a multi-gene panel analysis, and compared these data with available whole exome sequencing data from 415 men used as population controls. Moreover, we genotyped the two most frequent FANCM mutations (c.5101C>T and c.5791C>T) in 506 …

0301 basic medicineMaleMutation rateSettore MED/06 - Oncologia MedicaDNA Helicasemedicine.disease_causeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; Adult; Aged; Aged 80 and over; Biomarkers Tumor; Breast Neoplasms Male; Case-Control Studies; DNA Helicases; Genetic Predisposition to Disease; Genotype; Germ-Line Mutation; Humans; Italy; Male; Middle Aged; Risk Factors; Whole Genome Sequencing; Young Adult; Surgery0302 clinical medicineFANCMRisk Factorshemic and lymphatic diseasesGermline mutationGenotypeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; SurgeryFANCMMutation frequencyGeneticsAged 80 and overeducation.field_of_studyMutationGeneral MedicineMiddle AgedItaly030220 oncology & carcinogenesisMale breast cancerCase-Control StudieHumanAdultcongenital hereditary and neonatal diseases and abnormalitiesGenotypePopulationBreast Neoplasms Male03 medical and health sciencesYoung AdultGermline mutationBRCA1/2medicineBiomarkers TumorHumansGenetic Predisposition to DiseaseeducationGermline mutationsGerm-Line MutationAgedBreast cancer susceptibilityWhole Genome Sequencingbusiness.industryRisk FactorDNA Helicasesnutritional and metabolic diseasesmedicine.diseaseMale breast cancer030104 developmental biologyCase-Control StudiesSurgerybusiness
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Temporal dynamics of the tick Ixodes ricinus in northern Europe : epidemiological implications

2017

Background Tick-borne pathogens pose an increasing threat to human and veterinary health across the northern hemisphere. While the seasonal activity of ticks is largely determined by climatic conditions, host-population dynamics are also likely to affect tick abundance. Consequently, abundance fluctuations of rodents in northern Europe are expected to be translated into tick dynamics, and can hence potentially affect the circulation of tick-borne pathogens. We quantified and explained the temporal dynamics of the tick Ixodes ricinus in the northernmost part of its European geographical range, by estimating (i) abundance in vegetation and (ii) infestation load in the most common rodent speci…

0301 basic medicineMaleNymphIxodes ricinusTime FactorsPopulation dynamics030231 tropical medicineIxodes ricinusTickmedicine.disease_causeModels BiologicalRodent hostlcsh:Infectious and parasitic diseasesrodent host03 medical and health sciences0302 clinical medicinekansanterveysInfestationparasitic diseasesmedicineAnimalslcsh:RC109-216NymphPublic healthbiologyIxodesEcologyArvicolinaeseasonalityResearchRicinusfungiSeasonalitybiology.organism_classificationpopulaatiodynamiikkaTick InfestationsBank vole030104 developmental biologyInfectious DiseasesArvicolinaeLarvaParasitologyIxodesFemaleSeasons
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The burden and epidemiology of community-acquired central nervous system infections: a multinational study

2017

Ghaydaa, Shehata/0000-0002-3631-893X; Radic, Ljiljana Betica/0000-0002-8778-106X; Silva-Pinto, Andre/0000-0002-2077-3356; Cascio, Antonio/0000-0002-1992-1796; Bossi, Paolo/0000-0003-0135-0224; Stebel, Roman/0000-0001-6922-4465; Namani, Sadie/0000-0002-2411-8623; Chan, Phillip/0000-0002-4071-4409; Hargreaves, Sally/0000-0003-2974-4348; Artuk, Cumhur/0000-0003-0827-990X; Harxhi, Arjan/0000-0001-8518-7377; Larsen, Lykke/0000-0002-4113-4182; Uysal, Serhat/0000-0002-4294-5999 WOS: 000407582200010 PubMed: 28397100 Risk assessment of central nervous system (CNS) infection patients is of key importance in predicting likely pathogens. However, data are lacking on the epidemiology globally. We perfor…

0301 basic medicineMaleOutcome AssessmentAdverse Clinical Outcomemedicine.disease_causeCentral nervous system infections ; burden ; epidemiologyMedical microbiologyCentral Nervous System InfectionsOutcome Assessment Health CareEpidemiology80 and overAged 80 and overbiologyAge FactorsGeneral MedicineMiddle AgedCommunity-Acquired InfectionsInfectious Diseases[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyPopulation SurveillanceFemaleNeuroborreliosisHuman Immunodeficiency VirusMicrobiology (medical)Adultmedicine.medical_specialtyTuberculosisSettore MED/17 - Malattie Infettive030106 microbiologyBrain AbscessCentral Nervous System InfectionNeurosyphilisMycobacterium tuberculosis03 medical and health sciencesYoung AdultInternal medicineStreptococcus pneumoniaeJournal ArticlemedicineHumansAgedRetrospective Studiesbusiness.industryVaricella zoster virusmedicine.diseasebiology.organism_classificationHealth CareCross-Sectional StudiesCentral Nervous System DiseaseBrain AbsceHuman Immunodeficiency ViruImmunologybusiness
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