Search results for "ADO"

showing 10 items of 13500 documents

NKX2-1 New Mutation Associated With Myoclonus, Dystonia, and Pituitary Involvement

2018

Background: NKX2-1 related disorders (also known as brain-lung-thyroid syndrome or benign hereditary chorea 1) are associated with a wide spectrum of symptoms. The core features are various movement disorders, characteristically chorea, less frequently myoclonus, dystonia, ataxia; thyroid disease; and lung involvement. The full triad is present in 50% of affected individuals. Numerous additional symptoms may be associated, although many of these were reported only in single cases. Pituitary dysfunction was ambiguously linked to NKX2-1 haploinsufficiency previously. Case Presentation: We examined two members of a family with motor developmental delay, mixed movement disorder (myoclonus, dyst…

0301 basic medicinePediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesMovement disordersAtaxialcsh:QH426-470NKX2-1 geneCase Reportbenign hereditary choreapituitary03 medical and health sciences0302 clinical medicineBenign hereditary choreamyoclonus dystoniaHypogonadotropic hypogonadismmedicineGeneticschoreaGenetics (clinical)Dystoniabusiness.industryChoreabrain-lung-thyroid syndromemedicine.diseasenervous system diseaseslcsh:Genetics030104 developmental biologyNKX2-1 related disordersempty sellaMolecular Medicinemedicine.symptombusinessHaploinsufficiencyMyoclonus030217 neurology & neurosurgeryFrontiers in Genetics
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A meta-analysis of the validity of FFQ targeted to adolescents.

2015

AbstractObjectiveThe present work is aimed at meta-analysing validity studies of FFQ for adolescents, to investigate their overall accuracy and variables that can affect it negatively.DesignA meta-analysis of sixteen original articles was performed within the ASSO Project (Adolescents and Surveillance System in the Obesity prevention).SettingThe articles assessed the validity of FFQ for adolescents, compared with food records or 24 h recalls, with regard to energy and nutrient intakes.SubjectsPearson’s or Spearman’s correlation coefficients, means/standard deviations, kappa agreement, percentiles and mean differences/limits of agreement (Bland–Altman method) were extracted. Pooled estimates…

0301 basic medicinePercentileAdolescentDatabases FactualMedicine (miscellaneous)Subgroup analysisFFQDiet SurveysStandard deviationValidityCorrelation03 medical and health sciencesStatisticsNutrition and DieteticHumansMeta-analysiObesityMathematicsObesity prevention030109 nutrition & dieteticsNutrition and DieteticsLimits of agreementPublic Health Environmental and Occupational HealthReproducibility of ResultsResearch PapersMeta-analysisMental RecallEnergy IntakeKappaPublic health nutrition
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DNA methylation links prenatal smoking exposure to later life health outcomes in offspring

2019

Background Maternal smoking during pregnancy is associated with adverse offspring health outcomes across their life course. We hypothesize that DNA methylation is a potential mediator of this relationship. Methods We examined the association of prenatal maternal smoking with offspring blood DNA methylation in 2821 individuals (age 16 to 48 years) from five prospective birth cohort studies and perform Mendelian randomization and mediation analyses to assess whether methylation markers have causal effects on disease outcomes in the offspring. Results We identify 69 differentially methylated CpGs in 36 genomic regions (P value < 1 × 10−7) associated with exposure to maternal smoking in adolesc…

0301 basic medicinePhysiologyraskausDiseaseBioinformaticsEpigenesis Genetic/dk/atira/pure/core/keywords/icepCohort Studies0302 clinical medicinePregnancyGTP-Binding Protein gamma SubunitsEpidemiologySCHIZOPHRENIADiseaseLongitudinal StudiesProspective StudieskohorttitutkimusGenetics (clinical)Maternal smokingGenetics & HeredityRISK0303 health sciencesDNA methylationSmokingWIDEMethylationASSOCIATIONMiddle AgedDNA-metylaatio3. Good healthCausalityPREGNANCYOncologyMaternal ExposureSchizophreniaPrenatal Exposure Delayed Effects030220 oncology & carcinogenesisDNA methylationkausaliteettilifecourseLife course approachFemaleICEPLife Sciences & BiomedicineAdultTOBACCO-SMOKEMediation (statistics)medicine.medical_specialtyAdolescentOffspringBirth weightPersistenceYoung Adult03 medical and health sciencestupakointiterveysvaikutuksetMendelian randomizationGeneticsmedicineHumansMolecular BiologyMETAANALYSIS030304 developmental biologyPregnancyScience & TechnologyIDENTIFICATIONbusiness.industryMATERNAL CIGARETTE-SMOKINGResearchMediationLife courseMendelian Randomization Analysismedicine.diseaseBIRTH-WEIGHT030104 developmental biologyCpG Islandsbusiness030217 neurology & neurosurgeryGenome-Wide Association StudyDevelopmental Biology
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The morphogenetically active polymer, inorganic polyphosphate complexed with GdCl 3 , as an inducer of hydroxyapatite formation in vitro

2015

Inorganic polyphosphate (polyP) is a physiological polymer composed of tens to hundreds of phosphate units linked together via phosphoanhydride bonds. Here we compared the biological activity of polyP (chain length of 40 phosphate units), complexed with Gd(3+) (polyP·Gd), with the one caused by polyP (as calcium salt) and by GdCl3 alone, regarding their potencies to induce hydroxyapatite (HA) formation in SaOS-2 cells in vitro. The three compounds, GdCl3, polyP and polyP·Gd were found to be non-toxic at concentrations up to at least 30μM. Selecting a low, 5μM, concentration it was found that polyP·Gd significantly induced HA formation, as determined by Alizarin Red S staining and by quantit…

0301 basic medicinePolymerschemistry.chemical_elementGadolinium02 engineering and technologyCalciumBiochemistry03 medical and health scienceschemistry.chemical_compoundPolyphosphatesCell Line Tumorotorhinolaryngologic diseasesHumansneoplasmsSaos-2 cellsPharmacologychemistry.chemical_classificationDose-Response Relationship DrugChemistryPolyphosphateBiological activitypathological conditions signs and symptoms021001 nanoscience & nanotechnologyPhosphatedigestive system diseasesIn vitroDurapatitesurgical procedures operative030104 developmental biologyEnzymeBiochemistryAlkaline phosphatase0210 nano-technologyBiochemical Pharmacology
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Diagnostic Targeted Resequencing in 349 Patients with Drug-Resistant Pediatric Epilepsies Identifies Causative Mutations in 30 Different Genes

2017

Targeted resequencing gene panels are used in the diagnostic setting to identify gene defects in epilepsy. We performed targeted resequencing using a 30-genes panel and a 95-genes panel in 349 patients with drug-resistant epilepsies beginning in the first years of life. We identified 71 pathogenic variants, 42 of which novel, in 30 genes, corresponding to 20.3% of the probands. In 66% of mutation positive patients seizures onset occurred before age 6 months. The 95-genes panel allowed a genetic diagnosis in 22 (6.3%) patients that would have otherwise been missed using the 30-gene panel. About 50% of mutations were identified in genes coding for sodium and potassium channel components. SCN2…

0301 basic medicineProbandMaleCDKL5Drug Resistancemedicine.disease_causeBioinformaticsEpilepsyAnticonvulsantSTXBP1Age of OnsetChildGenetics (clinical)AlleleMutationepilepsy; next-generation sequencing; gene panel; mutationPhenotypeMagnetic Resonance ImagingSettore MED/39 - Neuropsichiatria Infantile3. Good healthPhenotypeChild PreschoolAnticonvulsantsFemaleSequence AnalysisHumanAdolescentGenotypeGenetic Association StudieBiologyMECP203 medical and health sciencesGeneticgene panelGeneticsmedicineHumansGenetic Predisposition to DiseasePreschoolGeneAllelesGenetic Association StudiesGene Expression ProfilingInfant NewbornComputational BiologyInfantMolecular Sequence AnnotationDNASequence Analysis DNANewbornmedicine.disease030104 developmental biologyepilepsynext-generation sequencingmutation
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Mutations in the GLA Gene and LysoGb3: Is It Really Anderson-Fabry Disease?

2018

Anderson-Fabry disease (FD) is a rare, progressive, multisystem storage disorder caused by the partial or total deficit of the lysosomal enzyme &alpha

0301 basic medicineProbandMaleDiseasemedicine.disease_causeSphingolipidCatalysilcsh:Chemistry0302 clinical medicineGla geneFabry disease; GLA gene; LysoGb3MedicineChildlcsh:QH301-705.5Spectroscopychemistry.chemical_classificationGeneticsAlleleAged 80 and overMutationComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineMiddle AgedPhenotype3. Good healthComputer Science ApplicationsPhenotypeChild PreschoolFemaleHumanAdultAdolescentGenotypeGlycolipidCatalysisArticleInorganic Chemistry03 medical and health sciencesYoung Adultotorhinolaryngologic diseasesHumansPhysical and Theoretical ChemistryMolecular BiologyGeneGLA geneAllelesAgedFabry diseaseSphingolipidsbusiness.industryOrganic ChemistryInfant NewbornLysoGb3InfantBiomarkerFabry disease; gla gene; lysogb3; adolescent; adult; aged; aged 80 and over; alleles; amino acid substitution; biomarkers; child; child preschool; fabry disease; female; genotype; glycolipids; humans; infant; infant newborn; male; middle aged; phenotype; sphingolipids; young adult; alpha-galactosidase; mutationmedicine.diseaseFabry disease030104 developmental biologyEnzymechemistrylcsh:Biology (General)lcsh:QD1-999Amino Acid Substitutionalpha-GalactosidaseMutationGlycolipidsbusiness030217 neurology & neurosurgeryBiomarkersInternational Journal of Molecular Sciences
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HCN1 mutation spectrum: from neonatal epileptic encephalopathy to benign generalized epilepsy and beyond

2018

International audience; Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control neuronal excitability and their dysfunction has been linked to epileptogenesis but few individuals with neurological disorders related to variants altering HCN channels have been reported so far. In 2014, we described five individuals with epileptic encephalopathy due to de novo HCN1 variants. To delineate HCN1-related disorders and investigate genotype-phenotype correlations further, we assembled a cohort of 33 unpublished patients with novel pathogenic or likely pathogenic variants: 19 probands carrying 14 different de novo mutations and four families with dominantly inherited variants segre…

0301 basic medicineProbandMaleModels MolecularPotassium Channels[SDV]Life Sciences [q-bio]Medizinmedicine.disease_causeEpileptogenesisMembrane PotentialsEpilepsy0302 clinical medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMissense mutationChildGeneticsMutationMiddle AgedPhenotype3. Good healthTransmembrane domainclinical spectrum; epilepsy; HCN1; intellectual disability; ion channelintellectual disabilityChild PreschoolEpilepsy GeneralizedFemaleSpasms InfantileAdultAdolescentCHO CellsBiology03 medical and health sciencesYoung AdultCricetulusHCN1medicineAnimalsHumansGeneralized epilepsyGenetic Association StudiesAgedInfantmedicine.diseaseElectric Stimulationclinical spectrum030104 developmental biologyMutationion channelMutagenesis Site-DirectedepilepsyNeurology (clinical)030217 neurology & neurosurgery
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Confirmation of PDZD7 as a Nonsyndromic Hearing Loss Gene.

2016

Objective PDZD7 was identified in 2009 in a family with apparent nonsyndromic sensorineural hearing loss. However, subsequent clinical reports have associated PDZD7 with digenic Usher syndrome, the most common cause of deaf-blindness, or as a modifier of retinal disease. No further reports have validated this gene for nonsyndromic hearing loss, intuitively calling correct genotype-phenotype association into question. This report describes a validating second case for biallelic mutations in PDZD7 causing nonsyndromic mild to severe sensorineural hearing loss. It also provides detailed audiometric and ophthalmologic data excluding Usher syndrome in both the present proband (proband 1) and the…

0301 basic medicineProbandMalemedicine.medical_specialtyHeterozygoteAdolescentHearing lossUsher syndromeHearing Loss SensorineuralOtoacoustic Emissions SpontaneousAudiologyCompound heterozygosity03 medical and health sciencesSpeech and Hearing0302 clinical medicineotorhinolaryngologic diseasesmedicineEvoked Potentials Auditory Brain StemHumansGenetic Predisposition to DiseaseChildAllelesmedicine.diagnostic_testbusiness.industryAudiogramSequence Analysis DNAmedicine.diseaseMinor allele frequency030104 developmental biologyOtorhinolaryngologyMutationAudiometry Pure-ToneSensorineural hearing lossFemaleAudiometrymedicine.symptombusinessCarrier Proteins030217 neurology & neurosurgeryEar and hearing
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The expression and prognostic relevance of programmed cell death protein 1 in tongue squamous cell carcinoma

2020

Background Programmed cell death protein 1 (PD‐1) is an immune checkpoint receptor which plays an important role in a patient´s immune responses to microbial and cancer antigens. It is expressed in tumor infiltrating lymphocytes (TILs) with many different malignancies. The aim of the study was to evaluate PD‐1 expression and its prognostic value in tongue cancer. Methods The data of tongue squamous cell carcinoma (TSCC) patients (N=81) treated in Tampere University Hospital between 1999‐2013 was used. Control data consisted of patients with non‐malignant tongue mucous membrane lesions (N=48). The formalin‐fixed paraffin‐embedded samples were stained immunohistochemically and scanned via dig…

0301 basic medicineProgrammed Cell Death 1 Receptorbiomarkkerittongue squamous cell carcinomaLYMPHOCYTES0302 clinical medicineImmunology and AllergyEPIDEMIOLOGYReceptorDISSECTIONAged 80 and over11832 Microbiology and virologyLIGAND 1 PD-L1Mucous membranemolekyylitGeneral MedicineMiddle AgedCANCER3. Good healthTongue Neoplasmsmedicine.anatomical_structure030220 oncology & carcinogenesisimmunohistochemistryCarcinoma Squamous CellSURVIVALImmunohistochemistrysyöpätauditProgrammed cell death protein 1 (PD-1)Microbiology (medical)AdultAdolescentPathology and Forensic Medicine03 medical and health sciencesYoung AdultImmune systemAntigenTonguePOOR-PROGNOSISmedicineBiomarkers TumorHumansNECKAgedmolecular markerbusiness.industryHUMAN-PAPILLOMAVIRUSCancerennusteetprogrammed cell death protein 1 (PD‐1)medicine.diseaseImmune checkpoint030104 developmental biologyCancer researchT-CELLSprognosis3111 Biomedicinebusiness
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Accelerated telomere attrition in children and teenagers with α1-antitrypsin deficiency.

2016

Numerous studies have shown that oxidative stress accelerates telomere shortening in several lung pathologies. Since oxidative stress is involved in the pathophysiology of α1-antitrypsin deficiency (AATD), we hypothesised that telomere shortening would be accelerated in AATD patients. This study aimed to assess telomere length in AATD patients and to study its association with α1-antitrypsin phenotypes.Telomere length, telomerase activity, telomerase reverse transcriptase (hTERT) expression and biomarkers of oxidative stress were measured in 62 children and teenagers (aged 2–18 years) diagnosed with AATD and 18 controls (aged 3–16 years).Our results show that intermediate-risk (MZ; SZ) and …

0301 basic medicinePulmonary and Respiratory MedicineOncologyMalemedicine.medical_specialtyTelomeraseAdolescentmedicine.disease_causeBody Mass Index03 medical and health sciencesInternal medicinealpha 1-Antitrypsin DeficiencymedicineHumansTelomerase reverse transcriptaseChildLungTelomeraseTelomere ShorteningAlpha 1-antitrypsin deficiencybusiness.industryCase-control studyTelomeremedicine.diseaseMolecular biologyPathophysiologyTelomereOxidative Stress030104 developmental biologyPhenotypeSpirometryCase-Control StudiesChild PreschoolBiomarker (medicine)FemalebusinessOxidative stress
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