Search results for "neonata"

showing 10 items of 586 documents

DNA Methylation Analysis to Unravel Altered Genetic Pathways Underlying Early Onset and Late Onset Neonatal Sepsis. A Pilot Study

2021

Background: Neonatal sepsis is a systemic condition widely affecting preterm infants and characterized by pro-inflammatory and anti-inflammatory responses. However, its pathophysiology is not yet fully understood. Epigenetics regulates the immune system, and its alteration leads to the impaired immune response underlying sepsis. DNA methylation may contribute to sepsis-induced immunosuppression which, if persistent, will cause long-term adverse effects in neonates.Objective: To analyze the methylome of preterm infants in order to determine whether there are DNA methylation marks that may shed light on the pathophysiology of neonatal sepsis.Design: Prospective observational cohort study perf…

Male0301 basic medicinelcsh:Immunologic diseases. AllergyNeonatal intensive care unitgenetic structuresImmunologyPilot ProjectsLate onsetAdaptive ImmunityBioinformaticsCohort StudiesDiagnosis DifferentialSepsissepsis03 medical and health sciences0302 clinical medicineHumansImmunology and AllergyMedicineProspective StudiesEpigeneticsOriginal ResearchGenomeDNA methylationimmunosuppressionNeonatal sepsisbusiness.industryInfant Newbornneonatology and pediatric intensive careMethylationmedicine.diseaseImmunity Innate030104 developmental biologyinflammation030220 oncology & carcinogenesisDNA methylationBiomarker (medicine)FemaleNeonatal Sepsisbusinesslcsh:RC581-607Infant PrematureFrontiers in Immunology
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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The impact of diet during adolescence on the neonatal health of offspring: evidence on the importance of preconception diet. The HUNT study

2020

Background: Emerging evidence suggests that parents' nutritional status before and at the time of conception influences the lifelong physical and mental health of their child. Yet little is known about the relationship between diet in adolescence and the health of the next generation at birth. This study examined data from Norwegian cohorts to assess the relationship between dietary patterns in adolescence and neonatal outcomes. Methods: Data from adolescents who participated in the Nord-TrA¸ndelag Health Study (Young-HUNT) were merged with birth data for their offspring through the Medical Birth Registry of Norway (MBRN). Young-HUNT1 collected data from 8980 adolescents between 1995 and 19…

MaleAdolescentOffspringDeclarationMedicine (miscellaneous)030209 endocrinology & metabolismNorwegianHelsinki declaration03 medical and health sciences0302 clinical medicineEnvironmental healthHunt studyFood choiceneonatal outcomesFood QualityMedicineHumansInfant Health030212 general & internal medicineNeonatal healthadolescentsResearch ethicsbusiness.industrypreconceptionNorwayHUNT studyMental healthlanguage.human_languagenutritionNeonatal outcomesAdolescent BehaviorCohortlanguageFemalePreconception CarebusinessDemography
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Differential expression of PGC-1α and metabolic sensors suggest age-dependent induction of mitochondrial biogenesis in Friedreich ataxia fibroblasts.

2011

11 pages, 6 figures. PMID:21687738[PubMed] PMCID: PMC3110204

MaleAgingMitochondrial DiseasesMitochondrial MyopathyUbiquinoneCardiomyopathylcsh:MedicineMitochondrionAMP-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAntioxidantsAdenosine TriphosphateAMP-activated protein kinaseTrinucleotide RepeatsFibrosisMolecular Cell BiologyChildlcsh:ScienceHeat-Shock ProteinsRegulation of gene expressionMultidisciplinaryMovement DisordersbiologyNeuromuscular DiseasesMiddle AgedCatalasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyMitochondriaDNA-Binding ProteinsNeurologyDisease ProgressionMedicineFemalemedicine.symptomSignal TransductionResearch ArticleAdultcongenital hereditary and neonatal diseases and abnormalitiesAtaxiaAdolescentMitochondrial ProteinsmedicineGeneticsHumansBiologyAllelesGlutathione PeroxidaseSuperoxide Dismutaselcsh:RHuman GeneticsFibroblastsmedicine.diseaseMolecular biologyOxidative StressMitochondrial biogenesisGene Expression RegulationFriedreich Ataxiabiology.proteinFrataxinlcsh:QEnergy MetabolismReactive Oxygen SpeciesTranscription FactorsPLoS ONE
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Immunological investigations in two brothers with ataxia telangiectasia Louis-Bar

1976

Two of three brothers with the classical signs of ataxia telangiectasia were investigated for their immunological disorders at the ages of 13 and 16 years, respectively. The elder brother also suffers from autoimmune hemolytic anemia, a complication which has not yet been described in the course of ataxia telangiectasia. Immunological investigations made in both brothers showed a reduction in the number and function of T lymphocytes. The number of B lymphocytes was normal, among which there were cells staining for IgA, although serum IgA was absent. It seems possible that this phenomenon is caused by a disturbance in the process of maturation of lymphoid cells with a lack of differentiation…

MaleB-Lymphocytescongenital hereditary and neonatal diseases and abnormalitiesAdolescentbusiness.industryT-LymphocytesPlasma CellsGeneral MedicineSerum igamedicine.diseaseImmunoglobulin AAtaxia TelangiectasiaIMMUNE DEFICIENCY DISEASEPediatrics Perinatology and Child HealthImmunologyAtaxia-telangiectasiamedicineHumansRadiology Nuclear Medicine and imagingAnemia Hemolytic AutoimmuneAutoimmune hemolytic anemiaComplicationbusinessEuropean Journal of Pediatrics
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Distinct Xp11.2 breakpoints in two renal cell carcinomas exhibiting X;autosome translocations

1995

Several human renal cell carcinomas with X;autosome translocations have been reported in recent years. The t(X; I)(p11.2;q21) appears to be a specific primary anomaly, suggesting that tumors with this translocation form a distinct subgroup of RCC. Here we report two new cases, one with a t(X;10)(p11.2;q23), the other with a t(X;1)(p11.2;p34). The common breakpoint in Xp11.2 suggests that they belong to the above-mentioned subset of RCC. Using FISH in conjunction with X-specific YAC clones, we demonstrate that the two new cases exhibited distinct breakpoints within Xp11.2. (C) 1995 Wiley-Liss, Inc.

MaleCancer Researchmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesX ChromosomeChromosomal translocationBiologyTranslocation GeneticCLASSIFICATIONCHILDGeneticsmedicineCarcinomaHumansDe rol van chromosoomafwijkingen en (anti-)oncogenen in humane tumorenCarcinoma Renal CellGeneralLiterature_REFERENCE(e.g.dictionariesencyclopediasglossaries)In Situ Hybridization FluorescenceX chromosomeAgedGeneticsAutosomeBreakpointCytogeneticsKaryotypeADENOCARCINOMAMiddle Agedmedicine.diseaseMolecular biologyTUMORSCYTOGENETICSKidney NeoplasmsChromosome BandingAdenocarcinomaThe role of chromosomal aberrations and (anti-)oncogenes in human tumoursGenes, chromosomes & cancer
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Complete congenital heart block is associated with increased autoantibody titers against calreticulin.

1996

Complete congenital heart block (CCHB) is associated with anti-Ro/SS-A and anti-La/SS-B antibodies. Calreticulin, a calcium-binding, multi-functional protein of the endoplasmic reticulum with C-terminal KDEL-sequence, is not part of the Ro/SS-A ribonucleoprotein complex. In this study anti-calreticulin autoantibody responses in serum samples from 18 infants with CCHB, their mothers and in a control group of 11 anti-Ro/SS-A or anti-La/SS-B positive infants without heart block and their mothers were analysed. Specific enzyme-linked immunosorbent assays were performed. Nine out of 18 sera with CCHB contained IgG anti-calreticulin antibodies. Four sera of those with IgG antibodies also had IgM …

MaleClinical BiochemistryBlotting WesternEnzyme-Linked Immunosorbent AssayBiochemistryAutoantigensImmunopathologymedicineHumansNeonatal lupus erythematosusAutoantibodiesAutoimmune diseaseLupus erythematosusbiologybusiness.industryCalcium-Binding ProteinsAutoantibodyInfant NewbornGeneral Medicinemedicine.diseaseConnective tissue diseaseHeart BlockImmunoglobulin MRibonucleoproteinsImmunoglobulin GImmunologybiology.proteinFemaleAntibodybusinessCalreticulinCalreticulinEuropean journal of clinical investigation
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Laboratory investigations in genetic syndromes: examples of clinical approach in the neonatal unit.

2010

Contiguous gene deletion syndromes: the importance of an accurate genetic definition for a careful clinical monitoring. Contiguous gene deletion syndromes are so named because the deletion manifests as a distinctive cluster of otherwise unrelated single-gene disorders in the same subject. An accurate genetic definition of the deleted region is extremely important for the appropriate management of these patients and for unravelling the function of the involved genes. The microarray-based comparative genomic hybridization (CGH arrays) analysis is the actual molecular method able to accurately define the bounds of a deleted region, since it allows an evaluation of DNA copy number alterations a…

MaleComparative Genomic Hybridizationgenetic syndrome neonategenetic syndromesDisorders of Sex DevelopmentGene DosageGenetic Diseases InbornInfant NewbornLaboratories HospitalEarly DiagnosisPhenotypeSettore MED/38 - Pediatria Generale E SpecialisticaIntensive Care Units NeonatalIntensive Care NeonatalChromosomes HumanHumansFemaleGenetic TestingGene Deletion
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Benign familial infantile epilepsy associated with KCNQ3 mutation: a rare occurrence or an underestimated event?

2020

Abstract Benign familial infantile epilepsy (BFIE) is the most genetically heterogeneous phenotype among early-onset familial infantile epilepsies. It has an autosomal dominant inheritance pattern with incomplete penetrance. Although PRRT2 is the most mutated gene detected in families with BFIE, other mutations in KCNQ2, SCN2A, and GABRA6 genes have also been described. To date, KCNQ3 mutations have been detected in only four patients with BFIE. Here, we describe the clinical pattern and course of an additional individual with BFIE associated with a novel missense heterozygous KCNQ3 c.1850G>C variant inherited by his unaffected father. The incidence of KCNQ3 mutations among BFIE patients…

MaleGABRA6Mutation Missensemedicine.disease_causeKCNQ3 Potassium ChannelEpilepsymutation.medicineHumansMissense mutationBFIEGeneticsBenign familial infantile epilepsyMutationKCNQ3biologybusiness.industryGenetic heterogeneityInfantGeneral Medicinemedicine.diseasePenetranceEpilepsy Benign NeonatalNeurologybenign familial infantile epilepsybiology.proteinincidenceNeurology (clinical)businessPRRT2
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Nuclear localization of the protein encoded by the Wilms’ tumor gene WT1 in embryonic and adult tissues

1993

ABSTRACT The human Wilms’ tumor gene WT1 encodes a putative transcription factor implicated in tumorigenesis and in specifying normal urogenital development. We have studied the distribution of WT1 protein and mRNA using immunohistochemistry and in situ hybridization. Monoclonal antibodies were raised against a peptide specific to the first alternative splice site of WT1. Two antibodies specifically reacted on Western blot to this WT1 isoform. Immunofluorescence localized WT1 protein to podocytes during mesonephric and metanephric development. In situ hybridization revealed a similar pattern of expression except that WT1 mRNA was also present in metanephric blastema and renal vesicles. Mess…

MaleGene isoformcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyBlotting WesternFluorescent Antibody TechniqueGene ExpressionUrogenital SystemIn situ hybridizationBiologyKidneyurologic and male genital diseasesPolymerase Chain ReactionInternal medicineGene expressionmedicineHumansRNA MessengerWT1 ProteinsMolecular BiologyTranscription factorIn Situ HybridizationCell NucleusMessenger RNAGranulosa CellsSertoli Cellsurogenital systemfungiZinc FingersWilms' tumormedicine.diseasefemale genital diseases and pregnancy complicationsWilms Tumor ProteinCell biologyDNA-Binding ProteinsCell nucleusmedicine.anatomical_structureEndocrinologyMesonephrosFemaleTranscription FactorsDevelopmental BiologyDevelopment
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