Search results for "Family health"

showing 10 items of 78 documents

Familial aggregation of tumors and detection of hereditary non-polyposis colorectal cancer in 3-year experience of 2 population-based colorectal-canc…

1995

The clinical data of 2 population-based registries, located in areas with different incidence rates of colorectal cancer, were used in order to assess the role of familial factors in the pathogenesis of these tumors. The occurrence of tumors in family members was investigated in 389 subjects with colorectal cancer registered in Modena (Northern Italy, an area characterized by a high incidence of colorectal malignancies) between 1984 and 1986; similar information was obtained in 213 patients with tumors of the large bowel registered in Ragusa (Sicily, Southern Italy, an area of similar magnitude and with low incidence rates for these tumors) in the 3-year period 1988 to 1990. In both series,…

MaleCancer Researchmedicine.medical_specialtyColorectal cancerPopulationRisk FactorsInternal medicineEpidemiologyPrevalenceMedicineHumansRegistriesRisk factoreducationAgedFamily Healtheducation.field_of_studybusiness.industryIncidence (epidemiology)IncidenceCancerFamily aggregationmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisLynch syndromeSurgerynot availableOncologyItalyEvaluation Studies as TopicCase-Control StudiesFemalebusinessColorectal NeoplasmsInternational journal of cancer
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Fibrinogen Naples I (Bβ A68T) Nonsubstrate Thrombin-Binding Capacities

2001

Fibrinogen Naples I (Bbeta A68T) is characterized by defective thrombin binding and fibrinopeptide cleavage at the fibrinogen substrate site in the E domain. We evaluated the fibrinogen of three homozygotic members of this kindred (II.1, II.2, II.3) who have displayed thrombophilic phenotypes and two heterozygotic subjects (I.1, I.2) who were asymptomatic. Electron microscopy of Naples I fibrin networks showed relatively wide fiber bundles, probably due to slowed fibrin assembly secondary to delayed fibrinopeptide release. We evaluated 125I-thrombin binding to the fibrin from subjects I.1, I.2, II.1, and II.2 by Scatchard analysis with emphasis on the high-affinity site in the D domain of f…

MaleCleavage (embryo)FibrinogenFibrinEpitopeRadioligand AssayThrombinmedicineHumansFibrinopeptideBinding siteFamily Healthchemistry.chemical_classificationFibrinBinding SitesbiologyFibrinogens AbnormalThrombinSequence Analysis DNAHematologyMolecular biologyEnzymeBiochemistrychemistryMicroscopy Electron Scanningbiology.proteinFemaleProtein Bindingmedicine.drugThrombosis Research
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Functioning of family system in pediatric oncology during treatment phase.

2012

The study focuses on parents’ psychological implications caused by the treatment of their children suffering from tumor. It investigates some specific mothers’ resource factors such as their strategies of coping and the perception of their own family functioning in terms of cohesion and adaptability. The study was performed with 34 mothers of children suffering from acute lymphoblastic leukemia(ALL),duringthetreatmentphase.TheusedtoolsweretheCopingOrientationtoProblem Experienced—New Italian Version, to investigate coping strategies, and the Family Adaptability and Cohesion Evaluation Scale-III, to analyze both real and ideal perception of family functioning. The data related to coping, show h…

MaleCoping (psychology)media_common.quotation_subjectLymphoblastic LeukemiaFamily functioningcompliance coping behavior family pediatric oncology psychology/psychiatry quality of life/psychosocial treatmentMothersMedical OncologyPediatricsAdaptabilityDevelopmental psychologySocial supportPerceptionAdaptation PsychologicalAntineoplastic Combined Chemotherapy ProtocolsPediatric oncologyMedicineHumansChildmedia_commonFamily Healthbusiness.industrySocial SupportHematologyPrecursor Cell Lymphoblastic Leukemia-LymphomaOncologyPediatrics Perinatology and Child HealthAptitudeFemalebusinessPediatric hematology and oncology
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In-frame deletion in the seventh immunoglobulin-like repeat of filamin C in a family with myofibrillar myopathy.

2009

Myofibrillar myopathies (MFMs) are an expanding and increasingly recognized group of neuromuscular disorders caused by mutations in DES, CRYAB, MYOT, and ZASP. The latest gene to be associated with MFM was FLNC; a p.W2710X mutation in the 24th immunoglobulin-like repeat of filamin C was shown to be the cause of a distinct type of MFM in several German families. We studied an International cohort of 46 patients from 39 families with clinically and myopathologically confirmed MFM, in which DES, CRYAB, MYOT, and ZASP mutations have been excluded. In patients from an unrelated family a 12-nucleotide deletion (c.2997_3008del) in FLNC resulting in a predicted in-frame four-residue deletion (p.Val…

MaleFilaminsDNA Mutational AnalysisImmunoblottingMolecular Sequence DataImmunoglobulinsmacromolecular substancesBiologymedicine.disease_causeFilaminArticle03 medical and health sciences0302 clinical medicineContractile ProteinsMuscular DiseasesMyofibrilsGeneticsmedicineHumansFLNCAmino Acid SequenceMyopathyRepeated sequenceMuscle SkeletalGenePeptide sequenceGenetics (clinical)030304 developmental biologyRepetitive Sequences Nucleic AcidSequence DeletionGeneticsFamily Health0303 health sciencesMutationSequence Homology Amino AcidMicrofilament Proteinsmedicine.diseaseMolecular biologyImmunohistochemistry3. Good healthMicroscopy ElectronMutationFemalemedicine.symptom030217 neurology & neurosurgeryLimb-girdle muscular dystrophyEuropean journal of human genetics : EJHG
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Next-generation sequencing confirms the implication of SLC24A1 in autosomal-recessive congenital stationary night blindness.

2015

Congenital stationary night blindness (CSNB) is a clinically and genetically heterogeneous retinal disorder which represents rod photoreceptor dysfunction or signal transmission defect from photoreceptors to adjacent bipolar cells. Patients displaying photoreceptor dysfunction show a Riggs-electroretinogram (ERG) while patients with a signal transmission defect show a Schubert-Bornschein ERG. The latter group is subdivided into complete or incomplete (ic) CSNB. Only few CSNB cases with Riggs-ERG and only one family with a disease-causing variant in SLC24A1 have been reported. Whole-exome sequencing (WES) in a previously diagnosed icCSNB patient identified a homozygous nonsense variant in SL…

MaleGenes RecessiveSodium-Calcium ExchangerNight BlindnessElectroretinographyMyopiaHumansExomeGenetic Predisposition to DiseaseAmino Acid SequenceSLC24A1Family HealthHigh-throughput sequencingBase SequenceSequence Homology Amino AcidSettore MED/30 - Malattie Apparato VisivoHomozygoteHigh-Throughput Nucleotide SequencingEye Diseases HereditaryGenetic Diseases X-LinkedPedigreeNight BlindneMutationFemaleCongenital stationary night blindneHumanClinical genetics
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A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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Cathepsin C gene: First compound heterozygous patient with Papillon-Lefèvre syndrome and a novel symptomless mutation.

2001

Papillon-Lefevre syndrome (PLS) has recently been shown to be caused by mutations in the cathepsin C gene resulting in periodontal disease and palmoplantar keratosis. Thirteen different homozygous mutations have been characterised in PLS patients of different ethnic origin. In the present paper, a PLS patient is described who carries two novel mutations (706G>T and 872G>A) in the paternal and maternal chromosomes, respectively. This is the first compound patient described so far. In addition, a novel symptomless mutation (458C>T) in the cathepsin C gene is described in three homozygous individuals. Thus, not all mutations should be considered as a cause of disease, whether case studies or g…

MaleHeterozygoteHaim–Munk syndromeDNA Mutational AnalysisMolecular Sequence DataMutation MissensePapillon–Lefèvre syndromeBiologyCompound heterozygositymedicine.disease_causePapillon-Lefevre DiseaseCathepsin CCathepsin CPapillon-Lefevre DiseaseGene FrequencyGeneticsmedicineHumansAlleleAllele frequencyAllelesGenetics (clinical)Family HealthGeneticsMutationDNAmedicine.diseaseMutationFemale
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Partial replication of a DRD4 association in ADHD individuals using a statistically derived quantitative trait for ADHD in a family-based association…

2007

Contains fulltext : 52515.pdf (Publisher’s version ) (Closed access) BACKGROUND: Previous research found an association between single nucleotide polymorphisms (SNPs) in the promoter region of DRD4 and statistically derived phenotypes generated from attention-deficit/hyperactivity disorder (ADHD) symptoms. We sought to replicate this finding by using the same methodology in an independent sample of ADHD individuals. METHODS: Four SNPs were genotyped in and around DRD4 in 2631 individuals in 642 families. We developed a quantitative phenotype at each SNP by weighting nine inattentive and nine hyperactive-impulsive symptoms. The weights were selected to maximize the heritability at each SNP. …

MaleLinkage disequilibriumGenetics and epigenetic pathways of disease [NCMLS 6]Databases FactualMedizinNeuroinformatics [DCN 3]Severity of Illness Index0302 clinical medicinePerception and Action [DCN 1]Determinants in Health and Disease [EBP 1]ChildPromoter Regions GeneticGenetics0303 health sciencesEuropePhenotypeChild PreschoolFemalemedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]medicine.medical_specialtyAdolescentSingle-nucleotide polymorphismQuantitative trait locusImpulsivityMental health [NCEBP 9]Polymorphism Single NucleotideGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesQuantitative Trait HeritableCognitive neurosciences [UMCN 3.2]Genetic modelmental disordersmedicineAttention deficit hyperactivity disorderSNPHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersPsychiatryBiological Psychiatry030304 developmental biologyFamily HealthReceptors Dopamine D4Heritabilitymedicine.diseaseGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivity030217 neurology & neurosurgeryBiological psychiatry
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Linkage disequilibrium of MTHFR genotypes 677C/T-1298A/C in the German population and association studies in probands with neural tube defects(NTD).

1999

A number of studies have demonstrated that the common polymorphism 677CT in the gene encoding 5, 10-methylenetetrahydrofolate reductase (MTHFR) leads to a thermolabile variant with decreased enzyme activity and to mildly elevated plasma homocysteine. 677TT homozygosity was shown to be more frequent in NTD probands compared with controls in some studies. Recently, another polymorphism, 1298AC, in the MTHFR gene was described and combined heterozygosity 677CT/1298AC was suggested to be an additional risk factor for NTD. The present study examines the genotype and haplotype distribution of the two polymorphisms in the German population and evaluates the impact on NTD individuals and their rela…

MaleLinkage disequilibriumGenotypePopulationLinkage DisequilibriumFetusGene FrequencyGermanyHumansNeural Tube DefectseducationAllele frequencyGenetics (clinical)AllelesMethylenetetrahydrofolate Reductase (NADPH2)Genetic associationGeneticsFamily Healtheducation.field_of_studyOxidoreductases Acting on CH-NH Group DonorsPolymorphism GeneticbiologyHaplotypeTransmission disequilibrium testDNAGenotype frequencyPedigreeHaplotypesMethylenetetrahydrofolate reductaseCase-Control StudiesPopulation SurveillanceMutationbiology.proteinFemaleAmerican journal of medical genetics
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Neurophysiology in preschool improves behavioral prediction of reading ability throughout primary school.

2009

BACKGROUND: More struggling readers could profit from additional help at the beginning of reading acquisition if dyslexia prediction were more successful. Currently, prediction is based only on behavioral assessment of early phonological processing deficits associated with dyslexia, but it might be improved by adding brain-based measures. METHODS: In a 5-year longitudinal study of children with (n = 21) and without (n = 23) familial risk for dyslexia, we tested whether neurophysiological measures of automatic phoneme and tone deviance processing obtained in kindergarten would improve prediction of reading over behavioral measures alone. RESULTS: Together, neurophysiological and behavioral m…

MaleLongitudinal studyAgingmedia_common.quotation_subjectMismatch negativityNeuropsychological TestsLateralization of brain functionDevelopmental psychologyDyslexiaCommunication disorderPhoneticsPredictive Value of TestsmedicineHumansLanguage disorderNervous System Physiological PhenomenaLongitudinal StudiesChildEvoked PotentialsBiological Psychiatrymedia_commonFamily HealthSchoolsDyslexiaCognitionElectroencephalographymedicine.diseaseReadingAptitudeFemalePsychologyBiological psychiatry
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