Search results for "Disposition"

showing 10 items of 832 documents

Cardiomyopathy due to PRDM16 mutation: First description of a fetal presentation, with possible modifier genes

2020

PRDM16 (positive regulatory domain 16) is localized in the critical region for cardiomyopathy in patients with deletions of chromosome 1p36, as defined by Gajecka et al., American Journal of Medical Genetics, 2010, 152A, 3074-3083, and encodes a zinc finger transcription factor. We present the first fetal case of left ventricular non-compaction (LVNC) with a PRDM16 variant. The third-trimester obstetric ultrasound revealed a hydropic fetus with hydramnios and expanded hypokinetic heart. After termination of pregnancy, foetopathology showed a eutrophic fetus with isolated cardiomegaly. Endocardial fibroelastosis was associated with non-compaction of the myocardium of the left ventricle. Exom…

AdultHeart Defects CongenitalMalemedicine.medical_specialtyCardiomyopathyBiologyLabor PresentationGenetic HeterogeneityPregnancyExome SequencingGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseGenetics (clinical)Exome sequencingGeneticsFetusGenes ModifierGenetic heterogeneityInfant NewbornEndocardial fibroelastosisMiddle AgedFetal Presentationmedicine.diseasePedigreeDNA-Binding ProteinsMutationMedical geneticsFemaleCardiomyopathiesTranscription FactorsAmerican Journal of Medical Genetics Part C: Seminars in Medical Genetics
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Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Not All Floating-Harbor Syndrome Cases are Due to Mutations in Exon 34 of SRCAP

2013

International audience; Floating-Harbor syndrome (FHS) is a rare disorder characterized by short stature, delayed bone age, speech delay, and dysmorphic facial features. We report here the molecular analysis of nine cases, fulfilling the diagnostic criteria for FHS. Using exome sequencing, we identified SRCAP as the disease gene in two cases and subsequently found SRCAP truncating mutations in 6/9 cases. All mutations occurred de novo and were located in exon 34, in accordance with the recent report of Hood et al. However, the absence of SRCAP mutations in 3/9 cases supported genetic heterogeneity of FH syndrome. Importantly, no major clinical differences were observed supporting clinical h…

AdultHeart Septal Defects VentricularMaleDNA Mutational AnalysisBiologyShort statureCraniofacial Abnormalitiesgenetic heterogeneity03 medical and health sciencesExonGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildFloating-Harbor syndromeGenetics (clinical)Exome sequencingGrowth Disorders030304 developmental biologyDisease geneGeneticsAdenosine Triphosphatases0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsGenetic heterogeneity030305 genetics & heredityBone ageExonsmedicine.diseaseSRCAP3. Good healthFloating–Harbor syndromeSpeech delayMutationFemalemedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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No Association between Mannose-Binding Lectin Alleles and Susceptibility to Chronic Hepatitis B Virus Infection in German Patients

1998

Variants of the mannose-binding lectin (MBL) have been shown to be associated with low serum concentrations of the protein and to predispose to bacterial, fungal and viral infections. A recent small study on 33 Caucasian patients had suggested that a mutation at codon 52 of the MBL gene is associated with chronic hepatitis B virus (HBV) infection. Exon 1 of the MBL gene was amplified by PCR in 61 patients with chronic HBV infection, 28 patients with acute infection and in 60 controls. MBL variants were detected by subsequent restriction enzyme digestion and agarose gel electrophoresis. The occurrence of the codon 52 mutation in patients with chronic HBV infection did not differ significantl…

AdultImmunologychemical and pharmacologic phenomenamedicine.disease_causePolymerase Chain ReactionVirusExonHepatitis B ChronicGeneticsmedicineHumansGenetic Predisposition to DiseaseProspective StudiesAlleleGeneAllelesGenetics (clinical)Mannan-binding lectinElectrophoresis Agar GelMutationbiologyLectinDNAHepatitis Bbacterial infections and mycosesMBL deficiencymedicine.diseaseVirologyCollectinsAcute DiseaseMutationImmunologybiology.proteinCarrier ProteinsExperimental and Clinical Immunogenetics
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Inflammation, Longevity, and Cardiovascular Diseases: Role of Polymorphisms of TLR4

2006

The total burden of infection at various sites may affect the progression of atherosclerosis, the risk being modulated by host genotype. The role of lipopolysaccaride receptor TLR4 is paradigmatic. It initiates the innate immune response against gram-negative bacteria; and TLR4 polymorphisms, as ASP299GLY, suggested to attenuate receptor signaling, have been described. We demonstrated that TLR4 ASP299GLY polymorphism shows a significantly lower frequency in patients affected by myocardial infarction compared to controls, whereas centenarians show a higher frequency. Thus, people genetically predisposed to developing weak inflammatory activity, seem to have fewer chances of developing cardio…

AdultLipopolysaccharidesMaleHeterozygoteTime Factorsmedia_common.quotation_subjectmedicine.medical_treatmentLongevityMyocardial InfarctionEnzyme-Linked Immunosorbent AssayInflammationBiologyGeneral Biochemistry Genetics and Molecular BiologyAMIHistory and Philosophy of SciencemedicineHumansGenetic Predisposition to DiseaseTLR4Interleukin 6media_commonInflammationPolymorphism GeneticInnate immune systemInterleukin-6General NeuroscienceLongevityInterleukinHeterozygote advantageMiddle AgedToll-Like Receptor 4CytokineAcute DiseaseMutationImmunologyTLR4biology.proteinFemalemedicine.symptomAnnals of the New York Academy of Sciences
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Expression and prognostic significance of insulin‑like growth factor-2 receptor in human hepatocellular carcinoma and the influence of transarterial …

2019

Hepatocellular carcinoma (HCC) is one of the most common human malignancies, the incidence of which is growing worldwide. The prognosis of HCC is very poor and it is often accompanied by a high rate of recurrence. Conventional chemotherapeutic approaches are largely inefficient. In order to develop novel effective methods for the early detection and prognosis of HCC, novel markers and therapeutic targets are urgently required. The present study focused on the effects of the expression of the tumor suppressor gene insulin‑like growth factor‑2 receptor (IGF2R) on patient survival and tumor recurrence in patients with HCC; this study paid specific attention to the influence of transarterial ch…

AdultLiver CirrhosisMale0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyCarcinoma HepatocellularCirrhosisTumor suppressor geneKaplan-Meier EstimatePolymorphism Single NucleotideDisease-Free SurvivalReceptor IGF Type 203 medical and health sciences0302 clinical medicineInternal medicinemedicineCarcinomaHumansGenetic Predisposition to DiseaseChemoembolization TherapeuticAgedAged 80 and overOncogenebusiness.industryLiver NeoplasmsCase-control studyCancerGeneral MedicineMiddle AgedPrognosismedicine.diseaseMolecular medicinedigestive system diseases030104 developmental biologyOncologyCase-Control Studies030220 oncology & carcinogenesisHepatocellular carcinomaFemaleNeoplasm Recurrence LocalbusinessFollow-Up StudiesOncology Reports
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Haplotypes of the caspase-1 gene, plasma caspase-1 levels, and cardiovascular risk.

2006

Caspase-1 processes the interleukin (IL)-1β and IL-18 inactive precursors to the biologically active cytokines that are known to have proatherogenic effects. The present study investigated the genetic variability of the CASP1 gene and plasma levels of caspase-1 in relation to cardiovascular risk. In Europeans, 3 tag SNPs captured 4 common haplotypes of the CASP1 gene. Among these, the A in6 allele of the G+7/in6A polymorphism was less frequent in 246 cases with myocardial infarction and a parental history of disease than in 253 controls free of familial history of disease (0.13±0.02 versus 0.20±0.02; P =0.005). However, in a larger case/control study (n=1774), these effects are borderline …

AdultMale/dk/atira/pure/subjectarea/asjc/1300/1314medicine.medical_specialtyPathologyGenotypePhysiologyPopulationMyocardial Infarction/dk/atira/pure/subjectarea/asjc/2700/2705Single-nucleotide polymorphismCoronary Artery DiseaseBiologyPolymorphism Single NucleotideRisk AssessmentCoronary artery diseaseCohort StudiesGene FrequencyPolymorphism (computer science)Internal medicinemedicineHumansGenetic Predisposition to DiseaseProspective StudiesAlleleeducationProspective cohort studyAgededucation.field_of_studyVascular diseaseHazard ratioCaspase 1Interleukin-18Genetic VariationMiddle Agedmedicine.diseaseEndocrinologyHaplotypesCardiovascular DiseasesCase-Control StudiesFemaleCardiology and Cardiovascular MedicineFollow-Up StudiesCirculation research
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Genetic screening for MC4R gene identifies three novel mutations associated with severe familiar obesity in a cohort of Spanish individuals

2019

Abstract MC4R gene is a hypothalamic satiety control mediator in which mutations cause a monogenic form of obesity. The aim of this study was to perform a genetic screening to identify variations in the entire region of MC4R gene. A total of 236 unrelated and severely obese patients (BMI ≥ 40 kg/m2) with Spanish ancestry and severe overweight familiar history have been enrolled into the study. Seven MC4R gene variants were identified in the heterozygous state in 21 patients. Coding variants p.Thr101Ile and p.Ala259Asp are new and variants p.Ser30Phe, p.Val103Ile and p.Ile251Leu were previously described. Two variants have been also observed in the promoter region of the MC4R gene; the c.-24…

AdultMale0301 basic medicineAdolescentObesity phenotypeIn silicoDNA Mutational AnalysisMutation MissenseOverweightBiologymedicine.disease_causePolymorphism Single NucleotideCohort StudiesYoung Adult03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingGeneGenetic Association StudiesGeneticsMutationPromoterGeneral MedicineMiddle Agedmedicine.diseaseObesityObesity MorbidPedigree030104 developmental biologySpainCase-Control Studies030220 oncology & carcinogenesisCohortReceptor Melanocortin Type 4Femalemedicine.symptomGene
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Further delineation of a rare recessive encephalomyopathy linked to mutations in GFER thanks to data sharing of whole exome sequencing data

2017

Background Alterations in GFER gene have been associated with progressive mitochondrial myopathy, congenital cataracts, hearing loss, developmental delay, lactic acidosis and respiratory chain deficiency in 3 siblings born to consanguineous Moroccan parents by homozygosity mapping and candidate gene approach (OMIM#613076). Next generation sequencing recently confirmed this association by the finding of compound heterozygous variants in 19-year-old girl with a strikingly similar phenotype, but this ultra-rare entity remains however unknown from most of the scientific community. Materials and methods Whole exome sequencing was performed as part of a "diagnostic odyssey" for suspected mitochon…

AdultMale0301 basic medicineHeterozygoteCandidate geneAdolescentdata sharingMitochondrial diseaseCompound heterozygosityBioinformaticsYoung Adult03 medical and health sciencesMitochondrial myopathyMitochondrial EncephalomyopathiesExome SequencingGeneticsHumansMedicineGenetic Predisposition to DiseaseOxidoreductases Acting on Sulfur Group Donorswhole-exome sequencingChildExomeCytochrome ReductasesGenetics (clinical)Exome sequencing[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryGFERDisease gene identificationmedicine.diseasePedigree3. Good health030104 developmental biologymitochondrial conditionMutationCongenital cataractsFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsbusinessClinical Genetics
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Cholelithiasis in Patients with Gaucher Disease type 1: Risk Factors and the Role of ABCG5/ABCG8 Gene Variants

2016

Background & Aim: Patients with Gaucher disease type 1 (GD1) show an altered lipid profile and a certain degree of insulin resistance, which might contribute to cholelithiasis (CL) and could possibly be associated with ABCG5/ABCG8 gene variants. We aimed to investigate the prevalence of CL in Caucasian adult patients with GD1 and the possible risk factors, including gene variants of the ABCG5/ABCG8 genes.
 Methods: 61 Caucasian patients with GD1 (38 female/23male), aged 18-62 years and 61 healthy subjects matched for age, gender and BMI, without CL, for comparison of lipid profiles. Data before start of enzyme replacement therapy (ERT) were recorded: clinical, haematological, sever…

AdultMale0301 basic medicineHeterozygotemedicine.medical_specialtyAdolescentLipoproteinsmedicine.medical_treatmentSplenectomyABCG8030105 genetics & heredityGastroenterologyWhite PeopleYoung Adult03 medical and health sciencesInsulin resistanceGene FrequencyCholelithiasisRisk FactorsInternal medicineGenotypePrevalencemedicineHumansEnzyme Replacement TherapyGenetic Predisposition to DiseaseATP Binding Cassette Transporter Subfamily G Member 5Genetic Association StudiesGaucher Diseasemedicine.diagnostic_testRomaniabusiness.industryATP Binding Cassette Transporter Subfamily G Member 8HomozygoteGastroenterologyCase-control studyGenetic VariationEnzyme replacement therapyMiddle Agedmedicine.diseaseCross-Sectional StudiesPhenotypeCase-Control StudiesGlucosylceramidaseFemaleLipid profilebusinessDyslipidemiaJournal of Gastrointestinal and Liver Diseases
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