Search results for "Phenotype"

showing 10 items of 1875 documents

Circulating levels of adipose products and differences in fat distribution in the ovulatory and anovulatory phenotypes of polycystic ovary syndrome.

2009

Central fat distribution is increased in anovulatory women with polycystic ovary syndrome (PCOS) compared with ovulatory PCOS and matched controls. Among secreted adipocytokines, this is reflected mainly in lower levels of adiponectin.

AdultLeptinOvulationmedicine.medical_specialtySettore MED/09 - Medicina Internaendocrine system diseasesmedia_common.quotation_subjectAdipokineAdipose tissueBiologyAnovulationInsulin resistanceAdipokinesInternal medicinemedicineBody Fat DistributionHumansNicotinamide PhosphoribosyltransferaseOvulationmedia_commonAdiponectinLeptinnutritional and metabolic diseasesObstetrics and Gynecologymedicine.diseasePolycystic ovaryfat distribution; polycystic ovary syndromeLipidsfemale genital diseases and pregnancy complicationsEndocrinologyC-Reactive ProteinPhenotypeReproductive Medicinefat distributionCase-Control StudiesFemaleAdiponectinInsulin ResistanceWaist CircumferenceRetinol-Binding Proteins PlasmaAnovulationPolycystic Ovary SyndromeFertility and sterility
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Liver cirrhosis associated with heterozygous alpha-1-antitrypsin deficiency type Pi MS and autoimmune features.

1995

Patients with homozygous protease inhibitor (Pi) type ZZ or a few rare M-like types may develop liver cirrhosis due to intracellular storage of alpha-antitrypsin (AAT), whereas some patients with heterozygous Pi MZ or SZ normally present with transient abnormal liver function tests in childhood. We report a 42-year-old obese patient who developed liver cirrhosis in association with heterozygous Pi MS (AAT) deficiency. Immunohistological and electron microscope examination showed storage of AAT in the hepatocytes. Interestingly, autoimmune features in this patient suggest that abnormal immune responses may contribute to the pathology of chronic liver disease.

AdultLiver CirrhosisMalecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyHeterozygoteCirrhosisT-LymphocytesAlpha (ethology)medicine.disease_causeAutoimmunityAutoimmune DiseasesImmunoenzyme TechniquesInternal medicinealpha 1-Antitrypsin DeficiencyPiMedicineHumansProtease inhibitor (pharmacology)ObesityAutoimmune diseaseAlpha 1-antitrypsin deficiencybusiness.industryGastroenterologymedicine.diseaseTrypsin deficiencyFlow CytometryAlcoholismMicroscopy ElectronEndocrinologyPhenotypeLiveralpha 1-AntitrypsinCytokinesbusinessDigestion
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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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Whole genome paired-end sequencing elucidates functional and phenotypic consequences of balanced chromosomal rearrangement in patients with developme…

2019

BackgroundBalanced chromosomal rearrangements associated with abnormal phenotype are rare events, but may be challenging for genetic counselling, since molecular characterisation of breakpoints is not performed routinely. We used next-generation sequencing to characterise breakpoints of balanced chromosomal rearrangements at the molecular level in patients with intellectual disability and/or congenital anomalies.MethodsBreakpoints were characterised by a paired-end low depth whole genome sequencing (WGS) strategy and validated by Sanger sequencing. Expression study of disrupted and neighbouring genes was performed by RT-qPCR from blood or lymphoblastoid cell line RNA.ResultsAmong the 55 pat…

AdultMale0301 basic medicineCandidate geneAdolescentDNA Copy Number VariationsDevelopmental Disabilities030105 genetics & heredityGenomeTranslocation GeneticStructural variationChromosome BreakpointsStructure-Activity RelationshipYoung Adult03 medical and health sciencessymbols.namesakeposition effectGeneticsHumansChildGeneGenetic Association StudiesGenetics (clinical)Paired-end tagComputingMilieux_MISCELLANEOUSchromosomal rearrangementsChromosome AberrationsGene RearrangementWhole genome sequencingGeneticsSanger sequencingwhole genome sequencingbiologystructural variationInfantNFIXPhenotype030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbiology.proteinsymbolsFemaleBiomarkers
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Identification of a novel LMF1 nonsense mutation responsible for severe hypertriglyceridemia by targeted next-generation sequencing

2016

Background Severe hypertriglyceridemia (HTG) may result from mutations in genes affecting the intravascular lipolysis of triglyceride (TG)-rich lipoproteins. Objective The aim of this study was to develop a targeted next-generation sequencing panel for the molecular diagnosis of disorders characterized by severe HTG. Methods We developed a targeted customized panel for next-generation sequencing Ion Torrent Personal Genome Machine to capture the coding exons and intron/exon boundaries of 18 genes affecting the main pathways of TG synthesis and metabolism. We sequenced 11 samples of patients with severe HTG (TG>885 mg/dL–10 mmol/L): 4 positive controls in whom pathogenic mutations had pre…

AdultMale0301 basic medicineCandidate geneEndocrinology Diabetes and MetabolismDNA Mutational AnalysisNonsense mutationPanel-based NGS sequencing030204 cardiovascular system & hematologyBiologymedicine.disease_causeDNA sequencing03 medical and health sciencessymbols.namesakeExon0302 clinical medicineNutrition and DieteticInternal MedicinemedicineHumansGeneHypertriglyceridemiaSanger sequencingGeneticsMutationNutrition and DieteticsLMF1 geneNonsense mutationHigh-Throughput Nucleotide SequencingInfantMembrane ProteinsIon semiconductor sequencingMiddle AgedIon torrent PGM sequencingPhenotype030104 developmental biologyChild PreschoolsymbolsFemaleCardiology and Cardiovascular MedicineJournal of Clinical Lipidology
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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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Characterization of γδ T cells in intestinal mucosa from patients with early onset or long standing inflammatory bowel disease and their correlation …

2019

Abstract Background and Aims Inflammatory bowel disease [IBD] is a complex chronic inflammatory disease of the human gut with no clear aetiology. Traditionally, dysregulated adaptive immune responses play an important role even though accumulating evidence suggests a role also for innate immunity. Because of the well-known plasticity of γδ T cells, we investigated their percentage occurrence, phenotypic features and effector functions in the intestinal mucosa of early-onset and long-standing IBD patients, as compared to healthy subjects. Methods Fresh biopsies from 30 Crohn’s disease and ulcerative colitis patients were obtained and digested, and cells were analysed by flow cytometry. Resul…

AdultMale0301 basic medicineNecrosisAdolescentBiopsyT-LymphocytesInflammatory bowel disease03 medical and health sciences0302 clinical medicineImmune systemIntestinal mucosainflammatory bowel diseasemedicineHumansgamma delta T cellsIntestinal MucosaAgedAged 80 and overInnate immune systembusiness.industryGastroenterologyGeneral MedicineMiddle AgedFlow CytometryInflammatory Bowel Diseasesmedicine.diseaseUlcerative colitisPhenotype030104 developmental biologyImmunologyFemaleTumor necrosis factor alphaInterleukin 17medicine.symptombusinessBiomarkers030215 immunology
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Phenotype and natural history of inherited neuropathies caused byHSJ1c.352+1G>A mutation

2015

Mutations in the HSJ1 ( Heat-Shock Protein J1 ) gene, also called DNAJB2 (DnaJ (Hsp40) homologue, subfamily B, member 2), have been recently described as a cause of hereditary neuropathies. The HSJ1 c.352+1G>A mutation in homozygote state has been reported as the causative mutation in a single family with autosomal recessive distal hereditary motor neuropathy (dHMN).1 Since then, two other families with different HSJ1 mutations have been described: one with a dHMN phenotype and the other with a Charcot-Marie-Tooth disease type 2 (CMT2) phenotype.2 We identified the HSJ1 c.352+1G>A mutation in 10 patients who underwent long-lasting follow-up. We describe their phenotype and clinical evolutio…

AdultMale0301 basic medicineNeural ConductionCell Cycle ProteinsNeurological examinationDisease03 medical and health sciencessymbols.namesake0302 clinical medicineCharcot-Marie-Tooth DiseasemedicineHumansGeneHeat-Shock ProteinsExome sequencingAdaptor Proteins Signal TransducingGenetic testingGeneticsSanger sequencingmedicine.diagnostic_testbusiness.industryNuclear ProteinsMiddle AgedPhenotypePsychiatry and Mental healthPhenotype030104 developmental biologySpainMutationMutation (genetic algorithm)symbolsFemaleSurgeryNeurology (clinical)Hereditary Sensory and Motor Neuropathybusiness030217 neurology & neurosurgeryJournal of Neurology, Neurosurgery & Psychiatry
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Hypoxia-Inducible Factor 2α Mutation-Related Paragangliomas Classify as Discrete Pseudohypoxic Subcluster

2016

Contains fulltext : 172720.pdf (Publisher’s version ) (Open Access) Recently, activating mutations of the hypoxia-inducible factor 2alpha gene (HIF2A/EPAS1) have been recognized to predispose to multiple paragangliomas (PGLs) and duodenal somatostatinomas associated with polycythemia, and ocular abnormalities. Previously, mutations in the SDHA/B/C/D, SDHAF2, VHL, FH, PHD1, and PHD2 genes have been associated with HIF activation and the development of pseudohypoxic (cluster-1) PGLs. These tumors overlap in terms of tumor location, syndromic presentation, and noradrenergic phenotype to a certain extent. However, they also differ especially by clinical outcome and by presence of other tumors o…

AdultMale0301 basic medicineOriginal articleCancer ResearchAdolescentMicroarraySDHBSDHABiologylcsh:RC254-282Oxidative PhosphorylationParagangliomaYoung Adult03 medical and health sciences0302 clinical medicineParagangliomaBasic Helix-Loop-Helix Transcription FactorsmedicineJournal ArticleCluster AnalysisHumansChildHypoxiaAgedGeneticsGene Expression ProfilingVascular damage Radboud Institute for Molecular Life Sciences [Radboudumc 16]Middle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePhenotypeGene Expression Regulation NeoplasticGene expression profiling030104 developmental biologyHypoxia-inducible factors030220 oncology & carcinogenesisMutationFemaleSDHDTranscriptomeProtein BindingNeoplasia
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Mutations in theMORC2gene cause axonal Charcot–Marie–Tooth disease

2015

Charcot-Marie-Tooth disease (CMT) is a complex disorder with wide genetic heterogeneity. Here we present a new axonal Charcot-Marie-Tooth disease form, associated with the gene microrchidia family CW-type zinc finger 2 (MORC2). Whole-exome sequencing in a family with autosomal dominant segregation identified the novel MORC2 p.R190W change in four patients. Further mutational screening in our axonal Charcot-Marie-Tooth disease clinical series detected two additional sporadic cases, one patient who also carried the same MORC2 p.R190W mutation and another patient that harboured a MORC2 p.S25L mutation. Genetic and in silico studies strongly supported the pathogenicity of these sequence variant…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyGene ExpressionSchwann cellSural nerveBiologyFasciculationMiceYoung Adult03 medical and health sciences0302 clinical medicineAtrophySural NerveCharcot-Marie-Tooth DiseasemedicineAnimalsHumansAxonAgedGenetic heterogeneityInfantSensory lossMiddle Agedmedicine.diseaseSciatic NerveAxonsPedigreePhenotype030104 developmental biologymedicine.anatomical_structureMutationFemaleNeurology (clinical)Myokymiamedicine.symptomNeuroscience030217 neurology & neurosurgeryTranscription FactorsBrain
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