Search results for "HETEROZYGOTE ADVANTAGE"

showing 10 items of 56 documents

Gene Expression and Apoptosis Levels in Cumulus Cells of Patients with Polymorphisms of FSHR and LHB Undergoing in Vitro Fertilization Program

2017

Background/Aims: FSH receptor (FSHR) Ala307Thr and Asn680Ser and LHβ chain (LHB) Trp28Arg and Ile35Thr polymorphisms affect the response to pharmacological ovarian stimulation with r-FSH in women undergoing assisted reproductive treatment (ART). Here, we evaluated the expression level of selected genes involved in follicle maturation and the possible onset of apoptosis in cumulus cells of patients with single and double FSHR and LHB polymorphisms, as potential markers of oocyte competence. Methods: Cumulus cells from 36 stimulated patients were collected and SNP genotyping performed by PCR. Gene expression was evaluated through real-time PCR, and apoptosis estimated via TUNEL assay, and cle…

0301 basic medicineApoptosis; Cumulus cells; FSHR; Gene expression; LH; Polymorphism; PhysiologyLHPhysiologyApoptosislcsh:PhysiologyGonadotropin-Releasing Hormone0302 clinical medicineGene FrequencyFSHRGene expressionlcsh:QD415-436Settore BIO/06 - Anatomia Comparata E CitologiaCells CulturedIn Situ Hybridization Fluorescence030219 obstetrics & reproductive medicinelcsh:QP1-981Caspase 3Apoptosis; Cumulus cells; FSHR; Gene expression; LH; Polymorphismmedicine.anatomical_structureCumulus cellReceptors FSHDNA fragmentationFemaleSignal TransductionAdultHeterozygotemedicine.medical_specialtyendocrine systemGenotypeGranulosa cellCumulus cellsDNA FragmentationFertilization in VitroBiologyReal-Time Polymerase Chain ReactionBuserelinPolymorphism Single Nucleotidelcsh:Biochemistry03 medical and health sciencesFollicleInternal medicinemedicineHumansPolymorphismApoptosiHeterozygote advantageLuteinizing Hormone beta SubunitOocyte030104 developmental biologyEndocrinologyHaplotypesApoptosisMultivariate AnalysisOocytesGene expressionFollicle-stimulating hormone receptorProto-Oncogene Proteins c-aktCellular Physiology and Biochemistry
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Haploinsufficiency of ARFGEF1 is associated with developmental delay, intellectual disability, and epilepsy with variable expressivity

2021

PURPOSE: ADP ribosylation factor guanine nucleotide exchange factors (ARFGEFs) are a family of proteins implicated in cellular trafficking between the Golgi apparatus and the plasma membrane through vesicle formation. Among them is ARFGEF1/BIG1, a protein involved in axon elongation, neurite development, and polarization processes. ARFGEF1 has been previously suggested as a candidate gene for different types of epilepsies, although its implication in human disease has not been well characterized.METHODS: International data sharing, in silico predictions, and in vitro assays with minigene study, western blot analyses, and RNA sequencing.RESULTS: We identified 13 individuals with heterozygous…

0301 basic medicineGeneticsCandidate geneHeterozygoteEpilepsyADP ribosylation factorIn silicoHeterozygote advantageHaploinsufficiency030105 genetics & heredityBiologymedicine.disease03 medical and health sciencesEpilepsy030104 developmental biologyIntellectual DisabilitymedicineGuanine Nucleotide Exchange FactorsHumansGuanine nucleotide exchange factorHaploinsufficiencyGenetics (clinical)MinigeneGenetics in Medicine
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Clinical and hormonal characteristics in heterozygote carriers of congenital adrenal hyperplasia

2020

Abstract Non-classical congenital adrenal hyperplasia (NC-CAH) includes a group of genetic disorders due to a broad class of CYP21A2 variants identifying a disease-causing ‘C’ genotype. The heterozygous carriers of CYP21 mutations are at increased risk of developing clinically evident hyperandrogenism, even though clinical and laboratory characteristics are still underestimated. With the aim of obtaining a more accurate delineation of the phenotype of heterozygous carrier of CAH, we analyzed clinical, biochemical and molecular characteristics in a cohort of Sicilian subjects. Fifty-seven females with biallelic and monoallelic CYP21A2 variants classifying NC-CAH (24) and heterozygous carrier…

0301 basic medicineHirsutismHydrocortisoneendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryPhysiologyOverweighturologic and male genital diseasesBiochemistrySettore MED/13 - Endocrinologia0302 clinical medicineEndocrinologySettore BIO/10 - BiochimicaGenotypeMedicineChildhirsutismPolycystic ovaryfemale genital diseases and pregnancy complications030220 oncology & carcinogenesisCohortMolecular MedicineFemalemedicine.symptomAdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAdolescentYoung Adult03 medical and health sciencesHumansCongenital adrenal hyperplasiaMolecular BiologyHeterozygous carrierAdrenal Hyperplasia Congenitalbusiness.industryHyperandrogenismCongenital adrenal hyperplasianutritional and metabolic diseasesHeterozygote advantageCell BiologyOverweightmedicine.diseaseOligomenorrhea17OHProgesterone deficiency030104 developmental biologyMutationSteroid 21-HydroxylaseHyperandrogenismbusinessThe Journal of Steroid Biochemistry and Molecular Biology
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Maternal eNOS deficiency determines a fatty liver phenotype of the offspring in a sex dependent manner

2016

ABSTRACT Maternal environmental factors can impact on the phenotype of the offspring via the induction of epigenetic adaptive mechanisms. The advanced fetal programming hypothesis proposes that maternal genetic variants may influence the offspring's phenotype indirectly via epigenetic modification, despite the absence of a primary genetic defect. To test this hypothesis, heterozygous female eNOS knockout mice and wild type mice were bred with male wild type mice. We then assessed the impact of maternal eNOS deficiency on the liver phenotype of wild type offspring. Birth weight of male wild type offspring born to female heterozygous eNOS knockout mice was reduced compared to offspring of wil…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyHeterozygoteNitric Oxide Synthase Type IIIOffspringBiology03 medical and health sciencesGenomic ImprintingMiceSex FactorsEnosInternal medicineFetal programmingmedicineAnimalsEpigeneticsMolecular BiologyGeneFatty liverWild typeHeterozygote advantageDNA Methylationmedicine.diseasebiology.organism_classificationFatty LiverMice Inbred C57BL030104 developmental biologyEndocrinologyPhenotypeKnockout mouseeNOSCarbohydrate MetabolismFemaleEpigeneticsInstitut für ErnährungswissenschaftmetabolismResearch Paper
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Clinical and biochemical characteristics of individuals with low cholesterol syndromes: A comparison between familial hypobetalipoproteinemia and fam…

2017

Background The most frequent monogenic causes of low plasma cholesterol are familial hypobetalipoproteinemia (FHBL1) because of truncating mutations in apolipoprotein B coding gene (APOB) and familial combined hypolipidemia (FHBL2) due to loss-of-function mutations in ANGPTL3 gene. Objective A direct comparison of lipid phenotypes of these 2 conditions has never been carried out. In addition, although an increased prevalence of liver steatosis in FHBL1 has been consistently reported, the hepatic consequences of FHBL2 are not well established. Methods We investigated 350 subjects, 67 heterozygous carriers of APOB mutations, 63 carriers of the p.S17* mutation in ANGPTL3 (57 heterozygotes and …

0301 basic medicineMaleHepatic steatosisSettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematologymedicine.disease_causeANGPTL3 gene; APOB gene; Familial combined hypolipidemia; Familial hypobetalipoproteinemia; HDL cholesterol; Hepatic steatosis; Low cholesterol syndromesHypobetalipoproteinemiasExon0302 clinical medicineHDL cholesterolANGPTL3Nutrition and DieteticFamilial hypobetalipoproteinemiaGeneticsMutationNutrition and Dieteticsbiologyhepatic steatosisHomozygoteANGPTL3 geneMiddle AgedLow cholesterol syndromesPhenotypePhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineANGPTL3 gene; APOB gene; familial combined hypolipidemia; familial hypobetalipoproteinemia; HDL cholesterol; hepatic steatosis; low cholesterol syndromesmedicine.medical_specialtyHeterozygoteLow cholesterol syndromeHepatic steatosi03 medical and health sciencesInternal medicineInternal MedicinemedicineHumansAPOB geneFamilial combined hypolipidemiaGeneAgedAngiopoietin-Like Protein 3Apolipoproteins Bbusiness.industryHeterozygote advantagemedicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsMutationbiology.proteinlow cholesterol syndromesSteatosisbusiness
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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The neuroanatomy of Eml1 knockout mice, a model of subcortical heterotopia

2018

Symposium issue: Human Cortex Developmentidentifiant wos: 000482426800014; International audience; The cerebral cortex is a highly organized structure responsible for advanced cognitive functions. Its development relies on a series of steps including neural progenitor cell proliferation, neuronal migration, axonal outgrowth and brain wiring. Disruption of these steps leads to cortical malformations, often associated with intellectual disability and epilepsy. We have generated a new resource to shed further light on subcortical heterotopia, a malformation characterized by abnormal neuronal position. We describe here the generation and characterization of a knockout (KO) mouse model for Eml1,…

0301 basic medicineMale[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]heterotopiaHistology[SDV.BA] Life Sciences [q-bio]/Animal biologyClassical Lissencephalies and Subcortical Band HeterotopiasBiologyCorpus callosum03 medical and health sciences0302 clinical medicinemedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Animals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Progenitor cellMolecular BiologyEcology Evolution Behavior and SystematicsMice Knockout[SDV.BA]Life Sciences [q-bio]/Animal biologyBrainHeterozygote advantageCell BiologyOriginal Articlesmouse model of developmental disordersmedicine.diseasecortical malformationsCorticogenesisDisease Models Animal030104 developmental biologymedicine.anatomical_structureHeterotopia (medicine)Cerebral cortexKnockout mouseFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AnatomyNeuroscienceMicrotubule-Associated Proteins030217 neurology & neurosurgeryDevelopmental BiologyNeuroanatomy
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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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Mutation analyses in 17 patients with deficiency in acid β-galactosidase: three novel point mutations and high correlation of mutation W273L with Mor…

2001

An inherited deficiency in beta-galactosidase can result in GM1 gangliosidosis, with several phenotypes of generalized or chronic psychomotor deterioration, as well as in Morquio disease type B, a characteristic mucopolysaccharidosis free of neurological symptoms. We performed mutation analyses in 17 juvenile and adult patients from various European regions with a deficiency in beta-galactosidase and skeletal abnormalities. Fifteen of these had the Morquio B phenotype and have remained neurologically healthy until now while the two others exhibited psychomotor retardation of juvenile onset. A two-base substitution (851-852TG--CT; W273L) was present in 14 of the 15 Morquio B cases. Even if o…

AdultMaleAdolescentMucopolysaccharidosisDNA Mutational AnalysisRestriction MappingMutation MissenseBiologyGeneticsmedicineHumansPoint MutationMissense mutationRNA MessengerChildGenetics (clinical)DNA PrimersGeneticsPsychomotor retardationReverse Transcriptase Polymerase Chain ReactionPoint mutationMucopolysaccharidosis IVHeterozygote advantageMiddle Agedbeta-Galactosidasemedicine.diseasePhenotypePedigreePhenotypeGLB1Child PreschoolMutation (genetic algorithm)Femalemedicine.symptomHuman Genetics
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Influence of genetic variation at the apo A-I gene locus on lipid levels and response to diet in familial hypercholesterolemia

1998

We have examined the apo AI - 75 (G/A) and apo AI + 83(MspI +/-) polymorphisms at the APOA1 gene locus for associations with plasma lipid levels and response to an NCEP-I diet in 69 (44 women, 25 men) heterozygotes for familial hypercholesterolemia (FH). Subjects were studied at baseline (after consuming for one month a diet with 35%, fat, 10% saturated, and 300 mg/day cholesterol) and after 3 months of an NCEP-I diet. No gender-related differences for any of the lipid variables examined were found and the data were analyzed for men and women combined. For the apo AI - 75 (G/A) polymorphism, there were 51 G/G and 18 G/A subjects. At baseline, G/A subjects showed significantly lower total ch…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BCholesterol VLDLLocus (genetics)Familial hypercholesterolemiaHyperlipoproteinemia Type IIchemistry.chemical_compoundInternal medicineGenetic variationAPOA1 GenemedicineHumansAlleleAllelesGeneticsPolymorphism GeneticApolipoprotein A-IbiologyCholesterolCholesterol HDLGenetic VariationHeterozygote advantageCholesterol LDLmedicine.diseaseLipidsDietEndocrinologychemistrybiology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAtherosclerosis
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