Search results for " Mutation"

showing 10 items of 1212 documents

Germline copy number variation in theYTHDC2gene: does it have a role in finding a novel potential molecular target involved in pancreatic adenocarcin…

2014

Abstract: Objective: The vast majority of pancreatic cancers occurs sporadically. The discovery of frequent variations in germline gene copy number can significantly influence the expression levels of genes that predispose to pancreatic adenocarcinoma. We prospectively investigated whether patients with sporadic pancreatic adenocarcinoma share specific gene copy number variations (CNVs) in their germline DNA. Patients and methods: DNA samples were analyzed from peripheral leukocytes from 72 patients with a diagnosis of sporadic pancreatic adenocarcinoma and from 60 controls using Affymetrix 500K array set. Multiplex ligation-dependent probe amplification (MLPA) assay was performed using a s…

Malecopy number variations germline alteration pancreatic cancer susceptibility YTHDC2 geneDNA Copy Number VariationsSettore MED/06 - Oncologia MedicaClinical BiochemistryAdenocarcinomaBiologyGermlinePancreatic cancerDrug DiscoverymedicineHumansGenetic Predisposition to DiseaseMultiplexProspective StudiesMultiplex ligation-dependent probe amplificationCopy-number variationAlleleGeneGerm-Line MutationAgedAdenosine TriphosphatasesAged 80 and overPharmacologyPharmacology. TherapyDNA HelicasesMiddle Agedmedicine.diseaseMolecular biologyPancreatic NeoplasmsCase-Control StudiesMolecular MedicineAdenocarcinomaFemaleMultiplex Polymerase Chain ReactionRNA HelicasesExpert Opinion on Therapeutic Targets
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Germline deletion of Cetn1 causes infertility in male mice

2013

Centrins are calmodulin-like Ca2+-binding proteins that can be found in all ciliated eukaryotic cells from yeast to mammals. Expressed in male germ cells and photoreceptors, centrin 1 (CETN1) resides in the photoreceptor transition zone and connecting cilium. To identify its function in mammals, we deleted Cetn1 by homologous recombination. Cetn1−/− mice were viable and showed no sign of retina degeneration suggesting that CETN1 is nonessential for photoreceptor ciliogenesis or structural maintenance. Phototransduction components localized normally to the Cetn1−/− photoreceptor outer segments, and loss of CETN1 had no effect on light-induced translocation of transducin to the inner segment.…

Maleendocrine systemLight Signal TransductionCentrioleChromosomal Proteins Non-HistoneSpermiogenesisBiologyMice03 medical and health sciencesRetinal Rod Photoreceptor CellsCiliogenesismedicineAnimalsBasal bodyTransducinSpermatogenesisGerm-Line MutationInfertility MaleCentriolesSequence Deletion030304 developmental biologyMice KnockoutGenetics0303 health sciencesSpermatidCalcium-Binding ProteinsCell Cycle030302 biochemistry & molecular biologyCell DifferentiationCell BiologySpermatidsCell biologyMice Inbred C57BLmedicine.anatomical_structureCentrinFemalesense organsTransducinResearch ArticleVisual phototransductionJournal of Cell Science
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Two novel mutations in the human thyroid peroxidase (TPO) gene: genetics and clinical findings in four children

2009

UNLABELLED We report four children originating from two unrelated German families with congenital hypothyroidism (CH) due to mutations in the thyroid peroxidase (TPO) gene. Three female siblings (family 1) were found to be compound heterozygous for two mutations, a known mutation in exon 9 (W527C), and a mutation in exon 8 (Q446H), which has not been described before. In the second family we identified a boy with goitrous CH, who had a novel homozygous mutation in the TPO gene in exon 16 (W873X). All children of family 1 were diagnosed postnatally by newborn screening. The case of the boy of family 2 has already been reported for the in utero treatment of a goiter with hypothyroidism. CONCL…

Maleendocrine systemmedicine.medical_specialtyMutation MissenseThyrotropinGene mutationCompound heterozygositymedicine.disease_causeIodide PeroxidaseUltrasonography PrenatalExonChild DevelopmentThyroid peroxidaseInternal medicineCongenital HypothyroidismmedicineHumansMissense mutationGeneticsMutationNewborn screeningbiologybusiness.industryInfant NewbornInfantGeneral MedicineFetal Bloodmedicine.diseaseCongenital hypothyroidismEndocrinologyCodon NonsenseChild PreschoolPediatrics Perinatology and Child Healthbiology.proteinFemalebusinessActa Paediatrica
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Clinical manifestations of Fabry disease in children: data from the Fabry Outcome Survey.

2006

Background Fabry disease is a rare X-linked disorder caused by deficient activity of the enzyme alpha-galactosidase A. This produces progressive lysosomal accumulation of globotriaosylceramide throughout the body, leading to organ failure and premature death. Aim Here, we present the clinical manifestations of Fabry disease in children enrolled in FOS--the Fabry Outcome Survey--a European database of the natural history of Fabry disease and the effects of enzyme replacement therapy with agalsidase alfa (Replagal). Methods Currently, there are 545 patients in FOS, from 11 European countries. We analysed the baseline demographic and clinical characteristics of 82 of these patients (40 boys, 4…

Malemedicine.medical_specialtyAbdominal painPediatricsHeterozygoteAdolescentDNA Mutational AnalysisGlobotriaosylceramidechemistry.chemical_compoundOutcome Assessment Health CaremedicineHumansAge of OnsetChildStrokebusiness.industryVascular diseaseGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryAngiokeratomaIsoenzymeschemistryChild Preschoolalpha-GalactosidasePediatrics Perinatology and Child HealthFabry DiseaseFemaleAge of onsetmedicine.symptombusinessActa paediatrica (Oslo, Norway : 1992)
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Hunter disease before and during enzyme replacement therapy.

2011

Mucopolysaccharidosis type II (Hunter disease) is a lysosomal storage disease attributable to X-linked deficiency of the enzyme α-L-iduronate-sulfatase. Because of this deficiency, glycosaminoglycanes accumulate in various tissues and body fluids. We describe three patients representing the broad spectrum of Hunter disease and their response to enzyme replacement therapy. Patient 1 did not manifest central nervous system involvement, patient 2 manifested moderate neurologic disease, and patient 3 had already manifested a severe neurologic course during early infancy. In all patients, improvements in visceral organ size, physical capacity, and gastrointestinal functioning were reported. More…

Malemedicine.medical_specialtyAdolescentmedicine.drug_classAntibioticsCentral nervous systemIduronate SulfataseBiologyGastroenterologyFrameshift mutationYoung AdultDevelopmental NeuroscienceInternal medicinemedicineLysosomal storage diseaseMissense mutationHumansEnzyme Replacement TherapyMucopolysaccharidosis type IIYoung adultChildGlycosaminoglycansMucopolysaccharidosis IIInfant NewbornInfantEnzyme replacement therapyOrgan Sizemedicine.diseaseSurgeryGastrointestinal Tractmedicine.anatomical_structureNeurologyChild PreschoolPediatrics Perinatology and Child HealthNeurology (clinical)Nervous System DiseasesPediatric neurology
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Pgc-1α and Nr4a1 Are Target Genes of Circadian Melatonin and Dopamine Release in Murine Retina

2015

Purpose The neurohormones melatonin and dopamine mediate clock-dependent/circadian regulation of inner retinal neurons and photoreceptor cells and in this way promote their functional adaptation to time of day and their survival. To fulfill this function they act on melatonin receptor type 1 (MT1 receptors) and dopamine D4 receptors (D4 receptors), respectively. The aim of the present study was to screen transcriptional regulators important for retinal physiology and/or pathology (Dbp, Egr-1, Fos, Nr1d1, Nr2e3, Nr4a1, Pgc-1α, Rorβ) for circadian regulation and dependence on melatonin signaling/MT1 receptors or dopamine signaling/D4 receptors. Methods This was done by gene profiling using qu…

Malemedicine.medical_specialtyDopamineDNA Mutational AnalysisBiologyMelatonin receptorRetinaMelatoninMiceDopamineInternal medicinemedicineNuclear Receptor Subfamily 4 Group A Member 1AnimalsCircadian rhythmReceptorMelatoninRegulation of gene expressionDNAAdaptation PhysiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaeye diseasesCircadian RhythmMice Inbred C57BLEndocrinologyGene Expression RegulationDopamine receptorMutationFemalesense organsSignal transductionhormones hormone substitutes and hormone antagonistsmedicine.drugSignal TransductionTranscription Factors
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Murine expression and mutation analyses of the prostate androgen-regulated mucin-like protein 1 (Parm1) gene, a candidate for human epispadias.

2012

Abstract Background Epispadias is the mildest phenotype of the human bladder exstrophy–epispadias complex (BEEC), and presents with varying degrees of severity. This urogenital birth defect results from a disturbance in the septation process, during which separate urogenital and anorectal components are formed through division of the cloaca. This process is reported to be influenced by androgen signaling. The human PARM1 gene encodes the prostate androgen-regulated mucin-like protein 1, which is expressed in heart, kidney, and placenta. Methods We performed whole mount in situ hybridization analysis of Parm1 expression in mouse embryos between gestational days (GD) 9.5 and 12.5, which are e…

Malemedicine.medical_specialtyEpispadiasTime Factorsmedicine.drug_classDNA Mutational AnalysisIn situ hybridizationEpispadiasBiologymedicine.disease_causeAndrogen-Binding ProteinAndrologyMiceInternal medicinePlacentaGeneticsmedicineAnimalsHumansTissue DistributionGenital tubercleGeneIn Situ HybridizationMutationProstateGene Expression Regulation DevelopmentalGeneral MedicineSequence Analysis DNAAndrogenmedicine.diseaseMucin-Like Protein 1Endocrinologymedicine.anatomical_structurePhenotypeFemale
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Branch retinal vein occlusion associated with the 20210 G-to-A prothrombin variant.

2000

Purpose To describe a case of branch retinal vein occlusion (BRVO) in a patient who tested positive for the 20210 A allele of the prothrombin (PT) gene. Methods A 48-year-old man had visual loss in the right eye secondary to BRVO confirmed by ophthalmoscopy and fluorescein angiography. His medical history was not remarkable for common risk factors for retinal occlusive diseases. Results Laboratory tests for hypercoagulability were positive for PT 20210 A variant. The patient's family tested negative for the PT variant. Conclusions Laboratory tests for coagulopathy, including the PT 20210 A variant, should be added to the examination of patients with central or BRVO, especially if most commo…

Malemedicine.medical_specialtyEye diseaseVisual AcuityBlindnessOphthalmoscopy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOphthalmologyRetinal Vein OcclusionCoagulopathyMedicineHumansPoint MutationFluorescein AngiographyClotting factormedicine.diagnostic_testbusiness.industryGenetic VariationRetinalGeneral MedicineMiddle Agedmedicine.diseaseFluorescein angiographyThrombosisSurgeryOphthalmologychemistry030221 ophthalmology & optometryBranch retinal vein occlusionProthrombinbusiness030217 neurology & neurosurgeryEuropean journal of ophthalmology
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Missense mutations in the coagulation factor XII (Hageman factor) gene in hereditary angioedema with normal C1 inhibitor.

2006

Hereditary angioedema is characterized by recurrent skin swelling, abdominal pain attacks, and potentially life-threatening upper airway obstruction. The two classic types are both caused by mutations within the complement C1 inhibitor gene. A recently described new type does not show a deficiency of C1 inhibitor and affects almost exclusively women. We screened twenty unrelated index patients with this new type of hereditary angioedema for mutations in the coagulation factor XII gene. Two different missense mutations were identified in exactly the same position within exon 9 of the F12 gene. 'Mutation 1' (1032C-->A), encountered in five patients, predicts a threonine-to-lysine substitution…

Malemedicine.medical_specialtyGenetic LinkageBiophysicsMutation MissenseCoagulation Factor XIImedicine.disease_causeBiochemistryC1-inhibitorInternal medicinemedicineMissense mutationHumansHereditary Angioedema Type IIIAngioedemaMolecular BiologyMutationFactor XIIAngioedemabiologyChemistryCell Biologymedicine.diseasePedigreeEndocrinologyHereditary angioedemaImmunologyFactor XIIbiology.proteinFemalemedicine.symptomComplement C1 Inhibitor ProteinBiochemical and biophysical research communications
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Late-onset myasthenia gravis - CTLA4(low) genotype association and low-for-age thymic output of naïve T cells.

2014

Abstract Late-onset myasthenia gravis (LOMG) has become the largest MG subgroup, but the underlying pathogenetic mechanisms remain mysterious. Among the few etiological clues are the almost unique serologic parallels between LOMG and thymoma-associated MG (TAMG), notably autoantibodies against acetylcholine receptors, titin, ryanodine receptor, type I interferons or IL-12. This is why we checked LOMG patients for two further peculiar features of TAMG – its associations with the CTLA4 high/gain-of-function  +49A/A genotype and with increased thymic export of naive T cells into the blood, possibly after defective negative selection in AIRE-deficient thymomas. We analyzed genomic DNA from 116 …

Malemedicine.medical_specialtyGenotypeThymomaT-LymphocytesImmunologyDNA Mutational AnalysisRecent Thymic EmigrantLate onsetCell CountThymus GlandBiologyPeripheral blood mononuclear cellWhite PeopleGene FrequencyInternal medicineGenotypeMyasthenia GravismedicineImmune ToleranceImmunology and AllergyHumansCTLA-4 AntigenGenetic Predisposition to DiseaseGenetic Association StudiesAgedPeripheral tolerance inductionAged 80 and overPolymorphism GeneticThymocytesT-cell receptor excision circlesAutoantibodyCell DifferentiationThymus NeoplasmsMiddle Agedmedicine.diseaseMyasthenia gravisEndocrinologyImmunologyFemaleJournal of autoimmunity
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