Search results for " and neonatal diseases and abnormalities"

showing 10 items of 344 documents

Age-Related Lipid Metabolic Signature in HumanLMNA-Lipodystrophic Stem Cell-Derived Adipocytes

2015

Lamin A (LMNA)-linked lipodystrophies belong to a group of clinical disorders characterized by a redistribution of adipose tissue with a variable range of metabolic complications. The leading cause of these disorders is the nonphysiological accumulation of the lamin A precursor, prelamin A. However, the molecular mechanisms by which prelamin A induces the pathology remain unclear.The aim of this study is to use an experimental LMNA-lipodystrophy model based on human mesenchymal stem cell (hMSC)-derived adipocytes that accumulate prelamin A to gain deeper insights into the mechanisms governing these diseases.Prelamin A-induced or -noninduced hMSC-derived adipocytes were obtained from healthy…

AdultMaleAgingcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentLipodystrophyLipolysisEndocrinology Diabetes and MetabolismCellular differentiationClinical BiochemistryAdipose tissueMitochondrionBiologyBiochemistryLMNAYoung AdultEndocrinologyInternal medicineAdipocytesmedicineHumansMetabolomicsLipolysisintegumentary systemStem CellsBiochemistry (medical)Mesenchymal stem cellnutritional and metabolic diseasesCell DifferentiationMiddle AgedLamin Type ALipid MetabolismEndocrinologyMetabolomeFemaleStem cellLaminThe Journal of Clinical Endocrinology & Metabolism
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Combined aortic and mitral stenosis in mucopolysaccharidosis type I-S (Ullrich-Scheie syndrome)

1999

The genetic mucopolysaccharidosis syndromes (MPS) are autosomal recessive inborn errors of metabolism. Heart valve involvement in MPS is not uncommon but only a few case reports of successful cardiac surgery are available. In particular, reports of combined aortic and mitral stenosis associated with MPS type I-S are very rare. Both type I and type VI MPS are associated with significant left sided valvar heart disease that requires surgical valve replacement because of irregular valve thickening, fibrosis, and calcification. A 35 year old man had severe mitral valve stenosis after successful surgical replacement of a stenotic aortic valve. Valvar heart disease was investigated by cardiac ult…

AdultMaleAortic valvecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyMucopolysaccharidosis Imedicine.medical_treatmentCase ReportMitral valve stenosisValve replacementMitral valveInternal medicineMucopolysaccharidosis IHumansMitral Valve StenosisMedicinecardiovascular diseasesHeart valvebusiness.industrynutritional and metabolic diseasesAortic Valve Stenosismedicine.diseaseEchocardiography Doppler ColorCardiac surgerySurgerymedicine.anatomical_structureEchocardiographyAortic valve stenosiscardiovascular systemCardiologyMitral ValveCardiology and Cardiovascular MedicinebusinessHeart
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Both rare and de novo copy number variants are prevalent in agenesis of the corpus callosum but not in cerebellar hypoplasia or polymicrogyria.

2013

Agenesis of the corpus callosum (ACC), cerebellar hypoplasia (CBLH), and polymicrogyria (PMG) are severe congenital brain malformations with largely undiscovered causes. We conducted a large-scale chromosomal copy number variation (CNV) discovery effort in 255 ACC, 220 CBLH, and 147 PMG patients, and 2,349 controls. Compared to controls, significantly more ACC, but unexpectedly not CBLH or PMG patients, had rare genic CNVs over one megabase (p = 1.48×10−3; odds ratio [OR] = 3.19; 95% confidence interval [CI] = 1.89–5.39). Rare genic CNVs were those that impacted at least one gene in less than 1% of the combined population of patients and controls. Compared to controls, significantly more AC…

AdultMaleCancer ResearchMicrocephalycongenital hereditary and neonatal diseases and abnormalitiesAdolescentDNA Copy Number Variationslcsh:QH426-470Developmental DisabilitiesPopulationGenome-wide association studyBiologyNervous System MalformationsCorpus callosumPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineCerebellummental disordersGeneticsPolymicrogyriamedicineHumansCopy-number variationChildAgenesis of the corpus callosumeducationMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsExome sequencing030304 developmental biologyGenetics0303 health scienceseducation.field_of_studyGenome HumanInfant NewbornInfantMiddle Agedmedicine.disease3. Good healthMalformations of Cortical Developmentlcsh:GeneticsChild PreschoolFemaleAgenesis of Corpus Callosum030217 neurology & neurosurgeryResearch ArticleGenome-Wide Association StudyPLoS Genetics
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Push-and-Pull Enteroscopy Using the Double-Balloon Technique (Double-Balloon Enteroscopy) for the Diagnosis of Meckel's Diverticulum in Adult Patient…

2006

Meckel's diverticulum (MD) occurs in 2-3% of the population. Although the clinical, histopathologic, and radiologic features of the complications of MD are well known, the diagnosis may be difficult before surgery.Three patients (age 22-34 yr, two women) presenting with gastrointestinal (GI) bleeding of obscure origin underwent multiple endoscopic and radiologic tests including capsule endoscopy and Tc-99m pertechnetate scintigraphy before push-and-pull enteroscopy using a double-balloon technique (double-balloon enteroscopy). Double-balloon enteroscopy was performed in all three patients using oral and anal approaches to evaluate the entire intestine. In one case, MD was detected using the…

AdultMaleEnteroscopycongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyGastrointestinal bleedingGI bleedingBalloondigestive systemEndoscopy GastrointestinalCatheterizationDouble-balloon enteroscopymedicineHumansMeckel's diverticulumHepatologymedicine.diagnostic_testbusiness.industryGastroenterologymedicine.diseaseSurgeryEndoscopyEndoscopes GastrointestinalMeckel DiverticulumFemaleGastrointestinal HemorrhagebusinessDiverticulumThe American Journal of Gastroenterology
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A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation.

2007

X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with …

AdultMaleMicrocephalycongenital hereditary and neonatal diseases and abnormalitiesGermline mosaicismLocus (genetics)BiologyMicrophthalmiaFrameshift mutationGenetic linkageGenes X-LinkedIntellectual DisabilityGeneticsmedicineMissense mutationHumansMicrophthalmosAbnormalities MultipleFrameshift MutationGenetics (clinical)GeneticsChromosomes Human XNuclear ProteinsGenetic Diseases X-LinkedSyndromemedicine.diseasePedigreeLenz microphthalmia syndromeDNA-Binding ProteinsChild PreschoolMicrocephalyFemaleCarrier ProteinsGene DeletionEuropean journal of human genetics : EJHG
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High prevalence of BRCA1 deletions in BRCAPRO-positive patients with high carrier probability.

2007

Mutation screening of the BRCA1 and BRCA2 genes in probands with familial breast/ovarian cancer has been greatly improved by the multiplex ligation-dependent probe amplification (MLPA) assay able to evidence gene rearrangements not detectable by standard screening methods. However, no criteria for selection of cases to be submitted to the MLPA test have been reported yet. We used the BRCAPro software for the selection of familial breast/ovarian cancer probands investigated with the MLPA approach after negative BRCA1/2 conventional mutation screening. One hundred and seventy-seven probands were investigated for germline BRCA1/2 mutations after assessment of genetic risk using BRCAPro. Proban…

AdultMaleOncologyProbandcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyendocrine system diseasesBreast NeoplasmsGermlineBreast Neoplasms MaleGermline mutationBreast cancerRisk FactorsInternal medicinePrevalenceHumansMedicineGenetic Predisposition to DiseaseMultiplexMultiplex ligation-dependent probe amplificationskin and connective tissue diseasesAgedSequence DeletionOvarian NeoplasmsGeneticsBRCA1 Proteinbusiness.industryGenetic Carrier ScreeningProstatic NeoplasmsHematologyMiddle Agedmedicine.diseaseBRCA1 BRCA2 BRCAPro breast cancer MLPA ovarian cancerPedigreeOncologyMutation (genetic algorithm)FemalebusinessOvarian cancerSoftware
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Gastric outlet obstruction in a neonate because of Peutz-Jeghers syndrome

2012

Neonatal detection of Peutz-Jeghers syndrome is unusual with only 2 cases previously reported in the literature. We describe a neonate presenting with gastric outlet obstruction owing to 2 large Peutz-Jeghers polyps. The child's father and grandmother were known to have Peutz-Jeghers syndrome. On the ninth day of life, the infant underwent colonoscopy, abdominal exploration, and complete surgical resection of 3 polyps. The postoperative course was uneventful, and the patient was discharged home at the age of 3 weeks on full oral feeds. This is the first case report of inherited Peutz-Jeghers syndrome causing gastric outlet obstruction in a neonate.

AdultMalePolyhydramniosSurgical resectioncongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyDay of lifePeutz-Jeghers SyndromeColonoscopyPeutz–Jeghers syndromePolypsPregnancyStomach NeoplasmsAbdominal explorationmedicineHumansskin and connective tissue diseasesmedicine.diagnostic_testGastric Outlet Obstructionbusiness.industryInfant NewbornGastric outlet obstructionGeneral Medicinemedicine.diseasedigestive system diseasesSurgeryPediatrics Perinatology and Child HealthFemaleSurgerybusinessJournal of Pediatric Surgery
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A new germline mutation in BRCA1 gene in a sicilian family with ovarian cancer

2005

A group of 103 sicilian patients with hereditary and familiar breast and/or ovarian cancer were screened for Breast Cancer 1 gene (BRCA1) mutations by direct sequencing PCR products spanning the coding region and partial intronic regions of the BRCA1 gene. In this study, we report a new germline mutation in BRCA1 gene, not previously reported in the BIC database, in a woman with ovarian cancer at 46 years old. Mother's proband has been diagnosed the same histotype of ovarian cancer at 42 age. The mutational analyses that shown a 4843delC frameshift mutation in exon 16 of BRCA1 gene was extended to other family members including the proband's brother and her two sons. Direct automatic sequen…

AdultMaleProbandcongenital hereditary and neonatal diseases and abnormalitiesCancer Researchendocrine system diseasesGenetic counselingCystadenocarcinomaGenes BRCA1BiologyFrameshift mutationExonGermline mutationBreast cancermedicineHumansGenetic Predisposition to DiseaseFrameshift MutationSicilyGerm-Line MutationOvarian NeoplasmsBRCA1 Direct automatic sequencing Germline mutation Ovarian cancerGeneticsMiddle Agedmedicine.diseasePedigreeOncologyMutation (genetic algorithm)Cancer researchFemaleOvarian cancerBreast Cancer Research and Treatment
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GAA trinucleotide repeat expansion in variant Friedreich's ataxia families.

1997

Phenotypic variants in Friedreich's ataxia include late onset, preservation of the lower limbs tendon reflexes, and slow progression. We describe clinical and electrophysiological features from three families with Friedreichlike phenotypes. Friedreich's ataxia diagnosis was confirmed by finding two allelic expansions of the GAA trinucleotide repeat at the X25 gene. In family 1 both patients had a late-onset phenotype with preservation of knee and ankle jerks, lack of cardiomyopathy, and preserved H reflex. One of them did not have electrophysiologic evidence of sensory axonal neuropathy. Patients from family 2 showed variability in the age of onset, and 2 out of 3 affected children had hype…

AdultMaleReflex Stretchcongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtySensory axonal neuropathyAtaxiaPhysiologyGenetic LinkageAction PotentialsLate onsetBiologyH-ReflexCellular and Molecular NeuroscienceDegenerative diseaseTrinucleotide RepeatsPhysiology (medical)medicineHumansNeurons AfferentChildAllelesLegGenetic VariationDNACardiomyopathy Hypertrophicmedicine.diseasePedigreePeripheral neuropathyFriedreich AtaxiaReflexDisease ProgressionFemaleNeurology (clinical)medicine.symptomAge of onsetTrinucleotide repeat expansionMusclenerve
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Gly114Asp mutation of rhodopsin in autosomal dominant retinitis pigmentosa

1995

Two autosomal dominant retinitis pigmentosa families of different origin were screened for rhodopsin mutations using the method of single strand conformation polymorphism and direct sequencing. We found a CGG-CAG substitution in codon 114 of rhodopsin in both families. This change predicted the replacement of a glycine by an aspartic acid and suggested that this change is the cause of the disease in these families.

AdultMaleRhodopsincongenital hereditary and neonatal diseases and abnormalitiesAdolescentgenetic structuresMolecular Sequence DataGlycinemedicine.disease_causeAutosomal dominant retinitis pigmentosaRetinitis pigmentosaAspartic acidmedicineHumansPoint MutationAmino Acid SequenceCodonMolecular BiologyGenes DominantGeneticsAspartic AcidMutationPolymorphism GeneticBase SequencebiologyDirect sequencingSingle-strand conformation polymorphismCell BiologyMiddle Agedmedicine.diseasePedigreeRhodopsinGlycinebiology.proteinFemalesense organsRetinitis PigmentosaMolecular and Cellular Probes
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