Search results for "Smith-Lemli-Opitz Syndrome"

showing 4 items of 4 documents

Oral manifestations of Smith-Lemli-Opitz syndrome: a paediatric case report.

2009

ABSTRACT. Background The Smith-Lemli-Opitz Syndrome (SLOS) is an autosomal recessive genetic disorder, characterised by multiple congenital malformations, dysmorphic facial features and mental retardation. SLOS is caused by a genetically inherited deficiency of the enzyme 7-dehydrocholesterol Δ7reductase (7-DHC reductase), the catalyst involved in the final step of cholesterol biosynthesis, with the consequence of an increased serum levels of 7-DHC and generalised cholesterol deficiency. Case Report A 5-year-old female child was referred to the Department of Paediatric Dentistry of the University of Palermo for caries, gingivitis and malocclusion. The medical history revealed the diagnosis …

Settore MED/28 - Malattie OdontostomatologicheChild PreschoolOpen BiteSmith-Lemli-Opitz Syndrome Cholesterol metabolism 7-dehydrocholesterol reductase Craniofacial manifestationsDental ProphylaxisHumansFemaleDental CariesOral HygieneGingivitisFollow-Up StudiesSmith-Lemli-Opitz Syndrome
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A novel mutation of the DHCR7 gene in a sicilian compound heterozygote with Smith-Lemli-Opitz Syndrome

2005

Introduction: Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive disorder of cholesterol biosynthesis, resulting from deficient 7-dehydrocholesterol reductase (3β-hydroxysterol Δ7-reductase) activity, the enzyme responsible for conversion of 7-dehydrocholesterol to cholesterol. SLOS is most common among people of European descent, with a reported incidence of 1 per 20 000–60 000 newborns, depending on the diagnostic criteria and the reference population. More than 80 different mutations have been identified in several hundred patients. In Italy, SLOS appears to be a rare condition, probably because of underdiagnosis. Method: We analyzed by direct sequencing the 7-dehydrocholesterol…

Malecongenital hereditary and neonatal diseases and abnormalitiesHeterozygoteOxidoreductases Acting on CH-CH Group DonorsMutation MissenseBiologyReductaseCompound heterozygosityExonmedicineMissense mutationHumansGeneSicilyGeneticsnutritional and metabolic diseasesInfantGeneral Medicinemedicine.diseaseHuman geneticsPedigreeSmith-Lemli-Opitz SyndromeOxidoreductases Acting on CH-CH Group DonorSmith–Lemli–Opitz syndromeMutation (genetic algorithm)Human
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The ins and outs of cholesterol in the vertebrate retina

2010

Thematic Review Series: Lipids and Lipid Metabolism in the Eye; International audience; The vertebrate retina has multiple demands for utilization of cholesterol and must meet those demands either by synthesizing its own supply of cholesterol or by importing cholesterol from extraretinal sources, or both. Unlike the blood-brain barrier, the blood-retina barrier allows uptake of cholesterol from the circulation via a lipoprotein-based/receptor-mediated mechanism. Under normal conditions, cholesterol homeostasis is tightly regulated; also, cholesterol exists in the neural retina overwhelmingly in unesterified form, and sterol intermediates are present in minimal to negligible quantities. Howe…

QD415-436Degeneration (medical)BiologyBlood–brain barrierBiochemistryRetina03 medical and health scienceschemistry.chemical_compoundSmith-Lemli-Opitz syndrome0302 clinical medicineEndocrinology[SDV.IDA]Life Sciences [q-bio]/Food engineeringmedicineAnimalsHumans[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineeringcholesterol/biosynthesis;eye/retina;Smith-Lemli-Opitz syndrome030304 developmental biologychemistry.chemical_classification0303 health sciencesRetinaCholesterolThematic ReviewBiological TransportCell Biologycholesterol/biosynthesismedicine.diseaseSterolDe novo synthesisCholesterolmedicine.anatomical_structureEnzymechemistryBiochemistryBlood-Brain BarrierSmith–Lemli–Opitz syndromeeye/retinaVertebrates030221 ophthalmology & optometrylipids (amino acids peptides and proteins)sense organs
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Mild phenotypes in a series of patients with Opitz GBBB syndrome with MID1 mutations

2004

Contains fulltext : 48815.pdf (Publisher’s version ) (Closed access) Opitz syndrome (OS; MIM 145410 and MIM 300000) is a congenital midline malformation syndrome characterized by hypertelorism, hypospadias, cleft lip/palate, laryngotracheoesophageal (LTE) abnormalities, imperforate anus, developmental delay, and cardiac defects. The X-linked form (XLOS) is caused by mutations in the MID1 gene, which encodes a microtubule-associated RBCC protein. In this study, phenotypic manifestations of patients with and without MID1 mutations were compared to determine genotype-phenotype correlations. We detected 10 novel mutations, 5 in familial cases, 2 in sporadic cases, and 3 in families for whom it …

Malemedicine.medical_specialtyUbiquitin-Protein LigasesBiologymedicine.disease_causeGastroenterologyG/BBB SYNDROMEFAMILIESGenomic disorders and inherited multi-system disorders [IGMD 3]Genotype-phenotype distinctionInternal medicineGeneticsmedicineHumansHypertelorismGeneGenetics (clinical)GeneticsFamily HealthX-linked Opitz syndromeMutationMID1Nuclear ProteinsGenetic Diseases X-LinkedExonsOpitz G/BBB Syndromemedicine.diseasePhenotypeGENEPedigreeSmith-Lemli-Opitz SyndromePhenotypeGenetic defects of metabolism [UMCN 5.1]HypospadiasMutationMicrotubule ProteinsFemalephenotypic variabilityXP22medicine.symptomImperforate anusFunctional Neurogenomics [DCN 2]BBBTranscription FactorsAmerican Journal of Medical Genetics. Part A
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