Search results for "neon"

showing 10 items of 760 documents

The impact of genetic diseases on neonatal and pediatric care

2019

The impact of genetic diseases on the pediatric population in clinical practice is remarkable and their prevalence has rapidly increased in the last 50 years. A wide diffusion of modern diagnostic techniques has implemented early diagnosis and consequently the precocious start of effective support therapies which have determined an increased survival rate and quality of life. The percentage of genetics anomalies in children hospitalized is really high and amounts to at least 50% of hospital pediatric admissions. Over 5% of stillborn babies, without other known causes, have genetic disorders, and it goes up to 50% in the case of visible malformations.

Genetic anomalieGenetic diseaseNeonatal careNeonatal infection
researchProduct

Genetics of the Charcot-Marie-Tooth disease in the Spanish Gypsy population: the hereditary motor and sensory neuropathy-Russe in depth

2012

Four private mutations responsible for three forms demyelinating of Charcot-Marie-Tooth (CMT) or hereditary motor and sensory neuropathy (HMSN) have been associated with the Gypsy population: the NDRG1 p.R148X in CMT type 4D (CMT4D/HMSN-Lom); p.C737_P738delinsX and p.R1109X mutations in the SH3TC2 gene (CMT4C); and a G>C change in a novel alternative untranslated exon in the HK1 gene causative of CMT4G (CMT4G/HMSN-Russe). Here we address the findings of a genetic study of 29 Gypsy Spanish families with autosomal recessive demyelinating CMT. The most frequent form is CMT4C (57.14%), followed by HMSN-Russe (25%) and HMSN-Lom (17.86%). The relevant frequency of HMSN-Russe has allowed us to inv…

GeneticsProbandcongenital hereditary and neonatal diseases and abnormalitiesWeaknesseducation.field_of_studyHaplotypePopulationBiologymedicine.diseaseTooth diseaseDistal sensory lossGeneticsmedicinemedicine.symptomeducationHereditary motor and sensory neuropathyFounder mutationGenetics (clinical)Clinical Genetics
researchProduct

Mitochondrial DNA variations in patients with Type 2 (non-insulin dependent) diabetes mellitus and a Welsh control population

1999

The LDL-receptor gene point mutation FH-Genoa/Palermo is the most frequent mutation responsible for Familial Hypercholesterolemia in Sicily. The mutation does not introduce or abolish any useful restriction site. We establish a GeneComb-based strategy to identify this mutation in a population of Sicilian unrelated clinically diagnosed FH probands. The method was very sensitive and specific; 12 out of 90 (13.3%) unrelated FH probands were found to carry the FH-Genoa/Palermo mutation. According to these results, the FH-Genoa/Palermo is the more frequent LDL-receptor gene mutation among the Sicilian FH patients. Moreover FH-Genoa/Palermo is the mutation cluster to date more represented in Sout…

GeneticsProbandcongenital hereditary and neonatal diseases and abnormalitieseducation.field_of_studyPoint mutationPopulationnutritional and metabolic diseasesFamilial hypercholesterolemiaGene mutationBiologymedicine.diseaseRestriction siteLDL receptorMutation (genetic algorithm)Geneticsmedicineskin and connective tissue diseaseseducationGenetics (clinical)Human Mutation
researchProduct

Cytogenetic response induced by interferon alpha in the myeloproliferative disorder with eosinophilia, T cell lymphoma and the chromosomal translocat…

1998

Cytogenetic response induced by interferon alpha in the myeloproliferative disorder with eosinophilia, T cell lymphoma and the chromosomal translocation t(8;13)(p11;q12)

Geneticscongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchAlpha interferonChromosomal translocationHematologyBiologymedicine.diseaseCytogenetic ResponseLymphomaOncologyhemic and lymphatic diseasesCancer researchmedicineEosinophiliaT-cell lymphomamedicine.symptomLeukemia
researchProduct

Imprint switching on human chromosome 15 may involve alternative transcripts of the SNRPN gene

1996

Imprinting on human chromosome 15 is regulated by an imprinting centre, which has been mapped to a 100–kb region including exon 1 of SNRPN. From this region we have identified novel transcripts, which represent alternative transcripts of the SNRPN gene. The novel exons lack protein coding potential and are expressed from the paternal chromosome only. We have also identified intragenic deletions and a point mutation in patients who have Angelman or Prader–Willi syndrome due to a parental imprint switch failure. This suggests that imprint switching on human chromosome 15 may involve alternative SNRPN transcripts.

Geneticscongenital hereditary and neonatal diseases and abnormalitiesChromosome 15ExonAlternative splicingHappy puppet syndromeGeneticsBiologyImprinting (psychology)Genomic imprintingGeneSNRPN GeneNature Genetics
researchProduct

Indication of a common origin of German and American Families with Familial Amyloidneuropathy Typ II

1999

Abstract The classification of familial amyloid neuropathies (FAP) is traditionally based on clinical and regional aspects. In the last 10 years more than 40 mutations of the transthyretin gene have been found to be responsible for different clinical forms of amyloidosis including familial FAP.FAP II is caused by a mutation on the codon 58 of the transthyretin gene. Only two american kindreds (the Maryland/German and the Ohio family) have previously been reported with FAP II starting in the 3rd or 4th decade by sensory disturbances of the hands typically as a carpal tunnel syndrome. We report on a german family with FAP II from the rhine river area south of Mainz. Four members with typical …

Geneticscongenital hereditary and neonatal diseases and abnormalitiesMutationPathologymedicine.medical_specialtybusiness.industryAmyloidosisHaplotypeGeneral Medicinemedicine.disease_causemedicine.diseaseTransthyretin Genedigestive system diseaseslanguage.human_languageGermanPsychiatry and Mental healthAmyloid NeuropathyNeurologyGenetic linkagemedicinelanguageNeurology (clinical)businessneoplasmsDer Nervenarzt
researchProduct

Novel <b><i>VANGL1</i></b> Gene Mutations in 144 Slovakian, Romanian and German Patients with Neural Tube Defects

2012

Neural tube defects (NTDs) are a group of congenital malformations of the central nervous system occurring at an average rate of 1 per 1,000 human pregnancies worldwide. Numerous genetic and environmental factors are discussed to be relevant in their etiology. In mice, mutants in >200 genes including the planar cell polarity (PCP) pathway are known to cause NTDs, and recently, heterozygous mutations in the human <i>VANGL1</i> gene have been described in a small subset of patients with NTDs. We performed a <i>VANGL1</i> mutation analysis in 144 unrelated individuals with NTDs from Slovakia, Romania and Germany and identified 3 heterozygous missense mutations: c.613…

Geneticscongenital hereditary and neonatal diseases and abnormalitiesMutationbusiness.industryMutantCentral nervous systemNeural tubeGene mutationmedicine.disease_causemedicine.anatomical_structureGeneticsMutation testingmedicineMissense mutationbusinessGeneGenetics (clinical)Molecular Syndromology
researchProduct

Hutchinson Gilford Progeria Syndrome: A Therapeutic Approach via Adenoviral Delivery of CRISPR/cas Genome Editing System

2015

Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare human genetic disease caused by mutations in the LMNA gene. LMNA codes for structural components of the nuclear lamina. Alterations of nuclear lamina lead to a very variable class of diseases known as laminopathies. In detail, HGPS manifests a severe premature ageing phenotype due to the accumulation of a dominant negative form of lamin-A called progerin. With current treatments, the life expectancy of HGPS patients does not exceed their second decade. Death is usually due to cardiovascular complications. Recently, a new technology for mammals in vivo gene editing has been developed: the clustered regularly interspaced short palindromic …

Geneticscongenital hereditary and neonatal diseases and abnormalitiesProgeriaintegumentary systemCas9Genetic enhancementnutritional and metabolic diseasesLamin-ABiologyProgerinmedicine.diseaseSettore MED/13 - EndocrinologiaLMNACRISPR/CasGenome editingSettore BIO/13 - Biologia Applicataembryonic structuresmedicineHGPSCRISPRLaminJournal of Genetic Syndromes & Gene Therapy
researchProduct

αααanti-4.2 Haplotype and heterozygous β° thalassemia in a Sicilian family

1985

The presence of the αααanti-4.2 haplotype and heterozygous β° thalassemia in a Sicilian family is described. These findings confirm the presence in Italy of a leftward deletion (−α4.2) and indicate that this may not be rare. Furthermore, although the β thalassemia determinant in this family has a severe expression, the interaction with the triplicated α gene does not necessarily express itself as thalassemia intermedia.

Geneticscongenital hereditary and neonatal diseases and abnormalitiesThalassemiaHaplotypeBiologymedicine.diseaseHuman geneticslanguage.human_languageHemoglobinopathyhemic and lymphatic diseasesGene duplicationGeneticslanguagemedicineGlobinGeneSicilianGenetics (clinical)Human Genetics
researchProduct

Epidemiological study of nonsyndromic hearing loss in Sicilian newborns

2007

Deafness is caused by a variety of facts, genetic and environmental. Regarding the acquired causes, deafness can be the consequence of prenatal infections, acoustic or cerebral trauma, and the use of ototoxic drugs. Deafness can be the only manifestation (nonsyndromic forms) or it may occur together with other phenotypic findings (syndromic forms). The majority of nonsyndromicdeafness has a genetic basis [Van Camp et al., 1997]. In recent years, deafness and hearing loss have assumed a clinical importance in the study of congenital disorders [Morton et al., 1991]. The clinical interest for hearing loss is supported by the social impact that this disorder has; if not treated, delays in the d…

GenotypeHearing lossHearing Loss SensorineuralDNA Mutational AnalysisNonsense mutationBiologyGene mutationConnexinsneonate deafness geneticExonNeonatal ScreeningGene Frequencyotorhinolaryngologic diseasesGeneticsmedicineHumansGenetic TestingSicilyGeneGenetics (clinical)Chromosome 13GeneticsSplice site mutationInfant NewbornGenetic VariationStop codonConnexin 26PhenotypeMutationmedicine.symptomAmerican Journal of Medical Genetics Part A
researchProduct