Search results for " Dysplasia"

showing 10 items of 206 documents

The spondylometaphyseal dysplasias. A tentative classification.

1991

The spondylometaphyseal dysplasias constitute a very complex group of disorders. In addition to the Kozlowski type, three subgroups can be distinguished by the appearance of the femoral neck. In the first group (A) the changes are severe with absent ossification of the femoral neck and coxa vara. In the second group (B) the changes of the femoral neck are moderate and in the third (C) mild metaphyseal irregularities are only visible. This classification is not definitive but tries to put order in this confusing section of constitutional bone diseases.

MaleBone diseaseAdolescentCoxa varaOsteochondrodysplasiasmedicineHumansRadiology Nuclear Medicine and imagingChildFemoral neckbusiness.industryOssificationFemur NeckInfantAnatomymedicine.diseaseHandmedicine.anatomical_structureSpondylometaphyseal dysplasiaDysplasiaChild PreschoolPediatrics Perinatology and Child HealthFemaleSpinal Diseasesmedicine.symptombusinessPediatric radiology
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A retrospective analysis of myelodysplastic syndromes with thrombocytosis: reclassification of the cases by WHO proposals.

2004

Myelodysplastic syndromes (MDS) show occasionally thrombocytosis, common feature of myeloproliferative diseases (MPD), with the overlapping of both disorders. Classically, thrombocytosis has been associated with some MDS subtypes: refractory anaemia with ringed sideroblasts (RARS), 5q- syndrome and those MDS with 3q chromosome rearrangements. The recent WHO classification recognises an unclassifiable MDS/MPD category including some of these disorders. Our aim is to determine the frequency of presentation, subtype classification and chromosome abnormalities of MDS with thrombocytosis diagnosed in our institution. Between 1990 and 2003 we studied 317 SMD patients according to FAB and WHO revi…

MaleCancer ResearchPathologymedicine.medical_specialtyRefractory anemia with ringed sideroblastsWorld Health OrganizationAge Distributionhemic and lymphatic diseasesInternal medicinemedicineHumansSurvival analysisAgedRetrospective StudiesAged 80 and overThrombocytosisThrombocytosisbusiness.industryMyelodysplastic syndromesRetrospective cohort studyHematologyMiddle Agedmedicine.diseaseSurvival AnalysisOncologyInternational Prognostic Scoring SystemDysplasiaKaryotypingMyelodysplastic SyndromesFemalebusinessRefractory cytopenia with multilineage dysplasiaLeukemia research
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Multifocal aplasia cutis congenita, distal limb hemimelia, and cutis marmorata telangiectatica in a patient with Adams-Oliver syndrome.

1992

Summary We describe an 18-month-old boy with multifocal scalp defects over the posterior parietal region combined with an underlying defect of the skull, left lower limb distal hemimelia and generalized cutis marmorata telangiectatica, consistent with a diagnosis of Adams–Oliver syndrome (aplasia cutis congenita with distal transverse limb defects).

MaleCutis marmorataPathologymedicine.medical_specialtyDermatologyAplasia cutis congenitaEctromeliaEctodermal DysplasiamedicineHemimeliaHumansAbnormalities MultipleTelangiectasisSkinLegScalpbusiness.industryInfantAplasiaAnatomySyndromemedicine.diseasebody regionsSkullmedicine.anatomical_structureScalpmedicine.symptombusinessAdams–Oliver syndromeThe British journal of dermatology
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The deletion of six amino acids at the C-terminus of the alpha 1 (II) chain causes overmodification of type II and type XI collagen: further evidence…

1996

We have identified an 18 bp deletion in exon 49 of the type II procollagen gene (COL2A1) in a patient with Kniest dysplasia. The deletion is located at the very C-terminus of the helical domain and removes two of three Gly-Pro-Pro triplets at positions 1007-1012, which are thought to be involved in helix formation and stability. Morphological investigation of an iliac crest biopsy showed large inclusions in the endoplasmic reticulum of chondrocytes, reflecting impaired secretion of type II collagen. Electrophoretic analysis of collagens extracted from cartilage or synthesised by cultured chondrocytes showed that type II and also type XI procollagen molecules containing mutant alpha 1 (II) c…

MaleDNA Mutational AnalysisMolecular Sequence DataMutantType II collagenBiologyOsteochondrodysplasiasChondrocyteIliumExonKniest dysplasiaGeneticsmedicineHumansAmino Acid SequencePeptide sequenceCells CulturedGenetics (clinical)Sequence DeletionInclusion BodiesGeneticsBase SequenceC-terminusExonsmedicine.diseaseMolecular biologyProcollagen peptidaseCartilagemedicine.anatomical_structureGenesChild PreschoolCollagenEndoplasmic Reticulum RoughProcollagenResearch ArticleJournal of Medical Genetics
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Mutations inWNT10Aare frequently involved in oligodontia associated with minor signs of ectodermal dysplasia

2012

Ectodermal dysplasias (ED) are a clinically and genetically heterogeneous group of hereditary disorders that have in common abnormal development of ectodermal derivatives. Hypohidrotic ectodermal dysplasia (HED) is characterized by abnormal development of eccrine sweat glands, hair, and teeth. The X-linked form of the disease, caused by mutations in the EDA gene, represents the majority of patients with the hypohidrotic form. Autosomal dominant and autosomal recessive forms are occasionally seen, and result from mutations in at least three genes (WNT10A, EDAR, or more rarely EDARADD). We have screened for mutations in EDAR (commonly involved in the hypohidrotic form) and WNT10A (involved in…

MaleEctodermal dysplasiaGenotypeMolecular Sequence Datamedicine.disease_causeCompound heterozygosityEctodermal DysplasiaGeneticsmedicineHumansAmino Acid SequenceHypohidrotic ectodermal dysplasiaGenetic Association StudiesGenetics (clinical)AnodontiaGeneticsMutationEDARADDEdar ReceptorGenetic heterogeneitybusiness.industrymedicine.diseaseWnt ProteinsHypodontiaPhenotypeMutationFemaleEctodysplasin AbusinessSequence AlignmentAmerican Journal of Medical Genetics Part A
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Evaluation of cell proliferation rate in non-dysplastic leukoplakias

2008

Objective: Analyze whether the most frequent cases of non-dysplastic leukoplakias, hyperkeratosis (H), acanthosis (A), and hyperkeratosis with acanthosis (HA) have similar cell proliferation rates and to compare them with epithelial dysplastic (ED) leukoplakias and normal oral epithelium (NOE).Study design: The sample comprised 10 cases of normal oral epithelium, 10 cases of hyperkeratosis, 10 cases of acanthosis, 10 cases of hyperkeratosis with acanthosis and 10 cases of epithelial dysplasia. The mean number of AgNORs per nucleus (mAgNOR) and the mean percentage of cells with 1, 2, 3 and 4 or more AgNORs per nucleus (pAgNOR) were recorded. Results: The results of mAgNOR showed differences …

MaleEpithelial dysplasiaPathologymedicine.medical_specialtyHyperkeratosisAcanthosisHyperkeratosisEpithelial dysplasiaAcanthosisBasal (phylogenetics)Biological profileProliferation rateOral and maxillofacial pathologyHumansMedicineLeucoplasia bucalGeneral DentistryCell proliferationCell ProliferationLeukoplakiabusiness.industryAntigens NuclearProliferação celularMiddle Agedmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Doencas [Mucosa bucal]AgNORstomatognathic diseasesOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASPatologia bucalFemaleSurgeryLeukoplakia OralbusinessLeukoplakia
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Sedaghatian congenital lethal metaphyseal chondrodysplasia—observations in a second Iranian family and histopathological studies

1987

In 1980, Sedaghatian described in two brothers and one sister a neonatally lethal disorder associated with slight rhizomelic limb shortness, mild platyspondyly, and severe metaphyseal dysplasia. Here data are presented on another Iranian infant with the Sedaghatian syndrome who died on day 4 and was found to have histologic evidence of severe epimetaphyseal dysplasia. The occurrence in children of both sexes in one instance, born to normal parents who were first cousins, and currently apparent confinement of the disorder to Iranians suggests that the Sedaghatian syndrome is an autosomal recessive trait with high gene frequency in Iranians. This may be a more complexly pleiotropic syndrome t…

MaleGeneticsmedicine.medical_specialtyDepressed nasal bridgeMetaphyseal chondrodysplasiabusiness.industryInfant NewbornShort neckConsanguinityIranOsteochondrodysplasiasmedicine.diseaseMetaphyseal dysplasiaDermatologyMicrophthalmiaBone and BonesAutosomal recessive traitCartilageDysplasiaotorhinolaryngologic diseasesmedicineHumansbusinessGenetics (clinical)American Journal of Medical Genetics
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Acromesomelic dysplasia Maroteaux type maps to human chromosome 9.

1998

SummaryAcromesomelic dysplasias are skeletal disorders that disproportionately affect the middle and distal segments of the appendicular skeleton. We report genetic mapping studies in four families with acromesomelic dysplasia Maroteaux type (AMDM), an autosomal recessive osteochondrodysplasia. A peak LOD score of 5.1 at recombination fraction 0 was obtained with fully informative markers on human chromosome 9. In three of the four families, the affected offspring are products of consanguineous marriages; if it is assumed that these affected offspring are homozygous by descent for the region containing the AMDM locus, a 6.9-cM AMDM candidate interval can be defined by markers D9S1853 and D9…

MaleGenotypeGenetic LinkageLocus (genetics)Chromosome 9ConsanguinityBiologyOsteochondrodysplasiasGenetic determinismBone and BonesConsanguinityGene mappingmedicineGeneticsHumansGenetics(clinical)OsteochondrodysplasiaGenetics (clinical)GeneticsChromosome 9Chromosome Mappingmedicine.diseaseOsteochondrodysplasiaPedigreeRadiographyMappingAcromesomelic dysplasia Maroteaux typeFemaleChromosome 20Lod ScoreChromosomes Human Pair 9Acromesomelic dysplasiaResearch ArticleMicrosatellite Repeats
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PI3K/AKT pathway mutations cause a spectrum of brain malformations from megalencephaly to focal cortical dysplasia

2015

Malformations of cortical development containing dysplastic neuronal and glial elements, including hemimegalencephaly and focal cortical dysplasia, are common causes of intractable paediatric epilepsy. In this study we performed multiplex targeted sequencing of 10 genes in the PI3K/AKT pathway on brain tissue from 33 children who underwent surgical resection of dysplastic cortex for the treatment of intractable epilepsy. Sequencing results were correlated with clinical, imaging, pathological and immunohistological phenotypes. We identified mosaic activating mutations in PIK3CA and AKT3 in this cohort, including cancer-associated hotspot PIK3CA mutations in dysplastic megalencephaly, hemimeg…

MaleHemimegalencephalyPathologymedicine.medical_specialtyAKT3HemimegalencephalyPhosphatidylinositol 3-KinasesmedicinePTENHumansMegalencephalyPI3K/AKT/mTOR pathwaybiologyBrainOriginal ArticlesCortical dysplasiamedicine.diseaseDEPDC5MegalencephalyMalformations of Cortical DevelopmentDysplasiabiology.proteinFemaleNeurology (clinical)Proto-Oncogene Proteins c-aktSignal Transduction
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A novel mutation of gene CBFA1/RUNX2 in cleidocranial dysplasia.

2007

Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal dysplasia characterised by abnormal clavicles, patent sutures and fontanelles, supernumerary teeth, short stature, and a variety of other skeletal changes. The disease gene is CBFA1/RUNX2, which is mapped to chromosome 6p21. Inactivation of the CBFA1/RUNX2 gene by mutations is involved in the skeletal defects that occur in patients with CCD. CBFA1/RUNX2 controls the differentiation of precursor cells into osteoblasts and is essential for membranous as well as endochondral bone formation. In this study of a 14-yr-old boy with typical CCD phenotype, the authors found a novel CBFA1/RUNX2 gene mutation. All of the amplified segment…

MaleHeterozygoteAdolescentDNA Mutational AnalysisCore Binding Factor Alpha 1 SubunitPolymerase Chain ReactionPedigreeAdolescent Chromosomes Human Pair 6 Cleidocranial Dysplasia/genetics* Cleidocranial Dysplasia/pathology Codon Nonsense/genetics* Core Binding Factor Alpha 1 Subunit/genetics* DNA Mutational Analysis DNA Primers/chemistry Female Gene Silencing Heterozygote Humans Male Pedigree Point Mutation* Polymerase Chain Reactioncleidocranial dysplasiaCodon NonsenseCBFA1/RUNX2HumansPoint MutationChromosomes Human Pair 6Femalegene mutationGene SilencingCleidocranial DysplasiaDNA Primers
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