Search results for "neonatal"

showing 10 items of 581 documents

Dystroglycan regulates structure, proliferation and differentiation of neuroepithelial cells in the developing vertebrate CNS.

2007

AbstractIn the developing CNS α- and β-dystroglycan are highly concentrated in the endfeet of radial neuroepithelial cells at the contact site to the basal lamina. We show that injection of anti-dystroglycan Fab fragments, knockdown of dystroglycan using RNAi, and overexpression of a dominant-negative dystroglycan protein by microelectroporation in neuroepithelial cells of the chick retina and optic tectum in vivo leads to the loss of their radial morphology, to hyperproliferation, to an increased number of postmitotic neurons, and to an altered distribution of several basally concentrated proteins. Moreover, these treatments also altered the oriented growth of axons from retinal ganglion c…

musculoskeletal diseasesCentral Nervous Systemcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtySuperior Colliculianimal structuresCellular differentiationNeuroepithelial CellsStem cellsDevelopmentDystrophin-associated protein complexRetinal ganglionAxonal growthMuscular DystrophiesRetina03 medical and health sciences0302 clinical medicineInternal medicineDystroglycanmedicineAnimalsDystroglycansMolecular BiologyCell Shape030304 developmental biologyCell Proliferation0303 health sciencesRetinabiologyfungiCell DifferentiationCell BiologyMuscular dystrophymusculoskeletal systemCell biologyNeuroepithelial cellmedicine.anatomical_structureEndocrinologyRNAiVertebratesbiology.proteinBasal laminaPikachurinStem cellChickens030217 neurology & neurosurgeryDevelopmental BiologyDevelopmental biology
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Bioengineered in vitro 3D model of myotonic dystrophy type 1 human skeletal muscle

2021

Abstract Myotonic dystrophy type 1 (DM1) is the most common hereditary myopathy in the adult population. The disease is characterized by progressive skeletal muscle degeneration that produces severe disability. At present, there is still no effective treatment for DM1 patients, but the breakthroughs in understanding the molecular pathogenic mechanisms in DM1 have allowed the testing of new therapeutic strategies. Animal models and in vitro two-dimensional cell cultures have been essential for these advances. However, serious concerns exist regarding how faithfully these models reproduce the biological complexity of the disease. Biofabrication tools can be applied to engineer human three-dim…

musculoskeletal diseasesDistròfia muscularcongenital hereditary and neonatal diseases and abnormalitiesCellular differentiation0206 medical engineeringBiomedical EngineeringBioengineering02 engineering and technologyBiologyBiochemistryMyotonic dystrophyBiomaterials3D cell culturemedicineMyocyteTissue engineeringMyopathyMyogenesisSkeletal muscleGeneral MedicineMuscular dystrophy021001 nanoscience & nanotechnologymedicine.disease020601 biomedical engineering3. Good healthCell biologymedicine.anatomical_structureEnginyeria de teixitsCell culturemedicine.symptom0210 nano-technologyBiotechnologyBiofabrication
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Mechanical activity of small and large intestine in normal and mdx mice: a comparative analysis.

1999

The aim of this study was to compare the motor pattern (recorded as changes in intraluminal pressure) of isolated duodenum and proximal colon between dystrophic mdx and normal mice. When duodenal recordings from control preparations were compared with mdx mice there was no significant difference in the spontaneous motor pattern, responses to electrical nerve stimulation or sensitivity to pharmacological agents. Colonic segments from mdx mice showed a more complex motor pattern, consisting of contractions with amplitude and frequency similar to those of controls and by additional contractions with lower amplitude and higher frequency. Moreover, 70% of the colonic preparations from mdx mice d…

musculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyNerve stimulationPhysiologyColonDuodenumDuchenne muscular dystrophyIn Vitro TechniquesInhibitory postsynaptic potentialNitric oxidechemistry.chemical_compoundMiceReference ValuesInternal medicineIntestine SmallmedicineAnimalsLarge intestineProximal colonIntestine LargeEndocrine and Autonomic SystemsChemistrySignificant differenceGastroenterologyAnatomyMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseElectric StimulationBiomechanical PhenomenaMice Inbred C57BLmedicine.anatomical_structureEndocrinologyDuodenumMice Inbred mdxGastrointestinal MotilityNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
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Sicilian pistachio (Pistacia vera L.) nut inhibits expression and release of inflammatory mediators and reverts the increase of paracellular permeabi…

2014

Background Dietary approaches to control inflammatory bowel diseases (IBD) may include proanthocyanidin-rich foods. Our previous research showed that a hydrophilic extract from Sicilian pistachio nut (HPE) contains sub- stantial amounts of proanthocyanidins and possesses anti- inflammatory activities. Purpose We studied the effects of HPE and of its poly- meric proanthocyanidin fraction (PPF) in a cell model that simulated some conditions of IBD, consisting of interleukin (IL)-1b-stimulated Caco-2 cells. Methods HPE was prepared by Pistacia vera L. nuts, and PPF was isolated from HPE by adsorbance chromatogra- phy. Proanthocyanidins were quantified as anthocyanidins after acidic hydrolysis.…

musculoskeletal diseasesPistachio nut Inflammation Intestinal epithelium Polyphenols Proanthocyanidinscongenital hereditary and neonatal diseases and abnormalitiesCellInterleukin-1betaAnti-Inflammatory AgentsMedicine (miscellaneous)BiologyPharmacologyPermeabilityCell membraneSettore BIO/10 - BiochimicamedicineHumansNutsProanthocyanidinsViability assayIntestinal MucosaCell ProliferationNutrition and DieteticsPistaciaInterleukin-6Interleukin-8NF-kappa BEpithelial Cellsbiology.organism_classificationIntestinal epitheliumIntestinesmedicine.anatomical_structureProanthocyanidinBiochemistryCaco-2Cyclooxygenase 2Paracellular transportPistaciaCaco-2 Cells
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The revised ghent nosology; reclassifying isolated ectopia lentis

2014

Inherited ectopia lentis (EL) is most commonly caused by Marfan syndrome (MFS), a multisystemic disorder caused by mutations in FBN1. Historically the diagnosis for patients with EL who have no systemic features of MFS is isolated EL (IEL). However, the Ghent nosology for MFS was updated in 2010 and made some important alterations. In particular, patients with EL and a FBN1 mutation are now categorically diagnosed with MFS, if their mutation has previously been described with aortic dilation/dissection. This carries significant systemic implications, as many patients previously diagnosed with IEL are now reclassified. We provide a review of all published cases of IEL caused by FBN1 mutation…

musculoskeletal diseasesProbandMarfan syndromeNosologycongenital hereditary and neonatal diseases and abnormalitiesPediatricsmedicine.medical_specialtybusiness.industrymedicine.disease3. Good healthDissectionGeneticsMedicineIn patientChinese familyAortic dilationbusinessEctopia lentisGenetics (clinical)Clinical Genetics
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Muscleblind, BSF and TBPH are mislocalized in the muscle sarcomere of a Drosophila myotonic dystrophy model

2012

SummaryMyotonic dystrophy type 1 (DM1) is a genetic disease caused by the pathological expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene. In the DMPK transcripts, the CUG expansions sequester RNA-binding proteins into nuclear foci, including transcription factors and alternative splicing regulators such as MBNL1. MBNL1 sequestration has been associated with key features of DM1. However, the basis behind a number of molecular and histological alterations in DM1 remain unclear. To help identify new pathogenic components of the disease, we carried out a genetic screen using a Drosophila model of DM1 that expresses 480 interrupted CTG repeats, i(CTG)480, and a collection of…

musculoskeletal diseasesSarcomerescongenital hereditary and neonatal diseases and abnormalitiesNeuroscience (miscellaneous)lcsh:MedicineMedicine (miscellaneous)RNA-binding proteinGenes InsectBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically Modifiedchemistry.chemical_compoundImmunology and Microbiology (miscellaneous)RNA interferencelcsh:PathologymedicineMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophyGeneticsMuscleslcsh:RAlternative splicingNuclear ProteinsRNA-Binding ProteinsEpistasis Geneticmedicine.diseaseDisease Models AnimalchemistryGene Knockdown TechniquesDrosophilaFemaleRNA InterferenceTrinucleotide repeat expansionTrinucleotide Repeat ExpansionDrosophila Proteinlcsh:RB1-214Genetic screenResearch ArticleDisease Models & Mechanisms
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A possible susceptibility locus for bipolar affective disorder in chromosomal region 10q25--q26.

2000

In an attempt to identify susceptibility loci for bipolar affective disorder, we are currently conducting a systematic genome screen with highly polymorphic microsatellite markers at an average marker spacing of 10 cM in a series of 75 families, comprising 66 families from Germany, eight families from Israel, and one family from Italy. The families were ascertained through index cases with bipolar affective disorder. The distribution of diagnoses is as follows: 126 individuals with bipolar I disorder, 40 with bipolar II disorder, 14 with schizoaffective disorder of the bipolar type, 40 individuals with recurrent unipolar depression, 51 with a minor psychiatric diagnosis, and two individuals…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesBipolar DisorderLocus (genetics)Nuclear FamilyCellular and Molecular NeurosciencemedicineHumansGenetic Predisposition to DiseaseBipolar disorderMolecular BiologyGeneticsFamily HealthChromosomes Human Pair 10Chromosome MappingGene Localizationmedicine.diseaseSib pairseye diseasesbody regionsPsychiatry and Mental healthChromosomal regionSusceptibility locussense organsPsychologyManic depressionMicrosatellite RepeatsMolecular psychiatry
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A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA b…

2002

The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (ste…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairTranscription GeneticDNA damageDNA repairBiologyGene productMicechemistry.chemical_compoundGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNA PrimersMice KnockoutBase SequenceHomozygoteDNA HelicasesDeoxyguanosinenutritional and metabolic diseasesBase excision repairMolecular biologyOxidative StressDNA Repair EnzymesBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineDNA glycosylaseDNADNA DamageNucleotide excision repairOncogene
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The Skull in Achondroplasia

1988

The growth disorder in achondroplasia results from abnormalities of endochondral bone formation. Cranial abnormalities originate from the occipital bone, the only region where enchondral bone is formed.

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMuscular hypotoniaThanatophoric dysplasiabusiness.industryOccipital boneAnatomymedicine.diseaseEndochondral bone formationSkullmedicine.anatomical_structuremedicineAchondroplasiabusinessJugular foramen
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Molecular Effects of the CTG Repeats in Mutant Dystrophia Myotonica Protein Kinase Gene

2008

Myotonic Dystrophy type 1 (DM1) is a multi-system disorder characterized by muscle wasting, myotonia, cardiac conduction defects, cataracts, and neuropsychological dysfunction. DM1 is caused by expansion of a CTG repeat in the 3 untranslated region (UTR) of the Dystrophia Myotonica Protein Kinase (DMPK) gene. A body of work demonstrates that DMPK mRNAs containing abnormally expanded CUG repeats are toxic to several cell types. A core mechanism underlying symptoms of DM1 is that mutant DMPK RNA interferes with the developmentally regulated alternative splicing of defined pre-mRNAs. Expanded CUG repeats fold into ds(CUG) hairpins that sequester nuclear proteins including human Muscleblind-lik…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesThree prime untranslated regionAlternative splicingBiologyMolecular biologyArticleExonchemistry.chemical_compoundCell nucleusmedicine.anatomical_structurechemistryGene expressionGeneticsmedicineGene silencingMBNL1Nuclear proteinGenetics (clinical)Current Genomics
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