Search results for "ATAL"

showing 10 items of 10591 documents

Sp1 transcription factor interaction with accumulated prelamin a impairs adipose lineage differentiation in human mesenchymal stem cells: essential r…

2012

Abstract Lamin A (LMNA)-linked lipodystrophies may be either genetic (associated with LMNA mutations) or acquired (associated with the use of human immunodeficiency virus protease inhibitors [PIs]), and in both cases they share clinical features such as anomalous distribution of body fat or generalized loss of adipose tissue, metabolic alterations, and early cardiovascular complications. Both LMNA-linked lipodystrophies are characterized by the accumulation of the lamin A precursor prelamin A. The pathological mechanism by which prelamin A accumulation induces the lipodystrophy associated phenotypes remains unclear. Since the affected tissues in these disorders are of mesenchymal origin, we…

congenital hereditary and neonatal diseases and abnormalitiesLipodystrophySp1 Transcription FactorCellular differentiationAdipose tissueBiologyLMNAHumansProtein PrecursorsTranscription factorOriginal Articles and ReviewsAdipogenesisintegumentary systemSecretory VesiclesMesenchymal stem cellnutritional and metabolic diseasesNuclear ProteinsCell DifferentiationMesenchymal Stem CellsCell BiologyGeneral MedicineLamin Type ALipid MetabolismCell biologyExtracellular MatrixBiochemistryAdipose TissueGene Expression RegulationAdipogenesisDifferentiationMutationMesenchymal stem cellsTranscription factorStem cellExperimental modelsLaminDevelopmental BiologyStem cells translational medicine
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Studies on the interaction of C1q,a subcomponent of the first component of complement, with porins fromSalmonella minnesotaincorporated into artifici…

1990

AbstractPurified outer membrane proteins (OMP) of Salmonella minnesota, Re-form, were incorporated into liposomes. These induced in macrophages a chemiluminescence signal identical to that of the intact Re-form. This signal was abolished by preincubation of porin-containing liposomes with purified C1q. Incorporation of isolated OMP into black lipid membranes (BLM) resulted in channel-formation which could not be inhibited by isolated C1q. Additionally, incubation of OMP-containing liposomes with BLM resulted in pore-formation within the BLM. This was amplified when lipid A was present within the liposomes. Preincubation of OMP-containing liposomes with purified C1q abolished pore-formation …

congenital hereditary and neonatal diseases and abnormalitiesLuminescenceMacrophageLipid BilayersBiophysicsSynthetic membranePorinschemical and pharmacologic phenomenaBiochemistryIon ChannelsMembrane PotentialsLipid AMiceSalmonellaStructural BiologyGeneticsAnimalsHumansBlack lipid membraneLipid bilayerMolecular BiologyC1qCells CulturedMice Inbred BALB CLiposomeurogenital systemChemistryComplement C1qMacrophagesElectric Conductivitynutritional and metabolic diseasesMembranes ArtificialCell BiologyLiposomeKineticsCholesterolMembraneMembrane proteinBiochemistryOuter membrane proteinPorinPhosphatidylcholinesbacteriaBacterial outer membraneBacterial Outer Membrane ProteinsFEBS Letters
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Cytotoxicity investigations of plasma sprayed calcium phosphate coatings

1994

One potential alternative material to replace hydroxyapatite (HAp) as a coating material for plasma-sprayed coatings on implants for hip replacement is fluorapatite (FAp). FAp has advantages over HAp regarding the capability of being chemically stable during the coating process. This leads to surface coatings containing high apatite rates with a mechanical stability (bond strength, microhardness) comparable to HAp. From the technical point of view the production of FAp coatings is well investigated, although studies on biocompatibility of FAp coatings are fewer. This paper reports the production of HAp and FAp coatings with varying solubilities by plasma spraying and their in vitro cytotoxi…

congenital hereditary and neonatal diseases and abnormalitiesMaterials scienceBiocompatibilityBond strengthMetallurgyFluorapatiteBiomedical EngineeringBiophysicsBioengineeringElectrolyteengineering.materialCell morphologydigestive system diseasesApatiteBiomaterialschemistry.chemical_compoundstomatognathic systemchemistryChemical engineeringCoatingvisual_artvisual_art.visual_art_mediumengineeringFluorideJournal of Materials Science: Materials in Medicine
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Safety of Dietary Guanidinoacetic Acid: A Villain of a Good Guy?

2021

Guanidinoacetic acid (GAA) is a natural amino acid derivative that is well-recognized for its central role in the biosynthesis of creatine, an essential compound involved in cellular energy metabolism. GAA (also known as glycocyamine or betacyamine) has been investigated as an energy-boosting dietary supplement in humans for more than 70 years. GAA is suggested to effectively increase low levels of tissue creatine and improve clinical features of cardiometabolic and neurological diseases, with GAA often outcompeting traditional bioenergetics agents in maintaining ATP status during stress. This perhaps happens due to a favorable delivery of GAA through specific membrane transporters (such as…

congenital hereditary and neonatal diseases and abnormalitiesNutrition and DieteticsNutrition. Foods and food supplyGlycinetoxicitynutritional and metabolic diseasesReviewMCDARisk AssessmentVDP::Medisinske Fag: 700::Helsefag: 800::Ernæring: 811creatineDietary SupplementsneuromodulationAnimalsHumansTX341-641methylationEnergy MetabolismhyperhomocysteinemiaHomocysteineAgedFood ScienceNutrients
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A girl with inverted triplication of chromosome 3q25.3 → q29 and multiple congenital anomalies consistent with 3q duplication syndrome

2005

We report a newborn girl with intrachromosomal triplication of 3q25.3 --> q29 (mosaicism) who died at the age of 3.5 weeks due to her malformations. She demonstrated disproportionate short stature with short limbs, a prominent and hairy forehead, thick eyebrows, synophrys, small upturned nose, full cheeks, micrognathia, and low set malformed and posteriorly rotated ears, short and webbed neck, hydrocephalus, Dandy-Walker malformation, spina bifida, complex heart defect (ventricular and atrial septal defect, malrotation, and interrupted aortic arch), omphalocele, polycystic kidneys, postaxial polydactyly of left hand, and generalized hirsutism; all signs have been associated with the dup(3q)…

congenital hereditary and neonatal diseases and abnormalitiesOmphaloceleSpina bifidaInterrupted aortic archAnatomyBiologymedicine.diseaseShort statureChromosome 3GeneticsmedicineWebbed neckmedicine.symptomTrisomyFull cheeksGenetics (clinical)American Journal of Medical Genetics Part A
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Enzyme replacement and gene therapy for mucopolysaccharidoses: current progress and future directions

2015

Introduction: Mucopolysaccharidoses (MPS) are lysosomal storage disorders caused by the deficiency of enzymes that are responsible for the stepwise degradation of complex carbohydrates, the glycosaminoglycans. Whereas in the past the treatment of MPS consisted mainly of palliative care, enzyme replacement therapy (ERT) is now possible for some MPS disorders, and in the future many other therapeutic options will become available.Areas covered: This review, based on personal experience and the currently available literature, will give an overview on the efficacy and limitations of ERT and will discuss new therapeutic approaches, such as anti-inflammatory drugs, substrate reduction therapy, ch…

congenital hereditary and neonatal diseases and abnormalitiesPalliative carebusiness.industryHealth PolicyGenetic enhancementmedicine.medical_treatmentnutritional and metabolic diseasesLysosomal storage disordersHematopoietic stem cell transplantationEnzyme replacement therapyBioinformaticsImmunologymedicinePharmacology (medical)Substrate reduction therapybusinessPharmacology Toxicology and Pharmaceutics (miscellaneous)Expert Opinion on Orphan Drugs
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GLI3 is rarely implicated in OFD syndromes with midline abnormalities

2011

A range of phenotypes including Greig cephalopolysyndactyly and Pallister-Hall syndromes (GCPS, PHS) are caused by pathogenic mutation of the GLI3 gene. To characterize the clinical variability of GLI3 mutations, we present a subset of a cohort of 174 probands referred for GLI3 analysis. Eighty-one probands with typical GCPS or PHS were previously reported, and we report the remaining ninety-three probands here. This includes nineteen probands (twelve mutations) who fulfilled clinical criteria for GCPS or PHS, forty-eight probands (sixteen mutations) with features of GCPS or PHS but who did not meet the clinical criteria (sub-GCPS and sub-PHS), twenty-one probands (six mutations) with featu…

congenital hereditary and neonatal diseases and abnormalitiesPallister-Hall SyndromeKruppel-Like Transcription FactorsNerve Tissue ProteinsBiologyBioinformaticsArticlePolydactylyMutationGLI3Mutation (genetic algorithm)GeneticsHumansAbnormalities MultipleSyndactylyGenetics (clinical)Human Mutation
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Genetic features of neuroblastic tumors associated with opsoclonus-myoclonus syndrome opens up the possibility for detection in peripheral blood

2016

Opsoclonus–myoclonus syndrome (OMS) is a rare paraneoplastic, postinfectious, or parainfectious or idiopathic acute neurological syndrome in children and adults. OMS is characterized by involuntary...

congenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyGeneral NeuroscienceBiologymedicine.diseaseNeuroblastic TumorPeripheral bloodnervous system diseases03 medical and health sciences0302 clinical medicineCirculating tumor DNA030220 oncology & carcinogenesisOpsoclonus myoclonus syndromeImmunologymedicineNeurological syndromePharmacology (medical)Neurology (clinical)030217 neurology & neurosurgeryExpert Review of Neurotherapeutics
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B and T lymphocytes are affected in lysosomal disorders--an immunoelectron microscopic study.

1991

Circulating lymphocytes of four patients with mucopolysaccharidoses II and IIIA, four patients with juvenile neuronal ceroid-lipofuscinosis, one patient each with glycogenosis type II, infantile neuronal ceroid-lipofuscinosis, and Gaucher disease were classified by immunoelectron microscopy as B or T lymphocytes. Disease-specific lysosomal inclusions as well as non-specific lysosomal organelles, especially Gall bodies were identified in B and T lymphocytes. These non-quantitative studies indicate that both B and T lymphocytes participate in the lysosomal storage process.

congenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyHistologyImmunoelectron microscopyMucopolysaccharidosisT-LymphocytesCentral nervous systemVacuoleBiologyPathology and Forensic MedicinePhysiology (medical)OrganellemedicineLysosomal storage diseaseHumansMicroscopy ImmunoelectronB-Lymphocytesnutritional and metabolic diseasesT lymphocytemedicine.diseasemedicine.anatomical_structureNeurologyNeuronal ceroid lipofuscinosisNeurology (clinical)Metabolism Inborn ErrorsNeuropathology and applied neurobiology
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Expression of hMLH1 and hMSH2 proteins in ameloblastomas and tooth germs

2017

Background Mismatch repair proteins (MMRPs) are a group of nuclear enzymes that participate in the repair of base mismatches that occur during DNA replication in all proliferating cells. The most studied MMRPs are hMSH2 and hMLH1, which are known to be highly expressed in normal tissues. A loss of MMRPs leads to the accumulation of DNA replication errors in proliferating cells. Ki-67 is a biomarker regarded to be the gold-standard tool for determining cell proliferation by immunohistochemical methods. The aim of this study was to investigate the immunohistochemical expression of hMLH1, hMSH2 and Ki-67 proteins in ameloblastomas and tooth germs, to contribute to the understanding of the deve…

congenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyhMSH2hMLH1Ameloblastoma03 medical and health sciencesTooth germsGERMEN DENTARIO0302 clinical medicinemedicineHumansHOMOLOGO 1 DE LA PROTEINA MutL (1)AmeloblastomaGeneral DentistryTooth GermsOral Medicine and PathologyAmeloblastomasbiologyCell growthResearchDNA replicationTooth Germnutritional and metabolic diseases030206 dentistry:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseImmunohistochemistryJaw NeoplasmsANTIGENO Ki-67PROTEINA 2 HOMOLOGA a MutS (1)digestive system diseasesKi-67 AntigenMutS Homolog 2 ProteinAMELOBLASTOMAOtorhinolaryngology030220 oncology & carcinogenesisKi-67UNESCO::CIENCIAS MÉDICASbiology.proteinKi-67Biomarker (medicine)ImmunohistochemistrySurgeryDNA mismatch repairMutL Protein Homolog 1Medicina Oral Patología Oral y Cirugia Bucal
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