Search results for " Type A"

showing 10 items of 67 documents

F-contractions of Hardy–Rogers-type and application to multistage decision

2016

We prove fixed point theorems for F-contractions of Hardy–Rogers type involving self-mappings defined on metric spaces and ordered metric spaces. An example and an application to multistage decision processes are given to show the usability of the obtained theorems.

010101 applied mathematicsCombinatoricsApplied Mathematics010102 general mathematicslcsh:QA299.6-433F-contractions of Hardy–Rogers type and application to multistage decision processeslcsh:Analysis0101 mathematicsType (model theory)01 natural sciencesAnalysisMathematicsNonlinear Analysis: Modelling and Control
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A High Throughput Phenotypic Screening reveals compounds that counteract premature osteogenic differentiation of HGPS iPS-derived mesenchymal stem ce…

2016

AbstractHutchinson-Gilford progeria syndrome (HGPS) is a rare fatal genetic disorder that causes systemic accelerated aging in children. Thanks to the pluripotency and self-renewal properties of induced pluripotent stem cells (iPSC), HGPS iPSC-based modeling opens up the possibility of access to different relevant cell types for pharmacological approaches. In this study, 2800 small molecules were explored using high-throughput screening, looking for compounds that could potentially reduce the alkaline phosphatase activity of HGPS mesenchymal stem cells (MSCs) committed into osteogenic differentiation. Results revealed seven compounds that normalized the osteogenic differentiation process an…

0301 basic medicineCell typecongenital hereditary and neonatal diseases and abnormalitiesPhenotypic screeningInduced Pluripotent Stem CellsRetinoic acidTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundProgeriaOsteogenesis[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]medicineHumansInduced pluripotent stem cellChildIsotretinoinGeneticsProgeriaMultidisciplinaryintegumentary systemGuided Tissue RegenerationMesenchymal stem cellnutritional and metabolic diseasesAging PrematureCell DifferentiationMesenchymal Stem Cellsmedicine.diseaseProgerinAlkaline PhosphataseLamin Type A3. Good healthCell biologyHigh-Throughput Screening Assays030104 developmental biologychemistryGene Expression Regulation[ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Alkaline phosphataseScientific Reports
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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Consensus recommendation for a diagnostic guideline for acid sphingomyelinase deficiency

2017

Disclaimer: This diagnostic guideline is intended as an educational resource and represents the opinions of the authors, and is not representative of recommendations or policy of the American College of Medical Genetics and Genomics (ACMG). The information should be considered a consensus based on expert opinion, as more comprehensive levels of evidence were not available in the literature in all cases. Background: Acid sphingomyelinase deficiency (ASMD) is a rare, progressive, and often fatal lysosomal storage disease. The underlying metabolic defect is deficiency of the enzyme acid sphingomyelinase that results in progressive accumulation of sphingomyelin in target tissues. ASMD manifests…

0301 basic medicineGuias de prática clínica como assuntomedicine.medical_specialtyConsensusLysosomal storage disorderClinical Decision-MakingMEDLINEDiseaseDiagnosis Differential03 medical and health sciencesSpecial Article0302 clinical medicineInternal medicinemedicineHumansacid sphingomyelin deficiencyGenetic TestingDisease management (health)Intensive care medicineDoenças de Niemann-PickGenetics (clinical)PulmonologistsGenetic testingmedicine.diagnostic_testbusiness.industryNiemann-Pick disease types A and BEvidence-based medicineGuidelineNiemann-Pick Disease Type BNiemann-Pick Disease Type A030104 developmental biologyEndocrinologyPhenotypeSphingomyelin PhosphodiesteraseMutationPractice Guidelines as TopicMedical geneticslysosomal storage disorderbusiness030217 neurology & neurosurgeryAlgorithmsBiomarkersAcid sphingomyelin deficiency
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Dopamine, Noradrenaline and Serotonin Receptor Densities in the Striatum of Hemiparkinsonian Rats following Botulinum Neurotoxin-A Injection.

2017

Abstract Parkinson’s disease (PD) is characterized by a degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) that causes a dopamine (DA) deficit in the caudate-putamen (CPu) accompanied by compensatory changes in other neurotransmitter systems. These changes result in severe motor and non-motor symptoms. To disclose the role of various receptor binding sites for DA, noradrenaline, and serotonin in the hemiparkinsonian (hemi-PD) rat model induced by unilateral 6-hydroxydopamine (6-OHDA) injection, the densities of D1, D2/D3, α1, α2, and 5HT2A receptors were longitudinally visualized and measured in the CPu of hemi-PD rats by quantitative in vitro receptor autorad…

0301 basic medicineMalemedicine.medical_specialtyApomorphine5-HT2A receptorNeurotoxinsSubstantia nigraMotor ActivityFunctional LateralityAntiparkinson Agents03 medical and health sciences0302 clinical medicineDopamine receptor D1Parkinsonian DisordersDopamine receptor D3DopamineInternal medicinemedicineAnimalsddc:610Longitudinal StudiesBotulinum Toxins Type ARats WistarReceptorOxidopamine5-HT receptorChemistryGeneral NeuroscienceDopaminergicCorpus StriatumReceptors Neurotransmitter030104 developmental biologyEndocrinologyDopamine Agonists030217 neurology & neurosurgerymedicine.drugNeuroscience
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An Integrated Pharmacophore/Docking/3D-QSAR Approach to Screening a Large Library of Products in Search of Future Botulinum Neurotoxin A Inhibitors

2020

Botulinum toxins are neurotoxins produced by Clostridium botulinum. This toxin can be lethal for humans as a cause of botulism

0301 basic medicineModels MolecularBotulinum ToxinsDatabases FactualNeuromuscular transmissionQuantitative Structure-Activity RelationshipPharmacologymedicine.disease_cause01 natural sciencesType Alcsh:ChemistryModelsClostridium botulinumbotulinum neurotoxin ABotulismBotulinum Toxins Type Alcsh:QH301-705.5Spectroscopyfood and beveragesGeneral MedicineBotulinum neurotoxinComputer Science ApplicationsdockingPharmacophoreQuantitative structure–activity relationshipStatic ElectricityChemicalbotulinum neurotoxin A virtual screening docking 3D-QSAR molecular dynamicsMolecular Dynamics SimulationArticleCatalysisInorganic ChemistrySmall Molecule Libraries03 medical and health sciencesDatabasesmedicinePhysical and Theoretical ChemistryMolecular BiologyFactual3D-QSARVirtual screening010405 organic chemistrybusiness.industryfungiOrganic ChemistryMolecularHydrogen Bondingmedicine.diseasevirtual screeningmolecular dynamics0104 chemical sciences030104 developmental biologyModels Chemicallcsh:Biology (General)lcsh:QD1-999Docking (molecular)Clostridium botulinumbusinessInternational Journal of Molecular Sciences
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Recommendations for clinical monitoring of patients with acid sphingomyelinase deficiency (ASMD)

2018

Abstract Background Acid sphingomyelinase deficiency (ASMD), a rare lysosomal storage disease, results from mutations in SMPD1, the gene encoding acid sphingomyelinase (ASM). As a result, sphingomyelin accumulates in multiple organs including spleen, liver, lung, bone marrow, lymph nodes, and in the most severe form, in the CNS and peripheral nerves. Clinical manifestations range from rapidly progressive and fatal infantile neurovisceral disease, to less rapidly progressing chronic neurovisceral and visceral forms that are associated with significant morbidity and shorter life span due to respiratory or liver disease. Objectives To provide a contemporary guide of clinical assessments for di…

0301 basic medicinemedicine.medical_specialtyEndocrinology Diabetes and MetabolismDisease030105 genetics & heredityBiochemistryArticle03 medical and health sciencesLiver disease0302 clinical medicineEndocrinologyQuality of lifeInternal medicineGeneticsmedicineLysosomal storage diseaseHumansEnzyme Replacement TherapyMolecular BiologyMonitoring PhysiologicPatient monitoringClinical Trials as TopicAcid sphingomyelinase deficiencyASMDLungbusiness.industryDisease ManagementEnzyme replacement therapyNiemann-Pick Disease Type Amedicine.diseasePhenotypemedicine.anatomical_structureMutationPractice Guidelines as TopicQuality of LifeBone marrowAcid sphingomyelinasebusinessRisk Reduction Behavior030217 neurology & neurosurgerymedicine.drugMolecular Genetics and Metabolism
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In Silico Conformational Features of Botulinum Toxins A1 and E1 According to Intraluminal Acidification

2022

International audience; Although botulinum neurotoxins (BoNTs) are among the most toxic compounds found in nature, their molecular mechanism of action is far from being elucidated. A key event is the conformational transition due to acidification of the interior of synaptic vesicles, leading to translocation of the BoNT catalytic domain into the neuronal cytosol. To investigate these conformational variations, homology modeling and atomistic simulations are combined to explore the internal dynamics of the sub-types BoNT/A1 (the most-used sub-type in medical applications) and BoNT/E1 (the most kinetically efficient sub-type). This first simulation study of di-chain BoNTs in closed and open s…

<i>Clostridium botulinum</i>; botulinum toxin; molecular dynamics; residue protonation; homology modeling[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM][SDV.BBM.BS] Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM]Health Toxicology and Mutagenesismolecular dynamichomology modelingresidue protonation[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsHydrogen-Ion ConcentrationToxicology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologySettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)molecular dynamics[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsGangliosidesSolventsClostridium botulinumbotulinum toxinBotulinum Toxins Type A[SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology[INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM][INFO.INFO-BI] Computer Science [cs]/Bioinformatics [q-bio.QM]
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Double inlet left ventricular main chamber, subaortic small left sided right ventricle and interrupted aortic arch type A. What operation is indicate…

1987

A case of a 23 year old female patient who suffered from the complex congenital heart lesion of a double inlet left ventricular main chamber, subaortic small left sided right ventricle and interrupted aortic arch type A is reported. With equally high blood pressures, the perfusion in the upper half of the body was maintained through the ascending aorta while the lower half and the lungs were supplied through the pulmonary artery and a patent ductus arteriosus (PDA). Angiographically, the bulbo-ventricular foramen appeared to be nonrestrictive. However, distinct signs of muscular subaortic stenosis were detected. The hemodynamic status principally allowed surgical correction when this became…

AdultHeart Defects CongenitalPulmonary and Respiratory MedicineAortic archmedicine.medical_specialtyHeart VentriclesAorta ThoracicAfterloadInternal medicinemedicine.arteryDuctus arteriosusAscending aortaMethodsmedicineHumansAortabusiness.industryPalliative CareInterrupted aortic arch type Amedicine.anatomical_structureDescending aortaPulmonary arterycardiovascular systemCardiologyFemaleSurgeryCardiology and Cardiovascular MedicinebusinessThe Thoracic and Cardiovascular Surgeon
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Age-Related Lipid Metabolic Signature in HumanLMNA-Lipodystrophic Stem Cell-Derived Adipocytes

2015

Lamin A (LMNA)-linked lipodystrophies belong to a group of clinical disorders characterized by a redistribution of adipose tissue with a variable range of metabolic complications. The leading cause of these disorders is the nonphysiological accumulation of the lamin A precursor, prelamin A. However, the molecular mechanisms by which prelamin A induces the pathology remain unclear.The aim of this study is to use an experimental LMNA-lipodystrophy model based on human mesenchymal stem cell (hMSC)-derived adipocytes that accumulate prelamin A to gain deeper insights into the mechanisms governing these diseases.Prelamin A-induced or -noninduced hMSC-derived adipocytes were obtained from healthy…

AdultMaleAgingcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentLipodystrophyLipolysisEndocrinology Diabetes and MetabolismCellular differentiationClinical BiochemistryAdipose tissueMitochondrionBiologyBiochemistryLMNAYoung AdultEndocrinologyInternal medicineAdipocytesmedicineHumansMetabolomicsLipolysisintegumentary systemStem CellsBiochemistry (medical)Mesenchymal stem cellnutritional and metabolic diseasesCell DifferentiationMiddle AgedLamin Type ALipid MetabolismEndocrinologyMetabolomeFemaleStem cellLaminThe Journal of Clinical Endocrinology &amp; Metabolism
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