Search results for "skeletal disease"

showing 10 items of 845 documents

Increased Muscleblind levels by chloroquine treatment improve myotonic dystrophy type 1 phenotypes in in vitro and in vivo models

2019

Myotonic dystrophy type 1 (DM1) is a life-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG trinucleotide repeat in the 3′ UTR of the DMPK gene. The mutant RNA forms insoluble structures capable of sequestering RNA binding proteins of the Muscleblind-like (MBNL) family, which ultimately leads to phenotypes. In this work, we demonstrate that treatment with the antiautophagic drug chloroquine was sufficient to up-regulate MBNL1 and 2 proteins in Drosophila and mouse (HSA LR ) models and patient-derived myoblasts. Extra Muscleblind was functional at the molecular level and improved splicing events regulated by MBNLs in all disease models. In vivo,…

0301 basic medicinemusculoskeletal diseasesMaleRNA SplicingRNA-binding proteinBiologyMyotonic dystrophychloroquinemuscleblindMyoblasts03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivomedicineAutophagyMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophytherapyMultidisciplinarymyotonic dystrophyMusclesRNANuclear ProteinsRNA-Binding ProteinsChloroquinemedicine.diseaseMyotoniaCell biologyDNA-Binding ProteinsDisease Models Animal030104 developmental biologyPhenotypechemistryPNAS PlusRNA splicingDrosophilaFemaleTrinucleotide repeat expansion030217 neurology & neurosurgery
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miR-23b and miR-218 silencing increase Muscleblind-like expression and alleviate myotonic dystrophy phenotypes in mammalian models

2018

Functional depletion of the alternative splicing factors Muscleblind-like (MBNL 1 and 2) is at the basis of the neuromuscular disease myotonic dystrophy type 1 (DM1). We previously showed the efficacy of miRNA downregulation in Drosophila DM1 model. Here, we screen for miRNAs that regulate MBNL1 and MBNL2 in HeLa cells. We thus identify miR-23b and miR-218, and confirm that they downregulate MBNL proteins in this cell line. Antagonists of miR-23b and miR-218 miRNAs enhance MBNL protein levels and rescue pathogenic missplicing events in DM1 myoblasts. Systemic delivery of these “antagomiRs” similarly boost MBNL expression and improve DM1-like phenotypes, including splicing alterations, histo…

0301 basic medicinemusculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesScienceMyoblasts SkeletalGeneral Physics and AstronomyMice TransgenicBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineRNA interferencemicroRNAmedicineMBNL1Gene silencingAnimalsHumansMyotonic DystrophyGene SilencingRNA Messengerlcsh:ScienceMuscle Skeletal3' Untranslated RegionsMultidisciplinaryThree prime untranslated regionAlternative splicingQRNA-Binding ProteinsGeneral Chemistrymedicine.diseaseMyotoniaCell biologyUp-RegulationAlternative SplicingDisease Models AnimalMicroRNAs030104 developmental biologyPhenotypechemistrylcsh:Q030217 neurology & neurosurgeryHeLa CellsNature Communications
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Apert Syndrome With FGFR2 758 C > G Mutation: A Chinese Case Report

2018

Background: Apert syndrome is considered as one of the most common craniosynostosis syndromes with a prevalence of 1 in 65,000 individuals, and has a close relationship with point mutations in FGFR2 gene.Case report: Here, we described a Apert syndrome case, who was referred to genetic consultation in our hospital with the symptom of craniosynostosis and syndactyly of the hands and feet. Craniosynostosis, midfacial retrusion, steep wide forehead, larger head circumference, marked depression of the nasal bridge, short and wide nose and proptosis could be found obviously, apart from these, ears were mildly low compared with normal children and there was no cleft lip and palate. Mutation was i…

0301 basic medicinemusculoskeletal diseasesPediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNasal bridgelcsh:QH426-470Case ReportApert syndromeCraniosynostosis03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGeneticsmedicineSyndactylyGenetics (clinical)NoseSanger sequencingbusiness.industryPoint mutationmedicine.diseaseexons sequencingcraniosynostosislcsh:Genetics030104 developmental biologymedicine.anatomical_structureFGFR2genetic mutationsymbolsMolecular Medicinebusiness030217 neurology & neurosurgeryApert syndromeFrontiers in Genetics
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Association between ribs shape and pulmonary function in patients with Osteogenesis Imperfecta

2019

Graphical abstract

0301 basic medicinemusculoskeletal diseasesVital capacityPulmonary functionMedicinaKyphosisScoliosisPulmonary function testing03 medical and health sciencesFEV1/FVC ratio0302 clinical medicinemedicineRespiratory functionLung volumeslcsh:Science (General)ComputingMethodologies_COMPUTERGRAPHICSRib cagelcsh:R5-920Geometric morphometricsMultidisciplinarybusiness.industryAnatomymedicine.diseasemusculoskeletal system030104 developmental biologyScoliosis030220 oncology & carcinogenesisRib cageOriginal ArticleOsteogenesis imperfectaThoracic spinebusinesslcsh:Medicine (General)lcsh:Q1-390Journal of Advanced Research 21: 177-185 (2020)
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Therapeutic Potential of AntagomiR-23b for Treating Myotonic Dystrophy

2020

Myotonic dystrophy type 1 (DM1) is a chronically debilitating, rare genetic disease that originates from an expansion of a noncoding CTG repeat in the dystrophia myotonica protein kinase (DMPK) gene. The expansion becomes pathogenic when DMPK transcripts contain 50 or more repetitions due to the sequestration of the muscleblind-like (MBNL) family of proteins. Depletion of MBNLs causes alterations in splicing patterns in transcripts that contribute to clinical symptoms such as myotonia and muscle weakness and wasting. We previously found that microRNA (miR)-23b directly regulates MBNL1 in DM1 myoblasts and mice and that antisense technology (“antagomiRs”) blocking this microRNA (miRNA) boost…

0301 basic medicinemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMyotonic dystrophyArticleantagomiR03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymicroRNAMedicineMBNL1AntagomirProtein kinase AmiRNAmyotonic dystrophybusiness.industrylcsh:RM1-950Muscle weaknessmedicine.diseaseMyotoniaMbnl1030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisRNA splicingCancer researchHSALR miceMolecular Medicinemedicine.symptomDM1antisense oligonucleotidesbusinessMolecular Therapy: Nucleic Acids
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Autoantibodies in Spondyloarthritis, Focusing on Anti-CD74 Antibodies

2019

Spondyloarthritis (SpA) is an inflammatory rheumatic disease with diverse clinical presentation. The diagnosis of SpA remains a big challenge in daily clinical practice because of the limitation in specific biomarkers of SpA, more biomarkers are still needed for SpA diagnosis and disease activity monitoring. In the past, SpA was considered predominantly as auto-inflammatory disease vs. autoimmune disease. However, in recent years several researches demonstrated a broad autoantibody response in SpA patients. Study also indicated that mice lack of ZAP70 in T cell develop SpA featured inflammation. These studies indicated the autoimmune features of SpA and gave rise to the potential use of aut…

0301 basic medicinemusculoskeletal diseaseslcsh:Immunologic diseases. AllergyCD74autoantibodiesdiagnosisImmunologyAutoimmunityDiseaseAutoantigensAutoimmune DiseasesPathogenesis03 medical and health sciences0302 clinical medicineHypothesis and TheorySpondylarthritismedicineImmunology and AllergyHumansHeat-Shock ProteinsAutoimmune diseasebiologybusiness.industryChinese patientsAutoantibodyHistocompatibility Antigens Class IIspondyloarthritismedicine.diseaseClinical PracticeAntigens Differentiation B-LymphocyteProtein Phosphatase 2Cstomatognathic diseases030104 developmental biology14-3-3 ProteinsROC CurveImmunologybiology.proteinBiomarker (medicine)Antibodybusinessbeta 2-Microglobulinlcsh:RC581-607Biomarkers030215 immunologyanti-CD74 autoantibodyFrontiers in Immunology
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A Strongyloides stercoralis infection presenting as arthritis of sternoclavicular joint

2016

Strongyloides stercoralis (S. stercoralis) is a parasite, endemic in tropical, subtropical, and also not rarely in temperate regions, that infects up to 100 million people worldwide [1]. Patients m...

0301 basic medicinemusculoskeletal diseasesmedicine.medical_specialty030106 microbiologySternoclavicular jointArthritisStrongyloides stercoralis03 medical and health sciences0302 clinical medicineRheumatologyInternal medicineStrongyloidesmedicineReactive arthritis030212 general & internal medicinebiologybusiness.industryArthritismedicine.diseasebiology.organism_classificationhumanitiesRheumatologyStrongyloidiasismedicine.anatomical_structureStrongyloidesImmunologyStrongyloides Arthritis Rheumatologybusinesshuman activities
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Gene variants of osteoprotegerin, estrogen-, calcitonin- and vitamin D-receptor genes and serum markers of bone metabolism in patients with Gaucher d…

2018

Anca Zimmermann,1 Radu A Popp,2 Heidi Rossmann,3 Simona Bucerzan,4 Ioana Nascu,4 Daniel Leucuta,5 Matthias M Weber,1 Paula Grigorescu-Sido41Department of Endocrinology and Metabolic Diseases, 1st Clinic and Polyclinic of Internal Medicine, University of Mainz, Mainz, Germany; 2Department of Medical Genetics, University of Medicine and Pharmacy, Cluj-Napoca, Romania; 3Institute for Clinical Chemistry and Laboratory Medicine, University of Mainz, Mainz, Germany; 4Center of Genetic Diseases, 1st Pediatric Clinic, University of Medicine and Pharmacy, Cluj-Napoca, Romania; 5Department of Medical Informatics and Biostatistics, University of Medicine and Pharmacy, Cluj-Napoca, RomaniaPurpose: Oste…

0301 basic medicinemusculoskeletal diseasesmedicine.medical_specialtyTherapeutics and Clinical Risk ManagementOsteoporosisGaucher diseasegene variantsCalcitriol receptorBone remodeling03 medical and health sciencesOsteoprotegerinInternal medicineGenotypecalcitonin receptormedicinevitamin D receptorPharmacology (medical)General Pharmacology Toxicology and PharmaceuticsCalcitonin receptorOriginal ResearchChemical Health and Safetybiologybusiness.industryGeneral Medicinemedicine.diseaseosteoporosis030104 developmental biologyEndocrinologyosteoprotegerinOsteocalcinbiology.proteinbusinessSafety ResearchEstrogen receptor alphaTherapeutics and Clinical Risk Management
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The Vitamin D Receptor Regulates Glycerolipid and Phospholipid Metabolism in Human Hepatocytes.

2020

The vitamin D receptor (VDR) must be relevant to liver lipid metabolism because VDR deficient mice are protected from hepatosteatosis. Therefore, our objective was to define the role of VDR on the overall lipid metabolism in human hepatocytes. We developed an adenoviral vector for human VDR and performed transcriptomic and metabolomic analyses of cultured human hepatocytes upon VDR activation by vitamin D (VitD). Twenty percent of the VDR responsive genes were related to lipid metabolism, including MOGAT1, LPGAT1, AGPAT2, and DGAT1 (glycerolipid metabolism)

0301 basic medicinemusculoskeletal diseasesmedicine.medical_specialtyVitaminesLithocholic acidMice Knockout ApoECèl·luleslcsh:QR1-502Phospholipidvitamin DBiochemistryCalcitriol receptorlcsh:MicrobiologyArticle03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineBiomolèculesDownregulation and upregulationInternal medicinelipid metabolismmedicinepolycyclic compoundsAnimalsHumansvitamin D receptorMolecular BiologyPhospholipidsTriglyceridesPhosphatidylethanolaminedigestive oral and skin physiologyhuman hepatocytesLipid metabolismMetabolismHep G2 Cells030104 developmental biologyEndocrinologychemistryGene Expression Regulation030220 oncology & carcinogenesisHepatocytesReceptors Calcitriollipids (amino acids peptides and proteins)IntracellularBiomolecules
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Biplanar ultrasound investigation of in vivo Achilles tendon displacement non-uniformity

2019

The Achilles tendon is a common tendon for the medial and lateral gastrocnemius and soleus muscles. Non‐uniform Achilles tendon regional displacements have been observed in vivo which may result from non‐uniform muscle loading and intratendinous shearing. However, prior observations are limited to the sagittal plane. This study investigated Achilles tendon tissue displacement patterns during isometric plantarflexor contractions in the coronal and sagittal planes. Fourteen subjects (5 female, 9 male, 26 ± 3 year) performed maximal isometric plantarflexor contractions with the knee in full extension and flexed to 110°. An ultrasound transducer positioned over the free Achilles tendon collecte…

030110 physiology0301 basic medicinemusculoskeletal diseasesIsometric exerciseKnee JointArticle03 medical and health sciences0302 clinical medicineIn vivoMedicineDisplacement (orthopedic surgery)ta315sub-tendonAchilles tendonultrasoundbusiness.industryUltrasoundultraääni030229 sport sciencesAnatomymusculoskeletal systemSagittal planemedicine.anatomical_structurespeckle trackingCoronal planetriceps suraeultraäänitutkimuskantajännebusiness
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