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showing 10 items of 2571 documents

Some critical remarks on the paper “A note on the metrizability of tvs-cone metric spaces” / Некоторые критические замечания о работе «Заметки о метр…

2018

This short and concise note provides a detailed exposition of the approach and results established by (Lin et al, 2015, pp.271-279). We show that the obtained results are not particularly surprising and new. Namely, using an old result due to K. Deimling it is indicated that tvs-cone metric spaces over solid cones are actually cone metric spaces over normal solid cones. Hence, there are only cone metric spaces over normal solid cones or over normal non-solid cones. One question still unanswered is whether an ordered topological vector space with a non-normal non-solid cone exists. / В представленных, в данной статье, заметках приведен подробный обзор методов и полученных результатов исследо…

metrizabilannormalanUnon-normaltvp-konusni metrički prostormetrizableненормальныйEngineering (General). Civil engineering (General)нормальныйnormalтвп-коническое метрическое пространствоtvs-cone metric spaceMilitary Sciencesolidметризуемостьnije normalanTA1-2040конус с непустой внутренностьюkonus sa nepraznom unutrašnjošćuVojnotehnički Glasnik
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Hands-feet wireless devices: Test-retest reliability and discriminant validity of motor measures in Parkinson's disease telemonitoring

2022

Background Telemonitoring, a branch of telemedicine, involves the use of technological tools to remotely detect clinical data and evaluate patients. Telemonitoring of patients with Parkinson's disease (PD) should be performed using reliable and discriminant motor measures. Furthermore, the method of data collection and transmission, and the type of subjects suitable for telemonitoring must be well defined. Objective To analyze differences in patients with PD and healthy controls (HC) with the wearable inertial device SensHands-SensFeet (SH-SF), adopting a standardized acquisition mode, to verify if motor measures provided by SH-SF have a high discriminating capacity and high intraclass corr…

motor function assessmentFootParkinson's diseasesubclinical motor abnormalitieswearable sensorsReproducibility of ResultstelemonitoringParkinson DiseaseGeneral MedicineWearable Electronic DevicesNeurologyHumansbiomechanical parametersSettore MED/26 - NeurologiaNeurology (clinical)telemedicineGait
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The assessment of skeletal status in young patients with Turner syndrome by 2 densitometric techniques: Phalangeal quantitative ultrasound and dual e…

2018

Background. Studies using dual energy X-ray absorptiometry (DXA) demonstrate a reduction in bone mineral density (BMD) in children and adolescents with Turner syndrome (TS). However, these studies do not take into account changes in bone size, which influence BMD in the case of short-statured patients. Phalangeal quantitative ultrasound (phQUS) measurements have shown an ability to reveal changes due to skeletal growth, aging, and bone and mineral disorders. There is limited data on bone mineral status in girls with TS assessed by 2 different techniques, i.e., DXA and phQUS. Objectives. The aim of this study was to investigate the potential negative impact of TS on bone status and to assess…

musculoskeletal diseases0301 basic medicineAdolescentmedicine.medical_treatmentMedicine (miscellaneous)Turner Syndromedual energy X-ray absorptiometry030209 endocrinology & metabolismGeneral Biochemistry Genetics and Molecular BiologyBone and Bones03 medical and health sciencesFinger PhalangesFractures Bonequantitative ultrasound0302 clinical medicineAbsorptiometry PhotonBone DensityTurner syndromeInternal MedicinemedicinePrevalenceHumansPharmacology (medical)Reference populationChildGenetics (clinical)Dual-energy X-ray absorptiometryReduction (orthopedic surgery)UltrasonographyBone mineralmedicine.diagnostic_testbusiness.industryfracturesmedicine.diseaseQuantitative ultrasound030104 developmental biologyNormal boneChild PreschoolReviews and References (medical)Lumbar spineFemalebusinessNuclear medicineAdvances in clinical and experimental medicine : official organ Wroclaw Medical University
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RNA-mediated therapies in myotonic dystrophy

2018

Myotonic dystrophy 1 (DM1) is a multisystemic neuromuscular disease caused by a dominantly inherited 'CTG' repeat expansion in the gene encoding DM Protein Kinase (DMPK). The repeats are transcribed into mRNA, which forms hairpins and binds with high affinity to the Muscleblind-like (MBNL) family of proteins, sequestering them from their normal function. The loss of function of MBNL proteins causes numerous downstream effects, primarily the appearance of nuclear foci, mis-splicing, and ultimately myotonia and other clinical symptoms. Antisense and other RNA-mediated technologies have been applied to target toxic-repeat mRNA transcripts to restore MBNL protein function in DM1 models, such as…

musculoskeletal diseases0301 basic medicinePharmacologycongenital hereditary and neonatal diseases and abnormalitiesMessenger RNAMyotonin-protein kinaseRNABiologymedicine.diseaseMyotoniaMyotonic dystrophyMyotonin-Protein KinaseCell biology03 medical and health sciences030104 developmental biologyDrug DiscoverymedicineAnimalsHumansMyotonic DystrophyRNARNA MessengerTrinucleotide repeat expansionGeneLoss functionDrug Discovery Today
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Myotonic dystrophy: candidate small molecule therapeutics

2017

Myotonic dystrophy type 1 (DM1) is a rare multisystemic neuromuscular disorder caused by expansion of CTG trinucleotide repeats in the noncoding region of the DMPK gene. Mutant DMPK transcripts are toxic and alter gene expression at several levels. Chiefly, the secondary structure formed by CUGs has a strong propensity to capture and retain proteins, like those of the muscleblind-like (MBNL) family. Sequestered MBNL proteins cannot then fulfill their normal functions. Many therapeutic approaches have been explored to reverse these pathological consequences. Here, we review the myriad of small molecules that have been proposed for DM1, including examples obtained from computational rational …

musculoskeletal diseases0301 basic medicineTherapeutic gene modulationcongenital hereditary and neonatal diseases and abnormalitiesMutantComputational biologyBiologyMyotonic dystrophyMyotonin-Protein Kinase03 medical and health sciences0302 clinical medicineTrinucleotide RepeatsDrug DiscoveryGene expressionmedicineAnimalsHumansMyotonic DystrophyGenePharmacologyRegulation of gene expressionGeneticsDrug RepositioningRational designmedicine.diseaseSmall moleculeHigh-Throughput Screening Assays030104 developmental biologyGene Expression RegulationDrug Design030217 neurology & neurosurgeryDrug Discovery Today
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Derepressing muscleblind expression by miRNA sponges ameliorates myotonic dystrophy-like phenotypes in Drosophila

2016

AbstractMyotonic Dystrophy type 1 (DM1) originates from alleles of the DMPK gene with hundreds of extra CTG repeats in the 3′ untranslated region (3′ UTR). CUG repeat RNAs accumulate in foci that sequester Muscleblind-like (MBNL) proteins away from their functional target transcripts. Endogenous upregulation of MBNL proteins is, thus, a potential therapeutic approach to DM1. Here we identify two miRNAs, dme-miR-277 and dme-miR-304, that differentially regulate muscleblind RNA isoforms in miRNA sensor constructs. We also show that their sequestration by sponge constructs derepresses endogenous muscleblind not only in a wild type background but also in a DM1 Drosophila model expressing non-co…

musculoskeletal diseases0301 basic medicineUntranslated regioncongenital hereditary and neonatal diseases and abnormalitiesMotor ActivityBiologyMyotonic dystrophyArticle03 medical and health sciences0302 clinical medicineRNA IsoformsmicroRNAmedicineAnimalsDrosophila ProteinsMyotonic DystrophyRegulation of gene expressionGeneticsMultidisciplinaryWild typeNuclear Proteinsmedicine.diseaseMicroRNAsDrosophila melanogasterPhenotype030104 developmental biologyGene Expression RegulationFlight AnimalTrinucleotide Repeat ExpansionTrinucleotide repeat expansion030217 neurology & neurosurgeryDrosophila ProteinScientific Reports
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Expanded CCUG repeat RNA expression in Drosophila heart and muscle trigger Myotonic Dystrophy type 1-like phenotypes and activate autophagocytosis ge…

2016

AbstractMyotonic dystrophies (DM1–2) are neuromuscular genetic disorders caused by the pathological expansion of untranslated microsatellites. DM1 and DM2, are caused by expanded CTG repeats in the 3′UTR of the DMPK gene and CCTG repeats in the first intron of the CNBP gene, respectively. Mutant RNAs containing expanded repeats are retained in the cell nucleus, where they sequester nuclear factors and cause alterations in RNA metabolism. However, for unknown reasons, DM1 is more severe than DM2. To study the differences and similarities in the pathogenesis of DM1 and DM2, we generated model flies by expressing pure expanded CUG ([250]×) or CCUG ([1100]×) repeats, respectively, and compared …

musculoskeletal diseases0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesRNA SplicingScienceGene ExpressionBiologyMyotonic dystrophyMyotonin-Protein KinaseArticle03 medical and health sciencesGene expressionAutophagymedicineAnimalsMyotonic DystrophyMuscle SkeletalGeneDNA Repeat ExpansionMultidisciplinaryMyocardiumQRIntronRNAArrhythmias CardiacDNA Repeat Expansionmedicine.diseaseMolecular biologyDisease Models AnimalCell nucleus030104 developmental biologymedicine.anatomical_structureRNA splicingMedicineDrosophilaLocomotionScientific Reports
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Mild Aerobic Exercise Training Hardly Affects the Diaphragm ofmdxMice

2017

In the mdx mice model of Duchenne Muscular Dystrophy (DMD), mild endurance exercise training positively affected limb skeletal muscles, whereas few and controversial data exist on the effects of training on the diaphragm. The diaphragm was examined in mdx (C57BL/10ScSn-Dmdmdx) and wild-type (WT, C57BL/10ScSc) mice under sedentary conditions (mdx-SD, WT-SD) and during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days (training: 5 d/wk for 6 weeks), diaphragm muscle morphology and Cx39 protein were assessed. In addition, tissue levels of the chaperonins Hsp60 and Hsp70 and the p65 subunit of nuclear factor-kB (NF-kB) were measured in diaphragm, gastrocnemius, and q…

musculoskeletal diseases0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyNecrosisPhysiologyDuchenne muscular dystrophyClinical Biochemistry03 medical and health sciences0302 clinical medicineEndurance trainingInternal medicineDiaphragm musclemedicineAerobic exercisebusiness.industryRegeneration (biology)Cell BiologyAnatomymusculoskeletal systemmedicine.diseaseDiaphragm (structural system)Hsp70030104 developmental biologyEndocrinologymedicine.symptombusiness030217 neurology & neurosurgeryJournal of Cellular Physiology
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Lack of Dystrophin Affects Bronchial Epithelium inmdxMice

2016

Mild exercise training may positively affect the course of Duchenne Muscular Dystrophy (DMD). Training causes mild bronchial epithelial injury in both humans and mice, but no study assessed the effects of exercise in mdx mice, a well known model of DMD. The airway epithelium was examined in mdx (C57BL/10ScSn-Dmdmdx) mice, and in wild type (WT, C57BL/10ScSc) mice either under sedentary conditions (mdx-SD, WT-SD) or during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days of training (5 d/wk for 6 weeks), epithelial morphology and markers of regeneration, apoptosis, and cellular stress were assessed. The number of goblet cells in bronchial epithelium was much lower…

musculoskeletal diseases0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyTUNEL assayPhysiologyDuchenne muscular dystrophyRegeneration (biology)Clinical BiochemistryCell BiologyBiologymedicine.diseaseEpithelium03 medical and health sciences030104 developmental biologyEndocrinologymedicine.anatomical_structureApoptosisInternal medicineImmunologymedicinebiology.proteinRespiratory epitheliumMuscular dystrophyDystrophinJournal of Cellular Physiology
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Interaction of allopurinol with phenprocoumon in man.

1977

Conditions in two patients on long-term phenprocoumon (Marcumar®) treatment are reported who had signs of phenprocoumon overdosage when given simultaneously allopurinol. The determination of phenprocoumon plasma concentrations in one patient showed that phenprocoumon accumulates for several weeks during treatment with allopurinol. Signs of phenprocoumon overdosage thus can appear long time after starting allopurinol treatment.

musculoskeletal diseasesAdultMalecongenital hereditary and neonatal diseases and abnormalitiesAllopurinolMyocardial InfarctionAllopurinolPharmacologyPhenprocoumonDrug DiscoveryMedicineHumansDrug InteractionsBlood CoagulationGenetics (clinical)integumentary systembusiness.industrynutritional and metabolic diseasesGeneral Medicine4-HydroxycoumarinsDrug interactionMiddle AgedPlasma concentrationPhenprocoumonMolecular MedicineBlood Coagulation TestsbusinessMathematicsmedicine.drugKlinische Wochenschrift
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