Search results for "CHON"

showing 10 items of 1866 documents

Moderate exercise in mice improves cancer plus chemotherapy-induced muscle wasting and mitochondrial alterations

2019

Cancer cachexia is a multifactorial syndrome characterized by anorexia, body wasting, and muscle and adipose tissue loss, impairing patient's tolerance to anticancer treatments and survival. The aim of the present study was to compare the effects induced in mice by tumor growth alone (C26) or in combination with chemotherapy [C26 oxaliplatin and 5-fluorouracil (oxfu)] and to evaluate the potential of moderate exercise. Oxfu administration to C26 mice exacerbated muscle wasting and triggered autophagy or mitophagy, decreased protein synthesis, and induced mitochondrial alterations. Exercise in C26 oxfu mice counteracted the loss of muscle mass and strength, partially rescuing autophagy and m…

0301 basic medicineMaleCachexiamedicine.medical_treatmentPGC-1αMitochondrionliikuntaBiochemistryMice0302 clinical medicineNeoplasmsMitophagyautophagy; cancer cachexia; mitochondria; PGC-1α; survival; Biotechnology; Biochemistry; Molecular Biology; Geneticsta315WastingMice Inbred BALB C3. Good healthmitochondriaMuscular AtrophyFemalemedicine.symptomBiotechnologycancer cachexiamedicine.medical_specialtyautophagyAntineoplastic AgentsAnorexiasurvivalCachexia03 medical and health sciencesInternal medicinePhysical Conditioning AnimalGeneticsmedicineAnimalsMuscle SkeletalMolecular BiologyChemotherapysyöpähoidotbusiness.industryAutophagyCancermedicine.diseaseta3122030104 developmental biologyEndocrinologyQuality of Lifekoe-eläinmallitbusinessEnergy Metabolismlihassurkastumasairaudet030217 neurology & neurosurgeryFASEB Journal
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Odiparcil, a potential glycosaminoglycans clearance therapy in mucopolysaccharidosis VI—Evidence from in vitro and in vivo models

2020

International audience; Mucopolysaccharidoses are a class of lysosomal storage diseases, characterized by enzymatic deficiency in the degradation of specific glycosaminoglycans (GAG). Pathological accumulation of excess GAG leads to multiple clinical symptoms with systemic character, most severely affecting bones, muscles and connective tissues. Current therapies include periodic intravenous infusion of supplementary recombinant enzyme (Enzyme Replacement Therapy-ERT) or bone marrow transplantation. However, ERT has limited efficacy due to poor penetration in some organs and tissues. Here, we investigated the potential of the β-D-xyloside derivative odiparcil as an oral GAG clearance therap…

0301 basic medicineMaleMucopolysaccharidosis type VIRespiratory SystemAdministration OralGlycosaminoglycanRats Sprague-DawleyWhite Blood CellsMice0302 clinical medicineOral administrationAnimal CellsMedicine and Health SciencesGlycosidesCells CulturedConnective Tissue CellsGlycosaminoglycansMultidisciplinaryMucopolysaccharidosis VIChemistryChondroitin SulfatesQRMucopolysaccharidosis VIAnimal Models3. Good healthTracheamedicine.anatomical_structureExperimental Organism SystemsConnective Tissue[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyMedicineFemaleBiological CulturesCellular TypesAnatomyCellular Structures and OrganellesResearch Articlemedicine.medical_specialtyImmune CellsScienceImmunologyDermatan SulfateMouse ModelsIn Vitro TechniquesResearch and Analysis Methods03 medical and health sciencesModel OrganismsIn vivoInternal medicinemedicineAnimalsHumansBlood CellsCartilageBiology and Life SciencesEndothelial CellsKidneysCell BiologyRenal SystemFibroblastsCell CulturesIn vitroMice Mutant StrainsRatsMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyBiological TissueCartilageCell cultureAnimal Studies[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyCattleLysosomes030217 neurology & neurosurgery
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Melatonin enhances neural stem cell differentiation and engraftment by increasing mitochondrial function

2017

Mendivil-Perez, Miguel et al.

0301 basic medicineMaleParkinson's diseaseCellMice TransgenicBiologyMitochondrionTransplantmedicine.disease_causeMelatonin03 medical and health sciencesMice0302 clinical medicineEndocrinologyAlzheimer DiseasemedicineAnimalsreproductive and urinary physiologyMelatoninNeuronsNeural stem cellsATP synthaseGraft SurvivalCell Differentiationmedicine.diseaseAntigens DifferentiationNeural stem cellnervous system diseasesCell biologyMitochondriaTransplantation030104 developmental biologymedicine.anatomical_structurenervous systemOxidative stressbiology.proteinParkinson’s diseaseNeuroscienceAlzheimer’s disease030217 neurology & neurosurgeryOxidative stressmedicine.drug
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Short-Term Effects of Microglia-Specific Mitochondrial Dysfunction on Amyloidosis in Transgenic Models of Alzheimer's Disease.

2018

Reduction of mitochondrial activity is a subtle and early event in the pathogenesis of Alzheimer’s disease. Mitochondrial damage and consequentially enhanced production of reactive oxygen species is particularly occurring in the vicinity of amyloid plaques. Since all cells are affected by mitochondrial damage, analyses of cell type-specific effects are challenging. To study the impact of mitochondrial alterations on microglial activity in a homogeneous genetic background, we generated bone marrow chimeras of irradiated 46-days-old APP-transgenic mice. For reconstitution, bone marrow from CX3CR1-eGFP mice with mitochondria of either non-obese diabetic or C57BL/6J animals was utilized. Succes…

0301 basic medicineMalePathologymedicine.medical_specialtyMitochondrial DiseasesAmyloidCellGreen Fluorescent ProteinsCX3C Chemokine Receptor 1Mice TransgenicPlaque AmyloidBiologyMitochondrionPathogenesis03 medical and health sciencesAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseMice Inbred NODCX3CR1medicinePresenilin-1AnimalsHumansMicrogliaGeneral NeuroscienceAmyloidosisCalcium-Binding ProteinsMicrofilament ProteinsGeneral MedicineAmyloidosismedicine.diseaseMitochondriaMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureFemaleBone marrowMicrogliaGeriatrics and Gerontology030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Microvesicles from Human Adipose Tissue-Derived Mesenchymal Stem Cells as a New Protective Strategy in Osteoarthritic Chondrocytes

2018

[EN] Background/Aims: Chronic inflammation contributes to cartilage degeneration during the progression of osteoarthritis (OA). Adipose tissue-derived mesenchymal stem cells (ADMSC) show great potential to treat inflammatory and degradative processes in OA and have demonstrated paracrine effects in chondrocytes. In the present work, we have isolated and characterized the extracellular vesicles from human AD-MSC to investigate their role in the chondroprotective actions of these cells. Methods: AD-MSC were isolated by collagenase treatment from adipose tissue from healthy individuals subjected to abdominal lipectomy surgery. Microvesicles and exosomes were obtained from conditioned medium by…

0301 basic medicineMalePhysiologyCell SurvivalAdipose tissue-derived mesenchymal stem cellsAdipose tissueInflammationNitric OxideExtracellular vesiclesChondrocytelcsh:PhysiologyDinoprostonelcsh:Biochemistry03 medical and health sciencesChondrocytesOsteoarthritismedicineHumanslcsh:QD415-436Cells CulturedAgedInflammationlcsh:QP1-981ChemistryMesenchymal stem cellMesenchymal Stem CellsMiddle AgedExtracellular vesiclesChondrocyteMicrovesiclesMatrix MetalloproteinasesCell biology030104 developmental biologymedicine.anatomical_structureAdipose TissueCytokinesFemalemedicine.symptom
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Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

2020

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. M…

0301 basic medicineMaleProtein metabolismMedicine (miscellaneous)MitochondrionEnergy homeostasis03 medical and health scienceschemistry.chemical_compoundNile tilapia0302 clinical medicineAdjuvants ImmunologicmedicineAnimalsHomeostasisInsulinCarnitineProtein kinase ACells CulturedZebrafishNutrition and DieteticsbiologyCarnitine O-PalmitoyltransferaseChemistryFatty AcidsProtein turnoverProteinsMetabolismCichlidsDNACytochromes bbiology.organism_classificationMitochondria030104 developmental biologyGlucoseBiochemistryMutationHepatocytesNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgerymedicine.drugMethylhydrazinesThe Journal of nutrition
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Skeletal muscle Heat shock protein 60 increases after endurance training and induces peroxisome proliferator-activated receptor gamma coactivator 1 α…

2016

AbstractHeat shock protein 60 (Hsp60) is a chaperone localizing in skeletal muscle mitochondria, whose role is poorly understood. In the present study, the levels of Hsp60 in fibres of the entire posterior group of hindlimb muscles (gastrocnemius, soleus and plantaris) were evaluated in mice after completing a 6-week endurance training program. The correlation between Hsp60 levels and the expression of four isoforms of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) were investigated only in soleus. Short-term overexpression of hsp60, achieved by in vitro plasmid transfection, was then performed to determine whether this chaperone could have a role in the activa…

0301 basic medicineMaleTime FactorsPPARgammaPeroxisome proliferator-activated receptorExosomesMiceendurance trainingMyocytechemistry.chemical_classificationMultidisciplinarytrainingbiologyHsp60Mitochondriamedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle Fibers Fast-TwitchHsp60; skeletal muscle; training; PPARgamma; PGC1αHSP60[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Oxidation-Reductionmedicine.medical_specialtyanimal structureschemical and pharmacologic phenomenacomplex mixturescachexiaArticleCell Line03 medical and health sciencesEndurance trainingHeat shock proteinInternal medicinePhysical Conditioning AnimalPGC1αCoactivatormedicineAnimals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]skeletal muscleMuscle SkeletalSettore BIO/16 - Anatomia UmanafungiSkeletal muscleChaperonin 60030104 developmental biologyEndocrinologychemistryGene Expression RegulationChaperone (protein)biology.proteinPhysical EnduranceBiomarkersTranscription FactorsScientific Reports
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VEGF-B gene therapy inhibits doxorubicin-induced cardiotoxicity by endothelial protection

2016

Congestive heart failure is one of the leading causes of disability in long-term survivors of cancer. The anthracycline antibiotic doxorubicin (DOX) is used to treat a variety of cancers, but its utility is limited by its cumulative cardiotoxicity. As advances in cancer treatment have decreased cancer mortality, DOX-induced cardiomyopathy has become an increasing problem. However, the current means to alleviate the cardiotoxicity of DOX are limited. We considered that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesis, physiological cardiac hypertrophy, and ischemia resistance, could be an interesting candidate for prevention of DOX-induced cardiotoxicity …

0301 basic medicineMaleVEGFBVascular Endothelial Growth Factor BAnthracyclineAdipose Tissue WhiteCardiomyopathyheart failureApoptosisheart030204 cardiovascular system & hematologyPharmacologyta3111Mitochondria Heart03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsmedicinepolycyclic compoundscancerAnimalsDoxorubicinTube formationCardiotoxicityMultidisciplinaryAntibiotics Antineoplasticbusiness.industryta1184MyocardiumEndothelial CellsGenetic TherapyBiological Sciencesmedicine.diseaseCardiotoxicity3. Good healthVascular endothelial growth factorMice Inbred C57BL030104 developmental biologychemistryLiverDoxorubicinHeart failureendothelial cellArteriogenesisbusinessmedicine.drugDNA Damage
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Impact of elosulfase alfa in patients with morquio A syndrome who have limited ambulation: An open-label, phase 2 study.

2017

Efficacy and safety of elosulfase alfa enzyme replacement therapy (ERT) were assessed in an open-label, phase 2, multi-national study in Morquio A patients aged ≥5 years unable to walk ≥30 meters in the 6-min walk test. Patients received elosulfase alfa 2.0 mg/kg/week intravenously for 48 weeks. Efficacy measures were functional dexterity, pinch/grip strength, mobility in a modified timed 25-foot walk, pain, quality of life, respiratory function, and urine keratan sulfate (KS). Safety/tolerability was also assessed. Fifteen patients received elosulfase alfa, three patients discontinued ERT due to adverse events (two were grade 3 drug-related adverse events, the other was not drug-related), …

0301 basic medicineMaleWalkingchemistry.chemical_compoundGrip strengthGALNS protein0302 clinical medicineElosulfase alfaQuality of lifeActivities of Daily LivingRespiratory functionFunctional abilityChildGenetics (clinical)education.field_of_studyMucopolysaccharidosis IVChondroitinsulfatases3. Good healthRespiratory Function TestsTreatment OutcomeTolerability6.1 PharmaceuticalsOriginal ArticleFemalePatient Safetyphysical enduranceGALNS protein human [supplementary concept]Adultsafetymedicine.medical_specialtyAdolescentClinical Trials and Supportive ActivitiesPopulationClinical Sciences03 medical and health sciencesYoung Adultmobility limitationClinical ResearchInternal medicinemedicineGeneticsHumansEnzyme Replacement TherapyAdverse effecteducationhuman [supplementary concept]Exercisebusiness.industryEvaluation of treatments and therapeutic interventionsOriginal Articles030104 developmental biologychemistryKeratan SulfateQuality of LifeSelf Reportbusiness030217 neurology & neurosurgeryBiomarkers
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