Search results for " Inbred mdx"

showing 10 items of 20 documents

Increased calcium influx is responsible for the sustained mechanical tone in colon from dystrophic (mdx) mice

2001

Abstract Background & Aims: Proximal colon from dystrophic mice develops spontaneous tone increment, but the mechanisms involved in its development have not been investigated. This study examined whether alterations in the properties of cell membrane calcium channels and/or sarcoplasmic reticular (SR) Ca 2+ -adenosine triphosphatase (ATPase) contribute to tone development. Methods: Effects of calcium-free solution, nifedipine, pinaverium (calcium channel blockers), and cyclopiazonic acid (CPA; SR Ca 2+ -ATPase inhibitor) on the contractile activity of colon from mdx and control mice were determined. Results Calcium-free solution abolished spontaneous contractions in both preparations, but d…

Malemedicine.medical_specialtyIndolesNifedipineColonSarcoplasmchemistry.chemical_elementCalciumMuscular DystrophiesCalcium in biologyMicechemistry.chemical_compoundNifedipineInternal medicinemedicineAnimalsHepatologyVoltage-dependent calcium channelCalcium channelGastroenterologyPinaveriumMice Inbred C57BLEndocrinologychemistryMice Inbred mdxCalciumCyclopiazonic acidMuscle Contractionmedicine.drugGastroenterology
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Myogenic NOS and endogenous NO production are defective in colon from dystrophic (mdx) mice.

2001

The aim of the present study was to evaluate whether alterations in the distribution and/or function of nitric oxide synthase (NOS) could be involved in the development of the spontaneous mechanical tone observed in colon from dystrophic ( mdx) mice. By recording the intraluminal pressure of isolated colon from normal mice, we showed that Nω-nitro- l-arginine methyl ester (l-NAME) increased the tone, even in the presence of tetrodotoxin. The effect was prevented by l-arginine, nifedipine, or Ca2+-free solution. In colon from mdx mice, l-NAME was ineffective. Immunohistochemistry revealed that the presence and distribution of neuronal (nNOS), endothelial, and inducible NOS isoforms in smooth…

Malemedicine.medical_specialtyPhysiologyRatónColonDuchenne muscular dystrophyEndogenyNitric OxideNitric oxidechemistry.chemical_compoundMiceReference ValuesPhysiology (medical)Internal medicineGene expressionmedicineAnimalsHepatologybiologyGastroenterologyMuscle Smoothmedicine.diseaseImmunohistochemistryPathophysiologyNitric oxide synthaseMice Inbred C57BLMuscular Dystrophy DuchenneEndocrinologychemistrybiology.proteinMice Inbred mdxImmunohistochemistryNitric Oxide SynthaseAmerican journal of physiology. Gastrointestinal and liver physiology
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Evidence for a role of inducible nitric oxide synthase in gastric relaxation of mdx mice

2006

Alterations of gastric mechanical activity have been reported in mdx mouse, animal model for Duchenne muscular dystrophy. This study examined if alterations in the vasoactive intestinal polypeptide (VIP) system are present in mdx stomach. Gastric mechanical activity was recorded in vitro as changes of endoluminal pressure and neurally or pharmacologically evoked relaxations were analysed in mdxvs normal stomach. Reverse-transcription polymerase chain reaction was used to detect inducible nitric oxide synthase (iNOS) expression. Relaxations to sodium nitroprusside in mdx stomach showed no difference in comparison with normal preparations. In normal stomach, VIP produced relaxation, which was…

Malemedicine.medical_specialtymdx mousePhysiologyMuscle RelaxationVasoactive intestinal peptideNitric Oxide Synthase Type IIStimulationDUCHENNES MUSCULAR-DYSTROPHYSettore BIO/09 - FisiologiaNitric oxidechemistry.chemical_compoundMiceOrgan Culture TechniquesInternal medicineQuinoxalinesmedicineAnimalsRNA MessengerEnzyme InhibitorsReceptorOxadiazolesbiologyEndocrine and Autonomic SystemsReverse Transcriptase Polymerase Chain ReactionStomachStomachGastroenterologySMOOTH-MUSCLE CELLSMuscle SmoothPEPTIDE RELEASENitric oxide synthaseMuscular Dystrophy DuchenneDisease Models AnimalEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl Esterchemistrybiology.proteinMice Inbred mdxReceptors Vasoactive Intestinal PeptideSodium nitroprussideIminesmedicine.drugVasoactive Intestinal Peptide
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Recovery of Damaged Skeletal Muscle in mdx Mice through Low-intensity Endurance Exercise

2013

The lack of dystrophin in mdx mice leads to cycles of muscle degeneration and regeneration processes. Various strategies have been proposed in order to reduce the muscle-wasting component of muscular dystrophy, including implementation of an exercise programme. The aim of this study was to examine how low-intensity endurance exercise affects the degeneration-regeneration process in dystrophic muscle of male mdx mice. Mice were subjected to low-intensity endurance exercise by running on a motorized Rota-Rod for 5 days/week for 6 weeks. Histomorphological analysis showed a signifi cant reduction of measured inflammatory-necrotic areas in both gastrocnemius and quadriceps muscle of exercised m…

Malemusculoskeletal diseasesmedicine.medical_specialtyBlotting WesternConnexinPhysical Therapy Sports Therapy and RehabilitationDegeneration (medical)Settore BIO/09 - FisiologiaConnexinsMiceRandom Allocationdystrophic muscle muscle regeneration muscle injury connexin connexin 39 muscle strengthEndurance trainingPhysical Conditioning AnimalInternal medicinemedicineAnimalsRegenerationOrthopedics and Sports MedicineMuscle StrengthMuscular dystrophyMuscle SkeletalbiologyMuscle fatiguebusiness.industrySkeletal muscleAnatomyMuscular Dystrophy Animalmedicine.diseaseExercise TherapyMice Inbred C57BLmedicine.anatomical_structureEndocrinologyMuscle FatigueMice Inbred mdxPhysical Endurancebiology.proteinmedicine.symptomDystrophinbusinessBiomarkersMuscle ContractionMuscle contraction
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Exercise restores decreased physical activity levels and increases markers of autophagy and oxidative capacity in myostatin/activin blocked mdx mice

2013

The importance of adequate levels of muscle size and function and physical activity is widely recognized. Myostatin/activin blocking increases skeletal muscle mass but may decrease muscle oxidative capacity and can thus be hypothesized to affect voluntary physical activity. Soluble activin receptor IIB (sActRIIB-Fc) was produced to block myostatin/activins. Modestly dystrophic mdx mice were injected with sActRIIB-Fc or PBS with or without voluntary wheel running exercise for 7 wk. Healthy mice served as controls. Running for 7 wk attenuated the sActRIIB-Fc-induced increase in body mass by decreasing fat mass. Running also enhanced/restored the markers of muscle oxidative capacity and autoph…

medicine.medical_specialtyPhysiologyActivin Receptors Type IIEndocrinology Diabetes and MetabolismBlotting WesternCitrate (si)-SynthaseMyostatinMotor ActivityHematocritMuscle hypertrophyEatingHemoglobinsMice03 medical and health sciences0302 clinical medicinePhysical Conditioning AnimalPhysiology (medical)Internal medicineAutophagymedicineAnimalsMuscle Skeletalta315Creatine KinaseAdiposity030304 developmental biology0303 health sciencesbiologymedicine.diagnostic_testTumor Necrosis Factor-alphaBody WeightAutophagySkeletal muscleDNAActivin receptorMyostatinActivinsMice Inbred C57BLmedicine.anatomical_structureEndocrinologyHematocritMice Inbred mdxbiology.proteinCreatine kinaseTumor necrosis factor alphaOxidation-Reduction030217 neurology & neurosurgeryAmerican Journal of Physiology-Endocrinology and Metabolism
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Myostatin/activin blocking combined with exercise reconditions skeletal muscle expression profile of mdx mice

2015

Duchenne Muscular Dystrophy is characterized by muscle wasting and decreased aerobic metabolism. Exercise and blocking of myostatin/activin signaling may independently or combined counteract muscle wasting and dystrophies. The effects of myostatin/activin blocking using soluble activin receptor-Fc (sActRIIB-Fc) administration and wheel running were tested alone or in combination for seven weeks in dystrophic mdx mice. Expression microarray analysis revealed decreased aerobic metabolism in the gastrocnemius muscle of mdx mice compared to healthy mice. This was not due to reduced home-cage physical activity, and was further downregulated upon sActRIIB-Fc treatment in enlarged muscles. However…

muscular dystrophymedicine.medical_specialtyDuchenne muscular dystrophyActivin Receptors Type IIRecombinant Fusion Proteinsphysical activityMyostatinBiologyta3111BiochemistryMuscle hypertrophy03 medical and health sciencesGastrocnemius muscleMice0302 clinical medicineEndocrinologyoxidative metabolismInternal medicinePhysical Conditioning AnimalGene expressionmedicineSTAT5 Transcription FactorAnimalsmuscle hypertrophyMuscular dystrophyPhosphorylationta315Muscle SkeletalMolecular BiologyWasting030304 developmental biologyInhibin-beta Subunits0303 health sciencesPhysical activitySkeletal muscleMyostatinmusculoskeletal systemmedicine.diseaseMuscular dystrophymRNA profilingEndocrinologymedicine.anatomical_structurebiology.proteinMice Inbred mdxOxidative metabolismMuscle hypertrophymedicine.symptom030217 neurology & neurosurgery
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Gastric emptying, small intestinal transit and fecal output in dystrophic (mdx) mice.

2009

Duchenne muscular dystrophy (DMD), which results from deficiency in dystrophin, a sarcolemma protein of skeletal, cardiac and smooth muscle, is characterized by progressive striated muscle degeneration, but various gastrointestinal clinical manifestations have been observed. The aim was to evaluate the possible impact of the dystrophin loss on the gastrointestinal propulsion in mdx mice (animal model for DMD). The gastric emptying of a carboxymethyl cellulose/phenol red dye non-nutrient meal was not significantly different at 20 min from gavaging between wild-type and mdx mice. The intestinal transit and the fecal output were significantly decreased in mdx versus normal animals, although th…

musculoskeletal diseasesCell physiologyDuchenne muscular dystrophyMalecongenital hereditary and neonatal diseases and abnormalitiesmdx mousemedicine.medical_specialtyPhysiologyDuchenne muscular dystrophySettore BIO/09 - FisiologiaMiceIn vivoInternal medicineIntestine SmallMedicineAnimalsmdx mouseMuscular dystrophyDefecationSarcolemmabiologyGastric emptyingbusiness.industryMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseMice Inbred C57BLDisease Models AnimalEndocrinologyGastric Emptyingbiology.proteinFecal outputMice Inbred mdxIntestinal transitbusinessDystrophinGastrointestinal MotilityThe journal of physiological sciences : JPS
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Mechanical activity of small and large intestine in normal and mdx mice: a comparative analysis.

1999

The aim of this study was to compare the motor pattern (recorded as changes in intraluminal pressure) of isolated duodenum and proximal colon between dystrophic mdx and normal mice. When duodenal recordings from control preparations were compared with mdx mice there was no significant difference in the spontaneous motor pattern, responses to electrical nerve stimulation or sensitivity to pharmacological agents. Colonic segments from mdx mice showed a more complex motor pattern, consisting of contractions with amplitude and frequency similar to those of controls and by additional contractions with lower amplitude and higher frequency. Moreover, 70% of the colonic preparations from mdx mice d…

musculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyNerve stimulationPhysiologyColonDuodenumDuchenne muscular dystrophyIn Vitro TechniquesInhibitory postsynaptic potentialNitric oxidechemistry.chemical_compoundMiceReference ValuesInternal medicineIntestine SmallmedicineAnimalsLarge intestineProximal colonIntestine LargeEndocrine and Autonomic SystemsChemistrySignificant differenceGastroenterologyAnatomyMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseElectric StimulationBiomechanical PhenomenaMice Inbred C57BLmedicine.anatomical_structureEndocrinologyDuodenumMice Inbred mdxGastrointestinal MotilityNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
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Duodenal contractile activity in dystrophic (mdx) mice: reduction of nitric oxide influence.

2003

The present study was undertaken to analyse duodenal contractility in adult dystrophic (mdx) mice. The spontaneous changes of the isometric tension and the responses of longitudinal duodenal muscle to nonadrenergic, noncholinergic (NANC) nerve stimulation and to exogenous drugs were compared between normal and mdx mice. Duodenal segments from mdx mice displayed spontaneous contractions with higher frequency than normals. N omega-nitro-L-arginine methyl ester (L-NAME) increased the frequency of contractions in normals without affecting that in mdx mice. In normals, NANC nerve stimulation elicited a transient relaxation abolished by L-NAME. In mdx mice a frank relaxation was not observed, the…

musculoskeletal diseasesMalemedicine.medical_specialtyNerve stimulationPhysiologyDuodenumInhibitory pathwayIsometric exerciseIn Vitro TechniquesInhibitory postsynaptic potentialNitric OxideSettore BIO/09 - FisiologiaNitric oxideContractilityDystrophinchemistry.chemical_compoundMiceSmooth muscleInternal medicinemedicineSpontaneous contractionAnimalsNeuroscience (all)biologyDose-Response Relationship DrugEndocrine and Autonomic SystemsIntestinal relaxationGastroenterologymusculoskeletal systemMice Inbred C57BLEndocrinologychemistrybiology.proteinMice Inbred mdxmdx miceSodium nitroprussideDystrophinGastrointestinal Motilitytissuesmedicine.drugMuscle ContractionNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
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Combined effect of AAV-U7-induced dystrophin exon skipping and soluble activin Type IIB receptor in mdx mice.

2012

Adeno-associated virus (AAV)-U7-mediated skipping of dystrophin-exon-23 restores dystrophin expression and muscle function in the mdx mouse model of Duchenne muscular dystrophy. Soluble activin receptor IIB (sActRIIB-Fc) inhibits signaling of myostatin and homologous molecules and increases muscle mass and function of wild-type and mdx mice. We hypothesized that combined treatment with AAV-U7 and sActRIIB-Fc may synergistically improve mdx muscle function. Bioactivity of sActRIIB-Fc on skeletal muscle was first demonstrated in wild-type mice. In mdx mice we show that AAV-U7-mediated dystrophin restoration improved specific muscle force and resistance to eccentric contractions when applied a…

musculoskeletal diseasesmdx mousemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesDuchenne muscular dystrophyActivin Receptors Type IIGenetic VectorsMyostatinBiologyDystrophin03 medical and health sciencesMice0302 clinical medicineInternal medicineGeneticsmedicineMyocyteAnimalsMuscular dystrophyMuscle SkeletalMolecular Biology030304 developmental biology0303 health sciencesBody WeightSkeletal muscleExonsGenetic TherapyDependovirusMuscular Dystrophy Animalmedicine.diseasemusculoskeletal system3. Good healthMice Inbred C57BLEndocrinologymedicine.anatomical_structureImmunologybiology.proteinMice Inbred mdxMolecular MedicineITGA7Dystrophin030217 neurology & neurosurgeryMuscle ContractionHuman gene therapy
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