Search results for " Muscle"

showing 10 items of 1495 documents

Spontaneous mechanical activity and evoked responses in isolated gastric preparations from normal and dystrophic (mdx) mice

2002

This study examined whether alterations of the spontaneous and evoked mechanical activity are present in the stomach of the mdx mouse, the animal model for Duchenne muscular dystrophy. The gastric mechanical activity from whole-organ of normal and mdx mice was recorded in vitro as changes of intraluminal pressure. All gastric preparations developed spontaneous tone and phasic contractions, although the tone of the mdx preparations was significantly greater. Atropine reduced the tone of the two preparations by the same degree. Nomega-nitro-l-arginine methyl ester (l-NAME) significantly increased the tone and spontaneous contractions only in the stomach from normal animals, but did not affect…

MaleNitroprussideDuchenne muscular dystrophymedicine.medical_specialtymdx mouseContraction (grammar)PhysiologyDuchenne muscular dystrophyTetrodotoxinCholinergic AgonistsSettore BIO/09 - FisiologiaContractilityMicechemistry.chemical_compoundOrgan Culture TechniquesInternal medicinemedicineAnimalsNitric Oxide Donorsmdx mouseAnesthetics LocalEnzyme InhibitorsNeuroscience (all)Endocrine and Autonomic SystemsChemistryStomachStomachGastroenterologyMuscle SmoothNitric oxideAnatomyMuscular Dystrophy AnimalGastric smooth musclemedicine.diseaseElectric StimulationMuscular Dystrophy DuchenneGastric mechanical activityAtropineNG-Nitroarginine Methyl Estermedicine.anatomical_structureEndocrinologyMice Inbred mdxTetrodotoxinCholinergicCarbacholMuscle Contractionmedicine.drug
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Inhibitory purinergic transmission in mouse caecum: Role for P2Y1 receptors as prejunctional modulators of ATP release

2007

Using conventional microelectrode recording techniques, we investigated, in the circular muscle of the mouse caecum, the neurotransmitter(s) involved in the neurally-evoked inhibitory junction potentials (IJPs) and the existence of possible prejunctional mechanisms controlling neurotransmitter release. Electrical field stimulation with single pulses elicited IJPs, consisting only of a "fast" hyperpolarization, while using train stimuli (30-50 Hz) the initial fast hyperpolarization was followed by a slower hyperpolarization. The fast and the slow component were selectively antagonized by apamin, a blocker of calcium-activated potassium channels, and N(omega)-nitro-l-arginine methyl ester (l-…

MaleP2Y receptormedicine.medical_specialtyAntineoplastic AgentsSuraminNitric OxideApaminSettore BIO/09 - FisiologiaSynaptic TransmissionEnteric Nervous SystemMembrane PotentialsMiceReceptors Purinergic P2Y1chemistry.chemical_compoundAdenosine TriphosphateInternal medicinePurinergic P2 Receptor AntagonistsmedicineAnimalsPPADSReceptorCecumMembrane potentialReceptors Purinergic P2General NeurosciencePurinergic receptorMembrane ProteinsHyperpolarization (biology)Electric StimulationReceptors Purinergic P2Y12Potassium channelMice Inbred C57BLEndocrinologyApaminchemistryBiophysicsenteric nerves intestinal muscle ATP purinergic receptors inhibitory junction potentialsNeuroscience
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The effects of the Nordic hamstring exercise on sprint performance and eccentric knee flexor strength: A systematic review and meta-analysis of inter…

2021

Objectives: The primary aim of this study was to investigate the effects of the Nordic hamstring exercise (NHE) on sprint performance (i.e., 5, 10 and 20 m) and explore associations between study characteristics and sprint outcomes in team sport players. Secondary aims were to (1) investigate the effects of the NHE on eccentric strength of the knee flexors (ESKF) with categorical subgroup analysis to determine differences between recreationally, well-trained individuals and young athletes, (2) determine the relation between ESKF and sprint performance in team sport players, and (3) explore the effect of study characteristics (i.e., weekly volume, time duration and body mass) on ESKF.Methods…

MalePROTOCOLmedicine.medical_specialtyTeam sporteducationPsychological interventionSTRAIN INJURYPhysical Therapy Sports Therapy and RehabilitationSubgroup analysisHamstring MusclesAthletic PerformanceRunningACTIVATION03 medical and health sciences0302 clinical medicineBiasNordic hamstring exerciseMedicineEccentricHumansOrthopedics and Sports MedicineKnee030212 general & internal medicineKINEMATICSSPEEDLOWER-EXTREMITY STRENGTHRISKSprint timebiologybusiness.industryAthletesMuscle strengthMALE SOCCER PLAYERSTeam Sports030229 sport sciencesbiology.organism_classificationEccentric strength of knee flexorsSprintMeta-analysisPhysical therapyFemalebusinesshuman activitiesHamstringPhysical Conditioning HumanJournal of Science and Medicine in Sport
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Survival of patients with spinal muscular atrophy type 1.

2013

BACKGROUND: Spinal muscular atrophy type 1 (SMA1) is a progressive disease and is usually fatal in the first year of life. METHODS: A retrospective chart review was performed of SMA1 patients and their outcomes according to the following choices: letting nature take its course (NT); tracheostomy and invasive mechanical ventilation (TV); continuous noninvasive respiratory muscle aid (NRA), including noninvasive ventilation; and mechanically assisted cough. RESULTS: Of 194 consecutively referred patients enrolled in this study (103 males, 91 females), NT, TV, and NRA were chosen for 121 (62.3%), 42 (21.7%), and 31 (16%) patients, respectively. Survival at ages 24 and 48 months was higher in …

MalePalliative careDatabases Factualmedicine.medical_treatmentKaplan-Meier EstimateSpinal Muscular Atrophies of ChildhoodSeverity of Illness IndexCohort StudiesRetrospective StudieCause of DeathPalliative CarePrognosisSpinal muscular atrophy type 1Child PreschoolHome mechanical ventilationBreathingFemaleLong survivalSurvival AnalysiPediatric palliative careHumanmedicine.medical_specialtyPrognosiMechanical assisted coughRisk AssessmentStatistics NonparametricArts and Humanities (miscellaneous)medicineRespiratory muscleConfidence IntervalsHumansDecompensationSurvival analysisRetrospective StudiesMechanical ventilationNoninvasive Ventilationbusiness.industryInfant NewbornOxygen Inhalation TherapyInfantSpinal muscular atrophymedicine.diseaseRespiration ArtificialSurvival AnalysisConfidence intervalSurgeryPediatrics Perinatology and Child HealthCohort StudiebusinessConfidence IntervalPediatrics
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Ceramide inhibits Kv currents and contributes to TP-receptor-induced vasoconstriction in rat and human pulmonary arteries

2011

et al.

MalePatch-Clamp TechniquesPhysiologyReceptors ThromboxaneSpider Venoms030204 cardiovascular system & hematologyMuscle Smooth VascularMembrane Potentialschemistry.chemical_compound0302 clinical medicineHypoxic pulmonary vasoconstrictionVasoconstrictor AgentsProtein Kinase C0303 health sciencesAniline Compounds3. Good healthSphingomyelin Phosphodiesterasemedicine.anatomical_structurePotassium Channels Voltage-GatedCirculatory systemmedicine.symptomSphingomyelinSignal TransductionBlood vesselmedicine.medical_specialtyCeramidePhosphinesMyocytes Smooth MusclePulmonary ArteryBiologyCeramidesBenzylidene Compounds03 medical and health sciencesInternal medicinemedicineAnimalsHumansRats Wistar030304 developmental biologyCell BiologySphingolipidRatsHEK293 CellsEndocrinologychemistryVasoconstriction15-Hydroxy-11 alpha9 alpha-(epoxymethano)prosta-513-dienoic AcidVascular resistanceVascular ResistancePeptidesVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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Upregulation of activin-B and follistatin in pulmonary fibrosis: a translational study using human biopsies and a specific inhibitor in mouse fibrosi…

2014

Background: Activins are members of the TGF-ß superfamily of growth factors. First, we identified by expression array screening that activin-B and follistatin are upregulated in human idiopathic pulmonary fibrosis (IPF). Next, we wanted to clarify their specific role in lung fibrosis formation. Methods: We used specific antibodies for activin-A and -B subunits and follistatin to measure and localize their levels in idiopathic pulmonary fibrosis and control lung biopsies. To inhibit activin signaling, we used soluble activin type IIB receptor fused to the Fc portion of human IgG1 (sActRIIB-Fc) in two different mouse models of pulmonary fibrosis. Results: Activin-B and follistatin mRNA levels…

MalePathologyFollistatinPulmonary FibrosisPROTEINCell CountQuadriceps MuscleACTIVATIONIdiopathic pulmonary fibrosisMiceBMP-7FibrosisPulmonary fibrosisfollistatinInhibin-beta SubunitsGREMLINImmunity Cellularmedicine.diagnostic_testbiologyactivinsPIRFENIDONEPirfenidonerespiratory systemidiopathic pulmonary fibrosisMouse fibrosis model3. Good healthUp-RegulationActivinsmedicine.anatomical_structureACUTE EXACERBATIONmouse fibrosis modelembryonic structuresGROWTHBronchoalveolar Lavage Fluidhormones hormone substitutes and hormone antagonistsmedicine.drugResearch ArticleSignal TransductionPulmonary and Respiratory MedicineEXPRESSIONmedicine.medical_specialtyendocrine systemRecombinant Fusion ProteinseducationIdiopathic pulmonary fibrosisRespiratory MucosaAlveolar cellsINFLAMMATIONmedicineAnimalsHumansRNA MessengerLungbusiness.industrymedicine.diseaserespiratory tract diseasesMice Inbred C57BLPulmonary AlveoliDisease Models AnimalBronchoalveolar lavageProtein Biosynthesis3121 General medicine internal medicine and other clinical medicinebiology.proteinbusinessFollistatin
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A new familial congenital myopathy in children with desmin and dystrophin reacting plaques.

1995

In 5 children with a progressive congenital myopathy representing 3 different families, unusual histological, immunohistochemical and ultrastructural changes in skeletal muscle have been found. Histologically, this myopathy was characterized by the presence of fine hyaline plaques devoid of oxidative as well as ATPase enzyme activities. At the ultrastructural level plaques were composed of helical filaments and amorphous dense material. Helical filament storage corresponded to strong desmin as well as ubiquitin immunoreactivity. In addition they were also dystrophin positive. The exclusive appearance of desmin, ubiquitin and dystrophin positive plaques in muscle specimens from 5 children em…

MalePathologymedicine.medical_specialtyAdolescentImmunocytochemistryBiologyDesminDystrophinMyofibrilsBiopsymedicineHumansMyopathyChildUbiquitinsHyalinemedicine.diagnostic_testMusclesSkeletal muscleNeuromuscular Diseasesmedicine.diseaseCongenital myopathyImmunohistochemistryMicroscopy Electronmedicine.anatomical_structureNeurologyChild Preschoolbiology.proteinDesminFemaleNeurology (clinical)medicine.symptomDystrophinJournal of the neurological sciences
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Prenatal diagnosis of infantile neuronal ceroid-lipofuscinosis: a combined electron microscopic and molecular genetic approach.

1995

Based on two unrelated index patients afflicted with INCL, fetal chorion tissues were studied from subsequent pregnancies of the two respective mothers resulting in the prenatal diagnosis of INCL in two of the three pregnancies. Documentation of INCL was based on electron microscopy and DNA studies of the biopsied chorion tissue, later confirmed in the two affected fetuses after termination of their pregnancies by demonstrating INCL-specific lipopigments in post-mortem tissues, in the liver of both aborted fetuses and, additionally, in spleen and skeletal muscle of one of the affected fetuses. The autolysis of the aborted tissues, however, precluded a systematic documentation of all affecte…

MalePathologymedicine.medical_specialtyCell typeBiopsyInfantile neuronal ceroid lipofuscinosisSpleenPrenatal diagnosisBiologyConsanguinityDevelopmental NeuroscienceNeuronal Ceroid-LipofuscinosesPregnancyPrenatal DiagnosisBiopsymedicineHumansreproductive and urinary physiologyFetusmedicine.diagnostic_testAborted FetusSkeletal muscleInfantAbortion InducedGeneral MedicineChorionDNAmedicine.diseasePedigreeMicroscopy Electronmedicine.anatomical_structureLiverembryonic structuresPediatrics Perinatology and Child HealthFemaleNeurology (clinical)Braindevelopment
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Heterozygous nonsense SCN5A mutation W822X explains a simultaneous sudden infant death syndrome.

2008

The sudden, unexpected, and unexplained death of both members of a set of healthy twins (simultaneous sudden infant death syndrome (SSIDS)) is defined as a case in which both infants meet the definition of sudden infant death syndrome individually. A search of the world medical literature resulted in only 42 reported cases of SSIDS. We report the case of a pair of identical, male, monozygotic twins, 138 days old, who suddenly died, meeting the full criteria of SSIDS and where a genetic screen was performed, resulting in a heterozygous nonsense SCN5A mutation (W822X) in both twins. Immunohistochemistry was performed on cardiac tissue samples utilizing polyclonal antibodies anti-Na+ CP type V…

MalePathologymedicine.medical_specialtyNav1.5 protein functionv1.5 protein functionmedia_common.quotation_subject2734Nonsense mutationNonsenseNa+ channel functionMuscle ProteinsSocio-culturaleBiology+Nav1.5 protein function; Na+ channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutation; Codon Nonsense; Diseases in Twins; Humans; Infant; Male; Muscle Proteins; NAV1.5 Voltage-Gated Sodium Channel; Sodium Channels; Sudden Infant Death; 2734Sudden deathSodium ChannelsNAV1.5 Voltage-Gated Sodium ChannelPathology and Forensic MedicinePathogenesisSCN5A gene mutationDiseases in TwinsmedicineHumansSimultaneous sudden infant death syndromeSCN5A gene mutationW822X mutationNa+ channel functionNav1.5 protein functionNaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein function CodonMolecular BiologyCellular localizationmedia_commonSimultaneous sudden infant death syndromeSettore BIO/16 - Anatomia UmanaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein functionW822X mutationInfantCell BiologyGeneral MedicineSudden infant death syndromeNonsenseTerminal deoxynucleotidyl transferaseCodon NonsenseImmunohistochemistryNa; v; 1.5 protein function; Na; +; channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutationchannel functionSudden Infant Death
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A Paucisymptomatic Neuromuscular Disease Mimicking Type III 5q-SMA With Complex Rearrangements in the SMN Gene

2013

Spinal muscular atrophy is an autosomal-recessive neuromuscular disorder, causing progressive proximal weakness and atrophy of the voluntary muscles. More than 96% of the spinal muscular atrophy patients show a homozygous absence of exons 7 and 8, or exon 7 only, in SMN1, the telomeric copy of the SMN gene. We report a young male patient with neurogenic symptoms and sparse muscle fiber atrophy, suggestive of a mild form of type III spinal muscular atrophy. He was found to be a carrier of intragenic mutations in both copies of the SMN gene, exhibiting a homozygous duplication of exons 7 and 8 in SMN1 and a homozygous deletion of exon 8 as well as a heterozygous deletion of exon 7 in SMN2. H…

MalePathologymedicine.medical_specialtyNeuromuscular diseaseBiopsyDNA Mutational AnalysisSMN1Spinal Muscular Atrophies of ChildhoodBiologyQuadriceps MuscleDiagnosis DifferentialMice03 medical and health sciencesExonAtrophyGene duplicationmedicineAnimalsHumansChildSequence Deletion030304 developmental biology0303 health sciences030305 genetics & heredityNeuromuscular DiseasesSpinal muscular atrophymedicine.diseaseSMA*ImmunohistochemistrySurvival of Motor Neuron 1 ProteinMolecular biologynervous system diseasesSmn geneSurvival of Motor Neuron 2 ProteinMuscular AtrophyPhenotypeMutationPediatrics Perinatology and Child HealthNeurology (clinical)Journal of Child Neurology
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