Search results for "DLIM"

showing 4 items of 44 documents

Redox regulation of E3 ubiquitin ligases and their role in skeletal muscle atrophy

2015

Muscle atrophy is linked to reactive oxygen species (ROS) production during hindlimb-unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of our study was to determine the mechanism by which ROS cause muscle atrophy and its possible prevention by allopurinol, a well-known inhibitor of XO widely used in clinical practice, and indomethacin, a nonsteroidal anti-inflammatory drug. We studied the activation of p38 MAP Kinase and NF-?B pathways, and the expression of two E3 ubiquitin ligases involved in proteolysis, the Muscle atrophy F-Box (MAFb) and Muscle RING Finger-1 (MuRF-1). Male Wistar rats (3 mold) conditioned by 14 days of hindlimb unloading (n=18),…

Soleus musclemedicine.medical_specialtySkeletal muscleAllopurinolHindlimbBiologymedicine.disease_causemedicine.diseaseBiochemistryMuscle atrophychemistry.chemical_compoundmedicine.anatomical_structureEndocrinologyAtrophychemistryBiochemistryPhysiology (medical)Internal medicinemedicinemedicine.symptomXanthine oxidaseOxidative stressmedicine.drugFree Radical Biology and Medicine
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Capillary enlargement, not sprouting angiogenesis, determines beneficial therapeutic effects and side effects of angiogenic gene therapy.

2010

Aims Currently, it is still unclear which mechanisms drive metabolic benefits after angiogenic gene therapy. The side-effect profile of efficient angiogenic gene therapy is also currently incompletely understood. In this study, the effects of increasing doses of adenoviral (Ad) vascular endothelial growth factor-A (VEGF-A) were evaluated on vascular growth, metabolic benefits, and systemic side effects. Methods and results Adenoviral vascular endothelial growth factor-A or AdLacZ control was injected intramuscularly (109–1011 vp/mL) or intra-arterially (5 × 1011 vp/mL) into rabbit ( n = 102) hindlimb muscles and examined 6 or 14 days later. Blood flow, tissue oedema, metabolic benefits, and…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyAngiogenesisGenetic VectorsNeovascularization PhysiologicEnzyme-Linked Immunosorbent Assayta3111Injections IntramuscularAdenoviridaeNeovascularizationchemistry.chemical_compoundInternal medicinemedicineAnimalsMuscle SkeletalUltrasonography InterventionalSprouting angiogenesisDose-Response Relationship Drugbusiness.industryGene Transfer TechniquesMetabolic acidosisGenetic Therapymedicine.diseaseCapillariesHindlimbVascular endothelial growth factorVascular endothelial growth factor AEndocrinologychemistryLac OperonCirculatory systemRabbitsmedicine.symptomCardiology and Cardiovascular MedicinebusinessPerfusionEuropean heart journal
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Cisplatin-induced peripheral neuropathy: neuroprotection by erythropoietin without affecting tumour growth

2007

This study examined the dose-dependent efficacy of erythropoietin (EPO) for preventing and/or treating cisplatin (CDDP) induced peripheral neurotoxicity (CINP), and its influence on tumour treatment and growth. Rats received eight intraperitoneal (ip) injections of 2 mg/kg CDDP twice weekly. EPO co-administered (50 or 10 microg/kg ip, three times/week) had a dose-dependent effect, partially preventing CINP, but 0.5 microg/kg ip was not effective. The neuroprotective effect lasted at least 5 weeks after the last dose of EPO and CDDP. In addition, EPO (50 microg/kg ip three times/week) after the last injection of CDDP still induced a significant recovery of CINP. In a separate experiment in r…

medicine.medical_specialtyCancer ResearchPeripheral neuropathyNeural ConductionNeurophysiologyAntineoplastic AgentsHindlimbHematocritNeuroprotectionAntineoplastic AgentInternal medicinemedicinePathologyAnimalsRats WistarErythropoietinCisplatincisplatin; Erythropoietin; peripheral neuropathy; tumor growthmedicine.diagnostic_testDose-Response Relationship Drugbusiness.industryAnimalNeurotoxicityPeripheral Nervous System DiseasesMammary Neoplasms ExperimentalTumour growthHematologymedicine.diseaseRatsHindlimbDose–response relationshipPeripheral neuropathyEndocrinologyOncologyHematocritErythropoietinRatFemalePeripheral Nervous System DiseaseCisplatinbusinessCell Divisionmedicine.drug
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Increased pain and neurogenic inflammation in mice deficient of neutral endopeptidase

2009

The complex regional pain syndrome (CRPS) is characterized by enhanced neurogenic inflammation, mediated by neuropeptides. Neutral endopeptidase (NEP) is a key enzyme in neuropeptide catabolism. We used NEP knock out (ko) mice to investigate whether NEP deficiency leads to increased pain behavior and signs of neurogenic inflammation after soft tissue trauma with and without nerve injury. After chronic constriction injury (CCI) of the right sciatic nerve, NEP ko mice were more sensitive to heat, to mechanical stimuli, and to cold than wild type mice. Tissue injury without nerve injury produced no differences between genotypes. After CCI, NEP ko mice showed increased hind paw edema but lower …

medicine.medical_specialtyHot TemperaturePainSubstance PEnzyme-Linked Immunosorbent AssayCalcitonin gene-related peptideSubstance PEndothelin 1lcsh:RC321-571chemistry.chemical_compoundMiceCGRP catabolismEdemaInternal medicinePhysical StimulationMedicineAnimalsEdemaMuscle SkeletalNeprilysinlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPain MeasurementSkinMice KnockoutNeurogenic inflammationEndothelin-1business.industryCCIfungiNerve injurymedicine.diseaseNeutral endopeptidaseEndothelin 1Sciatic NerveHindlimbCold TemperatureMice Inbred C57BLComplex regional pain syndromeEndocrinologyNeurologychemistryAnesthesiaNeprilysinmedicine.symptomNeurogenic InflammationbusinessSkin TemperaturePrimarily cold CRPSNeurobiology of Disease
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