Search results for "MITO"

showing 10 items of 2513 documents

Rationale, design, and baseline characteristics in Evaluation of LIXisenatide in Acute Coronary Syndrome, a long-term cardiovascular end point trial …

2015

BACKGROUND: Cardiovascular (CV) disease is the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Furthermore, patients with T2DM and acute coronary syndrome (ACS) have a particularly high risk of CV events. The glucagon-like peptide 1 receptor agonist, lixisenatide, improves glycemia, but its effects on CV events have not been thoroughly evaluated.METHODS: ELIXA (www.clinicaltrials.gov no. NCT01147250) is a randomized, double-blind, placebo-controlled, parallel-group, multicenter study of lixisenatide in patients with T2DM and a recent ACS event. The primary aim is to evaluate the effects of lixisenatide on CV morbidity and mortality in a population …

Malemedicine.medical_specialtyAcute coronary syndromePopulationLIXisenatide610 Medicine & healthHypoglycemiaPlacebop38 Mitogen-Activated Protein Kinases11171 Cardiocentro Ticino2705 Cardiology and Cardiovascular Medicinelaw.inventionSettore MED/13 - EndocrinologiaAcute Coronary Syndrome; Aged; Cardiovascular Diseases; Double-Blind Method; Female; Glucagon-Like Peptide 1; Humans; Male; Middle Aged; Peptides; Placebos; Protein Kinase Inhibitors; Research Design; p38 Mitogen-Activated Protein Kinases; Cardiology and Cardiovascular MedicinePlacebosLixisenatidechemistry.chemical_compoundRandomized controlled trialDouble-Blind MethodlawGlucagon-Like Peptide 1Internal medicineJournal ArticlemedicineHumansComparative StudyMyocardial infarctionAcute Coronary SyndromeeducationProtein Kinase InhibitorsAgededucation.field_of_studybusiness.industryUnstable anginaResearch Support Non-U.S. Gov'tta3121Middle Agedmedicine.diseaseSurgeryMulticenter StudychemistryCardiovascular DiseasesResearch DesignRandomized Controlled TrialCardiologyFemaleCardiology and Cardiovascular MedicinebusinessPeptides
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Effects of training on regional substrate oxidation in the hearts of ageing rats.

1989

23-month-old male rats were trained by running for 20 weeks. The oxidation rates of succinate, glutamate+malate, palmitoylcarnitine, and pyruvate and the activities of lactate dehydrogenase, citrate synthase, isocitrate dehydrogenase and cytochrome oxidase were measured in the subendocardium and subepicardium and in the right ventricle. Regional differences of substrate oxidation rates in the myocardium of old sedentary or trained rats were less than in young rats, suggesting that regional differences in the cardiac work load disappear during ageing. Training did not improve oxidation rates, in contradiction to some previous results.

Malemedicine.medical_specialtyAgingCitrate (si)-SynthaseElectron Transport Complex IVchemistry.chemical_compoundLactate dehydrogenaseInternal medicinePhysical Conditioning AnimalmedicineCitrate synthaseCytochrome c oxidaseAnimalsPalmitoylcarnitinebiologyL-Lactate DehydrogenaseMyocardiumBody WeightGlutamate receptorHeartRats Inbred StrainsOrgan SizeIsocitrate DehydrogenaseRatsmedicine.anatomical_structureIsocitrate dehydrogenaseEndocrinologychemistryAgeingVentriclebiology.proteinGeriatrics and GerontologyOxidation-Reduction
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Growth hormone replacement therapy prevents sarcopenia by a dual mechanism: improvement of protein balance and of antioxidant defenses.

2013

The aim of our study was to elucidate the role of growth hormone (GH) replacement therapy in three of the main mechanisms involved in sarcopenia: alterations in mitochondrial biogenesis, increase in oxidative stress, and alterations in protein balance. We used young and old Wistar rats that received either placebo or low doses of GH to reach normal insulin-like growth factor-1 values observed in the young group. We found an increase in lean body mass and plasma and hepatic insulin-like growth factor-1 levels in the old animals treated with GH. We also found a lowering of age-associated oxidative damage and an induction of antioxidant enzymes in the skeletal muscle of the treated animals. GH…

Malemedicine.medical_specialtyAgingSarcopeniaIGF-1. Mitochondrial biogenesis Myostatin p70S6KHormone Replacement TherapyMyostatinProtein degradationmedicine.disease_causeAntioxidantsInternal medicineMedicineAnimalsRats WistarMuscle Skeletalbiologybusiness.industryProtein turnoverSkeletal muscleProteinsmedicine.diseaseMitochondria MuscleRatsSomatropinEndocrinologymedicine.anatomical_structureMitochondrial biogenesisSarcopeniaGrowth Hormonebiology.proteinBody CompositionGeriatrics and GerontologybusinessOxidative stressThe journals of gerontology. Series A, Biological sciences and medical sciences
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Mitochondria from females exhibit higher antioxidant gene expression and lower oxidative damage than males

2003

We have investigated the differential mitochondrial oxidative stress between males and females to understand the molecular mechanisms enabling females to live longer than males. Mitochondria are a major source of free radicals in cells. Those from female rats generate half the amount of peroxides than those of males. This does not occur in ovariectomized animals. Estrogen replacement therapy prevents the effect of ovariectomy. Mitochondria from females have higher levels of reduced glutathione than those from males. Those from ovariectomized rats have similar levels to males, and estrogen therapy prevents the fall in glutathione levels that occurs in ovariectomized animals. Oxidative damage…

Malemedicine.medical_specialtyAntioxidantOvariectomymedicine.medical_treatmentMitochondria LiverMitochondrionBiologymedicine.disease_causeDNA MitochondrialBiochemistryAntioxidantsGene Expression Regulation EnzymologicSuperoxide dismutasechemistry.chemical_compoundRNA Ribosomal 16SPhysiology (medical)Internal medicinemedicineAnimalsRats WistarDNA Primerschemistry.chemical_classificationGlutathione PeroxidaseReverse Transcriptase Polymerase Chain ReactionSuperoxide DismutaseGlutathione peroxidaseEstrogensGlutathioneGlutathionePeroxidesRatsOxygenOxidative StressEndocrinologychemistryOvariectomized ratbiology.proteinRNAFemaleDismutaseReactive Oxygen SpeciesOxidation-ReductionOxidative stressFree Radical Biology and Medicine
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Hydralazine is a powerful inhibitor of peroxynitrite formation as a possible explanation for its beneficial effects on prognosis in patients with con…

2005

The hemodynamic and anti-ischemic effects of nitroglycerin (GTN) are rapidly blunted as a result of the development of nitrate tolerance. Hydralazine has been shown to prevent tolerance in experimental and clinical studies, all of which may be at least in part secondary to antioxidant properties of this compound. The antioxidant effects of hydralazine were tested in cell free systems, cultured smooth muscle cells, isolated mitochondria, and isolated vessels. Inhibitory effects on the formation of superoxide and/or peroxynitrite formation were tested using lucigenin and L-012 enhanced chemiluminescence as well as DHE-fluorescence. The peroxynitrite scavenging properties were also assessed by…

Malemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentBiophysicsMitochondrionBiochemistryAntioxidantsMitochondrial ProteinsNitroglycerinchemistry.chemical_compoundPeroxynitrous AcidInternal medicinemedicineAnimalsHumansLucigeninRats WistarMolecular BiologyHeart FailureSuperoxideAldehyde Dehydrogenase MitochondrialMicrofilament ProteinsDrug ToleranceFree Radical ScavengersCell BiologyAldehyde DehydrogenaseHydralazineHydralazinePhosphoproteinsPrognosismedicine.diseaseReactive Nitrogen SpeciesMitochondriaRatsOxidative StressEndocrinologychemistryHeart failureIsosorbide dinitrateReactive Oxygen SpeciesCell Adhesion MoleculesPeroxynitritemedicine.drugBiochemical and Biophysical Research Communications
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Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice

2012

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by…

Malemedicine.medical_specialtyBiliary cirrhosisMAP Kinase Kinase 2ApoptosisBiologymedicine.disease_causeProinflammatory cytokineMitogen-Activated Protein Kinase 14MiceCholestasisInternal medicinemedicineAnimalsCyclin D1Cyclin B1Cell ProliferationCytokinesisMice KnockoutHepatologyLiver Cirrhosis BiliaryHepatologymedicine.diseaseMice Inbred C57BLSurvival RateDisease Models AnimalOxidative Stressmedicine.anatomical_structureEndocrinologyLiverHepatocyteChronic DiseaseDisease ProgressionHepatocytesTumor necrosis factor alphaOxidative stressSignal TransductionTransforming growth factorHepatology
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Mildronate, the inhibitor of l-carnitine transport, induces brain mitochondrial uncoupling and protects against anoxia-reoxygenation

2013

Abstract The preservation of mitochondrial function is essential for normal brain function after ischaemia-reperfusion injury. l -carnitine is a cofactor involved in the regulation of cellular energy metabolism. Recently, it has been shown that mildronate, an inhibitor of l -carnitine transport, improves neurological outcome after ischaemic damage of brain tissues. The aim of the present study was to elucidate the mitochondria targeted neuroprotective action of mildronate in the model of anoxia-reoxygenation-induced injury. Wistar rats were treated daily with mildronate ( per os ; 100 mg/kg) for 14 days. The acyl-carnitine profile was determined in the brain tissues. Mitochondrial respirati…

Malemedicine.medical_specialtyBioenergeticsCell RespirationMitochondrionBiologyNeuroprotectionCarnitine transportAdenosine TriphosphateCarnitineInternal medicineRespirationmedicineAnimalsCarnitineRats WistarHypoxiaPharmacologyBrainMetabolismMitochondriaRatsOxygenCitric acid cycleNeuroprotective AgentsEndocrinologyCarnitine AcyltransferasesAcyl Coenzyme AMethylhydrazinesmedicine.drugEuropean Journal of Pharmacology
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Chemoembolization for primary liver cancer

2002

Abstract Aims: For most patients with primary liver cancer surgical treatment is not feasible and prognosis without treatment is poor. We aimed to assess the morbidity and efficacy of transarterial chemoembolization (TACE) with lipiodol and mitomycin C in these patients in a prospective case-control study. Methods: From August 1996 to May 2000 22 patients with non-resectable hepatocellular carcinoma were treated with TACE. In case of radiological or tumour-marker response, treatment was repeated after 4–6 weeks, up to seven times per patient. Results: Morbidity was 23% and usually minor, no patient died within 30 days of treatment. A decrease in size of the reference tumour or constant tumo…

Malemedicine.medical_specialtyCarcinoma HepatocellularMitomycinmedicine.medical_treatmentGastroenterologyInternal medicinemedicineHumansProspective StudiesEmbolizationChemoembolization TherapeuticSurvival rateAgedAged 80 and overChemotherapyAntibiotics Antineoplasticbusiness.industryLiver NeoplasmsMitomycin CIodized OilGeneral MedicineMiddle Agedmedicine.diseaseSurgerySurvival RateOncologyCase-Control StudiesRadiological weaponHepatocellular carcinomaLipiodolFemaleSurgeryalpha-FetoproteinsComplicationbusinessmedicine.drugEuropean Journal of Surgical Oncology (EJSO)
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Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: a severe fatty acid oxidation disorder

1994

3-Hydroxyacyl-CoA dehydrogenase deficiency is a newly recognised fatty acid oxidation disorder with a usually fatal outcome. We present a further patient who presented with hypoketotic hypoglycaemia, hepatopathy, secondary carnitine deficiency and increased plasma long-chain acylcarnitines. 3-Hydroxydicarboxylic aciduria was present and the diagnosis confirmed in cultured skin fibroblasts. Our patient is compared with those reported in the literature with respect to clinical symptoms, differential diagnosis and possible therapeutic regimens.

Malemedicine.medical_specialtyCardiomyopathyLipid Metabolism Inborn ErrorsFatal OutcomeInternal medicineCarnitineMedicineHumansBeta oxidationchemistry.chemical_classificationCultured skinbusiness.industryLiver DiseasesInfant Newborn3-Hydroxyacyl CoA DehydrogenasesMitochondrial MyopathiesClinical Enzyme Testsmedicine.diseaseDehydrogenase deficiencyHypoglycemiaEnzymeEndocrinologychemistrySecondary carnitine deficiencyPediatrics Perinatology and Child HealthDifferential diagnosisbusinessCardiomyopathiesLong-Chain-3-Hydroxyacyl-CoA DehydrogenaseEuropean journal of pediatrics
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Ursodeoxycholic acid protects against secondary biliary cirrhosis in rats by preventing mitochondrial oxidative stress

2004

Ursodeoxycholic acid (UDCA) improves clinical and biochemical indices in primary biliary cirrhosis and prolongs survival free of liver transplantation. Recently, it was suggested that the cytoprotective mechanisms of UDCA may be mediated by protection against oxidative stress, which is involved in the development of cirrhosis induced by chronic cholestasis. The aims of the current study were 1) to identify the mechanisms involved in glutathione depletion, oxidative stress, and mitochondrial impairment during biliary cirrhosis induced by chronic cholestasis in rats; and 2) to determine the mechanisms associated with the protective effects of UDCA against secondary biliary cirrhosis. The find…

Malemedicine.medical_specialtyCirrhosisCardiolipinsGlutamate-Cysteine LigaseBiliary cirrhosisPopulationBiologymedicine.disease_causeMembrane Potentialschemistry.chemical_compoundPrimary biliary cirrhosisInternal medicinemedicineCardiolipinAnimalsRats Wistareducationeducation.field_of_studyCholestasisHepatologyLiver Cirrhosis BiliaryUrsodeoxycholic AcidCystathionine gamma-LyaseGlutathionemedicine.diseaseGlutathioneUrsodeoxycholic acidMitochondriaPeroxidesRatsOxidative StressEndocrinologyLiverchemistryChronic DiseaseHepatocytesOxidation-ReductionOxidative stressmedicine.drugHepatology
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