Search results for "Malo"

showing 10 items of 815 documents

Paraoxonase-1 deficiency is associated with severe liver steatosis in mice fed a high-fat high-cholesterol diet: a metabolomic approach.

2013

Oxidative stress is a determinant of liver steatosis and the progression to more severe forms of disease. The present study investigated the effect of paraoxonase-1 (PON1) deficiency on histological alterations and hepatic metabolism in mice fed a high-fat high-cholesterol diet. We performed nontargeted metabolomics on liver tissues from 8 male PON1-deficient mice and 8 wild-type animals fed a high-fat, high-cholesterol diet for 22 weeks. We also measured 8-oxo-20-deoxyguanosine, reduced and oxidized glutathione, malondialdehyde, 8-isoprostanes and protein carbonyl concentrations. Results indicated lipid droplets in 14.5% of the hepatocytes of wild-type mice and in 83.3% of the PON1-deficie…

Malemedicine.medical_specialtyBiologymedicine.disease_causeDiet High-FatBiochemistrychemistry.chemical_compoundMiceLipid dropletInternal medicineNonalcoholic fatty liver diseasemedicineAnimalsMetabolomicsAmino AcidsOrotic AcidTriglycerideLipid peroxideAryldialkylphosphataseGeneral Chemistrymedicine.diseaseMalondialdehydeLipid MetabolismGlutathioneFatty LiverMice Inbred C57BLOxidative StressEndocrinologyCholesterolGlucosechemistryLiverUrea cycleSteatosisOxidative stressBiomarkersJournal of proteome research
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REDUCED OXIDATIVE STRESS DURING ACELLULAR REPERFUSION OF THE RAT LIVER AFTER HYPOTHERMIC OSCILLATING PERFUSION

1999

Background ATP resynthesis during reperfusion after liver preservation has been shown to be well correlated with the function of transplanted grafts. Nevertheless, the advantages of a cellular energy charge loading during the preservation period are yet not fully understood. This study evaluates the effects of different nucleotide levels at the end of preservation on metabolic changes and oxidative stress during reperfusion. Methods Two experimental groups were chosen reflecting different energy charge states after preservation: static cold storage for 10 hr and hypothermic oxygenated oscillating perfusion for 10 hr. In both experimental groups, normothermic ex vivo acellular reperfusion ov…

Malemedicine.medical_specialtyCold storageHypothermiaLipid peroxidationSuperoxide dismutasechemistry.chemical_compoundSuperoxidesMalondialdehydeRats Inbred BNInternal medicinemedicineAnimalsEnergy chargeLiver preservationCryopreservationTransplantationbiologyTumor Necrosis Factor-alphaChemistrySuperoxideLiver cellOrgan PreservationMalondialdehydeLiver GlycogenRatsPerfusionOxidative StressEndocrinologyLiverBiochemistryReperfusionbiology.proteinLipid PeroxidationBiomarkersTransplantation
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Vitamin D status is linked to biomarkers of oxidative stress, inflammation, and endothelial activation in obese children.

2012

To examine vitamin D, parathyroid hormone, and serum calcium-phosphorus levels relationships to biomarkers of oxidative/nitrosative stress, inflammation, and endothelial activation, potential contributors for vascular complications in obese children.Cross-sectional clinical study of 66 obese Caucasian children aged 7 to 14 years. Cardiovascular risk factors were assessed. Malondialdehyde and myeloperoxidase as measures of oxidative stress, and plasma nitrite+nitrate, urinary nitrate, and 3-nitrotyrosine as markers of nitrosative stress were measured. Adipocytokines, inflammatory molecules (high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α), endothelial activati…

Malemedicine.medical_specialtyEndotheliumAdolescentNitrogenParathyroid hormoneInflammationmedicine.disease_causeEndothelial activationchemistry.chemical_compoundRisk FactorsInternal medicinemedicineVitamin D and neurologyHumansObesityVitamin DChildInflammationbusiness.industryPhosphorusMalondialdehydeVascular endothelial growth factorOxidative Stressmedicine.anatomical_structureEndocrinologyCross-Sectional StudieschemistryCardiovascular DiseasesParathyroid HormonePediatrics Perinatology and Child HealthCalciumFemaleEndothelium Vascularmedicine.symptombusinessOxidative stressBiomarkersThe Journal of pediatrics
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Atorvastatin treatment increases plasma bilirubin but not HMOX1 expression in stable angina patients.

2015

In vitro and animal studies indicate that statins increase heme oxygenase-1 gene (HMOX1) expression, which then, presumably, increases plasma bilirubin concentration. However, clinical confirmation that statins concomitantly increase HMOX1 expression and plasma bilirubin concentration is lacking. We hypothesized that in patients with stable angina atorvastatin therapy (20 mg/day for 10 weeks) concomitantly increases total bilirubin concentration and HMOX1 expression, as assessed non-invasively by plasma analysis.In 44 patients with stable angina plasma concentrations of total bilirubin, HMOX1 mRNA and HMOX1 protein were measured before and after the statin treatment, as well as plasma conce…

Malemedicine.medical_specialtyHMOX1BilirubinAtorvastatinClinical BiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundInternal medicinemedicineAtorvastatinHumanscardiovascular diseasesAngina StableRNA MessengerIncreased total bilirubinHemeBilirubinGeneral MedicineMiddle AgedMalondialdehydeEndocrinologychemistryProteolysislipids (amino acids peptides and proteins)FemaleAnimal studiesHeme Oxygenase-1Lipoproteinmedicine.drugScandinavian journal of clinical and laboratory investigation
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Lasting downregulation of the lipid peroxidation enzymes in the prefrontal cortex of mice susceptible to stress-induced anhedonia

2015

International audience; Antioxidant enzymes and lipid peroxidation in the brain are involved in neuropsychiatric pathologies, including depression. 14- or 28-day chronic stress model induced a depressive syndrome defined by lowered reward sensitivity in C57BL/6J mice and changed gene expression of peroxidation enzymes as shown in microarray assays. We studied how susceptibility or resilience to anhedonia is related to lipid peroxidation in the prefrontal cortex (PFC). With 14-day stress, a comparison of the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and accumulation of malondialdehyde (MDA) revealed a decrease of the first two measures in suscepti…

Malemedicine.medical_specialtyImipramineAnhedoniaLipid peroxidationDown-RegulationMotor ActivityMicroarrayHippocampusImipraminePrefrontal cortexGene Expression Regulation EnzymologicSuperoxide dismutaseLipid peroxidationFood PreferencesMiceBehavioral Neurosciencechemistry.chemical_compoundNeurochemicalMalondialdehydeInternal medicinemedicineAnimalsChronic stresschemistry.chemical_classificationGlutathione PeroxidasebiologySuperoxide Dismutasebusiness.industryGene Expression ProfilingGlutathione peroxidaseAnhedoniaResilience PsychologicalCatalaseMalondialdehydeAggressionEndocrinologychemistrybiology.protein[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]medicine.symptombusinessChronic stress depression modelStress Psychologicalmedicine.drug
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Involvement of nitric oxide-soluble guanylyl cyclase pathway in the control of maximal dentate gyrus activation in the rat.

2006

Summary Nitric oxide=soluble Guanylyl cyclase (NO=sGC) pathway on the maximal dentate gyrus activation (MDA) was studied in rats. The cerebral NO levels were modified by administrating 7-Nitroindazole (7-NI), a selective inhibitor of neuronal NOS, and L-arginine, a precursor of the synthesis of NO. 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a specific inhibitor of the NO-sGC pathway, was administered to study the involvement of cGMP pathway. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle; MDA parameters studied were: onset time, MDA duration and post-stimulus afterdischarge (AD) duration. 7-NI caused an increase of M…

Malemedicine.medical_specialtyIndazolesArginineNitric Oxide Synthase Type IIIReceptors Cytoplasmic and NuclearKeywords: Maximal dentate activation nitric oxide cGMP modulationArginineNitric OxideNitric oxidechemistry.chemical_compoundSoluble Guanylyl CyclaseInternal medicineMalondialdehydeQuinoxalinesmedicineAnimalsEnzyme InhibitorsRats WistarReceptorBiological PsychiatryOxadiazolesDentate gyrusNitric Oxide Synthase Type IIIIontophoresisRatsElectrophysiologyPsychiatry and Mental healthMetabolic pathwayEndocrinologyNeurologychemistryGuanylate CyclaseDentate GyrusNeurology (clinical)Signal transductionSoluble guanylyl cyclaseSignal TransductionJournal of neural transmission (Vienna, Austria : 1996)
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Temporomandibular chronic dislocation : the long-standing condition

2016

Background The temporomandibular joint (TMJ) dislocation can be categorised into three groups: acute, habitual or recurrent and long-standing. The long-standing or protracted lower jaw dislocation refers to a condition that persists for more than one month without reduction. There are a great variety of methods for its treatment, from the manual or non-surgical, to surgical ones like the indirect approach (conservative surgical approach) and direct approach (open joint). Additional procedures in unsuccessful cases may include extra-articular orthognathic techniques to correct a malocclusion until joint replacement. Material and Methods We report four new cases with a minimum of 6 weeks disl…

Malemedicine.medical_specialtyJoint replacementmedicine.medical_treatmentJoint DislocationsReview03 medical and health sciences0302 clinical medicineDislocation (syntax)medicineHumansInitial treatmentJoint dislocation030223 otorhinolaryngologyGeneral DentistryReduction (orthopedic surgery)Orthodonticsbusiness.industryOpen surgery030206 dentistryMiddle AgedTemporomandibular Joint Disordersmedicine.disease:CIENCIAS MÉDICAS [UNESCO]SurgeryTemporomandibular jointOrofacial Pain-TMJDmedicine.anatomical_structureJawOtorhinolaryngologySpainUNESCO::CIENCIAS MÉDICASFemaleSurgeryMalocclusionbusinessMalocclusion
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Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid.

2004

Decreased body fat mass and liver steatosis have been reported in mice fed diets containing the conjugated linoleic acid trans-10,cis-12-C18:2 (CLA2), but not in those fed diets containing cis-9,trans-11-C18:2 (CLA1). Because the decrease in fatty acid (FA) oxidation may cause fat accumulation, we questioned whether the effects of both CLAs on enzyme activities and mRNA expression were related to liver FA oxidation. To address this question, 7-wk-old male C57BL/6J mice were fed for 4 wk a diet supplemented with 1% CLA1, CLA2, or cis-9-C18:1 (control) esterified as triacylglycerols. In CLA2-fed mice, the proportions of CLA2 in the total FA of liver lipids were substantially lower than those …

Malemedicine.medical_specialtyLinoleic acidConjugated linoleic acidMedicine (miscellaneous)Mitochondria LiverBiologychemistry.chemical_compoundMiceDietary Fats UnsaturatedInternal medicinemedicineAnimalsLinoleic Acids ConjugatedCarnitineRNA MessengerEnzyme InhibitorsUnsaturated fatty acidTriglycerideschemistry.chemical_classificationNutrition and DieteticsCarnitine O-PalmitoyltransferaseEsterificationReverse Transcriptase Polymerase Chain ReactionFatty liverFatty AcidsFatty acidmedicine.diseaseFatty LiverMalonyl Coenzyme AMice Inbred C57BLEndocrinologychemistryBiochemistryLiverCarnitine palmitoyltransferase IOxidation-ReductionPolyunsaturated fatty acidmedicine.drug
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Oxidant/antioxidant status in obese children compared to pediatric patients with type 1 diabetes mellitus.

2009

Codoner-Franch P, Pons-Morales S, Boix-Garcia L, Valls-Belles V. Oxidant/antioxidant status in obese children compared to pediatric patients with type 1 diabetes mellitus. Background: Type 1 diabetes (T1D) mellitus and obesity are recognized risk factors for cardiovascular disease (CVD). A common mechanism underlying an increased risk for endothelial dysfunction in these two metabolic diseases is oxidative stress. Objective: To evaluate and compare the oxidant/antioxidant defense systems in children affected with T1D or obesity in order to determine the importance of oxidative stress before the emergence of complications. Subjects: Children with T1D (n = 20) or obesity (n = 22), without com…

Malemedicine.medical_specialtyLipid PeroxidesAntioxidantErythrocytesAdolescentEndocrinology Diabetes and Metabolismmedicine.medical_treatmentalpha-TocopherolProtein oxidationmedicine.disease_causeLipid peroxidationProtein Carbonylationchemistry.chemical_compoundInternal medicineMalondialdehydeInternal MedicinemedicineHumansObesityProspective StudiesChildRetrospective Studieschemistry.chemical_classificationType 1 diabetesGlutathione Peroxidasebusiness.industryGlutathione peroxidaseMalondialdehydemedicine.diseasebeta CaroteneObesityGlutathioneOxidative StressEndocrinologyDiabetes Mellitus Type 1chemistryPediatrics Perinatology and Child HealthFemaleLipid PeroxidationbusinessOxidative stressPediatric diabetes
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Protective effect of N-acetylcysteine on ischaemia-induced myocardial damage in canine heart.

1991

The glutathione redox pathway is an important antioxidant system in the myocardium. N-Acetylcysteine is a low molecular weight glutathione precursor that has been used clinically to replenish glutathione stores. The present study was aimed at evaluating the protective effect of N-acetylcysteine on myocardial damage resulting from permanent coronary occlusion (without reperfusion) in anaesthetized dogs. N-Acetylcysteine (150 mg kg−1 i.v.) administered 2 min before occlusion rerduced infarct size in dogs subjected to 24 h ischemia. The infarct size as a percentage of the area at risk was 86.8 ± 3.6% (n = 11) in control (salinetreated) dogs and 68.2 ± 2.4% (n = 7; P < 0.05 vs control) in N-ace…

Malemedicine.medical_specialtyMean arterial pressureTime FactorsIschemiaMyocardial InfarctionHemodynamicsCoronary DiseaseAcetylcysteinechemistry.chemical_compoundDogsInternal medicineCoronary CirculationmedicineAnimalsMyocardial infarctionPharmacologybusiness.industryGeneral MedicineGlutathionemedicine.diseaseMalondialdehydeGlutathioneAcetylcysteineDisease Models AnimalchemistryCoronary occlusionAnesthesiaCardiologyFemalebusinessmedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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