Search results for "hydrogenase"

showing 10 items of 575 documents

Continuous Normothermic Ex Vivo Kidney Perfusion Is Superior to Brief Normothermic Perfusion Following Static Cold Storage in Donation After Circulat…

2016

Hypothermic preservation is known to cause renal graft injury, especially in donation after circulatory death (DCD) kidney transplantation. We investigated the impact of cold storage (SCS) versus short periods of normothermic ex vivo kidney perfusion (NEVKP) after SCS versus prolonged, continuous NEVKP with near avoidance of SCS on kidney function after transplantation. Following 30 min of warm ischemia, kidneys were removed from 30-kg Yorkshire pigs and preserved for 16 h with (A) 16 h SCS, (B) 15 h SCS + 1 h NEVKP, (C) 8 h SCS + 8 h NEVKP, and (D) 16 h NEVKP. After contralateral kidney resection, grafts were autotransplanted and pigs followed up for 8 days. Perfusate injury markers such a…

Malemedicine.medical_specialtyBrain DeathTissue and Organ ProcurementSus scrofaUrologyCold storageRenal function030230 surgery03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLactate dehydrogenasemedicineImmunology and AllergyAnimalsPharmacology (medical)Kidney transplantationTransplantationCreatinineintegumentary systembusiness.industryOrgan Preservationmedicine.diseaseKidney TransplantationSurgeryTransplantationCold TemperaturePerfusionchemistryTissue and Organ Harvesting030211 gastroenterology & hepatologybusinessPerfusionEx vivoAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
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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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Protection effect of endurance training against reoxygenation-induced injuries in rat heart

1990

Endurance training by swimming (219-229 h) resulted in a significant protection against hypoxia/reoxygenation-induced injuries in Langendorff-perfused rat hearts. The protection was manifested as improved flow characteristics and a smaller release of creatine kinase into the perfusate. The concentration of thiobarbituric acid reactive substances (TBARS) was lower in the trained than in the respective control hearts. The trained hearts also showed a lower reoxygenation-induced increase in TBARS. The myocardium of the right ventricle and that of the left subepimyocardium were the most affected by reoxygenation. The swimming program induced a decrease in the activities of catalase and glutath…

Malemedicine.medical_specialtyHeart DiseasesPhysiologyThiobarbituric acidGlutathione reductaseGlucosephosphate DehydrogenaseSuperoxide dismutasechemistry.chemical_compoundEndurance trainingPhysical Conditioning AnimalPhysiology (medical)Internal medicineTBARSAnimalsMedicineHypoxiaSwimmingbiologySuperoxide Dismutasebusiness.industryMyocardiumRats Inbred StrainsGlutathioneThiobarbituratesGlutathioneRatsOxygenEndocrinologychemistryPhysical Endurancebiology.proteinGlutathione disulfideCreatine kinaseLipid PeroxidationbusinessJournal of Applied Physiology
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Exhaustive physical exercise and acid hydrolase activity in mouse skeletal muscle

1978

Adult, untrained NMRI mice were exhausted on a motor-driven treadmill by an intermittent-type running programme. Serial cryostate sections for the staining of NADH-tetrazolium reductase, beta-glucuronidase, beta-N-acetylglucosaminidase, and beta-glycerophosphatase activities and for making hematoxylin-eosin staining were cut from m. quadriceps femoris 1, 2, 3, 5, 7, and 15 days after physical exhaustion. A strong increase in the activities of beta-glucuronidase and beta-N-acetylglucosaminidase was observed 7 days after exhaustion and the activity changes, which were similar for the both glycosidases, were more prominent in the highly oxidative red compared to less oxidative white fibres. Ac…

Malemedicine.medical_specialtyHistologyHydrolasesPhysical ExertionConnective tissuePhysical exerciseBiologyMiceMuscular DiseasesInternal medicineAcetylglucosaminidasemedicineAnimalsMyocyteMolecular BiologyGlucuronidaseHistocytochemistryMusclesNADPH DehydrogenaseSkeletal muscleExtremitiesCell BiologyGeneral MedicinePhosphoric Monoester HydrolasesStainingMedical Laboratory TechnologyEndocrinologymedicine.anatomical_structureBiochemistryGlycerophosphatesbiology.proteinAnatomyGeneral Agricultural and Biological SciencesMyofibrilHomeostasisAcid hydrolaseHistochemistry
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Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus

2007

Abstract Objective HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. Methods and results In male Wistar rats, diabetes was induced by streptozotocin (STZ, 60mg/kg). In STZ rats, atorvastatin feeding (20mg/kg/d, 7 weeks), normalized vascular dysfunction as analyzed by isometric tens…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIGTP cyclohydrolase INitric Oxide Synthase Type IIReductaseArticleDiabetes Mellitus ExperimentalCytochrome P-450 Enzyme SystemEnosInternal medicineAtorvastatinmedicineAnimalsNADH NADPH OxidoreductasesPyrrolesRats WistarEndothelial dysfunctionGTP CyclohydrolaseNADPH oxidasebiologyStem CellsBody WeightMicrofilament ProteinsTetrahydrobiopterinPhosphoproteinsmedicine.diseasebiology.organism_classificationBiopterinRatsEnzyme ActivationIntramolecular OxidoreductasesVasodilationNitric oxide synthaseDisease Models AnimalOxidative StressTetrahydrofolate DehydrogenaseDiabetes Mellitus Type 1EndocrinologyHeptanoic AcidsHMG-CoA reductaseNADPH Oxidase 1biology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesDiabetic Angiopathiesmedicine.drugAtherosclerosis
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Oxidative Inhibition of the Mitochondrial Aldehyde Dehydrogenase Promotes Nitroglycerin Tolerance in Human Blood Vessels

2007

Objectives We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels. Background The hemodynamic effects of GTN are rapidly blunted by the development of tolerance, a phenomenon associated with increased formation of reactive oxygen species (ROS). Recent studies suggest that ROS-induced inhibition of ALDH-2 accounts for tolerance in animal models. Methods Segments of surgically removed arteria mammaria and vena saphena from patients undergoing coronary bypass surgery were used to examine the vascular responsiveness to GTN and the endothelium-dependent vas…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilator AgentsMyocardial InfarctionAldehyde dehydrogenaseVasodilationPharmacologyDrug Administration ScheduleTissue Culture TechniquesNitroglycerinIn vivoEnosmedicineHumansSaphenous VeinEndothelial dysfunctionMammary ArteriesAgedbiologybusiness.industryAldehyde Dehydrogenase MitochondrialDrug ToleranceAldehyde Dehydrogenasemedicine.diseasebiology.organism_classificationAcetylcholineSurgeryOxidative Stressmedicine.anatomical_structureCirculatory systemcardiovascular systembiology.proteinFemaleAnimal studiesbusinessCardiology and Cardiovascular Medicinecirculatory and respiratory physiologyBlood vesselJournal of the American College of Cardiology
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Comparison of enzyme phenotypes in human bladder tumours and experimentally induced hyperplastic and neoplastic lesions of the rat urinary bladder. A…

1988

The expression of a number of enzymes involved in drug metabolism, membrane function etc. was compared in hyperplastic and neoplastic lesions of the rat bladder and in human bladder tumours. Transitional cell carcinomas (TCC) in both rat and Man were characterized by decreased alkaline phosphatase (ALP) and increased gamma-glutamyl transpeptidase (GGT), beta-glucuronidase (beta-G1), succinate dehydrogenase (SD) and glucose-6-phosphate dehydrogenase (G6PD) activities. In addition, binding for antibodies specific for different cytochrome P-450 species (UT50, PB3a, MC1, MC2) and microsomal epoxide hydrolase (mEHb) was elevated in both murine and human tumours. Comparison of the enzyme phenotyp…

Malemedicine.medical_specialtyPathologyUrinary BladderGlucosephosphate DehydrogenaseInternal medicinemedicineAnimalsHumansNeoplastic transformationEnzyme inducerGlucuronidaseCarcinoma Transitional CellUrinary bladderHyperplasiabiologyHistocytochemistrySuccinate dehydrogenasegamma-GlutamyltransferaseHyperplasiamedicine.diseaseAlkaline PhosphataseImmunohistochemistryRats Inbred F344RatsSuccinate DehydrogenaseEndocrinologymedicine.anatomical_structurePhenotypeUrinary Bladder NeoplasmsMicrosomal epoxide hydrolasebiology.proteinImmunohistochemistryDrug metabolismVirchows Archiv. B, Cell pathology including molecular pathology
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Nitric oxide synthase in the hypothalamic suprachiasmatic nucleus of rat: evidence from histochemistry, immunohistochemistry and Western blot; and co…

1995

Nitric oxide (NO) is a neuroactive substance of high potency. Physiological results revealed the involvement of NO in circadian regulation of rats. Since neuronal structures containing NO-synthase (NOS) were previously not found in the circadian oscillator, the hypothalamic suprachiasmatic nucleus (SCN), in this species but are present in the hamster, we investigated the distribution of NO-producing structures in the rat SCN by Western blot analysis, immunohistochemistry of NOS, and by histochemistry (NADPH-diaphorase (NADPH-d) activity of NOS). Western blot analysis of SCN homogenates from rat (and, for comparison, hamster) showed a NOS-like immunoreactive (-LI) protein band of apparent mo…

Malemedicine.medical_specialtyPhodopusBlotting WesternVasoactive intestinal peptidePopulationHamsterNitric OxideNitric oxideRats Sprague-Dawleychemistry.chemical_compoundWestern blotCricetinaeInternal medicinemedicineAnimalseducationMolecular BiologyNeuronseducation.field_of_studybiologymedicine.diagnostic_testSuprachiasmatic nucleusGeneral NeuroscienceNADPH DehydrogenaseColocalizationImmunohistochemistryMolecular biologyRatsNitric oxide synthaseEndocrinologynervous systemchemistryFluorescent Antibody Technique Directbiology.proteinFemaleSuprachiasmatic Nucleussense organsNeurology (clinical)Nitric Oxide SynthaseVasoactive Intestinal PeptideDevelopmental BiologyBrain Research
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Inflammation, muscle damage and post-race physical activity following a mountain ultramarathon

2021

BACKGROUND: The study aimed at exploring whether muscle membrane disruption, as a surrogate for muscle damage, and inflammation recovery following a mountain ultramarathon (MUM) was related with race performance and post-race physical activity. METHODS: Blood samples were obtained from thirty-four athletes (29 men and 5 women) before a 118-km MUM, immediately after and three and seven days post-race. Creatine kinase (CK), lactate dehydrogenase (LDH) and C-reactive protein (CRP) were compared between faster (FR) and slower (SR) runners. Physical activity performed during the week following the MUM was objectively analyzed using accelerometers and compared between FR and SR. RESULTS: CK was s…

Malemedicine.medical_specialtyPhysical activityMarathon RunningPhysical Therapy Sports Therapy and RehabilitationInflammationMuscle damageC-reactive proteinchemistry.chemical_compoundrecoveryInternal medicineLactate dehydrogenasemedicineaccelerometryHumansOrthopedics and Sports MedicineMuscle membraneCreatine KinaseExerciseInflammationbiologybusiness.industrycreatine kinaseMuscleslactate dehydrogenaseLight intensityEndocrinologychemistryAthletesPhysical Endurancebiology.proteinFemaleCreatine kinasemedicine.symptombusiness
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