Search results for "Phosphor"

showing 10 items of 1952 documents

Effects of Acute Handling Stress on Whitefish Coregonus lavaretus After Prolonged Exposure to Biologically Treated and Untreated Bleached Kraft Mill …

2000

Exposure of fish to water of impaired quality has been shown to disrupt the function of the hypothalamo-pituitary-interrenal (HPI) axis and alter the interpretation of data from field studies due to the varying effects of handling and delayed sampling on exposed and reference animals. In the present study, juvenile whitefish, Coregonus lavaretus, were exposed for 6 weeks to diluted (4-8%) untreated and biologically treated bleached kraft mill effluent (BKME) and their response to acute handling was investigated. Liver microsomal EROD activity and glycogen phosphorylase (GPase) activity, in addition to gill Na+-K+-ATPase activity, and blood hemoglobin and hematocrit levels were increased in …

Papermedicine.medical_specialtyTime FactorsPhosphorylasesHealth Toxicology and MutagenesisBiologyHematocritToxicologyWaste Disposal FluidSpecimen HandlingHemoglobinsGlycogen phosphorylasechemistry.chemical_compoundfoodCoregonus lavaretusInternal medicineCytochrome P-450 CYP1A1medicineAnimalsAnimal HusbandrySalmonidaeGlycogenmedicine.diagnostic_testfood.dishFishesReproducibility of ResultsGeneral Medicinebiology.organism_classificationPollutionRed blood cellEndocrinologymedicine.anatomical_structureHematocritchemistryEnzyme InductionToxicityHemoglobinWater Pollutants ChemicalArchives of Environmental Contamination and Toxicology
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Effects of pharmacological agents on the lifespan phenotype of Drosophila DJ-1beta mutants.

2010

Mutations in the DJ-1 gene cause autosomal recessive, early-onset Parkinsonism. The DJ-1 protein exerts a protective role against oxidative stress damage, working as a cellular oxidative stress sensor, and it seems to regulate gene expression at different levels. In Drosophila, two DJ-1 orthologs have been identified: DJ-1β and DJ-1β. Several studies have shown that loss of DJ-1β function causes Parkinson's disease (PD)-like phenotypes in flies such as age-dependent locomotor defects, reduced lifespan, and enhanced sensitivity to toxins that induce oxidative stress, like the herbicide paraquat. However, no dopaminergic neurodegeneration is observed. These results suggested that both locomot…

ParaquatDopamineMutantOxidative phosphorylationBiologymedicine.disease_causeAntioxidantsLipid peroxidationchemistry.chemical_compoundParkinsonian DisordersGeneticsmedicineAnimalsGeneticschemistry.chemical_classificationReactive oxygen speciesNeurodegenerationDopaminergicBrainParkinson DiseaseGeneral Medicinemedicine.diseasePhenotypeCell biologyOxidative StressPhenotypechemistryMutationDrosophilaReactive Oxygen SpeciesOxidative stressGene
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Sistemic calciphylaxis and thrombotic microangiopathy in a kidney transplant patient: Two mixing fatal syndromes?

2012

Abstract Abnormalities in calcium and phosphorus metabolism are common and metabolic bone diseases develop often in patients with chronic renal failure (CRF). Effective clinical management includes measures to control phosphorus retention and prevent hyperphosphataemia, to maintain serum calcium concentrations within the normal range and to prevent excess parathyroid hormone (PTH) secretion by the judicious use of vitamin D sterols. Certain of these interventions, however, appear to increase the risk of soft tissue and vascular calcification in patients with End Stage Renal Disease (ESRD), so current therapeutic approaches are thus being re-evaluated in an effort to limit these risks. Patie…

Parathyroidectomymedicine.medical_specialtyPathologyCalciplhylaxisThrombotic microangiopathymedicine.medical_treatmentHemolitic Huremic SyndromeSettore MED/08 - Anatomia PatologicaGastroenterologyPhosphorus metabolismEnd stage renal diseaseInternal medicineSettore MED/35 - Malattie Cutanee E VenereemedicineHumansKidney transplantationSettore MED/14 - NefrologiaCalciphylaxisThrombotic Microangiopathiesbusiness.industryCalciphylaxisEnd Stage Renal Disease; Hemolitic Huremic Syndrome; CalciplhylaxisGeneral MedicineModels Theoreticalmedicine.diseaseKidney TransplantationSettore MED/18 - Chirurgia GeneraleSecondary hyperparathyroidismEnd Stage Renal DiseasebusinessCalcificationMedical Hypotheses
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Lipid nanoparticles as delivery vehicles for the Parietaria judaica major allergen Par j 2

2011

Maria Luisa Bondì1,*, Giovanna Montana2,*, Emanuela Fabiola Craparo3, Roberto Di Gesù3, Gaetano Giammona3, Angela Bonura2, Paolo Colombo21Istituto per lo Studio dei Materiali Nanostrutturati, 2Istituto di Biomedicina ed Immunologia Molecolare, Consiglio Nazionale delle Ricerche, 3Laboratory of Biocompatible Polymers, Dipartimento di Scienze e Tecnologie Molecolari e Biomolecolari Stembio, Università di Palermo, Palermo, Italy *These authors contributed equally to this workAbstract: Parietaria pollen is one of the major causes of allergic reaction in southern Europe, affecting about 30% of all allergic patients in this area. Specific immunotherapy is the only…

ParietariaMembrane lipidsBiophysicsPharmaceutical Sciencerecombinant allergensEnzyme-Linked Immunosorbent AssayBioengineeringmedicine.disease_causelaw.inventionBiomaterialsMembrane LipidsAllergenlawInternational Journal of NanomedicineParietaria judaica (Par j)Drug DiscoverySolid lipid nanoparticlemedicineHumansParticle SizePyrophosphatasesOriginal ResearchPlant ProteinsDrug Carriersallergic rhinitisbiologyPhosphoric Diester HydrolasesChemistryOrganic ChemistryRhinitis Allergic SeasonalGeneral MedicineAllergensbiology.organism_classificationMolecular biologyRecombinant ProteinsBasophilssolid lipid nanoparticlesBiochemistrySettore CHIM/09 - Farmaceutico Tecnologico Applicativodrug deliveryDrug deliveryParietaria judaicaRecombinant DNAsolid lipid nanoparticles Parietaria judaica (Par j) drug delivery recombinant allergens specific immunotherapy allergic rhinitis.NanoparticlesEmulsionsImmunotherapyDrug carrierspecific immunotherapyInternational Journal of Nanomedicine
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Hypothesis: can N-acetylcysteine be beneficial in Parkinson's disease?

1999

Based on the finding of decreased mitochondrial complex I activity in the substantia nigra of patients with Parkinson's disease, we propose that the consequent reduction of ATP synthesis and increased generation of reactive oxygen species may be a possible cause of nigrostriatal cell death. Since sulfhydryl groups are essential in oxidative phosphorylation, thiolic antioxidants may contribute to the preservation of these proteins against oxidative damage. In the present paper, we hypothesize that treatment with a sulfur-containing antioxidant such as N-acetylcysteine may provide a new neuroprotective therapeutic strategy for Parkinson's disease.

Parkinson's diseaseAntioxidantmedicine.medical_treatmentModels NeurologicalSubstantia nigraOxidative phosphorylationPharmacologyBiologyMitochondrionNeuroprotectionGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationAcetylcysteineAdenosine TriphosphatemedicineNAD(P)H Dehydrogenase (Quinone)HumansGeneral Pharmacology Toxicology and Pharmaceuticschemistry.chemical_classificationReactive oxygen speciesParkinson DiseaseGeneral Medicinemedicine.diseaseCorpus StriatumAcetylcysteineMitochondriaSubstantia NigraNeuroprotective AgentschemistryReactive Oxygen SpeciesNeurosciencemedicine.drugLife sciences
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Modulation of voltage-gated K(+) channels Kv11 and Kv1 4 by forskolin.

2002

Forskolin (FSK) affects voltage-gated K + (Kv) currents in different cell types, but it is not known which of the various subunits form FSK-sensitive Kv channels. We compared the effect of the compound at Kv1.1 and Kv1.4 channels ectopically expressed in HEK 293 cells. Low FSK concentrations induced a phosphorylation-dependent potentiation of Kv1.1 currents. At higher concentrations, this effect was superimposed by a fast, cAMP-independent channel block. Kv1.4 currents were inhibited with lower potency by FSK but were not modified by phosphorylation. The variable effect of the compound might help to distinguish between Kv subunits expressed by native cells.  2002 Elsevier Science Ltd. All …

Patch-Clamp TechniquesPotassium ChannelsStereochemistryBiologyMembrane PotentialsCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineCyclic AMPHumansPatch clampPhosphorylationProtein kinase ACells CulturedPharmacologyFrequency-shift keyingForskolinDose-Response Relationship DrugHEK 293 cellsColforsinCyclic AMP-Dependent Protein KinasesElectrophysiologyElectrophysiologyKineticsMechanism of actionchemistryPotassium Channels Voltage-GatedBiophysicsPhosphorylationKv1.4 Potassium Channelmedicine.symptomKv1.1 Potassium ChannelIon Channel GatingAlgorithmsNeuropharmacology
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Analysis of phosphorylation-dependent modulation of Kv1.1 potassium channels.

2003

The voltage-gated potassium channel Kv1.1 contains phosphorylation sites for protein kinase A (PKA) and protein kinase C (PKC). To study Kv1.1 protein expression and cellular distribution in regard to its level of phosphorylation, the effects of PKA and PKC activation on Kv1.1 were investigated in HEK 293 cells stably transfected with Kv1.1 (HEK 293/1). Without kinase activation, HEK 293/1 cells carry unphosphorylated Kv1.1 protein in the plasma membranes, whereas large amounts of phosphorylated and unphosphorylated Kv1.1 protein were located intracellularly. Activation of PKA resulted in phosphorylation of intracellular Kv1.1 protein, followed by a rapid translocation of Kv1.1 into the pla…

Patch-Clamp TechniquesPotassium Channelscomplex mixturesCell LineCellular and Molecular NeuroscienceHumansnatural sciencesProtein phosphorylationPatch clampPhosphorylationProtein kinase AProtein kinase CProtein Kinase CPharmacologyurogenital systemKinaseChemistryHEK 293 cellsAntibodies MonoclonalCyclic AMP-Dependent Protein KinasesPotassium channelCell biologyEnzyme ActivationKineticsProtein Transportnervous systemBiochemistryPotassium Channels Voltage-GatedPhosphorylationbiological phenomena cell phenomena and immunityKv1.1 Potassium ChannelIon Channel GatingNeuropharmacology
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IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
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Molecular mechanisms linking amyloid β toxicity and Tau hyperphosphorylation in Alzheimer׳s disease

2015

Neurofibrillary tangles (aggregates of cytoskeletal Tau protein) and senile plaques (aggregates mainly formed by amyloid β peptide) are two landmark lesions in Alzheimer׳s disease. Some researchers have proposed tangles, whereas others have proposed plaques, as primary lesions. For a long time, these were thought of as independent mechanisms. However, experimental evidence suggests that both lesions are intimately related. We review here some molecular pathways linking amyloid β and Tau toxicities involving, among others, glycogen synthase kinase 3β, p38, Pin1, cyclin-dependent kinase 5, and regulator of calcineurin 1. Understanding amyloid β and Tau toxicities as part of a common pathophys…

Pathologymedicine.medical_specialtyAmyloid beta-PeptidesbiologyChemistryKinaseNeurodegenerationTau proteinBACE1-AStau Proteinsmedicine.diseaseProtein Aggregation PathologicalBiochemistryBiochemistry of Alzheimer's diseaseAlzheimer DiseaseGSK-3Physiology (medical)mental disordersmedicinebiology.proteinCancer researchPIN1HumansSenile plaquesPhosphorylationFree Radical Biology and Medicine
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Current Experience in Testing Mitochondrial Nutrients in Disorders Featuring Oxidative Stress and Mitochondrial Dysfunction: Rational Design of Chemo…

2014

An extensive number of pathologies are associated with mitochondrial dysfunction (MDF) and oxidative stress (OS). Thus, mitochondrial cofactors termed "mitochondrial nutrients" (MN), such as alpha-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and L-carnitine (CARN) (or its derivatives) have been tested in a number of clinical trials, and this review is focused on the use of MN-based clinical trials. The papers reporting on MN-based clinical trials were retrieved in MedLine up to July 2014, and evaluated for the following endpoints: (a) treated diseases; (b) dosages, number of enrolled patients and duration of treatment; (c) trial success for each MN or MN combinations as reported by authors. The…

Pathologymedicine.medical_specialtyMitochondrial Diseasesmitochondrial nutrientsCoenzymesoxidative phosphorylationReviewPharmacologyMitochondrionBiologyControlled studiesmedicine.disease_causeChemopreventionCatalysislcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundmitochondrial dysfunctionmedicineAnimalsHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCoenzyme Q10Clinical Trials as TopicOrganic ChemistryGeneral Medicine3. Good healthComputer Science ApplicationsMitochondriaClinical trialOxidative Stresslcsh:Biology (General)lcsh:QD1-999chemistrymitochondrial dysfunction and oxidative streKrebs cycleOxidative stressmitochondrial nutrient
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