Search results for "Phosphor"

showing 10 items of 1952 documents

Calcium-enriched bread for treatment of uremic hyperphosphatemia

2004

Abstract Objective To assess phosphate-binding efficacy of a new food product, bread with unusually high calcium content (Ca-bread). Design and setting A randomized parallel group trial in the university hospital outpatient dialysis unit. Patients Fifty-three randomly selected uremic patients who met the following inclusion criteria: (1) required maintenance hemodialysis treatment, (2) were not to receive vitamin D throughout the study, (3) were nondiabetic, and (4) were diagnosed with hyperphosphatemia. Intervention Fifty-three patients were randomized into 2 groups: control group (n = 26), which received calcium acetate as a phosphate binder throughout the study, and Ca-bread group (n = 2…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentElemental calciumMedicine (miscellaneous)chemistry.chemical_elementAcetatesCalciumPhosphatesHyperphosphatemiachemistry.chemical_compoundAnimal scienceRenal DialysismedicineVitamin D and neurologyHumansUremiaNutrition and Dieteticsbusiness.industrydigestive oral and skin physiologyfood and beveragesBreadCalcium CompoundsMiddle Agedmedicine.diseasePhosphateDiet RecordsSurgeryPhosphate binderCalcium DietarychemistryNephrologyFood FortifiedCalcium CompoundsPatient CompliancePhosphorus DietaryCalciumFemaleHemodialysisbusinessJournal of Renal Nutrition
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats.

1997

The effects of insulin on the rates of glucose disposal were studied in soleus muscles isolated from hyper- or hypothyroid rats. Treatment with triiodothyronine for 5 or 10 days decreased the sensitivity of glycogen synthesis but increased the sensitivity of lactate formation to insulin. The sensitivity of 3-O methylglucose to insulin was increased only after 10 days of treatment and was accompanied by an increase in the sensitivity of 2-deoxyglucose phosphorylation; however, 2-deoxyglucose and glucose 6-phosphate in response to insulin remained unaltered. In hypothyroidism, insulin-stimulated rates of 3-O-methylglucose transport and 2-deoxyglucose phosphorylation were decreased; however, a…

Malemedicine.medical_specialtymedicine.medical_treatmentClinical BiochemistryBiological Transport ActiveBiologyCarbohydrate metabolismIn Vitro TechniquesBiochemistryHyperthyroidismDinoprostonechemistry.chemical_compoundHypothyroidismInternal medicinemedicineAnimalsInsulinGlycolysisDrug InteractionsLactic AcidPhosphorylationRats WistarGlycogen synthaseMuscle SkeletalHexokinaseInsulinGlucose transporterGeneral MedicineMetabolismRatsCortisoneEndocrinologyGlucosechemistryBasal (medicine)Growth Hormonebiology.proteinTriiodothyronineGlycolysisGlycogenEuropean journal of clinical investigation
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Elevated plasma level of visfatin/pre-b cell colony-enhancing factor in male oral squamous cell carcinoma patients

2012

Objectives: Visfatin, also known as nicotiamide phosphoribosyltransferase or pre-B cell colony enhancing factor, is a pro-inflammatory cytokine whose serum level is increased in various cancers. In this study, we investigated whether plasma visfatin levels were altered in patients with oral squamous cell carcinoma (OSCC). The relation ship between plasma visfatin levels and the pretreatment hematologic profile was also explored. Study Design: Plasma visfatin concentrations were measured through ELISA in OSCC patients and control sub- D esign: Plasma visfatin concentrations were measured through ELISA in OSCC patients and control sub- esign: Plasma visfatin concentrations were measured throu…

Malemedicine.medical_specialtymedicine.medical_treatmentNicotinamide phosphoribosyltransferaseOdontologíaHematocritPathogenesischemistry.chemical_compoundWhite blood cellInternal medicineCarcinomaMedicineHumansProspective StudiesNicotinamide PhosphoribosyltransferaseGeneral DentistryMouth neoplasmOral Medicine and Pathologymedicine.diagnostic_testbusiness.industryMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseCiencias de la saludstomatognathic diseasesEndocrinologymedicine.anatomical_structureCytokineOtorhinolaryngologychemistryUNESCO::CIENCIAS MÉDICASAbsolute neutrophil countCarcinoma Squamous CellSurgeryResearch-ArticleMouth Neoplasmsbusiness
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Nitric oxide metabolites, leukocyte activation markers and oxidative status in dialyzed subjects.

2008

<i>Aims:</i> Our purpose was to evaluate, in a group of 42 end-stage renal disease patients who regularly undergo hemodialysis, some indexes of leukocyte activation, nitric oxide metabolites (NOx) and other parameters that reflect the oxidative stress before and after a standard hemodialysis session. <i>Methods:</i> Elastase and myeloperoxidase (MPO) were determined by means of ELISA. The NO production was evaluated by a micromethod which measures the concentration of NOx. The oxidation of polyunsaturated fatty acids was evaluated in plasma by detection of thiobarbituric acid-reactive substances (TBARS). Total antioxidant status (TAS) was obtained using spectrophotom…

Malemedicine.medical_treatmentActivation markersOxidative phosphorylationHemodialysis Oxidative status Nitric oxide Elastase MyeloperoxidasePharmacologyNitric OxideThiobarbituric Acid Reactive SubstancesAntioxidantsNitric oxidechemistry.chemical_compoundRenal DialysisLeukocytesmedicineHumansAgedPeroxidasechemistry.chemical_classificationbiologyElastaseHematologyGeneral MedicineMiddle AgedOxidative StressEnzymechemistryNephrologyMyeloperoxidaseImmunologybiology.proteinKidney Failure ChronicFemaleHemodialysisLeukocyte Elastase
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Neuroimmune and Mu-Opioid Receptor Alterations in the Mesocorticolimbic System in a Sex-Dependent Inflammatory Pain-Induced Alcohol Relapse-Like Rat …

2021

Evidence concerning the role of alcohol-induced neuroinflammation in alcohol intake and relapse has increased in the last few years. It is also proven that mu-opioid receptors (MORs) mediate the reinforcing properties of alcohol and, interestingly, previous research suggests that neuroinflammation and MORs could be related. Our objective is to study neuroinflammatory states and microglial activation, together with adaptations on MOR expression in the mesocorticolimbic system (MCLS) during the abstinence and relapse phases. To do so, we have used a sex-dependent rat model of complete Freund’s adjuvant (CFA)-induced alcohol deprivation effect (ADE). Firstly, our results confirm that only CFA-…

Malemedicine.medical_treatmentFreund's AdjuvantReceptors Opioid mualcohol deprivation effectNitric Oxide Synthase Type IImicroglianeuroinflammationRats Sprague-DawleyRecurrenceLimbic SystemImmunology and AllergypainPhosphorylationReceptormedia_commonMicrogliaAlcohol AbstinencealcoholMicrofilament ProteinsNF-kappa BBrief Research ReportInterleukin 10AlcoholismCytokinemedicine.anatomical_structureCytokinesFemaleμ-opioid receptorInflammation Mediatorsmedicine.medical_specialtyNeuroimmunomodulationmedia_common.quotation_subjectImmunologyPrefrontal CortexSex FactorsDownregulation and upregulationInternal medicinemedicineAnimalsNeuroinflammationbusiness.industryCalcium-Binding ProteinsAbstinenceRC581-607EndocrinologyCyclooxygenase 2mu-opioid receptorImmunologic diseases. AllergybusinessFrontiers in Immunology
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A non-redundant role for OX40 in the competitive fitness of Treg in response to IL-2.

2010

OX40 stimulation is known to enhance activation of effector T cells and to inhibit induction and suppressive function of Treg. Here we uncovered a novel role of OX40 in sustaining Treg competitive fitness in vivo, during repopulation of lymphopenic hosts and reconstitution of BM chimeras. Defective expansion of OX40-null Treg diminished their ability to suppress inflammation in a model of lymphopenia-driven colitis. OX40-mediated promotion of Treg fitness spanned beyond lymphopenic environments, as endogenous Treg in OX40-null mice showed decreased accumulation during thymic development, enhanced susceptibility to antibody-mediated depletion and defective turnover following thymectomy. In v…

Malemedicine.medical_treatmentImmunologyBlotting Westernchemical and pharmacologic phenomenaEndogenyInflammationSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryMiceSuppressor of Cytokine Signaling 1 ProteinLymphopeniaOX40; Treg; IL-2.medicineSTAT5 Transcription FactorImmunology and AllergyAnimalsOX40PhosphorylationReceptorSTAT5Cell ProliferationMice KnockoutbiologyEffectorCell growthSuppressor of cytokine signaling 1hemic and immune systemsReceptors OX40IL-2.ColitisFlow Cytometrycytokinescompetitive fitnessSpecific Pathogen-Free OrganismsThymectomyMice Inbred C57BLTregRadiation ChimeraImmunologybiology.proteinInterleukin-2costimulatory moleculesmedicine.symptomcompetitive fitness; costimulatory molecules; cytokines; treg
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Abnormalities of mitochondrial functioning can partly explain the metabolic disorders encountered in sarcopenic gastrocnemius.

2007

International audience; Aging triggers several abnormalities in muscle glycolytic fibers including increased proteolysis, reactive oxygen species (ROS) production and apoptosis. Since the mitochondria are the main site of substrate oxidation, ROS production and programmed cell death, we tried to know whether the cellular disorders encountered in sarcopenia are due to abnormal mitochondrial functioning. Gastrocnemius mitochondria were extracted from adult (6 months) and aged (21 months) male Wistar rats. Respiration parameters, opening of the permeability transition pore and ROS production, with either glutamate (amino acid metabolism) or pyruvate (glucose metabolism) as a respiration substr…

Malemuscle atrophyMESH : Cell Aging[SDV]Life Sciences [q-bio]MESH : Reactive Oxygen SpeciesMitochondrion0302 clinical medicineGlycolysisMESH: AnimalsMESH : Muscle SkeletalMESH : Fatty AcidsCellular SenescencePhospholipidsMESH: Superoxide Dismutasereactive oxygen speciesMESH : Free Radicals0303 health sciencesMESH: Muscle SkeletalMESH : RatsFatty Acidsfatty acid profile of mitochondrial lipidsMESH: Reactive Oxygen SpeciesPyruvate dehydrogenase complexMESH: Fatty Acidsmitochondria[SDV] Life Sciences [q-bio]BiochemistryMESH: Cell AgingMESH: CalciumMESH : MitochondriaCell agingPyruvate decarboxylationmedicine.medical_specialtyFree RadicalsMESH: RatsCellular respirationMESH: MitochondriaMESH : MaleCell Respirationchemistry.chemical_elementOxidative phosphorylationBiologyCalciumMESH : Rats WistarMESH : Phospholipids03 medical and health sciencesMESH: Free RadicalsInternal medicinemedicineAnimalsMESH : Superoxide DismutaseRats WistarMuscle SkeletalMESH : Calcium030304 developmental biologyMESH: Phospholipidscalciumpermeability transition poreSuperoxide Dismutaseagingaging;calcium;fatty acid profile of mitochondrial lipids;mitochondria;muscle atrophy;permeability transition pore;reactive oxygen species;Animals;Calcium;Cell Aging;Cell Respiration;Fatty Acids;Free Radicals;Male;Mitochondria;Muscle;Skeletal;Phospholipids;Rats;Wistar;Reactive Oxygen Species;Superoxide DismutaseCell BiologyMESH: Rats WistarMESH: MaleRatsEndocrinologychemistryMESH : Cell RespirationMESH : AnimalsMESH: Cell Respiration030217 neurology & neurosurgery
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Preventing bone loss during androgen deprivation therapy for prostate cancer: Early experience with neridronate

2005

Abstract Objective: Androgen-deprivation therapy (ADT) is the usual treatment for locally advanced or metastatic prostate cancer. Osteoporosis is a common complication of ADT. The aim of our study was to evaluate the efficacy of neridronate, a relatively new bisphosphonate to prevent bone loss during androgen ablation. Methods: Sixty patients with prostate cancer and osteoporosis were enrolled and randomly assigned to 2 different treatment regimes: group A (30 patients) treated with maximum androgenic blockage (MAB), and group B (30 patients) treated with bicalutamide 150mg. Each group was divided in 2 subgroups A1–A2 and B1–B2. All patients received calcium and cholecalciferol supplements …

Malemusculoskeletal diseasesmedicine.medical_specialtyDeoxypyridinolineBone densityBicalutamideUrologymedicine.medical_treatmentOsteoporosisUrologyImmunoenzyme TechniquesTosyl CompoundsAndrogen deprivation therapyProstate cancerchemistry.chemical_compoundAbsorptiometry PhotonBone DensityNitrilesmedicineHumansNeridronic acidAnilidesTestosteroneAmino AcidsVitamin DChromatography High Pressure LiquidAgedAged 80 and overDiphosphonatesEstradiolbusiness.industryProstatic NeoplasmsAndrogen AntagonistsPhosphorusBisphosphonatemedicine.diseaseSurgeryTreatment OutcomechemistryParathyroid HormoneOsteoporosisCalciumDrug Therapy CombinationbusinessBiomarkersFollow-Up Studiesmedicine.drug
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Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independen…

2011

OBJECTIVE: Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein. METHODS AND RESULTS: Immunoblotting studies revealed a marked reduction in p27-phospho-Ser10 in atheroscleroti…

Malerho GTP-Binding ProteinsRHOAMoesinMiceApolipoproteins ERadixinSerinemedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein kinase ACell ProliferationFoam cellMice Knockoutrho-Associated KinasesbiologyArteriesAtherosclerosismedicine.diseaseCell biologyMice Inbred C57BLDisease Models AnimalAtheromaCase-Control StudiesImmunologyDisease Progressionbiology.proteinPhosphorylationFemalerhoA GTP-Binding ProteinCardiology and Cardiovascular MedicineCyclin-Dependent Kinase Inhibitor p27Foam CellsSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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