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showing 10 items of 2099 documents

PURINE AND PYRIMIDINE NUCLEOTIDES IN THE BRAIN OF NORMAL AND CONVULSANT RATS

1969

— Purine and pyrimidine nucleotides were measured in the brain of normal and electroshocked rats after chromatographic separation on ion-exchange resin of mono-, di- and tri-phosphorylated derivatives. CMP, IMP and NAD did not show any significant quantitative change. Adenine nucleotides showed an abrupt change followed by a rapid return to the control value. GTP was the only purine nucleotide exhibiting a relatively slow return to its starting concentration. The greatest percentage increase after electroshock was observed in UMP, which returned to its control value only after 5 min; UDPCoenzymes (i.e. UDPA plus UDPG) showed a relatively small drop during the development of the seizure and …

MalePurineGTP'Uracil NucleotidesCytosine NucleotidesTritiumBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundAdenosine TriphosphateSeizuresAdenine nucleotideAnimalsNucleotidechemistry.chemical_classificationChromatographyElectroshockAdenine NucleotidesNucleotidesChemistryBrainNADGuanine NucleotidesUridineRatsPyrimidinesBiochemistryPurinesConvulsantIon Exchange ResinsNAD+ kinasePyrimidine NucleotidesJournal of Neurochemistry
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Activation of P2Y receptors by ATP and by its analogue, ADPbetaS, triggers two calcium signal pathways in the longitudinal muscle of mouse distal col…

2008

Our previous research showed that ATP and adenosine 5'-O-2-thiodiphosphate (ADPbetaS) induce contractile effects in the longitudinal muscle of mouse distal colon via activation of P2Y receptors which are not P2Y(1) or P2Y(12) subtypes. This study investigated the nature of the P2Y receptor subtype(s) and the mechanisms leading to the intracellular calcium concentration increase necessary to trigger muscular contraction. Motor responses of mouse colonic longitudinal muscle to P2Y receptor agonists were examined in vitro as changes in isometric tension. ATP or ADPbetaS induced muscular contraction, which was not affected by P2Y(11) or P2Y(13) selective antagonists. Calcium-free solution or th…

MalePurinergic P2 Receptor Agonistsmedicine.medical_specialtyP2Y receptormedicine.drug_classColonchemistry.chemical_elementCalcium channel blockerCalcium-Transporting ATPasesCalciumBiologyCholinergic AgonistsIn Vitro TechniquesCalcium in biologyMiceAdenosine TriphosphateInternal medicinemedicineAnimalsInositol 145-Trisphosphate ReceptorsCalcium SignalingEnzyme InhibitorsReceptorPharmacologyRyanodine receptorReceptors Purinergic P2Muscle SmoothRyanodine Receptor Calcium Release ChannelThionucleotidesCalcium Channel BlockersAdenosineAdenosine DiphosphateMice Inbred C57BLEndocrinologychemistryType C Phospholipasesmedicine.symptomMuscle contractionmedicine.drugMuscle ContractionEuropean journal of pharmacology
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Involvement of the P2X7 purinergic receptor in colonic motor dysfunction associated with bowel inflammation in rats

2014

Background and Purpose Recent evidence indicates an involvement of P2X7 purinergic receptor (P2X7R) in the fine tuning of immune functions, as well as in driving enteric neuron apoptosis under intestinal inflammation. However, the participation of this receptor in the regulation of enteric neuromuscular functions remains undetermined. This study was aimed at investigating the role of P2X7Rs in the control of colonic motility in experimental colitis. Experimental Approach Colitis was induced in rats by 2,4-dinitrobenzenesulfonic acid. P2X7R distribution was examined by immunofluorescence analysis. The effects of A804598 (selective P2X7R antagonist) and BzATP (P2X7R agonist) were tested on co…

MalePurinergic P2X Receptor AntagonistsInflammatory Diseaseslcsh:MedicineInflammationGastroenterology and HepatologyBiologyInflammatory bowel diseaseSettore BIO/09 - FisiologiaGuanidinesPurinergic P2X Receptor AgonistsRats Sprague-DawleyImmune systemAdenosine TriphosphatemedicineMedicine and Health SciencesAnimalsP2X7 purinergic receptorColitisReceptorlcsh:SciencePurinergic P2X Receptor AgonistsPharmacologyNeuronsMultidisciplinaryPurinergic receptorlcsh:RBenzenesulfonatesMuscle Smoothmedicine.diseaseColitisRatsDisease Models AnimalImmunologyQuinolineslcsh:QP2X7 Purinergic Receptor Bowel Inflammation colonReceptors Purinergic P2X7medicine.symptomPurinergic P2X Receptor AntagonistsResearch Article
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Elimination of Ehrlich tumours by ATP-induced growth inhibition, glutathione depletion and X-rays

1995

ATP-induced tumour growth inhibition is accompanied by a selective decrease in the content of the tripeptide glutathione (GSH) within the cancer cells in vivo. Depletion of cellular GSH sensitizes tumours to chemotherapy and radiation, but the usefulness of this depletion depends on whether the levels of GSH can be reduced in the tumour relative to normal tissues. We report here that administration of ATP in combination with diethylmaleate and X-rays leads to complete regression of 95% of Ehrlich ascites tumours in mice. This shows that an aggressive tumour can be eliminated by using a therapy based on modulation of GSH levels in cancer cells.

MaleRadiation-Sensitizing AgentsGlutamate-Cysteine Ligasemedicine.medical_treatmentAntineoplastic AgentsTripeptideBiologyGeneral Biochemistry Genetics and Molecular BiologyMicechemistry.chemical_compoundAdenosine TriphosphateIn vivoMethionine SulfoximinemedicineAnimalsButhionine sulfoximineEnzyme InhibitorsCarcinoma Ehrlich TumorButhionine SulfoximineChemotherapyX-RaysMaleatesGeneral MedicineGlutathioneHydrogen-Ion ConcentrationCombined Modality TherapyGlutathionechemistryBiochemistryCancer cellCancer researchGrowth inhibitionAdenosine triphosphateCell DivisionNature Medicine
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Regulation of phospholipase D activity in synaptosomes permeabilized with Staphylococcus aureus alpha-toxin.

1998

In order to investigate the regulation of presynaptic phospholipase D (PLD) activity by calcium and G proteins, we established a permeabilization procedure for rat cortical synaptosomes using Staphylococcus aureus alpha-toxin (30-100 microg/ml). In permeabilized synaptosomes, PLD activity was significantly stimulated when the concentration of free calcium was increased from 0.1 microM to 1 microM. This activation was inhibited in the presence of KN-62 (1 microM), an inhibitor of calcium/calmodulin-dependent kinase II (CaMKII), but not by the protein kinase C inhibitor, Ro 31-8220 (1-10 microM). Synaptosomal PLD activity was also stimulated in the presence of 1 microM GTPgammaS. When Rho pro…

MaleStaphylococcus aureusCell Membrane PermeabilityG proteinBacterial ToxinsBiophysicschemistry.chemical_elementCalciumBiologyIn Vitro TechniquesBiochemistryClostridium difficile toxin Bchemistry.chemical_compoundHemolysin ProteinsStructural BiologyStaphylococcus aureus α-toxinCa2+/calmodulin-dependent protein kinaseSynaptosomeGeneticsPhospholipase DPhospholipase D activityAnimalsRats WistarMolecular BiologyProtein kinase CSynaptosomePhospholipase DRho proteinCalcium/calmodulin-dependent protein kinase IICell BiologyBrefeldin AMolecular biologyRatsEnzyme Activationenzymes and coenzymes (carbohydrates)BiochemistrychemistryGuanosine 5'-O-(3-Thiotriphosphate)lipids (amino acids peptides and proteins)CalciumSynaptosomesFEBS letters
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Effect of Thyroid Hormones on Urea Biosynthesis and Related Processes in Rat Liver*

1988

The results of the few studies on the effect of the thyroid status on nitrogen metabolism have been inconclusive and/or contradictory. In an attempt to elucidate this important relationship, we have studied the effect of experimental hypo- and hyperthyroidism on urea biosynthesis and related processes. We have found that the capacity of the liver to synthesize urea was increased in hypothyroid rats, as were the activities of the urea cycle enzymes; there were also changes in the activities of some related enzymes and in the levels of intermediates and amino acids. Isolated hepatocytes from these rats showed an increased capacity for urea synthesis. In hyperthyroid rats the picture was more …

MaleThyroid Hormonesendocrine systemmedicine.medical_specialtyendocrine system diseasesCarbamoyl-Phosphate Synthase (Ammonia)HyperthyroidismIodide PeroxidaseGlucagonchemistry.chemical_compoundEndocrinologyGlutamatesHypothyroidismBiosynthesisAmmoniaInternal medicineCyclic AMPmedicineAnimalsUreaAmino AcidsOrnithine Carbamoyltransferasechemistry.chemical_classificationCatabolismRats Inbred StrainsMetabolismGlucagonRatsAmino acidThyroxineEndocrinologymedicine.anatomical_structureLiverchemistryBiochemistryUrea cycleHepatocyteUreaTriiodothyroninehormones hormone substitutes and hormone antagonistsEndocrinology
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Dynamics of complement activation in aHUS and how to monitor eculizumab therapy.

2014

Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic complement abnormalities/anti–complement factor H antibodies, which paved the way to treatment with eculizumab. We studied 44 aHUS patients and their relatives to (1) test new assays of complement activation, (2) verify whether such abnormality occurs also in unaffected mutation carriers, and (3) search for a tool for eculizumab titration. An abnormal circulating complement profile (low C3, high C5a, or SC5b-9) was found in 47% to 64% of patients, irrespective of disease phase. Acute aHUS serum, but not serum from remission, caused wider C3 and C5b-9 deposits than control serum on unstimulated human microvascular endotheli…

MaleTime FactorsClinical Trials and ObservationsComplement Membrane Attack Complexurologic and male genital diseasesBiochemistryGlomerulonephritisInside BLOOD Commentaryhemic and lymphatic diseasesMembranoproliferative glomerulonephritisMonoclonalHumanizedComplement ActivationAtypical Hemolytic Uremic SyndromeEndothelial CellHematologyRemission Inductionfood and beveragesHematologyComplement C3Eculizumabmedicine.anatomical_structureFactor HFemalecomplementaHUS eculizumabmedicine.drugMembranoproliferativeHumanmedicine.medical_specialtyEndotheliumMonitoringTime FactorGlomerulonephritis MembranoproliferativeImmunologyBiologyAntibodies Monoclonal HumanizedAntibodiesInternal medicineAtypical hemolytic uremic syndromemedicineHumansPhysiologicMonitoring PhysiologicAdenosine Diphosphate RiboseEndothelial CellsCell Biologymedicine.diseaseComplement systemImmunologyAdenosine Diphosphate Ribose; Antibodies Monoclonal Humanized; Atypical Hemolytic Uremic Syndrome; Complement Activation; Complement C3; Complement Membrane Attack Complex; Endothelial Cells; Female; Glomerulonephritis Membranoproliferative; Hemolytic-Uremic Syndrome; Humans; Male; Remission Induction; Time Factors; Monitoring Physiologic; Hematology; Biochemistry; Cell Biology; ImmunologyHemolytic-Uremic SyndromeComplement membrane attack complexBlood
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Toxicological investigations in a fatal and non-fatal accident due to hydrogen sulphide (H2S)poisoning

2019

Hydrogen sulphide (H2S) is one of the most toxic natural gas and represents a not rare cause of fatal events in workplaces. We report here a serious accidental poisoning by hydrogen sulphide inhalation involving six sailors. Three of them died while the other three survived and were transported to the emergency room. No greenish discolouration of the body, that could be a feature of these type of deaths, was observed at autopsy. Given that blood and/or urine H2S detection does not allow to discriminate if it is related to inhalation or to putrefactive processes, the determination of thiosulphate, H2S main metabolite, is decisive. The succession of fatal events reported here can be rebuilt b…

MaleTime FactorsPoison controlAutopsyFatal accidentBrain EdemaUrine01 natural scienceschemistry.chemical_compound0302 clinical medicineThiosulfateHydrogen sulphideMedicineHydrogen SulfideThiosulfateAir PollutantsOccupational accidentInhalationFatal poisoningMiddle AgedPulmonary edemaFatal poisoning; Hydrogen sulphide; Non-fatal poisoning; Occupational accident; Thiosulphate; Administration Inhalation; Adult; Air Pollutants; Brain Edema; Emphysema; Humans; Hydrogen Sulfide; Hyperemia; Italy; Male; Middle Aged; Military Personnel; Pulmonary Edema; Thiosulfates; Time Factors; Accidents OccupationalOccupationalMilitary PersonnelInhalationItalyAir PollutantAnesthesiaAdministrationNon-fatal poisoningHumanAdultTime FactorThiosulphateThiosulfatesHyperemiaPulmonary EdemaHydrogen sulphidePathology and Forensic Medicine03 medical and health sciencesAdministration InhalationHumansAccidents Occupational030216 legal & forensic medicineEmphysemabusiness.industry010401 analytical chemistrymedicine.disease0104 chemical scienceschemistryAccidentsbusinessLaw
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In situ hybridization of dihydroxyacetone phosphate acyltransferase, the regulating enzyme involved in plasmalogen biosynthesis

2005

International audience; In situ hybridization can be carried out using different methods. The experimenter has to choose various parameters: the type of tissue fixation, the time of incubation, and the duration of the exposure time. All these parameters are determinant for the sensitivity and the resolution of this technique. This publication of technical aspects described different experiments performed for in situ hybridization on liver tissue. We may conclude on the parameters to optimize each step of the hybridization procedure. Moreover, this technique could be transposed to the brain and applied to little structures with a light expression of DHAP-AT.

MaleTime FactorsTissue FixationLIVERPlasmalogenIn situ hybridizationIn Vitro TechniquesBiologySensitivity and Specificity03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBiosynthesisLiver tissueAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerRats WistarBRAINMolecular Biology030304 developmental biologyDihydroxyacetone phosphateIN SITU HYBRIDIZATIONchemistry.chemical_classification0303 health sciencesBase SequenceReverse Transcriptase Polymerase Chain ReactionRatsMolecular hybridizationEnzymechemistryBiochemistryDIHYDROXYACETONE PHOSPHATE ACYLTRANSFERASEAcyltransferaseAcyltransferases030217 neurology & neurosurgeryPLASMALOGENSubcellular Fractions
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Transdermal iontophoresis of dexamethasone sodium phosphate in vitro and in vivo: effect of experimental parameters and skin type on drug stability a…

2010

The aim of this study was to investigate the cathodal iontophoresis of dexamethasone sodium phosphate (DEX-P) in vitro and in vivo and to determine the feasibility of delivering therapeutic amounts of the drug for the treatment of chemotherapy-induced emesis. Stability studies, performed to investigate the susceptibility of the phosphate ester linkage to hydrolysis, confirmed that conversion of DEX-P to dexamethasone (DEX) upon exposure to samples of human, porcine and rat dermis for 7 h was limited (82.2+/-0.4%, 72.5+/-4.8% and 78.6+/-6.0% remained intact) and did not point to any major inter-species differences. Iontophoretic transport of DEX-P across dermatomed porcine skin (0.75 mm thic…

MaleTime FactorsVomitingSwineSkin AbsorptionPharmaceutical ScienceAntineoplastic AgentsPharmacologyAdministration CutaneousHigh-performance liquid chromatographyDexamethasoneGlucocorticoids/administration & dosage/pharmacokineticsDexamethasone Sodium PhosphatePharmacokineticsDrug StabilitySpecies SpecificityIn vivoAnimalsHumansSkin/metabolismVomiting/chemically induced/prevention & controlRats WistarGlucocorticoidsTransdermalSkinddc:615IontophoresisDose-Response Relationship DrugChemistryHydrolysisGeneral MedicineAntineoplastic Agents/adverse effectsPermeationIontophoresisRatsDose–response relationshipDexamethasone/administration & dosage/analogs & derivatives/pharmacokineticsBiotechnologyNuclear chemistry
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