Search results for "blotting"

showing 10 items of 899 documents

Functionally active complement proteins C6 and C7 detected in C6- and C7-deficient individuals

1991

SUMMARYTwo sensitive sandwich ELISAs based on monoclonal antibodies directed to native C6 and C7 allowed the detection and quantitation of these complement proteins in 20 out of 37 serum samples from individuals who had previously been classified as deficient in these proteins as assessed by immunochemical and/or functional assays. Furthermore, serum from four C6-deficient and one combined C6-/C7-deficient individual showed an increase in the terminal complement complex (TCC) and a decrease in native C6 and C7 after complement activation as assayed by specific ELISAs. Despite their (incomplete) deficiencies, these individuals therefore possess functionally active terminal complement protein…

Blood Bactericidal Activitymedicine.drug_classImmunoblottingImmunologyEnzyme-Linked Immunosorbent AssayBiologyMonoclonal antibodyComplement Hemolytic Activity AssaySpecimen Handling03 medical and health sciences0302 clinical medicineTerminal complement complexImmunopathologymedicineHumansImmunology and AllergyComplement ActivationVolume concentration030304 developmental biology0303 health sciencesTemperatureZymosanAntibodies MonoclonalComplement deficiencyComplement C9Serum samplesmedicine.diseaseMolecular biologyComplement C7Complement C63. Good healthComplement (complexity)Complement systemImmunologyElectrophoresis Polyacrylamide GelResearch Article030215 immunologyClinical and Experimental Immunology
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Role of NO-synthases and cyclooxygenases in the hyperreactivity of male rabbit carotid artery to testosterone under experimental diabetes.

2009

Abstract Cardiovascular disease is the major cause of morbidity and mortality in diabetic patients, which in turn is also associated with low levels of serum testosterone. The working hypothesis was that diabetes might modify the mechanisms involved in the vascular actions of testosterone in isolated rabbit carotid arteries. Testosterone (10 −8 –3 × 10 −4  M) induced a concentration-dependent relaxation of precontracted carotid arteries, which was higher in diabetic than in control rabbits. In control rabbits neither endothelium removal nor the nitric oxide synthase (NOS) inhibitor N G -nitro- l -arginine ( l -NOArg, 10 −5  M) modified the relaxant action of testosterone, and the cyclooxyge…

Blood GlucoseCarotid Artery DiseasesMalemedicine.medical_specialtyArginineEndotheliumCharybdotoxinNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIVasodilationProstacyclinNitric OxideNitroarginineDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Internal medicinemedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsTestosteronePharmacologybiologyDose-Response Relationship Drugbusiness.industryTestosterone (patch)EpoprostenolNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureCarotid ArteriesApaminCyclooxygenase 2cardiovascular systembiology.proteinPotassiumCalciumCyclooxygenaseEndothelium VascularRabbitsbusinessDiabetic Angiopathiesmedicine.drugPharmacological research
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High pancreatic n-3 fatty acids prevent STZ-induced diabetes in fat-1 mice: inflammatory pathway inhibition.

2011

OBJECTIVE Because of confounding factors, the effects of dietary n-3 polyunsaturated fatty acids (PUFA) on type 1 diabetes remain to be clarified. We therefore evaluated whether fat-1 transgenic mice, a well-controlled experimental model endogenously synthesizing n-3 PUFA, were protected against streptozotocin (STZ)-induced diabetes. We then aimed to elucidate the in vivo response at the pancreatic level. RESEARCH DESIGN AND METHODS β-Cell destruction was produced by multiple low-doses STZ (MLD-STZ). Blood glucose level, plasma insulin level, and plasma lipid analysis were then performed. Pancreatic mRNA expression of cytokines, the monocyte chemoattractant protein, and GLUT2 were evaluate…

Blood GlucoseFatty Acid DesaturasesMalemedicine.medical_specialtyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentBlotting WesternMice TransgenicBiologyProinflammatory cytokineDiabetes Mellitus Experimentalchemistry.chemical_compoundMiceInternal medicineFatty Acids Omega-3Internal MedicinemedicineAnimalsInsulinCaenorhabditis elegans ProteinsUnsaturated fatty acidLipoxinReverse Transcriptase Polymerase Chain ReactionInsulinTranscription Factor RelAStreptozotocinImmunohistochemistryLipidsNitric oxide synthasemedicine.anatomical_structureEndocrinologyMetabolismchemistryHyperglycemiabiology.proteinGLUT2FemalePancreasmedicine.drugSignal TransductionDiabetes
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ERK1 and ERK2 activation modulates diet-induced obesity in mice

2017

IF 3.112; International audience; Obesity is a worldwide problem, and dietary lipids play an important role in its pathogenesis. Recently, Erk1 knock-out (ERK1(-/-)) mice have been shown to exhibit low preference for dietary fatty acids. Hence, we maintained Erk1(-/-) mice on a high-fat diet (HFD) to assess the implication of this mitogen-activated protein (MAP) kinase in obesity. The Erk1(-/-) mice, fed the HFD, were more obese than wild-type (WT) animals, fed the same diet. Erk1(-/-) obese mice gained more fat and liver mass than WT obese animals. No difference was observed in daily food and energy intake in HFD-fed both group of animals. However, feed efficiency was higher in Erk1(-/-) t…

Blood GlucoseMale0301 basic medicinemedicine.medical_treatmentMice ObeseBiochemistryMicechemistry.chemical_compoundPhosphorylationBeta oxidationCells CulturedMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionGeneral MedicineLipidsFatty acid synthaseLiverLipogenesisHomeostatic model assessmentmedicine.medical_specialtyBlotting WesternBiologyDiet High-FatReal-Time Polymerase Chain Reaction03 medical and health sciencesInsulin resistanceInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerObesity[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyInflammationTriglycerideLipogenesisInsulinBody WeightLipid Metabolismmedicine.diseaseObesityMice Inbred C57BL030104 developmental biologyEndocrinologychemistrybiology.proteinMAP kinaseInsulin ResistanceBiochimie
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Mechanisms involved in the relaxant action of testosterone in the renal artery from male normoglycemic and diabetic rabbits.

2009

Kidney disease is a frequent complication in diabetes, and significant differences have been reported between male and female patients. Our working hypothesis was that diabetes might modify the vascular actions of testosterone in isolated rabbit renal arteries and the mechanisms involved in these actions. Testosterone (10(-8) to 10(-4)M) induced relaxation of precontracted arteries, without significant differences between control and diabetic rabbits. Both in control and diabetic rabbits endothelium removal inhibited testosterone relaxant action. In arteries with endothelium, incubation with indomethacin (10(-5)M), N(G)-nitro-l-arginine (10(-5)M) or tetraethylammonium (10(-5)M) did not modi…

Blood GlucoseMalemedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIProstacyclinVasodilationNitroarginineMuscle Smooth VascularDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Renal ArteryEnosInternal medicinemedicine.arteryDiabetes mellitusmedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsProstaglandins ITestosteroneRenal arteryPharmacologybiologyDose-Response Relationship Drugbusiness.industryTetraethylammoniumTestosterone (patch)medicine.diseasebiology.organism_classificationVasodilationEndocrinologymedicine.anatomical_structureCyclooxygenase 2Cyclooxygenase 1PotassiumCalciumEndothelium VascularRabbitsbusinessmedicine.drugSignal TransductionPharmacological research
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Dual role of the p38 MAPK/cPLA2 pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists.

2013

p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influ…

Blood PlateletsCancer ResearchcPLA2p38 mitogen-activated protein kinasesImmunologyBlotting Westernp38 Mitogen-Activated Protein KinasesPiperazinesNitrophenolsCellular and Molecular NeurosciencePhospholipase A2Crotalid VenomsHumansLectins C-Typeddc:610Cells CulturedMembrane Potential MitochondrialplateletSulfonamidesbiologyKinaseGroup IV Phospholipases A2Biphenyl CompoundsapoptosisConvulxinCell BiologyFlow Cytometryp38 MAP kinaseCell biologyApoptosisMitogen-activated protein kinasebiology.proteinPhosphorylationOriginal ArticleSignal transductionReactive Oxygen SpeciesSignal TransductionCell deathdisease
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Amyloid precursor protein in platelets of patients with Alzheimer disease: effect of acetylcholinesterase inhibitor treatment.

2001

BACKGROUND:Amyloid precursor protein (APP) forms with apparent molecular weights of 130, 110, and 106 kd are present in human platelets. It has been demonstrated that Alzheimer disease (AD) is specifically associated with a decreased APP forms ratio in platelets. OBJECTIVE:To investigate whether acetylcholinesterase (AChE) inhibitor treatment modifies the ratio of platelet APP forms in patients with AD. PATIENTS AND METHODS:From a large sample of patients with probable AD, 30 with mild to moderate AD were selected. Each patient underwent a clinical evaluation including the Mini-Mental State Examination (MMSE) and platelet APP forms analysis at baseline and after 30 days. During this interva…

Blood PlateletsMalemedicine.medical_specialtyIsoformmedicine.drug_classBlotting WesternAlzheimer disease; biomarker; platelet; Amyloid Precursor Protein; Isoformchemistry.chemical_compoundAmyloid beta-Protein PrecursorArts and Humanities (miscellaneous)PiperidinesDonepezil HydrochlorideInternal medicinemental disordersAmyloid precursor proteinMedicineHumansPlateletDonepezilLongitudinal StudiesDonepezilCholinesteraseAgedamyloid alzheimer diseaseplateletbiologybusiness.industryMiddle AgedAcetylcholinesteraseEndocrinologychemistryAcetylcholinesterase inhibitorEnzyme inhibitorIndansAmyloid Precursor Proteinbiology.proteinbiomarkerSettore MED/26 - NeurologiaFemaleNeurology (clinical)Cholinesterase InhibitorsAlzheimer diseasebusinessmedicine.drugFollow-Up Studies
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Amelioration of spinal cord compressive injury by pharmacological preconditioning with erythropoietin and a nonerythropoietic erythropoietin derivati…

2006

Object Spinal cord injury (SCI) is a devastating clinical syndrome for which no truly efficacious therapy has yet been identified. In preclinical studies, erythropoietin (EPO) and its nonerythropoietic derivatives asialoEPO and carbamylated EPO have markedly improved functional outcome when administered after compressive SCI. However, an optimum treatment paradigm is currently unknown. Because the uninjured spinal cord expresses a high density of EPO receptor (EPOR) in the basal state, signaling through these existing receptors in advance of injury (pharmacological preconditioning) might confer neuroprotection and therefore be potentially useful in situations of anticipated damage. Methods…

Blotting WesternAsialoglycoproteinsPharmacologyNeuroprotectionCentral nervous system diseaseImmunoenzyme TechniquesRats Sprague-DawleySpinal cord compressionReceptors ErythropoietinMedicineAnimalsReceptorSpinal cord injuryErythropoietinSpinal Cord InjuriesAnalysis of Variancebusiness.industryGeneral MedicineSpinal cordmedicine.diseaseErythropoietin receptorRatsDisease Models Animalmedicine.anatomical_structureNeuroprotective AgentsErythropoietinImmunologybusinessmedicine.drugJournal of neurosurgery. Spine
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DNA methylation and histone acetylation of rat methionine adenosyltransferase 1A and 2A genes is tissue-specific.

2000

Methionine adenosyltransferase (MAT) catalyzes the biosynthesis of S-adenosylmethionine (AdoMet). In mammals MAT activity derives from two separate genes which display a tissue-specific pattern of expression. While MAT1A is expressed only in the adult liver, MAT2A is expressed in non-hepatic tissues. The mechanisms behind the selective expression of these two genes are not fully understood. In the present report we have evaluated MAT1A and MAT2A methylation in liver and in other tissues, such as kidney, by methylation-sensitive restriction enzyme digestion of genomic DNA. Our data indicate that MAT1A is hypomethylated in liver and hypermethylated in non-expressing tissues. The opposite situ…

Blotting WesternBiologyIn Vitro TechniquesKidneyBiochemistryHistonesHistone methylationAnimalsRats WistarEpigenomicsDNA methylationMyocardiumAnti-acetylated H4Kidney metabolismAcetylationCell BiologyMethylationMethionine AdenosyltransferaseDNA MethylationMolecular biologyRatsBlotting SouthernHistoneHistone acetylationLiverOrgan SpecificityMethionine AdenosyltransferaseHistone methyltransferaseDNA methylationbiology.proteinMethionine adenosyltransferaseGene expressionSpleenThe international journal of biochemistrycell biology
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Differentiative pathway activated by 3-aminobenzamide, an inhibitor of PARP, in human osteosarcoma MG-63 cells

2004

AbstractThis study describes the molecular mechanism by which treatment with 3-AB, a potent inhibitor of PARP, allows human osteosarcoma MG-63 cells to restrict growth and enter differentiation. Our findings show that in MG-63 cells, aberrant gene expression keeps Rb protein constitutively inactivated through hyperphosphorylation and this promotes uncontrolled proliferation of the cells. After 3-AB-treatment, the poly(ADP-ribosyl)ation of nuclear proteins markedly decreases and this results in an increase in both the hypophosphorylated active form of Rb and pRb/E2F complexes. These effects are accompanied by G1 arrest, downregulation of gene products required for proliferation (cyclin D1, β…

Blotting WesternBiophysicsHyperphosphorylationCell Cycle ProteinsPoly(ADP-ribose) Polymerase InhibitorsCell cycleRetinoblastoma ProteinBiochemistryPARPRb proteinCyclin D1Downregulation and upregulationStructural BiologyCell Line TumorGene expressionGeneticsHumansImmunoprecipitationOsteopontinEnzyme InhibitorsPhosphorylationE2FMolecular BiologyDNA PrimersAdenosine Diphosphate RiboseOsteosarcomaBase SequencebiologyReverse Transcriptase Polymerase Chain ReactionG1 PhaseCell DifferentiationCell BiologyCell cycleFlow Cytometry3-ABE2F Transcription FactorsChromatinDNA-Binding ProteinsGene Expression RegulationDifferentiationBenzamidesbiology.proteinCancer researchTranscription FactorsFEBS Letters
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