Search results for "FRAGMENTS"

showing 10 items of 422 documents

Cellular Prion Protein Participates in Amyloid-β Transcytosis across the Blood—Brain Barrier

2012

The blood—brain barrier (BBB) facilitates amyloid-β (Aβ) exchange between the blood and the brain. Here, we found that the cellular prion protein (PrPc), a putative receptor implicated in mediating Aβ neurotoxicity in Alzheimer's disease (AD), participates in Aβ transcytosis across the BBB. Using an in vitro BBB model, [125I]-Aβ1–40 transcytosis was reduced by genetic knockout of PrPc or after addition of a competing PrPc-specific antibody. Furthermore, we provide evidence that PrPc is expressed in endothelial cells and, that monomeric Aβ1–40 binds to PrPc. These observations provide new mechanistic insights into the role of PrPc in AD.

Amyloid βanimal diseasesBiologyBrief CommunicationBlood–brain barrierModels BiologicalMiceAlzheimer Diseasemental disordersmedicineAnimalsPrPC ProteinsPrion proteinReceptorCells CulturedAmyloid beta-PeptidesNeurotoxicitymedicine.diseaseMolecular biologyPeptide FragmentsIn vitronervous system diseasesCell biologymedicine.anatomical_structureNeurologyTranscytosisBlood-Brain BarrierGene Knockdown Techniquesbiology.proteinNeurology (clinical)AntibodyTranscytosisCardiology and Cardiovascular MedicineProtein BindingJournal of Cerebral Blood Flow & Metabolism
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The sea urchin embryo: a model to study Alzheimer's beta amyloid induced toxicity.

2009

Abstract Alzheimer’s disease (AD) is the most common form of dementia. The cause of AD is closely related to the accumulation of amyloid beta peptide in the neuritic plaques. The use of animal model systems represents a good strategy to elucidate the molecular mechanism behind the development of this pathology. Here we use the Paracentrotus lividus embryo to identify molecules and pathways that can be involved in the degenerative process. As a first step, we identified the presence of an antigen related to the human APP, called Pl APP. This antigen, after gastrula stage, is processed producing a polypeptide of about 10 kDa. By immunohistochemistry we localized the Pl APP antigen in some ser…

AmyloidAmyloid betaBiophysicsApoptosisBiochemistryNervous SystemParacentrotus lividusAlzheimer Diseasebiology.animalAnimalsHumansSenile plaquesAntigensMolecular BiologySea urchinCaspaseTUNEL assayAmyloid beta-Peptidesbiologybiology.organism_classificationPeptide FragmentsRecombinant ProteinsCell biologyBiochemistryApoptosisCaspasesModels Animalbiology.proteinParacentrotusParacentrotus lividusAmyloid-betaOligomers Fibrillar aggregatesApoptosisAnimal modelArchives of biochemistry and biophysics
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Structural analysis of copper(I) interaction with amyloid β peptide

2019

Abstract The N-terminal fragment of Aβ (β = beta) peptide is able to bind essential transition metal ions like, copper, zinc and iron. Metal binding usually occurs via the imidazole nitrogens of the three His residues which play a key role in the coordination chemistry. Among all the investigated systems, the interaction between copper and Amyloid β assume a biological relevance because of the interplay between the two copper oxidation states, Cu(II) and Cu(I), and their involvement in redox reactions. Both copper ions share the ability to bind Amyloid β. A huge number of investigations have demonstrated that Cu(II) anchors to the N-terminal amino and His6, His13/14 imidazole groups, while …

AmyloidSilverCoordination spherechemistry.chemical_elementPeptide010402 general chemistrySilver(I)01 natural sciencesBiochemistryRedoxCoordination complexInorganic ChemistryMetalchemistry.chemical_compoundCoordination ComplexesImidazoleHistidineAmino Acid SequenceHistidinechemistry.chemical_classificationAmyloid beta-Peptides010405 organic chemistryChemistryStructureCopperPeptide Fragments0104 chemical sciencesCrystallographyCoordinationvisual_artvisual_art.visual_art_mediumCopper(I)CopperProtein BindingJournal of Inorganic Biochemistry
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Angiotensin Receptor Neprilysin Inhibition Compared With Enalapril on the Risk of Clinical Progression in Surviving Patients With Heart Failure

2015

Background— Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. Methods and Results— We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of med…

Angiotensin receptorVascular damage Radboud Institute for Health Sciences [Radboudumc 16]receptorsTetrazolesheart failureAngiotensin-Converting Enzyme InhibitorsKaplan-Meier EstimateSacubitrilAngiotensin; Heart failure; Neprilysin; Receptors; Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; Double-Blind Method; Enalapril; Heart Failure; Humans; Kaplan-Meier Estimate; Natriuretic Peptide Brain; Neprilysin; Peptide Fragments; Risk Factors; Stroke Volume; Survivors; Tetrazoles; Treatment Outcome; Troponin; Disease Progression; Medicine (all); Cardiology and Cardiovascular Medicine; Physiology (medical)AngiotensinEnalaprilRisk FactorsEnalapril/therapeutic useNatriuretic Peptide BrainHeart Failure/bloodSurvivorsReceptorNeprilysinAminobutyrates: Systèmes cardiovasculaire & respiratoire [D03] [Sciences de la santé humaine]Troponin/bloodTroponinAngiotensin Receptor Antagonists/therapeutic useDrug CombinationsAngiotensin-Converting Enzyme Inhibitors/therapeutic useTreatment OutcomeTetrazoles/therapeutic useCardiologyDisease ProgressionValsartanNeprilysinHeart Failure/blood/drug therapy/physiopathologyCardiology and Cardiovascular Medicinemedicine.drugReceptormedicine.medical_specialtyHeart failureneprilysinAngiotensin Receptor Antagonistsreceptors angiotensinDouble-Blind MethodPhysiology (medical)Internal medicineRenin–angiotensin systemmedicineHumansheart failure neprilysin receptors angiotensinEnalaprilbusiness.industryBiphenyl CompoundsStroke Volumemedicine.diseasePeptide FragmentsEndocrinologyAminobutyrates/therapeutic useStroke Volume/physiologyHeart failureNatriuretic Peptide Brain/blood: Cardiovascular & respiratory systems [D03] [Human health sciences]businessNeprilysin/antagonists & inhibitorsPeptide Fragments/bloodSacubitril ValsartanBiomarkersBiomarkers/blood
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Identification of epitopes of Mycobacterium tuberculosis 16-kDa protein recognized by human leukocyte antigen-A*0201 CD8(+) T lymphocytes.

2002

CD8(+) T cells could make an important contribution to protection against tuberculosis (TB), but the antigenic determinants recognized in the context of major histocompatibility complex class I molecules remain ill defined. Our aim was to identify nonamer peptides derived from the acr/16-kDa antigen. Two immunogenic peptides (p21-29 and p120-128) were identified by their ability to elicit cytotoxic CD8(+) T cells from juvenile patients recovering from TB. Epitope-specific recognition was demonstrated by the lysis of both Mycobacterium tuberculosis-infected and peptide-pulsed macrophages, the release of cytotoxic granules, and interferon-gamma and tumor necrosis factor-alpha production. CD8(…

Antigens Differentiation T-LymphocyteCytotoxicity ImmunologicMalePore Forming Cytotoxic ProteinsT cellEpitopes T-LymphocyteHuman leukocyte antigenCD8-Positive T-LymphocytesMajor histocompatibility complexEpitopeInterferon-gammaImmune systemAntigenBacterial ProteinsHLA-A2 AntigenmedicineImmunology and AllergyCytotoxic T cellHumansChildTuberculosis PulmonaryMembrane GlycoproteinsbiologyHLA-A AntigensPerforinTumor Necrosis Factor-alphaMacrophagesMycobacterium tuberculosisFlow CytometryPeptide FragmentsMolecular WeightInfectious Diseasesmedicine.anatomical_structureImmunologybiology.proteinFemaleCD8The Journal of infectious diseases
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Efficacy and safety of bempedoic acid for the treatment of hypercholesterolemia: A systematic review and meta-analysis

2020

Background Bempedoic acid is a first-in-class lipid-lowering drug recommended by guidelines for the treatment of hypercholesterolemia. Our objective was to estimate its average effect on plasma lipids in humans and its safety profile. Methods and findings We carried out a systematic review and meta-analysis of phase II and III randomized controlled trials on bempedoic acid (PROSPERO: CRD42019129687). PubMed (Medline), Scopus, Google Scholar, and Web of Science databases were searched, with no language restriction, from inception to 5 August 2019. We included 10 RCTs (n = 3,788) comprising 26 arms (active arm [n = 2,460]; control arm [n = 1,328]). Effect sizes for changes in lipids and high-…

Apolipoprotein BPublication Ethics030204 cardiovascular system & hematologyCardiovascularGastroenterologyLipoprotein particleMedical and Health SciencesBiochemistrychemistry.chemical_compoundDatabase and Informatics Methods0302 clinical medicineMathematical and Statistical TechniquesAnticholesteremic Agents Apolipoproteins B Cholesterol Cholesterol LDL Clinical Trials Phase II as Topic Clinical Trials Phase III as Topic Dicarboxylic Acids Fatty Acids Humans Hypercholesterolemia Peptide Fragments Randomized Controlled Trials as TopicLipid and Blood Pressure Meta-Analysis Collaboration (LBPMC) Group and the International Lipid Expert PanelMedicine and Health SciencesDicarboxylic Acids030212 general & internal medicineDatabase SearchingResearch IntegrityRandomized Controlled Trials as Topicmedicine.diagnostic_testbiologyAnticholesteremic AgentsStatisticsFatty AcidsRDrugsGeneral MedicineMetaanalysisSerious Mental IllnessLipidsPhase III as TopicMental HealthCholesterolPhysical SciencesMedicineResearch Articlemedicine.medical_specialtyRMScience PolicyLipoproteinsHypercholesterolemiaBempedoic acid hypercholesterolemia lipid profile hsCRPResearch and Analysis MethodsLDL03 medical and health sciencesClinical Trials Phase II as TopicInternal medicineGeneral & Internal MedicinemedicineHumansClinical TrialsStatistical MethodsApolipoproteins BPharmacologyPlasma Proteinsbusiness.industryCholesterolPhase II as TopicStatinsBiology and Life SciencesProteinsOdds ratioCholesterol LDLConfidence intervalPeptide FragmentschemistryClinical Trials Phase III as Topicbiology.proteinUric acidCreatine kinaseLipid profilebusinessDigestive DiseasesMathematicsPLoS Medicine
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Amyloid-β toxicity and tau hyperphosphorylation are linked via RCAN1 in Alzheimer's disease.

2011

Amyloid-β peptide (Aβ) toxicity and tau hyperphosphorylation are hallmarks of Alzheimer’s disease (AD). How their molecular relationships may affect the etiology, progression, and severity of the disease, however, has not been elucidated. We now report that incubation of foetal rat cortical neurons with Aβ up-regulates expression of the Regulator of Calcineurin gene RCAN1, and this is mediated by Aβ-induced oxidative stress. Calcineurin (PPP3CA) is a serine-threonine phosphatase that dephosphorylates tau. RCAN1 proteins inhibit this phosphatase activity of calcineurin. Increased expression of RCAN1 also causes up-regulation of glycogen synthase kinase-3beta (GSK3β), a tau kinase. Thus, incr…

Apolipoprotein EAdultMuscle Proteinstau ProteinsBiologymedicine.disease_causeTransfectionArticleDephosphorylationGlycogen Synthase Kinase 3GSK-3Alzheimer DiseasemedicineAnimalsHumansLymphocytesPhosphorylationRNA Small InterferingGSK3BCells CulturedChromatography High Pressure LiquidRegulation of gene expressionCerebral CortexNeuronsAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaGeneral NeuroscienceCalcineurinIntracellular Signaling Peptides and ProteinsGeneral MedicineMiddle Agedmedicine.diseaseEmbryo MammalianMolecular biologyGlutathionePeptide FragmentsCell biologyRatsCalcineurinDNA-Binding ProteinsPsychiatry and Mental healthClinical PsychologyOxidative StressGene Expression RegulationFemaleGeriatrics and GerontologyAlzheimer's diseaseOxidative stressJournal of Alzheimer's disease : JAD
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Role for NK1 and NK2 receptors in the motor activity in mouse colon

2007

The present study examined the effects induced by endogenous and exogenous activation of NK(1) and NK(2) receptors on the mechanical activity of mouse proximal colon. Experiments were performed in vitro recording the changes in intraluminal pressure from isolated colonic segments. Electrical field stimulation in the presence of atropine and guanethidine produced a small relaxation, followed by nonadrenergic noncholinergic (NANC) contraction. SR140333, NK(1) receptor antagonist, or SR48968, NK(2) receptor antagonist, significantly reduced the contraction, although SR48968 appeared more efficacious. The co-administration of SR140333 and SR48968 virtually abolished the NANC contraction. [Sar(9…

AtropineAgonistmedicine.medical_specialtyContraction (grammar)Colonmedicine.drug_classNeurokinin AMuscarinic AntagonistsTetrodotoxinSubstance PSettore BIO/09 - FisiologiaNK1 receptorNitric oxideMicechemistry.chemical_compoundNeurokinin-1 Receptor Antagonistsnitric oxideInternal medicinemedicineAnimalsNK2 receptorReceptorGuanethidinePharmacologyAntagonistReceptors Neurokinin-2Receptors Neurokinin-1Electric StimulationPeptide FragmentsMice Inbred C57BLEndocrinologychemistryTetrodotoxinNANC contractionCholinergicTachykininMuscle ContractionSodium Channel Blockersmedicine.drugEuropean Journal of Pharmacology
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Endotoxin inhibits gastric emptying in rats via a capsaicin-sensitive afferent pathway.

2001

The effects of endotoxin on gastric emptying of a solid nutrient meal and the neural mechanisms involved in such a response were investigated in conscious rats. The intraperitoneal (i.p.) administration of E. coli endotoxin (40 mug/kg) significantly reduced the 4-h rate of gastric emptying of a standard solid nutrient meal. Ablation of primary afferent neurons by systemic administration of high doses of capsaicin (20+30+50 mg/kg s.c.) to adult rats did not modify the rate of gastric emptying in control animals but prevented the delay in gastric transit induced by endotoxin. Local application of capsaicin to the vagus nerve rather than application of capsaicin to the celiac ganglion signific…

AtropineLipopolysaccharidesMaleendotoxinmedicine.medical_specialtyCalcitonin Gene-Related PeptidePharmacology toxicologyMuscarinic AntagonistscapsaicinRats Sprague-Dawleychemistry.chemical_compoundgastric emptyingtransitNeurons EfferentCalcitonin Gene-Related Peptide Receptor AntagonistsInternal medicinemedicineAnimalsDrug InteractionsCGRPNeurons AfferenttachykininsPhentolamineAfferent PathwayAdrenergic alpha-AntagonistsPharmacologyMealAfferent PathwaysGastric emptyingdigestive oral and skin physiologyGeneral MedicinePeptide FragmentsRatsEndocrinologychemistryGastric EmptyingCapsaicinCapsaicinNaunyn-Schmiedeberg's archives of pharmacology
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On the opioid receptor subtype inhibiting the evoked release of 3H-noradrenaline from guinea-pig atria in vitro

1986

1. Guinea-pig isolated atria were incubated and loaded with 3H-(−)-noradrenaline. The intrinsic nerves were stimulated with trains of 5 or 35 field pulses (4 Hz), and the evoked efflux of 3H-noradrenaline and of total tritium was determined in the presence of atropine, corticosterone, desipramine, and phentolamine by liquid scintillation spectrometry. 2. Ethylketocyclazocine (1.4 nmol/l, IC50), MR 2033 (9.1 nmol/l), dynorphin A (1–13) (25 nmol/l, peptidase inhibitors present), etorphine (71 nmol/l), and [d-Ala2, d-Leu5]-enkephalin (>10 μmol/l, peptidase inhibitors present) inhibited the stimulation-evoked efflux of 3H-noradrenaline in a concentration-dependent manner, but not morphine up to…

Atropinemedicine.medical_specialtyEthylketocyclazocinemedicine.drug_classGuinea PigsPopulationEthylketocyclazocine(+)-NaloxoneIn Vitro TechniquesPharmacologyBinding CompetitiveDynorphinsNorepinephrinechemistry.chemical_compoundOpioid receptorInternal medicinemedicineAnimalsCyclazocineHeart AtriaPhentolamineeducationEndogenous opioidPharmacologyeducation.field_of_studyMorphineNaloxoneMyocardiumReceptors Opioid kappaDesipramineEtorphineDynorphin AGeneral MedicineEnkephalin Leucine-2-AlaninePeptide FragmentsBenzomorphansEndocrinologyEtorphineOpioidchemistryReceptors OpioidSynapsesCorticosteroneEnkephalin Leucinemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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