Search results for "Locke"

showing 10 items of 332 documents

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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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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AT1-receptor blockade by telmisartan upregulates GTP-cyclohydrolase I and protects eNOS in diabetic rats.

2008

Several enzymatic sources of reactive oxygen species (ROS) were described as potential reasons of eNOS uncoupling in diabetes mellitus. In the present study, we investigated the effects of AT1-receptor blockade with chronic telmisartan (25 mg/kg/day, 6.5 weeks) therapy on expression of the BH4-synthesizing enzyme GTP-cyclohydrolase I (GCH-I), eNOS uncoupling, and endothelial dysfunction in streptozotocin (STZ, 60 mg/kg iv, 7 weeks)-induced diabetes mellitus (type I). Telmisartan therapy did not modify blood glucose and body weight. Aortas from diabetic animals had vascular dysfunction as revealed by isometric tension studies (acetylcholine and nitroglycerin potency). Vascular and cardiac RO…

Blood GlucoseMalemedicine.medical_specialtyNitric Oxide Synthase Type IIImedicine.disease_causeBiochemistryBenzoatesReceptor Angiotensin Type 1chemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineDiabetes MellitusAnimalsTelmisartanEndothelial dysfunctionRats WistarXanthine oxidaseGTP CyclohydrolaseNADPH oxidasebiologySuperoxideBody WeightNADPH Oxidasesmedicine.diseaseStreptozotocinbiology.organism_classificationMitochondriaRatsUp-RegulationEnzyme ActivationOxidative StressEndocrinologychemistrybiology.proteinBenzimidazolesTelmisartanAngiotensin II Type 1 Receptor BlockersOxidative stressmedicine.drugFree radical biologymedicine
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MitoKATP-channel opener protects against neuronal death in rat venous ischemia.

2005

OBJECTIVE: Mitochondrial adenosine triphosphate-dependent potassium (mitoK ATP ) channels are present in the brain, and several reports have shown their neuroprotective, preconditioning effect against an ischemic insult. The role of mitoK ATP channels in the penumbra area has not been studied thoroughly. In a model of venous ischemia, widespread penumbra-like low flow areas are created, which are susceptible to cortical spreading depression. Thus, we studied effects of mitoK ATP channels on infarct size in this model. METHODS: Male Wistar rats were subjected to two-vein occlusion by photochemical thrombosis of two adjacent cortical veins combined with KCI-induced cortical spreading depressi…

Brain InfarctionMalemedicine.medical_specialtyPotassium ChannelsPhotochemistryIschemiaBrain EdemaPotassium ChlorideIschemiaInternal medicinemedicineDiazoxideLaser-Doppler FlowmetryAnimalsChannel blockerDrug InteractionsRats WistarNeuronsAnalysis of VarianceCell Deathbusiness.industryPenumbraCortical Spreading DepressionDiazoxidemedicine.diseaseCerebral VeinsPotassium channelRatsTolerance inductionDisease Models AnimalNeuroprotective AgentsCerebral blood flowRegional Blood FlowAnesthesiaCortical spreading depressionCardiologySurgeryNeurology (clinical)businessHydroxy AcidsAnti-Arrhythmia AgentsDecanoic Acidsmedicine.drugNeurosurgery
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Stability of charge-pump phase-locked loops : the hold-in and pull-in ranges

2020

The problem of design and analysis of synchronization control circuits is a challenging task for many applications: satellite navigation, digital communication, wireless networks, and others. In this article the Charge-Pump Phase-Locked Loop (CP-PLL) electronic circuit, which is used for frequency synthesis and clock generation in computer architectures, is studied. Analysis of CP-PLL is not trivial: full mathematical model, rigorous definitions, and analysis still remain open issues in many respects. This article is devoted to development of a mathematical model, taking into account engineering aspects of the circuit, interpretation of core engineering problems, definition in relation to m…

CP-PLLPFDcontrol of phase synchronizationsäätöteoriaphase-frequency detectorcharge-pumpsäätötekniikkaphase-locked loopselektroniset piiritnonlinear analysispull-in rangematemaattiset mallithold-in range
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Nonlinear Analysis of Charge-Pump Phase-Locked Loop : The Hold-In and Pull-In Ranges

2021

In this paper a fairly complete mathematical model of CP-PLL, which reliable enough to serve as a tool for credible analysis of dynamical properties of these circuits, is studied. We refine relevant mathematical definitions of the hold-in and pull-in ranges related to the local and global stability. Stability analysis of the steady state for the charge-pump phase locked loop is non-trivial: straight-forward linearization of available CP-PLL models may lead to incorrect conclusions, because the system is not smooth near the steady state and may experience overload. In this work necessary details for local stability analysis are presented and the hold-in range is computed. An upper estimate o…

CP-PLLvärähtelythidden oscillationsphase-locked loopsVCO overloadelektroniset piiritGardner conjecturecharge-pump PLLmatemaattiset mallit
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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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Excitotoxic Hippocampal Membrane Breakdown and its Inhibition by Bilobalide: Role of Chloride Fluxes

2003

We have previously shown that hypoxia and N-methyl-D-aspartate (NMDA) receptor activation induce breakdown of choline-containing phospholipids in rat hippocampus, a process which is mediated by calcium influx and phospholipase A (2) activation. Bilobalide, a constituent of Ginkgo biloba, inhibited this process in a potent manner (Weichel et al., Naunyn-Schmiedeberg's Arch. Pharmacol. 360, 609-615, 1999). In this study, we used fluorescence microscopy and radioactive flux measurements to show that bilobalide does not interfere with NMDA-induced calcium influx. Instead, bilobalide seems to inhibit NMDA-induced fluxes of chloride ions through ligand-operated chloride channels. In our experimen…

Calcium IsotopesMaleN-Methylaspartatemedicine.drug_classGlycineCyclopentanes44'-Diisothiocyanostilbene-22'-Disulfonic AcidIn Vitro TechniquesHippocampusChlorideCholinechemistry.chemical_compoundChloridesBilobalideFurosemideExcitatory Amino Acid AgonistsmedicineAnimalsCholineDrug InteractionsPharmacology (medical)Channel blockerRats WistarDiureticsFuransCell MembraneGeneral MedicineReceptor antagonistPyrrolidinonesRatsPsychiatry and Mental healthGinkgolidesnervous systemchemistryBiochemistryDIDSPotassiumChloride channelBiophysicsNMDA receptorCalciumDiterpenesDizocilpine MaleateExcitatory Amino Acid AntagonistsSynaptosomesmedicine.drugPharmacopsychiatry
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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