Search results for "beta"

showing 10 items of 3374 documents

Beta-adrenoceptor-mediated facilitation of endogenous noradrenaline release from rat isolated trachea.

1994

Overflow of endogenous noradrenaline from rat isolated trachea was evoked by electrical field stimulation (3 Hz, 540 pulses) in the presence of yohimbine, desipramine and tyrosine. Isoprenaline 100 nmol/l increased the evoked overflow of noradrenaline by about 65%. This effect was antagonized by propranolol (100 nmol/l) and the beta 2-selective adrenoceptor antagonist ICI 118,551 (100 nmol/l), but not by the beta 1-selective adrenoceptor antagonist CGP 20712 A (100 nmol/l). The beta 2-selective adrenoceptor agonist formoterol (1-100 nmol/l) also facilitated the evoked overflow of noradrenaline, but maximally by only about 25% at 10 nmol/l, i.e. formoterol behaved as a partial agonist at the…

medicine.medical_specialtyAdrenergic beta-AntagonistsIndomethacinAdrenergicPropranololIn Vitro TechniquesPartial agonistNorepinephrine (medication)Rats Sprague-DawleyNorepinephrineAdrenergic AgentsIsoprenalineInternal medicineReceptors Adrenergic betamedicineAnimalsPharmacologyChemistryAntagonistGeneral MedicineElectric StimulationYohimbineRatsTracheaEndocrinologycardiovascular systemFemaleFormoterolmedicine.drugSignal TransductionNaunyn-Schmiedeberg's archives of pharmacology
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Management of Blood Pressure and Heart Rate in Patients with Acute Stroke

2017

BACKGROUND: Stroke represent one of the most devastating of all neurological diseases, affecting about 15 million people per year and is an important cause of morbidity and mortality worldwide and currently the leading cause of adult disability in developed countries. Blood pressure and heart rate may undergo several modifications in patients with both ischemic and hemorrhagic stroke in fact raised blood pressure levels may lead to cerebral edema, hematoma expansion or hemorrhagic transformation and in contrast low blood pressure can lead to increased cerebral infarction or perihematomal ischemia. In addition, ECG abnormalities and cardiac arrhythmias, especially atrial fibrillation, are re…

medicine.medical_specialtyAdrenergic beta-AntagonistsIschemiaInfarctionBlood Pressureheart rate monitoringSudden death03 medical and health sciences0302 clinical medicineHeart RateInternal medicineDrug DiscoverymedicineHumansAcute strokehemorrhagic strokecardiovascular diseasesDiureticsStrokePharmacologyCerebral infarctionbusiness.industrymiocardial infarctionAtrial fibrillationmedicine.diseaseStrokeblood pressure modulationBlood pressure030220 oncology & carcinogenesisHeart failureAcute Diseaseperihematomal ischemiaCardiologybusiness030217 neurology & neurosurgeryCurrent Pharmaceutical Design
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OGT and OGA expression in postmenopausal skeletal muscle associates with hormone replacement therapy and muscle cross-sectional area

2013

Protein glycosylation via O-linked N-acetylglucosaminylation (O-GlcNAcylation) is an important post-translational regulatory mechanism mediated by O-GlcNAc transferase (OGT) and responsive to nutrients and stress. OGT attaches an O-GlcNAc moiety to proteins, while O-GlcNAcase (OGA) catalyzes O-GlcNAc removal. In skeletal muscle of experimental animals, prolonged increase in O-GlcNAcylation associates with age and muscle atrophy. Here we examined the effects of hormone replacement therapy (HRT) and power training (PT) on muscle OGT and OGA gene expression in postmenopausal women generally prone to age-related muscle weakness. In addition, the associations of OGT and OGA gene expressions with…

medicine.medical_specialtyAgingGlycosylationTime Factorsmedicine.drug_classPlyometric ExerciseBiologyta3111N-AcetylglucosaminyltransferasesBiochemistryGene Expression Regulation EnzymologicEndocrinologyDownregulation and upregulationInternal medicineGene expressionGeneticsmedicineHumansMuscle StrengthRNA Messengerta315Muscle SkeletalMolecular BiologyFinlandGlyceraldehyde 3-phosphate dehydrogenasePlyometric power trainingEstrogen Replacement Therapyta1182Age FactorsMuscle weaknessSkeletal muscleta3141Cell BiologyMiddle Agedbeta-N-AcetylhexosaminidasesMuscle atrophyPostmenopausePhenotypeTreatment OutcomeEndocrinologymedicine.anatomical_structureEstrogenbiology.proteinFemaleMuscle atrophymedicine.symptomProtein Processing Post-TranslationalMuscle ContractionMuscle contraction
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Effect of sodium bicarbonate and beta-alanine supplementation on maximal sprint swimming

2013

Background. This study examined the effect of simultaneous supplementation of extracellular buffer sodium bicarbonate (SB) and intracellular buffer beta-alanine (BA) on maximal sprint swimming. Methods. Thirteen competitive male swimmers completed 4 different treatments (placebo [PL], SB, BA + PL, and BA + SB) in a crossover procedure. PL or SB supplementation (0.3 g/kg body weight) was ingested 60 min before two maximal 100-m freestyle swims that were performed with a passive recovery of 12-min between each swim. Because of the known long washout period for carnosine, four weeks of BA supplementation (4.8 g per day) was started after the first week of PL or SB supplementation and performan…

medicine.medical_specialtyAlkalosisPassive recoverybeta-AlanineCarnosineErgogenic aidergogenic aidchemistry.chemical_compoundAnimal sciencemedicineBlood lactatealkaloosiSodium bicarbonateNutrition and Dieteticsbusiness.industryanaerobinen kuormitusergogeeninen apukeinoAlkalosismedicine.diseaseanaerobic exercisechemistrySprintAnaerobic exercisePhysical therapyalkalosisbufferbusinessAnaerobic exercisehuman activitiesBufferpuskuriResearch ArticleFood ScienceJournal of the International Society of Sports Nutrition
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Estradiol or genistein prevent Alzheimer's disease-associated inflammation correlating with an increase PPAR gamma expression in cultured astrocytes.

2009

Inflammation has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD). The main inflammatory players in AD are the glial cells which initiate the inflammatory response. One of the earliest neuropathological changes in AD is the accumulation of astrocytes at sites of A beta deposition. It is desirable to find methods of tipping the balance towards anti-inflammatory state. Estrogenic compounds have shown anti-inflammatory and also antioxidant activity. Astrocytes were pretreated with 17-beta estradiol or with genistein, and 48 h later treated with 5 microM amyloid beta (A beta) for 24 h. We found that A beta induces inflammatory mediators, such as cyclooxygenase 2 (…

medicine.medical_specialtyAmyloid betaInterleukin-1betaGenisteinPeroxisome proliferator-activated receptorNitric Oxide Synthase Type IIInflammationEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsMolecular BiologyProtein Kinase InhibitorsCells Culturedchemistry.chemical_classificationCerebral CortexAmyloid beta-PeptidesbiologyDose-Response Relationship DrugEstradiolTumor Necrosis Factor-alphaGeneral NeuroscienceInterleukinEstrogensGenisteinPeptide FragmentsRatsPPAR gammaEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationCyclooxygenase 2Astrocytesbiology.proteinNeurogliaTumor necrosis factor alphaNeurology (clinical)medicine.symptomDevelopmental BiologyAstrocyteBrain research
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Analysis of molecular mechanisms and anti-tumoural effects of zoledronic acid in breast cancer cells

2012

Zoledronic acid (ZOL) is the most potent nitrogen-containing bisphosphonate (N-BPs) that strongly binds to bone mineral and acts as a powerful inhibitor of bone resorption, already clinically available for the treatment of patients with osteolytic metastases. Recent data also suggest that ZOL, used in breast cancer, may provide more than just supportive care modifying the course of the disease, though the possible molecular mechanism of action is still unclear. As breast cancer is one of the primary tumours with high propensity to metastasize to the bone, we investigated, for the first time, differential gene expression profile on Michigan Cancer Foundation-7 (MCF-7) breast cancer cells tre…

medicine.medical_specialtyAngiogenesismedicine.medical_treatmentBlotting WesternAngiogenesis InhibitorsAntineoplastic AgentsBreast NeoplasmsBiologyReal-Time Polymerase Chain ReactionZoledronic AcidZOL FN1 TGF-b1 THBS-1 invasion breast cancerBone resorptionThrombospondin 1Transforming Growth Factor beta1breast cancerBreast cancerTGF-β1Internal medicineThrombospondin 1medicineHumansBone ResorptionCell ProliferationMatrigelDiphosphonatesFN1Gene Expression ProfilingImidazolesCancerOriginal ArticlesCell BiologyZOLBisphosphonateMicroarray Analysisinvasionmedicine.diseaseFibronectinsUp-RegulationGene Expression Regulation NeoplasticEndocrinologyZoledronic acidTHBS-1MCF-7 CellsCancer researchMolecular MedicineFemalemedicine.drug
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Oxidative stress and endothelial dysfunction: therapeutic implications.

2011

In a previous issue of Annals of Medicine, we presented evidence in support of the concept that an abnormally increased production of reactive oxygen species plays a central role in the genesis and progression of cardiovascular disease. While a number of preclinical lines of evidence support this concept, and despite the results of many studies suggesting a beneficial impact of antioxidant drugs on endothelial function, large clinical trials have failed to demonstrate a benefit of antioxidants on cardiovascular outcomes. Studies exploring the possibility that classical antioxidants such as vitamin C, vitamin E, selenium, or folic acid may improve the prognosis of patients with cardiac disea…

medicine.medical_specialtyAntioxidantEndotheliummedicine.medical_treatmentAdrenergic beta-AntagonistsAngiotensin-Converting Enzyme InhibitorsDiseaseBioinformaticsmedicine.disease_causeNitric OxideAntioxidantsInternal medicinemedicineHumansEndothelial dysfunctionVitamin Cbusiness.industryVitamin EGeneral Medicinemedicine.diseaseClinical trialOxidative StressEndocrinologymedicine.anatomical_structureCardiovascular DiseasesEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersOxidative stressAnnals of medicine
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Control of murine hair follicle regression (catagen) by TGF‐β1in vivo

2000

The regression phase of the hair cycle (catagen) is an apoptosis-driven process accompanied by terminal differentiation, proteolysis, and matrix remodeling. As an inhibitor of keratinocyte proliferation and inductor of keratinocyte apoptosis, transforming growth factor beta1 (TGF-beta1) has been proposed to play an important role in catagen regulation. This is suggested, for example, by maximal expression of TGF-beta1 and its receptors during late anagen and the onset of catagen of the hair cycle. We examined the potential involvement of TGF-beta1 in catagen control. We compared the first spontaneous entry of hair follicles into catagen between TGF-beta1 null mice and age-matched wild-type …

medicine.medical_specialtyApoptosisBiochemistryAndrologyMiceTransforming Growth Factor betaHair cycleInternal medicineIn Situ Nick-End LabelingGeneticsmedicineAnimalsHumansMolecular BiologyhirsutismMice KnockoutTUNEL assayintegumentary systembiologyChemistryTransforming growth factor betamedicine.diseaseHair follicleMice Inbred C57BLbody regionsmedicine.anatomical_structureEndocrinologybiology.proteinHuman hair growthKeratinocyteHair FollicleCell DivisionBiotechnologyTransforming growth factorThe FASEB Journal
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PPAR in Cardiovascular Disorders

2016

Peroxisome proliferation-activated receptors (PPARs) are ligand-inducible transcription factors that, upon binding their ligands, translocate into the nucleus, where they regulate transcription of numerous genes that have the peroxisome proliferator response element (PPRE) in the promoter region [1]. In humans, there are 3 PPAR isoforms: PPAR-α, PPAR-β/δ, and PPAR-γ. The isoforms have partially overlapping spectra of activity and are differently expressed in organs and tissues [2]. PPAR-α is expressed mostly in tissues characterized by high catabolic activity, including skeletal muscle, liver, proximal tubular cells in kidneys, and brown fat. This PPAR isoform regulates components of β-oxid…

medicine.medical_specialtyArticle SubjectPeroxisome proliferator-activated receptor030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationInternal medicineDrug DiscoverymedicineGlucose homeostasisPharmacology (medical)Beta oxidationlcsh:QH301-705.5chemistry.chemical_classificationFatty acid metabolismLipid metabolismPeroxisomeEndocrinologyEditorialchemistrylcsh:Biology (General)Rosiglitazonemedicine.drugPPAR Research
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Physical exercise neuroprotects ovariectomized 3xTg-AD mice through BDNF mechanisms.

2014

Postmenopausal women may be more vulnerable to cognitive loss and Alzheimer's disease (AD) than premenopausal women because of their deficiency in estrogens, in addition to their usually older age. Aerobic physical exercise has been proposed as a therapeutic approach for maintaining health and well-being in postmenopausal women, and for improving brain health and plasticity in populations at high risk for AD. To study the neuroprotective mechanisms of physical exercise in a postmenopausal animal model, we submitted previously ovariectomized, six-month old non-transgenic and 3xTg-AD mice to three months of voluntary exercise in a running wheel. At nine months of age, we observed lower grip s…

medicine.medical_specialtyBehavioral testsEndocrinology Diabetes and MetabolismOvariectomyP-CREBPhysical exerciseMice Transgenictau ProteinsCREBNeuroprotectionGrip strengthAmyloid beta-Protein PrecursorMiceEndocrinologyCognitionAlzheimer DiseaseInternal medicinePhysical Conditioning AnimalNeuroplasticitymedicinePresenilin-1DementiaAnimalsApathy3xTg-AD miceBiological PsychiatryNeuronsFrailtybiologyEndocrine and Autonomic SystemsBrain-Derived Neurotrophic FactorPhysical exerciseAlzheimer's diseaseCatalasemedicine.diseaseMice Inbred C57BLPsychiatry and Mental healthDisease Models AnimalBDNFEndocrinologyNeuroprotective AgentsCytoprotectionbiology.proteinOvariectomized ratFemalemedicine.symptomPsychologySignal TransductionPsychoneuroendocrinology
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