Search results for "beta"

showing 10 items of 3374 documents

P2‐220: Cholesterol and amyloid‐beta: Evidence for a cross‐talk between astrocytes and neuronal cells

2011

medicine.medical_specialtybiologyEpidemiologyAmyloid betaChemistryCholesterolHealth PolicyPsychiatry and Mental healthCellular and Molecular Neurosciencechemistry.chemical_compoundEndocrinologyDevelopmental NeuroscienceInternal medicinebiology.proteinmedicineNeurology (clinical)Geriatrics and GerontologyAlzheimer's & Dementia
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Enzyme replacement therapy in Fabry disease: Comparison of agalsidase alfa and agalsidase beta

2008

medicine.medical_specialtybusiness.industryEndocrinology Diabetes and MetabolismUrologyEnzyme replacement therapymedicine.diseaseBiochemistryFabry diseaseAGALSIDASE BETAEndocrinologyGeneticsmedicinebusinessMolecular BiologyAgalsidase alfaMolecular Genetics and Metabolism
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Survival and causes of death in 2,033 patients with non-transfusion-dependent β-thalassemia

2021

medicine.medical_specialtybusiness.industryThalassemiabeta-ThalassemiaMEDLINEHematologymedicine.diseaseInternal medicineCause of DeathTransfusion dependencemedicineHumansBlood TransfusionBlood Transfusion; Cause of Death; Humans; beta-ThalassemiabusinessLetters to the EditorHaematologica
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Hematopoietic Peripheral Circulating Blood Stem Cells As an Independent Marker of Good Transfusion Management in Patients with Beta-Thalassemia

2015

Abstract Aim Aim of the current study was to prospectively evaluate the potential role of peripheral circulating CD34+ stem cells as new independent marker of appropriate hemopoietic balance in patients with thalassemia major and intermedia. Materials and methods Peripheral blood samples from patients with thalassemia major (TM) and intermedia (TI) were drawn. Peripheral circulating CD34+ stem cells, CF-GEMM, CFU-GM and BFU-GM were assayed with monoclonal antibodies for CD34 and clonogenic tests, according to standard procedures and ISHAGE method (BD stem cell enumeration kit, Becton Dickinson; H4434, Stem Cell Technology). Demographic and clinical data were recorded from each enrolled subj…

medicine.medical_specialtybusiness.industryThalassemiamedicine.medical_treatmentImmunologySplenectomyCD34Becton dickinsonBeta thalassemiaCell BiologyHematologymedicine.diseaseBiochemistryGastroenterologyHaematopoiesisInternal medicineCirculating Hematopoietic stem cells beta-thalassemiatrasfusionmedicineStem cellClonogenic assaybusinessBlood
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Statins stimulate the production of a soluble form of the receptor for advanced glycation end products

2013

The beneficial effects of statin therapy in the reduction of cardiovascular pathogenesis, atherosclerosis, and diabetic complications are well known. The receptor for advanced glycation end products (RAGE) plays an important role in the progression of these diseases. In contrast, soluble forms of RAGE act as decoys for RAGE ligands and may prevent the development of RAGE-mediated disorders. Soluble forms of RAGE are either produced by alternative splicing [endogenous secretory RAGE (esRAGE)] or by proteolytic shedding mediated by metalloproteinases [shed RAGE (sRAGE)]. Therefore we analyzed whether statins influence the production of soluble RAGE. Lovastatin treatment of either mouse alveol…

medicine.medical_specialtyendocrine system diseasesADAM10Receptor for Advanced Glycation End ProductsBeta-CyclodextrinsQD415-436PharmacologyBiochemistryCell LineRAGE (receptor)MiceEndocrinologyGlycationInternal medicinediabetic complicationsmedicineAnimalsHumansSecretionLovastatincardiovascular diseasesReceptors ImmunologicReceptorResearch ArticlesDose-Response Relationship DrughypercholesterolemiaChemistrybeta-CyclodextrinsHEK 293 cellsTricarboxylic Acidsnutritional and metabolic diseasesCell BiologyBridged Bicyclo Compounds HeterocyclicADAM 10CholesterolFarnesyl-Diphosphate FarnesyltransferaseEndocrinologySolubilitycardiovascular systemLovastatinHydroxymethylglutaryl-CoA Reductase Inhibitorsatherosclerosishuman activitiesmedicine.drugJournal of Lipid Research
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Regulated Proteolysis of RAGE and AβPP as Possible Link Between Type 2 Diabetes Mellitus and Alzheimer's Disease

2009

Epidemiological studies have linked type 2 diabetes mellitus (T2DM) with an increased risk of developing Alzheimer's disease (AD). In T2DM, the elevated blood glucose level promotes formation of advanced glycation end products (AGEs). The receptor for AGEs (RAGE) is a type I membrane-protein and is also able to import amyloid-beta (Abeta) from the blood across the blood-brain-barrier into the brain. Oligomeric Abeta peptides disturb synaptic function in the brain and are believed to contribute to the development of AD. Abeta peptides are released from the amyloid-beta protein precursor (AbetaPP) after sequential proteolysis by beta- and gamma-secretases but alpha-secretase-mediated cleavage…

medicine.medical_specialtyendocrine system diseasesProteolysisReceptor for Advanced Glycation End ProductsAmyloid beta-Protein PrecursorAlzheimer DiseaseGlycationInternal medicinemental disordersmedicineAnimalsHumansReceptors ImmunologicProtein precursorProtein kinase AReceptorAmyloid beta-Peptidesmedicine.diagnostic_testChemistryGeneral Neurosciencenutritional and metabolic diseasesGeneral MedicinePsychiatry and Mental healthClinical PsychologyCholesterolEndocrinologyDiabetes Mellitus Type 2EctodomainPeptide transportAmyloid Precursor Protein SecretasesGeriatrics and GerontologySignal transductionJournal of Alzheimer's Disease
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Clinical and genetic update of corneal dystrophies.

2019

The International Committee for Classification of Corneal Dystrophies (IC3D) distinguishes between 22 distinct forms of corneal dystrophy which are predominantly autosomal dominant, although autosomal recessive and X-chromosomal dominant patterns do exist. Before any genetic examination, there should be documentation of a detailed corneal exam of as many affected and unaffected family members as possible, because detailed phenotypic description is essential for accurate diagnosis. Corneal documentation should be performed in direct and indirect illumination at the slit lamp with the pharmacologically dilated pupil. For the majority of the corneal dystrophies, a phenotype-genotype correlatio…

medicine.medical_specialtygenetic structuresGenetic ExaminationCorneal dystrophyCollagen Type ITransforming Growth Factor beta1Cellular and Molecular NeuroscienceCorneaOphthalmologyGenotypemedicineHumansGenetic Predisposition to DiseaseCorneal Dystrophies Hereditarybusiness.industryEpithelium Cornealmedicine.diseasePhenotypeeye diseasesSensory SystemsCollagen Type I alpha 1 ChainOphthalmologyEpithelial recurrent erosion dystrophymedicine.anatomical_structuresense organsDifferential diagnosisbusinessTGFBIExperimental eye research
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Renin-Angiotensin System Blockade and Mortality in Patients With Hypertension and COVID-19 Infection

2020

To determine the effect renin-angiotensin system blockers on the outcome in patients with hypertension and concurrent COVID-19 infection, we searched PubMed, the Cochrane Library, and Google Scholar for relevant articles. Twelve studies with a total of 16,101 patients met the inclusion criteria. The mortality rate among the users of angiotensin converting enzyme inhibitors or angiotensin receptor blockers was 12.15% and in non-users it was 14.56% (risk ratio 0.70, 95% CI [0.53-0.91], P < 0.007). There was no difference in the risk of death between the use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers (risk ratio 1.09, 95% CI [0.90 -1.32]). We conclude tha…

medicine.medical_specialtyhypertensionCoronavirus disease 2019 (COVID-19)PopulationPneumonia ViralAngiotensin-Converting Enzyme Inhibitors030204 cardiovascular system & hematologyCochrane LibraryGastroenterologyArticleRenin-Angiotensin System03 medical and health sciencesAngiotensin Receptor AntagonistsBetacoronavirus0302 clinical medicineInternal medicineRenin–angiotensin systemmedicineHumansPharmacology (medical)In patient030212 general & internal medicineeducationPandemicsPharmacologyeducation.field_of_studybiologybusiness.industrySARS-CoV-2Mortality rateCOVID-19Angiotensin-converting enzymerenin-angiotensin-aldosterone systemRelative riskbiology.proteinCardiology and Cardiovascular MedicinebusinessCoronavirus InfectionsAngiotensin II Type 1 Receptor BlockersJournal of Cardiovascular Pharmacology and Therapeutics
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α-secretase mediated conversion of the amyloid precursor protein derived membrane stub C99 to C83 limits Aβ generation

2009

The Swedish mutation within the amyloid precursor protein (APP) causes early-onset Alzheimer's disease due to increased cleavage of APP by BACE1. While beta-secretase shedding of Swedish APP (APPswe) largely results from an activity localized in the late secretory pathway, cleavage of wild-type APP occurs mainly in endocytic compartments. However, we show that liberation of Abeta from APPswe is still dependent on functional internalization from the cell surface. Inspite the unchanged overall beta-secretase cleaved soluble APP released from APP(swe) secretion, mutations of the APPswe internalization motif strongly reduced C99 levels and substantially decreased Abeta secretion. We point out t…

medicine.medical_specialtymedia_common.quotation_subjectEndocytic cycleCHO CellsTransfectionBiochemistryAmyloid beta-Protein PrecursorCellular and Molecular NeuroscienceCricetulusCricetinaeInternal medicinemental disordersmedicineAmyloid precursor proteinAnimalsHumansBiotinylationProtein Interaction Domains and MotifsSecretionInternalizationSecretory pathwaymedia_commonAmyloid beta-PeptidesbiologyChemistryP3 peptidePeptide FragmentsCell biologyEndocrinologyGene Expression RegulationAlpha secretaseMutationbiology.proteinAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseJournal of Neurochemistry
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Clinical pharmacokinetics of atenolol — A review

1982

Atenolol is a hydrophilic betareceptor blocking drug, which is predominantly eliminated via the kidneys, only about 5% of the atenolol is metabolised by the liver. After oral administration atenolol is incompletely absorbed from the intestine, so about 50% of the beta blocker are finally biovailable. In plasma only 3% of atenolol are protein-bound. There exists a linear relationship between the atenolol plasma levels and the degree of beta blocking effect measured by inhibition of the exercise-induced tachycardia. No correlation was found between plasma levels of atenolol and blood pressure lowering activity of the drug. After oral administration elimination half life of atenolol is calcula…

medicine.medical_specialtymedicine.drug_classAdministration OralBiological AvailabilityRenal functionPharmacologyKidneyIntestinal absorptionPropanolaminesPharmacokineticsRenal DialysisOral administrationInternal medicinemedicineHumansDrug InteractionsPharmacology (medical)cardiovascular diseasesBeta blockerPharmacologyChemistryLiver DiseasesKidney metabolismAtenololKineticsEndocrinologyAtenololIntestinal AbsorptionInjections IntravenousKidney DiseasesBiological half-lifecirculatory and respiratory physiologymedicine.drugEuropean Journal of Drug Metabolism and Pharmacokinetics
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