Search results for "ACID"

showing 10 items of 13107 documents

Inhibition of intracellular Ca2+ release by a Rho-kinase inhibitor for the treatment of ischemic damage in primary cultured rat hippocampal neurons.

2008

The effects of hydroxy fasudil, a specific Rho-kinase inhibitor, on behavior and brain neuronal activity in animal studies have been described previously. However, whether a Rho-kinase inhibitor can directly protect neurons against ischemic damage and the molecular mechanisms underlying these effects are poorly understood. The present work was designed to investigate the effect of hydroxy fasudil against oxygen-glucose deprivation (OGD) induced acute neuronal injury and the underlying mechanisms in vitro. Pretreatment with hydroxy fasudil at 5 and 10 microM could concentration-dependently improve cell viability and decrease Lactate dehydrogenase (LDH) level in extracellular solution of neur…

medicine.medical_specialtyExcitotoxicityIntracellular SpaceGlutamic AcidBiologymedicine.disease_causeNeuroprotectionHippocampusCalcium in biologyPotassium ChlorideRats Sprague-DawleyCalcium imagingAdenosine TriphosphateIschemiaInternal medicine1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinemedicineAnimalsHypoxiaProtein Kinase InhibitorsCells CulturedPharmacologyNeuronsrho-Associated KinasesDose-Response Relationship DrugCalcium channelFasudilGlutamate receptorRatsEndocrinologyGlucoseRho kinase inhibitorCalciumEuropean journal of pharmacology
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Hipercolesterolemia familiar homocigota: adaptación a España del documento de posición del grupo de consenso sobre hipercolesterolemia familiar de la…

2015

Homozygous familial hypercholesterolaemia (HoFH) is a rare life-threatening disease characterized by markedly elevated circulating levels of low-density lipoprotein cholesterol (LDL-C) and accelerated, premature atherosclerotic cardiovascular disease (ACVD). The Consensus Panel on Familial Hypercholesterolaemia of the European Atherosclerosis Society (EAS) has recently published a clinical guide to diagnose and manage HoFH (Eur Heart J. 2014;35:2146-57). Both the Spanish Society of Atherosclerosis (SEA) and Familial Hypercholesterolaemia Foundation (FHF) consider this European Consensus document of great value and utility. However, there are particularities in our country which advise to ha…

medicine.medical_specialtyEzetimibeHomozygous familial hypercholesterolaemiaDiagnosisMedicinePharmacology (medical)Lipoprotein cholesterolNational healthEzetimibabusiness.industryAtherosclerotic cardiovascular diseaseDiagnósticoAféresisStatinsHipercolesterolemia familiar homocigotaLomitapidaEzetimibeLomitapidePatient managementLDL apheresisFamily medicineEuropean atherosclerosis societylipids (amino acids peptides and proteins)ApheresisCardiology and Cardiovascular MedicinebusinessEstatinasmedicine.drug
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Farber disease (acid ceramidase deficiency) epidemiology: literature review and patient cohort data indicate moderate and attenuated phenotypes are l…

2017

medicine.medical_specialtyFarber diseasePathologybusiness.industryEndocrinology Diabetes and Metabolismmedicine.diseaseBiochemistryPhenotypeAcid Ceramidase Deficiency03 medical and health sciences0302 clinical medicineEndocrinology030220 oncology & carcinogenesisInternal medicineCohortEpidemiologyGeneticsMedicinebusinessMolecular Biology030217 neurology & neurosurgeryMedical literatureMolecular Genetics and Metabolism
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Potential involvement of fas and its ligand in the pathogenesis of Hashimoto's thyroiditis

1997

The mechanisms responsible for thyrocyte destruction in Hashimoto's thyroiditis (HT) are poorly understood. Thyrocytes from HT glands, but not from nonautoimmune thyroids, expressed Fas. Interleukin-1β (IL-1β), abundantly produced in HT glands, induced Fas expression in normal thyrocytes, and cross-linking of Fas resulted in massive thyrocyte apoptosis. The ligand for Fas (FasL) was shown to be constitutively expressed both in normal and HT thyrocytes and was able to kill Fas-sensitive targets. Exposure to IL-1β induced thyrocyte apoptosis, which was prevented by antibodies that block Fas, suggesting that IL-1β-induced Fas expression serves as a limiting factor for thyrocyte destruction. Th…

medicine.medical_specialtyFas Ligand Proteinmedicine.medical_treatmentThyroid GlandApoptosisPolymerase Chain ReactionThyroiditisFas ligandPathogenesisImmunoenzyme TechniquesInternal medicinemedicineTumor Cells CulturedHumansRNA Messengerfas ReceptorCells CulturedNucleic Acid Synthesis InhibitorsProtein Synthesis InhibitorsMultidisciplinaryMembrane GlycoproteinsChemistryThyroidThyroiditis AutoimmuneInterleukinAntibodies Monoclonalmedicine.diseaseFas receptorRecombinant ProteinsCytokinemedicine.anatomical_structureEndocrinologyApoptosisCytokinesInterleukin-1
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Efficacy, safety and tolerability of combined low-dose simvastatin-fenofibrate treatment in primary mixed hyperlipidaemia.

2007

In order to assess the long-term (12 months) efficacy and safety of fenofibrate administered with simvastatin in the treatment of primary mixed hyperlipidaemia, we conducted a study that compared increasing dosages of these drugs in subgroups of men and women belonging to a clinical sample of outpatients. This was an open study carried out in patients with primary mixed hyperlipidaemia (lipoprotein phenotype IIb) who needed a combined therapeutic approach because of their poor response to a single-drug regimen with an HMG-CoA reductase inhibitor (simvastatin). Thus, a fibrate (fenofibrate) was added to the therapy. The study lasted 12 months. Forty-five patients (mean age: 58.9 ± 11.3 years…

medicine.medical_specialtyFenofibrateDosemedicine.drug_classbusiness.industrynutritional and metabolic diseasesGeneral MedicineFibratePharmacologyGastroenterologyDiscontinuationRegimenTolerabilitySimvastatinInternal medicinemedicinelipids (amino acids peptides and proteins)Pharmacology (medical)Adverse effectbusinessmedicine.drugClinical drug investigation
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Fibratos: efectos farmacológicos

2012

Fibrates have demonstrated efficacy in modifying the various parameters of atherogenic dyslipidemia. The best known fibrate is fenofibrate, which is indicated for the treatment of hypertriglyceridemia with or without low high-density lipoprotein cholesterol (HDL-c) and the treatment of atherogenic dyslipidemia in patients with statin intolerance or contraindications. Fenofibrate is also indicated in association with statins in patients with high cardiovascular risk when HDL-c and triglyceride (TG) concentrations are poorly controlled. The lipid-lowering effects of fenofibrate are mediated by activation of the nuclear transcription factor PPARα, which leads to an increase of lipolysis and pl…

medicine.medical_specialtyFenofibrateStatinTriglyceridebusiness.industrymedicine.drug_classCholesterolHypertriglyceridemiaFibratePharmacologymedicine.diseaseTransaminasechemistry.chemical_compoundEndocrinologychemistryInternal medicinemedicineLipolysislipids (amino acids peptides and proteins)Pharmacology (medical)Cardiology and Cardiovascular Medicinebusinessmedicine.drugClínica e Investigación en Arteriosclerosis
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Histometric investigations of placental villi in cases of unexpected fetal acidosis.

1994

It is not unusual that, after an apparently uneventful pregnancy and birth, postpartal analysis of fetal blood unexpectedly reveals the presence of peripartal acidosis, a finding that is inexplicable on the basis of routine observation of the placenta. Using computer-assisted histometric procedures, it is possible to make a quantitative assessment with respect to the maturity and differentiation of villi, thus casting light on the functional anatomy of these structures. 89 single-birth pregnancies were grouped in accordance to the pH of blood in the umbilical artery (pre-acidosis, acidosis, non acidotic). In acidotic newborns, there is an absolute reduction in the surface area of the placen…

medicine.medical_specialtyFetal acidosisPlacentaPhysiologyPathogenesisFetal Organ MaturityPregnancyInternal medicinePlacentamedicine.arterymedicineHumansDiagnosis Computer-AssistedMaternal-Fetal ExchangeAcidosisFetusPregnancybusiness.industryHistological TechniquesInfant NewbornObstetrics and GynecologyUmbilical arterymedicine.diseaseFetal Diseasesmedicine.anatomical_structureEndocrinologyPediatrics Perinatology and Child HealthChorionic villiFemalemedicine.symptomChorionic VillibusinessAcidosisJournal of perinatal medicine
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Fracture incidence and characterization in patients on osteoporosis treatment: The ICARO study

2006

None of the available osteoporosis therapies have been shown to completely abolish the risk of fractures. In clinical practice, the outcome may be even poorer. In 880 patients prescribed with antiresorptives (alendronate, risedronate, and raloxifene) for >1 year, a fragility fracture was recorded in 8.9%/year of them. This incidence is considerably higher than that observed in randomized clinical trials, and it was significantly related to poor compliance and lack of supplementation with calcium and vitamin D. Introduction: Osteoporotic fracture is one of the most important public health concerns among the elderly. Currently available therapies have been shown to significantly decrease the …

medicine.medical_specialtyFracture riskEndocrinology Diabetes and MetabolismOsteoporosisIncidence; FRACTURETreatment resistancelaw.inventionCalcium and vitamin D intake Fracture risk Osteoporosis Treatment compliance Treatment resistancecalcium and vitamin d intake; fracture risk; osteoporosis; treatment compliance; treatment resistanceFractures BoneRandomized controlled trialRisk FactorslawInternal medicineCalcium and vitamin D intakemedicineVitamin D and neurologyHumansOrthopedics and Sports MedicineRaloxifeneVitamin DAgedRetrospective StudiesAlendronateBone Density Conservation Agentsbusiness.industryIncidenceIncidence (epidemiology)Etidronic AcidRetrospective cohort studyMiddle Agedmedicine.diseaseCalcium and vitamin D intake Fracture incidence Fracture risk Osteoporosis Treatment compliance Treatment resistanceFRACTUREFracture incidenceSurgeryItalyRaloxifene HydrochlorideRisedronic acidOsteoporosisFemaleObservational studyTreatment compliancebusinessRisedronic Acidmedicine.drug
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Prooxidative toxicity and selenoprotein suppression by cerivastatin in muscle cells

2012

Statins are the most widely used drugs for the treatment of hypercholesterolemia. In spite of their overall favorable safety profile, they do possess serious myotoxic potential, whose molecular origin has remained equivocal. Here, we demonstrate in cultivated myoblasts and skeletal muscle cells that cerivastatin at nanomolar concentrations interferes with selenoprotein synthesis and evokes a heightened vulnerability of the cells toward oxidative stressors. A correspondingly increased vulnerability was found with atorvastatin, albeit at higher concentrations than with cerivastatin. In selenium-saturated cells, cerivastatin caused a largely indiscriminate suppression of selenoprotein biosynth…

medicine.medical_specialtyGPX1Cell SurvivalPyridinesMevalonic AcidMevalonic acidBiologyToxicologyCell LineMyoblastsMiceSeleniumchemistry.chemical_compoundInternal medicineAtorvastatinmedicineAnimalsMyocytePyrrolesSelenoproteinseducationchemistry.chemical_classificationeducation.field_of_studySelenoprotein NEbselenSkeletal muscleCerivastatinHydrogen PeroxideGeneral MedicineRatsOxidative StressEndocrinologymedicine.anatomical_structureGene Expression RegulationchemistryHeptanoic AcidsSelenoproteinHydroxymethylglutaryl-CoA Reductase Inhibitorsmedicine.drugToxicology Letters
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Statin-Induced Liver Injury Involves Cross-Talk between Cholesterol and Selenoprotein Biosynthetic Pathways

2009

Statins have become the mainstay of hypercholesterolemia treatment. Despite a seemingly clear rationale behind their use, the inhibition of HMG-CoA reductase, these compounds have been shown to elicit a variety of unanticipated and elusive effects and side effects in vivo. Among the most frequently noted side effects of statin treatment are elevations in liver enzymes. Here, we report our finding that atorvastatin, cerivastatin, and lovastatin at clinically common concentrations induce a selective, differential loss of selenoprotein expression in cultured human HepG2 hepatocytes. The primarily affected selenoprotein was glutathione peroxidase (GPx), whose biosynthesis, steady-state expressi…

medicine.medical_specialtyGPX1Thioredoxin-Disulfide ReductaseStatinPyridinesmedicine.drug_classAtorvastatinBiologyGPX4tert-ButylhydroperoxideCell Line TumorInternal medicineAtorvastatinmedicineHumansPyrrolesLovastatinSelenoproteinsPharmacologychemistry.chemical_classificationGlutathione Peroxidaseintegumentary systemCytotoxinsGlutathione peroxidaseCerivastatinIsoenzymesCholesterolEndocrinologychemistryHeptanoic AcidsHepatocytesMolecular MedicineLovastatinSelenoproteinHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesSignal Transductionmedicine.drugMolecular Pharmacology
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