Search results for " STRESS"

showing 10 items of 3936 documents

Circulating miR-130a, miR-27b, and miR-210 in Patients With Peripheral Artery Disease and Their Potential Relationship With Oxidative Stress: A Pilot…

2016

Some emerging risk factors such as oxidative stress biomarkers and microRNAs (miRs) may add additional value to the established risk factors for peripheral artery disease (PAD). We enrolled 27 patients with PAD and 27 age-matched controls. We examined the levels of a series of miRs (miR-130a, miR-27b, and miR-210) in serum samples. The level of well-established oxidative stress biomarkers, such as lipid hydroperoxides, isoprostanes, hemeoxygenase-1 (HO-1) and reduced glutathione, was also measured in plasma and their relationship with the miRs was determined. Levels of miR-130a, miR-27b, and miR-210 were significantly increased in patients with PAD when compared to the controls. The level …

0301 basic medicineOncologyMalemedicine.medical_specialtyLipid PeroxidesStatistics as TopicPilot ProjectsDisease030204 cardiovascular system & hematologyIsoprostanesmedicine.disease_cause03 medical and health scienceschemistry.chemical_compoundPeripheral Arterial Disease0302 clinical medicineIsoprostaneRisk FactorsInternal medicinemicroRNAmedicineHumansPilot ProjectIn patientAgedoxidative streHeme OxygenasemicroRNALipid Peroxidebusiness.industryRisk FactorBiomarkerGlutathioneMiddle AgedGlutathioneHeme oxygenaseMicroRNAsOxidative Stress030104 developmental biologychemistryBiomarker (medicine)FemaleCardiology and Cardiovascular MedicinebusinessBody mass indexOxidative stressBiomarkersHeme Oxygenase-1Human
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Oxidative signature of cerebrospinal fluid from mild cognitive impairment and Alzheimer disease patients

2015

Abstract Background Several studies suggest that pathological changes in Alzheimer’s disease (AD) brain begin around 10–20 years before the onset of cognitive impairment. Biomarkers that can support early diagnosis and predict development of dementia would, therefore, be crucial for patient care and evaluation of drug efficacy. Although cerebrospinal fluid (CSF) levels of Aβ42, tau, and p-tau are well-established diagnostic biomarkers of AD, there is an urgent need to identify additional molecular alterations of neuronal function that can be evaluated at the systemic level. Objectives This study was focused on the analysis of oxidative stress-related modifications of the CSF proteome, from …

0301 basic medicineOncologyPathologyDiseasephysiology (medical)medicine.disease_causeProtein oxidationtau proteins0302 clinical medicineCerebrospinal fluidmiddle aged80 and overoxidative stresshumansAged 80 and overamyloid beta-peptidesredox proteomicsagedfemale030220 oncology & carcinogenesisBiomarker (medicine)Alzheimer's diseaseAlzheimer diseaseAPOEmedicine.medical_specialtyoxidation-reductionproteomeCSFmolecular sequence data03 medical and health sciencesmalecognitive dysfunctionInternal medicinemental disordersmedicineDementiabiochemistryprotein oxidationbusiness.industrypeptide fragmentscase-control studiesCase-control studybiomarkersmedicine.diseaseAPOE; biomarkers; CSF; extracellular chaperones; protein oxidation; redox proteomics; aged; aged 80 and over; Alzheimer disease; amino acid sequence; amyloid beta-peptides; apolipoproteins E; biomarkers; case-control studies; cognitive dysfunction; female; humans; male; middle aged; molecular sequence data; oxidation-reduction; oxidative stress; peptide fragments; proteome; tau proteins; biochemistry; physiology (medical)extracellular chaperonesamino acid sequence030104 developmental biologybusinessOxidative stressapolipoproteins E
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Protein misfolding, amyotrophic lateral sclerosis and guanabenz: Protocol for a phase II RCT with futility design (ProMISe trial)

2017

IntroductionRecent studies suggest that endoplasmic reticulum stress may play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS) through an altered regulation of the proteostasis, the cellular pathway-balancing protein synthesis and degradation. A key mechanism is thought to be the dephosphorylation of eIF2α, a factor involved in the initiation of protein translation. Guanabenz is an alpha-2-adrenergic receptor agonist safely used in past to treat mild hypertension and is now an orphan drug. A pharmacological action recently discovered is its ability to modulate the synthesis of proteins by the activation of translational factors preventing misfolded protein accumula…

0301 basic medicineOncologyPathologyamyotrophic lateral sclerosisamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; adrenergic alpha-2 receptor agonist s; age of onset; amyotrophic lateral sclerosis; disease progression; double-blind method; endoplasmic reticulum stress; guanabenz; humans; italy; medical futility; neuroprotective agents; proteostasis deficienciesamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Medicine (all)randomized clinical trial guanabenzHelsinki declaration0302 clinical medicineProtocolAdrenergic alpha-2 Receptor Agonists1506Amyotrophic lateral sclerosisAge of OnsetGuanabenzMedicine (all)amyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein responseNeurodegenerationamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response;amyotrophic lateral sclerosis; guanabenz; motor neurone disease; neuromuscular disease; randomized clinical trial; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis DeficienciesGeneral Medicineunfolded protein responseEndoplasmic Reticulum StressRiluzoleNeuroprotective AgentsNeurologyTolerabilityItalyDisease Progression1713GuanabenzMedical Futilitymedicine.drugmedicine.medical_specialtyamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis Deficiencies; Medicine (all)Neuroprotection03 medical and health sciencesmotor neurone diseaseDouble-Blind MethodInternal medicinemedicineHumansProteostasis Deficienciesbusiness.industryAmbientaleneuromuscular diseaserandomized clinical trialmedicine.diseaseClinical trial030104 developmental biologybusiness030217 neurology & neurosurgery
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A free radical theory of frailty.

2018

The free radical theory of ageing provided an intellectual framework for many laboratories working on ageing. However, experimental and clinical evidence showing that high doses of antioxidants do not have an effect on ageing or on age-associated diseases, cast doubts on the validity of this theory. Data from our own laboratory show that oxidative damage does not correlate with age, especially in the geriatric population, but rather with the frailty state. This has led us to postulate the free radical theory of frailty that proposes that oxidative damage is associated with frailty, but not with chronological age itself. Superoxide dismutase deficient mice are more frail than controls. But m…

0301 basic medicineOncologymedicine.medical_specialtyAgingFree Radicalsmedicine.disease_causeBiochemistrySuperoxide dismutase03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicineDeficient mouseHigh dosesMedicineAnimalsHumansFree-radical theory of agingGeriatricsbiologyFrailtybusiness.industryChronological ageOxidative Stress030104 developmental biologyAgeingbiology.proteinbusiness030217 neurology & neurosurgeryOxidative stressFree radical biologymedicine
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Sympathetic, metabolic adaptations, and oxidative stress in autism spectrum disorders: How far from physiology?

2018

Autism spectrum disorders (ASD) is a complex and multifaceted neurobehavioral syndrome with no specific cause still identified, despite the worldwide increasing (prevalence for 1,000 children from 6.7 to 14.6, between 2000 and 2012). Many biological and instrumental markers have been suggested as potential predictive factors for the precocious diagnosis during infancy and/or pediatric age. Many studies reported structural and functional abnormalities in the autonomic system in subjects with ASD. Sleep problems in ASD are a prominent feature, having an impact on the social interaction of the patient. Considering the role of orexins (A and B) in wake-sleep circadian rhythm, we could speculate…

0301 basic medicineOrexin-APhysiologyAutism spectrum disorders (ASD); Heart rate (HR); Heart rate variability (HRV); Orexin-A; Oxidative stress; Physiology; Physiology (medical)Case ReportAutism spectrum disorders (ASD); Heart rate (HR); Heart rate variability (HRV); Orexin-A; Oxidative stressmedicine.disease_causelcsh:PhysiologyHeart rate (HR)03 medical and health sciences0302 clinical medicinePhysiology (medical)Heart ratemental disordersmedicineHeart rate variabilityCircadian rhythmlcsh:QP1-981business.industryPediatric agemedicine.diseaseAutism spectrum disorders (ASD)Pathophysiology030104 developmental biologyOxidative stressAutismOxidative streAutism spectrum disorders (ASD); Heart rate (HR); Heart rate variability (HRV); Orexin-A; Oxidative stress;Skin conductancebusinessNeuroscienceHeart rate variability (HRV)030217 neurology & neurosurgeryOxidative stress
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Two-Week Aflibercept or Erlotinib Administration Does Not Induce Changes in Intestinal Morphology in Male Sprague–Dawley Rats But Aflibercept Affects…

2019

Gastrointestinal toxicity is a frequently observed adverse event during cancer treatment with traditional chemotherapeutics. Currently, traditional chemotherapeutics are often combined with targeted biologic agents. These biologics, however, possess a distinct toxicity profile, and they may also exacerbate the adverse effects of traditional chemotherapeutics. In this study, we aimed to characterize the gastrointestinal and metabolic changes after a 2-week treatment period with aflibercept, an antiangiogenic VEGFR decoy, and with erlotinib, a tyrosine-kinase inhibitor. Male rats were treated either with aflibercept or erlotinib for 2 weeks. During the 2-week treatment period, the animals in …

0301 basic medicineOriginal articleCancer ResearchBevacizumabANTITUMOR-ACTIVITYmedicine.medical_treatmentBEVACIZUMAB3122 CancersAdipose tissuePharmacologylcsh:RC254-282TOXICITY03 medical and health sciences0302 clinical medicinemedicineOXIDATIVE STRESSCOMBINATIONAdverse effectAfliberceptChemotherapyIntestinal permeabilitybusiness.industryCHEMOTHERAPYmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthMETASTATIC COLORECTAL-CANCER1ST-LINE TREATMENT030104 developmental biologyOncology030220 oncology & carcinogenesisCELLSACIDToxicityErlotinibbusinessmedicine.drug
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Increased basal antioxidant levels in RCAN1 - deficient mice lowers oxidative injury after acute paraquat insult.

2020

RCAN1 is an inhibitor of the phosphatase calcineurin, which is involved in the regulation of oxidative stress and apoptosis, among other important cell processes. Here we have used RCAN1 deficient mice (RCAN1-/-) to elucidate its role after an acute oxidative insult such as paraquat injection. We have observed that RCAN1-/- mice show less oxidative damage than wildtype (WT) mice after treatment. Under basal conditions, RCAN1-/- animals express more calcineurin, heme oxygenase-1, Nrf2, and catalase compared to WT mice (controls). This may explain the less severe effect of paraquat treatment on RCAN1-/- mice compared to WT. We showed that oxidative stress is involved in the early stages of ap…

0301 basic medicineParaquatmedicine.medical_specialtyAntioxidantmedicine.medical_treatmentMuscle ProteinsOxidative phosphorylationmedicine.disease_causeBiochemistryAntioxidants03 medical and health scienceschemistry.chemical_compoundMiceParaquatInternal medicinemedicineAnimals030102 biochemistry & molecular biologybiologyCalcineurinGeneral MedicineGlutathioneCalcineurinDNA-Binding ProteinsOxidative Stress030104 developmental biologyEndocrinologychemistryCatalaseApoptosisbiology.proteinOxidative stressFree radical research
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Enhanced activity of glycolytic enzymes in Drosophila and human cell models of Parkinson's disease based on DJ-1 deficiency

2020

ABSTRACTParkinson’s disease (PD) is a neurodenerative debilitating disorder characterized by progressive disturbances in motor, autonomic and psychiatric functions. The pathological hallmark of PD is the loss of dopaminergic neurons in the substantia nigra pars compacta, which causes striatal dopamine deficiency. Although most PD cases are sporadic (iPD), approximately 5-10% of all patients suffer from monogenic PD forms caused by highly penetrant rare mutations segregating with the disease in families (fPD). One of the genes linked to monogenic PD is DJ-1. Mutations in DJ-1 cause autosomal recessive early-onset forms of fPD; however, it has been shown that an over-oxidized and inactive for…

0301 basic medicineParkinson's diseaseProtein CarbonylationProtein Deglycase DJ-1MutantNerve Tissue ProteinsSubstantia nigraBiologymedicine.disease_causeBiochemistryNeuroprotection03 medical and health sciences0302 clinical medicinePhysiology (medical)medicineAnimalsDrosophila ProteinsHumansGlycolysisGeneLoss functionPars compactaChemistryDopaminergicParkinson Diseasemedicine.diseasePhenotypeCell biologyOxidative Stress030104 developmental biologyDrosophilaGlycolysis030217 neurology & neurosurgeryOxidative stressFree Radical Biology and Medicine
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Identification of potential therapeutic compounds for Parkinson's disease using Drosophila and human cell models.

2017

Abstract Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease. It is caused by a loss of dopaminergic neurons in the substantia nigra pars compacta, leading to a decrease in dopamine levels in the striatum and thus producing movement impairment. Major physiological causes of neurodegeneration in PD are oxidative stress (OS) and mitochondrial dysfunction; these pathophysiological changes can be caused by both genetic and environmental factors. Although most PD cases are sporadic, it has been shown that 5–10% of them are familial forms caused by mutations in certain genes. One of these genes is the DJ-1 oncogene, which is involved in an early…

0301 basic medicineParkinson's diseaseProtein Deglycase DJ-1Drug Evaluation PreclinicalSubstantia nigraNerve Tissue ProteinsBiologymedicine.disease_causeBiochemistryAnimals Genetically Modified03 medical and health sciences0302 clinical medicineDopaminePhysiology (medical)Cell Line TumorDrug DiscoverymedicineAnimalsDrosophila ProteinsHumansGeneticsMutationPars compactaNeurodegenerationDopaminergicParkinson Diseasemedicine.diseaseDisease Models AnimalOxidative Stress030104 developmental biologyGene Knockdown TechniquesMutationCancer researchDrosophila030217 neurology & neurosurgeryOxidative stressLocomotionmedicine.drugFree radical biologymedicine
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Reductive Stress: A New Concept in Alzheimer's Disease

2015

Reactive oxygen species play a physiological role in cell signaling and also a pathological role in diseases, when antioxidant defenses are overwhelmed causing oxidative stress. However, in this review we will focus on reductive stress that may be defined as a pathophysiological situation in which the cell becomes more reduced than in the normal, resting state. This may occur in hypoxia and also in several diseases in which a small but persistent generation of oxidants results in a hormetic overexpression of antioxidant enzymes that leads to a reduction in cell compartments. This is the case of Alzheimer's disease. Individuals at high risk of Alzheimer's (because they carry the ApoE4 allele…

0301 basic medicinePathologymedicine.medical_specialtyAntioxidantmedicine.medical_treatmentDiseaseBiologymedicine.disease_cause03 medical and health sciencesAlzheimer DiseasemedicineAnimalsHumanschemistry.chemical_classificationReactive oxygen speciesResting state fMRIHormesisHypoxia (medical)medicine.disease030104 developmental biologyNeurologychemistryImmunologyNeurology (clinical)medicine.symptomAlzheimer's diseaseOxidation-ReductionOxidative stress
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