Search results for "H30"

showing 10 items of 1587 documents

Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtu…

2020

A number of aging-related disorders (ARD) have been related to oxidative stress (OS) and mitochondrial dysfunction (MDF) in a well-established body of literature. Most studies focused on cardiovascular disorders (CVD), type 2 diabetes (T2D), and neurodegenerative disorders. Counteracting OS and MDF has been envisaged to improve the clinical management of ARD, and major roles have been assigned to three mitochondrial cofactors, also termed mitochondrial nutrients (MNs), i.e., alpha-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and carnitine (CARN). These cofactors exert essential-and distinct-roles in mitochondrial machineries, along with strong antioxidant properties. Clinical trials have mostly…

0301 basic medicineAgingAntioxidantUbiquinonemedicine.medical_treatmentmitochondrial nutrientsReviewoptic neuropathiesType 2 diabetesPharmacologyMitochondrionmedicine.disease_causeAntioxidantslcsh:Chemistrychemistry.chemical_compound0302 clinical medicineCardiovascular Diseaseoxidative stressaging-related disorderslcsh:QH301-705.5SpectroscopyThioctic AcidMitochondrial nutrientNeurodegenerative DiseasesGeneral MedicineComputer Science ApplicationsMitochondriaCardiovascular DiseasesAntioxidantmedicine.drugHumanCatalysisAging-related disorderCell LineInorganic Chemistry03 medical and health sciencesCarnitinemedicineAnimalsHumansMicrobiomeCarnitinePhysical and Theoretical ChemistryMolecular BiologyCoenzyme Q10business.industryAnimalOrganic ChemistryOxidative Stremedicine.diseaseClinical trial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryDiabetes Mellitus Type 2MicrobiomeOptic neuropathiebusinessMitochondrial dysfunction030217 neurology & neurosurgeryOxidative stress
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IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

2021

This article belongs to the Collection Insulin-Like Growth Factors in Development, Cancers and Aging.

0301 basic medicineAgingApoptosisHaploinsufficiencyMice0302 clinical medicineBiology (General)Insulin-Like Growth Factor ICell DeathapoptosisGeneral Medicine3. Good healthCochleaCytokinesmedicine.symptomHaploinsufficiencyNoise-induced hearing lossmedicine.medical_specialtyHeterozygoteHearing lossQH301-705.5InflammationArticleARHLProinflammatory cytokine03 medical and health sciencesInternal medicinemedicineotorhinolaryngologic diseasesAnimalsRNA MessengerProtein kinase BCochleaInflammationbusiness.industryGene Expression ProfilingAKTTGFβ1Auditory Thresholdmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologyGene Expression RegulationHearing Loss Noise-InducedAgeingSynapsesIL1βJNKbusinessNoise030217 neurology & neurosurgeryBiomarkersNIHL
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Electrical activity controls area-specific expression of neuronal apoptosis in the mouse developing cerebral cortex

2017

Programmed cell death widely but heterogeneously affects the developing brain, causing the loss of up to 50% of neurons in rodents. However, whether this heterogeneity originates from neuronal identity and/or network-dependent processes is unknown. Here, we report that the primary motor cortex (M1) and primary somatosensory cortex (S1), two adjacent but functionally distinct areas, display striking differences in density of apoptotic neurons during the early postnatal period. These differences in rate of apoptosis negatively correlate with region-dependent levels of activity. Disrupting this activity either pharmacologically or by electrical stimulation alters the spatial pattern of apoptos…

0301 basic medicineAgingMouseStimulationCell CountSomatosensory systemMice0302 clinical medicineAnesthesiaBiology (General)whisker deafferentationCerebral CortexNeuronsNeocortexCaspase 3General NeuroscienceQRapoptosisMotor CortexGeneral MedicineAnatomyactivity patternsmedicine.anatomical_structurecell deathCerebral cortexMedicinePrimary motor cortexMotor cortexResearch ArticleProgrammed cell deathQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesmedicineAnimalsSensory deprivationdevelopmentGeneral Immunology and MicrobiologySomatosensory CortexElectrophysiological Phenomena030104 developmental biologyDevelopmental Biology and Stem Cellsnervous systemAnimals NewbornNeuroscience030217 neurology & neurosurgeryNeuroscienceeLife
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Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening

2018

Loss of function of dyskerin (DKC1), NOP10 and TIN2 are responsible for different inheritance patterns of Dyskeratosis congenita (DC; ORPHA1775). They are key components of telomerase (DKC1 and NOP10) and shelterin (TIN2), and play an important role in telomere homeostasis. They participate in several fundamental cellular processes by contributing to Dyskeratosis congenita through mechanisms that are not fully understood. Presence of oxidative stress was postulated to result from telomerase ablation. However, the resulting disturbed redox status can promote telomere attrition by generating a vicious circle, which promotes cellular senescence. This fact prompted us to study if acute loss of …

0301 basic medicineAgingTelomeraseTelomere-Binding ProteinsClinical BiochemistryCell Cycle ProteinsBiologymedicine.disease_causeBiochemistryDyskeratosis CongenitaDyskerin03 medical and health sciencesTelomere HomeostasisRibonucleoproteins Small NucleolarmedicineHumanslcsh:QH301-705.5TelomeraseCellular SenescenceTelomere ShorteningRibonucleoproteinlcsh:R5-920TelomeropathiesOrganic ChemistryNuclear ProteinsShelterinmedicine.diseaseMolecular biologyTelomereCell biologyOxidative Stress030104 developmental biologylcsh:Biology (General)DNA damageRNA InterferenceAntioxidantlcsh:Medicine (General)Oxidative stressDyskeratosis congenitaResearch PaperHeLa CellsRedox Biology
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Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

2020

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidati…

0301 basic medicineAircraftmedicine.medical_treatmentClinical BiochemistryBlood Pressure1308 Clinical Biochemistrymedicine.disease_causeBiochemistryMice0302 clinical medicineMedicineEndothelial dysfunctionlcsh:QH301-705.5lcsh:R5-920NADPH oxidasebiologyCytokineHypertensionmedicine.symptomlcsh:Medicine (General)Arterial hypertensionmedicine.medical_specialtyArticles from the Special Issue on Impact of environmental pollution and stress on redox signaling and oxidative stress pathways; Edited by Thomas Münzel and Andreas Daiber10208 Institute of Neuropathology610 Medicine & healthInflammation03 medical and health sciencesInternal medicineEnvironmental noise exposureAnimalsNeuroinflammationInflammationbusiness.industryOrganic ChemistryEndothelial functionmedicine.diseaseAngiotensin IIMice Inbred C57BLOxidative Stress030104 developmental biologyEndocrinologyBlood pressurelcsh:Biology (General)Vascular oxidative stressbiology.protein570 Life sciences; biologyEndothelium Vascularbusiness030217 neurology & neurosurgeryOxidative stress1605 Organic ChemistryRedox Biology
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Expression of Alpha-Enolase (ENO1), Myc Promoter-Binding Protein-1 (MBP-1) and Matrix Metalloproteinases (MMP-2 and MMP-9) Reflect the Nature and Agg…

2019

Breast cancer is a complex and heterogeneous disease: Several molecular alterations cause cell proliferation and the acquisition of an invasive phenotype. Extracellular matrix (ECM) is considered essential for sustaining tumor growth and matrix metalloproteinases (MMPs) have been identified as drivers of many aspects of the tumor phenotype. Mounting evidence indicates that both &alpha

0301 basic medicineAlpha-enolaseENO1Kaplan-Meier EstimateMatrix metalloproteinasemedicine.disease_causeMetastasisExtracellular matrixlcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopybiologyMMP-2General MedicineComputer Science ApplicationsDNA-Binding ProteinsGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisDisease ProgressionMatrix Metalloproteinase 2FemaleMMP-9Breast NeoplasmsCatalysisArticleInorganic Chemistry03 medical and health sciencesBreast cancerbreast cancerCell Line TumormedicineBiomarkers TumorHumansPhysical and Theoretical ChemistryMBP-1Molecular BiologyCell ProliferationTumor Suppressor ProteinsOrganic ChemistryCancermedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Phosphopyruvate HydrataseCancer cellbiology.proteinCancer researchCarcinogenesisInternational Journal of Molecular Sciences
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Tocotrienol Affects Oxidative Stress, Cholesterol Homeostasis and the Amyloidogenic Pathway in Neuroblastoma Cells: Consequences for Alzheimer’s Dise…

2016

One of the characteristics of Alzheimer´s disease (AD) is an increased amyloid load and an enhanced level of reactive oxidative species (ROS). Vitamin E has known beneficial neuroprotective effects, and previously, some studies suggested that vitamin E is associated with a reduced risk of AD due to its antioxidative properties. However, epidemiological studies and nutritional approaches of vitamin E treatment are controversial. Here, we investigate the effect of α-tocotrienol, which belongs to the group of vitamin E, on AD-relevant processes in neuronal cell lines. In line with the literature, α-tocotrienol reduced the ROS level in SH-SY5Y cells. In the presence of tocotrienols, cholesterol…

0301 basic medicineAlzheimer´s diseasemedicine.medical_treatmentvitamin Eγ-secretasemedicine.disease_causeAntioxidantslcsh:ChemistryNeuroblastomachemistry.chemical_compoundAβ degradation0302 clinical medicineβ-secretaselcsh:QH301-705.5SpectroscopyNeuronschemistry.chemical_classificationbiologyTocotrienolsGeneral Medicinetocopherol3. Good healthComputer Science ApplicationsCholesterolNeuroprotective AgentsTocotrienolmedicine.medical_specialtyAmyloidamyloid-βNeuroprotectionArticleGene Expression Regulation EnzymologicCatalysisCell LineInorganic Chemistry03 medical and health sciencesAlzheimer DiseaseInternal medicinemedicineHumanstocotrienolPhysical and Theoretical ChemistryMolecular BiologyReactive oxygen speciesAmyloid beta-PeptidesCholesterolVitamin EOrganic Chemistrytocotrienol; vitamin E; Alzheimer´s disease; amyloid-β; tocopherol; Aβ degradation; β-secretase; γ-secretaseOxidative Stress030104 developmental biologyEndocrinologychemistrylcsh:Biology (General)lcsh:QD1-999biology.proteinAmyloid Precursor Protein SecretasesReactive Oxygen SpeciesAmyloid precursor protein secretase030217 neurology & neurosurgeryOxidative stressInternational Journal of Molecular Sciences
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Direct Sensing of Nutrients via a LAT1-like Transporter in Drosophila Insulin-Producing Cells

2016

Summary Dietary leucine has been suspected to play an important role in insulin release, a hormone that controls satiety and metabolism. The mechanism by which insulin-producing cells (IPCs) sense leucine and regulate insulin secretion is still poorly understood. In Drosophila, insulin-like peptides (DILP2 and DILP5) are produced by brain IPCs and are released in the hemolymph after leucine ingestion. Using Ca2+-imaging and ex vivo cultured larval brains, we demonstrate that IPCs can directly sense extracellular leucine levels via minidiscs (MND), a leucine transporter. MND knockdown in IPCs abolished leucine-dependent changes, including loss of DILP2 and DILP5 in IPC bodies, consistent wit…

0301 basic medicineAmino Acid Transport Systemsheavy-chainmedicine.medical_treatmentInsulinsamino acid transporter0302 clinical medicinegenetics [Drosophila Proteins]cytology [Drosophila melanogaster]Glutamate DehydrogenaseHemolymphInsulin-Secreting Cellsmetabolism [Drosophila melanogaster]HemolymphDrosophila;Drosophila insulin-like peptides;amino acid transporter;food;glutamate dehydrogenase;glycemia;growth;insulin-producing cells;minidiscs;starvationDrosophila ProteinsProtein Isoformsmetabolism [Calcium]genetics [Insulins]genetics [Amino Acid Transport Systems]lcsh:QH301-705.5minidiscsGene knockdowncytology [Larva]pancreatic beta-cellglutamate dehydrogenaseBrainmetabolism [Hemolymph]secretionDrosophila melanogasterBiochemistryLarvaAlimentation et NutritionDrosophilaLeucineSignal Transductionglucose-transportgenetics [Glutamate Dehydrogenase]genetics [Protein Isoforms]growthamino-acidsmetabolism [Drosophila Proteins][SDV.BC]Life Sciences [q-bio]/Cellular BiologyNutrient sensingmetabolism [Larva]Biologyinsulin-producing cellsArticleGeneral Biochemistry Genetics and Molecular Biologymetabolism [Amino Acid Transport Systems]metabolism [Insulins]03 medical and health sciencesLeucineparasitic diseasesmedicineFood and NutritionAnimalsddc:610cytology [Insulin-Secreting Cells]cardiovascular diseasesAmino acid transporterMnd protein Drosophilaadministration & dosage [Leucine]metabolism [Protein Isoforms]Ilp5 protein Drosophilacytology [Brain]foodGlutamate dehydrogenaseInsulinNeurosciencesstarvationGlucose transportermetabolism [Insulin-Secreting Cells]glutamate-dehydrogenasel-leucineglycemia030104 developmental biologyGene Expression Regulationlcsh:Biology (General)metabolism [Brain]metabolism [Glutamate Dehydrogenase]Neurons and Cognitionmetabolism [Leucine]CalciumDrosophila insulin-like peptidesmetabolismfat-cells030217 neurology & neurosurgeryCell Reports
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The Role of Osteoprotegerin and Its Ligands in Vascular Function

2019

International audience; The superfamily of tumor necrosis factor (TNF) receptors includes osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The OPG/RANKL/RANK system plays an active role in pathological angiogenesis and inflammation as well as cell survival. It has been demonstrated that there is crosstalk between endothelial cells and osteoblasts during osteogenesis, thus establishing a connection between angiogenesis and osteogenesis. This OPG/RANKL/RANK/TRAIL system acts on specific cell surface receptors, which are then able to transmit their signals to other intracellular comp…

0301 basic medicineAngiogenesismedicine.medical_treatmentReview030204 cardiovascular system & hematologyLigandslcsh:ChemistryTNF-Related Apoptosis-Inducing Ligand0302 clinical medicineReceptorlcsh:QH301-705.5Cellular SenescenceSpectroscopyReceptor Activator of Nuclear Factor-kappa BbiologyChemistryvascular diseaseGeneral MedicineComputer Science ApplicationsProtein Transportmedicine.anatomical_structureCytokineRANKLTumor necrosis factor alphaDisease Susceptibilitymedicine.symptomProtein BindingSignal Transductionmusculoskeletal diseasesProteasome Endopeptidase ComplexEndotheliumendotheliumNeovascularization PhysiologicInflammationCatalysisInorganic ChemistryStructure-Activity Relationship03 medical and health sciencesOsteoprotegerin[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyMyocardiumRANK LigandOrganic ChemistryEndothelial Cells030104 developmental biologylcsh:Biology (General)lcsh:QD1-999osteoprotegerinOPG/RANKL/RANKCancer researchbiology.proteinBlood VesselsBiomarkers
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Role of Regular Physical Activity in Neuroprotection against Acute Ischemia

2020

One of the major obstacles that prevents an effective therapeutic intervention against ischemic stroke is the lack of neuroprotective agents able to reduce neuronal damage; this results in frequent evolution towards a long-term disability with limited alternatives available to aid in recovery. Nevertheless, various treatment options have shown clinical efficacy. Neurotrophins such as brain-derived neurotrophic factor (BDNF), widely produced throughout the brain, but also in distant tissues such as the muscle, have demonstrated regenerative properties with the potential to restore damaged neural tissue. Neurotrophins play a significant role in both protection and recovery of function followi…

0301 basic medicineAngiogenesismyokinesphysical activityReviewneurotrophinsAntioxidantsBrain Ischemialcsh:Chemistry0302 clinical medicineNeurotrophic factorsneuronal recoverylcsh:QH301-705.5SpectroscopybiologyGeneral MedicineNeuroprotectionComputer Science ApplicationsAcute DiseaseNeurotrophinmedicine.symptomNeurotrophinTraumatic brain injuryIschemiaInflammationNeuroprotectionCatalysisInorganic Chemistry03 medical and health sciencesHormesisMyokineMyokinemedicineischemic strokeAnimalsHumansPhysical and Theoretical ChemistryExerciseMolecular Biologybusiness.industryOrganic Chemistrymedicine.disease030104 developmental biologylcsh:Biology (General)lcsh:QD1-999inflammationbiology.proteinBrain-derived neurotrophic factor (BDNF)businessNeuroscience030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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