Search results for "BLAST"

showing 10 items of 2136 documents

Biotensegrity of the Extracellular Matrix: Physiology, Dynamic Mechanical Balance, and Implications in Oncology and Mechanotherapy

2014

Cells have the capacity to convert mechanical stimuli into chemical changes. This process is based on the tensegrity principle, a mechanism of tensional integrity. To date, this principle has been demonstrated to act in physiological processes such as mechanotransduction and mechanosensing at different scales (from cell sensing through integrins to molecular mechanical interventions or even localized massage). The process involves intra- and extracellular components, including the participation of extracellular matrix (ECM) and microtubules that act as compression structures, and actin filaments which act as tension structures. The nucleus itself has its own tensegrity system which is impli…

Cancer Researchneuroblastoma.Mechanism (biology)extracellular matrixIntegrinReview ArticleBiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensBioinformaticslcsh:RC254-282Neuroblastic TumorbiotensegrityExtracellular matrixneuroblastomaOncologyTensegritymechanotherapyExtracellularbiology.proteincancerMechanotransductionMechanotherapyNeuroscience
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miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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Radiation-induced vascular changes in the intracranial irradiation field in medulloblastoma survivors: An MRI study

2019

While survival times after treatment of medulloblastoma are increasing, little is known about radiochemotherapy (RCT)-induced cerebrovascular changes. High resolution vessel wall imaging (VWI) sequences are an emerging tool for the evaluation of cerebrovascular diseases. We performed VWI in medulloblastoma long-term survivors to screen for late sequelae of RCT.Twenty-two pediatric medulloblastoma survivors (mean age 25.8 years (10-53 years); 16.3 years (mean) post primary RCT (range 1-45 years)) underwent 2D VWI-MRI. Vessel wall thickening, contrast enhancement and luminal narrowing were analyzed. The findings were correlated with the patients' radiation protocols.Vessel wall changes were o…

Carotid Artery DiseasesMalemedicine.medical_specialtyAdolescentHigh resolutionRadiation induced030218 nuclear medicine & medical imaginglaw.invention03 medical and health sciences0302 clinical medicineCancer SurvivorsRandomized controlled triallawmedicine.arteryHumansMedicineRadiology Nuclear Medicine and imagingCerebellar NeoplasmsChildRadiation InjuriesMedulloblastomabusiness.industryMean ageHematologyCerebral ArteriesIntracranial Arteriosclerosismedicine.diseaseMagnetic Resonance ImagingOncologyCerebrovascular CirculationChild Preschool030220 oncology & carcinogenesisFemaleRadiologyThickeningCranial IrradiationInternal carotid arterybusinessCarotid Artery InternalMagnetic Resonance AngiographyAfter treatmentMedulloblastomaRadiotherapy and Oncology
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Staphylococcal alpha-toxin: repair of a calcium-impermeable pore in the target cell membrane

2000

Staphylococcal alpha-toxin forms heptameric pores that render membranes permeable for monovalent cations. The pore is formed by an amphipathic beta-barrel encompassing amino acid residues 118-140 of each subunit of the oligomer. Human fibroblasts are susceptible to alpha-toxin but are able to repair the membrane lesions. Thereby, toxin oligomers remain embedded in the plasma membrane and exposed to the extracellular medium. In this study, we sought to detect structural changes occurring in the pore-forming sequence during lesion repair. Single cysteine substitution mutants were labelled with the environmentally sensitive fluorochrome acrylodan and, after mixing with wild-type toxin, incorpo…

Cell Membrane PermeabilityCalmodulinStaphylococcusBacterial ToxinsMicrobiologyCell membraneHemolysin Proteinschemistry.chemical_compoundmedicineExtracellularHumansLymphocytesLipid bilayerMolecular BiologyCells CulturedCytochalasin DbiologyCell MembraneLipid metabolismFibroblastsSpectrometry Fluorescencemedicine.anatomical_structureMembraneBiochemistrychemistrybiology.proteinBiophysicsCalciumCysteineMolecular Microbiology
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Central nicotinic receptors, neurotrophic factors and neuroprotection

2000

The multiple combinations of nAChR subunits identified in central nervous structures possess distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely ind…

Cell SurvivalAgonist-antagonistCentral nervous systemReceptors Nicotiniccomplex mixturesNeuroprotectionBehavioral NeuroscienceNeurotrophic factorsmental disordersmedicineAnimalsHumansNerve Growth FactorsAcetylcholine receptorNeuronsRegulation of gene expressionbiologymusculoskeletal neural and ocular physiologyBrainHaplorhinimedicine.diseaseRatsNeuroprotective Agentsmedicine.anatomical_structurenervous systembiology.proteinFibroblast Growth Factor 2sense organsAlzheimer's diseasePsychologyNeuroscienceNeurotrophinBehavioural Brain Research
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Induction of programmed cell death in human retinoblastoma Y79 cells by C2-ceramide.

1998

C2-ceramide, a cell-permeable analogue of ceramide, induced significant, dose- and time-dependent death in human retinoblastoma Y79 cells. Dying cells strongly displayed the morphology of apoptosis as characterized by microscopic evidence of cell shrinkage, membrane blebbing, nuclear and chromatin condensation and degeneration of the nucleus into membrane-bound apoptotic bodies. Upon induction of apoptosis Y79 cells evidence early phosphatidylserine externalization, as shown by annexin V-FITC. Apoptosis was also assessed by monitoring changes in cell granularity by staining with the combined fluorescent dyes acridine orange and ethidium bromide. C2-ceramide induced these morphological chang…

Cell SurvivalBlotting WesternRetinoblastomaProteinsApoptosisDNA FragmentationCeramidesC2-ceramideNucleosomesSphingomyelin PhosphodiesteraseBacterial ProteinsProto-Oncogene Proteins c-bcl-2SphingosineOkadaic AcidTumor Cells CulturedHumansTumor Suppressor Protein p53Interleukin-1Molecular and cellular biochemistry
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Biocompatible hydrogels based on hyaluronic acid cross-linked with a polyaspartamide derivative as delivery systems for epithelial limbal cells.

2011

The aim of this work was to evaluate the potential use of hydrogels based on hyaluronic acid (HA) chemically cross-linked with α,β-poly(N-2-hydroxyethyl) (2-aminoethylcarbamate)-D,L-aspartamide (PHEA-EDA) as substitutes for the amniotic membrane able to release limbal cells for corneal regeneration. Hydrogels, shaped as films, with three different molar ratios (X) between PHEA-EDA and HA (X = 0.5, 1.0 and 1.5) have been investigated. First, it has been evaluated their swelling ability, hydrolytic resistance in simulated physiological fluid and cell compatibility by using human dermal fibroblasts chosen as a model cell line. Then adhesion studies in comparison with collagen gel, have been pe…

Cell SurvivalContact LensesDrug CompoundingCellPharmaceutical ScienceCell LineGlycosaminoglycanchemistry.chemical_compoundDrug Delivery SystemsHyaluronic acidPolymer chemistrymedicineCell AdhesionPolyaminesAnimalsHumansAmnionHyaluronic AcidCell adhesionAspartameEpithelial CellsHydrogelsFibroblastsIn vitroCoculture Techniquesmedicine.anatomical_structurechemistryCell cultureSelf-healing hydrogelsBiophysicssense organsCollagenRabbitsImmortalised cell lineInternational journal of pharmaceutics
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Differential regulation of apoptosis-associated genes by estrogen receptor alpha in human neuroblastoma cells

2012

Purpose: The neuroendocrinology of female sex hormones is of great interest for a variety of neuropsychiatric disorders. In fact, estrogens and estrogen receptors (ERs) exert neuromodulatory and neuroprotective functions. Here we investigated potential targets of the ER subtype alpha that may mediate neuroprotection and focused on direct modulators and downstream executors of apoptosis. Methods: We employed subclones of human neuroblastoma cells (SK-N-MC) stably transfected with one of the ER subtypes, ERalpha or ERbeta. Differences between the cell lines regarding the mRNA expression levels were examined by qPCR, changes on protein levels were examined by Western Blot and immunocytochemist…

Cell SurvivalEstrogen receptorApoptosisCaspase 3BiologyNeuroprotectionRats Sprague-DawleyNeuroblastomaDevelopmental NeuroscienceCell Line TumorAnimalsEstrogen Receptor betaHumansGene silencingAdaptor Proteins Signal TransducingNeuronsCaspase 3Estrogen Receptor alphaTransfectionMolecular biologyRatsUp-RegulationDNA-Binding ProteinsProto-Oncogene Proteins c-bcl-2NeurologyCell cultureApoptosisCancer researchNeurology (clinical)Apoptosis Regulatory ProteinsEstrogen receptor alphahormones hormone substitutes and hormone antagonistsTranscription FactorsRestorative Neurology and Neuroscience
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Effects of vinblastine, leucine, and histidine, and 3-methyladenine on autophagy in Ehrlich ascites cells.

1990

The microtubule inhibitor vinblastine causes accumulation of autophagic vacuoles in many cell types. In hepatocytes, many of the accumulated vacuoles are nascent, which has been interpreted to suggest that vinblastine acts by inhibiting the fusion of hydrolase-containing lysosomes with early autophagic vacuoles. However, our previous results suggested that, in Ehrlich ascites cells, vinblastine causes accumulation mainly of older autophagic vacuoles (AVs). This study was undertaken to further characterize the mode of action of vinblastine in these cells. The vinblastine-accumulated AVs were quantified by electron-microscopic morphometry. In addition, the effects of inhibitors of autophagic …

Cell SurvivalPhagocytosisClinical BiochemistryVacuoleProtein degradationBiologyVinblastinePathology and Forensic MedicinePhagocytosisMicrotubuleLeucineLysosomemedicineAutophagyTumor Cells CulturedAnimalsHumansHistidineCarcinoma Ehrlich TumorChildMolecular BiologyAdenineAutophagyVinblastineCell biologyMicroscopy Electronmedicine.anatomical_structureBiochemistryLeucinemedicine.drugExperimental and molecular pathology
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