Search results for " inhibition"

showing 10 items of 435 documents

Synthesis and Biological Properties of Benzothiazole, Benzoxazole, and Chromen-4-one Analogues of the Potent Antitumor Agent 2-(3,4-Dimethoxyphenyl)-…

2008

New fluorinated 2-aryl-benzothiazoles, -benzoxazoles, and -chromen-4-ones have been synthesized and their activity against MCF-7 and MDA 468 breast cancer cell lines compared with the potent antitumor benzothiazole 5. Analogues such as 9a, b and 12a, d yielded submicromolar GI50 values in both cell lines; however, none of the new compounds approached 5 in terms of antitumor potency. For 5, binding to the aryl hydrocarbon receptor appeared to be necessary but not sufficient for growth inhibition.

BenzoxazolesBicyclic moleculebiologyStereochemistryCell CycleAntineoplastic AgentsBreast NeoplasmsBenzoxazoleAryl hydrocarbon receptorChemical synthesisIn vitroStructure-Activity Relationshipchemistry.chemical_compoundReceptors Aryl HydrocarbonchemistryBenzothiazoleCell Line TumorDrug Discoverybiology.proteinHumansMolecular MedicineStructure–activity relationshipBenzopyransBenzothiazolesGrowth inhibitionJournal of Medicinal Chemistry
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Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ?accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. "Regulated cell death" (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to…

Biochemical Manifestations of Cell DeathISCHEMIA-REPERFUSION INJURYApoptosisReviewTransduction (genetics)0302 clinical medicineCASPASE INHIBITION SWITCHESAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction610 Medicine & healthCaspaseTUMOR-NECROSIS-FACTOR0303 health sciencesSettore BIO/17biologySettore BIO/11NeurodegenerationSettore BIO/13APOPTOSIS3. Good healthMedicina Básicacell death030220 oncology & carcinogenesiscell death; Morphologic Aspects of Cell Death; Biochemical Manifestations of Cell DeathSignal transductionDOMAIN-LIKE PROTEINIntracellularHumanSignal TransductionNecroptosiCYTOCHROME-C RELEASEOUTER-MEMBRANE PERMEABILIZATIONProgrammed cell deathCIENCIAS MÉDICAS Y DE LA SALUDSettore BIO/06Inmunología610 Medicine & healthCELL DEATHNOQ-VD-OPH03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEddc:570Terminology as TopicAPOPTOSIS-INDUCING FACTORMIXED LINEAGE KINASEmedicineAnimalsHumansAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction; Molecular Biology; Cell BiologyMorphologic Aspects of Cell DeathSettore BIO/10Molecular Biology030304 developmental biologyAnimalCell growthApoptosiBiology and Life SciencesCell Biologymedicine.diseaseMITOCHONDRIAL PERMEABILITY TRANSITIONApoptosisImmunologybiology.proteinNeuroscienceCell death and differentiation
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Determination of lectin-cell-binding parameters by a new agglutination technique.

1992

We applied a recently described technique which is based on a light transmission/scattering method to determine the association characteristics of the Geodia lectin to sheep erythrocytes. The agglutination assays were performed in a total volume of 3 ml with 5.4 x 10(6) erythrocytes/ml. At a concentration of 360 ng/ml 50% of the lectin molecules were bound to the cells within the first 10 s of incubation. Scatchard analyses revealed an association constant (K(a)) of 0.9 +/- 0.1 x 10(8) M-1 and a number of 3.8 +/- 0.6 x 10(6) lectin binding sites on one erythrocyte. The method was also successfully applied to determine quantitatively the inhibitory potential of sugars competing with cell sur…

BiochemistryAgglutination techniquechemistry.chemical_compoundLectinsmedicineAnimalsLactoseIncubationchemistry.chemical_classificationScatchard plotChromatographySheepbiologyChemistryLectinHemagglutination TestsHemagglutination Inhibition TestsPoriferaRed blood cellAgglutination (biology)Kineticsmedicine.anatomical_structureReceptors MitogenImmunologyCalibrationbiology.proteinGlycoproteinProtein BindingBiological chemistry Hoppe-Seyler
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The Essential Oil of Thymbra capitata and its Application as A Biocide on Stone and Derived Surfaces

2019

Many chemicals used nowadays for the preservation of cultural heritage pose a risk to both human health and the environment. Thus, it is desirable to find new and eco-friendly biocides that can replace the synthetic ones. In this regard, plant essential oils represent effective alternatives to synthetic substances for the preservation of historical monuments. Thymbra capitata (syn. Thymus capitatus) is a medicinal and aromatic plant growing in the Mediterranean area and endowed with important pharmacological properties related to its essential oil. Among them, the antimicrobial ones make the T. capitata essential oil an ideal candidate for industrial applications

BiocideStone surface<i>Thymbra capitata</i>02 engineering and technologyPlant Science01 natural sciencesThymbra capitataessential oillaw.inventionchemistry.chemical_compoundHuman healthfoodstone surfaceslawnatural biocideThymbra capitataCarvacrolSettore BIO/15 - Biologia FarmaceuticaEcology Evolution Behavior and SystematicsEssential oilSettore CHIM/02 - Chimica FisicaEcology010405 organic chemistryChemistrybiological inhibitionBotanySettore CHIM/06 - Chimica Organicacultural heritage021001 nanoscience & nanotechnologyPulp and paper industryfood.food0104 chemical sciencesbiodeteriogensPickering emulsionQK1-989CapitataBiodeteriogenMediterranean areaThymus capitatus0210 nano-technologyPlants
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NOVEL COMPOSED GALACTOSYLATED NANODEVICES CONTAINING A RIBAVIRIN PRODRUG AS HEPATIC CELL-TARGETED CARRIERS FOR HCV TREATMENT

2013

In this paper, we describe the preparation of liver-targeted nanoparticles potentially able to carry to hepatocytes a ribavirin (RBV) prodrug, exploiting the presence of carbohydrate receptors in the liver (i.e., ASGPR in hepatocytes). These particles were obtained starting from a galactosylated phospholipid-polyaminoacid conjugate. This latter was obtained by chemical reaction of ALPHA, BETA -poly(N-2-hydroxyethyl) (2-aminoethylcarbamate)-DL-aspartamide (PHEA-EDA) with 1,2-dipalmitoyl-sn-glycero-3-phosphoethanolamine-N-(succinyl) sodium salt (DPPE), and subsequent reaction with lactose, obtaining PHEA-EDA-DPPE-GAL copolymer. To enhance the entrapment into obtained nanostructures, a hydroph…

Biomedical EngineeringPharmaceutical ScienceMedicine (miscellaneous)NanoparticleBioengineeringAntiviral AgentsDiffusionNon-competitive inhibitionNanocapsulesMaterials TestingRibavirinHumansGeneral Materials ScienceProdrugschemistry.chemical_classificationGalactoseHep G2 CellsProdrugCarbohydrateVirologyCombinatorial chemistryHepatitis CIn vitroGalactosylated Nanoparticles Hepatic Cell-Targeted Carriers Active Targeting Ribavirin Tripalmitate Hepatitis C.EnzymechemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoDrug deliveryConjugate
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An overview of doping in sports

2019

The history of doping field can be outlined in three major stages: (1) early stage in which drug abuse took place during sports performance and competition and gas chromatography was used for its detection; (2) approximately in the 1970s when androgenic anabolic steroids were introduced; (3) In the recent era when the fields of biochemistry, physiology, toxicology, genomics, genetics, immunology, and molecular biology were integrated and applied routinely. Advanced omics technology and gene doping age may be applied in near future. This review will discuss commonly abused materials, both their adverse and harmful effects, and the alleged benefits in conjunction with the current standards in…

Bioquímicaprotein synthesis[SDV]Life Sciences [q-bio]anabolic androgenic steroidsPharmacologyProtein chemistry01 natural sciencesDopaje03 medical and health sciencesCondensed Matter::Materials SciencePhysics::Popular PhysicsBlood dopingerythropoiesis-stimulating agentsGene dopinghuman urineCondensed Matter::SuperconductivityToxicologíaComputer Science::Multimediaaromatase inhibition030304 developmental biology0303 health sciencesAromatase inhibitionbody compositionChemistryexogenous growth hormone010401 analytical chemistryMedicina deportivaskeletal muscle massAnabolic-Androgenic SteroidsSkeletal muscle massGenética3. Good health0104 chemical sciencesautologous blood transfusionsCondensed Matter::Strongly Correlated Electronshuman activitiesClinical psychology
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The transcriptional programme of contact-inhibition.

2010

Proliferation of non-transformed cells is regulated by cell-cell contacts, which are referred to as contact-inhibition. Vice versa, transformed cells are characterised by a loss of contact-inhibition. Despite its generally accepted importance for cell-cycle control, little is known about the intracellular signalling pathways involved in contact-inhibition. Unravelling the molecular mechanisms of contact-inhibition and its loss during tumourigenesis will be an important step towards the identification of novel target genes in tumour diagnosis and treatment. To better understand the underlying molecular mechanisms we identified the transcriptional programme of contact-inhibition in NIH3T3 fib…

Blotting WesternClone (cell biology)Cell Cycle ProteinsBiologyBiochemistryMiceComplementary DNATranscriptional regulationAnimalsMolecular BiologyGeneRegulator geneOligonucleotide Array Sequence AnalysisContact InhibitionReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleContact inhibitionCell BiologyFibroblastsFlow CytometryMolecular biologyGene expression profilingNIH 3T3 CellsDNA microarraySignal TransductionJournal of cellular biochemistry
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Influence of different biomaterials on the viability of Aggregatibacter actinomycetemcomitans

2011

Abstract Objectives The aim of the present in vitro study was to evaluate the effects of different biomaterials used for regenerative periodontal surgery on the growth of the periodontopathogen Aggregatibacter actinomycetemcomitans . Methods Three commercially available biomaterials of synthetic origin (hydroxyapatite/beta-tricalcium phosphate, nanostructured hydroxyapatite paste, oily calcium hydroxide suspension), a bovine-derived xenograft as well as an enamel matrix derivative (EMD) were added in different concentrations to calibrated suspensions of A. actinomycetemcomitans ATCC 43718/33384 (serotype b/c). Equal aliquots (0.1 ml) for the viability assay were taken after 5 min, 1 h, 3 h,…

Calcium PhosphatesBone MatrixBiocompatible MaterialsRegenerative MedicineAggregatibacter actinomycetemcomitansMicrobiologyCalcium HydroxideAgar platechemistry.chemical_compoundDental Enamel ProteinsMaterials TestingEnamel matrix derivativeAnimalsViability assayLeast-Squares AnalysisGeneral DentistryColony-forming unitMicrobial ViabilityCalcium hydroxidebiologyAggregatibacter actinomycetemcomitansCell BiologyGeneral Medicinebiology.organism_classificationAntimicrobialNanostructuresDurapatiteOtorhinolaryngologychemistryLinear ModelsCattleGrowth inhibitionArchives of Oral Biology
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TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.

2007

The aryl hydrocarbon receptor (AhR) is a transcription factor involved in physiological processes, but also mediates most, if not all, toxic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Activation of the AhR by TCDD leads to its dimerization with aryl hydrocarbon nuclear translocator (ARNT) and transcriptional activation of several phase I and II metabolizing enzymes. However, this classical signalling pathway so far failed to explain the pleiotropic hazardous effects of TCDD, such as developmental toxicity and tumour promotion. Thus, there is an urgent need to define genetic programmes orchestrated by AhR to unravel its role in physiology and toxicology. Here we show that TCDD …

Cancer ResearchAryl hydrocarbon receptor nuclear translocatorPolychlorinated Dibenzodioxinscyclin AProto-Oncogene Proteins c-junCyclin DCyclin Acell cycle controlCyclin ATetrachlorodibenzodioxinModels BiologicalDownregulation and upregulationGeneticsAnimalsRNA Small InterferingMolecular BiologyTranscription factorAryl hydrocarbon receptorCells CulturedbiologyContact InhibitionContact inhibitionCell cycleAryl hydrocarbon receptorRatsAdult Stem CellsLiverReceptors Aryl Hydrocarbonliver oval cellsbiology.proteinCancer researchJunDOncogene
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Bortezomib: a new pro-apoptotic agent in cancer treatment.

2010

Bortezomib is a proteasome inhibitor. It targets the ubiquitin-proteasome pathway with subsequent inhibition of the degradation of proteins involved in cell cycle regulation and cancer cell survival. The best known molecular mechanism concerns the inhibition of IkappaB breakdown and the related stabilization of NFkappaB, thus preventing its translocation to the nucleus for the activation of downstream pathways. Bortezomib is the only drug in this class which has been approved for clinical use. It has shown an efficient antitumor effect in a phase III clinical trial (APEX) involving relapsed multiple myeloma patients. Response rate, time to progression and overall survival have been improved…

Cancer ResearchCell cycle checkpointSettore MED/06 - Oncologia MedicaAntineoplastic AgentsApoptosisPharmacologyDexamethasoneBortezomibMiceNeoplasmshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoverymedicineAnimalsHumansDexamethasoneMultiple myelomaPharmacologyproteasome inhibitionClinical Trials as TopicNeovascularization Pathologicbusiness.industryBortezomibCell CycleNF-kappa Bsolid tumorsmedicine.diseaseBoronic AcidsClinical trialBortezomib; solid tumors; proteasome inhibition.OncologyApoptosisPyrazinesCancer cellProteasome inhibitorCancer researchMultiple MyelomabusinessProteasome InhibitorsBortezomib solid tumors proteasome inhibitionmedicine.drug
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