Search results for " Shock"

showing 10 items of 691 documents

Regional labor markets in Finland: Adjustment to total versus region-specific shocks

2005

This article analyses regional labor market adjustment in the Finnish provinces during 1976-2000. We investigate the inter-relations of employment, unemployment, labor force participation, and migration to see how a change in region-specific and total labor demand is adjusted. The analysis reveals that region-specific labor demand shocks adjust mainly via participation, whereas total shocks are adjusted by unemployment. The region-specific component of labor demand shock has shorter-lived effects on unemployment and participation, but its effect on employment is permanent. Conversely, total shocks leave no permanent effect. Migration is more important in the region-specific case where, afte…

Labour economicsSecondary labor marketmedia_common.quotation_subjectGeography Planning and DevelopmentLabor demandEnvironmental Science (miscellaneous)Excess supplyShock (economics)Region specificjel:J6UnemploymentEconomicsLabor market employment unemployment migration shock adjustmentjel:R23media_commonPapers in Regional Science
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HSP27 controls GATA-1 protein level during erythroid cell differentiation.

2010

AbstractHeat shock protein 27 (HSP27) is a chaperone whose cellular expression increases in response to various stresses and protects the cell either by inhibiting apoptotic cell death or by promoting the ubiquitination and proteasomal degradation of specific proteins. Here, we show that globin transcription factor 1 (GATA-1) is a client protein of HSP27. In 2 models of erythroid differentiation; that is, in the human erythroleukemia cell line, K562 induced to differentiate into erythroid cells on hemin exposure and CD34+ human cells ex vivo driven to erythroid differentiation in liquid culture, depletion of HSP27 provokes an accumulation of GATA-1 and impairs terminal maturation. More spec…

LeupeptinsPyridines[SDV]Life Sciences [q-bio]Cellular differentiationCellHSP27 Heat-Shock ProteinsAntigens CD34Biochemistryp38 Mitogen-Activated Protein Kinases0302 clinical medicineTransforming Growth Factor betahemic and lymphatic diseasesChlorocebus aethiopsGATA1 Transcription FactorPhosphorylationComputingMilieux_MISCELLANEOUSCells CulturedHeat-Shock Proteins0303 health sciencesbiologyImidazolesCell DifferentiationHematology[SDV] Life Sciences [q-bio]medicine.anatomical_structure030220 oncology & carcinogenesisembryonic structuresCOS CellsRNA InterferenceSignal transductionProteasome InhibitorsProtein BindingProteasome Endopeptidase ComplexImmunologyImmunoblotting03 medical and health sciencesHsp27Erythroid CellsHeat shock proteinmedicineAnimalsHumansTranscription factor030304 developmental biologyCell NucleusInterleukin-6UbiquitinationCell BiologyTransforming growth factor betaMolecular biologyChaperone (protein)biology.proteinK562 CellsHeLa CellsMolecular ChaperonesBlood
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Bank-specific shocks and aggregate leverage: Empirical evidence from a panel of developed countries

2020

International audience; This paper investigates the link between shocks in the banking sector and aggregate leverage measured by the credit-to-GDP gap. Using a balanced panel of 15 countries for the period 1989–2016, we exploit the approach due to Gabaix (2011) and consider banking granular shocks as an indicator of banking distress. Using methods that account for potential endogeneity, we find that banking shocks Granger-cause aggregate leverage. In particular, banking shocks tend to increase the level of leverage and cause departures of the credit-to-GDP ratio from its long-term trend.

Leverage (finance)ExploitMonetary economics[SHS]Humanities and Social SciencesPanel VARGranger causalityGranularity model0502 economics and businessBanking shocksEconomicsEndogeneityEmpirical evidence040101 forestryCredit-to-GDP gap050208 finance05 social sciences1. No poverty04 agricultural and veterinary sciences[SHS.ECO]Humanities and Social Sciences/Economics and FinanceBanking sector8. Economic growthGranger causality0401 agriculture forestry and fisheriesGeneral Economics Econometrics and FinanceDeveloped countryFinanceJournal of Financial Stability
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Interaction of TLR2 and TLR4 ligands with the N-terminal domain of Gp96 amplifies innate and adaptive immune responses.

2006

Activation of dendritic cells by ligands for Toll-like receptors (TLR) is a crucial event in the initiation of innate and adaptive immune responses. Several classes of TLR ligands have been identified that interact with distinct members of the TLR-family. TLR4 ligands include lipopolysaccharide derived from different Gram-negative bacteria and viral proteins. Recent reports have demonstrated the TLR-mediated activation of dendritic cells by heat shock proteins (HSPs). However, doubts were raised as to what extent this effect was due to lipopolysaccharide contaminations of the HSP preparations. We re-examined this phenomenon using Gp96 or its N-terminal domain, nominally endotoxin-free (0.5 …

LipopolysaccharidesLipopolysaccharideBiologyCD8-Positive T-LymphocytesBiochemistrychemistry.chemical_compoundMiceImmune systemDogsHeat shock proteinAnimalsHumansReceptorMolecular BiologyInflammationMice Inbred BALB CInnate immune systemMembrane GlycoproteinsCCL18Cell BiologyToll-Like Receptor 2Cell biologyEndotoxinsMice Inbred C57BLToll-Like Receptor 4TLR2BiochemistrychemistryTLR4The Journal of biological chemistry
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Doxycycline Reduces Mortality to Lethal Endotoxemia by Reducing Nitric Oxide Synthesis via an Interleukin‐10‐Independent Mechanism

1998

It was demonstrated that doxycycline protected BALB/c mice injected intraperitoneally with bacterial lipopolysaccharide (LPS) against lethal septic shock. Doxycycline (at 1.5 mg/kg) exerted its protective effect by inhibiting nitrate production by an interleukin-10-independent mechanism. Experiments carried out in vitro also indicated that doxycycline inhibited NO synthesis by LPS-activated macrophages without inducing any significant modification in interleukin-10 release. These data suggest that the direct inhibition of nitrate release is the main mechanism of the antiinflammatory activity of doxycycline in septic shock.

LipopolysaccharidesLipopolysaccharidePharmacologyNitric OxideNitric oxideMicechemistry.chemical_compoundmedicineAnimalsImmunology and AllergyDoxycyclineMice Inbred BALB CNitratesSeptic shockMacrophagesInterleukinmedicine.diseaseShock SepticEndotoxemiaAnti-Bacterial AgentsInterleukin-10Interleukin 10Infectious DiseaseschemistryDoxycyclineShock (circulatory)ImmunologyLiberationFemalemedicine.symptommedicine.drugThe Journal of Infectious Diseases
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The adenosine deaminase inhibitor erythro-9-[2-hydroxyl-3-nonyl]-adenine decreases intestinal permeability and protects against experimental sepsis: …

2008

Introduction The treatment of septic conditions in critically ill patients is still one of medicine's major challenges. Cyclic nucleotides, adenosine and its receptors play a pivotal role in the regulation of inflammatory responses and in limiting inflammatory tissue destruction. The aim of this study was to verify the hypothesis that adenosine deaminase-1 and cyclic guanosine monophosphate-stimulated phosphodiesterase inhibition by erythro-9-[2-hydroxyl-3-nonyl]-adenine could be beneficial in experimental endotoxicosis/sepsis. Method We used two established animal models for endotoxicosis and sepsis. Twenty-four male Wistar rats that had been given intravenous endotoxin (Escherichia coli l…

LipopolysaccharidesMaleLipopolysaccharideAdenosine DeaminasePharmacologyCritical Care and Intensive Care MedicinePermeabilitySepsisExcretionMicechemistry.chemical_compoundSepsisAdenosine Deaminase InhibitorsmedicineAnimalsProspective StudiesRats WistarPhosphodiesterase inhibitorIntestinal permeabilitybusiness.industrySeptic shockAdenineResearchmedicine.diseaseAdenosineRatsIntestinal AbsorptionchemistryImmunologyFemaleAdenosine Deaminase Inhibitorbusinessmedicine.drugCritical Care
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Glycyrrhetinic Acid Reverses the Lipopolysaccharide-Induced Hypocontractility to Noradrenaline in Rat Aorta: Implications to Septic Shock

2014

Abstract.: Septic shock and associated vascular hyporeactivity to vasoconstrictor agonists remain a major problem of critical care medicine. Here we report that glycyrrhetinic acid (GA), the active component of licorice, effectively restores vascular contractility in the model of lipopolysaccharide (LPS)-treated rat aorta. GA was as effective as the NO synthase inhibitor NG-nitroarginine methylester. GA did not affect the vascular NO levels (measured by EPR spin trapping) and relaxations to l-arginine in LPS-treated rings as well as relaxation to S-nitroso-Nacetylpenicillamine in control rings. Thus, GA may represent an interesting alternative to NO synthase inhibitors in sepsis-associated …

LipopolysaccharidesMaleLipopolysaccharideArgininePharmacologychemistry.chemical_compoundNorepinephrinemedicine.arteryActive componentNo synthaseGlycyrrhizaMedicineAnimalsEnzyme InhibitorsRats WistarAortaPharmacologyVascular contractilityAortabusiness.industrySeptic shocklcsh:RM1-950medicine.diseaseShock SepticEpr spin trappinglcsh:Therapeutics. PharmacologychemistryBiochemistryVasoconstrictionMolecular MedicineGlycyrrhetinic AcidNitric Oxide SynthasebusinessPhytotherapyJournal of Pharmacological Sciences
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HSP60 and CpG-DNA-oligonucleotides differentially regulate LPS-tolerance of hepatic Kupffer cells

2004

Background/aims: Hepatic Kupffer cells (KC) are major regulators of the immune response to gut-derived bacterial products; uncontrolled activation of KC by bacterial components is of pathogenic relevance in alcoholic hepatitis and septic shock. Methods: We examined the role of bacterial lipopolysaccharide (LPS), bacterial and autologous HSP60 and bacterial DNA, which are recognized by innate Toll-like receptors, during activation of murine KC. Results: In cultivated KC, autologous HSP60 induced a state of LPS-hyporesponsiveness; bacterial DNA did not mitigate the response to subsequent LPS-challenge in vitro; in contrast, pre-treatment of mice with bacterial DNA even significantly increased…

LipopolysaccharidesMaleLipopolysaccharideKupffer CellsImmunologyGene ExpressionGalactosamineReceptors Cell SurfaceCell LineMicrobiologyMicechemistry.chemical_compoundImmune systemImmunityHeat shock proteinAnimalsImmunology and AllergyInterleukin 6Cells CulturedbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAlanine TransaminaseChaperonin 60Macrophage ActivationToll-Like Receptor 9DNA-Binding ProteinsToll-Like Receptor 4LiverOligodeoxyribonucleotideschemistryToll-Like Receptor 9Immunologybiology.proteinFemaleHSP60Tumor necrosis factor alphaLiver FailureImmunology Letters
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Tiratricol neutralizes bacterial endotoxins and reduces lipopolysaccharide-induced TNF-alpha production in the cell.

2008

Contains fulltext : 70610.pdf (Publisher’s version ) (Closed access) The screening of a commercially available library of compounds has proved a successful strategy for the identification of a lead compound in a drug discovery programme. Here, we analysed 880 off-patent drugs, which initially comprised the Prestwick Chemical library, as sources of bacterial endotoxin neutralizers. We identified 3,3',5-triiodo-thyroacetic acid (tiratricol) as a non-antibacterial compound that neutralizes the toxic lipopolysaccharide.

LipopolysaccharidesendotoxinLipopolysaccharideCelllipopolysaccharide-antagonistsBiology:Enginyeria dels materials [Àrees temàtiques de la UPC]BiochemistryCell LineChemical libraryMicrobiologyLipid ASepsissepsisMiceStructure-Activity Relationshipchemistry.chemical_compoundtumour necrosis factor-alphaDrug DiscoveryEscherichia colimedicineAnimalsDrugs--Designlipid APharmacologyTriiodothyroacetic acidMedicaments -- DissenyTumor Necrosis Factor-alphaDrug discoveryOrganic Chemistrylipopolysaccharidetumour necrosis factor-amedicine.diseaseAnti-Bacterial AgentsEndotoxinsmedicine.anatomical_structurechemistryTriiodothyronineMolecular Medicineseptic shockLead compoundImmunity infection and tissue repair [NCMLS 1]
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Heat shock response in yeast involver changes in both transcription rates and mRNA stabilities

2011

We have analyzed the heat stress response in the yeast Saccharomyces cerevisiae by determining mRNA levels and transcription rates for the whole transcriptome after a shift from 25uC to 37uC. Using an established mathematical algorithm, theoretical mRNA decay rates have also been calculated from the experimental data. We have verified the mathematical predictions for selected genes by determining their mRNA decay rates at different times during heat stress response using the regulatable tetO promoter. This study indicates that the yeast response to heat shock is not only due to changes in transcription rates, but also to changes in the mRNA stabilities. mRNA stability is affected in 62% of …

Llevat de cervesaTranscription GeneticEstrès oxidatiuRNA StabilitySaccharomyces cerevisiaeGene Expressionlcsh:MedicineYeast and Fungal ModelsRNA-binding proteinSaccharomyces cerevisiaeModels BiologicalGenètica molecularModel OrganismsTranscripció genèticaGenome Analysis ToolsTranscription (biology)Gene Expression Regulation FungalYeastsHeat shock proteinMolecular Cell BiologyGeneticsCluster AnalysisRNA MessengerHeat shocklcsh:ScienceBiologyGeneTranscription factorHeat-Shock ProteinsMultidisciplinaryBase SequenceOrganisms Genetically ModifiedbiologySystems Biologylcsh:RRNA FungalLlevats -- GenèticaGenomicsbiology.organism_classificationMolecular biologyFunctional GenomicsCell biologyRegulonRNAlcsh:QGenome Expression AnalysisHeat-Shock ResponseResearch ArticleTranscription Factors
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