Search results for "EMBER"

showing 10 items of 549 documents

Pharmacogenetic Study of ABCB1 and CYP3A5 Genes During the First Year Following Heart Transplantation Regarding Tacrolimus or Cyclosporine Levels

2011

Pharmacogenetics explains part of the interindividual variability in drug responses. Many published works about the effects of single nucleotide polymorphisms (SNPs) on immunosuppressive drug blood levels present contradictory results. We evaluated the SNPs in ABCB1 (glycoprotein P) and CYP3A5 (metabolic enzyme) genes, seeking correlate them with tacrolimus or cyclosporine levels during the first year after heart transplantation. One blood sample was obtained from each of 41 patients: 26 treated with cyclosporine and 15 with tacrolimus. We characterize the SNPs rs1045642, 1128503, 2032582, 2235013, 2235033, 2229109, 3213619, 9282564 in ABCB1 and rs10264272, 776746 in CYP3A5 genes using the …

Linkage disequilibriummedicine.medical_specialtyATP Binding Cassette Transporter Subfamily BGenotypemedicine.medical_treatmentSingle-nucleotide polymorphismBiologyPharmacologyPolymorphism Single NucleotideGastroenterologyLinkage DisequilibriumTacrolimusGene FrequencyInternal medicineGenotypemedicineCytochrome P-450 CYP3AHumansDrug Dosage CalculationsATP Binding Cassette Transporter Subfamily B Member 1CYP3A5Heart transplantationTransplantationTacrolimusPhenotypeImmunosuppressive drugPharmacogeneticsSpainCyclosporineHeart TransplantationSurgeryDrug MonitoringImmunosuppressive AgentsPharmacogeneticsTransplantation Proceedings
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Probabilistic and fuzzy logic in clinical diagnosis

2007

In this study I have compared classic and fuzzy logic and their usefulness in clinical diagnosis. The theory of probability is often considered a device to protect the classical two-valued logic from the evidence of its inadequacy to understand and show the complexity of world [1]. This can be true, but it is not possible to discard the theory of probability. I will argue that the problems and the application fields of the theory of probability are very different from those of fuzzy logic. After the introduction on the theoretical bases of fuzzy approach to logic, I have reported some diagnostic argumentations employing fuzzy logic. The state of normality and the state of disease often figh…

Logicbusiness.industrymedia_common.quotation_subjectfungiProbabilistic logicProbability TheoryFuzzy logichumanitiesProbabilistic logic Fuzzy logic truth diagnosisFuzzy Logicstomatognathic systemProbabilistic logic networkClinical diagnosisDiagnosisEmergency MedicineInternal MedicineHumansMedicineArtificial intelligenceClinical MedicinebusinessMembership functionNormalitymedia_commonInternal and Emergency Medicine
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Is There Life Outside of the European Union? Lower Silesians’ Opinions About the Alternatives to the EU Membership

2017

This paper answers the question about the alternatives to the European Union membership (and its consequences) conceptualised by the inhabitants of Lower Silesia. To achieve this goal, this text delivers and discusses the empirical data, both quantitative and qualitative, answering the sub-questions if and how their lives have changed as a result of the accession to the EU as well as what are the alternatives, namely: How would our lives have looked like if Poland had not joined the EU in 2004? The article is empirical at its heart. It is built on some fresh data from an extensive research project conducted in 2014 – at the occasion of the tenth anniversary of the EU ‘big bang’ enlargement.…

Lower SilesiaEuropean Union membershipalternativesYearbook of Polish European Studies
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Novel Stability Criteria for T--S Fuzzy Systems

2014

In this paper, novel stability conditions for Takagi-Sugeno (T-S) fuzzy systems are presented. The so-called nonquadratic membership-dependent Lyapunov function is first proposed, which is formulated in a higher order form of both the system states and the normalized membership functions than existing techniques in the literature. Then, new membership-dependent stability conditions are developed by the new Lyapunov function approach. It is shown that the conservativeness of the obtained criteria can be further reduced as the degree of the Lyapunov function increases. Two numerical examples are given to demonstrate the effectiveness and less conservativeness of the obtained theoretical resul…

Lyapunov functionpolynomialsFuzzy setStability (learning theory)Lyapunov function; membership-dependent; stability; Takagi-Sugeno (T-S) fuzzy system; Control and Systems Engineering; Computational Theory and Mathematics; Artificial Intelligence; Applied Mathematicssymbols.namesakevectorsTakagi-Sugeno (T-S) fuzzy systemComputer Science::Systems and ControlArtificial IntelligenceControl theoryLyapunov equationLyapunov redesignLyapunov methodsMathematicsLyapunov functionDegree (graph theory)membership-dependentstability criteriaApplied Mathematicseducational institutionsFuzzy control systemstabilityStability conditionsComputational Theory and MathematicsControl and Systems Engineeringfuzzy systemssymbolsIEEE Transactions on Fuzzy Systems
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Acidosis induces multi-drug resistance in rat prostate cancer cells (AT1) in vitro and in vivo by increasing the activity of the p-glycoprotein via a…

2008

Because solid growing tumors often show hypoxia and pronounced extracellular acidosis, the aim of this study was to analyze the impact of an acidotic environment on the activity of the p-glycoprotein (pGP) and on the cellular content and cytotoxicity of the chemotherapeutic drug daunorubicin in the AT1 R-3327 Dunning prostate carcinoma cell line cultured in vitro and in vivo. In vitro, extracellular acidosis (pH 6.6) activated p38 and ERK1/2 and thereby induced daunorubicin resistance via a pronounced activation of pGP. De-novo protein synthesis was not necessary and analysis of transport kinetics indicated a fast and persistent pGP activation at pH 6.6 (when compared with 7.4). Intracellul…

MAPK/ERK pathwayMaleCancer Researchmedicine.medical_specialtyDaunorubicinPharmacologyp38 Mitogen-Activated Protein KinasesIn vivoInternal medicinepolycyclic compoundsmedicineExtracellularAnimalsATP Binding Cassette Transporter Subfamily B Member 1Extracellular Signal-Regulated MAP KinasesProtein Kinase CP-glycoproteinAcidosisCell ProliferationbiologyCaspase 3DaunorubicinProstatic NeoplasmsBiological activityHydrogen-Ion ConcentrationIn vitroDrug Resistance MultipleRatscarbohydrates (lipids)Enzyme ActivationEndocrinologyOncologyDrug Resistance Neoplasmbiology.proteinmedicine.symptomAcidosisNeoplasm Transplantationmedicine.drugInternational journal of cancer
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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The nuclear receptor PPARγ selectively inhibits Th17 differentiation in a T cell–intrinsic fashion and suppresses CNS autoimmunity

2009

T helper cells secreting interleukin (IL)-17 (Th17 cells) play a crucial role in autoimmune diseases like multiple sclerosis (MS). Th17 differentiation, which is induced by a combination of transforming growth factor (TGF)-beta/IL-6 or IL-21, requires expression of the transcription factor retinoic acid receptor-related orphan receptor gamma t (ROR gamma t). We identify the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) as a key negative regulator of human and mouse Th17 differentiation. PPAR gamma activation in CD4(+) T cells selectively suppressed Th17 differentiation, but not differentiation into Th1, Th2, or regulatory T cells. Control of Th17 differentia…

MESH: Nuclear Receptor Subfamily 1 Group F Member 3Helper-InducerReceptors Retinoic AcidT-LymphocytesMESH: Interleukin-17Cellular differentiationRetinoic AcidPeroxisome proliferator-activated receptorNeurodegenerativeInbred C57BLMedical and Health SciencesMiceInterleukin 210302 clinical medicineGroup FRAR-related orphan receptor gammaMESH: Nuclear Receptor Co-Repressor 2Receptors2.1 Biological and endogenous factorsThyroid HormoneImmunology and AllergyMESH: AnimalsAetiologyEncephalomyelitisPromoter Regions Geneticchemistry.chemical_classificationOrphan receptor0303 health sciencesReceptors Thyroid HormoneInterleukin-17Cell DifferentiationT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 33. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureMESH: Repressor Proteins[SDV.IMM]Life Sciences [q-bio]/ImmunologyInterleukin 17MESH: Cell Differentiationmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisNuclear Receptor Subfamily 1Member 31.1 Normal biological development and functioningT cellImmunologyBiologyAutoimmune DiseasePromoter RegionsExperimental03 medical and health sciencesGeneticUnderpinning researchMESH: Mice Inbred C57BLInternal medicineMESH: Promoter Regions GeneticGeneticsmedicineAnimalsHumansNuclear Receptor Co-Repressor 2MESH: Receptors Thyroid HormoneMESH: T-Lymphocytes Helper-InducerMESH: Encephalomyelitis Autoimmune ExperimentalMESH: Mice030304 developmental biologyMESH: Receptors Retinoic AcidMESH: HumansInflammatory and immune systemNeurosciencesBrief Definitive ReportCorrectionMESH: Multiple SclerosisBrain DisordersMice Inbred C57BLPPAR gammaRepressor ProteinsEndocrinologyMESH: PPAR gammaNuclear receptorchemistryMESH: DNA-Binding Proteins030217 neurology & neurosurgeryAutoimmuneJournal of Experimental Medicine
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Cloning and expression of genes involved in conidiation and surface properties of Penicillium camemberti grown in liquid and solid cultures.

2008

International audience; Based on bioinformatic data on model fungi, the rodA and wetA genes encoding, respectively, a RodA hydrophobin protein and the WetA protein involved in conidiation mechanisms, were PCR-cloned and characterized for the first time in Penicillium camemberti. These results, completed by a sequence of the brlA gene (available in GenBank), which encodes a major transcriptional regulator also involved in the conidiation mechanism, were used to compare, by qRT-PCR, the expression of the three genes in liquid and solid cultures in a synthetic medium. While expression of the brlA and wetA genes increased dramatically in both culture conditions after 4 days of growth, expressio…

MESH: Sequence Analysis DNAMESH : Spores FungalMESH : Molecular Sequence DataConidiationMESH: Amino Acid SequenceMESH: Base SequenceGene Expression Regulation FungalGene expressionMESH : Fungal ProteinsCloning MolecularFungal proteinMESH : Amino Acid SequenceMESH : Sequence AlignmentGeneral MedicineSpores FungalMESH: MyceliumCell biologyWetaPenicillium camembertiMESH: Fungal ProteinsMESH : HydrophobicityHydrophobic and Hydrophilic InteractionsMESH : MyceliumMESH: Gene Expression Regulation FungalHyphaMESH : Cloning MolecularHydrophobinMolecular Sequence DataMESH: Sequence AlignmentBiologyMicrobiologyMicrobiologyFungal ProteinsMESH: Spores FungalMESH : Gene Expression Regulation FungalMESH: Cloning Molecular[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceMolecular BiologyGene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: PenicilliumMESH: HydrophobicityMESH: Molecular Sequence DataBase SequenceMyceliumPenicilliumSequence Analysis DNAMESH : Penicilliumbiology.organism_classificationCulture MediaMESH: Culture MediaMESH : Base SequenceMESH : Culture MediaSequence AlignmentMESH : Sequence Analysis DNA
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Antigen-processing machinery breakdown and tumor growth.

2000

Defects in the major histocompatibility complex (MHC) class I antigen-processing machinery (APM) have been described in tumors of different histology. Murine data suggest that defects in the MHC class II APM might also be associated with malignant transformation of human cells. This article describes the pathophysiology of the MHC class I and II APM, reviews APM abnormalities in tumor cells and discusses their role in the escape of tumor cells from in vitro recognition by T cells.

MHC class IIAntigen PresentationProteasome Endopeptidase ComplexbiologyAntigen processingImmunologyAntigen presentationHistocompatibility Antigens Class IHistocompatibility Antigens Class IIATP-binding cassette transporterMajor histocompatibility complexIn vitroMalignant transformationCysteine EndopeptidasesATP Binding Cassette Transporter Subfamily B Member 3Multienzyme ComplexesNeoplasmsMHC class IImmunologybiology.proteinCancer researchAnimalsHumansATP-Binding Cassette TransportersImmunology today
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