Search results for "R1"

showing 10 items of 1016 documents

Immunoprofiles and DNA methylation of inflammatory marker genes in ulcerative colitis-associated colorectal tumorigenesis

2021

Immunological and epigenetic changes are interconnected and contribute to tumorigenesis. We determined the immunoprofiles and promoter methylation of inflammation-related genes for colitis-associated colorectal carcinomas (CA-CRC). The results were compared with Lynch syndrome (LS)-associated colorectal tumors, which are characterized by an active immune environment through inherited mismatch repair defects. CA-CRCs (n = 31) were immunohistochemically evaluated for immune cell scores (ICSs) and PDCD1 and CD274 expression. Seven inflammation-associated genes (CD274, NTSR1, PPARG, PTGS2, PYCARD, SOCS1, and SOCS2), the repair gene MGMT, and eight standard marker genes for the CpG Island Methyl…

MaleCarcinogenesismedicine.disease_causeBiochemistry0302 clinical medicineIntestinal MucosaDNA Modification Methylases0303 health sciencesMUCOSADNA methylationtulehdusinflammation-associated genesPYCARDMethylationMiddle AgedLynch syndromeQR1-502EPIGENETICS3. Good healthDNA-metylaatioGene Expression Regulation NeoplasticPhenotypecolon cancerepigenetiikka030220 oncology & carcinogenesisimmuunivasteDNA methylationFemaleColorectal NeoplasmsCANCERSINSTABILITYsuolistosyövätBiology3121 Internal medicineMicrobiologyArticle03 medical and health sciencesmedicineHumansEpigeneticsLynchin oireyhtymäMolecular Biologyneoplasms030304 developmental biologypaksusuolisyöpäulcerative colitisInflammationCpG Island Methylator PhenotypeTumor Suppressor Proteinshaavainen koliittimedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseasesDNA Repair EnzymesLynch syndrome3121 General medicine internal medicine and other clinical medicineMutationimmune cell scoreCancer research1182 Biochemistry cell and molecular biologyColitis UlcerativeCpG IslandsField cancerizationCarcinogenesisBiomarkers
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Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats.

2020

Minimal hepatic encephalopathy is associated with changes in the peripheral immune system which are transferred to the brain, leading to neuroinflammation and thus to cognitive and motor impairment. Mechanisms by which changes in the immune system induce cerebral alterations remain unclear. Extracellular vesicles (EVs) seem to play a role in this process in certain pathologies. The aim of this work was to assess whether EVs play a role in the induction of neuroinflammation in cerebellum and motor incoordination by chronic hyperammonemia. We characterized the differences in protein cargo of EVs from plasma of hyperammonemic and control rats by proteomics and Western blot. We assessed whether…

MaleCerebellumtnfαhepatic encephalopathyArticleExtracellular VesiclesImmune systemWestern blotmedicineAnimalsHumansHyperammonemiaRats WistarReceptorlcsh:QH301-705.5NeuroinflammationInflammationMicrogliamedicine.diagnostic_testbusiness.industryTumor Necrosis Factor-alphaHyperammonemiaGeneral Medicinetnfα receptor tnfr1medicine.diseaseRatsMotor Skills DisordersDisease Models Animalmedicine.anatomical_structurelcsh:Biology (General)glial activationTumor necrosis factor alphaNervous System DiseasesTNF alpha receptor TNFR1businessNeuroscienceTNF alpha
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The default mode network and the working memory network are not anti-correlated during all phases of a working memory task

2015

INTRODUCTION:\ud \ud The default mode network and the working memory network are known to be anti-correlated during sustained cognitive processing, in a load-dependent manner. We hypothesized that functional connectivity among nodes of the two networks could be dynamically modulated by task phases across time.\ud METHODS:\ud \ud To address the dynamic links between default mode network and the working memory network, we used a delayed visuo-spatial working memory paradigm, which allowed us to separate three different phases of working memory (encoding, maintenance, and retrieval), and analyzed the functional connectivity during each phase within and between the default mode network and the …

MaleCingulate cortexComputer scienceFunctional magnetic resonance imagingCINGULATE CORTEX0302 clinical medicinePrefrontal cortexALZHEIMERSDefault mode networkCerebral CortexDefault mode network; female; Functional magnetic resonance imaging; Working memoryMultidisciplinarymedicine.diagnostic_testArtificial neural networkQ05 social sciencesRCognitionHuman brainFUNCTIONAL CONNECTIVITYFLUCTUATIONSMagnetic Resonance ImagingMemory Short-Termmedicine.anatomical_structurefemaleCerebral cortexConnectomeMedicineSettore MED/26 - NeurologiaAlzheimer's diseasedefault mode network; working memory; functional magnetic resonance imaging; functional connectivity; Brain networksResearch ArticleHumanCognitive psychologyAdultBrain networksScienceRETRIEVALPosterior parietal cortex050105 experimental psychologyYoung Adult03 medical and health sciencesPARIETAL CORTEXTask-positive networkEncoding (memory)ConnectomemedicineHumans0501 psychology and cognitive sciencesMODULATIONBRAIN-FUNCTIONResting state fMRIWorking memoryWorking memorymedicine.diseaseR1COMPONENTDefault mode networkRESTING-STATEFunctional magnetic resonance imaging030217 neurology & neurosurgery
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Spasmolytic Effects of Aphanizomenon Flos Aquae (AFA) Extract on the Human Colon Contractility.

2021

The blue-green algae Aphanizomenon flos aquae (AFA), rich in beneficial nutrients, exerts various beneficial effects, acting in different organs including the gut. Klamin® is an AFA extract particularly rich in β-PEA, a trace-amine considered a neuromodulator in the central nervous system. To date, it is not clear if β-PEA exerts a role in the enteric nervous system. The aims of the present study were to investigate the effects induced by Klamin® on the human distal colon mechanical activity, to analyze the mechanism of action, and to verify a β-PEA involvement. The organ bath technique, RT-PCR, and immunohistochemistry (IHC) were used. Klamin® reduced, in a concentration-dependent manner, …

MaleColonmotility discomfortMethysergideGene ExpressionPharmacologyArticle-PEAContractilityTAAR1medicineSerotonin receptor antagonistAphanizomenonHumansTX341-641Myenteric plexusAgedhuman colon contractilityAged 80 and overBiological ProductsAFA extractNutrition and DieteticsDose-Response Relationship DrugChemistryNutrition. Foods and food supplyParasympatholyticsEPPTBMuscle SmoothKlamin®Middle AgedKlamin<sup>®</sup>ImmunohistochemistryMechanism of actionDietary SupplementsEnteric nervous systemFemalePeristalsismedicine.symptomBiomarkersβ-PEAFood Sciencemedicine.drugMuscle ContractionNutrients
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A human leucocyte antigen-DR1 transgene confers susceptibility to experimental allergic encephalomyelitis elicited by an epitope of myelin basic prot…

2003

Much evidence now indicates that human leucocyte antigen (HLA) class I and class II transgenic (Tg) mice can be of value in analysing HLA-restricted presentation of T-cell epitopes relevant to experimental models of autoimmune diseases. One area where this has been applied is the characterization of myelin epitopes presented by HLA class II molecules in experimental model of multiple sclerosis (experimental allergic encephalomyelitis (EAE)). As a first step towards humanized disease models in HLA Tg mice, we have analysed immune response of lymph node cells of HLA-DR1 Tg mice immunized with the human myelin basic protein (MBP) peptides 13–33, 87–106 and 139–154 bound by HLA-DR1. We report h…

MaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEncephalomyelitisTransgeneImmunologyMolecular Sequence DataEpitopes T-LymphocyteMice TransgenicHuman leukocyte antigenEpitopeMyelinMiceImmune systemmedicineAnimalsHumansGenetic Predisposition to DiseaseAmino Acid SequencebiologyHLA-DR1 AntigenMyelin Basic ProteinGeneral Medicinemedicine.diseaseIn vitroPeptide FragmentsMyelin basic proteinDisease Models Animalmedicine.anatomical_structureImmunologybiology.proteinFemaleLymph NodesScandinavian journal of immunology
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Mutual Antagonism between Circadian Protein Period 2 and Hepatitis C Virus Replication in Hepatocytes

2013

BackgroundHepatitis C virus (HCV) infects approximately 3% of the world population and is the leading cause of liver disease, impacting hepatocyte metabolism, depending on virus genotype. Hepatic metabolic functions show rhythmic fluctuations with 24-h periodicity (circadian), driven by molecular clockworks ticking through translational-transcriptional feedback loops, operated by a set of genes, called clock genes, encoding circadian proteins. Disruption of biologic clocks is implicated in a variety of disorders including fatty liver disease, obesity and diabetes. The relation between HCV replication and the circadian clock is unknown.MethodsWe investigated the relationship between HCV core…

MaleGastroenterology and hepatologyCircadian clockHepacivirusVirus ReplicationHepatitisMolecular cell biologyCellular Stress ResponsesMultidisciplinaryViral Core ProteinsQMechanisms of Signal TransductionRPeriod Circadian ProteinsMiddle AgedHepatitis CCLOCKPER2ARNTLInfectious hepatitisLiverMedicineInfectious diseasesRNA ViralFemaleResearch ArticleSignal TransductionPER1AdultHistologyFeedback RegulationGenotypeSciencePeriod (gene)DNA transcriptionViral diseasesGenome ViralBiologyCell LineCell Line TumorGeneticsHumansBiologyLiver diseasesAgedVirologyHepatocytesPeriod Circadian ProteinsGene expressionARNTL2PLoS ONE
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Loss of striatal type 1 cannabinoid receptors is a key pathogenic factor in Huntington's disease.

2010

Endocannabinoids act as neuromodulatory and neuroprotective cues by engaging type 1 cannabinoid receptors. These receptors are highly abundant in the basal ganglia and play a pivotal role in the control of motor behaviour. An early downregulation of type 1 cannabinoid receptors has been documented in the basal ganglia of patients with Huntington's disease and animal models. However, the pathophysiological impact of this loss of receptors in Huntington's disease is as yet unknown. Here, we generated a double-mutant mouse model that expresses human mutant huntingtin exon 1 in a type 1 cannabinoid receptor-null background, and found that receptor deletion aggravates the symptoms, neuropatholog…

MaleHuntingtinCannabinoid receptorCell Survivalmedicine.medical_treatmentBlotting WesternMice TransgenicBiologyMotor ActivityGrowth Hormone-Releasing HormoneMiceReceptor Cannabinoid CB1medicineCannabinoid receptor type 2AnimalsDronabinolReceptorBrain-derived neurotrophic factorNeuronsAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemMagnetic Resonance ImagingCorpus StriatumHuntington DiseaseRotarod Performance TestGPR18Neurology (clinical)CannabinoidNeuroscienceBrain : a journal of neurology
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A Polymorphism in the Crhr1 Gene Determines Stress Vulnerability in Male Mice

2014

Chronic stress is a risk factor for psychiatric disorders but does not necessarily lead to uniform long-term effects on mental health, suggesting modulating factors such as genetic predispositions. Here we address the question whether natural genetic variations in the mouse CRH receptor 1 (Crhr1) locus modulate the effects of adolescent chronic social stress (ACSS) on long-term stress hormone dysregulation in outbred CD1 mice, which allows a better understanding of the currently reported genes × environment interactions of early trauma and CRHR1 in humans. We identified 2 main haplotype variants in the mouse Crhr1 locus that modulate the long-term effects of ACSS on basal hypothalamic-pitui…

MaleHypothalamo-Hypophyseal SystemGenotypeGene ExpressionPituitary-Adrenal SystemLocus (genetics)Single-nucleotide polymorphismRegulatory Sequences Nucleic AcidBiologyBinding CompetitivePolymorphism Single NucleotideReceptors Corticotropin-Releasing HormoneMiceEndocrinologyGene FrequencyGenetic predispositionAnimalsHumansGenetic Predisposition to DiseaseChronic stressCRHR1 GeneGeneIn Situ HybridizationSocial stressGeneticsBehavior AnimalTriazinesHaplotypeHaplotypesPituitary GlandPyrazolesFemaleGene-Environment InteractionCorticosteroneStress PsychologicalSignal TransductionEndocrinology
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Social defeat-induced increase in the conditioned rewarding effects of cocaine: Role of CX3CL1

2019

Abstract Social stress is associated with higher vulnerability to drug use, as it enhances the reinforcing effects of psychostimulants in rodents. Furthermore, continued or severe stress induces a proinflammatory state of microglial activation and augmented cytokine production. The aim of the present work was to evaluate the role of fractalkine [C-X3-C motif ligand 1 (CX3CL1)], an inflammatory chemokine, in the increased conditioned rewarding effects of cocaine in animals exposed to social defeat stress. In addition, we measured the signaling cascade pathway of CX3CL1 in the hippocampus (HPC) (including p-ERK/ERK, p-p38/p38 MAPK, p-p65/p65 NFκB and p-CREB/CREB ratios). The glutamate recepto…

MaleMAPK/ERK pathwaymedicine.medical_specialtyCREBSocial DefeatSocial defeatMice03 medical and health sciences0302 clinical medicineCocaineDopamine Uptake InhibitorsRewardInternal medicineConditioning PsychologicalCX3CR1AnimalsMedicineCX3CL1Biological PsychiatryMice KnockoutPharmacologySocial stressbiologyChemokine CX3CL1business.industryGlutamate receptorConditioned place preference030227 psychiatryMice Inbred C57BLEndocrinologybiology.proteinbusinessProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Dectin-1 Stimulation of Hematopoietic Stem and Progenitor Cells Occurs In Vivo and Promotes Differentiation Toward Trained Macrophages via an Indirec…

2020

Invasive candidiasis is an increasingly frequent cause of serious and often fatal infections. Understanding host defense is essential to design novel therapeutic strategies to boost immune protection against Candida albicans. In this article, we delve into two new concepts that have arisen over the last years: (i) the delivery of myelopoiesis-inducing signals by microbial components directly sensed by hematopoietic stem and progenitor cells (HSPCs) and (ii) the concept of “trained innate immunity” that may also apply to HSPCs. We demonstrate that dectin-1 ligation in vivo activates HSPCs and induces their differentiation to trained macrophages by a cell-autonomous indirect mechanism. This p…

MaleMyeloidbeta-Glucanshematopoietic stem and progenitor cellstlr2BiologyMicrobiologyHost-Microbe Biology03 medical and health sciencesMicetrained immunity0302 clinical medicineImmune systemVirologymedicineAnimalsLectins C-TypeProgenitor cell030304 developmental biologyMice Knockout0303 health sciencesInnate immune systemStem CellsCandidiasisCell DifferentiationHematopoietic Stem CellsImmunity InnateToll-Like Receptor 2QR1-502Cell biologymacrophagesTransplantationMice Inbred C57BLTLR2Haematopoiesismedicine.anatomical_structureMyeloid Differentiation Factor 88Femalecandida albicansBone marrowdectin-1030215 immunologyResearch ArticleSignal TransductionmBio
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