Search results for "ck"

showing 10 items of 18632 documents

Maternal eNOS deficiency determines a fatty liver phenotype of the offspring in a sex dependent manner

2016

ABSTRACT Maternal environmental factors can impact on the phenotype of the offspring via the induction of epigenetic adaptive mechanisms. The advanced fetal programming hypothesis proposes that maternal genetic variants may influence the offspring's phenotype indirectly via epigenetic modification, despite the absence of a primary genetic defect. To test this hypothesis, heterozygous female eNOS knockout mice and wild type mice were bred with male wild type mice. We then assessed the impact of maternal eNOS deficiency on the liver phenotype of wild type offspring. Birth weight of male wild type offspring born to female heterozygous eNOS knockout mice was reduced compared to offspring of wil…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyHeterozygoteNitric Oxide Synthase Type IIIOffspringBiology03 medical and health sciencesGenomic ImprintingMiceSex FactorsEnosInternal medicineFetal programmingmedicineAnimalsEpigeneticsMolecular BiologyGeneFatty liverWild typeHeterozygote advantageDNA Methylationmedicine.diseasebiology.organism_classificationFatty LiverMice Inbred C57BL030104 developmental biologyEndocrinologyPhenotypeKnockout mouseeNOSCarbohydrate MetabolismFemaleEpigeneticsInstitut für ErnährungswissenschaftmetabolismResearch Paper
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Outcome of melanoma patients with elevated LDH treated with first-line targeted therapy or PD-1-based immune checkpoint inhibition.

2020

Abstract Background Elevated lactate dehydrogenase (LDH) is a known predictive and prognostic factor for a poor outcome in patients with metastatic melanoma. It is unclear whether first-line targeted therapy (TT) or immune checkpoint inhibition (ICI) is more beneficial in melanoma patients with elevated LDH because prospective studies in this area are lacking. Methods This multicentre retrospective cohort study was conducted at 25 melanoma centres worldwide to analyse progression-free survival (PFS) and overall survival (OS) among melanoma patients with elevated LDH. The role of confounders was addressed by using inverse probability of treatment weighting. Results Among 173 BRAFV600-mutant …

0301 basic medicineMaleCancer Researchmedicine.medical_specialtymedicine.medical_treatmentProgrammed Cell Death 1 ReceptorMedizinGastroenterologyTargeted therapy03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansProspective cohort studyImmune Checkpoint InhibitorsMelanomaAgedRetrospective Studiesbusiness.industryMelanomaConfoundingRetrospective cohort studyMiddle Agedmedicine.diseasePrognosisImmune checkpoint3. Good healthBlockadeSurvival Rate030104 developmental biologyOncologyCTLA-4030220 oncology & carcinogenesisDrug Therapy CombinationFemaleImmunotherapybusinessFollow-Up StudiesEuropean journal of cancer (Oxford, England : 1990)
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Intratumoral immunosuppression profiles in 11q-deleted neuroblastomas provide new potential therapeutic targets

2021

In this issue, Coronado et al. attempt to improve our understanding of the factors affecting the response to immunotherapy in a large subset of high‐risk neuroblastoma with hemizygous deletion of chromosome 11q. By using several computational approaches, the authors study potential transcriptional and post‐transcriptional pathways that may affect the response to immunotherapy and further be leveraged therapeutically in a biomarker‐directed fashion.

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentRetinoic acidchemistry.chemical_compoundNeuroblastoma0302 clinical medicineTumor Microenvironment11q deletion anti-GD2 immunotherapy combination immunotherapy immune cell infiltration miRNAs neuroblastomaMedicineeducation.field_of_studyimmune cell infiltration11q deletionImmunosuppressionGeneral Medicinelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPatologiaNeoplasm ProteinsmicroRNAsSurvival Rateanti‐GD2 therapyOncology030220 oncology & carcinogenesiscombination immunotherapymiRNAsMolecular Medicineimmune checkpoint inhibitionFemaleImmunotherapyChromosome Deletionanti‐GD2 immunotherapyPopulationlcsh:RC254-282Disease-Free Survival03 medical and health sciencesImmune systemNeuroblastomaGeneticsImmune ToleranceHumanseducationRetrospective Studiesbusiness.industryChromosomes Human Pair 11Immunotherapymedicine.diseaseImmune checkpointBlockade030104 developmental biologychemistryCancer researchCommentarybusiness
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Synergistic action of CB1 and 5-HT2B receptors in preventing pilocarpine-induced status epilepticus in rats

2019

Abstract Endocannabinoids (eCBs) and serotonin (5-HT) play a neuromodulatory role in the central nervous system. Both eCBs and 5-HT regulate neuronal excitability and their pharmacological potentiation has been shown to control seizures in pre-clinical and human studies. Compelling evidence indicates that eCB and 5-HT systems interact to modulate several physiological and pathological brain functions, such as food intake, pain, drug addiction, depression, and anxiety. Nevertheless, there is no evidence of an eCB/5-HT interaction in experimental and human epilepsies, including status epilepticus (SE). Here, we performed video-EEG recording in behaving rats treated with the pro-convulsant age…

0301 basic medicineMaleCannabinoid receptormedicine.medical_treatmentPharmacologySettore BIO/09 - Fisiologia0302 clinical medicineStatus Epilepticus5-HT2BEEGStatus epilepticuPilocarpineCalcium Channel BlockersEndocannabinoid systemCB1Clinical applicationNeurologyPilocarpinemedicine.symptommedicine.drugReceptorAM251AgonistSerotoninEndocannabinoid systemmedicine.drug_classMorpholinesCannabinoid receptors; Clinical applications; EEG; Endocannabinoid system; Serotonin; Status epilepticus; Synergistic interactions; Animals; Benzoxazines; Calcium Channel Blockers; Male; Morpholines; Muscarinic Agonists; Naphthalenes; Pilocarpine; Rats; Rats Sprague-Dawley; Receptor Cannabinoid CB1; Receptor Serotonin 5-HT2B; Serotonin 5-HT2 Receptor Agonists; Status EpilepticusStatus epilepticusClinical applicationsMuscarinic AgonistsNaphthaleneslcsh:RC321-57103 medical and health sciencesmedicineAnimalsCannabinoid receptorslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCannabinoidbusiness.industryAntagonistSynergistic interactionsBenzoxazinesRats030104 developmental biologySerotoninCannabinoidSprague-Dawleybusiness030217 neurology & neurosurgerySerotonin 5-HT2 Receptor Agonists
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CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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Endothelial Dab1 signaling orchestrates neuro-glia-vessel communication in the central nervous system.

2018

Developing the bloodbrain barrier During development, signals need to be dynamically integrated by endothelial cells, neurons, and glia to achieve functional neuro-glia-vascular units in the central nervous system. During cortical development, neuronal Dab1 and ApoER2 receptors respond to a guidance cue called reelin. Studying mice, Segarra et al. found that Dab1 and ApoER2 are also expressed in endothelial cells (see the Perspective by Thomas). The integration of reelin signaling in endothelial cells and neurons facilitates the communication between vessels, glia, and neurons that is necessary for the correct positioning of neurons during cortical development. This integration is also impo…

0301 basic medicineMaleCell signalingLow-density lipoprotein receptor-related protein 8EndotheliumCell Adhesion Molecules NeuronalCentral nervous systemNeovascularization PhysiologicNerve Tissue ProteinsCell Communication03 medical and health sciencesMiceCell MovementmedicineAnimalsReelinLDL-Receptor Related ProteinsCerebral CortexMice KnockoutNeuronsRetinaExtracellular Matrix ProteinsMultidisciplinarybiologyIntegrin beta1Serine EndopeptidasesRetinal VesselsDAB1Reelin Protein030104 developmental biologymedicine.anatomical_structurenervous systemCerebral cortexBlood-Brain Barrierbiology.proteinFemaleEndothelium VascularLamininNeuroscienceNeurogliaGene DeletionSignal TransductionScience (New York, N.Y.)
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Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification

2020

International audience; Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromo…

0301 basic medicineMaleCerebellumPathology[SDV]Life Sciences [q-bio]recessive brain calcificationMice0302 clinical medicineCognitive declineAge of OnsetChildGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSBrain Diseasesprimary familial brain calcificationMalalties neurodegenerativesBrainFahr diseaseCalcinosisOCLNNeurodegenerative DiseasesHuman brainMiddle AgedPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structureKnockout mouseFemalemedicine.symptomAdultmedicine.medical_specialtyAdolescentGenes RecessiveNeuropathologyBiologyCalcificacióCalcification03 medical and health sciencesBasal Ganglia DiseasesReportGeneticsmedicineAnimalsHumansAllelesSLC20A2Cerebellar ataxiaknock out mouse modelmedicine.diseaseJAM2030104 developmental biologyFahr disease; familial idiopathic basal ganglia calcification; JAM2; JAM3; knock out mouse model; MYORG; OCLN; primary familial brain calcification; recessive brain calcification; SLC20A2familial idiopathic basal ganglia calcificationJAM3MYORGXenotropic and Polytropic Retrovirus ReceptorCell Adhesion Molecules030217 neurology & neurosurgeryCalcification
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Genome-wide association study of non-alcoholic fatty liver and steatohepatitis in a histologically characterised cohort☆

2020

Background & Aims: Genetic factors associated with nonalcoholic fatty liver disease (NAFLD) remain incompletely understood. To date, most genome-wide association studies (GWASs) have adopted radiologically assessed hepatic triglyceride content as the reference phenotype and so cannot address steatohepatitis or fibrosis. We describe a GWAS encompassing the full spectrum of histologically characterised NAFLD. Methods: The GWAS involved 1,483 European NAFLD cases and 17,781 genetically matched controls. A replication cohort of 559 NAFLD cases and 945 controls was genotyped to confirm signals showing genome-wide or close to genome-wide significance. Results: Case-control analysis identified…

0301 basic medicineMaleCirrhosis17-Hydroxysteroid DehydrogenasesFibrosiVARIANTLOCIPROGRESSIONGenome-wide association studyDiseaseBioinformaticsDISEASECohort Studies0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsGWASINCREASED RISKCONFERS SUSCEPTIBILITYeducation.field_of_studyFatty liverNASHMiddle Aged3. Good healthNAFLD; NASH; Fibrosis; GWAS; PNPLA3; TM6SF2; GCKR; HSD17B13; SNPPhenotypeLiver030211 gastroenterology & hepatologyFemaleLife Sciences & BiomedicineGCKRAdultPopulationSNP610 Medicine & healthGastroenterology and HepatologyPolymorphism Single NucleotideTM6SF2HSD17B1303 medical and health sciencesNAFLDmedicineGastroenterologiHumansGenetic Predisposition to DiseaseeducationPNPLA3Adaptor Proteins Signal TransducingScience & TechnologyGastroenterology & HepatologyHepatologybusiness.industrynutritional and metabolic diseasesMembrane ProteinsLipasemedicine.diseaseFibrosisPOLYMORPHISMLEPTIN RECEPTOR GENE030104 developmental biology3121 General medicine internal medicine and other clinical medicineCase-Control StudiesHuman medicineSteatosisSteatohepatitisbusinessTM6SF2Genome-Wide Association StudyJournal of Hepatology
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Assessment of Targeted Next-Generation Sequencing as a Tool for the Diagnosis of Charcot-Marie-Tooth Disease and Hereditary Motor Neuropathy

2016

Charcot-Marie-Tooth disease is characterized by broad genetic heterogeneity with >50 known disease-associated genes. Mutations in some of these genes can cause a pure motor form of hereditary motor neuropathy, the genetics of which are poorly characterized. We designed a panel comprising 56 genes associated with Charcot-Marie-Tooth disease/hereditary motor neuropathy. We validated this diagnostic tool by first testing 11 patients with pathological mutations. A cohort of 33 affected subjects was selected for this study. The DNAJB2 c.352+1G>A mutation was detected in two cases; novel changes and/or variants with low frequency (50 known disease-associated genes. Mutations in some of these gene…

0301 basic medicineMaleDiseaseBioinformaticsDNA sequencingPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseaseMedicineHumansGeneGeneticsbusiness.industryGenetic heterogeneityHaplotypeCase-control studyHigh-Throughput Nucleotide SequencingReproducibility of ResultsHSP40 Heat-Shock Proteins030104 developmental biologyHaplotypesCase-Control StudiesMutation (genetic algorithm)MutationMolecular MedicineFemalebusinessHereditary Sensory and Motor Neuropathy030217 neurology & neurosurgeryFounder effectMolecular Chaperones
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Targeting aurora kinase B alleviates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury.

2019

Peripheral nerve injury elicits spinal microgliosis, contributing to neuropathic pain. The aurora kinases A (AURKA), B (AURKB), and C (AURKC) are potential therapeutic targets in proliferating cells. However, their role has not been clarified in microglia. The aim of this study was to examine the regulation of aurora kinases and their roles and druggability in spinal microgliosis and neuropathic pain. Sprague-Dawley rats received chronic constriction injury (CCI). Gene expression of aurora kinases A-C was evaluated by quantitative RT-PCR and western blot, respectively, in spinal cords at 1, 3, 7, and 14 days after CCI. AURKB gene and protein expression was up-regulated concomitantly with th…

0301 basic medicineMaleDown-RegulationGene ExpressionMicrogliosisBiochemistryRats Sprague-Dawley03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePeripheral Nerve InjuriesMedicineAnimalsAurora Kinase BAURKB GeneEnzyme InhibitorsGene knockdownMicrogliabusiness.industryKinaseSpinal cordRatsDisease Models Animal030104 developmental biologymedicine.anatomical_structureSpinal CordGene Knockdown TechniquesPeripheral nerve injuryNeuropathic painCancer researchNeuralgiaMicrogliabusiness030217 neurology & neurosurgeryJournal of neurochemistryReferences
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