Search results for "L1"

showing 10 items of 831 documents

High serum CXCL10 in Rickettsia conorii infection is endothelial cell ă mediated subsequent to whole blood activation

2016

International audience; Background: The pathophysiological hallmark of Rickettsia conorii (R. ă conorii) infection comprises infection of endothelial cells with ă perivascular infiltration of T-cells and macrophages. Although ă interferon (IFN)-gamma-induced protein 10 (IP-10)/CXCL10 is induced ă during vascular inflammation, data on CXCL10 in R. conorii infection is ă scarce. ă Methods: Serum CXCL10 was analyzed in two cohorts of southern European ă patients with R. conorii infection using multiplex cytokine assays. The ă mechanism of R. conorii-induced CXCL10 release was examined ex vivo ă using human whole blood interacting with endothelial cells. ă Results: (i) At admission, R. conorii …

0301 basic medicineAdultMalemedicine.medical_treatmentT-Lymphocytes030106 microbiologyImmunologyInflammationBiologyBoutonneuse FeverBiochemistryMonocytesCohort Studies03 medical and health sciencesBlood serum[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesmedicineImmunology and AllergyCXCL10HumansInterleukin 8Molecular BiologyWhole bloodAgedAged 80 and overEndothelial CellsHematologyMiddle Agedbiology.organism_classification3. Good healthEndothelial stem cellChemokine CXCL10Rickettsia conorii030104 developmental biologyCytokineImmunologyFemalemedicine.symptomRickettsia conorii
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IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

2021

This article belongs to the Collection Insulin-Like Growth Factors in Development, Cancers and Aging.

0301 basic medicineAgingApoptosisHaploinsufficiencyMice0302 clinical medicineBiology (General)Insulin-Like Growth Factor ICell DeathapoptosisGeneral Medicine3. Good healthCochleaCytokinesmedicine.symptomHaploinsufficiencyNoise-induced hearing lossmedicine.medical_specialtyHeterozygoteHearing lossQH301-705.5InflammationArticleARHLProinflammatory cytokine03 medical and health sciencesInternal medicinemedicineotorhinolaryngologic diseasesAnimalsRNA MessengerProtein kinase BCochleaInflammationbusiness.industryGene Expression ProfilingAKTTGFβ1Auditory Thresholdmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologyGene Expression RegulationHearing Loss Noise-InducedAgeingSynapsesIL1βJNKbusinessNoise030217 neurology & neurosurgeryBiomarkersNIHL
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“Pro-youthful” factors in the “labyrinth” of cardiac rejuvenation

2016

IF 3.350; International audience; The mechanisms of aging and senescence include various endogenous and exogenous factors. Among cardiovascular diseases, heart failure is a typical age-related disease. New strategies to restore cardiomyocyte cells have been reported: endogenous substances that can regenerate the heart's cardiomyocytes have been described: follistatin like 1 (FSTL1), growth-differentiation factor 11 (GDF11) and insulin-like growth factor 1 (IGF-I). Manipulation of the different anti and pro-pathways is essential to discover new approaches to regenerative therapies. (C) 2016 Elsevier Inc. All rights reserved.

0301 basic medicineAgingStem-Cellsmedicine.medical_treatmentEndogenyCardiovascular-DiseaseBioinformaticsBiochemistryEndocrinologyFollistatin-Like 1Myocytes CardiacInsulin-Like Growth Factor Ibiology[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyGrowth differentiation factorGrowth-Factor-I3. Good healthIGF-IGrowth Differentiation FactorsBone Morphogenetic ProteinsCardiacMouse HeartSenescencemedicine.medical_specialtyFollistatin-Related ProteinsGene-Expression[ SDV.MHEP.GEG ] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyFSTL1Mammalian Heart03 medical and health sciencesMyocardial-InfarctionInternal medicineGeneticsmedicineHumansRegenerationRejuvenationMolecular BiologyHeart FailureYoung BloodTelomerase ExpressionRegeneration (biology)Growth factorCell Biologymedicine.disease030104 developmental biologyEndocrinologyHeart failureGDF11GDF11biology.proteinFollistatin
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Effects of Chronic Dopamine D2R Agonist Treatment and Polysialic Acid Depletion on Dendritic Spine Density and Excitatory Neurotransmission in the mP…

2016

Dopamine D2 receptors (D2R) in the medial prefrontal cortex (mPFC) are key players in the etiology and therapeutics of schizophrenia. The overactivation of these receptors contributes to mPFC dysfunction. Chronic treatment with D2R agonists modifies the expression of molecules implicated in neuronal structural plasticity, synaptic function, and inhibitory neurotransmission, which are also altered in schizophrenia. These changes are dependent on the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a plasticity-related molecule, but nothing is known about the effects of D2R and PSA-NCAM on excitatory neurotransmission and the structure of mPFC pyramidal n…

0301 basic medicineAgonistMaleDendritic spineArticle SubjectGlycoside Hydrolasesmedicine.drug_classDendritic SpinesPrefrontal CortexNeural Cell Adhesion Molecule L1NeurotransmissionInhibitory postsynaptic potentialbehavioral disciplines and activitiesSynaptic Transmissionlcsh:RC321-571Rats Sprague-Dawley03 medical and health sciences0302 clinical medicineDopamineDopamine receptor D2PhenethylaminesmedicineAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryChemistryReceptors Dopamine D2Pyramidal CellsGlutamate receptorRats030104 developmental biologyNeurologynervous systemDopamine AgonistsSialic AcidsNeural cell adhesion moleculeNeurology (clinical)Neuroscience030217 neurology & neurosurgerymedicine.drugResearch ArticleNeural plasticity
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Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice

2019

The CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interle…

0301 basic medicineApolipoprotein Emedicine.medical_specialtyRegulatory T cellCCL1030204 cardiovascular system & hematologyCCR8T-Lymphocytes RegulatoryReceptors CCR8Chemokine CCL1Mice03 medical and health sciencesApolipoproteins ETh2 Cells0302 clinical medicineInternal medicineLeukocytesmedicineSplenocyteAnimalsMolecular BiologyInflammationMice KnockoutChemistryTh1 CellsAtherosclerosisInterleukin-10Mice Inbred C57BLTregInterleukin 10030104 developmental biologyEndocrinologymedicine.anatomical_structureIL-10CytokinesCardiology and Cardiovascular MedicineCCR8Intravital microscopyCCL1LipoproteinJournal of Molecular and Cellular Cardiology
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Ubiquitin-Dependent And Independent Signals In Selective Autophagy.

2015

Selective autophagy regulates the abundance of specific cellular components via a specialized arsenal of factors, termed autophagy receptors, that target protein complexes, aggregates, and whole organelles into lysosomes. Autophagy receptors bind to LC3/GABARAP proteins on phagophore and autophagosome membranes, and recognize signals on cargoes to deliver them to autophagy. Ubiquitin (Ub), a well-known signal for the degradation of polypeptides in the proteasome, also plays an important role in the recognition of cargoes destined for selective autophagy. In addition, a variety of cargoes are committed to selective autophagy pathways by Ub-independent mechanisms employing protein-protein int…

0301 basic medicineAutophagosomebiologyUbiquitinGABARAPAutophagyUbiquitinationCell BiologyBAG3BioinformaticsCell biology03 medical and health sciences030104 developmental biologyProteasomeUbiquitinProteolysisbiology.proteinAutophagyAnimalsHumansTarget proteinATG16L1Signal TransductionTrends in cell biology
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Activin A Signaling Regulates IL13Rα2 Expression to Promote Breast Cancer Metastasis

2019

Metastatic dissemination of cancer cells to distal organs is the major cause of death for patients suffering from the aggressive basal-like breast cancer (BLBC) subtype. Recently, we have shown that interleukin 13 receptor alpha 2 (IL13Rα2) is a critical gene that is overexpressed in a subset of BLBC primary tumors associated with poor distant metastasis-free survival (DMFS) and can promote extravasation and metastasis of breast cancer cells to the lungs. However, the upstream signaling mechanisms that promote aberrant IL13Rα2 expression during tumor progression remain unknown. Driven by our previously published gene expression microarray data derived from a well-characterized cell line mod…

0301 basic medicineCancer ResearchBiologymigrationlcsh:RC254-282MetastasisIL13Rα203 medical and health sciencesbreast cancer0302 clinical medicineBreast cancermedicinemetastasisOriginal ResearchCancerActivin receptorActivin Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMetastatic breast cancerPrimary tumor030104 developmental biologyOncologyTumor progression030220 oncology & carcinogenesisCancer cellCancer researchFrontiers in Oncology
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Immunotherapy in non-small-cell lung cancer: a bridge between research and clinical practice

2018

Lung cancer has been historically considered a poorly immunogenic disease because of the few evidence of immune responses in affected patients and the limited efficacy of immunomodulating strategies. Recent understanding of the molecular mechanisms leading to cancer immune evasion has allowed the development of a new class of drugs called immune checkpoint inhibitors, which reactivate host responses with outstanding clinical benefits in a portion of patients with non-small-cell lung cancer. In this review, we briefly summarize the basis of immunogenicity and immune escape of cancer, with specific focus on non-small-cell lung cancer, mechanisms underlying immune checkpoint inhibitors effica…

0301 basic medicineCancer ResearchLung NeoplasmsSettore MED/06 - Oncologia Medicamedicine.medical_treatmentProgrammed Cell Death 1 Receptorimmune checkpoint inhibitorDiseaseNSCLCBioinformaticsB7-H1 Antigenimmune checkpoint inhibitorsTranslational Research Biomedical0302 clinical medicineCarcinoma Non-Small-Cell LungPD-1clinical studiesNSCLC; PD-1; PD-L1; biomarkers; cancer immunogenicity; clinical studies; immune checkpoint inhibitors; translational researchMolecular Targeted TherapybiologyImmunogenicityGeneral Medicinecancer immunogenicityOncology030220 oncology & carcinogenesisbiomarkerCytokinesImmunotherapyPD-L1chemical and pharmacologic phenomena03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemPD-L1Biomarkers TumormedicineHumansLung cancerbusiness.industryImmunitybiomarkersCancerImmunotherapymedicine.disease030104 developmental biologytranslational researchTumor EscapeMutationbiology.proteinTumor Escapebusinessclinical studieFuture Oncology
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Primary and metastatic brain cancer genomics and emerging biomarkers for immunomodulatory cancer treatment

2018

Abstract: Recent studies with immunomodulatory agents targeting both cytotoxic T-lymphocyte protein 4 (CTLA4) and programmed cell death 1 (PD1)/programmed cell death ligand 1 (PDL1) have shown to be very effective in several cancers revealing an unexpected great activity in patients with both primary and metastatic brain tumors. Combining anti-CTLA4 and anti-PD1 agents as upfront systemic therapy has revealed to further increase the clinical benefit observed with single agent, even at cost of higher toxicity. Since the brain is an immunological specialized area it's crucial to establish the specific composition of the brain tumors' micro environment in order to predict the potential activit…

0301 basic medicineCancer ResearchSettore MED/06 - Oncologia Medicamedicine.medical_treatmentBiomarkers; Brain; CTLA4; Immunotherapy; Metastasis; PD1/PDL1GenomicsMetastasiMetastasisMetastasisImmunomodulation03 medical and health sciences0302 clinical medicinemedicineBiomarkers TumorCytotoxic T cellAnimalsHumansCTLA4Primary (chemistry)business.industryPD1/PDL1Brain NeoplasmsImmunogenicityBrainBiomarkerImmunotherapyGenomicsmedicine.diseaseCancer treatment030104 developmental biology030220 oncology & carcinogenesisToxicityCancer researchImmunotherapyHuman medicinebusinessBiomarkersSeminars in cancer biology
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Daunorubicin reduces MBNL1 titration by expanded CUG repeat RNA and rescues cardiac dysfunctions in a Drosophila model of myotonic dystrophy

2018

International audience; Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant DMPK transcripts containing expanded CUG repeats. Pathogenic RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations of RNA metabolism. Cardiac dysfunction represents the second most common cause of death in DM1 patients. However, the contribution of MBNL titration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resemble cardiac defects observed in patients. We als…

0301 basic medicineCardiac function curvecongenital hereditary and neonatal diseases and abnormalitiesDaunorubicin[SDV]Life Sciences [q-bio]Neuroscience (miscellaneous)Medicine (miscellaneous)BiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmunology and Microbiology (miscellaneous)medicineMBNL1Daunorubicin HydrochlorideRNAmedicine.diseaseTrinucleotide repeat disorder3. Good healthCell biology[SDV] Life Sciences [q-bio]030104 developmental biologychemistryTrinucleotide repeat expansion030217 neurology & neurosurgerymedicine.drug
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