Search results for "OSA"

showing 10 items of 9388 documents

Infant gut microbiota modulation by human milk disaccharides in humanized microbiome mice

2021

Human milk glycans present a unique diversity of structures that suggest different mechanisms by which they may affect the infant microbiome development. A humanized mouse model generated by infant fecal transplantation was utilized here to evaluate the impact of fucosyl-α1,3-GlcNAc (3FN), fucosyl-α1,6-GlcNAc, lacto-N-biose (LNB) and galacto-N-biose on the fecal microbiota and host–microbiota interactions. 16S rRNA amplicon sequencing showed that certain bacterial genera significantly increased (Ruminococcus and Oscillospira) or decreased (Eubacterium and Clostridium) in all disaccharide-supplemented groups. Interestingly, cluster analysis differentiates the consumption of fucosyl-oligosacc…

0301 basic medicineMaleBifidobacterium longuminfant fecal microbiotaMicrobiologiaRC799-869Gut floraAcetatesDisaccharidesFecesMice0302 clinical medicinelacto-n-biosefluids and secretionsRuminococcus gnavusRNA Ribosomal 16SEubacteriumgalacto-n–bioseBifidobacteriumbiologyGastroenterologyDiseases of the digestive system. Gastroenterologylacto-N-biosegalacto-N–biosefucosyl-α-1ButyratesInfectious Diseases030211 gastroenterology & hepatologyFemaleResearch ArticleResearch PaperMicrobiology (medical)AdultDNA Bacterialhumanized mouse modelInfants Malaltiesshort-chain fatty acidsMicrobiologyMicrobiology03 medical and health sciencesfucosyl-α-16-N-acetylglucosamineYoung AdultAnimalsHumans6-n-acetylglucosamineMicrobiomeBacteriaMilk HumanRuminococcusInfant NewbornInfantAkkermansiafucosyl-α-13-N-acetylglucosaminebiology.organism_classificationcytokinesGastrointestinal Microbiome3-n-acetylglucosamineMice Inbred C57BL030104 developmental biologyshort-chain fatty acidscytokineshuman milk oligosaccharides
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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A phase I dose-escalation study of IMAB362 (Zolbetuximab) in patients with advanced gastric and gastro-oesophageal junction cancer

2018

Introduction IMAB362 (Zolbetuximab) is a chimeric monoclonal antibody that binds to Claudin-18.2, a target antigen specific to cancer cells. In vitro, IMAB362 mediates cell death through antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity; thus, IMAB362 may serve as a potent, targeted immunotherapeutic agent. Methods This first-in-human phase I study enroled adult patients (N = 15) with advanced gastric or gastro-oesophageal junction cancer into five sequential single dose-escalation cohorts (33, 100, 300, 600, and 1000 mg/m2) following a 3 + 3 design. Safety/tolerability, including determination of maximum tolerated dose and recommended phase II dose, were the pr…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyTime FactorsEsophageal NeoplasmsMaximum Tolerated Dosemedicine.medical_treatmentMedizinGastroenterologyAntibodies Monoclonal/administration & dosage03 medical and health sciences0302 clinical medicineAntineoplastic Agents ImmunologicalPharmacokineticsAntineoplastic Agents Immunological/administration & dosageStomach NeoplasmsInternal medicineGermanymedicineHumansDrug Dosage CalculationsAdverse effectInfusions IntravenousAgedbusiness.industryCancerAntibodies MonoclonalEsophagogastric Junction/drug effectsImmunotherapyMiddle Agedmedicine.diseaseLatviaddc:030104 developmental biologyTreatment OutcomeOncologyTolerabilityResponse Evaluation Criteria in Solid Tumors030220 oncology & carcinogenesisToxicityDisease ProgressionFemaleStomach Neoplasms/drug therapyEsophagogastric JunctionEsophageal Neoplasms/drug therapybusinessProgressive disease
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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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Cohesin-dependent regulation of gene expression during differentiation is lost in cohesin-mutated myeloid malignancies.

2019

Cohesin complex disruption alters gene expression, and cohesin mutations are common in myeloid neoplasia, suggesting a critical role in hematopoiesis. Here, we explore cohesin dynamics and regulation of hematopoietic stem cell homeostasis and differentiation. Cohesin binding increases at active regulatory elements only during erythroid differentiation. Prior binding of the repressive Ets transcription factor Etv6 predicts cohesin binding at these elements and Etv6 interacts with cohesin at chromatin. Depletion of cohesin severely impairs erythroid differentiation, particularly at Etv6-prebound loci, but augments self-renewal programs. Together with corroborative findings in acute myeloid le…

0301 basic medicineMaleCohesin complexChromosomal Proteins Non-HistoneImmunologyGene DosageCell Cycle ProteinsBiologyRegulatory Sequences Nucleic AcidBiochemistryHistones03 medical and health sciences0302 clinical medicineNeoplasmshemic and lymphatic diseasesCell Line TumorBiomarkers TumorHumansTranscription factorRegulation of gene expressionHematopoietic stem cell homeostasisMyeloid NeoplasiaMyeloproliferative DisordersCohesinProto-Oncogene Proteins c-etsGene Expression Regulation LeukemicETS transcription factor familyMyeloid leukemiafood and beveragesCell BiologyHematologyHematopoietic Stem CellsCell biologyChromatinHematopoiesisRepressor Proteins030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMutationFemalesense organsbiological phenomena cell phenomena and immunityNeoplasm GradingBLOOD CommentaryProtein BindingBlood
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NKp46-expressing human gut-resident intraepithelial Vδ1 T cell subpopulation exhibits high antitumor activity against colorectal cancer

2019

γδ T cells account for a large fraction of human intestinal intraepithelial lymphocytes (IELs) endowed with potent anti-tumor activities. However, little is known about their origin, phenotype and clinical relevance in colorectal cancer (CRC). To determine γδ IEL gut-specificity, homing and functions, γδ T cells were purified from human healthy blood, lymph nodes, liver, skin, intestine either disease-free or affected by CRC or generated from thymic precursors. The constitutive expression of NKp46 specifically identifies a new subset of cytotoxic Vδ1 T cells representing the largest fraction of gut-resident IELs. The ontogeny and gut-tropism of NKp46pos/Vδ1 IELs depends both on distinctive …

0301 basic medicineMaleColorectal cancerImmunotherapy AdoptiveMice0302 clinical medicineSex Hormone-Binding GlobulinCytotoxic T cellAntigens LyIntestinal MucosaIntraepithelial LymphocytesInnate immunityAged 80 and overGastroenterologyAge FactorsReceptors Antigen T-Cell gamma-deltaGeneral MedicineMiddle AgedPhenotypemedicine.anatomical_structure030220 oncology & carcinogenesisDisease ProgressionFemaleColorectal NeoplasmsResearch ArticleAdultColonT cellImmunologyT cellsBiologydigestive systemColorectal cancer; Gastroenterology; Immunology; Innate immunity; T cells03 medical and health sciencesYoung AdultIleummedicineAnimalsHumansAgedNeoplasm StagingTumor microenvironmentInnate immune systemNatural Cytotoxicity Triggering Receptor 1medicine.diseaseColorectal cancer030104 developmental biologyCancer researchIntraepithelial lymphocyteHoming (hematopoietic)T-Lymphocytes Cytotoxic
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Preferential uptake of polyunsaturated fatty acids by colorectal cancer cells

2020

AbstractAlthough a growing body of evidence suggests that colorectal cancer (CRC) is associated with alterations of fatty acid (FA) profiles in serum and tumor tissues, available data about polyunsaturated fatty acid (PUFA) content in CRC patients are inconclusive. Our study showed that CRC tissues contained more PUFAs than normal large intestinal mucosa. However, serum levels of PUFAs in CRC patients were lower than in healthy controls. To explain the mechanism of PUFA alterations in CRC, we measured FA uptake by the colon cancer cells and normal colon cells. The levels of PUFAs in colon cancer cell culture medium decreased significantly with incubation time, while no changes were observed…

0301 basic medicineMaleColorectal cancerlcsh:MedicineCell membrane0302 clinical medicinelipid metabolismIntestinal Mucosalcsh:SciencePhospholipidschemistry.chemical_classificationMultidisciplinaryChemistryfood and beveragespolyunsaturated fatty acidColon cancermedicine.anatomical_structure030220 oncology & carcinogenesisFatty Acids UnsaturatedFemalelipids (amino acids peptides and proteins)Colorectal NeoplasmsHT29 CellsPolyunsaturated fatty acidmedicine.medical_specialtyColoncolorectal cancerArticleIncubation period03 medical and health sciencesHT29 CellsInternal medicineCell Line TumormedicineHumansAgedCell ProliferationCell Membranelcsh:RFatty acidmedicine.diseaseeye diseasesdigestive system diseases030104 developmental biologyEndocrinologyCell cultureCancer cellLipidomicslcsh:Qsense organsScientific Reports
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Antibiotic resistance and population structure of cystic fibrosis Pseudomonas aeruginosa isolates from a Spanish multi-centre study

2017

The first Spanish multi-centre study on the microbiology of cystic fibrosis (CF) was conducted from 2013 to 2014. The study involved 24 CF units from 17 hospitals, and recruited 341 patients. The aim of this study was to characterise Pseudomonas aeruginosa isolates, 79 of which were recovered from 75 (22%) patients. The study determined the population structure, antibiotic susceptibility profile and genetic background of the strains. Fifty-five percent of the isolates were multi-drug-resistant, and 16% were extensively drug-resistant. Defective mutS and mutL genes were observed in mutator isolates (15.2%). Considerable genetic diversity was observed by pulsed-field gel electrophoresis (70 p…

0301 basic medicineMaleCystic FibrosisAntibiotic resistanceArray tubeMulti-locus sequence typing (MLST)medicine.disease_causeGenotypePharmacology (medical)ChildGeneticseducation.field_of_studyMolecular EpidemiologyVirulencePseucforrumus aeruginosaGeneral MedicineMiddle AgedMutS DNA Mismatch-Binding ProteinElectrophoresis Gel Pulsed-FieldInfectious DiseasesChild PreschoolPseudomonas aeruginosaFemalemedicine.drugMicrobiology (medical)AdultAdolescentGenotype030106 microbiologyPopulationVirulenceBiologyCystic fibrosisMicrobiology03 medical and health sciencesYoung AdultAntibiotic resistanceDrug Resistance BacterialmedicineHumansPseudomonas InfectionsTypingeducationGenetic diversityPseudomonas aeruginosaGenetic VariationMutL ProteinsSpainColistinMultilocus Sequence Typing
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TRPM8 Channel Activation Reduces the Spontaneous Contractions in Human Distal Colon

2020

The transient receptor potential-melastatin 8 (TRPM8) is a non-selective Ca2+-permeable channel, activated by cold, membrane depolarization, and different cooling compounds. TRPM8 expression has been found in gut mucosal, submucosal, and muscular nerve endings. Although TRPM8 plays a role in pathological conditions, being involved in visceral pain and inflammation, the physiological functions in the digestive system remain unclear as yet. The aims of the present study were: (i) to verify the TRPM8 expression in human distal colon

0301 basic medicineMaleGene ExpressionPharmacologySettore BIO/09 - Fisiologialcsh:ChemistryTissue Culture Techniqueschemistry.chemical_compound0302 clinical medicineIntestinal MucosaReceptorlcsh:QH301-705.5Spectroscopyhuman colon contractilityAged 80 and overTetraethylammoniumDepolarizationGeneral MedicineIberiotoxinMiddle AgedComputer Science Applications030220 oncology & carcinogenesisTetrodotoxinFemaleMuscle ContractionAgonistSerotoninmedicine.drug_classColonTRPM Cation ChannelsTetrodotoxinApaminCatalysisArticleInorganic Chemistry03 medical and health sciencesIBSmedicineTRPM8HumansPhysical and Theoretical ChemistryMolecular BiologyAgedOrganic ChemistryMuscle SmoothTetraethylammonium chloridePhosphinic Acids1-[Diisopropyl-phosphinoyl]-alkane (DIPA)030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999ApaminTRPM-8PeptidesInternational Journal of Molecular Sciences
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