Search results for "Iso"

showing 10 items of 22430 documents

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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Blockade of nitric oxide signalling promotes resilience to the effects of social defeat stress on the conditioned rewarding properties of MDMA in mice

2020

Abstract MDMA abuse continues being a serious problem in our society. Environmental factors, such as stress, increase the vulnerability of individuals to develop drug abuse and we have observed that exposure to social defeat (SD) stress alters the sensitivity of mice to the rewarding effects of MDMA in the conditioned place preference (CPP) paradigm. In the present study, we evaluated the role of the nitric oxide (NO) pathway in the effects of SD on the rewarding properties of MDMA. Three groups of mice were treated with an inhibitor of NO synthesis, 7-nitroindazole (0, 7.25 and 12.5 mg/kg), before each exposure to SD and place conditioning with MDMA (1.25 mg/kg) on PND 54, 56, 58, and 60. …

0301 basic medicineMaleCancer Researchmedicine.medical_specialty7-NitroindazoleIndazolesMDMAPhysiologyN-Methyl-34-methylenedioxyamphetamineClinical BiochemistryHippocampusMice Inbred StrainsStriatum030204 cardiovascular system & hematologyNitric OxideBiochemistrySocial defeat03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineSocial defeatInternal medicineConditioning Psychologicalmental disordersmedicineAnimalsPrefrontal cortex7-NitroindazoleSocial stressDose-Response Relationship Drugbusiness.industryMDMANitric oxideConditioned place preferenceConditioned place preference030104 developmental biologyEndocrinologychemistrybusinessStress Psychologicalpsychological phenomena and processesmedicine.drugSignal Transduction
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Plasma heme oxygenase-1 is decreased in peripheral artery disease patients.

2016

Peripheral artery disease (PAD) is a common manifestation of atherosclerosis. A number of emerging risk factors, including oxidative stress biomarkers, free radicals and heat shock proteins, may add to the established risk factors for cardiovascular disease (CVD). The present study assessed surrogate markers of oxidative stress, including total reduced glutathione (GSH), lipid hydroperoxides (LOOH), isoprostanes, heme oxygenase‑1 (HO‑1) and metabolic biomarkers, such as adiponectin and lactate, in PAD patients (n=27). Healthy age‑matched volunteers (n=27) served as controls. GSH and LOOH were evaluated by measuring total thiol groups and iron oxidation, respectively, by spectrophotometric a…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyAdipokineOxidative phosphorylationBiologyIsoprostanesmedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compoundPeripheral Arterial DiseaseInternal medicineGeneticsmedicineHumansAnkle Brachial IndexMolecular BiologyAgedAdiponectinGlutathioneMiddle Agedmedicine.diseaseIsoprostanesGlutathioneHeme oxygenaseOxidative Stress030104 developmental biologyEndocrinologyOncologychemistryImmunologyMolecular MedicineFemaleAdiponectinLipid PeroxidationOxidative stressDyslipidemiaBiomarkersHeme Oxygenase-1Molecular medicine reports
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CD19 Isoforms Enabling Resistance to CART-19 Immunotherapy Are Expressed in B-ALL Patients at Initial Diagnosis.

2017

Supplemental Digital Content is available in the text.

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT-LymphocytesEpitopes T-LymphocyteT-Cell Antigen Receptor SpecificityImmunotherapy AdoptiveEpitopeCohort StudiesExon0302 clinical medicineimmune system diseasesImmunology and AllergyMedicineProtein IsoformsChildAged 80 and overbiologyCD19CART-19B-ALLMiddle AgedPrecursor Cell Lymphoblastic Leukemia-Lymphomaepitope-lossmedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisChild PreschoolComputingMethodologies_DOCUMENTANDTEXTPROCESSINGFemaleClone (B-cell biology)Gene isoformAdultAdolescentRecombinant Fusion ProteinsImmunologyAntigens CD19Receptors Antigen T-CellCancer VaccinesCD1903 medical and health sciencesYoung AdultAntigenHumansAgedPharmacologybusiness.industryInfant NewbornisoformsInfantImmunotherapy030104 developmental biologyImmunologybiology.proteinClinical StudyTumor EscapeBone marrowbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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Heterozygous deletion of the LRFN2 gene is associated with working memory deficits

2016

International audience; Learning disabilities (LDs) are a clinically and genetically heterogeneous group of diseases. Array-CGH and high-throughput sequencing have dramatically expanded the number of genes implicated in isolated intellectual disabilities and LDs, highlighting the implication of neuron-specific post-mitotic transcription factors and synaptic proteins as candidate genes. We report a unique family diagnosed with autosomal dominant learning disability and a 6p21 microdeletion segregating in three patients. The 870 kb microdeletion encompassed the brain-expressed gene LRFN2, which encodes for a synaptic cell adhesion molecule. Neuropsychological assessment identified selective w…

0301 basic medicineMaleCandidate genefamilyspeechHippocampal formationRats Sprague-Dawley0302 clinical medicineBorderline intellectual functioningNeuropsychological assessmentChilddisordersGenetics (clinical)Cells Culturedadhesion-like moleculesMembrane Glycoproteinsmedicine.diagnostic_testLearning DisabilitiesBrainMagnetic Resonance Imaging3. Good healthPedigreeMemory Short-TermBrain sizeFemaleAdultHeterozygotenmda receptorautismNerve Tissue ProteinsBiologyReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesFluorodeoxyglucose F18[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyexpressionGeneticsmedicineAnimalsHumansMemory DisorderslanguageGenetic heterogeneityWorking memoryMembrane Proteinsdown-syndromeRats030104 developmental biologyEndophenotypePositron-Emission TomographySynapsesshort-termRadiopharmaceuticalsNeuroscience030217 neurology & neurosurgeryGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Cannabinoid receptor expression in non-small cell lung cancer. Effectiveness of tetrahydrocannabinol and cannabidiol inhibiting cell proliferation an…

2020

Background/Objective Patients with non-small cell lung cancer (NSCLC) develop resistance to antitumor agents by mechanisms that involve the epithelial-to-mesenchymal transition (EMT). This necessitates the development of new complementary drugs, e.g., cannabinoid receptors (CB1 and CB2) agonists including tetrahydrocannabinol (THC) and cannabidiol (CBD). The combined use of THC and CBD confers greater benefits, as CBD enhances the effects of THC and reduces its psychotropic activity. We assessed the relationship between the expression levels of CB1 and CB2 to the clinical features of a cohort of patients with NSCLC, and the effect of THC and CBD (individually and in combination) on prolifer…

0301 basic medicineMaleCannabinoid receptorLung NeoplasmsPulmonologymedicine.medical_treatmentGene ExpressionBiochemistryLung and Intrathoracic TumorsReceptor Cannabinoid CB20302 clinical medicineContractile ProteinsReceptor Cannabinoid CB1Epidermal growth factorCarcinoma Non-Small-Cell LungMedicine and Health SciencesCannabidiolDronabinolAged 80 and overMultidisciplinaryChemistryQRDrugsMiddle AgedCancer Cell MigrationCell MotilityOncologyCell Processes030220 oncology & carcinogenesisMedicinelipids (amino acids peptides and proteins)Femalemedicine.drugResearch ArticleAdultEpithelial-Mesenchymal TransitionScienceChronic Obstructive Pulmonary DiseaseCell Migration03 medical and health sciencesCell Line Tumormental disordersmedicineGeneticsHumansEpithelial–mesenchymal transitionTetrahydrocannabinolCell ProliferationAgedA549 cellPharmacologyCannabinoid Receptor AgonistsPsychotropic DrugsCell growthCannabinoidsorganic chemicalsCancers and NeoplasmsBiology and Life SciencesProteinsCell Biologydigestive system diseasesActinsrespiratory tract diseasesNon-Small Cell Lung CancerCytoskeletal Proteins030104 developmental biologyA549 CellsCancer researchCannabinoidCannabidiolDevelopmental BiologyPLoS ONE
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12q14.3 microdeletion involving HMGA2 gene cause a Silver-Russell syndrome-like phenotype: a case report and review of the literature

2020

Abstract Background Silver-Russell Syndrome (SRS) is a genetic disorder characterized by intrauterine and postnatal growth restriction and normal head circumference with consequent relative macrocephaly. Addictional findings are protruding forehead in early life, body asymmetry (of upper and lower limbs) and substantial feeding difficulties. Although several genetic mechanisms that cause the syndrome are known, more than 40% of patients with a SRS-like phenotype remain without an etiological diagnosis. In the last few years, different clinical reports have suggested that mutations or deletions of the HMGA2 gene can be responsible for a SRS-like phenotype in patients with negative results of…

0301 basic medicineMaleCase Report030105 genetics & heredityBioinformaticsHMGA2 gene03 medical and health sciencesHMGA2parasitic diseasesmedicineHumansGeneChromosome 12biologybusiness.industrySilver–Russell syndromeNetchine-Harbison clinical scoring systemHMGA2 Proteinlcsh:RJ1-570Genetic disorderlcsh:PediatricsFailure to thrivemedicine.diseasePhenotypeSilver-Russell Syndrome030104 developmental biologyPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolFailure to thriveEtiologybiology.proteinmedicine.symptombusinessGene DeletionItalian Journal of Pediatrics
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Regulation of PDE5 expression in human aorta and thoracic aortic aneurysms

2019

AbstractAneurysms and dissections affecting thoracic aorta are associated with smooth muscle cell (SMC) dysfunction. NO/cGMP signaling pathway in smooth muscle cells has been shown to be affected in sporadic thoracic aortic aneurysms. We analyzed the mRNA levels of PDE5, a cGMP-hydrolyzing enzyme highly expressed in aortic SMCs, that regulates arterious vascular tone by lowering cGMP levels. We found that aortic tissue obtained from Marfan, tricuspid and bicuspid thoracic aneurysms expressed lower levels of PDE5 mRNA compared to control aortas. In particular, we found that affected aortas showed lower levels of all the PDE5A isoforms, compared to control aortas. Transfection of vascular SMC…

0301 basic medicineMaleCelllcsh:MedicineStimulationMuscle Smooth VascularAortic aneurysmchemistry.chemical_compound0302 clinical medicinePDE5 expression human aorta and thoracic aortic aneurysmsMyocyteThoracic aortalcsh:ScienceSettore BIO/16MultidisciplinaryTransfectionMiddle AgedIsoenzymesmedicine.anatomical_structurecardiovascular systemFemaleGene isoformAdultmedicine.medical_specialtyMyocytes Smooth MuscleArticleGene Expression Regulation EnzymologicNitric oxide03 medical and health sciencesmedicine.arteryInternal medicinemedicineHumansSettore MED/05 - Patologia ClinicaAgedCyclic Nucleotide Phosphodiesterases Type 5Aortic Aneurysm Thoracicbusiness.industrylcsh:Rmedicine.disease030104 developmental biologyEndocrinologychemistryRisk factorsthoracic aortic aneurysmslcsh:QAngiogenesisPDE5business030217 neurology & neurosurgery
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Prevalence and determinants of non-alcoholic fatty liver disease in lifelines: A large Dutch population cohort

2017

BACKGROUND & AIMS Non-alcoholic fatty liver disease is an increasing health issue that develops rather unnoticed with obesity, type 2 diabetes mellitus and metabolic syndrome. We investigated prevalence, determinants and associated metabolic abnormalities of non-alcoholic fatty liver disease in the largest population-based cohort to date. METHODS Biochemical characteristics, type 2 diabetes mellitus and metabolic syndrome were determined in the Lifelines Cohort Study (N = 167,729), a population-based cohort in the North of the Netherlands. Non-alcoholic fatty liver disease was defined as Fatty Liver Index (FLI)≥60. Exclusion criteria were age <18 years, immigrants, missing data to assess FL…

0301 basic medicineMaleCirrhosislcsh:MedicineGastroenterologyBiochemistryGLOMERULAR-FILTRATION-RATESTEATOHEPATITISWhite Blood Cells0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsAnimal CellsPrevalenceMedicine and Health SciencesDiabetes diagnosis and managementlcsh:ScienceNetherlandsMETABOLIC SYNDROME2. Zero hungerINSULIN-RESISTANCEMultidisciplinaryLiver DiseasesFatty liverMiddle AgedLipids3. Good healthType 2 DiabetesCholesterolHypertension030211 gastroenterology & hepatologyFemaleAnatomyCellular TypesResearch ArticleAdultmedicine.medical_specialtyHbA1cEndocrine DisordersImmune CellsImmunologyUNITED-STATESGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansHemoglobinHEPATIC STEATOSISHepatitisBlood Cellsbusiness.industryCholesterol HDLlcsh:RType 2 Diabetes MellitusBiology and Life SciencesProteinsRenal SystemCell Biologymedicine.diseaseDiagnostic medicineFatty LiverSERUM CREATININE VALUESRENAL-DISEASE030104 developmental biologyEndocrinologyCross-Sectional StudiesDiabetes Mellitus Type 2ATHEROSCLEROSISHyperglycemiaMetabolic DisordersRISK-FACTORSlcsh:QSteatohepatitisMetabolic syndromebusiness
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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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