Search results for " mac"

showing 10 items of 3066 documents

H-ferritin and proinflammatory cytokines are increased in the bone marrow of patients affected by macrophage activation syndrome

2017

Summary Macrophage activation syndrome (MAS) is hyperinflammatory life-threatening syndrome, associated typically with high levels of serum ferritin. This is an iron storage protein including heavy (H) and light (L) subunits, categorized on their molecular weight. The H-/L subunits ratio may be different in tissues, depending on the specific tissue and pathophysiological status. In this study, we analysed the bone marrow (BM) biopsies of adult MAS patients to assess the presence of: (i) H-ferritin and L-ferritin; (ii) CD68+/H-ferritin+ and CD68+/L-ferritin+; and (iii) interleukin (IL)-1β, tumour necrosis factor (TNF) and interferon (IFN)-γ. We also explored possible correlations of these re…

0301 basic medicineBiopsymedicine.medical_treatment0302 clinical medicineBone MarrowcytokineImmunology and AllergyInterleukinBlood ProteinsSyndromeMiddle AgedC-Reactive ProteinCytokinemedicine.anatomical_structureCytokinesTumor necrosis factor alphaInflammation Mediatorsmedicine.symptommacrophage activation syndromeAdultImmunologyAntigens Differentiation MyelomonocyticInflammationmacrophageBiologyProinflammatory cytokine03 medical and health sciencesAntigens CDmedicineHumansAgedRetrospective StudiesInflammation030203 arthritis & rheumatologyMacrophagesferritinOriginal ArticlesMacrophage Activationmedicine.diseaseFerritinSettore MED/16 - Reumatologia030104 developmental biologyMacrophage activation syndromeApoferritinsImmunologybiology.proteinBone marrowCytokine; Ferritin; Hyperferritinaemic syndrome; Macrophage; Macrophage activation syndrome; Immunology and Allergy; Immunologycytokine; ferritin; hyperferritinaemic syndrome; macrophage; macrophage activation syndromehyperferritinaemic syndrome
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A clinical review on megalencephaly: A large brain as a possible sign of cerebral impairment

2017

Megalencephaly and macrocephaly present with a head circumference measurement 2 standard deviations above the age-related mean. However, even if pathologic events resulting in both megalencephaly and macrocephaly may coexist, a distinction between these two entities is appropriate, as they represent clinical expression of different disorders with a different approach in clinical work-up, overall prognosis, and treatment. Megalencephaly defines an increased growth of cerebral structures related to dysfunctional anomalies during the various steps of brain development in the neuronal proliferation and/or migration phases or as a consequence of postnatal abnormal events. The disorders associate…

0301 basic medicineBrain development030105 genetics & hereditymacrocephalybrain dysfunction large head macrocephaly megalencephaly metabolic disorders03 medical and health sciences0302 clinical medicinemedicinemegalencephalymetabolic disordersHumansMegalencephaly10. No inequalitybrain dysfunctionbusiness.industryMedicine (all)Macrocephalybrain dysfunction; large head; macrocephaly; megalencephaly; metabolic disorders; Humans; Observational Studies as Topic; Megalencephaly; Medicine (all)General Medicinemedicine.diseaseHead circumferenceObservational Studies as Topiclarge headMeasurement 2medicine.symptombusinessNeuroscience030217 neurology & neurosurgery
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CD36 gene is associated with intraocular pressure elevation after intravitreal application of anti-VEGF agents in patients with age-related macular d…

2017

IF 1.886; International audience; Background: The wet form of age-related macular degeneration (AMD) is characterized by pathological vascularization of the outer retinal layers. The condition responds to treatment with antibodies against vascular endothelial growth factor (VEGF), but the patients receiving such anti-VEGF therapy sometimes show undesirable acute short-term increases in the intraocular pressure (IOP). The cause of this adverse effect is unknown, and here, we are testing a hypothesis that it is related to CD36 gene polymorphisms.Materials and Methods: A group of 134 patients with AMD were given three therapeutic doses of anti-VEGF antibody (ranibizumab) at monthly intervals. …

0301 basic medicineCD36 AntigensMaleVascular Endothelial Growth Factor AIntraocular pressuregenetic structuresreceptorGlaucomaAngiogenesis InhibitorsthrombospondinPolymerase Chain Reactionpolymorphismchemistry.chemical_compound0302 clinical medicineGenotypeGenetics (clinical)Schlemm´s canalVascular endothelial growth factorIntravitreal InjectionsFemalemedicine.drugmedicine.medical_specialtyPolymorphism Single Nucleotide03 medical and health sciencesTonometry Ocular[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyOphthalmologyRanibizumabmedicineHumansAdverse effectIntraocular PressureAgedbusiness.industryGlaucomaRetinalMacular degenerationmedicine.diseaseeye diseasesOphthalmology030104 developmental biologychemistryPediatrics Perinatology and Child Health030221 ophthalmology & optometryWet Macular DegenerationOcular Hypertensionsense organsRanibizumabbusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyOphthalmic genetics
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A Pan-Cancer Approach to Predict Responsiveness to Immune Checkpoint Inhibitors by Machine Learning

2019

Immunotherapy by using immune checkpoint inhibitors (ICI) has dramatically improved the treatment options in various cancers, increasing survival rates for treated patients. Nevertheless, there are heterogeneous response rates to ICI among different cancer types, and even in the context of patients affected by a specific cancer. Thus, it becomes crucial to identify factors that predict the response to immunotherapeutic approaches. A comprehensive investigation of the mutational and immunological aspects of the tumor can be useful to obtain a robust prediction. By performing a pan-cancer analysis on gene expression data from the Cancer Genome Atlas (TCGA, 8055 cases and 29 cancer types), we …

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatmentimmunology-pancancerimmune checkpoint inhibitorContext (language use)Machine learningcomputer.software_genrelcsh:RC254-282Article03 medical and health sciences0302 clinical medicinemedicineExtreme gradient boostingPan cancerbusiness.industryCancerImmunotherapylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMatthews correlation coefficientmedicine.diseaseSupport vector machine030104 developmental biologymachine learningOncology030220 oncology & carcinogenesisArtificial intelligencebusinesscomputerCancers
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Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma.

2016

ABSTRACT Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged in vivo exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine i…

0301 basic medicineCancer ResearchMethyltransferasesteatohepatitisDecitabineBiologyDecitabineDNA methylation Decitabine guadecitabine hepatocellular carcinoma (HCC) histone macroH2A1 steatohepatitishepatocellular carcinoma (HCC)03 medical and health scienceschemistry.chemical_compoundCDKN2AmedicineEpigeneticsMolecular BiologyneoplasmsDNA methylationGuadecitabineguadecitabinehistone macroH2A1steatohepatitidigestive system diseases3. Good healthDemethylating agent030104 developmental biologychemistryHypomethylating agentDNA methylationCancer researchResearch Papermedicine.drug
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LC3-Associated Phagocytosis (LAP): A Potentially Influential Mediator of Efferocytosis-Related Tumor Progression and Aggressiveness

2020

One aim of cancer therapies is to induce apoptosis of tumor cells. Efficient removal of the apoptotic cells requires coordinated efforts between the processes of efferocytosis and LC3-associated phagocytosis (LAP). However, this activity has also been shown to produce anti-inflammatory and immunosuppressive signals that can be utilized by live tumor cells to evade immune defense mechanisms, resulting in tumor progression and aggressiveness. In the absence of LAP, mice exhibit suppressed tumor growth during efferocytosis, while LAP-sufficient mice show enhanced tumor progression. Little is known about how LAP or its regulators directly affect efferocytosis, tumor growth and treatment respons…

0301 basic medicineCancer ResearchPhagocytosisReviewtumor cell apoptosislcsh:RC254-28203 medical and health sciences0302 clinical medicinemedicineCytotoxic T cellEfferocytosisefferocytosistumor immune responseTumor microenvironmentbusiness.industrydigestive oral and skin physiologyCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensM2 macrophage activation030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer cellLAPCancer researchbusinesshuman activitiesFrontiers in Oncology
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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Overview of General and Discriminating Markers of Differential Microglia Phenotypes.

2020

Inflammatory processes and microglia activation accompany most of the pathophysiological diseases in the central nervous system. It is proven that glial pathology precedes and even drives the development of multiple neurodegenerative conditions. A growing number of studies point out the importance of microglia in brain development as well as in physiological functioning. These resident brain immune cells are divergent from the peripherally infiltrated macrophages, but their precise in situ discrimination is surprisingly difficult. Microglial heterogeneity in the brain is especially visible in their morphology and cell density in particular brain structures but also in the expression of cell…

0301 basic medicineCentral nervous systemInflammationReviewBiologylcsh:RC321-571M1/M2 phenotype03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineImmune systemneurotoxicitymedicineCytotoxic T celllcsh:Neurosciences. Biological psychiatry. NeuropsychiatrypolarizationMicrogliaRegeneration (biology)Neurotoxicityinfiltrating macrophagesmedicine.diseasePhenotype030104 developmental biologymedicine.anatomical_structureinflammationCellular Neuroscienceregenerationmicroglial heterogeneitymedicine.symptomNeuroscience030217 neurology & neurosurgeryFrontiers in cellular neuroscience
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Mass Spectrometry Imaging Differentiates Chromophobe Renal Cell Carcinoma and Renal Oncocytoma with High Accuracy

2020

Background: While subtyping of the majority of malignant chromophobe renal cell carcinoma (cRCC) and benign renal oncocytoma (rO) is possible on morphology alone, additional histochemical, immunohistochemical or molecular investigations are required in a subset of cases. As currently used histochemical and immunohistological stains as well as genetic aberrations show considerable overlap in both tumors, additional techniques are required for differential diagnostics. Mass spectrometry imaging (MSI) combining the detection of multiple peptides with information about their localization in tissue may be a suitable technology to overcome this diagnostic challenge. Patients and Methods: Formalin…

0301 basic medicineChromophobe Renal Cell Carcinoma610610 Medicine & healthmass spectrometry imagingBiologyCross-validationMass spectrometry imagingOncocytic renal tumors03 medical and health sciences0302 clinical medicineproteomics10049 Institute of Pathology and Molecular PathologymedicineRenal oncocytomachromophobe renal cell carcinomabusiness.industrymedicine.diseaseLinear discriminant analysisRandom forestSupport vector machine030104 developmental biologyOncology030220 oncology & carcinogenesis2730 OncologyDifferential diagnosisNuclear medicinebusinessrenal oncocytomaResearch PaperJournal of Cancer
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Cohesive Model for the Simulation of Crack Initiation and Propagation in Mixed-Mode I/II in Composite Materials

2019

A cohesive element able to connect and simulate crack growth between independently modeled finite element subdomains with non-matching meshes is proposed and validated. The approach is based on penalty constraints and has several advantages over conventional FE techniques in disconnecting two regions of a model during crack growth. The most important is the ability to release portion of the interface that are smaller than the local finite element length. Thus, the growth of delamination is not limited to advancing by releasing nodes of the FE model, which is a limitation common to the methods found in the literature. Furthermore, it is possible to vary the penalty parameter within the cohes…

0301 basic medicineCommercial softwareCohesive elementMaterials science030102 biochemistry & molecular biologyInterface (computing)Delamination02 engineering and technologyFinite element . Cohesive element . Penalty method . Composite materials . Delamination . Mixed-mode propagation021001 nanoscience & nanotechnologyMixed modeFinite element method03 medical and health sciencesSettore ING-IND/14 - Progettazione Meccanica E Costruzione Di MacchineCeramics and CompositesPenalty methodPolygon meshComposite material0210 nano-technology
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