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showing 10 items of 13935 documents

Characteristics and Clinical Outcome of Breast Cancer Patients with Asymptomatic Brain Metastases

2020

Background: Brain metastases (BM) have become a major challenge in patients with metastatic breast cancer. Methods: The aim of this analysis was to characterize patients with asymptomatic BM (n = 580) in the overall cohort of 2589 patients with BM from our Brain Metastases in Breast Cancer Network Germany (BMBC) registry. Results: Compared to symptomatic patients, asymptomatic patients were slightly younger at diagnosis (median age: 55.5 vs. 57.0 years, p = 0.01), had a better performance status at diagnosis (Karnofsky index 80&ndash

0301 basic medicineCancer Researchmedicine.medical_specialtyNeoplasm metastasisMetastasePrognoseContext (language use)lcsh:RC254-282AsymptomaticGastroenterologyArticle03 medical and health sciencesbreast cancer0302 clinical medicineBreast cancerbrain metastasesInternal medicineBrustkrebsasymptomaticMedicineClinical significanceddc:610Treatment outcomeHirnmetastasePerformance statusbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMetastatic breast cancer030104 developmental biologyRisk factorsOncologyLead time bias030220 oncology & carcinogenesisCohortBreast neoplasmsmedicine.symptombusinessDDC 610 / Medicine & healthCancers
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Genetic susceptibility to angiotensin-converting enzyme-inhibitor induced angioedema: A systematic review and evaluation of methodological approaches.

2019

Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II which causes vasoconstriction. ACE inhibitors reduce blood pressure by inhibiting ACE. A well-known adverse drug reaction to ACE inhibitors is ACE inhibitor-induced angioedema (ACEi-AE). Angioedema is a swelling of skin and mucosa, which can be fatal if the airway is compromised. We have performed a systematic review of the evidence suggesting that genetic polymorphisms are associated with ACEi-AE and evaluated the methodological approaches of the included studies. The Cochrane Database of Systematic Reviews, Google Scholar, and PubMed were searched. Studies investigating the association between genetic markers and…

0301 basic medicineCandidate geneHeredityACE inhibitorsGenome-wide association studyAngiotensin-Converting Enzyme InhibitorsBioinformatics030226 pharmacology & pharmacyBiochemistryDatabase and Informatics Methods0302 clinical medicineOutcome Assessment Health CareMedicine and Health SciencesDatabase SearchingMultidisciplinarybiologyQRDrugsEnzyme inhibitorsGenomicsResearch AssessmentGenetic MappingSystematic reviewResearch DesignMedicinemedicine.symptomResearch ArticleSystematic ReviewsScienceResearch and Analysis Methods03 medical and health sciencesAdverse ReactionsGenetic predispositionmedicineGenome-Wide Association StudiesGeneticsHumansGenetic Predisposition to DiseaseAngioedemaPharmacologyEvolutionary BiologyPolymorphism GeneticAngioedemaBiology and life sciencesPopulation Biologybusiness.industryCase-control studyComputational BiologyCorrectionAngiotensin-converting enzymeHuman GeneticsGenome AnalysisAngiotensin II030104 developmental biologyHaplotypesCase-Control Studiesbiology.proteinEnzymologyGenetic PolymorphismbusinessPopulation GeneticsPloS one
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Comparison of Migratory and Resident Populations of Brown Trout Reveals Candidate Genes for Migration Tendency

2018

Abstract Candidate genes associated with migration have been identified in multiple taxa: including salmonids, many of whom perform migrations requiring a series of physiological changes associated with the freshwater–saltwater transition. We screened over 5,500 SNPs for signatures of selection related to migratory behavior of brown trout Salmo trutta by focusing on ten differentially migrating freshwater populations from two watersheds (the Koutajoki and the Oulujoki). We found eight outlier SNPs potentially associated with migratory versus resident life history using multiple (≥3) outlier detection approaches. Comparison of three migratory versus resident population pairs in the Koutajoki…

0301 basic medicineCandidate geneTroutPopulationlife-history strategyFresh WaterSingle-nucleotide polymorphismPolymorphism Single NucleotideLife history theoryEvolution Molecular03 medical and health sciencesBrown troutsmoltificationOsmoregulationtaimenbrown troutpopulaatiotsalmonidsGeneticsAnimalsSeawatermigration tendency14. Life underwaterSalmoeducationgenesEcology Evolution Behavior and SystematicsSmoltificationmigratory populationseducation.field_of_studyvaelluskalatgeenitbiologyta1184RADseqbiology.organism_classificationTrout030104 developmental biologyEvolutionary biologypopulaatiogenetiikkata1181Animal Migrationmigratory behaviorresident populationsSalmonidaeResearch ArticleGenome Biology and Evolution
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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Localization of the cannabinoid type-1 receptor in subcellular astrocyte compartments of mutant mouse hippocampus

2018

Astroglial type‐1 cannabinoid (CB1) receptors are involved in synaptic transmission, plasticity and behavior by interfering with the so‐called tripartite synapse formed by pre‐ and post‐synaptic neuronal elements and surrounding astrocyte processes. However, little is known concerning the subcellular distribution of astroglial CB1 receptors. In particular, brain CB1 receptors are mostly localized at cells' plasmalemma, but recent evidence indicates their functional presence in mitochondrial membranes. Whether CB1 receptors are present in astroglial mitochondria has remained unknown. To investigate this issue, we included conditional knock‐out mice lacking astroglial CB1 receptor expression …

0301 basic medicineCannabinoid receptormedicine.medical_treatmentImmunoelectron microscopyNeurotransmissionBiologyHippocampusImmunoenzyme Techniques03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineReceptor Cannabinoid CB1Glial Fibrillary Acidic ProteinTripartite synapsemedicineAnimalsMicroscopy ImmunoelectronReceptorMice KnockoutGlial fibrillary acidic proteinmusculoskeletal neural and ocular physiologyfood and beveragesMitochondriaCell biology030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyAstrocytesbiology.proteinlipids (amino acids peptides and proteins)Cannabinoidpsychological phenomena and processes030217 neurology & neurosurgeryAstrocyte
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Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
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Inflammatory Response Mechanisms of the Dentine–Pulp Complex and the Periapical Tissues

2021

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The fron…

0301 basic medicineCarcinogenesisRoot canalReviewimmune responselcsh:Chemistryodontoblast0302 clinical medicinePulpitislcsh:QH301-705.5SpectroscopyTissue homeostasisOdontoblastsPeriapical TissueIntracellular Signaling Peptides and ProteinsGeneral MedicineComputer Science ApplicationsCell biologyPeriradicularmedicine.anatomical_structureCarcinoma Squamous CellMouth NeoplasmsChemokinescarious lesionPeriapical GranulomaConnective tissueDental CariesBiologyNitric OxideCatalysisInorganic Chemistry03 medical and health sciencestertiary dentinestomatognathic systemAntigens NeoplasmmedicineAnimalsHumansddc:610Physical and Theoretical ChemistryApical foramenMolecular BiologyDental PulpRadicular CystNeuropeptidesOrganic ChemistryPulpitisMesenchymal Stem CellsComplement System Proteins030206 dentistryFibroblastsmedicine.diseasestomatognathic diseases030104 developmental biologyOdontoblastlcsh:Biology (General)lcsh:QD1-999DentinPulp (tooth)Nerve NetPeriapical PeriodontitisInternational Journal of Molecular Sciences
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mRNA-binding protein tristetraprolin is essential for cardiac response to iron deficiency by regulating mitochondrial function

2018

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specifically Ndufs1 in complex I and Uqcrfs1 in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP, Uqcrfs1 levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion of Ttp …

0301 basic medicineCardiac responseCardiac function curveIron-Sulfur ProteinsTristetraprolinMitochondria HeartCell Line03 medical and health sciencesElectron Transport Complex IIIMiceTristetraprolinmedicineAnimalschemistry.chemical_classificationMice KnockoutReactive oxygen speciesMultidisciplinaryNDUFS1MyocardiumNADH DehydrogenaseIron deficiencyIron Deficienciesmedicine.diseaseCell biology030104 developmental biologychemistryPNAS PlusCoenzyme Q – cytochrome c reductaseOxidation-ReductionFunction (biology)
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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

2017

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective…

0301 basic medicineCarotid Artery DiseasesMalePathologymedicine.medical_specialtyNecrosisCardiology030204 cardiovascular system & hematologyBiologyC-Mer Tyrosine KinaseProinflammatory cytokine03 medical and health sciencesMiceNecrosis0302 clinical medicineProto-Oncogene ProteinsmedicineAnimalsHumansEfferocytosisMice Knockoutc-Mer Tyrosine KinaseBrief ReportFibrous capReceptor Protein-Tyrosine KinasesGeneral MedicineMERTKPlaque Atherosclerotic030104 developmental biologymedicine.anatomical_structureReceptors LDLApoptosisProteolysisFemalemedicine.symptomTyrosine kinase
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Hepatitis C Virus Eradication by Direct Antiviral Agents Improves Carotid Atherosclerosis in patients with Severe Liver Fibrosis.

2018

Abstract BACKGROUND AND AIM: Recent studies suggest an association between HCV infection and cardiovascular damage, including carotid atherosclerosis, with a possible effect of HCV clearance on cardiovascular outcomes. We aimed to examine whether HCV eradication by direct antiviral agents (DAA) improves carotid atherosclerosis in HCV-infected patients with advanced fibrosis/compensated cirrhosis. MATERIALS AND METHODS: One hundred eighty-two consecutive HCV patients with advanced fibrosis or compensated cirrhosis were evaluated by virological, anthropometric and metabolic measurements. All patients underwent DAA-based antiviral therapy according to AISF/EASL guidelines. Intima-media thickne…

0301 basic medicineCarotid atherosclerosisCarotid Artery DiseasesMalemedicine.medical_specialtyCirrhosisSVRSustained Virologic ResponseHepatitis C virusHepacivirusmedicine.disease_causeGastroenterologyAntiviral AgentsCarotid Intima-Media Thickness03 medical and health sciencesLiver disease0302 clinical medicineRisk FactorsInternal medicineDiabetes mellitusmedicineGlucose homeostasisHumansIn patientProspective StudiesDAAHepatologybusiness.industryHepatitis C ChronicMiddle Agedmedicine.disease030104 developmental biologyTreatment OutcomeATHEROSCLEROSISHCVcardiovascular system030211 gastroenterology & hepatologyFemalebusinessDirect actingFollow-Up Studies
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