Search results for "10040"

showing 10 items of 11 documents

Association of prestroke metformin use, stroke severity, and thrombolysis outcome

2020

ObjectiveTo evaluate whether pretreatment with metformin (MET) is associated with less stroke severity and better outcome after IV thrombolysis (IVT), we analyzed a cohort of 1,919 patients with stroke with type 2 diabetes mellitus in a multicenter exploratory analysis.MethodsData from patients with diabetes and ischemic stroke treated with IVT were collected within the European Thrombolysis in Ischemic Stroke Patients (TRISP) collaboration. We applied propensity score matching (PSM) to obtain balanced baseline characteristics of patients treated with and without MET.ResultsOf 1,919 patients with stroke with type 2 diabetes who underwent IVT, 757 (39%) had received MET before stroke (MET+),…

Malemedicine.medical_specialtymedicine.medical_treatment610 Medicine & health030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineFibrinolytic AgentsModified Rankin ScaleInternal medicineDiabetes mellitusEpidemiologymedicineHumansHypoglycemic AgentsThrombolytic Therapycardiovascular diseases10064 Neuroscience Center ZurichStrokeAgedRetrospective Studiesbusiness.industryRecovery of Function10060 Epidemiology Biostatistics and Prevention Institute (EBPI)ThrombolysisMiddle Agedmedicine.diseaseMetformin10040 Clinic for Neurology3. Good healthMetforminStroke2728 Neurology (clinical)Diabetes Mellitus Type 2Propensity score matchingCohortFemaleNeurology (clinical)business030217 neurology & neurosurgerymedicine.drugNeurology
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Differential expression of the tumor suppressor A-kinase anchor protein 12 in human diffuse and pilocytic astrocytomas is regulated by promoter methy…

2013

The scaffold protein A-kinase anchor protein 12 (AKAP12) exerts tumor suppressor activity and is downregulated in several tumor entities. We characterized AKAP12 expression and regulation in astrocytomas, including pilocytic and diffusely infiltrating astrocytomas. We examined 194 human gliomas and 23 normal brain white matter samples by immunohistochemistry or immunoblotting for AKAP12 expression. We further performed quantitative methylation analysis of the AKAP12 promoter by MassARRAY® of normal brain, World Health Organization (WHO) grade I to IV astrocytomas, and glioma cell lines. Our results show that AKAP12 is expressed in a perivascular distribution in normal CNS, strongly upregula…

AdultMalePathologymedicine.medical_specialtyAdolescent2804 Cellular and Molecular NeuroscienceA Kinase Anchor ProteinsCell Cycle Proteins610 Medicine & healthAstrocytomaBiologyPathology and Forensic MedicineCellular and Molecular NeuroscienceGliomamedicineHumansChildPromoter Regions GeneticneoplasmsAgedAged 80 and overRegulation of gene expressionPilocytic astrocytomaBrain NeoplasmsInfantAstrocytomaGeneral MedicineMethylationDNA MethylationMiddle AgedAKAP12medicine.diseaseUp-Regulationnervous system diseases10040 Clinic for NeurologyGene Expression Regulation Neoplastic2734 Pathology and Forensic Medicine2728 Neurology (clinical)nervous systemNeurologyChild Preschool2808 NeurologyDNA methylationCancer researchImmunohistochemistryFemaleNeurology (clinical)Neoplasm Grading
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Nuclear actin aggregation is a hallmark of anti-synthetase syndrome-induced dysimmune myopathy

2015

Objective: To analyze antisynthetase syndrome–associated myositis by modern myopathologic methods and to define its place in the spectrum of idiopathic inflammatory myopathies (IIMs). Methods: Skeletal muscle biopsies from antisynthetase syndrome–associated myositis and other IIMs from different institutions worldwide were analyzed by histopathology, quantitative PCR, and electron microscopy. Results: Myonuclear actin filament inclusions were identified as a unique morphologic hallmark of antisynthetase syndrome–associated myositis. Nuclear actin inclusions were never found in dermatomyositis, polymyositis, sporadic inclusion body myositis, autoimmune necrotizing myopathy associated with si…

Pathologymedicine.medical_specialtyBiopsyIntranuclear Inclusion Bodies10208 Institute of Neuropathology610 Medicine & healthAntisynthetase syndromeBiologyPolymyositisSensitivity and SpecificityNecrosisPerimysialmedicineHumansMyopathyMuscle SkeletalMyositisMyositisDermatomyositisActin cytoskeletonmedicine.diseaseAutoimmune necrotizing myopathyActins10040 Clinic for NeurologyActin Cytoskeleton2728 Neurology (clinical)Immunology570 Life sciences; biologyNeurology (clinical)medicine.symptom
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Tolerance without clonal expansion: self-antigen-expressing B cells program self-reactive T cells for future deletion.

2008

Abstract B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by abl…

T-LymphocytesProgrammed Cell Death 1 ReceptorAutoimmunityAntigens CD/biosynthesisAntigens CD5/geneticsAutoantigensInterleukin 21MiceImmunology and AllergyCytotoxic T cellHomeostasisCTLA-4 AntigenIL-2 receptorAntigens Differentiation/biosynthesisB-LymphocytesAntigens CD/geneticsB-Lymphocytes/immunologyT-Lymphocytes/metabolismNatural killer T cellCell biologymedicine.anatomical_structureHomeostasis/immunology2723 Immunology and AllergyAntigens CD5/biosynthesisAntigens Differentiation/geneticsAntigens CD5/immunologyT cellImmunologyAntigens CD/immunologyClonal Deletion610 Medicine & healthchemical and pharmacologic phenomenaMice TransgenicBiologyAutoantigens/biosynthesisCD5 AntigensAutoimmunity/physiologyAutoantigens/immunologyAntigens CDmedicineAnimalsB-Lymphocytes/metabolismAntigen-presenting cellCell Proliferation2403 ImmunologyAntigens Differentiation/immunologyGene Expression Regulation/immunologyCD40Clonal Deletion/physiologyT-Lymphocytes/immunologyAntigens Differentiation10040 Clinic for NeurologyB-1 cellGene Expression Regulationbiology.protein
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The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
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Recanalization Therapies in Acute Ischemic Stroke Patients Impact of Prior Treatment With Novel Oral Anticoagulants on Bleeding Complications and Out…

2015

Background— We explored the safety of intravenous thrombolysis (IVT) or intra-arterial treatment (IAT) in patients with ischemic stroke on non-vitamin K antagonist oral anticoagulants (NOACs, last intake <48 hours) in comparison with patients (1) taking vitamin K antagonists (VKAs) or (2) without previous anticoagulation (no-OAC). Methods and Results— This is a multicenter cohort pilot study. Primary outcome measures were (1) occurrence of intracranial hemorrhage (ICH) in 3 categories: any ICH (ICH any ), symptomatic ICH according to the criteria of the European Cooperative Acute Stroke Study II (ECASS-II) (sICH ECASS-II ) and the National Institute of Neurological Disorders and Stroke …

MaleBrain Ischemia/blood/drug therapyVitamin Kmedicine.medical_treatmentendovascular proceduresAnticoagulants/administration & dosage/adverse effects/classification/therapeutic useAdministration OralPilot ProjectsTissue plasminogen activatorBrain IschemiaCohort Studies2737 Physiology (medical)Atrial Fibrillation80 and overThrombolytic TherapyVitamin K/antagonists & inhibitorsStrokethrombolytic therapyAged 80 and overIncidenceAtrial fibrillationThrombolysisMiddle Aged3. Good healthvitamin K antagonistsTreatment OutcomeAdministrationAcute DiseaseCohortCerebral Hemorrhage/chemically induced/epidemiologyFemaleCardiology and Cardiovascular MedicineAtrial Fibrillation/complicationsmedicine.drugOralmedicine.medical_specialtyanticoagulantsnon-vitamin K antagonist oral anticoagulantsFactor Xa Inhibitors/administration & dosage/adverse effects/therapeutic useintracranial hemorrhagesintra-arterial treatment610 Medicine & healthAntithrombins2705 Cardiology and Cardiovascular MedicineDabigatranFibrinolytic AgentsPhysiology (medical)Internal medicinemedicineischemic strokeHumansAgedCerebral HemorrhageIntracerebral hemorrhageFibrinolytic Agents/therapeutic usebusiness.industryAntithrombins/administration & dosage/adverse effects/therapeutic usemedicine.diseaseddc:616.810040 Clinic for Neurologyanticoagulants; endovascular procedures; intra-arterial treatment; intracranial hemorrhages; ischemic stroke; non-vitamin K antagonist oral anticoagulants; thrombolytic therapy; vitamin K antagonistsPropensity score matchingbusinessFactor Xa InhibitorsCirculation
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ERGO: A pilot study of ketogenic diet in recurrent glioblastoma

2014

Limiting dietary carbohydrates inhibits glioma growth in preclinical models. Therefore, the ERGO trial (NCT00575146) examined feasibility of a ketogenic diet in 20 patients with recurrent glioblastoma. Patients were put on a low-carbohydrate, ketogenic diet containing plant oils. Feasibility was the primary endpoint, secondary endpoints included the percentage of patients reaching urinary ketosis, progression-free survival (PFS) and overall survival. The effects of a ketogenic diet alone or in combination with bevacizumab was also explored in an orthotopic U87MG glioblastoma model in nude mice. Three patients (15%) discontinued the diet for poor tolerability. No serious adverse events attri…

MaleCancer ResearchStatement (logic)medicine.medical_treatmentSalvage treatmentPilot ProjectsBioinformaticsGastroenterologyMicegliomaClinical endpoint1306 Cancer ResearchglucoseArticlesMiddle AgedCombined Modality TherapyBevacizumabTreatment OutcomeTolerabilityOncologyketogenic dietFemale2730 OncologyDiet Ketogenicmedicine.drugAdultmedicine.medical_specialtyBevacizumabMice NudeAntineoplastic Agents610 Medicine & healthMistakeRecurrent GliomaBiologyAntibodies Monoclonal HumanizedInternal medicineGliomamedicineAnimalsHumansddc:610Adverse effectAgedbusiness.industryRecurrent glioblastomaGeneral surgeryKetosisNeoplasms Experimentalmedicine.diseaseSurvival Analysis10040 Clinic for NeurologySurgeryQuality of LifeNeoplasm Recurrence LocalKetosisGlioblastomabusinessmetabolismfeasibilityKetogenic dietInternational Journal of Oncology
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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Randomized phase III study of whole-brain radiotherapy for primary CNS lymphoma

2015

Objective: This is the final report of a phase III randomized study to evaluate whole-brain radiotherapy (WBRT) in primary therapy of primary CNS lymphoma (PCNSL) after a median follow-up of 81.2 months. Methods: Patients with newly diagnosed PCNSL were randomized to high-dose methotrexate (HDMTX)–based chemotherapy alone or followed by WBRT. We hypothesized that the omission of WBRT would not compromise overall survival (OS; primary endpoint), using a noninferiority design with a margin of 0.9. Results: In the per-protocol population (n = 320), WBRT nonsignificantly prolonged progression-free survival (PFS) (median 18.2 vs 11.9 months, hazard ratio [HR] 0.83 [95% confidence interval (CI) 0…

MaleOncologyAntimetabolites Antineoplasticmedicine.medical_specialtyLymphomamedicine.medical_treatmentPopulationMedizin610 Medicine & healthDisease-Free Survivallaw.inventionCentral Nervous System NeoplasmsRandomized controlled triallawInternal medicinemedicineClinical endpointHumanseducationAgededucation.field_of_studyChemotherapybusiness.industryHazard ratioAntineoplastic ProtocolsMiddle AgedCombined Modality TherapyConfidence interval10040 Clinic for NeurologyRadiation therapyMethotrexateTreatment Outcome2728 Neurology (clinical)MethotrexateNeurology (clinical)Cranial Irradiationbusinessmedicine.drug
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Endothelial GLP-1 (Glucagon-Like Peptide 1) Receptor Mediates Cardiovascular Protection by Liraglutide In Mice With Experimental Arterial Hypertension

2019

Supplemental Digital Content is available in the text.

0301 basic medicineMalemedicine.medical_specialtyhypertensionBlotting WesternInflammationBlood Pressure030204 cardiovascular system & hematologyangiotensin IImedicine.disease_causeGlucagon-Like Peptide-1 Receptor1005403 medical and health sciencesMice0302 clinical medicine10030Internal medicinemedicineoxidative stressAnimalsHypoglycemic AgentsReceptor10111Cells CulturedMice KnockoutliraglutideLiraglutidebusiness.industryBasic SciencesType 2 Diabetes MellitusEndothelial CellsAtherosclerosisGlucagon-like peptide-1Angiotensin II3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology10040inflammationComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRNAmedicine.symptomCardiology and Cardiovascular Medicinebusiness10024Oxidative stressmedicine.drug
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