Search results for "granulocyte colony-stimulating factor"

showing 10 items of 68 documents

Granulocyte-macrophage colony-stimulating factor induces cytokine secretion by human polymorphonuclear leukocytes.

1989

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known as an inducer of proliferation and functional activation of myeloid cells. This study was carried out to characterize the effects of GM-CSF on polymorphonuclear leukocytes (PMN) more extensively. Using Northern blot analysis, we show that PMN are able to accumulate mRNAs for different cytokines, including tumor necrosis factor-alpha (TNF-alpha); G-CSF, and M-CSF, all of which are involved in inflammation and hematopoiesis. Biological assays and immunoassays demonstrate that PMN translate these mRNAs, except TNF-alpha, into secretory proteins. However, the expression of these cytokines is dependent on stimulation by exogenous…

Macrophage colony-stimulating factorNeutrophilsT cellInflammationBiologyBiological FactorsMiceColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineAnimalsHumansRNA MessengerGrowth SubstancesTumor Necrosis Factor-alphaMacrophage Colony-Stimulating FactorLymphokineGranulocyte-Macrophage Colony-Stimulating FactorGeneral MedicineColony-stimulating factorRecombinant ProteinsRetractionCell biologymedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyCytokinesTumor necrosis factor alphaCytokine secretionmedicine.symptomResearch Articlemedicine.drugJournal of Clinical Investigation
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Production of macrophage-, granulocyte-, granulocyte-macrophage- and multi-colony-stimulating factor by peripheral blood cells

1989

The specific cell sources and signals for induction of various colony-stimulating factors (CSF) in peripheral blood mononuclear cells (PBMC), purified T lymphocyte and monocyte (Mo) populations have been investigated. In the absence of exogenous activating stimuli, human PBMC, T cells and Mo failed to produce stable cytoplasmic mRNA for CSF for macrophages (M-CSF or CSF-1), for granulocytes (G-CSF), for granulocytes and macrophages (GM-CSF) and for multilineage CSF [multi-CSF, interleukin (IL) 3] and thus failed to release CSF proteins. However, after stimulation with phorbol myristate acetate and phytohemagglutinin, M-, G-, GM- and multi-CSF mRNA became detectable in PBMC, resulting in the…

Macrophage colony-stimulating factorT-Lymphocytesmedicine.medical_treatmentImmunologyGranulocyteBiologyPeripheral blood mononuclear cellMonocytesColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineHumansImmunology and AllergyMacrophageRNA MessengerGrowth SubstancesMacrophage Colony-Stimulating FactorMonocyteGranulocyte-Macrophage Colony-Stimulating FactorT lymphocyteMolecular biologyGranulocyte macrophage colony-stimulating factorCytokinemedicine.anatomical_structureImmunologyInterleukin-3medicine.drugEuropean Journal of Immunology
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Incidence and risk factors of post-engraftment invasive fungal disease in adult allogeneic hematopoietic stem cell transplant recipients receiving or…

2015

Studies that analyze the epidemiology and risk factors for invasive fungal disease (IFD) after engraftment in alloSCT are few in number. This single-center retrospective study included 404 alloSCT adult recipients surviving > 40 days who engrafted and were discharged without prior IFD. All patients who received >= 20 mg/day of prednisone were assigned to primary oral prophylaxis (itraconazole or low-dose voriconazole). The primary end point was the cumulative incidence (CI) of probable/proven IFD using the European Organization for Research and Treatment of Cancer and Mycoses Study Group (EORTC/MSG) criteria. The independent prognostic factors after multivariate analyses were used to constr…

MaleAntifungal AgentsTransplantation ConditioningPremedicationmedicine.medical_treatmentMULTICENTERAdministration OralHematopoietic stem cell transplantationEchinocandinsCOMPETING RISKCaspofunginRisk FactorsCause of DeathINFECTIONGranulocyte Colony-Stimulating FactorEPIDEMIOLOGYCumulative incidenceTreatment FailureFramingham Risk ScoreIncidenceIncidence (epidemiology)Hematopoietic Stem Cell TransplantationHematologyMiddle AgedAllograftsHematologic NeoplasmsVORICONAZOLEDrug Therapy CombinationFemaleASPERGILLOSISRisk assessmentFungemiamedicine.drugAdultmedicine.medical_specialtyNeutropeniaANTIFUNGAL PROPHYLAXISNeutropeniaRisk AssessmentITRACONAZOLEMedication AdherenceImmunocompromised HostLipopeptidesYoung AdultAmphotericin BInternal medicinemedicineAspergillosisHumansAgedRetrospective StudiesVoriconazoleTransplantationbusiness.industryRetrospective cohort studyFLUCONAZOLETriazolesmedicine.diseaseSurvival AnalysisSurgeryMycosesPatient CompliancebusinessSCT
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Sustained telomere erosion due to increased stem cell turnover during triple autologous hematopoietic stem cell transplantation.

2007

Telomeres cap chromosomal ends and are shortened throughout a lifetime. Additional telomere erosion has been documented during conventional chemotherapy or hematopoietic stem cell transplantation. Previous studies of stem cell transplantation reported variable amounts of telomere shortening with inconsistent results regarding the persistence of telomere shortening. Here we have prospectively studied telomere length and proliferation kinetics of hematopoietic cells in aggressive non-Hodgkin lymphoma patients who underwent a four-course high-dose chemotherapy protocol combined with triple autologous stem cell transplantation. We observed sustained telomere shortening in hematopoietic cells af…

MaleCancer ResearchTransplantation Conditioningmedicine.medical_treatmentHematopoietic stem cell transplantationAntibodies Monoclonal Murine-DerivedAutologous stem-cell transplantationAntineoplastic Combined Chemotherapy ProtocolsGranulocyte Colony-Stimulating FactorLymphocytesProspective StudiesCellular SenescenceEtoposideMyelopoiesisLymphoma Non-HodgkinAntibodies MonoclonalHematologyMiddle AgedTelomereCombined Modality TherapyHaematopoiesisVincristineFemaleStem cellRituximabCell DivisionPrednisoloneTransplantation AutologousDrug Administration ScheduleGeneticsmedicineHumansMolecular BiologyCyclophosphamideChemotherapyPeripheral Blood Stem Cell Transplantationbusiness.industryCell BiologyMyeloablative Agonistsmedicine.diseaseHematopoietic Stem CellsTelomereLymphomaTransplantationClinical Trials Phase III as TopicDoxorubicinImmunologyCancer researchbusinessGranulocytesExperimental hematology
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Disseminated fusariosis in immunocompromised patients

2011

Immunocompromised patients are at high risk of developing serious disseminated infections by opportunistic fungi (Aspergillus, Candida, and Fusarium spp), which frequently present as cutaneous lesions, sometimes as a first sign. Prolonged and deep neutropenia, immunodepressive treatments (systemic steroids and chemotherapy) and severe T-cell immunodeficiency are the most important risk factors. We report 2 patients with acute lymphoblastic leukemia, who developed multiple tender erythematous skin lesions on their legs and arms during chemotherapy treatment. Skin biopsies for histology and culture studies established the diagnosis of Fusarium infection. They received treatment with systemic …

MaleFusariummedicine.medical_specialtyAntifungal Agentsmedicine.medical_treatmentDermatologyNeutropeniaImmunocompromised HostYoung AdultFatal OutcomeAmphotericin BGranulocyte Colony-Stimulating FactormedicineHumansYoung adultImmunodeficiencyVoriconazoleChemotherapyAspergillusbiologybusiness.industryMortality rateMiddle AgedPrecursor Cell Lymphoblastic Leukemia-LymphomaTriazolesmedicine.diseasebiology.organism_classificationDermatologyPyrimidinesFusariosisImmunologyFemaleVoriconazolebusinessmedicine.drugEuropean Journal of Dermatology
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Neuroprotective effect of Fn14 deficiency is associated with induction of the granulocyte-colony stimulating factor (G-CSF) pathway in experimental s…

2010

Using a transgenic mouse model of ischemic stroke we checked for a possible interaction of antiphospholipid antibodies (aPL) which often cause thromboses as well as central nervous system (CNS) involvement under non-thrombotic conditions and the TWEAK/Fn14 pathway known to be adversely involved in inflammatory and ischemic brain disease. After 7 days, infarct volumes were reduced in Fn14 deficient mice and were further decreased by aPL treatment. This was associated with strongest increase of the endogenous neuroprotective G-CSF/G-CSF receptor system. This unexpected beneficial action of aPL is an example for a non-thrombogenic action and the double-edged nature of aPL.

MaleGenetically modified mouseImmunologyMice TransgenicBiologyNeuroprotectionReceptors Tumor Necrosis FactorBrain IschemiaMiceRandom AllocationTissue factorimmune system diseasesAntiphospholipid syndromeGranulocyte Colony-Stimulating FactormedicineAnimalsHumansImmunology and AllergyneoplasmsStrokeLupus anticoagulantmedicine.diseaseMice Inbred C57BLDisease Models AnimalNeurologyTWEAK ReceptorReceptors Granulocyte Colony-Stimulating FactorImmunologyAntibodies AntiphospholipidTumor necrosis factor alphaNeurology (clinical)Inflammation MediatorsGranulocyte colony-stimulating factor receptorSignal TransductionJournal of Neuroimmunology
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Distribution of the hematopoietic growth factor G-CSF and its receptor in the adult human brain with specific reference to Alzheimer's disease

2013

The granulocyte colony-stimulating factor (G-CSF), being a member of the hematopoietic growth factor family, is also critically involved in controlling proliferation and differentiation of neural stem cells. Treatment with G-CSF has been shown to result in substantial neuroprotective and neuroregenerative effects in various experimental models of acute and chronic diseases of the central nervous system. Although G-CSF has been tested in a clinical study for treatment of acute ischemic stroke, there is only fragmentary data on the distribution of this cytokine and its receptor in the human brain. Therefore, the present study was focused on the immunohistochemical analysis of the protein expr…

MaleHistologyHematopoietic growth factorCentral nervous systemNeuroprotectionAlzheimer DiseaseGranulocyte Colony-Stimulating FactormedicineHumansMolecular BiologyEcology Evolution Behavior and SystematicsAgedAged 80 and overNeuronsbiologyBrainOriginal ArticlesCell BiologyHuman brainMiddle AgedImmunohistochemistryNeural stem cellmedicine.anatomical_structureCase-Control StudiesReceptors Granulocyte Colony-Stimulating FactorImmunologybiology.proteinFemaleChoroid plexusAnatomyGranulocyte colony-stimulating factor receptorNeuroscienceDevelopmental BiologyNeurotrophinJournal of Anatomy
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Bone marrow failure by cytomegalovirus is associated with an in vivo deficiency in the expression of essential stromal hemopoietin genes.

1997

Bone marrow (BM) failure associated with cytomegalovirus (CMV) infection is a feared complication after clinical BM transplantation. Experiments in long-term BM cultures have indicated that BM stromal cells (BMSC) are targets of productive CMV infection, but an in situ infection of BM stroma remained to be documented, and the pathomechanism is open to question. Here we describe a murine in vivo model of lethal CMV aplastic anemia (CMV-AA). The reconstitution of hematopoietic progenitor cells expressing stem cell factor (SCF) receptor was found to be defective in CMV-AA. While murine CMV replication in permissive parenchymal tissues is cytolytic, the hematopoietic cord was found to be a site…

MaleStromal cellImmunologyGene ExpressionStem cell factorBiologyHematopoietic Cell Growth FactorsMicrobiologyMiceBone MarrowVirologyGranulocyte Colony-Stimulating FactormedicineAnimalsRNA MessengerAplastic anemiaMice Inbred BALB CStem Cell FactorInterleukin-6Hematopoietic Cell Growth FactorsBone marrow failureAnemia Aplasticmedicine.diseaseHematopoiesisTransplantationHaematopoiesisProto-Oncogene Proteins c-kitmedicine.anatomical_structureInsect ScienceImmunologyCytomegalovirus InfectionsFemaleBone marrowResearch Article
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Continuous Intravenous Administration of Granulocyte-Colony-Stimulating Factors—A Breakthrough in the Treatment of Cancer Patients with Febrile Neutr…

2021

(1) Background: Febrile neutropenia (FN) remains one of the most challenging problems in medical oncology and is a very severe side effect of chemotherapy. Its late consequences, when it is recurrent or of a severe grade, are dose reduction and therapy delays. Current guidelines allow the administration of granulocyte-colony-stimulating factors (G-CSF) for profound FN (except for the case when a pegylated form of G-CSF is administrated with prophylactic intention) in addition to antibiotics and supportive care. (2) Methods: This is a prospective study that included 96 patients with confirmed malignancy, treated with chemotherapy, who developed FN during their oncological therapy, and were h…

Malemedicine.medical_specialtyMedicine (General)Side effectmedicine.medical_treatmentNeutropeniaG-CSFfebrilechemotherapyGastroenterologyArticleProcalcitoninR5-920NeoplasmsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsGranulocyte Colony-Stimulating FactormedicineHumansneutropeniacancerProspective StudiesProspective cohort studyFebrile NeutropeniaChemotherapybiologybusiness.industryStandard treatmentC-reactive proteinGeneral Medicinemedicine.diseasebiology.proteinAdministration IntravenousFemalebusinessFebrile neutropeniaGranulocytesMedicina
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The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis.

2005

G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong anti-apoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neurona…

Malemedicine.medical_specialtyProgrammed cell deathNeutrophilsCellular differentiationApoptosisBiologyLigandsBrain IschemiaBrain ischemiaInternal medicineGranulocyte Colony-Stimulating FactormedicineAnimalsHumansGranulocyte Precursor CellsNerve TissueRats WistarReceptorAutocrine signallingStem CellsNeurogenesisCell DifferentiationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseNeural stem cellCell biologyRatsStrokeDisease Models AnimalEndocrinologyBlood-Brain BarrierReceptors Granulocyte Colony-Stimulating FactorStem cellResearch ArticleThe Journal of clinical investigation
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