Search results for "Growth factor"

showing 10 items of 1300 documents

Sequential BMP7/TGF-β1 signaling and microbiota instruct mucosal Langerhans cell differentiation

2018

Capucha et al. demonstrate that mucosal Langerhans cell (LC) differentiation from pre–dendritic cells and monocytes involves consecutive BMP7 and TGF-β1 signaling in separate anatomical locations. Moreover, mucosal microbiota regulates the development of LCs that in turn shape microbial and immunological homeostasis.

Male0301 basic medicineLangerhans cellBone Morphogenetic Protein 7ImmunologyReceptor Transforming Growth Factor-beta Type IBiologyArticle311Transforming Growth Factor beta1Mice03 medical and health sciencesDownregulation and upregulation319Langerhans cell differentiationmedicineAnimalsHumansImmunology and AllergyLectins C-TypeImmunity MucosalResearch ArticlesBone Morphogenetic Protein Receptors Type IMice KnockoutLamina propriaintegumentary systemMicrobiotaStem CellsMouth MucosaMucous membraneCell DifferentiationEpitheliumUp-RegulationCell biologyMice Inbred C57BLBone morphogenetic protein 7Mannose-Binding Lectins030104 developmental biologymedicine.anatomical_structureLangerhans CellsAntigens SurfaceSignal transductionTranscriptomeSignal TransductionJournal of Experimental Medicine
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Pathological significance and prognostic value of surfactant protein D in cancer

2018

Surfactant protein D (SP-D) is a pattern recognition molecule belonging to the Collectin (collagen-containing C-type lectin) family that has pulmonary as well as extra-pulmonary existence. In the lungs, it is a well-established opsonin that can agglutinate a range of microbes, and enhance their clearance via phagocytosis and super-oxidative burst. It can interfere with allergen–IgE interaction and suppress basophil and mast cell activation. However, it is now becoming evident that SP-D is likely to be an innate immune surveillance molecule against tumor development. SP-D has been shown to induce apoptosis in sensitized eosinophils derived from allergic patients and a leukemic cell line via …

Male0301 basic medicineLung NeoplasmsDatasets as Topic0302 clinical medicineEpidermal growth factorNeoplasmsImmunology and AllergyRNA NeoplasmOriginal ResearchCancerOvarian NeoplasmsInnate immunitySurfactant protein DBioinformatics analysiPrognosisPulmonary Surfactant-Associated Protein DImmunohistochemistryTumor microenvironment030220 oncology & carcinogenesisAdenocarcinomaFemaleCancersBreast NeoplasmHumanlcsh:Immunologic diseases. AllergyPrognosiImmunologyBreast NeoplasmsBiology03 medical and health sciencesImmune systemBioinformatics analysisStomach NeoplasmsStomach NeoplasmBiomarkers TumormedicineHumansComputer SimulationLung cancerTumor microenvironmentOvarian NeoplasmComputational BiologySurfactant protein DCancermedicine.diseaseSurvival AnalysisLung NeoplasmImmune surveillance030104 developmental biologyCancer researchNeoplasmBioinformatics analysis; Cancers; Immune surveillance; Immunohistochemistry; Innate immunity; Surfactant protein D; Tumor microenvironment; Immunology and Allergy; Immunologylcsh:RC581-607Ovarian cancer
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Additive effects of cherlerythrine chloride combination with erlotinib in human non-small cell lung cancer cells

2017

Several studies implicate that lung cancer progression is governed by the interaction between epidermal growth factor receptor (EGFR) signaling and protein kinase C (PKC) pathways. Combined the targeting of EGFR and PKC may have an additive or synergistic effects in lung cancer treatment. The aim of this study is to explore the potential utility by inhibiting these two pathways with the combination of erlotinib and chelerythrine chloride in non-small cell lung cancer (NSCLC) cell lines. The erlotinib-less sensitive cell lines SK-MES-1 and A549 were treated with erlotinib or chelerythrine by themselves or in combination with each other. The cell viability, clonogenic survival, cell migration…

Male0301 basic medicineOncologyCell signalingLung NeoplasmsCancer Treatmentlcsh:MedicineApoptosisMice SCIDSignal transductionLung and Intrathoracic TumorsMicechemistry.chemical_compoundMice Inbred NODCarcinoma Non-Small-Cell LungMedicine and Health SciencesEpidermal growth factor receptorPhosphorylationlcsh:ScienceErlotinib HydrochlorideMultidisciplinaryCell DeathbiologyPharmaceuticsChemistrySignaling cascadesFlow CytometryErbB ReceptorsCell MotilityOncologyCell ProcessesDrug Therapy CombinationErlotinibSignal transductionEGFR signalingResearch Articlemedicine.drugmedicine.medical_specialtyMAPK signaling cascadesCell MigrationErlotinib Hydrochloride03 medical and health sciencesDrug TherapyCell Line TumorInternal medicinemedicineAnimalsHumansViability assayLung cancerBenzophenanthridineslcsh:RCancers and NeoplasmsBiology and Life SciencesCell Biologymedicine.diseaseXenograft Model Antitumor AssaysNon-Small Cell Lung Cancerrespiratory tract diseases030104 developmental biologyChelerythrineApoptosisCancer researchbiology.proteinlcsh:QDevelopmental BiologyPLOS ONE
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A Phase Ib Dose-Escalation Study of the Safety, Tolerability, and Pharmacokinetics of Cobimetinib and Duligotuzumab in Patients with Previously Treat…

2017

Abstract Lessons Learned Cobimetinib and duligotuzumab were well tolerated as single agents and in combination with other agents. The cobimetinib and duligotuzumab combination was associated with increased toxicity, most notably gastrointestinal, and limited efficacy in the patient population tested. Background KRAS-mutant tumors possess abnormal mitogen-activated protein kinases (MAPK) pathway signaling, leading to dysregulated cell proliferation. Cobimetinib blocks MAPK signaling. The dual-action antibody duligotuzumab (MEHD7945A) inhibits ligand binding to both epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 3 (HER3). Blockade of EGFR/HER3 and inhibitio…

Male0301 basic medicineOncologyMAPK/ERK pathwayCancer ResearchReceptor ErbB-3MAP Kinase Kinase 1Administration Oralmedicine.disease_causechemistry.chemical_compound0302 clinical medicinePiperidinesAntineoplastic Combined Chemotherapy ProtocolsMedicineProspective StudiesEpidermal growth factor receptor31biologyMiddle AgedErbB ReceptorsTreatment OutcomeOncologyTolerability030220 oncology & carcinogenesisFemaleDrug EruptionsKRASmedicine.symptomColorectal NeoplasmsSignal TransductionAdultmedicine.medical_specialty4HypokalemiaAcneiform eruptionProto-Oncogene Proteins p21(ras)03 medical and health sciencesAcneiform EruptionsInternal medicineHumansAdverse effectAgedNeoplasm StagingCobimetinibDose-Response Relationship Drugbusiness.industryClinical Trial Resultsmedicine.disease030104 developmental biologychemistryAstheniaImmunoglobulin Gbiology.proteinAzetidinesbusinessProgressive diseaseThe Oncologist
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Relationships of growth factors, proinflammatory cytokines, and anti-inflammatory cytokines with long-term clinical results of autologous bone marrow…

2017

Aim The aim of the study was to test the hypothesis suggesting that the pre-intervention levels of proinflammatory cytokines, anti-inflammatory cytokines, and angiogenic growth factors predict the long-term clinical results of autologous bone marrow-derived mononuclear cell (ABMMC) transplantation in patients with primary ST elevation myocardial infarction (STEMI). Methods and results From 2003 to 2006, a total of 62 patients with primary STEMI were enrolled in an open randomized study registered under the title ESTABOMA. Patients were randomized into two groups: group 1 included patients treated with percutaneous coronary intervention (PCI) and ABMMC transplantation (n = 28); group 2 compr…

Male0301 basic medicinePhysiologyCardiovascular ProceduresCell Transplantationmedicine.medical_treatmentMyocardial InfarctionSocial Scienceslcsh:Medicine030204 cardiovascular system & hematologyPathology and Laboratory MedicineVascular MedicineGastroenterologyAnginaEndocrinology0302 clinical medicineImmune PhysiologyMedicine and Health SciencesBlood and Lymphatic System ProceduresPsychologyMyocardial infarctionlcsh:ScienceImmune ResponseBone Marrow TransplantationInnate Immune SystemMultidisciplinaryCardiac TransplantationAnginaMiddle AgedBrain natriuretic peptidesurgical procedures operativeCytokinesIntercellular Signaling Peptides and ProteinsFemaleInflammation MediatorsResearch Articlemedicine.medical_specialtySocial PsychologyImmunologyCardiologySurgical and Invasive Medical ProceduresTransplantation AutologousProinflammatory cytokine03 medical and health sciencesSigns and SymptomsDiagnostic MedicineGrowth FactorsInternal medicineчрескожное коронарное вмешательствоmedicineHumanscardiovascular diseasesInflammationTransplantationEndocrine Physiologybusiness.industrylcsh:RBiology and Life SciencesPercutaneous coronary interventionOrgan TransplantationMolecular Developmentmedicine.diseaseпровоспалительные цитокиныинфаркт миокардаTransplantation030104 developmental biologyImmune SystemHeart failureImmunologyConventional PCIтрансплантация мононуклеарных клетокlcsh:Qbusinessаутологичная трансплантация костного мозгаDevelopmental BiologyStem Cell Transplantation
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Compromised Neurotrophic and Angiogenic Regenerative Capability during Tendon Healing in a Rat Model of Type-II Diabetes

2017

Metabolic diseases such as diabetes mellitus type-II (DM-II) may increase the risk of suffering painful connective tissue disorders and tendon ruptures. The pathomechanisms, however, by which diabetes adversely affects connective tissue matrix metabolism and regeneration, still need better definition. Our aim was to study the effect of DM-II on expressional changes of neuro- and angiotrophic mediators and receptors in intact and healing Achilles tendon. The right Achilles tendon was transected in 5 male DM-II Goto-Kakizaki (GK) and 4 age-matched Wistar control rats. The left Achilles tendons were left intact. At week 2 post-injury, NGF, BDNF, TSP, and receptors TrkA, TrkB and Nk1 gene expre…

Male0301 basic medicinePhysiologyGene Expressionlcsh:MedicineSubstance PCardiovascular PhysiologyTendonsEndocrinology0302 clinical medicineNerve Growth FactorMedicine and Health SciencesHomeostasisMedicinelcsh:ScienceMammalsAchilles tendonMultidisciplinarybiologyAnimal ModelsAnatomyReceptors Neurokinin-1musculoskeletal systemTendonmedicine.anatomical_structureExperimental Organism SystemsConnective TissueVertebratesAnatomyResearch ArticleNeurotrophinmedicine.medical_specialtyWistar RatsEndocrine DisordersNeovascularization PhysiologicConnective tissueResearch and Analysis MethodsRodentsAchilles Tendon03 medical and health sciencesModel OrganismsTendon InjuriesInternal medicineTissue RepairDiabetes MellitusGeneticsAnimalsReceptor trkBRats WistarReceptor trkABrain-derived neurotrophic factorWound Healingbusiness.industryBrain-Derived Neurotrophic Factorlcsh:RScleraxisOrganismsBiology and Life SciencesRatsTenomodulinDisease Models AnimalBiological Tissue030104 developmental biologyNerve growth factorEndocrinologyDiabetes Mellitus Type 2Metabolic DisordersAmniotesbiology.proteinlcsh:QAngiogenesisPhysiological Processesbusiness030217 neurology & neurosurgeryDevelopmental BiologyPLOS ONE
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Lean NAFLD: A Distinct Entity Shaped by Differential Metabolic Adaptation

2020

Background and Aims: Nonalcoholic fatty liver disease (NAFLD) affects a quarter of the adult population. A significant subset of patients are lean, but their underlying pathophysiology is not well understood. Approach and Results: We investigated the role of bile acids (BAs) and the gut microbiome in the pathogenesis of lean NAFLD. BA and fibroblast growth factor (FGF) 19 levels (a surrogate for intestinal farnesoid X receptor [FXR] activity), patatin-like phospholipase domain containing 3 (PNPLA3), and transmembrane 6 superfamily member 2 (TM6SF2) variants, and gut microbiota profiles in lean and nonlean NAFLD were investigated in a cohort of Caucasian patients with biopsy-proven NAFLD (n …

Male0301 basic medicineReceptors Cytoplasmic and NuclearGut floraMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisNonalcoholic fatty liver diseasebiologyMiddle AgedNAFLD; bile acids; fibrosis; gut microbiota; leanPhospholipases A2 Calcium-IndependentFemale030211 gastroenterology & hepatologyfibrosiAdultmedicine.medical_specialtydigestive systemBile Acids and SaltsCyclic N-Oxides03 medical and health sciencesThinnessInternal medicineNAFLDmedicinebile acidAnimalsHumansbile acidsHepatologygut microbiotabusiness.industryFGF15fibrosisnutritional and metabolic diseasesFGF19leanmedicine.diseasebiology.organism_classificationNAFLD fibrosis lean bile acids gut microbiotadigestive system diseasesGastrointestinal MicrobiomeFibroblast Growth FactorsMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyFarnesoid X receptorSteatohepatitisbusinessTropanesTM6SF2
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Adverse Effects of Diabetes Mellitus on the Skeleton of Aging Mice

2016

In the present study, the possibility that a diabetic (DM) status might worsen age-related bone deterioration was explored in mice. Male CD-1 mice aged 2 (young control group) or 16 months, nondiabetic or made diabetic by streptozotocin injections, were used. DM induced a decrease in bone volume, trabecular number, and eroded surface, and in mineral apposition and bone formation rates, but an increased trabecular separation, in L1-L3 vertebrae of aged mice. Three-point bending and reference point indentation tests showed slight changes pointing to increased frailty and brittleness in the mouse tibia of diabetic old mice. DM was related to a decreased expression of both vascular endothelial …

Male0301 basic medicineSenescenceAgingmedicine.medical_specialtyBone densityOsteoporosisDiabetes Mellitus ExperimentalBone remodelingMice03 medical and health scienceschemistry.chemical_compoundSDG 3 - Good Health and Well-beingBone DensityOsteogenesisDiabetes mellitusInternal medicineAnimalsMedicineLumbar Vertebraebusiness.industryStreptozotocinmedicine.diseaseVascular endothelial growth factor030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistryOsteoporosisBone RemodelingBone marrowGeriatrics and GerontologyTomography X-Ray Computedbusinessmedicine.drugThe Journals of Gerontology Series A: Biological Sciences and Medical Sciences
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EGFR gene copy number decreases during anti-EGFR antibody therapy in colorectal cancer

2018

Epidermal growth factor receptor (EGFR) gene copy number (GCN) increase is associated with a favorable anti-EGFR antibody treatment response in RAS wild-type metastatic colorectal cancer. However, there are limited and comparative data regarding the EGFR GCN in primary colorectal cancer tumors and corresponding metastases or the effect of anti-EGFR antibody treatment on EGFR GCN in recurrent disease. In addition, little is known about the potential EGFR GCN changes during anti-EGFR therapy in comparison with other treatment regimens. EGFR GCN was analyzed by EGFR immunohistochemistry-guided silver in situ hybridization in primary and corresponding recurrent local or metastatic tumors from 8…

Male0301 basic medicineTime FactorsColorectal cancerBLOCKADEGene DosageCetuximabmedicine.disease_causeAntineoplastic Agents Immunological0302 clinical medicinePREDICTS RESPONSEMedicineHETEROGENEITYBENEFITCopy-number variationEpidermal growth factor receptorIn Situ Hybridization FluorescenceAged 80 and overbiologyPanitumumabvasta-aineetMiddle AgedImmunohistochemistry3. Good healthErbB ReceptorsGene Expression Regulation NeoplasticTreatment OutcomeRAS MUTATIONSChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleKRASAntibodyColorectal NeoplasmsAdultgene copy numbermedicine.drug_classCETUXIMAB THERAPY3122 Cancerssilver in situ hybridizationDown-Regulationcolorectal cancerIn situ hybridizationAdenocarcinomaMonoclonal antibodyta3111Pathology and Forensic MedicineProto-Oncogene Proteins p21(ras)03 medical and health sciencesKRASHumansWILD-TYPEMETAANALYSISAgedRetrospective Studiessyöpähoidotbusiness.industrymedicine.diseaseta3122Blockadeperäsuolisyöpä030104 developmental biologymonoclonal antibodyMutationCancer researchbiology.protein3111 BiomedicineNeoplasm Recurrence Localbusinessepidermal growth factor receptorACQUIRED-RESISTANCEHuman Pathology
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Translating intracarotid artery transplantation of bone marrow-derived NCS-01 cells for ischemic stroke: Behavioral and histological readouts and mec…

2019

Abstract The present study used in vitro and in vivo stroke models to demonstrate the safety, efficacy, and mechanism of action of adult human bone marrow‐derived NCS‐01 cells. Coculture with NCS‐01 cells protected primary rat cortical cells or human neural progenitor cells from oxygen glucose deprivation. Adult rats that were subjected to middle cerebral artery occlusion, transiently or permanently, and subsequently received intracarotid artery or intravenous transplants of NCS‐01 cells displayed dose‐dependent improvements in motor and neurological behaviors, and reductions in infarct area and peri‐infarct cell loss, much better than intravenous administration. The optimal dose was 7.5 × …

Male0301 basic medicinecell lofunctional recoverymedicine.medical_treatmentBasic fibroblast growth factorCell- and Tissue-Based TherapyPharmacologycerebral ischemia03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBone Marrowmental disordersmedicinecytokineAnimalsHumansinfarctcell losslcsh:QH573-671cell transplantationStrokeIschemic Strokelcsh:R5-920business.industrylcsh:CytologyMesenchymal stem cellCell BiologyGeneral MedicineStem-cell therapymedicine.diseaseNeural stem cellcytokinesRatsTransplantation030104 developmental biologymedicine.anatomical_structurechemistrymotor deficitsEnabling Technologies for Cell‐based Clinical TranslationBone marrowStem cellbusinesslcsh:Medicine (General)030217 neurology & neurosurgeryStem Cell TransplantationDevelopmental Biology
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