Search results for "Models"

showing 10 items of 8211 documents

Targeting Angiogenesis in Biliary Tract Cancers: An Open Option

2017

Abstract: Biliary tract cancers (BTCs) are characterized by a bad prognosis and the armamentarium of drugs for their treatment is very poor. Although the inflammatory status of biliary tract represents the first step in the cancerogenesis, the microenvironment also plays a key role in the pathogenesis of BTCs, promoting tumor angiogenesis, invasion and metastasis. Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer. Recent studies evaluated the genomic landscape of BTCs and…

0301 basic medicineMAPK/ERK pathwayVascular Endothelial Growth Factor AAngiogenesisDrug Evaluation PreclinicalTyrosine kinase inhibitorAngiogenesis InhibitorsReviewFibroblast growth factorCatalysiMetastasisAntineoplastic Agentlcsh:Chemistrychemistry.chemical_compoundangiogenesis0302 clinical medicinetyrosine kinase inhibitorsMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyClinical Trials as TopicMonoclonal antibodieNeovascularization Pathologicvascular endothelial growth factorComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineComputer Science ApplicationsVascular endothelial growth factorGene Expression Regulation NeoplasticAngiogenesiChemistryBiliary Tract NeoplasmsTreatment OutcomeBiliary Tract Neoplasm030220 oncology & carcinogenesismonoclonal antibodiesTyrosine kinaseAngiogenesis InhibitorHumanSignal TransductionProtein Kinase InhibitorAntineoplastic Agentsbiliary tract cancersBiologyModels BiologicalAngiogenesis; Biliary tract cancers; Monoclonal antibodies; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Biliary Tract Neoplasms; Clinical Trials as Topic; Drug Evaluation Preclinical; Gene Expression Regulation Neoplastic; Genetic Variation; Humans; Models Biological; Neovascularization Pathologic; Protein Kinase Inhibitors; Signal Transduction; Treatment Outcome; Vascular Endothelial Growth Factor A; Molecular Targeted Therapy; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisInorganic Chemistry03 medical and health sciencesIn vivomedicineAnimalsHumansPhysical and Theoretical ChemistryGallbladder cancerMolecular BiologyProtein Kinase InhibitorsBiologyAnimalOrganic ChemistryGenetic Variationmedicine.disease030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Immunologyangiogenesis; biliary tract cancers; monoclonal antibodies; tyrosine kinase inhibitors; vascular endothelial growth factorCancer researchBiliary tract cancerInternational Journal of Molecular Sciences
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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A rare disease and education : Neurofibromatosis type 1 decreases educational attainment

2021

Rare heritable syndromes may affect educational attainment. Here, we study education in neurofibromatosis 1 (NF1) that is associated with multifaceted medical, social and cognitive consequences. Educational attainment in the Finnish population‐based cohort of 1408 individuals with verified NF1 was compared with matched controls using Cox proportional hazards model with delayed entry and competing risk for death. Moreover, models accounting for the effects of cancer at age 15–30 years, parental NF1 and developmental disorders were constructed. Overall, the attainment of secondary education was reduced in individuals with NF1 compared to controls (hazard ratio 0.83, 95%CI 0.74–0.92). History …

0301 basic medicineMale030105 genetics & heredityNeoplasmsneurofibromatosis 1ChildGenetics (clinical)FinlandLearning DisabilitiesHazard ratioCognitionVocational educationChild Preschooleducational attainmentCohortEducational StatusFemaleOriginal ArticleAdultopintomenestyscongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1Adolescentrare diseaseneurofibromatoosiAffect (psychology)multiorgan syndromeschool performance03 medical and health sciencesRare DiseaseskoulutustasoGeneticsmedicineHumansEducation Graduateharvinaiset tauditNeurofibromatosisneoplasmsProportional Hazards ModelsVocational Educationperinnölliset tauditProportional hazards modelbusiness.industrySiblingsOriginal Articlesmedicine.diseaseEducational attainmenteye diseasesnervous system diseases030104 developmental biologybusinessDemographyFollow-Up Studies
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Myeloid cells do not contribute to gender-dependent differences in disease outcome in murine cutaneous leishmaniasis.

2015

Gender-associated differences in the outcome of infections are well known. Apart from behavior-released differences in their incidence, immunological factors also contribute to disease outcome. The underlying mechanisms are often unknown. Here, we show that in murine experimental leishmaniasis, female mice develop larger skin lesions that harbor significantly more parasites, exhibit increased parasite dissemination to visceral organs associated with a shift towards T helper (Th) 2 immunity with increased levels of IL-4. Antigen presenting cells (APC) responsible for T cell priming, such as macrophages or dendritic cells, were not involved in the process. Additionally, in adoptive transfer e…

0301 basic medicineMaleAdoptive cell transferMyeloidStromal cellT cellImmunologyLeishmaniasis CutaneousBiology03 medical and health sciencesMice0302 clinical medicineImmune systemTh2 CellsCutaneous leishmaniasismedicineAnimalsHumansCell LineageMyeloid CellsAntigen-presenting cellTh1-Th2 BalanceCells CulturedCell DifferentiationDendritic cellmedicine.diseaseHormonesMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureImmunologyDisease ProgressionFemaleSexDisease SusceptibilityInterleukin-4Stromal Cells030215 immunologyCellular immunology
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Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin.

2021

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. A minority of affected patients develops inflammation, subsequently fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCC is a leading cause of cancer-related death. An increased number of senescent cells correlate with age-related tissue degeneration during NAFLD-induced HCC. Senolytics are promising agents that target selectively senescent cells. Previous studies showed that whereas a combination of the senolytic drugs dasatinib and quercetin (D + Q) reduced NAFLD in mice, D + Q lacked efficacy in removing doxorubicin-induced…

0301 basic medicineMaleAgingCirrhosisDasatiniblcsh:MedicineBiochemistrySenolytics.Liver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseSenotherapeuticsNonalcoholic fatty liver diseaseDiethylnitrosamineCancerlcsh:CytologyLiver Diseases3. Good healthDasatinib030220 oncology & carcinogenesisHepatocellular carcinomaDisease ProgressionQuercetinmedicine.symptomLiver diseasemedicine.drugShort ReportInflammationDiet High-Fat03 medical and health sciencesmedicineAnimalsObesitylcsh:QH573-671SenolyticMolecular BiologyInflammationbusiness.industrySenolyticslcsh:RCell Biologymedicine.diseasedigestive system diseasesMice Inbred C57BLDisease Models Animal030104 developmental biologyGene Expression RegulationCancer researchbusinessCell communication and signaling : CCS
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Modulation of brain PUFA content in different experimental models of mice.

2016

International audience; The relative amounts of arachidonic acid (AA) and docosahexaenoic acid (DHA) govern the different functions of the brain. Their brain levels depend on structures considered, on fatty acid dietary supply and the age of animals. To have a better overview of the different models available in the literature we here compared the brain fatty acid composition in various mice models (C57BL/6J, CD1, Fat-1, SAMP8 mice) fed with different n-3 PUFA diets (deficient, balanced, enriched) in adults and aged animals. Our results demonstrated that brain AA and DHA content is 1) structure-dependent; 2) strain-specific; 3) differently affected by dietary approaches when compared to gen…

0301 basic medicineMaleAgingClinical Biochemistryfat-1 miceHippocampuschemistry.chemical_compoundMice0302 clinical medicineCerebellumDocosahexaenoic acid (DHA)fatty-acid-compositionFood science2. Zero hungerchemistry.chemical_classificationCerebral CortexArachidonic Acidanxiety-like behaviordocosahexaenoic acidaccelerated mouse samBiochemistryDocosahexaenoic acidArachidonic acid (AA)Arachidonic acidFemaleFatty acid compositionSAMP8 miceBrain regionsPolyunsaturated fatty acidN-3 PUFAdiet-induced obesityDocosahexaenoic AcidsHypothalamusPrefrontal CortexBiology03 medical and health sciencesrat-brainDietary Fats UnsaturatedGenetic modelAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyN 3 pufaBrain Chemistryage-related-changesFatty acidCell BiologyModels Theoreticalgene-expressiondepressive-like behaviorMice Inbred C57BL030104 developmental biologychemistry030217 neurology & neurosurgeryBrain StemProstaglandins, leukotrienes, and essential fatty acids
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Analysis of allergic immune responses in humanized mice.

2015

Nowadays, more than 25% of the population in industrial countries are affected by IgE-mediated (atopic) allergic diseases such as allergic rhinitis, asthma and atopic eczema. Due to intensive research on basis of in vitro studies with human immune cells and different murine in vivo models of allergy fundamental mechanisms of allergic immune responses have been elucidated during the last years. However, human studies are restricted and the immune system of mice differs from the human immune system in several aspects so that the transferability of experimental results from mice to men is limited. Humanized mice represent a new tool to analyze the interaction of human immune cells under physio…

0301 basic medicineMaleAllergyBiomedical ResearchImmunologyPopulationInflammationMice SCIDImmunoglobulin ET-Lymphocytes Regulatory03 medical and health sciencesMice0302 clinical medicineImmune systemHypersensitivityMedicineAnimalsHumanseducationAsthmaeducation.field_of_studyTransplantation Chimerabiologybusiness.industryImmunoglobulin Emedicine.diseaseIn vitroAsthmaDisease Models Animal030104 developmental biologyDesensitization ImmunologicHumanized mouseImmunologybiology.proteinFemalemedicine.symptombusiness030215 immunologyCellular immunology
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The concerted amyloid-beta clearance of LRP1 and ABCB1/P-gp across the blood-brain barrier is linked by PICALM

2018

The accumulation of neurotoxic amyloid-beta (Aβ) in the brain is a characteristic hallmark of Alzheimer's disease (AD). The blood-brain barrier (BBB) provides a large surface area and has been shown to be an important mediator for removal of brain Aβ. Both, the ABC transporter P-glycoprotein (ABCB1/P-gp) and the receptor low-density lipoprotein receptor-related protein 1 (LRP1) have been implicated to play crucial roles in Aβ efflux from brain. Here, with immunoprecipitation experiments, co-immunostainings and dual inhibition of ABCB1/P-gp and LRP1, we show that both proteins are functionally linked, mediating a concerted transcytosis of Aβ through endothelial cells. Late-onset AD risk fact…

0301 basic medicineMaleAmyloid betaSwineImmunologyPrimary Cell CultureATP-binding cassette transporterBlood–brain barrierClathrinArticlePICALM03 medical and health sciencesBehavioral NeuroscienceMice0302 clinical medicineAlzheimer DiseasemedicineAnimalsATP Binding Cassette Transporter Subfamily B Member 1Mice KnockoutAmyloid beta-PeptidesbiologyEndocrine and Autonomic SystemsChemistryTumor Suppressor ProteinsPhosphatidylinositol bindingBrainEndothelial CellsLRP1Peptide FragmentsCell biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureTranscytosisReceptors LDLBlood-Brain BarrierMonomeric Clathrin Assembly Proteinsbiology.proteinTranscytosis030217 neurology & neurosurgeryLow Density Lipoprotein Receptor-Related Protein-1Brain, Behavior, and Immunity
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Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.

2017

Abstract Context Angiopoietin-like 3 (ANGPTL3) deficiency in plasma due to loss-of-function gene mutations results in familial combined hypobetalipoproteinemia type 2 (FHBL2) in homozygotes. However, the lipid phenotype in heterozygotes is much milder and does not appear to relate directly to ANGPTL3 levels. Furthermore, the low-density lipoprotein (LDL) phenotype in carriers of ANGPTL3 mutations is unexplained. Objective To determine whether reduction below a critical threshold in plasma ANGPTL3 levels is a determinant of lipoprotein metabolism in FHBL2, and to determine whether proprotein convertase subtilisin kexin type 9 (PCSK9) is involved in determining low LDL levels in this conditio…

0301 basic medicineMaleApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryBiochemistryLipoprotein particlePCSK9Cohort StudiesHypobetalipoproteinemiaschemistry.chemical_compoundEndocrinologyANGPTL3biologyChemistryMiddle AgedPedigreeLipoproteins LDLPhenotypeKexinlipids (amino acids peptides and proteins)FemaleANGPTL3; familial combined hypolipidemia; PCSK9Lipoproteins HDLAdultmedicine.medical_specialtyHeterozygoteBlotting Western03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseClinical Research ArticlesAgedAngiopoietin-Like Protein 3Apolipoproteins BCholesterolPCSK9Biochemistry (medical)medicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsLDL receptorMultivariate AnalysisMutationbiology.proteinLinear Modelsfamilial combined hypobetalipoproteinemiaHypobetalipoproteinemiaAngiopoietinsLipoprotein
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