Search results for "patho"

showing 10 items of 10772 documents

Relationship between -889 C/T polymorphism in interleukin-1A gene and risk of chronic periodontitis : evidence from a meta-analysis with new publishe…

2017

Background Periodontitis results from an inflammatory response caused by accumulative microorganisms in periodontal sites. Several factors are involved in pathogenesis of periodontitis, for example the -889 C/T polymorphism in interleukin-1A gene. This study aimed to evaluate the relationship between this polymorphism and risk of development of chronic periodontitis by a meta-analysis based in new published findings. Material and Methods Thereunto a review in literature was performed in the electronic biomedical and education databases (Cochrane Library, Google Scholar, MEDLINE and PubMed) to studies published before August 2, 2015, the abstracts were evaluated and the data extraction perfo…

0301 basic medicineFunnel plotmedicine.medical_specialtyPathologyReviewCochrane LibraryGastroenterology03 medical and health sciences0302 clinical medicineRisk FactorsPolymorphism (computer science)Interleukin-1alphaInternal medicineHumansMedicineGeneral DentistryPeriodontitisPolymorphism GeneticOral Medicine and Pathologybusiness.industry030206 dentistryOdds ratioPublication biasmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Chronic periodontitis030104 developmental biologyOtorhinolaryngologyMeta-analysisChronic PeriodontitisUNESCO::CIENCIAS MÉDICASSurgerybusiness
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Microevolutionary response of a gut nematode to intestinal inflammation.

2017

7 pages; International audience; Parasitic helminths interfere with the immune response of their hosts to establish long-lasting, chronic infections. While favorable to the parasite, the capacity to dampen the immune response can also provide a benefit to the host in terms of reduced risk of immune disorders and immunopathology. The immunomodulatory role of nematodes has been exploited in clinical trials to treat a number of inflammatory and immune diseases. However, how parasites adapt to an inflammatory environment remains a poorly explored question. Here, we conducted a serial passage experiment where the gut nematode Heligmosomoides polygyrus was maintained for nine generations in mice …

0301 basic medicineGastrointestinal DiseasesInflammationHost-Parasite InteractionsRodent Diseases03 medical and health sciencesMice0302 clinical medicineImmune systemSerial passageImmunopathology[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosismedicine[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyAnimalsAdaptationStrongylida InfectionsInflammationExperimental evolutionNematospiroides dubiusbiologyHost (biology)Life history traitsbiology.organism_classificationColitisBiological Evolution3. Good health030104 developmental biologyInfectious DiseasesNematodeExperimental evolutionImmunologybacteria[SDV.IMM]Life Sciences [q-bio]/ImmunologyParasitologyHeligmosomoides polygyrusmedicine.symptomSerial passage030215 immunology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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Use of deep learning methods to translate drug-induced gene expression changes from rat to human primary hepatocytes

2020

In clinical trials, animal and cell line models are often used to evaluate the potential toxic effects of a novel compound or candidate drug before progressing to human trials. However, relating the results of animal and in vitro model exposures to relevant clinical outcomes in the human in vivo system still proves challenging, relying on often putative orthologs. In recent years, multiple studies have demonstrated that the repeated dose rodent bioassay, the current gold standard in the field, lacks sufficient sensitivity and specificity in predicting toxic effects of pharmaceuticals in humans. In this study, we evaluate the potential of deep learning techniques to translate the pattern of …

0301 basic medicineGene ExpressionGene Expression Regulation/drug effectsPathology and Laboratory MedicineConvolutional neural networkTOXICITYMachine LearningVoeding Metabolisme en GenomicaTime Measurement0302 clinical medicineGene expressionMedicine and Health SciencesMeasurementClinical Trials as TopicMultidisciplinaryArtificial neural networkPharmaceuticsQRMetabolism and GenomicsTOXICOGENOMICS030220 oncology & carcinogenesisMetabolisme en GenomicaMedicineEngineering and TechnologyNutrition Metabolism and GenomicsHepatocytes/drug effectsAlgorithmsResearch ArticleComputer and Information SciencesClinical Trials as Topic/statistics & numerical dataNeural NetworksGenetic ToxicologyTOXICOLOGYSciencePredictive ToxicologyComputational biologyBiologyComputer03 medical and health sciencesDose Prediction MethodsDeep LearningVoedingArtificial IntelligenceIn vivoGeneticsLife ScienceAnimalsHumansGeneNutritionbusiness.industryDeep learningBiology and Life SciencesGold standard (test)REPRESENTATIONSRats030104 developmental biologyGene Expression RegulationHepatocytesArtificial intelligenceNeural Networks ComputerToxicogenomicsbusinessNeuroscience
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Analysis of the expression of SDF-1 splicing variants in human colorectal cancer and normal mucosa tissues

2016

C-X-C motif chemokine ligand 12 (CXCL12), also termed stromal cell-derived factor-1 (SDF-1) is a small protein 8-14 kDa in length that is expressed as six isoforms, consisting of SDF-1α, SDF-1β, SDF-1γ, SDF-1δ, SDF-1ε and SDF-1θ. All six isoforms are encoded by the single CXCL12 gene on chromosome 10. This gene regulates leukocyte trafficking and is variably expressed in a number of normal and cancer tissues. The potential role of the novel CXCL12 splice variants as components of the CXCR4 axis in cancer development is not fully understood. The present study aimed to analyze the expression profile of the various SDF-1 isoforms and SDF-1 polymorphisms, and the association with the clinicopat…

0301 basic medicineGene isoformCancer ResearchPathologymedicine.medical_specialtyOncogeneArticlesBiologymedicine.diseasePrimary tumorCXCR403 medical and health sciences030104 developmental biology0302 clinical medicineOncologyTumor progression030220 oncology & carcinogenesisGenotypemedicineCancer researchGene polymorphismTumor markerOncology Letters
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The Multifaced Role of STAT3 in Cancer and Its Implication for Anticancer Therapy

2021

Signal transducer and activator of transcription (STAT) 3 is one of the most complex regulators of transcription. Constitutive activation of STAT3 has been reported in many types of tumors and depends on mechanisms such as hyperactivation of receptors for pro-oncogenic cytokines and growth factors, loss of negative regulation, and excessive cytokine stimulation. In contrast, somatic STAT3 mutations are less frequent in cancer. Several oncogenic targets of STAT3 have been recently identified such as c-myc, c-Jun, PLK-1, Pim1/2, Bcl-2, VEGF, bFGF, and Cten, and inhibitors of STAT3 have been developed for cancer prevention and treatment. However, despite the oncogenic role of STAT3 having been…

0301 basic medicineGene isoformSTAT3 Transcription FactorCarcinogenesistumor suppressorPIM1Antineoplastic AgentsReviewBiologyCatalysisstatInorganic ChemistrySTAT3lcsh:Chemistry03 medical and health sciences0302 clinical medicineNeoplasmsDrug DiscoverymedicineAnimalsHumanscancerNeoplasm InvasivenessMolecular Targeted TherapyPhysical and Theoretical ChemistrySTAT3Molecular BiologyTranscription factorlcsh:QH301-705.5SpectroscopyNeovascularization PathologicOrganic ChemistryAlternative splicingtumor promoterCancerGeneral Medicinemedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplastic030104 developmental biologylcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisCancer researchbiology.proteinSTAT proteinInternational Journal of Molecular Sciences
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Sensory neuropathy in progressive motor neuronopathy(pmn)mice is associated with defects in microtubule polymerization and axonal transport

2016

Motor neuron diseases such as amyotrophic lateral sclerosis (ALS) are now recognized as multi-system disorders also involving various non-motor neuronal cell types. The precise extent and mechanistic basis of non-motor neuron damage in human ALS and ALS animal models remain however unclear. To address this, we here studied progressive motor neuronopathy (pmn) mice carrying a missense loss-of-function mutation in tubulin binding cofactor E (TBCE). These mice manifest a particularly aggressive form of motor axon dying back and display a microtubule loss, similar to that induced by human ALS-linked TUBA4A mutations. Using whole nerve confocal imaging of pmn × thy1.2-YFP16 fluorescent reporter …

0301 basic medicineGeneral NeuroscienceMotor neuronBiologymedicine.disease3. Good healthPathology and Forensic MedicineMicrotubule polymerizationTubulin binding03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systemDorsal root ganglionmedicineAxoplasmic transportNeurology (clinical)NeuronAxonAmyotrophic lateral sclerosisNeuroscience030217 neurology & neurosurgeryBrain Pathology
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IL-17A mediated endothelial breach promotes metastasis formation

2015

Abstract The role of the IL23/IL17A axis in tumor–immune interactions is a matter of controversy. Although some suggest that IL17A-producing T cells (TH17) can suppress tumor growth, others report that IL17A and IL23 accelerate tumor growth. Here, we systematically assessed the impact of IL17A-secreting lymphocytes in several murine models of tumor lung metastasis. Genetic fate mapping revealed that IL17A was secreted within lung metastases predominantly by γδ T cells, whereas TH17 cells were virtually absent. Using different tumor models, we found Il17a−/− mice to consistently develop fewer pulmonary tumor colonies. IL17A specifically increased blood vessel permeability and the expression …

0301 basic medicineGenetically modified mouseCancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsEndotheliumImmunologyMelanoma ExperimentalVascular permeability610 Medicine & healthBiology10263 Institute of Experimental ImmunologyCapillary Permeability03 medical and health sciencesCarcinoma Lewis LungCell Line TumormedicineCell AdhesionAnimals1306 Cancer ResearchCell adhesionMice Knockout2403 ImmunologyLungMelanomaInterleukin-17Transendothelial and Transepithelial MigrationEndothelial Cellsmedicine.diseaseMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureCell culture570 Life sciences; biologyInterleukin 17Endothelium VascularNeoplasm Transplantation
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Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation.

2017

Organ fibrosis is characterized by a chronic wound-healing response, with excess deposition of extracellular matrix components. Here, collagen type I represents the most abundant scar component and a primary target for antifibrotic therapies. Liver fibrosis can progress to cirrhosis and primary liver cancer, which are the major causes of liver related morbidity and mortality. However, a (pro-)collagen type I specific therapy remains difficult and its therapeutic abrogation may incur unwanted side effects. We therefore designed tetracycline-regulated procollagen alpha1(I) short hairpin (sh)RNA expressing mice that permit a highly efficient inducible knockdown of the procollagen alpha1(I) gen…

0301 basic medicineGenetically modified mouseLiver CirrhosisPathologymedicine.medical_specialtyCirrhosisInflammationMice TransgenicCollagen Type ISmall hairpin RNAExtracellular matrix03 medical and health sciencesMiceFibrosismedicineAnimalsRNA Small InterferingMolecular BiologyCells CulturedGene knockdownExtracellular Matrix ProteinsChemistryMouse Embryonic Stem CellsFibroblastsmedicine.diseaseProcollagen peptidaseDisease Models Animal030104 developmental biologyGene Expression RegulationGene Knockdown TechniquesCancer researchmedicine.symptomProcollagenMatrix biology : journal of the International Society for Matrix Biology
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Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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Gradual development of psoriatic skin lesions by constitutive low-level expression of IL-17A

2016

Psoriasis is a common chronic inflammatory skin disease restricted to humans. The understanding of its pathogenesis has long been hampered by the lack of suitable chronic mouse models. The cytokine IL-17A has emerged as a key player in epithelial immune responses and the defense against extracellular pathogens. Moreover, enhanced expression of IL-17A can turn pathologic and is closely associated with psoriasis. In this study, we generated a novel transgenic mouse model that recapitulates many characteristics of psoriasis. DC-1L-17A(ind) mice with constitutive low-level expression of IL-17A by CD11c(+) cells gradually develop skin lesions during adult life. The lesions preferentially occur a…

0301 basic medicineGenetically modified mousemedicine.medical_treatmentImmunologyCD11cInflammationAnimals Genetically ModifiedPathogenesisMice03 medical and health sciences0302 clinical medicineImmune systemSDG 3 - Good Health and Well-beingPsoriasismedicineAnimalsHumansPsoriasisCells CulturedSkinbusiness.industryInterleukin-17Dendritic Cellsmedicine.diseaseCD11c AntigenDisease Models Animal030104 developmental biologyCytokineImmunologyCytokinesInterleukin 17medicine.symptombusiness030215 immunologyCellular Immunology
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