Search results for " Models"

showing 10 items of 4240 documents

Energy compensation and adiposity in humans

2021

Publisher Copyright: © 2021 The Authors Understanding the impacts of activity on energy balance is crucial. Increasing levels of activity may bring diminishing returns in energy expenditure because of compensatory responses in non-activity energy expenditures.1–3 This suggestion has profound implications for both the evolution of metabolism and human health. It implies that a long-term increase in activity does not directly translate into an increase in total energy expenditure (TEE) because other components of TEE may decrease in response—energy compensation. We used the largest dataset compiled on adult TEE and basal energy expenditure (BEE) (n = 1,754) of people living normal lives to fi…

Calorie030309 nutrition & dieteticsEnergy balanceRA773SDG 3 – Goede gezondheid en welzijnCardiovascularMedical and Health SciencesOral and gastrointestinalCompensation (engineering)RC12000302 clinical medicineWeight lossenergy compensationAdiposityCancer0303 health sciencesexerciseCONSTRAINTBiological SciencesStrokeIAEA DLW database groupEXERCISE PHYSICAL-ACTIVITYmedicine.symptomGeneral Agricultural and Biological SciencesINTERVENTIONSEnergy (esotericism)WEIGHT-LOSS030209 endocrinology & metabolismMASSBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAffordable and Clean EnergySDG 3 - Good Health and Well-beingTotal energy expenditureClinical Researchdaily energy expendituremedicineVDP::Matematikk og Naturvitenskap: 400::Basale biofag: 470HumansBASALObesityMetabolic and endocrineenergy management modelsNutritionHomo sapiensBIRDSactivityPsychology and Cognitive Sciencesmedicine.diseaseObesitytrade-offsMETABOLIC-RATESBasal metabolic ratebasal metabolic rate1182 Biochemistry cell and molecular biologyDemographic economics3111 Biomedicineweight lossEnergy MetabolismEnergy IntakeEXPENDITUREDevelopmental Biology
researchProduct

Myeloid-Derived Suppressor Cells in Multiple Myeloma: Pre-Clinical Research and Translational Opportunities

2014

Immunosuppressive cells have been reported to play an important role in tumor-progression mainly because of their capability to promote immune-escape, angiogenesis, and metastasis. Among them, myeloid-derived suppressor cells (MDSCs) have been recently identified as immature myeloid cells, induced by tumor-associated inflammation, able to impair both innate and adaptive immunity. While murine MDSCs are usually identified by the expression of CD11b and Gr1, human MDSCs represent a more heterogeneous population characterized by the expression of CD33 and CD11b, low or no HLA-DR, and variable CD14 and CD15. In particular, the last two may alternatively identify monocyte-like or granulocyte-lik…

Cancer ResearchAngiogenesisCD33MDSCInflammationReview Articlelcsh:RC254-282Immune systemImmunesuppressionmedicinecancerimmunosuppressionbusiness.industryAcquired immune systemlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenspreclinical modelsmedicine.anatomical_structuremyelomaOncologyTumor progressionImmunologyMyeloid-derived Suppressor CellBone marrowmedicine.symptombusinesspre-clinical modelsFrontiers in Oncology
researchProduct

Role of two sequence motifs of mesencephalic astrocyte-derived neurotrophic factor in its survival-promoting activity

2015

AbstractMesencephalic astrocyte-derived neurotrophic factor (MANF) is a prosurvival protein that protects the cells when applied intracellularly in vitro or extracellularly in vivo. Its protective mechanisms are poorly known. Here we studied the role of two short sequence motifs within the carboxy-(C) terminal domain of MANF in its neuroprotective activity: the CKGC sequence (a CXXC motif) that could be involved in redox reactions, and the C-terminal RTDL sequence, an endoplasmic reticulum (ER) retention signal. We mutated these motifs and analyzed the antiapoptotic effect and intracellular localization of these mutants of MANF when overexpressed in cultured sympathetic or sensory neurons. …

Cancer ResearchCell SurvivalImmunologyMutantAmino Acid MotifsIntracellular SpaceGolgi ApparatusSuperior Cervical GanglionBiologyRats Sprague-DawleyCellular and Molecular Neurosciencesymbols.namesakeMiceStructure-Activity RelationshipMutant proteinNeurotrophic factorsGanglia SpinalExtracellularAnimalsCysteineNerve Growth FactorsEtoposideSequence DeletionEndoplasmic reticulumprosurvival proteinsta1182Cell BiologyGolgi apparatusMolecular biologyRecombinant ProteinsStrokeDisease Models AnimalProtein Transportmesencephalic astrocyte-derived neurotrophic factorNeuroprotective AgentsMutationsymbolsOriginal ArticleSequence motifIntracellularCell Death and Disease
researchProduct

The impact of oophorectomy on survival from breast cancer in patients with CHEK2 mutations

2022

BACKGROUND: To estimate the impact of oophorectomy and other treatments on the survival of breast cancer patients with a CHEK2 mutation. METHODS: Women with Stage I–III breast cancer who were treated at 17 hospitals in Poland were tested for four founder mutations in the CHEK2 gene. 974 women (10%) were positive for a CHEK2 mutation. Control patients without a CHEK2 mutation were selected from a database of patients treated over the same time period. Information on treatments received and distant recurrences were retrieved from medical records. Treatments included chemotherapy, hormonal therapy (tamoxifen) and radiation therapy. Oophorectomies were performed for the treatment of breast canc…

Cancer ResearchCheckpoint Kinase 2OncologyRisk FactorsOvariectomyMutationHumansBreast NeoplasmsFemaleGenetic Predisposition to DiseaseArticleProportional Hazards Models
researchProduct

Intracellular coexpression of CXC- and CC– chemokine receptors and their ligands in human melanoma cell lines and dynamic variations after xenotransp…

2014

Abstract Background Chemokines have been implicated in tumor progression and metastasis. In melanoma, chemokine receptors have been implicated in organ selective metastasis by regulating processes such as chemoattraction, adhesion and survival. Methods In this study we have analyzed, using flow cytometry, the systems formed by the chemokine receptors CXCR3, CXCR4, CXCR7, CCR7 and CCR10 and their ligands in thirteen human melanoma cell lines (five established from primary tumors and eight established from metastasis from different tissues). WM-115 and WM-266.4 melanoma cell lines (obtained from a primary and a metastatic melanoma respectively) were xenografted in nude mice and the tumors and…

Cancer ResearchChemokine receptorIntracellular SpaceBiologyCCL7LigandsChemokine receptorMiceReceptors CCRCell Line TumorGeneticsAnimalsHumansCCR10CXC chemokine receptorsCCL13MelanomaReceptors CXCRChemotaxisCell MembraneImmunohistochemistry3. Good healthCXCL2Disease Models AnimalOncologyChemokineCancer researchHeterograftsXenotransplantationCC chemokine receptorsCell lineCCL21Research ArticleBMC Cancer
researchProduct

T Cells Expressing Receptor Recombination/Revision Machinery Are Detected in the Tumor Microenvironment and Expanded in Genomically Over-unstable Mod…

2021

AbstractTumors undergo dynamic immunoediting as part of a process that balances immunologic sensing of emerging neoantigens and evasion from immune responses. Tumor-infiltrating lymphocytes (TIL) comprise heterogeneous subsets of peripheral T cells characterized by diverse functional differentiation states and dependence on T-cell receptor (TCR) specificity gained through recombination events during their development. We hypothesized that within the tumor microenvironment (TME), an antigenic milieu and immunologic interface, tumor-infiltrating peripheral T cells could reexpress key elements of the TCR recombination machinery, namely, Rag1 and Rag2 recombinases and Tdt polymerase, as a poten…

Cancer ResearchDatasets as TopicT-Cell Antigen Receptor SpecificityCD8-Positive T-LymphocytesMice0302 clinical medicineTumor MicroenvironmentRecombinaseT-cell receptorBreastRNA-SeqT Cells T Cell Receptor Recombination/Revision Machinery Tumor MicroenvironmentCancerAged 80 and overMice KnockoutRecombination GeneticNuclear Proteinshemic and immune systemsMiddle AgedDNA-Binding Proteins030220 oncology & carcinogenesisFemaleSingle-Cell AnalysisMutL Protein Homolog 1AdultImmunologyReceptors Antigen T-CellT cellsBreast Neoplasmschemical and pharmacologic phenomenaSettore MED/08 - Anatomia PatologicaBiologyRecombination-activating gene03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemAntigenDNA NucleotidylexotransferaseRAG2AnimalsHumansSettore MED/05 - Patologia ClinicaAgedHomeodomain ProteinsTumor microenvironmentT-cell receptorDisease Models AnimalImmunoeditingCancer researchDNA Damage030215 immunology
researchProduct

Erratum to “Time trends and short term projections of cancer prevalence in France” [Cancer Epidemiol. 56 (2018) 97–105]

2018

IF 2.888 (2017); International audience

Cancer ResearchEpidemiologyTime trendsbusiness.industryPublished ErratumMEDLINECancerTime trends[SDV.CAN]Life Sciences [q-bio]/Cancermedicine.diseaseShort-term projectionsTerm (time)Projection scenariosOncologyPrevalenceMedicineFlexible modelsbusinessCancer prevalenceDemographyCancer Epidemiology
researchProduct

Stochastic Loss of Silencing of the Imprinted Ndn/NDN Allele, in a Mouse Model and Humans with Prader-Willi Syndrome, Has Functional Consequences

2013

Genomic imprinting is a process that causes genes to be expressed from one allele only according to parental origin, the other allele being silent. Diseases can arise when the normally active alleles are not expressed. In this context, low level of expression of the normally silent alleles has been considered as genetic noise although such expression has never been further studied. Prader-Willi Syndrome (PWS) is a neurodevelopmental disease involving imprinted genes, including NDN, which are only expressed from the paternally inherited allele, with the maternally inherited allele silent. We present the first in-depth study of the low expression of a normally silent imprinted allele, in path…

Cancer ResearchHeterozygotelcsh:QH426-470Apnea[SDV]Life Sciences [q-bio]Nerve Tissue ProteinsBiologyEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineGeneticsAnimalsHumansEpigeneticsAlleleImprinting (psychology)Promoter Regions GeneticMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and SystematicsAlleles030304 developmental biologyGeneticsMice Knockout0303 health sciencesBrainNuclear ProteinsPhenotypeAllelic exclusionDisease Models Animallcsh:GeneticsGene Expression RegulationDNA methylationGenomic imprintingPrader-Willi Syndrome030217 neurology & neurosurgeryResearch Article
researchProduct

Dysfunction of Oskyddad causes Harlequin-type ichthyosis-like defects in Drosophila melanogaster.

2020

Prevention of desiccation is a constant challenge for terrestrial organisms. Land insects have an extracellular coat, the cuticle, that plays a major role in protection against exaggerated water loss. Here, we report that the ABC transporter Oskyddad (Osy)—a human ABCA12 paralog—contributes to the waterproof barrier function of the cuticle in the fruit fly Drosophila melanogaster. We show that the reduction or elimination of Osy function provokes rapid desiccation. Osy is also involved in defining the inward barrier against xenobiotics penetration. Consistently, the amounts of cuticular hydrocarbons that are involved in cuticle impermeability decrease markedly when Osy activity is reduced. …

Cancer ResearchLife CyclesEmbryologyMutantCell MembranesATP-binding cassette transporterQH426-470Biochemistry0302 clinical medicineLarvaeAnimal WingsLoss of Function MutationMedicine and Health SciencesDrosophila ProteinsAnimal AnatomyGenetics (clinical)Barrier functionSkin0303 health sciencesbiologyDrosophila MelanogasterEukaryotaAnimal ModelsHarlequin IchthyosisLipidsCell biologyInsectsExperimental Organism SystemsEmbryology and OrganogenesisDrosophilaDrosophila melanogasterCellular Structures and OrganellesAnatomyIntegumentary SystemEmbryologie et organogenèseDrosophila ProteinAutre (Sciences du Vivant)Research Article[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]ArthropodaResearch and Analysis Methods03 medical and health sciencesModel OrganismsExtracellularGeneticsAnimalsABCA12DesiccationMolecular BiologyEcology Evolution Behavior and Systematics030304 developmental biologyEmbryosfungiOrganismsBiology and Life SciencesCell Biologybiology.organism_classificationInvertebrates[SDV.BDD.EO]Life Sciences [q-bio]/Development Biology/Embryology and Organogenesisbiology.proteinAnimal StudiesATP-Binding Cassette TransportersEpidermisZoology030217 neurology & neurosurgeryIchthyosis LamellarDevelopmental BiologyPLoS Genetics
researchProduct

cIAP1 regulates TNF-mediated cdc42 activation and filopodia formation

2013

International audience; umour necrosis factor-α (TNF) is a cytokine endowed with multiple functions, depending on the cellular and environmental context. TNF receptor engagement induces the formation of a multimolecular complex including the TNFR-associated factor TRAF2, the receptor-interaction protein kinase RIP1 and the cellular inhibitor of apoptosis cIAP1, the latter being essential for NF-κB activation. Here, we show that cIAP1 also regulates TNF-induced actin cytoskeleton reorganization through a cdc42-dependent, NF-κB-independent pathway. Deletion of cIAP1 prevents TNF-induced filopodia and cdc42 activation. The expression of cIAP1 or its E3-ubiquitin ligase-defective mutant restore…

Cancer ResearchLung NeoplasmsBlotting WesternFluorescent Antibody Techniquemacromolecular substancesCDC42BiologyTransfectionInhibitor of Apoptosis ProteinsMice03 medical and health sciences0302 clinical medicineCell AdhesionGeneticsAnimalsHumansImmunoprecipitationNeoplasm InvasivenessPseudopodia[SPI.NANO]Engineering Sciences [physics]/Micro and nanotechnologies/Microelectronicscdc42 GTP-Binding ProteinMolecular Biology030304 developmental biology0303 health sciencesTumor Necrosis Factor-alphaActin cytoskeleton reorganizationCell PolarityActin remodelingSurface Plasmon ResonanceActin cytoskeletonCell biologyActin CytoskeletonDisease Models AnimalHEK293 CellsCdc42 GTP-Binding Protein030220 oncology & carcinogenesisNIH 3T3 CellsHeterografts[ SPI.NANO ] Engineering Sciences [physics]/Micro and nanotechnologies/MicroelectronicsPseudopodiaSignal transductionFilopodiaSignal TransductionOncogene
researchProduct